Pulmonary Regurgitation (Pulmonic Regurgitation)

Updated: Jun 28, 2018
Author: Tarek Ajam, MD, MS; Chief Editor: Richard A Lange, MD, MBA 


Practice Essentials

Pulmonary or pulmonic regurgitation (PR) is defined as an abnormal reversal of blood flow from the pulmonary artery into the right ventricle. Most often, PR is not the primary process but a finding secondary to an underlying process, such as pulmonary hypertension or dilated cardiomyopathy. 

Signs and symptoms

Patients with PR are typically asymptomatic prior to the onset of right ventricular (RV) dysfunction. Symptoms consist of exertional dyspnea and fatigue. With the progression of RV dysfunction, the onset of atrial and ventricular arrhythmias, palpitations, and syncope may occur.  

The murmur is in early diastole and it may increase in intensity with inspiration. With more signicant PR, an ejection murmur in systole may be heard and a third heart sound may be present.

Significant PR can be associated with the following symptoms:

  • Distended neck veins
  • Palpable pulmonary artery pulsation 
  • Pedal edema
  • Hepatosplenomegaly
  • Ascites
  • Syncope
  • Lightheadedness


Echocardiography generally confirms the diagnosis of PR, which also provides an evaluation of the mechanism, cause, and severity of the valve disease. In addition, echocardiography provides information about the hemodynamic effects and the assessment of associated disorders, such as pulmonary artery hypertension. PR severity is determined by jet width, density, and deceleration rate. Patients with moderate or greater PR should also undergo evaluation with cardiovascular magnetic resonance imaging (CMRI) to provide a quantitative assessment of PR and of RV size and function. 

Imaging studies

  • Radiography
  • Echocardiography
  • Computed tomography scanning
  • CMRI


PR is seldom severe enough to warrant special treatment. It is recommended to treat the underlying etiologies that cause severe PR. When right-sided heart failure due to PR cannot be ameliorated by medical therapy, surgical reconstruction or replacement of the pulmonic valve is an appropriate option. 

The following are indications for surgical pulmonic valve replacement:

  • Severe, symptomatic PR
  • Asympatomatic severe PR with severe RV dilatation and/or dysfunction, or symptomatic atrial and/or ventricular arrythmias; dysfunction on CMRI with a RV end-diastolic volume above 150 mL/m 2, an end-systolic volume over 80 mL/m 2, and an ejection fraction below 47%
  • Severe PR and progressive tricuspid valve regurgitation


The pulmonic valve is normally a thin tricuspid structure that prevents blood from regurgitating into the right ventricle (RV) once it is ejected into the low-pressure pulmonary circulation. Pulmonary or pulmonic regurgitation (PR) refers to retrograde flow from the pulmonary artery into the RV during diastole. Physiologic (trace to mild) PR is present in nearly all individuals, particularly in those with advanced age. However, pathologic conditions that produce excessive and clinically significant regurgitation can result in impairment of RV function and eventual clinical manifestations of right-sided volume overload and heart failure. Most often, PR is not the primary process but a finding secondary to an underlying process such as pulmonary hypertension or dilated cardiomyopathy.


Pulmonary or pulmonic regurgitation (PR) or incompetence of the pulmonic valve occurs by one of three basic pathologic processes: dilatation of the pulmonic valve ring, acquired alteration of the pulmonic valve leaflet morphology, or congenital absence or malformation of the valve. PR leads to right ventricular (RV) volume overload, which will subsequently lead to RV enlargement and RV dysfunction. In time, PR will lead to tricuspid regurgitation.


Significant pulmonary or pulmonic regurgitation (PR) occurs variably as a complication of various conditions.

The most common causes for a leaky pulmonary valve is pulmonary hypertension or a congenital heart defect (most commonly tetralogy of Fallot).

Less common causes of PR include the following:

Primary and pulmonary hypertension

Primary pulmonary hypertension occurs in approximately 1 per 500,000 cases. This diagnosis can be made only after all other causes have been excluded. Primary causes include iatrogenic, infective endocarditis, systemic (carcinoid disease), immune-mediated (rheumatic heart disease), and congenital heart disease.[1, 2]

Secondary pulmonary hypertension (multiple causes) is the most common cause of pulmonic regurgitation in adults. Secondary or functional PR occurs in patients with nromal pulmonic valve who have severe pulmonary arterial hypertension and/or pulmonary artery dilatation.[3]

Tetralogy of Fallot

Tetralogy of Fallot, especially with congenital absence of the pulmonary valve, or postoperative following surgical repair of this condition (eg, pulmonary valvotomy), commonly cause significant PR.[4]

Infective endocarditis

In rare cases, infective endocarditis results in significant PR. It may occur in an intravenous/injection drug user or in an individual with an atrial septal defect and a large left-to-right intracardiac shunt.

Rheumatic and carcinoid heart diseases

In rheumatic heart disease leading to significant PR, the pulmonary valve is affected following mitral, aortic, and tricuspid valve involvement.

For more information on carcinoid heart disease, see Carcinoid Lung Tumors and Intestinal Carcinoid Tumor.


Medications that act via serotoninergic pathways may result in significant PR (eg, methysergide, pergolide, fenfluramine).

Disorders that dilate the pulmonic valve ring to create valvular incompetence

Disorders that dilate the pulmonic valve ring to create valvular incompetence are the most common cause of PR and include primary or secondary pulmonary hypertension, dilatation of the pulmonary trunk in Marfan syndrome or Takayasu arteritis, and idiopathic causes.

Acquired disorders that alter pulmonic valve morphology

Acquired conditions that alter pulmonic valve morphology include the following:

  • Rheumatic heart disease: In most cases, the other valves (ie, mitral, aortic, tricuspid) are also substantially affected.

  • Trauma from a Swan-Ganz catheter: This cause is unusual, but it can result if the catheter tip is withdrawn across the pulmonic valve with the balloon inflated.

  • Complications related to therapeutic balloon catheter dilation of a stenotic pulmonic valve (eg, pulmonary balloon valvuloplasty): Such complications are not uncommon; however, in most cases, the degree of regurgitation is clinically insignificant, rendering pulmonic valve balloon catheter dilation a safe and effective treatment for moderate to severe pulmonic stenosis in adult and pediatric patients.

  • Complications of surgical repair of pulmonic stenosis[5]  or congenital heart disease, such as tetralogy of Fallot[6, 7]

  • Syphilis infection

  • Carcinoid heart disease: The heart is affected in up to 60% of patients in whom carcinoid heart disease has metastasized to the liver, most commonly manifesting as valvular disease. In a series of 74 patients, the pulmonic valve was involved in 88%.[8] Of those affected, 49% exhibited significant pulmonic stenosis, and 81% had significant PR.

Congenital disorders that produce an incompetent pulmonic valve

These include complete absence of the pulmonic valve and valvular abnormalities (eg, fenestrations or redundant leaflets).


United States

Physiologic pulmonary or pulmonic regurgitation (PR) is present in nearly all individuals and is a normal echocardiographic finding. PR detected by physical examination is not a normal finding in healthy adults. Congenital PR and congenital absence of the pulmonic valve are rare conditions.


No difference in international incidence is known.

Race-, sex-, and age-related demographics

No racial or ethnic predilection exists.

The differing frequency of PR between men and women corresponds to the specific etiology resulting in this condition.

Except for congenital absence of the pulmonic valve, which is more likely to cause right-sided ventricular decompensation early in life, the age at which clinical symptoms of PR occur is variable and is primarily related to the underlying process causing the PR. Patients are usually in their third or fourth decade of life at presentation, typically with severe PR that is manifested by surgical repair.


The prognosis for patients with severe pulmonary or pulmonic regurgitation (PR) depends on the presence or absence of right ventricular (RV) dysfunction, pulmonary artery dilatation, and symptoms.

Most patients with with PR following repair of tetralogy of Fallot carry an excellent prognosis. However there is a late mortality that is related to RV dysfunction.[4, 9]  Residual PR is an important determinant of outcome, as it may contribute to RV hypertrophy and dysfunction, a propensity for arrhythmias, and an increased risk for sudden cardiac death.[10, 11]

In general, survival is not significantly affected by mild to moderate PR. If the PR is severe, the RV is initially able to compensate for the volume overload state, and the state may remain well compensated for years. However, persistently elevated RV volumes may eventually cause RV dilatation and, finally, failure.

As previously stated, the various disorders causing pulmonary hypertension are the most common causes of clinically significant PR. The principal prognostic indicators of mortality in PR associated with pulmonary hypertension are (1) the severity and duration of the pulmonary hypertension at the time of diagnosis and (2) the RV response to the state of volume overload.

In all etiologies of pulmonary hypertension, early diagnosis that allows for intervention to slow or reverse the cause of pulmonary hypertension is essential, although, in many cases, diagnosis is difficult and requires a high degree of clinical suspicion.

In primary pulmonary hypertension, the pathologic process is often insidious, and symptoms manifest at an advanced disease state, resulting in an average survival period of 2.5 years from the time of diagnosis.

In congenital regurgitation of the pulmonic valve, the prognosis depends upon the initial severity, progression of the regurgitation, and the ability of the RV to adapt to volume overload. Usually, the degree of regurgitation in this condition is no more than moderate, so no clinical sequelae occur. Congenital absence of the pulmonic valve, a much rarer condition, confers an increased risk of morbidity and mortality because of more severe regurgitation, and it usually warrants pulmonic valve replacement for improved prognosis.

Morbidity, mortality, and complications

As noted, the morbidity and mortality rates associated with pulmonic regurgitation vary considerably, depending on the underlying etiology.

Severe pulmonary valve regurgitation may result in RV enlargement, systolic dysfunction, and death.[4, 12, 13]  Complications of severe PR may lead to right-sided heart failure (itself a complication of RV volume overload), thromboembolic events, hepatic congestion, systolic dysfunction, arrhythmias, and death. 

Other complications are related to the underlying disease processes resulting in PR.

After a pulmonic valve replacement, infective endocarditis and structural valve failure are signifcant long-term complications.[14]

Patient Education

Carefully explain to patients that pulmonary or pulmonic regurgitation (PR) is in essence a leaky pulmonary valve. The pulmonary valve helps control the flow of blood passing from the heart to the lungs. Thus, a leaky pulmonary valve permits blood to flow back into the heart chamber before it returns to the lungs and becomes oxygenated.

If symptoms occur, patients should be reviewed by their physicians. Although there is little available on the risk of endocarditis following pulmonary valve surgery, the current recommendation is to provide antibiotic prophylaxis before dental or urologic procedures.




Pulmonary or pulmonic regurgitation (PR) is seldom clinically significant. There are usually no early symptoms that would be noticed by the patient. Eventually,the lower right chamber of the heart can become enlarged and dysfunctional due to the valve problem or pulmonary hypertension. Rarely, this can progress to heart failure. 

Symptoms of right-sided heart failure can occur when the severity and duration of the regurgitation result in right ventricular (RV) enlargement and decompensation. Dyspnea on exertion is the most common complaint. Easy fatigability, light-headedness, peripheral edema, chest pain, palpitations, and frank syncope may occur in patients with any cause of right-sided heart failure and do little to elucidate its etiology. Patients who experience these symptoms may attribute them to poor physical fitness or anxiety, delaying evaluation until their condition worsens. In more advanced presentations of right-sided heart failure, abdominal distention secondary to ascites, right upper quadrant pain secondary to hepatic distention, and early satiety may occur.

Other symptoms specific to the underlying disease process causing PR may occur. Such disease processes include connective-tissue disease, infective endocarditis, carcinoid heart disease, rheumatic heart disease, and primary or secondary pulmonary hypertension. For example, hemoptysis is generally not associated with PR per se, but in severe pulmonary hypertension causing PR, it may occur as a result of the associated pulmonary arteriole rupture and hemorrhage and/or parenchymal inflammation.

Physical Examination

The cardiac examination of pulmonary or pulmonic regurgitation (PR) varies with the severity and cause of the PR. 

Jugular venous pressure (JVP) is usually increased. Often, an increased A wave is present, but this may be less apparent when significant tricuspid regurgitation with a dominant V wave is also present. When right ventricular (RV) enlargement is present, a palpable impulse (lift or heave) is usually present at the left lower sternal border. Palpable pulmonary artery pulsation at the left upper sternal border may be present in the setting of significant pulmonary artery dilatation. With significant pulmonary hypertension, pulmonic valve closure can be palpated.

Signs of PR that can be detected on clinical examination include a unique murmur. In PR, the murmur begins in early diastole, and it is most audible in the left second and third interspaces. The intensity of the murmur increases during inspiration. The pulmonic component of the second heart sound (P2) is inaudible in the absence of a pulmonic valve, whether congenital or secondary to surgical resection. PR associated with pulmonary hypertension has a more high pitched and blowing decrescendo murmur with an accentuated P2 component of the second heart sound; with increased RV end-diastolic volume, the ejection time is increased, P2 is delayed, and the S2 split is widened.

A low-pressure regurgitant flow across the pulmonic valve, as occurs when the pulmonary arterial pressure is normal, is heard as a brief, decrescendo early diastolic murmur at the upper left sternal border. It is made louder by squatting or inspiration and softer by Valsalva maneuvers or expiration. An S3 or S4 may be noted at the left mid-to-lower sternal border because of the presence of RV hypertrophy or failure and is augmented by inspiration.

With more significant PR, the may be a systolic ejection murmur audible in the left upper sternal border from increased RV stroke volume. An accentuated RV impulse may be present. The JVP is typically normal.

The Graham Steell murmur of pulmonary hypertension is a high-pitched, early diastolic decrescendo murmur noted over the left upper-to-left midsternal area and is a result of high-velocity regurgitant flow across an incompetent pulmonic valve. The regurgitant flow murmur may be present during the whole of diastole because there is a pulmonary-to-RV pressure gradient throughout this time period. Typically, the murmur occurs in severe pulmonary hypertension when the pulmonary artery systolic pressure is more than 60 mm Hg. The quality of this high-pitched early decrescendo diastolic murmur is identical to that of aortic insufficiency. However, the peripheral manifestations of aortic insufficiency are absent. The associated findings of tricuspid regurgitation are frequently present, that is, prominent JVP with surging V waves, holosystolic murmur at the lower left sternal border (louder with inspiration), and enlarged, pulsatile liver.

Stages of Progression of Valvular Heart Disease

The American Heart Association and American College of Cardiology (AHA/ACC) has four stages in its classification of progression of valvular heart disease (VHD), as follows[1] :

  • Stage A (at risk): Patients who have risk factors for developing VHD
  • Stage B (progressive): Patients with progressive VHD (mild to moderate severity and asymptomatic)
  • Stage C (asymptomatic severe): Asymptomatic patients with criteria for VHD; C1 comprises asymptomatic patients with severe VHD and left (LV) or right ventricle (RV) compensation, whereas C2 consists of asymptomatic patients with severe VHD plus LV or RV decompensation  
  • Stage D (symptomatic severe: Patients who are symptomatic due to VHD


Diagnostic Considerations

As with any cardiovascular diagnosis, it is important to document the presence and extent of pulmonary or pulmonic regurgitation (PR), the treatment options considered and undertaken (including antibiotic prophylaxis for dental and other procedures), and the plans for follow-up care.

Other conditions to be considered in patients with suspected PR include the following:

  • Marfan syndrome

  • Rheumatic heart disease

  • Carcinoid heart disease

  • Aortic insufficiency: The Graham Steell murmur of pulmonary hypertension is identical in quality to that of the early diastolic murmur in aortic insufficiency. They must be differentiated.


Pregnancy is usually well tolerated in patients with PR, including those who have had surgical repairs for tetralogy of Fallot, except when right-sided heart failure is present that cannot be medically controlled.

Infective endocarditis

Pulmonic valve endocarditis is almost always associated with immunosuppressed states, intravenous/injection drug abuse, and/or congenital heart disease. The risk of endocarditis is thought to chiefly depend on two factors: the presence of high-velocity flow that injures the endothelium by shear forces or the jet impact and exposure to infective organisms. In a series of 186 patients from a congenital heart disease registry with varying degrees of pulmonary and/or tricuspid regurgitation and normal pulmonic and tricuspid valves, investigators observed that the occurrence of pulmonic and tricuspid valve endocarditis was extremely low.[15] The study, however, was not large enough to resolve the question of endocarditis risk in this group, and the authors still advised antibiotic prophylaxis against endocarditis.

The American Heart Association (AHA) recommendations on prevention of infective endocarditis do not support the necessity for antibiotic prophylaxis in pulmonic regurgitation for otherwise structurally normal pulmonic valves, especially if no diastolic murmur is audible (see Infective Endocarditis). However, PR in congenital heart malformations, acquired valvular dysfunction as in rheumatic heart disease, complex cyanotic heart disease, prosthetic valves, and prior bacterial endocarditis comprise moderate- to high–risk conditions that warrant antibiotic prophylaxis.[16, 17, 18]

Differential Diagnoses



Approach Considerations

Pulmonary or pulmonic regurgitation (PR) should be considered in patients with an early diastolic murmur and in patients with right ventricular (RV) enlargement. PR should also be considered in patients who have a history of valvotomy/valvectomy, balloon pulmonary valvuloplasty performed for RV outflow tract obstruction, and in patients with repaired tetralogy of Fallot. When PR is suspected, echocardiography generally confirms the diagnosis and provides an evaluation of its cause and severity. For moderate or severe PR, cardiovascular magnetic resonance imaging (CMRI) is reasonable to provide quantitative assessment of the PR and of RV size and function.

Computed tomography (CT) scanning can be used to evaluate the right heart size and function, but it is generally not used unless there is a contraindication to CMRI, such as the presence of an implanted cardiac device.

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 PR or RV dysfunction.[19]  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 PR compared to those with insignificant or mild PR (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 RV end-diastolic pressure.[19]  The investigators reported 32.15 pg/mL was the optimal BNP cut-off level for considering pulmonary valve replacement.

Exercise testing may provide prognostic information and assist in deciding the timing of valve replacement in symptomatic patients. It is also reasonable in selected asymptomatic severe patients with valvular heart disease (VHD) to confirm the absence of symptoms, to assess the hemodynamic response to exercise, or to determine prognosis.[1]

2014 American Heart Association and American College of Cardiology (AHA/ACC) recommendations

The AHA/ACC recommends the following for diagnosis and follow-up in those VHD (all class I)[1] :

  • Transthoracic echocardiography (TTE) for the initial evaluation of patients with known or suspected VHD for confirmation of the diagnosis, establishment of the cause, determination of the severity and prognosis, and assessment of hemodynamic consequences and timing of interventions
  • TTE for patients with known VHD and any changes in symptoms of physical examination findings
  • Periodic TTE monitoring in asymptomatic patients with known VHD at intervals based on the valve lesion, severity, and ventricular size and function
  • Cardiac catherization for hemodynamic assessment in symptomatic patients in the setting of inconclusive findings with noninvasive studies or in the presence of a discrepancy between results of noninvasive testing and physical examination regarding severity of the valve lesion

Plain Radiography

With severe pulmonary or pulmonic regurgitation (PR), patients may have dilatation of the pulmonary trunk and central pulmonary arteries. Prominent central pulmonary arteries with enlarged hilar vessels and loss of vascularity in the peripheral lung fields ("pruning") suggests severe pulmonary hypertension. In addition, the right ventricle is usually enlarged.

Fluoroscopy and Catheterization

Cardiac catheterization is usually not necessary for the diagnosis of pulmonary or pulmonic regurgitation (PR), but it 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 computed tomography angiography is 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 PR.


Two-dimensional echocardiography (2DE) and M-mode echocardiography can reveal right ventricular (RV) hypertrophy and dilatation. RV volume overload may induce a characteristic abnormal septal wall motion, which appears as flattening of the septum during diastole. Conversely, RV 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 can 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 identifying pulmonary or pulmonic regurgitation (PR). In trivial-to-mild PR, the jet is central and narrow. In moderate-to-severe PR, the width of the jet increases, as does the penetration of the jet into the RV outflow tract. In free or open PR (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 electrocardiogram), 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.[20, 21]

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.

In a study that evaluated the utility of pulmonary arterial end-diastolic forward flow (EDFF) late after repair of tetralogy of Fallot in 399 patients to predict a restrictive RV, Kutty et al noted that while EDFF was common in this group, its presence and extent varied between  echocardiography and cardiac magnetic resonance imaging (CMRI), and it had an association with greater PR and larger RV size but no relationship with markers of poor RV compliance (eg, right atrial enlargement).[22]  The investigators suggested that additional mechanisms beyond RV compliance have a role in EDFF.

Cardiac Magnetic Resonance Imaging (CMRI)

Cardiac magnetic resonance imaging (CMRI) has shown promise based on studies of pulmonary or pulmonic regurgitation (PR). CMRI has excellent temporal and spacial resolution and can provide an accurate estimation of the severity of the regurgitation, the mechanism of the regurgitation, and right ventricular (RV) size and function. However, size and time constraints limit the use of CMRI in clinical practice.

In a retrospective study (2000-2015) of 63 patients with postintervention native valve PR and two or more CMRIs, El-Harasis et al noted clinical characteristics of a low-risk group for rapid progression of RV enlargement included those with PR without an RV end-diastolic volume index (RVEDVi) above 130 mL/m2 and/or without moderate or more severe tricuspid regurgitation.[23]  The investigators indicated that this subgroup of patients may be appropriate for clinical and echocardiographic follow-up, with potentially infrequent CMRI follow-up.


Electrocardiography (ECG) may demonstrate findings of right ventricular (RV) 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. RV hypertrophy may be present by ECG criteria.

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

  • Tall R wave in V1 or qR in V1

  • R wave greater than S wave in V1

  • R wave progression reversal in the precordial leads

  • Inverted T wave in the anterior precordial leads

  • Right axis deviation

  • Right atrial enlargement


Mild-to-moderate pulmonary or pulmonic regurgitation (PR) on echocardiography does not require any follow-up or intervention if the patient is asymptomatic with normal right ventricular (RV) size and function.

For severe PR, the valve anatomy is distorted or has absent leaflets, and annular dilatation is present. In addition, the valve hemodynamics include color jet filling the RV outflow tract, as well as the presence of a continuous wave jet density and contour in addition to dense laminar flow with a steep deceleration slope that may terminate abruptly.[1, 24] Hemodynamic consequences include paradoxical septal motion and RV enlargement. Symptoms include none or variable, and they depend on the cause of the PR and RV function.[1, 24]



Approach Considerations

Pulmonary or pulmonic regurgitation (PR) is seldom severe enough to warrant special treatment because the right ventricle normally adapts to low-pressure volume overload without difficulty. High-pressure volume overload leads to right-sided heart strain and, ultimately, heart failure.

Treatment for PR is usually focused on the underlying cause that created the valve problem (eg, pulmonary hypertension). Underlying etiologies causing severe PR, whether congenital or acquired, must be treated to prevent or reverse right-sided heart strain and failure that may further complicate the clinical picture. 

If pulmonary hypertension is identified with PR, determining the etiology is essential to institute appropriate therapy as expeditiously as possible. For example, primary pulmonary hypertension, secondary pulmonary hypertension due to thromboembolism, severe mitral stenosis, and pulmonary carcinomatosis can all manifest as severe pulmonary hypertension with PR. A discussion of therapeutic interventions in pulmonary hypertension by etiology is beyond the scope of this article. Refer to the articles for each entity under Differentials for a detailed discussion of treatment options.

The need for surgical replacement of the pulmonary valve is very rare.

Transfer requirements are the same as in heart failure.

Consider consultation with cardiologists for patients with right-sided heart failure in the presence of severe PR.

Medical Care

No aspect of medical management of heart failure is uniquely applicable to pulmonary or pulmonic regurgitation (PR), and the discussion of management of right-sided heart failure is beyond the scope of this article. In general, similar approaches to those used in the treatment of patients with left-sided congestive heart failure can be useful. In some circumstances, such as in patients with pulmonary hypertension, vasodilator therapies must be very carefully considered and monitored. In addition, therapies aimed toward the underlying etiology may also reduce PR (see Heart Failure).

Aspects of inpatient care are primarily governed by the treatment indicated for the particular disorder that causes PR. As previously mentioned, if heart failure is present that is due to or exacerbated by PR, usual heart failure management applies.

The American Heart Association and the American College of Cardiology (AHA/ACC) continually updates their guidelines on the management of patients with valvular heart disease.[1, 16]

As noted earlier, the AHA recommendations on prevention of infective endocarditis do not support the necessity for antibiotic prophylaxis in pulmonic regurgitation for otherwise structurally normal pulmonic valves, especially if no diastolic murmur is audible (see Infective Endocarditis). However, PR in congenital heart malformations, acquired valvular dysfunction as in rheumatic heart disease, complex cyanotic heart disease, prosthetic valves, and prior bacterial endocarditis comprise moderate- to high–risk conditions that warrant antibiotic prophylaxis.[16, 17, 18]

Surgical Care

When right-sided heart failure due to pulmonary or pulmonic regurgitation (PR) from an abnormal pulmonic valve cannot be ameliorated by medical management, appropriate options include surgical reconstruction or replacement of the pulmonic valve, preferably with a bioprosthetic valve. Bioprosthetic valves with a logevity up to approximately 15 years after implantation are usually preferred over mechanical valve protheses.[14]  Continuing advances in technology include investigational novel valves for use in larger, nonconduit, outflow tracts (vs fixed-dimension conduits) and the addition of a hybrid surgical and transcatheter approach to pulmonary valve implantation.[25]

Although congenital PR is usually well tolerated, the much more rare congenital absence of the pulmonic valve usually requires pulmonic valve replacement (PVR). Young adults with PVR are likely to require further surgery because protheses have a limited life span. 

Patients should be considered for surgery when both greater than moderate PR and progressive right ventricular (RV) dilatation are present. Delaying surgery may lead to irreverisble RV dysfunction. When PVR is performed, there is reduction of RV size and improved function. However, RV function may not recover in PVR that is performed late. 

The following are indications for surgical PVR[26] :

  • Severe, symptomatic PR
  • Asympatomatic severe PR with severe RV dilatation and/or dysfunction or symptomatic atrial and/or ventricular arrythmias; dysfunction on cardiac magnetic resonance imaging with RV end-diastolic volume above 150 mL/m 2, an end-systolic volume over 80 mL/m 2, and an ejection fraction below 47%
  • Severe PR and progressive tricuspid valve regurgitation

Percutaneous implantation

Relatively recently, percutaneous intervention for dysfunctional RV outflow tract conduits has become available. The intermediate-term results have shown that percutaneous bioprosthetic valve implantation is a reasonable option for patients with dysfunctional RV outflow tract conduits, especially those with high surgical risk. Freedom from valve dysfunction or reintervention following percutaneous bioprosthetic valve placement was 93.5% at 1 year.[27]

Diet and Activity


No specific dietary recommendations exist for pulmonary or pulmonic regurgitation (PR). However, patients who have heart failure symptoms may benefit from a salt-restricted diet.


Because PR is usually of a mild to moderate degree, restriction of athletic activities is unnecessary. Follow-up echocardiographic studies can provide data to assess for changes in PR and right ventricular functional status to more objectively base activity-limitation recommendations.


Patients with underlying conditions such as mtiral stenosis, left ventricular dysfunction, and pulmonary hypertension should be treated. 

Specific comments on deterrence and prevention of pulmonary or pulmonic regurgitation (PR) in general are not found in the literature, except in the context of the specific entities, such as those listed under Etiology, that can cause this condition.

Periodic echocardiographic follow-up is appropriate when significant PR is present for clinicians to better manage the condition over the long term and to help decide when interventions may be warranted.

Long-Term Monitoring

Patients with moderate or severe pulmonary or pulmonic regurgitation (PR) should be seen annually to observe for changes in symptoms and for echocardiography. Adults with repaired tetralogy of Fallot should also be evaluated annually. 

Following pulmonic valve repair, patients require an inital transthoracic echocardiogram to assess baseline valve hemodynamics. Anticoagulation is required for all patients with a mechanical valve prosthesis. For those with a bioprosthesis, administration of 3 to 6 months of oral anticoagulation is recommended.[28]

Regurgitation may worsen with time. Therefore, periodic echocardiographic reassessment with Doppler color flow studies provides a longitudinal comparison of the progression of both the regurgitation and right ventricular size and function. In cases of significant PR, exercise capacity should be assessed and quantitated serially, observing for a change or decrease in function, the goal being to accurately assess the need and potential timing for surgical repair.



Medication Summary

Medications are directed according to the specific etiology resulting in pulmonary or pulmonic regurgitation in addition to the treatment of heart failure (if present). Complete discussions regarding medication use in the specific etiologies noted previously may be found in the respective Medscape Drugs and Diseases articles (see Heart Failure). Infective endocarditis antibiotic prophylaxis should be considered for patients whose PR is due to valve leaflet abnormalities.