Pleural effusions have a major impact on the cardiorespiratory system. This article reviews the pathophysiological effects of pleural effusions and pleural drainage, their relationship with breathlessness, and highlights key knowledge gaps.
The basis for breathlessness in pleural effusions and relief following thoracentesis is not well understood. Many existing studies on the pathophysiology of breathlessness in pleural effusions are limited by small sample sizes, heterogeneous design and a lack of direct measurements of respiratory muscle function. Gas exchange worsens with pleural effusions and improves after thoracentesis. Improvements in ventilatory capacity and lung volumes following pleural drainage are small, and correlate poorly with the volume of fluid drained and the severity of breathlessness. Rather than lung compression, expansion of the chest wall, including displacement of the diaphragm, appears to be the principle mechanism by which the effusion is accommodated. Deflation of the thoracic cage and restoration of diaphragmatic function after thoracentesis may improve diaphragm effectiveness and efficiency, and this may be an important mechanism by which breathlessness improves. Effusions do not usually lead to major hemodynamic changes, but large effusions may cause cardiac tamponade and ventricular diastolic collapse. Patients with effusions can have impaired exercise capacity and poor sleep quality and efficiency.
Pleural effusions are associated with abnormalities in gas exchange, respiratory mechanics, respiratory muscle function and hemodynamics, but the association between these abnormalities and breathlessness remains unclear. Prospective studies should aim to identify the key mechanisms of effusion-related breathlessness and predictors of improvement following pleural drainage.
aCentre for Asthma, Allergy and Respiratory Research, School of Medicine and Pharmacology, University of Western Australia
bPleural Medicine Unit, Lung Institute of Western Australia
cDepartment of Respiratory Medicine, Sir Charles Gairdner Hospital
dPhysiotherapy Unit, Lung Institute of Western Australia
eDepartment of Physiotherapy, Sir Charles Gairdner Hospital
fSchool of Physiotherapy and Exercise Science, Curtin University
gCentre for Sleep Science, School of Anatomy, Physiology and Human Biology, University of Western Australia
hWest Australian Sleep Disorders Research Institute, Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
Correspondence to Dr Rajesh Thomas, MBBS, FRACP, Department of Respiratory Medicine, B Block, QE II Medical Centre, Perth, WA 6009, Australia. Tel: +61 93463333; fax: +61 8 93462816; e-mail: firstname.lastname@example.org
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