Episode #2 – RV (patho)physiology
Follow Karl-Philipp Rommel (Leipzig, Germany) as he shares insights on physiology relevant to diagnosing and treating TR-related right heart failure.
In this video you will learn:
– to recall the unique physiology of right ventricular function
– to understand the implications of RV pressure and volume load using the pressure-volume-loop framework
– to illustrate the concept of right ventricular-pulmonary arterial (RV-PA) coupling ratio

More resources from the PCR Tricuspid Focus Group: https://www.pcronline.com/Cases-resources-images/Zoom-on/Tricuspid-Focus-Group-Content

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And this is the second part of our series discussing physiology relevant for diagnosis and treatment of tricuspid regation related right heart failure and here I want to take a deeper dive into right ventricular physiology together we want to recall the unique physiology of right VC function understand implication of different loading conditions and

Illustrate the concept of righten to pulmonary arterial coupling the right ventricle has a complex shape and contracts in three separate mechanisms the movement of the free wall towards the septum produces a battos effect then there is traction of the free wall secondary to LV constraction and then there is longitudinal shortening which accounts

For the the majority of normal RV function however this might not hold true in the setting of RV dysfunction standard clinical assessment often relies on onedimensional assessment of RV function as tapsy or tissue velocity at the lateral TripIt anulus both predominantly quantifying longitudinal function in order to comprehensively

Assess RV function we need to use a multi metric approach as Illustrated here for example with echocardiography or more advanced modalities like cardiac magnetic resonance imaging considering the right ventricle functional unit you can also apply the pressure volume Loop framework which describes the instantaneous changes in pressures and volumes during the cardiac

Cycle the width of the loop corresponds to the stroke volume the height of the loop represents the peak systolic pressure and it shows you four discrete phases of the cardiac cycle The Filling phase the bottom the injection phrase here at the top and the isobolic contraction phase and isobolic relaxation phase to the

Side of it systolic properties of the right ventricle can be summarized by the slope here of the antolic pressure volume relationship or an systolic elastin and as this um slope here becomes steeper the contractility increases the diastolic properties of the right ventricle are represented by the and diastolic pressure volume

Relationship this the curve that actually hugs The Filling phase here of the right ventricle and one of the main advantages of pressure volume Loop assessment is that systolic and diastolic properties can be assessed in a load independent fashion the pressure volume diagram also helps to characterize right ventricular

Energetics here you see the area within the pressure volume Loop represents the stroke work and together with the potential energy this equals the pressure volume Loop area which is directly and linearly related to myocardial oxygen consumption the pressure volume Loop diagram also informs on pulmonary arterial properties and RV AP the load

AP load is presented here by the effective arterial elastin which is the line that connects coordinates at and diast and coordinates it and syy and as the slope of that line increases after also increases right V cha pulmonary arterial coupling then is a concept indexing ventricular contractility to its after load

And on the PV Lo it can be summarized as the ratio of the antolic elastin here resembling contractility to the effective arterior elastance resembling after load and conceptually it’s it describes a hemodynamic state where mechanical stroke work is most efficiently transferred to the pulmonary vasculature and practically it helps you determine

Whether RV function is adequately compensated for specific loading conditions a such can use this concept to describe the disease progression but also evaluate RV compensation relative to abnormal RV loading and as the acquisition of invasive pressure volume Loops is not feasible on a large scale and clinical practice we usually rely on non-invasive

Surrogates the most commonly used here is the ratio of tapsy over PA systolic pressure or right ventricular systolic pressure um which had been initially evaluated for left heart failure patients but now let’s see what happens when we introduce tricuspid regurgitation in this model from the purple Loop here with no

Trasp reg to the yellow loop with torrential TR you see that the stroke volume progressively increases but keep in mind this results from an increase in regurgitant volume while actually the RV forward stro volume decreases in addition stroke work increases but importantly RV and Pa pressures tend to

Decline these effect is even more pronounced when modeling Progressive tricuspid regurgitation in abnormal right abnormal right ventricle you see here um in dark purple no TR to Yellow torrential TR the stroke volume doubles and this also means that TR causes a reduction in energetic efficiency in this case for reduced cardiac output the

Stroke work actually increases by a factor of two another interesting aspect when interpreting rvpa coupling in TR patients is then what that one has to come to understand that the presence of TR is associated with the reduction in RV afterload since the ejection occurs partly towards um low impedance Outlet namely the

A so here you can see this is Illustrated here in this pressure volume Loops here again no TR here with the dark purple to torrential TR uh in yellow the effective material elastance resembling afterload actually decreases in slope meaning that afterload is decreasing however contractility is not expected to change

Significantly and all this summarizes the mechanisms by which TR can create right hard failure namely volume overload besides volume overload there are other mechanisms by which rart failure might be induced among them are fact s associated with impaired intrinsic contractility or as we typically see in our patients a pressure

Overload and you probably have come across this 50-year-old concept of right afterload sensitivity that says that for a given increase in pressure the RV um decreases more in stroke volume than the LV however pressure levels of the system IC and Pulmonary vasculature obviously differ and when we plot

Changes in stroke volume as a function of percentage changes of peak pressures the RV and the LV curves are not that different really questioning this existing Paradigm in addition these changes really apply to acute conditions and in chronic conditions the RV has enormous potential to adapt this function to

Altered loading conditions and this is nicely Illustrated here in um our patients characterized as pressure volume overloaded or volume overloaded or controls and we see here that uh patients with a pressure volume overload actually have the highest Baseline contractility as indicated here by steep slope of the an systolic elastin much

Higher than the controls and notably the patients with the volume Overload at the lowest Baseline contractility and both patients with pressure and volume overload actually showed no increase of the contractility with exercise meaning that they do not have a contra contractile Reserve as opposed to Patient control patients actually increases increase their

Contractility and these observations together suggest that chronic RV volume overload is at least as detrimental for RV function as pressure over overload um which has been considered in a setting of TR related rard failure and to conclude the section RV function exhibits a unique physiology RVP coupling describes how

Well RV function is compensated for given after load trasp gradutation induces RV volume overload reduces energetic efficiency and effective afterload chronic RV volume overload is characterized by low cont tra low RV contractility and low RV contractile reserve and with that I thank you and hope you to see you the next Video

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