The electrocardiogram in large pericardial effusion: the forgotten "P" wave and the influence of tamponade, size, etiology, and pericardial thickness on QRS voltage.

There are varying reports on the electrocardiogram in pericardial effusions. Some correlate low QRS voltage with tamponade and the size of the effusion while others do not. Low voltage also appears to vary with the etiology. There are no reports on the influence of pericardial thickness or changes in the P voltage. The authors studied 43 patients with large effusions of whom 26 had tuberculosis and the remaining had viral/idiopathic etiology. Pericardial thickness was measured at chest computed tomography. They found no correlation between the low QRS voltage and tamponade, size of the effusion, etiology, or pericardial thickness. Low voltage of the P wave and T-wave changes were more frequent than low QRS voltage.

Tuberculous pericardial effusion: features, tamponade, and computed tomography.

The clinical features with particular reference to tamponade and mediastinal adenopathy were studied in tuberculous pericardial effusion. Tamponade is a frequent complication and the recognition of tuberculous etiology can be difficult. Involvement of the pericardium is mostly from mediastinal lymph nodes that have not been studied. This was a prospective cohort study. All patients had large effusions, and underwent pericardiocentesis and chest computed tomography. Patients with tuberculosis had specific therapy. Others with viral/idiopathic effusion served as controls for the computed tomography studies. There were 26 patients with tuberculosis: 18 had tamponade on echocardiography. All had symptoms. Fever (n = 23) and dyspnea (n = 20) were the most frequent presenting symptoms. Pericardial rub was heard in 14, and 3 had enlarged cervical or axillary nodes. Pulmonary tuberculosis was present in 6. Tuberculin skin test measured 17 +/- 3.3 mm. The biopsy specimen showed a granuloma in 22 of 24. All 26 had mediastinal lymph nodes > 10 mm with a mean size of 19.5 +/- 8.6 mm that disappeared (81%) or regressed (19%) on treatment (p < 0.001). Aortopulmonary nodes were most frequently enlarged (65.4%) and hilar the least. Three required pericardiectomy. At follow-up all were doing well. None with viral/idiopathic effusion had lymph node enlargement. Fever, dyspnea, and tamponade were frequent with tuberculosis. The prognosis was good with specific therapy. Mediastinal nodes were enlarged in all and only with tuberculosis and not with viral/idiopathic effusion. Nodes disappeared or regressed with treatment. In the appropriate clinical context, mediastinal lymph node enlargement on chest computed tomography along with a strongly positive skin test results could help in the diagnosis of a tuberculous etiology of pericardial effusion.

Tuberculous pericardial effusion--mediastinal lymph glands: the cause and clue to the etiology.

BACKGROUND: Tuberculous pericardial effusion is most often due to the spread of tuberculosis from the mediastinal lymph glands; however, no attempt has yet been made to study these glands. We studied the mediastinal glands in proven tuberculous pericardial effusion patients and hypothesized that the findings may be of use in the etiological diagnosis of pericardial effusion. METHODS AND RESULTS: We studied 45 patients with large pericardial effusion or tamponade. All underwent chest computed tomographic studies that were reviewed by radiologists blinded to the diagnosis. Of these 45 patients, 27 had tuberculosis and 18 had viral or idiopathic effusion. Pericardial biopsy was done in 25/27 and tuberculin skin test in 22/27 patients with tuberculosis, and all received specific treatment. In patients with tuberculosis the skin test measured 17+/-3.3 mm. All 27 had mediastinal lymph glands > or = 10 mm in size. The mean size of the mediastinal glands was 19.5+/-8.6 mm and the mean number was 2.5+/-1.2. The aortopulmonary glands were the most frequently enlarged (63%), and hilar the least often (14.8%). The glands showed a hypodense center in 52% of the patients. On follow-up of 15.8+/-10.4 months, glands were not seen in 80.9%, and were smaller in size in 19%; none had a hypodense center. Marked lymphadenopathy was not seen in any patient with viral/idiopathic pericardial effusion. Two had glands < or = 5 mm in size. CONCLUSIONS: Only patients with tuberculosis had substantial mediastinal lymph gland enlargement and not those with viral or idiopathic pericardial effusion. Such glands disappeared or regressed on treatment. In the appropriate clinical context, marked nonhilar mediastinal lymphadenopathy on chest computed tomographic studies along with a strongly positive tuberculin skin test could be of value in the noninvasive diagnosis of pericardial effusion due to tuberculosis.