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Heart failure results when cardiac output is inadequate for the needs of the body. A poorly understood defect in cardiac contractility is complicated by multiple compensatory processes that further weaken the failing heart. The drugs used in heart failure fall into three major groups with varying targets and actions.
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Heart failure is an extremely serious cardiac condition associated with high mortality. The fundamental physiologic defect in heart failure is a decrease in cardiac output relative to the needs of the body, and the major manifestations are dyspnea and fatigue. The causes of heart failure are still not completely understood. In some cases, it can be ascribed to simple loss of functional myocardium, as in myocardial infarction. It is frequently associated with chronic hypertension, valvular disease, coronary artery disease, and a variety of cardiomyopathies. More than one third of the cases are associated with a reduction of cardiac contractile force and ejection fraction (systolic failure, heart failure with reduced ejection fraction [HFrEF]). Another large group of cases is caused by stiffening or other changes in the ventricles that prevent adequate filling during diastole; ejection volume (stroke volume) is reduced but ejection fraction is normal (diastolic failure, heart failure with preserved ejection fraction [HFpEF]). The remaining cases can be attributed to a combination of systolic and diastolic dysfunction.
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The severity of heart failure is traditionally indicated on the New York Heart Association (NYHA) scale, which places patients at step I if symptoms occur only with maximal exercise, steps II and III with symptoms that occur with marked (II) or mild (III) exercise, and step IV if severe symptoms are present at rest. The natural history of heart failure is characterized by a slow deterioration of cardiac function, punctuated by episodes of acute cardiac decompensation that are often associated with pulmonary or peripheral edema or both (congestive heart failure).
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The reduction in cardiac output is best shown by the ventricular function curve (Frank-Starling curve; Figure 13–1). Changes in the ventricular function curve reflect some compensatory responses of the body and demonstrate some of the responses to drugs. As ventricular ejection decreases in HFrEF, the end-diastolic fiber length increases, as shown by the shift from point A to point B in Figure 13–1. Operation at point B is intrinsically less efficient than operation at shorter fiber lengths because of the increase in myocardial oxygen requirement associated with increased fiber tension and length (see Figure 12–1).
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