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CARONARY ARTERY

DISEASE & CONGESTIVE

HEART FAILURE

Margaret Xaira R. Mercado RN

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CORONARY ARTERY DISEASE

(CAD)

Refers to a variety of disease pathologic

conditions causing narrowing or

obstruction of coronary arteries, therefore

decreasing blood supply to themyocardium (decreased perfusion to

myocardial tissue leads to an inadequate

myocardial oxygen supply)

Results from central narrowing large and

medium-sized coronary arteries due tointimal plaque formation

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Atherosclerosis (deposits of cholesterol

and lipids within the walls of the artery)is the major causative factor. It may

manifest as angina pectoris or MI.

Increased potential for thrombosis and

embolism to occur Significant if 50% of the left coronary

arterial lumen is reduced or 75% of the

other coronary artery

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RISK FACTORS

a. Age: above 30-50

b. Sex: male and postmenopausal women

c. Race: nonwhites have higher mortality

rates

d. Family history of CAD

e. Hypertension

f. Diabetes milletus

g. Smoking

h. Obesity

i. Sedentary lifestyle

j. Hyperlipidemia

k. Elevated serum uric acid levels

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PATHOPHYSIOLOGY

Fatty streakformation in thevarcular intima

T-cells andmonocytes ingestlipids in the area

of deposition

AtheromaNarrowing of the

arterial lumen

Reducedcoronary blood

flow

Myocardialischemia

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CONGESTIVE HEART FAILURE

Refers to the inability of the heart to pump

an adequate supply of blood to meet the

metabolic needs of the body

A syndrome of systemic or pulmonarycirculatory congestion caused by

decreased myocardial contractility

resulting in inadequate cardiac output to

meet oxygen demands

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COMMON TYPES

a. Left-sided heart failure

b. Right-sided heart failure

The right-sided failure is commonly due toleft-sided failure (cor pulmonale)

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NEW YORK HEART ASSOCIATIONS

CLASSIFICATION OF HEART FAILURE

CLASS 1

Ordinary physical activity does

not cause chest pain and fatigue

No pulmonary congestion

Asymptomatic

No limitation in activities of daily

living (ADL)

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CLASS 2

Slight limitation in ADLs

No symptom at rest

(+) symptom with increased activity

Basilar crackles and S3 heart sound

CLASS 3

Marked limitation in ADLs

Comfortable at rest but symptoms

present in less than ordinary activities

CLASS 4

Symptoms are present at rest

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ETIOLOGY OF CHF

a. Decreased cardiac contractility due to

cardiac diseases (CAD, MI,

cardiomyopathy)

b. Valvular heart diseases

c. Hypertensive heart disease

d. Dysrhythmias

e. Cor pulmonale secondary to lung

diseases

f. Pericardial tamponade andpericarditis

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LEFT-SIDED HEART FAILURE

Left ventricular damage usually due to MI,hypertension, ischemic heart disease, aortic valve

stenosis, or mitral stenosis

Left ventricular damage causes blood to back-up

through the left atrium and into the pulmonary veins.Increased pressure causes transaction into the

interstitial tissues to the lungs with resultant

pulmonary congestion

The congestion occurs primarily in the lungs leading

to the symptoms referable to the pulmonary systems.

Blood flow from the left ventricle is diminished,

causing decreased flow to the brain, kidneys and

tissues

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ASSESSMENT

RESIPIRATORY SYSTEM

Dyspnea on exertion

Paroxysmal nocturnal dyspnea

Orthopnea Adventitious breath sounds: pulmonary

crackles/rales (moist), possible bronchial

wheezing

Cough with pinkish, frothy to blood-tingedsputum

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CARDIOVASCULAR SYSTEM

Peripheral and central cyanosis with pallor

of the skin Tachycardia with S3 heart sound, PMI

displaced laterally

Decreased peripheral pulses and capillary

refill longer than 3 seconds

OTHER MANIFESTATIONS

Cool extremities

Muscle weakness, malaise, easyfatigability

Insomnia and restlessness

Oliguria

Signs of cerebral anoxia

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DIAGNOSTIC TESTS

CXR: cardiac hypertrophy (cardiomegaly),vascular congestion of the lung fields

2D ECHOCARDIOGRAPHY: increased

size of cardiac chamber

ECG: may identify cardiac hypertrophy

ABG: decreased partial oxygen pressure

(PaO2), increased partial carbon dioxide

pressure (PaCO2)

PULSE OXIMETER: decreased SaO2

PAP & PWP (pulmonary artery pressure &

pulmonary wedge pressure): increased

depends on the degree of heart failure

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RIGHT-SIDED HEART FAILURE

Weakened right ventricle is unable to

pump blood into the pulmonary system;

systemic venous congestion occurs as

pressure builds-up

Caused by left-sided heart failure, right

ventricular infarction, atherosclerotic

heart disease, chronic obstructive

pulmonary disease (COPD), pulmonic

stenosis, or pulmonary embolism

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PATHOPHYSIOLOGY

Right ventricularfailure

Blood pooling in the

venous circulation

Increasedhydrostatic pressure

Peripheral ede a

Right ventricularfailure

Blood pooling

Venouscongestion in thekidney, liver and

GIT

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ASSESSMENTSYSTEMIC MANIFESTATIONS:

Distended neck vein (jugular venous

distention)

Bounding pulses

Peripheral dependent pitting edema

Ascites

Hepatomegaly

Oliguria

Weight gain Cool extremities

Anorexia

Nausea

Body weakness

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DIAGNOSTIC TESTS

CHEST XRAY: cardiomegaly

ELECTROCARDIOGRAM (ECG): cardiac

hypertrophy

2D ECHOCARDIOGRAM: hypokinetic heart,

increased size of cardiac chambers

ABG: decreased partial pressure of oxygen

PULSE OXIMETER: decreased oxygen

saturation

LIVER ENZYME: increased ALT (SGPT)

PCWP is increased in left-sided CHF and CVP

is increased in right-sided CHF

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NURSING INTERVENTIONS

1. Monitor and improve clients cardiopulmonary stateAssess respiratory status assess breath sounds for

presence of adventitious breath sounds

Provide adequate ventilation when CHF progresses to

pulmonary edemaadminister O2 therapy

maintain client on semi or high foelwrs position to

improve chest expansion

Monitor ABG

Monitor the hemodynamic parameters: heart rate and

rhythm, CVP and PCWP

Weigh client daily and monitor for fluid retention

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2. Increase cardiac output

monitor VS

ECG and hemodynamic monitoring administer digitalis as ordered and monitor

effects

administer vasodilators as ordered

3. Provide physical and emotional rest

maintain a quiet and relaxed environment

maintain bed rest with limited activity to

provide adequate rest periods to preventfatigue

Organize nursing care around rest periods

Assess level of anxiety

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4. Prevent complications of immobility

Assist the client in active/assistive ROM or perform

passive ROM

Apply anti-embolic stockings to prevent deep vein

thrombosis (as ordered)

5. Reduce/eliminate edema

Obtain daily weights and report if the client gains 3

pounds or more per day (indicates fluid retention)

Maintain adequate intake and output recording

Assess for peripheral edema

Measure abdominal girths daily

Monitor electrolyte levels

Monitor CVP and PCWP readings

Administer diuretics as ordered

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6. Provide meticulous skin care

7. Provide other dependent nursing

interventions:

Determination and elimination/control of

underlying cause

Sodium restricted diet to decrease fluid

retention and cardiac workload If medical therapy is unsucessful, intra-

aortic balloon pump, cardiac

transplantation, or mechanical hearts may

be employed Drug therapy: cardiac glycosides, diuretics,

vasodilators and anti-lipidemics

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8. Provide client teaching and discharge

planning:

Monitoring self daily for signs andsymptoms of CHF: pedal edema, weight

gain of 1-2lbs in a 2-day period, dyspnea,

loss of appetite, cough

Medication regimen: Name, purpose,

dosage, frequency, and side-effects (i.e.,

digitalis, diuretics)

Prescribed dietary meal planning: low/

restricted sodium; small, frequent meals

Avoidance of fatigue and planning for restperiods

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PHARMACOLOGY

VASODILATORS

Acts to directly relax vascular muscle tone

causing a decrease in blood pressure with

pooling of blood in the veins

Decrease preload and afterload

ACE INHIBITORS

Agents that block the conversion of

angiotensin I to angiotensin II causing

blockage of vasoconstriction and decreased

blood volume

Decrease afterload

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DIURETICS

Employed to decrease the blood volumecausing a decrease in venous return and

blood pressure

Decrease preload and afterload

BETA STIMULATORS

Stimulates the beta receptors in the

sympathetic nervous system, thereby

increasing the myocardial contraction

(positive inotropic effect)

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CARDIOTONIC DRUGS

Agents that affect the intracellular

calcium levels in the heart muscles

leading to increased cardiac output,

increased renal blood flow, increased

perfusion and increased urineformation

Include cardiac glycosides and the

phosphodiesterase inhibitors