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. 2016 May 24;86(21):1950-6.
doi: 10.1212/WNL.0000000000002696. Epub 2016 Apr 22.

Pathophysiologic differences in cerebral autoregulation after subarachnoid hemorrhage

Gabriela A Santos  1 , Nils Petersen  1 , Amir A Zamani  1 , Rose Du  1 , Sarah LaRose  1 , Andrew Monk  1 , Farzaneh A Sorond  1 , Can Ozan Tan  2
Affiliations

Pathophysiologic differences in cerebral autoregulation after subarachnoid hemorrhage

Gabriela A Santos et al. Neurology. .

Abstract

Objective: To understand the physiologic basis of impaired cerebral autoregulation in subarachnoid hemorrhage (SAH) and its relationship to neurologic outcomes.

Methods: The cohort included 121 patients with nontraumatic SAH admitted to a neurointensive critical care unit from March 2010 to May 2015. Vasospasm was ascertained from digital subtraction angiography and delayed cerebral ischemia (DCI) was defined as new cerebral infarction on high-resolution CT. Cerebral blood flow and beat-by-beat pressure were recorded daily on days 2-4 after admission. Autoregulatory capacity was quantified from pressure flow relation via projection pursuit regression. The main outcome was early alterations in autoregulatory mechanisms as they relate to vasospasm and DCI.

Results: Forty-three patients developed only vasospasm, 9 only DCI, and 14 both. Autoregulatory capacity correctly predicted DCI in 86% of training cohort patients, generalizing to 80% of the patients who were not included in the original model. Patients who developed DCI had a distinct autoregulatory profile compared to patients who did not develop secondary complications or those who developed only vasospasm. The rate of decrease in flow was significantly steeper in response to transient reductions in pressure. The rate of increase in flow was markedly lower, suggesting a diminished ability to increase flow despite transient increases in pressure.

Conclusions: The extent and nature of impairment in autoregulation accurately predicts neurologic complications on an individual patient level, and suggests potentially differential impairments in underlying physiologic mechanisms. A better understanding of these can lead to targeted interventions to mitigate neurologic morbidity.

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Figures

Figure 1
Figure 1. Five hemodynamic markers of cerebral autoregulatory capacity
Falling slope (rate of blood flow decrease in response to a decrease in pressure), lower and upper limits of autoregulation (within which pressure fluctuations are counter-regulated), autoregulatory effectiveness (slope within autoregulatory range; lower gain indicates more effective autoregulation), and rising slope (rate of increase in flow in response to increases in pressure). Data from reference 22.
Figure 2
Figure 2. Pressure–flow relation in patients with subarachnoid hemorrhage
DCI = delayed cerebral ischemia.
Figure 3
Figure 3. Secondary complications, markers of cerebral autoregulatory capacity, and associated physiologic mechanisms
Contributions of cerebral autoregulatory capacity to secondary complications (A) and contribution of neurogenic and myogenic mechanisms to each marker (B, data from reference 23). DCI = delayed cerebral ischemia.
See this image and copyright information in PMC

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