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Dysfunctional breathing (DB) is a disabling condition which affects the biomechanical breathing pattern and is challenging to diagnose. It affects individuals in many circumstances, including those without underlying disease who may even be athletic in nature. DB can also aggravate the symptoms of those with established heart or lung conditions. However, it is treatable and individuals have much to gain if it is recognized appropriately. Here we consider the role of cardiopulmonary exercise testing (CPET) in the identification and management of DB. Specifically, we have described the diagnostic criteria and presenting symptoms. We explored the physiology and pathophysiology of DB and physiological consequences in the context of exercise. We have provided examples of its interplay with co-morbidity in other chronic diseases such as asthma, pulmonary hypertension and left heart disease. We have discussed the problems with the current methods of diagnosis and proposed how CPET could improve this. We have provided guidance on how CPET can be used for diagnosis, including consideration of pattern recognition and use of specific data panels. We have considered categorization, e.g., predominant breathing pattern disorder or acute or chronic hyperventilation. We have explored the distinction from gas exchange or ventilation/perfusion abnormalities and described other potential pitfalls, such as false positives and periodic breathing. We have also illustrated an example of a clinical pathway utilizing CPET in the diagnosis and treatment of individuals with suspected DB.

Pulmonary rehabilitation (PR) for people with COPD leads to clinically significant improvements in quality of life and exercise capacity [1]. In England and Wales, UK, in 2013–2014, only 15% of eligible patients were referred (51% from primary care), of whom 31% did not attend assessment [2]. We aimed to generate a theory-informed understanding of enablers and barriers to PR referral and uptake from primary care., Healthcare service and patient barriers contribute to low referral to and uptake of pulmonary rehabilitation (PR). Solutions should support skilled clinician–patient conversations and span primary care–PR boundaries to prevent disjointed working. http://bit.ly/2PVKHZf

We describe two cases of patients with emphysema who, in the lead up to hyperinflation intervention, developed pneumonia with significant physiological, anatomical, functional and quality of life improvement observed following. This directly goes against the natural history of both disease processes, demonstrating the benefit resulting from infective autobullectomy. Keywords: COPD, Autobullectomy, Lung volume reduction

Cardiovascular and skeletal muscle manifestations constitute important comorbidities in COPD, with systemic inflammation proposed as a common mechanistic link. Fibrinogen has prognostic role in COPD. We aimed to determine whether aortic stiffness and quadriceps weakness are linked in COPD, and whether they are associated with the systemic inflammatory mediator—fibrinogen. Aortic pulse wave velocity (aPWV), quadriceps maximal volitional contraction (QMVC) force and fibrinogen were measured in 729 patients with stable, Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages II–IV COPD. The cardiovascular and muscular manifestations exist independently (P=0.22, χ2). Fibrinogen was not associated with aPWV or QMVC (P=0.628 and P=0.621, respectively), making inflammation, as measured by plasma fibrinogen, an unlikely common aetiological factor.

Cardiovascular disease is a common comorbidity and cause of mortality in chronic obstructive pulmonary disease. A better understanding of mechanisms of cardiovascular risk in chronic obstructive pulmonary disease patients is needed to improve clinical outcomes. We hypothesized that such patients have increased arterial stiffness, wave reflections, and subclinical atherosclerosis compared with controls and that these findings would be independent of smoking status and other confounding factors. A total of 458 patients with a diagnosis of chronic obstructive pulmonary disease and 1657 controls (43% were current or ex-smokers) with no airflow limitation were matched for age, sex, and body mass index. All individuals underwent assessments of carotid–femoral (aortic) pulse wave velocity, augmentation index, and carotid intima–media thickness. The mean age of the cohort was 67±8 years and 58% were men. Patients with chronic obstructive pulmonary disease had increased aortic pulse wave velocity (9.95±2.54 versus 9.27±2.41 m/s; P P P

Levetiracetam is widely regarded as a benign antiepileptic drug, compared to older antiepileptic medication. We report a case of eosinophilic pneumonia due to levetiracetam use in a non-smoking woman aged 59 years with no previous respiratory history. Our patient presented with exertional breathlessness and marked desaturation on exertion. She displayed 'reverse bat-wing' infiltrates on her chest radiograph and peripheral eosinophilia on a complete blood count. Her symptoms, radiology and peripheral eosinophilia resolved completely with cessation of levetiracetam and a course of prednisolone. This is the first report of isolated eosinophilic pneumonia due to levetiracetam. Other reports of levetiracetam-induced eosinophilia describe drug rash, eosinophilia and systemic symptoms (DRESS syndrome). Detection of pulmonary drug reactions requires a careful drug history and high index of suspicion. Identifying and reporting a causative agent is crucially important, as cessation of the drug is essential for resolution of the syndrome.