EFFECTS OF SIMULATED MOUTH-TO-MOUTH VENTILATION DURING EXTERNAL CARDIAC COMPRESSION OR ACTIVE COMPRESSION-DECOMPRESSION IN A SWINE MODEL OFWITNESSED CARDIAC-ARREST

Study objective: To assess the effects of simulated mouth-to-mouth (MT M) ventilation on blood gases, gas exchange, and minute ventilation du ring external cardiac compression (ECC) or active compression-decompre ssion (ACD) in a swine model of witnessed cardiac arrest and bystander CPR. Methods: Twenty swine were anesthetized, intubated, ventilated w ith room air, and monitored for aortic and right atrial pressure and b lood 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 t ubes open to air, whereas those in the MTM group were mechanically ven tilated with a gas mixture of 16% oxygen and 4% carbon dioxide. Arteri al and venous Po-2, Pco(2), and pH values; oxygen consumption (VO2); c arbon dioxide production (Vco(2)); and minute ventilation (V-E) were m easured at baseline and 1, 5, 9, and 13 minutes after induction of car diac arrest. Results: MTM ventilation did not alter arterial or venous Po-2 values in comparison with room air but did result in higher arte rial Pco(2) values at 5 and 9 minutes (although the mean Pco(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 Po-2 values were g reater in the ACD than the ECC groups at 5, 9, and 13 minutes, althoug h ail groups maintained acceptable Po-2 (mean values 2 60 mm Hg [8.0 k Pa]) through 9 minutes of CPR and through 13 minutes in all but the EC C-room air group. Pco(2) values were lower in the ACD groups beyond 1 minute, with the ACD-room air group showing extreme hyperventilation ( mean Pco(2) less than or equal to 20 mm Hg [2.7 kPa]). MTM ventilation resulted in negative Vo(2) and Vco(2) for the first few minutes, refl ecting changes in pulmonary gas stores. As equilibrium was approached, Vo(2) and Vco(2) approached zero in all groups, reflecting low cardia c output. MTM ventilation did not improve V-E over room air at any tim e during ACD. It did improve V-E during ECC, but only at the 12th inte rval. Conclusion: In this swine model of witnessed CPR, simulated MTM ventilation was not beneficial for blood gases, gas exchange, or venti lation during ECC or ACD CPR.