Pulmonary valve velocity–time integral
PV VTI (transvalvular) · Continuous-wave Doppler across the pulmonary valve, parasternal short axis and subcostal; use several windows
Normal range & thresholds
Normal transpulmonary peak velocity <1.0–1.5 m/s (native valve). Pulmonary stenosis severity: mild peak velocity <3 m/s (peak gradient <36 mmHg); moderate 3–4 m/s (36–64 mmHg); severe >4 m/s (peak gradient >64 mmHg).[25]
Bioprosthetic and valve-in-valve pulmonary valves normally run at higher velocities than a native valve; interpret against the specific prosthesis type and size, and against the patient’s own baseline study — the first post-implant study is the reference for all later ones.[20,21]
Bioprosthetic and valve-in-valve pulmonary valves normally run at higher velocities than a native valve; interpret against the specific prosthesis type and size, and against the patient’s own baseline study — the first post-implant study is the reference for all later ones.[20,21]
Pathophysiology
Pulmonary valve VTI is the integral of transvalvular velocity and enters the continuity equation for pulmonary valve area exactly as the aortic VTI does for the aortic valve. Right-sided gradients are even more flow-sensitive than left-sided ones, because the right ventricle operates on a steep part of its pressure–flow relation: a modest rise in cardiac output produces a disproportionate rise in gradient. In prosthetic and valve-in-valve pulmonary valves this flow dependence, combined with pressure recovery in a compliant pulmonary artery, is why Doppler gradients routinely exceed catheter gradients.[20,25]
Raised by
- Valvular pulmonary stenosis — congenital (commonest), rheumatic (rare), carcinoid
- Prosthetic or homograft stenosis; degeneration of a bioprosthesis; valve-in-valve with a small effective orifice
- Supravalvular or branch pulmonary artery stenosis; conduit stenosis after tetralogy or Ross procedure
- High flow without obstruction — left-to-right shunt, anaemia, thyrotoxicosis, pregnancy, fever, exercise: the most important non-obstructive cause
- Dynamic subvalvular (infundibular) obstruction, including double-chambered RV
Lowered by
- RV systolic failure — a severely obstructed valve with a failing RV generates a deceptively low gradient
- Low-output states, hypovolaemia, tamponade
- Severe tricuspid regurgitation reducing forward flow
- After relief of obstruction (valvuloplasty, valve replacement)
- Severe pulmonary regurgitation shortens the diastolic pressure equalisation but does not itself lower the systolic velocity
Technique & pitfalls
- Interrogate from the parasternal short axis and the subcostal window; alignment is often better subcostally, especially in hyperinflated chests.
- Trace the outer edge of the dense CW envelope; report peak velocity, peak and mean gradients, and VTI.
- Always report the heart rate and the flow state. A gradient measured during fever, anaemia or tachycardia is not comparable with a resting one — this is the dominant source of spurious ‘progression’ in prosthetic pulmonary valve follow-up.
- For a prosthesis, report the Doppler velocity index (RVOT VTI / PV VTI) as well as absolute gradients — the ratio is far less flow-dependent.[20,21]
- Distinguish valvular from subvalvular obstruction by pulsed Doppler mapping along the RVOT: a dagger-shaped, late-peaking envelope indicates dynamic infundibular obstruction.
- Interpret every prosthetic study against the patient’s own early post-operative baseline.
Pseudo-change & artefact
- High-flow states — the commonest cause of an apparently rising prosthetic gradient, and it resolves when the flow state is corrected.
- Pressure recovery in the pulmonary artery inflates Doppler gradients relative to catheter gradients, particularly with small conduits and valve-in-valve implants.[20]
- Angle error — underestimates; a single window is not enough.
- Contamination by the tricuspid regurgitation jet (which is holosystolic and higher velocity).
- Distal branch stenosis raising the velocity without valvular disease.
- In serial follow-up, a change of window or of operator can create an apparent change of 20–30%.
Treatment thresholds
- Severe valvular pulmonary stenosis (peak gradient >64 mmHg, peak velocity >4 m/s) → balloon pulmonary valvuloplasty, which is the treatment of choice for a domed non-dysplastic valve (class I); surgery for a dysplastic valve or associated lesions.[25]
- Intervention is also indicated at lower gradients when there are symptoms, RV dysfunction, right-to-left shunting through a patent foramen, or arrhythmia.[25]
- Prosthetic pulmonary valve or conduit stenosis: a rising mean gradient with a falling Doppler velocity index, particularly with RV dilatation or dysfunction, prompts reintervention — increasingly transcatheter valve-in-valve.[20,25]
- After tetralogy of Fallot repair, the dominant lesion is usually pulmonary regurgitation, and the intervention triggers are RV volumes (RVEDVi ≥160 mL/m², RVESVi ≥80 mL/m² by CMR), not the transvalvular gradient.[25]
Next step
- Next: localise the obstruction (subvalvular, valvular, supravalvular, branch) by pulsed Doppler mapping and 2D imaging; quantify pulmonary regurgitation.
- Then: assess RV size, wall thickness and function, and estimate RV systolic pressure from the TR jet.
- Then: CMR for RV volumes and pulmonary regurgitant fraction, and CT or angiography for branch and conduit anatomy.
- Then: catheterisation with direct pull-back gradients before intervention — the invasive gradient, not the Doppler gradient, is the operative reference in conduits and prostheses.
Drugs
- No drug treats pulmonary valve stenosis — the lesion is mechanical.
- Correct high-flow states (anaemia, thyrotoxicosis, sepsis) before judging severity.
- Beta-blockers reduce dynamic infundibular obstruction, when that is the mechanism.
- Diuretics relieve congestion in the failing RV but do not change the valve.
- Endocarditis prophylaxis applies to prosthetic and repaired valves.
Reversibility
Native valvular pulmonary stenosis is one of the most completely reversible lesions in adult cardiology: balloon valvuloplasty of a domed valve typically drops the gradient by 70–90% immediately, with excellent long-term durability and regression of RV hypertrophy over months to years; the trade-off is progressive pulmonary regurgitation. Prosthetic and conduit stenosis is relieved immediately by valve-in-valve implantation or surgical replacement. Nothing regresses spontaneously.[25]