pathophysiology question on heart

ok, let's piece these out one at a time.

filling pressure is just the pressure that is in the ventricles at the end of diastole. for a given volume delivered to a ventricle, pressure can be lower if the ventricle is nice and soft and flexible and empty, ready to accept a new load, than if it's hard and scarred up or has leftover blood in it from the last systole because the av is hard to open or because its contractility was so lousy that it didn't empty well. another term that is used could be "preload," pre- meaning "before systole," and load, well, being the load of blood delivered to the ventricle that it is gonna have to move out in systole. you can measure load as weight or volume, but the way we look at it is by measuring the pressure that occurs there. pressure changes tell us what's going on in there.

first, let's look at the blood flow in a linear fashion.

body > veins > vena cava > right atrium > tricuspid valve > right ventricle > pulmonic valve > pulmonary artery > lungs >pulmonary vein > left atrium > mitral valve > left ventricle > aortic valve > arteries > body

think about when the valves between two chambers are open. by definition, each chamber must be at the same pressure, right? so, at the end of diastole, just before systole, the pressure in the lv is the same as la pressure is the same as the pressure in the pulmonary vein (no valve in the way there) and in the pulmonary capillary bed. and since there are no valves in the pulmonary capillary bed, tracking backwards, you can see that lv end diastolic pressure equals end-diastolic pulmonary artery pressure, which is, conveniently, what we look at when we are wondering what's going on in the left heart.

ok. now, why do we care about lv end-diastolic (filling) pressure? for that, i wish i could draw you a nice little curve here. i can't, so i will describe it and you will draw it on a piece of paper to look at while we chat.

horizontal axis: label this "preload" or any other term you like. filling pressure, pa diastolic pressure is the same thing (see above) and you can even extrapolate all the way back to central venous pressure, for a rough trend-setting bit of data.

the vertical axis you will call "cardiac output," or "blood pressure," because the line we are going to draw is going to explain something really cool.

start lowish on the left, near the vertical axis-- low filling pressure means low bp. think: hemorrhage, hypovolemia, makes your bp low, right?

slant the line upwards to the right, showing that blood pressure (cardiac output) increases the more blood you put into the heart. (tank up that hypovolemic guy, and bp improves.) but at some point, that upward-going curve peaks, flattens out...and then it drops as the preload keeps increasing. this is because cardiac muscle is like a rubber band-- the more you stretch it, the harder it contracts...to a point, at which point it gets too stretched out and actually contracts less well. draw a little asterisk at the top of that curve, where it starts to fall, then let it fall a little bit. that asterisk marks the best cardiac output you can get-- preload and output are optimal for that heart. beyond that point, where the line slopes downwards, lies congestive heart failure- the heart is too full, has more than it can handle, and it fails. (this is, btw, called the frank-starling law of the heart, and you just drew the frank-starling curve) pressure backs up into the pulmonary capillary bed making the lungs get wet and heavy. this is when people get diuretics (to decrease that excessive preload) and drugs to improve their contractility.

of course, if contractility is lousy because of coronary artery disease, previous mi, or whatever, this whole curvy line thing will kinda slide over to the left-- the myocardium will fail with lower pressures than it would if it had better contractility. better contractility (a right shift) means it will handle more preload (higher filling pressures) and make better bp out of it. draw a second curve to the right of the first one, parallel to it, to see that. with me so far?

your instructor is partly right, but just didn't give you a very full explanation. i think you can see how cad will give you higher filling pressures-- when the heart is failing a bit, it goes past the top of its curve more easily because its contractility is diminished.

mitral stenosis will, in fact, decrease your lv preload, but it will increase pressures back into the lungs and, eventually, the right heart, because of the resistance to flow from the right side to the lv. mitral regurgitation, on the other hand, will result in higher filling pressures because when the ventricle contracts in systole, some of the blood goes backwards, leaving excess sloshing around between the atrium and ventricle; the ventricle will have to accept a higher reload at diastole, and it doesn't like it. over the top of the curve again.

well, i hope this hasn't confused you. i used to tell my students they had to know this because we saw lots of people with all sorts of deficits, but if they didn't have hearts and lungs, they were dead and we didn't have to take care of them anymore. works in every possible area you could work, except pathology:d. please ask me if i've confused you anywhere.

GrnTea.

Thank you so much for your explanation. I think I kinda get the concept now except the CAD part.

Here’s the part I understood.

the filling pressure is the end-of diastole pressure in the ventricle, referred as preload. And this filling pressure is equal to the pulmonary artery pressure. So, if there is increase in the filling pressure, pulmonary artery pressure increases as well.

Mitral stenosis inhibits complete emptying of left atrium, so the pressure builds up in the lungs. Mitral regurgitation increases filling pressure because it has to accept a higher reload at diastole.

I’m still shaky on the concept of CAD relationship with the filling pressure.

So for the CAD, since the highest peak point of filling pressure is reached faster than in a healthy heart, it causes the pulmonary hypertension (this is what I understood so far).

But, in fact, CAD’s actual filling pressure is lower than in a healthy heart, right? Because if the curve is shifted to the left, the highest point comes first, which is at a lower number in the horizontal axis. It’s just reaching the highest peak filling pressure sooner, causing the pulmonary hypertension more easily? So when you say, “how CAD will give you higher filling pressure,” does this mean it’s just reaching the filling pressure in a much faster rate?

Once again, thank you so much for helping me out…. I’m really feeling hopeless with myself not understanding this…

cad is coronary artery disease, which makes the myocardium short on blood supply (the myocardium is, interestingly, the only muscle that doesn't get blood flow when it works-- when the myocardium pumps in systole, the coronary arteries are smushed shut, and when they are relaxing in diastole, that's when the coronaries fill).

so if your myocardium is poorly-fed and -oxygenated, its contractility is going to be suboptimal. does that help?

do you have a particular concern about pulmonary hypertension? i ask because although the pressures in the lung (and pulmonary artery) do rise in chf, we don't usually think of that as a pulmonary hypertension diagnosis per se; we think of it as chf. pulmonary hypertension has many different causes, like congenital cardiac malformations that expose the right-sided vessels to (the much higher) left-sided pressures, and destructive pulmonary disease (much fewer alveolar walls/less capillary capacity to carry the same amount of blood -> higher pressures).

Wow...great explanation. This will be very handy to me one day!

GrnTea,

Thank you so much for your detailed explanation. Now I can understand a little better :)

You really are a savior!!!