Document Server@UHasselt >
Research publications >
Please use this identifier to cite or link to this item:
|Title: ||Is there a relationship between cerebral oxygenation after cardiac arrest and outcome?|
|Authors: ||Meex, I.|
De Deyne, C.
|Issue Date: ||2012|
|Citation: ||EUROPEAN JOURNAL OF ANAESTHESIOLOGY, 29, p. 49-49|
|Abstract: ||Background: After cardiac arrest (CA), neurological outcome might be influenced by cerebral perfusion. Near‐infrared spectroscopy (NIRS) makes it possible to continuously monitor the absolute cerebral tissue oxygen saturation (SctO2). Using four wavelengths of laser light, absolute determination of oxygenated and deoxygenated hemoglobin in the cerebral microvasculature is provided. Validated by correlation between SctO2 and jugular bulb saturation, threshold for cerebral ischemia is estimated at SctO2‐values of 55%. In this study, cerebral tissue oxygen saturation (SctO2) was measured during the first 24 hours after cardiac arrest (CA).Patients and methods: After IRB approval, 23 patients were monitored during the first hours after cardiac arrest (induction, maintenance and recovery of therapeutic hypothermia). Cold saline (30 ml/kg) was administered as soon as possible after hospital admission. Therapeutic hypothermia (TH) (33°C) was induced by endovascular or surface cooling. All patients were sedated (propofol/remifentanil) for the duration of hypothermia. SctO2‐monitoring was applied before start of TH.Results: Of the 23 patients, 12 (52%) patients survived the hospital stay. Eight of these survivors were discharged without any neurological deficit (CPC1). Two (9%) patients died within the first day after admission due to hemodynamic shock. Nine (39%) patients died during admission as a consequence of post‐ischemic brain damage.Values for cerebral oxygenation in non‐survivors started at 66% (± 7). Within three hours, SctO2 gradually declined to 55% (± 4) and remained below this critical value for cerebral ischemia for one hour. Thereafter, SctO2 started to increase to reach baseline values at 12 hours after start of monitoring. The decrease in SctO2 was not correlated with a change in hemodynamic parameters (MAP start: 76 mmHg; 3u: 91 mmHg) or systemic oxygenation (SpO2 start: 96%; 3h: 100%).Patients who survived the hospital stay, started at SctO2 values of 68% (± 4). SctO2 decreased to 59% (± 5) within two hours, but increased again to baseline values within four hours after the start of monitoring. In the following hours, SctO2 further increased up to 70% (± 3).Conclusion: In the first hours after CA cerebral oxygenation showed a decrease in SctO2. A significant difference in start values between survivors and non‐survivors was not observed. But, SctO2‐values decreased below the critical limit of 55% in non‐survivors.|
|Type: ||Journal Contribution|
|Appears in Collections: ||Research publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.