AV BlocksBundle 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)

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Heart rate generated by SA node and ectopic sites (beats per minute):

oSA Node @ 60-100oAtrial cells @ 55-60oAV node @ 45-50oBundle of His @ 40-45-50oBundle branches @ 40-45-50oPurkinje cells @ 35-40oVentricular myocardium @ 30-35

Ventricular TachycardiaA 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 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 infarction of myocardial tissue is not generally uniformuniform, 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 possible for strands of cells to survive within the infarcted area.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 depolarization and repolarization properties may differ significantly from repolarization properties may differ significantly from unaffected tissue adjacent to the infarctunaffected tissue adjacent to the infarct.

These are the conditions in which re-entrant loops re-entrant loops arisearise and and the commonest mechanism triggering VTthe 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’.7

Definition and classification of VT

Ventricular tachycardia is present when more more than three consecutive ventricular (broad) than three consecutive ventricular (broad) complexes occur in sequence at a rate of, or complexes occur in sequence at a rate of, or greater than, >100 beats per minutegreater than, >100 beats per minute [100-250 bpm].

Forms of VT:Non-sustained VT: Non-sustained VT: A self terminating run of VT, self terminating run of VT,

less than < 30 seconds in durationless than < 30 seconds in duration, Sustained VT : Sustained VT : episode episode of VT greater than > 30 of VT greater than > 30

seconds in duration, or an episode requiring seconds in duration, or an episode requiring clinical intervention for terminationclinical intervention for termination..

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Q: Why sometimes it is difficult to differentiate SVT and VTA: 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.

How to differentiate broad complex SVT and VT? By knowing ECG signs of atrioventricular atrioventricular dissociation dissociation ((AV) dissociationAV) dissociation specific only for VT!!!! specific only for VT!!!! 9

RBBB + SVT=Broad Complex SVT

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.III. P wave activity fused with components of the P wave activity fused with components of the broad complexbroad 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 non-refractory 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 P wave activity fused with components of the broad complex broad complex tachycardia of VT: P waves show P waves show no fixed relationship with the QRS complexesno 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 practice, evidence of AV dissociation in a broad complex tachycardia, in a broad complex tachycardia, strongly strongly favoursfavours aa “diagnosis of VT” “diagnosis of VT”. .

Evidence of AV dissociation is detectable Evidence of AV dissociation is detectable on the ECG in approximately 50% of on the ECG in approximately 50% of cases of VTcases 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 high rates achieved in this arrhythmiaarrhythmia, 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 outputloss of cardiac output 15

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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 requiredHow 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

Ventricular Flutter

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• 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)

V. Fibrillation

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Atrioventricular BlockDysfunction 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 recognized1st Degree2nd Degree

3rd Degree (aka Complete)23

Mobitz Type 1aka Wenkenbach

Mobitz Type 2 Untypable with

Conduction ratio2:1

Untypable High GradewithConduction ratio3:1; 4:1; etc.

First Degree Heart Block PR interval > 200ms (five small squares) P wave before each QRS complex

CausesIncreased vagal toneAthletic trainingInferior MIMitral valve surgeryMyocarditis (e.g. Lyme disease)HypokalaemiaAV nodal blocking drugs (beta-blockers,

calcium channel blockers, digoxin, amiodarone)

May be a normal variantClinical significanceDoes not cause haemodynamic

disturbanceNo specific treatment is required

First Degree Heart Block

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 constantThe 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

Dropped beat5:4

AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon) - read the comments t the slide!

AV Block: 2nd degree, Mobitz IClinical significanceMobitz 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 IIIntermittent 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)

HyperkalaemiaDrugs: 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 ventriclesPerfusing 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

intervalSecond 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': 'High-grade':      Consecutive P waves dropped [@ least [@ least

2 Consecutive P waves FAIL to conduct to Ventricular 2 Consecutive P waves FAIL to conduct to Ventricular MyocardiumMyocardium.].]

Third degree Heart Block: [AV dissociation]No P waves transmitted to the ventricular myocardium 39

Bundle Branch Blocks

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Under normal all regions of the ventricular myocardium are depolarized within 0.12 seconds or 3 small squaresWhen 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.

“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)

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: Right Bundle Branch Block

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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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)

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 Damage to the left bundle branch in this situation tends to be permanent following resolution tends to be permanent following resolution of the of the acute MIacute MI. The chronic ST changes associated with . The chronic ST changes associated with LBBB then LBBB then make interpretation of the ECG at any make interpretation of the ECG at any subsequent presentations with chest pain difficultsubsequent 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]

LBBB (left bundle branch block)