Right ventricular myocardium
Fascicles, Purkinje, muscle
Thin-walled crescentic chamber activated through the right bundle and moderator band slightly after the septum and LV apex. Its small mass contributes little to the normal QRS, so RV disease is inferred from axis, V1 morphology and repolarisation rather than voltage.
Traced from the start
Detail
- Activation
- RV free wall and outflow tract are among the last regions to depolarise; the RVOT and posterobasal LV end the QRS
- Arterial supply
- RCA (acute marginal branches) for the free wall; LAD for the anterior RV and apex
- Action potential
- RV epicardium has the largest transient outward K+ current (Ito), the substrate for Brugada and J-wave patterns in V1–V3
When it goes wrong
Loss-of-function SCN5A sodium-channel mutation reducing RVOT epicardial depolarisation (Brugada syndrome)
Coved ST elevation of 2 mm or more with inverted T in V1–V2 (type 1), unmasked by fever, flecainide or ajmaline; polymorphic VT/VF during sleep in young men; an ICD is the only proven therapy
Desmosomal mutation (plakophilin-2) with fibrofatty replacement of the RV free wall (arrhythmogenic RV cardiomyopathy)
Epsilon wave and T inversion in V1–V3, LBBB-morphology VT with exercise, sudden death in young athletes
Acute RV pressure load from massive pulmonary embolism
S1Q3T3, new RBBB, T inversion V1–V4, right axis deviation and sinus tachycardia
RV infarction from proximal RCA occlusion with inferior MI
ST elevation in V4R, hypotension with clear lungs and a raised JVP; preload-dependent — give fluids, avoid nitrates
Practise this structure
1 question in the bank tagged Cardiac Muscle.