Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation.

Cardiopulmonary resuscitation (CPR) has been thought to produce blood flow by compression of the heart between the sternum and spine, termed "external cardiac massage," but there has been-no direct experimental documentation of this proposed mechanism. Micromanometric pressure recordings were synchronized with cineangiograms during mechanical CPR in 17 dogs with induced ventricular fibrillation. Chest compression produced equivalent pressure increases in the aorta (Ao) and right atrium (RA) (Ao 32 + 14 mm Hg, RA 30 ± 14 mm Hg; NS), a linear relationship between aortic and intrapleural pressures (r = 0.87, p < 0.001) over a wide range of induced pressures, cineangiographic blood flow through both left-heart chambers, and a pressure gradient (21 ± 14 mm Hg) between all intrathoracic cardiovascular compartments and the jugular veins that resulted from closure of venous valves at the thoracic inlets. Simultaneous chest compression and lung inflation significantly increased all intrathoracic vascular pressures, the aortojugular venous gradient (42 ± 13 mm Hg,p < 0.05 vs chest compression alone), electromagnetically determined carotid arterial blood flow (1.75 ± 0.81 ml/min/kg vs 0.51 ± 0.27 mI/min/kg during chest compression alone, p < 0.005), and angiographic left-heart flow. We conclude that blood flow during CPR results principally from an increased intrathoracic pressure and that there is selective flow to the brachiocephalic vascular bed because of the arteriovepous gradient produced by venous valves at the thoracic inlets. Greater intrathoracic pressure resulting from simultaneous inflation and compression improves left-heart flow. The left heart is therefore a conduit, not a pump, during CPR.