This study was conducted to determine the effects of high pressure interposed ventilations during cardiopulmonary resuscitation (CPR). Cardiac output was measured by a modified indicator dilution technique in eight anesthetized, intubated mongrel dogs. Positive pressure ventilations (12/min, 80% O 2 ) were interposed after every five chest compressions (performed at 62/min) by a mechanical chest compressor (Thumper ® ). On repeated trials in the same animal, ventilation pressures from 10-50 cm of H 2 O were tested in randomized sequence, while the technique of chest compression was held constant. Arterial blood gases immediately after resuscitation were monitored. Increasing ventilation pressure had surprisingly little effect on cardiac output during CPR, although blood gases were profoundly altered. For ventilation pressures of 10, 20, 30, 40, and 50 cm of H 2 O, producing mean tidal volumes 23, 38, 61, 83, and 94 ml/kg; cardiac output remained nearly constant, averaging 21, 25, 23, 26, and 24 ml/min/kg. Corresponding mean post-resuscitation pH was 7.24, 7.41, 7.51, 7.56, and 7.53; PCO 2 was 41, 26, 18, 16, and 15 torr. The post-resuscitation arterial oxygen tension was greater than 100 torr at all ventilation pressures except 10 cm of H 2 O. Interposed ventilations of pressure and volume more than adequate to prevent acidosis during CPR did not impair artificial cardiac output. If anything, cardiac output was slightly improved by more forceful ventilation.2