Hemodynamic Instability After Cardiac Surgery: Transesophageal Echocardiographic Diagnosis of a Localized Pericardial Tamponade Fabio Sangalli, MD,* Luisa Colagrande, MD,† Bruna Manetti, MD,* Leonello Avalli, MD,* Simona Celotti, MD,* Paolo Maniglia, MD,* Francesco Formica, MD,† Giovanni Paolini, MD, PhD,† and Antonio Pesenti, MD, PhD*
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ERICARDIAL TAMPONADE represents a rare yet potentially life-threatening complication after cardiac surgery.1 It may present with peculiar characteristics that make the diagnosis particularly difficult if clinicians rely only on clinical and hemodynamic data, because the classic features of pericardial tamponade are absent, or at least blunted, in this setting. Conversely, transesophageal echocardiography (TEE) allows a rapid diagnosis and the prompt institution of appropriate therapeutic options. CASE PRESENTATION A case of a 76-year-old woman with a history of ischemic heart disease and chronic mitral valve regurgitation is presented. Her preoperative transthoracic echocardiogram (TTE) showed moderate-to-severe mitral regurgitation, moderate tricuspid regurgitation with pulmonary hypertension (pulmonary artery pressure 50 mmHg), and moderately depressed left ventricular systolic function (ejection fraction 43%). She underwent elective surgery for coronary artery bypass grafting and valve repair. She received a left internal thoracic artery graft to the left anterior descending artery, an annuloplasty ring (Carpentier Physio size 28 mm; Edwards Lifesciences, Irvine, CA) plus a quadrangular resection of the posterior leaflet of the mitral valve, and an annuloplasty ring (Edwards Mc3 size 32 mm) to the tricuspid valve. Routine surgery was performed, with closure of the pericardium and placement of 2 mediastinal and 2 pleural drains. The intraoperative course was uneventful. At the end of surgery, she was transferred to the intensive care unit in stable condition with dopamine and nitrates. In the subsequent hours, her hemodynamics showed an adequate systolic arterial pressure (110 mmHg), normal-to-high heart rate (95 beats/min), and central venous pressure (13 mmHg). Metabolic acidosis, with elevated blood lactate, and gas exchange impairment developed. A pulmonary artery catheter was placed, which revealed a severely reduced cardiac index (1.3 L/min/m2) and mixed venous oxygen saturation (43%); pulmonary artery occlusion pressure (13 mmHg) and pulmonary arterial pressure (32/10 mmHg) were both normal. Central venous pressure values were confirmed as previously assessed from the central venous catheter (13 mmHg). A TTE was performed; it confirmed the reduced systolic function of the left ventricle, no mitral valve regurgitation, mild residual tricuspid regurgitation, and no evidence of pericardial effusion. Because of the unclear hemodynamic data interpretation, a TEE was obtained that revealed a large clot (3.5 ⫻ 5.2 cm) localized in the pericardial cavity around the right atrium at the base of the heart (Fig 1). This caused a localized pericardial tamponade, partially obliterating the right atrium during diastole. The patient went back to the operating room to undergo a surgical revision and hemostasis of the pericardial space. The presence of a large clot (250 mL) was confirmed, and prompt evacuation led to an immediate improvement in hemodynamic function. The patient was transferred back to the intensive care unit in stable condition and subsequently recovered uneventfully. DISCUSSION
This case underlines the peculiar characteristics frequently associated with postsurgical pericardial effusions. A certain degree of pericardial effusion is frequently encountered after
cardiac surgery, but its progression to pericardial tamponade is uncommon, accounting for about 2% of all cardiac patients1,2; these figures are also consistent with the authors’ experience (F. Sangalli, unpublished data, 2004). In a large prospective single-institution study, Pepi et al1 observed a loculated effusion in 57.8% of the investigated patients. The effusion magnitude was variable, and in only 1.6% it was defined as large (ie, more than 10 mm maximal length). In only 3 of 803 consecutive patients studied, the loculated effusion led to pericardial tamponade and only 1 among these patients experienced a large pericardial clot compressing the right atrium.1 Most classic clinical and echocardiographic signs of pericardial tamponade are not present in a vast majority of patients with loculated effusions.3 Pulsus paradoxus is typically absent in patients with isolated right-heart tamponade and so are transmitral and transtricuspidal flow respiratory variations. This is possibly because of the constantly higher left ventricular filling pressure.4 Localized right-heart tamponade has been characterized by right atrial pressure in excess of pulmonary capillary wedge pressure, along with the following signs that may also be consistent with right ventricular dysfunction: low cardiac output, low blood pressure, and prominent neck veins.5 In the present patient, filling pressures were equalized and their absolute values were not particularly high. Mediastinal drains were in place and working well, with bleeding within normal limits, making the possibility of a relevant pericardial effusion theoretically unlikely. The poor preoperative systolic function, moreover, made the diagnosis of right ventricular dysfunction seem more plausible. This point is of paramount importance for the acute management of the patient because it leads to profound differences in the treatment of similar clinical pictures. It is widely accepted that, under certain circumstances, “filling” pressures obtained with right-heart catheterization may be inaccurate in reflecting the volume status of the patient.6 Such “uncoupling” among pressures and volumes may occasionally lead to errors in the evaluation and treatment of such patients, and evidence exists that
From the Departments of *Anesthesia and Intensive Care and †Cardiac Surgery, Ospedale San Gerardo dei Tintori, University of MilanoBicocca, Monza, Italy. Address reprint requests to Fabio Sangalli, MD, U.O.S. di Anestesia e Terapia Intensiva Cardiochirurgica, Dipartimento di Anestesia e Rianimazione, Ospedale San Gerardo, via Pergolesi 33, I-20052 Monza (MI), Italy. E-mail:
[email protected] © 2005 Elsevier Inc. All rights reserved. 1053-0770/05/1906-0015$30.00/0 doi:10.1053/j.jvca.2004.12.007 Key words: echocardiography, postoperative care, pericardial tamponade, complications of cardiac surgery
Journal of Cardiothoracic and Vascular Anesthesia, Vol 19, No 6 (December), 2005: pp 775-776
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Fig 1. Midesophageal 4-chamber view, slightly rotated clockwise to expose the right chambers. The right atrium is almost completely obliterated by the extrinsic compression exerted by the clot.
TEE provides more accurate diagnoses in cardiac surgical patients.7,8 TTE is often difficult to carry out properly in the immediate postoperative period because of chest tubes, supine
position, and positive-pressure ventilation. Even if the introduction of harmonic tissue imaging has greatly improved the quality of images, a complete examination is seldom possible and the apical position is normally the only available window. The present patient revealed a large loculated clot along the right atrium free wall, a difficult site to explore properly with TTE because of its location in the far field of the acoustic window. Furthermore, in the setting of valve surgery, because of the presence of artifacts produced by sutures and prostheses, TEE is strongly indicated. Multiple reports exist on the utility of TEE in properly diagnosing the etiology of hemodynamic instability in critically ill patients,9 particularly after cardiac surgery,10,11 and evaluating the effects of therapy. Even the data obtained after placement of a pulmonary artery catheter were inconclusive, revealing only a low-output syndrome but no clear data suggesting the diagnosis of pericardial tamponade. In conclusion, knowledge of the pathophysiology of postoperative pericardial effusions is essential when treating cardiac surgical patients, and a high index of suspicion must always be maintained toward this diagnosis because only a prompt diagnosis can lead to immediate treatment, and improvement, whereas even modest delays may have deleterious consequences on the outcome of the patient.
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