This translational research initiative focused on the physiology of cardiopulmonary resuscitation (CPR) initiated by a clinical observation of consistent hyperventilation by professional rescuers in out-of-hospital cardiac arrest. This observation generated scientific hypotheses that could only ethically be tested in the animal laboratory.
To examine the hypothesis that excessive ventilation rates during performance of CPR by overzealous but well-trained rescue personnel causes a significant decrease in coronary perfusion pressure and an increased likelihood of death.
In the in vivo human aspect of the study, we set out to objectively and electronically record rate and duration of ventilation during performance of CPR by trained professional rescue personnel in a prospective clinical trial in intubated, adult patients with out-of-hospital cardiac arrest. In the in vivo animal aspect of the study, to simulate the clinically observed hyperventilation, nine pigs in cardiac arrest were ventilated in a random order with 12, 20, or 30 breaths/min, and physiologic variables were assessed. Next, three groups of seven pigs in cardiac arrest were ventilated at 12 breaths/min with 100% oxygen, 30 breaths/min with 100% oxygen, or 30 breaths/min with 5% CO2/95% oxygen, and survival was assessed.
Ventilation rate and duration in humans; mean intratracheal pressure, coronary perfusion pressure, and survival rates in animals.
In 13 consecutive adults (average age, 63 +/- 5.8 yrs) receiving CPR (seven men) the average ventilation rate was 30 +/- 3.2 breaths/min (range, 15 to 49 breaths/min) and the average duration of each breath was 1.0 +/- 0.07 sec. The average percentage of time in which a positive pressure was recorded in the lungs was 47.3 +/- 4.3%. No patient survived. In animals treated with 12, 20, and 30 breaths/min, the mean intratracheal pressures and coronary perfusion pressures were 7.1 +/- 0.7, 11.6 +/- 0.7, 17.5 +/- 1.0 mm Hg/min (p < .0001) and 23.4 +/- 1.0, 19.5 +/- 1.8, 16.9 +/- 1.8 mm Hg (p = .03) with each of the different ventilation rates, respectively (p = comparison of 12 breaths/min vs. 30 breaths/min for mean intratracheal pressure and coronary perfusion pressure). Survival rates were six of seven, one of seven, and one of seven with 12, 30, and 30 + CO2 breaths/min, respectively (p = .006).
Despite seemingly adequate training, professional rescuers consistently hyperventilated patients during out-of-hospital CPR. Subsequent hemodynamic and survival studies in pigs demonstrated that excessive ventilation rates significantly decreased coronary perfusion pressures and survival rates, despite supplemental CO2 to prevent hypocapnia. This translational research initiative demonstrates an inversely proportional relationship between mean intratracheal pressure and coronary perfusion pressure during CPR. Additional education of CPR providers is urgently needed to reduce these newly identified and deadly consequences of hyperventilation during CPR. These findings also have significant implications for interpretation and design of resuscitation research, CPR guidelines, education, the development of biomedical devices, emergency medical services quality assurance, and clinical practice.