Key result
External chest compression delays aortic flow behind pressure by ~40 ms, supporting an intrathoracic pressure mechanism.
Why the study?
Do different modes of external chest compression alter aortic flow, pressure relations, and aortic diameter compared to sinus rhythm and internal cardiac massage in dogs?
Do different modes of external chest compression alter aortic flow, pressure relations, and aortic diameter compared to sinus rhythm and internal cardiac massage in dogs?
p-value: p=<0.001
External chest compression generates blood flow via fluctuations in intrathoracic pressure rather than stroke volume-induced increases in aortic pressure and diameter.
Aortic flow and pressure relations and aortic diameter were examined during sinus rhythm, internal cardiac massage, vest cardiopulmonary resuscitation, conventional manual cardiopulmonary resuscitation and high impulse manual cardiopulmonary resuscitation in 14 anesthetized large dogs. During sinus rhythm and during internal cardiac massage, ascending aortic flow and pressure increased simultaneously and the rise in ascending aorta pressure preceded the rise in descending aortic pressure by (mean +/- SEM) 28 +/- 4 and 30 +/- 1 ms, respectively. In contrast, during vest, conventional and high impulse cardiopulmonary resuscitation, ascending aortic flow lagged behind the initial rise in aortic pressure by 40 +/- 4 to 46 +/- 4 ms and ascending and descending aortic pressure increased simultaneously (p less than 0.001 for each external compression mode versus sinus rhythm and internal massage). The ratio of pulse pressure to stroke volume increased by an order of magnitude during all modes of external chest compression (p less than 0.001 versus sinus rhythm and internal massage) and aortic diameter decreased during vest and high impulse cardiopulmonary resuscitation (p less than 0.05 versus sinus rhythm and internal massage). The hemodynamics of external chest compression depart from the normal physiologic sequence of stroke volume-induced increase in aortic pressure and diameter. The rise in aortic pressure precedes flow into the aorta, stroke volume does not fully account for pulse pressure, and aortic diameter decreases during chest compression. These data support the hypothesis that blood flow is due to fluctuations in intrathoracic pressure for high impulse as well as vest and conventional cardiopulmonary resuscitation.
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Guerci et al. (1989) studied Cardiac arrest / CPR models (n=14). External chest compression (vest, conventional manual, high impulse manual CPR) vs. Sinus rhythm and internal cardiac massage was evaluated on Aortic flow and pressure relations and aortic diameter (p=<0.001). External chest compression caused ascending aortic flow to lag behind the initial rise in aortic pressure by 40-46 ms (P<0.001 vs sinus rhythm), supporting an intrathoracic pressure mechanism.
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