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00ECG-FM 2/10/05 7:45 PM Page 2

F. A. Davis Company • Philadelphia

ECG

otes

Purchase additional copies of this book

at your health science bookstore or

directly from F. A. Davis by shopping

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A Davis’s Notes Book

Shirley A. Jones, MS Ed, MHA, EMT-P

Interpretation and Management Guide

ECG

otes

Interpretation and Management Guide

00ECG-FM 2/10/05 7:45 PM Page i

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00ECG-FM 2/10/05 7:45 PM Page ii

BASICS

ECGS

12-LEAD

MEDS/

SKILLS

CPR

ACLS

TEST

STRIPS

TOOLS

Waterproof and Reusable

Wipe-Free Pages

Write directly onto any page of ECG Notes with
a ballpoint pen. Wipe old entries off with an
alcohol pad and reuse.

Place 2

Sticky Notes

here

for a convenient and refillable note pad

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OSHA Compliant

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00ECG-FM 2/10/05 7:45 PM Page iii

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00ECG-FM 2/10/05 7:45 PM Page iv

BASICS

Anatomy of the Heart

The heart, located in the mediastinum, is the central structure of

the cardiovascular system. It is protected by the bony structures
of the sternum anteriorly, the spinal column posteriorly, and the
rib cage.

♥

Clinical Tip: The cone-shaped heart has its tip (apex) just

above the diaphragm to the left of the midline. This is why we
may think of the heart as being on the left side, since the
strongest beat can be heard or felt here.

01ECG-Tab 01 2/4/05 3:57 PM Page 1

BASICS

Endocardium

Parietal
pericardium

Myocardium
(heart muscle)

Epicardium
(visceral pericardium)

Fibrous pericardium
(pericardial sac)

Pericardial cavity

Layers of the Heart

The pericardial cavity contains a small amount of lubricating fluid to

prevent friction during heart contraction.

01ECG-Tab 01 2/4/05 3:57 PM Page 2

BASICS

Pulmonary semilunar

valve

Aortic semilunar

valve

Tricuspid

valve

Fibrous

skeleton

Mitral valve

Posterior

Coronary artery

Heart Valves

Properties of Heart Valves

■

Fibrous connective tissue prevents enlargement of valve
openings and anchors valve flaps.

■

Valve closure prevents backflow of blood during and after
contraction.

The atria have been removed in this superior view.

01ECG-Tab 01 2/4/05 3:57 PM Page 3

BASICS

Brachiocephalic

artery

Superior vena cava

Left common carotid artery

Left subclavian artery

Aortic arch

Right
pulmonary artery

Right
pulmonary veins

Right atrium

Inferior vena cava

Tricuspid

valve

Pulmonary
semilunar valve

Left pulmonary artery

Left atrium

Left pulmonary veins

Mitral valve

Left ventricle

Aortic semilunar
valve

Interventricular
septum

Apex

Chordae
tendineae

Right
ventricle

Papillary
muscles

Heart Chambers and Great Vessels

01ECG-Tab 01 2/4/05 3:57 PM Page 4

2005

Davis.

BASICS

Aorta

Left coronary artery

Anterior
descending branch

Coronary sinus

Posterior
artery and
vein

Small

cardiac vein

Right coronary artery

Circumflex branch

Great cardiac
vein

Right coronary vein

Coronary Arterial Circulation

(A) Anterior view

(B) Posterior view

01ECG-Tab 01 2/4/05 3:57 PM Page 5

2005

Davis.

Anatomy of the Cardiovascular System

The cardiovascular system is a closed system consisting of

blood vessels and the heart. Arteries and veins are connected
by smaller structures in which electrolytes are exchanged
across cell membranes.

Blood Vessel Structures

BASICS

Tunica

externa

External elastic

lamina

Tunica

media

Internal elastic

lamina Endothelium (lining)

Artery

Arteriole

Endothelial

cells

Smooth

muscle

Precapillary

sphincter

Capillary

Blood flow

Venule

Vein

Valve

Tunica
intima

Tunica
externa

Tunica
media

01ECG-Tab 01 2/4/05 3:57 PM Page 6

Arterial Circulation

Arteries (excluding the pulmonary artery) transport oxygenated blood.

BASICS

Occipital

Internal carotid

Vertebral

Brachiocephalic

Aortic arch

Maxillary

Facial

External carotid

Common carotid

Subclavian

Axillary

Pulmonary

Celiac

Left gastric

Hepatic

Splenic

Superior

mesenteric

Abdominal aorta
Right common

iliac

Internal iliac

External iliac

Femoral

Popliteal

Anterior tibial

Posterior tibial

Intercostal

Brachial

Renal

Gonadal
Inferior mesenteric

Radial

Ulnar

Deep palmar arch

Superficial
palmar arch

Deep femoral

01ECG-Tab 01 2/4/05 3:58 PM Page 7

BASICS

Superior sagittal sinus

Inferior sagittal sinus

Straight sinus

Transverse sinus

Vertebral

External jugular

Internal jugular

Subclavian

Brachiocephalic

Pulmonary

Hepatic

Hepatic portal

Left gastric

Renal

Splenic

Inferior
mesenteric

Internal iliac

Femoral

External iliac

Great saphenous

Popliteal

Small saphenous

Anterior tibial

Anterior facial

Superior vena cava

Axillary

Cephalic

Hemiazygos

Intercostal

Inferior vena cava

Brachial

Basilic

Gonadal

Superior

mesenteric

Dorsal arch

Volar digital

Dorsal arch

Common iliac

Venous Circulation

Veins (excluding the pulmonary vein) carry blood low in oxygen and high

in carbon dioxide.

01ECG-Tab 01 2/4/05 3:58 PM Page 8

Physiology of the Heart

Mechanics of Heart Function

Process

Action

Cardiac cycle

Systole

Diastole

Stroke

volume (SV)

Cardiac

output (CO)

Properties of Cardiac Cells

Property

Ability

Automaticity

Excitability

Conductivity

Contractility

BASICS

Sequence of events in 1 heartbeat. Blood is

pumped through the entire cardiovascular
system.

Contraction phase—usually refers to

ventricular contraction.

Relaxation phase—the atria and ventricles are

filling. Lasts longer than systole.

Amount of blood ejected from either ventricle

in a single contraction. Starling’s Law of the
Heart states that degree of cardiac muscle
stretch can increase force of ejected blood.
More blood filling the ventricles

↑ SV.

Amount of blood pumped through the

cardiovascular system per min.
CO

SV Heart rate (HR)

Generates electrical impulse independently,

without involving the nervous system.

Responds to electrical stimulation.

Passes or propagates electrical impulses

from cell to cell.

Shortens in response to electrical

stimulation.

01ECG-Tab 01 2/4/05 3:58 PM Page 9

BASICS

Dominant pacemaker of the heart, located in

upper portion of right atrium. Intrinsic rate
60–100 bpm.

Direct electrical impulses between SA and AV

nodes.

Part of AV junctional tissue. Slows

conduction, creating a slight delay before
impulses reach ventricles. Intrinsic rate
40–60 bpm.

Transmits impulses to bundle branches.

Located below AV node.

Conducts impulses that lead to left ventricle.

Conducts impulses that lead to right ventricle.

Network of fibers that spreads impulses

rapidly throughout ventricular walls.
Located at terminals of bundle branches.
Intrinsic rate 20–40 bpm.

Bundle of His

Left bundle
branch

Purkinje
fibers

Right bundle
branch

AV Node

SA node

Internodal
pathways

Electrical Conduction System of the Heart

Conduction System Structures and Functions

Structure

Function and Location

Sinoatrial (SA)

node

Internodal

pathways

Atrioventricular

(AV) node

Bundle of His

Left bundle

branch

Right bundle

branch

Purkinje system

Conduction system of the heart.

01ECG-Tab 01 2/4/05 3:58 PM Page 10

Electrical Conduction System of the Heart

Electrophysiology

Action

Effect

Depolarization

The electrical charge of a cell is altered

by a shift of electrolytes on either side
of the cell membrane. This change
stimulates muscle fiber to contract.

Repolarization

Chemical pumps re-establish an internal

negative charge as the cells return to
their resting state.

Depolarization and

repolarization of the heart.

♥

Clinical Tip: Mechanical

and electrical functions of
the heart are influenced by
proper electrolyte balance.
Important components of
this balance are sodium,
calcium, potassium, and
magnesium.

BASICS

Ventricular

depolarization

Ventricular

repolarization

Atrial

depolarization

01ECG-Tab 01 2/4/05 3:58 PM Page 11

BASICS

The Electrocardiogram (ECG)

■

An ECG is a series of waves and deflections recording the
heart’s electrical activity from a certain “view.”

■

Many views, each called a lead, monitor voltage changes
between electrodes placed in different positions on the body.

■

Leads I, II, and III are bipolar leads, which consist of two
electrodes of opposite polarity (positive and negative). The
third (ground) electrode minimizes electrical activity from
other sources.

■

Leads aVR, aVL, and aVF are unipolar leads and consist of a
single positive electrode and a reference point (with zero
electrical potential) that lies in the center of the heart’s
electrical field.

■

Leads V

–V

are unipolar leads and consist of a single positive

electrode with a negative reference point found at the
electrical center of the heart.

■

Voltage changes are amplified and visually displayed on an
oscilloscope and graph paper.

■

An ECG tracing looks different in each lead because the
recorded angle of electrical activity changes with each lead.

■

Several different angles allow a more accurate perspective
than a single one would.

■

The ECG machine can be adjusted to make any skin electrode
positive or negative. The polarity depends on which lead the
machine is recording.

■

A cable attached to the patient is divided into several
different-colored wires: three, four, or five for monitoring
purposes, or ten for a 12-lead ECG.

■

Incorrect placement of electrodes may turn a normal ECG
tracing into an abnormal one.

♥

Clinical Tip: Patients should be treated according to their

symptoms, not merely their ECG.

♥

Clinical Tip: To obtain a 12-lead ECG, four wires are attached

to each limb and six wires are attached at different locations on
the chest. The total of ten wires provides twelve views (12
leads).

01ECG-Tab 01 2/4/05 3:58 PM Page 12

Limb Leads

Electrodes are placed on the right arm (RA), left arm (LA), right

leg (RL), and left leg (LL). With only four electrodes, six leads
are viewed.

■

Standard leads: I, II, III

■

Augmented leads: aVR, aVL, aVF

Standard Limb Lead Electrode Placement

BASICS

01ECG-Tab 01 2/4/05 3:58 PM Page 13

BASICS

III

Standard Limb Leads

Elements of Standard Limb Leads

Positive

Negative

View of

Lead

Electrode

Heart

Lateral

Inferior

III

Inferior

01ECG-Tab 01 2/4/05 3:58 PM Page 14

Augmented Limb Leads

Elements of Augmented Limb Leads

Lead

Positive Electrode

View of Heart

aVR

None

aVL

Lateral

aVF

Inferior

BASICS

aVR

aVL

aVF

01ECG-Tab 01 2/4/05 3:58 PM Page 15

BASICS

Midclavicular
line

Anterior
axillary line

Midaxillary
line

Chest Leads

Standard Chest Lead Electrode Placement

Elements of Chest Leads

Lead

Positive Electrode Placement

View of Heart

4th Intercostal space to

Septum

right of sternum

4th Intercostal space to

Septum

left of sternum

Directly between V

and V

5th Intercostal space at

left midclavicular line

Level with V

at left anterior

Lateral

axillary line

Level with V

at left midaxillary line

Lateral

01ECG-Tab 01 2/4/05 3:58 PM Page 16

Electrode Placement Using a 3-Wire Cable

Electrode Placement Using a 5-Wire Cable

♥

Clinical Tip: Five-wire telemetry units are commonly used to monitor

leads I, II, III, aVR, aVL, aVF, and V

in critical care settings.

BASICS

01ECG-Tab 01 2/4/05 3:58 PM Page 17

BASICS

Modified Chest Leads

■

Modified chest leads (MCL) are useful in detecting bundle branch
blocks and premature beats.

■

Lead MCL

simulates chest lead V

and views the ventricular septum.

■

Lead MCL

simulates chest lead V

and views the lateral wall of the left

ventricle.

Lead MCL

electrode placement.

Lead MCL

electrode placement.

♥

Clinical Tip: Write on the rhythm strip which simulated lead

was used.

01ECG-Tab 01 2/4/05 3:58 PM Page 18

The Right-Sided 12-Lead ECG

■

The limb leads are placed as usual but the chest leads are a
mirror image of the standard 12-lead chest placement.

■

The ECG machine cannot recognize that the leads have been
reversed. It will still print “V

–V

” next to the tracing. Be sure

to cross this out, and write the new lead positions on the ECG
paper.

The Right-Sided 12-Lead ECG

Chest Leads

Position

4th Intercostal space to left of sternum

4th Intercostal space to right of sternum

Directly between V

and V

5th Intercostal space at right midclavicular line

Level with V

at right anterior axillary line

Level with V

at right midaxillary line

♥

Clinical Tip: Patients with an acute inferior MI should have

right-sided ECGs to assess for possible right ventricular
infarction.

BASICS

Midclavicular

line

axillary line

Midaxillary

line

01ECG-Tab 01 2/4/05 3:58 PM Page 19

BASICS

Spinal

column

Left

shoulder

The 15-Lead ECG

Areas of the heart that are not well visualized by the six chest

leads include the wall of the right ventricle and the posterior
wall of the left ventricle. A 15-lead ECG, which includes the
standard 12 leads plus leads V

, V

, and V

, increases the

chance of detecting an MI in these areas.

The 15-Lead ECG

Chest

Electrode

View

Leads

Placement

of Heart

5th Intercostal space in right

Right ventricle

anterior midclavicular line

Posterior 5th intercostal space

Posterior wall

in left midscapular line

of left ventricle

Directly between V

and spinal

Posterior wall

column at posterior 5th

of left ventricle

intercostal space

♥

Clinical Tip: Use a 15-lead ECG when the 12-lead is normal

but the history is still suggestive of an acute infarction.

01ECG-Tab 01 2/4/05 3:58 PM Page 20

BASICS

1 mm

0.1 mv

0.04 sec

Constant speed of 25 mm/sec

0.20 sec

5 mm

0.5 mv

Small

box

Large

box

Q S

QT Interval

Interval

Segment

QRS

Interval

Isoelectric

line

Recording of the ECG

Components of an ECG Tracing

01ECG-Tab 01 2/4/05 3:58 PM Page 21

BASICS

First wave seen
Small rounded, upright (positive) wave

indicating atrial depolarization (and
contraction)

Distance between beginning of P wave and

beginning of QRS complex

Measures time during which a depolariza-

tion wave travels from the atria to the
ventricles

Three deflections following P wave

Indicates ventricular depolarization (and
contraction)

Q Wave: First negative deflection
R Wave: First positive deflection
S Wave: First negative deflection after R wave

Distance between S wave and beginning of

T wave

Measures time between ventricular

depolarization and beginning of
repolarization

Rounded upright (positive) wave following

QRS

Represents ventricular repolarization

Measured from beginning of QRS to end of

T wave.

Represents total ventricular activity.

Small rounded, upright wave following

T wave

Most easily seen with a slow HR.
Represents repolarization of Purkinje fibers.

Electrical Components

Deflection

Description

P Wave

PR Interval

QRS Interval

ST Segment

T Wave

QT Interval

U Wave

01ECG-Tab 01 2/4/05 3:58 PM Page 22

Methods for Calculating Heart Rate

Heart rate is calculated as the number of times the heart beats

per minute. It usually measures ventricular rate (the number of
QRS complexes) but can refer to atrial rate (the number of P
waves). The method chosen to calculate HR varies according to
rate and regularity on the ECG tracing.

Method 1: Count Large Boxes

Regular rhythms can be quickly determined by counting the

number of large graph boxes between two R waves. That
number is divided into 300 to calculate bpm. The rates for the
first one to six large boxes can be easily memorized.
Remember: 60 sec/min divided by 0.20 sec/large box

300

large boxes/min.

Counting large boxes for heart rate. The rate is 60 bpm.

BASICS

100

300 150

01ECG-Tab 01 2/4/05 3:58 PM Page 23

BASICS

Method 2: Count Small Boxes

Sometimes it is necessary to count the number of small boxes

between two R waves for fast heart rates. That number is
divided into 1500 to calculate bpm. Remember: 60 sec/min
divided by 0.04 sec/small box

1500 small boxes/min.

Examples: If there are six small boxes between two R waves:

1500/6

250 bpm.

If there are ten small boxes between two R waves:
1500/10

150 bpm.

Methods 1 and 2 for Calculating Heart Rate

Number of

Large Boxes

Rate/Min

Small Boxes

Rate/Min

300

750

150

500

100

375

300

250

214

186

167

150

136

125

115

107

100

♥

Clinical Tip: Approximate rate/min is rounded to the next-

highest number.

01ECG-Tab 01 2/4/05 3:58 PM Page 24

BASICS

Method 3: Six-Second ECG Rhythm Strip

The best method for measuring irregular rates with varying R-R intervals is to count the

number of R waves in a 6-sec strip and multiply by 10. This gives the average number of bpm.

Using 6-sec ECG rhythm strip to calculate heart rate. Formula: 7

10 70 bpm

♥

Clinical Tip:

If a rhythm is extremely irregular, it is best to count the number of R-R intervals

per 60 sec (1 min).

01ECG-Tab 01 2/4/05 3:58 PM Page 25

2005

Davis.

BASICS

ECG Interpretation

Analyzing a Rhythm

Component

Characteristic

Rate

Regularity

P Waves

PR Interval

QRS Interval

QT Interval

Dropped beats

The bpm is commonly the ventricular rate.
If atrial and ventricular rates differ, as in a

-degree block, measure both rates.

Normal: 60–100 bpm
Slow (bradycardia):

60 bpm

Fast (tachycardia):

100 bpm

Measure R-R intervals and P-P intervals.
Regular: Intervals consistent
Regularly irregular: Repeating pattern
Irregular: No pattern

If present: Same in size, shape, position?
Does each QRS have a P wave?
Normal: Upright (positive) and uniform
Inverted: Negative
Notched: P

′

None: Rhythm is junctional or ventricular.

Constant: Intervals are the same.
Variable: Intervals differ.
Normal: 0.12–0.20 sec and constant

Normal: 0.06–0.10 sec
Wide:

0.10 sec

None: Absent

Beginning of R wave to end of T wave
Varies with HR.
Normal: Less than half the R-R interval

Occur in AV blocks.
Occur in sinus arrest.

01ECG-Tab 01 2/4/05 3:58 PM Page 26

Component

Characteristic

Pause

QRS Complex

grouping

Notes:

BASICS

Compensatory: Complete pause following a

premature atrial contraction (PAC),
premature junctional contraction (PJC), or
premature ventricular contraction (PVC)

Noncompensatory: Incomplete pause

following a PAC, PJC, or PVC

Bigeminy: Repeating pattern of normal

complex followed by a premature
complex

Trigeminy: Repeating pattern of 2 normal

complexes followed by a premature
complex

Quadrigeminy: Repeating pattern of 3

normal complexes followed by a
premature complex

Couplets: 2 Consecutive premature

complexes

Triplets: 3 Consecutive premature

complexes

01ECG-Tab 01 2/4/05 3:58 PM Page 27

ECGs

Sinoatrial (SA) Node Arrhythmias

■

Upright P waves all look similar.

Note: All ECG strips in this tab were recorded in lead II.

■

PR intervals and QRS complexes are of normal duration.

Normal Sinus Rhythm (NSR)

Rate: Normal (60–100 bpm)
Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

A normal ECG does not exclude heart disease.

02ECG-Tab 02 2/4/05 3:58 PM Page 28

2005

Davis.

Sinus Bradycardia

■

Results from slowing of the SA node.

Rate: Slow (

60 bpm)

Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Sinus bradycardia is normal in athletes and during sleep. In acute MI, it may be

protective and beneficial or the slow rate may compromise cardiac output. Certain
medications, such as beta blockers, may also cause sinus bradycardia.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 29

2005

Davis.

Sinus Tachycardia

■

Results from increased SA node discharge.

Rate: Fast (

100 bpm)

Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Sinus tachycardia may be caused by exercise, anxiety, fever, hypoxemia,

hypovolemia, or cardiac failure.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 30

2005

Davis.

Sinus Arrhythmia

■

The SA node discharges irregularly.

■

The R-R interval is irregular.

Rate: Usually normal (60–100 bpm); frequently increases with inspiration and decreases with

expiration

Rhythm: Irregular; varies with respiration
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

The pacing rate of the SA node varies with respiration, especially in children

and elderly people.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 31

2005

Davis.

ECGs

3 - Sec pause/ arrest

Sinus Pause (Sinus Arrest)

■

The SA node fails to discharge and then resumes.

■

Electrical activity resumes either when the SA node resets itself or when a lower latent
pacemaker begins to discharge.

■

The pause (arrest) time interval is not a multiple of the normal P-P interval.

Rate: Normal to slow; determined by duration and frequency of sinus pause (arrest)
Rhythm: Irregular whenever a pause (arrest) occurs
P Waves: Normal (upright and uniform) except in areas of pause (arrest)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Cardiac output may decrease, causing syncope or dizziness.

02ECG-Tab 02 2/4/05 3:58 PM Page 32

2005

Davis.

Sinoatrial (SA) Block

■

The block occurs in some multiple of the P-P interval.

■

After the dropped beat, cycles continue on time.

Rate: Normal to slow; determined by duration and frequency of SA block
Rhythm: Irregular whenever an SA block occurs
P Waves: Normal (upright and uniform) except in areas of dropped beats
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Cardiac output may decrease, causing syncope or dizziness.

ECGs

Dropped beat

02ECG-Tab 02 2/4/05 3:58 PM Page 33

2005

Davis.

Atrial Arrhythmias

■

P Waves differ in appearance from sinus P waves.

■

QRS Complexes are of normal duration.

Wandering Atrial Pacemaker (WAP)

■

Pacemaker site transfers from the SA node to other latent pacemaker sites in the atria and
the AV junction and then moves back to the SA node.

Rate: Normal (60–100 bpm)
Rhythm: Irregular
P Waves: At least three different forms, determined by the focus in the atria
PR Interval: Variable; determined by focus
QRS: Normal (0.06–0.10 sec)

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 34

2005

Davis.

Multifocal Atrial Tachycardia (MAT)

■

This form of WAP is associated with a ventricular response of

100 bpm.

■

MAT may be confused with atrial fibrillation (A-fib); however, MAT has a visible P wave.

Rate: Fast (

100 bpm)

Rhythm: Irregular
P Wave: At least three different forms, determined by the focus in the atria
PR Interval: Variable; depends on focus
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

MAT is commonly seen in patients with COPD but may also occur in acute MI.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 35

2005

Davis.

Premature Atrial Contraction (PAC)

■

A single complex occurs earlier than the next expected sinus complex.

■

After the PAC, sinus rhythm usually resumes.

Rate: Depends on rate of underlying rhythm
Rhythm: Irregular whenever a PAC occurs
P Waves: Present; in the PAC, may have a different shape
PR Interval: Varies in the PAC; otherwise normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

In patients with heart disease, frequent PACs may precede paroxysmal

supraventricular tachycardia (PSVT), A-fib, or A-flutter.

ECGs

PAC

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2005

Davis.

Atrial Tachycardia

■

A rapid atrial rate overrides the SA node and becomes the dominant pacemaker.

■

Some ST wave and T wave abnormalities may be present.

Rate: 150–250 bpm
Rhythm: Regular
P Waves: Normal (upright and uniform) but differ in shape from sinus P waves
PR Interval: May be short (

0.12 sec) in rapid rates

QRS: Normal (0.06–0.10 sec) but can be aberrant at times

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 37

2005

Davis.

Supraventricular Tachycardia (SVT)

■

This arrhythmia has such a fast rate that the P waves may not be seen.

Rate: 150–250 bpm
Rhythm: Regular
P Waves: Frequently buried in preceding T waves and difficult to see
PR Interval: Usually not possible to measure
QRS: Normal (0.06–0.10 sec) but may be wide if abnormally conducted through ventricles

♥

Clinical Tip:

SVT may be related to caffeine intake, nicotine, stress, or anxiety in healthy

adults.

ECGs

P wave buried in T wave

02ECG-Tab 02 2/4/05 3:58 PM Page 38

2005

Davis.

Paroxysmal Supraventricular Tachycardia (PSVT)

■

PSVT is a rapid rhythm that starts and stops suddenly.

■

For accurate interpretation, the beginning or end of the PSVT must be seen.

■

PSVT is sometimes called paroxysmal atrial tachycardia (PAT).

♥

Clinical Tip:

The patient may feel palpitations, dizziness, lightheadedness, or anxiety.

ECGs

Sudden onset of SVT

02ECG-Tab 02 2/4/05 3:58 PM Page 39

2005

Davis.

Atrial Flutter (A-flutter)

■

AV node conducts impulses to the ventricles at a 2:1, 3:1, 4:1, or greater ratio (rarely 1:1).

■

Degree of AV block may be consistent or variable.

Rate: Atrial: 250–350 bpm; ventricular: slow or fast
Rhythm: Usually regular but may be variable
P Waves: Flutter waves have a saw-toothed appearance
PR Interval: Variable
QRS: Usually normal (0.06–0.10 sec), but may appear widened if flutter waves are buried in QRS

♥

Clinical Tip:

The presence of A-flutter may be the first indication of cardiac disease.

♥

Clinical Tip:

Signs and symptoms depend on ventricular response rate.

ECGs

Flutter waves

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2005

Davis.

Atrial Fibrillation (A-fib)

■

Rapid, erratic electrical discharge comes from multiple atrial ectopic foci.

■

No organized atrial contractions are detectable.

Rate: Atrial: 350 bpm or greater; ventricular: slow or fast
Rhythm: Irregular
P Waves: No true P waves; chaotic atrial activity
PR Interval: None
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

A-fib is usually a chronic arrhythmia associated with underlying heart disease.

♥

Clinical Tip:

Signs and symptoms depend on ventricular response rate.

ECGs

Irregular R-R intervals

02ECG-Tab 02 2/4/05 3:58 PM Page 41

2005

Davis.

ECGs

Delta

wave

Wolff-Parkinson-White (WPW) Syndrome

■

In WPW an accessory conduction pathway is present between the atria and the ventricles.
Electrical impulses are rapidly conducted to the ventricles.

■

These rapid impulses create a slurring of the initial portion of the QRS called the delta wave.

Rate: Depends on rate of underlying rhythm
Rhythm: Regular unless associated with A-fib
P Waves: Normal (upright and uniform) unless A-fib is present
PR Interval: Short (

0.12 sec) if P wave is present

QRS: Wide (

0.10 sec); delta wave present

♥

Clinical Tip:

WPW is associated with narrow-complex tachycardias, including A-flutter and

A-fib.

02ECG-Tab 02 2/4/05 3:58 PM Page 42

2005

Davis.

ECGs

Inverted P wave

Absent P wave

Junctional Arrhythmias

■

The atria and SA node do not perform their normal pacemaking functions.

■

A junctional escape rhythm begins.

Junctional Rhythm

Rate: 40–60 bpm
Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)

02ECG-Tab 02 2/4/05 3:58 PM Page 43

2005

Davis.

Accelerated Junctional Rhythm

Rate: 61–100 bpm
Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Monitor the patient, not just the ECG, for clinical improvement.

ECGs

Absent P wave

02ECG-Tab 02 2/4/05 3:58 PM Page 44

2005

Davis.

Junctional Tachycardia

Rate: 101–180 bpm
Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Signs and symptoms of decreased cardiac output may be seen in response to

the rapid rate.

ECGs

Retrograde P wave

02ECG-Tab 02 2/4/05 3:58 PM Page 45

2005

Davis.

Junctional Escape Beat

■

An escape complex comes later than the next expected sinus complex.

Rate: Depends on rate of underlying rhythm
Rhythm: Irregular whenever an escape beat occurs
P Waves: None, inverted, buried, or retrograde in the escape beat
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)

ECGs

Junctional escape beats

02ECG-Tab 02 2/4/05 3:58 PM Page 46

2005

Davis.

Premature Junctional Contraction (PJC)

■

Enhanced automaticity in the AV junction produces PJCs.

Rate: Depends on rate of underlying rhythm
Rhythm: Irregular whenever a PJC occurs
P Waves: Absent, inverted, buried, or retrograde in the PJC
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Before deciding that isolated PJCs may be insignificant, consider the cause.

ECGs

PJC

02ECG-Tab 02 2/4/05 3:58 PM Page 47

2005

Davis.

ECGs

Ventricular Arrhythmias

■

QRS complex is

0.10 sec. P Waves are absent or, if visible, have no consistent relationship

to the QRS complex.

Idioventricular Rhythm

Rate: 20–40 bpm
Rhythm: Regular
P Waves: None
PR Interval: None
QRS: Wide (

0.10 sec), bizarre appearance

♥

Clinical Tip:

Idioventricular rhythm may also be called agonal rhythm.

02ECG-Tab 02 2/4/05 3:58 PM Page 48

2005

Davis.

Accelerated Idioventricular Rhythm

Rate: 41–100 bpm
Rhythm: Regular
P Waves: None
PR Interval: None
QRS: Wide (

0.10 sec), bizarre appearance

♥

Clinical Tip:

Idioventricular rhythms appear when supraventricular pacing sites are

depressed or absent. Diminished cardiac output is expected if the heart rate is slow.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 49

2005

Davis.

Premature Ventricular Contraction (PVC)

■

Usually PVCs result from an irritable ventricular focus.

■

PVCs may be uniform (same form) or multiform (different forms).

■

The pause following a PVC may be compensatory or noncompensatory.

Rate: Depends on rate of underlying rhythm
Rhythm: Irregular whenever a PVC occurs
P Waves: None associated with the PVC
PR Interval: None associated with the PVC
QRS: Wide (

0.10 sec), bizarre appearance

♥

Clinical Tip:

Patients may sense the occurrence of PVCs as skipped beats. Because the

ventricles are only partially filled, the PVC frequently does not generate a pulse.

ECGs

PVC

02ECG-Tab 02 2/4/05 3:58 PM Page 50

2005

Davis.

ECGs

Premature Ventricular Contraction: Uniform (same form)

Premature Ventricular Contraction: Multiform (different forms)

02ECG-Tab 02 2/4/05 3:58 PM Page 51

2005

Davis.

Premature Ventricular Contraction: Ventricular Bigeminy (PVC every other beat)

Premature Ventricular Contraction: Ventricular Trigeminy (PVC every 3rd beat)

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 52

2005

Davis.

Premature Ventricular Contraction: Ventricular Quadrigeminy (PVC every 4th beat)

Premature Ventricular Contraction: Couplets (paired PVCs)

ECGs

Couplets

02ECG-Tab 02 2/4/05 3:58 PM Page 53

2005

Davis.

Ventricular Tachycardia (VT): Monomorphic

■

QRS complexes in monomorphic VT have the same shape and amplitude.

Rate: 100–250 bpm
Rhythm: Regular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (

0.10 sec), bizarre appearance

♥

Clinical Tip:

It is important to confirm the presence or absence of pulses because

monomorphic VT may be perfusing or nonperfusing.

♥

Clinical Tip:

Monomorphic VT will probably deteriorate into VF or unstable VT if sustained

and not treated.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 54

2005

Davis.

Ventricular Tachycardia (VT): Polymorphic

■

QRS complexes in polymorphic VT vary in shape and amplitude.

■

The QT interval is normal or long.

Rate: 100–250 bpm
Rhythm: Regular or irregular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (

0.10 sec), bizarre appearance

♥

Clinical Tip:

It is important to confirm the presence or absence of pulses because

polymorphic VT may be perfusing or nonperfusing.

♥

Clinical Tip:

Consider electrolyte abnormalities as a possible etiology.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 55

2005

Davis.

Torsade de Pointes

■

The QRS reverses polarity and the strip shows a spindle effect.

■

This rhythm is an unusual variant of polymorphic VT with normal or long QT intervals.

■

In French the term means “twisting of the points.”

Rate: 200–250 bpm
Rhythm: Irregular
P Waves: None
PR Interval: None
QRS: Wide (

0.10 sec), bizarre appearance

♥

Clinical Tip:

Torsade de pointes may deteriorate to VF or asystole.

♥

Clinical Tip:

Frequent causes are drugs that prolong QT interval and electrolyte

abnormalities such as hypomagnesemia.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 56

2005

Davis.

Ventricular Fibrillation (VF)

■

Chaotic electrical activity occurs with no ventricular depolarization or contraction.

■

The amplitude and frequency of the fibrillatory activity can be used to define the type of
fibrillation as coarse, medium, or fine.

Rate: Indeterminate
Rhythm: Chaotic
P Waves: None
PR Interval: None
QRS: None

♥

Clinical Tip:

There is no pulse or cardiac output. Rapid intervention is critical. The longer the

delay, the less the chance of conversion.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 57

2005

Davis.

Pulseless Electrical Activity (PEA)

■

Monitor shows an identifiable electrical rhythm, but no pulse is detected.

■

Rhythm may be sinus, atrial, junctional, or ventricular in origin.

■

PEA is also called electromechanical dissociation (EMD).

Rate, rhythm, P waves, P-R interval, and QRS: Reflect underlying rhythm.

♥

Clinical Tip:

Potential causes of PEA are pulmonary embolism, MI, acidosis, tension

pneumothorax, hyper- and hypokalemia, cardiac tamponade, hypovolemia, hypoxia,
hypothermia, and drug overdose (i.e., cyclic antidepressants, beta blockers, calcium channel
blockers, digoxin).

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 58

2005

Davis.

Asystole

■

Electrical activity in the ventricles is completely absent.

Rate: None
Rhythm: None
P Waves: None
PR Interval: None
QRS: None

♥

Clinical Tip:

Always confirm asystole by checking the ECG in two different leads. Also,

search to identify underlying ventricular fibrillation.

♥

Clinical Tip:

Seek to identify the underlying cause as in PEA.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 59

2005

Davis.

Atrioventricular (AV) Blocks

■

AV blocks are divided into three categories: first-, second-, and third-degree.

First-Degree AV Block

Rate: Depends on rate of underlying rhythm
Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Prolonged (

0.20 sec)

QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

Usually AV block is benign, but if associated with an acute MI, it may lead to

further AV defects.

ECGs

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2005

Davis.

Second-Degree AV Block

Type I (Mobitz I or Wenckebach)

■

P-R intervals become progressively longer until one P wave is totally blocked and produces
no QRS. After a pause, during which the AV node recovers, this cycle is repeated.

Rate: Depends on rate of underlying rhythm
Rhythm: Irregular
P Waves: Normal (upright and uniform)
PR Interval: Progressively longer until one P wave is blocked and a QRS is dropped
QRS: Normal (0.06–0.10 sec)

♥

Clinical Tip:

This rhythm may be caused by medication such as beta blockers, digoxin, and

calcium channel blockers. Ischemia involving the right coronary artery is another cause.

ECGs

Blocked beat

02ECG-Tab 02 2/4/05 3:59 PM Page 61

2005

Davis.

Second-Degree AV Block

Type II (Mobitz II)

■

Conduction ratio (P waves to QRS complexes) is commonly 2:1, 3:1, or 4:1.

■

QRS complexes are usually wide because this block usually involves both bundle branches.

Rate: Atrial rate (usually 60–100 bpm); faster than ventricular rate
Rhythm: Atrial regular and ventricular irregular
P Waves: Normal (upright and uniform); more P waves than QRS complexes
PR Interval: Normal or prolonged but constant
QRS: Usually wide (

0.10 sec)

♥

Clinical Tip:

Resulting bradycardia can compromise cardiac output and lead to complete AV

block. This rhythm often occurs with cardiac ischemia or an MI.

ECGs

02ECG-Tab 02 2/4/05 3:59 PM Page 62

2005

Davis.

ECGs

Third-Degree AV Block

■

Conduction between atria and ventricles is absent because of electrical block at or below the
AV node.

■

“Complete heart block” is another name for this rhythm.

Rate: Atrial: 60–100 bpm; ventricular: 40–60 bpm if escape focus is junctional,

40 bpm if

escape focus is ventricular

Rhythm: Usually regular, but atria and ventricles act independently
P Waves: Normal (upright and uniform); may be superimposed on QRS complexes or T waves
PR Interval: Varies greatly
QRS: Normal if ventricles are activated by junctional escape focus; wide if escape focus is

ventricular

02ECG-Tab 02 2/4/05 3:59 PM Page 63

2005

Davis.

Bundle Branch Block (BBB)

■

Either the left or the right ventricle may depolarize late, creating a “notched” QRS complex.

Rate: Depends on rate of underlying rhythm
Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Usually wide (

0.10 sec) with a notched appearance

♥

Clinical Tip:

Commonly, BBB occurs in coronary artery disease.

ECGs

Notched QRS

02ECG-Tab 02 2/4/05 3:59 PM Page 64

2005

Davis.

Artificial Cardiac Pacemakers

■

Electronically stimulate the heart in place of the heart’s own
pacemaker.

■

May be preset to stimulate the heart’s activity continuously or
intermittently.

Temporary Pacemaker

■

Paces the heart through epicardial, transvenous, or
transcutaneous routes. The pulse generator is located externally.

Permanent Pacemaker

■

Its circuitry sealed in an airtight case, the pacemaker is
implanted in the body. Uses sensing and pacing device leads.

Single-Chamber Pacemaker

■

One lead is placed in the heart and paces a single heart chamber
(either atrium or ventricle).

Dual-Chamber Pacemaker

■

One lead is placed in the right atrium and the other in the right
ventricle. The atrial electrode generates a spike that should be
followed by a P wave, and the ventricular electrode generates a
spike followed by a wide QRS complex.

Pacemaker Modes

■

Fixed rate (asynchronous): Discharges at a preset rate (usually
70—80 bpm) regardless of the patient’s own electrical activity.

■

Demand (synchronous): Discharges only when the patient’s heart
rate drops below the pacemaker’s preset (base) rate.

♥

Clinical Tip: Pacemaker patients may receive defibrillation, but

avoid placing the defibrillator paddles or pads closer than 5 inches
from the pacemaker battery pack.

ECGs

02ECG-Tab 02 2/4/05 3:59 PM Page 65

ECGs

Artificial Pacemaker Rhythm

Rate:

Varies according to preset pacemaker rate

Rhythm:

Regular for asynchronous pacemaker; irregular for demand pacemaker

P waves:

None produced by ventricular pacemaker. Sinus P waves may be seen but are unrelated
to QRS. Atrial or dual-chamber pacemaker should have P waves following each atrial
spike.

P-R interval:

None for ventricular pacer. Atrial or dual-chamber pacemaker produces ventricular spike
at constant interval from P wave.

QRS:

Wide (

0.10 sec) following each ventricular spike in paced rhythm. Patient’s own

electrical activity may generate QRS that looks different from paced QRS complexes. If
atrially paced only, may be within normal limits.

Single-Chamber Pacemaker Rhythm—Atrial

Pacemaker spike

02ECG-Tab 02 2/4/05 3:59 PM Page 66

2005

Davis.

ECGs

Pacemaker spike

Atrial pacemaker spike

Ventricular pacemaker spike

Single-Chamber Pacemaker Rhythm—Ventricular

Dual-Chamber Pacemaker Rhythm—Atrial and Ventricular

02ECG-Tab 02 2/4/05 3:59 PM Page 67

2005

Davis.

Pacemaker Malfunctions

Malfunction

Reason

Failure to fire

Failure to capture

Failure to sense

♥

Clinical Tip:

A pacemaker spike—a mark on the ECG projecting upward or downward from the baseline—

indicates that the pacemaker has fired.

♥

Clinical Tip:

A pacemaker is said to be in capture when a spike produces an ECG wave or complex.

Pacemaker Failure to Sense

ECGs

Pacemaker spikes are absent. The cause may be a dead battery or a disruption in the

connecting wires.

Pacemaker spikes are present, but no P wave or QRS complex follows the spike. Turning

up the pacemaker’s voltage often corrects this problem.

The pacemaker fires because it fails to detect the heart’s intrinsic beats, resulting in

abnormal complexes. The cause may be a dead battery, decrease of P wave or QRS
voltage, or damage to a pacing lead wire.

02ECG-Tab 02 2/4/05 3:59 PM Page 68

2005

Davis.

Artifact

■

Artifacts are ECG deflections caused by influences other than the heart’s electrical activity.

Loose Electrodes

Baseline Varies with Respiration

ECGs

02ECG-Tab 02 2/4/05 3:59 PM Page 69

2005

Davis.

ECGs

Regular R-R intervals

60-Cycle Interference

Muscle Artifact

02ECG-Tab 02 2/4/05 3:59 PM Page 70

2005

Davis.

ECGs

♥

Clinical Tip:

Never confuse muscle ar

tifact with

A-fib if the rh

ythm is regular

Notes:

02ECG-Tab 02 2/4/05 3:59 PM Page 71

The 12-Lead ECG

■

The most commonly used clinical ECG system is the 12-lead
ECG. It consists of the following leads: I, II, III, aVR, aVL, aVF,
V

, V

, and V

. Both limb and chest electrodes are

used to record 12-lead ECGs.

■

Measurements are central to 12-lead ECG analysis. The height
and depth of waves can be important in the diagnosis of
certain conditions, including MI or ventricular hypertrophy.

■

The direction of ventricular depolarization is an important
factor in determining the axis of the heart.

■

In the case of MI, multiple leads are necessary to recognize its
presence and determine its location. If large areas of the heart
are affected, the patient can develop cardiogenic shock.

■

ECG signs of an MI are best seen in the reflecting leads—
those facing the affected surface of the heart. Reciprocal leads
are in the same plane but opposite the area of the MI; they
show a “mirror image” of the electrical complex.

■

Prehospital EMS systems may use 12-lead ECGs to discover
signs of acute myocardial infarction, such as ST segment
elevation, in preparation for in-hospital administration of
thrombolytic drugs.

■

Once a 12-lead ECG is performed, a 15-lead, or right-sided,
ECG may be used for an even more comprehensive view if it
appears that the right ventricle or posterior portion of the
heart has been affected.

♥

Clinical Tip: Always compare the patient’s current 12-lead

ECG with the previous one.

12-LEAD

03ECG-Tab 03 2/4/05 3:59 PM Page 72

12-LEAD

Left

lung

Right

lung

R Wave Progression

■

Normal ventricular depolarization in the heart progresses
from right to left and from front to back.

■

In a normal heart the R wave becomes taller and the S wave
becomes smaller as electrical activity moves across the heart
from right to left. This phenomenon is called R wave
progression.

■

Alteration in the normal progression of the R wave may be
seen in left ventricular hypertrophy, COPD, left bundle branch
block, or anteroseptal MI.

Normal R wave progression in chest leads V

–V

03ECG-Tab 03 2/4/05 3:59 PM Page 73

12-LEAD

180

–90

–30

120

150

–150

III

aVF

aVR

aVL

aVF

xis

evia

tion

iat

ion

Left

Devia

tio

Electrical Axis of the Heart

The electrical axis is the sum total of all electrical currents

generated by the ventricular myocardium during depolarization.
Analysis of the axis may help to determine the location and
extent of cardiac injury, such as ventricular hypertrophy, bundle
branch block, or changes in the position of the heart in the chest
(from, e.g., pregnancy or ascites).

The direction of the QRS complex in leads I and aVF determines

the axis quadrant in relation to the heart.

♥

Clinical Tip: Extreme right axis deviation is also called

indeterminate, “no man’s land,” and “northwest.”

03ECG-Tab 03 2/4/05 3:59 PM Page 74

12-LEAD

Anterior wall

Anterior view

Lateral

wall

Septal wall

Inferior wall

Anterior view

Posterior view

I lateral

aVR

V1 septal

II inferior

aVL lateral

V2 septal

lateral

III inferior

aVF inferior

V3 anterior

lateral

Ischemia, Injury, or Infarction in

Relation to the Heart

Location of MI by ECG Leads

♥

Clinical Tip: Lead aVR is a nondiagnostic lead and does not

show any change in an MI.

♥

Clinical Tip: An MI may not be limited to just one region of

the heart. For example, if there are changes in leads V

and V

(anterior) and in I, aVL, V

, and V

(lateral), the MI is called an

anterolateral infarction.

03ECG-Tab 03 2/4/05 3:59 PM Page 75

Progression of an Acute Myocardial Infarction

An acute MI is a continuum that extends from the normal state

to a full infarction:

■

Ischemia—Lack of oxygen to the cardiac tissue, represented
by ST segment depression, T wave inversion, or both

■

Injury—An arterial occlusion with ischemia, represented by ST
segment elevation

■

Infarction—Death of tissue, represented by a pathological Q
wave

♥

Clinical Tip: Once the acute MI has ended, the ST segment

returns to baseline and the T wave becomes upright, but the Q
wave remains abnormal because of scar formation.

12-LEAD

Infarction

Injury

Ischemia

Normal

03ECG-Tab 03 2/4/05 3:59 PM Page 76

ST Segment Elevation and Depression

■

A normal ST segment represents early ventricular repolarization.

■

Displacement of the ST segment can be caused by various conditions
listed below.

ST segment is at baseline.

ST segment is elevated.

ST segment is depressed.

Primary Causes of ST Segment Elevation

■

ST segment elevation

1 mm in the limb leads and 2 mm in the

chest leads indicates an evolving acute MI until there is proof to the
contrary. Other primary causes:

◆ Early repolarization (normal variant in young adults)

◆ Pericarditis

◆ Ventricular aneurysm

◆ Pulmonary embolism

◆ Intracranial hemorrhage

Primary Causes of ST Segment Depression

■

Myocardial ischemia

■

Left ventricular hypertrophy

■

Intraventricular conduction defects

■

Medication (e.g., digitalis)

■

Reciprocal changes in leads opposite the area of acute injury

12-LEAD

03ECG-Tab 03 2/4/05 3:59 PM Page 77

12-LEAD

aVR

aVL

III

aVF

Normal 12-Lead ECG

♥

Clinical Tip: A normal ECG does not rule out any acute

coronary syndrome.

03ECG-Tab 03 2/4/05 3:59 PM Page 78

12-LEAD

aVR

aVL

III

aVF

Anterior Myocardial Infarction

■

Occlusion of the left coronary artery—left anterior descending
branch

■

ECG changes: ST segment elevation with tall T waves and
taller-than-normal R waves in leads V

and V

♥

Clinical Tip: Anterior MI frequently involves a large area of

the myocardium and can present with cardiogenic shock,
second-degree AV block type II, or third-degree AV block.

03ECG-Tab 03 2/4/05 3:59 PM Page 79

12-LEAD

aVR

aVL

III

aVF

Inferior Myocardial Infarction

■

Occlusion of the right coronary artery—posterior descending
branch

■

ECG changes: ST segment elevation in leads II, III, and aVF

♥

Clinical Tip: Be alert for symptomatic sinus bradycardia, AV

blocks, hypotension, and hypoperfusion.

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12-LEAD

aVR

aVL

III

aVF

Lateral Myocardial Infarction

■

Occlusion of the left coronary artery—circumflex branch

■

ECG changes: ST segment elevation in leads I, aVL, V

, and V

♥

Clinical Tip: Lateral MI is often associated with anterior or

inferior wall MI. Be alert for changes that may indicate
cardiogenic shock or congestive heart failure.

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12-LEAD

aVR

aVL

III

aVF

Septal Myocardial Infarction

■

Occlusion of the left coronary artery—left anterior descending
branch

■

ECG changes: pathological Q waves; absence of normal R
waves in leads V

and V

♥

Clinical Tip: Septal MI is often associated with an anterior

wall MI.

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12-LEAD

aVR

aVL

III

aVF

Posterior Myocardial Infarction

■

Occlusion of the right coronary artery (posterior descending
branch) or the left circumflex artery

■

Tall R waves and ST segment depression possible in leads V

, V

, and V

■

ST segment elevation in true posterior leads, V

and V

♥

Clinical Tip: Diagnosis may require a 15-lead ECG because a

standard 12-lead does not look directly at the posterior wall.

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12-LEAD

aVR

aVL

III

aVF

Left Bundle Branch Block

■

QRS

0.10 sec

■

QRS predominantly negative in leads V

and V

■

QRS predominantly positive in V

and V

and often notched

■

Absence of small, normal Q waves in I, aVL, V

, and V

■

Wide monophasic R waves in I, aVL, V

, V

, and V

♥

Clinical Tip: Patients may have underlying heart disease,

including coronary artery disease, hypertension,
cardiomyopathy, and ischemia.

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12-LEAD

aVR

aVL

III

aVF

Right Bundle Branch Block

■

QRS

0.10 sec

■

QRS normal or deviated to the right

■

Slurred S wave in leads I and V

■

RSR’ pattern in lead V

with R’ taller than R

♥

Clinical Tip: Patients may have underlying right ventricular

hypertrophy, pulmonary edema, cardiomyopathy, congenital
heart disease, or rheumatic heart disease.

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Emergency Medications

This list is a reference list only. It is not meant to be exhaustive

in clinical content.

♥

Clinical Tip: Always consult an authoritative, current

reference about dose, dilution, route and rate of administration,
and interactions before administering medications, especially
IV medications. Have a second licensed person independently
check dose calculations, preparation, original orders, and
infusion pump programming.

ACE INHIBITORS

(Angiotensin-converting Enzyme Inhibitors)

(Antihypertensive)

Common Agents: Captopril, enalapril, lisinopril, ramipril.
Indications: MI, hypertension (HTN), congestive heart failure

(CHF), heart failure without hypotension, ST segment
elevation, left ventricular dysfunction after MI.

Dose: See individual order and drug for route and dosage.

Usually not started in emergency department, but within 24
hr after fibrinolytic therapy has been completed and blood
pressure (BP) has stabilized.

Contraindications: Lactation, pregnancy, angioedema,

hypersensitivity to ACE inhibitors, serum potassium

mEq/L.

Side Effects: Tachycardia, dizziness, headache, fatigue,

hypotension, hyperkalemia.

Precautions: Reduce dose in renal failure.

ADENOSINE

(Adenocard, Adenoscan) (Antiarrhythmic)

Indications: Narrow-complex tachycardias and PSVT.
Dose: 6 mg rapid intravenous push (IVP) over 1–3 sec followed

by a 20-mL bolus of normal saline. Give 12 mg by IVP in 1–2
min if needed. A third dose of 12 mg IVP may be given in 1–2
min, max. 30 mg.

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Contraindications: Hypersensitivity, sick sinus syndrome, 2nd-

or 3rd-degree AV block (unless a functional artificial
pacemaker is present), drug- or poison-induced tachycardia.

Side Effects: Flushing, dizziness, bronchospasm, chest pain or

tightness, bradycardia, AV block, asystole, ventricular ectopic
beats, VF.

Precautions: Ineffective in treating A-fib, A-flutter, or VT. Avoid

in patients receiving dipyridamole and in patients with
asthma or unstable angina.

AMIODARONE

(Cordarone, Pacerone) (Antiarrhythmic)

Indications: Wide- and narrow-complex tachycardia,

polymorphic VT, shock-refractory VF or pulseless VT, SVT,
PSVT.

Dose: Cardiac arrest 300 mg (diluted in 20–30 mL D5W) IVP;

consider additional 150 mg IVP in 3–5 min. Wide- and narrow-
complex tachycardia (stable) 150 mg IVP over first 10 min (15
mg/min)—may repeat infusion of 150 mg IVP every 10 min as
needed; slow infusion of 360 mg IV over next 6 hr (1 mg/min);
maintenance infusion of 540 mg over next 18 hr (0.5 mg/min).
Max. cumulative dose: 2.2 g IV in 24 hr.

Contraindications: Bradycardia, hypersensitivity, cardiogenic

shock, 2nd- or 3rd-degree AV block.

Side Effects: Vasodilation, hypotension, visual impairment,

hepatotoxicity, pulmonary toxicity, CHF; may prolong QT
interval, producing torsade de pointes.

Precautions: Avoid concurrent use with procainamide. Correct

hypokalemia and hypomagnesemia if possible before use.
Draw up amiodarone through a large-gauge needle to reduce
foaming. For slow or maintenance IV infusion, mix
medication only in glass bottle containing D5W and
administer through an in-line filter.

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ASPIRIN

(Acetylsalicylic Acid) (Antiplatelet)

Indications: Acute coronary syndrome, symptoms suggestive

of cardiac ischemia.

Dose: 162–325 mg PO non-enteric coated for antiplatelet effect.

Give within minutes of onset.

Contraindications: Known allergy to aspirin, pregnancy.
Side Effects: Anorexia, nausea, epigastric pain, anaphylaxis.
Precautions: Active ulcers and asthma, bleeding disorders, or

thrombocytopenia.

ATROPINE

(Antiarrhythmic, Anticholinergic)

Indications: Symptomatic sinus bradycardia, asystole, PEA with

rate

60 bpm, cholinergic drug toxicity and mushroom

poisoning (antidote).

Dose: Cardiac arrest 1 mg IVP every 3–5 min (may give through

endotracheal (ET) tube at 2.0–3.0 mg diluted in 10 mL normal
saline, max. 0.03–0.04 mg/kg. Bradycardia 0.5–1.0 mg IVP
every 3–5 min, max. 0.03–0.04 mg/kg.

Contraindications: A-fib, A-flutter, glaucoma, asthma.
Side Effects: Tachycardia, headache, dry mouth, dilated pupils,

VF or VT.

Precautions: Use caution in myocardial ischemia and hypoxia.

Avoid in hypothermic bradycardia and in 2nd-degree (Mobitz
type II) and 3rd-degree AV block.

BETA BLOCKERS

(Antihypertensive)

Common Agents: Atenolol, esmolol, labetalol, metoprolol,

propranolol.

Indications: MI, unstable angina, PSVT, A-fib, A-flutter, HTN.
Dose: See individual order and drug for route and dosage.
Contraindications: HR

60 bpm, systolic BP 100 mm Hg,

2nd- or 3rd-degree AV block, left ventricular failure.

Side Effects: Hypotension, dizziness, bradycardia, headache,

nausea and vomiting.

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Precautions: Concurrent use with calcium channel blockers,

such as verapamil or diltiazem, can cause hypotension. Use
caution in patients with a history of bronchospasm or cardiac
failure.

CALCIUM CHLORIDE

(Minerals/Electrolytes/Calcium Salt)

Indications: Hyperkalemia, hypocalcemia, hypermagnesemia;

antidote to calcium channel blockers and beta blockers; given
prophylactically with calcium channel blockers to prevent
hypotension.

Dose: Hyperkalemia and antidote to calcium channel blocker

8–16 mg/kg (usually 5–10 mL) slow IVP, may be repeated as
needed. Given prophylactically prior to IV calcium channel
blockers 2–4 mg/kg (usually 2 mL) slow IVP.

Contraindications: Hypercalcemia, VF, digoxin toxicity, renal

calculi.

Side effects: Bradycardia, asystole, hypotension, VF, nausea

and vomiting.

Precautions: Incompatible with sodium bicarbonate.

DIGOXIN IMMUNE FAB

(Fragment Antigen Binding) (Digibind)

(Antidote to Digoxin, Digitoxin)

Indications: Symptomatic digoxin toxicity or acute ingestion of

unknown amount of digoxin.

Dose: Dependent on serum digoxin levels. One 40-mg vial binds

to approximately 0.6 mg of digoxin. Dose typically
administered over 30 min.

Contraindications: Allergy only, otherwise none known.
Side Effects: Worsening of CHF, A-fib, hypokalemia; increased

serum digoxin levels.

Precautions: Allergies to sheep proteins or other sheep

products.

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DIGOXIN

(Lanoxin) (Inotropic, Antiarrhythmic)

Indications: To slow ventricular response in A-fib or A-flutter, as

a positive inotrope in CHF, pulmonary edema. May be used as
an alternative drug for PSVT.

Dose: Loading dose of 10–15

g/kg, administered over 5 min.

Maintenance dose determined by body size and renal
function.

Contraindications: Hypersensitivity, uncontrolled ventricular

arrhythmias, AV block, idiopathic hypertrophic subaortic
stenosis (IHSS), constrictive pericarditis.

Side Effects: Arrhythmias, particularly VF and AV block;

bradycardia; fatigue; nausea and vomiting; blurred or yellow
vision; headache; hypersensitivity; hypokalemia.

Precautions: Avoid electrical cardioversion of stable patients. If

the patient’s condition is unstable, use lower current settings
such as 10–20 J. Use cautiously in elderly patients. Correct
electrolyte abnormalities, monitor digoxin levels, monitor for
clinical signs of toxicity.

DILTIAZEM

(Cardizem) (Calcium Channel Blocker)

Indications: A-fib, A-flutter, PSVT refractory to adenosine with

narrow QRS complex and adequate BP.

Dose: 15–20 mg (0.25 mg/kg) IVP over 2 min. May repeat in 15

min at 20–25 mg (0.35 mg/kg) IVP over 2 min. Start
maintenance drip at 5–15 mg/hr and titrate to HR.

Contraindications: Drug- or poison-induced tachycardia, wide-

complex tachycardia of uncertain origin, rapid A-fib and A-
flutter with Wolff-Parkinson-White syndrome, sick sinus
syndrome, 2nd- and 3rd-degree AV block (unless a functional
artificial pacemaker is present).

Side Effects: Hypotension, bradycardia (including AV block),

chest pain, ventricular arrhythmias.

Precautions: Severe hypotension in patients receiving beta

blockers, hepatic injury, renal disease.

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DOPAMINE (INTROPIN)

(Vasopressor, Inotropic)

Indications: Symptomatic bradycardia and hypotension,

cardiogenic shock.

Dose: Continuous infusions (titrate to patient response): Low

dose 1–5

g/kg/min; moderate dose 5–10 g/kg/min (cardiac

doses); high dose 10–20

g/kg/min (vasopressor doses). Mix

400 mg/250 mL in normal saline, lactated Ringer’s solution, or
D5W (1600

g/mL).

Contraindications: Pheochromocytoma, uncorrected

tachycardia, cardiogenic shock with CHF.

Side Effects: Tachyarrhythmias, angina, hypotension,

palpitations, vasoconstriction, dyspnea, nausea and vomiting.

Precautions: Hypovolemia, MI. Adjust dosage in elderly

patients and in those with occlusive vascular disease. Ensure
adequate hydration prior to infusion. Taper slowly. Do not mix
with sodium bicarbonate. Use care with peripheral
administration; infiltration can cause tissue necrosis. Central
line is preferred.

EPINEPHRINE

(Adrenalin) (Adrenergic Agonist)

Indications: Cardiac arrest: PEA, asystole, pulseless VT, VF;

severe hypotension; symptomatic bradycardia; anaphylaxis;
severe allergic reactions.

Dose: Cardiac arrest 1 mg IVP (10 mL of 1:10,000 solution) every

3–5 min; follow each dose with 20 mL IV flush; higher doses
(up to 0.2 mg/kg) may be used if 1-mg dose fails. Give 2.0–2.5
mg diluted in 10 mL normal saline if administering by ET
tube. For continuous infusion add 30 mg (30 mL of 1:1000
solution) to 250 mL normal saline or D5W, run at 100 mL/hr,
and titrate to response. Profound bradycardia or hypotension
2–10

g/min IV (add 1 mg of 1:1000 solution to 500 mL

normal saline or D5W and infuse at 1–5 mL/min).
Anaphylaxis/asthma 0.1–0.5 mg SC or IM of 1:1000 solution
every 5–15 min, may be followed by 1–4

g/min continuous

infusion.

Contraindications: Hypersensitivity to adrenergic amines,

hypovolemic shock, coronary insufficiency.

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EPINEPHRINE

(Continued)

Side Effects: Angina, HTN, tachycardia, VT, VF, nervousness,

restlessness, tremors, weakness, headache, nausea.

Precautions: Use caution in HTN and increasing heart rate

(may cause increased myocardial oxygen demand). Higher
doses can contribute to postarrest cardiac impairment, but
they may be required to treat poison- or drug-induced shock.

FIBRINOLYTIC AGENTS

(Thrombolytic, Fibrinolytic)

Common Agents: Alteplase (Activase, t-PA), anistreplase

(Eminase), reteplase (Retavase), streptokinase (Streptase),
tenecteplase (TNKase).

Indications: Within

12 hr from onset of symptoms of acute

MI. Alteplase is the only fibrinolytic agent approved for acute
ischemic stroke and must be started

3 hr from onset of

symptoms.

Dose: See individual order and drug for route and dosage.
Contraindications: Active internal bleeding within 21 days

(except menses), neurovascular event within 3 months, major
surgery or trauma within 2 weeks, aortic dissection, severe
(uncontrolled) HTN, bleeding disorders, prolonged
cardiopulmonary resuscitation (CPR), lumbar puncture within
1 week.

Side Effects: Hypotension, reperfusion, arrhythmias, heart

failure, headache, increased bleeding time, deep or superficial
hemorrhage, flushing, urticaria, anaphylaxis.

Precautions: Use cautiously in patients with severe renal or

hepatic disease.

FUROSEMIDE

(Lasix) (Diuretic, Loop Diuretics)

Indications: CHF with acute pulmonary edema, hypertensive

crisis, postarrest cerebral edema, hepatic or renal disease.

Dose: 0.5–1.0 mg/kg slow IVP over 1–2 min, may repeat at 2

mg/kg slow IVP over 1–2 min.

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Contraindications: Hypersensitivity (cross-sensitivity with

thiazides and sulfonamides may occur), uncontrolled
electrolyte imbalance, hepatic coma, anuria, hypovolemia.

Side Effects: Severe dehydration, hypovolemia, hypotension,

hypokalemia, hyponatremia, hypochloremia, hyperglycemia,
dizziness, ototoxicity.

Precautions: Use cautiously in severe liver disease

accompanied by cirrhosis or ascites, electrolyte depletion,
diabetes mellitus, pregnancy, lactation, risk for ototoxicity
with increased dose or rapid injection. Monitor electrolytes
closely.

IBUTILIDE

(Corvert) (Antiarrhythmic)

Indications: SVT, including A-fib and A-flutter; most effective for

conversion of A-fib or A-flutter of short duration.

Dose: Patients

≥60 kg 1 mg IVP over 10 min, may repeat same

dose in 10 min. Patients

60 kg 0.01 mg/kg IVP over 10 min,

may repeat same dose in 10 min.

Contraindications: Known hypersensitivity, history of

ventricular arrhythmias including torsade de pointes.

Side Effects: Headache, nausea and vomiting.
Precautions: Monitor ECG for 4–6 hr after administration, with

defibrillator nearby. Correct electrolyte abnormalities prior to
use. If A-fib

48 hr, anticoagulation is required before

cardioversion with ibutilide.

ISOPROTERENOL

(Isuprel) (Sympathomimetic, Beta-

Adrenergic Agonist)

Indications: Symptomatic bradycardia, refractory torsade de

pointes unresponsive to magnesium, bradycardia in heart
transplant patients, beta blocker poisoning.

Dose: IV infusion: mix 1 mg/250 mL in normal saline, lactated

Ringer’s solution, or D5W, run at 2–10

g/min, and titrate to

patient response. In torsade de pointes titrate to increase
heart rate until VT is suppressed.

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ISOPROTERENOL

(Continued)

Contraindications: Cardiac arrest, concurrent use with

epinephrine (can cause VF or VT), poison- or drug-induced
shock (exception: beta blocker poisoning).

Side Effects: Anxiety, tachycardia, palpitations, skin flushing.
Precautions: May increase myocardial ischemia, tachycardia,

restlessness. High doses are harmful except in beta blocker
overdose.

LIDOCAINE

(Xylocaine) (Antiarrhythmic, Anesthetic)

Indications: VF or pulseless VT, stable VT, wide-complex

tachycardia of uncertain origin, wide-complex PSVT.

Dose: Cardiac arrest from VF or VT 1.0–1.5 mg/kg IVP (or 2–4

mg/kg via ET tube), may repeat 0.5–0.75 mg/kg IVP every 5–10
min, max. 3 mg/kg. Stable VT, wide-complex tachycardia of
uncertain origin use 0.5–0.75 mg/kg and up to 1.0–1.5 mg/kg,
may repeat 0.5–0.75 mg/kg every 5–10 min; max. total dose
3.0 mg/kg. If conversion is successful, start an IV infusion of
1–4 mg/min (30–50

g/kg/min) in normal saline or D5W.

Contraindications: Prophylactic use in acute MI, advanced AV

block, hypotension, Wolff-Parkinson-White syndrome,
hypersensitivity to amide-type local anesthetics.

Side Effects: Confusion, seizures, hypotension, bradycardia,

cardiovascular collapse, respiratory arrest.

Precautions: CHF, respiratory depression, shock. Reduce

maintenance dose (not loading dose) in presence of impaired
liver function or left ventricular dysfunction or in the elderly.
Stop infusion if signs of toxicity (prolonged PR interval, QRS
widening, or CNS changes) develop.

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MAGNESIUM SULFATE

(Electrolyte, Antiarrhythmic)

Indications: Torsade de pointes, VF refractory to lidocaine,

digoxin-induced VT/VF.

Dose: Cardiac arrest (in hypomagnesemia or torsade de

pointes) 1–2 g (2–4 mL of a 50% solution) diluted in 10 mL of
D5W IVP. Digoxin-induced VT or VF 1–2 g IVP. Torsade de
pointes (non-cardiac arrest) load with 1–2 g mixed in 50–100
mL of D5W infused over 5–60 min IV, then infuse 0.5–1.0 g/hr
IV (titrate to control torsade). Acute MI load with 1–2 g mixed
in 50–100 mL of D5W over 5–60 min IV, then infuse 0.5–1.0
g/hr IV for up to 24 hr.

Contraindications: Hypermagnesemia, hypocalcemia, renal

disease, AV block, toxemia of pregnancy 2 hr prior to delivery.

Side Effects: Hypotension, bradycardia, cardiac arrest,

respiratory depression, altered level of consciousness (LOC),
flushed skin, diaphoresis.

Precautions: Renal insufficiency, occasional fall in BP with

rapid administration. Monitor serum magnesium levels.

MORPHINE

(Opioid Agonist Analgesic)

Indications: Chest pain unrelieved by nitroglycerin, CHF and

dyspnea associated with pulmonary edema.

Dose: 2–4 mg IVP (over 1–5 min) every 5–30 min.
Contraindications: Hypersensitivity, heart failure due to

chronic lung disease, respiratory depression, hypotension.

Side Effects: Respiratory depression, hypotension, nausea and

vomiting, bradycardia, altered LOC, seizures.

Precautions: Administer slowly and titrate to effect. Reverse

with naloxone (0.4–2.0 mg IVP). Use caution in cerebral
edema and pulmonary edema with compromised respiration.

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NITROGLYCERIN

(Nitrostat, Nitrolingual Pumpspray)

(Antianginal, Nitrate)

Indications: Angina, CHF associated with acute MI,

hypertensive crisis.

Dose: Sublingual route, 0.3–0.4 mg (1 tablet), repeat every 5

min, max. 3 doses/15 min. Aerosol, spray for 0.5–1.0 sec at 5-
min intervals (provides 0.4 mg/dose), max. 3 sprays/15 min.
IVP at 12.5–25.0

g (if no sublingual or spray used). IV

infusion: mix 25 mg/250 mL (100

g/mL) in D5W, run at 5–20

g/min, and titrate to desired response.

Contraindications: Hypersensitivity, systolic BP

90 mm Hg;

severe bradycardia or severe tachycardia; sildenafil (Viagra),
tadalafil (Cialis), vardenafil (Levitra) within 24 hr; right
ventricular infarction.

Side Effects: Hypotension with secondary tachycardia,

syncope, headache, flushed skin.

Precautions: Do not mix with other medications; titrate IV to

maintain systolic BP

90 mm Hg. Mix only in glass IV bottles

and infuse only through tubing provided by manufacturer;
standard polyvinyl chloride tubing can bind up to 80% of the
medication, making it necessary to infuse higher doses.

OXYGEN

(Gas)

Indications: Cardiopulmonary emergencies with shortness of

breath and chest pain, cardiac or respiratory arrest.

Dose: Nasal cannula 1–6 L/min (24%–44% oxygen), Venturi mask

4–8 L/min (24%–40% oxygen), simple mask 5–8 L/min
(40%–60% oxygen), partial rebreathing mask 6–15 L/min
(35%–60% oxygen), nonrebreathing mask 6–15 L/min
(60%–90% oxygen), bag-valve-mask 15 L/min (up to 100%
oxygen).

Contraindications: Emphysema (deliver

35% oxygen unless

severely hypoxic), hyperventilation.

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Side Effects: Drying of respiratory mucosa, possible

bronchospasm if oxygen is extremely cold and dry. Oxygen
supports combustion and can fuel a fire.

Precautions: Respiratory arrest in patients with hypoxic drive.

Patient needs an airway and adequate ventilation before
oxygen is effective.

PROCAINAMIDE

(Pronestyl) (Antiarrhythmic)

Indications: Recurrent VT or VF, PSVT refractory to adenosine

and vagal stimulation, rapid A-fib with Wolff-Parkinson-White
syndrome, stable wide-complex tachycardia of uncertain
origin, maintenance after conversion.

Dose: 20 mg/min IV infusion or up to 50 mg/min under urgent

conditions, max. 17 mg/kg loading dose. Maintenance IV
infusion: mix 1 g/250 mL (4 mg/mL) in normal saline or D5W,
run at 1–4 mg/min.

Contraindications: 2nd- and 3rd-degree AV block (unless a

functioning artificial pacemaker is in place), torsade de
pointes, hypersensitivity.

Side Effects: Hypotension, widening QRS, headache, nausea

and vomiting, flushed skin, seizures, ventricular arrhythmias,
AV block, cardiovascular collapse, arrest.

Precautions: Monitor BP every 2–3 min while administering

procainamide. If QRS width increases by 50% or more, or if
BP decreases to

90 systolic, stop drug. Reduce total dose to

12 mg/kg and maintenance infusion to 1–2 mg/min if cardiac
or renal dysfunction is present. Use cautiously in myasthenia
gravis and in hepatic or renal disease and with drugs that
prolong QT interval (e.g., amiodarone, sotalol).

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SODIUM BICARBONATE

(Alkalizing Agent, Buffer)

Indications: Prolonged resuscitation with effective ventilation;

hyperkalemia; diabetic ketoacidosis; cocaine toxicity; tricyclic
antidepressant, diphenhydramine, or acetylsalicylic acid
overdose; metabolic acidosis; shock associated with severe
diarrhea.

Dose: 1 mEq/kg IVP, may repeat 0.5 mEq/kg every 10 min.
Contraindications: Metabolic and respiratory alkalosis,

hypocalcemia, renal failure, peptic ulcer, hypertension,
convulsions, hypercarbic acidosis.

Side Effects: Hypokalemia, metabolic alkalosis, seizures,

tetany.

Precautions: CHF, renal disease, cirrhosis, toxemia, concurrent

corticosteroid therapy. Not recommended for routine use in
cardiac arrest patients because adequate ventilation and CPR
are the major “buffer agents” in cardiac arrest. Incompatible
with many drugs; flush line before and after administration.

VASOPRESSIN

(Pitressin Synthetic) (Vasopressor, Hormone)

Indications: Vasodilatory (septic) shock, an alternative to

epinephrine in shock-refractory VF and pulseless VT.

Dose: Cardiac arrest 40 units IVP single dose.
Contraindications: Seizures, heart failure, asthma, coronary

artery disease (CAD), migraine, allergy to beef or pork
protein, chronic renal failure with increased blood urea
nitrogen (BUN).

Side Effects: Dizziness, headache, nausea and vomiting, MI,

chest pain, abdominal cramps, diaphoresis,
bronchoconstriction, anaphylaxis, coma, convulsions.

Precautions: Coronary artery disease (may precipitate angina

or MI), renal impairment; potent peripheral vasoconstrictor.

VERAPAMIL

(Calan, Isoptin) (Calcium Channel Blocker,

Antiarrhythmic, Antihypertensive)

Indications: PSVT (with narrow QRS and adequate BP)

refractory to adenosine, rapid ventricular rates in A-fib,
A-flutter, or MAT.

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Dose: 2.5–5.0 mg slow IVP over 2 min; may give second dose, if

needed, of 5–10 mg IVP in 15–30 min, max. dose 20 mg. An
alternative second dose is 5 mg IVP every 15 min, max. dose
30 mg.

Contraindications: A-fib with Wolff-Parkinson-White syndrome,

wide-complex tachycardia of uncertain origin, 2nd- or 3rd-
degree AV block (unless a functioning artificial pacemaker is
in place), sick sinus syndrome, hypotension, severe CHF,
cardiogenic shock.

Side Effects: Hypotension, exacerbation of CHF with left

ventricular dysfunction, bradycardia, AV block.

Precautions: Concurrent oral beta blockers, CHF, impaired

hepatic or renal function; may decrease myocardial
contractility. In geriatric patients administer dose slowly over
3 min.

Emergency Medical Skills

DEFIBRILLATION

Indications: VF or pulseless VT.
Energy Levels: Adult monophasic energy levels first shock 200

J, second shock 200–300 J, third shock 360 J; continue at 360
J for further shocks. Biphasic energy level shocks use lower
energy levels, approximately 150 J.

Application: Use handheld paddles or remote adhesive pads.

Always use a conducting gel with paddles and apply firm
pressure to chest to ensure good skin contact. Dry skin if wet,
shave excessive hair.

Methods: Manual or automated.
Precautions: Place paddles and pads several inches away from

an implanted pacemaker.

♥

Clinical Tip: May be used on children aged 1–8 years. But

always use pediatric paddles or pads and follow pediatric
protocols.

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MANUAL DEFIBRILLATION

A manual defibrillator is used to restore a normal heart rhythm.

For a patient experiencing sudden cardiac arrest, first use the
ECG tracing to verify that the rhythm is either VF or pulseless
VT, and then manually deliver an electric shock to the heart.

Procedure

1. Verify patient is in cardiac arrest, with no pulse or

respiration. Have someone provide CPR, if possible, while
the defibrillator is obtained and placed next to the patient.

2. Turn on defibrillator; verify all cables are connected.
3. Turn “lead select” to “paddles” or “defibrillator.”
4. Select initial energy level for an adult to 200 J.
5. Paddles: Use conducting gel and place on apex (lower left

chest, midaxillary) and sternum (right of sternum,
midclavicular).
Pads: Place in same locations as you would put paddles.

6. Verify rhythm as VF or pulseless VT.
7. Say, “Charging defibrillator, stand clear!”
8. Charge defibrillator.

04ECG-Tab 04 2/4/05 4:00 PM Page 100

101

9. Say, “I’m going to shock on three. One, I’m clear; two,

you’re clear; three, everybody’s clear.” Perform visual sweep
to assure all rescue personnel are clear of patient, bed, and
equipment.

10. Discharge defibrillator, reassess rhythm, and refer to

appropriate treatment algorithm for resulting rhythm.

AUTOMATIC EXTERNAL DEFIBRILLATOR (AED)

An AED is a small, lightweight device used by both professionals

and laypersons to assess heart rhythm by computer analysis. If
necessary, it administers an electric shock to restore a normal
rhythm in patients with sudden cardiac arrest. A shock is
administered only if the rhythm detected is VF or VT.

Procedure

1. Verify patient is in cardiac arrest, with no pulse or

respiration. Have someone provide CPR, if possible, while the
AED is obtained and placed next to the patient.

2. Turn on AED. Follow voice prompts or visual messages.
3. Open adhesive pads and attach pads to cables.
4. Attach pads to right sternal border and apex or as

pictured on each of the AED electrodes (see preceding manual
defibrillation figure).

5. Clear patient and stop CPR.
6. Press analyze button, if present.
7. If shock is advised, say, “I’m going to shock on three. One,

I’m clear; two, you’re clear; three, everybody’s clear.” Perform
visual sweep to ensure rescue personnel are not touching
patient or equipment. Press shock button. Reanalyze after
shock and continue as prompted by the AED.

8. If no shock is advised, check for a pulse. If no pulse,

start CPR.

♥

Clinical Tip: Fully automatic AED analyzes the rhythm and

delivers shock if indicated.

♥

Clinical Tip: Semiautomatic AED analyzes the rhythm and

tells operator that shock is indicated. If it is indicated, operator
initiates shock.

MEDS/

SKILLS

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102

CARDIOVERSION

(Synchronized)

Indications: Unstable tachycardia (altered LOC, dizziness, chest

pain, hypotension).

Energy Levels: 100 J, 200 J, 300 J, 360 J.
Application: Use handheld paddles or remote adhesive pads.

Always use a conducting gel with paddles. For conscious
patients explain the procedure and use a medication for
sedation. Consider 2.5–5.0 mg of midazolam (Versed) or 5
mg diazepam (Valium).

Methods: Place defibrillator in synchronized (sync) mode.

Charge to appropriate level. Say, “I’m going to shock on
three. One, I’m clear; two, you’re clear; three, everybody’s
clear.” Perform visual sweep and press shock button. Reassess
and treat according to appropriate algorithm.

Precautions: Reactivation of sync mode is required after each

attempted cardioversion. Defibrillators default to
unsynchronized mode. Place paddles and pads several inches
away from an implanted pacemaker.

♥

Clinical Tip: Sync mode delivers energy just after the R wave

to avoid stimulation during the refractory, or vulnerable, period.

TRANSCUTANEOUS PACING

Indications: Symptomatic bradycardia unresponsive to

atropine, bradycardia with ventricular escape rhythms,
symptomatic 2nd-degree AV block type II, or 3rd-degree AV
block.

Pacing Modes: Demand mode (synchronous) pacer senses the

patient’s heart rate and paces only when the heart rate falls
below the level set by the clinician. Fixed mode
(asynchronous) pacer cannot sense the heart rate, and the
pacer operates at the rate set by the clinician. Rate selection
is 30–180 bpm. Output is adjustable 0–200 mA. Pulse duration
varies from 20 to 40 ms.

Contraindications: Not effective in VF or pulseless VT.
Side Effects: Chest muscle contraction, burns, chest

discomfort.

Precautions: Make sure pads have good skin contact to achieve

capture and avoid burns.

MEDS/

SKILLS

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103

MEDS/

SKILLS

Female patients:
Position electrode
under breast

Anterior

Posterior

Placement of anterior-posterior pacemaker pads.

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104

MEDS/

SKILLS

PRECORDIAL THUMP

Indications: VF or pulseless VT; can cause depolarization and

return the heart to an organized rhythm. Cardiac arrest must
be witnessed.

Method: Sharply strike the midsternal area of the chest from a

height of 10–12 inches with a fist. Recheck pulse and rhythm.

Contraindications: Should not be used in infants or children.
Side Effects: Fractured ribs or sternum.
Precautions: Position the fist (thumb side up) and arm parallel

to the long axis of the sternum to avoid injuring adjacent ribs.

CAROTID SINUS MASSAGE

(Vagal Maneuver)

Indications: Can increase vagal nerve stimulation and slow SVT,

or even convert SVT to NSR, without severe hemodynamic
compromise.

Method: Supine position, head tilted to either side with neck

hyperextended. Place index and middle fingers over the
carotid artery below the angle of the jaw, as high on the neck
as possible. Massage the artery for 5–10 sec by firmly
pressing on it and rubbing.

Contraindications: Unequal carotid pulses, carotid bruits,

cervical spine injury, or history of cerebrovascular accident
(CVA) or carotid atherosclerosis.

Side Effects: Slow HR or AV block, PVCs, VT, VF, syncope,

seizure, hypotension, nausea or vomiting, stroke.

Precautions: Be sure patient is receiving oxygen and an IV is in

place. Never massage both arteries simultaneously.

04ECG-Tab 04 2/4/05 4:00 PM Page 104

Sternocleido-

mastoid

muscle

Carotid
sinus nerve

Carotid
body

Vagus nerve

Right common
carotid artery

Cardiac
plexus

105

MEDS/

SKILLS

Carotid sinus massage.

♥

Clinical Tip: Each carotid pulse should be palpated and

auscultated before the procedure to maintain safety measures.

♥

Clinical Tip: Alternate vagal maneuvers include coughing,

bearing down, holding breath.

04ECG-Tab 04 2/4/05 4:00 PM Page 105

CPR Skill Performance

Compression/

Rate of

Depth of

Pulse

Hand

CPR

Ventilation

Compressions

Check

Position for

Method

Ratio

(min)

(in.)

(artery)

Compressions

Adult, 1

rescuer

Adult, 2

rescuers

Child, 1

rescuer

Child, 2

rescuers

Infant, 1

rescuer

Infant, 2

rescuers

Newborn

106

CPR

15:2

5:1

3:1

100

≥100

≥120

–2

1–1

–1

Carotid

Brachial

Femoral

Brachial

Femoral

Brachial

Femoral

Heels of 2 hands

over lower half of
sternum

Heels of 2 hands

over lower half of
sternum

Heel of 1 hand over

lower half of
sternum

Heel of 1 hand over

lower half of
sternum

2 fingers over lower

half of sternum

2 fingers over lower

half of sternum

2 fingers over lower

half of sternum

05ECG-Tab 05 2/4/05 4:01 PM Page 106

2005

Davis.

107

CPR

CPR: Adult (older than 8 yr)

1. Check for unresponsiveness. Gently shake or tap person.

Shout, “Are you OK?”

2. If no response, call for an AED, summon help, call a

code, or call 911. Send second rescuer, if available, for help.

3. Position person supine on a hard, flat surface. Support

head and neck, loosen clothing, and expose chest.

4. Open airway by the head tilt–chin lift method or, if spinal

injury is suspected, use the jaw thrust method.

5. Look, listen, and feel for breathing for up to 10 sec.
6. If person is breathing, place in recovery position.
7. If person is not breathing, begin rescue breaths. Using a

bag-valve-mask or face mask, give two slow breaths (2 sec
each). Be sure that chest rises.

8. If the chest does not rise, reposition the head and the chin and

jaw, and give two more breaths. If chest still does not rise,
follow instructions for unconscious adult with an
obstructed airway (p 112).

9. Assess carotid pulse for signs of circulation. If signs of

circulation are present but person is still not breathing,
continue to give rescue breaths at the rate of one every 5 sec.

10. If pulse and signs of circulation are not present, begin

compressions. Place heel of your hand 2 finger-widths above
xiphoid process; place heel of the second hand over the first.
Keep elbows locked, lean shoulders over hands, and firmly
compress chest 1

–2 inches. Give 15 compressions.

Compress at a rate of 100 per min.

11. Continue to give 2 breaths followed by 15 compres-

sions. After about 1 min (or at the 4th cycle of 15:2) check
pulse and other signs of circulation. If circulation resumes but
breathing does not or is inadequate, continue rescue
breathing.

12. If breathing and circulation resume, place person in recovery

position and monitor until help arrives.

♥

Clinical Tip: The compression rate is the speed of the

compressions, not the actual number of compressions per min.
Compressions, if uninterrupted, would equal 100/min.

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108

CPR

CPR: Child (1–8 yr)

1. Check for unresponsiveness. Gently shake or tap child.

Shout, “Are you OK?”

2. If no response send a second rescuer, if available, for help.
3. Position child supine on a hard, flat surface. Support head

and neck, loosen clothing, and expose chest.

4. Open airway by the head tilt–chin lift method or, if spinal

injury is suspected, use the jaw thrust method.

5. Look, listen, and feel for breathing for up to 10 sec.
6. If child is breathing, place in recovery position.
7. If child is not breathing, begin rescue breaths. Using a bag-

valve-mask or face mask, give two slow breaths (1–1

sec

each). Be sure the chest rises.

8. If the chest does not rise, reposition the head and the chin

and jaw and give two more breaths. If chest still does not
rise, follow instructions for unconscious child with an
obstructed airway (p 113).

9. Assess carotid pulse for signs of circulation. If signs of

circulation are present but child is still not breathing, continue
to give rescue breaths at the rate of one every 3 sec.

10. If pulse and signs of circulation are not present, begin

compressions. Place heel of one hand 2 finger-widths above
xiphoid process. Keep elbow locked, lean shoulders over
hand, and firmly compress chest 1–1

in. Give 5

compressions. Compress at a rate of 100 per min.

11. Continue to give 1 breath followed by 5 compressions.

After about 1 min of CPR, check pulse and other signs of
circulation. If rescuer is alone and no signs of circulation are
present, call for an AED, summon help, call a code, or
call 911. If circulation resumes but breathing does not or is
inadequate, continue rescue breathing.

12. If breathing and circulation resume, place child in recovery

position and monitor until help arrives.

♥

Clinical Tip: It is not always necessary to wait 1 min before

calling for help if you are alone. If you know a child has had a
cardiac arrest due to heart failure, request immediate help
including a defibrillator.

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109

CPR

CPR: Infant (under 1 yr)

1. Check for unresponsiveness. Gently rub infant’s back or

sternum. Never shake an infant.

2. If no response send a second rescuer, if available, for help.
3. Position infant supine on a hard, flat surface. Support head

and neck, loosen clothing, and expose chest.

4. Open airway by the head tilt–chin lift method (do not

overextend head or airway will become obstructed). If spinal
injury is suspected, use jaw thrust method.

5. Look, listen, and feel for breathing for up to 10 sec.
6. If infant is breathing, place in recovery position.
7. If infant is not breathing, begin rescue breaths. Using a

bag-valve-mask or face mask, give two slow breaths (1–1

sec each). Be sure that chest rises.

8. If the chest does not rise, reposition the head and the chin

and jaw and give two more breaths. If chest still does not
rise, follow instructions for unconscious infant with
an obstructed airway (p 114).

9. Assess brachial or femoral pulse for signs of circulation.

If signs of circulation are present but infant is still not breath-
ing, continue rescue breaths at the rate of one every 3 sec.

10. If pulse and signs of circulation are not present, begin

compressions. Place two fingers of one hand 2 finger-
widths above xiphoid process. Firmly compress chest

–1 in.

Give five compressions. Compress at a rate of

≥100 per

min.

11. Continue to give one breath followed by five

compressions. After about 1 min of CPR, check pulse and
other signs of circulation. If rescuer is alone and no signs of
circulation are present, call for an AED, summon help,
call a code, or call 911. If circulation resumes but breathing
does not or is inadequate, continue rescue breathing.

12. If breathing and circulation resume, place infant in recovery

position and monitor until help arrives.

♥

Clinical Tip: Chest compressions must be adequate to

produce a palpable pulse during resuscitation.

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110

CPR

Obstructed Airway: Conscious Adult

or Child (1 yr or older)

Signs and Symptoms

■

Grabbing at the throat with one or both hands

■

Inability to speak; high-pitched crowing sounds

■

Wheezing, gagging, ineffective coughing

1. Determine that airway is obstructed. Ask, “Are you

choking? Can you speak?”

2. Let person know you are going to help.
3. Stand behind choking person and wrap your arms

around his or her waist. For someone who is obese or
pregnant, wrap arms around chest.

4. Make a fist. Place thumb side of fist in middle of

abdomen just above navel. Locate middle of sternum for
obese or pregnant persons.

5. Grasp fist with your other hand.
6. Press fist abruptly into

abdomen using an
upward, inward thrust.
Use a straight thrust back for
someone who is obese or
pregnant.

7. Continue thrusts until object

is dislodged or person loses
consciousness.

8. If person loses

consciousness, treat as
unconscious adult or child
with an obstructed airway
(pp 112–113).

Heimlich maneuver for adult or child.

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111

CPR

Obstructed Airway: Conscious

Infant (younger than 1 yr)

Signs and Symptoms

■

Inability to breathe or cry

■

High-pitched crowing sounds

■

Sudden wheezing or noisy breathing
1. Determine that airway is obstructed.
2. Lay infant down on your forearm, with the chest in your

hand and the jaw between your thumb and index finger.

3. Using your thigh or lap for support, keep infant’s head

lower than his or her body.

4. Give five quick, forceful blows between shoulder

blades with your palm.

5. Turn infant over to be face up on your other arm. Using

your thigh or lap for support, keep infant’s head lower than
his or her body.

6. Place two fingers on center of sternum just below nipple

line.

7. Give five quick thrusts down, depressing chest

–1

in. each time.

8. Continue sequence of five back blows and five chest

thrusts until object is dislodged or infant loses
consciousness. If infant loses consciousness, treat as
unconscious infant with an obstructed airway (p 114).

Heimlich maneuver for infant.

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112

Obstructed Airway: Unconscious

Adult (older than 8 yr)

Signs and Symptoms

■

Failure to breathe

■

Inability to move air into lungs with rescue breaths

■

Cyanosis

1. Establish unresponsiveness. Gently shake or tap person.

Shout, “Are you OK?”

2. If no response, call for an AED, summon help, call a

code, or call 911. Send second rescuer, if available, for
help.

3. Position person supine on a hard, flat surface. Support

head and neck, loosen clothing, and expose chest.

4. Open airway by the head tilt–chin lift method or, if spinal

injury is suspected, use the jaw thrust method.

5. Look, listen, and feel for breathing for up to 10 sec.
6. If person is not breathing, begin rescue breaths. If the

chest does not rise, reposition the head and the chin and jaw,
and attempt to ventilate.

7. If ventilation is unsuccessful and chest still does not rise,

begin abdominal thrusts. Straddle thighs or kneel to side
for someone who is obese or pregnant. Place heel of hand in
middle of abdomen just above umbilicus (middle of sternum
if person is obese or pregnant).

8. Place other hand on top of first hand and give five quick

thrusts inward and upward.

9. Open mouth by placing thumb over tongue and index finger

under chin. Perform a finger sweep to try to remove
object.

10. Repeat steps 6 through 9 until rescue breaths are effective.

Then continue steps for CPR.

♥

Clinical Tip: The most common cause of airway obstruction

is the tongue.

CPR

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113

Obstructed Airway: Unconscious Child (1–8 yr)

Signs and Symptoms

■

Failure to breathe

■

Inability to move air into lungs with rescue breaths

■

Cyanosis

1. Check for unresponsiveness. Gently shake or tap child.

Shout, “Are you OK?”

2. If no response send a second rescuer, if available, for help.
3. Position child supine on a hard, flat surface. Support head

and neck, loosen clothing, and expose chest.

4. Open airway by the head tilt–chin lift method or, if spinal

injury is suspected, use the jaw thrust method.

5. Look, listen, and feel for breathing for up to 10 sec.
6. If child is not breathing, begin rescue breaths. If the chest

does not rise, reposition the head and the chin and jaw, and
attempt to ventilate.

7. If ventilation is unsuccessful and chest still does not rise,

begin abdominal thrusts. Straddle child’s thighs. Place
heel of hand in middle of abdomen just above umbilicus.

8. Place other hand on top of first hand and give five quick

thrusts inward and upward.

9. Open child’s mouth by placing thumb over tongue and index

finger under chin. If object is visible and loose, perform
a finger sweep and remove it. Do not perform a blind
finger sweep.

10. If airway obstruction is not relieved after 1 min and rescuer is

alone, call for an AED, summon help, call a code, or
call 911.

11. Repeat steps 6 through 9 until rescue breaths are effective.

Then continue steps for CPR.

♥

Clinical Tip: Avoid compression of the xiphoid process.

CPR

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114

Obstructed Airway: Unconscious

Infant (younger than 1 yr)

Signs and Symptoms

■

Inability to breathe, high-pitched noises

■

Inability to move air into lungs with rescue breaths

■

Cyanosis

1. Check for unresponsiveness. Gently rub infant’s back or

sternum. Never shake an infant.

2. If no response send a second rescuer, if available, for help.
3. Position infant supine on a hard, flat surface. Support head

and neck, loosen clothing, and expose chest.

4. Open airway by the head tilt–chin lift method, or, if spinal

injury is suspected, use the jaw thrust method.

5. Look, listen, and feel for breathing for up to 10 sec.
6. If infant is not breathing, begin rescue breaths. If the chest

does not rise, reposition the head and the chin and jaw, and
attempt to ventilate.

7. If ventilation is unsuccessful and chest still does not rise, begin

back blows.

8. Lay infant down on your forearm, with the chest in your hand

and the jaw between your thumb and index finger.

9. Using your thigh or lap for support, keep infant’s head lower

than his or her body. Give five quick, forceful blows
between shoulder blades with your palm.

10. Turn infant over to be face up on your other arm. Using your

thigh or lap for support, keep infant’s head lower than his or
her body. Place two fingers on center of sternum just below
nipple line. Give five quick thrusts down, depressing chest

–1 in. each time.

11. Open infant’s mouth by placing thumb over tongue and index

finger under chin. If object is visible and loose, perform a
finger sweep and remove it. Do not perform a blind
finger sweep.

12. If airway obstruction is not relieved after 1 min and rescuer is

alone, call for an AED, summon help, call a code, or call
911.

13. Repeat steps 6 through 11 until rescue breaths are effective.

Then continue steps for CPR.

CPR

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115

CPR and Obstructed Airway Positions

Head tilt–chin lift (adult or child).

Jaw thrust maneuver.

Bag-valve-mask.

Head tilt–chin lift (infant).

Universal choking sign.

Abdominal thrusts.

CPR

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116

ACLS

Ventricular Fibrillation or

Pulseless Ventricular Tachycardia

Signs and Symptoms

■

Unresponsive state

■

No respiration, pulse, or BP

1. Establish unresponsiveness with no respiration or pulse.
2. Deliver a precordial thump if cardiac arrest is witnessed

and a defibrillator is not immediately available.

3. Begin CPR with high-flow oxygen.
4. Defibrillate at 200 J (or equivalent biphasic energy).
5. Defibrillate at 200–300 J (or equivalent biphasic energy).
6. Defibrillate at 360 J (or equivalent biphasic energy).
7. Intubate and establish IV.
8. Administer epinephrine 1 mg (10 mL of 1:10,000) IVP

(follow with 20 mL IV flush), repeat every 3–5 min; give
2.0–2.5 mg diluted in 10 mL normal saline if administering
via ET tube; or administer a single dose of vasopressin 40
U IVP.

9. Defibrillate at 360 J (or equivalent biphasic energy) within

30–60 sec after each dose of medication. Pattern should be
drug, shock; drug, shock. Consider the following anti-
arrhythmics for shock-refractory VF or VT:

10. Administer amiodarone 300 mg (diluted in 20-30 mL D5W)

IVP; or lidocaine 1.0–1.5 mg/kg IVP, 2-4 mg/kg by ET tube.

11. Repeat initial antiarrhythmic for shock-refractory VF or VT:

amiodarone 150 mg IVP; or lidocaine 0.5–0.75 mg/kg IVP,
repeat lidocaine every 5–10 min, max. 3 mg/kg.

12. Administer magnesium sulfate 1–2 g (2–4 mL of a 50%

solution) diluted in 10 mL of D5W IVP in polymorphic VT,
torsade de pointes, or suspected hypomagnesemia.

13. If no response, consider procainamide 30–50 mg/min IV

infusion, max. 17 mg/kg; or sodium bicarbonate 1 mEq/kg
IVP, may repeat 0.5 mEq/kg every 10 min.

♥

Clinical Tip: Do not delay defibrillation.

♥

Clinical Tip: If vasopressin is used, wait 10–20 min before

administering epinephrine.

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117

ACLS

Thrombosis (pulmonary)

Thrombosis (coronary)

Tension pneumothorax

Tamponade (cardiac)

Tablets (drug overdose)

Pulseless Electrical Activity

Signs and Symptoms

■

Unresponsive state

■

No respiration, pulse, or BP

■

Identifiable electrical rhythm on monitor but no pulse

1. Establish unresponsiveness with no respiration or pulse.
2. Begin CPR with high-flow oxygen.
3. Intubate and establish IV.
4. Consider and treat possible causes: pulmonary embolism,

MI, acidosis, tension pneumothorax, hyper- or hypokalemia,
cardiac tamponade, hypovolemia, hypoxia, hypothermia,
drug overdose (e.g., cyclic antidepressants, beta blockers,
calcium channel blockers, digoxin).

5. Administer epinephrine 1 mg (10 mL of 1:10,000) IVP, repeat

every 3–5 min; give 2.0–2.5 mg diluted in 10 mL normal
saline if administering by ET tube.

6. Administer atropine 1 mg IVP if ECG rate is

60 bpm.

Repeat every 3–5 min as needed to a total dose of 0.03–0.04
mg/kg. May be given by ET tube at 2–3 mg diluted in 10 mL
normal saline.

7. Consider fluid challenge of 500 mL normal saline, especially

in suspected hypovolemia.

8. If no response, consider sodium bicarbonate 1 mEq/kg IVP,

may repeat 0.5 mEq/kg every 10 min.

♥

Clinical Tip: Sodium bicarbonate may be harmful in

hypercarbic acidosis.

♥

Clinical Tip: Memory aid for causes of PEA:

Five “H” Causes

Five “T” Causes

Hypothermia

Hyperkalemia/hypokalemia

Hydrogen ion (acidosis)

Hypoxia

Hypovolemia

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118

Asystole

Signs and Symptoms

■

Unresponsive state

■

No respiration, pulse, or BP

■

ECG shows flat line; no electrical activity

1. Establish unresponsiveness with no respiration or pulse.
2. Begin CPR with high-flow oxygen.
3. Intubate and establish IV.
4. Consider and treat possible causes: pulmonary embolism,

MI, acidosis, tension pneumothorax, hyper- or
hypokalemia, cardiac tamponade, hypovolemia, hypoxia,
hypothermia, drug overdose (e.g., cyclic antidepressants,
beta blockers, calcium channel blockers, digoxin).

5. If condition remains unchanged, begin immediate

transcutaneous pacing if equipment is available.

6. Administer epinephrine 1 mg (10 mL of 1:10,000) IVP,

repeat every 3–5 min; give 2.0–2.5 mg diluted in 10 mL
normal saline if administering by ET tube.

7. Administer atropine 1 mg IVP, repeat every 3–5 min as

needed, to a total dose of 0.03–0.04 mg/kg. May be given
by ET tube at 2–3 mg diluted in 10 mL normal saline.

8. If no response, consider sodium bicarbonate 1 mEq/kg IVP,

may repeat 0.5 mEq/kg every 10 min.

9. If asystole persists, consider quality of resuscitation,

identification of reversible causes, and support for
termination protocols.

♥

Clinical Tip: Do not delay transcutaneous pacing; it takes

priority over medication.

♥

Clinical Tip: Always confirm asystole by checking the ECG in

two different leads. Also, search to identify underlying VF.

♥

Clinical Tip: Study local policy to learn established criteria

for stopping resuscitation efforts.

ACLS

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119

Ischemic Chest Pain

Signs and Symptoms

■

History of acute MI or angina

■

Chest pain or discomfort

■

Pain spreading to neck, shoulders, arms, or jaw

■

Nausea, diaphoresis, shortness of breath

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, start IV, and

obtain 12-lead ECG.

4. Administer aspirin 162–325 mg.
5. Administer nitroglycerin by sublingual route 0.3–0.4 mg (1

tablet), repeat every 5 min, max. 3 doses/15 min; or
administer aerosol spray for 0.5–1.0 sec at 5-min intervals
(provides 0.4 mg per dose).

6. Nitroglycerin administration requires BP >100 mm Hg

systolic.

7. Repeat nitroglycerin (see step 5) until chest pain is relieved,

systolic BP falls below 100 mm Hg, or signs of ischemia or
infarction are resolved.

8. If chest pain is not relieved by nitroglycerin, administer

morphine 2–4 mg IVP (over 1–5 min) every 5–30 min. Do
not administer morphine if systolic BP is

100 mm Hg.

♥

Clinical Tip: Patients should not be given nitroglycerin if they

have taken sildenafil (Viagra), tadalafil (Cialis), or vardenafil
(Levitra) in the last 24 hr. The use of nitroglycerin with these
medications may cause irreversible hypotension.

♥

Clinical Tip: Diabetic patients and women frequently present

with atypical symptoms (e.g., weakness, fatigue, complaints of
indigestion).

ACLS

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Bradycardia

Signs and Symptoms

■

Pulse rate

60 bpm

■

AV block

■

Hypotension, altered mental status, pulmonary edema, shock

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. In 2nd-degree (Mobitz type II) or 3rd-degree AV block,

proceed directly to step 5, transcutaneous pacing;
otherwise administer atropine 0.5–1.0 mg IVP every 3–5
min, max. 0.03–0.04 mg/kg.

5. If patient remains symptomatic or has 2nd-degree (Mobitz

type II) or 3rd-degree AV block, sedate patient and begin
transcutaneous pacing, if available.

6. If no response, consider dopamine with continuous

infusions (titrate to patient response) of 5–20

g/kg/min.

Mix 400 mg/250 mL in normal saline, lactated Ringer’s
solution, or D5W.

7. If patient is still hypotensive with severe bradycardia,

consider epinephrine infusion, 2–10

g/min IV (add 1 mg of

1:1000 to 500 mL normal saline and infuse at 1–5 mL/min).

8. If still no response, consider isoproterenol, IV infusion: mix

1 mg in 250 mL normal saline, lactated Ringer’s solution, or
D5W with rate of 2–10

g/min, titrate to patient response.

♥

Clinical Tip: If patient is symptomatic, do not delay

transcutaneous pacing while waiting for atropine to take effect
or for IV access.

♥

Clinical Tip: Use atropine with caution in a suspected acute

MI; atropine may induce rate-related ischemia.

♥

Clinical Tip: If patient is asymptomatic but has 2nd-degree

(Mobitz type II) or 3rd-degree AV block, use transcutaneous
pacemaker until transvenous pacer is placed.

ACLS

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Tachycardia—Unstable

Signs and Symptoms

■

Altered level of consciousness

■

Chest pain or discomfort, palpitations

■

Shortness of breath, diaphoresis

■

Hypotension, pulmonary edema, crackles, rhonchi, jugular
vein distention, peripheral edema

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. Establish that serious signs and symptoms are related to

the tachycardia.

5. If ventricular rate is

150 bpm, prepare for immediate

synchronized cardioversion.

6. Premedicate with a sedative plus an analgesic whenever

possible.

7. Administer synchronized cardioversion at 100 J (or

equivalent biphasic energy).

8. If no response, administer synchronized cardioversion at

200 J (or equivalent biphasic energy).

9. If no response, administer synchronized cardioversion at

300 J (or equivalent biphasic energy).

10. If no response, administer synchronized cardioversion at

360 J (or equivalent biphasic energy).

11. If the unstable tachycardia converts to VF or pulseless VT,

treat with immediate defibrillation and follow algorithm for
VF and pulseless VT.

♥

Clinical Tip: Reactivate sync mode before next attempted

cardioversion.

♥

Clinical Tip: If a tachycardia is VT or torsade de pointes, it

may rapidly deteriorate to VF.

♥

Clinical Tip: A-flutter and PSVT may respond to lower energy

levels such as 50 J (or equivalent biphasic energy).

ACLS

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122

Wide-Complex Tachycardia—Stable

Monomorphic VT

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. May go directly to step 8, cardioversion.

For Impaired Cardiac Function

5. Administer amiodarone 150 mg IVP over 10 min (15 mg/min),

may repeat infusion of 150 mg IVP every 10 min as needed; or
administer lidocaine 0.5–0.75 mg/kg IVP (may use up to
1.0–1.5 mg/kg), repeat 0.5–0.75 mg/kg IVP every 5–10 min,
max. 3 mg/kg.

6. If rhythm converts to sinus rhythm, begin infusion of rhythm-

converting agent: amiodarone, slow infusion of 360 mg IV
over the next 6 hr (1 mg/min) with maintenance infusion of
540 mg over the next 18 hr (0.5 mg/min); or start lidocaine
infusion of 1–4 mg/min (30–50

g/kg/min).

7. If rhythm does not convert, prepare for immediate

cardioversion.

8. Premedicate with sedative plus analgesic agent whenever

possible.

9. Administer synchronized cardioversion incrementally at 100 J,

200 J, 300 J, then 360 J (or equivalent biphasic energy).

For Normal Cardiac Function

5. Follow steps 1–4 above.
6. Otherwise, consider procainamide or sotalol.
7. Other acceptable medication is amiodarone or lidocaine.

Notes:

ACLS

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Wide-Complex Tachycardia—Stable

Polymorphic VT

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. May go directly to step 8, cardioversion.

For Impaired Cardiac Function
5. Administer amiodarone 150 mg IVP over first 10 min (15

mg/min), may repeat infusion of 150 mg IVP every 10 min as
needed; or administer lidocaine 0.5–0.75 mg/kg IVP (may use
up to 1.0–1.5 mg/kg), repeat 0.5–0.75 mg/kg IVP every 5–10 min,
max. 3 mg/kg.

6. If rhythm converts to sinus rhythm, begin infusion of rhythm-

converting agent: amiodarone, slow infusion of 360 mg IV over
the next 6 hr (1 mg/min) with maintenance infusion of 540 mg
over the next 18 hr (0.5 mg/min); or start lidocaine infusion of
1–4 mg/min (30–50

g/kg/min).

7. If rhythm does not convert, prepare for immediate cardiover-

sion.

8. Premedicate with sedative plus analgesic agent whenever

possible.

9. Administer synchronized cardioversion incrementally at 100 J,

200 J, 300 J, then 360 J (or equivalent biphasic energy).

For Normal Cardiac Function
If possible, measure QT interval before onset of VT; it cannot be

obtained in sustained VT. Torsade de pointes is an example of
polymorphic VT with an abnormally prolonged QT interval.

Normal QT Interval

Prolonged QT Interval

Correct electrolytes

Treat ischemia

Consider (any one): beta

blockers, lidocaine,
amiodarone, procainamide,
or sotalol.

ACLS

Correct electrolytes

Treat ischemia

Consider (any one):

magnesium, overdrive
pacing, isoproterenol,
phenytoin, or lidocaine.

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124

Narrow-Complex Tachycardia—Stable

Paroxysmal Supraventricular Tachycardia

Signs and Symptoms

■

If present, hypotension, syncope, or limited ability to exercise

■

Patient may be asymptomatic.

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. Attempt vagal maneuvers (e.g., carotid sinus massage,

Valsalva maneuver).

5. If rhythm has not converted to sinus rhythm, administer

adenosine 6 mg rapid IVP over 1–3 sec followed by a 20-mL
bolus of normal saline.

6. If rhythm still has not converted, repeat adenosine 12 mg IVP

in 1–2 min. A third dose of 12 mg IVP may be given after
another 1–2 min, max. 30 mg.

For Impaired Cardiac Function

7. If still no response and patient has serious signs and

symptoms with ventricular rate

150 bpm, prepare for

immediate cardioversion.

8. Premedicate with sedative plus analgesic agent whenever

possible.

9. Administer synchronized cardioversion incrementally at 100

J, 200 J, 300 J, then 360 J (or equivalent biphasic energy).

10. If rhythm still has not converted, consider digoxin,

amiodarone, or diltiazem.

For Normal Cardiac Function

7. Follow steps 1–6 above.
8. Consider in order of priority an AV blocker (beta blocker,

calcium channel blocker, digoxin), cardioversion, and an
antiarrhythmic (procainamide, amiodarone, sotalol).

ACLS

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Narrow-Complex Tachycardia—Stable

Junctional Tachycardia

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. Attempt vagal maneuvers (e.g., carotid sinus massage,

Valsalva maneuver).

5. If rhythm has not converted to sinus rhythm, administer

adenosine 6 mg rapid IVP over 1–3 sec followed by a 20-mL
bolus of normal saline.

6. If rhythm still has not converted, repeat adenosine 12 mg IVP

in 1–2 min. A third dose of 12 mg IVP may be given after
another 1–2 min, max. 30 mg.

For Impaired Cardiac Function

7. If still no response consider amiodarone, 150 mg IVP over 10

min (15 mg/min), may repeat infusion of 150 mg IVP every 10
min as needed.

8. Do not attempt cardioversion.

For Normal Cardiac Function

7. Follow steps 1–6 above.
8. Consider a beta blocker, calcium channel blocker, or

amiodarone.

9. Do not attempt cardioversion.

♥

Clinical Tip: Avoid carotid massage in patients at risk for

carotid atherosclerosis.

Notes:

ACLS

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126

Narrow-Complex Tachycardia—Stable

Ectopic or Multifocal Atrial Tachycardia

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. Attempt vagal maneuvers (e.g., carotid sinus massage,

Valsalva maneuver).

5. If rhythm has not converted to sinus rhythm, administer

adenosine 6 mg rapid IVP over 1–3 sec followed by a 20-mL
bolus of normal saline.

6. If rhythm still has not converted, repeat adenosine 12 mg IVP

in 1–2 min. A third dose of 12 mg IVP may be given after
another 1–2 min, max. 30 mg.

For Impaired Cardiac Function

7. If still no response, consider amiodarone 150 mg IVP over 10

min (15 mg/min), may repeat infusion of 150 mg IVP every 10
min as needed.

8. Consider diltiazem 15–20 mg (0.25 mg/kg) IVP over 2 min.

May repeat in 15 min at 20–25 mg (0.35 mg/kg) IVP over 2
min. Start maintenance drip at 5–15 mg/hr and titrate to HR.

9. Do not attempt cardioversion.

For Normal Cardiac Function

7. Follow steps 1–6 above.
8. Consider a beta blocker, calcium channel blocker, or

amiodarone.

9. Do not attempt cardioversion.

Notes:

ACLS

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127

ACLS

To control rate

Diltiazem (or another calcium channel

blocker) or metoprolol (or another beta
blocker)

To convert rhythm

Urgent cardioversion (

24 hr): IV heparin,

transesophageal echocardiography to
exclude atrial clot, cardioversion (within
24 hr), then anticoagulation (4 wk); or
delayed cardioversion (

3 wk):

anticoagulation (3 wk), then
cardioversion, then anticoagulation (4 wk)

To control rate

Diltiazem, digoxin, or amiodarone

To convert rhythm

Urgent cardioversion (

24 hr): IV heparin ,

transesophageal echocardiography to
exclude atrial clot, cardioversion (within
24 hr), then anticoagulation (4 wk); or
delayed cardioversion (

3 wk):

anticoagulation (3 wk), then
cardioversion, then anticoagulation (4 wk)

Narrow-Complex Tachycardia—Stable

Atrial Fibrillation or Atrial Flutter

1. Establish responsiveness.
2. Measure vital signs, including oxygen saturation.
3. Supply oxygen, begin cardiac monitoring, and start IV.
4. If rate or rhythm has not converted, proceed to the following tables:

Agents Used in Normal Cardiac Function

Duration

≤ 48 hr

Duration

48 hr

To control rate

Diltiazem (or another

calcium channel
blocker) or metoprolol
(or another beta blocker)

To convert rhythm

Recommended:

cardioversion
Or consider:
procainamide,
amiodarone, ibutilide,
flecainide, propafenone

Agents Used in Impaired Cardiac Function

Duration

≤ 48 hr

Duration

48 hr

To control rate

Diltiazem, digoxin, or

amiodarone

To convert rhythm

Recommended:

cardioversion
Or consider:
amiodarone

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128

Narrow-Complex Tachycardia—Stable

Atrial Fibrillation or Atrial Flutter with

Wolff-Parkinson-White Syndrome

tables:

To Control Rate and Rhythm

Agents Used in Normal Cardiac Function

Duration

≤ 48 hr

Duration

48 hr

Recommended:

cardioversion
Or consider:
amiodarone,
procainamide,
flecainide, pro-
pafenone, sotalol

Agents Used in Impaired Cardiac Function

Duration

≤ 48 hr

Duration

48 hr

Recommended:

cardioversion
Or consider:
amiodarone

♥

Clinical Tip: Do not use adenosine, beta blockers, calcium

channel blockers, or digoxin with A-fib or A-flutter associated
with WPW.

ACLS

Urgent cardioversion (

24 hr): IV

heparin, transesophageal
echocardiography to exclude atrial
clot, cardioversion (within 24 hr), then
anticoagulation (4 wk); or delayed
cardioversion (

3 wk):

anticoagulation (3 wk), then cardio-
version, then anticoagulation (4 wk)

Urgent cardioversion (

24 hr): IV heparin,

transesophageal echocar-diography to
exclude atrial clot, cardioversion (within
24 hr), then anticoagulation (4 wk); or
delayed cardioversion (

3 wk): anticoa-

gulation (3 wk), then cardioversion,
then anticoagulation (4 wk)

06ECG-Tab 06 2/4/05 4:01 PM Page 128

129

Notes:

ACLS

06ECG-Tab 06 2/4/05 4:01 PM Page 129

ECG Test Strip 1

Note: All ECG strips in this tab were recorded in lead II.

ECG Test Strip 2

130

TEST

STRIPS

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ECG Test Strip 3

ECG Strip 1

ECG Strip 2

ECG Strip 3

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

TEST

STRIPS

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Case Study One: A 66-year-old woman with a history of heart disease is found unresponsive.

This is an unwitnessed cardiac arrest with the initial rhythm shown in ECG strip 4. CPR is
initiated while the defibrillator is charged. Strip 5 shows the rhythm following defibrillation.
Because the first defibrillation was unsuccessful, the machine is charged a second time. The
next rhythm is shown in strip 6.

ECG Strip 4 Interpretation:

ECG Strip 5 Interpretation:

ECG Strip 6 Interpretation:

ECG Test Strip 4

TEST

STRIPS

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ECG Test Strip 5

ECG Test Strip 6

TEST

STRIPS

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ECG Test Strip 7

ECG Test Strip 8

TEST

STRIPS

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ECG Test Strip 9

ECG Strip 7

ECG Strip 8

ECG Strip 9

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

135

TEST

STRIPS

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136

Case Study Two: A 72-year-old man is complaining of dizziness and anxiety. Strip 10 shows his

initial rhythm. An IV is started and the patient is given oxygen, but his vital signs become
unstable (strip 11). An IVP of adenosine is given and his condition stabilizes with the final
rhythm, shown in strip 12.

ECG Strip 10 Interpretation:

ECG Strip 11 Interpretation:

ECG Strip 12 Interpretation:

ECG Test Strip 10

TEST

STRIPS

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ECG Test Strip 11

ECG Test Strip 12

TEST

STRIPS

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ECG Test Strip 13

ECG Test Strip 14

TEST

STRIPS

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TEST

STRIPS

ECG Test Strip 15

ECG Strip 13

ECG Strip 14

ECG Strip 15

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

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ECG Test Strip 16

ECG Test Strip 17

TEST

STRIPS

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TEST

STRIPS

ECG Test Strip 18

ECG Strip 16

ECG Strip 17

ECG Strip 18

Rate:

Rhythm: Rhythm:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

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ECG Test Strip 19

ECG Test Strip 20

TEST

STRIPS

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TEST

STRIPS

ECG Test Strip 21

ECG Strip 19

ECG Strip 20

ECG Strip 21

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

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144

Case Study Three:

A 44-year-old man complains of severe chest pain. He has diaphoresis, a

BP of 80/60, and 24 respirations per min. The initial rhythm, recorded by the paramedics, is
shown in strip 22. An IV is started and the patient is given oxygen. Because his condition is
unstable, he receives sedation and cardioversion (strip 23). There is no change, and
cardioversion is performed a second time (strip 24).

ECG Strip 22 Interpretation:

ECG Strip 23 Interpretation:

ECG Strip 24 Interpretation:

ECG Test Strip 22

TEST

STRIPS

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ECG Test Strip 23

ECG Test Strip 24

TEST

STRIPS

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ECG Test Strip 25

ECG Test Strip 26

TEST

STRIPS

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TEST

STRIPS

ECG Test Strip 27

ECG Strip 25

ECG Strip 26

ECG Strip 27

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

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ECG Test Strip 28

ECG Test Strip 29

TEST

STRIPS

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TEST

STRIPS

ECG Test Strip 30

ECG Strip 28

ECG Strip 29

ECG Strip 30

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

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ECG Test Strip 31

ECG Test Strip 32

TEST

STRIPS

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ECG Test Strip 33

ECG Strip 31

ECG Strip 32

ECG Strip 33

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

TEST

STRIPS

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ECG Test Strip 34

ECG Test Strip 35

TEST

STRIPS

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TEST

STRIPS

ECG Test Strip 36

ECG Strip 34

ECG Strip 35

ECG Strip 36

Rate:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

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154

ECG Test Strip 37

ECG Test Strip 38

TEST

STRIPS

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155

TEST

STRIPS

ECG Test Strip 39

ECG Strip 37 Interpretation:

ECG Strip 38 Interpretation:

ECG Strip 39 Interpretation:

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156

ECG Test Strip 40

ECG Test Strip 41

TEST

STRIPS

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ECG Test Strip 42

ECG Strip 40

ECG Strip 41

ECG Strip 42

Rate:

Rhythm: Rhythm:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

TEST

STRIPS

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ECG Test Strip 43

ECG Test Strip 44

TEST

STRIPS

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ECG Test Strip 45

ECG Strip 43

ECG Strip 44

ECG Strip 45

Rate:

Rhythm: Rhythm:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

TEST

STRIPS

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ECG Test Strip 46

ECG Test Strip 47

TEST

STRIPS

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ECG Test Strip 48

ECG Strip 46

ECG Strip 47

ECG Strip 48

Rate:

Rhythm: Rhythm:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

TEST

STRIPS

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ECG Test Strip 49

ECG Test Strip 50

TEST

STRIPS

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TEST

STRIPS

ECG Test Strip 51

ECG Strip 49

ECG Strip 50

ECG Strip 51

Rate:

Rhythm: Rhythm:

Rhythm:

P Waves:

PR Interval:

QRS:

Interpretation:

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164

TEST

STRIPS

Rate: 34 bpm

Rhythm: Regular

P Waves: None

PR Interval: None

QRS: 0.20 sec

Interpretation:

Idioventricular
rhythm

Rate: Ventricular 150 bpm,

atrial 280 bpm

Rhythm: Regular

P Waves: Flutter waves

PR Interval: Variable

QRS: 0.08 sec

Interpretation: Atrial flutter

with 2:1 conduction

Answers to ECG Test Strips

ECG Strip 1

ECG Strip 2

ECG Strip 3

Rate: 35 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: Sinus

bradycardia

ECG Strip 4 Interpretation: Ventricular fibrillation

ECG Strip 5 Interpretation: VF with defibrillation converting back to same rhythm

ECG Strip 6 Interpretation: VF with defibrillation converting to sinus rhythm at 68 bpm

Notes:

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165

ECG Strip 7

ECG Strip 8

ECG Strip 9

Rate: 115 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.12 sec

QRS: 0.10 sec

Interpretation: Sinus

tachycardia

ECG Strip 10 Interpretation: Paroxysmal supraventricular tachycardia—initial junctional rhythm

at 48 bpm converting to supraventricular tachycardia at 250 bpm

ECG Strip 11 Interpretation: SVT at 250 bpm

ECG Strip 12 Interpretation: SVT at 250 bpm converting to a sinus rhythm at 100 bpm

Notes:

TEST

STRIPS

Rate: None

Rhythm: None

P Waves: None

PR Interval: None

QRS: None

Interpretation:

Asystole

Rate: 115 bpm

Rhythm: Regular

P Waves: None

PR Interval: None

QRS: Wide (

0.12 sec), bizarre

Interpretation: Ventricular

tachycardia—monomorphic

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ECG Strip 13

ECG Strip 14

ECG Strip 15

Rate: 41 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.20 sec

QRS: 0.24 sec

Interpretation: Sinus brady-

cardia with a bundle branch
block

ECG Strip 16

ECG Strip 17

ECG Strip 18

Rate: Atrial

350 bpm,

ventricular 88–115 bpm

Rhythm: Irregular

P Waves: None

PR Interval: None

QRS: 0.12 sec

Interpretation: Atrial

fibrillation

166

TEST

STRIPS

Rate: Basic rate 79 bpm

Rhythm: Irregular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.08 sec

Interpretation: Sinus rhythm

with sinus pause/arrest

Rate: 58 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.32 sec

QRS: 0.08 sec

Interpretation: Sinus

bradycardia with
1st-degree AV block

Rate: Atrial 60 bpm

Rhythm: Atrial regular

P Waves: Normal

PR Interval: None

QRS: None

Interpretation: P Wave

asystole

Rate: Basic rate 68 bpm

Rhythm: Irregular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.08 sec

Interpretation: Sinus rhythm

with premature ventricular
contractions—triplets

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167

ECG Strip 19

ECG Strip 20

ECG Strip 21

Rate: 65 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.20 sec

QRS: 0.08 sec

Interpretation: Normal

sinus rhythm with U wave

ECG Strip 22 Interpretation: VT—monomorphic

ECG Strip 23 Interpretation: VT—monomorphic with cardioversion converting to same rhythm

ECG Strip 24 Interpretation: VT—monomorphic with cardioversion converting to a sinus rhythm

at 65 bpm

Notes:

TEST

STRIPS

Rate: 214 bpm

Rhythm: Regular

P Waves: None

PR Interval: None

QRS: Wide (

0.12 sec),

bizarre

Interpretation: VT—

monomorphic

Rate: Basic rate 35 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.08 sec

Interpretation: Sinus

bradycardia with ventricular
bigeminy

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ECG Strip 25

ECG Strip 26

ECG Strip 27

Rate: Pacing spikes 68 bpm

Rhythm: Regular pacing

spikes

P Waves: None

PR Interval: None

QRS: None

Interpretation: Pacemaker—

100% failure to capture,
underlying rhythm asystole

ECG Strip 28

ECG Strip 29

ECG Strip 30

Rate: 50–75 bpm

Rhythm: Irregular

P Waves: Normal

PR Interval: 0.12–0.28 sec

QRS: 0.08 sec

Interpretation: 2nd-degree

AV block Type I

TEST

STRIPS

Rate: Atrial 125 bpm,

ventricular 44 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: 2nd-degree AV

block Type II with 3:1
conduction

Rate: 200–250 bpm

Rhythm: Irregular

P Waves: None

PR Interval: None

QRS: Wide (

0.12 sec), bizarre

Interpretation: VT—torsade de

pointes

Rate: None

Rhythm: None

P Waves: None

PR Interval: None

QRS: None

Interpretation: Loose

electrodes

Rate: Basic rate 68 bpm

Rhythm: Irregular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: Sinus rhythm

with multiform PVCs—
couplets

07ECG-Tab 07 2/4/05 4:02 PM Page 168

2005

Davis.

169

TEST

STRIPS

ECG Strip 31

ECG Strip 32

ECG Strip 33

Rate: 68 bpm

Rhythm: Regular

P Waves: Upright with pacing

spikes

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: Atrial

pacemaker with 100%
capture

ECG Strip 34

ECG Strip 35

ECG Strip 36

Rate: 48 bpm

Rhythm: Regular

P Waves: Inverted

PR Interval: 0.12 sec

QRS: 0.08 sec

Interpretation: Junctional

rhythm

Rate: Atrial 75 bpm,

ventricular 48 bpm

Rhythm: Regular

P Waves: Normal,

superimposed on QRS and
T waves

PR Interval: Varies

QRS: 0.16 sec

Interpretation: 3rd-degree AV

block

Rate: 250 bpm

Rhythm: Irregular

P Waves: None

PR Interval: None

QRS: Wide (

0.12 sec),

bizarre

Interpretation: VT—

polymorphic

Rate: Indeterminate

Rhythm: Irregular

P Waves: None

PR Interval: None

QRS: None

Interpretation: VF

Rate: Atrial

≥350 bpm,

ventricular 94–167 bpm

Rhythm: Irregular

P Waves: None

PR Interval: None

QRS: 0.10 sec

Interpretation: A-fib

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170

ECG Strip 37 Interpretation: Agonal rhythm at 22 bpm

ECG Strip 38 Interpretation: Pacemaker failure to capture. When the pacemaker voltage is

increased, there is capture at pacemaker spike 4.

ECG Strip 39 Interpretation: Junctional bradycardia at 38 bpm converting to sinus bradycardia

at 38 bpm

Notes:

ECG Strip 40

ECG Strip 41

ECG Strip 42

Rate: 75 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.08 sec

Interpretation: Normal

sinus rhythm

TEST

STRIPS

Rate: Basic rate 79 bpm

Rhythm: Irregular

P Waves: Normal

PR Interval: 0.20 sec

QRS: 0.10 sec

Interpretation: Sinus

rhythm with ventricular
trigeminy

Rate: Basic rate 68 bpm

Rhythm: Irregular

P Waves: Normal; none

associated with premature
junctional contraction

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: Sinus rhythm

with PJCs at beats 4 and 6

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171

ECG Strip 43

ECG Strip 44

ECG Strip 45

Rate: 75 bpm

Rhythm: Regular

P Waves: Upright with

pacing spike

PR Interval: 0.20 sec

QRS: 0.16 sec

Interpretation: Atrial-

ventricular pacemaker

ECG Strip 46

ECG Strip 47

ECG Strip 48

Rate: 88 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.12 sec

QRS: 0.12 sec

Interpretation: Sinus

rhythm with ST segment
elevation

TEST

STRIPS

Rate: 75 bpm

Rhythm: Regular

P Waves: Not visible

PR Interval: Not measurable

QRS: Not measurable

Interpretation: Sinus

rhythm with muscle
artifact

Rate: 68 bpm

Rhythm: Irregular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: Sinus rhythm

with two premature atrial
contractions (beats 2 and 7)

Rate: 250 bpm

Rhythm: Regular

P Waves: Buried in T waves

PR Interval: Not measurable

QRS: 0.08 sec

Interpretation: SVT

Rate: 136 bpm

Rhythm: Regular

P Waves: Not visible

PR Interval: Not measurable

QRS: 0.10 sec

Interpretation: Sinus

tachycardia with muscle
artifact

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172

ECG Strip 49

ECG Strip 50

ECG Strip 51

Rate: 71 bpm

Rhythm: Regular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: Sinus rhythm

with ST segment depression

Notes:

TEST

STRIPS

Rate: Basic rate 79 bpm

Rhythm: Irregular

P Waves: Normal

PR Interval: 0.16 sec

QRS: 0.10 sec

Interpretation: Sinus rhythm

with two SA blocks

Rate: 107 bpm

Rhythm: Regular

P Waves: Notched (P prime)

PR Interval: 0.20 sec

QRS: 0.12 sec

Interpretation: Sinus

tachycardia with P

′ wave

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173

Notes:

TEST

STRIPS

07ECG-Tab 07 2/4/05 4:02 PM Page 173

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174

TOOLS

Troubleshooting ECG Problems

■

Place leads in the correct position. Incorrect placement can give
false readings.

■

Avoid placing leads over bony areas.

■

In patients with large breasts, place the electrodes under the
breast. Accurate tracings are obtained through the least amount
of fat tissue.

■

Apply tincture of benzoin to the electrode sites if the patient is
diaphoretic. The electrodes will adhere to the skin better.

■

Shave hair at the electrode site if it interferes with contact
between the electrode and skin.

■

Discard old electrodes and use new ones if the gel on the back of
the electrode dries.

Cable Connections

It is important to know if you are using an American or European cable

for ECG monitoring. The colors of the wires differ as shown below.

Monitoring Cable Connections

U.S.A.

Connect to

Europe

White

Right arm

Red

Black

Left arm

Yellow

Red

Left leg

Green

Right leg

Black

Brown

Chest

White

Patient Cable

Monitoring cables contain varying numbers of wires.

3- and 4-wire cables: Allow a choice of limb and augmented leads.
5-wire cable: Allows a choice of limb and augmented leads plus a

chest lead.

10-wire cable: Records a 12-lead ECG.

08ECG-Tab 08 2/4/05 4:03 PM Page 174

175

TOOLS

Patient ECG Record

Patient Name: _______________________________________________

Sex

Heart rate: ________ bpm

■

Normal (60–100 bpm)

■

Bradycardia (

60 bpm)

■

Tachycardia (

100 bpm)

Rhythm

■

Regular

■

Irregular

■

P waves

P Waves (form)

■

Normal (upright and uniform)

■

Inverted

P wave associated with QRS

PR interval normal (0.12–0.20 sec)

P waves and QRS complexes associated with one another

Y N

QRS Interval

■

Normal (0.6–0.10 sec)

■

Wide (

0.10 sec)

Are the QRS complexes grouped or not grouped?

Are there any dropped beats?

Is there a compensatory or noncompensatory pause?

QT interval:

Interpretation:

08ECG-Tab 08 2/4/05 4:03 PM Page 175

176

TOOLS

HEART RATE 1 Cycle from reference arrow (25 mm/s)

150 100

75 60

125

HEART RATE 2 Cycles from reference arrow (25 mm/s)

400

200150

125100

300

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177

TOOLS

HEART RATE 3 Cycles from reference arrow (25 mm/s)

100

125

150

200

300

400

Inches

08ECG-Tab 08 2/4/05 4:03 PM Page 177

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178

Abbreviations

ACE

angiotensin-converting enzyme

AED

automatic external defibrillator

A-fib

atrial fibrillation

A-flutter

atrial flutter

ARDS

acute respiratory distress syndrome

atrioventricular

BBB

bundle branch block

blood pressure

bpm

beats per min

BUN

blood urea nitrogen

CAD

coronary artery disease

CHF

congestive heart failure

cardiac output

COPD

chronic obstructive pulmonary disease

CPR

cardiopulmonary resuscitation

CVA

cerebrovascular accident

ECG

electrocardiogram

EMD

electromechanical dissociation

endotracheal

FAB

fragment antigen binding

heart rate

HTN

hypertension

IHSS

idiopathic hypertrophic subaortic stenosis

intramuscular

intravenous

IVP

intravenous push

left arm

left leg

LOC

level of consciousness

MAT

multifocal atrial tachycardia

MCL

modified chest lead

myocardial infarction

NSR

normal sinus rhythm

PAC

premature atrial contraction

PAT

paroxysmal atrial tachycardia

PEA

pulseless electrical activity

TOOLS

08ECG-Tab 08 2/4/05 4:03 PM Page 178

179

PJC

premature junctional contraction

by mouth

PSVT

paroxysmal supraventricular tachycardia

PVC

premature ventricular contraction

right arm

right leg

sinoatrial

subcutaneous

stroke volume

SVT

supraventricular tachycardia

ventricular fibrillation

ventricular tachycardia

WAP

wandering atrial pacemaker

WPW

Wolff-Parkinson-White

TOOLS

08ECG-Tab 08 2/4/05 4:03 PM Page 179

180

Selected References

1. Cummins, RO (ed.): ACLS Provider Manual. American Heart

Association, Dallas, 2002.

2. Deglin, JH, Vallerand, AH: Davis’s Drug Guide for Nurses, ed

8. FA Davis, Philadelphia, 2003.

3. Deglin, JH, Vallerand, AH: Med Notes. FA Davis, Philadelphia,

2004.

4. Myers, E: RNotes. FA Davis, Philadelphia, 2003.

5. Myers, E, Hopkins, T: MedSurg Notes. FA Davis, Philadelphia,

2004.

6. Physicians’ Desk Reference, ed 59. Thomson Healthcare,

Montvale, NJ, 2005.

7. Scanlon, VC, Sanders, T: Essentials of Anatomy and

Physiology, ed 4. FA Davis, Philadelphia, 2003.

8. Stapleton, ER, et al. (eds.): BLS for Healthcare Providers.

American Heart Association, Dallas, 2001.

9. Taber’s Cyclopedic Medical Dictionary, ed 19. FA Davis,

Philadelphia, 2001.

TOOLS

09ECG-Ref 2/4/05 4:03 PM Page 180

181

Illustration Credits

Pages 2, 3, 4, 5, 6, 7, 8, from: Scanlon, Essentials of Anatomy and

Physiology, ed 4. F.A. Davis, Philadelphia, 2003.

Pages 10, 11, 16, 19, 73, 100, 111, 115 from: Myers, MedSurg

Notes. F.A. Davis, Philadelphia, 2004.

Pages 28–64, 66–70, 130–163 from: Armstrong Medical

Industries, Inc. Lincolnshire, IL.

TOOLS

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182

TOOLS

Accelerated idioventricular

rhythm, 49, 49f

Accelerated junctional rhythm,

44, 44f

ACE (angiotensin-converting

enzyme) inhibitors, as emer-
gency cardiac medications,
86

Acute MI. See Infarction,

myocardial.

Adenosine, as emergency

cardiac medication, 86–87

Adult, cardiopulmonary resus-

citation of, 106t, 107
conscious, emergency

management of obstructed
airway in, 110

Heimlich maneuver in, 110f
unconscious, emergency

management of obstructed
airway in, 112

AED (automated external

defibrillator), 101

A-fib (atrial fibrillation), 41, 41f,

140f, 153f, 166, 169
management of, 127

in Wolff-Parkinson-White

syndrome, 128

A-flutter (atrial flutter), 40, 40f,

131f, 164
management of, 127

in Wolff-Parkinson-White

syndrome, 128

Agonal rhythm, 154f, 170
Airway obstruction, emergency

management of, 110–114,
115f

in conscious adult, 110
in conscious child, 110
in conscious infant, 111
in unconscious adult,

112

in unconscious child, 113
in unconscious infant, 114
via Heimlich maneuver,

110f, 111f

universal sign of, 115f

Amiodarone, as emergency

cardiac medication, 87

Angiotensin-converting

enzyme (ACE) inhibitors, as
emergency cardiac medica-
tions, 86

Anterior myocardial infarction,

79, 79f

Arrest, sinus, 32, 32f, 138f, 166
Arrhythmia(s), 28–59, 29f–59f

atrial, 34–42, 34f–42f
junctional, 43–47, 43f–47f
sinoatrial node, 28–33,

29f–33f

sinus, 31, 31f
ventricular, 48–59, 48f–59f

Arterial circulation, 7f

coronary, 5f

Artifacts, 69, 69f, 70, 70f

muscle, 70f, 158f, 161f, 171

Index

Note: Page numbers followed by f refer to illustrations and

pages followed by t refer to tables.

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Aspirin, as emergency cardiac

medication, 88

Asystole, 59, 59f, 134f, 140f,

165, 166
management of, 118

Atrial arrhythmias, 34–42,

34f–42f

Atrial contraction(s), prema-

ture, 36, 36f, 159f, 171

Atrial fibrillation (A-fib), 41,

41f, 140f, 153f, 166, 169
management of, 127

in Wolff-Parkinson-White

syndrome, 128

Atrial flutter (A-flutter), 40, 40f,

131f, 164
management of, 127

in Wolff-Parkinson-White

syndrome, 128

Atrial pacemaker, wandering,

34, 34f

Atrial tachycardia, 37, 37f

multifocal, 35, 35f

Atrioventricular block(s),

60–64, 60f–64f
first-degree, 60, 60f, 139f,

166

Mobitz I, 61, 61f, 148f, 168
Mobitz II, 62, 62f, 146f, 168
second-degree, 61, 61f, 62,

62f, 146f, 148f, 168

third-degree, 63, 63f, 150f,

169

Wenckebach, 61, 61f

Atrioventricular node, 10
Atropine, as emergency

cardiac medication, 88

Augmented limb leads, in elec-

trocardiography, 15, 15f

Automated external defibrilla-

tor (AED), 101

Automaticity, of cardiac cells,

AV. See Atrioventricular

entries.

Bag-valve mask, in airway

management, 115f

BBB (bundle branch block), 64,

64f, 138f, 166
left, 84, 84f
right, 85, 85f

Beta blockers, as emergency

cardiac medications, 88–89

Bicarbonate, as emergency

cardiac medication, 98

Bigeminy, ventricular, 52, 52f,

143f, 167

Block(s), atrioventricular,

60–64, 60f–64f

first-degree, 60, 60f, 139f,

166

Mobitz I, 61, 61f, 148f, 168
Mobitz II, 62, 62f, 146f, 168
second-degree, 61, 61f, 62,

62f, 146f, 148f, 168

third-degree, 63, 63f, 150f,

169

Wenckebach, 61, 61f

bundle branch, 64, 64f, 138f,

166
left, 84, 84f
right, 85, 85f

sinoatrial, 33, 33f, 162f, 172

Blood vessel structures, 6, 6f
Bradycardia, 120

junctional, 155f, 170

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TOOLS

Bradycardia (Continued)

management of, 120
sinus, 29, 29f, 130f, 138f,

139f, 143f, 164, 166, 167
junctional bradycardia

converting to, 155f, 170

with muscle artifact, 161f,

171

Bundle branch(es), 10
Bundle branch block (BBB), 64,

64f, 138f, 166
left, 84, 84f
right, 85, 85f

Bundle of His, 10

Cable connections, in electro-

cardiography, 17, 17f, 174

Calcium chloride, as emer-

gency cardiac medication,
89

Cardiac anatomy, 1, 1f–5f, 3
Cardiac electrophysiology,

9–11, 10f–11f, 74, 74f. See
also Electrocardiography
(ECG).

Cardiac ischemia, 76, 76f. See

also Infarction, myocardial.
chest pain due to, manage-

ment of, 119

Cardiopulmonary resuscitation

(CPR), 106t, 107–109, 115f
by one rescuer, 106t
by two rescuers, 106t
of adult, 106t, 107
of child, 106t, 108
of infant, 106t, 109
of newborn, 106t

Cardiovascular system, 6, 6f–8f

Cardioversion, 102
Carotid sinus massage,

104–105, 105f

Chambers of heart, 4f
Chest compressions, in CPR,

106t, 107, 108, 109

Chest leads, in electrocardiog-

raphy, 16, 16f, 18, 18f

Chest pain, ischemic, manage-

ment of, 119

Child, cardiopulmonary resus-

citation of, 106t, 108
conscious, emergency

management of
obstructed airway in, 110

Heimlich maneuver in, 110f
unconscious, emergency

management of
obstructed airway in, 113

Chin lift, in airway manage-

ment, 115f

Choking. See Airway obstruc-

tion.

Circulation, arterial, 7f

coronary, 5f

venous, 8f

Complex, 21

QRS, 22, 27

Complex width, tachycardia

management in relation to,
122, 123, 124–128

Conduction system, of heart,

10–11, 10f–11f. See also
Electrocardiography (ECG).

Conductivity, of cardiac cells, 9
Conscious patient, emergency

management of obstructed
airway in, 110, 111

Contractility, of cardiac cells, 9

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Contraction(s), atrial, prema-

ture, 36, 36f, 159f, 171
junctional, premature, 47,

47f, 157f, 170

ventricular, premature, 50,

50f
couplet (paired), 53, 53f,

149f, 168

every 2nd beat (bigemi-

nal), 52, 52f, 147f,
163

every 3rd beat (trigemi-

nal), 52, 52f, 156f, 170

every 4th beat

(quadrigeminal), 53,
53f

multiform, 51, 51f
paired (couplet), 53, 53f,

149f, 168

triplet, 141f, 166
uniform, 51, 51f

Coronary arterial circulation,

Couplet PVCs (paired PVCs),

53, 53f, 149f, 168

CPR. See Cardiopulmonary

resuscitation (CPR).

Defibrillation, 99–101, 100f

automated external, 101
manual, 100

Depolarization, 11
Digoxin, as emergency cardiac

medication, 90

Digoxin toxicity, antidote for,

Diltiazem, as emergency

cardiac medication, 90

Dopamine, as emergency

cardiac medication,
91

Dropped beats, 26

ECG. See Electrocardiography

(ECG).

Electrical activity, pulseless,

58, 58f
management of, 117
mnemonics for causes of,

117

Electrical axis deviation, of

heart, 74, 74f

Electrical conduction system,

of heart, 10–11, 10f–11f. See
also Electrocardiography
(ECG).

Electrocardiography (ECG),

12–13, 21f

cable connections in, 17, 17f,

174

electrode placement in,

13–20, 13f–20f
loose, artifact due to, 69f,

148f, 168

fifteen-lead, 20, 20f
heart rate calculation via,

23–24, 23f, 25f, 176f,
177f

interpretation of results of,

22, 26–27

as abnormal, 28–64,

29f–64f. See also
Arrhythmia(s) and
specific patterns.

as artifactual. See

Artifacts.

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TOOLS

Electrocardiography (Cont’d)

as diagnostic yield in

suspected MI, 79–83,
79f–83f

as pacemaker rhythms, 66,

66f, 67f, 150f, 158f, 169,
171

on patient’s record, 175

leads used in, 13–20, 13f–20f
monitoring cables in, 174
troubleshooting in, 174
twelve-lead, 19, 19f, 72, 78,

78f

Emergency medical skills,

99–115

Emergency medications, 86–99
Endocardium, 2f
Epinephrine, as emergency

cardiac medication, 91–92

Escape beat, junctional, 46,

46f

Excitability, of cardiac cells, 9
External defibrillator, auto-

mated, 101

Fibrillation, atrial, 41, 41f, 140f,

153f, 166, 169

management of, 127

in Wolff-Parkinson-White

syndrome, 128

ventricular, 57, 57f, 132f,

133f, 151f, 164, 169
management of, 116

Fibrinolytic agents, as emer-

gency cardiac medications,
92

Fifteen-lead electrocardiogra-

phy, 20, 20f

First-degree atrioventricular

block, 60, 60f, 139f, 166

Flutter, atrial, 40, 40f, 131f,

164
management of, 127

in Wolff-Parkinson-White

syndrome, 128

Furosemide, as emergency

cardiac medication, 92–93

Great vessels of heart, 4f

H mnemonic, for causes of

pulseless electrical activity,
117

Head tilt, in airway manage-

ment, 115f

Heart, anatomy of, 1, 1f–5f, 3

cells of, properties of, 9
chambers of, 4f
coronary arteries of, 5f
electrical axis deviation of,

74, 74f

electrical conduction system

of, 10–11, 10f–11f. See also
Electrocardiography
(ECG).

great vessels of, 4f
ischemia of, 76, 76f. See also

Infarction, myocardial.
chest pain due to,

management of, 119

layers of, 2f

infarct sites in. See

Infarction, myocardial.

physiology of, 9
valves of, 3, 3f

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Heart rate, methods of calcu-

lating, 23–24, 23f, 25f, 176f,
177f

Heimlich maneuver, 110f, 111f

Ibutilide, as emergency cardiac

medication, 93

Idioventricular rhythm, 48, 48f,

130f, 164
accelerated, 49, 49f

Infant, cardiopulmonary resus-

citation of, 106t, 109
conscious, emergency

management of
obstructed airway in, 111

Heimlich maneuver in, 111f
unconscious, emergency

management of
obstructed airway in, 114

Infarction, myocardial, 75, 76,

79–83
anterior, 79, 79f
electrocardiographic

evidence for, 79–83,
79f–83f

inferior, 80, 80f
lateral, 81, 81f
posterior, 83, 83f
propagation of, 76, 76f
septal, 82, 82f

Inferior myocardial infarction,

80, 80f

Interval(s), 21

PR, 22, 26
QRS, 26
QT, 22, 26

Ischemia, cardiac, 76, 76f. See

also Infarction, myocardial.

chest pain due to, manage-

ment of, 119

Isoproterenol, as emergency

cardiac medication, 93–94

Jaw thrust, in airway manage-

ment, 115f

Junctional arrhythmias, 43–47,

43f–47f

Junctional bradycardia, 155f,

170

Junctional contraction(s),

premature, 47, 47f, 157f, 170

Junctional escape beat, 46, 46f
Junctional rhythm, 43, 43f

accelerated, 44, 44f

Junctional tachycardia, 45, 45f

management of, 125

Lateral myocardial infarction,

81, 81f

Left bundle branch, 10
Left bundle branch block, 84,

84f

Lidocaine, as emergency

cardiac medication, 94

Limb leads, in electrocardiog-

raphy, 13–15, 13f–15f

Loose electrode(s), artifact due

to, 69f, 148f, 168

Magnesium sulfate, as emer-

gency cardiac medication, 95

Manual defibrillation, 100
Massage, carotid sinus,

104–105, 105f

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MAT (multifocal atrial tachycar-

dia), 35, 35f

Medical skills, emergency,

99–115

Medications, emergency,

86–99

MI. See Myocardial infarction.
Mobitz I atrioventricular block,

61, 61f, 148f, 168

Mobitz II atrioventricular block,

62, 62f, 146f, 168

Monitoring cables, in electro-

cardiography, 174

Monomorphic ventricular

tachycardia, 54, 54f, 135f,
142f, 143f, 145f, 165, 167
management of, 122

Morphine, as emergency

cardiac medication, 95

Multifocal atrial tachycardia

(MAT), 35, 35f

Multiform premature ventricu-

lar contraction, 51, 51f

Muscle artifacts, 70f, 158f, 161f,

171

Myocardial infarction, 75, 76,

79–83
anterior, 79, 79f
electrocardiographic

evidence for, 79–83,
79f–83f

inferior, 80, 80f
lateral, 81, 81f
posterior, 83, 83f
propagation of, 76, 76f
septal, 82, 82f

Myocardium, 2f

acute infarction of. See

Myocardial infarction.

Narrow-complex tachycardia,

management of, 124–128

Newborn, cardiopulmonary

resuscitation of, 106t

Nitroglycerin, as emergency

cardiac medication, 96

Obstructed airway, emergency

management of, 110–114,
115f

in conscious adult, 110
in conscious child, 110
in conscious infant, 111
in unconscious adult, 112
in unconscious child, 113
in unconscious infant,

114

via Heimlich maneuver,

110f, 111f

universal sign of, 115f

One-rescuer cardiopulmonary

resuscitation, 106t

Oxygen, as emergency cardiac

medication, 96–97

P wave, 22, 26
PAC(s) (premature atrial

contraction[s]), 36, 36f, 159f,
171

Pacemaker, atrial, wandering,

34, 34f

Pacemaker device(s), 65

malfunction of, 68, 68f, 146f,

154f, 168, 170

Pacemaker rhythm, 66, 66f,

67f, 150f, 158f, 169, 171

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Pacing, transcutaneous, 102,

103f

Pain, ischemic, management

of, 119

Paired PVCs (couplet PVCs),

53, 53f, 149f, 168

Paroxysmal supraventricular

tachycardia (PSVT), 39, 39f,
136f, 165
management of, 124

Pause, sinus, 32, 32f, 138f, 166
PEA (pulseless electrical activ-

ity), 58, 58f
management of, 117
mnemonics for causes of,

117

Pediatric patient, cardiopul-

monary resuscitation of,
106t, 108, 109
conscious, emergency

management of
obstructed airway in, 110,
111

Heimlich maneuver in, 110f,

111f

unconscious, emergency

management of
obstructed airway in, 113,
114

Pericardium, 2f
PJC(s) (premature junctional

contraction[s]), 47, 47f, 157f,
170

Polymorphic ventricular tachy-

cardia, 55, 55f, 152f, 169
management of, 123

Posterior myocardial infarc-

tion, 83, 83f

PR interval, 22, 26

Precordial thump, 104
Premature atrial contraction(s)

(PAC[s]), 36, 36f, 159f, 171

Premature junctional contrac-

tion(s) (PJC[s]), 47, 47f, 157f,
170

Premature ventricular contrac-

tion(s) (PVC[s]), 50, 50f
couplet (paired), 53, 53f,

149f, 168

every 2nd beat (bigeminal),

52, 52f, 143f, 167

every 3rd beat (trigeminal),

52, 52f, 156f, 170

every 4th beat (quadrigemi-

nal), 53, 53f

multiform, 51, 51f
paired (couplet), 53, 53f,

149f, 168

triplet, 141f, 166
uniform, 51, 51f

Procainamide, as emergency

cardiac medication, 97

PSVT (paroxysmal supraven-

tricular tachycardia), 39, 39f,
136f, 165
management of, 124

Pulseless electrical activity

(PEA), 58, 58f
management of, 117
mnemonics for causes of,

117

Pulseless ventricular tachycar-

dia, management of, 116

Purkinje system, 10
PVC(s) (premature ventricular

contraction[s]), 50, 50f
couplet (paired), 53, 53f,

149f, 168

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PVC(s) (Continued)

every 2nd beat (bigeminal),

52, 52f, 143f, 157

every 3rd beat (trigeminal),

52, 52f, 156f, 170

every 4th beat (quadrigemi-

nal), 53, 53f

multiform, 51, 51f
paired (couplet), 53, 53f,

149f, 168

triplet, 141f, 166
uniform, 51, 51f

Q wave, 22
QRS complex, 27
QRS interval, 22, 26
QT interval, 22, 26
Quadrigeminy, ventricular, 53,

53f

R wave, propagation of, 73, 73f
Rate component, in rhythm

evaluation, 26

Regularity component, in

rhythm evaluation, 26

Repolarization, 11
Resuscitation, cardiopul-

monary, 106t, 107–109, 115f
by one rescuer, 106t
by two rescuers, 106t
of adult, 106t, 107
of child, 106t, 108
of infant, 106t, 109
of newborn, 106t

Rhythm. See also

Arrhythmia(s).
agonal, 154f, 170

idioventricular, 48, 48f, 130f,

164
accelerated, 49, 49f

junctional, 43, 43f

accelerated, 44, 44f

pacemaker, 66, 66f, 67f, 158f,

159f, 169, 171

sinus, 28, 28f, 156f, 170

with muscle artifact, 158f,

171

with premature atrial

contractions, 159f,
171

with premature junctional

contractions, 157f,
170

with premature ventricular

contractions, 141f, 149f,
156f, 166, 168, 170

with sinoatrial block, 162f,

172

with sinus pause/arrest,

138f, 166

with ST segment depres-

sion, 162f, 172

with ST segment eleva-

tion, 160f, 171

with U wave, 142f, 167

Right bundle branch, 10
Right bundle branch block, 85,

85f

Right-sided twelve-lead elec-

trocardiography, 19, 19f

SA. See Sinoatrial entries.
Second-degree atrioventricular

block, 61, 61f, 62, 62f, 146f,
148f, 168

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Segment(s), 21

ST, 22

depression of, 77, 77f, 162f,

172

elevation of, 77, 77f, 160f,

171

Septal myocardial infarction,

82, 82f

Sinoatrial block, 33, 33f, 162f,

172

Sinoatrial node, 10
Sinoatrial node arrhythmias,

28–33, 29f–33f

Sinus arrest (sinus pause), 32,

32f, 138f, 166

Sinus arrhythmia, 31, 31f
Sinus bradycardia, 29, 29f,

130f, 138f, 139f, 143f, 164,
166, 167
junctional bradycardia

converting to, 155f, 170

with muscle artifact, 161f,

171

Sinus pause (sinus arrest), 32,

32f, 138f, 166

Sinus rhythm, 28, 28f, 156f,

170
with muscle artifact, 158f,

171

with premature atrial

contractions, 159f,
171

with premature junctional

contractions, 157f, 170

with premature ventricular

contractions, 141f, 149f,
156f, 166, 168, 170

with sinoatrial block, 162f,

172

with sinus pause/arrest, 138f,

166

with ST segment depression,

162f, 172

with ST segment elevation,

160f, 171

with U wave, 142f, 167

Sinus tachycardia, 30, 30f,

134f, 163f, 165, 172

Sodium bicarbonate, as emer-

gency cardiac medication,
98

ST segment, 22

depression of, 77, 77f, 162f,

172

elevation of, 77, 77f, 160f,

171

Stable narrow-complex tachy-

cardia, management of,
124–128

Stable wide-complex tachycar-

dia, management of, 122,
123

Supraventricular tachycardia

(SVT), 38, 38f, 137f, 160f,
165, 171
paroxysmal, 39, 39f, 136f,

165
management of, 124

T mnemonic, for causes of

pulseless electrical activity,
117

T wave, 22
Tachycardia, atrial, 37, 37f

multifocal, 35, 35f

junctional, 45, 45f

management of, 125

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Tachycardia (Continued)

monomorphic ventricular,

54, 54f, 135f, 142f, 143f,
145f, 165, 167
management of, 122

multifocal atrial, 35, 35f
narrow-complex, manage-

ment of, 124–128

paroxysmal supraventricular,

39, 39f, 136f, 165
management of, 124

polymorphic ventricular, 55,

55f
management of, 123

sinus, 30, 30f, 134f, 163f, 165,

172

stable, management of,

122–128

supraventricular, 38, 38f,

137f, 160f, 165, 171
paroxysmal, 39, 39f, 136f,

165
management of, 124

unstable, management of,

121

ventricular, 54, 54f, 55,

55f
monomorphic, 54, 54f,

135f, 142f, 143f, 145f,
165, 167
management of, 122

polymorphic, 55, 55f, 152f,

169
management of, 123

pulseless, management of,

116

wide-complex, management

of, 122, 123

Third-degree atrioventricular

block, 63, 63f, 150f, 169

Thump, precordial, 104
Torsade de pointes, 56, 56f,

147f, 168

Transcutaneous pacing, 102,

103f

Trigeminy, ventricular, 52, 52f,

156f, 170

Triplet PVCs, 141f, 166
Troubleshooting, in electrocar-

diography, 174

Twelve-lead electrocardiogra-

phy, 19, 19f, 72, 78, 78f

Two-rescuer cardiopulmonary

resuscitation, 106t

U wave, 22, 142f, 167
Unconscious patient, emer-

gency management of
obstructed airway in, 112,
113, 114

Uniform premature ventricular

contraction, 51, 51f

Universal sign, of airway

obstruction, 115f

Unstable tachycardia, manage-

ment of, 121

Vagal maneuver(s), 105

carotid sinus massage as,

104–105, 105f

Valves of heart, 3, 3f
Vasopressin, as emergency

cardiac medication, 98

Venous circulation, 8f

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Ventricular arrhythmias, 48–59,

48f–59f

Ventricular bigeminy, 52, 52f,

143f, 167

Ventricular contraction(s),

premature, 50, 50f
couplet (paired), 53, 53f,

149f, 168

every 2nd beat (bigeminal),

52, 52f, 143f, 167

every 3rd beat (trigeminal),

52, 52f, 156f, 170

every 4th beat (quadrigemi-

nal), 53, 53f

multiform, 51, 51f
paired (couplet), 53, 53f,

149f, 168

triplet, 141f, 166
uniform, 51, 51f

Ventricular fibrillation (VF), 57,

57f, 132f, 133f, 151f, 164, 169
management of, 116

Ventricular quadrigeminy, 53,

53f

Ventricular tachycardia (VT),

54, 54f, 55, 55f
monomorphic, 54, 54f, 135f,

142f, 143f, 145f, 165, 167
management of, 122

polymorphic, 55, 55f, 152f,

169
management of, 123

pulseless, management of,

116

Ventricular trigeminy, 52, 52f,

156f, 170

Verapamil, as emergency

cardiac medication, 98–99

VF (ventricular fibrillation), 57,

57f, 132f, 133f, 151f, 164, 169
management of, 116

VT (ventricular tachycardia),

54, 54f, 55, 55f
monomorphic, 54, 54f, 135f,

142f, 143f, 145f, 165, 167
management of, 122

polymorphic, 55, 55f, 152f,

169
management of, 123

pulseless, management of,

116

Wandering atrial pacemaker,

34, 34f

Wave(s), 21

P, 22, 26
Q, 22
R, propagation of, 73, 73f
T, 22
U, 22, 142f, 167

Wenckebach atrioventricular

block, 61, 61f

Wide-complex tachycardia,

management of, 122, 123

Wolff-Parkinson-White (WPW)

syndrome, 42, 42f
management of, 128

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