EFFECTS OF HYPEROXIC VENTILATION ON HEMODILUTION-INDUCED CHANGES IN ANESTHETIZED DOGS

BACKGROUND: In subjects who have undergone acute preoperative normovol emic hemodilution (ANH), intraoperative hemorrhage is generally treate d by immediate return of autologous blood collected during ANH. Simply increasing blood oxygen content by hyperoxic ventilation (HV, inspira tory fraction [FiO(2)] 1.0) might compensate for the acute anemia, all ow further ANH, and delay onset of autologous blood return. STUDY DESI GN AND METHODS: This study 1) evaluated the effects of HV (FiO(2) 1.0) upon ANH to a hemoglobin (Hb) concentration of 7 g per dL in anesthet ized dogs ventilated with room air and 2) compared the effects of subs equent profound ANH (Hb, 3 g/dL) with and without an intravenous perfl uorocarbon emulsion (perflubron 60% wt/vol) versus those of autologous red cell transfusion. The results of the entire study are presented i n two parts. Organ tissue oxygenation was assessed in skeletal muscle and liver, and systemic oxygenation status was evaluated. Myocardial c ontractility was deduced from left ventricular pressure-volume relatio nship. Seven of 22 dogs underwent further hemodilution while breathing 100-percent O-2, for a determination of the Hb concentration at which HV-induced effects were abolished. RESULTS: HV completely reversed th e ANH-induced increase in cardiac index (4.6 +/- 0.7 vs. 3.8 +/- 0.9 L /min/m(2) before and during HV; p<0.05) and partially reversed the dec rease in systemic vascular resistance (1784 +/- 329 vs. 2087 +/- 524 d yn x cm(-5) x sec x m(-2); p<0.05). Despite unchanged global O-2 deliv ery, organ tissue oxygenation improved during HV (mixed venous partial pressure of O-2: 40 +/- 3 vs. 59 +/- 7 torr; coronary venous pressure of O-2: 30 +/- 4 vs. 43 +/- 6 torr; p<0.05; liver surface: 31 +/- Il vs. 39 +/- 13 torr; skeletal muscle surface: 30 +/- 14 vs. 41 +/- 22 t orr; p<0.05). This improvement was due to an increased contribution of physically dissolved O-2 in plasma to O-2 delivery (3.2 +/- 0.2% befo re HV vs. 14.6 +/- 1% during HV; p<0.05) and O-2 consumption (whole bo dy: 6 +/- 1% vs. 47 +/- 8%, p<0.05; myocardium: 4.3 +/- 0.9% vs. 31 +/ - 6%, p<0.05). The beneficial effects of HV were lost after an additio nal volume-compensated exchange of 19 percent of blood volume (Hb, 5.6 g/dL). CONCLUSION: In anesthetized dogs ventilated with room air and hemodiluted to a Hb of 7 g per dL, simple oxygen therapy by HV (FiO(2) 1.0) rapidly improves tissue oxygenation and permits extended hemodil ution to Hb of 5.8 g per dL until the HV-induced effects are lost.