houseman teaching

1. ECG
Houseman
Teaching
Emergency
Department
Hospital Ampang

2. ECG BASICS

3. System For Reporting
3 Initial Features:
• Rate (and regularity)
• Rhythm
• Axis
Waves and Intervals: PQRST
• P wave, PR interval
• QRS complexes
• ST segment
• T waves
• QT interval

4. Calibration
• Should be calibrated to 25mm/sec and l0mm/mV
• Calibration spike = 1 mV for 0.2 sec
• 1 large square = 200msec
• 1 small square = 40msec

5. Calculating rate
• Alternatively, count the number of QRS complexes in the rhythm strip
and multiply by 6. (ECGs record over 10 seconds)
• Heart Rate = Number of QRS complexes x 6

6. What is the heart rate?

7. What is the heart rate?

8. Rhythm
What do we mean when describing
rhythm?
• The place where the action potential
starts.
•Sinus rhythm ➔ the action potential
starts at the sinus node.

9. Rhythm
What is a normal rhythm?
• Sinus rhythm
How do you know if the heart is in sinus rhythm?
• The SA node is in the top right of the right atrium.
• The impulse will spread downwards, forwards and to the left.
Therefore, in sinus rhythm:
• P waves upright: lead II
• P waves inverted: lead aVR
• Each P wave looks the same (within the same lead).

10. What is the rhythm?
• Upright in lead II?
• Inverted in lead aVR?

11. What is the rhythm?
• Upright in lead II? Initially sinus rhythm
• Inverted in lead aVR? P waves changed (arrow) ➔ no longer in sinus rhythm

12. Cardiac axis
What is the cardiac axis?
•The average direction of the electrical potential during depolarisation
of the ventricles.
Could calculate an axis any part of the ECG (e.g. the P wave axis or the T
wave axis).
Normal range of the QRS axis?

14. Cardiac axis

15. Cardiac axis

16. The P Wave
Physiology: atrial depolarization
In sinus rhythm:
• P waves upright: lead II
• P waves inverted: lead aVR
• Same shape
Check:
• Size - e.g. Tall in right atrial enlargement (>2.5mm)
• Shape - e.g. Bifid in left atrial enlargement
• Followed by a QRS - e.g. heart block

17. PR interval
Start of P wave to start of QRS complex.
Physiology: atrial depolarisation and contraction
Normal range:
• 120-200msec (3-5 small squares)
Abnormalities:
• Prolonged (> 1 big square) - Heart (AV) block
• Short (<3 small squares) - Pre-excitation (e.g. WPW)

18. What is the PR interval?

19. What is the PR interval?

20. QRS complex
Physiology: ventricular depolarisation
Look for:
1. Width (narrow or wide)
2. Height
3. Shape
i. Q waves
ii. R wave progression
iii. Bundle branch blocks
Normal QRS duration?
• < 120msec (3 smaII squares)

21. QRS complex
Why is it important to note that the QRS complex is narrow?
• Narrow QRS ➔ normal VENTRICULAR conduction
(Action Potential: AV node ➔ Bundle of His ➔ Bundle Branches ➔ Purkinje
fibres)
• Wide QRS ➔ abnormal ventricular conduction
(bundle branch block, ventricular origin, accessory pathway, etc.)
A wide QRS complex will cause ST-segment and T wave changes.
What is the significance of the QRS height?
• Tall QRS complex ➔ ventricular hypertrophy

22. Q Waves
• Definition: If the FIRST deflection of the QRS complex is downwards
➔ Q wave
Physiology: normal left to right depolarisation of the septum.
• Usually seen in the left sided leads (I, aVL, V5-6)

23. Abnormal Q Waves
Pathological if any of:
• >40msec ( l small square).
• >2mm deep (may be a normal variant in leads Ill and aVR).
• >25% of the height of the following QRS.
• Present in leads V l -3.
Basically, Q waves are abnormal if they're big.
Most commonly due to previous myocardial infarction.
• Permanent so cannot tell the age of the infarction.

24. Are there abnormal Q waves?

25. Are there abnormal Q waves?

26. Are there abnormal Q waves?

27. Are there abnormal Q waves?

28. R wave progression - Chest Leads
• Ventricles depolarize down and towards the LEFT
• Right sided leads (V1) -> Negative
• Left sided leads (V6) -> Positive
- Should be a smooth transition
- When R>S this is labelled the transition point
- Normal transition point in V3-V4.
- Abnormal R wave progression in anterior MI, LVH, RVH, others.

30. ST Segment
 Physiology: no electrical activity
- ventricles are depolarised
 Look for:
a) Elevation
b) Depression
c) Shape (concave up, concave down, horizontal, etc.)
lschaemia can cause ST elevation or depression
Many other causes:
• Pericarditis, LBBB, benign early repolarisation, L VH, L V aneurysm, etc.

31. Are the ST segments deviated?

32. Are the ST segments deviated?

33. Are the ST segments deviated?

34. Are the ST segments deviated?

35. T Waves
Physiology:
• Ventricular repolarisation.
Anything that disrupts depolarisation usually affects repolarisation
Abnormal T waves in:
• lschaemia
• Bundle branch blocks, ventricular hypertrophy, any prolonged QRS

36. T Waves
Check:
• Orientation: (upright or inverted)
• Height
Usually inverted in Vl and aVR
- Occasionally inverted in V2 and inferior leads (II, Ill and aVF) - non-
specific.

37. QT interval
• Start of the QRS complex until the end of T wave.
• Physiology: ventricular depolarisation and repolarization.
- Varies with heart rate.
Corrected heart rate
Prolonged if:
• QTc >440msec in men
• QTc >460msec in women
QTc >500msec is associated with an increased risk of Torsades de Pointes VT

38. Is the QT interval normal?

39. Is the QT interval normal?

40. Sample ECGS

41. ECG 1

43. ECG 2

45. ECG 3

47. ECG 4

49. ECG 5

51. ECG 6

53. TACHYARRYTHMIAS

54. Tachyarrhythmias
• Tachycardia Definition: HR > 100
• Treatment depends on:
• Presence or absence of hemodynamic compromise
• Type of tachycardia
• Look for:
• Wide vs Narrow complex
• Regular vs Irrefular
• P waves

55. Types of Tachycardias
• Narrow-complex tachycardia
• Atrial Fibrillation (AF) – irregular
• Atrial flutter
• Sinus tachycardia
• SVT
• Wide-complex tachycardias
• Ventricular tachycardia
• SVT with aberrancy
• SVT with pre-excitation (eg: Wolf-
Parkinson-White)

56. Identify The Origin Of A Beat
• Use the P wave and QRS morphology
to identify where a beat originated
• Example: Sinus beats
• Sinus P wave (upright in ll and
inverted in aVR)
• Followed by a normal QRS

57. • Sinus beats:
• Normal P wave
• Normal (narrow) QRS
• Atrial Beats:
• Abnormal P wave
• Normal (narrow) QRS
• Junctional (AV nodal) Beats:
• P wave absent (buried in QRS), or
• Abnormal P wave just before/after
QRS
• Narrow QRS
• Ventricular beats:
• Wide QRS, abnormal T wave
• No P wave

60. Atrial Fibrillation
• Disorganised activation of the atria (termed fibrillation)
• No P waves – unstable baseline
• Irregular ventricular rate
• ECG features:
• Irregularly irregular rhythm
• No P waves
• Unstable baseline – may have fine or coarse ‘fibrillatory wave’
• Narrow QRS complex (unless other conduction pathology)

61. Atrial Fibrillation
• This is the most common sustained arrhytmia
• Treatment of AF can be complicated
• Rate control
• Rhythm control
• Stroke risk and anticoagulation – CHA2DS2-VASc Score

64. Atrial Flutter
• Re-entry circuit in right atrium
• Organised atrial activity  P waves
• Atrial rate usually ~ 300
• Usually a 2:1 AV block  ventricular rate 150
• ECG features:
• Narrow complex tachycardia
• Ventricular rate 150 with atrial rate 300
• Flutter waves  “sawtooth pattern” – best seen i
n
ll, lll, aVF
• May resemble P waves in V1

66. Wolff-Parkinson-White Syndrome = AVRT
• An accessory pathway allows conduction of electrical impulse into the
ventricles at a site other than the AV node.
• This allows “pre-excitation” of the ventricles  delta wave
• ECG features:
• Short PR interval (<120msec)
• Delta wave (slurred upstroke of the QRS complex)
• Slight prolongation of the QRS complex
• ST and T wave changes
• Tachycardias arise from re-entry pathways involving the accessory
pathway

68. Supraventricular Tachycardia (SVT)
• Technically, this refers to any tachycardia originating in the atria or AV node
• Every example so far has been a type of SVT
• Sometimes SVT is used to imply AVNRT
• ECG features:
• Narrow complex tachycardia – unless other conduction defect
• May be regular or irregular

70. V
QRS Complexes: Wide
Regular vs Irregular: Regular
, . P waves: Absent
I 1- •• - ••
- ---
y _ _ _[
-
1
1 •·-- -, - ·J
-
Interpretation: Ventricular Tachycardia
1
1
w
.i
, . . . .. ..... - - ..
• ••• • • ••
l
I I

71. Wide Complex Tachycardia
• Ventricular Tachycardia until proven otherwise!!
• Differentials
• Ventricular tachycardia
• Supraventricular tachycardia with aberrancy (eg Bundle branch block)
• Supraventricular tachycardia with pre-excitation (WPW)

72. Ventricular Tachycardia (VT)
• Ventricular origin  wide complex
• Defined as ≥ 3 ventricular beats (>30 sec = sustained VT)
• Types
• Monomorphic VT  all QRS complexes about the same shape
• Polymorphic VT (torsades de pointes)  changing QRS amplitude (appears t
o
rotate)
• Shockable rhytm

73. VT vs SVT with aberrancy
• Many different criteria to help clarify this. None are perfect
• The following may help:
• AV dissociation
• Fusion beats
• Capture beats
• Extreme axis deviation (‘northwest axis’)
• If in doubt  treat as VT

75. Ventricular Fibrillation (VF)
• Shockable rhythm
• Chaotic irregular baseline
• No identifiable P, QRS or T wave
• Amplitude decreases with time: course VF  fine VF  a
s
y
s
t
o
l
e

77. Conduction Disease and
Bradyarrhythmias

78. Cardiac Conduction System

79. Conduction Disease
• Normal conduction:
• SA node ➔ AV node ➔ Bundle of His/
Purkinje system
• Disease at the AV node:
• ➔ AV block (heart block)
• Disease in the bundle branches of fascicles:
• ➔ Bundle Branch blocks
• ➔Fascicular blocks
• If no impulse arrives at all ➔ Escape
rhythm

80. Escape Rhythms
• If the SA node does not fire, another area may take over
• ➔ Escape rhythm/ beats
• The more distal the origin of the escape rhythm, the slower the rate:
• SA node: 70-80 bpm
• AV node: 40-60 bpm
• Purkinje fibres/ventricles: 15-40 bpm

81. Identify The Origin Of A Beat
• Use the P wave and QRS
morphology to identify where a
beat originated.
• Example: Sinus beats
• Sinus P wave (upright in ll and
inverted in aVR)
• Followed by a normal QRS

82. • Sinus beats:
• Normal P wave
• Normal (narrow) QRS
• Atrial Beats:
• Abnormal P wave
• Normal (narrow) QRS
• Junctional (AV nodal) Beats:
• P wave absent (buried in QRS), or
• Abnormal P wave just before/after
QRS
• Narrow QRS
• Ventricular beats:
• Wide QRS, abnormal T wave
• No P wave

84. Heart Block (AV nodal block)
• Conduction disease of the AV node.
• Conceptually:
• 1st Degree AV block – every P wave is
conducted (but slower than usual)
• 2nd Degree AV block – some P waves are
conducted
• 3rd Degree AV block – no P waves are
conducted

85. 1st Degree AV Block
• Every P wave is followed by a QRS
• PR interval > 200msec (> 1 big square)
• PR interval is constant

86. 2nd Degree AV block
• Mobitz l (Wenckebach):
• PR interval lengthens progressively followed by a dropped beat and
then the PR interval resets

87. 2nd Degree AV block
• Mobitz ll:
• PR interval constant
• Occasional non-conducted P waves
• Variable or may occur in set ratios e.g 2:1

88. 3rd Degree AV Block (Complete Heart Block)
• No P waves are conducted
• Complete AV dissociation ➔ No correlation between P waves and
QRS complexes
• Regular P waves (may be obscured by QRS or T waves)
• Regular QRS complexes – usually wide (ventricular escape)

89. Bundle Branch Blocks
• Lead to abnormal ventricular
conduction ➔ Wide QRS
• QRS complex > 120msec (3 small
squares)
• The T waves may be abnormal/inverted
• The ST segments may be abnormal

90. Left Bundle Branch Block
• Deep S waves in V1-3  W shape
• Tall notched R wave in V5-6  M shape
• Wide QRS > 120msec
• ST segment and T wave changes (T
wave opposite to QRS = appropriate
discordance)
• Left axis deviation
• The classic M and W shapes are
unfortunately rare

92. Right Bundle Branch Block
• RSR’ pattern in V1-3 – the M shape
• Wide slurred S wave in V6 – the W shape
• Wide QRS > 120msec
• Normal axis
• Even if there is no M shape, if the QRS is
wide and the last part of QRS is upright
in V1  RBBB

94. Fascicular Block (Hemiblock)
• The left bundle branch divides into:
• Left anterior fascicle
• Left posterior fascicle
• Left anterior fascicular block (LAFB)  left a
x
i
s
deviation
• Left posterior fascicular block (LPFB)  righ
t
axis deviation
• Together with the right bundle branch, there
are three fascicles that conduct through the
ventricles

95. LAFB LPFB

96. Bifascicular Block
• Examine the ECG
• RBBB plus left axis deviation 
RBBB + LAFB
• RBBB plus right axis deviation 
RBBB + LPFB
• These are bifascicular blocks (they
involve 2 fascicles)

97. Bifascicular Block

99. Trifascicular Block
• Examine the ECG:
• Bifascicular block + heart block (eg:
Mobitz ll)  incomplete trifascicular
block
• Two fascicles are blocked (you know
this by seeing the bifascicular block)
• The third fascicle is starting to fail (you
know this by seeing the heart block)
• Therefore trifascicular block

102. Paced Rhythms
• Keep an eye out pacing spikes (arrowed)
• Ventricular pacing will cause a wide QRS

103. Myocardial ischemia

104. Myocardial ischemia
If the patient has chest pain, ask yourself: STEMI or not a STEMI?
• STEMls require urgent management
• Don't forget non-cardiac causes
Certain STEMls and STEMI equivalents may be subtle
• Posterior STEMI
• Left bundle branch block
• Paced rhythms
• Right ventricular STEMI
• Wellen 's syndrome
• LMCA occlusion

105. STEMI/Reperfusion criteria
Chest pain > 30 min and <12 hours
ECG:
• Persistent ST elevation ≥1mm in 2 contiguous limb leads, or
• Persistent ST elevation ≥2mm in 2 contiguous chest leads, or
• New or presumed new left bundle branch block
Myocardial infarct likely from history

106. STEMI or not STEMI?

107. ECG ischemic changes
• ECG changes in ischemia:
1 . Hyperacute T waves ( early)
2. ST-segment elevation/ depression
3. Q waves
4. T wave inversion
Should be present in 2 contiguous
(side by-side) leads
• You won't miss a STEMI if you look for
these 4 features!

108. Localise the infarct
• Each lead looks at the heart from a different angle.

111. Which region of the heart is ischemic?

112. Which region of the heart is ischemic?

113. Which region of the heart is ischemic?

114. Which region of the heart is ischemic?

115. STEMI or not a STEMI?

116. Posterior STEMI
• Look for reciprocal changes in the anterior leads (Vl -3). I
• ST depression in V l -3 I
• Tall, broad (>30msec) R waves
• Upright T waves
• Dominant R wave in V2

117. • These are the same ECG changes
of a STEMI that have been flipped.
• ST elevation ➔ ST depression
• Q waves ➔ dominant R waves
•Inverted T waves ➔ upright T
waves
• Flip the paper over and look
through the back
• This makes a posterior STEMI look
like a normal STEMI

118. Posterior ECG
• To confirm: do a posterior ECG:
• Only 0.5mm of ST elevation is
required for diagnosis of STEMI!

120. STEMI or not a STEMI?

122. Right Ventricular Infarct
Why is this important not to miss?
• Susceptible to hypotension and nitrates (GTN) can worsen this

123. Right Ventricular Infarct
Consider a RV infarct in all cases of inferior Ml.
• Inferior surface of the heart is supplied the posterior descending artery
• The PDA arises from the RIGHT coronary in 90% of people
ECG Features:
• ST Elevation in lead Ill > lead II
• ST Elevation in V l > V2
• ST Elevation in lead V l
Right sided ECG

126. STEMI or not a STEMI?

127. Wellens Syndrome
ECG Changes:
• Deeply inverted {75%} or biphasic {25%} T waves in V2-3
• The rest of the ECG may be normal
Highly specific for critical stenosis of the proximal LAD.
• Often do poorly with medical therapy
Pathophysiology: transient anterior ischaemia
• Patients may be pain free and have an otherwise normal ECG

130. STEMI or not STEMI?

131. lschaemia in LBBB or Paced Rhythms
• Old LBBB + new chest pain? ➔
Consider Sgarbossa Criteria
Modified Sgarbossa Criteria
• Concordant ST elevation ≥ 1 mm in ≥
1 lead
• Concordant ST depression ≥ 1 mm in
≥ 1 lead of V1-V3
•Proportionally excessive discordant
STE in ≥ 1 lead anywhere with ≥ 1 mm
STE, as defined by ≥ 25% of the depth
of the preceding S-wave

134. STEMI or not a STEMI?

135. LMCA

136. Left Main Coronary Artery (LMCA) Occlusion
• ECG features:
• Widespread ST depression - mostly leads I, II and V 4-6
• ST elevation in aVR > 1 mm
• ST elevation in aVR > V1
These are not specific findings.
However should be taken seriously in a patient with chest pain.

137. SUMMARY
• Hyperacute T waves
• ST segment
elevation/depression
• Q Waves
• T wave insertion
ECG changes in ischemia