1.

Discuss different Acute Biologic Crisis conditions together with the roles
and responsibilities of the nurse in the care of the following.
•Cardiac failure - Acute Myocardial infarction
• Acute pulmonary failure
• Acute renal failure
• Stroke
• Increased Intracranial pressure
• Metabolic emergencies – e.g. DKA/HHNK
• Massive Bleeding
• Extensive surgeries
• Extensive Burns
• Emerging illnesses (SARS, Avian Flu)
• Multiple injuries
2. Use critical thinking in the management of these cases
3. Familiarize with the different treatment modalities and equipments used
Acute Biologic Crisis
Condition that may result to patient
mortality if left unattended in a brief
period of time.

Condition that warrants immediate

attention for the reversal of disease
process and prevention of further
morbidity and mortality.
 1. Coronary Artery Disease &
Acute Coronary Syndromes
Most Common cause of cardiovascular
disability and death.

It refers to a spectrum of illnesses that

range from the least life threatening to
the most life threatening acute coronary
syndrome(AMI/ Heart attack).
 Coronary Artery Disease &
Acute Coronary Syndromes
Incomplete occlusion of the
coronary arteries lead to Angina
(ischemia)
Complete occlusion of the coronary
arteries lead to Myocardial Infarction
The heart will pump harder to meet
the O2 demand leading to Congestive
Non Modifiable Risk Factors of
CAD/ ACS
Age
Gender
Race
Heredity
Modifiable Risk Factors of CAD/
ACS tachycardia
Stress norepinephrine
vasoconstriction
Diet
Na, cholesterol & fat CVD
Circulation, maintains vascular tone&
enhances release of chemical activators
Exercise that prevent blood clotting

Vasoconstriction & Myocardial

Cigarette Smoking spasm of arteries. demand

Alcohol 20 ml = vasodilation 30 ml = vasoconstriction

As a result of Systemic vascular

Hypertension resistance
Modifiable Risk Factors of CAD/ ACS
Accumulation of fatty
Hyperlipidimia plaques

Glucose cannot be transported into the

Diabetes Mellitus cells due to insulin insufficiency or
Increases resistance to insulin
Obesity Increase cardiac workload

Personality Type or
BehavioralType
Factors
A – competitive, impatient, aggressive
has been correlated to CAD

Contraceptive Pills
Cardiovascular Assessment
Chest Pain
Most common
Due to Ischemia or MI
Precipitated by stress or can be relieved
by Nitroglycerin (NTG)
In MI, it is more intense, unrelated to
activities and can’t be relieved by NTG
If it occurs during breathing, suspect
respiratory problems
Rough diagram of pain zones in myocardial
infarction (dark red = most typical area, light
red = other possible areas, view of the
chest).
Cardiovascular Assessment
Dyspnea
subjective feeling (inability to get enough
air).
Dyspnea on exertion is due to increased O2
myocardial demand.
Orthopnea is related to blood pooling in the
pulmonary bed; suspect Pulmonary Edema
Any sudden or acute dyspnea may be a sign
of Pulmonary Embolism
Tightness of Chest
Cardiovascular Assessment
Cough/sputum
Mucoid and foamy sputum can be a sign of
CHF
Pink-tinged frothy appearance may signal
Pulmonary Edema.
Whitish, viral infection
Change in color other than the above
mentioned may signify bacterial infection.
Cardiovascular Assessment
Cyanosis
Bluish discoloration of the skin and
mucous membrane
Sat O2 is below 90%

Fatigue
May be due to Anemias or related to
decreased Cardiac Output
Cardiovascular Assessment
Palpitations
Awareness of rapid or irregular heart beat
Autonomic Nervous System and Adrenal
Glands response (stress)

Syncope
Transient loss of consciousness
Due to decreased cerebral tissue perfusion
Cardiovascular Assessment
Edema
Due to: Increased Hydrostatic Pressure
(HP)
Decreased Colloidal Oncotic
Pressure (COP)
Obstructed Lymphatic or
Vascular System
Related to Inflammatory reaction
Types of Edema
Bilateral edema
= CHF or Renal Failure
Unilateral edema
= Vascular or Lymphatic
obstruction
Non-pitting edema
= Inflammatory

Pitting edema
= HP and
COP derangement
Cardiovascular Assessment
Skin
Color, temperature, hair growth,
nails, capillary refill
spooning of fingers /clubbing of
fingers
Clubbing of Fingers
Cardiovascular Assessment
Heart rate – 60-100
Rhythm – regular or irregular
Bruits and Thrills – murmurlike; vascular
in origin
- palpate a thrill, auscultate a bruit
Blood Pressure
Jugular venous pressure
Cardiovascular Assessment
Cardiac rate and rhythm
Tachycardia = ↑ 100 beats/minute
Bradycardia = ↓ 60 beats/minute
Arrhythmias = irregular rate and
rhythm
Cardiovascular Assessment
Murmurs - turbulence of blood flow; if
positive watch out for FVE; normal until 1 year
old
Pericardial Friction Rub -“squeaking
sound”; suspect pericardial effusion if this is
heard
Muffled Heart Sound - if positive rule out
Cardiac Tamponade and other similar problems
like Effusion
Laboratory & Diagnostic Test
Complete Blood Count- RBC suggest tissue
oxygenation.
Elevated WBC may indicate infectious heart
disease and MI.
Erythrocyte Sedimentation Rate (ESR)- Its
is elevated in infectious heart disorder or MI.
Normal range: Males: 15-20mm/hr
Females: 20-30 mm/hr
Laboratory & Diagnostic Test
Blood Coagulation Test:
1.Prothrombin Time (PT, Pro Time)- It
measures time required for clotting to occur.
Used to evaluate effectiveness of COUMADIN.
Normal range 11-16 secs.
2.Partial Thromboplastin Time (PTT)- Best
screening test for disorders of coagulation.
Used to determine the effectiveness of
HEPARIN. Normal Range: 60-70 secs.
Laboratory & Diagnostic Test
Blood Urea Nitrogen (BUN)- Indicator of
renal function
Normal Range: 10-20mg/dl (5-25mg/dl is also
accepted).
Blood Lipids:
1.Serum Cholesterol: 150-200mg/dl
2.Serum Triglycerides: 140-200mg/dl.
Laboratory & Diagnostic Test
Serum Enzymes Studies
1.Aspatate Aminotransferase(AST)- Elevated
level indicates tissue necrosis. Normal Range:
7-40mu/ml
2.CK-MB- Elevated 4-6hrs from the onset of
infarction; peaks 24-36 hrs. returns to normal
4-7 days.
Normal Range: males: 50-325mu/ml; Females:
50-250mu/ml
Laboratory & Diagnostic Test
Serum Enzymes Studies
3. Lactic Dehydogenase (LDL)- Onset: 12hrs;
Peak: 48hrs; returns to normal: 10-14 days
4. Hydroxybuterate Dehydroxynase (HBD)- it is
valuable in detecting silent MI because it is
elevated for a long period of time.
Onset: 10-12hrs; Peaks: 48-72hrs; Returns to
Normal 12-13 days
Laboratory & Diagnostic Test
Serum Enzymes Studies
5. Troponin- Most specific lab test to
detect MI. Troponin has 3
compartments: I,C, &T .
Troponin I persist for 4-7 days.
Angina Myocardial Infarction
Chest Pain- tightness & Severe crushing,
heaviness stabbing chest pain
Relieved quickly:3- Not relieve by rest and
15min by rest or medication
sublingual nitrogen.
Initiated by physical Pain last longer >20min
exertion or stress
Radiation may or may May or may not have
not be present radiation of pain
Frequently associated
with shortness of breath
Laboratory & Diagnostic Test
Serum Electrolytes/ Blood Chemistry:
1.Sodium (Na)
2.Potassium (K)
3.Calcium (Ca)
4.Magnessium (Mg)
5.Glucose
6.Glycosylated Hemoglobin (Hemoglobin A1c)
 Laboratory & Diagnostic Test
ECG/ EKG- ST segment elevation and T
wave inversion
Diagnostic Test
Radiologic Findings
Chest X-Ray
Normal
Cardiomegaly
Signs of CHF
Diagnostic Test
Hemodynamic Monitoring
Swan-Ganz Catheterization
Right side of the heart
Pulmonary artery pressure
Pulmonary artery occlusive pressure
Right atrial pressure

Cardiac output
Swan-Ganz
Catheterization
Diagnostic Test
Coronary
Angiogram
 allows to
visualize
narrowings or
obstructions
therapeutic
measures can
follow
Goal:
Pain relief
Reduction of myocardial
oxygen consumption
Prevention and treatment of
complications
Intervention
Admit to the CCU/ ICU
Activity
Day 1: bed rest, if stable
Day 2-3: bed rest, but patient
may be allowed to sit on a chair
for 15-20 minutes
Early mobilization is
recommended for
uncomplicated AMI
Intervention
Monitoring Vital Signs
First 6 hours- q30-60 minutes
Next 24 hours- q 2 hours
Thereafter q 4 hours
Diet
NPO: 1st 24 hours
If stable low salt, low cholesterol
diet
Intervention
IV Fluids
D5W to KVO
If unable to take food/
fluid per orem
1000ml/8 hours
K supplement
Intervention
Pain Medication
Morphine SO4 (2-5mg/IV dose)
Potent analgesic
Peripheral venous vasodilation

Pulmonary venous distention

Inferior wall MI: may increase vagal

discharge
Tranquilizres
To decrease anxiety
Diazepam (5-10 mg per
IV/orem)
Laxative
To prevent straining during
defecation
Lactulose (HS)
Drugs to Limit Infarct Size
Beta Blockers
Hyperdynamic states, HPN w/o
evidence of heart failure
Reduce myocardial oxygen
consumption by decreasing: BP. Heart
Rate, Myocardial Contractility and
calcium output.
Ex: Propranolol, Metoprolol, Atenolol
Nursing Consideration:
1.Assess Pulse Rate before administration;
withhold if bradycardia is present.
2.Administer with food, may cause GI upset.
3.Do not administer with asthma it causes
Bronchoconstriction.
4.Do not give to patient with DM, it causes
hypoglycemia.
5.Antidote for Beta Blocker poisoning is
Glucagon
Nitrates
Act by augmenting perfusion at the border
of ischemic zone.
Generalized vasodilation
Reducing myocardial O2 demand
Lowering preload
Lowering afterload
Ex: IV Nitroglycerine, Sublingual
Niotroglycerine, Oral/Transdermal
Nitroglycerine
Nursing Considerations:
1.Only a maximum of 3 doses at 5 min. interval.
2.Offer sips of water before giving it
sublingually.
3.Store the medication in a cool, dry place; use
dark /amber container.
4.If side effects is noticed do not discontinue the
drug this is usual in the first few doses of
medication.
5.Rotate skin sites for nitro patch.
ACE inhibitors
reduce mortality rates after MI.
Administer ACE inhibitors as soon as
possible
ACE inhibitors have the greatest benefit in
patients with ventricular dysfunction.
Continue ACE inhibitors indefinitely after
MI.
Angiotensin-receptor blockers may be used
as an alternative
adverse effects, such as a persistent cough,
Aspirin and/or antiplatelet
therapy

Continue aspirin indefinitely

Clopidogrel may be used as
an alternative only if
resistance or allergy to
aspirin.
Nursing Considerations:
1.Assess for signs and symptoms of
Bleeding.
2.Avoid straining at stool to avoid rectal
bleeding.
3.It should be given with food.
4.Observe for toxicity- Tinnitus (ringing
of ears).
5.May cause Bronchoconstriction-
Observe for wheezing.
Heparin
1.Assess for S/S of Bleeding.
2.Keep Protamine Sulfate available.
3.If used SQ. do not aspirate to
prevent hematoma formation.
4.Monitor for PTT or APTT
5.Used for a maximum of 2 weeks.
Coumadin (Warfarin Sodium)
1.Assess for bleeding
2.Keep Vitamin K available.
3.Monitor for Prothrombin Time
4.Do not give together with aspirin to
prevent bleeding.
5.Minimize green leafy vegetables in
the diet.
thombolytic therapy
The effectiveness:
highest in the first 2 hours
After 12 hours, the risk associated with
thrombolytic therapy outweighs any benefit
contraindicated
unstable angina and NSTEMI

and for the treatment of individuals with evidence

of cardiogenic shock
streptokinase, urokinase, and alteplase
(recombinant tissue plasminogen activator, rtPA),
reteplase, tenecteplase
Surgical Care
Percutaneous Transluminal Coronary
Angioplasty
-treatment of choice
PCI provides greater coronary patency
lower risk of bleeding
and instant knowledge about the
extent of the underlying disease.
A specially designed balloon – tipped
catheter is inserted uder flouroscopic
guidance and advance to the site of the
obstruction.
 Intravascular Stenting
Biologic Stent is produced through
coagulation of collagen, ellastin and
other tissues in the vessel wall by
laser, photocoagulation or radio
frequency.
It is done to prevent restenosis after
Percutaneous Transluminal Coronary
Angioplasty.
Emergent or urgent
coronary artery graft
bypass surgery (CABG)
is indicated
angioplasty fails
Severe narrowing of 1
or more coronary
artery.
Commonly used:
Saphenous vein and
internal mamary artery.
Complications
Inflammation
Mechanical
Electrical abnormalities
Cardiac Rehabilitation
A process which a person restored to
health and maintains optimal physiologic,
psychosocial and recreational functions.
Begins with the moment a client is
admitted to the hospital for emergency
care, it continues for months and even
years after the client is discharged from
the health care facility.
Goals of Rehabilitation:
1.To live as full, vital and productive life as
possible.

2.Remain within the limits of the heart’s

ability to respond to activity and stress.
Activities:
 Exercise may gradually
implemented from the hospital
onwards.
 Exercise session is terminated if
any one of the following occurs:
cyanosis, cold sweats, faintness,
extreme fatigue, severe dyspnea,
pallor, chest pain, PR more than
100/ min., dysrhythmias greater
than 160/95mmHg.
Teaching and Counseling
Self management education guide.
Control hypertension with
continued medical supervision.
Diet
Weight reduction program
Progressive exercise
Stress management techniques
Resumption of sexual activity
after 4-6 weeks from discharge, if
appropriate.
Teaching guide on resumption of
sexual activities:
Assume less fatiguing position.
The non- MI partner take the active
role
Take nitroglycerine before sexual
activity
If dyspnea, chest pain or palpitations
occur, moderation should be
observed; if symptom persist stop
sexual activity.
Develop other means of sexual
expression.
ACUTE RENAL
FAILURE Rapid
onset of oliguria
(<400 ml /day) ,
with severe rise in
BUN & creatinine
(Azotemia –
accumulation of
nitrogen in blood )
Acute renal failure is
classified as pre renal,
intra renal or post renal.
All conditions that lead to
pre renal failure impair
blood flow to the kidneys
(renal perfusion), resulting
in a decreased glomerular
filtration rate and
increased tubular
resorption of sodium and
water. Intra renal failure
results from damage to the
Onset – 1-3 days with ^ BUN and creatinine and
possible decreased UOP
Oliguric – UOP < 400/d, ^BUN,Crest, Phos, K,
may last up to 14 d
Diuretic – UOP ^ to as much as 4000 mL/d but no
waste products, at end of this stage may begin to
see improvement
Recovery – things go back to normal or may
remain insufficient and become chronic
Complications ARF
Hyperkalemia – most
dangerous complication,
may lead to cardiac arrest if
rise in K+ is too fast
Nursing Care ARF
Daily Weight
CVP monitoring
Diuretic as prescribed
Low protein, K,Na &
high carbohydrate diet
Nursing Care ARF
Emergency
management of
Hyperkalemia : insulin
& dextrose
Kayexalate enema
Chronic Renal failure
Chronic irreversible
progressive reduction of
functioning renal tissue
Common causes CRF
Diabetic nephropathy
Hypertensive nephropathy
Glomerulonephritis
Chronic pyelonephritis
Stages CRF
1. Reduced Renal Reserve high
BUN no clinical symptoms yet
2. Renal insufficiency- mild
Azotemia – impaired urine
concentration , nocturia
Stages CRF
3. Renal failure – Severe
azotemia, acidosis,concentrated
urine, severe anemia &
electrolyte imbalances
CRF systemic SS
Hyper K, Hypernatremia,
Hypocalcemia
Anemia
Anorexia, nausea & vomiting
CRF systemic SS
Ammoniacal breath
Immunosuppression
HTN, CHF
Pulmonary edema
Severe pruritus
Peripheral neuropathy
Uremic amaurosis
Nursing Care ESRD
Low Protein, Low Na diet
Prepare client for
peritoneal / hemodialysis
Monitor Anemia
Nursing Care ESRD
Administer epoietin alpha
(Epogen), diuretics,
antihypertensives as
prescribed
Kidney transplant
Peritoneal Dialysis
Peritoneal Dialysis
Hemodialysis
HEMODIALYSIS: Is the
diffusion of dissolved particles
from the blood into the dialysate
bath of the hemodialysis
machine across the
semipermeable membrane of the
dialyzer.
Hemodialysis requires vascular
access:
Subclavian vein/ Femoral vein
(temporary)
Arteriovenous fistula,
arteriovenous shunt,/
arteriovenous graft
( Permanent)
Hemodialysis
Hemodialysis
Nursing Management:
Assess the integrity of the
hemodialysis access site
Monitor VS
Assess client for fluid
overload
Nursing Management:

Weigh the client before and after

the dialysis treatment ( to
determine fluid loss)
Hold meds that can be dialyzed
off
Monitor for SS of Shock &
Disequilibrium syndrome
Complication: Disequilibrium
Syndrome – is the rapid change in
composition of extracellular fluid
where the solutes of the blood are
removed from the blood faster than
that of the CSF, causing osmotic
movement of fluid into the CSF
causing cerebral edema.
Nursing Management: Disequilibrium syndrome:

Assess for Nausea & vomiting

Assess for headache
Restlessness, agitation & or
confusion
Watch out for seizures
Nursing Management: Disequilibrium syndrome:

Notify physician if SS of
disequlibrium syndrome occurs
Reduce environmental stimuli
Dialyze the patient at a shorter period
and at a slower rate
Kidney Transplant
Cell destruction of the
layers of the skin and
resultant depletion of fluid
and electrolytes
Types of Burns
Thermal : exposure to flame
Chemical: exposure to strong
acids or alkali
Electrical: Caused by electrical
strong electrical current results in
internal tissue injury
Burn Depth:
Superficial thickness burn (1st
degree)- mild to severe erythema
of skin, blanches with pressure –
heals in 3-7 days
Partial thickness burn(2nd degree) –
large blisters; painful heals 2-3
weeks
Burn Depth:

Full thickness burns (3rd degree) –

white yellow deep red to black
(eschar) disruption of blood flow,
no pain; scarring and wound
contractures will develop.
Grafting is required; healing takes
weeks to months
Burn Depth:
Deep full thickness burn (4th
degree) – Involves injury to
muscle and bone= appears
black(eschars) – hard and
inelastic healing takes weeks to
months; grafts are required
Nursing Diagnosis
Decreased Cardiac output
Related to Fluid shifts
Rule Of 9
Head and neck 9%
Anterior trunk 18%
( chest-9 abdomen-9)
Posterior trunk-18%
Rule Of 9
Arms 9% each (forearms
only or upper arms only
4.5%)
Legs – 18% each
Perineum-1%
Rule of 9
PARKLAND (BAXTER)
FORMULA FOR FLUID
REPLACEMENT
 4ml Lactated Ringer’s sol x
Kg body mass x total
percentage of body surface
burned
PARKLAND (BAXTER)

•1st 8 hours = ½ of total 24

hour fluid replacement
•next 8 hours = ¼ of
total
•last 8 hours= ¼ of total
A man Suffered from a 3rd degree burn involving
the head and neck, front of the torso (chest &
abdomen), and whole left arm. Weight is 50 kg

Calculate the:
TBSA burned
24 hour fluid replacement in ml
1st 8 hours fluid replacement
2nd 8 hour
remaining 8 hour
TBSA:
Head & neck= 9%
front of torso = 18%
Whole left arm = 9%
TBSA burned 36%
24 hour replacement:
Parkland Baxter formula
4mlX 50 kgs x (TBSA)36%

= 7200 ml
1 8 hours :
st

7200 ml
2
= 3600 ml = 1st 8 hours
2 8 hours & remaining 8
nd

hours respectively :
3600 ml
2
= 1800 ml = 2nd 8 hours
= 1800 ml = last 8 hours
MANAGEMENT OF BURNS:
Administer fluids as prescribed
Maintain a high calorie, high
protein diet
Monitor intake and output
Monitor for infections of burn site
Burn Medications:
Nitrofurazone ( Furacin) –
broad spectrum antibiotic
ointment or cream – used when
bacterial resistance to other
drugs is a problem : apply 1/16
inch thick film directly to burn
Burn Medications:
Mafenide ( Sulfamylon) – water
soluble cream bacteriostatic gr + -
bacteria- apply 1/16 inch directly to
burn – notify physician if
hyperventilation occurs as this drug
may ppt. metabolic acidosis.
Burn Medications:
Silver Sulfadiazene
( Silvadene) – cream Broad spectrum
to gr+ - ; does not cause metabolic
acidosis – keep burn covered at all
times with Sulfadiazine – (1/16 inch
thick);
 Monitor CBC – causes leukopenia
Burn Medications:
Silver Nitrate – Antiseptic
solution against gr-, dressings are
applied to the burn and then kept
moist with Silver nitrate ; used on
extensive burns that may
precipitate fluid and electrolyte
imbalance.
DKA( Diabetic Ketoacidosis) / HHNS
( Hyperglycemic
Hyperosmolar Nonketotic Syndrome)

DKA- Is a life threatening

complication of DM type 1 =
develops because of severe insulin
deficiency
 MANIFESTATATIONS
1. Hyperglycemia
2. Dehydration
3. Electrolyte loss and
acidosis
 CAUSE; Missed insulin
dose, or infection
HHNS- SIMILAR TO dka WITH
EXTTREME hyperglycemia except
that in HHNS there is no acidosis.
This is for DM type 2
ASSESSMENT:
Blood glucose – 300 – 800
mg/dl
Low bicarbonate & low
pH
Dehydration
ASSESSMENT:
Mental status changes
Neurological deficits
Seizures

NURSING INTERVENTION:
Administer Insulin IV push 5-10 units
1st then IV infusion
NURSING INTERVENTION:
Restore Fluids ( administer fluids as
prescribed)
Treat dehydration w/ rapid
infusion of NSS or .45% saline
when blood glucose reaches 250-
300 mg/dl D5NS, or D5 .45%Saline
is used
NURSING INTERVENTION:
Always use infusion pump for IV
insulin
Monitor serum potassium ( initially
as a result of acidosis Hyperkalemia
is present upon admin of insulin K+
level drops)
NURSING INTERVENTION:
Monitor LOC= too rapid decrease in
blood glucose may cause cerebral
edema
THYROID CRISIS – (THROID
STORM/ Thyrotoxicosis)- Acute life
threatening condition that occurs in a
client with uncontrollable
hyperthyroidism – maybe a result of
manipulation of thyroid gland during
surgery(release of thyroid hormones to
bloodstream)
THYROID CRISIS –
(THROID STORM/
Thyrotoxicosis)-
Causes: Undiagnosed , untreated
hyperthyroidism, infection,
trauma
Medical management:
Antithyroid medications;
beta blockers; glucocorticoids
& iodides are given before
surgery to prevent thyroid
crisis
Medical management:
Antithyroid meds: Iodide,
Propylthiouracil, Methimazole
Iodides/ Iodine = Reduce the
vascularity of the thyroid gland
before thyroidectomy,
Medical management:
Iodides= used in the treatment of
thyroid storm because it enables the
storage of TH in the thyroid gland.

However it is given only for 10-14

days Because eventually it looses its
effect on the thyroid gland.
NURSING INTERVENTION:
ASSESSMENT : elevated Temp
( high fever); tachycardia; agitation;
tremors
Maintain a patent airway
Administer antithyroid meds as
prescribed ( sodium iodide solution)
Monitor VS
 MULTI ORGAN
DYSFUNCTION SYNDROME
(MODS)
SEPSIS, DEAD TISSUE,
PNEUMONITIS,
PANCREATITIS

RESPIRATORY FAILURE
INTUBATION (maybe stable
for 7-14 days)

MALFUNCTION of GI
 SEEDING OF BACTERIA
FR. GI TO OTHER ORGANS

HYPERMETABOLIC
STATE
HYPERMETABOLIC STATE
(hyperglycemia, hyperlactacidemia,
ulceration in GI- seeding of bacteria
from GI to other organs)
(skin breakdown, loss of muscle mass,
delayed healing of surgical wounds)
(mortality rate 60%)
 LIVER FAILURE
(jaundice)
RENAL FAILURE
(mortality rate 90-100%)
 Criteria for
Diagnosis of MODS
 Cardiovascular Failure
presence of 1 or more of the ff:
<54 bpm
Systolic < 60 mm Hg
Vtach/ V fib
pH < 7.24
Respiratory Failure
RR < 5/min
RR> 49/min
Renal Failure presence of 1 or
more of the ff:
Output < 479 ml/24 hr or < 159 ml/ 8 hr
BUN > 100mg/dl
Crea > 3.5mg/dl
Hematologic Failure presence of
1 or more of the ff:
WBC < 1000 uL
Platelets < 20,000
HCT < 20%
 Hepatic failure presence of both
of the FF:
Bilirubin > 6 mg %
PT > 4 sec over control in absence
of anticoagulation (normal PT – 11-12sec)
Neurologic Failure
GCS < 6 in absence of sedation
Medical Management:
Control of infection w/ antibiotics
( common MRSA & Vancomycin
resistant
Aggressive pulmonary care mech
vent & O2 (intubation)
Enteral (NGT) feeding
Nursing Management
Limited : effective client & family
coping
The only way to keep your hea

Mark Twain