Medical School · Year 1 · Cardiovascular · includes a quiz and discussion video

Lecture 12: Cardiac Arrhythmias

Unit 1.7: Cardiovascular System

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the mechanisms of arrhythmia formation
2. Classify arrhythmias by site of origin and rate
3. Recognize common arrhythmias on ECG
4. Explain the clinical significance of various arrhythmias
5. Describe the principles of arrhythmia management
6. Apply antiarrhythmic drug mechanisms to clinical scenarios

Mechanisms of Arrhythmias

Cardiac arrhythmias arise from two fundamental abnormalities: disorders of impulse formation and disorders of impulse conduction. Understanding these mechanisms provides the foundation for diagnosis and treatment.

Abnormal impulse formation encompasses enhanced automaticity and triggered activity. Enhanced normal automaticity occurs when pacemaker cells develop steeper phase 4 depolarization, reaching threshold earlier and accelerating their intrinsic rate. This can occur in the SA node (sinus tachycardia) or in latent pacemakers in the AV junction or ventricular conduction system. Abnormal automaticity occurs when non-pacemaker cells, such as working myocytes, develop spontaneous depolarization—a phenomenon that can occur in ischemic or damaged tissue. Triggers for enhanced automaticity include ischemia, elevated catecholamine levels, and hypokalemia.

Triggered activity refers to abnormal depolarizations that occur as a consequence of a preceding action potential. Early afterdepolarizations (EADs) occur during phase 2 or phase 3 of the action potential, before repolarization is complete. They are associated with conditions that prolong the action potential, including long QT syndrome (congenital or drug-induced), hypokalemia, and bradycardia. EADs can trigger polymorphic ventricular tachycardia (torsades de pointes). Delayed afterdepolarizations (DADs) occur during phase 4, after repolarization is complete. They result from intracellular calcium overload, which activates a transient inward current. DADs are associated with digitalis toxicity, catecholamine excess, and heart failure. If DADs reach threshold, they trigger action potentials that can initiate arrhythmias.

Reentry is the most common mechanism of sustained tachyarrhythmias. Reentry requires three conditions: an anatomic or functional circuit providing a pathway for the impulse, unidirectional block in one limb of the circuit preventing normal conduction, and slow conduction in the alternate pathway allowing time for the originally blocked tissue to recover excitability. When these conditions are met, an impulse can travel around the circuit continuously, activating the heart repetitively. Reentrant circuits may be anatomic (fixed pathways as in Wolff-Parkinson-White syndrome or post-infarction ventricular tachycardia) or functional (dynamically determined by tissue properties).

Conduction block can occur at any level of the conduction system. SA nodal block or sinus arrest results from failure of impulse generation or exit from the sinus node. AV nodal block causes varying degrees of dissociation between atrial and ventricular activity. Bundle branch block results from conduction failure in the specialized ventricular conduction system.

<image>Panel A: Enhanced automaticity shown as a graph of membrane potential versus time comparing normal and enhanced automatic rhythms with steeper phase 4 slope reaching threshold earlier. Panel B: Triggered activity showing an early afterdepolarization occurring during phase 3 associated with long QT syndrome, and a delayed afterdepolarization occurring during phase 4 associated with calcium overload. Panel C: Reentry mechanism showing a circular pathway with two limbs, normal conduction in one limb, and unidirectional block in the other limb. Panel D: Completion of the reentrant circuit with slow retrograde conduction through the unblocked limb and recovery of excitability in the blocked limb, with the three requirements for reentry labeled.</image>

Classification of Arrhythmias

Arrhythmias are classified by rate and by anatomic origin. By rate, bradyarrhythmias are rhythms with heart rate below 60 beats per minute, while tachyarrhythmias exceed 100 beats per minute. By origin, supraventricular arrhythmias arise above the bundle of His (sinus node, atria, or AV junction), while ventricular arrhythmias arise below the bundle of His.

Supraventricular tachyarrhythmias include sinus tachycardia (enhanced automaticity of the sinus node in response to physiologic stimuli), atrial fibrillation (chaotic atrial activation from multiple simultaneous reentrant wavelets), atrial flutter (organized macro-reentrant circuit in the right atrium), AV nodal reentrant tachycardia (reentry utilizing dual AV nodal pathways), AV reciprocating tachycardia (reentry utilizing an accessory pathway as in Wolff-Parkinson-White syndrome), and focal atrial tachycardia (enhanced automaticity or micro-reentry within atrial tissue).

Ventricular arrhythmias include premature ventricular complexes (isolated ectopic beats from ventricular foci), ventricular tachycardia (three or more consecutive ventricular beats at a rate exceeding 100 per minute), and ventricular fibrillation (chaotic ventricular activation producing no effective cardiac output). Ventricular tachycardia may be monomorphic (uniform QRS morphology, usually from a single focus or fixed reentrant circuit) or polymorphic (varying QRS morphology, suggesting multiple foci or a shifting reentrant circuit). Torsades de pointes is a specific form of polymorphic ventricular tachycardia associated with long QT syndrome.

<image>Panel A: Hierarchical classification dividing arrhythmias by rate into bradyarrhythmias below 60 bpm and tachyarrhythmias above 100 bpm, and by origin into supraventricular and ventricular. Panel B: Supraventricular tachyarrhythmias with ECG patterns: sinus tachycardia with regular narrow QRS, atrial fibrillation with irregularly irregular rhythm, atrial flutter with sawtooth waves, and AVNRT with P waves buried in QRS. Panel C: AVRT with regular narrow or wide QRS depending on conduction direction, shown with anatomical reference to accessory pathways. Panel D: Ventricular arrhythmias with ECG patterns: PVCs with wide QRS without preceding P wave, monomorphic VT with uniform wide QRS, polymorphic VT with varying complexes, and VF with chaotic irregular waveform.</image>

Bradyarrhythmias

Sinus bradycardia is defined as sinus rhythm with a rate below 60 beats per minute. The ECG shows normal P waves with normal PR interval, simply at a slow rate. Sinus bradycardia may be physiologic in athletes or during sleep, or it may result from medications (beta-blockers, calcium channel blockers), hypothyroidism, increased vagal tone, or sinus node disease. Treatment is needed only when bradycardia causes symptoms; options include atropine for acute symptomatic bradycardia and permanent pacing for chronic symptomatic disease.

Sick sinus syndrome encompasses a spectrum of sinus node dysfunction including inappropriate sinus bradycardia (rate too slow for physiologic conditions), sinus arrest (complete failure to generate impulses for prolonged periods), and tachy-brady syndrome (alternating periods of tachyarrhythmias and bradyarrhythmias, often atrial fibrillation alternating with sinus bradycardia). Sick sinus syndrome typically requires permanent pacemaker implantation when symptomatic.

AV blocks represent impaired conduction from atria to ventricles and are classified by degree. First-degree AV block shows prolonged PR interval (greater than 200 ms) with all P waves conducted to the ventricles. This is usually benign and requires no treatment. Second-degree AV block includes two patterns. Mobitz type I (Wenckebach) shows progressive PR prolongation until a P wave fails to conduct, then the cycle repeats. The block is typically at the AV node, often responds to atropine, and is usually benign. Mobitz type II shows constant PR intervals with sudden failure of conduction—a P wave is simply not followed by a QRS. This pattern indicates infranodal disease (in the His bundle or bundle branches), does not respond to atropine, and carries high risk of progression to complete heart block. Third-degree (complete) AV block shows complete absence of conduction between atria and ventricles, with atria and ventricles beating independently (AV dissociation). The ventricular escape rhythm is usually slow (20-40 bpm if originating below the His bundle) and unreliable. Complete heart block typically requires permanent pacing.

Treatment of acute symptomatic bradycardia includes atropine (blocks vagal input to the AV node, effective for nodal block), transcutaneous or transvenous pacing for emergency situations, and occasionally isoproterenol as a temporizing measure. Chronic symptomatic bradycardia requires permanent pacemaker implantation.

<image>Panel A: First-degree AV block ECG showing regular rhythm with prolonged PR interval greater than 200 ms but all P waves conducted to QRS complexes, with block localized to the AV node. Panel B: Second-degree Mobitz type I Wenckebach showing progressive PR prolongation followed by a dropped beat, then the cycle repeats with reset PR interval, with block at the AV node. Panel C: Second-degree Mobitz type II showing constant PR intervals with sudden absence of QRS after one P wave, with infranodal block location and high-risk annotation. Panel D: Third-degree complete AV block showing P waves marching at atrial rate 75 and QRS complexes at ventricular rate 35 with complete AV dissociation, with block at the His-Purkinje level.</image>

Supraventricular Tachycardias

Sinus tachycardia represents accelerated firing of the sinus node in response to physiologic demands. The ECG shows normal P wave morphology and axis at a rate exceeding 100 bpm. Sinus tachycardia is not a primary arrhythmia but rather a normal response to stimuli such as exercise, fever, anxiety, pain, anemia, hyperthyroidism, or hypovolemia. Treatment addresses the underlying cause rather than the tachycardia itself.

Atrial fibrillation is the most common sustained arrhythmia, characterized by chaotic, disorganized atrial activation. The mechanism involves multiple simultaneous reentrant wavelets wandering through the atrial tissue. On ECG, P waves are absent, replaced by an irregular fibrillatory baseline, and the ventricular response is irregularly irregular—the hallmark of atrial fibrillation. Risk factors include hypertension, heart failure, valvular disease (particularly mitral stenosis), hyperthyroidism, and age. Atrial fibrillation has two major clinical consequences: symptoms from rapid or irregular heart rate and risk of thromboembolism due to blood stasis in the non-contracting left atrial appendage.

Management of atrial fibrillation addresses three goals. Rate control uses AV nodal blocking agents (beta-blockers, non-dihydropyridine calcium channel blockers, or digoxin) to slow the ventricular response. Rhythm control attempts to restore and maintain sinus rhythm using antiarrhythmic drugs, electrical cardioversion, or catheter ablation. Stroke prevention is essential because of the high thromboembolic risk; the CHA₂DS₂-VASc score stratifies stroke risk and guides anticoagulation decisions. Anticoagulation with warfarin or direct oral anticoagulants is indicated for most patients with atrial fibrillation.

Atrial flutter is an organized macro-reentrant arrhythmia, most commonly utilizing a circuit in the right atrium that travels through the cavotricuspid isthmus (typical flutter). The atrial rate is characteristically around 300 bpm, and the ventricular rate depends on the degree of AV block—typically 150 bpm with 2:1 block, 100 bpm with 3:1 block, or variable. The ECG shows characteristic "sawtooth" flutter waves, most apparent in the inferior leads. Management parallels atrial fibrillation, with the addition that catheter ablation of the cavotricuspid isthmus is highly effective (greater than 90% success) for typical flutter.

Paroxysmal supraventricular tachycardia includes two common reentrant arrhythmias that present similarly: sudden onset of regular, rapid, narrow-complex tachycardia. AV nodal reentrant tachycardia (AVNRT) is the most common form, utilizing dual AV nodal pathways—a slow pathway and a fast pathway—to create a reentrant circuit entirely within the AV node. The ECG shows regular narrow QRS complexes at 150-250 bpm, with P waves often buried within or appearing just after the QRS. AV reciprocating tachycardia (AVRT) utilizes an accessory pathway (such as the Kent bundle in Wolff-Parkinson-White syndrome) as one limb of the reentrant circuit. During tachycardia, the impulse typically conducts antegrade through the AV node and retrograde through the accessory pathway (orthodromic AVRT), producing a narrow QRS. In sinus rhythm, patients with WPW show the classic triad of short PR interval, delta wave (slurred upstroke of the QRS), and wide QRS due to ventricular pre-excitation via the accessory pathway.

Acute management of AVNRT and orthodromic AVRT is identical: vagal maneuvers (Valsalva, carotid massage) may terminate the arrhythmia by slowing AV nodal conduction. If ineffective, adenosine produces transient AV nodal block and terminates most episodes. Beta-blockers or calcium channel blockers can also be used. Importantly, in patients with WPW who develop pre-excited atrial fibrillation (rapid wide-complex irregular tachycardia), AV nodal blocking agents are contraindicated because they may allow uninhibited rapid conduction over the accessory pathway, potentially causing ventricular fibrillation. Procainamide or electrical cardioversion should be used instead. Catheter ablation is curative for both AVNRT (modification of the slow pathway) and AVRT (ablation of the accessory pathway) with success rates exceeding 95%.

<image>Panel A: Atrial fibrillation ECG showing absent P waves, irregular fibrillatory baseline, and irregularly irregular QRS complexes, with mechanism illustration of multiple wandering reentrant wavelets in the left atrium. Panel B: Atrial flutter ECG showing regular sawtooth flutter waves at 300 per minute with 2:1 conduction producing ventricular rate of 150 bpm, with mechanism showing a macro-reentrant circuit through the cavotricuspid isthmus. Panel C: AVNRT ECG showing regular narrow QRS tachycardia at 180 bpm with P waves buried as pseudo r-prime in V1, with mechanism showing dual AV nodal pathways creating a reentrant circuit. Panel D: WPW/AVRT showing sinus rhythm ECG with short PR, delta wave, and wide QRS, and tachycardia ECG showing narrow QRS orthodromic AVRT using the AV node for antegrade and accessory pathway for retrograde conduction.</image>

Ventricular Arrhythmias

Premature ventricular complexes (PVCs) are ectopic beats arising from ventricular tissue. The ECG shows wide QRS complexes (greater than 120 ms) without preceding P waves, typically followed by a compensatory pause. PVCs may result from automaticity, triggered activity, or micro-reentry. In the absence of structural heart disease, PVCs are generally benign. However, frequent PVCs (greater than 10-20% of beats), multiform PVCs, or PVCs in the setting of structural heart disease warrant evaluation. Symptomatic PVCs can be treated with beta-blockers or catheter ablation.

Ventricular tachycardia (VT) is defined as three or more consecutive ventricular beats at a rate exceeding 100 bpm. Monomorphic VT shows uniform QRS morphology and usually results from a fixed reentrant circuit, often around scar tissue from prior myocardial infarction. Polymorphic VT shows varying QRS morphology and suggests multiple foci, ischemia, or long QT syndrome. Nonsustained VT lasts less than 30 seconds and terminates spontaneously. Sustained VT persists for 30 seconds or longer or requires intervention for termination due to hemodynamic compromise.

Distinguishing wide-complex tachycardia as VT versus supraventricular tachycardia with aberrant conduction is clinically critical because VT carries higher risk and different treatment implications. Features favoring VT include AV dissociation (P waves marching independently of QRS complexes), capture beats or fusion beats (intermittent normal conduction), very wide QRS (greater than 160 ms), concordance in precordial leads (all QRS complexes pointing in the same direction), and history of structural heart disease (the strongest predictor). When in doubt, treat wide-complex tachycardia as VT.

Torsades de pointes is a specific polymorphic VT characterized by QRS complexes that appear to twist around the baseline. It is associated with long QT syndrome, whether congenital or acquired. Acquired long QT results from drugs (many antiarrhythmics, antibiotics, antipsychotics), electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), or bradycardia. Treatment of torsades involves withdrawing offending drugs, correcting electrolytes (magnesium is first-line even if levels are normal), and increasing heart rate (temporary pacing or isoproterenol) to shorten the QT interval. Defibrillation is required if the arrhythmia persists.

Ventricular fibrillation is chaotic, disorganized ventricular activity that produces no cardiac output—it is cardiac arrest. The ECG shows irregular, chaotic waveforms without discernible QRS complexes. VF requires immediate CPR and defibrillation; survival decreases by approximately 10% with each minute of delay in defibrillation. Epinephrine and amiodarone are adjunctive medications, but defibrillation is the definitive treatment.

<image>Panel A: PVC shown as normal sinus beats interrupted by a wide bizarre QRS complex without preceding P wave, followed by compensatory pause, with severity indicator noting usually benign. Panel B: Monomorphic VT showing regular wide-complex tachycardia at 200 bpm with uniform QRS morphology and AV dissociation with P waves marching independently, with severity indicator noting dangerous. Panel C: Torsades de pointes showing polymorphic VT with QRS complexes rotating around the baseline in a sinusoidal pattern, preceded by prolonged QT interval, with severity indicator noting life-threatening. Panel D: Ventricular fibrillation showing chaotic irregular waveform with no identifiable QRS complexes and no cardiac output, requiring immediate defibrillation.</image>

Long QT Syndrome

Long QT syndrome is characterized by prolonged ventricular repolarization (QTc greater than 450 ms in men, greater than 460 ms in women) and risk of torsades de pointes and sudden cardiac death. The prolonged QT interval reflects delayed repolarization, which creates conditions favorable for early afterdepolarizations and triggered arrhythmias.

Congenital long QT syndrome results from mutations in genes encoding cardiac ion channels. The most common subtypes differ in the affected channel and clinical triggers. LQT1 results from mutations in KCNQ1, which encodes the slow component of the delayed rectifier potassium current (IKs). Events are typically triggered by exercise, particularly swimming. LQT2 results from mutations in KCNH2, encoding the rapid component of the delayed rectifier potassium current (IKr). Events are triggered by emotional stress or sudden auditory stimuli. LQT3 results from mutations in SCN5A, encoding the cardiac sodium channel. These mutations cause persistent inward sodium current during the plateau phase. Events occur during sleep or rest.

Acquired long QT syndrome is more common than congenital forms and results from drugs, electrolyte abnormalities, or bradycardia. Many drugs prolong the QT interval by blocking potassium channels, including class Ia and class III antiarrhythmic drugs, certain antibiotics (fluoroquinolones, macrolides), antipsychotics, and some antiemetics. Hypokalemia, hypomagnesemia, and hypocalcemia all prolong repolarization. Bradycardia increases action potential duration and therefore QT interval.

Management of long QT syndrome depends on the underlying cause and risk stratification. For acquired long QT, the offending drug should be discontinued and electrolytes corrected. For congenital long QT, beta-blockers are first-line therapy for LQT1 and LQT2, reducing arrhythmic events by preventing catecholamine-triggered events. For LQT3, sodium channel blockers (mexiletine) may be beneficial, and beta-blockers are less effective. Implantable cardioverter-defibrillators are indicated for high-risk patients, including those with prior cardiac arrest, syncope despite beta-blocker therapy, or very prolonged QT intervals.

<image>Panel A: ECG showing markedly prolonged QT interval measured from QRS onset to T wave end, with comparison of normal QT versus prolonged QT and correction formula using RR interval. Panel B: Three congenital long QT subtypes: LQT1 with KCNQ1 gene and IKs reduction triggered by exercise, LQT2 with KCNH2 gene and IKr reduction triggered by emotional stress, and LQT3 with SCN5A gene and persistent sodium current triggered at rest. Panel C: Action potential diagram with extended plateau phase in long QT showing where early afterdepolarizations arise and initiate torsades de pointes. Panel D: Common acquired causes including QT-prolonging drugs, electrolyte abnormalities such as low potassium, magnesium, and calcium, and bradycardia.</image>

Antiarrhythmic Drugs

The Vaughan-Williams classification organizes antiarrhythmic drugs by their primary mechanism of action, though most drugs have multiple effects.

Class I drugs block cardiac sodium channels, reducing the rate of phase 0 depolarization and slowing conduction. Class Ia drugs (quinidine, procainamide, disopyramide) produce moderate sodium channel block and also block potassium channels, prolonging repolarization and the QT interval. They can cause torsades de pointes. Class Ib drugs (lidocaine, mexiletine) produce weak sodium channel block with rapid binding kinetics, preferentially affecting ischemic tissue. They have minimal effect on the QT interval. Class Ic drugs (flecainide, propafenone) produce strong sodium channel block, markedly slowing conduction and widening the QRS complex. They are contraindicated in structural heart disease because of proarrhythmic risk.

Class II drugs are beta-blockers, which reduce sympathetic input to the heart. They decrease automaticity and slow AV nodal conduction. Beta-blockers are among the safest antiarrhythmic drugs and are first-line therapy for many supraventricular and ventricular arrhythmias.

Class III drugs block potassium channels, prolonging repolarization and the refractory period. This increases the action potential duration and the QT interval. Amiodarone is the most commonly used class III drug and also has class I, II, and IV properties. It is effective for both atrial and ventricular arrhythmias but has significant toxicities (thyroid, pulmonary, hepatic, neurologic). Sotalol combines class III effects with beta-blockade. Dofetilide and ibutilide are pure class III agents. All class III drugs carry risk of torsades de pointes.

Class IV drugs are non-dihydropyridine calcium channel blockers (verapamil, diltiazem), which block L-type calcium channels. They slow conduction through the AV node and are useful for rate control in atrial fibrillation and for terminating AV nodal-dependent arrhythmias.

Other antiarrhythmic agents do not fit neatly into the Vaughan-Williams classification. Adenosine activates A₁ receptors, producing transient AV nodal block, and is first-line for terminating AVNRT and AVRT. Digoxin has vagotonic effects that slow AV nodal conduction. Atropine blocks muscarinic receptors, increasing heart rate and AV conduction in vagally-mediated bradycardia. Magnesium is effective for torsades de pointes through unclear mechanisms.

Proarrhythmia—the paradoxical worsening of arrhythmias by antiarrhythmic drugs—is a significant concern. Class Ia and III drugs can cause torsades de pointes by prolonging the QT interval. Class Ic drugs can cause sustained ventricular tachycardia in patients with structural heart disease (the CAST study demonstrated increased mortality with flecainide and encainide in post-MI patients). Any antiarrhythmic drug can cause bradycardia or conduction block.

<image>Panel A: Cardiac action potential with phases 0 through 4 labeled, showing Class I sodium channel blockers acting on phase 0 with subgroups Ia producing moderate block plus K block with QRS and QT prolongation, Ib producing weak block with minimal ECG effect, and Ic producing strong block with QRS widening. Panel B: Class II beta-blockers reducing phase 4 slope and nodal tissue depolarization. Panel C: Class III potassium channel blockers prolonging phase 3 repolarization, extending action potential duration and QT interval, and Class IV calcium channel blockers reducing calcium-dependent nodal depolarization. Panel D: Drug reference table listing example drugs for each class with ECG effects and major adverse effects, highlighting proarrhythmia risk including torsades for Ia and III and VT in structural heart disease for Ic.</image>

Device Therapy

Permanent pacemakers are indicated for symptomatic bradyarrhythmias that are not reversible. Indications include symptomatic sinus node dysfunction (sick sinus syndrome), symptomatic or high-grade AV block (Mobitz type II, third-degree), and certain neuromuscular diseases with conduction abnormalities.

Pacemaker function is described by the NBG code, where the first letter indicates the chamber paced (A for atrium, V for ventricle, D for dual), the second letter indicates the chamber sensed, the third indicates the response to sensing (I for inhibit, T for trigger, D for dual), and the fourth indicates rate-responsive capability (R). VVI mode paces and senses the ventricle, inhibiting pacing when native activity is detected—a simple mode for patients in chronic atrial fibrillation. DDD mode paces and senses both chambers, providing physiologic AV synchrony—the standard mode for patients with intact atrial function. DDDR adds rate responsiveness based on activity sensors.

Implantable cardioverter-defibrillators (ICDs) provide protection against sudden cardiac death from ventricular tachyarrhythmias. ICDs can deliver anti-tachycardia pacing (rapid pacing to terminate VT), cardioversion (synchronized shock for VT), and defibrillation (unsynchronized shock for VF). They also provide backup bradycardia pacing.

ICD indications include secondary prevention (survived cardiac arrest or hemodynamically significant sustained VT) and primary prevention in high-risk patients. Primary prevention indications include heart failure with ejection fraction ≤35% on optimal medical therapy, hypertrophic cardiomyopathy with high-risk features, arrhythmogenic right ventricular cardiomyopathy, and congenital long QT syndrome with high-risk features.

Cardiac resynchronization therapy (CRT) is a specialized form of pacing for heart failure patients with ventricular dyssynchrony. By pacing both ventricles (typically with leads in the right ventricle and coronary sinus to pace the left ventricle), CRT restores coordinated contraction. Indications include symptomatic heart failure with ejection fraction ≤35%, left bundle branch block, and QRS duration ≥150 ms. CRT reduces mortality and improves symptoms and ejection fraction.

<image>Panel A: Pacemaker with leads in the right atrium and right ventricle and pulse generator in the pectoral region, with NBG code positions explained including chamber paced, chamber sensed, response to sensing, and rate modulation. Panel B: Common pacing modes VVI and DDD with descriptions, and ICD with shock coil on ventricular lead capable of anti-tachycardia pacing, cardioversion, defibrillation, and backup pacing. Panel C: ICD indications for secondary prevention after survived VT/VF and primary prevention with EF 35% or less, and cardiomyopathies. Panel D: CRT with three leads in right atrium, right ventricle, and coronary sinus for biventricular pacing, restoring synchrony with indications of EF 35% or less, LBBB, and QRS 150 ms or greater.</image>

Catheter Ablation

Catheter ablation is an invasive procedure that destroys arrhythmogenic tissue using radiofrequency energy or cryotherapy delivered through intracardiac catheters. This approach can be curative for many arrhythmias.

The electrophysiology study (EPS) that precedes ablation involves placing multiple electrode catheters in the heart to map electrical activation and identify the arrhythmia mechanism and location. Programmed electrical stimulation can induce arrhythmias for characterization. Electroanatomic mapping systems create three-dimensional reconstructions of cardiac chambers with color-coded activation patterns.

Ablation success rates vary by arrhythmia. AVNRT ablation targets the slow AV nodal pathway with success rates exceeding 95% and low risk of inadvertent complete heart block. AVRT/WPW ablation targets the accessory pathway, with similar success rates. Atrial flutter ablation creates a line of block across the cavotricuspid isthmus, with success rates exceeding 90%. Atrial fibrillation ablation is more complex, typically involving electrical isolation of the pulmonary veins (the source of triggers in most cases); single-procedure success rates are 70-80%, with some patients requiring multiple procedures. Ventricular tachycardia ablation targets reentrant circuits, often involving scar tissue; success depends on substrate complexity and is lower than for supraventricular arrhythmias.

Complications of catheter ablation include vascular complications at the access site (hematoma, arteriovenous fistula), cardiac perforation and tamponade (0.5-1% risk), stroke (particularly with left atrial procedures), pulmonary vein stenosis (with atrial fibrillation ablation), and heart block (with procedures near the AV node).

<image>Panel A: Electrophysiology laboratory setup with patient on table, fluoroscopy, and electroanatomic mapping display, with electrode catheters entering through the femoral vein and positioned in the coronary sinus, His bundle region, and right atrium. Panel B: Ablation targets for specific arrhythmias including AVNRT at the slow pathway, WPW at the accessory pathway, and atrial flutter across the cavotricuspid isthmus. Panel C: Ablation for atrial fibrillation showing pulmonary vein isolation with circumferential lesions, and VT ablation targeting substrate with scar border zone lesions. Panel D: Success rates listed as AVNRT/AVRT greater than 95%, flutter greater than 90%, AF 70-80% single procedure, and VT variable by substrate, with complications and approximate rates.</image>

Clinical Approach to Arrhythmias

The approach to narrow-complex tachycardia begins with assessing hemodynamic stability. If the patient is unstable (hypotensive, altered mental status, ischemic symptoms), proceed immediately to synchronized cardioversion. If stable, attempt vagal maneuvers (Valsalva, carotid sinus massage) to slow or terminate the arrhythmia. If unsuccessful, administer adenosine 6 mg IV push followed by 12 mg if needed—this will terminate most reentrant SVTs or reveal the underlying atrial rhythm in atrial fibrillation or flutter. Once the mechanism is identified (AVNRT, AVRT, atrial flutter, atrial fibrillation, or atrial tachycardia), proceed with appropriate management.

The approach to wide-complex tachycardia requires treating it as ventricular tachycardia until proven otherwise, especially in patients with structural heart disease. Assess hemodynamic stability. If unstable, proceed immediately to cardioversion (synchronized if organized, unsynchronized if VF or pulseless VT). If stable, consider pharmacologic treatment with amiodarone or procainamide. Obtain a 12-lead ECG and look for features distinguishing VT from SVT with aberrancy. Do not use adenosine routinely in wide-complex tachycardia, as it may cause hypotension in VT. Avoid AV nodal blockers in pre-excited atrial fibrillation.

Cardiac arrest rhythms are classified as shockable (VF, pulseless VT) or non-shockable (asystole, pulseless electrical activity). For VF or pulseless VT, deliver unsynchronized defibrillation immediately, then resume CPR for 2 minutes before rhythm check. Administer epinephrine 1 mg IV every 3-5 minutes and amiodarone 300 mg IV after the first shock (with an additional 150 mg for refractory VF). For asystole or PEA, provide CPR, give epinephrine, and search for reversible causes (hypoxia, hypovolemia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, and thrombosis).

<image>Panel A: Narrow-complex tachycardia pathway: assess stability, if unstable proceed to cardioversion, if stable attempt vagal maneuvers then adenosine to identify mechanism and treat accordingly. Panel B: Wide-complex tachycardia pathway: treat as VT, if unstable proceed to cardioversion, if stable use amiodarone or procainamide and determine VT versus SVT with aberrancy. Panel C: Cardiac arrest algorithm for shockable rhythms: VF or pulseless VT requiring defibrillation plus CPR plus epinephrine plus amiodarone. Panel D: Non-shockable cardiac arrest algorithm: asystole or PEA requiring CPR plus epinephrine plus treatment of reversible causes including the Hs and Ts.</image>

Summary

Arrhythmias arise from abnormal impulse formation (enhanced automaticity, triggered activity) or abnormal impulse conduction (reentry, block). Bradyarrhythmias include sinus bradycardia, sick sinus syndrome, and AV blocks of varying degrees. High-grade AV blocks typically require permanent pacing.

Supraventricular tachycardias include sinus tachycardia (physiologic response), atrial fibrillation (chaotic atrial activity with irregularly irregular ventricular response), atrial flutter (organized macro-reentrant atrial tachycardia with sawtooth waves), and AVNRT and AVRT (reentrant tachycardias involving the AV node or accessory pathways). Atrial fibrillation management addresses rate control, rhythm control, and stroke prevention.

Ventricular arrhythmias range from benign PVCs to life-threatening VT and VF. Torsades de pointes is polymorphic VT associated with long QT syndrome. Magnesium and correction of underlying causes are first-line treatment.

Antiarrhythmic drugs are classified by mechanism: class I (sodium channel blockers), class II (beta-blockers), class III (potassium channel blockers), class IV (calcium channel blockers). All antiarrhythmics carry proarrhythmic risk.

Device therapy includes pacemakers for bradycardia, ICDs for prevention of sudden cardiac death, and CRT for heart failure with dyssynchrony. Catheter ablation is curative for many arrhythmias, with highest success rates for AVNRT, AVRT, and atrial flutter.

Key Terms

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