5. • Sinus bradycardia (35 bpm) in a 15-year old girl with anorexia
nervosa.
• Note the prominent U waves in the precordial leads, a common
finding in sinus bradycardia.
9. • Mobitz I AV block
• Progressive prolongation of PR interval, with a subsequent non-
conducted P wave
• Repeating 5:4 conduction ratio of P waves to QRS complexes
• Relatively constant P-P interval despite irregularity of QRS complexes
10. • The first clue to the presence of Mobitz I AV block on this ECG is the
way the QRS complexes cluster into groups, separated by short
pauses. This phenomenon usually represents 2nd-degree AV block or
non-conducted PACs; occasionally SA exit block.
11.
12. • Intermittent non-conducted P waves without progressive
prolongation of the PR interval.
• The PR interval in the conducted beats remains constant
• The P waves ‘march through’ at a constant rate
• The RR interval surrounding the dropped beat(s) is an exact multiple
of the preceding RR interval (e.g. double the preceding RR interval for
a single dropped beat, triple for two dropped beats, etc)
13.
14. • 2:1 AV block - Fixed
• The atrial rate is approximately 75 bpm.
• The ventricular rate is approximately 38 bpm.
• Non-conducted P waves are superimposed on the end of each T
wave.
• Could be 3:1 , 4:1
17. • Complete Heart Block:
• Atrial rate is ~ 60 bpm
• Ventricular rate is ~ 27 bpm
• None of the atrial impulses appear to be conducted to the ventricles
18.
19. • Atrial fibrillation:
• Irregularly irregular rhythm
• No P waves
• Variable ventricular rate
• Coarse fibrillatory waves are visible in V1
20.
21. • Atrial Flutter with 2:1 Block
• Narrow complex tachycardia
• Regular atrial activity at ~300 bpm
• Loss of the isoelectric baseline
• “Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF
• Upright flutter waves in V1 that may resemble P waves
• Ventricular rate depends on AV conduction ratio ( 2:1)
22.
23. • There are inverted flutter waves in II, III + aVF at a rate of 260 bpm
• There are upright flutter waves in V1-2 (= anticlockwise circuit)
• There is 4:1 block, resulting in a ventricular rate of 65 bpm
• Saw tooth apperence.
27. High Lateral STEMI
• ST elevation is present in the high lateral leads (I and aVL).
• There is also subtle ST elevation with hyperacute T waves in V5-6.
• There is reciprocal ST depression in the inferior leads (III and aVF)
with associated ST depression in V1-3 (which could represent anterior
ischaemia or reciprocal change).
28.
29. Inferior STEMI:
• ST elevation in II, III and aVF.
• Q-wave formation in III and aVF.
• Reciprocal ST depression and T wave inversion in aVL
30.
31. • Posterior extension is suggested by:
• Horizontal ST depression in V1-3
• Tall, broad R waves (> 30ms) in V2-3
• Dominant R wave (R/S ratio > 1) in V2
• Upright T waves in V2-3
32.
33. • Marked ST elevation in V7-9 with Q-wave formation confirms
involvement of the posterior wall, making this an inferior-lateral-
posterior STEMI (= big territory infarct!).
34. • Posterior leads
• Leads V7-9 are placed on the
posterior chest wall in the following
positions (see diagram below):
• V7 – Left posterior axillary line, in
the same horizontal plane as V6.
• V8 – Tip of the left scapula, in the
same horizontal plane as V6.
• V9 – Left paraspinal region, in the
same horizontal plane as V6.
35.
36. • This is case if Inferior STEMI.
• How do we suspect RV infarction?
39. • There is ST elevation in V4R
consistent with RV infarction
• The most useful lead is V4R,
which is obtained by placing the
V4 electrode in the 5th right
intercostal space in the mid-
clavicular line
43. LBBB
QRS duration ≥ 120ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Absence of Q waves in lateral leads
Prolonged R wave peak time > 60ms in leads V5-6
44.
45. RBBB
QRS duration > 120ms.
RSR’ pattern in V1-3 (“M-shaped” QRS complex).
Wide, slurred S wave in lateral leads (I, aVL, V5-6).
46.
47. • Regular, broad complex tachycardia.
• Uniform QRS complexes within each lead — each QRS is identical
(except for fusion/capture beats).
• Very broad QRS (~200 ms)
48.
49. • Polymorphic ventricular tachycardia (PVT) is a form of ventricular
tachycardia in which there are multiple ventricular foci with the
resultant QRS complex varying in amplitude, axis, and duration. The
most common cause of PVT is myocardial ischaemia/infarction.