Cardiovascular effects of acute normovolemic hemodilution in rats with disopyramide-induced myocardial depression

Abstract

The effect of myocardial depression on the circulatory response to acute normovolemic hemodilution (hematocrit 23%) with hetastarch was evaluated in 28 anesthetized Sprague-Dawley rats. Cardiac output was recorded using an electromagnetic flow probe. Mild, moderate, and severe myocardial depression were achieved by infusing disopyramide 50, 75, and 85 mg/kg. This resulted in a dose-dependent decrease in cardiac output (r = -0.73, p less than 0.05) and mean arterial pressure (r = -0.65, p less than 0.05), and an increase in left ventricular end-diastolic pressure (r = 0.77, p less than 0.05) and total peripheral resistance (r = 0.46, p less than 0.05). Following hemodilution, cardiac output and mean arterial pressure were significantly lower and total peripheral resistance significantly higher in animals with myocardial depression compared with saline anemic controls. These differences were dose-dependent for cardiac output (r = -0.83, p less than 0.05), mean arterial pressure (r = -0.68, p less than 0.05), and total peripheral resistance (r = 0.51, p less than 0.05). Although control animals were able to significantly increase their cardiac output and stroke volume after hemodilution compared with baseline, animals with severe myocardial depression were unable to do so. This resulted in marked hypotension after hemodilution in controls compared with severely depressed animals. The results suggest a diminished ability of the pharmacologically depressed heart to tolerate acute normovolemic hemodilution.

Cardiac mechanoenergetic cost of elevated plasma viscosity after moderate hemodilution

“…These results are in agreement with the work reported by Estafanous et al and Shinoda et al in their control group, but differ from that Murray et al , who found that hemodilution slightly increases MAP and HR [10, 23, 29]. The marked decrease in SVR and SVH after HVPE hemodilution implies geometrical change in the vasculature to explain the reduced resistance, compared to LVPE.…”

Continuous haemodynamic monitoring using transoesophageal Doppler during acute normovolaemic haemodilution in patients with coronary artery disease

“…The individual flow compared with filling pressure curves reflected the large variability in haemodynamic response to ANH, regardless of preoperative left ventricular ejection fraction. Likewise, previous studies performed in patients with CAD and in animals with a myocardial infarct or disopyramide‐induced myocardial insufficiency, have indicated that the increase in cardiac output during ANH was largely independent of ventricular function [33, 34].…”

Acute Normovolemic Hemodilution in Cardiac Surgery

“…43 Acute administration of negative inotropic agents like anti-arrhythmic drugs or β-blocking agents will also reduce the cardiac output response to ANH. 25,44 In the postoperative period, tolerance of patients with altered myocardial function will closely depend on the potential recovery of their cardiac function and, again, on the level of metabolic demand.…”