HEMODILUTION SIGNIFICANTLY DECREASES TOLERANCE TO ISOFLURANE-INDUCED CARDIOVASCULAR DEPRESSION

Background: Hemodilution is used to reduce the need for allogenic bloo d transfusion. The aim of this study was to evaluate to what extent ac ute extreme normovolemic hemodilution affects the circulatory response to isoflurane. Methods: Ten midazolam-fentanyl-pancuronium anesthetiz ed pigs were exposed to isoflurane at end-tidal concentrations of 0, 0 .5, 1.0, 1.5 and 2%, before and after extreme normovolemic hemodilutio n (hematocrit 33+/-3% and 11+/-1%, respectively). Systemic and myocard ial hemodynamics and oxygen delivery and consumption were measured. Re sults: 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 bloo d pressure (MAP) (from 130+/-13 to 91+/-13 mmHg, P<0.01) and a decreas e 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). m in(-1) (P<0.01) before hemodilution. Likewise, systemic vascular resis tance 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 i soflurane 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 ox ygen delivery enough to cause delivery-dependent oxygen consumption an d hyperlactemia; and at 2% isoflurane, myocardial blood flow became in sufficient, as indicated by myocardial lactate production. Conclusions : 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 compens ate for the myocardial depression, and also contributed to a criticall y low arterial blood pressure; 2) A decrease in cardiac output produce d delivery-dependent oxygen consumption and hyperlactemia; and 3) A de crease in myocardial blood flow caused myocardial ischemia which may h ave exacerbated the myocardial depression. (C) Acta Anaesthesiologica Scandinavica 41 (1997).