Right ventricular fractional area change

FAC · RV-focused apical 4-chamber; trace RV endocardium at end-diastole and end-systole, including trabeculae and moderator band

Normal range & thresholds

Pathophysiology

Raised by

• Hyperdynamic circulation, sepsis, anaemia, thyrotoxicosis
• Severe tricuspid regurgitation (large area change with a low forward output — falsely reassuring)
• Inotropes; exercise

Lowered by

• Pulmonary hypertension and chronic pressure overload
• RV infarction, myocarditis, sarcoid, amyloid, ARVC
• Acute pulmonary embolism (typically with apical sparing — the McConnell pattern)
• Chronic lung disease, ARDS, positive-pressure ventilation
• Advanced left heart failure; post-LVAD RV failure
• Sepsis-associated RV dysfunction

Technique & pitfalls

• Trace the endocardium from the tricuspid annulus, along the free wall to the apex, back along the interventricular septum to the annulus, and close across the annular plane.
• Include the trabeculations and the moderator band inside the cavity trace — the 2025 guideline is explicit, and excluding them lowers FAC artefactually.^[3]
• Use the RV-focused view; a foreshortened or LV-optimised view distorts both areas.
• End-diastole is the largest area, end-systole the smallest.
• Report FAC alongside TAPSE, S′ and strain; discordance is common and clinically meaningful.
• Poor free-wall endocardial definition is the practical limitation — consider contrast or move to strain or 3D.

Pseudo-change & artefact

• Endocardial dropout in the RV free wall — the most frequent technical problem.
• Foreshortening; off-axis planes.
• Excluding trabeculae from the trace (falsely low) or tracing epicardially (falsely high).
• Severe TR raising the area change without improving forward flow.
• Load dependence: falls with hypovolaemia and with positive-pressure ventilation.
• Arrhythmia and cycle-to-cycle variation — average multiple beats in AF.
• Blindness to RVOT dysfunction, as above.

Treatment thresholds

• Tricuspid regurgitation intervention: FAC contributes, with TAPSE and free-wall strain, to defining the severe RV dysfunction that excludes a patient from transcatheter tricuspid therapy in the 2025 ESC/EACTS guidelines.^[6]
• Pulmonary hypertension: RV function is a core element of the multiparametric risk table that determines initial dual versus triple therapy and the timing of referral for transplantation.^[8]
• Acute pulmonary embolism: RV dysfunction defines intermediate risk and drives the decision to monitor rather than discharge, and to reperfuse if deterioration occurs.^[8]
• LVAD candidacy: a low FAC predicts post-implant right heart failure and may lead to planned biventricular support.^[11]
• No isolated FAC value triggers therapy by itself.

Next step

• Next: RV free-wall longitudinal strain — more sensitive, more reproducible and more prognostic than FAC, and abnormal earlier.
• Then: 3D RV ejection fraction where available (normal ≥45%), which includes the outflow tract.
• Then: CMR for the reference-standard RV ejection fraction and for tissue characterisation.
• Then: pursue the cause — pulmonary pressures and PVR, thromboembolic imaging, right heart catheterisation, ARVC evaluation with the Task Force criteria.

Drugs

• Same as for TAPSE: the therapy is directed at the load and at the underlying disease, not at the number.
• Pulmonary vasodilators in group 1 disease and in operated CTEPH; diuretics for congestion; revascularisation for RV infarction.^[8]
• Positive-pressure ventilation and high PEEP reduce FAC — a management effect, not a disease effect.
• Inotropes (dobutamine, milrinone, levosimendan) raise it acutely in decompensated right heart failure.

Reversibility