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(Circulation. 1996;93:272-276.)
© 1996 American Heart Association, Inc.

Articles

Air Travel and Adults With Cyanotic Congenital Heart Disease

Eric Harinck, MD, PhD; Paul A. Hutter, MD; Theo M. Hoorntje, MD; Marinus Simons, MD; Avram A. Benatar, MD; Johan C. Fischer, PhD; Dagmar de Bruijn; Erik Jan Meijboom, MD, PhD

From Wilhelmina University Children's Hospital (E.H., P.A.H., A.A.B., J.C.F., D.d.B., E.J.M.), Utrecht, Netherlands; Netherlands Aerospace Medical Centre (M.S.); and Academic Hospital Maastricht (T.M.H.), Maastricht, Netherlands.

Correspondence to Paul A. Hutter, MD, Wilhelmina University Children's Hospital, PO Box 18009, 3501 CA Utrecht, Netherlands.

	Abstract

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Background Concern has been expressed that a reduction of partial oxygen pressure during flight in commercial aircraft may induce dangerous hypoxemia in patients with cyanotic congenital heart disease.

Methods and Results To evaluate the validity of this concern, the transcutaneous SaO₂ was measured in 12 adults with this type of heart disease and 27 control subjects during simulated commercial flights of 1.5 and 7 hours in a hypobaric chamber. Ten of those patients and 6 control subjects also were evaluated during two actual flights of approximately 2.5 hours in a DC-10 and an A-310, respectively. During the prolonged simulated and actual flights, the capillary blood pH, gases, and lactic acid were analyzed in the patients and during one of the actual flights also in the control subjects. During the simulated flights the SaO₂ was at all times lower in the patients than in the control subjects. However, the maximal mean actual percentage decrease, as compared with sea level values, did not exceed 8.8% in either patients or control subjects. During the actual flights, this maximal decrease in the patients was 6%. In-flight reduction of the capillary PO₂ was considerable in the control subjects but not in the patients. It is our hypothesis that the lack of a significant decrease of the PO₂ in the patients might possibly be due to a high concentration of 2.3 diphosphoglycerate in the red cells. The flights had no influence on the capillary blood pH, PCO₂, bicarbonate, or lactic acid levels in either patients or control subjects.

Conclusions Atmospheric pressure changes during commercial air travel do not appear to be detrimental to patients with cyanotic congenital heart disease.

Key Words: heart disease • oxygen • air travel

	Introduction

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Physicians are often consulted by their patients with pulmonary or cardiovascular disease regarding their medical fitness to fly as passengers in commercial aircraft. In-flight atmospheric conditions in commercial jet aircraft may approach altitude equivalents of 6000 to 8000 ft (1829 to 2438 m).^{1 2 3} In healthy people this causes a marked decrease in the arterial PO₂ but only a mild reduction of the arterial oxygen saturation. Therefore, aircraft passengers are usually unaware of their temporary mild hypoxemic state.^{4 5}

General concern has been expressed that such cabin altitudes may induce dangerous hypoxemia in patients with chronic pulmonary obstructive disorders and cardiopulmonary disease. Certain guidelines on air travel are available for those patients entirely based on studies involving patients with chronic parenchymal pulmonary disease.^{3 6 7 8 9 10 11} Current guidelines on air travel for patients with CCHD are extrapolated from those studies because there are no scientific data available on this subject for these cardiac patients.^{1 12 13}

To ascertain the clinical and metabolic effects of air travel on patients with CCHD, we conducted a study whereby a group of adults with this type of heart disease was subjected to simulated air travel in a hypobaric chamber and to actual flights in commercial jet aircraft.

	Methods

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Patients
Twelve patients (6 men, 6 women) with CCHD volunteered for this investigation. Their mean age was 21 years (range, 16 to 26). Eight had concomitant irreversible pulmonary vascular disease (Table 1). One patient with ventricular septal defect and irreversible pulmonary vascular disease was not cyanosed at rest, but there was mild cyanosis on exertion. The Hb levels varied from 9.6 to 15.6 mmol/L (mean, 12.5 mmol/L) (15.9 to 25.9 g%; mean, 20.8 g%) and the hematocrits from 0.50 to 0.77 L/L (mean, 0.62 L/L). The mean corpuscular volume of the erythrocytes was within the high normal range in each patient, which excluded overt anemia as a result of iron-deficient erythropoiesis. None had evident cardiac failure or pulmonary parenchymal disease. One patient was an occasional smoker. As a precautionary measure, supplemental oxygen was available on the simulated and actual flights. In addition, medical facilities were taken on board the aircraft for resuscitation and advanced life support.

View this table: [in this window] [in a new window]   Table 1. Types of Congenital Heart Disease of Study Patients, n=12

This study was in agreement with the rules set out by the ethical review board of the Wilhelmina Children's Hospital. Informed consent was obtained from patients, parents, and control subjects.

Simulated Air Travel
Twelve patients were subjected to a simulated short flight of 1.5 hours and subsequently 10 of them for a prolonged simulated flight of 7 hours in a hypobaric chamber. The maximal CA attained under normal flying conditions with commercial pressurized jet aircraft is 8000 ft (2438 m).¹ For this reason, an atmospheric pressure compatible with that altitude was maintained for 45 minutes during the short simulated flight and for 6 hours during the prolonged simulated flight.

Twenty-seven young air pilots were investigated as control subjects during two other simulated flights under identical conditions. Their mean age was 23 years (range, 18 to 32). Fifteen participated in the short flight and 12 in the prolonged simulated flight. They were all male and all nonsmokers. None of the control subjects or the patients showed any signs of anxiety before or during the experiments.

The SaO₂ and heart rate were continuously monitored with a pulse oximeter (Nellcor N-20), and the blood pressure was measured (Criticon Dinamap 1846) at intervals of 15 to 30 minutes. Mean values of repeated measurements were used in the calculations. Seven patients additionally volunteered to have the capillary blood pH, gases, and lactic acid levels measured before and at the end of maximal CA during the prolonged simulated flight.

Actual Air Travel
The investigations during the actual flights were carried out in a DC-10 from Amsterdam-Schiphol to Malaga (Spain) and after a stay-over of two nights back in an Airbus A-310. The 10 patients who were studied during the prolonged simulated flight also participated in this investigation. Six attendants served as control subjects. Apart from some excitement common in inexperienced air travelers, there were no signs of obvious anxiety or fatigue during the study. To minimize the non–flight-related stress, transport to and from the airport was arranged by coach and at the airport by courtesy cars. The transport of luggage was taken care of by the charter company and airport personnel. The total duration of both flights was approximately 2.5 hours. During the outbound flight, a maximal CA of 6000 ft (1829 m) was attained for 97 minutes and on the return flight 5830 ft (1767 m) for 75 minutes. The cabin altitudes were obtained from the cockpit crew. Throughout both flights, the SaO₂ and the heart rate of the patients were continuously monitored (Nellcor N-20 P). Capillary blood samples for blood pH, gases, and lactic acid analysis were taken from the patients and the control subjects before the outbound flight, in the last 45 minutes of maximal CA, and after disembarkation. On the return flight, capillary blood samples were taken from the patients before embarkation, during the first and the last 30 minutes of maximal CA. For logistic reasons, the SaO₂ could not be measured in the control subjects during the outbound and return flights. For the same reason, capillary blood samples could only be collected from the control subjects on the outbound flight.

Laboratory Methods
All blood samples were obtained by finger stab by skilled laboratory technicians and immediately stored at 4°C to 5°C. The analyses were performed between 30 minutes and 3 hours after the blood was collected. To evaluate whether the time lag between blood sampling and analyses influenced the results, five capillary blood samples from each of 6 volunteers were collected in the Children's Hospital before the study. The first sample was analyzed immediately after collection. The remainder was stored at 4°C to 5°C and analyzed at hourly intervals up to 4 hours. The delay between collection and analysis had no influence on the results. The average of two measurements of each sample during the clinical investigation was taken for the calculations. The capillary blood pH and gases were measured with an IL 1306 blood gas analyzer. The analyzer and gas mixtures for calibration and measurement were transported to Malaga for prompt analyses. For the lactic acid analyses, the blood was centrifuged before storage. The hematocrits were electronically determined.

The bias of the pulse oximeters that we used was within 2% of the true SaO₂. This equipment is also reliable for monitoring patients during air travel.^{4 14}

Statistical Analysis
The statistical analysis was carried out with a t test for paired samples for the individual variations within the group of patients or control subjects and the unpaired t test for comparison between patients and control subjects.

	Results

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Simulated Flights
A short, transient earache occurred in one patient during the "descent" of the short simulated flight, but otherwise no untoward clinical effects were noted. There were no significant changes in the heart rate and blood pressure. Compared with the initial sea level values, a statistically significant decrease of the SaO₂ was observed at maximal CA of 8000 ft (Table 2). The mean SaO₂ decrease from sea level to maximal CA during the short simulated flights was 7.5% in the patients (P<.001) and 8.0% in the control subjects (P<.001). Expressed as a percentage of sea level value, the SaO₂ decreased by 8.5% in the patients and by 8.2% in control subjects. Throughout the investigation, the SaO₂ was higher in the control subjects than in the patients, but there was no significant difference between the actual percentage decrease after 6 hours at maximal CA (P=.63). During the prolonged "flight," the mean SaO₂ decrease at maximal CA compared with that of the sea level value was 7.6% in the patients and 6.8% in the control subjects. Expressed as a percentage from the sea level values, the SaO₂ decreased by 8.8% in the patients and 7.0% in the control subjects. The duration of maximal CA had no significant influence on the SaO₂ reduction (P=.22). The post–simulation flight mean SaO₂ of both patients and control subjects did not significantly differ from the pre–simulation flight values (P=.16 and .11, respectively). This was observed on both short and prolonged simulated flights. The most striking individual SaO₂ reduction was 14% (89% to 75%) in one patient and 11% (96% to 85%) in one control subject. The lowest sea level SaO₂ measured was 69% in one of the patients who also reached the lowest individual SaO₂ of 65% at maximal CA.

View this table: [in this window] [in a new window]   Table 2. Transcutaneous Oxygen in Control Subjects and Patients During Simulated Flights

The patient who was acyanotic at rest participated both in the simulated and the actual flights. His sea level SaO₂ was >95%, which accounts for the high individual maximal SaO₂ values of the patients in Tables 2 and 4.

View this table: [in this window] [in a new window]   Table 4. Transcutaneous Oxygen Saturation of Patients During Commercial Air Travel

The results of the capillary blood pH, gas, and lactic acid analyses are shown in Table 3. The mean capillary PO₂ decrease was 5.4 mm Hg, or 9.7% of the initial sea level value (P=.01). The maximal individual decrease of the capillary PO₂ was 12 mm Hg (14%), which occurred in the patient who was acyanotic at rest and who had the highest sea level capillary PO₂ (86 mm Hg). The lowest individual capillary PO₂ measured was 40 mm Hg at sea level and 35 mm Hg at maximal CA in the same patient. The mean lactic acid level increased from 2.0 mmol/L at sea level to 4.2 mmol/L (P=.002). The capillary pH, the actual bicarbonate, the mean base excess, and the PCO₂ remained statistically unchanged.

View this table: [in this window] [in a new window]   Table 3. Capillary Blood Gases, pH, and Lactic Acid Levels in Patients at Sea Level and After 6 Hours at Maximum Cabin Altitude During a 7-Hour Simulated Flight

Actual Air Travel
During the flights, no clinical problems were noted. All patients had a reduction of the SaO₂ at maximal CA compared with the sea level values on both flights (Table 4). The actual mean SaO₂ decrease was 2.8% on the outbound and 4.8% on the return flight (P<.001). Expressed as a percentage from the initial sea level value, the SaO₂ decreased by 3.3% during the outbound and by 5.7% during the return flight. After the initial reduction of SaO₂ at maximal CA, there were no further significant changes throughout the flights at that altitude. There was no statistically significant difference between the mean SaO₂ values at sea level before and after the outbound flight (P=.42) and a 1.1% difference on the return flight (P=.04). The lowest values of the SaO₂ recorded were 77% in two patients at sea level and maximal CA in the same patients (70% and 71%).

The results of the capillary blood pH, gases, and lactic acid analyses are presented in Table 5. In the control subjects, there was a considerable reduction of the mean capillary PO₂ of 15 mm Hg at maximal CA during the outbound flight compared with the sea level value (P<.001). Expressed as a percentage of the preflight sea level value, the mean capillary PO₂ decreased by 19%. There was no statistically significant difference between the mean capillary PO₂ at sea level before and after the flights. In the patients, there was an unexpected mean increase of 1.3 mm Hg in the capillary PO₂ at maximal CA during the outbound and a mean decrease of 3.1 mm Hg during the return flight. However, these changes were not statistically significant (P=.49 and .74). There were no statistically significant changes in the capillary pH, the PCO₂, the actual bicarbonate values, the mean base excess, or the lactic acid levels during the flights in either patients or control subjects.

View this table: [in this window] [in a new window]   Table 5. Capillary Blood Gases, pH, and Lactic Acid Levels in Patients and Control Subjects During Commercial Air Travel

	Discussion

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At CAs of 6000 to 8000 ft (1829 to 2438 m), these being the respective average and maximal CAs reached in commercial air travel, the atmospheric partial oxygen pressure in the cabins falls considerably as compared with sea level. Healthy people have little difficulty in adapting to this change and tolerate it by increasing ventilation. This physiological compensatory mechanism at acutely increased altitudes moderates the fall in arterial PO₂.^{4 5 15} This has been a cause for concern in patients with chronic obstructive pulmonary disease.^{3 6 7 8 9 10 11 12} The ability of these patients to increase ventilation is limited. Therefore, many physicians either prescribe in-flight supplemental oxygen for patients who are likely to develop an arterial PO₂ of 50 mm Hg or less at any airborn altitude or else advise against flying.^{1 3 11 12} The average resting arterial PO₂ of the patients who participated in the various studies on air travel and chronic pulmonary disease was above 65 mm Hg.^{3 6 7 8 9 10} Fear of dangerous hypoxemia in patients with CCHD during flight is particularly understandable, as their resting arterial PO₂ at sea level is commonly below 65 mm Hg and often close to or on the steep slope of the Hb-O₂ dissociation curve. A considerable decrease in arterial PO₂ during flight, as occurs in healthy people, could jeopardize the patient's health. Consequently, they are also often discouraged from flying, forbidden to fly, or advised that in-flight supplementary oxygen must be available.^{12 13}

Our results show that although the sea level SaO₂ in the patients was much lower than in the control subjects, the actual decrease during maximal CA followed similar patterns. The mean SaO₂ decrease at maximal CA compared with sea level values was less during the actual flights than the simulated flights. This can be explained by the difference of the maximal CA between the actual and the simulated flights.

During the actual flight, the capillary PO₂ markedly decreased in the control subjects at maximal CA, which was to be expected from other studies.^{4 5} The capillary PO₂ of the patients did not follow a similar pattern. At maximal CA during the prolonged simulated flight, only a small decrease occurred. During the return flight, we observed a slight decrease of the capillary PO₂ in the patients and an unexpected mean increase during the outbound flight; however, these differences had no statistical significance. In an attempt to explain the absence of a statistically significant decrease in the mean capillary PO₂ in the patients during the actual flights, one may speculate on several factors. The mean decrease during the simulated flight was small; therefore, an even smaller reduction was expected during the actual flights because the maximal CA was markedly lower during the actual flights than during the simulated flight. Furthermore, the capillary PO₂ is easily influenced, for instance, by small differences in peripheral capillary perfusion in the extremities of patients with a high hematocrit or by slight changes of the patient's condition and by unavoidable laboratory errors. Any of these factors and particularly a combination of them may explain the absence of a statistically significant decrease. However, the results clearly indicate that the commonly feared hazardous decrease of the capillary PO₂ and SaO₂ in these patients during air travel does not occur.

There is no direct explanation for these observations. One possible mechanism that may be postulated is the presence of a high level of organic phosphates in the red cells of the patients. Native high altitude residents have as a reaction to their chronic hypoxemia a high DPG concentration in their red cells.^{13 16} The more severe the hypoxemia the greater the amount of DPG.¹⁶ A high concentration of DPG in the red cells causes a rightward shift of the Hb-O₂ dissociation curve, which is particularly beneficial to patients whose arterial PO₂ is situated on the steep slope of this curve. A high content of DPG in the red cells decreases the affinity of Hb for oxygen, rendering Hb-bound oxygen more readily available to body tissues. This means a rapid unloading of oxygen for small changes in oxygen tension.^{13 16} When persons normally residing at sea level altitude are exposed to high altitudes, the DPG increases considerably in a few days because of the induced hypoxemia.¹⁶ The DPG was not measured in our patients, but it seems reasonable to assume that their severe chronic hypoxemia has caused a permanent elevation of this organic phosphate in their red cells, at least in 9 of the 10 patients. In support of this hypothesis is the observation that in the one patient with a normal SaO₂ (>95%) and capillary PO₂ at sea level, the drop in these variables at maximal CA was consistent with the control subjects, suggesting an oxygen dissociation curve similar to the control subjects.

Acute exposure to high altitudes leads to increased ventilation and eventually to respiratory alkalosis. Respiratory alkalosis causes a leftward shift of the Hb-O₂ dissociation curve, which could counteract the rightward shift caused by a high concentration of DPG in the red cells. However, patients with CCHD and native high altitude residents have a blunted ventilatory response to hypoxemia.^{13 17} Therefore, this physiological mechanism will not come into operation. Consequently, these patients maintain the benefit of the rightward shift when exposed to in-flight hypoxic stress.

On the basis of our results, it appears that commercial air travel itself is well tolerated by patients with CCHD. Therefore, the restrictions and recommendations in air travel guidelines for patients with chronic pulmonary disease should not be applied to patients with CCHD. In-flight supplemental oxygen does not seem to be automatically indicated when their arterial PO₂ is or may be expected to decrease below 50 mm Hg. In these patients, the hypoxemia is increased by the right-to-left shunt and not by diminished gas exchange in the lungs. Therefore, supplemental oxygen is unlikely to influence the state of their hypoxemia.

The results of this study should not be regarded as an automatic entry to air travel for all patients with CCHD. When counseling these patients for their fitness to participate in commercial air travel, their clinical condition must be taken into account. For instance, because of uncontrollable rhythm disturbances and/or (threatening) cardiac failure or because of psychological instability, the patient may be so compromised that the non–flight-related stresses alone could be a contraindication for air travel.

The main problems that patients with CCHD have to cope with when traveling by air are the non–flight-related stresses, which can be very fatiguing and must not be underestimated. Some specific recommendations for those patients include adequate transportation to and from the airport; traveling with a companion who knows the patient's needs and can help with the handling of the luggage; early arrangements of a courtesy car, a special service provided by most airports and airlines; and maintenance of ample nonalcoholic fluids. The last recommendation is of particular importance for patients with a high hematocrit. During the flight, the humidity in any type of pressurized jet aircraft is very low, and thirst is a poor indicator of dehydration under these circumstances.¹⁸

Conclusions
Our data indicate that most patients with CCHD can enjoy the convenience of air travel, provided that adequate preparatory arrangements are made.

	Selected Abbreviations and Acronyms

 

CA = cabin altitude CCHD = cyanotic congenital heart disease DPG = 2.3 diphosphoglycerate Hb = hemoglobin

	Acknowledgments

 
This study was supported by the Netherlands Heart Foundation, grant 44 004. We thank Martinair Holland for the provision of the air accommodation and the catering during the prolonged simulated flight.

Received December 8, 1994; revision received July 27, 1995; accepted August 25, 1995.

	References

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Harinck, E. Articles by Jan Meijboom, E. Search for Related Content PubMed PubMed Citation Articles by Harinck, E. Articles by Jan Meijboom, E. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Congenital Heart Defects Hazardous Substances DB LACTIC ACID OXYGEN