Origins of symptoms in heart failure

Chronic heart failure is accompanied by disabling symptoms, poor quality of life, and marked exercise limitation. Despite being initiated by a reduction in left ventricular pump function, the syndrome that develops in treated heart failure is one in which a vast array of noncardiac abnormalities develop, many of which may limit exercise in their own right, and some of which may lead to progressive deterioration in left ventricular performance and prognosis. The conventional explanations for the development of symptoms and exercise limitation in heart failure are now seen as being inadequate in many respects. Exercise is usually limited by either dyspnea or muscular fatigue, and it was originally thought the former reflected elevated pulmonary capillary wedge pressures producing pulmonary congestion and edema, whereas the latter was due to inadequate cardiac output, leading to poor muscular perfusion. Recent evidence has shown, however that there is little correlation between left ventricular function and exercise Limitation; that the limiting symptoms can be changed by relatively minor alterations in the exercise test procedure; and that the hemodynamic characteristics of patients do not predict; whether fatigue or dyspnea is the predominant symptom. Abnormal peripheral blood flow, endothelial dysfunction, abnormal skeletal muscle structure and function, and skeletal muscle wasting all appear better correlated with symptom generation in heart failure than hemodynamic status. An early metabolic change in skeletal muscle, due in part to abnormal muscle metabolism, activates work-sensitive neural afferents (ergoreceptors) in the muscle, which reflexly increase sympathetic drive, ventilation, and generalized vasoconstriction as well as being prime candidates for carrying the fatigue signal to the cortical centers. Treatments that correct skeletal muscle abnormalities in chronic heart failure, such as ACE inhibitors and physical training, have been shown to improve exercise tolerance and to reduce both fatigue and dyspnea in addition, such treatments, in particular exercise training of muscle, reduce the overactivity of the work-sensitive ergoreceptors, giving a possible mechanism for both the generation of symptoms and the beneficial response to treatments that improve either muscle blood flow or metabolism in heart failure. The importance of peripheral factors in chronic heart failure stresses the multiorgan nature of this syndrome.