Introduction to ECG/EKG for General Doctors & Medical students

1. Introduction to
ECGs/EKG
BARAL AKSHAY KUMAR.
Hospital Physician
Specialist
Anesthesiologist

2. 1
Discussion Topics
0 ECG Monitoring Basics a
Standardized Methods & Devices
a Components & Measurements of the
ECG Complex
0 ECG Analysis

3. 2
Objectives
n To learn how to properly set up your ECG leads. a To
Learn What a lead is. a To learn the anatomy of a
normal ECG.
0 To define Normal Sinus Rhythm.
0TO quantify the various components of a normal ECG

4. 3
ECG Monitoring
a Recording of Electrical Activity
a Uses Bipolar or Unipolar leads
The ECG DOES NOT provide a recording
or evaluation of Mechanical Activity!!!

5. 4
0 The five lead ECG is becoming a standard feature
on all new monitors.
0The 12 leads you can monitor are:
I II III
aVR,aVL,aVF and V1,V2,V3.V4,V5 &V6 0 This allows
more precise diagnosis of cardiac events
5

7. Precordial Leads
6

9. Precordial Leads

10. This is a 12 lead ECG or simply 12
different views of the heart.
10

14. In Emergency
0 Patients can be monitored with only 2 Leads
attached.
These is done either with the Defibrillator Paddles
or with Defibrillator Patches

15. Note the placement in each case is upper right
and lower left chest which will sandwich the heart
in between the electrodes.

16. Which coincidentally is one of the correct
placements for defibrillation and will also work for
external pacing .
16

17. 13
Remember all that an ECG is looking at is
the electrical activity and electical activity
is not always associated with contraction.

18. So never forget to check a manual pulse in
an emergency.
18

19. The Normal Conduction System

21. 60-100 i 40-60 t
beats/min beats/min
Sinoatrial Atrioventricular
node node

22. Left
bundle
branch
I
20-40 beats/min
Right bundle
branch

24. Time Sequences on ECG Strips
The strip is read from
left to right in seconds

25. and up and down on
millivolts.
Standardized
Methods & Devices
sECG Paper
24

26. s Device Paper Speed 0
Device Calibration
0 Electrode Placement 0
Variations Do Exist!

27. Rule of 300
Take the number of “big boxes” between
neighboring QRS complexes, and divide this into
300. The result will be approximately equal to the
rate.
Although fast, this method only works for regular
rhythms.

28. What is the heart rate?

29. What is the heart rate?
(300 / 1.5) = 200 bpm

30. The Rule of 300
It may be easiest to memorize the following table:
# of big boxes Rate
1 300
2 150
3 100

31. 4 75
5 60
6 50

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33. Sinus Bradycardia

34. Sinus Tachycardia

35. May be caused by exercise, fever,
hyperthyroidism

36. Sinus Arrhythmia

37. Seen in young patients
Secondary to breathing
Heart beats faster

38. Atrial Flutter

39. Atrial Flutter

40. Atrial Fibrillation

41. Atrial Fibrillation

42. racing shows irregularly irregular
rhythm with no P waves
Ventricular rate is 40

43. Atrial Tachycardia
Tracing shows regular ventricular rate with
P waves that are different from sinus

44. P waves
• Ventricular rate is usually 150 to 250 bpm

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46. Rhythm

47. Rate is 40 to 100 bpm
Ventricular

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49. Ventricular Fibrillation

50. Right Bundle Branch Block

52. Normal Complexes and Segments

54. J Point

56. Ischemia

57. Measurements

59. ST-Segment Elevation

61. ST Segment Depression
Can be characterised as:-

62. D
Downsloping
0 Upsloping 0
Horizontal
JPotbt
Horizontal STUpsloping STDownsloping ST
The J point occurs at the end of the QRS comples.
I he ST segment begins at the J point and extends to a user defined interval
ST Segment Depression

63. EKG Changes: Ischemia ^
Acute Injury^ Infarction

65. Evolution of Transmural Infarction

66. Transmural Infarction
t— Before coronary occlusion —< -— Onset and first several hours

67. First and second days
Transmural infarction
nearly complete. Some
ischemia and injury may
be present at borders
Transmural infarction
complete
Infarcted tissue replaced by
fibrous scar, sometimes bulging
(ventricular aneurysm)

68. Evolution of a Subendocardial
Infarction

70. After several
First several days weeks or months
Some subendocardial muscle dies, Lesion heals Some subendocardial
but lesion does not extend through fibrosis may occur but does not
entire heart wall involve entire thickness of heart wall
R wave persists T wave
ST segment
but may diminish may or may notinversion and
somewhat return to normalmay occur T wave
CT

71. Hyperacute T waves

72. Anterior infarct
Occlusion of proximal left anterior
descending coronary artery
Significant Q waves and T wave inversions in
leads I, V2) V3 and V4
Anterior Septal (Left

73. Anterior Descending)

74. Inferior infarct
Occlusion of right
coronary artery
Significant Q waves and T wave inversions in leads II,
III and aVF. With lateral damage, changes also may
be seen in leads V5 and V6
Inferior (Right Coronary

77. Summary
a Basic physiology of the conduction system
0 Origin of a normal EKG 0 Systematic
approach to reading an EKG

78. 0 Major abnormalities when reading an EKG

79. Irani'S lOmm/mV 4€Hz 005B 12SL 237 CID: 1 HD: 123 EDT: 10:45 28-DEC-2006 ORDE

80. Referred bv :t by: s. G’ JRL1 lEV.
rfTTTTT
nm/5 1 Omni mV 40Hz 005B 12SL 235 CID! 1 16:26 05-SEP-2005 ORDEE

83. ECG Analysis
a An ECG is a diagnostic tool, NOT a
treatment
a No one was ever cured by an
ECG!!
Treat the PATIENT not the Monitor!!!

84. 60
THANK
YOU
61