All you need to know about CARDIAC ARRHYTHMIAS!

Summary

Join our comprehensive on-demand teaching session about Cardiac Arrhythmias. Under the guidance of experts Johanne Li and Khadeejah Hullemuth, learn everything from the basic underlying physiology of the cardiac rhythm, to identifying and recognizing features of different arrhythmias in clinical scenarios. Brush up on your understanding of ECG interpretations, learn how to apply ALS guidelines for managing arrhythmias, and be prepared for any quick-fire questions that will be thrown your way during the session. Perfect for current medical students, this session is reviewed by doctors to ensure accuracy. Don't miss out on this opportunity to enhance your diagnostic technique and core understanding of cardiac arrhythmias!

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Description

Welcome to Teaching Things!

We're excited to bring you this high-yield teaching series, designed to help you ace both your written and practical exams.

This tutorial will focus on Arrhythmias, covering key differentials such as SVTs and Atrial Fibrillation to ensure you're well-prepared.

The session will be led by Khadeejah and Johanne, both medical students in their clinical years at UCL, who are passionate about delivering practical, exam-focused content.

Don’t forget to fill out the feedback form after the tutorial—we value your input! And remember, you can access recordings of all past tutorials on our page.

Learning objectives

Comprehend the fundamental physiology that guides the cardiac rhythm to correctly interpret ECG readings.
Demonstrate the ability to recognize common clinical presentations of various arrhythmias and establish their related diagnostic procedures.
Identify and interpret primary features of different cardiac arrhythmias observed in an ECG reading and discuss their clinical significance.
Understand and apply the Adult Life Support (ALS) guidelines for managing common cardiac arrhythmias.
Analyze the different types of arrhythmias, their pathogenesis, and potential treatments, to provide comprehensive patient care.

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EVERYTHING YOU NEED TO KNOW ABOUT CARDIAC ARRHYTHMIAS Johanne Li and Khadeejah Hullemuth Here’s what we do: ■ Weekly tutorials open to all! ■ Focussed on core presentations and teaching diagnostic technique If you’re new here… ■ Bstudentsl students, for medical ■ Reviewed by doctors to ensure W elcome to accuracy T eaching ■ We’ll keep you updated about our Things! upcoming events via email and groupchats!TOPIC ONE Khadeejah HullemuthLearning Objectives: 1. To recap the basic underlying physiology of the cardiac rhythm 2. To be able to identify common presentations and clinical vignettes of common arrhythmias 3. To recognise the features of different arrhythmias on ECG 4. To understand and apply ALS guidelines for managing arrhythmiasQuick ﬁre question! Which of these is the dominant pacemaker? A. Atria B. AV node C. Bundle of His D. SA node E. Purkinje ﬁbresQuick ﬁre question! Which of these is the dominant pacemaker? A. Atria B. AV node C. Bundle of His D. SA node E. Purkinje ﬁbresWhy is this important?Cardiac cycle 1. SA node excited - atria contracts (P wave) 2. Triggers the AV node, delivers a slow action potential (to allow ventricles to ﬁll) 3. AV node triggers the bundle of HisCardiac cycle 1. SA node excited - atria contracts (P wave) 2. Triggers the AV node, delivers a slow action potential (to allow ventricles to ﬁll) 3. AV node triggers the bundle of His 4. Impulse conducts down bundle of his to right and left bundle branches and through the purkinje ﬁbres to have a FAST depolarisation - ventricles contractCardiac cycle 1. SA node excited - atria contracts (P wave) 2. Triggers the AV node, delivers a slow action potential (to allow ventricles to ﬁll) 3. AV node triggers the bundle of His 4. Impulse conducts down bundle of his to right and left bundle branches and through the purkinje ﬁbres to have a FAST depolarisation - ventricles contract 5. Ventricles then repolarise - relax (T wave) Where does it all go wrong?! Some other slightly rogue things Supraventricular Ventricular ConductionQuick ﬁre question! Which of these is NOT a supraventricular rhythm? A. Torsades de Pointes B. Sinus tachycardia C. Atrial ﬂutter D. Supraventricular tachycardia (SVT) E. Wolff-Parkinson-White (WPW) syndromeQuick ﬁre question! Which of these is NOT a supraventricular rhythm? A. Torsades de Pointes B. Sinus tachycardia C. Atrial ﬂutter D. Supraventricular tachycardia (SVT) E. Wolff-Parkinson-White (WPW) syndrome Where does it all go wrong?! Some other slightly rogue things Supraventricular Ventricular Conduction Supraventricular arrhythmias Name of What it looks like Actions arrhythmia Sinus arrhythmia Differing lengths between p waves Nothing (normal) Sinus tachycardia Like sinus rhythm, but faster Adult Tachycardia guidelines - Resus Council 2021 Sinus bradycardia Like sinus rhythm, but slower (under 60bpm for Adult Bradycardia guideliens - Resus Council 2021 adults) Atrial fibrillation Irregularly irregular rhythm with no p waves Depends on if acute or chronic. Acute = oral anticoagulation and possible chemical cardioversion Atrial flutter ‘Saw tooth’ Consult with cardiology + anticoagulate Supraventricular Narrow complex, regular tachycardia with no p Vasovagal manouevres → IV adenosine → electrical tachycardia waves cardioversion Wolf Parkinson White Short PR interval + ‘delta waves’ (slow upstroke of Radiofrequency ablation of accessory pathway QRS)Quick ﬁre question! What type of rhythm abnormalities occur as a result of disturbances between the AV node and the bundle of His? A. Sinus bradycardia B. Ventricular ﬁbrillation C. Ectopic beats D. Heart block E. Pulseless electrical activityQuick ﬁre question! What type of rhythm abnormalities occur as a result of disturbances between the AV node and the bundle of His? A. Sinus bradycardia B. Ventricular ﬁbrillation C. Ectopic beats D. Heart block E. Pulseless electrical activity Where does it all go wrong?! Some other slightly rogue things Supraventricular Ventricular Conduction Name of Causes What it looks like Actions arrhythmia 1st degree heart block Inferior MI, hyperkalemia, Long PR interval Nothing / Reverse underlying iatrogenic (CCB, thiazide cause diuretics and digoxin) 2nd degree heart block (Mobitz ● inferior MI PR gets longer and longer and If they’re an athlete - nothing type 1) ● calcium channel blockers, longer until one just happens without a QRS following it Stop precipitating drugs digoxin, beta blockers ● athletes due to high vagal Adult Bradycardia guidelines tone 2nd degree heart block (Mobitz Surgery Every p wave is followed by a Permanent pacemaker type 2) Autoimmune conditions QRS then there is a non-conducted p wave 3rd degree heart block (aka Inferior MI No relationship between p Transcutaneous pacing complete heartblock) Idiopathic fibrosis waves and QRS complexes Bundle branch block ASD, blood clots, HTN Causes an ‘M’ or a ‘W’ shape in Cardiac resynchronisation the QRS complexes deviceECG practice What does this ECG show: A. Ventricular tachycardia B. 3rd degree heart block C. Ventricular ﬁbrillation D. Torsade de Pointes E. Wolf Parkinson WhiteECG practice What does this ECG show: A. Ventricular tachycardia B. 3rd degree heart block C. Ventricular ﬁbrillation D. Mobitz type II E. Wolf Parkinson White Where does it all go wrong?! Some other slightly rogue things Supraventricular Ventricular Conduction Name of What it looks like Actions arrhythmia Ventricular tachycardia (VT) Broad complex tachycardia Adult Tachycardia guidelines Ventricular ﬁbrillation (VF) Chaotic, irregular deflections BLS / ALS with no p waves Torsades de pointes ‘Twisting’ changes of IV magnesium sulphate amplitude around the isolectric line Can deteriorate to VF so needs to be managed ASAPHelpful videos! https://www.youtube.com/watch?v=EqUfgffJx_8 https://www.youtube.com/watch?v=RuxKTCv_s0MPART 2 Johanne LiTachycardia (>100bpm) Regular: equally spaced, repeating patternT achycardia (>100bpm) Regular: equally spaced, repeating pattern Sinus tachycardia Anxiety Pain ● Regular rhythm Fever ● Upright and regular P waves Shock ● 1 P wave for each QRST achycardia (>100bpm) Regular: equally spaced, repeating pattern Sinus tachycardia Regularly Irregular: unequal beats Atrial ﬂutter Regularly irregular (pattern● Sawtooth baseline ● Regular QRS ● 2:1 conductionT achycardia (>100bpm) Regular: equally spaced, repeating pattern Sinus tachycardia Regularly Irregular: unequal beats Irregularly Regularly irregular irregular (Sporadic) (pattern) Atrial ﬂutter Atrial ﬁbrillation: absent P waves, irregular R-RSVT vs VT Origin of electrical circuit dysfunction AF: atria SVT: above ventricles (atria or AVN) VT: ventricles SVT Narrow QRS, no clear P waves VT Wide QRS SBA 55yo M presents to A&E with a sudden onset of palpitations and mild chest discomfort. He has a past medical history of hypertension but no known heart disease. On examination, his HR is 160bpm with a BP of 130/85. His ECG shows the following: What is the most likely presentation? A) Sinus tachycardia B) Atrial ﬁbrillation C) Atrial ﬂutter D) 1st degree heart block E) Ventricular tachycardia SBA 55yo M presents to A&E with a sudden onset of palpitations and mild chest discomfort. He has a past medical history of hypertension but no known heart disease. On examination, his HR is 160bpm with a BP of 130/85. His ECG shows the following: What is the most likely presentation? A) Sinus tachycardia B) Atrial ﬁbrillation C) Atrial ﬂutter D) 1st degree heart block E) Ventricular tachycardiaAtrial ﬁbrillation ● Cardiac causes: HTN, CAD, HF, CHD, peri/myocarditis Pathophysiology: ● Non-cardiac causes: hyperthyroidism, electrolyte imbalance, sleep ● Irregular atrial conduction apnoea/COPD, alcohol excess, stimulants leads to sporadic signalling via the AVN ● atria:ventricular rate of 2:1 Risk factors: Classiﬁcation: ● Blood remains in the ● Age (>60yo) ● 1st detected episode ventricles for longer = incr. ● Family Hx ● Recurrent ● Obesity ○ Paroxysmal risk of clot formation ● = Incr. risk of stroke ○ Persistent ● Permanent Presentation: ● palpitations, dyspnoea, chest pain ● apical-to-radial pulse deﬁcit ● variable intensity of ﬁrst heart soundGoing back to our gentleman… 55yo M, A&E, sudden onset palpitations + mild chest discomfort PMHx: HTN O/E: HR 160, BP 130/85 Stable or unstable? Acute management UNSTABLE/DECOMPENSATED STABLE 1. A-E assessment 1. Treat reversible causes: infection, 2. 3 synchronised DC shocks hydration, electrolytes, endocrine 3. Correct electrolyte abnormalities abnormalities 2. Rate vs Rhythm control 3. Reducing stroke risk E.g atenolol, Rate control: Rhythm control: Rate control not offered if: propranolol Pharmacological cardioversion - Reversible cause BB Rate limiting CCB or - HF thought to be primarily caused by AF Digoxin Electrical cardioversion - New-onset AF within the past 48 hours - A rhythm-control strategy is felt to be more Diltiazem or suitable clinically non‑paroxysmal AF verapamilSBA 55yo M presents to A&E with a sudden onset of palpitations and mild chest discomfort. He has a past medical history of hypertension but no known heart disease. On examination, his HR is 160bpm with a BP of 130/85. Before commencing his treatment, which risk scores should be calculated? A) CHA2DS2-VASc only B) CHA2DS2-VASc and ORBIT C) CHA2DS2-VASc, ORBIT and FRAX D) ORBIT only E) ORBIT and FRAXSBA 55yo M presents to A&E with a sudden onset of palpitations and mild chest discomfort. He has a past medical history of hypertension but no known heart disease. On examination, his HR is 160bpm with a BP of 130/85. Before commencing his treatment, which risk scores should be calculated? A) CHA2DS2-VASc only B) CHA2DS2-VASc and ORBIT C) CHA2DS2-VASc, ORBIT and FRAX D) ORBIT only E) ORBIT and FRAXRisk scoring: CHA2DS2- VSc Score ≥2: offer DOAC (apixaban, dabigatran, rivaroxaban) or warfarin if contraindicated Score of 1: consider DOAC if M with concurrent AFRisk scoring: ORBIT NICE: Do not withhold anticoagulation solely based on a person's age or falls riskSBA A 65yo F with a past medical history of coronary artery disease collapses in the with a ventricular tachycardia.CG shows broad-complex tachycardia consistent What is the most appropriate next step in management? A) Administer amiodarone IV B) Perform immediate synchronised cardioversion C) Start chest compressions and deliver unsynchronised deﬁbrillation D) Administer atropine 1 mg IV E) Administer adenosine 6 mg IVSBA A 65yo F with a past medical history of coronary artery disease collapses in the with a ventricular tachycardia.CG shows broad-complex tachycardia consistent What is the most appropriate next step in management? A) Administer amiodarone IV B) Perform immediate synchronised cardioversion C) Start chest compressions and deliver unsynchronised deﬁbrillation D) Administer atropine 1 mg IV E) Administer adenosine 6 mg IVShockable rhythms ● Broad QRS complex ● Absent P waves ● Chaotic, irregular ﬁbrillatory waves ● Absent QRS, absent P waves Non-shockable rhythms Adult Advanced Life Support (ALS) Recognise signs of arrest: unresponsive, Commence CPR at a abnormal/no breathing, no pulse 1. 2. depth of 5-6 cm or ⅓ of the chest wall Call for senior help, emergency response, and get a deﬁbrillator ratio of 30 compressions to 2 breaths Shockable (VF, PVT) ● Administer shock 1 Non-shockable (asystole, PEA) ● Return to CPR for 2 minutes, rhythm check ● Resume CPR for 2 minutes ● Administer shock 2 ● Return to CPR for 2 minutes, rhythm check ● Administer 1mg IV Adr immediately ● Administer shock 3, Adr 1mg IV + amiodarone 300mg IV ● Repeat 1mg every 3-5 minutes ● Administer 1mg Adr every 3-5 minutes after alternate shocks Lidocaine 100mg IV may be used if amiodarone is not available https://cks.nice.org.uk/topics/cardiac-arrest-out-of-hospital-care/management/advanced-life-support-adult/ SBA initiated, and the ECG shows pulseless electrical activity (PEA). The advanced lifes support (ALS) team begins resuscitation, and the team leader asks for a review of potential reversible causes. What is the most likely cause? A) Hyponatraemia B) Hyperthermia C) Hypoxia D Hypocalcaemia E) Hyperglycaemia SBA A 54yo M collapses at home, and emergency services ﬁnd him incardiac arrest. CPR is initiated, and the ECG shows pulseless electrical activity. The ALS team begins resuscitation, and the team leader asks for a review of potential reversible causes. What is the most likely cause? A) Hyponatraemia B) Hyperthermia C) Hypoxia D Hypocalcaemia E) Hyperglycaemia THANKS FOR W ATCHING! on Medall and see you next week! Tutor 1: Khadeejah Hullemuth Tutor 2: Johanne Li