Introduction:
Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest but the optimal target to reach for mean arterial pressure (MAP) remains to be determined.
Hypothesis:
We hypothesized that MAP levels modify cerebral hemodynamics during E-CPR. Accordingly, we tested two MAP targets (65-75
vs
80-90 mmHg) in a porcine model of E-CPR.
Methods:
Pigs were anesthetized and instrumented for the evaluation of cerebral and systemic hemodynamics. They were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Electric attempts of defibrillation were then delivered until resumption of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min with a standardized volume expansion in both groups. The dose of epinephrine was set to reach either a standard or a high MAP target level (65-75
vs
80-90 mmHg, respectively). Animals were followed during 120 min after ROSC.
Results:
Six animals were included in both groups. After cardiac arrest, MAP was maintained at the expected level (Figure). During E-CPR, high MAP transiently improved carotid blood flow as compared to standard MAP. This blood flow progressively decreased after ROSC in high vs standard MAP, while intra-cranial pressure increased. Interestingly, this was associated with a significant decrease in cerebral oxygen consumption (26±8
vs
54±6 L O
2
/min/kg at 120 min after ROSC, respectively; p<0.01) (Figure). The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, became positive in high MAP (0.47±0.02) vs standard MAP group (-0.16±0.10), demonstrating altered cerebral autoregulation with high MAP.
Conclusion:
Increasing MAP above 80 mmHg with epinephrine aggravates cerebral hemodynamics after E-CPR.
Figure:
Mean arterial pressure (MAP), cerebral blood flow and oxygen consumption (*, p<0.05)