History
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] :
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Stage A (at risk): Patients who have risk factors for developing VHD
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Stage B (progressive): Patients with progressive VHD (mild to moderate severity and asymptomatic)
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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
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Stage D (symptomatic severe: Patients who are symptomatic due to VHD
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Continuous-wave signal of transpulmonary flow in severe pulmonary regurgitation. Courtesy of Wikimedia Commons [AMC Echolab, AMC, The Netherlands].
