Abstract

We investigated cardiopulmonary effects of dopamine in patients with acute respiratory failure. Specifically, we wished to test the hypothesis that left ventricular filling pressure (Pcwp) would increase when cardiac output (CO) increased with dopamine. Dopamine (range, 5.5 to 20 micrograms/kg/min) increased blood pressure (BP) (p less than 0.001) Pcwp, CO, and stroke volume (SV) (p less than 0.005). Mean Pcwp increased (p less than 0.005) 45% with dopamine, from 11 to 16 mmHg. Qs/Qt increased with dopamine in association with an increase in mixed venous O2 tension, and arterial O2 tension remained constant. In 8 of these patients, left ventricular end-diastolic volume (LVEDV) and end-systolic volume (ESV) were measured using scintigraphic techniques. The LVEDV increased (p less than 0.01) in each patient after the administration of dopamine, and the mean change was from 134 to 163 ml. Although BP and LV afterload increased in each patient, there was no consistent change in LVESV after dopamine administration, i.e., ESV decreased in 1 patient, remained constant in 3, and increased in 4. Accordingly, because afterload increased in all patients and ESV did not, dopamine probably increased contractility. Because EDV increased in all patients, we concluded that the increase in SV with dopamine is explained by a combination of inotropic and peripheral vascular effects.

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