Right ventricular infarction

Reviewed and revised 10 June 2014


  • Suspect in all patients with inferior STEMI
  • Right ventricular infarction complicates up to 40% of inferior STEMIs
  • Isolated RV infarction is extremely uncommon
  • cardiac MRI studies indicate that a significant minority of anterior MIs have RV involvement as well


  • typically results from acute coronary syndrome, involving the right coronary artery
  • proximal lesions mayinvolve the right atrial branch, with the loss of augmented right atrial contraction
  • may result from systemic hypotension
  • so-called ‘RV infarction’ often does not progress to Q wave infarction because of greater resistance to ischemia than the LV:
    • pulmonary circulation is approximately one-tenth the length of systemic circulation, and a 5-mmHg perfusion gradient is sufficient
    • the thin RV free wall allows the biphasic perfusion of coronary blood, with approximately equal contributions during systole and diastole
    • right ventricle has rich collaterals from the left anterior descending artery in addition to right coronary artery (RCA) blood flow
  • may be mimicked by a ‘stunned’ or ‘hibernating’ RV


Classically presents with:

  • ischaemic chest pain
  • bradycardia
  • hypotension
  • clear lungs
  • distended neck veins and Kussmaul sign may be present


  • ventricular septal rupture
  • hypoxemia from right-to-left shunting
  • hypotension from ventricular interdependence
  • high-grade atrioventricular block
  • vagal nerve-mediated bradycardia
  • ventricular tachycardia


ECG findings (may be transient, 50% resolve by 10 hours)

  • ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle
  • ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle
  • ST elevation in V1 > the magnitude of ST elevation in V2; combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI
  • ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed
  • confirmed by ST elevation in right-sided chest leads (V3R-V6R) — V4R is usually sufficient because ST elevation in V4R has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83%


  • cardiac biomarkers (e.g. troponin)


  • evidence of RV dysfunction, regional wall abnormalities, exclude other causes
  • technically challenging as RV cannot be completely visualized in any single 2D view


  • cardiac MRI and 3D echo are emerging modalities


  • call Code STEMI if appropriate
  • attend to ABCs
  • Oxygenate to SpO2 94-98%
  • Analgesia
  • Avoid nitrates (preload sensitive)
  • IV fluid boluses for hypotension if estimated CVP <15 mmHg (avoid fluid excess, the dilated RV may impair LV function due to ventricular interdependence)
  • maintenance of an adequate heart rate and atrioventricular synchrony
  • early revascularisation (transfer to cath lab or thrombolysis)
  • refractory cases should be treated as for other other causes of RV failure


  • From the thrombolytic era:
    • inferior MI 6.3% mortality
    • inferior MI + RV infarction 17% mortality, addition of RV mortality has a RR of 2.6
  • late revascularization is associated with higher RV dysfunction and complications


Journal articles

  • Inohara T, Kohsaka S, Fukuda K, Menon V. The challenges in the management of right ventricular infarction. Eur Heart J Acute Cardiovasc Care. 2013 Sep;2(3):226-34. PMC3821821.


CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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