Asymmetry of critical closing pressure following head injury

OBJECTIVE: Critical closing pressure (CCP) is the arterial pressure below which the vessels collapse. Hypothetically it is the sum of intracranial pressure (ICP) and vessel wall tension in the cerebral circulation. This study investigated transhemispherical asymmetry of CCP by studying its correlation with radiological findings on computed tomography (CT) scans in head injury patients. METHOD: ICP, arterial blood pressure, and middle cerebral artery blood flow velocity were recorded daily in 119 ventilated patients. Waveforms were processed to calculate CCP. CT scans were analysed according to a system based on the Marshall classification. RESULTS: Left-right differences in CCP correlated with midline shift on the CT scan (r = 0.48; p<0.02). Asymmetry of CCP also corresponded with the side of the head lesion (p<0.007) and the side of the craniotomy where it was performed (p<0.006). Absolute CCP weakly correlated with brain swelling (r = -0.23; p<0.03) and arterial pressure (r = 0.21; p<0.02) but did not correlate with ICP. Cerebral perfusion pressure calculated as the difference between mean arterial pressure and CCP did not correlate with outcome, but "traditional" cerebral perfusion pressure (mean arterial pressure minus intracranial pressure) did. CONCLUSIONS: Critical closing pressure is disturbed by localised brain lesions. Its asymmetry corresponds to asymmetrical findings on CT scans. CCP seems to describe vascular resistance better than ICP.     

Association between intracranial, arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

OBJECTIVE: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation. METHODS: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1-14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording. RESULTS: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p 相似文献   

Association between intracranial,arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

Abstract

Objective: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation.

Methods: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1–14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording.

Results: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p ≤ 0.04, multiple regression analysis). Correlations between intracranial and arterial pulse pressure amplitudes were weakly related to PRx (Pearson's correlation coefficient: 0.16; p=0.01), but were not related to the indices of cerebral autoregulation Mx (Pearson's correlation coefficient: 0.07) and Sx (Pearson's correlation coefficient: 0.04).

Conclusions: In this cohort of pressure recordings, we found no evidence of a correlation between intracranial and arterial blood pressure amplitudes. The correlation appeared not to be related to the state of cerebral autoregulation, although a weak correlation was found with pressure reactivity index PRx.     

Critical Closing Pressure During Intracranial Pressure Plateau Waves

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.     

Impact of intracranial pressure and cerebral perfusion pressure on severe disability and mortality after head injury

Objective  To investigate the relationships between intracranial pressure (ICP), cerebral perfusion pressure (CPP), and outcome after traumatic brain injury. Material and Methods  A retrospective analysis of prospectively recorded data from 429 patients after head injury requiring intensive treatment on the Neuroscience Intensive Annex and the Neuro Critical Care Unit, Cambridge, UK. ICP, CPP, and arterial blood pressure (ABP) were continuously recorded. Mean values of pressures were compared to outcome assessed at 6 months after injury (using the Glasgow Outcome Scale). Results  The mortality rate was greater in those having mean ICP greater than 20 mmHg (17% below versus 47% above; p<0.00001). The mortality rate was dramatically increased for CPP below 55 mmHg (81% below versus 23% above; p<0.0001). For values of CPP greater than 95 mmHg, favorable outcome was less frequent (50% below versus 28% above; p<0.033). The rate of severe disability showed the tendency to increase with CPP (r=0.87; p=0.02), suggesting that a higher CPP does not help in achieving favorable outcomes. ICP was greater in those who died in comparison to those who survived (27±19 mmHg versus 16±6 mmHg; p<0.10–7), and CPP was lower (68±21 versus 76±10 mmHg; p<0.0002). There was no difference between mean ICP and CPP in good/moderate and severe disability outcome groups. Conclusion  High ICP is strongly associated with fatal outcome. Excessive CPP seems to reduce the probability of achieving a favorable outcome following head trauma.     

Critical closing pressure determined with a model of cerebrovascular impedance

Critical closing pressure (CCP) is the arterial blood pressure (ABP) at which brain vessels collapse and cerebral blood flow (CBF) ceases. Using the concept of impedance to CBF, CCP can be expressed with brain-monitoring parameters: cerebral perfusion pressure (CPP), ABP, blood flow velocity (FV), and heart rate. The novel multiparameter method (CCPm) was compared with traditional transcranial Doppler (TCD) calculations of CCP (CCP1). Digital recordings of ABP, intracranial pressure (ICP), and TCD-based FV from previously published studies of 29 New Zealand White rabbits were reanalyzed. Overall, CCP1 and CCPm showed correlation across wide ranges of ABP, ICP, and PaCO2 (R=0.93, P<0.001). Three physiological perturbations were studied: increase in ICP (n=29) causing both CCP1 and CCPm to increase (P<0.001 for both); reduction of ABP (n=10) resulting in decrease of CCP1 (P=0.006) and CCPm (P=0.002); and controlled increase of PaCO2 (n=8) to hypercapnic levels, which decreased CCP1 and CCPm, albeit insignificantly (P=0.123 and P=0.306 respectively), caused by a spontaneous significant increase in ABP (P=0.025). Multiparameter mathematical model of critical closing pressure explains the relationship of CCP on brain-monitoring variables, allowing the estimation of CCP during cases such as hypercapnia-induced hyperemia, where traditional calculations, like CCP1, often reach negative non-physiological values.     

A Continuous Correlation Between Intracranial Pressure and Cerebral Blood Flow Velocity Reflects Cerebral Autoregulation Impairment During Intracranial Pressure Plateau Waves

Background

In the healthy brain, small oscillations in intracranial pressure (ICP) occur synchronously with those in cerebral blood volume (CBV), cerebrovascular resistance, and consequently cerebral blood flow velocity (CBFV). Previous work has shown that the usual synchrony between ICP and CBFV is lost during intracranial hypertension. Moreover, a continuously computed measure of the ICP/CBFV association (Fix index) was a more sensitive predictor of outcome after traumatic brain injury (TBI) than a measure of autoregulation (Mx index). In the current study we computed Fix during ICP plateau waves, to observe its behavior during a defined period of cerebrovascular vasodilatation.

Methods

Twenty-nine recordings of arterial blood pressure (ABP), ICP, and CBFV taken during ICP plateau waves were obtained from the Addenbrooke’s hospital TBI database. Raw data was filtered prior to computing Mx and Fix according to previously published methods. Analyzed data was segmented into three phases (pre, peak, and post), and a median value of each parameter was stored for analysis.

Results

ICP increased from a median of 22–44 mmHg before falling to 19 mmHg. Both Mx and Fix responded to the increase in ICP, with Mx trending toward +1, while Fix trended toward ?1. Mx and Fix correlated significantly (Spearman’s R = ?0.89, p < 0.000001), however, Fix spanned a greater range than Mx. A plot of Mx and Fix against CPP showed a plateau (Mx) or trough (Fix) consistent with a zone of “optimal CPP”.

Conclusions

The Fix index can identify complete loss of cerebral autoregulation as the point at which the normally positive CBF/CBV correlation is reversed. Both CBF and CBV can be monitored noninvasively using near-infrared spectroscopy (NIRS), suggesting that a noninvasive method of monitoring autoregulation using only NIRS may be possible.     

A synopsis of brain pressures: which? when? are they all useful?

OBJECTIVE: In addition to intracranial pressure (ICP) and cerebral perfusion pressure (CPP), there are many more brain-related measures defined as 'pressures'. Cerebral intra-tissue pressure, critical closing pressure, 'optimal' CPP, non-invasive CPP (nCPP) and non-invasive ICP (nICP), interhemispherical pressure gradients are the modalities which currently attract more attention in the management of head injured patients. METHODS: This review summarizes the most important points related to the 'brain pressures' applied in clinical practice, and it is based both on the literature and the authors' own experience. RESULTS: While ICP and CPP monitoring remains the cornerstone of head injury management, derived pressures are gaining clinical significance. 'Optimization' of CPP provides a rational compromise between the 'Critical Closing Pressure-oriented protocol' and the 'Lund concept', and it allows individualized tailoring of cerebral hemodynamics. Non-invasive ICP and CPP are practical surrogates for invasive monitoring especially in the early stages of trauma management. CCP and pressure gradients are promising prognostication tools. DISCUSSION: Most of the derived brain pressures cannot be assessed at the bedside without a dedicated computer tool. Some practical and theoretical aspects about the measurement, signal analysis, estimation process, accuracy and interpretation need further researching and refinement.     

Preliminary experience of the estimation of cerebral perfusion pressure using transcranial Doppler ultrasonography

OBJECTIVE: The direct calculation of cerebral perfusion pressure (CPP) as the difference between mean arterial pressure and intracranial pressure (ICP) produces a number which does not always adequately describe conditions for brain perfusion. A non-invasive method of CPP measurement has previously been reported based on waveform analysis of blood flow velocity measured in the middle cerebral artery (MCA) by transcranial Doppler. This study describes the results of clinical tests of the prototype bilateral transcranial Doppler based apparatus for non-invasive CPP measurement (nCPP). METHODS: Twenty five consecutive, paralysed, sedated, and ventilated patients with head injury were studied. Intracranial pressure (ICP) and arterial blood pressure (ABP) were monitored continuously. The left and right MCAs were insonated daily (108 measurements) using a purpose built transcranial Doppler monitor (Neuro Q(TM), Deltex Ltd, Chichester, UK) with software capable of the non-invasive estimation of CPP. Time averaged values of mean and diastolic flow velocities (FVm, FVd) and ABP were calculated. nCPP was then computed as: ABPxFVd/FVm+14. RESULTS: The absolute difference between real CPP and nCPP (daily averages) was less than 10 mm Hg in 89% of measurements and less than 13 mm Hg in 92% of measurements. The 95% confidence range for predictors was no wider than +/-12 mm Hg (n=25) for the CPP, varying from 70 to 95 mm Hg. The absolute value of side to side differences in nCPP was significantly greater (p<0.05) when CT based evidence of brain swelling was present and was also positively correlated (p<0.05) with mean ICP. CONCLUSION: The device is of potential benefit for intermittent or continuous monitoring of brain perfusion pressure in situations where the direct measurement is not available or its reliability is in question.     

Continuous Monitoring of Cerebrovascular Reactivity Using Pulse Waveform of Intracranial Pressure

Background

Guidelines for the management of traumatic brain injury (TBI) call for the development of accurate methods for assessment of the relationship between cerebral perfusion pressure (CPP) and cerebral autoregulation and to determine the influence of quantitative indices of pressure autoregulation on outcome. We investigated the relationship between slow fluctuations of arterial blood pressure (ABP) and intracranial pressure (ICP) pulse amplitude (an index called PAx) using a moving correlation technique to reflect the state of cerebral vasoreactivity and compared it to the index of pressure reactivity (PRx) as a moving correlation coefficient between averaged values of ABP and ICP.

Methods

A retrospective analysis of prospective 327 TBI patients (admitted on neurocritical care unit of a university hospital in the period 2003?C2009) with continuous ABP and ICP monitoring.

Results

PAx was worse in patients who died compared to those who survived (?0.04?±?0.15 vs. ?0.16?±?0.15, ??²?=?28, p?2?=?6, p?=?0.01).

Conclusions

PAx is a new modified index of cerebrovascular reactivity which performs equally well as established PRx in long-term monitoring in severe TBI patients, but importantly is potentially more robust at lower values of ICP. In view of establishing an autoregulation-oriented CPP therapy, continuous determination of PAx is feasible but its value has to be evaluated in a prospective controlled trail.     

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

The methods for continuous assessment of cerebral autoregulation using correlation, phase shift, or transmission (either in time- or frequency-domain) were introduced a decade ago. They express dynamic relationships between slow waves of transcranial Doppler (TCD), blood flow velocity (FV) and cerebral perfusion pressure (CPP), or arterial pressure (ABP). We review a methodology and clinical application of indices useful for monitoring cerebral autoregulation and pressure-reactivity in various scenarios of neuro-critical care. Facts: Poor autoregulation and loss of pressure-reactivity are independent predictors of fatal outcome following head injury. Autoregulation is impaired by too low or too high CPP when compared to autoregulation with normal CPP (usually between 60 and 85 mmHg; and these limits are highly individual). Hemispheric asymmetry of the bi-laterally assessed autoregulation has been associated with asymmetry of CT scan findings: autoregulation was found to be worse ipsilateral to contusion or lateralized edema causing midline shift. The pressure-reactivity (PRx index) correlated with a state of low CBF and CMRO₂ revealed using PET studies. The PRx is easier to monitor over prolonged periods of time than the TCD-based indices as it does not require fixation of external probes. Continuous monitoring with the PRx can be used to direct CPP-oriented therapy by determining the optimal CPP for pressure-reactivity. Autoregulation indices are able to reflect transient changes of autoregulation, as seen during plateau waves of ICP. However, minute-to-minute assessment of autoregulation has a poor signal-to-noise ratio. Averaging across time (30 min) or by combining with other relevant parameters improves the accuracy. Myths: It is debatable whether the TCD-based indices in head injured patients can be calculated using ABP instead of CPP. Thresholds for functional and disturbed autoregulation dramatically depends on arterial tension of CO₂—therefore, comparison between patients cannot be performed without comparing their PaCO₂. The TCD pulsatility index cannot accurately detect the lower limit of autoregulation. Missing Links: We still do not know whether autoregulation-oriented therapy can be understood as a consensus between CPP-directed protocols and the Lund-concept. What are the links between endothelial function and autoregulation indices? Can autoregulation after head injury be improved with statins or EPO, as in subarachnoid hemorrhage? In conclusion, monitoring cerebral autoregulation can be used in a variety of clinical scenarios and may be helpful in delineating optimal therapeutic strategies.     

Comparison of frequency and time domain methods of assessment of cerebral autoregulation in traumatic brain injury

The impulse response (IR)-based autoregulation index (ARI) allows for continuous monitoring of cerebral autoregulation using spontaneous fluctuations of arterial blood pressure (ABP) and cerebral flow velocity (FV). We compared three methods of autoregulation assessment in 288 traumatic brain injury (TBI) patients managed in the Neurocritical Care Unit: (1) IR-based ARI; (2) transfer function (TF) phase, gain, and coherence; and (3) mean flow index (Mx). Autoregulation index was calculated using the TF estimation (Welch method) and classified according to the original Tiecks'' model. Mx was calculated as a correlation coefficient between 10-second averages of ABP and FV using a moving 300-second data window. Transfer function phase, gain, and coherence were extracted in the very low frequency (VLF, 0 to 0.05 Hz) and low frequency (LF, 0.05 to 0.15 Hz) bandwidths. We studied the relationship between these parameters and also compared them with patients'' Glasgow outcome score. The calculations were performed using both cerebral perfusion pressure (CPP; suffix ‘c'') as input and ABP (suffix ‘a''). The result showed a significant relationship between ARI and Mx when using either ABP (r=−0.38, P<0.001) or CPP (r=−0.404, P<0.001) as input. Transfer function phase and coherence_a were significantly correlated with ARI_a and ARI_c (P<0.05). Only ARI_a, ARI_c, Mx_a, Mx_c, and phase_c were significantly correlated with patients'' outcome, with Mx_c showing the strongest association.     

Relationship of Vascular Wall Tension and Autoregulation Following Traumatic Brain Injury

Background

The vascular wall tension (WT) of small cerebral vessels can be quantitatively estimated through the concept of critical closing pressure (CrCP), which denotes the lower limit of arterial blood pressure (ABP), below which small cerebral arterial vessels collapse and blood flow ceases. WT can be expressed as the difference between CrCP and intracranial pressure (ICP) and represent active vasomotor tone. In this study, we investigated the association of WT and CrCP with autoregulation and outcome of a large group of patients after traumatic brain injury (TBI).

Methods

We retrospectively analysed recordings of ABP, ICP and transcranial Doppler (TCD) blood flow velocity from 280 TBI patients (median age: 29 years; interquartile range: 20–43). CrCP and WT were calculated using the cerebrovascular impedance methodology. Autoregulation was assessed based on TCD-based indices, Mx and ARI.

Results

Low values of WT were found to be associated with an impaired autoregulatory capacity, signified by its correlation to FV-based indices Mx (R = ?0.138; p = 0.021) and ARI (R = 0.118; p = 0.048). No relationship could be established between CrCP and any of the autoregulatory indices. Neither CrCP nor WT was found to correlate with outcome.

Conclusions

Impaired autoregulation was found to be associated with a lower WT supporting the role of vasoparalysis in the loss of autoregulatory capacity. In contrast, no links between CrCP and autoregulation could be identified.     

Cerebral vasomotor reactivity testing in head injury: the link between pressure and flow

BACKGROUND: It has been suggested that a moving correlation index between mean arterial blood pressure and intracranial pressure, called PRx, can be used to monitor and quantify cerebral vasomotor reactivity in patients with head injury. OBJECTIVES: To validate this index and study its relation with cerebral blood flow velocity and cerebral autoregulation; and to identify variables associated with impairment or preservation of cerebral vasomotor reactivity. METHODS: The PRx was validated in a prospective study of 40 head injured patients. A PRx value of less than 0.3 indicates intact cerebral vasomotor reactivity, and a value of more than 0.3, impaired reactivity. Arterial blood pressure, intracranial pressure, mean cerebral perfusion pressure, and cerebral blood flow velocity, measured bilaterally with transcranial Doppler ultrasound, were recorded. Dynamic cerebrovascular autoregulation was measured using a moving correlation coefficient between arterial blood pressure and cerebral blood flow velocity, the Mx, for each cerebral hemisphere. All variables were compared in patients with intact and impaired cerebral vasomotor reactivity. RESULTS: No correlation between arterial blood pressure or cerebral perfusion pressure and cerebral blood flow velocity was seen in 19 patients with intact cerebral vasomotor reactivity. In contrast, the correlation between these variables was significant in 21 patients with impaired cerebral vasomotor reactivity, whose cerebral autoregulation was reduced. There was no correlation with intracranial pressure, arterial blood pressure, cerebral perfusion pressure, or interhemispheric cerebral autoregulation differences, but the values for these indices were largely within normal limits. CONCLUSIONS: The PRx is valid for monitoring and quantifying cerebral vasomotor reactivity in patients with head injury. This intracranial pressure based index reflects changes in cerebral blood flow and cerebral autoregulatory capacity, suggesting a close link between blood flow and intracranial pressure in head injured patients. This explains why increases in arterial blood pressure and cerebral perfusion pressure may be useful for reducing intracranial pressure in selected head injured patients (those with intact cerebral vasomotor reactivity).     

Monitoring of Cerebral Autoregulation

Pressure autoregulation is an important hemodynamic mechanism that protects the brain against inappropriate fluctuations in cerebral blood flow in the face of changing cerebral perfusion pressure (CPP). Static autoregulation represents how far cerebrovascular resistance changes when CPP varies, and dynamic autoregulation represents how fast these changes happen. Both have been monitored in the setting of neurocritical care to aid prognostication and contribute to individualizing CPP targets in patients. Failure of autoregulation is associated with a worse outcome in various acute neurological diseases. Several studies have used transcranial Doppler ultrasound, intracranial pressure (ICP with vascular reactivity as surrogate measure of autoregulation), and near-infrared spectroscopy to continuously monitor the impact of spontaneous fluctuations in CPP on cerebrovascular physiology and to calculate derived variables of autoregulatory efficiency. Many patients who undergo such monitoring demonstrate a range of CPP in which autoregulatory efficiency is optimal. Management of patients at or near this optimal level of CPP is associated with better outcomes in traumatic brain injury. Many of these studies have utilized the concept of the pressure reactivity index, a correlation coefficient between ICP and mean arterial pressure. While further studies are needed, these data suggest that monitoring of autoregulation could aid prognostication and may help identify optimal CPP levels in individual patients.     

Monitoring cerebral autoregulation after head injury. Which component of transcranial Doppler flow velocity is optimal?

Background

Cerebral autoregulation assessed using transcranial Doppler (TCD) mean flow velocity (FV) in response to various physiological challenges is predictive of outcome after traumatic brain injury (TBI). Systolic and diastolic FV have been explored in other diseases. This study aims to evaluate the systolic, mean and diastolic FV for monitoring autoregulation and predicting outcome after TBI.

Methods

300 head-injured patients with blood pressure (ABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), and FV recordings were studied. Autoregulation was calculated as a correlation of slow changes in diastolic, mean and systolic components of FV with CPP (Dx, Mx, Sx, respectively) and ABP (Dxa, Mxa, Sxa, respectively) from 30 consecutive 10?s averaged values. The relationship with age, severity of injury, and dichotomized 6?months outcome was examined.

Results

Association with outcome was significant for Mx and Sx. For favorable/unfavorable and death/survival outcomes Sx showed the strongest association (F?=?20.11; P?=?0.00001 and F?=?13.10; P?=?0.0003, respectively). Similarly, indices derived from ABP demonstrated the highest discriminatory value when systolic FV was used (F?=?12.49; P?=?0.0005 and F?=?5.32; P?=?0.02, respectively). Indices derived from diastolic FV demonstrated significant differences (when calculated using CPP) only when comparing between fatal and non-fatal outcome.

Conclusions

Systolic flow indices (Sx and Sxa) demonstrated a stronger association with outcome than the mean flow indices (Mx and Mxa), irrespective of whether CPP or ABP was used for calculation.     

Cerebral autoregulation in patients with obstructive sleep apnea syndrome during wakefulness

Background and purpose:  Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for stroke. Impairment of cerebral autoregulation may play a potential role in the pre-disposition to stroke of OSAS patients. In this study, we aimed to assess dynamic cerebral autoregulation (DCA) during wakefulness in OSAS patients and a group of matched controls.
Methods:  Patients and controls were examined in the morning after an overnight complete polysomnography. Mean cerebral blood flow velocity (CBFV) in the middle cerebral artery and mean arterial blood pressure (ABP) were continuously recorded using transcranial Doppler and Finapres. DCA was assessed using the Mx autoregulatory index. Mx is a moving correlation coefficient between mean CBFV and mean ABP. More positive value of Mx indicates worse autoregulation.
Results:  Eleven OSAS patients (mean age ± SD; 52.6 ± 7.9) and 9 controls (mean age ± SD; 49.1 ± 5.3) were enrolled. The mean apnea–hypopnea index (AHI) in the OSAS group was of 22.7 ± 11.6. No significant difference was found between the two groups as for age, body mass index, mean ABP and endtidal CO₂ pressure. Cerebral autoregulation was impaired in OSAS patients compared with controls (Mx index: 0.414 ± 0.138 vs. 0.233 ± 0.100; P  = 0.009). The severity of autoregulation impairment correlated to the severity of the sleep respiratory disturbance measured by the AHI ( P  = 0.003).
Conclusion:  Cerebral autoregulation is impaired in patients with OSAS during wakefulness. Impairment of cerebral autoregulation is correlated with the severity of OSAS.     

Continuous monitoring of cerebrovascular autoregulation: a validation study

BACKGROUND: Continuous monitoring of dynamic cerebral autoregulation, using a moving correlation index of cerebral perfusion pressure and mean middle cerebral artery flow velocity, may be useful in patients with severe traumatic brain injury to guide treatment, and has been shown to be of prognostic value. OBJECTIVE: To compare an index of dynamic cerebral autoregulation (Mx) with an index of static cerebral autoregulation (sRoR). METHODS: Mx was validated in a prospective comparative study against sRoR, using 83 testing sessions in 17 patients with traumatic brain injury. sRoR and Mx were calculated simultaneously during pharmacologically induced blood pressure variations. RESULTS: Mx was significantly correlated with sRoR (R = -0.78, p < 0.05). Nine patients were found to have failure of cerebral autoregulation, with an sRoR value < 50%. If an Mx value of 0.3 was used as the cut off point for failure of cerebral autoregulation, this index had 100% sensitivity and 90% specificity for demonstrating failure of autoregulation compared with the sRoR. An increase in cerebral blood flow velocity correlated significantly with Mx (R = 0.73, p < 0.05) but not with cerebral perfusion pressure (R = 0.41). CONCLUSIONS: Dynamic and static cerebral autoregulation are significantly correlated in traumatic brain injury. Cerebral autoregulation can be monitored continuously, graded, and reliably assessed using a moving correlation analysis of cerebral perfusion pressure and cerebral blood flow velocity (Mx). The Mx index can be used to monitor cerebral blood flow regulation. It is useful in traumatic brain injury because it does not require any external stimulus.     

Temporal changes in cerebral tissue oxygenation with cerebrovascular pressure reactivity in severe traumatic brain injury

Objective

To investigate the temporal relationship between cerebrovascular pressure reactivity and brain tissue oxygenation in patients with severe head injury.

Methods

In 40 patients, brain tissue oxygenation and intracranial pressure were monitored. Time‐averaged values for intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and brain tissue oxygenation (PtiO₂) were computed. The pressure reactivity index (PRx) was calculated. The mean values of the variables were obtained at the 6‐h and 72‐h post‐injury time points, and the difference between the two time points for each of the variables was denoted as delta (δ).

Results

Of the 40 patients, 32 were survivors and 8 were non‐survivors. Statistically significant differences were present between these two groups with regard to δMAP (p = 0.013), ICP at 6 h (p = 0.027), CPP at 72 h (p = 0.018), δCPP (p = 0.033), PRx at 6 h (p = 0.029), PRx at 72 h (p = 0.002), PtiO₂ at 72 h (p<0.0005) and δPtiO₂ (p = 0.023) values, reflecting an improvement with time in survivors and a deterioration with time in non‐survivors. In non‐survivors, the magnitude of change in PtiO₂ and CPP with time correlated in a negative linear fashion (p = 0.042 and 0.029, respectively) with the change in PRx with time, whereas no such relationship was seen in survivors.

Conclusion

The severity of brain tissue oxygenation derangement correlates with increasing cerebrovascular dysautoregulation in patients succumbing to severe head injury, supporting the utility of PRx as a monitoring variable and the rationale for a target‐driven approach to head injury management.Cerebral ischaemia is a critical contributory factor to secondary brain injury after trauma. In the presence of an unstable cerebral perfusion pressure (CPP), the autoregulatory cerebrovascular reactivity attempts to maintain an adequate cerebral blood flow. Increasing CPP may result in raised or lowered intracranial pressure (ICP), depending on whether cerebral autoregulation is preserved. Rosner et al¹ have described how increases in CPP within the autoregulatory range lead to compensatory vasoconstriction to maintain a stable cerebral blood flow. In so doing, cerebral blood volume and thus ICP levels fall. However, outside of these autoregulatory limits, a pressure‐passive scenario exists where increases in CPP lead to vasodilatation and a rise in ICP. Investigators have defined an index comparing arterial blood pressure (ABP) and ICP to quantify this relationship between CPP and ICP, known as the pressure reactivity index (PRx).^2,3 If a rise in ABP (and hence CPP) leads to a parallel increase in ICP, a good correlation exists, and the PRx is positive. However, in the face of intact cerebral autoregulatory capacity, vasoconstriction in the face of rising CPP leads to a drop in ICP, and hence PRx approaches zero or takes a negative value. Measurement of PRx could thus form the basis for target‐driven management, as ABP can be manipulated.Clinical studies on patients with head injury have shown the feasibility of continuous monitoring of local brain tissue oxygenation (PtiO₂) as a variable for cerebral oxygenation.^4,5,6 Despite the limitations of such a local method of measurement, PtiO₂ indicates global cerebral oxygenation when the monitoring is carried out in a relatively uninjured part of the brain.⁶ The presence of autoregulation disturbance could conceivably lead to disturbance in oxygen tension in the tissue of interest by virtue of blood flow metabolism uncoupling as PtiO₂ reflects the net balance between oxygen supply and demand at the tissue level.⁷We hypothesised that a worsening PRx indicative of increasing dysautoregulation during the temporal course of monitoring is related to mortality, and this may arise from specific patterns of change in various physiological variables including PtiO₂.