Hemodynamic and cardiac metabolic effects of inotropic stimulation with dobutamine in patients with coronary artery disease

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Abstract
The hemodynamic and myocardial metabolic effects of two intravenous doses (5 and 10 ug/kg/min) of dobutamine were measured in 15 patients with congestive heart failure secondary to coronary artery disease. Dobutamine at 5 μg/kg/min induced an increase in peak rate of left ventricular pressure rise (dp/dtmax) from 1004 ± 261 to 1386 ± 469 mm Hg × s−1, coronary sinus blood flow (CSF) from 98 ± 34 to 128 ± 60 ml/min and myocardial oxygen consumption (MVO2) from 10.5 ± 3.8 to 14.3 ± 6.9 ml/min. It decreased mean left ventricular end-diastolic pressure (LVEDP) from 24 ± 6 to 20 ± 8 mm Hg. All changes were significant (P < 0.01). No significant changes occurred in mean heart rate, left ventricular systolic pressure, arterio-coronary venous oxygen content difference and mean myocardial lactate extraction rate. Dobutamine at 10 μg/kg/min further increased dp/dtmax to 1545 ± 408 mm Hg × s−1, CSF to 146 ± 75 ml/min and MVO2 to 17 ± 9.1 ml/min. Because mean heart rate also increased significantly from 73 ± 15 to 90 ± 23 beats/min it is possible that the concomitant increase in myocardial oxygen demand was no longer offset by the reduction in preload (further decrease of LVEDP to 18 ± 7 mm Hg). Thus, myocardial oxygen demand was inadequately met, myocardial lactate extraction rate decreased significantly (34 ± 16 to 14 ± 20%, P < 0.01) and signs of myocardial ischemia developed in three of the 15 patients. For this reason, heart rate should be monitored closely if dobutamine is given to patients with limited capacity to increase myocardial blood flow and oxygen delivery to the myocardium.

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