Following many forms of cardiac injury, including myocardial infarction, surgery, or trauma, a syndrome of pericarditis, pleuritis, and rarely pneumonitis may develop over the ensuing 1-12 weeks. This process is called Dressler’s syndrome and may be seen in 1-3% of patients following myocardial infarction and up to 30% of cardiac surgery patients. Symptoms include pericardial and pleuritic chest pain, and signs of fever, pericardial or pleural friction rub, and elevated white blood cell count and sedimentation rate are typically seen. Pleural effusions occur in 60-80% of cases, and 50% have an enlarged cardiac silhouette due to pericardial effusion. The pleural effusion is exudative with high protein (usually 3 g/100 ml), pH (7.40), lactate dehydrogenase, and red blood cell count. The etiology of Dressler’s syndrome is unknown but is thought to be due to an antibody-mediated response to myocardial antigens exposed upon injury. Treatment is supportive with nonsteroidals or corticosteroids.
A patient presents with fevers, hempotysis, and multiple pulmonary infiltrates with central radiolucencies on chest x-ray. What is the diagnosis?
Right-sided endocarditis with septic pulmonary emboli. Cardiac disease may lead to pulmonary embolism in the setting of right-sided endocarditis affecting the tricuspid valve. Rarely, septic emboli may arise from indwelling catheters in the superior vena cava. Right-sided endocarditis accounts for 5-10% of all cases of endocarditis and is most often seen in intravenous drug abusers. The most common infecting organism is Staphylococcus aureus, although Streptococcus, gram-negative, and Candida species also may be involved. The radiographic appearance is very characteristic and includes multiple, patchy, ill-defined densities scattered throughout the lung fields, especially in the periphery. They may appear to change in number and size on serial x-rays, reflecting the ongoing shower of emboli to the lungs. Cavitation is seen in 25% of patients.
What are the pulmonary effects of various cardiovascular drugs? Angiotensin-converting enzyme inhibitors cause cough in approximately 15% of all patients but twice as frequently in women than men. The mechanism is not known. (3-blockers are well-known in their ability to precipitate bronchospasm in patients with asthma and occasionally bronchitis. The drugs procainamide and hydralazine may cause a lupus-like syndrome in susceptible individuals. With procainamide, the reaction is much more common and involves a positive antineutrophil antibody test in 50-80% of patients, with 30-40% developing pulmonary infiltrates and 40-50% having pleuropericardial disease. The latter manifestations are rare with hydralazine. Amiodarone causes pulmonary toxicity, with 5-15% of treated patients developing a severe pneumonitis, which is fatal in 5-10%. This side effect is dose-dependent, usually occurring only in patients who have been treated with 400 mg/day for 4 months.
What are the main pulmonary complications of cardiac surgery?
Atelectasis, pneumonia, and exacerbation of COPD. Atelectasis and pneumonia are usually due to the inability of the patient to cough adequately or deep breathe following surgery, often because of the pain of the thoractomy and the heavy use of analgesics and sedatives. These complication are less common following median sternotomy than after lateral thoracotomy. Left lower lobe atelectasis may also be due to concomitant phrenic nerve dysfunction, which may result from
mechanical injury or from the cooling associated with cardioplegia. Phrenic nerve function usually recovers within the first 30 days to 1 year but may take as long as 2 years. Bronchospasm may be worsened. Pleural effusions are also common. Some special pulmonary concerns in cardiac transplant surgery, in addition to those above, include postoperative elevations in pulmonary vascular resistance and the numerous infectious complications associated with immunosuppression.
Differentiate dyspnea due to cardiac disease from that due to pulmonary disease.
This is a common clinical problem, as many patients have concomitant cardiac and pulmonary disease, often in association with cigarette smoking. The most important feature in distinguishing these two etiologies is clues of underlying disease. Thus, a history of angina, hypertension, or previous myocardial infarction, together with signs of heart failure on examination, make cardiac disease more likely; whereas a history of bronchitis and heavy smoking, with diminished breath sounds on examination, and a normal cardiac silhouette with hyperinflated lungs on chest x-ray suggest primary pulmonary disease. In many cases, however, further testing including pulmonary function, arterial blood gases, and a cardiac function assessment with echocardiography or radioisotope scanning, are necessary. Exercise testing with measurement of expired gases can be helpful in difficult cases.
Can the pattern of dyspnea help distinguish between cardiac and pulmonary causes? Yes and no. Paroxysmal nocturnal dyspnea (PND) is thought to be specific for heart failure, but patients with COPD may also complain of PND due to the development of increased secretions upon lying down. Asthmatics may also have PND due to nocturnal worsening of bronchospasm. Orthopnea is likewise not specific for congestive heart failure because COPD patients sometimes complain of orthopnea due to partial loss of diaphragmatic and accessory muscle function when supine. Sleep apnea is often associated with hypertension or left-heart failure, but secondary pulmonary hypertension may result from years of hypoxia. Cheyne-Stokes respirations, or periodic breathing, is characteristic of left ventricular dysfunction and rarely associated with pulmonary disease per se. A recent study of patients with congestive heart failure and Cheyne-Stokes respirations found that such patients were more likely to have awake hypocapnia due to hyperventilation. Such patients may complain of PND during periods of hyperpnea.
Can pulmonary function predict cardiovascular morbidity and mortality?
Yes. Recent studies have shown an inverse relationship between pulmonary function, as measured by FEV, or FVC, and the incidence of coronary artery disease and congestive heart failure, independent of cigarette smoking. One explanation for these findings is that decreased pulmonary function is a marker of centripetal obesity and decreased physical activity, which are themselves related to increased insulin resistance, lower high-density lipoproteins, and higher triglycerides. Hyperinsulinemia is associated with increased sympathetic nervous activity and therefore may result in increased risk of hypertension and myocardial infarction.
How can heart disease cause an exudative pleural effusion? Photo Gallery
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