Systolic pulmonary artery pressure
SPAP (RVSP) · Derived: SPAP = 4 × (TR Vmax)2 + estimated right atrial pressure
Normal range & thresholds
Normal <35 mmHg at rest (many laboratories use ≤30 mmHg in the young; the upper limit rises with age and body mass index). In the 2025 ASE diastolic algorithm, PASP ≥35 mmHg is the abnormal threshold that parallels a TR velocity ≥2.8 m/s.[2,3]
Important caveat: the 2022 ESC/ERS guidelines base echocardiographic probability on TR velocity rather than on estimated SPAP, precisely because adding an estimated right atrial pressure adds error without adding information. Report both, and make clear which one you are asking the reader to act on.[8]
Important caveat: the 2022 ESC/ERS guidelines base echocardiographic probability on TR velocity rather than on estimated SPAP, precisely because adding an estimated right atrial pressure adds error without adding information. Report both, and make clear which one you are asking the reader to act on.[8]
Pathophysiology
SPAP equals RV systolic pressure when there is no pulmonary or RVOT obstruction, and RV systolic pressure is recovered from the TR jet plus right atrial pressure. It rises through three distinct mechanisms that the number cannot distinguish: raised pulmonary venous pressure transmitted backwards from the left heart (postcapillary, group 2 — the commonest), raised pulmonary vascular resistance (precapillary), and raised pulmonary blood flow (shunt, high-output states). Treatment differs completely between the three, which is why an SPAP without a mechanism is a clinically incomplete result.[8]
Raised by
- Group 2 — left heart disease: HFrEF, HFpEF, mitral and aortic valve disease. The commonest cause in every unselected echo laboratory
- Group 3 — lung disease and hypoxia: COPD, interstitial disease, obstructive sleep apnoea, obesity hypoventilation, high altitude
- Group 4 — chronic thromboembolic pulmonary hypertension
- Group 1 — pulmonary arterial hypertension: idiopathic, heritable, connective tissue disease, congenital shunts, portopulmonary, HIV, drug- and toxin-induced
- Group 5 — multifactorial: sarcoid, haematological disease, chronic renal failure
- High-flow states: shunts, anaemia, thyrotoxicosis, arteriovenous fistula (including dialysis access)
Lowered by
- Normal pulmonary circulation
- Falsely low with severe RV failure or torrential tricuspid regurgitation — see card 30
- Hypovolaemia; over-estimation of a low right atrial pressure
- After effective treatment of the underlying cause
Technique & pitfalls
- Every technical rule from card 30 applies, and one more: the estimated right atrial pressure must be measured, not assumed. Substituting a habitual ‘5 mmHg’ is a common and avoidable source of error.
- Report as a range or with the RA pressure stated separately, e.g. ‘TR velocity 3.2 m/s, gradient 41 mmHg, estimated RA pressure 8 mmHg, SPAP ≈49 mmHg’.
- Subtract the transpulmonary gradient when there is pulmonary or RVOT stenosis; otherwise the number describes RV pressure, not pulmonary artery pressure.
- Correlation with invasive measurement is only moderate — within ±10 mmHg in about two-thirds of patients, with both over- and underestimation common. Say so when the number is near a decision point.[8]
- Do not diagnose pulmonary hypertension on echo. Assign a probability and refer.[8]
Pseudo-change & artefact
- Every artefact of the TR jet, plus every error in the right atrial pressure estimate — the two compound.
- Pulmonary or RVOT stenosis (SPAP overestimated unless the gradient is subtracted).
- Severe RV failure and torrential TR (underestimated).
- Study performed during pain, anxiety, exertion, hypoxaemia, or immediately after fluid administration.
- Positive-pressure ventilation.
- Reporting a single point value with no indication of its uncertainty — a presentational artefact that changes clinical behaviour.
Treatment thresholds
- Asymptomatic severe primary mitral regurgitation: resting SPAP >50 mmHg is an accepted trigger for mitral valve surgery (class IIa) — the clearest place where this number alone changes management.[6,7]
- Mitral stenosis: pulmonary hypertension supports intervention in patients with equivocal symptoms, and SPAP >50 mmHg with severe mitral stenosis is a recognised indication for balloon mitral valvuloplasty.[6,7]
- Diastolic function: PASP ≥35 mmHg (TR velocity ≥2.8 m/s) is a primary variable in the 2025 ASE algorithm.[2]
- Pulmonary hypertension: the probability assessment, not the SPAP value, determines referral for catheterisation; SPAP is then used for follow-up rather than diagnosis.[8]
- Pre-operative and pre-transplant assessment: severe pulmonary hypertension changes operative risk, influences LVAD and transplant candidacy, and may exclude transcatheter tricuspid intervention.[6,11]
Next step
- Next: establish the mechanism — assess the left heart thoroughly before attributing the pressure to the pulmonary vasculature.
- Then: PAAT, RVOT notching and the estimated PVR to distinguish flow, resistance and venous hypertension.
- Then: pulmonary function tests, high-resolution CT and V/Q scanning.[8]
- Then: right heart catheterisation with a wedge pressure — without it, precapillary and postcapillary disease cannot be separated, and treating the wrong one is harmful.[8]
Drugs
- Group 2: treat the left heart — diuretics, GDMT, valve intervention. Pulmonary vasodilators are contraindicated and cause pulmonary oedema.[8]
- Group 1: endothelin receptor antagonists, PDE-5 inhibitors, riociguat, prostacyclin pathway agents; calcium-channel blockers only in documented vasoreactive responders.[8]
- Group 3: oxygen, treatment of the lung disease, CPAP for sleep apnoea.
- Group 4: lifelong anticoagulation, pulmonary endarterectomy, balloon pulmonary angioplasty, riociguat.[8]
- Raised by: fluid overload, hypoxaemia, hypercapnia, acidosis, and drugs implicated in pulmonary arterial hypertension.
Reversibility
Depends on the group. Group 2 is often dramatically reversible: SPAP falls by 20–40 mmHg after decongestion, and after mitral valve intervention most patients normalise within 3–6 months — even very high pre-operative pressures, which is why severe pulmonary hypertension is not a contraindication to mitral intervention. Acute pulmonary embolism largely normalises with reperfusion. CTEPH after endarterectomy: substantial and often near-complete. Group 1: partially reversible in responders, with the fall in pressure and the rise in cardiac output the key treatment targets; established plexogenic remodelling does not reverse.[6,8]