Pressure-volume index as a function of cerebral perfusion pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 377-380 ◽  
Author(s):  
W. John Gray ◽  
Michael J. Rosner
Keyword(s):  
Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Complex Function ◽  
Volume Index ◽  
Content Type ◽  
Adult Cats ◽  
Hydrogen Clearance ◽  
Fine Print

✓ The pressure-volume index (PVI) was measured in six adult cats while cerebral perfusion pressure (CPP) was reduced from normal levels to below the autoregulatory range by a continuous infusion of adenosine triphosphate. Anesthesia was induced with methohexital and maintained with an N2O:O2 (70%:30%) mixture. Body temperature, hematocrit, and PaCO2 were held constant throughout each experiment. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. At CPP levels over 50 mm Hg, CBF remained relatively constant despite changes in CPP. Within this range, the PVI varied directly with CPP (PVI = 0.24 ml + 0.0013 mm Hg CPP). Below the autoregulatory range, CBF fell progressively with further decreases in CPP; in this range, PVI was found to increase as CPP fell (PVI = 0.84 ml − 0.0071 mm Hg CPP). These results indicate that the PVI is a complex function of CPP, varying directly with CPP within the autoregulatory range and indirectly with CPP below the autoregulatory range.

Pressure-volume index as a function of cerebral perfusion pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 369-376 ◽  
Author(s):  
W. John Gray ◽  
Michael J. Rosner
Keyword(s):  
Body Temperature ◽  
Linear Relationship ◽  
Cerebral Perfusion Pressure ◽  
Adenosine Triphosphate ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Volume Index ◽  
Content Type ◽  
Adult Cats ◽  
Fine Print

✓ The pressure-volume index (PVI) was measured as a function of cerebral perfusion pressure (CPP) in 12 adult cats. Anesthesia was induced with methohexital in six animals and with pentobarbital in six animals; all were maintained on an N2O:O2 (70%:30%) mixture. The CPP was either increased in 10-torr increments using norepinephrine or decreased by a combination of adenosine triphosphate and hemorrhage in subgroups. Three estimations of PVI were made at each level of CPP. The PaCO2, body temperature, and hematocrit were controlled at normal levels throughout. In both groups there was a linear relationship between PVI and CPP with increasing CPP being reflected by a rise in PVI. This relationship was more marked in the methohexital group: PVI = 0.37 ml + 0.0005 mm Hg CPP in the pentobarbital group, and PVI = 0.14 ml + 0.0019 mm Hg CPP in the methohexital group. These results indicate that the PVI is not independent of CPP but is a function of CPP and is profoundly influenced by anesthesia.

Is cerebral perfusion pressure a major determinant of cerebral blood flow during head elevation in comatose patients with severe intracranial lesions?

2000 ◽  
Vol 92 (4) ◽  
pp. 606-614 ◽  
Author(s):  
Jean-Jacques Moraine ◽  
Jacques Berré ◽  
Christian Mélot
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pressure Gradient ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Head Elevation ◽  
Intracranial Lesions ◽  
Fine Print

Object. Head elevation as a treatment for lower intracranial pressure (ICP) in patients with intracranial hypertension has been challenged in recent years. Therefore, the authors studied the effect of head position on cerebral hemodynamics in patients with severe head injury.Methods. The effect of 0°, 15°, 30°, and 45° head elevation on ICP, cerebral blood flow (CBF), systemic arterial (PsaMonro) and jugular bulb (Pj) pressures calibrated to the level of the foramen of Monro, cerebral perfusion pressure (CPP), and the arteriovenous pressure gradient (PsaMonro − Pj) was studied in 37 patients who were comatose due to severe intracranial lesions. The CBF decreased gradually with head elevation from 0 to 45°, from 46.3 ± 4.8 to 28.7 ± 2.3 ml · min−1 · 100 g−1 (mean ± standard error, p < 0.01), and the PsaMonro − Pj from 80 ± 3 to 73 ± 3 mm Hg (p < 0.01). The CPP remained stable between 0° and 30° of head elevation, at 62 ± 3 mm Hg, and decreased from 62 ± 3 to 57 ± 4 mm Hg between 30° and 45° (p < 0.05). A simulation showed that the 38% decrease in CBF between 0° and 45° resulted from PsaMonro − Pj changes for 19% of the decrease, from a diversion of the venous drainage from the internal jugular veins to vertebral venous plexus for 15%, and from CPP changes for 4%.Conclusions. During head elevation the arteriovenous pressure gradient is the major determinant of CBF. The influence of CPP on CBF decreases from 0 to 45° of head elevation.

Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury

2000 ◽  
Vol 92 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Niels Juul ◽  
Gabrielle F. Morris ◽  
Sharon B. Marshall ◽  
_ _ ◽  
Lawrence F. Marshall
Keyword(s):  
Head Injury ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Neurological Deterioration ◽  
Double Blind ◽  
Content Type ◽  
Fine Print

Object. Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate.Methods. The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-d-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.4% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP ≥ 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg.Conclusions. Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurological Function ◽  
Content Type ◽  
No Reflow ◽  
No Reflow Phenomenon ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Effect of reduced cerebral perfusion pressure on cerebral blood flow following inhibition of nitric oxide synthesis

1998 ◽  
Vol 89 (3) ◽  
pp. 448-453 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Nitric Oxide Synthesis ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. The authors tested the hypothesis in a porcine model that inhibition of nitric oxide synthesis during reduced cerebral perfusion pressure (CPP) affected the relative cerebral blood flow (CBF) and the cerebrovascular resistance. Methods. The CPP was reduced by inducing high cerebrospinal fluid pressure and hemorrhagic hypotension. With continuous blood and intracranial pressure monitoring, relative CPP was estimated using the laser Doppler flowmetry technique in nine pigs that received 40 mg/kg nitro-l-arginine methyl ester (l-NAME) and in nine control animals. The l-NAME caused a decrease in relative CBF (p < 0.01) and increases in cerebrovascular resistance (p < 0.01), blood pressure (p < 0.05), and CPP (p < 0.001). During high intracranial pressure there were no significant differences between the treated animals and the controls. After hemorrhage, there was no significant difference between the groups initially, but 30 minutes later the cerebrovascular resistance was decreased in the control group and increased in the l-NAME group relative to baseline (p < 0.05). Combined hemorrhage and high intracranial pressure increased the difference between the two groups with regard to cerebrovascular resistance (p < 0.05). Conclusions. These results suggest that nitric oxide synthesis inhibition affects the autoregulatory response of the cerebral circulation after cardiovascular compensation has taken place. Nitric oxide synthesis inhibition enhanced the undesirable effects of high intracranial pressure during hypovolemia.

Dimethyl sulfoxide in experimental brain injury, with comparison to mannitol

1980 ◽  
Vol 53 (1) ◽  
pp. 58-62 ◽  
Author(s):  
Frederick D. Brown ◽  
Lydia M. Johns ◽  
Sean Mullan
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Brain Injury ◽  
Dimethyl Sulfoxide ◽  
Rhesus Monkeys ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Missile Injury ◽  
Fine Print

✓ The effects of dimethyl sulfoxide therapy were studied in rhesus monkeys following a standardized occipitofrontal missile injury. This therapy resulted in substantially higher blood pressure, cerebral perfusion pressure, blood flow, and oxidative metabolism than those of a group of monkeys that had been treated similarly with mannitol, and than those of an untreated group.

Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients with brain trauma

2005 ◽  
Vol 102 (2) ◽  
pp. 311-317 ◽  
Author(s):  
Tim Howells ◽  
Kristin Elf ◽  
Patricia A. Jones ◽  
Elisabeth Ronne-Engström ◽  
Ian Piper ◽  
...  
Keyword(s):  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Regression Line ◽  
Brain Trauma ◽  
Treatment Protocols ◽  
Content Type ◽  
Arterial Blood ◽  
Pressure Reactivity ◽  
Fine Print

Object. The aim of this study was to compare the effects of two different treatment protocols on physiological characteristics and outcome in patients with brain trauma. One protocol was primarily oriented toward reducing intracranial pressure (ICP), and the other primarily on maintaining cerebral perfusion pressure (CPP). Methods. A series of 67 patients in Uppsala were treated according to a protocol aimed at keeping ICP less than 20 mm Hg and, as a secondary target, CPP at approximately 60 mm Hg. Another series of 64 patients in Edinburgh were treated according to a protocol aimed primarily at maintaining CPP greater than 70 mm Hg and, secondarily, ICP less than 25 mm Hg for the first 24 hours and 30 mm Hg subsequently. The ICP and CPP insults were assessed as the percentage of monitoring time that ICP was greater than or equal to 20 mm Hg and CPP less than 60 mm Hg, respectively. Pressure reactivity in each patient was assessed based on the slope of the regression line relating mean arterial blood pressure (MABP) to ICP. Outcome was analyzed at 6 months according to the Glasgow Outcome Scale (GOS). The prognostic value of secondary insults and pressure reactivity was determined using linear methods and a neural network. In patients treated according to the CPP-oriented protocol, even short durations of CPP insults were strong predictors of death. In patients treated according to the ICP-oriented protocol, even long durations of CPP insult—mostly in the range of 50 to 60 mm Hg—were significant predictors of favorable outcome (GOS Score 4 or 5). Among those who had undergone ICP-oriented treatment, pressure-passive patients (MABP/ICP slope ≥ 0.13) had a better outcome. Among those who had undergone CPP-oriented treatment, the more pressure-active (MABP/ICP slope < 0.13) patients had a better outcome. Conclusions. Based on data from this study, the authors concluded that ICP-oriented therapy should be used in patients whose slope of the MABP/ICP regression line is at least 0.13, that is, in pressure-passive patients. If the slope is less than 0.13, then hypertensive CPP therapy is likely to produce a better outcome.

Cerebral perfusion pressure, intracranial pressure, and head elevation

1986 ◽  
Vol 65 (5) ◽  
pp. 636-641 ◽  
Author(s):  
Michael J. Rosner ◽  
Irene B. Coley
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Pressure Waves ◽  
Content Type ◽  
Arterial Blood ◽  
Head Elevation ◽  
Adequate Hydration ◽  
Fine Print

✓ Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20° to 30°, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10° of head elevation from 0° to 50°. For every 10° of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 ± 3.4 mm Hg (mean ± standard error of the mean)) always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0° head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.

Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood

1976 ◽  
Vol 44 (3) ◽  
pp. 353-358 ◽  
Author(s):  
Albert N. Martins ◽  
Norwyn Newby ◽  
Thomas F. Doyle ◽  
Arthur I. Kobrine ◽  
Archimedes Ramirez
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Subarachnoid Injection ◽  
Ischemic Encephalopathy ◽  
Hydrogen Clearance

✓ The hydrogen clearance method was used to measure total and focal cerebral blood flow (CBF) in the monkey before and for 5 hours after a simulated subarachnoid hemorrhage (SAH). Some monkeys also received 0.2 to 1.0 mg/kg phentolamine intracisternally 3 hours after SAH. Results show that SAH did not change cerebrovascular resistance, but as cerebral perfusion pressure decreased, CBF fell transiently. Phentolamine injected intracisternally 3 hours after SAH produced a significant fall in arterial blood pressure; cerebrovascular resistance did not change but CBF decreased significantly. These data indicate that intracisternal phentolamine cannot be considered potentially useful to treat ischemic encephalopathy after SAH.

Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: a microdialysis study

1998 ◽  
Vol 89 (6) ◽  
pp. 971-982 ◽  
Author(s):  
Paul Vespa ◽  
Mayumi Prins ◽  
Elizabeth Ronne-Engstrom ◽  
Michael Caron ◽  
Ehud Shalmon ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebral Microdialysis ◽  
Extracellular Glutamate ◽  
Content Type ◽  
The Mean ◽  
Fine Print

Object. To determine the extent and duration of change in extracellular glutamate levels after human traumatic brain injury (TBI), 17 severely brain injured adults underwent implantation of a cerebral microdialysis probe and systematic sampling was conducted for 1 to 9 days postinjury. Methods. A total of 772 hourly microdialysis samples were obtained in 17 patients (median Glasgow Coma Scale score 5 ± 2.5, mean age 39.4 ± 20.4 years). The mean (± standard deviation) glutamate levels in the dialysate were evaluated for 9 days, during which the mean peak concentration reached 25.4 ± 13.7 (µM on postinjury Day 3. In each patient transient elevations in glutamate were seen each day. However, these elevations were most commonly seen on Day 3. In all patients there was a mean of 4.5 ± 2.5 transient elevations in glutamate lasting a mean duration of 4.4 ± 4.9 hours. These increases were seen in conjunction with seizure activity. However, in many seizure-free patients the increase in extracellular glutamate occurred when cerebral perfusion pressure was less than 70 mm Hg (p < 0.001). Given the potential injury-induced uncoupling of cerebral blood flow and metabolism after TBI, these increases in extracellular glutamate may reflect a degree of enhanced cellular crisis, which in severe head injury in humans appears to last up to 9 days. Conclusions. Extracellular neurochemical measurements of excitatory amino acids may provide a marker for secondary insults that can compound human TBI.

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