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Acute right ventricular dilation and echocardiographic volume overload following pericardiocentesis for relief of cardiac tamponade
Brief
1266
4.
5.
6.
I.
8.
9.
10.
11.
Communications
American
Bruce RA: Exercise testing of patients with coronary heart disease. Principles and normal standards for evaluation. Ann Clin Res 3:323, 1971. Dunn RF, Freedman B, Bailey IK, Bernstein L, Kelly DT: Exercise thallium imaging: Location of perfusion abnormalities in single vessel coronary disease. J Nucl Med 21:717, 1980. McLaughlin PR, Martin R, Doherty P, Daspit S, Gloris M, Haskell W, Lewis S, Kriss JP, Harrison DC: Reproducibility of thallium-201 myocardial imaging. Circulation 55:497, 1977. Thadani U, West RO, Mathew TM, Parker JO: Hemodynamits at rest and during supine and sitting bicycle exercise in patients with coronary artery disease. Am J Cardiol 39:776, 1977. Levey M, Rozanski A, Valovis R, Ford D, Morris D, Pantaleo N, Maddahi J, Swan HJC, Berman D: Comparative ability of upright and supine bicycle exercise electrocardiography to detect coronary artery disease (abstr). Am J Cardiol 49:945, 1982. Currie P, Kelly M, Pitt A: Is it valid to compare the sensitivity of a supine exercise nuclear imaging procedure with that of an erect exercise ECG (abstr)? Aust NZ J Med 12:668, 1982. Freeman MR, Berman DS, Staniloff H, Elkayam U, Maddahi J, Swan HJC, Forrester J: Comparison of upright and supine bicycle exercise in the detection and evaluation of extent of coronary artery disease by equilibrium radionuclide ventriculography. AM HEART J 102:182, 1981. Manyari DE, Kostuk WJ, Purves PP: Left and right ventricular function at rest and during bicycle exercise in the supine and sitting positions in normal subjects and patients with coronary artery disease: Assessment by radionuclide ventriculography. Am J Cardiol 51:36, 1983.
Acute right ventricular dilation and echocardiographic volume overload following pericardiocentesis for relief of cardiac tamponade William F. Armstrong, M.D., Harvey Feigenbaum, M.D., and JamesC. Dillon, M.D. Indianapolis, Znd.
June, 1984 Heart Journal
Recently, this phenomenonhas been noted with radionuelide angiographyP We report here the finding of acute right ventricular (RV) dilation and development of an echocardiographicRV volume overload pattern in three of six patients after removal of pericardial fluid for relief of cardiac tamponade. Exemplary cases. A 13-year-old white boy (patient No. 5, Table I) wasadmitted to the hospital with a diagnosisof germinal cell tumor. On admission,he was in mild respiratory distress. Heart rate was 130 bpm and blood pressure was 60/50 mm Hg with a palpable paradox. Two-
dimensional echocardiography @DE) revealed a large pericardial effusion with RV collapsesuggestinghemodynamic compromise.7Pericardiocentesis was performed, and 1400ml of serosanguineous fluid wasremoved. Immediately after pericardiocentesis, 2DE was repeated. The right ventricle was markedly dilated and interventricular septal motion was consistent with a RV volume overload pattern. Following pericardiocentesis,heart rate remained elevated at 140 bpm; blood pressurewas 90/70 mm Hg without paradox. Marked jugular venous distention persisted and a RV gallop was noted. Right heart catheterization revealed equalization of diastolic pressures at 40 mm
Hg. Repeat pericardiocentesis was performed and an additional 700 ml fluid was removed. The clinical picture of jugular venous distention with right heart gallop persisted.On the fifth hospital day, the patient wastaken to the operating room where a pericardial window was created. The resected pericardium was noted to be inflamed but wasnot thickened. The patient experienced gradual resolution of symptoms and evidence of venous congestionresolved. He was dischargedfollowing therapy of the malignancy. A 26-year-old white woman (patient No. 6, Table I) was admitted to the hospital in marked respiratory distress. Past medical history wassignificant for Hodgkins disease treated 11 years previously with chemotherapy and mediastinal radiation. She had no history of cardiovascular diseaseand had previously had multiple normal cardiovascular examinations. At the time of admission, the patient was an acutely ill and cachetic white woman.
The normal pericardium exerts a restraining influence on the size of the cardiac chambers.’ Dilation of the right ventricle has been reported after surgical removal of the pericardium for treatment of constrictive pericarditis and in cases of congenital absence of the pericardium.2-5
Blood pressurewas 70/50 mm Hg and heart rate was 120 bpm. An echocardiogram demonstrated the presence of moderate pericardial effusion with abnormal RV free wall motion suggestinghemodynamic compromise(Fig. 1).7A flow-directed right heart catheter documented elevation and equilibration of diastolic pressuresconsistent with cardiac tamponade. Pericardiocentesiswas performed, at which time 200 ml of serosanguineous
From Indiana
the Krannert University
Institute of Cardiology, School of Medicine.
Department
of Medicine,
Supported in part by the Herman C. Krannert Fund, Indianapolis, Ind., Grants HL-06308 and HL-07182, and by Clinical Investigator Award HL 01041-02 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.; by the American Heart Association, Indiana Affiliate, Indianapolis, Ind.; and by the Whitaker Foundation, Camp Hill, Pa. Reprint requests: William F. Armstrong, of Medicine, University Hospital N562,926 IN 46223.
M.D., Indiana W. Michigan
University School St., Indianapolis,
fluid was removed.
The systolic blood pressuresubsequently rose to 120 mm Hg; however, right heart pressuresremained elevated. Repeat M-mode and 2DE, performed immediately after pericardiocentesis, revealed increase in RV dimension from 1.2 cm to 2.6 cm. Left ventricular internal dimension decreasedfrom 3.8 cm to 3.1 cm. Interventricular septal motion becameabnormal, demonstrating the characteristic early systolic anterior motion of the interventricular septum, seen in RV volume overload (Fig. 2). 2DE revealed a markedly dilated right ventricle, with diastolic
Volume Number
107 6
Brief Communications
1267
Fig. 1. M-mode echocardiogram from patient No. 6 at time of diagnosis of cardiac tamponade. There is moderate anterior and posterior pericardial effusion (PE). Right ventricular (RV) dimension is 1.1 cm and (LV) is 3.8 cm. Immediately after onset of electrical systole (arrow), the left ventricular dimension interventricular septum moves posteriorly. This is the normal motion pattern of the interventricular septum.
“flattening” of the interventricular septum, also consistent with RV volume overload (Fig. 3). The records, from January, 1981, to December, 1982, of the echocardiographic laboratory at the Indiana University Hospital were reviewed to identify patients who had undergone pericardiocentesis for relief of cardiac tamponade and who had been studied with either M-mode or 2DE within 24 hours of pericardiocentesis. Clinical records were reviewed to insure accuracy of the diagnosis of cardiac tamponade and to obtain information for clinical correlation. All M-mode and 2DEs were reviewed by two experienced echocardiographers. RV volume overload was defined on M-mode echocardiography aa dilation of the RV cavity in diastole (>2.3 cm), in association with abnormal motion of the interventricular septmng The abnormal motion had to consist of brisk anterior motion of the interventricular septum immediately after onset of electrical systole, associated with appropriate thickening of the interventricular septum. On 2DE, RV volume overload was defined as the combination of subjective dilation of the right ventricle in association with the characteristic “flattening” of the interventricular septum throughout diastole, and restitution of normal, circular left ventricular geometry with onset of systole? Including the two index cases, six patients were identified who met the study criteria. Five of the six patients
Table
I. Clinical
Patient
Age
and echographic Etiology
M-Breast
1 2 3 4 5*
65 21 32 26 13
Histo M-Germ cell M-Brea$t M-Testicular
6*
26
Radiation
features
Amount of fluid (ml)
800
Type
Echo
RVVO
300 1100 900 1400
2D, MM 2D, MM7 2D, MM? 2Dt MM? 2Dt
++ + +
200
MM? 2Dt
+
Histo = histoplasmosis; M = malignancy; MM = M-mode echocardiography; 2D = two-dimensional echocardiography; Amount fluid = volume of fluid removed at the time of pericardiocentesis; RVVO = right ventricular volume overload. *Index case. tStudy showing evidence of right ventricular volume overload.
had been examined personally by one of the authors. Both M-mode and 2DE were performed in five; one patient had only 2DE performed after pericardiocentesis. The salient demographic data are presented in Table I. At the time of pericardiocentesis, all patients had clinical evidence of cardiac tamponade with jugular venous distention, hypotension, and pulsus paradoxus. Three patients underwent flow-directed right heart catheterization, and in each the findings were characteristic of cardiac tamponade. Follow-
1268
Brief
Communication-s
June, 1984 Heart Journal
American
---?t”
v”’
‘i
“V
V
9-9-82
Fig. 2. Patient No. 6. M-mode echocardiogram recorded after removal of 200 ml of fluid from the pericardium. Motion of the interventricular septum (IVS) is now markedly abnormal. After onset of electrical systole (arrow), the IVS moves briskly anteriorly. This is the characteristic motion seenin RV volume overload. Additionally, RV internal dimension has increasedto 2.6 cm.
ing pericardiocentesis, marked symptomatic relief was experienced by five of the six patients. Patient No. 6 achieved only minimal relief after pericardiocentesisand subsequently died of respiratory insufficiency from uncontrolled pneumonia. Clinically, no patient had evidenceof either an atrial septal defect or tricuspid regurgitation. Definite echocardiographicevidence of RV volume overload, with RV dilation and abnormal septal motion, was seen in three patients. Two other patients had equivocal evidence of RV volume overload. Both of these patients had serial dilation of the right ventricle; however, the abnormality of septal motion was nonspecific, with only minimal anterior motion at the onset of systole. This variant of abnormal septal motion has been described previously in patients with congenital absence of the pericardium or following pericardectomy.2 Comments. The pericardium exerts a restraining influenceon cardiac chamberswith respect to both geometry and potential for dilation.’ Dilation of cardiac chambers hasbeennoted after pericardectomy, where dilation of the right and/or left ventricle has been recognizedat the time of surgery3,4or noted postoperatively with echocardiography.2 Additionally, the rare finding of congenital absence of the pericardium is characterized echocardiographically by a dilated right ventricle and abnormal septal motion as
is seenin RV volume overload.2Excessivecardiac motion and unconventional orientation of the echo beam have been offered as an explanation. The use of 2DE in our study should negate both of these effects Although systolic anterior septal motion on M-mode echocardiography could be an artifact of cardiac motion, the septal flattening seen with 2DE cannot be explained as such. Becauseof the short-term nature of this study, we are unable to state the duration of this effect. In one patient, the RV volume overload pattern had only partially resolved 3 days after pericardiocentesis.That the acute right heart dilation is more than an incidental finding is suggestedby patient No. 5, in whom clinical evidence of right heart failure, including jugular venous distention, RV gallop, and persistent elevation of right heart pressures, was noted. The slow resolution of elevated right heart pressures suggests a component of RV failure prompted by acute dilation. A delay in normalization of pressuresis well described after surgical pericardectomy and has beenpresumedto he secondary to delay in return of normal myocardial function due to atrophy produced by long-standing constrictive process.3.5The failure of right heart pressuresto normalize promptly after pericardiocentesisalso has been previously recognized.‘” I1 This phenomenonpreviously hasbeen ascribedto the presence
Volume Number
107 6
Brief Communications 1269 creation of a pericardial window are against this mechanism. Additionally, the echocardiographicwall motion was purely that of RV volume overload and not that of pericardial constriction.‘3 In a recent report of RV volumesand function studied with radionuclide techniques, dilation of the right ventricle was noted after therapeutic pericardiocentesis.Furthermore, in this study RV ejection fraction decreasedor failed to increaseappropriately after removal of pericardial fluid. This is consistent with the presenceof a component of RV failure.6 To our knowledge, the casespresented in this brief report constitute the only description of pathologic RV volume overload occurring in the setting of an intact pericardium following pericardiocentesis.We hypothesize that in a patient with cardiac tamponade,the combination of the pericardium and the contained fluid exerts a restraining effect on chamber sizes. After removal of pericardial fluid, the effective intrapericardial volume is increasedin relation to the cardiac volume, thus allowing dilation of the most distensible cardiac chamber, the right ventricle. In effect, removing a large volume of pericardial fluid has the sameeffect as actual removal of the pericardium. In conclusion, we have reported three instancesof right heart dilation and development of a pathologic RV volume overload pattern echocardiographically in patients following pericardiocentesisfor relief of cardiac tamponade. Two further patients had equivocal evidence of RV volume overload. Only one patient, in our series of six studied immediately after pericardiocentesis,did not have someevidence of acute RV dilation and abnormal septal motion. REFERENCES
1. Shahetai R, Mangiardi L, Bhargava V, Ross J, Higgins CB: The pericardium and cardiac function. Prog Cardiovasc Dis 22:107, 1979. 2. Payvandi MN, Kerber RE: Echocardiography in congenital and acquired absence of the pericardium: An echocardiographic mimic of right ventricular volume overload. Circulation 53:86, 1976. 3. Chambliss JR, Jaruszewski EJ, Brofman BL, Martin JF, Feil H: Chronic cardiac compression (chronic constrictive pericarditis). Circulation 4:816, 1951. 4. Heuer GJ, Stewart HJ: The surgical treatment of chronic constrictive pericarditis. Surg Gynecol Obstet 66:979, 1939. Viola AR: The influence of pericardectomy on the hemody5. Fig. 3. 2DE recorded immediately after pericardiocentenamics of chronic constrictive pericarditis. Circulation sis in patient No. 6. A, End-diastolic frame recorded at 48:1038,1973. ECG position A in the rhythm strip. The right ventricle is 6. Manyari DE, Kostuk WJ, Purves P: Effect of pericardiocenmarkedly dilated. The normal circular geometry of the left tesis-on right and left ventricular function and volumes in ventricle has been distorted; there is marked “flattening” nericardial effusion. Am J Cardiol 52:159, 1983. of the interventricular septum at end diastole (arrow7. Armstrong WF, Schilt BF, Helper DJ, Dillon JC, Feigenbaum H: Diastolic collapse of the right ventricle with cardiac heads). B, Early systole as timed from the ECG. The tamponade: An echocardiographic study. Circulation septal geometry has returned to normal and the septum 65:1491, 1982. has moved anteriorly (arrowheads) as the left ventricle 8. Diamond MA, Dillon JC, Haine CL, Chang S, Feigenbaum H: assumesa normal circular configuration. Echocardiographic features of atrial septal defect.. Circulation 43:129, 1971. 9. Weyman AE, Warm S, Feigenbaum H, Dillon JC: Mechanism of abnormal septal motion in patients with right ventricular of a constrictive component to the pericardial disease.‘1s12 volume overload. Circulation 54:179, 1976. Although a component of pericardial constriction cannot 10. Reddy PS, Curtiss EI, O’Toole JD, Shaver JA: Cardiac be fully excluded in our patients, the apparent gradual tamponade: Hemodynamic observations in man. Circulation return to normal of pressuresand, in oneinstance (patient 56:265, 1978. No. 5), the absenceof pericardial thickening at the time of 11. Kerber RE, Gascho JA, Litchfield R, Wolfson P, Ott D,
June,
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American
PandianNG: Hemodynamic effectsof volumeexpansionand nitroprussidecomparedwith pericardiocentesis in patients with acute cardiac tamponade.N Engl J Med 307:929, 1982. 12. Hancock EW: Subacuteeffusive-constrictivepericarditis. Circulation43:183,1971. 13. GibsonTC, Grossman W, McLaurin LP, MoosS,CraigE: An echocardiographic study of the interventricular septumin constrictivepericarditis.Br Heart J 38~738,1976.
Contrast echocardiographic documentation of paradoxical
embolism
David M. Rodgers, M.D., Surender Singh, M.D., and Steven G. Meister, M.D. Philadelphia, Pa.
Paradoxical thromboembolism is an uncommon disorder in which a venousthrombus crossesan intracardiac defect and causesan arterial embolism. The mortality is very high, and the diagnosisis most often made at autopsy.’ Diagnosisduring life requires a high index of suspicion, and may be life-saving. We report the diagnosisof paradoxicd embolism during life by the use of contrast two-dimensional echocardiography (2DE). A 78-year-old woman was in good health until 2 days prior to admission,when shedeveloped acute dyspnea. On the night prior to admission she experienced the acute onset of slurred speech and right-sided weakness.This From the Medical College Division of Cardiology: and Reprint requests: 31, Philadelphia,
of Pennsylvania Chestnut Hill
David M. Rodgers, PA 19118.
M.D.,
Department Hospital. 8815
Germantown
of Medicine, Ave.,
Suite
Heart
1984 Journal
persisted, and shewasbrought to the emergencyroom by her family. Physical examination revealed a heart rate of 136 bpm, respiratory rate 40/min, and blood pressure 100/80 mm Hg. The temperature was normal. The neck veins were distended. The lung fields were clear to auscultation. Cardiac examination was normal. There wastrace ankle edema. Neurologic examination revealed aphasia and right hemiparesis.ECG was normal except for sinus tachycardia. Chest roentgenogram revealed an uncoiled aorta. The pulmonary vasculature was normal, and there were no pulmonary infiltrates. Arterial oxygen saturation on room air was 68% and rose to only 81% while the patient was breathing 80% oxygen by face mask. Lung scan revealed multiple segmental perfusion defects. A diagnosis of acute pulmonary embolism was made and paradoxical cerebral embolismwas suspected.Accordingly, the patient was started on intravenous heparin. 2DE examination (Varian 3000) revealed an enlarged right ventricle and right atrium, reversed septal motion, and a normal left ventricle. Saline injection into a brachial vein confirmed the presenceof a right-to-left intracardiac shunt*,” (Fig. 1). Inferior vena cava ligation was advised, but was refused by the patient’s family. On the third hospital day, repeat ECG revealed acute anterior myocardial infarction. Right heart catheterization and pulmonary arteriography were performed on the fourth hospital day. A patent foramen ovale was crossedand revealed mean left atria1 pressureof 19 mm Hg. The mean right atria1 pressure was 16 mm Hg, right ventricular pressure was 60/22 mm Hg, and pulmonary artery pressurewas 60/30 mm Hg. Oximetry and indicator dye dilution curves revealed no intracardiac shunt. Pulmonary cineangiography demonstrated filling defects in both main pulmonary arteries and their branches, confirming the lung scan diagnosisof multiple pulmonary emboli. Repeat 2DE now
Fig. 1. A, Apical four-chamber view showingan enlarged right ventricle (RV) and right atrium (RA). B, After saline injection. There is dropout on the stop frame, but saline bubbles are evident in the left ventricle (LV), indicated by the arrow. LA = left atrium.
1266
4.
5.
6.
I.
8.
9.
10.
11.
Communications
American
Bruce RA: Exercise testing of patients with coronary heart disease. Principles and normal standards for evaluation. Ann Clin Res 3:323, 1971. Dunn RF, Freedman B, Bailey IK, Bernstein L, Kelly DT: Exercise thallium imaging: Location of perfusion abnormalities in single vessel coronary disease. J Nucl Med 21:717, 1980. McLaughlin PR, Martin R, Doherty P, Daspit S, Gloris M, Haskell W, Lewis S, Kriss JP, Harrison DC: Reproducibility of thallium-201 myocardial imaging. Circulation 55:497, 1977. Thadani U, West RO, Mathew TM, Parker JO: Hemodynamits at rest and during supine and sitting bicycle exercise in patients with coronary artery disease. Am J Cardiol 39:776, 1977. Levey M, Rozanski A, Valovis R, Ford D, Morris D, Pantaleo N, Maddahi J, Swan HJC, Berman D: Comparative ability of upright and supine bicycle exercise electrocardiography to detect coronary artery disease (abstr). Am J Cardiol 49:945, 1982. Currie P, Kelly M, Pitt A: Is it valid to compare the sensitivity of a supine exercise nuclear imaging procedure with that of an erect exercise ECG (abstr)? Aust NZ J Med 12:668, 1982. Freeman MR, Berman DS, Staniloff H, Elkayam U, Maddahi J, Swan HJC, Forrester J: Comparison of upright and supine bicycle exercise in the detection and evaluation of extent of coronary artery disease by equilibrium radionuclide ventriculography. AM HEART J 102:182, 1981. Manyari DE, Kostuk WJ, Purves PP: Left and right ventricular function at rest and during bicycle exercise in the supine and sitting positions in normal subjects and patients with coronary artery disease: Assessment by radionuclide ventriculography. Am J Cardiol 51:36, 1983.
Acute right ventricular dilation and echocardiographic volume overload following pericardiocentesis for relief of cardiac tamponade William F. Armstrong, M.D., Harvey Feigenbaum, M.D., and JamesC. Dillon, M.D. Indianapolis, Znd.
June, 1984 Heart Journal
Recently, this phenomenonhas been noted with radionuelide angiographyP We report here the finding of acute right ventricular (RV) dilation and development of an echocardiographicRV volume overload pattern in three of six patients after removal of pericardial fluid for relief of cardiac tamponade. Exemplary cases. A 13-year-old white boy (patient No. 5, Table I) wasadmitted to the hospital with a diagnosisof germinal cell tumor. On admission,he was in mild respiratory distress. Heart rate was 130 bpm and blood pressure was 60/50 mm Hg with a palpable paradox. Two-
dimensional echocardiography @DE) revealed a large pericardial effusion with RV collapsesuggestinghemodynamic compromise.7Pericardiocentesis was performed, and 1400ml of serosanguineous fluid wasremoved. Immediately after pericardiocentesis, 2DE was repeated. The right ventricle was markedly dilated and interventricular septal motion was consistent with a RV volume overload pattern. Following pericardiocentesis,heart rate remained elevated at 140 bpm; blood pressurewas 90/70 mm Hg without paradox. Marked jugular venous distention persisted and a RV gallop was noted. Right heart catheterization revealed equalization of diastolic pressures at 40 mm
Hg. Repeat pericardiocentesis was performed and an additional 700 ml fluid was removed. The clinical picture of jugular venous distention with right heart gallop persisted.On the fifth hospital day, the patient wastaken to the operating room where a pericardial window was created. The resected pericardium was noted to be inflamed but wasnot thickened. The patient experienced gradual resolution of symptoms and evidence of venous congestionresolved. He was dischargedfollowing therapy of the malignancy. A 26-year-old white woman (patient No. 6, Table I) was admitted to the hospital in marked respiratory distress. Past medical history wassignificant for Hodgkins disease treated 11 years previously with chemotherapy and mediastinal radiation. She had no history of cardiovascular diseaseand had previously had multiple normal cardiovascular examinations. At the time of admission, the patient was an acutely ill and cachetic white woman.
The normal pericardium exerts a restraining influence on the size of the cardiac chambers.’ Dilation of the right ventricle has been reported after surgical removal of the pericardium for treatment of constrictive pericarditis and in cases of congenital absence of the pericardium.2-5
Blood pressurewas 70/50 mm Hg and heart rate was 120 bpm. An echocardiogram demonstrated the presence of moderate pericardial effusion with abnormal RV free wall motion suggestinghemodynamic compromise(Fig. 1).7A flow-directed right heart catheter documented elevation and equilibration of diastolic pressuresconsistent with cardiac tamponade. Pericardiocentesiswas performed, at which time 200 ml of serosanguineous
From Indiana
the Krannert University
Institute of Cardiology, School of Medicine.
Department
of Medicine,
Supported in part by the Herman C. Krannert Fund, Indianapolis, Ind., Grants HL-06308 and HL-07182, and by Clinical Investigator Award HL 01041-02 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.; by the American Heart Association, Indiana Affiliate, Indianapolis, Ind.; and by the Whitaker Foundation, Camp Hill, Pa. Reprint requests: William F. Armstrong, of Medicine, University Hospital N562,926 IN 46223.
M.D., Indiana W. Michigan
University School St., Indianapolis,
fluid was removed.
The systolic blood pressuresubsequently rose to 120 mm Hg; however, right heart pressuresremained elevated. Repeat M-mode and 2DE, performed immediately after pericardiocentesis, revealed increase in RV dimension from 1.2 cm to 2.6 cm. Left ventricular internal dimension decreasedfrom 3.8 cm to 3.1 cm. Interventricular septal motion becameabnormal, demonstrating the characteristic early systolic anterior motion of the interventricular septum, seen in RV volume overload (Fig. 2). 2DE revealed a markedly dilated right ventricle, with diastolic
Volume Number
107 6
Brief Communications
1267
Fig. 1. M-mode echocardiogram from patient No. 6 at time of diagnosis of cardiac tamponade. There is moderate anterior and posterior pericardial effusion (PE). Right ventricular (RV) dimension is 1.1 cm and (LV) is 3.8 cm. Immediately after onset of electrical systole (arrow), the left ventricular dimension interventricular septum moves posteriorly. This is the normal motion pattern of the interventricular septum.
“flattening” of the interventricular septum, also consistent with RV volume overload (Fig. 3). The records, from January, 1981, to December, 1982, of the echocardiographic laboratory at the Indiana University Hospital were reviewed to identify patients who had undergone pericardiocentesis for relief of cardiac tamponade and who had been studied with either M-mode or 2DE within 24 hours of pericardiocentesis. Clinical records were reviewed to insure accuracy of the diagnosis of cardiac tamponade and to obtain information for clinical correlation. All M-mode and 2DEs were reviewed by two experienced echocardiographers. RV volume overload was defined on M-mode echocardiography aa dilation of the RV cavity in diastole (>2.3 cm), in association with abnormal motion of the interventricular septmng The abnormal motion had to consist of brisk anterior motion of the interventricular septum immediately after onset of electrical systole, associated with appropriate thickening of the interventricular septum. On 2DE, RV volume overload was defined as the combination of subjective dilation of the right ventricle in association with the characteristic “flattening” of the interventricular septum throughout diastole, and restitution of normal, circular left ventricular geometry with onset of systole? Including the two index cases, six patients were identified who met the study criteria. Five of the six patients
Table
I. Clinical
Patient
Age
and echographic Etiology
M-Breast
1 2 3 4 5*
65 21 32 26 13
Histo M-Germ cell M-Brea$t M-Testicular
6*
26
Radiation
features
Amount of fluid (ml)
800
Type
Echo
RVVO
300 1100 900 1400
2D, MM 2D, MM7 2D, MM? 2Dt MM? 2Dt
++ + +
200
MM? 2Dt
+
Histo = histoplasmosis; M = malignancy; MM = M-mode echocardiography; 2D = two-dimensional echocardiography; Amount fluid = volume of fluid removed at the time of pericardiocentesis; RVVO = right ventricular volume overload. *Index case. tStudy showing evidence of right ventricular volume overload.
had been examined personally by one of the authors. Both M-mode and 2DE were performed in five; one patient had only 2DE performed after pericardiocentesis. The salient demographic data are presented in Table I. At the time of pericardiocentesis, all patients had clinical evidence of cardiac tamponade with jugular venous distention, hypotension, and pulsus paradoxus. Three patients underwent flow-directed right heart catheterization, and in each the findings were characteristic of cardiac tamponade. Follow-
1268
Brief
Communication-s
June, 1984 Heart Journal
American
---?t”
v”’
‘i
“V
V
9-9-82
Fig. 2. Patient No. 6. M-mode echocardiogram recorded after removal of 200 ml of fluid from the pericardium. Motion of the interventricular septum (IVS) is now markedly abnormal. After onset of electrical systole (arrow), the IVS moves briskly anteriorly. This is the characteristic motion seenin RV volume overload. Additionally, RV internal dimension has increasedto 2.6 cm.
ing pericardiocentesis, marked symptomatic relief was experienced by five of the six patients. Patient No. 6 achieved only minimal relief after pericardiocentesisand subsequently died of respiratory insufficiency from uncontrolled pneumonia. Clinically, no patient had evidenceof either an atrial septal defect or tricuspid regurgitation. Definite echocardiographicevidence of RV volume overload, with RV dilation and abnormal septal motion, was seen in three patients. Two other patients had equivocal evidence of RV volume overload. Both of these patients had serial dilation of the right ventricle; however, the abnormality of septal motion was nonspecific, with only minimal anterior motion at the onset of systole. This variant of abnormal septal motion has been described previously in patients with congenital absence of the pericardium or following pericardectomy.2 Comments. The pericardium exerts a restraining influenceon cardiac chamberswith respect to both geometry and potential for dilation.’ Dilation of cardiac chambers hasbeennoted after pericardectomy, where dilation of the right and/or left ventricle has been recognizedat the time of surgery3,4or noted postoperatively with echocardiography.2 Additionally, the rare finding of congenital absence of the pericardium is characterized echocardiographically by a dilated right ventricle and abnormal septal motion as
is seenin RV volume overload.2Excessivecardiac motion and unconventional orientation of the echo beam have been offered as an explanation. The use of 2DE in our study should negate both of these effects Although systolic anterior septal motion on M-mode echocardiography could be an artifact of cardiac motion, the septal flattening seen with 2DE cannot be explained as such. Becauseof the short-term nature of this study, we are unable to state the duration of this effect. In one patient, the RV volume overload pattern had only partially resolved 3 days after pericardiocentesis.That the acute right heart dilation is more than an incidental finding is suggestedby patient No. 5, in whom clinical evidence of right heart failure, including jugular venous distention, RV gallop, and persistent elevation of right heart pressures, was noted. The slow resolution of elevated right heart pressures suggests a component of RV failure prompted by acute dilation. A delay in normalization of pressuresis well described after surgical pericardectomy and has beenpresumedto he secondary to delay in return of normal myocardial function due to atrophy produced by long-standing constrictive process.3.5The failure of right heart pressuresto normalize promptly after pericardiocentesisalso has been previously recognized.‘” I1 This phenomenonpreviously hasbeen ascribedto the presence
Volume Number
107 6
Brief Communications 1269 creation of a pericardial window are against this mechanism. Additionally, the echocardiographicwall motion was purely that of RV volume overload and not that of pericardial constriction.‘3 In a recent report of RV volumesand function studied with radionuclide techniques, dilation of the right ventricle was noted after therapeutic pericardiocentesis.Furthermore, in this study RV ejection fraction decreasedor failed to increaseappropriately after removal of pericardial fluid. This is consistent with the presenceof a component of RV failure.6 To our knowledge, the casespresented in this brief report constitute the only description of pathologic RV volume overload occurring in the setting of an intact pericardium following pericardiocentesis.We hypothesize that in a patient with cardiac tamponade,the combination of the pericardium and the contained fluid exerts a restraining effect on chamber sizes. After removal of pericardial fluid, the effective intrapericardial volume is increasedin relation to the cardiac volume, thus allowing dilation of the most distensible cardiac chamber, the right ventricle. In effect, removing a large volume of pericardial fluid has the sameeffect as actual removal of the pericardium. In conclusion, we have reported three instancesof right heart dilation and development of a pathologic RV volume overload pattern echocardiographically in patients following pericardiocentesisfor relief of cardiac tamponade. Two further patients had equivocal evidence of RV volume overload. Only one patient, in our series of six studied immediately after pericardiocentesis,did not have someevidence of acute RV dilation and abnormal septal motion. REFERENCES
1. Shahetai R, Mangiardi L, Bhargava V, Ross J, Higgins CB: The pericardium and cardiac function. Prog Cardiovasc Dis 22:107, 1979. 2. Payvandi MN, Kerber RE: Echocardiography in congenital and acquired absence of the pericardium: An echocardiographic mimic of right ventricular volume overload. Circulation 53:86, 1976. 3. Chambliss JR, Jaruszewski EJ, Brofman BL, Martin JF, Feil H: Chronic cardiac compression (chronic constrictive pericarditis). Circulation 4:816, 1951. 4. Heuer GJ, Stewart HJ: The surgical treatment of chronic constrictive pericarditis. Surg Gynecol Obstet 66:979, 1939. Viola AR: The influence of pericardectomy on the hemody5. Fig. 3. 2DE recorded immediately after pericardiocentenamics of chronic constrictive pericarditis. Circulation sis in patient No. 6. A, End-diastolic frame recorded at 48:1038,1973. ECG position A in the rhythm strip. The right ventricle is 6. Manyari DE, Kostuk WJ, Purves P: Effect of pericardiocenmarkedly dilated. The normal circular geometry of the left tesis-on right and left ventricular function and volumes in ventricle has been distorted; there is marked “flattening” nericardial effusion. Am J Cardiol 52:159, 1983. of the interventricular septum at end diastole (arrow7. Armstrong WF, Schilt BF, Helper DJ, Dillon JC, Feigenbaum H: Diastolic collapse of the right ventricle with cardiac heads). B, Early systole as timed from the ECG. The tamponade: An echocardiographic study. Circulation septal geometry has returned to normal and the septum 65:1491, 1982. has moved anteriorly (arrowheads) as the left ventricle 8. Diamond MA, Dillon JC, Haine CL, Chang S, Feigenbaum H: assumesa normal circular configuration. Echocardiographic features of atrial septal defect.. Circulation 43:129, 1971. 9. Weyman AE, Warm S, Feigenbaum H, Dillon JC: Mechanism of abnormal septal motion in patients with right ventricular of a constrictive component to the pericardial disease.‘1s12 volume overload. Circulation 54:179, 1976. Although a component of pericardial constriction cannot 10. Reddy PS, Curtiss EI, O’Toole JD, Shaver JA: Cardiac be fully excluded in our patients, the apparent gradual tamponade: Hemodynamic observations in man. Circulation return to normal of pressuresand, in oneinstance (patient 56:265, 1978. No. 5), the absenceof pericardial thickening at the time of 11. Kerber RE, Gascho JA, Litchfield R, Wolfson P, Ott D,
June,
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American
PandianNG: Hemodynamic effectsof volumeexpansionand nitroprussidecomparedwith pericardiocentesis in patients with acute cardiac tamponade.N Engl J Med 307:929, 1982. 12. Hancock EW: Subacuteeffusive-constrictivepericarditis. Circulation43:183,1971. 13. GibsonTC, Grossman W, McLaurin LP, MoosS,CraigE: An echocardiographic study of the interventricular septumin constrictivepericarditis.Br Heart J 38~738,1976.
Contrast echocardiographic documentation of paradoxical
embolism
David M. Rodgers, M.D., Surender Singh, M.D., and Steven G. Meister, M.D. Philadelphia, Pa.
Paradoxical thromboembolism is an uncommon disorder in which a venousthrombus crossesan intracardiac defect and causesan arterial embolism. The mortality is very high, and the diagnosisis most often made at autopsy.’ Diagnosisduring life requires a high index of suspicion, and may be life-saving. We report the diagnosisof paradoxicd embolism during life by the use of contrast two-dimensional echocardiography (2DE). A 78-year-old woman was in good health until 2 days prior to admission,when shedeveloped acute dyspnea. On the night prior to admission she experienced the acute onset of slurred speech and right-sided weakness.This From the Medical College Division of Cardiology: and Reprint requests: 31, Philadelphia,
of Pennsylvania Chestnut Hill
David M. Rodgers, PA 19118.
M.D.,
Department Hospital. 8815
Germantown
of Medicine, Ave.,
Suite
Heart
1984 Journal
persisted, and shewasbrought to the emergencyroom by her family. Physical examination revealed a heart rate of 136 bpm, respiratory rate 40/min, and blood pressure 100/80 mm Hg. The temperature was normal. The neck veins were distended. The lung fields were clear to auscultation. Cardiac examination was normal. There wastrace ankle edema. Neurologic examination revealed aphasia and right hemiparesis.ECG was normal except for sinus tachycardia. Chest roentgenogram revealed an uncoiled aorta. The pulmonary vasculature was normal, and there were no pulmonary infiltrates. Arterial oxygen saturation on room air was 68% and rose to only 81% while the patient was breathing 80% oxygen by face mask. Lung scan revealed multiple segmental perfusion defects. A diagnosis of acute pulmonary embolism was made and paradoxical cerebral embolismwas suspected.Accordingly, the patient was started on intravenous heparin. 2DE examination (Varian 3000) revealed an enlarged right ventricle and right atrium, reversed septal motion, and a normal left ventricle. Saline injection into a brachial vein confirmed the presenceof a right-to-left intracardiac shunt*,” (Fig. 1). Inferior vena cava ligation was advised, but was refused by the patient’s family. On the third hospital day, repeat ECG revealed acute anterior myocardial infarction. Right heart catheterization and pulmonary arteriography were performed on the fourth hospital day. A patent foramen ovale was crossedand revealed mean left atria1 pressureof 19 mm Hg. The mean right atria1 pressure was 16 mm Hg, right ventricular pressure was 60/22 mm Hg, and pulmonary artery pressurewas 60/30 mm Hg. Oximetry and indicator dye dilution curves revealed no intracardiac shunt. Pulmonary cineangiography demonstrated filling defects in both main pulmonary arteries and their branches, confirming the lung scan diagnosisof multiple pulmonary emboli. Repeat 2DE now
Fig. 1. A, Apical four-chamber view showingan enlarged right ventricle (RV) and right atrium (RA). B, After saline injection. There is dropout on the stop frame, but saline bubbles are evident in the left ventricle (LV), indicated by the arrow. LA = left atrium.