vectorial analysis of ECG- Physiological basis

1. ECG- VECTORIAL ANALYSIS

2. DISCUSSED UNDER…
• Principles of vectors
• Vectorial analysis of potentials
• Vectorial analysis of each wave in ECG
• Vectorcardiogram
• Mean electrical axis- significance
• Applied aspects- abnormalities

3. PRINCIPLES OF VECTORIAL ANALYSIS
• Current flows in a particular direction in the heart during
the cardiac cycle.
• A vector is an arrow that points in the direction of the
electrical potential generated by the current flow.
• Arrowhead in the positive direction.
• Length of arrow is
proportional to the voltage
of the potential

4. RESULTANT VECTOR IN THE HEART
• Long elliptical arrows- current flows between the
depolarized areas inside the heart and the non
depolarized areas on the outside of the heart.
• Some current also flows inside the heart chambers
directly from the depolarized areas toward the still
polarized areas.

5. • More current flows downward from the base of
the ventricles toward the apex.
• Instantaneous mean vector- summated vector
of the generated potential at a particular
instant
• Long black arrow drawn
through the centre of
the ventricles from the
base toward the apex

6. DIRECTION OF A VECTOR
• A vector, exactly horizontal and directed toward the person’s
left side- direction of 0 degrees- Zero reference point
• The scale of vectors rotates clockwise
• Above and straight downward- +90 degrees
• Straight vector from person’s
left to right- +180 degrees
• Straight upward- −90 (or +270) degrees.

7. • Mean QRS vector- In normal heart, the average direction of
the vector during spread of the depolarization wave through
the ventricles
• It is about +59 degrees
• Apex of the heart remains positive with respect to the base of
the heart

8. AXIS FOR EACH LIMB LEAD
• Direction from negative electrode to positive electrode
• Axis of lead I - 0 degrees
- The electrodes lie in horizontal direction
- The positive electrode to the left
• Lead II- +60 degrees
• Lead III- axis of +120 degrees
• Lead aVR - +210 degrees
aVF - +90 degrees
aVL - −30 degrees
HEXAGONAL REFERENCE SYSTEM

9. VECTORIAL ANALYSIS OF POTENTIALS
1. A partially depolarized heart- vector A represents the
instantaneous mean vector
Direction- +55 degrees
Voltage - 2millivolts (length of vector A)
• Line is drawn to represent the axis of lead I in the 0-degree
direction.

10. • Projected vector (B)- Line perpendicular to the axis of lead I is
drawn from the tip of vector A
• Arrow of this projected vector points toward the positive end
of the lead I axis (wave recorded in lead I is positive)

11. 2. Heart with left side depolarizing more rapidly than right
• Vector A- electrical potential and its axis at a given instant during
ventricular depolarization
• Instantaneous vector- Direction- +100 degrees
Voltage - 2 millivolts.
• Projected vector B- perpendicular line from the tip of vector A to
the lead I axis
• It is very short
• In the negative direction

12. • Recording in lead I will be negative (below the zero
line in the ECG)
• Voltage recorded will be less - about −0.3 millivolts.

13. • Vector in the heart is in a direction almost perpendicular to
the axis of the lead- the voltage recorded in the ECG of this
lead is very low.
• Vector- the same axis as the lead axis- the entire voltage of
the vector will be recorded.

14. VECTORIAL ANALYSIS OF POTENTIALS
OF EACH WAVE
• Vector A- instantaneous electrical potential of a partially
depolarized heart
• Perpendicular lines are drawn from the tip of vector A to the
axes of the three different standard leads
• Projected vector B- potential in lead I
• Projected vector C- potential in lead II
• Projected vector D- potential in lead III

15. • Projected vectors point in the positive directions- record in
the ECG is positive
• Potential in - Lead I (vector B) is about one half that in the
heart
- Lead II (vector C), it is almost equal to that in the
heart
- Lead III (vector D), it is about one third that in
the heart

16. VECTORIAL ANALYSIS OF THE
NORMAL ECG
• DEPOLARIZATION OF THE VENTRICLES—THE QRS COMPLEX
• First part of the ventricles to become depolarized is the left
endocardial surface of the septum
• Depolarization spreads rapidly to involve both endocardial
surfaces of the septum

17. • Then depolarization spreads along the endocardial
surfaces of the two ventricles
• Finally, it spreads through the ventricular muscle to
the outside of the heart

18. • Instantaneous mean electrical potential of the ventricles is
represented by vector superimposed on the ventricle
• Positive vector- recording in the ECG above zero line
• Negative vector- recording below the zero line.

19. • 0.01 second after the onset of depolarization
• Vector is short because only a septum is depolarized.
• All electrocardiographic voltages are low.
• Heart vector extends in the same direction as the
axis of lead II- voltage in lead II is more

20. • 0.02 second after onset of depolarization- ventricular
muscle mass has become depolarized- heart vector is
long
• Voltages in all electrocardiographic leads have
increased

21. • 0.035 second after onset of depolarization- vector is
becoming shorter
• Voltages are lower - electronegativity of outside apex,
neutralizing much of the positivity on the other epicardial
surfaces of the heart.
• Axis of the vector- shift toward the left side of the chest (left
ventricle is slightly slower to depolarize than is the right
ventricle)
• Ratio of the voltage in lead I to that in lead III is increasing

22. • 0.05 second after onset of depolarization- vector points
toward the base of the left ventricle
• Short vector because only a minute portion of the ventricular
muscle yet to be depolarised.
• Direction of the vector changes- the voltages recorded in
leads II and III are both negative
• Voltage of lead I is still positive

23. • 0.06 second after onset of depolarization
• Entire ventricular muscle mass is depolarized- no
current flows around the heart and no electrical
potential is generated.
• The vector becomes zero, and the voltages in all
leads become zero.

24. Q WAVE
• Slight negative depression at the beginning of QRS complex- is
the Q wave.
• Caused by initial depolarization of the left side of the septum
before the right side
• It creates a weak vector from left to right for a fraction of a
second before the usual base-to-apex vector occurs

25. VENTRICULAR REPOLARIZATION
T WAVE
• 0.15 second after ventricular depolarisation,
repolarization begins
• Completes at about 0.35 second.
• This repolarization causes the T wave in the ECG.

26. • Septum and endocardial areas of the ventricular muscle
depolarize first.
• Repolarization first occurs in the entire outer surface of the
ventricles (apex of the heart)
• Septum and other endocardial areas have a longer period of
contraction than external surfaces of the heart.
• Endocardial areas- repolarize last.
• This sequence of repolarization is caused by:
- High blood pressure inside the ventricles during contraction
- Reduces coronary blood flow to the endocardium

27. • Positive end of the overall ventricular vector during
repolarization is toward the apex of the heart
• Outer apical surfaces of the ventricles repolarize before the
inner surfaces
• So the normal T wave in all three bipolar limb leads is positive

28. • Five stages of repolarization of the ventricles are denoted by
progressive increase of the light tan areas
• Vector extends from the base of the heart toward the apex
and disappears in the last stage.
• First, the vector is small because the area of repolarization is
small.
• Vector later becomes stronger because of greater degrees of
repolarization.

29. • Vector becomes weaker again because the areas of
depolarization decreases- total quantity of current flow
decreases.
• Vector is greatest when about half the heart is in the polarized
state and about half is depolarized.
• 0.15 second- repolarisation completes- T wave of the ECG is
generated

30. DEPOLARIZATION OF THE
ATRIA - P WAVE
• Begins in the sinus node and spreads in all directions over the
atria
• Electronegativity is at the point of entry of the superior
venacava where the SA node lies (depolarizes much before
the musculature)
• Spread of depolarization in atrial
muscle is slow (no Purkinje system)
• Direction of initial depolarization
is denoted by the black vector

31. • Direction is generally in the positive directions of the
axes of the three standard bipolar limb leads
• ECGs recorded from the atria during depolarization-
positive in all three of these leads

32. REPOLARIZATION OF THE ATRIA—THE
ATRIAL T WAVE
• Repolarization in atria that also begins at SA nodal region
(depolarized first)
• Region around the sinus node becomes positive with respect to
the remainder of the atria.
• So atrial repolarization vector is backward to the vector of
depolarization.

33. • ECG- the atrial T wave appears at the same time of
QRS complex
• So totally obscured by the large ventricular QRS
complex
P
Ta

34. VECTORCARDIOGRAM
• Vector of current flow through the heart changes rapidly
• Vector increases and decreases in length (increasing and
decreasing voltage)
• Vector changes direction (changes in the average direction of
the electrical potential)
• Vectorcardiogram depicts these changes at different times
during the cardiac cycle

35. • Point 5 is the zero reference point, and this point is the
negative end of all the successive vectors.
• Positive end of the vector remains at the zero point before
depolarization
• Ventricular depolarization, the positive end of the vector
leaves the zero reference point.
• Septum- depolarized, the vector extends downward toward
the apex of the ventricles- shown by positive end of vector 1.

36. • Ventricular muscle becomes further depolarized, the vector
becomes stronger
• Vector 2 of represents the state of depolarization of the
ventricles about 0.02 second after vector 1.
• Vector 3- 0.02 second later
• Vector 4 occurs in another 0.01 second.
• Ventricles become totally depolarized, and the vector
becomes zero once again

37. MEAN ELECTRICAL AXIS OF THE
VENTRICULAR QRS AND ITS SIGNIFICANCE
• Ventricular depolarization- the direction of the electrical
potential (negative to positive) is from the base of the ventricles
toward the apex.
• Mean electrical axis- direction of the potential during
depolarization is called the of the ventricles.
• The mean electrical axis of the normal ventricles is 59 degrees.

38. DETERMINING THE ELECTRICAL AXIS
FROM STANDARD LEAD ECG
• In normal ECG- net potential and polarity of the recordings in
leads I and III are noted
• Lead I- positive recording
• Lead III- recording is mainly positive and partly negative
• Negative potential is subtracted from the positive part of the
potential to determine the net potential

39. • Net potential for leads I and III is plotted on the axes of the
respective leads
• Perpendicular lines drawn from the apices of leads I and III
• Apex of the mean QRS vector- Intersection of these two
perpendicular lines
• Intersection of the lead I and lead III axes represents the
negative end of the mean vector

40. • The approximate average potential represented by the length
of this mean QRS vector
• Mean electrical axis is represented by the direction of the
mean vector.
• Thus, the orientation of the mean electrical axis of the normal
ventricles- 59 degrees positive (+59 degrees).

41. APPLIED ASPECTS

42. ABNORMAL VENTRICULAR CONDITIONS
THAT CAUSE AXIS DEVIATION
• Axis can swing even in a normal heart from 20 degrees- 100
degrees.
• The causes of the normal variations
1. Anatomical differences in the Purkinje fibres
2. Anatomical differences in musculature of different
hearts

43. LEFT AXIS DEVIATION
• Change in the Position of the Heart in the chest.
• Heart is angulated to the left, the mean electrical axis of the heart
also shifts to the left.
• Such shift occurs in:
(1) at the end of deep expiration
(2) when a person lies down
(3) quite frequently in obese people (increased visceral adiposity)

44. RIGHT AXIS DEVIATION
• Angulation of the heart to the right causes the mean electrical
axis of the ventricles to shift to the right.
• This shift occurs:
(1) at the end of deep inspiration,
(2) when a person stands up
(3) normally in tall, lanky people whose hearts hang
downward.

45. AXIS DEVIATION IN HYPERTROPHY
• Hypertrophy of One Ventricle- axis of the heart shifts toward
the hypertrophied ventricle
• Due to:
- Greater quantity of muscle exists on the hypertrophied
side of the heart than on the other side (greater electrical
potential on that side)
- More time is required for the depolarization wave to
travel through the hypertrophied ventricle

46. • Normal ventricle becomes depolarized considerably in
advance of the hypertrophied ventricle
• A strong vector from the normal side of the heart toward the
hypertrophied side
• Axis deviates toward the hypertrophied ventricle

47. VECTORIAL ANALYSIS OF LEFT AXIS
DEVIATION IN LVH
• Vectorial analysis of this ECG- left axis deviation pointing in
the −15-degree direction.
• Causes:
1. Hypertension - LVH
2. Aortic valvular stenosis- LVH
3. Aortic valvular regurgitation- LVH
4. Congenital heart conditions causing LVH

48. VECTORIAL ANALYSIS OF RIGHT AXIS
DEVIATION IN RVH
• The ECG of right axis deviation, to an electrical axis of 170
degrees, which is 111 degrees to the right of the normal 59-
degree mean ventricular QRS axis.
• Due to:
1. Hypertrophy of the right ventricle as a result of
congenital pulmonary valve stenosis.
2. Congenital heart conditions causing hypertrophy of the
right ventricle (TOF and VSD)

49. BUNDLE BRANCH BLOCK CAUSES AXIS
DEVIATION
• Lateral walls of the two ventricles depolarize at almost the
same instant
• So potentials generated by the two ventricles- neutralizes
each other.
• In bundle branch block- cardiac impulse
spreads through the normal ventricle first
• So depolarization potentials do not
neutralize each other

50. VECTORIAL ANALYSIS OF LEFT AXIS
DEVIATION IN LBBB
• LBBB- left bundle branch is blocked
• Left ventricle depolarization remains 0.1 second slower than
right ventricle
• Strong vector projects from the right ventricle toward the left
ventricle.
• Left axis deviation of about −50 degrees occurs because the
positive end of the vector points toward the left ventricle.

51. QRS complex prolongation in LBBB
• Slowness of impulse conduction- duration of the QRS
complex is greatly prolonged
• Excessive widths of the QRS waves in ECG
• Prolonged QRS complex differentiates bundle branch
block from hypertrophy.

52. VECTORIAL ANALYSIS OF RIGHT AXIS
DEVIATION IN RBBB
• Left ventricle depolarizes far more rapidly than does the right
ventricle (0.1 second before)
• Strong vector develop towards the right ventricle
• Causes intense right axis deviation occurs.
• Vector axis of +105 degrees instead of the normal +59 degrees
• Prolonged QRS complex because of slow conduction.

53. ABNORMAL VOLTAGES OF THE QRS
COMPLEX
INCREASED VOLTAGE IN THE STANDARD BIPOLAR LIMB LEADS
• Voltages is measured from the peak of the R wave to the bottom
of the S wave
• Normal- varies from 0.5 and 2.0 millivolts
• Lead III- lowest voltage and lead II- highest voltage
• High-voltage ECG- sum of the voltages of all the QRS complexes
of the three standard leads is greater than 4 mV

54. CAUSE OF HIGH-VOLTAGE QRS
COMPLEXES
• Hypertrophy of the muscle in response to excessive load
(increased muscle mass)
• Eg: Pulmonary stenosis- RVH
Hypertension - LVH
• The increased quantity of muscle generates increased
electricity around the heart.
• Potentials recorded in the electrocardiographic leads are
considerably greater than normal

55. DECREASED VOLTAGE OF THE
ELECTROCARDIOGRAM
• Caused by Cardiac Myopathies (diminished muscle mass)
• Most common cause- old myocardial infarctions
• Depolarization wave to move through the ventricles slowly
• Also shows prolongation of the QRS complex along with the
decreased voltage.
• Local delays of impulse conduction and reduced voltages due
to loss of muscle mass throughout the ventricles

56. DECREASED VOLTAGE CAUSED BY
CONDITIONS SURROUNDING THE HEART
Pericardial effusion
• Extracellular fluid conducts electrical currents with great ease
• Effusion effectively short-circuits the electrical potentials
generated by the heart, decreasing the electrocardiographic
voltages

57. Pleural effusion
• Decreases voltages in the ECGs- conduction loss in fluid
Pulmonary emphysema
- Conduction of electrical current through the lungs is
depressed due to excessive quantity of air in the lungs.
- Lungs envelops the heart than normal- act as an insulator
to prevent spread of electrical voltage from the heart to
the surface

58. PROLONGED QRS COMPLEX
CARDIAC HYPERTROPHY OR DILATION
• The QRS complex lasts as long as depolarization continues to
spread through the ventricles
• Prolonged conduction of the impulse through the ventricles
always causes a prolonged QRS complex (one or both
ventricles are hypertrophied or dilated)
• QRS complex in hypertrophy or dilation of the left or right
ventricle prolonged upto 0.09 to 0.12 second (normal 0.06-
0.08)

59. PURKINJE SYSTEM BLOCK
• Purkinje fibers- blocked, impulse is conducted by the
ventricular muscle
• Decreases the velocity of impulse conduction to one third
• Complete block- duration of the QRS complex is usually
increased to 0.14 second or greater
• Always pathological if prolonged beyond 0.12 seconds

60. BIZARRE QRS COMPLEXES
• Bizarre patterns of the QRS complex caused by two conditions:
(1) Destruction of cardiac muscle in various areas with
replacement of this muscle by scar tissue
(2) Multiple small local blocks- causing rapid shifts in
voltages and axis deviations.
• Causes double or even triple peaks in some leads

61. CURRENT OF INJURY
• Damage to the heart muscle- part remains partially or totally
depolarized all the time.
• Current of injury- Current flows between the pathologically
depolarized and the normally polarized areas
• Injured part of the heart is negative- emits negative charges into
the surrounding fluids
• Cause current of injury are:
(1) most common cause- Local coronary occlusions(Ischemia
of local areas of heart muscle)
(2) mechanical trauma (membranes- so permeable)
(3) infectious processes that damage the muscle membranes

62. EFFECT OF CURRENT OF INJURY ON THE
QRS COMPLEX
• A small area in the base of the left ventricle is newly infarcted in
the figure
• Abnormal negative current still flows from the infarcted area at
the base of the left ventricle and spreads to rest parts
• The vector of this current of injury 125 degrees, the negative
end toward the injured muscle

63. • Before the QRS complex begins, this vector causes:
- Lead I- An initial record-below the zero potential line,
(negative end of the lead I axis)
- Lead II- the record is positive- above the line (positive
terminal of axis)
- Lead III- record is positive- the projected vector-(positive
terminal of axis)
• Voltage of the current of injury in lead III is much greater than in
either lead I or lead II

64. • As normal process- septum first becomes depolarized; then the
depolarization spreads down to the apex and back toward the
base
• The last portion of the ventricles to become totally depolarized
is the base of the right ventricle
• At the end of the depolarization, all the ventricular muscle is in a
negative state (no net current flow)
• Both injured heart muscle and the contracting muscle are
depolarized.

65. • Repolarization- all of the heart finally repolarizes, except the
area of permanent depolarization (injured base of the left
ventricle)
• Repolarization causes a return of the current of injury again

66. ‘J’ POINT- ZERO REFERENCE POTENTIAL
• ECG machines can determine current when no net current is
flowing around the heart.
• Due to many stray currents exist in the body, such as currents
from skin potentials and from differences in ionic
concentrations in different fluids of the body.
• These stray currents make it impossible to predetermine the
exact zero reference level in the ECG.

67. • To determine the zero potential level:
Note the exact point at which the wave of depolarization
completes its passage through the heart (end of the
QRS complex)
• At this point, whole of ventricles have become depolarized,
including damaged and normal parts (no current is flowing
around the heart)
• Current of injury disappears at this point
• Potential of the electrocardiogram at this instant is at zero
voltage.
• This point is known as the “J point” in the ECG

68. • Analysis of the electrical axis of the injury potential caused by
a current of injury:
• A horizontal line is drawn in the ECG for each lead at the level
of the J point.
• This is the zero potential level in the ECG from which all
potentials caused by currents of injury measured

69. J POINT IN PLOTTING AXIS OF INJURY
POTENTIAL
• ECGs (leads I and III) from an injured heart. Both records show
injury potentials.
• The J point of each of these two ECGs is not on the same line
as the T-P segment.
• Horizontal line has been drawn through the J point- zero
voltage level
• Injury potential- difference between the voltage of the before
P wave and zero voltage level (J point)

70. • In lead I, the recorded voltage of the injury potential is above
the zero potential level and is therefore positive
• Lead III, the injury potential is below the zero voltage level
and therefore is negative

71. • The respective injury potentials in leads I and III are plotted on
the coordinates of these leads
• Resultant vector extends from the right side of the ventricles
toward the left and slightly upward, with an axis of about −30
degrees

72. CORONARY ISCHEMIA CAUSING
INJURY POTENTIAL
• Insufficient blood flow depresses the metabolism of the
muscle by:
(1) lack of oxygen
(2) excess accumulation of carbon dioxide
(3) lack of sufficient food nutrients.
• Also repolarization of the muscle membrane cannot occur in
areas of severe myocardial ischemia.
• Heart muscle does not die because the blood flow is sufficient
to maintain life of the muscle
• But not sufficient to cause normal repolarization of the
membranes.

73. • So an injury potential continues to flow during the T-P portion
of each heart cycle.
• Strong current of injury flows from the infarcted area of the
ventricles during the T-P interval
• So one of the important diagnostic features of ECGs after acute
coronary thrombosis is the current of injury
• ECG in the three standard bipolar limb leads and in one chest
lead (lead V2) from acute anterior wall MI

74. • Most important diagnostic feature- intense injury potential in
chest lead V2
• A strong negative injury potential during the T-P interval is
found
• The negative end of the injury potential vector in this heart is
against the anterior chest wall.
• The current of injury is emanating from the anterior wall of
the ventricles- anterior wall infarction.

75. • On analysis the injury potentials is negative potential in lead I
and a positive potential in lead III.
• The resultant vector of the injury potential in the heart is
about +150 degrees
• Negative end pointing toward the left ventricle
• Positive end pointing toward the right ventricle.
• Current of injury is coming mainly from the left ventricle- from
the anterior wall of the heart.

76. POSTERIOR WALL INFARCTION
• If a zero potential reference line is drawn through the J point
of the chest lead V2 (potential of the current of injury is
positive)
• Vector- Positive end- direction of the anterior chest wall
Negative end- away from the chest wall
• The current of injury is coming from the back of the heart-
diagnose posterior wall infarction.
• Injury potentials from leads II and III is negative in both leads.

77. • The resultant vector of the injury potential is about −95
degrees, with the negative end pointing downward and the
positive end pointing upward.
• Chest lead indicate injury on the posterior wall of the heart
• Injury potentials in leads II and III, is in the apical portion of
the heart
• Infarct is near the apex on the posterior wall of the left
ventricle suspected.

78. INFARCTION IN OTHER PARTS OF THE
HEART
• Demonstration of locus of any infarcted area emitting a
current of injury is done by the above method
• In such vectorial analysis:
- Positive end of the injury potential
vector points toward the normal
cardiac muscle
- Negative end points toward the
injured portion of the heart that is
emitting the current of injury.

79. RECOVERY FROM ACUTE CORONARY
THROMBOSIS
• ECG- V3 chest lead with acute post: wall MI, showing changes
from the day of the attack to 1 week, 3 weeks, and 1 year later.
• Injury potential is strong after the acute attack (the T-P segment
is displaced positively from the S-T segment), disappears later.
• This is the usual recovery pattern after acute myocardial
infarction of moderate degree (new collateral coronary blood
flow re-establish appropriate nutrition)

80. OLD RECOVERED MYOCARDIAL
INFARCTION
• ECG shows leads I and III after anterior infarction and leads I
and III after posterior infarction about 1 year later
• Anterior MI- Q wave- at the beginning of the QRS complex in
lead I in anterior infarction (loss of muscle mass in the
anterior wall of the left ventricle)
• Posterior MI - Q wave- at the beginning of the QRS complex in
lead III (loss of muscle in the posterior apical part of the
ventricle)

81. SPATIAL QRS-T ANGLE
• The SA is the angle of deviation between two vectors:
- Spatial QRS-axis- electrical potential by ventricular
depolarization
- Spatial T-axis- electrical potential ventricular
repolarization
• In healthy individuals- the direction of ventricular depolarization
and repolarization is relatively reversed- sharp SA.
• The mean, normal SA in healthy young adult females and males
is 66° and 80°
• In ECG analysis, the SA is categorized into:
Normal (below 105°)
Borderline abnormal (105–135°)
Abnormal (greater than 135°)

82. • A broad SA results when the heart undergoes
pathological changes and is reflected in a discordant
ECG
• The SA is a sensitive marker of repolarization
aberrations
• It is clinically applied in predicting cardiac morbidity
and mortality.

83. NORMAL P WAVE MORPHOLOGY
LEAD- II
• The right atrial depolarisation wave (brown)
precedes that of the left atrium (blue).
• The combined depolarisation wave, the P wave, is
less than 120 ms wide and less than 2.5 mm high

84. ABNORMALITIES OF P WAVE
• Peaked P waves (> 0.25 mV) suggest right atrial enlargement, cor
pulmonale- chronic obstructive pulmonary disease
• Increased amplitude- hypokalemia, right atrial enlargement
• Decreased amplitude- hyperkalemia
• P-wave prolonged- left and right atrial hypertrophy
• Bifid P waves (P mitrale) indicate left-atrial abnormality - e.g.
dilatation or hypertrophy.

85. RIGHT ATRIAL ENLARGEMENT
LEAD II
• In right atrial enlargement, right atrial depolarisation lasts
longer than normal- waveform extends to the end of left atrial
depolarisation.
• Right atrial depolarisation peak now falls on top of that of the
left atrial depolarisation wave.
• The combination of these two waveforms produces a tall
peaked P waves (> 2.5 mm)
• ‘P pulmonale’- seen in cor pulmonale

86. LEFT ATRIAL ENLARGEMENT – LEAD II
• Left atrial depolarisation lasts longer than normal- amplitude
remains unchanged.
• Height of the resultant P wave remains within normal limits
but its duration is longer than 120 ms.
• A notch (broken line) near its peak may or may not be present
(“P mitrale”).
• Seen in Mitral stenosis

87. Biphasic P waves
• Interatrial conduction over posterior interatrial connections-
posterior‐to‐anterior propagation of excitation in the left atrium-
positive or isoelectric P waves
• Interatrial conduction over Bachmann's bundle only-
anterior‐to‐posterior activation of the left atrium
biphasic P waves in the same leads

88. ABNORMALITIES IN THE T WAVE
• T wave is normally positive in all the standard bipolar limb
leads
• It is caused by repolarization of the apex and outer surfaces of
the ventricles ahead of the intraventricular surfaces
• T wave becomes abnormal when the normal sequence of
repolarization does not occur.

89. SLOW CONDUCTION OF THE
DEPOLARIZATION WAVE- T WAVE
• Delayed conduction in the left ventricle resulting from left
bundle branch block- QRS prolonged
• This delayed conduction causes the left ventricle to become
depolarized about 0.08 second after depolarization of the
right ventricle
• Strong mean QRS vector to the left is generated

90. • The right ventricle begins to repolarize long before the left
ventricle- strong positivity in the right ventricle and negativity
in the left ventricle
• Mean axis of the T wave is now deviated to the right, which is
opposite the mean electrical axis of the QRS complex
• Conduction of the depolarization impulse through the
ventricles is greatly delayed- T wave is almost always of
opposite polarity to that of the QRS complex.

91. SHORTENED DEPOLARIZATION- T-WAVE
ABNORMALITIES
• If the base of the ventricles exhibit an abnormally short
period of depolarization
• Base of the ventricles would repolarize ahead of the apex
• Vector of repolarization would point from the apex toward the
base of the heart
• So T wave in all three standard leads would be negative
• Shortened period of depolarization is sufficient to cause
marked changes in the T wave

92. • Mild ischemia- most common cause of shortening of depolarization
• Ischemia- in one area of the heart- depolarization decreases
• Due to :-
- Chronic progressive coronary occlusion
- Acute coronary occlusion
- Relative coronary insufficiency- during exercise
• Mild coronary insufficiency detected by exercise and record the
ECG- changes in T waves noted

93. BIPHASIC ‘T WAVE’
• Digitalis is a drug used during coronary insufficiency to
increase the strength of cardiac muscle contraction.
• Overdose of digitalis- depolarization duration in one part of
the ventricles may be increased
• Nonspecific T wave changes can occur- inversion or biphasic T
waves
• Changes in the T wave during digitalis administration are
often the earliest signs of digitalis toxicity.

94. REFERENCES
• Guyton and Hall Textbook of Medical Physiology 13th edition
• Boron Medical Physiology 3rd Edition
• Ganong's Review of Medical Physiology 26th Edition
• Berne & Levy Physiology 7th Edition
• Harrison’s textbook of internal medicine-
19th edition

95. THANK YOU…!