Epidemiology
and Pathophysiology
HEART
FAILURE
Clinical Overview
Epidemiology
and Pathophysiology
As cardiac function decreases, the heart depends on three major compensatory mechanisms in order to maintain adequate cardiac output.7,9 Although these responses will maintain cardiac function at relatively normal levels for a period of time, they all have limited capacity. If the causative factor of the reduced function (for instance, decreased contractility) persists, the heart will eventually fail.
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The sympathetic nervous system is activated within seconds of a change in cardiac output, and serves as an immediate support mechanism.7 •Norepinephrine released into the myocardium maintains cardiac output by increasing both heart rate and contractility,•Norepinephrine released into the vascular beds causes vasoconstriction which redistributes blood away from nonessential organs to coronary and cerebral circulation.•Increases in systemic vascular resistance due to the peripheral vasoconstriction can help support blood pressure which may be reduced (BP = CO x TPR).6,9 |
Activation of the renin-angiotensin-aldosterone (RAA) system rapidly kicks in with heart failure, due to decreased renal perfusion caused by both a reduction in cardiac output and redistribution of blood away from nonessential organs (kidney).7,9 The kidney retains sodium and water in response to the perception of ineffective blood volume. The perception of decreased blood volume and the increase in sympathetic nervous activity stimulates renin release from the juxtaglomerular cells in the kidneys.
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In comparison to the rapid onset of sympathetic activation and RAA stimulation, ventricular hypertrophy, an increase in cardiac muscle mass, occurs more slowly. •May be stimulated by increases in preload or afterload or by decreases in contractility.7 •An important mechanism for improving contractile function•Hypertrophied cells that are exposed to continued stress eventually become fibrotic and inadequate in maintaining cardiac function. |
Vicious Cycle of Heart Failure
The compensatory mechanisms in heart failure eventually initiate a
vicious cycle which leads to continued worsening and downward
spiraling of the heart failure state. The peripheral vasoconstriction
mediated by increased sympathetic activity, angiotensin II, and other
possible mechanisms such as arginine vasopressin (AVP) causes an
increase in systemic vascular resistance or afterload. Afterload
resists myocardial fiber shortening and further decreases cardiac
output, which leads to further increases in sodium and water
retention and sympathetic nervous activity.7
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