Pathophysiology of dyspnoea in pleural effusion

Abstract

Pleural effusion induces an increase in pleural pressure, resulting in a cascade of changes in the physiological parameters of the thoracic cavity. These changes include increased volume of the rib cage, abnormal gas exchange, impaired respiratory mechanics, and abnormal diaphragmatic movements. Such alterations have a significant clinical impact, including the development of specific symptoms such as dyspnoea. Dyspnoea secondary to pleural effusion has a complex physiopathology. Notably, the severity of dyspnoea often shows a poor correlation with effusion size and may not improve after fluid drainage. The symptomatic relief experienced by patients after fluid drainage is largely attributed to improvements in the length–tension relationship of the respiratory muscles. Importantly, dyspnoea in these cases results from the abnormal shape and restricted motion of the ipsilateral hemidiaphragm, coupled with an increased compensatory respiratory drive aimed at preserving adequate ventilation. Fluid drainage reduces diaphragmatic distension, restoring diaphragmatic mobility, reducing inspiratory neural drive, and enhancing the neuromechanical coupling of the diaphragm, all of which contribute to dyspnoea relief. This review explores current evidence regarding the pathophysiological mechanisms underlying dyspnoea in pleural effusion and the therapeutic effects of thoracentesis.