Key result
Short-term vasodilators increase exercise cardiac output ~19% without improving oxygen consumption or lactate metabolism.
Why the study?
Does short-term treatment with vasodilators (hydralazine or prazosin) improve cardiac output, oxygen consumption, and lactate metabolism during exercise in patients with chronic heart failure?
Does short-term treatment with vasodilators (hydralazine or prazosin) improve cardiac output, oxygen consumption, and lactate metabolism during exercise in patients with chronic heart failure?
Short-term vasodilator therapy in chronic heart failure increases cardiac output during exercise but does not improve oxygen consumption or lactate metabolism, explaining the lack of acute improvement in exercise tolerance.
Answers are grounded in this paper and cite their sources.
Does not support acute vasodilator use to boost exercise tolerance in HF; hypothesis-generating for hemodynamic-metabolic dissociation.
Short-term vasodilators increase exercise cardiac output without an increase in exercise tolerance when administered to chronic heart failure patients.This study was designed to examine cardiac out- put, oxygen consumption, and lactate metabolism during exercise in chronic heart failure.Thirteen patients participated in 17 studies during control exercise (C) and during vasodilator exercise after short-term treat- ment with either hydralazine (H) or prazosin (P).Cardiac output increased during exercise both with hydralazine (C = 5.8 2.3 1/min, H = 6.9 i 2.3 1/min; p < 0.001) and with prazosin (C = 5.9 ± 2.3 1/min, P = 7.6 ± 2.7 1/min; p < 0.005).Oxygen consumption did not change during exercise either with hydralazine (C = 663 249 ml/min, H = 651 ± 200 mI/min; p > 0.10) or with prazosin (C = 696 ± 246 ml/min, P= 734 245 ml/min; p > 0.10).Peak blood lactate did not change either with hydralazine (C = 49.7 i 24.2 mg/dl, H = 44.0 ± 21.4 mg/dl; p > 0.05) or with prazosin (C = 33.8± 16.5 mg/dl, P = 32.1 i 12.2 mg/dl; p > 0.10).Vasodilators did not change the rate of lactate disappearance during recovery from exercise.We conclude that short-term administration of vasodilators increased cardiac output during exercise but did not improve nutritional flow to exercising muscle.However, chronic administration of vasodilators with sustained improvement in cardiac output may allow the readjustment of peripheral mechanisms that control the nutritional flow of muscle in order to take advantage of improved cardiac perfor- mance caused by vasodilators.IN PREVIOUS REPORTS on the exercise hemodynamics and exercise capacity of chronic heart failure patients administered short-term oral vasodilators," 2 we noted that hydralazine and prazosin increased cardiac output during exercise, but did not increase exercise tolerance.It seemed paradoxical to us that improvement of a fundamental abnormality of chronic heart failure -low cardiac outputshould not result in improvement of exercise tolerance.Data concerning changes in oxygen con- sumption and muscle metabolism should clarify these disparate effects of short-term vasodilators.In this study we examined changes in the metabolism of oxy- gen and lactate during exercise and during recovery from exercise as affected by short-term oral vasodilators. Methods PatientsThirteen patients who had chronic, stable, severe heart failure of either coronary heart disease (nine patients) or idiopathic cardiomyopathy (four patients) etiology were studied.The mean patient age was 60 years (range 44-80 years).Each patient had clinical and laboratory evidence of chronic heart failure, in-
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Rubin et al. (1980) studied chronic heart failure (n=13). Short-term vasodilators (hydralazine or prazosin) vs. Control exercise was evaluated on Cardiac output during exercise (p=<0.001). Short-term administration of vasodilators increased cardiac output during exercise (hydralazine 6.9 vs 5.8 L/min, p<0.001) but did not improve oxygen consumption or lactate metabolism.
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