Etomidate Adversely Alters Determinants of Left Ventricular Afterload in Dogs with Dilated Cardiomyopathy

We tested the hypothesis that etomidate produces similar alterations in left ventricular (LV) afterload in dogs with normal LV function or dilated cardiomyopathy.Dogs were instrumented for LV and aortic pressures, and aortic blood flow. LV afterload was measured with aortic input impedance and quantified with a three-element Windkessel model. In one group of experiments, dogs (n = 6) were paced at 240 bpm for 18 +/- 2 days (mean +/- SEM). Hemodynamic data were recorded in sinus rhythm in the conscious state and during etomidate anesthesia (5, 10, and 20 mg [center dot] kg-1 [center dot] h-1). Identical experiments were conducted in a separate group of chronically instrumented dogs not subjected to LV pacing (n = 6). No changes in heart rate and arterial and LV pressures were observed during etomidate anesthesia in cardiomyopathic dogs. There were decreases in arterial and LV systolic pressure during the administration of 20 mg [center dot] kg-1 [center dot] h-1 etomidate to dogs with normal LV function. Etomidate significantly (P < 0.05) increased total arterial resistance (R; 3220 +/- 290 dynes [center dot] s [center dot] cm-5 during control to 6110 +/- 790 dynes [center dot] s [center dot] cm-5 during 10 mg [center dot] kg (-1) [center dot] h-1) and characteristic aortic impedance (Zc; 141 +/- 22 dynes [center dot] s [center dot] cm-5 during control to 161 +/- 23 dynes [center dot] s [center dot] cm-5 during 20 mg [center dot] kg-1 [center dot] h-1) and decreased total arterial compliance (C; 0.70 +/- 0.15 mL/mm Hg during control to 0.45 +/- 0.07 mL/mm Hg during 10 mg [center dot] kg-1 [center dot] h-1) in cardiomyopathic but not healthy dogs. Etomidate markedly reduced mean aortic blood flow (2.26 +/- 0.17 L/min during control to 1.39 +/- 0.20 L/min during 10 mg [center dot] kg-1 [center dot] h-1) and increased the time constant of LV relaxation (54 +/- 3 ms during control to 74 +/- 9 ms during 20 mg [center dot] kg-1 [center dot] h-1) in dogs with LV failure. Arterial pressure is maintained during etomidate anesthesia in the presence of LV dysfunction as a result of increases in R and Zc and decreases in C. These deleterious increases in LV afterload further compromise LV systolic and diastolic performance in dogs with dilated cardiomyopathy. Implications: The results of this investigation indicate arterial pressure is maintained during etomidate anesthesia as a consequence of increases in left ventricular (LV) afterload that further diminish LV systolic and diastolic performance in the presence of impaired LV function. (Anesth Analg 1998;86:932-8)