05. Right Ventricular (RV) Myocardial Infarction

Definition/Etiology 

  • Right ventricular myocardial infarction (RVMI) is usually caused by proximal occlusion of the right coronary artery (RCA). This limits blood flow to the RV marginal branches, which are the primary blood supply to right ventricle.
  • RVMI complicates 30-50% of inferior STEMIs and is associated with higher mortality compared to a similar infarction territory involving the left ventricle alone.

Pathophysiology 

  • The spectrum of disease seen in RVMI depends on the extent and territory of both the RV infarction and LV infarction.
  • Hemodynamic effects:
    • An ischemic RV can become dilated and stiff with decreased RV output, which can impair LV preload, resulting in decreased cardiac output.
    • An ischemic RA can reduce RV filling.
    • RV infarction is almost always accompanied by LV infarction given that a proximal RCA occlusion in a right-dominant coronary system will affect the PDA, and subsequent LV dysfunction can further reduce cardiac output.
  • Arrhythmic complications:
    • The SA nodal artery arises from the RCA, and the AV node is partially supplied by the RCA. Therefore, these patients can present with bradycardia and/or AV nodal block.
  • Mechanical complications:
    • Tricuspid regurgitation can result from papillary muscle rupture or dilation of the tricuspid annulus.
    • Ventricular septal rupture can occur as a result of ischemia to the interventricular septum.

Evaluation 

  • Physical exam: elevated JVP, hypotension, and clear lungs. This constellation of findings indicates RV failure and may also occur in pulmonary embolism and cardiac tamponade.
  • ECG: 1mm ST elevation in V4R is sensitive (88%) and specific (78%). Other causes of elevations in right sided EKG leads include pulmonary embolism, pericarditis, and antero-septal MI.
    • Consider RV infarction in inferior STEMI and obtain right-sided ECG leads to understand the extent and distribution of infarction.
  • Echo: useful for evaluating wall motion abnormalities and tricuspid valve function.

Management 

  • In general, management of RVMI is similar to management of STE-ACS (including dual antiplatelet therapy, statin therapy, anticoagulation, and reperfusion).
  • Given the decreased LV preload in RVMI, gentle IV fluids (i.e. 250 mL aliquots) can be considered if the JVP is low or normal to achieve a JVP between 10-12 cm. However, in patients with elevated JVP or other evidence of right heart failure, additional volume loading can worsen RV output by pushing the RV further off its Frank-Starling curve. Fluids should be administered ONLY in the aforementioned setting. Multiple liters of fluid are almost never indicated and can be detrimental.
  • Drugs that decrease preload (e.g. nitrates, diuretics, opioids) should generally be avoided.
  • Drugs that decrease heart rate, AV conduction, and contractility (e.g. beta-blockers and calcium channel blockers) should be used with caution in hemodynamically stable patients and avoided in hemodynamically unstable patients.
  • Cardiogenic shock should be managed per the standard algorithm (see section Cardiogenic Shock). Note that right-sided mechanical circulatory support devices are experimental at this time and should be used in conjunction with experts at the institution.
  • Transcutaneous pacer pads should be applied and atropine should be at the bedside in case of unstable bradyarrhythmia or AV block.
  • While RVMI increases short-term morbidity and mortality, emergent PCI significantly improves outcomes, and over the long-term, many have near-complete recovery of RV function.

References 

Haji SA, Movahed A.  Right ventricular infarction--diagnosis and treatment. Clin Cardiol. 2000 Jul;23(7):473-82.

O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. Journal of the American College of Cardiology. 2013;61(4):e78-e140. doi:10.1016/j.jacc.2012.11.019

Zehender, M, Kasper, W, Kauder, E, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993; 328:981.