In-patient management of Atrial disorders ( A-FIB and A-Flutter)



This on-demand teaching session is aimed at medical professionals and covers understanding of the mechanisms of atrial flutter and atrial fibrillation, clinical history and examination of patients with atrial fibrillation, investigation required in assessing patients with atrial fibrillation, treatment options available, causes of AF and its potential clinical presentations, and current approaches to restoring Sinus rhythm and controlling the ventricular rate in patients. Throughout the session, the speaker will use two case studies to discuss diagnosis and treatment options in detail and answer questions at the end. Join this session to gain a comprehensive understanding of AF and its management.
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In this session we will cover the following:


  • To understand the mechanisms of atrial flutter and atrial fibrillation
  • To describe the clinical history and examination of These patients
  • To understand the investigations required in the assessment.
  • To understand the treatment options available


  • To describe the potential causes of AF
  • To present to you cases showing various clinical presentations of AF which will help you understand how to decide on anticoagulation for patients
  • To describe the current approaches to restoring sinus rhythm and controlling the ventricular rate in patients with AF.

Learning objectives

Learning Objectives: 1. To understand the mechanisms of atrial flutter and atrial fibrillation. 2. To be able to describe the clinical history, examination and investigation of patients with atrial fibrillation. 3. To know the treatment options available for atrial fibrillation. 4. To be able to decide on anti-coagulation for patients based on the CHADS score. 5. To explain to patients the potential causes of atrial fibrillation and the current approaches to restoring sinus rhythm and controlling the ventricular rate.
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Computer generated transcript

The following transcript was generated automatically from the content and has not been checked or corrected manually.

and we have with us today. Hello. Good evening, everybody. Can you all see me clearly? Hi. Good evening. Uh, today I shall give a presentation on the atrial conduction disorders, atrial flutter and atrial fibrillation, which are both commonly abbreviated A f. I'd like to thank my former colleague, Doctor Promise Ferry for inviting me to give this talk. So let's just get the formal parts out of the way. Uh, the names of the session to understand the mechanisms of atrial flutter and atrial fibrillation to describe the clinical history and examination of patients with atrial fibrillation To understand the investigation required in assessing patients with atrial fibrillation to understand the treatment options available for atrial fibrillation. My objective by the end of the session will be to describe the potential causes of air to present to you. Case is showing various clinical presentations of a F which will help understand how to decide on anti coagulation for patients and then to describe the current approaches to restoring Sinus rhythm and controlling the ventricular rate in patients with a F. So, our first case, uh, in our first case, we have Janet. Janet is a 69 year old lady, and she presents to the emergency room by ambulance, complaining of palpitations and feeling lightheaded. She has been out for dinner, celebrating her 50th wedding anniversary with her husband and friends. That evening, at the end of celebrations, she stood up and, while walking towards the exit of the restaurant, felt that her heart was racing away in her chest. Naturally, she blamed the alcohol and staggered towards the car, where she swooned into the arms of her husband without losing consciousness. I never want to really suffer fainting spells and generally and well, she asked her husband to call 999, and an ambulance was dispatched their location in the emergency department. You find out that she's previously fit and well. She has had two Children born by normal delivery and never had any surgical operations to date. She has no known allergies and takes over the counter paracetamol occasionally for lower back pain, but doesn't need to see her GP regularly or require any regular medications. She is up to date on cardio vascular screening. On arrival, she appears diaphoretic and pale, somewhat clammy, but she feels warm to touch. Her pulse is irregular and irregular at 160 BPM. Her capillary feel time is less than two seconds and her jugular venous pulse shows absent a waves. She appears to be acyanotic. Her heart sounds normal with no murmurs to Auscultation. And the apex beat is not displaced. She has no features of edema. Blood tests, lying standing BP and the c G are requested. The results show that there was no significant drop in her postural BP with the line BP 114 over 82. Understanding BP 112 over 84. Her bloods were also essentially normal. As you can see, we then move onto looking at her E C G and her EKG shows an irregular, narrow, complex tachycardia. The P waves are irregular, and the are intervals are variable. As a result, you make a diagnosis of new onset atrial fibrillation. The nurse acts whether you would like the patient to have any intravenous fluids. Does she need any fluids at this time? Does she need any electrolyte replacement? Um, in in this instance, uh, the answer is probably no. Her electrolytes are all normal and and she's well hydrated. Um, so in this instance, she's placed on the cardiac monitor and she's moved to the majors department from the resuscitation department. So considering her treatment, what should be considered doing next? Well, in the department, various vehicle maneuvers were tried, and the carotid massage was also tried, but she remained symptomatic of her palpitations. Occasionally there was slowing down of the rate, but her heart rate generally remained variable and high. There was certainly no sustained response to any attempts at vehicle maneuvers because the heart rhythm was irregular, and it was clear to see that this was atrial fibrillation as an adenosine was not tried because this was not a super ventricular tachycardia. After about 15 minutes of attempts, you ask for her repeat observations, which was follows. Her respiratory rate is now 16, her saturations and 99% on room air. Her heart rate has come down to 125 and her BP is 121 over 78. Her chest X ray is normal. A repeat EKG also confirms atrial fibrillation. Uh, the emergency department consultant arise and acts for a hand over, which is given. He acts that you consider whether the patient can be given some sort of drug treatment and be transferred to the ambulatory care department. You make the call, but they stayed that she remains to tachycardia for a transfer there. And actually you consider a drug treatment. Having made the diagnosis of a F with fast ventricular response rate, you speak to your senior and discuss the treatments at the end of the 15 minute conversation about the benefits of rate control, rhythm restoration and anti coagulation. He states to you that in many patients, a f will self terminate and treatment is only needed if the patient has prolonged symptoms and the need for anti coagulation is based upon the child's fast score. You once again ask the nurse to repeat the observations, and she tells you that the patient feels better when you go to the patient. She starts to apologize, and she asked if she can go home. Her heart rate is now 84 BPM. Now, at this point in time, is it safe to discharge her? What needs to be addressed? Certainly with a chads score of two, she would benefit from anti coagulation. You also need to explain to her that moderate long term alcohol intake and acute intoxication are both associated with atrial fibrillation. You agree on a plan to discharge her with care of her GP and request an appointment for discussion of anti coagulation, and at this time, she has no further questions. Okay, At this point in time, I just want to check to see if there are any questions. Lovely. So I'll now move on to our second patient. But just before I move on to him, I just want to give you a bit of an understanding about atrial conduction disorders. And atrial conduction disorders are classed as super ventricular arrhythmias, and I want you to remember that these are not to be confused with the more devastating ventricular arrhythmias, which include ventricular tachycardia and ventricular fibrillation. Okay, so these are super ventricular arrhythmias, and it is also worthwhile to point out at this time that arrhythmias can occur in patients who have a pre existing heart block and heart blocks have various degrees, so a patient can have an arrhythmia who has a coexisting first degree. A second degree mobiles type one a second degree mobitz type two or even third degree heart block. The super ventricular arrhythmias, however, are a heterogenous generous group of diseases of the conduction system. Um, these are diseases which run from the Sinoatrial node through the Atria down to the atrioventricular node. These diseases tend to be caused by the presence of either ectopic focus of conduction abnormal conduction circuits or the presence of abnormal pathways. And in this group there are about seven disorders atrial flutter, atrial fibrillation, the two conditions which we're going to be talking about. And then the less common atrial tachycardia paroxysmal supraventricular tachycardia, S V t multifocal atrial tachycardia Does atrioventricular node all reentry tachycardia and then finally, wolf Parkinson White syndrome. It is worth noting at this point in time, just for academic reasons. Um, that a V nodal reentry tachycardia operates because there are two pathways with in the navy node one is a slow pathway and one is a fast pathway, and electrical currents can pass down one pathway and then cause reentry. However, in wolf Parkinson white syndrome, the pathway exists outside the HIV node. So with that in mind, let's just move on to our second case remember our first case was was a lady who had symptomatic new onset atrial fibrillation, which self terminated. Now you've now been asked to Clark in a patient by the name of Mark. He's a 72 year old. He's a retired Laurie driver from all the Hampton as a young man in the late 19 sixties. Uh, he did like many people in that generation. He sang a lot of music and did a lot of recreational drug drugs. He can't recall most of the drugs that he took, probably because he took LSD. Um, and he continues to drink through his twenties, drinking alcohol heavily and smoking up to about 15 cigarettes today. At that time, he was working in carpentry and in construction. He met his wife in his thirties and his alcohol intake reduced. But it fluctuated. Um, it was heaviest that social gatherings. And on holidays, um, he decided at the age of 38 to stop smoking and then again at the age of 40 and in his forties, he put on considerable weight. He took on a much more sedentary job because he was exhausted from working in construction work when he was 45 years old. He went to, well, man checking his GP. And he was only diagnosed with having hypertension. But he saw his GP infrequently on these. In frequent visits, he was always asked to consider treatment. He would always discuss losing weight, and on one occasion he decided to purchase a bicycle. Now, at 53 years old and he's 72 now, he had a stemi non ST elevation myocardial infarction and required emergency percutaneous angioplasty. Following this emergency procedure, it was recommended that he should have a bypass surgery. So he went on to have bypass surgery. After his bypass surgery about 20 years ago, he took life a lot more slowly. He decided to take early retirement. At the age of 53. He moved to Florida. And then two years ago, he returned to the UK Um, after his return, he is now, uh, enrolled in a GP, and he admits to his GP that he's taking amlodipine. And that might, um, valsartan of his BP. Um, this is something which was started, of course, in Florida. But he says that he never had any follow up by his cardiac surgeons. What he was told was You've been treated and you should not go out and eat a Mediterranean diet and and reduce the amount of red wine which you decided to have. Um, in the last few weeks, though, he's been investigated for COPD because he's developed a cough and shortness of breath. While he was at this appointment for Spirometry, he noticed that he was having some palpitations and and he had been having palpitations on and off for several weeks. So he mentioned this. The physiologist You kindly performed an EKG and that EKG showed a F with a left bundle branch block. The physiologist therefore commended to him that there were abnormalities with the voltage on the BCG, Um, but said with his body size, his smoking history, it was difficult for him to elaborate further without doing an echocardiogram, and this would have to be requested by his doctor, so not having a clue what any of that meant. He returned home waiting for his next GP appointment, and he told his wife that he might have a condition called atrial fibrillation. He might now have a condition called COPD, and he might have problems with his heart in addition to his previous hypertension and previous stemi. So while waiting to see his GP, he develops episodes of chest tightness and discomfort. One night his wife noticed that he's becoming very breathless and that his palpitations are not abating and he cannot get comfortable. So she calls up her niece, who is a student nurse. Um, she explains that, uh, he's been getting these episodes of chest tightness and chest discomfort. They're they're not. They're not probably musculoskeletal in nature. Um, sometimes they're related to coughing. Sometimes they come on at rest, Sometimes they occur with physical activity. Um, but he hasn't noticed that they're associated with any particular strenuous activity. Um, and as she said, they're happening at rest in bed. So she didn't think that they were musculoskeletal in nature. These episodes of discomfort, um, and and alongside that, the breathlessness. This is the reason why, uh, he was having investigations for COPD, but her her niece was more astute and decided that she should call 999 because she felt that these episodes of chest pain represented angina. And he could be having silent heart attacks and on the verge of dipping into pulmonary edema. So he arrives in the accident in emergency department in the recess, and by now he's critically ill. He's pale, his hands are now cold and clammy, and it's important to distinguish that he has cold peripheries. Uh, unlike Janet, who had warm peripheries, his capillary refill time is prolonged at five seconds, unlike Janet, who's had a capillary refill time of less than two seconds, Uh, and his wife, of course, is faring and can see that he's getting more and well by the minute. His breathing is noisy and distressed. He is restless, and he's coughing up frothy sputum. Um, so she's taken aside by a nurse to the waiting room and his observation show how well he is. His respiratory rate is 30. His saturations are 74% on 60% liters via non rebreathe mask. His heart rate is 240 his BP is hypertensive 65/40. When you examine him, you notice Yes, his pulse is weak, thready and irregular. He has bilateral crepitations on his chest and his JVP is elevated by four centimeters when you listen to his chest Now, having moved on from the examination of the neck and of the pulse is you can hear a pan systolic murmur, and you know that this murmurs mitral regurgitation because it's being heard in the mitral area. And you also noticed that his apex is displaced. It's displaced, inferior early, and it's displaced to the left And when you're listening to the heart sounds, although it's somewhat difficult to hear heart sounds because of the mitral regurgitation, um, you feel that you certainly can hear a first heart sound, the second heart sound and the third heart sound giving a Gallup rhythm on further examination. He doesn't have that much in the way of peripheral, uh, edema, and he has no signs of the cities. Um, you know, he's otherwise well, in terms of his his temperature. He is afebrile and his GCS is thought to be, as I said before, 13 out of 15, because his eyes are less responsive and he's speaking in a confused way. So he loses one point on his I response and one point on his verbal response. He's still able to obey most commands normally, so he's undergone a portable chest X ray, which has shown pulmonary edema and he's had an EKG done, which I can show you there, and he has been catheterized, and what we can see on this CCG is a first of all. It's somewhat irregular. It's difficult to say that each of these are intervals are exactly the same. It's certainly tachycardia. So in terms of rate, there's a tachycardia, and in terms of rhythm, it is slightly irregular. So we have to look to see if there any discernible P waves to see if this is atrial fibrillation. And there do appear to be plenty of P waves. In fact, there seems to be a P wave nestled into almost every T wave on the rhythm strip at the bottom. Uh, we can certainly see a number of peer waves. And given his previous history of left bundle branch block, we know that he has a history of a F. He has a history of left bundle branch block, and these P waves are occurring at very frequent intervals. And if we try to do a ratio of the P ways, we'll find that they're occurring probably in ratios ranging from 1 to 1322 or 2 to 1 they're quite variable, but this is atrial flutter. So in terms of how we therefore manage him, it will all depend on our knowledge that this is atrial flutter and not atrial fibrillation, and it can be difficult to distinguish between the two. All right? No. A diagnosis of fast classical atrial flutter with aberrant conduction with variable. Every node conduction block was made. I'll repeat that again. Fast classical atrial flutter with aberrant conduction with a variable every node conduction block. Okay, your consultant explains what this means to you that this means that the patient is experiencing a super ventricular tachycardia. It's coming from above the IV node, which in this case is atrial flutter when the flutter waves reached the IV nodes. Sometimes each beat is transmitted through the ventricles in a 1 to 1 fashion, and sometimes every other beat is blocked by what is called a V node refractory nous. So you may get a 2 to 1 ratio, and occasionally it's more bizarre than that because he already has a left bundle branch block from before. His QRS complex is will be wide, as opposed to the usual situation where atrial flutter is associated with a narrow, complex tachycardia. So in your mind, you're probably confused. This is a broad, complex tachycardia, but it is a chore flatter. So just remember, you have to know if your patient has a left bundle branch block. All right, bundle branch block before to know if this is a broad, complex tachycardia or a narrow, complex tachycardia. Alternatively, if they're discernible P waves and it appears to be flatter, then it's more likely that this is a narrow, complex tachycardia or, as I should probably say, a super ventricular tachycardia. The reason why we use the terminology of narrow and broad, broad complex comes down to the management of this patient. So this patient now needs to be treated on the LS protocol, which is the protocol which we use in all hospitals. The first thing in any ls protocol is always to call for help. Okay, and in this case, we will be calling for a cardiac arrest or a medical emergency team call. Okay, so that's the first thing that you should do when you're when you're given this sort of information that you made this clinical assessment, um, try to get senior help and try to get help from those who can probably help the patient the most so cardiac arrest or a med call. And then we're going to follow the ABC, the approach which we've already followed. We know that the airway isn't particularly compromised, but it could become compromised if the patient's level of consciousness falls. In terms of the breathing, there's inadequate ventilation and long hike along perfusion. Uh, the patient is tachypnea. The patient has hypoxia, and this is despite additional supplemental oxygen, so this needs to be addressed immediately. Remember, with the A B C D approach we address, and then we go back and re assess, and then we address again if there's still a problem. So this patient needs supplemental oxygen. So while we are seeing a patient who is Perry arrest, we sometimes have to think to ourselves. Well, could could the peri cardiac arrest be related, actually two respiratory arrest. So we always try to optimize the patient's oxygenation, so this patient needs more than we can give them with 60% oxygen via non rebreathe mask, and we could consider high flow oxygen. But this patient probably would be better off being intubated and ventilated. Okay. And then we, of course, move on to see which is tachycardia and hypertension, which are features of cardiogenic shock in association with cool, clammy peripheries, a prolonged capillary refill time, um, and and and an obvious precipitant. So this needs to be addressed once the hypoxia has been addressed. So you have called for help. You've done exactly the right thing called for help and critical care outreach, And I two are both on the way. You know that, Mark. In addition to having fast, the F is showing adverse features these adverse features a cardiogenic shock and pulmonary edema. And in the peri arrest situation, we use the ls algorithm for narrow, complex tachycardia when managing h A flutter. Okay, we're following this because we know the underlying rhythm is a f not VT. Remember, VT hardly ever skipped beats, except if we're seeing escape beats or fusion beats. Okay, but that's for a different discussion. All right? So moving on the anesthesia rise and ask whether the gentleman remains for resuscitation and begins to assess his fitness for I see you. He speaks to Mark and says to him that even though he has had a bypass in the past and he has coronary artery disease probably related to smoking, and that he has poorly controlled hypertension for several years that at the age of 72 he would still consider taken into I see you. But he probably will need to have some more investigations into his heart and into his lungs as his GP had already commenced. He says that if treatment is successful, he will definitely need to go to I t. U. So in this situation you have a patient who you have now intubated and ventilated and who continues to show signs of cardiogenic shock. The treatment is immediate DC cardioversion with 50 to 100 and 20 Jules of biphasic energy. Okay, we can start at 50 and we can then increase up to 70 90. We try to give only about three shocks, but generally we start with a lower energy delivery because it often is successful, particularly with in atrial fibrillation. Atrial flutter. I must apologize. H a flutter. Now, in terms of sedating the patient, the patient will usually require some propofol, midazolam and fentanyl. So post I see you care is going to be essential because this is a patient who for a long time is going to be to anesthetize, to be able to protect their airway. So it is essential that we have the help of I see you on, uh, in terms of managing the post resuscitation patient. Now, I just want to clarify that in this situation there's no rate control measure which is appropriate. There is no role at all for rate control. Reversing hypoxia and lifesaving cardioversion is required to restore this patient to Sinus rhythm in every effort to prevent imminent cardiac arrest. So we don't think about rate control. This is a rhythm control strategy, and it's a life saving rhythm control strategy. Now, um, in terms of ongoing care, he goes to intensive care and on intensive care. We would usually consider whether our patients need further investigations if they presented with a flutter rhythm. Um so most patients will have thyroid function tests. Uh, most patients will need to have an echocardiogram. Uh, some patients will need to be considered for a cardiac angiogram or a cardiac MRI. Um, and we sometimes consider renal or adrenal MRI to look for renal artery stenosis or adrenal tumors in patients with resistant hypertension. And this goes along side category catecholamine screening. Okay, Now for Mark. He was intubated, taken to intensive care, and his echocardiogram showed grade three diastolic dysfunction. It also showed left ventricular hypertrophy. And the combination of these two things are quite indicative of hypertensive heart disease. Um, in terms of his left ventricle, it was also impaired and dilated. Um, and there were regional wall motion abnormalities consistent with an ischemic cardiomyopathy. Um, these areas of regional motion abnormalities were consistent with the previous MRI, as opposed to an acute Am I, um however, when we check serial troponin levels, they were persistently elevated. And in the context of such a tacky arrhythmia requiring DC cardioversion, it was difficult to interpret those troponin levels. Okay, so this is one of those situations where you can check troponin levels, they're elevated. And it's difficult to say whether there had been a cardiac event that triggered or not because there's likely to going to be a rise because of how devastating this tacky arrhythmia actually was in a patient who had been otherwise relatively well, no, I just want to point at this point in time that following DC cardioversion anti coagulation needs to be given for a minimum of four weeks. This is due to the really high risk that follows DC cardioversion in the emergency setting. Um, this cardio embolism generally will occur in the first four days and in some studies is reported as high as up to seven days after cardioversion. So the first week is the really important week to look out for symptoms of a stroke or other peripheral embolization. Um, however, we we anticoagulated for a minimum of four weeks or longer, depending, of course, upon the patient. Such adverse risk score. Because Mark has been taken to intensive care and he was initially treated in the recess department. We decided to give him low molecular weight heparin at the treatment dose. No, while he was there on on intensive care, um, he happened to be seen by a medical registrar who also worked at the cardiology registrar. And he was listed for a coronary angiogram. Um, he felt that the diagnosis of acute and stemi could not be ignored. Um, and with him having, uh, what he felt was a newly documented left bundle branch block Although, of course, this was documented by the physiologist before and the presence of the race troponin there was enough evidence, really for him to have a repeat angiogram. Also, he hadn't had an angiogram since his CABG was done almost 20 years ago. Um, the the angiogram showed no new stenosis requiring any intervention, and his grafts remained all well, patent. Okay, um, so there's there's no coronary artery disease which has triggered his atrial flutter. All right, so he's diaries. He's given IV diuretics. He's now commenced on heart failure treatment because in terms of his ejection fraction, um, this is found to be low. He has heart failure. Um, And when we're starting patients on heart failure treatment, Um, our our our use of beta blockers tends to be a lot more cautious. We tend to start with a dose of 1.25 mg, for instance of bisoprolol. So he was just started on that. And then we up titrate, usually in 1 to 2 week intervals, or longer if we actually can can afford that time. Um, he makes some somewhat slow progress. Eventually step down to see. See you. Um, so at this point in time. I think it's worthwhile checking. Of course, that no one has any questions. Just discuss a little bit about the physiology of atrial flutter. Now, as you can see in this diagram, um, there's a a circuit which has been drawn here in red arrows, and the first part of this circuit is this almost vertical curve. And this is traveling from the office of the coronary Sinus, which is the main vein, which drains the heart. Um, so that's draining blood back into the right atrium. Um, this. Sit alongside a ridge of tissue to it's left called the Eustation Ridge, and you'll see that there's this ridge of tissue in between the Eustation Ridge and the Tricuspid valve. And those red arrows indicate the way how flutter waves tend to propagate themselves in typical atrial flutter. It originates from a focus, which is anterior to the origin of the coronary Sinus. It propagates along and is muscle tissue, which is bordered anteriorly by the analysts of the Tricuspid valve and posteriorly by the Eustation Ridge and then superior early by the crystal term analysis. And you can see the crystal terminal is is very close to the left atrial appendage. Now, for those of you who don't understand the anatomy, of course, the Eustation Ridge is going to be separating the non muscular part of the right atrium, which includes the vena cava, uh, from the more muscular part of the right atrium, which is the pectoral muscle. So in terms of the electrical focus, we are no longer seeing electrical activity being generated from the essay node which, as you all know, lies closer to the SV. See, electrical activity is being generated from around the coronary Sinus propagating up towards the Christian terminals and from there moving into the pectoral muscle, which is the muscular part of the right atrium. And it is this kind of electrical activity propagating in this sort of counter clockwise direction. This is what causes flutter ways because these flutter waves tend to occur at a very fast rate and because they're traveling in a counterclockwise way. In typical flutter, we start to see negative anyways in leads to three and a V f. Okay, so in typical flutter, there's a counter clockwise mechanism and we get negative P waves and needs to three and a V F uh, the opposite, of course, of this is what's called reverse typical flutter, which is much less frequent but that shows positive P waves and needs to three and a V F so negative P waves in typical flutter. Positive P waves in reverse. Typical flutter. The other kind of flutter, which we tend to see, is a typical flutter and with atypical, flatter, flatter ways are originating from focuses, which can be anywhere within the left or the right atrium. But not this flutter, which we describe as Christmas dependent flutter, which is seen in typical flutter, which can be either counterclockwise mechanism, which is the typical one. Typical typical flutter, or a clockwise mechanism, which is the reverse Typical flutter. I hope that was easy enough to understand in terms of the physiology, and you'll hear that we're discussing macro reentrant circuit. So these are relatively large circuits and they're located within the right atrium. Unless, of course, we're dealing with an atypical flutter, which can be left or right atrium. So we've had an introduction to Janet. We've had an introduction to Mark. Um uh, we've discussed a bit about the physiology of atrial flutter, so we can move on to our next consultation with Janet. And she has come now to see you as a private patient. And she's asking, How did she get your fibrillation? Does she need to continue with anti coagulation? Can she pass a fibrillation on to others? And what options for rate or rhythm control are for the best quality of life and the least impact on her life? So, of course, you explain to her a f is a common condition which occurs more commonly as we age. But there are certain factors which are associated with this. Um, in her case, of course, we're unable to find any of the traditional respiratory cardiovascular causes, and you also reassure her. Of course, that is not a transmissible condition. Um, while she's been waiting to see you, she's had further episodes. She had an episode that lasted five days and an episode that lasted three days, all within the space of the last two weeks. And these are causing her palpitations. Uh, she usually does Pilates, but when she gets palpitations during Pilates has occurred. Um, she's unable to do them because she gets breathless. Um, she went to see her GP. Um, you did advise her from that emergency consultation to start anti coagulation to see her GP. Um, so she's been commenced on apixaban 5 mg. Um, and of course, she wants to know she needs to continue this lifelong, Um, And of course, the easy answer is, Well, if your risk changes, then we can change our mind. But at the moment, within your current strategy, you need to be anticoagulated because if you're at risk growth profile and your risk score is two, then you benefit from anti coagulation. And this is as simply as one needs to explain it, that in terms of risk scores and in terms of how much you can benefit from being anticoagulated if your score is one or if your score is two or if your score is three, anything one or above, you need anti coagulation. No. Will this come at a risk? Um, and and this is the reason why we do has bled scores hemorrhages scores, which look at other factors, which could increase your risk of bleeding. But despite a risk factor for bleeding despite ongoing bleeding, despite despite, um, High has bled score or hemorrhages, score identifying a patient for anti coagulation is important because a patient who has high risk with a F we'll see benefit from anti coagulation, and this is what all of the trials have shown. So it is offered. But the decision has to, of course, be based on risk. So if the patient has active bleeding, then prophylaxis against a stroke may not at that point in time be considered to be as important. Remember, we use treatment dose anti coagulation for treating venous thromboembolism for treating DVT and pulmonary emboli. And we're using a similar dose of anti coagulant to treat a F in an attempt to prevent patients having strokes long term. Um so the indication is slightly softer indication. And then the rationale for stopping anticoagulants in this situation is easy to to meet. It's it's easy to identify patients who need to stop your anti coagulation if they're bleeding and they have a F. So it's usually a simpler decision to make Okay, but nonetheless, you explain to her that she has a chads score of two, so her risk goes up from about 9.6% of having a stroke per year to about 2.9%. And you explain to her that as she gets older, the risk of stroke in the general population will go up, but that her risk of having a stroke goes up exponentially, and therefore the risk of the risk of having a stroke goes up. And therefore the need for anticoagulations also goes up. So when your patient ask you if they need anti coagulation for F, and then if they need to take it for the rest of their life, invariably your answer is going to be yes. However, there may be times when that that anti coagulation needs to be discontinued because of unexplained bleeding or active bleeding. Actually, before I move on to this bit about the physiology, I think it's just worthwhile just going back to talk about the options for treatment a bit more. Um, I know that's probably a question many of you have and and certainly from the evidence and from the guidelines which were given, um, no acthar preferable to warfarin. And patients who have non valvular A F, um, and patients who have valvular a F warfarin is superior in terms of preventing patients from having a stroke. And remember that this prevention of stroke and thromboembolic uh, complications such as embolism to the heart embolism. Uh, two other vital organs. Prevention of systemic embolization is the rationale for our treatments. Okay. And prevention of stroke is superior with warfarin for patients who have valvular a f and prevention of stroke for patients with non valvular A f is superior with a no ac. Okay, All right, now there are There are reasons why you might not be able to give your patients, you know, ac, um and then, yes, we can choose to give them warfarin, but we have to accept that we have not given them the recommended best treatment now, in terms of preference for for NOACs, there is building evidence that if you're going to be anticoagulated for a F, the best impact in terms of preventing stroke is derived from using a six, even which is given at the 5 mg twice daily dose, um, or using a full dose, the bigger tran um that 150 mg twice daily dose. Obviously, both of these are twice daily medications, and that has to be taken into account when, when offering patients medications, but they offer the best efficacy. Um, lower low dose dabigatran 1 10, which might have to be offered if the patient has renal impairment, low dose of eczema, which may have to be offered if the patient has renal impairment or has low weight. Or is it a certain age or a combination of all those things that we should probably see a combination of all those things rather than any of the individual findings? Um, as well as rivaroxaban and edoxaban. Um, just don't seem to be standing up in the head to head comparisons. So, um, without doubting for anyone, particular anticoagulant apixaban and the pegintron tend to have the most favorable profile. It also helps the bigger trend that it has a reversal agent idea. This is a map. Um, and apixaban, of course, has a reversal agent, which is a dexa alpha and that can also be used for rivaroxaban. The result as to whether it's, uh, safe to use in the oxygen toxicity or bleeding associated with the oxygen, I should say, Um, but of course, with warfarin, warfarin has always been a relatively, um, good drug to use because it can be monitored. It can be monitored using the I N R. Levels or the prothrombin times. Um, and in addition, the anticoagulant effect of warfarin can generally be reversed by using vitamin K or various prothrombin complex concentrates. So, um, in terms of the choice, really, Um, you can say to your patient I can offer you what's best. Or you can say to your patient I can offer you what I'm allowed to because of your age and your renal function. Or you can say to your patient, I'm going to offer you something which can be monitored, and in some cases it's all of those things that you're offering your patient now. You also need to explain to your patients that they might develop certain intolerance to certain tablets so a patient might decide to go for a oxygen, and they might just develop a rash with the doxepin and decide to switch. And you may therefore go to Rivaroxaban, and they might tolerate that quite well. So specific intolerances might make your patient decide to switch, Um, and it's also a fairly understandable if a patient doesn't want there to be too much impact on their activities of daily living that might be caused by having to take medications at specific times. Um, this might affect compliance, and it might just be annoying for the patient. Um, so you explain that different tablets are available. Um, and you also even can explain that some tablets are larger than others. So if they have difficulty swallowing a large tablet, then they can probably switch to a smaller tablet. Okay, So in terms of treatments, the issues which we need to address, of course, are the patient's age, their renal function, their weight and whether they have valvular a f those specific issues determine if your patient needs to have anything other than what we discuss, which is probably apixaban or dabigatran at full doses. Um, if they can tolerate it and if they have no intolerance, is okay. So for Janet, it's easy for us to explain that she has paroxysmal atrial fibrillation. Uh, and the best option from all the trials and the treatments, which have the best evidence. Our rate control strategies. Uh, using beta blockers are rate limiting calcium channel blockers. It's as simple as that. The best evidence is for those medications. Um, other options then have less evidence for them. And therefore you should see those options therefore as second line options, rather than necessarily options which provide your patients for a better quality of life. Because if you're going to be offering your patients sotalol or flecainide, which are also options that they can use. Because sotalol, of course, is a beta blocker, you have to explain to them why they have to take sotalol multiple times of the day. Unlike the metoprolol and the Livalo. Um, and you have to explain that they need to have some EKG monitoring because sotalol can cause QT prolongation. Um, you may decide, Hey, I'll try flecainide. But of course, Flecainide also has to be given along side the beta blocker. So while it can be used as a pill in the pocket, strategy is being used as a pill in the pocket strategy, really in those patients in whom beta blockers have failed or in whom diltiazem or verapamil has failed. Now, of course, the other big thing about that is, can your patient tolerate a beta blocker? Can your patient tolerate a rate limiting calcium channel blocker and the main thing with with beta blockers, of course, is that they can cause bronchospasm so in patients who have severe asthma. Um, certainly patients who have frequent eye to it in attendance is you really have to think twice about using a beta blocker is probably discouraged in terms of the calcium channel blockers. They shouldn't really be used in patients who have heart failure. So in patients who have established heart failure who need rate control for their A. F, um, we probably need to rely on a beta blocker in that instance, um, beyond that in terms of rate control. Um, uh, we we don't really have other options that are first line or second line. The next line then would be the digoxin. And the use of digoxin really needs to be limited to elder elderly or sedentary patients. Now, I said, elderly and then I I There's a proviso to using it in the elderly. In the elderly, Digoxin can have significant toxicity. Um, they have more renal dysfunction. Um, and elderly patients tend to have lower body weight, so you have to be careful when choosing digoxin for an elderly patient. But your elderly patients is typically going to be the patient who is sedentary, in whom digoxin might actually have an effect. But for patients who are ambulance, digoxin will not have an effect, and you will still rely upon use of a beta blocker or a calcium channel blocker. Where the junction, of course, is useful is in patients who have low blood pressures. Where use of a beta blocker calcium channel blocker, um, is limited, Uh, and there's very little in the way of dose escalation in order to control tachycardia. So if your patient is hypertensive, which usually would indicate that they're probably getting a lot of symptoms when they're ambulatory and they probably would be sedentary anyway in your hypertensive patient, Um, and that's not your shocked patient. Of course, you're relatively hypertensive patient considered use of digoxin alongside the beta blocker calcium channel blocker. If it can be tolerated, Um, but we try to avoid using digoxin first line. It certainly isn't our first line drug for a F. So I know it's a typical practice when you're on nights and you see an elderly patient and they're going in fast deaf, uh, to just load them with the jocks in before considering giving a beta blocker. But certainly you can consider using a low dose of metoprolol instead as your first line option. Um, it's the best option. No, Um, there are, of course, other options. Um, there is propafenone as well, and propafenone is a very good drug to use in patients who have new onset a f new onset CHF. So they never had any real palpitations are now getting symptoms, and you've caught it early. Um, so So if you can identify a patient who was new onset A F and you can identify that they don't have heart failure, propafenone is also a good option. All right, so we've got beta blockers, calcium channel blockers, digoxin and propafenone. Um, and I also mentioned flecainide being used as a pill in the pocket. Um, but of course, Flecainide isn't really a pill in the pocket for rate control. It's more for rhythm restoration. I can see that. It's a lot of pharmacology, so I'm quickly going to move off of pharmacology, and I can see the time is also catching up with this, so I'm just going to quickly move on to the ablation. I just wanted to tell you about a half ablation because if ablation can restore Sinus rhythm and a patient and render them symptom symptom free in about 90% of cases at about one year. And certainly the pulmonary vein isolation procedure that's pulmonary vein. Isolation has a cure rate of about 80% when used in selected cases of focal dependent A F in addition to a F ablation DC cardioversion is also a very successful tool in restoring a patient. Is Sinus rhythm okay? So when you're thinking about who to refer for a F ablation, you have to realize that a F ablation is successful in relatively selected patients. So typically the younger patient who has not had a F for a long time. Um, and that's probably the kind of person you thinking about for propafenone. And also, when you do the echocardiogram, the HMO sizes are relatively normal. That's the typical patient who will probably get the most benefit from a F because, uh, from an ablation procedure, Um, but if you're patient isn't typical, uh, you're you're you know you're a patient who's a typical successful candidate for ablation. You might then consider a DC cardioversion and and DC cardioversion can definitely be used in patients who have pacemakers. It can also be used in patients who have heart failure in an attempt to restore Sinus rhythm. Okay, Um, in addition, I won't go on to discuss the chemical cardioversion options, but they include drugs like dronedarone and amiodarone, and they also include drugs like dofetilide ibutilide and run a colon. And when I mentioned dofetilide, I want to mention that alongside propafenone because as those drugs which, um uh, they can actually cause proarrhythmic states, um and and they can induce VT, Um, particularly towards a deep, uh, and they can cause significant electrolyte disturbances. So when you're thinking about doing chemical cardioversion, you need to be thinking about having your patient in the CCU unit, where they can have constant monitoring and where they can have constant checks of the electorate levels, because it's essential that they're monitored and replaced while having that treatment to restore Sinus rhythm. I mentioned ibutilide and vernacular and, um, and dofetilide. These, of course, on dronedarone are agents you might not have heard much about. They are on the market and they are available within the European Union. But we have far more experience with amiodarone, and we tend only to use amiodarone inpatient with heart failure. Because DC cardioversion is so much more successful. An ablation is so much more successful in those patients with normal hearts. So amiodarone has kind of taken the place in rhythm control in patients who have established heart failure. Um, so last year, I just go through this very quickly because I had a little bit about, uh, physiology about a f Just have a look at this diagram. You can see the atria left and right, separated by the septum. And you can obviously see this, uh, mitral and tricuspid valves and you can see the sinoatrial node up by the SV. See, And that's obviously normally conduction runs via the sinoatrial node, uh, down through the atria through conduction tissues. And you can see here they're drawn in about three pathways, and then these pathways eventually join up around the atrioventricular node and then conduction passes through. But here, in this schematic, we can see that we've got these haphazard arrows. And these arrows are micro entry entry circuits, as opposed to the macro reentry circuits we saw in atrial flutter and here. They have conveniently drawn some of these micro reentry circuits just around the pulmonary veins and therefore pulmonary veins within the left atrium. So whereas flutter tends to be is most dependent, it tends to occur within the right atrium, close enough to the sinoatrial node to make you think that it's actually being propagated in the right way with atrial fibrillation. The current are actually being generated in most cases from around the ostium of the pulmonary veins. So this is where a F is coming from. In most of our patients, however, it can come from other areas within the left atrium and also within the right atrium. And this is the basis for the surgical correction of a F surgical ablation procedures which were done before known as males procedures where the the entire atrial would be, uh, surgically incised in an attempt to interrupt these these pathways through the atrium and the conduction of these abnormal um uh atrial beats. Um, so we have this, um, theory that these folks are coming from the pulmonary veins. But if we have multiple folk, I, um the difficulty is that this can make an attempt to ablate these folks, I more challenging when they're coming from the pulmonary veins. Balloon. Cryo ablation is a technique that can be used to ablate the pulmonary veins, and this is known as pulmonary vein isolation. You, of course, get some emails from Janet, and she's not pleased she's had palpitations while on um, not even while on any medications. Just while I'm thinking about taking Lexapro law, she's heard that a friend, Barbara, like steak flecainide. So she's thinking about that. Um, she's going to go see your GP and, of course, her GP right back to you, asking why she came to see her in the first place. Um, she thinks that she's a bit anxious, so she's even considering giving the propranolol. Aw, um, At least though Janet agrees to take the Eliquis, which is probably the most important invention, if one thing you take away from this talk remember, anti coagulation is the most important intervention. What we do to restore Sinus rhythm is or to restore heart rate is less important. So, um, this slide, of course, was a long slide dedicated to the cardiac kind of causes of a F. I just want you to know that in essence, if the atria is stretched because the valves aren't working or the ventricle isn't working, so blood never leaves the atrium or the patient has hypertension, so the blood in the ventricle can't get out into the aorta. So it's pumping backwards or they have pulmonary hypertension. So lots of pressure is going into the atrium all the time. Um, there are they have tumors are thrown by sitting there. Then that will cause a F if there's ischemia, whether that be from ventricular ischemia or coronary disease that can cause a F coronary disease is a rare cause of a F. And if there is inflammation of the heart of the lining of the heart, particularly pericarditis, um, then that can cause a f. Okay. So patients who have had surgery recently who may have had certain viral infections like Coxsackie be, or bacterial infections that can cause bacterial pericarditis or who have collagen vascular diseases are always at risk of getting atrial fibrillation. And then we go back to our gentleman mark. So after I t u, he was stepped down to see see you seen by the heart team, and he was given heart failure treatment, and that consisted of a beta blocker entresto and the paranoia and dapagliflozin, all of which are drugs that are shown to improve patient outcomes who have heart failure. And they decided to ditch the rest of the anti hypertensives because those wouldn't offer him a prognostic benefit. Um, he tried metoprolol, but unfortunately, he had some chest symptoms in terms of breathlessness. Um, he had further investigations by the respiratory team and had a CTPE a um it was diagnosed with COPD and he had a couple of rounds of antibiotics and some COPD treatment. Um, but because he hadn't managed with the Metoprolol and they felt that his COPD was particularly mild, they thought, Well, try a slightly more but a selective drug know that he's had his chest treated. And so they started nebivolol and this was started and maximize his treatment at 3.75 mg. And that was stopped because he was getting too much bradycardia and too much in the way of hypertension. Remember, this is being used to treat heart failure is not being used to treat flutter because he's already been cardioverted. He's not having any more atrial flutter where Just uptitrating heart failure medications. Which happened to be first line treatment for atrial flutter. Um, and he was felt to be a high risk. So he definitely needs to have apixaban. And that's based on his chart past score of three. Um, I won't go through this. This is an extremely long slide. Talking about the noncardiac cause is of a f, uh, The only thing to realize is that it increases with age. So, uh, not 0.1% of people who are 55 10% of people who are over 80. And then obviously you have the respiratory causes, which can cause pericarditis, use of stimulant drugs, diabetes and hypothyroidism and pheochromocytoma. And rarely we get subarachnoid hemorrhage is and strokes causing your, uh, a F and also rarely in some families. DCF is an inherited condition. Uh, we've heard of paroxysmal a fib where episodes last less than seven days and persistent a f where they last for more than seven days. But anything that lasts more than 12 months is known as a purse. Longstanding, persistent, permanent F, on the other hand, occurs when the doctor and the patient both decided to stop treatment. So when assessing your patient, just remember the key features are to look for patients with palpitations, chest pain, shortness of breath. Who've had syncope or who are presenting with edema. They'll have an irregular, irregular pulse. They may have a murmur. Uh, they may have displacement of the heart apex, and they may have an S three sounds Congestive heart failure. They may have surgical scars from before they may have signs of right sided heart failure, such as a powerful liver ascites peripheral edema. They may have an elevated jugular, venous pulse, tricuspid insufficiency and loud pee too suggestive of pulmonary hypertension. Or they may have pulmonary edema and pleural effusion suggested left ventricular failure. In essence, we're looking for a scheming heart disease, valvular heart disease, congenital heart disease, heart failure, pulmonary hypertension or signs that the patient may have had previous cardiac surgery. And of course, we need to ask them about any previous interventions that they might have had Janet returns. All of her tests are normal. She starts diltiazem 240 mg once a day modified release alongside her apixaban. And you say that you will see her at any point in time. Mark hasn't been getting on so well. After two years, he's had a number of admissions to the hospital for heart for diuretics. He's been getting breathlessness at rest, and he's had a number of arrhythmias. He had another episode of atrial flutter, and then he had some fibrillation. So to treat his flutter, he underwent another DC cardioversion, which again was successful. And then he had an atrial flutter ablation because it came back that then was successful and flutter. Ablation, as you can imagine, is a lot easier than fibrillation ablation with flutter ablation. If it is typical, flutter were only ablating that is, muscle tissue around the tricuspid valve. He needed to have a flutter ablation. Then he went on to have a fibrillation ablation. But that wasn't particularly successful, so it was decided to then do an HIV node ablation. And the point of doing the Navy node ablation is to stop all of the different signals that are coming down from the atrial going through into the ventricle, and that stops the rapid ventricular response rate. But what it does is it makes the patient profoundly bradycardic, and in a situation where your patient has a bundle branch block, they will adopt a ventricular response rate that is probably going to be around 30 to 40. Um, so it's essential that once you put in an IV node ablation, uh, that your patient either has a backup pacemaker or you insert a pacemaker to control the ventricular response rate. He, however, of course, has had a CRT device put in because it was felt that he should have a CRT device for management of his heart failure. So every node ablation was done after the ablation, which was done after a flat ablation, uh, which was done after two loss of DC cardioversion. After that, Martin decided he had had enough, and he felt that he now should be redeemed as having a permanent A F. But he wasn't giving up on treatment for is a F. He felt that he needed to discuss with his consult and the need for a left atrial appendage closure device. And this obligates the need for long term anti graduation but should really only be used in patients who have high risk of bleeding. Janet tried a number of medications. She even went private and she went to get an implantable loop recorder implanted. Um, because she just felt that she should have one. She opted not to try flecainide or propafenone, which were offered to her because she didn't like the thought of the risks involved that they might actually need. Um, there would there would be a need for her to go into a CCU and monitor and have additional blood test. She didn't want to have a chemical cardioversion. Um, because of the risk profile is presented the potential for liver and thyroid toxicities, Um, and the need for an inpatient stay. And she didn't want to have a general anesthetic either, because a general anesthetic is essentially in doing a DC cardioversion. Um, so that left her only with the option for an ablation, which can be done under local anesthetic. So this was done by pulmonary vein isolation, and she was discharged, and she remains symptom free and in Sinus rhythm. So at six months, she opted to have her anti coagulation stopped. Um, thank you all for your time. Thank you all for attending. Um, if any of you want to do any further reading on atrial fibrillation, um, I suggest that you you check the guidelines published by the resuscitation UK Advanced Life Support. Um, there's also several, uh, bits of information that can be, um, got from either the American Heart Association guidelines. European Cardiology Society guidelines. British Heart Society. Of course, nice is also published guidelines, and there's plenty of information available in the B n f thank you all very much and enjoy your evening. Hi. Um, so much about that, um, to change. It was really educational at all. Um, if anyone has any questions rhetorical, pop them into the chart. I know they're over time while we are also open answering a few questions with anything at all. Um, it's a few more minutes to see if anyone has been questioned. Well, often keeps coming in, so that's wonderful this year. So, um, so the part, the presentation itself and kind of content will be available, Um, here on the platform. So it could. It's not going to be available tomorrow or Sunday. Um, depending on when that is assaulted by the other members of the same. Um, over the next few weeks, you'll have teaching by some consulting about various topics and what we also offer