Ducros Laurent, Vicaut Eric, Soleil Christian, Le Guen Morgan, Gueye Papa, Poussant Thomas, Mebazaa Alexandre, Payen Didier, Plaisance Patrick
Department of Anesthesiology and Critical Care, Lariboisière University Hospital, Paris, France.
J Emerg Med. 2011 Nov;41(5):453-9. doi: 10.1016/j.jemermed.2010.02.030. Epub 2010 Apr 24.
Infusion of a vasopressor during cardiopulmonary resuscitation (CPR) in humans increases end decompression (diastolic) arterial blood pressure, and consequently increases vital organ perfusion pressure and survival. Several vasoactive drugs have been tested alone or in combination, but their hemodynamic effects have not been investigated clinically in humans.
We tested the hypothesis that epinephrine (1 mg) co-administered with vasopressin (40 IU) ± nitroglycerin (300 μg) results in higher diastolic blood pressure than epinephrine alone.
A prospective, randomized, double-blinded controlled trial in the prehospital setting. The study included 48 patients with witnessed cardiac arrest. Patients received either epinephrine alone (E alone) or epinephrine plus vasopressin (E+V) or epinephrine plus vasopressin plus nitroglycerin (E+V+N). A femoral arterial catheter was inserted for arterial pressure measurement.
The primary end point was diastolic blood pressure during CPR, 15 min after the first drug administration (T = 15 min).
After exclusions, a total of 44 patients were enrolled. Diastolic blood pressures (mm Hg) at T = 15 min were not statistically different between groups (median [interquartile range]: 20 [10], 15 [6], and 15 [13] for E alone, E+V, and E+V+N, respectively. The rate of return of spontaneous circulation was 63% (n = 10) in the epinephrine group, 43% (n = 6) in the epinephrine plus vasopressin group, and 36% (n = 5) in the triple therapy group (NS).
Addition of vasopressin or vasopressin plus nitroglycerin to epinephrine did not increase perfusion blood pressure compared to epinephrine alone in humans in cardiac arrest, suggesting the absence of benefit in using these drug combination(s).
在对人类进行心肺复苏(CPR)期间输注血管加压药可提高舒张期(减压期)动脉血压,从而增加重要器官灌注压并提高生存率。已经单独或联合测试了几种血管活性药物,但尚未在人体中对其血流动力学效应进行临床研究。
我们检验了以下假设,即肾上腺素(1毫克)与血管加压素(40国际单位)±硝酸甘油(300微克)联合使用比单独使用肾上腺素可导致更高的舒张压。
一项在院前环境中进行的前瞻性、随机、双盲对照试验。该研究纳入了48例目击心脏骤停患者。患者接受单独使用肾上腺素(仅E组)或肾上腺素加血管加压素(E + V组)或肾上腺素加血管加压素加硝酸甘油(E + V + N组)治疗。插入股动脉导管以测量动脉压。
主要终点是首次给药后15分钟(T = 15分钟)心肺复苏期间的舒张压。
排除后,共纳入44例患者。T = 15分钟时,各组间舒张压(毫米汞柱)无统计学差异(中位数[四分位间距]:仅E组为20[10],E + V组为15[6],E + V + N组为15[13])。肾上腺素组自主循环恢复率为63%(n = 10),肾上腺素加血管加压素组为43%(n = 6),三联疗法组为36%(n = 5)(无统计学差异)。
在心脏骤停的人体中,与单独使用肾上腺素相比,在肾上腺素中添加血管加压素或血管加压素加硝酸甘油并未增加灌注血压,这表明使用这些药物组合并无益处。