Restoring coronary perfusion pressure before defibrillation after chest compression interruptions

Recent studies have shown that blood flow during closed-chest cardiopulmonary resuscitation (CPR) results primarily from generalized changes in intrathoracic pressure rather than direct compression of the heart. Since ascending aortic and right atrial pressures rise and fall synchronously and to comparable levels during CPR, we hypothesized that the absence of a pressure difference across the coronary vascular bed during CPR precludes coronary blood flow. To test this hypothesis, we compared high-fidelity ascending aortic and right atrial pressures and carotid and coronary blood flow (electromagnetic flowmeters) during closed-chest CPR in 12 fibrillating dogs. Chest compression force was increased from 40 to 140 pounds in 20-pound increments using a pneumatic chest compression device. Although ascending aortic and right atrial pressures were always similar, high-compression-force CPR produced small mean pressure differences across the coronary vascular bed (5.6 +/- 0.8 mm Hg [+/- SEM] at 140 pounds). These pressure differences were accompanied by low levels of coronary blood flow. However, coronary flow was less than 1% control (prearrest) values whenever chest compression force was less than 100 pounds, and carotid flow exceeded coronary flow under all conditions (carotid and coronary flows at 140 pounds = 26.2 +/- 6.4% and 4.3 +/- 2.0% of prearrest values, respectively, p less than 0.01). We conclude that generalized changes in intrathoracic vascular pressures during closed-chest CPR promote carotid but not coronary blood flow. High-compression-force CPR produces small pressure differences across the coronary vascular bed, allowing low levels of coronary flow. However, even high-compression-force CPR is over six times more effective in maintaining carotid flow than coronary flow