Transcript CARDIAC ARRHYTHMIAx

By Dr. Zahoor
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CARDIAC ARRHYTHMIA
First we will have quick look at the
physiology
 SA Node is the pace maker of the heart
and is under control of ANS
(Sympathetic and Parasympathetic)
 Heart has its conductive tissue
SA Node – Internodal fibers – AV Node
– Bundle of HIS – Bundle branches
(RBB and LBB) – Purkinje fibers
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CONDUCTIVE TISSUE OF HEART
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CARDIAC ARRHYTHMIA

If the sinus rate (SA Node) becomes unduly
slow then lower center may assume the
role of pacemaker, this is known as ESCAPE
RHYTHM

Impulse may arise from
- AV Node (Nodal Rhythm) or
HIS bundle (Junctional Rhythm) or
Ventricles (Idioventricular Rhythm)
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CARDIAC ARRHYTHMIA
What is CARDIAC ARRHYTHMIA?
 It is the disturbance of electrical rhythm
of the heart.
Why Arrhythmia occur?
 They are often due to structural heart
disease, but may also occur due to
abnormal conduction
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CARDIAC ARRHYTHMIA
Normal heart rate (HR)
60-100/min
 HR > 100/min is called Tachycardia
 HR < 60/min is called Bradycardia

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CARDIAC ARRHYTHMIA

Arrhythmia may be
1. Supraventricular
i- Sinus (SA Node)
ii- Atrial
iii- Atrioventricular nodal re-entrant
tachycardia (AVNRT)
2. Ventricular
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CARDIAC ARRHYTHMIA
Important
 Supraventricular rhythm produces
narrow QRS complex. Why?
Because ventricles are depolarized
through AV Node and Bundle of His.
 Ventricular rhythm produce wide,
bizarre QRS complex because
ventricles are depolarized in an
abnormal sequence
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SUPRAVENTRICULAR
ARRHYTHMIA
i. SA NODE
Sinus Arrhythmia
 Heart rate increases during inspiration and
slows during expiration, it is called sinus
arrhythmia. More commonly seen in
children. It is physiological.
Sinus Bradycardia
 Sinus rate < 60/min, may occur in healthy
people at rest, athlete or it may be
pathological e.g. hypothyroidism, increased
intracranial pressure
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CAUSES OF SINUS BRADYCARDIA
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SUPRAVENTRICULAR
ARRHYTHMIA
Sinus Tachycardia - Physiological
 Sinus rate > 100/min usually due to
increased sympathetic activity
associated with emotion, exercise,
pregnancy
OR
It may be pathological e.g.
hyperthyroidism, heart failure
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CAUSES OF SINUS TACHYCARDIA
- Some pathological causes
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ii. ATRIAL TACHYARRHYTHMIA
Atrial Tachyarrhythmia may be
1. Atrial extra systole/premature
beat/ectopic beat
2. Atrial Tachycardia
3. Atrial flutter
4. Atrial fibrillation
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ATRIAL TACHYARRHYTHMIA
1. Atrial extra systole
 When there is atrial extra systole, it usually causes
no symptoms, but can give the sensation of miss
beat or abnormally strong beat
Atrial Ectopic Beats – 3rd 4th and 6th complexes
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ATRIAL TACHYARRHYTHMIA
1. Atrial extra systole
 ECG shows premature beat, P wave
has different morphology. Why?
Because atria are activated from an
abnormal site ( but QRS is normal)
 Effect – usually no consequence but
very frequent atrial ectopic beat may
lead to AF
 Treatment – beta blockers can be used
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ATRIAL TACHYARRHYTHMIA
2. Atrial tachycardia
 Heart rate is 140-250/min, it is due to atrial
automaticity, digoxin toxicity

ECG produces narrow complex tachycardia
(QRS is narrow) with abnormal P wave
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ATRIAL TACHYARRHYTHMIA
2. Atrial Tachycardia
Treatment
 Beta blockers – they reduce automaticity
 If ventricular response is rapid, A..V node
blocking drugs (calcium blockers e.g.
verapamil)
 Cathetor ablation to target the ectopic site in
case of recurrent atrial tachycardia
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ATRIAL TACHYARRHYTHMIA
3. Atrial Flutter
 Atrial rate is approximately 300/min and
usually associated with 2:1, 3:1 or 4:1 A.V
block (with heart rate of 150, 100, or 75/min)

ECG shows saw – toothed flutter waves. It is
narrow complex tachycardia
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ATRIAL TACHYARRHYTHMIA
3. Atrial Flutter
Management
 Beta blocker, verapamil, digoxin can be
used to control the ventricular rate
 To restore sinus rhythm, we use direct
current, DC cardio version or
Amiodarone IV
 Catheter ablation – 90% chance of
complete cure
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation (AF)
 It is due to abnormal automatic firing in the
atria
 In AF – atria beat rapidly
 Atrial rate 350 to 500/min but in
uncoordinated and ineffective manner
 The ventricles are activated irregularly at a
rate determined by conduction through the
AV Node. This produces irregularly
irregular pulse
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation

ECG shows no P-wave but fibrillation
waves. QRS complex is normal but
coming at irregular interval
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation
 It may be
1. Paroxysmal (intermittent, self terminating
episode)
2. Persistent (prolonged episode)
3. Permanent
 AF causes are – coronary artery disease,
valvular heart disease, hypertension,
hyperthyroidism, alcohol, idiopathic (lone
AF)
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation
Causes
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ATRIAL TACHYARRHYTHMIA
4. Atrial Fibrillation
Do ECG, echo cardiogram, thyroid function
test
Management
1. Paroxysmal AF
 Paroxysmal AF may not require treatment.
Beta blockers are used
 Other drugs used are digoxin, verapamil to
limit the heart rate by blocking AV node
 Ablation is used for ectopic focus
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ATRIAL TACHYARRHYTHMIA
Management
2. Persistent AF and 3. Permanent AF
 There are two ways to treat
i). Rhythm control – to restore and maintain
sinus rhythm by DC cardioversion (after the
administration of anti coagulants)
Indication – when AF is present < 3months,
patient is young, no structural heart
disease
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ATRIAL TACHYARRHYTHMIA
Management ( cont )
2. Persistent and Permanent AF (cont)
ii). Rate control using treatment to
control ventricular rate and prevent
embolic complication
 Drugs used are digoxin, beta blocker,
calcium antagonist e.g. verapamil or
diltiazem (they act by increasing AV
node delay)
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ATRIAL TACHYARRHYTHMIA
Prevention of thromboembolism in AF
 Loss of atrial contraction and left atrial
dilatation causes stasis of blood in left
atrium and may lead to thrombus
formation. It predisposes the patient to the
stroke.
 Treatment advised
- Warfarin – it decreases the risk by 62%
- Aspirin – it decreases the risk by 22%
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SUPRAVENTRICULAR
TACHYCARDIA (SVT)
iii. Atrioventricular nodal re-entrant
tachycardia (AVNRT)- Junctionalarryhythmias
 These tachycardia are due to re-entry in
a circuit involving AV node.
 It produces regular tachycardia with a
rate of 120-240/min. Episode may last
from few seconds to many hours
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SUPRAVENTRICULAR
TACHYCARDIA (SVT)
HR 180/min
Management
 Carotid sinus pressure – it increases vagal tone
 IV adenosine or verapamil will restore sinus rhythm in most
cases
 Beta blockers
 DC cardio version if SVT with hemodynamic compromise
 Catheter abalation
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WOLFF – PARKINSON WHITE
SYNDROME (WPW Syndrome)

In WPW Syndrome, there is abnormal
band of conductive tissue which
connects atria to the ventricles. It is like
Purkinje tissue that conducts very
rapidly and is called accessory pathway
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WOLFF – PARKINSON WHITE
SYNDROME (WPW Syndrome)
ECG shows short PR and slurring of QRS
complex called Delta wave
Treatment
 Carotid sinus pressure
 IV adenosine
 Catheter abalation in symptomatic patient
For prophylaxis
- Amiodarone, flecainide (they slow the
conduction in the accessory pathway)

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VENTRICULAR TACHYARRYTHMIA

They are
1. Ventricular ectopic beats
2. Ventricular Tachycardia (VT)
3. Ventricular Fibrillation (VF)
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VENTRICULAR TACHYARRYTHMIA
1. Ventricular ectopic beat (extra systole,
premature beat)
 In ventricular ectopic beat, QRS is broad
and bizarre because ventricles are
activated by abnormal focus
 QRS may be unifocal (identical), when they
arise from single ectopic focus or QRS may
be multi focal (varying morphology) as they
arise from multiple foci
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VENTRICULAR TACHYARRYTHMIA
Ventricular ectopic beat (extra systole,
premature beat)
QRS Complex (arrows) are broad, bizarre with no preceding P
wave
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VENTRICULAR TACHYARRYTHMIA
Ventricle ectopic beat may occur in
Healthy subject – more prominent at rest and
disappear at exercise
 Treatment in symptomatic patient - beta blocker
Ventricular ectopic beat in Heart Disease
 Occur during acute MI
 Heart failure
 Digoxin toxicity
 Mitral valve prolapse
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2. VENTRICULAR TACHYCARDIA (VT)

ECG shows tachycardia with broad, abnormal
QRS complex with a rate of > 120/min
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VENTRICULAR TACHYCARDIA (VT)
Common causes of VT
 Acute MI
 Cardiomyopathy
 Chronic IHD with poor LV function
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VENTRICULAR TACHYCARDIA (VT)
Treatment of VT
 Synchronized DC cardio version shock, if
systolic BP < 90mmHg
 If VT is well tolerated then
- IV Amiodarone as bolus and then continuous
infusion
- IV lidocaine
Note – Correct hypokalaemia, hypomagnesaemia,
acidosis and hypoxaemia
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TORSADES DEPOINTES
(VENTRICULAR TACHYCARDIA)

This type of VT occurs in patients who
have prolonged QT interval
(hypocalcaemia, hypomagnesaemia,
hypokalaemia)

ECG shows bradycardia with long QT
interval followed by VT, rapid, irregular
QRS complex
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3. Ventricular Fibrillation (VF)
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3. Ventricular Fibrillation (VF)
It is life threatening, medical emergency
There is very rapid, irregular ventricular
activation with no pumping of blood
 Patient is pulseless, becomes rapidly
unconscious and respiration ceases
(Cardiac arrest)
 Can lead to death in minutes
Treatment
1- Defibrillation
2- CPR


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HEART BLOCKS
First degree AV Block
 In first degree heart block, AV conduction is
delayed. PR interval is prolonged > 0.2
second
 It rarely causes symptoms
First Degree AV Block
Prolonged PR interval 0.26 second
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HEART BLOCKS
Second degree AV Block
 In this condition, some impulse from atria to
ventricle fail to conduct, therefore, drop beat
occur.
 There are two types
1. Wenchebach’s Phenomenon or Mobitz
type I
2. Mobitz type II
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1. Wenckebach’s phenomenon
or Mobitz type I
Here PR interval progressively
increases, until P wave is not
followed by QRS (drop beat)
Wenchebach’s Phenomenon or Mobitz type I
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2. Mobitz type II – second degree AV block
Here PR interval remains constant but
some P wave are not conducted
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HEART BLOCKS
Third degree (complete) AV block
 There is no conduction taking place through
AV node, therefore atria and ventricle beat
independently

Atrial rate may be 80/min, ventricular rate
38/min
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AV BLOCK
Treatment
 For second and third degree AV block
 Atropine 0.6mg IV, repeated as necessary
 If it fails – temporary pacemaker
 Permanent pacemaker is indicated in
patients with chronic Mobitz type II second
degree heart block and third degree AV
block because of risk of asystole and
sudden death
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Thank you
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