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Pulmonic Regurgitation Workup

  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Richard A Lange, MD, MBA  more...
Updated: Feb 17, 2015

Laboratory Studies

Japanese investigators suggest that evels of plasma brain natriuretic peptide (BNP) have the potential to be useful for postsurgical long-term monitoring of patients with tetralogy of Fallot who are under consideration for pulmonary valve replacement to correct pulmonary regurgitation or right-ventricular dysfunction.[5] In their study of 33 patients who underwent repair of tetralogy of Fallot, significantly higher plasma BNP levels were found not only in patients with moderate-severe pulmonary regurgitation compared to those with insignificant or mild pulmonary regurgitation (P = 0.013.) but also in patients with cardiac symptoms compared to asymptomatic patients (P = 0.005).

Following pulmonary valve replacement, there was a significant reduction in mean BNP levels, and the plasma BNP level correlated with the right-ventricular end-diastolic pressure.[5] The investigators reported 32.15 pg/mL was the optimal BNP cut-off level for considering pulmonary valve replacement.


Plain Radiography

Plain radiographs change little with pulmonic regurgitation unless tricuspid regurgitation also occurs, in which case cardiomegaly and enlargement of the right-sided heart contour are observed.

Prominent central pulmonary arteries with enlarged hilar vessels and loss of vascularity in the peripheral lung fields ("pruning") suggests severe pulmonary hypertension.


Fluoroscopy and Catheterization

Cardiac catheterization is usually not necessary for diagnosis but may be helpful in determining the underlying etiology and for determining coexisting conditions that may influence treatment and/or repair decisions.

Pulmonary artery angiography may reveal evidence of multiple pulmonary emboli as a cause of pulmonary hypertension when the degree of clinical suspicion is high. Ventilation/perfusion scanning or CT angiography is now more commonly performed in most hospitals. Pulmonary emboli must be excluded before the diagnosis of primary pulmonary hypertension is possible.

If pressure measurements are performed, the pulmonary artery and right ventricular pressure curves equalize in late diastole in individuals with severe pulmonary regurgitation.



Two-dimensional echocardiography (2DE) and M-mode echocardiography can reveal right ventricular hypertrophy and dilatation. Right ventricular volume overload may induce a characteristic abnormal septal wall motion, which appears as flattening of the septum during diastole. Conversely, right ventricular pressure overload usually appears as flattening of the septum during systole. The lack of a pulmonic valve or valve deformities can be noted with 2DE, but the pulmonic valve apparatus typically appears unremarkable. In some cases, pulmonic ring dilatation with poor valve leaflet coaptation may be observed.

Doppler techniques are used to visualize the regurgitant flow. These techniques are useful to directly visualize regurgitant jets, measure the flow velocities of the regurgitant jets, and accurately estimate pulmonary pressures. Regurgitation that persists throughout diastole suggests the presence of pulmonary hypertension, whereas regurgitation that diminishes earlier in diastole suggests more normal pulmonary arterial pressures. Normally, peak flow velocity across the pulmonic valve is achieved within 140 milliseconds of systole. With pulmonary hypertension, the peak flow velocity is reached faster. The shortening of the interval within which the peak velocity is reached (acceleration time) is linearly inversely proportional to the severity of the pulmonary hypertension.

Color flow Doppler echocardiography is the mainstay for recognizing pulmonic regurgitation. In trivial-to-mild pulmonic regurgitation, the jet is central and narrow. In moderate-to-severe pulmonic regurgitation, the width of the jet increases, as does the penetration of the jet into the right ventricular outflow tract. In free or open pulmonic regurgitation (usually due to congenitally absent pulmonic valve), color Doppler can miss the jet altogether due to the brisk and laminar regurgitant flow.

Using pulsed wave and continuous wave Doppler, pulmonary artery systolic and diastolic pressures can be calculated. Pulmonary artery systolic pressure can be estimated (using continuous wave Doppler) in the presence of tricuspid regurgitation by measuring the peak regurgitant flow velocity across the tricuspid valve, converting it to a pressure gradient (by use of the modified Bernoulli equation), and then adding the gradient to an estimate of the right atrial pressure.

Pulmonary artery diastolic pressure can be estimated by measuring the end-diastolic regurgitant flow velocity across the pulmonic valve (at the QRS complex on the ECG), converting it to a pressure gradient, and then adding the gradient to the estimated right atrial pressure. Both pulmonary artery systolic pressure and diastolic pressure are predictors of cardiac status and outcome.[6, 7]

Pulmonary arterial mean pressure can also be estimated by converting the early diastolic regurgitation velocity to a pressure gradient, and then adding it to the estimated right atrial pressure.


Cardiac Magnetic Resonance Imaging (CMRI)

CMRI has shown promise based on recent studies of pulmonary regurgitation. CMR has excellent temporal and spacial resolution and can provide accurate estimation of the severity of regurgitation, mechanism of regurgitation, and right ventricular size and function. However, size and time constraints limit the use of CMR in clinical practice.



ECG may demonstrate findings of right ventricular dilatation (occurs either while in a compensated volume overload state or in a decompensated pressure overload state), including incomplete right bundle branch block and right axis deviation. Right ventricular hypertrophy may be present by ECG criteria.

In the presence of right ventricular hypertrophy (representing a compensated state of pressure overload), the following may be present:

  • Tall R wave in V 1 or qR in V 1
  • R wave greater than S wave in V 1
  • R wave progression reversal in the precordial leads
  • Inverted T wave in the anterior precordial leads
  • Right axis deviation
  • Right atrial enlargement
Contributor Information and Disclosures

Xiushui (Mike) Ren, MD Cardiologist, The Permanente Medical Group; Associate Director of Research, Cardiovascular Diseases Fellowship, California Pacific Medical Center

Xiushui (Mike) Ren, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Society of Echocardiography

Disclosure: Nothing to disclose.


Lauralyn B Cannistra, MD, FACC Director of Echocardiography Lab and Cardiac Rehabilitation, Assistant Professor, Department of Medicine, Memorial Hospital of Rhode Island, Brown University School of Medicine

Lauralyn B Cannistra, MD, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Anesthesiologists, American Society of Echocardiography, Rhode Island Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Marschall S Runge, MD, PhD Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine

Marschall S Runge, MD, PhD is a member of the following medical societies: American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Texas Medical Association, Southern Society for Clinical Investigation, American Federation for Clinical Research, Association of Professors of Medicine, Association of Professors of Cardiology, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association

Disclosure: Received honoraria from Pfizer for speaking and teaching; Received honoraria from Merck for speaking and teaching; Received consulting fee from Orthoclinica Diagnostica for consulting.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.


The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous author Pablo J Saavedra, MD, to the development and writing of this article.

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