Right Ventricular Infarction Treatment & Management

  • Author: Claudia Dima, MD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Mar 29, 2011
 

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]

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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]

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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]

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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.

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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]

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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]

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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]

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Contributor Information and Disclosures
Author

Claudia Dima, MD  Fellow in Interventional Cardiology, Department of Cardiology, Banner Good Samaritan Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

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

Disclosure: Nothing to disclose.

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.

Specialty Editor Board

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.

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 Interventional Cardiology Fellowship Program, Henry Ford Hospital

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

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

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Table. Sensitivity and Specificity of More Than 1 mm of ST-Segment Elevation in V1, V3 R, and V4 R
Leads Sensitivity (%) Specificity (%)
V12892
V3 R6997
V4 R9395
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