Development of severe hypoxaemia in chronic obstructive pulmonary disease patients at 2,438m (8,000 ft) altitude. C.C. Christensen, M. Ryg, O.K. Refvem, O.H. Skjùnsberg. #ERS Journals Ltd 2000. ABSTRACT: The arterial oxygen tensions (Pa,O 2 ) in chronic obstructive pulmonary disease (COPD) patients travelling by air, should, according to two different guidelines, not be lower than 7.3 kPa (55 mmHg) and 6.7 kPa (50 mmHg), respectively, at a cabin pressure altitude of 2,438 m (8,000 ft). These minimum in-flight Pa,O 2 values are claimed to correspond to a minimum Pa,O 2 of 9.3 kPa (70 mmHg) at sea-level. The authors have tested whether this limit is a safe criterion for predicting severe in-flight hypoxaemia.The authors measured arterial blood gases at sea-level, at 2,438 m and at 3,048 m (10,000 ft) in an altitude chamber at rest and during light exercise in 15 COPD patients with forced expiratory volume in one second (FEV1) <50% of predicted, and with sea-level Pa,O 2 >9.3 kPa.Resting Pa,O 2 decreased below 7.3 kPa and 6.7 kPa in 53% and 33% of the patients, respectively, at 2,438 m, and in 86% and 66% of the patients at 3,048 m. During light exercise, Pa,O 2 dropped below 6.7 kPa in 86% of the patients at 2,438 m, and in 100% of the patients at 3,048 m. There was no correlation between Pa,O 2 at 2,438 m and preflight values of Pa,O 2 , FEV1 or transfer factor of the lung for carbon monoxide.In contrast to current medical guidelines, it has been found that resting arterial oxygen tension >9.3 kPa at sea-level does not exclude development of severe hypoxaemia in chronic obstructive pulmonary disease patients travelling by air. Light exercise, equivalent to slow walking along the aisle, may provoke a pronounced aggravation of the hypoxaemia. Eur Respir J 2000; 15: 635±639.

To test the applicability of indirect estimation of daily energy expenditure from average daily heart rate (HR) and individual O2-intake/heart rate (VO2/HR) regression lines in subjects with metabolic disorders, VO2/HR regression lines were determined on 2 consecutive days in 17 subjects (five healthy, five with obesity, five with untreated thyrotoxicosis, two with anorexia nervosa). Daily energy expenditure was calculated by means of the average 24 h HR. Generally, there was a high correlation coefficient for the relationship between VO2 and HR, but the slopes and intercepts varied considerably from day to day, leading to poor agreement between duplicate estimates of energy expenditures, and not infrequently to physiologically meaningless values. Further studies, comprising determination of the VO2/HR regression lines in three different body positions on 7 different days in one experienced test subject showed great variability of the VO2/HR regression lines, both in the same position and in different positions. The applied procedure seems unsuitable for metabolic studies in individual patients who engage in ordinary daily activities with low energy expenditure.

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BackgroundThe reduced pressure in the aircraft cabin may cause significant hypoxaemia and respiratory distress in patients with chronic obstructive pulmonary disease (COPD). Simple and reliable methods for predicting the need for supplemental oxygen during air travel have been requested. Objective To construct a pre-flight evaluation algorithm for patients with COPD. Methods In this prospective, cross-sectional study of 100 patients with COPD referred to hypoxia-altitude simulation test (HAST), sea level pulse oximetry at rest (SpO 2 SL ) and exercise desaturation (SpO 2 6MWT ) were used to evaluate whether the patient is fit to fly without further assessment, needs further evaluation with HAST or should receive in-flight supplemental oxygen without further evaluation. HAST was used as the reference method. Results An algorithm was constructed using a combination of SpO 2 SL and SpO 2 6MWT . Categories for SpO 2 SL were >95%, 92e95% and <92%, the cut-off value for SpO 2 6MWT was calculated as 84%. Arterial oxygen pressure (PaO 2 HAST ) <6.6 kPa was the criterion for recommending supplemental oxygen. This algorithm had a sensitivity of 100% and a specificity of 80% when tested prospectively on an independent sample of patients with COPD (n¼50). Patients with SpO 2 SL >95% combined with SpO 2 6MWT $84% may travel by air without further assessment. In-flight supplemental oxygen is recommended if SpO 2 SL ¼92e95% combined with SpO 2 6MWT <84% or if SpO 2 SL <92%. Otherwise, HAST should be performed. Conclusions The presented algorithm is simple and appears to be a reliable tool for pre-flight evaluation of patients with COPD.

Pulmonary hypertension (PH) in patients with chronic obstructive pulmonary disease (COPD) has traditionally been explained as an effect of hypoxaemia. Recently, other mechanisms, such as arterial remodelling caused by inflammation, have been suggested. The aim of this study was to investigate whether exercise-induced PH (EIPH) could occur without concurrent hypoxaemia, and whether exercise-induced hypoxaemia (EIH) was regularly accompanied by increased pulmonary artery pressure or pulmonary vascular resistance index (PVRI).Pulmonary haemodynamics in 17 patients with COPD of varying severity, but with no or mild hypoxaemia at rest, were examined during exercise equivalent to the activities of daily living (ADL) and exhaustion.EIPH occurred in 65% of the patients during ADL exercise. Pulmonary arterial pressure during exercise was negatively correlated with arterial oxygen tension, but EIPH was not invariably accompanied by hypoxaemia. Conversely, EIPH was not found in all patients with EIH. The resting PVRI was negatively correlated with arterial oxygen tension during ADL exercise, but an elevated PVRI without EIH occurred in 35% of the patients.In conclusion, exercise-induced pulmonary hypertension occurred during exercise equivalent to the activities of daily living in chronic obstructive pulmonary disease patients with no or mild hypoxaemia at rest. Although pulmonary artery pressure and arterial oxygen tension were negatively correlated during exercise, a consistent relationship between hypoxaemia and pulmonary hypertension could not be demonstrated. This may indicate that mechanisms other than hypoxaemia contribute significantly in the development of pulmonary hypertension in these patients. Eur Respir J 2004; 24: 580-586