Cardiac Electrophysiology and Arrhythmia management

⚡ Cardiac electrophysiology explains how the heart generates and conducts electrical impulses, and why abnormal impulse formation or conduction causes arrhythmias. 🫀 Understanding the physiology makes ECG interpretation much easier: every arrhythmia comes from a problem with automaticity, triggered activity, re-entry, or conduction block.

📖 Overview

• 🫀 The normal heartbeat begins in the sinoatrial (SA) node, spreads through the atria, slows at the atrioventricular (AV) node, then travels rapidly via the His–Purkinje system to the ventricles.
• 📉 Arrhythmias occur when impulses are generated abnormally, conducted abnormally, or both.
• ⚠️ Clinical importance depends not just on the rhythm itself, but on haemodynamic effect, underlying structural heart disease, symptoms, and risk of sudden cardiac death.

🧬 Core Electrophysiology

• Resting membrane potential 🔋: Cardiac cells maintain a negative intracellular potential, mainly due to potassium gradients.
• Depolarization ⚡: A positive inward current makes the cell membrane less negative and triggers an action potential.
• Repolarization 🔄: Outward potassium currents restore the resting potential.
• Refractory period 🚧: After depolarization, tissue cannot immediately be re-excited. This protects against tetany and shapes arrhythmia behaviour.

⚙️ Action Potentials

• Fast-response tissues 🏎️: atrial muscle, ventricular muscle, Purkinje fibres.
  • Phase 0: rapid Na+ influx → fast depolarization.
  • Phase 1: brief early repolarization.
  • Phase 2: plateau due to balance of Ca2+ influx and K+ efflux.
  • Phase 3: repolarization from outward K+ current.
  • Phase 4: resting membrane potential.
• Slow-response tissues 🐢: SA node and AV node.
  • Depolarization depends more on Ca2+ channels than fast sodium channels.
  • These cells have spontaneous phase-4 depolarization, which creates automaticity.

🧠 Why This Matters Clinically

• 💊 Sodium-channel blockers mainly affect fast tissues → slow conduction through atrial/ventricular myocardium and widen QRS if excessive.
• 💊 Calcium-channel blockers mainly affect nodal tissue → slow AV nodal conduction.
• 💊 Beta-blockers reduce sympathetic stimulation → slow sinus rate, reduce AV conduction, and reduce triggered arrhythmias.
• 💊 Potassium-channel blockers prolong repolarization and refractory period → may terminate re-entry but can also prolong QT and provoke torsades.

📡 Normal Conduction System

• SA node 🌟: normal pacemaker, usually 60–100 bpm at rest.
• Atrial conduction 🫀: gives the P wave.
• AV node ⏸️: physiological delay allows ventricular filling.
• His bundle / bundle branches / Purkinje fibres ⚡: rapid ventricular activation gives a narrow QRS when conduction is normal.

📈 ECG Correlation

• P wave = atrial depolarization.
• PR interval = atrial to ventricular conduction, mainly across the AV node.
• QRS complex = ventricular depolarization.
• ST segment + T wave = ventricular repolarization.
• QT interval = total ventricular depolarization and repolarization time.

🧩 Mechanisms of Arrhythmia

• 1. Abnormal automaticity 🌱: ectopic pacemaker fires spontaneously (for example atrial ectopics, ventricular ectopics).
• 2. Triggered activity 🎯: afterdepolarizations produce extra beats; classically seen with long QT / torsades or digoxin toxicity.
• 3. Re-entry 🔁: impulse repeatedly circles around a conduction pathway; this is the key mechanism in many SVTs, atrial flutter, and scar-related VT.
• 4. Conduction block 🚫: impulse delay or failure, causing bradycardia or facilitating re-entry.

🫀 Major Arrhythmia Categories

• Bradyarrhythmias 🐌: sinus bradycardia, sinus node dysfunction, AV block.
• Supraventricular tachyarrhythmias (SVT) ⚡: AVNRT, AVRT, focal atrial tachycardia, atrial flutter, atrial fibrillation.
• Ventricular arrhythmias 🚨: ventricular ectopics, non-sustained VT, sustained VT, ventricular fibrillation.

🐌 Bradyarrhythmias

• Sinus bradycardia: may be physiological (athletes, sleep) or pathological (drugs, hypothyroidism, ischaemia, sick sinus syndrome).
• AV block:
  • First-degree AV block: prolonged PR, all P waves conducted.
  • Second-degree Mobitz I: progressive PR prolongation then dropped beat.
  • Second-degree Mobitz II: dropped beats without progressive PR prolongation → more concerning.
  • Third-degree AV block: AV dissociation.
• ⚠️ Persistent complete or high-grade AV block is a major pacing indication. :contentReference[oaicite:1]{index=1}

⚡ Tachyarrhythmia Framework

• Ask 3 questions:
  • 1. Is the patient unstable? 😵
  • 2. Is the QRS narrow or broad? 📏
  • 3. Is the rhythm regular or irregular? ⏱️
• 🚨 If there are life-threatening features such as shock, syncope, myocardial ischaemia, or heart failure, follow the adult tachyarrhythmia algorithm and perform urgent synchronized cardioversion where indicated. :contentReference[oaicite:2]{index=2}

🚑 Unstable Tachyarrhythmia

• ⚠️ Signs of instability:
  • 💥 Shock
  • 🧠 Syncope / severe pre-syncope
  • ❤️ Chest pain / myocardial ischaemia
  • 🌊 Heart failure / pulmonary oedema
• 🔌 Synchronized DC cardioversion is usually required for unstable tachyarrhythmia with a pulse. :contentReference[oaicite:3]{index=3}

🔹 Narrow-Complex Regular Tachycardia

• Usually AVNRT, AVRT, or atrial tachycardia.
• 🧘 Vagal manoeuvres first.
• 💉 If ineffective, give adenosine if there is no evidence of pre-excitation. Resuscitation Council UK recommends 6 mg rapid IV bolus, then 12 mg, then 18 mg if needed. :contentReference[oaicite:4]{index=4}
• 🧠 Adenosine transiently blocks AV nodal conduction, so it terminates AV node–dependent rhythms and may unmask atrial activity.

🔸 Narrow-Complex Irregular Tachycardia

• Most commonly atrial fibrillation.
• Could also be atrial flutter with variable block or multifocal atrial tachycardia.
• 💊 In stable AF, initial management often focuses on rate control unless there is a strong reason for rhythm control. NICE recommends beta-blockers as first-line long-term rate control in most people. :contentReference[oaicite:5]{index=5}

🌀 Atrial Fibrillation (AF)

• Mechanism 🔁: multiple re-entrant wavelets and ectopic activity, often from the pulmonary veins, create chaotic atrial activation.
• ECG 📉: absent organized P waves, irregularly irregular ventricular rhythm.
• Symptoms 😵: palpitations, breathlessness, fatigue, chest discomfort, syncope, or asymptomatic incidental finding.
• Clinical importance ⚠️: stroke risk, heart failure, tachycardia-mediated cardiomyopathy.

💊 AF Management Principles

• 1. Stroke prevention 🧠: anticoagulation according to stroke and bleeding risk assessment.
• 2. Rate control ⏱️: often first-line using a beta-blocker or rate-limiting calcium-channel blocker where appropriate. NICE recommends a standard beta-blocker first-line, except in people with asthma or other contraindications. :contentReference[oaicite:6]{index=6}
• 3. Rhythm control 🔄: consider if symptoms persist despite rate control, in first presentation, younger patients, tachycardia-mediated cardiomyopathy, or when rhythm strategy is preferred. NICE includes cardioversion and catheter ablation within rhythm-control pathways. :contentReference[oaicite:7]{index=7}
• 4. Treat triggers 🩺: sepsis, hyperthyroidism, alcohol excess, PE, ischaemia, post-op state, electrolyte disturbance.

🛡️ Anticoagulation in AF

• 📊 NICE recommends stroke risk assessment using the CHA₂DS₂-VASc score and bleeding risk assessment using the ORBIT score. :contentReference[oaicite:8]{index=8}
• 💊 If anticoagulation is indicated, DOACs are generally preferred over warfarin for most non-valvular AF patients in UK practice. :contentReference[oaicite:9]{index=9}
• 🚫 Do not stop anticoagulation solely because AF is no longer clinically detectable; NICE says decisions should still be based on stroke risk, bleeding risk, and preferences. :contentReference[oaicite:10]{index=10}

🧭 AF: Acute vs Chronic Thinking

• Acute AF often reflects a trigger: infection, surgery, electrolyte disturbance, MI, PE, alcohol, thyrotoxicosis.
• Chronic AF needs a structured long-term plan: anticoagulation, symptom control, echo if indicated, and management of comorbidities.
• ⏳ Duration matters because cardioversion of AF >48 h without appropriate anticoagulation increases embolic risk. :contentReference[oaicite:11]{index=11}

🟦 Atrial Flutter

• 🔁 Usually caused by a macro-re-entrant circuit in the right atrium.
• 📈 ECG classically shows saw-tooth flutter waves, often best seen in inferior leads.
• Management overlaps with AF:
  • rate control
  • anticoagulation assessment
  • cardioversion if indicated
  • catheter ablation is often highly effective

🔄 AVNRT and AVRT

• AVNRT = re-entry within or around the AV node.
• AVRT = re-entry using an accessory pathway (e.g. Wolff–Parkinson–White syndrome).
• 📉 ECG during tachycardia is often a regular narrow-complex tachycardia.
• 🧘 Vagal manoeuvres and adenosine are first-line acute treatments in stable AV node–dependent tachycardia. :contentReference[oaicite:12]{index=12}
• ⚠️ In pre-excited AF, AV nodal blockers can be dangerous because they may increase conduction through the accessory pathway; urgent specialist help is needed. :contentReference[oaicite:13]{index=13}

🟫 Broad-Complex Tachycardia

• 🚨 Assume broad-complex tachycardia is ventricular tachycardia (VT) until proven otherwise, especially in older patients or those with structural heart disease.
• Causes include:
  • VT
  • SVT with bundle branch block
  • pre-excited tachycardia
  • drug / electrolyte-related conduction delay
• ⚠️ If unstable → synchronized cardioversion. :contentReference[oaicite:14]{index=14}

🚨 Ventricular Tachycardia (VT)

• Monomorphic VT 🔁: usually due to re-entry around a scar, commonly after myocardial infarction.
• Polymorphic VT 🌪️: changing QRS morphology; if associated with prolonged QT it is called torsades de pointes.
• Non-sustained VT: self-terminates within 30 seconds.
• Sustained VT: lasts >30 seconds or causes instability.

🛠️ VT Management

• 🚑 Unstable VT with pulse → synchronized DC cardioversion. :contentReference[oaicite:15]{index=15}
• 💉 Stable regular broad-complex tachycardia may be approached using the adult tachyarrhythmia algorithm and specialist input.
• 🧠 Long-term management depends on cause and recurrence risk:
  • treat ischaemia / heart failure / electrolyte abnormalities
  • beta-blockers
  • amiodarone in selected patients
  • catheter ablation
  • ICD for sudden death prevention where indicated
• ESC ventricular arrhythmia guidance strongly supports ICD and ablation strategies in selected high-risk groups. :contentReference[oaicite:16]{index=16}

🌪️ Torsades de Pointes

• Usually occurs with QT prolongation.
• Causes:
  • 💊 drugs (antiarrhythmics, antipsychotics, macrolides, etc.)
  • 🧪 low K+, low Mg2+, low Ca2+
  • 🧬 congenital long QT syndromes
  • 🐌 bradycardia
• Management principles:
  • stop QT-prolonging drugs
  • correct electrolytes
  • give IV magnesium
  • increase heart rate if needed in recurrent episodes

💥 Ventricular Fibrillation (VF)

• ⚡ Completely disorganized ventricular activation → no effective cardiac output.
• 🚨 Treated as cardiac arrest with immediate defibrillation and ALS protocol. :contentReference[oaicite:17]{index=17}

🩻 Ectopic Beats

• Atrial ectopics 🌟: often benign, may trigger SVT or AF.
• Ventricular ectopics / PVCs 💢: common and often benign, but frequent PVCs can be associated with symptoms or PVC-induced cardiomyopathy.
• ESC notes ECG and echocardiography are important in PVC evaluation, and treatment is usually driven by symptoms or PVC burden. :contentReference[oaicite:18]{index=18}

🧪 Reversible Causes of Arrhythmia

• 🫁 Hypoxia
• 🧪 Electrolyte disturbance (K+, Mg2+, Ca2+)
• ❤️ Ischaemia / infarction
• 🦠 Sepsis
• 🫀 Heart failure
• 🦋 Thyroid disease
• 🍷 Alcohol / stimulants / recreational drugs
• 💊 Medication toxicity (digoxin, antiarrhythmics, QT-prolonging drugs)

💊 Antiarrhythmic Drugs: Practical Logic

• Beta-blockers 🛡️: useful for AF rate control, catecholamine-mediated arrhythmias, post-MI protection.
• Rate-limiting calcium-channel blockers ⏸️: diltiazem/verapamil for selected SVTs and AF rate control; avoid in some heart failure settings.
• Adenosine ⚡: diagnostic and therapeutic for regular narrow-complex tachycardia if no pre-excitation. :contentReference[oaicite:19]{index=19}
• Amiodarone 🌪️: broad antiarrhythmic effects but significant long-term toxicities (thyroid, liver, lung, cornea, skin).
• Digoxin 🐢: slows AV nodal conduction, sometimes useful in AF with heart failure, but less effective during high sympathetic tone.
• Class Ic drugs 🎯: can be useful in selected patients but are generally avoided in significant structural heart disease because of pro-arrhythmic risk.

🔌 Cardioversion, Ablation, Devices

• Electrical cardioversion ⚡: used for unstable tachyarrhythmia and selected stable AF/flutter cases.
• Catheter ablation 🧵: definitive or highly effective for many SVTs, atrial flutter, some AF, and selected VT.
• Permanent pacemaker 🔋: used for symptomatic bradycardia, high-grade AV block, and some conduction disease. :contentReference[oaicite:20]{index=20}
• ICD 🚨: prevents sudden death in selected patients at high risk of ventricular arrhythmia. :contentReference[oaicite:21]{index=21}

🧠 Bedside ECG Pattern Recognition

• Regular narrow fast rhythm → think AVNRT/AVRT/atrial tachycardia.
• Irregular narrow fast rhythm → think AF first.
• Saw-tooth atrial activity → think flutter.
• Broad regular fast rhythm → think VT until proven otherwise.
• Broad polymorphic rhythm + long QT → think torsades.
• AV dissociation, capture beats, fusion beats → support VT diagnosis.

🩺 Clinical Assessment in Arrhythmia

• Ask:
  • When did it start? ⏰
  • Any syncope or chest pain? ⚠️
  • Any structural heart disease? 🫀
  • Any stimulant / alcohol / drug trigger? 🍷💊
  • Any family history of sudden death? 🧬
• Examine:
  • pulse rate and regularity
  • blood pressure
  • signs of heart failure
  • thyroid status
  • evidence of systemic illness
• Investigations:
  • 12-lead ECG
  • telemetry / ambulatory monitoring
  • echo
  • U&E, Mg, TFTs, troponin if indicated
  • consider cardiac MRI or EP referral in selected cases

⚠️ Dangerous Arrhythmia Red Flags

• 😵 Syncope during exertion or with palpitations.
• 🧬 Family history of sudden cardiac death.
• 🫀 Known cardiomyopathy or prior MI.
• 📉 Broad-complex tachycardia.
• ⏳ Markedly prolonged QT.
• 💔 High-grade AV block.
• 🌊 Arrhythmia causing heart failure, ischaemia, or shock.

💡 High-Yield Teaching Points

• 🧠 Unstable rhythm = treat the patient first, name the rhythm second.
• 📏 Narrow vs broad and regular vs irregular are the first ECG sorting questions.
• 🔁 Most paroxysmal SVTs are re-entrant.
• 🚨 Broad-complex tachycardia is VT until proven otherwise.
• 🛡️ AF management has 3 pillars: stroke prevention, rate/rhythm control, and trigger treatment.
• 🔋 Persistent complete heart block usually needs pacing.
• 🧪 Always correct K+ and Mg2+ in arrhythmia patients.

📚 References

• NICE Guideline NG196 – Atrial fibrillation: diagnosis and management
• NICE CKS – Atrial fibrillation: New-onset or acute AF
• NICE CKS – Atrial fibrillation: Paroxysmal, persistent, or permanent AF
• Resuscitation Council UK – Adult Advanced Life Support Guidelines
• Resuscitation Council UK – Adult tachyarrhythmia algorithm
• ESC Guidelines – Ventricular arrhythmias and sudden cardiac death
• ESC Guidelines – Supraventricular tachycardia
• ESC/ACC summary – Cardiac pacing and CRT