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I've been emailed a few times about the ECG in 20 Seconds Method. This is an approach to reading the ECG, I put together years ago, mostly to help myself read the ECG and not miss things. There is nothing new and groundbreaking about this. It has the elements of the classic ECG approach. Some say it is too simple, but that's its greatest strength!......
What is special about this method, is that it allows us to learn a basic algorithm, that looks for the most important ECG findings. You won't pick up everything with this, but you will pick up those important ECG changes that will have the highest yield for your patient, like the sneaky ischaemia, differentiating a lethal from non-lethal arrhythmia. It gives you the confidence to read ECG's. Why did I call it 'ECG in 20 Seconds'? Because it only takes 20 seconds to pick up the abnormalities in the algorithm. You can then sit down and spend a few minutes sorting them. ​Below are the basic elements. For a more detailed approach login and go to the ECG in 20 seconds page. 
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We look at a lot of ECG's and we do a lot of troponins, however the most important thing we are going to do in the patient who presents with chest pain is take a good history. Regardless of a normal troponin or a normal ecg, if the patient has a very good history for acute coronary syndrome, we have to admit that patient, or at least watch them and do serial testing. The low risk group that we clear with rapid rule-out criteria, are just that, low risk on history. Here is an example of a patient who presents to the emergency department with chest pain. Please rank the following in terms of likelihood for predicting a myocardia infarction, or at least ischaemia.
 ANSWER
CASE A patient presents to the emergency department with chest pain and you put a pre-test probability of x% on that chest pain being ischaemic. How does it change with the following? DOES IT INCREASE OR DECREASE THE CHANCE THAT THIS IS ISCHAEMIC PAIN?
The table below looks at the PPV and Likelihood ratios of predictors for AMI  Reference
Body R et al. The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes. Resuscitation 81 (2010) 281-286. A 6 week old is brought to your rural emergency department with several days history of irritability and poor feeding. On history there was poor/no antenatal care and the child was a home birth. On examination the child is afebrile, with a tachycardia and is haemodynamically stable. There is a 4/6 holosystolic murmur on cardiac auscultation and bilateral lung crepitations. An ecg is done and is shown below. Please answer the following:
 WHAT Does the ECG show?
The rate is 138. Normal P waves The QRS's in V4-5 overlap, indicating a Left Ventricular Hypertrophy. This is most likely due to a Vetriculoseptal defect (VSD) WHAT is the most likely diagnosis
This is a VSD. VSD's cause a left to right shunt. Over time they result in pulmonary hypertension and right ventricular hypertrophy, which then reverses the shunt. This can lead to Eisenmenger's syndrome, resulting in cyanosis and heart failure. At 4 to 6 weeks, the features of heart failure begin to appear. what investigations would you like to order?
The diagnosis has almost been made clinically. We already have an ECG. We need a Chest-Xray, which may show cardiomegaly and a cardiac echo to follow. STEMI mimics(1) are important to understand, because in taking the time to investigate the mimic, we can miss opportunity for early treatment of the real disease. Unlike STEMI equivalents, which have been covered previously, some of the mimics are not as serious. Here are some examples. 1. Normal ST ElevationThis can be in 2 forms, where in both the ST segment is concave:
The ECG below is from a male who presents with chest pain. It is normal.  (3) 2. Benign Early Repolarisation (BER)This condition is present in a younger population group and amongst athletes. There are three types:
Point notch with elevation STE with concave up morphology V2-V6, II, III, avF usually < 2mm No reciprocal changes Symmetrical Concordant T wave STE/T-wave height <0.25 in V6 Benign Early Repolarisation may not be that benign, being associated with serious arrhythmias in some studies.  BER Source: Cardiac Bootcamp Online Course 3. PericarditisDiffuse STE ST/T-wave >0.25 There are 4 stages in pericarditis:
 Pericarditis. Source: Cardiac Bootcamp Live Course  4. LBBBST-T and QRS discordant. STE is concave and <5mm 5. HyperkalaemiaPeaked T waves Downsloping ST segment. 6. Brugada SyndromeType I: Coved Pattern
 Type I Coved Pattern Brugada(4) Type II: Saddle-back
 Type II Saddle-Back pattern Brugada(4) 7. Pulmonary EmbolismCan present with STE in Precordial leads A more common presentation of right ventricular injury is STE in V1-V3 and/or ST depression of V4-V6. Theories for why STE occurs in the precordial leads include:
 (7) References
A 28 yo patient presents to the emergency department complaining of palpitations of 2 hours duration. He has no other symptoms and has no past medical history of note. He is afebrile, with a respiratory rate of 14 a heart rate of 237bpm and a blood pressure of 119/67. An ECG is done and is shown below. What does the ECG show and what is your diagnosis? Is it Ventricular Tachycardia?  ANSWER
This is a wide 'ish' complex tachycardia at a rate of 237bpm. There is a RBBB morphology. The axis is extreme. If we use the 120 CRAM formula to see if it VT: Faster than 120bpm (but not too fast)- It is faster than 120. Wider than 120ms- It is borderline. Concordance: No Initial R wave in aVR: No AV Dissociation: No Morphology: RBBB pattern however there is an rsR pattern not indicative of VT R/S > 1 I would consider this more likely to be Supraventricular Tachycardia (SVT) with a RBBB, even with the axis as it is. How would you manage this haemodynamically stable patient? (a) Adenosine (b) Cardioversion (c) Sotalol IV (d) Amiodarone ANSWER
This can be a difficult question to answer. For those who prefer cardioversion in every patient with a WCT, that's a very appropriate approach.. However, is there any harm in giving Adenosine? There are 3 things to consider:
The patient was given Adenosine and reverted as shown below. Was this an Idiopathic Ventricular Tachycardia. How do you differentiate it from Ventricular tachycardia or from an SVT with aberrancy?  What is Idiopathic Ventricular Tachycardia?Idiopathic Ventricular Tachycardia (VT), occurs in structurally normal hearts and comprises about 10% of VT cases. This is a more benign form of VT, with patients rarely suffering from sudden cardiac death. Definitive treatment includes medications or ablation. Patients presenting to the emergency department with this arrhythmia, can be cardioverted and some will respond to AV nodal blockers such as Adenosine or Calcium Channel Blockers or Beta Blockers. However, even if the arrhythmia reverts with these, the patient should still be discussed with cardiology, especially if they fit the particular ECG patterns discussed below. Idiopathic VT can be mistaken for a supra ventricular tachycardia(SVT) with aberrancy and it will respond in some cases to AV nodal blockers, just like an SVT with aberrancy, so beware. However there are some distinct differences in morphology and axis, that allow us to identify it. Classifications can be confusing. For simplicity we can classify them as:
I recently gave a webinar on wide complex tachycardias(WCT) and other ECGs. Here are 4 WCT ECGs for you to try. The question I would like you to answer is simple:
Is this Ventricular Tachycardia (VT)? ​Then watch the 4 minute video with the answers, below.
ECG 1
An elderly patient who is hypotensive and has had a collapse/fall is found to have a WCT on the monitor. This ECG is done. Is this VT? 
ECG 2
A 19 yo woman presents with palpitations. An ECG is done which shows this WCT. Is this VT? 
ECG 3
A 58 yo patient present to the Emergency Department complaining of palpitations. Is this VT? 
ECG 4
A 60 yo male presents with palpitations. Is this VT? 
THE ANSWERS
We know that Left Ventricular Hypertrophy (LVH) when diagnosed on an ECG, is associated with a higher mortality and cardiovascular morbidity. The gold standard for diagnosis is Cardiac Echocardiography, or ventricular mass measurements by MRI. The ECG however can provide a helpful screening tool for patients, alerting us for the need for further investigations. How do you determine if the ECG shows LVH? MEMBERS go to LVH under the ECG section to read about:
The SEAMENS' SIGN This is a new proposed sign from the recent literature(1). The Seamens Sign is as follows: If any of the QRS Complexes in the precordial leads in a 12 lead ECG, touch or cross another QRS complex, this is defined as LVH. This was a retrospective chart review of 2184 patient records in a Quartenary Centre and looked at consecutive patients with an ECG and a trans thoracic echocardiogram, performed within 90 days of each other. The Primary Endpoint was to determine if the Seamens' Sign was non inferior in confirming LVH compared to other criteria. Conclusion When compared to the Sokolow-Lyon criteria and the Cornell criteria for males, the Seamens' Sign was non-inferior in confirming LVH on an ECG. Below is the example.  Syncope is not uncommon, occurring in up to 25% of children before 18 years of age. Most causes are benign, however we need to be aware of the of 3 major groups as these can be very serious diagnoses:
Definition of Syncope Syncope in children and adults is a symptom, not a condition. It is up to us to determine the cause. The definition of syncope involves three components:
CaseA 12 yo presents to the emergency department. He is unwell and has had some episodes of syncope. His investigations in the ED result in the diagnosis of Viral Encephalitis. He develops the rhythm shown below and at the same time drops his conscious state. What does the ECG show? What is the diagnosis? What would you do now?  What is the diagnosis?
Ventricular Tachycardia Do you have an approach to Paediatric Syncope?Below you will find my approach to the child with syncope. Read more on this on the website, and also watch the video lecture.  Watch the Lecture A 40 yo male is brought in by ambulance following a collapse His GCS at the scene was 3 Paramedics found his rhythm to be VT? and he was given 11 shocks and 5mg of Adrenaline in total. On arrival he has an undetectable BP. He is maxed out on an adrenaline infusion. He has an LMA and has spontaneous assisted respirations The ECG is shown below. What do you think are the important changes  What would you treat this patient with, acutely? He is maxed out on an adrenaline infusion. (a)Adrenaline (b)Calcium Gluconate (c)Amiodarone (d)Potassium (e)Atropine ANSWER
The answer is d. This is the ECG of hypokalaemia. Notice the PR prolongation, ST depression and U waves. See the ECG changes below. . . . . .  What are the causes of this condition?
What is the treatment? Was it really VT or something else? What is the issue with Adrenaline in this case? A 38 yo male presents with sharp stabbing central chest pain. It changes with breathing. He feels worst when he is lying down. He is haemodynamically stable. An ECG is done. What does it show?  WHAT DOES THE ECG SHOW? Using the ECG in 20 Seconds Approach:
 REMEMBER: When looking for ST elevation or depression, use the T-P line as the isoelectric line.
DIAGNOSIS The diagnosis is most likely pericarditis. The history is very indicative of that. The characteristics of the pain ie., that is it worst on lying down indicate pericarditis. Although there appears to be a pleuritic component, there is no real other history of a PE and the ECG does not show a right axis or S1Q3T3 etc. In the ECG itself:
 WHAT TO DO NEXT
Who needs admission and who can be discharged?
What is Spodick's Sign and how good is it? What are the stages of Pericarditis? What is the treatment? Is there a role for glucocorticoids? |
AuthorDr Peter Kas 
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