1. Electrocardiogram Interpretation
ISMAIL HAMAM, MD
DEPARTMENT OF CARDIOLOGY
JORDAN UNIVERSITY HOSPITAL

2. Objectives To review Basic Concepts for the 12-Lead ECG
To know Normal Criteria for the ECG
To perform a Systematic Approach to ECG Interpretation.
To discuss a deferent Rhythms on the 12-Lead ECG

3. Basic Concepts
The heart is a pump with an electrical conduction system
2 basic types of cardiac cells in the heart
1. Myocardial cells or “muscle” cells
2. Specialized cells of the conduction system or “pacemaker” cells

4. The Electrical Cycle 1.The S-A Node generates an action potential.
2. The action potential
propagates in the atria
and causes a contraction.
It is also transmitted to
the AV Node.
3.The action potential is
delayed at the A-V Node.
4.The action potential is
transmitted to the ventricles
and causes contraction

5. The electrocardiogram (ECG) is a standardize way to measure and display the electrical activity of the heart.
Physicians can diagnose problems with the heart by analyzing its ECG and comparing it to the ECG

6. 12-lead ECG Simultaneous measurements from: – Three limb leads
– Three augmented limb leads
– Six chest leads
Process data from all leads to obtain ECG waveform

7. Structure of a 12-Lead Recording
The three standard or limb leads 1,2 and 3 have been in use since the late 1800’s, but the augmented limb leads aVR, aVL and aVF, and the precordial or chest leads V1-6 only came into use in the 1930’s.
The six precordial electrodes create a six-lead image of the heart on the transverse plane .Each of the pericardial leads is unipolar (1 electrode constitutes a lead).

8. Limb leads are three electrodes that are placed on the two arms and left leg create a 360o six-lead electrical image of the heart on the frontal plane on the ECG recording (1, 2, 3, aVR, aVL, aVF).
The lead on the right leg is system ground.
Accurate lead placement is important. Malposition can lead to significant interpretation errors, especially while comparing serial recordings from the same patient.

10. Limb Leads Lead Relative angle l: RA-LA 0° ll: RA-LL 60° lll: LA-LL
120°

11. Augmented Limb Leads: aVR = (LA-LL) vs. RA(+) aVL = (RA-LL) vs. LA(+)
aVF = (RA-LA) vs. LL(+)

12. Locating the leads The four limb leads are placed on the four limbs.
V1 in the 4th intercostal space adjacent to the right sternum.
V2 in the 4th intercostal space adjacent to the left sternum.
V4 in the 5th intercostal space in the mid- clavicular line.
V6 90o to the sternal axis at the same level as V4 and on the mid- axillary line.
V3 halfway between V2 and V4.
V5 halfway between V4 and V6, in the anterior axillary line.

14. Paper Speed and Voltages
Time is measured for cardiac heartbeats in milliseconds on the x-axis.
The standard 12-lead recording is made with the paper running through the machine at rate of 25 mm/sec.
This produces tracings along the X-axis with a duration of 40 msec/mm (“one small square”), or 200 msec for each 5 mm thick line (“one large square”) .
Strength of the electrical signal from the heart is measured in millivolts on the y-axis.
The ECG normally records a gain of 1 mV/cm on the Y-axis .

15. paper Paper speed = 25mm / second Voltage Time .1 mv .5 mv .04 seconds

16. Standard 12-lead electrocardiogram

17. The ECG Complex Component Physiologic Correlation P wave
Atrial depolarization
PR interval
AV node refractory period
PR segment
Atrial repolarization
QRS complex
Ventricular depolarization
J point
End of ventricular depolarization
ST segment
Blood flow from the ventricles
T wave
Ventricular repolarization
U wave
Uncertain
TP Segment
Rest prior to next heartbeat cycle

18. Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
Impulse delayed
at AV node
Impulse passes to
heart apex; ventricular
excitation begins
Ventricular excitation
complete
SA node
AV node
Bundle
branches
Purkinje
fibers

19. Normal Criteria for the ECG
P wave
≤ 110 msec. <0.25 mvolts in the limb leads.
Upright in 1, 2, aVF, V4-6.
Inverted in aVR.
Leads 1-3: single peak, or two peaks if they are < 40 msec apart.
Second half in V1 positive.

20. PR interval PR segment 120 - 200 msec. Usually measure in lead 2.
Shorter at faster rates and younger persons.
Longer in larger hearts and older persons.
PR segment
Usually isoelectric

21. QRS complex < 120 msec. And > 0.5 mV in all the limb leads.
> 1.0 mV in all of the precordial leads
Measure in the lead with the longest QRS duration.
Any initial upward deflection means that an R wave, not a Q wave, is present.
R wave increases in amplitude across the precordial leads, usually becoming larger in voltage than the S wave in V2 - V4 (transition zone) in adult

22. Limb lead QRS axis
Net electrical vector of ventricular
contraction
-30o to +105o
Overweight: more leftward, Thin: more rightward.

23. ST segment Usually within 1 mm of the isoelectric baseline.
Horizontal, with a smooth entry to the T wave.
Limb leads: isoelectric in 75% of normal persons; in the remaining 25% slight elevation is more common.
Precordial leads: slight elevation in 90% of normal persons, more common in men, usually in V2 and V3, where it can reach 3 mm.
ST depression is rare in 1, 2, and aVF in normal persons, and is considered abnormal in the precordial lead

24. T wave < 0.5 mvolts in the limb leads.
< 1.0 mvolt in the chest leads.
More gradual slope in the first half than the second half.
Upright in 1, 2 and V4-6 , inverted in aVR, variable in all other leads.
Upright, flat or slightly inverted in 3.
Upright in aVL, aVF if QRS > 0.5 mV.
Can be inverted in V1-2 in adult men, V1-3 in adult women (shallowly in V3).
Always upright in V5-V6.

25. TP segment U wave QT interval
Varies with the heart rate, age and gender.
Usually less than half the RR interval at normal sinus rates (65-90 bpm).
TP segment
Usually isoelectric
Can be used as a baseline reference like the PR segment.
U wave
Usually 5-25% the amplitude of the T wave.
Usually same polarity as the T wave.

26. The Normal EKG (ECG)

27. A Systematic Approach to Electrocardiogram Interpretation.
Step 1
To know the age, gender and history of the patient
Step 2
Standardization.
Y-axis (voltage, normally one millivolt per cm
X-axis (rate of recording, normally 25 mm/sec, or 200 msec/5 mm).

28. Step 3
Rate.
Calculate the rate by knowing that the Y-axis standardization is 25 mm/sec.
One small square (1 mm) is 40 msec in duration.
Therefore 2.5 cm represents one second.

29. Count the number of complexes across the 25 cm page (10 seconds), multiply by 6 and you get the average rate per one minute.
This is a useful way to estimate rate for irregular features.
Count the large squares between P waves for atrial rate and R waves for ventricular rate
300 ÷ number of large squares = number of beats/min

30. Step 4 Rhythm Identify P waves and QRS complexes.
Is the RR interval regular or irregular?
Note whether the QRS complex is wide (> 3 mm or 120 msec) or narrow.
Observe for -- rate, P wave and QRS complex synchrony, RR interval regularity, and width of the QRS complex – you can begin to sort out the rhythm.
Look for extra complexes such as premature atrial, junctional and ventricular contractions.

31. Normal sinus rhythm Rate 60 – 100 bpm Rhythm Regular
P wave Upright, normal
P-R – 0.20 sec
QRS – 0.12 sec
P : QRS Rasio 1: 1

32. 12 lead ECG

33. Step 5 Axis
Each of the 12 leads on the ECG has a different pattern because each lead views the hearts electrical axis from a different position
Atrial and ventricular depolarization and repolarization generate an electric current known as an electrical axis or vector (different from the axis of a lead)
The electrical current of a heartbeat normally flows from the SA node into the ventricles, roughly toward the positive pole of lead 2.
The normal range -30o to 105o but varies with age.

34. Limb lead axis.

35. Left axis deviation (LAD) any age group. -30o to -90o.
Right axis deviation (RAD) in adults. +90o to +180o.
Extreme axis deviation (EAD) any age group. -90o to -180o.

36. Step 6 P Waves. PR interval QRS Complex. Duration of PR interval
Note the width, height and shape of the P waves.
PR interval
Duration of PR interval
Dose PR segment is isoelectric
QRS Complex.
Note the width, height, shape and pattern of the complex.
Always assess Q waves relative to other clinical information
If Q waves are not clearly diagnostic, then call them “nondiagnostic”.

37. ST Segments
Study the ST segments separately from the T waves first, then together with the T waves.
Look for deviation from the baseline, and shape of the ST segment. Shapes include flat, upsloping, downsloping, curved and straight.
Note where the ST segment is relative to baseline 2 mm (80 msec) after the J point.
Note carefully how the ST segment enters the T wave: is it smooth, or does it have an ominous abrupt entry?

38. Measuring ST Segments
ST measurement = vertical difference between the isoelectric line + end of QRS complex, the “J” point”

39. ST segment elevation = >1 mm (>0
ST segment elevation = >1 mm (>0.1 mV) above baseline after the J point
ST segment elevation due to severe injury temporary until ischemia resolved or injured heart tissue heals or dies
ST segments elevate in leads facing the injury
ST segments depress in leads opposite (reciprocal ) leads

40. T Waves
Note height and shape of the T waves. Shapes include smooth symmetry, asymmetry sharp peaking, inversion, and biphasic.
Check again for the way the ST segment enters the T wave.
QT Interval
Calculate the QT interval to spot unusually short or long duration.

41. Sinus Tachycardia Causes Fever Pain Anxiety Hypoxia CHF
Fright or stress

42. Rate
Rhythm regular
P wave upright, normal
P-R sec
QRS sec
P: QRS ratio 1: 1

43. Sinus Bradycardia Causes Normal in athletes Increased vagal tone
Sinus node disease
Hypothermia
Acute MI
Drug effect (digoxin, CCB , BB)

44. Rate less than 60 bpm
Rhythm regular
P wave upright, normal
P-R sec
QRS sec
P: QRS ratio 1: 1

45. Junctional Rhythm Causes Digitalis toxicity Acute MI Ischemia Hypoxia
Post valve surgery

46. Sinus node and atria fail to pace the heart.
AV junction paces at → 40-60/min
No P wave or PR interval < 0.12, QRS normal

47. Idioventricular Rhythm
Causes
SA node and AV node fail to initiate rhythm. MI
Digoxin toxicity
Metabolic imbalance
Dying heart

48. Sinus node, atria, and AV junction fail to pace
Sinus node, atria, and AV junction fail to pace. Ectopic pacemaker in the ventricles paces at → 20-40/min
No P wave, QRS wide, ST & T waves often abnormal

49. AV Blocks First degree AV block Causes
May be normal findings especially in athletes
Myocardial ischemia injuring the AV node or junction
Medication :quinidine, BB, CHB, digoxin, and amiodaron
Acute MI
Rheumatic heart disease
Increased vagal tone

50. Usually normal rate , regular
PR interval is prolonged > 0.20
Normal QRS
P: QRS Ratio 1:1

52. Second degree AV block Causes
Ischemic damage below the AV node, involving the bundle of his or the bundle branch
Drugs , digoxin ,BB
Increased vagal tone

53. Mobitz type I (Wenckebach)
Progressive prolongation of PR interval until P wave fails to conduct to the ventricle
Progressive shortening of RR interval until P wave is not conducted
The RR interval containing the nonconducted
P wave is shorter than the sum of two PP intervals

54. Acute inferior myocardial infarction with atrioventricular
block, second degree–Mobitz type I (Wenckebach),

55. AV block, second degree–Mobitz type II
There are intermittent nonconducted P waves with no evidence of atrial prematurity
In conducted beats, PR intervals stay constant
The RR interval containing the nonconducted P wave is equal to two PP intervals

56. Sinus rhythm with atrioventricular block, second degree–Mobitz type II, and right bundle branch block.

57. Third degree AV block
Causes
Ischemic damage
Post cardiac surgery
Chronic degenerative changes of the conduction system
Drugs, digoxin ,BB

58. Independent atrial and ventricular activities
Atrial rate faster than ventricular rate
Ventricular rhythm maintained by a junctional or idioventricular escape rhythm or ventricular pacemaker
When the ventricular rate is faster than the atrial rate, AV dissociation (not AV block)

60. Superventricular Tachycardia
Ectopic focus in atria or AV junction paces the heart
or Abnormal conduction thru AV node
or Accessory pathway
P wave or no P wave, QRS narrow or wide,
rate > 150/min

62. Ventricular Tachycardia
Ectopic pacemaker in ventricles paces the heart
No P wave, QRS wide and bizarre

65. Premature Ventricular Contractions
QRS Duration
QRS duration - depolarization of right and left ventricles, from the endocardium to epicardium
Normal QRS duration sec
QRS duration > sec, a conduction delay exists in the bundle branches, Purkinjie network or ventricular myocardium, or ventricular ectopic conduction exists

66. PVC’s, premature ventricular complexes:
the premature beat originates in an ectopic
focus in one ventricle, it depolarizes that
ventricle, then the other
No P wave, QRS wide & bizarre, ST often abnormal, T wave often opposite the rhythm
Multifocal PVC’s come from more than one ectopic focus, each foci has a different shape

67. 1 PVC = a PVC
2 PVC’s = couplet
3 PVC’s = triplet
4 PVC’s = ventricular tachycardia
Every 2nd PVC = bigeminy
Every 3rd PVC = trigeminy
Bigeminy or trigeminy can refer to any ectopic beat so clarify -
eg. bigeminal PVC’s or bigeminal PAC’s, etc.

72. ST Segments

73. Other Common Causes of ST Segment Elevation
Coronary artery vasospasm
Acute pericarditis
Ventricular aneursym
Hyperkalemia
Non-specific ST-T wave changes

74. ST Segment Depression
ST segment depression = > 1 mm below baseline after the J point
ST segment depression due to severe ischemia temporary until ischemia resolved or heart tissue heals
ST segments depress in leads facing the ischemia
ST segments elevate in opposite (reciprocal) leads

76. Other Common Causes of ST Segment Depression
Left and right ventricular hypertrophy
Left and right bundle branch block
Digitalis in therapeutic and toxic doses

77. Acute MI Facing Leads Opposite Leads
Anterior
Septal V1-V None
Anterior V3-V None
Lateral I, aVL, & V5 or V II, III, & aVF
Inferior II, III, & aVF I & aVL
Posterior V7,V8, V9 on 18 lead V1-V4
Right Ventricle V4R None

80. Thank you