Right Ventricular Infarction

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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]

For more information, see Myocardial Infarction.

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 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 if 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, 10] In general, any major reduction in blood supply to the right ventricular free wall portends an adverse prognosis in association with this disorder.

Epidemiology

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.[11]

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.[12, 13, 10, 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 are 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]

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,[21] 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.[22, 23] 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.[24]

Physical Examination

The classic clinical triad of right ventricular infarction includes distended neck veins, clear lung fields, and hypotension.[25]

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.

Approach Considerations

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. Cardiac MRI is the most sensitive method to assess right ventricular function, but, because of logistical issues, it is rarely used for critically ill patients.[30]

For more information, see Imaging in Myocardial Infarction.

Echocardiography

Echocardiography is useful as a modality to rule out pericardial disease and tamponade, which are the major disorders in the differential diagnosis of 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.[21]

Echocardiography can detect shunting through a patent foramen ovale. It has a sensitivity of 82% and a specificity of 93% in detecting right ventricular infarction when right ventricular scintigraphy is used as the comparative standard.[26]

In the vast majority of patients with right ventricular infarction, the wall motion abnormalities that are initially manifested on echocardiography reverse themselves within 3 months.[27]

The use of tissue Doppler 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.[28]

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 or greater suggests the presence of a right ventricular infarction.[29]

Angiography and Scintigraphy

Gated equilibrium radionuclide angiography and technetium-99m pyrophosphate scintigraphy are useful in diagnosing right ventricular infarction noninvasively.[24] 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.[6, 14]

Electrocardiography

All patients with inferior wall myocardial infarction should have a right-sided ECG. ST-segment elevation in lead V4 R 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.[2, 7, 16, 31] The ST-segment elevation is transient, disappearing in less than 10 hours following its onset in half of patients. The table below demonstrates the sensitivity and specificity of more than 1 mm of ST-segment elevation in V1, V3 R, and V4 R.[32]

Table. Sensitivity and Specificity of More Than 1 mm of ST-Segment Elevation in V1, V3 R, and V4 R


View Table

See Table

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.[33, 34] 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.[21] 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.[35]

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.[36]

In the setting of right ventricular infarction, pulmonary capillary wedge pressure may be misleading and may 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.[37]

Other interesting hemodynamic features of right ventricular infarction include the following:

Some of these hemodynamic derangements superficially resemble those of restrictive or constrictive physiology.

Approach Considerations

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. In patients with right ventricular dysfunction and shock, the focus is on ensuring adequate right-sided filling pressures. If cardiogenic shock persists after optimization of right ventricular end-diastolic pressure, inotropic therapy should be instituted.

Concomitant left ventricular dysfunction may necessitate use of an intra-aortic balloon pump and/or nitroprusside infusion for afterload reduction.

Because of the critical role of atrioventricular synchrony and atrial transport in maintaining cardiac output, atrioventricular sequential pacing is the modality of choice when a pacemaker is required.[39]

Right Ventricular Dysfunction and Shock

Right ventricular failure may limit filling via a decrease in CO, ventricular interdependence, or both. Treatment of patients with right ventricular dysfunction and shock has traditionally focused on ensuring adequate right-sided filling pressures to maintain CO and adequate left ventricular preload; however, patients with cardiogenic shock due to right ventricular dysfunction have very high right ventricular end-diastolic pressure, often greater than 20 mm Hg.

This elevation of right ventricular end-diastolic pressure may result in shifting of the interventricular septum toward the left ventricular cavity, which raises left atrial pressure but impairs left ventricular filling due to the mechanical effect of the septum bowing into the left ventricle. This alteration in geometry also impairs left ventricular systolic function. Therefore, the common practice of aggressive fluid resuscitation for right ventricular dysfunction in shock may be misguided.[17] Careful administration of fluid boluses, used in conjunction with noninvasive or invasive assessment of cardiac output, is recommended (500-1000 mL); no further volume challenge is needed if no effect.[30]

Inotropic Therapy in Cardiogenic Shock

Inotropic therapy is indicated for right ventricular failure when cardiogenic shock persists after right ventricular end-diastolic pressure has been optimized.[38, 30] Inotropes should be used until more data are available. Right ventricular 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.

Inotropes that can be used in right ventricular failure are dobutamine, milrinone, levosimendan (approved only in Europe), norepinephrine, and, possibly, low-dose vasopressin. Avoid dopamine and phenylephrine. Consider combination therapy with inhaled nitric oxide.[30]

Hemodynamic Monitoring

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.

Early Treatment Survival Benefit

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.[9, 10, 32, 33, 40, 41] 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.[42]

Inhaled Nitric Oxide

The use of inhaled nitric oxide has been of interest to treat patients with right ventricular infarctions complicated by cardiogenic shock. The principle behind this 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.[43] The combination of inhaled nitric oxide with dobutamine is best supported by current evidence in the treatment of acute right ventricular failure.[30]

Beta-blocking agents and angiotensin-converting enzyme inhibitors improve right ventricular hemodynamics in patients with biventricular failure and have theoretical benefits in isolated right ventricular failure, but their role in the latter is poorly studied.[30]

Valve Replacement and Repair

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.[43]

Mechanical circulatory support can be also used, including a left ventricular assist device (LVAD), right ventricular assist device (RVAD), or biventricular ventricular assist device.[30]

Medication Summary

The goals of pharmacotherapy for right ventricular infarction are to reduce morbidity and prevent complications. Agents included in treatment are cardiovascular agents such as dobutamine and tissue plasminogen activators such as alteplase.[4, 8]

In addition, agents such as levosimendan (Simdax), a calcium sensitizer, have been developed for hospitalized patients with acutely decompensated heart failure. Levosimendan is not available in the United States and is only approved in Europe.

Dobutamine (Dobutrex)

Clinical Context:  Dobutamine produces vasodilation and increases the inotropic state. At higher dosages, this agent may cause increased heart rate, exacerbating myocardial ischemia.

Milrinone

Clinical Context:  Milrinone is a bi-pyridine positive inotrope and vasodilator with little chronotropic activity. It is different in mode of action from both digitalis glycosides and catecholamines. It selectively inhibits phosphodiesterase type III (PDE III) in cardiac and smooth vascular muscle, resulting in reduced afterload, reduced preload, and increased inotropy.

Class Summary

Inotropic therapy is indicated for right ventricular failure when cardiogenic shock persists after right ventricular end-diastolic pressure has been optimized. Inotropes should be used until more data are available. Dobutamine is an inotropic agent used to improve right ventricular contractility and maintain cardiac output.

Alteplase (Activase)

Clinical Context:  Alteplase is a tissue plasminogen activator used in the management of acute myocardial infarction, acute ischemic stroke, and pulmonary embolism. Heparin or aspirin may be administered with and after alteplase infusions to reduce the risk of rethrombosis. The safety and efficacy of concomitant administration of heparin or aspirin during the first 24 hours after symptom onset have not been investigated.

Reteplase (Retavase)

Clinical Context:  Reteplase is a recombinant plasminogen activator that forms plasmin after facilitating cleavage of endogenous plasminogen. It is used in the management of acute myocardial infarction. Heparin or aspirin may be administered with and after reteplase infusions.

Class Summary

Tissue plasminogen activators bind to fibrin and convert plasminogen to plasmin, which in turn initiates local fibrinolysis with limited systemic proteolysis. Thrombolytic therapy may contribute to an early survival benefit in patients presenting within 6 hours of onset of onset of inferior wall myocardial infarction with right ventricular involvement diagnosed by ECG or other noninvasive criteria.

Norepinephrine (Levophed)

Clinical Context:  Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. It increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia.

Class Summary

Adrenergic agonists stimulate beta- and alpha-adrenergic receptors, causing increased contractility and heart rate, as well as vasoconstriction. These actions increase systemic blood pressure and coronary blood flow.

Vasopressin (Pitressin)

Clinical Context:  Vasopressin increases water resorption at the distal renal tubular epithelium (ADH effect). It promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). Vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

Class Summary

Antidiuretic hormone analogs increase cyclic adenosine monophosphate (cAMP), increasing water permeability at the renal tubules. An example of this analog is vasopressin, which is a direct vasoconstrictor without inotropic or chronotropic effects.

Author

Claudia Dima, MD, FACC, Interventional Cardiology

Disclosure: Nothing to disclose.

Coauthor(s)

Ashish Pershad, MD, Consulting Staff, Heart and Vascular Center of Arizona

Disclosure: Nothing to disclose.

David L Coven, MD, PhD, Assistant Professor of Clinical Medicine, Columbia University College of Physicians and Surgeons; Director, Cardiology Outpatient Clinic, St Luke's Site, Attending Physician, Department of Medicine, Division of Cardiology, St Luke's-Roosevelt Hospital Center

Disclosure: Nothing to disclose.

Kenneth B Desser, MD, Clinical Professor, Director of Cardiology Fellowship, Banner Good Samaritan Medical Center, Phoenix, Arizona

Disclosure: Nothing to disclose.

Specialty Editors

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

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Chief Editor

Eric H Yang, MD, Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona

Disclosure: Nothing to disclose.

Additional Contributors

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

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Leads Sensitivity (%) Specificity (%)
V12892
V3 R6997
V4 R9395