Effects of Simulated Mouth-to-Mouth Ventilation During External Cardiac Compression or Active Compression-Decompression in a Swine Model of Witnessed Cardiac Arrest

Abstract

Study objective: To assess the effects of simulated mouth-to-mouth (MTM) ventilation on blood gases, gas exchange, and minute ventilation during external cardiac compression (ECC) or active compression-decompression (ACD) in a swine model of witnessed cardiac arrest and bystander CPR. Methods: Twenty swine were anesthetized, intubated, ventilated with room air, and monitored for aortic and right atrial pressure and blood gas sampling. After 1 minute of ventricular fibrillation cardiac arrest, ECC or ACD was manually performed at a rate of 100 per minute for 12 minutes. Animals in the room air group had their endotracheal tubes open to air, whereas those in the MTM group were mechanically ventilated with a gas mixture of 16% oxygen and 4% carbon dioxide. Arterial and venous P o 2, P co 2, and pH values; oxygen consumption (VO 2); carbon dioxide production (V co 2); and minute ventilation (V E) were measured at baseline and 1, 5, 9, and 13 minutes after induction of cardiac arrest. Results: MTM ventilation did not alter arterial or venous P o 2 values in comparison with room air but did result in higher arterial P co 2 values at 5 and 9 minutes (although the mean P co 2 was 40 mm Hg or less [5.3 kPa] in all groups) and significant central venous hypercarbic acidosis at 9 and 13 minutes. Arterial P o 2 values were greater in the ACD than the ECC groups at 5, 9, and 13 minutes, although all groups maintained acceptable P o 2 (mean values ≥ 60 mm Hg [8.0 kPa]) through 9 minutes of CPR and through 13 minutes in all but the ECC–room air group. P co 2 values were lower in the ACD groups beyond 1 minute, with the ACD–room air group showing extreme hyperventilation (mean P co 2 ≤ 20 mm Hg [2.7 kPa]). MTM ventilation resulted in negative V o 2 and V co 2 for the first few minutes, reflecting changes in pulmonary gas stores. As equilibrium was approached, V o 2 and V co 2 approached zero in all groups, reflecting low cardiac output. MTM ventilation did not improve VE over room air at any time during ACD. It did improve V E during ECC, but only at the 12th interval. Conclusion: In this swine model of witnessed CPR, simulated MTM ventilation was not beneficial for blood gases, gas exchange, or ventilation during ECC or ACD CPR. [Engoren M, Plewa MC, Buderer NF, Hymel G, Brookfield L: Effects of simulated mouth-to-mouth ventilation during external cardiac compression or active compression-decompression in a swine model of bystander cardiac arrest. Ann Emerg Med May 1997; 29:607-616.]