HOWTO READ ~|~ — dbbeibdd AN ECG ey U v — Ri NT CTSSTEP 1: Clinical history a——— Bunlorn page * Verify brief history * Compare tracing with old records (if available) * First look: “lay of the land” STEP 2: Technical quality and calibration 10mm =imv * Check technical quality oS tn= te * Check paper speed (25 mm/s ?) * Check calibration (10 mm/mV ?) STEP 3: Rate | Rate Slow Fast < 60 bpm aictonen > 100 bpm Bradycardia pm Tachycardia Sinus Rhythm * mostly regular * sinus arrhythmia AZ See * P wave - neg. inaVR - pos. in Il, Ill, aVF if P wave is not upright in lead II consider * arm lead reversal (P, QRS & T wave neg. in lead I) * dextrocardiaSTEP 4: Rhythm diagnosis * Rhythm regular or irregular? AFib (irregular), AFI (occasionally irregular), AV block (irregular with partial AV block) * P waves present or absent? * QRS narrow or wide? * rate P: rate QRS relation? (rate P = rate QRS, rate P > rate QRS, rate QRS > rate P) Rhythm regular / irregular Slow J Fast < 60 bpm P waves P waves > 100 bpm. Bradycardia present absent Tachycardia * Sinus brady- Normal * * Sinus tachy- cardia ¥ sinus * aluier _ cardia * Escape rhythm rhythm. Supraventric. * AV Block sachycarda * Ventricular MD,Sun Bunlorn page tachycardia STEP 5: Determine QRS axis in frontal plane Quick and easy way = 4 |eaui a i LAH :rS in Lead II and aVF and Lead III LPH : rS in Lead | and aVL Abbreviations: AFib: atrial fibrillation; AFI: atrial flutter; pos: positive; neg: negative; LAH: left anterior hemiblock; LPH: left posterior hemiblockSTEP 6A: Measurement of PR interval PR interval Cc PR interval Short PR Normal Prolonged PR <0.12s 0.12-0.20 s with preserved J AV conduction >0.20s *WPW T * Low atrial rhythm 7 7] * Upper AV Ne roped beats; junctional rhythm * Normal variant * Dropped beats * No AV conduction Sun Bunlorn page STEP 6B: Measurement of QRS complex: duration a QRS duration (QRSd) auation QRSd Normal QRsd QRSd wide <0.105 >0.10s and 0128 <0.12s ° t ¥ * i - * Sinus rhythm: Consider incom RBBB or LBBB plete BBB * No sinus rhythm: * Intraventricular ventricular conduction disorder rhythm or VTSTEP 6C: Measurement of QRS complex: voltage QRS voltage High QRS voltage Low QRS voltage SV1+RV6>35 mm Amplitude of all QRS com- Rinl>15mm plexes in limb leads < 5 mm R>aVL>11mm or < 10 mm in the precor- T dial leads 4 LVH * Pericardial effusion (triad T of low voltage, tachycardia, electrical alternans) Exclude: * Pleural effusion * Ventricular pacing (look for * Emphysema (COPD) pacemaker stimuli) * Pneumothorax * Hyperkalemia (if prolonged 4 Marked obesity QRS) ‘ Previous maseve MI i * Look for delta wave (WPW) myopathy. Mateo caldo: * Hypothyroidism The absence of LVH on ECG * Infiltrative myocardial disease means nothing, if present COPD: chronic obstructive pulmonary disease; LVH is likely. MI: myocardial infarction; LVH: left ventricular hypertrophy STEP 7A: Look at R wave progression in precordial leads Normal R wave vs Causes of slow R Progression saqeen eNO wave progression: * Anterior myocardial infarction * Incorrect lead placement (in obese women) * LVH, * LBBB, * WPW * Dextrocardia * Tension pneumothorax with mediastinal shift *C ital heart di LH: ett ventricular hypertrophy; LBBB: left bundle branch block; WPW: Wolff. Parkinson-WhiteSTEP 7B: Look at R wave progression in precordial leads Reversed R wave progression bf STEP 8: QT Interval QTc = corrected QT interval QTc (s) = QT interval (s) V RR interval (s) This describes abnormal R waves in lead V1 that pro- gressively decrease in amplitude if the QRS is narrow. This pattern may occur with a number of conditions, including RVH, posterior (or posterolateral) Ml, dextro- cardia (in concert with a limb lead reversal pattern), mis- placed leads and rarely as a normal variant. If the QRS. is wide, a dominant R wave in V1 may be caused by RBBB or WPW. MI: myocardial infarction; RBBB: right bundle branch block; WPW: Wollf-Parkinson-White syndrome; RVH: right ventricular hypertrophy; RR interval Normal QTc < 440 ms slightly larger values are acceptable in women MD,Sun Bunlorn page Short QTc < 330 ms Increased risk of Causes AF & VF * Congenital (requires family history) * Acquired - drug toxicity - electrolyte imbalance Long QTc = 460 ms t Abbreviatic if OTe 20 ome & EAD = early aterdepolarization TAP (after short-long-| f= atnaltoivaton short sequence) VF = ventricular fibrillation The QT interval is a measure of ventricular action potential duration. It decreases when the heart rate increases. _STEP 9: U wave * small deflection (0.5 mm), immediately following the T wave * usually same polarity as T wave * possibly orainating rom Purkinje network * best seen in lead V2 and V3 and during slow rate Normal u Prominent U wave \ A Hypokalemia Inverted U wave * Myocardial ischemia * LV volume overload STEP 10: P wave -P waves are best seen in lead II and V1 P wave Normal P wave * lead || < 0.12 s and < 2.5mm * lead V1 biphasic P wave too wide Lead Il 2 0.12 s & notched Prominent negative ter- minal forces in lead V1 P wave too tall P peaked in lead Il P > 2.5 mm in inferior leads P > 1.5 mm in lead V1 P wave negative in inferior leads (II, Ill, AVF) Retrograde P wave ? Ectopic beat ? pa Ectopic beat ? P wave funnySTEP 11: T wave Normal T wave * T wave same polarity as main QRS deflection *T wave is upright in |, Il, V3 to V6 *T wave always inverted in aVR T wave inversion in V1 to V3 * Common finding in children and adolescents * Infrequently found in healthy adults Is not associated with adverse outcome if T waves are normal in other leads * Hyperacute T wave High amplitude - may be seen 5-30 min after T waves onset of MI - broad-based T wave - round summit | |, [V3] * Hyperkalemia (best seen in precordial leads) - narrow-based T wave - tenting of T wave MD,Sun Bunlorn page Abnormal T waves Inverted Biphasic. Flatten T waves T waves T waves Camel hump T waves Severe Hidden P waves hypokalemia embedded in T wave prominent U wave - sinus tachycardia fused to end of the - various types of heart block T waveSTEP 12: ST segment *The typical ST segment duration is usually around 0.08 s (80 ms). * Usually flat and isoelectric and should essentially level with PR and TP segments. “The ventricles remain depolari- zed during the ST segment. * It is usually difficult to determine exactly where the ST segment ends and the T wave begins. Therefore the relationship between ST segment and T wave should be evaluated together. The most important cause of ST segme! abnormality (elevation or depression) is myocardial ischemia or infarction. QRS complex at segnrent T wave Pe cconaNenses > \Junction. or “J” point oy > Action Doten- ial repola- rization depola- rization nt The diagnosis of AMI and severe ischemia depend on the ~ careful assessment of the ST segment. - AMI: acute myocardial infarction ST segment depression ST segment elevation * Ischemia (most common) * Subendocardial infarction * Reciprocal changes asso- ciated with AMI * Drug effects digitalis ischemia effects or early MI | Scooping of the ST segment * AMI (convex ST segment elevation) * Transmural ischemia * Ventricular aneurysm (ST ele- vation does not subside after * Pericarditis AMI pericarditis Abbreviations MI: myocardial infarction AMI: acute myocardial infarctionSTEP 13: ST elevation MI (STEMI) ECG diagnosis of STEMI * Limb leads: ST segment elevation = 1 mm (0.1 mV) * Precordial leads: ST segment elevation = 2 mm (0.2 mV) * Elevations must be present in anatomically contiguous leads Inferior Lateral Septal Anterior Il, Ill, aVF | 1,aVL,V5,V6} V1, v2 V3, V4 * An approximation of the infarction size can be assessed from the extent of ST elevation. * Of note: Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. Look for reciprocal changes of ST depression in leads opposite the area undergoing injury For example in acute transmural inferior ischemia, the direction of the ST vector faces the injured area (resulting in a ST elevation in leads Il, Ill, aVF) while the tail of the ST vec- tor faces anatomically opposite sites where it causes ST segment depres- sion (lead aVL and lead |). The significance of these reciprocal changes or mirror-images is unclear but they are useful diagnostically by providing confirmatory evidence for the diagnosis of STEMI. Mirror-image changes do not occur in pericarditis An acute STEMI can present with upwardly concave ST elevation, so the mere fact that ST elevation is upwardly concave does NOT mean that a condition other than ischemia is present.ST elevation due to ischemia or infarction: Focus on contiguous leads and those showing reciprocal changes! One must be well versed in recognizing the so-called ECG mimics of acute myocardial infarction. The development of reciprocal changes during STEMI helps the differentiation from the listed conditions: ECG mimics of AMI: * Left ventricular hypertrophy (LVE) * Left bundle branch block ( * Paced rhythm BB) * Early repolarization * Pericarditis * Hyperkalemia * Ventricular aneurysm Paced Ventricular Rhythm aneurysm 3 S+R>35mm Evolution of STEMI MD,Sun Buniorn page Sometimes the earliest presentation of AMI is the hyperacute T wave, which is treated the same as ST elevation. In prac- tice this is rarely seen Pathologic Q waves may appear within hours or may take more than 24 hr. The T wave will generally become inver- ted in the first 24 hr, as ST elevation begins to resolve Note : Tong-term changes In the first few hours the ST segments usually begin to rise Long-term changes of EGG include persistent Q waves (in 90% of cases) and persistent inverted T waves ays Persistent ST elevation is rare except in the presence of a ventricular aneurysm Abbreviation: AMI: acute myocardial infarctionHOW TO READ AN 6 STEP 14: Non-ST elevation MI (NSTEMI) * The ECG sign of non-STEMI is ST segment depression *ST segment depression seen in subendocardial ischemia or infarction can take on different patterns. The most typical is a horizontal or downsloping depression (A, B, C). Upsloping ST depression (D) is less specific. de Ha Hal * Upsloping depression of less than 1 mm at 80 ms beyond the J point (E) is simply J point depression and not ST segment depression. newhat vague bu n¢ it's notin * Depression is reversible if ischemia is only transient but depression persists if ischemia is severe enough to produce infarction. * T wave inversion with or without ST segment depression is sometimes seen but not ST segment elevation or new Q waves. * The nonspecific ST-T wave changes should be evaluated with old ECGs because myocardial ischemia is not a static process. GUIDELINES 1. ST Elevation New ST elevation at the J point in 2 contiguous leads with the following cut-points: Age and gender specific ! * 20.1 mV in all leads except leads V2-V3 in men and women * in leads V2-V3: = 0.2 mV in men 2 40 years and 2 0.25 mV in men < 40 years * in leads V2-V3; 2 0.15 mV in women 2. ST Depression and T wave changes * New horizontal or down-sloping ST segment depression 2 0.05 mV in 2 contiguous leads * and/or T wave inversion 2 0.1 mV in 2 contiguous leads with prominent R wave or R/S ratio > 1STEP 15: Additional information * In the chronic phase of myocardial infarction, Q waves are regarded as a sign of irreversible necrosis. ° However, about 50% of patients presenting within 1 hour of onset of ST elevation acute coronary syndrome already have Q waves in the leads with ST elevation, especially in the anterior leads. ° These Q waves may be transient and not necessarily represent irreversible damage. ° They may represent transient loss of electrical activity in the region at risk (“myocardial concussion”). “Thus, Q waves on presentation may reflect either irreversible damage and/or a large ischemic zone. * Request right-sided leads for the diagnosis of right ventricular (RV) myocardial infarction (MI) if ECGs show acute inferior MI, anterio- lateral and posterior MI. *The 12-lead ECG may suggest RV MI if the magnitude of ST elevation in V1 > the magnitude of ST elevation in V2. “The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI. * In the acute phase of myocardial infarction, ST elevation is the key to the diagnosis and therapy. * The presence of Q waves is far less important for diagnosis and treatment. Indeed, the early diagnosis does not depend on Q waves. * Any Q wave in leads V2-V3 > 0.02 s (20 ms) or QS complex or *Q wave = 0.03 s (30 ms) and = 0.1 mV deep or QS complex in leads I, II, aVL, aVF or in V4-V6 or in any 2 contiguous lead grouping (I, aVL, V1-V6, Il, Ill, aVF) or * R wave 2 0.04 s (40ms) in V1-V2 and R/S = 1 with concordant positive T wave (in absence of conduction defect) Abbreviations: LVH: left ventricular hypertrophy; LBBB: leit bundle branch block MI: myocardial infarctionSTEP 16: Early repolarization Early repolarization (ER) is defined as J point elevation with the terminal QRS showing either: * notching (a positive deflection on terminal QRS complex) or * slurring (on the downslope portion of the QRS complex) | i | | [-] Various patterns of early repo- larization The changes tend to disappear with tachycardia. MD,Sun Bunlorn page Early repolarization has recently been subject to much research because of the association of sudden death and malignant arrhythmias in patients with cer- tain specific ECG features. The common form of early repolarization with a high ST take-off in the right precordial leads is considered benign and common, especially in athletes. | | | * There is a typical concave upward ST segment ele- vation (1-4 mm), prominent symmetrical T waves and absence of reciprocal ST depression. * These features are present in at least two conti-guous leads. * It is generally a benign entity commonly seen in young men. The characteristics of ER may persist for many years. It is important to discern ER from ST segment elevation due to other causes such as ischemia. Cardiac ischemia is a dynamic process with a changing ECG while | the ECG of ER generally remains stable. A changing ECG favors ischemia.Inferolateral Early Repolarization (ER) Inferolateral ER is characterized by a deflection in the R wave descent (slurred pattern) or a positive deflection with a secondary “r’ (notching pattern) in the terminal part of the QRS complex in at least two inferior leads (Il, Ill, AVF), in two lateral leads (1, aVL, V4 to V6) or in both. * A pattern of > 0.2 mV in two inferior (II, Ill, aVF) leads has been shown to impart a higher risk of malignant arrhythmia and sudden death. * Early repolarization > 1 mV of horizontal or des- cending ST segment also carries a higher risk of sudden death. * The management of asymptomatic patients with ‘Atter Juntiila Md et al. high risk ECG forms of early repolarization is un- European Heart Journal resolved. 2012; 3 : 2639 A Smiley face with concave ST segment elevation is showing a happy face because a concave form may be benign as in early repolarization. Convex ST elevation superimposed on a face as before, produces a frowny sad face because of the poor prognosis (because of acute myocardial infarction).STEP 17: Congestive heart failure As congestive heart failure (CHF) is the outcome of many pathophysiologic disorders, the ECG may show a large variety of abnormalities. Occasionally the ECG is normal. However, CHF is unlikely if the ECG is entirely normal. In other words, a normal ECG does not rule out CHF. The ECG abnormalities in CHF may be seen in many disorders. They consist of left ventricular hypertrophy, atrial and ventricular arrhythmias, atrioventricular and intraventricular conduction abnormalities, evidence of myocardial ischemia and infarction, right ventricular hypertrophy and atrial abnormalities. No specific ECG feature is indicative of heart failure Teme Atrial fibrillation is present in 25% of patients with cardiomyopathy, especial- ly elderly patients with severe heart failure. The prognosis is worse for pa- tients with atrial fibrillation, ventricular tachycardia, or left bundle branch block. The presence of left bundle branch block with right axis deviation almost always indicates the presence of cardiomyopathy. Heart failure pa- tients with implanted cardiac devices may show a paced rhythm with no diagnostic features of left ventricular function. A prominent negative component of the P wave in lead V1 reflects elevated left ventricular end-diastolic pressure. The negativity may subside with the relatively early improvement of heart failure. In CHF, peripheral edema may be associated with a decrease in amplitude (voltage) and duration of the QRS complex and the QT interval. These changes may hide important underlying abnormalities such as bundle branch block. The QRS and QT interval return to their baseline values when peripheral edema has subsided. The QRS abnormalities correlate with weight gain (peripheral edema). The mechanism of the attenuation of the ECG amplitude with peripheral edema is based on an increase in the electrical conductivity (i.e. decrease of resistivity) resulting in decrease of ECG voltage as per Ohm's law. Thus, QRS and even P wave changes (in V1) can be used in the follow-up of heart failure therapy.During congestive heart failure with peripheral edema there is shortening of the QRS and QT interval. The ECG triad suggestive of CHF is characterized by low voltage in the limb leads, and high voltage in the precordial leads, and an R/S ratio < 1 in lead V4. There is a modest sensitivity and good specificity. The absence of the ECG triad does not exclude heart failure ! ECG triad of congestive heart fallure * Relatively low QRS voltage in all six limb leads (< 0.8 mV) * High QRS voltage in precordial leads (S in V1 or S in V2 and R in V5 or R in V6 > 3.5 mV) * Poor R wave progression with R/S ratio < 1 in lead V4 aVR v1 u aVL v2 "9 | | VI a ml aVF V3, 4| | —— \—_——- ECG showing atrial fibrillation and the typical features of the congestive heart failure triad. oarActivation of the Activation of the Recovery wave ventricles‘QRS Complex T Wave Activation of the Recovery wave: ventriclesHold your finger on the crown.