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Extreme environments—flying, altitude, diving 

Extreme environments—flying, altitude, diving
Extreme environments—flying, altitude, diving

Stephen Chapman

, Grace Robinson

, John Stradling

, Sophie West

, and John Wrightson

Page of

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date: 29 November 2021

Lung disease and flying


Flying presents problems for three reasons:

  • Extra hypoxia

  • Volume changes in gas compartments

  • Closed environment and disease transmission.

Extra hypoxia

Some more recent airplanes may be pressurized to the equivalent of about 5, 000ft (1, 500m). This gives an atmospheric pressure of about 85kPa and an FiO2 of about 18kPa, compared with 21kPa at sea level. In normal subjects, this causes inconsequential falls in PaO2 and SaO2. However, many companies pressurize to the minimum allowed 8, 000ft (e.g. Boeing 767—7, 900ft or 2, 400 m, the same as some of the lower ski resorts in Colorado), equivalent to an FiO2 of 16kPa (equivalent to breathing 15% O2 at sea level), and, even in normal subjects, the SaO2 may fall to 90% or so. The new Airbus 380 is pressurized to 5, 000ft (1, 500m), and the new Boeing 787 to 6, 000ft (1, 800 m).

Patients with lung disease and a degree of hypoxia will be nearer the steep part of the Hb dissociation curve and will experience bigger proportional falls in O2 carriage by the blood. The estimated PaO2 at 8, 000ft (2, 400m) (the lowest cabin pressurization likely to be encountered) is empirically estimated by the formula:

Estimated PaO2 at 8,000ft (2,400m)= (0.24 × PaO2 at sea level)+(2.7 × FEV1/VC)+3

For example, if sea level PaO2 = 8kPa, FEV1/VC = 0.40, estimated PaO2 = 6kPa.

This is a rough approximation and will vary considerably from patient to patient, particularly due to differences in hypoxic drive. An alternative is to give the patient a hypoxic challenge for 15min minimum, and measure the PaO2/SaO2. This is most easily achieved by feeding a 40% Venturi mask with 100% nitrogen, which simulates a little under 8, 000ft (2, 400m) (equivalent to 16% O2). There is no evidence this predicts whether a patient will, or will not, run into trouble. Recently, Edvardsen et al. confirmed that the result of a hypoxic challenge test in patients with moderate to severe COPD did not predict whether they developed symptoms during a flight, although the pre-flight MRC dyspnoea score did predict symptoms. Those that had supplemental O2 had fewer symptoms, regardless of the simulated hypoxia testing.

Empirically, O2 is often prescribed if the in-flight PaO2 at 8, 000ft (2, 400m), estimated from the above equation or by experimentation, is <6.6kPa or 85% SaO2. Others have used SaO2 during a 6MWT to try and improve the ability to predict SaO2 during 15% hypoxia testing. None of this is evidence-based, so a simple recommendation based on sea level oximetry measurements is likely to be as valid, in conjunction with further information such as how disabled the patient is already by shortness of breath, their previous flight experience, length of proposed flight, time since last exacerbation, and importance of the trip to the patient, etc.

The suggestions in Box 26.1 are similar to BTS guidelines, which are a little more complex and consider comorbidities. 2L/min via nasal cannulae, or 28% Venturi mask, is usually sufficient to raise SaO2 to sea level equivalent. Airlines vary over charging for this; allow at least a month to arrange it (see British Lung Foundation (BLF) reference under Further information for each airline’s procedure). A MEDIF form or equivalent will require completion by the GP or specialist. Occasionally, patients are allowed to bring their own O2 on board as hand luggage. Some airlines prohibit using O2 during take-off and landing.

Volume changes in gas compartments

Ascent to the equivalent of 5, 000ft (1, 500m) increases gas trapped in compartments by 20%, ascent to 8, 000ft (2, 400m) by nearly 40%. A pneumothorax or non-communicating bullae therefore increases by this amount; patients with current pneumothoraces should not fly. It used to be advised not to fly within 6 weeks of a pneumothorax (slightly higher chance of recurrence and lack of adequate emergency treatment on board). This has recently been changed to 1 week after full radiographic resolution, or 2 weeks in the case of a traumatic pneumothorax. Patients having had recent thoracic surgery (for whatever reason) are now advised they can fly once recovered from the surgery itself (previously advised to wait 2 weeks). None of this is evidence-based, and the true risks of ignoring these guidelines are not known. It is probable that the risk of a second pneumothorax, in the absence of definitive management (pleurodesis, etc.), is only high enough to worry about in patients with pre-existing lung disease who should be made aware of this higher risk.

Closed environment

Patients with infectious diseases, such as TB, should not fly. There seems to be a significant risk of infecting others.

Further information

Edvardsen A et al. COPD and air travel: does hypoxia-altitude simulation testing predict in flight respiratory symptoms? Eur Respir J 2013;42:1216–23.Find this resource:

Edvardsen A et al. High prevalence of respiratory symptoms during air travel in patients with COPD. Respir Med 2011;105:50–6.Find this resource:

Cottrell JJ. Aircraft cabin pressures. Chest 1988;98:81.Find this resource:

British Thoracic Society guidelines: Extreme environments—flying, altitude, diving Editorial: Extreme environments—flying, altitude, diving

BTS patient advice leaflet. Extreme environments—flying, altitude, diving

Coker R et al. Is air travel safe for those with lung disease? Eur Respir J 2007;30:1057–63.Find this resource:

BLF patient advice. Extreme environments—flying, altitude, diving

BLF information on oxygen and airlines. Extreme environments—flying, altitude, diving

Altitude sickness


of acute mountain or high altitude sickness are not precise but include several symptoms provoked by the hypoxia.


Some of the pathophysiology is well understood and explains some of the symptoms and signs. These largely fall into two categories, minor and major.


Due to hyperventilation/hypocapnia/alkalosis/cerebral vasoconstriction provoked by the hypoxia, and include:

  • Light-headedness/fatigue

  • Numbness/tingling of extremities

  • Nausea/vomiting and anorexia

  • Headache

  • Insomnia/sleep disturbance

  • Periodic ventilation during sleep.

These symptoms are common, develop over 6–12h after arrival, and affect at least a quarter of those flying to Colorado for a skiing holiday (altitude 2,400–3,400m, ~10,000ft, barometric pressure 70kPa, inspired O2 tension 14.5kPa, average SaO2 on arrival 89–90%). Most of the symptoms are due to a respiratory hypocapnic alkalosis and resolve as the kidney retains [H+] and excretes [HCO3], returning pH towards normal. This allows further hyperventilation, and the rise in SaO2 helps resolve any of the symptoms due to the hypoxia itself. This scenario tends to be common in those with a higher hypoxic drive (measured at sea level, as it encourages greater hypocapnia and alkalosis). Confusingly, these symptoms may also indicate the early development of the more major category.


Those due to the hypoxia itself. These are more serious, can develop rapidly, and tend to occur more in those with a lower hypoxic drive. There is also a genetic component influencing susceptibility, related to the ACE gene. In high altitude pulmonary oedema (HAPE), the hypoxia provokes a non-uniform pulmonary vasoconstriction, raising PAP; hence some pulmonary capillaries are unprotected and receive the full rise in PAP. Fluid leakage into alveoli, pulmonary oedema, and capillary damage (with pulmonary haemorrhage) produce clinically apparent disease. The dominant symptoms/signs are:

  • Extra breathlessness/cough

  • Cyanosis

  • Blood-tinged frothy sputum

  • Crackles on auscultation/raised JVP.

In high altitude cerebral oedema (HACE), hypoxia also causes increased cerebral blood flow, cerebral oedema, retinal haemorrhages, cerebral thrombosis, and petechial haemorrhages. The dominant symptoms are:

  • Ataxia (may be the first sign)

  • Confusion/disorientation/hallucinations/behavioural change

  • Severe headache/reduced conscious level

  • Papilloedema.

Both HAPE and HACE are potentially fatal.


Risk factors are mainly the rate and degree of altitude attained. Keep ascent to ≤300m (1, 000 ft)/day, and rest every third day. The minor form of altitude sickness is likely to resolve spontaneously over a few days with simple symptomatic treatment, analgesics, and plenty of hydration. However, prophylaxis, or early treatment on symptom appearance, with acetazolamide is very effective, as are limiting further ascent and encouraging descent. Acetazolamide provokes a mild metabolic acidosis (by reducing [H+] availability for excretion in the distal tubule) and ‘pre-acclimatizes’ the subject to allow greater hyperventilation in response to hypoxia without the usual alkalosis. It is recommended when rapid ascent to altitudes ≥2, 500m (8, 200ft) is unavoidable (such as a package ski trip to Aspen). 500mg/day (slow release) for the 2 days prior to ascent is probably adequate for most subjects (or as treatment after symptoms develop). The commonest side effect is a harmless and reversible tingling of the extremities.


has been shown to reduce the periodic breathing at night (by reducing the arousals that help maintain the periodicity) and does not appear to worsen the hypoxia or reduce vigilance levels the following day.

The best predictor of severe altitude sickness is a prior episode. It may be possible to predict likely severe problems, based on sea level estimates of a poor hypoxic response, but this has not been fully validated.

The management of the more severe forms of altitude sickness that tend to occur with rapid ascent to over 4, 000m (13, 000ft), pulmonary and cerebral oedema, is urgent.

Management of severe altitude sickness


  • Sit upright, and keep warm

  • Nifedipine (20mg bd up to qds + loading dose, 10mg sublingually) to reduce PAP

  • Acetazolamide may help by also reducing PAP as well as increasing the effective ventilatory response to altitude hypoxia.


  • Dexamethasone (4mg qds + loading dose, 8mg) to reduce cerebral oedema.

Improvement is usually rapid once inspiratory O2 tension is raised. Prophylaxis for this severe form of altitude sickness is controversial, but graded ascent is important; acetazolamide probably helps, and nifedipine is used by some, particularly if there is a history of a previous episode.

Further information

Information for doctors/patients. Extreme environments—flying, altitude, diving

Information for patients. Extreme environments—flying, altitude, diving

Information for patients and doctors. Extreme environments—flying, altitude, diving

Luks AM et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med. 2010;21:146–55.Find this resource:



Increased recreational diving has raised the awareness of respiratory problems at depth. These can essentially be divided into five:

  • Barotrauma, e.g. ruptured bullae and pneumothorax

  • Worsening of pre-existing disorder whilst at depth, e.g. asthma

  • Nitrogen gas evolved from solution in body fluids (the ‘bends’)

  • Breath-hold diving and ascent hypoxia

  • Pulmonary oedema.


Barotrauma (second commonest cause of death in SCUBA divers after drowning)

During descent, any air-containing cavity in the body will be compressed by the rise in external pressure. If there is any communication with the airways (e.g. middle ear, lung bullae), then gas will slowly move into the airspace. On ascent, the airspace will expand and, if air cannot escape quickly enough, may lead to rupture of the eardrum or the bullae. A tension pneumothorax can be rapidly fatal in this situation. Obstructive lung diseases in general can predispose to ruptured alveoli. In addition to pneumothoraces, the escaped air can produce a pneumomediastinum, causing chest pain, and a radiolucent band (air in the pericardium) along the cardiac border on CXR. Breathing 100% O2 will clear this air more quickly. Air emboli can also occur and produce a wide range of symptoms; hyperbaric O2 may be required.

Pre-existing lung disease

The onset of asthma during a dive can be disastrous and may be provoked by the dry gases breathed from SCUBA gear (self-contained underwater breathing apparatus). See British Sub-Aqua Club (BSAC) recommendations on asthma and diving (see Box 26.2). Many lung diseases, such as CF, COPD (FEV1 <80% predicted), fibrotic lung disease, previous pneumothorax (with no pleurodesis), and lung bullae, are considered contraindications to diving. However, recently, BSAC has adopted the pragmatic approach of accepting that, in individuals with a history of spontaneous pneumothorax, who have had no pneumothorax for 5y, the risk of pulmonary barotrauma is small and not significantly greater than for many in the general population, e.g. smokers. Such individuals may dive, provided that a CT scan of the chest and lung function tests (including flow–volume loops) show no reason to suggest that there is significant residual lung disease.

The bends or caisson disease

(caisson is an underwater air chamber in which people work) During periods of high pressure, extra nitrogen dissolves into the blood and other tissue fluids. This takes many minutes. On ascent, this nitrogen literally bubbles off. If the amount coming out of solution is too great, nitrogen bubbles act as emboli and limit blood flow. This produces micro-infarction, with activation of inflammatory and clotting cascades and damage to several organs, e.g. joints, spinal cord, brain. Limited diving times and slow ascents reduce this problem, as do breathing mixtures containing helium, rather than nitrogen. Severe cases require treatment in hyperbaric chambers.

Breath-hold diving

During breath-hold diving, increased pressure on the chest elevates alveolar and arterial PO2. This extends breath-hold time, particularly with prior hyperventilation to reduce PaCO2. During the dive, O2 is used and PO2 falls. On ascent, with rarefaction of the thoracic gas, PO2 falls quickly, with possible loss of consciousness and drowning.

Pulmonary oedema

has been reported whilst SCUBA diving in cold water, but the mechanism is not clear.

Further information

Aberdeen emergency number for hyperbaric chambers. Extreme environments—flying, altitude, diving 07831 151523 (Extreme environments—flying, altitude, diving 0845 4086008 in Scotland). Extreme environments—flying, altitude, diving and Extreme environments—flying, altitude, diving

Plymouth Diving Disease Research Centre. Extreme environments—flying, altitude, diving (24h helpline and register of hyperbaric chambers). Extreme environments—flying, altitude, diving 01752 209999. Email

BTS guidelines (2003). Extreme environments—flying, altitude, diving

Diving and medical conditions. Extreme environments—flying, altitude, diving

Diving and asthma/pneumothorax. Extreme environments—flying, altitude, diving

Cochard G et al. Pulmonary oedema in scuba divers. Undersea Hyperb Med 2005;32:39–44.Find this resource: