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Page 16 of 24 Rao. Vessel Plus 2022;6:22 https://dx.doi.org/10.20517/2574-1209.2021.105

murmur. The BP and pulses are unremarkable. As alluded to above, there are no peripheral signs of AR.

ECG typically demonstrates right bundle branch block, especially if the PR is due to previously operated
tetralogy of Fallot. RVH may also be seen. Chest roentgenogram may either demonstrate evidence for prior
surgery (for example, sternal wires) or aneurismal dilatation of pulmonary arteries (in patients with the
syndrome of absent pulmonary valve). Echocardiogram will show RV volume overload in the presence of
moderate to severe PR and demonstrates other heart defects. Doppler examination shows reversed Doppler
flow velocity in the RV outflow tract. Color flow mapping documents the PR and helps quantify the degree
of PR.

The most frequent cause of PR is prior surgical repair of tetralogy of Fallot. Surgical pulmonary valvotomy
and balloon pulmonary valvuloplasty for valvar PS are the other causes. Historical information of the
previous operation or catheter intervention and the scar of previous surgery are useful hints in the patient
assessment. Syndrome of the absence of pulmonary valve, usually associated with other defects such as
tetralogy of Fallot or VSD should also be considered in the differential. Chest X-ray may suggest aneurismal
dilatation of the PAs. But echocardiogram demonstrates all the features of the syndrome, namely, VSD,
pulmonary valve ring narrowing, absent or rudimentary pulmonary valve leaflets, systolic pressure gradient
across the pulmonary valve, PR, and massive dilatation of the main, right, and left PAs. Cardiac
catheterization and angiography are not necessary for the diagnosis, but if performed, confirm the above
findings.

Pulmonary regurgitation murmur of pulmonary hypertension
The early diastolic decrescendo murmur of pulmonary hypertension, referred to as Graham Steel’s murmur,
is auscultated best at LUSB and LMSBs. However, it exhibits a high pitch similar to AR murmur. Increased
RV impulse, single 2nd heart sound, and ejection systolic click along the left sternal border indicative of
pulmonary hypertension are also found on examination. Infrequently, a murmur of TR may be heard.
While the high-pitched quality of this murmur is similar to that of AR, the location of the murmur is at the
LUSB, and there are no peripheral signs of AR.

RVH is present in the ECG. Echo-Doppler studies demonstrate a dilated and hypertrophied RV. Elevated
RV/PA pressures may be documented on the basis of TR and PR jet velocities. In addition, the heart defect
causing pulmonary hypertension is also identified.

Mid-diastolic murmurs
Mid-diastolic murmurs (Figure 3; middle) are more difficult to appreciate because they are low-pitched
murmurs, they are of low intensity (Grade I-II/VI), and are typically confined to a small part of the
precordium. These murmurs are secondary to increased blood flow through a normal atrioventricular (AV)
valve (during the rapid filling phage of the ventricles) or due to a normal amount of blood flow through a
narrowed AV valve. The mid-diastolic murmurs related to flow across the mitral valve are auscultated better
at an area somewhat internal to the apex, while those related to flow across the tricuspid valve are
auscultated at the LLSB. Both murmurs are heard best when using the stethoscope’s bell for auscultation.
The etiology of both AV valve mid-diastolic flow murmurs is shown in [Table 7]. There are no distinctive
features of these murmurs that can differentiate the mid-diastolic murmurs from one another; however,
findings in history and physical examination are useful in the differential diagnosis.

Large flow across the mitral valve
Increased flow across the mitral valve is produced either by augmented pulmonary blood flow secondary to