Cardiol Rev. 2022 Dec 28. doi: 10.1097/CRD.0000000000000469. Online ahead of print.
Patients with cardiac disease frequently develop pleural effusions; the incidence is approximately 500,000 cases per year in the United States. These effusions often represent important clinical events for patients, indicating that either there has been an acute change in the patient's clinical status or the patient's chronic management program needs review. These effusions usually develop in both the right and left hemithorax but can be unilateral. The pathogenesis involves increased fluid transfer from parietal pleural capillaries into the pleural space and possibly decreased pleural fluid uptake into parietal pleural lymphatic structures. The increased fluid transfer develops due to increased capillary pressure secondary to elevated venous outflow pressure and secondary to decreased lymphatic flow into central vessels secondary to heart failure. Most pleural effusions associated with heart failure are transudates, but 20% to 25% have increased protein and lactate dehydrogenase levels suggesting an exudative process. Additional testing can clarify the situation and requires calculation of the serum albumin to pleural fluid albumin gradient or measurement of N-terminal pro-brain natriuretic peptide in the pleural fluid. An albumin gradient of greater than 1.2 g/dL suggests that the fluid is a transudate. The presence of a pleural effusion in a hospitalized patient at discharge is associated with an increased likelihood of rehospitalization and mortality within the next year. Patients with large symptomatic pleural effusions may require therapeutic thoracentesis. Recurrence of symptomatic effusions presents a management dilemma that might require repeated thoracenteses, indwelling intrapleural catheter placement, or other management steps used in advanced chronic heart failure.