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Department of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, CanadaCentre for Heart, Lung, & Vascular Health, School of Health and Exercise Sciences, University of British Columbia – Okanagan, Kelowna, BC, Canada
Department of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, CanadaDivision of Critical Care Medicine, Department of Medicine, University of British Columbia, Vancouver, BC, Canada
Lack of agreement between optimal mean arterial pressure determination using pressure reactivity index versus cerebral oximetry index in hypoxic ischemic brain injury after cardiac arrest.
Significant work has been undertaken using the pressure reactivity index (PRx) to identify patient-specific perfusion thresholds (optimal mean arterial pressure, MAPOPT). Our research group demonstrated feasibility of MAPOPT determination in hypoxic ischemic brain injury (HIBI) patients using PRx and more importantly, established a relationship between perfusion within proximity to MAPOPT and improved brain tissue oxygenation (PbtO2).
Therefore, our study used PRx derived MAPOPT as the gold standard to which non-invasive methodologies were compared, specifically near infrared spectroscopy (NIRS) based cerebral oximetry index (COx).
Lack of agreement between optimal mean arterial pressure determination using pressure reactivity index versus cerebral oximetry index in hypoxic ischemic brain injury after cardiac arrest.
Lack of agreement between optimal mean arterial pressure determination using pressure reactivity index versus cerebral oximetry index in hypoxic ischemic brain injury after cardiac arrest.
For physiologic validity, COx requires the regional saturation of oxygen (rSO2) from NIRS to accurately reflect cerebral blood flow (CBF) or brain oxygenation.
The accuracy of rSO2 as a surrogate of CBF or brain oxygenation is predicated upon normal oxygen uptake from the cerebral microvasculature into the brain parenchyma. However, a proportion of HIBI patients exhibit an inability to offload oxygen from the cerebral microvasculature into the parenchyma, termed diffusion limitation.
In this setting, the ratio of oxygenated vs deoxygenated hemoglobin and the resultant rSO2, would be elevated independent of CBF and not reflect the true degree of brain hypoxia or CBF. Indeed, we demonstrate no relationship between PbtO2 and rSO2 (Fig. 1A) further adding credence to the inability of rSO2 to reflect brain oxygenation.
Fig. 1A. Depicted is a linear regression analysis between PbtO2 (y – axis) and rSO2 (x – axis). The light greylines represent summary lines for each individual patient and the dark line represents the overall linear regression analysis across the entire cohort. Fig. 1B. An individual patient example of neuromonitoring physiologic variables (y – axis) over time (5 minute intervals on x – axis) in the post-cardiac arrest patient. The top panel reveals cerebral perfusion pressure (CPP, mmHg) showing a precipitous drop from ∼ 85 mmHg to 65 mmHg. The nadir of the CPP decrease is associated with a concomitant decrease in the brain tissue oxygenation (PbtO2, mmHg) in the second panel. The bottom 2 panels demonstrate stagnant values of right and left regional oxygen saturation (rSO2, %) in the setting of the decrease in CPP and PbtO2.
further highlighting the discordance between rSO2 and cerebrovascular physiology. We have shown that while PbtO2 jugular venous bulb oxygen saturation are correlated with MAP, rSO2 is not, in HIBI.
These results are concordant with the COMACARE study, a randomized control trial of high MAP (80-100 mmHg) vs. normal-low MAP (65-75 mmHg), which did not demonstrate significant differences in rSO2 between study groups.
Lack of agreement between optimal mean arterial pressure determination using pressure reactivity index versus cerebral oximetry index in hypoxic ischemic brain injury after cardiac arrest.
On an individual patient level, we demonstrate a precipitous decrease in the cerebral perfusion pressure (CPP) with a concomitant decrease in PbtO2 but stable bilateral rSO2 values, thereby revealing rSO2 does not seem to reflect brain oxygenation nor does it correlate with CPP, a primary determinant of CBF (Fig. 1B).
Collectively, our results with the known limitations of NIRS suggest significant more work is required to validate NIRS as a potential monitor of CBF, brain oxygenation or, autoregulation in HIBI. The allure of non-invasive and generalizable monitoring must be tempered with consideration of the accuracy of the data that is produced and its reflection of true cerebral physiology in health and disease. We thank Drs. Skrifvars and Aneman for their thoughtful and insightful review of our manuscript and hope to work together to reconcile the utility of NIRS as a monitoring tool in HIBI.
Funding
Dr. Sekhon is supported by the Vancouver Coastal Health Research Institute Clinician Scientist Award. Dr. Griesdale is funded by the Michael Smith Foundation for Health Research Health Professional Award.
Conflicts of interest
None.
Acknowledgement
This work was funded by the Canadian Institute for Health Research and Heart and Stroke Foundation of Canada.
References
Hoiland R.L.
Sekhon M.S.
Cardim D.
et al.
Lack of agreement between optimal mean arterial pressure determination using pressure reactivity index versus cerebral oximetry index in hypoxic ischemic brain injury after cardiac arrest.
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