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eMedicine Specialties > Cardiology > Coronary Artery Disease

Right Ventricular Infarction

Claudia Dima, MD, Cardiology Fellow, Banner Good Samaritan Medical Center
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

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.

Differential Diagnoses

Cardiomyopathy, Hypertrophic
Pulmonary Embolism
Cardiomyopathy, Restrictive
Pulmonary Hypertension, Primary
Cor Pulmonale
Pulmonary Hypertension, Secondary
Endomyocardial Fibrosis
Tricuspid Regurgitation
Pericarditis, Acute
Pericarditis, Constrictive
Pneumothorax

Workup

Imaging Studies

  • In the appropriate clinical setting, a diagnosis of right ventricular infarction can be made using noninvasive techniques, or the patient may require right ventricular catheterization and hemodynamic monitoring.
  • Echocardiography is useful as a modality to rule out pericardial disease and tamponade, which are the major differential diagnoses in the setting of a right ventricular infarction.
    • Right ventricular dilatation, abnormal right ventricular wall motion, paradoxical motion of the interventricular septum, and tricuspid regurgitation are echocardiographic features of right ventricular infarction.
    • As might be expected, tricuspid regurgitation in this setting is detected more frequently by ultrasound than by auscultation of a tricuspid regurgitation murmur.
    • Echocardiogram can detect shunting through a patent foramen ovale.
    • Echocardiogram has an 82% sensitivity and 93% specificity in detecting right ventricular infarction when right ventricular scintigraphy is used as the comparative standard.24
    • In the vast majority of patients with right ventricular infarction, the wall motion abnormalities initially manifest on echocardiography reverse within 3 months.25
    • The use of tissue Doppler in echocardiography has also increased, providing another means to detect right ventricular infarction. A decrease in the systolic velocity at the tricuspid annulus not only allows for diagnosis of right ventricular infarction but also suggests worse mortality outcome.26
    • Another echocardiographically obtained value that can aid in diagnosis of right ventricular infarction is the myocardial performance index (MPI). MPI is derived from the sum of the isovolumic relaxation and contraction time divided by the ejection fraction. An abnormally elevated MPI of >0.30 suggests the presence of a right ventricular infarction.27
  • Gated equilibrium radionuclide angiography and technetium 99m pyrophosphate scintigraphy are useful in diagnosing right ventricular infarction noninvasively.28 In the case of radionuclide angiography, the right ventricle is demonstrated to be enlarged and poorly contractile, with a reduced ejection fraction. When technetium 99m pyrophosphate is employed, the right ventricular free wall is "hot," indicating significant infarction.

Other Tests

  • Electrocardiography
    • All patients with inferior wall myocardial infarction should have a right-sided ECG. ST-segment elevation in lead V4R is the single most powerful predictor of right ventricular involvement, identifying a high-risk subset of patients in the setting of inferior wall myocardial infarction.29 The ST-segment elevation is transient, disappearing in less than 10 hours following its onset in half of patients. The following table demonstrates the sensitivity and specificity of more than 1 mm of ST-segment elevation in V1, V3 R, and V4 R.30 Sensitivity and Specificity of more than 1 mm of ST-Segment Elevation in V1, V3 R, and V4 R
      LeadsSensitivity (%)Specificity (%)
      V1 2892
      V3 R6997
      V4 R9395
    • Isolated right ventricular infarct is extremely rare and may be interpreted erroneously as left ventricular anteroseptal infarction on ECG because of ST-segment elevation in leads V1 -V4.31,32 Some have suggested that the differential diagnosis between the 2 abnormalities can be distinguished by using vectorial analysis. The mean ST-segment vector in right ventricular infarction usually is directed anteriorly and to the right (>100°).
    • In an anteroseptal left ventricular infarct, the mean ST-segment vector is oriented leftward between -30° and -90° thus, analysis of the frontal and horizontal plane axis of the mean ST-segment vector can distinguish electrocardiographically between myocardial infarction at these 2 sites.33 There has also been some discussion about right ventricular infarctions giving rise to an epsilon wave. However, because of the low voltage of this wave, low sensitivity, and low specificity, this electrocardiographic feature is of little value in daily practice.34
  • Hemodynamic monitoring
    • Disproportionate elevation of right-sided filling pressures when compared with left-sided hemodynamics represents the hallmark of right ventricular infarction.
    • Accepted hemodynamic criteria for right ventricular infarction include right atrial pressure greater than 10 mm Hg, right atrial–to–pulmonary capillary wedge pressure ratio greater than 0.8, or right atrial pressure within 5 mm Hg of the pulmonary capillary wedge pressure. These values may manifest only after volume loading.35
    • In the setting of right ventricular infarction, pulmonary capillary wedge pressure may be misleading and not accurately reflect left ventricular end-diastolic volume but rather impaired left ventricular filling due to bowing of the interventricular septum into the left ventricle.36
    • Other interesting hemodynamic features of right ventricular infarction include the following:
      • Prominent y descent of the right atrial pressure
      • Increase in venous or right atrial pressure with inspiration (ie, Kussmaul sign)
      • Exaggeration of the normal inspiratory decline in systemic arterial pressure (ie, pulsus paradoxus)
      • Elevation of right ventricular filling pressure with early diastolic dip and plateau
  • Some of these hemodynamic derangements superficially resemble those of restrictive or constrictive physiology.

Treatment

Medical Care

Right ventricular infarction should always be considered in any patient who has inferior wall myocardial infarction and associated hypotension, especially in the absence of rales.

RV failure may limit filling via a decrease in CO, ventricular interdependence, or both. Treatment of patients with RV dysfunction and shock has traditionally focused on ensuring adequate right-sided filling pressures to maintain CO and adequate LV preload; however, patients with cardiogenic shock due to RV dysfunction have very high RV end-diastolic pressure, often greater than 20 mm Hg. This elevation of RV end-diastolic pressure may result in shifting of the interventricular septum toward the LV cavity, which raises left atrial pressure but impairs LV filling due to the mechanical effect of the septum bowing into the LV. This alteration in geometry also impairs LV systolic function. Therefore, the common practice of aggressive fluid resuscitation for RV dysfunction in shock may be misguided. Excess volume loading in patients with RV infarction may also cause or contribute to cardiogenic shock.

Inotropic therapy is indicated for RV failure when cardiogenic shock persists after RV end-diastolic pressure has been optimized.37 Inotropes should be used until more data is available. RV end-diastolic pressure of 10-15 mm Hg has been associated with higher output than lower or higher pressures, but marked variability exists in optimal values. 
 
If hypotension persists, consider hemodynamic monitoring with a pulmonary artery catheter, keeping in mind the following admonitions concerning right ventricular perforation. 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.
 
Concomitant left ventricular dysfunction may necessitate use of an intraaortic balloon pump and/or nitroprusside infusion for afterload reduction.
 
Because of the critical roles of atrioventricular synchrony and atrial transport in maintaining cardiac output, atrioventricular sequential pacing is the modality of choice when a pacemaker is required.38
 
Achieving early reperfusion: Current available evidence indicates that patients presenting within 6 hours of onset of inferior wall myocardial infarction with right ventricular involvement diagnosed by ECG or other noninvasive criteria have a definite early survival benefit from thrombolytic therapy or coronary angioplasty.39,40 Scant data exist regarding improvement in patients who present later than 12 hours after onset, and these patients most likely would do well with a conservative management strategy, considering the often spontaneous resolution of right ventricular dysfunction.41
 
Recently, the use of inhaled nitric oxide has been of interest to treat patients with RV infarctions complicated by cardiogenic shock. The principle behind this experimental treatment is that by specifically decreasing pulmonary vascular resistance without compromising systemic vascular resistance, the filling of the left ventricle can be improved with a resultant improvement of systemic cardiac output. Utilization of inhaled nitric oxide in this setting has been associated with rapid improvement of hemodynamics.42

Surgical Care

Severe tricuspid regurgitation in the setting of acute right ventricular infarction can be managed with either valve replacement or repair with angioplasty rings, because the incompetent valve may serve as a mechanical impediment to maintenance of adequate cardiac output. Finally, should a patient develop arterial hypoxemia secondary to right-to-left shunting at the atrial level, then an atrial septal defect–occluding device should be considered immediately. However, if for any reason, a delay occurs in placement of the occluding device, inhaled nitric oxide can decrease the right-to-left shunting and increase systemic oxygenation.42 Pericardiectomy has been used in extreme cases.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Cardiovascular agents

Dobutamine is an inotropic agent used to improve right ventricular contractility and maintain cardiac output. Sodium nitroprusside reduces afterload.


Dobutamine (Dobutrex)

Produces vasodilation and increases inotropic state. At higher dosages, may cause increased heart rate, exacerbating myocardial ischemia.

Dosing

Adult

0.5 mcg/kg/min IV initial; titrate until desired effect attained

Pediatric

Administer as in adults

Interactions

Beta-adrenergic blockers antagonize effects; general anesthetics may increase toxicity

Contraindications

Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis; atrial fibrillation or flutter

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution following MI; hypovolemic state should be corrected before using


Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of heart. At higher doses, may exacerbate myocardial ischemia by increasing heart rate. Infusion rates >10 mcg/kg/min may lead to cyanide toxicity.

Dosing

Adult

0.3-0.5 mcg/kg/min IV initial infusion; use 0.5 mcg/kg/min increments and titrate to desired effect; average dose is 1-6 mcg/kg/min

Pediatric

Administer as in adults

Interactions

Coadministration with other hypotensive agents may have additive effects

Contraindications

Documented hypersensitivity; subaortic stenosis; idiopathic hypertrophic subaortic stenosis; decreased cerebral perfusion; arteriovenous shunt or coarctation of aorta (eg, compensatory hypertension); atrial fibrillation or flutter

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside has ability to lower blood pressure and should be used only in patients with mean arterial pressures >70 mm Hg

Tissue plasminogen activators

These agents bind to fibrin and convert plasminogen to plasmin, which in turn initiates local fibrinolysis with limited systemic proteolysis.


Alteplase (Activase)

Tissue plasminogen activator (t-PA) used in management of acute myocardial infarction, acute ischemic stroke, and pulmonary embolism. May administer heparin or aspirin with and after alteplase infusions to reduce risk of rethrombosis. Safety and efficacy of concomitant administration of heparin or aspirin during first 24 h after symptom onset have not been investigated.

Dosing

Adult

0.9 mg/kg (not to exceed 90 mg) IV infusion over 60 min with 10% of total dose administered as initial IV bolus over 1 min

Pediatric

Not established

Interactions

Anticoagulants and antiplatelets may increase risk of bleeding; heparin with and after alteplase infusions reduces risk of rethrombosis—either heparin or alteplase may cause bleeding complications

Contraindications

Documented hypersensitivity; active internal bleeding; cerebrovascular accident or stroke within last 2 mo; intracranial or intraspinal surgery or trauma; intracranial hemorrhage on pretreatment evaluation; suspicion of subarachnoid hemorrhage; intracranial neoplasm; arteriovenous malformation or aneurysm; bleeding diathesis; severe uncontrolled hypertension

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following alteplase administration (when managing acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH

Miscellaneous

Medicolegal Pitfalls

Most litigation involving right ventricular infarction, as with myocardial infarction as a whole, involves missing the diagnosis rather than specific errors in treating the condition. In fact, more malpractice awards are for this reason than for any other diagnosis and usually involve emergency physicians, since they are involved in the initial evaluation of the patient seeking treatment for chest pain. Moreover, claims also arise from not providing appropriate therapy in a timely manner, which has increased in importance because of time-sensitive therapies that have become the standard of care.

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Keywords

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

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

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Rex C Liu, MD to the development and writing of this article.

Further Reading

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