LV volumes and ejection fraction

LVEDV, LVESV, LVEF · Biplane method of discs (modified Simpson) from non-foreshortened apical 4- and 2-chamber views

Normal range & thresholds

Pathophysiology

Raised by

• LVEDV ↑: chronic AR, chronic primary MR, shunts, DCM, ischaemic remodelling, endurance athlete, bradycardia, high-output states
• LVESV ↑: any cause of reduced contractility, plus pressure overload — the earliest volume signal of true systolic failure
• LVEF apparently ↑: severe MR, hyperdynamic sepsis/anaemia/thyrotoxicosis, HCM, small hypercontractile ventricle, dobutamine

Lowered by

• LVEDV ↓: hypovolaemia, tamponade, constriction, restrictive/infiltrative disease, severe MS, HCM, severe RV pressure overload
• LVEF ↓: ischaemic and non-ischaemic cardiomyopathy, myocarditis, cardiotoxic chemotherapy, tachycardia-induced, stress (takotsubo), sepsis, thyroid disease, alcohol, sustained arrhythmia, afterload mismatch in severe hypertension or aortic stenosis
• Dyssynchrony (LBBB, RV pacing) — a mechanical, partly reversible cause

Technique & pitfalls

• Use a non-foreshortened apex: the commonest single error in all of echocardiography, and it under-measures volumes while over-measuring ejection fraction.
• Trace the blood–tissue interface, excluding papillary muscles and trabeculae, at end-diastole (largest) and end-systole (smallest).
• Use ultrasound-enhancing agent whenever two or more contiguous segments are not seen — class I practice, not a luxury.^[17,27]
• Report the method (2D biplane / contrast / 3D) in the report line; a change of method looks exactly like a change of patient.
• Teichholz and fractional shortening are invalid whenever wall motion is regional; they extrapolate a whole ventricle from one basal chord.^[1,42]
• In AF, average at least 5 consecutive cycles, or use beats with comparable preceding RR intervals.

Pseudo-change & artefact

• Foreshortening (→ falsely high LVEF), endocardial dropout, and inclusion of trabeculae.
• Contrast studies give volumes 10–20% larger — a ‘deterioration’ that is pure method.
• Load: acute afterload reduction raises LVEF; hypovolaemia lowers volumes and can raise LVEF.
• Heart rate and rhythm, post-extrasystolic potentiation, and the beat chosen in AF.
• Inter-observer variability of LVEF by 2D echo is ±5–8 percentage points — larger than several guideline thresholds, which is the main argument for adding strain or CMR near a decision point.
• Eyeballed ‘visual EF’ reported as a number without tracing.

Treatment thresholds

• LVEF ≤40% → full guideline-directed medical therapy for HFrEF (class I): ARNI/ACEi, beta-blocker, MRA, SGLT2 inhibitor.^[11,12]
• LVEF ≤35% after ≥3 months of optimal therapy, NYHA II–III, expected survival >1 year → primary-prevention ICD (class I in ischaemic, class I–IIa in non-ischaemic).^[11,38]
• LVEF ≤35% + sinus rhythm + LBBB ≥150 ms → CRT (class I).^[39]
• Aortic stenosis: severe AS with LVEF <50% → AVR (class I) regardless of symptoms — and even an ejection fraction in the 50–60% range carries excess mortality in severe AS;^[85] low-flow low-gradient AS is defined by stroke volume index <35 mL/m².^[5,6,7]
• Aortic regurgitation: LVEF ≤55% (2025 ESC/EACTS) or ≤50–55% (ACC/AHA), or LVESVi >45 mL/m², → surgery in asymptomatic severe AR.^[6,7]
• Primary MR: LVEF ≤60% → surgery (class I) — the deliberately ‘high’ threshold, because a normal-looking EF is already abnormal when the ventricle empties into the left atrium.^[6,7]
• Secondary MR: COAPT-like anatomy with LVEF 20–50% and persistent symptoms on GDMT → TEER (class I, 2025 ESC/EACTS).^[6,64]
• Cardio-oncology: LVEF fall ≥10 points to <50% = cancer-therapy-related cardiac dysfunction → cardioprotection and multidisciplinary review.^[15]

Next step

• Next: repeat with an ultrasound-enhancing agent if any doubt; add GLS in the same sitting.
• Then: CMR for the reference-standard volumes, scar burden and aetiology — particularly when the decision is an ICD or when echo and clinical picture disagree.
• Then: ischaemia/viability assessment (stress echo, perfusion CMR, coronary angiography) in any newly reduced LVEF; then rhythm review (rate control, PVC burden >10%, dyssynchrony).
• Then: re-image at 3 months of optimal therapy before committing to device therapy — a substantial minority recover above the threshold.

Drugs

• Improve LVEF / reduce volumes: ARNI (PROVE-HF: LVEF +9.4 points, LVEDVi −7.9 mL/m² at 12 months)^[68]; SGLT2 inhibitors (EMPA-TROPISM: LVEF +6.0 points, LVESV −26.6 mL at 6 months)^[69]; beta-blockers; MRAs; CRT in dyssynchrony.
• Reduce LVEF: anthracyclines, trastuzumab, immune-checkpoint inhibitors, VEGF and proteasome inhibitors, high-dose alcohol, cocaine/amphetamines, some tyrosine-kinase inhibitors, chronic non-dihydropyridine calcium blockers in decompensated HFrEF.^[15]
• Transiently raise LVEF without improving outcome: inotropes — do not mistake a dobutamine ejection fraction for recovery.

Reversibility