ECG Proff.Sumit Kr Ghosh Dept of Internal Medicine Medical College 88 College Street Kolkata

1. ECG
Dr. Sumit Kr. Ghosh
Asst. Professor
Department of Medicine
Medical College & Hospital,

2. INTRODUCTION
Graphic representation of electrical activities of heart
Resting ECG
Exercise ECG / TMT
24-hr ECG / Holter

4. READING ECG
• Rate
• Rhythm
• Axis
• Lie & Rotation
• Voltage
• Waves & Intervals
• Abnormalities

5. ECG PAPER

6. STANDARDISATION
• 1mv will produce deflection of 10 mm / 1
cm
• Stylus should have an appropriate pressure

7. WAVES & INTERVAL
P Q R S T > 5mm
q r s < 5mm
P
Q
R
S
T
U
J-point
J
δ
PR
QRS
ST
QT
TP
PP & RR

8. LEADS
Lead = paired electrode
12 leads
Limb leads Precordial leads
Frontal or Coronal plane leads Horizontal plane leads
Bipolar unipolar (low EP) unipolar
I, II, III aVR, aVL, aVF v1, v2, v3, v4, v5, v6
rt side septum lt side
I, avL, v5, v6 : lateral wall
II, III Avf : inferior wall
Long leads
V7, v8, v9
V1r – v9r
3v1 – 3v9
Esophageal leads

9. Resultant vector
• Towards lead : positive / upward deflection
• Away from lead : negative / downward deflection
• Perpendicular to lead : equiphasic deflection

10. RATE
Ventricular rate vs Atrial rate
Rate = 1500/ no of small square = 300/no of
large square
Depends on speed of ECG paper
Usual speed = 90m/hr =1.5m/min
No of QRS complex in 1 min = HR

11. RHYTHM
• Regular :
~ Sinus
~ Nodal
~ Idioventricular
• Irregular :
~ Regularly irregular
~ Irregularly irregular

12. AXIS
• Normal axis : 0 to +90 degree (most cases +40 to +60 degree)
• LAD : 0 to -90 degree (slight LAD : 0 to -30 degree
marked LAD : -30 to -90 degree )
• RAD : +90 to ± 180 degree
• Inderminate / NW axis : -90 to ± 180 degree
an expression of :
- marked RAD
- marked LAD
- discharge of ectopic
ventricular pacemaker

13. AXIS DETERMINATION
• Lead I,II & III
• Pairs of perpendicular leads
• Perpendicular to the lead where R=S
• In degree
I II III
↑ ↑ ↑ Normal
↑ ↑ ↓ ↓ LAD
↓ ↑ ↑ RAD

14. +
+
_
_ I
aVF
0± 180
- 90
+ 90
NORMAL AXIS RAD LAD INDETERMINATE AXIS

15. EASY TO REMEMBER
I (left) aVF (right)
↑ ↑ Normal
↑ ↓ LAD
↓ ↑ RAD
↓ ↓ Indeterminate

16. LAD
• LAHB
• LBBB
• Inf wall MI
• Pacing from apex of RV/LV
• WPW
Isolated LVH does not cause
LAD
RAD
• RV dominance
- acq. Rt heart disease :
pulm embolism
chr. Cor pulmonale
- cong. heart disease :
TOF
• Anterolateral MI
• LPHB
• WPW

17. LIE & ROTATION
• LIE : in frontal plane [ vertical (90 degree) to horizontal (0 degree )
• Rotation : in horizontal plane
~ Clockwise – persistent S waves in v5, v6
~ Anti-clockwise – R waves in v2

18. P - WAVE
• Atrial activity (RA earliar than LA)
• Best seen in lead II & v1
• Normal duration : 0.08 s – 0.1 s (not > 0.11 s)
• Normal amplitude : not > 2 mm ( max – 2.5 mm)
• Diphasic in v1
• Inverted in aVR (normally), wrong electrode placement,
dextrocardia, retrograde atrial activation
• Absent : Atrial fibrillation, nodal rhythm, hyperkalemia
• P-pulmonale : tall & peaked (amplitude > 2.5 mm) » » RAH
• P-mitrale : wide & notched (duration > 0.11 s) » » LAH
• P-tricuspidale

19. QRS COMPLEX
• Ventricular depolarisation
Q-wave : initial negative deflection
septal depolarisation :: from left to right
R-wave : depolarisation of venticular muscle mass
S-wave : depolarisation of postero-basal part of left
ventricle, superiormost part of ventricular septum
• High amplitude : RVH / LVH
• Low amplitude : Low voltage complex
(< 5 mm in limb leads & < 10 mm in precordial leads)
Standardisation is important
• Taller in v5 than v6

20. QRS COMPLEX
QRS in precordial leads

21. T-WAVE
• Ventricular repolarisation
• Blunt apex with 2 asymerical limbs :
proximal limb shallower than distal
• Tall –peaked : hyperkalemia
• Tall- wide : hyperacute stage of MI
• Inverted : IHD, Ventricular strain, CVA
• Flat : thick chest wall, emphysema,
pericardial effusion, hypokalemia

22. U-WAVE
• Positive deflection after T & before P of
next cycle
• Slow repolarisation of Purkinje’s fibres,
septum, papillary muscles but uncertain
• Mid-precordial leads – v2 to v4
• Prominent : hypokalemia
• Inverted / absent : diastolic overload /
myocardial dysfunction

23. P-R INTERVAL
• Beginning of P-wave to beginning of QRS
complex
• Intra-atial, AV nodal & His-Purkinje coduction
• Normal duration : 0.12 – 0.20 s
• Prolonged : Acute rheumatic fever, 1st
degree
AV block
• Progressive prolongation : Mobitz type-I (2nd
degree AV block) » » Wenckebach phenomenon
• Shortened : WPW syndrome, AV nodal rhythm

24. QRS INTERVAL
• Total ventricular depolarisation
• Beginning of Q-wave ( beginning of P-wave,
if no Q-wave present) to termination of S-
wave
• Normal duration : usually not > 0.09 sec
(range 0.05-0.11 s)
• Prolonged : Intaventricular conduction defect
or BBB
≥ 0.12 sec » » complete BBB
• Intrinsicoid deflection / ventricular activation
time : time taken for an impulse to traverse
myocardium
VAT normally not > 0.02 s in v1, v2
& not > 0.04 s in v5, v6

25. ST SEGMENT
• End of QRS complex to beginning of T
• Normal ST segment merges smoothly & imperceptibly with
proximal limb of T : difficult to separate
• Time interval between ventricular depolarisation &
repolarisation
• Isoelectric to TP segment
• Elevated :
~ with upward convexity : AMI, coronary spasm, LV
Aneurysm
~ with upward concavity : acute pericarditis
• Depressed :
~ oblique/plane/sagging : CAD
~ mirror image of correction mark : digitalis effect
~ upward convexity : strain pattern
• End of QRS complex & beginning of ST segment : J point

26. QT INTERVAL
• Beginning of Q to end of T
• Ventricular depolarisation + repolarisation
• Corrected QT or QTc : as QT changes with heart rate
• Bazett’s formula :
QT interval
√RR interval
It should be ≤ 0.44 s
Prolonged : acute rheumatic carditis, hypokalemia,
hypocalcemia, drugs
Shortened : hypercalcemia, digitalis, hyperthermia
QTc =

27. PP & RR INTERVAL
• PP interval : distance between 2 successive P waves
- reflects atrial rate
• RR interval : distance between 2 successive R waves
- reflects ventricular rate
• Normally PP = RR

29. Atrial hypertrophy :
LAH : P-mitrale
RAH : P- pulmonale
Bi-atrial hypertrophy
Ventricular hypertrophy :
LVH
RVH
Bi-ventricular hypertrophy

30. LVH
• Voltage criteria :
~ Sv1 + Rv6 > 35
~ Sv1 / Rv6 ≥ 20
~ Rv6 ≥ Rv5
~ RI ≥ 15
~ RaVL ≥ 11
~ Rall(12) > 175
• Horizontal heart
• VAT in v5/v6 > 0.04 s
• Strain pattern in I, aVL, v5, v6
LAD is not a criteria for isolated LVH
• Pressure overload LVH
• Volume overload LVH

31. RVH
• Voltage criteria :
~ R > S
~ Rv1 > 5 mm
~ persistent Sv5 / Sv6
• Usually RAD (most common & at times only manifestation); but axis
may be normal
• Vertical heart
• VAT in v1 > 0.02 s
• Strain pattern in v1, Avr
• Associated P-pulmonale may be there

32. BIVENTRICULAR HYPERTROPHY
• LVH + RAD
• LVH + Clockwise rotation
• Tall Rv6 + tall Rv1 ( R > S)

34. CORONARY INSUFFICIENCY
• Impaired coronary blood flow : present all the time :
absolute
• Increased demand : present time to time : relative
• ST depression : horizontality, upward sloping, plane,
downward sloping
• ST elevation : coronary vasospasm
more severe than ST depression
• T wave :
~ symmetrical limbs with sharp vertex : coronary
insufficiency
~ asymmetrical limbs with blunt vertex : strain, digitalis
effect
• Inverted U

35. MYOCARDIAL INFARCTION

36. ECG CHANGES
• Hyperacute phase
~ increased amplitude of R wave
~ increased VAT
~ slope elevation of ST segment
~ tall & wide T
• Fully evolved phase
~ pathological Q
~ ST elevation with upward convexity
~ symmetrical T inversion
• Chronic stabilized phase
~ pathological Q
~ ST segment & T may be normal or
point towards coronary insuffiency
Indicative & reciprocal changes

37. AMI
LV RV
v1 & v4R
Anterior wall
Extensive anterior wall
I, aVL, v1 to v6
Anterolateral wall
I, aVL, v4 to v6
Anteroseptal wal
v1 to v4
Apical wall
V5,V6
Inferior wall
II, III, aVF
Posterior wall
mirror-image change
in v1 to v3, esp v2

38. PATHOLOGICAL Q
• Present in indicative leads
• 0.04s in duration
• >4 mm deep
• >1/4th
of R wave magnitude
Physiological Q
• Septal depolarisation from left to right
• Present in lateral leads I, aVL, v5,v6
Loss of Q : early feature of LBBB
Deep Q with giant negative T : HOCM

41. • Sinus rhythm : 60-100 beats/min
• Sinus arrythmia (sinus node rate can change with
inspiration/expiration, especially in younger people
variation of the P-P interval from one beat to the
next by at least 0.12 seconds
• Sinus tachycardia : regular sinus rhythm with sinus
node rate > 100/min
• Sinus bradycardia : regular sinus rhythm with sinus
node rate < 60 / min

42. Similarities :
Premature
Ectopic
Etiology
Dissimilarities :
SVPB VPB
Focus in Atrium ( other than SA
node)
Ventricle
QRS complex Morphology similar
Narrow
Morphology dissimilar
Wide
ST-T No significant change Usually displaced in
opposite direction of QRS
Compensatory pause Incomplete Complete
APC / SVPB vs. VPC / VPB

43. SUPRAVENTRICULAR
TACHYARRYTHMIA
SVTs from a sinoatrial source:
• Inappropriate sinus tachycardia
• Sinoatrial node reentrant tachycardia (SANRT)
SVTs from an atrial source:
• Ectopic (unifocal) atrial tachycardia (EAT)
• Multifocal atrial tachycardia (MAT)
• Atrial fibrillation with a rapid ventricular response
• Atrial flutter with a rapid ventricular response
SVTs from an atrioventricular source (junctional tachycardia):
• AV nodal reentrant tachycardia (AVNRT) or junctional reciprocating
tachycardia (JRT)
• AV reentrant tachycardia (AVRT) - visible or concealed (including
Wolff-Parkinson-White syndrome)
• Junctional ectopic tachycardia

44. PAT / PSVT / AVNRT
• A run of rapidly repeated SVPBs ( usually ≥ 3 )
• Narrow QRS
• Rate around 160-220/ min
• Usually 1:1 conduction; sometimes AV block associated
(PAT with block)
• Prolonged PR
• Management : carotid sinus massage, adenosine,
verapamil, DC cardioversion

45. Atrial fibrillation
• Chaotic atrial excitation & contraction
• Atrial rate 350-600 / min
• No definite P; replaced by ‘f’ wave
• Irregularly irregular ventricular rhythm
• Narrow QRS
• Etiology :
• Management :

46. Atrial flutter
• Regular atrial contraction
• Atrial rate 220-350 / min
• Ventricular rate ½ - ¼ th of atrial rate; may be
irregular; QRS complex : normal morphology
• “Saw-toothed” appearance; flutter wave

47. VENTRICULAR
TACHYARRYTHMIA
VT
VFl
VF
VPC
Bigeminy : alternate sinus beat & VPC
Trigeminy : 2 sinus beat followed by VPC
Couplets / pairs : 2 successive VPCs
VT : ≥ 3 consecutive VPCs with rate >100

48. VT
Sustained VT : >30s in duration & symptomatic :
generally requires termination by anti-tachycardia
pacing techniques
Non-sustained VT : episodes are short (≥3 beats) and
terminate spontaneously
Monomorphic VT : regular rate and rhythm and fixed
shape or morphology of the ECG trace
Polymorphic VT : irregular in rate and rhythm and has
varying shapes or morphologies on the ECG
Monomorphic VT may deteriorate into polymorphic
VT to VF

49. VFl
• High frequency (250- 350/min) beats
• The ECG signal looks like sinusoidal or ‘sine-
like wave’ form
• High rate of contraction of heart chambers : time
of blood flow into the chamber becomes very
small : very little blood flows to body
• The person who is experiencing VFl is close to
unconsciousness

50. VF
• Most dangerous arrythmia
• Ventricular rate 350-450/min
• Totally uncoordinated : no discriminate waves :
totally irregular, bizarre & deformed deflections
of varying width, height & shape
• No audible heart sounds, no palpable pulse
• Treatment : immediate electrical defibrillation
• If lucky to survive from VT, chance of VF in near
future

51. ATRIOVENTRICULAR
CONDUCTION DEFECTS
• 1st
degree
• 2nd
degree
~ Mobitz type I
~ Mobitz type II
~ Constant / fixed AV block
• 3rd
degree / Complete block

52. 1st
degree
Prolonged PR interval (>0.2 s)
2nd
degree
Mobitz type I
Mobitz type II
Constant / fixed AV block
3rd
degree / Complete block
No SA impulse pass through AV
node
Idioventricular rhythm
No synchrony between atrial rhythm
& ventricular rhythm
Mobitz type I Mobitz type II
More common Less common
Benign Serious
Inf wall MI Ant wall MI
Proximal to
bundle of His
Distal to bundle of
His
Prognosis better Prognosis worse

53. INTERVENTRICULAR
CONDUCTION DEFECTS
• Unilateral bundle branch block ( LBBB,
RBBB)
• Peripheral block ( LAHB, LPHB, Septal
block)
• Bifascicular block
• Trifascicular block

54. BBB

55. LBBB
• M pattern or M-shaped complexes in lead I, aVL, v5, v6
• Absent Q
• ST depression with T inversion
• QRS interval more or less 0.12s
• Usually LAD
• Usually VAT prolonged
Most cases have organic heart disease
Recent onset LBBB : think of AMI
Presence of Q in lateral leads : never LBBB

56. RBBB
• RSR’ pattern in v1, v2, aVR, v3R
• ST depression with T inversion
• Wide & slurred S in I, aVL, v5, v6
• QRS interval more or less 0.12 s
• Usually VAT prolonged
Commoner than LBBB, often without any
cardiac diseases

57. LAHB
• LAD
• qR in I, aVL & rS in II, III, aVF
LPHB
• RAD
• qR in II, III, aVF

58. Bifascicular block
• RBBB + LAHB
• RBBB + LPHB
• LAHB + LPHB
Trifascicular block
• LAD + RBBB + Prolonged PR