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INTERNAL MEDICINE
CARDIOLOGY
ECG
Prepared by : Dr. Abdullahi Muktar Abdikadir
GROSS ANATOMY ELECTROCARDIOGRAM An ECG provides an assessment of the electrical activity of the heart. The heart rate, rhythm, axis, intervals, ischemia, and chamber enlargement can be evaluated ECG LEADS 1: Chest leads 2: Limb leads LIMB LEADS NORMAL ECG Rate Normal adult heart rate (HR) is 60–100 beats/min (bpm). HR <60 bpm is bradycardia. Heart rate >100 bpm is tachycardia. Common causes of sinus bradycardia are 1: physical fitness, sick sinus syndrome, drugs, vasovagal attacks, acute myocardial infarction (MI), and ↑ intracranial pressure. Common causes of sinus tachycardia are anxiety, anemia, pain, fever, sepsis, congestive heart failure (CHF), pulmonary embolism, hypovolemia, thyrotoxicosis, carbon dioxide (CO2) retention, and sympathomimetics. Rhythm Sinus rhythm: Normal rhythm that originates from the sinus node. It is characterized by a P wave (upright in leads II, III, and aVF; inverted in lead aVR) preceding every QRS complex and a QRS complex following every P wave. Sinus arrhythmia is a sinus rhythm originating from the sinoatrial (SA) node with cyclical beat-to- beat variation (>120 milliseconds [msec]) in the P- P interval and a constant P-R interval, which results in an irregular ventricular rate. It is common in young adults and is considered a normal variant. Axis The QRS axis represents the direction in which the mean QRS current flows. It can be determined by examining the QRS in leads I, II, and aVF Intervals PR interval: Normally 120 to 200 msec (3–5 small boxes). Prolonged = delayed atrioventricular (AV) conduction (eg, first-degree heart block). Short = fast AV conduction down accessory pathway (eg, Wolff-Parkinson-White [WPW] syndrome). QRS interval: Normally <120 msec. A normal Q wave is <40 msec wide and <2 mm deep. Ventricular conduction defects can cause a widened QRS complex (>120 msec) Left bundle-branch block (LBBB): Deep S wave and no R wave in V1 (“W” shaped); wide, tall and broad, or notched (“M”-shaped) R waves in I, V5, and V6 . A new LBBB is pathologic, and it may be suggestive of acute MI. However, this is not diagnostic in isolation. Rather, the Modified Sgarbossa Criteria (see key fact) should be used for the ECG diagnosis of acute MI in this situation (higher sensitivity and specificity). KEY FACT Smith-Modified Sgarbossa Criteria are used to diagnose MI in the presence of LBBB should be suspected in a patient with LBBB and the following ECG findings: Concordant ST elevation (STE) ≥1 mm in ≥1 lead Concordant ST depression ≥1 mm in ≥1 lead of V1– V3 Excessive discordant STE in ≥1 lead with ≥1 mm STE, where excessive discordance is defined as STE to the maximum QRS amplitude ratio ≥25% Right bundle-branch block (RBBB): RSR′ complex (“rabbit ears;” “M”-shaped); qR or R morphology with a wide R wave in V1; QRS pattern with a wide S wave in I, V5, and V6 QT interval: Normally QTc (the QT interval corrected for extremes in heart rate) is 380 to 440 msec (QTc = QT/√RR). QTc may be prolonged (QTc >440 msec) due to acquired causes, including electrolyte derangements (↓ K+, ↓ Ca2+, ↓ Mg2+) and medications (macrolides, fluroquinolones, opioids, ondansetron, Classes Ia [quinidine, procainamide] and III [sotalol, amiodarone] antiarrhythmic drugs). Congenital causes include long QT syndrome (LQTS), an underdiagnosed disorder that predisposes to ventricular tachyarrhythmias (eg, torsade de pointes) and sudden cardiac death (SCD, see later). Within hours, peaked T-waves and ST-segment changes (either depression or elevation). Within 24 hours, T-wave inversion and ST-segment resolution. Within a few days, pathologic Q waves (>40 msec or more than one-third of the QRS amplitude). Q waves usually persist, but may resolve in 10% of patients. Because of this, Q waves signify either acute or prior ischemic events. Non–Q-wave infarcts (also known as subendocardial infarcts) have ST and T changes without Q waves. In a normal ECG, R waves increase in size compared to the S wave between leads V1 and V5. Poor R-wave progression refers to abnormalities in this pattern (eg, reversed progression [R in V2 > V3], transition point beyond V4, R in V3 <3 mm) and can be a sign of new or prior anterior infarction, although it is not specific. Chamber Enlargement Atrial enlargement: Right atrial abnormality (P pulmonale): Generally, the right atrium (RA) depolarizes before the left. Right atrial enlargement (due to pulmonary hypertension [eg, chronic obstructive, pulmonary disease, tetralogy of Fallot, tricuspid atresia]) causes slowed conduction; therefore peak right atrial depolarization coincides with left. This results in increased P-wave amplitude (>2.5 mm in lead II). Left atrial abnormality (P mitrale): Left atrial enlargement causes prolonged left atrial (LA) depolarization, increased P-wave duration (>120 msec in lead II), and sometimes a V-shape occurs in P wave (also in lead II) . Also, the P wave in lead V1 may have a large negative deflection (>1 small square wide and 1 small square deep in a standard tracing). Commonly seen in isolation in mitral stenosis or associated with LV hypertrophy Amplitude of S in V1 + R in V5 or V6 is >35 mm. Alternative criteria: The amplitude of R in aVL + S in V3 is >28 mm in men or >20 mm in women. Usually associated with ST depression and T-wave changes. Causes include hypertension (most common), aortic stenosis/regurgitation, mitral regurgitation, coarctation of the aorta, and hypertrophic cardiomyopathy. Right ventricular hypertrophy (RVH): Right-axis deviation and an R wave in V1 >7 mm. Causes pulmonary hypertension, pulmonary embolism, chronic lung disease (cor pulmonale), mitral stenosis, and congenital heart disease (eg, tetralogy of Fallot, pulmonary stenosis). KEY FACT Axis deviation can be a sign of ventricular enlargement MNEMONIC “D ARMS PITS” Diastolic Murmurs Aortic Regurgitation Mitral Stenosis Pulmonary Insufficiency Tricuspid Stenosis END OF THE LECTURE