Systolic function and exercise capacity are unrelated in chronic heart failure, but overlapping hemodynamic abnormalities in the heart, lung, and skeletal muscle lead to exercise intolerance.
Exercise intolerance in chronic heart failure is multifactorial, involving diastolic dysfunction, skeletal muscle abnormalities, vasodilatory defects, and neurohumoral changes, rather than just systolic dysfunction.
PURPOSE: To synthesize information on hemodynamic determinants of exercise capacity in patients with chronic heart failure. DATA IDENTIFICATION: Relevant studies published from the mid-1960s to the present were identified by a manual search of the English-language literature and by bibliographic review of pertinent articles. STUDY SELECTION: Both controlled and observational studies that reported measures of either exercise time or oxygen uptake and hemodynamic variables in patients with heart failure were reviewed for quality and included when relevant to the discussion. DATA EXTRACTION: Key conclusions or data, or both, were extracted from each article and described. DATA SYNTHESIS: Exercise intolerance is a hallmark of chronic congestive heart failure. Studies have emphasized central factors and indices of systolic ventricular function, but poor relations have been consistently found between these measurements and exercise capacity. Recent data suggest that diastolic function (that is, ventricular filling and compliance) is an important factor affecting the ability to increase cardiac output and determining exercise capacity, but this issue needs further study. A clearer picture of histologic and biochemical abnormalities in skeletal muscle has recently emerged; patients with heart failure show greater glycolysis, reduced oxidative phosphorylation, and reduced oxidative enzyme activity. Vasodilatory abnormalities in heart failure were first described more than 20 years ago, and such abnormalities may underlie recently reported reductions in skeletal muscle blood flow during exercise. Relative hyperventilation is commonly observed during exercise in patients with heart failure and is related to ventilation-perfusion mismatching in the lung due to a higher-than-normal fraction of physiologic dead space. Neurohumoral abnormalities include reductions in beta-receptor density and sensitivity and contribute to reduced inotropic and chronotropic responses to exercise. CONCLUSIONS: Systolic function and exercise capacity are unrelated in patients with chronic heart failure, but many hemodynamic abnormalities (including those in the heart, lung, and skeletal muscle) overlap, which leads to exercise intolerance in these patients.
Myers et al. (Sun,) conducted a review in Chronic heart failure. Hemodynamic determinants was evaluated on Exercise capacity. Systolic function and exercise capacity are unrelated in chronic heart failure, but overlapping hemodynamic abnormalities in the heart, lung, and skeletal muscle lead to exercise intolerance.
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