1. AV Blocks Bundle Branch Blocks
Associate Professor
Dr. Alexey Podcheko
Spring 2015

2. 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)
-Right Bundle Branch Block
-Complete Left Bundle Branch Block (LBBB)

3. Heart rate generated by SA node and ectopic sites (beats per minute):SA
Atrial 55-60
AV 45-50
Bundle of
Bundle
Purkinje 35-40
Ventricular 30-35

4. 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.

5. 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.

7. 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’.

8. 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 [ 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.

9. 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.
How to differentiate broad complex SVT and VT? By knowing ECG signs of atrioventricular dissociation (AV) dissociation  specific only for VT!!!!
RBBB + SVT=Broad Complex SVT

10. 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:
Recognition of a normal QRS complex (aka capture beat) in a run of broad complex tachycardia
A fusion QRS complex
P wave activity fused with components of the broad complex

11. 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. 

12. 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! 

13. 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.

14. 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. 

15. 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

17. 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!

18. Ventricular Flutter

19. 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)

22. 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”

23. Classification of AV Blocks
Three degrees of AV block are recognized
1st Degree
2nd Degree
3rd Degree (aka Complete)
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.

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

25. 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
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

26. 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
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
Other Features
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 RR interval progressively shortens with each beat 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

27. AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon) - read the comments t the slide!
The first clue to the presence of Wenckebach AV block on this ECG is the way the QRS complexes cluster into groups, separated by short pauses (This phenomenon usually represents 2nd-degree AV block or non-conducted PACs; occasionally SA exit block).
At the end of each group is a non-conducted P wave; the PR interval progressively increases from one complex to the next.
The Wenckebach pattern here is repeating in cycles of 5 P waves to 4 QRS complexes (5:4 conduction ratio).
The increase in PR interval from one complex to the next is subtle. However, the difference is more obvious if you compare the first PR interval in the cycle to the last.
 The P-P interval is relatively constant despite the irregularity of the QRS complexes.

28. 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.

29. 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)

30. 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.

32. 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.
LITFL | ECG Library | ECG Basics | AV Block: 2nd degree, Mobitz II
AV Block: 2nd degree, Mobitz II
Definition
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, treble for two dropped beats, etc).
Example of Mobitz II
Arrows indicate “dropped” QRS complexes (i.e. non-conducted P waves)
Mechanism
Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node).
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).
Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd degree AV block is produced by intermittent failure of the remaining fascicle (“bilateral bundle-branch block”).
In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.
In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes.
Unlike Mobitz I, which is produced by progressive fatigue of the AV nodal cells, Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse.
There may be no pattern to the conduction blockade, or alternatively there may be a fixed relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block. 
Causes of Mobitz II
Anterior MI (due to septal infarction with necrosis of the bundle branches).
Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease).
Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)
Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).
Autoimmune (SLE, systemic sclerosis).
Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).
Hyperkalaemia.
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.
Clinical Significance
Mobitz II is much more likely than Mobitz I to be associated with haemodynamic 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.

33. 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.

34. 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.
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.

35. Interpretation: AV Block 2nd degree, Untypable High Grade with Conduction ratio 3:1 (3 P waves and 1 QRS complex)

36. 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

39. 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]
No P waves transmitted to the ventricular myocardium

40. 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.

41. “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)

42. : Right Bundle Branch Block

43. RBBB (right bundle branch block)”:

44. Causes of RBB Block: RBBB on the ECG may arise secondary to
a chronic increase in right ventricular pressure (for example, in primary pulmonary hypertension or cor pulmonale) or
an acute rise in right ventricular pressure in, for example, acute pulmonary embolism
new onset RBBB may be observed in myocardial infarction secondary to obstruction of LAD

46. 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

47. LBBB (left bundle branch block)
-no q waves in V6, I - R wave notch may be small or invisible

48. 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!

49. 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.

50. :Left Bundle Branch Block
[…“right-sided” precordial leads…]
[…“left-sided”...]
[“various” leads]

51. LBBB (left bundle branch block)