Isolated right atrial tamponade by serous fluid simulating tricuspid stenosis

Isolated right atrial tamponade by serous fluid simulating tricuspid stenosis

Isolated Right Atrial Tamponade by Serous Fluid Simulating Tricuspid Stenosis RAPHAEL ZAHLER, M.D. WARREN BREISBLATT, M.D. SABET HASHIM, M.D. CHARLES...

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Isolated Right Atrial Tamponade by Serous Fluid Simulating Tricuspid Stenosis

RAPHAEL ZAHLER, M.D. WARREN BREISBLATT, M.D. SABET HASHIM, M.D. CHARLES KLEINMAN, M.D. RENE LANGOU, M.D. New Haven, Connecticut

Echocardiography is a key diagnostic tool in the recognition of pericardial tamponade. A 56-year-old man in whom severe dyspnea developed 22 days after cardiac surgery is described. Echocardiography suggested tricuspid valve disease but showed no pericardial abnormalities. Catheterization revealed functional stenosis of a normal tricuspid valve caused by loculated serous pericardial fluid. The diagnosis of cardiac tamponade is usually made by physical examination and corroborated by the finding of pericardial fluid on echocardiography, a highly sensitive test. In contrast, loculated effusions, often associated with hemopericardium or clot, are sometimes difficult to diagnose. We report a case of isolated right atrial tamponade that appeared suddenly on the 22nd day after cardiac surgery and, unlike previously reported cases, was caused by nonbloody fluid. It is of additional interest because echocardiography suggested tricuspid valve disease but no pericardial abnormalities. Catheterization, however, demonstrated severe extrinsic compression of right-sided structures with hemodynamic evidence of obstruction to flow from right atrium to right ventricle.

CASE REPORT

From the Departments of Medicine, Surgery, and Pediatrics, Yale University School of Medicine, New Haven, Connecticut. Requests for reprints should be addressed to Dr. Raphael Zahler, Yale University School of Medicine, 333 Cedar Street, Fitkin 3, New Haven, Connecticut. Manuscript accepted August a, 1984.

A 56-year-old man underwent coronary artery bypass grafting on November 17, 1983; the pericardium was left open. The patient’s postoperative course was essentially uneventful, and he was discharged on November 29. On December 9, severe exertional dyspnea and right-sided pleuritic chest pain developed. Results of physical examination were notable for a heart rate of 92 beats per minute and blood pressure of 1 lo/80 mm Hg with pulsus paradoxus of 10 to 12 mm Hg. There was markedly increased jugular venous distension without clear-cut respiratory variation. The chest was clear; no pericardial rub or gallop was present. Electrocardiography showed old Q waves and T wave inversions in leads II, Ill, and aVF, and S-T depression in leads V4 to Vg, which was new. Posteroanterior chest radiography (Figure 1) revealed striking deformity of the right heart border without gross abnormality on the lateral view. Laboratory studies, including serial determinations of cardiac enzymes, gave normal results. Echocardiography performed on the day of admission showed a massively enlarged right atrium seen on the apical four-chamber view (Figure 2) without evidence of pericardial fluid. The tricuspid valve appeared markedly abnormal with thickening and decreased mobility of the septal leaflet; results of pulsed Doppler study were suggestive of tricuspid regurgitation and stenosis. In addition, there was decreased left ventricular contractility and paradoxic septal motion. The patient was taken to the cardiac catheterization laboratory on December 12. Hemodynamic studies were performed with a balloon-tipped

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Figure 1. Posteroanterior days later (right).

Figure 2. Echocardiograms text for comments.

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artery bypass, shortly before discharge

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catheter inserted through a left antecubital vein. The superior vena caval pressure was 15 to 17 mm Hg, increasing to 18 to 21 mm Hg on inspiration, and was equal to the right atrial pressure; there were no V waves. Right ventricular pressure was 16 to 20/O to 3 mm Hg; simultaneous central venous and 3) demonstrated a mean right ventricular tracings (Figure gradient of 10 mm Hg with a peak gradient of 14 mm Hg across the tricuspid valve. Right atrial angiography was 4). performed in the right anterior oblique position (Figure Most of the enlarged right heart border seen on fluoroscopy failed to fill with contrast medium; the superior vena cava was also not opacified. Contrast medium was seen to reflux into

the azygous vein and a markedly dilated inferior vena cava. There was a narrow communication between the right atrium and the right ventricle and only a small amount of contrast medium was seen to enter the ventricle. There was no evidence of intracavitary thrombosis. At surgery, a tense serous effusion was found inferior to the right ventricle and lateral to the right atrium separated from the remainder of the pericardial cavity by adhesions. After 500 ml of fluid was removed, the central venous pressure fell from 20 to 10 to 12 mm Hg. Postoperative echocardiography (Figure 2) showed a normal right atrial/right ventricular junction and normal ventricular septal motion.

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Figure 3. Simultaneous pressure tracings at time of catheterization. EKG = electrocardiogram; RV = right ventricular pressure; SVC = superior vena caval pressure.

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COMMENTS

A recent series of patients with late postoperative pericardial tamponade has been reported at our institution [ 11; none of these had localized tamponade, and the fluid was serosanguineous (hematocrit greater than 8 percent) in all cases. Earlier series of late tamponade [2,3] found bloody fluid in nearly all cases; echocardiography, when performed, showed no tricuspid valve abnormalities. The first published report of isolated right atrial tamponade appeared in 1980 [ 41; the diagnosis was made post-mortem, and at autopsy the right atrium was compressed to a narrow slit by a large hematoma. Five other cases of right atrial tamponade have been reported recently [5-81, all caused by bloody fluid or clot. In four of these, a gradient across the tricuspid valve was documented; echocardiography, when performed, showed no tricuspid valve abnormalities. In three of five cases, the diagnosis was made postmortem. A correct noninvasive diagnosis of our patient’s problem rested strongly on clinical suspicion and the sudden marked change on chest radiography. Physical findings suggested systemic venous hypertension, but classic signs of tamponade were absent. The patient’s marked exertional dyspnea was evidently secondary to reduced cardiac output caused by obstruction to right ventricular filling. An interesting aspect of this case is the false-negative echocardiographic result. What appeared to be a large right atrium on echocardiography consisted mostly of pericardial fluid at surgery. The thin right atrial wall was not visualized, in contrast to the thicker ventricular walls that usually form the sonographic interface and allow pericardial fluid to be detected. This may be a result of the limited examination ‘window” in this patient, which allowed visualization of the right atrium in only one tomographic plane. The abnormal echographic appearance of this morphologically normal tricuspid valve probably represents compression of the atrioventricular groove abutting the distorted valve orifice. It is also possible that the region labeled “tricuspid October

valve” in Figure 2 represents compressed right atrial wall, and the region labeled ‘VA” is actually effusion, but this does not fit as well with the angiographic findings. Localized cardiac tamponade can be a late complication of cardiac surgery. Two-dimensional echocardiography can sometimes fail to disclose the presence of serous pericardial fluid abutting the atrial cavities.

Figure 4. Right atrial angiogram (posteroanterior position). AZV = azygous vein; WC = inferior vena cava; RA = right atrium; RVOT = right ventricular outflow tract.

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REFERENCES 1.

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