Pathophysiology of Heart Failure

Initially, myocardial dysfunction and the attendant reduction of forward cardiac output lead to expansion of intravascular volume and activation of neurohumoral systems, particularly the sympathetic nervous system and the renin—angiotensin system (Figure 33-1). These compensatory responses maintain perfusion to vital organs by increasing left ventricular preload, stimulating myocardial contractility, and increasing arterial tone. Acutely, these mechanisms help to sustain cardiac output by allowing the heart to operate at higher end-diastolic volumes, leading to increased stroke volume; concomitant peripheral vasoconstriction allows for regional redistribution of the cardiac output to critical organs. Unfortunately, each of these compensatory responses will also promote disease progression. Expansion of the intravascular volume and elevated ventricular chamber volumes lead to increased diastolic and systolic wall stress; these changes in turn impair myocardial energetics and induce hypertrophic remodeling. Neurohumoral activation leads to arterial and venous constriction; the former increases left ventricular afterload (thereby compromising left ventricular stroke volume) and the latter increases preload, thereby exacerbating both diastolic and systolic wall stress. In addition, the neurohumoral effectors (such as nor-epinephrine [NE] and angiotensin II [AngII]) may act directly on the myocardium to promote unfavorable remodeling by causing myocyte apoptosis, abnormal gene expression, and alterations in the extracellular matrix.

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