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Cardiac Arrhythmias: Atrial Fibrillation, Supraventricular Tachycardia, and Ventricular Tachycardia

Cardiovascular7 min read1,388 wordsintermediateUpdated 3/13/2026
Contents

Cardiac arrhythmias are abnormalities in the heart's electrical conduction system that result in irregular heart rhythms. The three major categories covered here represent distinct pathophysiological mechanisms and clinical implications.

Atrial Fibrillation (AF)

Atrial fibrillation is the most common sustained cardiac arrhythmia, characterized by chaotic, irregular atrial electrical activity with an atrial rate of 400-600 beats per minute. [HIGH_YIELD] AF affects approximately 6 million Americans and is projected to affect 12.1 million by 2030. The prevalence increases dramatically with age, affecting <1% of individuals under 60 years but >9% of those over 80 years.

Supraventricular Tachycardia (SVT)

Supraventricular tachycardia encompasses arrhythmias originating above the ventricles with heart rates typically 150-250 bpm. The most common forms include:

  • Atrioventricular nodal reentrant tachycardia (AVNRT) - 60% of SVTs
  • Atrioventricular reentrant tachycardia (AVRT) - 30% of SVTs
  • Atrial tachycardia - 10% of SVTs

[CLINICAL_PEARL] SVT has a bimodal age distribution with peaks in young adults (20-30 years) and elderly patients (>65 years).

Ventricular Tachycardia (VT)

Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate >100 bpm (typically 150-250 bpm). VT can be:

  • Sustained (≥30 seconds or hemodynamically significant)
  • Non-sustained (<30 seconds)
  • Monomorphic (uniform QRS morphology) or Polymorphic (varying QRS morphology)

[KEY_CONCEPT] VT is associated with structural heart disease in 80-90% of cases, most commonly ischemic cardiomyopathy.

Atrial Fibrillation

Pathophysiology: AF results from abnormal automaticity and multiple reentrant circuits within the atria, often triggered by ectopic foci in the pulmonary veins. Risk factors include:

  • Hypertension (most common)
  • Heart failure
  • Coronary artery disease
  • Valvular disease
  • Hyperthyroidism

Clinical Presentation:

  • Palpitations (most common symptom)
  • Fatigue and exercise intolerance
  • Dyspnea
  • Chest discomfort
  • Dizziness or syncope
  • [HIGH_YIELD] Up to 30% of patients are asymptomatic

Supraventricular Tachycardia

Pathophysiology: SVT mechanisms include:

  • Reentry (AVNRT, AVRT) - most common
  • Enhanced automaticity (atrial tachycardia)
  • Triggered activity (digitalis toxicity)

Clinical Presentation:

  • Sudden onset and termination of palpitations
  • Chest pain or pressure
  • Dyspnea
  • Dizziness or lightheadedness
  • Neck pounding sensation (cannon A waves)
  • Diaphoresis

[CLINICAL_PEARL] The abrupt onset and termination of symptoms strongly suggests AVNRT or AVRT rather than sinus tachycardia.

Ventricular Tachycardia

Pathophysiology: VT typically results from:

  • Reentry within ventricular myocardium (most common in ischemic heart disease)
  • Abnormal automaticity (catecholaminergic polymorphic VT)
  • Triggered activity (torsades de pointes)

Clinical Presentation:

  • Palpitations
  • Chest pain
  • Dyspnea
  • Dizziness or syncope
  • Cardiac arrest (in sustained VT)
  • [KEY_CONCEPT] Hemodynamic tolerance varies greatly depending on ventricular function and rate
ArrhythmiaTypical Rate (bpm)OnsetDurationKey Symptoms
AF110-180Gradual/suddenPersistent/paroxysmalFatigue, DOE
SVT150-250AbruptMinutes to hoursPalpitations, chest pressure
VT150-250SuddenSeconds to sustainedSyncope, cardiac arrest

Electrocardiographic Criteria

Atrial Fibrillation ECG Criteria:
  • Irregularly irregular rhythm
  • Absence of P waves
  • Fibrillatory waves (f-waves) at 400-600/min
  • Variable ventricular response (typically 110-180 bpm if untreated)
SVT ECG Criteria:
  • Regular narrow QRS tachycardia (QRS <120 ms)
  • Heart rate 150-250 bpm
  • P waves may be hidden in QRS or T waves
  • Abrupt onset and termination

[HIGH_YIELD] AVNRT: Pseudo R' in lead V1, pseudo S waves in inferior leads [HIGH_YIELD] AVRT: Visible P waves with short RP interval (<100ms)

Ventricular Tachycardia ECG Criteria:
  • Wide QRS tachycardia (QRS ≥120 ms)
  • Heart rate >100 bpm (typically 150-250)
  • AV dissociation (when visible)
  • Concordance in precordial leads
  • Morphology criteria (LBBB or RBBB pattern)

Diagnostic Algorithm

Wide QRS Tachycardia (≥120 ms) | v AV Dissociation Present? | Yes | No/Uncertain | | VT v Morphology Analysis | VT Criteria Present? | Yes | No | | VT SVT with aberrancy

Diagnostic Workup

Initial Assessment:

  • 12-lead ECG (during arrhythmia if possible)
  • Complete blood count, comprehensive metabolic panel
  • Thyroid function tests
  • Troponin levels
  • Echocardiography

Advanced Testing:

  • Holter monitoring or event monitoring for paroxysmal arrhythmias
  • Electrophysiology study for recurrent SVT or VT
  • Stress testing for exercise-induced arrhythmias
  • Cardiac MRI for suspected structural heart disease

[CLINICAL_PEARL] In hemodynamically stable wide QRS tachycardia, assume VT until proven otherwise - VT is far more common than SVT with aberrancy.

Atrial Fibrillation Management

Rate vs Rhythm Control Strategy

Rate Control (preferred in most patients):

  • Beta-blockers: Metoprolol, atenolol (first-line)
  • Non-dihydropyridine calcium channel blockers: Diltiazem, verapamil
  • Digoxin: Reserve for heart failure patients

Rhythm Control:

  • Class IC agents: Flecainide, propafenone (normal heart)
  • Class III agents: Amiodarone, sotalol (structural heart disease)
  • Catheter ablation: For symptomatic, drug-refractory AF
Anticoagulation in AF

[HIGH_YIELD] Use CHA₂DS₂-VASc score for stroke risk stratification:

  • Score ≥2: Recommend anticoagulation
  • Score 1: Consider anticoagulation
  • Score 0: No anticoagulation needed

Anticoagulant Options:

  • Warfarin: INR target 2.0-3.0
  • DOACs: Apixaban, rivaroxaban, dabigatran, edoxaban (preferred)

SVT Management

Acute Termination Algorithm

Hemodynamically Stable SVT | v Vagal Maneuvers | v Adenosine 6 mg IV push | No response? | v Adenosine 12 mg IV push | No response? | v Rate Control Agents (Metoprolol, Diltiazem)

[CLINICAL_PEARL] Valsalva maneuver is most effective when performed with legs elevated and followed by rapid supine positioning.

Long-term Management:
  • Catheter ablation: Curative for AVNRT/AVRT (>95% success)
  • Prophylactic medications: Beta-blockers, calcium channel blockers

Ventricular Tachycardia Management

Acute Management

Hemodynamically unstable: Immediate synchronized cardioversion

Hemodynamically stable monomorphic VT:

  1. Amiodarone 150 mg IV over 10 minutes
  2. Procainamide 20-50 mg/min (if no heart failure)
  3. Lidocaine 1-1.5 mg/kg IV (if ischemic)

Polymorphic VT/Torsades de Pointes:

  • Magnesium sulfate 2g IV
  • Correct electrolyte abnormalities
  • Remove offending medications
  • Consider isoproterenol or temporary pacing
Long-term Management:
  • ICD implantation for sustained VT with structural heart disease
  • Antiarrhythmic drugs: Amiodarone, sotalol
  • Catheter ablation for recurrent monomorphic VT
  • Beta-blockers for all patients with ischemic cardiomyopathy

[KEY_CONCEPT] The 2017 ACC/AHA Guidelines emphasize shared decision-making and quality of life considerations in arrhythmia management.

Atrial Fibrillation Complications

Thromboembolic Complications

Stroke Risk: AF increases stroke risk 5-fold

  • [HIGH_YIELD] Left atrial appendage is the source of 90% of AF-related emboli
  • Risk persists even with restored sinus rhythm
  • Silent AF detected on monitoring devices still requires anticoagulation
Heart Failure
  • Tachycardia-induced cardiomyopathy can develop with poor rate control
  • AF and heart failure have bidirectional relationship
  • Rate control <110 bpm is usually adequate
Prognosis
  • Mortality: 1.5-2x increased risk compared to sinus rhythm
  • Quality of life: Significantly impacted by symptoms
  • Progression: Paroxysmal → Persistent → Permanent AF over time

SVT Complications

Acute Complications
  • Hemodynamic compromise (rare with structurally normal heart)
  • Myocardial ischemia in patients with CAD
  • Heart failure in patients with underlying cardiomyopathy
Long-term Effects
  • Tachycardia-induced cardiomyopathy (with incessant SVT)
  • Reduced quality of life due to recurrent episodes
  • Excellent prognosis with successful ablation

[CLINICAL_PEARL] WPW syndrome with AF can degenerate to ventricular fibrillation - avoid AV nodal blocking agents.

Ventricular Tachycardia Complications

Immediate Life-threatening Complications
  • Ventricular fibrillation (VT storm)
  • Cardiogenic shock
  • Sudden cardiac death
Long-term Complications
  • Progressive heart failure due to underlying structural disease
  • Recurrent VT episodes
  • ICD shocks and associated anxiety/depression
Prognosis by Etiology
VT TypeUnderlying Disease5-Year MortalityTreatment
Ischemic VTPrior MI15-25%ICD + optimal medical therapy
Non-ischemic VTDilated cardiomyopathy10-20%ICD + heart failure management
Idiopathic VTStructurally normal heart<5%Ablation or medical therapy
ARVD/CRight ventricular dysplasia10-15%ICD + activity restriction

[KEY_CONCEPT] Primary prevention ICDs reduce mortality by 23% in patients with EF ≤35% despite optimal medical therapy (per ACC/AHA Guidelines).

Monitoring and Follow-up
  • Regular device interrogation for ICD patients
  • Echocardiographic monitoring for ventricular function
  • Electrolyte monitoring with antiarrhythmic drugs
  • Anticoagulation monitoring for AF patients on warfarin
!

High-Yield Key Points

1

Atrial fibrillation is the most common sustained arrhythmia, requiring stroke risk stratification using CHA₂DS₂-VASc score and anticoagulation for scores ≥2

2

Wide QRS tachycardia should be assumed to be ventricular tachycardia until proven otherwise, as VT is far more common than SVT with aberrancy

3

SVT can be terminated acutely with vagal maneuvers and adenosine, with catheter ablation offering >95% cure rates for AVNRT and AVRT

4

Hemodynamically unstable ventricular tachycardia requires immediate synchronized cardioversion, while stable monomorphic VT is treated with IV amiodarone

5

Primary prevention ICDs reduce mortality by 23% in patients with EF ≤35% despite optimal medical therapy and are indicated for ischemic cardiomyopathy >40 days post-MI

6

Torsades de pointes (polymorphic VT) is treated with IV magnesium, electrolyte correction, and removal of QT-prolonging medications

References (6)

[1]

January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation. Circulation. 2019.

[2]

Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Circulation. 2018.

[3]

McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med. 2014. PMID: 25176015.

PMID: 25176015
[4]

McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction. N Engl J Med. 2019. PMID: 31535829.

PMID: 31535829
[5]

Maron DJ, Hochman JS, Reynolds HR, et al. Initial Invasive or Conservative Strategy for Stable Coronary Disease. N Engl J Med. 2020. PMID: 32227755.

PMID: 32227755
[6]

Eikelboom JW, Connolly SJ, Bosch J, et al. Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. N Engl J Med. 2017. PMID: 28498692.

PMID: 28498692

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