Auscultatory and Phonocardiographic Assessment of Fallot's Tetralogy

Abstract

A clinical and phonocardiographic study has been made on 62 cases of Fallot's tetralogy in order to determine the value of auscultation and phonocardiography in assessing the severity of the stenosis. The severity of the tetralogy, as determined by clinical methods, was correlated with the length and loudness of the murmur and other auscultatory signs. Increasingly severe stenosis was shown to be associated with a shorter, earlier, and softer systolic murmur. In extreme tetralogy, the murmur was invariably soft and very short, being confined to early systole and ending in midsystole. An aortic ejection sound was usually audible and the second sound invariably loud and single. In severe tetralogy, the murmur was usually loud and short, with its crescendo before midsystole and termination before the aortic second sound. A pulmonary component was never audible. In moderate cases, the murmur was loud and longer, with its crescendo at midsystole and termination before or at the aortic second sound, which was never obscured by the murmur. A very soft pulmonary component was only rarely recorded. In mild cases, the murmur was loud and more prolonged with the crescendo in the latter half of systole and extension into, but rarely much beyond, the aortic component. Although at times loud at the aortic component, the murmur totally obscured this sound in only 1 case. A pulmonary component was frequently recorded and often heard; it was extremely soft and localized, but occasionally relatively loud. Splitting was always wide (average 0.09 second). The loud, long murmur reflected good pulmonary flow; the audible or recordable pulmonary component, a relatively normal pulmonary arterial pressure. Since the length and loudness of the systolic murmur reflect the volume rate of blood ejected through the stenosis, auscultation is believed to be a most valuable method of assessing both the severity of stenosis and fluctuations in blood flow, which may result from changes in systemic resistance and tonus of the infundibulum of the right ventricle. The change in murmur during cyanotic or syncopal attacks has thrown considerable light on the mechanism of such attacks.