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A 78 yo patient male presents with palpitations. He has no chest pain or shortness of breath. His heart rate is 138bpm and he was haemodynamically stable. His ECG is shown. Describe and interpret the ECG.  BRIEF ANSWER
The diagnosis is atrial flutter. Do you know how to pick it? Do these patients need anticoagulation? Below is the post treatment ECG. 
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A 48 yo male presents to the emergency department with a complaint of a rapid heart rate. He has been known to be in this before and is usually on Sotalol, but has not taken any for two days. He has also been drinking heavily the night before. He states that at 7.15 that morning he felt his heart start to race suddenly. His ECG is shown below. What is your diagnosis?  This ECG shows an atrial tachycardia with atrial rate of 120bpm. The p waves are inverted in III and aVF, which is abnormal. This is a unifocal atrial tachycardia. It can occur in structurally normal and abnormal hearts. it arises from a particular part of the atrium and its location can be diagnosed by the axis of the p waves. Below is another example:  This is someone at a rate of 120bpm. Notice the inverted p’s in lead III. Again, this is unifocal atrial tachycardia.
Clinical Presentation The usual presentation is one of palpitations, but may be that of syncope, or cardiac failure if the patient has been in the rhythm long enough. Workup An ECG and electrolytes to ensure no abnormalities and a full blood count to exclude anaemia. Very few other investigations are needed in the emergency department. Perhaps a chest xray if lung pathology is suspected. The patient should have an echocardiogram, to look for structural abnormalities, but this can be as an outpatient. Management The unifocal atrial tachycardia can be treated like an SVT. The general treatment for this condition is:
Introduction When we assume that every wide complex tachycardia is Ventricular Tachycardia(VT) our sensitivity for picking up VT is 100%. In the emergency department setting, this is a must! We use electricity on all of these patients because it is safe and effective. We can try adenosine, in case it’s a supra ventricular tachycardia(SVT) but only if it’s a regular rhythm. Our specificity in this scenario lags, however in our favour, is that fact that 80% of WCT is VT. If we wanted to determine if an ECG is showing VT, we have a range of rules at our disposal, including Brugada and Vereckei, that give a respectable specificity, but it’s still in the mid 80%. A new validated rule The VT Score, uses 7 criteria, some of which we already use, to diagnose VT. A specificity of 100% is reached when 4 or more criteria are satisfied(1).  The Seven Criteria are as follows: NOTE: Before we start I would add that the rate should be greater than 120 beats per minute for us to start considering VT. 1. Dominant Initial R wave in V1. This can be notched(the original rabbit’s ear) provided the notch is on the descending limb.  2. Initial r > 40 ms in V1 or V2: assess in predominantly negative QRS complexes. Look for a ‘fat’ initial r in rS in V1. It can also include variations such as: RS with high ‘r’ amplitude, rS with notched r  3 Notched S in V1. The notch can be at the beginning, in the middle or near the nadir of the S wave.(This has been known as Josephson’s Sign)  4. Initial R wave in aVR. The QRS in aVR must start with a large R wave. it can be notched. (This comes from the Vereckei(2) criteria).  5. Lead II R wave Peak time(RWPT) > or equal to 50ms. This is the time from the beginning of QRS to first change in direction.  6. Lack of RS in V1-V6.(Brugada Criterion(3)). This is similar to saying that there is concordance.  7. Atrioventricular Dissociation. This is indicated where a fast ventricular activity iOS not related to atrial depolarisation.  Source: LITFL LETS MAKE IT EASIER TO REMEMBER:
A 6 week old baby is brought into the emergency department by her mother with irritability and poor feeding. She is afebrile and her examination reveals bilateral crepitations in the chest and a systolic murmur. What does the ECG show and what is the likely diagnosis?  The ECG is usually quite straightforward to analyse if we remember 2 things:
In any child presenting this way, we need to think of:
Rate: just count the number of complexes and multiply by 6 ( an ECG takes 10 seconds to print). Rate = 23 x 6 = 138, which is acceptable Rhythm: For sinus rhythm, there must be a P wave before each QRS and the P wave must be upright in II and inverted in aVR. If not, then it is not sinus rhythm and the pacemaker is in the low right/left atrium This is sinus rhythm QRS: is it too tall or too small, ie is there hypertrophy? Remember that in the child the is right ventricle is dominant. To judge hypertrophy look at V6. If the R wave intersects the baseline of the V5 tracing above, then there is LVH In terms of Right Ventricular Hypertrophy, in adults it is usually hidden by the left ventricle, however in children the clues are in V1. There is RVH if there is an rsR pattern in V1, or a pure R wave in V1 after 6 months. It is also helpful to look at the R wave to S wave ratio. Remember that the young heart is right heart dominant, so you would expect that the R wave is more predominant than the S wave in the right leads, however if the opposite is true, then there is left ventricular hypertrophy. The QRS is normally +ve in aVF
This shows Left Ventricular Hypertrophy. The heart is left heart dominant rather than right heart dominant, which we would expect in this age group. With the murmur and the crepitations and the left heart dominance, this is most likely VSD(left to right shunt). ST-T: The T wave is upright for the first week of life, then is inverted until adolescence. This is normal. Intervals: PR- In anyone, an interval > 0.2 sec is abnormal
This ECG is of a patient with VSD. Paeds referral is needed for further investigation including an Echo and bloods. Treatment may include:
The Case A 40 yo is brought to the emergency department with the following vitals:
The patient has a known history of IVDU and has been found in a chair, not rousable. She has fluids and inotropes and antibiotics and she has the ECG shown. What are your differential diagnoses for this patient? What is the most likely diagnosis? The computer says acute AMI. Could it be? Let’s look at the ECG  Rate 106
Is it sinus?– P waves are upright in II and inverted in aVR; Yes Is there a P for every QRS? Yes QRS: Is it tall/small?: It’s about right, there is no hypertrophy. Is it wide/narrow? It’s narrow Is it of abnormal morphology ie., delta wave? No Is it clumped?(just incase we miss a Mobitz- but it’s not slow enough) No ST-T Remember the baseline is the T-P line If we look we see that there is some ST elevation in some areas of the ECG of about 1mm, although this is difficult to gauge as the T wave goes straight into the p wave. The most visible abnormality is the inverted T waves. What causes inverted T waves?As this is an adult patient we can overlook the T wave inversion of childhood. Other prominent causes are:
The PR is normal and the QT is very prolonged. PACING Spikes: None. Putting it all together, what would seem the most probable diagnosis?Before we look at the most likely diagnoses. One differential to entertain is an overdose, however there are no signs of classic QRS widening of Na channel blockade, or a terminal R wave in aVR. It might be an AMI, there is no evidence of hypertrophy, the patient is not behaving like they have a PE, but they may have raised intracranial pressure given the decreased conscious state. The decreased conscious state may be simply due to low blood pressure. The patient is also febrile. Why? Remember this patient has a history of IVDU, so infective endocarditis is a consideration. The patient may also have meningitis. The fever may also be secondary to stroke as we know that about 50% of stroke develop a fever, which in itself is a marker of severity and marker of mortality. Let’s narrow it down to 2 causes, AMI and raised intracranial pressure. Raised intracranial pressure ECG’s have deep T wave inversion and a prolonged QT. I’m thinking this is an intracranial event, especially if the fever is due to this. Echo showed a myocardium, not contraction properly, with clean valves, so it may be AMI. However the CT gave the diagnosis with large subarachnoid haemorrhage. This is a neurocardiogenic phenomenon when the heart is affected by deranged autonomic supply coming from a stroke. A fascinating case mixed with electrolyte abnormalities etc. I hope you enjoyed it. A 31 yo female presents to the emergency department with pleuritic chest pain. The patient is 19/40 gestation and no medical conditions. The history of the event is that the patient was sitting on the couch and developed left shoulder and then left chest pleuritic chest pain. There was no history of trauma, or fevers, cough or wheeze and the patient had no history of a DVT. Clinical examination was normal. Basic blood tests were done that showed: CRP 4 D-Dimer 0.71 mg/L Na 134/ K 4.1/ HCO3 19/ Creat 61/ eGFR 90 WCC 10.4/ Neut 6.3/ High sensitivity troponin 3 Vitals were HR 80bpm, BP 122/70 SpO2 100% on RA. What is your working diagnosis so far? An ECG was done as shown below. The resident reported it as normal. What does it show and what is your diagnosis?  ANSWER
This is a normal sinus rhythm ECG, with good R wave progression. The only finding of note is S1Q3T3 Take Part in the Poll What are some of the important ECG changes seen in Pulmonary Embolism?
What did the YEARS Study tell us? In 2017, we were given a new approach to looking at PE and the D-dimer(2) They used a clinical decision rule which consisted of 3 items:
In the non-pregnant patient:
 (2) The Pregnancy Adapted algorithm from 2019(3) is shown below:  WHAT HAPPENED TO THE PATIENT?It was decided that although pleuritic chest pain was all that the patient had, there was nothing else to explain the symptom. The D-dimer was > 500, so the patient was sent for a CTPA. It was negative. The patient was discharged for GP followup. Members, go to the section on PE in the course and on the ECG's of PE to see more. References
This week I have 4 questions for you. 3 are ECGs you must know and the fourth is a simple question on what you should look for in the QRS complex, when reading the ECG. Enjoy. Hope to see you at the Live Cardiac Bootcamp Course on the Gold Coast in January 2022. Congratulations to everyone who has purchased the Online Cardiac Course and thank you for all the great comments. New sections added regularly.. ECG 1A 69 year old woman presents with dyspnoea. Her ECG is shown below. Describe the ECG and interpret the changes by giving your most likely diagnosis.  Perm J. 2011 Fall; 15(4): 75. ANSWER
The diagnosis is most likely a pulmonary embolism. There are 3 main ECG changes seen on this ECG.
ECG 2In my ECG in 20 seconds method, what are the 4 things to look for when looking at the QRS? ANSWER
1. Are they TALL or are they small? When looking at the QRS complex look to see if there is any evidence of hypertrophy. The Sokolow-Lyon method is the one I use. It allows rapid reading. I add the amplitudes of the S wave of V1 to the R wave or V5 or to V6. Are the QRS complexes small? ie., is there something between them and the reading electrodes? This may be fluid or fat. Pericardial or pleural effusions are the ones to consider. Small complexes and tachycardia, should always make us think of a pericardial effusion. 2. Are they Wide or narrow? Here I am looking to see what the cause of a wide complex is. Sometimes we couple this question with fast or slow. For example, slow rates with a wide complex may be associated with a complex being initiated outside the atrioventricular node. If a complex passes through the AV node, it is narrow. Wide complex fast rhythms may be due to a number of causes including ventricular tachycardia, hyperkalaemia, Na channel blockade, ischaemia and more. 3. Do they have abnormal morphology? This is really referring to the delta wave of WPW 4. Are they clumped? This is a step I have included to ensure we don't miss a Moritz block( which we would normally look for in the previous step). In mobitz blocks, we often (not always) see a clumping of the QRS waveforms. This reminds us to go back and look for a Moritz Block more closely. ECG 3A 54 yo male presents with chest pain, that radiates into his jaw. He has a previous history of an AMI 10 years previously and also has hypertension, diabetes and hypercholesterolaemia. An ECG is done. Does this patient need to go to the Cath lab? What is the 'sign' seen here?  Image courtesy of Dr Louise Cullen. ANSWER
This is a'The South African Flag Sign'. The patient had an obstructed diagonal artery.
ECG 4A 64 yo male presents with chest pain. What are the important ECG changes and what other ECGs would you perform?  ANSWER
The ECG shows ST depression in leads V1-V3. The anterior leads show reciprocal ecg changes, as no leads look directly at the posterior part of the heart.
Posterior leads are done here and the ECG is shown below. This is another STEMI Equivalent. This patient needs to go to the Cath lab. 
I've done a presentation on these ECGs before. One of my young doctors asked if I could make an ECG of them. Here it is. It's just over 12 minutes and a bit of fun. Enjoy and hope to see you at the Cardiac Bootcamp Live Course.
The arrhythmia from Hell! Everyone stresses about wide complex tachycardias(WCT). In the Cardiac Bootcamp Course we make it simple. A recent article in JAMA Internal Medicine looked at the ECG features that differentiated VT from SVT. In the course you learn my 120CRAM rule. Let's see what this paper found. Cerantola M et al. Diagnostic Approach to Wide Complex Tachycardia. JAMA Intern Med 2021 Sep 1;181(9):1231-1233 A few points of summary from this article. 90% of patients with a WCT and a history of myocardial infarction, will be in Ventricular Tachycardia(VT). We know that about 80% of WCT is VT, so it is a safe assumption. But there are a few other things to take into account. The ECG factors that were associated with VT included: A. AV Dissociation, Capture and Fusion Beats B. Positive QRS in aVR C. QRS Concordance in the precodial leads D. QRS duration > 160ms E. A deflection in the initial portion of the QRS  Causes of WCTThere are really only a few causes of Wide Complex Tachycardia:
What's my 120CRAM formula?120: This is a critical number. The rate must be faster than 120bpm and wider than 120ms. However BEWARE, if the QRS is too wide always think of HYPERKALAEMIA. C: Concordance R: Dominant R wave in aVR A: AV dissociation M: Morphology which includes capture and fusion beats and an Rsr pattern in V1 and a QS in V6 ( refer to the section on Wide Complex Tachycardia in the Course) Below is a slide from the course.  Do you have a simple failsafe approach to arrhythmias? You must have your own simple approach. Members can go to the 'Narrow Complex Tachycardias' section to view my simple algorithm approach to the fast and slow rhythms. An old boss of mine used to have what he called 'The 2am in the morning' approach to airway drug doses, so that it was simplified and minimised errors, when you were called in at that time. It's important to have a similar simple approach to arrhythmias. Here is my approach. It comes back to some simple questions. If the rhythm is fast (>100 bpm) there are some critical questions to ask. Is it Narrow? If Yes:
What are the causes of wide complex tachycardia:
Given that 80% of wide complex rhythms are Ventricular Tachycardia(VT), we can settle on that for most patients. However there are a few things to remember about VT:
 What does the ecg below show?  This is WPW with Atrial Fibrillation. The rate in some areas is 300 bpm. If you have any rate faster than 250bpm in an adult, there must be an accessory pathway. It is irregularly irregular. Some complexes are wide and others are narrow, as some pass through the AV node and others via the accessory pathway. See below:  How do we manage this condition? If we used Procainamide, that would be fine, as it preferentially blocks the accessory pathway. What we cannot use, is an AV nodal blocker, such as a beta or calcium channel blocker, or Amiodarone. If we did this all the impulses would be conducted down the accessory pathway and the heart would go into ventricular fibrillation. What if we applied the simple algorithm approach? We don't need to know what the diagnosis is.... that's the benefit of having an approach like this. Just follow the flow....  Let's try one more, then you can go to the course and do a bundle of examples. What is the diagnosis of the ECG below?  It is a fast, narrow complex tachycardia. It is AVN re-entry tachycardia. What if you weren't sure of what to do? What would the algorithm say?  Remember to develop your own approach or just use mine. It's very satisfying when you have a simple approach. You can then add all the other learnings to this.
Join me for an a fun approach to really understanding arrhythmias, when I cover 'Rule the Arrhythmia' at the Cardiac Bootcamp on the Gold Coast on January 18 2022, |
AuthorDr Peter Kas 
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