This overview of ECG essentials aims to help ED doctors (new to the department or existing as a refresher!) feel more confident in interpreting ECGs. I trust you are all familiar with the basics - if you'd like a recap grab a copy of 'ECGs made easy' from the library or scroll through life in the fast lane: https://litfl.com/ecg-library/basics/ Here we will focus on identifying ECGs that require immediate management and what that entails...
Emergency ECGs ST elevation myocardial infarction An acute STEMI requires urgent review; if you think a patient fits the criteria for PCI then your nearest PCI centre needs to be contacted ASAP. Time is myocardium!
Acute anterolateral ST elevation myocardial infarction
Anterior-inferior myocardial infarction
Striking features: - ST elevation present on lead II, III, AvF, as well as V1 - V5 - Q waves in III, AvF, V1 - V3
Left bundle branch block
Striking features - QRS >12oms i.e. broad QRS complexes - Broad R waves and absence of Q waves in I, AvL, V5 - V6 (lateral leads)
Understanding LBBB Usually the septum is activated from left -> right which produces small Q waves in the lateral leads. However, in LBBB the direction is reversed as the left bundle is 'blocked' (indicating a left coronary artery thrombus which supplies the left bundle), the electrical activity runs down the right bundle to the right ventricle, and then to the left ventricle via the septum. This process extends the QRS duration >120ms and removes the Q waves from the lateral leads Also, as the ventricles are activated in sequence rather than at the same time this produces a notch appearance in the R wave. WiLLiaM = LBBB
**PCI Criteria** Criteria for PCI referral (in the presence of chest pain starting <12 hours ago)
ST-elevation >2mm in 2 contiguous (next to each other) CHEST leads
ST-elevation >1mm in 2 contiguous LIMB leads
New LBBB (presume new if no previous ECG)
STEMI management If you see what you think is a STEMI on an ECG what should you do?
Show a senior doctor
Review the patient - how are the observations. Ensure they are being monitored and having bloods taken and a cannula inserted
ABCDE assessment, maintain oxygen sats 94 - 98%
GTN and opiates for analgesia
Asprin 300mg (if not already given by crew)
Liaise with our local PCI cardiology team - state at beginning of the referral you have a patient with STEMI/LBBB for consideration of PCI
There have been case reports of patients who have COVID presenting with or concurrently having STEMIs so remember to have this on your radar!
Fast AF - Atrial Fibrillation
Atrial fibrillation is an atrial (supraventricular) tachycardia with uncoordinated atrial activation which consequently leads to deterioration in atrial mechanical function. The ECG will have absent P waves and an irregular ventricular (QRS) response
Many patients we see will have Atrial fibrillation - for the purpose of Emergency ECGs we are only acutely worried if they are in fast AF. Fast AF can lead to ventricular failure, cardiac ischaemia and thromboembolic events if not dealt with quickly.
Management depends on 2 main things 1. Is the AF existing/permanent or new onset (defined by NICE as within 48hours3) 2. If the patient is showing any adverse features of - Chest pain/myocardial infarction - Shock - Syncope - Heart failure
Management 1. New onset AF or adverse features - electrical DC cardioversion 2. AF permanent and NO adverse features - pharmacological agents should be used to control the rate. This includes beta-blockers or rate-limiting calcium antagonists. If these are contraindicated amiodarone is used. 3. AF in Wolff-Parkinson-White has different management due to the differences in conduction pathways... Ask a senior - Flecainide may be used or DC cardioversion
Supraventricular Tachycardia - SVT
Tachycardias arising from above the bundle of His, producing a regular narrow-complex tachycardia. AF is technically an SVT, but is generally managed and classified separately.
There are different classifications of Supraventricular tachycardias > Sinus tachycardia (usually in response to stimulus eg. hypovolaemia, sepsis) > Atrioventricular nodal re-entry tachycardia (AVNRT) - occurs due to a re-entry circuit next to the AV node. > Atrioventricular re-entry tachycardia - usually due to Wolff-Parkinson-White syndrome (an accessory pathway between the atria and ventricles can set-up a re-entry circuit > Atrial flutter - usually at a rate of 2:1 so HR shows a fairly fixed 150bpm
Management- depends on whether the patient is haemodynamically stable If stable: > Try vagal manoeuvres: valsalva or carotid sinus massage can terminate the rhythm. See here for how to most successfully valsalva - the REVERT trial was a locally run trial with significantly improved results from their modified valsalva rather than standard valsalva alone. > Adenosine 6mg as a rapid IV bolus through a large cannula followed by a quick 20ml saline flush > If no success repeat adenosine at 12mg, this can be done twice if no response > Consider IV Verapamil if no success BUT discuss with senior / medics prior If unstable prepare for electrical cardioversion, in the meantime Adenosine can be tried if this will not delay treatment.
Complete or third degree heart block occurs when the atrial activity is not conducted to the ventricles; the atria and ventricles are working independently of each other and pumping asynchronously.
This correlates on the ECG with P waves not being paired with a QRS complex. There will be a separate P wave or atrial rate, and a QRS or ventricular rate.
The above ECG also shows complete heart block - the P waves are quite small and harder to identify, however you can see that they do not correlate with a QRS complex. The ventricular rate is maintained by a slow ventricular escape rhythm. This shows that it can be tricky to identify complete heart block, however in an ECG that is bradycardic always remember the basics - is the P wave followed by a QRS complex?
This is an emergency and classified as an unstable bradycardia as patients are at high risk of ventricular standstill and sudden cardiac death
Management 1. Atropine 500mcg IV bolus. Can be repeated up to 6x giving a total of 3mg. Atropine works by antagonizing the action of the parasympathetic neurotransmitter acetylcholine at muscarinic receptors. It blocks the action of the vagus nerve at the SA and AV nodes which increases sinus automaticity and facilitates AV node conduction. 2. Pacing should be commenced if bradycardia with adverse signs persists despite Atropine. Transcutaneous pacing can be painful so sedation is likely to be required. Transcutaenous pacing is a temporary measure and plans for a transvenous pacing wire should be urgently arranged with cardiology (intensivists may also have the skillset required) 3. If there is a delay in pacing other drugs can be tried; Isoprenaline infusion - seems to be our regional cardiologists' preference, can be given peripherally in emergencies, see infusion regimen in resus. Adrenaline 2-10mcg per minute is an alternative, or occasionally dobutamine - ideally both given via central access but can be given peripherally short term in extremis. Glucagon 1-2mg can be tried if bradycardia is secondary to a beta blocker overdose.
Summary On this page we have covered the striking ECG findings and urgent management of - STEMI - Left bundle branch block - Fast AF - Supraventricular tachycardia - Complete heart block
When presented with an ECG always remember the basics and ask how the patient is.
If they are showing any adverse features of - Chest pain - Shock - Syncope - Heart failure... they require urgent review!
If in doubt always ask a senior :-)
Please test your knowledge with the quiz below... until you get full marks, share any ecg you are asked to review with a with a senior ED doctor if you have any doubts at all about it.