Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression

Prior studies in dogs indicate that (1) blood flow during cardiopulmonary resuscitation results from the induced rise in intrathoracic pressure rather than from direct cardiac compression, and (2) maneuvers that increase intrathoracic pressure lead to increased carotid blood flow. Therefore, a system was devised for administering cyclical increases in intrathoracic pressure without lung overinflation for use during cardiac arrest. Ventilation at high airway pressure (60 to 100 mm Hg) was performed simultaneously with chest compression at a rate of 40/min in seven dogs with cardiac arrest. Airway pressure returned to the atmospheric level between compression-ventilation periods to allow venous return. This new technique was compared with conventional cardiopulmonary resuscitation both with and without sustained abdominal compression by binding. Peak chest compression force was held constant during all forms of resuscitation. Carotid blood flow was higher during simultaneous compression-ventilation resuscitation than with conventional resuscitation both without abdominal binding (mean ± standard error of the mean 18.7 ± 4.7 versus 5.1 ± 1.08 ml/min, p < 0.05) and with abdominal binding (28.6 ± 3.5 versus 13.8 ± 3.4 ml/min, p < 0.001). Carotid blood flow before cardiac arrest was 142 ± 26 ml/min. Carotid flow could be further increased over that during simultaneous compression-ventilation resuscitation with abdominal binding by interposing 20 mm Hg negative airway pressure between compression-ventilation periods. Similar results were obtained in six pigs and one baboon with cardiac arrest. Oxygenation and removal of carbon dioxide were adequate after 10 min of simultaneous compression-ventilation resuscitation. Although coronary blood flow was low with both techniques, left circumflex coronary flow was significantly greater with simultaneous compression-ventilation resuscitation (3.7 ±0.5 ml/min) than with conventional resuscitation (1.1 ± 0.5 ml/min, p < 0.01). Thus, in animals with cardiac arrest simultaneous compression-ventilation resuscitation can substantially increase carotid blood flow over that obtained with conventional cardiopulmonary resuscitation. Negative airway pressure added between compression-ventilation periods and abdominal binding can further augment carotid flow.