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Schoenthal, Tison David

University of British Columbia

Hypoxic ischemic brain injury (HIBI) is the resultant cerebral injury acquired after cardiac arrest stemming from cerebral ischemia during circulatory arrest and reperfusion following return of spontaneous circulation. Regrettably, HIBI outcomes remain poor, with survivors commonly experiencing neurological disabilities and neuropsychiatric sequelae. A cornerstone of HIBI management focusses on optimizing cerebral oxygen delivery and utilization. Central to this objective, the manipulation of arterial blood gases has come under scrutiny as a potential therapeutic approach, specifically the implementation of normobaric hyperoxia and mild hypercapnia. In study 1, normobaric hyperoxia was administered in post-cardiac arrest HIBI patients for 6 hours, targeting an arterial oxygen tension (PaO₂) of 200–300mmHg. Patients were monitored with jugular venous bulb oximetry, near infrared spectrometry and hemodynamic bedside monitoring in the ICU, with arterial and jugular venous blub blood samples taken at baseline, 2-, 4-, and the 6- hour mark, and following the resumption of normoxemia (PaO₂ 80–120mmHg) with additional blood samples taken at the 12- and 24-hour marks. The jugular venous oxygen saturation and regional saturation of oxygen did not increase during exposure to normobaric hyperoxia. Neurofilament light, a blood-based biomarker reflecting axonal injury, was significantly elevated at the 6-hour mark. In study 2, mild hypercapnia was administered for 2 hours in post-cardiac arrest HIBI patients who were monitored with transcranial Doppler ultrasound (TCD), jugular venous bulb oximetry and hemodynamic bedside monitoring. Baseline serum and plasma samples were taken from the in situ arterial and jugular venous bulb catheters, and then repeated at the 1- and 2- hour marks. TCD was also conducted in 15 healthy humans who were exposed to mild hypercapnia for control comparisons. Arterial CO₂ levels significantly increased during the study; however, no differences were seen in the jugular venous bulb oxygen saturation or cerebral oxygen extraction fraction. The cerebral arterio-venous difference of ubiquitin carboxyl hydrolase L1, a biomarker of neuron cell body injury, decreased at the 1-hour mark. HIBI patients also demonstrated decreased cerebrovascular reactivity and conductance compared to healthy humans when exposed to mild hypercapnia.

Text

2023-12-18

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/86973

Experimental Medicine

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/4.0/