Pulmonic Valve

The pulmonic valve is frequently incompletely visualized by TTE. Evaluation relies on a combination of 2D imaging, color Doppler, and spectral Doppler.

Assess the valve from the parasternal short-axis, RV outflow, and subcostal views.

Routine Assessment¶

Evaluate:

Leaflet thickness and mobility
Doming or restricted excursion
Subvalvular, valvular, or supravalvular obstruction
Pulmonic regurgitation
Main and proximal branch pulmonary arteries
RV size, hypertrophy, and systolic function
RVOT size and Doppler profile

Normal pulmonic flow velocity is generally <1.5 m/s.

Pulmonic Stenosis¶

Pulmonic stenosis is usually congenital. Less common causes include:

Carcinoid heart disease
Rheumatic disease
Prior surgical or transcatheter intervention
Endocarditis
External compression

Congenital valvular stenosis typically produces systolic doming with commissural fusion. Poststenotic dilation of the main pulmonary artery may be present.

Use color Doppler to identify the site of flow acceleration. Record CW Doppler through the RVOT and pulmonic valve from the window producing the highest velocity.

\[ \text{Peak gradient} = 4(V_{max})^2 \]

Severity¶

Severity	Peak velocity	Peak gradient
Mild	<3.0 m/s	<36 mm Hg
Moderate	3.0–4.0 m/s	36–64 mm Hg
Severe	>4.0 m/s	>64 mm Hg

Pulmonary valve area is not routinely used because accurate measurement is difficult and poorly validated.

Level of Obstruction¶

Valvular: flow acceleration begins at the valve; doming leaflets may be present
Subvalvular: acceleration begins within the RVOT
Supravalvular: acceleration begins in the main or branch pulmonary artery
Dynamic infundibular: late-peaking, dagger-shaped Doppler envelope

The peak Doppler gradient is an instantaneous gradient and may exceed the peak-to-peak gradient measured during catheterization.

Pulmonic Regurgitation¶

Trace or mild pulmonic regurgitation is common and usually physiologic.

Pathologic PR may result from:

Prior repair of tetralogy of Fallot
Pulmonary valvotomy or balloon valvuloplasty
Pulmonary hypertension
Carcinoid heart disease
Endocarditis
Congenital valve abnormalities
Surgical or transcatheter prosthetic valve dysfunction

Severity Assessment¶

PR severity should integrate color Doppler, CW Doppler, pulmonary artery flow, and RV remodeling.

Parameter	Mild PR	Severe PR
Jet width	Narrow	Broad; occupies most of RVOT
Jet width/RVOT width	<25%	>50–65%
CW density	Faint or incomplete	Dense
CW deceleration	Slow	Steep
Pressure half-time	Usually >500 ms	Often <100 ms
Jet duration	Usually holodiastolic	May terminate early
Branch PA flow	No significant reversal	Diastolic flow reversal
RV size	Normal	Usually dilated in chronic PR

A short pressure half-time or early termination reflects rapid equalization of pulmonary artery and RV diastolic pressures. These findings may also occur with elevated RV diastolic pressure and should not be used alone.

Severe chronic PR produces RV volume overload:

RV dilation
Diastolic septal flattening
Progressive RV systolic dysfunction
Tricuspid annular dilation and secondary TR

In acute severe PR, the RV may not yet be dilated.

Pulmonary Hypertension¶

Pulmonary hypertension commonly causes functional PR with a dilated pulmonary annulus.

Pulmonary artery end-diastolic pressure may be estimated from the PR end-diastolic velocity:

\[ PAEDP = 4(PR_{ED})^2 + RAP \]

Mean pulmonary artery pressure may be estimated from the early peak PR velocity:

\[ mPAP = 4(PR_{peak})^2 + RAP \]

These estimates require a complete, well-aligned PR Doppler envelope.

RVOT acceleration time is measured from the onset to the peak of systolic pulmonary flow:

105 ms is generally normal
Shortening supports increased pulmonary vascular resistance
Mid-systolic notching supports increased pulmonary vascular impedance

Acceleration time evaluates pulmonary hemodynamics rather than pulmonic valve stenosis severity.

Carcinoid Heart Disease¶

Typical findings include:

Thickened and retracted pulmonic leaflets
Restricted systolic and diastolic motion
Mixed pulmonic stenosis and regurgitation
Associated tricuspid valve involvement

The valve may remain fixed in a partially open position.

Suggested Reporting¶

The pulmonic valve is not well visualized. Doppler interrogation demonstrates no significant pulmonic stenosis or regurgitation.

The pulmonic valve demonstrates systolic doming with restricted excursion. Peak velocity is ___ m/s with a peak gradient of ___ mm Hg, consistent with ___ pulmonic stenosis.

Severe pulmonic regurgitation is present with a broad regurgitant jet, rapid CW deceleration, and diastolic flow reversal in the branch pulmonary arteries. The RV is ___ dilated with ___ systolic function.

Mild pulmonic regurgitation is present, likely physiologic.

There is flow acceleration within the RVOT rather than at the pulmonic valve, consistent with subvalvular obstruction.

Key Points¶

Pulmonic stenosis severity is based primarily on peak velocity and gradient.
Identify whether obstruction is subvalvular, valvular, or supravalvular.
Severe PR may terminate before end-diastole because of rapid pressure equalization.
RV dilation is the major consequence of chronic severe PR.
RVOT acceleration time reflects pulmonary vascular hemodynamics, not valve stenosis.
Trace or mild PR is commonly physiologic.