Effects of positive end-expiratory pressure on intracranial pressure in dogs with intracranial hypertension

1981 ◽  
Vol 55 (5) ◽  
pp. 704-707 ◽  
Author(s):  
Jon S. Huseby ◽  
John M. Luce ◽  
Jeffrey M. Cary ◽  
Edward G. Pavlin ◽  
John Butler
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Clinical Situation ◽  
Positive End Expiratory Pressure ◽  
Content Type ◽  
Neurosurgical Patients

✓ Positive end-expiratory pressure (PEEP) is used to improve oxygenation in patients with the adult respiratory distress syndrome. Nevertheless, this treatment may increase intracranial pressure (ICP) and be detrimental to certain neurosurgical patients. This clinical situation was simulated by administering PEEP to dogs with normal and elevated ICP. Increases in PEEP increased ICP in all animals. However, the presence of intracranial hypertension diminished the increase in ICP seen at a given level of PEEP. Cerebral perfusion pressure also fell less in the presence of intracranial hypertension than it did in its absence, although in the former situation cerebral perfusion pressure was at the lower limits of the range of cerebral autoregulation. These findings suggest that PEEP is no more detrimental to patients with elevated ICP than it is to patients whose ICP is normal, assuming that their cerebral autoregulation is not impaired.

Continuous monitoring of cerebral oxygenation in acute brain injury: injection of mannitol during hyperventilation

1990 ◽  
Vol 73 (5) ◽  
pp. 725-730 ◽  
Author(s):  
Julio Cruz ◽  
Michael E. Miner ◽  
Steven J. Allen ◽  
Wayne M. Alves ◽  
Thomas A. Gennarelli
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebral Oxygenation ◽  
Jugular Bulb ◽  
Oxyhemoglobin Saturation ◽  
Content Type ◽  
Closed Head Trauma

✓ Global cerebral oxygenation, perfusion pressure, and expired pCO2 were continuously monitored in 10 adults with acute severe closed head trauma. Cerebral oxygenation was monitored by fiberoptic catheter oximetry, which allowed simultaneous measurements of arterial and jugular bulb oxyhemoglobin saturation. Intracranial pressure levels over 20 mm Hg were recorded several times in all patients, in spite of sedation, muscle paralysis, and profound hyperventilation. Intracranial hypertension was frequently associated with oligemic cerebral hypoxia, identified as abnormally low jugular oxygen saturation in the presence of normal arterial oxygenation. Intracranial hypertension was then managed with intravenous administration of mannitol boluses, which yielded simultaneous decreases in intracranial pressure and increases in cerebral oxygenation to highly statistically significant levels. Monitoring cerebral oxygenation was clinically useful because it allowed identification of impaired cerebral oxygenation even when cerebral perfusion pressure was normal. It is therefore proposed as a new monitoring technique, to supplement conventional monitoring of cerebral perfusion pressure.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 318-322 ◽  
Author(s):  
Lawrence F. Marshall ◽  
David I. Graham ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.

Transcranial Doppler ultrasonography in raised intra-cranial pressure and in intracranial circulatory arrest

1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski
Keyword(s):  
Intracranial Pressure ◽  
Brain Death ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Transcranial Doppler ◽  
Cerebral Perfusion ◽  
Doppler Ultrasonography ◽  
Perfusion Pressure ◽  
Circulatory Arrest ◽  
Transcranial Doppler Ultrasonography

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.

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.

Effects of increased intracranial pressure on cerebral blood volume, blood flow, and oxygen utilization in monkeys

1975 ◽  
Vol 43 (4) ◽  
pp. 385-398 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
Michael E. Phelps ◽  
Robert A. Ratcheson
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Metabolic Rate ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Cerebral Perfusion ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Cerebral Metabolic Rate

✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulation was reached at a higher CPP (CPP ∼ 80 torr) than when an increase in ICP was employed (CPP ∼ 30 torr).

scholarly journals Comparison of static and dynamic cerebral autoregulation under anesthesia influence in a controlled animal model

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245291
Author(s):  
Alexander Ruesch ◽  
Deepshikha Acharya ◽  
Samantha Schmitt ◽  
Jason Yang ◽  
Matthew A. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Animal Model ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Phase Lag ◽  
Arterial Blood

The brain’s ability to maintain cerebral blood flow approximately constant despite cerebral perfusion pressure changes is known as cerebral autoregulation (CA) and is governed by vasoconstriction and vasodilation. Cerebral perfusion pressure is defined as the pressure gradient between arterial blood pressure and intracranial pressure. Measuring CA is a challenging task and has created a variety of evaluation methods, which are often categorized as static and dynamic CA assessments. Because CA is quantified as the performance of a regulatory system and no physical ground truth can be measured, conflicting results are reported. The conflict further arises from a lack of healthy volunteer data with respect to cerebral perfusion pressure measurements and the variety of diseases in which CA ability is impaired, including stroke, traumatic brain injury and hydrocephalus. To overcome these differences, we present a healthy non-human primate model in which we can control the ability to autoregulate blood flow through the type of anesthesia (isoflurane vs fentanyl). We show how three different assessment methods can be used to measure CA impairment, and how static and dynamic autoregulation compare under challenges in intracranial pressure and blood pressure. We reconstructed Lassen’s curve for two groups of anesthesia, where only the fentanyl anesthetized group yielded the canonical shape. Cerebral perfusion pressure allowed for the best distinction between the fentanyl and isoflurane anesthetized groups. The autoregulatory response time to induced oscillations in intracranial pressure and blood pressure, measured as the phase lag between intracranial pressure and blood pressure, was able to determine autoregulatory impairment in agreement with static autoregulation. Static and dynamic CA both show impairment in high dose isoflurane anesthesia, while low isoflurane in combination with fentanyl anesthesia maintains CA, offering a repeatable animal model for CA studies.

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.

Effects of nifedipine on intracranial pressure in neurosurgical patients with arterial hypertension

1988 ◽  
Vol 69 (2) ◽  
pp. 213-215 ◽  
Author(s):  
Akio Tateishi ◽  
Takanobu Sano ◽  
Hiroshi Takeshita ◽  
Toshihisa Suzuki ◽  
Hisao Tokuno
Keyword(s):  
Intracranial Pressure ◽  
Arterial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Neurological Signs ◽  
Arterial Blood ◽  
Neurosurgical Patients ◽  
The Mean ◽  
Made In

✓ The effects of nifedipine, 20 mg administered via a nasogastric tube, on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were examined. Nifedipine was administered to treat arterial hypertension (> 180 mm Hg, systolic). Ten measurements were made in eight patients with cerebrovascular disease or head trauma. The mean arterial blood pressure (MABP) and ICP were measured before and for 30 minutes after the administration of nifedipine. The MABP gradually decreased and reached its lowest value at approximately 10 minutes after initiation of nifedipine administration, and thereafter remained unchanged. The MABP decreased significantly from 128 ± 8 (mean ± standard deviation) to 109 ± 7 mm Hg, and the CPP decreased from 105 ± 11 to 84 ± 10 mm Hg. The ICP increased by 1 to 10 mm Hg in eight of 10 measurements, and the mean change of ICP from 19 ± 7 to 22 ± 6 mm Hg was statistically significant. These changes were not accompanied by alterations in neurological signs. The results suggest that enteral nifedipine produces a small but statistically significant increase in ICP. Accordingly, neurological signs must be closely observed to detect deterioration, which can be caused by an increase in ICP and/or a decrease in CPP.

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