Bradyarrhythmias

Risalina Myrtha
Department of Cardiology and Vascular Medicine
Faculty of Medicine, Universitas Sebelas Maret/ RSUD Dr. Moewardi

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 Physiologic
phenomenon

A bradycardia is a heart
Cardiac
rate of <60 beats/min causes

Non cardiac
causes

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 Introduction

Meek S and Morris F, 2003, ABC of Clinical Electrocardiography 3

 Typical Symptoms of Bradycardia
Persistent bradycardia Intermittent bradycardia
Due to cerebral Perfusion
Easy fatiguability Syncope, pre-syncope
Irritability, lassitude, inability to Dizziness, vertigo
concentrate
Apathy, forgetfulness, cognitive Light-headedness, blurred vision
impairment
Dizziness, vertigo
Due to other mechanisms
Shortness of breath, heart failure Sudden dyspnoe and chest pain
unrelated to exercise
Reduced exercise capacity Palpitation (irreguler beats)
(chronotropic incompetence)

2013 ESC guidelines on cardiac pacing and CRT 4

Sinus Node Dysfunction

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 SND
secondary to a
pathological condition
Intrinsic involving the sinus node
proper

Causes of SND

caused by depression of
sinus node function by
Extrinsic external factors such as
drugs or autonomic
influences

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 • Inappropriate Sinus bradycardia
• Sinus pauses or sinus arrest
ECG Features
• Sinoatrial exit block
• Tachycardia-bradycardia syndrome
• Chronotropic incompetence

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 Sinus Bradycardia
The electrocardiogram shows a P wave before every QRS complex, with a normal P wave
axis (that is, upright P wave in lead II). The PR interval is at least 0.12 s. Sinus rate <60 bpm

Sinus bradycardia (less than 60 beats/min) is considered abnormal when it is persistent,

unexplained,and inappropriate for physiological circumstances.

Sinus bradycardia slower than 40 beats/min (not associated with sleep or physical
conditioning) is generally considered abnormal

The sinus bradycardia is inappropriate when it is unusually slow, is persistent, and does
not increase sufficiently with exercise

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 • the sinus node continues to discharge at
regular intervals, but some impulses are
SA Exit blocked and are unable to reach the
surrounding atria.
Block

Complete absence of an entire P-QRS-T complex

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 First Degree SA Exit Block
First degree SA exit block is manifested by an increased time for the impulse generated by
the SA node to reach and cause contraction of the atrial myocardium.

Because SA node depolarization produces no deflection on the surface ECG, these blocks can be
diagnosed only by specialized sinus node recordings. Thus, the ECG demonstrates normal sinus
rhythm

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 Second degree SA Exit Block
Intermittent failure of the sinus impulse to exit the sinus node with Wenckebach
periodicity of the P wave

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 Third degree SA Exit Block

Absence of P waves owing to failure of the sinus impulse to conduct to the atrium

Long pauses resulting in lower pacemaker escape rhythm.It cannot be differentiated

from sinus arrest on a 12-lead ECG. The ECG records only the escape rhythm.

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 Sinus Arrest/ Pause
The terms sinus arrest and sinus pause are often used interchangeably. In sinus arrest,
the sinus node is unable to generate impulses regularly

x x x x *

The pause is not an exact multiple of the preceding P-P interval but is random in
duration

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 vs SA Exit Block
Sinus Arrest/Pause vs

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 Tachycardia-Bradycardia Syndrome
Tachycardia-bradycardia syndrome, frequently referred to as sick sinus syndrome, is a common
manifestation of SND, and it refers to the presence of intermittent sinus or junctional
bradycardia alternating with atrial tachyarrhythmias

Tachycardia Bradycardia

Tachycardia – bradycardia syndrome

• Common in sick sinus syndrome
• Characterized by bursts of atrial tachycardia interspersed with periods of bradycardia
• Paroxysmal atrial flutter or fibrillation may also occur, and cardioversion may be followed by
a severe bradycardia

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 Tachycardia-Bradycardia Syndrome

Tachycardia Bradycardia

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 Chronotropic Incompetence

an abnormally slow heart rate response to exercise manifesting as a less than normal increase in
the sinus rate at each stage of exercise, with a plateau at less than 70% to 75% of the age-
predicted maximum heart rate (220 − age) or an inability to achieve a sinus rate of 100 to 120
beats/min at maximum effort.
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Atrioventricular (AV) Block

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 First degree AV
Block

Mobitz type I
AV Second degree
Mobitz type II
Block AV Block
Advanced/ high
grade

Third degree AV
Block

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 First Degree AV Block

PR interval longer than 200 milliseconds following a normally timed (nonpremature)

P wave. All P waves are conducted, but with delay; each P wave is followed by a QRS complex
with a constant, prolonged PR interval

Shade, 2008; Issa ZF, Miller JM., Zipes DP, 2012 20

 Second Degree AV Block

intermittent failure of AV conduction is present (i.e., one or more atrial

impulses that should be conducted fail to reach the ventricles)

Type 1 Type 2

Issa ZF, Miller JM., Zipes DP, 2012 21

 Second Degree AV Block Type I (Mobitz Type 1)

Progressive prolongation of the PR interval before failure of an atrial impulse to conduct to the
ventricles. The PR interval immediately after the nonconducted P wave returns to its baseline
value, and the sequence begins again

Shade, 2008; Issa ZF, Miller JM., Zipes DP, 2012 22

 Second Degree AV Block Type II (Mobitz Type 2)

a constant (normal or prolonged) PR interval of all conducted P waves, followed by

sudden failure of a P wave to be conducted to the ventricles

Shade, 2008; Issa ZF, Miller JM., Zipes DP, 2012 23

 Advanced 2:1 second Degree AV Block

2:1 AV block is an example of advanced second-degree AV block. In 2:1 block, every other
P wave is conducted alternating with every other P wave that is blocked. The QRS
complexes may be narrow or wide
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Advanced 2nd degree AV Block 3:1 and higher

The conduction ratio refers to the number of P waves that are blocked before a P wave is
conducted. Thus, a 3:1 conduction ratio implies that of three consecutive P waves, only
one is conducted
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 Third Degree AV Block

there is complete failure of conduction between the atria and ventricles, with
complete independence of atrial and ventricular contractions. The P waves bear no
relation to the QRS complexes and usually proceed at a faster rate.

Shade, 2008; Meek S and Morris F, 2003. 26

 Third Degree AV Block

Complete AV Block with narrow QRS complex

Shade, 2008; Meek S and Morris F, 2003. 27

 Third Degree AV Block

Complete AV Block with wide QRS complex

Shade, 2008; Meek S and Morris F, 2003. 28

Localizing AV Block

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Comparison of AV Block Localization

AV Nodal Infra-nodal
PR prolongs prior to block Sudden block without PR
prolongation
Escape rate 40-60 bpm Escape rate <40 bpm
QRS <120 ms QRS >120 ms
Stable hemodynamically Often unstable
hemodynamically
Responds to atropine Poor response to atropine

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 Intraventricular Conduction Defect
Types Examples
Unifascicular block Left anterior fascicular block (LAFB)
Left posterior fascicular block (LPFB)
Right bundle branch block (RBBB)
Bifascicular block Left bundle branch block (LBBB)
RBBB+LAFB
RBBB+LPFB
Trifascicular block Definite Alternating BBB
RBBB + alternating fascicular block
RBBB + Mobitz type II second degree AVB
Possible Complete AV block with ventricular escape
rhythm
Any bifascicular block with first or second
degree AVB

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 Right Bundle Branch Block

Right bundle branch block, showing the

wave of depolarisation spreading to the
right ventricle through non-specialised
conducting tissue

Meek S and Morris F, 2003, ABC of Clinical Electrocardiography 32

 Right Bundle Branch Block
Diagnostic criteria of RBBB
• QRS duration >0.12 s
• A secondary R wave (R’) in V1 or V2
• Wide slurred S wave in leads I, V5,
and V6
Associated feature
• ST segment depression and T wave
inversion in the right precordial
leads

Meek S and Morris F, 2003, ABC of Clinical Electrocardiography 33

RBBB + Anterior STEMI

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 Left Bundle Branch Block

Left bundle branch block is most

commonly caused by coronary artery
disease, hypertensive heart disease, or
dilated cardiomyopathy. It is unusual
for left bundle branch block to exist in
the absence of organic disease.

Meek S and Morris F, 2003, ABC of Clinical Electrocardiography 35

 Left Bundle Branch Block
Diagnostic criteria of LBBB
• QRS duration >0.12 s
• Broad monophasic R wave in leads 1, V5, and V6
• Absence of Q waves in leads V5 and V6

Associated feature
• Displacement of ST segment and T wave in an
opposite direction to the dominant deflection of
the QRS complex (appropriate discordance)
• Poor R wave progression in the chest leads
• RS complex, rather than monophasic complex, in
leads V5 and V6
• Left axis deviation—common but not invariable
finding

Meek S and Morris F, 2003, ABC of Clinical Electrocardiography 36

Sgarbossa Criteria
• Concordant ST
elevation > 1mm in leads
with a positive QRS
complex (score 5)
• Concordant ST
depression > 1 mm in
V1-V3 (score 3)
• Excessively discordant ST
elevation > 5 mm in
leads with a -ve QRS
complex (score 2).

A total score of ≥ 3 is
reported to have a
specificity of 90% for
diagnosing myocardial
infarction.

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 Sgarbossa Criteria
2

5
3

A total score of ≥ 3 is reported to have a specificity of 90% for diagnosing

myocardial infarction. 38
 Left Anterior Fascicular Block
LAFB occurs when the sinus impulse is delayed or interrupted within the left anterior
fascicle.

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Inferior Myocardial Infarction

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 Left Posterior Fascicular Block
LPFB occurs when conduction across the left posterior fascicle is delayed or interrupted.
It is the least common among all intraventricular conduction abnormalities.

The hallmark of LPFB is a shift in the electrical axis of the QRS complex to the right of
90o.
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Right ventricular hypertrophy

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 Bifascicular Block
Right Bundle Branch Block + Left Anterior Fascicular Block

Right bundle branch block is recognized by the presence of wide QRS complexes measuring 0.12
seconds with rR or rsR in V1 and wide S waves in V6. Left anterior fascicular block is diagnosed
by the presence of left axis deviation of –600 in the frontal leads.
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 Bifascicular Block
Right Bundle Branch Block + Left Posterior Fascicular Block

There is right bundle branch block with rR pattern in V1 and RS in V6. Left posterior fascicular
block is diagnosed by the presence of right axis deviation of 1200 in the frontal plane.

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 Trifascicular Block
Left Bundle Branch Block + Mobitz type II Second Degree AV Block

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 Trifascicular Block
RBBB + LPFB + 2:1 Second degree AV Block

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 Assess appropriateness for clinical condition.
HR typically <50 bpm if bradyarrythmia

Identify and treat underlying cause

•Maintain patent airway; assist breathing as necessary
•Oxygen (if hypoxemic)
•Cardiac monitor to identify rhythm; monitor BP and oximetry
•IV access
•12-lead ECG if available; don’t delay therapy

Persistent bradyarrhythmia causing

NO •Hypotension?
Monitor and •Acutely altered mental status?
observe •Signs of shock?
•Ischemic chest discomfort?
•Acute Heart failure

YES

Atropin iv dose (first dose: 0,5 mg bolus, repeat every 3-5 minutes,
maximum 3 mg)

If atropin ineffective:
Transcutaneous pacing OR
Dopamin iv infusion: 2-10 mcg/kg/min OR
Epinephrine IV infusion 2-10 mcg per min

Consider:
Expert consultation
Transvenous pacing 47
• References:
– Baltazar RF., 2009. Basic and bedside electrocardiography
– Morris F, Edhouse J, Brady WJ, Camm J, 2003. ABC of Clinical
Electrocardiography
– Mithilesh KD., Zipes DP., 2012. Electrocardiography of Arrhythmias: A
Comprehensive Review
– ESC, 2013. Guideline on Cardiac Pacing and CRT

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