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Late isolated left ventricular tamponade
Late isolated left ventricular tamponade Clinical, hemodynamic, and echocardiographic manifestations of a previously unreported postoperative complication A unique case of late postoperative left ventricular tamponade, hemodynamically indistinguishable .from severe left ventricular failure. is reported in a patient I month after an apparently uncomplicated aortic valve replacement. An echo-free space behind the left ventricle led to surgical exploration and successful resolution of the disease process. To our knowledge, this is the first documented case of isolated left ventricular tamponade in the literature. The findings highlight the importance of postoperative echocardiography in the evaluation of the patient having cardiac surgery.
Michael R. Jones, M.D., Donald L. Vine, M.D., Michael Attas, M.D., and Edward P. Todd, M.D., Ph.D., Lexington, Ky.
P
ericardial tamponade complicates 3.4 to 8.8 percent of all open-heart procedures.v " The majority of these cases occur in the immediate postoperative period and usually pose no special diagnostic difficulties. Pericardial tamponade occurring in the late postoperative period is much less frequent, with only 43 cases having been described in the literature. 1-13 Cardiac tamponade produced by the localized effect of fluid or clot is the least frequently reported and most diagnostically evasive presentation of tamponade after open-heart operations. Four such cases have been found in the literature, only two of which occurred in the late postoperative period. 7, 14, 15 The reported case occurred in the late postoperative period and is to our knowledge the first documented instance of isolated postoperative left ventricular tamponade in the literature.
Case report A 55-year-old man underwent aortic valve replacement and mycotic aneurysmectomy in October, 1976. The pericardium was left open and drainage was established with two anterior mediastinal tubes. The immediate postoperative course was uncomplicated. Mediastinal tubes drained 445 ml. From the Divisions of Cardiology and Cardio-Thoracic Surgery, University of Kentucky College of Medicine, Lexington. Ky. Received for publication June 6, 1978. Accepted for publication July 13, 1978. Address for reprints: Michael R. Jones, M.D., University of Kentucky Medical Center, Department of Medicine, Division of Cardiology, Room MN670, 800 Rose St., Lexington, Ky. 40506.
142
of serosanguineous fluid before they were removed on the second postoperative day. Coumadin was begun on the second postoperative day, and the prothrombin time was 23.8 seconds (control 12.1 seconds) on the seventh postoperative day when the patient was discharged. On Dec. 15, 1976, the twenty-ninth postoperative day, the patient was seen at a follow-up examination. He was noted to have an asymtomatic right pleural effusion on chest roentgenogram and a posterior pericardial effusion on echocardiogram (Fig. I). The patient was begun on a regimen of digitalis and furosemide for suspected congestive heart failure and returned home only to note the gradual onset of progressively severe dyspnea, for which he was admitted to another hospital on Dec. 20, 1976. Pulmonary edema was diagnosed at that time and treatment was begun with oxygen and diuretics. Despite this, pulmonary edema worsened and hypotension developed over the next 48 hours. The patient was transferred to the University of Kentucky Medical Center on the thirty-sixth postoperative day. When admitted to this hospital, the patient was markedly dyspneic and somnolent. Blood pressure was 70/50 mm. Hg and pulsus paradox us was not appreciated. The heart rate was 120 beats per minute and the respiratory rate was 28 breaths per minute. Neck veins were not distended. An active point of maximal impulse was palpated 2 to 3 cm. lateral to the midclavicular line in the fifth left intercostal space. The aortic prosthetic sounds were crisp and no murmurs were heard. Rales were noted over the entirety of both lung fields. The liver was palpable and nontender at the right costal margin. The extremities were cool and mottled and edema was absent. Chest roentgenogram revealed an increased cardiothoracic ratio unchanged from that of a week earlier, persistence of the right pleural effusion, and pulmonary venous congestion. An electrocardiogram revealed sinus tachycardia (rate 120) but was otherwise unchanged from previous tracings showing left ventricular hypertrophy. Electrical altemans was absent. The prothrombin time was 33.2 seconds (control 12.6 seconds).
0022-5223179/010142+05$00.50/0 © 1979 The C. V. Mosby Co.
Volume 77 Number 1
January, 1979
Left ventricular tamponade
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Fig. 1. Echocardiographic sweep from the left ventricle to the aorta on the twenty-ninth postoperative day. A large posterior pericardial effusion (PE) is demonstrated. MV, Mitral valve. AV, Aortic prosthesis. LA, Left atrium. Calibration markers = I em.
Fig. 2. Echocardiogram obtained on the thirty-sixth postoperative day immediately prior to cardiac catheterization. A large posterior pericardial effusion (PE) and systolic anterior motion of the mitral valve (arrow) are noted. MV, Mitral valve. RV, Right ventricle. LV, Left ventricle. S, Septum. EP, Epicardium. Calibration markers = I em. An echocardiogram showed an echo-free space behind the left ventricle. This space was obliterated at the level of the left ventricular-left atrial junction, an indication of pericardial rather than pleural effusion. This size of space was noted to have increased since the tracing obtained I week earlier. Systolic anterior motion (SAM) of the mitral valve was also noted. A chest tube inserted into the right pleural space drained approximately 300 mi. of blood-tinged fluid. A repeat echocardiogram (Fig. 2) was unchanged, further substantiat-
ing the diagnosis of pericardial fluid. Attempts at pericardiocentesis via a subxyphoid approach with electrocardiographic monitoring were unsuccessful. The patient was then taken to the cardiac catheterization laboratory for hemodynamic evaluation. At cardiac catheterization, the central aortic pressure was 80/60 mm. Hg with a 6 mm. Hg respiratory variation in systolic blood pressure. Right heart catheterization (Fig. 3) disclosed markedly elevated pulmonary capillary wedge and
The Journal of
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Jones et al.
~ RA
Thoracic and Cardiovascular Surgery
M JVJ RV
PA
- 50
~ :~
- 10 -0
pew
Fig. 3. Right-sided heart pressures obtained at cardiac catheterization. Equilibration of diastolic pressures, the hallmark of cardiac tamponade, is absent. EKG. Electrocardiogram. RA, Right atrium. RV, Right ventricle. PA, Pulmonaryartery. pew, Pulmonary capillary wedge. Pressures are in millimeters of mercury. pulmonary artery diastolic pressures (28 mm. Hg). Mean right atrial and right ventricular end-diastolic pressures were slightly elevated (10 mm. Hg) but well below the pulmonary capillary wedge and pulmonary artery diastolic pressures. Cardiac output by the thermodilution technique was 2.40 L. per minute (1.28 L. per minute per square meter). An aortic root injection revealed no aortic insufficiency, and findings on coronary angiography were normal. Whereas catheterization data suggested severe left ventricular failure, the echocardiographic finding of a large posterior echo-free space suggested left ventricular compression by loculated pericardial effusion and prompted surgical exploration. The mediastinum was explored through a small subxyphoid incision. No fluid or clot was found anterior to the heart. The heart was adherent to the diaphragmatic portion of the pericardium, but after these adhesions had been taken down a large posterior space containing fluid under pressure was opened. The patient's blood pressure immediately increased from 70/40 to 160/80 mm. Hg and the mean pulmonary capillary wedge pressure fell to 10 mm. Hg. A chest tube was placed into this space and the incision was closed. The postoperative course was uncomplicated. A repeat echocardiographic examination on the seventh postoperative day revealed no evidence of pericardia! fluid, and SAM of the mitral valve was no longer present (Fig. 4).
Discussion Case histories of 43 patients with tamponade occurring from 7 days to 3 months after operation have been reported. Seven of these patients have died of this complication for a mortality rate of 16 percent.t"!" There appears to be no consistent pattern in the early postoperative course of these patients that will serve to predict those who are at high risk for this complication. Although many authors reported finding pericardial and mediastinal clots at the time of reoperation, no instances of hemodynamic abnormalities attributable to compression of one part of the heart were described until 1966, when Yacoub and associates':' reported on
two cases caused by left atrial compression by clot. In both instances the clinical picture was one of low cardiac output in the immediate (I to 2 hours) postoperative period; cardiac tamponade was not seriously considered in the differential diagnosis because of the absence of an elevated central venous pressure and paradoxical pulse. In both cases, exploration and removal of clot compressing the left atrium resulted in relief of hemodynamic embarrassment.':' Hill and colleagues, 7 in 1969, reported a case of pulmonary outflow obstruction with a 24 mm. Hg gradient across the pulmonary outflow tract 8 days after mitral valve replacement. Surgical exploration with removal of clot resulted in the disappearance of the gradient, and the patient made an uneventful recovery. Simpkin's group;" in 1973, described a patient followed for continuing malaise, chest pain, and cardiomegaly during the second and third months following repair of an atrial septal defect. The central venous pressure was not elevated and pulsus paradoxus was not present. The patient had acute hemodynamic decompensation after practolol was given to correct a junctional tachycardia, and surgical exploration revealed a loculated posterior pericardial effusion. After drainage of the effusion the patient became hemodynamically stable and made an uneventful recovery. This case appears somewhat similar to the one reported here, but closer comparison is not possible because hemodynamic and echocardiographic data were not reported. The case reported here is unique. The patient presented on the thirty-sixth postoperative day with clinical and hemodynamic evidence of left ventricular failure, pulmonary edema, and low cardiac output. The findings classically associated with pericardial tamponade, in which fluid compression is distributed equally about the heart, were absent. 16 - 18 The apical impulse was distinct, radiographic heart size was unchanged from previous examinations, electrocardiographic voltage was not decreased, and electrical alternans was absent. Most importantly, equalization of diastolic pressures was absent, with right ventricular diastolic pressure being only slightly elevated and well below the pulmonary artery diastolic and pulmonary capillary wedge pressures. The small pulsus (6 mm. Hg) was not diagnostically helpful. The hemodynamic findings of hypotension, reduced cardiac output, and a markedly elevated pulmonary capillary wedge pressure were indicative of left ventricular failure or obstruction to left ventricular inflow. The identification of a large posterior pericardial effusion, however, suggested left ventricular tamponade by loculated pericardial effusion and the diagnosis was surgically confirmed.
Volume 77
Left ventricular tamponade
Number 1 January. 1979
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Fig. 4. Echocardiogram obtained 7 days after the drainage of loculated posterior pericardial effusion. In comparison to earlier tracings, pericardial effusion and systolic anterior motion of the mitral valve are absent. LV , Left ventricle. MV, Mitral valve. P, Pericardial echoes. Calibration markers = I em. The usefulness of echocardiography in determining the correct diagnosis in this case merits special attention. There have been only two previously reported echocardiograms from patients having late postoperative pericardial tamponade. 5 , 6 In neither was there an anterior echo-free space, but unlike the present case, both patients had the usual hemodynamic findings of cardiac tamponade and were successfully treated by pericardiocentesis. Accordingly, posterior pericardial effusion in the absence of anterior effusion does not appear to indicate loculation . Echocardiographic features suggesting tamponade, such as right ventricular compression and abnormal respiratory variation of ventricular dimensions or mitral valve E-F slope, 19-21 were not reported in earlier cases and were not found in the present case. Systolic anterior motion (SAM) of the mitral valve was noted in this case. Although "pseudo SAM" has been previously described in patients with a heart "swinging" in a large pericardial effusion, " the SAM noted in this case appears to be true SAM, in that it does not merely reflect exaggerated posterior wall motion. True SAM, similar to that of obstructive cardiomyopathy ." has been reported in a number of disease states 24 - 26 including hypovolemic shock'" and conditions associated with an increased ejection frac tion . 28 These latter observations of SAM occurring in a small , hypercontractile left ventricle may explain its occurrence in this case, in which a loculated effusion restricted ventricular filling . Although the significance
of SAM in the context of postoperative pericardial tamponade requires further clarification, its absence before clinical decompensation and resolution following surgical decompression suggests a relationship between the observed hemodynamic and echocardiographic abnormalities. In the postoperative patient with a large posterior pericardial effusion and signs of left ventricular failure , loculated pericardial effusion with restriction to left ventricular filling should be considered . The additional finding of SAM of the anterior leaflet of the mitral valve may indicate significant hemodynamic embarrassment, but the clinical usefulness of this latter observation remains to be determined.
2
3 4 5
REFERENCES Engelman RM, Spencer FC, Reed GE, Tice DA: Cardiac tamponade following open-heart surgery. Circulation 41, 42:(Suppl 2): 165-171, 1970 Radley-Smith R, Gonzalez-Lavin L, Somerville J: Pericardial effusion with tamponade following anastomosis of the ascending aorta to the right pulmonary artery (Waterston's operation). J THORAC CARDIOVASC SURG 60:565-574, 1970 Nelson RM, Jenson CB, Smoot WM: Pericardial tamponade following open-heart surgery. J THORAC CARDJOVASC SURG 58:510-516, 1969 Craddock DR, Logan A. Fadali A: Reoperation for hemorrhage following cardiopulmonary bypass. Br J Surg 55:17-20, 1968 Merrill W, Donahoo JS, Brawley RK, Taylor D: Late cardiac tamponade. A potentially lethal complication of
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7
8
9
10
II
12
13 14 15
16
17
Jones et al.
open-heart surgery. 1 THORAC CARDIOVASC SURG 72: 929-932, 1976 Fernando HA, Friedman HS, Lejam F, Sakurai H: Late cardiac tamponade following open-heart surgery. Detection by echocardiography. Ann Thorac Surg 24: 174-177, 1977 Hill 10, Johnson DC, Miller GE, Kerth wr, Gerbode F: Latent mediastinal tamponade after open-heart surgery. Arch Surg 99:808-814, 1969 Somerville 1, Yacoub M, Ross ON, Ross K: Aorta to right pulmonary artery anastomosis (Waterstons operation) for cyanotic heart disease. Circulation 39:593-602, 1969 Fraser DG, Ullyot 01: Mediastinal tamponade after open-heart surgery. 1 THORAC CARDIOVASC SURG 66: 629-631, 1973 Berger RL, Loveless G, Warner 0: Delayed and latent postcardiotomy tamponade. Ann Thorac Surg 12:22-28, 1971 Prewitt TA, Rackley CE, Wilcox BR, Scatlift JH, Young DT: Cardiac tamponade as a late complication of openheart surgery. Am Heart 176:139-141, 1968 Scott RAP, Drew CE: Delayed pericardial effusion with tamponade after cardiac surgery. Br Heart 1 35: 13041306, 1973 Ellison LH, Kirsh MM: Delayed mediastinal tamponade after open heart surgery. Chest 65:64-66, 1974 Yacoub MH, Cleland WP, Deal CW: Left atrial tamponade. Thorax 21:305-309, 1966 Simpkin P, Brown AH, Ersoz A, Braimbridge MY: Chronic left heart tamponade. 1 THORAC CARDIOVASC SURG 65:531-533, 1973 Spodick DH: Acute cardiac tamponade. Pathologic physiology, diagnosis, and management. Progr Cardiovasc Dis 10:64-96, 1967 Shabetai R, Fowler NO, Guntheroth WG: The hemodynamics of cardiac tamponade and constrictive pericarditis. Am 1 Cardiol 26:480-489, 1970
The Journal of Thoracic and Cardiovascular Surgery
18 Weeks KR, Chatterjee K, Block S, Matloff 1M, Swan H1C: Bedside hemodynamic monitoring. Its value in the diagnosis of tamponade complicating cardiac surgery. 1 THoRAc CARDIOVASC SURG 71:250-252, 1976 19 D'Cruz lA, Cohen HC, Prabhu R, Glick G: Diagnosis of cardiac tamponade by echocardiography. Circulation 52:460-465, 1975 20 Seattle HP, Adolph Rl, Fowler NO, Engel P, Agruss NS, Levenson NI: Echocardiographic study of cardiac tamponade. Circulation 56:951-959, 1977 21 Schiller NB, Botvinick EH: Right ventricular compression as a sign of cardiac tamponade. Circulation 56:774779, 1977 22 Nanda NC, Gramiak R, Gross CM: Echocardiography of cardiac valves in pericardial effusion. Circulation 54: 500-504, 1976 23 Shah PM, Gramiak R, Kramer DH: Ultrasound localization of left ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy. Circulation 40:3-11, 1969 24 Nanda NC, Gramiak R, Manning lA, Lipchik EO: Echocardiographic features of subpulmonic obstruction in dextro-transposition of the great vessels. Circulation 51:515-521, 1975 25 Davis RH, Feigenbaum H, Chang S, Knecke LL, Dillon 1: Echocardiographic manifestations of discrete subaortic stenosis. Am 1 Cardiol 33:277-280, 1974 26 Feigenbaum H: Echocardiography, Philadelphia, 1976, Lea & Febiger, Publishers, pp 137-138 27 Buckley BH, Fortuin Nl: Systolic anterior motion of the mitral valve without asymmetric septal hypertrophy. Chest 69:694-696, 1976 28 Mintz GS, Kotler MN, Segal BL, Parry WR: Systolic anterior motion of the mitral val ve in the absence of asymmetric septal hypertrophy. Circulation 57:256-263, 1978
Michael R. Jones, M.D., Donald L. Vine, M.D., Michael Attas, M.D., and Edward P. Todd, M.D., Ph.D., Lexington, Ky.
P
ericardial tamponade complicates 3.4 to 8.8 percent of all open-heart procedures.v " The majority of these cases occur in the immediate postoperative period and usually pose no special diagnostic difficulties. Pericardial tamponade occurring in the late postoperative period is much less frequent, with only 43 cases having been described in the literature. 1-13 Cardiac tamponade produced by the localized effect of fluid or clot is the least frequently reported and most diagnostically evasive presentation of tamponade after open-heart operations. Four such cases have been found in the literature, only two of which occurred in the late postoperative period. 7, 14, 15 The reported case occurred in the late postoperative period and is to our knowledge the first documented instance of isolated postoperative left ventricular tamponade in the literature.
Case report A 55-year-old man underwent aortic valve replacement and mycotic aneurysmectomy in October, 1976. The pericardium was left open and drainage was established with two anterior mediastinal tubes. The immediate postoperative course was uncomplicated. Mediastinal tubes drained 445 ml. From the Divisions of Cardiology and Cardio-Thoracic Surgery, University of Kentucky College of Medicine, Lexington. Ky. Received for publication June 6, 1978. Accepted for publication July 13, 1978. Address for reprints: Michael R. Jones, M.D., University of Kentucky Medical Center, Department of Medicine, Division of Cardiology, Room MN670, 800 Rose St., Lexington, Ky. 40506.
142
of serosanguineous fluid before they were removed on the second postoperative day. Coumadin was begun on the second postoperative day, and the prothrombin time was 23.8 seconds (control 12.1 seconds) on the seventh postoperative day when the patient was discharged. On Dec. 15, 1976, the twenty-ninth postoperative day, the patient was seen at a follow-up examination. He was noted to have an asymtomatic right pleural effusion on chest roentgenogram and a posterior pericardial effusion on echocardiogram (Fig. I). The patient was begun on a regimen of digitalis and furosemide for suspected congestive heart failure and returned home only to note the gradual onset of progressively severe dyspnea, for which he was admitted to another hospital on Dec. 20, 1976. Pulmonary edema was diagnosed at that time and treatment was begun with oxygen and diuretics. Despite this, pulmonary edema worsened and hypotension developed over the next 48 hours. The patient was transferred to the University of Kentucky Medical Center on the thirty-sixth postoperative day. When admitted to this hospital, the patient was markedly dyspneic and somnolent. Blood pressure was 70/50 mm. Hg and pulsus paradox us was not appreciated. The heart rate was 120 beats per minute and the respiratory rate was 28 breaths per minute. Neck veins were not distended. An active point of maximal impulse was palpated 2 to 3 cm. lateral to the midclavicular line in the fifth left intercostal space. The aortic prosthetic sounds were crisp and no murmurs were heard. Rales were noted over the entirety of both lung fields. The liver was palpable and nontender at the right costal margin. The extremities were cool and mottled and edema was absent. Chest roentgenogram revealed an increased cardiothoracic ratio unchanged from that of a week earlier, persistence of the right pleural effusion, and pulmonary venous congestion. An electrocardiogram revealed sinus tachycardia (rate 120) but was otherwise unchanged from previous tracings showing left ventricular hypertrophy. Electrical altemans was absent. The prothrombin time was 33.2 seconds (control 12.6 seconds).
0022-5223179/010142+05$00.50/0 © 1979 The C. V. Mosby Co.
Volume 77 Number 1
January, 1979
Left ventricular tamponade
143
Fig. 1. Echocardiographic sweep from the left ventricle to the aorta on the twenty-ninth postoperative day. A large posterior pericardial effusion (PE) is demonstrated. MV, Mitral valve. AV, Aortic prosthesis. LA, Left atrium. Calibration markers = I em.
Fig. 2. Echocardiogram obtained on the thirty-sixth postoperative day immediately prior to cardiac catheterization. A large posterior pericardial effusion (PE) and systolic anterior motion of the mitral valve (arrow) are noted. MV, Mitral valve. RV, Right ventricle. LV, Left ventricle. S, Septum. EP, Epicardium. Calibration markers = I em. An echocardiogram showed an echo-free space behind the left ventricle. This space was obliterated at the level of the left ventricular-left atrial junction, an indication of pericardial rather than pleural effusion. This size of space was noted to have increased since the tracing obtained I week earlier. Systolic anterior motion (SAM) of the mitral valve was also noted. A chest tube inserted into the right pleural space drained approximately 300 mi. of blood-tinged fluid. A repeat echocardiogram (Fig. 2) was unchanged, further substantiat-
ing the diagnosis of pericardial fluid. Attempts at pericardiocentesis via a subxyphoid approach with electrocardiographic monitoring were unsuccessful. The patient was then taken to the cardiac catheterization laboratory for hemodynamic evaluation. At cardiac catheterization, the central aortic pressure was 80/60 mm. Hg with a 6 mm. Hg respiratory variation in systolic blood pressure. Right heart catheterization (Fig. 3) disclosed markedly elevated pulmonary capillary wedge and
The Journal of
144
Jones et al.
~ RA
Thoracic and Cardiovascular Surgery
M JVJ RV
PA
- 50
~ :~
- 10 -0
pew
Fig. 3. Right-sided heart pressures obtained at cardiac catheterization. Equilibration of diastolic pressures, the hallmark of cardiac tamponade, is absent. EKG. Electrocardiogram. RA, Right atrium. RV, Right ventricle. PA, Pulmonaryartery. pew, Pulmonary capillary wedge. Pressures are in millimeters of mercury. pulmonary artery diastolic pressures (28 mm. Hg). Mean right atrial and right ventricular end-diastolic pressures were slightly elevated (10 mm. Hg) but well below the pulmonary capillary wedge and pulmonary artery diastolic pressures. Cardiac output by the thermodilution technique was 2.40 L. per minute (1.28 L. per minute per square meter). An aortic root injection revealed no aortic insufficiency, and findings on coronary angiography were normal. Whereas catheterization data suggested severe left ventricular failure, the echocardiographic finding of a large posterior echo-free space suggested left ventricular compression by loculated pericardial effusion and prompted surgical exploration. The mediastinum was explored through a small subxyphoid incision. No fluid or clot was found anterior to the heart. The heart was adherent to the diaphragmatic portion of the pericardium, but after these adhesions had been taken down a large posterior space containing fluid under pressure was opened. The patient's blood pressure immediately increased from 70/40 to 160/80 mm. Hg and the mean pulmonary capillary wedge pressure fell to 10 mm. Hg. A chest tube was placed into this space and the incision was closed. The postoperative course was uncomplicated. A repeat echocardiographic examination on the seventh postoperative day revealed no evidence of pericardia! fluid, and SAM of the mitral valve was no longer present (Fig. 4).
Discussion Case histories of 43 patients with tamponade occurring from 7 days to 3 months after operation have been reported. Seven of these patients have died of this complication for a mortality rate of 16 percent.t"!" There appears to be no consistent pattern in the early postoperative course of these patients that will serve to predict those who are at high risk for this complication. Although many authors reported finding pericardial and mediastinal clots at the time of reoperation, no instances of hemodynamic abnormalities attributable to compression of one part of the heart were described until 1966, when Yacoub and associates':' reported on
two cases caused by left atrial compression by clot. In both instances the clinical picture was one of low cardiac output in the immediate (I to 2 hours) postoperative period; cardiac tamponade was not seriously considered in the differential diagnosis because of the absence of an elevated central venous pressure and paradoxical pulse. In both cases, exploration and removal of clot compressing the left atrium resulted in relief of hemodynamic embarrassment.':' Hill and colleagues, 7 in 1969, reported a case of pulmonary outflow obstruction with a 24 mm. Hg gradient across the pulmonary outflow tract 8 days after mitral valve replacement. Surgical exploration with removal of clot resulted in the disappearance of the gradient, and the patient made an uneventful recovery. Simpkin's group;" in 1973, described a patient followed for continuing malaise, chest pain, and cardiomegaly during the second and third months following repair of an atrial septal defect. The central venous pressure was not elevated and pulsus paradoxus was not present. The patient had acute hemodynamic decompensation after practolol was given to correct a junctional tachycardia, and surgical exploration revealed a loculated posterior pericardial effusion. After drainage of the effusion the patient became hemodynamically stable and made an uneventful recovery. This case appears somewhat similar to the one reported here, but closer comparison is not possible because hemodynamic and echocardiographic data were not reported. The case reported here is unique. The patient presented on the thirty-sixth postoperative day with clinical and hemodynamic evidence of left ventricular failure, pulmonary edema, and low cardiac output. The findings classically associated with pericardial tamponade, in which fluid compression is distributed equally about the heart, were absent. 16 - 18 The apical impulse was distinct, radiographic heart size was unchanged from previous examinations, electrocardiographic voltage was not decreased, and electrical alternans was absent. Most importantly, equalization of diastolic pressures was absent, with right ventricular diastolic pressure being only slightly elevated and well below the pulmonary artery diastolic and pulmonary capillary wedge pressures. The small pulsus (6 mm. Hg) was not diagnostically helpful. The hemodynamic findings of hypotension, reduced cardiac output, and a markedly elevated pulmonary capillary wedge pressure were indicative of left ventricular failure or obstruction to left ventricular inflow. The identification of a large posterior pericardial effusion, however, suggested left ventricular tamponade by loculated pericardial effusion and the diagnosis was surgically confirmed.
Volume 77
Left ventricular tamponade
Number 1 January. 1979
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Fig. 4. Echocardiogram obtained 7 days after the drainage of loculated posterior pericardial effusion. In comparison to earlier tracings, pericardial effusion and systolic anterior motion of the mitral valve are absent. LV , Left ventricle. MV, Mitral valve. P, Pericardial echoes. Calibration markers = I em. The usefulness of echocardiography in determining the correct diagnosis in this case merits special attention. There have been only two previously reported echocardiograms from patients having late postoperative pericardial tamponade. 5 , 6 In neither was there an anterior echo-free space, but unlike the present case, both patients had the usual hemodynamic findings of cardiac tamponade and were successfully treated by pericardiocentesis. Accordingly, posterior pericardial effusion in the absence of anterior effusion does not appear to indicate loculation . Echocardiographic features suggesting tamponade, such as right ventricular compression and abnormal respiratory variation of ventricular dimensions or mitral valve E-F slope, 19-21 were not reported in earlier cases and were not found in the present case. Systolic anterior motion (SAM) of the mitral valve was noted in this case. Although "pseudo SAM" has been previously described in patients with a heart "swinging" in a large pericardial effusion, " the SAM noted in this case appears to be true SAM, in that it does not merely reflect exaggerated posterior wall motion. True SAM, similar to that of obstructive cardiomyopathy ." has been reported in a number of disease states 24 - 26 including hypovolemic shock'" and conditions associated with an increased ejection frac tion . 28 These latter observations of SAM occurring in a small , hypercontractile left ventricle may explain its occurrence in this case, in which a loculated effusion restricted ventricular filling . Although the significance
of SAM in the context of postoperative pericardial tamponade requires further clarification, its absence before clinical decompensation and resolution following surgical decompression suggests a relationship between the observed hemodynamic and echocardiographic abnormalities. In the postoperative patient with a large posterior pericardial effusion and signs of left ventricular failure , loculated pericardial effusion with restriction to left ventricular filling should be considered . The additional finding of SAM of the anterior leaflet of the mitral valve may indicate significant hemodynamic embarrassment, but the clinical usefulness of this latter observation remains to be determined.
2
3 4 5
REFERENCES Engelman RM, Spencer FC, Reed GE, Tice DA: Cardiac tamponade following open-heart surgery. Circulation 41, 42:(Suppl 2): 165-171, 1970 Radley-Smith R, Gonzalez-Lavin L, Somerville J: Pericardial effusion with tamponade following anastomosis of the ascending aorta to the right pulmonary artery (Waterston's operation). J THORAC CARDIOVASC SURG 60:565-574, 1970 Nelson RM, Jenson CB, Smoot WM: Pericardial tamponade following open-heart surgery. J THORAC CARDJOVASC SURG 58:510-516, 1969 Craddock DR, Logan A. Fadali A: Reoperation for hemorrhage following cardiopulmonary bypass. Br J Surg 55:17-20, 1968 Merrill W, Donahoo JS, Brawley RK, Taylor D: Late cardiac tamponade. A potentially lethal complication of
I 46
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7
8
9
10
II
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13 14 15
16
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Jones et al.
open-heart surgery. 1 THORAC CARDIOVASC SURG 72: 929-932, 1976 Fernando HA, Friedman HS, Lejam F, Sakurai H: Late cardiac tamponade following open-heart surgery. Detection by echocardiography. Ann Thorac Surg 24: 174-177, 1977 Hill 10, Johnson DC, Miller GE, Kerth wr, Gerbode F: Latent mediastinal tamponade after open-heart surgery. Arch Surg 99:808-814, 1969 Somerville 1, Yacoub M, Ross ON, Ross K: Aorta to right pulmonary artery anastomosis (Waterstons operation) for cyanotic heart disease. Circulation 39:593-602, 1969 Fraser DG, Ullyot 01: Mediastinal tamponade after open-heart surgery. 1 THORAC CARDIOVASC SURG 66: 629-631, 1973 Berger RL, Loveless G, Warner 0: Delayed and latent postcardiotomy tamponade. Ann Thorac Surg 12:22-28, 1971 Prewitt TA, Rackley CE, Wilcox BR, Scatlift JH, Young DT: Cardiac tamponade as a late complication of openheart surgery. Am Heart 176:139-141, 1968 Scott RAP, Drew CE: Delayed pericardial effusion with tamponade after cardiac surgery. Br Heart 1 35: 13041306, 1973 Ellison LH, Kirsh MM: Delayed mediastinal tamponade after open heart surgery. Chest 65:64-66, 1974 Yacoub MH, Cleland WP, Deal CW: Left atrial tamponade. Thorax 21:305-309, 1966 Simpkin P, Brown AH, Ersoz A, Braimbridge MY: Chronic left heart tamponade. 1 THORAC CARDIOVASC SURG 65:531-533, 1973 Spodick DH: Acute cardiac tamponade. Pathologic physiology, diagnosis, and management. Progr Cardiovasc Dis 10:64-96, 1967 Shabetai R, Fowler NO, Guntheroth WG: The hemodynamics of cardiac tamponade and constrictive pericarditis. Am 1 Cardiol 26:480-489, 1970
The Journal of Thoracic and Cardiovascular Surgery
18 Weeks KR, Chatterjee K, Block S, Matloff 1M, Swan H1C: Bedside hemodynamic monitoring. Its value in the diagnosis of tamponade complicating cardiac surgery. 1 THoRAc CARDIOVASC SURG 71:250-252, 1976 19 D'Cruz lA, Cohen HC, Prabhu R, Glick G: Diagnosis of cardiac tamponade by echocardiography. Circulation 52:460-465, 1975 20 Seattle HP, Adolph Rl, Fowler NO, Engel P, Agruss NS, Levenson NI: Echocardiographic study of cardiac tamponade. Circulation 56:951-959, 1977 21 Schiller NB, Botvinick EH: Right ventricular compression as a sign of cardiac tamponade. Circulation 56:774779, 1977 22 Nanda NC, Gramiak R, Gross CM: Echocardiography of cardiac valves in pericardial effusion. Circulation 54: 500-504, 1976 23 Shah PM, Gramiak R, Kramer DH: Ultrasound localization of left ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy. Circulation 40:3-11, 1969 24 Nanda NC, Gramiak R, Manning lA, Lipchik EO: Echocardiographic features of subpulmonic obstruction in dextro-transposition of the great vessels. Circulation 51:515-521, 1975 25 Davis RH, Feigenbaum H, Chang S, Knecke LL, Dillon 1: Echocardiographic manifestations of discrete subaortic stenosis. Am 1 Cardiol 33:277-280, 1974 26 Feigenbaum H: Echocardiography, Philadelphia, 1976, Lea & Febiger, Publishers, pp 137-138 27 Buckley BH, Fortuin Nl: Systolic anterior motion of the mitral valve without asymmetric septal hypertrophy. Chest 69:694-696, 1976 28 Mintz GS, Kotler MN, Segal BL, Parry WR: Systolic anterior motion of the mitral val ve in the absence of asymmetric septal hypertrophy. Circulation 57:256-263, 1978