January 1, 1984
View Full PaperEffects of dobutamine on left ventricular performance and myocardial metabolic demands in patients with ischemic heart disease
Key Result
Dobutamine infusion improved left ventricular performance in patients with ischemic heart disease without a major increase in left ventricular oxygen consumption or marked aggravation of ischemia.
Structured PICO
Does dobutamine improve left ventricular performance without significantly increasing myocardial metabolic demands in patients with ischemic heart disease?
P
Population
16 patients with coronary artery disease undergoing cardiac catheterization, evaluated for hemodynamic and metabolic responses to dobutamine infusion.
I
Intervention
Continuous intravenous infusion of dobutamine from 2.5 to 10 μg/kg/min with dosage increments of 2.5 μg/kg at 15-minute intervals.
C
Comparator
Baseline measurements prior to dobutamine infusion.
O
Outcome
Left ventricular performance (cardiac index, left ventricular stroke work index, mean systolic ejection rate, left ventricular end-diastolic pressure) and myocardial metabolic demands (left ventricular oxygen consumption, myocardial lactate extraction).surrogate
Dobutamine improves left ventricular performance in patients with ischemic heart disease without a major increase in left ventricular oxygen consumption, particularly in those with severe left ventricular dysfunction.
Abstract
Abstract Sixteen patients with coronary artery disease undergoing cardiac catheterization were studied. Eleven had previous infarcts and the patients were divided into two groups: In group I were 7 patients with no left ventricular dysfunction, no increase in ventricular size, or symptoms of congestive failure; group II included 9 patients with ventricular dysfunction, increased ventricular size, and 7 of the 9 had congestive failure. Each patient underwent a continuous infusion of dobutamine from 2.5 to 10 μUg/kg min ‐1 with dosage increments of 2.5 μUg/kg at 15‐minute intervals. Systemic and coronary hemodynamic measurements were obtained at the end of the 5 and 10 μUg/kg min ‐1 infusion doses. Left ventricular performance improved (higher cardiac index, left ventricular stroke work index and mean systolic ejection rate, and lower left ventricular end‐diastolic pressure), while heart rate, mean arterial pressure, and coronary sinus blood flow increased after dobutamine in the 16 patients. While patients in both groups had a rise in cardiac index, a reduction in left ventricular end‐diastolic pressure, an unchanged mean arterial pressure and a rise in coronary blood flow, only patients in group I had a significant increase in heart rate, and only patients in group II had significant increases in left ventricular stroke work index and mean systolic ejection rate, and a significant reduction in systemic vascular resistance. Left ventricular oxygen consumption did not increase significantly in either group. However, 5 patients showed a decreased myocardial lactate extraction after 10 μUg/kg min ‐1 of intravenous dobutamine, 3 from group I and 2 from group II. These 5 patients had less ventricular dysfunction than patients with a normal lactate response to intravenous dobutamine. We conclude that the improvement in left ventricular performance observed after dobutamine administration in patients with ischemic heart disease is not usually associated with a major increase in left ventricular oxygen consumption or with marked aggravation of myocardial ischemia. This appears to be particularly true in patients with relatively severe left ventricular dysfunction.