To the Editor:
The recent multicenter prospective observational study by Dres et al.1 examining the impact of pleural effusions on liberation from mechanical ventilation showed that 13% of their patients had a pleural effusion at the time of ventilator weaning, but that there was no relationship to the successful discontinuation of ventilation. Indeed, in their discussion on the potential reasons why pleural effusions might influence ventilator weaning failure, they identified three principal mechanisms. The first of these was the impact on respiratory mechanics, suggesting that large pleural effusions could reduce the end-expiratory lung volumes. The second mechanism was linked with the potential for pleural effusions to have an impact on the impairment of gas exchange, stating that associated lung collapse caused by the effusion could increase hypoxemia due to ventilation perfusion mismatch or intrapulmonary shunting. The third mechanism that they outlined related to the potential impact on cardiac filling pressures, with pleural effusions potentially increasing these filling pressures, and as a result, weaning-induced pulmonary edema. We contend that this last mechanism seems far less likely given that it would have to be the result of a significant leftward shift of the interventricular septum or some another cause of left-sided systolic or diastolic dysfunction. What is far more common is that pleural effusions often are the consequence of high left atrial pressure (i.e., forming due to hydrostatic forces), and therefore represent the same underlying pathophysiologic state, that is heart failure or fluid overload. The elevated left atrial pressure, when coupled with increased venous return that occurs with reduced intrathoracic pressures during weaning, may result in pulmonary edema.
Furthermore, the authors failed to elaborate on a potentially even more important and mechanically simple mechanism; namely, mechanical compression of the lung by the effusion that could subsequently increase the pulmonary vascular resistance. Indeed, it is well known that pulmonary vascular resistance is optimal at functional residual capacity.2 Anything that reduced this functional residual capacity (such as a pleural effusion) could increase pulmonary vascular resistance, and subsequently cause right ventricular dysfunction,3 leading to an impairment in the ability to successfully wean from ventilation. However, because they did not measure pulmonary artery pressures, nor have an identified subset of patients with preexisting right ventricular dysfunction, they were not able to determine whether pleural effusions would have a negative impact on this patient subset. Indeed, this subset of patients is increasingly common and as a result, their negative study (i.e., not being able to demonstrate that pleural effusions had any impact on weaning), should likely be specifically applied to the nonpulmonary hypertensive patient, with no preexisting right ventricular dysfunction.
The authors declare no competing interests.