MARCH 1979
The American
Journal
of CARDIOLOGY” VOLUME NUMBER
43 3
CLINICAL STUDIES
Right Ventricular Infarction Clinical Diagnosis and Differentiation From Cardiac Tamponade and Pericardial Constriction
BEVERLY LORELL, MD ROBERT C. LEINBACH, MD, FACC GERALD M. POHOST, MD, FACC HERMAN K. GOLD, MD, FACC ROBERT E. DINSMdRE, MD, FACC ADOLPH M. HUTTER, Jr., MD, FACC JOHN 0. PASTORE, MD, FACC ROMAN W. DESANCTIS, MD, FACC Boston, Massachusetts
From the Department of Medicine, Massachusetts General Hospital (Cardiac Unit), and Harvard Medical School, Boston, Massachusetts. This study was supported in part by Grant HL-17665 from the U. S. Public Health Service, Bethesda, Maryland. Manuscript received May 2, 1978; revised manuscript received October 20, 1978, accepted October 25, 1978. Ad&ess for reprints: Roman W. DeSanctis, MD, Cardiac Unit, Massachusetts General Hospital, Soston, Massachusetts 021 14.
Twelve patients with a clinical diagnosis of right ventricular infarction are described. All had acute inferior wall myocardial infarction associated with the bedside-findings of jugular venous distension, clear lungs on auscultatlon, and arterial hypotension. Hemodynamically, there was elevation of right-sided filling pressures not explained by normal or minimally elevated pulmonary wedge pressures. Four patients had an incorrect diagnosis of acute cardiac tamponade. However, a review of the data showed that the hemodynamic features of right ventricular infarction more closely resemble those of pericardial constriction, a point that may be helpful in distinguishing right ventricular infarction from cardiac tamponade. Invasive and noninvasive techniques that exclude the presence of pericardial fluid and suggest enlargement and abnormal contractility of the right ventricle were helpful in establishing the diagnosis of right ventricular infarction in several patients.
Right ventricular infarction should be suspected when there is evidence of right ventricular dysfunction in the setting of acute inferior myocardial infarction.lp2 Clinically significant right ventricular infarction is characterized by an elevated systemic venous pressure, clear lungs and, frequently, arterial hypotension. Hemodynamically, right ventricular filling pressures are equal to or greater than those of the left ventricle.3y4 Recent studies utilizing data from hemodynamic measurements and cardiac radionuclide imaging suggest that right ventricular damage may be present in as many as 19 to 43 percent of patients with acute inferior myocardial infarction.5-s However, right ventricular infarction is still often unrecognized and, as indicated in this report, may be misdiagnosed as acute cardiac tamponade. In this paper we describe 12 patients with the clinical diagnosis of right ventricular infarction seen at the Massachusetts General Hospital between January 1971 and September 1977. Four of the 12 were erroneously thought to have acute cardiac tamponade. Our report particularly emphasizes the clinical diagnosis of right ventricular infarction and its differentiation from acute cardiac tamponade.
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465
RIGHT VENTRICULAR
INFARCTION-LORELL
ET AL.
TABLE I Clinical and Hemodynamic Characteristics of 12 Patients With Suspected dight Ventricular Infarction Pressor Agents*
Pressures PA
Case
Age (yr)
no.
& Sex
ECG
BP
1
55M
f 5”
1:; %!
IMI lPMl IPMI IMI IPMI
98150 75150 90160 92/60 90/60
Yes Yes No Yes No
12 :z
--/12 215
33/14 24/17 20/a -112 -/15
6 s’
61M 64M
IMI IMI
70140 loo/75 100/80
Yes Yes
::
30115 25/16
63M 54M 69F
IMI IPMI IPMI IPMI
No ES Yes No Yes
::
53F
82146 96172 78/50 110150 i 04180
28/14 1 2817 -
am
1: ::;: 12
RA
RV
::
33/12 24/;7
:; 1:
PCW
PVR
Cl
::
1.0 1.5
8 :;
184 112 118 I
23/11 25115 25/16
:;
28115 -/a 25/4 30112
::: 1.9
Discharged Died Discharged Discharged Died
-
2.9 -
Discharged Discharged Died
::9
76 -
lir
< 13
1% 136
& 2.0
Discharged Discharge& chronic right ventricular failure Discharged
15
* Infusion of pressor agents during hemodynamic measurements. + Patient 11 was restudied by right heart catheterization 7 days after infarction. BP = blood pressure (mm Hg); Cl = cardiac index (liters/min per m*); ECG = electrocardiogram; IMI = inferior myocardial infarction; IPMI = inferoposterior myocardial infarction; PA = pulmonary arterial pressure (mm Hg); PCW = pulmonary capillary wedge pressure (mm Hg); PVR = pulmonary vascular resistance (dynes set cms5); RA = mean right atrial pressure (mm Hg); RV = right ventricular pressure (mm Hg).
Methods Patients: The records of 306 patients with electrocardiographic evidence of acute inferior or inferoposterior infarction admitted to the Myocardial Research and Ischemic SCOR units between January 1971 and September 1977 were retrospectively reviewed. The following criteria were used to identify patients with suspected right ventricular infarction: (1) acute inferior or inferoposterior infarction on electrocardiography; (2) jugular venous pressure estimated or measured to be higher than 10 cm HzO; (3) clear lungs on auscultation; and (4) absence of interstitial pulmonary edema or infiltrates on chest X-ray films. We recognized that elevation of pulmonary wedge pressure precedes the appearance of abnormal chest X-ray film findings. Therefore, we also required documentation of right heart filling pressures greater than or within 2 mm Hg of the pulmonary wedge pressure. No patient was included who had a history of lung,disease or clinical or electrocardiographic evidence of chronic car pulmonale. Of the 306 patients, 8 met the defined criti& for right ventricular infarction. Four patients who were seen in con-
TABLE II Characteristics of Seven Patients With Equalization of EndDiastolic Pressures
Case no.
Pulsus Paradoxus’ (mm Hg)
Kussmaul’s Sign+
1
25
Yes
: 5 :
20 10 14 No No 12-15
zl Yes No
9
z,o
RVEDP DipPlateauf:
Tamponade Syspected§
Yes Yes No Yes No Yes Yes
Yes Yes No Yes NO ves No
Results Clinical Features
* lnspiratory fall in systolic arterial pressure recorded by indwelling arterial catheter. + lnspiratory rise in mean right atrial pressure. t Abnormal early diastolic dip and plateau configuration of the right ventricular pressure tracing. 5 Initial incorrect diagnosis of cardiac tamponade. RVEDP = right ventricular end-diastolic pressure.
466
March 1979
The American Journal of CARDIOLOGY
sultation by physicians on the cardiac service and who met the criteria for right ventricular infarction were added to the group. Diagnostic procedures: Right-sided filling pressures were measured using flow-directed balloon catheters in all 12 patients. Left ventricular filling pressures were determined from the pulmonary wedge pressure; the left ventricular end-diastolic pressure was also measured in three patients. Pressure tracings were recorded using either Hewlett-Packard transducers and recorders, or Gould multichannel Brush ink recoiders. Cardiac output was determined using the Fick method in three cases and the thermodilution method in the others. In three cases, coronary arteriography was performed with the Sones technique. Cineangiography was performed in three cases by injection of contrast medium into the right atrium. Echocardiograms in four cases were obtained with an SKI 2OH echograph and Honeywell strip recorder, using the technique and range of normal values of cavity dimensions described by FeigenbaGm and Chang.g Multiple gated blood pool imaging performed in three patients utilized a Searle Pho Gamma III camera and the MGH Numedics computer system, or an Ohio Nuclear’Series 400 gamma camera and an MDS PAD computer system. Right heart chamber size and contactility were assessed relative to that of the left ventricle by two experienced obsepvers. The right atrium and ventricle were judged as “markedly dilated,” “mildly dilated” or “normal,” and their contractility was scored as “akinetic,” “ markedly hypokinetic” or “normal.” The two observers agreed in all cases on scoring of size and contractility. The swe scoring system was used to assess the right atria1 cineangiograms.
History and symptoms: The clinical and hemodynamic findings of the 12 patients with suspected right ventricular infarction are shown in Table I; there were 8 men and 4 women, whose ages ranged from 53 to 87 years. Three patients had a history of prior heart disease. Oue patient had chronic angina, one patient (Case
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RIGHT VENTRICULAR INFARCTION-LORELL ET AL.
11) had a history of partial pericardiectomy for cardiac tamponade 15 years before infarction and one patient had a previous inferior myocardial infarction. The presenting complaint was typical crushing chest pain in 10 patients, and nausea with diaphoresis in 2. Four patients had collapsed at home and required emergency resuscitation. No patient had a history of chronic lung disease that could have contributed to right ventricular dysfunction. Clinical findings:: The interval between electrocardiographic diagnosis of acute inferior infarction and hemodynamic evaluation ranged from 2 to 72 hours. All patients were described as appearing severely ill. All patients were initially hypotensive (systolic pressure less than 100 mm Hg) and oliguric with urinary output of less than 30 ml/hour, and all had cool mottled limbs. Four patients were mentally obtunded. Pericarditis, evident as a pericardial friction rub, was noted in 11 patients. With the exception of Case 11, chest X-ray films showed no cardiac enlargement or pulmonary edema. The initial rhythm was normal sinus in seven patients, sinus bradycerdia in one patient, Wenckebach atrioventricular (A-V) block in one, and complete A-V block in three patients.
KUSSMAUl’S SIGN AND PULSUS PARADOXUS
ECG
RACYAL ARTERY
mmfig
RIGHT
ATRfUlW mm Hg
FIGURE 1. Case 2. Simultaneous radial arterial and right atrial pressure tracings demonstrating pulsus paradoxus and Kussmaul’s sign in a patient initially thought to have cardiac tamponade. The phasic fall in systemic arterial pressure that occurred during inspiration corresponds with a.phasic rise in right atrial pressure during inspiration. ECG = electrocardiogram.
ECG
FIGURE 2. Case 9. The right atrial and right ventricular pulse tracings were sequentially recorded, and the pulmonary arterial tracing was recorded after a short delay. The right atrial pressure is elevated, and the wave form shows an X’ and prominent Y descent. There is an early diastolic dip-plateau configuration of the right ventricular pressure tracing. The pulmonary arterial systolic pressure is not elevated, and the right ventricular pulse pressure is narrow, suggesting poor systolic function of the right ventricle. ECG = electrocardiogram.
--l-T-r-200 mmffg 400
Radial Artery -JLb-J-ku
0 40
mmHg
Right Atri’f Pressure
Ri@htVefltrkufarPressure
20
FIGURE 3. Acute cardiac tamponade without right ventricular infarction (compare with Fig. 2). As in Figure 2, the right atrial (RAP) and right ventricular pressure @VP) tracings were sequentially recorded. The right atrial pressure is elevated, but the right atrial wave form is relatively flat and the Y descent is nearly obliterated. Note that a steep early diastolic dip-plateau configuration is not present in the right ventricular pulse tracing. ECG = electrocardiogram; PAP = pulmonary arterial pressure.
mm Hg
20
~ 1
JfMJLl
OL
March 1979
The American Journal of CARDIOLOGY
Volume 43
467
RIGHT VENTRICULAR INFARCTION-LORELL
RW(
ET AL.
..~.l......l.l..~l....‘~.
FIGURE 4. Case 9. Echocardiographic study of the right (RV) and left ventricles (LV) just below the level of the free edge of the mitral valve leaflets. The right ventricle is enlarged. The interventricularseptum (IVS) thickens poorly in systole, and it appears to move paradoxically away from the left ventricle in systole. There is no evidence of a pericardial effusion. CW = chest wall; ECG = electrocardiogram; LVPW = left ventricular posterior wall.
Hemodynamic data: To clarify the etiology of the bedside findings of right-sided heart failure, right heart catheterization was performed. The right atrial pressure in the 12 patients ranged from 11 to 18 (average 14) mm Hg, and the right ventricular diastolic pressure, measured in 7 patients, ranged from 12 to 17 (average 14) mm Hg. Right ventricular systolic pressures varied from 24 to 33 (average 28) mm Hg. The pulmonary arterial systolic pressures ranged from 20 to 33 (average 26) mm Hg. The pulmonary wedge pressures ranged from 8 to 16 (average 12) mm Hg. The pulmonary vascular resistance could be calculated in six patients, and ranged from 15 to 136 (average 108) dynes set cme5. In each of the three patients (Cases 4,6 and 9) studied with coronary arteriography the right coronary artery was completely occluded; in addition, Patient 4 had 90 percent diameter narrowing of the left main coronary artery and Patient 9 had a 60 percent luminal narrowing of the left circumflex artery. Seven patients had equilibration of the right atrial, pulmonary diastolic and pulmonary wedge pressures suggesting pericardial disease (Table II). In this subgroup, radial artery monitoring showed pulsus
paradoxus greater than 10 mm Hg in five patients. Two of the seven patients had an abnormal inspiratory rise in mean right atrial pressure (Kussmaul’s sign) (Fig. 1). Although pressure tracing contours may be difficult to assess because of “overshoot” in the absence of high fidelity micromanometer catheters, we observed that five of the seven patients had a right ventricular tracing with a striking early diastolic dip and plateau configuration and a right atria1 tracing with a steep Y descent (Fig. 2 and 3). Echocardiography: Additional. studies were performed in several patients to evaluate further the right ventricle and exclude the presence of pericardial fluid. Echocardiograms (obtained in Cases 5, 8, 9 and 11) showed no pericardial effusion, but in each of the four cases showed right ventricular end-diastolic cavity enlargement, defined in this laboratory as greater than 14 mm/m2 (Fig. 4). In two studies, poor systolic septal thickening and abnormal systolic anterior septal motion were recorded. Multiple gated blood pool imaging: This procedure, performed in Cases 9,10 and 11, showed in each study marked dilatation of the right ventricle relative to the left ventricle, and akinesia or marked hypokinesia of the body of the right ventricle (Fig. 5). The right ventricular apex also appeared markedly hypokinetic in two studies. The right atrium was only mildly dilated in one study, but in the other two appeared markedly dilated and hypokinetic. Each study showed paradoxjcal systolic motion of the septum away from the left ventricle. The left ventricular inferior and inferoapical walls appeared mildly or markedly hypokinetic in the studies. The left ventricular ejection fraction was greater than 50 percent in each imaging study. Right atria1 cineangiography: Marked right ventricular dilatation relative to left ventricular size was also seen in the right atria1 cineangiograms (Cases 5,8 and 11) (Fig. 6). In each cineangiogram, the body of the right ventricle appeared markedly hypokinetic, and the inferobasal right ventricular wall appeared mildly hypokinetic. In each study, the right atrium appeared markedly enlarged, and in two it appeared severely hypokinetic. Levophase opacification showed left ventricular inferior wall akinesia in two studies, and posterobasal wall akinesia in the other study. Hospital Course
Arrhythmias: Initial serious management problems included disturbances of cardiac rhythm and hypo-
FlGURE 5. Case 9. Left anterior oblique gated cardiac blood pool images in end-systole and enddiastole. The diagram at left shows the location of the cardiac chambers. The right ventricle (RV) is markedly dilated and pborly contractile. By comparison, the left ventricle (LV) has normal size and contractilii. RA = right atrium.
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ET AL
END SYSTOLE
END-DIASTOLE
FIGURE 6. Case 5. End-diastolic (left) and end-systolic (right) frames from a right atrial cineangiogram in a posteroanterior projection performed in a patient initially thought to have cardiac tamponade. The right atrium (RA) and right ventricle (RV) are markedly enlarged. The study demonstrated generalized right ventricular hypokinesia and akinesia of the inferobasaf right ventricular wall. PA = pulmonary artery.
tension. Nine of the 12 patients required temporary demand pacemakers for correction of severe bradycardia or complete A-V block. Five patients required intermit.tent demand pacing for more than 5 days. Atrial fibrillation or flutter occurred in six patients and was treated with digoxin. Lidocaine or procainamide, or both, was given to four patients for frequent premature ventricular beats or ventricular tachycardia. Hypotension: Hypotension was not alleviated by correction of bradycardia alone in any patient. Expansion of the intravascular volume was tried initially in all patients. It successfully corrected hypotension and oliguria in three patients whose fluid intake ranged from 2,500 to 6,300 ml/day for the first 48 hours. Nine patients were also treated with dopamine, isoproterenol or norepinephrine, or combinations of these, and improvement occurred in six of the nine. In three of these patients, intraaortic balloon counterpulsation was used, but its efficacy was difficult to assess because other measures were used simultaneously. However, in Case 9 multiple paired hemodynamic measurements obtained with and without counterpulsation showed that the counterpulsation resulted in the expected decrease in left ventricular filling pressure but did not significantly change the cardiac index or right-sided pressures. Acute cardiac tamponade: This was initially incorrectly diagnosed in four patients on the basis of the bedside findings and the catheterization findings of equilibration of end-diastolic pressures. In three of the four, subxyphoid pericardiocentesis was attempted. Early in our experience, one patient subsequently underwent pericardial exploration performed during cardiopulmonary bypass, for suspected myocardial rupture, but no bleeding point or evidence of rupture
was found. In the other patients, the diagnosis was clarified with echocardiography or right atria1 cineangiography, which excluded the presence of pericardial fluid and showed dilatation and abnormal contractility of the right ventricle. Later in the hospital course, nine patients had evanescent right-sided pleural effusions in the absence of interstitial edema, and two had murmurs of tricuspid insufficiency, an infrequent finding in inferior infarction that may be due to papillary muscle damage or functional regurgitzation.lOJ1 Mortality: Three patients died in the hospital. All had progressive deterioration of cardiac output and experienced terminal ventricular arrhythmias. Autopsy was permitted only in Case 4, and showed fibrinous pericarditis and total occlusion of the right coronary artery with insignificant atherosclerosis of the other coronary arteries. An infarction of 36 to 48 hours’ age involved the right and left posterior ventricular walls, part of the ant,erior right ventricular wall, and the right atrium. Nine patients were discharged from the 14 to 30th hospital day. In one patient (Case 11 with the history of part,ial pericardiectomy) chronic right ventricular failure developed, and one patient died suddenly at home 3 months later.
Discussion Incidence of right ventricular infarction: Myocardial infarction is generally regarded as an ischemic injury of the left ventricle. That the right ventricle can be the site of major damage from acute myocardial infarction has been recognized clinically only recently.S When present, right ventricular infarction is almost invariably associated with inferior infarction because the posterior wall of the right ventricle and the inferior
March1979
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wall of the left ventricle share a common blood supply, usually the right coronary artery.12 In an analysis of 236 necropsy patients with transmural myocardial infarction, Isner and Roberts13 emphasized that right ventricular infarction occurred exclusively in those patients with both transmural posterior (“inferior”) infarction of the left ventricle and infarction of the posterior ventricular septum. Right ventricular infarction was observed in 14 percent of the 236 patients with transmural infarction, occurring in none of the 97 patients with anterior infarction and in 24 percent of the 139 patients with posterior (“inferior”) infarction. This incidence is comparable with that reported in an older necropsy series14 of 2,000 patients with transmural infarction in which right ventricular infarction was associated with left ventricular infarction in 13.8 percent of cases. It appears that the incidence rate of clinically significant right ventricular infarction is considerably lower than the incidence rate found at autopsy. Thus, we recognized only eight cases of right ventricular infarction among 306 patients with acute inferior myocardial infarction, an incidence rate of 2.6 percent. However, this is undoubtedly a minimal incidence in light of the rigid criteria we used for selecting cases. Subtle clinical signs of right ventricular infarction might easily be overlooked at the bedside. Clinical diagnostic features and differentiation from cardiac tamponade and constrictive pericardial disease: Recently Cohn and co-workers3 drew attention to the important features of right ventricular infarction: an elevated systemic venous pressure, the absence of pulmonary edema, and a low cardiac output. Their patients had the hemodynamic findings of elevated right-sided filling pressures and normal or modestly elevated left-sided filling pressures. Our 12 patients exhibited similar clinical and hemodynamic findings. An unusual aspect of our experience was the incorrect diagnosis of cardiac tamponade in four patients, all of whom were seen before the clinical features of right ventricular infarction were appreciated. In the presence of pericarditis, which was noted in 11 of our 12 patients, the constellation of an elevated systemic venous pressure, hypotension, and the occasional occurrence of a paradoxical pulse-all secondary to severe right ventricular dysfunction-could be mistaken for cardiac tamponade. In addition, 7 of our 12 patients had an equilibration of diastolic pressures as measured in the pulmonary wedge position, pulmonary artery, right ventricle and right atrium. However, on carefully reviewing our hemodynamic data in these seven patients, we were struck by the fact that the findings more closely resembled those of constrictive pericardial disease than those of cardiac tamponade. Five of the seven patients had a well preserved and steep right atria1 Y descent, and the right ventricular pressures showed an early diastolic dip and plateau configuration. These findings are much more prevalent in constrictive disease than in cardiac tamponade, where the right atria1 Y descent is usually attenuated or ab-
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sent, and right ventricular pressure tracings rarely show a prominent dip and plateau configuration.15-l7 Kussmaul’s sign-that is, an inspiratory rise in mean right atria1 pressure-was documented in two patients. This finding is sometimes present with constrictive disease but is unusual in cardiac tamponade.lsJg It is possible that the hemodynamic findings in right ventricular infarction that resemble the findings in constrictive disease are indeed manifestations of right ventricular dysfunction combined with the restraining effects of the pericardium. The use of newer noninvasive methods and the occasional application of right atria1 cineangiography
are valuable in the diagnosis of right ventricular infarction because they demonstrate the diminished systolic performance of the right ventricle. Thus, right atria1 cineangiography and multiple gated blood pool imaging permit qualitative assessment of right ventricular size and contractility. The dilated and poorly contracting right-sided chambers observed with these techniques in five of our patients differ strikingly from the small, vigorously contracting chambers seen in both cardiac tamponade and constrictive pericarditis, in which the problem is ordinarily that of limited ventricular filling with unimpaired systolic emptying. Thallium-201 and technetium-99m pyrophosphate scintigraphy are promising methods for detecting right ventricular infarction and may supplement studies that suggest right ventricular dysfunction.8 We also found echocardiography a useful bedside technique in distinguishing between right ventricular
infarction and cardiac tamponade. In tamponade, the presence of pericardial fluid can be demonstrated and, in some patients, the exaggerated inspiratory filling and expiratory compression of the right ventricle associated with tamponade can be detected.20,21 In our four patients with right ventricular infarction studied with echocardiography, right ventricular end-diastolic dimensions were uniformly increased. It is not clear to us whether the abnormal septal motion detected by both the echocardiographic and imaging studies was due to ischemic septal damage or to dilatation of the right ventricle. Differentiation from pulmonary embolism: In addition to differentiation from acute cardiac tamponade, the differential diagnosis of acute right ventricular failure and systemic hypotension in the setting of acute myocardial infarction should also include acute pulmonary embolism. However, normal or minimally elevated pulmonary vascular resistance measurements and pulmonary arterial systolic pressure measurements help to exclude massive pulmonary embolism sufficient to cause right ventricular failure.22 In our patients, the pulmonary vascular resistance and pulmonary arterial systolic pressure measurements were normal or minimally elevated. Hence the marked right ventricular failure could only have been due to right ventricular dysfunction from the infarction. In patients who might have elevation of the pulmonary arterial pressures, such as those with chronic pulmonary disease, even a modest elevation of the pulmonary arterial pressure might cause
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RIGHT VENTRICULAR INFARCTION-LORELL ET AL.
of any dysfunction of the right ventricle that occurred subsequent to its infarction. Treatment: The management of our patients included correction of bradyarrhythmias and an initial trial of intravascular volume expansion that appeared to correct hypotension and oliguria in 3 of the 12 patients. In right ventricular infarction, it seems reasonable to attempt initial expansion of the intravascular volume because the right ventricle may be functioning almost as a passive conduit. The use of pressor and inotropic agents and volume expansion appeared to reverse hypotension in six of the nine patients. However, our series is too small to permit recommendation of specific agents; indeed, drugs that increase pulmonary vascular resistance by causing pulmonary vasoconstriction could conceivably worsen right ventricular failure. enhancement
Systemic afterload reduction induced by intraaortic balloon counterpulsation has been useful in treating
severe left ventricular dysfunction secondary to myocardial infarction. Intraaortic balloon counterpulsation reduces left ventricular filling pressures and cardiac work and augments cardiac output. In our experience, intraaortic balloon counterpulsation did not appear to benefit the three patients with right ventricular infarction in whom it was tried. This is not surprising, because the major beneficial hemodynamic effects of
intraaortic balloon counterpulsation would appear to be exerted primarily on the systemic arterial circulation and the left ventricle, rather than on the pulmonary arterial circulation and the right ventricle. Prognosis: The mortality rate in this series of 12 patients was high: Three of the 12 patients died in the hospital of irreversible cardiac failure and terminal ventricular arrhythmias, and 1 died suddenly at home 3 months later. However, there is much to suggest on the basis of our experience and that of others that this outcome is unusually poor. Our hospital is a referral center for patients with severe complications of acute myocardial infarction, and several of the patients were transferred here for treatment of hypotension. Thus, these 12 patients represent a cluster of unusually sick patients with right ventricular infarction. Certainly the very large incidence of right ventricular involvement detected with noninvasive radionuclide studies in patients with inferior myocardial infarction compared with the relatively small number who manifest severe problems from right ventricular dysfunction would indicate that the overall prognosis is substantially better than that in our series.8 Acknowledgment We gratefully acknowledge the assistance of Theresa Flynn, RN.
References 1. Lassers BW, George M, Anderton JL, Higgens MR, Philp MB: Left ventricular failure in acute myocardial infarction. Am J Cardiol 2551 l-522, 1970. 2. Rackley CE, Russell RO: Right ventricular function in acute myocardial infarction. Am J Cardiol33:927-929, 1974 3. Cohn JN, Guiha NH, Broder MI, Limas CJ: Right ventricular infarction. Clinical and hemodynamic features. Am J Cardiol 33: 209-214, 1974 4. Rotman M, Ratliff NB, Hawley J: Right ventricular infarction: a haemodynamic diagnosis. Br Heart J 36:941-944, 1974 5. Al-Sadir J; Falicov R, Zahavi I, Brooks H, Resnekov L: Right ventricular dysfunction in acute inferior myocardial infarction (abstr). Circulation 48:Suppl lV:IV-59, 1973 6. Rlgo P, Murray M, Taylor DR, Weisfekfl ML, Kelly DT, Strauss HW, Pitt B: Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction. Circulation 52:268-274, 1975 7. Sharpe DN, Botvinick EH, Shames DM, Schiller NB, Massie BM, Chatter@ K, Parmley WW: The noninvasive diagnosis of right ventricular infarction. Circulation 57:483-490, 1978 8. Wackers FJ, Lie KI, Sokole EB, Res J, Van Der Schoof JB, Durrer D: Prevalence of right ventricular involvement in inferior wall infarction assessed with myocardial imaging with thallium-201 and technetium-99m pyrophosphate. Am J Cardiol 42:358-362, 1978 9. Feigenbaum H: Echocardiography. Philadelphia, Lea & Febiger, 1976, p 464 10. McAllister RG, Friesinger GC, Sinclair-Smith BC: Tricuspid regurgitation following inferior myocardial infarction. Arch Intern Med 136:95-99, 1976 11. Zone DD, Bottl RE: Right ventricular infarction with tricupsid insufficiency and chronic right heart failure. Am J Cardiol 37:
445-448, 1978 12. Wade WG: The pathogenesis of infarction of the right ventricle. Br Heart J 21:545-554, 1959 13. lsner JM, Roberts WC: Right ventricular infarction complicating left ventricular infarction secondary to coronary artery disease. Am J Cardiol 42:885-894, 1978 14. Warfman WB, Hellerslein HK: The incidence of heart disease in 2.000 consecutive autopsies. Ann Intern Med 28:41-65, 1948 15. Shabetai R, Fowler NO, Guntheroth WG: The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 26:480-489, 1970 16. Shabetai R: The pathophysiology of cardiac tamponade and constriction, In Pericardial Diseases (Spodick DH, ed). Philadelphia, FA Davis, 1976, p 83-84 17. Moscovitz H: Pericardial constriction versus cardiac tamponade. Am J Cardiol 26546, 1970 18. Guntheroth WG, Morgan BC, Mullins GL: Effect of respiration on venous return and stroke volume in cardiac tamponade. Circ Res 20.381-390, 1967 19. Shabetai R: The pathophysiology of cardiac tamponade and constriction. In Ref 16, p 74-75 20. Horowitz MS, Schultz CS, Stinson EB, Harrison DC, Popp RL: Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 50:239-247, 1974 21. Schiller NB, Botvinick EH: Right ventricular compression as a sign of cardiac tamponade: an analysis of echocardiographic ventricular dimensions and their clinical implications. Circulation 56:774779, 1977 22. Dalen JE, Banas J, Brooks HL, Evans GL, Paroskos JA, Dexter L: Resolution rate of acute pulmonary embolism in man. N Engl JMed230:1194-1199.-1969
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The American
Journal
of CARDIOLOGY” VOLUME NUMBER
43 3
CLINICAL STUDIES
Right Ventricular Infarction Clinical Diagnosis and Differentiation From Cardiac Tamponade and Pericardial Constriction
BEVERLY LORELL, MD ROBERT C. LEINBACH, MD, FACC GERALD M. POHOST, MD, FACC HERMAN K. GOLD, MD, FACC ROBERT E. DINSMdRE, MD, FACC ADOLPH M. HUTTER, Jr., MD, FACC JOHN 0. PASTORE, MD, FACC ROMAN W. DESANCTIS, MD, FACC Boston, Massachusetts
From the Department of Medicine, Massachusetts General Hospital (Cardiac Unit), and Harvard Medical School, Boston, Massachusetts. This study was supported in part by Grant HL-17665 from the U. S. Public Health Service, Bethesda, Maryland. Manuscript received May 2, 1978; revised manuscript received October 20, 1978, accepted October 25, 1978. Ad&ess for reprints: Roman W. DeSanctis, MD, Cardiac Unit, Massachusetts General Hospital, Soston, Massachusetts 021 14.
Twelve patients with a clinical diagnosis of right ventricular infarction are described. All had acute inferior wall myocardial infarction associated with the bedside-findings of jugular venous distension, clear lungs on auscultatlon, and arterial hypotension. Hemodynamically, there was elevation of right-sided filling pressures not explained by normal or minimally elevated pulmonary wedge pressures. Four patients had an incorrect diagnosis of acute cardiac tamponade. However, a review of the data showed that the hemodynamic features of right ventricular infarction more closely resemble those of pericardial constriction, a point that may be helpful in distinguishing right ventricular infarction from cardiac tamponade. Invasive and noninvasive techniques that exclude the presence of pericardial fluid and suggest enlargement and abnormal contractility of the right ventricle were helpful in establishing the diagnosis of right ventricular infarction in several patients.
Right ventricular infarction should be suspected when there is evidence of right ventricular dysfunction in the setting of acute inferior myocardial infarction.lp2 Clinically significant right ventricular infarction is characterized by an elevated systemic venous pressure, clear lungs and, frequently, arterial hypotension. Hemodynamically, right ventricular filling pressures are equal to or greater than those of the left ventricle.3y4 Recent studies utilizing data from hemodynamic measurements and cardiac radionuclide imaging suggest that right ventricular damage may be present in as many as 19 to 43 percent of patients with acute inferior myocardial infarction.5-s However, right ventricular infarction is still often unrecognized and, as indicated in this report, may be misdiagnosed as acute cardiac tamponade. In this paper we describe 12 patients with the clinical diagnosis of right ventricular infarction seen at the Massachusetts General Hospital between January 1971 and September 1977. Four of the 12 were erroneously thought to have acute cardiac tamponade. Our report particularly emphasizes the clinical diagnosis of right ventricular infarction and its differentiation from acute cardiac tamponade.
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TABLE I Clinical and Hemodynamic Characteristics of 12 Patients With Suspected dight Ventricular Infarction Pressor Agents*
Pressures PA
Case
Age (yr)
no.
& Sex
ECG
BP
1
55M
f 5”
1:; %!
IMI lPMl IPMI IMI IPMI
98150 75150 90160 92/60 90/60
Yes Yes No Yes No
12 :z
--/12 215
33/14 24/17 20/a -112 -/15
6 s’
61M 64M
IMI IMI
70140 loo/75 100/80
Yes Yes
::
30115 25/16
63M 54M 69F
IMI IPMI IPMI IPMI
No ES Yes No Yes
::
53F
82146 96172 78/50 110150 i 04180
28/14 1 2817 -
am
1: ::;: 12
RA
RV
::
33/12 24/;7
:; 1:
PCW
PVR
Cl
::
1.0 1.5
8 :;
184 112 118 I
23/11 25115 25/16
:;
28115 -/a 25/4 30112
::: 1.9
Discharged Died Discharged Discharged Died
-
2.9 -
Discharged Discharged Died
::9
76 -
lir
< 13
1% 136
& 2.0
Discharged Discharge& chronic right ventricular failure Discharged
15
* Infusion of pressor agents during hemodynamic measurements. + Patient 11 was restudied by right heart catheterization 7 days after infarction. BP = blood pressure (mm Hg); Cl = cardiac index (liters/min per m*); ECG = electrocardiogram; IMI = inferior myocardial infarction; IPMI = inferoposterior myocardial infarction; PA = pulmonary arterial pressure (mm Hg); PCW = pulmonary capillary wedge pressure (mm Hg); PVR = pulmonary vascular resistance (dynes set cms5); RA = mean right atrial pressure (mm Hg); RV = right ventricular pressure (mm Hg).
Methods Patients: The records of 306 patients with electrocardiographic evidence of acute inferior or inferoposterior infarction admitted to the Myocardial Research and Ischemic SCOR units between January 1971 and September 1977 were retrospectively reviewed. The following criteria were used to identify patients with suspected right ventricular infarction: (1) acute inferior or inferoposterior infarction on electrocardiography; (2) jugular venous pressure estimated or measured to be higher than 10 cm HzO; (3) clear lungs on auscultation; and (4) absence of interstitial pulmonary edema or infiltrates on chest X-ray films. We recognized that elevation of pulmonary wedge pressure precedes the appearance of abnormal chest X-ray film findings. Therefore, we also required documentation of right heart filling pressures greater than or within 2 mm Hg of the pulmonary wedge pressure. No patient was included who had a history of lung,disease or clinical or electrocardiographic evidence of chronic car pulmonale. Of the 306 patients, 8 met the defined criti& for right ventricular infarction. Four patients who were seen in con-
TABLE II Characteristics of Seven Patients With Equalization of EndDiastolic Pressures
Case no.
Pulsus Paradoxus’ (mm Hg)
Kussmaul’s Sign+
1
25
Yes
: 5 :
20 10 14 No No 12-15
zl Yes No
9
z,o
RVEDP DipPlateauf:
Tamponade Syspected§
Yes Yes No Yes No Yes Yes
Yes Yes No Yes NO ves No
Results Clinical Features
* lnspiratory fall in systolic arterial pressure recorded by indwelling arterial catheter. + lnspiratory rise in mean right atrial pressure. t Abnormal early diastolic dip and plateau configuration of the right ventricular pressure tracing. 5 Initial incorrect diagnosis of cardiac tamponade. RVEDP = right ventricular end-diastolic pressure.
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sultation by physicians on the cardiac service and who met the criteria for right ventricular infarction were added to the group. Diagnostic procedures: Right-sided filling pressures were measured using flow-directed balloon catheters in all 12 patients. Left ventricular filling pressures were determined from the pulmonary wedge pressure; the left ventricular end-diastolic pressure was also measured in three patients. Pressure tracings were recorded using either Hewlett-Packard transducers and recorders, or Gould multichannel Brush ink recoiders. Cardiac output was determined using the Fick method in three cases and the thermodilution method in the others. In three cases, coronary arteriography was performed with the Sones technique. Cineangiography was performed in three cases by injection of contrast medium into the right atrium. Echocardiograms in four cases were obtained with an SKI 2OH echograph and Honeywell strip recorder, using the technique and range of normal values of cavity dimensions described by FeigenbaGm and Chang.g Multiple gated blood pool imaging performed in three patients utilized a Searle Pho Gamma III camera and the MGH Numedics computer system, or an Ohio Nuclear’Series 400 gamma camera and an MDS PAD computer system. Right heart chamber size and contactility were assessed relative to that of the left ventricle by two experienced obsepvers. The right atrium and ventricle were judged as “markedly dilated,” “mildly dilated” or “normal,” and their contractility was scored as “akinetic,” “ markedly hypokinetic” or “normal.” The two observers agreed in all cases on scoring of size and contractility. The swe scoring system was used to assess the right atria1 cineangiograms.
History and symptoms: The clinical and hemodynamic findings of the 12 patients with suspected right ventricular infarction are shown in Table I; there were 8 men and 4 women, whose ages ranged from 53 to 87 years. Three patients had a history of prior heart disease. Oue patient had chronic angina, one patient (Case
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11) had a history of partial pericardiectomy for cardiac tamponade 15 years before infarction and one patient had a previous inferior myocardial infarction. The presenting complaint was typical crushing chest pain in 10 patients, and nausea with diaphoresis in 2. Four patients had collapsed at home and required emergency resuscitation. No patient had a history of chronic lung disease that could have contributed to right ventricular dysfunction. Clinical findings:: The interval between electrocardiographic diagnosis of acute inferior infarction and hemodynamic evaluation ranged from 2 to 72 hours. All patients were described as appearing severely ill. All patients were initially hypotensive (systolic pressure less than 100 mm Hg) and oliguric with urinary output of less than 30 ml/hour, and all had cool mottled limbs. Four patients were mentally obtunded. Pericarditis, evident as a pericardial friction rub, was noted in 11 patients. With the exception of Case 11, chest X-ray films showed no cardiac enlargement or pulmonary edema. The initial rhythm was normal sinus in seven patients, sinus bradycerdia in one patient, Wenckebach atrioventricular (A-V) block in one, and complete A-V block in three patients.
KUSSMAUl’S SIGN AND PULSUS PARADOXUS
ECG
RACYAL ARTERY
mmfig
RIGHT
ATRfUlW mm Hg
FIGURE 1. Case 2. Simultaneous radial arterial and right atrial pressure tracings demonstrating pulsus paradoxus and Kussmaul’s sign in a patient initially thought to have cardiac tamponade. The phasic fall in systemic arterial pressure that occurred during inspiration corresponds with a.phasic rise in right atrial pressure during inspiration. ECG = electrocardiogram.
ECG
FIGURE 2. Case 9. The right atrial and right ventricular pulse tracings were sequentially recorded, and the pulmonary arterial tracing was recorded after a short delay. The right atrial pressure is elevated, and the wave form shows an X’ and prominent Y descent. There is an early diastolic dip-plateau configuration of the right ventricular pressure tracing. The pulmonary arterial systolic pressure is not elevated, and the right ventricular pulse pressure is narrow, suggesting poor systolic function of the right ventricle. ECG = electrocardiogram.
--l-T-r-200 mmffg 400
Radial Artery -JLb-J-ku
0 40
mmHg
Right Atri’f Pressure
Ri@htVefltrkufarPressure
20
FIGURE 3. Acute cardiac tamponade without right ventricular infarction (compare with Fig. 2). As in Figure 2, the right atrial (RAP) and right ventricular pressure @VP) tracings were sequentially recorded. The right atrial pressure is elevated, but the right atrial wave form is relatively flat and the Y descent is nearly obliterated. Note that a steep early diastolic dip-plateau configuration is not present in the right ventricular pulse tracing. ECG = electrocardiogram; PAP = pulmonary arterial pressure.
mm Hg
20
~ 1
JfMJLl
OL
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RW(
ET AL.
..~.l......l.l..~l....‘~.
FIGURE 4. Case 9. Echocardiographic study of the right (RV) and left ventricles (LV) just below the level of the free edge of the mitral valve leaflets. The right ventricle is enlarged. The interventricularseptum (IVS) thickens poorly in systole, and it appears to move paradoxically away from the left ventricle in systole. There is no evidence of a pericardial effusion. CW = chest wall; ECG = electrocardiogram; LVPW = left ventricular posterior wall.
Hemodynamic data: To clarify the etiology of the bedside findings of right-sided heart failure, right heart catheterization was performed. The right atrial pressure in the 12 patients ranged from 11 to 18 (average 14) mm Hg, and the right ventricular diastolic pressure, measured in 7 patients, ranged from 12 to 17 (average 14) mm Hg. Right ventricular systolic pressures varied from 24 to 33 (average 28) mm Hg. The pulmonary arterial systolic pressures ranged from 20 to 33 (average 26) mm Hg. The pulmonary wedge pressures ranged from 8 to 16 (average 12) mm Hg. The pulmonary vascular resistance could be calculated in six patients, and ranged from 15 to 136 (average 108) dynes set cme5. In each of the three patients (Cases 4,6 and 9) studied with coronary arteriography the right coronary artery was completely occluded; in addition, Patient 4 had 90 percent diameter narrowing of the left main coronary artery and Patient 9 had a 60 percent luminal narrowing of the left circumflex artery. Seven patients had equilibration of the right atrial, pulmonary diastolic and pulmonary wedge pressures suggesting pericardial disease (Table II). In this subgroup, radial artery monitoring showed pulsus
paradoxus greater than 10 mm Hg in five patients. Two of the seven patients had an abnormal inspiratory rise in mean right atrial pressure (Kussmaul’s sign) (Fig. 1). Although pressure tracing contours may be difficult to assess because of “overshoot” in the absence of high fidelity micromanometer catheters, we observed that five of the seven patients had a right ventricular tracing with a striking early diastolic dip and plateau configuration and a right atria1 tracing with a steep Y descent (Fig. 2 and 3). Echocardiography: Additional. studies were performed in several patients to evaluate further the right ventricle and exclude the presence of pericardial fluid. Echocardiograms (obtained in Cases 5, 8, 9 and 11) showed no pericardial effusion, but in each of the four cases showed right ventricular end-diastolic cavity enlargement, defined in this laboratory as greater than 14 mm/m2 (Fig. 4). In two studies, poor systolic septal thickening and abnormal systolic anterior septal motion were recorded. Multiple gated blood pool imaging: This procedure, performed in Cases 9,10 and 11, showed in each study marked dilatation of the right ventricle relative to the left ventricle, and akinesia or marked hypokinesia of the body of the right ventricle (Fig. 5). The right ventricular apex also appeared markedly hypokinetic in two studies. The right atrium was only mildly dilated in one study, but in the other two appeared markedly dilated and hypokinetic. Each study showed paradoxjcal systolic motion of the septum away from the left ventricle. The left ventricular inferior and inferoapical walls appeared mildly or markedly hypokinetic in the studies. The left ventricular ejection fraction was greater than 50 percent in each imaging study. Right atria1 cineangiography: Marked right ventricular dilatation relative to left ventricular size was also seen in the right atria1 cineangiograms (Cases 5,8 and 11) (Fig. 6). In each cineangiogram, the body of the right ventricle appeared markedly hypokinetic, and the inferobasal right ventricular wall appeared mildly hypokinetic. In each study, the right atrium appeared markedly enlarged, and in two it appeared severely hypokinetic. Levophase opacification showed left ventricular inferior wall akinesia in two studies, and posterobasal wall akinesia in the other study. Hospital Course
Arrhythmias: Initial serious management problems included disturbances of cardiac rhythm and hypo-
FlGURE 5. Case 9. Left anterior oblique gated cardiac blood pool images in end-systole and enddiastole. The diagram at left shows the location of the cardiac chambers. The right ventricle (RV) is markedly dilated and pborly contractile. By comparison, the left ventricle (LV) has normal size and contractilii. RA = right atrium.
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END-DIASTOLE
FIGURE 6. Case 5. End-diastolic (left) and end-systolic (right) frames from a right atrial cineangiogram in a posteroanterior projection performed in a patient initially thought to have cardiac tamponade. The right atrium (RA) and right ventricle (RV) are markedly enlarged. The study demonstrated generalized right ventricular hypokinesia and akinesia of the inferobasaf right ventricular wall. PA = pulmonary artery.
tension. Nine of the 12 patients required temporary demand pacemakers for correction of severe bradycardia or complete A-V block. Five patients required intermit.tent demand pacing for more than 5 days. Atrial fibrillation or flutter occurred in six patients and was treated with digoxin. Lidocaine or procainamide, or both, was given to four patients for frequent premature ventricular beats or ventricular tachycardia. Hypotension: Hypotension was not alleviated by correction of bradycardia alone in any patient. Expansion of the intravascular volume was tried initially in all patients. It successfully corrected hypotension and oliguria in three patients whose fluid intake ranged from 2,500 to 6,300 ml/day for the first 48 hours. Nine patients were also treated with dopamine, isoproterenol or norepinephrine, or combinations of these, and improvement occurred in six of the nine. In three of these patients, intraaortic balloon counterpulsation was used, but its efficacy was difficult to assess because other measures were used simultaneously. However, in Case 9 multiple paired hemodynamic measurements obtained with and without counterpulsation showed that the counterpulsation resulted in the expected decrease in left ventricular filling pressure but did not significantly change the cardiac index or right-sided pressures. Acute cardiac tamponade: This was initially incorrectly diagnosed in four patients on the basis of the bedside findings and the catheterization findings of equilibration of end-diastolic pressures. In three of the four, subxyphoid pericardiocentesis was attempted. Early in our experience, one patient subsequently underwent pericardial exploration performed during cardiopulmonary bypass, for suspected myocardial rupture, but no bleeding point or evidence of rupture
was found. In the other patients, the diagnosis was clarified with echocardiography or right atria1 cineangiography, which excluded the presence of pericardial fluid and showed dilatation and abnormal contractility of the right ventricle. Later in the hospital course, nine patients had evanescent right-sided pleural effusions in the absence of interstitial edema, and two had murmurs of tricuspid insufficiency, an infrequent finding in inferior infarction that may be due to papillary muscle damage or functional regurgitzation.lOJ1 Mortality: Three patients died in the hospital. All had progressive deterioration of cardiac output and experienced terminal ventricular arrhythmias. Autopsy was permitted only in Case 4, and showed fibrinous pericarditis and total occlusion of the right coronary artery with insignificant atherosclerosis of the other coronary arteries. An infarction of 36 to 48 hours’ age involved the right and left posterior ventricular walls, part of the ant,erior right ventricular wall, and the right atrium. Nine patients were discharged from the 14 to 30th hospital day. In one patient (Case 11 with the history of part,ial pericardiectomy) chronic right ventricular failure developed, and one patient died suddenly at home 3 months later.
Discussion Incidence of right ventricular infarction: Myocardial infarction is generally regarded as an ischemic injury of the left ventricle. That the right ventricle can be the site of major damage from acute myocardial infarction has been recognized clinically only recently.S When present, right ventricular infarction is almost invariably associated with inferior infarction because the posterior wall of the right ventricle and the inferior
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wall of the left ventricle share a common blood supply, usually the right coronary artery.12 In an analysis of 236 necropsy patients with transmural myocardial infarction, Isner and Roberts13 emphasized that right ventricular infarction occurred exclusively in those patients with both transmural posterior (“inferior”) infarction of the left ventricle and infarction of the posterior ventricular septum. Right ventricular infarction was observed in 14 percent of the 236 patients with transmural infarction, occurring in none of the 97 patients with anterior infarction and in 24 percent of the 139 patients with posterior (“inferior”) infarction. This incidence is comparable with that reported in an older necropsy series14 of 2,000 patients with transmural infarction in which right ventricular infarction was associated with left ventricular infarction in 13.8 percent of cases. It appears that the incidence rate of clinically significant right ventricular infarction is considerably lower than the incidence rate found at autopsy. Thus, we recognized only eight cases of right ventricular infarction among 306 patients with acute inferior myocardial infarction, an incidence rate of 2.6 percent. However, this is undoubtedly a minimal incidence in light of the rigid criteria we used for selecting cases. Subtle clinical signs of right ventricular infarction might easily be overlooked at the bedside. Clinical diagnostic features and differentiation from cardiac tamponade and constrictive pericardial disease: Recently Cohn and co-workers3 drew attention to the important features of right ventricular infarction: an elevated systemic venous pressure, the absence of pulmonary edema, and a low cardiac output. Their patients had the hemodynamic findings of elevated right-sided filling pressures and normal or modestly elevated left-sided filling pressures. Our 12 patients exhibited similar clinical and hemodynamic findings. An unusual aspect of our experience was the incorrect diagnosis of cardiac tamponade in four patients, all of whom were seen before the clinical features of right ventricular infarction were appreciated. In the presence of pericarditis, which was noted in 11 of our 12 patients, the constellation of an elevated systemic venous pressure, hypotension, and the occasional occurrence of a paradoxical pulse-all secondary to severe right ventricular dysfunction-could be mistaken for cardiac tamponade. In addition, 7 of our 12 patients had an equilibration of diastolic pressures as measured in the pulmonary wedge position, pulmonary artery, right ventricle and right atrium. However, on carefully reviewing our hemodynamic data in these seven patients, we were struck by the fact that the findings more closely resembled those of constrictive pericardial disease than those of cardiac tamponade. Five of the seven patients had a well preserved and steep right atria1 Y descent, and the right ventricular pressures showed an early diastolic dip and plateau configuration. These findings are much more prevalent in constrictive disease than in cardiac tamponade, where the right atria1 Y descent is usually attenuated or ab-
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sent, and right ventricular pressure tracings rarely show a prominent dip and plateau configuration.15-l7 Kussmaul’s sign-that is, an inspiratory rise in mean right atria1 pressure-was documented in two patients. This finding is sometimes present with constrictive disease but is unusual in cardiac tamponade.lsJg It is possible that the hemodynamic findings in right ventricular infarction that resemble the findings in constrictive disease are indeed manifestations of right ventricular dysfunction combined with the restraining effects of the pericardium. The use of newer noninvasive methods and the occasional application of right atria1 cineangiography
are valuable in the diagnosis of right ventricular infarction because they demonstrate the diminished systolic performance of the right ventricle. Thus, right atria1 cineangiography and multiple gated blood pool imaging permit qualitative assessment of right ventricular size and contractility. The dilated and poorly contracting right-sided chambers observed with these techniques in five of our patients differ strikingly from the small, vigorously contracting chambers seen in both cardiac tamponade and constrictive pericarditis, in which the problem is ordinarily that of limited ventricular filling with unimpaired systolic emptying. Thallium-201 and technetium-99m pyrophosphate scintigraphy are promising methods for detecting right ventricular infarction and may supplement studies that suggest right ventricular dysfunction.8 We also found echocardiography a useful bedside technique in distinguishing between right ventricular
infarction and cardiac tamponade. In tamponade, the presence of pericardial fluid can be demonstrated and, in some patients, the exaggerated inspiratory filling and expiratory compression of the right ventricle associated with tamponade can be detected.20,21 In our four patients with right ventricular infarction studied with echocardiography, right ventricular end-diastolic dimensions were uniformly increased. It is not clear to us whether the abnormal septal motion detected by both the echocardiographic and imaging studies was due to ischemic septal damage or to dilatation of the right ventricle. Differentiation from pulmonary embolism: In addition to differentiation from acute cardiac tamponade, the differential diagnosis of acute right ventricular failure and systemic hypotension in the setting of acute myocardial infarction should also include acute pulmonary embolism. However, normal or minimally elevated pulmonary vascular resistance measurements and pulmonary arterial systolic pressure measurements help to exclude massive pulmonary embolism sufficient to cause right ventricular failure.22 In our patients, the pulmonary vascular resistance and pulmonary arterial systolic pressure measurements were normal or minimally elevated. Hence the marked right ventricular failure could only have been due to right ventricular dysfunction from the infarction. In patients who might have elevation of the pulmonary arterial pressures, such as those with chronic pulmonary disease, even a modest elevation of the pulmonary arterial pressure might cause
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of any dysfunction of the right ventricle that occurred subsequent to its infarction. Treatment: The management of our patients included correction of bradyarrhythmias and an initial trial of intravascular volume expansion that appeared to correct hypotension and oliguria in 3 of the 12 patients. In right ventricular infarction, it seems reasonable to attempt initial expansion of the intravascular volume because the right ventricle may be functioning almost as a passive conduit. The use of pressor and inotropic agents and volume expansion appeared to reverse hypotension in six of the nine patients. However, our series is too small to permit recommendation of specific agents; indeed, drugs that increase pulmonary vascular resistance by causing pulmonary vasoconstriction could conceivably worsen right ventricular failure. enhancement
Systemic afterload reduction induced by intraaortic balloon counterpulsation has been useful in treating
severe left ventricular dysfunction secondary to myocardial infarction. Intraaortic balloon counterpulsation reduces left ventricular filling pressures and cardiac work and augments cardiac output. In our experience, intraaortic balloon counterpulsation did not appear to benefit the three patients with right ventricular infarction in whom it was tried. This is not surprising, because the major beneficial hemodynamic effects of
intraaortic balloon counterpulsation would appear to be exerted primarily on the systemic arterial circulation and the left ventricle, rather than on the pulmonary arterial circulation and the right ventricle. Prognosis: The mortality rate in this series of 12 patients was high: Three of the 12 patients died in the hospital of irreversible cardiac failure and terminal ventricular arrhythmias, and 1 died suddenly at home 3 months later. However, there is much to suggest on the basis of our experience and that of others that this outcome is unusually poor. Our hospital is a referral center for patients with severe complications of acute myocardial infarction, and several of the patients were transferred here for treatment of hypotension. Thus, these 12 patients represent a cluster of unusually sick patients with right ventricular infarction. Certainly the very large incidence of right ventricular involvement detected with noninvasive radionuclide studies in patients with inferior myocardial infarction compared with the relatively small number who manifest severe problems from right ventricular dysfunction would indicate that the overall prognosis is substantially better than that in our series.8 Acknowledgment We gratefully acknowledge the assistance of Theresa Flynn, RN.
References 1. Lassers BW, George M, Anderton JL, Higgens MR, Philp MB: Left ventricular failure in acute myocardial infarction. Am J Cardiol 2551 l-522, 1970. 2. Rackley CE, Russell RO: Right ventricular function in acute myocardial infarction. Am J Cardiol33:927-929, 1974 3. Cohn JN, Guiha NH, Broder MI, Limas CJ: Right ventricular infarction. Clinical and hemodynamic features. Am J Cardiol 33: 209-214, 1974 4. Rotman M, Ratliff NB, Hawley J: Right ventricular infarction: a haemodynamic diagnosis. Br Heart J 36:941-944, 1974 5. Al-Sadir J; Falicov R, Zahavi I, Brooks H, Resnekov L: Right ventricular dysfunction in acute inferior myocardial infarction (abstr). Circulation 48:Suppl lV:IV-59, 1973 6. Rlgo P, Murray M, Taylor DR, Weisfekfl ML, Kelly DT, Strauss HW, Pitt B: Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction. Circulation 52:268-274, 1975 7. Sharpe DN, Botvinick EH, Shames DM, Schiller NB, Massie BM, Chatter@ K, Parmley WW: The noninvasive diagnosis of right ventricular infarction. Circulation 57:483-490, 1978 8. Wackers FJ, Lie KI, Sokole EB, Res J, Van Der Schoof JB, Durrer D: Prevalence of right ventricular involvement in inferior wall infarction assessed with myocardial imaging with thallium-201 and technetium-99m pyrophosphate. Am J Cardiol 42:358-362, 1978 9. Feigenbaum H: Echocardiography. Philadelphia, Lea & Febiger, 1976, p 464 10. McAllister RG, Friesinger GC, Sinclair-Smith BC: Tricuspid regurgitation following inferior myocardial infarction. Arch Intern Med 136:95-99, 1976 11. Zone DD, Bottl RE: Right ventricular infarction with tricupsid insufficiency and chronic right heart failure. Am J Cardiol 37:
445-448, 1978 12. Wade WG: The pathogenesis of infarction of the right ventricle. Br Heart J 21:545-554, 1959 13. lsner JM, Roberts WC: Right ventricular infarction complicating left ventricular infarction secondary to coronary artery disease. Am J Cardiol 42:885-894, 1978 14. Warfman WB, Hellerslein HK: The incidence of heart disease in 2.000 consecutive autopsies. Ann Intern Med 28:41-65, 1948 15. Shabetai R, Fowler NO, Guntheroth WG: The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 26:480-489, 1970 16. Shabetai R: The pathophysiology of cardiac tamponade and constriction, In Pericardial Diseases (Spodick DH, ed). Philadelphia, FA Davis, 1976, p 83-84 17. Moscovitz H: Pericardial constriction versus cardiac tamponade. Am J Cardiol 26546, 1970 18. Guntheroth WG, Morgan BC, Mullins GL: Effect of respiration on venous return and stroke volume in cardiac tamponade. Circ Res 20.381-390, 1967 19. Shabetai R: The pathophysiology of cardiac tamponade and constriction. In Ref 16, p 74-75 20. Horowitz MS, Schultz CS, Stinson EB, Harrison DC, Popp RL: Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 50:239-247, 1974 21. Schiller NB, Botvinick EH: Right ventricular compression as a sign of cardiac tamponade: an analysis of echocardiographic ventricular dimensions and their clinical implications. Circulation 56:774779, 1977 22. Dalen JE, Banas J, Brooks HL, Evans GL, Paroskos JA, Dexter L: Resolution rate of acute pulmonary embolism in man. N Engl JMed230:1194-1199.-1969
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