Cardiovascular Therapeutics
Arrhythmias
A comprehensive lecture note covering cardiac electrophysiology, antiarrhythmic drug classes,
supraventricular and ventricular arrhythmias, anticoagulation strategy, acute ACLS-style
management, and exam-focused review.
Common Clinical Focus
Atrial fibrillation
Rate vs Rhythm
AF symptom strategy
Danger Pattern
Wide complex equals VT until proven otherwise
QT Emergency
Torsades, treat with magnesium
1. Learning Objectives
- Describe the cardiac action potential and identify phases targeted by antiarrhythmic drugs.
- Classify antiarrhythmic medications by the Vaughan Williams system and explain their mechanisms.
- Differentiate supraventricular and ventricular arrhythmias by ECG pattern and clinical behavior.
- Select therapy for common arrhythmias including AF, AVNRT, AVRT, and ventricular tachycardia.
- Apply rate-control versus rhythm-control strategies in atrial fibrillation.
- Assess stroke risk and choose anticoagulation for atrial fibrillation.
- Recognize life-threatening arrhythmias and outline acute management steps.
- Identify proarrhythmic risks such as QT prolongation and Torsades de Pointes.
2. Introduction to Cardiac Electrophysiology
2.1. Cardiac Action Potentials
| Phase |
Ion Movement |
Description |
| Phase 0 |
Rapid sodium influx |
Fast depolarization in ventricular myocardium; Class I drugs act here. |
| Phase 1 |
Transient potassium efflux |
Early repolarization. |
| Phase 2 |
Calcium influx with potassium efflux |
Plateau phase that couples electricity to contraction. |
| Phase 3 |
Potassium efflux |
Rapid repolarization and QT behavior. |
| Phase 4 |
Resting membrane maintenance |
Resting state in working myocytes, spontaneous depolarization in pacemaker tissue. |
| Pacemaker Phase |
Ion Movement |
Description |
| Phase 4 |
Funny sodium current, then calcium influx |
Automatic spontaneous depolarization. |
| Phase 0 |
Calcium influx |
Depolarization in SA and AV nodal tissue. |
| Phase 3 |
Potassium efflux |
Repolarization. |
2.2. Conduction System of the Heart
| Structure |
Intrinsic Rate |
Main Function |
| SA node |
60-100 bpm |
Primary pacemaker |
| AV node |
40-60 bpm |
Delays atrioventricular conduction |
| Bundle of His |
Not primary pacemaker |
Connects AV node to ventricular system |
| Purkinje fibers |
20-40 bpm |
Rapid ventricular activation |
2.3. Mechanisms of Arrhythmogenesis
| Mechanism |
Description |
Examples |
| Abnormal automaticity |
Enhanced spontaneous depolarization outside normal pacemaker hierarchy |
Atrial tachycardia, some ventricular ectopy |
| Triggered activity |
Afterdepolarizations that reach threshold |
Torsades, digoxin toxicity |
| Reentry |
Circular impulse around a functional or anatomical circuit |
AVNRT, AVRT, atrial flutter, scar-related VT |
3. Classification of Antiarrhythmic Drugs
3.1. Class I: Sodium Channel Blockers
| Subclass |
Effect |
Examples |
Main Use |
Key Adverse Effects |
| Ia |
Moderate sodium blockade and prolonged repolarization |
Quinidine, procainamide, disopyramide |
Atrial and ventricular arrhythmias |
Torsades risk, lupus-like syndrome, anticholinergic effects |
| Ib |
Weak sodium blockade and shorter repolarization |
Lidocaine, mexiletine |
Ischemia-related ventricular arrhythmias |
CNS toxicity, dizziness, paresthesias, hypotension |
| Ic |
Strong sodium blockade with minimal repolarization effect |
Flecainide, propafenone |
AF rhythm control without structural heart disease |
Dangerous proarrhythmia in structural heart disease |
High-yield pearl: Class Ic agents are contraindicated in structural heart disease,
especially prior MI or reduced EF, because they increase mortality.
3.2. Class II: Beta-Blockers
| Aspect |
Details |
| Mechanism |
Reduce sympathetic tone, slow SA automaticity, and slow AV nodal conduction |
| Examples |
Metoprolol, atenolol, bisoprolol, propranolol, esmolol, carvedilol |
| Uses |
AF rate control, SVT suppression, ventricular arrhythmias, post-MI, heart failure |
| Risks |
Bradycardia, hypotension, fatigue, bronchospasm with non-selective agents |
3.3. Class III: Potassium Channel Blockers
| Aspect |
Details |
| Mechanism |
Prolong repolarization and refractory period by blocking potassium current, so QT lengthens |
| Examples |
Amiodarone, dronedarone, sotalol, dofetilide, ibutilide |
| Uses |
AF rhythm control and selected ventricular arrhythmias |
| Risk |
QT prolongation and Torsades, plus bradycardia and hypotension |
| Amiodarone Feature |
Key Point |
| Pharmacology |
Very long half-life with Class I, II, and IV crossover effects |
| Main uses |
AF, VT, VF |
| Major toxicity |
Pulmonary fibrosis, thyroid dysfunction, liver injury, neuropathy, corneal deposits, photosensitivity |
| Monitoring |
Chest imaging, thyroid studies, liver tests, and eye follow-up |
3.4. Class IV: Calcium Channel Blockers
- Agents: verapamil and diltiazem.
- Effect: slow AV nodal conduction and reduce nodal automaticity.
- Main uses: AF rate control, AVNRT, atrial tachycardia.
- Avoid in: HFrEF, severe bradycardia, advanced AV block, and AF with WPW.
3.5. Other Antiarrhythmic Agents
| Agent |
Role |
Key Reminder |
| Adenosine |
Acute termination of AVNRT and related narrow-complex SVT |
Rapid IV push, half-life under 10 seconds, transient flushing or asystole |
| Digoxin |
Rate control in AF, especially with heart failure or sedentary patients |
Narrow therapeutic index; toxicity can trigger arrhythmias |
| Magnesium |
First-line for Torsades de Pointes |
Give even if serum magnesium is normal |
4. Supraventricular Arrhythmias
4.1. Atrial Fibrillation
Atrial fibrillation is chaotic atrial activity with loss of effective atrial contraction and an
irregularly irregular ventricular response.
| ECG Feature |
Description |
| P waves |
No organized P waves; fibrillatory baseline |
| R-R pattern |
Irregularly irregular |
| Complications |
Stroke, heart failure, symptom burden, mortality |
| Type |
Definition |
Management Theme |
| Paroxysmal |
Self-terminates within 7 days |
Symptom-driven treatment |
| Persistent |
More than 7 days or requires intervention to stop |
Rate or rhythm control plus anticoagulation |
| Long-standing persistent |
Continuous more than 12 months |
Long-term strategy selection |
| Permanent |
No more rhythm-control attempts planned |
Rate control and anticoagulation |
Rate Control
- Beta-blockers are first-line for most patients.
- Diltiazem or verapamil can be used if EF is preserved.
- Digoxin is most useful in heart failure or more sedentary patients.
Rhythm Control
- No structural heart disease: flecainide or propafenone.
- Structural heart disease: amiodarone, dofetilide, or sotalol.
- Heart failure: amiodarone or dofetilide.
4.2. Atrial Flutter
- Macroreentrant rhythm with classic sawtooth flutter waves.
- Stroke risk and anticoagulation logic are similar to AF.
- Catheter ablation is highly effective and often curative.
4.3. AVNRT
- Most common paroxysmal SVT.
- Regular narrow-complex tachycardia, often 150-250 bpm.
- Stable sequence: vagal maneuvers, then adenosine, then AV nodal blockers.
4.4. AVRT and WPW
- Accessory pathway bypasses the AV node and supports reentry.
- WPW pattern shows delta wave, short PR interval, and pre-excitation.
- In AF with WPW, avoid AV nodal blockers such as verapamil, diltiazem, and digoxin.
4.5. Atrial Tachycardia
- Focal atrial rhythm with abnormal P-wave morphology.
- Usually treated with beta-blockers or calcium channel blockers.
- Catheter ablation can be curative when symptoms persist.
5. Ventricular Arrhythmias
5.1. Premature Ventricular Complexes
- Wide premature beat without a preceding P wave, usually followed by a compensatory pause.
- Low-burden asymptomatic PVCs often need reassurance only.
- Symptomatic or high-burden PVCs may respond to beta-blockers or ablation.
5.2. Ventricular Tachycardia
| Type |
Pattern |
Key Point |
| Monomorphic VT |
Uniform QRS morphology |
Often scar-related, especially after MI |
| Polymorphic VT |
Changing QRS morphology |
Can deteriorate quickly |
| Sustained VT |
More than 30 seconds or needs termination |
High sudden death risk |
| Non-sustained VT |
Self-terminates before 30 seconds |
Risk depends on structural disease context |
5.3. Ventricular Fibrillation
- Chaotic ventricular electrical activity with no organized cardiac output.
- Requires immediate defibrillation and ACLS.
5.4. Torsades de Pointes
- Polymorphic VT associated with prolonged QT.
- Common triggers include Class Ia and III drugs, electrolyte depletion, and congenital long QT.
- First-line treatment is magnesium sulfate 2 g IV.
6. Bradyarrhythmias and Conduction Disorders
6.1. Sinus Bradycardia
- Defined as sinus rate below 60 bpm.
- May be physiologic or drug-related.
- Symptomatic cases are treated with atropine, pacing, or long-term device therapy if persistent.
6.2. Atrioventricular Block
| Type |
ECG Finding |
Management |
| First-degree AV block |
PR interval above 200 ms |
Usually no treatment |
| Mobitz I |
Progressive PR prolongation until dropped beat |
Often observed |
| Mobitz II |
Fixed PR with intermittent dropped QRS |
Pacemaker indicated |
| Third-degree block |
AV dissociation with escape rhythm |
Urgent pacing then permanent pacemaker |
6.3. Bundle Branch Block
| Type |
ECG Clue |
Clinical Meaning |
| RBBB |
rSR' in V1-V2 with wide S in lateral leads |
Can be benign |
| LBBB |
Wide QRS with broad lateral R waves and absent lateral Q waves |
Often implies structural disease and may support CRT decisions |
7. Management Strategies
7.1. Rate Control vs. Rhythm Control
| Strategy |
Best Fit |
Main Tradeoff |
| Rate control |
Older, minimally symptomatic, persistent AF, structural disease |
Less drug toxicity but AF persists |
| Rhythm control |
Younger, symptomatic, early AF, heart failure needing sinus restoration |
More antiarrhythmic toxicity and hospitalization risk |
7.2. Anticoagulation in Atrial Fibrillation
| CHA2DS2-VASc Element |
Points |
| Congestive heart failure | 1 |
| Hypertension | 1 |
| Age 75 or older | 2 |
| Diabetes mellitus | 1 |
| Prior stroke or TIA | 2 |
| Vascular disease | 1 |
| Age 65-74 | 1 |
| Female sex | 1 |
| Drug |
Core Dosing Concept |
Key Point |
| Apixaban |
5 mg BID, or 2.5 mg BID if at least 2 dose-reduction criteria are present |
Often lower bleeding risk |
| Rivaroxaban |
20 mg daily, reduced if renal function is impaired |
Once daily but higher GI bleed tendency |
| Dabigatran |
Twice daily with renal adjustment |
Specific reversal agent exists |
| Warfarin |
INR target 2-3 |
Useful when DOACs are unsuitable |
7.3. Electrical Cardioversion
- Uses synchronized shocks for AF, atrial flutter, and organized unstable tachycardia.
- If AF has lasted at least 48 hours or duration is unknown, anticoagulate for 3 weeks first or perform TEE to exclude thrombus.
- Continue anticoagulation for at least 4 weeks after cardioversion when indicated.
7.4. Catheter Ablation
- Curative for AVNRT, AVRT, and typical atrial flutter.
- Used for symptomatic AF or recurrent VT when drugs are inadequate.
7.5. Implantable Devices
| Device |
Main Indications |
| Pacemaker |
Symptomatic bradycardia, sinus node dysfunction, AV block |
| ICD |
Secondary prevention after VT or VF arrest and selected primary prevention with low EF |
| CRT |
Heart failure with low EF, LBBB, and wide QRS |
8. Acute Management of Specific Arrhythmias
8.1. Narrow Complex Tachycardia (Stable)
| Step |
Intervention |
| 1 | Vagal maneuvers |
| 2 | Adenosine 6 mg rapid IV push, then 12 mg if needed |
| 3 | Verapamil or diltiazem |
| 4 | IV beta-blocker |
| 5 | Synchronized cardioversion if unstable or refractory |
8.2. Wide Complex Tachycardia (Stable)
| Scenario |
Management |
| Monomorphic VT |
Amiodarone, lidocaine, or procainamide |
| Polymorphic VT with prolonged QT |
Magnesium, electrolyte correction, stop QT-prolonging drugs, pacing if needed |
| Wide complex of uncertain origin |
Treat as VT; avoid routine AV nodal blockers |
8.3. Unstable Tachycardia
- Defined by hypotension, ischemic chest pain, shock, acute HF, or altered mental status.
- Use synchronized cardioversion for organized tachycardias.
- Use unsynchronized defibrillation for VF or unstable polymorphic VT.
8.4. Bradycardia
- Give atropine 0.5-1 mg IV, repeated up to 3 mg.
- If ineffective, move to pacing, dopamine, or epinephrine support.
- Permanent pacemaker is definitive for persistent symptomatic conduction disease.
9. Special Populations
9.1. Arrhythmias in Pregnancy
- SVT is common and adenosine is considered safe.
- Metoprolol, propranolol, and digoxin are commonly used.
- Avoid amiodarone when possible, and avoid warfarin early in pregnancy.
- Electrical cardioversion is safe when clinically needed.
9.2. Arrhythmias in Heart Failure
- Preferred rhythm-control agents are amiodarone and dofetilide.
- Avoid flecainide, propafenone, dronedarone, verapamil, and diltiazem in HFrEF.
- ICD and CRT decisions are often central to long-term management.
9.3. Arrhythmias in Renal Impairment
| Drug |
Renal Consideration |
| Dofetilide | CrCl-based dosing; avoid if CrCl is very low |
| Sotalol | CrCl-based dosing and QT monitoring |
| Flecainide | Reduce dose in impaired renal function |
| Digoxin | Reduce dose and monitor for toxicity carefully |
| DOACs | Adjust by creatinine clearance |
10. Patient Counseling Points
- Take medicines consistently: missing antiarrhythmic or rate-control doses can trigger recurrence.
- Report symptoms early: palpitations, syncope, chest pain, dyspnea, or dizziness may signal recurrence or toxicity.
- Watch QT interactions: always mention your antiarrhythmic drugs before starting anything new.
- Anticoagulation prevents stroke: take it regularly and seek care for bleeding or neurologic symptoms.
- Check pulse if instructed: persistent rates below 50 bpm should be reported.
- Amiodarone needs monitoring: lungs, thyroid, liver, vision, and sun protection matter.
- Pacemaker or ICD patients: carry device identification and report shocks or alerts.
11. Summary for Exam Preparation
High-yield memory anchors: Phase 0 equals sodium, Class Ic means no structural
heart disease, AF anticoagulation follows CHA2DS2-VASc, stable narrow-complex SVT gets adenosine,
wide-complex tachycardia is VT until proven otherwise, and Torsades gets magnesium first.
Vaughan Williams Overview
| Class |
Mechanism |
Examples |
Key Point |
| I | Sodium channel blockade | Procainamide, lidocaine, flecainide | Ic is dangerous in structural heart disease |
| II | Beta blockade | Metoprolol, esmolol | Core AF rate-control agents |
| III | Potassium channel blockade | Amiodarone, sotalol, dofetilide | QT prolongation and Torsades risk |
| IV | Calcium channel blockade | Verapamil, diltiazem | AV nodal blockers, avoid in HFrEF |
Quick Selection Table
| Arrhythmia |
First-Line |
Alternatives |
| AF rate control | Beta-blocker or CCB | Digoxin |
| AF rhythm control without SHD | Flecainide or propafenone | Dronedarone |
| AF rhythm control with SHD or HF | Amiodarone | Dofetilide, sometimes sotalol |
| AVNRT or AVRT acute | Vagal maneuvers then adenosine | CCB or beta-blocker |
| Stable VT | Amiodarone | Lidocaine or procainamide |
| Torsades | Magnesium | Pacing or isoproterenol if needed |