Targeted high mean arterial pressure aggravates cerebral hemodynamics after extracorporeal resuscitation in swine

Nicolas Polge,Pierre-Louis Leger,Rocio Fernandez,Bijan Ghaleh,Lionel Lamhaut,Renaud Tissier,Yael Levy,Alice Hutin,Keith Lurie,Matthias Kohlhauer,Guillaume Debaty,Fanny Lidouren

doi:10.1186/s13054-021-03783-3

Abstract

BackgroundExtracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest. However, the optimal target to reach for mean arterial pressure (MAP) remains to be determined. We hypothesized that MAP levels critically modify cerebral hemodynamics during E-CPR and tested two distinct targets (65–75 vs 80–90 mmHg) in a porcine model.MethodsPigs were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Defibrillations were then delivered until return of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min. The dose of epinephrine was set to reach a standard or a high MAP target level (65–75 vs 80–90 mmHg, respectively). Animals were followed during 120-min after ROSC.ResultsSix animals were included in both groups. During E-CPR, high MAP improved carotid blood flow as compared to standard MAP. After ROSC, this was conversely decreased in high versus standard MAP, while intra-cranial pressure was superior. The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, also demonstrated inverted patterns of alteration according to MAP levels during E-CPR and after ROSC. In standard-MAP, PRx was transiently positive during E-CPR before returning to negative values after ROSC, demonstrating a reversible alteration of cerebral autoregulation during E-CPR. In high-MAP, PRx was negative during E-CPR but became sustainably positive after ROSC, demonstrating a prolonged alteration in cerebral autoregulation after ROSC. It was associated with a significant decrease in cerebral oxygen consumption in high- versus standard-MAP after ROSC.ConclusionsDuring early E-CPR, MAP target above 80 mmHg is associated with higher carotid blood flow and improved cerebral autoregulation. This pattern is inverted after ROSC with a better hemodynamic status with standard versus high-MAP.

Highlights

Out-of-hospital cardiac arrest is the leading cause of mortality in western countries, with an extremely low survival and poor neurological outcome [1]
After 30 min of Extracorporeal cardiopulmonary resuscitation (E-CPR), all animals achieved return of spontaneous circulation (ROSC) after the first electric shock, except one animals which required a second shock in the standardMAP group
The total amount of epinephrine administered to achieve mean arterial pressure (MAP) target during the first 30 min of E-CPR was lower in standard-MAP vs high –MAP group (51 ± 13 vs 102 ± 21 μg/kg over 30 min)

Summary

Introduction

Out-of-hospital cardiac arrest is the leading cause of mortality in western countries, with an extremely low survival and poor neurological outcome [1]. (CPR) fails to achieve return of spontaneous circulation (ROSC). It allows restoring organ perfusion whilst the underlying etiology is identified and properly treated [2, 3]. The ideal hemodynamic management remains unclear during E-CPR, e.g., regarding optimal mean arterial pressure (MAP) target. There is no few specific data regarding cerebral hemodynamics at different MAP levels during E-CPR to our knowledge, despite its relevance as a determinant of cerebral outcome. A specific investigation of these parameters is of importance since brain circulation is peculiar with a proper autoregulation and cerebral dramatic metabolic changes after cardiac arrest. We hypoth‐ esized that MAP levels critically modify cerebral hemodynamics during E-CPR and tested two distinct targets (65–75 vs 80–90 mmHg) in a porcine model

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