This document provides an overview of normal cardiac impulse conduction and various cardiac arrhythmias based on electrocardiogram (ECG) findings. It describes the pacemaker tissues of the heart and normal P wave, PR interval, QRS complex, and ST-T wave patterns on ECG. Common arrhythmias are then summarized, including sinus bradycardia, sinus tachycardia, heart block, atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation. For each arrhythmia, the document outlines key ECG features and potential underlying causes. The goal of the document is to provide guidance on systematically interpreting ECGs

1. ECG INTERPRETATION
AND
ARRYTHMIAS
By Dr Victor Ngo Jia Tong
Supervised by Dr Michelle
TheMoreY
ouSee,The
MoreY
ouKnow

3. N
o
r
m
a
lI
m
p
u
l
s
eC
o
n
d
u
c
t
i
o
n
Sinoatrial node
A
Vnode
Bundle of His
Bundle Branches
Purkinje fibers

4. P
a
c
e
m
a
k
e
r
softheH
eart
● SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100
beats/minute.
● A
VNode - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.
● Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.

5. The P-wave indicates the electricalactivity
associatedwith contraction of the cardiac atria, the
heart's upperchambers.

6. ● The P-R interval is the delay
between the beginning of
activity in the atria and the
ventricles (atrio-ventricular
conduction time)

7. ● The QRS complex indicates the
onset of contraction of the
ventricles.

8. ST-T wave:ventricular
repolarization

9. The T-wave indicates when the
electrical activity associated with the
cells in the cardiac ventricle returns to
the resting state after electrical
activation -ventricular repolarization

10. The best way to interpret an ECG is to do it step-by-step
Rate
Rhythm
CardiacAxis
P – wave
PR - interval
QRS Complex
ST Segment
QT interval (Include T and U wave)
Other ECG signs

12. SINUS RHYTHM

14. ARRHYTHMIAS

15. Arrhythmia Formation
Arrhythmias can arise from problems in the:
• Sinus node
• Atrial cells
• A
Vjunction
• Ventricular cells

17. SANode Problems
The SANode can:
● fire too slow
● fire too fast
Sinus Bradycardia
Sinus Tachycardia
Sinus Tachycardia may be an appropriate
response to stress.

18. SINUS BRADYCARDIA

19. ● A sinus rate of less than 60 bpm
Normal in atheletes and elderly
● Causes: hypothermia,
hypothyroidism, raised ICP, drugs
( B blocker, Digitalis),acute
ischemia and infarction , chronic
degenerative changes eg:
fibrosis of atrium or sinus nodes
● Rx: asx; no treatment
● Rx: sx ; atropine /pacemaker

20. SINUS ARRYTHMIA

21. ● changing sinus node rate
with the respiratory cycle,
on inspiration and
expiration.
● Thus , during inspiration,
parasympathetic tone
falls and the heart rate
quickens and
● On expiration, the heart
rate falls.
● Normal- particularly in
children and young adult.

22. SINUS TACHYCARDIA

23. ● Sinus rate acceleration to
more than 100bpm
● Causes: fever, pain, anemia,
thyrotoxicosis, pregnancy,
emotion, exercise etc
● Rx: correction of condition
causing the tachycardia.
● B blocker may be used to
slow the rate

24. HEART BLOCK

25. 1
s
t Degree Heartblock
● Prolongation of PR interval > 0.2s ( > 5 small boxes)
● No drop beats
● Every atrial depolarization is followed by conduction to the ventricle but
with delay somewhere along the conduction pathway
● Depend on the cause, does not cause haemodynamic disturbance
● No specific treatment is required

26. ● Causes ; Increased
vagal tone, Athletic
training, Inferior MI,
Mitral valve surgery,
Myocarditis (e.g. Lyme
disease),Electrolyte
disturbances (e.g.
Hyperkalaemia),AV
nodal blocking drugs
(beta-blockers,
calcium channel
blockers, digoxin,
amiodarone), May be
a normal variant

27. 2nd Degree Heartblock MOBITZ I (WENCKENBACH)
●
● Constant atrial rate
● Ventricularrate :irregular,
● Progressive lengthening of PR interval, then failure of conductionof an atrial beat followed by a
conducted beatwith a short PR interval then repetitionof this cycle
● Veryrarely progressto complete heartblock
● Does not require pacing unless hemodynamically compromised

28. Causes of Wenckebachphenomenon
● Drugs: beta-blockers,calcium
channel blockers,digoxin,
amiodarone
● Increasedvagal tone (e.g.
athletes)
● InferiorMI
● Myocarditis
● Following cardiac surgery(mitral
valve repair,Tetralogyof Fallot
repair)

29. 2ND DEGREE HEART BLOCK MOBITZ II
● Atrial rate : regular and unaffected
● Ventricular rate : less than atrial rate
● PR interval is constant.
● P wave is normal , each will be followed by QRS except the blocked P
wave.
● Common site of block: His-Purkinjee system
● May progress to complete heart block
● Causes : degenerative disease of the conducting systems,Anteroseptal MI
● Rx: permanent pacemaker

30. Causes of Mobitz II
● Anterior MI (due to septal infarction with
necrosis of the bundle branches).
● Idiopathic fibrosis of the conducting system
(Lenegre’s or Lev’s disease).
● Cardiac surgery (especially surgery occurring
close to the septum, e.g. mitral valve repair)
● Inflammatory conditions (rheumatic fever,
myocarditis, Lyme disease).
● Autoimmune (SLE, systemic sclerosis).
● Infiltrative myocardial disease(amyloidosis,
haemochromatosis, sarcoidosis).
● Hyperkalaemia.
● Drugs: beta-blockers, calcium channel
blockers, digoxin, amiodarone

31. 3RD DEGREE HEART BLOCK
● Occurs when atrial contraction is normal but no beats are conducted to ventricles.
● Atrial rate :unaffected
● Ventricular rate: slower
● Atrial + ventricular rhythm are regular.
● Causes : MI ( usually transient), fibrosis around bundle of His
● Rx: Atropine 0.5 mg IV max 2 mg or transcutaneous pacing
● Persistent symptomatic ; permanent pacemaker

32. Causes ofcomplete heart block
The causes are the same as forMobitz I and
Mobitz II second degreeheart block.The most
important causes;
● Inferiormyocardial infarction
● AV-nodalblocking drugs (e.g.
calcium-channel blockers,
beta-blockers,digoxin)
● Idiopathic degenerationof the
conducting system (Lenegre’sorLev’s
disease)

33. Bradycardia(HR
< 60 bpm)
P waves
absent
P waves
present
P>QRS
P=QRS
Escape rhythms
(junctional and
ventricular)
Slow atrial
fibrillation
Irregular QRS Regular QRS
PR fixed
3rd Degree
Heart Block
Mobitz II
Progressive
lengthening of PR
Mobitz I
Sinus bradycardia
Sinus arrhythmia
2nd degree
Heart Block

35. ATRIALFIBRILLATION

36. ECG FEATURES
Irregularly irregular rhythm.
No P waves.
Absence of an isoelectric baseline.
Variable ventricular rate.
QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate
related aberrant conduction.
Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude
>0.5mm).
Fibrillatory waves may mimic P waves leading to misdiagnosis.
Commonly AF is associated with a ventricular rate ~ 110 – 160.
AF is often described as having ‘rapid ventricular response’ once the ventricular rate is > 100 bpm.
‘Slow’AFis a term often used to describe AFwith a ventricular rate < 60 bpm.
Causes of ‘slow’AFinclude hypothermia, digoxin toxicity, medications, and sinus node dysfunction.

38. RHYTHM CONTROL
Pharmacological or
electrical
cardioversion
Electrical
cardioversion
preferred when
patient
hemodynamically
unstable

41. R
A
T
E
C
O
N
T
R
O
L

44. ATRIALFLUTTER

45. ECG FEATURES
Narrow complex tachycardia
Regular atrial activity at ~300 bpm
Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF —may be more
easily spotted by turning the ECG upside down!
Flutter waves in V1 may resemble P waves
Loss of the isoelectric baseline

49. SUPRAVENTRICULAR
TACHYCARDIA

50. ECG FEATURES
Regular tachycardia ~140-280 bpm.
QRS complexes usually narrow (< 120 ms) unless pre-existing bundle branch
block, accessory pathway, or rate related aberrant conduction.
ST-segment depression may be seen with or without underlying coronary artery
disease.
QRS alternans – phasic variation in QRS amplitude associated with AVNRTand
AVRT, distinguished from electrical alternans by a normal QRS amplitude.
P waves if visible exhibit retrograde conduction with P-wave inversion in leads II,
III, aVF.
P waves may be buried in the QRS complex, visible after the QRS complex, or very
rarely visible before the QRS complex.

53. VENTRICULAR
TACHYCARDIA

54. ECG FEATURES
• broad QRS complexes (>0.14s)
• Ventricular rate 100-200/min.
• Fusion Beats
• AV dissociation
• Sustained – lasted more than 30 sec or associated with immediate hemodynamic
collapse

58. VENTRICULAR
FIBRILLA
TION

59. ECG FEATURES
Chaotic irregular deflections of varying amplitude
No identifiable P waves, QRS complexes, or T waves
Rate 150 to 500 per minute
Amplitude decreases with duration (coarse VF →fine VF)

62. THANKYOU