Ryu S-J, Lee S-J, Park C-H, Lee S-M, Lee D-H, Cho Y-S, Jung Y-H, Lee B-K, Jeung K-W
Department of Emergency Medicine, Chonnam National University Hospital, Gwangju, Korea.
Department of Emergency Medicine, Myongji Hospital, Goyang, Gyeonggi-do, Korea.
Acta Anaesthesiol Scand. 2016 Aug;60(7):1012-23. doi: 10.1111/aas.12728. Epub 2016 Apr 14.
We sought to investigate the utility of arterial pressure, end-tidal carbon dioxide (ETCO2 ), and central venous oxygen saturation (SCVO2 ) to guide compression depth adjustment. Thus, in a pig model of cardiac arrest, we observed these parameters during cardiopulmonary resuscitation (CPR) with optimal and suboptimal compression depths.
Sixteen pigs underwent three experimental sessions after induction of ventricular fibrillation. First, the animals received two 4-min CPR trials with either optimal (20% of the anteroposterior diameter) or suboptimal (70% of the optimal depth) compression depth. Second, the animals received two 5-min CPR trials with optimal compression depth, in which adrenaline (0.02 mg/kg) or saline placebo was administered. Third, the animals randomly received compression with either optimal or suboptimal depth during advanced cardiovascular life support.
The systolic arterial pressure reflected compression depth most accurately and immediately (area under the curve [AUC], 0.895-0.939 without adrenaline and 0.928-1.000 with adrenaline). Although the response of ETCO2 to the change in compression depth was 0.5 min slower than that of the systolic arterial pressure, the performance of ETCO2 was comparable with that of systolic arterial pressure. SCVO2 did not reflect compression depth. Adrenaline administration remarkably increased systolic arterial pressure, diastolic arterial pressure, and coronary perfusion pressure but did not affect the ETCO2 readings.
In a pig model of cardiac arrest, systolic arterial pressure reflected compression depth immediately and accurately. The performance of ETCO2 was comparable with that of systolic arterial pressure. SCVO2 did not reflect compression depth.
我们试图研究动脉压、呼气末二氧化碳分压（ETCO2）和中心静脉血氧饱和度（SCVO2）在指导按压深度调整方面的作用。因此，在猪心脏骤停模型中，我们在心肺复苏（CPR）期间以最佳和次优按压深度观察了这些参数。
16只猪在诱发室颤后进行了三个实验阶段。首先，动物接受两次4分钟的CPR试验，按压深度分别为最佳深度（前后径的20%）或次优深度（最佳深度的70%）。其次，动物接受两次5分钟的CPR试验，按压深度为最佳深度，其中一次给予肾上腺素（0.02mg/kg），另一次给予生理盐水安慰剂。第三，在高级心血管生命支持期间，动物随机接受最佳或次优深度的按压。
收缩压最能准确、即时地反映按压深度（曲线下面积[AUC]，未使用肾上腺素时为0.895 - 0.939，使用肾上腺素时为0.928 - 1.000）。虽然ETCO₂对按压深度变化的反应比收缩压慢0.5分钟，但其性能与收缩压相当。SCVO₂不能反映按压深度。给予肾上腺素显著提高了收缩压、舒张压和冠状动脉灌注压，但不影响ETCO₂读数。
在猪心脏骤停模型中，收缩压能即时、准确地反映按压深度。ETCO₂的性能与收缩压相当。SCVO₂不能反映按压深度。
