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Eur Respir J 2002; 20:300-305
Copyright ©ERS Journals Ltd 2002

Effect of hypobaric hypoxia on blood gases in patients with restrictive lung disease

C.C. Christensen1,2,3, M.S. Ryg2,3, O. Kåre Refvem3 and O. Henning Skjønsberg1

1 Dept of Pulmonary Medicine, Ullevål Hospital, Oslo, 2 Institute of Aviation Medicine, Blindern, Oslo and 3 Glittreklinikken, Hakadal, Norway

CORRESPONDENCE: C.C. Christensen, Glittreklinikken, 1488, Hakadal, Norway. Fax: 47 67075344. E-mail: carl.christian.christensen@nih.no

Keywords: air travel, cabin pressure altitude, commercial aircraft, hypoxia, oxygen, restrictive lung disease

Received: March 7, 2001
Accepted December 12, 2001


   Abstract
TOP
 Abstract
Methods
 Results
 Discussion
 Acknowledgements
 References
 
Several publications have reported effects of hypobaric conditions in patients with chronic obstructive pulmonary disease. To the current authors' knowledge, similar studies concerning patients with restrictive lung disease have not been published.

The effect of simulated air travel in a hypobaric chamber on arterial blood gases, blood pressure, and cardiac frequency during rest and 20 W exercise, and the response to supplementary oxygen in 17 patients with chronic restrictive ventilatory impairment has been investigated.

Resting oxygen tension in arterial blood (Pa,O2) decreased from 10.4±1.6 kPa at sea level to 6.5±1.1 kPa at 2,438 m simulated altitude, and decreased further during light exercise in all patients (5.1±0.9 kPa). Pa,O2 at this altitude correlated positively with sea-level Pa,O2 and transfer factor of the lung for carbon monoxide (TL,CO), and negatively with carbon dioxide tension in arterial blood (Pa,CO2). Pa,O2 increased to acceptable levels with an O2 supply of 2 L·min–1 at rest and 4 L·min–1 during 20 W exercise.

In conclusion, most of the patients with restrictive ventilatory impairment developed hypoxaemia below the recommended levels of in-flight oxygen tension in arterial blood during simulated air travel. Light exercise aggravated the hypoxaemia. Acceptable levels of oxygen tension in arterial blood, with only a minor increase in carbon dioxide tension in arterial blood, were obtained by supplementary oxygen.

Federal aviation regulations specify rules for commercial aircraft of a maximal cabin altitude of 2,438 m (8,000 feet) in order to avoid hypoxaemia in crew and passengers 1, 2. The oxygen saturation (Sa,O2) in healthy subjects will exceed 90% at this cabin altitude and only a slight reduction in mental performance will be observed 3–5.

Passengers with chronic obstructive pulmonary disease (COPD) may experience a severe decrease in arterial blood oxygen content at a cabin altitude of 2,438 m 6, 7. Three medical guidelines for COPD patients conclude that in-flight O2 supplementation should be considered if the O2 tension in arterial blood (Pa,O2) at 2,438 m altitude is <6.7 kPa (50 mmHg) 8, 9 or 7.3 kPa (55 mmHg) 10, respectively, since hypoxaemia below these levels is considered to be associated with increased risk of medical complications 11, 12. Several studies concerning preflight evaluation of COPD patients have suggested screening criteria based on sea-level blood gases, spirometry, and exercise capacity 8–10, 13–16. However, to the current authors' knowledge, similar studies concerning hypobaric conditions on patients with restrictive ventilatory impairment have not previously been performed.

The present investigation was carried out to study the influence of low atmospheric pressure on arterial blood gases in patients with chronic restrictive ventilatory impairment. In addition, the authors wanted to evaluate the effect of supplementary O2 on arterial blood gases and cardiovascular function under these conditions, both at rest and during light exercise. The exercise tests were performed because it is recommended that passengers take brief walks during long distance flights to avoid thromboembolic complications. Seventeen patients with chronic restrictive ventilatory impairment were studied at rest and during bicycle exercise (at a rate equivalent to slow walking along the aisle of an airplane) at sea level and at 2,438 m simulated altitude in a hypobaric chamber.


   Methods
TOP
 Abstract
 Methods
Results
 Discussion
 Acknowledgements
 References
 
Seventeen patients, 10 females and seven males, attending a rehabilitation programme were recruited for the study (group 1, table 1Go). They all suffered from chronic restrictive ventilatory impairment (total lung capacity (TLC) <95% confidence interval) 17, caused by either sequelae from tuberculosis (five patients), kyphoscoliosis (two patients), or lung fibrosis (sarcoidosis: three patients; fibrosing alveolitis: two patients; unspecified lung fibrosis: five patients). At the time of testing, all were in a stable phase of their disease. Two patients with mild hypertension received amlodipine (2.5 mg·day–1) or spironolactone (50 mg·day–1), and seven used oral or inhaled corticosteroids. Two had a history of myocardial infarction, without ventricular dysfunction. Patients with coexisting medical problems that might influence their physical capacity were excluded from the study. However, because analysis of blood pressures was performed after completion of the experiments, the authors failed to observe that one of the patients had a resting diastolic pressure of 118 mmHg on the day of the experiment. To test an equation for the prediction of in-flight Pa,O2 from preflight variables in these 17 patients, a separate group, consisting of 11 patients with chronic restrictive ventilatory impairment, was studied (group 2, table 2Go). The Regional Medical Ethics Committee approved the study, and written informed consent was obtained from all participants.


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  		Table 1— Lung function and arterial blood gases in 17 patients with chronic restrictive ventilatory impairment (group 1)

 

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  		Table 2— Lung function and arterial blood gases at rest at sea level in 11 patients with chronic restrictive ventilatory impairment (group 2)

 
Vital capacity (VC), forced expiratory volume in one second (FEV1), TLC, single-breath transfer factor of the lung for carbon monoxide (TL,CO) 18, and aerobic capacity were measured before the altitude experiment, as previously reported 7.

The experiments were performed with one patient and three technicians present in an air-conditioned (3 m3·min–1, 25°C) hypobaric altitude chamber (20 m3) with stable concentrations of O2 and carbon dioxide. In group 1, the subjects sat in a chair to use a cycle ergometer. After ≥10 min rest, they started cycling at 20 W, increasing by 10 W every 4 min, but here only responses during rest and 20 W exercise are reported. The procedure was performed in a random order at sea level and a simulated altitude of 2,438 m (8,000 ft), with 60 min rest between each exercise test. In group 2, the subjects were only exposed to hypobaric hypoxia (2,438 m) without exercise. Arterial blood samples were drawn every 4 min from a catheter in the radial artery. The samples were stored on melting ice in sealed syringes for 10–15 min before being sluiced out of the chamber and analysed for blood gases 7. The heart rhythm was continuously monitored, and arterial blood pressure was recorded through the catheter in the radial artery using a Mingograf 7 (Siemens-Elema, Solna, Sweden) and a Baxter TruWave disposable pressure transducer (Glendale, CA, USA).

After terminating the measurements at sea level and 2,438 m, the patients in group 1 were tested at 2,438 m at rest and during 20 W exercise with and without a supply of 100% O2 through a double nasal cannula. The O2 flow rates of 1, 2 and 4 L·min–1 were blinded for the patients. Arterial blood gases, intra-arterial blood pressure and cardiac frequency were measured at 4 min intervals. Two of the subjects did not participate in the study of supplementary O2, because they feared increased dyspnoea during a repeated exercise test.

Results are expressed as mean±sd. All variables, except Sa,O2, were normally distributed, and as a result, paired t-tests were used to evaluate differences between sea level and altitude. A Mann-Whitney test was used for Sa,O2. To test for combined effects, linear regression analysis of Pa,O2 (2,438 m) versus Pa,O2 (sea level), TL,CO (% of predicted 8), and Pa,CO2 (sea level) was performed, because of the significant bivariate correlations between the first and the latter three variables. The effect of O2 supply was tested using a two factor (rest versus exercise, and level of O2 supply) repeated measures analysis of variance (ANOVA), followed by contrasts between different flow rates. Two-tailed p-values <0.05 were considered statistically significant.


   Results
TOP
 Abstract
 Methods
 Results
Discussion
 Acknowledgements
 References
 
All subjects had a TLC <80% pred, as shown in table 1Go. Values for VC, FEV1 and TL,CO were also reduced to ~50% pred. All except one of the subjects were nonsmokers.

Individual values for arterial blood gases are presented in figure 1Go (a–c). There was a considerable decrease in Pa,O2 and Sa,O2 as the patients were taken from sea level to 2,438 m altitude (table 3Go). During 20 W exercise, Pa,O2 and Sa,O2 decreased markedly as compared to resting values, both at sea level and at 2,438 m (table 3Go). All subjects managed the work load (20 W) at sea level for ≥4 min, but at 2,438 m three subjects terminated after 2 min because of dyspnoea. In the figures showing 20 W exercise, blood values from these subjects are also included.



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  		Fig. 1.— Arterial blood gas values from 17 patients with chronic restrictive ventilatory impairment during rest and 20 W ergometer cycle exercise at sea level and at 2,438 m (8,000 feet) altitude. Individual ({triangleup}) and mean values ({circ}) of a) oxygen tension in arterial blood (Pa,O2), b) arterial oxygen saturation (Sa,O2) and c) carbon dioxide tension in arterial blood (Pa,CO2).

 

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  		Table 3— Blood gases and ventilation at rest and during 20 W exercise at sea level and 2,438 m simulated altitude (group 1)

 
There was a statistically significant decrease in resting Pa,CO2 from sea level to 2,438 m (table 3Go). During 20 W exercise, Pa,CO2 increased significantly at sea level, but not at altitude. Resting ventilation was not significantly different at sea level and at 2,438 m. During 20 W exercise, however, the ventilation at 2,438 m was significantly higher than at sea level (table 3Go).

The resting Pa,O2 at 2,438 m was correlated to both the sea-level Pa,O2 (r=0.73, p<0.001), TL,CO (r=0.59, p<0.02) and TL,CO in per cent of predicted values (r=0.69, p<0.01), and negatively correlated to Pa,CO2 (r=-0.55, p<0.05). There was no significant correlation between in-flight Pa,O2 and sea-level values of VC, FEV1, TLC, or aerobic capacity.

A multiple linear regression analysis of Pa,O2 (in kPa) at 2,438 m versus TL,CO and Pa,O2 at sea level gave the following equation:


(001)
with multiple r=0.88. The deviations from predicted Pa,O2 ranged from an overestimate of 1.0 kPa to an underestimate of 0.7 kPa and were normally distributed. Sea-level Pa,CO2 had no significant relation to Pa,O2 at altitude in the multiple regression. In group 2, no significant difference between measured in-flight Pa,O2 and Pa,O2 pred from the equation above (0.25±0.46 kPa, range –0.43–0.81 kPa) was observed. A comparison of measured and predicted Pa,O2 values at 2,438 m is shown in figure 2Go.



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  		Fig. 2.— Comparison of measured in-flight oxygen pressure in arterial blood (Pa,O2) and Pa,O2 pred from the equation Pa,O2 (2,438 m)=0.74+0.39xPa,O2 (sea level)+0.033xtransfer factor of the lung for carbon monoxide (% pred). {circ}: group 1; •: group 2.

 
By giving resting patients supplementary O2 (1 L·min–1) at 2,438 m, there was a statistically significant increase in Pa,O2 at rest and during exercise (fig. 3aGo). Further increases were observed at flow rates of 2 and 4 L·min–1. Likewise, Sa,O2 increased with increasing rates of O2 supply (fig. 3bGo). At rest and during exercise, Sa,O2 increased markedly when the O2 supply increased from 0 to 1 L·min–1, and increased further with 2 L·min–1. At a flow rate of 4 L·min–1, Sa,O2 increased relative to 2 L·min–1 during exercise, but not at rest. At rest, supplementary O2 resulted in a small but significant increase in Pa,CO2 at flow rates of 1 and 2 L·min–1, but no further increase at 4 L·min–1 (fig. 3cGo). During 20 W exercise, there was no increase in Pa,CO2 from 0 to 1 L·min–1, but a minor increase with 4 L·min–1 (fig. 3cGo).



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  		Fig. 3.— Effect of supplementary oxygen (O2) (mean±sem) in 15 patients with chronic restrictive impairment at 2,438 m (8,000 feet) simulated cabin altitude at rest ({circ}) and during 20 W ergometer cycle exercise (•). a) Oxygen tension in arterial blood (Pa,O2), b) arterial oxygen saturation (Sa,O2), c) carbon dioxide tension in arterial blood (Pa,CO2), d) systolic blood pressure (BPsys) and e) cardiac frequency (fC). *: p<0.05; **: p<0.01 compared to values without supplementary oxygen; #: p<0.05; ##: p<0.01 compared to values with supplementary oxygen at flow rate 1 L·min–1; : p<0.05; ¶¶: p<0.01 compared to values with supplementary oxygen at flow rate 2 L·min–1.

 
O2 supply at 2,438 m caused a decrease of ~9% in systolic blood pressure during 20 W exercise, but did not cause significant changes in blood pressure at rest (fig. 3dGo). Diastolic blood pressure was not affected by O2 supply. Resting cardiac frequency was reduced with an O2 supply of 2 L·min–1. During 20 W exercise the heart rate decreased ~8% with an O2 supply of 4 L·min–1 (fig. 3eGo).


   Discussion
TOP
 Abstract
 Methods
 Results
 Discussion
Acknowledgements
 References
 
Patients with various diseases leading to chronic restrictive ventilatory impairment developed pronounced hypoxaemia during simulated air travel at a cabin altitude of 2,438 m. The hypoxaemia was aggravated by light exercise, equivalent to slow walking along the aisle. The number of subjects was too small to evaluate each group of patients separately, but taken as a whole they seemed to respond to hypoxia in a similar manner. The spirometry and blood gas values showed an equal distribution among the different diagnoses, with a mean reduction in lung function parameters of ~50% pred. All patients included in the study were physically capable of travelling, and were thus potential aircraft passengers.

Guidelines for preflight medical evaluation are available for COPD patients 8–10, but not for other categories of lung patients. The intention of preflight medical evaluation is to avoid severe hypoxaemia provoked by the lowered cabin pressure in the aircraft. The lower limits for in-flight Pa,O2 (2,438 m), recommended in medical guidelines for COPD patients, are 7.3 kPa 10 and 6.7 kPa 8, 9, respectively, but it is not evident how these values have been established 11, 12. To the present authors' knowledge, studies on patients with restrictive ventilatory impairment at high altitude have not been published. According to the results presented here, these patients run a high risk of developing in-flight hypoxaemia, below the recommended levels. It was found that 82% expressed in-flight Pa,O2 values <7.3 kPa and 53% <6.7 kPa at rest. Even patients with Pa,O2 values close to normal at sea level, experienced a pronounced drop in Pa,O2 in the altitude chamber.

Effects of exercise at altitude have received little attention in the medical guidelines. However, passengers are recommended to take light exercise during longer flights to avoid thromboembolic complications 19. In this study, light exercise at sea level resulted in a reduced Pa,O2 compared to the resting situation, but none of the patients became severely hypoxaemic. However, the same level of exercise at 2,438 m resulted in a Pa,O2 level <6.7 kPa in all subjects, with a mean value of 5.1 kPa. In one patient with Pa,O2 9.4 kPa (sea level) at rest, the exercise Pa,O2 (2,438 m) was as low as 3.7 kPa.

Medical guidelines for COPD patients 8–10 recommend sea-level Pa,O2 as a reliable predictor of Pa,O2 at 2,438 m. Based on a study performed by the current authors on COPD patients in an altitude chamber, this recommendation could not be supported 7. In the present study, there was a significant correlation between Pa,O2 at sea level and Pa,O2 at 2,438 m, but only 53% of the variance of in-flight Pa,O2 could be accounted for by differences in sea-level Pa,O2. The prediction of Pa,O2 at 2,438 m could be improved by including TL,CO (% pred) in the regression, but in this study, sea-level Pa,O2 and TL,CO accounted for only 77% of the variance in Pa,O2 at 2,438 m. Even though the patients in group 2 showed no significant difference between measured in-flight Pa,O2 and Pa,O2 predicted from this regression, there is still a possibility of overestimating the in-flight Pa,O2 by using pre-flight parameters for prediction. Therefore, patients who might be particularly vulnerable to hypoxaemia should have priority to the limited resources of pre-flight evaluation under hypoxic conditions, either in a hypobaric chamber or testing by breathing a hypoxic gas mixture, as in the hypoxic altitude simulation test (HAST) 6. The current authors used a hypobaric chamber in the present investigation because it was easily accessibly. However, breathing a hypoxic gas at sea-level pressure gives similar results 20. Preflight evaluation might be offered to patients with accompanying heart disease and probably patients with hypercapnia, considering the observed negative correlation between pre-flight Pa,CO2 and in-flight Pa,O2. Hypercapnic patients might be less capable of increasing their ventilation in response to hypoxaemia. Conversely, preflight evaluation is controversial, and Naeije 21 recently pointed out that the benefit of such testing had never been documented.

At a cabin altitude of 2,438 m, an O2 supply of 2 L·min–1 on a nasal cannula increased the Pa,O2 (>8 kPa) and Sa,O2 (>92%) to acceptable levels in all subjects at rest, without causing alarmingly high levels of Pa,CO2 (range 4.2–6.8 kPa). There was a minor decrease in resting cardiac frequency and systolic blood pressure. During 20 W exercise at 2,438 m, equivalent to slow walking along the aisle, an O2 supply at 4 L·min–1 was sufficient to maintain Pa,O2>7.3 kPa and Sa,O2 >88% in all but two patients. There was a significant decrease in both cardiac frequency and systolic blood pressure at 20 W exercise, reflecting the improved oxygenation. There was only a minor increase in Pa,CO2 with this O2 flow (range 4.1–7.4 kPa).

The pronounced decrease in oxygen tension in arterial blood at altitude seems to contrast with the low level of medical emergencies among patients with pulmonary disease 21–23. This low incidence cannot be explained by a liberal prescription of supplementary oxygen. In a study among consultant respiratory physicians in England 24, approximately half of those measuring blood gas levels did not recommend in-flight supplementary oxygen unless the preflight oxygen tension in arterial blood was <8.0 kPa, and an additional 25% recommended that it should not be used unless the oxygen tension in arterial blood was <7.3 kPa. According to the results presented in this study, both chronic obstructive pulmonary disease 7 and restrictive lung patients with such preflight oxygen tension in arterial blood values will experience a decrease in oxygen tension in arterial blood to levels far below what is recommended in present guidelines 8–10. One reason could be that the cabin altitude during most flights is lower than at 2,438 m 25. However, the low frequency of medical emergencies indicate that these levels of hypoxaemia are generally well tolerated, and raises the question of whether the limit of acceptable in-flight oxygen tension in arterial blood should be reconsidered in future guidelines.


   Acknowledgements
TOP
 Abstract
 Methods
 Results
 Discussion
 Acknowledgements
References
 
The authors would like to the staff at the Institute of Aviation Medicine, Oslo, Norway, for helping with laboratory work and with controlling the hypobaric chamber during experiments.


   References
TOP
 Abstract
 Methods
 Results
 Discussion
 Acknowledgements
 References
 

  1. US Government Printing Office. Code of Federal Regulations. Title 14, Vol. 1, Part 25. 1527Washington, DC, US Government Printing Office, 1999.
  2. Harding RM, Mills JF. Problems of altitude I: Hypoxia and hyperventilation. BMJ 1983;286:1408–1410.
  3. Kelman GR, Crow TJ. Impairment of mental performance at a simulated altitude of 8,000 feet. Aerospace Med 1969;40:981–982.[Medline] [Order article via Infotrieve]
  4. McFarland RA. Human factors in relation to the development of pressurized cabins. Aerospace Med 1971;42:1303–1318.[Medline] [Order article via Infotrieve]
  5. DeHart RL. Fundamentals of aerospace medicine. 2nd EdnWashington Square, Lea Fabinger 600, 1996; pp. 96–97.
  6. Gong H Jr, Tashkin DP, Simmons MS. Hypoxia-altitude simulation test. Am Rev Respir Dis 1984;135:980–986.
  7. Christensen CC, Ryg M, Refvem OK, Skjønsberg OH. Development of severe hypoxaemia in COPD patients at 2,438 m (8,000 ft) altitude. Eur Respir J 2000;15:635–639.[Abstract]
  8. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995;152:S112–S113.
  9. Siafakas NM, Vermeire P, Pride NB, et al. Optimal assessment and management of chronic obstructive pulmonary disease (COPD): a consensus statement of the European Respiratory Society. Eur Respir J 1995;8:1398–1420.[CrossRef][ISI][Medline] [Order article via Infotrieve]
  10. Aerospace Medical Association, Air Transport Medicine Committee. Medical guidelines for air travel. Aviat Space Environ Med 1996;67:B1–B16.[Medline] [Order article via Infotrieve]
  11. Mills JF, Harding RM. Fitness to travel by air. BMJ 1983;286:1269–1271.
  12. AMA Commision on Emergency Medical Services. Medical aspects of transportation aboard commercial aircraft. JAMA 1982;247:1007–1011.[CrossRef][ISI][Medline] [Order article via Infotrieve]
  13. Gong H Jr. Advising pulmonary patients about commercial air travel. J Resp Dis 1990;11:484–499.
  14. Gong H, Lee Mark JA, Cowan MN. Pre-flight medical screenings of patients. Analysis of health and flight characteristics. Chest 1993;104:788–794.[Abstract/Free Full Text]
  15. Schwartz JS, Bencowitz HZ, Moser KM. Air travel hypoxaemia with chronic obstructive pulmonary disease. Ann Intern Med 1984;100:473–477.
  16. Vohra KP, Klocke RA. Detection and correction of hypoxaemia associated with air travel. Am Rev Respir Dis 1993;148:1215–1219.[ISI][Medline] [Order article via Infotrieve]
  17. American Thoracic Society. Lung function testing: selection of reference values and interpretative strategies. Am Rev Respir Dis 1991;144:1202–1218.[ISI][Medline] [Order article via Infotrieve]
  18. Quanjer PH. Standardized lung function testing. Bull Eur Physiopathol Respir 1983;19:39–44.
  19. Mercer A, Brown JD. Venous thromboembolism associated with air travel: a report of 33 patients. Aviat Space Environ Med 1998;69:154–157.[Medline] [Order article via Infotrieve]
  20. Dillard TA, Moores LK, Bilello KL, Phillips YY. The preflight evaluation. A comparison of the hypoxia inhalation test with hypobaric exposure. Chest 1995;107:352–357.[Abstract/Free Full Text]
  21. Naeije R. Preflight medical screening of patients. Eur Respir J 2000;16:197–199.[CrossRef][ISI][Medline] [Order article via Infotrieve]
  22. Rayman RB. Passenger safety, health and comfort: a review. Aviat Space Environ Med 1997;68:432–440.[Medline] [Order article via Infotrieve]
  23. Speizer C, Rennie C, Breton H. Prevalence of in-flight medical emergencies on commercial airlines. Ann Emerg Med 1989;18:26–29.[ISI][Medline] [Order article via Infotrieve]
  24. Coker RK, Patridge MR. Assessing the risk of hypoxia in flight: the need for more rational guidelines. Eur Respir J 2000;15:128–130.[Abstract]
  25. Cottrell JJ. Altitude exposures during aircraft flight. Flying higher. Chest 1988;93:81–84.[Abstract/Free Full Text]



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