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Central Hemodynamic Response to Exercise in Patients with Chronic Heart Failure
Section snippets
WHAT LIMITS EXERCISE IN CHRONIC HEART FAILURE?
A number of factors may contribute to exercise intolerance in CHF, including decreased cardiac output, decreased skeletal muscle blood flow, early anaerobic metabolism in muscle, increased pulmonary capillary wedge pressure, and excess pulmonary dead space and ventilation.10, 11, 12, 13 At present, the relative roles of each of these factors in causing exertional symptoms in this disorder have not been defined. Although increased pulmonary capillary wedge pressure is an important cause of
CENTRAL HEMODYNAMIC RESPONSE IN CHF
Previous studies in our laboratory have examined the central hemodynamic and metabolic responses to maximal upright exercise in 30 patients with severe systolic LV dysfunction (LV ejection fraction 24% ± 8%) and in 12 normal subjects.8 Although heart rate was increased in patients during submaximal exercise (Fig 3A), there was a 20% reduction in peak heart rate in patients when compared with normal subjects, despite near complete venous oxygen desaturation, and a high respiratory exchange ratio
ROLE OF THE FRANK-STARLING MECHANISM
Although measurements at rest have revealed abnormalities in diastolic function in patients with severe systolic LV dysfunction,32 studies in our laboratory by Higginbotham et al33 and by Shen et al34 suggest that use of the Frank-Starling mechanism plays an important role in augmenting stroke volume in a significant number of patients with this disorder. Left ventricular volumes at rest and during maximal upright exercise in patients with severe LV dysfunction (LV ejection fraction 21% ± 9%)
ROLE OF MITRAL REGURGITATION
Many patients with severe systolic dysfunction and CHF have secondary mitral regurgitation due to progressive ventricular dilation. Recent studies by Keren et al38 and Hamilton et al39 have demonstrated that ionotropic or vasodilator therapy may improve hemodynamics by reducing the mitral regurgitation fraction. It is possible that this is an important mechanism by which drug therapy improves cardiac output at rest or during exercise in dilated cardiomyopathy. Stevenson et al40 examined stroke
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This study was supported by grant H L-17670 from the National Heart, Lung and Blood Institute, Bethesda, Md, by General Medical Research Funds from the veterans Administration Medical Center, Durham, NC, and by grant MO1-RR-30, Division of Research Resources, General Clinical Research Centers Program, NIH. Dr. Sullivan was supported by a grant-in-aid and an established investigatorship from the American Heart Association.