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  • Title: Effects of simulated mouth-to-mouth ventilation during external cardiac compression or active compression-decompression in a swine model of witnessed cardiac arrest.
    Author: Engoren M, Plewa MC, Buderer NF, Hymel G, Brookfield L.
    Journal: Ann Emerg Med; 1997 May; 29(5):607-15. PubMed ID: 9140244.
    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 PO2, PCO2, and pH values; oxygen consumption (VO2); carbon dioxide production (VCO2); and minute ventilation (VE) 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 PO2 values in comparison with room air but did result in higher arterial PCO2 values at 5 and 9 minutes (although the mean PCO2 was 40 mm Hg or less [5.3 kPa] in all groups) and significant central venous hypercarbic acidosis at 9 and 13 minutes. Arterial PO2 values were greater in the ACD than the ECC groups at 5, 9, and 13 minutes, although all groups maintained acceptable PO2 (mean values > or = 60 mm Hg [8.0 kPa]) through 9 minutes of CPR and through 13 minutes in all but the ECC-room air group. PCO2 values were lower in the ACD groups beyond 1 minute, with the ACD-room air group showing extreme hyperventilation (mean PCO2 < or = 20 mm Hg [2.7 kPa]). MTM ventilation resulted in negative VO2 and VCO2 for the first few minutes, reflecting changes in pulmonary gas stores. As equilibrium was approached, VO2 and VCO2 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 VE 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.
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