1. This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student rotated under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Chairman of the Department of Medicine. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

2. ECG Changes in ischemic disease Presented by: Aliaa Ali Al Saffar Medical Student December 17, 2008

3. definition An electrocardiogram (ECG or EKG) is a recording of the electrical activity of the heart over time produced by an electrocardiograph, usually in a noninvasive recording via skin electrodes. An electrocardiogram (ECG or EKG) is a recording of the electrical activity of the heart over time produced by an electrocardiograph, usually in a noninvasive recording via skin electrodes.

4. Leads The word lead has two meanings in electrocardiography: it refers to either the wire that connects an electrode to the electrocardiograph, or (more commonly) to a combination of electrodes that form an imaginary line in the body along which the electrical signals are measured. The word lead has two meanings in electrocardiography: it refers to either the wire that connects an electrode to the electrocardiograph, or (more commonly) to a combination of electrodes that form an imaginary line in the body along which the electrical signals are measured.

5. When a depolarization wavefront (or mean electrical vector) moves toward a positive electrode, it creates a positive deflection on the ECG in the corresponding lead. When a depolarization wavefront (or mean electrical vector) moves toward a positive electrode, it creates a positive deflection on the ECG in the corresponding lead. When a depolarization wavefront (or mean electrical vector) moves away from a positive electrode, it creates a negative deflection on the ECG in the corresponding lead. When a depolarization wavefront (or mean electrical vector) moves away from a positive electrode, it creates a negative deflection on the ECG in the corresponding lead. When a depolarization wavefront (or mean electrical vector) moves perpendicular to a positive electrode, it creates an equiphasic (or isodiphasic) complex on the ECG. When a depolarization wavefront (or mean electrical vector) moves perpendicular to a positive electrode, it creates an equiphasic (or isodiphasic) complex on the ECG.

6. limb Leads I, II and III are the so-called limb leads. Leads I, II and III are the so-called limb leads. Lead I is a dipole with the negative (white) electrode on the right arm and the positive (black) electrode on the left arm. Lead I is a dipole with the negative (white) electrode on the right arm and the positive (black) electrode on the left arm. Lead II is a dipole with the negative (white) electrode on the right arm and the positive (red) electrode on the left leg. Lead II is a dipole with the negative (white) electrode on the right arm and the positive (red) electrode on the left leg. Lead III is a dipole with the negative (black) electrode on the left arm and the positive (red) electrode on the left leg. Lead III is a dipole with the negative (black) electrode on the left arm and the positive (red) electrode on the left leg.

7. Augmented limb Leads aVR, aVL, and aVF are augmented limb leads. Leads aVR, aVL, and aVF are augmented limb leads. Lead aVR or "augmented vector right" has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm. Lead aVR or "augmented vector right" has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm. Lead aVL or "augmented vector left" has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm. Lead aVL or "augmented vector left" has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm. Lead aVF or "augmented vector foot" has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg. Lead aVF or "augmented vector foot" has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg.

8. Diagram: Frontal Plane Leads

9. Precordial The precordial leads V1, V2, V3, V4, V5, and V6 are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. The precordial leads V1, V2, V3, V4, V5, and V6 are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. and these leads are considered to be unipolar. The precordial leads view the heart's electrical activity in the so-called horizontal plane.

10. Leads V1, V2, and V3 are referred to as the right precordial leads and V4, V5, and V6 are referred to as the left precordial leads. Leads V1, V2, and V3 are referred to as the right precordial leads and V4, V5, and V6 are referred to as the left precordial leads. The QRS complex should be negative in lead V1 and positive in lead V6. The QRS complex should show a gradual transition from negative to positive between leads V2 and V4. The equiphasic lead is referred to as the transition lead. When the transition occurs earlier than lead V3, it is referred to as an early transition. When it occurs later than lead V3, it is referred to as a late transition. There should also be a gradual increase in the amplitude of the R wave between leads V1 and V4. This is known as R wave progression. Poor R wave progression is a nonspecific finding. It can be caused by conduction abnormalities, myocardial infarction, cardiomyopathy, and other pathological conditions. The QRS complex should be negative in lead V1 and positive in lead V6. The QRS complex should show a gradual transition from negative to positive between leads V2 and V4. The equiphasic lead is referred to as the transition lead. When the transition occurs earlier than lead V3, it is referred to as an early transition. When it occurs later than lead V3, it is referred to as a late transition. There should also be a gradual increase in the amplitude of the R wave between leads V1 and V4. This is known as R wave progression. Poor R wave progression is a nonspecific finding. It can be caused by conduction abnormalities, myocardial infarction, cardiomyopathy, and other pathological conditions.

11. Characteristics of the Normal ECG 1. Measurement 2. Rhythm 3. Conduction 4. Waveform Description

12. Measurements Heart Rate: 60 - 100 bpm PR Interval: 0.12 - 0.20 sec QRS Duration: 0.06 - 0.10 sec QT Interval (QTc<0.40 sec)

15. 2. Rhythm: Normal sinus rhythm The P waves in leads I and II must be upright (positive) if the rhythm is coming from the sinus node.

16. Conduction Normal Sino-atrial (SA), Atrio-ventricular (AV), and Intraventricular (IV) conduction

18. Waveform Description P Wave and inverted in aVR A P wave must be upright in leads II and aVF and inverted in lead aVR to designate a cardiac rhythm as Sinus Rhythm. During normal atrial depolarization, the main electrical vector is directed from the SA node towards the AV node, and spreads from the right atrium to the left atrium. This turns into the P wave on the ECG, which is upright in II, III, and aVF and inverted in aVR A P wave must be upright in leads II and aVF and inverted in lead aVR to designate a cardiac rhythm as Sinus Rhythm. P duration < 0.12 sec P amplitude < 2.5 mm

19. P wave rate 60-100 pbm with <10% variation. P wave rate 60-100 pbm with <10% variation. Rate <60= sinus bradycardia Rate <60= sinus bradycardia Rate >100= sinus tachycardia Rate >100= sinus tachycardia Variation> 10%= sinus arrhythmia Variation> 10%= sinus arrhythmia

20. Abnormal P waves :- Right atrail hypertrophy Right atrail hypertrophy left atrail hypertrophy left atrail hypertrophy Atrial premature beat Atrial premature beat hyperkalaemia hyperkalaemia

21. Normal Sinus Rhythm

22. Sinus Bradycardia

23. SinusTachycardia

24. QRS Complex The QRS complex is a structure on the ECG that corresponds to the depolarization of the ventricles. QRS duration < 0.10 sec QRS amplitude is quite variable from lead to lead and from person to person. Two determinates of QRS voltages are: 1. Size of the ventricular chambers (i.e., the larger the chamber, the larger the voltage) 2. Proximity of chest electrodes to ventricular chamber (the closer, the larger the voltage)

25. For abnormally wide QRS: RBBB LBBB htperkalaemia

26. The electrical axis both I and aVF +ve = normal axis both I and aVF +ve = normal axis both I and aVF -ve = axis in the extreme right axis deviation both I and aVF -ve = axis in the extreme right axis deviation lead I -ve and aVF +ve right axis deviation lead I -ve and aVF +ve right axis deviation lead I +ve and aVF -ve lead I +ve and aVF -ve lead II +ve = normal axis lead II +ve = normal axis lead II -ve left axis deviation. lead II -ve left axis deviation.

27. causes of extreme right axis deviation. emphysema emphysema hyperkalaemia hyperkalaemia lead transposition lead transposition artificial cardiac pacing artificial cardiac pacing ventricular tachycardia ventricular tachycardia

28. causes of right axis deviation normal finding in children and tall thin adults normal finding in children and tall thin adults right ventricular hypertrophy right ventricular hypertrophy chronic lung disease even without pulmonary hypertension chronic lung disease even without pulmonary hypertension anterolateral myocardial infarction anterolateral myocardial infarction left posterior hemiblock left posterior hemiblock pulmonary embolus pulmonary embolus Wolff-Parkinson-White syndrome - left sided accessory pathway Wolff-Parkinson-White syndrome - left sided accessory pathway atrial septal defect atrial septal defect ventricular septal defect ventricular septal defect

29. causes of left axis deviation left anterior hemiblock left anterior hemiblock Q waves of inferior myocardial infarction Q waves of inferior myocardial infarction artificial cardiac pacing artificial cardiac pacing emphysema emphysema hyperkalaemia hyperkalaemia Wolff-Parkinson-White syndrome - right sided accessory pathway Wolff-Parkinson-White syndrome - right sided accessory pathway tricuspid atresia tricuspid atresia ostium primum ASD ostium primum ASD injection of contrast into left coronary artery injection of contrast into left coronary artery

30. QT interval QT interval The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Normal values for the QT interval are between 0.30 and 0.44 (0.45 for women) seconds. The most commonly used method for correcting the QT interval by dividing the QT interval by sequare root of preceeding R-R interval. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Normal values for the QT interval are between 0.30 and 0.44 (0.45 for women) seconds. The most commonly used method for correcting the QT interval by dividing the QT interval by sequare root of preceeding R-R interval.

31. Causes of long QT interval: MI, myocarditis, diffuse myocardial disease MI, myocarditis, diffuse myocardial disease Hypocalcaemia, hypotgyrodism Hypocalcaemia, hypotgyrodism Subarachnoid haemorrhage, intracerebral haemorrhage. Subarachnoid haemorrhage, intracerebral haemorrhage. Drugs (sotalol, amiodarone) Drugs (sotalol, amiodarone)

32. ST Segment and T wave The normal T wave is usually in the same direction as the QRS except in the right precordial leads. In the normal ECG the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR.

33. Causes of elevation of ST segment:- MI( anterior, inferior) MI( anterior, inferior) LBBB LBBB Normal varients (athletic heart) Normal varients (athletic heart) Acute pericarditis. Acute pericarditis. Causes of depression of ST segment: Causes of depression of ST segment: Myocardial ischaemia Myocardial ischaemia Digoxin effect. Digoxin effect. Ventricular hypertrophy Ventricular hypertrophy Acute post. MI, pulmonary embolus Acute post. MI, pulmonary embolus LBBB LBBB

34. Causes of tall T waves:- Hyperkalaemia. Hyperkalaemia. Hyperacute myocardial infarction. Hyperacute myocardial infarction. LBBB LBBB Causes of flattened or inverted T waves: Age, race. Age, race. hyperventilation hyperventilation Anxiety Anxiety LVH LVH PE PE Pericarditis, electrolyte imbalance. Pericarditis, electrolyte imbalance.

35. The normal U Wave: (the most neglected of the ECG waveforms) U wave amplitude is usually < 1/3 T wave amplitude in same lead U wave direction is the same as T wave direction in that lead U waves are more prominent at slow heart rates and usually best seen in the right precordial leads. Origin of the U wave is thought to be related to after depolarizations which interrupt or follow repolarization.

36. ECG changes in angina Resting ECG typically shows ST segment depression and T wave flattening or inversion during an attacks. Resting ECG typically shows ST segment depression and T wave flattening or inversion during an attacks. Exercise ECG testing is positive in about 75% of people with severe CAD; A normal test does not exclude the diagnosis. Exercise ECG testing is positive in about 75% of people with severe CAD; A normal test does not exclude the diagnosis.

37. ECG changes in MI MI's resulting from total coronary occlusion result in more homogeneous tissue damage and are usually reflected by a Q-wave MI pattern on the ECG. MI's resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by a non Q-wave MI pattern on the ECG. Two-thirds of MI's presenting to emergency rooms evolve to non-Q wave MI's, most having ST segment depression or T wave inversion.

38. Most MI's are located in the left ventricle. In the setting of a proximal right coronary artery occlusion, however, up to 50% may also have a component of right ventricular infarctionas well. Right- sided chest leads are necessary to recognize RV MI.

39. Acute anterior MI ST elevation in the anterior leads V1-6,I and AVL ST elevation in the anterior leads V1-6,I and AVL Reciprocal ST depression in the inferior leads Reciprocal ST depression in the inferior leads

40. Acute inferior MI ST elevation in the inferior leads II, III and aVF. ST elevation in the inferior leads II, III and aVF. Reciprocal ST depression in the anterior leads. Reciprocal ST depression in the anterior leads.

41. Acute posterior MI The mirror image of acute injery in leads V1-3 The mirror image of acute injery in leads V1-3 Tall R rave, tall upright Twave in leads V1-3. Tall R rave, tall upright Twave in leads V1-3. Usually associated with inferior and/or lateral wall MI. Usually associated with inferior and/or lateral wall MI.

42. Old Inferior MI A Q wave in lead III wider than 1mm. A Q wave in lead III wider than 1mm. A Q wave in lead AVF wider than 0.5 mm A Q wave in lead AVF wider than 0.5 mm A Q wave of any size in lead II. A Q wave of any size in lead II.

43. Anteroseptal MI The QS complexes, resolving ST segment elevation and T wave inversions in V1-2 are evidence for afully evolved anteroseptal MI. The inverted T waves in V3-5, I, aVL are also probably related to the MI.

44. Extensive Anterior/Anterolateral MI Significant pathologic Q-waves (V2-6, I, aVL) plus marked ST segment elevation are evidence for this large anterior/anterolateral MI. The exact age of the infarction cannot be determined without clinical correlation and previous ECGs, but this is likely a recent MI.

45. Postero-lateral MI The "true" posterior MI is recognized by pathologic R waves in leads V1-2. These are the posterior equivalent of pathologic Q waves (seen from the perspective of the anterior leads). Tall T waves in these same leads are the posterior equivalent of inverted T waves in this fully evolved MI. The loss of forces in V6, I, aVL suggest a lateral wall extension of this MI.

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