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.
