Abstract 11340: Increasing Mean Arterial Pressure or Cardiac Output in Comatose Out-of-Hospital Cardiac Arrest Patients Undergoing Targeted Temperature Management: Effects on Cerebral Tissue Oxygenation

Abstract

Introduction: There are few data regarding the effects of norepinephrine-uptitration on global and regional hemodynamics in cardiac intensive care patients. Methods: We prospectively studied 10 OHCA patients at our cardiac intensive care unit. The trial consisted of 5 phases. The first 4 phases were achieved by titrating norepinephrine to reach targets of mean arterial pressure (MAP). First a MAP of 65 mmHg, second 75 mmHg, third 85 mmHg, fourth 65 mmHg again. The fifth phase was with a constant MAP of 65 mmHg but aiming at an increased PaCO2 from 6.5-7.3 kPa to increase cardiac output. During each phase, 20 minutes steady state was achieved before measurements. We measured hemodynamic variables with a Swan-Ganz catheter, arterial and mixed venous blood gases, and near-infrared spectroscopy at the forehead (cerebral oxygen saturation). Results: To obtain a MAP at 85 mmHg, norepinephrine was increased from 0.11±0.02 to 0.18±0.02 μg · kg–1 · min–1 (P < 0.001). Norepinephrine uptitration significantly increased MAP, systemic vascular resistance and pulmonary artery pressure, without affecting cardiac output or heart rate. After phase 3, norepinephrine was decreased to basal values, and all variables returned to baseline. Increasing pCO2, resulted in a significant increase in cardiac output and cerebral oxygen saturation, while decreasing systemic vascular resistance. MAP (and NE dose) was unaffected by increasing pCO2. Conclusions: A short-term increase in MAP with norepinephrine in resuscitated OHCA-patients is associated with increased SVR and PVR without affecting cardiac output or NIRS of the brain. An increase in CO caused by an increase in pCO2 and thereby a decreased SVR increased NIRS potentially improving brain oxygenation.