DISPARITY OF ISOFLURANE EFFECTS ON LEFT AND RIGHT-VENTRICULAR AFTERLOAD AND HYDRAULIC-POWER GENERATION IN SWINE

The interaction between myocardial and vascular effects of anesthetics has a potential impact on how these drugs influence performance of th e heart. Most studies have focused on volatile anesthetic effects on t he left ventricle (LV) and systemic circulation. Whether the right ven tricle (RV) and pulmonary circulation respond in a similar fashion, ho wever, is unclear. In the present study, we therefore examined the dos e-related effects of isoflurane on LV and RV contractility and total a fterload and related changes to simultaneous effects on the hydraulic power generated by each chamber. Two groups of swine were studied: one received no additional treatment before isoflurane (LSO, n = 6), and the other received hexamethonium, atropine, and propranolol to produce autonomic blockade before isoflurane administration (ISO+AB, n = 4). For each experiment, measurements were made of RV and LV regional segm ent lengths and pressures, along with proximal aortic and pulmonary ar terial (PA) blood now and pressure during the administration of 0, 0.5 , 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC) isoflur ane. Contractility was assessed by calculating the regional preload re cruitable stroke work slope (PRSW). Afterload was characterized in bot h nonpulsatile and pulsatile terms by calculating aortic input impedan ce magnitude (Z). From these data, total arterial resistance (R), char acteristic impedance (Z(C)), and vascular compliance (C) were determin ed with reference to a three-element Windkessel model of the circulati on. Additionally, steady-state (W-ss), oscillatory (W-OS) and total (W -T) hydraulic power output of each ventricle was calculated. In the IS O group, isoflurane produced a nearly threefold greater decrease of pe ak systolic pressure in the LV than in the RV, yet the dose-related de crease of regional PRSW was virtually the same in both chambers. In th e aorta, isoflurane produced a maximal 25% reduction in R at 1.0 MAC a nd doubled C without a significant change in Z(C). Alternatively, PA R was increased from baseline at 1.0 and 1.5 MAC, whereas Z(C) was incr eased from all other values at 1.5 MAC. PA C was not altered by isoflu rane. in ISO+AB pigs, PA Z at baseline was higher than that evident in ISO animals but was not altered by isoflurane. In contrast, baseline aortic R was lower in ISO+AB pigs but was still modestly reduced by 1. 0 MAC isoflurane. In ISO animals, W-T and W-SS from both ventricles de monstrated dose-related deceases, but the reductions in LV W-T and W-S S were greater than those for the RV at all doses. Accordingly, the po wer requirement per unit flow decreased for the LV but remained consta nt for the RV. W-OS for both ventricles was also reduced by isoflurane . However, the LV W-OS to W-T ratio increased, which indicates that mo re power was lost to the system by pulsation. In contrast, reductions in RV W-T and W-OS were nearly parallel at all isoflurane doses, and t he W-OS to W-T ratio was unchanged. In the ISO+AB group, isoflurane-in duced alterations in LV and RV power characteristics were similar to t hose in the ISO group. These data indicate that, despite similar effec ts on biventricular contractility, isoflurane exerts qualitatively dif ferent effects on RV and LV afterload, in part via alteration in auton omic nervous activity, that influence the distribution of power output between steady-state and pulsatile components. Implications: In this study, we examined the effects of isoflurane on cardiac performance in swine and found that, although the drug depresses contraction of both the left and right ventricles similarly, it has different effects on forces that oppose the ejection of blood. These findings demonstrate t hat the two interdependent pumps that comprise the heart can be influe nced differently by anesthetic drugs.