Increasing mean arterial pressure or cardiac output in comatose out-of-hospital cardiac arrest patients undergoing targeted temperature management: Effects on cerebral tissue oxygenation and systemic hemodynamics

Johannes Grand,Sebastian Wiberg,Jesper Kjaergaard,Michael Wanscher,Christian Hassager

doi:10.1016/j.resuscitation.2021.08.037

Johannes Grand, Sebastian Wiberg + Show 3 more

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https://doi.org/10.1016/j.resuscitation.2021.08.037

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Journal: Resuscitation	Publication Date: Aug 27, 2021
Citations: 11	License type: cc-by

Affiliation: Rigshospitalet, Copenhagen University Hospital

Abstract

IntroductionFew data exist on the effects of increasing norepinephrine doses or increasing arterial CO2 (PaCO2) on hemodynamics and cerebral oxygenation in comatose out-of-hospital cardiac arrest (OHCA) patients. MethodsWe prospectively studied 10 resuscitated OHCA-patients undergoing targeted temperature management (36C°). The trial consisted of 5 phases with 20 minutes steady state in-between: Phase 1–4 were increasing doses of norepinephrine to reach targets of mean arterial pressure (MAP). First 65, second 75, third 85, fourth 65 mmHg again. In the fifth phase, MAP was constant while PaCO2 was increased to 6.5–7.3 kPa to increase cardiac output. Primary outcome was cerebral near-infrared spectroscopy (NIRS). Secondary outcomes were hemodynamic variables from Swan-Ganz catheters and blood samples from the radial artery and jugular bulb. ResultsTo reach a MAP at 85 mmHg, norepinephrine was increased from 0.11 ± 0.02 to 0.18 ± 0.02 µg/kg/min (P < 0.001). Norepinephrine uptitration significantly increased systemic vascular resistance (SVR) and pulmonary vascular resistance, without affecting cardiac output, heart rate or cerebral oxygenation.Increasing PaCO2, resulted in a significant increase in cardiac output and cerebral NIRS, but arterial-venous cerebral oxygen-uptake decreased. Norepinephrine demand to keep MAP at 65 mmHg was unaffected by increasing PaCO2. ConclusionsA short-term increase in MAP with norepinephrine in resuscitated comatose cardiac arrest-patients is associated with increased SVR and pulmonary vascular resistance without affecting cardiac output or cerebral NIRS. Increased cardiac output caused by an increase in PaCO2 increased cerebral NIRS, but not cerebral oxygen uptake.

Highlights

Few data exist on the eects of increasing norepinephrine doses or increasing arterial CO2 (PaCO2) on hemodynamics and cerebral oxygenation in comatose out-of-hospital cardiac arrest (OHCA) patients
During out-of-hospital cardiac arrest (OHCA), anoxic injury results in post-resuscitation challenges in the intensive care unit: Brain injury and coma, myocardial dysfunction, systemic inflammation leading to a sepsis-like syndrome with low systemic vascular resistance (SVR).[1,2]
Increasing PaCO2 in phase 5 resulted in a significant increase in cardiac output and cerebral near-infrared spectroscopy (NIRS), while decreasing SVR

Summary

Introduction

Few data exist on the eects of increasing norepinephrine doses or increasing arterial CO2 (PaCO2) on hemodynamics and cerebral oxygenation in comatose out-of-hospital cardiac arrest (OHCA) patients. During out-of-hospital cardiac arrest (OHCA), anoxic injury results in post-resuscitation challenges in the intensive care unit: Brain injury and coma, myocardial dysfunction, systemic inflammation leading to a sepsis-like syndrome with low systemic vascular resistance (SVR).[1,2] Vasopressors are needed to increase mean arterial pressure (MAP).[3,4] Association between low blood pressure after OHCA and poor outcome have been found in several studies,[5,6,7,8,9,10] but two pilot studies of higher MAP-targets did not show signs of benefit on surrogate outcomes.[11,12] International guidelines recommend treatment with vasopressors to avoid hypotension.[4] Despite being frequently used during post-resuscitation care, the hemodynamic and cerebral effects of changing vasopressor-dose in the clinical setting are sparsely studied in OHCA-patients. One study found less increase in neuron-specific enolase (NSE),[14] whereas the other study found no difference in NSE, but higher cerebral oxygenation.[15]

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