This document provides information on electrocardiograms (ECGs), including ECG paper layout, lead placement, interpretation steps, and how to locate infarcts based on ECG findings. Common arrhythmias are summarized, including definitions and treatments for sinus bradycardia, atrial fibrillation, heart blocks, premature ventricular contractions, ventricular tachycardia, and more. Overall health impacts and treatments are discussed for various rhythms.

1. ELECTROCARDIOGRAMs
(ECGs)

2. ECG paper
• Vertical dark lines- 5mm apart
• Vertical light lines- 1mm apart
• Horizontal dark lines-5mm apart
• Horizontal light lines- 1mm apart
• Large square- 5 X 5 mm
• Small square- 1 X 1 mm

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

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

5. CHEST LEADS
• V1- 4th intercostal space right to
sternal border
•V2- 4th intercostal space left to sternal
border
•V3- between V2 and V4
•V4- midclavicular line 5th intercostal
space
•V5- anterior axillary line
•V6-midaxillary line

6. Interpretation steps
Calibration should be 10mm
Paper speed should be 25mm/sec
Calculate HR and heart rhythm
Measure PR, QRS, QT, ST intervals

7. Location of infarcts
• V1-V3: Antero-septal
• V3-V4: Anterior
• V4-V6, lead I, aVL: Anterolateral
• V1-V6: Complete Anterior
• Lead I, aVL: lateral
• Lead II, III, aVF: inferior
• V1-V2: Posterior

8. NORMAL ECG

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

10. PROCESS
P Wave - Atrial depolarization and contraction

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

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

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

14. 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

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

16. PROCESS
T wave - Rapid phase of ventricular
repolarization

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

18. 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)

19. RATE
Methods:
300/ # of small boxes between RR

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

21. P WAVE ABNORMALITY

22. 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

24. 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

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

26. 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

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

28. QRS COMPLEX
• QRS Axis
• Normal duration of complex is < 0.12 s (3 small
squares)

29. 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

30. WIDE QRS COMPLEX

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

32. WIDE QRS COMPLEX

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

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

35. 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
Anatomical Site Lead with Abnormal EKG complexes Coronary Artery most often responsible
Inferior II, III, aVf RCA
Antero Septal V1-V2 LAD
Antero Apical V3-V4 LAD (distal)
Antero Lateral V5-V6, I, aVL CFX
Posterior V1-V2 (Tall R, Not Q) RCA

36. PATHOLOGICAL Q WAVES

37. 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)

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

39. 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: 565-72)
 S in V3 + R in aVL > 28 mm in men
 S in V3 + R in aVL > 20 mm in women
 Framingham criteria (Circulation,1990; 81:815-820)
 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

40. LVH
• Increased amplitude in height and depth

41. QT INTERVAL
• Calculate the corrected QT interval
- QTc = QT / RR = 0.42
- Normal = 0.42 s

42. 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

43. ST SEGMENT
Normal ST segment:
• No elevation or depression

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

45. ACUTE MI
• ST elevation in leads where MI occurs
• Look for reciprocal changes
(e.g. Ant MI look for ST depression in inferior leads)
Anatomical Site Lead with Abnormal EKG complexes Coronary Artery most often responsible
Inferior II, III, aVf RCA
Antero Septal V1-V2 LAD
Antero Apical V3-V4 LAD (distal)
Antero Lateral V5-V6, I, aVL CFX
Posterior V1-V2 (Tall R, Not Q) RCA

46. LOCATING THE DAMAGE

47. LOCATION: 12 LEAD

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

49. DIGOXIN EFFECT
• 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

50. 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.

51. 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

52. T WAVES
• Repolarization of the ventricles is signaled by
the T wave

53. TALL T WAVES
Causes:
• Hyperkalemia
• Hyperacute MI
• LBBB

54. 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

55. COMMON ARRHYTHMIAS
Location Bradyarrythmia Tacharrythmia
SA node Sinus Bradycardia Sinus tachycardia
Sick Sinus Syndrome
Atria Atrial Premature Beats
Atrial Flutter
Atrial Fibrillation
Paroxysmal SVT
Multifocal Atrial Tachycardia
AV node Conduction Blocks (1,2 and 3)
Jxal escape rhythm
Ventricles Ventricular escape rhytm Ventricular premature Beats
VT
Torsades de pointes
Ventricular Fibrillation

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

57. 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

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

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

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

61. 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

62. 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

63. 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)

64. 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

65. 1ST DEGREE AV BLOCK
• PR greater than 120 msec
• No hemodynamic complications
• Could progress to higher AV blocks

66. 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

67. 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

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

69. 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

70. 3RD DEGREE AV BLOCK (COMPLETE)
(CONT’D)
• Decreased cardiac output, compromised
coronary perfusion
• Treatment:
- Emergency
- Atropine
- Pacemaker

71. 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

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

73. 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

74. 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

75. 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

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

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

78. 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

79. SINUS ARREST

80. 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 - 0.20 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?