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Highlights the importance of using total lung capacity and arterial blood gas tensions to accurately diagnose and manage co-existing COPD and left ventricular failure.
The documentation of a 20.5% prevalence of heart failure (with ischaemic heart disease as the underlying cause in 20.2%) in stable chronic COPD1 is consistent with the observation made by Keistinen et al.2 that coronary heart disease was the cause of death in 26.7% of male patients with COPD. When establishing the diagnosis of COPD in patients with co-existing left ventricular failure (LVF), however, the authors of the present study should have relied not just on an FEV1/FVC ratio of <70% as their predecessors had done,3 but also on a concomitant increase in total lung capacity (TLC),4 given the fact that an FEV1/FVC ratio of <70% (which can be documented even in non-smokers with LVF), on its own, does not distinguish the obstructive lung defect of COPD from the obstructive lung defect of LVF.5 The distinction between the two can only be made on the basis that the obstructive lung defect of COPD is accompanied by an increase in TLC,4 whereas in LVF, airflow obstruction is accompanied by a fall in TLC due to lung stiffness attributable to alveolar oedema.5 Where the two conditions co-exist, the index of suspicion may be raised by the fact that ‘the TLC is not as high as expected for this level of airflow obstruction’,6 but to establish the presence of the COPD component beyond all doubt requires documentation of a high TLC either before the onset of LVF7 or after the resolution of pulmonary oedema.8 The identification of the co-existence of COPD and LVF also carries the responsibility to document the arterial blood gas tensions so that long-term oxygen therapy (LTOT) can be administered where appropriate,9,10 thereby avoiding the glaring errors of omission identified in a previous study where 50% of significantly hypoxaemic patients (with arterial oxygen tensions <7.3 kPa) characterized by the association of left ventricular ejection fraction (LVEF) <45% and stable COPD were not availed of what is now the British Thoracic Society Guidance on LTOT.10 Concomitant awareness of arterial carbon dioxide status also alerts frontline emergency medical staff about the potential dangers of uncontrolled oxygen therapy during exacerbations of COPD,11 and this is of even greater relevance when the co-existence of LVF and COPD is characterized by carbon dioxide retention (Table 2),3 given the widely prevalent practice of administering uncontrolled oxygen for exacerbations of LVF.
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Oscar M.P. Jolobe (2005) studied this question.
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