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Electrocardiography
&
Cardiac Arrhythmias
Saeed Oraii MD, Cardiologist
Interventional Electrophysiologist
Tehran Arrhythmia Clinic
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notes. To view them you can right
click on the screen, choose ‘Screen’
and then ‘Speaker Notes’.
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ECG
A graphic recording of electrical potentials
generated by the heart
A noninvasive, inexpensive and highly
versatile test
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Normal Pathway of Electrical Conduction
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Cardiac Action Potential
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Cardiac action potentials from different
locations have different shapes
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Electrophysiology
• Electric currents that spread through the
heart are produced by three components
– Cardiac pacemaker cells
– Specialized conduction tissue
– The heart muscle
• ECG only records the depolarization and
repolarization potentials generated by atrial
and ventricular myocardium.
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Electrocardiograph 1903
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Normal Electrocardiogram
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ECG Waveforms
Labeled alphabetically beginning with the P wave
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QRS-T Cycle Corresponds to
Different Phases of Ventricular
Action Potential
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Limb Leads
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Precordial Leads
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Position of Precordial Electrodes
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Precordial Leads
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3-D Representation of Cardiac
Electrical Activity
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Timing Intervals
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Vector Concept
• Cardiac depolarization and repolarization
waves have direction and magnitude.
• They can, therefore, be represented by
vectors.
• ECG records the complex spatial and
temporal summation of electrical potentials
from multiple myocardial fibers conducted
to the surface of the body.
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Limb Leads Directions
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Vector Concept
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Ventricular
Depolarization
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QRS Axis
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Determination of QRS Axis
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Direction of Propagation
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Determination of QRS Axis
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Determination of QRS Axis
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Main Vector
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Normal QRS Axis
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Left Axis Deviation
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Right Axis Deviation
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Major ECG Abnormalities
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Right Atrial
Enlargement
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Left Atrial
Enlargement
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Left Ventricular Hypertrophy
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Right Ventricular Hypertrophy
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RVH, RA enlargement
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Left Bundle Branch Block
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Left Bundle Branch Block
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Right Bundle Branch Block
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RBBB
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RBBB, RAD (Bifascicular Block)
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RBBB, LAD (Bifascicular Block)
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Myocardial Ischemia
• ECG is the cornerstone in the diagnosis of
myocardial ischemia
• Findings depend on several factors:
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Nature of the process, reversible vs. irreversible
Duration, acute vs. chronic
Extent, transmural vs. subendocardial
Localization, anterior vs. inferoposterior
Other underlying abnormalities
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Acute Ischemia
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Myocardial Infarction
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Acute Pericarditis
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Metabolic Abnormalities
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Hyperkalemia
K 6.9
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Same
patient
K 3.9
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Hypothermia, Osborn Wave
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Hypothermia, Corrected
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Right Axis Deviation
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Superior P Wave Axis
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Normal Sinus Rhythm
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Anterior MI
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RBBB and Inferior MI
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LA Enlargement and Prolonged
PR Interval
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LBBB
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LA Enlargement and Prolonged
PR Interval
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Left Anterior Hemiblock
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LVH and LA Enlargement
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Anterior MI
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Old Inferior MI
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RA Enlargement
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RBBB, LAH, Prolonged PR
(Trifascicular Block)
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RBBB and Inferior MI
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Cardiac Arrhythmias
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Normal Pathway of Electrical Conduction
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Normal Sinus Rhythm
• Normal and constant P wave contours
• Normal P wave axis
• Rate between 60 and 100 bpm
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Normal Sinus Rhythm
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Anatomical Aspects of Normal
Sinus Node
• Located at the superior anterolateral portion
of right atrium near its border with the
superior vena cava
• It is an epicardial structure near sulcus
terminalis
• From endocardial approach the closest
approach is near the superior end of crista
terminalis
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Sinus Node Function
•
•
•
•
•
The dominant cardiac pacemaker
Highly responsive to autonomic influences
Decreasing rate with vagal stimulation
Increasing rate with sympathetic activity
Normal sinus rate under basal conditions is
60-100 bpm.
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Sinus Tachycardia
• Sinus rhythm exceeding 100 bpm in adults
• Usually between 100 and 180 bpm but may
be higher with extreme exertion
• Maximum heart arte decreases wit age from
near 200 bpm to less than 140 bpm
• Gradual onset and termination
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Sinus Tachycardia
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Sinus Tachycardia
Causes
• Common in infancy and childhood
• Normal response to a variety of physiological and
pathological stresses
–
–
–
–
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Exertion, anxiety
Hypovolemia, anemia
Fever
Congestive heart failure
Myocardial ischemia
Thyrotoxicosis
• Drugs
• Inflammation
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Sinus Bradycardia
• Sinus rhythm at a rate less than 60 bpm
• Can result from excessive vagal or
decreased sympathetic tone as well as
anatomic changes in sinus node
• Frequently occurs in healthy young adults,
particularly well-trained athletes
• Sinus arrhythmia often coexists
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Sinus Bradycardia
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Sinus Bradycardia
Causes
•
•
•
•
•
•
•
•
Hypothyroidism
Drugs
During vomiting or vasovagal syncope
Increased intracranial pressure
Hypoxia, hypothermia
Infections
Depression
Jaundice
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Sinus Arrhythmia
• Phasic variation in sinus cycle length
• Maximum minus minimum sinus cycle
length exceeds 120 msec.
• May be considered the most common form
of arrhythmia
• Respiratory form is a normal event
• Common in the young esp. with slower
heart rates or enhanced vagal tone
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Sinus Arrhythmia
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Wandering Pacemaker
• Passive transfer of dominant pacemaker
focus from sinus node to latent pacemakers
in other atrial sites or AV junctional tissue
• Occurs in a gradual fashion over the
duration of several beats
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Wandering Pacemaker
ECG
• A cyclical increase in RR interval
• A PR interval that gradually shortens to less
than 120 msec
• A change in P wave contour that becomes
negative in lead I or II or is lost within the
QRS
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Wandering Pacemaker
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Inappropriate Sinus Tachycardia
• Persistent sinus tachycardia at rest or with
minimal exertion
• Usually occurs in otherwise healthy people
• More common in health care personnel
• May result from a defect in either
sympathetic or vagal nerve control of sinus
node automaticity or an abnormality of
intrinsic heart rate
• Some cases may need radiofrequency
ablation of sinus node
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Sinus Node Dysfunction
Mechanisms
• A disease affecting a limited amount of
tissue at or near the sinus node causing
dysfunction of impulse formation or
propagation or recovery from overdrive
suppression
• A disease affecting the atria in general that
consequently affects the sinus node function
and also frequently generates atrial
arrhythmias
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Sinus Node Dysfunction
ECG Manifestations
•
•
•
•
•
Sinus bradycardia
Sinus pauses
Sinus arrest
Atrial asystole
Sinus exit block
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Sinus Pause
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Sinoatrial Exit Block
1st and 2nd degree
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Sinus Node Dysfunction
Etiology
• Most often in elderly as an isolated
phenomenon
• Drugs
• Infiltration of atrial myocardium
• Interruption of blood supply
• Hypothyroidism, advanced liver disease,
severe hypoxia, acidemia …
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High Vagal Tone
•
•
•
•
Usually in the young
Normal heart rate response during exercise
Normal intrinsic heart rate
Bradycardia may be severe enough to cause
syncope (especially in familial form)
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Sick Sinus Syndrome
• A combination of symptoms (dizziness,
fatigue, confusion, syncope and congestive
heart failure) caused by sinus node dysfunction
• Atrial tachyarrhythmias may accompany
sinus node dysfunction
<bradycardia-tachycardia syndrome>
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Sick Sinus Syndrome
Clinical Manifestations
• Predominantly seen in the elderly
• Most patients with sinus node dysfunction
are asymptomatic
• Two types of presentations
– Syncope or near-syncope
– Fatigue or worsening heart failure
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Sick Sinus Syndrome
Diagnosis
•
•
•
•
Holter monitor recordings
Intrinsic heart rate by autonomic blockade
Sinus node recovery time
Sinoatrial conduction time
The most important step is to correlate symptoms
with ECG findings.
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Normal SNRT
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Abnormal SNRT
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SA Block during Overdrive Pacing
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Sinus Arrest after Termination of AF
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Loop Recorder Showed Junctional
Rhythm during Syncope
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Sinus arrest with syncope
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Therapy for Sick Sinus Syndrome
• Based mostly on symptoms and any clinical
documentation of cardiac arrhythmia
associated with these symptoms
• Drug therapy is rather limited
• Most effective treatment is pacing therapy
• Anticoagulation in certain situation
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Heart Block
•
•
•
•
Disturbance of impulse conduction
Transient or permanent
Due to anatomical or functional impairment
Must be distinguished from interference, a
normal phenomenon that is a disturbance of
impulse conduction caused by physiological
refractoriness due to inexcitability from a
preceding impulse
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AV Conduction Disturbances
Clinical Significance
• Heart block may be asymptomatic or lead to
syncope or cardiac arrest
• Clinical significance of conduction
abnormalities depend on:
– The site of disturbance
– The risk of progression to complete block
– The probability that a subsidiary escape rhythm
distal to the site of block develops and is stable
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AV Block
Types
• First degree AV block
• Second degree AV block
– Mobitz type I (Wenckebach)
– Mobitz type II
• Third degree block (Complete heart block)
• High degree (advanced) AV block
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First Degree AV Block
• Conduction time is prolonged but
all impulses are conducted.
• PR interval exceeds 0.2 sec in
adults
• Site of conduction delay may be
in the AV node (most
commonly), in the His-Purkinje
system or both.
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First Degree AV Block
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Second Degree AV Block
• Block of some atrial impulses at a time
when physiological interference is not
involved
• Non-conducted P waves can be infrequent
or frequent, at regular or irregular intervals,
and can be preceded by fixed or lengthening
PR intervals.
• The association of P with QRS is not
random.
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Mobitz Type I Second Degree AV
Block
• Also called Wenckebach block
• Typical type characterized by progressive
PR prolongation culminating in a nonconducted P wave
• Narrow QRS in most cases
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WB
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Wenckebach Block
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Wenckebach Block
• Atypical pattern in over half the cases
• The site of block is almost always in the AV
node.
• Generally benign and does not advance to
more advanced AV block
• Can occur in normal children and welltrained athletes
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Mobitz Type II Second Degree
AV Block
• PR interval remains constant prior to the
blocked P wave
• Commonly associated with bundle branch
blocks
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Mobitz Type II Second Degree
AV Block
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Mobitz Type II Second Degree
AV Block
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Mobitz Type II Second Degree
AV Block
• Site of block His-Purkinje system in most
case
• Often antedates the development of AdamsStokes syncope and complete AV block
• Never observed in normal people
• An indication for implantation of permanent
pacemaker even in asymptomatic cases
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2:1 AV Block
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2:1 AV Block
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2:1 AV block
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Complete AV block
• No atrial activity conducts to the ventricles
• AV dissociation is present. The atria and
ventricles are controlled by independent
pacemakers.
• Ventricular focus is usually located just
below the site of block.
• Higher sites are more stable with a more
faster escape rate.
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Complete AV block
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Complete AV block
Isorhythmic AV Dissociation
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Advanced AV block
Block in two or more consecutive P waves
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AV Conduction Disturbances
Etiology
• Degenerative diseases are the most common
causes
• A variety of other diseases may be
responsible: myocardial infarction, drugs,
acute infections, infiltrative diseases,
neoplasms, etc.
• Hypervagotonia
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Investigation of the
Site of AV
Conduction
Disease by
Electrophysiologic
Study (EPS)
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Cardiac Pacemakers
• The treatment of symptomatic
bradyarrhythmias is implantation of cardiac
pacemakers.
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Cardiac Pacing
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First Implanted Pacemaker
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Common Uses for Permanent
Pacemaker Therapy
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AV Block With Carotid Massage
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Long Asystole
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Sinus Pause
and
Junctional
Escape
Beats
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Sinus Pause
and Junctional Escape Beats
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BradycardiaTachycardia
Syndrome
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Mobitz Type I (Wenckebach)
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2:1 AV block
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Complete Heart Block
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Sinus Pause
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Sinus Arrhythmia
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Sinus Tachycardia
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Wandering Pacemaker
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Sinus Tachycardia
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Wandering Pacemaker
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Asystole and Junctional Escape
Rhythm
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Tachyarrhythmias
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Tachyarrhythmias
Mechanisms
Automaticity
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Tachyarrhythmias
Mechanisms
Triggered activity
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Tachyarrhythmias
Mechanisms
Reentry
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Premature
Complexes
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Ventricular Premature Complexes
Compensatory
Pause
Interpolated VPC
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Premature Complexes
• The most common arrhythmias
• Detected during 24h Holter monitoring in
over 60% of adults
• May cause palpitations or be asymptomatic
• May trigger more serious tachyarrhythmias
• May be associated with a normal heart or a
variety of cardiac disturbances
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Variability of Ventricular Ectopy with Age
• Effect of age on
probability (%) of
having more than a
given number of
PVCs per 24 hours
in subjects with
normal hearts.
60%
50%
> 0 PVCs
> 50 PVCs
> 100 PVCs
40%
30%
20%
10%
0%
10-29 30-39 40-49 50-59 60-69
Data from Kostis JB. Circulation.
1981;63(6):1353.
Age
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Ventricular Premature Complexes
• Without heart disease, PVCs have not been
shown to be associated with any increased
incidence in morbidity or mortality
• In the presence of underlying disease
(ischemia, heart failure …) they may add to
the risk of the disease. No treatment is,
however, shown to definitely decrease this
increased risk.
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Atrial Fibrillation
•
•
•
•
•
The most common sustained arrhythmia
Incidence increases progressively with age.
Prevalence: 0.4% of overall population
Mortality rate double that of control
AF is characterized by disorganized atrial
activity without discrete P waves
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Atrial
Fibrillation
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Atrial Fibrillation
• Undulating baseline or atrial deflections of
varying amplitude and frequency ranging
from 350 to 600 bpm.
• Irregularly irregular ventricular response.
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Atrial Fibrillation
• Morbidity related to:
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–
–
–
–
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Excessive ventricular rate
Pause following cessation of AF
Systemic embolization
Loss of atrial kick
Anxiety secondary to palpitations
Irregular ventricular rate
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Atrial Fibrillation
• Persistent AF usually in patients with
cardiovascular disease
– Valvular heart disease
– Hypertensive heart disease
– Congenital heart disease
• Paroxysmal AF may occur with acute hypoxia,
hypercapnia or metabolic or hemodynamic
derangements
• Normal people with emotional stress or surgery or
acute alcoholic intoxication
• Lone AF
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Atrial Fibrillation
• Therapeutic Goals:
– Control of ventricular rate
– Restoration and maintenance of sinus rhythm
– Prevention of thromboembolism
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Atrial Flutter
• Regular atrial tachyarrhythmia with atrial
rate between 250-350 bpm.
• Flutter waves are seen as saw-tooth like
atrial activity
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Atrial Flutter
• Atrial Flutter is a form of atrial reentry
localized to right atrium.
• Typically the ventricular rate is half the
atrial rate, but the ventricular response may
be 4:1, 2:1, 1:1 etc.
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Atrial Flutter Circuit
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Atrial Flutter
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Atrial Flutter
• Most often in patients with organic heart
disease
• Usually less long-lived than AF and may
convert to AF.
• Control of ventricular rate is difficult in
atrial flutter
• The most effective treatment is DC
cardioversion
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Paroxysmal Supraventricular
Tachycardia (PSVT)
• Usually at a rate of 150-250 bpm
• No organic heart disease in the majority
• Presentations
– Palpitations
– Chest discomfort,dyspnea, lightheadedness
– Frank syncope
– SCD
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PSVT
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PSVT
Mechanism
• Reentry in the vast majority
• Reentry may be localized to sinus node,
atrium, AV junction or a macroreentrant
circuit involving a bypass tract (WPW)
• In the absence of WPW, more than 90% are
due to reentry through AV node or a
concealed bypass tract
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AV Nodal Reentrant Tachycardia
(AVNRT)
• The most common form of paroxysmal
supraventricular tachycardia (about 70%)
• More common in women (66%)
• Usually a regular narrow QRS complex
tachycardia
• No P wave is usually evident during the
tachycardia. Retrograde P waves may
occasionally be seen at the end of QRS.
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Longitudinal Dissociation Within
AV Node
Atrium
Slow
Pathway
Fast
Pathway
His Bundle
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AVNRT
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AVNRT
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Preexcitation
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Wolff-Parkinson-White Syndrome
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AV Reentrant Tachycardia
(AVRT)
• Incorporates a bypass tract as part of the
tachycardia circuit.
• Surface ECG:
– Manifest with short PR interval and delta wave
(preexcitation)
– Concealed with normal ECG
• Prevalence of ECG pattern: 0.1% to 0.3%.
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AVRT
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Concealed Accessory Pathway
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PSVT
Treatment
• Vagal maneuvers particularly carotid sinus
massage
• AV nodal blocking drugs
–
–
–
–
Adenosine
Verapamil
Propranolol
Digoxin
• DC cardioversion if hypotensive
• Radiofrequency ablation
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Electrophysiologic Study (EPS)
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Catheter Positions at Fluoroscopy
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Intracardiac Recordings
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Radiofrequency Ablation (RFA)
Through
femoral vein
and right
atrium
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Loss of Delta during RF Burn
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Loss of Delta during Burn
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Ventricular Arrhythmias
Definitions
• Premature Ventricular beats
– Single beats
– Ventricular Bigeminy, the appearance of one PVC after each sinus
beat
– Couplets, two consecutive premature beats
– Triplets, three consecutive premature beats
– Salvos, runs of 3-10 premature beats
• Accelerated Idioventricular Rhythm (Slow VT), rate 60100 bpm
• Ventricular Tachycardia (VT), rate over 100 bpm
• Ventricular Flutter, regular large oscillations at a rate of
150-300 bpm
• Ventricular Fibrillation (VF), irregular undulations of
varying contour and amplitude
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Ventricular Tachycardia
Classification
• Duration
– Sustained VT defined as VT that persists for than 30 s
or requires termination because of hemodynamic
collapse
– Nonsustained VT, 3 beats to 30 s
• Morphology
– Monomorphic
– Polymorphic
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Salvos
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Sustained Monomorphic VT
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Sustained Polymorphic VT
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VT, Holter Recording
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VT
Presentations
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VT Etiology
• VT generally accompanies some form of
structural heart disease most commonly:
– Ischemic heart disease
– Cardiomyopathies
• Primary electrical abnormalities
– Long QT syndromes
– Brugada syndrome
• Idiopathic VT
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Electrocardiographic Differentiation of
VT vs. SVT with Aberrancy
•
•
•
•
•
•
Clinical history
AV dissociation
QRS morphology
QRS axis
Fusion beat
Capture beat
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A-V Dissociation, Fusion, and
Capture Beats in VT
V1
E
ECTOPY
F
C
FUSION
CAPTURE
Fisch C. Electrocardiography of Arrhythmias. 1990;134.
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Fusion and Capture Beats in VT
F
C
C
C
C
Fisch C. Electrocardiography of Arrhythmias. 1990;135.
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VT
Prognosis
• Depends on the underlying disease state
– 75% first year mortality in the first few weeks
after MI
– Poor prognosis in patients with left ventricular
dysfunction
– No increased risk in those with idiopathic VT
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Ventricular Fibrillation
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Sudden Death Syndrome
• Incidence
– 400,000 - 500,000/year in U.S.
– Only 2% - 15% reach the
hospital
– Half of these die before
discharge
• High recurrence rate
Tehran Arrhythmia Center
Underlying Arrhythmia of Sudden
Death
Primary
VF
8% Torsades
de Pointes
13%
VT
62%
Bradycardia
17%
Adapted from Bayés de Luna A. Am Heart J. 1989;117:151-159.
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Snapshot of Death
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Return of Life
Not the usual case !
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Clinical Substrates Associated with
VF Arrest
•
•
•
•
•
•
Coronary artery disease
Idiopathic cardiomyopathy
Hypertrophic cardiomyopathy
Long QT syndrome
RV dysplasia
Rarely: WPW syndrome
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VT/VF
Therapeutic Options
•
•
•
•
Antiarrhythmic drugs
Anti-tachycardia pacing
Radiofrequency ablation
Implantable defibrillators
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Earliest
Defibrillator
in Clinical
Use, 1899
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First Implantable Defibrillator
1970
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Thoracotomy
Lead System,
the technique
used at the
beginning
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Nonthoracotomy Lead System
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Pectoral Implantation
The Current Technique
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Tiered Therapy Defibrillators
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Defibrillator Function
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Interrogated ICD Event
VT, treated appropriately by burst pacing therapy
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Interrogated ICD Event
VT (CL 320ms), no response to burst pacing
therapy
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Interrogated ICD Event
VT (CL 320ms), cardioverted by DC shock
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Clinical Uses of Defibrillator
Therapy
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Congenital Long QT Syndrome
A Frequently Missed Diagnosis
Long QT Interval
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Long QT Interval
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Long QT Interval
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Clinical Manifestations
• Long QT syndrome is characterized by the
presence of a long QT interval (usually over 440
ms) and emergence of ventricular arrhythmias.
• The presenting arrhythmia is a polymorphic
ventricular tachycardia called ‘Torsade de
Pointes’.
• Patient present with recurrent syncope or sudden
cardiac death.
• Early diagnosis by ‘looking at ECG’ is critical!
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Torsade de Pointes
• Prolonged QT interval associated with a
polymorphic VT characterized by QRS
complexes that change in amplitude and
cycle length, giving the appearance of
oscillations around the baseline
• Congenital or acquired
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Brugada Syndrome
Definition
• Clinical-electrocardiographic diagnosis
based on:
- High incidence of sudden cardiac
death
- Structurally normal heart
- Characteristic ECG pattern
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ECG Abnormalities
• ST segment
elevation in V1-V3
• QRS complex
resembling RBBB
• J-point elevation
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Brugada ECG Pattern
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Brugada ECG Pattern
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History
• First time in 1986: a 3-year polish boy
• First presentation at NASPE meeting in
1991
• First paper by Pedro and Josep Brugada in
1992
• In the Philippines as “ bangungut”
• In Japan as “Pokkuri”
• In Thailand as “ Lai tai”, SUDS Circ. 1997
• Thai men correlated to Brugada, SUNDS
Hum. Mol. Gen. 2002
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Brugada Syndrome
 Prevalence in men (8:1 ratio males: females)
 Familial incidence (autosomal dominant with incomplete
penetrance ranging between 5 and 66 per 10 000)
 True prevalence is difficult to estimate as the ECG pattern is
often concealed.
 It is endemic in Southeast Asia including: Thailand, Japan,
Laos, Cambodia, Vietnam, the Philippines, and China.
 Appearance of arrhythmic events at an average age of 40
years
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Clinical Manifestations
 Sudden cardiac death
 Syncope, seizure, agonal respiration,
 Episodes at night during sleep with labored
respiration, agitation, loss of urinary control,
recent memory loss
 Most commonly occurs during sleep, in particular
during the early morning hours
 Early diagnosis is of utmost importance
 The only treatment is currently implantation of an
‘Implantable Cardioverter Defibrillator’.
Tehran Arrhythmia Center
Tehran Arrhythmia Center
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