impairs the ventricle’s ability to fill or to eject blood properly. Etiology The etiology of HF can be divided into the following three broad categories: 1. Anatomic or functional abnormalities of the coronary vessels, myocardium, or cardiac valves, of either sudden or gradual onset 2. Neurohormonal overexpression that causes activation of the adrenergic nervous system and renin-angiotensin system 3. Extracardiac factors that cause excessive demand on the cardiovascular system The most common diseases associated with HF are coronary artery disease, hypertension, and dilated cardiomyopathies Cardiomyopathy, the most common cause of HF, is a disease process of the myocardium that affects the heart’s pumping ability. Classification of heart muscle disease is complex; an expert panel defined cardiomyopathies as a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic. Cardiomyopathies either are confined to the heart or are part of generalized systemic disorders, often leading to cardiovascular death or progressive heart failurerelated disability. 5 Cardiomyopathies have been divided into two major groups: 1. Primary (including genetic, nongenetic, and acquired cardiomyopathies)confined to the heart muscle 2. Secondaryheart muscle involvement as part of a general or systemic disease or disorder Risk Factors. Many individuals with HF have antecedent hypertension or myocardial infarction (MI). Other risk factors include coronary artery disease, diabetes, renal disease, obesity, smoking, and increasing age. Pathophysiology HF is a clinical syndrome characterized by signs and symptoms of volume excess. Whereas there can be several causes of the HF, common pathophysiologic mechanisms characterize this important condition. Understanding these mechanisms is critical to selection of successful therapeutic interventions. Systolic Dysfunction: Heart Failure with Reduced Ejection Fraction Systolic dysfunction, which accounts for about half of all HF cases, is a decrease in both ejection fraction (40% or less) and cardiac output. In systolic dysfunction, when looking at a hemodynamic model, the three determinants of ventricular functionpreload, contractility, and afterloadare usually altered. Preload is the degree of myocardial fiber stretch at the end of ventricular filling. When the heart ejects subnormally, there is an increased volume of blood left in the ventricular chambers (increased left ventricular end-systolic volume). This excess volume leads to distention of the ventricles and increased interventricular pressure at the onset of diastole. Filling must then occur at higher pressures during diastole. At small increases of volume and pressure, nonfailing myocardial fibers have the intrinsic property of increasing their force of contraction in an attempt to revert the subsequent volume and pressure conditions of both heart ejection and filling back to normal. This intrinsic property also enables the heart to maintain cardiac output during states of pressure or volume overload. However, in the failing heart, the failing myocardial fibers are both excessively overloaded and stretched beyond lengths commensurate with the normal reflex-increased force of contraction. This results in left ventricular remodeling, with dilation and impaired contractility, and activation of the sympathetic and renin-angiotensin-aldosterone systems. The ventricular dysfunction in HFrEF is accompanied by a decrease in myocardial contractility, a reduction in ejection fraction, and often a reduction in stroke volume and cardiac output. If HF is left untreated, symptoms develop and worsen, with declining functional capacity, recurrent acute decompensated events, life-threatening arrhythmias, and pump failure. Effective treatment of HF, primarily pharmacotherapy, depends on the interruption of left ventricular remodeling and the pathophysiologic processes that accompany it. Afterload is the amount of left ventricular wall tension that develops during systole; it is determined by both the size of the ventricular chamber and the dynamic vascular resistance against which the heart contracts. According to Laplace’s law, an increase in the radius of the ventricle results in an increase in wall tension. Because systolic blood pressure closely approximates afterload, it [Show less]

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