2. Content
• AUTONOMIC NERVOUS SYSTEM
• CONDUCTION SYSTEM
• NORMAL INTERVALS
• INTRINSIC HEART RATE
• INTERFERENCE
• AV DISSOCIATION
• The Stokes-Adams syndrome
• FIRST DEGREE ,2ND DEGREE ,3RD AV Block
• High grade AV block
• ANS MEDIATED BRADYCARDIA
• SUMMARY
7. INTERFERENCE
• A normal phenomenon
• Physiologic refractoriness resulting from in-excitability secondary to a
preceding impulse
• Possible at any site where impulses are conducted
• Recognized most often
• Sinus node and atrium (SA block)
• The atria and ventricles (AV block)
• Intra-atrial block
• Intraventricular block
8. AV DISSOCIATION
COMPLETE
• PP regular or irregular
• RR regular or irregular
• There is no definite relation
between P and R
INCOMPLETE
• Ventricular capture
• Retrograde P conduction is
possible
10. Atrioventricular Dissociation
1. Slowing of the dominant pacemaker allows escape of a subsidiary
or latent pacemaker
2. Acceleration of a latent pacemaker
3. Complete AV block
4. Excess digitalis
1. Non-paroxysmal AV junctional tachycardia associated with SA or AV block
11. The Stokes-Adams syndrome
• First described in 1719
• Transient syncope
• Decreased cardiac output
• Mostly due to brady-arrythmia
• mostly marked in the advanced/high grade AV block
12. ATRIOVENTRICULAR BLOCK
• Disturbance of impulse conduction
• Site of block
• AV node
• His bundle
• Bundle branches :RBBB OR LBBB
• Anatomic(SSS,MI)
• Functional impairment(Interference ,electrolyte, drugs)
• Permanent or transient
13. CLASSIFICATION OF AV BLOCK :3 TYPES
• First-degree heart block
• P marry QRS but PR is prolonged ≥ 200 milli sec
• Second-degree heart block
• Mobitz type I (Wenckebach): Progressive lengthening of PP until a P is not
conducted
• Mobitz type II : Sudden block of a P in the AV node without prior measurable
lengthening of PR interval
• Third-degree block: No conduction through AV node
• High-grade heart block : Blockage of two or more consecutive P
impulses
• Retrograde conduction can still occur
14. First Degree Atrioventricular Block
• Every P precedes a QRS
• PR >0.20 sec
• PR intervals as long as 1.0 sec have been reported that can at times exceed the P-P interval, a
phenomenon known as skipped P waves
• PR interval prolongation
• Conduction delay in the AV node (A-H interval) most common
• In the His-Purkinje system (H-V interval)
• At both sites
• Acceleration of the atrial rate
• Enhancement of vagal tone
• Carotid massage can cause first-degree AV nodal block to progress to type I second-degree AV
block
• Mobitz type-I AV block can revert to a first-degree block with deceleration of the sinus rate
16. 2nd degree Atrioventricular Block
• Blocking of some atrial impulses
conducted to the ventricle
• No physiological interference
• With or without previous PR
prolongation
• It can occur in first degree AV
nodal block or Mobitz-I block or
Mobitz-II
• Distinction is must among three
for precise treatment
17. Anterograde block ±retrograde conduction
• Top :Unidirectional block
• Bottom: 1:1 retrograde
conduction is seen during
ventricular pacing at a rate of 70
beats/min. P waves are indicated
by arrowheads
18. • The non-conducted P wave can be intermittent or frequent, can occur at regular or
irregular intervals, and may be preceded by fixed or lengthening PR intervals
• A distinguishing feature is that conducted P waves relate to the QRS complex with
recurring PR intervals; that is, the association of P with QRS is not random
• Electrocardiographically, typical type I second-degree AV block is characterized by
progressive PR prolongation culminating in a nonconducted P wave
• Type II second-degree AV block, the PR interval remains constant before the blocked P
wave
• In both cases, the AV block is intermittent and generally repetitive
• Eponyms Mobitz type I and Mobitz type II are applied to the two types of block, whereas
Wenckebach block refers to type I block only
• Wenckebach block in the His-Purkinje system in a patient with a BBB can closely
resemble an AV nodal Wenckebach block, the site of Wenchekbach block most
commonly occurs in the AV node
19. Special about Type I 2ND degree AV block
• Sometimes actual conduction times are not apparent on the ECG
• PR prolongation in SA, junctional, or ventricular exit block can be difficult to recognize
• In a typical type I block, the increment in conduction time is greatest in the second beat
of the Wenckebach group, and the absolute increase in conduction time decreases
progressively over subsequent beats
• These features serve to establish the characteristics of classic Wenckebach group beats:
1. The interval between successive beats progressively decreases, although the conduction time
increases (but by a decreasing function)
2. The duration of the pause produced by the non-conducted impulse is less than twice the
interval preceding the blocked impulse (which is usually the shortest interval)
3. The cycle that follows the non-conducted beat (beginning the Wenckebach group) is longer than
the cycle preceding the blocked impulse
4. Although much emphasis has been placed on this characteristic grouping of cycles, primarily to
be able to diagnose a Wenckebach exit block, this typical grouping occurs in fewer than 50% of
patients with a type I Wenckebach AV nodal block.
20. Mobitz Type I :Ladder diagram of typical 4:3 atrioventricular
Wenckebach cycle
23. 2:1 AV block
1. A form of second-degree AV nodal block
2. Every other P wave is not followed by a QRS complex
3. Causes
1. Mobitz type I AV block
2. Mobitz type II AV block
3. First degree AV block with skipped P (PR >1sec)
4. If the cause is Mobitz II AV block ,patient needs pacemaker
implantation
24. 2:1 AV BLOCK
MOBITZ TYPE I AV BLOCK
• AV nodal
• Influenced by sympathetic and
parasympathetic modulation
• Becomes normal with exercise
• Atropine improves AV conduction
• Carotid sinus message suppress SA
node ,allows AV node to recover
• IV Adenosine suppress SA node
,improves AV node
MOBITZ TYPE II AV BLOCK
• The block is below the AV node
• Least influenced by maneuver
• Electrophysiology is diagnostic
•
25. High-Grade Atrioventricular Block
• Intermittent relationship between atrial and
ventricular activity
• Conduction that is more impaired than in
second-degree AV block
• Some studies define high-grade AV block as
Mobitz type II second-degree or third-degree
AV block
• The ventricular rhythm will not be regular
• Commonly, two or more consecutive non-
conducted P waves are noted on ECG
• acute coronary syndromes, rheumatic heart
disease, autoimmune disorders, myocarditis,
and infiltrative cardiomyopathies
• Clinical presentation, symptoms, and
outcomes are indistinguishable from third-
degree AV block
26. Third-Degree Atrioventricular Block
• No atrial activity is conducted to the ventricles
• Atria and ventricles are controlled by independent pacemakers
• Complete AV dissociation
• Atrial pacemaker
• Sinus or ectopic (tachycardia, flutter, or fibrillation)
• AV junctional focus occurring above the level of block with retrograde atrial
conduction
• Ventricular Pacemaker
• The region of the block can be above or below the His bundle bifurcation
27. Third-Degree Atrioventricular Block
• Sites of ventricular pacemaker activity that are in or closer to the His
bundle appear to be more stable and can produce a faster escape rate
than those located more distally in the ventricular conduction system
• The ventricular rate in acquired complete heart block is less than 40
beats/min
• Congenital complete AV block :HR>50/BPM
• The ventricular rhythm
• Regular
28. Third-Degree Atrioventricular Block
• The level of block
• AV node : congenital
• Bundle of His
• Distal to the His in the Purkinje system
• Block proximal to the His bundle generally exhibits normal QRS complexes and rates
of 40 to 60 beats/min because the escape focus that controls the ventricle arises in
or near the His bundle. In complete AV nodal block, the P wave is not followed by a
His deflection, but each ventricular complex is preceded by a His deflection
• His bundle recording can be useful to differentiate AV nodal from intrahisian block
• Intrahisian may carry a more serious prognosis than the AV nodal block
• Intrahisian block is recognized infrequently without invasive studies
•
29. Third-Degree Atrioventricular Block
• AV nodal block :Atropine generally speeds both the atrial and the ventricular
rate
• Exercise can reduce the extent of AV nodal block
• Acquired complete AV block occurs most often distal to the bundle of His
because of trifascicular conduction disturbance
• Each P wave is followed by a His deflection, and the ventricular escape
complexes are not preceded by a His deflection
• The QRS complex is abnormal, and the ventricular rate is generally less than
40 beats/min
• A hereditary form of conduction block caused by degeneration of the His
bundle and bundle branches has been linked to the SCN5A gene, which is also
responsible for LQT3
30. Congenital third-degree AV block
• A: Complete AV nodal block
• No P wave is followed by a His bundle
potential
• Ventricular depolarization is preceded
by a His bundle potential
• B: Atrial pacing at CL= 500 msec)
• fails to alter the cycle length of the
junctional rhythm
• C:Ventricular pacing at CL 700
msec
• Suppression of the junctional focus
results for almost 7 seconds
(overdrive suppression of
automaticity).
31. Autonomic Mediated Bradycardia
• Autonomic Mediated Bradycardia
• Sinus pauses
• Sinus arrest
• Sinus arrhythmia
• Type I AV block
• Intermittent complete block
• Excess parasympathetic activity
• Hypersensitive carotid sinus syndrome
• vasovagal syncope, cough syncope
• Stimulation of the Bezold-Jarisch receptors during an inferior MI
• Sympathetic withdrawal
32. ECG
• Ventricular asystole
• Sinus arrest or SA exit block
• AV block
• Less noticed because suppressed SA node, atria and AV node together
• AV junctional or ventricular escapes
• Heightened vagal tone
• Sympathetic withdrawal
33. Three types of neural mediated bradycardia
• Cardioinhibitory response
• Defined as ventricular asystole exceeding 3 seconds
• Asystole exceeding 3 seconds during carotid sinus massage is not common
but can occur in asymptomatic subjects
• Vasodepressor response
• Defined as a decrease in systolic blood pressure (SBP) of 50 mm Hg or
more without associated cardiac slowing or a decrease in SBP exceeding
30 mm Hg when the patient’s symptoms are reproduced
• Mixed
34. TREATMENT
• Atropine is vagolytic
• Symptomatic may benefit from pacemaker implantation
• Vasodepression
• Inhibition of sympathetic vasoconstrictor nerves and possibly from activation
of cholinergic sympathetic vasodilator fibers
• Atropine and pacing do not prevent the SBP decrease
• Elastic support hose and sodium-retaining drugs
• Asymptomatic :No treatment
• Avoid Digitalis, methyldopa, clonidine, and propranolol
