ARRHYTHMIA

S
MBCHB VI EU

DR D M
KILLINGO

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 THE BASICS – KNOW THE NORMAL
CARDIAC ELECTRICAL CONDUCTION
FIRST!

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3 07/11/20 03:10
 Normal Sinus Rhythm (NSR)

• Etiology: the electrical impulse is formed in the

SA node and conducted normally.
• This is the normal rhythm of the heart
• Other rhythms that do not conduct via the typical
pathway can be termed as arrhythmias.

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 NSR Parameters

• Rate 60 - 100 bpm

• Regularity Regular
• P waves Normal
• PR interval 0.12 - 0.20 s
• QRS duration 0.04 - 0.12 s
Any deviation from above is sinus tachycardia, sinus
bradycardia or an arrhythmia

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 Normal ECG Wave

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 Normal ECG
By convention, electrical pulses conducted
toward the ECG lead are positive those
conducted away are negative

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 The P wave
 Represents atrial
depolarization
 Duration is measure of time
required for depolarization to
spread through the atria to
the AV node
 Is usually upright in I, II, and
aVF
 Negative in aVR variable in
III, aVL

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 The PR interval
 Represents time required
for a supraventricular
impulse to depolarize the
atria, traverse the AV
node, and enter the
ventricle
 Normal is 0.12 to 0.20
seconds, greater than
0.20 is considered first
degree AV block

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 The QRS complex
Represents ventricular
depolarization
Q wave – first negative
deflection
R wave – first positive
deflection after a P wave
S wave – negative
deflection following an R
wave
Normal is between 0.06 and
0.12 sec
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 The ST segment
 The isoelectric segment
following depolarization and
preceding ventricular
repolarization
 From the end repolarization of
the QRS to the beginning of the
T wave
 In contrast to PR and QRS
intervals, the ST segment
length can be variable
 Elevation or depression of the
ST segment by 0.1 mV from
the baseline is abnormal

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 The T wave
Represents ventricular repolarization
T wave vector normally “tracks” with the QRS vector.
If QRS is predominantly negative an inverted T wave
is not necessarily abnormal

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 The QT interval
From the beginning of the QRS complex to the end of
the T wave
Represents electrical systole
Is usually <0.425 seconds duration when corrected for
heart rate (QTc = corrected QT interval)

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14 07/11/20 03:10
 ARRHYTHMIAS

 Definition: An arrhythmia is an abnormality or

disturbance in the rate or rhythm of the heartbeat.

Pathogenesis & Inducement of Arrhythmia

 Some physical condition
 Pathological heart disease
 Other systemic disease
 Electrolyte disturbance and acid-base imbalance
 Physical and chemical factors or toxicosis

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 Effect of electrolyte disturbance on cardiac rhythm
Hypocalcemia – prolonged QT interval, ST
segment, V Tach, Torsades
Hypercalcemia – shortened QT interval
Hypomagnesemia & Hypokalaemia– widened
QRS, prolonged PR, long QT, cardiac irritability
Hyperkalaemia: shortened QT interval, Widening
of the QRS complex, increase in the PR interval, and
bradycardia in the form of AV blocks occur as the
potassium level exceeds 7.0, Absence of the P waves and
eventually a "sine wave" pattern

16
07/11/20 03:10
 Arrhythmias: Site of origin
Arrhythmias can arise from problems in the sites:

• Sinus node Supraventricular

• Atrial cells
• AV junction

• Ventricular cells Ventricular

arrhythmias

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 Arrhythmias: classification
1.Broadly: Bradyrrhythmias & Tchyarrhythmias
2. Based on site of origin in conduction cycle
Sinus Rhythms
Premature Beats
Supraventricular Arrhythmias
Ventricular Arrhythmias
AV Junctional Blocks

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 SA Node pathology
The SA Node can:
fire too slow Sinus Bradycardia

fire too fast

Sinus Tachycardia

Sinus Tachycardia may be an appropriate

response to stress.
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 Sample Rhythm #1

• Rate? 30 bpm
• Regularity? regular
• P waves? normal
• PR interval? 0.12 s
• QRS duration? 0.10 s
Interpretation? Sinus Bradycardia
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 Sample Rhythm #2

• Rate? 130 bpm

• Regularity? regular
• P waves? normal
• PR interval? 0.16 s
• QRS duration? 0.08 s
Interpretation? Sinus Tachycardia
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 Atrial cell pathology (a)
Atrial cells can:
Fire occasionally Premature Atrial
from a focus Contractions
(PACs)
Fire continuously
due to a looping re-
entrant circuit Atrial Flutter

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 Premature Atrial Contractions

Etiology: Excitation of an atrial cell forms an

impulse that is then conducted normally
through the AV node and ventricles.
 These ectopic beats originate in the atria (but not in the SA
node), therefore the contour of the P wave, the PR interval,
and the timing are different than a normally generated
pulse from the SA node

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 Re-entrant pathway (AfL)
A re-entrant pathway
occurs when an impulse
loops and results in
self-perpetuating
impulse formation.

07/11/20 03:10 24
 Atrial cell pathogy (b)

Atrial cells can also:

• fire continuously from Multi-focal atrial
multiple foci or
tachycardia
•fire continuously due
to multiple micro re-
entrant “wavelets” Atrial Fibrillation

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 Atrial re-entrant wavelets (Afib)
Atrial tissue
•Multiple micro re-entrant
“wavelets” refers to
wandering small areas of
activation which generate
fine chaotic impulses.
• Colliding wavelets can,
in turn, generate new foci
of activation.

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 AV Junctional pathology

The AV junction can: Paroxysmal

fire continuously
Supraventricular
due to a looping re- Tachycardia
entrant circuit
block impulses
AV Junctional
coming from the SA Blocks
Node

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 Ventricular Cell Pathology

Ventricular cells can:

 fire occasionally from 1 Premature Ventricular
or more foci Contractions (PVCs)

 fire continuously due to

a looping re-entrant VentricularTachycardia
circuit

 fire continuously from

Ventricular Fibrillation
multiple foci

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 PVCs

Etiology: One or more ventricular cells are

depolarizing and the impulses are abnormally
conducting through the ventricles.

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 Sample Rhythm #3

• Rate? 75 bpm
• Regularity? Yes..but occasional irreg.(pvc)

• P waves? Normal (none for 7th QRS)

• PR interval? 0.14 s
• QRS duration? 0.08 s (but 7th wide)
30
•Interpretation?Sinus Rhythm with 107/11/20
PVC 03:10
 Take home message
When an impulse originates in a ventricle, conduction
through the ventricles will be inefficient and the QRS
will be wide and bizarre an
R wave and T wave always in opposite direction

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 Ventricular Conduction

Normal Abnormal
Signal moves rapidly through Signal moves slowly through
the ventricles =narrow the ventricles = wide bizzare
32complex QRS complex QRS complex 07/11/20 03:10
 Ventricular Tachycardia
  Rate Rhythm

Ventricular > 100 bpm Regular

Atrial None  

P-Wave Absent  

     

P-R Interval Absent  

> .10
QRS Complex  
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seconds 07/11/20 03:10
 Ventricular fibrillation

An electrocardiogram reflecting the irregular,

pulseless electrical activity of ventricular fibrillation

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 Arrhythmias of Clinical Importance

Tachyarrhythmias Bradyarrhythmias
Ventricular • Medication
Atrial • VT
AF
• AV block
A Flutter
• VF • SSS
Paroxs. SVT • Torsades
AVNRT
AVRT (WPW)
Multifocal atrial
tachycardia
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 Bradycardiarrythmias– Disturbances of
cardiac impulse conduction
Defined as HR less than 60 BPM
Occurs in heartblocks:
First degree AV heart block
Second degree
Mobitz I
Mobitz II
Unifasicular block
Rt bundle branch block
Lt bundle branch block
Third degree (trifascicular ) heart block

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 The wave of depolarization spreads normal ly from the
sinus node through the atria,
BUT upon reaching the AV node, it is held up for
longer than the usual time
- Asa result, the PR interval—the time between the start
of atrial depolarization and the start of ventricular
depolarization, a time period that encompasses the
delay at the AV node—is prolonged (>0.2 sec)

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 First degree AV block
Think of ischemia if it is a
new onset for the pt.
Can also be caused from
digitalis, aortic
regurgitation, increased
vagal tone
Usually asymptomatic
No Rx required

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 2nd degree AV block
Mobitz I (Wenckebach) progressive prolongtion of PR
until a beat is entirely blocked

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 Mobitz type I
Wenckebach block is almost always due to a block
within the AV node.
However, the electrical effects of Wenckebach block
are unique in that the block, or delay, is variable,
increasing with each ensuing impulse.
Each successive atrial impulse encounters a longer and
longer delay in the AV node until
one impulse (usually every third or fourth) fails to
make it through.

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 Mobitz type I

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 2nd degree AV block
Mobitz II
Sudden interruption of the conduction of an impulse
without prior prolongation of the PR

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 Mobitz type II
Mobitz type II block usual ly is due to a block below the
AV node in the His bundle.
It resembles Wenckebach block in that some, but not al l,
of the atrial impulses are transmitted to the ventricles.
 However, progressive lengthening of the PR interval does
not occur.
Instead, conduction is an all-or-nothing
phenomenon.

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 Mobitz type II

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 2nd degree AV block
Mobitz II
More serious than Mobitz I because it is more likely to
progress to complete heart block
More likely to require pacemaker

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 Third-Degree AV Block

The ultimate /complete Heart block (CHB)

No atrial impulses make it through to activate the
ventricles
The site of the block can be either at the AV node or
lower.
The ventricles respond to this dire situation by generating
an escape rhythm, usual ly an inadequate 30 to 45 beats
per minute (idioventricular escape).

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 CHB
The atria and ventricles continue to contract, but they
now do so at their own intrinsic rates, about 60 to100
beats per minute for the atria, and 30 to 45 beats per
minute for the ventricles.
In complete heart block, the atria and ventricles have
virtually nothing to do with each other, separated by
the absolute barrier of the complete conduction block.

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 CHB
Complete absence of conduction of impulse from atria
to ventricle
If block is proximal to AV node HR will be 45-55 BPM
If block is distal to AV node (infranodal) HR will be 30-
40 BPM with a wide QRS (ventricular in origin)
Can be caused by fibrotic degeneration, ischemia,
cardiomyopathy, ankylosing spondylitis, iatrogenic
(cardiac surgery), drugs, hyperkalemia
TX is pacing

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50 07/11/20 03:10
 CHB/ Third-degree AV block. The P waves appear at regular
intervals, as do the QRS complexes, but they have nothing to do
with one another. The QRS complexes are wide, implying a
ventricular origin.

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 Right bundle branch block (RBBB)
 Conduction block over the Right bundle branch which
is present in 1% of hospital patients
 May be seen in patients with pulmonary disease, ASD,
or increased Right ventricular pressures, PTE
 RBBB often clinically insignificant
 However look for and manage any significant
underlying disease

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 RBBB

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 RBBB
QRS complex
exceeds 0.1 second
Broad rSR complex
in V1 an V3

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 Left Bundle Branch Block (LBBB)

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 LBBB
Often associated with ischemic
heart disease, LVH/chronic HTN,
or valve disease
 LBBB may be a sign of MI

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 LBBB
QRS complex more
than 0.12 seconds
with wide notched R
waves in all leads

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 Bundle Branch Block and Repolarization
In both right and left bundle branch block, the
repolarization sequence is also affected.
In right bundle branch block, the right precordial leads will
show ST segment depression and T wave inversion, just
like the repolarization abnormalities that occur with
ventricular hypertrophy.
Similarly, in left bundle branch block, ST segment
depression and T wave inversion can be seen in the left
lateral leads

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 LBBB with repolarization abnormalities

ST segment depression and T wave inversion in lead V6 in a

patient with left bundle branch block.

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 Unifascicular block /Hemiblocks
 3 fascicles of the His-Perkinje system
 Right fascicle, Left anterior fascicle, Left posterior fascicle
 A block of one of the L fascicles can occur
 One of the L fascicles plus RBBB can lead to complete heart block

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 Left anterior hemi-block

Left anterior hemiblock ;Current flow down the left anterior fascicle is
blocked; hence, al l the current must pass down the posterior fascicle.
The resultant axis is redirected upward and leftward (left axis
deviation).
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 Left posterior hemiblock

Left posterior hemiblock. Current flow down the left posterior

fascicle is blocked; hence, al l the current must pass down the right
fascicle.anteriorly.The resultant axis is redirected downward and
rightward (right axis deviation).

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 Criteria for Hemiblock - Summary
 Hemi block is diagnosed by looking for left or right axis
deviation.
Left Anterior Hemi block
 1 Normal QRS duration and no ST segment or T wave changes
 2. Left axis deviation between -30° and -90°
 3. No other cause of left axis deviation is present.
Left Posterior Hemi block
 1. Normal QRS duration and no ST segment or T wave
changes
 2. Right axis deviation
 3. No other cause of right axis deviation is present.

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 Bifascicular Blocks ( either RBBB+LAF or LPF
Hemiblocks or LBB)

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 Bifascicular Blocks

This is an example of right bundle branch block combined with left anterior
hemiblock. Note the widened QRS complex and rabbit ears in leads V1 and
V2, characteristic of RBBB and the left axis deviation in the limb leads (the
QRS complex is predominantly positive in lead I and negative in lead AVF)
that suggests left anterior hemiblock
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 Causes of Bradycardia / Ddx
Hypovolemia,
Hypoxia,
Acidosis,,
 Hypothermia,
 Hyperkalemia,
Drug overdose e.g B-blockade
Tension pneumothorax,
 Increased ICP
Pesticide exposure,

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 Bradycardia ddx
Noxious surgical stimulation (ocular pressure,
scrotal/ovarian traction,
 Abdominal insufflation,
 Laryngoscopy,
 Pericardial Effusion,
Myocardial infarction,
carotid sinus stimulation,
 Narcotics,
Succinylcholine,
Sleep apnea,
Normal physiology of well-trained athlete,
Hypothyroidism .

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 Tachyarrhythmias

Heart rate greater than 100 BPM

Three key questions:
IS THE PATIENT STABLE?
Is the QRS narrow or wide?
Is the rhythm regular or irregular?

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 Tachycardia
Narrow complex Wide complex
Regular rhythm is Regular rhythm could
probably a reentrant be SVT with aberrant
tachycardia waveform or VT
Irregular rhythm is Irregular rhythm could
probably A fib or A be A fib with aberrant
flutter waveform, polymorphic
V tach, torsades

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 Narrow vs wide complex tachycardia

Narrow complex more likely from an atrial

origin
Aka SVT (supraventricular tachycardia)

Wide complex more likely from a ventricular

origin
VT more serious since the concern is that
the rhythm may degrade to V.Fib
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 Narrow complex tachycardia
i)Sinus Tachycardia
 Most common cause of tachycardia
 Rhythm originates from AV node in response to
stress
Hypovolemia
Pain
Fever
Exercise
Substance withdrawal
Agitation (in the ICU) . . . etc
 Treatment is to identify and treat the stressor (if
necessary)
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 Narrow complex tachycardia
ii)SupraVentricular Tachycardia (SVT)

 SVT can be loosely defined in 3 types

Atrial tachycardia-AV node passively conducts
impulse from atria to ventricles
A fib, A flutter, atrial tachycardia
Atrioventricular nodal reentrant tachycardia- re-
entrant focus is adjacent to AV node and AV node
propogates reentrant impulse
AV reentrant tachycardia-accessory pathway
bypasses the AV node e.g WPW, LGL, syndromes

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 Narrow complex (SVT) cont’d

Atrial tachycardia - ectopic atrial focus (outside the

atrial node) becomes irritable and can fire impulses
which override atrial rhythm.

 See P waves of different morphology

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 Narrow complex (SVT) cont’d

Atrial fibrillation with Rapid Ventricular Rate

Atrial depolarization rate is 400 –
600/minute
AV node acts as gatekeeper and only
conducts 100-180 of these depolarizations
each minute

Atrial Flutter - Atrial depolarization rate is

250-400/minute

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 Narrow complex tachycardia (SVT)

Atrial Fibrillation (AFib)

A flutter

Atrial flutter (AFL)

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76 07/11/20 03:10
 Narrow complex SVT
(A fib/A flutter)

Treatment
If patient is unstable tx is always cardioversion
50 J for A flutter, 100-200 for a fib
progressing to 200, 300, 360
For stable patients control rate with B blockers,
diltiazem, consider amiodorone for new onset

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 Narrow complex tachycardia (SVT)
(AVNRT & AVRT)

Reentry tachycardia requires

two pathways over which
impulses are conducted at
different velocities
Can originate adjacent to the
AV node
Pathway may completely
bypass AV node (giving rise
to WPW)

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 Narrow complex tachycardia (SVT)
(AVNRT & AVRT)
If the supraventricular tachycardia is due to AV node
reentry then it should be terminated by anything that
transiently blocks the AV node
Carotid massage
Valsalva
Adenosine
Definitive tx is ablation of the accessory pathway

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 Narrow complex tachycardia (SVT)
(AVNRT & AVRT)
Accessory pathway which bypasses AV node poses
risk for sudden cardiac death due to tachyarrhythmias
WPW syndrome on ECG has delta wave or slurred
deflection of beginning of QRS, QRS greater than 0.12
sec

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 Clinical manifestations
Will depend of type of arrhythmia and may
include:
 Palpitations
 Syncope
 If going fast enough, can precipitate cardiac
ischaemia and chest pain
 Cardiac failure
 Decreased level of consciousness
 Hypoperfusion of all organs
 Cardiac arrest

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 Management of arrhythmias

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 REMEMBER:
The response to a patient with dysrhythmia is
dependent on whether the patient is stable or
unstable for instance;
Bradycardia of 45 in an Olympic athlete is
acceptable for a BP of 120/80 but not for 60/40 !
A heart rate of 130 is NORMAL in an infant but
could cause an MI for a 78 year old hypertensive,
diabetic, smoker.

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 Management of unstable patients with
arrhythmias:

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86 07/11/20 03:10
 Anti-arrhythmia Agents
Anti-tachycardia agents
 E.g B-blockers, calcium channel
blockers, other anti-arrhythmic drugs
Anti-bradycardia agents
Isoprenaline
Epinephrine
Atropine
Aminophylline

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 Anti-tachycardia/anti-arrhythmic agents
 Modified Vaugham Williams classification
1. I class: Natrium channel blocker
2. II class: ß-receptor blocker
3. III class: Potassium channel blocker
4. IV class: Calcium channel blocker
5. Others: Adenosine, Digital

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 NOTE:
Prompt and appropriate management of
predisposing conditions such as
electrolyte disturbance may be all that is
required for the particular arrhythmia.

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 NON- PHARMACOLOGIC THERAPY
FOR ARRHYTHMIAS

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 Pacemakers
For patients with high degree SA/AVN
conduction abnormality
For patients with a high risk or personal
history of ventricular fibrillation

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 Cardioversion: For tachycardia
especially hemodynamic unstable
patient

Radiofrequency catheter ablation

(RFCA): For those tachycardia patients
(SVT, VT, AF, AFL)

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 ICD (implantable/internal cardiac
defibrillator)

For patients with a high risk or personal

history of ventricular fibrillation
Device delivers a defibrillating shock if V tach
or V fib is sensed.

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 SURGICAL Management of arrhythmias

Include MAZE procedure for A Fib and

surgery for congenital heart disease such as
ASD closure.

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