Background: Pleural effusion is common in routine medical practice and can be due to many different underlying diseases. Precise differential diagnostic categorization is essential, as the treatment and prognosis of pleural effusion largely depend on its cause. Methods: This review is based on pertinent publications retrieved by a selective search in PubMed and on the authors' personal experience. Results: The most common causes of pleural effusion are congestive heart failure, cancer, pneumonia, and pulmonary embolism. Pleural fluid puncture (pleural tap) enables the differentiation of a transudate from an exudate, which remains, at present, the foundation of the further diagnostic work-up. When a pleural effusion arises in the setting of pneumonia, the potential development of an empyema must not be overlooked. Lung cancer is the most common cause of malignant pleural effusion, followed by breast cancer. Alongside the treatment of the underlying disease, the specific treatment of pleural effusion ranges from pleurodesis, to thoracoscopy and video-assisted thoracoscopy (with early consultation of a thoracic surgeon), to the placement of a permanently indwelling pleural catheter. Conclusion: The proper treatment of pleural effusion can be determined only after meticulous differential diagnosis. The range of therapeutic options has recently become much wider. More data can be expected in the near future concerning diagnostic testing for the etiology of the effusion, better pleurodetic agents, the development of interventional techniques, and the genetic background of the affected patients.

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We aimed to characterise the association of pulmonary hypertension due to hypoventilation and exercise capacity, and the haemodynamic and functional changes under noninvasive ventilation.A retrospective analysis was carried out to assess haemodynamics and functional capacity in 18 patients with daytime pulmonary hypertension, due to hypoventilation, at baseline and after 3 months of noninvasive ventilation.Patients presented with a mean¡SD pulmonary artery pressure of 49¡13 mmHg, preserved cardiac index (3.2¡0.66 L?min -1 ?m -2 ), 6-min walking distance of 303¡134 m and severely elevated N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. Mean pulmonary artery pressure correlated negatively with maximum work rate (R5 -0.72; p50.03) and 6-min walking distance (R5 -0.62; p50.01). Following noninvasive ventilation we found a significant reduction of mean pulmonary artery pressure (-18 mmHg; p,0.001) and NT-proBNP levels (-2110 pg?mL -1 ; p50.001), and improvement in the 6-min walking distance (+66 m; p50.008) and maximum work rate (+18 W; p50.028). Changes in work rate correlated inversely with pulmonary artery pressure (R5 -0.75; p50.031).In this specific cohort with hypoventilation and severe pulmonary hypertension, pulmonary hypertension was associated with reduced exercise capacity. Following noninvasive ventilation, haemodynamics and exercise capacity improved significantly. @ERSpublications Pulmonary hypertension due to alveolar hypoventilation is associated with functional impairment and improved by NIPPV

Background: Patients with chronic thromboembolic pulmonary disease (CTED) have persistent pulmonary vascular obstruction and exercise intolerance without pulmonary hypertension at rest and may benefit from pulmonary endarterectomy. However, up to now, CTED has been poorly characterized. Objectives: This study aimed to analyze the exercise capacity and limiting factors in CTED. Methods: We compared right heart catheterization and cardiopulmonary exercise test results of patients with CTED [mean pulmonary artery pressure (mPAP) at rest <25 mm Hg, n = 10], chronic thromboembolic pulmonary hypertension (CTEPH, n = 31) and a control group (n = 41) presenting with dyspnea but normal pulmonary vascular imaging and excluded pulmonary hypertension. Results: Subjects with CTED show a reduced oxygen uptake [median 76/interquartile range (IQR) 22% pred.] and work rate (median 76/IQR 21 W). The work rate was significantly lower compared to control subjects (p = 0.04) but not significantly different from CTEPH patients (p = 0.66). Oxygen pulse and breathing reserve were normal. CTED subjects showed decreased end-tidal CO₂ at anaerobic threshold (28.4/4.3 mm Hg), an elevated VE/VCO₂ slope (42.5/23.5), breathing equivalents (EQO₂ 32.0/8.7, EQCO₂ 39.5/8.8), alveolar-capillary oxygen gradient (34.7/15.5 mm Hg) and capillary end-tidal carbon dioxide gradient (8.8/5.7 mm Hg) compared to control subjects (p < 0.001). The degree of limitation was similar to that in CTEPH. Conclusions: Despite an mPAP of <25 mm Hg, subjects with CTED show objective functional impairment and similar limitations to patients with CTEPH. Functional limitation is characterized by gas exchange disturbance and ineffective ventilation.