Isoflurane decreased total arterial resistance and increased compliance, whereas halothane increased compliance and characteristic aortic impedance without changing resistance.
What are the differential effects of isoflurane, halothane, and sodium nitroprusside on aortic input impedance and left ventricular afterload in a canine model?
Isoflurane and halothane differ in their effects on left ventricular afterload primarily through changes in arteriolar resistance rather than the mechanical characteristics of the aorta.
BACKGROUND: Systemic vascular resistance (the ratio of mean aortic pressure AP and mean aortic blood flow AQ) does not completely describe left ventricular (LV) afterload because of the phasic nature of pressure and blood flow. Aortic input impedance (Zin) is an established experimental description of LV afterload that incorporates the frequency-dependent characteristics and viscoelastic properties of the arterial system. Zin is most often interpreted through an analytical model known as the three-element Windkessel. This investigation examined the effects of isoflurane, halothane, and sodium nitroprusside (SNP) on Zin. Changes in Zin were quantified using three variables derived from the Windkessel: characteristic aortic impedance (Zc), total arterial compliance (C), and total arterial resistance (R). METHODS: Sixteen experiments were conducted in eight dogs chronically instrumented for measurement of AP, LV pressure, maximum rate of change in left ventricular pressure, subendocardial segment length, and AQ. AP and AQ waveforms were recorded in the conscious state and after 30 min equilibration at 1.25, 1.5, and 1.75 minimum alveolar concentration (MAC) isoflurane and halothane. Zin spectra were obtained by power spectral analysis of AP and AQ waveforms and corrected for the phase responses of the transducers. Zc and R were calculated as the mean of Zin between 2 and 15 Hz and the difference between Zin at zero frequency and Zc, respectively. C was determined using the formula C = (Ad.MAP).MAQ.(Pes-Ped)-1, where Ad = diastolic AP area; MAP and MAQ = mean AP and mean AQ, respectively; and Pes and Ped = end-systolic and end-diastolic AP, respectively. Parameters describing the net site and magnitude of arterial wave reflection were also calculated from Zin. Eight additional dogs were studied in the conscious state before and after 15 min equilibration at three equihypotensive infusions of SNP. RESULTS: Isoflurane decreased R (3,205 +/- 315 during control to 2,340 +/- 2.19 dyn.s.cm-5 during 1.75 MAC) and increased C(0.55 +/- 0.02 during control to 0.73 +/- 0.06 ml.mmHg-1 during 1.75 MAC) in a dose-related manner. Isoflurane also increased Zc at the highest dose. Halothane increased C and Zc but did not change R. Equihypotensive doses of SNP decreased R and produced marked increases in C without changing Zc. No changes in the net site or the magnitude of arterial wave reflection were observed with isoflurane and halothane, in contrast to the findings with SNP. CONCLUSIONS: The major difference between the effects of isoflurane and halothane on LV afterload derived from the Windkessel model of Zin was related to R, a property of arteriolar resistance vessels, and not to Zc or C, the mechanical characteristics of the aorta. No changes in arterial wave reflection patterns determined from Zin spectra occurred with isoflurane and halothane. These results indicate that isoflurane and halothane have no effect on frequency-dependent arterial properties.
Hettrick et al. (Tue,) reported a other. Isoflurane, halothane, and sodium nitroprusside vs. Conscious state (control) was evaluated on Aortic input impedance variables (characteristic aortic impedance, total arterial compliance, and total arterial resistance). Isoflurane decreased total arterial resistance and increased compliance, whereas halothane increased compliance and characteristic aortic impedance without changing resistance.