Cardiac Arrhythmias

Every normal heartbeat begins as a whisper of electricity in a cluster of cells no bigger than a grain of rice, spreads across two atria, pauses at a gatekeeper, then floods the ventricles in a fraction of a second. When that orderly electrical story is disrupted — a beat that comes too early, a rhythm that races or stalls, a signal that circles endlessly — we call it an arrhythmia. Some arrhythmias are utterly harmless (nearly everyone has occasional extra beats); others cause palpitations, faints, strokes, or sudden death within minutes. Understanding arrhythmias means understanding both the wiring diagram of the heart and the three ways that wiring can misbehave.

This page teaches you the mechanisms first, because once you understand why a rhythm goes wrong you can predict its ECG appearance and its treatment. We then work through the arrhythmias you must know cold for exams and clinical practice: atrial fibrillation, heart block, and the tachy- and bradyarrhythmias.

Learning Objectives

• Describe the normal cardiac conduction system and how it generates and coordinates a heartbeat.
• Explain the three fundamental mechanisms of arrhythmia: enhanced automaticity, triggered activity, and re-entry.
• Recognise and manage atrial fibrillation, including rate versus rhythm control and stroke prevention.
• Classify and grade the three degrees of heart block and know when a pacemaker is required.
• Distinguish narrow- from broad-complex tachycardias and outline emergency management including when to defibrillate.
• Appreciate the historical discovery of the conduction system and the invention of the pacemaker.

Quick Answer

A cardiac arrhythmia is any abnormality of heart rate or rhythm arising from disordered electrical impulse formation or conduction. Mechanistically arrhythmias arise from enhanced automaticity, triggered activity, or re-entry (a self-sustaining electrical circuit). Atrial fibrillation, the commonest sustained arrhythmia, is an irregularly irregular rhythm that raises stroke risk and is managed by rate or rhythm control plus anticoagulation guided by CHA2DS2-VASc. Bradyarrhythmias (sinus node disease, heart block) may need a permanent pacemaker; tachyarrhythmias are triaged by QRS width and haemodynamic stability. Any unstable tachyarrhythmia is treated with synchronised cardioversion, and pulseless VT or VF with immediate defibrillation. Correct diagnosis almost always rests on a good 12-lead ECG.

Where It Came From

For most of medical history the heartbeat was a mystery of pulse and sound, not electricity. The breakthroughs came in a remarkable half-century around 1900.

The conduction system was mapped anatomically by a string of investigators. In 1893 Wilhelm His Jr. described the muscular bridge crossing the fibrous ring between atria and ventricles — the bundle of His — proving that atria and ventricles are electrically connected by a discrete pathway, not by general muscle continuity. In 1906 Sunao Tawara traced that bundle down to its branches and the atrioventricular (AV) node. The same year Arthur Keith and Martin Flack, working in a Kent farmhouse laboratory, identified the sinoatrial (SA) node at the junction of the superior vena cava and right atrium — the heart's natural pacemaker. The Purkinje fibres had already been described by Jan Purkyně in 1839. Together these discoveries revealed the heart's wiring: SA node to atria to AV node to bundle of His to bundle branches to Purkinje network.

The tool that made arrhythmias visible was the electrocardiogram. Willem Einthoven perfected the string galvanometer around 1901–1903, defined the P, QRS and T waves, and won the 1924 Nobel Prize. Suddenly clinicians could see atrial fibrillation, heart block and ectopics on paper. The motivation throughout was intensely practical: patients were collapsing and dying from rhythms nobody could name.

The final chapter was treatment. Patients with complete heart block suffered Stokes-Adams attacks — sudden faints from the heart pausing — described by Robert Adams (1827) and William Stokes (1846). The need to keep such hearts beating drove the pacemaker. Paul Zoll demonstrated external electrical pacing in 1952; in 1958 Åke Senning and Rune Elmqvist implanted the first fully internal pacemaker in Arne Larsson (who went on to outlive both inventors, using 26 devices over 43 years). The defibrillator followed a parallel path, with Claude Beck achieving the first successful human defibrillation in 1947. These devices exist because understanding the wiring finally made it fixable.

The Normal Conduction System and How Rhythm Is Generated

The heartbeat is choreographed by specialised cells that generate and conduct impulses faster or slower than ordinary myocardium.

1. SA node (right atrium): the dominant pacemaker, firing about 60–100 times per minute at rest. Its cells have unstable resting membrane potentials that spontaneously drift upward (the "funny" current) until they reach threshold — this is automaticity.
2. Atria: the impulse spreads cell-to-cell, producing the P wave and atrial contraction.
3. AV node: the sole normal electrical connection to the ventricles. It deliberately delays the impulse (~0.1 s, seen as the PR interval), letting the ventricles fill before they contract, and it acts as a filter that protects ventricles from very fast atrial rates.
4. Bundle of His, bundle branches, Purkinje fibres: a high-speed cable system that delivers the impulse to both ventricles almost simultaneously, producing the narrow QRS complex and a coordinated squeeze.

A key safety feature is the hierarchy of pacemakers: if the SA node fails, the AV junction takes over (~40–60/min), and if that fails, the ventricles have a slow escape rhythm (~20–40/min). This backup explains why complete heart block often produces a slow but survivable rhythm rather than immediate arrest.

The Three Mechanisms of Arrhythmia

Almost every arrhythmia you will meet fits one of three mechanisms. Learn these and the rest is pattern recognition.

1. Enhanced or abnormal automaticity. Pacemaker cells fire too fast, or non-pacemaker cells acquire the ability to fire spontaneously — often driven by ischaemia, high catecholamines, hypoxia, or electrolyte disturbance. Examples: inappropriate sinus tachycardia, some atrial tachycardias, and accelerated idioventricular rhythm after a heart attack.

2. Triggered activity. Abnormal secondary depolarisations ("afterdepolarisations") ride on the back of a preceding beat. Early afterdepolarisations occur when repolarisation is prolonged (long QT) and can trigger torsades de pointes. Delayed afterdepolarisations arise from calcium overload — the mechanism of digoxin toxicity arrhythmias.

3. Re-entry. The commonest mechanism of sustained arrhythmias. An impulse, instead of dying out after activating the heart, finds a circular pathway and re-excites tissue that has just recovered, circling indefinitely. Re-entry needs two pathways with different conduction speeds and refractory periods, plus a trigger (often an ectopic beat) to start the loop. Re-entry drives AV nodal re-entrant tachycardia (AVNRT), atrial flutter (a large loop in the right atrium at ~300/min), most VT scar circuits, and the disorganised multiple wavelets of atrial fibrillation.

Worked example. A 25-year-old has sudden-onset regular palpitations at 180/min with a narrow QRS. This is classic AVNRT: the AV node has a slow and a fast pathway, and an ectopic beat set up a re-entry loop. Because the AV node is part of the circuit, blocking it terminates the arrhythmia — hence vagal manoeuvres or adenosine (which transiently blocks the AV node) can abruptly restore sinus rhythm.

Atrial Fibrillation

Atrial fibrillation (AF) is the most common sustained arrhythmia and a leading, preventable cause of stroke. The atria depolarise chaotically at 300–600/min, so there is no coordinated atrial contraction and no distinct P wave. The AV node passes impulses irregularly, giving the hallmark irregularly irregular ventricular rhythm with absent P waves on the ECG.

Two dangers flow from this. First, loss of the atrial "kick" reduces cardiac output and can precipitate heart failure. Second, stagnant blood in the fibrillating left atrium (especially the left atrial appendage) forms clots that embolise to the brain — AF causes roughly one in five ischaemic strokes.

Management has three pillars:

• Rate control: slow the ventricular response with a beta-blocker or a rate-limiting calcium channel blocker (diltiazem/verapamil); digoxin is an option in sedentary or hypotensive patients.
• Rhythm control: restore sinus rhythm by electrical cardioversion, antiarrhythmic drugs (flecainide in structurally normal hearts, amiodarone otherwise), or catheter ablation (pulmonary vein isolation). Rhythm control is favoured in younger, symptomatic patients and increasingly early after diagnosis.
• Stroke prevention: this is the single most life-saving step. Risk is scored with CHA2DS2-VASc (Congestive heart failure, Hypertension, Age 75+ = 2 points, Diabetes, prior Stroke/TIA = 2 points, Vascular disease, Age 65–74, Sex category female). Most patients with a score of 2 or more (1 or more in men) receive a direct oral anticoagulant (apixaban, rivaroxaban, dabigatran, edoxaban) or warfarin. Aspirin is not adequate stroke prevention in AF.

A crucial safety rule: if AF has been present more than 48 hours and you cardiovert without either 3 weeks of prior anticoagulation or a clot-excluding transoesophageal echo, restoring atrial contraction can dislodge a clot and cause a stroke.

Bradyarrhythmias and Heart Block

Bradyarrhythmia means a rate too slow for the body's needs (conventionally under 60/min). Two broad causes: the SA node fails to fire adequately (sinus bradycardia, sick sinus syndrome), or conduction is blocked between atria and ventricles (heart block).

Heart block is graded by how badly the AV node/His-Purkinje system conducts:

Degree	ECG finding	Clinical meaning
First-degree	PR interval prolonged (over 0.20 s), every P conducts	Usually benign; watch
Second-degree Mobitz I (Wenckebach)	PR lengthens progressively until a QRS is dropped	Usually AV node; often benign, may be vagal
Second-degree Mobitz II	Constant PR, then a sudden dropped QRS	His-Purkinje disease; unstable, often needs a pacemaker
Third-degree (complete)	P waves and QRS complexes independent (AV dissociation)	Ventricles rely on an escape rhythm; high risk, needs pacing

The key exam distinction is Mobitz I (progressive PR, benign, above the His) versus Mobitz II (sudden drop, dangerous, below the His and prone to progressing to complete block). Complete heart block classically causes Stokes-Adams attacks — abrupt loss of consciousness with a slow or absent pulse.

Management. Reversible causes first: stop AV-blocking drugs (beta-blockers, diltiazem, digoxin), correct hyperkalaemia and hypothyroidism, treat inferior MI (which can cause transient AV block). Symptomatic bradycardia is treated acutely with atropine, then transcutaneous or transvenous pacing if needed. Persistent high-grade block (Mobitz II, complete block, symptomatic sinus node disease) is the classic indication for a permanent pacemaker.

Tachyarrhythmias

A tachyarrhythmia is a heart rate over 100/min from an abnormal focus or circuit. The single most useful bedside classification is by QRS width on the 12-lead ECG.

Narrow-complex (QRS under 0.12 s) means the impulse reaches the ventricles through the normal His-Purkinje system, so the origin is supraventricular:

• Sinus tachycardia — a normal response to fever, exercise, pain, anaemia, hypovolaemia, thyrotoxicosis; treat the cause.
• AF / atrial flutter — irregular (AF) or regular with sawtooth flutter waves at ~150/min (flutter, typically 2:1 conducted).
• Supraventricular tachycardia (SVT) — usually AVNRT or AV re-entrant tachycardia (as in Wolff-Parkinson-White). Managed with vagal manoeuvres, then adenosine, then AV-nodal blockers; ablation is curative.

Broad-complex (QRS 0.12 s or more) should be assumed to be ventricular tachycardia (VT) until proven otherwise, especially in a patient with prior MI or structural heart disease. VT is a re-entry circuit or automatic focus in the ventricles; it can degenerate into ventricular fibrillation (VF) — chaotic, pulseless, fatal within minutes without defibrillation.

The decision that overrides everything is haemodynamic stability.

• Unstable (hypotension, chest pain, heart failure, reduced consciousness) with a pulse → synchronised DC cardioversion.
• Pulseless VT or VF → immediate unsynchronised defibrillation and CPR (the shockable arm of ACLS).
• Stable → time for a 12-lead ECG and drugs (e.g., amiodarone for VT; adenosine for regular narrow SVT).

Case vignette. A 68-year-old with a previous heart attack develops a regular broad-complex tachycardia at 170/min and a blood pressure of 80/50 with chest pain. This is unstable VT. Do not reach for adenosine or spend time debating SVT-with-aberrancy — deliver synchronised cardioversion after sedation, then correct electrolytes and start amiodarone.

Real-World Applications

• Emergency medicine: the tachy/brady algorithms above are core Advanced Life Support content used daily in resuscitation.
• Stroke prevention: detecting and anticoagulating AF (including with prolonged monitoring and now smartwatch ECG alerts) prevents thousands of disabling strokes.
• Devices: pacemakers restore rate in heart block and sinus node disease; implantable cardioverter-defibrillators (ICDs) abort VT/VF in high-risk patients; catheter ablation cures SVT, flutter and increasingly AF.
• Everyday relevance: palpitations are among the commonest reasons people present to primary care, and knowing the benign (ectopics, sinus tachycardia) from the sinister (VT, high-grade block) is a genuinely life-saving skill.

Common Mistakes

• "All broad-complex tachycardias in a stable patient are probably SVT with aberrancy." Wrong and dangerous. In a patient with structural heart disease the great majority are VT. Treating VT as SVT (e.g., with verapamil) can cause collapse. Default to VT unless you can prove otherwise.
• "Aspirin protects AF patients from stroke." Largely a myth. Aspirin is far inferior to anticoagulation for AF-related cardioembolic stroke and is no longer recommended for stroke prevention in AF. Use a DOAC or warfarin guided by CHA2DS2-VASc.
• "Mobitz I and Mobitz II are equally benign second-degree blocks." No. Mobitz I (Wenckebach) is usually benign and rarely needs pacing; Mobitz II reflects His-Purkinje disease, can progress abruptly to complete block, and usually warrants a pacemaker.
• (Bonus) "Adenosine or cardioversion should be given for any fast rhythm." Sinus tachycardia is a response, not a primary arrhythmia — cardioverting it is futile and you must treat the underlying cause (sepsis, bleeding, hypovolaemia).

Comparison and Connections

Feature	Atrial fibrillation	Atrial flutter	AVNRT (SVT)	Ventricular tachycardia
Rhythm	Irregularly irregular	Regular (usually)	Regular	Regular (usually)
QRS	Narrow	Narrow	Narrow	Broad
Rate	Variable	~150 (2:1)	150–250	120–250
P/atrial waves	Absent	Sawtooth flutter waves	Hidden in QRS	AV dissociation
Mechanism	Multiple re-entry wavelets	Single large re-entry loop	AV nodal re-entry	Ventricular re-entry/focus
First-line if stable	Rate control + anticoagulate	Rate control/ablate	Vagal, adenosine	Amiodarone

Re-entry links most of these; automaticity and triggered activity explain most of the rest. Note how the same mechanism (re-entry) produces very different ECGs depending on where the circuit sits — atrium, AV node, or ventricle.

Practice Questions

Recall

Q: Name the components of the cardiac conduction system in order. A: SA node to atrial myocardium to AV node to bundle of His to right and left bundle branches to Purkinje fibres to ventricular myocardium.

Understanding

Q: Why can adenosine terminate AVNRT but not atrial flutter? A: In AVNRT the AV node is an essential part of the re-entry circuit, so transiently blocking it (adenosine) breaks the loop. In atrial flutter the circuit is entirely within the atrium; blocking the AV node only slows ventricular response and unmasks the flutter waves, but does not stop the atrial circuit.

Application

Q: A 78-year-old with hypertension and diabetes has newly diagnosed AF. What is her CHA2DS2-VASc score and what does it mean? A: Age 75+ (2) + Hypertension (1) + Diabetes (1) + female sex (1) = 5. A score this high indicates a substantial annual stroke risk, so she should be started on a direct oral anticoagulant (after assessing bleeding risk).

Analysis

Q: An ECG shows progressively lengthening PR intervals followed by a dropped QRS, then the cycle repeats. Grade the block, localise it, and state whether a pacemaker is usually needed. A: Second-degree AV block, Mobitz type I (Wenckebach). It is usually within the AV node, frequently benign or vagally mediated, and generally does not require a permanent pacemaker unless the patient is symptomatic.

FAQ

Are palpitations always serious? No. Most palpitations are benign ectopic beats or sinus tachycardia. Red flags that warrant urgent assessment are syncope, palpitations during exertion, associated chest pain or breathlessness, or a family history of sudden cardiac death.

Can I feel my own arrhythmia? Often, but not always. AF may be felt as an irregular fluttering, SVT as a sudden fast regular pounding. Dangerous rhythms like VT may cause collapse rather than a felt palpitation, and some AF is completely silent — which is why it is sometimes only found after a stroke.

What is the difference between cardioversion and defibrillation? Cardioversion is a shock synchronised to the R wave, used for organised rhythms with a pulse (unstable AF, flutter, SVT, VT with a pulse). Defibrillation is an unsynchronised shock for pulseless VT and VF, where there is no organised QRS to synchronise to.

Does atrial fibrillation shorten life? Untreated, it raises the risk of stroke and heart failure. Well managed — with rate/rhythm control and appropriate anticoagulation — many people live normal lifespans. The anticoagulation is the part that most reduces serious harm.

Why does the AV node delay the impulse? The deliberate ~0.1 s pause lets the atria finish contracting and filling the ventricles before ventricular contraction, optimising stroke volume. It also protects the ventricles from following dangerously fast atrial rates such as in flutter or AF.

How long do pacemakers last? Modern pacemaker batteries typically last around 8–12 years before the generator is replaced in a minor procedure; the leads usually stay in place.

Quick Revision

• Three mechanisms: automaticity, triggered activity, re-entry (re-entry causes most sustained arrhythmias).
• Conduction order: SA node to atria to AV node to His to bundle branches to Purkinje.
• AF = irregularly irregular, no P waves; manage with rate/rhythm control + anticoagulation by CHA2DS2-VASc. Aspirin is not enough.
• Heart block: Mobitz I (progressive PR, benign) vs Mobitz II (sudden drop, dangerous); complete block causes Stokes-Adams attacks and needs pacing.
• Tachycardias: classify by QRS width; broad-complex = VT until proven otherwise.
• Unstable + pulse → synchronised cardioversion; pulseless VT/VF → immediate defibrillation.
• History: His, Tawara, Keith and Flack mapped the wiring; Einthoven made it visible; Zoll and Senning made it treatable.

Related Topics

Prerequisites

• Cardiology overview
• Cardiac physiology and the action potential (see ../../2._Physiology/index.md)

Related Topics

• Ischaemic heart disease and myocardial infarction (a major cause of VT and AV block)
• Heart failure (both cause and consequence of arrhythmia)
• Pharmacology of antiarrhythmic drugs (see ../../5._Pharmacology/index.md)

Next Topics

• Emergency management of cardiac arrest and ACLS (see ../../23._Emergency_Medicine/index.md)
• Cardiac devices: pacemakers and implantable defibrillators