HEART BLOCK

PRESENTER--- Dr Sibadatta Das

MODERATER----Dr Indu Khurana
INTRODUCTION

 A "heart block" is a disease in the electrical

system of the heart

.Heart Block is a type of bradycardia

(too-slow heartbeat) that also is called
atrioventricular, or AV block.
Cunducting system of heart

S.A.NODE
Intranodal INTRA ATRIAL
tracts TRACT OF
BACHMAN

A.V. NODE

BUNDLE OF HIS

PURKINJE FIBRES
MEASUREMENT

 Done mainly by 2 way

 1 ECG (Non interventional)
 2 his bundle electrogram
 (interventional)
ELECTRO CARDIO GRAM

 Extra corporial measurement of summed

electrical activity of intigrated myocardial
tissue
 Interpreted as different waves like
 P Q R, S ,T etc.
 Ventricular
depolarization

Atrial
depolarization
Ventricular
repolarization
HIS BUNDLE ELECTROGRAM

Recording of electrical activity

of heart by intra cardiac ring
electrode placed near the
tricuspid valve

From comparative study

Ventricular
With ECG accurate site of block
depolarization
can be calculated

Transmission
Of impulse
Activation Through
of AV node His bundle
Comparative study

This is done by calculating 3 intervals

PA Int:-conduction from SA node to

AV node
normal— (27 ms)

AH Int:-AV nodal conduction time

( 92 ms)

HV Int:-bundle conduction
( 43 ms)
DISEASE TARGETS
SA NODE DISTURBANCES

 Occurs mainly in 2 ways

 1. sinus failure (failure of
impulse generation)

 2. sinus exit block (failure of conductance of impulse to

 atrium)
manifestation
 Mostly presented in 2 way
 1.SICK SINUS SYNDROM
 mostly found in old patients
 Presented as sudden dizziness , fatigue , &
syncope
 ECG:
 persistent bradycardia i.e recognised by a pause which is multiple of
PP interval or progressive shortening of PPinterval followed by a pause
 TACHY-BRADY syndrome
•reentry of ventricular stimulation causing

• atrial tachycardia followed by a pause.

•Then started with a slower rate .

•Again &again the cycle is repeated.

investigation

 24 hr holter monitering is the chief mode.

 Interpretation shd be done cautiously as
hyper vagotonia in athelates & sleep sinus
pause causes the same pattern
 Accurate detection occurs throiugh sinus
node electrogram and calculating the sinus
recovery time indirectly
TREATMENT

 Most of the patients are symptom free

 Symptomatic patients are difficult to treat
 Oral theophylin is some how effective
 But most of the patients require pace maker
 Permanent pace maker is the T/t of choice in
recurrent symptomatic Pt.s
 Dual chamber pace maker is preferred as SA
node dysfunction is usually associated with
AV node dysfunction.
Affected AV Node

This is mainly affected by 3 ways

1. First degree AV block.
2. Second degree AV block.
3. Third degree AV block.
First degree AV block

 All the impulses from atria

reaches ventricle but delay
occurs in conduction.
 Etiology is not specified
 ECG is almost normal
except prolongation of PR
interval hence it is sited as
diagnostic criteria
 PR interval > 0.2s is almost
diagnostic
second degree AV block
(intermittent AV block)
 Not all impulses arising from atria reach
ventricle
 2 types
. Mobitz I
. Mobitz II
 Mobitz I
(Wenckebach AV block)
 PR interval gradually prolongs
till 1 P wave is dropped.
 After dropped P wave the PR
interval is shorter than the last
long PR interval.
 The difference between
longest & shortest PR interval
> 100 ms.
 ETIOLOGY :
 inferior wall infarction
 drug intoxications like digitalis,
β blockers, Ca channel
blockers etc.
 Mobitz II
 There is sudden stoppage of
conduction without previous
change in PR interval.
 So, 2 to 3 consecutive P wave
comes following 1 QRS complex
accordingly it is named as 2:1
or 3:1 block.
ETIOLOGY :
 Anteroseptal infarction
 calcific disease of fibrous
skeleton of heart
 Typically it has a tendency to
proceed towards complete heart
block
 THIRD DEGREE HEART BLOCK

 No atrial impulse conducted

into ventricle
 QRS complex comes alone
in ECG
 P wave has no relation with
the QRS complex
 Rate is
 as per AV node rhythm I;e
40-45/min with normal QRS
complex
 Or as per HIS-PURKINJE
rhythm i.e 15-40 /min with
wide QRS complex.
Bundle branch block
 Etiology – long standing HT
 severe valvular disease
 cardio myopathy

 Typical manifestations found in ECG is opposite direction of T wave to that

of QRS complex due to reverse direction of repolarization

 2 types

RIGHT BUNDLE-BRANCH BLOCK

LEFT BUNDLE-BRANCH BLOCK

 RIGHT BUNDLE-BRANCH BLOCK

•Electrical impulse cannot travel

through it to the right ventricle

• Activation reaches the right

•ventricle by proceeding from the
• left ventricle.
•It then travels through the septal
and right ventricular muscle mass
•This progress is, of course,
slower
•leads to a QRS-complex wider than
0.1 s
•QRS >0.12s is diagnostic
 RBBB causes an abnormal
terminal QRS-vector that is
directed to the right
ventricle (i.e., rightward and
anterior). This is seen in the
ECG as a broad terminal S-
wave in lead I.
 Another typical
manifestation is seen in
lead V1 as a double R-
wave. This is named an
RSR'-complex
 LEFT BUNDLE-BRANCH
BLOCK

The situation in left bundle-branch block (LBBB)

is similar, but activation proceeds in a direction
opposite to RBBB.

Again the duration criterion for complete block is QRS > 0.12s

.
Because the activation wave front travels
in more or less the normal direction.

However, because of the abnormal sites of initiation

of the left ventricular activation front and the
presence of normal right ventricular
activation the outcome is complex seen as a broad
and tall R-wave, usually in leads I, aVL, V5, or V6.
OTHER COMBINATIONS OF
BLOCK
 BIFASCICULAR BLOCK
RBB + Lt. Ant. Fascicle block
or
Rt. Ant. Fascicle block
 TRIFASCICULAR BLOCK
Bi fascicular block + PR prolongation etc.
CONCLUSION

 Still an enigma for medical science

 Highly unpredictable in character
 Through out monitoring is essential
 Non interventional T/t option is rare is present day
scenario.
 Hope is there for something better in future days.
REFERENCES

 Text book of physiology 1st- Indu khurana

 Review physiology 22nd-Ganong
 Physiology 13th- Samson wright
 Internal medicine16th- Harrison
 Clinical diagnosis of ECG- K.P. Mishra