Av block

1. AV DISSOCIATION
BY D.ANISHAA

2. • AV DISSOCIATION- independent/ dissociated activity of atria and vetricles.
• Not a primary disturbance of rhythm rather is a symptom of underlying rhythm
disturbances produced by one of three mechanism /combination which impairs
normal transmission of impulse from atria to ventricles.

3. LOCATION :
AV junction- CHB
INTERFERENCE FROM ACCELARATED LOWER PACEMAKER –VT/ AIVR

4. CLASSIFICATION
Type 1: AV Dissociation by Default
Slowing of dominant pacemaker– allows escape of subsidiary pacemaker
May occur in sinus bradycardia /sinus arrhythmia – permit independent AV
junctional rhythm to arise

5. • Sinus bradycardia
• High vagal tone
• beta-adrenergic blockers and calcium channel blockers

7. • Type II: ACCELARATION OF LATENT PACEMAKER:
Non paroxysmal AV junctional tachycardia
VT without retrograde atrial capture
• insults lead to an accelerated rate of the subsidiary pacemakers,
causing them to conduct preferentially.
Eg:
• Myocardial ischemia
• High catecholamine state
• Digitalis toxicity

9. TYPE III: COMPLETE AV block – which allows ventricles to beat under subsidiary
pacemakers- AV junctional / ventricular escape rhythm.
• Complete AV block- not synonymous with complete AV dissociation
• Patients with CHB – have AV dissociation
• Patients with complete AV dissociation may/may not have CHB

10. CHB
 When no atrial activity is conducted to ventricles.
 Atrial and ventricular activity are controlled by
independent pacemakers.
 Atrial pacemaker- sinus/ ectopic/ AV junctional
(above the block ) with retrograde atrial conduction.
 Ventricular pacemaker – below the level of block-
above/ below his bundle bifurcation.

11. • Block @ level of AV node- usually congenital
• Block within bundle of His / distal to His bundle in purkinje – usually acquired.

12. TYPE IV: COMBINATION OF CAUSES
DIGITALIS TOXICITY-
1.Down sloping ST depression with a characteristic “Salvador Dali sagging” appearance
2.Junctional AV nodal tachycardia
3.Ventricular tachycardia
4.Conduction block
5.Ventricular bigeminy rhythm
6.AV dissociation

13. COMPLETE VS INCOMPLETE AVD
• If a single pacemaker – establish control over atria/ventricles for one beat
(CAPTURE BEAT)/ Series of beats – NO AV DISSOCIATION for that period–
incomplete AV dissociation
Isorhythmic AV dissociation Interference AV dissociation
Severe sinus bradycardia Lower level pacemaker
Junctional escape rhythm Junctional / ventricular escape rhythm
Sinus rate = junctional rate Faster intrinsic rate

14. COMPLETE AV DISSOCIATION
When atria/ventricle –fails to respond to a single impulse for 1 beat /series of beats– AV
DISSOCIATION occurs for that period.
COMPLETE AV dissociation-
Eg: CHB,
Atrial rate > ventricular rate

17. ISORHYTHMIC AV DISSOCIATION
• When sinus rate is slowed & junctional rate is accelerated
• Slowed sinus rate = accelerated junctional rhythm
• Atria captured by sinus impulse
• Ventricles by junctional impulse.

18. INTERFERENCE
AV BLOCK-
 PRIMARY- anatomical defect /abnormal refractoriness of AV node
SECONDARY -AV BLOCK – due to interference with normal refractoriness of AV
node
• IPSIDIRECTIONAL interference
paroxysmal atrial tachycardia with first degree A-V block
atrial flutter with 2:1 A-V block.

19. INTERFERENCE AV DISSOCIATION
• Repetitive CONTRADIRECTIONAL INTERFERENCE- AV dissociation
Interference Dissociation—

20. ZONE OF INTERFERENCE

22. CHB AVD
DEFINITION
AV conduction
All atrial impulse –blocked
AV junction/ventricles –
compelled to initiate
alternate escape rhythm
affected
Ventricles dissociate itself
from atria by an
autonomous focus arising
from AV junction/ventricles.
intact
PATHOLOGY Pathological AV block
Degenerative , ischemic,
congenital, VHD
Physiological AV block
Due to ill-timed accelerated
lower pacemaker activity
CHB VS AVD

23. CHB AVD
BASIC HR Almost always in
bradycardia
Can occur @any HR
TACHYCARDIA:
Atrial tachycardia
Accelerated junctional
tachycardia
VT
All VVI pacemaker
rhythm
NORMAL RATE:
Early stages of SND
AIVR
BRADYCARDIA;
High vagal tone
Ischemic SA/AV nodes(
IWMI)

24. ATRIAL RATE VS
VENTRICULAR RATE
Atrial > ventricular rate Ventricular rate >/=
atrial rate
duration Often permanent
Drug /dyselectrolytemia-
reversible
Often transient
QRS width 50% narrow, 50% wide 90% narrow
Except VT
CAPTURE & FUSION
BEAT
Rare
If present- high grade
AVblock
common
PPI requirement Require PPI Rarely required

25. If VT is persistent – suppress SA node
Atrial depolarization & contraction during VT – complex
Hence P wave in VT can be
Totally absent
Occur antegrade
On QRS
Over T waves

26. • AV dissociation in VT – rarely manifested.
• In intact VA conduction
• VT – traverse AV junction– reset SA node/ set in semi depolarized state.

27. CLINICAL FEATURES
1.VARYING PULSE VOLUME:
Some atrial beats– contribute to ventricular filling--- varying ventricular volumes
2.REVERSE PULSUS PARADOXUS (IN ISORHYTHMIC AV DISSOCIATION):
Pulse volume decrease during expiration
Inspiration--- increase sinus rate – AV synchrony
Expiration – decrease sinus rate – junctional rhythm takes over--AV asynchrony

28. 2.JVP-Cannon waves
3.MR/TR:
Simultaneous contraction of atria & ventricle

29. MANAGEMENT
• Type I : increase sinus rate with sympathomimetics
• Type II: control tachyarrhythmias from subsidiary pacemakers
• Type III : PPI
• TYP IV: digoxin specific Ab ( digibind/digiFab)

30. THANK YOU