okay, starting off strong, apparently there’s a prevalence of five percent with this thing. five percent of all people have this, i guess? so what is it, though?
attack it’s an incomplete closure of the aortic VALVE, ohhh, right, okay, so this is a heart problem, and, i guess, not strictly an aortic problem. it’s aortic VALVE insufficiency. i’m already on board more than before. see, i’m learning, i’m learning, just like all of us here today.
anyway, yes, when the heart goes into diastole, the filling stage of the heartbeat, where it fills up with blood and prepares to pump it out, the aortic valve (which is supposed to close and prevent blood from flowing backward from the aorta, into which the heart pumps blood, back into the heart) doesn’t close all the way, so that means that...... the blood flows backwards from the aorta into the left ventricle..... hmmm..... just trying to wrap my head around that for a sec.... okay, so like.... if we’re filling up the heart, then yeah, the aorta is supposed to not be involved. we want the heart to fill up from the other direction. from the veins. it should fill from the veins. and if it’s getting filled from the aorta that’s a problem, and i have to believe that’s going to increase preload, or, in other words, the amount of blood that we have in the left ventricle at the beginning of systole. is that preload? do i still have my basic cardiology down? let’s just keep reading.
the incomplete aortic valve closure can be due to a primary disease of the actual valve, or due to a secondary problem which affects the supporting structures of the valve, like the aortic root or descending aorta. so there can be a primary or secondary cause.
most patients who have this disease develop it slowly....... it starts with progressive overloading of the left ventricle, which then causes some reeeeeeeeformation of the architecture of the heart, including hypertrophy of the left ventricular walls and enlargement of the chamber itself.
my anatomy professor just walked into the building, and she’s wearing all white, and she has to pull herself up the stairs using the railing. ummmm i have no comment for that, but i guess shoutout to her, in the smallest of ways, for, like, i guess, putting some effort into teaching me and my classmates this basic anatomy three years ago. anyway.
the most common causes of aortic insufficiency in the developed world issssss bicuspid aortic valve, which i think is usually congenital, as well as calcific aortic valve disease. in developing countries it’s more likely that someone will get aortic insufficiency after having rheumatic heart disease.
chronic AI can present with angina, orthopnea/PND, exertional dyspnea, and palpitations, especially while recumbent. a lot of jargon there. angina is like.... well, shit, i think, right now, in this moment, i can’t tell you a very good and snappy definition of angina. i’ll report back on that later. sorry. follow up for updates, i guess. damn. embarrassing. sorry. but i know orthopnea is like..... you can’t, umm.... it’s like shortness of breath while you’re lying down i think.... right?? my god.... and pnd is paroxysmal nocturnal dysuria....... dysuria????? holy shit, dude. i gotta look this up cuz this is embarrassing.
it’s paroxysmal nocturnal DYSPNEA. not dysuria. oh my god, i’m getting a flash of shame and embarrassment and anxiety at not having remembered that. and i’m also getting flashes of rage every few seconds because my laptop screen keeps automatically dimming. STOP FUCKING DIMMING YOU STUPID PIECE OF SHIT I GOTTA KEEP LOOKING AT YOU WHAT THE FUCK IS GOING ON???
pjjhhhh my fucking god dude i forgot what state this studying shit tends to put me in. i gotta take a deep sigh here before we move on. my god. sorry.
long story short with that last thing is that chronic AI can present with difficulty breathing, especially while lying down and at night. jesus christ. how hard was that.
and another thing. if it’s acute, it's usually because of infectious endocarditis, dilation of the ascending aorta, or blunt chest trauma, which can lead to cardiogenic shock and pulmonary edema. so we now know that it can be acute or chronic. fine. okay, great, fine.... ugh. man. shit. fuck. okay. moving. on.
when you do a cardiac exam, you might find that the heart is larger, which we call cardiomegaly, which we attribute to those architectural changes of the left ventricle due to it holding too much blood too much of the time.
you’ll also maybe see widened pulse pressure and a disasotlic murmur. this is easy to miss on initial exam, so keep an ear out for it, as it were.
when you do an echocardiogram, which you should do in all patients whom you suspect may have AI, or people with a bicuspid aortic valve, or a dilated ascending aorta, ..... i guess that’s not...... the sentence is just that.... that you SHOULD get an echo on these patients. i got nothing else to say about the results or anything. i guess you’re just checking the echo to diagnose it? to see if and how the blood is flowing? ummmm, okay, moving on, i guesss, shit, man,, , sorry i’m so fumbling this right now, ugh FUCK!!!!!
you can replace the valve and that improves survival in patients with acute AI from infective endocarditits. but that begs the question of can we replace the valve for people with chronic AI, or people with acute AI for other reasons than endocarditis? i’m asking too many questions. i’m being annoying. oh my god. fuck. oh my god.
the chronic management, okay, here’s the answer, the chronic management includes vasodilators which will slow down the flow of blood regurgitating form the aorta to the heart, and it will increase the forward flow of blood... you can also give venodilators which will decrease left ventricular preload, which there you go okay i’m vindicated for my assumption earlier about preload.... ummm...... okay, those also improve LV function and lower the stress on the LV walls... give nifedipine for asymptomatic patients with normal LV function and/or ACE inhibitors for symptomatic patients with chronic AI and hypertension or decreased LV function or CHF...... okay, so this one is kind of all over the place. thery’re just kind of doing whatever. like, why are we treating hypertension with this thing? when the problem is the valve, why not just go in and fix the valve? i think they’re about to tell us.
you replace the valve when the patient is symptomatic and has severe AI, regardless of how their LV is functioning. if the patient is asymptomatic but has severe AI, and their left ventricle is functioning at less than half capacity, then you replace............ if the patient is asymptomatic but has severe AI and normal LV function but has severe or progressively worsening LV dilation, this is a sign that things are just going to get worse and you can go ahead and replace the valve. okay, so i guess they’re somewhat conservative about replacing the valve but not overly conservative, as no one ever really is in medicine. even the most conservative treatment in medicine tends to be prettyyyy, shall we say, liberal........ using resources and making people patients, seemingly at..... well, not at random, but certainly not all that discriminatorily..... they love making people patients.... anyway... getting distracted here... let’s continue.
so, the whole definition of this thing is a disease of the aortic valve which prevents it from closing all the way while the heart is filling up with blood, which causes blood to flow from aorta to left ventricle. we said that already, but i guess saying it again can’t hurt us.
we said already that an acute AI is usually due to infectious endocarditis, dilation of ascending aorta, or blunt chest trauma. great. acute volume overload of left ventricle is not well tolerated. the heart doesn’t like it. that predisposes the patient to pulmonary edema (the blood is going to uhhhhh get pulled, or the fluid from it is going to get pulled somehow by the forces of physics into the lungs, and the lungs will then be all bogged down by fluid, hence the term pulmonary edema, and also uhhmmmmmm the patient will also be predisposed to reduced LV ejection fraction, aka the, ummm, ability of the left ventricle to do its job and eject blood from itself.... right, right.... right. okay. right.
most patients with chronic AI develop it slowly. they become symptomatic slowly, because the symptoms, i’m assuming, are resulting from theeeee, ummmm, left ventricle going through those architectural changes, which of course doesn’t happen overnight... it takes a minute to adjust.... yeah. yeah. okay. right. sure. yes. makes sense. it’s a muscle. the muscle gets too big when it gets overworked, but muscles take time to grow. right. we get it.
risk factors, how do you get it? you gotta ummmmmmm have a bicuspid aortic valve. that’s a good way to get it. be born with an aortic valve that has twooooo cusps instead of three. the three are typical, but two is not as many, and two cusps, two of those things that help the thing close... like, two flaps that stop the flow of blood.... are less effective than three flaps. that’s all.
however, we mention at this point that bicuspid aortic valve is more likely to cause aortic stenosis than regurgitation.... umm.... okay. not going to even begin to unpack that right now because i know that is a huge can of worms that if we need to open we will do later. later. much later. later on.
anyway, the other risk factor is calfcific aortic valve disease. if you find yourself having calcium deposits on your, ummmm, on your aorta, this can cause it to have strugglesssss, ummm, closing all the way during diatole. yes, right, of course.
other causes, as we said, include rheumatic heart disease in developing countries, ummmm, and dilation of the ascending aorta, however that happens. right, sure, of course, okay, right, then, yes, what next?
how does it develop? i feel we’ve already talked in depth about this as well. volume overload and high afterload on left ventricle. yes, because the aorta is insufficient to get all the blood out of itself, so the left ventricle has to pump harder to get all that blood out, and to get it past all the blood that is still in the aorta, you know.................... this is tolerated for years as the left ventricle does a good job working harder and getting larger, but we know how certain adaptations that initially help us can quickly turn into the harmful kind... you adapt to something for too long, and then you turn into someone you don’t recognize,,,, someone who is actually not as fit for survival as you might’ve thought.... you were working so hard to get through a hard time, only to find at the end that the changes you went through are deleterious to your own health... not going to dwell on that for too long or the metaphor will consume me.
chronic aortic regurgitation, yes, that’s the name of the game, that’s the name of the game of pathogenesis here..... then what else is there? there's a compensatory eccentric hypertrophy along with chamber dilation, right, like we already said, yes, of course.
with worsening aortic regurgitation, you will then have worsening left ventricular remodeling, of course, then increased interstitial fibrosis. the walls harden,,,, and decreasing left ventricle compliance, yes, it gets too hard, which raises the end-systolic volume and end-diastolic pressure, then this causes more cardoac dilation and decline in systolic function. the heart becomes too muscular, and then the muscle turns to fiber and just hardens... your heart litearlly hardens because it’s had to work too hard.. it becomes callous... and then it just forgets how to be a heart. sad, honestly, sad, and of course very poetic...
after this, the left atrial pressures increase along with pulmonary artery wedge and pulmonary arterial and right ventricular and atrial pressures. so basically the pressure builds in the left ventricle until it can’t tolerate all that pressure anymore, and now the pressure has to get outsourced to the rest of the heart, and now suddenly pressure is high everywhere, which leads the whole heart to just fail. sad!
but what actually happens to the real patient, you know what i mean? what are they coming in with and stuff? you should ask them specifically about, ummm...... ask them about, like..... signs of cardiogenic shock and signs of acute congestive heart failure... so that would include, i guess, like.... having trouble sleeping or feeling like they need to use more pillows to sleep, or they can’t get good breaths in, stuff like that, i guess? in terms of chronic AI, that might be asymptomatic for a long time, so it might be hard to pin down when someone has it, or when it even started. but it can present with angina.... now is when i have to look up angina, i fear, so i can know what i’m talking about.
right, actually, yes, like i thought, or like the inkling i had, angina just means chest pain, basically. they just mean chest pain. so the patient might come in with chest pain because of their increased oxygen demand due to all those changes happening in the left ventricle. and they’ll also have, like i said, that difficulty breathing while lying down, and difficulty breathing while exercising, and palpiatitons while lying down. so the problem reveals itself while you’re lying down, and that would be because..... well, i’m not really sure how to talk myself into that one yet. i’ll let that one simmer. you can, ummm... yeah, i guess, like, figure it out yourself, uh..... why would it be worse to lay down with a problem like this? when your heart... maybe gravity is a problem? like the gravity presses all the blood down into the heart more, and it’s already having to work so hard that if gravity works against it that could be harder? Maybe/??!?!?!?
on physical exam for these patients, you should look for a corrigan pulse, which means that there is a rapid swelling and falling of pulse when you palpate it. so like, you touch their wrist to feel the pulse, and then the pulse rapidly goes up and then down again...? why would that happen? anyway, another sign is the quincke sign, which i’ve never ever heard fof, which is an exaggerated pulsation of the capillaries in the nail besd. sure. then the de mussett sign, i’m unfamiilar, which is bobbing of the head with pulse. the head seems to beat right along with the heart. that’s awesome. rosenback sign is a pulsatile liver. becker sign is accentuated retinal artery pulsations. gerhard sign is a pulsatile spleen. so basically it’s like in this thing you can feel the heart beating everywhere in the body. if the heart is working that hard, you’ll feel it everywhere, i guess, is the long story short. you’ll also see, as we said, cardiomegaly with widened pulse pressure. also, the diastolic murmur which is easy to miss.
so like, just for my own synthesizing of my own understanding, we can think of this as like... the blood can go through the aortic valve just fine. it's not stenotic. there's not too little room for the blood to flow. the problem is the valve can't fully close, and blood falls back into the heart when it's not supposed to. so then you have extra blood getting pumped out when the time comes, which is why the pulses feel like they're bounding.
they found in a study that 28 of 100 patients had an AI murmur on echo. auscultation is highly specific for finding AI but not very sensitive. as in, you’re likely to get a false negative if you just do auscultation. like, if they have a murmur on auscultation, it’s probably the real thing, but if they don’t have a murmur on auscultation, you don't really know shit, still. when you’re auscultating, as in listening to their heart with a stethoscope, you gotta have the patient lean forward and have them exhale, then listen at the left sternal border. you’re looking for an austin flint murmur which happens in mid-to-late diastole and is low-pitched and rough.
when diagnosing AI, we should rule out other causes of heart failure and pulmonary disorders which lead to progressive dyspnea and activity intolerance, like COPD. the most common culprit.
to establish the diagnosis, we could consider doing labs for syphilis. they don’t specify why. we should also get an echo for all patients with signs/symptoms of AI or a bicuspid aortic valve, or a dilated ascending aorta. we’re trying to, first and foremost, make a correct diagnosis, then determine how severe the regurgitation is, then measure how big the LV is, then measure the LV systolic function........
how do we manage it? you can do AV replacement in acute cases. it improves survival in patients who have infective endocarditis-related acute AI. in terms of chronic management, we like giving vasodilators (they decrease regurgitant flow and increase forward flow) and venodilators (which decrease preload in the LV). these medications improve LV function by decreasing stress on the walls. if your patient is asymptomatic and has normal LV function, you can give nifedipine. if they are symptomatic and have hypertension or decreased LV function or CHF, give ACE inhibitors.
when do we do a valve replacement, though? when your patient is symptomatic with severe AI, no matter what their LV function is. asymptomatic patients with severe AI and LV function < 50% at rest also get a replacement. so do asymptomatic patients with severe AI and normal LV function but severe or worsening LV dilation. basically, even if they don’t have symptoms, but if theyyyyyy, if theyyyyyy have signs that their LV is working too hard as a result of the valve not working hard enough, let’s get ahead of things and just get that valve working and prevent problems from stacking up on each other.
finally, let’s discuss the prognosis...... the prognosis, as it were......................... asymptomatic patients whose LV are functioning remain asymptomatic, for the most part, even seven years after diagnosis. people tend to get more symptomatic as time goes on, but it’s chill, mostly. for people with moderate to severe AR, when they conservatively manage it, they have a fifty-fifty shot of surviving for 10 years. that’s a little alarming. but i guess, yeah, your heart is failing, so you can only fail for so long. that thing can only work so hard for so long. symptomatic patients and ones with LV dysfunction have a mortality rate of 25% per year. by the way, and this feels like a pretty important point, but it’s the one they chose to end on: once you develop symptoms, you’re going to die within 2-4 years unless you get the valve replacement. okay, damn, that’s a lot.
well, i’m just sitting here in a cafe, and it’s freezing. my butt is cold. but we persist. the next thing we’re going to learn about is
more valves