You mean lv end diastolic volume/pressure? Or do you mean end diastolic diameter.. These are all different terms but theyre all sort of interconnected (obviously more volume=more pressure=more stretch).. So ill explain some.
Well, assuming you're already familiar with the basics of what end diastolic volume is, and how it works.. For example, the frank starling mechanism, length tension relationship and how contractility and oxygen consumption are directly proportional.. We can dive a level deeper.
Higher end diastolic pressures are associated with changes in electrolytes. Specifically these conditions increase the levels of intracellular calcium, this is accomplished through the release od specialized neurotransmitters.
This calcium in term is a critical component in the interaction between actin and myosin... This alows for more contact points in the muscle fibers and hence more forceful contraction.
Unfortunately these increased levels of calcium means the cells have more electrolytes to manage in order to maintain an appropriate resting membrane potential.
Managing these elevated levels of calcium is accomomplished through channels in the membrane and via uptake of calcium in the sarcoplasmic reticulum.
All of these elecrolyte balancing processes are ACTIVE meaning they require de-phosphorylation of atp to reconfigure the responsible proteins.
In laymans terms.. More calcium means the body needs to use more ATP to get rid of it!
ATP is formed via the citric acid (Krebs) cycle, an aerobic metabolic process.. This means ATP is made from oxygen!
In order to make all this extra atp, the heart needs access to oxygen.. Which means it needs a steady supply of blood (somethinf heart failure patients dont often have), and it needs plenty of oxygen (also something heart failure patients tend to be deficient in)
If the heart doesnt have enough oxygen to make enough atp to keep all the "lights on".. Then it has to start picking and choosing which "lights" are gonna get shut down.
The end result? Tissues start to die, compensatory mechanisms start to kick in.. And what you wind up with is a process of ventricular remodeling that leaves alot of scar tissue and areas of heart muscle that function at a suboptimal level.
This of course also has the added pitfall of making the ventricle a bit stiffer, which further increases diastolic pressures.. Which further generates neurotransmitters, which free more calcium etc etc.. Until the patient.. Well you get the picture.
Hope it helps.
In terms of clinical management, these cases get tricky.. But thankfully modern medicine has some tools to use.
First thing we do is take care of any conditiom thats compromising the hearts ability to receive adequate blood flow or oxygen. This could be a blockage in an artery, a problem in the lungs or an electrical or anatomical issue, in any case it gets fixed.
Next we control the pressure. We use drugs such as aceinhibitors to lower arterial pressures. This forces blood into more distal systems.. Such as the arms and legs. It also reduces the pressure difference between the arterial and venous system and reduces the amount of blood flowing through the heart and hence end diastolic volume.
Thirdly when patients have high end diastolic pressures the heart compensates through compounds such as BNP (which is also a key marker for heart failure blood work) and ANP, which act in thd kidneys to help urinate some sodium. This helps in maintaining that electrolyte balance, with less consumption of ATP and takes out some fluid as well. When patients endogenous BNP and ANP is insufficient we have drugs available that function sort of like copycats and aid in this process.
If all that is still insufficient we gotta look at volume control.. Forcing fluid out through diuresis such as lasix, or through a system such as dialysis.
Unfortunately as we pump these patients full of these drugs we run into problems. Namely as we improve diastolic function we also lose alot of systolic function. So,we fix one problem but now we arent ejecting enough blood (a bigger problem). In this scenario we may have to add drugs that increase contractility basically by helping the body use what it has a bit better, for example we may want to open more calcium channels instead of simply increasing calcium comcentration, improving systolic function without the increased demand seen with simply increasing end diastolic pressure. A big go-to therapy here would,be biventricular pacing as well. We xan use a pacemaker to help,the heart mucle contract in a more 'organized' manner, allowing more blood to be ejected at systole. Extreme cases would require intervention through placement of a percutaneous or surgical device that helps patients pump blood.