4.7 Article

Early goal-directed haemodynamic optimization of cerebral oxygenation in comatose survivors after cardiac arrest: the Neuroprotect post-cardiac arrest trial

Journal

EUROPEAN HEART JOURNAL
Volume 40, Issue 22, Pages 1804-1814

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehz120

Keywords

Cardiac arrest; Haemodynamics

Funding

  1. Flemish government

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Aims During the first 6-12 h of intensive care unit (ICU) stay, post-cardiac arrest (CA) patients treated with a mean arterial pressure (MAP) 65 mmHg target experience a drop of the cerebral oxygenation that may cause additional cerebral damage. Therefore, we investigated whether an early goal directed haemodynamic optimization strategy (EGDHO) (MAP 85-100 mmHg, SVO2 65-75%) is safe and could improve cerebral oxygenation, reduce anoxic brain damage, and improve outcome when compared with a MAP 65 mmHg strategy. Methods and results A total of 112 out-of-hospital CA patients were randomly assigned to EGDHO or MAP 65 mmHg strategies during the first 36 h of ICU stay. The primary outcome was the extent of anoxic brain damage as quantified by the percentage of voxels below an apparent diffusion coefficient (ADC) score of 650.10(-6) mm(2)/s on diffusion weighted magnetic resonance imaging (at day 5 +/- 2 post-CA). Main secondary outcome was favourable neurological outcome (CPC score 1-2) at 180 days. In patients assigned to EGDHO, MAP (P < 0.001), and cerebral oxygenation during the first 12 h of ICU stay (P = 0.04) were higher. However, the percentage of voxels below an ADC score of 650.10(-6) mm(2)/s did not differ between both groups [16% vs. 12%, odds ratio 1.37, 95% confidence interval (CI) 0.95-0.98; P = 0.09]. Also, the number of patients with favourable neurological outcome at 180 days was similar (40% vs. 38%, odds ratio 0.98, 95% CI 0.41-2.33; P = 0.96). The number of serious adverse events was lower in patients assigned to EGDHO (P = 0.02). Conclusion Targeting a higher MAP in post-CA patients was safe and improved cerebral oxygenation but did not improve the extent of anoxic brain damage or neurological outcome.

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