11.3 Pulmonic Stenosis Assessment

Prove that the obstruction is valvular

Pulmonic stenosis, or PS, usually reflects congenital commissural fusion producing a doming valve with a narrow systolic opening. Dysplastic cusps may be thick and poorly mobile without doming. Less common acquired causes include rheumatic disease, carcinoid, or prior intervention. A high velocity near the pulmonic valve is not sufficient: subvalvular muscle bundles, dynamic RVOT narrowing, supravalvular MPA stenosis, branch stenosis, a conduit, or high flow can produce a similar CW signal.

Use 2-D sweeps from parasternal short-axis, PA-focused, subcostal, and modified apical windows. Record cusp number when genuinely seen, thickness, systolic mobility and doming, annular size, RVOT anatomy, MPA and branch caliber, and poststenotic dilation. Color should show the narrowest origin of the systolic jet. Step PW from proximal RVOT through the annulus and into the MPA; the first velocity increase localizes the obstruction. If PW aliases, move the gate proximally and distally rather than guessing from the mosaic.

Align spectral Doppler and calculate correctly

Use CW through the localized jet from every window that approaches parallel flow. Save the highest reproducible, complete envelope without angle correction. Trace the dense modal edge for peak velocity and mean gradient. The simplified Bernoulli equation converts peak velocity to maximum instantaneous pressure difference:

Peak gradient = 4V²

A velocity of 3.5 m/s gives 4 × 3.5² = 49 mm Hg. This Doppler maximum instantaneous gradient is not the same as the catheter peak-to-peak gradient, which compares nonsimultaneous chamber peaks and is usually lower. Name the Doppler quantity correctly. The machine-derived mean gradient averages instantaneous gradients across systole; it cannot be calculated by inserting mean velocity into 4V².

When proximal RVOT velocity is not negligible, use the expanded relation 4(V₂² − V₁²) rather than assuming V₁ is zero. This matters with serial obstruction, a tunnel, high flow, or substantial subvalvular acceleration. Match proximal and distal signals from representative beats. Do not add Doppler gradients from separate levels; pressure differences are not simple independent numbers when velocities and recovery interact.

Use velocity bands as one part of severity

ASE valve-stenosis guidance uses these conventional Doppler bands for valvular PS:

The category assumes a correctly localized, well-aligned jet and an interpretable flow state. High cardiac output from anemia, pregnancy, fever, or shunt can elevate velocity without a smaller anatomic orifice. Low output, severe RV dysfunction, or critical obstruction can yield a lower-than-expected gradient. Tachycardia, arrhythmia, respiration, and positive-pressure ventilation change right-sided filling and ejection. Record heart rate, rhythm, oxygen and ventilation conditions, and relevant loading; average protocol-defined beats in irregular rhythm. No single cutoff should overrule clearly discordant cusp anatomy or RV response.

Integrate the right-heart consequences

Chronic pressure overload produces RV hypertrophy, then possible dilation and systolic or diastolic dysfunction. Assess RV wall thickness, size, FAC, TAPSE, tissue Doppler s′, strain when available, RA size, IVC and systemic venous congestion, septal configuration, and secondary TR. Poststenotic MPA dilation supports a valvular high-velocity jet but is not a severity grade. Atrial shunting may decompress the right heart and alter flow; inspect the septum when RA pressure is high. Symptoms, exercise response, and serial change are interpreted by the physician with the anatomic and Doppler record.

Use the TR signal carefully. RV systolic pressure equals 4(TR velocity)² plus estimated RA pressure when the signal is valid. With no RVOT or pulmonic obstruction, RVSP can approximate pulmonary artery systolic pressure. In PS, however, the valve gradient separates RV and PA pressures, so RVSP must not be mislabeled PASP. A rough PA systolic estimate may subtract the obstruction gradient from RVSP only when measurements are compatible and no additional obstruction exists; severe TR, poor envelopes, branch disease, and different beats can invalidate that arithmetic.

A low TR velocity does not prove low RV pressure if the beam is misaligned or the jet is incomplete. Conversely, a high RVSP in severe PS describes RV pressure load, not pulmonary hypertension. Cross-check septal flattening, RV hypertrophy, PA flow, PR-derived pressures when valid, and the overall pulmonary-hemodynamic pattern. Right-heart catheterization or cross-sectional imaging may be needed when noninvasive data are discordant and management depends on exact pressures or anatomy.

Distinguish residual disease and associated lesions

After balloon valvuloplasty or surgery, document residual jet level and gradient, cusp or prosthetic motion, PR, annular and MPA anatomy, RV remodeling, and branch obstruction. A lower gradient with worsening PR may reflect a trade-off rather than complete normalization. In a conduit or prosthetic valve, apply the device-specific baseline and prosthetic guidance rather than native-valve cutoffs alone.

Before finalizing, verify that the highest CW signal corresponds to the lesion localized by PW and color, all measured envelopes are complete, proximal velocity was considered, and respiration and rhythm are documented. Reconcile Doppler category with cusp motion, poststenotic change, RV pressure load, function, and flow state. The RCS sonographer supplies a technically defensible integrated dataset; intervention decisions require clinical and multidisciplinary assessment.

RVSP is not PASP when PS is present

Pulmonic or RVOT obstruction creates a systolic pressure drop between RV and pulmonary artery. A valid TR-derived RVSP therefore describes RV pressure load and cannot be labeled pulmonary artery systolic pressure without accounting for the obstruction.