Using non-invasive techniques to explore personalized cerebral perfusion targets in critically ill patients
CCCF ePoster library. Lee K. 11/07/18; 234657; 87
Dr. Kevin Lee
Dr. Kevin Lee
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Cerebral autoregulation (CA) is a vascular reflex mechanism that responds to changes in systemic blood pressure in order to maintain constant cerebral blood flow. CA dysfunction during cardiac surgery, intracerebral hemorrhage and traumatic brain injury is associated with negative outcomes (1-3). Less is understood about CA function in the setting of critical illness. We recently showed that cerebral oxygenation during critical illness was associated with delirium, which may be related to CA dysfunction (4). We analyzed CA function in critically ill patients during the first 24-72 hrs in the ICU using near-infrared spectroscopy (NIRS)-based cerebral oximetry (5-9). We developed a novel approach to derive mean arterial pressure (MAP) targets that may help optimize cerebral perfusion in individual patients.


To identify putative MAP targets in critically ill patients using NIRS-based cerebral oximetry.


MAP and rSO2 were recorded simultaneously for up to the first 72 hours in ICU (n = 40 patients) by arterial catheter and NIRS, respectively. The cerebral oximetry index (COx) was computed as the moving Spearman correlation between MAP and rSO2 (Figure 1, 2). Positive COx values were taken to reflect CA dysfunction while near-zero or negative COx values reflect intact CA (5-7). We asked whether certain MAP values were associated with intact vs dysfunctional CA, and so binned the MAP values by COx (in bins of 0.05, from -1 to +1). This approach builds on previous research to identify optimal cerebral perfusion targets (5-11).


COx signals were variable between patients, with some patients exhibiting greater periods of CA dysfunction than others. In a separate parallel analysis, we found that CA dysfunction was associated with the subsequent development of delirium (data not shown). After sorting MAP values into their associated COx bins, the resulting plots adopted four general patterns: negative slope (n = 18/40 patients, Figure 3A), positive slope (2/40, Figure 3B), flat (13/40, Figure 3C) and complex (7/40, Figure 3D). Plots with either positive or negative slopes clearly showed certain MAP ‘danger’ zones that were associated with CA dysfunction (high COx values), as well as relative ‘safe’ zones (Figure 3A-B). Danger zones and safe zones were separated by 8 ± 4 mmHg on average, with average MAPs of 76 ± 8 mmHg and 82 ± 10 mmHg, respectively. MAP targets were not readily discernable in plots with flat or complex morphologies from the other half of our study subjects (Figure 3C-D). The basis for the different plot morphologies is presently unclear, but may be related to the patients’ position on the cerebral autoregulation curve.


We outlined an approach for identifying patient-specific MAP targets using NIRS-based cerebral oximetry. This strategy may help preserve cerebral blood flow and reduce the risk of negative neurocognitive outcomes. Our data demonstrate how patient-specific parameters can inform the identification of MAP targets on a case-by-case basis, and suggest that the classic MAP target of 65 mmHg during critical illness may need revisiting (12, 13). The ability to identify physiological targets in individual patients in real-time may allow precise personalized interventions that have the potential to improve outcomes for survivors of critical illness.


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