12th Department of Respiratory Medicine, Sotiria General Hospital, Athens, Greece.
Crit Care Med. 2012 Mar;40(3):861-8. doi: 10.1097/CCM.0b013e318232d8de.
To assess whether intermittent impedance of inspiratory gas exchange improves hemodynamic parameters, 48-hr survival, and neurologic outcome in a swine model of asphyxial cardiac arrest treated with active compression-decompression cardiopulmonary resuscitation.
Prospective, randomized, double-blind study.
Laboratory investigation.
Thirty healthy Landrace/Large-White piglets of both sexes, aged 10 to 15 wks, whose average weight was 19 ± 2 kg.
At approximately 7 mins following endotracheal tube clamping, ventricular fibrillation was induced and remained untreated for another 8 mins. Before initiation of cardiopulmonary resuscitation, animals were randomly assigned to either receive active compression-decompression cardiopulmonary resuscitation plus a sham impedance threshold device (control group, n = 15), or active compression-decompression cardiopulmonary resuscitation plus an active impedance threshold device (experimental group, n = 15). Electrical defibrillation was attempted every 2 mins until return of spontaneous circulation or asystole.
Return of spontaneous circulation was observed in six (40%) animals treated with the sham valve and 14 (93.3%) animals treated with the active valve (p = .005, odds ratio 21.0, 95% confidence interval 2.16-204.6). Neuron-specific enolase and S-100 levels increased in the ensuing 4 hrs post resuscitation in both groups, but they were significantly elevated in animals treated with the sham valve (p < .01). At 48 hrs, neurologic alertness score was significantly better in animals treated with the active valve (79.1 ± 18.7 vs. 50 ± 10, p < .05) and was strongly negatively correlated with 1- and 4-hr postresuscitation neuron-specific enolase (r = -.86, p < .001 and r = -.87, p < .001, respectively) and S-100 (r = -.77, p < .001 and r = -0.8, p = .001) values.
In this model of asphyxial cardiac arrest, intermittent airway occlusion with the impedance threshold device during the decompression phase of active compression-decompression cardiopulmonary resuscitation significantly improved hemodynamic parameters, 24- and 48-hr survival, and neurologic outcome evaluated both with clinical and biochemical parameters (neuron-specific enolase, S-100).
评估在窒息性心跳骤停猪模型中，使用主动按压-释放心肺复苏术（ACD-CPR）时，间歇性吸气气体交换阻抗是否能改善血流动力学参数、48 小时生存率和神经功能结局。
前瞻性、随机、双盲研究。
实验室研究。
30 只健康的长白-大白杂交公母猪，年龄 10 至 15 周，平均体重 19±2kg。
在气管插管夹闭后约 7 分钟，诱导心室颤动，然后再让其持续 8 分钟。在开始心肺复苏之前，动物随机分为接受 ACD-CPR 加假阻抗阈值装置（对照组，n=15）或 ACD-CPR 加主动阻抗阈值装置（实验组，n=15）。每 2 分钟尝试电除颤，直到自主循环恢复或出现心搏停止。
接受假瓣膜治疗的 6 只（40%）动物和接受主动瓣膜治疗的 14 只（93.3%）动物出现自主循环恢复（p=0.005，优势比 21.0，95%置信区间 2.16-204.6）。两组在复苏后 4 小时内神经元特异性烯醇化酶和 S-100 水平均升高，但假瓣膜治疗组升高更明显（p<0.01）。48 小时时，接受主动瓣膜治疗的动物的神经警觉评分明显更好（79.1±18.7 比 50±10，p<0.05），与 1 小时和 4 小时后复苏时神经元特异性烯醇化酶（r=-0.86，p<0.001 和 r=-0.87，p<0.001）和 S-100（r=-0.77，p<0.001 和 r=-0.8，p=0.001）值呈强烈负相关。
在这种窒息性心跳骤停模型中，在 ACD-CPR 的释放阶段使用阻抗阈值装置间歇性气道闭塞可显著改善血流动力学参数、24 小时和 48 小时生存率，并通过临床和生化参数（神经元特异性烯醇化酶、S-100）评估神经功能结局。
