Local vascular response during organ elevation. A model for cerebral effects of upright position and dural puncture

BACKGROUND: Dural puncture can be followed by postural headache and, in patients with cerebral infections, by brain stem herniation. The present study evaluates whether these complications may be related to the changes in hydrostatic pressure generated by the spinal fluid column when the dural sac surrounding the cerebrospinal tissue has been punctured. METHOD: An isolated cat skeletal muscle enclosed in a plethysmograph connected to a tube served as a model imitating the brain, the cranium and the spinal canal. We investigated effects of organ elevation on tissue pressure, venous collapse (venous outflow resistance) and tissue volume with closed "spinal" tube (intact dural sac) and open "spinal" tube (dural puncture), and effects of compliance of the draining veins. RESULTS: Organ elevation with closed "spinal" tube induced a decreased tissue pressure, whereas tissue pressure remained unchanged if arterial inflow pressure to the muscle was kept constant. Organ elevation with the "spinal" tube opened distally caused a significantly larger decrease in tissue pressure, venous dilation and disappearance of venous outflow resistance. Transcapillary filtration increased, and the filtration rate was higher with high than with low venous compliance. CONCLUSION: If our results are applicable to the brain, changing to an upright position following a lumbar dural puncture may generate a negative hydrostatic force and a negative interstitial cerebral pressure, causing an increased transvascular pressure and dilation of the cerebral outflow veins. The corresponding increase in cerebral blood volume may induce post-spinal headache, and the increased transcapillary pressure may cause increased fluid filtration and brain oedema if the blood-brain barrier is disrupted.     

Effects of hypotensive treatment with α2-agonist and β1-antagonist on cerebral haemodynamics in severely head injured patients

Therapy of post-traumatic brain oedema often includes preservation of high arterial blood pressure to avoid secondary ischaemic injuries to the brain. This practice can be questioned since high arterial blood pressure may aggravate brain oedema through raised hydrostatic capillary pressure, causing fluid filtration across the damaged blood-brain barrier. This latter view is in agreement with our clinical experience and therefore hypotensive therapy with an α₂-adrenergic agonist (clonidine) and a β₁-adrenergic antagonist (metoprolol) has become part of our treatment protocol for severely head injured patients to decrease the post-traumatic brain oedema. The present study is an attempt to analyse whether there are any direct local cerebrovascular effects of the hypotensive agents used, which also might influence intracranial pressure. Severely head injured patients were investigated. Heart rate, mean arterial blood pressure, intracranial pressure, cerebral blood flow and arterio-venous difference in oxygen content were measured before and after a bolus dose of clonidine (six patients) and metoprolol (nine patients).
Clonidine decreased mean arterial blood pressure and cerebrovascular resistance without affecting other parameters measured. Metoprolol decreased heart rate and mean arterial pressure, but had no effect on the cerebrovascular parameters.
The results show that clonidine and metoprolol have no, or only minor, direct influence on local cerebral haemodynamics in severely brain injured patients. This implies that if there is an intracranial pressure reducing effect of these drugs, as suggested, this must be due to other mechanisms, namely a reduction in capillary hydrostatic pressure secondary to decreased arterial blood pressure and heart rate.     

Cerebral venous blood outflow: a theoretical model based on laboratory simulation

OBJECTIVE: The cerebrovascular bed and cerebrospinal fluid circulation have been modeled extensively except for the cerebral venous outflow, which is the object of this study. METHODS: A hydraulic experiment was designed for perfusion of a collapsible tube in a pressurized chamber to simulate the venous outflow from the cranial cavity. CONCEPT: The laboratory measurements demonstrate that the majority of change in venous flow can be attributed to either inflow pressure when the outflow is open, or the upstream transmural pressure when outflow is collapsed. On this basis, we propose a mathematical model for pressure distribution along the venous outflow pathway depending on cerebral blood flow and intracranial pressure. The model explains the physiological strong coupling between intracranial pressure and venous pressure in the bridging veins, and we discuss the limits of applicability of the Starling resistor formula to the venous flow rates. The model provides a complementary explanation for ventricular collapse and origin of subdural hematomas resulting from overshunting in hydrocephalus. The noncontinuous pressure flow characteristic of the venous outflow is pinpointed as a possible source of the spontaneous generation of intracranial slow waves. CONCLUSION: A new conceptual mathematical model can be used to explain the relationship between pressures and flow at the venous outflow from the cranium.     

Alfentanil increases intracranial pressure when intracranial compliance is low

Intracranial pressure increases following the administration of alfentanil 1 mg are reported in five patients with suspected normal pressure hydrocephalus who were undergoing infusion of saline into a lateral ventricle to measure cerebrospinal fluid outflow resistance. The increase in intracranial pressure was accompanied by a fall in mean arterial pressure. These observations show that, when the intracranial compliance is reduced, alfentanil can cause considerable increases in intracranial pressure and decreases in cerebral perfusion pressure.     

Analysis of the ICP pulse-pressure relationship as a function of arterial blood pressure clinical validation of a mathematical model

Summary The influence of arterial blood pressure (ABP) on the intracranial pulse pressure relationship (PPR) was studied in 17 patients in 29 recordings, with a total period of registration of 71.5 hours. The relationship between ICP and ABP was analysed by sampling the data every 15 seconds during spontaneous fluctuations of both these variables, and the analysis was performed on the basis of a mathematical model which includes pulsatory components. MABP and ABP amplitude had an opposite effect on the slope of PPR. Flattening of the PPR slope was caused by a MABP increase or an ABP amplitude decrease. The slope became steeper with decreasing MABP or increasing ABP amplitude. In accordance with the theoretical assumptions the quotient MABP/ABP-AMP was found to be suitable to express these opposite effects on PPR. Qualitatively, the same pattern of reaction was found in all patients. Rapid changes in PPR occurring during monitoring can be explained by a change in MABP/ABP-AMP relationship, regardless whether ABP changes influence intracranial elastance or not. The breakpoint of the PPR was recorded only on two occasions and could be explained in one by the influence of ABP. Monitoring of PPR as a measure of intracranial elastance and correlation of PPR with the patient's condition it not permitted unless at least the influence of ABP is analysed in each individual case.Definitions of Abbreviations and Symbols ABP Arterial blood pressure - ABP-AMP Arterial blood pressure amplitude - c_a Elastance coefficient of intracranial arterial vessels - CSF Cerebrospinal fluid - C_v Compliance of the venous part of the vascular bed - CVP Central venous pressure - E_art Volume elasticity of intracranial arterial vessels - HR Heart rate - ICP Intracranial pressure - ICP-AMP Intracranial pressure amplitude - K_a Absorption rate of cerebrospinal fluid - K_s Secretion rate of cerebrospinal fluid - K_v Intracranial pressure volume curve determining parameter - MABP Mean arterial pressure - MICP Mean intracranial pressure - P_art Systemic arterial blood pressure - P_csf Cerebrospinal fluid pressure - P_ven Systemic venous pressure - ¯P ... Mean pressure - P Pressure amplitude or change in pressure - PPR Intracranial pulse pressure relationship - PVI Pressure volume index - RR Respiration rate - V Injected volume during a volume pressure test or the transient intracranial volume increase per cardiac cycle - VPR Volume pressure response - VPT Volume pressure test     

Colloidal Blood Volume Expansion During High Intracranial Pressure

Summary  This study tested the hypothesis that colloidal blood volume expansion could improve the cerebral circulation during high intracranial pressure. We studied cerebrovascular haemodynamic variables during high intracranial pressure with and without colloidal blood volume expansion in 12 pigs, whereas five pigs served as controls with intracranial pressure increase twice without colloidal blood volume expansion. Cerebral blood flow was measured with ultrasonic flowmetry on the internal carotid artery, and cerebral microcirculation with laser Doppler flowmetry. High intracranial pressure was induced by infusion of artificial cerebrospinal fluid into the cisterna magna. Blood volume expansion was obtained by infusion of albumin, 1 gram/kg. Albumin infusion caused increases in internal carotid artery blood flow (P<0.05) and cerebral perfusion pressure (P<0.005), while cerebral microcirculation and cerebrovascular resistance was unchanged. High intracranial pressure albumin infusion caused internal carotid artery blood flow (P<0.05) and cerebral perfusion pressure (P<0.001) to increase compared to high intracranial pressure without albumin infusion, while cerebrovascular resistance was unchanged. Cerebral microcirculation tended to increase, but this was not statistically significant (P=0.07). Augmentation of the intravascular blood volume during high intracranial pressure increased the arterial inflow to the brain and possibly the cerebral microcirculation by increasing the cerebral perfusion pressure. Our results tend to support that the effect of colloidal blood volume expansion is beneficial for the cerebral circulation during high intracranial pressure.     

Human craniovertebral dynamics

The human craniovertebral cavity, although practically completely surrounded by bone, is subject to relatively wide variations in pressure. The activity of the cerebrospinal fluid is dependent upon: (1) a stable production-absorption mechanism; (2) the phenomena occurring in the intracraniospinal veins which very sensitively reflect pressure changes to that fluid. The almost constantly shifting variations in pressure which occur in the cerebrospinal veins and which are secondary to pressure changes in the extracranio-vertebral veins, indicate the elastic nature of the craniovertebral cavity in contrast to the older conception of the closed box character of the cavity. Under most physiologic and many pathologic conditions, variations in cerebrospinal fluid pressure are readily explained by changes in venous pressure. It is only under unusual pathologic conditions that variations in osmotic pressure affect the level of the fluid pressure.Although the cerebral arteries have an intrinsic nerve supply, changes in caliber of the intracranial arteries probably rarely, if ever, disturb the normal cerebrospinal fluid pressure, except during severe abnormal states, such as during oxygen-carbon dioxide disequilibrium. It is true that these vessels react sensitively to changes in metabolites circulating in the body, metabolites, however, which remain remarkably constant under physiologic conditions. Even under very unusual conditions, it is difficult to effect changes in caliber of the cerebral arteries, and great and sudden increases in arterial pressure are necessary before the diameter of the cerebral arteries alters. Again, removal of fluid from the cistern does little, if anything, to the caliber of these vessels. On the other hand, during such procedures, marked changes occur in the size and pressure of the cerebral veins.If it is a dictum that the cerebrospinal fluid pressure is closely related to the venous pressure, it is also true that the cerebral blood flow is closely related to the arterial blood pressure and the width of the cerebral vascular bed. These two factors tend to keep the oxygenation of the brain at a steady state or within normal limits, so that, for example, a great fall in arterial pressure is compensated by a widening of the vascular bed. Thus, the blood flow may be slower, but the oxygen uptake by the brain is relatively greater. It is remarkable that unconsciousness or convulsions do not supervene until the cerebral arterial pressure falls to a level of approximately 20 mm. of mercury, at which point the oxygen saturation of the internal jugular blood is in the neighborhood of 20 volumes per cent. The difficulty in affecting the cerebral blood flow is again observed in states of increased intracranial pressure, which must be extremely high before collapse occurs. One of the most remarkable of the vascular adjustment mechanisms is the ability of the cerebral circulation to continue in the face of almost complete and prolonged venous obstruction. Under such conditions, the emissary pathways increase in their activity so that the cerebral venous pressure becomes partially adjusted, and the production-absorption mechanism becomes reestablished with a fall of cerebrospinal fluid pressure to its original level.These examples suffice to demonstrate the remarkable resiliency of the cerebral circulation during widely adverse circumstances.     

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.     

Acute changes in the dynamics of the cerebrospinal fluid system during experimental subarachnoid hemorrhage

Early changes in intracranial pressure (ICP), ICP volume index, and resistance to absorption of cerebrospinal fluid induced by experimental subarachnoid hemorrhage were studied in cats. After SAH, the ICP was slightly elevated, and there was a decrease in the buffering capacity of the intracranial space and a sharp rise in outflow resistance. During infusion of blood into the cisterna magna with a constant infusion rate, an extensive increase in ICP could be demonstrated in contrast to the infusion of saline, which caused only slight elevation of ICP. Furthermore, during blood infusion, the ICP level did not reach a plateau phase of pressure, as was demonstrated during infusion of saline. It is suggested that the marked increase in ICP during blood infusion into the subarachnoid space is caused by intracranial volume loading and the simultaneous increase in cerebrospinal fluid outflow resistance. It is concluded that the reported relationship between increased cerebrospinal fluid outflow resistance and increased ICP supports the hypothesis of a strong increase in ICP during subarachnoid hemorrhage in human subjects.     

Cerebral autoregulation among patients with symptoms of hydrocephalus

OBJECTIVE: To study the relationship between the resistance to cerebrospinal fluid (CSF) outflow and cerebral autoregulation. METHODS: We examined 35 patients who presented with ventricular dilation and clinical symptoms of communicating hydrocephalus. For all of these patients, CSF compensatory reserve was investigated by using a computerized infusion test, with simultaneous recording of blood flow velocity wave forms (by using transcranial Doppler ultrasonography) and arterial blood pressure (with a Finapress finger cuff). The resistance to CSF outflow was calculated as the absolute increase in intracranial pressure (interpolated over vasogenic waves) divided by the infusion rate (1.5 ml/min in most cases). The index of autoregulation was assessed as a correlation coefficient (moving time window of 5 min) between slow waves (with periods of 20 s to 2 min) in mean blood flow velocity and cerebral perfusion pressure. RESULTS: The mean intracranial pressure increased during the test, from 6 mm Hg (standard deviation, 6 mm Hg) to 20 mm Hg (standard deviation, 10 mm Hg) (P < 0.0001). The index of autoregulation was significantly correlated with the resistance to CSF outflow (r = -0.41, P < 0.03), indicating better autoregulation with greater resistance to CSF outflow. CONCLUSION: Patients presenting with ventricular dilation may exhibit either decreased (atrophy) or increased (normal-pressure hydrocephalus) resistance to CSF outflow. Increased resistance is correlated with preserved autoregulation. Patients with low resistance, suggesting brain atrophy, more often have disturbed autoregulation in the middle cerebral artery territory, as assessed by transcranial Doppler ultrasonography.     

Vascular components of cerebrospinal fluid compensation

OBJECT: The aim of the study was to assess how cerebrospinal fluid (CSF) pressure-volume compensation depends on cerebrovascular tone. METHODS: In 26 New Zealand White rabbits, intracranial pressure (ICP), arterial blood pressure, and basilar artery blood flow velocity were measured continuously. Saline was infused into the cranial subarachnoid space to assess CSF compensatory parameters: the resistance to CSF outflow, the elastance coefficient, and the amplitude of the ICP pulsatile waveform. Infusions were repeated on two different levels of CO2 concentration in the arterial blood (PaCO2), at normotension and hypotension, and after the death of the animal. An increase in PaCO2 from a mean of 27 to 48 mm Hg was accompanied by an 18% increase in the resistance to CSF outflow (p<0.005) and a 64% increase (p<0.05) in the elastance coefficient. A decrease in arterial blood pressure from a mean of 100 to 51 mm Hg caused a 25% decrease in CSF outflow resistance (p<0.01) but did not affect the elastance coefficient. Postmortem, a 23% decrease in the CSF outflow resistance was associated with a 102% decrease in the elastance coefficient. CONCLUSIONS: Cerebrovascular parameters have a limited but significant impact on CSF infusion studies. The vascular component of ICP may be identified as a significant factor contributing to this phenomenon. During infusion studies, physiological parameters influencing vascular conditions should be maintained as stable as possible.     

The effect of cerebrospinal fluid drainage on cerebral perfusion in traumatic brain injured adults

Cerebrospinal fluid drainage is a first line treatment used to manage severely elevated intracranial pressure (> or = 20 mm Hg) and improve outcomes in patients with acute head injury. There is no consensus regarding the optimal method of cerebrospinal fluid removal. The purpose of this investigation was to determine whether cerebrospinal fluid drainage decreases intracranial pressure and improves cerebral perfusion and to identify factors that impact treatment effectiveness. This study involved 31 severely head injured patients. Intracranial pressure and other indices of cerebral perfusion (cerebral perfusion pressure, cerebral blood flow velocity, and regional cerebral oximetry) were measured before, during, and after cerebrospinal fluid drainage. Arterial and jugular venous oxygen content was measured before and after cerebrospinal fluid drainage. Patients underwent three randomly ordered cerebrospinal fluid drainage protocols that varied in the volume of cerebrospinal fluid removed (1 mL, 2 mL, and 3 mL) for a total of 6 mL of cerebrospinal fluid removed. There was a significant change in the intracranial pressure from a mean at baseline of 26.1 mm Hg (SD = 4.4) to 22.1 mm Hg immediately after drainage. One third of patients experienced a decrease in the intracranial pressure below 20 mm Hg; in two patients the intracranial pressure dropped less than 1 mm Hg. The following factors predicted 61.5% of the variance in the responsiveness of intracranial pressure to drainage: vecuronium hypothermia, baseline cerebral perfusion pressure and acuity of illness. Cerebrospinal fluid drainage provides a transient decrease in intracranial pressure without a measurable improvement in other indices of cerebral perfusion.     

Applied cerebral physiology

This article reviews cerebral metabolism and blood flow, and the pressure dynamics within the cranial cavity. The brain functions within the confines of the cranial cavity and it is important to understand the dynamics of the parenchyma, cerebrospinal fluid and blood in relation to intracranial pressure (ICP) and metabolic needs. It requires an uninterrupted supply of oxygen and glucose to maintain its basal energy requirements and these are increased during periods of enhanced activity. Cerebral blood flow (CBF) is therefore critical for normal cerebral function. Its control is dictated by local intrinsic metabolic needs as well as extraneous factors such as arterial blood pressure, arterial carbon dioxide and oxygen tension, temperature and neural factors; all of which can be measured to guide therapy.     

Intracranial venous hypertension and the effects of venous outflow obstruction in a rat model of arteriovenous fistula

A model of rat arteriovenous fistula (AVF) was created using a proximal common carotid artery to distal external jugular vein anastomosis. Anatomical dissections revealed that the external jugular vein is the primary vessel draining intracranial venous blood. Physiological measurements were made with the AVF open and closed, and during venous outflow occlusion of the contralateral external jugular vein. Opening the AVF increased torcular pressure from 6.5 +/- 0.6 to 13.5 +/- 1.1 mm Hg and decreased mean arterial pressure from 82.7 +/- 1.8 to 62.8 +/- 1.8 mm Hg (both P less than .05), decreasing cerebral perfusion pressure from 76.2 +/- 1.7 to 49.3 +/- 2.2 mm Hg (P less than .05). Middle cerebral artery blood flow velocity (MCA BFV) decreased from 6.8 +/- 1.1 to 4.2 +/- 0.7 cm/s (P less than 0.05). In rats with an AVF, occlusion of venous outflow increased torcular pressure to 34.8 +/- 3.1 mm Hg (P less than 0.05), MCA BFV decreased to 1.8 +/- 0.5 cm/s (P less than 0.05), and severe ischemic changes were seen on the electroencephalogram. Under this condition, torcular pressure and systemic arterial pressure had a positive linear relationship (P less than 0.05), whereas in control rats torcular pressure and arterial pressure had no relationship. Restoration of cerebral perfusion pressure by release of venous outflow occlusion and AVF closure transiently increased MCA BFV to 69% above baseline (P less than 0.05). Histological examination 1 week after permanent venous outflow occlusion revealed venous infarction, subarachnoid hemorrhage, and severe brain edema in rats with an AVF but not in control rats without an AVF. This model of cerebrovascular steal with venous hypertension reproduces both hemodynamic and hemorrhagic complications of human AVF and emphasizes the importance of venous outflow obstruction and venous hypertension in the pathophysiology of these lesions.     

Magnetic resonance imaging quantification of compliance and collateral flow in late-onset idiopathic aqueductal stenosis: venous pathophysiology revisited

OBJECT: Findings in animal models of noncommunicating hydrocephalus have suggested that a reduction in compliance of the superior sagittal sinus, an elevation in venous outflow pressure, and the development of venous collateral flow may be associated with this condition. Although elevated venous pressure is known to cause hydrocephalus in children, this mechanism has fallen out of favor as a theory in adults. METHODS: Twenty-one patients with late-onset idiopathic aqueductal stenosis (LIAS) underwent magnetic resonance imaging with flow quantification measuring the degree of ventricular enlargement, sulcal compression, total blood inflow, superior sagittal/straight sinus outflow, aqueduct flow, arteriovenous delay (AVD), and the extent of collateral venous flow. Data obtained in these patients were compared with those obtained in 21 age-matched control individuals. RESULTS: There was a reduction in compliance in the patients with LIAS in whom the AVD decreased by 50% (p = 0.01). The arterial inflow and the straight sinus outflow were normal, but the sagittal sinus outflow was reduced by 23% (p = 0.001). This indicated that significant collateral venous outflow pathways were draining blood away from the superficial but not the deep drainage system. CONCLUSIONS: Similar to the animal models, patients with LIAS exhibit a reduced venous compliance and an elevation in venous collateral flow. Together, these findings suggest that an elevation in venous pressure may be associated with this disease process. A review of the literature has indicated that only subtle differences may exist in the pathophysiology among patients with LIAS, normal-pressure hydrocephalus, and idiopathic intracranial hypertension.     

A mathematical model of idiopathic intracranial hypertension incorporating increased arterial inflow and variable venous outflow collapsibility

OBJECT: A collapsible segment in the venous outflow has been noted in many patients with idiopathic intracranial hypertension (IIH). Mathematical modeling has shown that these collapsible segments can account for the elevated cerebrospinal fluid (CSF) pressures associated with IIH. However, the model required an elevated outflow resistance of up to 10 times normal to predict the CSF pressures actually found clinically. Measurement of blood flow in patients with IIH has shown that inflow rates vary, with higher rates noted in patients with lesser outflow stenoses. The aim of this work was to extend a simple model of cerebral hydrodynamics to accommodate a collapsible sinus and elevations in cerebral blood flow in accordance with in vivo measurements. METHODS: Forty patients with IIH underwent MR imaging in which the degree of stenosis on MR venography was compared with the total blood inflow by using MR flow quantification. The relative outflow resistance in IIH was estimated using the CSF opening pressure. The patients were compared with 14 age-matched control individuals. RESULTS: Patients were divided into 3 groups based on MR venography appearances (minimal stenosis, stenosis of 40-70% and > 70% stenosis). In vivo measurements suggested a relative resistance elevation of 2.5 times normal, 4.2 times normal, and 4.8 times normal in the 3 groups, respectively. There was an increased inflow of 1.56 times normal, 1.28 times normal, and 1.19 times normal in these groups. CONCLUSIONS: The model correctly predicted the CSF pressures noted in vivo, suggesting that high arterial inflow is required for patients with low-grade stenoses to be symptomatic.     

Focal brain edema associated with acute arterial hypertension

Acute arterial hypertension was studied in normal cats to determine its role in the formation of brain edema. Arterial hypertension was induced for 30 minutes by inflation of a balloon catheter situated in the descending aorta. Cerebral edema was evaluated by gross and microscopic observations, tissue water content by wet/dry weights, and blood-brain barrier (BBB) permeability by extravasation of horseradish peroxidase (HRP) and Evans blue dye. For 1 hour after the hypertensive insult, tissue pressure and regional cerebral blood flow (rCBF) were measured from the arterial boundary zone and from a non-boundary region, and intracranial pressure was recorded from the lateral ventricle as ventricular fluid pressure. Focal lesions with increased BBB permeability to Evans blue dye or HRP were usually located symmetrically in the cortex, corresponding to the occipitoparietal parts of the arterial boundary zones. The increase in water content was found only in areas of increased permeability. Tissue pressure increased simultaneously with the abrupt rise in blood pressure, and an increase in rCBF paralleled the elevation of blood pressure. Tissue pressure and rCBF returned to a steady state when blood pressure returned to normal. There were no differences in tissue pressure or rCBF between the arterial boundary zone and the non-boundary zone, even during arterial hypertension. In cerebral hemispheres examined 48 hours after the hypertensive challenge, brain edema had not continued to develop. The data indicate that acute arterial hypertension may produce focal brain edema with increased permeability of the BBB in the cortex of normal brain, particularly in the arterial boundary zones. The authors postulate that increased cerebral blood volume, high intraluminal pressure, and breakthrough of autoregulation play an important role in the formation of hypertensive brain edema.     

Epidural pulse waveform as an indicator of intracranial pressure dynamics

With an increase in intracranial pressure during epidural balloon inflation, epidural pulse waveform, which is polyphasic under normal conditions, becomes monotonous at about 30 mmHg. This change in waveform is considered closely related to the apparent increase in arterial driving pressure to the brain and to a disturbance of venous outflow. When cerebral vasodilatation is prominent, the waveform becomes monotonous at a significantly lower intracranial pressure. These findings correlate well with the results of spectral analysis of the pulse wave. The usefulness of change in epidural pulse waveform, which can indicate an alteration of intracranial pressure dynamics in a relatively low pressure range, is discussed with comparison to other techniques used to determine intracranial pressure dynamics.     

Effects of celiac plexus block on splanchnic circulation--II: Changes in the systemic hemodynamics and the blood flow of the liver and kidney in dogs

Effects of celiac plexus block (CPB) on systemic and splanchnic circulation, especially of liver and kidney, were investigated in twenty nine mongrel dogs. CPB was performed by an anterior approach through a catheter placed in a paraaortic compartment using 7 mg.kg-1 of 2% mepivacaine. Tissue blood flow measurement was performed by a hydrogen clearance method in eleven dogs, and vascular blood flow was measured in eighteen dogs by an electromagnetic flow meter. Swan-Ganz catheter was inserted to measure mean arterial pressure (ABP), heart rate (HR), central venous pressure (CVP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP) and cardiac output (CO). Then stroke volume (SV), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were calculated. Following CPB, ABP, HR, CVP and C.O. were significantly decreased at 7 to 9%. PAP decreased at 5%. PCWP, SV, SVR and PVR were unchanged. The hepatic arterial blood flow increased significantly, and portal venous blood flow decreased after CPB transiently, and then recovered to control value or to a higher level at 60min after CPB. The tissue blood flow of the liver tended to increase, but the change was not significant. In the kidney, both arterial and tissue blood flows increased significantly after CPB. The results suggest that following CPB, hepatic and renal tissue blood flows increased because of the increments of their arterial blood flows, unless a profound systemic hemodynamic depression occurred.     

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.