Heart Block

By

Dr. Shaaban Attiyah

Cardiologist

JGH

Introduction
Under normal condition, the SN is the pacemaker
function of the heart; which is a small comma
shaped of neuro-muscular tissue about 15mm
long & 5mm wide, lying in a groove
between the opening of the( the sulcus terminalis )
.SVC & the RA appendage
It supplied by the SN artery which is a branch
from either the RCA in about 60% of the
population or from the LCX in about 40% of the
population
The end of the SN fibers fuse with the
. surrounding atrial muscle fibers

The cardiac impulses are propagated from

;the SN through
Inter-atrial tract (Bachman bundle)-1
Is

a band of specialized muscle fibers that run from the

.SN to the LA
It conducts the cardiac impulse at rate of 1m/s

Inter-nodal tracts- 2

There are 3 bundles of specialized cells; the anterior,

.middle and posterior inter-nodal tracts

They connect the SN and AVN and conduct the cardiac

. impulse at a rate of 1m/s

AVN- 3
Is located in the posterior septal wall of the RA,
immediately behind the tricuspid valve adjacent to the
.opening of the coronary sinus
The rate of conduction of cardiac impulse in AVN is very
low, about 0.05m/s
;This extreme slow conduction may be due to
The sizes of the AVN fibers are smaller than the sizes of- 1
the normal atrial muscle fibers
The AVN fibers have resting membrane potential less -2
ve than the normal resting potential of the other cardiac
.muscle
Few gap junction connect the successive muscle cell in -3
AVN lead to great resistance to the conduction of
excitability from one cell to the next

Ventricular conduction-4
The impulses conducted through the AVN are
distributed to the ventricles over specialized
;fibers

AV bundle (bundle of His); is the continuation of the-1

AVN
and is located beneath the endocardium on
.the right-side
of the ventricular septum
Right-and Left bundle branches; Proceed on each side-2
of
the ventricular septum to their respective
.ventricles
The rate of cardiac impulse conduction in the AV bundle
and
its branches in about 1m/s

Continue

The AVN delayed the ventricular depolarization from 100150

ms after atrial depolarization.

This delay is important because ;

1- It delays the start of ventricular contraction till the end
of
atrial contraction which enhances the ventricular filling,
especially at the fast rate.
2- It protects the ventricles from the high pathological
atrial
rhythm.
The AVN can not conduct more than 150-200bpm

Continued
Purkinje fibers ; Arise from the bundle branches and- 3
extensively just
beneath the endocardium of both
ventricles, these cells have the
largest diameter in
the heart (70-80 um) & posses the highest
.conduction velocity of the cardiac impulse (4m/s)
This causes excitation of the whole ventricle as one unit
at the same
time leading to strong ventricular
.contraction
Ventriculal muscle depolarization ; occurs from the -4
. endocardial
surface to the epicardium
Depolarization initially reaches the surface of the heart at
.the apex and
the spread through the myocardium
The last area of the ventricle to depolarize is the base of
the LV
The conduction velocity of cardiac impulse in ventricular
myocardium is
about 1m/s

Factors affecting the cardiac conductivity

Nervous factors-1
Sympathetic stimulation increases the conductivity of the
cardiac impulse, while parasympathetic stimulation slow
.the conduction velocity
.Intense parasympathetic stimulation produces AVN block

Ions-2

Ca2+ ion ; hyper-calcaemia decreases the conduction

velocity of the cardiac impulse, while hypocalcemia
.increases it
K+ ion; hyperkalemia slow the conduction velocity of the
.cardiac impulse

Continued

Excess K+ ion concentration in extracellular fluid, block

the conduction
velocity of the cardiac impulse from the
.atria to the ventricles through the AV bundle
These changes lead to conduction disturbances e.g. Atrial
standstill, AVN block & increases cardiac ectopic activity
which may lead to VF

Drugs & chemicals- 3

Digitalis decreases the conduction velocity of the .cardiac impulse

Mild ischemia & hypoxia increases the conduction velocity of the

cardiac impulse while severe
ischemia & hypoxia decreases the
conduction
velocity of the cardiac impulse
Hypercapnia & acidosis decreases the conductivity of the cardiac
impulse, while hypocapnia and

Heart Block
SA block-1

First degree SA block*

Second degree SA block*
Third degree SA block*

AV block-2

First degree AV block*

Second degree AV block*
Third degree AV block*

Fascicular (intra-ventricular ) blocks-3

Unifascicular block*
Bifascicular block*
Trifascicular block*

SA block
.Is a minor arrhythmia that may become major
When SA block occurs, the SN fails to initiate one or more
stimuli or
there is a block or delay in the spread of
.the stimulus through the SN
into the atria
Therefore, neither the atria or the ventricles are
.stimulated & ECG
shows a long pause
;ECG

; SA block has been divided into several types

First-degree SA block; The ECG is not capable of-1

recording the electrical activity in the SN and this type of
.SA block cannot be recognized

Continued
Second-degree SA block; 2 types-2

Type 1; The PP interval become progressively shorter until

a long pause
occurs between two successive
.beats
Type 2 ; The long pause that occurs is a multiple of the
regular PP cycle.
If alternate beats drop out, the
heart rate will decrease to one
half and sinus
.bradycardia will occur
Third-degree SA block; is a characterized by standstill of -3
.the heart for a
variable period of time
It also called sinus arrest , sinus standstill, sinoatrial arrest
., sinoatrial
standstill and atrial standstill
.It may be transient or permanent
When a long period of SA block or sinus arrest occur, AV
.junctional or
ventricular escape beat may occur

Etiology
Second-degree SA block can be caused by excessive*
. vagal stimulation
in normal persons
; It also occur in many abnormal condition such as*
,acute myocarditis inferior infarction with occlusion of RCA and drugs such as digitalis , quinidine, acetyl choline,and .potassium salts
.It can also occur as apart of Sick Sinus Syndrome*
Third-degree SA block (sinus arrest ), does not occur
.* normally

Treatment
No specific treatment is needed if the pauses are short*
.and the patient does not have any symptoms
If the SA block is from drugs , the dosage should be*
.decreased or the
drugs stopped temporarily

If the patient has symptoms associated with slow heart*

rate or if the
SA block has produced frequent long
pauses ( with more than two
consecutive beats
missed ), atropine, isoproterenol, or even
.transvenous cardiac pacing may be necessary

AV block
First-degree AV block; during first-degree AV block, the*
conduction
time is prolonged but all impulses are
.conducted

Etiology

Degenerative changes in AV conduction system caused-1

;by
, aging , digitalis , exaggerated vagal tone & inferior ischemia .inflammation as myocarditis,& acute rheumatic fever .Cardiomyopathies-2

Continued

Second-degree AV block ; 3 forms*

Mobitz 1 ( wenckebach) ; is characterized by-1

progressive
lengthening
of conduction time until the impulse is not
.conducted

Mobitz 11 block ; sudden block of the-2

conduction of an
impulse without
.prior lengthening of the conduction time

Advanced second-degree AV block refers to-3

the distinct ECG finding of 2 or more consecutive
nonconducted sinus
.P-waves

Differences between type 1 & 11 seconddegree AV block

Type 11
( Mobitz 11)

Type 1 (Mobitz 1,
Wenchebach )

Infranodal ( intra-or
infra-Hisian )
Usually wide with
;infra-Hisian block
narrow with block
with intra-Hisian
block
Extensive AWMI
Degenerative
changes in His;purkinje system
Massive calcification
of mitral; or aortic

Usually AVN (supraHisian )

Usually normal in
width

Degenerative changes
; in AVN; IWMI
digitalis toxicity;
;
Myocarditis
Rheumatic fever ;

Site of
block
QRS
complexe
s

Causes

Type 11

Type 1

PR interval is usually*
normal
in duration &
constant in
.length
If PR interval is*
prolonged ,
the
duration of prolongation
is fixed
Blocked beat occur *
suddenly without
progressive
lengthening of the PR
interval

PR interval lengthen * ECG

progressively
until ventricular beat is
drpped
PR interval shortens*
.after
dropped beat
RR interval narrows
*
progressively up
to the
dropped
.
beat

RR interval of conducted* RR interval after the*

blocked beat
is
.beat is constant
always less than

Type 11
No effect

Type 1
May increase the
degree of block

Effect of
carotid
sinus
pressure
No effect
Frequently shortens
Effect of
PR interval & increase atropine
AV conduction
Escape focus infra-* Escape focus usually* Consequence
junctional
s of
;
junctional
(usually
progression
Narrow QRS*
ventricular )
complex; *Rate more to complete
Wide QRS *
heart block
than 45 bpm
;complex
Adams-Stoke attacks*
Rate less than 45*
uncommon
;bpm

Third-degree (complete )AV

block
.

Complete HB is an advanced form of block

.N0 impulse from the atria reaches the ventricles

Cardiac action is maintained by an escape rhythm
Escape rhythm arising in the bundle of His produces
.narrow QRS complexes at the rate of 50-60 bpm
Escape rhythm arising below the His bundle produces
.broad QRS complexes at the rate of 15-40bpm
. Exercise does not increase the heart rate

Clinical manifestation
In chronic CHB, pulse rate is slow (30-40bpm) , regular
. and does not vary with exercise
.First heart sound varies in intensity
.Wide pulse pressure
.Changing systolic blood pressure
Patient may be asymptomatic or may complain of
weakness or dyspnea if the heart rate is less than
.35bpm
Episodes of ventricular asystole may occur during periods
of transition from partial to complete heart block lasting
.several seconds to minutes

Continued
These episodes may cause cardiac syncope (also-called
Adams-Stokes
attacks)
These attacks often occur without warning, there is rapid
.loss of
consciousness and the patient may fall
Convulsions may occur if the heart does not begin to beat
again within
about 10 seconds and the death will result
if the arrest is prolonged

Management
HB complicating AMI
Acute IWMI is often complicated by transient AV -1
block which may
respond to atropine , 0.6mg
IV repeated as necessary, if it fails
.temporary pacemaker should be inserted
.In majority, AV block will resolve within 7-10 days
Second degree or CHB complicating anterior wall -2
infarction is usually a sign of extensive
.myocardial damage & carries a poor prognosis
Asystole often occurs & a temporary pacemaker
.should be inserted as soon as possible

If the patient presents with asystole, atropine -3

(0.6 mg iv repeated if
necessary) and
isoprenaline (1-5 mg in 500 ml 5% dextrose
infusion iv at minimum rate ) until a temporary
. pacemaker can be inserted

Continued

Chronic heart block

permanent pacemaker in patients with-1
symptomatic brady-arrhythmias with
complicating AV block
Asymptomatic first degree or Mobitz type 1-2
second degree AV block does not require
.treatment
Permanent pacemaker in patients with as a-3
symptomatic Mobitz type 11 second degree or
.complete heart block

Fascicular ( intra ventricular ) blocks

;A- Unifascicular block
types 4
.RBBB occur when right bundle of His is blocked- 1
LAH, occurs when anterior division of the left bundle of-2
.His is
blocked
LPH, occurs when posterior division of the left bundle of-3
His is blocked
LBBB, occurs when the left man branch of the bundle of- 4
His or both
branches ( anterior & posterior ) are
.blocked

Continued

B- Bifascicular block
types 2
RBBB with LAH or- 1
RBBB with LPH- 2

C- Trifascicular block
types 4

.Complete AV block with wide QRS complexes-1

RBBB with alternating LAH & with LPH-2
RBBB with LAH or LPH & with first or second-degree AV-3
.block
.Alternating right & left BBB-4