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The Bradyarrhythmias: Disorders

of the Atrioventricular Node


Cells located in the AV node

-sit at a relatively higher resting membrane potential than surrounding atrial


and ventricular myocytes

exhibit spontaneous depolarization during phase 4 of the action potential

-have slower phase 0 depolarization (mediated by calcium influx in nodal tissue)


than that seen in ventricular tissue (mediated by sodium influx)
Compromise AV
Node

Bradycardia

Ineffective Ventricular rates

fatigue, syncope, and (if subsidiary


pacemaker activity is insufficient) even
death
Disturbance in AV conduction
SA activation and atrial systole may occur at normal or
even accelerated rates
Ventricular activation is either slowed or nonexistent.
 Acquired and persistent failure of AV conduction
-incidence: 200 per million population per year

 Permanent pacing is the only reliable therapy for


symptoms arising from AV conduction block.
STRUCTURE AND PHYSIOLOGY OF THE AV NODE
 AV conduction axis is structurally complex, involving the atria and
ventricles as well as the AV node

AV NODE
- Subendocardial structure originating in the transitional zone
- (Composed of aggregates of cells in the posterior-inferior right
atrium)
- Compact AV node: ~1 x 3 x 5 mm
- Situated at the apex of triangle of Koch
- Triangle of Koch
Posterior: coronary sinus ostium
Anterior: septal tricuspid valve annulus
Superior: tendon of Todaro superiorly
BLOOD SUPPLY:
AV Bundle:
 AV Nodal Artery
 first perforator of the left anterior
descending cor. artery

Bundle Branches:
 septal perforators of the left anterior
desc. Cor. Artery
 branches of the posterior descending
cor. artery
Innervation:

AV Node
-highly innervated with postganglionic sympathetic and
parasympathetic nerves.

Bundle of His and Distal Conducting System


-minimally influenced by autonomic tone.
 AV node complex are heterogeneous
with a range of action potential profiles

 Transitional zones- composed of cells


that have an electrical phenotype between
those of atrial myocytes and cells of the
compact node

 Atrionodal transitional connections: may


exhibit decremental conduction – slowing of
conduction with increasingly rapid rates of
stimulation
Myocytes of compact Node
-resting membrane potentials ~ - 60mV
-Action Potentials:
-low amplitudes
-slow upstrokes of phase 0 (<10V/s), and phase 4
diastolic depolarization
-high-input resistance
-relatively insensitive to external [K+]
ETIOLOGY OF AV CONDUCTION DISEASE
 Heightened vagal tone during sleep or in well-conditioned
individuals  associated with all grades of AV block.
 Carotid sinus hypersensitivity, vasovagal syncope, and cough and
micturition syncope  associated with SA node slowing and AV
conduction block.
 Transient metabolic and endocrinologic disturbances as well as a
number of pharmacologic agents may produce reversible AV
conduction block.
ELECTROCARDIOGRAPHY AND
ELECTROPHYSIOLOGY OF
AV CONDUCTION BLOCK
Electrocardiography
-diagnose AV block
- characterizes the severity of the conduction disturbance
- localizes the block
 AV conduction block manifests as:
- slow conduction in its mildest forms
- failure to conduct, either intermittent or persistently, in more
severe varieties
First Degree AV Block
-PR interval >200 ms
-slowing of conduction through the AV junction
- site of delay is typically in the AV node but may be in the atria,
bundle of His, or His-Purkinje system.

 Wide QRS: delay in the distal conduction system

 Narrow QRS: delay in the AV node proper or, less


commonly, in the bundle of His
Second-degree AV block
 -intermittent failure of electrical impulse conduction from atrium to
ventricle.
Mobitz type I (Wenckebach)
 Periodic failure of conduction is characterized by:
-progressively lengthening PR interval,
-shortening of the RR interval,
- a pause that is less than two times the immediately preceding RR
Interval on ECG
 The ECG complex after the pause exhibits a shorter PR
interval than that immediately preceding the pause
Mobitz type I second-degree AV block. The PR interval prolongs before the
pause, as shown in the ladder diagram. The ECG
pattern results from slowing of conduction in the AV node
Type II second-degree AV block (Mobitz II)
 characterized by intermittent failure of conduction of the P
wave without changes in the preceding PR or RR intervals
 typically occurs in the distal or infra-His conduction system
 often associated with intraventricular conduction delays
 More likely to proceed to higher grades of AV block
 may be associated with a series of nonconducted P waves, referred
to as paroxysmal AV block
 Implies significant conduction system disease and is an indication
for permanent pacing.
Paroxysmal AV block. Multiple nonconducted P waves after a period of sinus bradycardia
with a normal PR interval.
Third-degree (Complete)AV block
-Complete failure of conduction from the block is most often distal to
the AV node
atrium to ventricle -Wide QRS –block in the distal
His or bundle branches
-Narrow QRS
High-grade AV block –block in the AV node or
proxiaml His
-AV block that is intermediate between - escape rhythm originating in
second degree and third degree the AV junction
DIAGNOSTIC TESTING
Aim: determine the level of
conduction block particularly in
asymptomatic patients

These may provide diagnostic


 slow conduction in the AV node
information: but have less effect on
 Vagal maneuvers infranodal tissue
 may even improve conduction
 carotid sinus massage due to a reduced rate of
activation of distal issues.

 Exercise
 Improve conduction through
 Administration of drugs such as the AV node
atropine and isoproterenol  impair infranodal conduction.
 Congenital CHB and a narrow QRS complex
-exercise typically increases heart rate

 Acquired CHB, particularly with wide QRS,


- do not respond to exercise with an increase in heart rate.
Electrophysiologic testing
- may be indicated in patients with syncope and suspected highgrade
AV block
- relevant if noninvasive testing does not reveal the cause of syncope
- if the patient has structural heart disease with ventricular
tachyarrhythmias as a cause of symptoms.

 provides more precise information regarding the location of AV


conduction block and permits studies of AV conduction under
conditions of pharmacologic stress and exercise.
 Recording of the His bundle electrogram
- a catheter is positioned at the superior margin of the tricuspid
valve annulus
- provides information about conduction at all levels of the AV
conduction axis
- reveals local atrial activity, the His electrogram, and local
ventricular activation
 When simultaneously recorded with body surface ECG traces,
intraatrial, AV nodal, and infranodal conduction times
can be assessed
Management of AV Conduction Block

 Temporary or Permanent
Artificial Pacing
-most reliable treatment for patients
with symptomatic AV conduction system
disease.

 Correction of electrolyte derangements


and ischemia
May INCREASE
 Inhibition of excessive vagal tone
Heart rate
 Withholding of drugs with AV nodal
blocking properties
 Block in AV Node:
- Atropine or Isoproterenol may be useful

most pharmacologic treatment may take some time


to initiate and become effective, temporary
pacing may be necessary
 TRANSCUTANEOUS PACING
-Cathode – placed anteriorly over the cardiac apex
-Anode – placed posteriorly between the spine and scapula
OR above the right nipple
- highly effective in acute setting
- duration is limited by patient discomfort and longer-term
failure to capture the ventricle owing to changes in lead
impedance
TRANS-VENOUS TEMPORARY PACING
-can be placed from the jugular or subclavian venous system
and advanced to the right ventricle, permitting stable
temporary pacing for many days

PERMANENT PACEMAKER
-required for conduction block distal to the AV node

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