Cardiac Arrhythmias�(Disorders of heart rhythm) and management

PROF S S DANBAUCHI

Objectives

• For the student to learn about normal propagation of cardiac impulses

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• To learn about abnormal formation and or propagation of cardiac impulses (arrhythmias or rhythm disorders)

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• To learn about investigations and treatment of arrhythmias

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• Investigations and Management of heart rhythm disorders

Cardiac Arrhythmias - Definition

● An abnormality of the cardiac rhythm is called a cardiac arrhythmia.

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● Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no symptoms at all.

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● There are two main types of arrhythmia:

bradycardia: the heart rate is slow (< 60 bpm).

tachycardia: the heart rate is fast (> 100 bpm).

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Definition and causes

• Arrhythmia is abnormal rhythm of the heart beat.
• The possible causes of arrhythmias are:
1. Abnormal rhythmicity of the pacemaker
2. Shift of the pacemaker to another place in the heart
3. Block of different parts of the conducting system
4. Abnormal pathway of impulses transmission
5. Spontaneous generation of spurious impulses in all parts of the heart.

Cardiac conduction system

Anatomy of the conducting system

Physiology of the normal heart

Normal conduction pathway:

1- SA node generates action potential and delivers it to the atria and the AV node

2- The AV node delivers the impulse to purkinje fibers

3- purkinje fibers conduct the impulse to the ventricles

Other types of conduction that occurs between myocardial cells:

When a cell is depolarized 🡪 adjacent cell depolarizes along

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Action potential of the heart:

In the atria, purkinje, and ventricles the AP curve consists of 5 phases

In the SA node and AV node, AP curve consists of 3 phases

Non-pacemaker action potential

Phase 0: fast upstroke

Due to Na⁺ influx

Phase 3: repolarization

Due to K⁺ efflux

Phase 4: resting membrane potential

Phase 2: plateu

Due to Ca⁺⁺ influx

Phase 1: partial repolarization

Due to rapid efflux of K⁺

N.B. The slope of phase 0 = conduction velocity

Also the peak of phase 0 = V_max

Effective refractory period (ERP)

It is also called absolute refractory period (ARP) :

• In this period the cell can’t be excited
• Takes place between phase 0 and 3

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Standard 12 lead ECG

ECG Basics�

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• How to Analyze a Rhythm

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• Normal Sinus Rhythm

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• Heart Arrhythmias

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• Diagnosing a Myocardial Infarction

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• Advanced 12-Lead Interpretation

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• The standardization of speed of paper (25 mm/sec) and Voltage (10 mm =1 mV)

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Normal Impulse Conduction

Sinoatrial node

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AV node

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Bundle of His

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Bundle Branches

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Purkinje fibers

The “PQRST”

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• P wave - Atrial depolarization

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• T wave - Ventricular repolarization

• QRS - Ventricular depolarization

Pacemakers of the Heart

• SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.

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• AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.

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• Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.

SAN

AVN

Impulse conduction

Impulses originate regularly at a frequency of 60-100 beat/ min

-100

-80

-60

-40

-20

0

20

Phase 0

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Phase 1

Phase 2

Phase 3

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Phase 4

Na⁺

ca⁺⁺

ATPase

mv

Cardiac Action Potential

Resting membrane Potential

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Na⁺

m

Na⁺

Na⁺

Na⁺

Na⁺

Na⁺

h

K⁺

ca⁺⁺

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K⁺

K⁺

K⁺

ca⁺⁺

ca⁺⁺

(Plateau Phase)

K⁺

K⁺

K⁺

Na⁺

K⁺

Depolarization

-100

-80

-60

-40

-20

0

20

Phase 0

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Phase 1

Phase 2

Phase 3

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Phase 4

Na⁺

ca⁺⁺

ATPase

mv

Cardiac Action Potential

R.M.P

Na⁺

m

Na⁺

Na⁺

Na⁺

Na⁺

Na⁺

h

K⁺

ca⁺⁺

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K⁺

K⁺

K⁺

ca⁺⁺

ca⁺⁺

(Plateau Phase)

K⁺

K⁺

K⁺

Na⁺

K⁺

Depolarization

Phase 4

(only in pacemaker cells

The ECG Paper

• Horizontally
• One small box - 0.04 s
• One large box - 0.20 s
• Vertically
• One large box - 0.5 mV

Reading 12-Lead ECGs

6 step approach for analyzing a 12-lead ECG.

• Calculate RATE
• Determine RHYTHM
• Determine QRS AXIS
• Calculate INTERVALS
• Assess for HYPERTROPHY
• Look for evidence of INFARCTION

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Normal sinus rhythm (NSR)

• Rate 60 - 100 bpm
• Regularity regular (rhythm)
• P waves normal
• PR interval 0.12 - 0.20 s
• QRS duration 0.04 - 0.12 s

Any deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia

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Arrhythmia

Arrhythmia /dysrhythmia: abnormality in the site of origin of impulse, rate, or conduction

If the arrhythmia arises from the ventricles it is called ventricular arrhythmia

If the arrhythmia arises from atria, SA node, or AV node it is called supra -ventricular arrhythmia

Classification of Arrhythmia

• Abnormal heart pulse formation
• Sinus arrhythmia
• Atrial arrhythmia
• Atrioventricular junctional arrhythmia
• Ventricular arrhythmia
• Abnormal heart pulse conduction
• Sinus-atrial block
• Intra-atrial block
• Atrio-ventricular block
• Intra-ventricular block
• Abnormal heart pulse formation and conduction

Mechnisms ofnesis

Delayed afterdepolarization

Early afterdepolarization

↑AP from SA node

AP arises from sites other than SA node

This is when the impulse is not conducted from the atria to the ventricles

1-This pathway is blocked

2-The impulse from this pathway travels in a retrograde fashion (backward)

3-So the cells here will be reexcited (first by the original pathway and the other from the retrograde)

Pathogenesis and Inducement �of Arrhythmia

• Some physical condition
• Pathological heart disease
• Other system disease
• Electrolyte disturbance and acid-base imbalance
• Physical and chemical factors or toxicosis, electrocution etc.

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Mechanisms of Cardiac Arrhythmias

Mechanisms of bradicardias:

Sinus bradycardia is a result of abnormally slow automaticity while bradycardia due to AV block is caused by abnormal conduction within the AV node or the distal AV conduction system.

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Mechanisms generating tachycardias include:

- Accelerated automaticity.

- Triggered activity

- Re-entry (or circus movements)

Atrial Arrhythmias

Sinus arrhythmia: 

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• A condition in which the heart rate varies with breathing.
• This is usually a benign condition

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SUPRAVENTRICULAR TACHYCARDIAS

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• Supraventricular tachycardia (SVTs) arise from the atrium or the atrioventricular junction.

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• Conduction is via the His-Purkinje system; therefore the QRS shape during tachycardia is usually similar to that seen in the same patient during baseline rhythm.

SVT

Sinus tachycardia  

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• A condition in which the heart rate is 100-160/min

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• Symptoms may occur with rapid heart rates including; weakness, fatigue, dizziness, or palpitations.

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• Sinus tachycardia is often temporary, occurring under stresses from exercise, strong emotions, fever, dehydration, thyrotoxicosis, anemia and heart failure.

• If necessary, beta-blockers may be used to slow the sinus rate, e.g. in hyperthyroidism

SINUS TACHYCARDIA

Sinus tachycardia converted to NSR

Atrial Arrhythmias

Premature supraventricular contractions or premature atrial contractions (PAC) 

• A condition in which an atrial pacemaker site above the ventricles sends out an electrical signal early. The ventricles are usually able to respond to this signal, but the result is an irregular heart rhythm.
• PACs are common and may occur as the result of stimulants such as coffee, tea, alcohol, cigarettes, or medications.
• Treatment is rarely necessary.

PAC

Atrial Arrhythmias

  Atrial flutter (HR 200-350/min) 

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• A condition in which the electrical signals come from the atria at a fast but even rate, often causing the ventricles to contract faster and increase the heart rate.
• When the signals from the atria are coming at a faster rate than the ventricles can respond to, the ECG pattern develops a signature "saw tooth" pattern, showing two or more flutter waves between each QRS complex.

Atrial Arrhythmias

Atrial flutter (TREATMENT)

• Treatment of the symptomatic acute paroxysm is electrical cardioversion.
• Patients who have been in atrial flutter more than 1-2 days should be treated in a similar manner to patients with atrial fibrillation and anticoagulated for 4 weeks prior to cardioversion.
• Recurrent paroxysms may be prevented by class Ic and class III agents
• The treatment of choice for patients with recurrent atrial flutter is radiofrequency catheter ablation

ATRIAL FLUTTER

Atrial flutter

• Is another condition which is caused by circus movement in the atria. But it is different from atrial fibrillation because the electrical impulses travel as a single signal always in ONE direction.
• In atrial flutter, when impulses reach the AV node they delay there. Therefore, every 2-3 beats of the atrium is for 1 beat of the ventricles.
• In the ECG we can see the flutter waves.

Flutter waves, with a very high atrial rate and low ventricular rate. 2 P waves for 1 QRS

P

P

P

P

P

P

QRS

QRS

QRS

Atrial Arrhythmias

Atrial fibrillation (AF) - 

• A condition in which the electrical signals come from the atria at a very fast and erratic rate. The ventricles contract in an irregular manner because of the erratic signals coming from the atria.
• The ECG shows normal but irregular QRS complexes, fine oscillations of the baseline (so-called fibrillation or f waves) and no P waves.
• Common causes include CAD, valvular heart disease, hypertension, hyperthyroidism and others. In some patients no cause can be found 'lone' atrial fibrillation.

ATRIAL FIBRILLATION

Types of fibrillation

• Atrial fibrillation: The atrium is not contracting & therefore losses its effect as a primer pump to eject the extra 25% of blood to the ventricles.
• The ECG is AF is irregularly irregular and there is no P wave

�The Wolf Parkinson White Syndrome (WPW)

► An abnormal band of atrial tissue connects the atria and ventricles and can electrically bypass the normal pathways of conduction; a re-entry circuit can develop causing paroxysms of tachycardia.

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► ECG shows:

- Short PR interval

- Delta wave on the upstroke of the QRS complex

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►Drug treatment includes flecainamide, amiodarone or disopyramide.

►Digoxin and verapamil are contraindicated.

►Transvenous catheter radiofrequency ablation is the treatment of choice.

WPW syndrome

Atrial Arrhythmias Management

• When atrial fibrillation is due to an acute precipitating event such as alcohol toxicity, chest infection or hyperthyroidism, the provoking cause should be treated.
• Strategies for the acute management of AF are ventricular rate control or cardioversion (± anticoagulation).
• Ventricular rate control is achieved by drugs which block the AV node
• Cardioversion is achieved electrically by DC shock or medically either by IV infusion of an anti-arrhythmic drug such as a class Ic or a class III agent

The choice depends upon:

• How well the arrhythmia is tolerated (is cardioversion urgent?)
• Whether anticoagulation is required before considering elective cardioversion
• Whether spontaneous cardioversion is likely (previous history? reversible cause?).

Atrial Arrhythmias Management

• Patients are anticoagulated with warfarin or NOACS for 4 weeks before cardioversion.
• Anticoagulants are used to minimize the risk of thromboembolism associated with cardioversion unless atrial fibrillation is of less than 1-2 days' duration.
• Transoesophageal echocardiography is being used to document the presence or absence of atrial thrombus as a guide to the necessity for long-term anticoagulation.

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Atrial Arrhythmias Management

• Long-term management of atrial fibrillation include two strategies:
• Rhythm control: antiarrhythmic drugs plus DC cardioversion plus warfarin
• Rate control: AV nodal slowing agents plus warfarin
• Recurrent paroxysms may be prevented by oral medication; class Ic agents are employed in patients with no significant heart disease and class III agents are preferred in patients with structural heart disease.
• Rate control is usually achieved by a combination of digoxin beta-blockers or calcium channel blockers (diltiazem or verapamil).

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Atrial Arrhythmias Management�

• Anticoagulation (target INR 2.0-3.0) This is indicated in patients with atrial fibrillation and one of the following major or two of the moderate risk factors:
• Major risk factors: Prosthetic heart valve, Rheumatic mitral valve disease, Prior history of CVA/TIA, Age > 75 years, Hypertension, Coronary artery disease with poor LV function
• Moderate risk factors: Age 65-75 years, Coronary artery disease but normal LV function, Diabetes mellitus.

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Ventricular Arrhythmias

Premature ventricular contactions (PVCs)

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• A condition in which an electrical signal originates in the ventricles and causes the ventricles to contract before receiving the electrical signal from the atria.
• ECG shows wide and bizarre QRS complex
• Early 'R-on-T' ventricular premature beats may induce ventricular fibrillation
• PVCs are not uncommon and often do not cause symptoms or problems.
• Treated only if symptomatic with beta-blockers.

Premature ventricular contractions (PVCs)

Types of premature beats

• Premature ventricular contraction (PVC): abnormal QRS complex
• prolonged( wide QRS)
• high voltage (tall QRS)
• T wave opposite the polarity of the QRS = Inverted

Premature Ventricular contraction

Prolonged/ high voltage QRS

Inverted T wave

Ventricular Tachyarrhythmias

Ventricular tachyarrhythmias can be

considered under the following headings:

• life-threatening ventricular tachyarrhythmias (Sustained ventricular tachycardia and ventricular fibrillation)
• torsades de pointes
• normal heart ventricular tachycardia
• non-sustained ventricular tachycardia
• ventricular premature beats

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Ventricular Arrhythmias

Ventricular tachycardia (VT)

• A condition in which an electrical signal is sent from the ventricles at a very fast but often regular rate.
• The ECG shows a rapid ventricular rhythm with broad (often 0.14 s or more), abnormal QRS complexes. AV dissociation may result in visible P waves

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Treatment: Ventricular Arrhythmias ��

• In hemodynamically compromised patients, emergency DC cardioversion may be required. If the blood pressure and cardiac output are well maintained, intravenous therapy with class I drugs or amiodarone is usually used.
• First-line drug treatment consists of lidocaine (50-100 mg i.v. over 5 minutes) followed by a lidocaine infusion (2-4 mg i.v. per minute). DC cardioversion is necessary if medical therapy is unsuccessful.

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Ventricular Tachycardia

Ventricular Arrhythmias

Ventricular fibrillation (VF) 

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• A condition in which many electrical signals are sent from the ventricles at a very fast and erratic rate. As a result, the ventricles are unable to fill with blood and pump.
• This rhythm is life-threatening because there is no pulse and complete loss of consciousness.
• The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes

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Ventricular fibrillation (VF) 

• A person in VF requires prompt defibrillation to restore the normal rhythm and function of the heart. It may cause sudden cardiac death. Basic and advanced cardiac life support is needed
• Survivors of these ventricular tachyarrhythmias are, in the absence of an identifiable reversible cause (e.g. acute myocardial infarction, severe metabolic disturbance), at high risk of sudden death. Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management of these patients

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Ventricular Fibrillation

Bradycardias

Sinus Bradycardia 

• Physiological variant due to strong vagal tone or atheletic training.
• Rate as low as 50 at rest and 40 during sleep.
• Common causes of sinus bradycardia include:
• Extrinsic causes ;Hypothermia, hypothyroidism, cholestatic jaundice and raised intracranial pressure. Drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs.
• Intrinsic causes; Acute ischaemia and infarction of the sinus node (as a complication of acute myocardial infarction). Chronic degenerative changes such as fibrosis of the atrium and sinus node (sick sinus syndrome).

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SINUS BRADYCARDIA

Bradycardias

Sick sinus syndrome 

• A condition in which the sinus node sends out electrical signals either too slowly or too fast. There may be alternation between too-fast and too-slow rates.
• This condition may cause symptoms if the rate becomes too slow or too fast for the body to tolerate.

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• Chronic symptomatic sick sinus syndrome requires permanent pacing (AAI), with additional antiarrhythmic drugs (or ablation therapy) to manage any tachycardia element.
• Thromboembolism is common in tachy-brady syndrome and patients should be anticoagulated unless there is a contraindication.

Impulse conduction block

1. Sinoatrial Block: the impulses are blocked in the SA node before reaching the atrial muscles. This will eliminate the P wave.
2. Atrioventricular Block: is caused when there is ischemia, compression or inflammation of the AV node or AV bundle.
3. Interventricular Block( RBBB or LBBB): in which impulses fail to reach part of the heart during heart cycle.

Atrioventricular (AV) Block

First degree A-V Block 

• Seldom of clinical significance, and unlikely to progress.
• ECG shows prolonged PR interval.
• May be associated with acute rheumatic fever, diphtheria, myocardial infarction or drugs as digoxin

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Atrioventricular (AV) Block

Second degree A-V Block 

Mobitz type I (Wenchebach phenomenon):

• Gradually increasing P-R intervals culminating in an omission.
• When isolated, usually physiological and due to increased vagal tone and abolished by exercise and atropine.

Mobitz type II

• The P wave is sporadically not conducted. Occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation.
• Pacing is usually indicated in Mobitz II block, whereas patients with Wenckebach AV block are usually monitored.

Atrioventricular (AV) Block

Third degree A-V Block 

• Common in elderly age groups due to idiopathic bundle branch fibrosis.
• Other causes include coronary heart disease, calcification from aortic valve, sarcoidosis or congenital.
• ECG shows bradycardia, P wave continue, unrelated to regular slow idioventricular rhythm.
• Treatment is permanent pacing.

Third Degree A-V block

Atrioventricular (AV) Block

Bundle Branch Block (BBB):

• Interruption of the right or left branch of the bundle of Hiss delays activation of the corresponding ventricle leading to broadening of the QRS complex
• Unlike right BBB, left BBB is always associated with an underlying heart disease.
• Both RT and LT BBB show wide deformed QRS complex. In RBBB there is rSR pattern in lead V1, while in LBBB there is a broad monophasic (or notched) R wave in leads V5 and V6.

INVESTIGATIONS- routine

• FBC and diff
• U & E, Creatinine
• Urine analysis
• Lipid profile
• CXR
• Angiography/Thallium scan

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SPECIFIC INVESTIGATIONS

• Standard resting ECG
• 24-48 Holter Monitoring, 30 days ECG monitoring
• Telemetry- ICU, CCU
• Telemetry from special pacemakers or ICDs
• Exercise ECG
• Electrophysiology- invasive procedures

MANAGEMENT OF ARRHYTHMIAS

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• Good history and physical examination/investigations
• Pharmacological therapy (Digoxin is not anti-arrhythmics)
• Cardioversion.
• Pacemaker therapy.
• Surgical therapy e.g. aneurysmal excision.
• Interventional therapy “ablation”.
• Treating the background disorder

Pharmacologic Rationale & Goals

• The ultimate goal of antiarrhythmic drug therapy:
• Restore normal sinus rhythm and conduction
• Prevent more serious and possibly lethal arrhythmias from occurring.
• Antiarrhythmic drugs are used to:
• decrease conduction velocity
• change the duration of the effective refractory period (ERP)
• suppress abnormal automaticity

Phase 0

Phase 1

Phase 2

Phase 3

Phase 4

R.M.P

(Plateau Phase)

Class I:

Na ⁺ channel blockers.

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Pacemaker potential

Class III:

K ⁺ channel blockers

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Class IV:

Ca ⁺⁺ channel blockers

Class II:

Beta blockers

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Classification of Anti-Arrhythmic Drugs

Antyarrhythmic drugs

• Most antiarrhythmic drugs are pro-arrhythmic (promote arrhythmia)
• They are classified according to Vaughan William into four classes according to their effects on the cardiac action potential

Compare between class IA, IB, and IC drugs as regards effect on Na⁺ channel & ERP

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• Sodium channel blockade:�   IC > IA > IB
• Increasing the ERP:�IA>IC>IB (lowered)

Because of K⁺ blockade

Class II ANTIARRHYTHMIC DRUGS �(β-adrenergic blockers)

Mechanism of action

• Negative inotropic and chronotropic action.
• Prolong AV conduction (delay)
• Diminish phase 4 depolarization 🡪 suppressing automaticity(of ectopic focus)

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Uses

• Treatment of increased sympathetic activity-induced arrhythmias such as stress- and exercise-induced arrhythmias
• Atrial flutter and fibrillation.
• AV nodal tachycardia.
• Reduce mortality in post-myocardial infarction patients
• Protection against sudden cardiac death

Class II ANTIARRHYTHMIC DRUGS

• Propranolol (nonselective): was proved to reduce the incidence of sudden arrhythmatic death after myocardial infarction
• Metoprolol
• reduce the risk of bronchospasm
• Esmolol:
• Esmolol is a very short-acting β₁-adrenergic blocker that is used by intravenous route in acute arrhythmias occurring during surgery or emergencies

selective

Class III ANTIARRHYTHMIC DRUGS�K⁺ blockers

• Prolongation of phase 3 repolarization without altering phase 0 upstroke or the resting membrane potential
• They prolong both the duration of the action potential and ERP
• Their mechanism of action is still not clear but it is thought that they block potassium channels

Uses:

• Ventricular arrhythmias, especially ventricular fibrillation or tachycardia
• Supra-ventricular tachycardia
• Amiodarone usage is limited due to its wide range of side effects

Summary

•An abnormality of the cardiac rhythm is called a cardiac arrhythmia.

•Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no symptoms at all.

• Some physical condition, pathological heart diseases, other system disease , electrolyte disturbance and acid-base imbalance, Physical and chemical factors or toxicosis, electrocution etc.

• The ultimate goal of antiarrhythmic drug therapy:

• Restore normal sinus rhythm and conduction
• Prevent more serious and possibly lethal arrhythmias from occurring.

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