Krismer A C, Lindner K H, Kornberger R, Wenzel V, Mueller G, Hund W, Oroszy S, Lurie K G, Mair P
Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Austria.
Anesth Analg. 2000 Jan;90(1):69-73. doi: 10.1097/00000539-200001000-00017.
The American Heart Association does not recommend epinephrine for management of hypothermic cardiac arrest if body core temperature is below 30 degrees C. Furthermore, the effects of vasopressin administration during hypothermic cardiac arrest are totally unknown. This study was designed to assess the effects of vasopressin and epinephrine on coronary perfusion pressure in a porcine model during hypothermic cardiac arrest cardiopulmonary resuscitation (CPR). Pigs were surface-cooled until their body core temperature was 26 degrees C. After 30 min of untreated cardiac arrest, followed by 3 min of basic life support CPR, 15 animals were randomly assigned to receive, at 5-min intervals, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 5), epinephrine (45, 45, and 200 microg/kg; n = 5), or saline placebo (n = 5). Compared with epinephrine, mean +/- SEM coronary perfusion pressure was significantly higher (P < 0.05) 90 s and 5 min after the first (35+/-4 vs 22+/-3 mm Hg and 37+/-2 vs 16+/-2 mm Hg) and the second vasopressin administration (40+/-5 vs 26+/-5 mm Hg and 36+/-5 vs 18+/-2 mm Hg, respectively). After the third drug administration, coronary perfusion pressure in the epinephrine group increased dramatically and was comparable to vasopressin. In the saline placebo group, coronary perfusion pressure was significantly lower (P < 0.05) than in the vasopressin and epinephrine groups. Six animals treated with epinephrine or vasopressin had transient return of spontaneous circulation, whereas all placebo animals died (P < 0.05). During CPR in severe hypothermia, administration of both vasopressin and epinephrine resulted in significant increases in coronary perfusion pressure when compared with placebo.
Our study was designed to assess the effects of vasopressin and epinephrine in a porcine model simulating cardiac arrest during severe hypothermia. This study demonstrates that the administration of both emergency drugs results in an increased perfusion pressure in the heart.
美国心脏协会不建议在体温低于30摄氏度时使用肾上腺素来处理低温性心脏骤停。此外,在低温性心脏骤停期间给予血管加压素的效果完全未知。本研究旨在评估在低温性心脏骤停心肺复苏(CPR)过程中,血管加压素和肾上腺素对猪模型冠状动脉灌注压的影响。将猪体表降温直至其体温达到26摄氏度。在未经处理的心脏骤停30分钟后,接着进行3分钟的基础生命支持CPR,然后将15只动物随机分组,每隔5分钟分别给予血管加压素(0.4、0.4和0.8 U/kg;n = 5)、肾上腺素(45、45和200 μg/kg;n = 5)或生理盐水安慰剂(n = 5)。与肾上腺素相比,首次给予血管加压素后90秒和5分钟时,平均±标准误冠状动脉灌注压显著更高(P < 0.05)(分别为35±4 vs 22±3 mmHg和37±2 vs 16±2 mmHg),第二次给予血管加压素后也是如此(分别为40±5 vs 26±5 mmHg和36±5 vs 18±2 mmHg)。在第三次给药后,肾上腺素组的冠状动脉灌注压急剧上升且与血管加压素组相当。在生理盐水安慰剂组中,冠状动脉灌注压显著低于血管加压素组和肾上腺素组(P < 0.05)。接受肾上腺素或血管加压素治疗的6只动物出现了短暂的自主循环恢复,而所有接受安慰剂治疗的动物均死亡(P < 0.05)。在严重低温状态下的CPR过程中,与安慰剂相比,给予血管加压素和肾上腺素均能显著提高冠状动脉灌注压。
我们的研究旨在评估在模拟严重低温期间心脏骤停的猪模型中血管加压素和肾上腺素的效果。本研究表明,给予这两种急救药物均可使心脏灌注压升高。