Ecg- Vector 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…!