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The aerobic exercise capacity of patients with chronic heart failure is frequently impaired because of inadequate O2 transport to working skeletal muscle. To determine whether hydralazine improves O2 transport to working muscle, we examined the effect of intravenous hydralazine on blood flow (measured by thermodilution) and metabolism in the leg during maximal upright bicycle exercise in 10 patients with chronic heart failure. Hydralazine increased maximal exercise cardiac output (5.6 +/- 0.7 to 6.7 +/- 0.6 l/min; p less than .01) and decreased systemic O2 extraction (79 +/- 3% to 65 +/- 2%; p less than .01) but did not alter maximal O2 uptake (787 +/- 105 vs 779 +/- 82 ml/min). Leg blood flow at maximal exercise increased from 1.6 +/- 0.2 to 2.1 +/- 0.4 l/min (p less than .03); the proportion of cardiac output delivered to the leg remained unchanged (59 +/- 3% vs 57 +/- 9%). This increase in flow was associated with a decrease in O2 extraction in the leg (84 +/- 2% to 79 +/- 2%; p less than .01) and no change in peak femoral venous lactate (59.1 +/- 7.4 vs 54.1 +/- 5.3 mg/dl), suggesting that there is functional or anatomic shunting of the augmented limb flow rather than delivery to metabolizing muscle. These data suggest that hydralazine augments flow to the exercising limb in patients with heart failure but that this augmented flow does not increase oxygen availability within working muscle.

Effect of hydralazine on perfusion and metabolism in the leg during upright bicycle exercise in patients with heart failure.