Transcript ECG signs of AV Blocks and Bundle Branch Blocks

AV Blocks
Bundle Branch
Blocks
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Associate Professor
Dr. Alexey Podcheko
Spring 2015
Learning Objectives
 To know ECG signs and causes of ventricular
tachycardia
 To know EKG signs and causes of
-1st degree AV blocks
-2nd degree AV blocks (4 subtypes)
-3rd degree AV blocks (2 subtypes)
 To know EKG signs and causes of
-Right Bundle Branch Block
-Complete Left Bundle Branch Block (LBBB)
 Heart rate generated by SA node and ectopic
sites (beats per minute):
o SA Node @ 60-100
o Atrial cells @ 55-60
o AV node @ 45-50
o Bundle of His @ 40-45-50
o Bundle branches @ 40-45-50
o Purkinje cells @ 35-40
o Ventricular myocardium @ 30-35
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Ventricular Tachycardia
 A tachycardia arising from a focus situated
below the bifurcation of the bundle of His is
termed ventricular tachycardia (VT).
 VT is characterized by wide QRS complexes of
0.12s or greater (and often much greater) in
duration – a.k.a. ‘broad complex’ tachycardia
 VT is extremely common, particularly in the
setting of acute coronary syndrome.
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 As infarction of myocardial tissue is not generally
uniform, at the margins of vascular territories there
may be a degree of overlap in blood supply between
vessels and it is possible for strands of cells to survive
within the infarcted area.
 Such a strand of viable tissue has lost much of its
cellular contacts due to the death of surrounding
tissue and for this reason depolarization and
repolarization properties may differ significantly from
unaffected tissue adjacent to the infarct.
 These are the conditions in which re-entrant loops
arise and the commonest mechanism triggering VT is
a 're-entry' circuit triggered by a ventricular ectopic.
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 Following an initial brief period of
irregularity at the time of onset, the
tachyarrhythmia tends to be
monotonously regular. When VT arises
from a single site in the ventricles and the
depolarization wave travels through the
chambers in a constant pattern, the QRS
complexes are all very similar in
morphology. This is termed
‘monomorphic ventricular tachycardia’.
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Definition and classification of VT
Ventricular tachycardia is present when more
than three consecutive ventricular (broad)
complexes occur in sequence at a rate of, or
greater than, >100 beats per minute [100-250
bpm].
Forms of VT:
Non-sustained VT: A self terminating run of VT,
less than < 30 seconds in duration,
Sustained VT : episode of VT greater than > 30
seconds in duration, or an episode requiring
clinical intervention for termination.
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Q: Why sometimes it is difficult to
differentiate SVT and VT
A: It is possible for a focus situated in the
supraventricular region to generate a broad complex
tachycardia if conduction of the depolarization wave
within the ventricles is abnormal.
RBBB + SVT=Broad Complex SVT
 How to differentiate broad complex SVT and VT? By
knowing ECG signs of atrioventricular
dissociation (AV) dissociation specific only for VT!!!!
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Q: What is the AV Dissociation?
A: When electrical events in the ventricles and atria
are occurring independently of one another, this
situation is referred to as AV dissociation.
Q: What are the three major findings on the ECG
consistent with AV dissociation:
I. Recognition of a normal QRS complex (aka
capture beat) in a run of broad complex
tachycardia
II. A fusion QRS complex
III. P wave activity fused with components of the
broad complex
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 1. Recognition of a normal
QRS complex, a capture
beat, in a run of broad
complex tachycardia. In
the presence of VT, a
capture beat represents a
rare P wave which has
arrived at the junction at a
point in time when the
conducting system and
ventricles are in a nonrefractory state. The
associated P wave triggering
the capture beat may or
may not be visible on the
readout.
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2. A fusion QRS complex may arise if the SA node,
uninfluenced by events in the ventricles, fires and
depolarization is transmitted into the conducting system just
as the ventricular focus discharges. The fusion QRS
complex generated will demonstrate features of both
sources of ventricular depolarization. Like the QRS
complexes of the underlying VT, it is bizarre in morphology
but bizarre in a different way!
 3. P wave activity fused with components of the
broad complex tachycardia of VT: P waves show
no fixed relationship with the QRS complexes,
indicating that the atria and ventricles are
depolarizing independently of one another.
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 In practice, evidence of AV dissociation
in a broad complex tachycardia, strongly
favours a “diagnosis of VT”.
Evidence of AV dissociation is detectable
on the ECG in approximately 50% of
cases of VT.
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Some clarifications regarding VT:
 The heart rate observed in VT is variable but most
commonly runs between 140 and 200 bpm. The
high rates achieved in this arrhythmia, with
impaired ventricular filling, are part of the reason
why it is so dangerous.
 Highly abnormal pattern of ventricular
depolarization is also a major contributor to
cardiovascular instability in VT.
 Highly deranged pattern of ventricular
depolarization may result in an equally deranged
pattern of ventricular myocardial contraction with
loss of cardiac output
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Ventricular Flutter
 Clinical Significance
• Extreme form of VT with loss of organized electrical
activity
• Associated with rapid and profound hemodynamic
compromise
• Usually short lived due to progression to ventricular
fibrillation
• As with ventricular fibrillation rapid initiation of advanced
life support is required
 How to Recognise Ventricular Flutter
• Continuous Sine Wave
• No identifiable P waves, QRS complexes, or T waves
• Rate usually > 200 beats / min
• The ECG looks identical when viewed upside down!
Ventricular Flutter
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V. Fibrillation
• Ventricular fibrillation (VF) is the the most important shockable
cardiac arrest rhythm.
• The ventricles suddenly attempt to contract at rates of up to 500
bpm.
• This rapid and irregular electrical activity renders the ventricles
unable to contract in a synchronised manner, resulting in
immediate loss of cardiac output.
• The heart is no longer an effective pump and is reduced to a
quivering mess.
• Unless advanced life support is rapidly instituted, this rhythm is
invariably fatal.
• Prolonged ventricular fibrillation results in decreasing waveform
amplitude, from initial coarse VF to fine VF and ultimately
degenerating into asystole due to progressive depletion of
myocardial energy stores.
 ECG Findings
• Chaotic irregular deflections of varying amplitude
• No identifiable P waves, QRS complexes, or T waves
• Rate 150 to 500 per minute
• Amplitude decreases with duration (coarse VF -> fine VF)
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Atrioventricular Block
 Dysfunction of the AV
node or diffuse damage
to components of the
ventricular conducting
system can result in a
delay or even failure of
transmission of atrial
depolarization into the
ventricular muscle mass.
This situation is referred
to as “atrioventricular or
AV block”
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Classification of AV Blocks
 Three degrees of AV block are recognized
1st Degree
2nd Degree
Mobitz Type 1
aka
Wenkenbach
Mobitz Type 2
Untypable
with
Conduction
ratio
2:1
Untypable
High Grade
with
Conduction
ratio
3:1; 4:1; etc.
3rd Degree (aka Complete)
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First Degree Heart Block
 PR interval > 200ms (five small squares)
 P wave before each QRS complex
First Degree Heart Block
Causes
 Increased vagal tone
 Athletic training
 Inferior MI
 Mitral valve surgery
 Myocarditis (e.g. Lyme disease)
 Hypokalaemia
 AV nodal blocking drugs (beta-blockers, calcium
channel blockers, digoxin, amiodarone)
 May be a normal variant
Clinical significance
 Does not cause haemodynamic disturbance
 No specific treatment is required
AV Block: 2nd degree, Mobitz I
(Wenckebach Phenomenon)
 Progressive prolongation of the PR interval culminating in a





non-conducted P wave
The PR interval is longest immediately before the dropped
beat
The PR interval is shortest immediately after the dropped
beat
The P-P interval remains relatively constant
The greatest increase in PR interval duration is
typically between the first and second beats of the cycle.
The Wenckebach pattern tends to repeat in P : QRS groups
with ratios of 3:2, 4:3 or 5:4
5:4
Dropped beat
AV Block: 2nd degree, Mobitz I (Wenckebach
Phenomenon) - read the comments t the slide!
AV Block: 2nd degree, Mobitz I
 Clinical significance
 Mobitz I is usually a benign rhythm, causing minimal
haemodynamic disturbance and with low risk of progression
to third degree heart block.
 Asymptomatic patients do not require treatment.
 Symptomatic patients usually respond to atropine.
 Permanent pacing is rarely required.
AV Block: 2nd degree, Mobitz II
 Intermittent non-conducted P waves without progressive prolongation of
the PR interval (compare this to Mobitz I).
 The PR interval in the conducted beats remains constant.
 The P waves ‘march through’ at a constant rate.
 The RR interval surrounding the dropped beat(s) is an exact multiple of
the preceding RR interval (e.g. double the preceding RR interval for a
single dropped beat)
AV Block: 2nd degree, Mobitz II
•While Mobitz I is usually due to a functional suppression
of AV conduction (e.g. due to drugs, reversible
ischaemia), Mobitz II is more likely to be due
to structural damage to the conducting system (e.g.
infarction, fibrosis, necrosis)
•In 75% of cases, the conduction block is located distal to
the Bundle of His, producing broad QRS complexes.
•In 25% of cases, the conduction block is located within
the His Bundle itself, producing narrow QRS complexes.
Causes of Mobitz II
 Anterior MI (due to septal infarction with necrosis
of the bundle branches)
 Cardiac surgery (especially surgery occurring
close to the septum, e.g. mitral valve repair)
 Inflammatory conditions (rheumatic fever,
myocarditis, Lyme disease)
 Hyperkalaemia
 Drugs: beta-blockers, calcium channel
blockers, digoxin, amiodarone.
Clinical Significance
 Mobitz II is much more likely than Mobitz I to be
associated with hemodynamic compromise, severe
bradycardia and progression to 3rd degree heart block.
 Onset of haemodynamic instability may be sudden and
unexpected, causing syncope (Stokes-Adams attacks)
or sudden cardiac death.
 The risk of asystole is around 35% per year.
 Mobitz II mandates immediate admission for cardiac
monitoring, backup temporary pacing and ultimately
insertion of a permanent pacemaker.
AV Block 2nd degree Untypable with
Conduction ratio 2:1 form
 Second degree heart block with a fixed ratio of P waves: QRS
complexes (e.g. 2:1)
•The atrial rate is approximately 75 bpm.
•The ventricular rate is approximately 38 bpm.
•Non-conducted P waves are superimposed on the
end of each T wave.
Interpretation: AV Block 2nd degree, Untypable High Grade
with Conduction ratio 3:1 (3 P waves and 1 QRS complex)
AV block: 3rd degree (complete heart block)
 No P waves transmitted to ventricles
 Perfusing rhythm is maintained by a junctional (narrow
QRS) or ventricular(broad QRS) escape rhythm.
 Patient may suffer ventricular standstill leading to syncope (if
self-terminating) or sudden cardiac death (if prolonged).
 Typically the patient will have severe bradycardia with
independent atrial and ventricular rates, i.e. AV dissociation.
 Ventricular heart rate between 20 to 40 bpm
Summary:
 First degree Heart Block:
 All P waves transmitted to ventricles with prolonged PR
interval
 Second degree Heart Block:
 Some P waves NOT transmitted to ventricles

Mobitz type I: progressive prolongation of PR
interval

Mobitz type II: constant PR interval
 'Untypable':
2:1 conduction ratio [i.e. 2 P wave: 1
QRS complex………………]
 'High-grade':
Consecutive P waves dropped [@ least
2 Consecutive P waves FAIL to conduct to Ventricular
Myocardium.]
 Third degree Heart Block: [AV dissociation]
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Bundle Branch Blocks
Under normal all regions of the
ventricular myocardium are
depolarized within 0.12 seconds or 3
small squares
When one of the bundle branches
is blocked, one of the ventricles
must be depolarized by signal
spreading by direct cell to cell
contact through myocardium.
 ECG finding in complete left
bundle branch block (LBBB) or right
bundle branch block (RBBB) is,
prolongation of the QRS complex to
or beyond 0.12s in duration.
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“RBBB (right bundle branch block)”:
The major changes are seen in leads V1 [or V2] and V6:
1. In the RBBB, depolarization of the right ventricle is delayed
and travels to the chamber by direct cell to cell contacts and
produces a wide “second” R wave in the lead V1 or V2 (rSR
-Rabbit Ear pattern)
2. Slurred S wave in V6
3. Overall positive QRS
complex in lead V1 (a
must!)
4. ST or T wave changes
in Right-sided Chest
leads (Electrical
phenomenon; Not
ischemia; Not infarction)
: Right Bundle Branch Block
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RBBB (right bundle branch block)”:
Causes of RBB Block:
 RBBB on the ECG may arise secondary to
1)a chronic increase in right ventricular pressure
(for example, in primary pulmonary hypertension
or cor pulmonale) or
2)an acute rise in right ventricular pressure in, for
example, acute pulmonary embolism
3)new onset RBBB may be observed in myocardial
infarction secondary to obstruction of LAD
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LBBB (left bundle branch block)
1. QRS duration equal to
or greater than 0.12s
2. Broad R waves (Small
Notch or M-shaped) in
lead I and V6 [or V5] with
No q waves
3. Broad & Deep S waves
in the septal leads [V1 or
V2]
4. Abnormal repolarization
with ST depression or
elevation in “various”
leads [Electrical
phenomenon; Not
ischemia ; Not infarction
LBBB (left bundle branch block)
-no q waves in V6, I
- R wave notch may be small or invisible
Causes of LBB Block:
 The presence of LBBB on an ECG is a highly
abnormal finding. Significant damage to the left
bundle branch is commonly seen in infarction
secondary to obstruction of the left anterior
descending artery and new onset LBBB may be the
presenting ECG abnormality in a patient with
anterior MI.
Damage to the left bundle branch in this situation
tends to be permanent following resolution of the
acute MI. The chronic ST changes associated with
LBBB then make interpretation of the ECG at any
subsequent presentations with chest pain difficult!
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 The left bundle branch may also be
damaged in diseases causing diffuse
damage to the left ventricle for example,
hypertension, myocarditis or
cardiomyopathy from whatever cause.
 In addition, during part of its course, the left
bundle branch has a close anatomical
relationship with the non-coronary cusp of
the aortic valve. Consequently, LBBB is seen
in diverse diseases of the aortic valve.
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:Left Bundle Branch Block
[…“right-sided” precordial leads…]
[…“left-sided”...]
[“various” leads]
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LBBB (left bundle branch block)