Objectives: In patients at risk of hypoxic ischemic brain injury following cardiac arrest, we sought to (i) characterize brain oxygenation and determine the prevalence of brain hypoxia, (ii) characterize autoregulation using the pressure reactivity index (PRx) and identify the optimal mean arterial pressure (MAPOPT), and (iii) assess the relationship between MAPOPT and brain tissue oxygenation (PbtO2). Design: Prospective interventional study. Setting: Quaternary intensive care unit. Patients: Adult patients with return to spontaneous circulation (ROSC) greater than 10 minutes and a post-resuscitation Glasgow Coma Score under 9 within 72 hours of cardiac arrest. Interventions: All patients underwent multimodal neuromonitoring which included: (i) PbtO2, (ii) intracranial pressure; (iii) jugular venous continuous oximetry (SjvO2); (iv) regional saturation of oxygen (rSO2) using near-infrared spectroscopy, and (iv) PRx based determination of MAPOPT, lower and upper limit of autoregulation. We additionally collected MAP, end tidal carbon dioxide (ETCO2) and temperature. All data were captured at 300 Hz using ICM+® brain monitoring software. Measurements and Main Results: Ten patients (7 males) were included with a median age 47 (range 20-71) and ROSC 22 minutes (12-36). The median duration of monitoring was 47 hours (15-88) and median duration from cardiac arrest to inclusion was 15 hours (6-44). The mean PbtO2 was 23 mmHg (SD 8) and the mean percentage of time with a PbtO2 below 20 mmHg was 38% (6-100). The mean PRx was 0.23 (0.27) and the percentage of time with a PRx greater than 0.3 was 50% (12-91). The mean MAPOPT, lower and upper of autoregulation were 89 mmHg (11), 82mmHg (8) and 96 mmHg (9), respectively. There was marked betweenpatient variability in the relationship between MAP and indices of brain oxygenation. As the patients' actual MAP approached MAPOPT, PbtO2 increased (p<0.001). This positive relationship did not persist when the actual MAP was above MAPOPT. Conclusions: Episodes of brain hypoxia in HIBI are frequent and perfusion within proximity of MAPOPT is associated with increased PbtO2. PRx can yield MAPOPT, lower and upper limit of autoregulation in patients following cardiac arrest.

Symptomatic deep CMs can be resected with acceptable morbidity and outcomes. Good preoperative modified Rankin Score and single hemorrhage are predictors of good long-term outcome.

Objectives: We sought to characterize 1) the difference in the diffusion gradient of cellular oxygen delivery and 2) the presence of diffusion limitation physiology in hypoxic-ischemic brain injury patients with brain hypoxia, as defined by parenchymal brain tissue oxygen tension less than 20 mm Hg versus normoxia (brain tissue oxygen tension > 20 mm Hg). Design: Post hoc subanalysis of a prospective study in hypoxic-ischemic brain injury patients dichotomized into those with brain hypoxia versus normoxia. Setting: Quaternary ICU. Patients: Fourteen adult hypoxic-ischemic brain injury patients after cardiac arrest. Interventions: Patients underwent monitoring with brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and jugular venous bulb oxygen saturation. Data were recorded in real time at 300Hz into the ICM+ monitoring software (Cambridge University Enterprises, Cambridge, United Kingdom). Simultaneous arterial and jugular venous bulb blood gas samples were recorded prospectively. Measurements and Main Results: Both the normoxia and hypoxia groups consisted of seven patients. In the normoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (sd, 9), 45 mm Hg (sd, 9), and 80 mm Hg (sd, 7), respectively. In the hypoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen to brain tissue oxygen tension gradient, and cerebral perfusion pressure were 14 mm Hg (sd, 4), 53 mm Hg (sd, 8), and 72 mm Hg (sd, 6), respectively. There were significant differences in the jugular venous bulb oxygen tension–brain oxygen tension gradient (16 mm Hg [sd, 6] vs 39 mm Hg sd, 11]; p < 0.001) and in the relationship of jugular venous bulb oxygen tension–brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing normoxia to hypoxia. Each 1 mm Hg increase in cerebral perfusion pressure led to a decrease in the jugular venous bulb oxygen tension–brain oxygen tension gradient by 0.36 mm Hg (95% CI, –0.54 to 0.18; p < 0.001) in the normoxia group, but no such relation was demonstrable in the hypoxia group. Conclusions: In hypoxic-ischemic brain injury patients with brain hypoxia, there is an elevation in the jugular venous bulb oxygen tension–brain oxygen tension gradient, which is not modulated by changes in cerebral perfusion pressure.