Standardization & Interpretation of ECG Dr Frijo Jose A.

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Standardization & Interpretation of ECG Dr Frijo Jose A

Transcript of Standardization & Interpretation of ECG Dr Frijo Jose A.

Page 1: Standardization & Interpretation of ECG Dr Frijo Jose A.

Standardization & Interpretation of ECG

Dr Frijo Jose A

Page 2: 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

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Mean Frontal Plane Axis

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Shifts to the left with increasing age

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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 ∆o V1- pure dominant R wave ± notch → Criterion 4

should be satisfied• J. Am. Coll. Cardiol. 2009;53;976-981;

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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.

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Complete LBBB

1. QRS ≥120 ms (Adults),>100 ms (4-16), >90 ms ( <4)2. Broad notched /slurred R wave - I, aVL, V5, V63. 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 QRS6. + T wave with upright QRS may be N (+ concordance)7. ↓ST and/or −T with −QRS (- concordance) -ABN

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Criteria for infarction in the presence of completeleft 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;

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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

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Nonspecific/UnspecifiedIntraventricular 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

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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

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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

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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

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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

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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)

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Peri-ischemic block

• transient ↑ in QRS duration accompanies the ST-segment deviation seen with acute injury

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Primary Repolarization Abnormalities

Abn in ST & T, without changes in depolarizationLocalized 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

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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

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Displacement of ST• usually measured at “J point,” and, in exercise

testing 80 ms after the J point

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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 MvLow -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

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• 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

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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;

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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

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• ↑ 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)

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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

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• 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

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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

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• 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

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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;

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

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• 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

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• 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

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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

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