Jasani M S, Salzman S K, Tice L L, Ginn A, Nadkarni V M
Department of Emergency Medicine, St. Christopher's Hospital For Children, Philadelphia, PA 19134-1095, USA.
Resuscitation. 1997 Aug;35(1):69-75. doi: 10.1016/s0300-9572(96)01094-5.
The effects of three anesthetic regimens on an established model of pediatric porcine hypoxic-hypercarbic arrest were examined. Twenty-four preadolescent miniature piglets were paralyzed, mechanically ventilated and anesthetized with one of three regimens: IM + IV pentobarbital (n = 8); IM + IV ketamine (n = 8); or IM ketamine+inhaled isoflurane (n = 8). Asphyxial cardiopulmonary arrest was induced and, after and 8 min cardiac arrest nonintervention interval, a standardized protocol of manual CPR with mechanical ventilation was performed. Outcome variables included incidence of ventricular fibrillation, time to cardiac arrest, endogenous plasma epinephrine levels and arteriovenous epinephrine gradients. IV Ketamine anesthesia produced the highest incidence of ventricular fibrillation (P < 0.01 vs. pentobarbital and isoflurane). Time to asphyxia induced cardiac arrest was greatest for the pentobarbital group (P < 0.05 vs. ketamine and isoflurane). During induction of asphyxial cardiac arrest (low cardiac flow), endogenous venous epinephrine accumulation was highest in the pentobarbital anesthetized group (P < 0.05). After 8 min of untreated cardiac arrest and 1 min of CPR (low flow), arterial epinephrine levels were highest in the ketamine group (P < 0.05). Endogenous epinephrine gradients were venous > arterial in all groups at the end of the 8 min cardiac arrest non-intervention interval (no flow). After 1 min of CPR, the gradients had either equalized or reversed to arterial > venous in all groups except for pentobarbital. As designed and expected, return of spontaneous circulation did not occur in any animal. We conclude that, in developing models of porcine asphyxial cardiopulmonary arrest and resuscitation to simulate pediatric human arrest, variations in anesthetic regimen produce significant differences in parameters that are important to consider: time to asphyxia induced cardiac arrest, fibrillation threshold, plasma epinephrine level and arteriovenous epinephrine gradient. Anesthetic effects need to be carefully considered and clearly explained to facilitate the interpretation of studies of interventions in cardiopulmonary arrest and resuscitation.
研究了三种麻醉方案对已建立的小儿猪缺氧 - 高碳酸血症性心脏骤停模型的影响。24只青春期前的小型仔猪被麻痹、机械通气，并采用以下三种方案之一进行麻醉：肌肉注射 + 静脉注射戊巴比妥（n = 8）；肌肉注射 + 静脉注射氯胺酮（n = 8）；或肌肉注射氯胺酮 + 吸入异氟烷（n = 8）。诱导窒息性心脏骤停，在8分钟心脏骤停非干预间隔后，进行标准化的手动心肺复苏并机械通气方案。结果变量包括室颤发生率、心脏骤停时间、内源性血浆肾上腺素水平和动静脉肾上腺素梯度。静脉注射氯胺酮麻醉导致室颤发生率最高（与戊巴比妥和异氟烷相比，P < 0.01）。戊巴比妥组窒息诱导心脏骤停的时间最长（与氯胺酮和异氟烷相比，P < 0.05）。在窒息性心脏骤停诱导期间（低心排血量），戊巴比妥麻醉组内源性静脉肾上腺素蓄积最高（P < 0.05）。未经治疗的心脏骤停8分钟和心肺复苏1分钟后（低流量），氯胺酮组动脉肾上腺素水平最高（P < 0.05）。在8分钟心脏骤停非干预间隔结束时（无血流），所有组内源性肾上腺素梯度均为静脉＞动脉。心肺复苏1分钟后，除戊巴比妥组外，所有组的梯度均已平衡或逆转至动脉＞静脉。按照设计和预期，任何动物均未出现自主循环恢复。我们得出结论，在开发猪窒息性心脏骤停和复苏模型以模拟小儿人类心脏骤停时，麻醉方案的差异会在一些重要参数上产生显著差异：窒息诱导心脏骤停的时间、颤动阈值、血浆肾上腺素水平和动静脉肾上腺素梯度。需要仔细考虑并清楚解释麻醉效果，以利于对心肺骤停和复苏干预研究的解读。
