Hayashida M, Orii R, Komatsu K, Du H L, Sato Y, Uchida K, Nagata O, Hanaoka K
Department of Anesthesiology, Faculty of Medicine, University of Tokyo.
Masui. 1998 Feb;47(2):161-7.
We investigated the relationship between cardiac output and PETCO2 as well as blood PCO2 in 10 patients undergoing cardiac surgery of long duration under high-dose fentanyl anesthesia. After anesthetic induction, the minute ventilation was kept constant at 10 ml.kg-1 x 10 cycles.min-1 and a pulmonary artery catheter was inserted. PETCO2, PaCO2 and cardiac index (CI) were measured simultaneously. PaCO2 was corrected for body temperature, and alveolar dead space-to-tidal volume ratio was calculated as VD/VTalv = (PaCO2-PETCO2)/PaCO2. After body, temperature became stabilized, the measurements were started and repeated every 10 to 20 minutes during the prebypass period. One hundred and eight sets of data were taken from 10 patients. PETCO2 correlated positively with CI. Similarly, PaCO2 correlated positively with CI, but VD/VTalv, did not correlate with CI. PETCO2 correlated closely and positively with PaCO2, but it correlated negatively and only marginally with VD/VTalv. When examined in individual patients, PaCO2 correlated positively with PETCO2 in all patients, while VD/VTalv correlated negatively with PETCO2 only in 3 patients. By multiple regression analysis, VD/VTalv change accounted for only 22.3 +/- 15.0% of PETCO2 change, while PACO2 or PaCO2 change accounted for 77.6 +/- 15.0% of PETCO2 change. Decreased CI was associated with decreased CO2 delivery from the tissue to the lung (DCO2) and PaCO2 decreased with decreasing DCO2. Decreased CI was also associated with decreased oxygen uptake (VO2), and PaCO2 decreased with decreasing VO2. A decrease in CI resulted in an increase in VA/Q, and PaCO2 decreased when VA/Q increased. PETCO2 decreased when cardiac output decreased. A decrease in PACO2 explained the decrease in PETCO2 better than an increase in VD/VT did. Decreased cardiac output might cause hypocapnia through decreased CO2 delivery to the lung, decreased CO2 production and/or increased ventilation-to-perfusion ratio.
我们研究了10例在大剂量芬太尼麻醉下接受长时间心脏手术患者的心输出量与呼气末二氧化碳分压(PETCO2)以及血二氧化碳分压(PCO2)之间的关系。麻醉诱导后,分钟通气量保持恒定在10 ml·kg-1×10次/分钟,并插入肺动脉导管。同时测量PETCO2、动脉血二氧化碳分压(PaCO2)和心脏指数(CI)。PaCO2进行体温校正,并计算肺泡死腔与潮气量比值,即VD/VTalv = (PaCO2 - PETCO2)/PaCO2。体温稳定后,开始测量,并在体外循环前期间每10至20分钟重复一次。从10例患者获取了108组数据。PETCO2与CI呈正相关。同样,PaCO2与CI呈正相关,但VD/VTalv与CI不相关。PETCO2与PaCO2密切正相关,但与VD/VTalv呈负相关且仅为轻度相关。在个体患者中检查时,所有患者的PaCO2与PETCO2呈正相关,而仅3例患者的VD/VTalv与PETCO2呈负相关。通过多元回归分析,VD/VTalv变化仅占PETCO2变化的22.3±15.0%,而肺泡气二氧化碳分压(PACO2)或PaCO2变化占PETCO2变化的77.6±15.0%。CI降低与组织向肺的二氧化碳输送量(DCO2)减少相关,且PaCO2随DCO2降低而降低。CI降低还与氧摄取量(VO2)减少相关,且PaCO2随VO2降低而降低。CI降低导致通气/血流比值(VA/Q)增加,且当VA/Q增加时PaCO2降低。心输出量降低时PETCO2降低。PACO2降低比VD/VT增加能更好地解释PETCO2降低。心输出量降低可能通过减少向肺的二氧化碳输送、减少二氧化碳产生和/或增加通气/血流比值导致低碳酸血症。