MS3 ECG Workshop Diagnostic Pearls

J.B. Esterson, MD

Ischemic ECG ChangesBoth of these can progress to MI

ST Depression (subendocardial injury):same as seen in Non-STEMI, but markers neg.

Symmetric T Inversion (transmural ischemia): i N STEMI b ksame as seen in Non-STEMI, but markers neg.

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ECG Presentations of A t C E tAcute Coronary Events

Acute IschemiaAcute Ischemia ST depressions (1 mm) or T inversions (2 mm) Biomarkers negativeg Prolonged = Unstable Angina

Acute Infarction ST Elevation MI (Q, Transmural)

Biomarkers may be positive Biomarkers may be negative if early (Injury)

Non-ST Elevation MI (Non-Q, Non-transmural) ST depressions (1 mm) or T inversions (2 mm) p ( ) ( ) Biomarkers positive

Stress-induced Ischemia(adapted from Thaler 1999)(adapted from Thaler, 1999)

AA

B

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EarlyEarly RepolarizationRepolarizationEarly Early RepolarizationRepolarization

J point and ST J point and ST nn ConcaveConcave upwardsupwards Most commonly Most commonly V 2V 2--44 No reciprocalNo reciprocal ST ST pp

AssociatedAssociated AssociatedAssociated J point slurring J point slurring oror notchingnotching Tall TTall T waveswaves Tall TTall T waveswaves No serial change; with exercise, ageNo serial change; with exercise, age

Usually HealthyUsually Healthy, no , no SxSx , male > female, young, athlete, male > female, young, athletey yy y y gy g Some evidence: Some evidence: sudden death Inferiorsudden death Inferior and ? and ? LateralLateral leadsleads

DDxDDx -- subepicardialsubepicardial injury (STEMI), injury (STEMI), pericarditispericarditispp j y ( ),j y ( ), pp

ST n: Pericarditis vs. MIST elevations allST elevations all leads (except aVR and isoelectricand isoelectric leads)

ST elevations regionalregional

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Right Bundle Branch BlockRight Bundle Branch Block(from Huszar, Basic Dysrhythmias, 1994)

Right Bundle Branch Block: Criteria

QRS prolongation t .12 sec Incomplete if < .12 sec.

Secondary R wave (R') in right precordial leads (especially V1) R' wave is wider and taller than the R wave

Wide S wave in lateral leads (I, aVL, V5-6)

Secondary ST-T changes (opposite direction)

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Left Bundle Branch BlockLeft Bundle Branch Block (from Huszar, Basic Dysrhythmias, 1994)

Left Bundle Branch Block: Criteria

QRS prolongation t .12 secp g

Absent Q wave lateral leads (I, V5-6)Absent Q wave lateral leads (I, V5 6)

Broad R wave I V5-6 Broad R wave I, V5-6 Usually slurred and notched

Secondary ST-T changes (opposite direction)

LAD common

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Injury - ECG Changesj y g

ST Elevation (transmural injury)

Not always truly transmural

Usually progresses to ST Elevation MI With elevated markers and pathologic Q With elevated markers and pathologic Q

Rarely can present as rest Variant Angina Rarely can present as rest Variant Angina (Prinzmetals Angina) without MI

Evolution of STEMI

Path. QPath. QT p

T upright

ST l

T pL ST n

Tall T ST nST normalLess ST n

Path. Q

Hyperacute Injury / Acute Evolving Old

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Left Ventricular HypertrophyLeft Ventricular Hypertrophy(adapted from Lilly, Pathophysiology of Heart Disease, 1998)

Left Ventricular Hypertrophy (LVH)

Increased QRS voltage (chest & limb leads best)

Secondary ST-T changes (Strain) commonSecondary ST T changes ( Strain ) common in left sided leads

b l l f i d i i ( ) Abnormal left axis deviation (LAD) Left atrial enlargement (LAE)Left atrial enlargement (LAE) QRS slight prolongation (up to .12)

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Right Ventricular HypertrophyRight Ventricular Hypertrophy(adapted from Lilly, Pathophysiology of Heart Disease, 1998

Typical RVH PatternTypical RVH Pattern(RV mass approaches LV mass)

Right axis deviation (usually > 110 q)Right axis deviation (usually > 110 ) RS ratio V1 > 1 (usually tall R) often qR Deep S waves left precordial leads Slight prolongation QRS duration (up to 12) Slight prolongation QRS duration (up to .12) Secondary ST-T changes (Strain) common

in right sided leads Occasional RAE (right atrial enlargement)Occasional RAE (right atrial enlargement)

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Hyperkalemiayp

T k d ll d 5 5

ECG Effect K+ Level T wave peaked, tall, and narrow > 5.5

QRS prolongation (T will widen) > 6.5

P wave p amplitude, n duration > 7.0

P-R interval n > 7.0

P wave disappears > 8.8

QRS sine wave (can occur earlier) > 8.8

Hyperkalemia (Lead II) Progression

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Atrial FibrillationAtrial FibrillationAtrial FibrillationAtrial Fibrillation

Atrial FibrillationAtrial FibrillationAtrial FibrillationAtrial Fibrillation

No definite P shape can be determined Atrial impulses very rapid and irregular, 400-700 bpm Fibrillatory waves coarse or fine

Ventricular response Always irregularly irregular (unless complete AV block)y g y g ( p ) Rate: untreated usually 100-180 QRS shape normal

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Atrial FlutterAtrial Flutter

BlockBlock

Atrial FlutterAtrial Flutter F (flutter) waves

Atrial FlutterAtrial Flutter( )

Shape: Saw tooth (undulating baseline) Rate: 250 350 bpm

QRS Shape: normal Rate: < F rate, may have variable block New onset usually 2:1 block (HR 150)

If 1:1 conduction, suspect WPW!

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Premature Ventricular Complexes Wide and different from sinus QRS

d d b Not preceded by premature P Morphology

Uniform Multiform

ST-T different from sinus Significance clinical setting

Ventricular Tachycardia 3 or more consecutive PVCs Abrupt onset and terminationAbrupt onset and termination Rate 140-200 QRS > 14 different from sinus QRS > .14, different from sinus Not preceded by P wave AV dissociation common AV dissociation common Differentiate from supraventricular

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2nd Degree AV Block Type I2nd Degree AV Block Type I(from Scheidt, 1983)

Second Degree AV Block, Type I

AV nodal site of blockAV nodal site of block Progressive PR n followed by non-conducted P

G d b i Grouped beating QRS usually narrow Transient. reversible

Excessive vagal toneg AV node ischemia / blocking drugs

Usually benign prognosisUsually benign prognosis Rarely progresses to 3rd degree AV block

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2nd Degree AV Block Type II2nd Degree AV Block Type II

Second Degree AV Block Type IIg yp

PR constant followed by non-conducted PPR constant followed by non conducted P Grouped beating

QRS ll id Hi P ki j QRS usually wide: His-Purkinje system Extensive disease Bi / Trifascicular block Progression to complete AV blockProgression to complete AV block

Slow escape ventricular rhythm Syncope / sudden death - pacemaker Syncope / sudden death - pacemaker

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Thi d D (C l t ) H t Bl kThird Degree (Complete) Heart Block

3rd Degree or Complete AV Block3rd Degree or Complete AV Block Sinus impulses do not activate the ventricle

3rd Degree or Complete AV Block3rd Degree or Complete AV Block Sinus impulses do not activate the ventricle Regular P-P intervals, regular R-R intervals

Variable PR inter als Variable PR intervals Atrial rate > ventricular rate

i i i d i dl QRS originates in AV Node, His, Bundles, Purkinje fibers, Ventricles

d i di i l Drugs, MI, conduction disease, congenital, hypertension, valvular, myocardial dis.

ll l d i l Rx: Pacer usually Px: related to etiology

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