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@kyliebaker888 @LMSaxhaug 1/Sorry if this is common knowledge (I know I wasn't asked) but if anyone is confused by diastology, perhaps this will help (what follows is the most basic explaination and reality is more complicated). Ventricular filling is mostly governed by 3 factors.
@kyliebaker888 @LMSaxhaug 2/ the factors are: 1)active relaxation or the detachment of the actin/myosin/troponin complex. The more Ca2+ in the cytosol the more linkage and the less ability of the fibers to "let go" thus less ability to relax. ATP is required to pump the Ca2+ out of the cytosol.
@kyliebaker888 @LMSaxhaug 3/ If something like ischemia reduces ATP production, this first factor is inhibited and relaxation is impaired. 2) the intrinsic "sponginess" of the ventricle. The ventrical, if allowed to relax (from factor 1) will like to "spring back" into its normal shape. This is suction!
@kyliebaker888 @LMSaxhaug 4/ 3) "Push" of blood into the ventricle from the left atria by LAP.
@kyliebaker888 @LMSaxhaug 5/ So, to summarize, the left ventricle is filled by a pressure differential between the LV and LA that is generated by either "suction" by the LV via factor 2, or a "push" of blood from pressures in the LA/pulmonary circulation. LV compliance/elastance is because of factor 1.
@kyliebaker888 @LMSaxhaug 6/ On to Doppler: PW Doppler measures velocities at the gate. Velocity represents pressure gradients as predicted by the Bernoulli principle, in this case the pressure difference between the LV and LA during diastole. E is passive filling, A is atrial kick of course.
@kyliebaker888 @LMSaxhaug 7/ However, whilst PW Doppler tells us what the pressure differential is between the LV and LA, it doesn't tell us if this pressure differential is due to LV suction (relative negative pressures generated by factor 2) or elevated LAP (push by factor 3).
@kyliebaker888 @LMSaxhaug 8/ When we see the diastolic PW progression, this is what we see: normal E>A. This is because factor 1, allows the LV to spring back to its relaxed shape and the LV/LA pressure differential is generated mostly by LV suction, rather than LA push as the LV springs back
@kyliebaker888 @LMSaxhaug 9/ Next is relaxation abnormality. E<A. Here, the LV doesn't "spring back" to its normal shape because factor 1 (the ATP dependent relaxation) is impaired, or the LV is less "springy." Now, there is a lack of suction, so the LV/LA pressure differential is reduced.
@kyliebaker888 @LMSaxhaug 10/ In this situation, LAP is generally not really elevated yet, so there is not significant "push" to generate a large LA to LV pressure. This is why the E wave is reduced-less pressure change. There still is a push from the LA, but because of decreased LV compliance, cont.
@kyliebaker888 @LMSaxhaug 11/ It takes longer for the pressures to equalize (affect of impaired factor 1), therefore a prolonged deceleration time.There's extra blood left over in the LA because the pressures equalize before the LA empties, so when the LA contracts, a LA "push" generates a tall A wave.
@kyliebaker888 @LMSaxhaug 12/ most of the time the LAP is normal here, but in reality, sometimes the LAP is actually a bit elevated. I think this is why there was the update from the 2009 to 2016 ASE diastolic classifications, but if the E<A and E is >50 cm/sec consider high LAP, grade 1a by 2009, 2 2016
@kyliebaker888 @LMSaxhaug 13/ On to Pseudonormalization: So now, LAP is on the rise and the "push" is generating the LA/LV pressure differential, rather than suction. E, being a measure of that pressure, increases. E doesn't care if the differential is generated by suck or push, it's just a pressure.
@kyliebaker888 @LMSaxhaug 14/ now the LV/LA pressure equalize at an elevated LV filling pressure, but the atria still generates a reasonable pressure gradient with contraction, just not as great as that generated by the "push" of the LAP. Thus we get the pseudonormal E>A.
@kyliebaker888 @LMSaxhaug 15/ Restrictive pattern is next: As the LV gets incredibly stiff and non compliant, the Increasingly elevated LAP generate a high LA/LV pressure gradient. The E is thus quite tall. The LV filling pressures are so high, the A wave cant make much more pressure-E:A >2:1 now.
@kyliebaker888 @LMSaxhaug 16/ another quick summary: PW Doppler measures velocity of blood flow-essentially pressure differentials to generate flow. But E can't tell you if this differential is due to suction or too much push, or the other way round. Critical point-cont!
@kyliebaker888 @LMSaxhaug 17/ E tells you something about the relative relationship of factor 2 and 3, but can't tell you about factor 1, if we are talking about the 3 primary factors if diastology. Another way to say this is E tells us pressure differentials, but the relaxation component is also there.
@kyliebaker888 @LMSaxhaug 18/ therefore, roughly, E=pressure/relaxation ability. Here's where tissue Doppler comes in. PW Doppler is meant to measure blood flow. Therefore, traditional PW Doppler is set up to filter Doppler signals out that aren't low amplitude and high velocities.
@kyliebaker888 @LMSaxhaug 19/ However, if we tell the US that we want to see high amplitude, low velocity Doppler signals, we can ignore blood flow and see how fast heart tissue moves. This is Tissue Doppler Imaging.
@kyliebaker888 @LMSaxhaug 20/ Because with tissue Doppler imaging (TDI) we are only looking at how fast tissue is moving, and not seeing blood flow, TDI doesn't give us much information about pressure differentials. It does, however tell us about how fast the LV can relax!
@kyliebaker888 @LMSaxhaug 21/ the faster the LV can relax, the more springy it is and the TDI velocities are faster. Stiff ventricles move slower (factors 1&2). So e' can be described as roughly e'=1/relaxation ability. Recall roughly, E=pressure change/relaxation ability.
@kyliebaker888 @LMSaxhaug 22/ with regard to e', as the ventricle gets stiffer the e' wave gets smaller. With regard to E, the velocity changes relative to the LA/LV pressure differential, which may be due to suck or push-which is a function of relaxation-that e' informs us about in a way that E can't.
@kyliebaker888 @LMSaxhaug 23/ if E=pressure/relaxation ability and e'=1/relaxation ability, then by dividing E by e' (the E/e' ratio), we cancel out the confounding relaxation ability and are left with something proprtional to only LAP, a very important clinical entity.
@kyliebaker888 @LMSaxhaug 24/ in summary, E and e' together inform us about ventricular stiffness and filling pressures. This ultimately has extremely important implications about LV diastolic function, arguably just as important as systolic function and there are multiple clinical applications here.
@kyliebaker888 @LMSaxhaug 25/25 Again, sorry to butt in uninvited on a conversation, especially if I only described what everyone already knew, but hopefully someone got something out of this!
