Air travel and COPD.
A proportion of them have chronic obstructive pulmonary disease (COPD) of varying severity, some of whom may experience significant psychological and physiological stress owing to hypoxia while flying.
It is a concern, particularly in COPD patients who live at the coast where the P[O.sub.2] is high, whether they will be compromised when the P[O.sub.2] diminishes. Commercial aircraft travel between 10 000 m and 13 500 m. However, Federal Aviation Administration requirements specify that the partial pressure in an aircraft should not be less than the partial pressure at an altitude of 2 540 m. (2) The Gauteng region is about 1 600 m above sea level; therefore the cabin pressure difference will be much less for COPD patients departing from that region than for those departing from a region at sea level.
Physiological response to hyperbaric hypoxia
The steps required for oxygen transportation from ambient air to cellular metabolism are numerous, and include: (i) alveolar ventilation; (ii) matching perfusion of blood with alveolar ventilation; (iii) diffusion of oxygen through the alveolar capillary membrane; (iv) circulatory ability, i.e. cardiac output of the right ventricle; and (v) compensatory oxygen binding to haemoglobin. Changes take place at each of these levels, but should there be an inability to compensate, the patient may be adversely affected by hyperbaric hypoxia.
Hyperventilation is the first compensatory mechanism used by the body for hypoxia. (3) At sea level the tracheal P[O.sub.2] is about 149 mmHg, but at 2 450 m it is about 108 mmHg, which represents a decrease of about 27.5%. At this level patients with more severe COPD will already be hyperventilating and may not be able to increase their respiratory rate further. With hyperventilation the alveolar carbon dioxide will diminish. This will decrease Air travel and COPD the ventilation drive--another factor that may decrease the ventilatory response.
The initial increase in ventilation is due first to an increase in tidal volume and then to an increase in respiratory rate. COPD patients have already increased their tidal volumes; their rate therefore starts to increase sooner than normal.
Ventilation-perfusion relationships are also affected by ascent to altitude. The hyperventilation is matched by the increase in cardiac output and therefore by pulmonary perfusion. Hypoxia and secondary pulmonary vasoconstrictions redistribute the blood flow to lung regions poorly perfused at sea level. This improves the ventilation-perfusion matching. (3)
Diffusion of oxygen through the alveolar-capillary membrane worsens at high altitude. Oxygen flux is dependent on the pressure gradient between the alveolus and the capillary membrane. This equilibrium is time dependent; therefore, as the Pa[O.sub.2] decreases with altitude, pulmonary transit time may not be adequate for equilibrium of oxygen to take place. This phenomenon is known as diffusion limitation of oxygen transfer of high altitude. (3) Diffusion limitation is exacerbated by exercise, when the pulmonary capillary transit time is further shortened. It is important that COPD patients should not walk around the aircraft more than is absolutely necessary. Attempts should be made to seat them near the toilets.
Cardiac output increases in a linear fashion with hypoxia in an attempt to sustain oxygen delivery owing to the decrease in arterial oxygen content. The increase is initially due to heart rate and then to stroke volume. Pulmonary vascular resistance increases with an increase in altitude owing to pulmonary vasoconstriction caused by hypoxia. This may be critical in COPD patients who may already have raised pulmonary arterial pressure and compromised right ventricular function.
Generally, the decrease in P[O.sub.2] represents a small decrease in Pa[O.sub.2] and a very small decrease in oxygen-carrying capacity, as it is on the flat part of the oxyhaemoglobin dissociation curve. However, in patients with cardiopulmonary disease and a lower baseline Pa[O.sub.2], the decrease in P[O.sub.2] at 2 500 m may cause a dramatically diminished Pa[O.sub.2] , as they may well be on the steep part of the curve.
Pre-flight medical assessment
The value of pre-flight medical assessment has frequently been shown. The Aerospace Medical Association and the British Thoracic Society (BTS) have published comprehensive guidelines for the evaluation and management of patients undertaking flights. (4,5)
A variety of tests have been used to identify patients at risk. These range from easily performed tests, such as arterial blood gas levels and a 6-minute walk test, to a highly sophisticated hypoxia altitude simulation test (HAST), where patients breathe a hypoxic gas mixture of 15.1% oxygen at sea level which simulates breathing air with a P[O.sub.2] of 108 mmHg (maximum allowable aircraft cabin pressure). As this test is difficult to perform, the simpler tests have been employed with acceptable results.
The single most important predictor of inflight Pa[O.sub.2] is the baseline Pa[O.sub.2] at ground level. A pre-flight Pa[O.sub.2] of 70 mmHg is considered to be adequate to achieve a Pa[O.sub.2] of 50 mmHg at an altitude of 2 540 m. It is recommended that an individual with a Pa[O.sub.2] of less than 50 mmHg receive supplemental oxygen during a flight. The BTS also recommends that any person with an Sp[O.sub.2] of less than 92% at sea level be given supplemental oxygen. If the Sp[O.sub.2] is between 92% and 95% and there are no other risk factors (see below), then the Pa[O.sub.2] must be above 70 mmHg. If not above 70 mmHg, ideally a HAST should be performed. If not feasible, a 6-minute walk test has been shown to correlate very well with the HAST. Patients who have an Sp[O.sub.2] of less than 85% during a standard 6-minute walk test should be provided with supplemental oxygen during a flight. (6)
Patients with an Sp[O.sub.2] of 92-95% and the following risk factors require supplemental oxygen:
* an [FEV.sub.1] of less than 50% predicted
* lung cancer
* associated restrictive lung disease
* an exacerbation of lung disease within the last 6 weeks
* cardiac or vascular disease
* ventilatory support.
Estimates of inflight Pa[O.sub.2] can also be determined by several formulae using a multivariate regression analysis:
Pa[O.sub.2] (alt) = 0.453 Pa[O.sub.2] (ground) + 0.386 ([FEV.sub.1] % predicted) + 2.44
If the patient has an acceptable [FEV.sub.1], but a very low diffusion capacity, the following equation should be used:
Pa[O.sub.2] (8 000 feet) = 0.74 + [0.39 Pa[O.sub.2] (sea level)] + [0.33 TLCO (% predicted)].
Patients normally require 2-3 litres/minute flow rate. Those already on supplemental oxygen require their rate to be increased by at least 33%. The aim of supplemental oxygen is to keep the Pa[O.sub.2] greater than 50 mmHg.
Patients are not allowed to bring their own cylinders on board aircraft. The airlines supply cylinders; obviously these arrangements should be made timeously. There are now also some FAA-approved portable oxygen concentrators available, but these must be cleared by the particular airline as policies differ.
Two final important points: remind patients to bring their own medicines and advise them to move around as little as possible during the flight (therefore they have to be seated near the toilets).
(1.) Select Committee on Science and Technology. Air Travel and Health. 5th report. London: Parliament, House of Lords, 2000.
(2.) Code of Federal Regulations. Title 14 CFR. Washington DC: US Government Printing Office, 1986.
(3.) Mortazavi A, Eisenberg MJ, Langleben D, Ernst P, Schiff RL. Altitude related hypoxia: Risk assessment and management for passengers on commercial aircraft. Aviat Space Environ Med 2003; 74(9): 922-927.
(4.) Air Transport Medicine Committee. Medical Guidelines for air travel. Aviat Space Environ Med 2003; 74: A1-9.
(5.) British Thoracic Society Standards of Care Committee. Managing passengers with respiratory disease planning air travel. BTS recommendations. Thorax 2002; 57: 289-304.
(6.) Mohr LC. Hypoxia during air travel in adults with pulmonary disease. Am J Med Sci 2008; 335(1): 71-79.
L P KRIGE, MB BCh, DOH, FCP (SA)
Private practitioner, Greenacres Hospital, Port Elizabeth
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|Title Annotation:||More about ... Pulmonology; chronic obstructive pulmonary disease|
|Publication:||CME: Your SA Journal of CPD|
|Date:||Apr 1, 2009|
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