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Abstract
Once the investigators established that excessive ventilation rates were a problem in the field, they returned to the laboratory to elucidate the significance of this phenomenon. To do so, they used a porcine model of cardiac arrest to explore the effect of hyperventilation on cardiac haemodynamics during cardiopulmonary resuscitation, and the likelihood of successful resuscitation. As expected, excessive ventilation rates (ie, 20 or 30 a minute) produced significantly higher mean intrathoracic pressures and lower coronary perfusion pressures than in animals that were ventilated at the AHA's recommended rate of 12 a minute. These differences were not only statistically significant, but clinically significant as well. Animals ventilated at 12 breaths a minute were much more likely to be successfully resuscitated (six of seven) than those who received 30 breaths a minute (one of seven). To assess whether these deleterious effects of hyperventilation were due to hypocapnoea or positive intrathoracic pressure, the researchers included a third group of seven pigs ventilated at 30 breaths a minute with 5% CO2. Such ventilation brought the animals' PCO^sub 2^ to normal, but failed to improve intrathoracic pressure, coronary perfusion pressure, or the odds of successful resuscitation (one of seven). This last finding strongly suggests that the adverse effects of hyperventilation are due to increased intrathoracic pressure and decreased coronary perfusion, not hypocapnoea.