Hypoxia, Hypocapnia and Spirometry at Altitude

1997 ◽  
Vol 92 (6) ◽  
pp. 593-598 ◽  
Author(s):  
Andrew J. Pollard ◽  
Peter W. Barry ◽  
Nick P. Mason ◽  
David J. Collier ◽  
Rachel C. Pollard ◽  
...  

1. Both hypoxia and hypocapnia can cause broncho-constriction in humans, and this could have a bearing on performance at high altitude or contribute to altitude sickness. We studied the relationship between spirometry, arterial oxygen saturation and end-tidal carbon dioxide (ETCO2) concentration in a group of healthy lowland adults during a stay at high altitude, and then evaluated the response to supplementary oxygen and administration of a β2 agonist 2. We collected spirometric data from 51 members of the 1994 British Mount Everest Medical Expedition at sea level (barometric pressure 101.2–101.6 kPa) and at Mount Everest Base Camp in Nepal (altitude 5300 m, barometric pressure 53–54.7 kPa) using a pocket turbine spirometer. A total of 205 spirometric measurements were made on the 51 subjects during the first 6 days after arrival at Base Camp. Further measurements were made before and after inhalation of oxygen (n = 47) or a β2 agonist (n = 39). ETCO2 tensions were measured on the same day as spirometric measurements in 30 of these subjects. 3. In the first 6 days after arrival at 5300 m, lower oxygen saturations were associated with lower forced expiratory volume in 1 s (FEV1; P < 0.02) and forced vital capacity (FVC; P < 0.01), but not with peak expiratory flow (PEF). Administration of supplementary oxygen for 5 min increased oxygen saturation from a mean of 81%–94%, but there was no significant change in FEV1 or FVC, whilst PEF fell by 2.3% [P < 0.001; 95% confidence intervals (CI) −4 to −0.7%]. After salbutamol administration, there was no significant change in PEF, FEV1 or FVC in 35 non-asthmatic subjects. Mean ETCO2 at Everest Base Camp was 26 mmHg, and a low ETCO2 was weakly associated with a larger drop in FVC at altitude compared with sea level (r = 0.38, P < 0.05). There was no correlation between either ETCO2 or oxygen saturation and changes in FEV1 or PEF compared with sea-level values. 4. In this study, in normal subjects who were acclimatized to hypobaric hypoxia at an altitude of 5300 m, we found no evidence of hypoxic broncho-constriction. Individuals did not have lower PEF when they were more hypoxic, and neither PEF nor FEV1 were increased by either supplementary oxygen or salbutamol. FVC fell at altitude, and there was a greater fall in FVC for subjects with lower oxygen saturations and probably lower ETCO2.

2012 ◽  
Vol 112 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Claire de Bisschop ◽  
Jean-Benoit Martinot ◽  
Gil Leurquin-Sterk ◽  
Vitalie Faoro ◽  
Hervé Guénard ◽  
...  

Lung diffusing capacity has been reported variably in high-altitude newcomers and may be in relation to different pulmonary vascular resistance (PVR). Twenty-two healthy volunteers were investigated at sea level and at 5,050 m before and after random double-blind intake of the endothelin A receptor blocker sitaxsentan (100 mg/day) vs. a placebo during 1 wk. PVR was estimated by Doppler echocardiography, and exercise capacity by maximal oxygen uptake (V̇o2 max). The diffusing capacities for nitric oxide (DLNO) and carbon monoxide (DLCO) were measured using a single-breath method before and 30 min after maximal exercise. The membrane component of DLCO (Dm) and capillary volume (Vc) was calculated with corrections for hemoglobin, alveolar volume, and barometric pressure. Altitude exposure was associated with unchanged DLCO, DLNO, and Dm but a slight decrease in Vc. Exercise at altitude decreased DLNO and Dm. Sitaxsentan intake improved V̇o2 max together with an increase in resting and postexercise DLNO and Dm. Sitaxsentan-induced decrease in PVR was inversely correlated to DLNO. Both DLCO and DLNO were correlated to V̇o2 max at sea level ( r = 0.41–0.42, P < 0.1) and more so at altitude ( r = 0.56–0.59, P < 0.05). Pharmacological pulmonary vasodilation improves the membrane component of lung diffusion in high-altitude newcomers, which may contribute to exercise capacity.


Author(s):  
Praveen S ◽  
Waris A

Retinopathy of prematurity (ROP) is an abnormal vascular proliferative disease of retina that affects preterm infants. It is a leading cause of childhood blindness worldwide despite improvement in neonatal care and management. Earlier ROP was found to be associated with oxygen therapy only. Now it was concluded that aetiology of ROP was multifactorial but three factors have shown significant association with ROP: low gestational age (GA), low birth weight (BW), prolonged exposure to supplementary oxygen following delivery. Several investigators reported that lower oxygen saturation targets at young post-gestational ages with increased oxygen saturation targets at older post gestational ages reduced the incidence of ROP. However previous clinical studies are not conclusive.


2000 ◽  
Vol 6 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Mary F. Shackelton ◽  
Christina M. Tondora ◽  
Susan Whiting ◽  
Michael Whitney

Homeopathic coca was tested among high altitude trekkers en route to the Mt. Everest base camp to determine its effect on mountain sickness symptoms. Study participants ( n = 24) took homeopathic coca while ascending from 8,000 ft. to 17,600 ft. Measurements included: heart rate, oxygen saturation, and a question naire detailing the occurrence and severity of symptoms. Questionnaire items regarding nausea, headaches, difficulty breathing while asleep all demonstrated statistical significance in the experimental group. Oxygen saturation in the exper imental group was significantly higher. In this placebo-controlled, single-blinded, non-randomized study, homeopathic coca significantly reduced the effects of altitude on trekkers in the experimental group when compared with placebo.


1989 ◽  
Vol 67 (1) ◽  
pp. 141-146 ◽  
Author(s):  
P. Bouissou ◽  
J. P. Richalet ◽  
F. X. Galen ◽  
M. Lartigue ◽  
P. Larmignat ◽  
...  

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R H Boeger ◽  
P Siques ◽  
J Brito ◽  
E Schwedhelm ◽  
E Pena ◽  
...  

Abstract Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) is an important regulator of systemic and pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis that increases in hypoxia, we aimed to investigate whether ADMA predicts the incidence of HAPH among Chilean frontiers personnel exposed to six months of CIH. We performed a prospective study of 123 healthy male subjects who were subjected to CIH (5 days at appr. 3,550 m, followed by 2 days at sea level) for six months. ADMA, SDMA, L-arginine, arterial oxygen saturation, systemic arterial blood pressure, and haematocrit were measured at baseline and at months 1, 4, and 6 at high altitude. Acclimatization to high altitude was determined using the Lake Louise Score and the presence of acute mountain sickness (AMS). Echocardiography was performed after six months of CIH in a subgroup of 43 individuals with either good (n=23) or poor (n=20) aclimatization to altitude, respectively. Logistic regression was used to assess the association of biomarkers with HAPH. 100 study participants aged 18.3±1.3 years with complete data sets were included in the final analysis. Arterial oxygen saturation decreased upon the first ascent to altitude and plateaued at about 90% during the further course of the study. Haematocrit increased to about 47% after one month and remained stable thereafter. ADMA continuously increased and SDMA decreased during the study course, whilst L-arginine levels showed no distinct pattern. The incidence of AMS and the Lake Louise Score were high after the first ascent (53 and 3.1±2.4, respectively) and at one month of CIH (47 and 3.0±2.6, respectively), but decreased to 20 and 1.4±2.0 at month 6, respectively (both p<0.001 for trend). In echocardiography, 18 participants (42%) showed a mean pulmonary arterial pressure (mPAP) greater than 25 mm Hg (mean ± SD, 30.4±3.9 mm Hg), out of which 9 (21%) were classified as HAPH (mPAP ≥30 mm Hg; mean ± SD, 33.9±2.2 mm Hg). Baseline ADMA, but not SDMA, was significantly associated with mPAP at month 6 in univariate logistic regression analysis (R = 0.413; p=0.007). In ROC analysis, a cut-off for baseline ADMA of 0.665 μmol/l was determined as the optimal cut-off level to predict HAPH (mPAP >30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. ADMA concentration increases during long-term CIH. It is an independent predictive biomarker for the incidence of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of high altitude pulmonary hypertension. Acknowledgement/Funding CONICYT/FONDEF/FONIS Sa 09I20007; FIC Tarapaca BIP 30477541-0; BMBF grant 01DN17046 (DECIPHER); Georg & Jürgen Rickertsen Foundation, Hamburg


1982 ◽  
Vol 100 (1) ◽  
pp. 147-157
Author(s):  
J B West

Hyperventilation is one of the most important features of acclimatization to high altitude. Resting ventilation at extreme altitudes increases up to fourfold and exercise ventilation for a given work level increases to the same extent. Hypoxic stimulation of the peripheral chemoreceptors is the chief mechanism for the hyperventilation but there is also evidence that central sensitization of the respiratory centres occurs. Permanent residents of high altitude have a blunted hypoxic ventilatory response compared to acclimatized lowlanders. Cardiac output increases in responses to acute hypoxia but returns to normal in acclimatized lowlanders. Oxygen uptake at extreme altitudes is markedly limited by the diffusion properties of the blood gas barrier. As a consequence the maximal oxygen consumption of a climber near the summit of Mount Everest is near his basal oxygen requirements. Maximal oxygen consumption is so sensitive to barometric pressure that it may be that day-to-day variations will affect the chances of a climber reaching the summit without supplementary oxygen.


1985 ◽  
Vol 58 (3) ◽  
pp. 978-988 ◽  
Author(s):  
G. E. Gale ◽  
J. R. Torre-Bueno ◽  
R. E. Moon ◽  
H. A. Saltzman ◽  
P. D. Wagner

To investigate the effects of both exercise and acute exposure to high altitude on ventilation-perfusion (VA/Q) relationships in the lungs, nine young men were studied at rest and at up to three different levels of exercise on a bicycle ergometer. Altitude was simulated in a hypobaric chamber with measurements made at sea level (mean barometric pressure = 755 Torr) and at simulated altitudes of 5,000 (632 Torr), 10,000 (523 Torr), and 15,000 ft (429 Torr). VA/Q distributions were estimated using the multiple inert gas elimination technique. Dispersion of the distributions of blood flow and ventilation were evaluated by both loge standard deviations (derived from the VA/Q 50-compartment lung model) and three new indices of dispersion that are derived directly from inert gas data. Both methods indicated a broadening of the distributions of blood flow and ventilation with increasing exercise at sea level, but the trend was of borderline statistical significance. There was no change in the resting distributions with altitude. However, with exercise at high altitude (10,000 and 15,000 ft) there was a significant increase in dispersion of blood flow (P less than 0.05) which implies an increase in intraregional inhomogeneity that more than counteracts the more uniform topographical distribution that occurs. Since breathing 100% O2 at 15,000 ft abolished the increased dispersion, the greater VA/Q mismatching seen during exercise at altitude may be related to pulmonary hypertension.


2018 ◽  
Vol 64 (1) ◽  
pp. 30-34
Author(s):  
Shahzaib Rehan ◽  
Harvey J Pynn ◽  
Ian Williams ◽  
Daniel S Morris

The effects of high altitude on the human vascular system are well described. This case demonstrates an interesting combination of vascular complications at high altitude which were both life- and sight-threatening. In May 2017, during an attempt on Mount Everest, a 58-year-old man was forced to descend from 8000 m because of adverse weather. He suffered significant frostbite of his right hand, later requiring termination of the distal phalanx of one of the affected digits. He also experienced increasing breathlessness and went on to develop pleuritic chest pain. A CT pulmonary angiogram performed upon return to sea level revealed multiple small sub-segmental pulmonary emboli. He was anticoagulated for three months and made a full recovery. The patient also reported visual loss in the left eye and on ophthalmic examination was found to have multiple retinal haemorrhages including a left macular haemorrhage, consistent with high altitude retinopathy. The retinal haemorrhages settled with conservative management. The vascular complications suffered by this patient demonstrate the potentially fatal changes that can occur at altitude. They also serve to act as a reminder for physicians, even at sea level of the potential complications in patients returning from high altitude.


2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P54-P54
Author(s):  
Axel Rolf Behnisch ◽  
Gerd Rasp ◽  
Klaus Mees

Objective The aim of this study was to measure DPOAEs in climbers on Mount Everest as a criterion for differential diagnosis of high altitude disease. The levels of distortion product otoacoustic emissions (DPOAEs) change at frequencies between 0,75 kHz and 1,5 kH along with intracranial pressure (ICP). DPOAEs are suggested for monitoring ICP changes. Methods In order to determine the etiology of DPOAE-level changes obtained in 6 climbers with severe acute mountain sickness, blood oxygen saturation was measured simultaneously, and a standard request form of Lake-Louis symptoms of high altitude disease was filled in with every DPOAE measurement. Data are presented from DPOAE measurements at frequencies of 1, 1.5, 2, 3 and 4 kHz during an ascent to Mount Everest (8848 m) up to an altitude of 7800 m. Results In all climbers, DPOA levels decreased at 4 kHz and 3 kHz with declining oxygen saturation (SaO2) at high altitude. That has been described in many prior animal studies. On the other hand, DPOAE at 1 kHz showed decreasing levels only with symptoms of high altitude disease (AMS). In one climber with severe symptoms of intracranial hypertension after the ascent to the high camp at 7800 m, decreasing DPOAE levels at 1 kHz were measured in the absence of declining blood oxygen saturation. The most pronounced decline of DPOAEs at 1 kHz was also seen on that occasion. Conclusions DPOAEs are suggested for detection of intracranial hypertension and early detection of high-altitude cerebral edema.


Sign in / Sign up

Export Citation Format

Share Document