P Wave

Right atrial enlargement/abnormality (P pulmonale)

P-wave amplitude > 2.5 mm in leads II, III, and aVF with P-wave duration < 0.12 sec; initial positive component of P-wave in lead VI > 1.5 mm; P-wave axis in frontal plane > +75°

Left atrial enlargement/abnormality (P mitrale)

P-wave duration ≥ 0.12 sec and P waves notched in leads I, II, and aVL; abnormal P terminal force in lead V1; P-wave axis in frontal plane is leftward of +15°

Biatrial enlargement/abnormality

Abnormal P terminal force combined with an initial positive P-wave component > 1.5 mm in lead Vl; combined wide (> 0.12 sec) and tall (> 2.5 mm) P waves in limb leads

QRS Complex

Left axis deviation

A frontal plane QRS between −30° and −90°

Right axis deviation (Table 3.3)

A frontal plane QRS between +90° and +270°

Low voltage

Sum of R and S waves in limb leads ≤ 5 mm; sum of R and S waves in precordial leads ≤ 10 mm

Poor R-wave progression

R waves are present in leads V1-V3 but magnitude of R waves in each of the 3 leads ≤ 3.0 mm, and LBBB, pre-excitation (WPW), or criteria for low voltage (above) are not present

rSR′ V1

rSR′ complex is of normal duration; primary R wave < 8 mm; R′ < 6 mm; R′/S ratio < 1

Electrical alternans

Regular alternation of amplitude of the P, QRS, and/or T waves in complexes originating from a single pacemaker

ST-T Findings/U Waves

J-point evaluation

1-4 mm upward displacement of ST segment at J junction with upward concavity; T waves are frequently tall, broad, and symmetric

Persistent juvenile T-wave pattern

T-wave inversion in V1 and V2 in an otherwise normal adult

Nonspecific ST-T abnormality

Slight ST depression, ST elevation, or isolated T-wave inversion or other abnormality that cannot be characterized as secondary to a specific abnormality

ST-T abnormalities associated with ventricular hypertrophy

LVH: ST depression with downward concavity and T-wave inversion in left precordial leads; same ST-T changes may be present in leads I, aVL if QRS axis horizontal, or in leads II, III, and aVF with a vertical axis

RVH: ST depression with downward concavity and T-wave inversion in right precordial leads

ST-T abnormalities associated with ventricular conduction abnormalities

LBBB: ST depression and T-wave inversion in left precordial leads

RBBB: ST depression and T-wave inversion in right precordial leads

Possible myocardial ischemia

Horizontal/downsloping ST depression with or without T-wave inversion in the absence of concomitant ST elevation in additional leads

Possible acute myocardial injury

Horizontal/concave downward ST-segment elevation with or without T-wave inversion; ST depression with upright T wave in leads V1-V2 (posterior wall injury); horizontal/downsloping ST depression with or without T-wave abnormalities in leads opposite those with the ST elevations can reflect ischemia or reciprocal change

ST-T abnormalities associated with acute pericarditis

Diffuse ST-segment elevation (concave upward) in multiple leads, especially leads I, II, and V5-V6; T wave remains concordant with direction of ST segment in early pericarditis

Digitalis effect

Flattening or inversion of T wave; “sagging” ST segment (down-sloping ST depression, concave upward); slight shortening of QT interval

Peaked T wave

T-wave amplitude > 6 mm in limb leads or > 10 mm in any precordial lead

Post-PVCT-wave abnormality

Nonspecific change in T-wave morphology of sinus beat following PVC

Prolonged QT interval

Corrected QT interval (QTc) = QT interval ÷ (sq root of R-R interval); upper limit of normal for QTc usually 0.44 sec; approximation formula: QT upper limit 0.40 sec for heart rate of 70, add/subtract 0.02 sec for every 10-beat increase/decrease in heart rate

U Waves

U waves

U wave usually ≤ 1.0 mm; amplitude is proportional to T wave; should be no greater than 25% of height of T wave; U-wave inversion in leads with a normally upright T wave are abnormal

1° AV block

Sinus rhythm with PR interval > 0.20 sec

2° AV block, Mobitz type I (Wenckebach block)

Sinus rhythm with progressive decremental lengthening of PR interval (and associated progressive shortening of R-R interval) until a P wave fails to conduct to the ventricles and a beat is dropped; resulting pause is sum of two P-P intervals

2° AV block, Mobitz type II

Sinus rhythm with constant PR interval and intermittent failure of P wave to conduct to the ventricles

3° AV block (complete heart block)

Complete absence of AV conduction; atrial rate > ventricular rate; atria and ventricles depolarize independently of each other

High-grade AV block

Sinus rhythm with conduction of P waves to ventricles in ratio ≥ 3:1; majority (but not all) of P waves fail to conduct to ventricles; identification of occasional conduction to ventricles defines the conduction abnormality as high-grade rather than complete AV block

Accelerated AV conduction

Sinus rhythm with PR interval < 0.12 sec and normal P-wave morphology and QRS duration

Wolff-Parkinson White (pre-excitation) syndrome

Sinus rhythm with PR interval < 0.12 sec, normal P-wave morphology, initial slurring (delta wave) prior to a wide QRS complex ≥ 0.11 sec, and secondary ST-T wave changes

Physiologic AV conduction delay associated with supraventricular tachyarrhythmias

Prolongation of PR interval with 1:1 conduction at atrial rates > 150 beat/min; Wenckebach phenomenon at atrial rates of 130-200 beat/min; 2:1 AV conduction at atrial rates > 200 beat/min in atrial tachycardia; Aflut; Afib with average ventricular response of 100-180 beat/min

Nonphysiologic AV conduction delay associated with supraventricular tachyarrhythmias

PR interval prolongation with 1:1 conduction at atrial rates of 100-150 beat/min; Wenckebach phenomenon at atrial rates of 100-130 beat/min; > 2:1 AV conduction ratio at atrial rates > 200 beat/min in atrial tachycardia and Aflut; Afib with an average ventricular response < 100 beat/min