Cerebrovascular autoregulation (CA) is an important hemodynamic mechanism that protects the brain against inappropriate fluctuations in cerebral blood flow in the face of changing cerebral perfusion pressure.
While most systems of the body show some degree of autoregulation, the brain is very sensitive to over- and underperfusion.
Brain perfusion is essential for life since the brain has a high metabolic demand. By means of cerebrovascular autoregulation the body is able to deliver sufficient blood containing oxygen and nutrients to the brain tissue for this metabolic need, and remove CO2 and other waste products.
However, due to the important influences of arterial carbon dioxide levels, cerebral metabolic rate, neural activation, activity of the sympathetic nervous system, posture, as well as other physiological variables, cerebral autoregulation is often interpreted as encompassing the wider field of cerebral blood flow regulation. This field includes areas such as CO2 reactivity, neurovascular coupling and other aspects of cerebral haemodynamics.
This regulation of cerebral blood flow is achieved primarily by small arteries, arterioles, which either dilate or contract under the influence of multiple complex physiological control systems.
Impairment of these systems may occur e.g. following stroke, trauma or anaesthesia, in premature babies and has been implicated in the development of subsequent brain injury.
Cerebral autoregulation disturbance after traumatic brain injury is associated with worse outcome.
Autonomic impairment after acute traumatic brain injury has been associated independently with both increased morbidity and mortality. Links between autonomic impairment and increased intracranial pressure or impaired cerebral autoregulation have been described as well. However, relationships between autonomic impairment, intracranial pressure, impaired cerebral autoregulation, and outcome remain poorly explored.
The non-invasive measurement of relevant physiological signals like cerebral blood flow, intracranial pressure, blood pressure, CO2 levels, cerebral oxygen consumption, etc. is challenging. Even more so, the subsequent assessment of the control systems. Much remains unknown about the physiology of blood flow control and the best clinical interventions to optimize patient outcome.
Pressure reactivity is a fundamental component of cerebral autoregulation that can be estimated using the pressure reactivity index, a correlation between slow arterial blood pressure, and intracranial pressure fluctuations.
Slow oscillations of cerebral hemodynamics (0.05-0.003 Hz) are visible in Multimodal neuromonitoring and may be analyzed to provide novel, surrogate measures of autoregulation. Near-infrared spectroscopy (NIRS) is an optical neuromonitoring technique, which shows promise for widespread clinical applicability because it is noninvasive and easily delivered across a wide range of clinical scenarios.
Twenty-seven sedated, ventilated, brain-injured patients were included in this observational study. Intracranial pressure, transcranial Doppler-derived flow velocity in the middle cerebral artery, and ipsilateral cerebral NIRS variables were continuously monitored. Signals were compared using wavelet measures of phase and coherence to examine the spectral features involved in reactivity index calculations. Established indices of autoregulatory reserve such as the pressure reactivity index (PRx) and mean velocity index (Mx) and the NIRS indices such as total hemoglobin reactivity index (THx) and tissue oxygen reactivity index (TOx) were compared using correlation and Bland-Altman analysis.
NIRS indices correlated significantly between PRx and THx (rs = 0.63, P < 0.001), PRx and TOx (r = 0.40, P = 0.04), and Mx and TOx (r = 0.61, P = 0.004) but not between Mx and THx (rs = 0.26, P = 0.28) and demonstrated wide limits between these variables: PRx and THx (bias, -0.06; 95% limits, -0.44 to 0.32) and Mx and TOx (bias, +0.15; 95% limits, -0.34 to 0.64). Analysis of slow-wave activity throughout the intracranial pressure, transcranial Doppler, and NIRS recordings revealed statistically significant interrelationships, which varied dynamically and were nonsignificant at frequencies <0.008 Hz.
Although slow-wave activity in intracranial pressure, transcranial Doppler, and NIRS is significantly similar, it varies dynamically in both time and frequency, and this manifests as incomplete agreement between reactivity indices. Analysis informed by a priori knowledge of physiology underpinning NIRS variables combined with sophisticated analysis techniques has the potential to deliver noninvasive surrogate measures of autoregulation, guiding therapy 1).
Early deterioration of CA significantly correlates with unfavorable clinical outcome and severity of angiographic vasospasm. Dynamic CA measurements might represent an important tool in stratifying therapy guidelines in patients after SAH 2).
Unfavorable outcomes for Traumatic Brain Injury (TBI) patients are more significantly associated with the duration of the single longest CA impairment episode at a high pressure reactivity index [PRx(t)] value, rather than with averaged PRx(t) values or the average time of all CA impairment episodes 3).