Abstract 163: Sodium Nitroprusside CPR Improves Vital Organ Perfusion and Resuscitation Outcomes in a Porcine Model of Ischemia Induced Pulseless Electrical Activity.
Introduction: We hypothesize that when standard (S-) CPR is unsuccessful in restoring spontaneous circulation during pulseless electrical activity (PEA), the combination of active compression decompression CPR with an inspiratory impedance threshold device, abdominal binding and large doses of sodium nitroprusside (SNP-CPR) may lead to successful resuscitation.
Methods: 9 female pigs, intubated and anesthetized had untreated ventricular fibrillation for 10 minutes followed by 3 minutes of chest compression only CPR (simulating bystander CPR) followed by 120J shocks (induction of PEA in all animals). S-CPR (continuous chest compressions with asynchronous ventilations [10 breaths/min]) was performed for 3 minutes. (simulating paramedic CPR). After documentation of a non-shockable rhythm on the ECG, 15 minutes after induction of cardiac arrest, SNP-CPR was initiated with 2mg of SNP given intravenously every 3 minutes. Aortic, right atrial pressures, end tidal CO2 and carotid blood flow (ml/min) were recorded. ANOVA was used for statistical analysis.
Results: Compared to S-CPR, SNP-CPR significantly improved coronary perfusion pressure (28±3 vs 12±4 mmHg), end tidal CO2 (23±4 vs 13±2 tor) and peak carotid blood flow (355±88 vs 91±32 mL/min) (p<0.05 for all). Systolic/diastolic aortic pressure significantly improved with SNP-CPR vs S-CPR (82±6/36±4 vs 41±4/15±3 mmHg, p<0.05 for both). 8/9 animals had successful return of spontaneous circulation with 5 animals demonstrating spontaneous electromechanical coupling after the second dose of SNP, requiring no further therapy.
Conclusions: SNP CPR is effective during PEA caused by prolonged ischemia as a “salvage” therapy when S-CPR fails and leads to electromechanical “coupling” with spontaneous resuscitation in a significant portion of animals.
- © 2010 by American Heart Association, Inc.