Alan E. Lindsay ECG Learning Center in Cyberspace

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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The standard 12-lead electrocardiogram is a representation of the heart’s electrical activity recorded from electrodes on the body surface. This section describes the basic components of the ECG and the lead system used to record the ECG tracings.

Topics for study:

What do they mean?

 P wave: the sequential activation (depolarization) of the right and left atria

QRS complex: right and left ventricular depolarization (normally the ventricles are activated simultaneously)

ST-T wave: ventricular repolarization

U wave: origin for this wave is not clear – but probably represents “afterdepolarizations” in the ventricles

PR interval: time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)

QRS duration: duration of ventricular muscle depolarization

QT interval: duration of ventricular depolarization and repolarization

RR interval: duration of ventricular cardiac cycle (an indicator of ventricular rate)

PP interval: duration of atrial cycle (an indicator of atrial rate)

It is important to remember that the 12-lead ECG provides spatial information about the heart’s electrical activity in 3 approximately orthogonal directions:

Each of the 12 leads represents a particular orientation in space, as indicated below (RA = right arm; LA = left arm, LF = left foot):

 Bipolar limb leads (frontal plane):

 Lead I: RA (-) to LA (+) (Right Left, or lateral)

Lead II: RA (-) to LF (+) (Superior Inferior)

Lead III: LA (-) to LF (+) (Superior Inferior)

 Augmented unipolar limb leads (frontal plane):

 Lead aVR: RA (+) to [LA & LF] (-) (Rightward)

Lead aVL: LA (+) to [RA & LF] (-) (Leftward)

Lead aVF: LF (+) to [RA & LA] (-) (Inferior)

 Unipolar (+) chest leads (horizontal plane):

 Leads V1, V2, V3: (Posterior Anterior)

Leads V4, V5, V6:(Right Left, or lateral)

Click here to see: Lead Placement Diagrams

II. A “Method” of ECG Interpretation

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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This “method” is recommended when reading all 12-lead ECG’s. Like the physical examination, it is desirable to follow a standardized sequence of steps in order to avoid missing subtle abnormalities in the ECG tracing, some of which may have clinical importance. The 6 major sections in the “method” should be considered in the following order:

1.      Measurements

2.      Rhythm Analysis

3.      Conduction Analysis

4.      Waveform Description

5.      Ecg Interpretation

6.      Comparison with Previous ECG (if any)

Click to view

 Heart rate (state atrial and ventricular, if different)

PR interval (from beginning of P to beginning of QRS)

QRS duration (width of most representative QRS)

QT interval (from beginning of QRS to end of T)

QRS axis in frontal plane (go to: “How To Determine Axis”)

Go to: ECG Measurement Abnormalities (Lesson IV) for description of normal and abnormal measurements

 State basic rhythm (e.g., “normal sinus rhythm”, “atrial fibrillation”, etc.)

Identify additional rhythm events if present (e.g., “PVC’s”, “PAC’s”, etc)

Consider all rhythm events from atria, AV junction, and ventricles

Go to: ECG Rhythm Abnormalities (Lesson V) for description of arrhythmias

 “Normal” conduction implies normal sino-atrial (SA), atrio-ventricular (AV), and intraventricular (IV) conduction.

The following conduction abnormalities are to be identified if present:

 SA block (lesson VI): 2nd degree (type I vs. type II)

AV block (lesson VI): 1st, 2nd (type I vs. type II), and 3rd degree

IV blocks (lesson VI): bundle branch, fascicular, and nonspecific blocks

Exit blocks: blocks just distal to ectopic pacemaker site

(Go to ECG Conduction Abnormalities (Lesson VI) for a description of conduction abnormalities)

 Carefully analyze the 12-lead ECG for abnormalities in each of the waveforms in the order in which they appear: P-waves, QRS complexes, ST segments, T waves, and… Don’t forget the U waves.

 P waves (lesson VII): are they too wide, too tall, look funny (i.e., are they ectopic), etc.?

QRS complexes: look for pathologic Q waves (lesson IX), abnormal voltage (lesson VIII), etc.

ST segments (lesson X): look for abnormal ST elevation and/or depression.

T waves (lesson XI): look for abnormally inverted T waves.

U waves (lesson XII): look for prominent or inverted U waves.

 This is the conclusion of the above analyses. Interpret the ECG as “Normal”, or “Abnormal”. Occasionally the term “borderline” is used if unsure about the significance of certain findings. List all abnormalities. Examples of “abnormal” statements are:

 Inferior MI, probably acute

Old anteroseptal MI

Left anterior fascicular block (LAFB)

Left ventricular hypertrophy (LVH)

Nonspecific ST-T wave abnormalities

Any rhythm abnormalities

 Example:

Click to view

 If there is a previous ECG in the patient’s file, the current ECG should be compared with it to see if any significant changes have occurred. These changes may have important implications for clinical management decisions.

III. Characteristics of the Normal ECG

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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It is important to remember that there is a wide range of normal variability in the 12 lead ECG. The following “normal” ECG characteristics, therefore, are not absolute. It takes considerable ECG reading experience to discover all the normal variants. Only by following a structured “Method of ECG Interpretation” (Lesson II) and correlating the various ECG findings with the particular patient’s clinical status will the ECG become a valuable clinical tool.

Topics for Study:

 Heart Rate: 60 – 90 bpm

 How to calculate the heart rate on ECG paper

PR Interval: 0.12 – 0.20 sec

QRS Duration: 0.06 – 0.10 sec

QT Interval (QT_c < 0.40 sec)

 Bazett’s Formula: QT_c = (QT)/SqRoot RR (in seconds)

Poor Man’s Guide to upper limits of QT: For HR = 70 bpm, QT<0.40 sec; for every 10 bpm increase above 70 subtract 0.02 sec, and for every 10 bpm decrease below 70 add 0.02 sec. For example:

 QT < 0.38 @ 80 bpm

QT < 0.42 @ 60 bpm

Frontal Plane QRS Axis: +90 ^o to -30 ^o (in the adult)

Normal sinus rhythm

The P waves in leads I and II must be upright (positive) if the rhythm is coming from the sinus node.

Normal Sino-atrial (SA), Atrio-ventricular (AV), and Intraventricular (IV) conduction

Both the PR interval and QRS duration should be within the limits specified above.

(Normal ECG is shown below – Compare its waveforms to the descriptions below)

Click to view

 P Wave

It is important to remember that the P wave represents the sequential activation of the right and left atria, and it is common to see notched or biphasic P waves of right and left atrial activation.

 P duration < 0.12 sec

P amplitude < 2.5 mm

Frontal plane P wave axis: 0^o to +75^o

May see notched P waves in frontal plane

QRS Complex

The QRS represents the simultaneous activation of the right and left ventricles, although most of the QRS waveform is derived from the larger left ventricular musculature.

 QRS duration < 0.10 sec

QRS amplitude is quite variable from lead to lead and from person to person. Two determinates of QRS voltages are:

 Size of the ventricular chambers (i.e., the larger the chamber, the larger the voltage)

Proximity of chest electrodes to ventricular chamber (the closer, the larger the voltage)

Frontal plane leads:

 The normal QRS axis range (+90 ^o to -30 ^o ); this implies that the QRS be mostly positive (upright) in leads II and I.

Normal q-waves reflect normal septal activation (beginning on the LV septum); they are narrow (<0.04s duration) and small (<25% the amplitude of the R wave). They are often seen in leads I and aVL when the QRS axis is to the left of +60^o, and in leads II, III, aVF when the QRS axis is to the right of +60^o. Septal q waves should not be confused with the pathologic Q waves of myocardial infarction.

Precordial leads: (see Normal ECG)

 Small r-waves begin in V1 or V2 and progress in size to V5. The R-V6 is usually smaller than R-V5.

In reverse, the s-waves begin in V6 or V5 and progress in size to V2. S-V1 is usually smaller than S-V2.

The usual transition from S>R in the right precordial leads to R>S in the left precordial leads is V3 or V4.

Small “septal” q-waves may be seen in leads V5 and V6.

ST Segment and T wave

In a sense, the term “ST segment” is a misnomer, because a discrete ST segment distinct from the T wave is usually absent. More often the ST-T wave is a smooth, continuous waveform beginning with the J-point (end of QRS), slowly rising to the peak of the T and followed by a rapid descent to the isoelectric baseline or the onset of the U wave. This gives rise to an asymmetrical T wave. In some normal individuals, particularly women, the T wave is symmetrical and a distinct, horizontal ST segment is present.

The normal T wave is usually in the same direction as the QRS except in the right precordial leads. In the normal ECG the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR.

Normal ST segment elevation: this occurs in leads with large S waves (e.g., V1-3), and the normal configuration is concave upward. ST segment elevation with concave upward appearance may also be seen in other leads; this is often called early repolarization, although it’s a term with little physiologic meaning (see example of “early repolarization” in leads V4-6):

Click to view

Convex or straight upward ST segment elevation (e.g., leads II, III, aVF) is abnormal and suggests transmural injury or infarction:

Click to view

ST segment depression is always an abnormal finding, although often nonspecific (see ECG below):

Click to view

ST segment depression is often characterized as “upsloping”, “horizontal”, or “downsloping”.

Click to view

  The normal U Wave: (the most neglected of the ECG waveforms)

 U wave amplitude is usually < 1/3 T wave amplitude in same lead

U wave direction is the same as T wave direction in that lead

U waves are more prominent at slow heart rates and usually best seen in the right precordial leads.

Origin of the U wave is thought to be related to afterdepolarizations which interrupt or follow repolarization.

IV. Abnormalities in the ECG Measurements

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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Click on the measurement abnormality you would like to study

In normal sinus rhythm, a resting heart rate of below 60 bpm is called bradycardia and a rate of above 90 bpm is called tachycardia.

(measured from beginning of P to beginning of QRS in the frontal plane)

 Normal: 0.12 – 0.20s

Short PR: < 0.12s

 Preexcitation syndromes:

 WPW (Wolff-Parkinson-White) Syndrome: An accessory pathway (called the “Kent” bundle) connects the right atrium to the right ventricle (see diagram below) or the left atrium to the left ventricle, and this permits early activation of the ventricles (delta wave) and a short PR interval.

Click to view

 LGL (Lown-Ganong-Levine): An AV nodal bypass track into the His bundle exists, and this permits early activation of the ventricles without a delta-wave because the ventricular activation sequence is normal.

AV Junctional Rhythms with retrograde atrial activation (inverted P waves in II, III, aVF): Retrograde P waves may occur before the QRS complex (usually with a short PR interval), in the QRS complex (i.e., hidden from view), or after the QRS complex (i.e., in the ST segment).

Ectopic atrial rhythms originating near the AV node (the PR interval is short because atrial activation originates close to the AV node; the P wave morphology is different from the sinus P)

Normal variant

Prolonged PR: >0.20s

First degree AV block (PR interval usually constant)

Intra-atrial conduction delay (uncommon)

Slowed conduction in AV node (most common site)

Slowed conduction in His bundle (rare)

Slowed conduction in bundle branch (when contralateral bundle is blocked)

Second degree AV block (PR interval may be normal or prolonged; some P waves do not conduct)

Type I (Wenckebach): Increasing PR until nonconducted P wave occurs

Type II (Mobitz): Fixed PR intervals plus nonconducted P waves

AV dissociation: Some PR’s may appear prolonged, but the P waves and QRS complexes are dissociated (i.e., not married, but strangers passing in the night).

(duration of QRS complex in frontal plane):

Normal: 0.06 – 0.10s

Prolonged QRS Duration (>0.10s):

QRS duration 0.10 – 0.12s

Incomplete right or left bundle branch block

Nonspecific intraventricular conduction delay (IVCD)

Some cases of left anterior or posterior fascicular block

QRS duration > 0.12s

Complete RBBB or LBBB

Nonspecific IVCD

Ectopic rhythms originating in the ventricles (e.g., ventricular tachycardia, pacemaker rhythm)

(measured from beginning of QRS to end of T wave in the frontal plane)

Normal: heart rate dependent (corrected QT = QT_c = measured QT ¸ sq-root RR in seconds; upper limit for QT_c = 0.44 sec)

Long QT Syndrome – “LQTS” (based on upper limits for heart rate; QT_c > 0.47 sec for males and > 0.48 sec in females is diagnostic for hereditary LQTS in absence of other causes of increased QT)

This abnormality may have important clinical implications since it usually indicates a state of increased vulnerability to malignant ventricular arrhythmias, syncope, and sudden death. The prototype arrhythmia of the Long QT Interval Syndromes (LQTS) is Torsade-de-pointes, a polymorphic ventricular tachycardia characterized by varying QRS morphology and amplitude around the isoelectric baseline. Causes of LQTS include the following:

Drugs (many antiarrhythmics, tricyclics, phenothiazines, and others)

Electrolyte abnormalities ( K⁺, Ca⁺⁺, Mg⁺⁺)

CNS disease (especially subarrachnoid hemorrhage, stroke, trauma)

Hereditary LQTS (e.g., Romano-Ward Syndrome)

Coronary Heart Disease (some post-MI patients)

 Click here for brief tutorial in Measuring QRS Axis

Normal: -30 degrees to +90 degrees

Abnormalities in the QRS Axis:

 Left Axis Deviation (LAD): > -30^o (i.e., lead II is mostly ‘negative’)

 Left Anterior Fascicular Block (LAFB): rS complex in leads II, III, aVF, small q in leads I and/or aVL, and axis -45^o to -90^o

Some cases of inferior MI with Qr complex in lead II (making lead II ‘negative’)

Inferior MI + LAFB in same patient (QS or qrS complex in lead II)

Some cases of LVH

Some cases of LBBB

Ostium primum ASD and other endocardial cushion defects

Some cases of WPW syndrome (large negative delta wave in lead II)

Right Axis Deviation (RAD): > +90^o (i.e., lead I is mostly ‘negative’)

Left Posterior Fascicular Block (LPFB): rS complex in lead I, qR in leads II, III, aVF (however, must first exclude, on clinical basis, causes of right heart overload; these will also give same ECG picture of LPFB)

Many causes of right heart overload and pulmonary hypertension

High lateral wall MI with Qr or QS complex in leads I and aVL

Some cases of RBBB

Some cases of WPW syndrome

Children, teenagers, and some young adults

Bizarre QRS axis: +150^o to -90^o (i.e., lead I and lead II are both negative)

Consider limb lead error (usually right and left arm reversal)

Dextrocardia

Some cases of complex congenital heart disease (e.g., transposition)

Some cases of ventricular tachycardia

V. ECG Rhythm Abnormalities

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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Topics for Study:

1. Introduction to rhythm analysis

2. Supraventricular arrhythmias

Premature atrial complexes
Premature junctional complexes
Atrial fibrillation
Atrial flutter
Ectopic atrial tachycardia and rythm
Multifocal atrial tachycardia
Paroxysmal supraventricular tachycardia
Junctional rhythms and tachycardias

3. Ventricular arrhythmias

Premature ventricular complexes (PVCs)
Aberrancy vs. ventricular ectopy
Ventricular tachycardia
Differential diagnosis of wide QRS tachycardias
Accelerated ventricular rhythms
Idioventricular rhythm
Ventricular parasystole

VI. ECG Conduction Abnormalities

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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Topics for Study

 1st Degree AV Block
 Type I (Wenckebach) 2nd Degree AV Block
 Type II (Mobitz) 2nd Degree AV Block
 Complete (3rd Degree) AV Block
 AV Dissociation

 Right Bundle Branch Block
 Left Bundle Branch Block
 Left Anterior Fascicular Block
 Left Posterior Fascicular Block
 Bifascicular Blocks
 Nonspecific Intraventricular Block
 Wolff-Parkinson-White Preexcitation

click here to view

This section considers all the important disorders of impulse conduction that may occur within the cardiac conduction system illustrated in the above diagram. Heart block can occur anywhere in the specialized conduction system beginning with the sino-atrial connections, the AV junction, the bundle branches and their fascicles, and ending in the distal ventricular Purkinje fibers. Disorders of conduction may manifest as slowed conduction (1^st degree), intermittent conduction failure (2^nd degree), or complete conduction failure (3^rd degree). In addition, 2^nd degree heart block occurs in two varieties: Type I (Wenckebach) and Type II (Mobitz). In Type I block there is decremental conduction which means that conduction velocity progressively slows down until failure of conduction occurs. Type II block is all or none. The term exit block is used to identify conduction delay or failure immediately distal to a pacemaker site. Sino-atrial (SA) block is an exit block. This section considers conduction disorders in the anatomical sequence that defines the cardiac conduction system; so lets begin . . .

 2^nd Degree SA Block: this is the only degree of SA block that can be recognized on the surface ECG (i.e., intermittent conduction failure between the sinus node and the right atrium). There are two types, although because of sinus arrhythmia they may be hard to differentiate. Furthermore, the differentiation is electrocardiographically interesting but not clinically important.

 Type I (SA Wenckebach): the following 3 rules represent the classic rules of Wenckebach, which were originally described for Type I AV block. The rules are the result of decremental conduction where the increment in conduction delay for each subsequent impulse gets smaller until conduction failure finally occurs. This declining increment results in the following findings:

 PP intervals gradually shorten until a pause occurs (i.e., the blocked sinus impulse fails to reach the atria)

The pause duration is less than the two preceding PP intervals

The PP interval following the pause is greater than the PP interval just before the pause

Differential Diagnosis: sinus arrhythmia without SA block. The following rhythm strip illustrates SA Wenckebach with a ladder diagram to show the progressive conduction delay between SA node and the atria. Note the similarity of this rhythm to marked sinus arrhythmia. (Remember, we cannot see SA events on the ECG, only the atrial response or P waves.)

click here to view

 Type II SA Block:

 PP intervals fairly constant (unless sinus arrhythmia present) until conduction failure occurs.

The pause is approximately twice the basic PP interval

click here to view

 Possible sites of AV block:

 AV node (most common)

His bundle (uncommon)

Bundle branch and fascicular divisions (in presence of already existing complete bundle branch block)

1^st Degree AV Block: PR interval > 0.20 sec; all P waves conduct to the ventricles.

click here to view

 2^nd Degree AV Block: The diagram below illustrates the difference between Type I (or Wenckebach) and Type II AV block.

click here to view

In “classic” Type I (Wenckebach) AV block the PR interval gets longer (by shorter increments) until a nonconducted P wave occurs. The RR interval of the pause is less than the two preceding RR intervals, and the RR interval after the pause is greater than the RR interval before the pause. These are the classic rules of Wenckebach (atypical forms can occur). In Type II (Mobitz) AV block the PR intervals are constant until a nonconducted P wave occurs. There must be two consecutive constant PR intervals to diagnose Type II AV block (i.e., if there is 2:1 AV block we can’t be sure if its type I or II). The RR interval of the pause is equal to the two preceding RR intervals.

 Type I (Wenckebach) AV block (note the RR intervals in ms duration):

click here to view

Type I AV block is almost always located in the AV node, which means that the QRS duration is usually narrow, unless there is preexisting bundle branch disease.

 Type II (Mobitz) AV block(note there are two consecutive constant PR intervals before the blocked P wave):

click here to view

Type II AV block is almost always located in the bundle branches, which means that the QRS duration is wide indicating complete block of one bundle; the nonconducted P wave is blocked in the other bundle. In Type II block several consecutive P waves may be blocked as illustrated below:

click here to view

 Complete (3^rd Degree) AV Block

 Usually see complete AV dissociation because the atria and ventricles are each controlled by separate pacemakers.

Narrow QRS rhythm suggests a junctional escape focus for the ventricles with block above the pacemaker focus, usually in the AV node.

Wide QRS rhythm suggests a ventricular escape focus (i.e., idioventricular rhythm). This is seen in ECG ‘A’ below; ECG ‘B’ shows the treatment for 3^rd degree AV block; i.e., a ventricular pacemaker. The location of the block may be in the AV junction or bilaterally in the bundle branches.

click here to view

 AV Dissociation (independent rhythms in atria and ventricles):

 Not synonymous with 3^rd degree AV block, although AV block is one of the causes.

May be complete or incomplete. In complete AV dissociation the atria and ventricles are always independent of each other. In incomplete AV dissociation there is either intermittent atrial capture from the ventricular focus or ventricular capture from the atrial focus.

There are three categories of AV dissociation (categories 1 & 2 are always incomplete AV dissociation):

1. Slowing of the primary pacemaker (i.e., SA node); subsidiary escape pacemaker takes over by default:

click here to view

2. Acceleration of a subsidiary pacemaker faster than sinus rhythm; takeover by usurpation:

click here to view

3. 2^nd or 3^rd degree AV block with escape rhythm from junctional focus or ventricular focus:

click here to view

In the above example of AV dissociation (3^rd degree AV bock with a junctional escape pacemaker) the PP intervals are alternating because of ventriculophasic sinus arrhythmia (phasic variation of vagal tone in the sinus node depending on the timing of ventricular contractions and blood flow near the carotid sinus).

 Right Bundle Branch Block (RBBB):

 “Complete” RBBB has a QRS duration >0.12s

Close examination of QRS complex in various leads reveals that the terminal forces (i.e., 2^nd half of QRS) are oriented rightward and anteriorly because the right ventricle is depolarized after the left ventricle. This means the following:

Terminal R’ wave in lead V1 (usually see rSR’ complex) indicating late anterior forces

Terminal S waves in leads I, aVL, V6 indicating late rightward forces

Terminal R wave in lead aVR indicating late rightward forces

The frontal plane QRS axis in RBBB should be in the normal range (i.e., -30 to +90 degrees). If left axis deviation is present, think about left anterior fascicular block, and if right axis deviation is present, think about left posterior fascicular block in addition to the RBBB.

“Incomplete” RBBB has a QRS duration of 0.10 – 0.12s with the same terminal QRS features. This is often a normal variant.

The “normal” ST-T waves in RBBB should be oriented opposite to the direction of the terminal QRS forces; i.e., in leads with terminal R or R’ forces the ST-T should be negative or downwards; in leads with terminal S forces the ST-T should be positive or upwards. If the ST-T waves are in the same direction as the terminal QRS forces, they should be labeled primary ST-T wave abnormalities.

The ECG below illustrates primary ST-T wave abnormalities (leads I, II, aVR, V5, V6) in a patient with RBBB. ST-T wave abnormalities such as these may be related to ischemia, infarction, electrolyte abnormalities, medications, CNS disease, etc. (i.e., they are nonspecific and must be correlated with the patient’s clinical status).

click here to view

 Left Bundle Branch Block (LBBB)

 “Complete” LBBB” has a QRS duration >0.12s

Close examination of QRS complex in various leads reveals that the terminal forces (i.e., 2^nd half of QRS) are oriented leftward and posteriorly because the left ventricle is depolarized after the right ventricle.

 Terminal S waves in lead V1 indicating late posterior forces

Terminal R waves in lead I, aVL, V6 indicating late leftward forces; usually broad, monophasic R waves are seen in these leads as illustrated in the ECG below; in addition, poor R progression from V1 to V3 is common.

click here to view

 The “normal” ST-T waves in LBBB should be oriented opposite to the direction of the terminal QRS forces; i.e., in leads with terminal R or R’ forces the ST-T should be downwards; in leads with terminal S forces the ST-T should be upwards. If the ST-T waves are in the same direction as the terminal QRS forces, they should be labeled primary ST-T wave abnormalities. In the above ECG the ST-T waves are “normal” for LBBB; i.e., they are secondary to the change in the ventricular depolarization sequence.

“Incomplete” LBBB looks like LBBB but QRS duration = 0.10 to 0.12s, with less ST-T change. This is often a progression of LVH.

 Left Anterior Fascicular Block (LAFB)… the most common intraventricular conduction defect

 Left axis deviation in frontal plane, usually -45 to -90 degrees

rS complexes in leads II, III, aVF

Small q-wave in leads I and/or aVL

R-peak time in lead aVL >0.04s, often with slurred R wave downstroke

QRS duration usually <0.12s unless coexisting RBBB

Usually see poor R progression in leads V1-V3 and deeper S waves in leads V5 and V6

May mimic LVH voltage in lead aVL, and mask LVH voltage in leads V5 and V6.

click here to view

In this ECG, note -75 degree QRS axis, rS complexes in II, III, aVF, tiny q-wave in aVL, poor R progression V1-3, and late S waves in leads V5-6. QRS duration is normal, and there is a slight slur to the R wave downstroke in lead aVL.

 Left Posterior Fascicular Block (LPFB)…. Very rare intraventricular defect!

 Right axis deviation in the frontal plane (usually > +100 degrees)

rS complex in lead I

qR complexes in leads II, III, aVF, with R in lead III > R in lead II

QRS duration usually <0.12s unless coexisting RBBB

Must first exclude (on clinical grounds) other causes of right axis deviation such as cor pulmonale, pulmonary heart disease, pulmonary hypertension, etc., because these conditions can result in the identical ECG picture!

 Bifascicular Blocks

 RBBB plus either LAFB (common) orLPFB (uncommon)

Features of RBBB plus frontal plane features of the fascicular block (axis deviation, etc.)

click here to view

The above ECG shows classic RBBB (note rSR’ in V1) plus LAFB (note QRS axis = -45 degrees, rS in II, III, aVF; and small q in aVL).

 Nonspecific Intraventricular Conduction Defects (IVCD)

 QRS duration >0.10s indicating slowed conduction in the ventricles

Criteria for specific bundle branch or fascicular blocks not met

Causes of nonspecific IVCD’s include:

 Ventricular hypertrophy (especially LVH)

Myocardial infarction (so called periinfarction blocks)

Drugs, especially class IA and IC antiarrhythmics (e.g., quinidine, flecainide)

Hyperkalemia

 Wolff-Parkinson-White Preexcitation

 Although not a true IVCD, this condition causes widening of QRS complex and, therefore, deserves to be considered here

QRS complex represents a fusion between two ventricular activation fronts:

 Early ventricular activation in region of the accessory AV pathway (Bundle of Kent)

Ventricular activation through the normal AV junction, bundle branch system

ECG criteria include all of the following:

click here to view

 QRS morphology, including polarity of delta wave depends on the particular location of the accessory pathway as well as on the relative proportion of the QRS complex that is due to early ventricular activation (i.e., degree of fusion).

Delta waves, if negative in polarity, may mimic infarct Q waves and result in false positive diagnosis of myocardial infarction.

VII. Atrial Enlargement

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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Topics for study:

 P wave amplitude >2.5 mm in II and/or >1.5 mm in V1 (these criteria are not very specific or sensitive)

Better criteria can be derived from the QRS complex; these QRS changes are due to both the high incidence of RVH when RAE is present, and the RV displacement by an enlarged right atrium.

 QR, Qr, qR, or qRs morphology in lead V1 (in absence of coronary heart disease)

QRS voltage in V1 is <5 mm and V2/V1 voltage ratio is >6 (Sensitivity = 50%; Specificity = 90%)

click here to view

In the above ECG, note the tall P waves in Lead II, and the Qr wave in Lead V1.

 P wave duration > 0.12s in frontal plane (usually lead II)

 Notched P wave in limb leads with the inter-peak duration > 0.04s

Terminal P negativity in lead V1 (i.e., “P-terminal force”) duration >0.04s, depth >1 mm.

Sensitivity = 50%; Specificity = 90%

click here to view

 Features of both RAE and LAE in same ECG

P wave in lead II >2.5 mm tall and >0.12s in duration

Initial positive component of P wave in V1 >1.5 mm tall and prominent P-terminal force

VIII. Ventricular Hypertrophy

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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Topics for study:

 The ECG criteria for diagnosing right or left ventricular hypertrophy are very insensitive (i.e., sensitivity ~50%, which means that ~50% of patients with ventricular hypertrophy cannot be recognized by ECG criteria). However, the criteria are very specific (i.e., specificity >90%, which means if the criteria are met, it is very likely that ventricular hypertrophy is present).

 General ECG features include:

 > QRS amplitude (voltage criteria; i.e., tall R-waves in LV leads, deep S-waves in RV leads)

Delayed intrinsicoid deflection in V6 (i.e., time from QRS onset to peak R is >0.05 sec)

Widened QRS/T angle (i.e., left ventricular strain pattern, or ST-T oriented opposite to QRS direction)

Leftward shift in frontal plane QRS axis

Evidence for left atrial enlargement (LAE) (lessonVII)

ESTES Criteria for LVH (“diagnostic”, >5 points; “probable”, 4 points)

CORNELL Voltage Criteria for LVH (sensitivity = 22%, specificity = 95%)

 S in V3 + R in aVL > 24 mm (men)

S in V3 + R in aVL > 20 mm (women)

Other Voltage Criteria for LVH

 Limb-lead voltage criteria:

 R in aVL >11 mm or, if left axis deviation, R in aVL >13 mm plus S in III >15 mm

R in I + S in III >25 mm

Chest-lead voltage criteria:

 S in V1 + R in V5 or V6 > 35 mm

Example 1: (Limb-lead Voltage Criteria; e.g., R in aVL >11 mm; note wide QRS/T angle)

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 Example 2: (ESTES Criteria: 3 points for voltage in V5, 3 points for ST-T changes)

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(Note also the left axis deviation of -40 degrees, and left atrial enlargement)

 General ECG features include:

 Right axis deviation (>90 degrees)

Tall R-waves in RV leads; deep S-waves in LV leads

Slight increase in QRS duration

ST-T changes directed opposite to QRS direction (i.e., wide QRS/T angle)

May see incomplete RBBB pattern or qR pattern in V1

Evidence of right atrial enlargement (RAE) (lessonVII)

Specific ECG features (assumes normal calibration of 1 mV = 10 mm):

 Any one or more of the following (if QRS duration <0.12 sec):

 Right axis deviation (>90 degrees) in presence of disease capable of causing RVH

R in aVR > 5 mm, or

R in aVR > Q in aVR

Any one of the following in lead V1:

 R/S ratio > 1 and negative T wave

qR pattern

R > 6 mm, or S < 2mm, or rSR’ with R’ >10 mm

Other chest lead criteria:

 R in V1 + S in V5 (or V6) 10 mm

R/S ratio in V5 or V6 < 1

R in V5 or V6 < 5 mm

S in V5 or V6 > 7 mm

ST segment depression and T wave inversion in right precordial leads is usually seen in severe RVH such as in pulmonary stenosis and pulmonary hypertension.

Example #1: (note RAD +105 degrees; RAE; R in V1 > 6 mm; R in aVR > 5 mm)

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 Example #2: (more subtle RVH: note RAD +100 degrees; RAE; Qr complex in V1 rather than qR is atypical)

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 Example #3: (note: RAD +120 degrees, qR in V1; R/S ratio in V6 <1)

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 In the presence of LAE any one of the following suggests this diagnosis:

      R/S ratio in V5 or V6 < 1

S in V5 or V6 > 6 mm

RAD (>90 degrees)

Other suggestive ECG findings:

 Criteria for LVH and RVH both met

LVH criteria met and RAD or RAE present

IX. Myocardial Infarction

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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Topics for study:

     When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with subendocardial or transmural ischemia, followed by necrosis, and eventual fibrosis (scarring) if the blood supply isn’t restored in an appropriate period of time. Rupture of an atherosclerotic plaque followed by acute coronary thrombosis is the usual mechanism of acute MI. The ECG changes reflecting this sequence usually follow a well-known pattern depending on the location and size of the MI. MI’s resulting from total coronary occlusion result in more homogeneous tissue damage and are usually reflected by a Q-wave MI pattern on the ECG. MI’s resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by a non Q-wave MI pattern on the ECG. Two-thirds of MI’s presenting to emergency rooms evolve to non-Q wave MI’s, most having ST segment depression or T wave inversion.

Most MI’s are located in the left ventricle. In the setting of a proximal right coronary artery occlusion, however, up to 50% may also have a component of right ventricular infarction as well. Right-sided chest leads are necessary to recognize RV MI.

In general, the more leads of the 12-lead ECG with MI changes (Q waves and ST elevation), the larger the infarct size and the worse the prognosis. Additional leads on the back, V7-9 (horizontal to V6), may be used to improve the recognition of true posterior MI.

The left anterior descending coronary artery (LAD) and it’s branches usually supply the anterior and anterolateral walls of the left ventricle and the anterior two-thirds of the septum. The left circumflex coronary artery (LCX) and its branches usually supply the posterolateral wall of the left ventricle. The right coronary artery (RCA) supplies the right ventricle, the inferior (diaphragmatic) and true posterior walls of the left ventricle, and the posterior third of the septum. The RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX.

Usual ECG evolution of a Q-wave MI; not all of the following patterns may be seen; the time from onset of MI to the final pattern is quite variable and related to the size of MI, the rapidity of reperfusion (if any), and the location of the MI.

 A. Normal ECG prior to MI

B. Hyperacute T wave changes – increased T wave amplitude and width; may also see ST elevation

C. Marked ST elevation with hyperacute T wave changes (transmural injury)

D. Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis)

 (Pathologic Q waves are usually defined as duration >0.04 s or >25% of R-wave amplitude)

E. Pathologic Q waves, T wave inversion (necrosis and fibrosis)

F. Pathologic Q waves, upright T waves (fibrosis)

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(includes inferior, true posterior, and right ventricular MI’s)

 Inferior MI

 Pathologic Q waves and evolving ST-T changes in leads II, III, aVF

Q waves usually largest in lead III, next largest in lead aVF, and smallest in lead II

Example #1: frontal plane leads with fully evolved inferior MI (note Q-waves, residual ST elevation, and T inversion in II, III, aVF)

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 Example #2: Old inferior MI (note largest Q in lead III, next largest in aVF, and smallest in lead II)

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 True posterior MI

 ECG changes are seen in anterior precordial leads V1-3, but are the mirror image of an anteroseptal MI:

 Increased R wave amplitude and duration (i.e., a “pathologic R wave” is a mirror image of a pathologic Q)

R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)

Hyperacute ST-T wave changes: i.e., ST depression and large, inverted T waves in V1-3

Late normalization of ST-T with symmetrical upright T waves in V1-3

Often seen with inferior MI (i.e., “inferoposterior MI”)

Example #1: Acute inferoposterior MI (note tall R waves V1-3, marked ST depression V1-3, ST elevation in II, III, aVF)

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 Example #2: Old inferoposterior MI (note tall R in V1-3, upright T waves and inferior Q waves)

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 Example #3: Old posterolateral MI (precordial leads): note tall R waves and upright T’s in V1-3, and loss of R in V6

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 Right Ventricular MI (only seen with proximal right coronary occlusion; i.e., with inferior family MI’s)

 ECG findings usually require additional leads on right chest (V1R to V6R, analogous to the left chest leads)

ST elevation, >1mm, in right chest leads, especially V4R (see below)

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 Anteroseptal MI

 Q, QS, or qrS complexes in leads V1-V3 (V4)

Evolving ST-T changes

Example: Fully evolved anteroseptal MI (note QS waves in V1-2, qrS complex in V3, plus ST-T wave changes)

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 Anterior MI (similar changes, but usually V1 is spared; if V4-6 involved call it “anterolateral”)

 Example: Acute anterior or anterolateral MI (note Q’s V2-6 plus hyperacute ST-T changes)

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 High Lateral MI (typical MI features seen in leads I and/or aVL)

 Example: note Q-wave, slight ST elevation, and T inversion in lead aVL

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(Note also the slight U-wave inversion in leads II, III, aVF, V4-6, a strong marker for coronary disease)

 MI + Right Bundle Branch Block

 Usually easy to recognize because Q waves and ST-T changes are not altered by the RBBB

Example #1: Inferior MI + RBBB (note Q’s in II, III, aVF and rSR’ in lead V1)

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 Example #2: Anteroseptal MI with RBBB (note Q’s in leads V1-V3, terminal R wave in V1, fat S wave in V6)

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 MI + Left Bundle Branch Block

 Often a difficult ECG diagnosis because in LBBB the right ventricle is activated first and left ventricular infarct Q waves may not appear at the beginning of the QRS complex (unless the septum is involved).

Suggested ECG features, not all of which are specific for MI include:

 Q waves of any size in two or more of leads I, aVL, V5, or V6 (See below: one of the most reliable signs and probably indicates septal infarction, because the septum is activated early from the right ventricular side in LBBB)

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 Reversal of the usual R wave progression in precordial leads (see above )

Notching of the downstroke of the S wave in precordial leads to the right of the transition zone (i.e., before QRS changes from a predominate S wave complex to a predominate R wave complex); this may be a Q-wave equivalent.

Notching of the upstroke of the S wave in precordial leads to the right of the transition zone (another Q-wave equivalent).

rSR’ complex in leads I, V5 or V6 (the S is a Q-wave equivalent occurring in the middle of the QRS complex)

RS complex in V5-6 rather than the usual monophasic R waves seen in uncomplicated LBBB; (the S is a Q-wave equivalent).

“Primary” ST-T wave changes (i.e., ST-T changes in the same direction as the QRS complex rather than the usual “secondary” ST-T changes seen in uncomplicated LBBB); these changes may reflect an acute, evolving MI.

 Recognized by evolving ST-T changes over time without the formation of pathologic Q waves (in a patient with typical chest pain symptoms and/or elevation in myocardial-specific enzymes)

Although it is tempting to localize the non-Q MI by the particular leads showing ST-T changes, this is probably only valid for the ST segment elevation pattern

Evolving ST-T changes may include any of the following patterns:

 Convex downward ST segment depression only (common)

Convex upwards or straight ST segment elevation only (uncommon)

Symmetrical T wave inversion only (common)

Combinations of above changes

Example: Anterolateral ST-T wave changes

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 These are ECG conditions that mimic myocardial infarction either by simulating pathologic Q or QS waves or mimicking the typical ST-T changes of acute MI.

 WPW preexcitation (negative delta wave may mimic pathologic Q waves)

IHSS (septal hypertrophy may make normal septal Q waves “fatter” thereby mimicking pathologic Q waves)

LVH (may have QS pattern or poor R wave progression in leads V1-3)

RVH (tall R waves in V1 or V2 may mimic true posterior MI)

Complete or incomplete LBBB (QS waves or poor R wave progression in leads V1-3)

Pneumothorax (loss of right precordial R waves)

Pulmonary emphysema and cor pulmonale (loss of R waves V1-3 and/or inferior Q waves with right axis deviation)

Left anterior fascicular block (may see small q-waves in anterior chest leads)

Acute pericarditis (the ST segment elevation may mimic acute transmural injury)

Central nervous system disease (may mimic non-Q wave MI by causing diffuse ST-T wave changes)

 The differential diagnosis of these QRS abnormalities depend on other ECG findings as well as clinical patient information

Poor R Wave Progression – defined as loss of, or no R waves in leads V1-3 (R £2mm):

 Normal variant (if the rest of the ECG is normal)

LVH (look for voltage criteria and ST-T changes of LV “strain”)

Complete or incomplete LBBB (increased QRS duration)

Left anterior fascicular block (should see LAD in frontal plane)

Anterior or anteroseptal MI

Emphysema and COPD (look for R/S ratio in V5-6 <1)

Diffuse infiltrative or myopathic processes

WPW preexcitation (look for delta waves, short PR)

Prominent Anterior Forces – defined as R/S ration >1 in V1 or V2

 Normal variant (if rest of the ECG is normal)

True posterior MI (look for evidence of inferior MI)

RVH (should see RAD in frontal plane and/or P-pulmonale)

Complete or incomplete RBBB (look for rSR’ in V1)

WPW preexcitation (look for delta waves, short PR)

X. ST Segment Abnormalities

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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Topics for study:

     Basic Concept: the specificity of ST-T and U wave abnormalities is provided more by the clinical circumstances in which the ECG changes are found than by the particular changes themselves. Thus the term, nonspecific ST-T wave abnormalities, is frequently used when the clinical data are not available to correlate with the ECG findings. This does not mean that the ECG changes are unimportant! It is the responsibility of the clinician providing care for the patient to ascertain the importance of the ECG findings.

Factors affecting the ST-T and U wave configuration include:

 Intrinsic myocardial disease (e.g., myocarditis, ischemia, infarction, infiltrative or myopathic processes)

Drugs (e.g., digoxin, quinidine, tricyclics, and many others)

Electrolyte abnormalities of potassium, magnesium, calcium

Neurogenic factors (e.g., stroke, hemorrhage, trauma, tumor, etc.)

Metabolic factors (e.g., hypoglycemia, hyperventilation)

Atrial repolarization (e.g., at fast heart rates the atrial T wave may pull down the beginning of the ST segment)

Ventricular conduction abnormalities and rhythms originating in the ventricles

“Secondary” ST-T Wave changes (these are normal ST-T wave changes solely due to alterations in the sequence of ventricular activation)

 ST-T changes seen in bundle branch blocks (generally the ST-T polarity is opposite to the major or terminal deflection of the QRS)

ST-T changes seen in fascicular block

ST-T changes seen in nonspecific IVCD

ST-T changes seen in WPW preexcitation

ST-T changes in PVCs, ventricular arrhythmias, and ventricular paced beats

“Primary” ST-T Wave Abnormalities (ST-T wave changes that are independent of changes in ventricular activation and that may be the result of global or segmental pathologic processes that affect ventricular repolarization)

 Drug effects (e.g., digoxin, quinidine, etc)

Electrolyte abnormalities (e.g., hypokalemia)

Ischemia, infarction, inflammation, etc

Neurogenic effects (e.g., subarrachnoid hemorrhage causing long QT)

 Normal Variant “Early Repolarization” (usually concave upwards, ending with symmetrical, large, upright T waves)

 Example #1: “Early Repolarization”: note high take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal ECG’s; the ST elevation in V2-6 is concave upwards, another characteristic of this normal variant.

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 Ischemic Heart Disease (usually convex upwards, or straightened)

 Acute transmural injury – as in this acute anterior MI

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 Persistent ST elevation after acute MI suggests ventricular aneurysm

ST elevation may also be seen as a manifestation of Prinzmetal’s (variant) angina (coronary artery spasm)

ST elevation during exercise testing suggests extremely tight coronary artery stenosis or spasm (transmural ischemia)

Acute Pericarditis

 Concave upwards ST elevation in most leads except aVR

No reciprocal ST segment depression (except in aVR)

Unlike “early repolarization”, T waves are usually low amplitude, and heart rate is usually increased.

May see PR segment depression, a manifestation of atrial injury

Other Causes:

 Left ventricular hypertrophy (in right precordial leads with large S-waves)

Left bundle branch block (in right precordial leads with large S-waves)

Advanced hyperkalemia

Hypothermia (prominent J-waves or Osborne waves)

 Normal variants or artifacts:

 Pseudo-ST-depression (wandering baseline due to poor skin-electrode contact)

Physiologic J-junctional depression with sinus tachycardia (most likely due to atrial repolarization)

Hyperventilation-induced ST segment depression

Ischemic heart disease

 Subendocardial ischemia (exercise induced or during angina attack – as illustrated below)

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Note: “horizontal” ST depression in lead V6

 ST segment depression is often characterized as “horizontal”, “upsloping”, or “downsloping”

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Note: “Upsloping” ST depression is not an ischemic abnormality

 Non Q-wave MI

Reciprocal changes in acute Q-wave MI (e.g., ST depression in leads I & aVL with acute inferior MI)

Nonischemic causes of ST depression

 RVH (right precordial leads) or LVH (left precordial leads, I, aVL)

Digoxin effect on ECG

Hypokalemia

Mitral valve prolapse (some cases)

CNS disease

Secondary ST segment changes with IV conduction abnormalities (e.g., RBBB, LBBB, WPW, etc)

XI. T Wave Abnormalities

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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The T wave is the most labile wave in the ECG. T wave changes including low-amplitude T waves and abnormally inverted T waves may be the result of many cardiac and non-cardiac conditions. The normal T wave is usually in the same direction as the QRS except in the right precordial leads (see V2 below). Also, the normal T wave is asymmetric with the first half moving more slowly than the second half. In the normal ECG (see below) the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR. The other leads are variable depending on the direction of the QRS and the age of the patient.

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 Q wave and non-Q wave MI (e.g., evolving anteroseptal MI):

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 Myocardial ischemia

Subacute or old pericarditis

Myocarditis

Myocardial contusion (from trauma)

CNS disease causing long QT interval (especially subarrachnoid hemorrhage; see below):

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 Idiopathic apical hypertrophy (a rare form of hypertrophic cardiomyopathy)

Mitral valve prolapse

Digoxin effect

RVH and LVH with “strain” (see below: T wave inversion in leads aVL, V4-6 in LVH)

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XII. Nice Seeing “U” Again

Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine

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The U wave is the only remaining enigma of the ECG, and probably not for long. The origin of the U wave is still in question, although most authorities correlate the U wave with electrophysiologic events called “afterdepolarizations” in the ventricles. These afterdepolarizations can be the source of arrhythmias caused by “triggered automaticity” including torsade de pointes. The normal U wave has the same polarity as the T wave and is usually less than one-third the amplitude of the T wave. U waves are usually best seen in the right precordial leads especially V2 and V3. The normal U wave is asymmetric with the ascending limb moving more rapidly than the descending limb (just the opposite of the normal T wave).

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 Prominent upright U waves

 Sinus bradycardia accentuates the U wave

Hypokalemia (remember the triad of ST segment depression, low amplitude T waves, and prominent U waves)

Quinidine and other type 1A antiarrhythmics

CNS disease with long QT intervals (often the T and U fuse to form a giant “T-U fusion wave”)

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(E.g., lead II, III, V4-6)

 LVH (right precordial leads with deep S waves)

Mitral valve prolapse (some cases)

Hyperthyroidism

Negative or “inverted” U waves

 Ischemic heart disease (often indicating left main or LAD disease)

 Myocardial infarction (in leads with pathologic Q waves)

During episode of acute ischemia (angina or exercise-induced ischemia)

Post extrasystolic in patients with coronary heart disease

During coronary artery spasm (Prinzmetal’s angina)

Nonischemic causes

 Some cases of LVH or RVH (usually in leads with prominent R waves)

Some patients with LQTS (see below: Lead V6 shows giant negative TU fusion wave in patient with LQTS; a prominent upright U wave is seen in Lead V1)

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