12- Atrial Fibrillation

Good day and welcome to the Aussie Med ED, the Australian medical education podcast where we get interviewed specialists in a variety of medical areas, asking their opinion on certain conditions, changing their insight into how they diagnose and treat that condition these COVID times as a way of replacing the relaxed discussion around the hospital by allowing the listener for questions to be answered, addressed on their behalf. I hope you enjoy the whole program. Welcome once again to Aussie Med ED . We start the new year 2021 with cardiology, in particular talking about atrial fibrillation. We speak to Dr. Cameron Singleton, who has expertise in cardiac electrophysiological procedures, including cardiac ablation and insertion of cardiac rhythm devices, and we look forward to hearing his approach to the assessment of a patient with atrial fibrillation and the treatment options involved. Not only would this information be useful for the general practitioner seeing a patient on a regular basis, but also for the medical student revising for their exams or preparing for the OSCE examination. I'm Gavin Nimon, I'm an orthopedic surgeon based in Adelaide and also a senior lecturer at the University of Adelaide involved in orthopedic musculoskeletal teachin g. I hope you enjoy the podcast series , and if so please feel free to subscribe, give us a like or review or tell your friends about it. We look forward to having you listen to our podcast series and we hope you find it enjoyable. I would like to begin this podcast by acknowledging the traditional custodians of the land, on which this podcast has been produced and pay my respects to the elders both past and present. It gives me great pleasure to introduce Dr. Cameron Singleton, a graduate of the University of Adelaide who has specialized in cardiology and held a fellowship position at the Royal Prince Alfred hospital specializing in cardiac electrophysiological procedures. He specializes in cardiac electrophysiological procedures including catheter ablations, as well as insertion of cardiac rhythm devices and resynchronization procedures. He practices both at the Flinders Medical Centre as well as privately at the Calvary Adelaide Hospital, at the Ashford hospital as well as Mt Barker and Strathalbyn peripheral clinics. It's a great pleasure to have Cameron on. Well welcome Cameron Singleton. It's great to have you on Aussie Med ED. We're going to talk about atrial fibrillation, or have chosen atrial fibrillation to talk about because it's the most common arrythmia. It would be excellent if we could start off by defining what types of arrythmias there are and if we can categorize them or how you would classify them,

Well, thanks for the invitation , in terms of arryhthmias, we normally think in terms of supra ventricular and ventricular, so supraventricular anything above the ventricles, obviously, so that's atrial fibrillation, atrial flutter, atrial tachycardia, SVT . Technically, any arrthythmia above the ventricles is an SVT but the term tends to be reserved more for re entry, SVT such as we see with Wolff-Parkinson -White, or atrial-ventriclar node reentry. So that's the full gamut of that sort of arrthythmia. And then there's ventricular arrhythmias. And we basically think of these in terms of ventricular tachycardia occurring in the context of a structurally normal heart and ventricular arrythmias occurring in the context of structuarlly abnormal heart, such as prior myocardial infarction, or cardiomyopathy of some sort,

OK so that's the general classification. Am I right in thinking atrial fibrillation is the most common one.

No doubt about that. The most common arrythmia in our community is atrial fibtrillation.

And how would they present?

Yeah, so the presentation of AF is very varied, it is th ought that occurs to that 1% of 40 year olds, but maybe 10% of eighty year old so it's certainly more common as we get older, but it also goes with a lot of other conditions. Obviously, that well known ones hypothyroidism will make you prone to extrapolation increasingly appreciate it is that sleep apnea will make people p rone to AF. Alcohol excess is another well known condition, or toxic metabolic situation that can predispose people to AF. We think of them in terms of paroxysmal (episodes that come and go), persistent (episodes that lasts and need a drug for termination or DC shock), Long term persistent or permanent where basically it is accepted that fibrillation can't be terminated, and the person will be perpetually in atrial fibrillation. Presentations, anything from rapid irregular palpitations that make people feel awful with chest pain and out of breath, feeling lousy and about to die, presyncopal, and no symptoms at all. We sometimes see people coming in with no symptoms at all going along, at 130 beats per minute in AF, totally unaware of it

Has the advent of the Fitbit or Apple Watch increased the presentation of these arrythmias and are people more aware because of these

People are certainly paying attention to their watches. In my own anecdotal experience. I'm not convinced that it's actually throwing up more cases, to be honest. We're certainly seeing more worried Well, who pay attention to what their phone says I'm not sure what to turn out any more true AF cases. But that's just my anecdotal. I don't know what the evidence is on that. That's just my own personal experience.

What's the complications of atrial fibrillation?

Yeah, so the dreaded complication really is thromboembolism, and this has been appreciated a lot more in recent years and in fact, a lot of work has been done on classifying stroke risk. We have the Chadvasc system, which helps us do a ready quick estimate of someone's thromboembolic stroke risk based on risk factors such as history of congestive heart failure, hypertension age (increasing age is a factor) diabetes history of CVA or TIA and vascular disease, a nd unfortunately women are more at risk of stroke than men. So female gender counts as a point on that stroke risk system. So absolutely urgent to sort out what that person's stroke risk is and make a decision about whether they need anticoagulation or not. And we generally would say a score of two or above on the Chadvasc and you need anti-coagulation unless you have a problem that rules you out from anticoagulation. And that would generally be a history of serious gi bleeding or, or serious cerebral bleeding. Even in that subset we look at left atrial appendage closure device, but thats for a followup topic and a bit more sophisticated. That's that's key we can get people with decompensating into heart failure from their AF, and it can precipitate ischaemia with chest pain and even non ST elevation myocardial infarctions are not uncommonly seen and people presenting with AF, due to the rapid rate and inefficient cardiac function resulting in poor perfusion and some ischemia and also syncope. AF itself rarely cause of syncope. But there is a situation where when people with paroxysmal AF terminates, you can get a post reversion pause, which can be quite prolonged and result in syncope. So AF itself hasn't caused syncope, its the pause upon termination. Most people often will end up needing a pacemaker. That's the most common presentation, which of course, depends on their co morbidity. So someone who has a very stiff ventricle with what we call diastolic dysfunction, so classically, a hypertrophic cardiomyopathy patient has a very stiff ventricle, so diastolic dysfunction , if they lose atrial contractions, with AF, they'll often be quite symptomatic, they'll get quite breathless in heart failure, because they depend on atrial contraction to push blood into the left ventricle. Whereas you've got your 40 year old, healthy individual who's just drank too much beer, because it's Australia day long weekend and they get AF, they're probably not going to go to heart failure. So I think the key is a big range of presentations, very important to, to first of all, deal with the immediate problem, my guess is there angina, heart failure is the person decompensating. That's immediate medical priority, but in the longer term, the priority is to make sure you appropriately assess and triage the person from a stroke risk point of view.

One question that comes to mind, obviously, as an orthopedic surgeon is, is the actual incidence of a thromboembolic event for the patient who actually stops the anticoagulation for a small period of time. Obviously, the most classic patient of ours will be someone who's a bit overweight, maybe has a history of bit of heart failure, and may be diabetic type two, and they've got some atrial fibrillation. What is the actual risk of stopping the anticoagulation? for five or six days?

Yeah, well, I guess a couple of things. First of all, I do come across patients who are advised to stop apixaban five or six days before surgery. And this is really not necessary, because they have gone within 48 hours. So you know, perhaps three days before a major operation will be reasonable, but there is no need to stop it five or six days, simply lengthening a period without anticoagulation for no real reason. So stop it no longer than is necessary. That would be the first point and I would say 72 hours is ample, then what we do is you look at the Chadvasc score. So if they Chadvasc score is 2, their annual stroke risk is about 2.2%, without anticoagulation. If their chadvasc their score is six, I think it comes out about five or 6% per year. So if you say well, that's 52 weeks. So if I've got someone who's got a chadvasc score of 2 right, they're 65, and they've got hypertension. So one point for hypertension, one point for being 65. And their annual stroke, which is 2%. Now 52 weeks, if you divide that by 50. That's .4% per week. And we're saying we're going to stop this stuff for less than half a week. So the chance of that person having a strike is .002 in that three days . So that's the value of the chadvasc score, because it gives you an idea what their annual stroke risk is. And then you can say, well, this person's got a score of 6, their annual stroke risk is 6%. Then stopping their anticoagulation may not be great. Maybe this is someone I should bridge with clexane, whilst the other person, their chadvasc score is 2, their stroke, which is 2% for the whole year. And I'm going to stop this stuff for three days. So what's that three out of 365 it's less than 1%. So their stroke which is going to be .002 or something , so they don't need bridging clexane. So in other words, look at the patient at their overall risk, one - hold anticoagulation to something scientifically proven two to three days, not six days. And secondly, look at the patient and see what their overall stroke risk is. A lot of them be relatively low, and that can be quite okay without bridging clexane for three days.

And of course, for those listening- the disclaimer, obviously, eachpatient, needs to be considered separately and assessed by their GP or their cardiologist in that scenario. Moving on, are there any other types of scales apart from the Chadvasc? Or is there other ones that you use as well? Or is that the the one?

I use that mostly? I mean, I think there's there's the Has-Bled, which looks at their bleeding risk, I must say, I don't use it on a day to day aspect very often, but the concepts are still there. And that is, what's their renal function like, how elderly are they? how frail are they ? how skinny are they and all these sorts of things? Of course, we make a decision about people who might be prone to falls. So if someone is a falls risk, that has to be factored in to the decisions about anticoagulation. In other words, you can't really protocolized management of atrial fibrillation, to look at the patient as a whole and make some judgment calls, that based on those working principles we've been discussing.

For the medical students who are listening, if they see a patient who presents with acute atrial fibrillation, what other things must you consider in working them up apart from the obvious cause of the chronic nature? Could there be acute elements or events that could happen? And what would be the screening that you do?

Yeah, well, we always want to know if they had been drinking too much. Again, you have to look at the person as a whole, but we're interested in know toxic things, alcohol excess , are they thyrotoxic, do they have sleep apnea, is this part and parcel of some other cardiaic conditions, ? cardiomyopathy, do they have coronary artery disease. So you know, all those other general cardiac history elements that you would take from any patient, particularly apply in the AF patient as well.

And what about the role of actually assessing for a heart attack , looking for troponins and doing serial ecgs

these people need ecgs as well, you sometimes get a troponin elevation purely as a consequence of the rapid ventricular rate, not due to any coronary atherosclerosis, it's often have the situation, someone might have moderate coronary disease that doesn't normally cause them any symptoms, unbeknownst to them, and any anybody else, for that matter. And they turn up with a HR of 170, from their AF. And they get a bit ischaemic from that, that's very common, if someone's coming along with an anterior infarct, with a STEMI(st elevation infarct), and they happen to have AF as well, I would hope that people would not miss the ST elevation on the ECG. So obviously, basic banded protocols of assessing cardiac patients with history examination, ECG would apply. So if someone's got an acute coronary syndrome, well, that'll be obvious on the ECG generally. Obviously, that personal journey complaint of anginal type symptoms or chest pain, ischemic type symptoms, but most of the patients that I see with if not in the context of acute infarct, and that's working in a public hospital and a number of very big private hospitals, the AF is generally not part of acute ischemic syndrome, or if it is that they're going to the cath lab to have their artery opened urgently. And often, if that happens, and you reperfuse the person, their AF spontaneously terminates within 24 hours anyway. S o of course, you must consider the acute ischemia as a driver of AF, but the overwhelming burden of AF out in the community is not that patient. It's the chronic defibrillator or the paroxysmal defibrillator with hypertension, sleep apnea, alcoholic excess, thyrotoxicosis or underlying cardiac condition or sometimes just alone, AF. You know we certainly get lots of people who have lone AF and you can't find any other associated cardiovascular cause that . That exists, but sometimes that depends on how hard you looks. If you look hard enough, you'll often find something, hypertension or sometimes quite thin skinny people who often end up having severe sleep apnea. And that's driving their AF.

So the treatment path of treating the atrial fibrillation, I presume, you'd go down both anticoagulation path as well as a try and correct the atrial fibrillation mode. Is that correct?

Correct. So so whenever any AF patient that you come across, there's always the decision tree, which is right control or rhythm control, so in other words, are we going to try and restore sinus rhythm in this person and do whatever it takes to restore sinus rhythm? And that's called rhythm control, or are we going to say now we're going to accept the atrial fibrillation and do rate control? Both patient groups will often need anticoagulation, but that's often the first decision point. I mean, you are going to anticoagulate, pretty much every AF person you meet acutely, really the people we don't only coagulate a CHADVASC 0-1 patients who you have no intention in cardioverting. You dont meetmany of those in the emergency dept or gp rooms. I guess you might get someone who is a paroxysmal fibrillator, who gets palpitations On & Off, they're mostly in sinus rhythm that you or somebody else has done a Holter monitor, and it shows paroxysmal episodes of fibrillation lasting couple of hours at a time. Their Chad score is 01, you're not going to any calculate them. There's a subset, but everybody else you probably going to anticoagulate because it Chad score is going to be two and the interesting thing is even if you can restore sinus rhythm, someone with a Chad score or two or higher, is still going to anticoagulant that person because the strike risk is considered to still exist, sinus rhythm or not, unless they're AF is part of an acute medical problem, such as post bypass AF. We do get people who've never had AF in their whole life, have a bypass. And then day three of the bypass get AF, lasts 72 hours , then go into sinus rhythm, those people got AF purely as a consequence of the surgery, with the inflammation and so on with the heart being handled and operated on. And if they've never had AF before, they've only got post operative AF, then we don't consider they need to be anticoagulated long term. They've had AF as a single self limiting episode out of some medical problems. So that's a good subset to bear in mind. If you've got some correctable medical problem, that's given you AF you correct that medical problem, you don't necessarily need to think of that person as an AF patient forevermore. So anyway, back to the patient group, the common ones we see yes, you want to get rate control, you want to antoicoagulate them. If they're compromised with chest pain, heart failure, really uncomfortable, you'll probably want to get them into sinus rhythm. And so we can do DC cardioversion, for that, or pharmacologic cardioversion to that but you have to be sure there's no thrombus in the heart. So how do you know that? Well, personally, if someone's been in AF more than about six hours, I'm not prepared to do a DC shock without knowing they're, they've got no clot there . So in the current era, we can do a transesophageal echocardiogram in most hospitals, relatively easy to get hold of on the day, the bigger hospitals and once there's no thrombus seen on TOE you can go on and cardiovert them the same day. So this is very commonly done at big hospitals. They turn up with AF, you keep them fasted, and you do the TOe, there's no clot, you go on and cardiovert them, they can potentially be discharged on the same day, because we can't assume that someone's notgot clot there. The alternative is if someone is stable and you see them in the GP practice and then you diagnose that AF and a little bit puffy, a little bit tired but they're okay. That patient group you can anticoagulate for four weeks, and then do the DC cardioversion without the need of a toe. Yoiu must have four weeks therapeutic anticoagulation before cardioversion or no evidence of thrombus on TOE for a cardioversion. So you have to factor that into how you manage patients.

And what's the anticoagulant you tend to use, or you'd recommend?

Well, I'm using apixaban pretty much all the time now five milligrams BD, for people with GFR is about 60. And between 25 and 60, GFR, 2.5mg bd. Under 25 GFR can use it and it's warfarin. Fortunately, there are not that many people out there with a GFR under 25, in our practice, so most of them you can manage with apixaban, which is so much easier for the patient than warfarin.

Which cardioversion to use. I know there's options of bi phasic versus monophasic, Just briefly describe those types of cardioversions and what the difference is.

I wouldn't be too fussed about that most defibrillators are now biphasic. I don't think there's too many monophasic out there anymore, and its just a more effective waveform for cardioversion. So you dont have to worry too much about that. Just get him to dial him up to 200 joules and deliver the shock. Must be synchronized. When you're cardiovert someone. you've got to synchronize the shock. If you don't synchronize and you deliver a shock you may be shocking on the vulnerable part of the cycle and shocking on the T wave which could precipitate ventricular fibrillation. I always go with 200 joules, I don't see any sense of mucking around 50 to 200, and almost always gets people out but make sure synchronize has been selected. So that shock is synchronized to the QRS and T wave appropriately. Why would you even bother this? Well, if you've got VF patient you don't want to synchronize, you got to be able to wear this option. VF don't sync to that the defibrillator will never see a QRS, will never deliver a shot. So you have to be able to deliver an unsynchronized shock in that situation. But for all are organized rhythms, they're always got to be synchronized. Sorry, go on about that. But that's a very important point.

that's good. That's what we want to hear.

More important is whether you select synchronized or not.

If we go on to the pharmocological versions of treatment for an atrial fibrillation, what are the main ones you're using is the digitoxin, still in favor,

I don't use digoxin at all. So if you're looking at rate control, then you use an AV blocking drug, beta blocker, or a calcium channel blocker is perfectly fine. If you're looking at a rhythmic drug, then you have to make a decision based on other patients. So people with structurally abnormal hearts, really the only drug I would use is amiodarone. People do use sotalol in that situation, but I think it's often disappointing, not not without potential for problems. Structurally normal heart, a lot of our AF patients have structurally normal heart other than a little bit of atrial l dilation but normal ventricles, flecanide is quite a good drug for those people, both IV and for chronic management orally, but you can't give that drug unless you know they have got a good left ventricle. And also, you want to be very careful, if there conduction systems, is not normal, bumndle branch block, etc. I wouldn't use it in that situation. Because being a sodium channel blocker, not great to give sodium channel blockers to these people . So flecanide is a good drug for people with good LV's and normal conduction system. And that's a large percentage of our AF patient group. Amiodarone is fine but I cant imagine that you want to give someone who's 50 this for the rest of their life, but it can be quite a very useful drug acutely and a lot of time we're just managing these people acutely and then reassessing what how we manage them in the longer term just because you gives it to someone acutely or for the first week, and that doesn't mean you're necessarily going to use that as long term treatment. And I guess that brings us to the next option which really is catheter ablation. So we do a lot of catheter ablation, for AF patients because the drug options are not perfect. And there are plenty of patients who prefer a catheter ablation, rather than indefinite treatment with drugs that have potentialfor problems. Right?

And what does that actually involve? Does that require an anaesthetic? Is it done under sedation?

The cornerstone for that type of case, is pulmonary vein isolation. So this is where with some energy source, in Australia, still mostly radiofrequency current or quite a lot of sensors using cryo freeze, we get rid of the electrical activity from the pulmonary veins where they join onto the left atrium, the procedure that in paroxysmal fibrillators done by people with good experience, in the cases, she'll get an 80% or better resolve the patient, if you get into persistent or long term fibrillation, the success rates drop off more like 50 to 70% success rates for that sort of procedure.

So that pulmonaryu vein junction to the heart is actually a main cause of AF

For setting of AF. And that was shown very nicely by a French cardiologist, probably mid 90s, who did the seminal work on this, I don't know if anyone still even knows why it works. But probably pulmonary isolation does a good job for many people with particularly paroxysmal AF nd in experienced hands, that do a lot of this work, it's a ve y low risk procedure. Now, ce tainly an option for people wh can only hold sinus rhythm wi h amiodarone, for example, a nic way to get them off ,to do the blation, or people may be hol ing sinus rhythm on flecanid . they dont want to be tak ng drugs at all. So it's cer ainly in our management arm ry.

Is that why sleep apnea is associated with atrial fibrillation because of the dilation of the pulmonary veins

I am in no way an expert with sleep apnoea. in it But as I understand it, people do desaturate their oxygen content, get high co2, they get atrial stretch, they get autonomic arousal, they're talking about this 50 times an hour, every hour every night, right? So I think if you were designing an experimental model with animals for extrapolation, I would probably want out hypoxia, acidosis. I want to see CO2 content , I want atrial stretch andautonomic activation. I would want all of these things to get my animal to go into AF. That's what sleep apnoea is. So it's not surprising that it leads into into AF and there's quite good data that optimal treatment of sleep apnea decreases cycle fibrillation, and also losing weight. It's been shown to help with minimize further problems with atrial fibrillation

weight reduction. is that because of fat content in the heart wallsor that because of the sleep apnea association

No it's not that.You probably need to speak to somebody else about the actual theory behind why weight loss decreases AF. I mean it seems to decrease AF independent of sleep apnea. So we want our patients who have AF to approach things from all directions. If they're drinking too much. You want to cut back how much alcohol they drink or abstain. They're overweight, we'd like them to lose weight. If they've got untreated sleep apnea. we'd like them to treat that. So these are all things that we can do in parallel with appropriate medical therapy and in a selected subset of procedural approach ablation approach.

Well, this is brilliant really appreciate the information provided today. Excellent rounded subjects on atrial fibrillation. It's beem great having you on on today on Aussie Med Ed and first interview for the New year. Thank you very much, Cameron

Okay.

The information provided today is designed to complement the information provided to you in your local region and should supplement your readings and teachings in that area. Please don't take it as the only way of treating this condition or assessing a condition, but really as one of various ways of assessing these conditions. Please be also be aware that the information provided today is really just general medical advice and isn't designed to actually be a source of medical information regarding your particular condition. Remember to consult your specialist or medical practitioner if you have concerns about a condition raised in this podcast. Thanks once again for listening to our podcast, Aussie Med Ed, the Australian medical education podcast. I have really enjoyed hosting this podcast. I hope you find it useful to hear a pragmatic approach to everyday conditions. If you have any questions or information you want to ask about us, or you'd like to put a suggestion for a topic, please don't hesitate to email us at Gavin@Med-Ed.com.au . once again, I hope you've enjoyed listening to it and we look forward to hosting it next fortnight when we introduce a new topic. Thank you