ACUTE BIOLOGICAL CRISIS

LOUIS CARLOS O. RODEROS

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 09/08/2018
ACUTE BIOLOGICAL CRISIS

 these are conditions that may result to

patient mortality if left unattended in a brief
period of time.

 These are conditions that warrants

immediate attention for the reversal of
disease process & prevention of further
morbidity & mortality.

5
 09/08/2018
Conditions:
1. Cardiac failure & dysrhythmias
2. Respiratory failures & ARDS
3. Renal Failure & ESRD
4. Burns
5. Hepatic coma
6. Diabetic ketoacidosis
7. Thyroid crisis & adrenal crisis
8. Multisystem organ failure & shock

6
 Ms. Jenneth E. dela Cerna, R.N.

09/08/2018 7
 CARDIOVASCULAR
DISORDERS

09/08/2018 8
• Enclosed within the inferior
mediastinum. THE HEART
• Enclosed by a double sac
of serous membrane –
Pericardium
Serous fluid
• Lubricating fluid that is
produced by the serous
pericardial membranes.
• Allows heart to beat easily.

Pericarditis:
• Decreased in the amount of
serous fluid adhesions

interfere with the

heart movement

9
3 LAYERS OF THE HEART WALLS:
1. Epicardium
 tightly hugs the external
surface of the heart.

2. Myocardium
 Consist of thick bundles of
cardiac muscle
 Contracts

3. Endocardium
 thin, glistening sheet of
endothelium that lines the
heart chambers.

Thursday, August 9, 2018 10

 CHAMBERS OF THE HEART
4 CHAMBERS:
1. ATRIA (2)
 Receiving chambers
 Not important in the
pumping activity
 Blood flow is under low
pressure

2. VENTRICLES (2)
 inferior, thick-walled
 Discharging chambers
 Contraction
propulsion of blood
circulation

Thursday, August 9, 2018 11

VALVES:
 Allow the blood flow in only one
direction through the heart
chambers.
1. ATRIOVENTRICULAR VALVES
 Between the atrial & ventricular
chambers on each side.
 Prevents the backflow of blood into
the atria during ventricular
contraction.
Bicuspid valve – mitral valve (left)
Tricuspid valve – right AV
Chordae tendinae – anchor the AV
valve flaps in a closed position
 Open during heart relaxation &
closed ventricular contraction.

Thursday, August 9, 2018 12

2. SEMILUNAR VALVES
• Guards the bases of the
two large arteries
• Pulmonary & aortic
semilunar valves
• Closed during heart
relaxation & open during
ventricular contraction.

Thursday, August 9, 2018 13

 UNoxygenated
blood enters the
atrium on the right
side of the heart.
Unoxygenated
blood comes in
from the top of the
body through the
superior vena
cava.
Unoxygenated
blood comes in
from the lower
body though the
inferior vena cava.

Thursday, August 9, 2018 14

 While the
unoxygenated
blood is in the
right atrium,
the tricuspid
valve is closed
to keep the
blood from
flowing down
to the
ventricle.

Thursday, August 9, 2018 15

 The atrium
contracts
and the
tricuspid
valve opens,
forcing the
blood down
into the
ventricle.

Thursday, August 9, 2018 16

 The tricuspid
valve closes
again so that
blood cannot
move back
up into the
atrium.

Thursday, August 9, 2018 17

 The ventricle
contracts.
This forces
the
unoxygenat
ed blood
through the
pulmonary
valve and
into the
pulmonary
arteries.

Thursday, August 9, 2018 18

 The right pulmonary
artery takes the
unoxygenated
blood to the right
lung.
The left pulmonary
artery takes the
unoxygenated
blood to the left
lung.
THE PULMONARY
ARTERIES ARE THE
ONLY ARTERIES THAT
CARRY
UNOXYGENEATED
BLOOD.

Thursday, August 9, 2018 19

In the lungs, the
carbon dioxide
in the blood
diffuses into the
alveoli.
The oxygen in
the lungs
diffuses into the
blood.
This is called gas
exchange.

Thursday, August 9, 2018 20

 Oxygenated
blood from the
lungs enters the
heart through
the left atrium.
The mitral valve
is closed to
keep the blood
from going into
the ventricle.

Thursday, August 9, 2018 21

 Oxygenated blood
from the right lung
returns to the heart
through the right
pulmonary vein.
Oxygenated blood
from the left lung
returns to the heart
through the left
pulmonary vein.
THE PULMONARY
VEINS ARE THE ONLY
VEINS THAT CARRY
OXYGENATED
BLOOD.

Thursday, August 9, 2018 22

 The left
atrium
contracts.
This forces
the
oxygenated
blood
through the
mitral valve
into the right
ventricle.

Thursday, August 9, 2018 23

 The mitral
valve closes
again. This
keeps the
oxygenated
blood from
moving
back up into
the atrium.

Thursday, August 9, 2018 24

 Oxygenated
blood is
forced into
the aorta to
be carried to
the rest of
the body.

Thursday, August 9, 2018 25

Oxygenated blood is
carried to all body
cells where oxygen
diffuses into the cells
and carbon dioxide
diffuses into the
blood.
Blood carrying
carbon dioxide then
returns to the heart.

Thursday, August 9, 2018 26

 And the
cycle
begins
again.

Thursday, August 9, 2018 27

 Meanwhile…
While the blood is
moving oxygen
and carbon
dioxide around, it is
also moving
nutrients, other
wastes, hormones,
and antibodies at
the same time.

Thursday, August 9,
28
2018
 CORONARY ARTERY DISEASE

 It is a heart disease due to impaired

coronary blood flow

disrupts the blood rich oxygen and

nutrients for metabolism

 Most common cause is

ATHEROSCLEROSIS

29
 Etiology:

Non- modifiable Modifiable Factors:

Factors:  Hyperlipidemia
 Age  Hypertension
 Gender  Cigarette smoking
 Family history  Diabetes mellitus
 Physical inactivity
 Obesity

30
 ATHEROSCLEROSIS
 Abnormal deposit
of fatty substances
and fibrous tissue
in the intima of the
blood vessel.

31
 ATHEROSCLEROSIS
PATHOPHYSIOLOGY:
Injury in the endothelial lining

Allows entry of lipids to the intima

Recruits monocytes and promote expression

of inflammatory mediators

Monocyte differentiate macrophages and

ingest LDL

32
 fatty streak or foam cells formation

Stimulates release of growth factors

Fibrous plaque formation

Foam cells increases in size becomes rigid,

calcified and fragile

Intimal ulceration

33
Platelet aggregation further increasing the
plaque

Narrowing of blood vessel lumen

Obstruction of blood flow

No or decrease blood supply

34
 ANGINA PECTORIS

 Clinical syndrome usually characterized by

episodes of pain and pressure in the
anterior chest.
 Increase O2 demand and decrease O2
supply.
 Usually a result of atherosclerosis.

35
Types of angina pectoris:
1. Stable angina
 a consistent pain that occurs on activity and
is relieve by rest.

2. Unstable angina
 increasing in frequency, duration and
intensity of pain at lower level of activity.

3. Prinzmetal angina
 result of coronary vasospasm

4. Silent angina
 ischemia occurs without at all

36
Clinical Manifestations:
a. Pain
b. Shortness of breath
c. Diaphoresis
d. Pallor
e. Weak or numbness of arm
f. Dizziness or lightheadedness
g. Feeling of impending doom
h. Choking or strangling sensation
i. Anxiety

37
Diagnostic tests:
1. ECG
2. 2D echocardiogram
3. Cardiac enzymes
4. CBC, ESR
5. Lipid levels
6. Exercise Stress Test
7. Cardiac catheterization & angiography

38
Medical management:
1. Oxygen therapy
2. Pharmacological treatment:
a. Nitrates

b. Beta-adrenergic blocker

c. Calcium channel blocker

d. Antiplatelet drugs

e. Antilipidemics

39
 3. Surgical management

A. CABG

40
41
B. PTCA

42
C. Laser angioplasty
- atherectomy

43
Nursing Management:
1. Lifestyle modification
2. Careful monitoring during anginal episodes
3. Keep nitroglycerin available for immediate
use.
4. Complete bed rest
5. Provide stress reduction activity

44
 MYOCARDIAL INFARCTION

09/08/2018
 Coronary occlusion, heart attack, & MI are
used synonymously, but the preferred term is
MI.

 characterized by the ischemic death of the

myocardium due to the reduced of absence
of blood flow.

45
CAUSES:

09/08/2018
1. Atherosclerosis

1. Complete occlusion of an artery by an embolus or

thrombus

2. Vasospasm of a coronary artery (constriction or

narrowing)

3. Decreased oxygen supply (acute blood loss,

anemia, or low blood pressure)

5. Increased demand for oxygen (from rapid HR,

thyrotoxicosis, or ingestion of cocaine)

Result: Profound imbalance exists between myocardial

oxygen supply & demand. 46
PATHOPHYSIOLOGY:

09/08/2018
occlusion/vasospasm

decreased diameter of the arterial wall

reduced/decreased blood supply

decreased oxygen supply to the

myocardium

NECROSIS 47
 09/08/2018
CLINICAL MANIFESTATIONS:

1. Sudden & persistent chest pain (despite rest

& medication is the primary presenting
symptom)
2. Anxious & restless
3. Cool, pale & moist skin
4. Tachycardia & tachypnea
5. Epigastric pain
6. Disorientation & confusion
7. Fainting & weakness
48
DIAGNOSTIC EVALUATIONS:

09/08/2018
1. ECG
2. 2D echocardiogram
3. Coronary angiography
4. Myocardial perfusion imaging with thallium-
201
5. Serial serum cardiac markers:
a. Creatine kinase (CK)
b. Lactic dehydrogenase (LDH)
c. Myoglobin
d. Troponin T & I 49
Cardiac Normal value with Acute Myocardial Infarction
enzyme

onset peak Duration

Troponin 0 ng/ml 3.5 – 7 hrs 4–6 days

(> 1.5 ng/ml is dx
for MI)

CPK 96 – 140 IU/L (F) 4 – 6 hrs 12 - 24 hrs 3-4 days

38 – 174 IU/L (M)

CPK MB 0 24 – 48 hrs 12 – 24 hrs 2–3 days

SGOT 6 – 18 IU/L (F) 12 – 18 hrs 24 – 48 hrs 3-4 days

7 – 21 IU/L (M)

LDH 70 – 180 mg/dl 24 – 48 hrs 3 – 6 days 7–10 days

50
Medical management:

09/08/2018
Goals: reperfusion of the necrotized area
a. To minimize myocardial damage
b. To preserve myocardial function
c. Prevent complications

1. Oxygen therapy
2. Pain control
 Opiate analgesic
a. Morphine sulfate (DOC)

 Vasodilator
a. Nitoglycerine

 Anxiolytic therapy
a. Benzodiazepine 51
 09/08/2018
3. Other pharmacologic therapy
 Thrombolytics
 to dissolve & lyse the thrombus in the coronary artery
(thrombolysis) allowing blood flow through the coronary
artery
 Do not affect the atherosclerotic lesion.
 Must be administered ASAP after the onset of symptoms that
indicate an AMI.

a. Streptokinase
 increases the amount of plasminogen activator thus increasing
the amount of both circulating & clot-bound plasminogen.
 Made from bacteria (risk of allergic reaction)
 Vasculitis is noted up to 9 days after adminstration.
 Not used if the patient received streptokinase in the past 6-12
months. 52
 09/08/2018
b. Tissue Plasminogen activator (t-PA)
 activates the plasminogen on the clot more than the
circulating plasminogen.
 Heparin can be used (to prevent another clot from formingh
at the same lesion site because t-PA dose not decrease the
clotting factors)

 Anticoagulants/antiplatelet
 Beta-adrenergic blockers
 Antidysrhythmics
 ACE inhibitors

4. Surgical management
 PTCA
 CABG
53
 09/08/2018
NURSING INTERVENTIONS:

1. Relieving chest pain.

2. Improving respiratory function.

3. Promoting adequate tissue perfusion.

4. Reducing anxiety.

5. Managing & monitoring potential complications

54
 Cardiac tamponade

09/08/2018
 is a rapid, unchecked increase in pressure in the pericardial
sac compressing the heart, impairing the diastolic filling,
reducing cardiac output

CAUSES:
1. Effusion
2. Hemorrhage due to trauma
3. Hemorrhage due to nontraumatic causes
4. Chronic renal failure
5. Connective tissue disorder
6. Acute myocardial infarction

55
Pathophysiology:

09/08/2018
accumulation of fluid in the pericardial sac

compression of the heart chambers

obstruction of blood flow into the ventricles

increase pressure in the pericardial sac

decreased venous return

reduces the amount of blood that can be pumped out

reduced cardiac output 56

 09/08/2018
Clinical manifestations:

1. Feeling of fullness within the chest ( from stretching of the

pericardial sac)
2. Elevated CVP with jugular vein distention (increased venous
pressure)
3. Shortness of breath
4. Pulsus paradoxus
5. Muffled heart sounds
6. Narrowed pulse pressure
7. Orthopnea
8. Diaphoresis
anxiety & restlessness
9. Cyanosis
10. Weak, rapid peripheral pulses
57
 09/08/2018
Diagnostic test:
1. Chest x-ray
2. ECG
3. Echocardiogram
4. CT scan or MRI

MEDICAL MANAGEMENT:
Goal: to relieve intrapericardial pressure & cardiac compression
1. Pericardiocentesis
2. Pericardiotomy
3. Insertion of a drain into the pericardial sac
4. Inotropic drugs
5. Blood transfusion
6. Protamine sulfate (heparin-induced tamponade)
7. Vitamin K administration (warfarin-induced tamponade) 58
 09/08/2018
Nursing responsibilities:

1. Monitor the cardiovascular & hemodynamic status frequently.

2. Monitor for pulsus paradoxus.
3. Watch closely for signs of increasing tamponade, increasing
dyspnea, & arrythmias.
4. Infuse IV solutions & inotropic drugs.
5. Administer oxygen therapy.
6. Monitor respiratory status.
7. Prepare for pericardiocentesis or thoracotomy.
8. Assess renal function status closely.
9. Monitor capillary refill time, LOC, peripheral pulses, & skin
temperature for evidence of diminished tissue perfusion.

59
 Cardiogenic shock

09/08/2018
 occurs when the heart cannot pump enough blood to supply
the amount of oxygen needed by the tissues.

 impairs tissue perfusion

CAUSES:
1. Myocardial infarction (most common)
2. Myocardial ischemia
3. End-stage cardiomyopathy
4. Myocarditis
5. Depression of myocardial contractility
6. Prolonged cardiac dysfunction
7. Acute mitral or aortic insufficiency
8. Ventricular septal defect
60
 09/08/2018
PATHOPHYSIOLOGY:

decreased contractility

decreased cardiac output

Myocardial ischemia

hypoxia

pulmonary pressure

pulmonary blood volume decreased BP

61
decreased coronary artery perfusion
 09/08/2018
Clinical manifestations:

1. Restlessness, confusion & agitation

2. Low blood pressure
3. Rapid & weak pulse
4. Cold & clammy skin
5. Rapid, shallow respirations
6. Increased respiratory crackles
7. Hypoactive bowel sounds
8. Oliguria
9. Narrowing pulse pressure
62
10.Dysrhythmias
 09/08/2018
Diagnostic tests:

1. Pulmonary artery pressure monitoring

2. ABG
3. ECG
4. Echocardiography
5. Serum cardiac enzymes
6. Cardiac catheterization

63
 09/08/2018
Medical management:

Goals:
 to increase cardiac output
 to improve myocardial perfusion
 to decrease cardiac workload

1. Intubation & mechanical ventilation

2. Supplemental oxygenation
3. Continuous cardiac monitoring
4. Maintaining at least 2 IV lines with large-gauge needles
5. IV fluids, crystalloids, colloids, or blood products
6. Strict bedrest
7. Mechanical assistance: IABP (Intra-aortic balloon pump)
64
 09/08/2018
7. Pharmacological therapy:
a. Vasodilator
b. Vasopressor
c. Diuretics
d. Inotropic drugs
e. Thrombolytics

NURSING RESPONSIBILITIES:
1. Monitor & record vital signs & peripheral pulses every 5
minutes until stable.
2. Assess the skin color & temperature.
3. Closely monitor PAP, PAWP & cardiac output.
4. Measure CVP.
5. Measure urine & output every through an indwelling catheter.
6. Monitor ABG, CBC & electrolyte levels.
65
7. Administer medications as ordered.
 09/08/2018
8. IABP:
 Move the client as little as possible.
 Never flex the “ballooned” leg at the hip.
 Never place the patient sitting position.
 Assess pedal pulses, skin temperature & color.
 Check the dressing over the insertion site for bleeding.

66
 09/08/2018
CONGESTIVE HEART FAILURE:
 Is the inability of the heart to pump enough blood to meet the
metabolic needs of the body.

 Results in intravascular & interstitial volume overload & poor

tissue perfusion.

 Most commonly occurs with disorders of cardiac muscle that

result in decreased contractile properties of the heart.

 Categories:
a. Left-sided failure
b. Right-sided failure
c. Systolic dysfunction
d. Diastolic dysfunction
67
 09/08/2018
Causes:

1. Myocardial dysfunction
 Coronary artery disease
 Ischemia
 Myocardial infarction
 Dilated cardiomyopathy

2. Arterial hypertension
3. Valvular heart disease

68
 09/08/2018
Etiologic factors:
1. Increased metabolic rate
2. Hypoxia
3. Anemia
4. Respiratory & metabolic acidosis
5. Cardiac dysrhythmias

69
 09/08/2018
PATHOPHYSIOLOGY:

1. Myocardial dysfunction
a. CAD
b. Ischemia
c. M.I . decreased blood flow to myocardium
d. Dilated cardiomyopathy
hypoxia - - - acidosis

necrosis

decreased contractility

CHF

70
 09/08/2018
2. Arterial hypertension increased workload of the heart

hypertrophy of myocardial muscle

fibers

decreased contractility of the

myocardium

decreased ability of the heart to

fill during diastole

increased amount of resistance

71
 09/08/2018
3. Valvular heart disease difficulty of blood in moving
forward

decreased ejection of the blood

increased pressure with in the heart

decreased myocardial contractility

pulmonary & venous congestion

72
 09/08/2018
• Left & right-sided dysfunction : word format

73
 09/08/2018
Compensatory mechanisms:
 all types of heart failure reduced cardiac output

triggers compensatory mechanism

at the expense of increased
ventricular work
a. Increased sympathetic activity
b. Renin-angiotensin aldosterone system
c. Ventricular dilation
d. Ventricular hypertrophy

74
 Clinical manifestations:
Left-sided Cardiac Failure:
1. Dyspnea on exertion
2. Paroxysmal nocturnal
dyspnea
3. Orthopnea
4. Cough
5. Pulmonary crackle
6. Lower than normal
oxygen saturation level
7. Restlessness & anxiety
8. Tachycardia/palpitations
9. Easily fatigued
10. Insomia
Right-sided Cardiac Failure:
1. Dependent edema
2. Weight gain
3. Hepatomegaly
4. Distended neck veins
5. Ascites
6. Anorexia & nausea
7. Nocturia
8. Weakness

09/08/2018 75
 09/08/2018
Diagnostic exam:

1. Chest x-ray
2. ECG
3. Liver & renal function test
4. ABG
5. Echocardiogram

76