Dr.

Randa AlHarizy

Prof. of Internal Medicine

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

SAN
AVN

mv 20
204060-

Phase 2
(Plateau Phase)

Depolarization

Cardiac Action
Potential

Phase 1

Phase 0

Phase 3

80-

Phase 4

Resting membrane
Potential
+
Na
Na
-100 +++++Na
Na
Na
Na

m
+

Na

++
caca
++
ca++

+
+ ++
KKK
K

K+

ca++

ATPase
+

Na

mv 20
204060R.M.P

Phase 2
(Plateau Phase)

Depolarization

Cardiac Action
Potential

Phase 1

Phase 0

Phase 4
only in)
pacemaker
cells

Phase 3

80-

-100

Phase 4
Na
Na
Na
Na
Na
Na

+
++
++
+

m
+

Na

++
caca
++
ca++

+
+ ++
KKK
K

K+

ca++

ATPase
+

Na

Cardiac Arrhythmias
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
:There are two main types of arrhythmia
. bradycardia: the heart rate is slow (< 60 b.p.m)
.tachycardia: the heart rate is fast (> 100 b.p.m)

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
:Mechanisms generating tachycardias include
. Accelerated automaticityTriggered activityRe-entry (or circus movements)-

ACCELERATED AUTOMATICITY
It occurs due to increasing the rate of diastolic
depolarization or changing the threshold
potential.
Abnormal automaticity can occur in virtually
all cardiac tissues and may initiate arrhythmias.
Such changes are thought to produce sinus
tachycardia, escape rhythms and accelerated
AV nodal (junctional) rhythms.

TRIGGERED ACTIVITY
Myocardial damage can result in oscillations of the
transmembrane potential at the end of the action potential.
These oscillations, which are called 'after depolarizations',
may reach threshold potential and produce an arrhythmia.
The abnormal oscillations can be exaggerated by pacing,
catecholamines, electrolyte disturbances, and some
medications.
Examples as atrial tachycardias produced by digoxin
toxicity and the initiation of ventricular arrhythmia in the
long QT syndrome.

Re-entry (or circus movement)

The mechanism of re-entry occurs when a 'ring' of cardiac tissue
surrounds an inexcitable core (e.g. in a region of scarred
myocardium). Tachycardia is initiated if an ectopic beat finds one
limb refractory () resulting in unidirectional block and the other
limb excitable. Provided conduction through the excitable limb ()
is slow enough, the other limb () will have recovered and will
allow retrograde activation to complete the re-entry loop. If the
time to conduct around the ring is longer than the recovery times
(refractory periods) of the tissue within the ring, circus movement
will be maintained, producing a run of tachycardia.
The majority of regular paroxysmal tachycardias are produced by
this mechanism.

Reentry Arrhythmias
Normal

Re-enterant
Tachycardia

Atrial Arrhythmias
Sinus arrhythmia:
A condition in which the heart rate varies with
breathing.
This is usually a benign condition

SUPRAVENTRICULAR TACHYCARDIAS

Supraventricular tachycardias (SVTs) arise from the

atrium or the atrioventricular junction.
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.

Causes of SVT
Tachycardia

ECG features

Comment

Sinus tachycardia

P wave morphology similar to sinus

rhythm

Need to determine underlying cause

AV nodal re-entry tachycardia (AVNRT)

No visible P wave, or inverted P wave

immediately before or after QRS
complex

Commonest cause of palpitations in patients

with normal hearts

AV reciprocating tachycardia (AVRT)

P wave visible between QRS and T

wave complexes

Due to an accessory pathway. If pathway

conducts in both directions, ECG during
sinus rhythm may be pre-excited

Atrial fibrillation

Irregularly irregular RR intervals and

absence of organized atrial activity

Commonest tachycardia in patients over 65

years

Atrial flutter

Visible flutter waves at 300/min (sawtooth appearance) usually with 2 : 1 AV

conduction

Suspect in any patient with regular SVT at

150/min

Atrial tachycardia

Organized atrial activity with P wave

morphology different from sinus rhythm

Usually occurs in patients with structural

heart disease

Multifocal atrial tachycardia

Multiple P wave morphologies (3) and

irregular RR intervals

Rare arrhythmia; most commonly associated

with significant chronic lung disease

Accelerated junctional tachycardia

ECG similar to AVNRT

Rare in adults

SVT
Sinus tachycardia
A condition in which the heart rate is 100-160/min
Symptoms may occur with rapid heart rates including;
weakness, fatigue, dizziness, or palpitations.
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

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.

PACs

SVT
Paroxysmal Supraventricular tachycardia [HR 160250/min]
Atrioventricular nodal re-entry tachycardia (AVNRT)
It usually begins and ends rapidly, occurring in repeated periods. This
condition can cause symptoms such as weakness, fatigue, dizziness,
fainting, or palpitations if the heart rate becomes too fast.
In AVNRT, there are two functionally and anatomically different
pathways within the AV node: one is characterized by a short effective
refractory period and slow conduction, and the other has a longer
effective refractory period and conducts faster.
In sinus rhythm, the atrial impulse that depolarizes the ventricles
usually conducts through the fast pathway.
If the atrial impulse (e.g. an atrial premature beat) occurs early when
the fast pathway is still refractory, the slow pathway takes over in
propagating the atrial impulse to the ventricles. It then travels back
through the fast pathway which has already recovered its excitability,
thus initiating the most common 'slow-fast', or typical, AVNRT.

AVNRT (continue)
The rhythm is recognized on ECG by normal regular QRS
complexes, usually at a rate of 140-240 per minute. Sometimes
the QRS complexes will show typical bundle branch block. P
waves are either not visible or are seen immediately before or
after the QRS complex because of simultaneous atrial and
ventricular activation.

SVT

Atrioventricular reciprocating tachycardia

(AVRT)
In AVRT there is a large circuit comprising the AV node, the His
bundle, the ventricle and an abnormal connection from the
ventricle back to the atrium. This abnormal connection is called
an accessory pathway or bypass tract.
Bypass tracts result from incomplete separation of the atria and
the ventricles during fetal development.
Atrial activation occurs after ventricular activation and the P
wave is usually clearly seen between the QRS and T complexes

PSVT
Acute Management
Patients presenting with SVTs and haemodynamic instability
require emergency cardioversion.
If the patient is haemodynamically stable, vagal manoeuvres,
including right carotid massage, Valsalva manoeuvre and
facial immersion in cold water can be successfully
employed.
If not successful, intravenous adenosine (up to 0.25 mg/kg) ,
verapamil 5-10 mg i.v. over 5-10 minutes, i.v. diltiazem, or
beta-blockers should be tried.
Long-term management
It includes ablation of an accessory pathway. Also,
verapamil, diltiazem & -blockers; are effective in 60-80%
of patients.

N.B.

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.
ECG shows:
- Short PR interval
- Delta wave on the upstroke of the QRS complex
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
Atrial flutter (HR200-350/min)
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 "sawtooth" 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 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

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 (continue)
Patients are anticoagulated with warfarin 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.

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 betablockers or calcium channel blockers (diltiazem or verapamil).

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.

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

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
Treatment: in haemodynamically 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. Firstline 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.

Ventricular Tachycardia

Ventricular Arrhythmias
Ventricular fibrillation (VF)

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
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 cardioverterdefibrillators (ICDs) are first-line therapy in the management of these patients

Ventricular Fibrillation

Ventricular Arrhythmias
-Torsades de pointes
This is a type of short duration tachycardia that reverts to sinus
rhythm spontaneously.
It may be due to:
- Congenital
- Electrolyte disorders e.g. hypokalemia, hypomagnesemia,
hypocalcemia.
- Drugs e.g. tricyclic antidepressant, class IA and III
antiarrhythmics.
It may present with syncopal attacks and occasionally ventricular
fibrillation.
QRS complexes are irregular and rapid that twist around the
baseline. In between the spells of tachycardia the ECG show
prolonged QT interval.

Torsade de Pointes in patient on Sotalol

Ventricular Arrhythmias
-Torsades de pointes
Acute management includes; correction of any electrolyte
disturbances, stopping of causative drug, atrial or ventricular
pacing, Magnesium sulphate 8 mmol (mg2+) over 10-15 min for
acquired long QT, IV isoprenaline in acquired cases and B
blockers in congenital types.
Long-term management of acquired long QT syndrome involves
avoidance of all drugs known to prolong the QT interval.
Congenital long QT syndrome is generally treated by betablockade, left cardiac sympathetic denervation, and pacemaker
therapy. Patients who remain symptomatic despite conventional
therapy and those with a strong family history of sudden death
usually need ICD therapy.

Ventricular Arrhythmias
Premature ventricular contractions (PVCs)
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)

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).

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.
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.

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

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.

Second Degree AV Block

Acute myocardial infarction may produce second-degree

heart block. In inferior myocardial infarction, close
monitoring and transcutaneous temporary back-up pacing
are all that is required. In anterior myocardial infarction,
second-degree heart block is associated with a high risk of
progression to complete heart block, and temporary pacing
followed by permanent pacemaker implantation is usually
indicated.

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.

Right BBB

Atrioventricular (AV) Block

:Bundle Branch Block (BBB)
Hemiblock
Delay or block in the divisions of the left bundle branch produces
a swing in the direction of depolarization (electrical axis) of the
heart. When the anterior division is blocked (left anterior
hemiblock), there is left axis deviation. Delay or block in the
postero-inferior division causes (right axis deviation).
Bifascicular block
This is a combination of a block of any two of the following: the
right bundle branch, the left antero-superior division and the left
postero-inferior division. Block of the remaining fascicle will
result in complete AV block.

Bifasicular Block [Rt BBB+ Lt anterior hemiblock

MANAGEMENT OF ARRHYTHMIAS

Pharmacological therapy.
Cardioversion.
Pacemaker therapy.
Surgical therapy e.g. aneurysmal excision.
Interventional therapy ablation.

Classification of Anti-Arrhythmic Drugs

:Class IV

Ca ++ channel blockers

Phase 2
(Plateau Phase)

Phase 1

:Class I
.Na + channel blockers

R.M.P

Phase 0

Phase 3

:Class III
K + channel blockers

:Class II
Beta blockers

Pacemaker potential
Phase 4

Classification of Antiarrhythmic Drugs

based on Drug Action
CLASS

ACTION

.I

Sodium Channel Blockers

DRUGS

.1A

Moderate phase 0 depression and

slowed conduction (2+); prolong
repolarization

Quinidine,
Procainamide,
Disopyramide

.1B

Minimal phase 0 depression and slow

conduction (0-1+); shorten
repolarization

Lidocaine

Marked phase 0 depression and slow

conduction (4+); little effect on
repolarization

Flecainide

.II

Beta-Adrenergic Blockers

Propranolol, esmolol

.III

K+ Channel Blockers
(prolong repolarization)

Amiodarone, Sotalol,
Ibutilide

.IV

Calcium Channel Blockade

Verapamil, Diltiazem

.1C

Implantable cardioverterdefibrillator

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YOU