PATHOPHYSIOLOGY OF

ARRHYTHMIAS

Belay E. MD
December 2015
 Objectives
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At the end of the lecture students should be able to:-

List common causes & risk factors of arrhythmias

Describe the pathophysiologic mechanisms of
common arrhythmias
Characteize common types of arrhythmias
 Outline
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Electrophysiology of the heart

Definition of arrhythmias

Etiology & risk factors

Pathophysiology of arrhythmias

Common types of arrhythmias

Summary
 Electrophysiology of heart
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 Electrophysiology..
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Cardiac cycle is the events that occur from the

beginning of one heart beat to the beginning of the
next
It is initiated by spontaneous generation of action
potential in the SA node
SA node is located in the superior lateral wall of the
right atrium near the opening of the SVC
 Electrophysiology
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The sequence of events can be grouped into:-

A. Mechanical events
A. Atrial & ventricular diastole(relaxation)
B. Atrial & ventricular systole (contraction)
B. Electrical events
Spontaneous discharge of action potential from the SA
node
Impulse is transmission
slowly to both atria
more rapidly to the AV node through intermodal fibres
Depolarization of atria represented by p wave
 Electrophysiology
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The AVN is the only electrical connection

AV nodal delay
The time needed for activation of the atria and the
AVN delay PR interval
Impulse is transmission to the His-Purkinje system
Rapid activation of ventricular muscle represented by
QRS wave
Re-polarization of ventricles represented by T wave
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Recovery of electrical excitability occurs more

slowly which inscribes a T wave
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 Electrophysiology.
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 Electrophysiology
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Cardiac muscle has three types of membrane ion

channels
Fast sodium channels
slow sodium-calcium channels
potassium channels
Cardiac myocytes exhibit long action potential
(200400 ms)
The most abundant superfamily of ion channels
expressed in the heart is voltage gated
 Electrophysiology
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Phase 1
Phase 2

Phase 0
Phase 3

Phase 4
 Definition of Arrhythmias
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A cardiac arrhythmia is an abnormality in the

timing or sequence of cardiac depolarization
There are two predominant types of cardiac
arrhythmias:
tachyarrhythmia, an abnormally rapid cardiac
rhythm (HR>100 bpm)
bradyarrhythmia, a slow cardiac rhythm (HR<60
bpm)
 Etiology & Risk Factors
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Arrhythmias are results of various underlying heart

conditions and other factors:
Ischemic heart disease
Congenital heart disease.

Sympathetic overstimulation

Cardiac hypertrophy and failure

Drug related

Electrolyte disturbances
 Etiology & Risk Factors
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Hypertensive heart diseases

Valvular heart disease

Cardiomyopathy

Pericarditis, carditis

Excessive stretch

Metabolic disturbance

COPD

Thyrotoxicosis
 Mechanism of Arrhythmogensis
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1. Disorder of impulse formation.

Abnormal automaticity.
Triggered Activity.
Earlyafter depolarization (EAD).
Delayed after depolarization (LAD).

2. Disorder of impulse conduction.

Re-entry.
Reflection.

3. Combined disorder.
 Disorder of impulse formation
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Abnormal automaticity:-
Automaticity is the ability to initiate spontaneous

impulses
In the normal heart, SA node is the predominant

pacemaker
Secondary pacemakers are in the atria, AV node,

His-Purkinje system, coronary sinus, and pulmonary

veins
Heart cells other than those of the SA node

depolarize faster than SA node cells, and take control

as the cardiac pacemaker
 Disorder of impulse formation
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Varity of factors affect automaticity of SA node:

Sympathetic nervous system automaticity

Parasympathetic nervous system automaticity

Hypokalemia automaticity

Ischemia & reperfusion automaticity

 Disorder of impulse formation
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Abnormal automaticity may underlie:-

Atrial tachycardia

Accelerated ventricular rhythms

Ventricular tachycardia

Automatic ventricular tachycardia.

 Disorder of impulse formation
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Triggered Activity:-
Triggered activity is an uncommon mechanism of

cardiac arrhythmias.
Impulse initiation is dependent on afterdepolarizations

(ADs)
ADS are membrane voltage oscillations that occur

during EADs or DADs action potential.

ADs could happen early or delayed
 Disorder of impulse formation
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It occurs when a preceding depolarization does not

repolarize completely before depolarizing again
EADs occur before the end of the action potential
(phases 2 and 3), interrupting repolarization.
DADs occur during phase 4 of the action potential
after completion of repolarization
 Disorder of impulse formation
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 Disorder of impulse formation
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Early afterdepolarizations (EAD)

The basis for EAD seems to involve the L-type

calcium channel
EADs are facilitated by increased repolarization

time (long QT interval)

Long QT intervals initiates in intracellular Ca2+

Drugs that prolong the QT interval, such as

erythromycin, quinidine, and procainamide

The ultimate effect of EADs may be in initiating

polymorphic ventricular tachycardia

 Disorder of impulse formation
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Hypokalemia, hypomagnesemia, bradycardia, and,

most commonly, drugs can predispose to the
generation of EADs
They prolong the action potential
 Disorder of impulse formation
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Delayed afterdepolarizations (DADs)

Arise during phase 4 of the action potential
2+
Elevated intracellular ca or by release of ca2+ from
the sarcoplasmic reticulum
HR, extracellular calcium, digitalis toxicity,
catecholamines, and ischemia can enhance DADs
DADs form the basis of digitalis arrhythmias,

idiopathic ventricular tachyarrhythmias & multifocal

atrial tachycardia
 Disorder of impulse conduction
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REENTRY
The most common arrhythmia mechanism

Defined as circulation of an activation wave around

an inexcitable obstacle
Two electrophysiologically dissimilar pathways for
impulse propagation around an inexcitable region
Unidirectional block occurs in one of the pathways

Region of excitable tissue exists at the head of the

propagating wave front
Reentry Mechanism
Electrical Impulse
Cardiac
Conduction
Tissue

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

1. Two distinct pathways that come together at beginning and end to

form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
Reentry Mechanism
Premature Beat Impulse
Cardiac
Conduction
Repolarizing Tissue
Tissue
(long refractory period)

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

1. An arrhythmia is triggered by a premature beat

2. The fast conducting pathway is blocked
because of its long refractory period so the beat
can only go down the slow conducting pathway
Reentry Mechanism
Cardiac
Conduction
Tissue

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

3. The wave of excitation from the premature beat

arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway
Reentry Mechanism
Cardiac
Conduction
Tissue

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

4. On arriving at the top of the fast pathway it finds the

slow pathway has recovered and therefore the wave of
excitation re-enters the pathway and continues in a
circular movement. This creates the re-entry circuit
 Disorder of impulse conduction
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Reentry underlay variety of arrhythmias:-

Atrial Reentry

atrial tachycardia
atrial fibrillation
atrial flutter
Atrio-Ventricular Reentry
Ventricular Re-entry
ventricular tachycardia
 Common types of arrhythmias
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Bradyarrhythmias
Bradycardia results from a failure of either impulse

initiation or impulse conduction

SA node dysfunction and AV conduction block are

the most common causes of pathologic bradycardia

Tachyarrhythmias
Rhythm that produces a ventricular rate >100 beats

per minute
Originate from myocardial foci or reentrant circuits
 Brady
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SINUS NODE DYSFUNCTION

Sinus bradycardia <45/min
SA exit block (First, second, third degree)
Sinus arrest
ATRIOVENTRICULAR BLOCK
First degree
Second degree
Third degree
Atrioventricularnode
His-Purkinje system
 Sinus Bradycardia
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Persistent rates less than 40 bpm while awake in

absence of physical conditioning
May also be manifested by the failure to accelerate
the sinus rate (lack of chronotropic response)
-blockers or calcium-channel blockers
 Sinoatrial Exit Block
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Impulse to the atrium can be delayed or interrupted

periodically with loss of P wave
Sinus node activity is not recorded on the surface
ECG
Severe SA block causes complete absence of sinus
P waves
 Sinus Arrest
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Sudden disappearance of P waves

Could be due to either SA exit block or cessation of
sinus node pacemaker function
 Atrioventricular Blocks
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Defined when some impulses are delayed or do not

reach the ventricle during sinus rhythm or sinus
tachycardia
AV nodal blocks can be caused by digitalis,
antiarrhythmic drugs, and vagal influences
 First Degree AV Block
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Prolonged atrioventricular conduction

Delay at the AV node results in prolonged PR

interval
PR interval>0.2 sec
 Second Degree AV Block Type 1
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(Wenckebach)

Increasing delay at AV node until a p wave is not

conducted.
Often comes post inferior MI with AV node ischemia
Gradual prolongation of the PR interval before a
skipped QRS. QRS are normal!
 Second Degree AV Block Type 2
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Intermittent Atrioventricular Conduction

Sudden loss of a QRS wave because p wave was

not transmitted beyond AV node. QRS are
abnormal!
May be precursor to complete heart block
 Third Degree AV Block
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No atrioventricular conduction
Complete failure of impulse propagation along the
AV conduction system
Necessitates emergence of a subsidiary pacemaker
distal to the site of block

Atria and ventricles beat independently

 Tachyarrhythmias
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Sinus tachycardia
Atrial fibrillation
Atrial flutter
Ventricular tachycardia
Monomorphic

Polymorphic (Torsades de pointe)

Ventricular fibrillation
 Sinus tachycardia
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Enhancement of normal automaticity seen in the

settings of increased adrenergic drive
PR interval is not prolonged despite acceleration of
the sinus rate
Pulse Rate increases
Physiologic sinus tachycardia
 Atrial fibrillation
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The most common sustained arrhythmia in adults

The incidence of AF increases with advancing age
During AF, the atria have disorganized, rapid,
irregular electrical activity exceeding 400 bpm
Ventricular response is also irregular and variable
(irregularly irregular)
Intra-atrial clot formation is promoted
Irregularity of the RR wave makes the diagnosis
 Atrial fibrillation
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Multiple wavelets of (micro)reentry

 Atrial fibrillation
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HTN, cardiomyopathy, valvular heart disease, sick

sinus, thyrotoxicosis, acute vagotonic episode,
acute alcohol intoxication, recovery phase of major
surgery
The ECG in AF is characterized by the lack of
organized atrial activity and the irregularly
irregular ventricular response
 Atrial Flutter
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Regular atrial rates ranging from 250 to 350 beats

per minute
sawtooth pattern in lead II
Usually a 2:1 conduction pattern
 Ventricular tachycardia
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 Ventricular tachycardia
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Impulse is initiated from the ventricle itself

Wide QRS
VT originates below the bundle of His at a rate
>100 beats per minute
Most VT patients have rates >120 beats per minute
 Ventricular Fibrillation
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Most common in acute MI, also drug overdose,

anesthesia, hypothermia & electric shock can
precipitate
Absence of ventricular complexes
Usually terminal event
 Summary
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Knowing the normal electrophysiology of the heart

has paramount importance to understand
arrhythmias
A cardiac arrhythmia is an abnormality in the
timing or sequence of cardiac depolarization
Two predominant types of cardiac arrhythmias
Arrhythmogensis is mainly due to abnormal
automaticity, triggered activity, or re-entry.
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Questions?
THE END
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THANK YOU