Pulmonary Regurgitation

Pulmonic regurgitation most often is an incidental benign finding, with a small amount of diastolic backflow across the pulmonic valve seen in most normal individuals. Pathologic pulmonic regurgitation usually is a result of congenital pulmonic valve disease, either untreated mild disease or residual regurgitation after pulmonic valve surgery. The most common cause of significant pulmonic regurgitation in adults is previous surgery for tetralogy of Fallot. Acquired pulmonic regurgitation is rare and is the result of endocarditis, carcinoid syndrome, or myxomatous valve disease. (Otto, Clinical Echocardiography 6e)

Mild pulmonary regurgitation is a normal variant. Acquired pulmonary regurgitation is rare. Causes include pulmonary hypertension, endocarditis, and carcinoid heart disease. Free pulmonary regurgitation is common after repair of tetralogy of Fallot. (Practical Perioperative TOE)

In the adult, acquired PR is most often seen in patients with pulmonary hypertension, which is often associated with dilatation of the pulmonary artery, right ventricle, right atrium, and hepatic veins. Specific valvular anomalies, such as bicuspid, hypoplasia, fenestrated, and prolapse of the pulmonary valve may occur in isolation but are more often associated with other congenital anomalies. Additional causes of PR include rheumatic or carcinoid heart disease, trauma, endocarditis, and pulmonary artery and annular dilation. (Oxford Critical Care Echo)

Severe PR although less common is observed with congenital PV anatomical abnormalities and of course after surgical valvotomy or balloon valvuloplasty. (EACVI Textbook of Echocardiography)

Pulmonary regurgitation is usually well tolerated for many years. However, over time, chronic volume overload causes progressive RV dilatation and dysfunction, with the potential for irreversible RV failure and sudden death due to ventricular arrhythmias. (Practical Perioperative TOE)

Severe pulmonary regurgitation leads to RV volume overload and functional tricuspid regurgitation. (Practical Perioperative TOE)

Chronic severe PR often is well tolerated for many years. More-than-moderate chronic PR produces RV volume overload, with increased end-diastolic volume, followed in time by an increase in end systolic volume and progressive deterioration of right ventricular function. (Oxford Critical Care Echo)

In severe pulmonary regurgitation, the PHT is short, often less than 100 ms, the jet is dense, and the RV is dilated and hyperdynamic. (EACVI Textbook of Echocardiography)

Most clinically important pulmonary regurgitation is seen after repair of congenital disease (notably Tetralogy of Fallot) or secondary to pulmonary hypertension. Work through it in order: define the valve morphology and mechanism, build severity from Doppler signs (remembering that severe low-pressure PR can look unimpressive on colour), assess the volume-loaded right ventricle and the pulmonary arteries, then integrate with CMR and the clinical context to inform the timing of pulmonary valve replacement.

Images of the pulmonary valve may be obtained from the PSAX view at the level of the aortic valve. With anterior angulation, the subcostal short axis view can also provide visualization of RVOT, including the pulmonary cusps. (Oxford Critical Care Echo)

Pulmonary regurgitation can be assessed with color flow Doppler in the midesophageal AV short-axis view or with spectral Doppler (if views are adequate) in the transgastric RV inflow-outflow or upper esophageal aortic arch short-axis view. Congenital disease or carcinoid involvement may result in thickening and deformity of the leaflets. (Practical Perioperative TOE)

Evaluation of pulmonic valve anatomy is limited in adult patients by poor acoustic access. With congenital disease, thickened, deformed leaflets are seen. In endocarditis, a valvular vegetation may be identified, although the pulmonic valve is involved least often. Carcinoid syndrome results in shortening and thickening of the pulmonic valve leaflet. (Otto, Clinical Echocardiography 6e)

Qualitative evaluation of PV to identify the mechanism of valvar dysfunction should include: description of the number of cusps; prolapse; dysplasia; absent of PV (atresia or agenesis). (EACVI Textbook of Echocardiography)

Distorted or absent leaflets, annular dilation, and the presence of a flail pulmonary valve typically indicate the presence of significant regurgitation. (Oxford Critical Care Echo)

Pulmonary regurgitation may be qualitatively assessed with color flow Doppler to estimate jet area and width and with CW Doppler to assess the intensity of the regurgitant signal. Holodiastolic flow reversal detected by PW Doppler in the main PA indicates significant regurgitation. (Practical Perioperative TOE)

In physiological regurgitation, the jet is usually small, centrally located, spindle-like in shape, and less than 10 mm in length. In contrast, pathological regurgitation is characterized by a longer duration of flow (holodiastolic) and a wider jet across the pulmonic valve. CFD is best measured immediately below the PV, from either the PSAX or subcostal view. (Oxford Critical Care Echo)

Mild pulmonic regurgitation is characterized by a narrow jet on color Doppler imaging. The CW Doppler signal is much less dense than the antegrade flow signal, and the diastolic slope is relatively flat. (Otto, Clinical Echocardiography 6e)

The color Doppler signal with severe pulmonic regurgitation often shows a uniform color (without variance) because the velocity of regurgitation is low and less than the Nyquist limit. Holodiastolic flow reversal is present in the main pulmonary artery when significant regurgitation is present and must be distinguished from diastolic flow reversal due to a patent ductus arteriosus. (Otto, Clinical Echocardiography 6e)

Pulmonary regurgitation can be quantified by comparing the jet width to the annulus diameter as mild (< 25%), moderate (26-50%), and severe (> 50%). In severe pulmonary regurgitation, the PHT is short, often less than 100 ms, the jet is dense, and the RV is dilated and hyperdynamic. (EACVI Textbook of Echocardiography)

Severe pulmonic regurgitation shows a wide color jet (at least 70% of outflow tract width); the CW Doppler signal is almost equal in density to antegrade flow with a steep diastolic deceleration, often reaching the zero baseline before the end of diastole. (Otto, Clinical Echocardiography 6e)

A jet width/RVOT ratio more than 65% is highly suggestive of severe PR. (Oxford Critical Care Echo)

A slow deceleration of the jet velocity occurs in mild PR, while a rapid deceleration rate occurs with increasing severity of PR. With increasing severity of PR, a rapid equalization of RV and PA pressures can occur before the end of diastole. Thus, there is an intense signal of 'to and fro' flow in the shape of a 'sine wave', with termination of flow in mid-to-late diastole. (Oxford Critical Care Echo)

Pulmonic Regurgitation: Echo Approach -- Severity of regurgitation: Jet width/annulus; Early termination of PR flow; Diastolic flow reversal in PR branches; Calculation of RF. (Otto, Clinical Echocardiography 6e)

With severe pulmonic regurgitation, color Doppler imaging is unimpressive because diastolic reverse flow is laminar and low in velocity. The pulsed or CW Doppler signal is diagnostic with diastolic reversal of flow equal in signal strength to antegrade flow, with the signal reaching the zero baseline before end-diastole, because of the equalization of pulmonic and RV diastolic pressures. (Otto, Clinical Echocardiography 6e)

Because the flow velocity is low, this finding often is missed on real-time viewing of the images, thus emphasizing the importance of frame-by-frame review when this diagnosis is suspected. (Otto, Clinical Echocardiography 6e)

With color flow Doppler imaging, the jet of pulmonary regurgitation is easily missed, as regurgitant flow is usually laminar and only present briefly during diastole, especially if free pulmonary regurgitation is present. (Practical Perioperative TOE)

This finding, however, is not specific for severe PR, as early and rapid equilibration of diastolic pressures is also seen in patients with low pulmonary artery end-diastolic pressure and/or elevated RV diastolic pressure (e.g. RV infarction). (Oxford Critical Care Echo)

Evaluation of RV size and systolic function on serial studies is particularly important, although quantitative CMR measurement of RV volumes and ejection fraction now is considered the optimal approach. (Otto, Clinical Echocardiography 6e)

Evaluation of the size and function of the RV in the absence of pulmonary hypertension provides indirect clues to the severity of PR. However, evidence of RV dilatation is not specific for severe PR. Nevertheless, its absence suggests a milder degree of PR. (Oxford Critical Care Echo)

Though not specific, the assessment of RV function is important, as the absence of RV dilatation or dysfunction suggest a milder degree of PR. (Oxford Critical Care Echo)

If imaging is technically difficult, consider cardiac magnetic resonance (CMR) or TEE. (Otto, Clinical Echocardiography 6e)

Additional problems that may be present and require surgical correction are a residual VSD, obstruction below or above the PV, and tricuspid regurgitation. The ascending aorta is commonly dilated but seldom needs replacement. (Practical Perioperative TOE)

Some patients with tetralogy of Fallot have pulmonary atresia and require a valved conduit from the right ventricle to the PA. A homograft pulmonary root, porcine pulmonary root, or valved Dacron tube graft may be used as a conduit. These conduits are prone to calcification, stenosis, and regurgitation. (Practical Perioperative TOE)

Assessment of the pulmonary artery (PA) and its bifurcation can be performed by withdrawing the probe to the ME ascending aorta short axis (ME ascending aortic SAX) view. (Oxford Critical Care Echo)

Pulmonic Regurgitation: Echo Approach -- Coexisting pulmonic stenosis: Pulmonic systolic velocity. (Otto, Clinical Echocardiography 6e)

In adults with a repaired tetralogy of Fallot, the VSD patch is evident, the aortic root is enlarged, and some degree of residual RV outflow obstruction usually persists. However, the major long-term issue in adults with surgically treated tetralogy of Fallot is late pulmonic regurgitation. (Otto, Clinical Echocardiography 6e)

The echocardiographic features of corrected tetralogy of Fallot are those of pulmonary regurgitation and RV dilatation and dysfunction. Reconstruction of the RVOT is usually achieved by placing a patch across the annulus of the PV, rendering it incompetent. Further surgery in adulthood for pulmonary regurgitation is common. (Practical Perioperative TOE)

However, over time, chronic volume overload causes progressive RV dilatation and dysfunction, with the potential for irreversible RV failure and sudden death due to ventricular arrhythmias. PV replacement is usually performed using a pulmonary homograft or a bioprosthetic porcine PV. A mechanical valve is not used due to the high risk of valve thrombosis. (Practical Perioperative TOE)

Pulmonary regurgitation following RV outflow tract repair resection is a common serious long-term complication with resultant chronic RV volume (and in this case additional pressure) overload and right heart failure. (Oxford Critical Care Echo)

Evaluation of RV size and systolic function on serial studies is particularly important, although quantitative CMR measurement of RV volumes and ejection fraction now is considered the optimal approach. (Otto, Clinical Echocardiography 6e)

The velocity in the pulmonic regurgitant curve reflects the pulmonary artery to RV diastolic pressure difference. The instantaneous end-diastolic pulmonary artery to RV gradient (calculated as 4v2) can be added to an estimate of RV diastolic pressure (from inferior vena cava size and respiratory variation) to provide an estimate of diastolic pulmonary artery pressure. (Otto, Clinical Echocardiography 6e)

The diastolic pulmonary arterial pressure (DPAP) can be estimated from the end-diastolic pulmonary regurgitation velocity using the modified Bernoulli equation: DPAP = 4 x (end-diastolic pulmonary regurgitation velocity)2 + mean RA pressure. (EACVI Textbook of Echocardiography)

The MPAP can also be estimated as 4 x (early pulmonary regurgitation velocity)2 + estimated mean RA pressure. (EACVI Textbook of Echocardiography)

The mean pulmonary arterial pressure (M) Vmax can be estimated from the early PR velocity and the pulmonary arterial diastolic pressure (D) Vmax from the end-diastolic PR velocity. (EACVI Textbook of Echocardiography)

This method is inaccurate in the presence of massive pulmonary regurgitation or in patients with very high right ventricular diastolic pressures because the velocities proximal and distal to the valve is comparable and violates the assumption of the modified Bernoulli equation. (Oxford Critical Care Echo)

Triage status: All ten targeted Q&A docs were filled with verbatim excerpts from the five mounted echo textbooks (Otto Clinical Echocardiography 6e, EACVI Textbook, Practical Perioperative TOE, Oxford Critical Care Echo, Essential Echocardiography). The orphan excerpts below were extracted but did not fit a single existing question; retained here for later triage.

Mild pulmonary regurgitation (PR) has been reported in 40-80% with normal PV and no structural heart disease. Acquired mild to moderate PR due to annular dilation is seen with pulmonary hypertension. (EACVI Textbook of Echocardiography)

Physiologic (trace-to-mild) pulmonary regurgitation (PR) with structurally normal pulmonary valves (PV) has been reported in up to 88% of patients with increasing prevalence with age. (Oxford Critical Care Echo)

VC width increases with increasing severity of pulmonary regurgitation, but formal cut-off values for the different severities are not available. (Oxford Critical Care Echo)

When compared with aortic flow, pulmonary flow by PW Doppler increases markedly in patients with severe PR, while in the situation of mild PR, pulmonary to aortic flow ratio is either normal or only slightly increased. (Oxford Critical Care Echo)

Note the massively dilated right ventricle in parasternal views accompanied by tricuspid regurgitation and pulmonary regurgitation. Spectral Doppler interrogation across the pulmonic valve confirms marked pulmonary regurgitation exceeding 2 m/s. (Essential Echocardiography)