1. Basic Clinical Electrocardiography Kitty Chan
School of Nursing,The Hong Kong Polytechnic University
Date: 2005

2. Objectives Upon completion of the session, the students should:
have developed a basic understanding of anatomy and of the physiology of cardiac conduction in relation to ECG interpretation;
have developed a systematic and pragmatic approach to ECG interpretation;
appreciate the clinical significance of ECG interpretation.

3. Indicative Readings
Wiegand, L-M D. J. & Carlson, K. K. (Eds.) (2005). American Association of Critical-Care Nurses AACN Procedure Manual for Critical Care. (5th ed.). Philadelphia: W B Saunders.
Section 8
Huszar, R. J. (2002). Basic Dysrhythmias: Interpretation & Management. (3rd Ed.). St Louis: Mosby.

4. The above two aspects will be the main focus of this module.
Introduction
The electrocardiogram [ECG] is a helpful in diagnosing cardiac & non-cardiac illnesses. It is also used to monitor the effects of therapeutic treatment.
Cardiac monitoring, or telemetry provides a continuous and real-time observation of the client’s cardiac rhythm. A single-strip ECG gives a prompt identification of life-threatening rhythms. In addition, abnormalities that are detected can serve as a basis for 12-Lead ECG or other investigations.
12-Lead ECG imparts more information, such as ischaemia and myocardial infarction.
The above two aspects will be the main focus of this module.
Of course, interpreting axis deviation & hypertrophies or other abnormalities is highly recommended.

5. Introduction
Electrical activities produce current that transmit through the heart conduction system. This is sensed and transformed into ECG waveforms. Depolarization and repolarization occurs in a precise sequence.
Normally, mechanical heart contraction follow to generate the cardiac output.
However, when disturbances arise, cardiac contraction may not be effective, and there may even be no contractions.
Therefore, always match the ECG rhythm with the patients’ clinical manifestation and complains.
Before we start interpreting ECG, the anatomy, cardiac cycle and electrophysiology are reviewed

6. Five Phases of the Depolarization-Repolarization Cycle
Response and Action Potential
Rapid Depolarization
A current is conducted from adjacent cells.
In response to a stimulus from connecting cells, a sodium channel opens
There is a rapid influx of Sodium into the cells
Calcium moves slowly into the cells
The cell membrane charge moves from -90mv to mv 1
Early Repolarization
Sodium channels close
The cells begin to return to a negative state 2
Plateau
The Calcium channels open
Slow influx of Calcium
Outflow of Potassium
Cell membrane potential is around 0mv 3
Rapid Repolarization
The Calcium channels close
Rapid outflow of Potassium
Cell membrane potential drops rapidly back to it resting membrane potential [RMP] 4
Resting
The Sodium pump is reactivated (* It depends on an adequate amount of Magnesium & Phosphate). Normal electrolytes distribution restored:
The Cell membrane is impermeable to Sodium
Potassium inside the cell & sodium outside the cell
The Resting Membrane Potential -90mv

7. Myocardial Transmembrane Potentials
Resting State
Rapid Depolarization
Early Repolarization
Rapid Repolarization
Potential milivolts    
Plateau
Action Potentials
Threshold Potentials
Mechanical Contraction
Absolute Refractory Period
Restoration of Balance
Sodium Pump K+
Na+
Relative Refractory Period
Cardiac
cell
Cell
membrane
Outside cell
Ca++
- - -
Fast Sodium Influx
Slow Calcium channel open  Plateau

8. Electrophysiological Properties
Properties of Cardiac Cells
Term
Electrophysiological Properties
Automaticity
Spontaneous Depolarization (Pacemaker Potential):
Cardiac cells initiate their own action potential WITHOUT a stimulus from another cell
A cell membrane allows Na+ & Ca++ ions to move in & prevents K+ from diffusing out. A NET build-up of positive ions inside the cell enables it to reach a threshold (TP) & depolarize
The slope of the pacemaker potential (i.e., the time it takes to reach TP) determines the automaticity of the cells
Excitability
Ability of a cell to depolarize in response to a stimulus:
The more negative the Resting Membrane Potential 
The LESS excitable is the cell;
The FASTER the conduction velocity
Conductivity
Ability of a cardiac cell to transmit an impulse
Refractoriness
The state of a cardiac cell: Regardless of the intensity of the stimulus (much stronger than normally required) to initiate repolarization

9. Electrophysiological Properties
Automaticity of Cardiac Cells
Cardiac Cells
Electrophysiological Properties
SA Node
Main Pacemaker:
Intrinsic firing at a rate of times/minute
Impulse generation is fastest & dominant
Impulse transmission follow specific path
AV Node
Slow Node:
Depolarizes at a rate of times/minute
Delays impulses from the SA node by 0.04 seconds
Generates impulses when the impulse generation function of the SA node pulse impairs
His-Purkinje Fibres
The Left & Right Bundle Branch conduct impulses at different speeds to synchronize the depolarization of the Left & Right Ventricles
Purkinje fibres are usually not activated unless the pulse transmission is blocked or not generated from higher pacemakers
Generates impulses & serves as a pacemaker at a rate of bpm or slower
The impulse transmission is chaotic

10. Pacemaker Action Potentials & Automaticity
Time (Second)
1.6
0.8
2.4
+ 10mV
-90mV
Membrane Potential
Threshold Potential
Action Potential
Resting Membrane Potential
-60mV
Pacemaker Potential: Spontaneous Depolarization
Automaticity in cardiac muscles:
a gradual  in K+ permeability  resting potential  Transmembranous Potential [TMP] reaches a threshold  Spontaneous depolarization occurs
SA node - shortest phase 4  dominates impulse generation

11. Pacemaker Action Potentials & Automaticity
Time (Second)
1.6
0.8
2.4
+ 10mV
-90mV
Membrane Potential
Threshold Potential
Action Potential
Resting Membrane Potential
-60mV
Steeper Slope: Automaticity Increase
Pacemaker Potential: Spontaneous Depolarization

12. Pacemaker Action Potentials & Automaticity
Time (Second)
1.6
0.8
2.4
+ 10mV
-90mV
Membrane Potential
Threshold Potential
Action Potential
Resting Membrane Potential
-60mV
Slope Decreases : Automaticity Decreases
Pacemaker Potential: Spontaneous Depolarization

13. Resting Membrane Potential
Effect of Change in RMP
Time (Second)
1.6
0.8
2.4
+ 10mV
-90mV
Membrane Potential
Threshold Potential
Action Potential
Resting Membrane Potential
-60mV TP
Bigger Difference
RMP
RMP Decreases (More Negative):
Cells are less excitable  Stronger stimulus required for depolarization  contractility weakens
This occurs in HYPOKalaemia

14. Resting Membrane Potential
Effect of Change in RMP
Time (Second)
1.6
0.8
2.4
+ 10mV
-90mV
Membrane Potential
Threshold Potential
Action Potential
Resting Membrane Potential
-60mV TP
RMP
Closer to TP
RMP Increases (Less Negative):
Cells are easily excitable  Depolarization occurs with a very weak stimulus contractility slow & ineffective
This occurs in HYPERKalaemia

15. Resting Membrane Potential
Effect of Change in TP
Time (Second)
1.6
0.8
2.4
+ 10mV
-90mV
Membrane Potential
Threshold Potential
Action Potential
Resting Membrane Potential
-60mV TP
RMP
Closer to RMP
TP Decreases:
Closer to RMP, the cells are more excitable  Depolarization occurs with a very weak stimulus contractility slow & ineffective
This occurs in HYPOCalaemia
 HYPERCALCAEMIA is a Positive Inotrope since it sustains & strengthens cardiac contractions

16. Electrical Conduction System
Sinoatrial (SA) Node
Interatrial conduction tract
(Bachmann Bundle)
Atrioventricular (AV) Node
AV Junction
Internodal atrial conduction tract
Bundle of His
Left Bundle Branch
Left posterior fascicle
Left anterior fascicle
Right Bundle Branch
Purkinje fibres

17. Wave Deflection & Current Direction
-ve ve
Electrical Waveform
Deflection
Toward the Lead
UPRIGHT
Away from the Lead
DOWNWARD
Perpendicular to the Lead
BIPHASIC

18. Cardiac Depolarization & Electrical Current
1. Atrial Depolarization
2. Septal vector
3. Apical vector & both ventricles
4. Remainder of the left ventricle
R. Resultant Cardiac Vector 1 4 2 R 3
A positive deflection (upstroke) Λ is recorded as depolarization proceeds towards the particular electrode & vice versa.

19. Limb Leads: Frontal Plane of the Heart Standard Bipolar Leads
Lead I + +
Lead II
Lead III +
Einthoven’s Equilateral Triangle
Inferior

20. Limb Leads: Frontal Plane of the Heart The Augmented Unipolar Leads
Lead aVR
Lead aVL x
Null Reference Point
Lead aVF
Null Reference Point: the negative reference for leads aVR, aVL, aVF & the precordial leads V1 - V6
(calculated from the right & left arm and right & left leg electrodes)

21. Hexaxial Reference Circle
For determining frontal plane axis deviation
aVF +900
-900
III +1200
-600
II +600
-1200
aVL
-300
+1500
aVR -1500
+300
LAD
Indeterminate
NORMAL
I 00
+1800
RAD

22. 12-Lead Electrode Placement
✼Precordial Leads are useful in detecting ST Changes & Aberrant Ventricular Conductions
Mid-Clavicular Line
Anterior Axillary Line
Mid-Axillary Line V1 V2 V3
V1 to V6: Corresponding sites for monitoring of MCL1 to MCL6 V6 V4 V5
Lateral Leads
Septal Leads
Anterior Leads
i.e., Electrode Placement at V6 equivalent of MCL6
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

23. Right-sided Chest Electrode Placement
Mid-Clavicular Line
Anterior Axillary Line
Mid-Axillary Line
V2R
V6R
V3R
V5R
V4R

24. Posterior Chest Electrode Placement
Left Paraspinal Line
Posterior Axillary Line
Mid-Axillary Line V6 V7 V8 V9
Wiegand & Calrson, 2004, p. 426

25. Cardiac Monitoring & Lead Placement
3-Lead-Wire system:
limited to leads I, II, III &
modified chest leads (MCL1-6)
For single-lead ECG monitoring, unless a specific part of the heart is under scrutiny, Lead II is usually chosen since both the positive & negative vectors are travelling in the same direction of cardiac impulse conduction, producing upright P & QRS complexes.

26. Cardiac Monitoring & Lead Placement
5-Lead-Wire system:
4 standardized electrodes corresponding to limbs leads I, II, III, aVR, aVL & aVF
placement of 5th chest leads provides 7 precordial lead options V1-V6 (1 at a time)

27. 1mm tall = 0.1mV of amplitude
1 Large Square
5 Large Squares
= 1 Second
1 Small Square
1mm tall = 0.1mV of amplitude
*Sweep speed of ECG & paper 25mm per second
5mm across = 0.2 second
1mm across
= 0.04 second

28. Normal ECG/EKG WaveformP T U R Q S
ST Segment
PR Interval
QT Interval
Lead II Q R S
ST Segment T P U
PR Interval
QT Interval

29. Normal ECG Waveforms & Configurations
Configuration & Duration (second)
Leads
Amplitude
Duration P
Rounded & Symmetrical
Amplitude cm
I, II, aVF, V4-V6
PR Interval
QRS
Q: Small & Non-significant
I, II, III, aVL, V4-V6
R: progressively higher in amplitude –
limb leads > 5mm
chest leads > 10mm
V2-V5, gradually diminish in V5-V6 ST
Curves gently into the proximal limb of the T wave
Isoelectric in ALL Leads
Elevation < 1mm & Depression < 0.5mm
J Point
Junction of QRS complex & the ST segment
T wave
Rounded & Symmetrical, amplitude:
limb leads< 5mm & chest leads < 10mm
Positive in I, II, V3-V6
Inverted in aVR QT
(<½ preceding RR)
U wave
Delayed depolarization of the purkinje system

30. P wave: Atrial Depolarization
rounded & symmetrical
sec
amplitude: mm
positive in Lead I, II, aVF & V4-V6
PR Interval:
sec P
PR INTERVAL
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

31. QRS: Ventricle Depolarization
Q waves is small & nonsignificant in leads I, II, III, aVL, V4-V6
R wave progressively higher in amplitude from V2-V4/V5 gradually diminish to V6
sec
amplitude: >5mm in limb leads; >10mm in Chest leads P
QRS
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

32. ST Segment: Isoelectric Line
Curves gently into the proximal limb of the T wave
Isoelectric in ALL Leads
elevation <1mm
depression <0.5mm
J Point:
The junction of QRS complex & the J point of the ST segment
deviates from the isoelectric line if an ST elevation/ depression exist P
QRS
J Point
ST SEGMENT
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

33. T wave: Ventricular Repolarization
QRS P QT T:
slightly rounded & symmetrical
positive in leads I, II, V3-V6
inverted in aVR
amplitude <5mm in limb leads & <10mm in chest leads
QT: ventricular refractory period
sec
* sec (<½ preceding RR)
U wave: delayed repolarization of the purkinje system
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

34. Sinus Rhythm
Sinus Rhythm

35. Normal Sinus Rhythm [NSR] Each P is followed by a QRS
Total in 6 seconds
Characteristics
P Waves: 7
Upright & amplitude 1mm
PR Interval
0.12 second
Each P is followed by a QRS
QRS Complex
7 (HR=70bpm)
Normal (0.12 second)
RR Interval
Regular
6 Seconds P

36. Each P is followed by a QRS
Sinus Bradycardia
Total in 6 seconds
Characteristics
P Waves: 5
Upright & amplitude 1mm
PR Interval
0.12 second
Each P is followed by a QRS
QRS Complex
5 (HR=50bpm)
Normal (0.12 second)
RR Interval
Regular
6 Seconds P
QRS Complex

37. Sinus Dysrhythmias Sinus Dysrhythmias Characteristics Sinus Pause
dropped P wave & SR resumed subsequently
Sinus Arrest /Sinoatrial Exit Block
SA node fails to initiate an impulse for  3 seconds
Sick Sinus Syndrome (SSS):
Paroxysmal or alternating sinus bradycardia & atrial tachycardia (brady-tachy syndrome)
Failure to HR to meet body demand

38. 
Atrial Dysrhythmias

39. SAW-TOOTH FLUTTER WAVES
Atrial Flutter
Total in 6 seconds
Characteristics
P Waves:
Varies
Saw-Tooth
QRS Complex
9 (HR=90bpm)
Normal
RR Interval
IRREGULAR
6 Seconds
QRS Complex
F F F F F F
F F F F
Identical undulating
SAW-TOOTH FLUTTER WAVES

40. Atrial Fibrillation [Fine AF] FIINE Fibrillatory Waves
Total in 6 seconds
Characteristics
P Waves:
Varies
FIINE Fibrillatory Waves
QRS Complex
HR bpm
Normal
RR Interval
IRREGULAR
6 Seconds

41. Atrial Fibrillation [Coarse AF] Coarse Fibrillatory Waves
Total in 6 seconds
Characteristics
P Waves:
Varies
Coarse Fibrillatory Waves
QRS Complex
HR 80bpm
Normal
RR Interval
IRREGULAR
6 Seconds

42. Atrial Dysrhythmias MAT (multifocal atrial tachycardia)
Atrial Dysrhythmias P’
MAT (multifocal atrial tachycardia)
Various P morphologies originate from multiple atrial ectopic foci
*(3 or more pacemaker sites)
Rate = bpm

43. Juntional Rhythm  6 Seconds QRS Complex Total in 6 seconds
Characteristics
P Waves:
QRS Complex 6
(HR=60bpm)
Normal
RR Interval
0.98 second
REGULAR 
6 Seconds
QRS Complex

44. Junctional Dysrhythmias
1o pacing from the AV node
Junctional Dysrhythmias

45. Re-Entry Phenomenon [1]
Non-uniform recovery from refractory period leading to re-entry circuit:
1. Slow conduction of impulses at a refractory zone → Unidirectional Block→ Detouring of Impulse
2. Activation & transmission of impulse via accessory pathway
3. Subsequent activation of impulse through the previously refractory zone (now recovered)
4. The reentry & activation of new impulses occur in a circuitry manner

46. Re-Entry Phenomenon [2]
Normal Impulse NOT yet fired from SAN
∴ AV Node NOT Reactivated
Unidirectional Block & Delayed Conduction within the circuit
Original impulse emerges & reenters the adjacent tissue (just recovered)
Recycles within the circuit
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

47. Ventricular Pre-excitation
AVNRT (AV Node Re-entry Tachycardia)
Micro-Circuits: At cellular level within the AV node with unidirectional block & the Purkinje fibers
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

48. Classic Ventricular Pre-excitation
delta wave
(slurred upstroke)
Wolf-Parkinson-White Syndrome:
pre-excitation via a Bundle of Kent without delay at the AV node
Depolarization occurs with AV impulse after normal delay
AVRT (AV Re-entry Tachycardia)-
Macro-Circuits: Antegrade travel through the AV node & retrograde across an accessory pathway
Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

49. PSVT (Paroxysmal Supraventricular Tachycardia)
*It is useful to capture the beginning of the PSVT to identify the re-entry loop, especially when aberrant conduction occurs & a wide bizarre QRS exists

50. Atrioventricular Blocks (Heart Block)

51. Heart Block 1o HB P PR Interval: Constant RR Interval: Constant
P:QRS Relationship -1:1
1o HB 1o P
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

52. Absence of QRS complex after P
Heart Block
Type I 2o HB (Wenkebach) 2o
Non-conduction
Absence of QRS complex after P P
PR Interval: Progressive lengthening
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

53. Heart Block Type II 2o HB sudden drop beat Advanced AV Block 3:1 Block
PR Interval: Constant
Advanced AV Block
3:1 Block
PR Interval: Constant
RR Interval: Constant
Regular drop beat(s)
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

54. Heart Block 3 o HB NO Relationship between P & QRS complex
R-R Interval Constant
P-P Interval Constant
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

55. Third Degree Heart Block & A-V Dissociation
Sinus Dysrhythmias, AV Conduction distrubances or Junctional/Ventricular Tachycardai may result in complete Atrioventricular (AV) Dissociation
Differentiate 3o HB & AV Dissociation:
3o HB
Atrial Rate > Ventricular Rate
AV Dissociation
Atrial Rate ≈ Ventricular Rate (slightly faster)
RARELY the Primary Problem

56. Right Bundle Branch Block
rSR’ pattern
Wide S wave
✼ RBBB: QRS  0.12 sec
T wave Inversion in V1 is common r R’
Late abnormal electrical vector leading to depolarization of right ventricle > (R’)
RBBB
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

57. Left Bundle Branch BlockV6
Large notched R wave
T wave inversion V1
QS WAVE: Wide negative QRS
LBBB
Impulse activates across the septum from Right to Left
Delayed & prolonged electrical vector toward the eft ventricle → notched R wave
✼LBBB: QRS  0.12 sec
Elevated ST is common in V1-V4
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

58. Hemi-/ Fascicular Blocks
Left Posterior Fasicular Block (LPFB)
Left Anterior Fasicular Block (LAFB)

59. Ventricular Dysrhythmias
Ventricular Dysrhythmias
Ectopic foci

60. Premature Ventricular Contractions (PVCs)
Group Beats
Couplet
Ventricular Tachycardia
Bigeminy
R-on-T
Trigeminy
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

61. Ventricular Dysrhythmias Ventricular tachycardia (monomorphic)
Ventricular Dysrhythmias
Ventricular tachycardia (monomorphic)
Torsades de pointes
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

62. Ventricular Dysrhythmias
Coarse V F
Fine V F
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

63. Ventricular Dysrhythmias
1. EMD (electromechanical dissociation):
*apparently normal ECG but no cardiac output/pulse generated
2. PEA (pulseless electrical activity)
3. Asystole
PEA
Asystole

64. Atrial & Ventricular Hypertrophies

65. Right Atrial Hypertrophies
P Pulmonale in Leads II, III & aVF : Direction: Upright Amplitude: ≥ 2.5mm
4mm

66. Left Atrial Hypertrophies
P-Mitrale in Lead I, II, V4-6
Biphasic P: duration > 0.10 second

67. Left Ventricular Hypertrophies
R wave in Lead I : 20mm S wave in Lead III: 20mm R [I] OR S [III] = 20mm (Fit criteria ≥ 20mm) R [I] + S [III] = 40mm (Fit criteria ≥ 25mm)
S wave in Lead V1 : 12mm R wave in Leads V5 & 6: 45 & 39mm, respectively S [V1] + R [V5] = 41mm (Fit criteria ≥ 35mm)

68. Normal 12-Lead Electrocardiogram
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

69. Acute Coronary Syndrome & Coronary Circulation
Coronary atherosclerosis poses the potential risk of plague rupture, mircroemboli & occlusive thrombus 
A spectrum of clinical syndromes will develop due to coronary artery occlusion:
1. Unstable angina
2. Non-Q MI
3. Q wave MI
4. Sudden cardiac arrest
Totora G J & Grabowski S R 2003 Principles of Anatomy and Physiology. 10th ed. New York: John Wiley & Sons.

70. Anterior View of Coronary Arteries
Arch of Aorta
Pulmonary Trunk
Left Coronary Artery [LCA]
Ascending Aorta
Left Atrium
Circumflex Coronary Artery [Cx]
Right Coronary Artery [RCA]
Left Anterior Descending Coronary Artery [LAD]
Right Atrium
Left Ventricle
Acute Marginal Artery
Right Ventricle
Posterior Descending Artery [RD]

71. Acute Subendocardial Ischaemia Acute Transmural Ischaemia
Myocardial Injury: Ischaemia and Infarction V5
Acute Subendocardial Ischaemia V5
Acute Transmural Ischaemia

72. Myocardial Injury:Ischaemia and Infarction
Ischaemic Zone
Injury Zone
Infarction Zone
Infarction  significant Q/QS wave
*absence of depolarization current from dead myocardial tissue
 facing lead recorded opposing electrical vector “through” infarcted area
Injury
 elevated ST
Ischaemia
 T wave inversion
* Reciprocal Effect on Opposite Leads
Recovery  ST & T wave return to normal
Lead I

73. Anterior View of Coronary Arteries
Coronary Circulation & Ischemic Changes
Lateral
I, aVL
Lateral
V5 & V6
Anterior
V3 & V4
Septal
V1 & V2
Inferior
II, III, aVF
Anterior View of Coronary Arteries

74. Myocardial Infarction & 12-Lead ECG

75. Anteroseptal Myocardiac Infarction
QS waves: V1 & V4 *(r waves absent)
ST segment elevation: V1-V4
EARLY ECG CHANGES: hours
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

76. Anteroseptal Myocardiac Infarction
2- 24 hours:
Maximal ST elevation
minimal Q wave formation
hours:
QS wave in V1-V4
ST returned to Baseline
T waves inversion
LATE ECG CHANGES
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

77. ST Changes Associated conditions: Myocardial injury or infarction
Normal ST
Associated conditions:
Myocardial injury or infarction
pericarditis
ventricular fibrosis, aneurysm
ventricular hypertrophy
digitalis effect
ST Depression
ST Elevation
Flat
Downsloping
Upsloping
Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

78. ECG Changes in Hypokalemia
Gradual ST depression
Flattened T wave
Tall U wave
Serum <K+ 3mEq/L
Serum <K+ 2.7mEq/L
Prolonged PR
U wave size increases
Serum <K+ 2.0mEq/L
Widened & Bizarre QRS complex
Marked ST depression
Inverted T

79. ECG Changes in Hyperkalemia
Peaked, narrow, bpm
Serum K+ > 5.5 mEq/L
Serum K+ progressive  6.5  8.0mEq/L
Loss of P wave & Bizarre QRS
Atrioventricular block, sinus arrest, VF , asystole

80. ECG Changes: Hypocalcemia/Hypercalcemia
Serum Ca++ < 8.5mg/dL
Lengthened ST
Lengthened QT
May cause Torsades de pointes
Serum Ca++ > 10.5mg/dL
Shortened ST
Shortened QT

81. ECG Changes: Hypomagnesemia/ Hypermagnesemia
Serum Mg++ < 1.5mEq/L
Lengthened QT
Broad & flattened T
often co-exist with hypokalemia
Serum Mg++ > 2.5mEq/L
Prolonged PR
Lengthened QT
QRS > 0.12sec

82. Systematic ECG Interpretation
1: Determine Dysrhythmia
Calculate HR
Determine the ventricular rhythm
Measure the RR regularity - variance < 0.12 second
(use a caliper or the paper-&-pencil method)
Identify & examine the P waves morphology
Measure the PR interval
Measure & Examine QRS complex morphology
Examine P:QRS correlation
Look for escape or dropped beats
Look for miscellaneous abnormalities
2: Identify Atrioventricular Block & Aberrant Conduction
3: Identify Axis Deviation & Hypertrophies
4: Determine MI - 12-Lead ECG overview

83. Heart Rate Calculation
1. Six Second Count Method:
Number of R-R intervals in a 6sec strip x 10 = HR bpm
2. R-R Interval Method:
HR bpm = 300  Number of Large Squares between the peaks of 2 consecutive R waves
6 second Interval
RR Interval

84. Heart Rate Calculation
3. Conversion table:
Number of Small Squares between the peaks of 2 consecutive R waves
4. Heart Rate Calculator Ruler Method:
HEART RATE CALCULATOR
* 3rd Complex from Arrow = bpm

85. Basic Dysrhythmias Interpretation Algorithms
P wave
Indeterminate
VENTRICULAR DYSRHYTHMIAS ALGORITHM
P-R normal
SINUS RHYTHM ALGORITHM
P-R > 0.2 s
HEART BLOCK ALGORITHM
Identifiable
Normal
P’ present or absent
QRS normal
Polymorphic
Irregular R-R
Irregular P-R
bpm
MULTIFOCAL ATRIAL TACHYCARDIA
Fibrillatory baseline
Flutter waves
Regular or irregular R-R
ATRIAL FIBRILLATION
ATRIAL FLUTTER
SUPRAVENTRICULAR TACHYCARDIA
P:QRS = 1:1
Regular R-R
Regular P-R HR
40-60
HR>100
60-100
ACCELERATED JUNCTINAL RHYTHM
JUNCTIONAL
RHYTHM
JUNCTINAL THCHYCARDIA

86. Sinus Dysrhythmias & Heart Blocks Algorithms
P-R interval normal sec.
P:QRS = 1:1
Regular atrial rhythm
Regular R-R HR
<60
Sinus Bradycardia
Sinus Tachycardia
60-100
Regular Sinus Rhythm
Irregular atrial rhythm
Irregular R-R
Sinus Arrhythmia
Progressive  PR
Regular non-conducted QRS
2o Heart Block
Wenkebach
Morbitz Type I
Constant prolonged PR HR
1o Heart Block
P > QRS
Constant  PR
Sudden dropped QRS
Morbitz Type II
No relationship ./. P & QRS
3o Complete Heart Block
P-R interval > 0.20sec.
P WAVE NORMAL

87. Ventricular Dysrhythmias Algorithms
Unidentifiable QRS
Coarse & or fine fibrillatory waves
Ventricular Fibrillation
Narrow-complex QRS ( 0.12 sec)
HR bpm
PSVT
Wide-complex QRS (>0.12 sec)
HR =
Accelerated Idioventricular Rhythm
HR< 40
Idioventricular Rhythm
HR:
Monomorphic
SVT & Aberrant Conduction
Polymorphic
Torsade de Pointes
Ventricular Tachycardia
P WAVE Indeterminate

88. QRS Axis Determination: Frontal Plane
There are a few methods for determining the Frontal Plane Axis and identifying any Axis Deviation. Each has its advantages.
The Quadrant method for locates deviation quickly & easily, while the Degree Method gives exact measurements.
Choose the one that is most suitable for you & practice reading 12-Lead ECG using the same method.
Once you are familiar with a method, you might try another one.

89. QRS Axis Determination: Frontal Plane
Quadrant Method:
Use Leads I & aVF
Locate the Main Deflection of the QRS complex
Axis
QRS complex
Lead I
Lead aVF
Normal
Upright in Both Leads
Left Axis Deviation
Upright
Points Downward
Right Axis Deviation
Indeterminate

90. QRS Axis Determination: Frontal Plane
Quadrant Method:
-90o
±180o
+0o
+90o

91. QRS Axis Determination: Frontal Plane
Degree Method:
Use Leads I & aVF
A negative wave (usually an S wave) is subtracted from the height of the R wave.
Plot the resultant vector on the hexaxial reference circle to locate the axis

92. QRS Axis Determination: Frontal Plane
Degree Method: Step 1

93. QRS Axis Determination: Frontal Plane
Degree Method: Step 2

94. QRS Axis Determination: Frontal Plane
Degree Method: Step 3

95. QRS Axis Determination: Frontal Plane
Null Plane Method:
Identify the equiphasic QRS
Locate the corresponding perpendicular lead
Map the axis that is parallel to this lead
The axis points to the predominant direction of either the positive or negative pole

96. Horizontal Axis Rotation
Dominance of Electrical Vector (Normal):
V3 : R > S
V4 : S > R
(V3 & V4 is the transition zone)
Identify the relationship of S-deflection & R-deflection in V1 to V6
Determine Axis Rotation:
Clockwise Rotation – Shift to V5 & V6
Counter-clockwise Rotation – Shift to V1 & V2

97. Clinical Significance of ECG Interpretation
Recognizing Life-threatening dysrhythmias is extremely important:
prompt interventions for cardiac arrest & cardiac compromise
restoration of haemodynamic stability
Familiarizing with anti-arrhythmic medications & life-saving measures are essential
Further readings:
Advanced Cardiac Life Support (ACLS) algorithms

98. Antiarrhythmic Therapy

99. References
Davis, D. (2001). Quick and Accurate: 12-Lead ECG Interpretation. (3rd Ed.). Philadelphia: Lippincott.
Huszar, R. J. (2002). Basic Dysrhythmias: Interpretation & Management. (3rd Ed.). St Louis: Mosby.
Huszar, R. J. (2002). Pocket Guide to Basic Dysrhythmias: Interpretation & Management. (3rd Ed.). St Louis: Mosby.
Jackson, K. (Ed.). (2002). ECG Interpretation made Incredibly Easy. (2nd Ed.). Springhouse: Springhouse.
Linda, D., Urden, K. & Stacy, M. E. L. (2002). Thelan’s critical care nursing: diagnosis and management. (4th ed.). St Louis: Mosby.
Lewis, K. M. (2000). Sensible ECG Analysis. Albany: International Thomson Publishng Company.

100. References
Paul, S. & Hebra, J. D. (1998). The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders.
Swearingen, P. L. & Keen, J. H. (2001). Manual of Critical Care Nursing: Nursing Interventions & Collaborative Management. (4th Ed.). St Louise: Lippincott.
Lead ECG Interpretation. Baltimore: Williams & Wilkins *CD-ROM

101. Journals
Adams-Hamoda, M. G., Caldwell, M. A., Stotts, N. A. & Drew, B. J. (2003). Factors to Consider When Analyzing 12-Lead Electrocardiograms for Evidence of Acute Myocardial Ischemia. American Journal of Critical Care, 12(1) 9-18.
Hutchisson, B., Cossy, S. & Wheeler, R., (1999). Basic Electrocardiogram Interpretation for the OR Nurse. AORN Journal, 69(1)
Henderson, N. (1997). Electrocardiography. Nursing Standard, 11(44)
Drew, B. J. (2002). Celebrating the 100th birthday of the electrocardiogram: Lessons learned from research in cardiac monitoring. American Journal of Critical Care, 11(4) 378.

102. Web Resources
Jenkins, D. & Gerrid, S. (2002). ECG Library. Retrieved July 20, 2005, from
Mysioki, F. (2003). McGill Medical Informatics. Electrocardiology and Cardiac Arrhythmias. Retrieved July 20, 2005, from McGill Univeristy, Physiology Department Web site:
SkillStat Learning Inc. (2005). SkillStat Learning Tools. Retrieved July 20, 2005, from
Scheinman, M. M. (n.d.). Supraventricular Tachycardias Tutorial. Retrieved July 20, 2005, from the Electrophysiology Service at UCSF in San Francisco, California Website:
Texas Arrhythmias Institute. (n.d.). Educational Material: Arrhythmias & Heart Failure. Retrieved July 20, 2005, from
Wong, R. (n.d.). Heart Sound Tutorial. Retrieved July 20, 2005, from The Harbor-UCLA Medical Center, Research lab of John Michael Criley, M.D. Website:
Yaniwitz, F. G. (2002). ECG Learning Center in Cyberspace. Retrieved July 20, 2005, from University of Utah School of Medicine, ECG Department Web site: