1. Heart Block Diagnosis, Ecg, and Aetiology Dr B A Animasahun

2. Case presentations
Introduction
Epidermiology
Types
Clinical features
Diagnosis

3. The normal conduction pathway

4. Conduction velocity Atrial Myocardium 1000mm/s AV node 200mm/s
His-purkinge System 4000mm/s
Ventricular myocard 400mm/s

5. Other levels of potential pacemaker sites are
AV node (NH region)
The ventricle
Have progressively lower automaticity than that of SA node
In SA node failure or excessive slowing, a lower pacemaker site takes over the pacemaker function (escape beat)

6. Definition of heart Block
AV (heart block) block is a disturbance in conduction between the normal sinus impulse and the ventricular response.
Severity varies

7. First degree
Second Degree
Third degree
Sinus Rhythm
Yes
In some
Drop beats No
some
QRS configuration
Normal

8. First degree Prolong cond 1:1
Second degree intermittent <1:1
Type I wenkeback block AV node
Type II Mobitz His- Pur
Third degree No conduction at all
Complete heart block
-Congenital
-Acquired

9. Case 1 Case 2 Master Y, 12 years Chest pain Palpitation x 5years
Headache on/off
syncopal attacks (3x in the last 5 years)
No family hx of sudden death
On Alupent in the last 2 years
PR of 53/min irregular
BP of 110/54
ECG- AR of 120, VR of 45, axis of +90
CXR = N
Echo= N
Admitted urgently for PPI
Discharged
Master D, 13 years
Giddiness
x2 weeks
Not on any medication
PR of 50/min irregular
BP of 110/60
ECG- AR of 120, VR of 50, axis of +90

10. Case 3 Case 4 Kum A, 10 years, F, 256870 Pre-op
CXR= RV apex, dilated hilar PAs
ECG= NSR, 80bpm, axis 90
RVH, No q in V6.
Echo= CoA with PDA
Repair of Coact + PDA ligation
Post up
JET initially
HR=
On Alupent
C/o syncopal attacks
Holter
Intermittent 2:1 AV block
Occational V Pc
still on observation
Kum San, 11years, F
Large VSD with severe PAH
Uneventful and in the ward
Irregular HR picked on ward round
ECG showed VT
Had cardiac arrest
Syncronised cardioversion
AV dissociation with ventricular ectopics
VVIR - stable

11. Case 5 Case 6 Baby S O, 23 months, F, 236281 Pre-op Echo A, D , S
Large prirmium ASD amounting to CA
Cleft MV
Grade II MR
Moderate TR
Interrupted IVC
Bilateral SVC
CXR= RV apex, dilated hilar PAs
ECG= NSR, 91bpm, superior axis
Had partial Av canal repair done
Developed persistent bradycardia
Pericardial pacemaker inserted after 3 weeks
Baby G, 5 months, F,
DILV
DORV
ASD, PS
VSD, PDA
Pre-op ECG= NSR
Had BT shunt on 23/03/09
On routine folllow up
HR= 50/min, regular
ECG= AR=120, VR= 50
VVIR done

13. Complete heart block
This is a defect in the electrical system of the heart in which impulses generated at the atrial( typically SAN) does not propagate to the ventricles,
Because the impulses is blocked an accessory pacemaker below the level of the block will typically activate the ventricle
This is known as escape rhythm

14. Two independent rhythm will be noted on ECCG
One will activate the atrial and create the p-wave
The second will activate the ventricle and produce the QRS complex, typically with a regular R-R interval.
PR intervall will be variable
Hallmark is no apparent relationship btw P wave and QRS complex

15. Pathophysiology Conduction block at the level of AV node
Bundle branch purkinje system
20% block occur within AV node
<20% block occur within His bundle
61% block occur below the His bundle

16. Duration of QRS complex depends on the site of the block and site of the escape rhythm pacemaker
AV node
escape from junctional pacemaker
rate of bpm
haemodynamically stable
heart increase in response to exercise and atropine.

17. When the block occur below the AV
-escape rhythm arise from His bundle or bundle branch purkinje system
-rate is < 45bpm
-generally haemodynamically unstable
-heart rate unresponsive to exercise and to atropine
Congenital complete heart block usually occur at the level of AV node.

18. Aetiology
Congenital
Acquired

19. Congenital heart block
A. Isolated
B. Associated with structural heart dx A
Transplacental passage of Anti-Ro and Anti- La (ribonuclear proteins)
Damae to the AV node by inflammation in the early stage and fibrosis later B.
Failure of the conduction system to develop

20. Congenital heart defects
AV canal defects
L-TGA
Left atrial isomerism
(Abnormalities of bulboventricular looping)- fibrous distruption btw Atrium and AV node or absence of penetrating bundles of the AV node
Holt- Oram syndrome- TBX5
NKx2.5
Storage disorders e.g Hurler’s and hunter’s syndrome

21. Physical examination Bradycardia Sign of CCF as a result of low CO
Tarchypnoea or Rs distress
Hypotension
Lethargy
If pt is having concormittant iscahemia
Anxiety, agitation, unease
Diaphoresis
Pale or pasty complexion
Regularised AF is the classical sign of CHB if due to digoxin toxicity

22. CAVB
Discoid skin lessions may be an associated finding
LCOS may manifest with Irritability, lethargy
Cool skin, mottling, cyanosis
Child with neonatal lupus can present with rash, neurological and hepatic maifestation, rash can occur some day after birth and is worsened by sun exposure
Annular or elliptical erythematous plaque canbe present on the skin, face,scalp and extremeties.
Those with structural heart disease may present with cyanosis, rs distress

24. Acquired Intracardiac surgery ( incidence now < 5%)
May be transient, risk of recurrence
ASD, VSD,TOF, TAPVC (cardiac) , MVR,
Relief of ventricular outflow obstruction in Hyp Cardio, single ventricle with a subaortic out flow chamber, konno procedure for relief of sub-aortic stenosis
Injury to the conducting system during RF
Ablation.

25. Cardiomyopathies and other infectious diseases
Lyme carditis
Trypanosoma cruzi infection
Acute rheumatic fever
Diphteria
Viral Myocarditis
Bacteria endocarditis
Metabolic
Severe hyperkalemia
Drugs
Class 1a, 1c,II,III,IV,Digoxin and other cardiac glycosides
Genetic disorders like-muscular dystropies, myotonic dystropies,
Kearns-sayre syndrome
Profound hypervagotonicity
Coronary iscahemia
MI in adults

26. Clincal features Most patients are symptomatic
Sym due to hypoperfusion
-fatique
-dizziness
-impaired exercise intolerance
-chest pain
Pt with narrow complex escape( escape above His bundle) are more likely to have minimal sym.

27. Pt are commonly profoundly symptomatic esp if a wide complex escape
Syncope
Confusion
Dyspnoea
Severe chest pain
Nausea, vomitting
Diasphoresis esp with MI
Sudden death

28. CAVB Mother may have hx of fetal loss
Mother is often completely asymptomatic or have diagnosis of collagen vascular disease e.g SLE, Sjogren syndrome
Incidental finding of bradycardia or hydrops fetalis
Newborn may present with hydrops
Newborn may also be asymptomatic or have near normal ventricular rates

29. Investigation ECG QT interval may be prolong
Holter Initially and periodically
Exercise testing regularly esp in those > 7yrs
Electrophysiologic studies- not done routinely
Histology- not routine

30. CXR-
Cardiomegaly,effusion, visceroatrial discordance, midline liver, rightward stomach bubble, dextrocardia
Echo- initially and periodically
Structural heart disease
Cardiac function, effusion
Eletrolyte-K
CBC
Anaemia, neutropenia,thrombocytopaenia

31. Neonatal lupus
Anti-Ro, anti-la- preferably ELISA in mother
Myocarditis
HIV
Cardiac troponins and BNP
Cardiomyopathy
Lysosomal storage disease-if hypertrophic
CHD
Pre and post ductal saturation
ABG
Heinz bodies-asplenia