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2025 ACC AHA guideline management cardiac arrhythmias antiarrhythmic drugs

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Arrhythmia and Antiarrhythmic Drugs: Easy Basics

Arrhythmia means an abnormal heart rhythm. The heart may beat:

Too fast: tachyarrhythmia (usually >100/min)
Too slow: bradyarrhythmia (usually <60/min)
Irregularly: beats come in an uneven pattern
From the wrong place: electrical activity starts outside the normal pacemaker

Visualize the heart as a house with electrical wiring

The heart is a muscular pump, but it works because of an electrical wiring system.

Think of the heart as a four-room house:

Right atrium
Right ventricle
Left atrium
Left ventricle

The electricity normally travels in one organized direction so the rooms contract in sequence and pump blood effectively.

Normal order:

SA node → atria → AV node → His bundle → bundle branches → Purkinje fibres → ventricles

1. Normal Cardiac Conduction System

SA node: the natural pacemaker

The sinoatrial (SA) node is in the right atrium. It normally produces about 60-100 impulses/minute.

Think of it as the main clock or conductor of an orchestra.

It tells the atria: “Contract now.”

AV node: the gatekeeper

The impulse then reaches the atrioventricular (AV) node.

The AV node delays the signal briefly. This delay allows the ventricles time to fill with blood before they contract.

Think of it as a traffic signal at a junction. It stops traffic for a moment so that the lower chambers do not contract too early.

His-Purkinje system: fast delivery network

After the AV node, electricity rapidly goes down the:

Bundle of His
Right and left bundle branches
Purkinje fibres

This triggers ventricular contraction.

Think of it as an express highway delivering a message to both ventricles at nearly the same time.

2. Why Arrhythmias Matter

A normal rhythm gives effective pumping. In an arrhythmia, the pump can become inefficient.

Example

Imagine a water pump that should compress rhythmically:

Pump... relax... pump... relax...

If it pumps too fast, too slowly, or chaotically:

pump-pump-pump-pump
or
pump... long pause... pump
or
random weak vibrations

then blood delivery to the brain, lungs, and body may fall.

This can cause:

Palpitations: awareness of heartbeat
Dizziness
Fatigue
Chest pain
Breathlessness
Syncope: fainting
Hypotension
Stroke
Cardiac arrest

Some arrhythmias are harmless. Others are immediately life-threatening.

3. Main Causes of Arrhythmias

A useful memory approach is to think: the heart's wiring is irritated, damaged, starved, or affected by chemicals.

Common causes:

Ischaemic heart disease / myocardial infarction
Lack of oxygen damages cardiac muscle and irritates electrical pathways.
Electrolyte imbalance
- Low potassium: hypokalaemia
- High potassium: hyperkalaemia
- Low magnesium: hypomagnesaemia
- Calcium abnormalities
Drugs and toxins
- Digoxin
- Antiarrhythmics
- Stimulants, including excess caffeine
- Alcohol
- Cocaine and amphetamines
Structural heart disease
- Heart failure
- Valvular disease
- Cardiomyopathy
Hypoxia
- Low oxygen, lung disease, severe anaemia, sleep apnoea
Endocrine causes
- Hyperthyroidism commonly causes atrial fibrillation
Stress, fever, pain, dehydration

4. How Arrhythmias Occur

There are three major mechanisms.

A. Abnormal automaticity

Normally, the SA node is the dominant pacemaker. Sometimes another area begins firing automatically.

Visualization

The SA node is the official school bell. If another classroom has a faulty bell that starts ringing by itself, students become confused.

This creates an ectopic focus, meaning an abnormal site producing impulses.

Example: premature atrial contractions or premature ventricular contractions.

B. Re-entry circuit

This is one of the most important mechanisms.

An electrical impulse travels in a loop and repeatedly stimulates the heart.

Visualization

Imagine a runner stuck on a circular track. Instead of leaving after one lap, they keep running round and round, repeatedly triggering contraction.

This can happen if:

One pathway conducts slowly
Another pathway is blocked in one direction but allows reverse conduction

Examples:

AV nodal re-entrant tachycardia (AVNRT)
Atrioventricular re-entrant tachycardia (AVRT), including Wolff-Parkinson-White syndrome
Atrial flutter
Some ventricular tachycardias

C. Triggered activity

An impulse occurs during or just after repolarization, when the heart cell should be resting.

Visualization

A phone should send one notification, but it glitches and sends repeated notifications before it resets.

Examples include arrhythmias related to:

Long QT interval
Low potassium or magnesium
Certain medicines
Digoxin toxicity

5. ECG Basics You Need Before Studying Arrhythmia

An ECG records the heart's electrical activity.

ECG part	What it represents	Simple image
P wave	Atrial depolarization	Atria receive the command to contract
PR interval	Travel through atria and AV node	Waiting at the AV-node traffic light
QRS complex	Ventricular depolarization	Ventricles receive the command to contract
T wave	Ventricular repolarization	Ventricles reset for the next beat
QT interval	Total ventricular electrical activity	Full work-and-recovery cycle

Important rule

Narrow QRS: rhythm likely begins above the ventricles
Wide QRS: rhythm may originate in the ventricles or be conducted abnormally

6. Important Arrhythmias

A. Sinus Bradycardia

Rate: <60/min
Rhythm: regular
Origin: SA node, but it fires slowly.

Example

A well-trained athlete may have a resting rate of 45/min without disease. But a patient who feels faint with pulse 35/min may have a dangerous bradycardia.

Causes

Athletes
Sleep
Drugs: beta-blockers, verapamil, diltiazem, digoxin
Hypothyroidism
Inferior myocardial infarction
Sick sinus syndrome

Treatment

Treat only if symptomatic or unstable.

For symptomatic bradycardia:

Atropine
Temporary pacing if needed
Correct the cause
Permanent pacemaker for persistent significant conduction disease

B. Sinus Tachycardia

Rate: >100/min
Rhythm: regular
Origin: SA node, but it fires rapidly.

This is usually a normal response, not the main disease itself.

Example

If someone is feverish, dehydrated, in pain, bleeding, anxious, or running, the SA node speeds up because the body needs more blood flow.

Treatment

Treat the cause:

Give fluids if dehydrated
Treat pain, fever, anaemia, infection, hypoxia, etc.

Do not simply suppress the rate without understanding why the body is asking for a faster heartbeat.

C. Premature Beats: Ectopics

Premature atrial contraction, PAC

An early beat starts in the atrium.

Premature ventricular contraction, PVC

An early beat starts in a ventricle and usually produces a broad, unusual QRS complex.

Visualization

It is like someone clapping early during a synchronized performance. One clap comes too soon, then there may be a short pause before the normal rhythm resumes.

Often benign, but frequent PVCs may need assessment, especially in people with structural heart disease or symptoms.

D. Supraventricular Tachycardia, SVT

SVT is a rapid rhythm originating above the ventricles. Usually it has a regular, narrow-complex tachycardia.

Typical rate: 150-250/min

Common types

AVNRT
AVRT
Atrial tachycardia

Example

A young person suddenly feels the heart racing at 180/min while sitting quietly. It starts abruptly and may stop abruptly. This “on-off switch” history strongly suggests a re-entry tachycardia.

Management if stable

Vagal manoeuvres
For example, modified Valsalva manoeuvre. This increases vagal activity and slows AV-node conduction.
Adenosine
If vagal manoeuvres fail and the rhythm is regular narrow-complex tachycardia.

Adenosine visualization

Adenosine is like temporarily closing the AV-node gate for a few seconds. If the circular electrical track needs the AV node, the loop breaks and normal rhythm returns.

It has a very short action. Patients may briefly feel chest pressure, breathlessness, flushing, or a feeling that the heart has stopped. These effects usually pass quickly.

If unstable

Urgent synchronized cardioversion.

E. Atrial Fibrillation, AF

AF is the most common sustained arrhythmia.

Instead of the atria contracting properly, many chaotic electrical signals make them quiver.

Visualization

Normally, the atria work like a coordinated group rowing a boat. In AF, everyone rows randomly. The atria quiver instead of producing a useful contraction.

ECG pattern

No clear P waves
Irregularly irregular rhythm
Usually narrow QRS

Why AF is important

Blood can stagnate in the left atrium, particularly the left atrial appendage, forming a clot. The clot can travel to the brain and cause ischaemic stroke.

Symptoms

Palpitations
Breathlessness
Fatigue
Dizziness
Some people have no symptoms

Treatment has three goals

1. Rate control

Slow the ventricular response.

Drugs include:

Beta-blockers, such as metoprolol
Diltiazem or verapamil in selected patients
Digoxin, particularly in some sedentary patients or those with heart failure

2. Rhythm control

Try to restore or maintain sinus rhythm, using:

Electrical cardioversion
Antiarrhythmic drugs such as flecainide, amiodarone, or others in selected patients
Catheter ablation in appropriate patients

3. Stroke prevention

Assess stroke risk and give anticoagulation where indicated.

Important distinction: anticoagulants prevent clot formation. They do not correct the rhythm.

F. Atrial Flutter

In atrial flutter, an electrical impulse repeatedly circles around the atrium in an organized loop.

Visualization

AF is like many people running randomly in a room. Flutter is like one person continuously running around a circular track.

ECG

Classic “saw-tooth” flutter waves.

The atrial rate may be around 300/min. The AV node blocks some impulses, so the ventricular rate may be around 150/min with 2:1 conduction.

Management principles are similar to AF: control rate, consider rhythm restoration, and evaluate need for anticoagulation.

G. Ventricular Tachycardia, VT

VT is a fast rhythm arising from the ventricles. It usually causes a broad-complex tachycardia.

Why VT is dangerous

The ventricles are pumping chambers. If they contract very fast and abnormally, they may not fill adequately. Cardiac output can collapse.

Example

A person with previous myocardial infarction develops sudden palpitations, dizziness, low blood pressure, and a wide-complex rhythm at 180/min. Assume VT unless proved otherwise.

Important safety rule

A broad-complex tachycardia should be treated as VT until proven otherwise, especially in a person with structural heart disease.

Management

Unstable with pulse: synchronized cardioversion
Pulseless VT: CPR + defibrillation + advanced life support
Stable VT: urgent expert assessment and antiarrhythmic therapy such as amiodarone, procainamide, or lidocaine depending on the situation and guideline

H. Ventricular Fibrillation, VF

VF is chaotic electrical activity in the ventricles. There is no effective contraction and therefore no cardiac output.

Visualization

VT is a pump working too fast and inefficiently. VF is a pump that has become a bag of trembling muscle with no coordinated pumping at all.

VF causes cardiac arrest.

Treatment

Immediate CPR
Immediate defibrillation
Advanced life support
Treat reversible causes

Defibrillation is not “starting” a stopped heart. It delivers a shock that stops chaotic electrical activity so that the natural pacemaker may regain control.

7. General Emergency Principle: Is the Patient Stable?

Do not look only at the ECG. Look at the patient.

Features of instability include:

Hypotension
Shock
Altered mental status
Ischaemic chest pain
Acute heart failure
Syncope or impending collapse

Easy rule

Unstable tachyarrhythmia with a pulse → synchronized cardioversion.
Pulseless VT/VF → defibrillation and CPR.

8. Antiarrhythmic Drugs

Antiarrhythmic drugs alter cardiac electrical conduction, automaticity, or repolarization.

They can be useful, but they can also cause proarrhythmia, meaning a drug intended to prevent an arrhythmia can sometimes trigger another dangerous rhythm.

Vaughan-Williams classification

Class	Main action	Main examples	Easy memory
I	Sodium-channel blockers	Flecainide, lidocaine, procainamide	I = sodium enters In
II	Beta-blockers	Metoprolol, propranolol, esmolol	II = block adrenaline
III	Potassium-channel blockers	Amiodarone, sotalol	III = prolong repolarization
IV	Calcium-channel blockers	Verapamil, diltiazem	IV = slow AV-node traffic
Other	Miscellaneous	Adenosine, digoxin, magnesium	Special tools

9. Class I: Sodium-Channel Blockers

These drugs reduce the fast sodium current in cardiac muscle, mainly affecting depolarization and conduction in atrial and ventricular tissue.

Visualization

Sodium is like the first fast push that starts the electrical wave in many heart cells. Blocking sodium channels makes the electrical message travel less easily.

Class IA

Examples:

Procainamide
Quinidine
Disopyramide

Effects:

Slow conduction
Prolong action potential duration
Prolong QT interval

Risk:

Torsades de pointes due to QT prolongation

A useful special point:

Procainamide may be used for some stable wide-complex tachycardias and selected cases of pre-excited atrial fibrillation under expert care.

Class IB

Examples:

Lidocaine
Mexiletine

Effects:

Preferential action in ventricular tissue, especially ischaemic tissue
Shorten action potential duration

Use:

Ventricular arrhythmias, particularly in certain acute settings

Class IC

Examples:

Flecainide
Propafenone

Effects:

Markedly slow conduction
Little effect on action potential duration

Use:

Selected atrial fibrillation or SVT patients with no significant structural heart disease

Important caution: Class IC drugs can be dangerous in people with prior myocardial infarction or structural heart disease because they may provoke serious ventricular arrhythmias.

10. Class II: Beta-Blockers

Examples:

Metoprolol
Bisoprolol
Atenolol
Propranolol
Esmolol
Carvedilol

How they work

They block beta-adrenergic stimulation from adrenaline and noradrenaline.

Visualization

Adrenaline is like pressing the accelerator of the heart. Beta-blockers reduce this accelerator effect.

They:

Slow SA-node firing
Slow AV-node conduction
Increase AV-node refractoriness
Reduce ectopic activity caused by stress hormones

Uses

Rate control in atrial fibrillation/flutter
Some SVTs
Prevention of arrhythmias after myocardial infarction
Catecholamine-triggered arrhythmias

Adverse effects

Bradycardia
Hypotension
Fatigue
May worsen bronchospasm in susceptible patients, especially non-selective beta-blockers
Can worsen acute decompensated heart failure in some situations

11. Class III: Potassium-Channel Blockers

Examples:

Amiodarone
Sotalol
Dofetilide
Ibutilide

How they work

They prolong repolarization and increase the refractory period.

Visualization

After a heartbeat, the cell must reset before responding again. Potassium-channel blockers lengthen the reset period, making it harder for an abnormal circuit to restart immediately.

Amiodarone

Amiodarone is a broad-spectrum antiarrhythmic. It has actions from more than one class, although it is traditionally placed in Class III.

Uses may include:

Atrial fibrillation rhythm control in selected patients
Ventricular tachyarrhythmias
Some resistant arrhythmias

Important adverse effects: remember “lungs, liver, thyroid, eyes, skin”

Pulmonary toxicity, including pneumonitis/fibrosis
Hepatotoxicity
Hypothyroidism or hyperthyroidism
Corneal deposits and optic problems
Photosensitivity and blue-grey skin discoloration
Bradycardia and QT prolongation
Many drug interactions

Amiodarone is powerful but requires monitoring.

Sotalol

Sotalol has beta-blocking and potassium-channel blocking effects.

Main concern:

QT prolongation and torsades de pointes

12. Class IV: Non-Dihydropyridine Calcium-Channel Blockers

Examples:

Verapamil
Diltiazem

These act mainly at the SA and AV nodes.

Visualization

If the AV node is the gatekeeper, calcium channels help it transmit messages. Verapamil and diltiazem make the gatekeeper slower and stricter.

Uses

Rate control in AF or flutter in appropriate patients
Some SVTs

Adverse effects

Bradycardia
Hypotension
Constipation, particularly with verapamil
Worsening heart failure in some patients

Important caution

Avoid combining verapamil or diltiazem with beta-blockers without careful supervision because both can excessively slow the heart or cause AV block.

They are also generally avoided in heart failure with reduced ejection fraction.

13. Other Important Drugs

Adenosine

Main use: regular narrow-complex SVT.

Very rapid onset
Very short duration
Temporarily blocks AV-node conduction

Visualization

It briefly locks the AV-node gate. If the tachycardia needs that gate to keep circulating, the rhythm stops.

Cautions:

May cause bronchospasm, so use carefully in asthma
Do not use casually in irregular or broad-complex tachycardias
In pre-excited AF, AV-nodal blockers can be dangerous because they may allow rapid conduction through an accessory pathway

Digoxin

Digoxin increases vagal tone and slows AV-node conduction.

Uses:

Rate control in AF in selected patients
Sometimes useful in heart failure with AF, especially when other options are unsuitable

Important points:

It does not work well for high sympathetic states, such as exercise or severe illness
It has a narrow therapeutic range
Toxicity can cause nausea, vomiting, confusion, visual changes, and many arrhythmias

Low potassium increases the risk of digoxin toxicity.

Magnesium sulfate

Main use:

Torsades de pointes
Correction of low magnesium

Torsades de pointes is a special polymorphic VT associated with prolonged QT interval.

Visualization

The ECG complexes seem to twist around the baseline, hence the name “twisting of the points.”

14. Easy Drug Selection Map

Clinical situation	Common immediate approach
Symptomatic bradycardia	Atropine, pacing if needed
Regular narrow SVT, stable	Vagal manoeuvre, then adenosine
AF with rapid rate, stable	Rate control with beta-blocker or diltiazem/verapamil in suitable patients
AF stroke prevention	Assess need for anticoagulation
Unstable tachyarrhythmia with pulse	Synchronized cardioversion
Pulseless VT/VF	CPR and defibrillation
Torsades de pointes	Magnesium, correct causes, manage QT prolongation
Wide-complex tachycardia	Treat as VT unless proven otherwise

15. High-Yield Memory Story

Imagine the heart as a city transport system.

SA node = central railway station that starts every train
Atria = local streets
AV node = toll gate that slows traffic
His-Purkinje system = express railway
Ventricles = factories that pump blood to the whole city

Arrhythmia happens when:

The central station sends trains too slowly or too quickly
Another station starts sending unauthorized trains
Traffic goes around in a circular route endlessly
The toll gate blocks too much traffic
The express railway is damaged
The whole transport system becomes chaotic, as in VF

Drugs act on different parts:

Beta-blockers reduce the accelerator effect of adrenaline
Verapamil/diltiazem slow the AV-node toll gate
Adenosine briefly closes the AV-node gate
Sodium-channel blockers slow electrical travel
Potassium-channel blockers lengthen the reset period
Amiodarone affects several electrical mechanisms and is powerful but toxic
Magnesium helps stabilize dangerous QT-related rhythms

16. Final One-Minute Summary

A normal heart rhythm starts in the SA node, pauses at the AV node, then activates ventricles through the His-Purkinje system.
Arrhythmias arise from abnormal automaticity, re-entry circuits, or triggered activity.
AF is irregularly irregular and increases stroke risk.
SVT is usually regular and narrow-complex, often treated with vagal manoeuvres or adenosine if stable.
VT is usually broad-complex and potentially dangerous.
VF causes cardiac arrest and requires immediate defibrillation.
In any arrhythmia, first ask: Is the patient unstable?
Antiarrhythmics can themselves cause arrhythmias, especially QT-prolonging drugs.
Never treat an ECG tracing alone. Treat the patient, identify the cause, and correct reversible triggers.

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