NCM106

2. 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

3. 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.

4. 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).

6. 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

7. Non Modifiable Risk Factors of
CAD/ ACS
Age
Gender
Race
Heredity

8. Modifiable Risk Factors of CAD/
tachycardia
ACS

Stress
Diet
norepinephrine
Na, cholesterol & fat
Cigarette Smoking
Hypertension
CVD
Circulation, maintains vascular tone&
enhances release of chemical activators
that prevent blood clotting
Exercise
Alcohol
vasoconstriction
Vasoconstriction &
spasm of arteries.
20 ml = vasodilation
As a result of
Myocardial
demand
30 ml = vasoconstriction
Systemic vascular
resistance

9. Modifiable Risk Factors of CAD/ ACS
Accumulation of fatty
plaques
Hyperlipidimia
Diabetes Mellitus
Obesity
Glucose cannot be transported into the
cells due to insulin insufficiency or
Increases resistance to insulin
Increase cardiac workload
Personality Type or
Type A – competitive,
Behavioral Factors toimpatient, aggressive
has been correlated CAD
Contraceptive Pills

10. 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

11. Rough diagram of pain zones in myocardial
infarction (dark red = most typical area, light
red = other possible areas, view of the
chest).

12. 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

13. Tightness of Chest

14. 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.

15. 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

16. 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

17. Cardiovascular Assessment
Edema
Due to: Increased Hydrostatic Pressure
(HP)
Decreased Colloidal Oncotic
Pressure (COP)
Obstructed Lymphatic or
Vascular System
Related to Inflammatory reaction

18. 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

19. Cardiovascular Assessment
Skin
Color, temperature, hair growth,
nails, capillary refill
spooning of fingers /clubbing of
fingers

20. Clubbing of Fingers

22. 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

23. Cardiovascular Assessment
Cardiac rate and rhythm
Tachycardia =
↑ 100 beats/minute
Bradycardia =
↓ 60 beats/minute
Arrhythmias
= irregular rate and
rhythm

24. 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

25. 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

26. 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.

27. 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.

28. 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

29. 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

30. 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.

33. Angina
Myocardial Infarction
Chest Pain- tightness & Severe crushing,
heaviness
stabbing chest pain
Relieved quickly:315min by rest or
sublingual nitrogen.
Not relieve by rest and
medication
Initiated by physical
exertion or stress
Pain last longer >20min
Radiation may or may
not be present
May or may not have
radiation of pain
Frequently associated
with shortness of breath

34. 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)

35. Laboratory & Diagnostic Test
ECG/ EKG- ST segment elevation and T
wave inversion

36. Diagnostic Test
Radiologic Findings
Chest X-Ray
Normal
Cardiomegaly
Signs of CHF

37. Diagnostic Test
Hemodynamic Monitoring
Swan-Ganz Catheterization
Right
side of the heart
Pulmonary
artery pressure
Pulmonary
artery occlusive pressure
Right atrial pressure
Cardiac output

39. Swan-Ganz
Catheterization

40. Diagnostic Test
Coronary
Angiogram
 allows to
visualize
narrowings or
obstructions
therapeutic
measures can
follow

41. Goal:
Pain relief
Reduction of myocardial
oxygen consumption
Prevention and treatment of
complications

42. 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

43. 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

44. Intervention
IV Fluids
D5W to KVO
If unable to take food/
fluid per orem
1000ml/8 hours
K supplement

45. Intervention
Pain Medication
Morphine SO4 (2-5mg/IV dose)
Potent
analgesic
Peripheral venous vasodilation
Pulmonary venous distention
Inferior wall MI: may increase vagal
discharge

46. Tranquilizres
To decrease anxiety
Diazepam (5-10 mg per
IV/orem)
Laxative
To prevent straining during
defecation
Lactulose (HS)

47. 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

48. 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

49. 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

50. 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.

51. 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,

52. Aspirin and/or antiplatelet
therapy
Continue aspirin indefinitely
Clopidogrel may be used as
an alternative only if
resistance or allergy to
aspirin.

53. 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 BronchoconstrictionObserve for wheezing.

54. 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.

55. 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.

56. 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

57. 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.

58. 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.

60. 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.

61. Complications
Inflammation
Mechanical
Electrical abnormalities

62. 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.

63. 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.

64. 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.

65. 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.

66. 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.

67. ACUTE RENAL
FAILURE Rapid
onset of oliguria
(<400 ml /day) ,
with severe rise in
BUN & creatinine
(Azotemia –
accumulation of
nitrogen in blood )

68. 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

69. 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

70. Complications ARF
Hyperkalemia
–
most
dangerous
complication,
may lead to cardiac arrest if
rise in K+ is too fast

71. Nursing Care ARF
Daily Weight
CVP monitoring
Diuretic as prescribed
Low protein, K,Na &
high carbohydrate diet

72. Nursing Care ARF
Emergency
management of
Hyperkalemia : insulin
& dextrose
Kayexalate enema

73. Chronic Renal failure
Chronic irreversible
progressive reduction of
functioning renal tissue

74. Common causes CRF
Diabetic nephropathy
Hypertensive nephropathy
Glomerulonephritis
Chronic pyelonephritis

75. Stages CRF
1. Reduced Renal Reserve high
BUN no clinical symptoms yet
2. Renal insufficiency- mild
Azotemia – impaired urine
concentration , nocturia

76. Stages CRF
3. Renal failure – Severe
azotemia, acidosis,concentrated
urine, severe anemia &
electrolyte imbalances

77. CRF systemic SS
Hyper K, Hypernatremia,
Hypocalcemia
Anemia
Anorexia, nausea & vomiting

78. CRF systemic SS
Ammoniacal breath
Immunosuppression
HTN, CHF
Pulmonary edema
Severe pruritus
Peripheral neuropathy
Uremic amaurosis

79. Nursing Care ESRD
Low Protein, Low Na diet
Prepare client for
peritoneal / hemodialysis
Monitor Anemia

80. Nursing Care ESRD
Administer epoietin alpha
(Epogen), diuretics,
antihypertensives as
prescribed
Kidney transplant

81. Peritoneal Dialysis

82. Peritoneal Dialysis

83. Hemodialysis

84. 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.

85. Hemodialysis requires vascular
access:
Subclavian vein/ Femoral vein
(temporary)
Arteriovenous fistula,
arteriovenous shunt,/
arteriovenous graft
( Permanent)

86. Hemodialysis

87. Hemodialysis

88. Nursing Management:
Assess the integrity of the
hemodialysis access site
Monitor VS
Assess client for fluid
overload

89. 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

90. 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.

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

92. 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

93. Kidney Transplant

94. Cell destruction of the
layers of the skin and
resultant depletion of fluid
and electrolytes

95. 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

96. 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

97. 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

98. 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

100. Nursing Diagnosis
Decreased Cardiac output
Related to Fluid shifts

101. Rule Of 9
Head and neck 9%
Anterior trunk 18%
( chest-9 abdomen-9)
Posterior trunk-18%

102. Rule Of 9
Arms 9% each (forearms
only or upper arms only
4.5%)
Legs – 18% each
Perineum-1%

103. Rule of 9

105. PARKLAND (BAXTER)
FORMULA FOR FLUID
REPLACEMENT
 4ml Lactated Ringer’s sol x
Kg body mass x total
percentage of body surface
burned

106. PARKLAND (BAXTER)
•1st 8 hours = ½ of total
hour fluid replacement
•next 8 hours = ¼ of
total
•last 8 hours= ¼ of total
24

107. 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

108. TBSA:
Head & neck= 9%
front of torso = 18%
Whole left arm = 9%
TBSA burned 36%

109. 24 hour replacement:
Parkland Baxter formula
4mlX 50 kgs x (TBSA)36%
= 7200 ml

110. 1 8 hours :
st
7200 ml
2
= 3600 ml = 1st 8 hours

111. 2 8 hours & remaining 8
hours respectively :
nd
3600 ml
2
= 1800 ml = 2nd 8 hours
= 1800 ml = last 8 hours

112. MANAGEMENT OF BURNS:
Administer fluids as prescribed
Maintain a high calorie, high
protein diet
Monitor intake and output
Monitor for infections of burn site

113. 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

114. 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.

115. 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

116. 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.

117. DKA( Diabetic Ketoacidosis) / HHNS
( Hyperglycemic
Hyperosmolar Nonketotic Syndrome)
DKA- Is a life threatening
complication of DM type 1 =
develops because of severe insulin
deficiency

118.  MANIFESTATATIONS
1. Hyperglycemia
2. Dehydration
3. Electrolyte loss and
acidosis
 CAUSE; Missed insulin
dose, or infection

119. HHNS- SIMILAR TO dka WITH
EXTTREME hyperglycemia except
that in HHNS there is no acidosis.
This is for DM type 2

120. ASSESSMENT:
Blood glucose – 300 – 800
mg/dl
Low bicarbonate & low
pH
Dehydration

121. ASSESSMENT:
Mental status changes
Neurological deficits
Seizures
NURSING INTERVENTION:
Administer Insulin IV push 5-10 units
1st then IV infusion

122. NURSING INTERVENTION:
Restore Fluids ( administer fluids as
prescribed)
Treat dehydration w/ rapid
infusion of NSS or .45% saline
when blood glucose reaches 250300 mg/dl D5NS, or D5 .45%Saline
is used

123. 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)

124. NURSING INTERVENTION:
Monitor LOC= too rapid decrease in
blood glucose may cause cerebral
edema

125. 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)

126. THYROID CRISIS –
(THROID STORM/
Thyrotoxicosis)Causes: Undiagnosed , untreated
hyperthyroidism, infection,
trauma

127. Medical management:
Antithyroid medications;
beta blockers; glucocorticoids
& iodides are given before
surgery to prevent thyroid
crisis

128. Medical management:
Antithyroid meds: Iodide,
Propylthiouracil, Methimazole
Iodides/ Iodine = Reduce the
vascularity of the thyroid gland
before thyroidectomy,

129. 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.

130. NURSING INTERVENTION:
ASSESSMENT : elevated Temp
( high fever); tachycardia; agitation;
tremors
Maintain a patent airway
Administer antithyroid meds as
prescribed ( sodium iodide solution)
Monitor VS

131. MULTI ORGAN
DYSFUNCTION SYNDROME
(MODS)
SEPSIS, DEAD TISSUE,
PNEUMONITIS,
PANCREATITIS
RESPIRATORY FAILURE

132. INTUBATION (maybe stable
for 7-14 days)
MALFUNCTION of GI

133. SEEDING OF BACTERIA
FR. GI TO OTHER ORGANS
HYPERMETABOLIC
STATE

134. 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%)

135. LIVER FAILURE
(jaundice)
RENAL FAILURE
(mortality rate 90-100%)

136. Criteria for
Diagnosis of MODS

137. Cardiovascular Failure
presence of 1 or more of the ff:
<54 bpm
Systolic < 60 mm Hg
Vtach/ V fib
pH < 7.24

138. 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

139. Hematologic Failure presence of
1 or more of the ff:
WBC < 1000 uL
Platelets < 20,000
HCT < 20%

140. 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

141. Medical Management:
Control of infection w/ antibiotics
( common MRSA & Vancomycin
resistant
Aggressive pulmonary care mech
vent & O2 (intubation)
Enteral (NGT) feeding

142. Nursing Management
Limited : effective client & family
coping

143. The only way to keep your hea
Mark Twain