1. 20 IMPORTANT ECGs
NOOR ATIKAH SAINI
080201033

2. Ecg 1
h/o: 60 years old man with 4 hours crushing chest pain

3. This ECG shows :
• Rate = 60/min
• Rhythm = sinus rhythm
• Axis = normal
• P wave = normal
• QRS complex = normal
• T wave = normal
• ST segment = elevated in the anterior leads
V1-V6, I and aVL
= reciprocal ST depression in the
inferior leads ( leads II,III, aVF)
• PR interval = normal
• QT interval = normal
Diagnosis = Acute Anterolateral Myocardial Infarction

4. Ecg 2 :
H/o: A 56 years old man with chest pain and vomiting for 90
minutes

5. This ECG shows :
• Rate = 50/min
• Rhythm = sinus
• Axis = normal
• P wave = normal
• QRS complex = normal
• T wave = normal
• ST segment = elevated in the inferior leads II,
III, aVF.
reciprocal ST depression in the
anterior leads ( V1-V4).
• PR interval = normal
• QT interval = normal
Diagnosis = Acute Inferior Myocardial Infarction

6. Ecg 3 :
H/o: A 78 years old lady with chest pain and collapse, BP 60/40

7. This ECG shows :
• Rate = 50/min
• Rhythm = sinus
• Axis = normal
• P wave = normal
• QRS complex = tall R wave in leads V1-V3
• T wave = tall upwright T wave in leads V1-V3
• ST segment = depression in anterior leads V1- V3
• PR interval = normal
• QT interval = normal
Diagnosis = Acute Posterior Myocardial Infarction

8. Summary :
1. Features of MI based on its site of infarction:
Changes Anterolateral Inferior MI Posterior MI
of ECG MI
ST •ST elevetion in •ST elevation ST elevation
segment leads V1-6, I in the leads in leads V1-3
and aVL II, III and aVF
•With ST •With ST
depression in depression in
leads II,III,aVF leads V1-V4
R wave - - Tall R wave in
leads V1-V3
T wave - - Tall T wave in
leads V1-3

9. Progression of Ischaemia to Injury to Infarction
ECG changes:
• Ischaemia = only T wave abnormalities
• Injury = T waves + ST segments abnormalities
• Infarction = T waves + ST segments + QRS complexes abnormalities

10. Ecg 4 :
H/o: A 64 years old man with breathlessness and a raised JVP

11. This ECG shows:
• Rate = 120 beats/min
• Rhythm = sinus
• Axis = normal
• P wave = normal
• QRS complex = normal
• T wave = small or inverted
• ST segment = widespread
• PR interval = normal
• QT interval = normal
Other features = alternating high and low voltages of all the ECG
waveforms
Diagnosis = Electrical alternans of pericardial effusion
The classic example is a pericardial effusion with the heart "swinging" in it
and changing its location and proximity to the chest wall (where the
electrodes are) from beat to beat.

12. electrical alternans/low voltage alternans:
=>alternate-beat variation in the direction, amplitude, and duration of any
component of the ECG waveform (ie, P, PR, QRS, R-R, ST, T, U).
Causes :
1. Physical : hypothermia
2. Infections : myocarditis, pericardial TB
3. Neoplasm : pericardial mesothelioma
4. Metabolic disorders : obesity, heart amyloidosis,haemochromatosis
cardiomyopathy
5. Structural disorders : pericardial effusion, cardiac temponade,
hydro/hemopericardium,pneumothorax
6. Poisoning : chronic alchoholism

13. 60 year old male with chronic kidney disease on
mantainance hemodialysis is brought to emergency
with breathlessness and volume overload

14.  Findings:
-sinus rhythm
-small or absent P wave
-long PR interval
-shortened ST segment
-normal axis
-broad QRS complexes
-tall tented T waves

15. Hyperkalemia
 Definition:plasma potassium level of 5.5mM
 Changes in hyperkalemia:
1.mild-prolongation of PR and QRS interval.
2.moderate-loss of Pwave and progressive
widening of QRS complex
3.severe-sine wave sinoaventricular rhythm

16.  Management:
-IV administration of glucose along with insulin
to encourage shift of potasium from EC to IC
compartment
-50ml of 50% glucose plus 10 unit of soluble
insulin as bolus
-500ml 20% glucose plus 10 unit of soluble
insulin as infusion over 6 – 12 hours

17. -10ml of 10% calcium gluconate IV slowly over 2-
5 min to stabilise myocardial cell
-50 – 100ml of 8.4% sodium bicarbonate IV
-nebulisation of beta agonist( salbutamol)
-if these measure fail hemodialysis is indicated

19.  Findings:
-sinus bradycardia
-long PR interval
-normal axis
-small T wave
-Presence of U wave (repolarization of papillary
muscles or purkinje fibres)
-ST segment deviation
-prolonged QT interval

20.  ECG changes of hypokalemia
-increased amplitude and width of Pwave
-prolongation of PR interval
-T wave flattening and inversion
-ST depression
-prominent U wave
-apparent long QT interval due to fusion of T and
U waves

21.  Hypokalemia
-causes:
1.Low PTH level:parathyroid
agenesis, destruction, reduced function
2.High PTH level:vit D deficiency, drugs, PTH
resistance syndrome, acute pancreatitis
-features
1.Asymptomatic
2.Paresthesia of fingers ,toes,circumoral regions
3.severe:seizure, carpopedal
spasm, bronchospasm, laryngospasm

22. Case 3
A 65 year old women with congestive cardiac
failure and on treatment come with the ECG.

23.  Findings:
-Abnormal rhythm
-inverted T wave
-downward sloping ST segment- reversed tick
sign
-depressed ST – J point
-shortened QT interval

24.  Digitalis effects
-digitalis is a drug used in CCF and to slow the
ventricular rate in atrial tachyarrhythmias
-digitalis effects is due to early recovery and
repolarisation of myocardial cells.
1.coved ST segment depression
2.flattened T wave
3.decreased QT interval

25.  Digitalis toxicity
-due to excessive amount of digitalis >2ng/ml
-features:
1.general symptoms-weakness, anorexia, nausea,
vomitting, visual effects and mental changes.
2.arrhythmias and conduction disturbance-
ventricular arrhythmia,bidirectional ventricular
tachycardia,AV junctional rhythm,sinus
bradycardia

26. -treatment:
1.prevention-baseline ECG, serum electrolyte,
BUN and creatinine.
2.definitive treatment depend on arrhythmia
minor-discontinuation of digitalis and careful
observation
serious-suppression with IV drugs lidocaine
-pacemaker in patient with complete
heart block
-digitalis binding antibody IV
(digoxin immune Fab)-lethal dose

27. A 40 year old male, asymptomatic came with
the ECG

28.  Findings :
-sinus rhythm
-inverted P wave in lead I
-increased PR interval
-right axis deviation
-QRS complexes get progressively smaller from
V1 to V6 with small R wave

29. Dextrocardia
 It is the condition in which the cardiac apex
is in the right side of the chest
 D/D
-accidental reversal of the left and right arm
electrodes
-situs inversus : congenital condition in which
major visceral organs are reversed from their
normal position

30. CASE #1
• A 27 year old female, Mrs. Terry, a
known case of α₁-
a nt i t r y ps i n
de f i c i e nc y ,
c o mp l a i n e d o f f e v e r ,
i nc r e a s e d
br e a t hl e s s ne s s a nd
COPD
wh e e z i n g s i n c e 3
da y s .

32. • Rhythm : sinus rhythm
• Axis : right axis deviation
• P wave : P pulmonale
( >2.5mm in lead II)

33. D/D for P pulmonale
Valvular Pulmonary Congenital
disease hypertension heart disease
• Tricuspid • COPD • Ebstein’s
stenosis • Pulmonary anomaly
• Tricuspid embolism
regurgitation • ILD
• Sleep apnoea
• LV systolic
dysfunction

34. EBSTEIN’S ANOMALY
-congenital condition
often associated with
WPW syndrome
ECG findings
- ‘Himalayan’ P wave
- prolong PR interval

35. ECG 2
40 y e a r o l d f e m a l e w i t h h i s t o r y o f
c h r o n i c b r e a t h l e s s n e s s

36. • Rhythm : irregularly irregular
• Axis : right axis deviation
• P wave : diminished
MITRAL STENOSIS

37. LA enlargement???

38. CASE #3
• A n 83-y e a r -o l d m a n w h o
i s a p p a r e n t l y
a s y mp t o ma t i c c a me
t o O P D .H e i s
r e g u l a r l y s e e n b y
y o u r c o l l e a g u e .
S i n c e y o u r
c o l l e a g u e i s o n
l e a v e ,t h i s p a t i e n t
a s k e d y o u r r e v i e w o n
h i s c u r r e n t h e a r t

39. ECG #3

40. • Rhythm : sinus rhythm
• Axis : left axis deviation
• P wave : biphasic
(2nd half of wave is –ve)
• QRS complex : deep S wave, tall R wave

41. DIAGNOSING LVH ON ECG
• Limb Leads (Low sensitivity, high specificity)
– R wave lead I + S wave lead III > 25 mm
– R wave aVL > 11mm
– R wave aVF > 20mm
– S wave in aVR > 14mm

42. ......
• Precordial Leads (High sensitivity, low
specificity)
– R wave V5 or V6 > 26mm
– R wave V5 or V6 + S wave in V1 > 35mm
– Largest R wave + largest S wave in precordial leads
> 45mm

43. ........
• The Sokolow-Lyon criterium
R in V5 / V6 + S in V1 > 35mm
• The Cornell criterium
R in aVL and S in V3 >28 mm in men
R in aVL and S in V3 >20 mm in women

44. ECG #4

45. CASE #4
• A 60-y e a r -o l d f e m a l e ,
k n o wn c a s e o f I HD,
p r e s e n t e d wi t h
pa l pi t a t i ons i n t he
O P D . O n e x a mi n a t i o n ,
h e r me a s u r e d
s y s t o l i c B P i s 80.

46. Tor s a de s de
Poi nt e s

47. TORSADES DE POINTES
(Polymorphic ventricular tachycardia)
• Acute management • Long-term management
1)Electrolyte 1)β-blockers
2)Drugs 2)Left cardiac sympathetic
3)Heart rate denervation
4)MgSo₄ 3)Pacemaker
5)IV isoprenaline

48. NUR SHUHAIZA BINTI SUPIAN
080201039

49. CASE 1
A 23 years old male with h/o episodes of palpitation

50. ECG FINDINGS:
 Normal rate
 Sinus rhythm
 Normal axis
 Short PR interval
 Slurred upstroke of QRS complex, best seen
in I, V4, V5
 Widened QRS complex due to „delta‟ wave
WPW SYNDROME

52.  one of several disorders of the conduction system of the
heart that are commonly referred to as pre-excitation
syndromes.
 majority of individuals with WPW remain asymptomatic
throughout their entire lives
 risk of sudden cardiac death associated with the syndrome.
 caused by the presence of an abnormal accessory electrical
conduction pathway between the atria and the ventricles
 Electrical signals travelling down this abnormal pathway
(known as the bundle of Kent) may stimulate the ventricles to
contract prematurely, resulting in a unique type of
supraventricular tachycardia referred to as an atrio-
ventricular reciprocating tachycardia.

53. CASE 2
A 50 years old male with h/o chest pain for 24 hours

54.  Sinus rhythm with ventricular bigeminy
 Normal rate and axis
 Bigeminy : every sinus beat is followed by a
ventricular premature beat
 No preceding P wave
 The coupling interval is usually constant
 Usually followed by compensatory pause
VENTRICULAR BIGEMINY

55. Compensatory pause:
The R-R interval between the beats directly
preceding and following the VPB is exactly
twice that of regular R-R interval
Common cause for ventricular bigeminy:
 May occur in normal individual
 Ischemic heart disease
 Digoxin toxicity
 Left ventricular dysfunction

56. CASE 3
A 40 years old female, bedridden for 48 hours, come
with c/o breathlessness

57.  Sinus tachycardia
 Normal rate
 Normal axis
 Prominent S wave in Lead I
 Small Q wave, inverted T wave in Lead III
S1 Q3 T3 PATTERN
ACUTE PULMONARY EMBOLISM

58. CASE 4
A 60 years old male, recently diagnosed with myocardial
infarction

59.  Rate increased (>100/min)
 Sinus rhythm
 Independent P wave
 Broad QRS complexes (>0.16s)
 beat to beat variability of the QRS
morphology
VENTRICULAR TACHYCARDIA

60. Fusion beat:
When one impulse originating from ventricle and a second
supraventricular impulse simultaneously activate the ventricular
myocardium
Capture beat:
Normal conduction momentarily “captured” control of
ventricular activation from VT focus

61. Brugada Criteria:
 Lack of an RS complex in the precordial leads
 Whether the longest interval in any precordial lead
from the beginning of the R wave to the deepest
part of the S wave when an RS complex is present
is greater than 100 ms
 Whether atrioventricular dissociation is present
 Whether both leads V1 and V6 fulfilled classic
criteria for ventricular tachycardia.

63.  Immediate cardioversion in synchronised
mode
 IV Amiodarone : given as bolus followed by
continuous infusion
 IV Lidocaine

65. AV BLOCKS
• FIRST DEGREE-
All impulses conducted, but delay present
(prolonged PR interval)
In
coronary artery disease,
drug toxicity(digoxin, CCB’s, β blockers)
electrolyte disturbances(hyperkalemia)
 acute rheumatic carditis,
 congenital heart diseases(ASD, Ebstein’s anomaly)

66. • SECOND DEGREE-
 Impulse completely fails to pass through the AV
node
 Mobitz type ll
 Wenkebach phenomenon/Mobitz type l
 Causes-
o Physiological- atheletes, vagotonic individuals
o Acute rheumatic carditis
o MI (eg inf wall, right ventricular)
o Acute diphtheric myocarditis
o Drugs- digitalis
o Idiopathic fibrosis of the conduction system
(Lenegre’s disease)

69. • THIRD DEGREE-
 Atrial contraction is normal, but no beats are
conducted to the ventricles
 Causes-
o Drugs-
o Acute MI
o Acute rheumatic carditis
o Congenital heart disease(ASD, VSD)

70. HOW TO DIAGNOSE
• LOOK FOR-
R-R INTERVAL
P WAVES
P-R INTERVAL

71. R-R INTERVAL
REGULAR IRREGULAR
P-R INTERVAL 2ND DEGREE
SAME VARIABLE P-R INTERVAL
1ST DEGREE 3RD DEGREE CHANGES FIXED
MOBITZ TYPE I TYPE II

72. CASE I
• 70 year old male, complains of
exercise intolerance

74. • RATE- normal
• RHYTHM- regular( dual rhythm)
• AXIS- normal
• P WAVE
• QRS COMPLEX
• T WAVE
• PR INTERVAL
• QRS INTERVAL

87. CASE II
• 90 year old male, presented
with syncope

89. Rhythm : sinus rhythm
Axis : normal
P wave :
QRS complex : wide
rsR’ pattern (M shaped) in V1, V2
•T wave : inversion in V1, V2
•wide, slurred S wave in L I and V5, V6
ST segment : depression in V1, V2
PR interval :
QT interval :

90. CAUSES
• acute myocardial infarction,
• acute pulmonary embolism,
• chronic cor pulmonale
• Congenital heart disease(ASD, VSD, Ebstein’s
anomaly)
• Myocarditis
• Cardiac contusion

91. CASE III
• 90 year old male presented with
sudden onset of chest pain and was
diagnosed to have myocardial
infarction

93. •Rhythm : sinus rhythm
•Axis : normal
•P wave :
•QRS complex :wide
small r waves followed by deep, wide and slurred S
waves in V1, V3;
•broad, notched or slurred (M shaped) R wave in L I,
aVL, V5, V6;
absence of q waves in L I, aVL, V5, V6;
•T wave : inversion
•ST segment :depression in L I, aVL, V5, V6
•PR interval :
•QT interval :

94. CAUSES
• Always pathological
• acute myocardial infarction,
• hypertensive heart disease
• dilated cardiomyopathy
• Aortic valve disease
• Drugs (quinidine).

95. CASE IV
• 90 year old male with a past history
of MI, which was complicated by
LBBB. He is currently asymptomatic

98. WHERE IS THE PACEMAKER ?
• Atrial pacing spikes- short vertical lines
preceding the P waves and best seen in lead III
• Ventricular pacing spikes- precede the QRS
complex and best seen in lead V2 , V3, V4 &
V5