Despite the widespread clinical application of cardiopulmonary resuscitation (CPR), the mechanism responsible for blood flow during this maneuver remains undefined, although it has been assumed that blood is squeezed from the heart by direct compression of the sternum. We studied the hemodynamics of CPR in 15 arrested dogs. During chest compression, pressures in the left ventricle, aorta, right atrium and pulmonary artery were essentially identical. These pressures were also equal to the intrathoracic pressure as estimated by an esophageal balloon catheter. Unequal transmission of pressures to the extrathoracic arterial and venous system resulted from collapse of the great veins at the thoracic outlet as intrathoracic pressures rose. This phenomenon gave rise to a peripheral arteriovenous pressure gradient and antegrade flow. When intrathoracic pressure was increased by maintaining the lungs fully inflated during chest compression, aortic systolic pressure rose from 27.3±4.0 mm Hg to 58.4±79 mm Hg (p < 0.001) and carotid blood flow increased from 9.0±2.2 ml/min to 28.6±5.9 ml/min (p<0.001). Increasing the intrathoracic pressure by tightly binding the abdomen to prevent paradoxical diaphragmatic motion during chest compression also resulted in a rise in aortic systolic pressure, from 29.4±3.2 to 57.7±7.7 mmHg (p<0.001), and an increase in carotid blood flow, from 14.5±8.1 ml/min to 32.3±9.7 ml/min (p<0.005). It appears that pressure generation and blood flow during CPR in the dog result from a generalized rise in intrathoracic pressure, not from direct cardiac compression. Maneuvers that raise the intrathoracic pressure can dramatically increase carotid blood flow during CPR.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)