Case Report Occult Cardiac Tamponade Detected by Transesophageal Echocardiography
KEITH H. BERGE, M.D., WILLIAM L. LANIER, M.D., Department ofAnesthesiology; GUY S. REEDER, M.D., Division of Cardiovascular Diseases and Internal Medicine
Transesophageal echocardiography is a safe, minimally invasive procedure that should be considered when the diagnosis of cardiac tamponade is a possibility and when conventional methods fail to provide conclusive diagnostic information. In this report, we describe a 74-year-old man in the intensive-care unit whose condition was unstable postoperatively because of an occult loculated pericardial effusion and cardiac tamponade. Routine noninvasive and invasive monitoring, including hemodynamic monitoring and transthoracic echocardlography, failed to confirm definitively the suspected diagnosis of cardiac tamponade. In addition, because of the hemodynamic instability of the patient, transporting him for definitive tests (such as fast computed tomographic scanning of the mediastinum, which could not be performed at the bedside) for assessment of cardiac tamponade was relatively contraindicated. In our patient, the diagnostic information obtained by transesophageal echocardiography may have been lifesaving.
Cardiac tamponade is a potentially life-threatening complication not only after cardiac and major vascular surgical intervention-? but also after placement of central venous and pulmonary artery catheters.v' In patients being monitored in an intensive-care unit, postoperative cardiac tamponade is usually diagnosed at the bedside by obtaining historical information and noninvasive and invasive hemodynamic data (for example, peripheral arterial, central venous, and pulmonary arterial blood pressures) andby performing a physical examination, routine chest radiography, and precordial echocardiography.v' Herein we describe a case of severe postsurgical hemodynamic compromise in which the clinical suggestion of cardiac tamponade was neither confirmed nor excluded by conventional diagnostic methods. In our patient, the definitive-s-and, we believe, lifesaving-diagnosis of cardiac tamponade at the bedside was possible only after transesophageal echocardiography was used. REPORT OF CASE A 74-year-old man who weighed 77 kg was admitted to the intensive-care unit after resection and repair of an expandAddress reprint requests to Dr. K. H. Berge, Department of Anesthesiology, Mayo Clinic, Rochester, MN 55905. Mayo Clin Proc 67:667-670, 1992
ing, symptomatic abdominal aortic aneurysm (6-cm diameter). The medical history included admission to the hospital 17 days earlier because of symptoms suggestive of myocardial ischemia. During this initial hospital admission, a subendocardial myocardial infarction was diagnosed on the basis of electrocardiographic changes and an increased plasma concentration of creatine kinase isoenzyme. Three days after admission, the patient underwent cardiac catheterization and coronary artery bypass grafting. His recovery, including the hemodynamic course, was uneventful, and he was dismissed to a rehabilitation facility. Fifteen days after the grafting procedure, excruciating abdominal pain and hypotension developed. After resuscitation with fluids, emergency abdominal ultrasonography revealed a 6-cm abdominal aortic aneurysm. Emergency resection and repair were performed during general anesthesia. Intraoperative anesthetic management included continuous invasive hemodynamic monitoring with use of a radial artery catheter and a pulmonary artery catheter (placed through the right internal jugular vein). The patient's intraoperative course was unremarkable. During the operation, volume replacement consisted of 3 liters of lactated Ringer's solution, 8 units of packed erythrocytes, 8 units of fresh frozen plasma, and 8 units of platelet concentrate. 667
668
TRANSESOPHAGEAL ECHOCARDIOGRAPHY AND CARDIAC TAMPONADE
On return to the intensive-care unit, the patient's systemic arterial blood pressure was 125/80 mm Hg and the heart rate was 100 beats/min during infusion of dopamine (2 Ilg/kg per min) and nitroglycerin (0.4 ug/min). During this period, the patient was mechanically ventilated by means of an endotracheal tube. Hemodynamic data obtained 4 hours after admission to the intensive-care unit were as follows: blood pressure, 82/52 mm Hg; heart rate, 109 beats/min; pulmonary artery pressure, 29/21 mm Hg; pulmonary capillary wedge pressure, 20 mm Hg; right atrial pressure, 17 mm Hg; cardiac output, 2.7 liters/min; cardiac index, 1.44 liters/min per m': and systemic vascular resistance index, 42 U· m-, The admitting resident physician in the intensive-care unit questioned the accuracy of the pulmonary artery pressure because of an "inability to wedge" the pulmonary artery catheter, despite chest radiographic evidence of proper placement of the catheter. Despite the increased pulmonary artery pressure, both the cardiac index and the urine output decreased during the ensuing 12 hours if crystalloid infusion was diminished. The team of physicians responsible for the care of the patient elected to continue intravascular volume expansion, assuming that the patient was hypovolemic and that the pulmonary artery catheter was providing misleading information. The next morning the patient remained mechanically ventilated; the cardiac index remained unexpectedly low, and the pulmonary artery pressure was still increased. Hemodynamic data were as follows: blood pressure, 137/63 mm Hg; heart rate, 112 beats/min; pulmonary artery pressure, 39/29 mm Hg; pulmonary capillary wedge pressure, 27 mm Hg; cardiac output, 4.38 liters/min; cardiac index, 2.33 liters/min per rn': systemic vascular resistance index, 35 U . m': and right atrial pressure, 24 mm Hg. Findings on an electrocardiogram obtained at this time were unchanged from those on the preoperative electrocardiogram. On the basis of these data and the hemodynamic trends of the previous evening, the possibility of cardiac tamponade was considered. Thus, emergency precordial echocardiography was performed. The examination was technically difficult because of the suboptimal acoustic windows available in this mechanically ventilated, supine patient. Although precordial echocardiography ruled out the presence of a substantial anterior collection of pericardial fluid (which might have been amenable to transthoracic needle aspiration), the results were considered inconclusive because they failed to exclude a loculated retrocardiac effusion (Fig. 1). The hemodynamic instability of the patient was a relative contraindication to transporting him to another site for a definitive test (such as fast computed tomography of the mediastinum) for assessment of cardiac tamponade. Therefore, transesophageal echocardiography was performed to enhance visualization of the retrocardiac structures. Transesophageal echocardiogra-
Mayo Clin Proc, July 1992, Vol 67
Fig. 1. Transthoracic echocardiograrn of74-year-old man obtained at bedside in the intensive-care unit. In this parasternal long-axis view, images are poor, but an echo-free area posterior to left ventricular free wall is possible (labeled ?PE). Despite numerous attempts at imaging this area, pericardial effusion could not be definitively diagnosed. No anterior echo-free space is evident. A = anterior; AV = aortic valve; I = inferior; LA = left atrium; LV = left ventricle; P = posterior; PE = pericardial effusion; RV = right ventricle; S = superior.
phy revealed a large loculated collection of pericardial fluid posterior to both ventricular chambers and posterior to the left atrium (Fig. 2). The collection of fluid extended around a portion of the right atrium but was not present anterior to the heart. Color flow imaging demonstrated blood flow from the surface of the heart into the pericardial effusion; however, injection of contrast medium into the right atrium failed to show passage of contrast (indocyanine green) into the effusion. Because of the compromised hemodynamic status and the presence of the bleeding source, the patient was urgently transported to a surgical suite, where the median sternotomy was reopened. At operation, a large, tense collection of bloody pericardial fluid was drained, and the cardiac index increased substantially (from 2.3 to 3.3 liters/min per rrr'). The volume of fluid drained during surgical intervention was not recorded. No myocardial perforation was evident. Because of extensive adhesions within the pericardial space, the surgical team neither completely dissected the pericardial tissues nor excessively mobilized the heart for better viewing of the posterior wall, to avoid damaging the vascular grafts. Instead, the posterior pericardial space was packed with thrombin (Parke-Davis)-soaked Gelfoam (The Upjohn
Mayo Clio Proc, July 1992, Vol 67
TRANSESOPHAGEAL ECHOCARDIOGRAPHY AND CARDIAC TAMPONADE
669
ventricular diastolic collapse," and certain characteristic Doppler inflow abnormalities." Although transthoracic echocardiography is usually diagnostic, the quality of images obtained from transthoracic acoustic windows is degraded by several factors, including surgical wound dressings, mechanical ventilation, and hemodynamic monitoring devices, in the intensive-care unit setting." In situations in which transthoracic echocardiographic data are inconclusive, transesophageal echocardiography may provide additional useful information. Transesophageal echocardiography has been shown to be safe and useful in the intensive-care unit setting.s?"! Typically, it offers vastly superior image quality in comparison with transthoracic echocardiography in the intensive-care unit setting; hence, diagnostic accuracy is improved.P-" The cause of the pericardial effusion in our patient was Fig. 2. Transesophageal two-dimensional echocardiogram of 74not determined conclusively. Two likely possibilities exist: year-old man obtained at bedside in the intensive-care unit. In this transgastric view, short-axis images of right ventricle and left ven- (1) cardiac perforation during placement of the pulmonary tricle are shown. Immediately posterior to both chambers is large, artery catheter or (2) gradual accumulation of fluid after loculated pericardial effusion, which was producing localized cardiac operation. Extensive retrospective review of the tamponade. A = anterior; L = left; LV = left ventricle; P = posterior; patient's medical records failed to reveal the precise onset of PE = pericardial effusion; R = right; RV = right ventricle. the clinical manifestations of cardiac tamponade. A physiologic profile consistent with tamponade was present at the Company), and the operative site was drained through two time of admission to the intensive-care unit after repair of the chest tubes. The patient's postoperative course was com- abdominal aortic aneurysm. Although it is possible that tamplicated by the development of a large alveolar-to-arterial ponade developed as a result of a catheter-induced cardiac perforation, the catheter placement was retrospectively deblood oxygen tension gradient and cardiac arrhythmias. Twenty-four days after drainage of the tamponade, the scribed as completely routine. Even though the incidence of patient was transferred from the intensive-care unit to a cardiac perforation during placement of a pulmonary artery rehabilitation unit, and he was ultimately dismissed from the catheter is not established in the medical literature, the incihospital to his home. Transthoracic echocardiography, dence of cardiac tamponade resulting from perforation durwhich was performed 6 weeks after the mediastinal fluid was ing placement of a central venous catheter ranges from 0.25 drained, showed normal cardiac function and no evidence of to 1.4%.3 In our patient, the alternative explanation is that the periresidual pericardial effusion. cardial effusion developed as a result of the coronary artery bypass grafting and had accumulated either immediately or gradually sometime before he underwent operation for an DISCUSSION Cardiac tamponade occurs when diastolic filling of the heart abdominal aortic aneurysm. Such an effusion may not have is impaired by fluid collecting in the pericardial space. compromised the patient's hemodynamic status to a suffiHemodynamic alterations suggestive of cardiac tamponade cient degree to be detected until it was unmasked by the include hypotension, pulsus paradoxus (an exaggeration of hemodynamic stress of the repair of the aneurysm and evaluthe normal decrease in systolic blood pressure during inspi- ated by the sophisticated monitoring used at that time. ration with either spontaneous or positive pressure ventila- D'Cruz and associates' described the occurrence of such tion"), and "equalization" of intracardiac diastolic pressures.' effusions in 13 of 140 patients studied prospectively who Other manifestations may include an enlarged cardiac underwent transthoracic echocardiography at a mean of 8 shadow evident on a routine chest roentgenogram' and elec- days after open-heart surgical treatment. Of the 13 patients, trical alternans on electrocardiograms.v' The definitive di- 5 had hemodynamic compromise sufficient to require surgiagnosis of cardiac tamponade usually necessitates echocar- cal drainage, and 5 had a loculated posterior effusion similar diography for demonstrating the presence and distribution of to that found in our patient. Those patients in whom the a pericardial effusion. Other echocardiographic findings effusions did not result in hemodynamic compromise were suggestive of cardiac tamponade include an inspiratory in- monitored with serial echocardiograms, and the effusions crease in right ventricular dimensions, right atrial and right gradually and spontaneously resolved.
670
TRANSESOPHAGEAL ECHOCARDlOGRAPHY AND CARDIAC TAMPONADE
In summary, we describe a critically ill patient in whom the diagnosis of perioperative cardiac tamponade was confirmed only after transesophageal echocardiography was used. On the basis of this experience, we recommend when cardiac tamponade is suspected and routine noninvasive and invasive monitoring procedures fail to provide conclusive diagnostic information, transesophageal echocardiography should be considered.
REFERENCES I. D'Cruz lA, Dick A, Pai GM, Kamath MV: Large pericardial effusion after cardiac surgery: role of echocardiography in diagnosis and management. South Med J 82:287-291, 1989 2. Chan K-L: Transesophageal echocardiography for assessing cause of hypotension after cardiac surgery. Am J Cardiol 62:1142-1143,1988 3. Karnauchow PN: Cardiac tamponade from central venous catheterization. Can Med Assoc J 135:1145-1147, 1986 4. Gravenstein JS, Paulus DA: Clinical Monitoring Practice. Second edition. Philadelphia, JB Lippincott Company, 1987, pp 147-148
Mayo Clin Proc, July 1992, Vol 67
Lorell BH, Braunwald E: Pericardial disease. In Heart Disease: A Textbook of Cardiovascular Medicine. Third edition. Edited by E Braunwald. Philadelphia, WB Saunders Company, 1988, pp 1492-1496 6. Shabetai R: Diseases of the pericardium. In The Heart: Arteries and Veins. Seventh edition. Edited by JW Hurst, RC Schlant, CE Rackley, EH Sonnenblick, NK Wenger. New York, McGraw-Hill Information Services Company, 1990, pp 1354-1355 7. Conahan TJ ill: Complications of cardiac surgery. In Cardiac Anesthesia. Vol 2. Second edition. Edited by JA Kaplan. Orlando, florida, Grune & Stratton, 1987, p 1113 8. Reeder GS: Pericardial disease: echocardiographic and hemodynamic aspects. Curr Opin Cardiol 4:417-422, 1989 9. Seward JB, Khandberia BK, Oh JK, Abel MD, Hughes RW Jr, Edwards WD, Nichols BA, Freeman WK, Tajik AJ: Transesophageal echocardiography: technique, anatomic correlations, implementation, and clinical applications. . Mayo Clin Proc 63:649-680,1988 10. Pearson AC, Castello R, Labovitz AJ: Safety and utility of transesophageal echocardiography in the critically ill patient. Am Heart J II 9:1083-1089, 1990 11. Oh JK, Seward JB, Khandberia BK, Gersh BJ, McGregor CGA, Freeman WK, Sinak LJ, Tajik AJ: Transesophageal echocardiography in critically ill patients. Am J Cardiol 66:1492-1495,1990 5.
KEITH H. BERGE, M.D., WILLIAM L. LANIER, M.D., Department ofAnesthesiology; GUY S. REEDER, M.D., Division of Cardiovascular Diseases and Internal Medicine
Transesophageal echocardiography is a safe, minimally invasive procedure that should be considered when the diagnosis of cardiac tamponade is a possibility and when conventional methods fail to provide conclusive diagnostic information. In this report, we describe a 74-year-old man in the intensive-care unit whose condition was unstable postoperatively because of an occult loculated pericardial effusion and cardiac tamponade. Routine noninvasive and invasive monitoring, including hemodynamic monitoring and transthoracic echocardlography, failed to confirm definitively the suspected diagnosis of cardiac tamponade. In addition, because of the hemodynamic instability of the patient, transporting him for definitive tests (such as fast computed tomographic scanning of the mediastinum, which could not be performed at the bedside) for assessment of cardiac tamponade was relatively contraindicated. In our patient, the diagnostic information obtained by transesophageal echocardiography may have been lifesaving.
Cardiac tamponade is a potentially life-threatening complication not only after cardiac and major vascular surgical intervention-? but also after placement of central venous and pulmonary artery catheters.v' In patients being monitored in an intensive-care unit, postoperative cardiac tamponade is usually diagnosed at the bedside by obtaining historical information and noninvasive and invasive hemodynamic data (for example, peripheral arterial, central venous, and pulmonary arterial blood pressures) andby performing a physical examination, routine chest radiography, and precordial echocardiography.v' Herein we describe a case of severe postsurgical hemodynamic compromise in which the clinical suggestion of cardiac tamponade was neither confirmed nor excluded by conventional diagnostic methods. In our patient, the definitive-s-and, we believe, lifesaving-diagnosis of cardiac tamponade at the bedside was possible only after transesophageal echocardiography was used. REPORT OF CASE A 74-year-old man who weighed 77 kg was admitted to the intensive-care unit after resection and repair of an expandAddress reprint requests to Dr. K. H. Berge, Department of Anesthesiology, Mayo Clinic, Rochester, MN 55905. Mayo Clin Proc 67:667-670, 1992
ing, symptomatic abdominal aortic aneurysm (6-cm diameter). The medical history included admission to the hospital 17 days earlier because of symptoms suggestive of myocardial ischemia. During this initial hospital admission, a subendocardial myocardial infarction was diagnosed on the basis of electrocardiographic changes and an increased plasma concentration of creatine kinase isoenzyme. Three days after admission, the patient underwent cardiac catheterization and coronary artery bypass grafting. His recovery, including the hemodynamic course, was uneventful, and he was dismissed to a rehabilitation facility. Fifteen days after the grafting procedure, excruciating abdominal pain and hypotension developed. After resuscitation with fluids, emergency abdominal ultrasonography revealed a 6-cm abdominal aortic aneurysm. Emergency resection and repair were performed during general anesthesia. Intraoperative anesthetic management included continuous invasive hemodynamic monitoring with use of a radial artery catheter and a pulmonary artery catheter (placed through the right internal jugular vein). The patient's intraoperative course was unremarkable. During the operation, volume replacement consisted of 3 liters of lactated Ringer's solution, 8 units of packed erythrocytes, 8 units of fresh frozen plasma, and 8 units of platelet concentrate. 667
668
TRANSESOPHAGEAL ECHOCARDIOGRAPHY AND CARDIAC TAMPONADE
On return to the intensive-care unit, the patient's systemic arterial blood pressure was 125/80 mm Hg and the heart rate was 100 beats/min during infusion of dopamine (2 Ilg/kg per min) and nitroglycerin (0.4 ug/min). During this period, the patient was mechanically ventilated by means of an endotracheal tube. Hemodynamic data obtained 4 hours after admission to the intensive-care unit were as follows: blood pressure, 82/52 mm Hg; heart rate, 109 beats/min; pulmonary artery pressure, 29/21 mm Hg; pulmonary capillary wedge pressure, 20 mm Hg; right atrial pressure, 17 mm Hg; cardiac output, 2.7 liters/min; cardiac index, 1.44 liters/min per m': and systemic vascular resistance index, 42 U· m-, The admitting resident physician in the intensive-care unit questioned the accuracy of the pulmonary artery pressure because of an "inability to wedge" the pulmonary artery catheter, despite chest radiographic evidence of proper placement of the catheter. Despite the increased pulmonary artery pressure, both the cardiac index and the urine output decreased during the ensuing 12 hours if crystalloid infusion was diminished. The team of physicians responsible for the care of the patient elected to continue intravascular volume expansion, assuming that the patient was hypovolemic and that the pulmonary artery catheter was providing misleading information. The next morning the patient remained mechanically ventilated; the cardiac index remained unexpectedly low, and the pulmonary artery pressure was still increased. Hemodynamic data were as follows: blood pressure, 137/63 mm Hg; heart rate, 112 beats/min; pulmonary artery pressure, 39/29 mm Hg; pulmonary capillary wedge pressure, 27 mm Hg; cardiac output, 4.38 liters/min; cardiac index, 2.33 liters/min per rn': systemic vascular resistance index, 35 U . m': and right atrial pressure, 24 mm Hg. Findings on an electrocardiogram obtained at this time were unchanged from those on the preoperative electrocardiogram. On the basis of these data and the hemodynamic trends of the previous evening, the possibility of cardiac tamponade was considered. Thus, emergency precordial echocardiography was performed. The examination was technically difficult because of the suboptimal acoustic windows available in this mechanically ventilated, supine patient. Although precordial echocardiography ruled out the presence of a substantial anterior collection of pericardial fluid (which might have been amenable to transthoracic needle aspiration), the results were considered inconclusive because they failed to exclude a loculated retrocardiac effusion (Fig. 1). The hemodynamic instability of the patient was a relative contraindication to transporting him to another site for a definitive test (such as fast computed tomography of the mediastinum) for assessment of cardiac tamponade. Therefore, transesophageal echocardiography was performed to enhance visualization of the retrocardiac structures. Transesophageal echocardiogra-
Mayo Clin Proc, July 1992, Vol 67
Fig. 1. Transthoracic echocardiograrn of74-year-old man obtained at bedside in the intensive-care unit. In this parasternal long-axis view, images are poor, but an echo-free area posterior to left ventricular free wall is possible (labeled ?PE). Despite numerous attempts at imaging this area, pericardial effusion could not be definitively diagnosed. No anterior echo-free space is evident. A = anterior; AV = aortic valve; I = inferior; LA = left atrium; LV = left ventricle; P = posterior; PE = pericardial effusion; RV = right ventricle; S = superior.
phy revealed a large loculated collection of pericardial fluid posterior to both ventricular chambers and posterior to the left atrium (Fig. 2). The collection of fluid extended around a portion of the right atrium but was not present anterior to the heart. Color flow imaging demonstrated blood flow from the surface of the heart into the pericardial effusion; however, injection of contrast medium into the right atrium failed to show passage of contrast (indocyanine green) into the effusion. Because of the compromised hemodynamic status and the presence of the bleeding source, the patient was urgently transported to a surgical suite, where the median sternotomy was reopened. At operation, a large, tense collection of bloody pericardial fluid was drained, and the cardiac index increased substantially (from 2.3 to 3.3 liters/min per rrr'). The volume of fluid drained during surgical intervention was not recorded. No myocardial perforation was evident. Because of extensive adhesions within the pericardial space, the surgical team neither completely dissected the pericardial tissues nor excessively mobilized the heart for better viewing of the posterior wall, to avoid damaging the vascular grafts. Instead, the posterior pericardial space was packed with thrombin (Parke-Davis)-soaked Gelfoam (The Upjohn
Mayo Clio Proc, July 1992, Vol 67
TRANSESOPHAGEAL ECHOCARDIOGRAPHY AND CARDIAC TAMPONADE
669
ventricular diastolic collapse," and certain characteristic Doppler inflow abnormalities." Although transthoracic echocardiography is usually diagnostic, the quality of images obtained from transthoracic acoustic windows is degraded by several factors, including surgical wound dressings, mechanical ventilation, and hemodynamic monitoring devices, in the intensive-care unit setting." In situations in which transthoracic echocardiographic data are inconclusive, transesophageal echocardiography may provide additional useful information. Transesophageal echocardiography has been shown to be safe and useful in the intensive-care unit setting.s?"! Typically, it offers vastly superior image quality in comparison with transthoracic echocardiography in the intensive-care unit setting; hence, diagnostic accuracy is improved.P-" The cause of the pericardial effusion in our patient was Fig. 2. Transesophageal two-dimensional echocardiogram of 74not determined conclusively. Two likely possibilities exist: year-old man obtained at bedside in the intensive-care unit. In this transgastric view, short-axis images of right ventricle and left ven- (1) cardiac perforation during placement of the pulmonary tricle are shown. Immediately posterior to both chambers is large, artery catheter or (2) gradual accumulation of fluid after loculated pericardial effusion, which was producing localized cardiac operation. Extensive retrospective review of the tamponade. A = anterior; L = left; LV = left ventricle; P = posterior; patient's medical records failed to reveal the precise onset of PE = pericardial effusion; R = right; RV = right ventricle. the clinical manifestations of cardiac tamponade. A physiologic profile consistent with tamponade was present at the Company), and the operative site was drained through two time of admission to the intensive-care unit after repair of the chest tubes. The patient's postoperative course was com- abdominal aortic aneurysm. Although it is possible that tamplicated by the development of a large alveolar-to-arterial ponade developed as a result of a catheter-induced cardiac perforation, the catheter placement was retrospectively deblood oxygen tension gradient and cardiac arrhythmias. Twenty-four days after drainage of the tamponade, the scribed as completely routine. Even though the incidence of patient was transferred from the intensive-care unit to a cardiac perforation during placement of a pulmonary artery rehabilitation unit, and he was ultimately dismissed from the catheter is not established in the medical literature, the incihospital to his home. Transthoracic echocardiography, dence of cardiac tamponade resulting from perforation durwhich was performed 6 weeks after the mediastinal fluid was ing placement of a central venous catheter ranges from 0.25 drained, showed normal cardiac function and no evidence of to 1.4%.3 In our patient, the alternative explanation is that the periresidual pericardial effusion. cardial effusion developed as a result of the coronary artery bypass grafting and had accumulated either immediately or gradually sometime before he underwent operation for an DISCUSSION Cardiac tamponade occurs when diastolic filling of the heart abdominal aortic aneurysm. Such an effusion may not have is impaired by fluid collecting in the pericardial space. compromised the patient's hemodynamic status to a suffiHemodynamic alterations suggestive of cardiac tamponade cient degree to be detected until it was unmasked by the include hypotension, pulsus paradoxus (an exaggeration of hemodynamic stress of the repair of the aneurysm and evaluthe normal decrease in systolic blood pressure during inspi- ated by the sophisticated monitoring used at that time. ration with either spontaneous or positive pressure ventila- D'Cruz and associates' described the occurrence of such tion"), and "equalization" of intracardiac diastolic pressures.' effusions in 13 of 140 patients studied prospectively who Other manifestations may include an enlarged cardiac underwent transthoracic echocardiography at a mean of 8 shadow evident on a routine chest roentgenogram' and elec- days after open-heart surgical treatment. Of the 13 patients, trical alternans on electrocardiograms.v' The definitive di- 5 had hemodynamic compromise sufficient to require surgiagnosis of cardiac tamponade usually necessitates echocar- cal drainage, and 5 had a loculated posterior effusion similar diography for demonstrating the presence and distribution of to that found in our patient. Those patients in whom the a pericardial effusion. Other echocardiographic findings effusions did not result in hemodynamic compromise were suggestive of cardiac tamponade include an inspiratory in- monitored with serial echocardiograms, and the effusions crease in right ventricular dimensions, right atrial and right gradually and spontaneously resolved.
670
TRANSESOPHAGEAL ECHOCARDlOGRAPHY AND CARDIAC TAMPONADE
In summary, we describe a critically ill patient in whom the diagnosis of perioperative cardiac tamponade was confirmed only after transesophageal echocardiography was used. On the basis of this experience, we recommend when cardiac tamponade is suspected and routine noninvasive and invasive monitoring procedures fail to provide conclusive diagnostic information, transesophageal echocardiography should be considered.
REFERENCES I. D'Cruz lA, Dick A, Pai GM, Kamath MV: Large pericardial effusion after cardiac surgery: role of echocardiography in diagnosis and management. South Med J 82:287-291, 1989 2. Chan K-L: Transesophageal echocardiography for assessing cause of hypotension after cardiac surgery. Am J Cardiol 62:1142-1143,1988 3. Karnauchow PN: Cardiac tamponade from central venous catheterization. Can Med Assoc J 135:1145-1147, 1986 4. Gravenstein JS, Paulus DA: Clinical Monitoring Practice. Second edition. Philadelphia, JB Lippincott Company, 1987, pp 147-148
Mayo Clin Proc, July 1992, Vol 67
Lorell BH, Braunwald E: Pericardial disease. In Heart Disease: A Textbook of Cardiovascular Medicine. Third edition. Edited by E Braunwald. Philadelphia, WB Saunders Company, 1988, pp 1492-1496 6. Shabetai R: Diseases of the pericardium. In The Heart: Arteries and Veins. Seventh edition. Edited by JW Hurst, RC Schlant, CE Rackley, EH Sonnenblick, NK Wenger. New York, McGraw-Hill Information Services Company, 1990, pp 1354-1355 7. Conahan TJ ill: Complications of cardiac surgery. In Cardiac Anesthesia. Vol 2. Second edition. Edited by JA Kaplan. Orlando, florida, Grune & Stratton, 1987, p 1113 8. Reeder GS: Pericardial disease: echocardiographic and hemodynamic aspects. Curr Opin Cardiol 4:417-422, 1989 9. Seward JB, Khandberia BK, Oh JK, Abel MD, Hughes RW Jr, Edwards WD, Nichols BA, Freeman WK, Tajik AJ: Transesophageal echocardiography: technique, anatomic correlations, implementation, and clinical applications. . Mayo Clin Proc 63:649-680,1988 10. Pearson AC, Castello R, Labovitz AJ: Safety and utility of transesophageal echocardiography in the critically ill patient. Am Heart J II 9:1083-1089, 1990 11. Oh JK, Seward JB, Khandberia BK, Gersh BJ, McGregor CGA, Freeman WK, Sinak LJ, Tajik AJ: Transesophageal echocardiography in critically ill patients. Am J Cardiol 66:1492-1495,1990 5.
