Ventricular–arterial coupling

Ea/Ees · Ratio of cards 48 and 49; with V₀ = 0 it equals ESV/SV

Normal range & thresholds

Optimal ≈0.5–1.0. Mechanical efficiency is maximal near 0.5 and stroke work near 1.0; values >1.0 indicate uncoupling ^[157].

Pathophysiology

Coupling describes whether the ventricle and arteries are matched: when arterial load exceeds ventricular elastance, energy is spent on pressure rather than flow, SV becomes afterload-sensitive and efficiency falls. Reduced coupling tracks adverse remodelling and outcome in chronic heart failure ^[156] and mortality in the cardiac ICU ^[192].

Raised by

• HFrEF (low Ees), severe hypertension with poor contractility, advanced AS with LV dysfunction

Lowered by

• Hyperdynamic states, vasodilation, regurgitant runoff; athletes

Technique & pitfalls

• Prefer single-beat Ees; report the method; interpret serially.

Pseudo-change & artefact

• The EF identity above; any volume or pressure error.

Treatment thresholds

No threshold defines therapy; the physiology supports afterload reduction in uncoupled HFrEF (GDMT) and BP control in HFpEF ^[11,12,157].

Next step

• Look for the dominant term: high Ea (arteries) or low Ees (ventricle).

Drugs

ARNI, RAAS blockade, SGLT2 inhibitors and vasodilators lower Ea; inotropes raise Ees.

Reversibility

Improves with reverse remodelling over months on GDMT.