Specifically: Deceleration of left ventricular contraction during systole produces an expansion pressure wave (pressure drop) just before valve closure. Is it conceivable that (under possibly pathological condition) the timing of the expansion wave may modulate the radial pulse pressure wave form (incident and reflected wave) into a type-C pressure wave form (wave forms according to Murgo et al. and Nichols et al.)? Is it possible that a pathological condition may thereby produce a radial waveform which is typically associated with a healthy CV system? Has anybody made such observation in practice?
Rapid end-systolic pressure drop and changes to valve patency would probably both have an effect on the wave impedance boundary conditions which regulate the way pulse waves (which are incident to the heart) will reflect back to the aorta. To model this effect would be complex.
@ Edward
Thanks for your thoughts on this. Modelling is actually what we are doing. We have replicated the arterial tree in a complex model of circuits representing the individual arterial segments. The hydraulic-electric analogy helps us to identify the key parameters of arterial function whereby we present in-vivo acquired pulse presure curves to the AI powered model and let the model reproduce the curves as faithfully as possible by modulating the parameters of compliance, resistance and inertia. Whar we see there are curves, specifically in young and very fit subjects, which do not show the second systolic peak at a very low end-systolic pressure. Since I saw the same curve in, admittedly very few, older and certainly unfit individuals, I began to suspect that pathologic conditions might present masquerading as a healthy profile. Would be nice to test this in diseased subjects.
Interesting- low ventricle end systolic pressure wont occur unless there is an ambient arterial bp which is also general low - so it should be encouraging to you how this model is seeing the low bp condition to be a property of healthy / fit subjects.
I hope with this explanation to be given a detailed answer When the cardiac cycle is divided into two stages of active rest stage. At the beginning of the active phase of electrical stimulation causes muscle contractions of the ventricles, resulting in the contraction of the ventricular pressure at constant volume increased with arterial pressure equal to the stage (beginning of systole) Avrty valves open and blood flows into Avrtatrial pressure fell below the mitral valve opens and blood into the left atrium
Left ventricular flow Shvdayn the right side of the heart also occur spontaneously
The location and relative magnitude of the first and the second aortic pressure peak is a matter of interaction between forward and backward flow and pressure waves.
Although forward waves are less variable (at least when speaking of their shape in their first moments), the amplitude and timing of their reflections is very complicated. Taking into consideration a number of paper about wave trapping, re-reflection, etc., only reflections originated somehow close to the ascending aorta are able to impact in a considerable manner the ascending aortic waveform, thus determining the type of the shape. High reflection patterns create type A waveform, while low reflections result in a more type C aortic pressure wave. It is important to underline that type A and type C refer to aortic waveform, and have not meaning at radial artery, although surely aortic shape influences the radial one.
Considering these wave phenomena, it is unlikely that a lumped model can faithfully reproduce all these very characteristics details of a specific person. What you can obtain is a lumped representation of the heart load, which will derive from the choice of the parameters describing resistance, inertance and elastic properties. As you will not deal with any local properties which would results in a subject-specific reflection patter, I think that you will not be able to differentiate between type A and type C aortic waveforms.
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