Cardiac arrhythmia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2] James Nasr[3]

Cardiac arrhythmias are a heterogeneous group of disorders caused by abnormal formation or conduction of cardiac electrical impulses. They may produce a heart rate that is abnormally slow, abnormally fast, or irregular and may arise from the atria, atrioventricular junction, ventricles, specialized conduction system, or an implanted cardiac device.^[1][2][3]

The clinical spectrum ranges from incidental premature complexes and physiologic rhythm variation to sustained ventricular tachycardia, ventricular fibrillation, cardiac arrest, and sudden cardiac death. Arrhythmias may also cause palpitations, syncope, myocardial ischemia, acute heart failure, tachycardia-mediated cardiomyopathy, systemic thromboembolism, and stroke.

This parent chapter summarizes the general classification, mechanisms, causes, evaluation, and management principles that apply across arrhythmia syndromes. Detailed diagnostic criteria and disease-specific management are addressed in the corresponding pages for individual arrhythmias.

Milestone	Clinical importance
Development of the electrocardiogram	Einthoven's electrocardiographic work established noninvasive recording of cardiac electrical activity and enabled rhythm classification.
Electrical defibrillation and cardiac pacing	External defibrillation, temporary pacing, and permanent pacemakers transformed the management of lethal tachyarrhythmias and symptomatic bradyarrhythmias.
Implantable cardioverter-defibrillator	Implantable defibrillation provided continuous detection and termination of malignant ventricular arrhythmias.[4]
Cardiac Arrhythmia Suppression Trial	CAST established that pharmacologic suppression of asymptomatic or mildly symptomatic ventricular ectopy after myocardial infarction with encainide or flecainide could increase mortality. Excess mortality was first reported in the preliminary 1989 publication and confirmed in the final 1991 analysis.[5][6]
Catheter ablation	Electrophysiologic mapping and catheter ablation enabled mechanism-directed treatment of accessory pathways, atrioventricular nodal reentry, atrial flutter, atrial fibrillation, and ventricular tachycardia.
Pulmonary-vein triggers of atrial fibrillation	Recognition that pulmonary-vein ectopy commonly initiates atrial fibrillation provided the basis for pulmonary-vein isolation.[7]

Arrhythmias are classified according to the ventricular rate, site of origin, QRS morphology, electrophysiologic mechanism, duration, and clinical context.

Category	Principal disorders
Bradyarrhythmias	Sinus bradycardia, sinus node dysfunction, sinoatrial block, sinus arrest, junctional or ventricular escape rhythms, and atrioventricular block
Normal-rate rhythm disturbances	Premature atrial, junctional, or ventricular complexes; bigeminy; parasystole; and selected forms of atrioventricular dissociation
Tachyarrhythmias	Sinus, atrial, junctional, atrioventricular reentrant, and ventricular tachyarrhythmias

Category	Examples	Clinical considerations
Supraventricular arrhythmias	Sinus tachycardia, focal or multifocal atrial tachycardia, atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, AV reentrant tachycardia, and junctional tachycardia	Usually produce a narrow QRS complex unless accompanied by pre-existing or rate-related aberrancy, ventricular pre-excitation, or ventricular pacing
Ventricular arrhythmias	Premature ventricular complexes, accelerated idioventricular rhythm, monomorphic or polymorphic ventricular tachycardia, torsades de pointes, and ventricular fibrillation	Usually produce a wide QRS complex and may cause severe hemodynamic compromise or sudden cardiac death
Wide-complex supraventricular tachycardia	Supraventricular tachycardia with bundle-branch aberrancy, ventricular pre-excitation, or ventricular pacing	Must be differentiated from ventricular tachycardia; an undifferentiated regular wide-complex tachycardia should generally be treated as ventricular tachycardia until proven otherwise

Mechanism	Description	Representative arrhythmias
Reentry	Repetitive propagation of an impulse through an anatomic or functional circuit containing regions with different conduction and refractory properties	AV nodal reentrant tachycardia, AV reentrant tachycardia, typical atrial flutter, scar-mediated monomorphic ventricular tachycardia, and many sustained tachyarrhythmias
Enhanced or abnormal automaticity	Accelerated spontaneous depolarization of normal pacemaker tissue or spontaneous depolarization of myocardial tissue that does not normally act as a pacemaker	Sinus tachycardia, focal atrial tachycardia, accelerated junctional rhythm, and accelerated idioventricular rhythm
Triggered activity	Impulse formation caused by afterdepolarizations that reach threshold	Torsades de pointes associated with early afterdepolarizations; digitalis-associated or catecholamine-mediated arrhythmias associated with delayed afterdepolarizations

Conduction disorders may coexist with arrhythmias but are not necessarily arrhythmias themselves. They include:

• First degree AV block
• Second degree AV block
• Third degree AV block
• Right bundle branch block
• Left bundle branch block
• Left anterior or posterior fascicular block
• Bifascicular conduction disease
• Nonspecific intraventricular conduction delay

Inherited channelopathies and cardiomyopathies with major arrhythmic manifestations include:

• Long QT syndrome
• Short QT syndrome
• Brugada syndrome
• Catecholaminergic polymorphic ventricular tachycardia
• Arrhythmogenic cardiomyopathy
• Andersen–Tawil syndrome
• Early repolarization syndrome
• Arrhythmia associated with hypertrophic cardiomyopathy

Normal cardiac activation begins in the sinoatrial node, spreads through the atrial myocardium, and reaches the atrioventricular node. After physiologic delay in the atrioventricular node, the impulse travels through the bundle of His, right and left bundle branches, fascicles, and Purkinje network to activate the ventricles in a coordinated sequence.

The sinus node normally generates impulses through spontaneous phase-4 depolarization. The atrioventricular node delays conduction and limits transmission of excessively rapid atrial impulses to the ventricles.

The cardiac action potential consists of phases 0 through 4 and is generated by coordinated sodium, calcium, and potassium currents.

Phase	Principal electrophysiologic event	Major currents
0	Rapid depolarization	Fast inward sodium current in atrial and ventricular myocardium; calcium-dependent depolarization in nodal tissue
1	Early repolarization	Transient outward potassium current
2	Plateau	Balance between inward L-type calcium current and outward potassium currents
3	Repolarization	Predominantly outward potassium currents
4	Resting membrane potential or spontaneous diastolic depolarization	Stable in working myocardium; spontaneous depolarization in pacemaker cells involving the funny current and calcium currents

Genetic or pharmacologic disruption of ion-channel function may alter conduction velocity, refractoriness, automaticity, and repolarization. Loss-of-function variants affecting potassium currents may prolong repolarization, whereas abnormal sodium-channel function may produce long-QT, Brugada, conduction-system, or overlapping phenotypes.

Reentry generally requires:

1. An anatomic or functional circuit
2. Unidirectional conduction block in one limb
3. Sufficiently slow conduction through an alternate pathway
4. Recovery of excitability in previously refractory tissue

Examples include atrioventricular nodal reentry, reentry involving an accessory pathway, cavotricuspid-isthmus-dependent atrial flutter, and scar-mediated ventricular tachycardia.

Enhanced automaticity may result from increased sympathetic tone, electrolyte abnormalities, ischemia, hypoxia, stretch, drugs, or injury to myocardial tissue. Abnormal automaticity commonly produces rhythms that demonstrate gradual acceleration and deceleration rather than abrupt initiation and termination.

Early afterdepolarizations occur during phases 2 or 3 of repolarization and are promoted by prolonged action-potential duration, bradycardia, electrolyte depletion, and QT-prolonging drugs. They may initiate torsades de pointes.

Delayed afterdepolarizations occur after repolarization and are associated with intracellular calcium overload. They may occur with digitalis toxicity, catecholamine excess, and catecholaminergic polymorphic ventricular tachycardia.

Fibrosis, myocardial scar, chamber dilation, myocyte hypertrophy, and altered gap-junction distribution may create regions of conduction slowing and nonuniform refractoriness. These changes facilitate reentry and help sustain arrhythmias.

Persistent atrial tachyarrhythmia can shorten atrial refractoriness and promote additional structural remodeling, supporting the clinical observation that prolonged atrial fibrillation becomes increasingly difficult to terminate and maintain in sinus rhythm.

Post-infarction scar may contain surviving myocardial bundles separated by fibrosis. These channels permit slow conduction and form the substrate for monomorphic ventricular tachycardia.

Sympathetic activation increases automaticity and triggered activity and may reduce ventricular fibrillation thresholds. It is particularly relevant to catecholaminergic polymorphic ventricular tachycardia and selected long-QT phenotypes.

Increased vagal tone slows sinoatrial and atrioventricular nodal conduction. Vagal maneuvers may terminate atrioventricular-node-dependent reentrant tachycardias but may also facilitate atrial fibrillation in susceptible patients.

Arrhythmias may arise from structural cardiac disease, ischemia, systemic illness, electrolyte or metabolic abnormalities, endocrine disorders, drugs, toxins, inherited disease, autonomic influences, or no identifiable structural cause.

Etiologic category	Examples	Common arrhythmic manifestations
Coronary artery disease and myocardial ischemia	Acute myocardial infarction, chronic ischemic scar, reperfusion	Sinus tachycardia, atrioventricular block, premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation
Cardiomyopathy	Dilated, hypertrophic, arrhythmogenic, restrictive, inflammatory, or infiltrative cardiomyopathy	Atrial fibrillation, conduction disease, ventricular tachycardia, and sudden cardiac death
Valvular heart disease	Mitral stenosis or regurgitation, aortic stenosis, and advanced multivalvular disease	Atrial fibrillation, atrial flutter, conduction disease, and ventricular arrhythmias
Congenital heart disease	Native malformation, postoperative scar, and Ebstein anomaly	Atrial tachycardia, macroreentrant atrial tachycardia, accessory-pathway-mediated tachycardia, and ventricular arrhythmias
Inflammatory or infiltrative disease	Myocarditis, cardiac sarcoidosis, and cardiac amyloidosis	Atrioventricular block, ventricular tachycardia, atrial arrhythmias, and sudden cardiac death
Cardiac surgery or intervention	Postoperative inflammation, atrial injury, ischemia, electrolyte shifts, and device-related causes	Postoperative atrial fibrillation, atrial flutter, bradyarrhythmia, and ventricular arrhythmia

• Hypokalemia may promote ventricular ectopy, QT-related proarrhythmia, and torsades de pointes.
• Hyperkalemia may cause sinus slowing, conduction block, QRS widening, ventricular arrhythmia, and asystole.
• Hypomagnesemia increases susceptibility to ventricular arrhythmias and potentiates hypokalemia-related proarrhythmia.
• Abnormal calcium concentrations alter repolarization and conduction.
• Acidemia, alkalemia, hypoxemia, and severe systemic metabolic disturbance may precipitate arrhythmias.
• Hypothermia may cause sinus bradycardia, conduction delay, atrial fibrillation, and ventricular arrhythmias.
• Hyperthermia may produce sinus tachycardia and catecholamine-mediated arrhythmias.

• Hyperthyroidism is associated with sinus tachycardia and atrial fibrillation.
• Hypothyroidism may cause sinus bradycardia and QT prolongation.
• Pheochromocytoma may produce catecholamine-mediated supraventricular or ventricular tachyarrhythmias.

• Pulmonary embolism
• Sepsis and critical illness
• Hypoxemic respiratory failure
• Obstructive sleep apnea
• Acute neurologic injury
• Major surgery
• Alcohol intoxication or binge alcohol exposure
• Stimulant exposure
• Autonomic dysfunction

Drug-induced arrhythmia should be considered when a new rhythm abnormality follows medication initiation, dose escalation, drug interaction, renal or hepatic deterioration, or development of electrolyte abnormalities.

Mechanism	Representative agents or exposures	Potential manifestations
QT prolongation and early afterdepolarizations	Class IA or III antiarrhythmic drugs, selected antimicrobials, antipsychotics, antiemetics, and methadone	QT prolongation and torsades de pointes
Sodium-channel blockade	Class I antiarrhythmic drugs, tricyclic antidepressants, and selected toxic ingestions	QRS widening, conduction block, monomorphic ventricular tachycardia, or ventricular fibrillation
Excess atrioventricular nodal blockade	Beta blockers, non-dihydropyridine calcium-channel blockers, digoxin, and interacting combinations	Sinus bradycardia, atrioventricular block, and hypotension
Digitalis toxicity	Digoxin accumulation or toxicity	Premature complexes, accelerated junctional rhythm, atrial tachycardia with block, bidirectional ventricular tachycardia, and other rhythm disturbances
Sympathomimetic effect	Cocaine, amphetamines, epinephrine, and inotropic drugs	Sinus tachycardia, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation
Cancer therapy-associated effects	Anthracyclines, selected tyrosine-kinase inhibitors, and arsenic trioxide	QT prolongation, atrial arrhythmia, ventricular arrhythmia, or arrhythmia secondary to cardiomyopathy

The continuously updated CredibleMeds database should be consulted when assessing the torsades-de-pointes risk of a medication.^[8]

CAST directly demonstrated excess mortality with encainide and flecainide in patients with recent myocardial infarction and ventricular ectopy, many of whom had left-ventricular dysfunction. Current guidelines consequently avoid class IC antiarrhythmic drugs in patients with prior myocardial infarction or significant ischemic heart disease and generally avoid them in clinically important structural heart disease. CAST did not directly study every form of structural heart disease, and observational data in selected patients with coronary disease but no prior myocardial infarction and preserved ventricular function remain hypothesis-generating rather than definitive.^[5][6][9]

Inherited arrhythmia syndromes include:

• Long-QT syndrome
• Brugada syndrome
• Catecholaminergic polymorphic ventricular tachycardia
• Short-QT syndrome
• Andersen–Tawil syndrome
• Arrhythmogenic cardiomyopathy
• Hypertrophic cardiomyopathy
• Familial progressive cardiac conduction disease
• Inherited dilated cardiomyopathies with prominent conduction or arrhythmic phenotypes

An apparently idiopathic arrhythmia may represent an incompletely expressed inherited syndrome. Family history and phenotype-directed genetic evaluation are important when arrhythmia occurs at a young age, during exertion, with characteristic ECG abnormalities, or in a family with unexplained sudden death.

Symptoms attributed to arrhythmia are often nonspecific. Documentation of the rhythm during symptoms is central to diagnosis.

Presentation	Features that increase suspicion for arrhythmia	Important alternatives	Principal evaluation
Palpitations	Sudden onset and termination, rapid regular pounding, irregular pulse, neck pounding, exertional episodes, or associated presyncope	Anxiety, panic symptoms, hyperthyroidism, anemia, fever, stimulant exposure, hypoglycemia, and heightened awareness of sinus rhythm	History, pulse examination, 12-lead ECG, laboratory testing when indicated, and ambulatory rhythm monitoring
Syncope	Abrupt loss of consciousness without prodrome, occurrence during exertion or while supine, preceding palpitations, structural heart disease, abnormal ECG, or family history of sudden death	Reflex syncope, orthostatic hypotension, seizure, hypoglycemia, intoxication, and cerebrovascular disease	ECG, orthostatic vital signs, structural evaluation, ambulatory monitoring, and selected electrophysiologic or neurologic testing
Sinus tachycardia	Persistent tachycardia disproportionate to the apparent physiologic stimulus	Pain, fever, hypovolemia, anemia, pulmonary embolism, sepsis, hyperthyroidism, hypoxemia, and medication or stimulant effects	Identify and treat the underlying physiologic or pathologic driver before diagnosing a primary sinus-node disorder
Wide-complex tachycardia	Prior myocardial infarction, cardiomyopathy, atrioventricular dissociation, capture or fusion complexes, or extreme axis abnormality	Supraventricular tachycardia with aberrancy, pre-excited tachycardia, electrolyte disturbance, and drug toxicity	Treat undifferentiated wide-complex tachycardia as ventricular tachycardia until an alternative mechanism is established
Chest discomfort or dyspnea	Symptoms occurring simultaneously with documented rapid or slow rhythm	Acute coronary syndrome, pulmonary embolism, heart failure, pulmonary disease, anemia, and panic symptoms	Hemodynamic assessment, ECG, cardiac biomarkers when indicated, and evaluation for structural or ischemic disease

The epidemiology of cardiac arrhythmia varies substantially by arrhythmia subtype, age, structural heart disease, and ascertainment method.

• Atrial fibrillation is the most common sustained arrhythmia.
• Approximately 10.55 million adults in the United States have atrial fibrillation, and prevalence is expected to continue increasing as the population ages.^[10]
• Atrial-fibrillation prevalence increases substantially with age.
• Ventricular tachyarrhythmias are major immediate mechanisms of sudden cardiac death.
• Bradyarrhythmias and conduction-system disease become increasingly common with aging and structural heart disease.

Risk factors vary by arrhythmia phenotype.

• Increasing age
• Sex-related differences that vary by arrhythmia phenotype
• Family history of arrhythmia, cardiomyopathy, or sudden cardiac death
• Pathogenic genetic variants
• Congenital heart disease
• Prior myocardial infarction or fixed myocardial scar

• Hypertension
• Obesity
• Obstructive sleep apnea
• Diabetes mellitus
• Heart failure
• Tobacco exposure
• Excessive alcohol consumption
• Stimulant or sympathomimetic exposure
• Physical inactivity and poor cardiorespiratory fitness
• Electrolyte abnormalities
• Uncontrolled thyroid disease

Risk-factor modification is an integral component of atrial-fibrillation management and may reduce arrhythmia burden, progression, and recurrence.^[1][11][12]

Very high levels of endurance exercise may be associated with selected atrial or ventricular arrhythmias in susceptible athletes, while regular moderate physical activity generally forms part of cardiovascular risk reduction. Exercise-associated syncope, exertional ventricular arrhythmia, or a family history of sudden death requires focused cardiovascular evaluation.

Evidence and recommendations for screening asymptomatic adults for atrial fibrillation differ among organizations. The U.S. Preventive Services Task Force has concluded that evidence is insufficient to determine the balance of benefits and harms of routine ECG-based screening in asymptomatic adults.^[13]

Targeted rhythm assessment may include pulse palpation, automated blood-pressure devices, single-lead ECG devices, wearable photoplethysmography, or intermittent ECG monitoring. A consumer-device alert is not by itself a definitive diagnosis; clinically actionable atrial fibrillation should be confirmed by review of an ECG-quality rhythm tracing.

Potential harms of screening include false-positive results, anxiety, unnecessary testing, incidental findings, and anticoagulation-related bleeding after uncertain or very low-burden device-detected episodes.

Preparticipation cardiovascular screening generally begins with a personal history, family history, and physical examination. The role of routine ECG screening varies by jurisdiction, sporting organization, and available expertise.

Abnormal findings, exertional syncope, exertional chest pain, unexplained exercise intolerance, complex ventricular ectopy, or a family history of premature sudden death should prompt further evaluation.

Clinical screening and phenotype-directed cascade testing should be considered in relatives of patients with a confirmed inherited channelopathy or arrhythmogenic cardiomyopathy. Evaluation may include:

• Three-generation family history
• Resting 12-lead ECG
• Exercise testing
• Ambulatory ECG monitoring
• Echocardiography or cardiac MRI
• Targeted testing for a known familial pathogenic or likely pathogenic variant

Genetic testing should be interpreted in conjunction with the clinical phenotype and appropriate genetic counseling.^[14]

Prognosis depends primarily on the arrhythmia, ventricular rate, duration, underlying myocardial substrate, comorbidities, and availability of effective treatment.

• Hemodynamic instability
• Syncope and traumatic injury
• Myocardial ischemia
• Acute or chronic heart failure
• Tachycardia-mediated cardiomyopathy
• Bradycardia-mediated low-output states
• Systemic thromboembolism
• Ischemic stroke
• Cardiac arrest
• Sudden cardiac death
• Adverse effects of antiarrhythmic drugs, anticoagulation, ablation, or implanted devices

Persistent or frequently recurrent tachyarrhythmia may cause left-ventricular systolic dysfunction. Improvement after control of the arrhythmia supports the diagnosis, although recovery may be incomplete and recurrence may rapidly reproduce ventricular dysfunction.

Atrial fibrillation and atrial flutter may lead to left-atrial or left-atrial-appendage thrombus and systemic embolization. Stroke-prevention decisions should be based on validated thromboembolic-risk assessment rather than apparent maintenance of sinus rhythm alone.^[1]

Sustained ventricular tachycardia and ventricular fibrillation are major immediate mechanisms of sudden cardiac death. Risk is highest in patients with prior cardiac arrest, sustained ventricular arrhythmia, significant ventricular dysfunction, ischemic scar, selected cardiomyopathies, or high-risk inherited arrhythmia syndromes.

Arrhythmias may be asymptomatic or produce intermittent symptoms that are absent during clinical evaluation.

• Palpitations
• Rapid, slow, forceful, or irregular heartbeat
• Presyncope or syncope
• Dizziness or lightheadedness
• Dyspnea
• Chest pressure or discomfort
• Fatigue
• Exercise intolerance
• Weakness
• Acute confusion in older or vulnerable patients
• Polyuria during selected supraventricular tachyarrhythmias

The history should establish:

• Abrupt versus gradual onset and termination
• Regular versus irregular sensation
• Episode duration and frequency
• Relationship to exertion, sleep, posture, meals, alcohol, caffeine, or emotional stress
• Associated syncope, chest pain, dyspnea, neurologic symptoms, or heart-failure symptoms
• Prior myocardial infarction, cardiomyopathy, valve disease, congenital heart disease, or cardiac surgery
• Current and recently discontinued medications
• Use of stimulants, alcohol, recreational drugs, or supplements
• History of thyroid, pulmonary, renal, or systemic illness
• Prior ECGs, monitors, cardioversion, ablation, pacemaker, or defibrillator
• Family history of cardiomyopathy, channelopathy, unexplained accidents, drowning, seizures, or premature sudden death

Urgent evaluation is required for:

• Syncope during exertion or while supine
• Arrhythmia accompanied by hypotension, ischemic chest discomfort, altered mental status, or acute heart failure
• Sustained wide-complex tachycardia
• Palpitations followed by syncope
• Documented ventricular tachycardia
• Marked QT prolongation with ventricular ectopy
• Family history of premature unexplained sudden death
• Arrhythmia associated with severe electrolyte abnormality or drug toxicity

The physical examination should determine hemodynamic stability and identify evidence of the rhythm, structural heart disease, or a systemic precipitant.

• Heart rate and rhythm
• Blood pressure and orthostatic measurements when appropriate
• Respiratory rate and oxygen saturation
• Peripheral pulse regularity and pulse deficit
• Fever or hypothermia

• Irregularly irregular pulse may suggest atrial fibrillation.
• Regular cannon A waves may occur with atrioventricular dissociation.
• Intermittent cannon A waves and variable first-heart-sound intensity may occur when atrial and ventricular contraction are dissociated.
• Murmurs may indicate valvular or congenital structural disease.
• Displaced apical impulse, gallop rhythm, elevated jugular venous pressure, edema, or pulmonary crackles may indicate cardiomyopathy or heart failure.

• Thyroid enlargement, tremor, hyperreflexia, or other findings of thyrotoxicosis
• Pallor suggesting anemia
• Findings of infection or sepsis
• Signs of pulmonary embolism or pulmonary disease
• Neurologic deficit suggesting embolic stroke
• Features of inherited syndromes or neuromuscular disease when clinically suspected

A modified Valsalva maneuver may terminate atrioventricular-node-dependent supraventricular tachycardia. Carotid sinus massage may be diagnostic or therapeutic in selected patients but should be avoided when carotid vascular disease, prior stroke, transient ischemic attack, or a carotid bruit creates concern for embolic risk.^[15]

Initial evaluation should answer the following questions:

1. Is the patient hemodynamically unstable?
2. Is the rhythm causing or contributing to myocardial ischemia, acute heart failure, syncope, or shock?
3. Is the rhythm supraventricular or ventricular?
4. Is the QRS complex narrow or wide?
5. Is the rhythm regular or irregular?
6. Is there an immediately reversible cause?
7. Is structural or inherited heart disease present?

A 12-lead electrocardiogram should be obtained during symptoms whenever possible.

Systematic assessment includes:

• Ventricular and atrial rates
• Rhythm regularity
• P-wave morphology and relationship to QRS complexes
• PR interval
• QRS duration, axis, and morphology
• QT and corrected QT interval
• Atrioventricular association or dissociation
• Premature complexes
• Pre-excitation
• Ischemic changes
• Brugada pattern or other channelopathy-associated findings
• Evidence of ventricular hypertrophy, myocardial scar, or conduction disease

An irregular wide-complex tachycardia raises concern for polymorphic ventricular tachycardia, atrial fibrillation with aberrancy, or pre-excited atrial fibrillation. A regular wide-complex tachycardia in a patient with structural heart disease is ventricular tachycardia unless convincingly demonstrated otherwise.

The monitoring method should be matched to symptom frequency.

Modality	Typical clinical use	Principal limitation
Continuous inpatient telemetry	Acute illness, high-risk symptoms, drug initiation, or active rhythm instability	Limited to the monitored hospitalization
Short-term Holter monitor	Daily or frequent symptoms; quantification of ectopy or rate control	Low yield when events are infrequent
Patch monitor	Continuous outpatient recording over several days to weeks	May not capture rare events
Patient-activated event monitor	Intermittent symptoms when the patient can activate the device	May miss abrupt syncope or asymptomatic episodes
Mobile cardiac outpatient telemetry	Near-real-time detection of clinically important arrhythmia	Cost, adherence, and false-positive alerts
Implantable loop recorder	Recurrent unexplained syncope or very infrequent suspected arrhythmia	Invasive implantation and potential signal misclassification
Consumer wearable or handheld ECG	Opportunistic documentation of intermittent rhythm symptoms	Requires clinical confirmation and may generate false-positive findings

Laboratory evaluation should be directed by the clinical context.

Test	Clinical purpose
Serum potassium, magnesium, and calcium	Detect reversible contributors to ectopy, conduction disturbance, QT prolongation, or ventricular arrhythmia
Renal function	Identify electrolyte disturbance and guide dosing of renally cleared antiarrhythmic drugs and anticoagulants
Hepatic function	Evaluate systemic illness and guide selected medication use
Thyroid-stimulating hormone with appropriate thyroid studies	Evaluate suspected thyroid-related tachyarrhythmia or bradyarrhythmia and monitor selected antiarrhythmic therapies
Complete blood count	Assess anemia, infection, or bleeding
Cardiac troponin	Evaluate suspected acute myocardial injury or ischemia; elevation is not specific for acute coronary occlusion
BNP or NT-proBNP	Support assessment of heart failure when clinically suspected
Toxicology testing	Evaluate suspected stimulant, medication, or toxic exposure
Digoxin concentration	Evaluate suspected digoxin toxicity; interpretation must consider timing of the sample

Transthoracic echocardiography is generally indicated when a newly recognized sustained arrhythmia, abnormal ECG, heart-failure finding, murmur, cardiomyopathy, or structural cardiac disease is suspected. Assessment commonly includes:

• Left- and right-ventricular size and systolic function
• Atrial size
• Valvular disease
• Ventricular hypertrophy
• Regional wall-motion abnormality
• Congenital or acquired structural abnormality
• Pericardial disease

Transesophageal echocardiography may be used to exclude left-atrial-appendage thrombus before cardioversion when atrial fibrillation or atrial flutter has persisted for more than 48 hours, has an unknown duration, or adequate preceding anticoagulation has not been established.^[1]

Cardiac CT may be used for:

• Pulmonary-vein and left-atrial anatomy before atrial-fibrillation ablation
• Left-atrial-appendage assessment and procedural planning
• Coronary assessment when ischemic disease is suspected
• Selected postprocedural complications
• Structural assessment when other imaging is inadequate or contraindicated

Cardiac magnetic resonance imaging provides ventricular functional assessment and myocardial tissue characterization. It is particularly useful when evaluating:

• Arrhythmogenic cardiomyopathy
• Myocarditis
• Cardiac sarcoidosis
• Infiltrative cardiomyopathy
• Nonischemic or ischemic myocardial scar
• Unexplained ventricular arrhythmia
• Substrate before selected ventricular-tachycardia ablation procedures

Late gadolinium enhancement identifies myocardial fibrosis or scar that may provide an arrhythmogenic substrate and may contribute to risk stratification.

• FDG-PET may support diagnosis and assessment of inflammatory activity in suspected cardiac sarcoidosis.
• Myocardial perfusion imaging may evaluate inducible ischemia when clinically appropriate.
• Chest radiography may identify cardiomegaly, pulmonary congestion, alternative pulmonary disease, or gross device-lead abnormalities.

An invasive electrophysiology study may establish the mechanism of an arrhythmia, assess conduction-system disease, induce suspected tachycardia, guide risk assessment in selected patients, and provide mapping for catheter ablation.

Electrophysiology study is not routinely required for every patient with palpitations or a documented arrhythmia. Its use depends on the suspected mechanism, clinical risk, diagnostic uncertainty, and whether ablation is being considered.

Management is determined by hemodynamic stability, arrhythmia mechanism, symptom burden, underlying structural disease, thromboembolic risk, and patient preferences.

Hemodynamic instability requires immediate treatment rather than prolonged diagnostic testing.

Features of instability include:

• Hypotension or shock
• Altered mental status
• Ongoing ischemic chest discomfort
• Acute pulmonary edema or severe heart failure
• Syncope or signs of critically impaired perfusion

A tachyarrhythmia with a pulse that is causing instability generally requires immediate synchronized cardioversion. Pulseless ventricular tachycardia and ventricular fibrillation require immediate defibrillation and cardiopulmonary resuscitation according to resuscitation protocols.

Symptomatic unstable bradycardia may require atropine, transcutaneous pacing, chronotropic medication, and preparation for transvenous pacing, depending on the underlying rhythm and response to initial treatment.

Reversible causes—including ischemia, hypoxemia, electrolyte abnormality, drug toxicity, and severe metabolic disturbance—should be treated concurrently.

For a stable patient:

1. Obtain and interpret a 12-lead ECG.
2. Determine whether the QRS complex is narrow or wide.
3. Determine whether the rhythm is regular or irregular.
4. Identify atrial activity and its relationship to the QRS complexes.
5. Correct reversible causes.
6. Select rate control, rhythm control, observation, or definitive ablation according to the specific rhythm and clinical context.

Atrioventricular nodal blocking drugs should not be administered to a patient with pre-excited atrial fibrillation because preferential blockade of the atrioventricular node may facilitate rapid conduction through the accessory pathway and precipitate ventricular fibrillation.^[1]

The Vaughan-Williams system provides a practical, although incomplete, classification of antiarrhythmic drugs.

Class	Principal action	Representative drugs	Major clinical cautions
IA	Moderate sodium-channel blockade with repolarization prolongation	Procainamide, quinidine, disopyramide	QRS or QT prolongation, torsades de pointes, hypotension, and drug-specific toxicities
IB	Sodium-channel blockade with preferential effect in depolarized or ischemic ventricular tissue	Lidocaine, mexiletine	Neurologic toxicity and limited effectiveness for many supraventricular arrhythmias
IC	Potent sodium-channel blockade and marked conduction slowing	Flecainide, propafenone	Avoid in patients with prior myocardial infarction or significant ischemic heart disease; generally avoid in clinically important structural heart disease. The direct randomized evidence for harm is strongest in the post-myocardial-infarction CAST population
II	Beta-adrenergic blockade	Metoprolol, propranolol, atenolol, esmolol	Bradycardia, atrioventricular block, hypotension, bronchospasm in susceptible patients, and worsening acute decompensated heart failure
III	Predominantly potassium-channel blockade and action-potential prolongation	Amiodarone, sotalol, dofetilide, ibutilide	QT prolongation and torsades risk with several agents; bradycardia; drug-specific organ toxicity and interactions
IV	Non-dihydropyridine calcium-channel blockade	Verapamil, diltiazem	Bradycardia, atrioventricular block, hypotension, negative inotropy, and danger in pre-excited atrial fibrillation or undifferentiated wide-complex tachycardia
Other	Mechanisms outside the four principal classes	Adenosine, digoxin, ivabradine	Drug selection depends on the specific arrhythmia; each agent has important rhythm-specific contraindications

Before initiating a QT-prolonging antiarrhythmic drug, clinicians should assess baseline QTc, potassium, magnesium, renal function, interacting medications, and relevant bradycardia or conduction disease.

Dofetilide requires monitored inpatient initiation. Sotalol initiation or reinitiation generally requires close ECG, renal-function, and electrolyte monitoring according to patient risk and applicable protocol.

Long-term amiodarone therapy requires surveillance for thyroid, hepatic, pulmonary, ocular, neurologic, dermatologic, and drug-interaction complications.

Rate control reduces the ventricular response without necessarily terminating the atrial rhythm. Rhythm control aims to restore and maintain sinus rhythm using cardioversion, antiarrhythmic drugs, catheter ablation, or a combination.

The choice between these strategies depends on:

• Arrhythmia type and duration
• Symptom burden
• Ventricular function
• Heart-failure status
• Structural or ischemic heart disease
• Previous treatment response
• Drug contraindications
• Likelihood of successful ablation
• Patient goals and preferences

In the EAST-AFNET 4 trial, early rhythm-control therapy in patients with atrial fibrillation diagnosed within the preceding year reduced the composite of cardiovascular death, stroke, or hospitalization for worsening heart failure or acute coronary syndrome compared with usual care (3.9 versus 5.0 events per 100 person-years; hazard ratio, 0.79).^[16]

Stroke prevention is a central component of atrial-fibrillation management.

• Thromboembolic risk should be assessed with a validated clinical risk model.
• Direct oral anticoagulants are generally preferred over warfarin for eligible patients with atrial fibrillation.
• Warfarin remains the established anticoagulant for patients with a mechanical prosthetic heart valve or clinically significant rheumatic mitral stenosis.
• Bleeding-risk assessment should identify modifiable bleeding factors but should not automatically be used to deny anticoagulation when the expected stroke-prevention benefit is substantial.
• Anticoagulation decisions should be based on thromboembolic risk and should not be discontinued solely because sinus rhythm appears to have been restored.^[1]

Catheter ablation is a definitive or rhythm-control treatment for many arrhythmias.

Arrhythmia	Principal ablation strategy	General role
AV nodal reentrant tachycardia	Slow-pathway modification	Highly effective definitive therapy for recurrent or symptomatic disease
Accessory-pathway-mediated tachycardia	Accessory-pathway ablation	Definitive treatment for recurrent AV reentrant tachycardia or clinically important pre-excitation
Typical atrial flutter	Cavotricuspid-isthmus ablation	Preferred definitive treatment in many symptomatic or recurrent cases
Atrial fibrillation	Pulmonary-vein isolation with additional substrate treatment when appropriate	First-line or early rhythm-control option in selected symptomatic patients and an option after drug failure or intolerance
Focal atrial tachycardia	Mapping and ablation of the focal source	Considered for recurrent, symptomatic, incessant, or tachycardia-mediated cardiomyopathy
Ventricular tachycardia	Mapping and elimination or isolation of critical ventricular arrhythmia substrate	Used for recurrent ventricular tachycardia, electrical storm, or drug-refractory disease; also supported as a first-line treatment strategy in selected patients with ischemic cardiomyopathy and ventricular tachycardia

The VANISH trial demonstrated that catheter ablation was superior to escalation of antiarrhythmic-drug therapy in patients with ischemic cardiomyopathy and recurrent ventricular tachycardia despite antiarrhythmic treatment.^[17]

The VANISH2 trial subsequently demonstrated that catheter ablation was superior to antiarrhythmic-drug therapy as an initial treatment strategy in patients with ischemic cardiomyopathy and clinically significant ventricular tachycardia. Ablation reduced the composite of death, ventricular-tachycardia storm, appropriate ICD shock, or treated sustained ventricular tachycardia (hazard ratio, 0.75; 95% confidence interval, 0.58–0.97).^[18]

In selected patients with atrial fibrillation and heart failure, catheter ablation may improve rhythm control and clinical outcomes compared with medical therapy alone.^[19]

Permanent pacing may be indicated for:

• Symptomatic sinus node dysfunction when symptoms correlate with bradycardia
• High-grade or complete atrioventricular block not caused by a reversible condition
• Selected symptomatic conduction disorders
• Selected neuromuscular or infiltrative disorders with progressive conduction disease
• Necessary medication therapy that produces clinically important bradycardia when no suitable alternative exists

The need for pacing should be based on the type of conduction disease, symptom correlation, reversibility, expected ventricular pacing burden, ventricular function, and anticipated progression.^[2]

Conduction-system pacing, including His-bundle or left-bundle-branch-area pacing, may preserve more physiologic ventricular activation in selected patients. Long-term comparative outcomes and optimal patient selection continue to evolve.

An implantable cardioverter-defibrillator may be indicated for:

• Secondary prevention after ventricular fibrillation or hemodynamically significant sustained ventricular tachycardia when no completely reversible cause is present
• Primary prevention in selected patients with persistently reduced left-ventricular ejection fraction despite appropriate guideline-directed therapy
• Selected high-risk inherited arrhythmia syndromes or cardiomyopathies

An ICD terminates malignant ventricular arrhythmias but does not prevent every arrhythmia from occurring. Antiarrhythmic drugs or ablation may still be required to reduce recurrent ventricular tachycardia and ICD shocks.

Primary-prevention decisions require disease-specific assessment of ventricular function, functional status, comorbidity, competing nonarrhythmic mortality, expected survival, and patient preferences.^[3]

Long-term management should include treatment of modifiable contributors:

• Blood-pressure control
• Weight management
• Evaluation and treatment of obstructive sleep apnea
• Diabetes management
• Alcohol reduction or abstinence when alcohol triggers or contributes to arrhythmia
• Smoking cessation
• Regular appropriate physical activity
• Correction of electrolyte abnormalities
• Treatment of thyroid disease
• Review of QT-prolonging or interacting medications

Primary prevention aims to prevent the first clinically significant arrhythmia or sudden-death event.

Potential strategies include:

• Control of hypertension, diabetes, obesity, and heart failure
• Prevention and treatment of coronary artery disease
• Avoidance of proarrhythmic drugs and combinations when safer alternatives exist
• Correction of electrolyte abnormalities
• Treatment of obstructive sleep apnea
• Reduction of excessive alcohol and stimulant exposure
• Primary-prevention ICD implantation in appropriately selected high-risk patients
• Identification and cascade screening of families with inherited arrhythmia syndromes
• Disease-specific exercise and medication counseling for inherited channelopathies

Secondary prevention after an arrhythmic event may include:

• ICD implantation after resuscitated ventricular fibrillation or sustained ventricular tachycardia when appropriate
• Catheter ablation to reduce recurrent arrhythmia
• Antiarrhythmic drug therapy
• Correction of reversible precipitants
• Guideline-directed therapy for ischemic heart disease, cardiomyopathy, or heart failure
• Anticoagulation for atrial fibrillation when thromboembolic risk warrants treatment
• Medication and activity counseling for inherited arrhythmia syndromes
• Family screening when an inherited disorder is suspected or confirmed

The NOAH-AFNET 6 and ARTESiA trials demonstrated that direct oral anticoagulants reduce ischemic stroke in patients with device-detected atrial fibrillation or atrial high-rate episodes but increase major bleeding. In a study-level meta-analysis of the two trials, anticoagulation reduced ischemic stroke (relative risk, 0.68; 95% confidence interval, 0.50–0.92) and increased major bleeding (relative risk, 1.62; 95% confidence interval, 1.05–2.50), without reducing cardiovascular or all-cause mortality.^[20]

The 2024 European atrial-fibrillation guideline states that direct oral anticoagulation may be considered in selected patients with device-detected subclinical atrial fibrillation who have elevated thromboembolic risk and no major bleeding-risk factors. The optimal episode duration or arrhythmia burden that should trigger treatment remains uncertain, and decisions should incorporate stroke risk, episode duration, vascular comorbidity, diagnostic certainty, and bleeding risk.^[21]

VANISH2 supports catheter ablation as an initial treatment strategy for ventricular tachycardia in selected patients with ischemic cardiomyopathy. Remaining uncertainties include generalizability to nonischemic cardiomyopathy, lower-risk ventricular-tachycardia populations, different antiarrhythmic-drug comparators, and centers with less ablation experience.^[18]

The overall mortality benefit of primary-prevention ICD therapy in nonischemic cardiomyopathy may vary with age, comorbidity, competing mortality, ventricular scar, and receipt of contemporary heart-failure therapy.

His-bundle and left-bundle-branch-area pacing provide more physiologic ventricular activation than conventional right-ventricular pacing in selected patients, but optimal indications and long-term comparative outcomes continue to develop.

Pulsed-field ablation has received regulatory approval and entered clinical practice as a nonthermal ablation modality, particularly for pulmonary-vein isolation. Its principal theoretical and observed advantage is preferential myocardial injury with reduced injury to selected adjacent structures. Remaining uncertainties include long-term lesion durability, comparative effectiveness, uncommon complications, and performance outside pulmonary-vein isolation.

1. Exertional or supine syncope, particularly in a patient with structural heart disease or a family history of sudden death, should be presumed potentially arrhythmic until adequately evaluated.
2. A consumer-wearable notification requires confirmation with an interpretable ECG tracing before a definitive arrhythmia diagnosis is made.
3. Persistent or frequently recurrent tachycardia may cause a potentially reversible cardiomyopathy.
4. Restoration of sinus rhythm does not by itself eliminate thromboembolic risk in atrial fibrillation.
5. The clinical significance of a rhythm depends not only on rate and morphology but also on symptoms, hemodynamic effect, underlying myocardial substrate, and reversibility.
6. Review medications, renal function, electrolytes, and drug interactions whenever a new arrhythmia or conduction abnormality develops.

CME Category::Cardiology