Extrapericardial cardiac compression syndrome

Extrapericardial cardiac compression syndrome

International Journal of Cardiology 113 (2006) 285 – 287 www.elsevier.com/locate/ijcard Letter to the Editor Extrapericardial cardiac compression sy...

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International Journal of Cardiology 113 (2006) 285 – 287 www.elsevier.com/locate/ijcard

Letter to the Editor

Extrapericardial cardiac compression syndrome Paul J. Swan, Fred M. Wu, Thom G. Dahle, Daniel A. Duprez * Division of Internal Medicine (P.J.S, T.A.D.), Cardiovascular Division (F.M.W, D.A.D), Department of Medicine, Medical School, University of Minnesota, VCRC-Room 270, 420 Delaware St SE, MMC 508, Minneapolis, MN 55455, United States Received 8 September 2005; accepted 20 September 2005 Available online 28 November 2005

Abstract A case report is described of a patient presenting with extrapericardial cardiac compression resulting from massive ascites. The history and electrocardiographic findings initially obscured the proper diagnosis. Extrapericardial cardiac compression syndromes resulting from massive ascites pose a particular challenge in that even when the diagnosis of tamponade is made, failure to recognize the true cause of impaired cardiac filling can lead to unnecessary instrumentation of an otherwise incidental pericardial effusion. This unique case is discussed with other group of conditions of pericardial compressive syndromes. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Extrapericardial; Cardiac compression syndrome; Tamponade

1. Case report A 68-year-old female with a recent diagnosis of portal and superior mesenteric vein thromboses, and a right adnexal mass was admitted to the hospital with increasing dyspnea on exertion, abdominal distention, and lower extremity swelling. On admission, she appeared to be in no acute distress. Her heart rate was 100 beats per minute, blood pressure 135/68 mm Hg, respirations of 16 per minute, and oxygen saturation of 96% on room air. Her physical exam was normal except for decreased breath sounds at the lung bases, tachycardia, distended abdomen with shifting dullness suggestive of ascites, and severe bilateral lower extremity edema. Later, she became acutely dyspneic and tachycardic. Her heart rate was 126 beats per minute, blood pressure 85 / 62 mm Hg, respirations 40 per minute, and oxygen saturation of 96% on high flow oxygen via face mask. Central venous pressure was measured at 19 mm Hg. On exam, the patient appeared to be in moderate respiratory distress, had distended neck veins and significantly diminished breath sounds at the lung bases. Auscul-

* Corresponding author. Tel.: +1 612 624 4948; fax: +1 612 626 4411. E-mail address: [email protected] (D.A. Duprez). 0167-5273/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2005.09.037

tation of the heart revealed tachycardia with regular rhythm and normal first and second heart sounds without murmur. Her abdominal distention and lower extremity edema was unchanged. Electrocardiogram showed sinus tachycardia with an S-wave in lead I, Q-wave in lead III, and flattening of the T-wave in lead III, suggestive of pulmonary embolism pattern (Fig. 1a). A computed tomography (CT) scan of the chest with contrast was obtained because of the concern for possible pulmonary embolus. There was no evidence of pulmonary embolus or pericardial effusion; however massive ascites was present with elevation of the hemidiaphragms and bilateral compression of the heart (Fig. 2). Repeat electrocardiogram showed the development of decreased voltage in all leads except V1 and V2 (Fig. 1b). She emergently underwent large volume paracentesis with removal of 5 L of fluid resulting in prompt improvement of her hemodynamic and respiratory status.

2. Discussion We present the first ever case report of a patient presenting with extrapericardial cardiac compression resulting from massive ascites. As can be seen, the history and

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Fig. 1. (a) Electrocardiogram illustrating S-wave in lead I, Q-wave in lead III, and flattening of the T-wave in lead III. (b) Electrocardiogram illustrating decreased voltage in all leads except V1 and V2.

electrocardiographic findings initially obscured the proper diagnosis. A complaint of acute-onset dyspnea in the context of a hypercoagulable condition, i.e. malignancy, and multiple previous venous thromboses, in conjunction with an EKG showing the classically described S-wave in lead I and Qwave and inverted T-wave in lead III, naturally suggested the diagnosis of pulmonary embolism [1]. However, the

Fig. 2. CT of chest with contrast illustrating massive ascites with elevation of the hemidiaphragms and bilateral compression of the heart.

urgently performed chest CT showed no evidence of filling defects within the pulmonary vasculature. Reexamination of the electrocardiogram in greater detail revealed an unusual pattern in that the majority of precordial leads exhibited low voltages with the conspicuous exception of lead V2. With this finding in mind, the chest CT was reviewed for evidence of a pericardial effusion only to reveal the dramatic hemidiaphragmatic elevation bilaterally with resultant cardiac compression. No pericardial effusion was noted. The low precordial voltages, it was apparent, were a result of attenuation by the hemidiaphragms lateral to the heart. Leads V1 and V2, on the other hand, were afforded an unobstructed measure of ventricular depolarization due to their location and therefore exhibited normal voltages (Fig. 1b). After paracentesis, with decreased elevation of the hemidiaphragms, voltages in the precordial leads normalized. The patient’s symptoms similarly improved supporting the diagnosis of a partial cardiac tamponade secondary to massive ascites. Cardiac tamponade, itself, is a well-known and welldescribed example of the pericardial compressive syndromes, a group of conditions which also includes pericardial constriction and effusive – constrictive pericarditis. Classically, it is characterized by the accumulation of fluid under pressure within the pericardium. The usual causes of tamponade include the entire spectrum of conditions which can lead to pericardial effusion – malignancy, infection, uremia, autoimmune conditions, and hypothyroid myxede-

P.J. Swan et al. / International Journal of Cardiology 113 (2006) 285 – 287

ma, to list a few – and those that result in acute intrapericardial hemorrhage such as trauma or aortic dissection. In such cases, diagnosis rests largely on clinical suspicion in conjunction with echocardiographic imaging. Definitive treatment includes either percutaneous drainage of the pericardial fluid or surgical pericardiotomy. In rarer situations, cardiac tamponade has been described to result from intrapericardial diaphragmatic hernias [2,3], both traumatic and iatrogenic, rupture of pancreatic pseudocysts into the pericardial space [4,5], and tension pneumopericardium, which can occur as a result of chest wall trauma [6], and esophago- [7], broncho- [8], or gastropericardial [9] fistulas. Treatment varies, of course, depending on the underlying abnormality. Less commonly, partial tamponade can arise due to extrapericardial compression of the heart. The most often reported cause for this condition is the presence of large pleural effusions [10,11]. The increased intrapleural pressure is transmitted to the pericardial space and impairs ventricular filling, thus mimicking the hemodynamic abnormalities of cardiac tamponade. In such cases, both clinical and echocardiographic signs of tamponade have been demonstrated. Drainage of the pleural fluid reliably results in resolution of these findings. In addition, there have been isolated case reports of extrapericardial cardiac compression resulting from conditions including anterior and posterior mediastinal hematomas and masses [12 –15]. Furthermore, cases of isolated left atrial compression resulting in respiratory symptoms have been reported in association with a variety of mediastinal pathology, including bronchogenic cysts, carcinomas, thymomas, and aortic aneurysms [16]. Gastroesophageal conditions, such as hiatal hernias with gastric volvulus [17,18] and two reports of herniated omentum [19], have led to extrapericardial cardiac compression post-operatively. What makes this case unique in comparison with the above-reported cases is that it is the only instance of cardiac compression resulting from a purely extrathoracic pathology. Furthermore, because ascites is commonly seen in association with some amount of pericardial effusion, extrapericardial cardiac compression syndromes resulting from massive ascites pose a particular challenge in that even when the diagnosis of tamponade is made, failure to recognize the true cause of impaired cardiac filling can lead to unnecessary instrumentation of an otherwise incidental pericardial effusion.

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