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- Chronic respiratory disease
- hypoxic challenge test
- fitness to fly test
- QTc interval
- acute hypoxia
- respiratory measurement
Current UK guidelines recommend administration of in-flight supplemental oxygen to patients with chronic respiratory disease who have sea level arterial oxygen saturations <92% or partial pressure of oxygen (Pao2) <6.6 kPa (50 mm Hg) during a hypoxic challenge fitness to fly test.1 Hypoxia has been shown to prolong cardiac repolarisation, assessed by the QT interval corrected for heart rate (QTc), and this may underlie the occurrence of potentially life-threatening cardiac arrhythmias2–4; however, few data exist about the cardiac response to hypoxia in patients with respiratory disease.
To establish whether hypoxia prolongs the QTc, potentially increasing the risk of significant arrhythmias in patients with respiratory disease, we analysed data from respiratory patients referred to our lung function department for fitness to fly testing.
Between 1 April 2008 and 27 February 2009, 101 patients (median age 57 years, range 20–87 years, 57.4% female) underwent hypoxic challenge (breathing 15% oxygen from a Douglas bag). Pulse oximetry was recorded continuously and an ECG recorded at baseline and after 15 min hypoxic exposure. In 65 patients (64.4%), capillary blood gases were analysed at the same time points. Further details are available online.
Disease aetiology was interstitial lung disease (39.6%), chronic obstructive pulmonary disease (COPD) (11.9%), bronchiectasis (11.9%), sarcoidosis (7.9%), cystic fibrosis (6.9%), systemic sclerosis (5.9%), asthma (5.0%), extrinsic allergic alveolitis (3.0%) and other chronic lung conditions (7.9%). Fifteen subjects (14.9%) had known cardiac disease.
Following hypoxic exposure, mean±SEM arterialised capillary Po2 decreased from 10.56±0.14 kPa to 6.82±0.09 kPa (p<0.001) and mean arterial oxygen saturation (Sao2) from 95.8±0.15% to 87.2±0.45% (p<0.001). Arterial carbon dioxide partial pressure, bicarbonate and transcutaneous carbon dioxide partial pressure also decreased (p<0.05, table 1).
Twenty patients (19.8%) became symptomatic during the test (combinations of dyspnoea, palpitations, nausea and dizziness). Eighty patients (79.2%) met the BTS criteria for use of supplemental oxygen in-flight.
Hypoxic challenge resulted in a significant increase in heart rate (from 83.2±1.48 bpm to 86.9±1.50 bpm; p<0.001) and decrease in PR interval (161.2±1.64 ms to 158.0±2.07 ms; p=0.02). In keeping, the QT interval decreased (357.8±4.08 ms to 348.8±3.49 ms; p<0.001). However, ECG frontal axis and QTc did not change (415.2±2.57 ms to 417.0±2.39 ms; p=0.50).
There was no correlation between changes in QTc and Pao2/Sao2. No patient suffered arrhythmias or ischaemic ECG changes. The presence of cardiac disease was not associated with differences in baseline measures or hypoxia response, including variation in QTc. ECG responses did not differ between those who had capillary blood gases performed (n=65) and those who did not (n=36; p>0.5 in all cases)
Exposure to acute hypoxia (15% fractional inspired oxygen) is not associated with significant changes in cardiac QTc in patients with chronic respiratory disease, in contrast to the QTc prolongation seen in healthy subjects at altitude.2 4 5 The absence of response might be due to hypoxic preconditioning6 7 or drug effects upon autonomic efferent response (eg, salmeterol, ipratropium) or through other means (eg, renin-angiotensin system antagonists8). Given the association between prolonged QTc and sudden death in COPD,9 these data are reassuring to patients with chronic lung disease who wish to fly. However, further studies are needed to confirm these findings, as well as the effects of prolonged hypoxia and exercise.
JS drafted the manuscript and all authors have significantly contributed to, read and approved the final manuscript.
These data were orally presented in part at the British Thoracic Society Winter Meeting 2009 and have been published in abstract form in Thorax 2009;64:Supplement IV.
Funding This work was supported by the NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London.
Competing interests None.
Provenance and peer review Not commissioned; not externally peer reviewed.
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