Ecg- Vector Analysis

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 C urrent 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. A rrowhead 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 L ong 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 T he scale of vectors rotates clockwise A bove 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 D irection 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) L ine 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 P erpendicular lines are drawn from the tip of vector A to the axes of the three different standard leads P rojected 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 F irst part of the ventricles to become depolarized is the left endocardial surface of the septum D epolarization 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 P ositive vector- recording in the ECG above zero line N egative 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 V oltages in all electrocardiographic leads have increased

21. 0.035 second after onset of depolarization- vector is becoming shorter V oltages are lower - electronegativity of outside apex, neutralizing much of the positivity on the other epicardial surfaces of the heart. A xis of the vector- shift toward the left side of the chest ( left ventricle is slightly slower to depolarize than is the right ventricle) R atio 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 E ntire 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 S light negative depression at the beginning of QRS complex- is the Q wave . C aused 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 C ompletes 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 O uter 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 V ector 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 E lectronegativity 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) D irection 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 V ector increases and decreases in length (increasing and decreasing voltage) V ector changes direction (changes in the average direction of the electrical potential) V ectorcardiogram 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. P ositive end of the vector remains at the zero point before depolarization V entricular 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. V entricular muscle becomes further depolarized , the vector becomes stronger V ector 2 of represents the state of depolarization of the ventricles about 0.02 second after vector 1. Vector 3- 0.02 second later V ector 4 occurs in another 0.01 second. V entricles 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 L ead I- positive recording L ead 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 I ntersection 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 M ean 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 A xis can swing even in a normal heart from 20 degrees- 100 degrees . The causes of the normal variations 1. A natomical 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 . H eart 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 A xis 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 L ateral 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 L eft ventricle depolarization remains 0.1 second slower than right ventricle S trong vector projects from the right ventricle toward the left ventricle. L eft 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 S lowness of impulse conduction- duration of the QRS complex is greatly prolonged E xcessive widths of the QRS waves in ECG P rolonged QRS complex differentiates bundle branch block from hypertrophy.

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

53. ABNORMAL VOLTAGES OF THE QRS COMPLEX INCREASED VOLTAGE IN THE STANDARD BIPOLAR LIMB LEADS V oltages 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 L ead 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 H ypertrophy 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. P otentials recorded in the electrocardiographic leads are considerably greater than normal

55. DECREASED VOLTAGE OF THE ELECTROCARDIOGRAM Caused by Cardiac Myopathies (diminished muscle mass) M ost common cause- old myocardial infarctions D epolarization wave to move through the ventricles slowly Also shows prolongation of the QRS complex along with the decreased voltage . L ocal 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 E xtracellular fluid conducts electrical currents with great ease E ffusion effectively short-circuits the electrical potentials generated by the heart, decreasing the electrocardiographic voltages

57. Pleural effusion D ecreases 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 P rolonged 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 D ecreases the velocity of impulse conduction to one third C omplete 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. C auses 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 A bnormal 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) - L ead II- the record is positive- above the line ( positive terminal of axis) - L ead 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) R epolarization 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) C urrent of injury disappears at this point P otential of the electrocardiogram at this instant is at zero voltage. This point is known as the “J point” in the ECG

68. A nalysis 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. T he J point of each of these two ECGs is not on the same line as the T-P segment. H orizontal line has been drawn through the J point- zero voltage level I njury 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 R esultant 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. H eart 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. S trong 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 N egative end pointing toward the left ventricle Positive end pointing toward the right ventricle. C urrent 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- P ositive end- direction of the anterior chest wall Negative end- away from the chest wall T he 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: - P ositive end of the injury potential vector points toward the normal cardiac muscle - N egative 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 . I njury 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) P osterior 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 I ncreased amplitude- hypokalemia , right atrial enlargement D ecreased 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. R ight 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 L eft atrial depolarisation lasts longer than normal- amplitude remains unchanged. H eight 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 B ase of the ventricles would repolarize ahead of the apex V ector of repolarization would point from the apex toward the base of the heart So T wave in all three standard leads would be negative S hortened 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 - A cute coronary occlusion - R elative coronary insufficiency- during exercise M ild coronary insufficiency detected by exercise and record the ECG- changes in T waves noted

93. BIPHASIC ‘ T WAVE’ D igitalis is a drug used during coronary insufficiency to increase the strength of cardiac muscle contraction. O verdose of digitalis- depolarization duration in one part of the ventricles may be increased Nonspecific T wave changes can occur- inversion or biphasic T waves C hanges 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- 19 th edition

95. THANK YOU…!