Auscultatory and Phonocardiographic Assessment of Pulmonary Stenosis with Intact Ventricular Septum

Abstract

A clinical and phonocardiographic study has been made on pulmonary and infundibular stenosis with intact ventricular septum, in order to determine the value of auscultation and phonocardiography in assessing the severity of the stenosis. There were 43 cases of pulmonary valve stenosis with intact ventricular septum and 8 cases of infundibular stenosis with intact ventricular septum. The severity of the stenosis, as determined by the right ventricular pressure, was correlated with the duration of right ventricular systole, as determined both by the length of the systolic murmur and the width of splitting of the second heart sound. It was shown that increasingly severe stenosis resulted in progressive lengthening of the murmur in relation to the aortic second sound and delay in pulmonary valve closure. Criteria were defined whereby the severity of the stenosis could be predicted; these proved more accurate than other clinical methods. In mild stenosis (RVP under 60 mm. Hg), the murmur was soft to loud in intensity, reached a crescendo in midsystole and ended before or at the aortic component of the second sound. The second sound was always abnormally split (average 0.05 second), and there was frequently a pulmonary ejection sound. In moderately severe stenosis (RVP 60 to 120 mm. Hg), the murmur was louder, the crescendo and duration greater, extending a short way beyond the aortic component, which it never obscured. Splitting was wider (average 0.07 second), and the pulmonary component was reduced in intensity. There was frequently a sharp, click-like first sound on expiration. In severe stenosis (RVP 120 to 180 mm. Hg), the murmur was loud with great delay in the crescendo and duration, resulting in a kite-shaped rather than a diamond-shaped configuration. It invariably extended well beyond the aortic component, which it either partially or completely buried. The murmur always ended before a very soft pulmonary component, which was widely separated from the aortic component (average 0.08 second). In very severe stenosis (RVP above 180 mm. Hg) the murmur was loud and so prolonged that it invariably obscured the aortic component, but ended before a very delayed (average 0.10 second) diminutive pulmonary component, which may or may not be heard. Whenever the aortic component was completely buried by the murmur, the great width of splitting could not be heard on auscultation, and phonocardiography was required for its detection. Thus, the length of murmur and the degree to which the aortic sound was buried were more useful auscultatory guides than the width of splitting in severe grades of stenosis. Whenever the aortic component was buried, a right ventricular pressure exceeding 120 mm. Hg could be predicted. Unusually wide splitting of the second sound was encountered in a few mild and moderately severe cases of valvular stenosis. These cases all had pronounced post-stenotic dilatation of the pulmonary artery to which the delay in pulmonary valve closure was attributed. In these cases prediction of severity from murmur length was more reliable than from width of splitting. Valvular and infundibular stenosis differed only in a few features. In infundibular stenosis, a pulmonary ejection sound was never encountered and the width of splitting was much greater than in valvular stenosis of comparable severity. The mechanism is discussed. The site of maximal intensity of the murmur was seldom helpful in differentiating valvular from infundibular stenosis. The increase in murmur length with increasing severity of stenosis was similar in both conditions.