Effect of Standard Cardiopulmonary Resuscitation on Cerebral Blood Flow and Coronary Perfusion Pressure in the Canine Model of Simulated Ventricular Tachycardia

PURPOSE: The purpose of this study was to evaluate the hemodynamic effects of external chest compression in state of the heart's beating. METHODS: Ten mongrel dogs were used in this study. Ventricular tachycardia was simulated by using a rapid ventricular pacing and ventricular rate was adjusted and maintained at the rate necessary to achieve a 50-mmHg fall in the baseline systolic aortic pressure. External chest compression was initiated after 4 minutes of simulated ventricular tachycardia and was continued for 4 minutes. Hemodynamic measurements, including the systolic and the diastolic aortic pressure, the right atrial pressure, the carotid blood flow, and the end tidal CO2 tension, were done at baseline, during the simulated ventricular tachycardia (VT), and during the simulated ventricular tachycardia with external chest compression (VT+ECC). RESULTS: The systolic aortic pressure, the diastolic aortic pressure, and the mean right atrial pressure were higher during VT+ECC than during VT (99+/-12 vs 92+/-8 mmHg, p=0.157, 59+/-8 vs 55+/-12 mmHg, p=0.140, and 23+/-8 vs 8+/-2 mmHg, p<0.001, respectively). The carotid blood flow was higher during VT+ECC than during VT (273+/-203 vs 136+/-76 mL/min., p=0.011). The calculated coronary perfusion pressure was lower during VT+ECC than during VT ( 26+/-8 vs 40+/-9 mmHg, p<0.001). The end tidal CO2 tension was not different between VT+ECC and VT. CONCLUSION: In the canine model of simulated ventricular tachycardia, external chest compression had a contradictory hemodynamic effect, including an increase in the cerebral blood flow and a decrease in the coronary perfusion pressure.

Hemodynamic Effect of Deformation of the Descending Thoracic Aorta by Precordial Chest Compression during Standard Cardiopulmonary Resuscitation in Humans

PURPOSE: There have been no reports concerning the role of the aorta in explaining why blood flow is low below the diaphragm and a pressure gradient is present between central and peripheral arteries during standard cardiopulmonary resuscitation (CPR). The aim of this study was to assess the morphologic changes of the descending thoracic aorta and its effect on aortic pressure during precordial chest compression in cardiac arrest victims. METHODS: Twelve patients with non-traumatic cardiac arrest (8 males, mean age: 58 years) were enrolled. Transesophageal echocardiography was performed to verify the morphologic changes of the descending thoracic aorta during standard manual CPR. The pressure gradient across the maximally compressed site of the aorta was measured by pullback tracing using a pigtail catheter. RESULTS: Focal compression and deformation of the descending thoracic aorta was uniformly observed in all patients during compression systole. The mean systolic blood pressure of the descending thoracic aorta proximal and distal to the maximally compressed site was 135+/-3 6 mmHg and 115+/-21 mmHg, respectively. The mean systolic pressure gradient across the maximally compressed site was 20.5+/-17.7 mmHg. During compression systole, the pressure gradient between the right atrium and the descending thoracic aorta proximal to the maximally compressed site during compression systole was 49 +/-1 2 mmHg while pressure gradient between the right atrium and the descending thoracic aorta distal to the maximally compressed site was 29+/-8 mmHg. CONCLUSION: We found that the descending thoracic aorta was focally compressed and that a pressure gradient developed across the maximally compressed site during compression systole. This may contribute to limiting blood flow to the subdiaphragmatic region during standard manual CPR in humans.