Pulmonary Regurgitation: Echocardiographic Assessment

Pulmonary regurgitation (PR), also called pulmonary insufficiency (PI), is retrograde diastolic flow of blood from the pulmonary artery back into the right ventricle, through an incompletely competent pulmonary valve.

A note on sourcing before starting: this page could not be cross-checked against the two valvular heart disease guidelines used elsewhere on this site. Searched directly, the 2025 ESC/EACTS guideline does not address pulmonary regurgitation at all, and the entire “Pulmonic Valve Disease” section of the 2020 ACC/AHA guideline consists of a single sentence: “See guidelines for the management of adults with congenital heart disease.” This isn’t an oversight on either society’s part — isolated PR is uncommon outside the congenital heart disease population, and the clinically important cases (typically following repair of tetralogy of Fallot or other right-ventricular-outflow-tract surgery) properly belong to dedicated ACHD guidance this site doesn’t currently have on hand. This tutorial is therefore built from standard echocardiography references rather than guideline-specific criteria — see the Zoghbi et al. 2017 ASE native regurgitation recommendations in particular for the severity criteria below.

Etiology

• Pulmonary hypertension — secondary to pulmonary valve annular/ring dilation from the elevated pressure
• Infective endocarditis
• Rheumatic heart disease
• Congenital abnormalities — tetralogy of Fallot, ventricular septal defect, and valvular pulmonic stenosis are all associated with PR, whether from the underlying lesion itself or its treatment
• Carcinoid heart disease
• Post-surgical repair — PR is a well-recognized, often expected consequence after pulmonary valve repair or balloon/surgical valvotomy, particularly following childhood repair of tetralogy of Fallot, where some degree of PR is frequently accepted as a trade-off for relieving the original stenosis

Signs and Symptoms

PR is often asymptomatic for years, given how well the right ventricle can initially tolerate chronic volume overload. When symptoms eventually develop, exertional dyspnea is the most common presentation.

Complications

Chronic, significant PR leads to right heart failure through sustained RV volume overload — the same underlying mechanism as any other significant right-sided regurgitant lesion, just applied to the pulmonary rather than tricuspid valve.

Cardiac Auscultation

• A low-pitched diastolic murmur along the 3rd or 4th intercostal space, adjacent to the left sternal border, accentuated with inspiration
• Graham Steell murmur — a distinct, high-pitched, blowing decrescendo murmur in the left parasternal region, associated with severe pulmonary hypertension (classically cited with a pulmonary artery systolic pressure above roughly 70 mmHg). This reflects PR occurring in the setting of significant pulmonary hypertension specifically, rather than PR from a structurally abnormal valve at normal pulmonary pressures.
• Wide splitting of S2
• A right-sided S3 and S4, both potentially accentuated with inspiration

Diagnostic Testing Beyond Echocardiography

• ECG — right ventricular hypertrophy and right bundle branch block
• Chest X-ray — an enlarged pulmonary artery and right ventricular enlargement

Echocardiographic Findings

M-Mode

• Right ventricular enlargement
• An RV volume overload pattern, with paradoxical septal motion
• Fine diastolic flutter of the tricuspid valve, from the regurgitant jet striking it
• Premature pulmonic valve opening — occurring at or before the QRS complex — is a sign specific to severe, acute PR, reflecting a rapidly rising RV diastolic pressure that exceeds pulmonary artery diastolic pressure before the next systole even begins

2D Echocardiography

• Identification of the anatomic basis for PR where present — endocarditis, a stenotic or previously repaired valve, or other structural findings
• Right ventricular dilation
• An RV volume overload pattern

Doppler Assessment

Pulsed-wave Doppler:

• Distinguishes physiologic from significant PR primarily by jet length: a physiologic jet is short (< 1 cm) and not holodiastolic
• A mapping technique, tracing how far the regurgitant color jet extends into the RVOT, supports severity assessment

Continuous-wave Doppler:

• Compare the regurgitant spectral display against the antegrade pulmonic outflow display
• Pulmonary artery end-diastolic pressure can be estimated from the end-diastolic regurgitant velocity, using the same simplified Bernoulli approach applied to other regurgitant lesions

Color flow Doppler:

• Assess the length and width of the regurgitant jet
• Proximal acceleration (flow convergence) indicates at least moderate-to-severe PR

Severity Assessment

These criteria are drawn from standard echocardiography references (notably the ASE’s 2017 native regurgitation recommendations), since — as noted above — they are not addressed in either VHD guideline reviewed for this page.

By jet length and pattern (PW and color flow Doppler):

Category	Jet length	Pattern
Physiologic	< 1 cm	Not holodiastolic
Borderline	1–2 cm	Holodiastolic
Clinically significant	> 2 cm	Holodiastolic, peak velocity > 1.5 m/s

By CW Doppler spectral density (a four-tier descriptive scale):

Grade	Spectral appearance
1+	Faint spectral tracing
2+	Clearly visible spectral tracing
3+	Dense tracing, less dark than antegrade flow
4+	Dense tracing, as dark as or darker than antegrade flow

Important Considerations

• Physiologic PR is common in structurally and hemodynamically normal hearts and is not itself significant — the diagnostic task is distinguishing it from something clinically meaningful using the jet characteristics above, not treating any visible diastolic flow as abnormal.
• Severe PR is associated with right-sided heart failure and progressive RV enlargement over time, which is why serial monitoring of RV size matters in patients with known significant PR — particularly those followed after childhood repair of right-ventricular-outflow-tract lesions, where the timing of pulmonary valve replacement is guided substantially by progressive RV dilation.
• Consider the differential for a diastolic murmur at the left sternal border — aortic regurgitation can produce a similarly located diastolic murmur, and the two should be distinguished on imaging even when the auscultatory findings overlap.
• Pulmonary hypertension and PR often coexist, and Graham Steell’s murmur together with directly assessed pulmonary artery pressures should guide how much of the clinical picture is driven by elevated pulmonary pressure versus primary valve disease.