Medical-Surgical Nursing 1

Medical-Surgical Nursing
Fluids and Electrolytes

 Fluids
60% of an adult’s body weight is water
Factors affecting body fluid composition:
1. Age
2. Gender
3. Body fat
Fluid Compartments in the body:
1. Intracellular space
-fluid in the cells
-approximately 2/3 of the total body water
-primarily located in the skeletal muscle mass
2. Extracellular Space
-body fluid outside the cells
-divided into:
a. intravascular
>contains plasma
>approximately 3L out of 6L blood volume
b. interstitial
>fluid that surrounds the cells
>approximately 11-12L in an average adult
c. transcellular
>smallest division of the ECF
>approximately 1L of fluid
>CSF, synovial, pericardial, pleural,
intraocular
 Electrolytes
2 types:
1. Cations
-sodium, potassium, calcium, magnesium and
hydrogen ions
2. Anions
-phosphate, bicarbonate, chloride
 3 Pressures Important in the Maintenance of
Fluid Balance
1. hydrostatic pressure
2. osmotic pressure
3. oncotic pressure
 Regulation of Body Fluid Compartments
1. Osmosis and Osmolality
2. Diffusion
3. Filtration
4. Sodium-Potassium Pump
 Routes of Gains and Losses
1. Kidneys
>approximately 1L in an average adult
>1mg/kg/hour
2. Skin
>may vary from 0 – 1000ml or more
3. Lungs
>approximately at 400ml a day
4. GI tract
>at 100 – 200ml a day
Laboratory Tests for Evaluating Fluid Status
1. Osmolality
serum Na x 2= glu/18 +BUN/3= Approx value of serum
osmolality
Osmolarity
2. BUN
10 – 20mg/dl or 3.5 – 7 mmol/L
3. Creatinine
0.7 – 1.5 mg/dl or 60 – 130mmol/L
4. Hematocrit
males: 0.44 - 0.52 females: 0.39 - 0.47
5. Urine Sodium
50 – 220mEq/24 hours
Homeostatic Mechanisms
1. Kidneys
-filters 170L of blood a day
-excretes only 1.5L of urine/24 hours
2. Heart and Blood Vessel Functions
3. Lungs
4. Pituitary Function
5. Adrenal Functions
6. Parathyroid Functions
7. Baroreceptors
a. high pressure baroreceptors
-in the aortic arc and carotid sinus
-in the juxtaglomerular cells of the nephron
b. low pressure baroreceptors
-in the cardiac atria (left atrium)
8. Renin - Angiotensin - Aldosterone System
Liver > Angiotensinogen > Angiotensin (kidneys)
renin
Angiotensin 2 (lungs) > Aldosterone (adrenals)
ACE
9. ADH and Thirst
10. Osmoreceptors
11. Atrial Natriuretic Peptide
-at 20 – 77pg/ml (20 -77ng/L)
 Third Space Fluid Shift
 Fluid Volume Deficit
Dehydration
>causes:
a. inadequate intake
b. abnormal fluid losses
c. other causes
-diabetes insipidus
-osmotic diuresis
-hemorrhage
-coma
>signs and symptoms:
weight loss, poor skin turgor, oliguria,
concentrated urine, postural hypotension
rapid heart rate, decreased CVP, cool
clammy skin, inc temperature
>assessment:
BUN and Crea
Hematocrit
Serum elecrolytes
Urine specific gravity
Fluid Challenge Test
>management:
a. oral route of fluid replacement
-preferred method
b. IV route
-isotonic then hypotonic
c. monitoring
-weight, intake and output, V/S, CVP
level of consciousness, breath
sounds and skin color
>nursing management:
a. prevent fluid volume deficit
b. correct fluid volume deficit
 Fluid Volume Excess
-isotonic expansion of body water
>cause:
a. abnormal retention of water and sodium
>s/sx:
a. edema b. distended neck veins
c. crackles g. increased CVP
d. tachycardia h. increased weight
e. increased BP i. increased urine output
f. increased PP j. shortness of breath
>assessment:
BUN CXR
Hematocrit
Serum Osmolality
Serum Electrolytes
>management:
a. withholding excessive administration of
IVF
b. diuretics
c. restriction of oral fluids (sodium)
1. Pharmacologic Therapy
2. Hemodialysis
3. Nutritional Therapy
a. preventing fluid volume excess
b. detecting and controlling fluid volume
excess
c. teaching patients about edema
 Sodium Deficit
-refers to serum sodium level below 135mEq/L
>causes:
a. vomiting d. fistulas
b. diarrhea e. sweating
c. diuretics f. dilutional hyponatremia
>s/sx:
similar to dehydration
>assessment:
serum sodium of less than 135mEq/L
urine sodium
SIADH - >20mEq/L
sodium loss - <20mEq/L
>management:
a. sodium replacement
-by mouth, NGT or through
parenteral route
-parenterally, must not exceed
12mEq/L in 24 hours > osmotic
demyelination
b. SIADH
-give Demeclocycline or Lithium
c. water restriction
-safer than sodium replacement
 Sodium Excess
-sodium level higher than 145mEq/L
-can occur in patients with normal fluid volume or in
those with FVE or FVD
>causes:
a. gain of sodium in excess of water
(administration of hypertonic saline)
b. loss of water in excess of sodium
(unconscious, cognitively impaired
individuals, diarrhea,hyperventilation,
burns, diabetes insipidus, heat stroke
and sea water drowning)
>signs and symptoms:
predominantly neurologic (cellullar
dehydration)
Management:
>serum sodium should be reduced at a rate of 0.5-
1mEq/L
1. IVF Therapy
-hypotonic solution or isotonic non saline solution
2. Diuretics
3. Desmopressin Acetate
Nursing Management:
1. Look for the hidden sources of sodium
2. Monitor for: body temperature, thirst and level of
consciousness
3. Prevent hypernatremia
4. Correct hypernatremia
 Potassium Deficit
-potassium serum level <3.5mEq/L
causes:
>alkalosis, GI losses, hyperaldosteronism,
potassium losing diuretics, other drugs
(corticosteroids, amphotericin B, carbenicillin
and sodium penicillin), insulin hypersecretion,
inability or unwillingness to eat a normal diet,
magnesium depletion, Cushing’s syndrome
signs and symptoms:
>fatigue, anorexia, nausea, vomiting, muscle
weakness, leg cramps, decreased bowel motility,
paresthesias, dysrhythmias and increased
sensitivity to digitalis, glucose intolerance
Confirmatory tests:
1. Decreased serum potassium
2. ECG changes
-flat or inverted T waves and depression of the
ST segments
-elevation of the U waves
3. Metabolic Alkalosis
4. Urine potassium concentration of >20mEq/24 hours
Medical Management:
1. Potassium replacement therapy
-if without abnormal potassium loss, 40-80mEqs/day
-oral (Kalium Durule) or IV (K chloride, K phosphate or
K acetate)
Nursing Management:
1. Monitoring for s/sx or progression of hypokalemia
2. Preventing hypokalemia
3. Correcting hypokalemia
4. Administering IV potassium
-after adequate urine flow
-20mEqs/hour or less
-30-40mEqs/L and below unless severe
 Potassium Excess
-less common but more severe than hypokalemia
-causes:
>renal failure, excessive intake of potassium,
infection, hyporaldosteronism and Addison’s
disease, medications (KCl, heparin, ACE
inhibitors, NSAIDS and K sparing diuretics) and
acidosis
-clinical manifestations:
>dysrhythmias, skeletal muscle weakness and
paralysis
>CNS and PNS involvement
>Flaccid quadriplegia, respiratory and speech
muscle paralysis
Confirmatory tests:
1. ECG
-peaked, narrow T waves, ST segment
depression and a shortened QT interval
-prolonged PR interval then absence of P wave
2. ABG
3. Serum potassium level increase
Medical Management:
1. Monitoring of serum potassium with ECG findings
2. Emergency pharmacologic therapy
>calcium gluconate or calcium chloride
>sodium bicarbonate
>insulin and glucose
>beta 2 agonist
3. Dialysis
Nursing Management:
1. Monitoring
2. Preventing hyperkalemia
3. Correcting hyperkalemia
Pseudohyperkalemia
>use of tourniquet in an exercising muscle
>marked leukocytosis and thrombocytosis
>familial pseudohyperkalemia
 Calcium Deficit
-less than 8.5mg/dl of calcium in the serum
-causes:
>hypoparathyroidism
>those who received citrated blood
>pancreatitis, renal failure
>vitamin D deficiency, magnesium deficiency
>medullary thyroid carcinoma
>low albumin levels, alkalosis and alcohol abuse
-signs and symptoms:
>tetany, seizures and mental changes
-confirmatory test:
>ECG- prolonged QT interval
Management:
1. Administer calcium salts
-calcium carbonate, calcium chloride, calcium
gluceptate
Risks:
a. Sloughing of tissues
b. Bradycardia then cardiac arrest
c. Digitalis toxicity
2. IVF but not normal saline or solutions containing
phosphates and bicarbonate
3. Vitamin D therapy
4. Aluminum hydroxide, calcium acetate, calcium
carbonate
5. Nutritional therapy
6. Screen for and treat hypomagnesemia
Nursing Management:
1. Monitor hypocalcemia for patients at risk
2. Airway management
3. Seizure precaution
4. Patient education
-caffeine and alcohol decreases absorption
-nicotine increases excretion
-medications to decrease bone loss
(alendronate, raloxifene and calcitonin)
Calcium Excess
-with high mortality rate
-causes:
>malignancies and hyperparathyroidism
>immobilization
>use of Thiazide diuretics
>milk-alkali syndrome
>Vitamin A and D intoxication
*proportional to the elevation of serum calcium
>muscle weakness, incoordination, anorexia and
constipation
>cardiac arrest
>dehydration
>abdominal and/or bone pain
>abdominal distention and paralytic ileus
>excessive urination then polyuria
>s/sx of PUD
>changes in the LOC and mental status
*hypercalcemic crisis
Laboratory tests:
1. Serum calcium determination
2. ECG
- shortening of the QT interval and ST segment
- prolongation of the PR interval
- dysrhythmias
3. Double antibody PTH test
4. X-Ray - osteoporosis
5. Sulkowitch test
Management:
1. Pharmacologic therapy
-dilute the serum calcium and promote its exc.
(normal saline, administer phosphates, diuretics,
calcitonin)
-Cancer treatment
-Corticosteroid therapy
> to decrease bone turnover and tubular
reabsorption
-Biphosphonates (pamidronate)
>causes myalgia, pyrexia and decreased WBC
-Mithramycin
>causes thrombocytopenia and nephrotoxicity and
hepatotoxicity
-IV phosphates should be used with caution
>Phospho-Soda, Neutra-Phos
Nursing Management:
1. Monitor the s/sx
2. Increase mobility
3. Increase oral fluid intake
Chloride Deficit
-serum chloride level below 96mEq/L
-causes:
>chloride deficient formulas, salt restricted diets
>GI tube drainage, severe vomiting and diarrhea
>hypokalemia, hyponatremia and metabolic
alkalosis
(hyperexcitability of muscles, tetany,
hyperactivity of deep tendon reflexes, weakness,
twitching, muscle cramps, cardiac
dysrhythmias, seizures and coma)
-lab tests:
>serum chloride determination
>serum potassium and sodium determination
>ABG
>urine chloride level decrease (normal value-
110-250mEq/L)
-medical management:
>chloride replacement
normal saline and half strength saline
>reevaluate the use of diuretics
>nutritional therapy
tomato juice, salty broth, canned
vegetables, processed meats and fruits
>restriction of free water intake
>ammonium chloride
-nursing management
>monitoring of intake and output, ABG
determination values, serum electrolyte
levels, LOC, muscle strength and
movement
>vital signs and respiratory assessments
>patient education as regards to replacement
therapy
Chloride Excess
-serum chloride level higher than 106mEq/L
-associated with hypernatremia, bicarbonate loss
and metabolic acidosis
-causes:
>loss of bicarbonate (GI and/or renal)
>metabolic acidosis, hypervolemia and
hypernatremia
(tachypnea, weakness, lethargy, deep rapid
respirations, diminished cognitive ability and
hypertension)
>decrease in CO, dysrhythmias and coma
-lab tests:
>serum sodium and chloride determination
>ABG- Bicarbonate less than 22mEq/L
-normal anion gap (8-12mEq/L)
>urine chloride concentration greater than
250mEq/L
>IVF therapy
-Lactated Ringer’s Solution
>IV sodium bicarbonate
>Diuretics
>Fluids, sodium and chloride restriction
-nursing management:
>monitoring V/S, ABG, I&O
>assessment of neurologic, respiratory and
cardiac functions
>patient education as regards to nutrition
Acid-Base Balance
 Normal blood pH
-7.35 to 7.45
 Blood pH compatible with life
-6.80 to 7.80
 Buffer Systems
-maintains the blood pH by removing or releasing

H+ ions
1. Bicarbonate-Carbonic Acid Buffer System
-the major extracellular buffer system
-Bicarbonate to Carbonic Acid Ratio is 20:1
2. Phosphate Buffer System
3. Plasma proteins, RBC and Hemoglobin
Organs involved in HCO3-H2CO3 System:
1. Kidneys
-activation is slower (hours to days) but more
efficient
-has the ability to regenerate and reabsorb or
excrete bicarbonates
-has the ability to retain or excrete H+
-in acidosis: excrete H+ and conserve bicarbonate
-in alkalosis: retain H+ and excrete bicarbonate
-cannot compensate in renal failure
2. Lungs
-adjust ventilation in response to CO2 content of
the blood
-activation is faster but less efficient
Acute and Chronic Metabolic Acidosis
(Base Bicarbonate Deficit)
-low pH; low plasma bicarbonate
-causes:
>gain of hydrogen ions or loss of bicarbonate
-2 forms:
A. High Anion Gap Acidosis
-due to the accumulation of the
unmeasured anions (phosphates, sulfates
and proteins)
B. Normal Anion Gap Acidosis (hyperchloremic
acidosis)
-due to the direct loss of bicarbonates
>diarrhea >diuretics
>lower intestinal fistulas >renal ins.
>excessive administration of chloride
>excessive administration of parenteral
solution without bicarbonate
>headache, confusion, drowsiness
>increased respiratory rate and depth
>nausea and vomiting
>peripheral vasodilatation and decreased CO
>decreased BP, cold and clammy skin,
dysrhythmias and shock
-lab tests:
>ABG - low bicarbonate level and a low pH
>Serum potassium determination
>Anion Gap Calculation
>ECG
>Eliminate excessive sources of chloride
>Sodium bicarbonate
-if pH is less than 7.1
-if bicarbonate is less than 10mEq/L
>Serum potassium monitoring and reversal of
potential hypokalemia
>Reversal of potential hypocalcemia
>Sodium Bicarbonate
>Dialysis
Acute and Chronic Metabolic Alkalosis
(Base Bicarbonate Excess)
-high pH; high plasma bicarbonate concentration
-causes:
(due to gain of bicarbonates or loss of hydrogen
ions)
>vomiting or gastric suction- most common
>diuretics- loop and thiazides
>hyperaldosteronism and Cushing’s syndrome
>excessive alkali ingestion or administration
>villous adenoma and cystic fibrosis
>decreased calcium ionization
(tingling of the fingers, toes, dizziness
and hypertonic muscles)
>depressed respirations
>atrial arrhythmias then ventricular arrhythmias
>decreased motility then paralytic ileus
-lab tests:
>ABG - pH greater than 7.45
- bicarbonate greater than 26mEq/L
>Serum potassium determination
>Urinary chloride levels
>Chloride replacement (KCl)
>IVF containing sufficient sodium and chloride
>H2R antagonists- in GI suctioning
>Carbonic Anhydrase Inhibitors
>I&O monitoring
Acute and Chronic Respiratory Acidosis
(Carbonic Acid Excess)
-pH is less than 7.35; paCO2 is higher than 42mmHg
-causes:
(due to inadequate excretion of CO2 > elevated
plasma CO2 > elevated plasma H2CO3)
>acute pulmonary edema >sedative overdose
>aspiration of foreign body >severe pneumonia
>atelectasis >RDS
>pneumothorax >MG, GBS
>increased HR, RR, BP, mental cloudiness and
feeling of fullness in the head
>ventricular fibrillation
>increased intracranial pressure, papilledema,
dilated conjunctival blood vessels
>hyperkalemia
-lab tests:
>ABG
>Serum electrolyte determination
>Chest X-Ray
>ECG
>Drug screen for overdose
>Pharmacologic
*bronchodilators *thrombolytics
*antibiotics *anticoagulants
>Pulmonary hygiene
>Adequate hydration
>Supplemental O2 with caution
>Mechanical ventilation
Acute and Chronic Respiratory Alkalosis
(Carbonic Acid Deficit)
-arterial pH of greater than 7.45; PaCO2 of less
than 38mmHg
-causes:
(due to hyperventilation > blowing off of CO2 >
decreased plasma carbonic acid concentration)
>extreme anxiety, hypoxemia, early phase of
Aspirin intoxication, gram negative
bacteremia and inappropriate ventilator
settings
>chronic hepatic insufficiency, cerebral tumors
>lightheadedness, inability to concentrate
>numbness and tingling from reduced ionized
calcium
>tinnitus, loss of consciousness
>tachycardia, atrial and ventricular arrhythmias
-lab tests:
>ABG
>Serum electrolyte determination
-management:
>breath slowly or into a closed system
>sedatives
Acid – Base Disturbances and Compensation
Disorder Initial Event Compensation
Respiratory ↑PaCO2;↑or N Kidneys eliminate H+

Acidosis HCO3;↓ pH & retain HCO3
Respiratory ↓PaCO2;↓or N Kidneys conserve H+

Alkalosis HCO3;↑pH & excrete HCO3
Metabolic ↓or N PaCO2; ↓Lungs eliminate

Acidosis ↓HCO3;↓ pH CO2 & conserve
HCO3
Metabolic ↑or N PaCO2; Lungs ↓to↑ PaCO2,
Alkalosis ↑HCO3;↑ pH kidneys conserve H+
Burns
Autograft Escharotomy
Heterograft Fasciotomy
Homograft Rule of Nines
Carboxyhemoglobin
4 Major Goals Relating to Burns
1. Prevention
2. Institution of lifesaving measures for the severely
burned person.
3. Prevention of disability and disfigurement through
early, specialized, individual treatment.
4. Rehabilitation through reconstructive surgery and
rehabilitation programs.
Burn Categories Burns are sustained through
1. Thermal 1. Conduction
2. Chemical 2. Electromagnetic radiation
3. Radiation
Skin destruction can lead to;
1. Increased fluid loss 4. Scarring, change in body image
2. Infection 5. Compromised immunity
3. Hypothermia 6. Changes in function
Classification of burns:
A. According to burn depth:
1. Superficial Partial Thickness (Similar to First Degree
Burn)
-causes:
*sunburn *low intensity flash
-involves the epidermis and possibly a portion of
the dermis
*tingling *pain that is soothed by
*hyperesthesia cooling
*reddened *possibly blisters
*minimal or no
edema
-complete recovery within a week; no scarring
-peel off
2. Deep Partial thickness (Similar to Second Degree
Burn)
-causes:
*scalds
*flash flame
-involves the epidermis, upper dermis, portion of the
deeper dermis
-s/sx:
*pain *sensitive to cold air
*hyperesthesia *blistered, weeping surface
*broken epidermis *edema
-recovery in 2-4 weeks
-some scarring and depigmentation contractures
-infection may convert it to full thickness
3. Full Thickness (Similar to Third Degree)
-causes:
*flame
*prolonged exposure to hot liquids
*electric current
*chemical
-involves the epidermis, entire dermis and
sometimes subcutaneous tissue, may involve
connective tissue, muscle and bone
-s/sx:
*pain free *hemolysis
*shock *entrance and exit wounds
*hematuria *broken skin with exposed
*edema fats
-eschar sloughs
-grafting necessary
-scarring and loss of contour and function;
contractures
-loss of digits or extremity possible
Physiologic Responses to Burns
Local Pathophysiologic Response
-if only less than 25% of the TBSA is involved
Local and Systemic Pathophysiologic Response
-if more than 25% of the TBSA is involved
-maximal if burns cover 60% or more of the TBSA
1. Cardiovascular Response
fluid loss > hypovolemia > decreased cardiac output >
decreased BP > decreased perfusion and oxygen delivery
> onset of burn shock > sympathetic response >
peripheral vasoconstriction > further decrease in the
CO
-the greatest volume of fluid leak occurs in 24 – 36
hours after the burn, peaking at 6 – 8 hours
-basically caused by increased capillary permeability
-diuresis occurs for several days to 2 weeks
2. Burn Edema
-swelling maximal after 24 hours
-begins to resolve 1-2 days post burn
-completely resolved after 7-10 days post injury
Edema > pressure on the small blood vessels
and nerves of distal extremity > ischemia >
3. Effects on Fluids and Electrolytes and Blood Volume
-evaporative loss through the burn wound (3-5 L)
-hyponatremia (dilutional due to fluid shift from
interstitial to intravascular space)
-hyperkalemia due to massive cell destruction
*later results in hypokalemia due to dilution caused
by fluid shift
-anemia due to blood loss and hemolysis
(though may be seen as polycythemia due to
excessive plasma loss)
4. Pulmonary Response
-inhalation injury > release of histamine, serotonin and
thromboxane > catecholamine release > hypoxia
-atelectasis may be present due to decreased surfactant
-types of pulmonary injury:
*upper airway injury
-results from direct heat and edema
*inhalation injury below the glottis
-usually results from carbon monoxide poisoning
-respiratory acidosis may occur over the first 5 days after
the burn
-indicators of a possible pulmonary damage;
*hx indicating that burn occurred in an enclosed space
*burns of the face and neck
*singed nasal hair
*hoarseness, voice change, dry cough, stridor
*bloody sputum
*Labored breathing or tachypnea
*Erythema or blistering of the oral or pharyngeal
mucosa
-possible consequences will be respiratory failure and
acute respiratory distress syndrome
4. Other Systemic Responses
-hemolysis and muscle damage > release of hemoglobin
and myoglobin > acute tubular necrosis and renal failure
-decreased immune response > sepsis
-loss of skin tissue > altered thermoregulation >
hypothermia > later hyperthermia due to
hypermetabolism
-sympathetic hyperactivity > paralytic ileus and Curling’s
ulcer
Management:
1. Emergent/ Resuscitative Phase of Burn Care
A. On the scene Care
-airway, breathing and circulation
-disability, exposure and fluid resuscitation
-duration (from onset of injury to completion of
fluid resuscitation
-priorities:
*first aid
*prevention of shock
*prevention of respiratory distress
*detection and treatment of concomitant
injuries
*wound assessment and initial care
-emergency procedures at the burn scene:
*extinguish the flames
*cool the burn
*remove restrictive objects
*cover the wound
*irrigate chemical burns
B. Emergency Medical Management:
-transport to the nearest hospital > life-saving
measures
-ABC
-humidification, bronchodilation, mucolytic agents,
coughing
-ET tube insertion and assisted ventilation
-continuous positive airway pressure
-assessment for head and neck injuries
-burn wound management
-IV access, CVP insertion
-indwelling urinary catheter insertion
-baseline data
-tetanus prophylaxis
-adequate pain relief
C. Transfer to Burn Center
D. Management of Fluid Loss and Shock
-fluid replacement therapy
-fluid requirements
Problems Associated:
>Acute Resp and Renal Failure
>Distributive Shock
> Compartment Syndrome
2. Acute or Intermediate Phase of Burn Care
-begins 48 to 72 hours after the burn injury
-goals:
A. Infection Prevention
-Staphylococcus, Pseudomonas, Proteus, E.
coli, and Klebsiella
-Candida is also being implicated
-3 characteristics of burn wound sepsis:
*100,000 bacteria/gram of tissue
*inflammation
*sludging and thrombosis of dermal blood
vessels
-early enteral feeding can be used for prevention
B. Wound Cleaning
-hydrotherapy
>use of tap water
>temperature of water should be
maintained at 37.8C
>room temperature should be maintained
at 26.6-29.4C
>should be limited to a 20-30 minute
period
C. Topical Antibacterial therapy
-criteria for choosing antibiotics:
*effective against gram negative organisms
*clinically effective
*penetrates the eschar but without systemic
toxicity
*does not lose its effectiveness
*cost effective, available and acceptable
*easy to apply
-examples:
1. Silver sulfadiazine
2. Silver Nitrate
3. Mafenide Acetate
D. Wound Dressing
E. Dressing Changes
F. Wound Debridement
-2 goals:
*to remove tissue contaminated by bacteria
*to remove devitalized tissue or burn eschar in
preparation for grafting and wound healing
G. Pain Management
H. Nutritional Support
Shock
-types:
1. Hypovolemic Shock
2. Cardiogenic Shock
3. Circulatory Shock (Distributive Shock)
> Septic Shock
> Neurogenic Shock
> Anaphylactic Shock
*Obstructive Shock
-Effect of shock to normal cellular functions
-Vascular Responses
1. Central Regulatory Mechanisms
2. Local Regulatory Mechanisms
-Blood Pressure Regulation
BP= CO x TPR CO= SV x HR
>Maintained by:
a. nervous system
b. endocrine system
c. chemicals
>Maintain tissue/organ perfusion:
a. MAP= systolic BP + 2 (diastolic BP)
3
*should exceed 70-80 mmHg
-Stages of Shock
1. Compensatory Stage
>BP is maintained within normal limits due to the
effect of normally functioning regulatory mechanisms
>s/sx:
*metabolic acidosis *mental status
change
*tachypnea
>medical management:
a. identify the cause of shock
b. correction of shock
c. support of the regulatory mechanisms
a. monitoring tissue perfusion
*LOC *urine output
*V/S *skin
*laboratory values
b. reducing anxiety
c. promoting safety
2. Progressive Stage
-exhaustion of the compensatory mechanisms
*myocardial depression
*increased capillary permeability
-assessment and dxtic findings:
a. respiratory effects
hypoxemia and hypercarbia
intense inflammatory response
decreased surfactant production
acute respiratory distress syndrome
(acute lung injury, shock lung, non cardiogenic
pulmonary edema)
b. cardiovascular effects
dysrhythmias
myocardial infarction
cardiac depression
c. neurologic effects
decreased cerebral perfusion
*mental status change
*behavioral change
*pupillary dilation
d. renal effects
MAP<80mmHg
acute renal failure
e. hepatic effects
decreased blood flow
less ability to perform hepatic functions
f. gastrointestinal effects
decreased blood flow
*PUD
*bloody diarrhea
*sepsis
g. hematologic
DIC
shock
a. depends on the type of shock
b. depends on the decompensation of the organ
systems
Management Common To All Types Of Shock
a. optimize intravascular volume
b. supporting the pumping action of the heart
c. improving the competence of the vascular
system
Nursing Management:
a. preventing complications
b. promoting rest and comfort
c. supporting family members
3. Irreversible Stage
-severe organ damage
-can no longer respond to treatment
-survival is less likely
a. same with the progressive stage
a. same with progressive shock
b. moral support to the family
c. ethical issues (living will)
Clinical Findings in the Stages of Shock
Finding Compensatory Progressive Irreversible
BP normal Systolic <80 Mechanical or
-90mmHg pharma support
HR >100bpm >150bpm erratic, asystole
Respiration >20 breaths/ Rapid, shallow Intubation

min crackles
Skin cold, clammy Mottled, Jaundice
petechiae
Urine decreased 0.5ml/kg/hr anuria, needs
Output dialysis
Mentation confusion Lethargy Coma
Finding Compensatory Progressive Irreversible
A/B Balance Resp Alkalosis Met Acidosis Profound
Acidosis
HYPOVOLEMIC SHOCK
-most common type of shock
-characterized by decreased intravascular volume of
15-25%
-predisposing factors:
External: Fluid Losses Internal: Fluid Shifts
a. trauma a. hemorrhage
b. surgery b. burns
c. vomiting c. ascites
d. diarrhea d. peritonitis
e. diuresis e. dehydration
f. diabetes insipidus
>goals:
a. restore intravascular volume
b. redistribute fluid volume
c. correct the underlying cause
*pharmacologic therapy
desmopressin anti-emetic
insulin anti-diarrhea
a. administering blood and fluids safely
CARDIOGENIC SHOCK
-due to cardiac failure
-either coronary and non coronary
Coronary Factors Non Coronary Factors
a. myocardial infarction a. cardiomyopathies
b. valvular damage
c. cardiac tamponade
d. dysrhythmias
a. anginal pain
b. hemodynamic instability
c. dysrhythmias
a. correction of underlying cause
b. initiation of first line treatment
*supplemental oxygen *vasoactive medications
*controlling chest pain *controlling HR
*selected fluid support *mechanical cardiac
support
c. pharmacologic therapy
*dobutamine *nitroglycerine
*dopamine *vasoactive meds
*anti-arrhythmic meds
d. fluid therapy
a. preventing cardiogenic shock
b. administering meds and IV fluids
c. maintaining mechanical devices
d. enhancing safety and comfort
CIRCULATORY SHOCK
vasodilation
maldistribution of blood volume
decreased venous return
decreased stroke volume
decreased cardiac output
decreased tissue perfusion
A. Septic Shock
-risk factors:
a. immunosuppression
b. extremes of age d. chronic illness
c. malnutrition e. invasive procedures
a. pharmacologic therapy
b. nutritional therapy
a. supportive to the medical management
B. Neurogenic Shock
-occurs due to the loss of sympathetic tone
a. spinal cord injury c. depressant meds
b. spinal anesthesia d. hypoglycemia
a. restoring sympathetic tone
a. elevate the head of the bed 30 degrees
( in spinal/epidural anesthesia)
b. immobilize the patient
(in spinal cord injury)
c. elastic compression stockings
d. feet elevation
e. heparin/low molecular weight heparin
f. pneumatic compression of the legs
g. passive ROM
C. Anaphylactic Shock
antigen-antibody reaction brought about by severe
allergic reaction
provokes mast cells to release chemical mediators like

histamine and bradykinin
widespread vasodilatation and capillary permeability

a. drug sensitivity c. bee sting allergy
b. transfusion reaction d. latex sensitivity
a. removal of the causative agent
b. restore vascular tone (epinephrine)
c. antihistamines and bronchodilators
a. assess for previous hypersensitivity reactions
b. prevention of future exposure to antigens
c. identification of new antigens
d. patient education
RENAL DISEASES
Terms:
1. aldosterone 9. hematuria
2. antidiuretic hormone 10. nocturia
3. anuria 11. oliguria
4. bacteriuria 12. proteinuria
5. clearance 13. pyuria
6. dysuria 14. Valsalva Leak Point
7. frequency Maneuver
8. GFR 15. vesicoureteral reflux
Test of Urine Specific Gravity:

1. Osmolality 2. Specific gravity
Kidneys
-retroperitoneal organs
-120 – 170g
-12cm long, 6cm wide and 2.5cm thick
-with 8 – 18 pyramids
-with 4 -13 minor calyces
-with 2 – 3 major calyces
-with protective structures:
a. Pararenal fat
b. Gerota’s fascia
c. Perirenal fat
d. Renal capsule
Nephron
-basic structural and functional unit of the kidney
 3 Processes of Urine Formation
1. Glomerular Filtration
2. Tubular Reabsorption
3. Tubular Secretion
 Renal function begins to decrease at a rate of 1%
each year at 30.
A. Acute Pyelonephritis
-bacterial infection of the renal pelvis, tubules and
interstitial tissue
-an ascending infection
a. vesico-ureteral reflux
b. urinary tract obstruction
-enlarged kidney
-with abscess on the renal capsule and at the
cortico-medullary junction
-s/sx:
>fever and chills >costo-vertebral angle
>leucocytosis tenderness
>bacteriuria and >flank pain
pyuria dysuria >inc. urinary frequency
-dx:
>UTZ >Nuclear scan
>CT scan >IVP
>Urine Culture & Sensitivity Test
Medical Management:
a. uncomplicated
-no dehydration, no nausea and vomiting, no
sepsis
>2 weeks of oral antibiotics
Trimethoprim-Sulfamethoxazole
Ciprofloxacin
Gentamicin with or without Ampicillin
Third Generation Cephalosporins
>6 weeks of oral antibiotics if with relapse
*urine culture 2 weeks after antibiotic therapy
b. complicated
-pregnant patients
>hospitalization (antibiotics from IV to oral)
B. Chronic Pyelonephritis
-repeated acute pyelonephritis >> chronic
pyelonephritis
-no s/sx unless there’s an acute exacerbation
-kidneys scarred, contracted and non functional
fatigue polyuria
headache excessive thirst
anorexia weight loss
-diagnosis:
creatinine and BUN clearance
creatinine levels
intravenous pyelography
-complications:
a. ESRD
b. hypertension
c. formation of renal stones
-may be due to the presence of urea splitting
microorganisms
a. urine culture and sensitivity guided antibiotic
therapy
Nitrofurantoin
TMP-SMZ
a. monitoring
-I&O
b. oral fluids (3-4L/day)
c. symptomatic
-antipyretics
d. education
-advise bed rest
-prevention of UTI
C. Acute Glomerulonephritis
-primarily a disease of children older than 2 years old
-may affect any age
-causes:
>autoimmune
SLE
>streptococcal
Acute Post Streptococcal Glomerulonephritis
Acute Post Streptococcal Glomerulonephritis
-2 to 3 weeks after
>impetigo
>sorethroat
hematuria hypertension
tea colored urine headache, malaise, flank pain
proteinuria (+) kidney punch
inc serum BUN and crea congestion
anemia confusion, somnolence
edema and seizures
Group A Beta-Hemolytic Streptococcal Infection
Antigen-Antibody Reaction
Deposition in the Glomerulus
Increased Production of Epithelial Cells in the
Glomerulus
WBC Infiltration
Thickening
Scarring
Decreased GFR
-diagnosis:
a. kidney biopsy
b. electron microscopy
c. immunoflourescence analysis
d. Anti-Streptolysin O Titer
Anti-DNAse B Titer
e. Serum Complement Determination
-decreased
-will normalize in 2 – 8 weeks
IgA Nephropathy
-most common type of primary glomerulonephritis
-Inc IgA; with normal serum complement
-complications:
a. Hypertensive Encephalopathy
b. Heart Failure
c. Pulmonary Edema
Rapidly Progressive Glomerulonephritis
-patient deteriorates in weeks to months
-course is more severe and more rapid
Management To Glomerulonephritis
Goals:
1. Treat symptoms
2. Preserve renal function
3. Treat complications
a. antibiotics d. protein restriction
b. steroids e. sodium restriction
c. cytotoxic agents f. diuretics
g. dialysis
D. Chronic Glomerulonephritis
-components:
repeated acute glomerulonephritis
hypertensive nephrosclerosis
hyperlipidemia
chronic tubulo-interstitial injury
hemodynamically mediated glomerular sclerosis
-contraction of the kidneys to 1/5 of its original size
-deformed kidneys
-may result to ESRD
may be asymptomatic hypertension
inc BUN and Crea bipedal edema
retinal hemorrhages ophthalmoscopy
papilledema
weight loss
weakness and irritability
nocturia
GIT disturbances
anemia
heart failure
peripheral neuropathy, decreased DTR
pulsus paradosus
-diagnosis:
1. Urinalysis - fixed sp. Gravity at 1.010
proteinuria; urinary casts
2. serum chemistry
-hyperkalemia -hypoalbuminemia
-hyperphosphatemia -hypocalcemia
-hypermagnesemia
3. CBC
-anemia
4. Chest X-Ray
-cardiomegaly
-pulmonary edema
5. ECG
-left ventricular hypertrophy
-management:
1. treatment of hypertension
2. weight monitoring
3. give proteins of high biologic value
4. adequate calories
5. dialysis
1. monitoring
E. Nephrotic Syndrome
-components:
proteinuria hyperlipidemia
hypoalbuminemia
-causes:
a. chronic glomerulonephritis
b. diabetes mellitus
c. amyloidosis
d. SLE
e. multiple myeloma
f. renal vein thrombosis
edema (soft and pitting)
-eyes, dependent area and abdomen
malaise irritability
headache fatigue
-diagnosis:
1. Urinalysis
-proteinuria (3-3.5g/day)
-inc WBC
2. Protein Electrophoresis
Immunoelectrophoresis
3. Biopsy
4. AntiC1q antibodies (SLE)
-complications:
a. infection d. acute RF
b. thromboembolism e. pulmonary emboli
c. accelerated atherosclerosis
-management:
1. diuretics
2. ACE inhibitors
3. immunosuppressants
4. steroids
5. hypolipidemic agents
6. sodium restriction
7. CHON intake of 0.8g/kg/day
low saturated fats
 Urolithiasis
-stones or calculi in the urinary tract
-supersaturation of substances such as calcium
oxalate, calcium phosphate and uric acid
>depends on:
*the site of obstruction
*edema
*infection
-assessment and diagnosis
>IVP, Intravenous Urography
>Retrograde Pyelography
>UTZ
>serum chemistries and 24 urine tests
deficiency of citrate, mg
nephrocalcin & uropontin
dehydration
infection
Urolithiasis
urinary stasis
periods of immobility
hypercalciuria and hypercalcemia

-causes of hypercalcemia and hypercalciuria:
a. hyperparathyroidism
b. renal tubular acidosis
c. cancers
d. granulomatous disease
e. excessive intake of Vitamin D
f. excessive intake of milk and alkali
g. myeloproliferative disease
-substances other than calcium that may precipitate
and form stones
a. uric acid
-5%-10% of renal stones
-gout, myeloproliferative disorders
b. struvite
-15% of renal stones
-in persistently alkaline and ammonia rich
urine
(caused by urease-splitting bacteria)
-in neurogenic bladder, foreign bodies and
recurrent UTI
c. cystine
-1%-2% of renal stones
-hereditary defect in the renal absorption
-medicines that increases the risk of urolithiasis
a. acetazolamide d. laxatives
b. Vitamin D e. high doses of aspirin
c. antacids
-management:
a. eradicate the stone
b. determine the stone type
c. prevent nephron destruction
d. control infection
e. relieve any obstruction
>Opioid Analgesics
NSAIDs
>Hot Baths and Moist Heat to the flank
area
>Advise to increase oral fluid intake
(urine output of >2L/day is advisable)
-specific management:
1. Calcium stones
-restrict proteins and sodium in the diet
-acidify the urine using Ammonium chloride
or Acetohydroxamic Acid
-Cellulose sodium phosphate
(binds calcium from food)
-thiazide diuretics (if caused by inc PTH)
2. Uric Acid Stones
-low purine diet (shellfish, mushrooms,
asparagus, organ meats)
-Allopurinol
-alkalinize the urine
3. Cystine
-low protein diet
-penicillamine (to decrease excretion
through the urine)
4. Oxalate
-dilute the urine
-limit oxalate containing foods
(spinach, strawberries, rhubarb, tea,
peanuts and wheat bran)
-surgical management:
a. Ureteroscopy
b. Extracorporeal Shock Wave Lithotripsy
c. Percutaneous Nephrostomy or Nephrolithotomy
 Acute Renal Failure
-sudden and almost complete loss of renal function
*oliguria *normal urine output
*anuria *rising serum creatinine
and BUN
Categories of ARF
1. Prerenal
-shock
2. Intrarenal
-the result of actual parenchymal damage
-use of nephrotoxic drugs (NSAIDs and ACE inh)
3. Postrenal
-the result of an obstruction in the distal urinary tract
Four Clinical Phases of ARF

1. Initiation
-begins with the initial insult and ends when oliguria
develops
2. Oliguria
-rise in the serum of waste products of metabolism
-rise in serum potassium and magnesium
3. Diuresis
-with gradually increasing urine output
-renal function may still be markedly abnormal
4. Recovery Period
-improvement of renal function
-may take 3-12 months
-with normal laboratory values
-with permanent 1-3% reduction in GFR
Characteristics Prerenal Intrarenal Postrenal
Etiology hypoperfusion parenchymal obstruction

damage
BUN value increased increased Increased
Creatinine value increased increased Increased
Urine output decreased varies, often varies, may be
decreased decreased or
anuria
Urine sodium Decreased, Increased, Varies, often
<20mEq/L >40mEq/L <20mEq/L
Urinary Normal, few Abnormal Usually normal

Sediment hyaline casts casts
Characteristics Prerenal Intrarenal Postrenal
Urine osmolality Increased Abnormal Usually
to casts and normal
500mOms debris
Urine specific Increased Low normal, Varies
gravity 1.010
-associated problems:
*metabolic acidosis
*hyperphophatemia and hypocalcemia
*anemia
-prevention:
*prevention of exposure to nephrotoxic drugs
-aminoglycosides, cyclosporine,
amphotericinB
*serum BUN and creatinine monitoring
-management:
a. restore chemical balance and prevent
complications
b. identification and treatment of the underlying
cause
c. maintain fluid balance
-BP, CVP, serum and urine elect., fluid loses
d. monitoring for over hydration
-dyspnea, crackles, distended neck veins
-Furosemide, Ethacrynic Acid
e. dialysis
-to prevent serious complications
*hyperkalemia
*severe metabolic acidosis
*pericarditis
*pulmonary edema
f. pharmacologic
-cation exchange resin
(sodium polystyrene sulfonate-kayexalate)
-retention enema
-diuretic therapy
-low dopamine dose (1-3g/kg)
-phosphate binding agents (AlOH)
g. nutritional therapy
-give additional proteins (1g/kg/day during
the oliguric phase)
-high potassium and phosphate foods are
restricted (banana, citrus and coffee)
-potassium restricted to 20-40mEq/day
-sodium restricted to 2g/day
-may require parenteral nutrition
a. monitoring fluid and electrolyte balance
b. reducing metabolic rate
-bed rest, prevention of fever and infection
c. promoting pulmonary function
-assistance in changing positions
-advise to cough and deep breath
d. preventing infection
-asepsis
-avoid inserting an indwelling urinary
catheter
e. providing skin care
f. providing support
 Chronic Renal Failure
-is a progressive irreversible deterioration in renal
function
-with uremia or azotemia (severity of build up will be
proportional to the severity of s/sx)
-prognosis will be determined by the presence or
absence of hypertension and proteinuria
-causes:
*diabetes mellitus- most common
*hypertension
*chronic glomerulonephritis
*obstruction of the urinary tract
*polycystic kidney disease
*infections
- stages:
Stage 1
-Reduced Renal Reserve
-40%-75% loss of nephron function
-usually asymptomatic
Stage 2
-Renal Insufficiency
-75%-90% loss of nephron function
-increase in serum BUN and creatinine
-inability to concentrate urine
-anemia may develop
-with polyuria and nocturia
Stage 3
-End Stage Renal Disease
-<10% of nephron function remaining
-regulatory, excretory and hormonal
functions are lost
-requires dialysis
cardiovascular
*hypertension *pulmonary edema
*heart failure *pericarditis
dermatologic
*pruritus
*uremic frost (deposit of urea crystals)
GI and Neurologic s&sx
-assessment and diagnosis
a. glomerular filtration rate
creatinine clearance
b. serum electrolytes
c. ABG
d. CBC
-complications
a. Hyperkalemia
b. Pericarditis, Pleural Effusion and Cardiac
Tamponade
c. Hypertension
d. Anemia
e. Bone Disease
a. maintain kidney function and homeostasis
b. treat the underlying cause and contributory
factors
>medications >dialysis
>diet therapy
1. Pharmacologic Therapy
a. antihypertensives
> includes intravascular volume control
*fluid restriction
*sodium restriction
b. sodium bicarbonate
c. erythropoietin
>will achieve a Hct of 33%-38%
>IV or SC 3x a week
>takes 2-6 weeks to increase Hct
>A/R:
*hypertension
*increased clotting of vascular
access sites
*seizures
*depletion of body iron stores
d. iron supplementation
e. antiseizure agents
>Diazepam
>Phenytoin
f. antacids
>aluminum based antacids
neurologic symptoms
osteomalacia
>calcium carbonate
2. Nutritional Therapy
-regulation of protein intake
-regulation of fluid intake
(500-600ml more than the previous day’s 24
hour UO)
-regulation of sodium intake
-regulation of potassium
-adequate calories and vitamins
3. Dialysis
-to prevent hyperkalemia
a. avoid the complications of reduced renal
function
b. assess fluid status
c. identify potential sources of the imbalance
d. implement a dietary program
e. encourage self care and independence
Cardiovascular System
Definition of Terms
1. Preload – venous blood return; degree of stretch
of cardiac muscle fibers at the end of
diastole
2. Afterload – BP in artery; amt of resistance to
ejection of blood from ventricle
3. Depolarization – active; caused by entry of Na
while K exits cell
4. Repolarization – rest; caused by reentry of K to
the cell while Na exits
5. Systole – blood supply to all except the heart;
ventricular contraction from ejection of
blood from ventricles to pulmonary artery
and aorta
6. Diastole – blood supply to the heart; period of
ventricular relaxation resulting in
ventricular filling
7. Cardiac Output – blood volume per minute;
normal = 5L/min (resting adult heart)
8. Stroke Volume – blood volume per contraction;
normal = 70mL (resting heart)
9. Baroreceptors – nerve fibers located in the
aortic arch and carotid arteries that are
responsible for reflex control of BP
10. Postural/ Orthostatic Hypotension – result to
syncope (blood drops to brain = faint);
usually 10mmHg systolic or more
 Anatomy and Physiology
1. Heart Valves
2. Heart Chambers
3. Coronary Arteries
4. Cardiac Muscle
5. Cardiac Conduction System
6. Cardiac Hemodynamics
>Cardiac Pressures
*right ventricular systole *left ventricular systole
(15-25mmHg) (110-130mmHg)
*PA diastolic pressure *resting aortic pressure
(8-15mmHg) (80mmHg)
*4-12mmHg on both ventricles and atria at
the end of diastole
7. Cardiac Output
preload
afterload stroke volume
contractility
baroreceptors heart rate
 Gender Differences
1. resting rate
2. stroke volume higher in women
3. ejection fraction
4. conduction time is briefer in women
5. arteries occlude more easily in women with
atherosclerosis
6. effects of estrogen in cardiovascular system of
women
-regulation of vasomotor tone
-response to vascular injury
-good liver function
-increased coagulation proteins
-decreased fibrinolytic substances
 Diagnostic Work-ups
Purposes:
1. to aid in the diagnosis of diseases
2. for prognostication
3. to screen patients at risk of diseases
4. monitor serum concentration of meds
5. monitor therapeutic effects of meds
A. Cardiac Enzymes
>Creatine Kinase (CK)
*MB
-most specific enzyme for MI
-first enzyme level to rise in MI
*MM and BB
-other isoenzymes
>Lactate Dehydrogenase
-peaks 2-3days after MI
>Myoglobin
-starts to increase 1-3hours after MI; 4-12hours
(peak)
>Troponin I
-contractile proteins found in cardiac muscles
only
-starts to rise 3-4 hours after MI
-peaks in 4-24 hours and remain elevated for 1-3
weeks
B. Blood Chemistry
>Lipid Profile
*Total Cholesterol
-should be less than 200mg/dl
*Serum Lipoproteins
LDL - should be less than 130mg/dl
HDL - should be 35-65mg/dl in men
- should be less than 35 to 85mg/dl in F
TAG - should be 40-150mg/dl
Factors that may elevate TAG level:
1. obesity
2. alcohol use
3. diabetes
Factors that contribute variations in cholesterol level:
1. age 4. exercise 7. tobacco use
2. gender 5. genetics 8. stress level
3. diet 6. menopause
Factors that lower HDL level
1. smoking 4. physical inactivity
2. diabetes
3. obesity
>Serum Electrolytes
>BUN and Creatinine
>Serum Glucose Level
C. Coagulation Studies
>PTT
-effects of Heparin therapy
-intrinsic pathway
-1.5 to 2.5x of their baseline values
>PT
-effects of Warfarin therapy
-extrinsic pathway
-2.5-3.5x (INR)
D. Hematologic Studies
>CBC
-WBC monitoring in immunocompromised patient
after heart transplantation
-associated anemia will aggravate CAD
E. Chest X-Ray
-for the evaluation of the size, position and contour of
the heart
-cardiac and pericardial calcification
F. ECG
>Continuous ECG Monitoring
a. Hardwire Cardiac Monitoring
b. Telemetry
c. Transtelephoning
G. Cardiac Stress Testing
a. Exercise Stress Test
-by using a treadmill or stationary bike
b. Pharmacologic Stress Test
-by using Dipyridamole or Adenosine
c. Emotional Stress Test
Purposes of Cardiac Stress Test
>to evaluate CAD
>to determine the cause of chest pain
>to assess the functional capacity of the heart
after MI or surgery
>to evaluate the effectiveness of anti-anginal
drugs
>to evaluate dysrhythmias after physical exercise
>to determine specific goals for a fitness program
H. Echocardiography
-to determine:
a. pericardial effusions
b. etiology of heart murmurs
c. function of prosthetic heart valves
d. chamber size
e. ventricular wall motion
*Transesophageal Echocardiography
-with 6 hours of fasting prior
-IV line
-with local anesthetic and sedation
-BP and ECG monitoring
-after the study:
extension of fasting for another 4 hours
monitoring for 30 – 60 minutes
sorethroat for the next 24 hours
I. Radionuclide Imaging
>to evaluate:
a. coronary artery perfusion
b. myocardial ischemia and infarction
c. left ventricular function
>uses:
Thallium 201 emits gamma rays
Technetium 99m detected by scintillation
camera
>types:
a. Myocardial Perfusion Imaging
b. Computed Tomography
c. Positron Emission Tomography
d. Magnetic Resonance Imaging
J. Cardiac Catheterization
-catheter advancement guided by fluoroscopy
-to measure oxygen saturation and pressures on
right and left side of the heart
-needs:
a. IV line
b. BP and ECG monitoring
c. resuscitation equipment at bedside
-uses contrast agent (iodine based)
-complications: (right sided cardiac catheterization)
a. dysrhythmias d. cardiac perforation
b. venous spasm e. cardiac arrest
c. infection
-complications: (left sided cardiac catheterization)
a. dysrhythmias d. systemic embolization
b. MI
c. perforation
-nursing interventions (pre-op)
1. fasting for 8 – 12 hours
2. explain that the procedure will take 2 hours or
less
3. with mild to moderate sedation
4. explain the anticipated sensations (flushing,
5. ask the patient to breath deeply or hold the
breath
>to lower the diaphram for better
visualization
>ask the patient to cough
(to disrupt a dysrhythmia and to clear the
contrast agent from the arteries)
-nursing interventions (post-op):
1. observe the site for bleeding and hematoma
2. assess peripheral pulses on the same ext q
15mins for 4 hours then q 1 – 2 hours
3. evaluate temperature and color of the affected
extremity
4. ask the patient to report signs and symptoms
of arterial insufficiency (pain, numbness
and tingling)
5. monitor for dysrhythmias and vasovagal reaction
*bradycardia >may be
*hypotension precipitated by a
*nausea distended bladder
>prompt interventions:
-raise the feet and
legs
-administer IVF and IV
atropine
6. explain that the patient should be in supine
position for 2 – 6 hours
7. analgesics
8. report chest pain, bleeding and sudden
discomfort
9. increase fluid intake to flush out the dye
10. watch out for orthostatic hypotension
 Hemodynamic Monitoring
1. Central Venous Pressure
2. Pulmonary Artery Pressure
3. Intra-arterial BP Monitoring
Central Venous Pressure
-pressure in the vena cava or right atrium is used to:
a. assess right ventricular function
b. venous blood return to the right side of the
heart
-nursing interventions:
a. application of dry, sterile dressing
-should be dry and occlusive
b. chest x-ray to confirm placement
c. daily inspection for signs of infection
(complication)
d. watch out for air embolism (complication)
e. maintenance of the transducer in phlebotactic
axis
*normal range:
0 – 8 mmHg >>> Pressure Monitoring System
3 – 8 cmH2O >> Water Manometer System
Pulmonary Artery Pressure Monitoring
-assessment of left ventricular function
-etiology of shock
-response to vasoactive medications
-can measure:
1. CVP or right atrial pressure
2. pulmonary artery systolic and diastolic
pressure (25/9 mmHg)
3. Mean Pulmonary Artery Pressure (15mmHg)
4. Pulmonary Artery Wedge Pressure
(4.5 to 13 mmHg)
a. Maintenance of the transducer at phlebotactic
axis
b. Watch out for complications:
-infections
-pulmonary artery rupture
-pulmonary thromboembolism
-pulmonary infarction
-catheter kinking
-dysrhythmias
-air embolism
Intra-arterial BP Monitoring
-direct and continuous BP measurements
-ABG measurements
-to obtain blood samples
*after selection of an area (site)>> assess
collateral circulation
a. Allen’s test
b. Doppler test
a. observe asepsis
b. watch out for complications:
-local obstruction with distal ischemia
-external hemorrhage
-massive ecchymosis
-dissection
-air embolism
-blood loss
-pain
-arteriospasm
-infection
 Hypertension
-terms related:
>hypertensive emergency
>hypertensive urgency
>rebound hypertension
-types:
a. Primary Hypertension b. Secondary
Hypertension
-BP monitoring:
*normal BP >> recheck in 2 years
*high normal >> recheck in 1 year
*first stage >> confirm in 2 months
*second stage >> confirm in 1 month
*third stage >> confirm immediately
-as a sign
-as a risk factor
-as a disease
-risk factors:
a. smoking d. age older than 60 years
b. dyslipidemia e. gender (men)
c. diabetes mellitus f. family history of CVD
-hypothesis:
a. increased sympathetic activity
b. renin-angiotensin-aldosterone system
c. increased absorption of chloride
d. decreased vasodilation of arterioles
-complications:
a. myocardial infarction
b. heart failure
c. renal failure
d. stroke/ cerebro-vascular accident
e. impaired vision
-gerontologic considerations:
a. accumulation of atherosclerotic plaque
b. fragmentation of arterial elastins
c. increased collagen deposits
d. impaired vasodilatations
-diagnosis:
a. urinalysis f. creatinine clearance
b. blood chemistry g. renin level
c. 12-lead ECG h. 24 hour urine protein
d. chest x-ray
e. echocardiography
b. dietary therapy
a. patient education
>avoid risk factors
>promote healthy lifestyle
 Peripheral Arterial Occlusive Disease
-usually involves the segment of the aorta below the
renal artery to the popliteal artery
-risk factors:
a. age (elderly)
b. diabetes mellitus
a. intermittent claudication
b. coldness or numbness of the affected extremity
c. skin and nail changes
d. ulcerations and gangrene
e. bruits
f. diminished to absent peripheral pulses
g. muscle atrophy
*Pentoxyphylline
-increases RBC flexibility and
decreases blood viscosity
*Cilostazol
-inhibits platelet aggregation
-increases vasodilatation
-inhibits smooth muscle proliferation
*Aspirin, Ticlopidine, Clopidogrel
-antiplatelets
b. surgical management:
vascular grafting
endarterectomy
a. maintain circulation
*doppler
*pulses
*color q 1 hour x 8 hours
*temperature q 2 hours x
*capillary refill 24 hours
*motor and sensory
b. monitoring for potential complications
*urine output
*CVP & PR
*mental status
*hematoma
c. avoidance of leg crossing or dependency of
the lower extremity
d. reduce edema -elevate the affected
extremity
-exercise
e. stockings
-may not be necessary
 Upper Extremity Arterial Occlussive Disease
-due to:
a. atherosclerosis
b. trauma
-clinical management:
a. forearm claudication
b. poor motor function
-diagnosis
a. difference of 20mmHg of BP between 2 arms
b. duplex ultrasonography
c. transcranial doppler evaluation
-management:
a. surgery
*PTA
*carotid to subclavian artery bypass
*axillary to axillary bypass
*autogenous reimplantation of the
subclavian to carotid artery
 Aneurism
 Aortic Dissection
 Raynaud’s Phenomenon
 Deep Vein Thrombosis
Venous thrombosis
Thrombophlebitis/ Phlebothrombosis
-of unknown cause
-with predisposing factors:
(Virchow’s triad)
A. stasis of blood
>heart failure >vasodilators
>shock >immobility
B. vessel wall injury
>trauma >chemical irritation
C. altered blood coagulation
>abrupt withdrawal from anticoagulants
>OCP
>severe blood dyscrasias
-manifestations:
a. nonspecific
b. phlegmasia cerulea dolens
>massive iliofemoral venous thrombosis
>entire extremity is massively swollen,
tense, painful and cool to touch
*deep vein involvement
-edema of the affected extremity
-affected extremity is warmer to touch
-tenderness
*superficial vein involvement
-pain -redness
-tenderness -warmth
-assessment
a. history
>varicose veins >obese
>hypercoagulation >elderly
>neoplastic disease >OCP
>cardiovascular disease
>recent major surgery
b. physical assessment
-prevention
a. application of elastic compression stockings
b. use of intermittent pneumatic compression
device
c. positioning
d. exercise
-medical management
1. anticoagulation therapy
a. unfractionated heparin
-sc or iv (intermittent infusion) for 5-
7days
-given with Warfarin
-coagulation study monitoring
b. low molecular weight heparin
-with longer half life
-can be used in pregnant women
-less toxic
c. thrombolytic therapy
-alteplase, reteplase, t-PA
streptokinase
-should be given within the first three
-effects less significant after 5 days
-surgical management
>when pharmacologic therapy is contraindicated
a. thrombectomy
b. vena cava filter
-nursing management
a. assessing and monitoring anticoagulant
therapy
b. monitoring and managing potential
complications
>bleeding
>thrombocytopenia
>drug interactions
c. provide comfort
>bed rest
>elevation of the leg
>elastic compression stockings
>analgesics
>application of warm moist packs
d. intermittent pneumatic compression devises
>with 35 to 55 mmHg
e. positioning
>feet higher than the heart
f. exercises
>passive then active exercises
>deep breathing exercises
>early ambulation
*avoid sitting for more than 2 hours
*walking for at least 10minutes every
after 2 hours
 Varicose Veins
-abnormally dilated, tortuous, superficial veins
caused by the incompetent venous valves
-may occur in the lower extremities and esophagus
-predisposing factors
>old age
>pregnancy
>prolonged standing
>genetic predisposition
-has 2 types:
a. primary
-without involvement of the deep veins
b. secondary
-resulting from the obstruction of the deep
veins
-manifestations
>dull aches >increased muscle
>muscle cramps fatigue
>ankle edema
>feeling of heaviness
-assessment
a. duplex scan
b. air plethysmography
c. venography
-prevention
a. avoidance of wearing tight socks or
constricting panty girdle
b. avoidance of crossing the thighs
c. avoidance of prolonged standing
d. frequent position changes
e. elevating the affected extremity when tired
f. walking 1 to 2 miles each day
g. using the stairs instead of elevators
h. elastic compression stockings
i. weight reduction planning
-management
>surgery
>sclerotherapy
-with application of elastic compression
bandages for 5 days
Acquired Valvular Disorders
 Mitral Valve Prolapse
-usually produces no symptoms
-mostly in women
-mitral valve balloons back into the left atrium during
systole
-asymptomatic -palpitations
-shortness of breath -syncope
-light headedness -chest pain
-dizziness -anxiety
-diagnosis:
-mitral clicks
-murmur of mitral regurgitations
a. symptomatic
b. elimination of stimulants
c. anti-arrhythmic meds
d. beta blockers/ calcium channel blockers
a. condition can be genetically transmitted
b. use of prophylactic antibiotics
-for patients with systolic click and a
murmur
c. instruct to avoid stimulants
d. diet, activity and sleep
 Mitral Regurgitation
a. chronic- asymptomatic
b. acute - severe congestive heart failure
dyspnea
fatigue most common symptoms
weakness
palpitations
shortness of breath on exertion
cough
-diagnosis:
a. systolic murmur
b. echocardiography
similar to congestive heart failure
 Mitral Stenosis
-causes
rheumatic endocarditis
>dyspnea on exertion
>fatigue (low cardiac output)
>hemoptysis
>cough
-diagnosis:
>weak pulses
>diastolic murmur
-low pitched rumbling sound at the apex
>echocardiography
>ECG and cardiac catheterization with
angiography
-to determine the severity of mitral stenosis
a. prophylactic antibiotics
b. anticoagulants
c. treatment of CHF
d. surgery
-valvuloplasty
-valve replacement
 Aortic Regurgitation
-causes:
>endocarditis
>syphilis
>dissecting aneurism
>deterioration of an aortic valve replacement
>asymptomatic
>forceful heart beat (head and neck)
exertional dyspnea and fatigue
signs of left ventricular failure
-diagnosis:
>diastolic murmur (high pitched blowing sound)
>widened pulse pressure
>water hammer pulse
>echocardiography, ECG, MRI and cardiac
catheterization
a. antibiotic prophylaxis
b. valvuloplasty or valve replacement
 Aortic Stenosis
-cause:
*rheumatic endocarditis
>asymptomatic
>exertional dyspnea
>dizziness due to left ventricular
failure
>syncope
>chest pain
-diagnosis:
>systolic murmur
-loud, rough
-crescendo-decrescendo
>12 lead ECG

> echocardiography
-management:
a. antibiotic prophylaxis
b. valvuloplasty
c. valve replacement
Cardiac Dysrhythmias
 Sinus Node Dysrhythmias
1. Sinus Bradycardia
-causes:
*lower metabolic needs (hypothyroidism, hypothermia,
sleep)
*vagal stimulation (vomiting, suctioning, extreme pain)
*medications (calcium channel blockers, beta blockers)
*increased intracranial pressure
*myocardial infarction
-treatment:
*atropine sulfate
*catecholamines
2. Sinus Tachycardia
-causes:
*acute blood loss *pain
*anemia *hypermetabolic state
*shock *fever
*hypervolemia *anxiety
*hypovolemia *sympathomimetic meds
*congestive heart failure
-decreased diastolic filling
decreased cardiac output
-syncope -acute pulmonary edema
-decreased BP
-management:
a. Ca channel blockers
b. Beta blockers
3. Sinus Arrhythmias
-no significant hemodynamic effects
-not treated usually
 Atrial Dysrhythmias
1. Premature Atrial Complex

-begins before the next impulse of the SA node
-causes:
>caffeine, alcohol
nicotine
>stretched atrial myocardium
>anxiety
>hypokalemia
>hypermetabolic state
>atrial ischemia, injury or infarction
-management:
>directed toward the cause
2. Atrial Flutter
-only at the atrium at a rate of 250-400/minute
-therapeutic block at the AV node
-causes:
>advanced age >hypertension
>valvular heart disease >cardiomyopathy
>coronary artery disease >hyperthyroidism
>pulmonary disease
>acute moderate to heavy ingestion of alcohol
(holiday heart syndrome)
>aftermath of open heart surgery
*chest pain *low BP
*shortness of breath
-management:
>electrical cardioversion
>if stable
-digitalis
-beta blockers
-calcium channel blockers
3. Atrial Fibrillation
-rapid, disorganized and uncoordinated twitching of
atrial musculature
-with decreased stroke volume
-with decreased diastole >> decreased coronary
artery perfusion >> increase the risk of myocardial
ischemia
-increased risk of thrombus formation within the atria
>> embolism
-2 to 5x increased risk of stroke
-same causes as with atrial flutter
-s/sx:
*irregular palpitations *malaise
-treatment:
>same as with atrial flutter
>cardioversion (if present in less than 48 hours
unless the patient is on anticoagulant
treatment)
>anti-arrhythmic meds:
-amiodarone, flecainide, ibutilide
>adenosine (treatment and diagnosis)
>pacemaker insertion
 Ventricular Dysrhythmias
1. Premature Ventricular Complex

-an impulse that starts at the left ventricle and is
conducted through the ventricles before the next
normal sinus impulse
-causes:
*caffeine, nicotine and alcohol
*cardiac dysrhythmias and infarction
*increased workload to the heart (exercise,
fever, hypervolemia, heart failure,
tachycardia)
*digitalis toxicity
*hypoxia, acidosis
*electrolyte imbalances (hypokalemia)
-with danger of ventricular tachycardia if with MI
-bigeminy, trigeminy…
>asymptomatic
>with skipped beats
-treatment:
>treat the cause
Lidocaine- short term and immediate therapy
2. Ventricular Tachycardia
-3 or more PVCs in a row occurring at a rate
exceeding 100 beats/minute
-causes are similar to PVCs
-usually associated with CAD preceding to PVC
-an emergency: pulseless and unresponsive
-treatment:
>if stable:
-attach to ECG
>if unstable:
-cardioversion or defibrillation
3. Ventricular Fibrillation
-rapid but disorganized ventricular rhythm
-no atrial activity
-causes:
>electrical shock
>brugada syndrome
-normal heart, few or no risk factor for
CAD, and a family history of sudden
cardiac death
>no heartbeat
>no pulse
>no respiration
-management:
>immediate defibrillation
>vasoactive meds
>anti-arrhythmic meds
4. Ventricular Asystole
HEMATOLOGY
Hematologic System
1. Blood 2. Reticulo-endothelial
a. Plasma -liver
-albumin -spleen
-globulin -bone marrow
-fibrinogen
-electrolytes
-waste products
b. cellular component
-RBC
-WBC
-platelets
 Functions of the blood
a. carrier
-oxygen and nutrients
-waste products
b. hemostasis
 Hematopoiesis
a. intramedullary
b. extramedullary
 RBC
-approximately 8 micrometers
-flexible, can pass through a small blood vessel
-made up of hemoglobin (95% of cell mass)
 Erythropoietin
-response to low RBC count
-stimulate the BM
-for erythropoiesis
>requires iron, folic acid, pyridoxine and
cyanocobalamin
 Iron Stores and Metabolism
-diet:
>10-15 mg of elemental iron/day in a well
balanced diet
>only 0.5 to 1 mg is absorbed >> transferrin >>
normoblast >> hemoglobin
-total body iron content:
>3 grams
-normal concentration value:
>75-175ug/dl for males
>65-165 ug/dl for females
 Vitamin B12 and Folic Acid Metabolism
-required in the synthesis of DNA

ANEMIA
3 Broad Causes:
1. loss of RBC
2. inadequate production
3. increased destruction
1. Types of Anemia due to decreased production of
RBC
a. Iron Deficiency Anemia C. Folate Deficiency
b. Vitamin B12 deficiency D. Dec. Erythropoietin
2. anemia due to blood loss
3. Types of anemia due to increased destruction
(hemolytic)
a. altered erythropoiesis
>sickle cell anemia
>thalassemia
>hemoglobinopathies
b. hypersplenism
c. drug induced anemia
d. autoimmune anemia
 Clinical manifestations:
(fatigue- most common)

>severity depends on:
1. speed with which anemia has developed
2. duration of anemia
3. metabolic requirements of the individual
4. presence of other disorders
 Complications:
1. Congestive Heart Failure

2. Paresthesia
3. Confusion
 Nursing Diagnosis:
1. Activity Intolerance related to Fatigue, Weakness and

Generalized Malaise
2. Altered Nutrition: Less than body Requirements
related to Inadequate Intake of Essential Nutrients
3. Altered Tissue Perfusion r/t Inadequate Blood Volume
 Nursing Interventions:
1. Managing fatigue
-the most frequent symptom and complication
-profound impact on ones level of functioning and
quality of life
2. Maintain adequate nutrition
-well balanced diet
-avoidance of alcohol
-dietary teaching
-dietary supplements
3. Maintain adequate perfusion
-transfusion
-supplemental oxygen/vital signs monitoring
4. Complying with prescribed therapy
5. Monitoring and managing potential complications
a. CHF
b. paresthesia
c. confusion
Hypoproliferative Anemias
 Iron Deficiency Anemia
-causes:
>decreased dietary intake of iron
>blood loss
*menorrhagia
*PUD (alcoholics)
>smooth, sore tongue
>brittle and ridged nails
>angular cheilosis
-diagnosis:
a. BMA
b. serum ferritin/TIBC
c. peripheral blood smear (dec MCV)
d. CBC (dec Hgb and Hct)
-management:
a. Iron supplementation
(Ferrous SO4, Ferrous Fumarate or Ferrous
Gluconate)
-should be taken for 6-12 months
*if oral iron preparation is not tolerated, give
iron dextran (IM or IV)
-Nursing Management:
1. Diet
-should take foods rich in iron
*organ meats *green leafy vegetables
*beans *raisins
-should take foods rich in vitamin C
-take iron with an empty stomach
-if with GI distress, take with food (but absorption
will be decreased by 50%)
-liquid oral iron preparation
 Anemia in Renal Disease
-ESRD:
>less likely to develop unless serum creatinine
exceeds 3mg/dl
-Dialysis:
>may lose blood into the dializer >> folic acid
deficiency and iron deficiency
-Management:
1. Recombinant Erythropoietin
>A/R: HPN- may inc Hct by 33-38%
(dose needs to be titrated and administer anti-
HPN)
2. Oral iron and folic acid supplementation
 Anemia of Chronic Diseases
-due to chronic disease of inflammation, infection
and/or malignancy
-mild to moderate anemia
-insidious onset over a period of 6-8 weeks
-Hct seldom less than 25%
-Hgb seldom less than 9 g/dl
-erythropoietin levels are low
-moderate shortening of the RBC lifespan
-management:
>no need
>treatment of the underlying cause
 Aplastic Anemia
-may lead to pancytopenia
-damage to the BM stem cells
-replacement of the marrow with fat
-also has neutropenia and thrombocytopenia
-forms:
>congenital >idiopathic
>acquired
-clinical manifestations: (insidious onset)
>infection
>anemia
>bruising
-causes:
1. chemicals
-pesticides
-glue
2. medications
-antimicrobials (Chloramphenicol)
-gold compounds
-sulfonamides
-assessment and diagnosis:
1. BMA
1. BM transplant or Peripheral Stem Cell Transplant
2. Immunosuppressive therapy
3. Withdrawal of the offending agent
4. RBC and platelet transfusion
 Megaloblastic Anemia
-may lead to pancytopenia
-due to vitamin B12 and Folic Acid Deficiency
(abnormal DNA synthesis)
-Hgb may be as low as 4-5 gm/dl
-WBC count may be as low as 2000-3000/mm3
-platelet count of less than 50000/mm3
-RBC (increase in MCV)
 Folic Acid Deficiency
-causes:
*depletion in 4 months time without sufficient
folic acid in the diet (green leafy vegetables and
liver)
*increased folic acid requirement (pregnancy,
alcoholism and chronic blood loss)
 Cyanocobalamin deficiency
-causes:
*strict vegetarians (no meat or dairy products)
*absence of intrinsic factor
*faulty absorption in the ileum
Clinical manifestations:
a. Hemolytic s/sx
-unique to vit B12 def
b. GI and Nervous system effects
Assessment and Diagnostic Findings:
a. Schilling Test
a. increase folic acid in the diet and take 1 mg of
folic acid daily (IM for patients with
malabsorption)
b. Vit B12 replacement
-oral supplements
-fortified soy milk
*if with intrinsic factor deficiency and
malabsorption, monthly IM injection of
cyanocobalamin at a dose of 1000ug
a. mild jaundice
b. vitiligo
c. premature graying of the hair
d. smooth, red and sore tongue
e. unstable gait
f. impaired position and vibration sense
 Myelodysplastic Syndrome
-is a group of disorder of myeloid stem cells causing
dysplasia of one or more cell types
-most common feature is the dysplasia of the RBCs
>> macrocytic anemia (WBC & platelets may be
affected)
-may evolve into Acute Myeloid Leukemia
-types:
a. Primary
>more than 80% (elderly)
b. Secondary
a. variable
a. CBC
>RBC, WBC & platelets are decreased
b. decreased serum erythropoietin
a. bone marrow transplantation
b. blood transfusion (needs chelation of iron)
c. platelet transfusion
d. growth factors (G-CSF)
e. erythropoietin
1. prevention of infection
2. instructions on the risks of bleeding
*chelation therapy is best administered as a
subcutaneous infusion over 10-12 hours often at
night
*close monitoring of lab values for anticipation of
transfusion and determination of response to
growth factors
Hemolytic Anemias
 Sickle Cell Anemia
-a result of inheritance of sickle hemoglobin gene
-sickled Hgb
*crystal formation when exposed to low oxygen
tension, deformed, rigid and sickled RBC >
ischemia & infarction
-sickling process is intermittent (with exposure to low
oxygen tension and cold environment)
-assessment and diagnostic findings
>sickle cell trait:
*normal RBC
*normal WBC
*normal platelets
>sickle cell anemia
*decreased Hct
*sickled cells on smear
-confirmatory test:
Hemoglobin electrophoresis
*Hgb 7-10mg/dl
*jaundice
*enlargement of the bones of the face and the skull
*tachycardia, cardiac murmurs and enlarged heart
*dysrhythmias and heart failure
*susceptible to infection primarily pneumonia and
osteomyelitis
*chronic hemolysis and thrombosis >> ischemia and
necrosis of organs with slowed circulation (spleen,
lungs and CNS)
-complications:
1. stroke
2. infection
3. renal failure
4. impotence
5. heart failure
6. pulmonary hypertension
Sickle Cell Crisis
-3 types:
1. Very painful sickle cell crisis
> due to tissue hypoxia and necrosis
2. Aplastic crisis
> due to infection of human parvovirus
> Hgb decreases rapidly that the BM cannot
compensate
3. Sequestration Crisis
>pooling of sickled cells in an organ
*spleen >> splenic infarction >>
autosplenectomy
Acute Chest Syndrome
-decreased hemoglobin and hematocrit (rapid)
-fever
-tachycardia
-bilateral chest film infiltrate
-causes: -diagnostic tests:
*infection *CXR
*fat embolism *incentive spirometry
-treatment: *bronchoscopy
*antibiotics *phospholipase A2 det
*fluid restriction
*corticosteroid
*transfusion
>decreases phospholipase A2
-prognosis:
>usually diagnosed during childhood
>3 treatment modalities:
a. BM transplantation
b. Hydroxyurea
*increases the concentration of fetal Hgb
*decreases vaso-occlusive crisis
c. Long term RBC transfusion
Adverse Effects of Hydroxyurea
1. chronic suppression of WBC formation
2. teratogenesis
3. potential for later development of pregnancy
Complications of Transfusion
1. Iron Overload
-needs chelation therapy
2. poor venous access
3. alloimmunization due to repeated transfusion
*exchange transfusion
Treatment:
1. Supportive
>pain management
*folic acid supplementation
2. Prompt use of antibiotics
-nursing diagnosis:
1. Pain related to tissue hypoxia
2. Risk for infection
3. Powerlessness related to illness induced
powerlessness
4. Knowledge deficit regarding prevention of crisis
-goals:
1. Relief of pain
2. Decreased incidence of crisis
3. Enhanced self esteem and power
4. Absence of complications
1. Management of pain
2. preventing and managing infections
3. promoting coping skills
4. Minimizing knowledge deficit
5. Monitoring and managing potential complications
-leg ulcers
-priapism leading to impotence
-chronic pain and substance abuse
 Thalassemias
-a hereditary disorder associated with defective

hemoglobin chain synthesis
-characterized by microcytosis and hypochromia
-imbalance in the configuration of hemoglobin >>
increased rigidity of RBC >> hemolysis
-2 types:
(according to the globin chain diminished)
a. alpha thalassemia
-milder and often without symptoms
b. beta thalassemia
-more severe and lethal
Alpha Thalassemia
 Clinical Syndromes:
1. Silent Carrier
-asymptomatic
-deletion of a single alpha globin gene
-barely detectable reduction in alpha globin gene
synthesis
2. Alpha Thalassemia Trait
-deletion of 2 globin gene
-minimal or no anemia and no abnormal physical
signs
3. Hemoglobin H Disease
-deletion of the 3 out of 4 alpha globin gene
-hemoglobin H has extremely high O2 affinity
and therefore not useful for O2 exchange
-with moderately severe anemia
4. Hydrops fetalis
-most severe form
-deletion of the 4 alpha globin gene
-in the fetus > gamma globin chains in excess
form tetramers (hemoglobin Bart) > extremely
increased oxygen affinity > unable to deliver
oxygen to the tissues > severe anoxia
Beta Thalassemia
 Clinical Syndromes:
1. Thalassemia Major
-lead to severe transfusion dependent anemia
-severe anemia and first become manifested 6-
9mos after birth (hemoglobin synthesis switches
from HgbF to HgbA)
-if untransfused, Hgb may range between 3-
6gm/dl (with marked anisocytosis and microcytic,
hypochromic anemia)
-aggregated alpha chains are taken up by the spleen
-increased reticulocytes but erythropoiesis is
ineffective
-clinical course:
short or brief because of death at an early age
2. Thalassemia Minor
-resistant against falcifarum malaria
-asymptomatic and anemia is mild if present
 G6PD Deficiency
(G6PD is essential for membrane stability)
-would result to chronic hemolytic anemia
-hemolysis only when under stress, infection or due
to the use of certain medications (oxidant
drugs)
-inherited as X-linked disease
-oxidant drugs:
>anti-malarial agents
>sulfonamides
>nitrofurantoin
>analgesics (ASA, Phenacetin)
>thiazides
>chloramphenicol
>para-amino-salisylic acid
>vitamin K
>s/sx of hemolysis
*reticulocytosis *jaundice
*hemoglobinuria *pallor
-presence of Heinz bodies (taken up by the
spleen)
-assessment and diagnostic findings:
>qualitative assay for G6PD
a. withdrawal of the offending agent
b. transfusion
-only in severe hemolytic states
c. health education
-avoid triggering factors
 Hereditary Spherocytosis
-Is also a type of hemolytic anemia
-Abnormal permeability of RBC membrane >
spherocytosis > taken up by the liver > hemolysis
-treatment:
>surgical removal of the spleen (splenectomy)
 Immune Hemolytic Anemia
-due to exposure of RBCs to antibodies
formation of alloantibodies
destruction of RBCs
(intravascular hemolysis)
-usually result from hemolytic transfusion reactions
-RBCs may be destroyed also because of poor level
of suppressor lymphocytes > antibody formation
(IgG)
-2 types:
1. warm body antibodies
>bind to RBCs most active in warm conditions
>most common (IgG usually but sometimes IgA)
>mostly extravascular
2. Cold-body Antibodies
>react in cold environment
>usually IgM
>usually occur acutely during recovery from viral
infections, chronically with lymphoproliferative
disorder
>self limited intravascular hemolysis
(variable depending on the severity)
a. splenomegaly in 80% of cases
b. hepatomegaly
c. lymphadenopathy
d. jaundice
a. CBC
-decreased Hgb and Hct
b. peripheral blood smear
-increased reticulocytes
c. serum chemistry
-increased serum bilirubin
a. withdrawal of the offending agent
b. increased doses of corticosteroids (1
mg/kg/day)
c. blood transfusions
-slowly and cautiously (10-15ml for 20-
30mins)
d. splenectomy
e. immunosuppressive therapy
-if splenectomy and steroids fail
-cyclophosphamide (more rapid effect but
more toxic)
-azathioprine (less rapid effect but less
toxic)
f. Immunoglobulin administration
a. prevention of infection
*after splenectomy; during steroid and
immunosuppressive therapy
 Hereditary Hemochromatosis
-deposition of excessive iron in the liver,
myocardium, testes, thyroid and pancreas
-women are less affected than men
a. weakness
b. lethargy
c. arthralgia
d. weight loss
e. loss of libido
f. skin hyperpigmentation
g. cardiac dysrrhythmias and cardiomyopathy >
edema and dyspnea
h. endocrine involvement
*hypothyroidism *diminished libido
*hypogonadism
may lead to Hepatocellular Carcinoma
-diagnosis:
a. liver biopsy
-definitive test
a. therapeutic phlebotomy
-removing whole blood from a vein
-every 1–3 year period
a. diet low in iron is not that important
b. prevent liver injury such as alcoholism
c. alpha feto-protein determination
-serial screening test for hepatoma
d. monitor for signs and symptoms of organ
dysfunction
Polycythemia
 Polycythemia Vera or Primary Polycythemia
-may lead to Acute Myeloid Leukemia

-myeloid stem cells have escaped normal control
mechanisms
-Increased RBC count (predominating sign)
involvement of the spleen in hematopoiesis
fibrosis of the bone marrow
(burnt or spent phase)
>ruddy complexion
>splenomegaly
>pruritus (due to histamine)
>headache
>dizziness
>tinnitus due to an increased
>paresthesias blood volume
>fatigue
>blurred vision
>angina
>claudication due to increased blood
>dyspnea viscosity
>thrombophlebitis
>erythromyalgia - burning sensation of the
fingers and toes
1. increased RBC mass (nuclear medicine
procedure)
-normal in erythropoietin
2. normal oxygen saturation level
3. enlarged spleen
-other signs:
1. increased WBC and Platelet count
2. increased vitamin B12
3. increased alkaline phosphatase
-complication
1. thrombosis - may lead to stroke or MI
2. bleeding
1. therapeutic phlebotomy
>500ml once or twice weekly
>to reduce the blood cell mass
2. radioactive phosphorus
>to suppress marrow function but may
increase the risk of leukemia
1. patient education
>avoid Aspirin to decrease the risk
>minimize alcohol of bleeding
>cool or tepid water bath
-for itchiness
-antihistamines are not effective
 Secondary Polycythemia
-due to excessive production of erythropoietin
as a reaction to:
>smoking
>COPD
>cyanotic heart disease
>increased altitude
1. Therapeutic Phlebotomy
Leukopenia and Neutropenia
-may result from:
*ionizing radiation
*long term use of steroids
*uremia
*neoplasms
-diagnosis:
Absolute Neutrophil Count
= % neutrophils + % bands X total WBC count
100
infections
1. withdrawal of the offending agent
2. corticosteroids
3. withholding or decreasing the dose of chemotherapy
or radiotherapy
4. culture of blood, urine and sputum; CXR > monitoring
1. infection control
Bleeding Disorder
-vascular in origin >> localized
-platelets or coagulation factor defects >>
widespread
 Primary Thrombocythemia
-also called essential thrombocythemia

-stem cell disorder in the bone marrow
-platelet count >> 600,000/mm3
>> size is abnormal
increased RBC
increased WBC
>usually asymptomatic
>hemorrhage or vasooclusion of the microvasculature
>painful, burning, warmth and redness on the localized
area of the extremity (due to an increased platelet ct.)
-diagnosis:
>CBC and other blood tests
(not necessary to perform BMA and biopsy)
*median survival is 10 years
-medical management: (controversial)
1. Low Dose Aspirin
-in young patient without aggravating factors like
atherosclerosis, smoking and peripheral vascular disease
2. Hydroxyurea
-chemotherapeutic agents to lower down the platelet
count
Anagrelide
-more specific than Hydroxyurea
-side effects: severe headache
Alpha Interferon
-lower the platelet count by unknown mechanisms
-sc 3x a week
-very expensive
-side effects:
>fatigue >dizziness
>weakness >anemia
>memory defects >liver dysfunction
3. Platelet Pheresis
-to reduce platelets with transient effects
1. Patient education
>risk of bleeding and thrombosis
>signs of bleeding and thrombosis (visual
changes, tingling and weakness)
 Secondary Thrombocytosis
-increased platelet production

-an increase above 1 “M” count is rare
-platelet function is normal
>survival time is normal or increased
-triggering factors:
>chronic inflammatory disorders
>iron deficiency >acute hemorrhage
>malignant disease >splenectomy
 Idiopathic Thrombocytopenic Purpura
-affects all ages
-more common to children and women
-2 types:
a. acute
>predominantly in children
>often 1-6 weeks after a viral illness
>self-limited (remission within 6 months)
b. chronic
-hypothetical causes:
a. exposure to sulfa drugs, quinine
b. SLE
c. pregnancy
d. autoimmunity
a. platelets
>less than 20,000/mm3 or even less than
5,000/mm3
b. bruising, heavy menses and petechiae on the
extremities and trunk
*2 types of purpura
a. dry purpura
-simple bruising or petechiae
-tend to have fewer complications
b. wet purpura
-GIT bleeding
-hemoptysis
-intracranial bleeding
decreased platelet count
decreased megakaryocytes
-management:
a. safe platelet count
-risk of bleeding starts at a platelet count of
10,000/mm3 and below
b. withdrawal of the offending agent
c. immunosuppressive therapy
to inc -mainstay of short term treatment
plt ct -to block the binding receptors in
macrophages
*Prednisone 1mg/kg
-effective in 75% of cases
-can be used also for maintenance at a dose
of 2.5 to 10mg QOD
*Cyclophosphamide
*Azathioprine
*Dexamethasone
*Vincristine
d. intravenous immunoglobulin
-binding the receptors on the macrophages
-1g/kg for 2 days (very expensive)
e. splenectomy
-effective in 50% of cases
-at risk of sepsis (should receive vaccines)
*Pneumovax should be given
*Haemophilus influenzae B within 2-3 wks
*Meningococcal vaccines prior to proc
a. history taking
-viral infection
-intake of sulfa containing drugs
b. neurologic assessment
-in addition to physical examination
-vital signs: don’t use the rectal route
c. patient education
-s/sx of bleeding
-whom to contact in case of emergency
-avoidance of sulfa containing drugs
-compliance to pharmacologic therapy (tapering)
-frequency of monitoring the platelet count
d. avoid the risk of bleeding
-no constipation
-use electric razors only
-use soft bristled tooth brush
-refrain from vigorous sexual intercourse
e. education of the disadvantages of corticosteroid
treatment
-osteoporosis should receive Ca
-proximal muscle wasting and vit D
-dental caries supplements
-cataract formation
Pulmonary Disorders
 Acute Respiratory Distress Syndrome
-characteristics: (in the absence of LV Failure)
*sudden or progressive pulmonary edema
*increasing bilateral infiltrates on CXR
*hypoxemia refractory to oxygen
supplementation
*reduced lung compliance
-with a high mortality rate as high as 50-60%
-multiple organ system failure with sepsis (most
common cause of death)
acute lung injury
alveolar capillary leak
microvascular a. pulmonary edema surfactant

obstruction b. hyaline membrane defect
c. microatelectasis decreased
V/Q mismatch compliance
right to left shunt
pulmonary hypertension dyspnea
hypoxemia
increased dead space increased work of
increased minute ventilation breathing
-causes:
*aspiration (gastric acid)
*drug ingestion and overdose
*hematologic disorders
-DIC, massive transfusion
*prolonged inhalation of high concentrations of
O2, smoke or corrosive substance
*localized infection
*metabolic disorders (pancreatitis)
*shock
*major surgery
*fat or air embolism
*sepsis
*rapid onset of dyspnea
-12 to 48 hours after the initiating event
*arterial hypoxemia not responsive to O2 therapy
*pulmonary edema
-quickly worsen
-assessment and diagnostics:
*history and physical exam
-retractions and crackles
*CXR
*pulse oximetry
*ABG
-management:
a. identification and treatment of the underlying
condition
b. aggressive, supportive care
-intubation and mechanical ventilation
c. circulatory support
-IVF
d. nutritional support (35-45kcal/kg/day)
e. O2 inhalation
f. PEEP (positive end expiratory pressure)
-critical in ARDS
-improves the oxygenation
-increase the functional residual capacity
h. pharmacologic therapy
-interleukin-1 receptor antagonist
(anakinra)
-neutrophil inhibitors
-pulmonary specific vasodilators
-surfactant replacement therapy
-antisepsis therapy
-antioxidant therapy
-corticosteroids
a. close monitoring
b. respiratory modalities
-O2 inhalation, nebulizer therapy, chest
physiotherapy, ET intubation, suctioning,
mechanical ventilation and bronchoscopy
c. positioning
-to improve ventilation
d. reduce anxiety and agitation
-explain all procedure and provide care in a
calm and reassuring manner
e. continuous assessment (ventilator setting)
-presence of tube blockade by kinking or
retained secretions
-acute respiratory problems (pneumothorax)
-sudden hypoxemia
-ventilator malfunction
f. sedation
-to decrease the patient’s O2 consumption
-to allow the ventilator provide full respiratory
support
-to decrease anxiety
g. administration of neuromuscular blocking agents
-alternative to sedation
 Acute Respiratory Failure

-is a sudden life threatening deterioration of the gas
exchange function of the lung
-fall in arterial oxygen tension to less than 50mmHg and
a rise in CO2 tension to more than 50mmHg and
with an arterial pH of less than 7.35
-mechanisms:
*alveolar hypoventilation *V/Q mismatch
*diffusion abnormalities *shunting
-causes:
a. decreased respiratory drive
-severe brain injury
-brainstem lesions
-use of sedatives
-metabolic disorders (hypothyroidism)
b. dysfunction of the chest wall
-diseases of the muscles, nerves, spinal
cord and neuromuscular junction
c. dysfunction of the lung parenchyma
-pleural effusion
-upper airway obstruction
-pneumothorax
*all related to hypoxemia and hypoxia
restlessness dyspnea
fatigue air hunger
headache tachycardia and inc BP
confusion, lethargy, tachycardia,

tachypnea, central cyanosis
respiratory arrest
-management:
a. correct the underlying cause
b. restore adequate gas exchange (ET with
ventilator)
surfactant replacement therapy
antiseptic agents
antioxidant therapy
corticosteroids
c. nutritional therapy
 Chronic Obstructive Pulmonary Disease
-airflow limitation not fully reversible

-types:
a. chronic bronchitis
b. emphysema
A. Chronic Bronchitis
-cough with sputum for at least 3 months in each of
2 consecutive years
Smoke/environmental pollutants
Hypersecretion of mucus and inflammation
B. Emphysema
Destruction of the walls of distended alveoli
Impaired gas exchange
-2 types:
1. panlobular
>respiratory bronchiole, alveolar duct and alveoli are
destroyed
2. centrilobular
>destruction of the center of the secondary lobule
-risk factors:
1. environmental
>cigarette smoking
>prolonged and intense exposure to
occupational dusts and chemicals
>indoor air pollution
>outdoor air pollution
2. host
>alpha-1-antitrypsin deficiency
-3 primary symptoms:
a. cough
b. sputum
c. dyspnea on exertion
>spirometry
-complications:
a. respiratory failure
b. respiratory insufficiency
a. risk reduction
b. pharmacologic therapy
*bronchodilators
>MDI
>nebulization
>oral (pill or liquid)
beta adrenergic agonist
anticholinergic agents
methylxanthines
*corticosteroids
oral or IV (Beclomethasone, Fluticasone)
*vaccines
>influenzae and pneumococcal
*alpha-1-antitrypsin augmentation therapy
*antibiotics
*mucolytics
*antitussives
c. surgical management:
*bullectomy
*lung volume reduction surgery
*lung transplantation
a. patient education
*breathing exercises
*inspiratory muscle training
*activity pairing
*self care activities
*physical conditioning
*oxygen therapy
*nutritional therapy
*coping measures
 Asthma
-a reversible chronic inflammatory disease of the
airways
-triad:
*airway hyperresponsiveness
*mucosal edema
*excessive mucus production
*cough *wheezing
*chest tightness *dyspnea
-causes:
a. allergy- strongest predisposing factor
>seasonal (weed pollens, grass
>perennial (molds, dust, roaches)
b. airway irritants (perfumes, smoke, cold, heat)
c. exercise
d. stress or emotional upset
e. sinusitis
f. medications
g. viral respiratory tract infections
h. gastro-esophageal reflux
-pathophysiology
bronchospasm mucosal edema exc mucus secretion
bronchial muscle mucosal gland enlargement
hypertrophy thick tenacious secretions
alveolar hyperinflation
chronic asthma
(chronic airway inflammation)
airway subbasement membrane fibrosis
airway narrowing irreversible airflow
limitation
*cough usually at night or early in the
*dyspnea morning due to circadian
*wheezing variations
*diaphoresis *hypoxemia
*tachycardia *central cyanosis
*widened pulse pressure
-types according to severity:
A. Mild Intermittent
-symptoms <2 times a week
-asymptomatic and normal PEF between
exacerbations
-exacerbations are brief; intensity may vary
-night time symptoms <2 times a month
B. Mild persistent
-symptoms >2 times a week but <1 time a day
-exacerbations may affect activity
-night time symptoms >2 times a month
C. Moderate Persistent
-daily symptoms
-daily use of inhaled short acting beta2 agonist
-exacerbations affect activity
-exacerbations >2 times a week; may last days
-night time symptoms >1 time a week
D. Severe Persistent
-continual symptoms
-limited physical activity
-frequent exacerbations
-frequent night time symptoms
-assessment and diagnostics:
*clinical history and physical assessment
*sputum/blood tests
>eosinophilia
*serology
>elevated IgE
*ABG
>hypoxemia
>hypocapnia then hypercapnia
*pulse oximetry
>hypoxemia
-prevention:
a. identificaton and avoidance of allergens
-complications:
a. status asthmaticus
b. respiratory failure
c. pneumonia
d. atelectasis
a. Long Acting Medications
*corticosteroids
-most potent and effective
-inhaled preparations commonly causes
oral thrush
-fluticasone, beclomethasone,
budesonide
*mast cell stabilizer
-for mild to moderate asthma only
(prophylaxis)
- cromolyn sodium and nedocromil
*beta 2 agonist
-to control symptoms especially at night
-prophylaxis of exercise induced asthma
-salmeterol, albuterol, formoterol
*methylxanthines
-mild to moderate bronchodilator
-mainly for the relief of night time sx
(theophylline as mild anti-inflammatory)
*leukotriene modifiers (inhibitors)
-may be added or be used as an
alternative to inhaled corticosteroids
-zafirlukast, montelukast, zileuton
B. Quick Relief Medications
*short acting beta 2 agonist
-to relieve acute symptoms
-to prevent exercise induced asthma
-may be combined with an
anticholinergic
-salbutamol, combivent
(salbutamol+ipratropium bromide)
>management of asthma exacerbation
-early treatment and education of the patient
*quick relief medications
*corticosteroids
*O2 inhalation
*serial measurement of lung function
-peak flow meter (FEV)
 Status Asthmaticus
-severe and persistent asthma that does not
respond to conventional therapy
-may last longer than 24 hours
-causes:
*infection *dehydration
*anxiety *inc adrenergic blockage
*nebulizer abuse *irritants (aspirin)
-pathophysiology:
similar to bronchial asthma
*hypoxemia and respiratory alkalosis >>> respiratory
acidosis
similar to asthma
(extent of wheezing does not indicate the severity of
attack)
*pulmonary function study
-most accurate
*ABG
-respiratory alkalosis (most frequent finding)
*short acting beta adrenergic agonist and steroid
*O2 inhalation
*IVF
*mechanical ventilation
 Bronchiectasis
-is a chronic irreversible dilation of the bronchi and
bronchioles
-causes:
*airway obstruction
*diffuse airway injury
*pulmonary infections and complications
*genetic disorders (cystic fibrosis)
*abnormal host defense (ciliary dyskinesia)
*idiopathic causes
-pathophysiology:
chronic airway inflammation
bronchial wall damage
bronchial obstruction
(due to thick sputum)
bronchial distention and distortion
(localized; segmental/lobar-lower lobes usually)
inflammation of the peribronchial tissues
alveolar collapse
pulmonary scarring/fibrosis
*chronic cough
*excessive production of purulent sputum
*hemoptysis
*clubbing of the fingers
*repeated pulmonary infections
*history and physical assessment
-prolonged history of productive cough
*sputum exam
-consistently negative for tubercle bacilli
*CT scan
-bronchial dilatation
a. bronchial drainage
-to clear excessive secretions
-to prevent or control infection
*postural drainage
*bronchodilators
*bronchoscopy
*chest physiotherapy
b. smoking cessation
c. infection control
-antimicrobial therapy (year round)
-vaccination (influenza and pneumococcal
pneumonia)
d. surgery
-for patients who continue to expectorate large
volume of phlegm
-for patients with repeated bouts of pneumonia
and hemoptysis
*segmental resection
*lobectomy
*pneumonectomy
-complications:
*atelectasis *bronchopleural fistula
*pneumonia *empyema
a. supportive and symptomatic
b. assistance to clear secretions
c. patient education
-smoking cessation
-infection prevention
-postural drainage
-activity/rest
-nutrition
Pulmonary Edema
-abnormal accumulation of fluids in the lung tissue
and/or alveolar space
-a severe, life threatening condition
-causes:
*left ventricular failure
*hypervolemia
*sudden increase in the intravascular pressure in
the lungs (post operative pneumonectomy)
>flash pulmonary edema
*rapid re-inflation of the lungs after the
removal of air from a pneumothorax or
evacuation of fluid from a large pleural
effusion
>re-expansion pulmonary edema
>increasing respiratory distress
-dyspnea -central cyanosis
-hunger -confusion/stupor
>foamy, frothy, and often blood tinged
secretions
a. physical examination
>crackles
-initially in the base and posterior part of the
lungs
-progress toward the apices
>tachycardia
b. chest x-ray
>increased interstitial markings
c. pulse oximetry
d. arterial blood gas determination
a. correction of the underlying cause
b. vasodilators
c. inotropic agents
d. afterload or preload agents
e. contractility meds
f. diuretics and fluid restriction
g. oxygenation and mechanical ventilation
h. morphine
supportive to the medical management
 Pulmonary Hypertension
-systolic pulmonary artery pressure exceeding 30mmHg
-mean pulmonary artery pressure exceeding 25mmHg
-2 Types:
1. Primary Pulmonary Hypertension
-with no evidence of pulmonary or cardiac
disease or pulmonary embolism
-more common in women 20-40 y/o
-high mortality within 5 years of diagnosis
2. Secondary Pulmonary Hypertension
-more common
-secondary to existing cardiac and pulmonary
disease (hypoxemia)
-
Hypoxemia Hypercapnia Pulmonary Embolism
Pulmonary Artery Constriction
Increased Pulmonary Vascular resistance
Increased Right Ventricular Workload
Right Ventricular Hypertrophy
Right Ventricular Failure
*dyspnea
-main symptom initially with exertion then
eventually at rest
*substernal chest pain
*weakness *syncope
*fatigue *occasional hemoptysis
*right sided heart failure
-peripheral edema, ascites, neck vein
engorgement, liver engorgement,
crackles
*clinical history and physical examination
*CXR
*pulmonary function studies
-normal, or slight decrease in VC and
compliance
-mild decrease in diffusing capacity
*electrocardiogram
-right ventricular hypertrophy
-right axis deviation
-tall peaked T waves (inferior leads)
-tall R waves, ST segment depression, T wave
inversion (anterior leads)
*echocardiogram
-can assess the progression of the disease
*ventilation perfusion scan
-defects in the pulmonary vasculature such
as pulmonary emboli
*cardiac catheterization
-elevated pulmonary arterial pressure
*lung biopsy
-through thoracotomy or thoracoscopy
Goal:
1. to manage the underlying cardiac or
pulmonary condition
A. Supplemental Oxygen
-reverses vasoconstriction
-reduces pulmonary hypertension
B. Pulmonary Vasodilators
(calcium channel blockers, IV prostacyclin)
-reduces pulmonary vascular resistance
-increases the cardiac output
C. Anticoagulants if with cor
D. Fluid Restriction pulmonale
E. Diuretics
F. Cardiac Glycosides
G. Heart-Lung Transplantation
1. identify high risk patients
-COPD, pulmonary emboli, congenital heart
disease, mitral valve disease
2. monitor s/sx
3. administer oxygen therapy appropriately
4. home use oxygen supplementation
 Cor pulmonale
-characterized by:
a. right ventricular enlargement
b. pulmonary congestion
-causes:
a. COPD
-most frequent
b. deformities of the thoracic cage
c. massive obesity
d. primary embolism
e. disorders of the nervous system
f. disorders of the respiratory muscles
g. disorders of the chest wall
h. disorders of the pulmonary arterial tree
Lung Disease
Hypoxemia and Hypercapnia
Pulmonary Hypertension
Increased Work Load to the Right Ventricles
Right Sided Heart Enlargement
Right Sided Heart Failure
*s/sx of the underlying pulmonary disease
*s/sx of right sided heart failure
-management:
goals:
1. improvement of ventilation
2. treatment of the underlying lung disease
3. treatment of the manifestations of the heart
A. Continuous 24 Hour O2 Therapy
-improvement may require 4-6weeks
of O2 therapy
-monitor pulse oximetry and ABG
B. Chest Physiotherapy and Bronchial
Hygiene Maneuvers
C. Bronchodilators
D. ET Intubation and Mechanical
Ventilation
E. Bed Rest
F. Sodium Restriction
G. Diuretic Therapy
H. Digitalis Therapy
I. ECG Monitoring
*supportive to the medical management
 Pulmonary Embolism
-obstruction of the pulmonary artery or one of its
branches by a thrombus or thrombi
-causes:
*venous thrombosis
*atrial fibrillation
Occlusion of the Pulmonary Artery
Increased Alveolar Dead Space
Ventilation/Perfusion Imbalance
Hypoxemia and Hypercapnia
Pulmonary Hypertension
Right Ventricular Failure
Shock
*dyspnea
-most frequent symptom
*tachypnea
-most frequent sign
*chest pain
-sudden and pleuritic
-mimics angina pectoris
*anxiety, fever, tachycardia, apprehension, cough,
diaphoresis, hemoptysis, syncope
-less than 10% progresses to pulmonary infarction
a. Ventilation Perfusion Scan (test of choice)
b. Pulmonary Angiography (gold standard)
c. CXR
-infiltrates
-atelectasis
-pleural effusion
-elevation of the diaphragm
d. ECG
-sinus tachycardia
-PR interval progression
-non specific T wave changes
e. Peripheral Vascular Studies
f. ABG
-prevention:
*prevention of DEEP VEIN THROMBOSIS
-management:
a. Emergency Management
*Nasal O2 Therapy
*IV access
*Perfusion Scan, ABG, Hemodynamic
Measurements
*Dobutamine or Dopamine
*ECG
*Digitalis Glycosides, IV Diuretics and Anti-
arrhythmics when appropriate
*Blood Studies
*ET Intubation and Mechanical Ventilation
*Indwelling Urinary Catheter Insertion
*Small Doses of Sedatives or Morphine
b. General Management
*O2 therapy
*elastic compression stockings
*intermittent pneumatic leg compression
*elevation of the leg
c. Pharmacologic Management
*Anticoagulation Therapy
Heparin (IV bolus of 5T to 10T “U”
then infusion of 18U/kg/hour not to
exceed 600U/hour)
Warfarin (begun within 24 hours after
initiating Heparin therapy)
*Thrombolytic Therapy
Urokinase, Streptokinase, Alteplase
CI: CVA w/in the past 2 months
active bleeding w/in the past 10
days
recent labor & delivery
severe hypertension
d. Surgical Management:
*embolectomy
*interruption of the inferior vena cava
Teflon clips
a. Minimizing the risk of pulmonary embolism
b. Preventing thrombus formation
c. Assessing for potential pulmonary embolism
d. Monitoring thrombolytic therapy
e. managing pain
f. managing O2 therapy
g. relieving anxiety
h. monitoring for complications
i. post op nursing care
 Diabetic Ketoacidosis
-is caused by an absent or markedly inadequate
amount of insulin
-results in disorder in the metabolism of
carbohydrate, protein and fat
-3 main clinical features of DKA:
*hyperglycemia
*dehydration and electrolyte loss
*acidosis
*blood glucose level
-300 to 800 mg/dl
*serum bicarbonate
-0-15mEq/L
*serum pH
-low: 6.8-7.3
*PCO2
-low: 10-30mmHg
-reflects respiratory compensation for
acidosis
*ketone bodies
-elevated in the blood and in the urine
*electrolyte depletion
*BUN, creatinine, hgb and hct
-elevated due to water loss
-lack of insulin -decreased utilization
increased breakdown of fat of glucose by muscle,
increased fatty acids fat and liver
increased ketone bodies -increased production
-acetone breath of glucose by liver
-poor appetite hyperglycemia
-nausea
-blurred vision polyuria

acidosis dehydration
-nausea -weakness
-vomiting -headache
-abdominal pain increased thirst
increasingly rapid respirations
-prevention:
a. full compliance to the medical treatment of
diabetes mellitus
b. good hydration
c. good nutrition
d. monitoring of blood and urine ketones every
3-4 hours
-management:
a. rehydration
>6-10 L of IVF
>plain NSS or half strength saline
b. restoring electrolytes
>ECG monitoring
*reversing acidosis:
-insulin
*same as in DM
Addison’s Disease Cushing’s Syndrome
Sugar Hypoglycemia, Hyperglycemia,hypokalemia

hyperkalemia
Salt Hyponatremia Hypernatremia
Sex Decreased libido Sexual urge not merely
affected
Physical Not seen, more on Buffalo hump, moonface,
Appearance symptoms pitting edema, hirsutism,
breast atrophy, purple striae
on abdomen, easy bruising,
facial flushing, acne,
hyperpigmentation
Diet High Na, CHON, Low Na, CHO, fats but high
CHO intake except K CHON and K intake
Hyperthyroidism (Thyroid Hypothyroidism (Myxedema
Crisis) Coma)
Grave’s Disease; inc. amt. of Dec. T3T4; causes in adult –
T3&T4 myxedema, child cretinism
Inc. appetite – wt. loss due to Dec. appetite – wt. gain due to
inc. metabolism, heat decreased. metabolism, all VS
intolerance, all VS increase, decrease, decreased
exopthalmos-pathognomonic menstruation
symptom, amenorrhea
Inc. caloric diet; watch out for Dec. caloric diet, force fluid
thyrotoxicosis (triad):
b. Tachycardia
c. Hyperthermia
d. agitation
Meds: SSKI (Lugol’s solution), Meds: Levothyroxin (T4)

PTU prophylthiuracil synthroid
DKA HHNS
Acute complication of type1 Hyperglycemia w/o ketosis is
DM due to severe commonly on DM type2
hyperglycemia, leading to
CNS depression & coma
Polyuria, Polydipsia, Hypotension, extreme thirst,
Polyphagia, Glycosuria, dehydration, tachycardia,
Pathognomonic hypokalemia, hyponatremia
Sx:
>acetone breath– fruity odor
>kussmul’s respiration– rapid,
shallow breathing
Mx: monitor VS; I/O Tx: give insulin, inc. fluid
Meds: Insulin therapy (IV),
counteract acidosis – Na
HCO3

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Medical-Surgical Nursing 1

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Medical-Surgical Nursing

Fluids and Electrolytes

-maintains the blood pH by removing or releasing

Disorder Initial Event Compensation

Respiratory ↑PaCO2;↑or N Kidneys eliminate H+

Respiratory ↓PaCO2;↓or N Kidneys conserve H+

Metabolic ↓or N PaCO2; ↓Lungs eliminate

Respiration >20 breaths/ Rapid, shallow Intubation

provokes mast cells to release chemical mediators like

widespread vasodilatation and capillary permeability

Test of Urine Specific Gravity:

hypercalciuria and hypercalcemia

Four Clinical Phases of ARF

Etiology hypoperfusion parenchymal obstruction

Urinary Normal, few Abnormal Usually normal

baroreceptors heart rate

>12 lead ECG

1. Premature Atrial Complex

1. Premature Ventricular Complex

-required in the synthesis of DNA

(fatigue- most common)

1. Congestive Heart Failure

1. Activity Intolerance related to Fatigue, Weakness and

-a hereditary disorder associated with defective

-may lead to Acute Myeloid Leukemia

-also called essential thrombocythemia

-increased platelet production

alveolar capillary leak

microvascular a. pulmonary edema surfactant

 Acute Respiratory Failure

confusion, lethargy, tachycardia,

-airflow limitation not fully reversible

-blurred vision polyuria

Sugar Hypoglycemia, Hyperglycemia,hypokalemia

Meds: SSKI (Lugol’s solution), Meds: Levothyroxin (T4)

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