The document provides a comprehensive overview of electrocardiograms (ECGs), explaining their definition, history, types of leads, and interpretation techniques. Key topics include the sequence of electrical activation in the heart, heart rate determination methods, and various abnormalities that can be identified through ECG analysis. Additionally, it details the factors affecting ECG results, such as axis determination and common causes of changes in wave morphology.

1. ECG BASICS
DR SNEHAL

2. • DEFINITION: An ECG is recording(gram) of the electrical activity(electro)
generated by the cells of the heart(cardio) that reaches the body surface.
• It basically plots
---> Voltage on its vertical axis which is the summation of electrical activation
of all cardiac cells on the body surface. Indicates chamber enlargement and axis.
---> Time on its horizontal axis which indicates HR, Rhythm & intervals
during electrical activity.

3. HISTORY
• 1842 - Italian scientist Carlo Matteucci realizes that electricity is associated with the
heart beat.
• 1876 - Irish scientist Marey analyzes the electric pattern of frog’s heart.
• 1895 - William Einthoven , credited for the invention of EKG.
• 1906 - using the string electrometer EKG, William Einthoven diagnoses some heart
problems.
• 1924 - the noble prize for physiology/medicine is given to William Einthoven for his
work on EKG.
• 1938 - AHA and Cardiac society of Great Britain defined the position of chest leads.
• 1942- Goldberger increased Wilson’s Unipolar lead voltage by 50% and made
Augmented leads(aVR, aVL & aVF).

5. PACEMAKER CELLS

6. SEQUENCE OF ELECTRICAL ACTIVATION

7. ELECTROMECHANICAL COUPLING

8. ACTION POTENTIAL vs EKG

9. PLANES OF ECG

10. ECG LEADS
• The standard ECG has 12 leads:
---> 3 Standard Limb Leads which are bipolar – I, II, III
---> 3 Augmented Limb Leads which are unipolar– aVR, aVL, aVF
---> 6 Precordial Leads which are unipolar – V1 to V6
• The axis of a particular lead represents the viewpoint from which it looks at the
heart.
• The standard and augmented leads represent the heart’s orientation in frontal
plane.
• Precordial leads represent the heart’s orientation in transverse plane.

11. FRONTAL LIMB LEADS

12. AUGMENTED LIMB LEADS

15. TRANSVERSE PLANE LEADS

17. • The electrocardiogram records only Lead I & II and then calculate the voltage in
remaining leads in real time on the basis of Einthoven law
• I+III = II
• The algebraic outcome of the formulas for calculating the voltages in aV leads
from Lead I, II & III are:
 aVR = - ½ (I + II)
 aVL = I - ½ (II)
 aVF = II – ½ (I)
• Thus, aVR + aVL + aVF = 0

18. EKG CALIBRATION
EKG graphs:
• 1 mm small squares
• 5 mm large squares
Paper Speed:
• 25 mm/sec standard
Voltage Calibration:
• 10 mm/mV standard

19. ARTERIAL TERRITORY & EKG LEADS

20. INTERPRETATION
OF NORMAL ECG

21. Steps involved
• Heart Rate
• Rhythm
• Axis
• Wave morphology
• Intervals and segments analysis

23. • Electrical impulse that travels towards the electrode produces an upright
(“positive”) deflection.

24. Determining the Heart Rate
• Rule of 300
• Rule of 1500
• 10 second rule

25. Rule of 300
• 300 divided by number of big boxes between RR interval.
• EKG speed is 25mm/sec ---> 5 big box ---> so, per minute
is 5 x 60 = 300 box.
• This works only when rhythm is regular.
• Better applicable when HR < 100.

26. Rule of 1500
• 1500 divided by number of small boxes between RR
interval.
• Each big box contains 5 small boxes, hence 300 x 5 = 1500.
• Better applicable during tachycardia ( HR > 100).

27. Rule of 10
• Used when rhythm is irregular
• Rhythm strip runs for 10 sec ---> count number of QRS in
10sec strip & multiply by 6

29. Rhythm strip contains 20 QRS complexes
HR is 20 x 6 = 120

30. Axis determination
• The QRS axis represents the net overall direction of the heart’s electrical activity.
• Abnormalities of axis can hint at:
---> Ventricular enlargement
---> Conduction blocks (i.e. hemiblocks)

31. • Axis can be determined by two approach
 Quadrant approach
 Equiphasic approach

32. QRS genesis
• QRS complex represents ventricular depolarization.
• A deflection is only referred to as wave if it crosses the baseline.
• The first negative wave is called the Q-wave. If the first wave is not negative,
then the QRS complex doesn’t possess a Q-wave.
• All positive waves are referred to as R-waves. The first positive wave is R-wave,
the second positive wave is referred as R’-wave.
• Any negative wave appearing after a positive wave is referred as S-wave.
• Large waves are designated by their capital letters – Q, R, S.
• Small waves are designated by their lower case letters – q, r, s.

33. Contd..
• Ventricular septum receives fibers from left bundle branch and hence gets activated first.
• Hence, depolarization of septum proceeds from left to right. The vector is directed forward and
to right.
• The ventricular septum is relatively small, which is why lead V1 displays a small ‘r’ wave and
V5, V6 displays small negative ‘q’ wave.
• Electrical impulses then progresses to ventricular free walls via purkinje fibres from
endocardium to epicardium from the apical region.
• The endocardium depolarizes first with subsequent spread of action potential from one
contractile cell to another heading to the epicardium generating a myocardial vector which is
oriented downward and to left.
• Vector generated from RV doesn’t come to expression as it is drowned by the many times
larger vector generated by LV.
• Finally the basal part of the ventricle gets depolarized giving rise to a vector which is directed
backward and upward. It moves away from V5, V6 giving rise to small ‘s’ wave in V5 & V6.

35. Contd..
• q – waves are present only in leftward oriented leads – I, aVL, V5, V6.
• Presence of ‘q’ in V1, V2, V3 is pathological.
• Presence of ‘q’ wave in rightward oriented leads should not qualify for the
criteria of pathological ‘q’ wave.
• Pathological q-wave - > 40msec in width and > 25% of QRS amplitude present in
two contiguous lead.
• R-wave should progress from V1---->V5. Tallest in V5 & V6 having a dominant
R-wave.

36. Pathological q-waves other than infarction
• LVH / RVH
• Bundle branch blocks / Fascicular blocks
• Pre-excitation syndrome
• Left pneumothorax
• Acute cor pulmonale
• Cardiomyopathies
• Amyloidosis
• Dextrocardia
• perimyocarditis

37. Quadrant approach
• Examine the QRS complex in leads I and aVF to determine if they are
predominantly positive or predominantly negative. The combination should
place the axis into one of the 4 quadrants below:

38. LAD

39. RAD

41. Right axis deviation – negative in I & positive in
aVF

42. Lead I positive, Lead aVF negative but Lead II
positive ---> non pathologic LAD (Normal axis)

43. Equiphasic approach
• Most equiphasic QRS complex.
• Identified Lead lies 90° away from the equiphasic lead.
• The fact that QRS complex is equally positive and negative indicates that the net
vector is perpendicular to the axis of this particular lead.
• Next see if in perpendicular lead QRS is upright or negative.
• If upright, that is the QRS axis.
• If negative, move 90 degree away in the opposite direction of the perpendicular
lead.

44. Lead aVF is equiphasic --> perpendicular lead I is
positive --> axis is 0 degree

45. Lead II equiphasic --> lead aVL negative --> axis is
150 degree
• kjkg

46. Causes of axis deviation
LAD
• LBBB, LVH
• LAFB
• INFERIOR WALL MI
• WPW – right accessory pathway
• OSTIUM PRIMUM ASD
• TRICUSPID ATRESIA
• HYPERKALEMIA
• OBESITY
• RV PACING / ECTOPICS
• HIGH DIAPHRAGM – PREGNANCY, ASCITES
RAD
• RBBB, RVH
• LPFB
• ANTEERIOR WALL MI
• CHRONIC LUNG DISEASES
• PULMONARY EMBOLISM
• WPE - left accessory pathway
• OSTIUM SECUNDUM ASD
• LV PACING / ECTOPICS
• NORMAL VARIANT - TALL

47. ‘T’ wave morphology
• Represents repolarization.
• Same direction as the preceding QRS complex.
• Blunt apex with asymmetric limbs – longer ascending limb.
• Can be biphasic ( initial positive and terminal negative ) in Lead V1.
• When biphasic the terminal portion of the ‘T’ wave determines if it is positive or
negative.
• Diminish with age and larger in males than females.
• Amplitude: 0.5 mV in limb lead, 1.5 mV in precordial lead.
• Should not exceed > 2/3rd of preceding ‘R’ wave.
• Same axis as QRS.
• Inversion in V1--->V3 – normal variant in females.

48. ‘P’ wave morphology

49. ‘PR’ interval
• It is the time required for electrical impulse to travel from SA node to AV node &
AV nodal conduction delay.
• Major portion ( later 2/3rd ) reflects the conduction delay in AV node.
• Duration: 0.12 – 0.2 sec.
• Tends to increase with age.
• Controlled by balance between sympathetic and parasympathetic divisions of
ANS.

51. T wave inversion causes

52. ‘ST’ SEGMENT MORPHOLOGY
• Represents preliminary phase of repolarization.
• Forms ‘J’ point at its junction with QRS – forms a distinct angle with the
downslope of ‘R’ or upslope of ‘S’ wave.
• Proceeds horizontally and curves gently into ‘T’ wave.
• Located at same horizontal level as the baseline formed by ‘TP’ segment.
• Displacement upto 1mm ( upward or downward) is common in precordial leads
especially V1--->V3.
• Early repolarization variants are considered normal except in symptomatic and
high risk individuals.

53. Early repolarization syndrome variants

54. Non specific ST changes

55. Secondary repolarization abnormalities

56. Causes of ST segment elevation
• Acute MI
• Left bundle branch block (brugada)
• Acute pericarditis
• Benign early repolarization
syndrome
• Hyperkalemia
• LV aneurysm
• Brugada syndrome
• Pulmonary embolism
• Pneumothorax
• Aortic dissection
• Hypothermia
• CNS pathologies with raised ICT
• Prinzmetals’s angina
• Post electrical cardioversion
• Short QT syndrome ( V3 to V5)
• Cholecystitis / subdiaphragmatic
abscess
• Cocaine abuse
• Drugs- digoxin, isoprenaline,
quinidine, procainamide, TCA’s

57. Causes of ST segment depression
• Ischemia
• LVH
• Hypokalemia
• Hypomagnesemia
• ICH
• Digoxin effect
• Post electrical cardioversion
• Exercise and deep inspiration

58. ‘QT’ interval
• Represents duration of electrical activation and recovery of the ventricular
myocardium.
• Measurement: QT interval is best determined in a lead with an initial q wave by
tangential method.

59. Contd..
• QT interval is rate dependent. To ensure complete recovery from one cardiac
cycle before the next cardiac cycle begins, the duration of recovery must decrease
as the rate of activation increases.
• Therefore normality of QT interval can be determined only by correcting for the
heart rate ----> QTc
• Bazett: QTcB = QT/RR1/2
• Fridericia: QTcFri = QT/RR1/3
• Framingham: QTcFra = QT+0.154 (1−RR)
• Hodges: QTcH = QT+0.00175 ([60/RR]−60)
• Rautaharju: QTcR = QT−0.185 (RR−1) + k (k=+0.006 seconds for men and
+0 seconds for women)

60. Contd..
Normal QTc values:
• QTc is prolonged if > 440ms in men or > 460ms in women.
• QTc > 500 is associated with increased risk of torsades de pointes.
• QTc is abnormally short if < 350ms.
• A useful rule of thumb is that a normal QT is less than half the preceding RR
interval.

61. Causes for QT prolongation:
• Electrolytes – hypo K+, Mg2+, Ca2+
• Increasing age
• Females
• Bradycardia
• MI / LVF
• ROSC - post cardiac arrest
• Hypothermia
• Recent cardioversions
• Congenital long QT
• Raised ICT
• Hepatic dysfunction

62. Drugs causing QT prolongation

63. Short QT interval
• Digoxin effect
• Hypercalcemia
• Short QT syndromes

64. ECG change in dextrocardia
• Right axis deviation
• Positive QRS complexes (with upright P and T waves) in aVR
• Lead I: inversion of all complexes, aka ‘global negativity’ (inverted P wave,
negative QRS, inverted T wave)
• Absent R-wave progression in the chest leads (dominant S waves throughout)
• These changes can be reversed by placing the precordial leads in a mirror-image
position on the right side of the chest and reversing the left and right arm leads.
• D/D – Accidental lead reversal, specifically reversal of the left and right arm
electrode.

65. DEXTROCARDIA vs ARM LEAD REVERSAL