A 64-year-old man comes to the office due to worsening dyspnea on exertion for the past 3 months. The patient has had a nonproductive cough but no chest pain, fever, or chills. He was diagnosed with hypertension several years ago but takes no medications. Blood pressure is 160/96 mm Hg, pulse is 92/min, and respirations are 18/min. Physical examination shows bilateral inspiratory crackles as well as dullness to percussion and decreased breath sounds at the right lung base. Chest x-ray reveals a right-sided pleural effusion. Which of the following pleuropulmonary changes are most likely present in this patient?
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In the normal state, the pleural space contains a small amount of fluid (eg, 5-10 mL) that undergoes constant turnover, with the rate of inflow equivalent to the rate of outflow. The rate of inflow is determined by vascular hydrostatic pressure, vascular oncotic pressure, and vascular membrane permeability (ie, the Starling equation), whereas the rate of outflow is determined by the drainage capacity of the parietal pleural lymphatics. A pleural effusion results from an increased rate of pleural fluid inflow, a decreased rate of pleural fluid outflow, or a combination of the two.
This patient with progressive dyspnea on exertion, nonproductive cough, bilateral crackles on lung auscultation, and a right-sided pleural effusion most likely has decompensated heart failure (chronic, poorly controlled hypertension is a common cause). Pleural effusion in decompensated heart failure is primarily driven by backward transmission of pressure from the failing left ventricle to the pulmonary circulation, resulting in increased pulmonary capillary hydrostatic pressure and an increased rate of fluid inflow to the pleural space. Vascular permeability remains normal, as does vascular oncotic pressure (which is mostly determined by serum albumin concentration). Outflow through the parietal pleural lymphatics increases in response to the increased fluid inflow, but it is unable to keep up, resulting in development of pleural effusion.
(Choice A) Lung malignancy can cause pleural effusion via both an increased rate of inflow due to an inflammatory increase in vascular membrane permeability and a decreased rate of outflow due to obstruction of parietal pleural lymphatics.
(Choice B) All 4 of these changes encourage the development of pleural effusion and multiple disturbances would be required for such changes to take place (eg, lung malignancy [increased vascular permeability and decreased lymphatic flow] in the setting of both hypoalbuminemia [decreased oncotic pressure] and heart failure [increased hydrostatic pressure]).
(Choice C) Hypoalbuminemia (eg, due to nephrotic syndrome or malnutrition) causes pleural effusion due to an increased rate of pleural fluid inflow from reduced vascular oncotic pressure. As with decompensated heart failure, lymphatic flow increases but is unable to keep up with the increased inflow.
(Choice E) All 4 of these changes would discourage the development of pleural effusion.
Educational objective:
Pleural effusion results from an increased rate of fluid inflow from the nearby vasculature or a decreased rate of fluid outflow through the parietal pleural lymphatics. Decompensated heart failure causes pleural effusion primarily due to increased fluid inflow from increased pulmonary capillary hydrostatic pressure; lymphatic outflow increases but is unable to keep up with the increased inflow.