Med-Surg Nursing Notes

Health Maintenance Theory 3310
Contents
Unit 1: Chronicity with Related Concepts...................................................................................................................................................4
Unit 2: Introduction to the Care of the Paediatric Client.............................................................................................................................7
INTRODUCTION........................................................................................................................................................................................7
COMMUNITY............................................................................................................................................................................................8
Unit 3: Fluid & Electrolyte........................................................................................................................................................................10
FLUID.....................................................................................................................................................................................................10
ELECTROLYTES......................................................................................................................................................................................16
CASE STUDY FLUID & ELECTROLYTE................................................................................................................................................17
Unit 4: Principles of Hemodynamics.........................................................................................................................................................19
CLIENTS WITH HYPERTENSION..............................................................................................................................................................19
CASE STUDY HEMODYNAMICS...........................................................................................................................................................25
Unit 5: Pain Theory and Assessment.........................................................................................................................................................26
Unit 6: Care of the Client with Chronic Pain both Adult and Child.......................................................................................................29
Unit 7: Clients with Rheumatic Disorders.................................................................................................................................................37
ARTHRITIS..............................................................................................................................................................................................37
Unit 8: Paediatric Client with Upper Respiratory Disorders.....................................................................................................................42
Unit 9: Clients with Altered Endocrine Function......................................................................................................................................50
Unit 10: Head-to-Toe Sexuality and Illness............................................................................................................................................61
Unit 11: Clients with Altered Glucose Homeostasis (Diabetes Mellitus).................................................................................................63
Unit 12: Paediatric Client with Chronic Respiratory Disorders................................................................................................................70
ASTHMA.................................................................................................................................................................................................75
CYSTIC FIBROSIS....................................................................................................................................................................................79
Unit 13: Clients with Altered Nutrition and Absorption Liver and Pancreas.........................................................................................83
Unit 14: Adult Chronic Respiratory Disorders..........................................................................................................................................94
ACIDBASE BALANCE AND ARTERIAL BLOOD GASES (ABG)..............................................................................................................94
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)....................................................................................................................100
TUBERCULOSIS.....................................................................................................................................................................................104
Unit 15: Care of the Client with Hematologic and Immune Disorders...................................................................................................106
IMMUNE SYSTEM.................................................................................................................................................................................117
Unit 16: Care of the Client with Dysrhythmias.......................................................................................................................................122
Unit 17: Clients with Coronary Artery Disease and Acute Coronary Syndrome....................................................................................130
CORONARY ARTERY DISEASE (CAD)..................................................................................................................................................130
ACUTE CORONARY SYNDROME (ACS)................................................................................................................................................132
Unit 18: Clients with Heart Failure.........................................................................................................................................................146
CORONARY ARTERY DISEASE (CAD)..................................................................................................................................................146
Unit 19: Clients with Cancer...................................................................................................................................................................156
SURGERY..............................................................................................................................................................................................167

RADIATION THERAPY...........................................................................................................................................................................167
CHEMOTHERAPY..................................................................................................................................................................................170
BIOLOGIC THERAPY.............................................................................................................................................................................174
Unit 20: Clients with Seizure Disorders..................................................................................................................................................182
Unit 21: Clients with Altered Elimination (Acute & Chronic Renal Failure).........................................................................................188
ACUTE RENAL FAILURE (ARF)...........................................................................................................................................................190
CHRONIC KIDNEY DISEASE (CKD).....................................................................................................................................................192
DIALYSIS..............................................................................................................................................................................................195
Unit 22: Care of the Client with a Cerebro-Vascular Disorder................................................................................................................199
CARE OF THE UNCONSCIOUS PATIENT.................................................................................................................................................199
STROKE................................................................................................................................................................................................203
Unit 23: Care of the Client with Neuromuscular Disorders....................................................................................................................208
MULTIPLE SCLEROSIS (MS).................................................................................................................................................................208
GUILLIAN BARR.................................................................................................................................................................................210
MYASTHENIA GRAVIS..........................................................................................................................................................................211
PARKINSONS DISEASE........................................................................................................................................................................212

Unit 1: Chronicity with Related Concepts
Chronicity
The human response to symptoms that interrupt ones life and force the person to reshape their life. These human responses all vary
and may stem from various places.
Characteristics of chronicity:
Permanent or residual disability requiring rehabilitation.
Multiple and prolonged hospitalizations.
Symptoms (lasting at least 3 months) may develop gradually or be the result of treatment.
Periods of remission and exacerbation (the biggest hallmark characteristic).
Acute and/or long term complications.
The Epidemiology of Chronic Illness
The leading causes of death in Canada in 2004 (for all ages) were chronic illnesses:
1. Cardiovascular disease (e.g., MIs, hypertension)
2. Cancer
3. Respiratory disease (e.g., emphysema, COPD, asthma, etc.)
Before We Move On.
Think of a patient you cared for in gerontology (either community or in long term care). Did they have a history of chronic illness?
How did they cope with this? How about the family?
When dealing with patients it is important to assess how they are coping with the situation. If possible they should be encouraged to
find positive ways of coping if this is not already the case. The family is just as important as the patient and the HCP should take the
time to get to know them as well.
Chronicity
Acute Illness Sick Role
Exempt from normal responsibilities.
Dependency is expected.
There is an obligation for the sick person to want to be well.
Chronic Illness Impaired Role
Expected to maintain roles and responsibilities within limits of their illness.
Family and ill person expect a degree of independence and self-care.
Obligation is not to get well but make the most of capabilities.
Nursing interventions are generally directed towards the patients response to illness and not merely the disease.
Human Response to Health and Illness
1) Physiologic regulatory
This is known as homeostasis.
2) Pathophysiologic response
Occurs when the physiologic regulatory responses have either gone wrong or are insufficient.
3) Experiential
This includes not only the patients experiences but the familys as well.
4) Behavioural
These are the individuals behaviours towards the illness (e.g., getting angry). This often builds on the patients
experiential aspect.
How do you think a nurse can care for a patient at any of these levels?
Chronicity
Illness Trajectory
The course of an illness which requires "the combined efforts of the affected individual, family and health care provider in order
to shape it". Each illness has a trajectory or course, the details of which can only be partially determined ahead of time. The
trajectory depends upon the individual and the actions taken to shape that course.
Corbin and Strauss identified phases that represent different changes that an individual with a chronic condition can undergo
over the course of the illness. There may be day to day fluctuations within each of these phases where the affected individual may
experience upward, downward or stable periods for several weeks or months. The following is a synopsis of the phases of an
illness trajectory and the implications for nursing management.
o Corbin and Strauss 1991.
o Updated 2002 page 30 of your text.
Coping tasks change throughout course of illness.
Illness trajectory = course of illness.
Illness trajectory can be uncertain:
o Textbook trajectory (i.e., it progresses as expected)
o Patients perception of own trajectory
o Health care providers perception
o Actual trajectory of illness as it unfolds
Influences of the Trajectory:
o Individuals perception
o Familys perception
o Resources (recall the determinants of health, especially the social determinants of health)
o Past experiences
o Lifestyle, beliefs, values, culture
Its important to consider ones culture and lifestyle as these elements often do not change (e.g., a fatty diet in
certain cultures).
o Motivation (individual and family)
o Relationship with care provider
The trust established between the HCP and the patient is very important.
Phases of the Trajectory Appendix A

1) Pre-trajectory
This occurs before the illness shows up (e.g., constantly consuming a fatty diet).
Management: preventative teaching and attitudinal and lifestyle changes.
2) Trajectory onset
Signs and symptoms are present and there is a diagnostic period.
Management: teaching about diagnostic procedures, providing emotional support, and answering questions related to the
illness.
3) Crisis
Life-threatening situation occurs, requiring emergency care.
Management: providing emotional support to the individual and to the family, exploring factors that precipitated the
crisis, and teaching.
4) Acute
Active illness/complication that requires hospitalization once crisis has subsided (e.g., out of ICU).
Management: teaching regarding the incorporation of a new treatment regimen into their lifestyle.
5) Stable
The symptoms are controlled by the treatment regimen. They are days away from discharge.
Management: encourage adherence to the regimen so the highest level of functioning is achieved.
6) Unstable
Symptoms are not controlled by the regimen but hospitalization is not required. This may occur from not being cautious
to ones lifestyle. It will lead to comeback.
Management: teaching and assisting the individual and family to gain better control over the symptoms.
7) Comeback
Symptoms are controlled by revisions to the treatment regimen and additional support.
Management: support the individual and their family to continue adhering to the regimen plan. The goal is to maintain
control of the symptoms and extend remission state through the promotion of teaching.
8) Downward
Progressing deterioration characterized by increase disability. Weve been unsuccessful at controlling the issues. We can
no longer maintain any issues.
Management: anticipate physiological and psychological impact of deteriorative state. Assist the individual and their
family to readjust their activities to adapt to increasing deterioration.
9) Dying
Immediate weeks/days preceding death.
Management: providing comfort care and emotional support to individual and family.

Lets Work it Through
Carol is a 28 yr. old Aboriginal woman with a family Hx of type 2 diabetes.
o Pre-trajectory
At age 17, she experienced polyuria, and polydipsia. She was Dx with Type 1 diabetes.
o Trajectory
During the first four years after her diagnosis, Carol had multiple hospital admissions due to poor blood sugar control
(hyperglycemia and ketoacidosis). Carol attended University and graduated with a Fine Arts Degree.
o Crisis
Stable
At age 24, after years of trying various regimens and experimenting, Carol had good control of her blood sugars. She married
and pursued a career as an artist.
o Stable
At age 28 Carols career as an artist was at its peak. She was working long hours and traveled frequently. She started to
experience episodes of severe hypoglycemia that resulted in seizures and emergency Tx. Carol also reported having blurred vision
and numbness to her fingertips.
o Crisis
Downward
Family Trajectory
It is important to keep the family in mind!
There are predictable points of stress.
They vary in level of tolerance.
May use ineffective coping mechanisms.
Each member has a unique experience.
Implications of Chronicity
Managing chronic illness:
o Involves more than managing medical problems.
o Can pass through many different phases over the course of the disease.
o Requires persistent adherence to therapeutic regimens.
o It is a process of discovery.
o It is a collaborative process.
o It is expensive.
Everyday Concerns of Chronicity
Prevention
Alleviating and managing symptoms
Prevent, adapt, and manage disabilities
Prevent/manage crises and complications
Attain, maintain and regain stability
Validating self worth and family functioning
Coping Styles
1) Assess how individual/family dealt with illness in the past.
2) Determine what coping style they are using at this time.
Nursing Interventions
Trust!!! This can be done by talking with the patients and getting to know them.
Maximize patient and families sense of control.
Support style of coping.
Modify the environment to remove barriers.
Involve significant others.

Unit 2: Introduction to the Care of the Paediatric Client
INTRODUCTION
Balconies for Open Air Treatment
On the Flu Front Line
Outline
Roles within paediatric health
Snapshot of paediatric health care in Manitoba
o Hospital
o Community
Key concepts:
o Paediatric nursing vs. nursing of adults
o Family-centred care
o Growth and development
o Video
Introduction
Manitoba (2006) The Youngest province of all
o 19.6% of population <15 yrs ;
The town with highest proportion is Thompson, with 26.8% of their population being <15 years.
o National average = 17.7%
Key determinant of child health is SES.
Leading cause of hospital admissions for those <10 yrs is respiratory illnesses.
Northern Manitoba
First Nations
o 1 in 4 children on First Nations reserves live in poverty.
Refugees/immigrants
Concerning Determinants of Health Among First Nation Children
117 First Nations communities are under drinking water advisories.
There is 3x the number of children in care in 2010 (27, 500) than at the height of the residential schools in 1940.
Immunizations rates are 20% than average for all children.
Youth suicide more prevalent in First Nations Communities than among all youth in Canada.
Encouraging Sign of Change in First Nations Children
Breastfeeding is being widely practiced.
Aboriginal women are finishing secondary school and obtaining university degrees at a higher rate than the men.
Income gap between Aboriginal peoples and rest of Canada who have a Bachelors degree is narrowing.
How Does Poverty Affect a Childs Health?

They are more likely to have low birth weights,
suffer from malnutrition, and diabetes Type 2.
They are 2.5 times more likely to have a disability and least likely to access medical and community supports.
More likely not have benefit plans for drugs, vision and dental care.
Learning disabilities, emotional difficulties and behavioural problems.
As adults they are more likely to experience addictions, mental health difficulties, physical disabilities and premature death.
o They have higher rates of death due to unintentional injuries than other children.
Leading cause of death for those <20 yrs...

o Unintentional injury
Car accidents, drowning, etc.
o Intentional injury
Suicide and abuse (e.g., shaken
babies).
Males are more likely than females to
succeed in suicide attempts.
1996: of deaths for Canadians 0-19 yrs
o 48.9% <1 yr of age
This may sometimes occurs from co-bedding.
Youth suicide in Manitoba

Manitoba's program has life-saving impact
Province has 'moral duty' to help: Rondeau
Medically Complex Children
Some children are going home on GT and NG feeds. There are efforts trying to centralize the resources required for medically
complex children.
COMMUNITY
Community
Home Care
o Goal: Prevention of readmission or prolonged admission.
Paediatric Day Unit/Home IV Program
o The Home IV Program is quite small.
Other community resources (e.g., diabetes clinics)
Discharge planning
Infant Feeding Ward
On the Flu Front Line
Childrens Hospital
http://www.goodbear.mb.ca/hospital_tour.aspx
Tertiary care facility
o Next closest
# beds is 120.
~ length of stay is about 4-7 days.
# admissions 3,722 (2002) and 3,995 (2010).
# ER visits 3,000+.
# clinic visits 50,000?
# surgeries is ~6,000/year.
54 kids sent to hospital over CO scare
Paediatric Nursing vs. Nursing of Adults
The client
o Adults: typically the one adult
o Paediatric: the patient and the family (which may be parents, grandparents, aunts, uncles, etc.)
Pediatric assessment
o These assessments must include age appropriate vital signs.
o They are anatomically different as well (e.g., airways are closed off with lesser swelling than adults).
Health problems
o Unique to paediatrics
Bronchiolitis is more common in children.
o Frequency in paediatrics
o Signs and symptoms
Some children display different signs and symptoms than adults for similar problems.
o CPR/BLS
Pharmacokinetics (ADME)
Safe med administration
o All medications are delivered based on weight and surface area.
o Their physiology is also different than adults (e.g., blood proteins).
Family & caregiver dynamics
o Therapeutic relationship vs. Friendship
o Bonding vs. Conflict vs. Control
Families and children
o Variety and values
o Culturally different parenting? Parenting that is less than optimal? Parenting that is different? Parenting that may be
harmful??
Play!
o Child Life Specialists
Education
o Health
o Development
o Hospitalization
Growth and Development

Goal: optimum level of health
Age appropriate self-care care
Resources:
o Video
o Syllabus
Nursing applications of developmental theories
Effects of illness and hospitalization on children and families
o Key developmental stages
o Developmental norms
Alterations?
o Health related care and tasks:
Psychomotor tasks
Knowledge/education (i.e., use terminology theyll understand).
Decision making abilities
Family Centred Care (FCC)
What is FCC?
o Holistic health care
o Collaboration (i.e., with parents, other staff, other units, etc.)
o Family and child routines
o Advocacy
o Respect
o Benefits
Ethics and Advocacy
Parental decision-making
o Responsibilities
o Rights?
o Competencies?
Child decision-making
o Consent vs. assent
Abuse and neglect
Advocacy
o but peds
Teen Zone room at Cancer Care Manitoba

Adult Paediatric Patients
This may come about with individuals with disabilities (e.g., regarding weight).
Unit 3: Fluid & Electrolyte
FLUID
Homeostasis
State of equilibrium in the internal environment of the body.
The cardiovascular system is the most important system relating to homeostasis as it powers fluid movement.
Explain the relationship of homeostasis to body fluid. For example, how does the body maintain fluid balance in the blood when
we sweat or do not drink enough?
o The thirst mechanism will be triggered, prompting you to drink. In paediatrics, its important to ensure your patients are
adequately hydrated.
Water Content of the Body
iClicker Question:
Water:
a. Accounts for 60% of body weight in adult and children
b. Accounts for 70-80% of body weight in infants
c. Is greater % in women
d. Is greater % with increased fat
Bigger individuals have less fluid moving throughout the body.
Compartments (p. 9 Human Physiology by Sherwood)
Intracellular fluid (ICF) is where 2/3 of fluid is found.
Extracellular fluid (ECF) is comprised of:
o Intravascular (plasma): 25%
o Interstitial: 75%
Transcellular
o There is typically no fluid flowing in/out of these spaces. There is roughly 1L of fluid in these spaces (e.g., synovial
joints, peritoneal cavity, cerebrospinal fluid, etc.).
Question
Match the following descriptions with the mechanisms of fluid and electrolyte movement
a. Pressure exerted by proteins (4)
1. Facilitated Diffusion
b. ATP required (5)
2. Diffusion
c. Flow of water from low concentration to high solute
3. Osmotic pressure
concentration (6)
4. Oncotic pressure
d. Force exerted by fluid (7)
5. Active transport
e. Passive movement of molecules from a high
6. Osmosis
concentration to lower concentration (2)
7. Hydrostatic pressure
f. Uses a carrier molecule (1)
g. Force determined by osmolality of a fluid (3)
You need glucose and O2 to make ATP. Bi-products of Glycolysis and the Citric Acid Cycle are CO2 and H2O.
Mechanisms Controlling Fluid and Electrolyte Movement

Diffusion go with the flow
Osmosis fluid flow (the solutes do not move)
Facilitated diffusion need a carrier
Know these terms!
10
Active transport Na and K use this mechanism

Hydrostatic pressure term hydro should give it away
Oncotic pressure it is the force exerted by proteins (i.e., albumin the water magnet)
Osmosis
Going back to our question earlier, how do we maintain fluid volume (and essentially blood pressure) when we lose fluid either
through insensible volume loss or failure to replenish?
o Hydrostatic pressure shifts fluid out of the capillaries. When this happens, albumin is left behind in the capillaries.
When the levels of albumin start to rise due to all this fluid loss, it will draw fluid back in the capillaries (i.e., oncotic
pressure).
More on this later..
Think About This

Given what you know about oncotic pressure, what would happen if someone has excessive protein loss (e.g., kidney disease) or
deficient protein synthesis (e.g., liver disease) or deficient protein intake (e.g., malnutrition r/t ETOH abuse). Where is the plasma
fluid going? What would the person look like?
o Edema starts to be seen when 2-3 litres of fluid has shifted. There will be edema and a decrease in BP in this patient as
there is no protein to draw the water back in the capillaries.
o The edema will be everywhere but will be more prominent depending on the persons position.
Fluid Movement in Capillaries

Tell me again, what are the two major factors that determine the amount and direction of fluid movement between plasma and the
interstitial space?
1. Oncotic pressure
2. Hydrostatic pressure
Fluid Shifts
What happens when the fluid shifts from the plasma to interstitial?
o The cells will swell and there will be a decrease in plasma volume (which will lead to blood pressure and edema).
Interstitial fluid to plasma?
o The cells will shrivel and there will be an increase in plasma volume (which will lead to blood pressure).
If the fluid is in your blood, that fluid will be strained by the kidneys and excreted. If the fluid is in the interstitial space, it will
not be excreted and the patient will therefore gain weight.
The pressure in the lungs is quite low so it can take O2 in the body. Recall that blood pressure is 120/80, which is the pressure the
body has to overcome.
Question (use fig 18-8)

As fluid circulates through the capillaries, there is movement of fluid between the capillaries and the interstitium. In the following
descriptions, match the direction of fluid movement and the location of the movement in the capillary
a. Plasma hydrostatic pressure is less than plasma
1. Movement into capillary
oncotic pressure
2. Movement into interstitium
b. Interstitial hydrostatic pressure is lower than
3. Occurs at arterial end
plasma hydrostatic pressure
4. Occurs at venous end
c. Plasma hydrostatic pressure is less than
interstitial hydrostatic pressure
d. Plasma hydrostatic pressure is higher than
plasma oncotic pressure
Summary Fluid Spacing
First spacing
o Normal distribution of fluid in ICF and ECF.
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Second spacing
o Abnormal accumulation of interstitial fluid (e.g., edema).
Third spacing
o Fluid accumulation in part of body where it is not easily exchanged with ECF (e.g., ascites, edema with burns).
Burns often look shiny due to the edema.
Third Space Shifting

Shift of fluid from vascular space into an area where it is not available for physiologic processes.
Trapped fluid does not participate in normal functions of ECF.
Weight does not change.
Location: pleura, peritoneal/ascites, pericardial, joints, bowel obstruction.
Regulation of Water Balance

Review on your own:
Hypothalamic regulation
o The hypothalamus has many functions that assist in the adaptation to real and potential threats (e.g., it receives
information concerning physical trauma and pain by way of the spinothalamic pathway; pressure-sensitive input,
resulting from high or low blood pressure, is relayed to the hypothalamus from the baroreceptors located in the
carotid sinus).
It also secretes hormones that control the release of hormones from the anterior pituitary.
ADH, also called vasopressin, is a nonapeptide that is produced in the magnocellular system of the
hypothalamus, specifically within cells of the supraoptic and paraventricular nucleus. The hormone is synthesized
and packaged in neurosecretory granules with a protein, neurophysin. The granules flow along the axons of these
cells to the nerve endings in the posterior pituitary where they are stored. ADH is released from the nerve endings
by exocytosis in response to stimulation of the neurons.
Pituitary regulation
o Anterior Pituitary Hormones
FSH, LH, ACTH, TSH
(Tropic Hormones)
Prolactin
, GH
(Direct Hormones)
o Posterior Pituitary Hormones
As mentioned above, ADH/Vasopressin is synthesized in the hypothalamus and is transferred to the
posterior pituitary, where it is eventually released.
Adrenal cortical regulation
o Renin is synthesize in the kidneys and via the Renin-Angiotensin-Aldosterone system, causes an increase in water
retention.
Renal regulation
Cardiac regulation
Gastrointestinal regulation
Insensible water loss
Renin-Angiotensin-Aldosterone System (see Human Phys notes and p. 511 & 517 of Human Physiology)
Know
this!
Renin comes from the kidneys and goes to the liver where it converts to angiotensin-I. It then goes to the lungs to become
angiotensin-II. The kidneys secrete renin when the blood pressure is too low, which will stimulate water reabsorption.
The aldosterone draws Na+ back in the body, which is followed by water. This water comes firstly from the interstitial space, and
if there is not enough there it comes from the intracellular space (when there is no water in the tubules).
Aldosterone belongs to a class of hormones called mineralocorticoids, also produced by the adrenal glands. It helps maintain
blood pressure, water, and salt balance in the body by helping the kidney retain sodium and excrete potassium. When aldosterone
production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume and blood pressure to
drop.
12
CO
BP
Neural
respons
e
Renal
respons
e
Sympathetic
NS activated
Renin (kidneys)
+
Angiotensinogen
(liver)
Norepinephrin
e
-blockers, 1
blockers
ADH
Retains
water
Angiotensin
I + ACE
Vasoconstrictio
n
BP
Hormon
al
respons
e
Angiotensin II
Increases
blood volume
Vasoconstricti
on
Aldosterone
(adrenal
cortex)
BP
Retention of Na+
and water
Sympatholyti
cs
BP
blood
volume
BP
Renal response
o ACE is found in the blood vessel epithelium.
o ADH comes from the posterior pituitary (ACTH comes from the anterior pituitary).
o Aldosterone comes from the adrenal cortex.
o Angiotensin II antagonist/ACE inhibitor (ACEi) in BP
o Giving a diuretic will cause a decrease in volume, thus decreasing BP.
Receptors Responses
Adrenergic agonists
- Arterioles (vasoconstriction)
1 - Pupils (dilation)
- Prostate, bladder neck, ejaculation

2 - GI tract ( motility)
- Heart rate
1 - Contractility
- Automaticity
- Conduction
- Bronchioles (dilation)
2 - Arterioles (vasoconstriction)
- Conversion of glycogen to glucose
Note: 1 mostly involved with the heart.
Note: this drug should not be given to diabetics.
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1
agonists
Blood
vessels
Iris
Gut
Liver
Urinary
bladder
Piloerector
muscle
Sweat
glands
Vasoconstriction
Pupil
dilation
(mydriasis
)
Decreased
peristalsis
Glycogen
breakdow
n
Decreased
voiding
Goosebum
ps
Sweating
Blurred
vision
Constipati
on
Increased
blood
sugar
Urinary
retention
Reduction
in
congestio
n
Increase in
systemic vascular
resistance (SVR)
Increase
in blood
pressure
Nasal
decongestion
Ocular
decongestion
Hypertension
2 agonists
Bronchioles
Skeletal
muscles
Pancreas
Liver
Skeletal
muscle,
coronary,
and cerebral
circulation
Triggers
bronchodilati
on
Triggers fine
muscle
tremor
Increase
insulin
secretion
Trigers
glycogen
breakdown
Trigers
vasodilation
Fall in serum
K+ levels
Rise is blood
glucose level
Increase in
tissue
perfusion
Uterine
smooth
muscle
Heart
Induces
relaxation
Trigers
increased
rate and
force of
contraction
1 agonists
Juxtaglomerular
apparatus
Heart
muscle
Gut
Adipose
tissue
Increases
blood lipid
levels
Stimulates
renin
release
Increases
heart rate (+
chronotropic)
Increases
force of
contraction
(+
inotropic)
Decreases
peristalsis
Increase in
angiotensin
II
production
Increases in
cardiac
output and
workload
Increases in
cardiac
output and
workload
Constipatio
n
Increase in
blood
pressure
Increase in
blood
pressure
Increase in
blood
pressure
14

Other Terms to Know!
Tonicity
o Isotonic solutions
o Hypertonic solutions
o Hypotonic solutions
Hypovolemia
Hypervolemia
Dehydration
Edema
Fluid Assessment
History
o Conditions that affect F&E
Kidney problems, obesity, diabetes, endocrine disorders, metabolic disorders.
o Medications
Diuretics (e.g., loop and thiazide diuretics).
Loop diuretics will excrete Na+ and K+. Normal range of K+ is 3.5-5 mmol/L. The body cannot
tolerate large changes in K+ levels. It is important to look for patterns (e.g., in the last few days) and
not merely at a single point during the day.
o Abnormal loss
Nausea, vomiting, diarrhoea.
o Diet
Water, salt, proteins.
Strict vegan and vegetarian diets must have protein from another source (e.g., legumes, nuts, etc.).
A high sodium diet will cause an increase in water retention.
o Intake
Follow Canadas Food Guide.
Urine Volume/Concentration
1mL/kg/hr (range 0.5-2 mL/kg/hr)
Decreased urinary output (shock, renal/cardiac disease)
Increased urinary output (diabetes mellitus and diabetes insipidus)
Specific gravity
o Proportional to the amount of water in the body. This value is typically more important for that reason.
Urine Osmolality
o This is strictly the urine concentration.
In/Out/Weight
Accuracy NB
o In = ice, soup, ice cream
o Out = urine, feces, emesis, sputum
Note paediatric, weigh diapers.
Compare cumulative balance.
Frequency of checks depends on fluid status.
o WEIGHT 1kg = 1L of fluid.
o WEIGHT is the best way to monitor fluid balance!
Extracellular Fluid Volume Imbalances

Hypovolemia can occur with loss of normal body fluids (diarrhoea, fistula drainage, haemorrhage), decreased intake, or plasmato-interstitial fluid shift.
Hypervolemia may result from excessive intake of fluids, abnormal retention of fluids (CHF), or interstitial-to-plasma fluid shift.
Considerations in the Elderly

Decreased total body water risk of fluid-volume deficit (FVD)
Decreased ability to concentrate urine
Kidney function changes (i.e., less able to respond)
Possible reduced thirst response
Changes in skin integrity
o It makes it difficult to assess turgor.
Changes in cardiovascular function
o They are less likely to vasodilate, turn up the angiotensin system, etc.
15
Changes in GI tract
o Less able to absorb available fluids.
Modified Assessment for the Elderly

o Normal volume status patient may still have decreased skin turgor, tachy, orthostatic hypotension, dry mucous
membranes
o Use forehead or sternum
o Dorsal foot vein filling
Empty the vein and see how long it takes for it to fill.
o Check ability to obtain fluids (i.e., make sure patients always have water at the bedside)
o BP
o Temperature
Considerations in Children
Larger total body water.
Larger ECF (both interstitial and plasma)
Need more fluid intake and output relative to size.
Exchange more fluid across capillary membranes daily than adults.
Immature renal function (i.e., it may not conserve as much Na+).
Infant has greater body surface area.
Skin and GI considerations.
Cardiovascular considerations.
o They will have a lower BP.
NOTE:
o Infant is less able to handle large quantities of solute free water than an older child.
o Should use Pedialyte (contains electrolytes) rather than water.
o It is important to rehydrate SLOWLY with Pedialyte.
ELECTROLYTES
Electrolytes Review
Substances that dissociate in solution = ions
Cations = positive charged electrolytes
Anions = negatively charged electrolytes
Functions:
o Help regulate water & acid/base balance.
o Contribute to enzyme reactions.
o Essential to neuromuscular activity.
Sodium
Imbalances are typically associated with parallel changes in osmolality. That is because where ever sodium goes, water follows.
Plays a major role in:
o ECF volume and concentration.
o Generation and transmission of nerve impulses.
o Acid-base balance.
Potassium
Potassium major ICF cation.
90% of potassium intake is eliminated by the kidneys.
o If someone has kidneys problems, they are likely unable to eliminate K+. This will lead to issues with the heart as it
cannot tolerate changes in K+ levels.
Potassium is necessary for:
o Transmission and conduction of nerve impulses.
o Maintenance of normal cardiac rhythms (e.g., may affect pulse).
o Skeletal muscle contraction.
16

Electrolyte Disorders Signs and Symptoms
Electrolyte
Excess
Deficit
Sodium
Hypernatremia
Hyponatremia
(Na+)
Thirst
CNS
deterioration
CNS deterioration
Increase interstitial
fluid
Potassium
Hyperkalemia
Hypokalemia
(K+)
Ventricular
Bradycardia
fibrillation
ECG changes
ECG changes
CNS changes
CNS changes
*Notice how CNS changes affected by many electrolytes.
Calcium
Obtained from ingested foods.
More than 99% combined with phosphorus and concentrated in skeletal system.
Aids coagulation.
Bones are a readily available store of calcium.
Magnesium
50-60% contained in bone.
A coenzyme in metabolism of protein (protein synthesis) and carbohydrates.
Modifies nerve impulse transmission and skeletal muscle response. These patients may have twitching.

Electrolyte
Excess
2+
Calcium (Ca ) Hypercalcemia
Muscle weakness, decreased DTRs
Confusion, lethargy, coma
Arrhythmias, hypertension, increased digoxin
sensitivity*
Magnesium
(Mg2+)
Hypermagnesemia
Loss of DTRs (i.e., deep tendon reflexes)
Depression of CNS
Depression of neuromuscular function
Deficit
Hypocalcemia
Tetany
Chvosteks, Trousseaus muscle
twitching
CNS changes
EKG changes
Hypomagnesemia
Hyperactive DTRs
CNS changes
EKG changes
Phosphate
Phosphorus is primary anion in ICF.
Promotes energy storage and CHO, protein, and fat metabolism.
Deposited with calcium for bone and tooth structure.
Kidneys are major route of phosphate excretion.
Acts as hydrogen buffer in acid/base function (more on this later).

Electrolyte
Excess
Phosphate
Hyperphosphatemia
(PO4-)
Signs of tetany (due to hypocalcemia)
Deposition calcium phosphate precipitates in skin,
soft tissue, cornea, etc.
Deficit
Hypophosphatemia
Parasthesias
Muscle weakness
Confusion, delirium
Question
Several conditions will cause multiple imbalances of electrolytes. Identify three electrolyte imbalances that are caused by the
following:
17

a.
b.
c.
Hyperaldosteronism (e.g., if you had too much aldosterone, what would your electrolytes look like?)
Aldosterone is a hormone that is produced by the adrenal glands. It works primarily on kidney (renal) cells to
help maintain the balance of fluids and electrolytes in our bodies. It mainly works to control reabsorption of
sodium and chloride and secretion of potassium and hydrogen. If aldosterone production is not functioning
properly, there can be serious consequences to the heart, kidneys and electrolyte balance.
They would have hypernatremia, followed by hypokalemia.
Chronic Renal Failure
Hyperkalemia, hyperphosphatemia.
Loop and thiazide diuretics
H4 may have many kidney infections.
Protein Imbalances
Plasma proteins, particularly albumin, are significant determinants of plasma volume. Recall how older adults and children have
fewer albumins in their blood, making them more susceptible to drug toxicity from the free drug in the blood stream.
Having too much protein is rare.
CASE STUDY FLUID & ELECTROLYTE
Client Profile
Kathleen B., a 74 year old woman who lives alone, is admitted to the hospital because of weakness and confusion. She has a
history of chronic heart failure and chronic diuretic use.
Objective Data
Neurological: confusion, slow to respond to questioning, generalized weakness
Cardiovascular: BP 90/62, HR 112 and irregular, peripheral pulses weak; ECG indicates sinus tachycardia (normal wave but it is
fast)
Pulmonary: respirations 12 per minute and shallow
Additional findings: decreased skin turgor; dry mucous membranes
Significant Laboratory Results

Serum electrolytes:
Na+ 141 mmol/L
K+ 2.5 mmol/L
Cl 85 mmol/L
HCO3 43 mmol/L
Critical Thinking Questions

1) Evaluate Kathleens fluid volume and electrolyte status.
Fluid volume
o Decreased, AEB decreased skin turgor and dry mucous membranes, BP, HR.
o We can assume shes on loop diuretics.
Electrolyte status
o Confused, slow to respond to questioning, generalized weakness, weak and irregular pulses, sinus tachycardia.
Electrolyte
Normal
K.B.
V
levels
s Levels
erdict
Na+
135-145
141
N
mmol/L
mmol/L
ormal
K+
3.5-5
2.5
L
mmol/L
mmol/L
ow
Cl
98-106
85
L
mmol/L
mmol/L
ow
HCO3
24-30
43
H
mmol/L
mmol/L
igh
Mg2+
0.75-0.95
mmol/L
Calcium (serum)
2.18-2.58
total
mmol/L
Calcium (serum)
1.05-1.30
18

ionized
Albumin (serum)
Cholesterol
2)
3)
4)
5)
6)
mmol/L
35-50 g/L
<5.2
mmol/L
Osmolality
280-300
mmol/kg
Iron
11-32
mol/L
Which physical assessment findings support your analysis? Which laboratory results support your analysis? What is the most
likely etiology of these imbalances?
Physical assessment
o See above.
Lab values
o See table.
Etiology
Explain the reasons for Kathleens ECG changes.
Increased HR.
Why has Kathleens advanced age placed her at risk of a fluid imbalance?
With age comes certain physiological changes (e.g., decrease in plasma protein levels, decreased water volume,
decreased kidney function, decreased thirst).
Discuss the role of aldosterone in the regulation of fluid and electrolyte balance. How will changes in aldosterone affect
Kathleens fluid and electrolyte imbalances?
It works primarily on kidney (renal) cells to help maintain the balance of fluids and electrolytes in our bodies. It mainly
works to control reabsorption of sodium and chloride and secretion of potassium and hydrogen.
While she is in the hospital what daily assessments should be included in her plan of care?
Measure her I&O.
The K+ is dangerously low so that must be dealt with. Shell likely be on a KCl treatment.
Stop giving her diuretics.
Take her vital signs q4h.
19

Unit 4: Principles of Hemodynamics
CLIENTS WITH HYPERTENSION
Hemodynamics
Depends upon:
o Adequate blood volume.
o Adequate amount oxygen in blood.
o Effective pump (i.e., heart).
o Effective vessels (particularly the arteries).
o Effective nervous system.
Principles of Hemodynamics
Fluid flows from high to low pressure.
Pressure is generated by ventricular contraction.
Pressure gradient forces blood through arteries and capillaries into veins (recall hydrostatic and oncotic pressure).
Pressure gradient in pulmonary circulation are lower than systemic circulation.
Review from last class

Define the following:
o Hydrostatic pressure: the pressure a fluid exerts on the walls that contain it.
o Osmotic pressure: the force determined by the osmolality of a fluid.
o Oncotic pressure: the force generated by proteins on a fluid (e.g., albumin).
Hemodynamics
Cardiac oxygen consumption
o Myocardium high need for oxygen.
o Volume of O2 is determined by the amount and type of exercise.
o The heart takes ~60-70% of oxygen from arterial blood. The brain also requires a lot of O2.
Workload
o Increased O2 demand = increased flow of O2 blood
Cardiac Output
o CO = HR X SV
o Amount of blood pumped from the ventricles in 1 min.
o Why is cardiac output so vital?
It delivers oxygen, glucose, electrolytes, etc. to the body.
iClicker time
What is cardiac reserve?
a. Peripheral resistance encountered by the left ventricle
This is afterload.
b. The force opposing the movement of blood
Systemic vascular resistance.
c. Ability to increase cardiac output
We can increase it by 3-4 times.
d. The addition of the diastolic pressure to 1/3 of the pulse pressure
Mean arterial pressure (MAP)
It is the difference between the amount of blood in the ventricles and the amount they eject during systole.
Otto Frank & Ernest Starlings Law

The greater the stretch of the ventricles or a particular muscle, the greater the contractility...to a point. Think of a rubber
band...there comes a point where great stretching will cause it to lose its elasticity and it will not snap back.
Factors Affecting Stroke Volume

Preload
o The end of diastole (i.e., the amount of blood coming to the heart).
Contractility
o The hearts ability to contract (rate and amplitude of contractions).
20
Afterload
o The resistance that the ventricles have to pump against during systole.
General Factors Affecting Venous Return (i.e., Preload)

Pressure in peripheral blood vessels
o Blood volume
At any given time, there is roughly 16% of blood in the veins. When there is too much volume, a backup
occurs. This backup can remain in the systemic system, thus increasing blood pressure, or enter the lungs.
o Sympathetic tone
This is mainly the stretch and contractility of the heart.
o Muscle contraction
Compliance of ventricles
o Fibrosis
o Hypertrophy
This may occur if the heart pumps too hard for too long.
o Scar tissue
From myocardial infarction.
Diseases
o Renal failure
Contractility
Contractility is enhanced by:
o Catecholamines
Epinephrine and norepinephrine.
o Sympathetic Nervsous System (SNS)
o Meds
Digoxin: it increases the contractility and the heart rate slows down because the contractility is more efficient
Contractility depressed by:
o Hypoxia
The heart needs O2 to run optimally.
o Acidosis
Any increase in K+ depresses contractility because of the ions inability to repolarize is slower.
o Meds
Digitalis drugs: decrease the heart rate
Calcium channel blockers (CCB): Ca2+ is required for adequate contractility
Ejection Fraction
The percentage of blood that is ejected from the heart with each beat.
o ~67% +/ 9% is normal
When is someone symptomatic?
o Symptomatic with activity: <40% ejection fraction
o Symptomatic at rest: <25% ejection fraction
o These people may be tired, dizzy, and pale.
Afterload
Ventricular wall tension during systolic ejection.
With an increase in peripheral vascular resistance, the heart will have to work harder in order to overcome that pressure. With
time the heart will get stronger and enlarge. This is a problem because it will then affect the pre-load (i.e., the amount of blood
that can enter the heart during diastole).
Resistance to ejection of blood from ventricles.
Heart Rate
Autorhythmic, SA node is controlled by the ANS.
For a short period of time, a normal heart can increase its rate by 3.
Sustained HR over 180 bpm will lead to:
o Workload,diastole, CO
Its important to look at patterns!
21
Regulation of Heart Rate

Cardiovascular control centre
Baroreceptors
Chemoreceptors
What can affect the heart rate?
o Emotions: stress (prolonged), anger, anxiety.
o Medications: caffeine.
o Exercise
o Smoking (HR increases)
o Illness (HR increases)
Sympathetic (adrenergic) HR, BP, GI

motility
BP Regulation Mechanisms
The radius of the small arteries and arterioles is the principle factor
Parasympathetic (cholinergic) HR, BP,
determining vascular resistance. A small change in the radius will lead to
GI motility
Autonomic Nervous
big changes in the systemic vascular resistance (SVR).
System
The mechanisms that affect BP can affect the cardiac output, the
systemic vascular resistance, or both.
Short Term
o Involve SNS and vascular endothelium.
Sympatheti
Parasympathetic
c
SNS activity
HR and contractility
Widespread vasoconstriction of peripheral
arteries
Fight or
Rest and Digest
Flight
Promotes the release of renin
Net effect is to CO and SVR.
Changes in blood pressure are sense by baroreceptors.
NE activates receptors in the SA node, myocardium, and
Stressful
Quiet
situations
activities
vascular smooth muscle.
1, 2, and 1 cause vasoconstriction when stimulated.
2 causes vasodilation when stimulated.
The sympathetic vasomotor centre in the medulla
Expend
Conserve energy
interacts with the brain to control blood pressure.
energy
Baroreceptors are located in arteries and the arch of the
aorta. When stretched by an BP, they send inhibitory signals to the sympathetic vasomotor centre to BP by
the HR, the force of contraction, and vasodilating the peripheral arterioles. A in BP causes
baroreceptors to SNS activity. With prolonged hypertension, the baroreceptors sense the BP as normal
and will stop sending messages to the vasomotor centre.
Vascular endothelium
Nitric oxide (NO), a potent vasodilator, helps maintain low arterial tone and prevent platelet
aggregation.
Endothelin (ET) is an extremely potent vasoconstrictor.
o Active in seconds to hours.
o Do not return BP to normal.
o Lose efficiency within hours to days.
Long Term
o Involves renal and hormonal processes (e.g., renin-angiotensin-aldosterone system).
Renal system
The kidneys regulate BP by controlling Na+.
Prostaglandins are vasodilators secreted by the adrenal medulla.
Angiotensinogen (from liver) Renin (from kidney) Angiotensin-I ACE (in lungs) Angiotens
Angiotensin-II is a potent vasoconstrictor that can:

a. Constrict arterioles in order to BP.
b. Signal the adrenal cortex to produce aldosterone which Na+ reabsorption and thus water
rentetion.
Endocrine system
22
The hypothalamus synthesizes ADH and stores it in the posterior pituitary. When sodium levels rise, it
signals it to release the ADH in order to retain water and thus [Na+].
Active in days to weeks.
Hypertension - Definition
Hypertension is sustained elevation of BP.
o Systolic blood pressure 140 mm Hg.
o Diastolic blood pressure 90 mm Hg.
Canadian Hypertension Society stipulates normal BP is 120/80.
o www.hypertension.ca
Classification of Hypertension
Primary (Essential) Hypertension
o Elevated BP without an identified cause (relating to disease processes such as kidney failure or diabetes). Having a high
Na+ diet would still constitute primary hypertension.
o This accounts for the majority of cases.
Secondary Hypertension
o Elevated BP with a specific cause (relating to disease conditions).
Primary Hypertension
Several contributing factors:
o SNS activity
o Sodium intake
Processed foods, canned drinks, sauces, certain dairy products, etc.
The average adult should have roughly 1,500mg of sodium. This amount decreases with age.
o Excessive alcohol intake
Risk Factors for Hypertension

Alcohol consumption
Smoking (increases blood viscosity and thus the systemic
vascular resistance)
Genetics
Obesity
Ethnicity (e.g., Aboriginals and African Americans are
more likely of getting high blood pressure)
Age
Secondary Hypertension
Contributing factors:
o Coarctation of aorta
o Renal disease
o Endocrine disorders
o Neurologic disorders
These factors must be dealt with in order to get rid of the hypertension more permanently.
iClicker time
While performing blood pressure screening at a health fair, the nurse counsels which of the following visitors as having the
greatest risk for developing hypertension?
a. A 56-year-old man whose father died at age 62 from a stroke
b. A 30-year-old female advertising agent who is unmarried and lives alone
c. A 68-year-old man who uses herbal remedies to treat his enlarged prostate gland
d. A 43-year-old man who travels extensively for his job and exercises only on weekends
Clinical Manifestation of Hypertension

Dizziness
Headaches
Blurry/spotty vision
Tinnitus
Epistaxis (nosebleeds)
Dyspnea
Palpitations, angina
Fatigue, reduced activity tolerance
Hypertension Complications
23
The common complications are target organ diseases occurring in the:

o Heart
o Brain
o Kidney
o Eyes
There are typically twice as many vessels in the eyes of a person with severe hypertension.
Hypertensive heart disease
o Coronary artery disease (may lead to MIs)
The response-to-injury mechanism of atherogenesis suggests that hypertension disrupts the coronary artery
endothelium, thus exposing the intimal layer to activate white blood cells and platelets. The growth factors
released by the vascular endothelium will interact with the platelets and induce smooth muscle proliferation
within the lesion.
o Left ventricular hypertrophy
Sustained hypertension can increase the workload on the heart causing left ventricular hypertrophy. At first this
hypertrophy provides increased cardiac output; however, with time the increased contractility increases
myocardial work and oxygen consumption. When the heart can no longer meet the demands for myocardial
oxygen, heart failure develops.
o Heart failure
It occurs when the hearts compensatory adaptations are overwhelmed and can no longer pump enough blood to
meet the bodys metabolic needs. Contractility, stroke volume, and cardiac output are all diminished. The
client may complain of dyspnea on exertion and fatigue.
Left ventricular hypertrophy, especially coupled with coronary artery disease, will often develop into heart
failure.
Cerebrovascular disease
o Cerebral vascular accidents (CVA), transient ischemic attacks (TIA).
o Atherosclerosis is the most common cause of cerebrovascular disease. Should any plaque located in the arteries break
free, they could end up in the brain, producing a Thromboembolism which may lead to a stroke.
Peripheral vascular disease
o Hypertension speeds up the process of atherosclerosis.
o Intermittent claudication is a sign of PVD.
Nephrosclerosis
o Hypertension is one of the leading causes of end-stage renal disease (ESRD). Common lab indications of renal
dysfunction are microalbuminuria, proteinuria, elevated blood urea nitrogen (BUN) and serum creatinine levels.
o Scarring inside the kidneys, thus reducing their ability to function.
Retinal damage
Hypertension Assessment Review

History and physical examination
o Take BP in both arms and in different positions (e.g., sitting/standing) with an adequate amount of time between. When
charting, always report the higher pressure measured.
What are we going to ask? Examine?
o Family Hx
o Heart palpitations?
o Lifestyle (e.g., diet, smoking)
o Chest pain?
o Blurry vision?
o Dyspnea?
o Fatigue?
o
o Hypertension Diagnostic Studies
Routine urinalysis
o Is there protein or ketones in the urine?
Serum electrolytes
o K+, Na+, PO4-, Cl-.
BUN (blood urea nitrogen) and serum creatinine
o This measures kidney function.
Serum lipid profile
o Cholesterol (HDL, LDL) levels.
ECG
o This informs us about the electrical conductivity in the heart.
More extensive testing for identifiable causes is not generally indicated unless BP control is not achieved.
24
Testing for secondary hypertension is not usually done as most hypertension is primary.
o
o Collaborative Care Strategies for Adherence to Regimens
What can we do as nurses?
o Encourage patients to stick to their medication regimens, diet by giving them realistic targets. It is important that
medications are taken regularly!
o Empathy increases patient trust, motivation, and adherence to therapy.
Consider patients cultural beliefs and individual attitudes in formulating therapy.
o
Goal is to reduce overall cardiovascular risk factors and control BP by the least intrusive means possible.
Follow-up monitoring of the BP is very important.
o
Health History
o Medications
o BP consistently >140 mm Hg
o Functional health patterns
o Presence or absence of target organ damage and CVD
o
Lifestyle Modifications
o Dietary changes
o Limitation of alcohol intake
o Regular physical activity
o Avoidance of tobacco use
o Stress management
o
Nutritional Therapy
o Sodium restriction
o Diet rich in vegetables, fruit, and non-fat dairy products
o Calorie restriction if overweight
o
o
Drug Therapy
o Reduce systemic vascular resistance (SVR)
o Decrease volume of circulating blood
ACE inhibitors and angiotensin-receptor blockers (ARBs) are not given together!
o Diuretics
o Adrenergic inhibitors
o Direct vasodilators
o Angiotensin inhibitors
o Calcium channel blockers
o
Drug Therapy and Patient Teaching
o Identify, report, and minimize side effects
o Achieve and maintain the individually determined target BP
o Understand and implement the therapeutic plan
o Experience minimal or no side effects of therapy
o
o Ambulatory BP Monitoring (ABPM)
It is when patients will be given the tools required to measure their blood pressure at home as they may get the white coat
syndrome.
o
o Hypertension in Older Persons
More than two-thirds of people over 65 have hypertension.
This population has the lowest rates of BP control.
Treatment, including those with isolated systolic hypertension, should follow same principles outlined for general care of
hypertension.
o
25
o Hypertension Minority Populations

In general, treatment similar for all demographic groups.
Socioeconomic factors and lifestyle are important barriers to BP control.
Prevalence and severity of HTN increased in non-Caucasian population.
o
o Hypertensive Crisis
Severe, abrupt elevation in BP.
The rate of in BP is more important than the absolute value.
In patients with a history of HTN who have failed to comply with medications or who have been under-medicated.
o
o Hypertensive Crisis Clinical Manifestations
Hypertensive encephalopathy
Renal insufficiency
Heart failure
Pulmonary edema
Diaphoresis
o
o Hypertensive Crisis Nursing and Collaborative Management
Hospitalization
o IV drug therapy
o Monitor cardiac and renal function
o Neurologic checks
o Determine cause
o Education to avoid future crises
o
O
CASE STUDY HEMODYNAMICS
o
Joan is a lively 78-year-old Aboriginal woman who comes to your clinic for a follow-up visit. She was diagnosed with
HTN 2 months ago and was started on HCTZ 25 mg 4x/day. She stopped taking the pills as they made her dizzy and she
had to keep getting up at night to void. Her mother died from a CVA at age 70. Father died from MI at 67. Brother alivehas CAD, DM, and HTN. Initial vitals were BP: 160/102, P: 78, RR: 16, T: 37.
o
1) What is going on with Joan?
Her BP is high.
2) What clinical manifestations is she exhibiting?
Hypertension.
3) What should you do immediately? For discharge? Follow-up?
o
o
26

o
Unit 5: Pain Theory and Assessment
o Pain
Pain is one of the major reasons people seek health care.
Nurses have a central role in pain assessment and management.
o
o Nursing Roles
Assessing pain and communicating this information to other health care providers.
Ensuring the initiation of adequate pain relief measures.
Evaluating the effectiveness of these interventions.
o
o Magnitude of the Pain Problem
o Do not memorize numbers for test.
11-12% of Canadians aged 12 and over report moderates to severe pain interfering with ADLs.
Although 90% of cancer pain can be controlled, 40-80% of patients with cancer report moderate to severe pain.
50% of the elderly living in the community experience pain.
70% of the elderly living in personal care homes experience pain.
o
o Pain in Children
Headache (H/A) prevalence by:
o Age 7: 37-51%
o Age 7-15: 57-82%
Chronic knee pain: 11.3% boys, 12.6% girls
Fibromyalgia age 9 12: 57 per 100,000
Jaw pain 0.2 12%
o
o Patient Related Barriers to Pain Control
Belief that pain cannot be relieved.
Not wanted to be a complainer.
Not wanting to distract doctors from treating the illness.
Fear of addiction.
Fear of tolerance.
Fear of side effects.
o
o Health Care Provider Related Barriers to Pain Control
Pain relief is not seen as a treatment goal.
Inadequate or non-existent pain assessment due to lack of knowledge/skills.
Under-treatment.
Fear of addiction, sedation, respiration, depression, and other opioid side-effects.
Perceptual differences between patient and provider.
o
o Definition of Pain
Whatever the person experiencing the pain says it is, existing wherever the person says it does (McCaffery 1968).
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such
damage (International Association for the Study of Pain).
o Description of Pain
Subjective experience.
Patients experience and self-report is essential if possible.
Affected by culture, meaning of situation, individual factors.
o
o Pain & Cultural Influences
Culture influences expression and perception of pain.
Beliefs/attitudes affect how one interprets, perceives, and responds to injury/illness.
Pain may have a personal meaning influenced by culture.
Pain is under-estimated in minorities!
27
o It is very likely that a nurse will not treat their pain adequately.
o
o Nociception vs. Suffering
Suffering can occur independently of tissue damage.
o
o Nociception
Nociception is the activation of the primary afferent nerves with peripheral terminals (free nerve endings) that respond differently
to noxious (tissue-damaging) stimuli.
Nociceptors function primarily to sense and transmit pain signals.
o
o Suffering
State of severe distress associated with events that threaten the intactness of the person.
Pain is not synonymous with suffering.
o E.g., you can treat some pain with opioids, but you cannot treat suffering with opioids.
Suffering can occur in the presence or absence of pain.
Pain can also occur with or without suffering.
o
o Total Pain
Pain is a MULTI-DIMENSIONAL experience.
Need to consider all factors, not just physical. Other kinds of pain are nociceptive, somatic, visceral, neuropathic, behavioural,
sensory, cognitive, psychological.
o
These dimensions are
important!
o Dimensions of Pain Sensory
The sensory component of pain is the recognition of the sensation as painful.
Sensory-pain elements include:
o Pattern (i.e., location)
o Area (i.e., radiation)
o Intensity (e.g., pain scale; what is it now; what is the best it ever gets; what is the worst it ever gets)
o Nature (what does it feel like: this is very subjective is it aching, dull, burning, sharp, etc.)
Electricity: burning, shooting, tingling, etc.
o This could be from neuropathic pain, which requires a different set of medications than those required to deal with
visceral or somatic pain.
o
o Dimensions of Pain Affective
The affective component of pain refers to the emotional responses to the pain experience.
o Anger, fear, depression, anxiety, etc.
Someone who is very nervous and anxious will not deal with the pain as well as someone who is not.
o
o Dimensions of Pain Behavioural
The behavioural component of pain refers to the observable actions used to express or control the pain.
o Facial expressions such as grimacing
o Posturing
o A person adjusts their daily physical and social activities in response to pain
o
o Dimensions of Pain Cognitive
The cognitive component of pain refers to beliefs, attitudes, memories, and meaning attributed to pain.
Cognitions influence the ways in which a person responds to the pain and must be incorporated into the comprehensive treatment
plan.
This is different from the affective perspective.
o E.g. of a person who had a hip tumour that was cured. Should they get hip pain there in the future, that pain will be a lot
more anxiety provoking than that same pain in a person who never had the experience of the hip tumour.
Meaning of the situation! This cognitive element cannot be treated with opioids.
o
o Dimensions of Pain Sociocultural
The sociocultural dimension of pain encompasses factors such as demographics, support systems, social roles, and culture.
Age, gender, and education have been found to influence pain beliefs and coping strategies.
28
o
o Classification of Pain
According to its underlying pathology:
o Nociceptive pain physical
o Neuropathic pain electrical
Another way to classify pain:
o Acute
o Chronic
o
o Nociceptive Pain
Caused by damage to somatic or visceral tissue.
o Pain from a surgical incision.
o Arthritis.
o Cardiac ischemia.
Usually responsive to non-opioids as well as opioids.
o
o Somatic Pain
Aching or throbbing pain that is well localized.
Arises from bone, joint, muscle, skin, or connective tissue.
o
o Visceral Pain
May result from stimuli such as tumor involvement or obstruction.
Arises from internal organs such as the intestine and bladder.
o
o Neuropathic Pain
It is caused by damage or compression to nerve cells, or changes in spinal cord processing.
Described as burning, shooting, stabbing, or other terms that are electric in nature.
It can be sudden, intense, short-lived, or lingering.
It is not well controlled by opioid analgesics alone.
Treatment often includes the use of adjuvant analgaesics, including tricyclic antidepressants, anti-convulsants. By adding these
drugs, you can often decrease the opioid dose.
It can be centrally (e.g., fibromyalgia) or peripherally (e.g., shingles) generated.
E.g., shingles
o There is ongoing pathology in the nerve root.
o
o Acute and Chronic Pain
o Differences based on:
Causes
Course (acute pain has a shorter course; chronic pain lasts longer)
Manifestation
Treatment
o
o Acute Pain
Protective mechanism.
Informs of malfunction in the body.
Usually due to tissue damage.
Prevents further damage by limiting movement in injured area.
Time-limited: resolves when damage heals.
Even if severe, often tolerable b/c it is temporary (think of the process of labour).
As a nurse try get the patients mind on other things (e.g., walking about and moving other limbs if at all possible).
o
Sudden onset.
<3 months or as long as it takes for normal healing to occur.
Mild-to-severe pain (recall that this is subjective).
Generally can identify a precipitating event or illness (e.g., surgery).
o
29
Course of pain over time and goes away as recovery occurs.

Treatment includes analgesics for symptom control and treatment of the underlying cause.
o
Manifestations reflect sympathetic nervous system (recall fight or flight) activation:
o heart rate
o respiratory rate
o blood pressure
Pain control with eventual elimination is treatment goal.
o
o Chronic Pain
Multi-dimensional, complex phenomenon.
o Not that acute pain is not, it is just not around long enough to cause issues.
Chronic pain can be disabling
Often due to tissue damage (e.g., arthritis), but not always.
Can affect every aspect of individuals life.
Can become a condition in and of itself.
Autonomic/behavioural adaptation.
Lasts at least one month beyond the usual course of an acute disease or beyond a reasonable time for an injury to heal.
Unlike acute pain, chronic pain is not typically associated with a change in vital signs.
o
Gradual or sudden onset.
>3 month duration; may start as acute injury (e.g., back injury) or event but continues past the normal recovery time.
May not know cause of pain.
o
Typically pain does not go away; characterized by periods of waxing and waning.
Mostly behavioural manifestations:
o physical movement/activity.
With some chronic pain, for instance back pain, it is important to promote exercise. This may not be well
received by patients but it is in fact a great way to help recover.
o Fatigue.
o Withdrawal from others and social interaction.
o
Can be disabling and is often accompanied by anxiety and depression.
Treatment goals:
o Pain control to the extent possible.
o Focus on enhancing function and quality of life.
o
o Pain Assessment
o General Principles
Listen and trust
o This is difficult because what you see and what you hear does not always match. It is however, important to trust your
patient. They will in return trust you.
Use the total pain concept.
o Ensure you incorporate all aspects of pain.
Use measurement tools individually (e.g., faces, dolls, etc.).
Use open-ended questions and avoid leading questions (e.g., are you in pain?) unless necessary.
o E.g., is it burning or is it dull.
Recognize and observe signs of chronic pain (e.g., anxiety, pain, depression).
Pain is the 5th vital sign.
o
o Goals
Describe the patients key components when experiencing pain:
o Sensory
o Affective
o Behavioral
o Cognitive
30
o Sociocultural
o
o Pain Treatment
Exercise is a great way for people to deal with back pain.
All pain treatment is guide by the same underlying principles:
1. The patient must always be believed.
2. Every patient deserves adequate pain management.
3. Treatment must be based on the patients goals (these goals must be realistic).
4. Treatment plans should use a combination of drug and non-drug therapies.
5. A multidisciplinary approach is necessary to address all dimensions of pain (e.g., nurses, physicians, Chaplin, etc.).
6. All therapies must be evaluated to ensure they are meeting a patients goals.
If drugs have been administered, it is vital to return to see how they are coping.
7. Drug side effects must be prevented and/or managed.
8. Patient and family teaching should be a cornerstone to the treatment plan.s
o
o Unit 6: Care of the Client with Chronic Pain both Adult and Child
o Myths about Pain in the Elderly
Pain is a natural consequence of aging. FALSE
Pain perception/sensitivity decreases with age. FALSE
Potential side effects of narcotics make them too dangerous to use in the elderly. FALSE
o Administer low doses and take it from there. The half-life is longer but that is no reason not to give them any.
Pain is a symptom of depression. FALSE
o Depression is sometimes a symptom of pain.
Narcotics are totally inappropriate for all patients with chronic non-malignant pain. FALSE
o
o Myths about Pain in Children
Newborn /infants dont feel pain due to immature nervous system. FALSE
o The opposite is in fact the case (i.e., they feel more pain).
Infants dont remember pain. FALSE
Children cry out of fear not pain. FALSE
Children need to learn to tolerate a little pain. FALSE
Children can become addicted; therefore its best not to expose them to strong opioids. FALSE
o
o Pain in the Elderly
Chronic pain often results in:
o Depression
o Sleep disturbances
o mobility
o health care utilization
o Physical and social role dysfunctions
Pain assessment tools may need to be adapted for the older adults:
o Vertical scales are better than horizontal.
o Most elders prefer using words be sure you both understand what they mean.
o Body outline draw or point to pain.
o Faces if non-English speaking or illiterate.
o Colour scale darkest color most painful.
o
o Pain Assessment in Children
Pre-verbal children
o It is important to listen to the family. The parents know their child best, ask them questions.
Differentiating anxiety/fear/pain
Health care providers knowledge deficit in pain assessment of children
o Again, the parents are a great source of information.
Presence of other symptoms
Role of parents/family members
Frequent or chronic uncontrolled pain: learned helplessness
31
o
o Nursing Role Regarding Pain Management
Nurses are responsible for:
o Identifying the problem of inadequate pain management.
o Initial and ongoing assessment, communicate to colleagues.
o Develop plan of care with measurable goals and effective interventions.
o Implementing and coordinating pain management plan.
o Evaluating patient response & revising plan as needed.
o
o Nurses as Advocates
Pain must be recognized.
Nurse needs courage to be present.
Nurse must be ready to engage.
Nurse must be more empathetic than judgmental!
Nurse must be willing to educate self beyond nursing school education.
o
o Drug Therapy
Nursing role
o Obtain analgesic history
Ask them which medications they have taken in the last 24 hours.
When people have a migraine, they often have decreased gut motility, which will affect the drugs onset.
Differentiate between side-effects and allergies! For instance, nausea and constipation are side-effects of
morphine, not allergies.
Codeine: it is a pro-drug that metabolizes to morphine.
It is possible to be allergic to codeine but be able to take morphine. It is not possible to be allergic to
morphine and be able to take codeine. Some Asians lack the enzyme that breaks codeine down to
morphine.
o Codeine morphine
o 1/3 of Ethiopians and 1% of Caucasians are rapid metabolizers of codeine. This means that when
given codeine, their bodies will turn it into large amounts of morphine.
Opioid abusers have an altered threshold as their nervous system is shot.
o Opioid-induced neurtoxicity.
o Opioid-induced hyperalgesia: these people will require less drug!
o The cytochrome P450 pathway is used by codeine to turn into morphine.
o
o Paxil (an SSRI: anti-depressant) is a serious inhibitor of the Cytochrome P450 pathway! Many SSRIs will
inhibit the P450 pathway but Paxil is the strongest of the SSRIs. With that being said, a patient taking Paxil
and codeine (e.g., T3), they will not have any benefits of codeine as it will not get turned into morphine due to
the Cytochrome P450 pathway inactivation.
o
o Calculating equianalgesic dose
o Scheduling analgesic doses
o Titrating opioids
o Selecting from the prescribed analgesic drugs
o Monitoring and managing medication side effects
o Evaluating effectiveness of pain medication!
o Analgesic History
All medications used in past 24 hours.
PRN or scheduled use?
Current medications onset, duration, maximal analgesia.
Side effects, drug allergies, or phobias (i.e., many people are afraid to become addicted).
o
o Adjuvant Analgesic Therapy
Antidepressants
o Recall that they are also good to relieve headaches.
Anti-seizure agents
2-Adrenergic agonists
32
o These are not are commonly used.

Corticosteroids
o They are potent anti-inflammatory.
o Prednisone is anti-inflammatory.
Local anesthetics
o Some are used transdermally to relieve discomfort.
o
o Administration Routes
Opioids and other analgesic agents can be delivered via many routes:
o Oral
This is the preferred way. Not all patients are able to swallow, so other routes are used.
o Sublingual and buccal
Lipophilic drugs are typically placed sublingually.
o Intranasal
It is not as common but can be used.
Some medications can be placed intranasally to treat migraines.
o Rectal
It was quite common 20 years ago but it being used less frequently.
o Transdermal
The patches are great for certain patients (e.g., patients on stable, chronic pain) and deadly for others (e.g.,
children should never be given patches are the doses are too high; patients with acute pain should never get
patches; and for opioid-naive patients, that is, patients who have never used opioids).
Image 1
There is a rate-limiting membrane. To increase the rate, you must increase the SA. The medication
takes roughly 12-36 hours to reach the blood stream which is why it is not for acute pain. It takes 17
hours for the blood concentration to drop in half. With that said, if you realize that the dose is not
good, when you take the patch off, there is still medication subcutaneously that will enter the
bloodstream.
o Parenteral routes
These are commonly used.
o Intraspinal delivery
These are sometimes used (e.g., sometimes anginal pain; epidural in palliative care).
o Patient-controlled analgesia (PCA)
It is not nurse controlled. A nurse pushing the button is not allowed. The reason being that when the patient
gets too sedated, they will not be able to push the button.
This flexibility allows the health care provider to:
o Target a particular anatomic source of the pain.
o Achieve therapeutic blood levels rapidly.
o Avoid certain side effects.
o Provide analgesia to patients who are unable to swallow.
Fentanyl appears to have less constipation as a side-effect and can be used transdermally.
o
o Surgical Therapies
Nerve blocks
o Used to reduce pain by interrupting transmission of nociceptive input.
o Neural blockade with local anesthetics is sometimes used for perioperative pain.
o For intractable chronic pain when conservative therapies fail.
Performed for severe pain that is unresponsive to all other therapies.
Neurosurgical interventions for pain encompass 3 groups of procedures:
1. Implantation of drug-infusion systems
2. Neuroablation
3. Neuroaugmentation
o
o Non-Pharmacologic Therapy
Can reduce the dose of an analgesic required to control pain and thereby minimize side effects of drug therapy.
Some strategies are believed to alter ascending nociceptive input or stimulate descending pain modulation mechanisms.
Physical pain relief strategies:
o Acupuncture
33

This is good for pain and for nausea.
Application of heat and cold
They change the way the pain impulse is transmitted (partly through gaiting). Also, adding heat vasodilates the
vessels.
o Exercise!!
This has been shown to be very effective for many things, including pain relief.
Patients with disc problems can greatly benefit from exercise.
Sitting around and resting is therapeutic for very few things.
Exercise appears to reset the nervous system.
o Massage
Multiple mechanisms:
Release endorphins, loosen muscles, gait control, etc.
The problem here is the cost.
o Percutaneous electrical nerve stimulation (PENS)
Competes with the painful stimulus.
o Transcutaneous electrical nerve stimulation (TENS)
o Vibration
o Cognitive therapies:
Distraction
Hypnosis
There have been some instances where people have undergone elbow surgery, hip replacements, etc.
with hypnosis being the sole method of pain relief.
The brain is a powerful tool! If you use a thermostat as an analogy, if you can turn something up (e.g.,
your anxiety), you also have the power to turn it down!
Patients must be motivated! As a nurse, try turn negative instances into positive ones.
Placebos are very useful.
Imagery
Relaxation
Music
Humour
Cognitive Behaviour therapy (CBT)
o
o Pharmacologic Management of Pain
World Health Organization Analgesic Ladder
Principles:
o By the ladder
If someone comes in with extreme pain, you would not use Tylenol but rather a stronger drug (i.e., start higher
up on the ladder).
o By the clock
o By mouth
WHO Analgesic Ladder
o Step 1: non-opioids (NSAIDs, Tylenol)
o Step 2: weak opioids ( T3s, oxycodeine)
o Step 3: strong opioids (morphine, demerol, fentynal, dilaudid)
o All steps: appropriate adjunctive agents
o Demerol
It is NOT recommended for chronic pain.
Short half-life (i.e., 2 hours).
It is a poor analgesic.
Toxic metabolite: normeperidine
Normeperidine
o Long half-life (24-36 hours)
o It is NOT reversible with naloxone (i.e., Narcan)
o It can cause seizures
Should not use for >2 days or more than 600 mg/24 hours.
o
34

o
Any longer and you may develop seizures from normeperidine toxicity. Using Narcan will not reverse the pain as it will
only release the Demerol from the receptors, therefore increasing the number of available receptors for the
normeperidine.
o Equianalgesia
Lack of knowledge of this is a common reason for under or over medication of patients.
Analgesics have different per mg potencies: 10 mg Drug X not necessarily equal to 10 mg Drug Y.
Need to know drug equivalence to properly assess efficacy/side effects when changing to different analgesic.
o In general, 10mg of Dilaudid = 50-75 mg of Morphine (i.e., Dilaudid is 5-7.5x stronger than Morphine).
Incomplete cross-tolerance: decrease dose by 25-50% when switching to a different medication.
o
o Dose Scheduling
Around the clock (ATC) or as needed (PRN).
PREVENTION is the key.
o ATC meds for constant pain.
o Give PRN meds as soon as pain starts (i.e., intermittent pain).
o Less analgesic is needed if the preventative approach is used.
Need to tech patients the importance of prevention.
The breakthrough dose is roughly 10% of the daily dose (e.g., if their daily dose is 100mg of a drug, the breakthrough dose is
10mg).
o
o Opioid Titration
Need to give enough medication to have the desired effect with the least side effects (i.e., the right dose).
May need to change route, interval, dose, or drug to get that effect. In general:
o If still in pain likely under-medicated
o If very sedated may be over-medicated
o If in pain but sedated possible wrong drug for patient
Nurse says The patient states he is in pain but he sleeps all day...this is a possible instance of this.
o If relief is adequate but not lasting inadequate frequency or dose
o
o Drug Selection
Patients will often have a range of medication or more than one analgesic ordered.
o It is not necessary to have a large drug list on the Kardex (e.g., Dilaudid, Morphine, T3, and percoset).
Tylenol #3 i-ii tabs q4-6h prn
How to decide which one to use:
o WHO ladder
o Use drug appropriate for pain
o
o Route Selection
PO route usually preferable.
Avoid IM route as there is variable absorption, and can cause scar tissue.
Sub-lingual: some meds absorbed via this route.
Transdermal fentanyl.
Peak concentration 24-72 hours after application.
Concentration decreases by 50% in 17 hours after removal.
o
o
o What is NOT an Analgesic
Pherergan (promethazine)
Valium (diazepam)
Ativan (lorazepam)
o
o All will increase sedation without enhancing analgesia.
o
o Pharmacotherapy in the Elderly
Increased sensitivity to analgesics due to age-related changes that alter absorption, metabolism, distribution, and excretion of
drugs.
35
More likely to have relief from lower doses and side-effects from higher doses.
No one drug is preferable.
START LOW and GO SLOW!
o
o Pharmacotherapy in Children
Should be managed as aggressively as in adults.
Use basic pain management principles.
Can be more difficult to assess pain and side effects.
Codeine in kids turns into morphine afterr being metaolized in the liver. Serious adverse effects. Genetically determined how
fast of a drug metabolizer you are. Variability in how one handles the drug. 1 in 10 people wont enjoy any benfits from codeine.
30% failure rate in Ethiopians. Important to ask if they have taken it before and what happened.
o
o Nursing and Collaborative Management
Effective Communication
o Patients need to feel confident that their reporting of pain will be believed and will not be perceived as complaining.
o The nurse needs to communicate concern and assure the patient that he or she is committed to helping the patient.
o If pt goals are not realistic, need to discuss honestly and compassionately.
o
o Addiction APS, AAPM, ASAM, 2001
It is a primary (its own entity), chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing
its development and manifestations.
It is not continuously asking for medications.
It is a primary, chronic disease of the brain reward, motivation, meemory and related to circuitry,
Dysfunction in these circuits leads to charisteristic biological, psychological, social and spiritual manifestations.
This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviouds.
o
o Characterized by the 4 Cs
Addiction is characterized by behaviours that include one or more of the following:
o Impaired control over drug use
o Compulsive use
o Continued use despite harm
o Craving
o
o Addiction
Craving a drug at escalating doses despite physical, psychological, and social consequences.
Pre-occupation with obtaining & using a substance, the use of which results in decreased quality of life.
NOT defined by symptoms of withdrawal ALONE.
Withholding opioid analgesics from chemically dependent patients with pain has NEVER been shown to increase the likelihood
of recovery from addiction. McCaffery
o
o
36
o Tolerance Definitions APS, AAPM, ASAM, 2001

It is a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drugs
effects over time.
o
o Tolerance
Occurs with chronic exposure to a variety of drugs
Can happen with analgesic effect, relatively rare.
Happens with side effects (respiratory, nausea).
Develops faster with IV vs. PO meds
Increased need for analgesia is usually d/t disease progression.
May have more tolerance with history of abuse.
Approaches to managing tolerance
o the dose of the analgesic.
o Substitute another drug in same class.
o Add a drug from a different drug class to augment pain relief without side effects.
o
o Physical Dependence (APS, AAPM, ASAM, 2001)
It is a state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt
cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist.
o E.g., if you have taken prednisone for 30 days, you cannot simply stop it as the prednisone stops your endogenous
steroids. Abrupt cessation will cause you body to go in shock.
Physical Dependence
Physical dependence is an expected physiologic response to ongoing exposure to pharmacologic agents that is manifested by a
withdrawal syndrome that occurs when blood levels of the drug are abruptly
o
o Signs and Symptoms Opioid Withdrawal
First 24 hours
o Restlessness, restless sleep, rhinorrhea, dilated pupils
24-72 hours
o Twitching, muscle spasms, severe aches (back, abdomen. Legs)
o N/V, diarrhea, severe sneezing, cold like symptoms (Sx)
o Increase in all VS
o
o Pseudo-Addiction Syndrome
Patients attempt to obtain adequate analgesia is misunderstood as abnormal drug-seeking behaviour (Fuchs & Gamsa, 1997, p.
103).
Difference from true addiction: drug-seeking behaviour ceases when adequate analgesia obtained.
o
o Special Populations Patients with Substance Abuse Problems
Have the right to receive effective pain management.
Comprehensive pain assessment is imperative, including a detailed history, physical examination, psychosocial assessment, and
diagnostic workup to determine the cause of pain.
Goal of the pain assessment is to facilitate the establishment of a treatment plan that will relieve the individuals pain, as well as
prevent and minimize withdrawal symptoms.
Usually requires a multidisciplinary team approach.
Talk to addict.
Acknowledge addiction.
Deal with it by:
o Give Rx for 1 week not 6 months (i.e., short intervals).
o Give long acting medications.
o Use the patch (recall that they are good for patients with chronic pain).
Some patients use the patch if many different ways.
o
o Team/Collaborative Approach
Common goals
o Agreement on comfort/function goals for pain relief.
Common knowledge
37
Common language
o Pain rating scale, standardized tools.
Regular communication
Being honest with the patient.
o
o Ongoing, Consistent Evaluation
Monitoring the 4 As:
1. Analgesia (is there pain relief)
The problem is that deception is an inherent problem of addiction.
2. ADL (psychosocial functioning)
3. Adverse effects
When they come to the clinic/hospital, are they excessively sedated?
4. Aberrant drug taking behaviour
o
o Pain & Quality of Life: A Challenge
Talk to someone with chronic pain about:
o What quality of life means to them.
o How pain affects quality of life (QOL) for them and their family.
o How would life be different if they had no pain?
o
38

o
Unit 7: Clients with Rheumatic Disorders
o How to All these Conditions Mesh Together?

They are all connective tissue disorders.
o
O
ARTHRITIS
o Arthritis in General
There are >100 types of arthritis.
Arthritis = problems with the joints
o Leading cause of disability.
o 3 out of 5 Manitobans have arthritis.
o 600,000 Canadians cant work due to arthritis.
o
o Rheumatoid Arthritis (RA)
A chronic, systemic (i.e., it is not only in the joints) disease characterized by inflammation of connective tissue in the synovial
joints (i.e., joints containing fluid).
Must be able to distinguish between OA and RA.
o
o Etiology and Pathophysiology
Cause of RA is unknown.
Should blame EBV because causes abnormal IGG
Autoimmune etiology (i.e., the body is attacking itself and it does not stop; it may begin by attacking an antigen but once that
antigen is gone it turns to the bodys cell) is currently the most widely accepted.
Genetic Factors
o Genetic predisposition appears to be important in the development of RA, although a particular chromosome has yet to
be detected.
o Women get it and its generational
Because of the Human Leukocyte Antigen (HLA)
Autoimmunity
o Changes begin when a susceptible host experiences an initial immune response to an antigen.
o Joint changes from chronic inflammation begin when the hypertrophied synovial membrane invades the
surrounding tissues.
The neutrophils are the first cells to arrive at a site of tissue damage.
o Pannus (i.e., a highly vascular tissue) forms within the joint. This prevents the joint from being able to bend or move
freely (i.e., it has taken up space and shortens the ligaments).
o
o Clinical Manifestations Joints
Onset of RA is typically insidious (i.e., slow and gradual).
Non-specific manifestations may precede the onset of arthritic complaints.
o E.g., low grade fevers, stiffness in the morning, etc.
Stages:
1. Synovial inflammation
2. Continued inflammation
3. Destruction of bone and cartilage
At this point you will be able to notice RA on an X-ray (it will not be seen in stages 1 and 2, meaning that Xrays are not good for the early detection of RA).
At this point you have the spreading into other tissues.
4. Fibrous tissue formation
o
Joint symptoms occur symmetrically (unlike OA) and frequently.
o Small joints of the hands and feet.
o Larger peripheral joints (e.g., jaw issues leading to difficulties eating).
o Cervical spine.
Specific articular involvement (but recall that it is systemic).
o Pain
o Stiffness (particularly after periods of inactivity, for instance, sleeping)
This typically last 1 hour.
39

o
Limitation of motion
Caused by the Pannus
Signs of inflammation
o
o
o Extra-articular Manifestations of RA
o Fig. 66-5 Image of woman
Every single system is affected (we will cover 3 of them).
Carpal tunnel syndrome
o This is because the nodules formed will take up space.
o
o Clinical Manifestations Extra-articular Manifestations
Three most common:
1. Rheumatoid nodules
They get bigger due to extravasation and will eventually decrease in size. They are typically not removed
(unless they cause extreme pain or are likely to open up).
Rheumatoid factors: autoimmune disease (meaning that the body produces antibodies)
o If the rheumatoid factor is high, 25% of people will develop nodules, which grow everywhere
(including the heart, cervical spine, any organ, the throat, etc.). These nodules can open up, causing
extreme pain.
2. Sjgren syndrome
10-15% of people with RA will develop this syndrome.
It can happen as a disease itself but often comes as a complication of RA. They have burning, gritty eyes,
decreased tearing, and photosensitivity.
Some anti-inflammatory drugs will cause the same signs and symptoms seen in Sjgren syndrome.
3. Felty syndrome
This is the worst case scenario of rheumatoid nodules. They are everywhere in your major organs.
o
o Complications
Flexion contractures and hand deformities seen in the joints.
Nodular myositis (i.e., the nodules are growing in the muscles) and consequently muscle fibre degeneration.
o
o Deformities of RA
o A ulnar drift
o B Boutrier
o C Hallus valgus (different from a bunion as there is less bone)
o D Swann neck
o
o Complications
Cataract development and loss of vision.
Rheumatoid nodules can ulcerate, similar to pressure ulcers.
Hoarseness.
Bone destruction from nodules in the vertebral bodies.
Cardiopulmonary effects later in the disease.
Carpal tunnel syndrome.
o
o Diagnostic Studies
Accurate diagnosis essential because you want to start treatment as early as possible
Positive Rheumatoid Factor (RF), which are antibodies, in 80% of patients
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
o An elevated ESR is a sign of inflammation somewhere in the body (recall that this is characteristic of RA systemic).
o CRP responds to inflammation.
o
o Nursing Management
Goals are that the patient with RA will:
o Have satisfactory pain relief (look at this first).
o Have minimal loss of functional ability of the affected joints.
o Participate in planning and carrying out the therapeutic regimen.
o Maintain a positive self-image.
40
o Perform self-care to maximum amount possible.

o
o Collaborative Care Drug Therapy
Choice of drug depends on:
o Disease activity
o Patients level of function
o Lifestyle considerations
Cornerstone of RA treatment is pain relief.
Salicylates (e.g., aspirine), NSAIDS (e.g., ibuprofen, naproxene), Corticosteroids (they reduce inflammation; e.g., prednisone),
Immunosuppressants, Synvisc (its like getting a lube job in the synovial joints).
o Prednisone is an immunosuppressant which makes the patient more likely to get an infection that will go undetected as
the fever and other such immune responses will not be seen (e.g., an elderly man with a fever of 36 may rise to 36.7 if he
is taking corticosteroids).
Disease-modifying antirheumatic drugs (DMARDs).
o Potential to lessen the permanent effects of RA.
o These are anti-inflammatory drugs.
o COX-2 inhibitors (e.g., Celebrex, Viox which is no longer used as it causes heart attacks).
Celebrex has many side-effects but it is still used: weigh out the pros and cons.
Gold-therapy
o Gold is injected into the joints q3-4months.
Anti-malarial drugs (q6-12months)
o Side effects will adversely affect the liver.
o They may also give you psychotic illusions.
o
o Nursing Implementation Acute Intervention
Comprehensive program to meet goals
o Drug therapy
o Rest
o Joint protection (i.e., immobilize the joint, but not for >48 hours)
o Heat and cold applications
With an injury use cold first (in order to slow vasodilation) and heat after the first 24 hours.
o Exercise
The heat reduces stiffness.
o Patient and family teaching
There are many drugs going on and it is chronic.
o
o
41
o Osteoarthritis
Non-inflammatory disorder of the synovial joints (different from RA).
Slowly progressive.
More than 90% of adults are affected by age 40.
It occurs from damage to the cartilage.
Before 50 years, men are more likely to get OA. After 50 years, women are more likely to get OA due to menopause (i.e., in
bone mass and oestrogen levels).
o
Bodys attempts at repair cannot keep up with destruction (i.e., homeostasis becomes inadequate).
There are continued changes in collagen structure (its supposed to be white, soft, etc.) fissuring (at the level of the
chondrocytes) and erosion (the cartilage is not as pliable and it becomes yellow).
Central cartilage becomes thinner.
Cartilage and bony growth (osteophytes) increase at the joint margins (this causes the pain).
o During assessment you would feel crepitus.
o
o Clinical Manifestations
No systemic manifestations (unlike RA). There may still be heat, swelling, and other such signs of inflammation, but it is
localized within the joint in question.
Joint pain.
Most commonly involved joints:
o Distal interphalangeal (DIP)
o Proximal interphalangeal (PIP)
o Carpometacarpal joint of the thumb
o Weight-bearing joints (hips, knees)
o Metatarsophalangeal (MTP)
o Cervical and lower lumbar vertebrae
Deformity
o OA can also have nodules, like RA, only these nodes are painful (unlike RA, where the nodules are painless). As in RA,
these nodes are not typically removed.
o Heberdens nodes
DIP joints
o Bouchards nodes
Red and painful
PIP joints
o
Bone scan
CT
MRI
X-ray
o This is because there is a problem with the cartilage and the bone.
ESR
o Localized ESR.
CBC
o Interested in the WBC count (due to synovitis).
o
o Collaborative Care
No cure.
Pain and inflammation management.
o Cortisone joint injections.
Prevent disability.
Maintain and improve joint function.
Drug Therapy
o Based on the severity of symptoms.
Mild anangelsics can cause more damage
o
42
o
o iClicker Questions
o To preserve function and the ability to perform activities of daily living, the nurse teaches the client with OA to:
a. Plan less stressful ways to accomplish ADLs.
o
o Naproxene, indomethacin, and ibuprofen are in the same family of drugs.
o
o Gout
Metabolic disorder of purine (protein) metabolism.
It is very painful and typically hurts the big toe.
o
Primary Gout
o Hereditary error: the body cannot metabolize the purine.
Secondary Gout
o Acquired disorder: too much meat and alcohol.
There are high levels of uric acid (i.e., an overproduction or the body cannot excrete it).
Acute gout: 1 joint affected
Chronic gout: up to 4 joints affected
o
o Complications
Pain
Joint deformity
TOPHI
o Formation of uric acid. If you cant excrete uric acid, it comes together to form crystals which are deposited in the big
toe. It can also ulcerate which may lead to infection.
Kidney stones
o Which may lead to pylonephritis.
o
o Pharmacology
Anti-inflammatory agents
o Ibuprofen, aspirin, acetaminophen.
The TOPHI is not supposed to be in the joints so the body will try fight it off.
Uricosuric Drugs
o Allopurinol.
It blocks the production of uric acid.
o Probenecid.
Anti-gout that increases uric acid excretion.
Antibiotics increase the synthesis of uric acid so Probenecid is sometimes used before the antibiotics are given
to ensure their half-life is extended.
o
o Nutrition
Limit red meat (e.g., sardines, muscles, moose).
Limit alcohol.
o
o Nursing Care
Immobilize the joint in question (for no more than a week for any joint!).
Avoid pain.
ROM exercises after the joint has been immobilized for no more than a week.
Lots of fluids for kidney stones
o
o Systemic Lupus Erythematosus
Chronic multisystem inflammatory disease.
Associated with abnormalities of immune system (i.e., autoimmune issues).
o Involves the lymphocytes (e.g., B cells and T cells).
Affects skin, joints, serous membranes, and renal, hematologic, and neurologic systems.
Africans, Natives & Asians are 3x more likely to get it than Caucasians.
o It is typically seen in women of childbearing age.
43

o

Etiology is unknown.
Most probable causes:
o Genetic influence
o Hormones
o Environmental factors
o Certain medications
Onset occurs after onset of menarche.
Autoimmune reactions directed against constituents of cell nucleus, DNA.
Antibody response related to B and T cell hyperactivity.
o The DNA is harmed as it is the target of this illness. New skin cells created are different from the old cells.
The skin tends to be tough.
o
o Multisystem Involvement of SLE
It is everywhere!
o E.g., endocarditis, myocarditis, pleural effusions, etc., etc.
o
No specific test.
SLE is diagnosed primarily on a distinct criteria relating to patient history, physical examination, and laboratory findings.
o It often takes years before a diagnosis is done.
o
o Nursing Management/Nursing Implementation
Acute Intervention
o Pain is the main issue.
o Want to be vigilant for bleeding as all the basement membranes are weakened.
o Monitor weight (intake and output) as the kidneys may be infected.
o Monitor for lethargy.
o Drugs:
Anti-malarial, immunosuppressants.
Ambulatory and Home Care
o Every system is affected because we are dealing with connective tissue.
o Taking the medication does not mean it is going to be relieved
o They tend to have a butterfly rash.
o Lupus is exacerbated by the sun.
Lupus and pregnancy
o It is rare but people with lupus who get pregnant may have a child with neonatal lupus (this is extremely painful for the
child).
Psychosocial Issues
o
o Unit 8: Paediatric Client with Upper Respiratory Disorders
o Objectives
Growth and Development of the Paediatric Upper Airway
o Implications for:
Pathogenesis
Assessment
Nursing care
Describe the etiology, pathogenesis, clinical manifestations, therapeutic and nursing management for:
o Tonsillitis
o Otitis media
o Nasopharyngitis
o Pharyngitis
o Bronchiolitis
Croup
o Differentiate the major types
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o Etiology
o Clinical manifestations
o Therapeutic/nursing management
o Paediatric Upper Airway Differences
Smaller airways.
o Small amounts of secretions can block off the airway.
Smaller nasopharynx.
Rapidly growing lymph tissue.
Smaller nares.
Small oral cavity/large tongue.
High larynx and glottis.
Immature thyroid/cricoid and tracheal cartilage.
o This makes it easier to collapse.
Narrowest part of airway at cricoid cartilage (funnel shaped). Older child is vocal cords.
Underdeveloped respiratory muscles.
o They often use their abdominal muscles when breathing.
Upper A/W compliant, may narrow during inspiration.
Longer epiglottis.
Shorter trachea.
A/W increases in size and length after birth.
Steeper right mainstem bronchus.
Obligate nose breathers (for the first 4 weeks of life).
o Secretions in the nose make it hard to breathe. These patients will have their noses suctioned.
Chest wall more pliable.
Diaphragm primary chief muscle of inspiration.
o
o Why is this important?
Edema increases airway resistance 15X that of adult.
Proper positioning can open an airway.
o E.g., back rolls will be used when the child is lying down as this will force their airways open.
A paediatric airway can be quickly lost.
o
o Effects of Edema
o
o
o Why is this Important?
The primary type of arrest in children is respiratory arrest, often associated with loss of an airway.
Early recognition and treatment is essential.
Nurses are often the first to assess the paediatric patient.
Airway is the A in ABCs of Basic Life Support.
o
o Paediatric Respiratory Assessment
Never force a child to lie down.
Assess in the position they have chosen.
o Children often like to be in their parents lap. If theyre comfortable in their position, let them stay as such. Trying to
move them may cause them to get agitated and cause their airways to become closed off.
Care should be take with throat cultures or visual inspection
Keep with parent do not remove them from their parent.
45
Goal: to keep child calm!!!

History:
o Family Hx asthma, allergy, respiratory illnesses
o Previous wheezing episodes
o Environmental smoking
o Recent illness
o Medications to treat upper respiratory symptoms
General appearance-looks good/looks bad.
Work of breathing (WOB)
o Is there indrawing? Nasal flaring? Etc.
RR fast vs. slow
o
Age (PALS) o
Breaths per
minute
o
Infant <1 yr
o
30-60
o
Toddler 1-3
o
24-40
yrs
o
Preschool 4o
22-34
5 yrs
o
School age
o
13-30
6-12 yrs
o
Adolescent
o
12-16
13-18
o
Chest assessment/auscultation
Colour (check from centrally and peripherally)
Cough (e.g., sharp, deep, coarse, bark-like, etc.)
Behaviour changes
o It is important to document these changes.
Breathing pattern
o Apnea >20 sec. is dangerous.
Drooling
o They often drool because they cannot swallow
their secretions.
Quality of voice/cry
Able to speak in full sentence
Position of child
Weight loss or gain
Chest pain
Vomiting
o When they cough often and hard, the vomiting
reflex is triggered.
Poor appetite or feeding
Sleeping patterns
General Signs of Upper Airway Obstruction

Tachypnea (this is often accompanied with an increase in HR)
Increase respiratory effort
Change in voice
Stridor
o This is characteristic of upper airway obstructions (wheezing is a characteristic of a lower obstruction).
Poor chest rise
Poor air entry on auscultation
cyanosis
Tonsillitis
Etiology
Viral (causes most cases): Herpes simplex, Epstein-Barr, Cytomegalovirus, Adenovirus, and the Measles virus
Bacterial: Streptococcus pyogenes is the cause for most bacterial tonsillitis
Pathogenesis
Infection/inflammation of palatine tonsils.
Clinical Manifestations
Frequent throat infections
Breathing /swallowing difficulties
Fever/headache
Ear pain
Redness +/- white patches to anterior pillars
Enlargement of cervical lymph nodes
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Offensive mouth odour

Impaired sense of taste/smell
Persistent cough
Therapeutic Management
Diagnosis is based on clinical manifestations and visual inspection.
Antibiotics usually Penicillin.
Treatment: symptomatic (i.e., treatment of the symptoms).
Nursing Management
Symptomatic
Acetaminophen
Cool fluids/popsicle/soft foods
o Use cool to decrease inflammation.
Salt water gargle
o The Na+ helps draw fluid out of the tonsilar beds.
Rest
Teach to take all antibiotics
Surgical Intervention
Removal of the tonsils.
o >3 years of age
3 infection/year X 3 years
Chronic tonsillitis
Obstructive sleep apnea
Malformation
+/- adenoids (pharyngeal tonsils)
Post-op Nursing Management

Check for signs active bleeding (ooze, frank blood, frequency swallow)
TPR with sats
Check pulse and respirations q2h for two hours then q8h
BP, pulse and respirations if any signs of active bleeding and notify MD
Document fluid intake and ensure adequate fluid intake
o This is to keep the tonsil beds moist (i.e., they become more painful when dry).
Ice collar
Discharge
Pain management (e.g., Tylenol)
Fluid intake (e.g., cold fluids or soft food)
Activity restrictions
Complications
Follow-up appointment
Children are at a higher risk for bleeding 7-10 days following surgery.
Nasopharyngitis
Etiology
The common cold.
Most common illness of infancy and childhood.
Viral causes: rhinovirus and coronavirus.
Bacterial: streptococcus.
Pathogenesis
Pathogens spread when infected person touches hand of uninfected person.
Incubation 1-3 days.
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Symptoms
Lethargy/irritability
Poor feeding/no appetite
Fever
Sneezing
Nasal discharge
Headache
Dry irritated throat
Nursing Management
Symptomatic
Saline drops to nares of infants/suctioning
Humidifiers
Antipyretics
Decongestants over 6 months of age
Antihistamines
Encourage adequate fluid intake
Rest
Pharyngitis
Etiology
80% Viral: cause is a large number of enteroviruses
Bacterial: Strep. throat (group A beta-hemolytic Streptococcus)
Diagnosed with a throat swab (it is important to swab the entire throat, i.e., both sides).
Pathogenesis
Infection of pharynx +/- tonsils
Usually 4-7 year olds rare <1 year
Onset abrupt
Sore throat
Difficulty swallowing
Fever >38.3C
Headache
Tonsillar exudate +/ Abdominal pain
Tender nodes
Penicillin
Erythromycin (if allergic to penicillin)
If drooling or dehydrated need to be seen by MD emergently
Nursing Management
Symptomatic
Antibiotics bacterial (Pennicillin)
Acetaminophen
Cool fluids/popsicle
Salt water gargle
Rest
Teach to take all antibiotics
Otitis Media
Etiology
48
Unknown
Related to eustachian tube dysfunction (typically because its blocked)
May be related to upper respiratory infection
75-95% all children by 6 years of age will have had an ear infection.
Boys typically get it more than girls
Bacterial: streptococcus pneumoniae, Haemophilus influenzae, moraxella catarrhalis
Highest in winter months due to the increase in upper respiratory tract infections.
Pathogenesis
Infection
Mucous membranes of eustachian tubes edematous
Air flow blocked, causing fluid to accumulate
Fluid pulled into air space
Medium for pathogens
Tympanic membrane and fluid infected
Tympanic membrane: red/bulging/retracted
Ear pulling
Fever
Hearing loss
Irritability
Ear popping
Rupture of TM
Diagnosis based on otoscopic exam.
Antibiotics: Amoxicillin, Clavulin, Cefuroxime
Antibiotic use is controversial because it may be due to a viral upper respiratory tract infection.
Surgical Intervention
Children with bil. middle ear effusion and hearing deficiency > 20 decibels for >3 months
Myringotomy with
Typanostomy tube (T-tubes)
o Recommend ear plugs if going swimming.
Nursing Management
Centers on care of child at home
Antibiotics should see improvement in 24 hrs.
Prevention
Analgesia
Chew gum
Lie on unaffected side
Warm cloth
Bronchiolitis
Etiology
Viral: RSV respiratory syncytial virus (most common), Adenovirus
Bacterial
Most frequently in toddlers and preschoolers
Most severe if <6 months
< 2 months often hospitalized
Winter months - early spring
75-90% of PICU admissions
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2010-2011 Brionchiolitis Statistics
106 admissions
19 patients required PICU
9 admissions <28 days of age
44 admissions 1-6 months of age
23 admissions 6-12 months of age
30 admissions >1 year of age
52 admissions were from outside of Winnipeg
Factors Increasing Risk of RSV

Premature birth
Chronic illness/disease
o Chronic lung disease
o Haemodynamically significant CHD
o Cystic fibrosis or pulmonary hypoplasia
o Down syndrome
o Neuromuscular disease
o Severe immune compromise
Males
Low birth weight for gestational age
Young chronological age (<12 weeks the start of RSV season)
Enrolled in daycare
Presence of pre-school or school age children
Not breastfeeding
Exposure to tobacco smoke
Family history without eczema
Pathogenesis
Viruses invade bronchiole cells (lower respiratory tract)
Virus bursts Cell debris in airway
Edema from inflammatory process
Airway produces excessive mucous
Above causes obstruction of airways and diffusion impairment
Repeated in both lungs
Blocked airway stops expulsion of air, which leads to the wheezing/crackles
Air trapped below prevents normal gas exchange O2 less CO2 more
Respiratory failure
The virus can live on hospital gowns for up to 2 hours, 20-30 minutes on skin, and 6-7 hours on surfaces.
Nasal stuffiness
Cough
Fever
As progresses:
Wheeze
Deeper cough
Increased WOB (e.g., trach tugging, nasal flaring,
indrawing, etc.)
o Their respiratory rate may be in the 70s, 80s, 90s.
Off feeds
Bad cold
Immunization (Palivizumab) for high risk patients (it is a short risk immunization that is to be given monthly).
Isolation for all suspected cases.
See Bronchiloitis Order Sheet and Clinical Scoring tool.
Manitoba RSV Prophylaxis Eligibility Criteria

Premature infants <33 weeks gestational age and <6 months preceding start of RSV season.
<24 months of age with chronic lung disease (i.e., BPD bipulmonary displasia) and who have received oxygen therapy within 6
months preceding RSV season.
50
<24 months of age with hemodynamically significant heart disease as assessed by paediatric cardiology.
Infants born 33-35 weeks gestational age and are living in or will reside in remote Northern communities
Other children <24 months of age may be considered on individual basis (e.g.,Respirology, infectious diseases, cardiology,
genetics, or haematology/oncology).
Other infants born 33-35 weeks gestational age deemed to be at high risk for hospitalization for RSV:
o Born November 2010 to March 2011
o Male
o Small for gestational age (BW<10th percentile)
o Patient or sibling attends daycare
o >5 people living in the home
o 2 or more smokers in household
Vaccines do not necessarily mean that the child will not get any health issues. It does, however mean that the severity will be
decreased.
2011 Bronchiolitis Management

Trial of inhaled L-epinephrine should be initiated.
L-epi effective may be ordered as a prn.
o Hypertonic saline may be considered within first 24-28 hours scheduled q8hrs. Should be stopped after 48 hours
CAUTION: Asthma (as this will cause bronchospasms).
This is controversial.
Score child pre- and post-masks.
Supplemental oxygen (only if O2 sat is <89%)

o Goal to keep room air saturations >89%
o Frequency of oxygen saturations
Do not give the child nasal prongs as they are nasal breathers.
2L via nasal prongs in an infant is equivalent to CPAP. The pressure is too high.
Chest X-rays only if:
o <2 months of age
o Needing cardio respiratory monitoring and or continuous oximetry
o Requiring PICU admission
Nasal Suctioning
o <3 months of age
o >3 months of age prn basis
Droplet and Contact Isolation
o Glover, mask, gown.
Not recommended:
o Blood, urine and CSF cultures.
o IV antibiotics for non-toxic vigorous infants with a diagnosis of viral bronchiolitis.
o Systemic or inhaled steroids.
Measures to Reduce RSV Transmission In Hospital

Hand hygiene before and after.
Gloves, gowns, and masks.
Identify all persons with respiratory illness in outpatient areas.
Isolate or cohort with cold symptoms even if there are no positive results.
Screen/test for RSV.
Disinfect surfaces, including toys and books.
Measures to Reduce RSV Transmission In Home

Hand hygiene before and after.
Frequently wash childrens clothes, bedding, and toys.
Keep children away from crowded area and those who are sick, if parents are sick, minimize close contact with children (avoid
kissing).
Encourage and support breastfeeding.
Croup
51
Broad classification of upper airway illness.

Swelling of epiglottis and larynx.
Extends into trachea and bronchi.
Viral (most likely) or bacterial.
Children 6 months-5 years.
Late fall early spring.
Viral: spasmodic laryngitis, laryngotracheitis, laryngotrachoebronchitis.
Bacterial: bacterial tracheitis,epiglottitis.
Acute Spasmodic Laryngitis

Suspected viral
Afebrile
Mild respiratory distress
Barking-seal cough
3 months-3years
Least serious
Laryngotracheitis
Parainfluenza I or II, RSV, influenza
T <39C
Hoarseness
Barking-seal cough
Sore throat
Stridor
Progresses to laboured respirations
Most common
Laryngotracheobronchitis
parainfluenza I or II, RSV, influenza
T <39C
Hoarseness
Barking-seal cough
Sore throat
Stridor
Progresses to laboured respirations, increasing stridor, cyanosis
Most serious if untreated
Bacterial Tracheitis
Staphylococcus
Fever>39C
Barking-seal cough
Stridor
Purulent secretions
Guarded prognosis requires close observation
L-epinephrine
Dexamethasone
Antibiotics as appropriate (bacterial)
Cool air (i.e., open a window in the house, go for a car ride with the windows down, get a cool air humidifier)
Nursing Management
Frequent airway assessment due to the inflammation
Humidified O2 as tolerated
52
Administer antibiotics as ordered

Dont separate from family
Epiglottitis
H-flu (incidence less since vaccine introduced)
Fever>39C
Preceded by URTI (upper respiratory tract infection)
Intense sore throat
Drooling
Stridor
Increase HR and RR
Prefers sitting upright
Medical Emergency
o This is because the inflamed epiglottis can cause an obstruction.
o Looking at a lateral neck X-ray, you will see the characteristic thumb print of the swollen epiglottis.
Management
o Intubation
o Sedation
o IV fluids
o Antibiotics
o Cast arms when intubated so they will not try rip them out
Videos
RSV Patients
RSV and pertussis.
Unit 9: Clients with Altered Endocrine Function
Exam Information
Know the information that relates to the objections outlined in the syllabus.
Lecture Plan
Introduction and Review of Endocrine System
Care of the client with thyroid and parathyroid dysfunction
Care of the client with imbalances of hormones produced by the adrenal cortex
Care of the client with endocrine disorders characterized by excess and deficits in fluid volume
Endocrine System Review

It is a regulatory and secretory system. Endocrine glands secrete hormones directly into the bloodstream (different from
exocrine).
Synthesis and Release

Two reasons:
1. Physiologic change
The body is always trying to get back to homeostasis following physiologic changes (e.g., stress, temperature
changes, etc.)
2. Alterations in plasma concentration
If you have high levels of Na+, aldosterone will not be secreted.
Most common trigger:
o Negative feedback loop.
High levels of a particular hormone will cause inhibition of secretion. Oxytocin functions as a positive
feedback loop (i.e., oxytocin will continue to be secreted until the object is secreted).
Feedback Mechanism
Hypothalamus:
Releasing hormone
53
Anterior pituitary:
Stimulating hormones
Target endocrine gland:

Hormone
Effect!
Thyroid
When palpating for the thyroid, stand behind them, have their head turned to the side and swallow. In a healthy individual you
should not feel the thyroid.
It regulates metabolism. It produces T4 (thyroxine), T3 (triiodothyronine), and calcitonin. The measure is three T4 and TSH
levels. T3 is very potent and is not present in as large of quantities. These levels are important because it is important to
determine if a patient has primary or secondary thyroidism.
Hypothyroidism
Etiology and Pathophysiology
Iodine deficiency.
o Iodine is required for the thyroid gland to synthesize T3 and T4. Salt has been iodized but the reason there is deficiency is
because people are changing their lifestyles in the following ways:
Vegetarians do not consume meat and therefore consume soy as their protein. Soy blocks the uptake of iodine.
Atrophy is the end result of Hashimotos thyroiditis and Graves disease.
o These are autoimmune diseases.
Other reasons:
o Iatrogenic
Hyperthyroidism was treated and hypothyroidism was the result.
o Surgery
T4 is required for metabolism therefore hypothyroidism can lead to weight gain. This lack of metabolism will also lead to
lethargy.
Cardiovascular System
o There will be a decrease in CO so the body will compensate with an HR. A continuous increase in HR can lead to
cardiac hypertrophy. If a patient has cardiac hypertrophy, we may hear S4 sounds, murmurs.
o Decreased cardiac contractility.
o LDL levels because your metabolism has decreased, causing your cholesterol to stay in the body.
o Red blood cells are created every 120 days. If the body does not have the energy, these patients are likely to be anaemic.
Respiratory System
o breathing capacity.
GI System
o Slowed GI motility, leading to constipation (and thus a distended abdomen because the impacted feces are causing fluid
retention.
o Weight gain because the food energy you are consuming is not being used to help expel waste so it is accumulating.
Integumentary System
54
o The skin is going to be dry, thick, and cold (people with hypothyroidism always feel cold).
o The nails are brittle, the hair is going to be sparse because the body does not have the energy to make it.
Musculoskeletal System
o Slow reflexes, muscle aches and pain, fatigue, and slowed movement. Tired, can hardly move, slow, no energy,
extremely fatigued.
Nervous System
o The nervous system slows down (e.g., decreased neuron firing) leading to slowed speech and thought processes. If it
progresses without treatment, the patient may end up in a stupor or coma.
Reproductive System
o Infertility, amenorrhea, decreased libido.
Other:
o Increased risk of infection as the entire body has slowed, meaning that the neutrophils, considering they have even been
made, will take longer to get to the site of infection.
o These patients are highly sensitive to narcotics and sedatives. This is because the body is not excreting them and they are
staying in the body.
o High cholesterol not burning it constipated cant move/excrete it
o Anemic not making cells (red blood cells gone after 120 days)
Myxedema Coma
o If untreated, patients may end up in myxedema coma.
o Accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues. These polysaccharides attract water
from the intravascular space and the blood pressure drops. Hypovolemic!
o It is an emergency because there is a decrease in blood flow to the brain.
If you see this in a patient, give the patient oxygen!
Diagnostic Studies
Laboratory tests that measure TSH and free T4.
o Values correlated with symptoms confirm diagnosis.
Free T4
TSH Primary
The gland is not responding.
Free T4
TSH Secondary
The gland is not the problem here.
Other Tests:
o Elevated cholesterol.
o Goiter (which occurs as a compensative mechanism).
You will notice that goiter is a sign of body hypo- and hyperthyroidism.
Nursing Management/Nursing Assessment

Health History
What relevant information do you want to know to r/o hypothyroidism?
o Family history.
o Genetics.
o Are they from a country in which iodine intake is low?
Acute Intervention (i.e., myxedema coma)
o Airway (ABCs)
o Hormone replacement therapy (i.e., IV thyroxine).
o L-thyroxine which has to be taken daily for the rest of your life.
Hyperthyroidism
A sustained increase in synthesis and release of thyroid hormones by thyroid gland. Catabolism (breaking down) and building
again.
Common form is Graves disease.
Groiter with hypo or hyper compensation creates more tissue (same thing but different reasons).
You make antibodies that act autoimmune thyroid enlarges and you make more thyroxine.
Exophthamlmos big white protruding eyes that push them forward. All you see is white and they cant close them.
Free T4
TSH Secondary
The problem is outside of the gland.
Free T4
TSH Primary
The problem is the gland.
Other causes:
o Thyroiditis
55

o
o
o
o
Nodular goitre
Exogenous iodine excess
Pituitary tumors
Thyroid cancer

Graves' disease
o Autoimmune disease of unknown etiology.
It is normally initiated by a virus, which turns on the immune response. The problem here is that the immune
response never turns off and begins attacking the body once the virus is gone.
o Diffuse thyroid enlargement and excessive thyroid hormone secretion.
Cardiovascular system
o CO which will lead to systolic hypertension. This will also lead to murmurs, arrhythmias (as the contractility is not
strong enough), an increase in -adrenergic receptors (causing an increase sensitivity in catecholamine), and distant heart
sounds.
o The symptoms will be similar to hypothyroidism but for different reasons.
Exophthalmos
o Eyeballs forced outward and protrude.
o Impaired drainage from orbit, increasing fat and edema in retroorbital tissues which stretches the ligaments, causing the
eyes to push outward.
o Corneal surfaces become dry and irritated. (eye drops to help)(lot of white hyperthyroidism)
GI system
o Diarrhoea.
K+ levels will be high.
o appetite (with no associated weight gain).
*Although the elderly with hyperthyroidism have anorexia.
o thirst (as there is a lot of energy being made).
o Weight loss.
o Hepatomegaly (large liver) and splenomegaly (large spleen).
RBCs get broken down in the liver. With an increase in RBCs comes an increase in liver function.
The spleen stores both red and white blood cells. With the increase in metabolic rate due to the increase in T 4,
the body is making a lot more RBCs and WBCs and storing them in the spleen.
Integumentary system
o The skin will be warm and moist. The nails will be brittle and the hair will be sparse as the excess energy is going to
other things than hair and nail growth.
Musculoskeletal system
o Fatigue from continuously moving and trying to burn energy
o Muscle weakness
Nervous system
o Everything is being processed quicker. Your thoughts, movements, etc. all occur quicker and dont stop.
o Fine tremors
o Insomnia, phychotic
o Lability of mood, delirium
Reproductive system
o Menstrual irregularities
o Amenorrhea
o Decreased libido (by the time you think of it, the feeling is gone)
o Impotence
Other Clinical Manifestations
o Intolerance to heat
o Increased sensitivity to stimulant drugs
o Elevated basal temperature
Complications Thyrotoxic Crisis/Thyroid Storm/Thyroid Toxicosis

Acute, rare condition where all manifestations are heightened.
Life-threatening emergency/death rare when treatment initiated.
56
This may occur because:

o Patients stopped taking their medications.
o They may have hyperthyroidism that was not diagnosed.
o They may have fear.
Manifestations include:
o Restlessness
o Agitation
o Seizures
o Abdominal pain (this is due to the K+ levels)
o Nausea/vomiting/diarrhoea (this is due to the K+ levels)
o Coma
Treatment and therapy

o Reduce thyroid hormone levels and clinical manifestations.
o Therapy aimed at fever reduction, fluid replacement, and management of stressors.
Diagnostic Studies
Laboratory findings for TSH and free thyroxine.
Radioactive iodine uptake is indicated to differentiate Graves' disease from other forms of thyroiditis.
o Radioactive iodine is going to burn cells off. Not only is it used to differentiate between the two, it is used to treat
hyperthyroidism.
Collaborative Care
Drug Therapy
o Antithyroid drugs PTU and Tapazole
o Iodine
By giving exogenous iodine, the negative feedback mechanism will tell the gland to stop creating endogenous
iodine. Treatment is radioactive for non-pregnant adults in a storm or crisis. Blocks synthesis of thyroxine. Ptu
will stop conversion between T3s and T4s (more numerous). Short term tx is to give some excess iodine.
o -adrenergic blockers (e.g., Propanolol)
You want to decrease the HR.
o Radioactive Iodine Therapy (RAI)
The amount required is based on trial and error. By giving too much you risk killing all the thyroid cells,
essentially giving the patient hypothyroidism. Burnt out thyroid iotrogenic now you have hypothyroidism
now.
Surgical Therapy
o Subtotal thyroidectomy involves removal of significant portion of thyroid.
These patients will have high levels of thyroxin in the blood for ~72 hours following surgery.
Nutritional Therapy
o High-calorie may be ordered for hunger and prevention of tissue breakdown.
o Protein allowance 1-2 g/kg ideal body weight.
o Avoid caffeine, highly seasoned foods, and high-fibre foods (this will worsen the patients diarrhoea)(sensative to these
foods/stimulants).
Nursing Management/Nursing Assessment

Health History
What information do you need to know to r/o hyperthyroidism?
Objective Data
o Agitation, mood, phychosis
o Hyperthermia (the high temperatures may kill cells)
o Enlarged or nodular thyroid gland
o Eyelid retraction (this will cause dry eyes which may lead to corneal abrasions)
o Diaphoretic skin (patient may lose 2-3L of fluid/hr)
Acute thyrotoxicosis (thyroid storm)
o Administer medications (levothyroxine, citha)
o Monitoring cardiac arrhythmias
o Ensuring adequate oxygenation and IV fluids
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Monitor hormone (TSH, T4) balance periodically
Reduce caloric intake to prevent weight gain
Must know they will be hypothyroid for the rest of their life.
Avoid goitrogens (these are foods that can precipitate a hyperthyroid crisis)
E.g., sardines, strawberries, peanut shells.
TSH will be up if it is the gland. If it is not the gland the levels will be down.
o
o
o
o
Parathyroid Review
There are 4 pea-sized glands located around the thyroid gland. The secrete PTH (parathyroid hormone) which regulates Ca 2+ and
PO32-. When PTH is increase, it increases calcium levels by:
Control calcium and phosphorous (have an inverse relationship like sodium and potassium)
o Taking the calcium from the bones or gut (after activating vitamin D).
o Causes increased reabsorption from the kidneys. (may cause kidney stones)
o Synthesizes Vitamin D
Calcium stops the transport of Na+ during an action potential and assists in nerve impulses. Calcium is for muscle contraction.
Doesnt take part in the reaction but must be present. Issues with clotting.
Beta Blocker or Calcium Channel blocker difference?
PTH says calcium is low so PTH is secreted once calcium is normal so the PTH stops.
Hyperparathyroidism
Problems with calcium and phosphorus.
o levels of calcium in the body, therefore low phosphorus levels in the body (recall that they are inversely proportional).
Causes:
Most common benign tumour in one of the glands.
o Primary: Disorder of calcium, phosphate, and bone metabolism 80%
Problems with bone metabolism.
o Secondary: Vitamin D deficiencies, electrolyte deficiencies, chronic renal failure (CRF) hyperphosphatemia
o Tertiary: Hyperplasia and loss of negative feedback from circulating Calcium (compensatory response)
The problem with the feedback system is that it does not shut off.
Cardiovascular
Too much calcium = disrhythmias
Hypertensive too many particles and same amount of fluid (move fluid from second space into first space (IS
into first space)
Gastrointestinal
N and V, diarrhea to constipation, cells getting dyhydration (they shrink and potassium is coming out so K+
is rising in first space so you will get nausea and vomiting and then abdominal pain).
o More common in women 30-70 years. Peak 60-70 years.
Bones
o Osteoporosis as the calcium is being pulled out.
Kidney
o Kidney stones. Polyurea due to increased glomular filtration so you will pee more and your first space fluid goes down
and we pull from second space and cycles. (gotta start an IV once it goes through the kidneys they are going to excrete
it).
Neuromuscular
o Muscle weakness as the muscle is over-contracting. Abnormal gait, psychosis bc you are conducting too quickly.
GI
o Constipation, loss of appetite.
Severe
o Gastric ulcers, pancreatitis, cardiac changes (e.g., dysrhythmias) and renal failure.
Symptoms
Moans, groans, stones, and bones.
It is insiduous, meaning that it will develop over time.
Diagnosis
Excess serum Calcium.
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Low serum phosphorus.

Radioimmununoassay of parathyroid hormone show an increased level of PTH.
Increased alkaline phosphatase
Increased uric acid
Increased creatinine amylase
Treatment
Focus on symptom management.
Prevention of complications.
Close monitoring.
Pharmacologic:
o Calciumemtic agents Plicamycin (lowers the calcium levels within 48 hours)
o Biphosphonates (Fosamax)
Puts calcium back into the bones in order to prevent people from getting fractures.
It does not treat hyperparathyroidism as the PTH is still being secreted.
o Estrogen/progestin
Given to those with osteoporosis as it puts calcium back into the bones.
Surgical one or all glands (if you take them out we will have iotrogenic hypoparathyroidism)
Increase phosphate levels within the body in order to decrease calcium levels.
Hypoparathyroidism
Cause
Primarily iatrogenic (i.e., treatment of hyperparathyroidism).
Pseudohypoparathyroidism (genetic usually).
Acute symptoms: muscle cramps (due to low calcium levels)
o Sudden hypocalcaemia leads to tetany.
o Hyperkalcemia breathing from a paper bag breathe in CO2 will help short term.
Treatment
Normalize Ca2+ levels by administering calcium with Vitamin D. PTH expensive and IM so not convenient.
Mild treatment: breathe in a paper bag in order to CO2 levels, thus making the bodys internal conditions acidic. Recall that
acidosis prevents calcium from binding to albumin.
Administering a patient with synthetic PTH is not typically done because it is expensive and must be injected.
Question
If a client has hyperparathyroidism, the nurse should:
Encourage a daily intake of 4,000mL of fluid to flush out the calcium thus preventing kidney stone formation.
The nurse should NEVER encourage a patient to decrease their intake of calcium. The calcium is being taken from the bones
which may lead to osteoporosis.
Urine output go to bathroom in the morning diuretic from alcohol dehydrated

ADH secreted
Adrenal Disorders
There are two adrenal glands located on top of the kidneys.
There are two parts to the kidneys:
1. Adrenal medulla
epinephrine and norepinephrine
2. Adrenal cortex
Produces corticosteroids:
o Glucocorticoids
o Mineralcorticoids
o Androgens
Endogenous Corticosteroids (meaning inside)

Corticotropin releasing hormone
(hypothalamus)
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Corticotropin/ACTH
Corticosteroids
(adrenocorticoptropic hormone) (anterior pituitary)
(adrenal glands)
Corticosteroids
Main functions:
o Glucocorticoids
Main glucocorticoid: cortisol
Function: stress hormone that increases blood glucose levels by gluconeogenesis (i.e., formation of glucose
from a non-glucose source; supresses inflammation). Cons: suppresses immunce system, sickness.
o Mineralcorticoids
Main mineralcorticoid: aldosterone
Function: help regulate blood pressure by control sodium
High corticosteroid levels: hypertension and hyperglycaemia
Low corticosteroid levels: hypotension and hypoglycaemia
o Androgens
Increases weight gain and makes more prone to infection.
Cushing Syndrome
Caused by an excess of corticosteroids, particularly glucocorticoids (clinically).
Mot often because they received corticosteroids (using it as a treatment hydrocortisone for a number of diseases)(they end up with
Cushings).
Symptoms: Moon face, buffalo hump, weight gain (from the excess glucose stored as fat).
Most common cause:
o Iatrogenic administration of exogenous corticosteroids (e.g., hydroclorozone).
Treatment:
o Stop taking exogenous corticosteroids slowly. The reason being that when taking exogenous corticosteroids, your body
will stop making them. A sudden decrease in exogenous corticosteroids will leave the body without any (which can be
life-threatening).
85% of endogenous is due to ACTH-secreting pituitary tumour.
Other causes include adrenal tumors and ectopic ACTH production by tumors outside hypothalamic-pituitary-adrenal axis.
Common Characteristics
Weight gain and stretch marks (i.e., purple striae).
Acne (due to the excess oil; androgens, females will have more testosterone, men get female characteristics).
Moon face (from the weight gain).
Buffalo hump (fat storage).
Slow wound healing (corticosteroids suppress the immune response).
Bruising / atrophy we are stealing protein and using it for glucose.
Thinning of hair.
Diagnostic Studies
24-hour urine for free cortisol. (throw away first urine and collect everything from 6-6)
o Urine (not blood), because it gives a 24-hour pattern of how a person secretes cortisol.
o The first urine sample of the day is to be discarded and the following samples should be collected until 0700 hrs the
following morning.
Low-dose dexamethasone suppression test (give a low dose of dexamethasone at night time and draw it in the morning)
o Dexamethasone (corticosteroid)
o Will do a high dexamethasone test if the urine is borderline
o ACTH normal = fine, keeps coming or is high (problem not with the gland but outside the gland) low = normal
CT and MRI are used for tumor localization
Plasma ACTH may be low, normal, or elevated depending on problem.
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o
o
o
corticosteroids (from an exogenous source), plasma ACTH would be low because it is not secreted in the body.
If the anterior pituitary is the problem, there would be an in ACTH because the negative feedback is not working
properly.
If the problem lies outside the gland (e.g., lung), the ATCH levels could be normal.
corticosteroids
ACTH
Corticosteroids from exogenic source the negative

feedback will tell the CRH not to produce ACTH.
corticosteroids
ACTH
Anterior pituitary is the problem because it is secreting

ACTH despite the negative feedback loop telling it not to.
corticosteroids
Problem is occurring outside the glands (i.e., the lungs).
Normal ACTH
Have to give time via dose reduction or alternate days (20mg of prednisone). Drop doses each week or alternate days but cannot
be stopped abruptly.
Collaborative Care
If developed during use of corticosteroids:
o Gradual discontinuance.
o Reduction of dose.
o Conversion to alternate-day regimen.
Avoids potentially life-threatening adrenal insufficiency.
Goal is inhibition of adrenal function.
Drug therapy is indicated when surgery is contraindicated.
Mitotane (medical adrenalectomy) drug may be used, which will lower corticosteroid levels.
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Nursing Implementation
Monitor:
o VS
A client with an excess in mineralcorticoids (e.g., aldosterone) will have an increase in BP (they will be
hypertensive).
o Daily weight
Weight gain/loss related to the retention of sodium and water. In same clothes and same time of day.
o Glucose
It can increase within the body. Cortisol makes glucose from a new source expect them to be hyperglucemic. 46 usual glucose. If youre not diabetic BS should never be above 9.
Fever, swelling, redness, pain = symptoms of infection. Cortisol suppresses immune responses so they wont
appear extremely out of the norm (but it is for a Cushings Patient). want to monitor signs of infections..
o Signs and symptoms of infection
This is because corticosteroids are immunosuppressants.
o Signs and symptoms of thromboembolic phenomena
Clotting can occur due to the patient being hyperglycaemic but they are more likely to have adherence to
platelets.
Hydrocortisone iotrogenic
Emotional support
o May feel unattractive or unwanted.
Discharge instructions based on lack of endogenous corticosteroids
o Take their medications daily.
Throughout the day for glucocorticoids.
Once a day for mineralcorticoids.
o Wear a medical alert bracelet.
o Instruct them that they are at greater risk of infection.
o Must increase glucocorticoids when under periods of stress (so the body can respond to this stress).
Addisons Disease
Adrenocortical insufficiency from a primary cause.
Main reason a person gets Addisons disease is from autoimmunity.
o The gland itself is not secreting corticosteroids.
Other causes:
o TB (rare cases)
o Infarction
o Fungal infections
o AIDS
o Metastatic cancer
o Iatrogenic Addisons
Insidious onset.
o Progressive weakness, fatigue, weight loss, anorexia are primary features. (Primary in the gland, secondary outside of the
gland)
o Skin hyperpigmentation (high levels of ACTH secreted instead of other corticosteroids in its place)
Areas exposed to sun.
Pressure joints.
Over joints.
In creases of the body.
The effects of aldosterone will cause the following: (all low)
o Hypotension
o Hyponatremia
o Hyperkalemia
Acidosis because the K+ holds on to H+ and is unable to enter the cell.
o N/V
Due to hyperkalemia.
o Diarrhoea
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Due to hyperkalemia.
Cramping from the N and V and diarrhoea.
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Complications
Risk for life-threatening crisis caused by insufficient adrenocortical hormones or sudden, sharp decrease in these hormones.
o Triggered by stress following withdrawal of corticosteroid replacement therapy. Cannot respond to stress will go into
shock.
Severe manifestations of glucocorticoid and mineralocorticoid deficiencies
o Can lead to shock
o Circulatory collapse (due to the severely low BP)
o Clinical manifestations: hypotension, tachycardia, hypovolemia, pale, cyanosis, arrhythmias, dehydration,
hypoglycaemia, confusion, sweating, shakiness.
Primary
corticosteroids
ACTH
Gland is not working properly, ACTH to try fix the problem.

Hyperpigmentation of the skin is seen.
Secondary
corticosteroids
ACTH
ACTH increases with the hormones are down and are not secreted when hormones are up.
ACTH test without Addison the corticosteroid should go up if they dont go up there is a problem in the gland.
Diagnostic Studies
Subnormal levels of cortisol or levels fail to rise over basal levels with ACTH stimulation test.
o Indicate primary adrenal disease.
o Positive response to ACTH stimulation indicates functioning adrenal gland.
Abnormal lab findings:
o Hyperkalemia
o Hypochloremia
o Hyponatremia
o Hypoglycemia
o Anemia
o BUN
Indicates kidney failure because of low BP, low volume, glomerular filtration rate, blood flow to the
kidneys, and therefore signs of kidney failure. Hypotensive so kidneys dont diffuse.
Urine levels of cortisol are low
ECG
o Due to hyperkalemia, there is a risk for arrhythmias and an elevated T-wave. PQRS T=(repolarization) will take longer to
repolarize due to potassium
CT and MRI
o Check for tumours and cancer.
Collaborative Care
If the body is not producing the corticosteroids, they must have it administered.
o Hydrocortisone most commonly used as replacement therapy.
o Going to increase corticosteroids during a cycle fashion (three times per day) to match circadian rhythem.
Glucocorticoid dosage must be increased during times of stress to prevent Addisonian crisis.
Treatment directed at shock management.
o Isotonic fluid, put the head of the bed down.
(isotonic unless they have heart disease so NS 0.45%)
Frequent assessment (particularly BP, Temp, RR, HR, chest-CHF(no crackles) checks).
Medication
o Glucocorticoids usually given in divided doses (typically 3x per day).
Increase glucocorticoids during times of stress.
o Mineralcorticoids usually given once in the morning.
o Reflects normal circadian rhythm
Teach signs and symptoms of corticosteroid deficiency and excess and to report findings.
Instruct to wear Medic Alert bracelet at all times. (need to learn how to give themselves a hydrocortisone IM injections)
Provide handouts on medications causing increased need for glucocorticoids.
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65
Instruct on how to take BP and report findings.

Instruct to carry emergency kit with IM hydrocortisone, syringes, and instructions for use.
o Teach how to give IM injection to be used if going into stress.
ADH (Anti-diuretic Hormone)/Vasopressin
Hypothalamus
Senses serum osmolarity

Posterior Pituitary
Secretes ADH
Stimulates the reabsorption of H2O in the renal tubules

Kidney: reabsorbs fluid

serum osmolarity
Osmolarity more condesnsed particles. Increased serum osmolariy. Will act on posterior pituitary to produce increased ADH to
act on the kidney to bring back water. Norm is same particles with more fluid/water. Guess what? ADH stops. IfI bring back water
it means there is less water going out. Kidneys will do that and you will feel thirsty and it will shut off once we get enough water.
Dysfunction of ADH
Provides two extremes
o Diabetes Insipidus
o Syndrome of Inappropriate Antidiuretic Hormone Secretion-SIADH
o Normal Serum Osmolality 280-300mOsm/kg of water
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

The key is to watch Na+ levels!!
It brings fluid back because ADh is still being secreted so its going to increase ECF.
Continuous secretion of ADH
o Reabsorb fluid continuously, resulting in an increase in ECF.
What happens?
o Edema.
o Cells will rupture and there will be leaking.
o Dilutional hyponatremia (related to the dilution of solutes)
o High blood pressure
o Hypovolemia
o Symptoms relating to sodium:
Low Na+ levels so the cells keep pumping Na+ out of the cell to maintain the balance, which in turn forces K+ to
enter the cells.
Persons at risk:
o Neurological injury or damage.
o Some cancers.
Symptoms primarily related to changes in Na+ levels:
o Neurological
Increased cerebral edema; seizures; coma.
o GI
Nausea and vomiting. Diarrhea.
o GU
Low urine output and concentrated urine.
Risk
o Increased cranial pressure notice confusion first (pupillary changes are later and late)
o Seizures
o Coma
Lab test and diagnosis
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o
o
o
o
Decrease serum osmolality. (lots of fluid so osmolarity is down)

Increased urine osmolality. (little urine but concentrated
Decrease serum Na+.
Decrease haemoglobin and hematocrit. (dillutional!!)
Treatment and Nursing Care

o Underlying cause (treat)
o Severe fluid restriction (e.g., 800mL/day)
o Medications Declomycin; Butorphanol (stop the action of ADH)
o Lifestyle (reduce fluid intake)
o Medications (Samsca) inhibits the kidneys response to ADH
o Great mouth candy, gum, lip moisturizers, ice chips to lips
Aldosterone is inhibited when ADH is secreted and recycling the fluid. Sodium is not reabsorbed. New problem is sodium isnt
reabsorbed too much fluid and not enough sodium dillutional!
Diabetes Insipidus (DI)
Dying of Thirst: these patients have extremely clear urine and their bodies are losing all their fliud.
Lack of ADH.
Types and causes
o Central Neurogenic not producing ADH
o Nephrogenic kidney unresponsive to ADH
o Dispogenic/Psychogenic excessive water intake (common with schizophrenia)
Presentation Symptoms
Abrupt polyuria
Polydipsia
Dehydration
Needs a catheter way too much fluid and output.
Neurological
o Na+ levels are up related to hypernatremia. The K+ levels will therefore be low.
o If Na+ levels >160mmol/L the patient is at risk for seizures and coma.
Lab values
o Different for Primary/Psychogenic
Water deprivation test
o Used to distinguish between Central DI, Nephrogenic DI, and Dispogenic DI. The patient are instructed not to
consuming any water or smoke beginning at midnight. They are then given exogenous ADH. In a normal clients and
patients with Dispogenic DI, urine osmolality and plasma osmolality are normal after ADH administration. In clients
with Central DI, urine osmolality increases after ADH administration. In clients with Nephrogenic DI, there is little or
no response to the ADH.
o Lose 3-5% of body weight and then give ADH = if you dont have DI you should reduce less urine and osmolarity and
urine should rise. Osmolarity in urine shouldbe higher and you put out less urine. (should be more concentrated).
Treatment and Assessment

Pharmacological = DDAVP (Desmopressin Acetate) synthetic vasopressin (i.e., give the patient synthetic ADH).
Monitor VS, IandO, monitor edema, measure cerebral edema
Fluids (IV and PO)
Unit 10: Head-to-Toe Sexuality and Illness
Why do We Have to Know This?

It is a quality of life issue.
It is affected by different disease states.
Nurses provide holistic care (it is important not to overlook this aspect).
Important to patients and partners.
Someone has to ask!
o Many people are afraid to ask about this topic.
Head
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Depression
o For humans, touch is an absolutely essential need.
o Touch releases the hormone oxytocin (which is also released after birth to help the mother bond with her child). When
depressed, some people become hypersexual as their bodies want the oxytocin release. Some anti-depressant drugs (i.e.,
SSRIs) have terrible side-effects on peoples sexual health.
Substance abuse
o Mind-altering substances have the ability to make people feel sexy.
People who are high on cocaine feel horny and they just cant get enough.
People on crystal meth also feel intense desires for sex.
Head injury/Brain tumour
o People who have impaired sexual function due to a head injury will often have a change in personality (e.g., some
patients may become more demanding and also more violent with their demands).
Multiple sclerosis
o It is a neurological disease. Neurological processes are required for adequate sexual functioning.
o Some people have had sexual numbing in their genital region and later been diagnosed with MS.
Torso
Respiratory diseases (e.g., asthma, COPD)
o These may affect ones sexual function.
Cardiovascular disease
o If an otherwise healthy man in his 40s or 50s experiences erectile dysfunction, he should not take Viagra or other such
drugs. This may be a sign of cardiovascular disease (as smaller blood vessels are affected first) and blood tests should be
taken.
o Climbing two flights of stairs comfortably is the test of whether an individual is physically able to have sex.
Diabetes
o It is a disease of blood vessels and may affect ones ability to attain an erection.
Pelvis
Hysterectomy
o Blood vessels are often ruined during a hysterectomy.
Radical prostatectomy
Bowel disease (malignant or benign)
o The rectum supports the vagina during sexual intercourse. When a bowel resection has occurred, there is often less
support for the vagina, making sex more uncomfortable.
Combat Injury
Burns
Amputation
PTSD
o This is very common in individuals who have served.
o Hypervigilance, over-reactive, anxiety.
Closed brain trauma
Cancer
Childhood
Adult
Reproductive organs
All cancers
Body image; libido; hormonal changes; anatomical changes; functional changes
o 80% of cancer survivors experience sexual dysfunction, most often relating to body image (e.g., breast cancer, loss of
hair in men, breast enlargement in men).
PLISSIT Model
Permission
o Give the patient permission to talk about this.
Limited Information
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o Patients often want limited information.

Specific Suggestion
o Some patients may require a deeper level of suggestion (e.g., a man who gets chest pain upon exertion Take a whiff
of nitro beforehand to increase vasodilation).
Intensive Therapy
BETTER Model
Bring up the topic.
Explain you are concerned with quality of life issues, including sexuality.
Tell patients you will find appropriate resources to address their concerns.
Timing may not seem appropriate now, but they can ask for information or help at any time.
Educate patients about the side effects of their cancer treatment.
Record your assessment and intervention in the patient chart.
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Unit 11: Clients with Altered Glucose Homeostasis (Diabetes Mellitus)
Outline
Physiology and pathophysiology
Etiology
Classification and clinical manifestation
Diagnosis
Management
Acute complications
Chronic complications
Diabetes Mellitus
Insulin and Carbohydrate Metabolism
Its about protein and fat metabolism as well (i.e., not only carbohydrates).
Insulin
o Insulin is a hormone (i.e., small protein). It must be given via injection because its a protein and will become denatured
if swallowed (by the acid in the stomach).
o It is produced in the pancreas, specifically in the beta cells of the Islets of Langerhan.
o It is continuously secreted by the body, but greater amounts are secreted when food is consumed.
o Carrier molecule
o If I put it in the cell blood levels will go down stores in the liver and skeletal muscles as glucogen (increases
glycogen stores) (facilitated diffusion).
What are the effects of insulin on carbohydrate metabolism?
o To increase the rate of glucose metabolism.
o To decrease blood glucose concentration.
o To increase glycogen stores.
How?
o Via facilitated diffusion. It will not move glucose against a concentration gradient. Insulin helps glucose move into the
cell. Doesnt require actions but a carrier.
o Brain doesnt need it, liver doesnt need it muscle needs insulin. Brain needs available source of glucose (no other
kind). Fructose, glucose, galactose, sucrose.
Insulin and Fat Metabolism

How is insulin involved in fat metabolism?
o Promotes fatty acid synthesis by converting glucose into fatty acids (i.e., triglycerides).
o Also need to know how much protein theyre taking in.
o Triglycerides goes to the arteries and vessles anthrosclerosis (worst kind of fat) amputations and kidney disease.
Insulin and Protein Metabolism

How does insulin work in protein metabolism?
o Promotes the entry of amino acids into cells and inhibits the catabolism of protein.
o Inhibits the rate of gluconeogenesis (recall that cortisol causes gluconeogenesis).
o Inhibits cortisol
Counter Regulatory Hormones

What are the hormones that oppose the action of insulin?
o Glucagon
A hormone produced in the pancreas, specifically the alpha cells of the Islets of Langerhan.
It converts the glycogen into glucose.
Number one counter regulatory hormone (reverses hypoglycaemia)
o Epinephrine
It is very similar to glucagon, but the effect is not as strong.
Think fight vs. flight. Your body needs glucose to react.
o Cortisol
It raises blood glucose via gluconeogenesis.
o Growth hormone (Somatotropin)
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Released from the anterior pituitary.

Just think how much energy is required during a growth spurt.
Raises blood glucose levels
Somatostatin***
It inhibits insulin and glucagon! It is still considered to be a counter-regulatory hormone (despite it inhibiting
glucagon) because it inhibits insulin. Cmes from the anterior pituitary. Neither raises nor lowers.
Absence of Insulin
Results in:
o Hyperglycemia
The sugar will not enter the cells so it will accumulate in the blood.
o Lipolysis
If you cant get sugar into the cells, the body will respond by using fat for energy.
o Osmotic diuresis
The water from the ISF and cell will move into the plasma in order to balance out the extra glucose. This
increase in volume will increase the GFR, thus increasing urinary output.
This will lead to dehydration, which will lead to an increase in K+.
o Ketone bodies
This is a by-product of fat breakdown. It will also cause acidosis. This acidosis will interact with the fact that
there is an increase in K+.
Ketones in the urine imply ph is becoming more acidic 7.35-7.45. average is in the middle.
Diabetes Mellitus
Imbalance between insulin supply and demand.
It is characterized by hyperglycemia and is associated with abnormal carbohydrate, protein and fat metabolism.
Statistics
4.8% of Canadians have been diagnosed with diabetes. Many more have it but are not diagnosed.
Aboriginal people have a 3-5X higher incidence in developing Type II diabetes.
Children typically only ever had Type I diabetes, however this trend is changing due to obesity and lifestyle modifications.
o Refined foods (e.g., white flour, white bread) break down a lot faster than non-refined foods. This quick breakdown is
likely to lead to diabetes.
Risk Factors
Family history
o You cannot prove that diabetes has a gene, but family history is certainly a big factor (e.g., may be due to lifestyle).
Ethnicity
Obesity
o Especially central obesity (i.e., greater central obesity is linked with greater insulin resistance).
History of delivering infants weighing more than 9lbs.
Classification
Terms were created in 1997.
Type 1 diabetes (formerly known as insulin-dependent DM or juvenile)
Type 2 diabetes (formerly known as non-insulin dependent DM)
Gestational diabetes
Other types of glucose intolerance (e.g., Cushings syndrome, pancreatitis).
Type I Diabetes (Former Insulin-Dependent)

These people will always be on insulin and are also often young.
Etiology
Research suggests that it is an autoimmune disease.
The body is not producing any insulin.
Clinical Manifestations (3 Ps)

Polyuria
o Due to osmotic diuresis (from the hyperglycemia).
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Polydipsia
o The increase in urine volume will cause the person to be thirsty.
Polyphagia
o The cells are not getting the glucose so they keep triggering the body to consume food energy.
o Will lose weight.
Type II Diabetes
Etiology
Most prevalent. Lifestyle.
Main characteristic is insulin resistance.
Available insulin is unable to bind with cell receptor sites (very little of the insulin can bind to the receptor sites). The more fat
present, the greater the resistance of the receptors to insulin.
Blood sugar should never go above 9 (regardless of whether a meal was consumed).
Blood tests for blood sugar are in the capillaries.
Inappropriate release from the liver, the liver makes more. Glucogon works on the liver to make glucose. Adipose tissue produce
signy with prevent use of insulin.
Non-specific
o Persistent infection (e.g., yeast infections in women).
o Still produce insulin but there is a resistance.
Risk factors family hx, ethnicity, obesity (II), hx of macro infant (II), hypertension autoimmune (II), polycystic ovary
syndrome (II), acanthosis nigricans (II).
Both Type I and II Diabetes

Blurred vision
Tingling
Numbness or pain in the extremities
Slow wound healing
Diagnosis (see Appendix)

Normal fasting blood glucose is 3.8-6.1.
There are several ways a person can be diagnosed with diabetes.
1. If BS is greater than 11.1 on any given reading.
2. If BS is greater than 7 on two separate readings.
3. Glucose Tolerance Test (GTT): after fasting, you are given a sugar solution to drink and your BS is measured one and
two hours after the drink was consumed.
If it is greater than 11.1, the diagnosis of diabetes is made.
Gerontologic Considerations
Elevation of blood glucose levels appear in the 5th decade.
Management (Type I or Type II)

Main goal:
o Normalize insulin activity and blood glucose levels to reduce the development of vascular and neuropathic complications
(which occur with continuous uncontrolled BS). People do not die from diabetes; they die from the complications of
diabetes.
Components of Management
Nutrition
Exercise
Monitoring
Pharmacologic therapy
Education
To teach diet principles to help in meal planning (see Appendix).
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Diet and Weight Control

Exchange lists
o You can swap one carbohydrate for another (e.g., instead of having a bowl of porridge in the morning, have a different
source of carbohydrates).
o These lists may have different calorie values and servings depending on the patient. Portion control is important.
Food guide
Glycaemic index
o Certain foods have a higher index than others, meaning that they will spike a persons blood sugar faster than a food with
a lower index. The more a food is processed and altered, the greater the glycaemic index will be.
Other dietary concerns:
o Alcohol (provides empty calories)
o Sweeteners (makes you crave sugar), aspartame (ticks)
Exercise
Lowers blood glucose.
Improves circulation and muscle tone.
Increases resting metabolic rate.
Alters blood lipids.
Increases levels of HDLs.
Decreases total cholesterol and triglyceride levels.
Type I individuals cannot benefit from exercise unless they take insulin beforehand. It is also important that these people have a
sugar source on hand in case their BS levels drop dramatically. It should also be noted that these patients can experience a
hypoglycaemic reaction up to 48 hours following the period of exercise.
Type II individuals will benefit from exercise because it helps decrease insulin resistance. These patients who are taking
medications such as glyburide can also have a hypoglycaemic effect up to 48 hours following the exercise period. They should
also have a snack nearby.
Monitoring
Self monitoring of blood glucose requires:
o Good visual acuity
o Fine motor coordination
o Cognitive ability
o Comfort with technology
o Willingness
o Costs (the machines are free but the strips are very expensive)
Glycosylated Haemoglobin (Haemoglobin A)

(A1C) every 3 months
o It can give you the average of what someones blood glucose has been for the past 3 months (i.e., red blood cells are
destroyed every 120 days).
o This test is a way of determining if a patient is telling you the truth.
o This is also used to determine what actions will be taken regarding treatment.
o You would not expect a diabetic to have a fasting BS level of 6.1.
Urine Testing for Glucose

Used before self-monitoring was established.
Less expensive and not invasive.
Whats the difficulty?

Its not immediate (i.e., the treatment cannot be based on the value obtained because it has gone through the kidneys).
Medications will interfere with the results (e.g., aspirin, Vitamin C).
Urine Testing for Ketones

It is displaying lipolysis in a patient with Type I.
A person with Type II diabetes displaying ketones is indicating starvation.
The Atkins diet would cause people to have ketone bodies, which would make their environment more acidic.
73
Complications and breaking fats and becoming acidis and will go into diabetic acidosis (regular person means they are starving).
Pharmacological Therapy Type 1

Need exogenous insulin to be administered.
Appendix for Insulin and Actions!!!!
o Know the names, actions, categories, how long they will last, and when they start to work!
The more often insulin is given, the less likely complications will occur.
The Goal of Insulin Therapy

To mimic the normal pattern of insulin secretion as closely as possible in response to food intake and activity patterns.
Complications of Insulin
1) Local allergic reaction
Due to lipolysis. That is why we have intrasite and other such rotations.
74

2) Systemic allergic reactions (rare)
An anaphylactic response to the synthetic insulin is very rare.
Reactions to animal insulin are more common than synthetic insulin. For that reason, pork and beef insulin are no longer
used.
3) Insulin Resistance
Some patients may require 300 units in order to decrease their glucose.
4) Somogyi phenomena
Hyperglycaemic in am.
Typically around 0200-0300hrs, the person becomes hypoglycaemic. This will then lead to rebound hyperglycaemia,
which is what is measured in the am.
With that being said, encourage people to decrease their insulin before bed.
5) Dawn Phenomena
Hyperglycaemic in am.
These people are hyperglycemia all the time. It is therefore important to increase the insulin before bed.
With that being said, it is crucial to know whether or not your patient has Somogyi or Dawn phenomena.
6) Honeymoon period
Pharmacological Therapy Type 2

See Appendix for oral medications (e.g., glyburide, metformin).
Insulin may be needed if diet, exercise, and oral medications dont work.
Insulin may be needed in times of stress (i.e., illness, infection, pregnancy, surgery, etc.).
Nursing Management
Education
o Focus should be on self care.
These patients will know more about their diabetes than you. It is important to listen to them.
o Develop a diabetic teaching plan.
o General approach:
Basic, initial, or survival skills (e.g., diet, exercise). Teach the patient, and if they are avoiders, teach the family
(recall FCC).
Continuing education.
Foot care
o Always wear shoes (even in the house), check your feet daily, maintain eye care (recall
retinopathy) as the triglycerides will be deposited in the eyes, etc.
Teaching Strategies
Assess readiness to learn (e.g., avoider or approach style).
Assess coping strategies.
Ask about major concerns or fears.
Understand misconceptions.
Acute Complications of Diabetes

3 major complications
1. Hypoglycaemia
2. Diabetic Ketoacidosis (Diabetic Coma)
3. Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHS/HHNS/HHN)
Hypoglycaemia
Abnormally low blood glucose levels (2.7-3.3mmol/L).
Causes:
o Too much insulin
o Exercising too much
o Not consuming enough food
o Defect in the counter-regulatory hormones (e.g., glucagon, epinephrine, etc.).
Clinical Manifestations:
Adrenergic Symptoms (ANS)
75
o Sweating, HR, tremors, hunger, palpitations (from HR).

Central Nervous symptoms
o Confusion, stupor, coma.
The symptoms are similar to those in patients with alcohol intoxication.
Self-Monitoring Blood Glucose (SMBG) Very important to Offset Hypoglycaemia

Gerontologic Considerations:
o They may not have the visual acuity to use an acucheck machine.
o They may not have the finger dexterity.
o May not recognize the symptoms.
o With decreasing renal function it takes longer for oral anti-hyperglycaemic agents to be excreted.
o Skipping of meals.
Medical Management
Mild to Moderate
o Give 10-15mL of a fast acting simple carbohydrate (e.g., orange juice, coke, or other such products containing sugar).
o Retest the blood glucose in 15mins after treatment.
o If its greater than 4mmol/L, then give a protein and starch (e.g., peanut butter on whole wheat toast) or a meal.
o If that doesnt help it rise, administer another 10-15mL of a fast-acting carbohydrate.
If client unconscious
o Inject Glucagon 1mg subcutaneously or IM.
o After conscious, give simple sugar then protein starch snack.
Hypoglycemia is preventable always carry a simple sugar (Lifesavers were created for diabetics). Family and friends need to
know S&S and what to do.
Diabetic Ketoacidosis/Diabetic Coma

Caused by an absence or markedly inadequate amount of insulin.
Mortality rate is 1-3%.
This is typically seen in Type I diabetics because they have an absence of insulin. It can occur in Type II diabetics if they
consume a lot of alcohol.
Clinical features:
o Hyperglycaemia (from the lack of insulin)
o Dehydration and electrolyte loss (due to osmotic diuresis)
Since we are losing so much Na+, the K+ levels will be up. The more a person is dehydrated, the higher their K+
levels will be.
o Metabolic Acidosis (from the lypolysis ketone bodies)
The levels of H+ are high.
This can lead to respiratory acidosis.
These patients will have an increase in depth of breathing as they are trying to expel the CO2 (i.e., Kussmaul
respirations).
3 Main Causes:
1. Decreased or missed dose of insulin
2. Illness or infection
Stress hormones (cortisol) will be released, thus increase blood glucose levels.
3. Undiagnosed and untreated diabetes
Hyperglycemia
Blurred vision, weakness, headache
Orthostatic hypotension
Anorexia, N&V, abdominal pain
Acetone breath
Hyperventilation
Mental changes vary individually
Assessment and Diagnostic Findings
Blood glucose levels vary >14-44.4mmol/L
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Severity of DKA not necessarily related to the blood glucose level

o Ketones checked in both blood and urine.
o Electrolytes may be low, normal, or high depending on dehydration.
Prevention of DKA
Adherence to SICK DAY rules
o S = Sugar
o I = Insulin
o C = Carbohydrates
o K = Ketones
When people are under stress, their body will still be making glucose. For that reason, you should not tell a patient who is not
eating not to take their insulin (if anything, recommend a smaller dose).
Take insulin or oral antidiabetic agents as usual.

Test blood glucose and urine ketones q3-4h.
Report elevated blood glucose >16.6mmol/L or ketones.
May need to supplement normal insulin with Regular insulin/Toronto/Humulin-R (short acting insulin) q3-4h. A sliding scale
may be prescribed.
If usual meal plan cannot be followed, substitute soft foods 6-8 times per day.
If vomiting, diarrhoea, or fever persists, take liquids q1/2 -1hr to prevent dehydration. If unable to tolerate report to doctor.
Collaborative Care
Dehydration
o NS (no heart issues)
o NS (if patient has heart issues)
o If a patient has a blood glucose of 44 that has finally been lowered anywhere between 13-16, stop the NS and start
administering D5W. This is to prevent hyperglycaemic rebound of lowering the blood sugar too quickly.
Electrolyte Loss
o K+ may be given.
Acidosis
o Administer insulin.
This is based on how acidic this person is. Insulin helps put K+ back into the cells, therefore causing the H+ ions
to leave, thus creating a more basic environment. The insulin will also help the glucose to enter the cell,
decreasing lipolysis and azthus acidicosis.
o Arterial blood gases (ABGs) are done to determine ones acidity.
Hyperosmolar Hyperglycemic, Nonketotic Syndrome HHS

Hyperosmolarity and hyperglycaemia predominate with alterations to the sensorium.
o Hyperglycemia (their glucose values may be in the hundreds)
o Absent ketosis
o Dehydration (due to osmotic diuresis)
The dehydration seen in people with HHS is much more severe than in those with DKA.
The mortality rate is 40% from the severe dehydration.
o Hyperosmolality of plasma
How does HHS differ from DKA?
o The person still has enough insulin to prevent lipolysis (and thus ketoacidosis) but there is not enough insulin to lower
blood glucose levels.
o A Type II diabetic or a person who has not been diagnosed is likely to get HHS.
Hypotension
Profound dehydration
Tachycardia (the body is trying to move the little fluid in the body to the cells)
Variable neurologic signs
Assessment and Diagnostic Findings
Blood work including:
o Glucose, electrolytes, BUN CBC, serum osmolality and ABG
77

If youre hypotensive, the odds of getting acute renal failure are high.
LOC changes
The combination of increased osmolarity and hypotension will lead to this.
Collaborative Care
o Dehydration (NS D5W once blood glucose levels have reached 13-16)
o Electrolyte Loss
K+ levels will be high with extreme dehydration. Insulin will be given to drive both glucose and K + into the
cells.
The insulin will not be given based on acidity, but on the level of hyperglycaemia (different from DKA). The
insulin will be regulated by a sliding scale. Short-acting (regular insulin) will be used.
Being that the insulin will be putting the K+ into the cell, K+ replacement will have to be administered.
o
Chronic Complications of Diabetes

2 categories
1. Vascular both micro and macro
2. Neuropathic
Vascular
Macrovascular
o Damage to the large blood vessels providing circulation to the brain, heart and extremities.
Microvascular Complications
o Abnormal thickening of basement membrane in the capillaries by chronic hyperglycaemia. The constant sugars trying to
get through the vessels will damage the capillaries.
Retinopathy
Nephropathy
Even if the blood sugars have been well controlled, 50% of diabetics will get kidney damage.
Albumin in the urine (i.e., proteinuria) is a sign of kidney damage.
Neuropathic
40-50% of those with diabetes will develop detectable neuropathy within 10 yrs of onset.
Paresthesia
o Numbness, tingling, touch sensation not what it used to be.
Autonomic complications, sensory disturbances
o Polyneuropathies
The worst case is the inability to feel pain.
Infection
Defect in the mobilization of inflammatory cells and impairment of WBCs in phagocytosis.
o This makes the person more susceptible to infections.
Skin Complications.
o Acanthosis nigricans (dark ring around the neck caused from hyperinsulinism).
Note
Patients with Type I diabetes are typically very thin from lipolysis.
Assignment
Choose 1 case study.
Complete the focused assessment (typed).
Weve got to decide what the patient is being admitted with (otherwise its a fail).
80% is allocated for content.
o Do not waste time regurgitating the case study.
o Use as many references as needed, but tie up your own paper (i.e., do not have a paper full of quotes).
Unit 12: Paediatric Client with Chronic Respiratory Disorders
Paediatric Respiratory System

Asthma
78
Cystic fibrosis
Related pharmacology integrated
o Review notes from Pharmacology and texts; power point notes as a guide.
Immature systems
Smaller nares (OBSTRUCTION) (NOSE breathers)
Large tongue (POSITIONing important)
Underdeveloped sinuses (sometimes worriesome when children snore re sleep apnea)
Larger epiglottis prevents aspiration
Larynx and glottis sit igher and more anterior which makes them more likely to aspiration
Tracha shorter and funnel shapped
Narrowest part at cricoid cartilage until 8 yo resp arrest (contributes to cardiac failure)
Smaller narrow airways
Non compliant ribcage more cartilage than bone
Inspection and observation (positioning)(drooling sometimes normal r sometimes difficulty swallowing)

(inspiration active or passive function)
Auscultation all 3 lobes on rt and 2 on left (all the way down) listening for clear, quality, adventitious sounds.
Resp rates irregular, obligatory mouth breathers, color, muscle tones, apnea event is 20 seconds, systemic system
immaturity, bradycardia rate (RR chart in slides)
Retractions inward motions of chest wall, inward movements of the chest wall or tissues of the neck or sternum
during inspiration. Impairing and ineffective pattern to sustain breathing. Subcostal, intersturnal, intercostal (infants
dont have fat stores so easily visual)
Respiratoy distress
Tachypnea breathing rates more rapid than nomarl

Often a 1st sign of resp distress in infants
Pain, fever, going septic, any other resp symptoms?
Bradypnea
Breathing rates slower than normal.
Often an omnious sign in an acutely ill child
Resp failure to arrest (CPCP or BIPAP - ventilation)
Poor prognosis
Grunting air being forced out of a partial closed epiglottis to increase negative pressue and help gas exchange (big
red flag for Resp distress)
Combined with retractions indiciitive of pneumonia or cardiac conditions
Grunting could also be from abdominal paid or fever
Stridor upper airway obstruction croup, foreign body, congenitial abnormalities, upper airway edema (allergy)
Wheezing lower airway obstruction,
Ped assessment hx:

Doing before distress started? How long? Howd it start? Previous hx? Symptoms before or similar? Around anyone
ill? Their symptoms? Allergies? Immunizations up to date? Meds theyre on? Meds around the house too?
Otitis media inner ear

Acute or chronic condition
Eustachian tube (shorter more prone to obstructions, warm and moist for bacteria to grow) dysfunction and
obstrucction
Upper resp tract infections often have otitis media too
Winter
Risk factors young age, daycare, recurrent URTIs abnormalitis, not breatfed, bottle propping, pacifier use
79
Viral or bacterial? Cant tell.

Fluids and pathogns can travelfrom nose to middle ear
Remain due to horizontal position of ET
Invade mucosa
Clinical manifestations: tympanic membrane, red bulging-retracting, ear pulling, fever, hearing loss, irritability,
ear popping, rupture of TM
Therapeutic management
Tx with antibiotics based on age, reoccurance and severity. Amoxil first line therapy
Otis media surgery

Myringotomy with pressure equalizing (PE tubes) will improve hearing and speech
Nursing management
Supportive
Analgesia- no codeine
Heat
Antibitotics
Educate family good hand hygiene, flu vaccine/pneumonococcol, dont prop bottle, vit D
Nasopharyngitis etiology
Most common illness of infancy and childhoos
More commone in daycare and winter
Pathogenesis
Droplet or person to person contact
Incubation 1-3 days
Viral causes usually
Edema and increased mucuse production increased liklihood of obstruction or you could start viral and end up
with a secondary bacterial infection
Secondary bacterial infections
Self limiting 7-10 dyas
Symptoms
Lethargy
Irriatably
Fever,
Eating?
Sneezing
Nasal discharge
Headache
Dry irritated throat
Poor feeding/no appetite
Bulb suction
Humidifiers
Antipyretics
No cough and cold preparations unter 6 years of age
Fluids
rest
paryngitis etiology and pathogenesis

inflammation of the pharynx
80
viral
bacterial
abrupt onset
winter
clinical manifestations
sore throat
difficulty swallowing / voice
fever greater than 38.3
headache
bdominal pain
cervical adenopathy
soft palate petchiae
tonsillar exudate + or
theraputic management
antibiotics bacterial
analgesias
cool fluids
salt water gargle
rest
croup aka laryngotracheobronchitis

children 3 months to 3 years
viral- parainfluenza virus
late fall / winter
suden onset
croup pathogenesis
inflammation and edma cause obstruction of the upper airway
narrowing of the subglottic are
edema of the larynx
increased mucus producation
peaks 3-5 days
clinical fidnings
anxiety / restlessness
inbility to sleep
hoarse voice or barky cough
inspiratory stridor
subcostal, substernal retractions
fever
steeple sign on x ray
manaement
humidification
oral steroids (dxamethasone)
inhaled epinephrine
cool mist humidifier

cool air
do not disturb
fluids
anallgesiacs
epiglottitis etology
81
rapid obstructioairway that occludes the trachea life threatening emgency

bacterial
HIB vaccine
Age 2-7 yo
Sudden onset
Pathogenesis
Bacterial iasuion and cause inflammation and swelling of the epuction
Ssore thoat
High fever
Mufflvoice
Drooling
Stridor
Pain
Anxieity / not vigorous
Tripod position / resp distress
Epiglottis therapeutic management

Lateral neck xray (thumbs sign(
Antibiotics
Steroids
Intubation in controlled setting
Do not disturb
Upright position
NPO
Aanalgesia
Foreign body upper airway

4th leading cause of death aand hospitalization
Usually under one year
History of cough or choke

Cough
Drooling
Stridor
Hoarseness
Tripod position
Xray return for serial xrays

Watch stool
Endoscopy
Eductin and prevention

Food prep
Small parts testfixture or toilet paper roll (if it fits through its too small)
Pertussis aka whooping cough or aka hundred day cough
Highly contagious
Usually under 1 yo age
Unimmunized
Can go apneic or bradycardiac
Bordetalla pertusiis bacteria
Attaches to cilia
82
Releases toxins which dmaage cilia

Bordetalla pertusssis bactteria
Attaches to cireleases toxins which damage cilia and caus incubation period od usually 7-10 days
Dx nasopharynngeal swab for polymerase chain reaction testing
Droplet precautions
Observe for airway obstructions
High humidity oxygen
Suction
Encourage fluids
rest
anaphlaxis etiology
incidence unknonw (increasing)
epinepherine dispensed to aprox 1% of MB poulation
1/3 of childrens emerg visits
Seeing more reactions to milk proteins
Triggers
Food
Bees and hornets
Insect stings
Medications
Latex
Pathogenesis
Histamines aand secondary mediators released from mast cells and eosinophils following contact with allergen
Vasodilation
Anxiety, swelling, itchy, drooling, abnormal upper airway sounds, chest tightness, flushing, hives, abdominal cramps
Im epinepherine
Followed by dose of H1 antagonist such as ceterizine (reactine) or desloradetein (Aerius)
Child observed for 6 hours after for 2nd reaction
Use of epi pen teaching critical
teaching
80-110$ and expire annually
Assess airway, breathing and circulation
Epi pen
Hold is fist
Remove blue cap
Place orange end against mid outer thigh
Press quickly and firmly to hear a click
Hold for ten seconds
Remove and carefully carry to emergency dept
Avoid triggers
Epi should always be with child
Follow up with allergist
Further education
83
ASTHMA
Paediatrics
Alveoli (by the age of 12 the alveoli are adult-like)
Peripheral bronchioles
Smooth muscle
Muscles of respiration (the diaphragm is the largest breathing muscle).
Additional symptoms
o The childrens respiratory rate is higher than that of adults.
o The ribs and cartilage are flexible.
o The chest walls are more pliable.
o The epiglottis is closer to the palate.
Airway Edema
Edema
o More dangerous in paediatric airway.
o 1 mm of circumferential edema can resistance to airflow by 16x.
Cross sectional area by 75%
o The paediatric airway can by quickly lost!
Most common cause of cardiac arrest in children = respiratory arrest.
Asthma
Incidence
o 15.6% from 4 to 11 yrs of age.
o 8.3% 12 yrs of age.
The incidence is decreasing due to asthma education.
Hospitalization and death
Risk factors:
o Allergies (i.e., dust mites)
Etiology
o Familial and environmental
The 3 contributors to asthma are:
Mucous
production
Mucosal
Bronchiol
inflammation
constriction
The middle is when obstruction occurs.
Pharmacologic Interventions
Two main groups are:
1. Controllers
2. Relievers
Pathophysiology
Early response to trigger:
o Bronchial constriction.
o Increase smooth muscle response and bronchospasm.
Pharmacological interventions?
84
Later:
o * Mucosal inflammation
o Mucous production
Pharmacological interventions?
Continued hyper-reactivity
Early:
o Bronchiol constriction
Late:
o * Mucosal inflammation
o Mucous production
Continued hyper-reactivity
Triggers
What they are:
o Substance (allergen)
Trigger + IgE + mast cells
o Health conditions (non-allergic) that may cause an asthma attack:
Respiratory infections, fever.
Maintenance is the key to preventing asthma attacks.
o Other
What they are not
What is the role of nurses?
o Education!
Signs, Symptoms and Nursing Implications

Implications for diagnosis
Cough
o Non-productive (i.e., bronchospasm)/productive (mucous production assess the colour).
Air entry
o Wheezing
Tight chest
o This is sometimes referred to as a silent chest as the air can no longer enter the body.
Respiratory rate and work of breathing (WOB) will both increase.
o Keep in mind the normals for the age group.
Respiratory fatigue (the child with start to tire as there is not enough O2 entering the body).
Cardiac
o The heart rate will often increase as this is a side-effect of ventolin.
O2 and CO2
o Blood levels
O2 levels will decrease and CO2 levels will increase due to the chest constriction.
o Administration O2 typically up to 92%.
Hydration
o It may be impaired. In children you should see 1-2mL/kg/hr.
o Correction
Behaviour
Laboratory prn
o CBC (Complete blood count)
o White blood cell count
o Effect of ventolin on K+
This is important because ventolin causes K+ to move from the blood stream into the cells.
Special note: children <6 yrs of age are typically those admitted to the hospital.
o Asthma Predictive Index (API)
Helps determine who is likely to get asthma and how badly they will tend to be.
If a parent has asthma, it is likely that the children will also get asthma.
A history of wheezing without having a cold is a predictive indicator of asthma.
Canadian Criteria for Asthma Control
85
Characteristic
Daytime symptoms
Night time symptoms
Physical activity
Exacerbations
Absence from work or school due to
asthma
Need for fast-acting 2-agonist
FEV1 or PEF1
Frequency or
Value
<4 days/week
<1 night/week
Normal
Mind, infrequent
None
<4 doses/week
>90% personal
best
PEF diurnal variation2
<10-15%
1FEV1 = forced expiratory volume in 1s; PEF = peak expiratory flow.
2Diurnal variation is calculated as the highest PEF minus the lowest divided by the highest PEF multiplied by 100 for morning
and night (determined over a 2 week period).
Asthma Action Plan

http://www.asthma-education.com/content/images/stories/actionplan-nopeak.pdf
Green: medications used to control asthma will be effective
Red: medications are not enough, child should be brought to the hospital
Asthma Severity
See also box 46-13 in text
Care and treatment follows a stepwise progression based on age. Education must take place at every stage.
Example of Stepwise Assessment and Treatment
Educational Tools
Targeted resources:
o Asthma Action Plans
o Asthma diaries
Childrens Asthma Education Centre Wpg
o http://www.asthma-education.com/content/
Status Asthmaticus
It is a life-threatening emergency indicating that asthma is not being controlled.
Causes
o Seasonal factors (e.g., farmers burning fields, environmental pollution)
o Infections most common
o Self d/c drug therapy (typically seen in adolescents)
Symptoms
86

o
o
o
o
o
Ventolin being used more frequently (q2h instead of q3h).

IV corticosteroids are typically used.
Irritability due to hypoxia.
Little to no air entry heard on auscultation.
Respiratory arrest (rare).
Frequent Reasons for Poor Control

Insufficient patient education
o Under appreciation of disease severity.
o Assessment of family adherence (not everyone will adhere to the programs)
Assess financial ability to maintain ventolin use.
o Failure/inability to follow treatment guidelines.
Inappropriate therapy
Misunderstanding role/use/side effects of medication
o Insufficient anti-inflammatory use.
o Overuse of 2-agonists.
Difficulty using inhalation devices (spacers are often used in children to help the administration; this is becoming more popular in
adults as well).
Education and Discharge Care

Teach and reinforce at every opportunity.
In-depth education and action plan that involves the patient, family, and community care providers.
Pharmacologic Education
Refer to Pharmacology notes and text.
Two main groups are.
o Controllers and Relievers
When to use it depends on the severity.
When to change your plan depends on the action care plan.
ISMP: Acute Care (Nov 19, 2009)
Controller Medicines
Inhaled steroids are the most common controller medications.
o or prevent swelling and extra mucous inside the airways
o Work slowly
87
o Must be used every day!

o Most common side-effects
o It is important to encourage patients to rinse their mouth afterwards as thrush is common if this is not done.
o E.g., beclomethasone (QVAR), budesonide (Pulmicort), Fluticasone (FloVent)
Long Acting Bronchodilators (LABA)
o Salmeterol (Serevent)
o Formoterol (Oxeze)
Combination Medicines: Pros and Cons

fluticasone & salmerterol (Advair)
budesonide & formoterol (Symbicort)
Controller Medicines
Leukotriene Receptor Antagonists (LRA)
o E.g., montelukast (Singular).
o Increasingly popular for complex asthma, with persistent allergies.
Reliever Medicines
Action: reduces bronchoconstriction
Use: if the patient has to use it more than q4h, they should see a doctor
Side effects: HR, supraventricular tachycardia, the children will vibrate.
Salbutamol (Ventolin), Airomir, terbutaline (Bricanyl)
Inhalers
There are many type and varied techniques.
Cleaning
Ability to use (child development)
Valved spacer recommended
CYSTIC FIBROSIS
Metered disk inhaler
Spacer with mouthpiece

Turbuhaler
Diskus
Spacer with Mask
65 Roses
Health Problems with Cystic Fibrosis
Cystic fibrosis affects the bodys endocrine glands. The respiratory and GI systems
are affected.
Cystic Fibrosis Gene

Mutation in CFTR gene on chromosome #7
o Autosomal recessive (i.e., 25% chance of children being affected if both parents are carriers).
o >1800 mutations identified
o MB: 83% have homozygous mutation = (delta) F508
o Other gene mutations can modify the severity of the disease
There are classic and non-classic cases.
88
Stats (FYI Only)

CF gene carried by 1/31 persons
o Hutterite in Mb 1/~12
o Aboriginal 1/~90
Overall incidence 1/3500 live births
Exocrine Glands
Exocrine glands
o Exocrine glands and CF
o Sodium and chloride transport
Respiratory tract is affected (i.e., mucous becomes quite thick)
Pancreas
Sweat glands (there is a high content of salt on their skin)
Dehydration is a big problem in these children.
o See also text for detail.
Diagnosis
If symptomatic:
o Respiratory symptoms
o GI/nutrition:
4 Fs
Frothy, fat, foul, floaty stools
Meconium ileus
Failure to thrive (no matter how much they, they will not gain weight
There will be respiratory symptoms (e.g., wheezing)
o Median age at dx = ~ 6 months of age
How:
o Newborn screening and further evaluation.
o Sweat chloride via a pilocarpine test chemical.
o DNA testing for gene mutation.
Prognosis
Median life expectancy tends to be 37 years.
# Canadians with CF
# Manitobans with CF
Screening for CF
Genetic screening for most common mutation(s) all or high risk groups?
89
Prenatal
At birth:
o IRT: a leak of tryptic-like substances into the blood detected by the IRT blood test.
Canada Ont/Alberta/Sask
A first step only confirm with retest and/or DNA +/- sweat chloride
o The pancreas secretes trypsinogen which is converted into trypsin.
Goals of Treatment
1) Prevent or minimize pulmonary complications
2) Optimize growth and nutrition
3) Assist family/child in coping
There is no cure for CF.
Infection/Inflammation/Destruction
Airway
destruction
Airway infection
(colonization)
Airway
inflammati
on (WBC)
Mucous is very thick and destroys the cilia.
Infection is caused by the thick mucous sitting in the respiratory tract.
Inflammatory response (early and chronic).
Progressive destruction.
Numerous respiratory symptoms.
Respiratory issues is the major cause of death.
Expiration
Inspiration
A+B = healthy
C+D = CF
Transplant
Theres a lot of risk associated with transplantation. There is only a 50% chance of living after a transplant has taken place.
Physiotherapy
Respiratory:
o Multiple methods:
Positioning, pummelling, and blowing devices.
External manoeuvres such as huffing.
o Oscillatory vest (the vest vibrates and is extremely expensive) in conjunction with other techniques.
Other physiotherapy:
o Upper body strength.
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o
o
Musculoskeletal and pain issues.

Aerobic conditioning.
Respiratory Infections
Organisms:
o Staphylococcus aureus seen early
o Pseudomonas aeruginosa
*colonization = mortality
o Burkholderia cepacia (this is associated with a rapid respiratory deterioration)
Treatment
o Antibiotics (although the prolonged use may lead to antibiotic resistance).
Nutrition
CF interferes with the passage of pancreatic enzymes.
Poor fat absorption
o Stools tend to be bulky and oily (see 4 Fs above).
o Other GI symptoms.
Therapy
o Goal
o Up to 30% more calories and protein
o Pancreatic enzymes (e.g., pancrease)
o Vitamins A, D, E and K
Routes
o Breastfeeding is encouraged by supplemental calorie sources may be needed.
o Enteral access devices may also be required.
Additional Medications
rhDNAse/Pulmazone (costs roughly $16,000/year)
o Promotes mucous thinning. It only benefits 30% of patients.
Inhaled NS (this may irritate some children).
High dose Ibuprofen.
Additional Issues
Transition to adult health care (this is needed since the average age is increasing).
(Fertility)
o The sperm and eggs are affected (recall that it is an exocrine gland disorder).
Expansion of adult clinics.
Cystic Fibrosis Related Diabetes (CFRD)
o This is due to the pancreas being affected (i.e., insulin release).
Resources
o Financial
o Family
Cystic Fibrosis Adult Care Consensus Conference Report

No achievement highlights the striking developments of the past few decades in cystic fibrosis (CF) care more clearly than the
tremendous growth of the adult CF population.
Video 65 Red Roses

The excess salt is what causes an increase in mucous.
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Unit 13: Clients with Altered Nutrition and Absorption Liver and Pancreas
Review of Liver
There are 2 main lobes.
What else?
o There are 4 quadrants of the liver.
o It is located in the right upper quadrant.
You should not be able to feel it during an assessment (i.e., other than the lower edge).
o It will have a dull sound when percussed.
o A normal liver weighs 1.5kg in a male.
Hepatic circulation
o Hepatic Artery
Brings oxygenated blood to the liver.
o Portal Vein
Takes all the nutrients from the gut to the liver for phagocytosis to occur.
Portal hypertenstion the blood backs up to the spleen cause it cant go forward.
o Hepatic Vein
Bring deoxygenated blood (but it is in nutrients) to the inferior vena cava to be distributed to the body.
Functions:
1. Production of Bile
This is its only digestive function.
It makes 700-1,200mL per day. The bile is required for fat breakdown.
Comes together and emulsifies fat. Empties into the common bile duct.
No bile? Lot of fat gowing around fatty stool (not being emulsified) (frothy, floaty, foul, clay colored)
2. Carbohydrate Metabolism
The liver regulates blood glucose levels via gluconeogenesis.
If there is a problem with the liver, the patient may be lethargic.
Coverts monosaccarides to glucose.
3. Amino Acid Metabolism
There are 20 amino acids needed to make proteins.
It synthesizes non-essential amino acid (it makes 12 amino acids).
Non-essential amino acid synthesis
4. Deamination
Production of urea
Ammonia (NH4) is a toxic by-product of protein breakdown that will destroy brain cells.
The liver must convert the NH4 to urea so it can be excreted.
The deamination refers to the removal of NH4. Cant break it down? Pt will die.
5. Synthesis of Plasma Proteins
Over 50% of the plasma proteins are albumin. If the body cannot synthesize albumin there will be a decrease in
plasma volume as the oncotic pressure will not be great enough to draw fluid back in the plasma. This will lead
to edema and ascites (recall third space shifting). Keeps Water in the vessle. Its going to end up with third
space shifting. Hypervolemia.
Clotting factors (e.g., thrombin, prothrombin, fibrinogen) will also not be made. Dont make it? Bleeding.
Globulins are required to immune system functioning. They make antibodies. Make lipo-protiens to help
transfer fat. (stored in lymph). Liver doesnt work? All this is screwed (immune system)
6. Lipid Metabolism
The liver synthesizes lipoproteins (e.g., HDL, LDL, VLDL), which act as carrier molecules to get other
substances into the cells.
7. Formation of Bilirubin
Bilirubin is a pigment derived from the breakdown of haemoglobin (i.e., the breakdown of RBCs). Since it is
water insoluble, it is bound to albumin for its transport to the liver.
Red blood cell destruction (the heme is separated from the globulin).
Unconjugated Bilirubin + Albumin (this is not water soluble and can thus not be excreted)
Conjugated Bilirubin + Glucuronic Acid (this is water soluble and can be excreted by the kidneys)
If it is unable to conjugate, it will not be excreted and will lead to jaundice. It will also cause the feces to be
white.
8. Storage
It stores glucose in the form of glycogen.
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It stores the fat soluble vitamins (A, D, E, and K) as well as the B Vitamins (B12, B6, B1).
o The fat soluble vitamins are needed for clotting.
o The B vitamins are for:
Lack of B12 will lead to pernicious anaemia (i.e., large red blood cells as pernicious anaemia is
a type of megaloblastic anaemia).
For B12 to be absorbed, intrinsic factors are required in the stomach. People without
these factors will require injections of these factors.
B1 and B6 vitamins are required for adequate nerve function.
9. Detoxification & Metabolism of inactive hormones
It detoxifies and metabolizes the steroid hormones coming from the adrenal cortex (i.e., aldosterone, cortisol,
and androgens). (Not metabolizing cortisol will make glucose and Cushings), hypertension (aldosterone
running amuk), see below
o This will lead to aldosteronism and thus a lot of fluid retention. Since there are no albumins, it will
lead to third space shifting.
o Will need to detoxify. Tylenol one of the biggest culprits for liver failure.
o Fatty liver precurser to liver failure. Taking too much tylenol or drinking. Destroy the normal
structure of the cell.
10. Phagocytosis by Kupffer Cells
They are fixed macrophages (clean up cells) that also help bring the level of old RBCs down. Not working
bacteria end up in systemic circulation infections, septic.
Diagnostic Evaluation of Liver

Typically 70% of the liver is damaged before tests are abnormal. Recall that this is the one organ that can regenerate, so the
damage can be reversed. Tylenol and alcohol can both lead to fatty livers.
o Transaminases (ALT, AST)
These are the liver enzymes. They are elevated when there is damage.
o Prothrombin time (assessment of extrinsic coagulation)
This will increase with damage to the liver.
o Serum concentration of:
Alkaline phosphatase
Levels are with damage. This is an indication of liver or bone disease.
Proteins
Levels are .
Bilirubin
Levels are .
o Urine urobilinogen
Levels are .
Physical Assessment
o Splenomegaly
The blood cannot enter the liver and therefore gets backed up and goes into the spleen. In extreme cases the
blood will back up into the oesophagus.
o Palpable liver
Biopsy
o Once a biopsy has been completed, a simple dressing is not adequate, there must be pressure put down on it.
CT/MRI
Hepatitis
Description
Inflammation of the liver.
Acute viral hepatitis
o Most common cause of why someone will get hepatitis.
o Other causes.
Drugs (e.g., acetaminophen), alcohol, chemicals (e.g., aerosols), genetic, autoimmune diseases.
If a person overdoses on Tylenol, you want to try prevent liver failure by giving Mucomyst IV.
Types of infectious viral hepatitis:
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o
o
o
A, B, C, D (you can only have Hep D if you have Hep B), E, G

Liver widespread inflammation of the live
Pathophysiologic changes in the various types of viral hepatitis are similar.
Serologic Events in Hepatitis A Viral Infection (p. 1112)

Its an RNA virus that is transmitted via the fecal-oral route.
Research shows that 70% of people do not wash their hands after going to washroom.
The virus will be seen in the blood for only a very brief time (it is often not detected). About 3
weeks
after being infected, you will see the virus in the stool.
When you see Anti-HAV IgM in the blood, we know that antibodies have been created to fight
an acute infection at the present time. IgM is the first responding immunoglobulin.
Anti-HAV IgG levels will be seen roughly 8 months after either a past infection or a vaccination.
If you think youve been infected, get the vaccine and also take immunoglobulins in order to help fight the virus. If you think
youve been infected and have already gotten the vaccination, get the immunoglobulins.
Serological Events in Hepatitis B Viral Infection (p. 1113)
Hep B can live on a surface for up to 7 days. (up to 150 days)
It is a DNA virus that enters your cells and replicates.
It is transmitted:
o Percutaneuously (e.g., injections, IV drug users, blood transfusions)
o Permucosal
o Sexual
o Vertical (mother to child)
o Horizontal (via objects such as manicure tools)
HbeAg
HBs IgG (vaccine or disease), HBc IgG (has disease)
HBV-DNA
HBsAg
o There is a peak around 3 months of these antigens. A surface antigen does not respond to a surface antigen. For
hepatitis B, a core antibody responds to a surface antigen.
The immune response is by an Anti-HBc IgM, which indicates an immune response.
o Core antibody (Anti-HBc IgM) will response to a surface antigen (HBsAg).
Core antibody: c
Surface antigen: s
o levels of Anti-HBs IgG: means a vaccination occurred.
o levels of Anti-HBc IgG: means you have a previous infection.
In 5 months, the virus should be gone. If, after 6 months, the levels of HBsAg, HBeAg, HBV-DNA are present on two separate
occasions, you are a carrier. You may not display symptoms of an infection. Once you are a carrier, you will always be one and
are also likely to get liver damage. You will have had the acute symptoms are one point if you are a carrier.
Percutaneous transmit it through perinatal, needles, sexually, vertical (mother to child), horizontal (objects, dentist, pedicure,
sharing toothbrush, sharing a towel).
Can live outside of the body for 7 days on a dry surface.
95 % dont carry it. 5% do vertically 80% results in liver failure.
Etiology
Hepatitis C Virus (HCV)
o RNA virus
o Transmitted percutaneously (e.g., injections, IV drug users, and blood transfusions and haemodialysis prior to the
1990s).
o 80% of the people who have Hep C do not know they have it.
o These patients will also have co-infections (e.g., Hep B, HIV).
Hepatitis D Virus (HDV)
o Also called delta virus.
o Defective single-stranded RNA virus.
o It cannot survive on its own (i.e., it can only survive if Hep B is cured).
o Requires the helper function of HBV to replicate.
Not all patients with viral hepatitis have jaundice.
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Termed anicteric hepatitis

30% of patients with HBV dare asymptomatic and 80% with acute HCV are asymptomatic.
Most people with acute viral hepatitis recover completely without complications
Overal mortality rate <1%
By the time you start to see symptoms 70% of your liver is usually damamged.
Pathophysiology
Liver
o Widespread inflammation of liver (the cardinal signs of inflammation are present).
o Pathophysiologic changes in the various types of viral hepatitis are similar.
During an acute infection:
o Liver cell damage results in hepatic cell necrosis.
o Proliferation and enlargement of Kupffer cells (these macrophages will enlarge to take up the extra debris).
o Basophils and eosinophils come too (very big). Inflammation and swelling. Swelling of periportal areas.
o Inflammation of the periportal areas may interrupt bile flow (recall that bile is made in the liver and stored in the
gallbladder). If the bile cannot make it to the gallbladder it will sit in the liver and cause damage.
o Cholestasis may occur.
Systemic effects
o Acute Phase table 46-2
o Basophils release histamine (itchy)
o Lasts from 1-4 months
o Icteric or anicteric
o (fill in more)
o Rash (bile salts will come out of the skin)
o Angioedema
o Arthritis (because the liver is not excreting everything it should be)
o Fever
o Malaise
30% of patients with HBV asymptomatic and 80% of patients with acute HCV will be asymptomatic.
It doesnt matter which type of hepatitis is present, the body will go through all 3 phases.
1) Preicteric phase precedes jaundice (icteric means jaundice)

o Lasts from 1-21 days
o Anorexia
o Nausea
o Vomiting
o Abdominal discomfort
Right upper quadrant
This is like the abdominal phase in A and is therefore more pronounced in Hep A.
2) Icteric phase
o Lasts 2 to 4 weeks
o Characterized by jaundice
o Pruritus due to:
Bile salts
Inflammatory response
Increase in neutrophils, eosinophils, and basohpils, which produce histamines and cause pruritis. This
patient must therefore be given anti-histamines.
o The differential will give you the difference between WBCs.
3) Posticteric phase
o Begins as jaundice is disappearing
o Lasts weeks to months
o Malaise
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o
Easy fatigability!
This is because there are no stores of glycogen.
General considerations
o Not all patients with viral hepatitis have jaundice (i.e., termed anicteric hepatitis). For this reason it is important to treat
every patient as if they have Hepatitis.
See Appendix
Complications
Most patients with acute viral hepatitis recover completely with no complications.
Overall mortality rate <1%.
Fulminant hepatic failure.
o This is a syndrome. With continued damage in the liver will come liver failure.
Chronic hepatitis.
o This is like the carrier state.
Cirrhosis.
Hepatocellular carcinoma
Collaborative Care
No specific treatment or therapy for acute viral hepatitis.
No specific drug therapy antiemetics, diphenhydramine (benadryl).
Most patients can be managed at home.
Drug Therapy
No specific drug therapies.
Supportive therapy:
o Antiemetics (e.g., gravol, Maxeran)
o Diphenhydramine (e.g., Benadryl)
o Chloral hydrate (its a sedative used to decrease the metabolic rate and thus give the liver some time to rest)
Nutritional Therapy
No special diet is require, but:
o High-carbohydrate and protein for repair
o Low-fat (do not force the liver to have to make a lot of bile)
o Adequate calories
o Vitamin supplements (give the fat soluble vitamins and the B complexes)
Drug Therapy
Chronic hepatitis B
o -interferon
These are biologic modifiers that decrease the viral load. These may cause flu-like symptoms.
Have to take these all the time. Dont take them? Virus comes back another way. Then what youre taking wont
work. (e.g MRSA).
Chronic hepatitis C
o -interferon
o ribavirin (Rebetol)
o different drugs for different non genotypes 2/3
Prevention
Hepatitis A
o Hepatitis A vaccine
o Immunoglobulin (Ig) (Passive immunity if I had the vaccine)
o When travelling, do not consuming the water or foods that have come in contact with water (e.g., salad, cool foods, ice).
Hepatitis B
o Immunization
Most effective method.
Hepatitis C
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o
o
o
Currently no products to prevent HCV.

There are no vaccines (several vaccines are in development).
The virus can change and alter its shape.
Nursing Management Nursing Assessment

Past Health History
o Haemophilia (have you ever gotten blood transfusions).
o Exposure to infected persons.
o Ingestion of contaminated food or water.
Medications that can cause liver failure
o Acetaminophen
o Phenytoin
o Halothane (used in general anaesthetic)
o Methyldopa (anti-hypertensive)
o Which OTC herbs is the patient taking
IV drug and alcohol abuse
Weight loss
Dark urine
Fatigue
Right upper quadrant pain
Nursing Management Nursing Implementation

Acute Intervention
o Rest!!!
o Jaundice
Assess degree of jaundice.
Small, frequent meals to keep the energy level high.
o Dietary teaching
o Assessment for complications
o Regular follow-up for at least 1 year after diagnosis (this is to see if the patient is a carrier)
o Avoid alcohol
o Medication education
-interferon administered IM or SQ
Ribavarin - po
Numerous side effects (e.g., flu-like symptoms)
Description & Statistics Cirrhosis

A chronic, progressive disease of the liver. At this point there is so much scar tissue that the liver cannot regenerate itself.
13th leading cause of death for Canadians.
Highest incidence between 40-60 years.
Twice as common in men as in women (due to alcohol intake).
o There is a direct correlation between alcohol intake and liver damage.

Cell necrosis occurs.
Destroyed liver cells are replaced by scar tissue (this is the reason the liver cannot regenerate itself).
Normal architecture becomes nodular as opposed to its usually smooth consistency.
There are 4 types of cirrhosis:
1. Alcoholic (Laennecs) cirrhosis
There is a theoretical perspective that the cessation of alcohol drinking can reverse this type of cirrhosis.
2. Postnecrotic cirrhosis
Associated with viral hepatitis that is not cleared (i.e., a hepatitis carrier)
3. Biliary cirrhosis
Occurs in physical obstruction of the biliary tree.
4. Cardiac cirrhosis
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This is due to long-standing heart failure (especially the right side because the blood will not flow onward but
will back up into the inferior vena cava and then the liver).
Diagnostic Studies
Liver function tests
Liver biopsy
Liver scan
Liver ultrasound
Esophagogastroduodenoscopy
Prothrombin time
o Would expect an increase in prothrombin time. Can expect Coumadin and Heparin to be administered.
Testing of stool for occult blood
o This is when there may be blood in the stools but it will not been seen by the naked eye.
Manifestations of Liver Cirrhosis

Almost every single system is affected.
There is often portal hypertension.
Clinical Manifestations Early Manifestations of Hepatocellular Failure

Onset usually insidious (recall that by the time changes are noticed, 70% of the liver is damaged).
GI disturbances:
o Anorexia
o Dyspepsia (heartburn)
o Flatulence
o N-V, change in bowel habits
Clinical Manifestations Late Manifestations of Hepatocellular Failure

The changes are due to 2 causative mechanisms:
1. Hepatocellular failure
2. Portal hypertension
Jaundice
o This is because the bilirubin is unable to conjugate.
Skin
o
Spider angiomas (telangiectasia, spider nevi), palmar erythema (the old blood cells are not being broken down and are
thus stored in the hands), petechiae (due to bleeding).
Endocrine Disturbances
o This is because the hormones (e.g., aldosterone, cortisol, androgens) are not being metabolized. This increase in serum
hormones will cause problems (e.g., edema, male/female characteristics due to the increase in serum androgens). Low in
potassium. Hair distribution different.
Hematologic Disorders
o Due to the decrease in clotting factors and an inability to store vitamin K. These patients have an increased likelihood of
bleeding and anaemia. Prothrombin. Anemia. Low in thrombocytes (thombocytpenia). Spleenomegly. Lymphopenic.
Palmar erythema Circulating estrogen we arent circulating the corticosterioids (red hands) affect red blood cells.
Peripheral Neuropathy
o This is because we are no longer storing the B vitamins.
Complications Portal Hypertension

Characterized by:
o Increased venous pressure in portal circulation.
Since there is scar tissue, the body will work harder at pumping blood against this resistance.
Varicese (veins that get smaller and bursted veins are called bleeding varicese).
o Splenomegaly
o Esophageal varices
o Systemic hypertension
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Splenomegaly
o Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the
splenic vein.
o The spleen stores RBCs and 30% of platelets, which are used for clotting. Platelets live for 10 days (as opposed to 120
days for RBCs). It also stores lymphocytes (T-cells and B-cells) which are responsible for an immune response.
These patients will therefore have increased infections and risk of bleeding.
Esophageal Varices (i.e., dilated veins).
o Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus
and produces varices. An increase in pressure (e.g., cough, roughage) can cause these varices to burst.
Caput Medusae
o Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins
around the umbilicus. To try and reduce pressure in systemc circulation.
Peripheral Edema and Ascites
o Ascites:
Intraperitoneal accumulation of watery fluid containing small amounts of protein. The body cannot make
albumin, which is responsible for drawing fluid back into the vascular space. Hypoalbuminia and increased
aldosterone.
Hepatic Encephalopathy
o This is usually a terminal condition. Ammonia not going through due to portal pressure. Its backing up and getting
into circulation and gets through the blood brain barrier this will kill brain cells. Terminal Condition.
Asterixis encephalopathy you can see. (liver flap arms cant stay up/tremors)
Fetor Hepaticus
o Musty, sweetish odour detected on the patients breath (it typically smells like feces).
o From accumulation of digested by-products.
Collaborative Care Portal Hypertension

Rest (you do not want to put strain on the liver)
Avoidance of alcohol and anticoagulants (e.g., Plavix, Coumadin, Heparin)
Management of ascites
Prevention and management of esophageal variceal bleeding
Management of encephalopathy
Collaborative Care Ascites

High carbohydrate, low protein (for the ascites), low Na+ diet (if a patient has encephalopathy you might not want to give any
Na+).
Diuretics (this will help get rid of the edema but will not help the third space shifting). (potassium sparing aldosterone)
Paracentesis (insert a needle in the abdominal cavity to drain the third space shifting).
o It is important to drain it slowly as a quick drain would cause interstitial fluid to replace this fluid, causing a decrease in
BP. Albumin can be given if the patient does not have varices. Risk for infection and bleeding. Indication difficulty
breathing.
Portosystemic/Peritovenous Shunt
This is done to prevent multiple needles as the patient is at an increased risk of infection and bleeding.
Collaborative Care Esophageal Varices

Avoid alcohol, aspirin, and irritating foods (i.e., roughage foods such as apple skins and broccoli).
If bleeding occurs, stabilize patient and manage the airway.
Endoscopic sclerotherapy or ligation of the bleeding capillaries.
Balloon tamponade.
Esophageal Varices
Sengstaken-Blakemore Tube
o There are balloons down the side that put pressure on the capillaries when inflated in order to stop bleeding.
o This is a short-term treatment.
o Perienteral nutrition.
Portosystemic Shunts- Fig: 45-10
o This is a more long-term treatment.
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o
The splenic vein is shunted from the liver directly into the kidney. This puts the patient at a higher risk of septicaemia.
Collaborative Care Hepatic Encephalopathy

Goal: reduce NH3 formation
o Protein restriction (0-40g/day).
o Sterilization of GI tract with antibiotics (e.g., neomycin, flagyl).
There are a lot of bacteria in the GI tract that are made of protein. We do not want these bacteria (i.e., protein)
to enter the gut. This is important because the proteins will be broken down into NH3.
o Lactulose (Cephulac) traps NH3 in gut.
These patients will get if often (e.g., q4h). They are not getting this medication for BM purposes, so if the
patient develops diarrhoea, do not stop administering lactulose! That is because the lactulose is given to trap and
the NH3 and it is still possible for the patient to be constipated.
o Levodopa (anti-Parkinsons).
This is because you get shaking.
o Bleeding can also lead to encephalopathy as the blood is made of protein.
Drug Therapy
There is no specific drug therapy for cirrhosis.
Drugs are used to treat symptoms and complications of advanced liver disease.
Nutritional Therapy
Diet for patient without complications:
o High in calories (from carbohydrates)
o CHO
o Moderate to low fat
o Amount of protein varies with degree of liver damage
Check Case Study
Acute Pancreatitis
Review exocrine functions of the pancreas!!
o Pancreatic enzymes necessary for digestion to occur are amylase, protease, and lipase. These enzymes are carried in a
NaHCO3- solution in order to neutralize the HCl of the stomach.
o The hormone secretin (in the duodenum) signals the pancreas to secrete NaHCO3.
Acute Pancreatitis Definition (Figure 46)

An acute inflammatory process of the pancreas.
Degree of inflammation varies from mild edema to severe necrosis.
Exocrine function need ducts emptying in the nearest region. Produces amylase, lipase, and proteases from exocrine function.
Amylase protien, lipase fat, protases protein. These work in the dudenum (must be activated there). Alcohol is a
carbohydrate. Salvary amylase begins to break it down in the mouth. Secretin is a hormone that is produced in the duodenum that
signalsthe pancreas and bile and gall bladder that food is coming. This is in order to alert the stomach with the HcL is breaking
bonds and throwing it into the duodenum (its acidic and your Ph will be low) so secretin doesnt have time if alcohol is dumped
quickly by the stomach (includinng the acid) and the pancreas hasnt had time to send the enzymes. The enzymes travel in
NaHCO3 (sodium bicarbonate). Has to come with the enzymes to neutralize the acid. The stomach dumped it really quickly so
there isnt much time for the pancreas to get the stuff out this may damage the cells and ultimately will get inflammation from
damaging the duodenum and there will be swelling. Inflammation and swelling will also go up into the ducts. The enzymes with
the sodium bicarb cant get out due to swelling and inflammation. If they cant get out they will act on the pancreas
autodigestion of the pancreas. They eat away at the pancreas. The person will hav lots of hemmorage.
Acute Pancreatitis
The biggest reason for pancreatitis is alcohol abuse. Other reasons may be trauma, infection, drugs, autoimmunity, and following
surgery to the GI tract. Birth control.
If secretin is not secreted soon enough, NaHCO3- from the pancreas will not neutralize the HCl from the stomach. This is
problematic because if the chyme is released too soon into the duodenum, it will damage the pancreatic duct (thus causing
inflammation).
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Edematous pancreatitis
o Mild and self-limiting.
Necrotizing pancreatitis
o Degree of necrosis correlates with severity of manifestations.
Abdominal pain is the predominant symptom.
o Pain located in the left upper quadrant.
o Pain may be in the midepigastrium.
o Commonly radiates to the back.
Complications
Pseudocyst
o A cavity surrounding the outside of pancreas that is filled with necrotic products and liquid secretions.
o Abdominal pain.
o Palpable epigastric mass.
o Internal complications (pulmonary complications due to swollen cavity).
Pancreatic abscess
o A large fluid-containing cavity within the pancreas.
o Results from extensive necrosis in the pancreas.
o Large and seen as worse.
Pulmonary (this is because the diaphragm cannot drop if there is an inflamed organ directly below it)
o Pleural effusion
o Atelectasis
o Pneumonia
Cardiovascular
o Hypotension (there is a lot of inflammation which can lead to haemorrhage).
o (skin might give a blueish-greenish circulation).
Tetany (caused by hypocalcaemia)
o The reason for this hypocalcaemia is unknown.
Diagnostic Studies
Serum amylase
Lipase
Urinary amylase is low (this is because the serum amylase is also )
Other lab abnormalities
Why?
o Hyperglycaemia damage to islets of landerhands they may become diabetic (because the insulin is not being
produced), Hypocalcaemia (reason unknown)
o Hyperlipidemia (the excess glucose from the hyperglycaemia will turn into fat)
Collaborative Care
Objectives include:
o Relief of pain
o Prevention or alleviation of shock
o Reduction of pancreatic secretions
o Fluid and electrolyte balance
o Removal of the precipitating cause
Drug Therapy
Demerol (reduces the spasms), IV morphine (step 3 morphine pain) (step 2 moderate codeine pain)
Nitroglycerin or papaverine (give these vasodilators, even though the patient is hypotensive, because it relaxes smooth muscle)
(vasodilates) (severely hypotenzive do not give right? Right). Hypotensive or shock would not geet this (very constricted
hypertensive then yea).
Antispasmodics (spasms from pain) (Never give demerol for chronic pain). Too short lifed.
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Carbonic anhydrase inhibitor (carbonic anhydrase makes NaHCO3 , which would typically be useful but if it cannot leave the
pancreas there is no point). Its an enzyme this inhibits the production of NaHCO3.
Antacids you wont be eating so why produce acid in the stomach. Well give you antacids.
H2-receptor antagonists (decrease gastric acid) prevents the production of hydrochloric acid.
Collaborative Care
Nutritional Therapy
o NPO status initially to reduce pancreatic secretion (not for long or youll start breaking down muscle mass and stores)
o Small, frequent feedings
o High-carbohydrate, low-fat, high-protein diet because it is good for repair, low fat.
o Bland diet
o Supplemental fat-soluble vitamins
o Enteral feeding (J or G tubes)
o TPN risk of infection, clots, fat embolisms, etc.
o Supplemental commercial liquid preparations
o Total parenteral nutrition (TPN): it is pre-digested food inserted via a central line
o No caffeine or alcohol
Acute Intervention (risk of shock, risk of pneumonia, etc.)
o Monitor vital signs depending on the patient (e.g., q15min, q30min, q1hr)
Listen to the chest when doing vital signs!
o IV fluids
o Assess respiratory function
o Monitor for signs of hypocalcaemia (e.g., Trousseau and Chvotseks sign)
Ambulatory Home Care
o Physical therapy (due to muscle atrophy from not metabolizing protein).
o Counselling regarding abstinence from alcohol, caffeine, and smoking.
Notes
A person with acute pancreatitis can recover (i.e., the swelling will decrease and the pancreas will repair itself). Recall that the
main reason for acute pancreatitis is alcoholism.
Chronic Pancreatitis
Definition
Progressive destruction of the pancreas with fibrotic replacement of pancreatic tissue.
Strictures and calcifications may also occur in the pancreas.

Two major types:
1. Chronic obstructive pancreatitis
2. Chronic calcifying pancreatitis
Chronic Obstructive Pancreatitis

o Associated with biliary disease.
o Most common cause is inflammation of the sphincter of Oddi associated with cholelithiasis.
o Cancer of the ampulla of Vater.
o Cancer of the duodenum or pancreas.
Chronic Calcifying Pancreatitis
o Inflammation and sclerosis, mainly in the head of the pancreas and around the pancreatic duct.
o Most common form of chronic pancreatitis.
o May be referred to as alcohol-induced.
o Ducts are obstructed with protein precipitates.
o Precipitates block the pancreatic duct and eventually calcify.
o Calcification is followed by fibrosis and glandular atrophy.
o Pseudocysts and abscesses commonly develop pancreatitis.
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Abdominal pain
o Located in the same areas as in acute pancreatitis.
o Heavy, gnawing feeling, burning, and cramp-like.
Malabsorption with weight loss
Constipation
Mild jaundice with dark urine
Steatorrhea (floaty, frothy, foul, fatty stools: recall the 4 Fs) (we dont have lipase to break up the stool looks like oil and
water).
Diabetes mellitus (it can be caused by pancreatitis, but not the other way around)
Diagnostic Studies
Increased serum amylase
Increased serum bilirubin
Increased alkaline phosphatase (indication of inflammation in either the liver or bone)
Mild leukocytosis (the number of WBCs will be increased)
Elevated sedimentation rate (ESR) indication of inflammation (how quickly red blood cells are going to fall out suggests
inflammation or infection somewhere). (heavier because of inflammation or infection so they will fall out of solution quicker).
Secretin (in the duodenum) stimulation test
Hyperglycaemia
Arteriography (want to see what is going on with the blood vessels)
X-ray
Endoscopic Retrograde Cholangio Pancretography (ERCP) (inside, with a dye, in the bile duct and pancreatic duct)
Collaborative Care
Prevention of attacks
Relief of pain
Control of pancreatic exocrine and endocrine insufficiency (pt will need to take enzymes since they arent making them and they
will likely be diabetic and will need insulin)
Surgery (not many successful transplants pancreatic cancer is typically short lived).
Nursing Management
Focus is on chronic care and health promotion.
o Dietary control
o Control of diabetes (because pancreas is destroyed).
o Patient and family teaching
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Unit 14: Adult Chronic Respiratory Disorders
ACIDBASE BALANCE AND ARTERIAL BLOOD GASES (ABG)
Purpose
Arterial blood shows the make-up of blood before it is distributed to the tissues.
The radial artery is typically chosen. This is a very painful procedure.
By treating the underlying condition, the ABGs will typically resolve themselves.
pH
pH is measured on a scale from 1-14, with 1 being extremely acidic and 14 being extremely basic.
The pH is an indirect measure of H+ ion concentration.
Ratio of base (HCO3-) to acid (CO2).
o Bicarbonate is a weak base and carbon dioxide is a weak acid (i.e., the requirements for buffers).
Acids give up (donate) H+ ions, while bases pick up H+ ions.
The expected pH of the body is between 7.35-7.45 (i.e., slightly alkaline).
PaCo2 35-45 mmHg (resp component)
HCO3 22-26 mEq/L (metabolic component) (low is acidic; high alk)
Regulators of Acid/Base
Buffers (there are many buffers in the body used to maintain homeostasis).
o Lots of albumin in the body as buffers
Respiratory system (works to control the bodys acidic conditions via CO2 excretion or retention).
o This works faster than the renal system.
Renal system (works to control the bodys basic conditions via HCO3- by absorbing, retaining, or creating HCO3-).
o Metabolic system
o First buffers, then lungs, then kidneys
Buffers
Primary regulators of changes in acid-base balance.
Act immediately.
Present in blood and tissues.
Take up or release extra H+ ions (e.g., bicarbonate, proteins, globulins).
o Proteins are amphoteric (i.e., both acid and base properties) and are therefore very important regulators.
Respiratory System
Eliminates CO2.
Increased respirations leads to CO2 eliminated from body and CO2 in blood.
Decreased respirations leads to CO2 elimination from body and CO2 in blood.
Responds within minutes to hours to changes in acid/base.
Only 50%-75% effective as a buffer.
o In order to be completely balanced, you need both the respiratory and metabolic systems functioning.
Acid-Base Balance
CO2 + H2O
H2CO3
H+ + HCO3
H2CO3 (carbonic acid) is a weak acid.
Lungs
Respiratory
Fast
Kidneys
Metabolic
Slow
Renal System
Secretes hydrogen (H+) ions and reabsorbs bicarbonate (HCO3-) ions.
Reabsorption and secretion of electrolytes (e.g., Na+, Cl-, K+).
o In order to reabsorb sodium in the kidneys, there must first be the excretion of hydrogen.
o The bicarbonate plays an important role.
Responds within hours to days.
104
ABG Normal Values

pH 7.35-7.45 overall state (i.e., slightly alkaline).
PaCO2 35-45 mm Hg (respiratory component).
o Closer to 35mmHg = alkalotic.
o Closer to 45mmHg = acidotic.
HCO3 22-26 mEq/L (metabolic component).
o Closer to 22mmHg = acidotic
o Closer to 26mmHg = alkalotic
Exam Question!
PaO2 80-100 mmHg partial pressure of oxygen in arterial blood.

SaO2 96-100% arterial O2 saturation.
Oxygen Pressure (PaO2)

Oxygen molecules dissolved in plasma (i.e., not bound to haemoglobin) are free to impinge on the measuring oxygen electrode.
This "impingement" of free O2 molecules is reflected as the partial pressure of oxygen; if the sample being tested is arterial blood,
then it is the PaO2. Although the number of O2 molecules dissolved in plasma determines, along with other factors, how many
molecules will bind to haemoglobin, once bound the oxygen molecules no longer exert any pressure (bound oxygen molecules
are no longer free to impinge on the measuring electrode). Since PaO2 reflects only free oxygen molecules dissolved in plasma
and not those bound to haemoglobin, PaO2 cannot tell us "how much" oxygen is in the blood; for that you need to know how
much oxygen is also bound to haemoglobin, information given by the SaO2 and haemoglobin content.
Oxygen Saturation (SaO2)
Binding sites for oxygen are the heme groups, the Fe2+-porphyrin portions of the haemoglobin molecule. There are four heme
sites, and hence four oxygen binding sites, per haemoglobin molecule. Heme sites occupied by oxygen molecules are said to be
"saturated" with oxygen. The percentage of all the available heme binding sites saturated with oxygen is the haemoglobin oxygen
saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn't reveal how much oxygen is in the blood; for that we also
need to know the haemoglobin content.
The a refers to the pressure (P) or saturation (S) in the arteries. If you see an A, it refers to the alveoli.
A normal haemoglobin value is 120. It is possible to have a high SaO2, but if there is not a lot of haemoglobin for the O2 to bind
to, there may not be great PaO2 values.
iClicker Question
What of the following is true regarding SaO2 and PaO2?
a) SaO2 and PaO2 refer to the same thing.
False. SaO2 refers to oxygen saturation (i.e., the percentage of heme binding sites occupied by O 2), whereas PaO2 refers to
oxygen pressure (i.e., pressure exerted by O2 molecules not bound to haemoglobin).
b) SaO2 is the amount of Hgb saturated with oxygen.
c) PaO2 is the pressure of Hgb.
False. PaO2 is the pressure exerted by the O2 molecules not bound to haemoglobin.
d) PaO2 is measured with a pulse oximeter.
Interpretation of ABGs
Evaluate pH: this determines acidosis or alkalosis.
A pH value of 7.40 is in the middle of the normal range of 7.35-7.45.
o Value below 7.40 is moving towards acidosis.
o Value above 7.40 is moving towards alkalosis.
Evaluate respiratory component (PaCO2).

o If PaCO2 <35, the value is alkalotic.
o If PaCO2 >45, the value is acidotic.
Evaluate the metabolic component (HCO3-).
o If HCO3- >26 mEq/L, the value is alkalotic.
o If HCO3- <22 mEq/L, the value is acidotic.
Example:
o You have a pH of 7.44 (higher, therefore alkalosis), a PaCO2 35 (lower, therefore alkalosis) and an HCO3- value of 22
(lower, therefore acidosis).
o All these values are within normal limits, but they are all at the extreme ends of the norms.
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It is important to determine which component (PaCO2 or HCO3 ) matches the pH.

If the pH is decreased or increased is the underlying disorder respiratory or metabolic?
o You will look for the value that is on the scale of normal.
Respiratory
o pH, PaCO2
o pH, PaCO2
Metabolic
o pH, HCO3
o pH, HCO3
alkalosis
acidosis
alkalosis
acidosis
If both the respiratory and metabolic components match the pH, it may be a mixed disorder, which is rare, or there may have been
an issue with the ABG (i.e., the blood may have accidently been taken from a vein as opposed to an artery).
Determine Degree of Compensation

Absent or Uncompensated:
o pH is not within normal range (i.e., 7.35-7.45).
o The component that does not match the pH imbalance is still within its normal range (i.e., there is no effort made by the
body to try correct the altered pH value).
Partial:
o pH is not within normal range.
o The component that does not match the pH disorder is above or below the normal range (i.e., the body is trying to
regulate the pH to normal values).
Complete or Fully:
o pH is within the normal range and both components are either above or below normal range.
If appropriate, treat the underlying cause and then treat acid-base imbalance. Often times, once the underlying cause has been
treated, the acid-base imbalance will correct itself.
ABG Interpretation
Example #1:
We are in acidosis (i.e., low pH).
CO2 47 (normal range is 35-45 it is high and acidotic)
HCO3- 24 (normal range is 22-26 it is normal)
Since the pH is outside the range and the HCO3- is normal, we are not compensated (therefore partially compensated or
absent).
Ac Nor Alka
idi
mal
line
c
p
H
O2
HC
O3
The acidosis appears to be respiratory in nature (due to the CO2 value). Since the HCO3- value is within normal ranges, we have
uncompensated respiratory acidosis.
Steps to Acid-Base Analysis

pH
o Acidotic, alkalotic, or normal?
PaCO2
o High or low?
o Causing or compensating?
HCO3-
106

o
o
o
High, low, or normal?

Causing or compensating?
Short- or long-term problem?
Respiratory Acidosis
pH
low
PaCO2
high
What could cause this condition?
COPD, sedatives, overdose. pneumonia, anything that
causes hypoventilation, low resp rate, shallow breaths,
quiet death decreased resps
o
Respiratory Alkalosis
pH
high
PaCO2
low
o Hyperventilation (due to anxiety, pain, sepsis).
Metabolic Acidosis
Metabolic Alkalosis
pH
low
pH
high
HCO3
low
HCO3
high
o Kidney failure, overconsumption of antacids.
Kidney failure, diabetes (i.e., DKA). Drugs, meds,
overdosing,
More Fun with Acid-Base
Mixed diagnoses:
o More than one problem:
Acute and compensated respiratory acidosis.
Respiratory and metabolic acidosis.
If you treat the underlying cause, the acid-base imbalance will sort itself out.
Hyperkalemia
o H+ drives K+ out of cells into serum (recall that alkalosis cause K+ to enter the cells).
o Treat acidosis, hyperkalemia resolves.
iClicker Question
A client with an acid-base imbalance has an altered potassium level. The nurse recognizes that the potassium level is altered
because of which following reason?
a. Potassium is returned to extracellular fluid when metabolic acidosis is corrected.
False, K+ is returned to the cell when acidosis is corrected. Alkalotic conditions cause K+ to enter the cell.
b. Hyperkalemia causes alkalosis that results in potassium being shifted into the cells.
c. Acidosis causes hydrogen ions in the blood to be exchanged for potassium from the cells.
d. In alkalosis, potassium is shifted into extracellular fluid to bind excessive bicarbonate.
False, K+ is shifted into the cells during alkalosis.
Example #1
pH 7.36
PaCO2 67
PaO2 47
HCO3- 37
What is this? Fully compensated respiratory acidosis.
o Acidosis because the pH is lower on the normal scale.
o Respiratory in nature.
o Fully compensated (because both the CO2 and HCO3- are outside the normal ranges).
Ac
idi
c
Nor
mal
pH
Alka
line
107

O2
HC
O3-
Example #2
pH 7.18
PaCO2 38
PaO2 70
HCO3- 15
What is this? Absent/uncompensated metabolic acidosis.
o Acidosis.
o Metabolic.
o Absent/uncompensated because the CO2 is
normal. It cannot be fully compensated because
the pH is not within normal ranges.
Ac
idi
c
p
H
Nor
mal
H
C
O3-
Alka
line
CO2
Example #3
pH 7.58
PaCO2 35
PaO2 75
HCO3- 50
What is this? Uncompensated metabolic alkalosis.
o Alkalosis.
o Metabolic due to the HCO3-.
o Uncompensated because CO2 is normal.
108
Ac
idi
c
Nor
mal
pH
CO2
Alka
line
HC
O3-
Example #4
pH 7.60
PaCO2 30
PaO2 60
HCO3- 22
What is this? Uncompensated respiratory alkalosis.
o Alkalosis.
o Respiratory.
o Uncompensated.
Ac
idi
c
Nor
mal
Alka
line
Example #5
pH 7.28
PaCO2 28
PaO2 70
HCO3- 18
What is this? Partially compensated metabolic acidosis.
o Acidosis.
o Metabolic.
o Partially compensated (i.e., the CO2 is trying to
correct the acidity).
pH
CO2
HC
O3-
109
Ac
idi
c
p
H
Nor
mal
H
C
O3Case Studies
Case Study #1: Jeri
Alka
line
CO2
110
1) What ABGs do you expect?

Were expecting pneumonia due to the increased temperature, crackles in lower lobes, productive cough.
The temperature is not high enough to indicate sepsis.
Resp acidosis (think hes retaining CO2)
pH low
Sats are: 85
Pao2 are: 50
CO2 high (due to retention)
HCO3- maybe a change
Respiratory acidosis.
2) What is your treatment?
DB&C.
Increase fluids.
Antibiotics therapy.
Case Study #4: Alan

17 years old
History of:
o feeling bad
o fatigue
o constant thirst
o frequent urination
Blood sugar is 48 mmol/L
Respirations are 28 and deep
Breath has a fruity odour
His lungs are clear
1) What ABGs do you expect?

DKA.
Respirations 28 and deep: hes trying to compensate.
Metabolic acidosis.
pH acidosis
CO2 high
HCO3- low
Insulin
Electrolyte replacement/fluids
r/a
Case Study #5: Anthony

History of nausea and vomiting for the past week.
Has been self-medicating himself with baking soda to control his abdominal discomfort.
1) What ABGs do you expect? Metabolic alkalosis.

Dehydration.
There does not appear to be a corrective respiratory rate.
Wed expect him to be basic (i.e., high pH).

Normal CO2.
HCO3- high.
Give him an anti-emetic.
Treat electrolyte imbalances (i.e., hypokalemia).
Figure out N & V
111
Case Study #6
ABG results are: pH 7.20, PaCO2 58, PaO2 59, HCO3- 24
1) Describe a patient that would have these ABGs.

2) What is the treatment?
Case Study #7
1) Describe a patient that would have these ABGs.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
Case Study #8
1) Describe a patient that would have these ABGs, including

history and assessment.
Case Study #9
1) Describe a patient that would have these ABGs

COPD What it is?

It may also be referred to as chronic bronchitis or emphysema.
There is a problem with gas exchange, which leads to a decrease in O2 saturation. Your body will react by increasing its
respiratory rate and heart rate (to try increase O2 delivery to the tissues).
Pathologic changes in patients with COPD occur in the large (central) airways, the small (peripheral) bronchioles, and the lung
parenchyma.
Most cases of COPD are the result of exposure to noxious stimuli, most often cigarette smoke.
Characteristics:
o These patients have excess secretions and a decreased ability to excrete this phlegm.
o Bronchoconstriction.
o Airway spasms (i.e., continuous cough).
This is generally not reversible (with the exception of asthma), especially when a lot of damage has occurred.
Air gets trapped and we cant expel it. We have to make room somehow, so we press on the diaphragm and gets pushed down.
Intercostal cartilage as you get older become more calcified. Mostly d/t cigarette smoking (and being older). Smoking is bad.
Cigarette Smoking
80-90% of COPD deaths in North America are related to tobacco smoking.
~4,000 chemicals and gases inhaled with cigarettes.
Nicotine acts as a SNS stimulant.
o It causes vasoconstriction of the peripheral blood vessels which causes an increase in heart rate and workload. This will
lead to an increase in blood pressure.
Questions to ask patients with COPD:
o Do you experience SOB? When (i.e., how much exercise/how far/how long)?
o Do you have a cough? Is it productive? What does it look like? When does this occur (e.g., on exertion, in the morning,
during the night)?
o Do you get frequent colds/flues in the winter?
Inflammatory response goes on with cellular hyperplasia, ciliary activity cant move things through, build up of mucous. CO2
breathing in and less oxygen able to use for the rest of the body.
How much they smoke and for how long. Biggest questions to ask.
Have they tried to quit?
D/t hyperplasia crackles.
Decreases cilliary activity.

Cellular hyperplasia (i.e., increase in mucous/secretion production).
o This makes it harder for the body to move these excess secretions through a constricted airway.
Carbon monoxide.
o It replaces O2 at the receptor sites. This decreases the bodys ability to bring oxygen to the cells.
Involuntary smoke exposure (second hand smoke).
So how does cigarette smoking relate to COPD?
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Infection
Major contributing factor to the aggravation and progression of COPD.
Recurring infections impair normal defence mechanisms.
o The excess mucous trapped in the bottom of the lungs is a lot harder to excrete, which may lead to pneumonia.
Bacteria like moist dark areas. COPD + cough (say green sputum) pt may automatically be put on antibiotics because we know
they wont be able to move the secretions d/t COPD. Sometimes prophalyaxily. If you dont they may die vs resistant strains
(Catch 22 there).
Heredity
-Antitrypsin (AAT) deficiency is the only known genetic abnormality that leads to COPD.
AAT deficiency accounts from <1% of COPD. These patients will have COPD at a young age.
It breaks down the elastin in the lungs.
Normal Manifestations Associated with Aging

Gradual loss of elastic recoil.
Lungs become rounded and smaller.
Thinner alveolar walls contribute to loss of septal tissue and alveolar capillaries.
Arterial O2 levels decrease.
PaO2 falls as a rate of 4 mmHg for each decade of life, beginning after age 20.
Thoracic cage changes from osteoporosis and calcification of costal cartilages.
Combined with smoking is worse.

Thin walls is where gas exchange occurs. CO2 falls every decade.
Decreased ability to exchange gases so decreased PO2 now. Less capacity now.
Start using sternocleidomastoid and abdominals to breath. Body tries to compensate by making space.
Chapter 31 chart
Never give cough serums to COPD pts. We want them to cough. Most meds are inhaled meds.
Lots of people will have copd and chronic emphysema.
Dillate the airways, inhaled corticosteroids, antibiotics, oxygen (tanks homecare too)
Emphysema
There is a decrease in number of alveoli and the ones that are present enlarge, decreasing the surface area and ability to exchange
gas.
This destruction of alveoli is permanent.
Two Types (pg. 671)

1) Centrilobular
The central lobes are hyperinflated and the alveoli appear somewhat normal. boule are enlarged
2) Panlobular
The alveoli are all enlarged. boule are cauliflower like
The tripod position allows the chest to expand and help the person breathe.
Pathophysiology
There is a decrease in number of alveoli and the ones that are present enlarge, decreasing the surface area and ability to exchange
gas.
This destruction of alveoli is permanent.
What do bullae have to do with anything?
o They are cyst-like blobs in the alveoli that are fluid encapsulated.
How does the body compensate?
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o Changes in VS: RR, cardiac workload in order to circulate oxygenated blood.
What would this person look like?
o Emaciated (the body is working hard and using a lot of calories just to breathe; these patients are also not hungry)
o Tripod position
o Using all the respiratory muscles (e.g., intercostals, diaphragm, sternocleidomastoid)
Will hear hyper resonate sounds d/t trapped air. (99 Tactile fremulis)
Use of tripod muscles, accessory muscles
Weight loss less calories, more fluids, difficulty eating so need nutrient dense calories.
Earliest symptoms:
o Frequent productive cough during winter (especially at the change between fall and winter).
o Frequent respiratory infections.
Bronchospasm can occur at end of paroxysms of coughing (i.e., the inability to stop coughing).
Cough usually exacerbated by respiratory irritants or cold air.
Anything that disrupts air quality will bother these individuals.

Ensure you have a list of the resp infections over the past few years.
Fast acting puffer
Chronic Bronchitis
Description
o Presence of chronic or productive cough for 3 or more months in each of 2 successive years in a patient whom other
causes of chronic cough have been excluded (e.g., asthma).
Tend to do it within the first year. Will start them on things like ventolin, etc.
Narrow airways, hypersecretions, Co2 levels go up/elevated (responsible for the urge to breath), hypoventilating d/t
hypercapnia.
Hr increases, not very oxygenating blood = pulmonary vasoconstriction
Resp acidosis confusion, forgetful,
More red blood cells are present, will increase in viscosity (like jelly) of deoxygenated blood.
Too much preload, end up with pulmonary (right sided) failure
Pathophysiology
Hypoxemia ( O2), hypercapnia ( CO2), and respiratory acidosis (due to CO2) usually develop late in disease.
o The alveoli are working fine; they just cant enough O2 because of the mucous present.
o The body will increase their production of RBCs in order to have more receptor sites for O2. These patients will have a
very high haemoglobin.
o Acidosis will eventually cause vasoconstriction, which is problematic because there is also an increase in RBCs that will
try squeeze through a constricted vessel, therefore increase the BP.
Inflammatory swelling + thick mucous = narrowing of airway lumen and diminished airflow.
Cough is often ineffective to remove secretions.
o This is because there are no cilia to move the mucous and the patient is unable to take a deep breath.
Hyperplasia of mucus-secreting glands in the trachea and bronchi.

Increase in goblet cells (cells whose sole function is to secrete mucin, which dissolves in water to form mucus).
Disappearance of cilia.
Chronic.
Alveolar structures and capillaries are normal.
Cilia cant move things through, DB + C uses diaphragm muscles. May be able to move it around but wont be effective. Meds,
bronchodilator, mucolytics, chest physio,
Chronic Bronchitis
114
Knowing all of this, what do you think this person would look like?
Haemoglobin may reach 200 g/L or more.
o This is because of the lack of O2. Many of these haemoglobin molecules will not get the O2 they need.
Normal hgb (120-130) 200 is high.
Pt will be cyanotic
iClicker Question
When reviewing the arterial blood gases of a client with COPD, the nurse identifies late-stage COPD based on which of the
following results?
1. pH 7.26, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO3 30 mmol/L
False. The PaCO2 is high, but still within normal range. Wed expect it to be higher and also have a high HCO3-.
False. The pH is within normal range. We would expect an acidic pH due to the retention of CO2.
False. The pH is high and thus basic. We would expect an acidic pH due to the retention of CO2.
COPD
Complications
Cor Pulmonale (i.e., failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries
and right ventricle of the heart.)
Pulmonary Hypertension
Acidosis
Polycythemia (i.e., in RBCsdeveloped secondary to a resp problem)
o This blood is extremely viscous and may lead to pulmonary hypertension.
Distended neck veins (due to problems with the right side of the heart).
Hepatomegaly (due to portal hypertension) with upper quadrant tenderness.
Ascites (due to third space shifting).
Epigastric distress (due to the increase in pressure on the diaphragm).
S3 & S4 heart sounds.
hyperviscosity so extra heart sounds
Peripheral edema.
Weight gain.
Acute exacerbations of chronic bronchitis.
Peptic ulcer disease and GERD (due to ascites, and hypertension).
Pneumonia. and ? Part off Right sided failure are really important to tx before going into acute resp failure. ACP status important
re intubation.
Acute respiratory failure.
People with COPD have their breathing triggered by O2 levels (not CO2 levels as in normal, healthy individuals). If they have too
much O2, their breathing mechanism will not shut off altogether, as previously believed, but their breathing will be hindered.
Acute Respiratory Failure

Can be caused by cor pulmonale or discontinuation of bronchodilators or corticosteroid medication.
Need meds (broncho dilators, etc.) abrupt cessation can lead to resp distress. Need things like ventolin at minimum.
-adrenergic blockers may exacerbate respiratory failure in patient with asthmatic component.
o May cause bronchospasm so you dont want to give this to them
o Caution with beta blockers. Wheezing or asthmatic component beta blockers will be used cautiously.
Narcotics and sedatives can cause respiratory depression, making them a potential danger to people with COPD.
Diagnostic studies
What would you want to do?
o Vital signs
o Dark patches (pneumonia)
o PFTs litres you can breath in and inspiratory and expiratory capacity
115

Chest X-ray (although it will not show much early on; may reveal an enlarged heart)
Spirometry (i.e., the amount of air entering the lungs and the amount of air the lungs can expel with each expiration)
Residual volume (i.e., the amount of air that does not leave the lungs).
Cardiac tests
ABGs what will we find?

o
o
o
o
o pH decreased
o PaO2 decreased
o CO2 increased
o HCO3- increased (in time as a compensatory mechanism)(increasing trying to buffer acid and high CO2)
Typical findings include reduced FEV/FVC (forced expiratory volume/forced vital capacity) and increased residual volume and
total lung capacity.
Ratio of <70% suggests presence of obstructive lung disease.
Collaborative Care
Smoking cessation
Drug therapy
o Corticosteroids
o Bronchodilators (e.g., Ventolin) (some for large and some for small),
o Anticholinergic (e.g., Atrovent)
Check medication book.
inhaled epi
To prevent bronchospasms
O2 therapy
o O2 narcosis (too much O2). You want to keep this persons SaO2 around 92%.
Respiratory therapy
o Pursed-lip breathing (blowing out candle breathing)(this enables a person to expel more CO2).
o Diaphragmatic breathing.
o Chest physiotherapy (e.g., pummelling).
o Cough in the later afternoon in evening if asthmatic, other might be in the morning
Aerosol-nebulization therapy.
Nutritional therapy: high calories, high protein, avoid foods that may cause gas, small frequent meals
Nursing Management
Nursing Assessments
o Health history
o Physical assessment
What symptoms would you expect to find in an acute exacerbation of COPD?
Cough, sputum, SOB, may see a barrel chest, use of accessory muscles,
Crackles if there is bronchitis component, pale color, pulse elevated (depending on progression of disease), increased Co2 =
hypoventilating (urge suppressed),
Nursing Assessments
Acute exacerbation
What are you going to do about it?
o Activity (not to the point of tiring the patient).
o Pt may be leaning forward, keep HOB elevated,
o What would you expect to do for patients in these environments?
Encourage patient to pace themselves.
Encourage adherence to medication therapy.
Use several pillows to stay propped up while sleeping.
Get rest.
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TUBERCULOSIS
Mycobacterium tuberculosis
Kills more people worldwide than any other infectious disease.
19-34% of worlds population estimated to be infected.
8 million new cases each year with 3 million deaths.
Endemic of TB with HIV infection.
Multidose resistant strains of Mycobacterium tuberculosis.
It is reversible if treated early.
Vulnerable, overcrowding, new immigrant populations.
Airborne, droplet.
Tuberculosis
It is seen in developing countries, over-crowded housing, and with poor nutrition.
It is spread by airborne droplets (e.g., sneezing, coughing) that are inhaled after prolonged exposure.
It likes to grow down low in the lungs.
Ghon tubercle (i.e., the central portion of lesion).

o Undergoes necrosis characterised by a cheese-like appearance ( called caseous necrosis) or liquifactive necrosis,
where liquid drains into connecting bronchi and produces a cavity.
Healing of primary lesion occurs by resolution, fibrosis, and calcification. The granulation tissue surrounding the lesion may
become more fibrous and form a collagenous scar around the tubercle.
If the initial immune response is unsuccessful at controlling the organism, clinical disease results.
Early stages are usually free of symptoms!
Systemic symptoms:
o Fatigue
o Weight loss
o Malaise
o Low-grade fever (e.g., 38.1C)
o Anorexia
o Night sweats
Acute symptoms:
o High fever
o Pleuritic pain
o Chills
o Productive cough (especially blood)
o Generalized flu symptoms
o Bloody cough severely sick, people must take precautions when it comes to coughing,
o Initially flu-like symptoms, malaise, not hungry
o
o Complications
Military TB/Necrotic Ghon
o It has spread beyond the lungs and reached other organs.
Pleural effusion and empyema (puss in the lungs)
TB pneumonia
o
o These types of TB are hard to treat.
o
Skin testing (Mantoux) does not necessarily mean you have it, but that youve been exposed to it
Chest X-ray (this may reveal a Ghon complex)
Sputum studies
Bacteriologic studies
Gastric washings
CSF
Cultures
Nucleic Acid Amplification
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Different ways to check sputum (aside from CSF), sputum samples.
o Collaborative Care Active Disease

5 primary drugs used:
Newer drugs
1. INH
o Cipro
2. Rifamate
o Gloxin
3. Pyrazinamide
o Zagam
4. Streptomycin
o Priftin
5. Myambutol or Ethambutol
Direct Observation Therapy (DOT)
if they are unreliable or homeless, we will watch you take your meds. You dont have a choice; you must take your meds.
Collaborative Care
Latent TB infection
o Individual is infected with bacilli but is not actually ill.
o Usually treated with INH for 6-9 months.
Not ill but bacilli (not sick and not contagious) lots of nurses or a family if one member has tb
Vaccine
o Bacille Calmette-Gurin (BCG)
Efficacy not clear.
Screening programs in high risk groups.
Identify contact of patients with TB.
Teach:
o Tissues in paper bag then garbage (i.e., double bag Kleenex).
o Cover mouth when coughing/sneezing.
o Handwashing.
o Medicine regime and encourage compliance (it is necessary).
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Unit 15: Care of the Client with Hematologic and Immune Disorders
PTT and INR = 2-3times high. Antidote = vit K
Overview Structures and Functions
Hematology
o Study of blood and blood-forming tissues (e.g., bone marrow, the lymphatic system, and the spleen).
Bone Marrow: Produces ALL blood cells
Hematopoiesis
o Blood cell production that occurs within the bone marrow.
Red marrow
o Produces blood cells and this red marrow is found in flat (e.g., sternum, scapula) and irregular bones (i.e., not long
bone).
The sternum is typically not used any more for bone marrow aspiration because if the needle used to aspirate
the marrow slips, it will hit the left ventricle.
The pelvic girdle is typically used.
Donor has it more difficult
Blood
o Two major components:
1. Plasma
2. Plasma Proteins
The major proteins are albumins, globulins, fibrinogen-fibrin complexes.
o Blood cells
Erythrocytes (RBC), leukocytes (WBC), and platelets (i.e., thrombocytes)
*Development of Blood Cells
Stem cell
Erythroblast
Normoblast
Basophilic
metamyelocy
te
Reticulocyt
e
Basophil
(histamine
)
Erythrocyt
es (RBC)
Myeloblast
Eosinophilic
metamyeloc
yte
Monoblast
Neutrophilic
metamyelocy
te
Band cell
Monocytes
Lymphoblas
t
Megakaryoblast
Lymphocytes
Megakaryocy
te
Found in bone
marrow
Found in blood
Leukocytes (WBCs)
Thrombocytes
(platelets)
Eosinophil
Neutrophil
You should not see erythroblasts in the blood! This is only seen in the bone marrow. The reticulocyte will be seen in the blood
and will mature into an erythrocyte.
What would be worse to live without, monoblasts or myeoblasts? The myeoblasts, because this the second line of defence (i.e.,
the inflammatory response).
If you reduce the formation of RBCs, you may not have a lot of platelets.
3rd line of defense is the immune system
RBC live for 120 days
o WBC between 4-10,000
o Myloblasts = granlocytes
o Need leukocytes for inflammation
o Monoblasts and lymphocytes 3rd line of defence (in the blood, spleen, lympth nodes)
o
Types and Functions of Leukocytes
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Type
Cell Function
Granulocytes (Myeoblasts)
Neutrophils
Phagocytosis, early phase of inflammation
Eosinophils
Phagocytosis, parasitic infections
Basophils
Inflammatory response, allergic response
Agranulocytes
Lymphocytes (T cells)
Cellular, humoral immune response
Thelper cells, Tkiller cells
Monocytes
Phagocytosis; cellular immune response
If the eosinophils levels are increased, you can assume a parasitic infection.
Overview Structures and Functions

Spleen
o Hematopoietic (blood form only in fetal development)
o Filter (it filters old and defect red blood cells)
o Immune
The immune function is greatly affected when the spleen is removed.
o Storage (30% of the platelets are stored in the spleen)
Lymph system
o Transport interstitial fluid into the blood stream (protein and fat from the GI; and excess fluid created during times of
edema as a method of preventing edema)
o Filter
During times of infection, the lymph nodes are swollen and painful if the lymphatic system is functioning
optimally.
A swollen, non-painful lymph node is problematic.
The study of haematology evaluates the following 4 aspects:
1. The ability to transport O2 and CO2.
This is acid-base balance.
2. Coagulation of the blood.
3. Combating infections.
4. Removal of old and dead cells.
Anaemia
It is a broad category of disorders involving a deficiency of RBCs. It is not seen on its own (a lot of diseases come with anemia).
Anaemia is reflected in:
o Haemoglobin
This explains the O2 carrying capacity of the blood (recall that every haemoglobin molecule can carry 4 O2
molecules). Travels as carbolic acid (switches in the lungs to carbon dioxide).
Little volume = lots of cells hgb HIGH? Dehydrated?
Normal values:
Females: 120-160
Males: 140-180
o Hematocrit (Going to tell you if youre dilutional, or dehydrated)
The percentage of the pack cells (i.e., RBCs) to the total volume.
This is the value you want to look at to determine if someone is haemorrhaging.
Normal values:
Females: 38-47%
Males: 40-54%
o RBC count
Normal values:
Females: 4-4.5 million
Males: 4.5-6.5 million
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Classification by red cell morphology (recall that cytic means cell; chromic means haemoglobin)
o Cell size/HGB content
o Classification
o Decreased red blood cell production
o Increased red blood cell destruction
o Blood loss
There are many combinations possible:
Normocytic
Normochromic
Microcytic
Hypochromic
Macrocytic
Hyperchromic
o Tablee 33-1
o Types:
Normocytic Normochromic Anaemia
Normal cells and normal amount of haemoglobin.
This could be due to haemorrhage (i.e., acute blood loss), haemolysis, chronic renal disease,
pregnancy, aplastic anaemia, or other conditions that destroy RBCs.
Treatment: administer pack cells or blood.
Microcytic Normochromic Anaemia
Small cells with normal amount of haemoglobin.
Seen with tumours, infections, viral illnesses.
Macrocytic Normochromic Anaemia
Large cells and normal amount of haemoglobin.
This is also known as pernicious anaemia. There is a problem with B12. Recall that the gut has
intrinsic factors that will help the body absorb the vitamin B12. These patients will require monthly IM
injections. Orally if IF, injection if no IF
Cobalamin (Vitamin B12 deficiency), liver disease, folic acid deficiency.
Treatment: give patient B12.
Microcytic Hypochromic Anaemia
Small cells and low amount of haemoglobin.
Seen in iron and folic acid deficiency, thalasemia, lead poisoning, as well as slow bleeds (e.g.,
prolonged menstrual periods).
Treatment: give patient folic acid.
Classification by etiology/cause
o Dietary Deficient States
Deficiencies of B12, folic acid, and iron.
o Hereditary Disorders
Sickle cell anaemia, thalasemia.
o Bone Marrow Disease
The body could not be making enough, breaking too much down, or making too much.
Aclassic anaemia means that all blood types and cells are low.
o Bleeding States
Acute (e.g., haemorrhage)
Chronic (e.g., prolonged menstrual bleed)
o
o Key Features of Anaemia
Skin
o Pallor: due to reduced amount of haemoglobin and reduced blood flow to the skin.
o Jaundice: occurs due to the increased breakdown of RBCs which causes an accumulation of bilirubin.
o Pruritis: due to increased serum and skin bile salt concentrations.
o In addition to the skin, the sclera of the eyes should be evaluated for jaundice as it is a better representation of the
integumentary system.
CVS
o The CVS changes that are seen results from the hearts attempt to increase the distribution of O 2 via the blood to the
bodys cells.
o Cardiac output is maintained by increase the heart rate (as seen below) and stroke volume).
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o
Tachycardia (i.e., a compensatory mechanism) which may lead to palpitations, chest pain, and murmurs (because the
heart does not have the time to adequately fill before sending blood throughout the body). The decrease in blood
viscosity will also contribute to the murmurs and bruits.
A person with a murmur will have to take antibiotics before going to the dentist in order to prevent endocarditis.
In extreme cases, angina pectoris or an MI can occur if myocardial O2 needs are not met.
o
Lungs
o The pulmonary changes seen reflect the lungs attempt to increase the amount of O2 reaching the lungs.
o Dyspnea at rest, tachypnea, tire easily.
Neurologic
o Dizziness, syncope, headaches, and brain damage if the body does not get enough O2 (i.e., 3 minutes without O2 will lead
to brain death).
Other
o Chronic fatigue.
o
o Collaborative Management
History
o Recent blood loss or trauma; chronic liver, endocrine, or renal disease (including dialysis); medications; surgery or other
treatments.
Lab
o Haemoglobin (Hgb) and hematocrit (Hct) are both expected to be low.
RBC indices MCV, MCH, MCHC
MCV = mean cell volume (i.e., cell size)
MCH = mean cell haemoglobin (i.e., amount of haemoglobin)
MCHC = mean cell haemoglobin concentration (i.e., the saturation of haemoglobin)
TIBC and Serum Iron
TIBC = total iron-binding capacity (i.e., the amount of iron stored in places other than the serum)
Feritin in liver (called)
Reticulocyte count
You do not want a lot of reticulocytes. Too many reticulocytes will indicate that bone marrow is
sending out the RBCs too early.
o
o Treatment
This will depend on the cause (e.g., some types may require Vitamin B12, others folic acid, etc.).
o
o Polycythemia
This is an absolute increase in RBC mass.
Erythropoietin is a hormone produced by the kidneys in response to low levels of O2. It stimulates the production of erythrocytes.
Types:
o Primary (a.k.a., polycythemia Vera)
It is insidious disease due to a chromosomal mutation.
The RBCs, granulocytes, and platelets will be affected.
The erythropoietin will be either decreased or normal.
Splenomegaly and hepatomegaly are often manifested.
o Secondary
This is a normal physiologic response to hypoxia.
Long-distance athletes will often train in high altitudes so their bodies will have more red blood cells. These
red blood cells will last up to 120 days, meaning that when they get to a lower altitude, their muscles will have
more O2 available due to the increase in RBCs.
The erythropoietin will be increased.
o
o Clinical Manifestations & Complications Polycythemia Vera
Manifestations will be hypertension due to hypervolemia, and hyperviscosity.
o The body will move from second to first space shifting.
o The heart rate will be increased, there will be clotting problems (e.g., DVT)
o Blood vessels breaking as well as clotting.
o Headaches, dizziness, vertigo, tinnitus, and visual disturbances.
o
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1)
2)
3)
4)
Complications:
o Most serious stroke (due to a thrombus).
o Haemorrhage (due to the hypertension and the bursting of the over-distended vessels).
o Generalized pruritis (due to the increase in basophils).
Recall that the granulocyte production (i.e., basophils, neutrophils, and eosinophils) has increased.
o Uric acid is a by-product of cell breakdown (which is common as so many RBCs are being destroyed). A form of gout
may therefore be seen due to this increase in uric acid crystals. Hyperuricemia (increase of uric acid in the urine) may
also be exhibited.
o
o Diagnosis
CBC (it is expected that the RBC count is going to be increased)
Alkaline phosphatase (will increase as an indication of bone or liver disease)
Uric acid (will be increased; it is a by-product of protein breakdown)
Histamine (increased due to the increase in number of basophils)
Bone marrow (bone marrow aspiration would reveal increased number of erythroblasts)
Splenomegaly
o This is never found in secondary anaemia, only primary.
o The spleen is responsible for destroying old and defected blood cells, meaning that it is working harder to accommodate
all the extra RBCs and therefore increasing in size.
o Erythropoietin expecting it ti be high. Its released when you are hypoxic, primary its low or normal. Secondary its
high.
o
o Collaborative Management
Directed at reducing blood volume and viscosity and bone marrow activity.
Reduce hct to less than 45-48%
o
Phlebotomy
o Done until the hematocrit is near 50%.
Hydration if the person stands to become dehydrated
o I&O is extremely important.
Myelosuppressive Agents (e.g., Methotrexate)
o This is to suppress the bone marrow from producing a lot of RBCs.
Allopurinol (recall that this is anti-gout)
o Used to decreased your uric acid
Anti-platelet Agents (e.g., Plavix/ASA)
This person can become anaemic. Supplemental iron should not be given as the body will then start to make more RBCs.
o
o Thrombocytopenia
Thrombocytopenia is when platelet count is decreased.
o Normal 150,000L-440,000L.
o Thrombocytopenia <150,000L.
Normal Platelet function:
o Platelets form haemostatic plugs in a fibrin mesh in order to prevent bleeding/promote clotting.
o Normal lifespan of 10 days
Thrombocytopenia can be either inherited, as seen in Fanconi syndrome (pancytopenia) and hereditary thrombocytopenia, or
acquired, as seen in aplastic anaemia, chronic alcoholism, and other conditions.
o
o Causes
Failed Platelet production
Certain drugs (e.g., myelosuppressant), radiation, leukemia.
Increased Platelet destruction
Autoimmune disorders, alcohol, sepsis.
Loss of Platelets
Haemorrhage.
Intravascular Dilution
o
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o Implications
>50,000L potential haemorrhage from minor trauma (e.g., nose bleed).
10-50,000L spontaneous bleeding.
<10,000L often fatal, severe bleeding risk.
o
o Signs and Symptoms
Purpura, which is a combination of ecchymosis and haemorrhages.
Petechiae and blood blisters are usually seen.
o
o Sites to Monitor
Generally limited to skin and mucous membranes.
Arms, legs, upper chest and neck.
o
o Treatment
Withdraw or treat stimulus (e.g., drugs, therapy).
Precautions to avoid bleeding.
Corticosteroids (they suppress the immune response).
Administer platelets.
o Except during DIC = Disseminated Intravascular Coagulation, which occurs during abdominal surgery.
Attempts to clot, but it doesnt work, so it just results in a bigger hemmorahge.
Splenectomy.
o
o Immune Thrombocytopenia Purpura (previously known as Idiopathic Thrombocytopenia Purpura) ITP
It is an autoimmune disease causing platelet destruction (#1 reason why this disease happens)
Acute
o Occurs in patients with acute, post-viral infections (e.g., chicken pox).
Chronic
o Is typically linked with HIV and Lupus.
The platelets are coated with antibodies, which, when passed through the spleen are seen as foreign and destroyed by
macrophages. Platelets typically survive for 8-10 days; however, in patients with ITP, the lifespan of the platelets is between 1-3
days.
o
Fever
Enlarged spleen
Bleeding mouth, nose
Risk factors such as HIV
o
o Diagnosis
History and lab
Includes all medications, including OTC and herbal medications
Bone marrow aspiration
o The megakaryocytes will be high because the thrombocytes are being destroyed from the autoimmune process. This will
cause the body to increase the megakaryocyte production.
Decreased platelet count
If bleeding decreased Hgb and Hct
Idiopathic Thrombocytopenia Purpura
o
o Treatment
Bleeding precautions (apply pressure)
Oral corticosteroids (e.g., prednisone) help suppress the immune function of the spleen. In addition, corticosteroids suppress
antibody formation. (suppress immune sytem)
IV Immunoglobulins (as the person has developed antibodies) (more at risk for infection)
Blood replacement therapy (never give with abdominal sx d/t dic risk, can give constuient blood)
Splenectomy
Avoid use of ASA anti-platelet inhibitor, dont t take otc St. Johns wort.
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o
o
o
o Note
An antidote for heparin is Vitamin K.
o
o Heperain Induced Thrombocytopenia and Thrombosis Syndrome/HITTS
Platelet destruction(possible immune response of body rejecting heparin so will need to give more and more heparin. If INR is
really high - Antidote is Protamine Zinc.
Vascular endothelial injury
Exchanging blood more serious
Believed to be an immune mediated response to heparin
Treatment d/c heparin, plasmaapheresis (exhchanging plasma more serious), individual reaction, INR raises significantly ,
protamine zinc to reveerse.
Thrombocytopenia
50,000 potential haemorrhage from minor trauma
10-50,000 spontaneous bleeding
<10,000 often fatal, severe bleeding risk.
o
o Neutropenia
It is a decrease in number of neutrophils (i.e., <1,000-1,500 L). Granulocytes in particular.
It may be a primary hematologic disorder but it is more often associated with other disorders:
o Ca chemotherapy
o SLE
Chemotherapy kills fast growing cells.
o Adverse drug reactions
o Mononucleosis its transient
o TB
o Reasons for becoming Neutropenic: Drug therapy, haematological disrders, leukemia, HIV, autoimmune disorders,
infections, severe sepsis, bone marrow infiltration, transfusion reactions, dialysis.
o
o Skin first line of defence, then immune system (neutrophils) very at risk for infections.
o
o Know aplastic anemia low everything.
o
Depends on severity
o Diminished phagocyte response
There is diminished phagocytosis (i.e., inflammatory response), thus making the patient more susceptible to
infection. Might think UTI. Must get sample. If suspected of neutropenia dont wait. Dont want to mask a
fever either. Temp is 38 or 38.5 for fever. Treat or they will die. Cant wait for the results. Tx immediately. Dx:
differentials (wbc with differential including ANC (absolute neutrophil count), hgb, hct, reticulocyte count and
platelets, drug hx, bone marrow aspiration)
o Fever
The cardinal signs of inflammation are not greatly exaggerated. For example, the patients temperature may rise
from 36.8C to 37C.
o Infection
If the urine is cloudy and smells, send a sample down for C&S but start antibiotics immediately (i.e., broad
spectrum antibiotics) as the patient may be dead by the time the C&S comes back from the lab. Once the results
come back, use an antibiotic specific to the cause.
o Changes in mentation
The person may become septic (i.e., infection flowing through the blood). Since there is no acute inflammation
response, this person may not have a fever.
o
o Diagnosis
CBC with differential (i.e., to differentiate between the WBCs).
Bone marrow aspiration.
o
o Collaborative Care/Nursing Management
Determine cause / Remove offending agent (e.g., the chemotherapy).
Prophylactic, therapeutic antibiotics
Administer granulocyte stimulating drug (G-CSF and GM-CSF)
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Reverse isolation, screen visitors, only cooked food, more at risk for fungal infections
Granulocyte infusion (i.e., neutrophils, basophils, eosinophils).
Neupogen.
o It is a stimulant for the bone marrow to produce more neutrophils.
This patient will be on reverse isolation (wash your hands, wear a mask)!
o Protecting the patient from us
If the patient is given raw fruit, ensure they have been washed with soap and water.
Notify a doctor is you notice a possible elevated temperature.
o
o Leukemia
A group of malignant disorders affecting the blood and blood-forming tissues of:
o Bone marrow
o Lymph system
o Spleen
Occurs in all age groups.
Results in an accumulation of dysfunctional cells because of a loss of regulation in cell division.
Fatal if untreated.
o Progressive.
Patients who are leukemic, are also going to be anemic and have a lot of bleeding (making lots of WBC so not making as many
RBC and platelets)
o
No single causative agent.
It occurs most likely due to a combination of factors (i.e., genetic and environmental influences).
o
o Classification
Cell maturity and nature of onset
o Acute
The cells are not mature (i.e., they are pushed out of the bone marrow too early).
o Chronic
The cells are mature.
Type of white blood cell (WBC)
o Granulocytes (i.e, basophils, eosinophils, neutrophils)(responsible for inflammation our second line of defense VERY
BAD Dont want this one)
o Agranulocytes (i.e., lymphocytes, monocytes)
o Types:
Acute lymphocytic leukemia (ALL)
Acute myelogenous leukemia (AML)
Also called acute nonlymphoblastic leukemia (ANLL). This type has the worst prognosis because it deals with
myeloblasts (i.e., the granulocytes), which are involved in inflammation.
o Chronic myelogenous leukemia (CML)
o Chronic lymphocytic leukemia (CLL)
o There are also some unclassified types, the prognosis of which is really, really poor as the drugs do not work.
o
o Acute Myelogenous Leukemia (AML) also referred to as Acute Non-Lymphoblastic Leukemia (ANLL)
One fourth of all leukemias.
o 85% of the acute leukemias in adults.
Abrupt, dramatic onset.
o Serious infections (as there is no inflammation process), abnormal bleeding (if a whole lot of white cells are made, the
body cannot make many platelets).
Characterized by uncontrolled proliferation of myeloblasts, the precursors of granulocytes.
o Hyperplasia of bone marrow and spleen (as they are working overtime to make the WBCs).
Clinical manifestations:
o Fatigue and weakness, headache, mouth sores, anaemia, bleeding, fever, and infection.
o
o Chronic Myelogenous Leukemia (CML) also referred to as Chronic Granulocytic Leukemia (CGL)
o
o
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Excessive development of mature neoplastic granulocytes in the bone marrow.

o These excess granulocytes move into the peripheral blood in massive numbers and ultimately infiltrate the liver and
spleen.
These cells contain a distinctive cytogenetic abnormality, the Philadelphia chromosome, which serves as a disease marker and
results from the translocation of genetic material between chromosomes 9 and 22.
The natural history of CML is a chronic, stable phase (can be 10+ years) followed by an acute, aggressive phase known as the
blastic phase. Even with adequate treatment, an individual with CML will progress to the blastic phase. Once this blastic phase
arrives, the patient has at most 6 weeks to live.
o
o Acute Lymphocytic Leukemia (ALL)
Most common type of leukemia in children and accounts for 15% of acute leukemia in adults. This has the best cure rate.
Immature lymphocytes (i.e., inflammatory response) proliferate in the bone marrow.
Fever is present in the majority of patients at the time of diagnosis.
Signs and symptoms may appear abruptly with bleeding and fever, or they may be insidious with progressive weakness, fatigue,
and bleeding tendencies.
Leukemic meningitis cause by arachnoid infiltration occurs in many clients with ALL.
o
o Chronic Lymphocytic Leukemia (CLL)
Characterized by the production and accumulation of functionally inactive but long-lived, mature-appearing lymphocytes.
The type of lymphocyte typically involved is the B cell.
o B cells are the antibody producing type. T cells disrupt membrane (killer cells)
The lymphocytes infiltrate the bone marrow, spleen, and liver.
Lymph node enlargement is noticeable throughout the body and there is an increase incidence of infection.
B cell CLL is considered to be identical to the mature B cell small lymphocytic lymphoma, a type of Non-Hodgkins lymphoma.
The prognosis is good. It is like CML without the blast phase.
o
The manifestations relate to problems caused by bone marrow failure. This results from over-crowding in the bone marrow due
to the increase in WBC formation. This will lead to anaemia, night sweats, fever, easy bruising, bone pain, thrombocytopenia
(and associated increased bleeding).Aplastic anemia.
Related to problems caused by leukemic cells infiltrating patients organs.
o Liver
o Brain
o Spleen
o Fever and night sweats are some of the clinical
o Lymph nodes
manifestations.
o Solid masses resulting from collections of leukemic cells called chloromas can also occur.
To diagnose and classify:
o Peripheral blood evaluation.
CBC with differential.
o Bone marrow evaluation.
o Lumbar puncture (looking for other hotspots)
o CT scan
To identify cell subtype and stage.
o The stage the person is at determines the treatment.
o
o Goal
Goal is to attain remission.
o Chemotherapeutic treatment.
Induction: aggressive, try to destroy WBCs in peripheral blood and bone marrow to restore normal
hematopoiesis
Care focused on neutropenia, thrombocytopenia and anemia
Intensification: Given for several months during postremission, same drugs as induction but higher doses
Conslidation: Started after remission is achieved, to eliminate remaining leukemic cells that are not clinically or
pathologically evident
Maintenance dose: Lower doses of drugs in induction
Rarely admin in AML
Different drugs to target cells at different point of cell development lower doses of multiple drugs
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Reduce toxicity and drug resistance
Bone Marrow and Stem Cell Transplantation.
It can be done with or without total body radiation. You want to get rid of all the blastic and leukemic cells first,
and then do a bone marrow transplant.
The procedure is always more effective with radiation, but not all patients are able to withstand this
radiation.
For the stem cell transplantation, it is placed in the blood, and it then enters the bone marrow.
Full remission: there are no signs of the disease (i.e., no night sweats, no palpable lymph nodes, no thrombocytopenia, peripheral
blood is normal, etc.).
Partial remission: there are no clinical signs of the disease, the peripheral blood is normal, but there are greater than 5% blast
cells within the bone marrow.
Minimal residual disease less evidence always remains
o
Bone Marrow and Stem Cell Transplantation
Many physical and psychological needs.
o Evokes great fear.
Family also needs help.
Balance demanding technical needs with a humanistic, caring approach.
o
o Lymphoma
This is the most common haematological cancer that occurs mostly in men between the teen years (15)-30 and 60 years onward
(i.e., bimodal age-specific incidence).
Definition:
o Malignant neoplasms originating in the bone marrow and lymphatic structures.
Two major types:
1. Hodgkins disease
2. Non-Hodgkins lymphoma (NHL)
This has the worst prognosis of the two.
o
o Hodgkins Disease
It is a malignant condition characterized by:
o A biopsy reveals the proliferation of abnormal giant, multinucleated cells called Reed Sternberg cells that are located in
the lymph nodes.
In adults, it is twice as likely to occur in men as in women.
o
o Etiology
Cause remains unknown.
Key factors:
o Infection with Epstein-Barr virus (EBV).
o Genetic predisposition (i.e., familial; there is not a particular gene).
o Exposure to occupational toxins.
Bimodal age-specific incidence. 15-30 and then greater than 50 (usually males)
o
o Pathophysiology
o
Normal structure of lymph nodes is destroyed by hyperplasia of monocytes and macrophages.

The main diagnostic feature if the presence of the Reed Sternberg cells in the lymph.
The disease is believed to arise in a single location.
o It originates in the lymph nodes in 90% of clients and spreads in adjacent lymphatics.
o It eventually infiltrates other organs such as the liver, spleen, and lungs.
o In roughly 2/3 of patients, the cervical lymph nodes are the first to be affected. If the detected node is above the
diaphragm, the prognosis is much better than if the detected lymph node is below the diaphragm because there are more
organs below the diaphragm that can be affected should the lymphoma spread. It is also easier to detect changes in
nodes above the diaphragm and the disease will remain confined to those lymphs nodes for a particular period of time
before spreading.
o Better prognosis if found above the diaphragm than if found below the lymph
o
128
Insidious onset.
Enlargement of cervical, axillary, or inguinal lymph nodes.
Nodes remain moveable, non-tender (recall that the tenderness only occurs during inflammation).
Painless nodes exert pressure on adjacent nerves, which may cause some discomfort.
o
May experience:
o Weight loss, fever, and night sweats occur and are known as the B symptoms. B symptoms are correlated with a worse
prognosis (i.e., Hodgkins + B symptoms).
o Fatigue, weakness, chills, tachycardia, palpitations followed by chest pain, dyspnea also occur.
o Alcohol induced pain at the located of the disease (for unknown reasons).
o Generalized pruritis (due to the granulocytes).
o Mediastinal node involvement.
Would expect to see cardiovascular problems, pulmonary problems.
Advanced cases:
o Hepatomegaly, splenomegaly.
o Anaemia (microcytic, hypochromic anaemia).
Since so many WBCs are being made, there is less focus towards making RBCs.
o Other physical signs vary depending on disease location.
If the cervical node is affected, it can lead to supra vena cava syndrome, hypertension, and coma.
If its below the diaphragm, it can be lead to spinal cord compression, hepatomegaly, splenomegaly, and bone
pain.
o
Peripheral blood analysis.
Lymph node biopsy (in order to check for Reed Sternberg cells).
Bone marrow examination.
Radiologic evaluation.
o Chest X-rays, CT scans, MRIs, PET scan (displays heat spots).
o
o Nursing & Collaborative Management
Using diagnostic studies, a stage of disease is determined.
Stages:
o A (without symptoms) & B (with symptoms) classification
Roman numeral (I to IV).
This reflects the location and disease extent.
o IVB is the worst.
Management focuses on selecting a treatment plan.
Radiation therapy
o 95% of stage I or II (for both A and B) patients are cured within 4-6 weeks of radiation.
Combination therapy
o ABVD = standard regimen for chemotherapy
o BEACOPP = aggressive regimen
o 90% of stage I or II patients 10 yr survival 2-4 cycles.
o Presence of B symptoms 4-6 cycles
o MOPP
o There are different cells growing at different stages, so combination therapy is used to wipe out that variety of cells.
Radiation and Chemotherapy
o Stage IIIA
High-dose chemotherapy and bone marrow or peripheral stem cell transplantation
o Stage IIIB and stage IV (A and B)
Once cured, there is a risk of secondary malignancies. The most common include:
o Acute lymphoblastic leukemia
o Non-Hodgkins lymphoma
o Solid tumours (in the lung, breast, brain)
o
o Nursing Considerations
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Skin (the radiation may cause burns)

o The skin should be washed with mild cleansers (i.e., treat the area like a burn).
Psychosocial considerations
o The young individuals will exhibit changes in their psychosocial aspect.
Fertility issues due to the chemotherapy
o Major concern.
o Men will usually become infertile. You want to inform the patient to wait at least 2 years before trying to conceive in
order to allow the cells to return to normal.
Long-term evaluation of patient
o
o Non-Hodgkins Lymphoma (NHL)
Heterogeneous group of malignant neoplasms of the immune system that affects all ages.
There is no hallmark characteristic of NHL as seen with the Reed Sternberg cells of Hodgkins lymphoma; however, all NonHodgkins lymphomas involve lymphocytes arrested in various stages of development.
NHL can originate outside the lymph nodes (different from Hodgkins lymphoma).
Classified according to:
o Different cellular characteristics.
You want an aggressive Non-Hodgkins Lymphoma because cancer drugs work better on fast growing cells.
o Lymph node characteristics.
o
Varies from slowly developing to rapidly progressive disease (preferred). There are no drugs that can treat the slowly developing
cells.
Types of NHLs:
o 90% B cell lymphomas
o 10% T cells lymphomas
Types of Non-Hodgkins Lymphoma:
1. Burkitts lymphoma
2. Reticulum cell sarcoma
3. Lymphosarcoma
o
Primary clinical manifestation:
o Painless lymph node enlargement.
o High grade lymphomas may have:
Lymphadenopathy (i.e., enlarged lymph nodes).
Constitutional B symptoms such as fever, night sweats, and weight loss.
By the time Non-Hodgkins is diagnosed, the disease has spread.
o
o Diagnosis
Peripheral blood is usually normal.
Diagnostic studies similar to Hodgkins. Barium enema, MRI, CTnto determine spread.
Lymph node biopsy establishes the cell type and pattern.
o Hodgkins: Reed Sternberg cells in the lymph nodes.
o Non-Hodgkins: No Reed Sternberg cells in the lymph nodes.
o
o Treatment
Radiation therapy.
Chemotherapy.
o AVBD, MOPP.
Going into remission is rare. Inpartial remission (take every two weeks the drugs under symptomatic)
More aggressive lymphomas are more responsive to treatment and are more likely to be cured.
o
o Once Symptomatic
Rituximab (a genetically made antibody for the CD20 antigen on the surface of normal and malignant B lymphocytes)
Cyclophosphamide
With or without prednisone
o
130

o
o
When the symptoms return, chemotherapy will no longer work. Stem cell transplant then nothing.
IMMUNE SYSTEM
o Immune System Review

What are the 3 Lines of Defence?
1. Chemical (e.g., saliva, HCl) and mechanical barriers (e.g., skin, cilia, sebaceous glands, lining of GI and GU tract)
2. Inflammatory response
It is non-specific (i.e., no memory component).
It distinguishes between an antigen and self.
3. Immune response
It is specific and has a memory (e.g., the second time an antigen is encountered, the response rate will be much
faster).
What are the Characteristics of the Immune Response?
o Phagocytic.
Antigen = immunogen = invador.
T-cells are involved.
o Humoral or immunoglobin-mediated.
B-cells are involved and antibodies are created.
o Cell-mediated.
Cytotoxic T-cells (TC cells)/Killer T-cells which mature in the thymus.
Kills cancer cells.
Helper T-cells (TH cells). The measurement is CD4+ cells.
Normal values are between 800-1,200 and they live for 100 days.
They help things get into the cell.
Suppressor T-cells (TS cells). The measurement is CD8 cells.
They help things get into the cell.
What are the Stages of Immune Response?
1. Recognition (i.e., the antigen as an invading event)
2. Proliferation
Every daughter cell from the proliferation will recognize the antigen.
3. Response
Humoral (B cells)
o Producing antibodies.
Cellular (T cells)
o Antigen attacked by the antibody.
4. Effector Stage
Coupling of the antigen and the particular cell from either a humoral or cellular response. This coupling
neutralizes the antigen.
What are the Key Organs?
1. Spleen (stores WBCs, RBCs and platelets)
2. Lymph nodes (lymphocytes located here and they act as filters)
3. Thymus
The hormone thymosin causes maturation of the lymphocytes. In the mediasteinum.
o
What factors affect the Immune System function?
1. Age (extremes: immature or no longer functioning)
2. Nutrition (proteins are needed to make antibodies)
3. Existence of other disease or injury (e.g., burns)
4. Cancer (large tumours will produce antigens which will combine with the antibodies and destroy them)
5. Medications (immunosuppressants [corticosteroids])
6. Radiation (killing off WBCs or stem cells)
o Appendix W
o
o Disorders of the Immune System
1) Immunopathology autoimmune diseases
2) Immunodeficiencies
a. Primary
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These deficiencies are hereditary. This is not discussed at length because these patients do not live long.
Cogenital or X-linked.
Secondary
This tends to be acquired. 70% of secondary immunodeficiencies occur in males. This encompasses anything
that interferes with the immune system.
There are times in which you want your immune system to be suppressed (e.g., organ transplant, autoimmune
diseases). The reason being that during a transplant, you do not want your body to reject the organ.
b.
o
o Immunosuppression (e.g. transplant)
Consequences
o Infections
1. Persistent or recurrent infections
2. Opportunistic
This occurs when your normal microflora take over.
3. Severe infections by organisms that are normally mild
E.g., Staphyloccocus aureus found on your skin may cause a small localized infection in a healthy
person but cause a flesh eating disease in a person who is immunocompromised.
Incomplete Recovery: the bug is never truly gone.
Increased incidence: cancers and tumours are more likely to occur. These cancers are thought to be viral in origin.
o
o Patient Education is Key Treatment
Immunosuppression is often intentional.
o Education is key (e.g., wash your hands all the time, avoid large crowds).
Protection against and treatment of diseases and infections. (may be taking prophylaxis antibiotics)
Immunostimulant drugs may have to be given in order to spark the immune system (e.g., Neupogen).
Bone Marrow Transplant is required if the immunosuppression was not intentional.
o
o Human Immunodeficiency Virus (HIV) Infection
o Significance of Problem
Globally
o 33 million living with HIV (2009).
In Canada
o 1 million
o 65,000 (2008).
o 2,300-4,300 diagnosed each year in Canada.
o RNA virus discovered in 1983.
o Virus binds to specific CDA receptor sites and then enters the cell. (loves T-cells)
o It attaches and injects the virus and an enzyme (reverse transcriptase).
o Injected into the nucleus (where your DNA is), reverse transcriptase decides not to make your own DNA but well make
our own DNA (the virus) single stranded DNA. Every cell will reproduce a daughter cell that is infected. Every cell
divides. Each one infected. You will lose billions of cells.
o Every cell you produce now will have that virus.
o Reverse transcriptase assists to make a single viral DNA.
o Virus enters the cell nucleus.
o
There is no vaccine available (as seen in Hepatitis C) because the virus mutates so quickly.
The rates of TB are a good indication of HIV infections. If you cannot test for HIV (e.g., in some countries, such as the Soudan,
testing for HIV is prohibited), test for TB to possibly get an indication (the reason being that TB is an opportunistic infection).
HIV used to be called Slims disease, as there is so much muscle wasting.
As of 2011, the majority of transmission occurs via heterosexual couples (and not homosexual couples).
o
o Side-Effects of HIV
Diarrhoea, changes in mentation, muscle wasting.
o
o Pathophysiology of HIV (17.1)
RNA virus was discovered in 1983 and is called a retrovirus because it replicates in a backwards manner (going from RNA to
DNA).
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The DNA does not open up to make RNA; instead, the RNA is used to make viral DNA. This viral DNA now becomes
part of your DNA. From this point on, every single cell that you make will contain some viral DNA.
There are two types of HIV (HIV-1 and HIV-2). Before 1990, people were testing blood for transfusion use for HIV-1 but not
HIV-2, causing people to have gotten HIV (i.e., HIV-2) from blood transfusions.
HIV destroys CD4 cells 3 ways:
Viral replication leaves holes in cell membranes
Infected cells fuse with other cells
Antibodies against HIV bind to the infected site
o
CD4+ counts are important measure of antibodies in patients with HIV: 800-1,200g/L is the normal range for CD 4+ cells. Healthy
CD4+ cells live for 100 days; HIV infected CD4+ cells live for only 2 days. Viral activity kills about one billion CD4+ cell per day.
Fortunately, the thymus and the bone marrow have the ability to replace the lost CD4+ cells for many years; however, there will
come a point whereby the HIV virus cells will kill more CD4+ cells than the body can make, leaving the body
immunocompromised and open for opportunistic infections.
gp120 Knobs on the virus bind to specific CD4+ receptor sites and then enters the cell.
o On TH-cells, there is a CD4+ (which is the measure of TH-cells) receptor site. This is the site that the gp120 knobs
located on the HIV virus bind to. Once bound, the HIV injects the core virus into the TH-cell.
o Once in the TH-cell, viral RNA is transcribed into a single strand of viral DNA with the assistance of reverse
transcriptase. The strand then copies itself, becoming double-stranded viral DNA.
o At this point, the viral DNA can enter the nucleus and, using an enzyme called integrase, splice itself into the genome,
becoming a permanent part of the cells genetic structure.
o
The virus replicates quickly (i.e., 108-109 cells per day). A major consequence of rapid replication is that copy errors are made,
causing mutations that contribute to difficulties in treatment and vaccine development.
The virus likes to stay in lymphoid tissue. Eventually, the HIV will cause significant damage to the lymph system and the virus
will spill into the blood.
o
HIV destroys CD4+ cells (i.e., TH-cells as they have more CD4+ receptors on their surface than any other cell containing CD4+
receptors on their surface) in 3 ways:
1. Viral replication includes a process called budding, which leaves holes in cell membranes. These holes allow the cell
content to leak out and die.
2. Infected cells fuse with other cells. This fusion process continues until many cells, some of which are not infected,
combine into a mass called a syncytium, that destroys all affected cells.
3. Antibodies against HIV bind to the infected cells and activate the complement system, which destroy the infected cells.
The problem is that your own cells are also being destroyed.
o
Up to 1 billion TH-cells can be destroyed per day.
o
o Dip is viremia (three weeks). You get a flu. It recovers because the immune system is still good. 2 ms later
recognizable antibodies being created.
o
o Viral Load in the Blood
o Viral load refers to the amount of virus in your blood. Upon infection, there is a small dip in the number of CD 4+ TH-cell
count. This dip will cause people to think they have the flu. There will also be a large increase in the viral load, which is
a process known as viremia (i.e., high number of viruses in the blood).
o If the body has a high number of antigens in the blood, it will respond by making antibodies.
o In time, the CD4+ cells will start to dramatically decrease (e.g., roughly 10 years) and the viral load will increase
dramatically. This is now considered to be AIDS (i.e., once the CD4+ count is 200). There is a second diagnosis
to AIDS (i.e., a CD4+ count of 200 or less + an opportunistic infection, typically PCP, Kaposis sarcoma, etc.). A person
diagnosed with Kaposis sarcoma or PCP, will typically also have HIV.
o The only treatment and ultimate goal is to keep the viral load low.
o
o Timeline for Untreated HIV Infection
o Many people do not go get tested as they merely think they have the flu.
o The test for HIV is to test for the level of antibodies. The problem is that it takes a while for the antibodies to build up
(the window period is between 3 weeks-2 months). This window period is known as early chronic infection. This is
followed by intermediate chronic infection (when the number of CD4+ cells starts to decrease) and late chronic
infection/AIDS.
o
o Acquired Immunodeficiency Syndrome (AIDS) 17.4
o
133
WHO criteria (Table 16-10 in text).

Immune system severely compromised.
Ratio of CD4+ to CD8+ is reversed from 2:1 to 1:2.
o CD8+ cells are suppressor cells. This is due to the great decrease in CD4+ cells.
Opportunistic diseases develop that contribute to disability and death.
Hepatitis B is 100x more virulent than HIV as it can live on surfaces for up to 7 days.
o
Rapid HIV antibody test results in 20min
Screening tests detect HIV-specific antibodies (see Fig16-1).
o May take up to 2 months before antibodies can be detected (window period).
Progression of the disease is monitored by CD4+ T-cell counts.
Lab tests measuring viral activity.
o Assess disease progression, viral load.
o EIA (enzyme immune assay)
o ELISA (enzyme linked immune assay)
o If a test comes up positive, a second test is done (best done at the same time of day that the first test was done).
If the second test is positive, a Western Blot test (i.e., a confirming test) is done.
A person with a high risk lifestyle (i.e., unprotected sex, sharing needles) will be brought back and tested in 3 months. If they are
not living a high risk lifestyle, they will be tested again in 6 months.
The anti-retroviral drugs have a lot of side-effects (e.g., diarrhoea).
All testing needs to include pre and post test education.
o
o Nursing Assessment
Dependent upon the stage of the disease.
o Prevention (this is key because there is no cure HIV)
o Treatment
o Terminal phase
o
o Nursing Management Implementation
Drug therapy for opportunistic diseases (Table 16-11)
o Delay or treat with adequate antiretroviral therapy.
This is done as early as possible (when CD4+ count hits 250). Many people would stop taking this HAART
(highly active anti-retroviral therapy) because of the many side-effects. The problem with this is that resistance
occurs quickly (as quickly as one missed dose)! Pregnant (doesnt matter what CD4 load is)
o Disease-specific prevention measures.
o
o Health Promotion
Prevention of HIV.
o Decreasing risks related to:
Sexual intercourse
Drug use
Perinatal transmission
Work
Pregnant women are started on HAART sooner. 95% of the babies with HIV will seroconvert within a year, which means that it
was the mothers antibodies that were being measured.
o
o HIV Testing and Counselling
All testing MUST be accompanied by pre- and post-test education.
Progression monitored by DX treatment slide.
o
o Antiretroviral Therapy
Multi-drug therapy reduces viral loads, but are complex, have interactions, and do not work for everyone.
o ART released in 1987.
o Federal guidelines suggest treatment be delayed until levels of immune suppression are observed.
o Debate about when to start ART. It is best to start it when the CD4+ levels are not too low, as CD4+ levels help the drug
take effect.
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HAART (highly active anti-retroviral therapy). Example: AZT.
Treatment decisions individualized
Combination ART (d/t side effects or resistance)
NRTIs, NNRTS & PI
Adherence to drug regimens is critical to:
o Prevent disease progression.
o Opportunistic disease.
o Viral drug resistance (as much as one missed dose can lead to drug resistance).
o People who do not want to take HAART, will be started on prophylactic antibiotics as a prevention for infection.
o
o Acute Exacerbations (once you have these you have AIDS)
Common opportunistic infections:
o Pneumocysits carinii pneumonia (PCP)
o Cryptococcal meningitis
o Cytomegalovirus retinitis
o Mycobacterium avium complex
o Candidiasis (in the mouth, oesophagus, vagina)
Encouraging people to eat yogurt with their antibiotics will help increase the number of normal microflora, thus
preventing thrush.
Common type of cancer:
o Kaposis sarcoma
There are blue-tumours from the sarcoma.
o
o Social Constructs Surrounding HIV
Negative social attitudes label patients.
Behaviours associated with HIV may be viewed as immoral and sometimes illegal.
Infected individuals can transmit the virus to others.
o
o Ambulatory and Home Care
Often experience anxiety, fear, diarrhoea, depression peripheral neuropathy, pain, nausea, vomiting, and fatigue.
Symptom management similar to other chronic illnesses.
Metabolic disorders have emerged.
Detect early and deal with symptoms.
o Hyperlipidemia, insulin resistance, and bone disease common.
o
o Terminal Care
Dementia is often present in final stages of HIV.
o AIDS-dementia complex and cognitive motor complex.
o
o
o
135

o
Unit 16: Care of the Client with Dysrhythmias
o 1iClicker Questions
o The component of the conduction system referred to as the pacemaker of the heart is the:
a) atrioventricular (AV) node.
b) sinoatrial (SA) node.
c) bundle of His.
d) bundle branches.
o
o The electrical stimulus of the cardiac cycle follows which sequence?
a) AV node SA node bundle of His
b) Bundle of His AV node SA node
c) SA node AV node bundle of His bundle branches
d) AV node SA node bundle of His bundle branches
o
o Review of Physiology Normal Heart Beat
The heart is made up of 2 types of cells:
1. Contractile cells
Make up 99% of cardiac muscle cells. These cells do not normally initiate their own action potentials.
2. Autorhythmic cells
Make up 1% of cardiac muscle cells. They do not contract but are specialized for initiating and conducting the
action potentials responsible for the contraction of the working cells.
They display pacemaker activity.
Cardiac autorhythmic cells (unlike any other type of cell) do not have a resting potential. The membrane
potential slowly depolarizes, or drifts, between action potentials. These cells initiate action potentials, which
then spread throughout the heart to trigger rhythmic beating without any nervous stimulation.
These cells are located in 4 different area of the heart:
1. The sinoatrial (SA) node
It is the normal pacemaker of the heart, located in the right atrium.
60-100 beats per minute (bpm).
o <60bpm = bradycardia.
o >100bpm = tachycardia.
2. The atrioventricular (AV) node
It is a small bundle of specialized cardiac cells located at the base of the right atrium near the
septum, just above the junction of the atria and ventricles.
Transmits pulses to ventricles.
Should the SA node suffer damage or trauma, the AV node will assume the role of pacemaker.
3. The bundle of His (atrioventricular bundle)
A tract of specialized cells that originate at the AV node and enters the interventricular
septum.
4. The Purkinje fibres
They are small terminal fibres that extend from the bundle of His and spread throughout the
ventricular myocardium.
Transmits pulses to the ventricles to make them contract.
o Normal Heart Beat
Effective electrical system.
Reacts to needs of body quickly.
Sometimes it breaks down, resulting in dysrhythmias (i.e., abnormal heart beats).
o
o Rhythm Identification and Treatment
Prompt assessment of abnormal cardiac rhythms, dysrhythmias, is crucial.
Conduction system.
Nervous control of the heart.
An ECG is the only accurate way to know exactly what is going on in the heart.
o Telemetry monitoring.
Heart palpitations (atrial flutter) may be transient.
o Review on Your Own
Electrophysiologic properties of the heart.
K+ out of the
cell
(repolarizatio
136
Action potential.
Na+ in the cell
o Every heart beat has its own action potential.
(depolarizatio
o Steps:
n)
0 = Depolarization
Sodium rushes into the ICF in large amounts; calcium
enters the ICF in smaller amounts.
1 = Early rapid repolarization
Sodium gates close and potassium gates open.
2 = Repolarization
Calcium moves into the ICF; potassium moves out of the
ICF (i.e., into the ECF).
3 = Repolarization
Polarized
Calcium channels close; potassium moves out of the ICF (i.e., into the ECF).
state
4 = Resting Membrane Potential/Polarized State
This is also a refractory period (i.e., a time during which depolarization cannot occur). The sodium
channels are blocked.
o There are two types of refractory periods:
1. Absolute refractory period
2. Relative refractory period
This is relative because of the T-wave.
o
o
Na+ in the cell
K+ out of the
(depolarizatio
cell
n)
(repolarizatio
Polarized
state
o
o
o
Big arrow: movement is fast

Small arrow: movement is slower
o
o Electrophysiologic Properties
Automaticity
o The ability to initiate an impulse spontaneously and continuously.
Excitability
o The hearts ability to receive the electrical impulses and contract.
Conductivity
o The hearts ability to transmit the impulse from one end of the heart to the other.
Contractility
o The hearts ability to respond to the electrical stimulus.
o
o *A problem with any of the four properties listed above will lead to dysrhythmias (i.e., abnormal heart rhythms).
o
o Refractory Periods
Many dysrhythmias are triggered at relative refractory periods.
o T wave most vulnerable.
Another action potential cannot take place during the absolute refractory period, but
o can, in some instances, take place during the relative refractory period.
T wave
o
o
o Dysrhythmias
They are abnormal heart rhythms.
137
It is important to watch for:

o Decreased CO in patients with dysrhythmias. This is exhibited by:
Pale diaphoretic skin.
Increased or decreased pulse.
The pulse may have skipped beats.
Decreased BP.
Changes in LOC (e.g., confusion).
This is different from a myocardial infarction.
o
o ECG
Displays of electrical action of heart.
It can detect rate, rhythm, conduction abnormalities, dig toxicity, and electrolyte imbalances (which will not appear on an ECG).
There are different kinds of ECGs.
o Example: 12 leads
This looks at the conductivity of the heart from 12 different views.
o
o Components of ECG
o *An ECG is printed on graph paper, with each block/square
Na+ in the cell
K+ out of the
(depolarizatio
o representing a unit of time.
cell
n)
o
(repolarizatio
P wave
o Atrial depolarization (60-100 bpm).
Polarized
PR interval
state
o Time it takes for the impulse to spread from the atria to ventricles.
QRS complex
o Ventricular depolarizing and atria repolarizing.
o This will become widened when there are problems.
T wave
o Ventricular repolarization.
ST segment
o Complete depolarize start repolarize.
QT interval
o Electrical systole.
U wave
o Abnormal, may follow T wave.
o It is important not to confusion a U wave with a new P wave.
o
Time between T and P wave
o Diastole.
ECG shows voltage of waves and duration of waves.
Voltage = info thickness of chamber walls.
Time = info about formation and conduction.
When you shock the heart,
you are essentially stopping and
restarting it.
o
o 1 = P wave
o 2 = P-Q segment
o 3 = QRS segment
o 4 = S-T segment
o 5 = T wave
o 6 = Q-T segment
o
o
138
o Anti-Arrhythmic Drugs
Class I Drugs that depress the upstroke of action potential
o Block influx of Na+ into cells in phase 0.
o Sodium channel blockers or fast channel blockers.
o These drugs are based on the patients weight.
o Procainamide, Quinidine.
o Lidocaine, Mexiletine.
o Encainide.
Class II -adrenergic receptor blockers
o Blocks -receptors and therefore the SNS, depresses depolarization, slows SA node impulses, increases atrial and AV
nodal refractories.
o General myocardial depressants.
o This leads to a slower and stronger heart rate.
o Atenolol, Metaprolol, Propranolol.
Class III Drugs that prolong repolarization
o Blocks K+ movement in phase 3, therefore prolonging repolarization and refractory period.
o Ventricular tachycardia (TxVT), ventricular fibrillation (VF), atrial flutter/fibrillation (AF/F) resistant to other treatment.
Ventricular tachycardia is life-threatening. This is why too much potassium is bad.
Normal K+ levels are 3.5-5mmol/L.
o Amiodarone, Bretylium, Sotalol
These drugs are all ACLS (Advanced Care Life Support) drugs.
Class IV Calcium-channel blockers
o Blocks Ca2+ in phase 2, calcium channel blockers, slow channel blockers, prolongs conductivity and increases refractory
period and AV node.
o Paroxismal supraventicular (TxPSVT), atrial flutter (AF).
o Diltiazem, Verapamil.
o Increased use will increase risk of mobidity and mortality
o
o Anti-Arrhythmic Drugs that Dont Fit Into Classes
Potassium-channel opener
o Adenosine: decreases conduction at AV node (PSVT, WPWS).
WPWS: Wolf-Parkinsons white syndrome.
Atropine: anti-cholinergic blocks vagal effect on SA and AV node Increases heart rate.
Digoxin: strengthens myocardial contraction and slows conduction at AV.
Epinephrine: acts on alpha and beta adrenergic receptor sites of SNS, helps restore NSR (Normal Sinus Rhythm) post cardiac
arrest.
Magnesium Sulfate: decreases excitability and conduction.
CAUTION overdose = cardiac standstill.
o 2 nurse checks are done.
o
o Dysrhythmias
Dysrhythmias are triggered by internal and external forces.
o Internal: electrolyte imbalances, oxygen deprivation (due to a lack of haemoglobin and thus lack of oxygen), acidosis,
etc.
o External: trauma, drugs, haemorrhage, stress (i.e., prolonged stress that increases the bodys metabolic demands), etc.
Dysrhythmias are characterized by:
o Alteration in impulse formation.
Rate, rhythm, ectopics (beats that are coming somewhere else).
o Alteration in conductivity.
Failure or delay impulse transmission heart blocks.
Cardiac rhythms are classified according to:
o Site of impulse formation.
o Site/degree of conduction block.
o
o
139

Supraventricular Rhythms
Question!
Normal Sinus Rhythm (NSR)
Sinus Arrhythmia (i.e., abnormal rhythm)
o Sick Sinus
o Sinus Tachycardia
o Sinus Bradycardia
Atrial Flutter
Atrial Fibrillation
o
o *The sinus node is the hearts pacemaker.
o **Check textbook notes for more information.
o
o Sinus Bradycardia
Sinus node discharges at a rate <60 bpm.
Significance:
o Hypotension with decreased CO.
Treatment:
o Consists of atropine.
o Pacemaker if the patient does not respond to other treatments.
ECG characteristics:
o Normal QRS complex.
o The entire thing is stretched out.
o
o Sinus Tachycardia
Discharge rate from the sinus node is and is >100bpm.
Significance:
o Dizziness (because there is not enough O2) and hypotension (there is not enough filling time).
o myocardial oxygen consumption with increased HR.
o Angina or increase in myocardial infarction size.
Treatment:
o Determined by underlying causes.
-adrenergic blockers (e.g., metoprolol, atenolol).
o The entire thing is condensed (there is no resting time).
o
o Atrial Flutter
It is an atrial tachyarrhythmia identified by recurring, regular, sawtooth-shaped flutter waves.
Associated with slower ventricular response.
Manifestations:
o Hypotension, dizziness.
Significance:
o High ventricular rates with atrial flutter can decrease CO.
o Risk of clot formation (this is due to the excess stasis).
Treatment:
o Primary goal is to slow ventricular response by increasing AV block.
o Electrical cardioversion (there is a smaller voltage used).
o Drugs:
Diltiazem, digoxin, and -adrenergic blockers.
Anti-coagulant therapy.
The patients pulse may feel normal for this reason.
o
o
o
Exam
140
o Atrial Fibrillation
Total disorganization of atrial activity without effective atrial contraction.
The arrhythmia may be chronic or intermittent.
Manifestations:
o Hypo- or hypertension (this depends on the CO).
Significance:
o Can result in decreased CO (due to ineffective atrial contractions and rapid ventricular response).
o Risk for stroke (due to stasis).
o Risk for heart failure or hypertension.
Treatment:
o Same as for atrial flutter.
o Multiple, short impulses.
o QRS complex is normal in shape but smaller (as the ventricles are not getting enough blood from the atria).
o
o First-Degree AV Block
It is a type of AV block in which every impulse is conducted to the ventricles, but the duration of AV conduction is prolonged.
Once the impulses move through the AV node, it is usually conducted normally through the ventricles.
Significance:
o May lead to other blocks.
No treatment.
o Rate is normal.
o Rhythm is regular.
o P wave is normal.
o PR segment is prolonged.
o QRS typically normal.
o
o Second-Degree AV Block Type 1
Includes gradual lengthening of the PR interval, which occurs because of prolonged AV conduction time (known as Wenckebachs
phenomenon).
Most commonly occurs at AV node, but can occur in His-Purkinje system.
Significance:
o Second-degree heart block is usually due to an inferior MI or ischemia.
o It may be a warning.
Treatment:
o Atropine.
o Pacemaker.
o Atrial rate is normal but ventricular rate may be slower as a result of dropped QRS complexes.
o Ventricular rhythm is irregular.
o
o Second-Degree AV Block Type 2
P wave is not conducted without progressive antecedent PR lengthening.
o It almost always occurs when bundle branch block is present.
It is a more serious type of block as a certain number of impulses from the sinus node are not conducted to the ventricles.
Type II AV block almost always occurs in the His-Purkinje system.
Significance:
o Often progresses to third-degree.
o May result in decreased CO due to BP and myocardial ischemia.
Treatment:
o Temporary drug measures to increase HR until pacemaker is available.
o Pacemaker.
o Atrial rate is normal.
o Sinus rhythm is regular but ventricular rhythm may be irregular.
o Third-Degree AV Heart Block
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Complete heart block.

There are no impulses from atria are conducted to ventricles.
Ventricular rhythm is an escape rhythm, and ectopic pacemaker may be above or below bifurcation of His bundle.
Significance:
o Reduced CO with ischemia and heart failure.
o Syncope.
Treatment:
o Pacemaker.
o Drugs used to temporarily increase HR and support blood pressure before pacemaker insertion.
o Atrial rate is normal. Ventricular rate depends on the site of the block. If it is in the AV node, the rate will be 40-60bpm,
if it is in the Purkinje fibres is will be 20-40bpm.
o Rhythms are usually normal (i.e., atrial and ventricular) but asynchronous.
o
o Premature Ventricular Contractions (PVC)
Contraction originating in an ectopic focus of the ventricles.
It is the premature occurrence of the QRS complex, which is wide and distorted in shape.
PVCs that are initiated from different foci appear different in contour from each other and are called multifocal PVCs.
Significance:
o Usually a benign in a client with a normal heart.
o In heart disease, PVCs may reduce CO and precipitate angina and heart failure.
o May represent ventricular irritability.
o May occur in reperfusion post thrombolytic therapy, or following percutaneous coronary intervention.
Treatment:
o Assessment of hemodynamic status.
o No treatment is typically required but medications are indicated should PVCs continue (especially into ventricular
tachycardia).
-adrenergic blockers, procainamide, amiodarone, or lidocaine.
o Rhythm is irregular because of premature beats.
o P wave is rarely visible because of the overlap between it and the QRS complex.
o
o Ventricular Tachycardia
Occurs when a run of three or more PVCs occurs.
Considered life-threatening because of decreased CO and the possibility of deterioration of ventricular tachycardia to ventricular
fibrillation.
Significance:
o Have been observed in patients with no evidence of heart disease.
o May cause severe decrease in CO (due to decreased diastolic filling).
o Result may be pulmonary edema, shock, and cerebral ischemia.
Treatment:
o IV procainamide, amiodarone or lidocaine is used.
o Synchronized cardioversion.
Synch with the rate of the AV-node.
o Rate is 100-250bpm.
o Rhythm may be regular or irregular.
o The ventricles take control as the pacemaker.
o
o
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o Ventricular Fibrillation
Severe derangement of the heart rhythm characterized on ECG by irregular undulations of varying contour and amplitude.
No effective contraction or CO occurs.
Significance:
o Results in unconsciousness, absence of pulse, apnea, and seizures.
o If untreated, patient will die.
Treatment:
o CPR and ACLS (advanced cardiac life support) with the use of defibrillation.
o Drug therapy.
o Hear rate is not measurable.
o Rhythm is irregular or chaotic.
o
o iClicker Question
o A client with a large myocardial infarction has been having premature ventricular contractions (PVCs) on his cardiac
monitor. Which pattern does the nurse recognize as being most characteristic of PVCs?
a) Irregular rhythm
b) Inverted T wave
o Characteristic of MIs.
c) Wide, distorted QRS complex
d) Increasingly long PR interval
o
o Sudden Cardiac Death
Death by an arrhythmia.
o
o Defibrillation
It is the most effective method of terminating ventricular fibrillation and ventricular tachycardia without a pulse.
It is most effective when the myocardial cells are not anoxic (i.e., having suffered damage due to hypoxia) or acidotic. For that
reason it is ideally performed within 15 to 20 seconds of onset of arrhythmia.
Defibrillation is accomplished by the passage of a direct current electrical shock through heart to depolarize cells. The intent is to
allow the SA node to resume the role of pacemaker.
The recommended energy for a first shock is 200J, with a second shock ranging between 200-300J as needed, and a third shock of
360J if defibrillation is unsuccessful. These shocks have been shown to cause myocardial damage, so it is important to start low
and work up as needed.
It is used in an emergency when the patient is unconscious.
o
o Cardioversion
It is not an emergency.
It is the therapy of choice for haemodynamically unstable ventricular or supraventricular tachyarrhythmias.
A synchronized circuit in the defibrillator is used to deliver a counter-shock that is programmed to occur during the with QRS
complex of the ECG.
Done on non-emergency basis.
During a cardioversion, the paitent is conscious, signs consent, start at 50J to 200J.
o
o Implantable Cardioverter-Defibrillator (ICD)
Treatment for life-threatening ventricular arrhythmias.
Education to the client receiving ICDs is extremely important.
o
o Pacemakers
They are pulse generators used to replace the SA node.
o Provide electrical stimulus to heart that cannot conduct own impulse to supply adequate CO.
o Used for transient and permanent conduction defects.
o They may have to be replaced over time.
o
o
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o
O
Unit 17: Clients with Coronary Artery Disease and Acute Coronary Syndrome
CORONARY ARTERY DISEASE (CAD)
o iClicker question A&P review

o Which of the following is a function of the right side of the heart?
a) Receives blood from lungs
b) Pumps blood to body
c) Receives blood from body
d) Supplies O2 to anterior wall
o
o Left coronary arteries feed left venricle dysrrhymias expected on left ventricle ventriclular dysrhymmias (vtachy, v
fib)
o Distupts conductions heart blocks (SA to AV Node) ventricluloar kill you fastest (zero cardiac output)(BP decreases
arteries coollapse on themselves)
o
o Coronary Arteries
The coronary arteries bring O2 blood to the heart.
Whats a Widow Maker?
o It is the name for a left, main coronary artery myocardial infarction.
o This leads to sudden cell death.
o
o Anatomy Review
4 electrophysiologic properties of heart:
1. Automaticity
2. Excitability of the heart to get excited
3. Conductivity ability to conduct from AV node to fibers
4. Contractility ability of the muscle to contract
Any compromised property will affect ejection fraction (i.e., the amount of blood the ventricles pump per beat), which is related
to cardiac output. Ejection fraction is measured as a percentage (see pg. 20 of notes).
o
o Atherosclerosis
It is hardening of the arteries due to the accumulation of fatty deposits that will eventually harden.
This is the result of having increased cholesterol levels for an extended period of time. A stroke or MI can occur if some of these
fatty deposits get dislodged and move to the brain or heart.
What does atheroma mean? Artery.
o
Atherosclerosis is the major cause of CAD.
o Characterized by a focal deposit of cholesterol and lipids, primarily within the intimal wall of the artery.
o C-reactive protein.
Blood test, autoimmune indicator of generalized inflammation. Not specific but gives an idea where the
inflammation is.
This is a non-specific marker for inflammation that is present in higher amounts in people with CAD.
This is a good indication of a potential MI.
o
Endothelial lining is altered as a result of chemical injuries.
o Hyperlipidemia (non-denuding)
There is plaque accumulating on the outside of the vessel walls, narrowing the vessel.
o Hypertension (denuding)
There is plaque accumulating on the outside of the vessel walls that eventually leak into the vessel, decreasing
the diameter of the vessel and forming a thrombin, which may possibly lead to a MI.
o
o Developmental Stages
Fatty streaks
o Small amounts of fat accumulation in the arteries.
Fibrous plaque
o Greater amounts of fat accumulation in the arteries.
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Complicated lesion
o Thrombus forms or can act ike a flap which may occulude the area or break off and travel somewhere and create a
partial or full occlution
o
o Endotherlial lining altered as a result of chemical injuries
o
Hyperlipidemia (nonendenuding
o
Hypertension (denuding)
o
o Response to endothelial injury can inject a dye and with another screen view occlusions and dan instrument with a
balloon that we can go in and smooshes these deposits to the side (plaque)
o Hyperension not usually enough
o Hyperlipidemia combine hypertension and boom increased pressure on thrombus
o Lipids attracted to coronary arteries
o
o Collateral Circulation
Growth of collateral circulation (i.e., creating of new, smaller arteries when the main ones become occluded) is attributed to two
factors:
1. The inherited predisposition to develop new vessels.
2. The presence of chronic ischemia.
Relation to age:
o Collateral circulation is typically seen in older individuals, as this process occurs with time.
o People who have MIs at a younger age are more like to die than their older counterparts as their bodies have not had a
chance to develop collateral circulation.
o
o Risk Factors for Coronary Artery Disease
Risk factors can be divided:
o Unmodifiable risk factors
Gender, ethnicity, age.
o Modifiable risk factors
Diet (low fat, high fibre, low sodium), smoking (stop), exercise (30 minutes/day is optimal), diabetes, alcohol
intake (increased intake stimulates the release of renin, which will eventually increase BP), stress.
o
o iClicker Question
o Which two risk factors for coronary artery disease increase the workload of the heart and increase myocardial oxygen
demand?
a) Hypertension and cigarette smoking
b) Elevated serum lipids and diabetes mellitus
c) Physical inactivity and elevated homocysteine levels
d) Obesity and smokeless tobacco use
o
o Health Promotion
Identification of high-risk persons.
o This is done through a history.
o Some people may want to have their lipids checked every 5 years.
Management of high-risk persons
o Physical fitness
o Nutritional therapy
o
o iClicker Question
o The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been effective
when the client states which of the following?
a) I should have some type of fish at least three times a week.
b) Most of my fat intake should be from olive oil or the oils in nuts.
c) If I reduce the fat in my diet to about 5% of my calories, I will be much healthier.
d) I should not eat any red meat such as beef, pork, or lamb.
o
o Health Promotion
Drug Therapy
o When do we start drug therapy?
145

Start with lifestyle modifications (e.g., exercise and diet). If the clients cholesterol is still high after 6 months,
drug therapy will be considered.
What do we usually start with? Why?
Statins (revolutionary drugs).
Sequestrians were used typically before statins came out; they are still sometimes used. They bind to lipids,
making them too large to be absorbed by the small intestine. They will then be excreted, causing the stools to
be more buoyant, frothy, and grey coloured.
o
o True or False
1) The leading theory of atherogenesis proposes that aging is the basic underlying cause of atherosclerosis.
o False lipids and hypertension
2) Endothelial alteration may be caused by chemical irritants such as hyperlipidemia or by hypertension.
o True
3) During development of the raised fibrous plaque, arterial wall changes may be initiated by carbon monoxide produced by
smoking.
o True
4) Partial or total occlusion of the coronary artery occurs during the stage of raised fibrous plaque.
o False (due to the complicated lesions)
5) Collateral circulation in the coronary artery is more likely to be present in the young client with CAD.
o False
o
o Case Study
o You are working in the internal medicine clinic of a large teaching hospital. Today your first patient is 70yearold J.M.
who has been coming to the clinic for several years for management of CAD, hypertension and anemia. A cardiac
catheterization done a year ago showed 50% occlusion of the circumflex artery. He has had episodes of dizziness for the
past 6 months and orthostatic hypotension, shoulder discomfort, and decreased exercise tolerance for the past 2 months.
On his last clinic visit 3 weeks ago, a chest xray and 12lead ECG were done, showing cardiomegaly and a left bundle
branch block (LBBB).
o Results of chemistries drawn at the time were as follows: Na 136 mmol/L, K 5.2 mmol/L, BUN 5.7 mmol/L, creatinine
120 mcmol/L, glucose 5.1 mmol/L, Cl 95 mmol/L, CBC: WBC 4.4x109/L, Hgb 105 mmol/L, Hct 31.4% and platelets
229x109/L.
o This morning his daughter has brought him to the clinic because he has had increased fatigue, significant swelling of his
ankles, and SOB for the past 2 days. His VS are 142/83, 105, 18, and 36.6C.
o
o General Information
o His vascular flow will not be good, and he has anaemia, meaning that they will have decreased vascular flow to
everything. The LBBB will decrease the CO. Cardiomegaly (enlarged heart) will lead to a decrease in heart filling.
o
o K+ levels are a little high (may lead to arrhythmias).
o Haemoglobin is low (this is due to his anaemia).
o
1) Knowing this history and seeing his condition this morning, what further questions are you going to ask J.M. and his daughter?
Does he have pain?
o Where is it? Is it radiating? What kinds of pain is it?
These questions are to rule out an MI.
Is his SOB while at rest or on exertion?
o Position while sleeping (e.g., how many pillows does he use).
Has he had any pallor, diaphoresis, pain, shortness of breath (how long has he had it for)
o This would be due to the increased K+.
o
O
ACUTE CORONARY SYNDROME (ACS)
o Acute Coronary Syndrome

Myocardial ischemia (i.e., cell death):
o O2 demand > O2 supply
o Results in cell death.
Myocardial ischemia typically comes about from CAD.
o
o Etiology and Pathophysiology ACS
146
st
Myocardial cyanosis occurs within the 1 10 seconds of coronary occlusion.

ECG changes will be seen immediately and the ECG characteristics will depend on the site of ischemia.
Total occlusion anaerobic metabolism and lactic acid accumulation.
o The accumulation of lactic acid is what causes pain.
o
o ECG Changes
o Ischema ST segment depression, T wave inversion, or both
o Injury ST segment elevation
o Infarction 0 Pathological Q wave
o
o Myocardial Infarction
Occurs as a result of sustained ischemia, causing irreversible cellular death (dead is dead). The majority of MIs occur in the left
ventricle.
Degree of altered function depends on a couple of thingswhat might they be?
o This depends on the part of the heart involved (i.e., its location, its size, etc.).
o
Contractile function of the heart stops in the areas of myocardial necrosis (the heart still receives signals but it has lost the ability
to respond).
Most involve the left ventricle (LV).
o The left coronary artery is responsible for this.
o
o
Subendocardial MI (non-Q wave MI)
o The damage has not penetrated through the entire thickness.
NSTEMI
o Non-ST elevation MI.
This occurs when the artery is partly occluded (typically from a thrombus).
It is not as serious as a STEMI.
Treatment: thrombolytics, anticoagulants.
STEMI
o ST elevation MI.
This is a complete occlusion of an artery.
Treatment: O2 therapy (as are all people with heart issues), morphine (it relaxes the body), thrombolytics (given
12 hours within occurrence of cardiac event).
If the patient will require a catheter, insert it before they are given thrombolytics to prevent unwanted
bleeding.
o
o Healing Process
Within 24 hours, leukocytes infiltrate the area of cell death.
Enzymes are released from the dead cardiac cells when should we see a rise in these enzymes? Which ones?
o Creatinine (CK) enzymes: onset of 3-4 hours; peak around 12 hours; and lasts around 24 hours.
This is the main enzyme checked as it helps give somewhat of a timeline.
o CKMB band.
o Troponin.
o Myoglobin.
o
Necrotic zone identifiable by ECG changes and nuclear scanning.
10 to 14 days after MI, scar tissue is still weak.
By 6 weeks after MI, scar tissue has replaced necrotic tissue.
o The area is said to be healed, but it is NOT as good as new.
What does the term ventricular remodelling mean?
o After an MI the body will try compensate for this loss muscle function. There will be hypertrophy of the ventricles (i.e.,
ventricular remodelling).
o
o Types of Angina
Stable Angina
o The heart is not getting enough blood flow.
147

The person will feel pain (with increased demands; pain will dissipate when the exercise or reason for increased demand
is stopped), SOB, and anxiety before the angina occurs.
o Treatment: nitro (it decreases the pre-load, relaxes the vessels, and decreases the workload of the heart).
Silent Ischemia
o The chest pains typically associated with ischemia are absent in this case.
o This may be seen in people with hypertension and diabetes.
o This is concerning because people will typically not seek assistance.
Prinzmetals Angina
o Temporary coronary artery spasm.
o This is common in people with Renauds, a history or migraine.
Nocturnal Angina
o Angina that occurs at night (not necessarily during sleep).
o The pathology is the same as in stable angina, only it is time-specific.
Angina Decubitus
o Chest pain when lying down that is alleviated when patient sits upright. Positional.
Unstable Angina
o Change in frequency and duration. It is unpredictable (i.e., it does not only come with activity).
o This will typically not resolve.
o ECG: there may be an ST depression.
o
What are the different symptoms?
o Unstable Angina
Why is this a problem?
What are some of the characteristics of unstable angina?
o It is unpredictable.
o
o Coronary Thrombogenesis Secondary to Plaque Production
Plaque starts to form in the arteries and will eventually completely occlude the vessel.
o
o iClicker Question
o Angina pectoris, the pain, most likely occurs with myocardial ischemia as a result of:
a. Death of myocardial tissue
b. Arrhythmias caused by cellular irritability
c. Lactic acid accumulation during anaerobic metabolism
d. Elevated pressure in the ventricles and pulmonary vessels
o
o Clinical Manifestations Angina
These patients almost never use the terms sharp or stabbing.
Usually does not change with position or breathing.
May complain of severe indigestion or burning.
Treatment: nitro.
o
o Match the Following Types of Angina with their Characteristics
1. Silent ischemia
h. Usually occurs in response to coronary artery spasm
2. Prinzmetals angina
(2)
3. Stable angina
i. Occurs only at night (4)
4. Nocturnal angina
j. May occurs in the absence of coronary artery
5. Unstable angina
disease(2)
6. Angina decubitus
o
a. Occurs only when the person is recumbent (6)
b. Usually precipitated by exertion (3)
c. Unpredictable and relieved by rest (5)
d. Prevalent in person with diabetes (1)
e. Characterized by progressive severity (5)
f. Occurs with same pattern of onset, duration, and
intensity (3)
g. Asymptomatic myocardial ischemia (1)
o
148

k.
l.
m.
n.
o.
p.
Occurs only when the person is recumbent (6)

q. Asymptomatic myocardial ischemia (1)
Usually precipitated by exertion (3)
r. Usually occurs in response to coronary artery spasm
Unpredictable and relieved by rest (5)
(2)
Prevalent in person with diabetes (1)
s. Occurs only at night (4)
Characterized by progressive severity (5)
t. May occurs in the absence of coronary artery
Occurs with same pattern of onset, duration, and
disease(2)
intensity (3)
o Clinical Manifestations Myocardial Infarction
Pain.
o Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration. It is typically sharp.
These characteristic of pain are the hallmark of an MI.
o
o Myocardial infarction occurs as a result of sustained ischemia, causing irreversable cellular death
o Dead is dead
o Degree of altered function depends on a couple of things size and location
o
o Subendocardial MI
o Damage has not penetrated through the entire thickness
o NSTEMI
o Non ST elevation MI Tx not as aggressive (disruption but not dcomplete occlusion)
o STEMI
o St elevation mi Cath lab ASAP
o
o Drugs throbolytics watch for brusiing, bleeding (start Ivs now or foleys in first)
o
o Healing process
o Within 24 hours leukocytes infiltrate the area of cell death
o Enzymes are released from the dead cardiac cells and it is these enzymes that we measure when we draw blood (CBC, WBC)
o Whch enzymes should we see? When? Figure 36-11 in text (chponen, ck peak at 24 hrs, myoglobin rises 1-3 hrs, cr chiase
o Healing process
o Necrotic zone identifiable by ecg changes and nuclear scanning..
o
o DX Angina
o cXR, ecg (ST depression), coronary angiography, serum lipid levels, cardiac markers, c-reactive protein (CRP) , treadmill
exercise testing
o
o Location of Chest Pain
Men
o Image
Different in women
o Complain of severe fatigue.
o Sleep disturbances.
o SOB.
o Anxiety.
o ~39% c/o chest pain.
o Jaw pain.
o Nausea and vomiting.
Can result from reflex stimulation of the vomiting center.
Tests to determine if a patient is having an MI:
o ECG.
o Cardiac enzymes.
o
Sympathetic nervous system stimulation
o catecholamines released during initial phases of MI.
Results in diaphoresis and vasoconstriction.
Vital sign changes:
o Fever (low grade ~38C).
o Increased heart rate initially (will decrease after about 1 day).
149
o Increased BP initially (will decrease after about 1 day).

Cardiovascular manifestations
o urine output
This is due to the lack of blood flow.
o Crackles
This is due to blood backing up.
o Hepatic engorgement
o Peripheral edema
EKG changes
o T wave inversion
ischemia
The T wave is important to watch because this is when there is a relative refractory period.
o ST segment elevation
injury
This is significantly elevated.
o Elongated Q wave
infarction
o
o Complications of Myocardial Infarction
Arrhythmias
o Ventricular arrhythmias are most common.
o PVCs are the most common cause of ventricular tachycardias, which, if untreated will lead to ventricular fibrillation.
Congestive Heart Failure
o This is due to a fluid backup.
Cardiogenic Shock
o A systolic of 40mmHg will likely lead to death.
o Increasing the patients blood volume is important (i.e., via IV fluids) as the nitrates administered will decrease the BP.
Papillary Muscle Dysfunction
o Responsible for the mitral valve.
o A murmur will be heard on auscultation.
Ventricular Aneurysm
o The ventricular walls are no good and start to thin. This will lead to bulges in the arteries, which will eventually lead to
rupturing.
Ventricular Septal Defect/Rupture
o This can happen in the second week post-MI.
Pericarditis
o Inflammation of the pericardium.
o Clinical manifestations:
Pain.
Cardiac tamponade.
Decreased heart filling.
Increased temperature (seen 2-3 days following an MI).
Dressler Syndrome
o Pericarditis, seen 2 weeks after an MI, which will lead to cell death.
o Changes in cardiac enzymes are seen with a new myocardial infarction, therefore, cardiac enzyme levels will not change.
o ECG changes will be seen.
Pulmonary Embolism
o Limitation of activity (i.e., bed rest) is important following an MI as we want to decrease myocardial oxygen demand.
o This may lead to a DVT.
o Diagnostic Studies Angina
Chest X-ray
o See the size of the heart.
ECG
o Check for disruptions in the hearts electrical activity.
o ECG should be different in patients with an angina but not with an MI.
Coronary angiography/nuclear imaging
o Determine where the blockage is located. Start in the femoral artery.
o A dye will be used, making the patient feel as though theyve been incontinent.
150
o When playing around with the arteries, it is possible for some clots to become loose.
Serum lipid levels
Cardiac markers
C-reactive protein (CRP)
Treadmill exercise testing
o
o iClicker Question
o The clients cardiac catheterization report reveals a 95% blockage of the LAD. The client is at greatest risk for an
infarction of the:
a. Lateral wall
b. Inferior wall
c. Anterior wall
d. Posterior wall
o
o Diagnostic studies Myocardial Infarction
Start with
o History of pain
Radiation, onset.
o Risk factors
o Health history
ECG
Serum cardiac markers
Other blood work?
o WBC count (sign of inflammation)
o Serum electrolytes (want to check K+ levels)
o C-Reactive Protein
o Creatinine, glucose
o
o Collaborative Care Angina
Treatment for stable angina:
o Nitrate therapy (vasodilation, decreasing pre-load)
o Stent placement
o Percutaneous coronary intervention (i.e., angiography)
o Atherectomy
o Laser angioplasty (i.e., reconstruction of the vessels)
o Myocardial revascularization
Drug Therapy
o Antiplatelet aggregation therapy
Aspirin (baby aspirin 81 mg): drug of choice
o -adrenergic blockers
Decreased heart workload.
o Calcium channel blockers
Decreased heart workload.
o Nitrates
Dilation of vessels
Percutaneous coronary intervention
o Surgical intervention alternative.
o Performed with local anaesthesia.
o Ambulatory 24 hours after the procedure.
Stent placement
o Used to treat abrupt or threatened abrupt closure and restenosis following PCI.
Atherectomy
o The plaque is shaved off using a type of rotational blade.
o Decreases the incidence of abrupt closure as compared with PCI.
Laser angioplasty
o Performed with a catheter containing fibres that carry laser energy.
o Used to precisely dissolve the blockage
151
Myocardial revascularization (CABG Coronary Artery By-pass Graft)

o Someones chest cavity is opened.
MIDCABG procedure
o This is left invasive.
o A camera is used to observe the chest cavity.
o
o Collaborative care Myocardial Infarction
Fibrinolytic (thrombolytic) therapy
o TPA
o These drugs start acting really fast and are not selective. Bleeding is a big concern (it will typically be seen in the
rectum, the gums, and urinary tract). If bleeding occurs, stop the medications immediately.
Cardiac catheterization
Percutaneous coronary intervention
Drug Therapy
o IV nitroglycerin
o IV anti-arrhythmic drugs
o IV morphine
o -adrenergic blockers
o Angiotensin-converting enzyme inhibitors
This decreases the blood pressure.
o Stool softeners
This will decrease strain during bowel movements.
Nutritional Therapy
o Diet restricted in saturated fats, trans-fats, and cholesterol.
o Low sodium.
o
o iClicker Question
o A client is admitted to the coronary care unit following a cardiac arrest and successful cardiopulmonary resuscitation at
his office. When reviewing the physicians admission orders, which of the following orders is it most important for the
nurse to question?
a. Oxygen at 4 L/min per nasal cannula.
b. Morphine sulphate 2 mg IV every 10 minutes until the pain is relieved.
c. Tissue plasminogen activator (t-PA) 100 mg IV infused over 3 hours.
d. IV nitroglycerin at 5 mcg/minute and increase 5 mcg/minute every 3-5 minutes.
o
o Angina and Myocardial Infarction Goals of Care
Relief of pain.
No progression of MI.
Immediate and appropriate treatment.
Cope with anxiety.
Modify risk factors once the patient has stabilized.
Rehabilitate.
o This is multidisciplinary (e.g., Refit Centre on Taylor).
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o Angina What can Nurses Do?
Acute Intervention
o Administration of oxygen
o Vital signs
o ECG (they are very non-invasive)
o Pain relief
o Patient teaching:
What is happening with the heart?
Factors that precipitate angina.
Risk factors.
Medications special ID?
Symptoms to report.
Avoid exposure to extremes of weather.
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o Myocardial Infarction What can Nurses Do?

Acute Intervention
o O2
o Morphine
o Continuous ECG
o Frequent vital signs
o Rest and comfort
Acute Intervention
o Anxiety
o Medications as needed
Diuretics, nitro, -blockers, anti-dysrhythmics.
o Emotional and behavioural reactions
o Communicate with the family
o Provide support
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o Rehabilitation
o Cardiac rehabilitation
o Physical exercise
o Resumption of sexual activity
Emotional readiness.
Physical training.
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o Evaluation
Pain level
Cardiac pump effectiveness
Anxiety control
Energy conservation
Health orientation
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o Sudden Cardiac Death
Unexpected death from cardiac causes.
Disruption in cardiac function.
Abrupt loss of cerebral blood flow.
Usually occurs within 1 hour of onset of symptoms.
Occurs secondary to natural causes.
Accounts for about 50% of all deaths from cardiovascular causes.
o
Mostly caused by ventricular arrhythmias.
Occurs less commonly as a result of primary LV outflow obstruction.
Risk factors:
o Male gender.
o Family history of premature atherosclerosis.
o Cigarette smoking.
o Diabetes mellitus.
o Hypercholesterolemia.
Diagnostic workup for determination of acute MI
o Cardiac markers
o ECG
24-hour Holter monitoring
Exercise stress testing
Electrophysiologic study (EPS)
Implantable cardioverter-defibrillator (ICD)
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Hypertension.
Cardiomegaly.
Ejection fraction < 40%.
History of ventricular arrhythmias.
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o iClicker Question
o What is the most significant factor in the positive outcome of a client with sudden cardiac death?
a. Absence of underlying heart disease
b. Rapid institution of emergency services and procedures
c. Performance of perfect technique in resuscitation procedures
d. Maintenance of 50% of normal cardiac output during resuscitation efforts
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o Gerontologic Consideration Coronary Artery Disease
Collagen and fat deposition.
Myofibrillar degeneration.
Endocardial thickening.
Calcification of the heart valves.
Degeneration of the conduction system.
Resting heart rate.
Loss of elastic fibres.
Systolic BP and SVR.
Circulating norepinephrine.
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o Women and Coronary Artery Disease
About 500,000 deaths occur in women per year.
Kills almost 10 times more women than breast cancer.
Manifest CAD 10 years later in life than men.
Most have symptoms present differently than men.
Diabetes mellitus found to be the single most powerful predictor of CAD in women.
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o Case Study #1 Martin
o 57 year old Martin came to ER at 02:44, c/o chest pain. His worried wife accompanied him. He stated he was seldom ill
but for the past 3 weeks hed had tightness in his chest & left arm pain. On admission he was SOB, pale & ashen &
nauseated. VS: BP 95/60, P 112 irregular, R 36, T 39, wheezes in chest.
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What are the pertinent facts of this case?
Chest pain, high respiratory rate, high temp, fast, irregular pulse, low BP, SOB, ashen, pale, and nauseated.
What nursing care issues/concerns should you address?
ECG, blood work, oxygen, when did this start, productive cough (i.e., pink, frothy sputum).
Need more detail about the pain (e.g., radiation, type of pain).
O2 sat?
What is your highest priority concern for this patient?
Deal with the patients chest pain.
Put patient on O2.
What should you be assessing for?
MI or angina:
o Perform an ECG.
o Ask pain questions: we know it radiates and hes had it for 3 weeks. How is the pain?
Angina and MI pain is differentiated based on when it occurs (i.e., at rest vs. on exertion).
What information is missing?
O2 saturations.
Medications taking.
Onset of pain.
What do you anticipate this patient will require for treatment?
Give patient nitro.
Oxygen therapy.
Take patients vital signs.
Give patient morphine.
ECG.
Blood work.
What assessments will the nurse need to anticipate/avoid complications to which the patient is susceptible?
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8) What specific teaching with the patient is required upon discharge?
Come in when signs and symptoms occur (e.g., chest pain).
Common complications.
Analgesics for the pain.
Antibiotics to treat the pericarditis.
9) What members of the health care team do you anticipate joining in the care for this patient?
10) How will you know your treatment/care has been effective?
If his symptoms disappear (e.g., no longer have SOB, edema, headaches, dizziness).
o
o Case Study #2 Hank
o Hank a 47 year old man was brought to the Churchill ER, by his wife, c/o severe indigestion. Hank has a 36 pack/year
smoking Hx, he has significant male pattern obesity, a barrel chest. VS BP 202/124, P 96, R18, T 36.8. Dr. orders include
O2 by NC to keep O2 Sat >90%. ASA 325 mg, IV NTG.
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1) What is the priority in Hanks care?
2) Are Hanks vital signs reasonable for a man his age? If not, what is wrong and why are they not normal?
No.
3) What information is missing?
Hx of hypertension?
Is he on/taking medications?
Hx of MIs?
Hx of CAD.
4) Identify 4 priority problems associated with the care of a patient like Hank.
a. Indigestion
b. BP
c. Potential COPD
5) What significant laboratory tests will be ordered and what will they reveal?
Cardiac markers.
Pink lady (i.e., viscous lidocaine and pepto-bismol).
Electrolytes.
Creatinine and urea.
6) How will you anticipate Hanks indigestion will be treated? What precautions must you follow when treating Hank for his
indigestion?
o
7) Angina is not always experienced as pain (as many people understand pain). How would you describe symptoms you want
Hank to warn you about?
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8) Hank is being treated medically for his CAD, what does this mean?
o
9) What other approaches may be used to treat CAD?
o
10) What specific teaching will Hank and his wife require prior to discharge?
When to comeback.
Teach smoking cessation.
Diet (low fat, low sodium) and exercise.
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o Coronary arteries, circulatiory
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o Cardiology 101 KNOW
o SBP / DBP
o Pulse Pressure
o MAP
o CVP
o LVEDP
o SVR or PVR,
o SV = stroke volume
o EF (% of blood from the left ventricle ejecting),
o CO or CI (Stroke ovlume x HR=Cardiac output = how much blood is moved in one minute), Cardiac index+ to calculate
cardiac output and divide by BMI
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Volume and Pressure

Mechanical structures
Electrical conduction
Fuel (oxygen and nutrients)
Volume and Pressure
Preload (starting) JVP (N or elevated; present someone filling with fluids we can see the jugular vein (overload), S3
(whoosing sounds or S3 sound when filling the heart which is a ventricular gallop and a sign of high pressures in the
ventricle S4is an atrial gallop), RAP or CVP (2-6mmHg), LVEDP (120/8 mmHg)
Afterload (pushing against to get blood out of the heart)
SBP (120 mmHG)
SVR = systemic vascular resistance (800-1200 dynes)
PVR = peripherial vascular resistance (more important)
Swan Ganz (PA) catheter into the right side used to measure pressures in the heart and calculate CO use to measure
using these tube to measure pressures.
Mechanical Structures
Heart valves
Stenosis tightening of the heart valves (increases afterload)
Regurgitation going back through valves wrong way or leaky valve (sounds like whooshing sound = murmurs)
Incompetent vale Endocarditis inflammation or infection on the valve that influences the ability to seal and can permanenemtly scar or
leak.
Chambers shape and size (ventricles and atrium)
Aortic Stenosis (outflow problems)
Tamponade fluid accumulating in the sac around the heart (usually fibrous and rigid with a little sereous fluid) the heart
relaxes and fills more but cant expand well in the rigid sac that is full of fluids. Emergency tx is to draw out the fluid
guided by US.
Malformation, genetic, birth defect
Electrical Conducation
Heart contracts on their own (they intrinsically contract on their own and heart muscles like to work with each other).
Electrical system helps the heart contract. Normal HR is 60-100 above is a sinus tachycardia or below is a sinus
bradycardia. Super high is a ventricular tachycardia.
SA node hits AV node and goes down the septum and down the bundle branch and then get a contraction from the apex
of the heart which initiates the ventricles and the heart twists itself a bit. EKG of note are: QRS to know about ellectrical
conducation in the heart. A wide QRS means it is slower. Faster shorter QRS.
Possible to lose conduction or timing or poor circulation lots can go wrong.
Heart failure pts prone to:
A fib (esp elderly or end stage) you can live with this but if you a fib too long, it doesnt move much so prone to develop
clots.
Atrial or vent tachycardia prone to low rhythems or bundle branch blocks (blocks are actual blocking of the
conducation or prolonging or losing the conducation altogether).
Atrial or Vent Arrthymias
Bundle Branch Blocks
Coronary Bloackage(physical blockage) vs heart block (electrical)
Complete heart block = type 1, type 2, type 3 (ventricles doing its own thing and atriums doing their own thing)
Oxygen and nutrients
Heart feeds itself first
Workload increases needs
Demand vs cardiac reserve. (cardiac reserve is how much you can overwork the heart and still make it keep it up) no
cardiac reserve could cause chest pain with the slightest movememt. Can help by giving oxygen and replenishing cardiac
reserve and give them rest and reduce the workload. Treat anemia to promote high quality of blood.
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Stress the heart leading to HF

#1 is ischemic disease ( vascular disease, diabetes, etc )
Hypertension (afterload is what the heart has to push against to pump blood)
Pulmonary Disease (affects the right side of the disease) Lungs can be sick and it becomes hard for the heart to push
blood through there.
Valvular disease stenosis, regurgitation, endocarditis
Anemia good oxygen capacity in blood, heart has to work harder to feed tissue.
Cardiomyopathy ischemic or other causes: etoh, viral, chemo, idiopathic (many origins).
More acutte cases:
MI partial death
Arrythmias long standing or prolonged tachycardia really overworking the heart and muscle is working and everything
is fast.
HTN crisis rapid increase in BP (pregnancy, drugs, etc.) afterload is just too heavy.
PE pulmonary embolis left isnt recieivng as much so stroke volume is down.
Ruptured papillary muscle regurgitation flow backwards
Myocarditis inflammation of the heart
Chemotherapy
Pregnancy extra workload (pre or clamsia)
Thyrotoxicosis drives the heart relentlessly
Cardiac compensation
HR + SV = CO
Go fastr
Fill up more
Squeeze harder (or carry more stuff)
Go Faster
SNS Stimulation due to low CO
Tachycardia, increased contractility, peripheral vasocontstriction, eventually counterproductive
Initial increased preload then increased after load (SVR)
Increased myocardial tissue oxygen demand ischemia
Shorter filling time ..
Fill up more
Neurohormonal
Decreased CO then RAAS
Starlings Law
Elongation of muscle fibres
Eventually less effective contraction
Early response (stretching of the heart)
Eventually will start showing wear and tear; it will stretch and get longer. Dont contract as well once theyre longer.
Huge and dilated.
Squeeze harder
Hypertrophy (higher duiastolic pressures ventricles wont relax)
Myocardial fibers thicken
Increased oxygen demand
Eventually thck, stiff ventricle (dilation and then thickening)
Less effective contraction
Poor coronary circulation
Prone to arrthmias
Poor relaxation for filling/small capacity
Later response
Cardiac remodeling changes to the heart architetcture
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Other compensations:
Endothelin potent vasocontrictor, NO
Cytokines inflammation depression
Atrial natriuretic peptides (ANP) and B-type natururetic peptide (BNP)
Naturesis excretion of NA in the urine
Counterbalanances aldosterone effect
BNP for monitoring HF
Cardiac compensation
Cardiac decompensation
Plus
Cardiac remodeling
Heart failure (immediately like an acute MI but chronic compensation can change the heart permanently)
Right sided heart failure:
Pt will look or symptoms will be: peripheral edema, Liver, kidneys, bowel and edema in ankles and hands and bellies.
Elevated liver function enzymes. JVP increased, fatigue and exhausted, no appetie. Rapid increase of water weight gain.
Left sided Heart Failure:
supposed to go to the body and lungs
Rapid breathing, SOB with activity and then at rest, nocturnal dyspnea, orthopnea (lay down and immediately have a
problem this is not the same as nocturnal dyspnea)
Other manifestations: fine crackles, pink frothy sputum (little blood), decreased aire entry to baes
Depression, confusion, altered memory and concentration
Arrhythmias fluttering in chest (tachy or brady)
Chest pressure or pain; diaphoresis
Positive HJR; S3, S4 present
Pallor, cyanoisis
Low BP, HR over 100
Lightheaded, dizzy, syncope
Nocturia
Upright assessment; JVP (up somewhat; down the jVP will go up automatically)
Chest xray cardiomegaly
On leads to the other
Right left
Biventricular failure
Cardiomyopathy
(not often it will just be one sided failure usually a mixture because its a cicuit or system).
Systolic Heart Filure
Inability to move blood forward
Unable to overcome SVR/PVR
Poor contraction
High afterload
Mechanical abnormalities
EF % of blood in ventricle that I am movving forward can still be compensating but the EF may be decreasing and
failing
Systolic ability staartss to fail (but Im going down hill slowly)
Diastolic Heart Failure
HF with preserved systolic function is now used
Stiff ventricle
Common to diabetes pts
Impaired filling pressures
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Venous engorgement
Little stressor tips really quickly into bd heart failure but where going along with diastolic heart failure.
NYHA Funcational Classification
Class I no limitation with oridinary changes, no symptoms
Calass II slight limitation of physical activities
Class III marked limiation of physical activities (a and B)
Class IV UNABLE TO CARRY OUT ANY PHYSICAL ACTIVITY without discomfort. Symptoms at rest. (hospital
or end stage)(caardiac cripple)
Regression of stages (can be a 4 then 1 than 3, etc.)
ACC/AHA HF Stages
Stage A high risk, no structural changes, no symptoms (want to catch; at risk)
Stage B structural changes, no symptoms (at least an episode of symptoms)
Stage C structural changes, past or present symptoms
Stage D structural changes, refractory symptoms, specialized interventions (end stage; heart reached maximal damage;
heart transplant and unmanageable heart failure)
No regressions of stages.
Case Study
Manifestations? CNS, CVS, Resp, GI, GU, P/S (biventricular)
Longer term (later stage)
Pleural effusions
Air hunger (palliative conceern)
Hypotension (particularly orthostatic)
Ventricular thrombus
Arrythmias (the more stretched out the more prone it iss to arrhthmias) (pacemakers, implantable defibulators)
- Tachy/brady
- High risk of sudden death
Longer term later stage
Mental changes (especially in the elderly)
Hepatomegaly (splenomegaly)
Renal failure (ace inhibitors hard on the kidneys watch creatine)
Gross ascites, anasarca (drains can be inserted peritoneal dialysis) (massive accumulation in the abd compressed the
bowel difficulty digesting food)
Anorexia
Muscle wasting common in late stages of heart failure (lose body mass)(immunological changes most likely culprit)
Function tatisnd trajectory:
NYHA Functional Classifications
ACC/AHA HF Stages
How do you classify and Stage? Pts know which class they are.
Tests:
Labs (cardiac enzymes, BNP, lytes (Potassium, magnesium, calcium, sodium, Creatinine), LFTs, T3/T4
(hyperthyroidism), CBC - hgb)
Hemodynamics blood pressure, pulse
ECG
CXR (enlrged heart, pleural effusion), Cardiac CT
Before tx: determine underlying cause
What do the tests tell you?
ECHO, MUGA, MRI (EF, architecture)
Cardiac catheterization (PCI) angiogram
Exercise Stress Test (debutamine drug to do the test)
6 Min Walk Test (how far can you walk in 6 min)
Sleep studies (obstructive apneic episodes during the night affects oxygen sats monitor on, orthopnea)
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NCP
Outline your intitial assessment H2T
CNS, CVS, Resp, GI, GU, P/S
Heart booklet/guidelines
Desired tx outcomes
Maintenance of adequate tissue oxygenation
Hemodynamic stability
Optimized fluid volume status (daily wt) (JVP down)
Minimized cardiac remodeling (get rid of alcohol, etc.)
Optimized functional sstatus (NYHA Class) ie. Symptom control
Medication adherance max dose titration, renal tolerance
Pt understanding of symptom maintenance and management (self-care)
Lifestyle modification (diet, obesity, smoking, exercise)
Knowledgeable family / community supports
(High potassium means failing kidneys)
#1 underlying cause ischemia***
HTN
Fluid Overload
Arrhythmias, electrolytes.
Medication therapy
ace inhibitors and beta blockers titrate!
Intolerant to either - > ARB
Intolerant to ACE-I/ARB
->nitrate/hydralazine
- tailor diuretic furosemide, metolozone
Electrolytes/creatinine within 7-10 days
If clinically stablee good! If not ->
Persistant NYHA II-IIIa on:
ACE-I and Beta Blcoker (ARB)
Tailored Diuretic
Then
Add ARB
Spironolactone or e[plerenone (MRA)
(**ACE-I + MRA + ARB not recommended)
If clinically stable good! If not ->
Digoxin )not a great ionotrope), nitrated increased
Other things to consider:
Statins
Antiplatelet agents
ACUTE/unstable
IV vasodilators
IV inotrpe (norepi, .
Devices and Interventions:
Revascularization (PTCA, Stent, CABG)
IABP
Pacer (temp/permananet)
ICD (implantable cardiaversion defibulator)
CRT (Cardiac resyncronization therapy for HF with some heart block where ventricles are not coordinated)
VAD (Ventricular assist device pump implanted with an external generator)
Transplant
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PTCA (percutaneous transluminal coronary angioplasty) in coronary artery through femoral artery up the left side of the
heart (very risky and controlled),
CABG take a vessel from another thigh or calf (vein) flip it around to change valves and move it to bypass the vessle
in the heart (Coronary artery bypass graph)
Intraaortic balloon pump temp lifesaving solution through artery into heart holds fluid and then deflates to allow
easy forward flow of the blood. Must be incredibly syncronized with how the heart contracts and it cant slide out of its
location.
Pacer/Pacemaker internal, external, temp with pain medication it delivers a shock each time. It will pace their heart.
Burnng or pain in chest in external pace
Temp goes into heart through another vein and can work for few days to get an internal pacer inserted via sx through the
vessles
Use vessle to attach patch to heart. Mimics the SV node.
Implantable cardioverter defibrillator and cardiac resyncronization therapy
- pacemaker clinic can monitor th pacers.
Will test pacemaker by setting it off.
CRT chambers are no longer coordinated
Carry a card in their wallet or have a bracelet or necklace what they have implanted.
Ventricular Assist Device implanted under ribs and physically pumps with th heart external device that requires lots
of power. Must carry the pack. Good for bridging to transplant.
Heart transplant steroid junkies, severe alcoholics,
Diet reduce obesity, controlled DM
Low salt
Fluid restriction
Daily weights (morning, dry, 2kg in two days)
Cardiac diet
Lifestyle diet, foo, stress, exercise, ADLs
Education self care
Family Caregivers:
Invaluable resource.
Consolidate notes..
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Unit 18: Clients with Heart Failure
CORONARY ARTERY DISEASE (CAD)
o Heart Failure
What is it?
o It is typically a grouping of symptoms, making it more of a syndrome than a disease in itself. It is characterized by
impaired cardiac pumping.
o It is viewed relating to anatomical location, that is, right and left sided heart failure, with the side pertaining to the
ventricles.
Left sided heart failure
Will affect the body systemically.
As the ventricles enlarge, they are less able to fill adequately, thus decreasing cardiac output.
Right sided heart failure
Will affect the lungs and pulmonary system.
Who is at greatest risk of developing heart failure?
o It is insidious and is therefore seen in the older populations.
o Individuals who have had a history of hypertension are also more susceptible to developing heart failure.
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Individuals who would have an increase in systemic vascular resistance for any particular reason, such as smokers, due
to the increase in blood viscosity, people with hyperlipidemia, and people with diabetes.
o Conditions that Exacerbate or Precipitate Heart Failure

Stress (i.e., long-term stress 3-5 years)
o This is because stress increases the cardiac output via an increased heart rate.
Dysrhythmias
o This is due to an increase in myocardial oxygen demand along with the hearts inability to effectively pump. The
ventricles will try compensate for these dysrhythmias, putting more strain on the heart.
Infection (on any sort)
o This will increase the bodys metabolic needs, causing the heart to have to pump more frequently.
Anaemia
o These patients have a decrease in O2-carrying capacity, therefore placing more stress on the heart (i.e., increased CO).
Thyroid disorder
o This predisposes patients to developing atherosclerosis. This can also impair the hearts contractility.
Pregnancy
o The blood volume has increased due to the child and there are is also an increase in metabolic demands.
Pagets disease
o This increases the bodys metabolic needs due to abnormal bone resorption.
Nutritional deficiency
o Thiamine (i.e., Vitamin B1) is essential for heart contractility. Patients with chronic alcohol abuse have a decrease in
thiamine in the body.
Pulmonary disease
o This is related to right-sided failure due to pulmonary hypertension.
Hypervolemia
o Increase in volume will increase the systemic vascular resistance, preload, and afterload.
o
o Etiology & Pathophysiology
It may be caused by any interference with normal mechanisms regulating cardiac output (CO).
CO depends on:
o Preload
The volume of blood present after diastole.
o Afterload
Associated with systemic vascular resistance.
o Myocardial contractility
Anything that affects contractility will alter the cardiac output.
o Heart rate
o Individuals metabolic state
o
o Pathology of Ventricular Failure Systolic Failure
This is the most common cause of CHF. It is a defect in the ventricles ability to contract.
The left ventricle loses its ability to generate enough pressure to eject blood forward.
The hallmark of systolic dysfunction is a in the left ventricular ejection fraction (i.e., the fraction of total ventricular filling
volume that is ejected with each contraction).
o This may be caused by impaired contractile function (i.e., an MI), increased afterload (e.g., hypertension),
cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disease).
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o There is a backup of blood during systole in patients with systolic
failure. This can lead to right-sided failure due to the backing up of
blood.
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o Pathology of Ventricular Failure Diastolic Failure
It is an impaired ability of the ventricles to fill during diastole.
Diastolic failure is characterized by high filling pressures and the end-result is pulmonary congestion due to a decrease in stroke
volume (i.e., the amount of blood expelled by the ventricles in one contraction) and impaired ventricular filling. There is
continuous venous engorgement in both the pulmonary and systemic vascular systems.
There is normal ejection fraction as the problem lies with heart filling (and not heart expulsion of blood to the body).
It is usually the result of left ventricular hypertrophy from chronic systemic hypertension.
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o Pathology of Ventricular Failure Mixed Systolic and Diastolic Failure
Seen in diseased states such as dilated cardiomyopathy.
There is biventricular failure (neither ventricle can compensate).
Patient has extremely poor ejection fractions.
This will lead to a decrease in cardiac output, decrease in blood pressure, and decrease in renal perfusion.
o
o 4 Basic Factors Causing Heart Failure
Increase in volume of blood to be pumped (i.e., problems with preload).
Increase in resistance against which blood must be pumped (i.e., problems with afterload).
Decreased contractility (e.g., dysrhythmias, patients with a history of MIs).
Decrease in filling of cardiac chambers (the chamber volume has decreased due to myocardial hypertrophy).
o
o iClicker Question
o A client with a history of chronic heart failure is hospitalized with severe dyspnea and a dry, hacking cough. She has
pitting edema in both ankles, and her vital signs are BP 170/100, P 92, and R 28. The nurse recognizes that the clients
symptoms indicate which of the following?
1. The venous return to the heart is impaired, causing a decrease in cardiac output.
2. There is impaired emptying of both the right and left ventricles, with low forward blood flow.
3. The right side of the heart is failing to pump enough blood to the lungs to provide systemic oxygenation.
4. The myocardium is not receiving enough blood supply through the coronary arteries to meet its oxygen demand.
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o Cardiac Reserve
It is the difference between the total amount of blood in the ventricles and the amount ejected during systole (i.e., stroke volume).
Not all the blood in the heart is expelled during ventricular contractions.
o During times of stress, the heart can increase its cardiac output with the help of this reserve.
o
o
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o Compensatory Mechanisms
o The overloaded heart resorts to certain compensatory mechanisms to try to maintain adequate cardiac output.
o
Ventricular dilation
o This is an enlargement of the chambers of the heart. It occurs when the pressure the heart chambers (typically the left
ventricle) is elevated over time. The muscle fibres of the heart stretch and increase their contractile force. This initially
increases the cardiac output and maintenance of arterial blood pressure and perfusion. This is an adaptive mechanism to
cope with increasing blood volume. With time this mechanism becomes inadequate as the elastic element of the muscle
fibres are overstretched and can no longer contract effectively, thus cardiac output.
Ventricular hypertrophy
o This is an increase in muscle mass and cardiac wall thickness in response to overwork and strain. This typically follows
persistent or chronic dilation. This will lead to an CO and maintenance of tissue perfusion but hypertrophic heart
muscle has poor contractility (i.e., the hearts ability to respond to an electrical stimulus).
Increased sympathetic nervous system stimulation
o SNS stimulation is often the first mechanism triggered in low CO states; however, it is the least effective compensatory
mechanism. Due to the inadequate stroke volume and CO, there is an increased release of epinephrine and
norepinephrine. This results in an increase in heart rate, myocardial contractility, and peripheral vasoconstriction, which
initially leads to an increase in HR and contractility, which increase the CO. Over time this becomes detrimental as it
increases the workload on the already weakened heart, which increases the hearts demand for O 2.
o The vasoconstriction increases the preload, which is problematic because the heart is already overloaded.
Neurohormonal responses
o A decrease in CO leads to a decrease in blood to the kidneys, which interpret this decreased flow as being a decreased
volume. The kidneys will release renin in response to a decrease in blood pressure. This will lead to vasoconstriction
and an increase in Na+ retention in the hopes of increase the blood pressure. Angiotensin-II will also secrete aldosterone,
which will cause Na+ retention and also increase the blood pressure.
o A decrease in blood flow to the brain causes the posterior pituitary to secrete ADH, which increases water retention and
thus the blood pressure.
o Natriuretic peptides are potent vasodilators.
Ventricular remodelling
o The neurohormonal response contributes to ventricular remodelling. This involves hypertrophy of the cardiac myocytes,
resulting in large, abnormal cells. This eventually leads to increased ventricular mass.
o
o *Cardiac compensation occurs when compensatory mechanisms succeed in maintaining adequate CO that is needed for
tissue perfusion. Cardiac decompensation occurs when these mechanisms can no longer maintain adequate CO.
o **Although these mechanisms are meant to be compensatory, their cumulative effects are harmful on the body because
the heart is unable to handle the compensatory effects.
o Clinical Manifestations of Heart Failure Depend Upon

Specific ventricle involved (e.g., right-, left-, or biventricular failure).
Precipitating causes of failure (e.g., hypertension, hyperlipidemia, high cholesterol, etc.).
o Once the precipitating factor is determined, we can help prevent future exacerbations (but not reverse any prior damage).
Duration of failure.
Patients underlying condition (e.g., history or atrial fibrillation).
o
o Classifications of Heart Failure
o CHF is usually manifested by biventricular failure, although one ventricle may precede the other in dysfunction.
Left-sided failure.
o Recall that this is the most common type of failure. It often leads to right-sided failure.
o Blood backs up into the left atrium and into the pulmonary veins which can lead to pulmonary congestion and edema.
o Most common cause is hypertension. Other causes include:
Cardiomyopathy
Rheumatic heart disease
CAD
Right-sided failure.
o The blood backs up into the right atrium and followed by the venous circulation.
o Signs and symptoms of a person with right-sided failure are due to venous congestion and include:
Peripheral edema.
Hepatomegaly.
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CHF can lead to severe hepatomegaly, especially with right ventricle failure. The liver lobules become
congested with venous blood and this hepatic congestion leads to impaired liver function.
Splenomegaly.
CHF can lead to splenomegaly, especially with right ventricle failure.
Jugular venous distension.
o The primary cause is left-sided failure (recall that one-sided heart failure will lead to biventricular failure). This is
because left-sided failure causes an increase in pulmonary congestion and increased pressure in the blood vessels of the
lungs (i.e., pulmonary hypertension). Eventually, chronic pulmonary hypertension results in right-sided hypertrophy and
failure.
o Cor pulmonale (i.e., right ventricular dilation and hypertrophy caused by pulmonary pathology (e.g., COPD)) may be a
cause of right sided-failure.
Forward & Backward failure.
o Based on the effect of circulation.
Forward failure: unable to propel the blood forward (i.e., during systole) due to decreased contractility. This
leads to an increase in sodium and water retention due to decreased renal perfusion and the release of renin.
Sodium and water are retained due to decreased renal perfusion.
Backward failure: unable to accommodate volume returning (i.e., preload) due to hypertrophy of the ventricles.
Sodium and water are retained due to decreased renal perfusion.
High output & Low output failure.
o High output failure: occurs when the cardiac output is normal or high but a condition exists that abnormally increases the
demand for oxygenated blood (e.g., hyperthyroidism, anaemia, pregnancy, arteriovenous fistulas, beriberi, and Pagets
disease).
o Low output failure: occurs when the cardiac output is low but the bodys demand of oxygen is normal (e.g., this may
occur due to ischemia coronary disease, hypertension, dilated cardiomyopathy, or valvular and pericardial disease).
Systolic & Diastolic failure.
o Systolic failure: the most common cause of CHF results from the hearts inability to pump blood (as the left ventricle
loses its ability to generate enough pressure to move blood past the aorta). It is a defect in the ability of the ventricles to
contract. The hallmark of systolic dysfunction is a decrease in the left ventricular ejection fraction. It is caused by
impaired contractile function (e.g., hypertension), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart
disease).
o Diastolic failure: it is an impaired ability of the ventricles to fill during diastole. Decreased filling will lead to decreased
stroke volume (and thus decreased CO). It is usually due to left ventricular hypertrophy from chronic systemic
hypertension, aortic stenosis, or hypertrophic cardiomyopathy.
o This is similar to forward and backward failure (i.e., forward failure = systolic failure and backward failure = diastolic
failure).
o
o Left-sided Heart Failure
o
o Right-sided Heart Failure
o Dyspnea (due to pulmonary
o
o Epigastric and RUQ
congestion)
abdominal pain
o Fatigue
o
o Increased abdominal girth
o Orthopnea, nocturia
o
o Anorexia
o Dry, hacking cough
o
o Bloating
o Pulmonary edema
o
o
o Acute Congestive Heart Failure Clinical Manifestations
Pulmonary edema.
o Agitation (due to decreased O2 to the brain).
o Pale or cyanotic.
o Cold, clammy skin.
o Severe dyspnea (the most common characteristic; due to severely impaired gas exchange).
o Tachypnea.
o Above is related to inadequate gas exchange as well as having fluid backing up into the lungs (more specifically, the
alveoli).
o Pulmonary Edema
o The pooling of blood in the lungs increases the hydrostatic pressure, pushing
the blood into the pulmonary interstitial space. This fluid will eventually
move into the alveoli. The most common cause of pulmonary edema is left
ventricular failure.
Every alveolus is surrounded by
lymphatics, which act as drains.
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o
o
o
This increase in pulmonary pressure due to a decrease in left ventricular efficiency results in engorgement of the
pulmonary vascular system. In order to help maintain a constant volume of the pulmonary extravascular fluid, the
lymphatic system increases its flow. This early stages is associated with a mild increase in the respiratory rate and a
decrease in PaO2.
If the pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move
into the interstitial space than the lymphatics can drain. Interstitial edema occurs at this point and severe tachypnea is
present.
Clients with pulmonary edema will be pale, agitated, and possible cyanotic. The skin is clammy and cold and the client
has severe dyspnoea, exhibited by the obvious use of accessory muscles, and orthopnea (i.e., severe dyspnea that is
relieved when seated upright). There may be frothy, blood-tinged, sputum upon coughing.
o
o Chronic Congestive Heart Failure Clinical Manifestations
Fatigue (due to decreased cardiac output, impaired circulation, tissue oxygenation, and anaemia)
Dyspnea
o Paroxysmal nocturnal dyspnea (PND) occurs when the client is asleep. It is caused by the reabsorption of fluid from
dependent body areas when the client is recumbent. The client will awaken in a panic and have feelings of suffocation as
well as the need to sit upright.
o Orthopnea.
These individuals are often sleeping with multiple pillows as lying supine is uncomfortable due to the PND.
Tachycardia (this is the body trying to compensate)
o It is one of the first symptoms. It occurs as a result of an increase in SNS stimulation.
Edema (this is due to a non-functional cardiac system)
Nocturia
o A person with chronic CHF who has decrease CO will also have impaired renal perfusion and decreased urinary output
during the day. When the person lies down at night, fluid movement from the interstitial spaces back into the circulatory
system is enhanced, which causes increase renal blood flow and diuresis.
Behavioural changes
o Cerebral circulation may be impaired with chronic CHF secondary to a in CO. The patient may display restlessness,
confusion, and attention span. This may be secondary to poor gas exchange and worsening renal failure.
Chest pain (this is similar to an angina-type pain due to a decrease in coronary perfusion)
Weight changes
o There will initially be weight gain, secondary to fluid retention; with time, the individuals may become too ill to eat and
will therefore lose weight. Renal failure may also contribute to fluid retention. In many cases, the persons weight loss
is masked by the edematous condition.
Skin changes (due to a general lack of circulation)
o Dusky appearance.
Cough (due to fluid build-up in the lungs)
o At first this will be a dry, hacking cough that is unrelieved by positional changes or over-the-counter medications. In
time (as the alveoli become flooded), the cough will be productive (i.e., pink and frothy).
Pulse Alterans (i.e., an alteration between a strong and weak pulse)
Enlargement of heart
o This is often due to the heart overworking for so long. This will lead to S3 and S4 heart sounds.
Atrial fibrillation
o These are common.
o The atrium quivers, leaving heart to pool in the ventricles and increases the likelihood of clot formation.
CheyneStokes Respiration
o An abnormal pattern of breathing characterized by alternating periods of apnea and deep, rapid breathing. This type of
breathing is typically seen as a person nears death (death breath).
o
o Heart Failure Complications
Pleural effusion
o The increase in pressure in the pleural capillaries leads to pleural effusions. This will be lead to dyspnea and bloodtinged frothy sputum.
Arrhythmias
o When the hearts chambers become enlarged, an alteration in the normal electrical pathway occurs, giving rise to atrial
fibrillation. The person may feel palpitations.
Left ventricular thrombus
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This is due to blood pooling from the atrial fibrillation. Clients with CHF and atrial fibrillation or very poor left
ventricular function should be on a regimen of anticoagulants (i.e., ejection fraction <20%).
Hepatomegaly
o This is due to the fluid backup in the heart, particularly due to right ventricular failure.
o
o Heart Failure Classification
The classification is based on the persons tolerance to physical activity.
o Class 1: No limitation of physical activity
This is the best time to start treating heart failure.
o Class 2: Slight limitation of physical activity (no limitations while at rest)
These limitations are due to dyspnea, SOB, and fatigue.
o Class 3: Marked limitation of physical activity (usually comfortable at rest)
These limitations are due to dyspnea, SOB, and fatigue.
o Class 4: Inability to carry on any physical activity without discomfort (symptoms may be present even at rest)
Any physical activity causes discomfort (e.g., going to the washroom is challenging).
o
o Heart Failure Diagnostic Studies
The primary goal in diagnosis is to determine the etiology (i.e., underlying cause). This may be done by:
o Physical exam (look at the liver, listen to heart sounds, check the respiratory system for shortness of breath)
o Chest xray (to check the hearts size)
o ECG (to determine the hearts contractility)
o Hemodynamic assessment (this is quite invasive and is not done often; it can determine if the patient has hyperlipidemia)
o Echocardiogram
o Stress testing (determines the hearts current condition)
o Cardiac catheterization (checks the patency of the cardiac arteries)
o Ejection fraction (EF)
There are 4 grades to left ventricular (LV) ejection fraction:
1. LVEF >60% (this is a normal left ventricular ejection fraction)
2. LVEF 40-60%
3. LVEF 20-40%
4. LVEF <20%
Once the underlying cause is determined, preventing the condition from worsening becomes important. It is not possible to erase
the damage that has occurred but further damage can be prevented.
o
Primary goal is to improve LV function by:
o Decreasing intravascular volume
Improves left ventricle function by reducing venous return.
Loop diuretic: drug of choice (e.g., Lasix).
It will be important to monitor the patients electrolyte status and blood pressure (as it may ).
o Decreasing venous return (i.e., preload)
Reduces the amount of volume returned to the left ventricle during diastole.
High Fowlers position (i.e., have the patient sitting upright at night while sleeping).
Leg position (do not have the legs above the heart; keep them down; never put the legs up as this will lead to
overload and is extremely problematic).
o Decreasing afterload
Decreasing afterload decreases pulmonary congestion as there is not as much fluid backing up.
IV nitroprusside (Nipride) Nitro, is a potent vasodilator that decreases both the preload and afterload.
Nesiritide (Natrecor)
ACE inhibitors (will help deal with the cough)
-blockers
Carvedilol (it helps prevent ventricular remodelling; lower the heart rate and contractions).
o Improving gas exchange and oxygenation
Decreases pulmonary congestion.
IV nitroprusside (Nipride).
Nesiritide (Natrecor).
IV morphine decreases oxygen demands.
Diuretics (Aldactone).
o
167
Aldactone/Spironolactone helps prevent the release of aldosterone, which leads to a decrease in Na+
and water reabsorption).
o Improving cardiac function
Hemodynamic monitoring for the following 3 drugs.
Digitalis.
It increases contractility but also increases myocardial oxygen demand.
Apical pulse must be >60bpm to receive this drug as it is a negative chronotropic and positive
inotropic.
Hold if the patients blood pressure is too low.
There are newer inotropics (e.g., dobutamine).
Dobutamine (this is not typically used on the average ward; it is usually in acute care settings).
o This drug enhances contractions but does not increase myocardial oxygen consumption.
o Reducing anxiety
Stress will exacerbate CHF.
Morphine.
This is not used for pain. It helps take the edge off and is used instead of sedatives as they will
decrease the patients respiration rate.
IV
inotropic
drugs.
Open vessels,
Enhance
contractility.
clear lungs,
Vasodilators.
and improves
ACE inhibitors.
heart rate
Prevent vasoconstriction.
o
Treat the underlying cause.
Maximize cardiac output.
Alleviate symptoms.
Oxygen treatment (especially at night).
Rest.
Biventricular pacing (this is typically done in more emergency-type situations when the patient experiences an HR).
Cardiac transplantation (severe; it is reserved for younger individuals).
o
o Chronic Heart Failure Drug Therapy
ACE inhibitors
o Prevent vasoconstriction by inhibiting the action of the angiotensin converting enzyme.
o They are the first line therapy for patients with CHF as they are useful in both systolic and diastolic failure.
Inotropic drugs
o They enhance heart contractility.
Vasodilators (e.g., nitro)
o It is the first line given to patients with heart failure (it is not for chest pain).
Diuretics
o The diuretics help decrease the fluid volume.
o The dose will increase with time and a combination of different diuretics is often used.
o Loop diuretics (e.g., Lasix) are the strongest type of diuretics.
Patients with allergies to sulfa drugs are cautioned against loop diuretics.
o Thiazide diuretics decrease the reabsorption of Na+, thus promoting its excretion along with water.
Adrenergic blockers
o Directly block the sympathetic nervous systems negative effects on the failing heart, such as increased heart rate.
o -adrenergic blockers must be started slowly as dizziness and edema are prevalent.
o Slows things down, enhances contractility of the heart.
o
o Question
o Match the following drugs used in the treatment of acute and chronic congestive heart failure with their therapeutic
effects.
a. Spironolactone (aldactone)................11
e. IV nitroprusside (nipride)..................6
b. IV nitroglycerin.................................4
f. Enalapril (vasotec).............................7
c. Digoxin (lanoxin)..............................10
g. Dopamine (Inotropin)........................5
d. Furosemide (lasix).............................8
h. Milrinone (Primacor).........................1
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i.
j.
k.
IV morphine......................................2
Carvedilol (Coreg).............................5
Nesirtide (natrecor)...........................3
1.
Improves cardiac contractions, decreases afterload,

and increases cardiac output
2. Dilates arterial and venous blood vessels in addition
to relieving anxiety
3. Recombinant form of a natriuretic peptide that
decreases preload and afterload
4. Primarily reduces preload and increases myocardial
oxygen supply
5. Directly blocks sympathetic nervous systems
negative effects on the failing heart
6. Potent vasodilator that decreases both preload and
afterload, increasing cardiac contractility and output
7. Decreases afterload by reducing levels of angiotensin
II and aldosterone
8. Primary effect is to decrease intravascular volume,
thus decreasing preload and improving left
ventricular function
9. Increases cardiac contractility but may increase
ventricular irritability
10. Increases cardiac contractility and output and slows
heart
11. Blocks action of aldosterone, decreasing intravascular
volume by sodium excretion, but retains potassium
l. Chronic Heart Failure Nutritional Therapy

Fluid restrictions are not commonly prescribed as the patients do not stick to it.
Sodium restriction (i.e., 2 g sodium diet) is very important. The average diet has between 3-7g of sodium.
o The amount of restriction depends on the severity of the heart failure and the potential of adherence (i.e., diets that
severely restrict the amount of sodium are not typically used as the likelihood of adherence to the poorly palatable food
is low).
Daily weights
o Same time each day.
o Wearing same type of clothing.
o Use same scale.
o If the client gains 1.4kg (i.e., 3lbs) within over 2-5 days, the primary health care provider should be called.
m.
n. Chronic Heart Failure Nursing Assessment
Past health history
Crackles (due to fluid in lungs)
Medications
Abdominal distension (due to ascites)
Functional health problems
Cold, diaphoretic skin
Tachypnea
Restlessness (due to lack of O2 to brain; check LOC)
Tachycardia
Chronic Heart Failure Overall goals

Peripheral edema (done by getting rid of fluid)
Shortness of breath (this should come with a decrease in fluid)
Exercise tolerance
Drug compliance
No complications (ideally)
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Acute intervention
o Establishment of quality of life goals.
o Symptom management.
They may feel as though they are drowning due to the pulmonary edema.
o Conservation of physical/emotional energy.
o Support systems.
Ambulatory and home care
o Teaching:
Psychological changes (inform the patient that these changes are likely to occur)
Exercisesaving behaviours (this is to conserve energy)
Medications
Environment
Evaluation
Respiratory status (first and foremost)
Sleep
Fluid balance (strict I&O are not done, but daily weights are taken to ensure there is no fluid retention occurring)
Activity tolerance
Anxiety control (they may feel as though they are drowning and will therefore be quite anxious)
Knowledge: disease process
Questions
A client with leftsided heart failure has oxygen at 4 L/min per nasal cannula, furosemide (Lasix) 40 mg po daily, spironolactone
(Aldactone) 25 mg po daily, and enalapril (Vasotec) 5 mg po bid. Which of the following actions is most important for the nurse
to implement?
1. Auscultate lung sounds.
2. Measure intake and output.
3. Assess skin turgor.
4. Draw a blood sample for arterial blood gases.
A client with chronic heart failure who is taking digoxin (Lanoxin) 0.25 mg po daily with furosemide (Lasix) 60 mg po daily
develops nausea and vomiting. Based upon these findings, what is the most appropriate intervention for the home care nurse?
1. Instruct the client to increase intake of high-potassium foods.
2. Notify the physician.
3. Perform a dipstick urine test for protein.
4. Ask the client to weigh himself each morning and call the nurse in 3 days.
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Unit 19: Clients with Cancer
Cancer
It is a group of more than 200 diseases characterized by uncontrolled and unregulated growth of cells.
Cancer is the second leading cause of death (second to heart disease).
Males: prostate cancer is the most common.
Females: breast cancer is the most common.
For both men and women, lung cancer is the deadliest type of cancer.
In Canada:
2 in 5 will be dx with cancer in their lifetime. 1 in 4 will die of cancer
At the beginning of 2009, 838,724 canadians alive who had been diagnosed with cancer in past 10 years.
A disease resulting from the interaction of multiple factors at the cellular, genetic, immunological and environmental levels.
Manitoba cancer statistics 2010

This year in Manitoba an estimated 6,200 new cases of cancer will be diagnosed and 2,800 cancer deaths are expected for this
year.
Breast cancer:
It is estimated that 800 new cases of breast cancer will be diagnosed this year and an estimated 220 women will die of the disease.
Prostate cancer:
An estimated 760 men will be diagnosed with prostate cancer this year. It is estimated that 180 men will die of prostate cancer.
Lung cancer:
Lung cancer remains the leading cause of cancer related deaths in both men and women in Manitoba.
It is estimated that 850 new cases of lung cancer will be diagnosed in Manitoba alone and that 780 people will die of lung cancer
this year.
Colorectal cancer:
Colorectal cancer is the third most common cancer diagnosed in both men and women.
In Manitoba, an estimated 820 people will be diagnosed with colorectal cancer this year. An estimated 350 people will die of the
disease.
An estimated 173,800 new cases of cancer (excluding about 75,500 non-melanoma skin cancers) and 76,200 deaths will occur in
Canada in 2010.
Approximately 83,900 Canadian women will be diagnosed with cancer and an estimated 36,200 women will die of cancer.
Approximately 90,000 Canadian men will be diagnosed with cancer and an estimated 40,000 men will die of cancer.
On average, 3,340 Canadians will be diagnosed with cancer every week.
On average, 1,470 Canadians will die of cancer every week.

The risk of cancer increases with age: 43% of new cancer cases and 61% of cancer deaths will occur among those who are at least
70 years old. However, cancer can occur at all ages.
Lung, prostate, breast and colorectal cancer account for 50% of all new cancer cases every year.
Lung cancer accounts for over a quarter (27%) of all cancer deaths each year.
Breast cancer accounts for over a quarter (28%) of new cancer cases in women.
Prostate cancer accounts for over a quarter (27%) of new cancer cases in men.
Prevalence
At the beginning of the year 2005, there were approximately 723,000 cases of cancer that had been diagnosed in the previous 10
years.
Survival
Based on 2002-2004 estimates, 62% of people are expected to survive for 5 years after their cancer diagnosis compared to the
general population of the same age and sex. Survival rates differ according to the type of cancer.
In Manitoba in 2010
Lung cancer
Colorectal cancer
o 850 new diagnoses
o 820 new diagnoses
o 780 deaths
o 350 deaths
Breast cancer
Prostate cancer
o 800 new diagnoses
o 760 new diagnoses
o 200 deaths
o 180 deaths
Estimated 6,200 new cancer diagnoses.
Estimated 2,800 cancer deaths.
In Canada
40% of women, 45% of men will develop cancer during their lifetimes.
o Approximately 1 in 4 will die of cancer.
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It is the leading cause of premature death.

o 1,026,600 PYLL (Potential Years of Life Lost) in 2004
32% of PYLL from all causes.
Statistics available at: www.cancer.ca
Paediatric Cancer
Much less common
Average of 1,271 new cases diagnosed in Canada.
Average of 208 deaths per year in Canada.
Most common types:
o 25% - Leukemia (most common: ALL)
o 18% lymphoma
o ~17% - Brain (gliomas, medulloblastomas)
o Less common:
Neuroblastoma
Wilms (kidney)
Sarcomas (rhabdomyosarcoma, osteosarcoma)
Survival Rates
Current 5-year overall survival:
o Adults: 65%
Death rate from breast cancer has decreased 24% since 1980.
o Children: 77%
1930s <30%
Leading theories and hypotheses of Tumorigenesis:

Clonal expansion. Multistep, mutagenesis, epigenetics, oncogene hypothesis, tumor suppressor gene, Knudsens two hit, cancer
stem cell hypothesis, immunosurveillance theory.
Development of Cancer
The following is a theoretical model to explain cancers development. The cause and development of each type of cancer are
likely to be multifactorial.
Growth factors will interact with its receptors to stimulate the cell.
Problems with cancer occur in and on the cell.
There are thought to be 3 main stages in the development of cancer:
1) Initiation
o Mutation of genetic structure (which can occur for many reasons) has the potential to develop into a clone of neoplastic
cells.
o Many carcinogens that enter the body are excreted; however, there are those that alter the bodys cells. If those cells do
not repair themselves or die, they will replicate into daughter cells, each of which will contain the alteration.
o Caused by things such as smoking
2) Promotion
o A single alteration of the genetic structure of a cell is not sufficient to result in cancer; however, the odds of cancer
development are increased with the presence of promoting agents (carcinogens).
o Promotion is characterized by the reversible (this characteristic distinguishes it from the initiation phase) proliferation of
altered cells.
o Promoting factors include dietary fat, obesity, cigarette smoking, alcohol consumption, and prolonged stress. The
withdrawal of these factors can reduce the risk of cancer development. Some carcinogens (known as complete
carcinogens) have the ability to initiate and promote the development of cancer (e.g., tobacco).
o A latent period is said to the time between the initial genetic alteration and clinical evidence of cancer. This period can
range between 1 and 40 years.
o A 0.5cm tumour is the smallest tumour that can be detected via MRI. A 1cm tumour is said to contain 1 billion cancer
cells.
3) Progression
o Progression is characterized by growth rate of the tumour, an increase in its invasiveness, and metastasis (i.e., the
spread of cancer from its original site to a distant site).
o Some cancers have certain sites in which they like to metastasize whereas others will metastasize randomly (e.g.,
melanoma). Frequent sites of metastasis are the lungs, brain, liver, bone, and adrenals (mnemonic: bball).
172

o
The metastatic process is a multistep process that begins with rapid growth of primary tumour. As the tumour increases
in size, it requires its own blood supply. This development of blood supply is critical for survival and is termed tumour
angiogenesis, which is promoted by tumour angiogenesis factors created by the cancer cells. Certain subsections of a
tumour are able to detach from the primary tumour and enter a different area of the body.
Biology of Cancer
Cancer is a group of many diseases of multiple causes that can arise in any cell of the body capable of evading regulatory controls
over proliferation and differentiation. Two major dysfunctions present in the process of cancer are defective cellular proliferation
(growth) and defective cellular differentiation.
Defects in Cellular Proliferation

Clonal Expansion Theory
DNA substituted or permanently rearranged
Once mutated cell can:
Die from damage or by initiating apoptosis
Can recognize damage and repair itself
Survive and pass on damage
Surviving mutated cells have potential to become malignant
Stem cell hypothesis
Sub-population of cells that are self-renewing
Normally, most tissues of the human adult contain a population of predetermined, undifferentiated cells known as stem cells.
Predetermined means that the stem cells of a particular tissue will ultimately differentiate and become mature, functioning cells of
that tissue and that tissue only. All cells of a tissue are controlled by an intracellular mechanism determining when cellular
proliferation is necessary. Under normal conditions, a state of dynamic equilibrium is maintained. Cellular proliferation is
typically only triggered in the presence of cellular degeneration or death. It may also be triggered when the body requires more
cells (e.g., more white blood cells in the presence of an infection). Cell proliferation originates in the stem cell and begins when
the stem cell enters the cell cycle.
Another explanation for the phenomenon of proliferation control of normal cells is contact inhibition (i.e., cells stop their
growth when their edges make contact with the edges of another cell). Cancer cells are characterized by a loss of contact
inhibition.
Cancer cells proliferate in the same manner and at the same rate as normal cells; however, cancer cells respond differently than
normal cells to the intracellular signals that regulate the state of dynamic equilibrium. Cancer cells divide indiscriminately and
haphazardly, sometimes producing more than two cells at the time of mitosis.
Growth without GO signals.
o Growth factors, cell-cell adhesion molecules, extracellular matrix components.
Ignoring STOP signals
o Loss of contact inhibition
Invade neighbouring cells, keep dividing.
o Loss of restrictive point control
Keep dividing without adequate nutrients.
Unlimited number of cell divisions: immortality.
Avoidance of APOPTOSIS (programmed cell death).
Induce angiogenesis.
http://www.cancerquest.org/cancer-hallmarks-introduction
Changes in Physical Properties of Cancer Cells

o The changes in cell behaviour that occur as cancer develops are, in part, dependent on changes in physical properties of
the cells. Some of the changes have been identified and may be used to identify cancer cells.
o Tumour cells display a characteristic set of features that distinguish them from normal cells. These traits allow the
individual cells to form a tumour mass and eventually to metastasize to other parts of the body. We will briefly consider
the changes that affect cell functions and then discuss some of the capabilities that must be acquired by the tumours as a
whole to enable them to grow and spread.
o A wide range of changes occur during the transformation of a normal cell to a cell capable of forming a cancerous
growth. All cancer cells acquire the ability to grow and divide in the absence of appropriate signals and/or in the
presence of inhibitory signals. There are also detectable changes in the physical properties of the cells. These changes
include the following:
Cytoskeletal changes
173
The distribution and activity of the microfilaments and microtubules may change. These alterations
change the ways in which the cell interacts with neighbouring cells and alter the appearance of the
cells. Changes in the cytoskeleton also affect cell adhesion and movement (motility).
Cell adhesion/motility
The reduction of cell:cell and cell:extracellular matrix adhesion allows large masses of cells to form.
As described in the section on cell division, cancer cells do not exhibit contact inhibition and are able
to continue to grow even when surrounded by other cells. The alterations in cell adhesion also impact
on the ability of the cells to move. Cancer cells must be able to move and migrate in order to spread,
and cell adhesion plays a major role in regulating cell movement.
Nuclear changes
The shape and organization of the nuclei of cancer cells may be markedly different from that of the
nuclei of normal cells of the same origin. This change in appearance may be useful in the diagnosis and
staging of tumours.
Enzyme production
Cancer cells often secrete enzymes that enable them to invade neighbouring tissues. These enzymes
digest away the barriers to migration and spread of the tumour cells.
Cancer cells that get past this have acquired the ability to avoid the cell death signals triggered by their abnormal behaviour.
Changes in Physical Properties of Cancer Cells
The changes in cell behavior that occur as cancer develops are, in part, dependent on changes in physical properties of the cells.
Some of the changes have been identified and may be used to identify cancer cells.
Tumor cells display a characteristic set of features that distinguish them from normal cells. These traits allow the individual cells
to form a tumor mass and eventually to metastasize to other parts of the body. We will briefly consider the changes that affect cell
functions and then discuss some of the capabilities that must be acquired by the tumors as a whole to enable them to grow and
spread.
A wide range of changes occur during the transformation of a normal cell to a cell capable of forming a cancerous growth. All
cancer cells acquire the ability to grow and divide in the absence of appropriate signals and/or in the presence of inhibitory
signals. There are also detectable changes in the physical properties of the cells. These changes include the following:
Cytoskeletal changes- The distribution and activity of the microfilaments and microtubules may change. These alterations
change the ways in which the cell interacts with neighboring cells and alter the appearance of the cells. Changes in the
cytoskeleton also affect cell adhesion and movement (motility).
Cell adhesion/motility- The reduction of cell:cell and cell:extracellular matrix adhesion allows large masses of cells to form. As
described in the section on cell division, cancer cells do not exhibit contact inhibition and are able to continue to grow even when
surrounded by other cells. The alterations in cell adhesion also impact on the ability of the cells to move. Cancer cells must be
able to move and migrate in order to spread, and cell adhesion plays a major role in regulating cell movement.
Nuclear changes- The shape and organization of the nuclei of cancer cells may be markedly different from that of the nuclei of
normal cells of the same origin. This change in appearance may be useful in the diagnosis and staging of tumors.
Enzyme production- Cancer cells often secrete enzymes that enable them to invade neighboring tissues. These enzymes digest
away the barriers to migration and spread of the tumor cells.
Cancer cells that get past this have acquired the ability to avoid the cell death signals triggered by their abnormal behavior.
Process of Tissue Invasion and Metastasis

Getting into the bloodstream: Altered adhesion and motility.
o Think of cellular velcro.
Cancer cells have lost the anchorage-dependent growth. Anchorage-dependent growth is that it must be attached
to a substrate to divide
Surviving in the bloodstream: Alteration in anchorage-dependent growth.
Co-opt platelets to use as shields.
Getting back into tissue: Extravasation and attraction to adhesion molecules in tissue.
Notes:
o Metastasis (e.g., bone or organ) are what cause death, not the cancer itself. Most cancers have a very predictable method
of spread.
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Stem cell theory

The theory essentially states that loss of intracellular control of proliferation results from the mutation of stem cells. The stem
cells DNA is substituted or permanently rearranged.
Once mutated, the stem cell can undergo different fates:
1. Cell can die from damage caused by the mutation or by initiating apoptosis [programmed cell death].
2. The cell can recognize the damage and repair itself.
3. The cell can survive and pass the damage on to future daughter cells.
Surviving mutated cells have potential to become malignant.
This theory is not complete as malignant stem cells can differentiate to form normal tissue cells.
Defects in Cellular Differentiation

Cellular differentiation is normally an orderly process that progresses from a state of immaturity to a state of maturity. Because
all cells are derived from the fertilized ova, all cells have the potential to perform all body functions. As cells differentiate, this
potential is repressed and the mature cell is capable of performing only specific functions. Once differentiated, a cell will not dedifferentiate.
Two types of genes that can be affected by mutation are proto-oncogenes and tumour suppressor genes. Proto-oncogenes are
normal cellular genes that are important regulators of normal cellular processes, such as promoting growth. Tumour suppressor
genes (e.g., p53) suppress growth. Mutations that alter the expression of proto-oncogenes can activate them to function as
oncogenes (i.e., tumour-inducing genes). Mutations that alter tumour suppressor genes render them inactive.
Proto-oncogenes have been described as genetic locks that keep the cell in its mature, functioning state. When unlocked (e.g., by
carcinogens), the abilities and properties the cell had while in the fetal development state are again expressed. Oncogenes
interfere with normal cell expression under some conditions, causing the cell to become malignant. This cell regains a fetal
appearance and function. For example, some cancer cells produce new proteins, such as those characteristic of embryonic and
foetal periods of life. These proteins located on the cell membrane include carcinoembryonic antigen (CEA) and -feto protein
(AFP).
Tumours can be classified as benign or malignant. In general, benign neoplasms are well differentiated and malignant neoplasms
range from well differentiated to undifferentiated.
Telomeres and Immortality

Normal cells are not immortal.
Drugs can inhibit telomerase (cancer cell)
Cancer Genetics 101

Proto-oncogenes
o They are normal cellular genes that are important regulators of normal cellular processes.
Its a Go signal. A mutation in a proto-oncogene becomes an oncogene.
o Mutations that alter their expression can activate them to act as oncogenes (tumour-inducing).
Tumour suppressor genes
o Suppress growth of tumours.
Its a Stop sign that does not work.
o Mutations render them inactive allowing tumours to develop.
Role of the Immune System

Immune response is to reject or destroy cells perceived as non-self. For example, cells from an organ transplant may be seen as
non-self cells and elicit an immune response. Similarly, cancer cells can be perceived as non-self cells and be rejected and
destroyed. The difference between an organ transplant and cancer is that the cancer cells have risen from the patients own cells,
and even though they are mutated, the immune response mounted against them may be inadequate to reject and destroy the
cancer.
Some cancer cells have changes on their surface antigens, which are known as tumour-associated antigens (TAAs). It is believed
that it is one of the functions of the immune system to respond to TAAs. This response to antigens of malignant cells is termed
immunologic surveillance.
o Immunologic surveillance:
Lymphocytes continually check cell surfaces, detect and destroy cells with abnormal or altered antigenic
determinants.
Involves cytotoxic T-cells (these are thought to have the most dominant role), natural killer cells, macrophages,
and B lymphocytes (i.e., every cell type involved in a normal immune response is used against tumour cells).
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T cells are also important in the production of cytokines (e.g., interleukin-2 and -interferon), which
stimulate T-cells, natural killer cells, B cells, and macrophages.
o Natural killer (NK) cells are able to directly lyse tumour cells spontaneously without any prior
sensitization. Their killing ability is boosted by -interferon.
o Macrophages also secrete cytokines (i.e., interleukin-1) and tumour necrosis factors (TNF).
Escape mechanisms by which cancer cells evade immune system:
o The process by which cancer cells evade the bodys immune system is known as immunological escape. Theorized
mechanisms by which cancer cells can escape immunological surveillance include:
1. Suppression of factors that stimulate T cells to react to cancer cells.
2. Weak surface antigens allow cancer cells to sneak through surveillance.
3. Development of tolerance of immune system to some tumour antigens.
4. Suppression of immune response to products secreted by cancer cells.
5. Induction of suppressor T cells by the tumour.
6. Blocking antibodies that bind TAAs, thus preventing their recognition by T cells.
Oncofoetal Antigens
o They are a type of tumour antigen found on both the surface and inside of cancer cells, as well as foetal cells. These
antigens are an expression of the shift of cancerous cells to a more immature metabolic pathway, an expression usually
associated with embryonic or foetal periods of life. The reappearance of foetal antigens in malignant disease is not well
understood, but it is thought to be a result of the cell regaining its embryonic capability to differentiate into many
different cell types. Examples of oncofoetal antigens include carcinoembryonic antigen (CEA) and -fetoprotein. CEA
levels are currently used to determine the efficacy of cancer treatment.
Immune system response is to reject or destroy cells perceived as nonself
Immunologic surveillance
o Lymphocytes continually check cell surfaces, detect and destroy cells with abnormalities
o Involves cytotoxic T-cell natural killer cells, macrophages, and B lymphocytes
Some cancer cells have changes on their surface antigens
o Tumor-associated antigens (TAAs)
Escape mechanisms by which cancer cells evade immune system
o Suppression of factors that stimulate T-cells
o Weak surface antigens allow cancer cells to sneak through surveillance
o Development of tolerance of immune system
o Suppression of immune response to products secreted by cancer cells
o Induction of suppressor T-cells
o Blocking antibodies that bind TAAs
Cell Biology:
Immortality: unlimited number of cell divisions
Growth without GO signals
Growth factors, cell-to-cell adhesion molecules, extracellular matrix components
Loss of contact inhibition: invade neighboring cells, keep dividing
Loss of restrictive point control: keep dividing without adequate nutrients
Loss of anchorage-dependent growth
Loss of cell cycle control
Avoidance of APOTOSIS (programmed cell death)
- apoptosis = auto destruct sequence (they dont self-destruct. They continue to grow.
- Angiogenesis can create their own blood supply. Secrete factors and androgen (vascular epidural growth factors)
Property
Characteristics of Cancer & Transformed Cells
Cytological changes
Increased size & number of nucleoli
Increased nuclear/cytoplasmic ratio
Altered cytoskeleton
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Immortality
Decreased density-dependent growth inhibition (loss of contact inhibit
Decreased requirement for serum
Loss of cell-cycle control
Reduced apoptosis
New surface antigens
New or altered glycoproteins
New or altered glycolipids
Altered cell growth
Changes in cell membrane
Altered Cell Growth

Immortality: unlimited number of cell divisions
Growth without GO signals
Growth factors, cell-to-cell adhesion molecules, extracellular matrix components
Loss of contact inhibition: invade neighboring cells, keep dividing
Loss of restrictive point control: keep dividing without adequate nutrients
Loss of cell cycle control
Avoidance of APOTOSIS (programmed cell death)
Telomeres and Immortality
Normal cells are not immortal: can only divide a limited number of times before senesce.
Telomeres: repeated DNA sequence & protective caps on each chromosome
Telomeres become smaller with each chromosomal replication
Telomerase is increased in cancer cells allows indefinite replication.
Process of Tissue Invasion & Metastasis

Getting into the bloodstream: altered adhesion and mobility
Surviving in the bloodstream: altered anchorage-dependent growth
Getting back into tissue: extravasation and attraction to adhesion molecules in metastatic site
Angiogenesis is important component
Types of Tumours
Benign neoplasms
o Well differentiated.
o Encapsulated.
o Expansive mode of growth.
o Characteristics similar to parent cell.
Malignant neoplasms
o Poorly differentiated.
o Infiltrative and expansive.
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Able to metastasize.
Frequent recurrence.
Moderate to marked vascularity.
Cells do not resemble parent cell.
Cells take on more foetal cell like appearance.
Causation of Cancer
External stimuli causing genetic mutation.
Age biggest factor. Lifetime of exposure.
o Carcinogens:
Chemicals:
Tobacco smoke, arsenic, EtOH (it is carcinogenic to the stomach, liver, pancreas, and breast), vinyl
chloride, benzene.
Exposure to viruses.
Immune system abnormalities.
Genetic abnormalities (inherited/heritable).
o Oncogenes, proto-oncogenes, tumour suppressor genes.
o Inherited genetic risk: 5-10% of cancers.
Chromosomal abnormalities (spontaneous: they are not passed down).
o Increased number of chromosomes, deletion, translocation, and breakage.
The Philadelphia chromosome is a switch between chromosomes 9 and 22.
o Genetic abnormalities are different from familial patterns.
Risk Factors
External stimuli (carcinogens)
o Diet colon cancer
Estimated that 1/3 all cancers and 90% of colon cancer are related to diet.
Tobacco small cell lung cancer (SCLC), oropharyngeal, bladder, cervical, gastric, lip, pancreatic, breast.
o As much as 50% of bladder cancer is related to smoking as a lot of carcinogens are excreted by the kidneys (meaning
that the carcinogens will sit in the bladder).
Bacteria H. pylori ulcers cancer risk.
UV radiation (e.g., from the sun) basal cell, squamous cell.
Chemicals
o Asbestos mesothelioma.
o Vinyl chloride liver.
o Arsenic sinuses, liver.
o Benzidine, aniline dyes bladder.
o Wool, leather, dust nasal sinuses.
Viruses
o Most common: HBV/liver cancer
o HTLV-1: T-cell lymphoma & T cell leukemia
o HTLV-2: Hairy cell leukemia
The prognosis is better with this type of cancer.
o Epstein Barr: Burkitts lymphoma
o HCV: liver cancer
o Human papilloma virus: cervical cancer
Immune System Abnormalities
o Immunosuppressive medications
Prednisone, cyclosporin, Immuran, etc.
Disorders affecting immune system
o Lupus, HIV/AIDS
Kaposis sarcoma is an AIDS-defining malignancy.
Age-related immune susceptibilities
o Children, Elderly
Inheritable Genetic Mutations
o BRCA-1: breast, ovarian, prostate
o BRCA-2: breast
o RB1: retinoblastoma (only in children up to the age of 2)
o
o
o
o
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This will lead to a tumour within the eye.
WT1: Wilms tumor (only in children)
Li Fraumeni (p53 suppressor mutation): breast, brain tumours, acute leukemia, soft tissue sarcomas, osteosarcomas, and
adrenal cortical carcinoma.
The off switch is broken, making the patient more likely to an array of tumours.
o Hereditary non-polyposis colorectal cancer
o Familial adenomatous polyposis
o Multiple Endocrine Neoplasia (MEN1, MEN2)
Prevention & Detection of Cancer

Up to 80% of cancers could be prevented if Canadians made healthier choices about:
o Tobacco.
o Diet.
o Exercise.
o Sexual practices (related to HPV, Hep B/C, etc.).
Reduce or avoid exposure to known or suspected carcinogens.
Eat balanced diet.
Exercise regularly.
Adequate rest.
Receive health examinations on a regular basis.
Early detection of cancer has a positive impact on prognosis.
o
o
Phase
Psychosocial Impact
Pre-diagnosis
Often caught off guard, sometimes suspected it
Diagnosis
Overwhelmed, info overload
Treatment
Dealing with S/E, life revolves around tx
Recovery
Re-entering normal world
Survivorship
Living beyond cancer
OR
Progression or recurrence
Approaching and dealing with death
Diagnosis
History and physical
o In many cases, the patients will have vague, non-specific symptoms which will lead them to see a health care provider.
Blood work
o A man with prostate cancer will test positive with a pregnancy test.
Tumour markers (e.g., oncofoetal antigens)
o As successful treatment progresses, the level of these markers will decrease.
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Proteins, antigens, ectopically produced hormones, receptors enzymes and genes or gene products that are tumor
derived (expressed by the tumor) or tumor associated (produced by normal tissue in response to the tumor). (Yarbro,
Wujcik & Gobel, 2011, p. 169)
o Not sensitive/specific enough for screening or diagnosis are adjuncts to other dx measures
Imaging: X-rays, CT, MRI, nuclear medicine, U/S
Visualization (endoscopy, cystoscopy)
Biopsy
o This is the gold standard in diagnosing cancer. The treatment is largely based on the pathologists report.
o In some cases, a chart may indicate presumed malignancy, but no biopsy will be done because this would only cause
distress to the patient as they already have serious health conditions.
Classification of Cancer
Cancer can be classified according to:
1. Anatomical site classification
2. Histological analysis classification/degree of differentiation (i.e., grading).
3. Extent of disease classification (i.e., staging).
Classifying cancer in such ways is intended to provide standardized ways to communicate the status of cancer within the health
care team, assist in finding the best treatment plan, evaluate the plan, help determine prognosis, and compare like groups for
statistical purposes.
HER2/neu (also known as ErbB-2) stands for "Human Epidermal growth factor Receptor 2
HER2 is a cell membrane surface-bound receptor tyrosine kinase and is normally involved in the signal transduction pathways
leading to cell growth and differentiation. It is encoded within the genome by HER2/neu, a known proto-oncogene. HER2 is
thought to be an orphan receptor, with none of the EGF family of ligands able to activate it. However, ErbB receptors dimerise on
ligand binding, and HER2 is the preferential dimerisation partner of other members of the ErbB family.[1] The HER2 gene is a
proto-oncogene located at the long arm of human chromosome 17(17q21-q22).[2]
In clinical usage, HER2/neu is important as the target of the monoclonal antibody trastuzumab (marketed as Herceptin).
Trastuzumab is effective only in cancers where the HER2/neu receptor is overexpressed. One of the mechanisms of how
trastuzumab works after it binds to HER2 is by increasing p27, a protein that halts cell proliferation.[8]
Anatomic Site Classification

In the anatomic classification of tumours, the tumour is identified by the tissue of origin, the anatomic site, and the behaviour of
the tumour (i.e., benign or malignant).
Carcinomas originate from embryonal ectoderm (skin and glands) and endoderm (mucous membrane linings of the respiratory
tract, GI tract, and genitourinary tract).
Sarcomas originate from embryonal mesoderm (connective tissue, muscle, bone, and fat).
Lymphomas and leukemias originate from the hematopoietic system.
If the disease is found distant from normal location it is identified as the primary cancer. For example, a person may have breast
cancer with brain metastasis. They will not be said to have brain cancer, unless the histology shows brain cancer cells.
Examples of tissues of origin:
o Carcinoma epithelial tissue
Adeno glandular/columnar
Squamous squamous
o Sarcoma connective tissue
Osteo bone
o Blastoma embryonal origin
o Teratoma germ cells
o Hematologic leukemia, lymphoma, myeloma
Histological Analysis Classification/Grading of Cells

In this type of grading, the appearance of cells and the degree of cell differentiation is evaluated:
o Grade 1: Cells differ slightly from normal cells (i.e., mild dysplasia) and are well differentiated.
o Grade 2: Cells more abnormal (i.e., moderate dysplasia) and moderately differentiated.
o Grade 3: Cells very abnormal (i.e., severe dysplasia) and poorly differentiated.
o Grade 4: Cells immature and primitive and undifferentiated; cell of origin difficult to determine.
Extent of Disease Classification/Staging of Cancer

o
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Classification systems are a means of categorizing the extent of disease into groupings that have clinical similarities rather than on
cell appearance. Its purpose is for treatment, research, and prognostication.
Clinical staging:
o Stage 0: cancer in situ (i.e., in a natural or original position)
o Stage 1: tumour limited to tissue of origin; localized tumour growth
o Stage 2: limited local spread
o Stage 3: extensive local and regional spread
o Stage 4: metastasis
If there is any metastasis, it is automatically stage 4.
This classification system has been used as a basis for staging cancer of the cervix and Hodgkins disease.
TNM Classification (one example of a classification system) there are MANY staging systems that are disease-specific.
This classification system is used to determine the extent of the disease process according to 3 parameters: tumour size (T),
degree of regional spread to the lymph nodes (N), and metastasis (M). After the extent of the disease is determined, the stage
classification is not changed. The original description of the extent of the tumour remains part of the original record.
o Tumour size
T0 No evidence of primary tumour
Tis Carcinoma in situ
T1-4 Ascending degrees of increase in tumour size and involvement
o Spread to lymph nodes
N0 No evidence of disease in the lymph nodes
N1-4 Ascending degrees of nodal involvement
Nx Regional lymph nodes unable to be assessed clinically
o Metastasis
M0 no evidence of distant metastases
M1-4 Ascending degrees of metastatic involvement of the host, including distant nodes
In general, the bigger the tumour, the greater the number of nodes, or the more metastasis, the worse the prognosis. Also, the
more primitive the cancer (i.e., the more the cell looks unlike healthy cells), the worse the prognosis.
Some cancers are also classified according to:

o Receptor status
Breast cancer: oestrogen, progesterone, HER2
o Chromosomal abnormalities
CML Philadelphia chromosome
o Tumour markers
Testicular cancer -fetoprotein, -HcG
Childhood Cancer
Children tend to develop different cancers than adults.
Usually embryonic in origin or due to oncogenes.
Major difference: immune system function.
Treatment protocols are prolonged (years vs. months).

E.g., leukemia:
Children develop ALL more commonly than adults.
Boys get more chemotherapy than girls as they are more susceptible to relapse.
Mortality rates have decreased dramatically since 1960s.
Nursing Care for Children with Cancer

Assessment.
o Physical, psychological, developmental, family.
Interventions.
o Nutrition, medication administration, hydration, infection prevention, pain management, measures to S/E.
Family care.
o Psychosocial support, information, referral to resources.
o
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Developmental Considerations
Impact of cancer and treatment is variable depending on age/stage of life and associated developmental tasks/roles.
Children
o Potential impact on normal growth and development, future health, schooling.
Young adult
o Potential impact on career choices, education, relapses, $$.
Middle adult
o Potential impact on family functioning, finances.
Older adult
o Potential impact on ability to live independently, finances, retirement plans.
Cancer Treatment
Curative therapy: eradication of disease using modalities appropriate to the type of cancer.
Control: disease is present but treatment is controlling growth.
Palliation: relief or control of symptoms and maintenance of quality of life.
In reality, treatment does not always fit into neat/discrete categories (e.g., BMT for multiple myeloma is life prolonging, not
curative; disease temporarily eradicated but relapse is certain, or may have partial remission with eventual progression.
Factors that determine treatment modality:

o Cancer type
o Location and size of tumour
o Extent of disease
o Performance status (overall physical functioning)
o Psychological status/need
o Patients goals/wishes
Cancer Treatment Modalities

Surgery
Radiation
Chemotherapy
Biological therapy
Targeted therapies
Hematopoeitic Therapy (supportive care)
Gene therapy
SURGERY
Surgical Therapy
Surgical therapy can be used for curative intent, for disease control, or for palliative reasons.
o Several principles are applicable when surgery is used to cure the disease process of cancer:
1. Cancer that arises from a tissue with a slow rate of cellular proliferation or replication is the most amenable to
surgical treatment.
2. A margin of normal tissue must surround the excised tumour.
3. Remove only as much as necessary and use adjuvant therapy. Less radical surgery is the current trend among
health care providers.
4. Preventative measures used to reduce surgical seeding of cancer cells.
5. Usual sites of regional spread may be removed.
Debulking is a procedure that may also be used when the tumour is attached to vital organs and cannot be completely removed. In
this case, as much tumour as possible is removed and the patient is then put on radiation and/or chemotherapy. This greatly
increases the effectiveness of the radiation/chemotherapy (as compared to no debulking).
RADIATION THERAPY
Radiation Therapy
It is the use of high energy particles or waves to treat disease.
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Degree of damage to cells/tissue depends upon:

o Type of cells/tissue
o Rate of division (rapidly dividing cells are more susceptible to radiation than cells that divide more slowly)
o Where the cells are in the cell cycle (i.e., cells are more resistant during the S phase than the M and G phases)
o Oxygenation level
Well oxygenated cells respond better to radiation than cells that are not well oxygenated.
o Degree of differentiation
The goal of radiation therapy can be either to cure the patient, maintenance of patient health, or palliative care.
The radiation breaks bonds in DNA, causing loss of proliferative capacity.

Radiation induces apoptosis (programmed cell death).
The plan is to deliver tumouricidal dose within limits of tolerance of surrounding normal tissues.
Normal tissues are usually able to recover better than cancer cells.
Methods of delivery:
o External beam radiation (teletherapy):
This is the most common form of treatment delivery; the client is never radioactive during this therapy.
o Internal radiation (brachytherapy)
This involves the implantation of radioactive materials directly into or near the tumour. Implants may be
temporary or permanent.
High dose rate (HDR) with remote loading.
Low dose rate implanted (temporary or permanent).
o E.g., Prostate seeds.
It is important to consider that these patients are radioactive.
Teletherapy and brachyterapy are often used in combination.
o Radiolabelled antibodies
Number of treatment depends on:
o Type of cancer
o Extent of disease
o Area being treated
o Dose
o Fractionation (i.e., how many pieces the dose is divided into)
The side-effects from radiation are due to radiation damage of normal cells in or around the treatment field.
o Factors affecting side-effects:
Treatment field/tumour location
Dose
Method of delivery
Individual factors
As a rule, whatever is in the way/path of radiation therapy will be destroyed.
Radiation Treatment Planning
Radiographic studies are done to define treatment area.
Simulation (to determine which dose the patient is to receive, the angle at which the radiation is to be delivered, etc.).
Markings, mould/forms/shields.
Side effects are d/t radiation damage of normal cells in or around the treatment field
Factors affecting S/E
o Treatment field/tumour location
o Dose
o Method of delivery
o Individual factors
Common Radiation Side-Effects

General:
o Radiodermatitis
o Fatigue
o Weight loss due to anorexia
o Myelosuppression (skull, sternum, long bones)
This is due to the decrease in WBCs.
Site-specific:
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o Depends on structures present in area of radiation treatment.
Nursing Management of General Radiation Effects

Radiodermatitis: wet/dry
o Erythema can occur 1-24 hours following a single treatment and is an acute response that is followed by dry
desquamation. If the rate of cellular sloughing is greater than the ability of new epidermal cells to replace dead cells,
wet desquamation occurs with the exposure of the dermis and oozing of serum. Dry reactions are uncomfortable and
result in pruritis and wet reactions results in discomfort and oozing.
o Skin care:
Dry reactions:
Use gentle soap (e.g., Ivory or Dove) with lukewarm water; do not rub.
Dry skin should be lubricated with non-irritating lotion or solution that contains no metal (be mindful
that antiperspirants contain metals), alcohol, perfume, or additives.
Wet reaction:
Must be kept clean and protected from further damage.
o Prevention of infection. assess skin, change drsg, notify MD if s/sx infection
o Facilitate wound healing. high protein diet, drsg changes
o Manage sx: pain, pruritus, wound exudate
o Protect irritated skin from extremes in temperature (forever).
This includes the use of heating pads, ice packs, and hot water bottles.
o While receiving radiation, avoid wearing constricting garments, harsh chemicals, and deodorants.
o The use of corticosteroids and hydrogen peroxide are contraindicated as they interfere with wound healing.
Fatigue
o LOTS of research on fatigue: models, causes, interventions
o Usually starts about 1-2/52 after tx starts and continues 1-2/52 after tx ends
o Rtx is 5/7 x 4-6/52 will likely need to take time off work
o Balance activity and rest
o Too much inactivity or activity will increase fatigue
o Encourage patient to identify times of day when they feel better and plan important activities for this time
o Rest before necessary activity (e.g. MD appt, kids activities)
o Ensure adequate nutrition using supplements if needed
o Consult HC, OT, PT to arrange assistance as needed
o It generally comes about during the third to fourth week of treatment, persists after treatment and finally subsides. It
may be due to the accumulation of by-products of cellular death (e.g., lactate, H+ ions, etc.).
o Encourage patient to identify times of the day when they are feeling better may assist them to understand their bodys
responses. Many patients may feel that this extreme fatigue is due to the treatment not working or that their cancer is
worsening and spreading. It is important to let them know fatigue is expected.
o Rest before activity.
o Arrange assistance with activity (home care, OT, PT).
o Maintain nutritional status.
o The wrong thing to do for fatigue is to lie down and rest!!!
Exercise (e.g., walking) is the best way to get rid of fatigue and prevent deconditioning.
Use the half rule of thumb:
For example, if a patient says that they only have enough energy to walk to the end of the driveway
and back, suggest walking half that distance twice daily.
Weight loss due to anorexia
o The reason for this is unknown, but one theory lies in the fact that macrophages release TNF and IL-1 in order to fight
off the cancer. TNF and IL-1 are both appetite suppressing are can cross the blood-brain barrier.
o Monitor carefully to minimize weight loss.
Weight twice weekly.
o Small, frequent, high-protein, high-calorie meals are better tolerated than large meals.
Some may need temporary feeding tube (e.g., patients with head & neck and oesophageal radiation).
Inserted prophylactically prior to start of Rtx
o Supplements are indicated in the anorexia is present or if other factors contribute to difficulty in eating.
o Anorexia peaks at the fourth week of treatment and resolves more quickly than fatigue when the treatment ends.
Nursing Management of Site-Specific Radiation Effects
Oral, Oropharynx, and Esophageal Reactions
o Teach patients to examine oral cavity.
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Dental work should be performed before initiation of radiation treatment.
Saliva substitutes are used to treat xerostomia (i.e., dry mouth); but patients have said that frequent, small doses of water
have the same effect.
o Oral care (i.e., tooth brushing and flossing) is critical, unless contraindicated by a low platelet count.
o Pain relief.
o Frequent feedings of soft, non-irritating, high-protein, high-calorie foods or temporary tube feeding.
o Avoidance of extremes in temperature, spicy foods, alcohol, and tobacco as they are severe upper GI tract irritants.
Pulmonary Effects
o Radiation pneumonitis: can be acute or develop 2-3 months after tx starts
o Pulmonary Fibrosis: occurs after 6-12 months, chronic, not reversible, can be fatal.
o Assess: cough, fever, hypoxia, exertional dyspnea
o Treatment:
o High-dose corticosteroids for acute pneumonitis
o Bronchodilators
o Oxygen (may need Home O2 if chronic fibrosis)
o Activity modification
o Codeine is more effective cough suppressant than OTC
o Treatment:
Bronchodilators
Cough suppressants
Activity modification
Oxygen
o Acute effects:
Acute pneumonitis (i.e., inflammation of the lung parenchyma/alveoli).
o Chronic effects:
Long-term pulmonary fibrosis.
o While radiating the lungs, the breasts are exposed to the radiation. For that reason they (and often the heart) are covered
with lead shields.
Gastrointestinal Effects
o Prophylactic administration of anti-emetics (nausea and vomiting can occur as soon as immediately following the first
treatment).
Anticipatory nausea and vomiting may occur and persist even after treatments have ceased, underscoring the
importance of prophylactic use of anti-emetics.
o Assess for signs and symptoms of alkalosis and dehydration if diarrhoea develops.
o I&O must be monitored.
o Non-irritating diet.
o Anti-diarrheal medications.
Reproductive Effects
o Gonads very sensitive to radiation
o Easier to shield testicles from pelvic radiation
o If one ovary spared may preserve fertility
o In Manitoba: Heartland Fertility Clinic offers:
o Egg, embryo, sperm cryopreservation
o Patient pays
o They prioritize cancer patient referrals
o Inform patient of expected sexual and reproductive side effects.
o Refer to counselling if needed.
o Sperm banking may be an option.
o Egg cryopreservation not yet an option.
o The ovaries and testicles are extremely sensitive to radiation.
If gyne radiation may develop dryness, atrophy
Lubricants, sexual activity/dilator to maintain vaginal patency
Impotence r/t prostate cancer tx
Effect on relationship from cancer experience
Sexuality counselor at CCMB: Dr. Anne Katz
Bone Marrow Effects
o When bones are affected, especially those containing large amount of bone marrow, such as bones in the pelvis, the
client may display a decrease in WBCs, RBCs, and platelets.
o
o
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Nursing Management in Patients with Radiation Treatment

Coping.
o Assist in planning for transportation, nutrition, and emotional support refer to community and institutional resources.
o Patient teaching of symptom management to maintain highest possible quality of life.
CHEMOTHERAPY
Chemotherapy
The use of cytotoxic medications to kill cancer cells
First drug: nitrogen mustard, 1940s
1960s/70s: platinum-based tx & combo chemtox
Goal: reduce and/or eliminate visible and invisible (micrometastases) disease
Cancer cells can develop resistance to chemotx
It is most often a SYSTEMIC therapy; therefore systemic side effects are expected. Chemotherapy works at the cellular level.
Drugs have expected side effects (e.g., nausea) that are to be managed aggressively. There are two types of chemotherapeutic
drugs: cell cycle-non-specific drugs and cell cycle phase-specific drugs. These two types of drugs are often administered in
combination with one another.
Drugs also have less common, unexpected toxicities (e.g., cardiotoxicity) assess carefully to allow for early identification.
Goal is to reduce and/or eliminate visible and invisible (micrometastases) cancer cells.
o Several factors determine response of cancer cells (e.g., mitotic rate of the tissue from which the tumour arises).
o Cancer cells can escape death by staying in the G0 phase (i.e., rest/non-active period).
o Main problem is the presence of drug-resistant resting and non-cycling cells.
Chemotherapy can be used in a number of ways:
o Primary therapy
o Adjuvant therapy
Women with breast cancer will often receive chemotherapy as an adjuvant.
o Neoadjuvant therapy (i.e., before other therapies)
This may be seen in order to shrink large masses before they can be removed.
o Combination therapy
Numerous regimens (recipes).
Important Issues Related to Chemotherapy

Should only be given by nurses with specific training in chemotherapy administration!!!
Other nurses should know:
o How to monitor the patient and infusion.
o How to give supplemental medications (meds in syllabus are examples).
o Safe handling of discarded bags and body fluids.
o Appropriate response to spills.
Nursing Role regarding Chemotherapy

ASSESSMENT & MANAGEMENT OF SIDE EFFECTS is a very important role!!
Know what to expect with patients regimen.
Be vigilant in assessment and aggressive in management.
ASSESSMENT & MANAGEMENT OF SIDE EFFECTS & TOXICITIES
o Know what to expect with patients regimen
o Be vigilant in assessment & aggressive in management
o Administer supportive care medications
E.g. anti-emetics, antibiotics, GCSF
o Report critical assessment data to MD asap
Some toxicities are not reversible
o Monitor lab results and tailor assessment
E.g. assess bldg if low platelets
Patient education is essential to decrease anxiety and ensure adherence to tx plan
o Tx protocol
o Supportive care
o Expected S/E, toxicities, monitoring parameters
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o Self care; activity restrictions

o If you do not know this information, connect patient with appropriate resource (e.g. Onc CNS/clinician)
Psychosocial assessment and support of patient and family is paramount
http://www.chemoready.ca/ - referred to on CCMB website as source of sx mgmt info
SHOULD ONLY BE GIVEN BY NURSES WITH SPECIFIC TRAINING IN CHEMOTHERAPY ADMINISTRATION
o This training is only available in places where the nurse is able to develop clinical competency in chemotherapy
administration. Can not take just for interest
Nurses without chemotherapy training should know:
o What kinds of medication the patient is getting
o How to monitor the patient and the infusion
o How to give supplemental meds (e.g. meds in syllabus)
o Safe handling of discarded bags & body fluids and response to accidental spills
Classification of Chemotherapeutic Agents

Alkylating agents
Nitrosoureas
Antimetabolites
Corticosteroids
Antitumor antibiotics
Hormone therapy
Plant alkaloids
Miscellaneous
Chemotherapy: Routes of Administration

Oral
IM (e.g., L-asparaginase given via IM greatly decreases the likelihood of the patient going into anaphylactic shock)
IV
o Intermittent
o Continuous Infusion
o bolus over min/hrs +/or CIVI over days
o Many chemotherapeutic drugs are vesicants, meaning that should accidental infiltration occur, severe local tissue
breakdown and necrosis is possible.
Intra-cavitary (e.g., bladder)
Intrathecal (i.e., into the CSF)
o ONLY CERTAIN DRUGS ARE OK VIA THIS ROUTE!!! OTHERS ARE FATAL (within 7-10 days)!!!
Intra-arterial
Subcutaneous: may be used for basal cell skin cancer
Topical (sometimes seen in certain types of skin cancer)
Central vascular access devices permit frequent, continuous, or intermittent administration or for vesicants.
o Can be used to administer additional fluids, supplemental medications, nutrition, and blood products.
Major types:
o Central line (subclavian)
o PICC
o Implanted infusion ports
Chemotherapy Regional Administration

Delivery of drug directly into the tumour site. This allows higher concentrations to be delivered with reduced systemic toxicity.
Types:
o Intrathecal or intraventricular (most common) most chemo agents cant cross BBB inject chemo directly into CSF.
An Ommaya reservoir is often used to ensure that equal drug distribution occurs.
o Intraarterial (i.e., the drugs are delivered to the tumour via the arterial vessels supplying it)
o Intraperitoneal
o Intravesical bladder (i.e., the medications are instilled directly into the bladder)
Chemotherapy Effects
Chemotherapeutic agents are cytotoxic to both normal and cancer cells.
The effects of chemotherapeutic drugs can either be acute, delayed, or chronic.
Bodys response to products of cellular destruction in circulation may cause fatigue, anorexia and taste alterations
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Each drug has unique S/E & toxicities

Combinations of drugs have the combined S/E & toxicities of all the drugs in the combination
Chemotherapeutic agents are cytotoxic to both normal and cancer cells including YOUR cells.
o Therefore, they require safe handling precautions there is a regional safe handling policy
Acute reactions:
o Vomiting prevent with anti-emetics.
Nausea and vomiting is important to treat with the first treatment. This is due to anticipatory nausea and
vomiting. Lorazepam is used to treat this.
o Allergic reactions may pre-medicate to prevent.
o Arrhythmias
Delayed effects:
o Mucositis
o Alopecia (i.e., loss of hair)
o Bone marrow suppression
Bleeding due to decreased platelets.
o Fatigue
Due to decreased Hgb (which will lead to fatigue) and other factors.
o Skin changes (this is because skin is a rapidly dividing tissue)
o Nausea and vomiting
o Diarrhoea
o Decreased white blood cells infection.
Chronic toxicities
o Unique to each medication
o Assess carefully to allow for early identification
o Damage to
o Heart: e.g. anthracyclines follow with serial MUGA, assess s/sx CHF, D/C meds if LV dysfunction. These meds have
maximum lifetime doses even in absence of cardiac dysfunction.
o Kidney: e.g. cisplatin, carboplatin monitor serum Urea/Cr & creatinine clearance (24 hour urine), monitor I/O
o Liver: e.g. - monitor LFTs, jaundice, edema
o Lungs: e.g. bleomycin follow with serial PFTs, assess resp fctn
o Bone marrow: most drugs can cause chronic bone marrow failure if used over a prolonged period of time follow with
CBC and bone marrow bx if signs of bone marrow failure
o Reproductive: sterility depends on drugs & dose, assisted fertility
o Damage to:
Heart (the ejection fraction will be effected)
(bone marrow failure may occur from repeated doses of chemotherapy)
Late Effects
o Risk for leukemias and other secondary malignancies
Radiation and chemotx can induce DNA damage that can lead to new malignancies other than original dx
o Secondary malignancies other than leukemia have been reported
Includes breast (esp women who had chest radiation without shielding prior to 1980s), uterine, thyroid, lung
o Secondary malignancies are usually tx-resistant
Acute reactions: immediate with infusion
Delayed effects: days to weeks after treatment
Chronic toxicity: known but not typically expected to occur with each patient; usually weeks/months/years after treatment
Late effects: years after treatment
Chemotherapy Treatment Plan

Drugs are usually given in combination according to specific, research-based protocols.
The administrations of drugs are usually given based on the following principles of combination chemotherapy:
1. The drugs used are effective against the cancer being treated.
2. When drugs are given in combination, a synergistic effect occurs.
3. The combination includes cell cycle phase-specific and cell cycle-non-specific drugs.
4. The combination includes drugs that have different toxic side-effects.
5. The combination of drugs that cause nadirs occurring at different time intervals.
The nadir is the lowest peripheral blood cell counts (especially WBCs) that occurs secondary to bone marrow
suppression. The nadir following most chemotherapy drugs occurs in 7-28 days.
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Most often given in combination according to specific research-based protocols

The drug combination therapies usually have acronyms:
o R-CHOP: Rituximab, Cyclophosphamide, Hydroxydaunorubicin (doxorubicin), Oncovin (vincristine), Prednisone
o ESHAP: EtopoSide, metHylprednisolone, Ara-C (cytarabine), cisPlatinum
o FEC: Flurouracil, Epirubicin, Cyclophosphamide
o FolFOX: FOLinic acid (leucovorin), 5-Fluorouracil, OXaliplatin
Patients are often part of clinical trials.
Doses are carefully calculated according to body surface area.
o Ht/Wt on chemo patient must be EXACT & MEASURED
Nursing Management of Patients Receiving Chemotherapy

One of the most important responsibilities of the nurse is that of differentiating between toxic side-effects of the drug and
progression of the malignant process.
The nurse must also differentiate between treatable side effects and toxicities requiring intervention.
Serious reactions must be reported to MD ASAP.
Some toxicities are not reversible.
Administration of anti-emetic drugs.
Monitor lab results, particularly WBCs, platelet, and RBCs.
Assess for signs of bleeding if platelet count falls below 50,000/l.
Patient education is essential to decrease anxiety and ensure adherence to treatment plant.
o Treatment protocol
o Supportive care
o Expected side effects, toxicities, monitoring parameters
o Self-care
o Activity restrictions
Psychosocial care.
Late Effects of Radiation and Chemotherapy

Risk for leukemias and other secondary malignancies.
Secondary malignancies other than leukemia have been reported.
o Includes breast, ovarian, uterine, thyroid, and lung cancers.
Secondary malignancies are usually resistant to therapy.
The risk of these secondary malignancies does not contraindicate the use of cancer treatment.
BIOLOGIC THERAPY
Biological therapy consists of agents that modify the relationship between the host and tumour by altering the biological response
of the host to the tumour cells.
Biological agents may affect the host-tumour relationship in 3 ways:
1. They have direct anti-tumour effects.
2. They restore, augment, or modulate the host immune system mechanism.
3. They have other biological effects, such as interfering with the cancer cells ability to metastasize or differentiate.
Biologic Therapy: Interferons

There are 3 types of this naturally occurring, complex protein: -, -, and -interferons.
Interferons are cytokines with antiviral, anti-proliferative, and immunodulatory properties.
They have been shown to increase the expression of tumour-associated antigens (TAAs), thus increasing the potential for an
immune response.
They are capable of modulating the response of other cytokines, such as IL-2 and TNF.
They must be administered via parenteral route only (not orally because they are proteins and would be broken down).
Side effects:
o Flu-like syndrome (i.e., fever, chills, myalgias,
o Lethargy
headaches)
o Depression
o Anorexia/weight loss
o Changes in cognitive function
o Fatigue
o Bone marrow suppression
o
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o Biologic Therapy: Interleukin-2 (IL-2)

Induce biologic activities that activate the immune system or alteration in functional capacity of cancer cells.
It also has the ability to activate or stimulate other cytokines.
Major toxicity of IL-2 therapy is capillary leak syndrome:
o It is the result of changes in permeability and vascular tone of the capillaries. This results in a fluid shift from
intravascular to extravascular space and results in intravascular fluid depletion.
o Additional toxicities include:
Renal, cardiovascular, pulmonary, GI, and integumentary toxicities
Bone marrow suppression
Changes in cognitive function
Interleukins are not widely used due to ++ toxicities.
o Nursing Management: Biologic Therapy
uses living organisms, substances derived from living organisms, or synthetic version of such substances to treat cancer.
(NCI, n.d.)
Approved: monoclonal antibodies, cytokines
Investigational: therapeutic vaccines, gene therapy, adoptive T-cell transfer
Nursing interventions for flu-like syndrome.
o Administration of acetaminophen before treatment and q4h after treatment.
o Monitor VS.
o Monitor blood work.
o Fatigue-related interventions.
o
o Targeted Therapy: Monoclonal Antibodies
drugs or other substances that block the growth & spread of cancer by interfering w. specific molecules involved in tumor
growth & progression. (NCI, n.d.)
drugs that interfere w. cell growth signaling or tumor b.v. development, promote the specific death of cancer cells, stimulate
the immune system to destroy specific cancer cells, & deliver toxic drugs to cancer cells. They are antibodies or
immunoglobulins produced by B lymphocytes that are capable of binding to specific targets on cell surface.
First molecular target: estrogen receptors in br ca
Selective estrogen receptor modulators (SERMs):
tamoxifen
Aromatase inhibitors:
exemestane, anastrazole, letrozole
Post-menopausal; pre-menopausal women produce enough on their own
The diagnostic use of monoclonal antibodies is primarily for the imaging of tumours.
Administered by infusion: can experience infusion-related symptoms (e.g., fever, chills, urticaria, nausea, diarrhoea, etc.).
There is also a risk, although rare, of anaphylaxis.
Increasingly used for cancer and a wide variety of other illnesses (rheumatoid arthritis, Crohns, psoriasis, etc.).
Side effects:
o Fatigue
o Bone marrow depression
o Capillary leak syndrome
o CNS effects
o Hepatotoxicity
o Cardiac dysfunction
o
o Targeted Therapy: Monoclonal Antibodies
Ab engineered to bind to specific targets on cell surface

IV
Also used for other illnesses (e.g. RA, Crohns psoriasis)
Risk of anaphylaxis with administration
Side Effect:
Fatigue
Capillary leak syndrome
Hepatotoxicity
Bone marrow suppression
CNS effects
Cardiac dysfunction
o Rituximab
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Chimeric (mouse/human) monoclonal antibody that targets CD20 cell surface receptor.
CD20 is present on B-cells
90% of NHL have CD20
o Bevacizumab
Monoclonal antibody that targets VEGF receptor and inhibits angiogenesis

o
Targeted Therapy: Tyrosine Kinase Inhibitors
Biological/Targeted Therapies
Monoclonal Antibodies:
Trastuzumab/Herceptin: HER-2+ breast ca, gastroesophageal junction adenoca
Cetuximab/Erbitux: squamous H & N, colorectal
Bevacizumab/Avastin: glioblastoma, NSCLS, met. colorectal & renal
Rituximab/Rituxan:
Tyrosine Kinase inhibitors:
Imatinib/Gleevec : CML, myelodysplatic/myeloproliferative, gastrointestinal stromal tumor
Dasatinib: CML, Philadelphia + ALL
Nilotinib: CML
Erlotinib/Tarceva: NSCLC, pancreatic
EGFR inhibitor:
Gefitinib/Iressa: NSCLC
mTOR inhibitors (mammalian target of rapamycin) a kinase enzyme:
Temsirolimus/Torisel: advanced renal cell
Everolimus/Afinitor:advanced renal
Retinoid (carboxylic acid form of Vitamin A) differentiating agent:
Tretinoin/Vesanoid: acute promyelocytic leukemia (can be very lethal from bleeding)
Proteasome inhibitor (promotes apoptosis):
Bortezomib/Velcade: multiple myeloma, mantle cell lymphoma
Angiogenesis inhibitors:
Thalidomide, lenalidomide/Revlimid: multiple myeloma
o
o Hematopoietic Therapy
Granulocyte Colony-stimulating Factors (G-CSF)
o Colony-stimulating factors (CSF) are a family of glycoproteins produced by various cells.
o These glycoproteins stimulate the production, maturation, regulation, and activation of cells in hematologic system.
o Hasten recovery from bone marrow depression or stimulate stem cell mobilization for transplantation.
o It is a supportive care measure rather than a treatment for cancer.
o Very important part of many cancer treatment protocols.
Erythropoietin is used more commonly in renal failure.
Platelet stimulating factors none on market in Canada.
Transfusions of RBC and platelets are more commonly used than growth factors in cancer treatment.
o
o Stem Cell (Blood) & Bone Marrow Transplantation (aka Hematopoietic Stem Cell Transplantation)
Myeloablative: use lethal doses of chemo/radiation.
o Administer large doses of chemo +/- radiation.
Eradicate diseased bone marrow (myeloablative).
Dose-escalation to treat disease outside bone marrow.
Stem cell rescue.
Engrafts and repopulates marrow with healthy donated cells or previously collected autologous cells.
Today we are also doing:
o Reduced intensity transplants.
o Non-myeloablative transplants.
o Both transplants depend on the graft-versus disease effect for success and use lower doses of chemo/radiation.
o Allows for older patients to receive treatment.
Other types of BMT:
o Reduced intensity
o Non-myeloablative
191

o
o
Both depend on the graft-versus-disease effect for success & use lower doses of chemo/radiation
Allows for older patients (up to 65) & those with certain co-morbid conditions to be transplanted
o
Allows use of very high doses of chemotherapy +/- radiation therapy.
Highest tolerable doses of chemotherapy.
Goal is to administer large doses of systemic therapy.
Eradicate diseased bone marrow (i.e., myeloablative).
Dose-escalation of disease outside bone marrow.
Bone marrow rescue is required after myeloablative therapy.
Engrafts and repopulates marrow with healthy donated cells or previously collected autologous cells.
Whether the disease is malignant or non-malignant, the goal of BMT is cure.
o BMT Complications
Graft-versus-host disease
o T-lymphocytes from donated marrow recognize recipient as foreign and attack organs such as skin, live and intestines
o Beneficial graft-versus-disease effect
T-lymphocytes also attack residual malignant cells
Essential component/benefit of BMT
Can induce this to treat early relapse
Reduce immunosuppression or give DLI
o
o Stem Cell Sources

Allogeneic
o Stem cells are acquired from a donor matched to the recipient (related or unrelated). There is a 1 in 4 chance of finding a
match with a sibling.
o Stems cells can be extracted from an individual and implanted in another individual within a few hours.
Autologous
o Patient receives their own stem cells that have been remove and stored.
Syngeneic
o Stem cells are removed from one identical twin and infused into the other as twins have identical human leukocyte
antigens (HLA).
Peripheral stem cell transplant
o Circulating stem cells are capable of repopulating bone marrow.
o Mobilization of stem cells from marrow to peripheral blood done using chemotherapy or hematopoietic growth factors.
Cord blood stem cells
o Umbilical cord blood can be typed and cryopreserved.
o May have insufficient numbers of stem cells to permit transplant to adults, can combine donors to transplant adult.
o More common in paediatric clients but there is growing interest in adults.
Bone marrow
o Harvested in or
o Less commonly done (<30% in Mb)
o
o Bone Marrow Transplantation (BMT) Complications
Infections are common:
o Pre-transplant screening.
o Prophylactic antibiotic therapy.
o Careful monitoring
o Additional antibiotics if infection develops.
Side effects and toxicities of chemo and radiation.
o
Graft-versus-host disease:
o T-lymphocytes from the donated marrow recognize the recipient as foreign and attack organs such as skin, liver, and
intestines.
o Beneficial graft-versus-disease effect T-lymphocytes also attack residual malignant cells.
Essential component/benefit of BMT.
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o
o Complications of Cancer and Treatment
Infection (the client may have neutropenia and may therefore not display the cardinal signs of inflammation)
Fatigue
Bleeding
Mucositis
Cachexia/Anorexia
o Malnutrition (once a weight loss of 10lbs has occurred it is difficult to maintain nutritional status).
o Altered taste sensations.
o
o Oncologic Emergencies (cancer equivalent of chest pain or GI bleed)
Can induce this to treat early relapse.

Reduce immunosuppression or give donor lymphocyte infusion (DLI).
Emergency
Sx
Tx
FNE/Septic Shock
T > 38, ANC , 0.5
Bld cultures
Urgent Abx
Assess focus: CXR, MSU
Hypercalcemia of
Malignancy
calcium
Pamidronate
Hydrate
TLS
K, uric acid
Prevent
Rasburicase
Hydrate/alkalinize
SIADH
Intra-vascular fluid excess

Dilutional hyponatremia
Fluid restriction
Treat cancer
DIC
Simultaneous bleeding and clotting

INR, decrease.
Tx underlying malignancy
Transfuse & anti-coagulate
Febrile (i.e., >38.5C at one measurement or >38C measured twice within an hour) neutropenia/Septic Shock
o They need antibiotics within 1 hour.
Obstructive emergencies:
o Spinal cord compression (SCC)
This occurs when there is the presence of a malignant tumour in the epidural space of the spinal cord.
o Superior Vena Cava Syndrome (SVC Syndrome)
This occurs when the superior vena cava is obstructed by the tumour.
o Metabolic emergencies:
o
o
o
o
Tumour Lysis Syndrome (TLS)

Syndrome of Inappropriate ADH (SIADH)
This leads to fluid overload and hyponatremia.
Disseminated Intravascular Coagulation (DIC)
This is typically only associated with one type of cancer.
Hypercalcemia of Malignancy
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Emergency
Sx
Tx
SCC
Below level of obstruction
Urgent radiation
Steroids
SVC syndrome
Upper body venous congestion: cyanosis, edema, decreased

LOC
Urgent chemo =/- Rtx

Steroids
Cardiac tamponade
Chest pain, SOB
Urgent chemo +/- Rtx

Pericardial window if effusion
Carotid artery
rupture
Exsanguination
Palliative control scene, sedation if

discussed prior with pt
Infiltrative emergencies:
o Cardiac Tamponade
Tumour is pressing on the heart.
o Carotid Artery Rupture
Cancer in the head and neck area can cause it to chew through the carotid artery. There is no management
possible.
Spinal Cord Compression
o
o Nutritional Problems:
o
o Symptoms:
N/V
Diarrhea
Anorexia/cachexia
Mucositis/dysphagia
Xerostomia
Taste changes
Fever/infection
Medication side effects
Disease effects
Fatigue
Edema/fluid retention
o Consequences:
Malnutrition d/t intake
Lytes, albumin, protein abnormal
Dehydration
Weight loss
Weight gain
Decreased wound healing
Fatigue
Weakness/difficulty ambulating
o
o Radiation Induced Xerostomia
o Nutritional Interventions
Manage symptoms optimally (n/v, pain)
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Adapt diet to patient needs

E.g. soft/pureed if mucositis or dysphagia, avoid dry foods (e.g. bread) if xerostomia, avoid malodorous foods if
N/V, increase protein
Have family bring food from home if preferred
Involve dietician
Monitor fluid & electrolyte balance
Monitor VS (dehydration)
Monitor weight
o
o Management of Cancer Pain
Patient report should always be believed and accepted as primary pain assessment data.
Drug therapy should be used following WHO analgesic ladder.
Non-pharmacologic interventions (e.g., relaxation therapy, imagery) can be effectively used.
Data such as vital signs and client behaviour are not reliable indicators of client pain, especially long-standing, chronic pain.
o
o Psychological Support
Emphasis on maintaining quality of life.
Adapting to different phases of treatment.
Patient/family education crucial.
Positive attitude of patient, family, and health care providers has significant positive impact on quality of life.
o May also influence prognosis.
o Careful how this is presented can make people feel guilty if unable to be positive.
o Maintain realistic hope. http://www.onsconnect.org/2013/03/reconnect/are-you-fostering-false-hope-in-your-patients
Empathic, open approach.
Listen actively to fears and concerns.
Provide relief from distressing symptoms.
Therapeutic relationship.
Assist patient in setting realistic short- term goals.
Assist in maintaining usual lifestyle patterns as possible.
Maintain realistic hope.
o
o Developmental Considerations
o
Stage
Potential Impact
Child/Teen
o G & D, future health, schooling, fertility, family $$ if parent needed to care for child at
home/hospital
Young Adult
Career choices, education, relationships, $$, fertility
Middle Adult
Family functioning, career/retirement plans, $$
195

o
Older Adult
Ability to live independently, $$, separation from spouse
Assessment:
Physical, psychological, developmental, family
How would you do an oral assessment on a 3 year-old with mucositis??
Interventions:
Nutrition/hydration: how to encourage if decreased appetite, nausea
Med administration: oral meds?
Infection prevention: crawling? Oral phase?
Pain/sx management: appropriate drugs/doses
School-age children: maintaining normalcy, keep up with class
Family care:
Parental psychosocial support
Information/resources
o
o
o Cancer: Gerontologic Considerations

Clinical manifestations may be mistaken for age-related changes and often ignored for that reason.
Organ function may affect ability to tolerate treatment may need dose adjustment
They are vulnerable to complications of cancer and cancer therapy.
The patients functional status is considered in treatment.
o
o Cancer Trajectory
o Phase
o Pre-diagnosis
o Diagnosis
o Treatment
o
o
o
o
Recovery
Survivorship
OR
Progression or recurrence
o
o
o
o
o
o
o
o
Psychosocial Impact
Often caught off guard, sometimes suspected it
Overwhelmed, information overload
Dealing with side-effects, life revolves around
treatment
Re-entering normal world
Living beyond cancer
Approaching and dealing with death
o
o Cancer Survivorship
Preferred term over cure
o Cure is a prophetic statement that cancer will never come back. Almost impossible to determine prospectively.
Refers to a dynamic process of living with, through, and beyond cancer.
o
o Treatment Goals:
Curative: eradication of disease using modalities appropriate to the type of cancer
Control: disease is present but treatment is controlling growth
Palliation: relief or control of symptoms and maintenance of quality of life
In reality, treatment does not always fit into neat/discrete categories e.g. BMT for multiple myeloma is life prolonging, not
curative; disease is temporarily eradicated but relapse is certain, or may have partial remission with eventual progression
Cancer survivorship care needs to take this into account
o
o Seasons of Survival
Acute
Extended survival
Permanent Survival
o Long-term disease free survival.
o
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o Survival Rates
838,724 people alive in 2009 who had cancer dx in previous 10 years.
Current 5-year overall survival
Adults: 63%
Range: Thyroid 98%, Pancreatic 8%
Death rate from breast cancer ing since 1980s, ~2.4% /year. 42% since 1986.
Children: 82%
1930s <30%
o
o Impact of Survival
Physiologic
o Disease recurrence: variable depending on diagnosis.
o Second malignancies low but real risk
o Long term effects:
Chronic S/E persisting beyond treatment:
Cognitive dysfunction, lymphedema, scars, ostomies, fatigue, N/V
o Late effects:
Occur months to years post treatment:
Cardiac changes, pulmonary fibrosis, cataracts, thyroid dysfunction, arthritis
Psychologic
o Fear of recurrence.
o Sense of vulnerability.
o Anxiety at cancer anniversaries.
o Body/self image changes.
o Sexuality issues.
Social
o Stigma.
o Perception of health by others (work, family).
o Employment issues, financial issues.
o Altered family roles/relationships.
o Loss of friends.
o Impact of Survival.
Spiritual
o Changes in priorities, values, lifestyle.
o Re-evaluation of goals, career.
o Search for meaning, enhanced meaning in life.
o Deepened sense of spirituality.
o Concerns about QOL, altered QOL.
o Increase self-acceptance.
o Increased passion or zest for life.
o Feel need to give back.
o Survivors guilt.
o
o Community resources (see slides 121-128)
o
o
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o
Unit 20: Clients with Seizure Disorders
o Outline
Definition
First aid
Etiology
Nursing care
Classifications and symptoms
Psychosocial issues
Diagnosis
Seizures
What is a seizure?
o Sudden disturbances of brain function that can cause:
Changes in involuntary muscle activity.
Behavioural and sensoral manifestations.
Alterations in consciousness/awareness
Partial or generalized seizures
Some just affect movement
Temporal lobe affects memory may cause hallucinations
to anxcessive and spontaneous electrical discharge of hyperexcited cells.

o Lowering of seizure threshold (e.g., fever lowers the seizure threshold, particularly in children and those with seizure
disorders).
Seizure Disorders
Two types:
1. Isolated, non-recurrent event, acute
Can occur due to drug use, alcohol, and fevers.
2. Epilepsy: chronic condition defined by the repeated (at least 2) and unprovoked seizure activity
Epilepsy is usually related to CNS disorders.
Having had one seizure increases the likelihood of seizures occurring again in the future.
The presence of 1 seizure does not constitute epilepsy.
Non-epileptic seizures could be d/t a biological event. Electrolyte disorders, hyper or hypo glycemia,
hypoxemia, alcohol withdrawl, massive sleep deprivation, excessive use of stimulnts, psychogenic conversion
disorder,acute head trauma, cns infection, 1 more.
Risk of recurrence
o For the points listed above, the risk of recurrence is highest in adults.
o Epilepsy is not hereditary; however, a personal past history of seizures is treated differently than in isolated cases.
Incidence:
o Highest during the first 10 years of life. The greatest incidence occurs in children <1 year of age.
o 10% of all people will have a seizure in their lifetime.
Goals of Treatment
The ultimate goal is to stop the seizures from occurring, but realistically speaking, this may not be possible due to different
etiologies. Maximum control of seizures is desired.
Maintain quality of life.
o Many seizure drugs have side-effects that may interfere with ones quality of life (e.g., sedation).
Etiology
Acquired (secondary); idiopathic/cryptogenic (i.e., the cause is unknown).
First month of life:
o Brain injury (e.g., asphyxia, birth trauma, intercranial haemorrhage)
Premature children are susceptible to intercranial haemorrhage.
o FAS
o Inborn errors of metabolism
o CNS infection (e.g., meningitis, encephalitis)
o Drug withdrawal (maternal)
Young Children
o Symptoms vary (e.g., sucking, yawning, lip smacking, staring, abnormal cry).
o Brodies seizures: http://www.youtube.com/watch?v=6Fje2AltD1A
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o Charlie having a seizure: http://www.youtube.com/watch?v=ndSpl7VPeL8

o Baby has seizures: http://www.youtube.com/watch?v=Ac17vTPGbl0
Older children:
o Above + degenerative disorders, idiopathic.
Adolescence/early adulthood
o Idiopathic (i.e., unidentifiable cause) the most common cause.
o Tumour.
o Trauma.
o Alcohol or other drug use/withdrawal.
Middle to later age:
o Above + vascular disease, degenerative disease.
International Classification (4)

Purpose of classifications is to guide diagnosis, assessment, and treatment.
1) Partial
a. Simple Partial
b. Complex Partial
2) Generalized (6 types)
3) Unclassified
4) Status epilepticus
Partial Seizures
Initiated in a localized area within brain.
1) Simple partial:
o No loss of consciousness. They are also likely to remember what happened.
o Symptoms vary: emotions (e.g., bliss), sensory response (e.g., visual disturbances), and motor response.
2) Complex partial:
o Most common type.
o Some alteration of LOC/awareness.
o Onset: blank stare, appears dazed or confused.
o Automatic, unorganized (they may be able to speak, but their sentences wont make sense), non-purposeful repetitive
movements, and lip-smacking.
o May have a post-dictal phase.
o May evolve into generalized.
Nursing care
o Remain calm and by their side.
o Turn the lights down/off.
o Ensure the surroundings are safe.
o Time the seizure.
Generalized Seizures
Convulsive or non-convulsive
Absence
Generalized
Status
Generalized Seizure Myoclonic

Juvenile Myoclonic Epilepsy
o Single or intermittent muscle contractions/jerks.
o May be associated with tonic-clonic or absence.
o Usually affects head, arms.
o "Myo (i.e., muscle) "clonus" (i.e., involuntary contraction and reaction).
Single, intermittent jerks.
o Usually occurs early in the morning or while sleeping (i.e., nocturnal).
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o No loss of consciousness.
o Quick recovery; excellent response to treatment.
Benign Myoclonic jerks
o Drowsy falling asleep.
o May occur from changes in visual perceptions (e.g., flickering lights, TV).
Absence seizures (formerly known as petit mal)
o Brief (2-10 seconds) lapse of consciousness making them hard to spot (an EEG is required for diagnosis).
o How to distinguish: age, frequency, and family history.
o Respond well to treatment.
o Some patients outgrow this type of seizure whereas others move onto the tonic/clonic seizures.
o http://www.youtube.com/watch?v=z9V2sNmIoJk
o http://www.youtube.com/watch?v=kawYuUeXg4U
o http://www.youtube.com/watch?v=DruJDZVO7Ko
o http://www.youtube.com/watch?v=H3iLQi6wt94
Tonic/clonic (formerly known as grand mal)
o Grand mal.
o Bilateral; lose consciousness.
o Tonic phase: muscle contraction/rigidity.
o Clonic phase: contraction and relaxation, intense jerking.
o When they regain consciousness they will be groggy and have a headache.
o Recovery time is different for everyone (may range from a few minutes to the entire day).
o http://www.youtube.com/watch?v=FSkwXUi6ie0
Post-dictal state
o http://www.youtube.com/watch?v=Tk6HyxSI4Ag
o Recovery
o Duration
Triggers
Role of triggers
Common triggers:
o Fatigue
o Fever/infection
o Stress
o Sleep deprivation
o Flashing lights
o
o
o
o
Photosensitivity
Prolonged use of video games/computer
Non-compliance with anti-epileptic drugs
(AEDs)
Hormonal changes (often associated with growth
spurts)
Action to take:
o Vigilance
o Emphasize normal family life
Jett Travolta
Died while taking a shower as a he hit his head during a shower.
Status-Epilepticus
Definition:
o Continuous generalized tonic-clonic activity with loss of consciousness for longer than 30 minutes, or two or more
discrete seizures without a return to baseline mental status.
or
o Continuous or intermittent seizures lasting longer than 5 minutes without full recovery of consciousness between
seizures.
During this time the patient will have an increased HR and BP as well as a decrease in SaO 2. This decrease in SaO2 can be very
dangerous if the patient is seizing for >5 minutes.
It most commonly occurs in children <2 years of age.
Nursing care:
o Check blood sugars.
They will often be hypoglycaemic as the body uses a lot of sugar during a seizure.
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o
o
o
Treat ABCs.
They may need help with ventilation.
They will have to be placed side-lying if they start vomiting.
Apply oxygen mask (even if their SaO2 appears normal) and monitor SaO2.
Monitor BP.
Common Etiologies
Acute (17-52%):
o Acute CNS infection
o Metabolic derangement
Hyperglycaemia, hypocalcaemia.
o Antiepileptic drug noncompliance, withdrawal or insufficient pharmacological treatment
o Antiepileptic drug overdose
o Non-antiepileptic drug overdose
o Prolonged febrile convulsion
o Trauma
Remote (16-39%)
o Cerebral migrational disorders
The brain lacks the grooves that develop with normal growth. This will alter the patients electrical conduction.
o Cerebral dysgenesis
o Perinatal hypoxic-ischemic encephalopathy
o Progressive neurodegenrative disorders
Idiopathic/cryptogenic (5-19%)
Objectives for Acute Management
Maintenance of adequate ABCs.
Termination of seizure and prevention of recurrence.
Diagnosis and initial therapy of life-threatening causes of status.
Arrangement of appropriate referral for ongoing care or transport to secondary centre.
Management of refractory status (i.e., period in time where the body does not respond to treatment).
Cell damage occurs after 30 minutes and is secondary to a decreased blood flow to the brain.
First Aid at Home/School (Pre-Hospital)

Remain calm: provide reassurance and emotional support.
Goal: protect from harm
o Lower to floor
o Move objects
o Recovery position
o Loosen tight clothing
o Call EMS (especially if this is an atypical seizure)
Family/school to be taught a rescue plan.
May have rescue meds:
o Drug classification
o Route(s):
Rectal, IV, orally, intranasally.
o Give at 3-5 min
We wait this long because the seizure may stop on its own within the first 4-5 minutes.
o Wait 2-5 min to work
o If not effective, call EMS
o Rural area: may call EMS at same time as rescue meds
o Examples of drugs: dilantin (i.e., phenytoin), lorazepam, diazepam (with this drug, if the first dose doesnt work, the
second one will typically not work. This drug also causes respiratory depression).
Call EMS if:
o Breathing px.
o Recurring seizure activity.
o First seizure.
Education of caregivers regarding care at home:
o How to respond.
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o
o
Helmet if recurrent seizures (e.g., >200 seizures/day).

Safe activities (e.g., riding a two-wheeled bicycle may not be safe, swimming lessons may also be ill advised).
Seizure Care in Hospital

ABC
Medications (first line vs. second line)
Causes
First Line Medications

Lorazepam
o Value of repeated doses.
o No IV access for lorazepam.
Other Drugs:
o Midazolam or diazepam
These drugs have a greater sedative effect than lorazepam.
Second Line Medication

Phenytoin/Fosphenytoin
o Preferred over phenobarb
o IV preferred
o Considerations
This drug is 60-80% effective.
Must be given over 20 minutes.
This drug cannot be given with dextrose (NS only).
o Fosphenytoin is preferred over phenytoin but it is more expensive and harder to come by.
Phenobarbital
o Greater incidence of respiratory depression.
o Routinely used for treatment of neonatal sz and for children already on phenytoin maintenance.
o Loading dose.
o Side effects.
Sedation, hypotension, and respiratory depression.
Paraldehyde
o Mechanism of action is unknown.
o Consider when other drugs have failed.
o Rectal route in dilution in oil is recommended but it can be given IV and IM
o Side effects:
Cough.
Sodium Valporate
o Second or third line treatment.
o Similar efficacy to phenytoin with fewer adverse effects. There is no respiratory or cardiovascular compromise.
o Dose-loading and maintenance.
Pyridoxine (Vitamin B6)
o For children <18 months sz may be caused by undiagnosed metabolic disorder.
o Dose.
Investigating Causes of Seizure

Most common cause of status epilepticus is prolonged febrile seizures.
Precipitating factors
Unclear etiology
o Serum electrolytes (Ca2+, bun, Mg2+, LFT, lactate and ammonia)
o CBC and C. diff
o Cultures (blood, urine and LP)
o Gases-cap or arterial
o Anticonvulsant levels
o Toxicology screening
o CT scan/MRI
o EEG
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Medications
Constant adjustments and on-going monitoring.
o Therapeutic index
o Long half-life
o Increase the drugs dose in small increments
o Serum levels
o When to discontinue
o Risk/benefit ratio
Drug interactions +++
Common side effects:
o Drowsiness, fatigue, nausea, clumsiness.
o Dilantin gingival hyperplasia.
o Teratogenic effects to be considered if contemplating pregnancy.
o Liver metabolizing enzymes.
Ketogenic Diet
This is used as a last effort to control seizures. The goal is to put the body in starvation mode.
Rigid and difficult to follow.

High in fat; low in carbohydrates and protein.
Minimize seizures resistant to AEDs.
Monitor blood sugars and urine ketones.
Restrictive and non-palatable.
Limited success.
Precise measurement and calculation.
Epilepsy Associated Problems

Cognitive dysfunction
risk of being victim to serious assault
Psychiatric problems:
o Mood disorders; anxiety
risk of suicide?
o Their quality of life is greatly decreased.
Mortality risk
Warning from FDA

Epilepsy and other illnesses for which antiepileptic drugs are prescribed are associated with an increased risk of suicidal thoughts
and behaviour. If suicidal thoughts or behaviour emerge during treatment with AEDs, the prescriber should consider whether
these symptoms may be related to the illness being treated.
All patients who currently are taking or starting on any antiepileptic drug for any indication should be monitored for notable
changes in behaviour that could indicate the emergence or worsening of suicidal thoughts or behaviour or depression.
Febrile Seizure
Does not = epilepsy.
Refer to text.
Characteristics:
o Generalized any kind.
o Associated with fever usually due to viral infection.
o Brief.
o Occur only once in 24 hours.
o 6 months to 5 years of age.
Diagnosis: by history and assessment.
Risk for recurrence,
Treatment:
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o Of seizure
o Do treat underlying cause
Many AED = teratogens
Psychosocial, Lifestyle Issues and Safety

Activities/vocation/lifestyle
o Lead normal lives with safety first
o E.g., bath vs. shower
o Seizures often unpredictable
o Usually occur at the worst time possible (trigger of stress)
Disclosure?
o Fear of embarrassment and stigma vs. safety
o Education of others (rescue medications?)
Sexuality and pregnancy
Drivers license
o Risk of suspension
Adolescence
o All of the above!! + risks of denial + anger + drugs + alcohol
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Unit 21: Clients with Altered Elimination (Acute & Chronic Renal Failure)
Review
Acute and chronic renal failure:
o Acute renal failure can lead to chronic renal failure. If treated early
enough, acute renal failure can be reversible.
Notes:
o Blood flow determines how the kidney will react (e.g., release of renin).
o Renal filtrate is very much like blood plasma.
Nephrons
o It is the basic structural unit of the kidney.
o It contains the Loop of Henle, the glomerulus, the Bowmans capsule, etc.
Formation of urine
Loop of Henle
o It is responsible for the reabsorption of Na+, Cl-, and water, which follows
sodium.
Primary function(s) of the kidney
o Filter blood.
o Regulates acid-base balance by controlling HCO3-.
o Reabsorption of sodium.
o It is one of the primary regulators of homeostasis in the body.
o 3-5L of blood is ejected from the heart in one minute.
~25% of this is seen by the kidneys.
4 Basic Kidney Processes

1. Filtration
2. Reabsorption
3. Secretion
4. Excretion
You want to see a urinary output of at least 30mL/hour (this
is an absolute minimum)!
Associated laboratory values
o Blood Urea Nitrogen (abbreviated as BUN)
Urea nitrogen, a by-product of protein metabolism, is
excreted primarily by the kidneys and therefore reflects kidney function.
Elevated BUN (a.k.a., azotemia) occurs in most renal diseases; also rises with GI bleeding, dehydration, a high
protein diet, and CHF.
Normal values:
Adults: 3.6-7.1 mmol/L
Children: 1.4-5.7 mmol/L
o Creatinine (abbreviated as Cr)
It is the by-product of the breakdown of creatine phosphate in muscle.
It is produced at a constant rate by the body and excreted by the kidneys.
Elevated creatinine occurs in renal impairment.
Creatinine level is a sensitive factor of renal function but is dependent on kidney function and muscle mass.
Patients with decreased muscle mass will not display a rise in creatinine as readily as those with more muscle
mass. For that reason, an estimated glomerular filtration rate (GFR) should be reported as well.
Normal values:
Adults
o Males: 53-106 mol/L
o Females: 44-97 mol/L
Children: 44-97 mol/L
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Review Kidney Functions
1) Regulatory
Regulates composition of body fluids.
Regulates total body fluid volume.
o This is where we have our K+ and Na+ exchange
Regulates acid-base balance.
Regulates BP.
o There is often a link between the function of kidneys and hypertension. ACE inhibitors are the drug of choice
to help this client.
2) Excretory
Excretes metabolites
o *Creatinine
These are the biggest indicators of kidney impairment. Kidney disease is the sole
o *Urea
reason the creatinine and urea levels would be increased.
o Sulphate
o Phosphate
o Uric acid
Excretes toxins and drugs
3) Endocrine/hormonal
Produces renin, which plays an important role in the regulation of BP via the renin-angiotensin system.
Produces erythropoietin.
o It stimulates the bone marrow to produce red blood cells.
Produces renal prostaglandin.
o Prostaglandi ns are vasodilators.
Produces an active form Vitamin D.
4) Catabolism
Degrades and catabolises insulin. With this in mind, individuals with kidney disease will require less insulin as the
insulin in their body is not being catabolised and excreted. This increased amount of insulin will stimulate the liver to
produce triglycerides, thus causing an increase in triglyceride levels.
Degrades and catabolises gastrin.
iClicker Questions
The client is admitted to a nursing unit from a long term care facility with a hematocrit of 0.56 (56%) and a serum sodium level of
152 mEq/L. Which condition would be a cause for these findings?
a) over-hydration
The sodium value is high.
b) anaemia
The hematocrit is a normal-high value (normal values are between 37-47% for women and a little higher for men).
c) dehydration
d) renal failure
The hematocrit is normal-high.
True or False
1) Glomerular filtration rate (GFR) is primarily dependent on adequate blood flow and adequate hydrostatic pressure.
True
2) The primary function of the kidney is to excrete nitrogenous waste products.
It does do that, but it is not the primary function. The primary function is to regulate volume, fluid and electrolyte
composition, etc.
3) Atrial natriuretic factor (ANF) is secreted by the right atrium when atrial blood pressure is low, and it blocks the action of
aldosterone.
False. ANF is secreted by the right atrium when atrial blood pressure is high. It then blocks the action of aldosterone.
4) Increased permeability in the glomerulus causes loss of proteins into the urine.
True
A client with an obstruction of the renal artery causing renal ischemia exhibits hypertension. One factor that may contribute to the
hypertension is:
a) Increased renin release
b) Increased ADH secretion
c) Decreased aldosterone secretion
Renin is secreted before aldosterone and both are responsible for an increase in blood pressure.
d) Increase synthesis and release of protaglandins
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A clinical situation in which the increased release of erythropoietin would be expected is:
a) Hypoxemia
b) Hypertension
c) Hyperkalemia
d) Fluid overload
ACUTE RENAL FAILURE (ARF)

Acute Renal Failure (Acute Kidney Injury)
It is a clinical syndrome characterized by a rapid loss of renal function with progressive azotemia (i.e., an accumulation of
nitrogenous waste products such as BUN).
Uremia is a condition in which renal function declines to the point that symptoms develop into multiple body systems. ARF is
often associated with oligouria, which is a decrease in urinary output <400mL/day. In about 50% of cases there is normal or
increased urinary output. Clients with oliguric ARF have a higher mortality rate.
Diagnosis of acute renal failure vs. renal failure is related to time duration.
o ARF develops in days and resolves within 6-8 weeks.
o CRF takes months/years to develop and is unrelenting in its course.
Renal failure cannot be reversed. The goal becomes to slow its progression.
Causes of ARF
They are divided according to similar pathogenesis into:
o Pre-renal (55-60% of all cases)
Due to factors external to the kidneys that reduce blood flow and lead to decreased glomerular perfusion and
filtration.
Hypovolemia (the most common cause), trauma, obstruction, and anything that decreases cardiac
output (e.g., MI, cardiac disease, etc.).
Pre-renal ARF can lead to intra-renal disease if the renal ischemia is prolonged.
o Renal/Intra-renal (30-40% of all cases)
Due to conditions that cause direct damage to the renal tissue (parenchyma), resulting in impaired nephron
function.
Glomerular nephritis, rhabdomyolysis, trauma, nephrotoxic drugs, and anything that affects the inside
of the kidneys. Strep throat and urinary tract infections can cause glomerular nephritis.
Acute tubular necrosis (ATN) is a type of intra-renal ARF caused by ischemia, `xins, or pigments.
o Post-renal (<5% of all cases)
Involve mechanical obstruction of urinary outflow. As the flow or urine is obstructed, it refluxes into the renal
pelvis, thus impairing kidney function.
Benign prostatic hyperplasia, kidney stones, prostate cancer, trauma, pylonephritis.
It is important to determine the cause of renal failure.
Treatment
Treatment must be prompt and appropriate. There is a 50% mortality rate.
iClicker Question
The nurse is admitting a client diagnosed with ARF. Which question would be most important for the nurse to ask during the
admission interview?
a) Have you recently traveled outside of Canada?
ARF is not caught.
b) Did you recently begin a vigorous exercise program?
The amount of exercise would have to be extremely vigorous (e.g., a triathalon).
c) Is there a chance you have been exposed to a virus?
A virus is generally not the cause.
d) What over-the-counter medications do you take regularly?
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Clinical Course of ARF
Pre- and post-renal ARF resolve quickly with the correction of the cause, but the intra-renal disease with ATN has a prolonged
course of recovery because actual parenchymal damage has occurred. There are also times during which recovery does not occur
and chronic kidney disease results.
1) Onset/Initiating Phase
Precipitous event (e.g., taking nephrotoxic drugs, a hypovolemic event such as a trauma).
2) Oliguric Phase (i.e., decrease in urine output: <400mL per day)
Recall that 30mL/hour is the absolute minimum urine output.
This is the most common initial manifestation of ARF. It is caused by a decrease in GFR.
~50% of people will not display this oliguric phase.
It is usually seen within 1-7days following the onset. It can last 1-2 weeks; can be up to 8 weeks or more.
BUN and creatinine.
Pre-renal oliguric phase:
o Increased specific gravity (i.e., >1.015).
o Na+ retention (and thus low Na+ concentration in the urine).
Intra-renal oliguric phase:
o Normal specific gravity (i.e., 1.010).
o High Na+ concentration in urine.
Fluid retention, edema, and weight gain.
Fluid and electrolyte imbalances.
Metabolic acidosis occurs as the kidneys are unable to produce ammonia that is used to bind the excess H +. This, couple
with the fact that the HCO3- in the kidneys is now being used to buffer the H+ (rather than ammonia) causes an acidotic
state.
Na+ spill as the damaged tubules are no longer able to retain Na+.
3) Diuresis
Over 2,000mL/day.
Marks return of glomerular filtration due to osmotic diuresis. The bodys ability to excrete waste products has returned
but the kidneys have not regained the ability to concentration urine.
BUN and creatinine begin to stabilize.
Risk of hypovolemia**.
o This can be determined by the patients blood pressure, their mucous membranes (check moisture), etc.
4) Recovery
Takes 3-12 months.
Begins when BUN is stable.
30% of those that recover do NOT recover normal GFR.

Death occurs commonly by bleed or infection.
o A patient would bleed due to anaemia (from a lack of erythropoietin). The increase in urea (that comes from the
oligouria phase) in the patient will decrease the patients platelets ability to coagulate.
o The white blood cells are altered due to the urea accumulation.
Case Studies
Karl is a healthy 42 year old bachelor who enjoys hunting by himself. While...
He has decreased urine output, possibly relating to decreased renal perfusion. He is at risk for acute renal failure.
What nursing measure would be beneficial for Karl?
o Fluids: strict I&O, daily weights, IV running to help replace the lost fluid
o Nutrition: low protein (as the BUN and creatinine [breakdown of creatine phosphate in the muscle][closest youre going
to measure the GFR] are high), low K+, increased carbohydrates for energy.
o Medications: medications to remove K+ (e.g., Kayexalate), ACEi (help slow the progression of acute renal failure),
diuretics.
o Dialysis: this may be started if the diuretics dont work (this is indicated when the GFR is decreased).
Clinical assessments:
o Vital signs, I&O.
Signs and symptoms of an elevated urea level:
o LOC, gout, pruritis.
Metabolic acidosis was developed as the H+ ions were not excreted and the HCO3- was not reabsorbed.
o This may lead to Kussmauls respirations (i.e., fast and deep respiratory rate).
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Clinical concerns during period of diuresis: hypovolemia, hypotension, electrolyte imbalances.

Therapies to lower K+: calcium gluconate, Kayexalate, K+ strict diet, loop diuretics.
Dee, 39 years old, had been controlling...
What might you suspect is wrong with Dee?
o Nephrotic syndrome.
What is the nursing priority for Dee and why?
1. Make sure there is often blood volume going to the kidneys.
2. Deal with the electrolyte imbalances.
3. Deal with the edema.
What other nursing interventions might be needed in the care of Dee?
o Diuretics.
What is the underlying cause of Dees condition?
o The protein is being spilled over into the urine.
CHRONIC KIDNEY DISEASE (CKD)
Chronic Renal Failure

It involves the progressive, irreversible destruction of the nephrons in both kidneys.
Usuaully no symptoms until GFR is 20% normal
Remaining nephrons hypertrophy to compensate
*Table 49.5
There are different stages, which are determined based on the level of kidney function. End-stage renal disease (ESRD), the last
stage, occurs when the GFR is <15mL/min.
It takes roughly 3 months for RBCs to be created.
Etiology
There is a high incidence of diabetes in Manitoba (30% of the patients with renal failure are diabetics)*
Hypertension*
Glomerulonephritis
Renal vascular disease
Pyelonephritis
Polycystic disease
There are usually no symptoms until the GFR is 20% of normal (i.e., 80% of the kidneys can be damaged before an individual
recognizes symptoms). This is because the remaining nephrons hypertrophy to compensate.
Clinical Course
1) Decreased renal reserve (stage 1)
Renal function 40-70% of normal.
Asymptomatic.
BUN and Cr are normal/high normal.
2) Renal insufficiency (stage 2)
GFR 60-89 mL/min. (Never going to ask about values)
Residual renal function 40% of normal.
Slight increase in BUN and Cr.
Polyuria with decreased ability to concentrate urine.
Anaemia (this is due to impaired erythropoietin production by the kidneys).
Symptoms worsen with stress (e.g., infection, emotional stress, etc.).
3) Chronic Renal Failure (stage 3-4)
GFR 15-59 mL/min.
15-20% normal function.
Azotemia (i.e., high BUN and Cr).
Metabolic acidosis due to a in ammonia excretion (this also leads to K + levels as acidosis prevents it from entering
the cells).
Fluid retention due to Na+ retention from a lack of its excretion.
Increased Na+, K+, and PO4- due to a lack of their excretion by the kidneys. PO4- also increases due to PTH release.
209
2+
Decreased Ca (due to a decrease in its absorption in the GI tract).

Severe anaemia (due to a lack of erythropoietin being made). It is classified as normocytic, normochromic.
Oliguria.
210

4) End Stage Renal Disease (ESRD) (stage 5)
15% residual renal function left.
GFR <15 mL/min.
Anuria.
Uremic syndrome (i.e., systemic manifestations associated with kidney disease).
Severe metabolic, fluid/electrolyte imbalance.
Requires dialysis or transplant.
Retained Substances
Urea
Hormones
Creatinine
Electrolytes (e.g., Na+, K+, PO4-)
Phenols
Water
iClicker Question
A client with an elevated BUN:
a) Has decreased urea in the urine.
b) May have non-renal tissue destruction.
c) Definitely has impaired renal function.
d) Will always have a rise in serum creatinine.
a. Note* BUN and Creatine will always be read together, BUN only reads the kidneys
Clinical Manifestations of Renal Failure

CNS
o Drowsiness, decreased LOC, and irritability due to an increase in waste products in the body, acidosis, and electrolyte
imbalances.
o Seizures and coma may result from a rapidly increasing BUN and hypertensive encephalopathy.
o Long term haemodialysis (HD) has led to dialysis dementia from the aluminum from the drugs. This is becoming less
common as the drugs no longer contain aluminum.
o Peripheral neuropathies CRF.
Muscle twitching, jerking, asterixis (i.e., hand-flapping tremor), and nocturnal leg cramps occur.
Restless legs syndrome that may be characterized as bugs crawling inside the leg.
o Effects of uremia on CNS
Poor memory.
Mood changes.
o Teaching implications
Slow
Reinforce
Family
CVS
1. Fluid overload (HF, edema X2)
Nursing management
Assessment****
o Crackles and wheezes in the lungs
Strict I&O
Daily weights (try do them at the same time)
Fluid and sodium restriction
Measures to decrease thirst
Diuretics
2. Hypertension
Related to renin-angiotensin-aldosterone system.
Antihypertensives.
ACE inhibitors.
3. Pericarditis
Chest pain, T, P, friction rub
4. Dysrhythmias
Related to:
Overload
Acidosis
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Electrolyte imbalance
Hypoxia
Respiratory
o Uremic lung aka pneumonitis (depressed cough reflex).
o Related to immune response.
o Leads to secondary infections.
o Pneumonia.
o Death.
o Pulmonary edema.
o SOB and Kussmauls breathing in order to excrete CO2.
Gastrointestinal
o Every part of the GI system is affected due to the mucosal inflammation due to the increase in urea.
o Nausea, vomiting, anorexia, hiccoughs.
o Bleeding and ulceration are prevalent due to irritation of the GI tract by waste products coupled with platelets.
o Uremic fetor (urinous odour of the breath).
o Stomatitis.
o Tongue yellow/brown.
o Altered sense of taste.
o Constipation/diarrhoea (due to K+).
o Altered CHO metabolism triglycerides.
o Nursing management r/t GI

Oral care
Anorexia often worse in AM
Dietary
Plan meals and fluid intake
High calorie
Teach regarding pre-dialysis binges:
Low/moderate protein
Reasons for restrictions.
Low phosphate
Effects of non-compliance.
Small frequent meals
Genitourinary
o urinary output or polyuria (unable to concentrate urine).
o Proteinuria, casts, hematuria, pyuria [py = pus].
o Intermittent catheterization.
o Oliguria, progress to anuria (<40 ml/day).
o Uremia affects libido.
Musculoskeletal
o Renal osteodystrophy is a result of Ca2+ and PO4- metabolism. There are 2 types in ESRD.
Osteomalacia: results from a lack of mineralization of newly formed bone. This can be due to hypocalcaemia
and/or increased levels of aluminum in the drugs used.
Osteitis fibrosa: results from Ca2+ reabsorption from the bone and replacement with fibrous tissue.
o The thyroid secretion PTH in response to a decrease in Ca2+ absorption (this is because the kidneys are unable to activate
vitamin D into its active form), which releases Ca2+ and PO4- from the bones. These two join, thus forming crystals in
the joints, muscles, eyes (which leads to uremic red eye), vessels, lungs, muscles, and myocardium.
o Spontaneous fractures
Dermatologic (Caused by the urea)
o Pale skin
o Uremic frost
o Yellow pigmentation (which is typically excreted
o Ecchymosis
and gives urine its yellow colour)
o Edema
o Dryness
o Dry brittle hair
o Pruritis (From the urea)
o Thin nails
o
o Nursing Management r/t skin disorders
Oatmeal baths
Antihistamines
Bath oil
Phosphate binders
Lanolin lotion
Endocrine Impairment
o Growth hormone.
o Testosterone.
o LH and FSH.
o Hypothyroidism manifestations.
o
o Lab Data
212
Serum
BUN and creatinine
Anaemia (Erythropoietin Epogen)
Hgb/Hct (decreased haemoglobin)
Coagulation defects
protein albumin
Hyperkalemia
Hypo/hypernatremia (edema, HF, HTN)
Magnesium imbalance
Calcium/phosphate imbalances (Ca++based phosphate binders)
Urine test
ABGs
o Bicarbonate IV, oral Shols solution (which is another form of bicarbonate)
o Monitor dysrhythmias, LOC
Management of hyperkalemia
o Diet (Leafy greens, bananas, etc.)
o Avoid catabolic states
o Transfuse during dialysis
o Kayexalate (cation-exchange resin)
o Glucose and insulin (shifts the K+ into the cell out of the vascular blood, where is cannot harm our hearts)
o K+ wasting diuretics
o Teach
o
o Other Major Concerns
1) Potential for infection.
o This is due to a change in leukocyte function.
o Altered immune response.
o Diminished inflammatory response.
2) Potential for injury related to diminished drug excretion.
o Drug toxicity digoxin antibiotics pain medications.
3) Psych-social aspects.
o Personal behavioural changes, emotional liability, withdraw, and depression.
o
o Diagnosis of Renal Failure
History
Physical
o Pre-renal (volume depletion)
o Renal (ischemia nephrotoxin)
o Post renal (obstruction)
Lab Work
o
o Diagnostic Tests
KUB
CT scan
IVP
Renal scan
Renal arteriogram
Blood work
U/S
Urinalysis
Management of ARF
ID, eliminate and treat
ACE Inhibitors
Monitor blood work (lytes)
Phosphate binders
Treat hyperkalemia
Monitor ABGs
o IV glucose and insulin
Diet restriction protein & phosphate/oliguric phase
o Calcium gluconate
Calorie requirements met by CHO
o Kayexalate
Dialysis
Diuretics
Diuresis phase: diet low in protein and CHO
Albumin
Management of CRF
213
Treat the Cause

Preserve existing renal function
Treat the consequences
Treat clinical manifestations
Conservative
Prevent complications
Aggressive (i.e., dialysis or transplant)
Provide for the patients comfort
DIALYSIS
Indications for Dialysis
Fluid overload.
Hyperkalemia.
Severe metabolic acidosis (determine by ABGs).
Uremic pericarditis.
Uremic encephalopathy (i.e., mental changes).
When the GFR <15mL/min.
Dialysis
It is the movement of fluid and molecules across a semi-permeable membrane from one compartment to another.
Purpose
Remove end-products of metabolism (i.e., metabolic wastes).
Remove excess fluid.
Restore electrolyte and acid balance.
Principles
Diffusion
Osmosis
Filtration (i.e., microfiltration)
Two Methods of Dialysis

Peritoneal dialysis (PD)
o Automated peritoneal dialysis (APD)
o Continuous ambulatory peritoneal dialysis (CAPD)
Haemodialysis (HD)
o Continuous Renal Replacement Therapy (CRRT)
Arterial or venous
Dialysis
Started when patients uremia can no longer be adequately managed conservatively.
Initiated when GFR <15 mL/min.
Peritoneal access is obtained by inserting a catheter through the anterior abdominal wall.
Complications of PD
Infection******
Bleeding
Abdominal/back pain
Protein loss
Outflow problems due to obstruction
Pulmonary complications
Hernias
3 Phases of Dialysis
Inflow (10 min)
Dwell (4-6 hrs)
Drain (15 min)
Effectiveness
Independence.
Ease of traveling.
Fewer dietary restrictions.
214

Greater mobility than HD.
Haemodialysis Vascular Access Sites
Shunts
Internal arterio-venous fistulas and grafts
Temporary vascular access
Continuous Renal Replacement Therapy (CRRT)
Haemodialysis Complications
Hypotension (#1 complication)
Muscle cramps
Loss of blood
Hepatitis
Sepsis
Disequilibrium syndrome
Effectiveness
It cannot fully replace the metabolic and hormonal functions of the kidneys.
It can ease many of the symptoms.
It can prevent certain complications.
Kidney Transplantation
Selection
o This is based on a variety of medical and psychosocial factors. Clients with cardiovascular disease and diabetes mellitus
are considered to be high risk. As are those who have displayed non-compliance with medication regimens, those who
are alcoholics, and those with drug addictions. The presence of hepatitis B or C is not a contraindication to
transplantation.
Histocompatability studies
Donor sources
o Polycystic kidney disease is hereditary, making other family members poor potential donors.
Treatment pre-, intra-, and post-op
o Pre-operation preparations include removing any dialysate from the
patient.
Complications
Acute Glomerulonephritis
Immunological processes involving the urinary tract predominantly affect the renal
glomerulus. The disease process results in glomerulonephritis, which affects both
kidneys equally.
There are 2 types of antibody-induced injury that can initiate glomerular damage.
1. The antibodies have specificity for antigens within the glomerular
basement membrane. Immunoglobulins and complement are deposited
along the basement membrane. Production of auto-antibodies (i.e.,
antibodies to ones own tissues) may be stimulated by a structural alteration in the glomerular basement membrane or by
a reaction of the basement membrane with an exogenous agent (e.g., hydrocarbon, virus).
2. The antibodies react with circulating non-glomerular antigens and are randomly deposited as immune complexes along
the glomerular basement membrane.
It is usually due to -haemolytic streptococci group A, which are nephrotoxic.
In both cases, the inflammation comes from the activation of complement.
Glomeruli become obstructed due to the inflammation which leads to a decrease in GFR.
Increase water and Na+.
Symptoms patients MAY have:
o Microscopic hematuria (if it is not microscopic, that is it can be seen by the naked eye, it may be bladder cancer)
o Hypertension & edema
o Excretion of formed elements (e.g., RBCs, WBCs, and casts)
o Oliguria (decrease in urine output)
o Transient anaemia
o Proteinuria
215
o Elevated BUN and creatinine

Treatment:
o LARGELY SUPPORTIVE and based on symptomatic relief.
BEDREST is recommended until the signs of glomerular inflammation (i.e., proteinuria, hematuria) and
hypertension subside.
Antihypertensives.
Antibiotics: typically penicillin (only if the Streptococcal infection is still present).
Protein restriction may be required if there is an elevated BUN.
Salt restriction.
Potassium restriction.
Nephrotic Syndrome
Nephrotic syndrome describes a clinical course that can be associated with a number of disease conditions. In adults, about one
third of clients with nephrotic syndrome will have a systemic disease such as diabetes or systemic lupus erythematosus (SLE).
The rest will be categorized as having idiopathic (i.e., arising spontaneously or having unknown origin) nephrotic syndrome.
The increased glomerular membrane permeability causes:
o Abnormal loss of protein (proteinuria)
o Hypoalbuminemia
Ascites and anasarca (i.e., generalized edema with accumulation of serum in the connective tissue) will develop
from severe hypoalbuminemia.
o Hyperlipidemia
This results from the decreased serum proteins which stimulates hepatic lipoprotein synthesis.
o Both lead to edema (due to decreased serum protein) and hypercoagulable state
Hypercoagulability and thromboembolism is potentially the most serious complication of nephritic syndrome.
Uremic Syndrome
Collective systemic responses to renal failure.
It is caused by retention of metabolic by-products.
iClicker Questions
Restriction of dietary protein may be indicated in management of acute post-streptococcal glomerulonephritis when the client has:
a. Hematuria
b. Proteinuria
c. Hypertension
d. Elevated BUN
Which following assessment would evaluate the effectiveness of treatment for the client with nephrotic syndrome?
a. Blood pressure q4h
b. Abdominal girth daily
c. Urine of each voiding for protein
d. Daily dietary protein intake
The edema associated with nephrotic syndrome occurs as a result of:
a. Hypercoagulability
b. Hyperalbuminemia
c. Decreased plasma oncotic pressure
d. Decreased glomerular filtration rate
216

Unit 22: Care of the Client with a Cerebro-Vascular Disorder
CARE OF THE UNCONSCIOUS PATIENT
Review
Levels of unconsciousness
o Check Appendix Y.
o The first sign that a patient has an increase in intracranial pressure is a change in level of consciousness. Another sign is
when the pupils are not the same size.
o The worst case scenario is when a patients pupils are fixed (this occurs from a lack of O2).
o Pinpoint pupils occur from pressure on the pons medulla.
Review assessment of cranial nerves
I.
Olfactory nerve
VII.
Facial nerve
II.
Optic nerve
VIII.
Vestibulocochlear/Auditory nerve
III.
Occulomotor nerve
IX.
Glossopharyngeal nerve
IV.
Trochlear nerve
X.
Vagus nerve
V.
Trigeminal nerve
XI.
Accessory/Spinal accessory nerve
VI.
Abducens nerve
XII.
Hypoglossal nerve
Review musculoskeletal positions
o Decorticate
o Decerebrate (more serious)
Components of the Brain

Cerebrospinal fluid (10%)
Intravascular blood (12%)
Brain tissue (78%)
Modified Monroe-Kellie doctrine

o It states that to keep the brain pressure constant, there must be some movement/shifting (i.e., compensatory mechanisms)
as the skull cannot expand (analogy of a locked vault). If one component , another must .
Regulation and Maintenance

Normal intracranial pressure is the pressure exerted by the total volume of brain tissue, blood, and CSF.
What are the mechanisms that maintain normal intracranial pressure?

o Cardiac function.
Arterial pressure.
Venous pressure.
o Positioning (i.e., sit upright, at least 30-45).
If a patient has shock and an increase in intracranial pressure, they may have to be put in a downward position
to help fix the shock first.
o Temperature.
o ABGs (particularly CO2 levels).
PaCO2 and PaO2.
Breathing is triggered by the amount of CO2 present in the body.
CO2 is a very potent vasodilator.
o So if CO2 levels increase, there will be an increase in blood flow due to vasodilation. This
will increase the ICP.
O2.
o SaO2 levels below 50% will act like CO2 (i.e., a vasodilator). = meaning increased ICP
o Intra-thoracic and intra-abdominal pressure (e.g., due to constipation).
The degree to which these factors affect the ICP depends on the brains ability to accommodate changes.
What are the factors that affect cerebral blood flow?
o Auto-regulation.
The brain has the ability to regulate its own blood flow by changing the diameter of the blood vessels. This
ensures that blood flow to the brain will always remain at a constant level.
If there is an increase in blood flow to the brain, the diameter will open; if there is a decrease in blood flow to
the brain, the diameter will close.
217

Mechanisms of Increased ICP
There are many causes of increased ICP, some of which are:
o Mass lesion
o Cerebral edema
o Head injury
o Brain inflammation
o Metabolic insult (e.g., DKA and HHS)
What factors influence increased ICP? (look at Fig. 58-3)

o Tissue injury will lead to inflammation (i.e., edema) and thus an increase in ICP.
o If there is a decrease in O2, the brain will switch to anaerobic respirations which will lead to a build-up of lactic acid.
Change in level of consciousness (this is the first thing that will occur).
Changes in vital signs (known as the Cushings triad).
o Increasing systolic blood pressure and decreasing diastolic blood pressure (i.e., widening pulse pressure).
o Bradycardia with a full and bounding pulse.
o Irregular respirations.
Ocular signs (i.e., cranial nerve III)
o The ocular signs are third, making it important not to wait for the pupils to change.
o Signs:
Having one dilated pupil. If the occulomotor nerve (i.e., cranial nerve III) is compressed, the pupil ipsilateral
(i.e., on the same side) to the mass of lesion will be dilated.
Pinpoint pupils indicate pressure on the pons medulla.
Papilledema, a choked optic disc seen on retinal exam, is also noted and is a non-specific sign associated with
long-standing increased ICP.
Decrease in motor function
o A contralateral (i.e., opposite side as the mass or lesion) hemiparesis or hemiplegia may be seen depending on the source
of the increased ICP.
o Decorticate Posturing
Arms come to the middle.
Theres an interruption in the voluntary motor tracts.
o Decerebrate Posturing
Palms are outward on the sides.
The nerve fibres are damaged.
Once the decerebrate posturing has occurred there is really no going back.
Headache
o Continuous headache that is worse in the morning and when the patient is lying.
Vomiting
o There is no nausea preceding the vomiting and it is projectile.
Complications
There are 2 major complications of uncontrolled ICP:
1. Inadequate cerebral perfusion
2. Cerebral herniation
With an increase in pressure, the brain will push downward (as the skull prevents it from moving anywhere else) and put pressure
on the medulla.
o This will lead to altered temperature (i.e., the patient will become extremely hot), pulse, and respiratory control.
The Unconscious Patient

Brain death
o Unresponsive coma no motor/reflex response (e.g., a sternum rubs will not do anything).
o EEG is isoelectric.
o No spontaneous respirations.
o Absent brain stem reflexes.
Diagnostic Studies
218
Aimed at identifying the underlying cause.

o MRI
o CT
o Cerebral angiography
o Lumbar punctures are not typically done when increased ICP is suspected because of the possibility of cerebral
herniation from the sudden release of pressure in the skull from the area above the lumbar puncture.
Collaborative Care
Drug therapy
o Mannitol, glycerol, and urea are all used as osmotic diuretics.
Mannitol is a sugar solution and strong diuretic that is kept in an incubator to prevent crystallization. This will
be given with loop diuretics. The mannitol will draw fluid out of the brain and the loop diuretics will help
excrete those excess fluids.
o Loop diuretics
o Corticosteroids
Decrease inflammation.
o Barbiturates
You want to slow the hypermetabolic state which will decrease the need for O2.
o Antiseizure drugs
The increase in pressure can lead to seizures.
Seizures can also occur if Na+ is below 125mmol/L or greater than 160mmol/L.
o Antipyretics
Nursing Management
Nursing Assessment
Subjective data from client or family members.
Glasgow Coma Scale.
o Vitals signs are completed q4h.
o Neurological tests are done q4h.
Vasomotor response.
Eye opening.
Muscle coordination.
o It is scaled up to 15 for adults.
When the patient scores 8, they have an increase in ICP.
The scale is a little different for children because of different developmental levels.
Neurological assessment.
o You typically only check the cranial nerves that are relevant to the patient.
Goals for a patient with increased ICP:
o Normalize the ICP.
o Maintain a patent airway.
Positioning (e.g., side-lying, chin-tuck with the chin being midline).
Adequate oxygenation.
The amount of O2 administered will be based on the ABGs.
Oral airway if the patient is unconscious.
Mouth care is very important due to the increased secretions.
o Maintain a normal fluid and electrolyte balance.

Give the patient IV fluids (i.e., NS or NS) to ensure they are normovolemic.
o Prevent complications secondary to immobility.
o CVS.
Observe for the Cushing triad (i.e., the widening pulse pressure, bradycardia, and irregular respirations).
219
Safety
o Side rails up.
o Patient side-lying.
o Ensure the environment is safe in case a seizure occurs.
o Changing positions.
o Have the patient blink to ensure the eyes dont dry out.
o Perform mouth care.
o Ensure there is a gag reflex.
o If a patient is tube feeding you want to check for residuals.
o If the blankets are too tight it may cause foot drop. This can be prevented if the patient is wearing shoes while in bed.
o The patient must be fed calories (e.g., TPN) to ensure they are not breaking down their protein.
GI & GU
o Catheters.
o Once the catheter is removed, put the patient on a schedule to retrain them.
Musculoskeletal
o Range of motion exercises as osteoporosis can occur from bed rest.
Skin
o Skin breakdown can be prevented by repositioning the client frequently.
o Skin assessments should be done frequently.
o Integumentary care and nutrition go hand-in-hand.
Psychosocial
o The patient in a coma is still able to hear what you are saying.
o Support the family.
Rehabilitation
Review
Anatomy of cerebral circulation and cerebral blood flow.
Review neurological assessments.
o Pupils unequal = increased ICP.
o Pinpoint = pressures on the pons medulla.
Terminology Review
Aphasia/Global aphasia
o Inability to express oneself (i.e., speak) as well as a loss of comprehension.
Brocas aphasia
o Inability to express oneself (i.e., speak). Anything that comes out of the mouth will be gibberish. They are able to
understand.
Wernickes aphasia
o Inability to comprehend the sounds or meaning of speech. They can express themselves but what they are saying will
not make any sense.
o This is often seen in patients with encephalopathy (liver failure).
Dysphasia (to be distinguished from dysphagia)
o Inability to arrange the words in proper order.
Apraxia
o Inability to carry out a motor activity in response to a command.
Dyspraxia
o Impairment of the ability to perform coordinated movements.
Anomia
o Difficulty in selecting the appropriate word.
Agnosia
o Unable to recognize objects by feeling them (while their eyes are closed). Their sensory stimuli are not good.
Unilateral neglect
o Typically affects the left side, which is a right-sided stroke (this greatly impacts safety). They cannot move their affected
sided. It is as though it does not belong to them.
A person with a left-sided stroke will lose the ability to speak.
o It is often accompanied by hemanopsia (i.e., the loss of peripheral vision; they only have central vision).
220
It is important not to approach people on their left side.

Anosognosia
o This is a worse form of unilateral neglect as the patients dont realize they are paralyzed (i.e., they still believe they can
use their affected side). This is a large safety concern.
Contracture
o Shortening of a muscle.
STROKE
Terminology
Brain attack
o Term increasingly being used to describe a stroke and communicate the urgency of recognizing stroke symptoms and
treating their onset as a medical emergency.
Stroke
It is the third most common cause of death in the Canada.
If people survive a stroke, it is the leading cause of serious, long-term disability.
Approximately 25% of individuals who have an initial stroke die within 1 year, even if treated with drugs such as t-Pa and
streptokinase.
In Canada, someone has a stroke every 10 minutes.
A stroke occurs when there is ischemia (i.e., inadequate blood flow to the brain) to a part of the brain or haemorrhage into the
brain that results in the death of brain cells.
o Transient ischemic attacks (TIA) are when there is ischemia to the brain for an extended period of time. When TIA lasts
for 24-48 hours, a stroke occurs.
Risk Factors
Non-modifiable:
o Age
2/3 of all strokes occur in people >65 years of age.
The incidence of a stroke doubles every decade after 55 years of age.
o Gender
The rate is equal among men and women until 75 years of age, after which there is a greater number of women
getting strokes (this is due to the fact that women are more likely to live longer than men).
Women are more likely to die from a stroke than a man.
o Race
Asians, Aboriginals, African Americans all have a greater likelihood than Caucasians due to their increased
incidences of diabetes.
o Genetic factors (i.e., heredity)
Modifiable:
o Hypertension*
o Hypercoagulability
Single most important risk factor.
o Hyperlipidemia
o Obesity
o Asymptomatic carotid stenosis
o Oral contraceptive use
o Diabetes mellitus
o Physical inactivity
o Heart disease, atrial fibrillation
o Sickle cell disease
o Heavy alcohol consumption
o Smoking
o Table 59-1
o
o Cerebral Arteries
There are 2 main arteries that feed the brain:
o Internal carotid arteries (anterior circulation)
o Vertebral arteries (posterior circulation)
The major branches of the internal carotid arteries are the middle cerebral and anterior cerebral arteries. The middle cerebral
artery is where most strokes occur. This is because there is a lot of branching in that area, making it a prime location for clot
deposition.
A lot of vision problems occur with strokes because the optic chiasm is located directly below the middle cerebral arteries.
221
In response to ischemia, a series of metabolic events (ischemic cascade) occur:

o Inadequate ATP production due to the lack of O2.
o Loss of ion homeostasis.
This is due to the anaerobic metabolism that starts to occur and the build-up of H + ions.
o Free radical formation (i.e., H+).
o Cell death.
If adequate blood flow can be restored early (<3 hours) and the ischemic cascade can be interrupted, less brain damage and less
neurologic function is lost.
Transient ischemic attack (TIA) is a temporary focal loss of neurologic function caused by ischemia.
o Most TIAs resolve within 3 hours.
If blood flow to the brain is totally interrupted:
o Neurologic metabolism is altered in 30 seconds.
o Metabolism stops in 2 minutes.
o Cellular death occurs in 5 minutes.
Collateral circulation may develop to compensate for a decrease in cerebral blood flow. It is also plays a role in determining the
degree of brain damage and functional loss when a stroke occurs.
o
Transient Ischemic
Attack (TIA)
o
o
Cerebrovascular
Accident (CVA)
24-48 hours
Neurological deficits
Completed Stroke
(following 72
hours of ischemia)
Stroke in evolution
o
o Transient Ischemic Attack (TIA)
It is a temporary focal loss of neurological function caused by ischemia of one of the vascular territories of the brain, lasting less
than 24 hours and often lasting less than 15 minutes. They may be due to microemboli that temporarily block the blood flow.
Most TIAs resolve within 3 hours.
o
o Types of Stroke
Strokes are classified based on the underlying pathophysiologic findings:
1. Ischemic stroke
o Ischemic strokes account for 85% of all strokes and result from inadequate blood flow to the brain from a partial or
complete occlusion of an artery.
a. Thrombotic stroke
These kinds of strokes account for 61% and they are usually preceded by TIAs. They occur due to
narrowing of the blood vessels by plaque. This narrowing increases the risk of a blood clot to occur.
b. Embolic stroke
Occurs when an embolus (i.e., blood clot) that is circulating in the blood gets caught in a cerebral
artery that is too small for it to pass through.
It is the second most common cause of strokes.
The client with an embolic stroke will have a sudden onset of symptoms (i.e., there are no warning
signs as in thrombotic strokes). With that in mind, these strokes are also more dangerous as collateral
circulation has not had a chance to develop. Recurrence of an embolic stroke is common unless the
underlying cause is aggressively treated.
2. Hemorrhagic stroke
o Hemorrhagic strokes account for 15% of all strokes. Results from bleeding into the brain tissue itself (i.e.,
intracerebral) or into the subarachnoid space or ventricles (i.e., subarachnoid).
a. Intracerebral haemorrhage
Results from bleeding the in brain tissue as result of a ruptured vessel. These ruptures may occur due
to trauma, or more commonly, hypertension.
Haemorrhage typically occurs during periods of activity as the heart rate and blood pressure rises.
o
222

b.
Subarachnoid haemorrhage
This occurs when there is intracranial bleeding into cerebrospinal fluid-filled space between the
arachnoid and pia mater membranes on the surface of the brain (or ventricles)
It is commonly caused by rupture of a cerebral aneurysm.
Most obvious effects of stroke include impairment of:
o Mobility
o Respiratory function
o Swallowing and speech
o Gag reflex
o Self-care abilities
o
o Motor Function
In a person with a right-sided stroke, their left side will be affected due to the neural pathways crossing over in the brain. This is
the contralateral side (i.e., opposite side as the stroke).
Characteristic motor deficits:
o Loss of skilled voluntary movement (i.e., akinesia).
o Impairment of integration of movements.
o Alterations in muscle tone.
o Alterations in reflexes (the initial hyporeflexia gradually progresses to hyperreflexia).
o
o Communication
This will occur in patients with a left-sided stroke.
Patient may experience:
o Aphasia (i.e., total loss of comprehension and use of language).
o Dysphasia (i.e., difficulty with comprehension and use of language).
o Dysarthria (i.e., a disturbance in the muscular control of speech).
o Expressive, receptive
o It can be classified as non-fluent or fluent.
o Impairments may involve pronunciation, articulation, and phonation.
o
o Affect
Affect is a persons facial expression. Patients who suffer a stroke may have difficulty controlling their emotions.
o
o Intellectual Function
Both memory and judgment may be impaired as a result of stroke.
o People with right-sided strokes will have really poor judgement.
Manifestations of Right-Brain and Left-Brain Stroke
Exam Question!
o
Right-brain damage
o
Left-brain damage
o
Paralyzed left side: hemiplegia (i.e., total or
o
Paralyzed right side: (hemiplegia)
partial paralysis of one side)
o
Often have proprioceptive damage (i.e., loss of o
Impaired speech; language aphasias
spatial awareness)
o
Spatial-perceptual deficits
o
Impaired right/left discrimination
o
Tends to deny or minimize problems
o
Slow performance; cautious
o
Rapid performance; short attention span
o
Aware of deficits: depression, anxiety
o
Impulsive; safety problems
o
Impaired comprehension related to language and math
o
Impaired judgment
o
o
Impaired time concepts
o
o Spatial-Perceptual Alterations
Stroke on the right side of the brain is more likely to cause problems in spatial-perceptual orientation.
There are 4 categories:
1. Incorrect perception of self and illness
2. Erroneous perception of self in space
This may be worsened by homonymous hemanopsia (i.e., blindness that occurs in the same half of the visual
field of both eyes).
3. Inability to recognize an object by sight, touch, or hearing (i.e., agnosia)
223

4.
5.
Inability to carry out learned sequential movements on command (i.e., apraxia)

Anasognosia- person with disability doesnt know that they have disability
o Elimination
Most problems with urinary and bowel elimination occur initially and are temporary if care was quickly initiated.
o
When symptoms of a stroke occur, diagnostic studies are done to:
o Confirm that it is a stroke.
o Identify the likely cause of the stroke (i.e., you do not want to give anticoagulants to a patient with a haemorrhagic
stroke).
CT is the primary diagnostic test used after a stroke.
o
Cerebral blood flow measures.
o Cerebral angiography
o Transcranial doppler
o Carotid angiography
o
Cardiac assessment:
o Electrocardiogram (want to check for dysrhythmias)
o Chest X-ray (want to check for emboli, pulmonary edema)
o Cardiac enzymes (want to see if the patient has had an MI)
o Echocardiography
o Holter monitor (does a continuous reading of the heart, whereas an ECG measures the heart at a point in time)
o
Additional studies:
o Complete blood count
o Platelets, PT (prothrombin time), APTT (activated partial thromboplastin time)
APTT is similar to INR.
o Electrolytes, blood glucose
o Renal and hepatic studies
A decreased GFR may lead to an increase risk of kidney failure. This is particularly likely in patients with
haemorrhagic stroke.
o Lipid profile
Recall that lipids are modifiable risk factors.
o
o Collaborative Care
Prevention
Priority for decreasing morbidity and mortality from stroke.
Surgical interventions for the patient with TIAs from carotid disease include:
o Carotid endarterectomy (rotor rooter)
o Transluminal angioplasty (i.e., reconstruction of a vein)
o Stenting (i.e., widen the vessel)
o Extracranial-intracranial bypass
The affected vessel is brought down, the poor piece excised, the two ends brought together, and the vessel is put
back in place.
o
o Acute Care
Goals for collaborative care during the acute phase are:
1. Preserving life.
The #1 priority is to check the airway!
2. Preventing further brain damage.
3. Reducing disability.
o
Etiology must be determined before treatment can occur.
o This is determined with the use of a CT scan.
Assessment findings:
o Altered level of consciousness
o Weakness, numbness, or paralysis
224

o
o
o
o
o
Speech or visual disturbances

Severe headache
or heart rate
Recall Cushings triad.
Respiratory distress
Unequal pupils
o
o
o
o
o
o
o
Hypertension
Recall the widening pulse pressure
associated with Cushings triad.
Facial drooping on affected side
Difficulty swallowing
Seizures
Bladder or bowel incontinence
Nausea and vomiting
Vertigo
Interventions Initial
o Ensure patient airway.
o Obtain CT scan immediately.
o Remove dentures.
o Perform baseline laboratory tests.
o Perform pulse oximetry.
o Position head midline with the chin down in
o Maintain adequate oxygenation.
order to prevent an increase in ICP.
o Elevate head of bed 30 if no symptoms of shock
o IV access with normal saline.
or injury are present.
o Maintain BP according to guidelines.
o Institute seizure precautions.
By decreasing the BP too quickly, you
o Anticipate thrombolytic therapy for ischemic
decreasing perfusion to the brain.
stroke.
o Remove clothing.
Recombinant tissue plasminogen activator (tPA) [tPA = clot buster] is used to:
o Reestablish blood flow through a blocked artery to prevent cell death in patients with acute onset of ischemic stroke
symptoms.
Thrombolytic therapy must be given within 3 hours of the onset of symptoms in order to decrease disability.
Surgical interventions for stroke include immediate evacuation of:
o Aneurysm-induced hematomas.
o Cerebellar hematomas (if >3 cm).
Drug Therapy
Mannitol (osmotic diuretic)
Anti-seizure
Loop Diuretics
Continuous anticoagulants (heparin, Coumadin)
Corticosteroids (dexamethasone)
Platelet Inhibitors (ASA, Ticlid, Plavix, Persantine)
Barbiturates
Calcium channel blockers
225

Nutrition
Hypermetabolic and hypercatabolic state.
o Increase need for glucose (glucose is the only sugar the brain can use).
o Keep patient normovolemic with NS or NS.
Rehabilitation Care
After the stroke has stabilized for 12-24 hours, collaborative care shifts from preserving life to lessening disability and attaining
optimal functioning.
Patient may be transferred to a rehabilitation unit.
Goals are that the patient will:
o Maintain adequate nutrition.
o Avoid complications of stroke:
Pressure ulcers.
Foot drop.
Muscle atrophy.
Osteoporosis.
Injuries from falls.
Catheters may cause urosepsis.
o Maintain effective personal and family coping.
Unit 23: Care of the Client with Neuromuscular Disorders
Neuromuscular Disorders Outline

This class will focus on chronic, progressive, degenerative disorders related to movement.
o Multiple Sclerosis*
o Parkinsons Disease*
o Guillain Barre
o Myasthenia Gravis
o Amyotrophic Lateral Sclerosis
o Huntingtons Disease (self study)
Anatomy Review
Functional unit of the nervous system is the neuron.
o This class will deal with the neurons taking the message from the brain to the muscle cells.
Neuron composition:
o Dendrites
o Axons
Myelinated
Myelinated axons increase the speed of conduction. This is further increased if Nodes of Ranvier are
present.
Unmyelinated
o Terminal end
MULTIPLE SCLEROSIS (MS)

Multiple Sclerosis
It is a chronic, progressive, degenerative disorder. It is also inflammatory and demyelinating (i.e., the message conduction is
either slowed or not transmitted).
Symptoms:
o Weakness, numbness, shaky, vision problems, forgetfulness, constipation, loss of bladder control, gait issues.
MS affect multiple areas of the body (including myelinated axons in all those body parts).
There is a high prevalence in Canada, particularly the prairies, especially Manitoba. Women are more prone to getting MS than
men. The most prevalent age group is between 15-50 (essentially the prime of life).
The exact cause of MS is unknown, although it is assumed to be an autoimmune response (the myelin is being attacked, which
may eventually lead to the damage of the axon itself).
o T-cells are activated which damage the myelin, which slows/blocks the impulse transmission.
There are often periods of exacerbation and remission. With the alternating of these periods, sclerosis starts to occur along the
axon.
MS: Diagnosis
It is primarily based on the clinical signs and symptoms.
o Since many of the signs and symptoms are vague, there must be 2 or more seemingly unrelated problems (e.g., eye
twitching and numbness in the right foot).
Once 2 or more signs and symptoms have occurred, an MRI will be done, which will show the damage along the axons.
The CSF may be monitored. If the patient has MS there will be an in Oligoclonal immunoglobulin G.
MS: Clinical Course

Typically: exacerbations and remissions.
Types:
o Relapsing-remitting:
There is a stepwise progression.
Medical/Nursing Management
Goals:
1. To treat/halt the disease process.
Drugs!!
o See Table 60-15
Immunomodulators
Avonex
Betaseron
Rebif
Copaxone
o New: Antegren
o New: Novantrone (this drug is used for patients with a progressive kind of MS)
Alemtuzamab
These two drugs were initially designed for patients with cancer.
2. To promote symptomatic relief
Regarding exacerbations:
o Immunosuppressives (e.g., Imuran, Cytoxan).
o Steroids (e.g., prednisone).
This will deal with the inflammatory element of the illness.
Regarding signs and symptoms:
o Related to cranial nerve dysfunction.
Diplopia/visual disturbances
Safety becomes a big issue in these patients.
Dysarthria
Rest is important for these patients.
Dysphagia
The diet will be important (i.e., what types of food can be handled).
Ataxia
Tremors
MS Signs and Symptoms

Related to Motor/Sensory Nerves
Weakness/paralysis
o Rest and safety are important issues.
o Exercise (i.e., physiotherapy) is important to keep their muscles going.
Numbness
Spasticity
o Medications (e.g., antispasmodics such as Zanaflex, baclofen).
Side-effects of antispasmodics will make the person drowsy. The newer age drugs will make the patient less
drowsy.
Fatigue
o Rest is important.
o Medications (e.g., ridiline).
Chronic pain
o Medications (e.g., antidepressants as adjuvant therapy).
Related to Bladder
There are usually two problems associated with the bladder.
o Spastic bladder
The patient will always have the urge.
Medications (antispasmotics).
o Hypotonic
The patient will have retention.
Treatment (straight catheter).
Related to Bowel
Constipation!!
o Treatment:
Increase activity.
Increase fibre in diet.
Related to Cognitive/Emotional Dysfunction

o
Cognitive
o Difficulty with word-finding.
Emotional
o This has both physical and psychological implications.
Related to Depression
Related to Cerebellar Dysfunction

They may have intention tremors (i.e., the patient will not tremor at all until they try perform a task, such as grab a glass of
water).
Safety is a huge problem.
Vertigo and dizziness are not uncommon.
Ataxia.
Related to Sexual Dysfunction

This may be one of the earliest symptoms in men (i.e., erectile dysfunction).
In women, a decreased libido may be seen.
MS Patient Teaching
Self-awareness!!
o Be aware of triggers (this is often seen in patients in patients with exacerbations and remissions).
Build resistance/maintain balance!
o Rest!
o Exercise (physiotherapy).
Avoid temperature extremes.
Avoid infection exposure.
Diet!
o Fibre and fluids.
o protein intake as the basal metabolic rate is very high.
Multidisciplinary team consult?
New/Alternative Therapies
Diets
Vitamins
Apitherapy
o Deliberate bee stings is a therapy (it is done following ice to numb the arm). This has to do with initiating an
inflammatory response.
Hyperbaric O2 therapy
o The idea is that the copious amounts of O2 will have a healing effect on the axons.
Vitamin D/sunshine!
Cannabis
Research: BMTs/stem cells; repair/grow myelin?
LATEST: CCSVI (Chronic Cerebrospinal Venous Insufficiency) a jugular venous obstruction?
Neuromuscular Transmission
I.
UMNs
II.
LMNs
III.
M/N Junction
a. This is where the axon meets the muscle cell.
I. Lower Motor Neurons

Takes the message from the spinal cord to the neuromuscular junction.
That is because it is the final common pathway.
Disruption?
o No reflexes.
Flaccid paralysis, which will lead to muscle atrophy.

GUILLIAN BARR
It is a post-infectious polyneuritis.
It occurs because the immune system is stimulated that results in the post-infectious polyneuritis.
It is similar to MS in that it affects the axon, but in this case the axons can regenerate.
CTQ: Key health history data?
o It is important to determine if infections occurred 2-3 weeks prior. It is typically triggered by a virus.
CTQ: Hallmark signs and symptoms.
o It is weakness and paralysis that starts at the feet and moves up bilaterally. It then recedes the way it came.
It starts at the toes and moves up to the nose.
o This is problematic because the diaphragm is involved, therefore cutting out their respiratory system.
Management: *CTQ: watch for the respiratory rate and effort (e.g., O2 sat).
o Supportive++
o IV immunoglobulin/plasmapheresis
o Recovery??
It generally recovers the way it came.
II. Upper Motor Neurons

Brain Spinal cord
Voluntary control
Disruption?
o Reflex arc is intact.
o Spastic paralysis.
o Hyperactive reflexes.
This is because the voluntary control is gone. There is a voluntary control to reflexes (i.e., the mechanism that
stops the reflex from getting out of control).
Amyotrophic Lateral Sclerosis (ALS)
o It is a progressive degeneration of motor neurons.
o This occurs in people between 40-70. They die due to respiratory issues.
o Signs and symptoms:
CTQ: Unique
Twitching in the face and tongue.
It starts distally before proximally and upper before lower.
Progressive weakness and paralysis.
Relentlessly progressive; there are no remissions.
They generally die in 2-6 years due to respiratory failure.
Cognition remains intact!
o Death: respiratory!
o CTQ: Key teaching point?
o There is no cure and really no successful treatment.
III. Myoneural Junction

Includes:
o Motor (axon) terminal.
o Muscle endplate.
Synapses
o Neurotransmitters
Acetylcholine (it is broken down by acetylcholinesterase)
Dopamine
MYASTHENIA GRAVIS
Definition: autoimmune disease of MNJ.

Pathophysiology: thymus gland autoimmune response
anti-ACh receptor antibodies receptor sites
CTQ: This will lead to fatigue with repeated use of a particular muscle.
CTQ: Hallmark signs and symptoms?
o It starts proximally and moves distally.
o Fatigue++
Is it with repetition? Does it resolve with rest?
o Ptosis
Eye drooping (early sign; can be bilateral or unilateral)
o Dysarthria
o Dysphagia
o Exacerbations and remissions
CTQ: Function best in the morning
Diagnosis:
o Gaze up!
In a patient with myasthenia gravis, the eyes will droop.
o Tensilon Test
It is a short-acting cholinergic/acetylcholine-like drug.
CTQ: Should always have atropine on hand when performing the tensilon test.
o ACh antibody titres
o Acetylcholine is the major neurotransmitter for the parasympathetic nervous system.
Treatment:
o Anti-Che meds
o Thymectomy
This is usually only done when the medications do not work. The success rate is very good.
o The medications must be given on time! Their food should be given shortly after their medications have been given.
Patient teaching
o Crises: Myasthenic vs. Cholinergic
o See Table 57-21
PARKINSONS DISEASE
CTQ: Degeneration of dopamine-producing neurons.

It typically occurs in people >50 years of age. 10% occurs in people <40 years of age.
It affects the basal ganglia and results in a depletion of dopamine.
Signs and symptoms:
o Slow/insidious onset. The problems are often associated with the aging process and are therefore ignored.
o Unilateral early.
o TRAP:
T tremor
The tremor is often in their hand, making it look like they are rolling a pill in their hand.
R rigidity
They walk very rigidly.
A akinesia/bradykinesia
The movements are slowed.
P posture
There is stooping while they walk as a mechanism to prevent falling.
o Blank stare
o Dysarthria
o Dysphagia
o salivation/drooling
o Depression
o Dementia
o Not affected
Vision/hearing.
Management
Goals: Balance dopamine and acetylcholine with the least amount of drugs.
Drugs!!
See Table 60-18

Sinemet CR
Levodopa and carbidopa.
o Note: on/off phenomenon
Surgical interventions:
o Neuroablation
o Deep Brain Stimulation (DBS)
Quality of life has greatly improved from DBS therapy.
o Transplantation
Neuromuscular Disorders & Multidisciplinary Team

Physiotherapy
Occupational therapy
o This will help people with their ADLs such as cooking, cleaning, getting dressed, etc.
Nutritionist/dietician
Social worker
Psychologist
Home care
Speech therapy
o Patients with dysarthria will greatly benefit from speech therapists.
Other?
o
o

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