1. ELECTROCARDIOGRAMs (ECGs)
Cardiac Wellness Institute of Calgary
Updated May 2010

2. Material to be Covered
ACSM’s Resource Manual for Guidelines for Exercise Testing and Prescription (6th ed.)
Chapter 27
Rapid Interpretation of EKG’s (6th ed.)

3. LEAD PLACEMENT Standard 12-lead ECG:
Limb Leads - 6 in all I, II, III, aVL, aVR, aVF
Chest leads - 6 in all V1,V2,V3,V4,V5,V6

4. LIMB LEADS
III II I
Bipolar + -
aVL
aVR
Augmented +
aVF

5. Along the horizontal plane:
CHEST LEADS
Along the horizontal plane:
V1 and V2 - Right side of the heart
V3 and V4 - Intraventricular septum
V5 and V6 - Left side of the heart

6. PROCESS
SA Node - Heart pacemaker; located in the RA; initiates next step

7. P Wave - Atrial depolarization and contraction
PROCESS
P Wave - Atrial depolarization and contraction

8. PROCESS
AV Node - Slows the depolarization of the atria; connects atria and ventricles electrically

9. PROCESS
QRS complex - ventricular depolarization; begins in Bundle of His

10. PROCESS

11. VENTRICULAR DEPOLARIZATION
His Bundle Left Bundle Branch & Right Bundle Branch Purkinje Fibers

12. VENTRICULAR DEPOLARIZATION
Q Wave - 1st downward wave of the complex
R Wave - 1st upward wave of the complex
S Wave - downward wave preceded by an upward wave

13. PROCESS
ST Segment - Initial plateau phase of ventricular repolarization

14. PROCESS
T wave - Rapid phase of ventricular repolarization

15. NORMAL ECG

16. RHYTHM Normal sinus rhythm: Each P wave is followed by a QRS
Regular or irregular

17. RATE P wave rate 60 - 100 bpm with <10% variation - Normal
Rate < 60 bpm = Sinus Bradycardia - Results from:
- Excessive vagal stimulation - SA nodal ischemia (Inferior MI)
Rate > 100 bpm = Sinus Tachycardia - Results from:
- Pain / anxiety - CHF - Volume depletion - Pericarditis - Chronotropic Drugs (Dopamine)

18. RATE
Methods:
Method 1 = 1500/ # of small boxes between RR
Method 2

19. P WAVE Normal: Height < 2.5 mm in lead II
Width < 0.11 s in lead II

20. P WAVE ABNORMALITY

21. P WAVE ABNORMALITIES Right atrial hypertrophy:
A P wave in lead II taller then 2.5 mm (2.5 small squares)
The P wave is usually pointed

23. P WAVE ABNORMALITIES
Left atrial abnormality (dilatation or hypertrophy):
M shaped P wave in lead II
Prominent terminal negative component to P wave in lead V1

24. P WAVE ABNORMALITIES Premature Atrial Complex (PAC):
An abnormal P wave (arrowed in figure below)
As P waves are small and rather shapeless, the difference in a PAC is usually subtle; the one shown here is a clear example
Occurs earlier than expected
Followed by a compensatory pause - but not a full compensatory pause

25. P WAVE ABNORMALITIES Hyperkalemia:
The following changes may be seen in hyperkalemia
- Small or absent P waves
- Atrial fibrillation
- Wide QRS
- Shortened or absent ST segment
- Wide, tall and tented T waves
- Ventricular fibrillation

26. P WAVE ABNORMALITIES Arrhythmias (will cover later):
Premature atrial complex (PAC)
Atrial flutter
Atrial fibrillation
Paroxysmal reentrant tachycardia (SVT)
Multifocal atrial tachycardia

27. PR INTERVAL
Normal PR interval:
0.12 to 0.20 s (3 - 5 small squares)

28. PR INTERVAL ABNORMALITIES
Shorter PR interval:
Wolf-Parkinson-White syndrome
- Short PR interval, less than 3 small squares (120 ms)
- Slurred upstroke to the QRS indicating pre- excitation (delta wave)
- Broad QRS
- Secondary ST and T wave changes

29. PR INTERVAL ABNORMALITIES
Long PR interval (will cover later):
AV blocks

30. QRS COMPLEX
QRS Axis
Normal duration of complex is < 0.12 s (3 small squares)
NO pathological Q waves
NO left or right ventricular hypertrophy

31. AXIS
Using leads I and aVF, the axis can be assigned to one of the four quadrants at a glance

32. AXIS - NORMAL
Both I and aVF +ve = NORMAL AXIS
Lead I +ve and aVF -ve If the axis is in the "left" quadrant take your second glance at lead II Lead II +ve = NORMAL AXIS Lead II -ve = LEFT AXIS DEVIATION

33. AXIS - LEFT AXIS DEVIATION
Left anterior hemiblock
Left ventricular hypertrophy
Q waves of inferior myocardial infarction
Artificial cardiac pacing
Emphysema
Hyperkalemia
Wolff-Parkinson-White syndrome - right sided accessory pathway
Tricuspid atresia
Ostium primum ASD
Injection of contrast into left coronary artery

34. AXIS - NORTHWEST TERRITORY
Both I and aVF -ve = axis in the NORTHWEST TERRITORY
Causes of “No man’s land”
- Emphysema
- Hyperkalemia
- Lead transposition
- Artificial cardiac pacing
- Ventricular tachycardia

35. AXIS - RIGHT AXIS DEVIATION
Lead I -ve and aVF +ve = RIGHT AXIS DEVIATION
Causes:
- Normal finding in children and tall thin adults - Right ventricular hypertrophy - Chronic lung disease even without pulmonary hypertension - Anterolateral myocardial infarction - Left posterior hemiblock - Pulmonary embolus - Wolff-Parkinson-White syndrome - left sided accessory pathway - Atrial septal defect - Ventricular septal defect

36. WIDE QRS COMPLEX Right Bundle Branch Block:
Wide QRS, more than 120 ms (3 small squares)
Secondary R wave in lead V1 (RSR)
Other features include slurred S wave in lateral leads and T wave changes in the septal leads

37. WIDE QRS COMPLEX

38. WIDE QRS COMPLEX Left Bundle Branch Block:
Wide QRS, more than 120 ms (3 small squares)
M shape QRS , R’R’

39. WIDE QRS COMPLEX

40. WIDE QRS Hyperkalemia: Changes that can be seen:
- Small or absent P waves
- Atrial fibrillation
- Wide QRS
- Shortened or absent ST segment
- Wide, tall and tented T waves
- Ventricular fibrillation

41. WIDE QRS
Ventricular rhythm (will cover later):

42. PATHOLOGICAL Q WAVES Q waves > 1mm
Their depth > 25% of the height of the QRS
Q waves in V6 and aVL (not pathological…small)
Look for anatomical site, ignore aVR

43. PATHOLOGICAL Q WAVES

44. NON Q WAVE MI
Not all MIs develop Q waves (up to 1/3 never do or they develop and resolve)
WHY?
Infarct was not complete (transmural)
Infarct occurred in a electrically “silent” area of the heart, where an EKG cannot record the injury
Acute Infarct (Q waves will eventually appear)

45. RIGHT VENTRICULAR HYPERTROPHY (RVH)
Right axis deviation
Deep S waves in the lateral leads
A dominant R wave in lead V1

46. LEFT VENTRICULAR HYPERTROPHY (LVH)
Sokolow + Lyon (Am Heart J, 1949;37:161)
S in V1+ R in V5 or V6 > 35 mm
Cornell criteria (Circulation, 1987;3: )
S in V3 + R in aVL > 28 mm in men
S in V3 + R in aVL > 20 mm in women
Framingham criteria (Circulation,1990; 81: )
R in aVL > 11mm, R in V4-6 > 25mm
S in V1-3 > 25 mm,
S in V1 or V2 + R in V5 or V6 > 35 mm,
R in I + S in III > 25 mm

47. LVH
Increased amplitude in height and depth

48. QT INTERVAL
Calculate the corrected QT interval QTc = QT / RR = Normal = 0.42 s

49. LONG QT INTERVAL Causes:
Myocardial infarction, myocarditis, diffuse myocardial disease
Hypocalcemia, Hypercalcemia (Short QT), hypothyrodism
Subarachnoid hemorrhage, intracerebral hemorrhage
Drugs (e.g. Sotalol, Amiodarone)
Heredity

50. ST SEGMENT
Normal ST segment:
No elevation or depression

51. ST ELEVATION Causes of elevation include:
Acute MI (eg. Anterior, Inferior, Lateral).
LBBB
Acute pericarditis
Normal variants (e.g. athletic heart, high-take off),

52. ACUTE MI Look for reciprocal changes
ST elevation in leads where MI occurs
Look for reciprocal changes
(e.g. Ant MI look for ST depression in inferior leads)

53. LOCATING THE DAMAGE

54. LOCATION: 12 LEAD

55. ST DEPRESSION Causes of depression include: Myocardial ischemia
Digoxin Effect
Ventricular Hypertrophy
Acute Posterior MI
Pulmonary Embolus
LBBB

56. DIGOXIN EFFECT Characteristic down-sloping ST depression Dysrhythmias
Shortened QT interval
Characteristic down-sloping ST depression
Dysrhythmias
- Ventricular / atrial premature beats
- PAT (paroxysmal atrial tachycardia) with variable AV block
- Ventricular tachycardia and fibrillation
- Many others

57. ACUTE POSTERIOR MI
The mirror image of acute injury in leads V1 - 3
(Fully evolved) tall R wave, tall upright T wave in leads V1 -V3
Usually associated with inferior and/or lateral wall MI
Mirror Test: Once you have determined an inferior (or other) MI has occurred, you begin looking for reciprocal changes. If there is ST depression in V1, V2, and V3, flip the EKG over and hold it up to the light.  Now read those leads flipped over.  Are there significant Q waves?  Is the ST segment elevated with a coved appearance?  Are the T waves inverted?  Answering yes tells you, there is a posterior infarct as well.

58. ST DEPRESSION In diagnosis with ischemia:
Looking for at least 1mm (1 square)
This can be
1. Upsloping
2. Horizontal (can be combined w/ 1 or 3)
3. Downsloping

59. T WAVES
Repolarization of the ventricles is signaled by the T wave

60. TALL T WAVES
Causes:
Hyperkalemia
Hyperacute MI
LBBB

61. SMALL, FLATTENED OR INVERTED T WAVES
Causes are plenty:
Ischemia, age, race, hyperventilation, anxiety
LVH, drugs, pericarditis, I-V conduction delay (RBBB),
Electrolyte disturbances
The most important thing to consider is INVERTED T waves associated with Ischemia

62. COMMON ARRHYTHMIAS

63. SINUS BRADYCARDIA Less than 60 bpm
If profound, could have decreased cardiac output
Treatment:
- None if uncomplicated - Atropine - Pacing

64. SINUS TACHYCARDIA Greater than 100 bpm
 Myocardial oxygen demand and may  coronary artery perfusion resulting in angina in CAD
Decreased cardiac output could be exhibited

65. SSS (SICK SINUS SYNDROME)
Deceased cardiac output, related to periods of excessive bradycardia, AV block and/or tachycardia
Treatment:
- Pacemaker
- Anti coagulation therapy

66. ATRIAL PREMATURE BEAT Can be in a healthy heart or with CAD
They are well tolerated because cardiac output is not altered

67. ATRIAL FLUTTER Saw toothed pattern; 200-350bpm atrial rate
Can convert to atrial fibrillation

68. ATRIAL FLUTTER (CONT’D)
People can feel flutter sensation… if short lived then no complication; however, with an increased ventricular rate, people can experience decreased cardiac output.
Treatment:
- Veramapril, vagal stimulation Digoxin (perhaps in combo with other drugs) Cardioversion or pacing

69. ATRIAL FIBRILLATION
Chaotic atrial dysrhythmia; atrial rate can be 350+ bpm
Higher ventricular response = cardiac output
Treatment:
- Drugs (Digitalis, Verapamil, Beta blocker) Anticoagulation therapy Cardioversion

70. PAROXYSMAL ATRIAL TACHYCARDIA OR SUPRAVENTRICULAR TACHYCARDIA
High ventricular rate
Inadequate ventricular filling time, decreased cardiac output, and inadequate myocardial perfusion time
Treatment:
- Prevent CHF - Carotid sinus massage to stimulate vagal response - Cardioversion - Drugs (Verapamil, Propranolol, and Digoxin)

71. MULTIFOCAL ATRIAL TACHYCARDIA
Irregular rhythm with multiple (at least 3) P wave morphologies in same lead with an irregular and usually rapid ventricular response.
Pulmonary disease, hypoxia.
Rate is greater than 100 bpm.
Treatment:
- Verapamil - Resolve causative disorder

72. 1ST DEGREE AV BLOCK PR greater than 120 msec
No hemodynamic complications
Could progress to higher AV blocks

73. 2ND DEGREE AV BLOCK MOBITZ TYPE 1 (WENCKEBACH)
PR interval progressively lengthens with each beat until it is completely blocked
If bradycardic, could have decreased cardiac output
Treatment:
- Only if brady (Atropine) - Rare pacemaker

74. 2ND DEGREE AV BLOCK MOBITZ TYPE 2
Rare, occurs with large ant MI
PR interval fixed and p waves occur in a regular ratio to QRS (atrial rate is regular) until conduction is blocked

75. 2ND DEGREE AV BLOCK MOBITZ TYPE 2 (CONT’D)
Symptoms of decreased cardiac output occur with slowing ventricular rate Could progress to complete block
Treatment:
- Atropine initially - Permanent pacemaker

76. 3RD DEGREE AV BLOCK (COMPLETE)
Atria and ventricles are independent of each other; no relationship present
Symptoms could include lightheadedness or syncope from decreased rate

77. 3RD DEGREE AV BLOCK (COMPLETE) (CONT’D)
Decreased cardiac output, compromised coronary perfusion
Treatment:
- Emergency
- Atropine
- Pacemaker

78. JUNCTIONAL ESCAPE RHYTHM
QRS complexes are not preceded by normal P waves, because the impulse originate below the SA node
Can cause a missed P wave, inverted or in the QRS

79. VENTRICULAR ESCAPE RHYTHM
Wide QRS complex (> 120ms)
Decreased cardiac output , lightheadedness and syncope due to decreased heart rate
Treatment:
- Atropine
- Electronic pacemaker

80. PREMATURE VENTRICULAR CONTRACTION (PVC)
Occasional PVC’s have minimal consequences
Increased frequency or multifocal PVCs can lead to ventricular tachycardia
Make sure it does not progress to more PVCs
Couplet is 2 PVCs in a row
Triplet is 3 PVCs in a row

81. VENTRICULAR BIGEMINY
Premature Ventricular contraction (PVC) in a bigeminal pattern
Can be trigeminy (every third is a PVC), quadrigeminy
Can be multifocal - increased irritability of the ventricle could lead to more severe dysrhythmia

82. VENTRICULAR TACHYCARDIA (VT)
More than 3 PVC’s in a row > 100bpm
Wide QRS, AV dissociation, QRS complex does not resemble typical bundle branch block
Irritable ventricle
Sustained VT is an emergency rhythm and could convert to ventricular fibrillation

83. VT
Decreased cardiac output , irritable ventricle
Treatment:
- Cardioversion Lidocaine or Procainamide to get NSR Emergent care Long term care: ICD (implantable cardioverter defibrillator)

84. TORSADES DE POINTES Form of VT – “twisting of the points”
People with prolonged QT interval are susceptible

85. VENTRICULAR FIBRILLATION
Chaotic activity of the ventricles
No effective cardiac output or coronary perfusion
Associated with severe myocardial ischemia.
Life-threatening - death occurs within 4 min.
Treatment:
- Immediate defibrillation
- CPR - Lidocaine, bretylium. epinephrine

86. SINUS ARREST

87. How to read the ECG Look at the whole tracing.
Rhythm: Is there a P wave before each QRS complex?
Yes: sinus rhythm No: AV junctional or heart block
Rate: Count boxes; use caliper, ruler
PR interval: Normal sec. or less
QRS complex: Skinny (0.10 sec. or less) or broad (BBB or ventricular)
ST segment: Isoelectric (normal), elevated or depressed
T wave: Upright, flat or inverted
Interpretation: Normal or abnormal.
Is the rhythm dangerous?