Acute Biologic Crisis

Heart Failure

-the inability of the heart to pump sufficient

blood to meet the needs of the tissues for
oxygen and nutrients.
Etiology:

1. Chronic Hypertension
2. Coronary Disease Artery-primary cause
of HF
3. Valvular Disease-blood has increasing
difficulty moving forward, increasing
pressure within the heart and increasing
cardiac workload
TYPES

1. Systolic Heart Failure

2. Diastolic Heart Failure
Left-Sided Cardiac Failure

Pulmonary congestion occurs when the left

ventricle cannot pump the blood out of the
chamber.
This
increases pressure in the left ventricle and
decreases the blood flow from the left atrium.
Left-Sided Cardiac Failure

Thepressure in the left atrium increases, which

decreases the blood flow coming from the
pulmonary vessels.
Theresultant increase in pressure in the
pulmonary circulation forces fluid into the
pulmonary tissues and alveoli; which impairs
gas exchange.
Clinical Manifestations:

Left-sided heart failure:

Pulmonary congestion
S3, or ventricular gallop,
Dyspnea, or shortness of breath
Orthopnea
Paroxysmal nocturnal dyspnea (pnd)
Pink (blood-tinged) frothy sputum
Oliguria
Clinical Manifestations:

Dizziness, lightheadedness, confusion,

restlessness, and anxiety
Palpitation
Fatigue
Right-Sided Cardiac Failure

When the right ventricle fails, congestion of the

viscera and the peripheral tissues
predominates.
This occurs because the right side of the heart
cannot eject blood and thus cannot
accommodate all the blood that normally
returns to it from the venous circulation.
Right-Sided Heart Failure:

Right Sided Heart Failure

Jugular vein distention
Edema of the lower extremities (dependent edema
Hepatomegaly
Ascites
Anorexia and nausea, and weakness and weight gain
due to retention of fluid
Diagnostics

Chest Xray (may show cardiomegaly or

vascular congestion)
Echocardiogram (shows decreased ventricular
function and decreased ejection fraction)
CVP (elevated in right-sided failure)
B-type natriuretic peptide (BNP) -is a marker of
ventricular dysfunction; >100 =CHF
Collaborative Management:

Medications:
Digitalis Therapy
-it is the major therapy for CHF
Collaborative Management:

Assess the heart rate before administration of digitalis. If

the heart rate is 60 bpm and below or 120 bpm and
above, withhold the drug. Bradycardia or rebound
tachycardia may occur.
Monitor serum K level. Hypokalemia enhances digitalis
toxicity.
Commonly used digitalis: Lanoxin (Digoxin),
Crystogdigin (Digitoxin),
Collaborative Management:

Evaluate effectiveness of digitalis:

-Increase CO
-Increased UO
-Stronger Pulse
-Lowering of BP
-Absence of crackles
Collaborative Management:

Digitalis Toxicity:
Bradycardia
GI Manifestations: Anorexia, Nausea and Vomiting,
Diarrhea
Dysrhythmias (most dangerous)
Altered visual perception (yellow or green vision; blurred
vision halos or rainbows
Antidote: Digoxin Immune Fab (Digibind)
Collaborative Management:

Diuretic Therapy
- The purpose of diuretic therapy is to decrease cardiac
workload by reducing circulating volume thereby
reducing preload.
- Assess for signs and symptoms of hypokalemia when
administering Thiazide and Loop diuretics.
Collaborative Management:

Diuretic Therapy
- Give potassium supplement and potassium rich foods
- Potassium rich food
- Diuretics are best administered early morning and or
early afternoon to prevent sleep pattern disturbance
related to nocturia.
Collaborative Management:

Diuretic Therapy
Thiazides (potassium-wasting)
Loop Diuretics (potassium-wasting)
Potassium-sparing
Collaborative Management:

Vasodilators
-to decrease afterload by decreasing resistance to
ventricular emptying
Nifedipine (CA channel blocker with vasodilator effect)
Captopril (Capoten) also has a vasodilator effect
Collaborative Management:

ACE inhibitors (eg, lisinopril [Prinivil, Zestril]

- ACE inhibitors promote vasodilation and diuresis
by decreasing afterload and preload
- Vasodilation reduces resistance to left
ventricular ejection of blood
Possible Nursing Diagnosis:

Activity intolerance r/t imbalance between oxygen

supply and demand secondary to decreased CO
Excess fluid volume r/t excess fluid/sodium intake or
retention secondary to CHF and its medical therapy
Anxiety r/t breathlessness and restlessness secondary to
inadequate oxygenation
Nursing Management

a. Acute phase
1. monitor and record BP, pulse, respirations, ECG and CVP to detect
changes in cardiac output
2. maintain client in sitting position to decrease pulmonary congestion and
facilitate improved gas exchange
3. auscultate heart and lung sounds frequently: increasing crackles,
increasing dyspnea, decreasing lung sounds indicate worsening failure
4. administer O2 as ordered to improve gas exchange and increase
oxygenation of blood; monitor arterial blood gases (ABG) as ordered to assess
oxygenation
Nursing Management

5. administer prescribed medications on accurate schedule

6. Monitor serum electrolytes to detect hypokalemia secondary to diuretic
therapy
7. monitor accurate input and output ( may require Foley cathether to allow
accurate measurement of urine output) to evaluate fluid status
8. if fluid restriction is prescribed, spread the fluid throughout the day to
reduce thirst
9. encourage physical rest and organized activities with frequent rest periods
to reduce the work of the heart
Nursing Management

10. provide a calm reassuring environment to decrease anxiety; this

decreases oxygen consumption and demands on the heart
11. educate client and family about the rationale for the regimen
12. establish baseline assessment for fluid status and functional abilities
13. monitor daily weights to evaluate changes in fluid status
14. assess at regular intervals for changes in fluid status or functional activity
level
Acute Myocardial
Infarction
Acute Myocardial Infarction (AMI)

Myocardial infarction (MI) is also known as Coronary Occlusion,

Heart Attack.
Death of heart tissue caused by lack of oxygenated blood flow
Formation of localized necrotic areas within the myocardium
Myocardial Infarction

REMEMBER:
Ischemic tissue progresses to
Injured tissue, which progresses to
Infarcted or dead tissue.
Causes

1. Coronary Atherosclerotic Heart Disease

2. Coronary Thrombosis/ Embolism
3. Decreased Blood flow with shock or
haemorrhage
4. Direct Trauma
Pathophysiology

Coronary artery blood flow is blocked by

atherosclerotic narrowing, thrombus formation
or persistent vasospasm; myocardium supplied
by the arteries is deprived of oxygen; persistent
ischemia may rapidly lead to tissue death
Clinical Manifestations

1. Acute substernal pain described as crushing

which may radiate to back or jaw
2. Levines sign (chest hand-clutching). This is
the universal sign of distress in agina pectoris and
MI.
Clinical Manifestations

3. Feeling of impending doom, restlessness

4. Shortness of breath
5. Shock
-Manifested by SBP <80mmHg, lethargic, cold
diaphoresis, peripheral cyanosis, weak pulse.
Clinical Manifestations

6. Oliguria
7. Gas pains around the heart, nausea and
vomiting
Clinical Manifestations

8. Fever-occurs within 24 hours and extens to 3-7 days

9. Acute Pulmonary Edema- dyspnea, orthopnea
Clinical Manifestations

8. Fever-occurs within 24 hours and extends to 3-7 days

9. Acute Pulmonary Edema- dyspnea, orthopnea
Diagnostics

1. Electrocardiogram (12-lead) capable of diagnosing

MI in 80% of patients, making it an indispensable,
noninvasive, and cost-effective tool.
-ST elevation, accompanied by T-wave inversion; and
later new pathologic Q wave
Diagnostics

2. Cardiac Enzymes Troponin I has been shown to be a

specific indicator of myocardial infarction. It appears 3-6
hours after MI, peaks at 16 hours and decreases in 9-10
days.
-elevated CK- MB isoenzymes and LDH
Diagnostics

1. WBC count leukocytosis (10,000/mm3 to 20,000/mm3)

appears on the second day after an MI and disappears
after 1 week
2. Tranesophageal Echocrdiography (TEE) is an imaging
technique in which transducer is placed against the
wall of the esophagus; the image of the myocardium is
clearer when the esophageal site is used.
Medications

1. Analgesic-priority
-Morphine Sulfate, Lidocaine, Nitroglycerine are
administered via IV. Morphine is Drug of Choice.

2. Thrombolytic therapy
-to disintegrate blood clot by activating the fibrinolytic
process.
e.g. Streptokinase, Urokinase, Tissue plasminogen
activator (TPA)
Medications

3. Anticoagulant & Antiplatelet meds-given after

thrombolytic therapy to maintain arterial patency.
INVASIVE CORONARY ARTERY
PROCEDURES

1. Percutaneous Transluminal Coronary Angioplasty

In PTCA, a balloon-tipped catheter is used to open blocked coronary
vessels and resolve ischemia.
The purpose of PTCA is to improve blood flow within a coronary artery by
compressing and cracking the atheroma.
PTCA is carried out in the cardiac catheterization laboratory.
INVASIVE CORONARY ARTERY
PROCEDURES

1. Percutaneous Transluminal Coronary Angioplasty

Hollow catheters called sheaths are inserted, usually in the femoral artery
Catheters are then threaded through the femoral artery, up through the
aorta, and into the coronary arteries.
When the catheter is properly positioned, the balloon is inflated with high
pressure for several seconds and then deflated. The pressure compresses
and often cracks the atheroma
Coronary Artery Stent

A stent is a metal mesh that provides structural support to a vessel at risk of

acute closure. The stent is positioned over the angioplasty balloon.
When the balloon is inflated, the mesh expands and presses against the
vessel wall, holding the artery open.
The balloon is withdrawn, but the stent is left permanently in place within
the artery.
Eventually, endothelium covers the stent and it is incorporated into the
vessel wall.
Coronary Artery Stent

Because of the risk of thrombus formation within the stent, the patient
receives antiplatelet medications, usually aspirin and clopidogrel.
Nursing Interventions: (PTCA)

Pre-Procedure:
1. Provide psychosocial support.
2. Assess for allergy of iodine or seafoods because the contrast medium used
is iodinated.
3. Obtain baseline v/s.
4. Npo to prevent n/v
5. Administer sedative as ordered
6. May experience warm or flushing sensation as the contrast medium is
injected.
Nursing Interventions: (PTCA)

After-Procedure:
1. Bed-rest
2. Monitor v/s and especially peripheral pulses
3. Monitor ECG
4. Apply pressure dressing and a small sandbag or ice over the punctured site to
prevent bleeding
5. Immobilize affected extremity in extension to promote circulation.
6. Monitor extremities for color, temperature, pulse and sensation.
Impaired circulation: pallor, cyanosis, cold skin, diminished pulse or pulselessness,
numbness and tingling sensation.
Nursing Interventions:

Promoting Oxygenation:
1. Avoid overfatigue, stop activity IMMEDIATELY in the presence of chest
pain, dyspnea, lightheadedness or faintness.
2. Administer O2
3. Monitor v/s
4. Position the patient in semi-fowlers
5. Monitor the following: ECG, VS, Effects of daily activities , Rate and Rhythm
6. Promote Rest
Nursing Interventions:

Promoting Comfort:
Relieve pain. Administer Morphine Sulfate as ordered.
The client is usually placed on bed rest with commode
Explain the purpose of CCU (Coronary Care Unit) for continuous monitoring
and safety
Nursing Interventions:

Promoting Activity
Gradual increase in activity is encouraged. After the first 24-48 hours, the
client may be allowed to sit on a chair for increasing periods of time may
ambulate 4th-5th day.

Promoting Nutrition and Elimination

Provide small, frequent feedings
Low calorie, low cholesterol, low sodium diet
Administer stool softener
CORONARY ARTERY BYPASS GRAFT
(CABG)

a surgical procedure in which a blood vessel from

another part of the body is grafted onto the occluded
coronary artery below the occlusion in such a way that
blood flow bypasses the blockage
the surgeon performs a median sternotomy and
connects the patient to the cardiopulmonary bypass
(CPB) machine.
CORONARY ARTERY BYPASS GRAFT
(CABG)

Next, a blood vessel from another part of the patients

body (eg, saphenous vein, left internal mammary
artery) is grafted distal to the coronary artery lesion,
bypassing the obstruction.
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.
Cardiac Rehabilitation

Goals of Rehabilitation:
1. To live as full, vital and productive life as possible.
2. Remain within the limits of the hearths ability to
respond to activity and stress.
Cardiac Rehabilitation

Progressive 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.
Exercise must be done twice a day for about 20 minutes.
Teaching and Counseling

Self-Management Education Guide: Discharge after MI

Discontinue Smoking
Control Hypertension
Weight reduction program
Progressive exercise
Stress management techniques
Resumption of sexual activity after 4-6 weeks from discharge, if appropriate.
Or when the client is capable of walking 1-2 flights of stairs without difficulty.
Teaching and Counseling

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.
Invasive Hemodynmaic
Monitoring
Central Venous Pressure

It is measured by positioning a catheter in the vena cava or right atrium

and connecting it to a pressure monitoring system.
Monitors blood volume, adequacy of venous return to the heart, pump
function of the right side of the heart.
the O level of the water manometer should be placed at the right, mid-
axillary, 4th ICS. This is the approximate level of the right atrium when the
client is in supine position.
Central Venous Pressure

Place the client in supine position or in the same position as during the
initial reading to get accurate readings. Position can affect CVP readings.
Practice strict asepsis to prevent infection.

Normal reading:
The normal CVP is 2 to 6 mm Hg
Central Venous Pressure
Pulmonary Artery Pressure Monitoring

PULMONARY ARTERY PRESSURE (PAP) AND PULMONARY CAPILLARY WEDGE

PRESSURE (PCWP)
SwanGanz catheter is inserted via antecubital vein into the right side of
the heart and is floated into the pulmonary artery.
It has four to five lumens to measure various cardiac pressures.
It reflects pressure in the left heart. Left-sided congestive heart failure may
lead to pulmonary edema. This causes congestion of blood in the
pulmonary artery (pulmonary hypertension)
Elevated PAP and PCWP indicate left side CHF
Pulmonary Artery Pressure Monitoring

Pulmonary artery catheters are balloon-tipped, flow-directed catheters

that have distal and proximal lumens.
Normal Range: PAP 4-12 mmHg
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