NITROUS-OXIDE REDUCES INSPIRED OXYGEN FRACTION BUT DOES NOT COMPROMISE CIRCULATION AND OXYGENATION DURING HEMODILUTION IN PIGS

Background: The use of nitrous oxide (N2O) during hemodilution has bee n questioned. Nitrous oxide reduces the inspired oxygen fraction (FIO2 ), depresses myocardial function and may reduce cardiac output (GO) an d systemic oxygen delivery (DO2SY). The aim of this study was to evalu ate the importance of the effects of nitrous bride on systemic and myo cardial circulation and oxygenation during extreme, acute, normovolemi c hemodilution. Methods: Ten midazolam-fentanyl-pancuronium anesthetiz ed pigs were exposed to 65% N2O before and after extreme isovolemic he modilution (hematocrit 33 +/- 1% and 10 +/- 1%, respectively). Systemi c and myocardial hemodynamics, oxygen delivery and consumption and blo od lactate were measured before (at FIO2 1.0 and 0.35) and during N2O exposure. Results: Hemodilution caused an increase in CO from 137 +/- 43 to 229 +/- 32 ml . kg(-1) . min(-1) (P<0.01), a decrease in systemi c vascular resistance (from 42 +/- 14 to 20 +/- 4 mmHg . L-1 . min(-1) , P<0.05), a decrease in mean arterial blood pressure (from 119 +/- 19 to 100 +/- 26 mmHg, P<0.05) and a decrease in DO2SY from 21.1 +/- 6.9 to 13.7 +/- 2.1 ml . kg(-1) . min(-1) (P<0.01). Cardiac venous blood flow increased by 135% (P<0.01) and cardiac venous saturation from 25 +/- 6 to 41 +/- 5% (P<0.05). After hemodilution, changing FIO2, from 1 .0 to 0.35 reduced arterial blood oxygen content from 59.4 +/- 3.7 to 52.3 +/- 5.1 ml . L-1 (P<0.01), mixed venous saturation (SvO(2)) from 75 +/- 9 to 47 +/- 7% (P<O.05) and DO2SY from 13.7 +/- 2.1 to 11.9 +/- 2.3 ml . kg(-1) . min(-1) (P<0.05). Dissolved oxygen at FIO2 = 1.0 an d FIO2 = 0.35 constituted 25.4 +/- 3.1% and 10.1 +/- 1.5%, respectivel y, of systemic oxygen delivery after hemodilution, compared with 10.7 +/- 1.2% and 3.9 +/- 0.5% before hemodilution (P<0.01). Left ventricul ar oxygen delivery and consumption were unchanged. Exposure to N2O did not affect mean arterial blood pressure or systemic vascular resistan ce before or after hemodilution. After hemodilution during N2O-exposur e, CO and DO2SY decreased by 9% (P<0.01 and P<0.05, respectively), but no changes in SvO(2), systemic oxygen uptake or arterial lactate were observed. The effect of N2O on myocardial oxygenation was similar bef ore and after hemodilution; cardiac venous blood flow, left ventricula r oxygen delivery and uptake decreased, but no animals showed left ven tricular lactate production. Conclusion: Nitrous oxide did not comprom ise systemic and myocardial circulation and oxygenation during acute n ormovolemic hemodilution in pigs. Possible adverse effects from the us e of nitrous oxide during hemodilution seem to be related to a reduced FIO2, reducing the safety margin for systemic oxygen delivery.