OBSERVATIONS OF VENTILATION DURING RESUSCITATION IN A CANINE MODEL

Background Fear of infection limits the willingness of laymen to do cardiopulmonary resuscitation (CPR). This study assessed the time course of change in arterial blood gases during resuscitation with only chest compression (no ventilation) in an effort to identify the time for which ventilation could be deferred. Methods and Results Aortic pressures and arterial blood gases were monitored in seven 20- to 30-kg dogs in ventricular fibrillation (VF) at 2-minute intervals during chest compression alone (no ventilation) at 80 to 100 compressions per minute. Before the induction of ventricular fibrillation, all animals were intubated and ventilated with room air, 10 mL/kg. The endotracheal tube was removed when VF was induced. Pre-VF arterial pH, PCO2, and O-2 saturation were (mean+/-SEM) 7.39+/-0.02, 27.0+/-1.5 mm Hg, and 97.5+/-0.5%, respectively, with aortic pressures being 143.2+/-5.7/116.2+/-4.6 mm Hg. At 4 minutes of chest compression alone, the corresponding values were 7.39+/-0.03, 24.3+/-3.1 mm Hg, and 93.9+/-3.0%, with an arterial pressure of 48.1+/-7.7/22.6+/-3.9 mm Hg. Mean minute ventilation during the fourth minute of CPR, measured with a face mask-pneumotachometer, was 5.2+/-1.1 L/min. Conclusions These data suggest that in the dog model of witnessed arrest, chest compression alone during CPR can maintain adequate gas exchange to sustain O-2 saturation >90% for >4 minutes. The need for immediate ventilation during witnessed arrest should be reexamined.