Akça O, Sessler D I, Delong D, Keijner R, Ganzel B, Doufas A G
Outcomes Research Institute, University of Louisville, KY 40202, USA.
Br J Anaesth. 2006 Jun;96(6):708-14. doi: 10.1093/bja/ael093. Epub 2006 May 4.
Tissue oxygenation is the primary determinant of wound infection risk. Mild hypercapnia markedly improves cutaneous, subcutaneous (s.c.), and muscular tissue oxygenation in volunteers and patients. However, relative contributions of increased cardiac output and peripheral vasodilation to this response remains unknown. We thus tested the hypothesis that increased cardiac output is the dominant mechanism.
We recruited 10 ASA III patients, aged 40-65 yr, undergoing cardiopulmonary bypass for this crossover trial. After induction of anaesthesia, a Silastic tonometer was inserted s.c. in the upper arm. S.C. tissue oxygen tension was measured with both polarographic electrode and fluorescence-based systems. Oximeter probes were placed bilaterally on the forehead to monitor cerebral oxygenation. After initiation of cardiopulmonary bypass, in random order patients were exposed to two arterial CO(2) partial pressures for 30 min each: 35 (normocapnia) or 50 mm Hg (hypercapnia). Bypass pump flow was kept constant throughout the measurement periods.
Hypercapnia during bypass had essentially no effect on Pa(CO(2)) , mean arterial pressure, or tissue temperature. Pa(CO(2)) and pH differed significantly. S.C. tissue oxygenation was virtually identical during the two Pa(CO(2)) periods [139 (50-163) vs 145 (38-158), P=0.335] [median (range)]. In contrast, cerebral oxygen saturation (our positive control measurement) was significantly less during normocapnia [57 (28-67)%] than hypercapnia [64 (37-89)%, P=0.025].
Mild hypercapnia, which normally markedly increases tissue oxygenation, did not do so during cardiopulmonary bypass with fixed pump output. This suggests that hypercapnia normally increases tissue oxygenation by increasing cardiac output rather than direct dilation of peripheral vessels.
组织氧合是伤口感染风险的主要决定因素。轻度高碳酸血症可显著改善志愿者和患者的皮肤、皮下及肌肉组织氧合。然而，心输出量增加和外周血管舒张对这种反应的相对贡献仍不清楚。因此，我们检验了心输出量增加是主要机制这一假设。
我们招募了10名年龄在40 - 65岁、接受体外循环的美国麻醉医师协会（ASA）III级患者进行这项交叉试验。麻醉诱导后，将一个硅橡胶张力计皮下插入上臂。用极谱电极和基于荧光的系统测量皮下组织氧张力。将血氧饱和度探头双侧置于前额以监测脑氧合。体外循环开始后，患者随机依次暴露于两种动脉血二氧化碳分压水平，每种水平持续30分钟：35（正常碳酸血症）或50 mmHg（高碳酸血症）。在整个测量期间，体外循环泵流量保持恒定。
体外循环期间高碳酸血症对动脉血二氧化碳分压、平均动脉压或组织温度基本无影响。动脉血二氧化碳分压和pH值有显著差异。在两个动脉血二氧化碳分压期间，皮下组织氧合实际上是相同的[139（50 - 163）对145（38 - 158），P = 0.335][中位数（范围）]。相比之下，正常碳酸血症期间脑氧饱和度（我们的阳性对照测量值）[57（28 - 67）%]显著低于高碳酸血症期间[64（37 - 89）%，P = 0.025]。
通常能显著增加组织氧合的轻度高碳酸血症，在固定泵输出的体外循环期间并未如此。这表明高碳酸血症通常通过增加心输出量而非直接扩张外周血管来增加组织氧合。
