Pulmonic (pulmonary) regurgitation (PR) is incompetency of the pulmonic valve causing blood flow from the pulmonary artery into the right ventricle during diastole. The most common cause is pulmonary hypertension. PR is usually asymptomatic. Signs include a decrescendo diastolic murmur. Diagnosis is by echocardiography. Usually, no specific treatment is necessary except for management of conditions causing pulmonary hypertension.
Secondary pulmonary hypertension (see Table 1: Classification of Pulmonary Hypertension) is by far the most common cause of PR. Less common causes are infective endocarditis, surgical repair of tetralogy of Fallot, idiopathic pulmonary artery dilation, and congenital valvular heart disease. Carcinoid syndrome, rheumatic fever, and catheter-induced trauma are rare causes. Severe PR is rare and most often results from an isolated congenital defect involving dilation of the pulmonary artery and pulmonary valve annulus.
PR may contribute to development of right ventricular (RV) dilatation and eventually RV dysfunction–induced heart failure (HF), but in most cases, pulmonary hypertension contributes to this complication much more significantly. Rarely, acute RV dysfunction–induced HF develops when endocarditis causes acute PR.
Symptoms and Signs
PR is usually asymptomatic. A few patients develop symptoms and signs of RV dysfunction–induced HF (see Classification).
Palpable signs are attributable to pulmonary hypertension and RV hypertrophy. They include a palpable pulmonic component (P2) of the 2nd heart sound (S2) at the left upper sternal border and a sustained RV impulse that is increased in amplitude at the left middle and lower sternal border.
On auscultation, the 1st heart sound (S1) is normal. The S2 may be split or single. When split, P2 may be loud and audible shortly after the aortic component of S2 (A2) because of pulmonary hypertension, or P2 may be delayed because of increased RV stroke volume. S2 may be single because of prompt pulmonic valve closing with a merged A2-P2 or, rarely, because of congenital absence of the pulmonic valve. An RV 3rd heart sound (S3), 4th heart sound (S4), or both may be audible with RV dysfunction–induced HF or RV hypertrophy; these sounds can be distinguished from left ventricular heart sounds because they are located at the left parasternal 4th intercostal space and because they grow louder with inspiration.
The murmur of PR due to pulmonary hypertension is a high-pitched, early diastolic decrescendo murmur that begins with P2 and ends before S1 and that radiates toward the mid-right sternal edge (Graham Steell murmur); it is heard best at the left upper sternal border with the diaphragm of the stethoscope while the patient holds the breath at end-expiration and sits upright. The murmur of PR without pulmonary hypertension is shorter, lower-pitched (rougher in quality), and begins after P2. Both murmurs may resemble the murmur of aortic regurgitation but can be distinguished by inspiration (which makes the PR murmur louder) and by Valsalva release. After Valsalva release, the PR murmur immediately becomes loud (because of immediate venous return to the right side of the heart), but the aortic regurgitation murmur requires 4 or 5 beats to do so. Also, a soft PR murmur may sometimes become even softer during inspiration because this murmur is usually best heard at the 2nd left intercostal space, where inspiration pushes the stethoscope away from the heart.
PR is usually incidentally detected during a physical examination or Doppler echocardiography done for other reasons. Mild PR is a normal echocardiographic finding that requires no action. An ECG and chest x-ray are obtained. Either may show signs of RV hypertrophy; chest x-ray typically shows evidence of conditions underlying pulmonary hypertension.
Treatment is management of the condition causing PR. Pulmonic valve replacement is an option if symptoms and signs of RV dysfunction–induced HF develop, but outcomes and risks are unclear because the need for replacement is so infrequent.
Last full review/revision November 2012 by Guy P. Armstrong, MD
Content last modified September 2013