scholarly journals Direct Measurement of Intracranial Pressure in Hypobaric Hypoxia: Implications for Acute Mountain Sickness

2016 ◽  
Vol 27 (3) ◽  
pp. 430
Author(s):  
Justin Lawley ◽  
Louis Whitworth ◽  
Benjamin Levine
Keyword(s):  
Intracranial Pressure ◽  
Direct Measurement ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

Elevated plasma S100B levels in high altitude hypobaric hypoxia do not correlate with acute mountain sickness

2014 ◽  
Vol 36 (9) ◽  
pp. 779-785 ◽  
Author(s):  
Craig D. Winter ◽  
Timothy R. Whyte ◽  
John Cardinal ◽  
Stephen E. Rose ◽  
Peter K. O’Rourke ◽  
...  
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Elevated Plasma ◽  
Mountain Sickness

Intracranial Pressure, High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 88 (s32) ◽  
pp. 26P-26P
Author(s):  
AD Wright ◽  
CHE Imray ◽  
MSC Morrissey ◽  
RJ Marchbanks ◽  
AR Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

Intracranial Pressure at High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 89 (2) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. Wright ◽  
C. H. E. Imray ◽  
M. S. C. Morrissey ◽  
R. J. Marchbanks ◽  
A. R. Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Raised Intracranial Pressure ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Pressure Changes ◽  
Serial Measurements

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.

Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude

2011 ◽  
Vol 300 (2) ◽  
pp. R428-R436 ◽  
Author(s):  
Charles S. Fulco ◽  
Stephen R. Muza ◽  
Beth A. Beidleman ◽  
Robby Demes ◽  
Janet E. Staab ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Performance ◽  
Hypobaric Hypoxia ◽  
Sham Group ◽  
Acute Mountain Sickness ◽  
Time Trial ◽  
Normobaric Hypoxia ◽  
Performance Decrement ◽  
Mountain Sickness ◽  
End Tidal

There is an expectation that repeated daily exposures to normobaric hypoxia (NH) will induce ventilatory acclimatization and lessen acute mountain sickness (AMS) and the exercise performance decrement during subsequent hypobaric hypoxia (HH) exposure. However, this notion has not been tested objectively. Healthy, unacclimatized sea-level (SL) residents slept for 7.5 h each night for 7 consecutive nights in hypoxia rooms under NH [ n = 14, 24 ± 5 (SD) yr] or “sham” ( n = 9, 25 ± 6 yr) conditions. The ambient percent O2 for the NH group was progressively reduced by 0.3% [150 m equivalent (equiv)] each night from 16.2% (2,200 m equiv) on night 1 to 14.4% (3,100 m equiv) on night 7, while that for the ventilatory- and exercise-matched sham group remained at 20.9%. Beginning at 25 h after sham or NH treatment, all subjects ascended and lived for 5 days at HH (4,300 m). End-tidal Pco2, O2 saturation (SaO2), AMS, and heart rate were measured repeatedly during daytime rest, sleep, or exercise (11.3-km treadmill time trial). From pre- to posttreatment at SL, resting end-tidal Pco2 decreased ( P < 0.01) for the NH (from 39 ± 3 to 35 ± 3 mmHg), but not for the sham (from 39 ± 2 to 38 ± 3 mmHg), group. Throughout HH, only sleep SaO2 was higher (80 ± 1 vs. 76 ± 1%, P < 0.05) and only AMS upon awakening was lower (0.34 ± 0.12 vs. 0.83 ± 0.14, P < 0.02) in the NH than the sham group; no other between-group rest, sleep, or exercise differences were observed at HH. These results indicate that the ventilatory acclimatization induced by NH sleep was primarily expressed during HH sleep. Under HH conditions, the higher sleep SaO2 may have contributed to a lessening of AMS upon awakening but had no impact on AMS or exercise performance for the remainder of each day.

scholarly journals The cerebral venous system and hypoxia

2016 ◽  
Vol 120 (2) ◽  
pp. 244-250 ◽  
Author(s):  
Mark H. Wilson ◽  
Christopher H. E. Imray
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Venous Outflow ◽  
Edema Formation ◽  
Care Environment ◽  
Fluid Production ◽  
High Altitude Cerebral Edema ◽  
Blood Inflow ◽  
Mountain Sickness

Most hypobaric hypoxia studies have focused on oxygen delivery and therefore cerebral blood inflow. Few have studied venous outflow. However, the volume of blood entering and leaving the skull (∼700 ml/min) is considerably greater than cerebrospinal fluid production (0.35 ml/min) or edema formation rates and slight imbalances of in- and outflow have considerable effects on intracranial pressure. This dynamic phenomenon is not necessarily appreciated in the currently taught static “Monro-Kellie” doctrine, which forms the basis of the “Tight-Fit” hypothesis thought to underlie high altitude headache, acute mountain sickness, and high altitude cerebral edema. Investigating both sides of the cerebral circulation was an integral part of the 2007 Xtreme Everest Expedition. The results of the relevant studies performed as part of and subsequent to this expedition are reviewed here. The evidence from recent studies suggests a relative venous outflow insufficiency is an early step in the pathogenesis of high altitude headache. Translation of knowledge gained from high altitude studies is important. Many patients in a critical care environment develop hypoxemia akin to that of high altitude exposure. An inability to drain the hypoxemic induced increase in cerebral blood flow could be an underappreciated regulatory mechanism of intracranial pressure.

scholarly journals Evidence for cerebral edema, cerebral perfusion, and intracranial pressure elevations in acute mountain sickness

2016 ◽  
Vol 6 (3) ◽  
Author(s):  
Dana M. DiPasquale ◽  
Stephen R. Muza ◽  
Andrea M. Gunn ◽  
Zhi Li ◽  
Quan Zhang ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Edema ◽  
Cerebral Perfusion ◽  
Acute Mountain Sickness ◽  
Mountain Sickness
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