eMedicine Specialties > Cardiology > Coronary Artery Disease

Right Ventricular Infarction

Author: Claudia Dima, MD, Cardiology Fellow, Banner Good Samaritan Medical Center
Coauthor(s): Ashish Pershad, MD, Consulting Staff, Heart and Vascular Center of Arizona; David L Coven, MD, PhD, Assistant Professor of Medicine, Columbia University College of Physicians and Surgeons; Attending Physician in Interventional Cardiology, St Luke's-Roosevelt Hospital Center; Kenneth Desser, MD, Director of Cardiology Fellowship, Clinical Professor, Department of Medicine, University of Arizona College of Medicine
Contributor Information and Disclosures

Updated: Oct 9, 2008

Introduction

Background

Right ventricular infarction was first recognized in a subgroup of patients with inferior wall myocardial infarctions who demonstrated right ventricular failure and elevated right ventricular filling pressures despite relatively normal left ventricular filling pressures. Increasing recognition of right ventricular infarction, either in association with left ventricular infarction or as an isolated event, emphasizes the clinical significance of the right ventricle to total cardiac function.

Interest in recognizing right ventricular infarction noninvasively has grown because of the therapeutic implications of distinguishing patients with right ventricular dysfunction from those with the more usual clinical presentation of left ventricular dysfunction. Patients with right ventricular infarctions associated with inferior infarctions have much higher rates of significant hypotension, bradycardia requiring pacing support, and in-hospital mortality than isolated inferior infarctions.1

Pathophysiology

The right ventricle is a thin-walled chamber that functions at low oxygen demands and pressure. It is perfused throughout the cardiac cycle in both systole and diastole, and its ability to extract oxygen is increased during hemodynamic stress. All of these factors make the right ventricle less susceptible to infarction than the left ventricle.

The posterior descending branch of the right coronary artery usually supplies the inferior and posterior walls of the right ventricle. The marginal branches of the right coronary artery supply the lateral wall of the right ventricle. The anterior wall of the right ventricle has a dual blood supply: the conus branch of the right coronary artery and the moderator branch artery, which courses from the left anterior descending artery.2

Interestingly, right ventricular infarction noted at necropsy usually involves the posterior septum and posterior wall rather than the right free wall. The relative sparing of the right ventricular anterior wall apparently arises from a high degree of collateralization. This collateral blood flow is thought to be derived from the thebesian veins and diffusion of oxygen directly from the ventricular cavity. A direct correlation exists between the anatomic site of right coronary artery occlusion and the extent of right ventricular infarction. Studies have demonstrated that more proximal right coronary artery occlusions result in larger right ventricular infarctions.3 On occasion, the right ventricle can be subjected to infarction from occlusion of the left circumflex coronary artery.4

Because the right ventricle is considered a low-pressure volume pump, its contractility is highly dependent on diastolic pressure. Hence, when contractility and associated diastolic dysfunction are impaired attendant to right ventricular infarction, the right ventricular diastolic pressure increases substantially and systolic pressure decreases. In such a scenario, concomitant left ventricular dysfunction, with increase in right ventricular afterload, is possible. In such a setting, right ventricular output can decrease dramatically, and the only driving force remaining is elevated right atrial pressure. In such a circumstance, the right ventricle serves as a poorly functioning conduit between the right atrium and the pulmonary artery.

Elevation of right atrial pressure secondary to right ventricular infarction has been noted to serve as a stimulus for secretion of atrial natriuretic factor. Increased levels of this polypeptide can be detrimental to normal left ventricular filling pressures. This occurs by virtue of the potent vasodilating, natriuretic, diuretic, and aldosterone-inhibiting properties of atrial natriuretic factor. Inappropriately elevated levels of atrial natriuretic factor may worsen the clinical syndrome of right ventricular infarction.5 The potential hemodynamic derangements associated with right ventricular infarction render the afflicted patient unusually sensitive to diminished preload (ie, volume) and loss of atrioventricular synchrony. These 2 circumstances can result in a severe decrease in right and, secondarily, left, ventricular output.6,7,8

Early thrombolysis or mechanical reperfusion of an occluded coronary artery resulting in right ventricular infarction is associated with prompt reduction in right atrial pressure. This is extremely important because persistently elevated right atrial pressure has been associated with increased in-hospital mortality rate when associated with myocardial infarction. The extent of right ventricular infarction varies greatly and is dependent on the site of occlusion of the right ventricular arterial supply. If occlusion occurs before the right ventricular marginal branches, and collateral blood flow from the left anterior descending coronary artery is absent, then the size of infarction generally is greater. Extent of infarction depends somewhat on flow through the thebesian veins.9 In general, any major reduction in blood supply to the right ventricular free wall portends an adverse prognosis in association with this disorder.

Frequency

United States

Isolated infarction of the right ventricle is extremely rare; right ventricular infarction usually is noted in association with inferior wall myocardial infarction. The incidence of right ventricular infarction in such cases ranges from 10-50%, depending on the series.10

The frequency of right ventricular infarction, which can be detected by right-sided precordial leads, in association with non–ST-segment elevation or non–Q-wave myocardial infarction is not known and currently is being investigated. Although right ventricular infarction is clinically evident in a sizable number of cases, the incidence is considerably less than that found at autopsy.11,12,13,14 A major reason for the discrepancy is the difficulty in establishing the presence of right ventricular infarction in living subjects. Additionally, right ventricular dysfunction and stunning frequently is of a transient nature, such that estimation of its true incidence is even more difficult.

Criteria have been set forth to diagnose right ventricular infarction; even when strictly employed, however, the criteria lead to underestimation of the true incidence of right ventricular infarction.15,16,17

Clinical

History

  • Although right ventricular infarction occurs in more than 30% of patients with inferior posterior left ventricular myocardial infarction, hemodynamically significant right ventricular infarction occurs in less than 10% of these patients.18,19
  • A right ventricular infarct should be considered in all patients who present with an acute inferior wall myocardial infarction, especially in the setting of a low cardiac output.
  • Patients may describe symptoms consistent with hypotension.
  • A subtle clue to the presence of hemodynamically significant right ventricular infarction is a marked sensitivity to preload-reducing agents such as nitrates, morphine, or diuretics.20
  • Other presentations include high-grade atrioventricular block, tricuspid regurgitation, cardiogenic shock, right ventricular free wall rupture, and cardiac tamponade.
  • Should a patient with right ventricular infarction experience unexplained hypoxia despite administration of 100% oxygen, right-to-left shunting at the atrial level in the presence of right ventricular failure and increased right atrial pressure must be considered.21,22 Despite its rarity, this complication of right ventricular infarction must always be considered when a patient with myocardial infarction is thought to have hypoxia secondary to clinically silent pulmonary emboli. The mechanism for right-to-left shunting in the absence of increased pulmonary arterial pressure resides in patency of the foramen ovale in association with poor right ventricular compliance and increased right atrial filling pressures.
  • Patients with extensive right ventricular necrosis are at risk for right ventricular catheter–related perforation, and passage of a floating balloon catheter or pacemaker must always be performed with great care in such a setting.

Physical

  • The classic clinical triad of right ventricular infarction includes distended neck veins, clear lung fields, and hypotension.23
  • Infrequent clinical manifestations include right ventricular third and fourth heart sounds, which are typically audible at the left lower sternal border and increase with inspiration.
  • On hemodynamic monitoring, disproportionate elevation of right-sided filling pressures compared with left-sided hemodynamics represents the hallmark of right ventricular infarction.

More on Right Ventricular Infarction

Overview: Right Ventricular Infarction
Differential Diagnoses & Workup: Right Ventricular Infarction
Treatment & Medication: Right Ventricular Infarction
Follow-up: Right Ventricular Infarction
References
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References

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Further Reading

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Keywords

right ventricle infarction, RVI, myocardial infarction, MI, right ventricular dysfunction, right coronary artery occlusion

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Contributor Information and Disclosures

Author

Claudia Dima, MD, Cardiology Fellow, Banner Good Samaritan Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

Ashish Pershad, MD, Consulting Staff, Heart and Vascular Center of Arizona
Ashish Pershad, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

David L Coven, MD, PhD, Assistant Professor of Medicine, Columbia University College of Physicians and Surgeons; Attending Physician in Interventional Cardiology, St Luke's-Roosevelt Hospital Center
David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Kenneth Desser, MD, Director of Cardiology Fellowship, Clinical Professor, Department of Medicine, University of Arizona College of Medicine
Disclosure: Nothing to disclose.

Medical Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Marschall S Runge, MD, PhD, Charles and Anne Sanders Distinguished Professor of Medicine, Chairman of Medicine, Vice Dean for Clinical Affairs, Chairman, Department of Medicine, University of North Carolina at Chapel Hill School of Medicine
Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association
Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD, Assistant Professor of Medicine, Director of Coronary Care Unit, University of North Carolina at Chapel Hill School of Medicine
Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Up to Date Royalty Review panel membership; pfizer Honoraria Speaking and teaching

 
 
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