scholarly journals Early brain swelling in acute hypoxia

2009 ◽  
Vol 107 (1) ◽  
pp. 244-252 ◽  
Author(s):  
David J. Dubowitz ◽  
Edward A. W. Dyer ◽  
Rebecca J. Theilmann ◽  
Richard B. Buxton ◽  
Susan R. Hopkins
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Acute Phase ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Brain Parenchyma ◽  
Phase Changes ◽  
Brain Swelling ◽  
Significant Difference

Acute mountain sickness (AMS) and high-altitude cerebral edema share common clinical characteristics, suggesting cerebral swelling may be an important factor in the pathophysiology of AMS. Hypoxia and hypocapnia associated with high altitude are known to exert strong effects on the control of the cerebral circulation, yet how these effects interact during acute hypoxia, and whether AMS-susceptible subjects may have a unique response, is still unclear. To test if self-identified AMS-susceptible individuals show altered brain swelling in response to acute hypoxia, we used quantitative arterial spin-labeling and volumetric MRI to measure cerebral blood flow and cerebrospinal fluid (CSF) volume changes during 40 min of acute hypoxia. We estimated changes in cerebral blood volume (CBV) (from changes in cerebral blood flow) and brain parenchyma swelling (from changes in CBV and CSF). Subjects with extensive high-altitude experience in two groups participated: self-identified AMS-susceptible ( n = 6), who invariably experienced AMS at altitude, and self-identified AMS-resistant ( n = 6), who almost never experienced symptoms. During 40-min hypoxia, intracranial CSF volume decreased significantly [−10.5 ml (SD 6.9), P < 0.001]. There were significant increases in CBV [+2.3 ml (SD 2.5), P < 0.005] and brain parenchyma volume [+8.2 ml (SD 6.4), P < 0.001]. However, there was no significant difference between self-identified AMS-susceptible and AMS-resistant groups for these acute-phase changes. In acute hypoxia, brain swelling occurs earlier than previously described, with significant shifts in intracranial CSF occurring as early as 40 min after exposure. These acute-phase changes are present in all individuals, irrespective of susceptibility to AMS.

scholarly journals Sustained high-altitude hypoxia increases cerebral oxygen metabolism

2013 ◽  
Vol 114 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Jia Guo ◽  
David D. Shin ◽  
Miriam Scadeng ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Altitude Hypoxia ◽  
Cerebral Oxygen Metabolism ◽  
High Altitude Hypoxia ◽  
Significant Difference

Acute mountain sickness (AMS) is a common condition occurring within hours of rapid exposure to high altitude. Despite its frequent occurrence, the pathophysiological mechanisms that underlie the condition remain poorly understood. We investigated the role of cerebral oxygen metabolism (CMRO2) in AMS. The purpose of this study was to test 1) if CMRO2 changes in response to hypoxia, and 2) if there is a difference in how individuals adapt to oxygen metabolic changes that may determine who develops AMS and who does not. Twenty-six normal human subjects were recruited into two groups based on Lake Louise AMS score (LLS): those with no AMS (LLS ≤ 2), and those with unambiguous AMS (LLS ≥ 5). [Subjects with intermediate scores (LLS 3–4) were not included.] CMRO2 was calculated from cerebral blood flow and arterial-venous difference in O2 content. Cerebral blood flow was measured using arterial spin labeling MRI; venous O2 saturation was calculated from the MRI of transverse relaxation in the superior sagittal sinus. Arterial O2 saturation was measured via pulse oximeter. Measurements were made during normoxia and after 2-day high-altitude exposure at 3,800 m. In all subjects, CMRO2 increased with sustained high-altitude hypoxia [1.54 (0.37) to 1.82 (0.49) μmol·g−1·min−1, n = 26, P = 0.045]. There was no significant difference in CMRO2 between AMS and no-AMS groups. End-tidal Pco2 was significantly reduced during hypoxia. Low arterial Pco2 is known to increase neural excitability, and we hypothesize that the low arterial Pco2 resulting from ventilatory acclimatization causes the observed increase in CMRO2.

scholarly journals Regional cerebral blood flow during acute hypoxia in individuals susceptible to acute mountain sickness

2008 ◽  
Vol 160 (3) ◽  
pp. 267-276 ◽  
Author(s):  
Edward A.W. Dyer ◽  
Susan R. Hopkins ◽  
Joanna E. Perthen ◽  
Richard B. Buxton ◽  
David J. Dubowitz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Regional Cerebral Blood ◽  
Mountain Sickness

New insights into ocular blood flow at very high altitudes

2009 ◽  
Vol 106 (2) ◽  
pp. 454-460 ◽  
Author(s):  
Martina M. Bosch ◽  
Tobias M. Merz ◽  
Daniel Barthelmes ◽  
Benno L. Petrig ◽  
Frederic Truffer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Edema ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Fundus Photography ◽  
Arterial Oxygen ◽  
High Altitudes ◽  
Choroidal Blood Flow

Little is known about the ocular and cerebral blood flow during exposure to increasingly hypoxic conditions at high altitudes. There is evidence that an increase in cerebral blood flow resulting from altered autoregulation constitutes a risk factor for acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) by leading to capillary overperfusion and vasogenic cerebral edema. The retina represents the only part of the central nervous system where capillary blood flow is visible and can be measured by noninvasive means. In this study we aimed to gain insights into retinal and choroidal autoregulatory properties during hypoxia and to correlate circulatory changes to symptoms of AMS and clinical signs of HACE. This observational study was performed within the scope of a high-altitude medical research expedition to Mount Muztagh Ata (7,546 m). Twenty seven participants underwent general and ophthalmic examinations up to a maximal height of 6,800 m. Examinations included fundus photography and measurements of retinal and choroidal blood flow, as well as measurement of arterial oxygen saturation and hematocrit. The initial increase in retinal blood velocity was followed by a decrease despite further ascent, whereas choroidal flow increase occurred later, at even higher altitudes. The sum of all adaptational mechanisms resulted in a stable oxygen delivery to the retina and the choroid. Parameters reflecting the retinal circulation and optic disc swelling correlated well with the occurrence of AMS-related symptoms. We demonstrate that sojourns at high altitudes trigger distinct behavior of retinal and choroidal blood flow. Increase in retinal but not in choroidal blood flow correlated with the occurrence of AMS-related symptoms.

scholarly journals Acupuncture Effects on Cerebral Blood Flow during Normoxia and Normobaric Hypoxia: Results from a Prospective Crossover Pilot Study

Technologies ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 102
Author(s):  
Oriana Pecchio ◽  
Massimo Martinelli ◽  
Giuseppe Lupi ◽  
Guido Giardini ◽  
Laura Caligiana ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Cerebrovascular Disorders ◽  
Sham Acupuncture ◽  
Normobaric Hypoxia ◽  
Acupuncture Points ◽  
Diastolic Velocity ◽  
Fraction Of Inspired Oxygen

Cerebral blood flow (CBF) is significantly influenced by exposure to hypoxia, both hypobaric and normobaric. Alterations in cerebral blood flow can play a crucial role in the pathogenesis of acute mountain sickness (AMS) and its symptoms, especially headache, dizziness, and nausea. Acupuncture has been proven to be effective in treating some cerebrovascular disorders and PC6 Nei Guan stimulation seems to enhance cerebral blood flow. Therefore, we have hypothesized that PC6 Nei Guan stimulation could affect CBF in acute hypoxia and could be used to contrast AMS symptoms. We evaluated blood flow in the middle cerebral artery (MCA) in normoxia, after 15 min in normobaric hypoxia (fraction of inspired oxygen (FiO2) 14%, corresponding to 3600 m a.s.l.) in basal conditions, and after PC6 Nei Guan stimulation, both by needle and by pressure. No comparisons with other acupuncture points and sham acupuncture were done. PC6 stimulation seemed to counteract the effects of acute normobaric hypoxia on end-diastolic velocity (EDV) in MCA, especially after acupuncture, and significantly reduced systolic and diastolic blood pressure. A rebalance of CBF could control some AMS symptoms, but further studies are necessary.

Effect of magnesium, high altitude and acute mountain sickness on blood flow velocity in the middle cerebral artery

2004 ◽  
Vol 106 (3) ◽  
pp. 279-285 ◽  
Author(s):  
Christopher LYSAKOWSKI ◽  
Erik VON ELM ◽  
Lionel DUMONT ◽  
Jean-Daniel JUNOD ◽  
Edömer TASSONYI ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
High Altitude ◽  
Blood Flow Velocity ◽  
Rescue Medication ◽  
Acute Mountain Sickness ◽  
Median Score ◽  
Magnesium Supplementation ◽  
Mountain Sickness

Cerebral blood flow is thought to increase at high altitude and in subjects suffering from acute mountain sickness (AMS); however, data from the literature are contentious. Blood flow velocity in the middle cerebral artery (MCAv) may be used as a proxy measure of cerebral blood flow. Using transcranial Doppler sonography, MCAv was measured during normo- and hyper-ventilation in subjects who participated in a trial that tested the effect of magnesium supplementation on the prevention of AMS. First, MCAv was recorded at 353 m (baseline). Subjects were then randomized to receive oral magnesium citrate and matching placebo. A second measurement was taken after a 24±2 h ascent from 1130 m to 4559 m (altitude I), and a third after a 20–24 h stay at 4559 m (altitude II). Using multivariate linear regression, an association was sought between MCAv and magnesium supplementation, subjects′ age and gender, altitude itself, a temporary stay at altitude, and the presence of AMS (Lake Louise Score >6 with ataxia, nausea and/or headache). Subjects with AMS had additional Doppler recordings immediately before and after rescue medication (oxygen, dexamethasone and acetazolamide). Forty-seven subjects had measurements at baseline, 39 (21 receiving magnesium and 18 placebo) at altitude I and 26 (13 receiving magnesium and 13 placebo) at altitude II. During hyperventilation, MCAv decreased consistently (for each measurement, P<0.001). Magnesium significantly increased MCAv by 8.4 cm·s-1 (95% confidence interval, 1.8–15), but did not prevent AMS. No other factors were associated with MCAv. Eleven subjects had severe AMS [median score (range), 11 (8–16)] and, after rescue medication, the median score decreased to 3 (range, 0–5; P=0.001), but MCAv remained unchanged (65±18 cm·s-1 before compared with 67±16 cm·s-1 after rescue medication; P=0.79). MCAv was increased in subjects who received magnesium, but was not affected by exposure to high altitude or by severe AMS.

Relationship of cerebral blood flow regulation to acute mountain sickness.

1989 ◽  
Vol 8 (3) ◽  
pp. 143-148 ◽  
Author(s):  
S M Otis ◽  
M E Rossman ◽  
P A Schneider ◽  
M P Rush ◽  
E B Ringelstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Flow Regulation ◽  
Blood Flow Regulation ◽  
Mountain Sickness ◽  
Relationship Of

scholarly journals Effect of acute hypoxia on regional cerebral blood flow: effect of sympathetic nerve activity

2014 ◽  
Vol 116 (9) ◽  
pp. 1189-1196 ◽  
Author(s):  
Nia C. S. Lewis ◽  
Laura Messinger ◽  
Brad Monteleone ◽  
Philip N. Ainslie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sympathetic Nerve ◽  
Regional Difference ◽  
Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Adrenergic Blockade ◽  
Percentage Increase ◽  
Nerve Activity ◽  
Global Cerebral Blood Flow

We examined 1) whether global cerebral blood flow (CBF) would increase across a 6-h bout of normobaric poikilocapnic hypoxia and be mediated by a larger increase in blood flow in the vertebral artery (VA) than in the internal carotid artery (ICA); and 2) whether additional increases in global CBF would be evident following an α1-adrenergic blockade via further dilation of the ICA and VA. In 11 young normotensive individuals, ultrasound measures of ICA and VA flow were obtained in normoxia (baseline) and following 60, 210, and 330 min of hypoxia (FiO2 = 0.11). Ninety minutes prior to final assessment, participants received an α1-adrenoreceptor blocker (prazosin, 1 mg/20 kg body mass) or placebo. Compared with baseline, following 60, 220, and 330 min of hypoxia, global CBF [(ICAFlow + VAFlow) ∗ 2] increased by 160 ± 52 ml/min (+28%; P = 0.05), 134 ± 23 ml/min (+23%; P = 0.02), and 113 ± 51 (+19%; P = 0.27), respectively. Compared with baseline, ICAFlow increased by 23% following 60 min of hypoxia ( P = 0.06), after which it progressively declined. The percentage increase in VA flow was consistently larger than ICA flow during hypoxia by ∼20% ( P = 0.002). Compared with baseline, ICA and VA diameters increased during hypoxia by ∼9% and ∼12%, respectively ( P ≤ 0.05), and were correlated with reductions in SaO2. Flow and diameters were unaltered following α1 blockade ( P ≥ 0.10). In conclusion, elevations in global CBF during acute hypoxia are partly mediated via greater increases in VA flow compared with ICA flow; this regional difference was unaltered following α1 blockade, indicating that a heightened sympathetic nerve activity with hypoxia does not constrain further dilation of larger extracranial blood vessels.

Physiology in Medicine: A physiologic approach to prevention and treatment of acute high-altitude illnesses

2015 ◽  
Vol 118 (5) ◽  
pp. 509-519 ◽  
Author(s):  
Andrew M. Luks
Keyword(s):  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Travel Medicine ◽  
Barometric Pressure ◽  
Time Frame ◽  
Low Oxygen ◽  
Organ Systems ◽  
Prevention And Treatment ◽  
Physiologic Responses

With the growing interest in adventure travel and the increasing ease and affordability of air, rail, and road-based transportation, increasing numbers of individuals are traveling to high altitude. The decline in barometric pressure and ambient oxygen tensions in this environment trigger a series of physiologic responses across organ systems and over a varying time frame that help the individual acclimatize to the low oxygen conditions but occasionally lead to maladaptive responses and one or several forms of acute altitude illness. The goal of this Physiology in Medicine article is to provide information that providers can use when counseling patients who present to primary care or travel medicine clinics seeking advice about how to prevent these problems. After discussing the primary physiologic responses to acute hypoxia from the organ to the molecular level in normal individuals, the review describes the main forms of acute altitude illness—acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema—and the basic approaches to their prevention and treatment of these problems, with an emphasis throughout on the physiologic basis for the development of these illnesses and their management.

Sign in / Sign up

Export Citation Format

Share Document