CHAPTER 81 Heart Failure

Heart failure (HF) is a debilitating cardiac syndrome characterized by dyspnea, poor exercise tolerance, and chronic fatigue along with high morbidity and mortality. Heart failure may be defined as the pathophysiologic state in which the heart is incapable of pumping a sufficient supply of blood to meet the metabolic requirements of the body or requires elevated ventricular filling pressures to accomplish this goal. The caveat about high filling pressures acknowledges that a failing heart may continue to maintain systemic perfusion via the compensatory Frank-Starling mechanism, resulting in the maintenance of normal stroke volume (SV) despite reduced ejection fraction (EF). Conversely, low filling pressure with hypoperfusion indicates a pump-priming problem distinct from cardiac disease. The American Heart Association (AHA) and American College of Cardiology (ACC) guidelines define HF related to systolic dysfunction as a left ventricular (LV) ejection fraction (LVEF) less than 40%. Diastolic dysfunction, a pathologic condition involving failure of ventricular relaxation with consequent high filling pressures, may exist in up to half of older individuals with HF. HF is a progressive and multifaceted disease that begins long before symptoms and signs are evident. A complex neurohormonal regulatory relationship exists between the heart and multiple organ systems. Feedback loops mediated through a variety of vasoactive substances secreted by the heart, autonomic nervous system, kidneys, adrenals, lungs, and vascular endothelium are most important. Perturbations of function in any of these organs affect the others (Fig. 81-1). Accordingly, the cardiovascular system should be viewed as a dynamic one, continually adapting to optimize organ perfusion. Dysfunction of the heart or any component of the cardiopulmonary system initiates adaptive neurohormonal activation of the sympathetic nervous system, renin-angiotensinaldosterone system (RAAS), natriuretic peptides, endothelin (ET), vasopressin, and other regulatory mechanisms. Neurohormonal activation initially compensates for circulatory system dysfunction. These mechanisms eventually lead to increased mechanical stress on the failing heart, however, causing maladaptive electrical and structural events, progressive cardiac fibrosis and apoptosis, and further impairment of systolic and diastolic function. This creates a vicious cycle of increasing myocardial dysfunction causing further neurohormonal modulation, leading to a progressive downward spiral. The degree of myocardial dysfunction depends on both the amount of primary myocardial disease and other pathologic conditions, particularly in the pulmonary, renal, and peripheral vascular systems. Understanding these underlying compensatory mechanisms is leading to progressive improvement in the management of HF, with a shift from a hemodynamic to a neurohormonal model. EPIDEMIOLOGY