Cerebrovascular Pressure Transmission Research Articles

Model-derived assessment of cerebrovascular resistance and cerebral blood flow following traumatic brain injury.

The published guidelines point out the need for the development of methods that individualize patient cerebral perfusion management and minimize secondary ischemic complications associated with traumatic brain injury. A laboratory method has been developed to determine model-derived assessments of cerebrovascular resistance (mCVR) and cerebral blood flow (mCBF) from cerebrovascular pressure transmission, and the dynamic relationship between arterial blood pressure (ABP) and intracranial pressure (ICP). The aim of this two-fold study is to (1) evaluate relative changes in the model-derived parameters of mCVR and mCBF with the corresponding changes in the pial arteriolar vascular parameters of pial arteriolar resistance (PAR) and relative pial arteriolar blood flow (rPABF); and (2) examine the efficacy of the proposed modeling methodology for continuous assessment of the state of cerebrovascular regulation by evaluating relative changes in the model-derived parameters of CBF and cerebrovascular resistance in relation to changes of cerebral perfusion pressure prior to and following fluid percussion brain injury. Changes of ABP, ICP, PAR, relative arteriolar blood flow (rPABF) and the corresponding model-derived parameters of mCBF and mCVR induced by acute hypertensive challenge were evaluated before and following fluid percussion injury in piglets equipped with cranial windows. Before fluid percussion, hypertensive challenge resulted in a significant increase of PAR and mCVR, whereas both rPABF and mCBF remained constant. Following fluid percussion, hypertensive challenge resulted in a significant decrease of PAR and mCVR and consistent with impaired cerebrovascular regulation. Hypertensive challenge significantly increased both rPABF and mCBF, which approximately doubled with increased CPP with correlation values of r = 0.96 (P < 0.01) and r = 0.97 (P <or= 0.01), respectively. The assessment of model-derived cerebrovascular resistance and CBF with changes of CPP provides a means to monitor continuously the state of cerebrovascular regulation.

A New Index Derived from the Cerebrovascular Pressure Transmission and Correlated with Consciousness Recovery in Severely Head-Injured Intensive Care Patients

In patients with serious head trauma, a moderate (20-25 mm Hg) mean level of intracranial pressure (ICP) may fail to distinguish patients with a real deteriorated intracranial status from those who are stable or improving. Because of these limitations, we analyzed the ICP curve in search of other relevant information regarding cerebrovascular pressure transmission. We looked for parameters with physiological meaning extracted from spectral analysis of cerebrovascular pressure transmission and correlated with consciousness recovery in patients with severe head injuries. A prospective cohort study was conducted in an intensive care unit of the University Hospital, Montpellier, France, from December 2003 to December 2005. Thirty consecutive patients admitted for severe head trauma were subjected to sedatives, mechanical ventilation, and intraparenchymatous recording of ICP and were evaluated with Glasgow Outcome Scale score. Simultaneous 60-s recordings of ICP and arterial blood pressure (BP) signals, beginning as soon as possible after head trauma, were repeated until death or clinical stabilization, every 15 min, with physicians blinded to the patients' data. Spectra of ICP and BP waveforms were computed with Fourier transform. Amplitudes of cardiac and respiratory harmonics were analyzed. Cardiac (or respiratory) gain was defined as the ratio of amplitudes of cardiac (or respiratory) harmonic of ICP to BP signals and referred to as Gc and Gr, respectively. Twenty of the 30 enrolled patients recovered consciousness (Glasgow Outcome Scale score = 3, 4, or 5). Gr/Gc averaged over the whole recording period performed better in discriminating consciousness recovery (area under receiver operating characteristic [ROC] curve: 0.98; 95% confidence interval [CI]: 0.91-1) than ICP (0.76; 95% CI: 0.54-0.97), cerebral perfusion pressure (0.75; 95% CI: 0.53-0.97) and Gc (0.77; 95% CI: 0.57-0.99) (P < 0.001 for each comparison). When considering the recording period 30 h posttrauma (hpt), 162 hpt, a value of Gr/Gc > or =4 was always associated with consciousness recovery, and the relative risk was equal to 9 (95% CI: 1.42-57.12). Gr/Gc, which characterizes the cerebrovascular transmission, better discriminates bad evolution than high values of ICP or low values of cerebral perfusion pressure in patients with severe head trauma. A reduction in Gr/Gc ratio might be an early alarm signaling worsening intracranial hemodynamic conditions.

Assessment of cerebrovascular resistance with a model of cerebrovascular pressure transmission

A method to assess continuous changes of cerebrovascular resistance based on a biomechanical model of cerebrovascular pressure transmission is developed. Such a method provides an end-point measure to assess new and/or existing management strategies during intensive-care management of patients with brain injury. Changes of both pial arteriolar resistance and cerebrovascular resistance derived by a physiologically based biomechanical model of cerebrovascular pressure transmission, the dynamic relationship between arterial blood pressure (ABP) and intracranial pressure (ICP), were compared to test the validity of the modeling procedure. Pressor challenge was administered to normoxic ( N = 5) and hypoxic ( N = 5) piglets equipped with closed cranial windows. Pial arteriolar diameters were used to compute arteriolar resistance. Percent change of pial arteriolar resistance (%ΔPAR) and percent change of model-derived cerebrovascular resistance (%ΔsCVR) in response to pressor challenge were computed. During intact cerebrovascular regulation and during hypoxia-induced impairment of cerebrovascular regulation, changes in pial arteriolar resistance were accurately predicted by the proposed modeling method designed to assess changes of cerebrovascular resistance.

Influence of hypercapnic vasodilation on cerebrovascular autoregulation and pial arteriolar bed resistance in piglets

Changes in both pial arteriolar resistance (PAR) and simulated arterial-arteriolar bed resistance (SimR) of a physiologically based biomechanical model of cerebrovascular pressure transmission, the dynamic relationship between arterial blood pressure and intracranial pressure, are used to test the hypothesis that hypercapnia disrupts autoregulatory reactivity. To evaluate pressure reactivity, vasopressin-induced acute hypertension was administered to normocapnic and hypercapnic (N = 12) piglets equipped with closed cranial windows. Pial arteriolar diameters were used to compute arteriolar resistance. Percent change of PAR (%DeltaPAR) and percent change of SimR (%DeltaSimR) in response to vasopressin-induced acute hypertension were computed and compared. Hypercapnia decreased cerebrovascular resistance. Indicative of active autoregulatory reactivity, vasopressin-induced hypertensive challenge resulted in an increase of both %DeltaPAR and %DeltaSimR for all normocapnic piglets. The hypercapnic piglets formed two statistically distinct populations. One-half of the hypercapnic piglets demonstrated a measured decrease of both %DeltaPAR and %DeltaSimR to pressure challenge, indicative of being pressure passive, whereas the other one-half demonstrated an increase in these percentages, indicative of active autoregulation. No other differences in measured variables were detectable between regulating and pressure-passive piglets. Changes in resistance calculated from using the model mirrored those calculated from arteriolar diameter measurements. In conclusion, vasodilation induced by hypercapnia has the potential to disrupt autoregulatory reactivity. Our physiologically based biomechanical model of cerebrovascular pressure transmission accurately estimates the changes in arteriolar resistance during conditions of active and passive cerebrovascular reactivity.

Mode Changes of Cerebrovascular Pressure Transmission Induced by Cerebral Vasodilation

Changes in the modes of cerebrovascular pressure transmission during cerebral vasodilation induced by hypercapnic challenge were examined as a means for developing the basis for a bedside method to evaluate regulation of cerebral blood flow. Recordings of arterial blood pressure (ABP) and intracranial pressure (ICP) obtained from a piglet preparation equipped with a cranial window were used to determine serial changes of the highest modal frequency (HMF) and dampening factor (DF) of a numerical system identification model of cerebrovascular pressure transmission. Resistance and compliance elements of a Windkessel model of ICP dynamics selected to provide the mathematical structure for the system identification modeling approach were also manipulated to obtain a match with HMF, DF, and the experimental and simulated recordings of ICP. During hypercapnic challenge, significant increases of ICP, pial arterial diameter (PAD) and partial pressure of arterial blood carbon dioxide increases, and a decrease of arterial pH were observed. Vasodilation changed the modes of the system identification model of cerebrovascular pressure transmission from a dominantly over-damped process to an under-damped one with a significant increase in HMF and decrease in DF. Simulations of the Windkessel circuit model required a decrease in the relative resistance and an increase in relative compliance of the arterial-arteriolar vascular bed consistent with the observed increases in PAD induced by vasodilation. Evaluation of changes in the modes of cerebrovascular pressure transmission may provide means of assessing the state of cerebrovascular vasodilation and autoregulation of cerebral blood flow in the clinical setting.

Cerebrovascular pressure transmission: Changes in highest modal frequency induced by vasodilation

Cerebrovascular pressure transmission: Changes in highest modal frequency induced by vasodilation

Evaluation of the mathematical assumption underlying numerical identification modeling of cerebrovascular pressure transmission

Evaluation of the mathematical assumption underlying numerical identification modeling of cerebrovascular pressure transmission

Assessment of cerebrovascular autoregulation: changes of highest modal frequency of cerebrovascular pressure transmission with cerebral perfusion pressure.

Development of a method to continuously assess cerebrovascular autoregulation of patients with traumatic brain injury would facilitate therapeutic intervention and thus reduce secondary complications. Changes in arterial blood pressure (ABP), intracranial pressure (ICP), cerebral blood flow velocity (CBFV), and pial arteriolar diameter (PAD) induced by acute pressor challenge (norepinephrine; 1 microg/[kg. min]) were evaluated in both uninjured and fluid percussion injured piglets equipped with cranial windows. The linear correlation coefficient and corresponding slope of the regression line of the relationship between highest modal frequency (HMF) of cerebrovascular pressure transmission of ABP to ICP and cerebral perfusion pressure (CPP) were determined for each challenge. For all uninjured piglets, pressor challenge resulted in an inverse relationship between HMF and CPP characterized by significant negative correlation values and negative corresponding regression line slopes with respective group mean values (+/-SD) of -0.50 (+/-0.14) and -0.6 (+/-0.44) Hz/mm Hg, respectively. Consistent with functional autoregulation of the uninjured preparations, pressor challenge resulted in a decrease of PAD, and CBFV remained relatively constant. For all injured piglets, pressor challenge resulted in direct relationship between HMF and CPP, characterized by positive correlation values and corresponding regression line slopes with group mean values of 0.48 (+/-0.21) and 1.13 (+/-2.08) Hz/mm Hg, respectively. Consistent with impaired autoregulation, PAD and CBFV increased during pressor challenge after brain injury. Evaluation of changes of the HMF of cerebrovascular pressure transmission with respect to CPP changes permits continuous monitoring of cerebral autoregulation.

Cerebrovascular pressure transmission analysis as a guide to the pathophysiology of raised intracranial pressure.

1. Raised intracranial pressure (ICP) is a major factor associated with morbidity and mortality in patients with severe head injury. Identifying the mechanisms responsible for raised ICP may be difficult and, as a result, treatment prescribed may be non-specific and often ineffective. 2. Research aimed at obtaining more information from measurement of ICP was initially focused on measurements of compliance. This was achieved by introducing fluid volume into the craniospinal compartment and measuring the response. Although shown to be clinically useful, associated technical problems have precluded the routine use of these measurements. 3. Cerebrovascular pressure transmission (CVPT) analysis has been suggested as an alternative method of deriving more information from the ICP wave-form. Pressure transmission across the cerebrovascular bed is assessed by a systems analysis approach whereby blood pressure and ICP wave-form pairs are resolved by fast Fourier transform analysis into component harmonic frequencies, each with a specific amplitude and phase. These are expressed as a ratio or 'transfer function' for each harmonic peak. 4. Laboratory models have identified specific CVPT patterns associated with various causes of raised ICP. These studies have been extended to clinical practice and have been used to define patterns of CVPT in head-injured patients, which may be used to identify mechanisms responsible for raised ICP, thus assisting in directing treatment strategy. Clinical usefulness of this technique in patient management is currently under investigation.

An experimental study of cerebrovascular resistance, pressure transmission, and craniospinal compliance.

To successfully match the treatment to the cause for raised intracranial pressure (ICP) after a severe head injury, it is important to know the underlying mechanism at a given moment for the raised pressure. In particular, it is important to distinguish between active cerebral vasodilation, indicating functional autoregulation, and a passive vascular dilation as the cause for raised ICP. An experimental study was performed in feline models of diffusely raised ICP (n = 6), of active arterial vasodilation caused by arterial hypercarbia (n = 6), and of passive arterial dilation caused by pharmacologically induced arterial hypertension (n = 6) to determine if wave form analysis of ICP can distinguish active from passive arteriolar vasodilation. Pulsatile pressure transmission from the blood pressure pulse to the ICP pulse (cerebrovascular pressure transmission [CVPT]), cerebrovascular resistance, and craniospinal compliance were measured simultaneously at each level of raised ICP, arterial hypercarbia, and arterial hypertension. Arterial hypercarbia, caused by both 5 and 10% inspired CO2 increased low-frequency CVPT, which was followed by an increasingly negative phase shift between the blood pressure and ICP wave form (P < 0.05). Diffusely raised ICP caused by intraventricular infusion of mock cerebrospinal fluid caused increased low-frequency CVPT (P < 0.01) but resulted in no overall change in phase shift, although the sign of the phase shift remained negative. After arterial hypertension, caused by the infusion of angiotensin II, where there was loss of myogenic tone, an increased low-frequency CVPT was accompanied by a positive phase shift (P < 0.01). These data demonstrate it may be possible to distinguish active arteriolar vasodilation from a passive loss of autoregulatory vascular tone through simultaneous measurement of the low-frequency CVPT and phase shift. Analysis of the ICP wave form provides information relevant to the management of raised ICP.

Systems analysis of cerebrovascular pressure transmission: an observational study in head-injured patients

In an observational study in head-injured patients, cerebrovascular pressure transmission was investigated using a systems analysis approach whereby the blood pressure (BP) waveform was used as a measure of an input stimulus to the cerebrovascular bed (CVB) and the intracranial pressure (ICP) waveform as the response to that stimulus. The transfer function is a measure of how much pressure is transmitted through the CVB at a given frequency and is calculated using Fourier analysis of the pressure waveforms. The transfer function allows quantification of the pressure transmission performance of the CVB, thus providing a basis for comparison between normal and abnormal function. Fifteen hundred samples of ICP and BP waveforms were collected from 30 head-injured patients via microcomputer. Off-line spectral analysis of the waveform database revealed four main classes of transfer function: those with an overall flat transfer function (curve type 1); those with an elevated low-frequency response (curve type 2); those with an elevated high-frequency response (curve type 3); and those exhibiting both an elevated low- and high-frequency response (curve type 4). Curve types 2 and 4 were most often associated with raised ICP (greater than 20 mm Hg), whereas curve types 1 and 3 were most often affiliated with ICP less than 15 mm Hg. Studies of this type may provide insight into the pathophysiology of the CVB and ultimately aid in the prediction and treatment of raised ICP.