The Bread and Butter of Cardiology: Common Cardiac Presentation
Serena
Welcome everyone to tonight's webinar. The bread and butter of cardiology, Common cardiac presentation. We are joined tonight by Presenters Dr Mahnoor Mian, Dr Kenneth Cho and Dr Vani Arjunamani. My name is Serena and I am your RACGP representative for this evening. Before we get started, I would like to make an acknowledgement of Country. We recognise the traditional custodians of the land and sea on which we live and work, and we pay our respects to elders past, present and emerging. I would also like to acknowledge any Aboriginal and Torres Strait Islander colleagues that have joined us online this evening. I would like to formally introduce you to our presenters for this evening. Dr Mahnoor is a Consultant Cardiologist with an interest in cardiac imaging. After completing her Bachelor of Medicine and University of Newcastle in 2016, she underwent basic physician and advanced training in cardiology at Liverpool Hospital. She obtained her FRACP and level A CTCA Specialist recognition in 2024 and is currently undertaking a high research degree in cardiac MRI and left ventricular non-compaction cardiomyopathy. Dr Kenneth is a Consultant Cardiologist with an interest in heart rhythm. After completing his Bachelor of Medicine at Western Sydney University, he completed a basic physician training followed by cardiology training at Saint Vincent and Liverpool hospitals. After obtaining FRACP in 2024, Kenneth is spending the next few years undertaking a high research degree in improved outcomes for patients with heart rhythm disorders. We are also joined by Vani who is our facilitator for this webinar. Dr Vani is a full time clinician for over a decade. She enjoys evidence based clinical disease management and preventative healthcare in high risk populations. As a RACGP supervisor, she emphasised the systematic approach to multi morbidity to her registrars. She champions general practice to medical students from the University of Sydney. Her passion is to encourage the chronic disease management as central to women's health. Welcome to all our speakers. I will now hand it over to Vani who will go over the learning objectives. Thank you.
Dr Vani Arjunamani
Thank you Serena. It is lovely to have you all here, and we are joined with Dr Ken Cho and Dr Mahnoor Mian. Today we are going to identify how to investigate key presentations of likely cardiac chest pain and their degree of urgency. We will also discuss how to conduct a thorough assessment and manage dyspnoea in the cardiac patient, including cardiac failure and pulmonary hypertension. We will also be discussing ECG interpretation and avoiding common errors. Therefore, we can integrate the knowledge of cardiac anatomy and physiology to the ECG interpretation. First I would like to pass on to Dr Mahnoor Mian for her presentation.
Dr Mahnoor Mian
Good evening everyone. We will get right into it. I will predominantly be talking about chest pain, and shortness of breath and what the red flags are, what to watch out for and how you would go about investigating patients. Now, chest pain is probably one of the most common presentations to general practices as well as emergency departments in Australia and what the European Society of Cardiology Guidelines Task Force defines it as, and a chest pain that is concerning or that should trigger an investigation is that that lasts for more than 15 minutes or recurs within an hour, and that is associated with other high risk symptoms, including sweating if it radiates to your shoulder or arm or complaints of indigestion. There are lots of guidelines out there. The main ones that we will be focusing on tonight are the American Heart Association guidelines, the European Society of Cardiology guidelines, as well as the Australian Heart Health Foundation and SCMR guidelines. The main take home messages are that most of the time chest pain could mean something else, and there are lots of differentials for chest pain as well. In an acute hospital setting, you would rely on high sensitivity Troponins. However, in a general practice, when you do not have those available, you would think about other clinical decision pathways that will go through, and it is also to be mindful that you want to identify patients that would benefit from further testing, those that are probably low risk and have a lower predictive value of testing, as well as being mindful of patients who do have existing coronary artery disease or women who tend to present with a lot more atypical symptoms. Now, depending on the nature of chest pain, increases or decreases your positive predictive value of the investigations that you will be performing or referring for. Typical what we call cardiac chest pain, and now another point is that we are moving away from calling pain typical or atypical, and we want to describe it as either cardiac, non-cardiac or likely cardiac. Cardiac chest pain would be central pressure. It is squeezing. It is heavy, and the key factor is it is associated with stress or exertion. Others can complain of a dull ache. Things that would make it less likely that the pain that patients are experiencing is due to cardiac ischaemia, if it is right sided, if it is sharp, if it is associated with movement, pleuritic in nature. Now, the various differential diagnoses of chest pain. Cardiac causes would be an acute myocardial infarction or angina. That being stable angina is chest tightness that is only on exertion whereas unstable angina would be chest tightness that you are getting on rest. Severe aortic stenosis and tachyarrhythmias as well. Other nonischaemic causes of chest pain include aortic dissections, pulmonary embolisms, myocarditis, pericarditis, or gastrointestinal causes and then non-cardiac causes are musculoskeletal, pneumonia, pleuritis, pneumothorax. This graph is from the Cardiac Society of Australia and New Zealand and the Heart Foundation back in 2016, and it just goes to show that the majority of presentations for the younger patients, usually low risk would be those less than 44. Nonspecific chest pain, as you can see as you get older, coronary atherosclerosis which is there in the orange it starts the likelihood of pain as a result of that starts to rise, but majority do remain to be non-specific in nature. Now another thing to be mindful of is sex differences in symptom presentation. Now, this was a systematic review and meta analysis of 27 studies that included greater than a million patients, and it showed that sex differences exist in symptom presentation in patients with confirmed ACS. While at the same time, there is that same overlap of symptoms such as central chest tightness, diaphoresis, left arm or shoulder pain, but you do see that women are a lot more likely to present with non-cardiac sounding chest pain so they have higher odds of presenting with pain between the shoulder blades, nausea or vomiting and breathlessness compared to men, and they also have lower odds of presenting with chest pain and diaphoresis compared to their male counterparts. Now when assessing a patient with chest pain, your money is always in the history, and then followed by that your next point of care test would be an ECG. In the acute setting obviously today, we are going to focus on stable patients, so not acute coronary syndromes. Now, not all patients would need further testing. This is from the American guidelines, the patients that are asymptomatic, so patients that do not complain of chest tightness, that do not complain of breathlessness regardless of whether or not they might have family history, they do not require any further testing. Those that are low risk, those that are less than 44, those that do not have any cardiovascular risk factors such as hyperlipidaemia, hypertension, diabetes, these will be your younger patients that complain of more pain on movement. Even in those, it is appropriate to not refer them for further testing. The ones that you really do want to investigate are your intermediate and high risk, and we will go through what scores that you can use that can aid. Now that is also backed up in our Australian guidelines where for those who are low risk, no further objective testing for coronary artery disease in particular is recommended. There are various scores that are developed alongside chest pain protocols, and it is to add structure in the process of evaluating patients, and they are generally used to guide disposition, and it just helps reduce unnecessary testing and reduces admissions to hospitals while maintaining high sensitivity for detection of acute myocardial injury in 30-day at max. Now there are multiple different scores out there if you were to look any up, but the ones that I have most commonly seen used in practice is the heart pathway. Now the HEART score was developed by a Dutch group, and what it does is, it calculates ten-year risk of fatal and non-fatal cardiovascular disease events for your patients. The heart score represents the patient's risk of developing a major adverse cardiac event, and that is defined as either a myocardial infarction or need for percutaneous coronary intervention or bypass grafting within six weeks of presentation. A score of less than three is your low risk patients, four to six is your intermediate and then greater than seven are your high risk patients. Now, obviously, a troponin in a primary care setting, it is actually not recommended. This would be more used in an emergency department, but it just helps you categorise your patients. Now, we would like to define those who do have existing coronary disease as either stable or unstable, and your stable patients are those that are either completely asymptomatic or they have symptoms on exertion only and can be managed with medical therapy, and your unstable patients are those who actively having an ACS who have symptoms at rest, who have symptoms that are not responsive to maximal medical therapy or if they have got left ventricular dysfunction or aortic stenosis as well. Now, the majority of our clinical practice these days is based on this landmark trial which was called the ischaemia trial, and it really changed the approach to stable coronary artery disease. So again, stable those who do not have symptoms or have symptoms on exertion only, and what it does is, it randomised about 5000 patients to optimal medical therapy or optimal medical therapy and revascularisation of their coronary artery disease, and what it found is that there was no significant difference at all between these two patient groups in terms of overall death with myocardial infarctions, and what it really showed was it stressed the importance of adherence to medical therapy and risk factor control, irrespective of whether or not patients end up undergoing revascularisation for their coronary artery disease. Now, the various options that we have of investigating patients who do not have non-existing coronary artery disease and different cardiologists will differ with their approach of what first line investigations they would like to use, but you have got the option between a CT coronary angiogram or some form of stress testing. Now, the most common form of stress testing is stress echocardiography. It is quite uncommon to perform stress testing, treadmill stress testing, ECG testing only, as the sensitivity and specificity is not quite as great as your other testing. There are pros and cons of either investigation option that you have. With CTCA, you do get anatomy. I do find that a lot of patients finding a lot more reassuring knowing exactly how much calcium they have, whether they have any calcium, and you can also look for other things like pericardial effusions if you have got large pulmonary embolism, you will see that on your CT coronary angiogram as well as your rare and malignant anomalous coronary arteries as well. With your stress testing, most commonly a stress echocardiogram, you get left ventricular function, right ventricular function as well. You can investigate for any valvular abnormalities whilst you are doing the echocardiogram part of the stress test, AND it also, going back to the ischaemia trial, even if patients do have underlying coronary artery disease that you might see on a CT coronary angiogram, if their stress testing is negative, you can manage them medically. The warranty period for your CT coronary angiogram is usually about two years that you can give your patients, and with a stress test, it will be one year given that it was an adequate good stress test. Now, depending on what a cardiologist investigation would be, some of the trials that did go and compare CT testing to functional testing. This was the promise trial, and the primary hypothesis was that clinical outcomes in patients assigned to anatomical testing would be superior to functional testing. This included about 10,000 patients, and it really showed that there is not much difference between both of them at all. Further trials that have been done are SCOT-HEART and PROMISE, and basically they had a similar approach of randomising patients into either CT coronary angiogram as first protocol or some form of stress testing. This randomised about 2000 patients. Again, it showed that there was not really much of a difference between two groups in terms of outcomes, but it did show that you did have a lot more patients being over investigated, and if you look at that highlighted part there, you did see that patients that with the Precision strategy that group of patients that did have quite high risk factors who did have quite cardiac sounding chest pain, when they did undergo cardiac catheterisation, their chance of having obstructive coronary artery disease requiring intervention was a lot higher than those who underwent testing in the absence of significant risk factors. Now, what are the clinical implications of all this, basically take home message messages are, if you have got low risk patients with a low pre-test probability of coronary artery disease, they most likely do not require further testing. In patients who have stable known coronary artery disease, CT may potentially be superior to assessing for risk prediction within the narrow range of a screening of ischaemia severity in the Ischaemia trial. Severity may not identify patients with stable ischaemic heart disease who may benefit from invasive management, and stress testing may be necessary to determine whether ischaemia is the likely cause of symptoms. In particular, a patient who does have known coronary artery disease. Now, another condition that we are learning a lot more about is angina with nonobstructive coronary arteries, and now this is becoming increasingly recognised, and it actually might affect quite a lot of patients who do undergo invasive coronary angiography for suspected ischaemic heart disease. Now these are essentially the patients who have got very typical sounding pain, but when they do end up going either coronary angiography or CT, they have got no obstructive coronary artery disease, and the working diagnosis of ANOCA is that you have got coronary microvascular dysfunction, and it also encompasses a range of a range of diagnoses, that includes microvascular spasm, endothelial dysfunction, epicardial coronary spasm as well as myocardial bridging, which would all result in the cardiac sounding pain that patients may experience, and you do see that a lot of these patients often face a high burden of symptoms and might have repeated presentations for two cardiologists, and the diagnosis of ANOCA is quite challenging, and not all hospitals routinely test for this, and the way you would test for it is doing Acetylcholine coronary reactivity testing during coronary angiogram, and that is why, a lot of patients go underdiagnosed as well, and there are various management options, but if you look at the treatment options for ANOCA, your first line is always going to be statin exercise, weight loss. I do find that patients tend to be quite scared of statins, but I highly encourage statin therapy, and then your second line is going to be your nitrate therapies as well as beta blockers, which would be first line for myocardial bridging. Now moving on to breathlessness. In regards to investigating breathlessness, your top differentials are either going to be cardiac or respiratory, and this is what the 2021 European Society of Cardiology guidelines actually recommend on how to investigate patients with suspected cardiac failure as a cause of their breathlessness, and now the first line recommendation is actually a BNP as well as a 12 lead ECG, a transthoracic echo, a chest x-ray and other blood testing for other conditions such as anaemia that may cause breathlessness, but you do not actually see a BNP being ordered first line, and that is because it is not Medicare debatable yet, and most of the time, when patients do present in the outpatient setting, they have had a full blood count. They may or may not have had a chest x-ray, and then when we see them, we perform a transthoracic echocardiogram or a stress echocardiogram, depending on what their history is. If they do present in a hospital setting, they will get a BNP most of the time, but depending on the patient and whether or not they are happy to pay for a BNP that is usually performed to support your diagnosis rather than help you come to the conclusion, and then usually if all your blood testing is inconclusive and you think that potentially cardiac ischaemia could be a cause of their breathlessness, you can pursue a CT coronary angiogram. Now what your BNP actually is, is the natural peptides are a class of structural proteins that have natural and diuretic effects, and they are released upon cardiac stretch. They inhibit the effects of the renin-angiotensin-aldosterone system and the sympathetic system that leads to vasodilation and induces diuresis, and it is actually NT-proBNP is one of the best indicators of the occurrence of cardiac failure and is considered an important prognostic factor related to mortality, and it is actually a lot more accurate than predicting mortality than your New York Heart Association clause. Now, there are lots of causes for an elevated BNP and your cardiac causes are going to be cardiac failure, coronary syndrome, right heart strain as well, which could be result of pulmonary hypertension, valvular heart diseases, atrial fibrillation, myocarditis, hypertrophic or restrictive or infiltrative cardiomyopathies, arrhythmias cardioversions and shocks, and then you have got non-cardiac causes as well. Now this was post-hoc analysis of the GUIDE-IT trial, which was a randomised trial and basically what it showed that serial ProBNP levels in chronic stable patients and heart failure served as a much better prognostic marker for cardiovascular death and hospitalisation, and that a change in your BNP level preceded any cardiac symptoms or hospitalisation by about 200 days on average, and the take home message is that change in BNP levels should warrant consideration of change in heart failure therapy, even in the absence of symptoms. Now what is a normal BNP? So currently we do not actually have any age or sex specific thresholds, and your BNP is very sensitive but not specific, now greater than 400 is definitely indicative of cardiac failure, but most of the time greater than 140 would be your normal assay depending on your lab and if it is greater than 140, you should consider investigating patients for cardiac failure taking into consideration other comorbidities as well. Now in terms of testing for pro-BNP in the outpatient setting, we have got new MBS item numbers which will make it a lot more helpful in diagnosing patients with cardiac failure as well as those who actually do warrant further investigation for cardiac disease who do present with breathlessness. At the moment, and you can order a BNP four times in any 12-month period to assess patients diagnosed with pulmonary arterial hypertension or to monitor disease progression, and then in patients with systemic sclerosis to assess the risk of pulmonary hypertension, you can order one to two times in any 12 month period, but from November of this year it can be useful have an item number for the diagnosis of heart failure outside the hospital. This will be perfect for patients that do present with breathlessness who do have a history of COPD, not your typical presentation for cardiac failure, but doing a quick BNP. If that is negative, then you can proceed investigating for other causes. When is your BNP the most helpful? It is got a high sensitivity and a negative predictive value, and it helps you avoid unnecessary echoes. It is usually in those patients I find most helpful if they have got normal ejection fraction, normal coronary arteries, and you want to evaluate is this heart failure with preserved ejection fraction? and what should you do if someone's levels are going up? It would be sending them back to their cardiologist to optimise their medical therapy or investigating for causes that might be contributing to the BNP rising, and it is also a guide for poor prognosis in patients who despite optimal medical therapy, have got rising levels in their BNP. Now, we do know that atrial fibrillation does cause your BNP levels to rise as well, and these Kaplan-Meier curves are of composite outcomes at two and a half years against baseline BNP levels, and you do see that there is an incremental risk associated with higher BNP levels, regardless of whether or not you have got atrial fibrillation and heart failure in across all four phenotypes. Now, what would an efficient diagnostic approach look like and this would be a lot more effective come November 1st when you can order a BNP in the outpatient setting without the patient having to pay for it, and that is, you have a patient presents with breathlessness along with your physical exam, your ECG, if you have access to one and a chest x-ray, you order a BNP as your first line investigation and if it is less than 100, it is not you can rule out cardiac failure, and consider alternative diagnoses. If it is between 100 to 400, now that is your kind of borderline area and you can have a suspicion of heart failure, but if it is greater than 400, very likely that the patient has heart failure, whether that is heart failure with reduced ejection fraction, preserved ejection fraction or pulmonary hypertension, which would be causing right heart strain. Now, these are the links to all the guidelines that were featured in the presentation, and I will hand over to Kenneth.
Dr Kenneth Cho
I think I have finished answering all the questions in the chat, but Mahnoor if you can take over the chat and I will share my presentation. Hello everyone. I thought could we have a short 20 to 25 minutes to go through ECGs. We would try to do something that was interactive. Use the Q&A function in the chat and either up-vote someone's answers or come up with your answers yourselves and we will just go through a few cases and illustrate a few things that might be useful to know as a GP or as a doctor anyway. This is the first case. These are all cases that have come through our service in the last year. This is the first one, a 78-year-old male for review following a syncope episode at home yesterday, and now he feels completely well, he rocks up and this is his ECG. What do people think if you can pop that in the Q&A chat? Somebody noted that there is a right bundle branch block. That is good. Lots of people noticed the right bundle branch block, and what that is that, if you can look at V1, the right bundle branch block, which is this. It is an RSR pattern in V1, and someone's mentioned at the PR interval that there is a P-wave. This is a P-wave and there is a long PR. What is that code in the chat. Good. Someone has mentioned atrial fibrillation when there are no P-waves, but in this case we can see a P-wave that is prolonged, that is called first degree AV block, and usually last thing is that yes, someone mentioned in lead three that there is a negative deflection in the QRS and T wave inversion that is associated with that, and so usually lead three is also positive, but when it is negative and lead one is positive and leads two negative, it is called left axis deviation, which is what the anonymous attendee has said. The combination of right bundle branch block and left axis deviation is bifascicular block, and when there is first degree AV block as well, some people call that trifascicular block, but does that matter for this patient who has had syncope. Whilst we are here because I felt that we would input some anatomy if this is the chest wall and this is the sternum, V1 is always on the right side of the sternum. V2 is always on the left side of the sternum, and as you go to your arm here, V6 is around here, and how are your hearts orientated? Is that your right ventricle? Is the anterior ventricle and the left ventricle that hits behind the right ventricle. So what happens in right bundle branch block is that the electrical impulse cannot go through that right bundle there and instead goes all the way around the heart, which is why you have this broad QRS and V1 and why V1 is positive because the electricity is going towards V1. That is just what we went through. This is called trifascicular block, and yes, you should consider a pacemaker, and the reason for that is that if you have right bundle branch block, left axis deviation, it means that the electrical wiring of the heart is degenerated, and so if you have symptoms then it suggests that it is degenerated enough that your heart rate goes too slow, decreases cardiac output and people faint, and this is illustrated in the ESC Guidelines that if you have bifascicular block unexplained syncope, you can have a pacemaker empirically even without further testing. Any questions about that case? No. We will move on. This is the second case. It is a 35-year-old gentleman, quite young and goes to the gym but has progressive dyspnoea and one syncopal episode. People want to write in the chat what they think of this ECG. Just like with every ECG, important to look at the rate, the rhythm, so look for P-waves and then look at abnormalities in any P-waves QRS, ST segments and The-waves. Someone wrote STEMI. Someone wrote Wolff-Parkinson-white, someone wrote Brugada, someone wrote mitral stenosis. I might just expand on some of these differentials, which are actually very, very good, and I think they are coming up with a common theme that people are looking at these anterior leads and they see that there is ST elevation or ST upsloping and then deep The-wave inversion, and they are concerned about that because obviously T-wave inversion one of the differentials is ischaemia. Someone also noted that the P-wave in lead two, instead of looking like a normal one shape is two shapes. The sinus node is in the right atrium, so this is the right atrium contracting. This is the left atrium contracting. Someone thought maybe mitral stenosis is putting pressure on the left atrium. Someone wrote HCM, which is actually the answer here, and we will talk about why and why this might be important, but because of these big QRS, I think that is why people are thinking maybe Wolff-Parkinson-White but it is actually HCM. There is big QRS patterns which make you think maybe there is hypertrophy of the chamber and this T-wave inversion that goes in the precordial leads, which is another name for V1 to V6. This The-wave inversion is classic for apical HCM. This is a condition that is quite important because you might think that this patient is quite young. His risk of coronary disease might be quite low, but actually apical HCM is a very important diagnosis to make especially if people have syncope. How does syncope happen in apical HCM? Well, what happens is that if you have your heart here, and you have your right atrium, left atrium, right ventricle and left ventricle in HCM, what happens is that part of the heart is very, very thick, which is why these QRS get very, very big because there is more muscle and so more electricity is generated, and people tend to faint because of one of two reasons. The first is that the thickness can stop blood from going out into the aorta, causing people to have syncope. That is called dynamic outflow obstruction. The other thing is that because the heart is so thick, it starts to scar, and whenever heart muscle scars, you can get ventricular arrhythmias happening and spinning around inside there which is obviously ventricular tachycardia. There are risk scores for patients with apical or any kind of hypertrophic cardiomyopathy, if they are high risk of developing VT, obviously VT is life threatening, people get a defibrillator to stop them from sudden cardiac death, so it is an example of apical HCM, and I think one takeaway from this session is that his symptoms and history are always key, and then you have got a mirror the findings of the ECG to your patients because not all T-wave inversion is ischaemia. On the topic of T-wave inversion, here is another one that is come through this year with some T-wave inversion. Where is it and is there anything else that you see that is a little bit unusual or suspicious? This is a 45-year-old lady with increasing breathlessness, no chest pain and some peripheral oedema. Someone has mentioned the T-wave inversion in the precordial leads, which is the there. It is good. To kind of think about some differentials about why this lady might be breathlessness. Someone has very astutely written pulmonary hypertension. I might just point out a few things. We talked about how if this is a cross section of the of the chest and this is the sternum here, and I am colouring in that V1 obviously is always on the right side of the sternum. V2 is on the left side of the sternum, and as you go towards your arm you have V3 V4 V5 V6. In pulmonary hypertension, which chamber of the heart pumps against the lungs, the right. That is right. In pulmonary hypertension, if this is the right heart, the right heart gets very thick because it is pumping blood against the large pressures of the lungs, and therefore more of the electricity goes towards V1 rather than V6, which is why V1 is positive here. Usually in most patients V1 is negative, but in patients with pulmonary hypertension, the V1 becomes positive because the right ventricle becomes hypertrophied. That was exactly what the echocardiogram showed. This patient had right ventricular hypertrophy right atrial hypertrophy, and this is another differential of T-wave inversion. This might be the last case of this particular finding, and before we move to other cases, this is a 72-year-old man and he presented with chest pain for several hours. Again go through, think about the the rate, the rhythm, the presence of P waves and QRS. We see people have mentioned ischaemia as a common theme. Some patients say some people say STEMI. Some people say Wellens, which is a form of acute coronary syndrome with subtotal occlusion and someone has written a PVC. I will just highlight the PVC. This is the PVC here. You can see that the QRS is broader. It is different morphology. The associated T-wave is different, which makes you think a PVC, which is correct. We spoke about how there is differentials for T-wave inversion. There is ischaemia, there is pulmonary hypertension with right ventricular hypertrophy, there is apical HCM and this one is ischaemia, and the reason that you think of ischaemia is obviously the clinical history is key. Like we talked about, if there is cardiac chest pain and ECG changes the first thing you think about is ischaemia. Someone has written STEMI, which is very close, but not completely accurate. With a STEMI you need more ST elevation, I mean contiguous leads with risk for depression, which you do not have, but this is Wellens's, which is a subtotal proximal LAD subtotal occlusion. If it was completely occluded, you get the STEMI pattern, but in a subtotally occluded, so almost occluded artery, you get this Wellens pattern, which is a good pattern to recognise. This patient of course should go straight to the emergency department, have aspirin loaded and should be going via ambulance rather themselves. I will just point out that someone wrote AV disassociation and that is probably because they have noticed these something to remember, a common pitfall that people can find themselves in is that they think a T-wave is a P-wave. You have to remember that every QRS is going to be associated with a T-wave, and you have to look up and down the lead so you can see that this T-wave is actually that blip there, so that is actually a T-wave there not a P-wave. Once again this is Wellens syndrome. It is a classic finding that it is important that we are all familiar with because these patients have to go straight to the emergency department via an ambulance loaded with aspirin. Ideally have some GTN. The next case, 77-year-old lady with some gastro symptoms, and some confusion, so people have put in a provisional diagnosis of hyperkalaemia. Could you explain why do you think hyperkalaemia. Very good. Tall T-waves, and then how should this patient be managed in the community and in the hospital? What is the risk with ECG changes with hyperkalaemia? Very good. Someone has written VT. So you can get ventricular arrhythmia. VF polymorphic VT. Very good. So that is good. This patient had a serum potassium of 7.0, should be in hospital and not only in hospital but in a monitored bed until the potassium improves and the ECG normalises because obviously, if the potassium is so high that it is affecting ventricular repolarization then then patients could be at risk of ventricular arrhythmia that can lead to cardiac death. That is very good. Someone mentioned calcium IV is good for stabilising the cardiac membrane, and all the other stuff for hyperkalaemia, absolutely critical. Very good. This might be the last case. So, 75-year-old gentleman tired and lethargic for a few days, some nausea, vomiting and abdominal pain. What do people think of the ECG? Someone has written complete heart block. You can go into third degree heart block, someone else has written very good differentials to have. For complete heart block to be a diagnosis, you would need to have P-waves. If there is no P-waves then you cannot really say that the atrium and the ventricles are disassociating because obviously with complete heart block, you have your atria pumping once and then twice then three times and there is no communication with the AV node, but for the differential of complete heart block, you need to see P-waves. Be interesting to see where people think they find P-waves, but I suspect that again, it is these that people think are P-waves, but these are not P-waves. What are they? Remember with EKGs, you do not just look across the other principal with EKGs, you do not just look across, you look up and down. What are these things here that we are highlighting? So these are T-waves. And we can see that every QRS has a T-wave and every QRS has to have a T-wave. You cannot have a QRS without T-wave. So if there are no P-waves, what rhythm could it be? And people have written now on the chat that it is atrial fibrillation, and that is correct. When there are no P-waves at all, and there is often a defibrillator equality that is atrial fibrillation, And then the question is what rhythm it is and it is slow AF. Is there a reason why a patient who feels tired with nausea, vomiting might develop slow atrial fibrillation? Digoxin toxicity. Exactly. yeah and that is that is a good point. If you have it is renally cleared, so if you have AKI then also atenolol, you can get slow AF. I guess the last point for this is something like complete heart block where you have your atria firing, complete AV disassociation and then your ventricles firing. Your ventricles are going to have a slow escape, but it is going to be regular. Whereas this is obviously irregularly irregular, which points you towards slow AF. That is all the ECGs we have had, but I suppose there are a few principles. The first principle that we covered is that if your QRS has a T-wave, so do not be fooled about there being extra P-waves because you have to have a T-wave with every QRS. The second principle we spoke about is do not just look left and right, look up and down, and the third principle is always correlated back to your patient because even if you might have similar ECG findings for example T-wave inversion, not every T-wave inversion is ischaemia, and it is important to keep an open mind and bring it back to the patient. So welcome any questions?
Dr Vani Arjunamani
Thank you so much both the speakers. You were very efficient. You have answered all the questions in the chat, but since we have got the people were mentioning sick sinus syndrome, Ken if I could ask you, how would you differentiate that?
Dr Kenneth Cho
I guess the first thing is sick sinus syndrome means that your sinus node, so maybe in your heart, you have a sinus node which is there, and sick sinus syndrome is when your sinus node is lazy, it is underactive, so in that situation what you have is P-wave, QRS, T-wave, long pause and then P-wave QRS T-wave. In this case, you can see that there is a QRS and a T-wave, but there is no P-wave, so it cannot be sick sinus syndrome. The important thing about the sinus node is that it is very vaguely, it is very mediated by sympathetic and parasympathetic activity. If people are active, obviously you get sinus tachycardia, which is very physiological, but if you snore, you have lots of sleep apnoea, you are on lots of drugs, then slow sinus rates can be physiological, so not necessarily a reason for pacing unless you have symptoms despite looking at reversible causes.
Dr Vani Arjunamani
There is another question here when to investigate RIGHT bundle branch block with bifascicular with no exercise symptoms.
Dr Kenneth Cho
The key with abnormal ECG findings is two-fold. The first is to really make sure that the patient is asymptomatic because you often have like 70 or 80 year old people who say they are asymptomatic, but they are not and they are just tolerating the symptoms, very common in the heart failure population, and the other thing is that it is important to look for underlying causes. Something like a bifascicular block or a left bundle, it can be benign but often it is associated with cardiomyopathy, so getting an echocardiogram is really reasonable. Some people have right bundle branch block important to compare to previous ECGs, but if they have had an echo before and they have had ongoing right bundle branch block easy to say that that is their physiological rhythm.
Dr Vani Arjunamani
Thank you. Thank you for that, Ken. Before I go into the question in the chat, I wanted to ask Dr Mian about given that you mentioned chest pain risk stratification in those studies, I mean, does it look at diabetics because they present so atypically? How would we manage that there?
Dr Mahnoor Mian
I think with diabetics, those would be the patients that you would classify as your intermediate high risk. So your low risk patients are really those who have got no cardiovascular risk factors, who are under the age of 40 and who have relatively non-cardiac chest pain. Diabetes would probably be one of the highest cardiovascular risk factors, so those would actually be the patients where if they were complaining of indigestion that happened on exertion that did not really sound like reflux or if they were getting breathless or if they were getting, their exercise tolerance was decreasing, and questions that you should be asking them is, if you climbed a flight of stairs, does that make you tired? And if their answer is yes and it is not related to any musculoskeletal conditions, then those would be patients that you would want to investigate.
Dr Vani Arjunamani
Great. Thanks. I am just going to come to the very last question by John Alex Tynan. It is coming to that same point. How do you investigate high risk but asymptomatic patient for ischaemic heart disease? I work with high risk populations, so subcontinental origin, Middle Eastern, they are in their 40s. They have had family history of premature cardiac death. Is it stress echo exercise, stress test or CTCA or what would both of you recommend?
Dr Mahnoor Mian
My approach for these patients and really the take home that we get for all our trials is aggressive risk factor modification. It would be if they are completely asymptomatic ensuring that their cholesterol is under control, educating them about statins and encouraging statin therapy. They do have a family history of premature cardiac death, screening them for familial hyperlipidaemia, and that will be through utilising your Dutch lipid scores, managing their high blood pressure and screening them for glucose intolerance. I can understand the anxiety and a lot of these patients that do come in and do want investigations, my investigation of choice usually for these patients would be if they have got hyperlipidaemia, I opt for a CT coronary angiogram and get a calcium score, and if they do not, then potentially a stress echo, but really, we do know that if they are completely asymptomatic, you can continue medical management and not investigate them.
Dr Kenneth Cho
I feel similarly with Mahnoor and it is actually a very like controversially hot topic perhaps, but I guess the underlying question is do stents save lives in patients who do not have any symptoms at all? and the most recent trials suggest, maybe stents do not actually save lives. Stents are very good for myocardial infarction and acute coronary syndrome, but for chronic stable angina, medical therapy is just as good, so that is why there is a paradigm you do these tests to help your medical therapy, but if they are completely asymptomatic, the tests are there to help medical therapy, not to put in stents unless it is a left main, for example which you might not get unless you do the test, and so there is a role for testing, but unlikely.
Dr Vani Arjunamani
This is a question I guess it can apply to both of you, role of aspirin versus any other antiplatelet in mortality benefits.
Dr Kenneth Cho
I might try first Mahnoor if you are happy. Even like the calcium score, which is good to delineate intermediate risk to low risk or high risk, if you have a very high calcium score, for example, for above 100 or above 400, there is a role in aspirin for preventing events, and I guess the other question about other anti-platelets it really depends on whether it is post-stent or pre-stent. Post-stent, there has been a movement towards not using aspirin and using a different antiplatelet, but for the sake of primary prevention, you can use aspirin if people have, for example, a high calcium score.
Dr Mahnoor Mian
I would agree with Ken on that. It really depends on the patient you have got in front of you and also taking into mind any bleeding risk factors that they may have and balancing the risk with that.
Dr Vani Arjunamani
In that high risk patient, aspirin is a definite yes because that is mostly what we will be seeing, so asymptomatic high risk, start them on aspirin?
Dr Mahnoor Mian
I think it really differs between cardiologists in different practices, and I think it is always the patient in front of you really.
Dr Vani Arjunamani
Okay great. So I will go back to the original question there for Holter monitors. We see this all the time. However, a burden of premature ventricular complexes, what does this mean, and does it require a cardiology review? So this is for a 43-year-old with a long history of anxiety. Both of you, I guess.
Dr Mahnoor Mian
I will tell you my approach to PVCs, but really, it depends on your PVC and depends on your ECG. The most useful thing to get in someone who does have a PVC is a 12-lead ECG and see where that PVC might be coming from, which is probably what our job would be, but the majority of PVCs, if someone who does not have a previous cardiac history of ischaemic heart disease and someone who does not have high risk symptoms such as syncope or a family history of cardiac death, most likely they are going to be benign.
Dr Kenneth Cho
Yeah. So I feel similarly. It depends where the PVC is and whether they have symptoms or not and whether what the consequences of the PVC is. If they are very symptomatic, there are different ways to get rid of PVCs. People use medications but you can find where the PVC is coming from and burn it. That is called ablation and that is often very good. If the patient is completely asymptomatic, when patient patients have high burden of PVCs, it is written like that, often it can mean that they have thousands and thousands or more than 10% burden, which can impact how the heart pumps and you can get something called a PVC cardiomyopathy where the heart gets weak because of all the irregular PVCs. So, I think if a patient does have high PVCs, I am worth, as Mahnoor said, going to a cardiologist seeing where the PVCs coming from and making sure that the echocardiogram does not have any consequences from that ie PVC mediated cardiomyopathy.
Dr Vani Arjunamani
I do not know if you have one final question is right bundle branch blocks always benign?
Dr Kenneth Cho
That sounds like a loaded question. So nothing can always be benign, but incomplete RBB can often be benign, and what I think we have demonstrated at least in the first ECG with, for example, if you have syncope and you have got some axis deviation, it can be a sign of underlying conduction disease. That is pathological.
Dr Vani Arjunamani
Okay. Great. I think we are 8:30. I will hand it back to you. Serena.
Serena
Thank you. I would like to extend my thanks to Mahnoor, Kenneth and Vani for presenting this evening, and also to everyone who joined us online. We do hope you enjoy the session and you also enjoy the rest of your evening. On another note, a friendly reminder this is a CPD activity, so to receive your CPD hours, you need to complete the survey following this webinar. Once the webinar ends, you will automatically be redirected to complete the survey. We will also be including the link to the survey in the following email that you will receive tomorrow. Whenever you choose to do the survey, you only need to complete it once. That brings us to the end of the session. Thank you and good night everyone.