The effects of isoflurane and halothane on left ventricular afterload in dogs with dilated cardiomyopathy.

UNLABELLED

The effects of volatile anesthetics, including isoflurane (ISO) and halothane (HAL), on determinants of left ventricular (LV) afterload have not been comprehensively described in experimental models of, or patients with, heart failure. We tested the hypothesis that ISO and HAL produce beneficial alterations in LV afterload when evaluated with aortic input impedance and interpreted using a three-element Windkessel model in dogs before and after development of pacing-induced cardiomyopathy. Hemodynamics and aortic pressure and blood flow waveforms were recorded in the conscious state and during 1.1- and 1.5-minimum alveolar anesthetic concentration (MAC) ISO and HAL anesthesia on separate days in chronically instrumented dogs (n = 6). Dogs were then paced at 220-240 bpm for 20 +/- 3 days (mean = SEM) to develop cardiomyopathy, and the experiments were repeated after pacing had been temporarily discontinued. ISO decreased mean arterial pressure (MAP), mean aortic blood flow (MAQ), and total arterial resistance (R) and increased total arterial compliance (C) and characteristic aortic impedance (Zc) in dogs before pacing. HAL decreased MAP and MAQ and increased C but did not alter R and Zc. Chronic rapid LV pacing increased HR and LV end-diastolic pressure and decreased MAP, LV systolic pressure, and the peak rate of increase of LV pressure. MAQ, C, R, and Zc were unchanged. ISO and HAL decreased arterial pressure but did not affect C and Zc in the presence of LV dysfunction. HAL, but not ISO, increased R at 1.1 MAC, which indicates that this drug increases resistance to LV ejection. In contrast to findings in normal dogs, these results indicate that neither ISO nor HAL reduce arterial hydraulic resistance to LV ejection or favorably improve the rectifying properties of the aorta in dogs with pacing-induced cardiomyopathy.

IMPLICATIONS

Isoflurane and halothane produce favorable alterations in the determinants of left ventricular afterload before, but not after, the production of experimental left ventricular dysfunction by sustained, rapid cardiac pacing in chronically instrumented dogs.