Volume-pressure Response Research Articles

The Intracranial Volume Pressure Response in Increased Intracranial Pressure Patients: Clinical Significance of the Volume Pressure Indicator

BackgroundFor patients suffering from primary brain injury, monitoring intracranial pressure alone is not enough to reflect the dynamic intracranial condition. In our previous study, a segment of the pressure-volume curve can be expressed by the parabolic regression model with single indicator “a”. The aim of this study is to evaluate if the indicator “a” can reflect intracranial conditions.MethodsPatients with traumatic brain injury, spontaneous intracranial hemorrhage, and/or hydrocephalus who had external ventricular drainage from January 2009 to February 2010 were included. The successive volume pressure response values were obtained by successive drainage of cerebral spinal fluid from intracranial pressure 20–25 mm Hg to 10 mm Hg. The relationship between withdrawn cerebral spinal fluid volume and intracranial pressure was analyzed by the parabolic regression model with single parameter “a”.ResultsThe overall mean for indicator “a” was 0.422 ± 0.046. The mean of “a” in hydrocephalus was 0.173 ± 0.024 and in severe intracranial mass with slender ventricle, it was 0.663 ± 0.062. The two extreme intracranial conditions had a statistical significant difference (p<0.001).ConclusionThe indicator “a” of a pressure-volume curve can reflect the dynamic intracranial condition and is comparable in different situations. A significantly larger indicator “a” with increased intracranial pressure is always observed in severe intracranial mass lesions with cerebral edema. A significantly smaller indicator “a” with increased intracranial pressure is observed in hydrocephalus. Brain computed tomography should be performed early if a rapid elevation of indicator “a” is detected, as it can reveal some ongoing intracranial pathology prior to clinical deterioration. Increased intracranial pressure was frequently observed in patients with intracranial pathology. The progression can be differentiated using the pattern of the volume pressure indicator.

The intracranial volume pressure response in increased intracranial pressure patients: Part 1. Calculation of the volume pressure indicator

The intracranial pressure (ICP) is usually continuously monitored in the management of patients with increased ICP. The aim of this study was to discover a mathematic equation to express the intracranial pressure-volume (P-V) curve and a single indicator to reflect the status of the curve. Patients with severe brain damage who had bilateral external ventricular drainage (EVD) from December 2008 to February 2010 were included in this study. The EVD was used as drainage of CSF and ICP monitor. The successive volume pressure response [6] values were obtained by successive drainage of CSF from ICP 20-25 to 10 mmHg. Parabolic, exponential, and linear regression models were designed to have a single parameter as the indicator to determine the P-V curves. The mean of parameter "a" in the exponential equation is 1.473 ± 0.054; in the parabolic equation, it is 0.332 ± 0.061; and in the linear equation, it is 1.717 ± 0.209. All regression equations of P-V curves had statistical significance (p < 0.005). Parabolic and exponential equations are closer to the original ICP curve than linear equation (p < 0.005). There is no statistically significant difference between parabolic and exponential regressions. The P-V curve can be expressed with linear, parabolic, and exponential regression models in increased ICP patients. The parabolic and exponential equations are more accurate methods to represent the P-V curve. The single parameter in the three regression equations can be compared in different conditions of one patient in clinical practice.

Inflation of a circular elastomeric membrane into a horizontally semi-infinite liquid reservoir of finite vertical depth: Quasi-static deformation model

Similar in both form and function to a classical circular membrane inflation experiment, cell-elastomer composite diaphragm inflation (CDI) experiments have recently been introduced as a methodology for exploring the mechanobiological properties of cell–cell anchoring junctions and cytoskeletal protein networks within a living epithelial sheet. Despite outward similarities, CDI experiments are unique from classical membrane inflation in that the loading associated with the inflation process, though axisymmetric, is inherently non-uniform. In order to better account for the effects of non-uniform loading in a CDI experiment, we introduce a model for the quasi-static inflation of a prestretched clamped circular isotropic incompressible hyperelastic membrane into a horizontally semi-infinite incompressible liquid reservoir of finite vertical depth. A set of coupled nonlinear first-order differential equations is shown to govern the inflation process. Assuming a Mooney–Rivlin (MR) constitutive model, the governing equations are formulated into a boundary value problem, and a procedure is developed for finding numerical solutions that quantify discrete membrane inflation states in terms of deformations, displacements, curvatures, stress resultants, and an inflation pressure distribution. Through iteration of the discrete state solution procedure, we further demonstrate how to generate a polynomial interpolating function that approximates the continuous volume–pressure response of a MR membrane. Select numerical examples are used to simulate the inflation response of a polydimethylsiloxane (PDMS) elastomer membrane used in an actual CDI experiment.

Monitoring of intracranial compliance: correction for a change in body position.

The objectives of our study were 1. to investigate whether the intracranial compliance changes with body position; 2. to test if the pressure-volume index (PVI) calculation is affected by different body positions; 3. to define the optimal parameter to correct PVI for changes in body position and 4. to investigate the physiological meaning of the constant term (P0) in the model of the intracranial volume-pressure relationship. Thirteen patients were included in this study. All patients were subjected to 2 to 3 different body positions. In each position, either classic bolus injection was performed for measurement of intracranial compliance and calculation of PVI or the new Spiegelberg compliance monitor was used to calculate PVI continuously. Four different models were used for calculating the constant pressure term P0 and the P0 corrected PVI values. Pressure volume index not corrected for the constant term P0 significantly decreased with elevating the patients head (r = 0.70, p < 0.0001). In contrast, volume-pressure response and ICP pulse amplitude did not change with position. Using the constant term P0 to correct the PVI we found no changes between the different body positions. Our results suggest that during the variation in body position there is no change in intracranial compliance but a change in hydrostatic offset pressure which causes a shifting of the volume-pressure curve along the pressure axis without its shape being affected. PVI measurements should either be performed only with the patient in the 0 degree recumbent position or that the PVI calculation should be corrected for the hydrostatic difference between the level of the ICP transducer and the hydrostatic indifference point of the craniospinal system close to the third thoracic vertebra.

A comparative study of the Spiegelberg Compliance Device with a manual volume-injection method: a clinical evaluation in patients with hydrocephalus

A new automated method of compliance measurement has been developed which may overcome some of the problems of the manual method. Measurement of craniospinal compliance in brain-injured patients offers the potential for early detection of raised intracranial pressure (ICP) before it rises to levels that may damage brain parenchyma. However, limitations of the existing manual volume pressure techniques have meant few centres routinely perform compliance testing.We report on the results of testing this new method against a manual volume pressure response method (VPR) in 10 patients with hydrocephalus. In this comparison study, 19 pairs of compliance measurements were obtained from 10 patients. The compliance values obtained ranged from 0.141 to 1.407 ml/mmHg.There was a good correlation between the two methods (r 2 =0.8508).The average bias in compliance between the two methods was 0.111 ml/mmHg (95% CL for the bias=0.0438, 0.1788) with the new method reading higher compliance than the manual method. These results indicate that the new automatic method of compliance measurement correlates well with an independent and classical measurement of compliance, and defines the bias and limits of agreement by which the new method measures craniospinal compliance in patients with hydrocephalus. Further work is needed to validate this device over a wider compliance range, especially at the lower compliance range often found in head injured patients. Studies are also required to determine the normal range of compliance values in the patient populations who undergo ICP monitoring. Research into determining which patient populations may benefit from continuous compliance measurement is warranted.

Effect of Cerebral Venous Congestion on the Pressure-Volume Index in the Evaluation of Intracranial Pressure Dynamics

Translocation of cerebrospinal fluid (CSF) between the intracranial and spinal subarachnoid space was blocked by ligating the cervical spinal core in eight cats under pentobarbital and nitrous oxide anesthesia, and the effects of cerebral venous congestion on the pressure-volume index (PVI), a measure relating the change in intracranial volume, and the logarithm of intracranial pressure (ICP) were evaluated. The changes in the volume-pressure response (VPR), a measure of intracranial elastance, were calculated simultaneously. Cerebral venous congestion was induced by lowering the head relative to the level of the heart by tilting the trunk of the animals to 20 degrees below horizontal. The presence of venous congestion was confirmed by an increase in the sagittal sinus pressure (SSP). The body position was shifted from horizontal prone (H1 group) to head-down tilt (D1 group) in four animals (group 1) and from head-down tilt (D2 group) to horizontal prone (H2 group) in the other four animals (group 2), and PVI and VPR were determined in each group. The changes in ICP and SSP with change of body position in group 1 were not significantly different from those in group 2, with both pressures changing by 7-8 mm Hg. PVI showed no significant differences between the H1 group and H2 group or between the D1 group and D2 group. The mean (+/- SEM) PVI for all measurements in the head-down tilt position (D1 and D2 groups) was significantly higher (0.50 +/- 0.02 ml; p < 0.01) than in the horizontal position (H1 and H2 groups; 0.35 +/- 0.02 ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Intracranial volume reserve determination using CT images, numerical analysis and lumbar infusion tests. An experimental study.

The epidural balloon compression model in the cat was used in intracranial volume reserve studies. The evaluation of the intracranial volume-pressure relations was based on the lumbar infusion test data: intracranial pressure, CSF outflow resistance, volume-pressure response and on CT images numerical analysis (CTINA) values. Two methods were applied and compared in the study: lumbar infusion test and CT images numerical analysis. The determinations were performed at the balloon volumes of 0.5 ml, 1.0 ml, and 1.5 ml. First statistically significant changes were found at the balloon volume of 0.5 ml i.e. the increase of CSF outflow resistance and volume-pressure response (data obtained in lumbar infusion test) and the decrease in CTINA values. The rise of intracranial pressure was less informative as it was observed at the balloon volume of 1.5 ml. Therefore CTINA seems to be a very useful noninvasive screening method in clinical studies of intracranial volume reserve.

Intracranial Volume-Pressure Relationship Following Flumazenil in Anesthetized Dogs

A series of infusions of mock cerebrospinal fluid (CSF) was used to determine intracranial volume-pressure relationships in 12 anesthetized dogs. Measures of intracranial volume-pressure relationships included (a) CSF pressure prior to volume infusion (Po), (b) peak CSF pressure (Pp) caused by volume injection, (c) intracranial compliance [C, calculated as the ratio of change of intracranial volume (DeltaLV) to change of CSF pressure (DeltaLP)], (d) the volume pressure response (VPR, a measure of elastance, calculated as the ratio of DeltaLP to DeltaLV), (e) the pressure-volume index (PVI, calculated as the ratio of DeltaLV to log Pp/Po), and (f) estimated intracranial compliance (Ce, calculated from PVI as 0.4343PVI/Po). Measurements were made before giving flumazenil and after flumazenil doses of 0.0025 and 0.16 mg/kg in dogs receiving midazolam and in dogs not receiving midazolam (controls). The midazolam and control groups were examined both when CSF pressure was normal and when CSF pressure was increased to approximately 35 cm H2O. In dogs receiving midazolam at normal CSF pressure, 0.16 mg/kg of flumazenil (but not 0.0025 mg/kg) increased Po (by 4 +/- 2 cm H2O) and PVI, decreased Ce, and did not significantly changes C or VPR. Neither does of flumazenil caused consistent changes in dogs receiving midazolam when CSF pressure was increased prior to giving flumazenil, or in dogs not receiving midazolam. It is concluded that, in the presence of a benzodiazepine effect, large does of flumazenil increase CSF pressure from preflumazenil values and may be interpreted as worsening the intracranial volume-pressure relationship when the relationship is assessed by measures strongly affected by Po (PVI and Ce) but not when the relationship is assessed by indices that are relatively independent of Po (C and VPR).

Intracranial volume-pressure relationship following thiopental or etomidate.

A series of infusions of mock cerebrospinal fluid (CSF) was used to determine intracranial volume-pressure relationships in 18 anesthetized dogs. Measures of intracranial volume-pressure relationships included 1) CSF pressure prior to volume infusion (P0), 2) peak CSF pressure (Pp) caused by volume injection, 3) intracranial compliance (C, calculated as the ratio of change of intracranial volume [delta V] to change of CSF pressure [delta P]), 4) the volume-pressure response (VPR, a measure of elastance, calculated as the ratio of delta P to delta V), 5) the pressure volume index (PVI, calculated as the ratio of delta V to log Pp/P0), and 6) estimated intracranial compliance (Ce, calculated from PVI as 0.4343 PVI/P0). Six of the 18 dogs (time controls) were studied during halothane (0.4%, end expired) and nitrous oxide (66%) in oxygen, six dogs were studied prior to and following each of two doses of thiopental (approximate cumulative doses were 10.5 and 25.5 mg/kg), and six dogs were studied prior to and following each of two doses of etomidate (approximate cumulative doses were 1.52 and 3.70 mg/kg). In the time controls P0, Pp, C, VPR, PVI, and Ce were steady throughout the experimental period. Thiopental decreased P0 (by 2-3 +/- 1 cmH2O) and Pp (by 2-4 +/- 2 cmH2O), increased Ce (by 0.02-0.03 +/- 0.01 ml/cmH2O), and did not change C, VPR, or PVI. Etomidate decreased P0 (by 3-4 +/- 1 cmH2O) and Pp (by 4-6 +/- 2 cmH2O), increased Ce (by 0.03-0.04 +/- 0.01 ml/cmH2O) and did not change C, VPR, or PVI.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulse amplitude and volume-pressure relationships in experimental hydrocephalus.

The bolus injection test was used to study the intracranial volume pressure relationships in an experimental population of normal and hydrocephalic dogs. Hydrocephalus was developed by means of an intracisternal injection of a kaolin powder solution. Hydrocephalic animals were tested a mean of 15 days after kaolin injection. The intraventricular pressure (ICPo) and amplitude of intraventricular pulse wave (AMPo) were measured at baseline steady-state. Pressure-volume index (PVI) and intracranial compliance (C) were calculated from bolus injection tests. The ICPo (p less than 0.01) and AMPo (p less than 0.001) were much higher in hydrocephalic animals and C decreased significantly (p less than 0.001). There were no statistical differences regarding PVI. A direct linear correlation was found between AMPo and ICPo (p less than 0.001) and between PVI and ICPo (p less than 0.05) but no correlations were found between PVI and AMPo. The regression analysis showed a non-linear correlation between C and ICPo (p less than 0.01) and between C and AMPo (p less than 0.001). The results of our experimental study suggest that: 1) pulse amplitude relates to the intracranial compliance, and 2) the intracranial compliance is a better parameter of the volume-pressure response than PVI.

A mathematical study of human intracranial hydrodynamics. Part 2--Simulation of clinical tests.

The mathematical model of human intracranial hydrodynamics proposed in a previous paper is here used to simulate the results of some dynamical tests of great clinical and physiological value and to analyze the blood flow pattern in the intracranial human basal arteries (especially in the internal carotid artery). Peak to peak amplitude of the blood flow waveform in the intracranial basal arteries, computed through the model, shows a significant increase at intracranial pressure levels above 50-60 mmHg, in accordance with recent experimental data. Moreover, diastolic blood flow appears to be largely sensitive to intracranial pressure changes during severe intracranial hypertension, whereas systolic blood flow is only slightly affected in this condition. The response of intracranial pressure to typical saline injection (volume-pressure response, steady state infusion and bolus injection tests) and to an abrupt obstruction in the extracranial venous drainage pathway is also well reproduced by the model. Finally, alterations in these responses, due to changes in some significant intracranial hydrodynamical parameters (i.e., the intracranial elastance coefficient and CSF outflow resistance) are presented.

DOES A BOLUS OF MANNITOL INITIALLY AGGRAVATE INTRACRANIAL HYPERTENSION?: A Study at Various Paco2 Tensions in Dogs

In two groups of anaesthetized dogs, with (n = 28) or without (n = 28) induced intracranial hypertension, we compared the effects on intracranial pressure (ICP) of the rapid administration of mannitol 2 g kg-1 i.v. at PaCO2 2.7, 4.0, 5.3, and 6.7 kPa (n = 7). In dogs with no induced intracranial hypertension, ICP increased during the administration of mannitol, reached a peak at 2 min after infusion, and then gradually decreased (P less than 0.05). More marked changes in ICP were observed in response to higher values of PaCO2 (P less than 0.05). In dogs with induced intracranial hypertension, the rapid infusion of mannitol caused an exponential decrease in ICP, without initial increase, which was significantly steeper at higher values of PaCO2 (P less than 0.05). This was followed by a more gradual decrease which achieved pre-balloon inflation values 10 min after infusion. We postulate that the absence of the initial increase in ICP is the result of a concomitant decrease in arterial pressure, a reduction in the volume-pressure response of the brain, the failure of mannitol to dilate further the cerebral arterial vascular bed and a hitherto unnoticed early water-drawing effect. Our study confirmed the safety of rapidly expanding the circulating blood volume with mannitol in circumstances of increased ICP in dogs.

206 ALTERATION OF BRAIN VOLUME-PRESSURE RESPONSE DURING OCTANOATE INFUSION IN RABBITS

Elevated serum concentrations of short chain fatty acids, including octanoate, are found in patients with Reye's Syndrome. Continuous intravenous infusion of octanoate in rabbits has been reported to result in similar clinical and chemical changes of Reye's Syndrome including hyperventilation, coma, seizures, increased intracranial pressure and hyperammonemia. To further evaluate the effect of octanoate on brain compliance we evaluated the brain volume-pressure response (VPR) during continuous octanoate infusion in rabbits. Volumes of 0.1ml were infused into the cisternal space of control rabbits (C) infused with normal saline and rabbits with continuous octanoate infusions at 1.5mmoles/hr (O). VPR was 1mmHg (C) vs 4mmHg (O). Time to recovery of initial intracranial pressure was 10 seconds (O). Both groups received pavulon 1mg/hr and were mechanically ventilated without changes in pH, pCO2 or pO2. Intracranial pressure (ICP) ranged 5-10mmHg and no differences were noted between (C) or (O) rabbits (p=ns). We conclude that continuous intravenous infusions of octanoate in rabbits 1) alter the brain VPR, and 2) do not produce elevations in ICP at 1.5mmoles/hr.

Intravesical ions, osmolality and pH influence the volume pressure response in the normal rat bladder, and this is more pronounced after DMSO exposure.

The influence of intravesical ions, osmolality, pH value, and active transurothelial NaCl-transport inhibition (furosemide) on the rat bladder volume-pressure response was studied according to the concept of a permeable urothelium and according to direct effects of osmolality and K+ on in vitro muscle preparations. It was found that the bladder capacity was decreased by K+, hyperosmolality and pH5, whereas it was increased by hypoosmolality, electrolyte-free media, furosemide and pH 8. The effects were found to be pronounced after dimethyl sulfoxide (DMSO) exposure. In this condition, furosemide showed less effect. It has been suggested that, especially in diseased bladders with increased permeability, frequent voiding and painful urge sensations are due to an enhanced urine access to nerve and muscle cells of the detrusor. On the other hand, frequent voiding reduces the urinary contact time within the bladder, thereby protecting from urine recirculation and thus from renal insufficiency. It has been further suggested that the bladder is not exclusively under central nervous control. As far as the present study is concerned, CO2, water, and normal saline do not seem to be appropriate urodynamic test media for providing the standard situation of bladder filling.

New intraventricular catheter for volume pressure response measurements.

Measurements of the volume-pressure response (VPR) to determine the relative position of a patient on the graphic volume-pressure curve have been used to derive clinically useful information. One reason that these measurements have not been used more frequently has been the fear of introducing infection into the ventricular system. We have designed an intraventricular catheter that allows repeated VPR measurements and reduces the risk of infection.

Changes in Intracranial Pressure and Compliance during Adenosine Triphosphate-induced Hypotension in Dogs

Intracranial pressure (ICP) was measured during induced hypotension with increasing doses of adenosine triphosphate (1-5 mg X kg-1 X min-1 ATP) in dogs without (group I) and with (group II) intracranial hypertension. After administration of 1 mg X kg-1 X min-1 ATP, ICP increased significantly from 11 +/- 4 mm Hg to 14 +/- 5 mm Hg (mean +/- SEM) (P less than 0.05; group I) and from 27 +/- 2 mm Hg to 38 +/- 6 mm Hg (P less than 0.05; group II), while mean arterial pressure (MAP) decreased from 103 +/- 10 mm Hg to 86 +/- 6 mm Hg (P less than 0.05; group I) and from 110 +/- 11 mm Hg to 90 +/- 11 mm Hg (P less than 0.05; group II). In both groups a slow decrease of ICP after the initial increase occurred with further lowering of MAP, but ICP remained significantly above control values even with a dose of 5 mg X kg-1 X min-1 ATP (P less than 0.05). Ventricular volume-pressure response curves (VPR) before and during intravenous infusion of 3 mg X kg-1 X min-1 ATP were constructed to determine changes in intracranial compliance (ICC). In both groups I and II ATP decreased ICC. On the basis of these results it is recommended that in the presence of intracranial mass lesions ATP should not be given to induce arterial hypotension before the dura is opened.

Influence of ketanserin, an antihypertensive agent with specific 5-HT2-receptor blocking activity, on intracranial pressure

During administration of ketanserin, a selective 5-HT2-receptor blocker, intracranial pressure (ICP) was measured in dogs without (group 1) and with (group 2) intracranial hypertension (ICP greater than 20 mm Hg). A bolus of 1 mg/kg body weight and subsequent infusion of 13.25 +/- 1.2 mg/kg of ketanserin decreased mean arterial pressure 35% +/- 18% in group 1 and 35% +/- 19% in group 2. In both groups, there was no change in ICP or in ventricular volume-pressure response curves (intracranial compliance [ICC]) after the administration of ketanserin. Ketanserin may be a safe antihypertensive drug for avoiding and treating hypertension in neurosurgical patients.

INFLUENCE OF URAPIDIL ON INTRACRANIAL PRESSURE AND INTRACRANIAL COMPLIANCE IN DOGS

During induced hypotension with urapidil, measurements of intracranial pressure and of the ventricular volume-pressure response (intracranial compliance) were obtained in dogs with and without intracranial hypertension. A bolus of urapidil 50 mg plus an infusion of urapidil 8.2 +/- 1.2 mg min-1 decreased mean arterial pressure by 22 +/- 10% from control in group I (without intracranial hypertension) and by 24 +/- 8% in group II (with intracranial hypertension). In both groups there was no change in intracranial pressure or in intracranial compliance after the administration of urapidil.

Effects of intravenous nitroglycerin on the intracranial pressure and volume pressure response.

Ventricular fluid pressure (VFP) and volume-pressure response were measured during nitroglycerin (NTG) infusion in nine patients anesthetized with N2O and fentanyl. The patients' ventilation was controlled, and PaCO2 was kept at 32 +/- 4 mm Hg. When an infusion of 0.01% NTG was given intravenously to decrease the mean blood pressure to 95.1%, 84.7%, and 78.2% of control, the VFP increased from control levels of 9.94 +/- 2.14 mm Hg to 12.89 +/- 2.25, 15.6 +/- 2.85, and 14.43 +/- 3.45 mm Hg, respectively. The volume-pressure response showed a significant increase when blood pressure decreased to 84.7% and 78.2% of control. These results suggest that intravenous NTG caused an increase in the intracranial pressure and a decrease in the intracranial compliance.

Effect of labetalol on intracranial pressure in dogs with and without intracranial hypertension.

Intracranial pressure measurements and ventricular volume pressure response curves were made during induced hypotension with labetalol, a combined alpha- and beta-adrenoceptor antagonist, in dogs without (group I) and with (group II) intracranial hypertension. The administration of 600 mg labetalol resulted in a percentage decrease of mean systemic arterial blood pressure (MAP) of 27% (+/- 10%) in group I, and 32% (+/- 9%) in group II from control values without changes in intracranial pressure and the ventricular volume pressure response curve. Larger decreases in MAP were not possible, even with a dose 3 times that clinically recommended. Labetalol may be a safe hypotensive agent to supplement neurolept analgesia, but it is not the drug of choice to induce deliberate hypotension.