- Email: [email protected]
Bedside recognition, incidence and clinical course of right ventricular infarction
Bedside Recognition, incidence and Clinical Course of Right Ventricular Infarction
GUILLERMO
B. CINTRON,
MD,
FACC
EDGARDO HERNANDEZ, MD, FACC ESTEBAN LINARES, MD, FACC JUAN M. ARANDA, MD, FACC San Juan, Puerto Rico
To evaluate the incidence, clinical characteristics and course of right ventricular infarction, 96 patients with an established diagnosis of acute myocardial infarction were evaluated during a 10 month study period. Of the 44 patients with acute inferior wall myocardial infarction, 16 had bedside evidence of right ventricular dysfunction. All had a positive Kussmaul’s sign, and 12 had either a right ventricular third or fourth heart sound. lnspiratory elevation of right atrial and right ventricular end-diastolic pressures was documented in nine patients. Ventricular fibrillation developed in one patient and advanced atrioventricular block in three. All 16 patients survived and were alive 3 months after infarction. The hospital course and 3 month survival rate were not different from those of the usual patient with inferior wall infarction. Approximately one third of the patients with inferior wall myocardial infarction have bedside evidence of right ventricular infarction, which usually does not alter short-term prognosis.
Since the initial description of right ventricular infarction, the clinical syndrome has been recognized with increasing frequency. The clinical picture described by Cohn et al.’ of acute inferior wall myocardial infarction with elevated systemic venous pressure, clear lungs, systemic hypotension and atrioventricular (A-V) block is well known. The diagnosis can be further documented with right heart catheterization or gated scintigraphy and technetium-99m pyrophosphate myocardial imaging.2J The clinical incidence of right ventricular infarction has been estimated to vary between 3 and 8 percent of all cases of myocardial infarction4 whereas pathologic and radionuclide studies have found a 24 to 37 percent incidence rate of right ventricular involvement in patients with inferior myocardial infarction. 3,5 Most authors have emphasized the invasive diagnostic procedures and serious complications of right ventricular infarction. This study was undertaken to evaluate, in a prospective fashion, the bedside clinical diagnosis, incidence and course of right ventricular infarction.
Methods
From the Cardiology Section, Medical Service, Veterans Administration Hospital, and Department of Medicine, University of Puerto Rico School of Medicine, San Juan, Puerto Rico. This work was supported in part by the Veterans Administration, Washington, D.C. Manuscript received June 5, 1980; revised manuscript received September 15, 1980. accepted October 6, 1980. Address for reprints: Guillermo Cintron. MD, Medical Service, Veterans Administration Hospital, GPO Box 4867, San Juan, Puerto Rico 00936.
224
February 1981
Study patients: During a 10 month study period all 96 patients admitted to the Coronary Care Unit of the San Juan Veterans Administration Hospital, Puerto Rico with the diagnosis of acute myocardial infarction were screened by one of us. The diagnosis of myocardial infarction was established by the clinical picture plus the usual electrocardiographic and serum enzyme criteria (elevation of serum glutamic oxaloacetic transaminase, lactic dehydrogenase and creatine kinase). The site of infarction was determined with electrocardiographic criteria.6 All patients were carefully examined for clinical signs of right ventricular dysfunction. Patients with acute inferior wall myocardial infarction and clinical evidence of new right ventricular dysfunction in the absence of pericardial disease, chronic pulmonary disease or chronic heart failure were considered to have right ventricular infarction. Hemodynamic studies: Such studies were obtained in some patients as part of an on-going research protocol.7 In the patients with clinical evidence of right
The American Journal of CARDIOLOGY
Volume 47
RIGHT VENTRICULAR
INFARCTION-CINTRON
ET AL.
/ ,POST
ventricular dysfunction who underwent hemodynamic studies, pressure tracings were obtained during continual expiration and inspiration in the right atrium, right ventricle and pulmonary artery. Pressures were measured with a Swan-Ganz catheter through a Statham P23-ID pressure transducer and recorded with an American Optical two channel recorder. The patients were maintained on a cardiology ward during the rest of their hospital stay. Follow-up: Follow-up information 3 months after the myocardial infarction was obtained from the clinical chart, by telephone or by personal interview. In approximately half of the patients (random selection), postconvalescence exercise testing was done using the standard Bruce protocol 3 months after the myocardial infarction. Results
FIGURE 1. Site of acute myocardial infarction in 96 patients. Shaded area represents patients with acute right ventricular infarction (WI). ANT = anterior; INF = inferior; LAT = lateral: POST = posterior.
Incidence: During the study period, 96 men were admitted with a documented diagnosis of acute myocardial infarction. Forty-seven had anterior myocardial infarction, 44 had inferior myocardial infarction and 4 had lateral and 1 posterior myocardial infarction (Fig. 1). Sixteen patients (16 percent) demonstrated new clinical evidence of right ventricular dysfunction and were considered to have right ventricular infarction. All of these patients had acute transmural inferior wall myocardial infarction. One third (36 percent) of all patients with inferior wall myocardial infarction had clinical evidence of right ventricular dysfunction. Clinical and hemodynamic data: The mean age of the 16 patients with right ventricular infarction was 55 years (Table I). Only 2 of the 16 had evidence of prior myocardial infarction. Nine patients had isolated inferior wall myocardial infarction and four had inferolateral and three inferoposterior infarction. Four patients had marked elevation of the central venous pressure (greater than 10 cm HsO) by clinical estimate. All 16 patients demonstrated a positive Kussmaul’s sign with distension of the jugular veins during inspiration.
Eleven patients had a right ventricular third heart sound and four had a right ventricular fourth heart sound. None of the patients had an audible murmur of tricuspid regurgitation. These clinical findings were present within 48 hours of admission to the coronary care unit and disappeared in all but two of the patients by the time of discharge from the hospital. Radiography was generally not helpful because only portable X-ray films were obtained; pulmonary congestion was observed in eight patients and cardiomegaly in seven. Ten of the 16 patients with right ventricular infarction underwent right heart catheterization. Res-
piratory variation of right atria1 and right ventricular pressures were recorded in nine patients. All nine patients demonstrated an inspiratory increase in mean right atria1 pressure and in right ventricular end-diastolic pressure (Fig. 2). Mean expiratory right atrial and right ventricular end-diastolic pressure was 7.8 f 1.2
TABLE I Clinical Features of 16 Patients With Riaht Ventricular Infarction
Case
Age (yr)
1 : 4
z: 54 49
:
z
; 9
:: 61 58
:: 12
2: 37
13 ::
:: 36
Prior Ml
Infarct Site
No No No Yes No No Yes No No No No No No No No No
Inf-lat Inf Inf Inf Inf-post Inf-lat Inf Inf-lat Inf Inf-post Inf Inf-lat Inf Inf Inf-post Inf
Estimated CVP (cm f-W) 5 : 12 t NA NA 12 10 :: 13 7 4 9
Right Kussmaul’s Sign Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes
s3
Yes Yes Yes No Yes Yes Yes No Yes No Yes Yes Yes No No Yes
Complications
s4
No No Yes Yes No Yes No No No No No Yes No No No No
RBBB None None VF None RBBB 2“AVB None None None None None 2”AVB 3”AVB None None
AVB = atrioventricular block; CVP = central venous pressure; Inf = inferior; lat = lateral; Ml = myocardial infarction; NA = not available; post = posterior: RBBB = right bundle branch block: VF = ventricular fibrillation.
February 1981
The American Journal of CARDIOLOGY
Volume 47
225
RlGUi
VENTP!C’:I_AP
INCA?C’!ON--S%‘TPON
CT
A:_.
identified a larger incidence of anatomic right ventricular infarction. This difference could be based on the fact that infarcts that involve a small amount of right ventricular muscle mass may not produce enough right ventricular dysfunction to become clinically apparent.
15-
Response of right-sided pressures to inspiration (Kussmaul’s sign): Experimental necrosis of the right
IO-
5MM
Exp.
Imp.
FIGURE 2. lnspiratory change in right atrial and right ventricular enddiastolic pressures in nine patients with right ventricular infarction. Open circles = pressure at expiration (Exp.); closed circles = pressure at inspiration (Insp.). Heavy line with arrowhead indicates mean value for the group.
mm Hg. Mean inspiratory right atria1 and right ventricular end-diastolic pressure was 12.5 f 1.2 mm Hg. The mean pulmonary arterial diastolic pressure in the group was 12.7 f 1.1 mm Hg. Clinical course: None of the patients exhibited clinical evidence of pericarditis, pericardial tamponade, shock or congestive heart failure during the hospital stay. Right bundle branch block developed in two patients, second degree A-V block in two and complete A-V block in one. No patient required a temporary pacemaker. Defibrillation was successful in one patient who manifested ventricular tachycardia and fibrillation. All patients survived the hospitalization and were alive 3 months after the acute myocardial infarction. Seven patients underwent exercise testing 3 months after the myocardial infarction. The mean maximal
work load achieved was 7.7 METS. This compares favorably with our previously reported value of 7 METS achieved by patients tested 12 weeks after uncomplicated convalescence from acute myocardial infarction.8 We compared the clinical course of the 16 patients with acute right ventricular infarction with that of 14 randomly selected patients during the same study period who had had an acute inferior wall myocardial infarction without clinical evidence of right ventricular dysfunction. The incidence of complications, duration of hospitalization and 12 week survival rate were similar in both groups. Discussion
The bedside diagnosis of right ventricular infarction has been based on the recognition of severe right ventricular dysfunction with resultant right-sided heart failure. The clinical recognition has thus been limited to cases in which right ventricular involvement has been very extensive. This may be the cause for the low reported incidence rate of clinical right ventricular infarction. Necropsy and radionuclide studies have
226
February 1961
The American Journal of CARDIOLOGY
ventricle has been proved to decrease the ability of the right ventricle to handle a volume load.4 Increasing the systolic load of the right ventricle has also been proved to result in abnormal right ventricular end-diastolic pressure in patients with right coronary artery disease.g A maneuver that would stress the right ventricle may thus help uncover any subclinical dysfunction. The simplest bedside maneuver to stress the right ventricle is inspiration. Normally, during inspiration, there is an increase in the venous return to the right side of the heart. At the same time, pulmonary vascular impedance is decreased during inspiration, thus facilitating right ventricular emptying. lo The inspiratory increase in venous return is so well handled by the healthy right ventricle that right ventricular end-diastolic pressure and right atria1 pressure decrease. This physiologic response is altered in right ventricular infarction and may be the earliest bedside sign of right ventricular infarction. It is of interest that none of our patients with acute anterior myocardial infarction and left ventricular failure had a positive Kussmaul’s sign. Recently, Coma-Canella and Lopez-Sendon’l also described the noncompliant nature of the right ventricle in patients with acute right ventricular infarction. This diastolic right ventricular dysfunction explains the right ventricular third and fourth heart sounds found in the majority of our patients. None of our 14 patients with inferior wall infarction and negative Kussmaul’s sign exhibited a third or fourth heart sound even though four had a pulmonary wedge pressure greater than 12 mm Hg. In some of our patients with a positive Kussmaul’s sign associated with acute inferior wall myocardial infarction, right-sided hemodynamic studies were obtained. We documented elevation of the right ventricular end-diastolic pressure during inspiration. This pressure is transmitted to the right atrium and hence to the jugular venous pulse, giving the characteristic response of Kussmaul’s sign. Most of our patients had a normal mean right atria1 pressure, which probably reflects their minor degree of right ventricular dysfunction. None of our patients had clinical signs or symptoms of pericardial disease. Pericardial effusion was excluded by M mode echocardiography in six of the patients with right ventricular infarction. Lore11 et all2 also emphasized this point of differential diagnosis of right ventricular infarction and pericardial disease. Clinical course and prognosis: The clinical course of our patients with right ventricular infarction was not different from the course of a random group of patients with acute inferior wall myocardial infarction without signs of right ventricular infarction. The 3 month survival rate was 100 percent in both groups. Performance
Volume 47
RIGHT VENTRICULAR
of the patients with right ventricular infarction on exercise testing 3 months after infarction was comparable with that of our usual patient with an uncomplicated myocardial infarction. This finding indicates that right ventricular infarction may not necessarily carry a bad prognosis, in contrast to data from other studieslJ,4 showing a large incidence of shock, A-V block and death in right ventricular infarction. This difference may again reflect the rather extensive myocardial damage needed to produce severe right ventricular failure. It appears that clinically right ventricular infarction presents a wide spectrum from a rather benign, uncomplicated entity to a catastrophic event with A-V block, shock and even death. Appropriate therapy in patients with acute right ventricular infarction and systemic hypoperfusion secondary to inadequate left ventricular filling pressure usually produces a satisfactory result. Clinical implications: Anatomic right ventricular infarction is seen in approximately one third of patients with acute inferior myocardial infarction. Careful
INFzARCTION-CINTRON
ET AL.
bedside physical diagnosis can identify these patients by demonstrating a positive Kussmaul’s sign plus a right ventricular third or fourth heart sound. Generally this is a benign condition. However, in some patients such severe right ventricular failure may develop that the resultant decrease in left heart venous return will decrease left ventricular output and cause systemic hypoperfusion. In these cases, expansion of intravascular volume and use of inotropic agents usually produce hemodynamic improvement. Therapeutic interventions that decrease right-sided venous return should be carefully monitored in patients with right ventricular infarction because these interventions will compromise right ventricular output with subsequent hemodynamic deterioration.lzS Acknowledgment We thank Brunilda Pena, RN, Martha Medina, RN and the medical house staff of the Veterans Administration Hospital, Puerto Rico, for their assistance, and Vilma Palanuk for secretarial support.
References 1. Cohn JN, Guiha NH, Broder MI, Limas CJ. Right ventricular infarction. Am J Cardiol 1974;33:209-14. 2. Rigo P, Murray M, Taylor DR, et al. Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction. Circulation 1975;52:268-74. 3. Wackers FJ, Lle KI, Soloke EB, Res J, Van der Schoot 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 1978;42:35862. 4. Cohn JN. Right ventricular infarction revisited. Am J Cardiol 1979;43:666-8. 5. lsner JM, Roberts WC. Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Am J Cardiol 1978;42:885-94. 6. The Criteria Committee of the New York Heart Association: Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Blood Vessels. 7th ed. Boston: Little, Brown, 1973;95-124. 7. Veterans Administration Cooperative Study of Vasodilators in Acute Myocardial infarction, Veterans Administration Cooperative Studies Program, Washington, DC.
8. Linares E, Clntron G, Perez J, Hernandez E, Gonzalez M, Aranda JM. Exercise treadmill testing in the early and convalescent period after acute myocardial infarction. Bol Asoc Med PR 1979;71: 228-9. 9. Berman JL, Green LH, Grossman W. Right ventricular diastolic pressure in coronary artery disease. Am J Cardiol 1979:44: 1263-8. 10. Curtiss El, Mathews RG, Shaver JA. Mechanism of the normal splitting of the second heart sound. Circulation 1975:51:15764. 11. Coma-Canella I, Lopez-Sendon J. Ventricular compliance in ischemic right ventricular dysfunction. Am J Cardiol 1980;45: 555-61. 12. Lorell 8, Leinbach RC, Pohost GM, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol 1979;43: 465-71. 13. Clark G, Strauss HD, Roberts R. Dobutamine vs furosemide in the treatment of cardiac failure due to right ventricular infarction. Chest 1980;77:220-3.
February 1981
The American Journal of CARDIOLOGY
Volume 47
227
GUILLERMO
B. CINTRON,
MD,
FACC
EDGARDO HERNANDEZ, MD, FACC ESTEBAN LINARES, MD, FACC JUAN M. ARANDA, MD, FACC San Juan, Puerto Rico
To evaluate the incidence, clinical characteristics and course of right ventricular infarction, 96 patients with an established diagnosis of acute myocardial infarction were evaluated during a 10 month study period. Of the 44 patients with acute inferior wall myocardial infarction, 16 had bedside evidence of right ventricular dysfunction. All had a positive Kussmaul’s sign, and 12 had either a right ventricular third or fourth heart sound. lnspiratory elevation of right atrial and right ventricular end-diastolic pressures was documented in nine patients. Ventricular fibrillation developed in one patient and advanced atrioventricular block in three. All 16 patients survived and were alive 3 months after infarction. The hospital course and 3 month survival rate were not different from those of the usual patient with inferior wall infarction. Approximately one third of the patients with inferior wall myocardial infarction have bedside evidence of right ventricular infarction, which usually does not alter short-term prognosis.
Since the initial description of right ventricular infarction, the clinical syndrome has been recognized with increasing frequency. The clinical picture described by Cohn et al.’ of acute inferior wall myocardial infarction with elevated systemic venous pressure, clear lungs, systemic hypotension and atrioventricular (A-V) block is well known. The diagnosis can be further documented with right heart catheterization or gated scintigraphy and technetium-99m pyrophosphate myocardial imaging.2J The clinical incidence of right ventricular infarction has been estimated to vary between 3 and 8 percent of all cases of myocardial infarction4 whereas pathologic and radionuclide studies have found a 24 to 37 percent incidence rate of right ventricular involvement in patients with inferior myocardial infarction. 3,5 Most authors have emphasized the invasive diagnostic procedures and serious complications of right ventricular infarction. This study was undertaken to evaluate, in a prospective fashion, the bedside clinical diagnosis, incidence and course of right ventricular infarction.
Methods
From the Cardiology Section, Medical Service, Veterans Administration Hospital, and Department of Medicine, University of Puerto Rico School of Medicine, San Juan, Puerto Rico. This work was supported in part by the Veterans Administration, Washington, D.C. Manuscript received June 5, 1980; revised manuscript received September 15, 1980. accepted October 6, 1980. Address for reprints: Guillermo Cintron. MD, Medical Service, Veterans Administration Hospital, GPO Box 4867, San Juan, Puerto Rico 00936.
224
February 1981
Study patients: During a 10 month study period all 96 patients admitted to the Coronary Care Unit of the San Juan Veterans Administration Hospital, Puerto Rico with the diagnosis of acute myocardial infarction were screened by one of us. The diagnosis of myocardial infarction was established by the clinical picture plus the usual electrocardiographic and serum enzyme criteria (elevation of serum glutamic oxaloacetic transaminase, lactic dehydrogenase and creatine kinase). The site of infarction was determined with electrocardiographic criteria.6 All patients were carefully examined for clinical signs of right ventricular dysfunction. Patients with acute inferior wall myocardial infarction and clinical evidence of new right ventricular dysfunction in the absence of pericardial disease, chronic pulmonary disease or chronic heart failure were considered to have right ventricular infarction. Hemodynamic studies: Such studies were obtained in some patients as part of an on-going research protocol.7 In the patients with clinical evidence of right
The American Journal of CARDIOLOGY
Volume 47
RIGHT VENTRICULAR
INFARCTION-CINTRON
ET AL.
/ ,POST
ventricular dysfunction who underwent hemodynamic studies, pressure tracings were obtained during continual expiration and inspiration in the right atrium, right ventricle and pulmonary artery. Pressures were measured with a Swan-Ganz catheter through a Statham P23-ID pressure transducer and recorded with an American Optical two channel recorder. The patients were maintained on a cardiology ward during the rest of their hospital stay. Follow-up: Follow-up information 3 months after the myocardial infarction was obtained from the clinical chart, by telephone or by personal interview. In approximately half of the patients (random selection), postconvalescence exercise testing was done using the standard Bruce protocol 3 months after the myocardial infarction. Results
FIGURE 1. Site of acute myocardial infarction in 96 patients. Shaded area represents patients with acute right ventricular infarction (WI). ANT = anterior; INF = inferior; LAT = lateral: POST = posterior.
Incidence: During the study period, 96 men were admitted with a documented diagnosis of acute myocardial infarction. Forty-seven had anterior myocardial infarction, 44 had inferior myocardial infarction and 4 had lateral and 1 posterior myocardial infarction (Fig. 1). Sixteen patients (16 percent) demonstrated new clinical evidence of right ventricular dysfunction and were considered to have right ventricular infarction. All of these patients had acute transmural inferior wall myocardial infarction. One third (36 percent) of all patients with inferior wall myocardial infarction had clinical evidence of right ventricular dysfunction. Clinical and hemodynamic data: The mean age of the 16 patients with right ventricular infarction was 55 years (Table I). Only 2 of the 16 had evidence of prior myocardial infarction. Nine patients had isolated inferior wall myocardial infarction and four had inferolateral and three inferoposterior infarction. Four patients had marked elevation of the central venous pressure (greater than 10 cm HsO) by clinical estimate. All 16 patients demonstrated a positive Kussmaul’s sign with distension of the jugular veins during inspiration.
Eleven patients had a right ventricular third heart sound and four had a right ventricular fourth heart sound. None of the patients had an audible murmur of tricuspid regurgitation. These clinical findings were present within 48 hours of admission to the coronary care unit and disappeared in all but two of the patients by the time of discharge from the hospital. Radiography was generally not helpful because only portable X-ray films were obtained; pulmonary congestion was observed in eight patients and cardiomegaly in seven. Ten of the 16 patients with right ventricular infarction underwent right heart catheterization. Res-
piratory variation of right atria1 and right ventricular pressures were recorded in nine patients. All nine patients demonstrated an inspiratory increase in mean right atria1 pressure and in right ventricular end-diastolic pressure (Fig. 2). Mean expiratory right atrial and right ventricular end-diastolic pressure was 7.8 f 1.2
TABLE I Clinical Features of 16 Patients With Riaht Ventricular Infarction
Case
Age (yr)
1 : 4
z: 54 49
:
z
; 9
:: 61 58
:: 12
2: 37
13 ::
:: 36
Prior Ml
Infarct Site
No No No Yes No No Yes No No No No No No No No No
Inf-lat Inf Inf Inf Inf-post Inf-lat Inf Inf-lat Inf Inf-post Inf Inf-lat Inf Inf Inf-post Inf
Estimated CVP (cm f-W) 5 : 12 t NA NA 12 10 :: 13 7 4 9
Right Kussmaul’s Sign Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes
s3
Yes Yes Yes No Yes Yes Yes No Yes No Yes Yes Yes No No Yes
Complications
s4
No No Yes Yes No Yes No No No No No Yes No No No No
RBBB None None VF None RBBB 2“AVB None None None None None 2”AVB 3”AVB None None
AVB = atrioventricular block; CVP = central venous pressure; Inf = inferior; lat = lateral; Ml = myocardial infarction; NA = not available; post = posterior: RBBB = right bundle branch block: VF = ventricular fibrillation.
February 1981
The American Journal of CARDIOLOGY
Volume 47
225
RlGUi
VENTP!C’:I_AP
INCA?C’!ON--S%‘TPON
CT
A:_.
identified a larger incidence of anatomic right ventricular infarction. This difference could be based on the fact that infarcts that involve a small amount of right ventricular muscle mass may not produce enough right ventricular dysfunction to become clinically apparent.
15-
Response of right-sided pressures to inspiration (Kussmaul’s sign): Experimental necrosis of the right
IO-
5MM
Exp.
Imp.
FIGURE 2. lnspiratory change in right atrial and right ventricular enddiastolic pressures in nine patients with right ventricular infarction. Open circles = pressure at expiration (Exp.); closed circles = pressure at inspiration (Insp.). Heavy line with arrowhead indicates mean value for the group.
mm Hg. Mean inspiratory right atria1 and right ventricular end-diastolic pressure was 12.5 f 1.2 mm Hg. The mean pulmonary arterial diastolic pressure in the group was 12.7 f 1.1 mm Hg. Clinical course: None of the patients exhibited clinical evidence of pericarditis, pericardial tamponade, shock or congestive heart failure during the hospital stay. Right bundle branch block developed in two patients, second degree A-V block in two and complete A-V block in one. No patient required a temporary pacemaker. Defibrillation was successful in one patient who manifested ventricular tachycardia and fibrillation. All patients survived the hospitalization and were alive 3 months after the acute myocardial infarction. Seven patients underwent exercise testing 3 months after the myocardial infarction. The mean maximal
work load achieved was 7.7 METS. This compares favorably with our previously reported value of 7 METS achieved by patients tested 12 weeks after uncomplicated convalescence from acute myocardial infarction.8 We compared the clinical course of the 16 patients with acute right ventricular infarction with that of 14 randomly selected patients during the same study period who had had an acute inferior wall myocardial infarction without clinical evidence of right ventricular dysfunction. The incidence of complications, duration of hospitalization and 12 week survival rate were similar in both groups. Discussion
The bedside diagnosis of right ventricular infarction has been based on the recognition of severe right ventricular dysfunction with resultant right-sided heart failure. The clinical recognition has thus been limited to cases in which right ventricular involvement has been very extensive. This may be the cause for the low reported incidence rate of clinical right ventricular infarction. Necropsy and radionuclide studies have
226
February 1961
The American Journal of CARDIOLOGY
ventricle has been proved to decrease the ability of the right ventricle to handle a volume load.4 Increasing the systolic load of the right ventricle has also been proved to result in abnormal right ventricular end-diastolic pressure in patients with right coronary artery disease.g A maneuver that would stress the right ventricle may thus help uncover any subclinical dysfunction. The simplest bedside maneuver to stress the right ventricle is inspiration. Normally, during inspiration, there is an increase in the venous return to the right side of the heart. At the same time, pulmonary vascular impedance is decreased during inspiration, thus facilitating right ventricular emptying. lo The inspiratory increase in venous return is so well handled by the healthy right ventricle that right ventricular end-diastolic pressure and right atria1 pressure decrease. This physiologic response is altered in right ventricular infarction and may be the earliest bedside sign of right ventricular infarction. It is of interest that none of our patients with acute anterior myocardial infarction and left ventricular failure had a positive Kussmaul’s sign. Recently, Coma-Canella and Lopez-Sendon’l also described the noncompliant nature of the right ventricle in patients with acute right ventricular infarction. This diastolic right ventricular dysfunction explains the right ventricular third and fourth heart sounds found in the majority of our patients. None of our 14 patients with inferior wall infarction and negative Kussmaul’s sign exhibited a third or fourth heart sound even though four had a pulmonary wedge pressure greater than 12 mm Hg. In some of our patients with a positive Kussmaul’s sign associated with acute inferior wall myocardial infarction, right-sided hemodynamic studies were obtained. We documented elevation of the right ventricular end-diastolic pressure during inspiration. This pressure is transmitted to the right atrium and hence to the jugular venous pulse, giving the characteristic response of Kussmaul’s sign. Most of our patients had a normal mean right atria1 pressure, which probably reflects their minor degree of right ventricular dysfunction. None of our patients had clinical signs or symptoms of pericardial disease. Pericardial effusion was excluded by M mode echocardiography in six of the patients with right ventricular infarction. Lore11 et all2 also emphasized this point of differential diagnosis of right ventricular infarction and pericardial disease. Clinical course and prognosis: The clinical course of our patients with right ventricular infarction was not different from the course of a random group of patients with acute inferior wall myocardial infarction without signs of right ventricular infarction. The 3 month survival rate was 100 percent in both groups. Performance
Volume 47
RIGHT VENTRICULAR
of the patients with right ventricular infarction on exercise testing 3 months after infarction was comparable with that of our usual patient with an uncomplicated myocardial infarction. This finding indicates that right ventricular infarction may not necessarily carry a bad prognosis, in contrast to data from other studieslJ,4 showing a large incidence of shock, A-V block and death in right ventricular infarction. This difference may again reflect the rather extensive myocardial damage needed to produce severe right ventricular failure. It appears that clinically right ventricular infarction presents a wide spectrum from a rather benign, uncomplicated entity to a catastrophic event with A-V block, shock and even death. Appropriate therapy in patients with acute right ventricular infarction and systemic hypoperfusion secondary to inadequate left ventricular filling pressure usually produces a satisfactory result. Clinical implications: Anatomic right ventricular infarction is seen in approximately one third of patients with acute inferior myocardial infarction. Careful
INFzARCTION-CINTRON
ET AL.
bedside physical diagnosis can identify these patients by demonstrating a positive Kussmaul’s sign plus a right ventricular third or fourth heart sound. Generally this is a benign condition. However, in some patients such severe right ventricular failure may develop that the resultant decrease in left heart venous return will decrease left ventricular output and cause systemic hypoperfusion. In these cases, expansion of intravascular volume and use of inotropic agents usually produce hemodynamic improvement. Therapeutic interventions that decrease right-sided venous return should be carefully monitored in patients with right ventricular infarction because these interventions will compromise right ventricular output with subsequent hemodynamic deterioration.lzS Acknowledgment We thank Brunilda Pena, RN, Martha Medina, RN and the medical house staff of the Veterans Administration Hospital, Puerto Rico, for their assistance, and Vilma Palanuk for secretarial support.
References 1. Cohn JN, Guiha NH, Broder MI, Limas CJ. Right ventricular infarction. Am J Cardiol 1974;33:209-14. 2. Rigo P, Murray M, Taylor DR, et al. Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction. Circulation 1975;52:268-74. 3. Wackers FJ, Lle KI, Soloke EB, Res J, Van der Schoot 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 1978;42:35862. 4. Cohn JN. Right ventricular infarction revisited. Am J Cardiol 1979;43:666-8. 5. lsner JM, Roberts WC. Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Am J Cardiol 1978;42:885-94. 6. The Criteria Committee of the New York Heart Association: Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Blood Vessels. 7th ed. Boston: Little, Brown, 1973;95-124. 7. Veterans Administration Cooperative Study of Vasodilators in Acute Myocardial infarction, Veterans Administration Cooperative Studies Program, Washington, DC.
8. Linares E, Clntron G, Perez J, Hernandez E, Gonzalez M, Aranda JM. Exercise treadmill testing in the early and convalescent period after acute myocardial infarction. Bol Asoc Med PR 1979;71: 228-9. 9. Berman JL, Green LH, Grossman W. Right ventricular diastolic pressure in coronary artery disease. Am J Cardiol 1979:44: 1263-8. 10. Curtiss El, Mathews RG, Shaver JA. Mechanism of the normal splitting of the second heart sound. Circulation 1975:51:15764. 11. Coma-Canella I, Lopez-Sendon J. Ventricular compliance in ischemic right ventricular dysfunction. Am J Cardiol 1980;45: 555-61. 12. Lorell 8, Leinbach RC, Pohost GM, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol 1979;43: 465-71. 13. Clark G, Strauss HD, Roberts R. Dobutamine vs furosemide in the treatment of cardiac failure due to right ventricular infarction. Chest 1980;77:220-3.
February 1981
The American Journal of CARDIOLOGY
Volume 47
227