Pape A, Steche M, Laout M, Wedel M, Schwerdel F, Weber C F, Zwissler B, Habler O
Department of Anesthesia, Intensive Care Medicine and Pain Therapy, University Hospital Frankfurt, Frankfurt/Main, Germany.
Eur Surg Res. 2013;51(3-4):156-69. doi: 10.1159/000357171. Epub 2013 Dec 31.
During acellular replacement of an acute blood loss, hyperoxic ventilation (HV) increases the amount of O2 physically dissolved in the plasma and thereby improves O2 supply to the tissues. While this effect could be demonstrated for HV with inspiratory O2 fraction (FiO2) 0.6, it was unclear whether HV with pure oxygen (FiO2 1.0) would have an additional effect on the physiological limit of acute normovolemic anemia.
Seven anesthetized domestic pigs were ventilated with FiO2 1.0 and subjected to an isovolemic hemodilution protocol. Blood was drawn and replaced by a 6% hydroxyethyl starch (HES) solution (130/0.4) until a sudden decrease of total body O2 consumption (VO2) indicated the onset of O2 supply dependency (primary endpoint). The corresponding hemoglobin (Hb) concentration was defined as 'critical Hb' (Hbcrit). Secondary endpoints were parameters of myocardial function, central hemodynamics, O2 transport and tissue oxygenation.
HV with FiO2 1.0 enabled a large blood-for-HES exchange (156 ± 28% of the circulating blood volume) until Hbcrit was met at 1.3 ± 0.3 g/dl. After termination of the hemodilution protocol, the contribution of O2 physically dissolved in the plasma to O2 delivery and VO2 had significantly increased from 11.7 ± 2 to 44.2 ± 9.7% and from 29.1 ± 4.2 to 66.2 ± 11.7%, respectively. However, at Hbcrit, cardiovascular performance was found to have severely deteriorated.
HV with FiO2 1.0 maintains O2 supply to tissues during extensive blood-for-HES exchange. In acute situations, where profound anemia must be tolerated (e.g. bridging an acute blood loss until red blood cells become available for transfusion), O2 physically dissolved in the plasma becomes an essential source of oxygen. However, compromised cardiovascular performance might require additional treatment.
在急性失血的无细胞替代过程中，高氧通气（HV）可增加血浆中物理溶解的氧气量，从而改善组织的氧气供应。虽然这种效应在吸入氧分数（FiO2）为0.6的高氧通气中得到了证实，但尚不清楚纯氧（FiO2 1.0）的高氧通气是否会对急性正常血容量性贫血的生理极限产生额外影响。
对7只麻醉的家猪进行FiO2 1.0通气，并实施等容血液稀释方案。抽血并用6%羟乙基淀粉（HES）溶液（130/0.4）替代，直至全身氧气消耗（VO2）突然下降表明出现氧气供应依赖（主要终点）。相应的血红蛋白（Hb）浓度被定义为“临界Hb”（Hbcrit）。次要终点是心肌功能、中心血流动力学、氧气运输和组织氧合的参数。
FiO2 1.0的高氧通气能够进行大量的血液与HES交换（循环血容量的156±28%），直至达到Hbcrit为1.3±0.3 g/dl。在血液稀释方案终止后，血浆中物理溶解的氧气对氧气输送和VO2的贡献分别从11.7±2%显著增加到44.2±9.7%，从29.1±4.2%显著增加到66.2±11.7%。然而，在Hbcrit时，发现心血管功能严重恶化。
FiO2 1.0的高氧通气在广泛的血液与HES交换过程中维持组织的氧气供应。在必须耐受严重贫血的急性情况下（例如在红细胞可用于输血之前度过急性失血期），血浆中物理溶解的氧气成为重要的氧气来源。然而，心血管功能受损可能需要额外的治疗。
