Pathologic ECG. Adelina Vlad, MD PhD

Transcription

1 Pathologic ECG Adelina Vlad, MD PhD

2 Basic Interpretation of the ECG 1) Evaluate calibration 2) Calculate rate 3) Determine rhythm 4) Determine QRS axis 5) Measure intervals 6) Analyze the morphology and interrelation of ECG elements (P, P-Q, Q, QRS, ST, T, QT) in frontal and in precordial leads 6) Asses for Hypertrophy OR 7) Look for evidence of Infarction

3 NSR Parameters Rate Regularity P waves PR interval QRS duration bpm regular normal s s Any deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia

4 Arrhythmia Formation Arrhythmias can arise from electrophysiological abnormalities in the: Sinus node Atrial cells AV junction Ventricular cells His Purkinje network

5 Mechanisms Underlying Arrhythmias Disorders of impulse formation Automatism Triggered activity Disorders of impulse conduction Partial and complete conduction block Unidirectional block with reentry Aberrant (accessory) conduction pathways

6 SA Node Problems The SA Node can: fire too slow (< 60 bpm) fire too fast (>100 bpm) Sinus Bradycardia Sinus Tachycardia The impulse is conducted normally Sinus Tachycardia may be an appropriate response to stress Both are abnormal Sinus Rhythms

7 Rate? Regularity? P waves? PR interval? QRS duration? 30 bpm regular normal 0.12 s 0.10 s Interpretation? Sinus Bradycardia

8 Rate? Regularity? P waves? PR interval? QRS duration? 130 bpm regular normal 0.16 s 0.08 s Interpretation? Sinus Tachycardia

9 Rare Sinoatrial Block The impulse from the sinus node is blocked before it enters the atrial muscle sudden cessation of P wave the impulse usually originates spontaneously in the atrioventricular node

10 Atrial cells can: Atrial Cell Problems fire occasionally from a focus Premature Atrial Contractions (PACs) fire continuously due to a looping re-entrant circuit Atrial Flutter

11 Rate? Regularity? P waves? 70 bpm occasionally irreg. 2/7 different contour PR interval? 0.14 s (except 2/7) QRS duration? 0.08 s Interpretation? NSR with Premature Atrial Contractions

12 Premature Atrial Contractions Deviation from NSR These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node Compensatory pause Pulse deficit due to a poor ventricular filling during the extrasystolic cycle

13 Premature Atrial Contractions PAC: Excitation of an atrial cell fires a premature impulse that is conducted normally through the AV node and ventricles When an impulse originating anywhere above the ventricles (SA node, atrial cells, AV node, Bundle of His) is conducted normally through the ventricles, the QRS will be narrow ( s)

14 Mechanisms Underlying Arrhythmias Disorders of impulse formation Automatism Triggered activity Disorders of impulse conduction Partial and complete conduction block Unidirectional block with reentry Aberrant (accessory) conduction pathways

15 Enhanced Automaticity Enhancement of normal automacity Development of automaticity in plain atrial or ventricular cells Can arise when the maximum diastolic potential becomes reduced to -50 mv and ICa may be operative at membrane potentials more negative than -70 mv, due to If Pathophysiologic states: increased catecholamines, electrolyte disturbances (e.g. hypokalemia), hypoxia or ischemia, mechanical stretch, drugs (e.g. digitalis)

16 Triggered Activity Requires the presence of an action potential Initiated by afterdepolarizations = depolarizing oscillations in membrane voltage induced by preceding AP Early afterdepolarizations (EAD) arise during phases 2 and 3 of AP Delayed afterdepolarizations (DAD) arise during phase 4 of AP When the after-depolarization reaches threshold, triggers a sequence of pacemaker-like action potentials that generate extrasystoles

17 EAD During a prolonged AP (bradicardia, hypokalemia, drugs that block outward K currents etc.) Ca++ channels recover from inactivation and can lead to a spontaneous depolarization

18 DAD Spontaneous release of Ca++ from SR during Ca++ overload (digitalis intoxication, injury-related cellular depolarization etc.) produces a transient inward current, Iti Iti is a composite current, resulting from - Na+/Ca++ exchange current - non-specific cation current that are activated by increased intracellular Ca++ concentration When large enough, Iti can produce a spontaneous AP DAD

19 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 70 bpm regular flutter waves none 0.06 s Atrial Flutter

20 Atrial Flutter Deviation from NSR No P waves; instead, flutter waves (note sawtooth pattern) are formed at a rate of bpm Only some impulses conduct through the AV node (usually every other impulse, resulting in an aprox. 150 ventricular bpm) Mechanism: Re-entrant pathway in the atria with every 2nd, 3rd or 4th impulse generating a QRS the others are blocked in the AV node

21 A re-entrant pathway (re-entrant excitation or circus movement) Is a wave of depolarization that travels in an endless circle Occurs when an action potential loops and results in self-perpetuating impulse formation Re-entry

22 Re entrant Excitation Re-entry has three requirements: (1) a closed conduction loop, (2) with unidirectional conduction, provided by a region of unidirectional block, (3) a sufficiently slow conduction of action potentials around the loop (relative to the path length and the action potential duration)

23 Unidirectional block Partial conduction block in which impulses travel in one direction, but not in the opposite one May arise as a result of a local depolarization or may be due to pathologic changes in functional anatomy

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25 When the pathway isn t long enough, the head of the reentrant impulse bites its own refractory tail, resulting in extinction of the excitation Pathway Length APD x Conduction Velocity APD action potential duration SHORT PATHWAY

26 The impulse can continue to travel around a closed loop, causing re-entrant excitation if: the pathway around the circle is long (dilated hearts) the velocity of conduction decreases (blockage of the Purkinje system, ischemia, hiperpotasemia etc.) the refractory period of the muscle is shortened (short APD) (drugs, such as epinephrine, or after repetitive electrical stimulation) Pathway Length > APD x Conduction Velocity APD action potential duration

27 Atrial Cell Problems Atrial cells can also: fire continuously from multiple foci or Atrial Fibrillation fire continuously due to multiple micro re-entrant wavelets

28 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 100 bpm irregularly irregular none none 0.06 s Atrial Fibrillation

29 Atrial Fibrillation Deviation from NSR No organized atrial depolarization, therefore no normal P waves; the P waves are replaced by f (fibrillatory) waves at a rate of bpm Atrial activity is chaotic (resulting in an irregularly irregular rate)

30 Atrial Fibrillation Mechanism: Multiple re-entrant wavelets conducted between the right and left atria Impulses are formed in a totally unpredictable fashion; the AV node allows some of the impulses to pass through at variable intervals (ventricular rhythm is irregularly irregular, and the rate about bpm)

31 Multiple micro re-entrant wavelets refers to wandering small areas of activation which generate fine chaotic impulses Atrial tissue They are generated by transmission of some of the depolarization waves around the heart in only some directions but not other directions This irregular pattern of impulse travel causes many circuitous routes for the impulses to travel results in an irregular pattern of patchy refractory areas in the heart many impulses traveling in all directions, some dividing and increasing the number of impulses, whereas others are blocked by refractory areas

32 The AV junction can: AV Junctional Problems fire continuously due to a looping re-entrant circuit fire occasionally from a focus block impulses coming from the SA node Paroxysmal Supraventricular Tachycardia (PSVT) Premature Junctional Contractions AV Junctional Blocks

33 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? bpm Regular regular Normal none 0.16 s none 0.08 s A-V Nodal Paroxysmal Tachycardia

34 PSVT Deviation from NSR The heart rate suddenly speeds up ventricular rate bpm; the P waves are lost or abnormal The paroxysm usually ends as suddenly as it began, with the pacemaker of the heart instantly shifting back to the sinus node PSVT: There are several types of PSVT but all originate above the bifurcation of the His bundle (therefore the QRS is usually narrow) Most common: abnormal conduction in the AV node (reentrant circuit looping in the AV node); P wave absent, covered by the QRS complex

35 Atrial Paroxysmal Tachycardia A PSVT with the abnormal impulse originating in the atria; the P wave is present, but modified

36 AV Premature Contractions Premature contractions fired from the A-V node or the A-V bundle The P wave is superimposed onto the QRS-T complex (no P wave on ECG) because the A-V impulse traveled at the same time towards atria and ventricles

37 1st Degree AV Block AV Nodal Blocks 2nd Degree AV Block, Type I 2nd Degree AV Block, Type II 3rd Degree AV Block

38 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 60 bpm regular normal 0.36 s 0.08 s 1st Degree AV Block

39 1st Degree AV Block Deviation from NSR PR Interval > 0.20 s Each P is followed by a QRS Etiology: Prolonged conduction delay in the AV node or bundle of His due to idiopathic fibrosis and sclerosis of the conduction system, ischemia, drugs (b-blockers, Ca channel blockers etc), increased vagal tone etc.

40 Rate? Regularity? P waves? PR interval? QRS duration? 50 bpm regularly irregular nl, but 4th no QRS lengthens 0.08 s Interpretation? 2nd Degree AV Block, Type I

41 2nd Degree AV Block, Mobitz Type I Deviation from NSR PR interval progressively lengthens with each beat until the atrial impulse is completely blocked (P wave not followed by QRS) Wenckebach phenomenon R-R intervals > P-P intervals Each successive atrial impulse encounters a longer and longer delay in the AV node until one impulse (usually the 3rd or 4th) fails to be conducted through the AV node

42 Rate? Regularity? P waves? PR interval? QRS duration? 75 bpm regularly irregular nl, 1 of 5 no QRS 0.14 s 0.08 s Interpretation? 2nd Degree AV Block, Type II

43 2nd Degree AV Block, Mobitz Type II Deviation from NSR Occasional P waves are completely blocked (P wave not followed by QRS), usually in a repeating cycle of every 3 rd (3:1 block) or 4 th (4:1 block) P wave Conduction is all or nothing (the PR interval remains constant)

44 High-Grade 2 nd Degree AV Block Every 2 nd or more P wave is blocked 2 P waves are never conducted in a row, therefore the distinction between Mobitz type I and Mobitz type II block is difficult to make

45 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? 40 bpm regular no relation to QRS none wide (> 0.12 s) 3rd Degree AV Block

46 3rd Degree AV Block Deviation from NSR The P waves are completely blocked in the AV junction; QRS complexes originate independently from below the junction no relationship between P and QRS The atria and ventricles form impulses independently of each other (AV dissociation) Escape rhythms originating above the bifurcation of the His bundle produce narrow QRS and a heart rate > 40 bpm below the bifurcation wide and bizarre QRS, heart rate < 40 bpm

47 Ventricular cells can: Ventricular Cell Problems fire occasionally from 1 or more foci Premature Ventricular Contractions (PVCs) fire continuously due to a looping re-entrant circuit Ventricular Tachycardia fire continuously from multiple foci Ventricular Fibrillation

48 Rate? Regularity? P waves? PR interval? QRS duration? 60 bpm occasionally irreg. none for 7th QRS 0.14 s 0.08 s (7th wide) Interpretation? Sinus Rhythm with 1 PVC

49 PVCs Deviation from NSR Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles

50 Ventricular Conduction Normal Signal moves rapidly through the ventricles Abnormal Signal moves slowly through the ventricles

51 A When an impulse originates in a ventricle, conduction is inefficient and the QRS is going to be wide and bizarre (A); T waves have an opposite polarity to the net polarity of the preceding QRS B The origin of the extrasystolic QRS axis points towards the site of the abnormal excitation (B)

52 Rate? Regularity? P waves? PR interval? QRS duration? 160 bpm regular none none wide (> 0.12 sec) Interpretation? Ventricular Tachycardia

53 Ventricular Tachycardia Deviation from NSR Impulse is originating in the ventricles (no P waves, wide QRS) > 3 consecutive ventricular beats at a rate > 120 bpm Can be regular, monomorphic or irregular, polymorphic Results from a re-entrant pathway looping in a ventricle (most common cause) or from abnormal foci or pathways Ventricular tachycardia can sometimes generate enough cardiac output to produce a pulse; at other times no pulse can be felt

54 Rate? Regularity? P waves? PR interval? QRS duration? Interpretation? none irregularly irreg. none none wide, if recognizable Ventricular Fibrillation

55 Ventricular Fibrillation Deviation from NSR Completely abnormal, with ultrarapid baseline undulations, irregular in timing and morphology Multiple wavelet reentrant electrical activity Rapid drop in cardiac output and death occurs if not quickly reversed

56 Electroshock Defibrillation

57 Basic Interpretation of the ECG 1) Evaluate calibration 2) Calculate rate 3) Determine rhythm 4) Determine QRS axis 5) Measure intervals 6) Analyze the ECG elements (P, P-Q, Q, QRS, ST, T, QT) and their interrelation in frontal and in precordial leads 6) Asses for Hypertrophy OR 7) Look for evidence of Infarction

58 4) Determine QRS Axis (The Electrical Axis of the Heart) Is the axis of the mean force during activation, measured in the frontal plane = mean QRS vector in the frontal plane Equals the sum of instantaneous activation vectors (corresponding to septum, apex, free walls and base activation)

59 Normal and Abnormal QRS Axis The normal QRS axis lies between -30 o and +90 o. A QRS axis that falls between -30 o and -90 o is abnormal and called left axis deviation o -120 o o -90 o -60 o -30 o A QRS axis that falls between +90 o and +150 o is abnormal and called right axis deviation. 180 o 150 o 120 o A QRS axis that falls between +150 o and -90 o is abnormal and called superior right axis deviation. o 90 o 60 o 0 o 30 o

60 Left Axis Deviation Left axis deviation in a hypertensive heart (hypertrophic left ventricle). Note the slightly prolonged QRS complex as well. Left axis deviation caused by left bundle branch block. Note also the greatly prolonged QRS complex.

61 Right Axis Deviation High-voltage electrocardiogram in congenital pulmonary valve stenosis with right ventricular hypertrophy. Superior right axis deviation and a slightly prolonged QRS complex also are seen. Right axis deviation caused by right bundle branch block. Note also the greatly prolonged QRS complex.

62 Intervals refers to the length of the PR and QT intervals and the width of the QRS complexes PR interval 5) Calculate Intervals < 0.12 s s > 0.20 s High catecholamine states Wolff-Parkinson-White Normal AV nodal blocks Wolff-Parkinson-White 1st Degree AV Block

63 Accessory Conduction Pathways Wolf-Parkinson-White (preexcitation) syndrome An accessory (aberrant) pathway conducts potential directly from A to V, providing a short circuit around the delay in the AV node Antegrade conduction occurs over both the accessory pathway and the normal conducting system The accessory pathway, being faster, depolarizes some of the V early short PR interval and a delta wave that prolongs QRS to > 0.1 s

64 Accessory conduction pathways in cases with Wolff Parkinson White syndrome. K, bundle of Kent; J, bundle of James; M, Mahaim fibres; the hatched area represents the atrioventricular border.

65 When the accessory pathway conducts in a retrograde direction can participate in reentrant tachycardia (PSVT)

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67 QTc interval < 0.44 s > 0.44 s Long QT Normal Long QT Torsades de Pointes A prolonged QT can be very dangerous. It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte abnormalities, CNS disease, post-mi, and congenital heart disease.

68 QT = 0.40 s RR = 0.68 s Square root of RR = 0.82 QTc = 0.40/0.82 = 0.49 s PR interval? QRS width? QTc interval? 0.16 seconds 0.08 seconds 0.49 seconds Interpretation of intervals? Normal PR and QRS, long QT

69 RR 23 boxes 17 boxes 10 boxes QT 13 boxes Normal QT Long QT QTc = QT/ RR Tip: Instead of calculating the QTc, a quick way to estimate if the QT interval is long is to use the following rule: A QT > half of the RR interval is probably long

70 QRS complex < 0.10 s s > 0.12 s Normal Incomplete bundle branch block Bundle branch block PVC Ventricular rhythm Incomplete bundle branch block 3 rd degree AV block with ventricular escape rhythm

71 Bundle Branch Blocks 1. QRS complex widens (> 0.12 sec) 2. QRS vector is oriented towards the area with delayed depolarization 3. QRS morphology changes (varies depending on ECG lead, and if it is a right vs. left bundle branch block) 4. Intrinsecoid deflection > 0.06 for RBBB and > 0.08 for LBBB 5. T wave inversion appears

72 QRS duration: < 0.12 s measured in the lead with the widest complex Intrinsecoid deflection: - measures the duration of transmural activation under the recording electrode of a precordial lead (V1, V2, V5, V6) - measured from the peak of the last R of the complex until the onset of the QRS complex - Normal values: < s in V1, V2 and < s in V5, V6 QRS ID ID

73 Right Bundle Branch Block What QRS morphology is characteristic? For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V 1 and V 2 ). V 1 Rabbit Ears

74 The terminal vector of ventricular depolarization, corresponding to delayed RV depolarization, is oriented anteriorly and to the right: rsr in V1 and qrs in V6 T wave in V1 is negative due to the delayed repolarization of the right ventricular wall (the vector is oriented posteriorly and to the left) qrs

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76 Left Bundle Branch Block Both early and later phases of ventricular depolarization are altered: both septal and left wall depolarization vectors are oriented posteriorly and to the left wide predominantly negative (QS) complexes in V1 and entirely positive complexes (wide, notched R) in V6 T wave has opposite polarity to the net QRS due to a repolarization vector oriented anteriorly and to the right QS

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78 6) Hypertrophy The ECG can reveal enlargement or hypertrophy of the four chambers of the heart: Right atrial enlargement (RAE) Left atrial enlargement (LAE) Right ventricular hypertrophy (RVH) Left ventricular hypertrophy (LVH)

79 Atrial Enlargement P wave changes (morphology, axis, amplitude) Due to Inlet ventricular valve stenosis (mitral - often, tricuspid - rare) or insufficiency Pulmonary hypertension Congenital heart diseases Heart failure

80 Right atrial enlargement P wave morphology: sharp, tall, symmetric in V1, V2, avf, II, III; if biphasic in V1, the positive initial deflection predominates P wave axis: P wave amplitude: II P > 2.5 mm, or V1 or V2 P > 1.5 mm > 1 ½ boxes (in height) > 2 ½ boxes (in height) A cause of RAE is RVH from pulmonary hypertension (P pulmonale)

81 Left atrial enlargement The P waves are broad (> 0.12 s) and often notched in lead I, avl, V5, V6 ; in lead V1 they have a deep and wide negative component In lead II, > 0.04 s (1 box) between notched peaks, or In V1, neg. deflection > 1 box wide x 1 box deep P wave axis: left deviation Normal Notched Negative deflection A common cause of LAE is Mi stenosis

82 Ventricular Hypertrophy Due to a pressure or volume load ECG abnormalities High voltage R, S waves QRS axis deviation Increased intrinsecoid deflection T-wave inversions

83 Left Ventricular Hypertrophy Normal Left Ventricular Hypertrophy The QRS complexes are very tall in the right panel (increased voltage)

84 Left Ventricular Hypertrophy Why is left ventricular hypertrophy characterized by tall QRS complexes? As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage. LVH Increased QRS voltage ECHOcardiogram

85 Left ventricular hypertrophy Take a look at this ECG. What do you notice about the axis and QRS complexes in leads V5, V6 and V1, V2? The deep S waves seen in the leads over the right ventricle and the tall R waves in the left leads are created because the heart is depolarizing left, superior and posterior (away from leads V1, V2, toward leads V5, V6) There is left axis deviation and there are tall R waves in V5, V6 and deep S waves in V1, V2

86 QRS amplitude = algebraic sum of the amplitudes of the component waves > 1 mv in one precordial lead, > 0.5 mv in a standard lead The amplitude of R and S waves it is used for the diagnosis of left ventricular hypertrophy: Sokolow-Lyon index: Sv1+ (Rv5 or Rv6) > 3.5 mv Cornell voltage criteria: Sv3 + SaVL 2.8 mv for men, 2.0 for women or of right ventricular hypertrophy: Rv1 > 0.7 mv, SV5 or V6 > 0.7 mv etc.

87 Left ventricular hypertrophy, diagnostic criteria: Most characteristic: increased QRS amplitude - R waves in left leads (I, avl, V5, V6) and S waves in the right leads (V1, V2) are oversized (and sometimes notched) Sokolow-Lyon index: SV1 + (RV5 or RV6) > 3.5 mv, RaVL > 1.1 mv Cornell voltage criteria: SV3 + SaVL > 2.8 mv and > 2.0 mv QRS duration > 0.11 s, ID > 0.05 s in V5, V6 QRS axis horizontal or with a left deviation ST depression and T inversion in leads with a tall R S = 13 mm R = 25 mm A common cause of LVH is systemic hypertension.

88 A 63 years old man has longstanding, uncontrolled hypertension. Is there evidence of heart disease from his hypertension? Yes, there is left axis deviation (positive in I, negative in II), left atrial enlargement (> 1 x 1 boxes in V1) and LVH (R in V5 = 27 + S in V2 = 10 > 35 mm).

89 Right Ventricular Hypertrophy Right axis deviation, tall R waves in V1, V2, T-wave inversions; P pulmonale can be observed as well

90 Right ventricular hypertrophy Tall R in avr, V1, V2 (R/S>1) and deep S in I, avl, V5 (V6): R in V1 > 0.7 mv, S in V5, V6 > 0.7 mv RV1 + SV5 > 1,05 mv ID > 0.03 s in V1,2 Right QRS axis deviation T-wave inversions Normal R waves in V1, V2 from a normal ECG and from a person with RVH RVH

91 7) Look for Evidence of Infarction ECG findings depend on The nature of the process Reversible ischemia Irreversible - infarction The duration: acute/ chronic The extent: Transmural Subendocardial Localization: anterior, inferoposterior ECG can identify other underlying abnormalities: ventricular hypertropy, conduction defects etc.

92 7) Look for Evidence of Infarction When analyzing a 12-lead ECG for evidence of an infarction one looks for the following: Abnormal Q waves ST elevation or depression Peaked, flat or inverted T waves ST elevation (or depression) in at least two leads is the earliest and most consistent ECG finding during AMI There are ST elevation (Q-wave) and non-st elevation (non-q wave) MIs

93 ST Elevation Elevation of the ST segment in at least 2 leads is consistent with a myocardial infarction Because blood flow is regional, the area of infarction are also regional specific ECG leads can provide the best view of the infarcted area

94 Views of the Heart Some leads get a good view of the: Anterior portion of the heart Leads V1 V4 Lateral portion of the heart Leads I, avl, V5, V6 Inferior portion of the heart Leads II, III, avf

95 Anterior Wall MI Can be recognized if there are changes in leads V 1 - V 4 that are consistent with a myocardial infarction

96 Inferior Wall MI ST segment is elevated in leads II, III and avf

97 Anterolateral MI This person s MI involves both the anterior wall (V 2 -V 4 ) and the lateral wall (V 5 -V 6, I, and avl)!

98 ST Elevation and non-st Elevation MIs When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply is not restored in an appropriate period of time. The ECG changes over time with each of these events

99 Mild ischemia increases K+ outflow shortens APD affected areas are repolarized before the rest of the myocardium changes of repolarization vector leading to T wave abnormalities

100 Severe, acute ischemia can reduce the resting membrane potential, shorten APD and decrease the slope and amplitude of phase 0 voltage gradient between normal and ischemic area current flows = diastolic and systolic injury currents

101 Transmural ischemia: overall ST vector shifts toward epicardial layers ST elevation, tall T waves in the overlying leads Subendocardial ischemia: overall ST vector shifts toward the inner layer and the ventricular cavity ST segment depression in the overlying leads

102 Necrosis decreased R amplitude or pathologic Q waves genesis due to loss of electric activity in the infarcted area

103 ECG Changes Ways the ECG can change include: ST elevation & depression T-waves Appearance of pathologic Q-waves peaked flattened inverted

104 ECG Changes and the Evolving MI There are two distinct patterns of ECG change depending if the infarction is: Non-ST Elevation ST Elevation ST Elevation (Transmural or Epicardial MI) Non-ST Elevation (Subendocardial or non-q-wave)

105 ST Elevation Infarction Diagram depicting an evolving infarction: A. Normal ECG prior to MI B. Ischemia from coronary artery occlusion results in ST elevation and peaked T-waves normal hours C. Infarction from ongoing ischemia results in marked ST elevation hours days D/E. Ongoing infarction with appearance of pathologic Q-waves; T-wave inversion may occur weeks months F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves of the clinical onset of an MI

106 ST Elevation Infarction ECG of an inferior MI: Look at the inferior leads (II, III, avf) What ECG changes do you see? ST elevation and Q-waves Extra credit: What is the rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!

107 Non-ST Elevation Infarction The ECG changes seen with a non-st elevation infarction are: Before injury Normal ECG Ischemia ST depression & T-wave inversion Infarction Fibrosis ST depression & T-wave inversion ST returns to baseline, but T-wave inversion persists

108 Non-ST Elevation Infarction Here s an ECG of an evolving non-st elevation MI: Note the ST depression and T-wave inversion in leads V 2 -V 6. Question: What area of the heart is infarcting? Anterolateral