Differential effects of isoflurane on regional right and left ventricular performances, and on coronary, systemic, and pulmonary hemodynamics in the dog.

The effects of isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right (RV) and left (LV) ventricular performance (ultrasonic dimension technique), and on coronary, systemic, and pulmonary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Isoflurane caused dose-dependent decreases in LV and RV dP/dt, and in myocardial segment shortening in the presence of unchanged heart rate, unchanged or increased (RV) preload, and unchanged (RV) or decreased (LV) afterload. RV and LV functions were affected differently: at a mean aortic pressure of 70 mmHg (mean inspired isoflurane 1.2%), RV end diastolic dimensions and pressure remained unchanged, whereas those of the LV decreased. At a mean aortic pressure of 55 mmHg (mean inspired isoflurane 1.8%), RV end diastolic dimensions and pressure increased above control, whereas those of the LV remained unchanged. Within the RV, inflow and outflow tract were affected quantitatively similarly, but dyssynchrony developed in four animals. Isoflurane caused dose-dependent decreases in coronary and systemic vascular resistances, but no change in pulmonary vascular resistance. At the lower concentration of isoflurane, coronary blood flow did not fall despite decreased LV and RV dP/dt, unchanged heart rate, unchanged or decreased preload, and unchanged or reduced afterload. The data indicate that isoflurane is a myocardial depressant and a potent coronary vasodilator. At both concentrations, LV function was better preserved than RV function, most likely due to the different effects of isoflurane on RV (unchanged) and LV (reduced) afterload.