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.

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.

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.

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.

Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury

1985 ◽  
Vol 63 (1) ◽  
pp. 43-48 ◽  
Author(s):  
A. David Mendelow ◽  
Graham M. Teasdale ◽  
Thomas Russell ◽  
John Flood ◽  
James Patterson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Neuronal Damage ◽  
Content Type ◽  
Made In

✓ Patients with severe head injury frequently have evidence of elevated intracranial pressure (ICP) and ischemic neuronal damage at autopsy. Mannitol has been used clinically to reduce ICP with varying success, and it is possible that it is more effective in some types of head injury than in others. The aim of the present study was to determine the effect of mannitol on ICP, cerebral perfusion pressure (CPP), and cerebral blood flow (CBF) in patients with severe head injury, and to discover if these effects differed in different types of injury. Measurements of CPP, ICP, and CBF were made in 55 patients with severe head injury. In general, the resting level of CBF was higher in patients with diffuse injury (mean 50.2 ml/100 gm/min) than in those with focal injury (mean 39.8 ml/100 gm/min). Mannitol consistently reduced ICP and increased CPP and CBF by 10 to 20 minutes after infusion. The lowest flows (31.8 ml/100 gm/min) were recorded from the most damaged hemispheres of patients with focal injuries and elevated ICP. The baseline levels of flow did not correlate with ICP, CPP, Glasgow Coma Scale score, or outcome. Only four of the 55 patients had a CBF of less than 20 ml/100 gm/min in either or both hemispheres. The few low CBF's in this and other studies may reflect the steady-state conditions under which measurements are made in intensive care units, and that these patients have entered a phase of reperfusion.

Cerebral blood flow regulation during experimental brain compression

1973 ◽  
Vol 39 (2) ◽  
pp. 186-196 ◽  
Author(s):  
J. Douglas Miller ◽  
Albert E. Stanek ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Brain Compression

✓ The effect of brain compression on cerebral blood flow was measured in 13 anesthetized, ventilated dogs by inflation of extradural balloons. The effects of the raised intracranial pressure, so produced, were correlated with the presence or absence of autoregulation of cerebral blood flow to induced changes of arterial pressure, which was tested immediately prior to each episode of inflation of the balloon. Cerebral blood flow was measured by a venous outflow method and monitored continuously, together with arterial and supratentorial intracranial pressure; arterial pCO2 and body temperature were held constant. Three stages were identified. When autoregulation to a change of arterial pressure was intact, initial inflation of the balloon did not reduce cerebral blood flow until the difference between arterial and intracranial pressure (which was taken to represent cerebral perfusion pressure) was less than 40 mm Hg. When autoregulation was impaired, which occurred after the first inflation of the balloon or was due to preceding arterial hypotension, raised intracranial pressure caused an immediate reduction of cerebral blood flow. At this stage of impaired autoregulation there was a tendency for hyperemia to develop on deflation of the balloon. Finally, after repeated inflation and deflation of the balloon, when brain swelling supervened, cerebral blood flow decreased steadily and failed to increase despite induced increases of arterial pressure and cerebral perfusion pressure.

Effects of graded hypotension on cerebral blood flow, blood volume, and mean transit time in dogs

1992 ◽  
Vol 262 (6) ◽  
pp. H1908-H1914 ◽  
Author(s):  
M. Ferrari ◽  
D. A. Wilson ◽  
D. F. Hanley ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Transit Time ◽  
Cerebral Perfusion ◽  
Pressure Range ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Mean Transit Time

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.

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.

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