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Right Ventricular Infarction Workup

  • Author: Claudia Dima, MD, FACC; Chief Editor: Eric H Yang, MD  more...
Updated: Nov 22, 2015

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,[26] but, because of logistical issues, it is rarely used for critically ill patients.[27]

Yaylak et al reported that a high neutrophil-lymphocyte ratio (NLR) is an independent predictor of right ventricular dysfunction in patients with acute inferior ST elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI).[28]

For more information, see Imaging in Myocardial Infarction.



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.[29]

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.[30]

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.[31]

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.[32]


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]

Tomala et al suggest that the angiographic result of index primary percutaneous coronary intervention (PCI) determines the presence of right ventricular (RV) infarction in patients with acute inferior myocardial infarction (MI).[26] In a multivariate regression analysis, thrombolysis in MI (TIMI) flow score below 2 in at least one RV branch after PCI was an independent angiographic predictor of RVMI, and TIMI flow below 3 in at least one RV branch before PCI was an independent angiographic predictor of ST-segment elevation of at least 1 mm in V4R. The only predictor of RVMI was TIMI flow less than 2 in at least one RV branch after PCI.[26]



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, 33] 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.[34]

Table. Sensitivity and Specificity of More Than 1 mm of ST-Segment Elevation in V1, V3 R, and V4 R (Open Table in a new window)

Leads Sensitivity (%) Specificity (%)
V1 28 92
V3 R 69 97
V4 R 93 95

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.[35, 36] 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.[37]


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.[38]

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.[39]

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.

Contributor Information and Disclosures

Claudia Dima, MD, FACC Interventional Cardiology

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

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, Massachusetts Medical Society

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.

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

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

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

Disclosure: Nothing to disclose.

Additional Contributors

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, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.


The authors and editors of Medscape Drugs & Diseases 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 V 1, V 3 R, and V 4 R
Leads Sensitivity (%) Specificity (%)
V1 28 92
V3 R 69 97
V4 R 93 95
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