Angelos M G, DeBehnke D J
Department of Emergency Medicine, Ohio State University, Columbus, USA.
Crit Care Med. 1995 May;23(5):925-30. doi: 10.1097/00003246-199505000-00022.
Previous studies suggest that epinephrine may alter the correlation of perfusion with measures of PCO2 during cardiopulmonary resuscitation. This study investigated the effects of epinephrine on PaCO2 and mixed venous PCO2 in a high-flow reperfusion model of cardiac arrest.
Prospective, block randomized, blinded, placebo-controlled, laboratory study.
Thirty mixed breed canines.
After a 12-min ventricular fibrillation cardiac arrest, 30 mixed breed canines were reperfused with standardized (3200 revolutions/min) cardiopulmonary bypass and were given placebo (n = 10), standard dose epinephrine (0.02 mg/kg; n = 10), or high-dose epinephrine (0.2 mg/kg; n = 10). Arterial and mixed venous blood gases, coronary perfusion pressure, pump flow and peripheral vascular resistance were compared between groups during the early reperfusion period using analysis of variance with a post hoc Tukey's multiple comparison test.
Baseline variables were similar between groups. With reperfusion, the high-dose epinephrine group had higher coronary perfusion pressures (p < .002), lower systemic pump flow (p < .01), and higher peripheral vascular resistance (p < .001). In the high-dose epinephrine group, both PaCO2 (high-dose epinephrine, 40 +/- 6 torr [5.3 +/- 0.8 kPa]; standard dose epinephrine, 45 +/- 7 torr [6.0 +/- 0.9 kPa]; placebo, 54 +/- 4 torr [7.2 +/- 0.5 kPa]; p < .01) and mixed venous PCO2 (high-dose epinephrine, 55 +/- 10 torr [7.3 +/- 1.3 kPa]; standard dose epinephrine, 57 +/- 9 torr [7.6 +/- 1.2 kPa]; placebo, 67 +/- 4 torr [8.9 +/- 0.5 kPa]; p < .05) were significantly decreased, and arterial pH, PaO2, and mixed venous PO2 were significantly increased compared with the placebo group.
In this model, when ventilation and CO2 production are constant, the decrease in PaCO2 with epinephrine is due to decreased pulmonary blood flow (flow to membrane oxygenator) and peripheral shunting.
先前的研究表明，在心肺复苏期间，肾上腺素可能会改变灌注与二氧化碳分压测量值之间的相关性。本研究在心脏骤停的高流量再灌注模型中，调查了肾上腺素对动脉血二氧化碳分压（PaCO2）和混合静脉血二氧化碳分压的影响。
前瞻性、区组随机、双盲、安慰剂对照的实验室研究。
30只混血犬。
在经历12分钟室颤性心脏骤停后，30只混血犬接受标准化（3200转/分钟）体外循环再灌注，并分别给予安慰剂（n = 10）、标准剂量肾上腺素（0.02 mg/kg；n = 10）或高剂量肾上腺素（0.2 mg/kg；n = 10）。在再灌注早期，采用方差分析及事后Tukey多重比较检验，比较各组之间的动脉血和混合静脉血气、冠状动脉灌注压、泵流量和外周血管阻力。
各组之间的基线变量相似。再灌注时，高剂量肾上腺素组的冠状动脉灌注压较高（p < .002），全身泵流量较低（p < .01），外周血管阻力较高（p < .001）。在高剂量肾上腺素组中，与安慰剂组相比，PaCO2（高剂量肾上腺素组为40±6托[5.3±0.8千帕]；标准剂量肾上腺素组为45±7托[6.0±0.9千帕]；安慰剂组为54±4托[7.2±0.5千帕]；p < .01）和混合静脉血二氧化碳分压（高剂量肾上腺素组为55±10托[7.3±1.3千帕]；标准剂量肾上腺素组为57±9托[7.6±1.2千帕]；安慰剂组为67±4托[8.9±0.5千帕]；p < .05）均显著降低，动脉血pH值、PaO2和混合静脉血氧分压均显著升高。
在该模型中，当通气和二氧化碳产生量保持恒定时，肾上腺素导致的PaCO2降低是由于肺血流量（流向膜式氧合器的流量）减少和外周分流所致。
