Right ventricular infarction

Reviewed and revised 10 June 2014

OVERVIEW

• 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

PATHOPHYSIOLOGY

• 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

CLINICAL FEATURES

Classically presents with:

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

Complications

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

INVESTIGATIONS

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%

Laboratory

• cardiac biomarkers (e.g. troponin)

Echocardiography

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

Other

• cardiac MRI and 3D echo are emerging modalities

MANAGEMENT

• 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

PROGNOSIS

• 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

References and links

LITFL

• CCC – Right ventricular failure
• ECG Library – Inferior STEMI
• ECG Library – Right ventricular infarction

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.

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