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

Introduction: Few 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.

Methods: We 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.

Results: To 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.

Conclusions: A 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.