Hemodilution significantly decreases tolerance to isoflurane-induced cardiovascular depression

Hemodilution is used to reduce the need for allogenic blood transfusion. The aim of this study was to evaluate to what extent acute extreme normovolemic hemodilution affects the circulatory response to isoflurane.

Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to isoflurane at end-tidal concentrations of 0, 0.5, 1.0, 1.5 and 2%, before and after extreme normovolemic hemodilution (hematocrit 33 +/- 3% and 11 +/- 1%, respectively). Systemic and myocardial hemodynamics and oxygen delivery and consumption were measured.

At zero end-tidal isoflurane concentration, hemodilution caused an increase in cardiac output (from 157 +/- 12 to 227 +/- 39 ml kg min-1, P < 0.01) a decrease in systemic vascular resistance (from 39 +/- 7 to 18 +/- 5 mmHg.L-1.min-1, P < 0.01) a decrease in mean arterial blood pressure (MAP) (from 130 +/- 13 to 91 +/- 13 mmHg, P < 0.01) and a decrease in systemic oxygen delivery (from 23.1 +/- 2.7 to 11.8 +/- 1.7 ml.kg-1.min-1, P < 0.01). When the end-tidal isoflurane concentration was increased from 0 to 2% after hemodilution, cardiac output decreased by 86 +/- 37 ml.kg-1.min-1, as compared with 36 +/- 20 ml.kg-1.min-1 (P < 0.01) before hemodilution. Likewise, systemic vascular resistance decreased with increasing isoflurane concentrations; at 2%, the decrease was 7 +/- 4 mmHg.L-1.min-1 after hemodilution and 18 +/- 5 mmHg.L-1.min-1 before hemodilution (P < 0.01). At an end-tidal isoflurane concentration of 2%, MAP had decreased to 43 +/- 6 mmHg after hemodilution, and to 61 +/- 15 mmHg before hemodilution (P < 0.01). After hemodilution, isoflurane concentrations above 1% decreased systemic oxygen delivery enough to cause delivery-dependent oxygen consumption and hyperlactemia; and at 2% isoflurane, myocardial blood flow became insufficient, as indicated by myocardial lactate production.

isoflurane-induced cardiovascular depression had adverse effects on cardiac output and oxygen delivery during extreme hemodilution because: 1) The vasodilatory effect of isoflurane was insufficient to compensate for the myocardial depression, and also contributed to a critically low arterial blood pressure; 2) A decrease in cardiac output produced delivery-dependent oxygen consumption and hyperlactemia; and 3) A decrease in myocardial blood flow caused myocardial ischemia which may have exacerbated the myocardial depression.