Heart Block ppt by siba

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

A.V. NODE

BUNDLE OF HIS

PURKINJE FIBRES

INTRA ATRIALTRACT OFBACHMAN

Intranodaltracts

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.

Atrial depolarization

Ventricular depolarization

Ventricular repolarization

HIS BUNDLE ELECTROGRAM Recording of electrical activity

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

From comparative studyWith ECG accurate site of block

can be calculated

Activation of AV node

Transmission Of impulseThroughHis bundle

Ventriculardepolarization

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 ventricularactivation 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