Peter G. Rogers

Effect of simulated commercial flight on oxygenation in patients with interstitial lung disease and chronic obstructive pulmonary disease

Background: Commercial aircraft cabins provide a hostile environment for patients with underlying respiratory disease. Although there are algorithms and guidelines for predicting in-flight hypoxaemia, these relate to chronic obstructive pulmonary disease (COPD) and data for interstitial lung disease (ILD) are lacking. The purpose of this study was to evaluate the effect of simulated cabin altitude on subjects with ILD at rest and during a limited walking task. Methods: Fifteen subjects with ILD and 10 subjects with COPD were recruited. All subjects had resting arterial oxygen pressure (Pao2) of >9.3 kPa. Subjects breathed a hypoxic gas mixture containing 15% oxygen with balance nitrogen for 20 minutes at rest followed by a 50 metre walking task. Pulse oximetry (Spo2) was monitored continuously with testing terminated if levels fell below 80%. Arterial blood gas tensions were taken on room air at rest and after the resting and exercise phases of breathing the gas mixture. Results: In both groups there was a statistically significant decrease in arterial oxygen saturation (Sao2) and Pao2 from room air to 15% oxygen at rest and from 15% oxygen at rest to the completion of the walking task. The ILD group differed significantly from the COPD group in resting 15% oxygen Sao2, Pao2, and room air pH. Means for both groups fell below recommended levels at both resting and when walking on 15% oxygen. Conclusion: Even in the presence of acceptable arterial blood gas tensions at sea level, subjects with both ILD and COPD fall below recommended levels of oxygenation when cabin altitude is simulated. This is exacerbated by minimal exercise. Resting sea level arterial blood gas tensions are similarly poor in both COPD and ILD for predicting the response to simulated cabin altitude.

Chronic cough in patients with sleep-disordered breathing

Chronic cough can be the sole presenting symptom for patients with obstructive sleep apnoea. We investigated the prevalence, severity and factors associated with chronic cough in patients with sleep-disordered breathing (SDB). We invited 108 consecutive patients who had been referred for evaluation of SDB to complete a comprehensive questionnaire on respiratory and sleep health, which included the Leicester Cough Questionnaire (cough specific quality of life; LCQ), Epworth Sleepiness Scale (ESS) and the Mayo Clinic gastro-oesophageal questionnaire. Chronic cough was defined as cough for a duration of >2 months. 33% of patients with SDB reported a chronic cough. Patients with a chronic cough had impaired cough related-quality of life affecting all health domains (mean±sem LCQ score 17.7±0.7; normal = 21). Patients with SDB and chronic cough were predominantly females (61% versus 17%; p<0.001) and reported more nocturnal heartburn (28% versus 5%; p = 0.03) and rhinitis (44% versus 14%; p = 0.02) compared to those without SDB. There were no significant differences in ESS, respiratory disturbance index, body mass index, or symptoms of breathlessness, wheeze, snoring, dry mouth and choking between those with cough and those without. Chronic cough is prevalent in patients with SDB and is associated with female sex, symptoms of nocturnal heartburn and rhinitis. Further studies are required to investigate the impact of continuous positive airway pressure therapy on cough associated with SDB to explore the mechanism of this association.

Abnormal ventilatory control in Parkinson's disease--further evidence for non-motor dysfunction.

There has been increasing recognition of pre-motor manifestations of Parkinsons disease (PD) resulting from early brainstem involvement. We sought to determine whether ventilatory control is abnormal. Patients with PD without respiratory disease were recruited. Spirometry, lung volumes, diffusing capacity and respiratory muscle strength were assessed. Occlusion pressure and ventilation were measured with increasing CO(2). Arterial blood gases were taken at rest and following 20 min exposure to 15% O(2). A linear correlation assessed associations between respiratory function and indices of PD severity. 19 subjects (17 males) with mild-moderate PD were studied (mean (SD) age 66 (8) years). Respiratory flows and volumes were normal in 16/19. Maximum inspiratory and expiratory pressures were below LLN in 13/19 and 15/19 respectively. 7/15 had a reduced ventilatory response to hypercapnia and 11/15 had an abnormal occlusion pressure. There was no correlation between impairment of ventilatory response and reduction in respiratory muscle strength. Response to mild hypoxia was normal and there were no associations between disease severity and respiratory function. Our findings suggest that patients with mild-moderate PD have abnormal ventilatory control despite normal lung volumes and flows.

Directly measured cabin pressure conditions during Boeing 747–400 commercial aircraft flights

Background and objectives:  In the low pressure environment of commercial aircraft, hypoxaemia may be common and accentuated in patients with lung or heart disease. Regulations specify a cabin pressure not lower than 750 hPa but it is not known whether this standard is met. This knowledge is important in determining the hazards of commercial flight for patients and the validity of current flight simulation tests.

Right heart function during simulated altitude in patients with pulmonary arterial hypertension.

Objective Patients with pulmonary arterial hypertension (PAH) are often recommended supplemental oxygen for altitude travel due to the possible deleterious effects of hypoxia on pulmonary haemodynamics and right heart function. This includes commercial aircraft travel; however, the direct effects and potential risks are unknown. Methods Doppler echocardiography and gas exchange measures were investigated in group 1 patients with PAH and healthy patients at rest breathing room air and while breathing 15.1% oxygen, at rest for 20 min and during mild exertion. Results The 14 patients with PAH studied were clinically stable on PAH-specific therapy, with functional class II (n=11) and III (n=3) symptoms when tested. Measures of right ventricular size and function were significantly different in the PAH group at baseline as compared to 7 healthy patients (p<0.04). There was no evidence of progressive right ventricular deterioration during hypoxia at rest or under exertion. Pulmonary arterial systolic pressure (PASP) increased in both groups during hypoxia (p<0.01). PASP in hypoxia correlated strongly with baseline PASP (p<0.01). Pressure of arterial oxygen correlated with PASP in hypoxia (p<0.03) but not at baseline, with three patients with PAH experiencing significant desaturation. The duration and extent of hypoxia in this study was tolerated well despite a mild increase in symptoms of breathlessness (p<0.01). Conclusions Non-invasive measures of right heart function in group 1 patients with PAH on vasodilator treatment demonstrated a predictable rise in PASP during short-term simulated hypoxia that was not associated with a deterioration in right heart function.

Maintenance of vital capacity during repetitive breath-hold in a spearfishing competition

Background and objective:  Cough and a reduction in vital capacity have recently been reported following breath‐hold dives to depths of 25–75 m. We sought to investigate whether repetitive dives to depths of less than 30 m would elicit similar effects.

Reduced hypoxic sympathetic response in mild Parkinson's disease: further evidence of early autonomic dysfunction.

The Braak staging hypothesis in Parkinson’s disease (PD) suggests that non-motor dysfunction may precede the classical motor symptoms, and this is supported by observations of postural hypotension, cardiac denervation, bowel dysmotility and hyposmia early in disease [1]. However, the effects of this process on the respiratory system, whose central control system resides mainly in the medulla, have been largely ignored. The dorsal motor nucleus of the vagus in the medulla is one of the earliest regions to accumulate alpha synuclein pathology. The dorsal medullary respiratory centre including the nucleus of the tractus solitarius receives afferent input from carotid and aortic chemoreceptors, which respond to a reduction in arterial oxygen tension and to an increase in arterial carbon dioxide. A reduced ventilatory response to hypoxia [2] and hypercapnia [3] has been reported in those with moderate PD, which was not related to peripheral muscle weakness or impairment in lung function. Dopaminergic therapy is standard in PD and its action on the dopamine receptors within the carotid body is not totally understood, but may affect both ventilatory and sympathetic control [4]. There is strong evidence that low-dose dopamine infusions reduce the ventilatory response to hypoxia in healthy normals and in those with heart failure [5,6]. This raises the question as to whether PD or the dopaminergic treatment was responsible for the previously observed reduced ventilatory drive in moderately advanced PD. We hypothesise that abnormalities in central respiratory control may be identifiable in mild PD due to the early pathological involvement of the medulla. We sought to assess the ventilatory and sympathetic response to hypoxia and hypercapnia before and after dopaminergic medication in patients with mild PD and compare to healthy normals. Patients with mild idiopathic PD were recruited from a hospitalbased PD outpatient clinic. Patients were excluded if they had any clinically significant respiratory or cardiovascular disease or a significant smoking history (>10 pack years). A history, including current medications and disease severity classifications off medications were documented. Ventilatory and sympathetic responses to progressive poikilocapnic hypoxia and isoxic hypercapnia were assessed via rebreathing methods (Vmax Encore, Sensormedics, Yorba Linda,

All that wheezes is not asthma: the value of curves

A 64-year-old woman, never smoker, with a history of fully treated tuberculosis at 20 years of age attended our department for lung function testing. She had recently experienced several episodes of intermittent breathlessness and wheeze presumed to be due to asthma and was referred to a respiratory physician following an emergency department visit during one of these episodes. She did not have any recent weight loss, night sweats, purulent sputum or haemoptysis. Her dyspnoea and wheeze (inspiratory and expiratory) had been refractory to inhaled corticosteroids and both short and long acting β2 agonists. Lung function using American …

The impact of severe lung disease on evidential breath analysis collection

BACKGROUND It is a legal requirement to supply a breath analysis sample when requested by Police at roadside checkpoints. The current device requires a 1L sample at 8L·min(-1). Court disputes commonly attribute respiratory disease for failure to produce a sample. OBJECTIVE To determine whether respiratory disease aetiology and/or severity precludes an adequate breath sample using a modern evidential breath analyser. METHODS Subjects performed breath analysis following standard Police procedure. Three efforts within 15min were allowed and any reasons for failure recorded. RESULTS 24 subjects with interstitial lung disease (ILD) and 26 subjects with chronic obstructive pulmonary disease (COPD) were studied and met minimum respiratory function criteria as per device specifications. 18 ILD subjects (75%) and 24 COPD subjects (92%) were able to provide a sample. All subjects with a vital capacity below 1.5L were unable to provide a sample. DISCUSSION In the balance of probabilities most patients with lung disease are able to supply an evidential breath sample. The exception is a very severe disease, particularly in volume limited patients.

Evidence of respiratory system remodelling in a competitive freediver

To the Editor: We present a healthy freediving subject with increasing lung volumes associated with repeated use of a technique used to enhance athletic performance. The repeated use of the technique over time appears to have altered respiratory system mechanics without any functionally important macroscopic lung damage, at least as evidenced by computed tomography scans and measures of gas exchange. Glossopharyngeal insufflation (GI) employs the glossopharyngeal structures to force air into the lungs above total lung capacity (TLC). It was developed to assist patients with diaphragm weakness in the era when polio was common [1]. Competitive freedivers have modified this technique to increase lung gas prior to apnoea [2], which has proven to enhance duration, distance and depth achieved while submersed. Lung barotrauma has been associated with GI [3, 4], which raises the possibility that use of this technique results in significant lung damage and long-term physiological impairment. The research data from a healthy competitive freediver who practised regular GI training was reviewed. This included longitudinal respiratory function and computed tomography images. On initial presentation in 2004, the subject was a 25-year-old male (186 cm, 90 …