Objective: 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.
Design: Prospective, randomized, double-blind study.
Setting: Laboratory investigation.
Subjects: Thirty healthy Landrace/Large-White piglets of both sexes, aged 10 to 15 wks, whose average weight was 19 ± 2 kg.
Interventions: 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.
Measurements and main results: 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.
Conclusions: 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).