Assessment of cerebral pressure autoregulation

Cerebral pressure autoregulation, a sensitive homeostatic mechanism important for the control of cerebral blood flow, is impaired by disease pathology and some drugs commonly used during anaesthesia. Therefore, the assessment of cerebral pressure autoregulation can help optimize cerebral blood flow in patients who have suffered neurological insults. In this article, we outline the means available for testing cerebral pressure autoregulation, thus allowing the reader to decide on the best strategy to adopt in their particular operating theatre and intensive care setting.     

Intracranial pressure and cerebral haemodynamics

Intracranial pressure (ICP) refers to the pressure within the skull, which is determined by the volumes of the intracranial contents; blood, brain and cerebrospinal fluid. Monro–Kellie homeostasis stipulates that a change in the total intracranial volume is accompanied by a change in the ICP, which is more precisely described by the ICP–volume relationship. Maintenance of a relatively constant ICP is essential for maintenance of the cerebral perfusion pressure (CPP), which in turn determines global cerebral blood flow (CBF). Although the physiological process of autoregulation ensures that CBF is tightly maintained over a range of CPPs, large increases in the ICP can result in severely impaired autoregulation, meaning that CBF may be compromised. In this review article we provide an overview of the physiological determinants of the ICP and CBF. We go on to illustrate how pathological states can compromise physiological compensatory mechanisms in order to potentially dangerous disturbances of the ICP and CBF.     

Intracranial pressure and cerebral haemodynamics

Intracranial pressure (ICP) refers to the pressure within the skull, which is determined by the volumes of the intracranial contents; blood, brain and cerebrospinal fluid. Monro–Kellie homeostasis stipulates that a change in the total intracranial volume is accompanied by a change in the ICP, which is more precisely described by the intracranial pressure–volume relationship. Maintenance of a relatively constant ICP is essential for maintenance of the cerebral perfusion pressure, which in turn determines global cerebral blood flow. Although the physiological process of autoregulation ensures that cerebral blood flow is tightly maintained over a range of cerebral perfusion pressures, large increases in the ICP can result in severely impaired autoregulation, meaning that cerebral blood flow may be compromised. In this review article we provide an overview of the physiological determinants of the ICP and cerebral blood flow. We go on to illustrate how pathological states can compromise physiological compensatory mechanisms in order to potentially dangerous disturbances of the ICP and cerebral blood flow.     

Intracranial pressure and cerebral haemodynamics

Intracranial pressure (ICP) refers to the pressure within the skull, which is determined by the volumes of the intracranial contents; blood, brain and cerebrospinal fluid. Monro–Kellie homeostasis stipulates that a change in the total intracranial volume is accompanied by a change in the ICP, which is more precisely described by the intracranial pressure–volume relationship. Maintenance of a relatively constant ICP is essential for maintenance of the cerebral perfusion pressure, which in turn determines global cerebral blood flow. Although the physiological process of autoregulation ensures that cerebral blood flow is tightly maintained over a range of cerebral perfusion pressures, large increases in the ICP can result in severely impaired autoregulation, meaning that cerebral blood flow may be compromised. In this review article we provide an overview of the physiological determinants of the ICP and cerebral blood flow. We go on to illustrate how pathological states can compromise physiological compensatory mechanisms in order to potentially dangerous disturbances of the ICP and cerebral blood flow.     

Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation

OBJECTIVE: Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS: Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS: We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 +/- 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION: Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and regional cerebral oxygen saturation in patients with cerebral hemorrhage

OBJECTIVE: To study the effects on cerebral dynamics and regional oxygenation (rSO2) of the semi-sitting position, with the head at either 30 degrees or 45 degrees, in surgery for cerebral hemorrhage. PATIENTS AND METHODS: We performed a prospective study of 10 patients undergoing surgery for cerebral hemorrhage under sedation and analgesia and with mechanical ventilation. Intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and rSO2 measured using near-infrared spectroscopy were recorded with the head in the supine position (0 degrees) and elevated to an angle of 30 degrees and then 45 degrees, following a stabilization period of 5 minutes. RESULTS: Mean (SD) ICP values were significantly lower in both semi-sitting positions than in the supine position: 2.8 (1.4) mm Hg lower at 30 degrees and 4.4 (1.4) mm Hg lower at 45 degrees. Mean CPP values were fell slightly when the head was elevated to 30 degrees (3.5 [3.1] mm Hg, P=.048); a greater reduction was achieved when the head was elevated 45 degrees (7.1 [4.8] mm Hg, P<.01). The greatest reduction in mean MAP values also occurred with the head elevated to 45 degrees (11.8 [4.6] mm Hg, P<.001). Mean rSO2 values fell when the head was elevated to 30 degrees and 45 degrees; the greatest reduction occurred when the head was elevated to 45 degrees (7% [2%], P<.001). There was a moderate correlation between CPP values and changes in rSO2 (r2=0.45, P<.001). CONCLUSION: Head elevation significantly reduces ICP and CPP in patients with cerebral hemorrhage. Head elevation also reduces rSO2, to a greater or lesser extent depending on the degree to which the head is elevated.     

Intracranial pressure and cerebral blood flow

Intracranial pressure (ICP) is determined by the volumes of brain, blood and cerebrospinal fluid within the skull, which is of course of fixed volume. The Monro–Kellie hypothesis states that an increase in volume of one of these components must be compensated for by a reduction in volume of one or both of the others. If this compensation is insufficient, then potentially fatal increases in ICP can occur. Maintenance of relatively constant ICP is essential for normal perfusion of the brain. Cerebral blood flow is regulated both globally, in order to prevent hypo- or hyper-perfusion resulting from changes in systemic arterial blood pressure, and locally, to meet the dynamic oxygen and substrate demands of different brain regions. Monitoring of ICP and the cerebral blood supply is possible through a variety of invasive and non-invasive techniques, and these techniques are already established in anaesthesia and intensive care medicine.     

异丙酚和普鲁卡因对颅内压及脑灌注压的影响

目的观察异丙酚、普鲁卡因对颅内压(ICP)和脑灌注压(CPP)的影响。方法25例脑肿瘤病人随机分成异丙酚组(D组)和普鲁卡因组(P组)。局麻下钻孔于颅骨及脑膜间安置SP-2000型颅内压监护仪，连续监测ICP，同时用Colin508连续监测MAP、HR及PETCO2。静注异丙酚2mg／kg后，输注异丙酚100～150pg·kg     

The effects of pipecuronium bromide on intracranial pressure and cerebral perfusion pressure

Twenty patients with expansive pathologic intracranial lesions, who were anesthetized with thiopental, nitrous oxide in oxygen, and fentanyl and mechanically ventilated to ensure normocarbia, received pipecuronium bromide 70 microg/kg i.v. Intracranial pressure (ICP), heart rate, arterial pressure, central venous pressure (CVP), EKG, and end-tidal CO2 were simultaneously recorded for 5 min before and for 15 min after administration of the muscle relaxant. No statistically significant changes in ICP and cerebral perfusion pressure were observed after administration of pipecuronium bromide. Cardiovascular stability was maintained during the study period except for a small, although significant, decrease of the CVP from 5.7 +/- 2.5 (SEM) to 5.0 +/- 2.5 mm Hg. These results, together with the long-lasting muscular effect of pipecuronium bromide, suggest that this new neuromuscular blocking agent may be used for muscle relaxation during neurosurgical operations in patients who have normal intracranial pressure at the time of administration of the drug.     

Cerebrovascular response to changes of cerebral venous pressure and cerebrospinal fluid pressure

Summary Using parietal cranial windows and multichannel videoangiometry, pial vessel responses were studied in cats during stepwise elevation of superior sagittal sinus pressure (P_SSS) to a level of 50 mmHg or reduction of CSF-pressure (P_CSF). P_CSF was monitored via a needle in the great cistern, known from previous studies to be identical to supratentorial CSF-pressure. During elevation of P_SSS, large and small pial veins dilated by 14±6.1% from resting diameter. Small arteries remained unresponsive until they were dilated by 9±2.1% at the level of P_SSS 50mmHg. Large arteries dilated by 18±5.5% at the level of P_SSS 50 mmHg. P_SSS was always approximately twice as high as P_CSF during increase of P_SSS. During reduction of P_CSF to– 5 mmHg, pial veins also dilated, by 7.4±1 % on the average. This observation suggests that normal P_CSF is a result of mainly venous vascular pressure, and that the level of normal venous pressure is not dictated by P_CSF but by the function and architecture of the cerebral vasculature. Since the rapid reduction of cerebral perfusion pressure CPP by elevation of venous pressure does not induce autoregulatory adjustment according to the level of CPP, but to the level of arterial transmural pressure, it is concluded, that the basic mechanism underlying autoregulation of CBF is myogenic.     

Estimation of critical closing pressure and cerebral perfusion pressure using transcranial Doppler

Editor—We read with interest the article by Sherman andcolleagues.¹ We would like to comment on the methods used toestimate critical closing pressure and cerebral perfusion pressure. The formula used to calculate critical closing pressure in thisarticle omits the influence of cerebrovascular wall tension.It actually equates critical closing pressure with intracranialpressure. As shown earlier, critical closing pressure consistsnot only of intracranial pressure but also of a factor representingarterial vascular wall tension.² Moreover, the method used tocalculate critical closing pressure can     

Circadian rhythm of cerebral perfusion pressure and intracranial pressure in head injury

The aim of the study was to determine if Cerebral Perfusion Pressure CPP and Intracranial Pressure ICP, in patients with head injury, has a circadian rhythm. CPP and ICP data of 13 patients were analysed using the Regressive and Iterative Cosinor methods. The Regressive Cosinor method did not detect a strong 24 hour rhythm. Therefore, the Iterative Cosinor method was used to seek rhythms with period not necessarily equal to 24 hours. Studying consecutive patient days by the Iterative cosinor method showed that rhythm is present but the rhythm period was often not 24 hours. A significant rhythm in the range of 20-30 hours was detected in eight patients for CPP 62 and in six patients for ICP 46. To validate the results real and surrogate time series were compared. The clinical implications of rhythmic data analysis are discussed.     

Extrapolation to zero-flow pressure in cerebral arteries to estimate intracranial pressure

Background. Cerebral perfusion pressure (CPP) is commonly calculatedfrom the difference between arterial blood pressure (AP) andintracranial pressure (ICP). ICP can be considered the effectivedownstream pressure of the cerebral circulation. Consequently,cerebral circulatory arrest would occur when AP equals ICP.Estimation of AP for zero-flow pressure (ZFP) may thus allowestimation of ICP. We estimated ZFP from cerebral pressure–flowvelocity relationships so that ICP could be measured by transcranialDoppler sonography. Methods. We studied 20 mechanically ventilated patients withsevere head injury, in whom ICP was monitored by epidural pressuretransducers. AP was measured with a radial artery cannula. Bloodflow velocity in the middle cerebral artery (V_MCA) ipsilateralto the site of ICP measurement was measured with a 2 MHz transcranialDoppler probe. All data were recorded by a microcomputer fromanalogue–digital converters. ZFP was extrapolated by regressionanalysis of AP–V_MCA plots and compared with simultaneousmeasurements of ICP. Results. ZFP estimated from AP–V_MCA plots was linearlyrelated to ICP over a wide range of values (r=0.93). There wasno systematic difference between ZFP and ICP. Limit of agreement(2 SD) was 15.2 mm Hg. Short-term variations in ICP wereclosely followed by changes in ZFP. Conclusion. Extrapolation of cerebral ZFP from instantaneousAP–V_MCA relationships enables detection of severely elevatedICP and may be a useful and less invasive method for CPP monitoringthan other methods. Br J Anaesth 2003; 90: 291–5     

Continuous cerebral compliance monitoring in severe head injury: its relationship with intracranial pressure and cerebral perfusion pressure

Summary Background. Cerebral compliance expresses the capability to buffer an intracranial volume increase while avoiding a rise in intracranial pressure (ICP). The autoregulatory response to Cerebral Perfusion Pressure (CPP) variation influences cerebral blood volume which is an important determinant of compliance. The direction of compliance change in relation to CPP variation is still under debate. The aim of the study was to investigate the relationship between CPP and compliance in traumatic brain injured (TBI) patients by a new method for continuous monitoring of intracranial compliance as used in neuro-intensive care (NICU).Method. Three European NICU’s standardised collection of CPP, compliance and ICP data to a joint database. Data were analyzed using an unpaired student t-test and a multi-level statistical model.Results. For each variable 108,263 minutes of data were recorded from 21 TBI patients (19 patients GCS≤8; 90% male; age 10–77 y). The average value for the following parameters were: ICP 15.1±8.9 mmHg, CPP 74.3±14 mmHg and compliance 0.68±0.3 ml/mmHg. ICP was ≥20 mmHg in 20% and CPP<60 mmHg for 10.7% of the time. Compliance was lower (0.51±0.34 ml/mmHg) at ICP≥20 than at ICP<20 mmHg (0.73±0.37 ml/mmHg) (p<0.0001). Compliance was significantly lower at CPP<60 than at CPP≥60 mmHg: 0.56±0.36 and 0.70±0.37 ml/mmHg respectively (p<0.0001). The CPP – compliance relationship was different when ICP was above 20 mmHg compared with below 20 mmHg. At ICP<20 mmHg compliance rose as CPP rose. At ICP≥20 mmHg, the relation curve was convexly shaped. At low CPP, the compliance was between 0.20 and 0.30 ml/mmHg. As the CPP reach 80 mmHg average compliance was 0.55 ml/mmHg., but compliance fell to 0.40 ml/mmHg when CPP was 100 mmHg.Conclusions. Low CPP levels are confirmed to be detrimental for intracranial compliance. Moreover, when ICP was pathological, indicating unstable intracranial equilibrium, a high CPP level was also associated with a low volume-buffering capacity.     

Simultaneous cerebral and spinal fluid pressure recordings

Summary Cerebrospinal fluid pulsation is likely to be responsible for the progression of some diseases, and it is differences in pressure which are significant in causing the imposition of energy upon tissues. The normal range of such differences has not been extensively documented. A technique for measuring intracranial and intraspinal pressures simultaneously in erect conscious patients is described. Normally the pressures are in a continual state of pulsation in response to changes in pressure in the arteries and veins. The measurements of CSF pressure fluctuations in response to normal cardiac pulsation, respiratory changes, coughing, Queckenstedt's test, and a variation of Valsalva's manoeuvre have been recorded, and the physiology has been discussed.     

Simultaneous cerebral and spinal fluid pressure recordings

Summary Simultaneous intraventricular and intraspinal pressure recordings in erect patients with obstructive lesions of the CSF pathways reveal differences in pressure which are frequently transitory and produced by pulsation. In nonacute cases without papilloedema but with suspected hindbrain hernia delay in equalization after pressure pulses may be demonstrated, and after Valsalva's manoeuvre differences between the head and the spine may be generated transiently and be responsible for clinical symptomatology. The particular clinical features related to hindbrain hernia are syringomyelia, cough headache, cough syncope, and lower cranial nerve signs with oscillopsia and cerebellar ataxia. Correction of the pressure dissociation is often associated with marked clinical improvement. It is suggested that this form of testing may be of relevance as an indication for operation and also for monitoring the progress of post-operative patients.     

Influence of nitroprusside on cerebral pressure autoregulation.

The authors studied 10 cats to assess the question of abolition of cerebral autoregulation attendant on the use of nitroprusside for hypotensive anesthesia. After the establishment of stable base line parameters, a continuous infusion of sodium nitroprusside was begun in a dose sufficient to maintain a mean systemic arterial pressure of 65 mm Hg. Infusion was continued for incremental periods of 30 seconds to 10 minutes, increasing the time of infusion by 30 seconds after each subsequent trial. At 10 seconds after the cessation of nitroprusside administration, intravenous dopamine was infused to raise the systemic arterial pressure to a mean of 100 mm Hg, and the subsequent response in intracranial pressure was recorded in each instance. In no animal was a loss of cerebral autoregulation noted when the nitroprusside infusion was maintained for 3 minute or less. When the infusion was maintained for 4 minutes or longer, cerebral autoregulation was lost in each animal, and the length of time to return of cerebral autoregulation correlated with the duration of nitroprusside infusion. Sodium nitroprusside disturbs the integrity of cerebral pressure autoregulation, and the onset and extent of this disturbance is a dose-dependent phenomenon.     

Brain tissue pressure in focal cerebral ischemia

Twenty-three anesthetized cats underwent permanent middle cerebral artery occlusion in a study of the relationships of regional cerebral blood flow, ventricular fluid pressure, brain tissue pressure, and ischemic edema formation. A pressure gradient of 8 mm Hg developed between ischemic tissue and normally perfused tissue during a 4-hour observation period after occlusion. Brain water accumulated as tissue pressure rose, while blood flow in the same area fell. The data suggest, but do not prove, that ischemic brain edema causes tissue pressure to rise focally, and that blood flow to the ischemic zone is compromised further by the resultant hydrostatic pressure gradient.