Bradyarrhythmia and

Atrioventricular Conduction
Disturbances
Agus Harsoyo, MD
Cardiovascular Intervensional and Clinical Cardiac
Electrophysiology Intervensional

Department of Cardiology
Gatot Soebroto Army Center Hopital
Jakarta
2012

Why Are Arrhythmias

Important?
Symptoms span palpitations, lightheadedness,
syncope (fainting) and cardiac arrest
May be the first manifestation of heart disease
May precipitate or exacerbate heart failure or
ischemia
Some
arrhythmias
can
predispose
to
intracardiac clot formation and embolic events
(stroke, myocardial infarction, peripheral
emboli)

EKG Assessment of
Arrhythmias
Is the rate slow (< 60 beats/min [>
5 big boxes])?
Is the rate fast (>100 beats/min [<
3 big boxes])?
What drives the P waves?
What drives the QRS complexes?
What is the relationship between Ps
and QRSs?

Sites of Disturbances in Impulse Formation

or Conduction Leading to Bradyarrhythmias
SA Node

AV Node
His-Purkinje
System

Components of Atrioventricular (AV) Conduction

HisPurkinje
System

Intraventricular
Conduction Disturbances

Intraventricular (His-Purkinje) Conduction System

(AV node)
His bundle
Right bundle branch

Left bundle branch

Septal fascicle
Left anterior fascicle

Left posterior
fascicle

Rule for QRS Width:

Any electrophysiologic process that engenders
a departure from synchronous activation
of the ventricles tends to widen the QRS

QRS Width: Synchronous vs. Asynchronous

Ventricular Activation
QRS
Normal synchronous
overlapping activation
of both ventricles:
On
time
Asynchronous
scenario I:

Head start
Asynchronous
scenario II:

Narrow

Late
Wide
On
time
(or late)
Wide

Generation of Narrow QRS Complex

( .10 sec [2.5 little boxes])
Horizontal
plane with
precordial
leads:

RV

LV

Intact Purkinje system

assures synchronous,
overlapping activation
of right ventricle (RV)
and left ventricle (LV)

Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

Late right ventricular

activation, with slow
muscle-to-muscle
conduction

RV is activated
via the left bundle

QRS Distortion Induced by RBBB

rSR
pattern

Initial QRS
inscription is
normal due to
normal LV activation

Broad
S wave

Note terminal rightward

delay with QRS widening
( .12 sec [3 little boxes],
with complete RBBB)

Complete RBBB Pattern

V1

rsR
complex

V6
Broad
S wave
(Lead I
similar)

Note T wave pointing in direction opposite to

late rightward component (2 repolarization effect)

Left Bundle Branch Block (LBBB)

Delayed left ventricular

activation, with slow
muscle-to-muscle
conduction

LV is activated
via the right bundle

QRS Distortion Induced by LBBB

Broad
monophasic
R wave

Broad
S wave

Entire QRS dominated by

marked leftward delay
and is wide ( .12 sec
[3 little boxes], with
complete LBBB)

Complete LBBB Pattern

V1

Broad
S wave

V6
Broad
R wave
(Lead I
similar)

Note absence of septal-q in V6; andT wave pointing

in direction opposite to QRS (2 repolarization effect)

Fascicular Blocks

Mean QRS Axis Quadrants in the Frontal Plane

()
Lead I
()

(+)

Lead AVF

(+)

Frontal Plane Mean QRS Axis Designatio

r S in Lead II
for Left Axis
Deviation

AVF

Left Anterior Fascicular (/Hemi-) Block (LAFB)

LV is activated via the
left posterior fascicle

1) Initial QRS forces

directed inferiorly
to the right
Left Axis
Deviation
(to -45
or beyond)

2) Bulk of QRS forces

directed superiorly
to the left

Lead I
Lead
AVF

3) Minimal or no
QRS widening

Left Anterior Fascicular (/Hemi-) Block (LAFB)

qR
I

rS

rS
II

III

Initial QRS forces directed rightward (negative in Lead I)

and inferiorly (positive in Leads II and III
Subsequent predominant forces directed leftward
(positive in I) and superiorly (negative in II and III)

Left Posterior Fascicular (/Hemi-) Block (LPFB)

LV is activated via the
left anterior fascicle

1) Initial QRS forces

directed superiorly
to the left
Right Axis
Deviation
(beyond
+90)

2) Bulk of QRS forces

directed inferiorly
to the right

Lead I
Lead
AVF

3) Minimal or no
QRS widening

Left Posterior Fascicular (/Hemi-) Block (LPFB)

rS

qR
II

qR
III

I
Initial QRS forces directed leftward (positive in Lead I)
and superiorly (negative in Leads II and III
Subsequent predominant forces directed rightward
(negative in I) and inferiorly (positive in II and III)

Bifascicular Block (RBBB + LAFB)

Site
of
RBB
B

RV is activated
from the left

Site of
LAFB
LV is activated via the
left posterior fascicle

Bifascicular Block (RBBB + LAFB)

Note RBBB
pattern plus
left axis
deviation of
unblocked
portion of QRS
(initial .06 sec
=1.5 little
boxes)

Bifascicular Block (RBBB + LPFB)

Site of
RBBB

LV is activated via the

left anterior fascicle

Site of
LPFB
RV is activated
from the left

Bifascicular Block (RBBB + LPFB)

Note RBBB
pattern plus
right axis
deviation of
unblocked
portion of QRS
(initial .06 sec
=1.5 little
boxes)

Non-Specific Intraventricular Conduction Block

Leads I & V1
inconsistent
with RBBB;
septal q in I
inconsistent
with LBBB

QRS .12 sec

without a
typical BBB
pattern

Causes of Intraventricular
Conduction Disturbances
Ischemic heart disease or cardiomyopathic
scarring
Degenerative changes in the conduction
system
Antiarrhythmic drugs that depress the
inward sodium current
Hyperkalemia (K)
Myocardial infection, infiltration (e.g., tumor)
Trauma (e.g., cardiac surgery)
Congenital abnormality

AV Block

Components of AV Conduction
AV
Node

HisPurkinje
System

AV Block - Definitions
First Degree: Prolonged
conduction time
Second Degree: Intermittent nonconduction
Third Degree: Persistent nonconduction

First Degree AV Block

(PR > .20 sec [1 big box])
II
P

.36
Site of delay most commonly the AV node,
localized to the His-Purkinje system

but may be

Second Degree AV Block - Type I

(Wenkebach or Mobitz I Block)

II

Block
Example of 3:2 conduction ratio; general pattern, n:n-1
Note PR prior to block and post-block
Characteristic of AV nodal site of block

Second Degree AV Block - Type I

(Wenkebach or Mobitz I Block)
II
P

Block

4:3 conduction ratio

Note first RR longer than second RR

Ladder Diagram of AV
Conduction
QRS
P

Schema of a Typical
4:3 AV Wenckebach Sequence

Second RR (VV) shortens due to diminution

in the increment of AV prolongation
Pause encompassing blocked beat < 2 x PP

Second Degree AV Block - Type I

V1
7:6 Conduction Ratio
Note atypical PR & RR features

Second Degree AV Block - Type I

(Repetitive Cycles)

II
4:3

4:3
Group beating

(Regularly irregular rhythm)

Second Degree AV Block - Type II

(Mobitz II)

II
P

Block

Block

Example of 3:2 conduction ratio; general pattern, n:n-1

Note fixed PR for all conducted beats
Characteristic of His-Purkinje system site of block

Second Degree AV Block - Type II

P
Block

4:3 conduction ratio

2:1 Second Degree AV Block Type I or Type II?

II

Is site of block within the AV node or His-Purkinje System?

EKG/Clinical Clues to site of

2:1 Second Degree AV block
Favoring AV Node

QRS narrow
Improves
with
exercise
(catecholaminefacilitated conduction)
Observed in setting of
increased vagal tone
(e.g., sleep) or AV
nodal
depressant
drugs

Rules-of-Thumb only

Favoring His-Purkinje System

QRS wide (BBB

patterns)
Unchanged (possibly
even precipitated)
during exercise
May improve with
heart rate slowing
during increased
vagal tone

Advanced Second Degree AV Block

(Block of 2 Consecutive P Waves)

II

3:1 conduction ratio, with ventricular rate in the 30s

Pacemaker Hierarchy
(Dominant vs Subsidiary/Escape Pacemakers)
Intrinsic Rate of Firing
SA
Node
(+Atria)

AV Junction
(=AVN/His Bundle)
Ventricles
(= Distal Purkinje System)

60-100 min1

40-60 min1

30-40 min1

Site of AV Block vs. Escape

Rhythm
AV Node: Junctional or ventricular
His-Purkinje System: Ventricular

Junctional and ventricular (=

idioventricular) escape beats or
rhythms
Are suppressed (inhibited) as long as their
intrinsic rates are overdiven by a faster
pacemaker tissue or rhythm process capturing
the heart
Become manifest (escape from suppression)
in the absence of faster competing rhythms
But, firing of these pacemakers at rates faster
than their upper-limit escape rates is
abnormal (i.,e., accelerated rhythm or
relative tachycardia )

EKG Appearance of Escape Beats

Narrow
QRS

Wide
QRS
P

Sinus
Rhythm

Atrial

Junctional

Ventricular

(Retrograde P waves require

intact retrograde AVN cond.)

QRS Width: Synchronous vs. Asynchronous

Ventricular Activation
QRS
Normal synchronous
overlapping activation
of both ventricles:
On
time
Asynchronous
scenario I:

Head start
Asynchronous
scenario II:

Narrow

Late
Wide

On
time
(or late)

Wide

Third Degree AV Block

(Complete Heart Block)
II
P

P waves at 60 beats/min
QRS complexes (junctional escape rhythm) at 45
beats/min
Atrial and ventricular activity are completely unrelated
Junctional escape rhythm suggests AV nodal site of block

Third Degree AV Block

(Complete Heart Block)
V1

P waves at 50-60 beats/min

QRS complexes (ventricular escape rhythm) at 35 beats/min
Atrial and ventricular activity are completely unrelated
Ventricular escape rhythm suggests His-Purkinje site of
block

Ladder Diagram of AV Dissociation

During Third Degree AV Block
Faster atrial rate

Slower ventricular (escape) rhythm

Note that impulses block anterogradely and retrogradely

within the AV conduction system

Unreliability of Ventricular Escape Rhythm

in Third Degree AV Block

(P)

P
15 s

No QRS complexes!

(P)

Physiologic AV Block
First and second degree AV block may occur
physiologically at an AV Nodal level:
in response to premature atrial impulses
or atrial tachyarrhythmias
in settings of increased vagal tone (e.g.,
sleep, Valsalva maneuver, well-trained
athletes)
BUT persistent 3rd degree AV block is
never physiologic

Causes of NON-Physiologic
AV Block
Ischemic heart disease, cardiomyopathy and
degenerative changes
Drugs that depress AV conduction
AV Node: digoxin, beta blockers, calcium
channel blockers, amiodarone
His-Purkinje System: Antiarrhythmic drugs
that depress the inward sodium current
Myocardial infection, infiltration (e.g., tumor)
Trauma (e.g., surgery; therapeutic ablation)
Congenital abnormalities

Sinus Bradyarrhythmias

Sinus Arrhythmia
Inspiration

SA nodal acceleration

Expiration

SA nodal deceleration

Pacemaker Hierarchy
(Dominant vs Subsidiary/Escape Pacemakers)
Intrinsic Rate of Firing
SA
Node
(+Atria)

AV Junction
(=AVN/His Bundle)
Ventricles
(= Distal Purkinje System)

60-100 min1

40-60 min1

30-40 min1

Sinus Bradycardia

II

P wave upright in leads I and II, just as in normal sinus rhythm

Causes of Sinus Bradycardia

Increased vagal tone
Drugs: beta blockers, calcium channel
blockers, amiodarone, digoxin (indirect
effect)
Myocardial ischemia/infarction
Hypothyroidism
Sick sinus syndrome degenerative/fibrotic atrial process

Sequence of P Wave Generation

Sinus
Node

SA
Junction

Non-visible process on the EKG

Atrium
(P wave)

Sinoatrial (SA) Exit Block Definitions

First Degree: Prolonged SA conduction time
(non-detectable on EKG; no missing P waves)
Second Degree: Intermittent non-conduction
(intermittent absence of P waves)
Third Degree: Persistent non-conduction
(complete absence of P waves; escape rhythms
only)

Second Degree SA Exit Block - Type I

(Wenkebach)
4:3 pattern
P

P
Missing
P wave

PP:
PP intervals shorten prior to block
Note unaffected, fixed PR intervals

Schema of a Typical 4:3 Second Degree

SA Exit Block (Type I) Sequence
Sinus
Node
SA
Junct.
A
Second PP (AA) shortens due to diminution
the increment of SA-A prolongation
Pause encompassing blocked beat < 2 x normal PP

in

Second Degree SA Exit Block - Type II

Missing
P wave
P

PP:
One P wave abruptly drops out on time

2:1 SA Exit Block

(Every Other P wave is Dropped)
X
P

2X
P

Atrial rate is abruptly cut in half

2X
P

X
P

Resolution of block

Sinus Arrest

Sinus bradycardia Sinus arrest Slow junctional escape rhythm

(with retrograde p waves)

Tachycardia-Bradycardia
(Form of Sick Sinus) Syndrome

Atrial Flutter

Atrial Flutter
terminates

Sinus arrest

Junctional
escape (tardy)

Sinus Arrest Asystole

Sinus rhythm

Sinus brady.
Sinus arrest
V. escape
rhythm

Failure of V.
escape rhythm
Asystole

P P P

P
P

Causes of SA Exit Block and

Sinus Pauses/Arrest
Increased vagal tone (very intense for sinus
arrest)
Drugs: beta blockers, calcium channel
blockers, amiodarone, digoxin (indirect effect)
Myocardial ischemia/infarction
Sick sinus syndrome
Sequela of open heart surgery

thank you