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EP on EP Episode 67: POTS and Autonomic Dysfunctio ...
EP on EP Episode 67
EP on EP Episode 67
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Hi, this is Eric Kostowski, and welcome to another segment of EP on EP. This is a special segment for me for two reasons. First of all, the topic is excellent. And most importantly, I've invited Dr. David Bended, who's professor of medicine at the University of Minnesota, to discuss POTS with us today. David and I trained together at Duke, and we've been friends for over four decades. So David, welcome to the show. Oh, thank you, Eric. Happy to be here. Now, let me start with something that may seem simple, but I'm thinking it may not be quite so easy. And that's the definition of POTS, because in the last couple of years, I've had more and more patients sent to me with a diagnosis of POTS, and then I go through whatever I think is the right workup, may not be, and I don't think they have POTS. So why don't you start off by telling us, is this a problem now, it's being overdiagnosed? And actually, how should one come to a diagnosis of POTS? Well, POTS is certainly being overdiagnosed. It's a condition that's been known for with different names for more than 100 years, but in the late 1990s, became popularized by a couple papers, and seemed by those experiences to explain a number of symptoms that patients were having that had previously been kind of difficult to deal with, namely feeling that their heart goes too fast, their brain isn't working quite right, stuff like that, very nonspecific complaints, for the most part. Now, doctors, when they encounter such complaints from patients, often think of this condition we call POTS. But in actuality, probably only about one in 10 patients who come with these nonspecific complaints, feeling palpitations, feeling weak, feeling tired, really have that particular diagnosis. So, POTS has to be diagnosed very specifically, and there are criteria, and the criteria typically are orthostatic tachycardia, over 120 beats a minute, or at least a 30-beat rise in heart rate from being seated, and in addition, no drop in blood pressure. So, very specific diagnoses are needed to establish true POTS, and everything else will fall in other diagnostic groups. David, that's great. Let me ask you this practically. You're in the office. I know you've talked about this in the past, and I think I'd like you to explain this to everyone. Do you need to send someone for a tilt table test, or can you actually do what's necessary in the office? It is not necessary to do a tilt table test. If you look at the heart rhythm guidelines, they don't even specify the method of which you show this orthostatic tachycardia. So, you could have a patient seated in the office, or lying on the exam table, and then ask them to get up and stand. They don't need to be rigid. They just stand comfortably for five minutes or so, and you can observe whether their heart rate goes up the 30 beats a minute, but it has to be above 100 when it gets there, and the drop in blood pressure, it has to be negligible. They generally say less than 20 millimeters of mercury. Establishing the heart rate in the clinic is not difficult, but to get a good blood pressure can be a problem, because sphygmomanometers are clumsy instruments. So, if you really want to do it in the office, you ought to use a non-invasive beat-to-beat blood pressure system. Those are widely available these days. I know you could probably go on this next question for a long time. Can you give me kind of the bottom line of what is the most recent thinking of why you get this? Because if the pressure doesn't fall, what's the stimulus, David, that makes the heart rate jump? So, the basic elements of the mechanism are not well known. We know that this can occur as a result of viral illnesses, autoimmune illnesses, trauma, surgery. So, there's a whole broad array of things that trigger the occurrence of true POTS. We suspect that the traumas, whether they're small or large, result in the release of neurohumors, histamines, other mast cell humors in some patients, that create an inadequate return of blood volume to the heart. So, they have some sequestration of blood in the lower extremities. Some people say the heart gets small as a result of that, but inadequate venous return is a consequence, perhaps, of all these chemical mediators that dilate lower extremity vessels. If you don't have enough venous return, the heart feels it has to beat faster. So, there's an element of that. There are some other less common mechanisms, including, for instance, inadequate reuptake of norepinephrine in the periphery. Nobody is really sure that there's any one mechanism that explains all these patients, but if you think inadequate venous return needs higher heart rate to maintain the brain operating way up high here, that's where the basic cardiovascular problem arises from. That's great. I have seen much more inappropriate signs of tachycardia than true POTS, but let me ask you this, without going into a huge tangent, which I know you can, you've written on this, and I've listened to your lecture on this. How often do you think there are these mixed syndromes where it's not just pure POTS or pure ISD? What is your sense of that? Well, I think there are a few instances in which POTS crosses over to many of the other conditions that we deem to be sort of autonomic dysfunction. So, POTS will even occasionally have vasovagal fangers. They'll occasionally have people that have ISD, inappropriate sinus tachycardia, but for the most part, POTS patients, I think, are not a crossover. If you have inappropriate sinus tachycardia, that's an important differential, at least an important component of the differential diagnosis. More often than not, POTS patients cross over to orthostatic hypotension. Okay. So, that is the biggest crossover group that I see. Yeah, and I think in keeping with that, that's really interesting because ironically, today in the office, I had somebody who came in with diagnosis of POTS and actually everything looked like it was ISD. So, I suspect that when patients tell doctors, you know, I get up and walk around and my heart rate jumps up, they jump to that diagnosis, I'm guessing, and actually it turns out to be ISD more than not. Yeah, actually, the cause of rapid heart beating in people, as you well know, is a large differential diagnosis. And to jump to POTS or any other of the rarer conditions is probably not the best way to go. Obviously, you know, you have to do all the basic bulwark of medicine before you get there, including checking their blood counts and their thyroid function and things of that, their conditioning. Deconditioning is a major problem. We've sent astronauts, very fit people up to space, they come back looking like a POTS patient. So, deconditioning is something that people don't like to admit to, but it can be an important component of the differential diagnosis. So, think through all those things that are sort of mundane, but important. No, no, I think you're absolutely right. Now, I'm going to come to the worst part of this, which you probably hate talking about, which is treatment. Because all I know is when I see on my list a new patient with POTS, all I really want to do is take the day off and hope one of my partners picks them up. I mean, true POTS, not someone who's misdiagnosed something. I find it a real challenge, personally, to treat. Can you give the viewers your tricks and how you go through what you use to treat these folks? Well, I think the important thing is to start again with the basics, not to necessarily jump to the biggest pharmacologic trick in your bag. So, most of these people need to be re-educated with respect to salt and volume intake. They, for some reason, require higher levels of intake of salt and volume than the average citizen. And so, I really encourage that. You know, I tell them that the American Heart Association worries about salt, but these folks with POTS need salt. They need volume. The volume should be electrolyte consumption. So, I tell them go and buy powder and drink at least 60 ounces a day, depending on how big the person is, of course. Do those things. Then the next step is actually more like physical rehabilitation. They need to do standing exercise and lower body isometric exercise. The isometric exercise was popularized by the rowing machine work at UT Southwestern, and I think it's a very important attribute of the therapeutic regimen. And after that, you might consider the use of drugs that slow the heart rate a little bit. Low-dose propranolol has been studied and looks helpful in some people. Evabradine, if you can get your hands on it, also does help. But don't forget to increase the body volume. Use fludrocortisone. It does create some problems with headache in people and a few other side effects, but generally well tolerated. Mitadrine to help constrict the lower bloody blood vessels that are presumably leaking a little bit and help to drive the blood back up towards the heart. We want to get venous return by hook or by crook. Anyway, we can do it because if the heart sees more venous return, it won't feel like it has to beat so fast. Those are the main tricks. One more is constrictive undergarments for people starting above the knee up to the waist, especially when you're in early stage treatment. Before they've got all this other stuff cooking and moving down the road, they can help them a lot with constrictive undergarments. And those are readily available. Some are nicely designed even and quite cool. You can get them on the internet. One last thing, David. Hope for these people down the road. I understand it's variable time, but do you find over time that a lot of these individuals will return to their pre-POTS state? The answer is yes. We just don't know ahead of time what the prognosis is in terms of timetable. So for instance, some of the slow onset, we assume post-infectious origins, can last for three to five years. Some of the more acute ones, post-surgery, post-trauma of some sort, are often of shorter duration. The most interesting current group that we just really don't understand are the COVID-19, post-COVID-19 subset. We're seeing more and more of those. We just simply don't know the natural history of that. And I think it may be like other viral illnesses may hang on, as they say, the long haul COVID patient for three to five years. So a lot to be learned yet about prognosis in all of these subsets of POTS. Terrific discussion, David. Thank you very, very much for joining the show. I always enjoy visiting with you, Eric. Thank you.
Video Summary
In this video, Eric Kostowski interviews Dr. David Bended about postural orthostatic tachycardia syndrome (POTS). They discuss the overdiagnosis of POTS and the specific criteria that are needed to establish a true diagnosis. Dr. Bended explains that a tilt table test is not necessary, and that the diagnosis can be made by observing orthostatic tachycardia and minimal drop in blood pressure. They also talk about the possible causes and mechanisms underlying POTS, including viral illnesses, autoimmune illnesses, trauma, and surgery. Treatment options discussed include re-education on salt and volume intake, physical rehabilitation, and the use of medications to slow heart rate and improve venous return. Dr. Bended also mentions that the prognosis for POTS varies and that some individuals may return to their pre-POTS state over time.
Keywords
postural orthostatic tachycardia syndrome
POTS
diagnostic criteria
treatment options
prognosis
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