Standardization & Interpretation of ECG Dr Frijo Jose A

Normal QRS Duration ↑with ↑ heart size Wider - precordial > limb leads Age- and gender-dependent Children <4 yrs -QRS ≥90 ms prolonged 4 -16 yrs –QRS ≥ 100 ms prolonged Adult males – N-QRS up to 110 ms J. Am. Coll. Cardiol. 2009;53;976-981;

Mean Frontal Plane Axis J. Am. Coll. Cardiol. 2009;53;976-981;

Shifts to the left with increasing age

Complete RBBB QRS ≥120 ms (>16 yrs), >100 ms (4-16 yrs), >90 ms (<4 yrs) rsr’, rsR’, or Rsr’ - V1 or V2. R’/r’ - Usually wider >R S duration > R or >40 ms (I&V6) Normal R peak time (V5 & V6) but >50 ms (V1) First 3 should be present to make ∆ V1- pure dominant R wave ± notch → Criterion 4 should be satisfied J. Am. Coll. Cardiol. 2009;53;976-981;

Incomplete RBBB QRS duration 110 -120 ms (adults), 90 - 100 ms (8 -16 yrs), 86 - 90 ms (<8 yrs) Other criteria - Same as for complete RBBB. J. Am. Coll. Cardiol. 2009;53;976-981;

Complete LBBB 1. QRS ≥120 ms (Adults),>100 ms (4-16), >90 ms ( <4) 2. Broad notched /slurred R wave - I, aVL, V5, V6 3. Absent q waves - I, V5, V6 (±q Avl) 4. R peak time > 60 ms in V5 & V6 but N in V1, V2,& V3 (when r+) 5. ST & T - Usually opposite in direction to QRS 6. + T wave with upright QRS may be N (+ concordance) 7. ↓ST and/or −T with −QRS (- concordance) -ABN but in Avl, a narrow q may be present in the absence of myocardial pathology.. 8. LBBB may change mean frontal QRS axis to Rt, to Lt, or to suprior, in some cases in a rate-dependent manner J. Am. Coll. Cardiol. 2009;53;976-981;

ST↑≥0.1 mV in leads with +QRS (concordant ST) Criteria for infarction in the presence of complete left bundle-branch block(GUSTO) ST↑≥0.1 mV in leads with +QRS (concordant ST) ST ↑≥ 0.5 mV in leads with −QRS (discordant ST) ST ↓≥ 0.1 mV in V1-V3 (concordant ST) Concordant ST changes -↑specificity but ↓ sensitivity Discordant ST changes - ↓↓ specificity ↓↓ sensitivity LBBB + concordant ST > 30-d mortality > LBBB + enzyme -- concordant ST changes J. Am. Coll. Cardiol. 2009;53;976-981;

Incomplete LBBB 1. QRS 110 -120ms (adults),90 - 100ms(8 -16), 80 - 90ms (<8) 2. Presence of LVH pattern 3. R peak time >60 ms in leads V4, V5, and V6 4. Absent q in I, V5, V6 J. Am. Coll. Cardiol. 2009;53;976-981;

Nonspecific/Unspecified Intraventricular Conduction Disturbance QRS >110ms (adults), >90ms (8 -16), >80ms (<8) without criteria for RBBB or LBBB Also RBBB criteria in precordial leads and LBBB criteria in limb leads, and vice versa J. Am. Coll. Cardiol. 2009;53;976-981;

Left Anterior Fascicular Block 1. Frontal plane axis -45°to -90° 2. qR pattern in aVL 3. R-peak time in aVL of ≥45 ms 4. QRS duration <120 ms These criteria do not apply to patients with CHD in whom LAD is present in infancy J. Am. Coll. Cardiol. 2009;53;976-981;

Left Posterior Fascicular Block 1. Frontal plane axis +90°to 180° (adults) 2. rS pattern in I and aVL 3. qR pattern in III and aVF 4. QRS <120 ms J. Am. Coll. Cardiol. 2009;53;976-981;

Preexcitation of WPW Type Whether preexcitation is full or not cannot be determined from surface ECG, but following criteria are suggestive of full preexcitation: 1. PR interval <120 ms during SR (adults) and <90 ms (children) 2. Delta wave 3. QRS >120 ms (adults) and > 90 ms (children) 4. Secondary ST and T wave changes J. Am. Coll. Cardiol. 2009;53;976-981;

Terms Not Recommended Mahaim-type preexcitation -because ∆ cannot be made with certainty with surface ECG Atypical LBBB, bilateral bundle-branch block, bifascicular block, and trifascicular block -because of great variation in anatomy and pathology producing such patterns Recommends that each conduction defect be described separately in terms of the structure or structures involved J. Am. Coll. Cardiol. 2009;53;976-981;

Peri-infarction block abnormal Q wave generated by a MI in Inf/lat leads, terminal portion of QRS- wide and directed opposite to Q wave (i.e., a QR complex in the inferior or lateral leads) J. Am. Coll. Cardiol. 2009;53;976-981;

A 59-year-old man with anterolateral pen-infarction block presented a history of myocardial infarction in January, 1965 and was hospitalized five months later with symptoms of left ventricular failure. The electrocardiogram demonstrates old anterior infarction. While the initial 0.04-second QRS vector points inferiorly and posteriorly, the terminal forces point superiorly. Slurring and notching in the early portion of the QRS complex in various leads are to be noted

Peri-ischemic block transient ↑ in QRS duration accompanies the ST-segment deviation seen with acute injury J. Am. Coll. Cardiol. 2009;53;976-981;

Primary Repolarization Abnormalities Abn in ST & T, without changes in depolarization Localized or diffuse ischemia, myocarditis, drugs, toxins, electrolyte abn-esp Ca & K Abrupt HR change, hyperventilation, body position, catecholamines, sympath stimulation or ablation of stellate ganglion, temp changes J. Am. Coll. Cardiol. 2009;53;976-981;

Secondary Repolarization Abnormalities Abn in ST & T →direct result of changes in sequence and/or duration of ventri depolarization manifested as changes in QRS shape and/or duration due to voltage gradients that are normally largely cancelled but become manifest when the changes in the sequence of depolarization alter the repolarization sequence BBBs, preexcitation, ectopics, paced V- complexes Primary and secondary repolarization abnormalities may occur concurrently. For example, ventricular hypertrophy is associated with changes in the shape and duration of the ventricular action potential of isolated ventricular cells, particularly on the endocardial surface (13). These changes may contribute to ST- and T-wave changes and are independent of the changes that are secondary to QRS-amplitude changes and prolongation of the QRS complex. A combination of primary and secondary repolarization abnormalities should also be considered when T-wave polarity does not change as anticipated by the changes in the QRS complex J. Am. Coll. Cardiol. 2009;53;976-981;

Displacement of ST usually measured at “J point,” and, in exercise testing 80 ms after the J point J. Am. Coll. Cardiol. 2009;53;976-981;

T-Wave Abnormalities T wave in I, II, aVL, and V2 - V6 Inverted −0.1 to − 0.5 Mv Deep negative − 0.5 to − 1.0 mV Giant negative <− 1.0 Mv Low -amplitude <10% of R-wave in same lead Flat - +0.1 to − 0.1 mV in leads I, II, aVL (with an R wave taller than 0.3 mV), and V4 to V6 J. Am. Coll. Cardiol. 2009;53;976-981;

Classification as slight or indeterminate T-wave abnormality Virtually impossible to develop a cause-specific classification for minor T-wave abn Classification as slight or indeterminate T-wave abnormality Overreader -analysis other features clinical condition prior ECGs J. Am. Coll. Cardiol. 2009;53;976-981;

T-Wave Alternans T-wave amplitude variations that alternate every 2nd beat Typically microvolt T-wave alternans rarely,more pronounced Latent instability of repolarization predictive of malign arrhythmias Generally not present at the resting state even in high-risk patients Stress test, requiring special equipment & analysis software- needed to provoke it J. Am. Coll. Cardiol. 2009;53;976-981;

The U Wave The U wave is a mechanoelectric pheno Frequently absent in limb leads & is most evident in V2 & V3 (0.33 mv or 11% of T wave) HR dependent Rarely present at rates >95 bpm Bradycardia enhances U-wave amplitude & present in 90% at HR< 65 bpm J. Am. Coll. Cardiol. 2009;53;976-981;

More recent information ↑ in U, usually in asso with ↓ST & a ↓in T-wave, may be due to quinidine-like effects & ↓K+ and that with more ↑ hypokalemia (<2.7), U may >T in same lead More recent information may be due to fusion of U with T rather than to an ↑U. Fusion of U with T also occurs in asso with an ↑ in sympath tone & in presence of a markedly ↑ QT as in LQTS ↓U(V2 - V5)→ abn(a/c ischemia/hypertension) J. Am. Coll. Cardiol. 2009;53;976-981;

The QT Interval QRS onset to end of T wave Onset of QRS -occur up to 20 ms earlier in V2, V3 than limb leads Some regard differences 50 ms up to 65 ms in QT measured in various leads being normal This value is reported to be less in women than in men J. Am. Coll. Cardiol. 2009;53;976-981;

If T & U are superimposed/cannot be separated→ When QT is measured in individual leads, lead showing ↑QT should be used (usually V2/V3) If T & U are superimposed/cannot be separated→ QT be measured in leads not showing U (aVR and aVL) or Downslope of T be extended by drawing a tangent to the steepest proportion of downslope until it crosses TP segment Might underestimate the QT interval J. Am. Coll. Cardiol. 2009;53;976-981;

QT Correction for Rate Linear regression functions rather than Bazett’s formula be used for QT-rate correction and method used for rate correction be identified in ECG analysis reports Rate correction of QT interval should not be attempted when RR interval variability is large, as with AF, or when identification of the end of the T wave is unreliable Relation between QT intervals and heart rates from 40 to 120 beats/min in rest electrocardiograms of men and a simple method to adjust QT interval values J Karjalainen, M Viitasalo, M Manttari, andV ManninenCentral Military Hospital, Helsinki, Finland. OBJECTIVES. The aim of this study was to establish the relation between QT intervals and a wide range of rest heart rates in men. These data provided the basis of a simple method for adjusting the QT interval for heart rate. BACKGROUND. Earlier correction equations give conflicting results, especially at low and high heart rates. METHODS. The QT intervals were measured in 324 electrocardiograms of healthy young men. The sample was weighted for low and high heart rates. A curve relating QT intervals and heart rates from 40 to 120 beats/min was constructed. The QT interval at 60 beats/min was used as the reference value, and an adjusting nomogram for different heart rates was created. The reliabilities of the nomogram and three earlier QT correction equations were tested in the study group and in 396 middle-aged men. RESULTS. The nomogram method presented (QTNc = QT + correcting number) adjusted the QT interval most accurately over the whole range of heart rates on the basis of smallest mean-squared residual values between measured and predicted QT intervals. The Fridericia formula (QTFc = QT/RR1/3) gave the best correction at low, but failed at high, heart rates. The linear regression equation (QTLc = QT + 0.154[1 - RR], Framingham Study) was reliable at normal, but failed at low and high, heart rates. The Bazett formula (QTc = QT/RR1/2) performed poorest at all heart rates. The relation between QT and RR intervals was determined by three linear regressions expressing the slopes 0.116 for heart rates < 60 beats/min, 0.156 for heart rates from 60 to 100 beats/min and 0.384 for heart rates > 100 beats/min. CONCLUSIONS. The QT-RR relation over a wide range of heart rates does not permit the use of one simple adjustment equation. A nomogram providing, for every heart rate, the number of milliseconds that the QT interval must be corrected gives excellent adjustment.  J. Am. Coll. Cardiol. 2009;53;976-981;

Prolonged QT: women ≥460 ms; men ≥450 ms Short QT (women & men) ≤390 ms In ventricular conduction defects- JT interval (QT duration– QRS duration) QT dispersion not be included in routine ECG reports J. Am. Coll. Cardiol. 2009;53;976-981;

Threshold Values for ST-Segment Changes For men ≥40 - abn J-point ↑ → 0.2 mV in V2 & V3 and 0.1 mV in others For men <40 - abn J-point ↑ → 0.25 mV in V2 & V3 For women - abn J-point ↑ → 0.15 mV in V2 & V3 and 0.1 mV in others For men & women - abn J-point ↑ → 0.05 mV in V3R & V4R, except for males <30 →0.1 For men & women - abn J-point ↑ → 0.05 mV in V7-V9 For men & women of all ages - abn J-point ↓ → 0.05 mV in V2 & V3 and 0.1 mV in all others J. Am. Coll. Cardiol. 2009;53;976-981;

Criteria for Acute Myocardial Infarction Any one of the following criteria • Detection of ↑and/or ↓ of markers (trop) with at least 1 value above 99th percentile of URL + evidence of myo ischaemia with at least 1 of the following: • Symptoms of ischaemia; • ECG changes indicative of new ischaemia (new ST-T changes or new LBBB) • Development of pathological Q waves in ECG • Imaging evidence of new loss of viable myo or new RWMA J. Am. Coll. Cardiol. 2007;50;2173-2195

• Sudden, unexpected cardiac death, involving cardiac arrest, often with symptoms suggestive of myo isch, and accompanied by new ST ↑ or new LBBB, and/or evidence of fresh thrombus by CAG and/or at autopsy, but death occurring at a time before appearance of cardiac biomarkers J. Am. Coll. Cardiol. 2007;50;2173-2195

• Patho findings of an a/c MI • For PCI in pts with N baseline trop, ↑of markers >99th percentile URL - peri-procedural M necrosis . By convention, ↑ of markers >3×99th percentile URL - PCI-related MI • For CABG in pts with N baseline trop, ↑ of markers >99th percentile URL - peri-procedural M necrosis. By convention, ↑ of markers >5×99th percentile URL plus either new path Q waves or new LBBB, or angiographically documented new graft or native CA occlusion, or imaging evidence of new loss of viable myocardium - CABG-related MI • Patho findings of an a/c MI J. Am. Coll. Cardiol. 2007;50;2173-2195

Criteria for Prior Myocardial Infarction Any one of the following criteria : • New patho Q waves ± symptoms • Imaging evidence of a region of loss of viable myo that is thinned & fails to contract, in absence of a non-ischaemic cause • Patho findings of a healed/healing MI J. Am. Coll. Cardiol. 2007;50;2173-2195

J. Am. Coll. Cardiol. 2007;50;2173-2195

J. Am. Coll. Cardiol. 2007;50;2173-2195