BACKGROUND: Critical closing pressure (CCP) denotes a threshold of arterial blood pressure (ABP) below which brain vessels collapse and cerebral blood flow ceases. Theoretically, CCP is the sum of intracranial pressure (ICP) and arterial wall tension (WT). The aim of this study is to describe the behavior of CCP and WT during spontaneous increases of ICP, termed plateau waves, in order to quantify ischemic risk. METHODS: To calculate CCP, we used a recently introduced multi-parameter method (CCPm) which is based on the modulus of cerebrovascular impedance. CCP is derived from cerebral perfusion pressure, ABP, transcranial Doppler estimators of cerebrovascular resistance and compliance, and heart rate. Arterial WT was estimated as CCPm-ICP. The clinical data included recordings of ABP, ICP, and transcranial Doppler-based blood flow velocity from 38 events of ICP plateau waves, recorded in 20 patients after head injury. RESULTS: Overall, CCPm increased significantly from 51.89 ± 8.76 mmHg at baseline ICP to 63.31 ± 10.83 mmHg at the top of the plateau waves (mean ± SD; p < 0.001). Cerebral arterial WT decreased significantly during plateau waves by 34.3% (p < 0.001), confirming their vasodilatatory origin. CCPm did not exhibit the non-physiologic negative values that have been seen with traditional methods for calculation, therefore rendered a more plausible estimation of CCP. CONCLUSIONS: Rising CCP during plateau waves increases the probability of cerebral vascular collapse and zero flow when the difference: ABP-CCP (the "collapsing margin") becomes zero or negative.
BACKGROUND: Critical closing pressure (CCP) denotes a threshold of arterial blood pressure (ABP) below which brain vessels collapse and cerebral blood flow ceases. Theoretically, CCP is the sum of intracranial pressure (ICP) and arterial wall tension (WT). The aim of this study is to describe the behavior of CCP and WT during spontaneous increases of ICP, termed plateau waves, in order to quantify ischemic risk. METHODS: To calculate CCP, we used a recently introduced multi-parameter method (CCPm) which is based on the modulus of cerebrovascular impedance. CCP is derived from cerebral perfusion pressure, ABP, transcranial Doppler estimators of cerebrovascular resistance and compliance, and heart rate. Arterial WT was estimated as CCPm-ICP. The clinical data included recordings of ABP, ICP, and transcranial Doppler-based blood flow velocity from 38 events of ICP plateau waves, recorded in 20 patients after head injury. RESULTS: Overall, CCPm increased significantly from 51.89 ± 8.76 mmHg at baseline ICP to 63.31 ± 10.83 mmHg at the top of the plateau waves (mean ± SD; p < 0.001). Cerebral arterial WT decreased significantly during plateau waves by 34.3% (p < 0.001), confirming their vasodilatatory origin. CCPm did not exhibit the non-physiologic negative values that have been seen with traditional methods for calculation, therefore rendered a more plausible estimation of CCP. CONCLUSIONS: Rising CCP during plateau waves increases the probability of cerebral vascular collapse and zero flow when the difference: ABP-CCP (the "collapsing margin") becomes zero or negative.
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