Korotkoff Sounds

Abstract

SUMMARYWe have studied Korotkoff sounds in 10 subjects by recording pressures and sounds simultaneously through a brachial arterial needle at locations both beyond and beneath the inflatable cuff. The Korotkoff sounds coincided with a small dip and ensuing steep rise in pressure immediately beyond the distal edge of the cuff. Sound intensity paralleled not only the rate and the acceleration of this steep ascent, but also the total pressure through which it was maintained. Pressures beneath the midportion of the cuff showed a more pronounced sharp initial negative dip, usually followed by a rapid reversal and steep rise, and the sounds were also recorded here in association with these rapid pressure changes. This study supports the hypothesis that the initial Korotkoff sound is produced by rapid changes of pressure both beneath and distal to the compressing cuff, sufficient in rate to impart sonic vibrations to the vessel wall and surrounding tissues. We have attempted to explain how these rapid pressure changes are produced.

Effect of respiration on Korotkoff sounds and oscillometric cuff pressure pulses during blood pressure measurement

“…Moreover, if respiration modulates the oscillometric pulses, this modulation could also affect the Korotkoff sounds associated with the blood pulse flowing through the brachial artery. One longstanding hypothesis on the genesis of Korotkoff sounds is that the sharp audible tapping sound is generated by the distension of the arterial wall caused by the changing transmural pressure gradient [4, 10, 16, 18]. It may therefore be speculated that if respiration modulates the pressure pulse, it might also influence the force deployed in opening the artery, which in turn may reflect on the amplitude of the Korotkoff sounds.…”

Compression of the brachial arteryin vivo

“…An occlusion cuff high up on the forearm is inflated to above systolic pressure. The internal pressure in the brachial artery distal to this cuff reduces over a few seconds to a pulseless non-flow, steady-state value generally between 30 and 70 mmHg (Tavel et al 1969).…”

Recent development of respiratory rate measurement technologies

“…Similar to PPG, the tissue volume changes the pressure of the OscP measurement site, which is reflected on the amplitude of OscP signal. Despite the debated genesis of Korotkoff sounds, it is widely supposed that KorS is generated by the distension of the arterial wall caused by the changing transmural pressure gradient (McCutcheon and Rushmer 1967, Tavel et al 1969, Ur and Gordon 1970, Venet et al 2000. The respiratory modulation of stroke volume will directly influence the force deployed in opening the artery and consequently the blood flow sound, reflected by the amplitude of the KorS signal.…”