THE CONTEXT
Reduced ventricular output triggers compensatory systems that can worsen loading conditions when ventricular function is impaired. Different mechanical abnormalities also produce distinct patterns of failure.
Neurohormonal vicious circle
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Reduced cardiac output activates the sympathetic nervous system and the renin–angiotensin–aldosterone system.
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These systems normally support cardiac function, but in impaired ventricular function their activation increases both preload and afterload.
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A further fall in cardiac output produces additional activation and a further rise in peripheral vascular resistance, establishing a vicious circle.
Reduced ventricular contractility
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Myocardial infarction can cause segmental dysfunction. In coronary artery disease, poorly contracting akinetic or dyskinetic segments can distort the contraction and relaxation of normal segments.
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Myocarditis or cardiomyopathy can produce global dysfunction with progressive ventricular dilatation.
Pressure overload
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Hypertension and aortic stenosis are listed with left heart failure; pulmonary hypertension and pulmonary valve stenosis are listed with right heart failure.
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Initially, concentric ventricular hypertrophy maintains normal output by generating a high systolic pressure.
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Later myocardial changes and increasing obstruction lead to failure with ventricular dilatation and rapid clinical deterioration.
Ventricular inflow obstruction
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Mitral and tricuspid stenosis are associated with a small, vigorous ventricle and a dilated, hypertrophied atrium.
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Atrial fibrillation is common and often causes marked deterioration because ventricular filling depends heavily on atrial contraction.
Volume overload and arrhythmia
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Mitral or aortic regurgitation causes left ventricular volume overload; an atrial septal defect causes right ventricular volume overload.
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Ventricular dilatation and hypertrophy support a high stroke volume and help maintain cardiac output, but secondary myocardial changes eventually impair contractility and worsen failure.
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Tachycardia limits adequate cardiac filling, reducing cardiac output and producing back pressure.