scholarly journals About interrelation of intracranial pressure and cerebral blood flow when positioning at patients with acute brain damage

2019 ◽  
Vol 18 (4) ◽  
pp. 4-10
Author(s):  
V. I. Gorbachev ◽  
N. V. Bragina ◽  
S. V. Gorbachev
Keyword(s):  
Blood Flow ◽  
Intensive Care ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Damage ◽  
Perfusion Pressure ◽  
Body Position ◽  
Slope Angle ◽  
Cerebral Damage ◽  
Bed Position

Changing of «head – of – the bed» position is a routine method of positioning the patient to correct intracranial hypertension. In intensive care units, the «head – of – the bed» position vary from 0 to 60 °, and there is no consensus on which of them is most effective. The review of the major publications in the domestic and foreign literature about the problem of interrelation between positioning and changes of intracranial pressure, system and cerebral hemodynamic in patients with brain damage including databases eLibrary, PubMed, with the key words «hyperthermia», « positioning», «slope angle of the head of bed», «intracranial pressure», «cerebral perfusion pressure», «cerebral blood flow», «brain damage», and their combination. It is believed that the majority of patients with cerebral damage, regardless of the etiological factor, is preferable to 15–30° «head – of – the bed» position. In some cases manipulation of the head of the bed can lead to irreversible ischemic damage, due to the reduction of system and perfusion pressure, and cerebral blood flow. Thus, the selection of the optimal body position in acute cerebral pathology remains a debated issue. In this way, individual tactics of positioning in patients with cerebral damage allows choosing the correct intensive care and improving the treatment results.

scholarly journals Cerebral Blood Flow in Patients with Intracranial Pressure Elevation due to Traumatic Brain Edema

1976 ◽  
Vol 3 (1) ◽  
pp. 35-37 ◽  
Author(s):  
W. A. Tweed ◽  
Jørn Overgaard
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Monitoring And Control ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
And Control

SUMMARY:The object of this study was to determine if traumatic brain edema (BE) and increased intracranial pressure (ICP) reduce cerebral blood flow (CBF). Two groups of patients were studied, one with slight BE and ICP less than 20 mm Hg., the other with pronounced BE and ICP over 20 mm Hg. Although ICP was higher and cerebral perfusion pressure lower in pro-nounced edema there was only a small and non-significant reduction in CBF and no difference in cerebro-vascular resistance. Since traumatic BE does not increase resistance to blood flow through the brain, cerebral perfusion can be maintained if an adequate perfusion pressure is established. This in turn, demands the monitoring and control of ICP.

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.

Experimental cerebral hemodynamics

1974 ◽  
Vol 41 (5) ◽  
pp. 597-606 ◽  
Author(s):  
Richard C. Dewey ◽  
Heinz P. Pieper ◽  
William E. Hunt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Brain Blood Flow ◽  
Vasomotor Tone ◽  
Vascular Bed ◽  
Critical Closing Pressure ◽  
Closing Pressure

✓ Application of Burton's concept of the critical closing pressure to experimental data on brain-blood flow in the monkey suggests that perfusion pressure, not vascular bed resistance, is the primary variable affecting cerebral blood flow. Perfusion pressure for the cerebral circulation is the mean arterial pressure minus the critical closing pressure (MAP — CCP). Vasomotor tone and intracranial pressure are the major determinants of the critical closing pressure. Changes in either of these variables, therefore, affect perfusion pressure and flow. Data on brain-blood flow at fixed vasomotor tone obtained over wide pressure ranges show little change in vascular bed resistance despite significant changes in flow. The diameter of resistance vessels probably does not change significantly throughout the normal physiological range of cerebral blood flow. The limits of the critical closing pressure in the anesthetized monkey are from 10 to 95 mm Hg. Using these limits, and beginning with the average values for MAP and CCP in 11 awake monkeys breathing room air, the authors present theoretical flow curves in response to changes in intracranial pressure and mean arterial pressure that closely approximate the data reported in man.

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