Mean pulmonary artery pressure

mean PAP · Estimated, not measured — from the pulmonary regurgitation early diastolic jet, from PAAT, or from SPAP

Normal range & thresholds

Normal ≤20 mmHg (invasively). Pulmonary hypertension is defined by mean PAP >20 mmHg at rest by right heart catheterisation, with precapillary disease requiring in addition a wedge pressure ≤15 mmHg and PVR >2 Wood units — both thresholds lowered by the 2022 ESC/ERS guidelines.^[8]
Echocardiographic estimates (all approximations):

From pulmonary regurgitation: mPAP = 4 × (early diastolic PR velocity)² + estimated RA pressure
From SPAP (Chemla): mPAP ≈ 0.61 × SPAP + 2 mmHg^[48]
From acceleration time (Mahan): mPAP ≈ 79 − (0.45 × PAAT)^[47]

End-diastolic PR velocity similarly estimates pulmonary artery diastolic pressure.

Pathophysiology

Mean pulmonary artery pressure is the product of flow and resistance plus the downstream (left atrial) pressure: mPAP = (cardiac output × PVR) + PAWP. All three terms are independent, and the same mean pressure can arise from a high flow with a normal vasculature, a normal flow with a remodelled vasculature, or a normal vasculature draining into a hypertensive left atrium. Because echocardiography cannot separate these terms, no echocardiographic estimate of mean PAP can establish the diagnosis or the group — it can only raise or lower the probability.^[8]

Raised by

The same five groups as for SPAP — left heart disease (much the commonest), lung disease and hypoxia, chronic thromboembolic disease, pulmonary arterial hypertension, and multifactorial causes
High-flow states: shunts, anaemia, thyrotoxicosis, arteriovenous and dialysis fistulae, liver disease
Exercise, altitude and volume loading (a physiological rise that does not by itself define disease)

Lowered by

Normal circulation
Falsely low whenever the pulmonary regurgitation jet is incomplete or poorly aligned, or with severe RV failure
After effective treatment of the underlying cause

Technique & pitfalls

The pulmonary regurgitation-derived estimate needs a complete, well-aligned continuous-wave PR envelope from the parasternal short axis — measure the early diastolic peak velocity for mean PAP and the end-diastolic velocity for diastolic PAP.
Add the estimated right atrial pressure; state it separately.
Cross-check with at least one independent method (Chemla from SPAP, or PAAT) and report the agreement or disagreement rather than one number.
Report the estimate as a range and label it an estimate. It should never be transcribed into a letter as if it were a catheter measurement.
In severe pulmonary regurgitation the early diastolic gradient equalises rapidly and the estimate degrades.

Pseudo-change & artefact

Incomplete or poorly aligned PR envelope — underestimates.
Errors in the right atrial pressure estimate, which propagate directly.
Regression formulae derived in specific populations applied to different ones — the Chemla and Mahan equations carry wide limits of agreement.
High flow states raise mean PAP without any vascular disease — the physiologically correct value, but clinically misleading if reported without the flow.
Severe RV failure lowers all derived pressures.
Positive-pressure ventilation, hypoxaemia and acidosis at the time of study.

Treatment thresholds

The formal definition of pulmonary hypertension itself: mean PAP >20 mmHg. Precapillary disease additionally requires PAWP ≤15 mmHg and PVR >2 WU; isolated postcapillary disease has PAWP >15 mmHg with PVR ≤2 WU; combined pre- and postcapillary has both raised. These are catheter definitions, and they determine who receives pulmonary vasodilator therapy.^[8]
Group 1 treatment strategy is then determined by risk stratification, in which the haemodynamics, RA area, RV function, six-minute walk distance and natriuretic peptides all participate; low-risk status is the treatment goal.^[8]
Transplant referral and the decision to start parenteral prostacyclin follow from persistent intermediate-high or high risk.^[8]
Cardiac surgery and transplantation: a high transpulmonary gradient and PVR affect operative risk and candidacy, and may require pre-transplant optimisation.^[11]
The echocardiographic estimate triggers none of these directly — it triggers the catheter.

Next step

Next: assemble the full echocardiographic probability — TR velocity, RV size and function, septal shape, PAAT and notching, IVC, RA area, pulmonary artery diameter.^[8]
Then: assess the left heart carefully; group 2 disease must be excluded before pursuing group 1.
Then: pulmonary function tests, arterial blood gases, high-resolution CT, and V/Q scanning in every unexplained case — CT pulmonary angiography alone misses chronic thromboembolic disease.^[8]
Then: right heart catheterisation at an expert centre, with vasoreactivity testing where the aetiology warrants it, before committing to therapy.^[8]

Drugs

Identical to the SPAP card, and the same warning: the treatment depends entirely on the group, and pulmonary vasodilators given for group 2 or much of group 3 disease cause harm.^[8]
Group 1: endothelin receptor antagonists, PDE-5 inhibitors or riociguat, prostacyclin pathway agents; upfront combination therapy is now standard, with the intensity set by risk status.^[8]
Group 4: anticoagulation, endarterectomy, balloon pulmonary angioplasty, riociguat.^[8]
Calcium-channel blockers only in documented acute vasoreactive responders — a small minority, and dangerous in the rest.^[8]

Reversibility

As for SPAP, and with the same group dependence. The point worth carrying into practice: the reversible components are flow and left atrial pressure, which respond within days to weeks; the fixed component is vascular remodelling. This is exactly what a right heart catheter separates and what echocardiography cannot. A patient whose pulmonary pressures fall with decongestion had a treatable postcapillary component; one whose pressures do not has vascular disease, and the distinction determines whether the next prescription helps or harms.^[8]