In hypertrophic cardiomyopathy, there is narrowing of the left ventricular outflow tract (LVOT) due to hypertrophy of the interventricular septum. During systole, the narrowing of the LVOT creates a more negative pressure due to the Venturi effect and sucks in the anterior mitral valve leaflet. This creates a transient occlusion of the LVOT, causing a midsystolic dip in the aortic waveform. Towards the end of systole, the ventricle is able to overcome the obstruction to cause the second rise in the aortic waveform.[2]
In severe aortic regurgitation, additional blood reenters the left ventricle during diastole. This added volume of blood must be pumped out during ventricular systole. The rapid flow of blood during systole is thought to draw the walls of the aorta together due to the Venturi effect, temporarily decreasing blood flow during midsystole.[2]
A recent paper theorized that an alternative explanation for pulsus bisferiens may be due to a forward moving suction wave occurring during mid-systole.[3]
^ abRiojas CM, Dodge A, Gallo DR, White PW (January 2016). "Aortic Dissection as a Cause of Pulsus Bisferiens: A Case Report and Review". Annals of Vascular Surgery. 30: 305.e1–5. doi:10.1016/j.avsg.2015.07.026. PMID26520426. This reference illustrates the normal and abnormal spectral waveform.
^ abMcGee SR (2018). "Chapter 15: Pulse Rate and Contour". Evidence-based physical diagnosis (Fourth ed.). Philadelphia, PA: Elsevier. pp. 95–108. ISBN978-0-323-50871-1. OCLC959371826.
