Right Ventricular Infarction: Specific Requirements of Management
Leo G. Horan
The principal cause of right ventricular infarction is atherosclerotic proximal occlusion of the right coronary artery. Proximal occlusion of this artery leads to electrocardiographically identifiable right-heart ischemia and an increased risk of death in the presence of acute inferior infarction. Clinical recognition begins with the ventricular electrocardiographic manifestations: inferior left ventricular ischemia (ST segment elevation in leads II, III and aVF), with or without accompanying abnormal Q waves and right ventricular ischemia (ST segment elevation in right chest leads V3R through V6R and ST segment depression in anterior leads V2 through V4). Associated findings may include atrial infarction (PR segment displacement, elevation or depression in leads II, III and aVF), symptomatic sinus bradycardia, atrioventricular node block and atrial fibrillation. Hemodynamic effects of right ventricular dysfunction may include failure of the right ventricle to pump sufficient blood through the pulmonary circuit to the left ventricle, with consequent systemic hypotension. Management is directed toward recognition of right ventricular infarction, reperfusion, volume loading, rate and rhythm control, and inotropic support. (Am Fam Physician 1999;60:1727-34.)
Clinicians sometimes encounter a patient who presents to the hospital with signs and symptoms of an acute myocardial infarction and is discovered, based on large ST segment elevations in leads II, III and aVF on the electrocardiogram (ECG), to be having an acute inferior myocardial infarction. In this situation, clinicians first need to determine if the occlusion is strictly a left ventricular (LV) infarction or if it is also jeopardizing the right ventricular (RV) free wall and septum. RV injury increases the risk of mortality in the elderly. Its recognition requires volume loading and rate and rhythm control, measures that otherwise are not part of the usual treatment of myocardial infarction.
Recognition and Diagnosis of Right Ventricular Infarction
Approximately one half of patients who present with signs and symptoms of acute inferior myocardial infarction have proximal occlusion of the dominant right coronary artery (RCA) and also show ECG signs of RV wall ischemia or infarction (Figure 1). Table 1 groups the branches of the four major segments of the RCA in descending order, along with the corresponding regions of perfusion and the ECG findings when these regions are underperfused. Occlusion sufficiently proximal to cause RV free wall injury also frequently compromises the blood supply to the sinoatrial node, atrium and atrioventricular (AV) node, producing such effects as sinus bradycardia, atrial infarction, atrial fibrillation and AV block (Figures 2 and 3).
Key ECG findings occur with RV and LV ischemic wall injuries. For injury of the LV wall, these findings are ST segment elevations and, possibly, abnormal Q waves in leads II, III and aVF. The appearance of abnormal Q waves (new, wider than previously seen or wider than 0.04 seconds) may be delayed several hours; indeed, if thrombolysis or angioplasty is used acutely, the development of Q waves may be completely aborted.1-4
When involvement of the RV free wall is suspected, clinicians are alerted by the presence of relative ST segment depression in lead V2 or V3 compared with lead V1 (Figure 1, top). If the ST segment depression in lead V2 is more than one half the amplitude of the ST segment elevation in lead aVF, the likely diagnosis is inferoposterior LV infarction with “reciprocal” ST segment depression in lead V2 but no RV involvement.5 However, confirmation of RV ischemia (or the clinical syndrome of RV stun or infarction) can be quickly obtained when right-sided leads V4R through V6R show ST segment elevations greater than 1 mm, or 0.1 mV (Figure 1, bottom). (The sites for right-sided leads are the mirror image of those for the usual left-sided leads: in the fifth right intercostal space, lead V4R is at the midclavicular line, lead V5R is at the anterior axillary line and lead V6R is at the midaxillary line.)
ECG identification of ischemic dysfunction is sufficient for immediate diagnosis and treatment.2 Most acute “RV infarctions” diagnosed by right- sided ST segment elevations do not progress to myocardial necrosis and subsequent scar formation. This accounts for the far lower percentage of autopsy-reported RV infarcts than clinically suspected RV infarcts.6-9 The latter group includes many patients with a stunned or hibernating RV free wall, which recovers more readily than a similarly injured LV wall. This more ready recovery occurs in part because of the rich collateral perfusion of the RV free wall and septum from the left coronary artery and the relatively greater penetration from the blood cavity by the thebesian veins. The work demand for the lower-pressure right circuit is also relatively less than that for the left circuit.
Although “RV infarction” sometimes is a misnomer, by current convention the term identifies the syndrome of acute ischemic RV dysfunction (Table 2). This syndrome is a significant clinical entity with a special pathophysiology and a well-delineated set of priorities for management.
With RV infarction, the ECG may show an acute anterior Q-wave pattern (leads V1 through V3) as well as a right-sided Q pattern (leads V3R through V6R). A number of case reports have described this pattern in association with known occlusion of a ventricular branch of the RCA following proximal angioplasty.10,11 RV involvement with physiologic stun and electrical shutdown may well include the RV portion of the interventricular septum and thus remove much of the septal contribution to the anteroseptal and right precordial R wave.
Clinicians should recognize that in the evolving picture of RV infarction, the appearance of Q waves in leads V1 through V3 does not necessarily require changing the clinical diagnosis to anteroseptal LV infarction. The patient may well have predominant RCA occlusion and RV infarction. Therefore, the clinical alert for the hemodynamic effects of RV infarction should remain in force.
RV involvement alters the in-hospital prognosis radically by overriding the linear relationship between survival and LV ejection fraction (which, in turn, relates inversely to LV infarct size).12 Not only does the paralyzed right heart fail to offer sufficient preload to the left ventricle, but proximal occlusion of the RCA sabotages the normal regular rate and rhythm controls to the whole heart, so that cardiogenic shock remains the primary immediate cause of death, especially in the elderly. To this is added the risk of ischemic rupture of the ventricular septum with RV infarct (Figure 4).12
Yet patients who survive the hospital period enjoy the relatively good long-term prognosis of patients with inferior infarction.6 A few such patients may later develop postinfarction angina, and other patients with proximal RCA stenosis without known RV infarction may also have chronic angina pectoris. Recognition of postinfarction ongoing RV ischemia may be accomplished using either a stress test with right-sided leads or a dobutamine (Dobutrex) echocardiographic stress test. These tests will show the signs of RV ischemic dysfunction, ST segment elevations in lead V4R or RV asynergy.13
Treatment Differing from That for Left Ventricular Infarction volume loading
Approximately one third to one half of patients with acute inferior LV infarction and accompanying RV infarction show the effects of LV volume underload (Table 3).14-16 For many years, physiologic experiments on the canine heart portrayed the right ventricle as a passive conduit for returning venous blood to the pulmonary circuit and on to the left atrium and ventricle. In humans it has become obvious that the pumping contribution of the right ventricle is significant. Acute underperfusion of the RV free wall and adjacent interventricular septum leads to a stunned, noncompliant RV myocardium.
Asynergy of the RV free wall (especially posteriorly and laterally) may be seen on echocardiography. Depending on the degree of ischemic damage, the hemodynamic effects may include elevated jugular venous pressure, a positive Kussmaul’s sign (paradoxically increased jugular pressure or distention on inspiration) and a noncompliant pattern of the right atrial pulse waveform similar to that of constrictive pericarditis.
Loss of RV contractility may lead to a serious deficit in LV preload with a resultant drop in cardiac output and consequent systemic hypotension-an undesirable complication in the presence of acute myocardial infarction. In contrast to the low output and congestive heart failure resulting from extensive LV infarction without RV involvement, which mandates parsimonious fluid administration, the volume-underload state in RV stun may require vigorous fluid administration.
A series of meticulous experimental occlusions of the canine RCA has shown that the response to reperfusion depends on the duration of the preceding ischemia.17,18 Early reperfusion leads to prompt improvement and subsequent recovery of RV free wall contraction and global RV function without any scar formation. Late reperfusion produces little acute return of RV free wall contractile function. Because resumed perfusion increases wall thickness, septal and free wall dyskinesis is reduced, and cavitary volume is diminished. These factors permit LV contraction to pull the passive right ventricle inward, and global function then improves. A further benefit is that necrosis and subsequent scar formation are minimized.16
The advantages of the right ventricle over the left ventricle in sustaining ischemic insult are listed in Table 4. These become reasons for extending the time window for assuming reversibility when RV infarction complicates inferior LV infarction. The other reasons are that in-hospital mortality and complication rates go up with RV infarction, thereby removing the traditional, more benign connotation from inferior myocardial infarction. Stepwise management of right ventricular infarction is presented in Table 5. (Additional information on terminology and dosages is also available.19)
Inotropic Support And Rate And Rhythm Control
Proximal occlusion of the RCA (Table 1) not only endangers right-sided atrial and ventricular pumping functions but also rate and conduction controls. If the response to fluid loading is not adequate, a trial of intravenous dobutamine is reasonable to increase contraction strength. The response should be confirmed by bedside echocardiography and cardiac output monitoring.20
Remembering the need for atrial contribution and the vulnerability of the hampered RV output to a slow rate, clinicians may turn to temporary AV pacing for symptomatic bradycardia (whether from sinus bradycardia or third-degree AV block). It is important to maintain AV synchrony from the outset. Thus, temporary AV sequential pacing should be considered in certain patients with RV infarction to provide the needed ventricular output for the fragile period of the first three or four hospital days.20 Later, permanent pacing may be indicated.21
The authors thank Judi Hubbard, Pat Orander and Lloyd Goodman, M.D., for their contributions to the manuscript.
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2. Zehender M, Kasper W, Kauder E, Schonthaler M, Geibel A, Olschewski M, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328:981-8.
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4. Giannitsis E, Potratz J, Wiegand U, Stierle U, Djonlagic H, Sheikhzadeh A. Impact of early accelerated dose tissue plasminogen activator on in- hospital patency of the infarcted vessel in patients with acute right ventricular infarction. Heart 1997; 77:512-6.
5. Lew AS, Laramee P, Shah PK, Maddahi J, Peter T, Ganz W. Ratio of ST- segment depression in lead V2 to ST-segment elevation in lead aVF in evolving inferior acute myocardial infarction: an aid to the early recognition of right ventricular ischemia. Am J Cardiol 1986;57:1047-51.
6. Kinch JW, Ryan TJ. Right ventricular infarction. N Engl J Med 1994;330:1211-7.
7. Horan LG, Flowers NC, Havelda CJ. Relation between right ventricular mass and cavity size: an analysis of 1500 human hearts. Circulation 1981;64:135-8.
8. Isner JM, Roberts WC. Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction. Am J Cardiol 1978;42:885-94.
9. Andersen HR, Falk E, Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol 1987;10:1223-32.
10. van der Bolt CL, Vermeersch PH, Plokker HW. Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary balloon angioplasty. The only true ‘model’ to study ECG changes in acute, isolated right ventricular infarction. Eur Heart J 1996;17:247-50.
11. Koh TW, Coghlan JG, Lipkin DP. Anterior ST segment elevation due to isolated right ventricular infarction during right coronary angioplasty. Int J Cardiol 1996;54:201-6.
12. Bueno H, Lopez-Palop R, Bermejo J, Lopez-Sandon JL, Delcan JL. In- hospital outcome of elderly patients with acute inferior myocardial infarction and right ventricular involvement. Circulation 1997;96:436-41.
13. San Roman JA, Vilacosta I, Rollan MJ, Castillo JA, Alonso J, Duran JM, et al. Right ventricular asynergy during dobutamine-atropine echocardiography. J Am Coll Cardiol 1997;30:430-5.
14. Mittal SR, Garg S, Lalgarhia M. Jugular venous pressure and pulse wave form in the diagnosis of right ventricular infarction. Int J Cardiol 1996; 53:253-6.
15. Cohen A, Guyon P, Johnson N, Chauvel C, Logeart D, Costagliola D, et al. Hemodynamic criteria for diagnosis of right ventricular ischemia associated with inferior wall left ventricular acute myocardial infarction. Am J Cardiol 1995;76:220-5.
16. Kinn JW, Ajluni SC, Samyn JG, Bates ER, Grines CL, O’Neill W. Rapid hemodynamic improvement after reperfusion during right ventricular infarction. J Am Coll Cardiol 1995;26:1230-4.
17. Laster SB, Ohnishi Y, Saffitz JE, Goldstein JA. Effects of reperfusion on ischemic right ventricular dysfunction. Disparate mechanisms of benefit related to duration of ischemia. Circulation 1994;90:1398-409.
18. Laster SB, Shelton TJ, Barzilai B, Goldstein JA. Determinants of the recovery of right ventricular performance following experimental chronic right coronary artery occlusion. Circulation 1993;88:696-708.
19. Alexander RW, Pratt CM, Roberts R. Diagnosis and management of patients with acute myocardial infarction. In: Alexander RW, Schlant RC, Fuster V, eds. Hurst’s The heart, arteries and veins. New York: McGraw-Hill, 1998:1345-433.
20. Ryan TJ, Anderson JL, Antman EM, Braniff BA, Brooks NH, Califf RM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction. J Am Coll Cardiol 1996;28:1328-428.
21. Dreifus LS, Fisch C, Griffin JC, Gillette PC, Mason JW, Parsonnet V. Guidelines for the implantation of cardiac pacemakers and antiarrhythmia devices. J Am Coll Cardiol 1991;18:1-13.
Major Sections of the Right Coronary Artery with Corresponding Regions
of Perfusion and ECG Findings for Underperfusion
Arterial segment Arterial branch Perfused region ECG effects of
Proximal segment SA nodal branch SA node Sinus bradycardia
Right atrial branch Atrial free wall Atrial infarct pattern,
Middle segment Lateral RV branches Lateral RV free wall ST
segment elevation; later,
Marginal RV branch Inferior (posterior) abnormal Q
waves in leads
RV free wall V3R through V6R
Distal segment AV nodal branch AV node AV block
Posterior descending Posterior lateral Posterior left ventricle
ST segment elevation; later,
segment LV branches Inferior septum, inferior abnormal
Q waves in leads
Posterior descending LV free wall II, III and aVF
ECG = electrocardiographic; SA = sinoatrial; RV = right ventricular; AV =
atrioventricular; LV = left ventricular.
Criteria for Acute Ischemic Right
Right-sided (leads V3R through V6R) ST segment elevation of greater than 1
Right ventricular asynergy as demonstrated by echocardiography or cardiac
Mean right arterial pressure of 10 mm Hg or greater, or a less than 5 mm Hg
difference from mean pulmonary capillary wedge pressure
(equivalent to left atrial pressure)
Noncompliant right atrial pressure waveform
pattern (steep and deep x and y descents)
Effects of Right Ventricular Ischemia
Systolic RV dysfunction 1/2
O RV CO 1/2 O LV CO
RV volume 1/2 septal shift
Diastolic RV dysfunction 1/2 O compliance 1/2
RVDP 1/2 septal shift 1/2 O LVDP 1/2 O LV CO
RAP 1/2 septal shift 1/2 O LAP 1/2 O LV CO
note: Pathophysiologically, RV ischemia ultimately leads to decreased
cardiac output from the left ventricle.
RV = right ventricle; 1/2 = implies; O = decreased; CO = cardiac output; LV
= left ventricle; = elevated; RVDP = right ventricular diastolic
pressure; LVDP = left ventricular diastolic pressure; RAP = right atrial
pressure; LAP = left atrial pressure.
Information from references 14 through 16.
Advantages of the Right Ventricle in Sustaining Reversible Ischemia
Variable Right ventricle Left ventricle
Systolic pressure Lower Higher
Wall stress Lower Higher
Oxygen consumption Less More
Wall thickness Thinner Thicker
Subendocardial resistance Less More
Coronary perfusion Diastolic and systolic Diastolic only
Stepwise Management of RV Infarction*
Recognition ST segment elevation in leads II, III and aVF plus ST segment
elevation in leads
V3R through V6R
Streptokinase (Streptase), 1.5 MU given IV over 60 minutes
rt-PA (recombinant alteplase [Activase]) given first in 15-mg
IV bolus, then 50 mg given
over 30 minutes followed by 35 mg given over 60 minutes
rt-PA given in 10-MU IV bolus, with 10-MU bolus given 30
Coronary bypass surgery
Volume loading Normal saline, 40 mL per minute given IV up to total of 2
L, keeping RA pressure at less
than 18 mm Hg; hemodynamic monitoring required
Inotropic support Dobutamine (Dobutrex), 2 to 5 [micro sign]g per kg per
IV, with dose increased every
5 to 10 minutes up to 15 to 20 [micro sign]g per kg per minute
Rate and rhythm Symptomatic bradycardia: atropine, 0.5 to 1 mg given IV
every 5 minutes up to total
control of 2.5 mg
AV block: AV sequential pacing (usually short term)
Complications LV ischemic dysfunction: judicious afterload reduction
angiotensin-converting enzyme inhibitors); volume restriction
Cardiogenic shock: aortic balloon pump
Interventricular septal rupture: emergency surgical repair
RV papillary muscle rupture and tricuspid regurgitation: emergency
MU = megaunit; IV = intravenous; rt-PA = recombinant tissue plasminogen
activator; RA = right atrial;
AV = atrioventricular; LV = left ventricular RV = right ventricular.
*-Successive steps usually imply lack of success with preceding step(s) or
increased severity of the patient’s condition. The preeminent first step
after recognition is reperfusion. Angioplasty presumes failed thrombolysis,
and coronary bypass surgery presumes failed angioplasty or the presence of
multivessel disease. Successful reperfusion returns RV function and
prevents the need for volume loading. When volume loading fails, inotropic
support may be required. When atropine fails to correct symptomatic
bradycardia or relieve AV block, pacing may be needed. The complications
and their strong countermeasures presume severe, unrelieved RV ischemic
damage. Additional information on terminology and dosages is available in
LEO G. HORAN, M.D., is clinical professor of medicine at Mercer University School of Medicine and consultant in cardiology at Memorial Medical Center, Savannah, Ga. He is also professor emeritus of medicine at the Medical College of Georgia, Augusta. His previous positions include chief of cardiology at the Department of Veterans Affairs Medical Center in Augusta. Dr. Horan is a graduate of Tulane University School of Medicine, New Orleans.
NANCY C. FLOWERS, M.D., is clinical professor of medicine at Mercer University School of Medicine, serving at the Memorial Medical Center on the Savannah campus. In addition, Dr. Flowers is professor emerita of medicine at the Medical College of Georgia. Her prior positions include chief of cardiology at the Department of Veterans Affairs Medical Center, Augusta. She received her medical degree from the University of Tennessee College of Medicine, Memphis.
Address correspondence to Leo G. Horan, M.D., 2 Priory Rd., Savannah, GA 31411. Reprints are not available from the authors.
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