Diminished cardiac output leads to decreased renal perfusion that in turn triggers the renin-angiotensin-aldosterone axis, increasing intravascular volume and pressures (Chapters 4 and 10). Unfortunately, with a failing heart, these compensatory effects exacerbate the pulmonary edema. With further progression of CHF, prerenal azotemia may supervene, with impaired excretion of nitrogenous wastes and increasing metabolic derangement. In severe CHF, diminished cerebral perfusion may manifest as hypoxic encephalopathy marked by irritability, diminished cognition, and restlessness that can progress to stupor and coma.
Treatment for CHF is typically focused—at least initially—on correcting the underlying cause, for example a valvular defect or inadequate cardiac perfusion. In lieu of such options, the clinical approach includes salt restriction or pharmacologic agents that variously reduce volume overload (e.g., diuretics), increase myocardial contractility (so-called “positive inotropes”), or reduce afterload (adrenergic blockade or inhibitors of angiotensin-converting enzymes). Angiotensin-converting enzyme inhibitors appear to benefit patients not only by opposing aldosteronemediated salt and water retention, but also by limiting cardiomyocyte hypertrophy and remodeling through uncertain mechanisms. Although cardiac resynchronization therapy (exogenous pacing of both the right and left ventricles) and cardiac contractility modulation (exogenous stimulation of cardiac muscle) have recently augmented the cardiologist’s armamentarium, CHF remains a serious cause of human morbidity and mortality.
Right-sided heart failure is usually the consequence of left-sided heart failure, since any pressure increase in the pulmonary circulation inevitably produces an increased burden on the right side of the heart. Consequently, the causes of right-sided heart failure include all of those that induce left-sided heart failure. Isolated right-sided heart failure is infrequent and typically occurs in patients with one of a variety of disorders affecting the lungs; hence it is often referred to as cor pulmonale. Besides parenchymal lung diseases, cor pulmonale also may arise secondary to disorders that affect the pulmonary vasculature, for example, primary pulmonary hypertension (Chapter 13), recurrent pulmonary thromboembolism, or conditions that cause pulmonary vasoconstriction (obstructive sleep apnea). The common feature of these disorders is pulmonary hypertension (discussed later), which results in hypertrophy and dilation of the right side of the heart. In cor pulmonale, myocardial hypertrophy and dilation generally are confined to the right ventricle and atrium, although bulging of the ventricular septum to the left can reduce cardiac output by causing outflow tract obstruction.
The major morphologic and clinical effects of pure right-sided heart failure differ from those of left-sided heart failure in that engorgement of the systemic and portal venous systems typically is pronounced and pulmonary congestion is minimal.
MORPHOLOGYLiver and Portal System. Theliverusuallyisincreasedinsizeandweight(congestive hepatomegaly). Acutsectiondisplaysprominentpassive congestion, apatternreferredtoasnutmeg liver (Chapter4);congestedcentrilobularareasaresurroundedbyperipheralpaler,noncongestedparenchyma.Whenleft-sidedheartfailureisalsopresent,severecentralhypoxiaproducescentrilobular necrosis inadditiontothesinusoidalcongestion.Withlong-standingsevereright-sidedheartfailure,thecentralareascanbecomefibrotic,creatingso-calledcardiac cirrhosis.