Page 580 - Cardiac Nursing

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556 PA R T IV / Pathophysiology and Management of Heart Disease

Table 24-1 ■ CONDITIONS ASSOCIATED WITH HEART FAILURE
Abnormal Abnormal Myocardial Increased Metabolic
Volume Load Pressure Load Abnormalities Filling Disorders Demand
Aortic valve Aortic stenosis Cardiomyopathy Mitral stenosis Anemias
incompetence Hypertrophic Myocarditis Tricuspid stenosis Thyrotoxicosis
Mitral valve cardiomyopathy Coronary heart disease Cardiac tamponade Fever
incompetence Coarctation of the aorta Ischemia Restrictive pericarditis Beriberi
Tricuspid valve Hypertension Infarction Restrictive cardiomyopathy Paget’s disease
incompetence Primary Arrhythmias Arteriovenous fistulas
Left-to-right shunts Secondary Toxic disorders Pulmonary emboli
Secondary hypervolemia Alcohol Systemic emboli
Cocaine
Administration of cardiac
depressants agents or
salt-retaining drugs

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(LV) function and neurohormonal regulation. Any disorder that morbidity and mortality. Four stages of HF were identified.
places the heart under an increased volume or pressure load or Stage A identifies the patient who is at high risk but has no
that produces primary damage or an increased metabolic demand structural heart disease; stage B refers to a patient with struc-
on the myocardium may result in HF (Table 24-1). Over the last tural heart disease but no symptoms of HF; stage C denotes the
decade there has been a primary shift in the etiology of HF with patient with structural heart disease and current or previous
coronary artery disease (CAD) surpassing hypertension or valvu- symptoms of HF; and stage D describes the patient with end-
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lar heart disease. As treatment modalities for both the acute and stage disease that requires special interventions (Fig. 24-1). The
chronic treatment of CAD improve, the number of patients living importance of this staging system arises from the fact that,
with CAD grows. while treatment options for HF have advanced in the last
Ventricular dysfunction begins with injury. It is vital for the decade, once myocyte, myocardial, and systemic changes have
clinician to identify the underlying and the precipitating causes begun, the only treatment option is altering the trajectory of
of HF. CAD is the underlying cause of HF in two thirds of pa- the syndrome as cure is seldom an option.
tients with systolic dysfunction. Hypertension is implicated in As the understanding of the mechanisms underlying both
both systolic and diastolic dysfunctions. Arrhythmias are com- the development and progression of the syndrome have
mon in patients with underlying structural heart disease; and evolved, much attention of late has been placed on identifying
they commonly precipitate an acute decompensation in pa- the factors that put patients at risk for developing the syndrome
tients with stable HF. These arrhythmias may take the form of (Table 24-2). While it is not surprising that advancing age, his-
tachyarrhythmias (most commonly atrial fibrillation), marked tory of CAD, MI, or hypertension are associated with develop-
bradycardia, degrees of heart block, and abnormal intraventric- ing HF, a robust association has been seen in patients with both
ular conduction, such as left bundle-branch block or ventricu- Type II diabetes mellitus (DM) 9,10 and obesity, and the subse-
lar arrhythmias. Other precipitating factors include systemic in- quent syndrome of HF. The worldwide epidemic of Type II DM
fections, anemias, and pulmonary emboli that all place and obesity make them potentially modifiable targets to reduce
increased metabolic and hemodynamic demand on the heart. incidence of HF.
Administration of cardiac depressants or salt-retaining drugs The clinical manifestations of acute and chronic failure de-
may precipitate HF; examples may include corticosteroids, pend on how rapidly the syndrome of HF develops. Acute HF
nondihydropyridine calcium-channel antagonists, and nons- may be the initial manifestation of heart disease but is more com-
teroidal anti-inflammatory drugs (NSAIDs). Alcohol is a po- monly an acute exacerbation of a chronic cardiac condition. The
tent myocardial depressant and may be responsible for the de- marked decrease in LV function may be caused by acute MI or
velopment of cardiomyopathy. Inappropriate reduction in acute valvular dysfunction. The events occur so rapidly that the
therapy is perhaps the most common cause of decompensation sympathetic nervous system compensation is ineffective, resulting
in a previously compensated patient, with reduction in phar- in the rapid development of pulmonary edema and circulatory
macological therapy or dietary excess of sodium. collapse (cardiogenic shock). Chronic HF develops over time and
is usually the end result of an increasing inability of physiologic
Stages of HF mechanisms to compensate.
The writing committee of the American College of Cardiology
and the American Heart Association (ACC/AHA) Task Force Low and High Cardiac Output Syndromes
decided to emphasize the evolution and progression of HF in In response to high blood pressure and hypovolemia, low cardiac
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their most recent revision of the guidelines. This classification output syndrome can appear. The word syndrome implies that the
recognizes that HF, like CAD, has established risk factors, that failure represents a reaction rather than a primary pathologic
the progression of HF has asymptomatic and symptomatic process. Low cardiac output syndrome is evidenced by impaired
phases, and that treatments prescribed at each stage can reduce peripheral circulation and peripheral vasoconstriction.