Exercise testing has assumed a position of growing importance in the assessment of patients with chronic congestive heart failure. The hemodynamic and neurohumoral adjustments that occur during dynamic exercise are very complex, but are basically designed to ensure that oxygen delivery is commensurate with oxygen demand. These responses are clearly altered in the presence of certain types of heart disease. Patients with chronic congestive heart failure have an attenuated heart rate and blood pressure response throughout exercise, but this is most clearly evident when the data are expressed as a percent of peak oxygen consumption (V̇O2) rather than as a function of absolute V̇O2. Likewise, the sympathetic response to exercise is altered in patients wiht heart failure. Plasma norepinephrine is normally augmented as a function of V̇O2 during exercise, but this augmentation occurs during the later stages (beyond 50% of peak V̇O2). Patients with congestive heart failure show a greater than normal augmentation of plasma norepinephrine during exercise when the data are expressed in terms of absolut V̇O2. However, when the data are expressed as a percent of peak V̇O2, there appears to be a relative attenuation of the sympathetic response to exercise. Current information suggests that increased plasma norepinephrine and renin activity during exercise in patients with heart failure are not directly related to a decrement in nutritive blood flow to skeletal muscles. The mechanisms responsible for exercise intolerance in patients with heart failure are not known, but do not seem directly related to a decrement in cardiac output or an increase in left ventricular filling pressure. The metabolic consequences of impaired nutritive blood flow during exercise may ultimately influence respiratory gas exchange to the extent that breathlessness and fatigue are experienced.
|Original language||English (US)|
|Issue number||6 II SUPPl.|
|State||Published - 1987|