The document provides an overview of electrocardiography (ECG) and ECG interpretation. It discusses the physiology of the heart and how the heart's electrical activity is recorded via an ECG. It explains ECG components such as P waves, QRS complex, T waves, and intervals like PR and QT. Methods for analyzing ECGs are presented, including assessing rhythm, rate, hypertrophy, axis, intervals, and ischemia patterns. Criteria for identifying left and right ventricular hypertrophy on ECGs are outlined.

1. Electrocardiogram
Basic Interpretation
Diagnosis of Ischemic Heart Diseases
Santi Silairatana, MD

2. Physiology of the Heart

3. Basic Function of the Heart
O2
CO2

4. Electromechanical Coupling Mechanism
⇣
Propagation of electrical current in conducting tissues
⇣
Electrical
Generation of electrical current
Depolarization of myocardial cells
Myocardial contraction
⇣
Increased intracardiac pressures
⇣
Blood flow in the circulation
Mechanical
⇣

5. Specialized Tissue of the Heart
Pacemaker cells & Conducting tissues
Intercalated striated muscle

6. Primary Pacemaker of the Heart: Sinoatrial (SA) Node
+20 mV
2
K+ channel opening
Outward current iK
0 mV
-20 mV
1
Rapid
Na+ channel
opening, INa
-40 mV
4
-60 mV
3
Action
ATPase
potential
pump
threshold
Na+-K+
Ca2+ channel opening
Inward current ICa
Na+ channel opening
Inward current If

7. Cardiac Electrical Activity
1
2
3
4
5
Sinus node
depolarization
Spreading to
atria via bundles
Atrioventricular node
depolarization
Atrial contraction
SA node
repolarization
Spreading to
His bundle
Spreading to
septum (LBB)

8. Cardiac Electrical Activity
6
7
8
9
10
Septal
depolarization
(Left —> Right)
Purkinje fiber
depolarization
Ventricular
myocardial
depolarization
Purkinje fiber
repolarization
Inner layer
ventricular
repolarization
Outer layer
ventricular
repolarization

9. Electrocardiography

10. Electrocardiography
A recording of
cardiac electrical activity
!
Amplitude
Vector
Time
!
Willem Einthoven
(1860-1927)
using conductivity
of the body to
the electrodes

11. Electrocardiograph Paper
Voltage
1mm
5mm
2x
1x
0.5x
Sens 0.5x = 5 mm/mV
Sens 1x = 10 mm/mV
Sens 2x = 20 mm/mV
Time
Recorder speed = 25 mm/sec
5 mm = 1/5 sec (0.2 sec)
1 mm = 1/25 sec (0.04 sec)

12. Electrocardiograph Leads: Why Many?
Left
Right
inferior
Apex

13. Electrocardiograph Leads
Use multiple leads
(electrodes)
to enhance
MULTI-DIMENSION
assessement
of the
cardiac activity

14. The Einthoven’s Triangle: Lead I, II, III
I
II
III

15. Additional Limb Leads: aVR, aVL, aVF
aVR
aVL
Wilson
central
terminal
aVF

16. Chest Leads: V3R, V4R, V1-V6, V7-9
Descending
aorta
Chest Leads
V1
V2
Left
lung
V3
V4
V5 V6
V6
LA
Recordings of electrical activity
in horizontal plane
Right
lung
RA
LV
RV
Sternum
V1
V2
V5
V3
V4

17. 12 Leads Electrocardiogram

18. Cardiac Physiology & ECG Correlations

19. Nomenclature of the ECG complex
QRS complex
T
P
ST
segment
PR
segment
PR interval
P
duration
QRS
duration
QT interval
U

20. ECG Complex & the Sequence of Activation
Ventricle
SA
AV node
Atrium
HB BB P

21. ECG and Electrical Vector

22. Atrial Depolarization
V6
the first half:
Right atrial
depolarization
the 2nd half:
Left atrial
depolarization
V1
Normal P wave:
Duration: ≤0.12 sec
Amplitude: <0.25 mV (2.5 mm)
V3

23. Septal Depolarization
In septal
depolarization,
electrical wavefront
spreads
from
Left —> Right
V6
V1
V3

24. Ventricular Depolarization
In ventricular
depolarization,
electrical wavefront
spreads
V6
from
Right —> Left
Anterior —> Posterior
Medial —> Lateral
V1
V3

25. Ventricular Repolarization
V6
1
V3
2
In ventricular repolarization,
electrical wavefront
spreads
from
Inner to outer

26. Systematic ECG Analysis & Interpretation

27. Rhythm: Sinus Rhythm
QRS complexes preceded by
P waves
Relatively constant PP interval
Each P waves are of the same configurations

28. Components of ECG “Read”
1
Rhythm
2
Rate
3
Axis
4
Chamber enlargement/hypertrophy
5
Intervals
6
Ischemia/infarction pattern

29. Heart (Atrial - Ventricular) Rate
R
RR interval 22 mm
HR = 1500/22
= 68 bpm
RR
interval
R
R
R
1 sec = 25 mm (small squares) or 5 large squares
60 sec = 1500 mm (small squares) or 300 large squares
Heart rate (/min) = 1500/RR interval (small square)
= 300/RR interval (Large square)

30. Heart Rate: Quick Look
0015010075 60 50
3
1
2
300/1 = 300 bpm
300/2 = 150 bpm
300/3 = 100 bpm
300/4 = 75 bpm
300/5 = 60 bpm
300/6 = 50 bpm
3
4
5
6
One big block = 1 sec (5 large boxes)
HR = No. of QRS complexes in 6 sec x 10

31. QRS Axis: Normal Axis
Extreme right
axis deviation
Left axis
deviation
-150o
aVR
-30o
aVL
0o
I
Right axis
deviation
120o
III
60o
II
90o
aVF
Normal axis

32. QRS Axis: Biphasic Method
-150o
aVR
-30o
aVL
0o
I
120o
III
60o
II
90o
aVF

33. QRS Axis: High QRS Amplitude Method
-150o
aVR
-30o
aVL
16 mm
0o
I
13 mm
120o
III
60o
II
90o
aVF
14 mm

34. Atrial Enlargement
“P Pulmonale”
Right atrial enlargement:
P wave amplitude > 2.5 mm
“P Mitrale”
Left atrial enlargement:
P wave duration > 3 mm (0.12 msec)
Notching of P wave

35. S V1,2ϩR V6
Grant
RϩS any precordial lead
Hancock et al
Ͼ40 mm
Ͼ35 mm
Grant66
R V5 : R V 6
Standardization and Interpretation of the ECG, Part V
Ͼ1.0
e253
Holt67
R, any precordial lead
Table 1.
Ͼ26 mm
McPhie70
S V2ϩR V4,5
Ͼ45 mm
Wolff77
R V5
First AuthorVof Study
R 6
Ͼ33 mm
Wilson76
Ͼ25 mm
Wilson76
Left Ventricular Hypertrophy
Criteria for Left Ventricular Hypertrophy
Amplitude
Limb lead voltage
Year of Study Publication
Combinations of limb and precordial voltage
(R I–S I)ϩ(S III–R III)
Ͼ16 mm
Lewis5
1914
RS aVFϩV2ϩV6 (Ͼ30 years)
Ͼ59 mm
Manning68
R IϩS III
Ͼ25 mm
Gubner6
1943
RS aVFϩV2ϩV6 (Ͻ30 years)
Ͼ93 mm
Manning68
RI
Ͼ15 mm
Gubner6 aVL (men)
S V3ϩR
1943
Ͼ28 mm
Casale8
R aVL
Ͼ11 mm
Sokolow7 aVL (women)
S V3ϩR
1949
Ͼ20 mm
Casale8
R aVF
Ͼ20 mm
Goldberger65
Total 12-lead voltage
1949
Ͼ175 mm
Siegel74
Q or S aVR
Ͼ19 mm
Schack73
1950
Combinations of voltage and nonvoltage
RϩS in any limb lead
Ͼ19 mm
Romhilt9
1968
Voltage-STT-LAA-axis-QRS duration
Point score
Romhilt9
Ͼ2436 mm/sec
Molloy71
Ͼ1742 mm/sec
Molloy71
Precordial lead voltage
(R aVLϩS V3)ϫQRS duration
Total
duration
Wilson76 12-lead voltageϫQRS 1944
S V1
Ͼ23 mm
S V2
Ͼ25 mm
S V1ϩR V5
Ͼ35 mm
S V1ϩR
Sokolow7 V5ϩS V5
1949
Ͼ25
Bozzi33
S V2ϩR V5,6
Ͼ45 mm
S V1,2
Romhilt72ϩR V6ϩS V6
1969
Ͼ25
Bozzi33
S V1,2ϩR V5,6
Ͼ35 mm
S IIIϩmax R/S any lead (men)
Murphy54
1984
Ͼ30
Gertsch32
S V1,2ϩR V6
Ͼ40 mm
S IIIϩmax R/S any lead (women)
Grant66
1957
Ͼ28
Gertsch32
RϩS any precordial lead
Ͼ35 mm
Criteria for use with right bundle-branch block
Grant66
1957
Ͼ29 mm
Vandenberg75
R V5 : R V 6
Ͼ1.0
Criteria for
Mazzoleni69 use with left anterior fascicular block
1964
Max
Holt67 R/S precordial lead (with LAD)
1962
R, any precordial lead
Ͼ26 mm
SV
McPhie170
1958
Ͼ2 mm
Vandenberg75
S V2ϩR V4,5
Ͼ45 mm
R 77
WolffV5,6
1956
Ͼ15 mm
Vandenberg75
R V5
Ͼ33 mm
Ͼ40 mm
Vandenberg75
R V6
Ͼ25 mm
S IIIϩmax R/S precordial (with LAD)
Wilson76
1944
RI
Wilson76
1944
Ͼ11 mm
Vandenberg75
Amplitudes are given in millimeters, where 1 mmϭ0.1 mV. LAD indicates left axis deviation.
Combinations of limb and precordial voltage
RS aVFϩV2ϩV6 (Ͼ30 years)
Ͼ59 mm
Manning68
1964

36. axis, left atrial abnormality, and QRS duration, in
diagnosing LVH in the presence of LBBB;
Identification of criteria that consistently outperform
Table 2. Criteria for Right Ventricular Hypertrophy
ic populations
other (semi)
cluding criteria and those that are only redundant; First Author
sFor pediatric patients, possible improvement of criteria
possible and
Amplitude
of Study
based on current sampling technology, wider demo- 78
Tall R V1
Ͼ6 mm
Myers
specific indicagraphic groups, and the use of more leads; and
Increased R:S ratio V1
Ͼ1.0
Myers78
g,The effectof day-to-day variation of voltage and other
follow-up of
Ͼ10 mm
Myers78
Deep S V5
criteria on the validity of LVH criteria.
78
Reduced R:S V5 to R:S V1
(R 1ϩS III)–(S IϩR III)
Ͻ0.04
Sokolow7
1949
Ͻ15 mm
Lewis5
1914
Butler51
1986
Max HypertrophyϾ6 mm
Right Ventricular R V , ϩmax S I,
when used in
Deep S V6
Ͼ3 mm
Myers
Tall R aVR
Ͼ4 mm
Sokolow7
ypicalRight Ventricular Hypertrophy
of LVH
Small S V1
Ͻ2 mm
Myers78
t ventricular
(RVH) causes a displacement 78
criteria of LVH hypertrophy5,6
Small R V
Ͻ3 mm
Myers
e QRS vector toward the right and anteriorly and often 78
Reduced R:S ratio V5
Ͻ0.75
Myers
, a delay in
essuch as QRS the R-waveR:S ratio V right precordial leads. 78
peak in
Reduced
Ͻ0.4
Myers
6
S duration, in
ever, considerable Reduced R:S ofto R:S V are often required to 7
degrees V RVH
Ͻ0.04
Sokolow
5
1
BB; the balance of right and left ventricular vectors,
ge
(R 1ϩS III)–(S IϩR III)
Ͻ15 mm
Lewis5
tly outperform
use the vector of left ventricular activation dominatesButler51
the
Max R V1,2ϩmax S I,
Ͼ6 mm
undant;
nce in the normal heart and even more so in the setting of
aVL–S V1
ment of criteria
H. wider demo-abilityR of the,6 ECG to detect RVH may be 7
Thus, the
V1ϩS V5
Ͼ10.5 mm
Sokolow
cted to
Ͼ0.035 sec
Myers78
ds; and be low. R peak V1 (QRS duration
ltage and criteria Ͻ0.12 derived from the amplitude of R
umerous other mostly sec)
Present
Myers
QR V1 the R-wave peak time in V have 78
S in leads I, V1, V6, and
1
proposed and areSupporting criteria
shown in Table 2. They have been
phy
RSR V1 (QRS duration
Present
12
Year of Study
aVL–S V1
Publication
R V1ϩS V5,6
Ͼ10.5 mm
Sokolow7
1949
R peak V1 (QRS duration
1948
Ͻ0.12 sec)
Ͼ0.035 sec
Myers78
1948
Present
Myers78
1948
1948
1948
QR V1
1948
Supporting criteria
1949
RSR V1 (QRS duration
1948
Ͼ0.12 sec)
1948
Present
SϾR in I, II, III
1948
Present
S I and Q III
1948
Present
1949
R:S V1ϾR:S V3,4
Present
1914
Negative T-wave V1
1986
through V3
Present
P II amplitude
1949
Ͼ2.5 mm
Amplitudes are given in millimeters, where 1 mmϭ0.1 mV.
1948
1948
and T-wave inversion in right precordial leads; as with LVH,
these ST-T abnormalities are better referred to as “secondary

37. PR Interval
QRS
complex
PR
P
segment
PR
interval
Prolonged PR (>200 msec):
First degree AV block
Normal Value:
0.12-0.20 msec (3-5 small squares)
The PR interval is the time from
the onset of the P wave to the start
of the QRS complex.
It reflects conduction through the
Atrioventricular (AV) junction
Shorted PR (<120 msec):
Pre-excitation syndrome

38. QT Interval
QRS
complex
U
QT interval
• The QT interval should be measured in either lead II or V5-6
• Several successive beats should be measured, with the
maximum interval taken
• Large U waves (> 1mm) that are fused to the T wave should be
included in the measurement
• Smaller U waves and those that are separate from the T wave
should be excluded
QT interval upper
normal limit (sec)
1.5
T
Heart rate
(bpm)
40
0.5
1.2
50
0.46
1
60
0.44
0.86
ST
segment
Measure RR
interval (sec)
70
0.4
0.8
75
0.38
0.75
80
0.37
0.67
90
0.35
0.6
100
0.34
0.5
120
0.31
0.4
150
0.25

39. Rate Corrected QT (QTc)
Estimation of QT interval
at a heart rate of 60 bpm
Bazett’s formula:
QTC = QT / √ RR
Fredericia’s formula:
QTC = QT / RR 1/3
Framingham formula:
QTC = QT + 0.154 (1 – RR)
Hodges formula:
QTC = QT + 1.75 (heart rate – 60)
Prolonged QTc (>440 msec):
Hypokalemia
Hypomagnesemia
Hypocalcemia
Hypothermia
Myocardial ischemia
Post-cardiac arrest
Increased intracranial pressure
Congenital long QT syndrome
Drugs
Short QTc (300-350 msec):
Hypercalcemia
Congenital short QT syndrome
Digoxin effect

40. ECG in Diagnosis of Ischemic Heart Diseases

41. Coronary Arteries for Myocardial Blood Supply
RCA
LCX
LAD

42. Acute Transmural Myocardial Infarction

43. ECG Change in Acute Transmural Myocardial Infarction
Ischemia/Infarction of myocardium
⇣
Failure of Na+-K+ ATPase pump
and protein channel
⇣
Decreased membrane potential
during action potential
⇣
Electrical gradient and current flow
to infarct area

44. ECG Criteria of Acute STEMI
ST segment amplitude (mm)
J point
Leads
Male
Female
Age <40
Age >40
V2 V3
2.5
2
1.5
V3R V4R
1
0.5
0.5
V7-V9
0.5
0.5
0.5
Others
1
1
1

45. ST Elevation VS Early Repolarization
Notching or slurring at the J-point
Concordant asymmetrical T wave
Concave upward ST elevation; <2 mm

46. ECG Evolution in Acute Transmural Myocardial Infarction
Normal ECG
Minutes to Hours
Hours to day
ST elevation
and Peaked T wave
Deepens Q wave
!
“Hyperacute
ST elevation”
Days to weeks
Return of ST segment
!
Inverted T wave
ST segment elevation Persistent Q wave
decreases
Months on
T wave returns
Q wave persists

47. required during mechanical revascularization procedures,
either by PCI or by coronary artery bypass grafting
(CABG). Elevated cTn values may be detected following
Anterior Myocardial Infarction
• results from occlusion of Left Anterior Descending (LAD) artery
• ST segment elevation with Q wave formation in the precordial
leads (V1-V6) ± the high lateral leads (I and aVL)
• Reciprocal ST depression in the inferior leads (II, III, aVF)
Septal Leads:
V1-V2
Anterior Leads:
V3-V4
Lateral Leads:
V5-V6, I, aVL
Anteroseptal:
V1-V4
Anterolateral:
V3-V6, I, aVL
Extensive anterior/anterolateral:
V1-V6, I + aVL

48. Acute Transmural Infarction: Anteroseptal Wall

49. Acute Transmural Infarction: Anterolateral Wall

50. Acute Transmural Infarction: Extensive Anterolateral Wall

51. Prediction of the Site of LAD Occlusion: Proximal VS Distal
Basal septal involvement:
ST elevation in aVR
ST elevation in V1 >2.5 mm
Complete RBBB
ST depression in V5
High lateral involvement:
ST elevation/Q wave in aVL
ST depression ≥1 mm in II, III, aVF

52. Proximal LAD Occlusion

53. Proximal LAD Occlusion
Reciprocal ST depression in II, III, aVF
High lateral involvement

54. Acute Transmural Infarction: Inferior Wall
• accounts for 40-50% of all myocardial infarctions
• Generally have a more favorable prognosis than anterior
myocardial infarction (2-9%)
• Up to 40% with a concomitant RV infarction
• Up to 20% with significant bradycardia due to 2nd or 3rd
degree AV block and higher mortality (>20%)
• may be associated with posterior wall infarction

55. Acute Transmural Infarction: Infero-posterior Wall
How to recognize an inferior STEMI
ST elevation in leads II, III and aVF
Progressive development of Q waves in II, III, aVF
Reciprocal ST depression in aVL (± lead I)

56. Acute Transmural Infarction: Inferior Wall

57. Prediction of the Culprit Artery: RCA VS LCX
Left Circumflex involvement:
ST elevation in lead II = lead III
No reciprocal ST depression in lead I
Signs of ST elevation in V5-V6, I , and aVL
Right Coronary involvement:
ST elevation in Lead III > lead II
Reciprocal ST depression in lead I
ST elevation in V1 and V3R-V4R

58. Acute Inferior STEMI: RCA as the Culprit
Reciprocal ST depression in lead I and aVL
ST segment elevation in lead II = lead III

59. Acute Inferior STEMI: LCX as the Culprit
Isoelectric ST segment in lead I
ST segment elevation in lead II = lead III

60. Acute Inferior STEMI: LAD as the Culprit

61. Left Ventricular Aneurysm
ECG features of LV aneurysm:
ST elevation seen >2 weeks after acute MI
Most commonly seen in the precordial leads
Convex or concave morphology
Presence of Q wave or QS pattern
Relatively small T wave

62. Acute Non-transmural Myocardial Infarction

63. ECG Change in Acute Non-transmural Myocardial Infarction
Horizontal
ST segment
depression
>1 mm
Down slope
ST segment
depression
J point >1 mm
Symmetrical
T wave inversion

64. Acute Nontransmural Myocardial Infarction

65. Acute Nontransmural Myocardial Infarction

66. Acute Nontransmural Myocardial Infarction

67. Thank You