Key result
Vasodilators increase cardiac output and oxygen transport but fail to alter VO2.
RCT (n=35)
Double-blind
Recent studies have suggested that oxygen consumption (VO2) may be dependent on systemic oxygen transport (SOT) in patients with the adult respiratory distress syndrome. To evaluate this relationship in patients with chronically impaired SOT, 2 groups underwent control right heart catheterization. Twenty-six patients with pulmonary hypertension (Group I) were then reevaluated after 48 h of treatment with a vasodilator, either hydralazine or nifedipine. Nine patients with refractory left ventricular failure (Group II) were first studied using nitroprusside, and 24 h later were begun on a double-blind drug protocol using either minoxidil or hydralazine. A significant correlation existed between control SOT and VO2 in both groups (r = 0.65, p less than 0.001). There were no changes in either group, however, in VO2 with vasodilator therapy, despite significant increases in cardiac output and SOT. We conclude that although resting oxygen consumption may be correlated with systemic oxygen transport when SOT is at low levels in stable patients with chronically impaired SOT, VO2 appears to be independent of SOT when oxygen delivery is increased by the administration of vasodilators.
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Chappell et al. (1983) conducted an RCT in Stable pulmonary hypertension or refractory left ventricular failure (n=35). Vasodilator therapy (hydralazine, nifedipine, nitroprusside, or minoxidil) vs. Control baseline prior to vasodilator administration was evaluated on Relationship between systemic oxygen transport (SOT) and oxygen consumption (VO2) (r = 0.65, p=<0.001). Vasodilator therapy increased cardiac output and systemic oxygen transport without changing VO2, despite a baseline correlation between transport and VO2 (r=0.65, p<0.001).
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