otherwise known as afib. i feel like this is one of those ones that we all hear about every now and then but which is not really well explained at all by the big pharma ads which are the source of our hearing about it, usually. unless you got like a grandpa who’s like "i got goaddamn afib." anyway, let’s learn about it officially, then.
narrowing i feel like this is also kind of an inefficient way of studying, and i might want to make it more efficient at some point here. but for now, since i’m not really doing anything else, let’s just like write about afib. what the hell, sure.
it’s defined as a “chaotic” atrial rhythm that replaces normal sinus activity leading to loss of coordinated atrial contraction. so it makes the atria of the heart beat out of rhythm with the rest of it. it impairs ventriucular filling and increases your risk of forming thrombi and having embolic events. it makes it more likely for blood to clot and for that blood to then go where it’s not supposed to go and gum up the works.
this is the most common sustained arrhythmia in adults, and you’re more likely to get it the older you are. there are currently about 2.3 million people in the US who have it. 80% of those people have some structural heart disease like coronary artery disease, hypertension, cardiomyopathy, or valvular disease. in the elderly, about 40% of cases are found incidentally—as in, the patient has no symptoms and they just happened to find the afib.
in terms of pathophysiology, fibrosis of the atria and other abnormalities in the structure of the heart muscle create a vulnerable setting in which afib can develop. an acute change in atrial wall tension can trigger the onset.
many patients present without any symptoms or just a kind of generalized fatigue. they’re tired and can’t explain why. if someone does have symptoms, it’s likely palpitations, dyspnea, chest discomfort, exercise intolerance, syncope, or worst of all, stroke or transient ischemic attack (mini-stroke).
what can happen if you have afib? the thing itself is not the killer. what kills is the complications, like stroke. the risk of stroke is five times higher than it is for someone without afib. we use the CHADS-VASc score to guide anticoagulation therapy, which is the treatment of choice for afib, cuz it prevents those thrombotic and embolic events like stroke. it doesn’t address the root of the problem but prevents the most deadly downstream consequences. if you don’t control your afib, as in addressing the root of the issue, you can develop heart failure or tachycardia-induced cardiomyopathy.
we diagnose it using ECG. it’s very plain to see on ECG as absent discrete P waves and an irregularly irregular rhythm. that’s the huge buzz term for afib: irregularly irregular. the heart just beats all weird. no rhyme or reason to it.
there are some different types of afib. one is paroxysmal, which only lasts about 48 hours or up to 7 days. then there’s persistent afib, which lasts more than a week or requires cardioversion. long-standing persistent lasts longer than a year, and permanent afib is the kind in which we don’t even bother pursuing rhythm-control. there is also valvular afib, which can result from a mechanical heart valve or moderate to severe mitral stenosis.
the goals of management, initially, are to stabilize hemodynamics (like blood pressure), control ventricular rate, prevent thromboembolism (leading to stroke), and consider rhythm control. rhythm control is being increasingly targeted early in disease course for symptomatic patients because it helps prevent the disease from progressing.
so what is it, exactly? it’s a supraventricular (as in, originating above the ventricles) tachyarrhythmia (as in, the heart is beating too fast and too weird) with disorganized atrial activation and ineffective atrial contraction. all of this leads to an irregularly irregular ventricular response and absent discrete P waves on ECG. it’s like... the origin of the heartbeat is all wrong, and it just fucks everything up.
zooming back in on pathophysiology, the trigger is a focal ectopy, as in, point
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procrastinant i got distracted yesterday. n--- came in and asked me what i was doing and i told him i’m learning about afib and he was like "oh, that’s one of those things that i’ve heard of but don’t actually know what it is. so what is it." and i said "it’s an irregularly irregular heartbeat" or something.... i told him.... i can’t quite remember at this point actually. i told him something..... that wasn’t sufficient to really explain it. but i did tell him the major thing, which is that itttttt makes you more likely to clot and then more likely to throw said clot somewhere like your brain, and it increases your risk of stroke.
and in fact i think that might be all we really need to know about this thing.
that’s something else i’ve been thinking about: how inefficient this way of studying really is, and how little from what i learn about these conditions i’ll be expected to regurgitate for this test........ like, do i really need to go into all these details?
you know, i think the best thing to do here is just to stay the course and edit accordingly. i don’t have to write every single thing down. for example, i don’t need to zoom in on the pathophysiology like i was about to. i can keep it the way it is right now and just keep talking about the important things. like..... for example........... afib can get modulated by acute triggers like illness, alcohol, and hyperthyroidism. all those things increase the stress on the atrial walls for some reason, which can cause afib. you stress out the wall and you get some fibrillation. i guess?
and then.... there’s this thing they put in quotes, this “afib begets afib.” what do they mean by that? it’s that..... something called electrical remodeling happens when you have afib.... so that...... there is sssssss sss s s changing of the circuits, i guess, in the span of hours to days, so the heart gets used to beating irregularly irregularly, i guess, and then over weeks and months there is literal structural remodeling like fibrosis and dilation of the atria. so here we have a shared thing from the previous things we were learning........ aortic stenosis and insufficiency. after a while, the heart gets used to doing weird shit, and it remodels itself to do weird shit even better. it’s like.... it learns how to do something and then it thinks that just because it’s learned something new, it should learn how to be the best at doing that new thing. but we have to remind the heart once again that just because you can doesn’t mean you should. just because you can beat irregularly irregularly doesn’t mean you should............ but the heart doesn’t really think like that, and it indeed does beat wrong. so afib begets afib, just like aortic valve issues beget heart disease. it’s a sad tale. the heart really does try, doesn’t it........
okay so what about hemodynamics and the forming of the thrombi? i wasn’t exactly clear on why that happens. but here’s our answer. in afib, there’s a loss of “atrial kick” which decreases our preload. okay, so basic physiology says that blood comes from the veins into the lefttttttttt atrium, right? yes, i think? no, right? yes, and then it goes from the left atrium to the lungs to the left ventricle, right???? yes, i think so? holy shit but is that even true? what about the ummmm..... no, i think it’s that it comes from the veins to the.... fucking.......... shit. i have to look this up. i’m so sorry.
yeah, right, so blood enters from the veins to the vena cava which then goes straight to the right atrium. the right atrium then sends blood to the right ventricle, and the right ventricle pumps the old deoxygenated blood to the lungs, then the lungs go to the left atrium and then to the left ventricle and then to the systemic circulation. so you start on the right when you’re coming from the veins. right. how many years is it going to take me to fully learn and remember that? maybe i’ll always have to remind myself of it. whatever, who cares. google isn’t going anywhere, is it? and am i going to have occasion after school ends to ever have to remember this?
i’m losing the plot. the loss of atrial kick means that......... i guess, like..... if the atrium is fibrillating, it’s harder to send blood to the ventricles, right, and then the blood just gets stuck in the atrium. and then blood when static tends to clot, so that’s how you form clots. because the atria aren’t kicking blood out fast enough. jesus. easy enough. i’m digressing so much today. it’s fine. we’re still learning.
the point is the left atrium is where clots form. there you go. in afib, clots tend to form in the left atrium, and then, and then, they will eventually escape to the left ventricle and then get sent to the systemic circulation. and we know how important it is to send blood to the brain. so the blood clot will get sent to the brain and that’s how you get a stroke. easy.
reviewing some general facts. afib is the most common sustained arrhythmia. it increases prevalence with age and with structural heart disease. it’s associated with hypertension, CAD, valve disease, heart failure, alcohol use, hyperthyroidism, lung disease, obesity, and sleep apnea. obesity and sleep apnea are very importantm, apparently. i know my dad is going to get fucking afib at some point. i keep trying to tell him to use the goddamn cpap but he doesn’t do it. he refuses. he’s going to get afib and die suddenly of a stroke, like overnight probably. who knows. whatever. fuck it.
damn, afib accounts for 15% of all strokes. crazy. it also causes heart failure exacerbations, and it can cause cardiomyopathy if it’s left uncontrolled.
it happens in stages. first you’re at risk, then you have pre-afib, then you are diagnosed, then it becomes recurrent, and then it’s permanent. a slippery slope as they say. we use this classification system to emphasize that there is an early stage in which we can modify risk factors (use the CPAP, DAD!).
CHADS-VASc is a term you hear a lot in the clinic or in the hospital or wherever. it’s a risk stratification tool for people with afib, and it tells you their risk of stroke. we use it to figure out what anticoagulation regimen to put afib patients on. since the clots form in the left atrium, remember, we’ll want to put the higher-risk patients on a medication to prevent their blood from clotting. we call them blood thinners sometimes.
CHADS-VASc, what does it mean? you get one or two points for each little thing in the acronym. a point for (C)ongestive heart failure, one for (H)ypertension, two for (A)ge above 75 or one for 65-74, one for (D)iabetes, two for previous (S)troke or CVA or thromboembolism, one for (VASc)ular disease, and then one for female sex. womp womp, ladies. you add up all the points you get and that’s your chads-vasc score. it only takes one or two points for us to start thinking about anticoagulation, which feels a little shady to me but i won’t get on my anti-big-pharma soap box right now. the definite indication for anticoagulation is a score of three or greater. we thin the blood unless there’s some other reason not to do it.
afib rarely just happens. you don’t just get it. there’s a reason, usually. a structural or systemic factor that makes your atrium want to remodel itself or become fibrotic or be electrically unstable. for example, 70% of afib patients have an intrinsic, cardiac cause. up to 70% of patients have a history of hypertension. because of the chronic pressure increase, your left atrium gets overly muscular just like the left ventricle has a tendency to do when the aortic valve is fucked up. we also said that aging leads to afib. the atrium progressively gets fibrotic with age and that makes it slower to conduct the electricity we need to make the heartbeat.
there are also some extrinsic factors causing afib, like hyperthyroidism (this just makes your heart beat faster, and a fast heartbeat can lead to afib i guess?), acute illness or stress (something really bad like sepsis, pulmonary embolism, surgery, or heart attack), stimulant exposure (like CAFFEINE or coke or meth).
another extrinsic thing that is important that i’ll give its own paragraph is something called “holiday heart.” holiday heart is when you drink a lot of alcohol and then get afib. and yes it does happen. alcohol is terrible guys!
if you’re a regular drinker, abstinence from alcohol reduces your chance of getting afib by 20%. i know it’s hard.
we are increasingly recognizing sleep apnea, obesity, and metabolic syndrome as modifiable risk factors for afib. managing these things improves our ability to control the heart rhythm.
now is when we talk about history and physical. you ask your patient about their symptoms and some of them will have none. some of them will have severe symptoms. commonly, there’s palpitations, dyspnea, fatigue, exercise intolerance, chest discomfort, lightheadedness, and syncope. feeling like you’re going to pass out. the elderly are often asymptomatic or have vague fatigue symptoms. afib is often found incidentally in the elderly. poor old heart.
sometimes a patient will come in with a stroke and that’ll be how you figure out they have afib.
you should ask your patients about history of hypertension, heart failure, murmurs, lung disease, hyperthyroidism, stimulant use, and alcohol use. instrinsic and extrinsic causes, people, remember.
on physical, the classic thing you’d find is an irregularly irregular pulse. just feel their wrist and you might find afib that way. if you see hypotension, pulmonary edema, ischemic chest pain, or syncope, you need to evaluate them for unstable afib which would require immediate cardioversion.
i’m so bored bro i wanna stop but i can just finish this one article it’s not going to kill me.
the goals of diagnosis are to find reversible triggers and figure out the status of the heart’s functional and structural disease. finally, we need to assess thromboembolic risk.
we get an ecg and find no discrete p waves, shaky horizontal lines, and the irregular R-R intervals. easy to find on ecg.
in terms of labs, let’s get a BMP, TSH to look for hyperthyroidism, BNP if we suspect herat failure, and figure out if they’re anemic before we start anticoags.
we can get an echo via TTE to look for chamber size, LV function, valve disease, and left atrial enlargement. if we’re thinking about cardioverting, we can also get a TEE to rule out left atrial thrombus. get a chest xray if you’re worried about pulmonary congestion or other lung disease.
look also, again, for the triggers: acute illness, metabolic disease, heart problems, or substance use.
in terms of acute management, we’ll do cardioversion if it’s unstable afib. if it’s lasted more than 48 hours or we don’t know how long, we’ll do anticoagulation and/or TEE before cardioverting to make sure we’re not just going to throw a clot somewhere when we electrocute the heart.
for stable afib, we wanna do rate control with a target heart rate less than 110 bpm. first-line is beta blockers like metoprolol. we can also use calcium channel blockers, though we avoid these in HFrEF. digoxin we don’t really use anymore, but can consider it for sedentary patients i guess.
we initiate anticoagulation promptly unless there’s a contraindication. use CHADS-VASc here, of course. we like DOACs more than warfarin unless someone has a mechanical valve or moderate-severe mitral stenosis.
for chronic management, of course the priority is stroke prevention. so we use chads-vasc to figure out oral anticoagulation. our options there are apixaban, rivaroxaban, dabigatran, and edoxaban. i hate talking drugs bruh this is so cringe to me. so let’s just move on.
oh god they’re talking about the watchman. this is a device we use for left atrial appendage occlusion. it’s like an umbrella that you can surgically place inside someone’s left atrium to block off the little zone where clots like to form. this is an alternative to systemic anticoagulation. i had a patient who had a watchman. she’s dead now. i’m sure it’s unrelated. i’m not trying to... er..... i’m not on a soap box here. i meant nothing by that. moving on.
i’m not anti-medicine. i’m just not pro-medicine. i’m.... i don’t know what i am. it doesn’t matter. this doesn’t matter. it’s not about me. sorry. moving on, really, for real.
for patients with afib, we want to reasses heart rate, rhythm, and anticoagulation at every visit. every year we will review the stroke and bleeding risk. we’ll also encourage self-monitoring like wearable ecgs when appropriate. there’s wearable ecgs? uhhhhhhhhhhhhhhhhh okay cool.
if the patient doesn’t have structural heart disease we can put them on flecainide, propafenone, dronedarone.... boring.......
afib is generally progressive. it starts as paroxysmal but ends up being persistent or permanent as the heart remodels itself. the rate of progression depends on your risk factors. having afib makes you up to twice as likely to die as someone who doesn’t have it, mainly becuase of stroke heart failure or other heart disease. rate and rhythm control along with anticoagulation reduces your risk of death.
afib makes you five times as likely to have an ischemic stroke. these strokes can be severe or disabling, so you should really check that chads-vasc. you don’t want to get disabled, right? or die?
in about 11% of people who have strokes of unknown origin (we call these “cryptogenic” because what the hell, sure, invent a word), we eventually figure out that they had subclinical afib. this thing can be a silent killer yall! it’s often paroxysmal and asymptomatic!
apparently we are “actively pursuing” a role for “wearable technologies.” fuck my life.
long story short, having afib, even if it’s intermittent or asymptomatic, “warrants aggressive risk-factor management and thromboembolic prophylaxis when indicated.” diagnose that afib, family, and start thinning that blood. that sounds fun, right?
i don’t know what i mean by any of this. i’m just so over studying already. it feels like it’s supposed to be the weekend but it’s wednesday. i’m just angsty. i believe in anticoagulation. i guess. no..... i don’t. yes i do? i don’t know what i believe in. let’s just move on. i’m sure it’s good. i’m sure they know what they’re doing. i’m sure anticoagulation saves lives and saving lives is still worthwhile it’s not meaningless it’s not just.... it’s not just pushing a rock up a hill, i’m sure, i’m sure it’s really worthwhile i’m sure it’s really important really valuable i’m sure western civilization is not a waste i’m sure this all means something i’m sure it’s all worth it.
let’s just.... be done here. the next thing will come when it’s ready. brugada syndrome. that’s what’s on the agenda. that’s what we’re doing next. i guess. i suppose. fuck. we’ll see. the list feels really long. i don’t know how long i can keep this up.
brugada