Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia

Changes in cardiac output in response to augmenting cardiac contractility, preload, and heart rate during enflurane anesthesia were examined in 12 open-chested dogs. Cardiac contractility was assessed by the slope of the end-systolic pressure-volume relation (E(max)). Dobutamine (3, 6, and 9 μg·kg^-1·min^-1) was administered to augment cardiac contractility. Autologous blood (5.0 and 10 mL/kg) was infused to increase preload. Atrial pacing was used to increase the heart rate by about 30%. Cardiac output decreased from 96 ± 4 (0% enflurane) (mean ± SE) to 73 ± 5 (1.7% enflurane) and to 46 ± 7 mL·kg^-1·min^-1 (3.4% enflurane), concomitantly with decreases in E(max) from 6.0 ± 1.2 (0% enflurane) to 4.5 ± 1.2 (1.7% enflurane) and to 2.5 ± 0.5 mm Hg/mL (3.4% enflurane). Dobutamine (3, 6, and 9 μg·kg^-1·min^-1) increased E(max) from 69% ± 7% (compared to 0% enflurane with no dobutamine) to 139% ± 15%, 167% ± 25%, and 183% ± 35% at 1.7% enflurane, and from 43% ± 8% to 78% ± 7%, 137% ± 20%, and 157% ± 22% at 3.4% enflurane, respectively. The decreases in cardiac output by 1.7% and 3.4% enflurane were reversed by the intravenous administration of 3 μg·kg^-1·min^-1 of dobutamine. Cardiac output was significantly increased by administration of 10 mL/kg of autologous blood at 1.7% enflurane, but did not significantly increase at 3.4% enflurane. Increasing the heart rate did not significantly increase cardiac output at 1.7% and 3.4% enflurane. The results of this study suggest that increasing cardiac contractility is the most effective therapeutic means of reversing circulatory depression during enflurane anesthesia.