PLEURAL EFFUSION IN HEART DISEASE
Pleural effusions commonly occur in patients with congestive heart failure (CHF). The effusions are a sequela of pulmonary venous hypertension and not the result of isolated systemic venous hypertension unless there is associated ascitic ﬂuid with transdiaphragmatic movement into the pleural space. With systolic or diastolic left-sided heart failure, pulmonary venous pressure increases, causing ﬂuid to move into the lung interstitium; the increased interstitial–pleural pressure gradient promotes the movement of ﬂuid between mesothelial cells into the pleural space. If pleural ﬂuid formation exceeds removal through the parietal pleural lymphatics, a pleural effusion will develop.
Pleural effusion from heart disease can also be caused by constrictive pericarditis, which is deﬁned by marked ﬁbrous thickening of the pericardium causing chronic cardiac compression. Causes of constrictive pericarditis include tuberculosis, cardiac surgery, connective tissue disease, radiation therapy, malignancies, and other infections (including viruses). Constrictive pericarditis results in limited ventricular diastolic ﬁlling. End-diastolic ventricular pressures and mean atrial pressures increase to virtually equal levels.
Patients with CHF present with the typical manifestations of orthopnea, paroxysmal nocturnal dyspnea, and dyspnea on exertion. Chest radiographs show evidence of pulmonary venous hypertension; extravascular lung water; and bilateral pleural effusions, with the right effusion typically being greater. A unilateral left pleural effusion in the patient with heart disease should suggest an alternate diagnosis.
Constrictive pericarditis is more common in men whose chief complaints include fatigue, dyspnea, weight gain, abdominal discomfort, and peripheral edema. The usual physical ﬁndings are sinus tachycardia, distant heart sounds, and prominent cervical neck veins that do not decrease with inspiration (Kussmaul sign). Chest radiographs reveal bilateral effusions with a normal heart size. In contrast to CHF, constrictive pericarditis results in ascites before the appearance of peripheral edema. A pulsus paradoxus is observed in most patients. The diagnosis is conﬁrmed by right-sided and left-sided heart catheterization demonstrating equalization of diastolic pressures.
Pleural effusion in CHF is the classic transudate. The total nucleated cell count is generally less than 500/L with a predominance of lymphocytes and mesothelial cells. The pH typically ranges from 7.45 to 7.55, and the glucose concentration is similar to the serum concentration. However, it is important to note that diuretic therapy may elevate both the protein and lactate dehydrogenase ratios into the exudative range in approximately 10% of patients. Use of the serum– pleural ﬂuid albumin gradient (serum minus pleural ﬂuid) helps determine whether the effusion is caused solely by CHF. If the albumin gradient is 1.2 g/dL, it is highly likely that the effusion is a transudate.
Pleural ﬂuid ﬁndings in patients with constrictive pericarditis are similar to those of CHF but may be exudative with effusive constriction from inﬂammatory pericarditis.
Management of patients with CHF is directed at decreasing pulmonary venous hypertension with diuretics, afterload reduction, digitalis, and salt restriction. Treatment of patients with constrictive pericarditis includes pericardiectomy.