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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/15020

Title: NIRS cerebral oxygenation monitoring during therapeutic hypothermia after cardiac arrest
Authors: Meex, I.
Jans, F.
Dens, J.
De Deyne, C.
Issue Date: 2012
Abstract: Background: Induced mild hypothermia improves survival and neurological outcome after CA. Using near‐infrared spectroscopy (NIRS), the FORE‐SIGHT® technology provides a non‐invasive continuous monitoring of absolute cerebral tissue oxygen saturation (SctO2). Four wavelengths of laser light determine levels of oxygenated and deoxygenated hemoglobin in the cerebral microvasculature. In this study, SctO2 was measured during the first 36 hours after CA.Methods: After IRB approval and with informed consent, data were collected from 23 patients admitted after cardiac arrest. Cold saline (30 ml/kg) was administered as soon as possible. TH (33°C) was induced by endovascular (Coolgard®) or surface (Arctic Sun®) cooling and maintained for 24 hours. All patients were sedated (propofol/remifentanil) for the duration of TH. NIRS‐sensors were bilaterally applied to the frontotemporal area before start of TH.Results: Of 23 patients, 11 patients did not survive until hospital discharge due to post‐ischemic brain damage. Twelve patients survived until hospital discharge (8 without any neurological impairment). Temperature at admission was 34,6°C (± 0.5°C). Patients reached target temperature (33°C) 4 hours after the induction of TH. Two patients died during maintenance of TH due to hemodynamic shock. In all patients, SctO2 started above 65%. Two and a half hours after induction of TH, SctO2 decreased with 9% (± 3%). The decrease in SctO2 during induction of TH was not associated with a major change in hemodynamic parameters (MAP before TH: 79 mmHg ± 19; at 33°C: 82 mmHg ± 9), nor with a major change in systemic oxygenation (SpO2 before TH: 99% ± 1; at 33°C: 97% ± 3). In patients who survived until hospital discharge, SctO2 returned to baseline values 3,5 hours after induction of TH, before the target temperature of 33°C was reached. In patients who did not survived the hospital stay, SctO2 remained lower than baseline values when target temperature was reached. In this group, SctO2 only returned to baseline values during maintenance of TH (10 hours after induction of TH). During maintenance of TH and rewarming (0,3°C), no further significant changes in SctO2‐values were observed.Conclusion: During induction of mild hypothermia after CA, a decrease in cerebral oxygenation was observed. Furthermore, there was a difference in oxygenation between hospital survivors and non‐survivors.
URI: http://hdl.handle.net/1942/15020
ISSN: 0265-0215
Category: M
Type: Journal Contribution
Appears in Collections: Research publications

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