Cardiac Arrhythmias (Complete)

❤️ Cardiac Arrhythmias — Causes, ECG Diagnosis and Management A comprehensive, compact guide for UK medical students, the UKMLA, foundation/IMT doctors and MRCP candidates. Arrhythmias arise from abnormal impulse formation, abnormal conduction, or both; management is determined by haemodynamic stability, ECG morphology, the underlying cause and thromboembolic/sudden-death risk. ⚠️ First principle: An unstable tachyarrhythmia generally requires urgent electrical treatment; life-threatening bradycardia requires the resuscitation pathway and possible pacing. Prescribing examples are adult educational doses: follow current RCUK, BNF and local specialist protocols.

Cardiac Conduction System and Normal Rhythm

The sinoatrial (SA) node initiates impulses that spread across the atria, pass through the atrioventricular (AV) node and His–Purkinje system, and depolarise the ventricles. Normal sinus rhythm has a P wave before each QRS complex, a constant PR interval and an appropriate rate.

• SA node: Primary pacemaker; intrinsic automaticity is altered by autonomic tone, drugs and metabolic disease.
• AV node: Slow, calcium-dependent conduction creates the PR interval and limits ventricular transmission during rapid atrial rhythms.
• His–Purkinje system: Rapid ventricular activation produces a narrow QRS, usually under 120 ms; bundle branch disease or ventricular origin widens the QRS.
• ECG intervals: PR normally 120–200 ms; QRS below 120 ms; QT varies with heart rate and must be corrected (QTc).
• Automaticity, triggered activity and re-entry: The three major mechanisms responsible for tachyarrhythmias.

💡 Clinical Pearl: A narrow QRS suggests ventricular activation through the normal His–Purkinje system; a broad QRS may arise from VT, bundle branch block, pacing or pre-excitation.

Mechanisms of Arrhythmia

• Increased automaticity: Enhanced spontaneous pacemaker firing; examples include sinus tachycardia and some focal atrial tachycardias.
• Abnormal automaticity: Latent pacemaker tissue develops spontaneous depolarisation during ischaemia or electrolyte disturbance.
• Triggered activity: Early afterdepolarisations occur with prolonged repolarisation and may initiate torsades de pointes; delayed afterdepolarisations can follow catecholamine excess or digoxin toxicity.
• Re-entry: An impulse circulates repeatedly around tissue with different conduction speeds and refractory periods; causes AVNRT, AVRT, typical atrial flutter and many monomorphic VTs.
• Substrate plus trigger: Scar, fibrosis, hypertrophy or an accessory pathway creates susceptibility; ectopy, ischaemia, electrolyte abnormalities or adrenergic stimulation precipitate the episode.

💡 Clinical Pearl: Monomorphic VT after myocardial infarction is commonly scar-related re-entry, whereas torsades is linked to abnormal repolarisation and early afterdepolarisations.

Causes and Reversible Triggers

• Cardiac disease: Acute coronary syndrome, old MI scar, heart failure, cardiomyopathy, myocarditis, valvular disease, congenital heart disease and postoperative inflammation.
• Physiological stress: Fever, sepsis, pain, hypovolaemia, haemorrhage, hypoxia, pulmonary embolism, anaemia and pregnancy.
• Endocrine/metabolic: Thyrotoxicosis, electrolyte disturbance (K, Mg, Ca), hypoglycaemia, acidosis and severe renal impairment.
• Drugs/toxins: Beta agonists, theophylline, digoxin, sympathomimetics, alcohol, cocaine, amphetamines, excess caffeine and medications prolonging QT.
• Bradycardia causes: Age-related conduction fibrosis, inferior MI, AV nodal blockers, hyperkalaemia, hypothyroidism, raised intracranial pressure and sleep-related vagal tone.
• Inherited disease: Channelopathies (long QT, Brugada, CPVT), inherited cardiomyopathy and familial conduction disease.

💡 Clinical Pearl: Treat the cause as well as the rhythm. Sinus tachycardia in sepsis is often a compensatory response; cardioverting or simply slowing it may harm the patient.

Clinical Presentation and Red Flags

• Symptoms: Palpitations, skipped beats, dizziness, presyncope, syncope, fatigue, reduced exercise tolerance, chest discomfort or dyspnoea.
• Haemodynamic compromise: Shock, severe or ongoing hypotension with syncope, myocardial ischaemia, acute pulmonary oedema, or immediately post-ROSC.
• High-risk history: Syncope during exertion or while supine, family history of sudden death under 40, known cardiomyopathy, congenital heart disease or prior ventricular arrhythmia.
• Examination: ABCDE, pulse regularity, BP, oxygen saturation, JVP, signs of heart failure, murmurs, perfusion and neurological status.
• History details: Abrupt versus gradual onset/offset; duration; frequency; exertional triggers; medicines; alcohol/stimulants; previous ECG; personal and family history.
• Immediate action: Monitor ECG, obtain 12-lead ECG where possible, gain IV access, correct reversible causes and summon senior/resuscitation help for instability.

💡 Clinical Pearl: Syncope associated with a palpitation immediately beforehand, exertion, structural heart disease or an abnormal ECG deserves urgent cardiac assessment.

Stepwise ECG Interpretation

• 1. Rate: Estimate the ventricular and atrial rate; compare them if P waves can be identified.
• 2. Regularity: Regular or irregular R–R intervals; irregularly irregular suggests AF, but irregular broad-complex rhythms have additional dangerous causes.
• 3. QRS duration: Narrow under 120 ms or broad 120 ms and above; initially presume a broad-complex tachycardia is VT until reliably established otherwise.
• 4. Atrial activity: Sinus P waves, flutter waves, absent discrete P waves, retrograde P waves or AV dissociation.
• 5. PR and QTc: Look for AV block, pre-excitation (short PR with delta wave) and prolonged QT.
• 6. Morphology: Capture/fusion beats and AV dissociation favour VT; compare with an old ECG for pre-existing bundle branch block.
• 7. Patient first: Do not delay emergency electrical treatment to complete the ECG analysis in a patient with adverse features.

💡 Clinical Pearl: A ventricular rate around 150/min with an apparently regular narrow QRS should prompt a search for 2:1 atrial flutter, not just “SVT”.

Investigations and Rhythm Monitoring

• Baseline: 12-lead ECG during symptoms, FBC, U&E, magnesium, calcium, thyroid tests when indicated, and troponin if ACS or injury is suspected.
• Echocardiography: Assess structural heart disease, LV/RV function, valves and atrial enlargement.
• 24–48-hour Holter: Useful when episodes occur daily; quantify ventricular ectopic burden and correlate symptoms.
• Patch/event recorder: Use for less frequent palpitations over days or weeks; select duration according to symptom frequency.
• Implantable loop recorder: Useful for infrequent unexplained syncope or suspected intermittent high-risk arrhythmia.
• Exercise ECG or imaging: Consider exertional symptoms, exercise-triggered arrhythmia or suspected ischaemia, after excluding contraindications.
• Cardiac MRI / electrophysiology: For suspected myocarditis, scar, inherited cardiomyopathy or specialist mechanism assessment.
• Family assessment: Consider genetic counselling, targeted testing and cascade screening for inherited arrhythmia syndromes.

Sinus Tachycardia

• ECG: Regular rhythm, sinus P wave before each QRS, usually rate above 100/min with gradual onset and resolution.
• Causes: Exercise, anxiety, pain, pyrexia, sepsis, haemorrhage, dehydration, anaemia, PE, hypoxia, thyrotoxicosis, stimulants and medication withdrawal.
• Assessment: Find the precipitant, examine perfusion and volume status, review ECG and blood results.
• Management: Treat the underlying cause: fluids when hypovolaemic, oxygen when hypoxaemic, antibiotics where indicated and analgesia. Do not routinely cardiovert or suppress the compensatory sinus rate.
• Inappropriate sinus tachycardia: Persistent symptomatic sinus tachycardia without an appropriate trigger is a diagnosis of exclusion; consider specialist management.

💡 Clinical Pearl: Sinus tachycardia is usually a sign, not a primary rhythm disorder.

Sinus Bradycardia

• ECG: Sinus P wave before each QRS at a rate below 60/min; can be normal during sleep and in trained athletes.
• Causes: Vagal tone, beta blockers, verapamil/diltiazem, digoxin, hypothyroidism, hypothermia, inferior MI and sinus node dysfunction.
• Assess: Symptoms, haemodynamics, medication history, electrolytes, ECG, thyroid function and evidence of reversible disease.
• Management: Asymptomatic physiological bradycardia often needs no intervention; symptomatic or unstable cases follow the bradyarrhythmia algorithm.
• Persistent symptomatic disease: Consider specialist assessment for permanent pacing where symptoms correlate with bradycardia.

Atrial and Ventricular Ectopic Beats

• Premature atrial complexes (PACs): Early atrial P wave, often with different morphology, followed by normal or sometimes aberrant QRS; may predispose to AF.
• Premature ventricular complexes (PVCs): Early broad QRS without a preceding conducted P wave, usually followed by a compensatory pause.
• Triggers: Caffeine, alcohol, sympathetic stimulation, electrolyte disturbance, myocardial ischaemia and structural heart disease.
• Investigations: ECG, ambulatory monitor to quantify ectopic burden, echocardiography if frequent/symptomatic or abnormal ECG; consider MRI if structural disease is suspected.
• Management: Reassurance for benign low-burden ectopy, treat triggers; beta blocker may improve symptoms; catheter ablation for selected highly symptomatic or high-burden PVCs.
• PVC cardiomyopathy: A sustained high PVC burden (often around 10% or more) can contribute to reversible LV dysfunction; interpret alongside ventricular function and morphology.

💡 Clinical Pearl: A PVC is not automatically dangerous. The important questions are burden, symptoms, LV function, morphology and evidence of structural heart disease.

Supraventricular Tachycardia: General Approach

• Definition: Tachyarrhythmia arising above the ventricles; includes AVNRT, AVRT, atrial tachycardia, flutter and AF, although “SVT” often refers to regular paroxysmal narrow-complex tachycardia.
• ECG: Regular narrow QRS in typical AVNRT/AVRT, with P waves frequently hidden or retrograde; abrupt onset and termination.
• Stable regular narrow-complex SVT: Modified Valsalva first; if unsuccessful, monitored adenosine 6 mg IV rapid bolus, then 12 mg, then 18 mg as in RCUK March 2026 algorithm, when appropriate.
• After failed adenosine: Consider specialist-guided verapamil or beta blocker if suitable, or synchronised cardioversion.
• Unstable patient: Synchronised cardioversion with appropriate sedation/anaesthesia if conscious and time permits.
• Contraindications / cautions: Adenosine can provoke bronchospasm; avoid in pre-excited AF or an irregular broad-complex rhythm; use caution with heart transplant and relevant drug interactions.

💡 Clinical Pearl: Adenosine briefly blocks AV nodal conduction. It may terminate AV node-dependent re-entry but often only unmasks flutter waves or atrial activity in atrial tachycardia.

AV Nodal Re-entrant Tachycardia (AVNRT)

• Mechanism: Re-entry within or adjacent to the AV node through dual fast and slow pathways; the commonest regular paroxysmal SVT in adults.
• ECG: Regular narrow-complex tachycardia, often 150–250/min, with buried or very short-RP retrograde P waves; pseudo-r' in V1 or pseudo-S in inferior leads may occur.
• Clinical features: Sudden palpitations, sometimes neck pounding from simultaneous atrial and ventricular contraction; usually haemodynamically tolerated.
• Acute management: Vagal manoeuvres then adenosine if stable; synchronised cardioversion if unstable.
• Prevention: Avoid triggers where relevant, consider beta blocker or non-dihydropyridine calcium blocker in suitable patients; slow-pathway catheter ablation is highly effective.

AV Re-entrant Tachycardia and Wolff–Parkinson–White

• Mechanism: An accessory atrioventricular pathway permits re-entry involving atria and ventricles; orthodromic AVRT generally has a narrow QRS, antidromic AVRT a broad QRS.
• WPW pattern: Short PR interval, delta wave (slurred initial QRS upstroke), broad QRS when manifest pre-excitation is present.
• WPW syndrome: Pre-excitation associated with symptomatic tachyarrhythmia.
• Major risk: AF conducted rapidly down an accessory pathway may degenerate to VF; ECG may be an extremely rapid irregular broad-complex tachycardia with variable QRS morphology.
• Stable orthodromic AVRT: Vagal manoeuvres/adenosine may be used when diagnosis is secure and pre-excited AF has been excluded, with monitoring and defibrillation available.
• Pre-excited AF: Urgent specialist help; electrical cardioversion if unstable; procainamide may be considered in selected stable patients.
• Avoid in pre-excited AF: Adenosine, beta blockers, verapamil, diltiazem, digoxin and IV amiodarone can be dangerous; do not use AV nodal blockade.
• Definitive management: Electrophysiological evaluation and accessory pathway ablation, particularly with symptomatic or high-risk pathways.

💡 Critical Safety Pearl: Irregular, very fast, wide-complex tachycardia in WPW is a potential pre-arrest rhythm: the main error is giving an AV nodal blocker.

Focal Atrial Tachycardia

• Mechanism: An ectopic atrial focus drives the atria independently of the sinus node; may arise from automaticity, triggered activity or micro-re-entry.
• ECG: Atrial rate often 100–250/min; abnormal P-wave axis or shape; possible warm-up/cool-down and variable AV conduction.
• Causes: Structural disease, postoperative scarring, pulmonary disease, catecholamine excess and digoxin toxicity.
• Management: Treat cause; rate control with beta blocker or suitable calcium blocker; adenosine may identify atrial activity but frequently does not terminate the mechanism; catheter ablation for recurrent symptomatic episodes.
• Clinical risk: Incessant atrial tachycardia may cause tachycardia-induced cardiomyopathy.

Atrial Fibrillation: Causes, Types and ECG

• Mechanism: Disorganised atrial activation, often initiated by pulmonary-vein triggers in an abnormal atrial substrate; loss of effective atrial contraction and irregular AV conduction.
• ECG: No consistent discrete P waves; irregularly irregular R–R intervals, usually narrow QRS unless aberrancy or pre-excitation.
• Phenotypes: First-diagnosed, paroxysmal (terminates within 7 days), persistent (over 7 days or requiring termination) and permanent (shared decision not to restore sinus rhythm).
• Causes: Hypertension, coronary disease, heart failure, valvular disease, obesity, OSA, hyperthyroidism, alcohol, infection, postoperative state and ageing.
• Clinical impact: Palpitations, fatigue, dyspnoea, stroke/systemic embolism, loss of atrial contribution to filling and tachycardia-mediated cardiomyopathy.
• Investigations: ECG confirmation, renal function, thyroid tests, FBC, echocardiography when structural assessment changes management, and assessment for triggers.
• Framework: Address comorbidities and risks, prevent stroke, choose rate/rhythm control, and reassess regularly.

💡 Clinical Pearl: Atrial fibrillation is both a rhythm problem and a long-term thromboembolic risk state; restoring sinus rhythm does not automatically remove the indication for anticoagulation.

AF: Stroke Risk and Anticoagulation

• UK stroke score: NICE NG196 uses CHA2DS2-VASc: heart failure 1, hypertension 1, age ≥75 = 2, diabetes 1, stroke/TIA/thromboembolism 2, vascular disease 1, age 65–74 = 1, female sex 1.
• NICE treatment threshold: Offer a DOAC when CHA2DS2-VASc ≥2 and bleeding risk is acceptable; consider for men with a score of 1. Do not anticoagulate solely for female sex.
• Bleeding risk: Use ORBIT under NICE to identify and modify bleeding risk; a high score prompts intervention and shared decision-making, not automatic withholding.
• Anticoagulant choice: DOAC usually preferred; use warfarin/VKA for mechanical prosthetic valves or moderate–severe rheumatic mitral stenosis. Check renal function using Cockcroft–Gault CrCl for drug dosing.
• Cardioversion timing: NICE guidance has historically allowed consideration of rhythm control for AF of definite onset under 48 h; ESC 2024 recommends a more cautious 24-hour threshold before elective cardioversion without ≥3 weeks of therapeutic anticoagulation or TOE exclusion of thrombus.
• After cardioversion: Anticoagulation for at least 4 weeks in most patients and indefinitely when stroke-risk criteria justify it, regardless of apparent sinus rhythm.
• Not substitutes: Aspirin is not an adequate alternative to oral anticoagulation for stroke prevention in AF.

💡 MRCP Pearl: NICE CHA2DS2-VASc and ESC CHA2DS2-VA scores are not identical. UK practice should use the local NICE pathway; distinguish emergency cardioversion for instability from elective cardioversion planning.

AF: Rate Control

• Objective: Reduce symptoms and avoid tachycardia-mediated cardiomyopathy; a resting rate below roughly 110/min is a reasonable initial lenient target for many stable patients, tightened if symptoms persist.
• First-line in suitable patients: Oral beta blocker (for example bisoprolol) or rate-limiting calcium blocker (diltiazem/verapamil) when LV systolic function permits.
• HFrEF: Use appropriately titrated beta blocker when stable; digoxin can be useful, especially when sedentary or BP limits other agents. Do not use verapamil/diltiazem in reduced EF or acutely decompensated HF.
• Digoxin limitations: Less effective during exertion or high sympathetic tone; monitor renal function, potassium, interacting drugs and toxicity.
• Acute AF with decompensated HF: Seek senior input. Avoid non-dihydropyridine calcium blockers; electrical cardioversion for instability, with carefully selected digoxin or amiodarone in specialist settings.
• Refractory rate control: Specialist consideration of rhythm control or AV node ablation with pacing.

AF: Rhythm Control and Cardioversion

• When to consider: Persistent symptoms despite good rate control, new-onset AF, tachycardia cardiomyopathy, selected HF patients, patient preference or unsuitable rate-control strategy.
• Electrical cardioversion: Synchronised shock under appropriate sedation or anaesthesia; immediate if life-threatening instability due to the rhythm.
• Pharmacological cardioversion: Flecainide in suitable patients without structural/ischaemic disease; amiodarone can be considered when structural heart disease is present; choose with cardiology expertise.
• Antiarrhythmic maintenance: Selected use of beta blockers, flecainide, dronedarone, sotalol or amiodarone according to heart disease, QT, renal function and interactions.
• Catheter ablation: Pulmonary vein isolation for symptomatic AF in selected patients; especially relevant for recurrent paroxysmal AF and some AF-related cardiomyopathy.
• Stroke prevention: Continue or stop long-term anticoagulation based on stroke risk and patient factors—not just ablation success or a normal follow-up ECG.
• Emergency nuance: Life-threatening unstable AF may require immediate cardioversion before the usual elective anticoagulation pathway; anticoagulate as soon as clinically appropriate.

Atrial Flutter

• Mechanism: Typical flutter is a macro-re-entrant circuit around the tricuspid annulus through the cavotricuspid isthmus.
• ECG: Sawtooth flutter waves, often prominent in II, III and aVF; atrial rate near 300/min; 2:1 conduction produces ventricular rate near 150/min.
• Causes: Structural heart disease, chronic lung disease, postoperative atrial scar and AF-related atrial disease.
• Acute treatment: Assess instability and provide synchronised cardioversion if required; otherwise careful rate control, sometimes difficult to achieve.
• Long-term: Cavotricuspid isthmus ablation is highly effective for typical flutter.
• Anticoagulation: Assess stroke risk as for AF; after flutter ablation, subsequent AF risk remains important.

💡 Clinical Pearl: Regular narrow-complex tachycardia at approximately 150/min should trigger the question: “Is this atrial flutter with 2:1 block?”

Multifocal Atrial Tachycardia (MAT)

• ECG: Irregular atrial tachycardia with ≥3 distinct P-wave morphologies, variable P–P and PR intervals, and an identifiable isoelectric baseline.
• Causes: Severe COPD, hypoxia, infection, theophylline, electrolyte disturbance or other acute illness.
• Management: Correct hypoxia and triggers, replace magnesium/potassium as needed; selected rate control if tolerated, usually guided by the underlying pulmonary and cardiac state.
• Key distinction: Unlike AF, discrete P waves of different shapes are present; routine AF cardioversion and anticoagulation are not indicated solely for MAT.

Broad-Complex Tachycardia: Differential

• Most important: VT must be assumed unless another diagnosis is confidently established, particularly in older patients, with previous MI or cardiomyopathy.
• Other causes: SVT with aberrant bundle branch conduction, pre-excited AVRT, ventricular pacing, severe hyperkalaemia or sodium-channel blocker toxicity.
• VT clues: AV dissociation, capture beats, fusion beats, extreme axis, concordance across chest leads, and atypical bundle branch morphology.
• Regular broad complex: Treat as monomorphic VT when uncertain; expert ECG interpretation and cardioversion planning.
• Irregular broad complex: Consider pre-excited AF, AF with bundle branch block, polymorphic VT and artefact; identify dangerous drug contraindications.
• Unstable: Synchronised cardioversion for organised tachycardia with a pulse; unsynchronised defibrillation for VF/pulseless VT or when synchronisation cannot be achieved in a life-threatening polymorphic rhythm.

💡 Critical Safety Pearl: Do not rely on the patient being awake and talking to rule out VT. Stable monomorphic VT is often initially well tolerated.

Monomorphic Ventricular Tachycardia

• Definition / ECG: At least 3 consecutive ventricular beats, usually broad and regular with a uniform QRS shape, often rate above 100/min.
• Causes: Old MI scar, dilated/arrhythmogenic cardiomyopathy, myocarditis, inherited disease or idiopathic outflow tract VT.
• Clinical presentation: Palpitations, presyncope, syncope, chest pain, hypotension and potentially cardiac arrest.
• Management if unstable: Immediate synchronised cardioversion; use sedation/anaesthesia if conscious and feasible; correct ischaemia and electrolytes.
• Stable monomorphic VT: RCUK March 2026 favours synchronised cardioversion for most; if sedation risks are high, expert-guided procainamide 10–15 mg/kg IV over 20 min (maximum 1 g), or amiodarone 300 mg IV over 10–60 min followed by 900 mg over 24 h when procainamide unsuitable.
• Prevention: Investigate scar or cardiomyopathy, optimise HF/ischaemia therapy, assess ICD indications and consider catheter ablation for recurrent VT.

💡 Clinical Pearl: Scar-related VT after MI may be haemodynamically stable, but recurrence and sudden-death risk require specialist evaluation.

Polymorphic VT and Torsades de Pointes

• Polymorphic VT: Changing QRS morphology and axis; may be associated with acute ischaemia or prolonged QT.
• Torsades: Polymorphic VT occurring in a prolonged-QT setting with characteristic twisting of QRS polarity around baseline.
• Causes of acquired QT prolongation: Low potassium, magnesium or calcium; bradycardia; QT-prolonging drugs; renal/hepatic drug accumulation.
• Immediate response: If pulseless or unstable with unsynchronisable rhythm, defibrillate according to ALS; stop offending medicines and urgently correct electrolytes.
• RCUK 2026 torsades regimen: Magnesium sulfate 8 mmol IV over 10 min; consider isoprenaline or temporary overdrive pacing for pause-dependent recurrent torsades with expert input.
• Avoid: Amiodarone and other QT-prolonging antiarrhythmics in long-QT-related torsades.
• Differentiate: Polymorphic VT with normal QT from acute ischaemia may require urgent coronary reperfusion and different antiarrhythmic strategy.

💡 Clinical Pearl: Torsades is a type of polymorphic VT, but not every polymorphic VT is torsades. The QT interval matters.

Ventricular Fibrillation and Pulseless VT

• Recognition: Cardiac arrest without a pulse; VF is chaotic electrical activity, while pulseless VT has organised fast ventricular complexes but no effective circulation.
• Treatment: Call 2222 in hospital; CPR, defibrillator pads and immediate unsynchronised shocks for shockable rhythm, with 2-minute CPR cycles.
• Defibrillation: Follow device-specific biphasic recommendations; RCUK generally specifies first shock ≥150 J for most biphasic waveforms, with escalation when appropriate.
• Adrenaline: 1 mg IV/IO after the third shock for shockable arrest, then every 3–5 min.
• Amiodarone: 300 mg IV/IO after three shocks; 150 mg after five shocks for recurrent/persistent VF/pVT. Lidocaine is an alternative where specified.
• Reversible causes: Four Hs and four Ts: hypoxia, hypovolaemia, hypo/hyperkalaemia or metabolic disturbance, hypothermia; tension pneumothorax, tamponade, toxins, thrombosis (coronary/pulmonary).
• After ROSC: Treat cause, assess for coronary occlusion, manage oxygenation, haemodynamics, temperature and neurological care.

PEA and Asystole

• PEA: Electrical activity without a palpable pulse or effective cardiac output; non-shockable.
• Asystole: Absent detectable ventricular electrical activity; check leads, gain and distinguish fine VF where uncertain.
• Treatment: CPR, oxygenation/ventilation, IV/IO access and adrenaline 1 mg as soon as possible then every 3–5 min.
• Do not shock: PEA and true asystole are non-shockable; defibrillation is not indicated.
• Reversible causes: Search actively for four Hs and four Ts, especially hypoxia, hypovolaemia, hyperkalaemia, pulmonary embolism and tamponade.
• P waves without QRS: Ventricular standstill can sometimes respond to pacing; identify on the tracing and seek specialist help.

RCUK 2026 Tachyarrhythmia Algorithm

• Initial: ABCDE, monitor ECG/BP/SpO2, 12-lead ECG if feasible, IV access, treat reversible causes and give oxygen if hypoxaemic.
• Life-threatening features: Shock, syncope with severe/ongoing hypotension, myocardial ischaemia, severe HF with pulmonary oedema, or immediately post-ROSC.
• Unstable tachyarrhythmia: Synchronised cardioversion up to 3 attempts; appropriate sedation/anaesthesia when conscious. If unsuccessful give amiodarone 300 mg IV over 10–20 min OR procainamide 10–15 mg/kg (maximum 1 g) over 20 min and repeat shock.
• Stable regular narrow-complex: Vagal manoeuvres, then adenosine 6 mg → 12 mg → 18 mg by rapid IV bolus when no pre-excitation; then specialist-guided beta blocker/verapamil or cardioversion.
• Stable irregular narrow-complex: Usually AF: select rate control based on EF, anticoagulation status and clinical context.
• Stable regular broad-complex: Treat as VT; synchronised cardioversion preferred; monitored antiarrhythmic option if sedation/anaesthesia presents excessive risk.
• Stable irregular broad-complex: Consider pre-excited AF and polymorphic VT; obtain expert advice, avoid AV nodal blockers if pre-excitation is suspected.
• Sinus tachycardia: Not covered by the peri-arrest tachyarrhythmia treatment pathway: correct the underlying cause rather than giving antiarrhythmics or cardioversion.

💡 Resuscitation Pearl: Electrical treatment depends on whether the patient has a pulse and whether the shock can be safely synchronised. Unstable organised VT with a pulse is cardioverted; VF/pulseless VT is defibrillated.

RCUK 2025 Bradyarrhythmia Algorithm

• Initial: ABCDE, monitor, 12-lead ECG, IV access, identify reversible causes and review rate-slowing medicines.
• Adverse features: Shock, syncope, myocardial ischaemia or severe heart failure; assess severity rather than treating the heart rate alone.
• Atropine: 500 micrograms IV; repeat every 3–5 min as needed to a maximum cumulative 3 mg for symptomatic bradycardia when appropriate.
• When atropine is ineffective: Consider isoprenaline infusion (starting 5 micrograms/min) or adrenaline infusion (2–10 micrograms/min) in a monitored setting while arranging pacing.
• High-degree block with broad QRS: Do not give atropine: it is unlikely to be effective and may worsen block; expedite pacing.
• Cardiac transplant: Avoid atropine; aminophylline 100–200 mg slow IV may be considered with specialist advice.
• Pacing: Transcutaneous pacing as a bridge to urgent transvenous pacing when instability persists.
• Additional causes: If beta blocker or calcium blocker toxicity suspected, seek toxicology advice; glucagon and other specific treatment may be relevant.
• Ongoing risk: Even after initial improvement, high-grade AV block, asystolic pauses or recent asystole merit monitoring and definitive pacing assessment.

Cardioversion, Defibrillation and Sedation

• Synchronised cardioversion: Shock timed to the R wave, avoiding delivery during the T wave; for unstable tachyarrhythmia with a pulse.
• Initial energy in RCUK guidance: AF: maximum defibrillator output is reasonable; atrial flutter/regular PSVT: 70–120 J; VT with a pulse: 120–150 J, increasing if needed.
• Defibrillation: Unsynchronised shock for VF, pulseless VT or critical polymorphic VT that cannot be safely synchronised.
• Sedation: Conscious cardioversion requires appropriately skilled anaesthesia/sedation and airway monitoring; do not allow avoidable delay in an immediately life-threatening situation.
• After shock: Reassess rhythm, pulse, BP and clinical response; treat underlying trigger and decide on recurrence prevention.

Sinus Node Dysfunction and Tachy–Brady Syndrome

• Mechanism: Degeneration or fibrosis of the SA node/atrial tissue produces inappropriate bradycardia, sinus pauses or chronotropic incompetence.
• Tachy–brady: Alternating AF or atrial tachyarrhythmias and symptomatic sinus pauses, sometimes after termination of AF.
• Features: Fatigue, dizziness, exercise intolerance, presyncope or syncope.
• Investigations: ECG, symptom-correlated Holter or loop recording, medicine review and echo as indicated.
• Management: Remove reversible rate-limiting factors; permanent pacemaker when symptoms are attributable to significant bradycardia/pauses.
• AF treatment: Pacing may permit necessary rate-control medication, but does not itself prevent AF-related stroke.

First-Degree and Second-Degree AV Block

• First-degree AV block: PR over 200 ms with every P wave conducted; usually observation unless symptoms, marked PR prolongation or underlying progressive disease.
• Mobitz I (Wenckebach): Progressive PR lengthening followed by a dropped QRS; usually AV nodal, often transient/vagal, but clinical context matters.
• Mobitz II: Fixed PR in conducted beats with sudden non-conducted P waves; often infranodal and more likely to progress to complete block.
• 2:1 AV block: Every second P wave blocked; cannot reliably distinguish Mobitz I from II on that strip alone, so assess QRS, context and conduction system disease.
• Causes: Age-related fibrosis, ischaemia, myocarditis, medications, electrolyte disturbance and infiltrative disease.
• Management: Assess symptoms and reversibility; Mobitz II and high-grade AV block usually need urgent specialist assessment and pacing, even if temporarily stable.

💡 Clinical Pearl: The important distinction is level of block and risk of progression, not simply the measured ventricular rate.

Complete Heart Block and High-Grade Block

• Complete AV block: Atria and ventricles beat independently; no P–QRS relationship, often with a slow escape rhythm.
• Narrow escape: Often junctional and may be relatively more stable.
• Broad escape: Often ventricular and may be unreliable, especially in acute anterior MI.
• Symptoms: Syncope (Stokes–Adams attacks), fatigue, hypotension, chest pain, heart failure or cardiac arrest.
• Acute management: Monitor closely, correct reversible causes, follow RCUK bradyarrhythmia pathway and prepare for transcutaneous/transvenous pacing when unstable.
• Definitive management: Permanent pacemaker for persistent or non-reversible high-grade or complete AV block in appropriate patients.
• MI distinction: Inferior MI often produces transient nodal block; anterior MI with infranodal block suggests extensive septal injury and worse prognosis.

Bundle Branch and Bifascicular Block

• Right bundle branch block: QRS ≥120 ms with rsR' or related morphology in V1 and broad terminal S waves in I/V6.
• Left bundle branch block: QRS ≥120 ms with broad/notched lateral R waves and predominantly negative V1; alters ST–T interpretation and may indicate structural disease.
• Bifascicular block: Usually RBBB with left anterior or left posterior fascicular block; important when accompanied by unexplained syncope.
• Clinical interpretation: Bundle branch block alone is not an indication for a pacemaker; investigate structural disease and symptom correlation.
• Syncope with conduction disease: Urgent specialist evaluation; ambulatory monitoring, electrophysiological testing or pacing may be required depending on findings.
• Heart failure: LBBB with wide QRS and reduced EF may identify patients eligible for CRT after appropriate optimisation.

Long QT Syndrome

• Mechanism: Prolonged ventricular repolarisation allows early afterdepolarisations and torsades; congenital or acquired.
• ECG: Prolonged rate-corrected QT; measure carefully and review T–U waves. A QTc around 500 ms or more raises particular concern in acquired disease.
• Causes: KCNQ1/KCNH2/SCN5A and other genetic variants, QT-prolonging medicines, hypokalaemia, hypomagnesaemia, hypocalcaemia and bradycardia.
• Symptoms: Syncope, seizure-like episodes, palpitations or sudden cardiac arrest.
• Management: Stop QT-prolonging drugs, replace electrolytes, specialist beta-blocker therapy (often nadolol/propranolol in congenital disease), exercise/trigger advice and ICD in selected high-risk patients.
• Acute torsades: Magnesium, correction of potassium and pacing/isoprenaline where appropriate for pause-dependent acquired forms.
• Family: Genetic counselling and screening when inherited syndrome suspected.

💡 Clinical Pearl: A prolonged QT may be masked by tachycardia or distorted by wide QRS. Always check the medication list and potassium, magnesium and calcium.

Brugada Syndrome, CPVT and Short QT

• Brugada syndrome: Coved ST elevation in V1–V3 in a characteristic type-1 pattern; arrhythmic syncope/VF risk. Fever can unmask the pattern; treat fever, avoid implicated drugs, and assess ICD need in high-risk patients.
• Catecholaminergic polymorphic VT (CPVT): Structurally normal heart at rest, exercise/emotion-triggered bidirectional or polymorphic ventricular arrhythmia, often in the young. Specialist beta blockade, exercise advice, flecainide/other interventions in selected cases.
• Short QT syndrome: Very short QT interval and inherited atrial/ventricular arrhythmia risk; specialist ECG/genetic evaluation and sudden death risk assessment.
• General red flags: Young patient with exertional syncope, unexplained seizure-like collapse or family history of premature sudden death requires assessment for inherited electrical disease.
• Family prevention: Refer to inherited cardiac conditions service for cascade screening and counselling.

Arrhythmias in Structural Heart Disease

• Previous MI: Ventricular scar supports re-entrant VT; acute ischaemia may precipitate VF or polymorphic VT.
• HFrEF / dilated cardiomyopathy: AF, frequent PVCs, conduction abnormalities, sustained VT and sudden death risk.
• Hypertrophic cardiomyopathy: AF can markedly impair ventricular filling; NSVT and specific risk factors guide sudden death assessment.
• Arrhythmogenic cardiomyopathy: Ventricular arrhythmias may precede overt heart failure; genetic evaluation and exercise restriction are important.
• Amyloidosis/sarcoidosis: AF, conduction disease and potentially ventricular arrhythmias; underlying diagnosis changes management.
• Myocarditis: Transient or persistent ventricular arrhythmia and conduction disease; investigate inflammation and LV function.
• Management principle: Treat underlying disease, optimise heart failure therapy and assess need for ICD, CRT or ablation rather than focusing on a single ECG episode.

Drug-Induced Arrhythmias and Electrolytes

• Hypokalaemia: Increases ectopy and ventricular arrhythmias; worsens digoxin toxicity and prolongs repolarisation.
• Hyperkalaemia: Peaked T waves, PR prolongation, loss of P waves, QRS widening and risk of sine-wave/arrest; ECG can be deceptively normal. Treat urgently per hyperkalaemia pathway.
• Hypomagnesaemia: Predisposes to torsades and refractory hypokalaemia.
• Hypocalcaemia: Prolongs QT; hypercalcaemia may shorten QT.
• Digoxin toxicity: Atrial tachycardia with block, junctional rhythms, bidirectional VT and AV block; assess ECG, renal function, K and drug interactions; consider digoxin-specific antibody fragments in severe toxicity.
• QT-prolonging medications: Some macrolides, fluoroquinolones, antipsychotics, antiemetics, methadone and class Ia/III antiarrhythmics; assess combinations and patient-specific risk.
• Sodium-channel blocker toxicity: Tricyclic antidepressants and some antiarrhythmics may widen QRS and cause VT; specialist toxicology management, often sodium bicarbonate in appropriate poisoning.

💡 Clinical Pearl: A “normal” serum potassium does not remove arrhythmia risk when QT-prolonging medicines, structural disease or profound bradycardia coexist.

Pacemakers: Indications and Complications

• What a pacemaker does: Detects intrinsic electrical activity and stimulates the heart when programmed pacing criteria are met; single-, dual-chamber and leadless systems exist.
• Common indications: Symptomatic sinus node dysfunction, persistent complete or Mobitz II AV block, selected bifascicular-block-associated syncope, and some post-procedural conduction disease.
• Not enough alone: An isolated slow rate during sleep or asymptomatic first-degree block generally does not mandate pacing.
• Dual chamber: Maintains AV synchrony when useful and atrial activity is appropriate.
• Complications: Pocket haematoma, infection, pneumothorax, lead displacement or failure, perforation, pacing-induced cardiomyopathy and device interactions.
• Pacemaker ECG: May show pacing spikes and broad paced QRS; pacing does not protect against VF unless combined with a defibrillator.
• Follow-up: Interrogation, battery/lead checks and infection precautions by a device team.

ICDs, CRT and Sudden Death Prevention

• ICD: Monitors and treats dangerous VT/VF with antitachycardia pacing or shocks; indicated for selected secondary and primary prevention populations.
• Secondary prevention: Consider after sustained VT/VF not attributable to a fully reversible cause, after specialist assessment.
• Primary prevention: Depends on LV function, underlying disease, duration of optimisation, predicted benefit and comorbidity; NICE TA314 and specialist risk models inform selection.
• CRT: Synchronises ventricular activation in selected HF patients with reduced EF and electrical dyssynchrony, especially LBBB with broad QRS.
• Complications: Inappropriate shocks, infection, lead failure, psychological burden and recurrent VT storm.
• Goals of care: Discuss device shocks and deactivation in advanced disease or palliative settings without equating this with withdrawal of all cardiac treatment.
• Family screening: Inherited cardiomyopathy/channelopathy may warrant assessment of first-degree relatives.

Catheter Ablation and Electrophysiology

• EP study: Uses intracardiac recordings and pacing to identify arrhythmia mechanism and conduction pathways.
• AVNRT: Slow-pathway ablation is highly effective with small but real AV block risk.
• AVRT/WPW: Accessory-pathway ablation can be curative, particularly for symptomatic or high-risk pre-excitation.
• Typical atrial flutter: Cavotricuspid isthmus ablation is usually very effective.
• AF: Pulmonary vein isolation by radiofrequency, cryoballoon or pulsed-field approaches in selected patients.
• PVC/VT: Ablation may reduce arrhythmia burden in focal PVCs or recurrent monomorphic scar-related VT.
• Risks: Bleeding, vascular damage, pericardial effusion/tamponade, stroke, heart block and procedure-specific complications.
• Outcome: Even after apparent successful AF ablation, anticoagulation is based on thromboembolic risk.

Arrhythmias in Older Adults and Frailty

• Common patterns: AF, sinus node disease, AV block, atrial ectopy and drug-associated bradycardia become more frequent with age.
• Multifactorial symptoms: Syncope may combine arrhythmia, postural hypotension, dehydration, autonomic dysfunction and medication effects.
• Medication review: Beta blockers, digoxin, amiodarone, verapamil/diltiazem, psychotropics and diuretics can interact or precipitate bradyarrhythmia/electrolyte disturbances.
• AF anticoagulation: Age and frailty alter bleeding risk and practical considerations but do not by themselves contraindicate anticoagulation; evaluate renal function, falls context, adherence and patient preferences.
• Pacemaker decisions: Base on documented rhythm–symptom relationship, reversibility, quality of life and goals of care.
• Digoxin: Use low maintenance doses when indicated and account for renal impairment, low body weight and interactions.
• Management goal: Prevent stroke and dangerous bradyarrhythmia while minimising postural symptoms, bradycardia, toxicity and treatment burden.

Postoperative, Pregnancy and Athlete Arrhythmias

• Postoperative AF: Common after cardiac/thoracic surgery and acute illness; address pain, volume status, infection, electrolytes, haemodynamics and stroke risk.
• Pregnancy: Sinus tachycardia and benign ectopy are common; SVT may be managed with vagal manoeuvres and selected agents with obstetric/cardiology support. Maternal haemodynamic instability requires urgent cardioversion.
• Pregnancy anticoagulation: DOACs are generally avoided; thrombosis prevention requires specialist pregnancy-specific plans.
• Athletes: Resting sinus bradycardia, first-degree block and some early repolarisation patterns may be physiological, but exertional syncope or complex ventricular arrhythmias require assessment.
• After cardiac surgery: AV block may be transient, but persistent significant block may need pacing; identify surgical complications and medication effects.

Syncope: Arrhythmic Versus Non-arrhythmic

• Arrhythmic clues: Abrupt collapse without warning, during exertion or while supine, palpitations immediately before syncope, structural heart disease or family history of sudden death.
• Vasovagal clues: Prolonged standing, warmth, nausea, sweating and gradual prodrome with prompt recovery on lying down.
• Orthostatic hypotension: Symptoms after standing, volume depletion, autonomic impairment or vasodilating drugs; check lying/standing BP when appropriate.
• Essential investigations: Witness history, medication review, 12-lead ECG, targeted orthostatic measurements and appropriate echocardiography/ambulatory ECG.
• NICE urgency: Syncope with abnormal ECG, heart failure, exertional syncope, family history of young sudden death, new unexplained breathlessness or a murmur warrants urgent cardiovascular referral.
• Monitoring choice: Frequent episodes: Holter; weekly: event monitoring; infrequent unexplained events: implantable loop recorder may be appropriate.

Two-Column Drug and Dose Table

Typical adult doses for teaching. All emergency IV treatments require monitoring and the current local resuscitation/BNF protocol; reduce or avoid agents according to renal function, comorbidities and contraindications.

💡 Clinical Pearl: DOAC dosing must use the appropriate licensed reduction criteria and renal assessment; never empirically halve the dose simply because a patient is older or frail.

Fast ECG Recognition: MRCP Patterns

• Irregularly irregular, no P waves: Atrial fibrillation.
• Regular narrow at ~150/min: Consider atrial flutter with 2:1 AV conduction.
• Abrupt regular narrow at 180/min with hidden P: AVNRT or orthodromic AVRT.
• Short PR with delta wave: Manifest pre-excitation/WPW pattern.
• Broad regular tachycardia, previous MI: Treat as VT until clearly proved otherwise.
• Polymorphic VT with prolonged QT: Torsades de pointes.
• P waves marching independently of QRS: Complete AV block or AV dissociation in VT; distinguish by ventricular rate and QRS context.
• Progressively lengthening PR then dropped beat: Mobitz I.
• Constant conducted PR with dropped QRS: Mobitz II, if rhythm meets strict diagnostic criteria.
• Three distinct atrial P-wave shapes with irregular tachycardia: Multifocal atrial tachycardia.
• Coved ST elevation V1–V3: Consider type-1 Brugada pattern.

High-Yield MRCP Teaching Pearls

• Patient before rhythm: Treat instability first and do not delay cardioversion for detailed ECG classification.
• Sinus tachycardia: Correct the cause; do not shock it.
• Regular narrow SVT: Vagal manoeuvres then monitored adenosine when appropriate.
• Irregular broad tachycardia: Exclude pre-excited AF before giving any AV nodal blocker.
• Stable VT: A patient can look comfortable despite a serious ventricular rhythm.
• QT: Amiodarone is inappropriate for long-QT-associated torsades.
• Bradycardia: Symptoms and conduction-system risk matter more than a numerical HR threshold.
• Atropine: Avoid in high-degree AV block with broad QRS; anticipate pacing.
• AF stroke prevention: Aspirin does not replace anticoagulation; assess ongoing need after cardioversion or ablation.
• Sustained VT/VF: Search for structural heart disease and consider ICD evaluation.
• Ablation: Potentially curative for AVNRT, AVRT and typical flutter; often symptom-improving for AF.
• Inherited risk: Exertional syncope or sudden death in a young relative is a major warning sign.

Guidelines and Further Reading

The following official resources should be checked for updates before using dose regimens clinically:

|Resuscitation Council UK: Adult ALS Guidelines 2025 — cardiac arrest, peri-arrest tachyarrhythmia and bradyarrhythmia guidance. |RCUK March 2026 adult tachyarrhythmia algorithm — current UK peri-arrest treatment pathway. |NICE NG196: Atrial Fibrillation — anticoagulation, rate and rhythm control and follow-up. |NICE CG109: Transient Loss of Consciousness — syncope red flags and ambulatory monitoring. |NICE TA314: Implantable Defibrillators and CRT — device indications. |ESC 2024 Atrial Fibrillation Guidelines — stroke prevention, cardioversion and ablation. |ESC Ventricular Arrhythmias / Sudden Death Guidelines — ventricular tachycardia and ICD decisions.

💡 Prescribing Safety: The current Resuscitation Council UK algorithm is designed for adult peri-arrest arrhythmias; specialist cardiology pathways and patient-specific contraindications still govern treatment outside those scenarios.