Stroke Volume: Normal stroke volume relies on

synchronous electrical stimulation to produce

an efficient pumping action. Rhythms originating

from ventricular foci cause the heart to contract

erratically, which reduces stroke volume and

ultimately lowers cardiac output.

You can use this basic understanding to organize all the

arrhythmias according to each one’s likelihood of causing

symptoms and therefore needing treatment. One such organizational scheme is called the Matrix of Clinical Impact, which

uses the two variables of Rate and Pacemaker Site (Figure B1).

Each of the basic arrhythmias is placed in its appropriate place on the matrix. They can then be clustered according to their threat to cardiac output. The three areas known

to produce symptoms are Bradycardias, Tachycardias, and

Ventricular Irritability.

Symptoms of Impaired Cardiac

Output

When cardiac output is diminished, it produces symptoms

in the patient. Regardless of which arrhythmia is causing

the problem, the symptoms of reduced cardiac output are

the same. These symptoms can include:

• Anxiety

• Chest pain

• Shortness of breath

• Diaphoresis

• Hypotension

• Cool, clammy skin

• Cyanosis

• Decreased consciousness

These symptoms are indications that cardiac output

is inadequate to perfuse body tissues. When you see these

symptoms, you know that perfusion is impaired and the

arrhythmia should be treated.

Treating Arrhythmias

ACLS Recommendations

The American Heart Association’s Advanced Cardiac Life

Support (ACLS) recommendations are the recognized standard

for treatment of arrhythmias associated with cardiac events

such as acute myocardial infarction and cardiac arrest. The

ACLS guidelines are prepared and kept current by leading

researchers and clinicians to provide detailed considerations

for management of all aspects surrounding treatment

of arrhythmias. The ACLS standards are published and

updated regularly and should be used as the guide for clinical

management of arrhythmias. The material presented here is an

introductory overview of management principles and should

not be used to direct clinical treatment.

General Treatment Principles

Arrhythmias are treated when they cause (or are likely to

cause) clinical symptoms. All patients with arrhythmias

or the potential for them should be monitored and receive

oxygen and a keep-open IV as a precaution. If arrhythmias

do occur, the patient’s various perfusion parameters (blood

pressure, pulses, skin, etc.) should be assessed to determine

impact on cardiac output. When arrhythmias cause symptoms, treatment should be initiated immediately.

Support Perfusion

In addition to treating the specific presenting arrhythmia, it

may be necessary to provide general supportive measures such

as ventilation to improve oxygenation, chest compression to

maintain circulation, and drugs to stabilize blood pressure.

Look for Correctable Underlying

Conditions

To enhance conversion of an arrhythmia, any contributing

conditions should be identified and corrected: bicarbonate

if the patient is acidotic, fluids if hypovolemic, oxygen if

hypoxic, and so on.

464 Appendix B

Figure B1 Matrix of Clinical Impact

Bradycardia Normal Tachycardia

RATE

Sinus Tachycardia

Atrial

Tachycardia

PACs

PJCs

Junctional

Tachycardia

Sinus Atrial Junctional

Junctional

Escape

Rhythm

Third-Degree

Heart Block

Idioventricular

Rhythm

Asystole

Supraventricular Ventricular

PACEMAKER SITE

BRADYCARDIAS & TACHYCARDIAS

Rates too fast or slow

VENTRICULAR IRRITABILITY

Causes inecient pumping

PVCs

Ventricular Tachycardia

Ventricular Fibrillation

Sinus Bradycardia

Sinus Arrhythmia

Wandering Pacemaker

Atrial Flutter

Atrial Fibrillation

Accelerated Junctional Rhythm

First-Degree Heart Block

Second-Degree Heart Block

Wenckebach

Normal Sinus Rhythm

Treatment Concepts

The old adage in electrocardiography is that you do not treat

rhythms, you treat patients. As you can see in Figure B1,

many arrhythmias produce no symptoms in the patient.

These rhythms do not require treatment, though they may

bear watching.

Treat the three groups that are likely to cause symptoms by removing the threat to cardiac output, as shown in

Figure B2.

The likelihood of any given arrhythmia producing

symptoms or causing clinical concerns depends on both rate

and pacemaker site. The expected significance and clinical

picture of each of the arrhythmias is shown in Figure B3.

Pathophysiology and Clinical Implications of Arrhythmias 465

Figure B2 Treatment Concepts

Rhythm Concept Treatment Goals

Tachycardias Heart rate is too fast to allow the ventricles to fill completely

before contraction.

• Slow the heart rate.

Bradycardias Heart rate is too slow to maintain cardiac output. • Speed up heart rate.

• When bradycardia is caused by block at the AV

node, the goal is to increase conduction through the

junction.

Ventricular Irritability Erratic ventricular contraction is not effective enough to

maintain stroke volume.

• Suppress irritable focus.

Figure B3 Arrhythmia Significance and Clinical Picture

Arrhythmia Significance Clinical Picture

NSR • Normal cardiac pattern • Does not produce symptoms

Sinus Bradycardia • Can reflect a normal, athletic heart

• Can precede blocks or Asystole

• Can precipitate escape rhythms or ventricular irritability

• Can be caused by AMI, vagal stimulation, increased

intracranial pressure

• Slow, regular pulse

• Can cause signs/symptoms of decreased cardiac

output

Sinus Tachycardia • Usually a compensatory response to fever, activity, pain,

anxiety, hypovolemia, heart failure, etc.

• Dangerous in AMI (can extend infarct)

• Rapid, regular pulse

• Probably asymptomatic

• Possibly palpitations, dyspnea

Sinus Arrhythmia • Common in children and young adults • Irregular pulse

• Rarely causes symptoms

Premature Atrial Complex • Usually benign

• Can be early sign of CHF

• Can lead to atrial tachyarrhythmias

• Causes include fatigue, hypoxia, dig-toxicity, caffeine,

ischemia, CHF, alcohol

• Irregular pulse

• Rarely causes symptoms

Wandering Pacemaker • Normal; often seen in very old, very young, or in athletes

• Persistence of junctional rhythm can indicate heart

disease

• Rarely causes symptoms

Atrial Tachycardia • Very dangerous in AMI or heart disease

• Commonly caused by dig-toxicity

• Rapid, regular pulse

• May show signs/symptoms of drop in cardiac output

• Can cause pulmonary edema, CHF, shock

Atrial Flutter • Rapid ventricular rate and loss of atrial kick can drop

cardiac output

• Risk of pulmonary and cerebral emboli

• Can cause CHF or myocardial ischemia

• Seen in CAD, rheumatic heart disease

• Pulse can be regular or irregular, fast or slow

• Rapid ventricular rate can cause signs/symptoms of

low cardiac output

Atrial Fibrillation • Very rapid rate can lead to CHF or myocardial ischemia

• Threat of pulmonary or cerebral emboli

• Commonly caused by dig-toxicity

• Irregular pulse, can be fast or slow

• Can have pulse deficit

• Can cause signs/symptoms of low cardiac output

Premature Junctional Complex • May precede AV block • Rarely causes signs/symptoms

Junctional Escape Rhythm • Failsafe mechanism

• Can be normal, as with athletes

• Slow pulse

• If rate is slow enough, can cause signs/symptoms of

low cardiac output

Accelerated Junctional Rhythm • Indicates irritable junction overriding normal pacemaker

• Often caused by AMI, open-heart surgery, myocarditis,

dig-toxicity

• Usually asymptomatic

Junctional Tachycardia • Indicates irritable junction overriding normal pacemaker

• Often caused by AMI, open-heart surgery, myocarditis,

dig-toxicity

• Rapid, regular pulse

• Can cause signs/symptoms of low cardiac output

First-Degree Heart Block • Can be caused by anoxia, ischemia, AV node

malfunction, edema following open-heart surgery,

dig-toxicity

• Can lead to more serious AV block

• Usually asymptomatic

Second-Degree Heart Block Type I

Wenckebach

• Common following inferior MI

• Can progress to more serious AV block

• Irregular pulse

• Usually asymptomatic

Second-Degree Heart Block Type II • Can be caused by anoxia, edema after open-heart

surgery, dig-toxicity, hyperkalemia, anterior MI

• Slow rate can cause signs/symptoms of low cardiac

output

466 Appendix B

Arrhythmia Significance Clinical Picture

Third-Degree Heart Block • Can progress to ventricular standstill • Very slow rate and abnormal pacemaker site

severely impair cardiac output

• Patients will frequently be unconscious from poor

perfusion

• Cardiac failure can follow quickly

Premature Ventricular Complex • Indicates ventricular irritability; increasing frequency

indicates increasing irritability

• Causes include ischemia/infarction, hypoxia, acidosis,

hypovolemia, electrolyte imbalance, caffeine, smoking,

alcohol

• PVCs considered to be extremely dangerous include:

—frequent, or increasing in frequency

—patterns (bigeminy, trigeminy, etc.)

—couplets

—runs

—R on T phenomenon

—multifocal

• Patients may feel PVCs and be distressed by them

• Pulse is irregular

• Perfusion is generally not impaired unless PVCs

become frequent

• Many adults have chronic PVCs from underlying

respiratory disease, smoking, caffeine, etc.

Ventricular Tachycardia • Can quickly progress to Ventricular Fibrillation • Patient will begin to lose consciousness as perfusion

drops

Ventricular Fibrillation • Lethal arrhythmia

• Indicative of extreme myocardial irritability

• Patient is clinically dead

Idioventricular Rhythm • Carries poor prognosis

• Often associated with large MI and damage to large

amount of ventricular muscle mass

• Patient is clinically dead

Asystole • Carries very poor prognosis

• Often seen after patient has been in arrest for some time

• Patient is clinically dead

Figure B3 (Continued)

467

Overview

IN THIS APPENDIX, you will learn how 12-lead EKGs are different from the basic arrhythmias

you learned in the first part of the book, and you will learn the uses and limitations of a 12-lead

EKG. You will learn the fundamental rules of electrocardiography, leads, and electrode placement.

Then you will explore vectors, vector relationships, and axis. Finally, you will learn the standardized

format for a printed 12-lead EKG. In general, you will learn everything you need to know to

understand what you are looking at when you first approach a 12-lead EKG.

12-Lead

Electrocardiography

Appendix C

468 Appendix C

The rhythm strips that you studied in the first part of

this book were single-lead strips. They all showed cardiac

activity from one angle (Lead II). A single-lead strip provides

enough information to analyze rate, determine pacemaker

control, identify conduction problems, and, ultimately,

to identify threats to perfusion.

A 12-lead EKG gives you twelve short strips, allowing

you to view electrical activity in the heart from twelve different

directions, both top to bottom and front to back. The added

angles provide a more complete picture of cardiac function.

In addition to information from the rhythm strip, the 12-lead

EKG enables you to locate tissue damage caused by myocardial

hypoxia and to determine whether the chambers are abnormally

enlarged as a result of valve problems or pulmonary disease.

It also provides more detailed information about conduction,

such as which branches of the conduction system are blocked

or whether the entire electrical flow is slightly off kilter, and it

can reveal certain metabolic and chemical abnormalities.

That much information packed into a single-page report

can be intimidating at first glance. But so was this book when

you first opened it, and by now you’re probably quite comfortable with rhythm strips. The same will happen with 12-lead

EKGs. Just take one step at a time. Don’t try to go from A to Z

in the first sitting. This appendix will take you from A to B, or

maybe C. From there, you can keep adding information from a

variety of sources until you have all the knowledge you want.

Fundamental Rules of

Electrocardiography

As you learn about 12-lead EKGs, remember the fundamental rules that apply to all tracings produced by EKG

machines:

• Current flowing toward a positive electrode creates an

upright deflection; current flowing away from a positive

electrode creates a downward deflection.

• Current flowing toward a negative electrode creates a

downward deflection; current flowing away from a

negative electrode creates an upright deflection.

• When the lead that detects the current is at right

angles (perpendicular) to the current, the line will be

isoelectric—that is, neither upright nor downward.

Leads and Electrode

Placement

Single-Lead Rhythm Strips

A lead is a combination of electrodes that reflects the flow of

electricity between two points on opposing sides of the heart.

Some leads have one positive and one negative electrode,

making them bipolar leads. Other leads have a single

positive electrode, but the opposing electrode is created

by combining other electrodes into a central terminal, an

electrically neutral point situated to reference the center of

the heart. Since only the positive electrode is polarized, these

leads are considered unipolar leads.

Regardless of whether a lead is unipolar or bipolar,

it provides information only in one dimension: it shows

only the view of the heart as seen between two points.

Many times, a single perspective is sufficient. It can tell you

whether the heart is beating, and, if so, you can identify the

underlying rate and rhythm. A single lead used for this purpose is called a monitoring lead.

When monitoring is all that’s needed, it is usually done

in Lead II. Lead II is also the most common lead used as the

rhythm strip on a 12-lead EKG.

Another popular monitoring lead is called Modified

Chest Left, or MCL . 1 MCL1 is a bipolar lead that can be

useful in differentiating rhythms with broad QRS complexes.

MCL1 requires different electrode positioning than Lead II:

the negative electrode goes on the left upper chest, with

the positive electrode at the right side of the sternum in the

fourth intercostal space (Figure C1). MCL1 is not included

on standard 12-lead EKGs.

Multiple Lead Recordings

You can learn more about the heart’s electrical function

by using multiple leads, each one providing a view that is

slightly different from other leads. By carefully positioning

electrodes on the skin over various areas of the heart, you

can see a more thorough picture of cardiac electrical activity.

Practically speaking, there are two dimensions in which

electrodes can be placed: up and down across the frontal

plane of the body and around the chest on the horizontal

plane (Figure C2). A standardized format has been developed that places six leads on each of these two planes,

Figure C1 Electrode Placement for MCL1

–

G

+

12-Lead Electrocardiography 469

Figure C2 Frontal and Horizontal Planes

Figure C3 Electrode Placement, Frontal Plane

RA LA

RL LL

Figure C4 The Standard Limb Leads

RA LA

LL

Figure C5 The Augmented Leads

RA LA

LL

aVR aVL

aVF

CT

thereby providing information from a total of twelve different angles. This conventional record is called a 12-lead

EKG. Once electrodes are placed in the standard locations,

the machine automatically measures flow between the electrodes needed to produce the desired lead.

Frontal Plane Leads

Four limb electrodes are used to view the frontal plane: right

arm (RA), left arm (LA), left leg (LL), and right leg (RL). The

limb electrodes are often placed on the anterior chest wall

(rather than limbs), both for convenience and in hopes of

reducing movement artifact (Figure C3).

These electrodes are used to produce the Standard Limb

Leads: I, II, and III (Figure C4). All of these are bipolar leads,

meaning they use both a positive and a negative electrode.

They view electrical flow as follows:

Lead I: right arm to left arm

Lead II: right arm to left leg

Lead III: left arm to left leg

The equilateral triangle formed by the standard limb

leads is called Einthoven’s Triangle.

By using a central terminal, it is possible to create three

more frontal leads, called Augmented Leads: augmented

voltage right arm (aVR), augmented voltage left arm (aVL),

and augmented voltage left leg (aVF) (Figure C5). (Note: The

F in aVF is for “foot,” to avoid confusion with aVL.)

The augmented leads are unipolar; they measure information from the central terminal to a positive electrode.

They view electrical flow as follows:

aVR: central terminal to right arm

aVL: central terminal to left arm

aVF: central terminal to left leg

The three standard limb leads and the three augmented

leads all view the heart from the frontal plane (Figure C6).

Horizontal Plane Leads

To visualize electrical flow on a horizontal plane (i.e., around

the circumference of the chest) we use additional electrodes

to create six more leads. These leads are called chest leads,

or Precordial leads (Figure C7).

Six different positive electrodes are used to produce

the six precordial leads. The leads are obtained by pairing

each positive electrode with the electrically neutral central terminal composed of the combined limb electrodes.

470 Appendix C

Thus, the precordial leads are unipolar, and they view current

flowing from the heart toward the chest wall.

To ensure accurate readings of chest leads, the precordial electrodes must be placed with care. The standardized

locations for the precordial electrodes are as follows:

V1: Right sternal border, fourth intercostal space

V2: Left sternal border, fourth intercostal space

V3: Midway between V2 and V4

V4: Midclavicular line, fifth intercostal space

V5: Anterior axillary line, fifth intercostal space

V6: Midaxillary line, fifth intercostal space

The six chest leads can be localized to provide information about specific areas of the heart: V1 and V2 view the

septum, V3 and V4 view the anterior myocardial wall, and

the lateral myocardial wall is reflected in V5 and V . 6

The precordial leads provide information on the horizontal plane. When combined with the leads of the frontal

plane, we see a more detailed view of the heart’s electrical

activity.

Vectors and Axis

Electrical Flow through the Heart

We think of the heart as having a single electrical flow that

goes roughly from the sinus node down toward the apex.

We’ve used large arrows to show how the direction of flow

changes slightly with rhythm changes. For example, with

junctional rhythms, the retrograde flow is shown by one

arrow from the AV junction up toward the sinus node, while

Figure C6 Frontal Plane Leads

Lead Lead Lead

Lead aVR Lead aVL Lead aVF

aVR aVL aVF

–

+

+ +

+ –

+

–

CT CT

+

CT

12-Lead Electrocardiography 471

Figure C7 Horizontal Plane Leads

V6

V5

V1

V4

V2

V3

a second arrow goes from the AV junction down through

the ventricles. These arrows are called vectors. They are

used to depict the direction of flow, with the point of the

arrow indicating the positive electrode. Vectors also indicate

magnitude; the larger the arrow, the greater the amplitude

of the flow.

There is one slight problem with our thinking at this

point. The heart doesn’t depolarize as a single event.

During each cardiac cycle, every depolarizing myocardial

cell generates its own current moving in all directions at once

and continuously changing direction. Each of these countless electrical currents has its own small vector showing its

magnitude and direction of flow. The much larger vector

we’re used to seeing is actually a combined vector of all

these various currents.

This larger, aggregate vector is called the axis, or the

sum direction of electrical flow. The axis of the heart as

a whole is called the mean QRS axis. The mean QRS

axis shows the overall direction of flow within the heart.

In a normal heart, the depolarization wave of the right

ventricle proceeds down and to the right. The much larger

left ventricle produces a stronger vector that goes down

and to the left. Thus, the combined vector of both ventricles,

the mean QRS axis, flows down and to the left, reflecting the

left ventricle’s larger muscle mass.

Lead Axis

Each lead also has its own axis. All the leads detect current

between two points on opposing sides of the heart. An

imaginary line between these two points is called the axis

of the lead. The axis of each lead is shown by an arrow,

or vector, drawn from its negative electrode (or a central

terminal) to its positive electrode.

The lead vectors are the physiologic basis for interpreting 12-lead EKGs. In a rhythm strip, you look at the wave

patterns and work backward to determine what went on

in the heart. The rules you use to draw your conclusions

are based on a single lead, Lead II, in which the vector

goes from the right atrium to the left ventricle. When the

P wave is inverted, you conclude that the vector was going

the wrong direction; thus, the impulse originated in the AV

junction.

The same principle applies when interpreting 12-lead

EKGs, except that now you will compare direction of flow

for electrodes placed in twelve different places, reflecting

472 Appendix C

twelve different lead vectors. Begin by learning how the

vectors of each lead relate to the others and to the vector of

the heart as a whole.

Interpretation of EKG Deflections

The heart’s current will cause deflections on the EKG according to the relationship between the lead’s axis and the heart’s

mean QRS axis (Figure C8).

• Complexes are most positive when lead axis and QRS

axis are parallel (or most negative if the current flows

toward the negative electrode).

• When lead axis and QRS axis are perpendicular, each

complex will be both upright and inverted (biphasic,

or equiphasic).

As depolarization spreads through the ventricles, the

changing vectors produce a QRS wave form reflecting the

axis of the particular lead in which it is viewed. The 12-lead

EKG displays the heart’s mean axis from twelve different

angles. Thus, the individual wave configurations will normally vary from one lead to the next. Before exploring these

differences, we must first review terms used to define some

of the specific waves and measurements (Figure C9).

Figure C8 EKG Deflections

–

An equiphasic deflection (equally positive and

negative) is produced when the lead axis is

perpendicular to the heart’s mean QRS axis.

The deepest negative deflection

is created when the lead axis is

parallel to the mean QRS axis and

current is flowing away from that

lead’s positive electrode.

The tallest positive deflection is

created when the lead axis is

parallel to the mean QRS axis

and current is flowing toward that

lead’s positive electrode.

+

Figure C9 Wave Definitions

R R R R

R´ R´

Q S Q S Q S QS

Intrinsicoid

Deflection

J Point

QT

Interval

12-Lead Electrocardiography 473

R Waves: All positive deflections within the QRS

complex are R waves.

If there are two R waves in the same complex, the

second is named prime (R′). Two R waves in the same

complex without an intervening S wave produce a pattern that is technically an RR′, though it is most commonly called a notched R wave, or “rabbit ears.”

NOTE: It is common to use upper and lowercase

letters to indicate the relative size of waves: uppercase

denotes large waves, while small waves are indicated

by lowercase. Thus, qRSr′ would indicate a small

Q wave, large initial R wave, large S wave, and small

second R wave. Many combinations are possible:

qR, Rs, rSR′, etc. For our purposes, we will use only

uppercase letters.

Q Waves: A negative deflection before the R wave is a Q.

S Waves: A negative deflection following an R wave is

an S.

QS Waves: If there is no R wave, the combined negative

deflection is a QS.

Intrinsicoid Deflection: This reflects the time it takes

for peak voltage to develop within the ventricles.

It is measured from the onset of the QRS to the peak

of the R wave. A prolonged intrinsicoid deflection

(> 0.06 second) is considered a “late R wave.”

J Point: This is the demarcation between the end of the

QRS complex and the beginning of the ST segment.

QT Interval: This reflects the total duration of

ventricular depolarization and repolarization. It is

measured from the beginning of the QRS complex

to the end of the T wave. The QT interval varies

with heart rate.

The presence or absence of individual wave forms is

determined by the vectors produced within the heart, relative to the axis of the lead being viewed.

Vector Relationships

Since the goal is to compare each lead’s axis to that of the

heart’s mean axis, we need to give them all a common reference point. We can do this by drawing a circle, with the

center being the AV node. For each lead, draw an arrow

from the center of the circle to that lead’s positive electrode. You will find that the vectors cross the perimeter of

the circle in increments of 30 degrees. Each arrow shows

the angle the vector has in its lead; thus, the vectors are

shown in relation to the heart and can be quantified in

terms of degrees. The first six leads show the vectors of the

frontal plane (Figure C10). The vectors of the six V leads,

showing the horizontal plane, can be similarly illustrated

(Figure C11).

Axis Deviation

This same format can be used to quantify the mean QRS

axis, the aggregate flow of electrical current through

the heart (Figure  C12). By dividing the circle into four

quadrants, we see that the QRS axis normally falls in the

lower right quadrant, between 0° and +90°. When the

heart is damaged, displaced, or enlarged, the electrical

flow changes, shifting the mean QRS axis. When the vector

shifts beyond the boundaries of normal, it is called axis

deviation. Axis deviation can be found in normal EKGs, or

it can be associated with myocardial infarction, ventricular

hypertrophy, or ventricular conduction defect.

Figure C10 Frontal Plane Vectors

–90°

–60°

–30°

+150° +30°

+120° +60°

–150°

–120°

+90°

+/–180° +/–0°

aVF

aVR aVL

474 Appendix C

Figure C11 Horizontal Plane Vectors

Spine

Right

Ventricle

Sternum

Left Ventricle

+120° +90° +75° +60°

+30°

+/–0°

V6

V5

V2 V3 V4 V1

Figure C12 Mean QRS Axis

–90°

–60°

–30°

+150° +30°

+120° +60°

–150°

–120°

+90°

+/–180° 0°

Extreme

Right Axis

Deviation

Left Axis

Deviation

Right Axis

Deviation

Normal

Axis

A shift in vector to the patient’s left (0° to −90° on the

circle) is called left axis deviation and can be associated

with left ventricular hypertrophy, hypertension, aortic stenosis, and other disorders affecting the left ventricle. When

the vector shifts to the patient’s right (+90° to +180°), it is

called right axis deviation and is suggestive of problems

in the right heart and pulmonary system. The upper left

quadrant, between + −/ 180° and −90°, is considered

extreme right axis deviation, or indeterminate axis.

Estimating QRS Axis

Understanding normal QRS axis, and recognizing abnormal deviations, is essential to accurate interpretation of

12-Lead Electrocardiography 475

lead vectors. However, the information gleaned from axis

analysis can be quite esoteric and can sidetrack you from

some of the more practical elements of basic 12-lead EKG

interpretation. For this reason, axis calculation has been

greatly simplified here.

A quick method for estimating axis relies on evaluating

leads I and aVF. In both these leads, the QRS complex is

normally upright. Axis deviation is indicated when the QRS

complex in either or both of these leads is negative—that

is, where the sum of the individual Q, R, and S waves is not

positive (Figure C13).

Standardized 12-Lead

EKG Format

Most 12-lead EKGs are printed in a standard format that

prints patient identifying information, computer measurements, and preliminary interpretations across the top,

followed by about 3 seconds of each lead. Any effort to

analyze a 12-lead EKG must necessarily begin with locating

lead layout. The transition between leads is often obscure,

so you won’t know what you’re looking at unless you know

the standard layout (Figure C14).

The standard layout places the twelve leads in four

columns of three rows each. Starting at the upper left,

you’ll read top to bottom, left to right. Column one holds

leads I, II, and III, and column two holds aVR, aVL, and

aVF. The V leads are in the last two columns; column three

holds V , 1 V ,2 and V , 3 and you’ll find V , 4 V , 5 and V6 in the

last column.

The last thing you see is a rhythm strip, usually lead II,

running across the bottom of the page. However, it is increasingly common to find the rhythm strip run in leads I, II,

and III simultaneously, occupying an entire second page of

the report.

Normal 12-Lead EKG

Before you can recognize abnormalities, you must first learn

to recognize normal. Because each lead has its own axis,

which may or may not align with the mean QRS axis, you

should expect to see a wide range of complexes from lead

to lead. A wave form that is normal for one lead could be

abnormal in another. The better you understand the electrical forces that produced the waves, the better you will

be able to remember what each lead normally looks like

(Figure C15).

Figure C13 Estimating QRS Axis

–90°

+90°

–/+180° 0°

EXTREME RIGHT

axis deviation produces

complexes that are negative

in both and aVF

LEFT

axis deviation produces

complexes that are negative

in aVF and upright in lead

RIGHT

axis deviation produces

complexes that are negative

in lead and upright in aVF

NORMAL

axis produces upright

complexes in both and aVF

QRS complexes are normally upright

in leads and aVF.

If the sum of deflections is negative

in either or both of these leads, axis

deviation is suggested.

aVF

aVF

ESTIMATING

QRS AXIS

476 Appendix C

Figure C14 Standard Layout of 12-Lead EKG

Patient Information: (Name, Date, Identifying Information, Computer Measurements, Interpretations)

hift in vector to the patient’s left (0° to −90° on the

circle) is called left axis deviation and can be associated

with left ventricular hypertrophy, hypertension, aortic stenosis, and other disorders affecting the left ventricle. When

the vector shifts to the patient’s right (+90° to +180°), it is

called right axis deviation and is suggestive of problems

in the right heart and pulmonary system. The upper left

quadrant, between + −/ 180° and −90°, is considered

extreme right axis deviation, or indeterminate axis.

Estimating QRS Axis

Understanding normal QRS axis, and recognizing abnormal deviations, is essential to accurate interpretation of

12-Lead Electrocardiography 475

lead vectors. However, the information gleaned from axis

analysis can be quite esoteric and can sidetrack you from

some of the more practical elements of basic 12-lead EKG

interpretation. For this reason, axis calculation has been

greatly simplified here.

A quick method for estimating axis relies on evaluating

leads I and aVF. In both these leads, the QRS complex is

normally upright. Axis deviation is indicated when the QRS

complex in either or both of these leads is negative—that

is, where the sum of the individual Q, R, and S waves is not

positive (Figure C13).

Standardized 12-Lead

EKG Format

Most 12-lead EKGs are printed in a standard format that

prints patient identifying information, computer measurements, and preliminary interpretations across the top,

followed by about 3 seconds of each lead. Any effort to

analyze a 12-lead EKG must necessarily begin with locating

lead layout. The transition between leads is often obscure,

so you won’t know what you’re looking at unless you know

the standard layout (Figure C14).

The standard layout places the twelve leads in four

columns of three rows each. Starting at the upper left,

you’ll read top to bottom, left to right. Column one holds

leads I, II, and III, and column two holds aVR, aVL, and

aVF. The V leads are in the last two columns; column three

holds V , 1 V ,2 and V , 3 and you’ll find V , 4 V , 5 and V6 in the

last column.

The last thing you see is a rhythm strip, usually lead II,

running across the bottom of the page. However, it is increasingly common to find the rhythm strip run in leads I, II,

and III simultaneously, occupying an entire second page of

the report.

Normal 12-Lead EKG

Before you can recognize abnormalities, you must first learn

to recognize normal. Because each lead has its own axis,

which may or may not align with the mean QRS axis, you

should expect to see a wide range of complexes from lead

to lead. A wave form that is normal for one lead could be

abnormal in another. The better you understand the electrical forces that produced the waves, the better you will

be able to remember what each lead normally looks like

(Figure C15).

Figure C13 Estimating QRS Axis

–90°

+90°

–/+180° 0°

EXTREME RIGHT

axis deviation produces

complexes that are negative

in both and aVF

LEFT

axis deviation produces

complexes that are negative

in aVF and upright in lead

RIGHT

axis deviation produces

complexes that are negative

in lead and upright in aVF

NORMAL

axis produces upright

complexes in both and aVF

QRS complexes are normally upright

in leads and aVF.

If the sum of deflections is negative

in either or both of these leads, axis

deviation is suggested.

aVF

aVF

ESTIMATING

QRS AXIS

476 Appendix C

Figure C14 Standard Layout of 12-Lead EKG

Patient Information: (Name, Date, Identifying Information, Computer Measurements, Interpretations)

III aVF V3 V6

Rhythm Strip

aVR V1 V4

II aVL V2 V5

I

Use the tracing in Figure  C15, along with its definition of features, to analyze the two normal tracings

in Figures C16 and C17. You may want to refer to these

“normal” EKGs as you explore the abnormalities discussed

in Appendix D.

Limitations of 12-Lead EKGs

Twelve-lead EKGs share two distinct limitations with singlelead rhythm strips:

1. They are representations of electrical activity. They provide information about the heart’s electrical status but

can’t tell us how the heart’s mechanical pump is functioning. Of course, we can draw conclusions when the

electrical patterns are clearly inadequate to produce

mechanical response.

2. They show us what happened when the recording was

made, but they don’t show what the heart did 5 minutes

later, and they can’t predict what it will do tomorrow.

Again, we can make some assumptions based on the

physiology underlying the electrical patterns.

The 12-lead EKG can provide more information about

cardiac activity than is possible with a single monitoring

strip. However, with 12-lead EKGs as well as rhythm strips

and all other diagnostic tools, it is important to assess the

patient and consider the context of current and previous

clinical circumstances. It is always the patient who receives

the treatment, not the EKG.

12-Lead Electrocardiography 477

Figure C15 Features of a Normal 12-Lead EKG

I

II

III

aVR

aVL

aVF

V1 V4

V5

V6

V2

V3

UPRIGHT COMPLEXES

•

•

TRANSITION

•

•

•

•

Q WAVES

•

PRECORDIAL T WAVES

•

•

All waves (P, QRS, and

T) are normally upright

in lead II.

Only in aVR is it normal

for the complexes to be

inverted.

Progressing from V1 to V6, the amplitude of R waves should increase, and the amplitude of S waves

should decrease.

In V1 you should see a small R and a large S.

In V6 you should see a small Q and a large R.

In V3 (or V4) the R and S waves should be approximately equal size (equiphasic).

Small Q waves are normal in the lateral leads

(I, aVL, V6).

V1 classically has a

small R wave and a

deeper S wave; the T

wave can be positive,

negative, or biphasic.

In V2 –V6 the T wave

should be positive; the

up-slope should be

smooth and gradual

(sharp angles are abnormal), and the downslope is slightly more

abrupt.

478 Appendix C

Figure C16 Normal 12-Lead Wave Forms—Example #1

aVR V1 V4

II aVL V2 V5

III aVF V3 V6

I

II

12-Lead Electrocardiography 479

Figure C17 Normal 12-Lead Wave Forms—Example #2

aVR V1 V4

II aVL V2 V5

III aVF V3 V6

I

II

480

Overview

IN THIS APPENDIX, you will begin to analyze and interpret what you see on a 12-lead EKG. You

will learn to recognize EKG changes caused by myocardial damage, chamber enlargement, bundle

branch block, and various other conditions such as pericarditis, digitalis toxicity, and abnormal

calcium or potassium levels. You will learn a methodical format for analyzing 12-lead EKGs.

Basic 12-Lead

Interpretation

Appendix D

From Appendix  C you know that the 12-lead EKG

provides information about cardiac rhythm and mean QRS

axis. The 12-lead EKG is also used routinely for a range

of other information. In this appendix, you will learn to

interpret a 12-lead EKG to determine all of the following:

• Myocardial Damage: age, extent, and location of

damage

• Bundle Branch Block: which branches of the ventricular

conduction system are blocked

• Chamber Enlargement: caused by dilation or

hypertrophy

• Miscellaneous Effects: drugs, electrolytes, pericarditis

Basic 12-Lead Interpretation 481

Figure D1 Grades of Myocardial Damage

Infarction

Ischemia

Injury

Figure D2 Extent of Infarction

Subendocardial

Partial thickness of Myocardium

Transmural

Full thickness of Myocardium

Myocardial Damage

Extent of Injury

When blood flow is obstructed within a coronary artery, the

portion of myocardial wall that was fed by the obstructed

vessel is deprived of oxygen and begins to die. The initial

lack of oxygen is called ischemia, and if allowed to continue,

it causes injury to the myocardium. If untreated, the tissues

eventually die completely—a condition called myocardial

infarction (Figure D1).

When the area of infarction extends completely

through the wall of the ventricle, the infarction is called

transmural. The term subendocardial has been used to

describe infarctions that extend only partially through the

wall (Figure D2).

Ischemic Changes on the EKG

The effects of ischemia appear on the EKG as changes in

Q waves, ST segments, and T waves as outlined below:

ST Segment: • depression

• elevation

T Wave: • peaking

• flattening

• inversion

Q Wave: • deepening and widening of Q waves

• loss of R wave resulting in deep

QS wave

These changes are considered ischemic changes and are

indicative of myocardial damage. They can be found alone or,

more commonly, in combination with one another to

produce a variety of patterns (Figure D3).

In infarctions that are limited to partial wall thickness

(subendocardial infarctions), the damage may be insufficient

to produce classically abnormal Q waves. For this reason, you

may see subendocardial infarctions referred to as “non-Q”

infarctions. In such situations the Q wave is not a diagnostic

feature.

Evolution of Ischemic Changes

Ischemic changes are the result of abnormal depolarization

around the area of damage. As the damage evolves, the

482 Appendix D Figure D3 Ischemic Changes

ST SEGMENT ST Elevation ST Depression

T WAVE Tall, Peaked T Wave Inverted T Wave

Q WAVE Deep Q Wave (with inverted T wave) Deep Q Wave (with loss of R wave) Q wave changes are not diagnostic in non-Q infarctions

Basic 12-Lead Interpretation 483

EKG continues to change (Figure D4). Thus, the EKG picture

will change over time and may show any combination of

these changes depending on when the tracing was made.

Generally speaking, the changes evolve as follows:

First Hours: Almost immediately, the ST segment

rises, and the T wave becomes more prominent; it

may be tall, peaked, or possibly inverted. You may

also see an increase in R wave amplitude.

First Day: Over the course of the first day or two, the

R wave begins to diminish, while the Q wave

becomes deeper and wider. The ST segment

elevation may increase. The T wave can be

upright, flattened, or inverted, but it usually

becomes less prominent.

First Week: Within a week or so, the ST segment

begins returning to normal, though the T wave

can remain inverted, upright, or flat. The most

prominent feature at this point is loss of the

R wave, resulting in a deep QS wave.

Months Later: Weeks or months later, the ST segment

returns to normal, though T wave abnormalities

can persist. The R wave may return partially, but

the Q wave often remains a permanent feature of

the EKG.

Infarction Location

Most infarctions cause damage to one or more walls of the

left ventricle. Abnormal depolarization in the damaged area

will cause ischemic changes in the leads directly over that

heart surface. Leads that correlate with myocardial surfaces

are called facing leads. By isolating ischemic changes in

facing leads, we can localize the area of damage.

Figure D4 Age of Infarction (Transmural MI)

FIRST HOURS

•

•

•

Tall, peaked, or inverted

T wave

Onset of ST elevation

Increased amplitude of

R wave

FIRST DAY

•

•

•

•

ST elevation

T wave is smaller

R wave begins to

diminish

Q wave begins to

deepen and widen

FIRST WEEK

•

•

•

ST begins returning

to normal

T wave can invert

Loss of R wave creates

deep QS wave

MONTHS LATER

•

•

•

•

Normal ST segment

T wave may remain

inverted

Partial R wave may

return

Q wave usually remains

484 Appendix D

The three heart surfaces most commonly damaged

by infarction are the anterior, lateral, and inferior walls

(Figure D5). See the facing lead clusters that correlate with

these surfaces in Figure D6.

Begin by looking across all the leads for ischemic changes.

Note the leads in which these changes are visible. The ischemic changes should correlate with the facing lead clusters.

Anterior wall damage is reflected by ischemic changes

in leads V –1 4 V (Figure  D7). When the changes are seen

only in V2 and/or V , 3 it indicates anteroseptal damage.

When both anterior (V –V ) 1 4 and lateral (V –V ) 5 6 leads

show ischemic changes, it indicates anterolateral damage

(Figure D8).

Lateral wall damage shows up as ischemic changes in

the lateral precordial leads (V5 and V6) and in left lateral limb

leads (I and aVL) (Figure D9).

Inferior wall damage creates ischemic changes in the

lower limb leads (II, III, and aVF) (Figure D10).

Figure D5 Infarction Location

ANTERIOR WALL

occlusion of

Left Anterior Descending

Coronary Artery

causes changes in leads

V1, V2, V3, V4

LATERAL WALL

occlusion of

Left Anterior Descending

or Circumflex Coronary Artery

causes changes in leads

I, aVL, V5, V6

INFERIOR WALL

occlusion of

Right

Coronary Artery

causes changes in leads

II, III, aVF

Figure D6 Localizing Myocardial Damage Using Facing Leads

Damage to These Surfaces . . .  Will Be Reflected in These Changing Lead

Clusters . . . 

Anterior V ,1 V , 2 V , 3 V4

Lateral I, aVL, V , 5 V6

Inferior II, III, aVF

Figure D7 Anterior Wall Facing Leads

These Leads . . .  Are Directly over These Surfaces . . . 

V1 anterior wall of the right ventricle

V , 2 V3 anterior wall over the septum

V , 3 V4 anterior wall of the left ventricle

Basic 12-Lead Interpretation 485

Figure D8 Anterior Wall Infarctions

Anterior

V1–V4

Anterolateral

V2–V6

Anteroseptal

V1–V2

Anterobasal

aVL

Apical

I, aVF, V2–V4

ANTERIOR Wall Infarction Leads V1–V4

aVR

aVL

aVF

V5

V6

486 Appendix D

Figure D9 Lateral Wall Infarctions

Lateral

I, aVL, V5, V6

LATERAL Wall Infarction Leads , aVL, V5, V6

III

aVR

aVF

II V2

V1 V4

V3

Basic 12-Lead Interpretation 487

Figure D10 Inferior Wall Infarctions

Inferior

II, III, aVF

INFERIOR Wall Infarction Leads , , aVF

aVR

aVL V2

V1 V4

V5

V3 V6