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Slide 1: Rapid ECG Interpretation Chih-L Han MD, PhD COR@vgh
Slide 2: The ECG is the oldest cardiologic test, but even 100 years after its inception, it continues as the most commonly used cardiologic test. Despite the advent of expensive and sophisticated alternatives, the ECG remains the most reliable tool for the confirmation of acute myocardial infarction (MI). The ECG—not CK-MB, troponins, echocardiogram, or SPECT or PET scan—dictates the timely administration of life-saving PCI or thrombolytic therapy. There is no test to rival the ECG in the diagnosis of arrhythmias, which is a common and bothersome clinical cardiologic problem. Also, the clinical diagnosis of pericarditis and myocardial ischemia is made mainly by ECG findings.
Slide 3: Electrical Activation of the Heart
Slide 4: Action Potential of Heart
Slide 5: How ECG deflection is formed?
Slide 6: ECG Signals
Slide 7: Cardiac Cycle
Slide 8: The Action Potential
Slide 9: Pharmacological effects
Slide 10: Instantaneous Vectors
Slide 11: Electrocardiogram
Slide 12: Variation in QRS Wave Form
Slide 13: Effects of Electrodes Position
Slide 14: Augmented Leads
Slide 15: Standard Limb Leads
Slide 16: Influence of Heart Positions
Slide 18: Clockwise and counterclockwise rotation Tall R wave LVH QRS Normal Variants RVH Loss of R waves or poor progression of R waves Amplitude of R waves from V2 to V4 Normal Q wave (duration < 0.04 sec and amplitude < 3 mm) Deep Q in hypertrophic cardiomyopathy Misplacement of leads Q wave
Slide 19: Clockwise and Counterclockwise Rotation
Slide 20: Pseudoinferior MI
Slide 21: Important Normal ECG Intervals and Parameters PR interval 0.12 to 0.2 second (up to 0.22 second in adults). P waves <3 small squares (0.12 second) in duration, and amplitude <3 mm. Upright in lead I, inverted in aVR (if opposite, suspect reversed arm leads† or dextrocardia) QRS duration 0.05 to 0.1 second; ≥0.1 second, consider incomplete LBBB, incomplete RBBB, or WPW syndrome Q waves Normally present in aVR; occasionally in V1 or in aVL (vertical heart) Often present in lead III: should be ≤0.04 second duration. Other leads except lead I: <0.04 second duration and ≤3 mm deep; lead I ≤1.5 mm in patients older than age 30. Q waves may be up to 5 mm deep in several leads in individuals age <30 R waves 30 0 to 6 mm, age >30 V3: 1 to 20 mm, age >30 • V1: 0 to 15 mm, age 12 to 20 0 to 8 mm, age 20 to V2: 0.2 to 12 mm, age <30 V2: 0.2 to 12 mm, age <30‡ (see Step 5, Fig. 2-16). V3: 1 to 20 mm, age >30.‡ ST segment Isoelectric or <1 mm elevation in limb lea • •
Slide 22: Important Normal ECG Intervals and Parameters cont’ T wave Inverted in aVR; upright in I, II, and V3 through V6. Variable in III, aVF, aVL, V1, and V2 Axis 0 degrees to +110 degrees age <40 −30 degrees to +90 degrees age >40 QT interval ST segment Isoelectric or <1 mm elevation in limb leads and <1 mm in precordial leads except for normal variant
Slide 23: Criteria for Low-Voltage QRS In all limb leads, the amplitude of the entire QRS complex (R + S) is <5 mm. In each of the precordial leads, the amplitude of the entire QRS complex (R+ S) is <10 mm Causes of Low-Voltage QRS Obesity Pericardial effusion Constrictive pericarditis Myxedema Amyloidosis and other restrictive cardiomyopathy and diffuse myocardial diseases Pleural effusion COPD
Slide 24: Step 1 Assess Rhythm first Rate
Slide 25: Step 2 Assess PR and QRS intervals for block Widening of the QRS duration RBBB LBBB
Slide 26: Step 3
Slide 27: Step 4
Slide 29: Step 6
Slide 30: Gothic Church
Slide 31: Step 7
Slide 32: Step 8
Slide 33: Step 9
Slide 34: Step 10
Slide 35: Hyperkalemia
Slide 36: Step 11
Slide 37: Dog Jimmy
Slide 38: Einthoven’s first ECG tracings
Slide 39: ECG Interpretation • Normal ECG • ECG within normal limits • Borderline ECG • Abnormal ECG
Slide 40: Exercise 1
Slide 41: Exercise 2
Slide 42: RBBB
Slide 43: Exercise 3
Slide 44: Exercise 4
Slide 45: LBBB
Slide 46: Exercise 5
Slide 47: Exercise 6
Slide 48: Exercise 7
Slide 49: Effect of Ligation of Coronary Artery
Slide 50: Cellular Mechanism of ECG Changes
Slide 52: T Wave peaking
Slide 53: T wave peaking cont’
Slide 54: Current of Injury
Slide 55: How Pathological Q formed?
Slide 57: Exercise 8
Slide 58: Exercise 9
Slide 59: Exercise 10
Slide 61: Exercise 11
Slide 62: Exercise 12
Slide 63: Exercise 13
Slide 64: Exercise 14
Slide 65: Normal variant: 1- to 2-mm ST segment elevation, mainly in leads V2 through V4, nonconvex, and with fishhook appearance. Common in African Americans: even 4-mm ST segment elevation Coronary artery spasm: ST returns to normal with nitroglycerin or with pain relief. LBBB: QRS >0.12 second and typical configuration Left ventricular aneurysm and known old infarct with old Q waves Chapter 6). Other Causes
Slide 66: Exercise 15
Slide 67: Exercise 16
Slide 68: Exercise 17
Slide 69: Exercise 18
Slide 70: Exercise 19
Slide 71: Causes of Poor R Wave Progression Improper lead placement. Late transition Anteroseptal or anteroapical MI LVH Severe chronic obstructive pulmonary disease, particularly emphysema HCM LBBB
Slide 72: Exercise 20
Slide 73: Exercise 21
Slide 74: Exercise 22
Slide 75: Exercise 23
Slide 76: Exercise 24
Slide 77: Exercise 25
Slide 79: Exercise 26
Slide 80: Exercise 27
Slide 81: Exercise 28
Slide 82: Torsades de point
Slide 83: Precipitating Factors of Torsades de point Antiarrhythmics known to increase the QT interval (e.g., quinidine, procainamide, amiodarone, disopyramide, sotalol) Tricyclic antidepressants and phenothiazines Histamine (H1) antagonists (e.g., astemizole, terfenadine) Antiviral and antifungal agents and antibiotics Hypokalemia, hypomagnesemia Insecticide poisoning
Slide 84: Precipitating Factors of Torsades de point Bradyarrhythmias Congenital long QT syndrome Subarachnoid hemorrhage Chloroquine, pentamidine Cocaine abuse
Slide 85: Subarachnoid Hemorrhage
Slide 86: Brugada syndrome
Slide 87: Electrical Alternans
Slide 88: Remember to always evaluate the ECG in the context of a patient’s symptoms. The presence of dynamic changes in the ECG should always be evaluated if possible.