A Practical Approach to Cardiovascular Medicine 1th 2011 EKG

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CHAPTER 22

ECG Interpretation

Marco Perez and Victor F. Froelicher Department of Internal Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, CA, USA

The 12 - lead ECG remains the most commonly used test in patients suspected of having cardiovascular disease. It supplies a wealth of information regard-ing the health of the conduction system, presence of structural abnormalities, such as hypertrophy, and signs of injury. The trick to reading a 12 - lead ECG is being methodical in approach and learning to recognize certain patterns. This chapter will assume prior knowledge about basic ECG function and will concentrate on a practical approach to reading the ECG.

Checklist

• Rate • Rhythm • Axis • Intervals: PR, QRS, QT • Hypertrophy: LV, RV, LA, RA • R - wave progression • Ischemia and injury: Q - waves, ST - and T - wave patterns • PR depression • Voltages: calibration, low voltage, and electrical alternans • Lead reversal • Clinical syndromes

Rate The normal adult heart rate (HR) is 60 – 100 bpm. • If a slow HR is seen, SA or AV nodal disease should be assessed (see

Chapter 18 ). • A fast HR should fl ag a check for a tachyarrhythmia (see Chapters 15 – 17 )

before calling the rhythm sinus tachycardia.

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A Practical Approach to Cardiovascular Medicine, First Edition. Edited by Reza Ardehali, Marco Perez, Paul Wang.© 2011 Blackwell Publishing Ltd. Published 2011 by Blackwell Publishing Ltd.

ECG Interpretation 273

Count the number of “ large boxes ” to quickly estimate heart rate. Memorize the HRs at each of the large boxes. In Figure 22.1 , three large boxes translates to 100 bpm. If the distance is somewhere between two large boxes, make an approximate estimate, e.g. four and a half large boxes would work out to be about half way between 75 and 60, or approximately 68.

Rhythm Sinus rhythm is determined when every P - wave is followed by a QRS complex, every QRS complex is preceded by a P - wave, and the P - wave is upright in II and biphasic in V1. If these criteria are not met, an attempt to identify the rhythm should be made:

Ask: • Fast or slow • Narrow or wide • Regular or irregular • Where are the Ps?

Figure 22.2 is not a comprehensive algorithm, but will identify the majority of arrhythmias.

If no clear pattern is present, remember to check for frequent premature atrial contraction (PACs) and premature ventricular contractions (PVCs).

Axis The normal QRS axis is between − 30 and + 90. If leads I and aVF are predomi-nantly positive then the axis is between 0 and + 90 (Figure 22.3 ). If lead I is positive and aVF is negative, lead II will help determine normal versus left axis deviation (Figure 22.3 ). A negative lead I and positive lead aVF means there is right axis deviation.

Intervals (Figure 22.4 ) • PR:

• 0.12 – 0.20 s • Measured from beginning of p to beginning of QRS • Quick read: less than one “ big box ”

Figure 22.1 Example ECG

274 Specialized Testing and Therapeutics

Figure 22.3 Determination of axis deviation

Positive in I Positive in

aVF

Determining axis quickly Axis First Second Tie

breakerNormal + I + aVF Normal + I – aVF + II LAD + I – aVF – II RAD – I + aVF “Northwest” – I – aVF

Positive in both I and aVF

Causes of left axis deviation (LAD): leftventricular hypertrophy (LVH), left bundlebranch block (LBBB), inferior myocardial infarction (MI)Diagnosis of exclusion: left anteriorfascicular block

Causes of right axis deviation (RAD): rightventricular hypertrophy (RVH), chronicobstructive pulmonary disease (COPD),pericardial effusion (PE), lead reversal,dextrocardia Diagnosis of exclusion: left posteriorfascicular block

Figure 22.2 Algorithm for arrhythmia identifi cation

Slow

QRS afterevery P

NonconductedP-waves

Regular IrregularMobitz I

or IINonconducted

PAC

Sinusbradycardia

Sinusarrest/PauseSA exit block

AVDissociation

Completeheartblock

Fast

Narrow Wide

Regular IrregularSVT withaberrancy

AVRT(antedromic)

VT

Sinustachycardia

atrialflutterAVNRTAVRT

AT

Atrialfibrillation

AFLvariable

blockMAT

frequentPAC


Figure 22.4 Intervals and bundle branch blocks

RBBB LBBB

• QRS: • Normal : < 0.10; prolonged: > 0.12 • Measured from beginning of QRS to end of QRS • Quick read: less than half of one “ big box ”

• QT: • 0.35 – 0.43 s • Measured from beginning of QRS to end of T - wave • Correct for HR: QTc = QT/(sqrt R – R) • Quick read: less than half the R – R interval

Bundle Branch Blocks In a prolonged QRS, identify the morphology (Figure 22.4 ): • Quick read: right bundle branch block (RBBB) looks like an “ M ” in V1 • Quick read: left bundle branch block (LBBB) looks like a “ V ” or “ W ” in V1

Hypertrophy

Left Ventricle There are several criteria that can be used, each with varying sensitivities and specifi cities. The best strategy is to choose a couple that can be remembered. A few are described below. • Cornell criteria: R in aVL + S in V3 > 28 mm in males or > 20 mm in females • Precordial lead criteria : S in V1 + R in V5 or V6 > 35 • Limb lead criteria : R in aVL ≥ 12


• Estes criteria: point system, cumbersome. Just remember discordant ST abnormalities, large left atrium, and left axis deviation associated with LVH are often seen

Right Ventricle Any of the following: • R > S in V1 • R in V1 ≥ 7 mm • rSR ′ in V1 with R ′ > 10

Left Atrium • Wide P ( > 0.12 s) in II or • Neg. P in V1 > 1 s × 1 mm

Right Atrium • Tall P ( > 2.5 mm) in II or • Pos. P in V1 > 1.5 mm

R - Wave Progression • Abnormal R - wave progression should be a fl ag that something is

abnormal. • Normally the R - wave starts off small in V1 and gradually enlarges

towards V6. • The transition where the R - wave is bigger than the S - wave is usually

V2 – V4.


• Late transition: LVH, COPD, anterior MI, LBBB, cardiomyopathy • Early transition: RVH, posterior MI, RBBB, Wolff – Parkinson – White

(WPW), precordial lead reversal • Reverse R - wave progression: dextrocardia, signifi cant anterior injury.

Ischemia and Injury: Q - Waves, ST - and T - Wave Patterns The leads can be grouped together according to anatomic distribution (Figure 22.5 ). Q - waves and ST elevations can then be localized based on this distribu-tion. Note that ST depressions and TWI can not be localized in this manner. • Pathologic Q - waves:

• Any Q - wave in V1 – V3 • Q > 1 mm deep and > 0.03 s in other leads • Must be present in two contiguous leads

• Signifi cant ST elevation (Figure 22.6 ): • Must be > 2 mm in V1 – V3 • STE > 1 mm in other leads • Must be present in two contiguous leads

• Ischemic ST depressions: • Horizontal or down sloping • At least 1 mm deep • Must be present in two contiguous leads

• Ischemic T - waves: • Deeply inverted • Biphasic (positive then negative).

Figure 22.5 Anatomic distribution of leads

Lateral

Inferior

I

II

III V3

V2

V1aVR

aVL

aVF V6

V5

V4

Anterior

Figure 22.6 Evolution of an ST elevation myocardial infarction

Acute Phase Evolving Phase Resolving Phase


PR Depression PR depression is due to abnormal atrial repolarization seen in acute pericar-ditis. PR elevation of 1 mm is seen in aVR, while PR depression and ST eleva-tion are seen in all other leads. If PR depression is seen, look for low voltages or electrical alternans as further clues of coexistent PE. PR depression is easily missed.

Voltages • Calibration :

• Make sure the voltage calibration bracket covers two “ large boxes ” • If the voltages are abnormally high or low, some ECG machines may

adjust the voltages to keep the tracings from overlapping. • Low voltages :

• QRS < 5 mm in all limb leads and < 10 mm in all precordial leads • Diagnosis: PE, COPD, obesity, infi ltrative cardiomyopathy, extensive MI,

myxedema • Electrical alternans (Figure 22.7 ):

• Alteration in amplitude from beat to beat, usually seen in QRS but can be noted of P - and T - waves

• Diagnosis: PE, deep respiration, heart failure, rheumatic heart disease, coronary artery disease (CAD).

Lead Reversal • Limb leads :

• Most common lead reversal is that of the left and right arms (Figure 22.8 ) This results in a negative P - wave, QRS and T - wave in I and aVL

Figure 22.7 Electrical alternans

Figure 22.8 Left and right arm lead reversal


Figure 22.9 Reversal of leads V2 and V5

• Rule out dextrocardia if this is seen (see below) • Other abnormally inverted limb leads, especially in lead III, are clues to

alternative types of lead reversals. • Precordial leads:

• Next most common lead reversal is that of any two precordial leads • This appears as a disruption in the normal R - wave progression, with a

sudden change in R - wave amplitude, followed by a return to normal progression (Figure 22.9 ).

Important Clinical ECG Patters Patterns to look out for in the appropriate clinical scenarios are listed below, and characteristic ECG patterns are shown in Figure 22.10 . • Hyperkalemia:

• Mild (5.5 – 6.5): peaked T - waves (limb leads > 6 mm, precordial leads > 10 mm), short QT

• Moderate (6.5 – 7.5): AV block, QRS widening • Severe ( > 7.5): P - wave fl attening, bundle branch block, ST elevation, VT/

VF, asystole. • Hypokalemia: QT prolongation, U - waves, ST depressions, AV block.

Figure 22.10 Characteristic ECG patterns

Delta wave Epsilon wave Osborne Brugada typeI

Dig scooping


• Digoxin effect: scooping of ST, abnormal TW, short QT, U - wave, prolonged PR.

• Digoxin toxicity: any arrhythmia, atrial fi brillation or tachycardia with AV block, junctional/idioventricular.

• Hypercalcemia: short QT, PR prolongation. • Hypocalcemia: prolonged QT, TW abnormalities. • Dextrocardia: inverted lead I (negative P, QRS and T - waves) and reverse

R - wave peak (RWP). • Chronic obstructive pulmonary disease: RVH, right axis deviation, right

atrial enlargement, late RWP, low voltages. • Pericardial effusion: S1Q3T3 (large S in I, deep Q in III, inverted T in III),

RBBB, inverted TW V1 – V3. • Hypertrophic obstructive cardiomyopathy:

• Large amplitude QRS, large Q - waves throughout, large R - wave in V1 • Left axis deviation, secondary ST/TW changes, left atrial enlargement

• Wolff – Parkinson – White: all of: • Delta wave • Short PR • Prolonged QRS.

• Myxedema: low voltages, sinus bradycardia, fl at TW, prolonged PR, electri-cal alternans.

• CNS disorder: deep TW inversions in precordium, prolonged QT, promi-nent U.

• Brugada: prolongation of the QRS complex with a RBBB morphology and a persistent ST elevation in leads V1 – V3. The morphology differs between the three subtypes.

• Arrhythmogenic right ventricular dysplasia: QRS may be prolonged with incomplete RBBB. TWI in V1 arrhythmogenic right ventricular dysplasia V3. Epsilon wave.

• Hypothermia : marked bradycardia, prolongation of PR, QRS, QT, Osborne waves, AF.

Lead Placement

Precordial Leads (Figure 22.11 ) • V1: fourth intercostal space, right of the sternum. • V2: fourth intercostal space, left of the sternum • V3: directly between leads V2 and V4 • V4: fi fth intercostal space at midclavicular line • V5: level with V4 at left anterior axillary line • V6: level with V5 at left midaxillary line

The four limb leads account for the six standard ECG limb vectors. The electrodes should be placed just above the wrists and ankles, although they can extend up to the shoulder or hips, respectively.


Figure 22.11 Lead placement

Mid clavicular line

Anterior axillary line

Mid axillary lineV1 V2

V3V4 V5 V6

CLINICAL PEARLS

• In RBBB: Q - waves and axis can still be interpreted, and LVH criteria followed;

standard criteria for RVH cannot be followed.

• In LBBB: Q - waves, axis, and LVH cannot be interpreted or standard injury criteria

used; discordant ST elevations > 5 mm or concordant ST depressions > 2 mm

suggest acute MI.

• Left anterior fascicle block (LAFB): unexplained left axis deviation + small Q - waves

in I, aVL, and small R in III.

• Left posterior fascicle block: unexplained right axis deviation + small Q - waves in II,

III, aVF, and small R in I. Rare compared to LAFB and often occurs with RBBB.

• Patients with inferior or posterior MI should have right precordial leads assessed.

Right - sided V4 ST elevation > 1 mm suggests RV infarct.

• Posterior infarcts: suspect when inferior infarct is seen. R > 0.04 ms and R > S

in V1.

• Post - syncope: make sure you assess for Wolff – Parkinson – White, long QT,

Brugada, complete heart block, Mobitz II and hypertrophic obstructive

cardiomyopathy pattern.

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A Practical Approach to Cardiovascular Medicine 1th 2011 EKG