INTODUCTION

TO
CARDIAC ARRYTHMIAS
M2 CLASS
Introduction.
The heart has the specialized conducting
tissue that forms the electrical component of
it.
It is the abnormal functioning of this system
that results in arrhythmias.
The abnormality could occur in a normal heart
or in a structurally abnormal heart.
When myocardial function is poor arrhythmias
tend to be more serious, symptomatic and
life threatening.
Definition of arrhythmias.
 A disorganized functioning of the specialized
conducting tissues of the heart or the cardiac
musculature resulting in the pulse being
irregular, abnormally fast or slow.
 There is a change in a normal, regular,

automatic, heart beat and rhythm to an

irregular beat and rhythm.
Normal conductive tissue
 SAN
 ATRIA
 SAN
 BUNDLE OF HIS
 PURKINGE FIBERS
 VENTRICLES
 The abnormalities could originate from any of
the above. Naturally SAN is the normal
pacemaker of the heart. Any other beat coming
from the lower subsidiary tissue is abnormal.
Classification of cardiac arrhythmia

The abnormality could be classified in terms :

 Origin (sinus/SAN, atrial, AVN, ventricular)
 Rate (bradycardia/tachycardia)
 Rhythm (regular or irregular)
 Conduction velocity (slow, fast, blocked)
 Sequence of heart activation (backward

sequence)
Cardiac conductors
SA Node and AV node cells are slow conductors .
 Activated by calcium.

 Blocked by calcium channel blockers such as

verapamil

Atrium, Bundle of His, and ventricle cells are fast

conductors.
 Activated by sodium.

 Blocked by sodium channel blockers (class 1 anti-

arrhythmics) such as quinidine, lidocaine and

propafenone.
Abnormalities in Rate
There are 2 main types:
 Bradycardia: the heart rate is slow(<60bpm)
 Tachycardia: fast heart rate >100bpm
 Tachycardia are more symptomatic when fast

and sustained.
Two types of tachycardia :
 Supraventricular (atria, atrioventricular node

or junctional arrhythmia). Has narrow QRS in

ECG ie below 0.10s
 Ventricular. Wide QRS > 0.12s
Mechanism of arrhythmias.
The mechanisms responsible for cardiac
arrhythmias are generally divided into:
 Disorders of impulse formation
 Disorders of impulse conduction
 Combination of both.
Classification of Arrhythmia based on
mechanism
A. Disorders of impulse formation
1. Sinus arrhythmia (SAN)
2. Atrial arrhythmia
3. Atrioventricular junctional arrhythmia
4. Ventricular arrhythmia
B. Disorders of impulse conduction
5. Sinus-atrial block
6. Intra-atrial block
7. Atrio-ventricular block
8. Intra-ventricular block
C. Disorders of impulse formation and
conduction
Disorders of Impulse formation
This can be:
1. Disorder of automaticity.

2. Trigger activity.

Abnormalities of automaticity:
 Result from a single cell problem
 Automaticity is the property of a fiber to initiate an impulse

spontaneously without need for prior stimulation. It is

characterized by:
 Inappropriate discharge rate of a normal pacemaker, the SA

node (eg sinus rate too fast or too slow)

 Discharge of an ectopic pacemaker that controls atria or

ventricular rhythm. Ectopic pacemakers are often called

latent or subsidiary pacemaker.
Accelerated automaticity
 Depolarization of cardiac muscle starts slowly
(after phase 4 diastolic depolarization or after-
depolarization) to approach threshold
potential. Once the threshold is reached action
potential takes off.
 This mechanism can be quickened by
increasing the rate of after-depolarization or
reducing threshold potential.
 Implicated in sinus tachycardia, escape rhythm,
and accelerated AV nodal (junctional) rhythm.
Triggered activity

 Triggered activity is initiated by after-depolarizations,

which are depolarizing oscillations in membrane voltage
induced by one or more preceding action potential.
 Thus, triggered activity is a pacemaker that results
consequent to a preceding impulse or series of impulses
without electrical quiescence occurring.
 The instability is due to cellular damage and the
unstable cell can depolarize easily and earlier to elicit
AP. This is the bases for atrial tachycardias produced by
Digoxin toxicity or ventricular arrhythmia caused by
long QT syndrome.
Cardiac Action potential
 Has phase 0 to 4.
 Phase 0: rapid depolarization. Opening of fast Na channel.
 Phase 1: Initial rapid repolarization. Closure of the fast Na
channel and transient opening of K channel. Phase 0 and 1
correspond to R and S waves in the ECG.
 Phase 2: Plateau phase. Balance between the inward movement
of Ca and outward movement of K, corresponds to ST segment
of the ECG.
 Phase 3: Repolarization. K channels remain open. Allows K to
build up outside the cell, causing the cell to repolarize.
Corresponds to T wave in the ECG.
 Phase 4: Resting phase. Associated to diastole portion of the
heart cycle. K outward channel though open, inwardly rectifying
K channel.
Action potential: After depolarization.
 Early after-depolarizations (EADs) arise from a
reduced level of membrane potential during
phases 2 (type 1 – augmented opening of Ca
channels) and 3 (type 2-augmented opening of
K channels) of the cardiac action potential.
 Late or delayed after-depolarizations (DADs)
occur after completion of repolarization (phase
4 – secondary to increase in cytosolic Ca
levels), generally at a more negative membrane
potential than that from which EADs arise.
Causes of EAD include:
 Low K blood level
 Slow heart rate
 Drug toxicity (ie quinidine causing Torsades de

pointes)
Causes of DAD:
1. Increase serum calcium level
2. Increase adrenaline levels
3. Digoxin toxicity.
DAD gives rise to premature beats.
Disorders of impulse conduction
Can be:
 Conduction block

 Re-entry

Abnormalities of conduction:
 Usually due to abnormal interaction between cells.

 Either of these mechanisms can result in

bradycardia or tachycardia.
 Slow automaticity -----sinus bradycardia

 Av block-----bradycardia due to conduction

block
Reentry or circus movement.
 This mechanism operates when a ring of
cardiac tissue surrounds a dead or scarred
myocardium.
 Excitation originating above the scar moves

on either side to join below the scar to

continue forward propagation.
 The speed of impulse propagation in the two

limbs are not same as one is faster than the

other.
Reentry cont
 If a block is on the faster limb, impulse may
reach the faster limb from the slower limb.
 When the blocked portion is bypassed, the

impulse will once again travel down via the

slow limb and a vicious cycle is set up.
 This is the bases of paroxysmal tachycardias.
Precipitants of Arrhythmia
 Some physical conditions eg. Electric shock,
hypoxia.
 Pathological heart disease eg CAD, HF.
 Other system diseases eg thyroid
dysfunction, COAD
 Electrolyte disturbances and acid-base
imbalance eg hypokaelemia
 Physical and chemical factors or toxicosis
Presentation of arrhythmias
 Asymptomatic
 Sudden death
 Syncope
 Heart failure
 Dizziness
 Palpitations.
Diagnosis of Arrhythmia
 Medical history
 Physical examination
 Laboratory test: This includes

specialized monitoring devises to

diagnose specific arrhythmias.
 ECG.
 CXR, ECHO, CHEMISTRY STUDIES,

THYROID FUNCTION TESTS, to diagnose

structural heart disease or cofounders.
Monitoring devices.
 For making specific diagnosis
 To monitor treatment efficacy.

 To monitor pacemaker effectiveness.

They include:
 Holter monitoring (worn over 24-48hours to pick up

abnormal BP or Pulse)
 Trans-telephonic event monitor (worn for several days and

abnormal impulse sent via telephone calls)

 Exercise testing (symptoms may appear or worsen)
 Signal average ECG (used in post-MI to evaluate risk of V.fib

or V.tach)
 Electrophysiologic testing placed on RA,AVN, BH, coronary

sinus. May undergo ablative therapy.

Therapy.
 Medical
 Interventional.
Medical – antiarrhythmic drugs.
 Modify rhythm and conduction in the heart.
 May aggravate or worsen arrhythmias

(proarrhythmic)
 Classified according to the effect on action

potential or the part of the heart where they

act.
 Used for symptomatic relief.
Voughan Williams classification
Class 1 (modifies Na channel). They increase mortality in
CAD, structural HD, LVD.
 1a: lengthens AP eg disopyramide

 1b: shortens AP eg lidocaine

 1c: no effect on AP eg flacainide, propafenone

Class 11: (B-blockers) prevent the effect of catecholamines.

Suppress AVN eg. Propranolol, metoprolol
Class 111: prolong AP and do not affect Na channel eg.
Amiodarone, Sotalol-also a B-blocker. May produce long QT
syndrome precipitated by hypokalaemia and diuretic use.
Safe in structural heart disease.
Class1V: Non-hydropyridine CCB. Reduce the plateau of AP.
Slow conduction in nodal tissues.
Classification according to site of
action.
 SAN: B-blocker, atropine, digitalis
 AVN: b-blocker, CCB, digitalis, adenosine
 Atrium: disopyramide, quinidine,

Procainamide, flacainide, amiodarone,

digitalis.
 Bypass tract: disopyramide, quinidine,

procainamide, flecainide, amiodarone

 Ventricle: disopyramide, quinidine,

procainamide, b-blocker, amiodarone.

Interventional
 Medical is for relief of symptoms and
effective in 70-90%.
 Interventional therapy: catheter ablation.
 Curative and most effective with minimal side

effects especially in SVTs.

Non-drug therapy

 Cardioversion: For tachycardia control

especially in hemodynamic unstable patient
 Radiofrequency catheter ablation (RFCA): For
those tachycardia patients (SVT, VT, AF, AFL)
 Artificial cardiac pacing: For bradycardia,
heart failure and malignant ventricular
arrhythmia patients.