Pulmonary and pleural complications of cardiac disease

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co