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 3rd Edition

ECG
Notes
Interpretation and Management Guide

Shirley A. Jones, MS Ed,

MHA, MSN, EMT-P, RN

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 1
Anatomy of the Heart
The heart, a fist-sized muscular organ 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. The heart is roughly conical, with the base of the cone at the
top of the heart and the apex (the pointed part) at the bottom. It is rotated
slightly counterclockwise, with the apex tipped anteriorly so that the back
surface of the heart actually lies over the diaphragm.

Location of the heart

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—the strongest beat can be heard or
felt there.

BASICS
 Pericardial cavity Dense fibrous
Areolar connective layer
Endocardium tissue Parietal
Areolar peri-
Endothelium tissue cardium
Meso-
Myocardium thelium
(cardiac
Base of
muscle
heart
tissue)
Heart wall
Pericardial
Layers of the Heart

cavity
Fibrous
pericardium

2
(pericardial sac)
Artery
Cut edge of Vein
pericardium
Areolar tissue Epicardium
Apex of B (visceral
Mesothelium pericardium)
heart
Connective tissue
BASICS A
A. Anterior view, B. Layers of the heart––Cross section.
 3
Heart—Anterior Surface

Left common
carotid artery
Brachiocephalic
trunk Left subclavian artery

Arch of aorta
Descending aorta
Ascending
aorta Ligamentum arteriosum

Superior Left pulmonary artery

vena cava
Pulmonary trunk

Auricle of Auricle of left atrium

right atrium
Fat in
anterior
intraventricular
Right sulcus
atrium

Left
ventricle
Fat in
coronary sulcus

Right
ventricle Apex

BASICS
 BASICS

Heart—Posterior Surface

Arch of aorta

Superior
vena cava
Left atrium

Left pulmonary Right

artery pulmonary
artery
Left pulmonary
veins Right
pulmonary
veins

Coronary
sinus
Right
atrium
Fat in
coronary
sulcus

Inferior
vena
cava

Left
ventricle

Right
ventricle

Fat in posterior
intraventricular sulcus

4
 5
Heart—Anterior Section (arrows show direction
of blood flow)

Brachiocephalic trunk
Left common carotid artery
Aortic arch
Left subclavian artery

Superior Ligamentum arteriosum

vena cava
Pulmonary trunk
Right
pulmonary Left pulmonary
arteries arteries

Pulmonary valve
Left atrium
Ascending
aorta Left pulmonary
Conus veins
arteriosus
Aortic semilunar
Fossa
valve
ovalis
Cusp of left AV
Right (mitral) valve
atrium
Left
Cusp of right ventricle
AV (tricuspid)
valve Trabeculae
Chordae carneae
tendineae
Papillary
Inferior muscle
vena cava

Right
ventricle Interventricular septum
Descending aorta

BASICS
 BASICS

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.

Pulmonary semilunar
valve

Coronary artery
Aortic semilunar
valve Tricuspid
valve

Fibrous
skeleton

Mitral valve

Posterior
Superior view with atria removed

6
 Coronary Arteries and Veins
The coronary arteries and veins provide blood to the heart muscle and the electrical conduction
system. The left and right coronary arteries are the first to branch off the aorta, just above the leaflets
of the aortic valve.
Aorta Coronary sinus
Left coronary artery
Anterior
descending branch
Circumflex branch
Great cardiac
vein
7

Posterior
artery and
vein
Small
Right coronary artery cardiac vein
A Right coronary vein B
(A) Anterior view (B) Posterior view

BASICS
 BASICS

Anatomy of the Cardiovascular System

The cardiovascular system is a closed system consisting of the heart and
all the blood vessels. Arteries and veins are connected by smaller struc-
tures that transport substances needed for cellular metabolism to body
systems and remove the waste products of metabolism from those same
tissues. Arteries carry blood away from the heart and, with the exception
of the pulmonary arteries, transport oxygenated blood. Veins move blood
toward the heart. With the exception of the pulmonary veins, they carry
blood that is low in oxygen and high in carbon dioxide.

Internal elastic
External elastic lamina Endothelium (lining)
lamina Tunica
media Artery
Tunica Arteriole
externa Endothelial
cells
Smooth
muscle
Precapillary
sphincter

Capillary

Tunica Blood flow

intima Venule
Tunica Vein
externa
Tunica
media

Valve
Blood vessels—Cross-section

8
 9
Cardiovascular System—Major Arteries

Maxillary
Occipital Facial
Internal carotid External carotid
Vertebral Common carotid
Brachiocephalic Subclavian
Axillary
Aortic arch
Pulmonary
Celiac Intercostal
Left gastric Brachial
Hepatic Renal
Splenic Gonadal
Superior Inferior mesenteric
mesenteric Radial
Abdominal aorta Ulnar
Right common Deep palmar arch
iliac
Internal iliac Superficial
External iliac palmar arch

Deep femoral
Femoral

Popliteal

Anterior tibial

Posterior tibial

BASICS
 BASICS

Cardiovascular System—Major Veins

Superior sagittal sinus
Inferior sagittal sinus
Straight sinus
Transverse sinus
Anterior facial Vertebral
External jugular
Superior vena cava
Internal jugular
Axillary Subclavian
Cephalic Brachiocephalic
Pulmonary
Hemiazygos
Hepatic
Intercostal
Hepatic portal
Inferior vena cava Left gastric
Brachial
Renal
Basilic
Splenic
Gonadal
Superior Inferior
mesenteric mesenteric

Common iliac Internal iliac

External iliac
Dorsal arch

Volar digital

Femoral
Great saphenous

Popliteal

Small saphenous

Anterior tibial

Dorsal arch

Physiology of the Heart

Normal blood flow through the heart begins at the right atrium, which
receives systemic venous blood from the superior and inferior venae
cavae. Blood passes from the right atrium, across the tricuspid valve, to
the right ventricle. It is then pumped across the pulmonary valve into the
pulmonary arteries.
10
 11
Outside the heart, the left and right pulmonary arteries distribute blood
to the lungs for gas exchange in the pulmonary capillaries. Oxygenated
blood returns to the left atrium through the left and right pulmonary veins.
After passing across the mitral valve, blood enters the left ventricle, where
it is pumped across the aortic valve, through the aorta, and into the coro-
nary arteries and the peripheral circulation.

Mechanics of Heart Function

Process Action
Cardiac cycle Sequence of events in 1 heartbeat. Blood is pumped
through the entire cardiovascular system.
Systole Contraction phase––usually refers to ventricular
contraction.
Diastole Relaxation phase––the atria and ventricles are filling.
Lasts longer than systole.
Stroke volume Amount of blood ejected from either ventricle in a
(SV) single contraction. Starling’s Law of the Heart states
that the degree of cardiac muscle stretch can increase
the force of ejected blood. More blood filling the
ventricles increases SV.
Cardiac output Amount of blood pumped through the cardiovascular
(CO) system per min. CO = SV × Heart rate (HR).

Properties of Cardiac Cells

Property Ability
Automaticity Generates electrical impulse independently, without
involving the nervous system.
Excitability Responds to electrical stimulation.
Conductivity Passes or propagates electrical impulses from cell
to cell.
Contractility Shortens in response to electrical stimulation.

BASICS
BASICS

Systolic and Diastolic Phases in the Heart

Aorta

Pulmonary
artery

Pulmonary
Superior vein
vena cava Left atrium
Right atrium Aortic valve
Pulmonary Mitral valve
valve Left ventricle
Tricuspid
valve Septum
Right ventricle
Papillary
Inferior muscle
vena cava

Diastole

Atrial systolic phase Ventricular systolic phase

12
 13
Electrical Conduction System of the Heart

Electrophysiology

Structure Function and Location

Sinoatrial (SA or Dominant pacemaker of the heart, located in upper
sinus) node portion of right atrium. Intrinsic rate 60–100 bpm.
Internodal Direct electrical impulses between the SA and AV
pathways nodes and spread them across the atrial muscle.
Atrioventricular Part of the AV junctional tissue, which includes
(AV) node some surrounding tissue plus the connected bun-
dle of His. The AV node slows conduction, creating
a slight delay before electrical impulses are carried
to the ventricles. The intrinsic rate is 40–60 bpm.
Bundle of His At the top of the interventricular septum, this bun-
dle of fibers extends directly from the AV node
and transmits impulses to the bundle branches.
Left bundle branch Conducts electrical impulses to the left ventricle.
Right bundle branch Conducts electrical impulses to the right ventricle.
Purkinje system The bundle branches terminate with this network
of fibers, which spread electrical impulses rapidly
throughout the ventricular walls. The intrinsic rate
is 20–40 bpm.

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.

BASICS
BASICS

Electrical Conduction System

of the Heart—cont’d

SA Node
Left bundle
Internodal branch
pathways
AV Node
Purkinje
Bundle of His fibers

Right bundle
branch
Conduction system of the heart

14
 15
Electrical Conduction System
of the Heart—cont’d
The Depolarization Process

(A) A single cell has depolarized. (B) A wave propagates from

cell to cell. (C) Wave propagation stops when all cells are
depolarized. (D) Repolarization restores each cell’s
normal polarity.

BASICS
BASICS

Progression of Depolarization Through the Heart

SA +
Node +
+
AV + +
Node
+
+ ++ +
+
+
+

Atrial Septal
depolarization depolarization

+
+ +
+ +
+ + +
+
+
+ + +

Apical Left ventricular

depolarization depolarization

16
 17
Correlation of Depolarization and Repolarization
With the ECG

P T

Q
S

Atrial Ventricular Ventricular

depolarization depolarization repolarization

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
 BASICS

The Electrocardiogram (ECG)

The body acts as a giant conductor of electrical current. Electrical activity
that originates in the heart can be detected on the body’s surface through
an electrocardiogram (ECG). Electrodes are applied to the skin to measure
voltage changes in the cells between the electrodes. These voltage changes
are amplified and visually displayed on an oscilloscope and graph paper.
■ 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 and 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 V1–V6 are unipolar leads and consist of a single positive electrode
with a negative reference point found at the electrical center of the heart.
■ An ECG tracing looks different in each lead because the recorded
angle of electrical activity changes with each lead. 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: It is important to keep in mind that the ECG shows only
electrical activity; it tells us nothing about how well the heart is work-
ing mechanically.
Clinical Tip: Patients should be treated according to their symp-
toms, 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 12 views (12 leads).

18
 19
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. These
leads include the standard leads––I, II, and III––and the augmented
leads––aVR, aVL, and aVF.

Standard Limb Lead Electrode Placement

OR

RA LA

RA LA

RL LL

RL LL

Standard Limb Leads

Leads I, II, and III make up the standard leads. If electrodes are placed on
the right arm, left arm, and left leg, three leads are formed. If an imaginary

BASICS
 BASICS

line is drawn between each of these electrodes, an axis is formed between

each pair of leads. The axes of these three leads form an equilateral trian-
gle with the heart in the center (Einthoven’s triangle).

RA I LA

II III

LL

Elements of Standard Limb Leads

Lead Positive Electrode Negative Electrode View of Heart

I LA RA Lateral
II LL RA Inferior
III LL LA Inferior

Clinical Tip: Lead II is commonly called a monitoring lead. It pro-

vides information on heart rate, regularity, conduction time, and ectopic
beats. The presence or location of an acute myocardial infarction (MI)
should be further diagnosed with a 12-lead ECG.

20
 21
Augmented Limb Leads
Leads aVR, aVL, and aVF make up the augmented leads. Each letter of
an augmented lead refers to a specific term: a = augmented; V = voltage;
R = right arm; L = left arm; F = foot (the left foot).

RA LA
aV L
R aV

aVF

LL

Elements of Augmented Limb Leads

Lead Positive Electrode View of Heart

aVR RA None
aVL LA Lateral
aVF LL Inferior

BASICS
 BASICS

Chest Leads
Standard Chest Lead Electrode Placement
The chest leads are identified as V1, V2, V3, V4, V5, and V6. Each electrode
placed in a “V” position is positive.

Midclavicular
line
Anterior
axillary line
Midaxillary
line

V6
V5
V1 V2
V3
V4

Elements of Chest Leads

Lead Positive Electrode Placement View of Heart

V1 4th Intercostal space to right of sternum Septum
V2 4th Intercostal space to left of sternum Septum
V3 Directly between V2 and V4 Anterior
V4 5th Intercostal space at left midclavicular line Anterior
V5 Level with V4 at left anterior axillary line Lateral
V6 Level with V5 at left midaxillary line Lateral

22
 23
Electrode Placement Using a 3-Wire Cable

RA LA

LL

Electrode Placement Using a 5-Wire Cable

RA LA

V1

RL LL

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

itor leads I, II, II, aVR, aVL, aVF, and V1 in critical care settings.

BASICS
 BASICS

Modified Chest Leads

■ Modified chest leads (MCL) are useful in detecting bundle branch
blocks and premature beats.
■ Lead MCL1 simulates chest lead V1 and views the ventricular septum.
■ Lead MCL6 simulates chest lead V6 and views the lateral wall of the
left ventricle.

Lead MCL1 electrode placement

Lead MCL6 electrode placement

Clinical Tip: Write on the rhythm strip which simulated lead was used.
24
 25
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 “V1–V6” next to the tracing. Be sure to cross this out
and write the new lead positions on the ECG paper.

Midclavicular
line
Anterior
axillary line
Midaxillary
line

V6R
V5R
V2R V1R
V3R
V4R

The Right-Sided 12-Lead ECG

Chest Leads Position

V1R 4th Intercostal space to left of sternum
V2R 4th Intercostal space to right of sternum
V3R Directly between V2R and V4R
V4R 5th Intercostal space at right midclavicular line
V5R Level with V4R at right anterior axillary line
V6R Level with V5R 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
 BASICS

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
V4R, V8, and V9, increases the chance of detecting an MI in these areas.

V9 Left
V8
shoulder

Spinal
column
V6

V4R V6 V8 V9

The 15-Lead ECG

Chest Leads Electrode Placement View of Heart

V4R 5th Intercostal space in right Right ventricle
anterior midclavicular line
V8 Posterior 5th intercostal space Posterior wall of
in left midscapular line left ventricle
V9 Directly between V8 and spinal Posterior wall of
column at posterior 5th 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.

26
 27
Recording of the ECG

Constant speed of 25 mm/sec

0.04 sec

1 mm 0.1 mv
Large
Small box
5 mm
box
0.5 mv

0.20 sec

Components of an ECG Tracing

QT Interval
R

P T U

Isoelectric
QS line
PR ST
Interval Segment
QRS
Interval

BASICS
 BASICS

Electrical Activity
Term Definition
Wave A deflection, either positive or negative, away from the
baseline (isoelectric line) of the ECG tracing
Complex Several waves
Segment A straight line between waves or complexes
Interval A segment and a wave

Clinical Tip: Between waves and cycles, the ECG records a baseline
(isoelectric line), which indicates the absence of net electrical activity.

Electrical Components
Deflection Description
P Wave First wave seen
Small, rounded, upright (positive) wave indicating
atrial depolarization (and contraction)
PR Interval Distance between beginning of P wave and beginning
of QRS complex
Measures time during which a depolarization wave
travels from the atria to the ventricles
QRS Complex 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
ST Segment Distance between S wave and beginning of T wave
Measures time between ventricular depolarization
and beginning of repolarization
T Wave Rounded upright (positive) wave following QRS
Represents ventricular repolarization
QT Interval Distance between beginning of QRS to end of T wave
Represents total ventricular activity
U Wave Small rounded, upright wave following T wave
Most easily seen with a slow HR
Represents repolarization of Purkinje fibers

28
 29
Methods for Calculating Heart Rate
Heart rate is the number of times the heart beats per minute (bpm). On an
ECG tracing, bpm is usually calculated as the number of QRS complexes.
Included are extra beats, such as premature ventricular contractions (PVCs),
premature atrial contractions (PACs), and premature junctional contrac-
tions (PJCs). The rate is measured from the R-R interval, the distance
between one R wave and the next. If the atrial rate (the number of
P waves) and the ventricular rate (the number of QRS complexes) vary,
the analysis may show them as different rates, one atrial and one ventric-
ular. The method chosen to calculate HR varies according to rate and reg-
ularity 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.

300 150 100 75 60 50

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

BASICS
 BASICS

Method 2: Count Small Boxes

The most accurate way to measure a regular rhythm is to count the num-
ber of small boxes between two R waves. 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 three small boxes between two R waves:
1500/3 = 500 bpm.
If there are five small boxes between two R waves:
1500/5 = 300 bpm.

Methods 1 and 2 for Calculating Heart Rate

Number of Number of
Large Boxes Rate/Min Small Boxes Rate/Min
1 300 2 750
2 150 3 500
3 100 4 375
4 75 5 300
5 60 6 250
6 50 7 214
7 43 8 186
8 38 9 167
9 33 10 150
10 30 11 136
11 27 12 125
12 25 13 115
13 23 14 107
14 21 15 100
15 20 16 94

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

number.

30
 31
Notes:
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BASICS
 Method 3: Six-Second ECG Rhythm Strip
The best method for measuring irregular heart rates with varying R-R intervals is to count the number of
R waves in a 6-sec strip (including extra beats such as PVCs, PACs, and PJCs) and multiply by 10. This
gives the average number of beats per minute.

32
Using a 6-sec ECG rhythm strip to calculate heart rate: 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).
BASICS
 33
ECG Interpretation

Analyzing a Rhythm

Component Characteristic
Rate The bpm is commonly the ventricular rate.
If atrial and ventricular rates differ, as in a
3rd-degree block, measure both rates.
Normal: 60–100 bpm
Slow (bradycardia): <60 bpm
Fast (tachycardia): >100 bpm
Regularity Measure R-R intervals and P-P intervals.
Regular: Intervals consistent
Regularly irregular: Repeating pattern
Irregular: No pattern
P Waves 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.
PR Interval Constant: Intervals are the same
Variable: Intervals differ
Normal: 0.12–0.20 sec and constant
QRS Interval Normal: 0.06–0.10 sec
Wide: >0.10 sec
None: Absent
QT Interval Beginning of QRS complex to end of T wave
Varies with HR
Normal: Less than half the RR interval
QTc Interval The QTc interval is the QT interval corrected for
the heart rate.
Formula for calculating QTc:
QTc = QT divided by the square root of the
R to R interval
Normal corrected QTc should be < 0.44 seconds.
Dropped beats Occur in AV blocks
Occur in sinus arrest

BASICS
BASICS

Analyzing a Rhythm—cont’d

Component Characteristic
Pause 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
QRS Complex Bigeminy: Repeating pattern of normal com-
grouping plex followed by a premature complex
Trigeminy: Repeating pattern of 2 normal com-
plexes followed by a premature complex
Quadrigeminy: Repeating pattern of 3 normal
complexes followed by a premature complex
Couplet: 2 Consecutive premature complexes
Triplet: 3 Consecutive premature complexes

Classification of Arrhythmias

Heart Rate Classification

Slow Bradyarrhythmia
Fast Tachyarrhythmia
Absent Pulseless arrest

Normal Heart Rate (bpm)

Age Awake Rate Mean Sleeping Rate

Newborn to 3 months 85–205 140 80–160
3 months to 2 years 100–190 130 75–160
2 to 10 years 60–140 80 60–90
>10 years 60–100 75 50–90

34
 Sinoatrial (SA) Node Arrhythmias
■ Upright P waves all look similar. Note: All ECG strips in Tab 2 were recorded in lead II.
■ PR intervals and QRS complexes are of normal duration.

Normal Sinus Rhythm (NSR)

35

Rate: Normal (60–100 bpm)

Rhythm: Regular
P Waves: Normal (upright and uniform)

ECGS
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.
Clinical Tip: This rhythm is generated by the sinus node, and its rate is within normal limits
(60–80 bpm).
 Sinus Bradycardia
■ The SA node discharges more slowly than in NSR.

36
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 pro-
ECGS

tective and beneficial, or the slow rate may compromise cardiac output. Certain medications, such
as beta blockers, may also cause sinus bradycardia. Sinus bradycardia may also be caused by vagal
stimulation, such as gagging, straining, and endotracheal suctioning, and by chronic ischemic heart
disease, sick sinus syndrome, hypothyroidism, and increased intracranial pressure.
 Sinus Tachycardia
37 ■ The SA node discharges more frequently than in NSR.

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 conditions such as fear, pain, exercise, anxiety, or

ECGS
fever. But it can also have a more significant pathological cause such as hypoxemia; hypovolemia and
dehydration; cardiac failure or recent MI; CHF; beta blocker withdrawal; hyperthyroidism; or nicotine,
alcohol, caffeine, and alcohol withdrawal.
 Sinus Arrhythmia
■ The SA node discharges irregularly.
■ The R-R interval is irregular.

38
Rate: Usually normal (60–100 bpm); frequently increases with inspiration and decreases with expira-
tion; may be <60 bpm
Rhythm: Irregular; varies with respiration; difference between shortest RR and longest RR intervals is
>0.12 sec
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
ECGS

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.
 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 slower latent pacemaker
begins to discharge.
■ The pause (arrest) time interval is not a multiple of the normal PP interval.

3.96 - sec pause/arrest

39

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)

ECGS
QRS: Normal (0.06–0.10 sec)
Clinical Tip: Cardiac output may decrease, causing syncope or dizziness.
 Sinoatrial (SA) Block
■ The block occurs in some multiple of the PP interval.
■ After the dropped beat, cycles continue on time.

Dropped beat
X

40
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)
ECGS

Clinical Tip: Cardiac output may decrease, causing syncope or dizziness.

 Atrial Arrhythmias
■ P waves differ in appearance from sinus P waves.
■ QRS complexes are of normal duration if no ventricular conduction disturbances are present.

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.
41

Rate: Normal (60–100 bpm)

ECGS
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)
Clinical Tip: WAP may occur in normal hearts as a result of fluctuations in vagal tone.
 Multifocal Atrial Tachycardia (MAT)
■ This form of WAP is associated with a ventricular response >100 bpm.
■ MAT may be confused with atrial fibrillation (A-fib); however, MAT has a visible P wave.

42
Rate: Fast (>100 bpm)
Rhythm: Irregular
P Wave: 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

Clinical Tip: MAT is commonly seen in patients with chronic obstructive pulmonary disease
(COPD) but may also occur in those with an acute MI.
 Premature Atrial Contraction (PAC)
■ A single contraction occurs earlier than the next expected sinus contraction.
■ After the PAC, sinus rhythm usually resumes.

PAC PAC
43

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)

ECGS
Clinical Tip: In patients with heart disease, frequent PACs may precede paroxysmal supraven-
tricular tachycardia (PSVT), atrial fibrillation (A-fib), or atrial flutter (A-flutter).
 Atrial Tachycardia
■ A rapid atrial rate overrides the SA node and becomes the dominant pacemaker.
■ Some ST segment and T wave abnormalities may be present.

44
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
 Supraventricular Tachycardia (SVT)
■ This arrhythmia has such a fast rate that the P waves may not be seen.

P wave buried in T wave

45

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
Clinical Tip: Some patients may experience angina, hypotension, lightheadedness, palpitations,
and intense anxiety.
 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).

Sudden onset of SVT

46
Rate: 150–250 bpm
Rhythm: Irregular
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
ECGS

Clinical Tip: The patient may feel palpitations, dizziness, lightheadedness, or anxiety.
 Atrial Flutter (A-flutter)
■ AV node conducts impulses to the ventricles at a ratio of 2:1, 3:1, 4:1, or greater (rarely 1:1).
■ The degree of AV block may be consistent or variable.

Flutter waves
47

Rate: Atrial: 250–350 bpm; ventricular: variable

Rhythm: Atrial: regular; ventricular: variable
P Waves: Flutter waves have a saw-toothed appearance; some may be buried in the QRS and not
visible
PR Interval: Variable
QRS: Usually normal (0.06–0.10 sec), but may appear widened if flutter waves are buried in QRS

ECGS
Clinical Tip: A-flutter may be the first indication of cardiac disease.
Clinical Tip: Signs and symptoms depend on ventricular response rate.
 Atrial Fibrillation (A-fib)
■ Rapid, erratic electrical discharge comes from multiple atrial ectopic foci.
■ No organized atrial depolarization is detectable.

Irregular R-R intervals

48
>350 bpm; ventricular: variable
Rate: Atrial: =
Rhythm: Irregular
P Waves: No true P waves; chaotic atrial activity
PR Interval: None
QRS: Normal (0.06–0.10 sec)
ECGS

Clinical Tip: A-fib is usually a chronic arrhythmia associated with underlying heart disease.
Clinical Tip: Signs and symptoms depend on ventricular response rate.
 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 slur the initial portion of the QRS; the slurred effect is called a delta wave.

Delta
wave
49

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

ECGS
Clinical Tip: WPW is associated with narrow-complex tachycardias, including A-flutter and A-fib.
 Junctional Arrhythmias
■ The atria and SA node do not perform their normal pacemaking functions.
■ A junctional escape rhythm begins.

Junctional Rhythm

Inverted P wave Absent P wave

50
Rate: 40–60 bpm
Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
ECGS

QRS: Normal (0.06–0.10 sec)

Clinical Tip: Sinus node disease that causes inappropriate slowing of the sinus node may exac-
erbate this rhythm. Young, healthy adults, especially those with increased vagal tone during sleep,
often have periods of junctional rhythm that is completely benign, not requiring intervention.
 Accelerated Junctional Rhythm

Absent P wave
51

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
 Junctional Tachycardia

Retrograde P wave

52
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
 Junctional Escape Beat
■ An escape complex comes later than the next expected sinus complex.

Junctional escape beats

53

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
 Premature Junctional Contraction (PJC)
■ Enhanced automaticity in the AV junction produces PJCs.

PJC PJC

54
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 whether isolated PJCs are insignificant, consider the cause.
ECGS
 Ventricular Arrhythmias
■ In all ventricular rhythms, the QRS complex is >0.10 sec. P Waves are absent or, if visible, have no
consistent relationship to the QRS complex.

Idioventricular Rhythm
55

Rate: 20–40 bpm

Rhythm: Regular
P Waves: None

ECGS
PR Interval: None
QRS: Wide (>0.10 sec), bizarre appearance
Clinical Tip: Diminished cardiac output is expected because of the slow heart rate. An idioven-
tricular rhythm may be called an agonal rhythm when the heart rate drops below 20 bpm. An ago-
nal rhythm is generally terminal and is usually the last rhythm before asystole.
 Accelerated Idioventricular Rhythm

56
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
 Premature Ventricular Contraction (PVC)
■ PVCs result from an irritable ventricular focus.
■ PVCs may be uniform (same form) or multiform (different forms).
■ Usually a PVC is followed by a full compensatory pause because the sinus node timing is not inter-
rupted. In contrast, a PVC may be followed by a noncompensatory pause if the PVC enters the sinus
node and resets its timing, enabling the following sinus P wave to appear earlier than expected.

PVC
57

Rate: Depends on rate of underlying rhythm

Rhythm: Irregular whenever a PVC occurs
P Waves: None associated with the PVC

ECGS
PR Interval: None associated with the PVC
QRS: Wide (>0.10 sec), bizarre appearance
Clinical Tip: Patients may sense PVCs as skipped beats. Because the ventricles are only partially
filled, the PVC frequently does not generate a pulse.
 Premature Ventricular Contraction: Uniform (same form)

58
Premature Ventricular Contraction: Multiform (different forms)
ECGS
 Premature Ventricular Contraction: Ventricular Bigeminy (PVC every 2nd beat)
59

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

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

60
Premature Ventricular Contraction: Couplets (paired PVCs)

Couplets
ECGS
 Premature Ventricular Contraction: R-on-T Phenomenon
■ The PVCs occur so early that they fall on the T wave of the preceding beat.
■ These PVCs occur during the refractory period of the ventricles, a vulnerable period because the
cardiac cells have not fully repolarized.
61

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

ECGS
QRS: Wide (>0.10 sec), bizarre appearance
Clinical Tip: In acute ischemia, R-on-T phenomenon may be especially dangerous because
the ventricles may be more vulnerable to ventricular tachycardia (VT), ventricular fibrillation (VF),
or torsades de pointes.
 Premature Contraction: Interpolated PVC
■ The PVC occurs between two regular complexes; it may appear sandwiched between two normal
beats.
■ An interpolated PVC does not interfere with the normal cardiac cycle.

Interpolated PVC

62
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
ECGS

QRS: Wide (>0.10 sec), bizarre appearance

 Ventricular Tachycardia (VT): Monomorphic
63 ■ In monomorphic VT, QRS complexes 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

ECGS
VT may be perfusing or nonperfusing.
Clinical Tip: Monomorphic VT will probably deteriorate into VF or unstable VT if sustained and
not treated.
 Ventricular Tachycardia (VT): Polymorphic
■ In polymorphic VT, QRS complexes vary in shape and amplitude.
■ The QT interval is normal or long.

64
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
ECGS

Clinical Tip: It is important to determine whether pulses are present because polymorphic VT
may be perfusing or nonperfusing.
Clinical Tip: Consider electrolyte abnormalities as a possible cause.
 Torsade de Pointes
■ The QRS reverses polarity, and the strip shows a spindle effect.
■ This rhythm is an unusual variant of polymorphic VT with long QT intervals.
■ In French, the term means “twisting of points.”
65

Rate: 200–250 bpm

Rhythm: Irregular
P Waves: None
PR Interval: None

ECGS
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 the QT interval, electrolyte abnormalities
such as hypomagnesemia, or the R-on-T phenomenon.
 Ventricular Fibrillation (VF)
■ Chaotic electrical activity occurs with no ventricular depolarization or contraction.
■ The amplitude and frequency of the fibrillatory activity can define the type of fibrillation as coarse,
medium, or fine. Small baseline undulations are considered fine; large ones are coarse.

66
Rate: Indeterminate
Rhythm: Chaotic
P Waves: None
PR Interval: None
ECGS

QRS: None
Clinical Tip: There is no pulse or cardiac output. Rapid intervention is critical. The longer the
delay, the less the chance for conversion.
 Pulseless Electrical Activity (PEA)
■ The monitor shows an identifiable electrical rhythm, but no pulse is detected.
■ The rhythm may be sinus, atrial, junctional, or ventricular.
■ PEA is also called electromechanical dissociation (EMD).
67

Rate: Reflects underlying rhythm

Rhythm: Reflects underlying rhythm
P Waves: Reflect underlying rhythm
PR Interval: Reflects underlying rhythm

ECGS
QRS: Reflects underlying rhythm
Clinical Tip: Potential causes of PEA are trauma, tension pneumothorax, thrombosis (pulmonary
or coronary), cardiac tamponade, toxins, hypokalemia or hyperkalemia, hypovolemia, hypoxia,
hypoglycemia, hypothermia, and hydrogen ion (acidosis).
 Asystole
■ Electrical activity in the ventricles is completely absent.

68
Rate: None
Rhythm: None
P Waves: None
PR Interval: None
QRS: None
Clinical Tip: Rule out other causes such as loose leads, no power, or insufficient signal gain.
ECGS

Clinical Tip: Seek to identify the underlying cause as in PEA. Also, search to identify VF.
 Atrioventricular (AV) Blocks
■ AV blocks are divided into three categories: first, second, and third degree.

First-Degree AV Block
69

Rate: Depends on rate of underlying rhythm

Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Prolonged (>0.20 sec)

ECGS
QRS: Normal (0.06–0.10 sec)
Clinical Tip: Usually a first-degree AV block is benign, but if associated with an acute MI, it may
lead to further AV defects.
Clinical Tip: Often AV block is caused by medications that prolong AV conduction; these include
digoxin, calcium channel blockers, and beta blockers.
 Second-Degree AV Block—Type I (Mobitz I or Wenckebach)
■ PR intervals become progressively longer until one P wave is totally blocked and produces no QRS
complex. After a pause, during which the AV node recovers, this cycle is repeated.

Blocked beat
X

70
Rate: Depends on rate of underlying rhythm
Rhythm: Atrial: regular; ventricular: irregular
P Waves: Normal (upright and uniform), more P waves than QRS complexes
PR Interval: Progressively longer until one P wave is blocked and a QRS is dropped
QRS: Normal (0.06–0.10 sec)
ECGS

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.
 Second-Degree AV Block—Type II (Mobitz II)
■ Conduction ratio (P waves to QRS complexes) is commonly 2:1, 3:1, or 4:1, or variable.
■ QRS complexes are usually wide because this block usually involves both bundle branches.
71

Rate: Atrial: usually 60–100 bpm; ventricular: slower than atrial rate
Rhythm: Atrial: regular; ventricular: regular or irregular
P Waves: Normal (upright and uniform); more P waves than QRS complexes
PR Interval: Normal or prolonged but constant
QRS: May be normal, but usually wide (>0.10 sec) if the bundle branches are involved

ECGS
Clinical Tip: Resulting bradycardia can compromise cardiac output and lead to complete AV
block. This rhythm often occurs with cardiac ischemia or an MI.
 Third-Degree AV Block
■ Conduction between atria and ventricles is totally absent because of complete electrical block at or
below the AV node. This is known as AV dissociation.
■ “Complete heart block” is another name for this rhythm.

72
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
ECGS

PR Interval: Varies greatly

QRS: Normal if ventricles are activated by junctional escape focus; wide if escape focus is ventricular
Clinical Tip: Third-degree AV block may be associated with ischemia involving the left coronary
arteries.
 Bundle Branch Block (BBB)
■ Either the left or the right ventricle may depolarize late, creating a “wide” or “notched” QRS complex.

Notched QRS
73

Rate: Depends on rate of underlying rhythm

Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Wide (>0.10 sec) with a notched appearance
Clinical Tip: Bundle branch block commonly occurs in coronary artery disease.

ECGS
 Artificial Cardiac Pacemakers
■ Artificial pacemakers electronically stimulate the heart in place of the heart’s own pacemaker.
■ Pacemakers 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. It uses sensing and
pacing device leads.

74
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 gener-
ates a spike that should be followed by a P wave, and the ventricular electrode generates a spike
ECGS

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: Patients with pacemakers may receive defibrillation, but avoid placing the defibril-
lator paddles or pads closer than 5 inches to the pacemaker battery pack.

Artificial Cardiac Pacemakers

75

Pacemaker Codes

Chamber Response to Programmable Response to

Chamber Paced Sensed Sensing Functions Tachycardia
A = Atrium A = Atrium T =Triggers P = Basic programs P = Pacing
V = Ventricle V = Ventricle pacing (rate and output) S = Shock
D = Dual (atrium D = Dual I = Inhibits M = Multiple D = Dual (pace
and ventricle) (atrium and pacing programs and shock)

ECGS
O = None ventricle) D = Dual C = Communication O = None
O = None (triggers (i.e., telemetry)
and inhibits) R = Rate response
O = None O = None
 Artificial Pacemaker Rhythm

Rate Varies according to preset pacemaker rate.

Rhythm Regular for asynchronous pacemaker; irregular for demand pacemaker unless
100% paced with no intrinsic beats.
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 follow-
ing each atrial spike.
PR Interval None for ventricular pacer. Atrial or dual-chamber pacemaker produces constant
PR intervals.
QRS Wide (>0.10 sec) following each ventricular spike in a pacemaker rhythm. The
patient’s own electrical activity may generate a QRS complex that looks different

76
from the paced QRSs. If atrially paced only, the QRS may be within normal limits.

Clinical Tip: Once an impulse is generated by the pacemaker, it appears as a spike, either above
or below the baseline (isoelectric line), on the ECG. The spike indicates that the pacemaker has fired.
Clinical Tip: A pacemaker is in capture when a spike produces an ECG wave or complex.
ECGS
 Single-Chamber Pacemaker Rhythm––Atrial

Pacemaker spike
77

Single-Chamber Pacemaker Rhythm—Ventricular

ECGS
Pacemaker spike
 Dual-Chamber Pacemaker Rhythm—Atrial and Ventricular

Atrial pacemaker spike Ventricular pacemaker spike

78
Notes:
________________________________________________________________________________________________
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________________________________________________________________________________________________
ECGS

________________________________________________________________________________________________
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________________________________________________________________________________________________
________________________________________________________________________________________________________
 Pacemaker Malfunctions

Malfunction Reason
Failure to pace Pacemaker spikes are absent. The cause may be a dead battery, a disruption in
the connecting wires, or improper programming.
Failure to capture Pacemaker spikes are present, but no P wave or QRS follows the spike. Turning
up the pacemaker’s voltage often corrects this problem. Lead wires should also
be checked—a dislodged or broken lead wire may not deliver the needed energy.
Failure to sense 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. One serious potential conse-
quence may be an R-on-T phenomenon.
Oversensing The pacemaker may be too sensitive and misinterpret muscle movement or other
79

events in the cardiac cycle as depolarization. This error resets the pacemaker
inappropriately, increasing the amount of time before the next discharge.

ECGS
 Pacemaker Failure to Capture

80
Pacemaker Failure to Sense
ECGS
 Pacemaker Oversensing
81

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

Loose Electrodes

82
ECGS
 Baseline Varies With Respiration
83

60-Cycle Interference

ECGS
 Muscle Artifact

Regular R-R intervals

84
Clinical Tip: Never confuse muscle artifact with A-fib if the rhythm is regular.
ECGS
 85
Notes:
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ECGS
 12-LEAD

The 12-Lead ECG

A standard 12-lead ECG provides views of the heart from 12 different
angles. This diagnostic test helps to identify pathological conditions, espe-
cially bundle branch blocks and T wave changes associated with ischemia,
injury, and infarction. The 12-lead ECG also uses ST segment analysis to
pinpoint the specific location of an MI.
The 12-lead ECG is the type most commonly used in clinical settings.
The following list highlights some of its important aspects:
■ The 12-lead ECG consists of the six limb leads—I, II, III, aVR, aVL, and
aVF—and the six chest leads—V1, V2, V3, V4, V5, and V6.
■ The limb leads record electrical activity in the heart’s frontal plane.
This view shows the middle of the heart from top to bottom. Electrical
activity is recorded from the anterior to posterior axis.
■ The chest leads record electrical activity in the heart’s horizontal
plane. This transverse view shows the middle of the heart from left to
right, dividing it into upper and lower portions. Electrical activity is
recorded from either a superior or an inferior approach.
■ Measurements are central to 12-lead ECG analysis. The height and
depth of waves can offer important diagnostic information in certain
conditions, including MI and ventricular hypertrophy.
■ The direction of ventricular depolarization is an important factor in
determining the axis of the heart.
■ In an 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 and fatal arrhythmias.
■ ECG signs of an MI are best seen in the reciprocal, or reflecting,
leads—those facing the affected surface of the heart. Reciprocal leads
are in the same plane but opposite the area of infarction; they show a
mirror image of the electrical complex.
■ Prehospital EMS systems may use 12-lead ECGs to discover signs of
acute MI, such as ST segment elevation, in preparation for in-hospital
administration of thrombolytic drugs.
■ After a 12-lead ECG is performed, a 15-lead, or right-sided, ECG may
be used for an even more comprehensive view if the right ventricle or
the posterior portion of the heart appears to be affected.

86
 87
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 smaller
as electrical activity crosses the heart from right to left. This phenom-
enon is called R wave progression and is noted on the chest leads.
■ Alteration in the normal R wave progression may be seen in left ventric-
ular hypertrophy, COPD, left bundle branch block, or anteroseptal MI.

Right Left
lung lung

V6

V5

V4
V1 V2 V3

Normal R wave progression in chest leads V1–V6

12-LEAD
 12-LEAD

Electrical Axis Deviation

■ 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 (e.g., from preg-
nancy or ascites).
■ The direction of the QRS complex in leads I and aVF determines the
axis quadrant in relation to the heart.

I
I
–90°
aVF aVF
Left
ight n Devi Axis
R
e iatio ati
on
aVR ev aVL
Axi trem

–30°
sD

–150°
Ex

180° I 0°
Righ
t

30°
Ax

is

De
Ax

150°
is

via a l
tion o r m
N
I
III II I
120° aVF 60°
aVF 90° aVF
Electrical axis of the heart

Clinical Tip: Extreme right axis deviation is also called indetermi-

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

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 89
Ischemia, Injury, and Infarction in Relation
to the Heart
Ischemia, injury, and infarction of cardiac tissue are the three stages
resulting from complete blockage in a coronary artery. The location of the
MI is critical in determining the most appropriate treatment and predicting
probable complications. Each coronary artery delivers blood to specific
areas of the heart. Blockages at different sites can damage various parts
of the heart. Characteristic ECG changes occur in different leads with each
type of MI and can be correlated to the blockages.

Lateral
wall

Anterior wall
Septal wall Inferior wall
Anterior view Anterior view Posterior view
Location of MI by ECG Leads

I lateral aVR V1 septal V4 anterior

II inferior aVL lateral V2 septal V5 lateral

III inferior aVF inferior V3 anterior V6 lateral

Clinical Tip: Lead aVR may 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 V3 and V4 (anterior) and leads I,
aVL, V5, and V6 (lateral), the MI is called an anterolateral infarction.

12-LEAD
 12-LEAD

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—Arterial occlusion with ischemia, represented by ST segment
elevation
■ Infarction—Death of tissue, represented by a pathological Q wave

Normal

Ischemia

Injury

Infarction

Clinical Tip: After 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.

90
 91
ST Segment Elevation and Depression
■ A normal ST segment represents early ventricular repolarization.
■ Displacement of the ST segment can be caused by the following
various conditions:

ST segment is at baseline.

ST segment is elevated.

ST segment is depressed.

Primary Causes of ST Segment Elevation

■ ST segment elevation exceeding 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 of ST segment elevation are:
■ 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
 12-LEAD

Notes:
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 93
The Normal 12-Lead ECG

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Clinical Tip: A normal ECG does not rule out an acute coronary
syndrome.

12-LEAD
 12-LEAD

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 V3 and V4.; reciprocal changes in II, III, and aVF

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

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.

94
 95
Inferior Myocardial Infarction
■ Occlusion of the right coronary artery—posterior descending branch
■ ECG changes: ST segment elevation in leads II, III, and aVF; reciprocal
ST segment depression in I and aVL

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Clinical Tip: Be alert for symptomatic sinus bradycardia, AV blocks,

hypotension, and hypoperfusion.

12-LEAD
 12-LEAD

Lateral Myocardial Infarction

■ Occlusion of the left coronary artery—circumflex branch
■ ECG changes: ST segment elevation in leads I, aVL, V5, and V6; recip-
rocal ST segment depression in V1, V2, and V3

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

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.

96
 97
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 V1 and V2

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Clinical Tip: Septal MI is often associated with an anterior wall MI.

12-LEAD
 12-LEAD

Posterior Myocardial Infarction

■ Occlusion of the right coronary artery (posterior descending branch)
or the left circumflex artery
■ Usually, tall R waves and ST segment depression in leads V1, V2, V3,
and V4; possible left ventricular dysfunction
■ You may need to view the true posterior leads, V8 and V9 (used in the
15-lead ECG), for definite diagnosis of an acute posterior MI. These
leads show ST segment elevation.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

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

dard 12-lead does not look directly at the posterior wall.
98
 99
Left Bundle Branch Block
■ QRS complex greater than 0.10 sec
■ QRS predominantly negative in leads V1 and V2
■ QRS predominantly positive in V5 and V6 and often notched
■ Absence of small, normal Q waves in I, aVL, V5, and V6
■ Wide monophasic R waves in I, aVL, V1, V5, and V6

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Clinical Tip: Patients may have underlying heart disease, including

coronary artery disease, hypertension, cardiomyopathy, and ischemia.

12-LEAD
 12-LEAD

Right Bundle Branch Block

■ QRS complex greater than 0.10 sec
■ QRS axis normal or deviated to the right
■ Broad S wave in leads I, aVL, V5, and V6
■ RSR’ pattern in lead V1 with R’ taller than R
■ qRS pattern in V5 and V6
■ ST segment to T wave distorted and in opposite direction to terminal
portion of QRS (this is not ST elevation or ST depression)
I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Clinical Tip: Patients may have underlying right ventricular hyper-

trophy, pulmonary edema, cardiomyopathy, congenital heart disease,
or rheumatic heart disease.
100
 101
Emergency Medications
This is a reference list only. It is not meant to be exhaustive in
clinical content. Drug dosages follow Advanced Cardiac Life
Support (ACLS) guidelines for adult patients and Pediatric
Advanced Life Support (PALS) guidelines for pediatric patients.
Before administering medications, especially IV medications,
always consult an authoritative, current reference about dose,
dilution, route, rate of administration, and interactions. Have a
second licensed person independently check dose calculations,
preparation, original orders, and infusion pump programming.
ACE Inhibitors
Class: Angiotensin-converting enzyme inhibitors.
Common Agents: Captopril, enalapril, lisinopril, ramipril.
Indications: MI, especially with ST elevation and with left ventricular
dysfunction; HTN; heart failure without hypotension.
Adult Dose: See individual order and drug for route and dosage.
Usually not started in the emergency department for an acute MI, but
within 24 hr after reperfusion therapy has been completed and BP has
stabilized.
Contraindications: Lactation, pregnancy, angioedema, hypersensitivity
to ACE inhibitors, hypotension.
Side Effects: Cough, dizziness, headache, fatigue, hypotension, hyper-
kalemia, renal insufficiency.
Precautions: Reduce dose in renal failure. Caution in severe aortic
stenosis, hypertrophic cardiomyopathy, unstented renal artery steno-
sis, severe CHF.
Adenosine (Adenocard)
Class: Antiarrhythmic.
Indications: Regular narrow-complex tachycardias, PSVT, and wide-
complex tachycardia only if regular and monomorphic.
Adult Dose: 6 mg IV in the antecubital or another large vein given rap-
idly over 1–3 sec followed by a 20-mL bolus of normal saline. If the
rhythm does not convert, give 12 mg by rapid IVP in 1–2 min if need-
ed. A third dose of 12 mg IVP may be given in another 1–2 min, maxi-
mum (max) total dose 30 mg.

MEDS
 MEDS

Adenosine (continued)
Pediatric Dose: 0.1 mg/kg (max 6 mg) IV/IO given rapidly over 1–3 sec
followed by a 5- to 10-mL bolus of normal saline. If the rhythm does
not convert, give 0.2 mg/kg (max 12 mg) IV/IO in 1–2 min if needed.
Contraindications: Hypersensitivity, sick sinus syndrome, second- or
third-degree AV block (unless a functioning pacemaker is present),
A-fib/A-flutter with underlying Wolff-Parkinson-White syndrome, drug-
or poison-induced tachycardia, bronchospastic lung disease.
Side Effects: Flushing; nausea; dizziness; headache; dyspnea; bron-
chospasm; chest pain or tightness; discomfort in neck, throat, or jaw;
bradycardia; AV block; asystole; ventricular ectopic beats; VF.
Precautions: Ineffective in treating A-fib, A-flutter, or VT. Less effective
in patients taking theophylline or caffeine. Reduce dose in patients
taking dipyridamole or carbamazepine or heart transplant patients.
Adenosine Diphosphate (ADP) Antagonists
Class: Antiplatelet agents––thienopyridines (clopidogrel and prasugrel),
cyclopentyltriazolopyrimidine (ticagrelor).
Common Agents: Clopidogrel (Plavix), prasugrel (Effient), ticagrelor
(Brilinta).
Indications: Antiplatelet therapy for acute coronary syndromes (ACS)
managed with percutaneous coronary intervention (PCI). Clopidogrel:
ACS, recent stroke, or peripheral arterial disease.
Adult Dose: See individual order and drug for dosage.
Contraindications: Acute pathological bleeding (e.g., peptic ulcer,
intracranial bleeding). Prasugrel: Also history of TIA or stroke. Ticagrelor:
Also history of intracranial hemorrhage, hepatic impairment.
Side Effects: Bleeding, thrombocytopenia purpura. Ticagrelor: Dyspnea,
increased serum creatinine. Stent thrombosis with premature discon-
tinuation of therapy.
Precautions: Increased risk of bleeding (chronic NSAID use, anticoagu-
lation therapy, thrombocytopenia, trauma/surgery), thienopyridine
hypersensitivity, severe hepatic impairment, severe renal impairment.
Prasugrel: Caution in patients ≥75 years old or patients <60 kg.
Ticagrelor: Patients with hyperuricemia or gouty arthritis, patients at
risk for bradycardia without pacemaker. Drugs must be withheld prior
to CABG or elective surgery––Clopidogrel and ticagrelor: 5 days; pra-
sugrel: 7 days. In patients at risk for stent thrombosis, consider bridg-
ing with IV glycoprotein IIb/IIIa inhibitor such as eptifibatide (Integrilin)
102
 103
while patient is off ADP antagonist; resume oral therapy as soon
as possible after surgery when risk for postoperative bleeding is
reduced.
Albuterol (ProAir, Proventil, Ventolin)
Class: Adrenergic beta2-agonist, bronchodilator.
Indications: Asthma, COPD, anaphylaxis (bronchospasm), hyperkalemia.
Adult Dose: For bronchospasm, metered-dose inhaler (MDI): 2 puffs
every 4–6 hr prn; nebulizer: 2.5 mg 3–4 times daily prn or 1.25–5 mg
every 4–8 hr prn. For severe bronchospasm and status asthmaticus:
5 mcg/min IV, titrate up every 15–30 min to 10–20 mcg/min. For
severe acute asthma exacerbation, MDI: 4–8 puffs every 20 min up
to 4 hr, then every 1–4 hr prn; nebulizer: 2.5–5 mg every 20 min for
3 doses, then 2.5–10 mg every 1–4 hr prn or 10–15 mg/hr by continu-
ous nebulizer.
Pediatric Dose: For bronchospasm, MDI 2 puffs every 4–6 hr prn;
nebulizer children 2–12 yr: 0.63–1.25 mg 3–4 times daily prn; nebulizer
children >–12 yr: 2.5 mg 3–4 times daily prn. For mild to moderate asth-
ma or anaphylaxis, hyperkalemia, MDI: 4–8 puffs every 20 min prn;
nebulizer, <20 kg: 2.5 mg every 20 min, >20 kg: 5 mg every 20 min.
For severe asthma exacerbation, MDI children <12 yr: 4–8 puffs every
20 min for 3 doses, then every 1–4 hr prn; MDI children > – 12 yr: 4–8
puffs every 20 min for up to 4 hr, then every 1–4 hr prn; nebulizer chil-
dren <12 yr: 0.15 mg/kg every 20 min for 3 doses, then 0.15–0.3 mg/kg
every 1–4 hr prn, or 0.5 mg/kg/hr by continuous nebulizer; nebulizer
children >– 12 yr: 2.5–5 mg every 20 min for 3 doses, then 2.5–10 mg ever
1–4 hr prn, or 10–15 mg/hr by continuous nebulizer.
Contraindications: Hypersensitivity, tachyarrhythmias, risk of abortion
during first or second trimester.
Side Effects: Angina, arrhythmias, palpitations, tachycardia, flushing,
dizziness, headache, insomnia, irritability, angioedema, rash, urticaria,
hypokalemia, hyperglycemia, asthma exacerbation, cough.
Precautions: Use of spacer with MDI is recommended. Caution in cardio-
vascular disease (arrhythmias, HTN, heart failure), diabetes (may increase
serum glucose), glaucoma (increased intraocular pressure), hyperthy-
roidism (may stimulate thyroid activity), hypokalemia (decreased serum
potassium), seizure disorders (CNS stimulation/excitation).

MEDS
 MEDS

Amiodarone (Cordarone, Pacerone)

Class: Antiarrhythmic, class III.
Indications: Management of life-threatening shock-refractory VF or VT,
recurrent hemodynamically unstable VT. Conversion of A-fib, SVT.
Control of rapid ventricular rate in pre-excited atrial arrhythmias.
Control of hemodynamically stable VT, polymorphic VT with normal
QT interval, or wide-complex tachycardia of uncertain origin.
Adult Dose: Cardiac arrest: 300 mg IV/IO; consider additional 150 mg
IV/IO in 3–5 min if needed. Wide- and narrow-complex tachycardia
(stable): 150 mg IV over first 10 min (15 mg/min)––may repeat infusion
of 150 mg IV 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.
Pediatric Dose: Cardiac arrest: 5 mg/kg IV/IO bolus (max 300 mg),
may repeat to max of 15 mg/kg (or 2.2 g in adolescents) in 24 hr;
Wide- and narrow-complex tachycardia (stable): 5 mg/kg IV/IO load
over 20–60 min (max 300 mg), may repeat to max of 15 mg/kg/day
(2.2 g/day in adolescents).
Contraindications: Hypersensitivity, cardiogenic shock, symptomatic
bradycardia or second- or third-degree AV block without functioning
pacemaker, severe sinus node dysfunction.
Side Effects: Vasodilation, hypotension, bradycardia, proarrhythmic
effects, 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 the medication only in
a glass bottle containing D5W or NS and administer through an
in-line filter using a volumetric pump. Use with caution in thyroid
disease, pulmonary disease, or hepatic impairment, and in patients
on warfarin.
Aspirin (Acetylsalicylic Acid, ASA)
Class: Antiplatelet.
Indications: Acute coronary syndrome, symptoms suggestive of car-
diac ischemia, post-percutaneous coronary interventions, A-fib, stroke,
peripheral arterial disease.

104
 105
Adult Dose: Acute coronary syndrome: 160–325 mg PO. Chewing the
tablet is preferable; use non–enteric-coated tablets for more rapid
antiplatelet effect. Give within minutes of onset of ischemic symptoms.
Other indications: 81–325 mg PO daily.
Contraindications: Known allergy to aspirin, third trimester of preg-
nancy, bleeding.
Side Effects: Anorexia, nausea, epigastric pain, bleeding, anaphylaxis.
Precautions: GERD, active ulcers, asthma, bleeding disorders, or
thrombocytopenia.
Atropine Sulfate
Class: Anticholinergic, parasympatholytic, vagolytic.
Indications: Symptomatic sinus bradycardia, junctional escape rhythm, or
second-degree type I block. Not likely to be effective in second-degree
type II or third-degree AV block with wide QRS complex.
Adult Dose: 0.5 mg IV given every 3–5 min as needed, max total dose
3 mg (0.04 mg/kg).
Pediatric Dose: 0.02 mg/kg IV/IO (min. dose 0.1 mg, max single dose
child 0.5 mg, max single dose adolescent 1 mg), may repeat dose
once, max total dose child 1 mg, max total dose adolescent 3 mg. May
give 0.04–0.06 mg/kg, flush with 5 mL normal saline if administering
by ET. Use ET route only if IV/IO access is not available.
Contraindications: Hypersensitivity, acute angle-closure glaucoma,
asthma, prostatic hypertrophy, myasthenia gravis.
Side Effects: Tachycardia, headache, dry mouth, nausea, constipation,
dilated pupils, flushing, hypotension.
Precautions: Use caution in myocardial ischemia and hypoxia. Avoid
in hypothermic bradycardia and in second-degree (Mobitz type II) and
third-degree AV block with wide QRS complex, asystole, bradycardic
PEA. Caution in colon disease, hepatic or renal impairment, hiatal
hernia, obstructive uropathy, hyperthyroidism.
Beta Blockers
Class: Beta blockers, antihypertensive, antiarrhythmic, antianginal.
Common Agents: Atenolol, esmolol, labetalol, metoprolol, propranolol.
Indications: MI, unstable angina, PSVT, A-fib, A-flutter, HTN, CHF.
Adult Dose: See individual order and drug for route and dosage.

MEDS
 MEDS

Beta Blockers (continued)

Contraindications: Heart rate <50 bpm, systolic BP <100 mm Hg,
second- or third-degree AV block or sick sinus syndrome without
functioning pacemaker, severe decompensated left ventricular failure,
cardiogenic shock. Nonselective beta blockers are contraindicated in
bronchospastic disease.
Side Effects: Hypotension, dizziness, bradycardia, headache, fatigue,
nausea and vomiting, depression.
Precautions: Concurrent use with calcium channel blockers, such as
verapamil or diltiazem, can cause hypotension. Use beta-1 selective
agents with caution in patients with a history of bronchospasm. Use
caution in thyroid disease, peripheral arterial disease, and diabetes
(monitor blood glucose levels frequently).
Calcium Chloride
Class: Minerals, electrolytes, calcium salt.
Indications: Hyperkalemia, hypocalcemia, hypermagnesemia; antidote
for calcium channel blocker or beta blocker overdose.
Adult Dose: 500–1000 mg (5–10 mL of a 10% solution) over 2–5 min IV;
may be repeated as needed.
Pediatric Dose: 20 mg/kg (0.2 mL/kg) IV/IO slow push during arrest or
if severe hypotension, repeat as needed.
Contraindications: Hypercalcemia, hypophosphatemia, VF, digoxin toxicity.
Side effects: Bradycardia, hypotension, hypomagnesemia, hypercalcemia,
VF, syncope, nephrolithiasis, flushing, dizziness, nausea and vomiting.
Precautions: Incompatible with sodium bicarbonate (precipitates).
Caution in patients with renal impairment, respiratory acidosis,
hypokalemia, hyperparathyroidism.
Digoxin (Lanoxin)
Class: Antiarrhythmic, cardiac glycoside.
Indications: To slow ventricular response in A-fib or A-flutter; rarely, as
a positive inotrope in CHF.
Adult Dose: Loading dose of 0.5 mg IV over 5 min, 0.25 mg IV in 6–8 hr
× 2. Maintenance dose determined by body size and renal function.
Contraindications: Hypersensitivity, uncontrolled ventricular arrhyth-
mias, AV block without functioning pacemaker, idiopathic hyper-
trophic subaortic stenosis (IHSS), constrictive pericarditis, A-fib with
Wolff-Parkinson-White syndrome.

106
 107
Side Effects: Accelerated junctional rhythm, atrial tachycardia with
block, AV block, asystole, VT, VF, ventricular bigeminy and trigeminy,
dizziness, weakness, 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 and patients with heart failure,
acute MI, renal impairment, and hypothyroidism. Correct electrolyte
abnormalities, monitor digoxin levels, monitor for clinical signs of toxicity.
Hypokalemia, hypomagnesemia, and hypercalcemia may precipitate
digitalis toxicity. Reduce digoxin dose by 50% in patients on amiodarone.
Digoxin Immune FAB (Fragment Antigen Binding)
(DigiFab)
Class: Antidote to digoxin and digitoxin.
Indications: Symptomatic digoxin toxicity or acute ingestion of
unknown amount of digoxin.
Adult Dose: Depends on serum digoxin levels. One 40-mg vial binds to
approximately 0.5 mg of digoxin. Dose is typically administered over
30 min.
Contraindications: Allergy only, otherwise none known. Allergy to
sheep proteins or other sheep products.
Side Effects: Worsening of CHF, rapid ventricular response in patients
with A-fib, hypokalemia, postural hypotension, increased serum digox-
in levels due to bound complexes (clinically misleading because
bound complex cannot interact with receptors).
Precautions: Heart failure, renal impairment.
Diltiazem (Cardizem)
Class: Calcium channel blocker, antiarrhythmic, class IV.
Indications: To control ventricular rate in A-fib and A-flutter; to termi-
nate PSVT (reentry SVT) refractory to adenosine with narrow QRS
complex and adequate BP.
Adult Dose: 15–20 mg (0.25 mg/kg) IV given over 2 min. May repeat in
15 min at 20–25 mg (0.35 mg/kg) IV given over 2 min. Start mainte-
nance 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, second- or third-degree

MEDS
 MEDS

Diltiazem (continued)
AV block (unless a functioning pacemaker is present), hypotension
with systolic BP less than 90 mm Hg, acute MI with pulmonary
congestion.
Side Effects: Hypotension, bradycardia (including AV block), chest
pain, ventricular arrhythmias, peripheral edema, flushing, heart failure,
syncope.
Precautions: Severe hypotension in patients receiving beta blockers.
Caution in patients with hepatic or renal disease, heart failure, hyper-
trophic cardiomyopathy.
Dobutamine
Class: Adrenergic direct-acting beta1-agonist, inotrope.
Indications: To increase myocardial contractility in patients with
decompensated heart failure with systolic BP 70–100 mm Hg and no
signs of shock.
Adult Dose: Continuous infusion (titrate to patient response):
2–20 mcg/kg/min, max 40 mcg/kg/min.
Pediatric Dose: Same as adult dose, titrate to patient response.
Contraindications: Hypersensitivity, idiopathic hypertrophic subaortic
stenosis (IHSS), suspected or known poison- or drug-induced shock.
Do not mix with sodium bicarbonate.
Side Effects: Tachycardia, HTN, hypotension, increased ventricular ectopy,
chest pain, palpitations, restlessness, headache, nausea, vomiting.
Precautions: Avoid in patients with systolic BP <100 mm Hg and signs
of shock; correct hypovolemia before use, if needed. MI: may increase
myocardial oxygen demand.
Dopamine (Intropin)
Class: Alpha-and beta1-adrenergic agonist, inotrope, vasopressor.
Indications: Symptomatic bradycardia and hypotension, cardiogenic
shock.
Adult Dose: Continuous infusion (titrate to patient response): low
dose 1–5 mcg/kg/min (renal dose); moderate dose 5–10 mcg/kg/min
(cardiac dose); high dose 10–20 mcg/kg/min (vasopressor dose). Mix
400 mg/250 mL in normal saline, lactated Ringer’s solution, or D5W
(1600 mcg/mL).
Pediatric Dose: Cardiogenic shock, distributive shock: 2–20 mcg/kg/min
IV/IO infusion, titrate to desired effect.

108
 109
Contraindications: Hypersensitivity to sulfites, pheochromocytoma, VF.
Side Effects: Tachyarrhythmias, angina, hypotension, palpitations,
vasoconstriction, dyspnea, headache, nausea and vomiting.
Precautions: Hypovolemia, MI. Adjust dosage in elderly patients and in
those with occlusive vascular disease. Ensure adequate IV volume
repletion with normal saline before infusion. Taper slowly. Do not mix
with sodium bicarbonate. Use care with peripheral administration;
infiltration with extravasation can cause tissue necrosis. A central line
is preferred. Use a volumetric infusion pump. Caution in patients with
occlusive vascular disease and patients taking MAO inhibitors.
Epinephrine (Adrenalin)
Class: Alpha-beta adrenergic agonist (sympathomimetic: inotrope,
vasopressor, bronchodilator).
Indications: Cardiac arrest: PEA, asystole, pulseless VT, VF; hypotension
with severe bradycardia. Anaphylaxis, severe asthma exacerbation.
Adult Dose: Cardiac arrest: 1 mg IV/IO (10 mL of 1:10,000 solution) every
3–5 min prn; follow each dose with 20 mL IV flush. Give 2.0–2.5 mg
diluted in 10 mL normal saline or sterile water if administering by ET
tube. Profound bradycardia or hypotension: 2–10 mcg/min IV infusion;
add 1 mg (1 mL of a 1:1000 solution) to 500 mL normal saline or D5W.
Anaphylaxis: 0.2–0.5 mg (1:1000 solution) IM (1:1000 solution) every
5–15 min prn or 0.1–0.25 mg (1:10,000 solution) IV every 5–15 min,
then 1–4 mcg/min IV prn. Severe asthma exacerbation: 0.3–0.5 mg
(1:1000 solution) SQ/IM every 20 min × 3 doses prn. Max 1 mg/dose.
Pediatric Dose: Cardiac arrest or symptomatic bradycardia: 0.01 mg/kg
(0.1 mL/kg) 1:10,000 IV/IO every 3–5 min as needed (max 1 mg; 10 mL).
Give 0.1 mg/kg (0.1 mL/kg) 1:1000, flush with 5 mL normal saline if
administering by ET tube. Use ET route only if IV/IO access is not
available. Repeat every 3–5 min as needed. Anaphylaxis: 0.01 mg/kg
(1:1000 solution) SQ/IM every 5–20 min × 3 doses prn or 0.01 mg/kg
(1:10,000 solution) IV × 1, then 0.1 mcg/kg/min IV prn. Severe asthma
exacerbation: 0.01 mg/kg (1:1000 solution) SQ/IM every 20 min × 3 doses
prn. Max 0.5 mg/dose.
Contraindications: Hypersensitivity to adrenergic amines, hypovolemic
shock, coronary insufficiency. No contraindication in cardiac arrest.
Side Effects: Angina, HTN, tachycardia, VT, VF, nervousness, restless-
ness, palpitations, tremors, weakness, diaphoresis, anxiety, headache,
nausea.

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Epinephrine (continued)
Precautions: Use caution in HTN and increasing heart rate (may cause
increased myocardial oxygen demand). Higher doses can contribute to
post-arrest cardiac impairment but may be needed to treat poison- or
drug-induced shock. Avoid mixing with alkaline solutions.
Fibrinolytic Agents
Class: Thrombolytic, fibrinolytic.
Common Agents: Alteplase (Activase, t-PA), reteplase (Retavase),
streptokinase (Streptase), tenecteplase (TNKase).
Indications: Acute ST elevation MI within the past 12 hr. Alteplase is
the only fibrinolytic agent approved for acute ischemic stroke and
must be started less than 3 hr from the onset of symptoms.
Adult 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 trau-
ma within 2 weeks, aortic dissection, severe (uncontrolled) HTN, bleed-
ing disorders, prolonged CPR, lumbar puncture within 1 week. History
of any intracranial bleeding, oral anticoagulation therapy, severe stroke.
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. Initiate bleeding precautions. Monitor patient for bleeding
complications.
Fondaparinux (Arixtra)
Class: Factor Xa inhibitor, anticoagulant.
Indications: To inhibit thrombin generation by inhibiting factor Xa in
patients with ACS; anticoagulation in patients with history of heparin-
induced thrombocytopenia (HIT); deep vein thrombosis (DVT) prophy-
laxis in patients undergoing orthopedic surgery or abdominal surgery;
pulmonary embolism (PE); acute DVT without PE.
Adult Dose: STEMI: 2.5 mg IV bolus followed by 2.5 mg SQ daily for up
to 8 days. Acute DVT/PE, acute thrombosis: 5–10 mg SQ daily (based on
body weight) up to 5–9 days, start coumadin therapy on first or second
day, discontinue fondaparinux when INR > – 2 for at least 24 hr. Other
uses: 2.5 mg SQ daily for up to 8 days (up to 10 days for abdominal
surgery, up to 11 days for hip replacement or total knee replacement

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surgery, up to 14 days for total hip or total knee arthroplasty or hip
fracture surgery).
Contraindications: Creatinine clearance <30 mL/min, hypersensitivity,
body weight <50 kg when used for prophylaxis, active major bleeding,
bacterial endocarditis, thrombocytopenia associated with positive in
vitro test for antiplatelet antibody in presence of fondaparinux.
Side Effects: Bleeding, edema, hypotension, insomnia, dizziness,
headache, rash, constipation, vomiting, diarrhea, urinary retention,
moderate thrombocytopenia.
Precautions: Increased risk of bleeding, creatinine clearance
30–50 mL/min, patients >75 years old, patients <50 kg being treated
for DVT/PE. Discontinue 24 hr before CABG and administer unfrac-
tionated heparin.
Furosemide (Lasix)
Class: Loop diuretic.
Indications: CHF with acute pulmonary edema, hypertensive crisis,
post-arrest cerebral edema, edema associated with hepatic or renal
disease.
Adult Dose: 0.5–1 mg/kg IV given over 1–2 min; may repeat at 2 mg/kg
IV given over 1–2 min. Alternative: 20–40 mg IV, increase by 20 mg IV
every 2 hr until desired response is obtained, max 160–200 mg/dose.
Pediatric Dose: 0.5–1 mg/kg IV/IO, may increase by 1 mg/kg IV every
2 hr until desired response is obtained, max 6 mg/kg/dose.
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, severe renal disease, gout. Risk for ototoxicity with
increased dose or rapid injection. Monitor electrolytes closely.
Glycoprotein IIB/IIIA Inhibitors
Class: Antiplatelet agents, GP IIb/IIIa inhibitors.
Common Agents: Abciximab (ReoPro), eptifibatide (Integrilin), tirofiban
(Aggrastat).

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Glycoprotein IIB/IIIA Inhibitors (continued)

Indications: Acute coronary syndromes managed medically (Eptifibatide
and Tirofiban) and those undergoing PCI (all three agents).
Adult Dose: See individual order and drug for dosage.
Contraindications: Hypersensitivity, active internal bleeding or bleed-
ing disorder within past 30 days, history of bleeding diathesis, history
of stroke within 30 days, history of hemorrhagic stroke, uncontrolled
HTN (systolic BP >200 mm Hg, diastolic pressure >110 mm Hg), major
surgery or trauma within 1 month, concomitant use of another GP IIb/IIIa
inhibitor, dependency on hemodialysis.
Side Effects: Bleeding, hypotension, thrombocytopenia.
Precautions: Patients at increased risk for bleeding, patients <70 kg,
platelet count <150,000/mm3, renal impairment. Discontinue > – 2–4 hr
prior to CABG. Abciximab (ReoPro) must be administered with aspirin
and heparin.
Heparin (Unfractionated Heparin [UFH])
Class: Anticoagulant.
Indications: Acute coronary syndromes (ACS): STEMI, NSTEMI, unsta-
ble angina (UA), during PCI; prophylaxis and treatment of thromboem-
bolic disorders such as DVT, pulmonary embolus; anticoagulant for
extracorporeal and dialysis procedures.
Adult Dose: ACS: 60 units/kg IV bolus, max 4000 units, followed by
continuous IV infusion of 12 units/kg/hr, max 1000 units/hr, check APTT
every 4–6 hr, adjust infusion to maintain APTT 50–70 sec for 48 hr or
until angiography. Thromboprophylaxis: 5000 units SQ every 8–12 hr.
Treatment of DVT/PE: 80 units/kg or 5000 unit IV bolus, followed by
continuous IV infusion of 18 units/kg/hr; adjust infusion to maintain
therapeutic APTT.
Pediatric Dose: Systemic heparinization for infants <1 year: 75 units/kg
IV over 10 min, followed by initial maintenance infusion of 28 units/kg/hr;
check APTT every 4 hr and adjust heparin dose to maintain APTT
60–85 sec. For children >1 year: 75 units/kg over 10 min, followed by
initial maintenance infusion of 20 units/kg/hr, adjust heparin to main-
tain APTT 60–85 sec.
Contraindications: Hypersensitivity, heparin-induced thrombocytope-
nia (HIT), severe thrombocytopenia, uncontrolled active bleeding
unless due to DIC; recent intracranial, intraspinal, or eye surgery;
uncontrolled HTN.

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Side Effects: Bleeding, HIT, thrombocytopenia, hyperkalemia, osteo-
porosis with use >6 mo.
Precautions: Patients at increased risk for bleeding; patients with
heparin resistance (antithrombin deficiency, increased heparin clear-
ance elevations in heparin-binding proteins, elevations in factor VIII
and/or fibrinogen). Female patients >60 yr old may require lower
doses. Check platelet count daily.
Ibutilide (Corvert)
Class: Antiarrhythmic, class III.
Indications: SVT, including A-fib and A-flutter; most effective for con-
version of A-fib or A-flutter of short duration (<
– 48 hr).
Adult Dose: Patients weighing 60 kg or more: 1 mg IV given over 10 min;
may repeat the same dose in 10 min if arrhythmia does not terminate.
Patients weighing <60 kg: 0.01 mg/kg IV given over 10 min; may repeat
the same dose in 10 min if arrhythmia does not terminate.
Contraindications: Known hypersensitivity, history of polymorphic VT,
QTc greater than 440 msec.
Side Effects: Nonsustained or sustained monomorphic or polymorphic
VT, torsade de pointes, AV block, CHF, HTN, headache, tachycardia,
hypotension, nausea and vomiting.
Precautions: Continuous ECG monitoring for 4–6 hr after administra-
tion or until QTc returns to baseline. Monitor for AV block. Skilled per-
sonnel and resuscitative equipment must be readily available. Correct
electrolyte abnormalities prior to use. If A-fib has lasted longer than
48 hr, anticoagulation is required before cardioversion with ibutilide.
Monitor QTc. Not recommended for chronic atrial fibrillation. Caution
in patients with heart failure or hepatic impairment.
Isoproterenol (Isuprel)
Class: Beta-adrenergic agonist.
Indications: Medically refractory symptomatic bradycardia when trans-
cutaneous or transvenous pacing is not available, refractory torsade
de pointes unresponsive to magnesium, bradycardia in heart trans-
plant patients, beta blocker poisoning.
Adult Dose: IV infusion: mix 1 mg/250 mL in normal saline, lactated
Ringer’s solution, or D5W, run at 2–10 mcg/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: Hypersensitivity to drug or sulfites, digitalis intoxi-
cation, angina, tachyarrhythmias, concurrent use with epinephrine
(can cause VF or VT).
Side Effects: Arrhythmias, cardiac arrest, hypotension, angina, anxiety,
tachycardia, palpitations, skin flushing, dizziness, tremors, headache,
nausea, vomiting, restlessness.
Precautions: May increase myocardial ischemia. Use caution in
patients with renal impairment, cardiovascular disease, distributive
shock, hyperthyroidism, diabetes. High doses are harmful except in
beta blocker overdose.
Lidocaine (Xylocaine)
Class: Antiarrhythmic, class Ib, local anesthetic.
Indications: Alternative to amiodarone in VF or pulseless VT. Use in
stable VT, wide-complex tachycardia of uncertain origin.
Adult Dose: Cardiac arrest from VF or VT: 1.0–1.5 mg/kg IV/IO (or
2–4 mg/kg via ET tube); may repeat 0.5–0.75 mg/kg IV/IO every
5–10 min, max dose 3 mg/kg. Stable VT, wide-complex tachycardia
of uncertain origin: 0.50–0.75 mg/kg up to 1.0–1.5 mg/kg; may
repeat 0.50–0.75 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 mcg/kg/min) in normal saline or D5W.
Pediatric Dose: 1 mg/kg IV/IO bolus. Give 2–3 mg/kg, flush with 5 mL
normal saline if administering by ET tube. Use ET route only if IV/IO
access is not available. Maintenance: 20–50 mcg/kg/min IV/IO infusion
(repeat bolus [0.5–1 mg/kg IV/IO] when infusion is initiated if bolus has
not been given within previous 15 min).
Contraindications: Prophylactic use in acute MI, advanced AV block
without functioning pacemaker, hypotension, Wolff-Parkinson-White
syndrome, hypersensitivity to amide local anesthetics.
Side Effects: Confusion, agitation, anxiety, tinnitus, blurred vision,
dizziness, tremors, hallucinations, seizures, hypotension, bradycardia,
cardiovascular collapse, respiratory arrest, slurred speech.
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 CNS
toxicity develop.

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Magnesium Sulfate
Class: Electrolyte, antiarrhythmic.
Indications: Torsade de pointes, hypomagnesemia, life-threatening
ventricular arrhythmias due to digitalis toxicity, status asthmaticus,
seizures.
Adult Dose: Torsade de pointes (cardiac arrest): 1–2 g IV (2–4 mL of
a 50% solution) diluted in 10 mL of D5W over 1–2 min. Torsade de
pointes (non–cardiac arrest with pulse): 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). Seizures: 2 g IV diluted in 10 mL of D5W
over 10 min.
Pediatric Dose: Torsade de pointes (cardiac arrest––pulseless VT):
25–50 mg/kg IV/IO bolus. Torsade de pointes (non–cardiac arrest
with pulses): 25–50 mg/kg IV/IO over 10–20 min. Status asthmaticus:
25–50 mg/kg/IV/IO over 15–30 min.
Contraindications: Hypermagnesemia, hypocalcemia, AV block.
Side Effects: HTN, bradycardia, cardiac arrest, respiratory depression,
altered LOC, flushed skin, diaphoresis, hypocalcemia, hyperkalemia,
hypophosphatemia.
Precautions: Renal insufficiency, occasional fall in BP with rapid admin-
istration. Monitor serum magnesium levels. Caution in patients with
myasthenia gravis. Correct concurrent hypokalemia and hypocalcemia.
Morphine Sulfate
Class: Opiate narcotic analgesic.
Indications: Chest pain unrelieved by nitroglycerin; CHF and dyspnea
associated with pulmonary edema.
Adult Dose: 2–4 mg IV (given over 1–5 min), administer every 5–30 min
as needed if hemodynamically stable; may repeat dose of 2–8 mg at
5- to 15-min intervals if needed.
Contraindications: Hypersensitivity, heart failure due to chronic lung
disease, respiratory depression, hypercarbia, hypotension, bowel
obstruction, severe asthma, acute or severe hypercarbia. Avoid in
patients with RV infarction.
Side Effects: Respiratory depression, hypotension, nausea and vomiting,
bradycardia, altered LOC, seizures, somnolence, dizziness, diaphoresis,
flushing, pruritus, dry mouth, urinary retention.
Precautions: Administer slowly and titrate to effect. Reverse with
naloxone (0.4–2.0 mg IV) if necessary. Use caution in cerebral edema

MEDS
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Morphine Sulfate (continued)

and pulmonary edema with compromised respiration. Use caution
with hypovolemic patients; be prepared to administer volume. Use
caution in renal and hepatic impairment, seizure disorder, CNS
depression, head injury, hypothyroidism, adrenal insufficiency, prosta-
tic hypertrophy, shock.
Naloxone (Narcan)
Class: Opioid antagonist.
Indications: Reversal of opioid overdose/toxicity unresponsive to oxygen
and ventilator support, such as respiratory and neurological depression.
Adult dose: Opioid overdose: 2 mg IV, IM, or SQ; may need to repeat
every 2-3 min up to 10 mg. Reversal of respiratory depression with
therapeutic opioid doses: 0.04–0.4 mg IV, IM, or SQ; may repeat until
ventilation is adequate, up to 0.8 mg. Postoperative reversal: 0.1–0.2 mg
IV every 2–3 min until adequate ventilation.
Pediatric dose: For total reversal, birth to 5 yr: 0.1 mg/kg IV every
2–3 min as needed, max 2 mg; >5 yr: 2 mg IV every 2–3 min prn up to
10 mg. For partial reversal: 0.001–0.005 mg/kg IV (1–5 mcg/kg), repeat
as needed every 2–3 min. For postoperative reversal: 0.01 mg/kg IV
every 2–3 min prn.
Contraindications: Hypersensitivity, meperidine-induced seizures.
Side Effects: Secondary to reversal (withdrawal) of narcotic analgesia
and sedation. Recurrent respiratory depression, pain, hypertension,
hypotension, irritability, agitation, diaphoresis, seizures.
Precautions: May precipitate symptoms of acute withdrawal in opioid-
dependent patients. Use caution in patients with a history of seizures
and patients with cardiovascular disease. Abrupt postoperative rever-
sal may cause nausea, vomiting, diaphoresis, tachycardia, hyperten-
sion, seizures, pulmonary edema, arrhythmias.
Nitroglycerin (Nitrostat, Nitrolingual [Pump spray])
Class: Antianginal, nitrate, vasodilator.
Indications: Acute coronary syndrome, angina, CHF associated with
acute MI, hypertensive urgency with ACS.
Adult Dose: Sublingual route, 0.3–0.4 mg (1 tablet); repeat every 3–5 min
if chest pain is not relieved, max 3 doses/15 min. Aerosol, spray for
0.5–1.0 sec at 3- to 5-min intervals (provides 0.4 mg/dose), max 3 sprays/
15 min. IV bolus administration at 12.5–25.0 mcg (if no sublingual or

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spray used). IV infusion: mix 25 mg/250 mL (100 mcg/mL) in D5W,
start at 5 mcg/min and titrate by 5 mcg/min every 3–5 min to 20 mcg/min.
If patient remains symptomatic, titrate by 10–20 mcg/min every 3–5 min,
max 200 mcg/min.
Pediatric Dose: 0.25–0.50 mcg/kg/min IV/IO infusion, titrate by
0.5–1 mcg/kg/min every 3–5 min as needed to typical dose range of
1–5 mcg/kg/min (max 20 mcg/kg/min).
Contraindications: Hypersensitivity, systolic BP less than 90 mm Hg,
pericardial tamponade, constrictive pericarditis, severe bradycardia or
severe tachycardia associated with hypotension; sildenafil (Viagra) or
vardenafil (Levitra) within 24 hr, tadalafil (Cialis) within 48 hr; right
ventricular infarction, increased intracranial pressure, hypertrophic
cardiomyopathy with outflow tract obstruction, restrictive cardiomy-
opathy, increased intracranial pressure.
Side Effects: Hypotension with reflex tachycardia, syncope, headache,
flushed skin, dizziness, paradoxical bradycardia.
Precautions: Do not mix with other medications; titrate IV to maintain
systolic BP above 90 mm Hg. Mix only in glass IV bottles and infuse
only through non-PVC tubing; standard polyvinyl chloride (PVC) tubing
can bind up to 80% of the medication, making it necessary to infuse
higher doses. Do not shake aerosol spray (affects metered dose).
Norepinephrine (Levophed)
Class: Alpha- and beta-adrenergic agonist, vasopressor.
Indications: Treatment of persistent shock after adequate volume replace-
ment, cardiogenic shock, low systemic vascular resistance shock, septic
shock, hemodynamically significant hypotension.
Adult Dose: Start at 0.1–0.5 mcg/kg/min, titrate to response up to
8–12 mcg/min, maintenance infusion usually 2–4 mcg/min. Use volu-
metric infusion pump.
Pediatric Dose: Start at 0.05–0.1 mcg/kg/min, titrate to response, up to
2 mcg/kg/min. Use volumetric infusion pump.
Contraindications: Hypovolemic shock prior to adequate volume
replacement, mesenteric or peripheral vascular thrombosis except as
emergency measure to maintain coronary and cerebral perfusion. Do
not administer in same line as alkaline solutions.
Side Effects: Arrhythmias, hypertension, headache, anxiety, dyspnea,
skin necrosis with extravasation.

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Norepinephrine (continued)
Precautions: Use caution in patients on MAO inhibitors as drug may
cause prolonged hypertension; infuse into large vein and avoid
extravasation; use caution in patients with ischemic heart disease:
increases myocardial oxygen consumption, may induce arrhythmias,
tachycardia, hypertension.
Oxygen
Class: Gas.
Indications: Cardiopulmonary emergencies with shortness of breath
and chest pain, cardiac or respiratory arrest, hypoxemia. Used to opti-
mize oxygen saturation <94%.
Adult and Pediatric Dose: Nasal cannula 1–6 L/min (21%–44% oxygen),
Venturi mask 4–12 L/min (24%–50% oxygen), simple mask 5–8 L/min
(40%–60% oxygen), partial rebreathing mask 6–10 L/min (35%–60%
oxygen), non-rebreathing mask 6–15 L/min (60%–100% oxygen), bag-
valve mask 15 L/min (95%–100% oxygen).
Contraindications: None reported.
Side Effects: Drying of respiratory mucosa, possible bronchospasm if
oxygen is extremely cold and dry. Oxygen supports combustion and
can fuel a fire. Hypoventilation in patients with severe COPD, pul-
monary fibrosis, oxygen toxicity.
Precautions: Respiratory arrest in patients with hypoxic respiratory
drive. The patient needs an airway and adequate ventilation before
oxygen is effective.
Procainamide (Pronestyl)
Class: Antiarrhythmic, class Ia.
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 con-
version. Stable monomorphic VT with normal QTc and preserved LV
function.
Adult Dose: 20 mg/min IV infusion or up to 50 mg/min under urgent
conditions, until arrhythmia is suppressed, 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.
Pediatric Dose: Atrial flutter, SVT, VT (with pulses): 15 mg/kg IV/IO load
over 30–60 min.

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Contraindications: Hypersensitivity, second- and third-degree AV block
(unless a functioning pacemaker is in place), prolonged QT interval,
torsade de pointes, hypersensitivity, systemic lupus erythematosus.
Side Effects: Hypotension, widening QRS, headache, nausea and vom-
iting, flushed skin, seizures, ventricular arrhythmias, AV block, cardio-
vascular collapse, arrest.
Precautions: Monitor BP every 2–3 min while administering pro-
cainamide. If QRS width increases by 50% or more, or if systolic BP
decreases to less than 90 mm Hg, stop the drug. Monitor for pro-
longed PR interval and AV block. Monitor for QT prolongation. May
precipitate or exacerbate CHF. Reduce the total dose to 12 mg/kg and
maintenance infusion to 1–2 mg/min if cardiac or renal dysfunction is
present. Use cautiously in heart failure, myasthenia gravis, and hepat-
ic or renal disease. Avoid concurrent use with drugs that prolong the
QT interval (e.g., amiodarone, sotalol).
Sodium Bicarbonate
Class: Alkalinizing agent, buffer.
Indications: Known preexisting hyperkalemia, bicarbonate-responsive
acidosis such as diabetic ketoacidosis or tricyclic antidepressant over-
dose, metabolic acidosis associated with prolonged resuscitation with
effective ventilation.
Adult Dose: 1 mEq/kg IV; may repeat 0.5 mEq/kg every 10 min. Dosing
is best guided by calculated base deficits or bicarbonate concentration
with arterial blood gas analysis if available.
Pediatric Dose: 1 mEq/kg IV/IO slow bolus. Dosing is best guided by
calculated base deficits or bicarbonate concentration with arterial
blood gas analysis, if available.
Contraindications: Metabolic and respiratory alkalosis,
hypochloremia, hypocalcemia, hypokalemia, hypercarbic acidosis,
hypernatremia, severe pulmonary edema.
Side Effects: Hypokalemia, hypocalcemia, hypernatremia, metabolic
alkalosis, edema, seizures, tetany, exacerbation of CHF, tissue hypoxia,
intracellular acidosis.
Precautions: CHF, renal disease, cirrhosis, hypernatremia, hypervolemia,
toxemia, concurrent corticosteroid therapy. Not recommended for rou-
tine use in cardiac arrest because adequate ventilation and CPR are the
major “buffer agents” in this case. Incompatible with many drugs;
flush the line before and after administration.

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Vasopressin (Pitressin)
Class: Vasopressor, hormone.
Indication: Cardiac arrest: an alternative to epinephrine in shock-
refractory VF and pulseless VT, PEA, and asystole. Vasodilatory shock/
septic shock.
Adult Dose: Cardiac arrest: 40 units IV/IO single dose to replace first or
second dose of epinephrine as an alternative. Vasodilatory shock:
0.01–0.04 units/min continuous IV infusion.
Pediatric Dose: Cardiac arrest: 0.4–1 unit/kg IV/IO, max 40 units.
Vasodilatory shock: 0.0002–0.002 unit/kg/min continuous IV infusion.
Contraindications: Hypersensitivity.
Side Effects: Bradycardia, HTN, angina, MI, arrhythmias, dizziness,
headache, nausea and vomiting, abdominal cramps, diaphoresis,
bronchoconstriction, anaphylaxis.
Precautions: Coronary artery disease (may precipitate angina or MI),
CHF, hepatic or renal impairment; seizure disorders, asthma, vascular
disease.
Verapamil (Calan, Isoptin)
Class: Calcium channel blocker, antiarrhythmic, class IV, antihypertensive.
Indications: PSVT (with narrow QRS and adequate BP) refractory to
adenosine; rapid ventricular rates in A-fib, A-flutter, and MAT.
Adult Dose: 2.5–5.0 mg IV over 2 min; may give second dose, if needed,
of 5–10 mg IV in 15–30 min, max dose 20 mg. An alternative second
dose is 5 mg IV every 15 min, max dose 30 mg.
Contraindications: A-fib with Wolff-Parkinson-White syndrome, wide-
complex tachycardia of uncertain origin, second- or third-degree AV
block (unless a functioning pacemaker is in place), sick sinus syn-
drome, hypotension, severe CHF, cardiogenic shock, concurrent IV beta
blocker, VT.
Side Effects: Hypotension, exacerbation of CHF with left ventricular
dysfunction, bradycardia, AV block, constipation, peripheral edema,
headache, dizziness, fatigue, paralytic ileus, hepatotoxicity.
Precautions: Concurrent oral beta blockers, CHF, impaired hepatic or
renal function, myasthenia gravis, muscular dystrophy, hypertrophic
cardiomyopathy with outflow tract obstruction; may decrease myocar-
dial contractility. In geriatric patients administer slowly over 3 min.

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Common Medication Formulas
Syringe: Desired dose of drug × Total volume
Amount to be Total dose of drug on hand
drawn up
IV: Calculating Volume to be infused × Drop (gtt) factor
gtt/min Total time in minutes
IV: Calculating Volume on hand × gtt factor × Desired dose
= gtt/min
infusion rate Total dose of drug on hand
(mg/min or Example: Administer 2 mg/min of lidocaine. To prepare
mcg/min) the infusion, mix 2 g (2000 mg) of lidocaine in 500 mL
of D5W with a drip set of 60 gtt/mL. Calculate the infu-
sion rate. 500 mL × 60 gtt/mL × 2 mg
= 30 gtt/min
2000 mg
IV: Rate of an 1. Count drops (gtt)/min and multiply by 60 min.
existing IV 2. Divide result by the drop (gtt) factor being used.

IV Fluid Drip Rate Table (gtt/min)

Rate: (mL/hr) ➜ TKO 50 75 100 125 150 175 200 250
10 gtt/mL set 5 8 13 17 21 25 29 33 42
12 gtt/mL set 6 10 15 20 25 30 35 40 50
15 gtt/mL set 8 13 19 25 31 37 44 50 62
20 gtt/mL set 10 17 25 33 42 50 58 67 83
60 gtt/mL set 30 50 75 100 125 150 175 200 250

MEDS
 Universal Formula––Figure Out Drip Rates
and Drug Amounts

122
MEDS

Note: The abbreviation mcg (microgram) means the same as µg (used in the above formula); mcg is used most commonly to prevent
medication errors.
 123

Emergency Medical Skills

Defibrillation
Indications: Ventricular fibrillation or pulseless VT.
Energy Levels: Use an adult biphasic energy level at 120–200 J (use
the manufacturer’s device-specific energy level) or deliver 360 J for a
monophasic energy level. Continue at a biphasic energy level of
120–200 J for further shocks or a monophasic energy level of 360 J.
Application: Dry moisture off skin; shave excessive hair, if necessary.
Use remote adhesive pads or handheld paddles. Always use a con-
ducting gel with paddles and apply firm pressure (15–25 pounds per
paddle) to the chest to ensure good skin contact.
Methods: Manual or automated.
Precautions: Place pads or paddles several inches away from an
implanted pacemaker or ICD.

Placement of paddles for defibrillation

Clinical Tip: Defibrillation may be used on infants younger than

1 year old and on children (1 yr to puberty). Always use pediatric pads
or paddles and follow pediatric protocols.

SKILLS
 SKILLS

Manual Defibrillation
A manual defibrillator is used to restore a normal heart rhythm. For a
patient experiencing sudden cardiac arrest, first assess for responsive-
ness, respiration, and pulse. Begin CPR. Verify that the rhythm is either VF
or pulseless VT, and then manually deliver an electric shock to the heart.
Procedure
1. Verify that the patient is in cardiac arrest, with no pulse or respira-
tion. Have someone provide CPR while the defibrillator is obtained
and placed next to the patient or left on the crash cart.
2. Turn on the defibrillator; verify that all cables are connected.
3. Turn “lead select” to “paddles” or “defibrillator.”
4. Pads: Place in locations specified for paddles. Roll pads on from top
to bottom edges to prevent air pockets. Paddles: Use conducting gel
or gel pads and place on the apex (lower left chest, midaxillary) and
sternum (right of sternum, midclavicular).
5. Remove oxygen away from patient and immediate vicinity.
6. Select the initial energy level for an adult to a biphasic energy level
of 120–200 J (use the manufacturer’s device-specific energy levels)
or a monophasic energy level of 360 J.
7. Verify rhythm as VF or pulseless VT.
8. Say, “Charging defibrillator, stand clear!”
9. Charge the defibrillator.
10. Say, “I’m going to shock on three. One, I’m clear; two, you’re clear;
three, everybody’s clear.” Perform a visual sweep to ensure all res-
cue personnel are clear of the patient, bed, and equipment and
oxygen is removed.
11. Discharge the defibrillator, reassess the rhythm, and refer to appro-
priate advanced cardiac life support protocol.

Automated External Defibrillator

An automated external defibrillator (AED) is a small, lightweight device
used by both professionals and laypersons to assess heart rhythm by
computer analysis. Using voice and visual prompts, it administers an
electric shock, if necessary, to restore a normal rhythm in patients
with sudden cardiac arrest. A shock is administered only if the rhythm

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detected is VF or pulseless VT. Automated external defibrillators are
available from medical device manufacturers and local pharmacies.
Although the AEDs all operate in basically the same way, external fea-
tures vary from model to model. Be sure to follow the manufacturer’s
recommendations.
Indications: Ventricular fibrillation or pulseless VT in adults, children,
and infants.
Dose: The AED will automatically select the energy dose for each defib-
rillation. Some devices are equipped with pediatric systems that
include a pad–cable system or a key to reduce the delivered energy to
a suitable dose for children.
Procedure
1. Verify that the patient is in cardiac arrest, with no pulse or respira-
tion. Have someone provide CPR while the AED is obtained and
placed next to the patient.
2. Power on the AED. Follow the voice prompts and visual messages.
3. Open the package of adhesive electrode pads and attach pads to the
patient’s bare chest.
4. Use adult pads for an adult and child pads for a child. If there are no
child pads available, you may use adult pads on a child, but be sure
the pads do not touch.
5. Attach one pad to the right sternal border (superior-anterior right
chest) and place the second pad over the left apex (inferior-lateral
left chest). Alternatively, follow the diagrams on each of the AED
electrodes.
6. Connect the pad cables to the AED.
7. Clear the patient and stop CPR. Remove oxygen, if applicable.
8. The AED may automatically analyze the patient’s rhythm or may be
equipped with an “analyze” button.
9. If a shock is advised, say, “I’m going to shock on three. One, I’m
clear; two, you’re clear; three, everybody’s clear.” Perform a visual
sweep to ensure rescue personnel are not touching the patient or
equipment. Remove oxygen, if applicable. Press the shock button.
10. Once the shock is delivered, continue CPR beginning with chest
compression.
11. After about 2 minutes of CPR, the AED will prompt you with further
verbal and visual cues.

SKILLS
 SKILLS

Clinical Tip: A fully automated AED analyzes the rhythm and deliv-
ers a shock, if one is indicated, without operator intervention once the
pads are applied to the patient.
Clinical Tip: A semiautomated AED analyzes the rhythm and tells
the operator that a shock is indicated. If it is, the operator initiates the
shock by pushing the shock button.

Cardioversion (Synchronized)
Indications: Unstable tachycardias (50 bpm with a perfusing rhythm).
The patient may present with an altered LOC, dizziness, chest pain, or
hypotension.
Energy Levels: Regular narrow QRS complex tachycardias (supraven-
tricular tachyarrhythmia)—generally requires less energy, 50 to 100 J
either biphasic or monophasic is often sufficient; narrow irregular
rhythm (atrial fibrillation)—120 to 200 J biphasic or 200 J monophasic.
If the initial cardioversion shock fails, the energy should be increased
in a stepwise fashion. Regular wide QRS complex tachycardias
(monomorphic ventricular tachycardia)—responds well to biphasic or
monophasic initial energies of 100 J. If there is no response to the first
shock, it may be reasonable to increase the dose in stepwise fashion.
Synchronized cardioversion must not be used for treatment of VF
because the device is unlikely to sense a QRS wave and thus a shock
may not be delivered. Synchronized cardioversion should also not be
used for pulseless VT or polymorphic VT (irregular VT). These rhythms
require delivery of high-energy unsynchronized shocks (i.e., defibrilla-
tion doses).
Application: Use remote adhesive pads or handheld paddles. Always
use a conducting gel with paddles. For conscious patients, explain the
procedure and use medication for sedation and analgesia. Consider
2.5–5.0 mg midazolam (Versed), or 5.0 mg diazepam (Valium), or
1–2 mcg/kg/min fentanyl IV, or anesthesia, if available.
Methods: Remove oxygen, if applicable. Place defibrillator in synchro-
nized (sync) mode. Observe marker on R wave to confirm proper
synchronization. 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 a visual sweep and ensure that oxygen is removed. Press
and hold shock button until shock is delivered. If using paddles, press

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and hold both discharge buttons simultaneously until shock is deliv-
ered. Reassess the patient and treat according to the appropriate
advanced cardiac life support protocol.
Precautions: Reactivate the “sync” mode after each attempted car-
dioversion; defibrillators default to the unsynchronized mode. Place
pads or paddles several inches away from an implanted pacemaker or
implantable cardioverter-defibrillator (ICD).
Clinical Tip: The “sync” mode delivers energy synchronizing with
the timing of the QRS complex to avoid stimulation during the refrac-
tory, or vulnerable, period of the cardiac cycle when a shock could
potentially produce VF.

Transcutaneous Pacing
Indications: A temporizing measure for symptomatic bradycardia (with
a pulse) unresponsive to atropine, bradycardia with ventricular escape
rhythms, symptomatic second-degree AV block type II, or third-degree
AV block.
Pacing Modes: Demand-mode (synchronous) pacemakers sense the
patient’s heart rate and pace only when the heart rate falls below
the level set by the clinician. Fixed-mode (asynchronous) pacemak-
ers cannot sense the heart rate and always operate at the rate set by
the clinician. Rate selections vary between 30 and 180 bpm. Output
is adjustable between 0 and 200 mA. Pulse duration varies from
20–40 ms.
Application: Pacemaker pads work most effectively if placed in an
anterior-posterior position on the patient.
Contraindications: Not effective in VF, pulseless VT, or asystole.
Side Effects: Chest muscle contraction, burns, and chest discomfort.
Precautions: Make sure pads have good skin contact to achieve cap-
ture and avoid burns.

SKILLS
 SKILLS

Anterior Posterior

Female patients:
Position electrode
under breast

Placement of anterior-posterior pacemaker pads.

Carotid Sinus Massage (Vagal Maneuver)

Indications: Can increase vagal nerve stimulation and slow SVT, or

even convert SVT to NSR, without severe hemodynamic compromise.
Should be performed only by qualified physicians due to the
risk for stroke.
Method: Place the patient in a supine position, head tilted to either side
with the neck hyperextended. Place your index and middle fingers
over the carotid artery just below the angle of the jaw, as high on the
neck as possible. Massage the artery for 5–10 sec by pressing it firmly
against the vertebral column and rubbing.

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Contraindications: Unequal carotid pulses, carotid bruits, cervical
spine injury, or history of cerebrovascular accident or carotid
atherosclerosis.
Side Effects: Slow HR or AV block, PVCs, VT, VF, syncope, seizure,
hypotension, nausea or vomiting, stroke.
Precautions: Be sure the patient is receiving oxygen and an IV is in
place. Never massage both arteries simultaneously. Resuscitation
equipment must be readily available.
Clinical Tip: Performed only by qualified physicians. Each carotid
artery should be palpated and auscultated before the procedure to
evaluate for contraindications to carotid sinus massage.
Clinical Tip: Alternate vagal maneuvers include encouraging the
patient to cough, bear down, blow through an obstructed straw, place
ice to the face, or hold his or her breath.

Carotid
sinus nerve

Carotid
body

Vagus nerve

Right common
carotid artery

Sternocleido-
mastoid Cardiac
muscle plexus
Carotid sinus massage

SKILLS
 Healthcare Provider Guidelines for CPR
Compression/ Rate of
CPR Ventilation Compressions Depth of Pulse Check Hand Position for
Method Ratio (min) Compressions (artery) Compressions
Adult, 1 30:2 100–120 At least 2.0 in Carotid Heels of 2 hands
rescuer (5 cm) on lower half of the
sternum
Adult, 2 30:2 100–120 At least 2.0 in Carotid Heels of 2 hands
rescuers (5 cm) on lower half of the
sternum
Child, 1 30:2 100–120 At least 1/3 Carotid or Heel of 1 or 2 hands
CPR

rescuer depth of femoral on lower half of the

130
chest (about sternum between
2.0 in [5 cm]) nipple line
Child, 2 15:2 100–120 At least 1/3 Carotid or Heel of 1 or 2 hands
rescuers depth of femoral over center of chest
chest (about between nipple line
2.0 in [5 cm])
Infant, 1 30:2 100–120 At least 1/3 Brachial 2 fingers over center
rescuer depth of of chest, just below
chest (about nipple line.
1.5 in [4 cm])
Infant, 2 15:2 100–120 At least 1/3 Brachial 2-thumbs-encircling-
rescuers depth of hands technique
chest (about over center of chest,
1.5 in [4 cm]) just below nipple line
 131
CPR: Adult (Age of puberty or older)
1. Ensure that the scene is safe. Check for unresponsiveness. Gently tap
the person’s shoulder. Ask, “Are you OK?”
2. Simultaneously assess the person's breathing and pulse.
■ Check for breathing. Is the breathing normal, no breathing, or
abnormal (only agonal gasps)?
■ Assess the carotid pulse and look for other signs of circulation
(no more than 10 sec). If signs of circulation are present but the
person is still not breathing, give rescue breaths at the rate of
10–12 breaths/min (1 breath every 5–6 sec).
3. In a sudden collapse, if you are alone and there is no response with
no breathing, abnormal breathing (only agonal gasps), and no pulse,
summon help, call a code, or phone 911 and get an automated
external defibrillator (AED), if available. Send a second rescuer, if
available, for help.
4. Position the person supine on a hard, flat surface.
5. If a pulse and signs of circulation are not present, begin chest
compressions.
■ Place the heel of one hand on the center of the chest over the
lower half of the sternum; place the heel of your other hand over
the first.
Firmly compress the chest at least 2.0 in (5 cm). Push hard and fast.
Give 30 compressions. Compress at a rate of 100–120/min. Ensure
complete chest recoil after each compression. Avoid leaning on the
chest between compressions.
6. If the person is not breathing, begin rescue breaths. Open the airway
by the head tilt–chin lift method or, if spinal injury is suspected, use
the jaw thrust method, if possible.
7. Using a face mask or barrier device, give 2 breaths (1 sec each) with
sufficient volume to cause the chest to rise. Do not overventilate.
Note: If the chest does not rise, reposition the head, chin, and jaw,
and give 2 more breaths. If the chest still does not rise, follow
instructions for unconscious adult with an obstructed airway.
8. Continue to give 30 compressions followed by 2 breaths until an AED
arrives. If an AED is unavailable, continue to give 30 compressions
followed by 2 breaths.

CPR
 CPR

9. If circulation resumes but breathing does not resume or is inadequate,

continue rescue breathing at 10–12 breaths/min (1 breath every 5–6 sec).
10. If adequate breathing and circulation resume, place the person in
the recovery position and monitor until help arrives.
Clinical Tip: Chest compressions should be interrupted infrequently
and for no longer than 10 seconds. Pulse checks, even to determine
return of spontaneous circulation (ROSC), should be minimized during
resuscitation.
Clinical Tip: When two rescuers are available, give cycles of 30 com-
pressions and 2 breaths for adult CPR. After every fifth cycle (2 min)
rescuers should switch roles to minimize rescuer fatigue because
compression rates and/or depth may become inadequate due to rec-
ognized or unrecognized fatigue. The switch should be accomplished
in less than 5 sec. If available, a bag-valve-mask device can be used
with two-rescuer CPR.

CPR: Child (1 yr to age of puberty)

1. Ensure that the scene is safe. Check for unresponsiveness. Gently tap
child’s shoulder. Ask, “Are you okay?”
2. Simultaneously assess the child's breathing and pulse.
■ Check for breathing. Is the breathing normal, no breathing, or
abnormal (only agonal gasps)?
■ Assess the carotid pulse and look for other signs of circulation
(no more than 10 sec). If signs of circulation are present but the
child is still not breathing, give rescue breaths at the rate of
12–20 breaths/min (1 breath every 3–5 sec).
3. If there is no response with no breathing or abnormal breathing
(only agonal gasps), send a second rescuer, if available, for help and
to get an AED, if available.
4. If you are alone, begin the steps for CPR.
5. Position the child supine on a hard, flat surface.
6. If a pulse and signs of circulation are not present, begin chest
compressions.
■ One hand: Place the heel of one hand on the center of the chest
over the lower half of the sternum.

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■ Two hands: Place the heel of one hand on the center of the chest
over the lower half of the sternum; place the heel of your other
hand over the first.
Firmly compress the chest at least one third the depth of the
chest (at least 2.0 in [5 cm]). Push hard and fast. Give 30 compres-
sions. Compress at a rate of 100–120/min. Ensure complete chest
recoil after each compression. Avoid leaning on the chest
between compressions.
7. If the child is not breathing, begin rescue breaths. Open the airway
by the head tilt–chin lift method or, if spinal injury is suspected, use
the jaw thrust method, if possible.
8. Using a face mask or barrier device, give 2 breaths (1 sec each) with
sufficient volume to cause the chest to rise. Do not overventilate.
Note: If the chest does not rise, reposition the head, chin, and jaw,
and give 2 more breaths. If the chest still does not rise, follow
instructions for unconscious child with an obstructed airway.
9. Continue cycles of 30 compressions followed by 2 breaths. After
the fifth cycle of 30:2 (2 min), if you are still alone and no signs of
circulation are present, summon help, call a code, or phone 911
and get an AED, if available.
10. If circulation is still not present, continue CPR, starting with chest
compressions until an AED is available. If an AED is unavailable,
continue to give 30 compressions followed by 2 breaths.
11. If circulation resumes but breathing does not resume or is inadequate,
continue rescue breathing at 12–20 breaths/min.
12. If adequate breathing and circulation resume, place the child in the
recovery position and monitor until help arrives.
Clinical Tip: If you are alone and know a child or infant has had a
sudden collapse because of heart failure, request immediate help
including an AED. Do not delay defibrillation.
Clinical Tip: When two rescuers are available, give cycles of
15 compressions and 2 breaths for child CPR.

CPR
 CPR

CPR: Infant (Younger than 1 yr)

1. Ensure that the scene is safe. Check for unresponsiveness. Gently
rub the infant’s back or tap the feet.
2. Simultaneously assess the infant's breathing and pulse.
■ Check for breathing. Is the breathing normal, no breathing, or
abnormal (only agonal gasps)?
■ Assess the brachial pulse and look for other signs of circulation
(no more than 10 sec). If signs of circulation are present but the
child is still not breathing, give rescue breaths at the rate of
12–20 breaths/min (1 breath every 3–5 sec).
3. If there is no response with no breathing or abnormal breathing
(only agonal gasps), send a second rescuer, if available, for help and
an AED, if available.
4. If you are alone, begin the steps for CPR.
5. Position the infant supine on a hard, flat surface.
6. If a pulse and signs of circulation are not present, begin chest
compressions.
■ Place two fingers of one hand over the center of the chest just
below the nipple line.
Firmly compress the chest at least one third the depth of the chest
(at least 1.5 in [4 cm]). Push hard and fast. Give 30 compressions.
Compress at a rate of 100–120/min. Ensure complete chest recoil after
each compression. Avoid leaning on the chest between compressions.
7. If the infant is not breathing, begin rescue breaths. Open the airway
by the head tilt–chin lift method or, if spinal injury is suspected, use
the jaw thrust method, if possible.
8. Using a face mask or barrier device, give 2 breaths (1 sec each) with
sufficient volume to cause the chest to rise. Do not overventilate.
Note: If the chest does not rise, reposition the head, chin, and jaw,
and give 2 more breaths. If the chest still does not rise, follow
instructions for unconscious infant with an obstructed airway.
9. Continue to give 30 compressions followed by 2 breaths. After
the fifth cycle of 30:2 (2 min), if you are still alone and no signs
of circulation are present, summon help, call a code, or phone 911
and get an AED, if available.
10. If circulation is still not present, continue CPR until the AED is
available. If an AED is unavailable, continue to give 30 compressions
followed by 2 breaths.
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11. If circulation resumes but breathing does not resume or is inadequate,
continue rescue breathing at 12–20 breaths/min.
12. If adequate breathing and circulation resume, place the infant in the
recovery position and monitor until help arrives.
Clinical Tip: When two rescuers are available, give cycles of
15 compressions and 2 breaths for infant CPR. Use the two-thumbs-
encircling-hands technique for chest compressions. If available, a
bag-valve-mask device can be used with two-person CPR.

Obstructed Airway: Conscious Adult or Child

(1 yr or older)
Clinical Presentation
■ Grabbing at the throat with one or both hands
■ Inability to speak; high-pitched crowing sounds
■ Wheezing, gagging, ineffective coughing
1. Determine that the airway is obstructed. Ask, “Are you choking?
Can you speak?”
2. Let the person know you are going to help.
3. Stand behind the choking person and wrap your arms around the
person’s waist. For someone who is obese or pregnant, wrap your
arms around the chest.
4. Make a fist. Place the thumb side of your fist in middle of the
person’s abdomen, just above the navel. Locate the middle of
the sternum for obese or pregnant persons.
5. Grasp your fist with your other hand.
6. Press your fist abruptly into the person’s abdomen using an
upward, inward thrust. Use a straight chest thrust back for
someone who is obese or pregnant.
7. Continue abdominal or chest thrusts until the object is dislodged
or the person loses consciousness.
8. If the person loses consciousness, treat as an unconscious adult
or a child with an obstructed airway.

CPR
 CPR

Abdominal thrusts for adult or child

Obstructed Airway: Conscious Infant

(younger than 1 yr)
Clinical Presentation
■ Inability to breathe or cry
■ High-pitched crowing sounds
■ Sudden wheezing or noisy breathing
1. Determine that the airway is obstructed. Notice if air exchange is
poor or does not occur.
2. Lay the infant down on your forearm, supporting the jaw between
your thumb and index finger and supporting the chest with your
hand and forearm.
3. Using your thigh or lap for support, keep the infant’s head lower
than the body.
4. Give five quick, forceful slaps between the shoulder blades with
the heel of your hand.
5. Turn the infant over to be face up on your other arm. Using your
thigh or lap for support, keep the infant’s head lower than the body.

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6. Place two fingers of one hand over the center of the chest just
below the nipple line.
7. Give five quick thrusts downward, depressing the chest by 1/3 (1.5 in)
its depth each time.
8. Continue the sequence of five back slaps and five chest thrusts
until the object is dislodged or the infant loses consciousness. If
the infant loses consciousness, treat as an unconscious infant with
an obstructed airway.

Back blows and chest thrusts for infant

Obstructed Airway: Unconscious Adult

(Age of puberty or older)
Clinical Presentation
■ Failure to breathe, cyanosis
■ Inability to move air into lungs with rescue breaths
1. Ensure that the scene is safe. Check for unresponsiveness. Gently
tap the person’s shoulder. Ask, “Are you OK?”
2. Simultaneously assess the person's breathing and pulse.
■ Check for breathing. Is the breathing normal, no breathing, or
abnormal (only agonal gasps)?
■ Assess the carotid pulse and look for other signs of circulation
(no more than 10 sec). If signs of circulation are present but the
person is still not breathing, give rescue breaths at the rate of
10–12 breaths/min (1 breath every 5–6 sec).

CPR
 CPR

3. In a sudden collapse, if there is no response with no breathing or

abnormal breathing (only agonal gasps) and you are alone, summon
help, call a code, or phone 911 and get an automated external defibril-
lator (AED), if available. Send a second rescuer, if available, for help.
4. Position the person supine on a hard, flat surface.
5. If a pulse and signs of circulation are not present, begin chest
compressions.
■ Place the heel of one hand on the center of the chest over the
lower half of the sternum; place the heel of your other hand
over the first.
Firmly compress the chest at least 2.0 in (5 cm). Push hard
and fast. Give 30 compressions. Compress at a rate of at least
100–120/min. Ensure complete chest recoil after each compres-
sion. Avoid leaning on the chest between compressions.
6. If the person is not breathing, begin rescue breaths. Open the air-
way by the head tilt–chin lift method or, if spinal injury is suspected,
use the jaw thrust method, if possible.
7. Using a face mask or barrier device, give 2 breaths (1 sec each) with
sufficient volume to cause the chest to rise. Do not overventilate.
If the chest does not rise, reposition the head, chin, and jaw, and
give 2 more breaths. If the chest still does not rise, each time the
airway is opened, look for an object in the person’s mouth. Only
use a finger sweep to remove material you see obstructing the
airway. Never perform a finger sweep if you do not see a foreign
body in the airway.
8. Continue to give 30 compressions followed by opening the airway,
looking for an object, and performing a finger sweep if object is
visible, and then attempt to give 2 breaths.
9. Continue these cycles until an AED arrives. If an AED is unavail-
able, continue to give 30 compressions followed by 2 breaths.
10. If circulation resumes but breathing does not resume or is inade-
quate, continue rescue breathing at 10–12 breaths/min (1 breath
every 5–6 sec).
11. If adequate breathing and circulation resume, place the person in
the recovery position and monitor until help arrives.
Clinical Tip: An airway obstruction is successfully removed if you see
and remove the object or feel air movement and see the chest rise
when you give breaths.

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Obstructed Airway: Unconscious Child
(1 yr to age of puberty)
Clinical Presentation
■ Failure to breathe, cyanosis
■ Inability to move air into lungs with rescue breaths
1. Ensure that the scene is safe. Check for unresponsiveness. Gently
tap child’s shoulder. Ask, “Are you okay?”
2. Simultaneously assess the child's breathing and pulse.
■ Check for breathing. Is the breathing normal, no breathing, or
abnormal (only agonal gasps)?
■ Assess the carotid pulse and look for other signs of circulation
(no more than 10 sec). If signs of circulation are present but the
child is still not breathing, give rescue breaths at the rate of
12–20 breaths/min (1 breath every 3–5 sec).
3. If there is no response with no breathing, and no pulse, abnormal
breathing (only agonal gasps), send a second rescuer, if available,
for help and an AED, if available.
4. If you are alone, begin the steps for CPR.
5. Position the child supine on a hard, flat surface.
6. If a pulse and signs of circulation are not present, begin chest
compressions.
■ One hand: Place the heel of one hand on the center of the chest
over the lower half of the sternum.
■ Two hands: Place the heel of one hand on the center of the
chest over the lower half of the sternum; place the heel of your
other hand over the first.
Firmly compress the chest at least one third the depth of the
chest (at least 2.0 in). Push hard and fast. Give 30 compressions.
Compress at a rate of at least 100–120/min. Ensure complete chest
recoil after each compression. Avoid leaning on the chest between
compressions.
7. If the child is not breathing, begin rescue breaths. Open the airway
by the head tilt–chin lift method or, if spinal injury is suspected,
use the jaw thrust method, if possible.
8. Using a face mask or barrier device, give 2 breaths (1 sec each) with
sufficient volume to cause the chest to rise. Do not overventilate.

CPR
 CPR

9. If the chest does not rise, reposition the head, chin, and jaw, and
give two more breaths. Each time the airway is opened, look for an
object in the child’s mouth. Only use a finger sweep to remove
material you see obstructing the airway. Never perform a finger
sweep if you do not see a foreign body in the airway.
10. Continue to give 30 compressions followed by opening the airway,
looking for an object, and performing a finger sweep if object is visi-
ble, and then attempt to give 2 breaths. After the fifth cycle of 30:2
(2 min), if you are still alone and no signs of circulation are present,
summon help, call a code, or phone 911 and get an AED, if available.
11. If circulation is still not present, continue CPR until the AED is
available. If an AED is unavailable, continue to give 30 compressions
followed by 2 breaths. After each fifth cycle of 30:2 (2 min), recheck
the pulse and look for other signs of circulation (no more than 10 sec).
12. If circulation resumes but breathing does not resume or is inadequate,
continue rescue breathing at 12–20 breaths/min.
13. If adequate breathing and circulation resume, place the child in the
recovery position and monitor until help arrives.
Clinical Tip: Never perform a blind finger sweep.

Obstructed Airway: Unconscious Infant

(younger than 1 yr)
Clinical Presentation
■ Inability to breathe, high-pitched noises
■ Inability to move air into lungs with rescue breaths
■ Cyanosis
1. Ensure that the scene is safe. Check for unresponsiveness. Gently
rub the infant’s back or tap the feet.
2. Simultaneously assess the infant's breathing and pulse.
■ Check for breathing. Is the breathing normal, no breathing, or
abnormal (only agonal gasps)?
■ Assess the brachial pulse and look for other signs of circulation
(no more than 10 sec). If signs of circulation are present but the
infant is still not breathing, give rescue breaths at the rate of
12–20 breaths/min (1 breath every 3–5 sec).

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 141
3. If there is no response with no breathing, abnormal breathing (only
agonal gasps), and no pulse, send a second rescuer, if available,
for help.
4. If you are alone, begin the steps for CPR.
5. Position the infant supine on a hard, flat surface.
6. If a pulse and signs of circulation are not present, begin chest
compressions.
■ Place two fingers of one hand over the center of the chest just
below the nipple line.
Firmly compress the chest at least one third the depth of the chest
(at least 1.5 in [4 cm]). Push hard and fast. Give 30 compressions.
Compress at a rate of at least 100–120/min. Ensure complete chest
recoil after each compression. Avoid leaning on the chest between
compressions.
7. If the infant is not breathing, begin rescue breaths. Open the airway
by the head tilt–chin lift method or, if spinal injury is suspected, use
the jaw thrust method, if possible.
8. Using a face mask or barrier device, give 2 breaths (1 sec each) with
sufficient volume to cause the chest to rise. Do not overventilate.
9. If the chest does not rise, reposition the head, chin, and jaw, and
give two more breaths. Each time the airway is opened, look for
an object in the infant’s mouth. Only use a finger sweep to remove
material you see obstructing the airway. Never perform a finger
sweep if you do not see a foreign body in the airway.
10. Continue to give 30 compressions followed by opening the airway,
looking for an object, and performing a finger sweep if object is
visible, and then attempt to give 2 breaths. After the fifth cycle of 30:2
(2 min), if you are still alone and no signs of circulation are present,
summon help, call a code, or phone 911 and get an AED, if available.
11. If circulation is still not present, continue CPR until the AED is
available. If an AED is unavailable, continue to give 30 compressions
followed by 2 breaths.
12. If circulation resumes but breathing does not resume or is inadequate,
continue rescue breathing at 12–20 breaths/min.
13. If adequate breathing and circulation resume, place the infant in the
recovery position and monitor until help arrives.
Clinical Tip: When you open an infant’s airway by the head tilt–chin lift
method, do not overextend the head or the airway will become obstructed.

CPR
 CPR

Opioid-Associated Life-Threatening
Emergency (Adult)
Clinical Presentation
■ Suspected Opioid Overdose
■ Unresponsiveness
1. Ensure that the scene is safe. Check for unresponsiveness. Gently
tap the person’s shoulder. Ask, “Are you OK?”
2. Simultaneously access the person’s breathing and pulse.
■ Check for breathing. Is the breathing normal, no breathing, or
abnormal (only agonal gasps)?
■ Assess the carotid pulse and look for other signs of circulation
(no more than 10 sec). If signs of circulation are present but the
person is still not breathing, give rescue breaths at the rate of
10–12 breaths/min (1 breath every 5–6 sec).
3. In a sudden collapse, if you are alone and there is no response
with no breathing or abnormal breathing (only agonal gasps) and
no pulse, summon help, call a code, or phone 911 and get an auto-
mated external defibrillator (AED) and naloxone, if available. Send
a second rescuer, if available, for help.
4. Position the person supine on a hard, flat surface.
5. If a pulse and signs of circulation are not present, begin chest
compressions.
■ Place the heel of one hand on the center of the chest over the
lower half of the breastbone; place the heel of your other hand
over the first.
Firmly compress the chest at least 2.0 in. Push hard and fast. Give
30 compressions. Compress at a rate of 100–120/min. Ensure com-
plete chest recoil after each compression. Avoid leaning on the
chest between compressions.
6. If the person is not breathing, begin rescue breaths. Open the
airway by the head tilt-chin lift method or, if spinal injury is
suspected, use the jaw thrust method, if possible.

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7. Using a face mask or barrier device, give 2 breaths (1 sec each) with
sufficient volume to cause the chest to rise. Do not overventilate.
Note: If the chest does not rise, reposition the head, chin, and jaw,
and give 2 more breaths. If the chest still does not rise, follow
instructions for unconscious adult with an obstructed airway.
8. Continue to give 30 compressions followed by 2 breaths until an
AED and naloxone arrive.
9. Administer naloxone as soon as it is available. Give 2 mg intranasal
or 0.4 mg IM. May repeat after 4 min.
10. Does the person respond?
■ Yes: If adequate breathing and circulation resume, place the per-
son in the recovery position and monitor until help arrives. If the
person stops responding, begin CPR and repeat naloxone.
■ No: Continue CPR and use the AED as soon as it is available.
Continue until the person responds or until advanced help
arrives.

CPR
 CPR

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 Recovery position.

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ACLS: Ventricular Fibrillation (VF) or Pulseless
Ventricular Tachycardia (VT)
Clinical Presentation
■ Unresponsive state
■ No respiration, pulse, or blood pressure (BP)
1. Establish unresponsiveness with no respiration or pulse. Call
for help.
2. Begin CPR, provide oxygen, and attach AED or monitor-defibrillator
when available without interrupting CPR.
3. When device is attached, stop CPR and assess rhythm. If shock is
advised when using an AED, defibrillate following the AED voice/
visual prompts. If using a manual monitor-defibrillator and the
rhythm is VF or pulseless VT, defibrillate at 120–200 J if using a
biphasic defibrillator following manufacturer’s device-specific
energy levels if known, or 200 J if unknown, or defibrillate at 360 J
if using a monophasic defibrillator.
4. Immediately resume CPR, beginning with compressions. Provide
five cycles (2 min) of uninterrupted CPR. During CPR, establish
IV or intraosseous (IV/IO) access. Prepare vasopressor dose
(epinephrine or vasopressin).
5. Assess rhythm. If the rhythm is shockable, follow AED voice/visual
prompts or defibrillate at same or higher energy for biphasic manual
defibrillator or at 360 J for a monophasic manual defibrillator.
6. Immediately resume CPR beginning with compressions and using
five cycles of 30 compressions and 2 breaths.
7. Consider insertion of an advanced airway (ET tube, LMA, King LT,
or Combitube) if basic airway management is inadequate. Once
an advanced airway is in place, compressions should be uninter-
rupted at a rate of at least 100–120/min, and ventilations should
be 10 breaths/min (1 breath every 6 sec). Use waveform capnog-
raphy to confirm and monitor ET tube placement.

ACLS
 ACLS

8. Administer epinephrine 1 mg (10 mL of 1:10,000) by the IV/IO

method; follow with 20-mL IV flush. Repeat every 3–5 min.
If no IV/IO access is available, give 2.0–2.5 mg (1:1000) epineph-
rine diluted in 5–10 mL normal saline or sterile water and admin-
ister by endotracheal (ET) tube every 3–5 min until IV/IO access is
available.
9. Continue CPR; check the rhythm every 2 min.
10. If the rhythm is still shockable, defibrillate as in step 5.
11. Immediately resume CPR; check the rhythm every 2 minutes.
Consider antiarrhythmics for shock-refractory VF or pulseless VT:
12. Administer amiodarone 300 mg IV/IO or lidocaine 1.0–1.5 mg/kg
IV/IO. Lidocaine should only be used as an alternative if the
patient is allergic to amiodarone or if amiodarone is unavailable.
13. Repeat antiarrhythmic therapy for shock-refractory VF or VT:
amiodarone 150 mg IV/IO in 3–5 min (use only one time); or
lidocaine 0.5–0.75 mg/kg IV/IO. Repeat lidocaine every 5–10 min,
maximum dose 3 mg/kg. Lidocaine should only be used as
an alternative if the patient is allergic to amiodarone or if
amiodarone is unavailable.
14. Consider magnesium sulfate 1–2 g (2–4 mL of a 50% solution)
diluted in 10 mL of D5W IV/IO, given over 1–2 min for cardiac
arrest caused by hypomagnesemia or torsade de pointes.
Clinical Tip: Do not delay defibrillation for a witnessed arrest. For
an unwitnessed arrest with a down time greater than 4–5 min, perform
2 min of CPR before defibrillation.
Clinical Tip: Airway must be secured and placement verified with
observation of chest rise and auscultation of breath sounds plus
a confirmatory device (exhaled CO2 detector). Monitor tube for
displacement during transport or whenever patient is moved.

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ACLS: Pulseless Electrical Activity (PEA)
Clinical Presentation
■ Unresponsive state
■ No respiration, pulse, or BP
■ Identifiable organized electrical rhythm on monitor but no pulse
1. Establish unresponsiveness with no respiration or pulse. Call for
help.
2. Begin CPR, provide oxygen, and attach manual monitor-defibrillator
when available without interrupting CPR.
3. When device is attached, stop CPR to assess rhythm. If organized
rhythm noted on monitor, immediately resume CPR beginning with
compressions. Establish IV/IO access.
4. During CPR, consider and treat possible causes:
■ Hypokalemia/hyperkalemia ■ Tension pneumothorax
■ Hypothermia ■ Thrombosis, pulmonary
■ Hypoxia ■ Thrombosis, coronary
■ Hypovolemia ■ Tamponade, cardiac
■ Hydrogen ion (acidosis) ■ Toxins
5. Continue CPR using five cycles of 30 compressions and 2 breaths;
check the rhythm every 2 minutes.
6. Consider insertion of an advanced airway (ET tube, LMA, King LT,
or Combitube) if basic airway management is inadequate. After an
advanced airway is in place, compressions should be uninterrupted at
a rate of at least 100/min, and ventilations should be 8–10 breaths/min
(1 breath every 6–8 sec). Use waveform capnography to confirm and
monitor ET tube placement.
7. If PEA persists, administer epinephrine 1 mg (10 mL of 1:10,000)
by the IV/IO method; follow with 20-mL IV flush. Repeat
every 3–5 min. If no IV/IO access is available, give 2.0–2.5 mg
(1:1000) epinephrine diluted in 5–10 mL normal saline or sterile
water and administer by endotracheal (ET) tube every 3–5 min
until IV/IO access is available.
8. Continue CPR; check the rhythm every 2 min.
9. If the rhythm is shockable with no pulse, follow VF/VT protocol.

ACLS
 ACLS

10. If the rhythm is not shockable with no pulse, resume CPR and
repeat steps 4–8.
11. If a stable ECG rhythm returns with adequate breathing and
circulation, monitor and reevaluate the patient.
Clinical Tip: PEA is frequently caused by potentially reversible condi-
tions and can be treated successfully if those conditions are identified
and corrected easily.

ACLS: Asystole
Clinical Presentation
■ Unresponsive state, no respiration, pulse, or BP
■ ECG shows flat line; no electrical activity
1. Establish unresponsiveness with no respiration or pulse. Call for
help.
2. Begin CPR, provide oxygen, and attach manual monitor-defibrillator
when available without interrupting CPR.
3. When device is attached, stop CPR to assess rhythm. If no electrical
activity (flat line or asystole) is noted on monitor, immediately
resume CPR beginning with compressions. Establish IV/IO access.
4. During CPR consider and treat possible causes:
■ Hypokalemia/hyperkalemia ■ Tension pneumothorax
■ Hypovolemia ■ Thrombosis, pulmonary
■ Hypoxia ■ Thrombosis, coronary
■ Hypothermia ■ Tamponade, cardiac
■ Hydrogen ion (acidosis) ■ Toxins
5. Continue CPR beginning with compressions and using five cycles
of 30 compressions and 2 breaths; check the rhythm every 2 min.
6. Consider insertion of an advanced airway (ET tube, LMA, King LT,
or Combitube) if basic airway management is inadequate. After
an advanced airway is in place, compressions should be uninter-
rupted at a rate of 100–120/min, and ventilations should be
10 breaths/min (1 breath every 6 sec). Use waveform capnography
to confirm and monitor ET tube placement.

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7. If asystole persists, administer epinephrine 1 mg (10 mL of 1:10,000)
by the IV/IO method; follow with 20 mL IV flush. Repeat every
3–5 minutes. If no IV/IO access is available, give 2.0–2.5 mg (1:1,000)
epinephrine diluted in 5–10 mL normal saline or sterile water and
administer by endotracheal (ET) tube every 3–5 minutes until IV/IO
access is available.
8. Continue CPR; check the rhythm every 2 min.
9. If the rhythm is shockable with no pulse, follow VF/VT protocol.
10. If the rhythm is not shockable with no pulse, resume CPR and
repeat steps 4–8.
11. If asystole persists, consider whether proper resuscitation proto-
cols were followed and reversible causes identified. If procedures
were performed correctly, follow local criteria for terminating
resuscitation efforts.
Clinical Tip:Transcutaneous pacing is not recommended for asystolic
cardiac arrest.
Clinical Tip: Study local policy to learn established criteria for stopping
resuscitation efforts.

ACLS: Acute Coronary Syndrome (ACS)

Clinical Presentation
■ History of coronary artery disease, angina, or acute myocardial
infarction (MI)
■ Chest pain or discomfort
■ Pain spreading to neck, shoulders, arms, jaw, or upper back
■ Sudden unexplained shortness of breath, weakness, fatigue with or
without chest pain/discomfort
■ Associated nausea, diaphoresis, lightheadedness, fainting
1. Establish responsiveness.
2. Perform primary ABCD survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen if oxygen saturation is <94%. Titrate to effect.

ACLS
 ACLS

5. Administer aspirin 160–325 mg orally (PO) if no history of aspirin

allergy. Aspirin 81 mg (times 4 tablets) is commonly given.
Chewing the tablet(s) is preferable; use nonenteric coated tablets
for antiplatelet effect. Give within minutes of onset.
6. Start an IV and attach a cardiac monitor. Obtain a 12-lead ECG.
7. If the 12-lead ECG shows ST segment elevation, notify the
attending physician. Begin the checklist for fibrinolytic therapy.
If possible, prehospital providers should transport the patient to
the closest facility with rapid coronary intervention capabilities.
8. Administer nitroglycerin by the sublingual route 0.3–0.4 mg
(1 tablet), repeated every 3–5 min for a total of three doses over
a 15-min interval, or administer aerosol spray for 0.5–1.0 sec at
3–5 min intervals (provides 0.4 mg per dose) not to exceed three
sprays in 15 min. Nitroglycerin administration requires a systolic
BP of 90 mm Hg or greater.
9. Repeat nitroglycerin (see step 8) until chest pain is relieved,
systolic BP falls below 90 mm Hg, or signs of ischemia or
infarction are resolved.
10. If chest pain is not relieved by nitroglycerin, administer morphine
2–4 mg IV (over 1–5 min). If symptoms are not resolved, adminis-
ter 2–8 mg every 5–15 min if hemodynamically stable. Do not
administer morphine if systolic BP is less than 90 mm Hg.
Clinical Tip: Do not delay rapid transport to a cardiac catheterization
laboratory for reperfusion. Consider fibrinolytic therapy within 30 minutes
if a cardiac catheterization laboratory is not immediately available.
Clinical Tip: Patients should not be given nitroglycerin if they have
taken sildenafil (Viagra) or vardenafil (Levitra) in the last 24 hours or
tadalafil (Cialis) within 48 hours. The use of nitroglycerin with these
medications may cause irreversible hypotension.
Clinical Tip: Nitroglycerin should be used with caution in patients
with an inferior MI with possible right ventricular involvement. It is
contraindicated with right ventricular MI, tachycardia, and bradycardia.
Clinical Tip: Diabetic patients, elderly patients, and women frequently
present with atypical symptoms (e.g., weakness, fatigue, complaints of
indigestion).

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ACLS: Bradycardia
Clinical Presentation
■ Heart rate less than 50 bpm in symptomatic patient.
■ Sinus bradycardia, junctional escape rhythm, or AV block
■ Symptoms of chest discomfort/pain, lightheadedness, dizziness,
dyspnea, tachypnea, presyncope, syncope.
■ Signs of hypoxemia, hypotension, diaphoresis, altered mental status,
congestive heart failure (CHF), shock
1. Establish responsiveness.
2. Perform primary ABCD survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen if oxygen saturation is <94%. Titrate to effect.
Start an IV and attach cardiac monitor to identify rhythm.
5. Obtain a 12-lead ECG.
6. If the patient is stable and asymptomatic with a heart rate less
than 50 bpm, monitor and observe for any changes.
7. If the patient is symptomatic with signs of poor perfusion, initiate
treatment.
8. Administer atropine 0.5 mg IV every 3–5 min, maximum total
dose 3 mg. In sinus bradycardia, junctional escape rhythm, or
second-degree AV block Wenckebach/Mobitz type I, atropine is
usually effective. In second-degree Mobitz type II or third-degree
AV block, atropine is likely to be ineffective; prepare for transcu-
taneous pacing.
9. If the patient fails to respond to atropine in step 8, sedate and
begin transcutaneous pacing (TCP) as a temporizing measure if
IV access is not available. TCP is painful and will require sedation/
analgesia in the conscious patient.
10. If the patient is hypotensive with severe bradycardia, or if TCP is
unavailable or ineffective, initiate drug therapy with a continuous
dopamine infusion starting at 2–10 mcg/kg/min (chronotropic or
heart rate dose) and titrate to patient response. Mix 400 mg/250 mL
in normal saline, lactated Ringer’s solution, or D5W (1600 mcg/mL).
An alternative may be an epinephrine infusion, 2–10 mcg/min IV (add
1 mg of 1:1000 in 500 mL normal saline and infuse at 1–5 mL/min).
Seek expert consultation and prepare for transvenous pacing.

ACLS
 ACLS

Clinical Tip: If the patient has symptoms, 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 lead to rate-induced ischemia.

ACLS: Tachycardia––Unstable
Clinical Presentation
■ Altered level of consciousness (LOC)
■ Symptoms of shortness of breath, diaphoresis, weakness, fatigue,
syncope or presyncope, chest discomfort or pain, palpitations
■ Signs of hypotension, shock, congestive heart failure, ischemic ECG
changes, poor peripheral perfusion
■ Heart rate typically > – 150 bpm
1. Establish responsiveness.
2. Perform primary ABCD survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen if oxygen saturation is <94%. Titrate to effect.
Start an IV and begin cardiac monitoring.
5. Establish that serious signs and symptoms are related to the
tachycardia.
6. If the patient is unstable and has symptoms with a heart rate –>150 bpm,
prepare for immediate synchronized cardioversion (patients with a
healthy heart are unlikely to be unstable if the ventricular rate is
less than 150 bpm; however, patients with cardiac disease may be
unstable with a heart rate less than 150 bpm). It is important to look
at the patient’s stability in addition to monitoring heart rate as criteria
for cardioversion.
7. Premedicate with a sedative plus an analgesic whenever possible.
8. Place the defibrillator in synchronized (sync) mode.

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9. Administer synchronized cardioversion at:
■ Narrow regular rhythm (supraventricular tachyarrhythmia
[SVT])—generally requires less energy, 50 to 100 J either
biphasic or monophasic is often sufficient; narrow irregular
rhythm (atrial fibrillation)—120 to 200 J biphasic or 200 J
monophasic. If the initial cardioversion shock fails, the energy
should be increased in a stepwise fashion.
■ Wide regular rhythm (monomorphic ventricular tachycardia)—
usually responds well to biphasic or monophasic initial ener-
gies of 100 J. If there is no response to the first shock, it may
be reasonable to increase the dose in a stepwise fashion.
10. If a regular narrow complex tachycardia is seen in an unstable
patient, consider administering adenosine before cardioversion.
■ Adenosine—6 mg IVP in the antecubital or other large vein
given rapidly over 1–3 seconds followed by a 20-mL bolus
of normal saline. If the rhythm has not converted in 1–2 min,
repeat adenosine at 12 mg IVP. If the rhythm still does not
convert, a third dose of 12 mg IVP may be given after another
1–2 min, maximum 30 mg.
11. If pulseless arrest develops, identify arrhythmia and follow
algorithm for VF/VT, PEA, or asystole.
Clinical Tip: Reactivate the “sync” mode before each attempted
cardioversion.
Clinical Tip: The “sync” mode delivers energy synchronizing with the
timing of the QRS complex to avoid stimulation during the refractory, or
vulnerable, period of the cardiac cycle when a shock could potentially
produce VF.
Clinical Tip: Synchronized cardioversion must not be used for treat-
ment of VF because the device is unlikely to sense a QRS wave, and
thus a shock may not be delivered. Synchronized cardioversion should
also not be used for pulseless VT or polymorphic VT (irregular VT).
These rhythms require delivery of high-energy unsynchronized shocks
(i.e., defibrillation doses).

ACLS
 ACLS

Narrow-Complex Tachycardia—Stable
Regular Rhythm
Clinical Presentation
■ No serious signs or symptoms related to the tachycardia
■ Regular ECG rhythm
■ QRS narrow (<0.12 sec)
■ Heart rate typically >– 150 bpm
1. Establish responsiveness.
2. Perform primary ABCD survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen if oxygen saturation is <94%. Titrate to effect.
Start an IV line, and attach cardiac monitor to identify rhythm.
Obtain a 12-lead ECG.
5. Attempt vagal maneuvers such as ice to the face (diving reflex),
holding the breath while bearing down (Valsalva maneuver), or
blowing through an obstructed straw.
6. If rhythm has not converted to sinus rhythm, administer adenosine
6 mg IV in the antecubital or other large vein given rapidly over
1–3 sec followed by a 20-mL bolus of normal saline.
7. If the rhythm has not converted in 1–2 min, repeat adenosine at
12 mg IV. If the rhythm still does not convert, a third dose of
12 mg IV may be given after another 1–2 min, maximum 30 mg.
8. If the rhythm still does not convert, it may be atrial flutter, atrial
tachycardia, multifocal atrial tachycardia, or junctional tachycardia.
Consider rate control using diltiazem or beta blockers. Obtain
expert consultation.
9. If the rhythm converts, observe the patient and treat any recurrence
with adenosine, diltiazem, or beta blockers. Obtain expert consultation.
Clinical Tip: If the patient’s condition becomes unstable during the
tachycardia, perform immediate synchronized cardioversion.
Clinical Tip: Use beta blockers with caution in patients with
obstructive pulmonary disease or congestive heart failure. Avoid use in
patients with bronchospastic disease.

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Wide-Complex Tachycardia—Stable
Regular Rhythm
Clinical Presentation
■ No serious signs and symptoms related to the tachycardia
■ Regular ECG rhythm
■ QRS wide (>0.12 sec)
■ Heart rate typically >– 150 bpm
1. Establish responsiveness.
2. Perform primary ABCD survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen if oxygen saturation is <94%. Titrate to effect.
Start an IV, and attach cardiac monitor to identify rhythm. Obtain a
12-lead ECG.
5. If the arrhythmia is VT, administer amiodarone 150 mg IV/IO over
10 minutes. May repeat every 10 minutes and start infusion at
1 mg/min for 6 hours, followed by 0.5 mg/min for 18 hours. Do not
exceed 2.2 g in 24 hours.
6. If the wide-complex tachycardia is regular, monomorphic, and
suspected to be SVT with aberrancy, administer adenosine 6 mg
IV in the antecubital or other large vein given rapidly over 1–3 seconds
followed by a 20-mL bolus of normal saline.
7. If the rhythm transiently slows or converts to a sinus rhythm, it
likely was SVT. However, if there was no effect after adenosine,
the rhythm is likely monomorphic VT or atrial fibrillation with
preexcitation and should be treated with amiodarone.
8. If pulseless arrest develops, identify arrhythmia and follow algorithm
for VF/VT.

ACLS
 ACLS

Immediate Post–Cardiac Arrest Care

Upon return of spontaneous circulation:
1. Provide oxygen to maintain oxygen saturation (94%–99% for optimal
oxygenation. Avoid hyperoxygenation and oxygen toxicity.
2. Unless awake and alert, the patient may require an advanced airway
and monitoring with waveform capnography.
■ Hyperventilation must be avoided.
■ Target end-tidal CO2 (PET CO2) should be 35–40 mm Hg, or
PaCO2 40–45 mm Hg.
3. Monitor vital signs.
■ Systolic blood pressure should be maintained at 90 mm Hg or
above, mean arterial pressure > – 65 mm Hg to optimize BP, cardiac
output, and perfusion.
■ Treat hypotension.
• If the systolic BP is <90 mm Hg, administer a 1- to 2-L fluid bolus
of normal saline or lactated Ringer’s.
• If necessary, the patient may be treated with a vasopressor
infusion: epinephrine, dopamine, or norepinephrine.
4. Consider and treat potentially reversible causes of cardiac arrest:
■ Hypokalemia/hyperkalemia ■ Tension pneumothorax
■ Hypovolemia ■ Thrombosis, pulmonary
■ Hypoxia ■ Thrombosis, coronary
■ Hypothermia ■ Tamponade, cardiac
■ Hydrogen ion (acidosis) ■ Toxins
5. Obtain a 12-lead ECG as soon as possible.
6. If the patient is comatose (lacking meaningful response to verbal
commands):
■ Initiate Targeted Temperature Management (TTM) with a targeted
temperature between 32°–36° C, selected and achieved, then main-
tained constantly for at least 24 hours.
7. If the patient rules in for an ST-elevation MI, or there is high suspicion
for an acute MI:
■ Arrange for prompt transport to a cardiac catheterization laboratory
for coronary reperfusion with possible percutaneous coronary
intervention, maintaining hypothermia.

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8. Maintain glycemic control.
■ Maintain blood glucose 144–180 mg/dL after arrest.
■ Avoid hypoglycemia.
9. Advanced critical care with development of a comprehensive plan of
care should be provided to all survivors of cardiac arrest to optimize
neurological, cardiopulmonary, and metabolic function.
■ Goal is return to patient’s prearrest functional status.
■ Use of appropriate tools to establish prognosis for patients requiring
continued advanced life support before determination to withdraw
life support.

Stroke
Clinical Presentation
■ Facial droop, arm or leg weakness/numbness, especially unilateral
■ Difficulty speaking or understanding, confusion
■ Sudden severe headache, visual disturbances, dizziness, loss of
balance or coordination
The importance of rapid recognition of stroke symptoms, immediate
activation of EMS, and rapid dispatch cannot be overemphasized.
EMS Response:
1. Support airway, breathing, and circulation.
■ Administer oxygen if needed (i.e., oxygen saturation <94%).
2. Perform prehospital stroke assessment.
■ Cincinnati Prehospital Stroke Scale.
3. Establish time when patient was last known to be normal or time of
symptom onset if known.
4. Rapid transport: Triage to a center capable of providing acute stroke
care if available.
5. Alert hospital.
■ Be sure hospital CT scan is functional.
6. Check patient’s glucose level.

ACLS
 ACLS

The following should be performed within first 60 min after patient has
arrived at emergency department:
Immediate general assessment and stabilization within first 10 min of
arrival:
1. Assess airway, breathing, circulation, and vital signs.
2. Administer oxygen if patient is hypoxemic.
3. Obtain IV access and blood samples.
4. Check glucose level.
■ Treat if indicated.
5. Perform initial neurological screening.
6. Activate stroke team.
7. Order emergent noncontrast CT scan or MRI of brain.
■ This is the most important test for a patient with a suspected acute
stroke.
8. Obtain 12-lead ECG.
Immediate neurological assessment by stroke team or designee within
first 25 min of arrival:
1. Review patient’s history and perform general physical exam.
2. Establish time of symptom onset or last time patient was known to be
normal.
3. Perform a neurological examination.
■ Use a stroke or neurological scale, such as the National Institutes
of Health Stroke Scale (NIHSS) or Canadian Neurological Scale.
4. Interpret CT scan within 45 min of arrival.
5. Does CT scan show hemorrhage?
If CT scan does not show hemorrhage, perform the following within the
first 45 min of arrival:
1. Review fibrinolytic inclusion, exclusion, and relative exclusion criteria.
2. Repeat neurological examination to determine whether patient’s
symptoms are improving/resolving or not.
3. If patient is a candidate for fibrinolytic therapy:
■ Review risks and benefits of fibrinolytic therapy with patient/family.
■ If patient/family agree, give rtPA within 60 min of arrival.
■ Do not give anticoagulants or antiplatelet treatment for 24 hours.
■ Begin post-rtPA stroke pathway.
■ Admit to stroke unit or intensive care unit.

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■ Initiate supportive therapy.
■ Treat comorbidities.
4. If patient is not a candidate for fibrinolytic therapy:
■ Administer aspirin (orally if the patient can swallow, or rectally if
the patient has difficulty swallowing).
■ Begin stroke pathway.
■ Admit to stroke unit or intensive care unit.
■ Initiate supportive therapy.
■ Treat comorbidities.
If CT scan shows hemorrhage, perform the following within the first
45 minutes of arrival:
1. No aspirin, anticoagulation, or fibrinolytic therapy.
2. Consult neurologist or neurosurgeon.
■ Consider transfer if such expertise is not available.
3. Initiate supportive therapy.
4. Begin stroke pathway within 60 min of arrival.
5. Admit to stroke unit or intensive care unit within 3 hours of arrival.
6. Treat comorbidities.

General Stroke Care

1. Begin stroke pathway.
2. Continue to support airway, breathing, and circulation.
■ Maintain oxygen saturation 94%–99%.
3. Cardiac monitoring for first 24 hours or longer, if indicated.
4. Avoid intravenous D5W or excessive fluid loading.
5. Monitor blood pressure.
■ Manage hypertension if systolic blood pressure is >220 mm Hg
or diastolic blood pressure is >120 mm Hg.
6. Monitor blood glucose.
■ Treat hyperglycemia.
7. Monitor temperature.
■ Treat fever with acetaminophen.
8. Perform dysphagia screening/swallow evaluation.
9. Monitor for complications of stroke and fibrinolytic therapy
(if administered).

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Cincinnati Prehospital Stroke Scale

Facial droop: Have patient show teeth or smile.
• Normal—Both sides of face move equally well.
• Abnormal—One side of face does not move as well as the other side.
Arm drift: Have patient close eyes and hold both arms straight out with
palms up for 10 sec
• Normal—Both arms move the same or do not move at all.
• Abnormal—One arm does not move or drifts down lower than the other.
Speech: Have the patient say “You can’t teach an old dog new tricks.”
• Normal—Patient uses correct words with no slurring.
• Abnormal—Patient slurs words, uses inappropriate words, or is unable
to speak.
Note: The presence of a single abnormality has a sensitivity of 59% and a specificity of 89%
when scored by prehospital providers.

Glasgow Coma Scale

Observation Response Score
Eye response • Opens spontaneously 4
• Opens to verbal commands 3
• Opens to pain 2
• No response 1
Best verbal response • Alert and oriented 5
• Disoriented but converses 4
• Uses inappropriate words 3
• Makes incomprehensible sounds 2
• No response 1
Best motor response • Reacts to verbal commands 6
• Reacts to localized pain 5
• Withdraws from pain 4
• Abnormal flexion 3
• Abnormal extension 2
• No response 1
Total score Normal 15
Score can range from 3 (lowest neurological function) to 15 (highest function).
Score 14–15: Mild dysfunction
Score 11–13: Moderate to severe dysfunction
Score ≤10: Severe dysfunction

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 161
PALS: Ventricular Fibrillation (VF) or Pulseless
Ventricular Tachycardia (VT)
Clinical Presentation
■ Pediatric patient
■ Unresponsive state
■ No respirations or only agonal respirations
■ No pulse
■ VF or pulseless VT on ECG monitor
1. Establish unresponsiveness with no respirations or only agonal
respirations with no pulse. Call for help.
2. Begin CPR. Provide oxygen as soon as available.
3. Attach an AED or monitor-defibrillator as soon as available without
interrupting CPR. Use pediatric pads or paddles if available and
indicated.
4. When device is attached, stop CPR, check rhythm, and defibrillate,
if advised.
■ If using an AED and shock is advised, defibrillate following AED
voice/visual prompts. Attach monitor-defibrillator as soon as
available to assess rhythm.
■ If using a manual monitor-defibrillator, assess the rhythm.
If rhythm is VF or pulseless VT, defibrillate at 2 J/kg using a
biphasic or monophasic defibrillator.
5. Immediately resume CPR, beginning with compressions.
■ Two-rescuer CPR: Cycles of 15 compressions followed by
2 breaths.
■ Provide 2 min of uninterrupted CPR.
6. During CPR, establish IV or IO access.
■ Prepare vasopressor dose (epinephrine).
7. Stop CPR and assess rhythm. Defibrillate if rhythm remains
shockable; follow AED voice/visual prompts or defibrillate
at 4 J/kg.
8. Immediately resume CPR, beginning with compressions, providing
2 min of uninterrupted CPR.

PALS
 PALS

9. Administer epinephrine 0.01 mg/kg IV/IO (0.1 mL/kg of 1:10,000);

follow with 20-mL IV flush.
■ Repeat every 3–5 min as needed.
■ If no IV/IO access is available and the patient has an endotra-
cheal (ET) tube in place, inject 0.1 mg/kg (0.1 mL/kg of 1:1,000)
epinephrine directly into ET tube followed by a 5-mL saline
flush.
■ Follow ET drug administration with ventilations to disperse drug
into small airways for absorption into pulmonary vasculature.
10. Insert an advanced airway (ET tube) if basic airway management
is inadequate.
■ Confirm tube placement without interrupting CPR.
■ After correct placement is confirmed, deliver uninterrupted
chest compressions at a rate of 100–120/min for 2 min and
deliver 10 breaths/min at a rate of 1 breath every 6 sec.
11. Continue CPR and check the rhythm every 2 min.
12. If rhythm remains shockable, defibrillate. Follow AED voice/visual
prompts or defibrillate at 4 J/kg.
■ May increase energy with subsequent shocks, if needed, up to a
maximum of 10 J/kg or adult maximum energy dose.
13. Immediately resume CPR beginning with compressions. Check the
rhythm every 2 min.
14. Consider antiarrhythmic drugs for shock-refractory VF or
pulseless VT:
■ Administer amiodarone 5 mg/kg IV/IO, or lidocaine 1 mg/kg
IV/IO if amiodarone is not available.
■ May repeat amiodarone 5 mg/kg IV/IO up to 2 times for
shock-refractory VF or VT to a maximum of 15 mg/kg.
■ If the arrhythmia is torsade de pointes, consider magnesium
sulfate 25–50 mg/kg IV/IO (maximum dose 2 g) bolus.
15. During CPR, consider and treat potentially reversible causes:
■ Hypoxia or ventilation ■ Trauma (hypovolemia,
problems increased ICP)
■ Hypovolemia ■ Tension pneumothorax
■ Hypothermia ■ Tamponade (cardiac)
■ Hypoglycemia ■ Toxins
■ Hydrogen ion (acidosis) ■ Thrombosis (pulmonary or
■ Hypokalemia/hyperkalemia coronary)

162
 163
16. If rhythm changes to asystole or PEA, follow asystole or PEA
protocol.
17. If rhythm converts to a stable ECG rhythm with return of sponta-
neous circulation, monitor and reevaluate the patient. Arrange for
transport to a critical care unit. The patient will need a comprehen-
sive plan of care.
Clinical Tip: In infants and young children, the cause of cardiac
arrest is more likely to be progressive respiratory failure or shock lead-
ing to an asphyxia arrest, rather than cardiac disease. Early recognition
and management of impending respiratory failure may prevent cardiac
arrest.
Clinical Tip: Signs of impending respiratory failure include tachyp-
nea, nasal flaring, intercostal and sternal retractions, grunting, and
seesaw breathing.
Clinical Tip: Use infant defibrillation pads or paddles for infants
weighing <10 kg. Use adult pads or paddles for infants/children
weighing ≥10 kg.
Clinical Tip: Advanced airway must be secured and placement ver-
ified with observation of bilateral chest expansion, auscultation of bilat-
eral breath sounds and lack of epigastric sounds, plus a confirmatory
device (exhaled CO2 detector). Use continuous waveform capnography
if available. If not available, use a colorimetric CO2 detector. Monitor
tube for displacement during transport or whenever the patient is
moved.
Clinical Tip: After an advanced airway is in place, chest compressions
should be delivered continuously without pausing for ventilations.
A breath is delivered every 6–8 seconds without regard to the phase of
chest compressions (downstroke vs. upstroke).

PALS
 PALS

PALS: Pulseless Electrical Activity (PEA)

Clinical Presentation
■ Pediatric patient
■ Unresponsive state
■ No respirations or only agonal respirations
■ Organized electrical rhythm on ECG monitor but no pulse
1. Establish unresponsiveness with no respirations or only agonal
respirations, no pulse. Call for help.
2. Begin CPR. Provide oxygen as soon as available.
3. Attach AED or monitor-defibrillator as soon as available without
interrupting CPR. Use pediatric pads or paddles if available and
indicated.
4. When device is attached, stop CPR.
■ If using an AED and no shock is advised, immediately resume
CPR beginning with compressions. Attach monitor-defibrillator as
soon as available to assess rhythm.
■ If using a manual monitor-defibrillator, assess the rhythm. If
rhythm is an organized rhythm, immediately resume CPR
beginning with compressions.
5. During CPR, establish IV or IO access.
■ Prepare vasopressor dose (epinephrine).
6. Stop CPR. Assess rhythm.
7. If PEA persists, administer epinephrine 0.01 mg/kg IV/IO (0.1 mL/kg
of 1:10,000); follow with 20 mL IV flush.
■ Repeat every 3–5 min as needed.
■ If no IV/IO access is available and the patient has an ET in place,
inject 0.1 mg/kg (0.1 mL/kg of 1:1,000) epinephrine directly into
ET tube, followed by a 5-mL saline flush. Follow ET drug admin-
istration with ventilations to disperse drug into small airways for
absorption into pulmonary vasculature.
8. Insert an advanced airway (ET tube) if basic airway management is
inadequate.
■ Confirm tube placement without interrupting CPR.
■ After correct placement is confirmed, deliver uninterrupted
compressions at a rate of 100–120/min for 2 min and deliver
10 breaths/min at a rate of 1 breath every 6 sec.

164
 165
9. During CPR, consider and treat potentially reversible causes:
■ Hypokalemia/hyperkalemia ■ Hydrogen ion (acidosis)
■ Hypovolemia ■ Tension pneumothorax
■ Hypoxia or ventilation ■ Tamponade, cardiac
problems ■ Toxins
■ Hypoglycemia ■ Thrombosis (pulmonary or
■ Hypothermia coronary)
10. Continue CPR; check the rhythm every 2 min.
11. If PEA persists, resume CPR and repeat steps 7, 9, and 10.
12. If rhythm becomes shockable with no pulse, follow VF/VT
protocol.
13. If rhythm changes to asystole, follow asystole protocol.
14. If rhythm converts to a stable ECG rhythm with return of sponta-
neous circulation, monitor and reevaluate the patient. Arrange for
transport to a critical care unit. The patient will need a comprehen-
sive plan of care.
Clinical Tip: PEA may be caused by potentially reversible condi-
tions (Hs and Ts) and may be treated successfully if those conditions
are identified and corrected early.
Clinical Tip: When IV/IO access is not available, drugs may be deliv-
ered via an ET tube in the intubated patient. Stop CPR, administer the
drug, flush with at least 5 mL normal saline, and deliver 5 consecutive
positive-pressure ventilations to ensure proper drug delivery to the
distal airways for absorption.

PALS: Asystole
Clinical Presentation
■ Pediatric patient
■ Unresponsive state
■ No respirations or only agonal respirations
■ No pulse
■ Flat line or agonal rhythm, no electrical activity on ECG monitor
1. Establish unresponsiveness with no respirations or only agonal
respirations, no pulse. Call for help.
2. Begin CPR. Provide oxygen as soon as available.

PALS
 PALS

3. Attach AED or monitor-defibrillator as soon as available without

interrupting CPR. Use pediatric pads or paddles if available and
indicated.
4. When device is attached, stop CPR.
■ If using an AED and no shock is advised, immediately resume
CPR beginning with compressions. Attach monitor-defibrillator as
soon as available to assess rhythm.
■ If using a manual monitor-defibrillator, assess the rhythm. If there
is no electrical activity (flat line or agonal rhythm), immediately
resume CPR beginning with compressions.
5. During CPR, establish IV or IO access.
■ Prepare vasopressor dose (epinephrine).
6. Stop CPR. Assess rhythm.
7. If asystole persists, administer epinephrine 0.01 mg/kg IV/IO
(0.1 mL/kg of 1:10,000); follow with 20-mL IV flush.
■ Repeat every 3–5 min as needed.
■ If no IV/IO access is available and the patient has an ET tube in
place, inject 0.1 mg/kg (0.1 mL/kg of 1:1,000) epinephrine directly
into ET tube, followed by a 5-mL saline flush. Follow ET drug
administration with ventilations to disperse drug into small
airways for absorption into pulmonary vasculature.
8. Insert an advanced airway (ET tube) if basic airway management is
inadequate.
■ Confirm tube placement without interrupting CPR.
■ After correct placement is confirmed, deliver uninterrupted
compressions at a rate of 100–120/min for 2 min and deliver
10 breaths/min at a rate of 1 breath every 6 sec.
9. During CPR consider and treat potentially reversible causes:
■ Hypokalemia/hyperkalemia ■ Trauma (hypovolemia,
■ Hypovolemia increased ICP)
■ Hypoxia or ventilation ■ Tension pneumothorax
problems ■ Tamponade, cardiac
■ Hypoglycemia ■ Toxins
■ Hypothermia ■ Thrombosis (pulmonary or
■ Hydrogen ion (acidosis) coronary)

166
 167
10. Continue CPR; check rhythm every 2 min.
11. If asystole persists, resume CPR and repeat steps 7, 9 and 10.
■ Consider whether proper resuscitation protocols were followed
and reversible causes were identified.
■ If procedures were performed correctly, follow local criteria for
terminating resuscitation efforts.
12. If rhythm is shockable with no pulse, follow VF/VT protocol.
13. If rhythm changes to an organized rhythm with no pulse, follow
PEA protocol.
14. If rhythm converts to a stable ECG rhythm with return of sponta-
neous circulation, monitor and reevaluate the patient. Arrange for
transport to a critical care unit. The patient will need a comprehen-
sive plan of care.
Clinical Tip: Emphasis must be on high-quality CPR, ensuring ade-
quate rate and depth of chest compressions with complete chest recoil
after each compression, minimizing interruptions in chest compres-
sions (no more than 10 seconds when necessary), and avoiding exces-
sive ventilation. Rotate chest compressor every 2 min to minimize
fatigue.
Clinical Tip: To calculate medication doses, use the pediatric
patient’s weight if known. If the weight is not known, use a pediatric
body-length tape with precalculated doses, which are based on the
50th percentile of weight for length (ideal body weight) for a reason-
able estimate of medication doses.
Clinical Tip: Family presence during resuscitation may be beneficial
to the family, providing an opportunity to say goodbye and facilitating
the grieving process when resuscitation attempts are unsuccessful.
Families should be offered this opportunity whenever possible.

PALS
 PALS

PALS: Bradycardia
Clinical Presentation
■ Pediatric patient
■ Heart rate less than 60 bpm
■ Respiratory distress or failure
■ Signs of shock with hypotension, diaphoresis, altered mental status
1. Establish responsiveness.
2. Perform primary ABCDE survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen, establish IV/IO access, and attach monitor-
defibrillator to identify rhythm.
5. Obtain 12-lead ECG if possible for more accurate rhythm
identification.
6. Assess for signs and symptoms.
■ If the patient is stable and asymptomatic with a heart rate
<60 bpm, support oxygenation and ventilation, monitor and
observe for any changes, and seek expert consultation.
■ If the patient is symptomatic with a heart rate <60 bpm and
signs of poor perfusion despite oxygenation and ventilation,
perform CPR.
7. If symptomatic bradycardia persists, administer epinephrine
0.01 mg/kg IV/IO (0.1 mL/kg of 1:10,000); follow with 20 mL IV
flush.
■ Repeat every 3–5 min as needed.
■ If no IV/IO access is available and the patient has an ET tube
in place, inject 0.1 mg/kg (0.1 mL/kg of 1:1,000) epinephrine
directly into ET tube, followed by a 5-mL saline flush. Follow
ET drug administration with ventilations to disperse drug into
small airways for absorption into pulmonary vasculature.
8. For increased vagal tone or primary AV block, administer a first
dose of atropine 0.02 mg/kg IV/IO.
■ May repeat every 3–5 min. Minimum single dose 0.1 mg,
maximum single dose 0.5 mg, maximum total dose 1 mg.
9. If the patient fails to respond to atropine, consider transthoracic
or transvenous pacing.
10. Identify and treat the cause of bradycardia.

168
 169
PALS: Tachycardia With Pulse, Narrow-Complex
QRS (<– 0.09 sec) With Adequate Perfusion
Clinical Presentation
■ Pediatric patient
■ Rapid heart rate
■ No serious symptoms with signs of adequate perfusion
1. Establish responsiveness.
2. Perform primary ABCDE survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen, establish IV/IO access, and attach monitor-
defibrillator to identify rhythm.
5. Obtain a 12-lead ECG if possible for more accurate rhythm
identification.
6. Assess for signs and symptoms.
■ If the patient is stable and asymptomatic, with a heart rate less
than 180 bpm for a child and less than 220 bpm for an infant,
the rhythm is probably sinus tachycardia, not SVT. Search for
and treat the underlying cause.
■ If the heart rate is ≥180 bpm for a child and ≥220 bpm for an
infant, the rhythm is probably SVT; consider vagal maneuvers.
7. If vagal maneuvers are ineffective and IV/IO access is available,
give adenosine 0.1 mg/kg IV/IO rapid push.
■ Maximum first dose 6 mg.
■ May double the first dose and give 0.2 mg/kg IV/IO rapid push.
■ Maximum second dose 12 mg.
8. Seek expert consultation. Search for and treat reversible causes.
9. If rhythm has not converted to sinus, consider administration of
amiodarone 5 mg/kg IV over 20–60 min or procainamide 15 mg/kg
IV over 30–60 min.
■ Do not administer amiodarone and procainamide together.
10. If medications are ineffective, or if patient becomes unstable,
attempt synchronized cardioversion at 0.5–1.0 J/kg.
■ If unstable tachycardia persists, increase to 2 J/kg. Premedicate
with a sedative plus an analgesic whenever possible but do not
delay cardioversion.

PALS
 PALS

PALS: Tachycardia With Pulse, Wide-Complex

QRS (>0.09 sec) With Adequate Perfusion
Clinical Presentation
■ Pediatric patient
■ Rapid heart rate
■ No serious symptoms with signs of adequate perfusion
1. Establish responsiveness.
2. Perform primary ABCDE survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen, establish IV/IO access, and attach monitor-
defibrillator to identify rhythm.
5. Obtain a 12-lead ECG if possible for more accurate rhythm
identification.
6. If rhythm is likely a supraventricular tachycardia with aberrancy
(wide QRS), seek expert consultation.
■ Give adenosine 0.1 mg/kg IV/IO rapid push.
■ Maximum first dose 6 mg.
■ May double the first dose and give 0.2 mg/kg IV/IO rapid push.
■ Maximum second dose 12 mg.
■ Search for and treat reversible causes.
7. If rhythm is likely ventricular tachycardia, seek expert consultation.
■ Prepare to administer amiodarone 5 mg/kg IV over 20-60 min or
procainamide 15 mg/kg IV over 30–60 min. Do not administer
amiodarone and procainamide together.
■ Search for and treat reversible causes.
8. If medications are ineffective, or if patient becomes unstable,
attempt synchronized cardioversion at 0.5–1.0 J/kg.
■ If unstable tachycardia persists, increase to 2 J/kg.
■ Premedicate with a sedative plus an analgesic whenever possible
but do not delay cardioversion.

170
 171
PALS: Tachycardia With Pulse, Narrow-Complex
QRS (<– 0.09 sec) With Poor Perfusion
Clinical Presentation
■ Pediatric patient
■ Altered LOC
■ Shortness of breath, diaphoresis, fatigue, syncope, poor perfusion
1. Establish responsiveness.
2. Perform primary ABCDE survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen, establish IV/IO access, and attach monitor-
defibrillator to identify rhythm.
5. Obtain a 12-lead ECG if possible for more accurate rhythm
identification.
6. Assess for signs and symptoms.
■ If the patient is stable and asymptomatic, with a heart rate
<180 bpm for a child and <220 bpm for an infant, normal
P waves present and varying R-R intervals, the rhythm is
probably sinus tachycardia, not SVT. Search for and treat the
underlying cause.
■ If the heart rate is ≥180 bpm for a child and ≥220 bpm for
an infant with absent P waves, regular rhythm and signs of
poor perfusion, the rhythm is probably SVT; consider vagal
maneuvers.
7. If vagal maneuvers are ineffective and IV/IO access is available,
give adenosine 0.1 mg/kg IV/IO rapid push.
■ Maximum first dose 6 mg.
■ May double first dose and give 0.2 mg/kg IV/IO rapid push.
■ Maximum second dose 12 mg.
■ Immediately follow each dose with 5- to 10-mL normal saline
flush.
8. If IV/IO access is not available or adenosine was ineffective, attempt
synchronized cardioversion at 0.5–1.0 J/kg.
■ If unstable tachycardia persists, increase to 2 J/kg.
■ Premedicate with a sedative plus an analgesic whenever possible
but do not delay cardioversion.

PALS
 PALS

9. If cardioversion is unsuccessful, seek expert consultation.

10. Prepare to administer either amiodarone 5 mg/kg IV/IO over
20–60 min or procainamide 15 mg/kg IV/IO over 30–60 min.
■ Do not routinely administer amiodarone and procainamide
together.
Clinical Tip: If there are visible P waves with a constant PR interval
and somewhat variable R-R intervals in an infant with a heart rate
<220/min or a child with a heart rate <180/min, the rhythm is probably
sinus tachycardia. The heart rate increases gradually rather than abruptly.
Correlate with the pediatric patient’s clinical history and always search
for and treat the cause.
Clinical Tip: If there are no visible P waves and therefore no meas-
urable PR interval, with a regular R-R interval in an infant with a heart
rate ≥220/min or a child with a heart rate ≥180/min, the rhythm is
probably SVT. The rate typically changes abruptly. Treat according to
the above algorithm.

PALS: Tachycardia With Pulse, Wide-Complex

QRS (>0.09 sec) With Poor Perfusion
Clinical Presentation
■ Pediatric patient
■ Altered LOC
■ Shortness of breath, diaphoresis, fatigue, syncope, poor perfusion
1. Establish responsiveness.
2. Perform primary ABCDE survey.
3. Measure vital signs, including oxygen saturation.
4. Administer oxygen, establish IV/IO access, and attach monitor-
defibrillator to identify rhythm.
5. Obtain a 12-lead ECG if possible for more accurate rhythm
identification.
6. If the patient is experiencing cardiopulmonary compromise with a
rapid heart rate and wide QRS complex, the rhythm is presumed to
be ventricular tachycardia.
■ Prompt synchronized cardioversion is indicated.
■ Attempt synchronized cardioversion at 0.5–1 J/kg; if unstable
tachycardia persists, increase to 2 J/kg.
172
 173
■ Premedicate with a sedative plus an analgesic whenever possible
but do not delay cardioversion.
7. If the patient does not exhibit signs of cardiopulmonary compromise,
consider adenosine if the wide-complex tachycardia is regular and
monomorphic.
■ Give adenosine 0.1 mg/kg IV/IO rapid push (maximum first dose
6 mg).
■ May double the first dose and give 0.2 mg/kg IV/IO rapid push.
■ Maximum second dose 12 mg.
8. If cardioversion or adenosine is unsuccessful, seek expert
consultation.
9. Prepare to administer either amiodarone 5 mg/kg IV/IO over
20–60 min or procainamide 15 mg/kg IV/IO over 30–60 min.
■ Do not routinely administer amiodarone and procainamide
together.
Clinical Tip: Wide-complex tachycardia is a relatively uncommon
rhythm in children; however, it can be seen in children with heart
disease, drug ingestion (tricyclic antidepressants), and hyperkalemia.

PALS: Immediate Post–Cardiac Arrest Care

1. Upon return of spontaneous circulation, assess responsiveness,
perform primary ABCDE survey and secondary assessment. Measure
vital signs, including oxygen saturation.
2. Airway, breathing:
■ Provide oxygen to maintain oxygen saturation 94%–99% for optimal
oxygenation.
■ Wean oxygen within the range of 94%–99% if oxygen is 100% to
prevent hyperoxemia and associated oxidative injury.
■ Unless awake and alert, the patient may require an advanced
airway and monitoring with waveform capnography.
■ Hyperventilation must be avoided. Target end-tidal CO2 should be
35–40 mm Hg.

PALS
 PALS

3. Circulation:
■ Assess for presence of shock.
■ Treat persistent shock with 20 mL/kg IV/IO boluses of normal
saline or lactated Ringer’s. Consider smaller boluses (10 mL/kg) if
poor cardiac function is suspected.
■ If hypotensive shock persists, consider vasopressor infusion with
epinephrine, dopamine, or norepinephrine.
■ If normotensive shock, consider dobutamine, dopamine, epinephrine,
or milrinone.
4. Consider and treat potentially reversible causes of cardiac arrest:
■ Hypokalemia/hyperkalemia ■ Trauma (hypovolemia,
■ Hypovolemia increased ICP)
■ Hypoxia or ventilation ■ Tension pneumothorax
problems ■ Tamponade, cardiac
■ Hypoglycemia ■ Toxins
■ Hypothermia ■ Thrombosis (pulmonary or
■ Hydrogen ion (acidosis) coronary
5. Obtain a chest radiograph to confirm ET tube placement, assess
pulmonary status, and evaluate heart size.
6. Obtain a 12-lead ECG as soon as possible.
7. For patients who are comatose in the first several days after cardiac
arrest, temperature should be monitored continuously and fever
should be treated aggressively.
8. If the patient remains comatose, maintain Targeted Temperature
Management (TTM) for either 5 days of normalthermia (36°C–37.5°C)
or 2 days of continuous hypothermia (32°C–34°C) followed by 3 days
of normothermia.
9. Monitor the patient for pain, agitation, and seizures; initiate
appropriate treatment if present.
10. Monitor the patient for hypoglycemia and initiate appropriate
treatment if present.
11. Advanced critical care with development of a comprehensive plan of
care should be provided to all survivors of cardiac arrest to optimize
neurological, cardiopulmonary, and metabolic function.

174
 ECG Test Strip 1
Note: All ECG strips in Tab 9 were recorded in lead II.
175

ECG Test Strip 2

STRIPS
TEST
 ECG Test Strip 3

176
ECG Strip 1 ECG Strip 2 ECG Strip 3
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 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 defib-
rillator 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

177

STRIPS
TEST
 ECG Test Strip 5

178
ECG Test Strip 6
STRIPS
TEST
 ECG Test Strip 7
179

ECG Test Strip 8

STRIPS
TEST
 ECG Test Strip 9

180
ECG Strip 7 ECG Strip 8 ECG Strip 9
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 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

181

STRIPS
TEST
 ECG Test Strip 11

182
ECG Test Strip 12
STRIPS
TEST
 ECG Test Strip 13
183

ECG Test Strip 14

STRIPS
TEST
 ECG Test Strip 15

184
ECG Strip 13 ECG Strip 14 ECG Strip 15
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 16

185

ECG Test Strip 17

STRIPS
TEST
 ECG Test Strip 18

186
ECG Strip 16 ECG Strip 17 ECG Strip 18
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 19

187

ECG Test Strip 20

STRIPS
TEST
 ECG Test Strip 21

188
ECG Strip 19 ECG Strip 20 ECG Strip 21
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 Case Study Three: A 44-year-old man complains of severe chest pain. He has diaphoresis, BP of 80/60
mm Hg, and 24 respirations/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

189

STRIPS
TEST
 ECG Test Strip 23

190
ECG Test Strip 24
STRIPS
TEST
 ECG Test Strip 25

191

ECG Test Strip 26

STRIPS
TEST
 ECG Test Strip 27

192
ECG Strip 25 ECG Strip 26 ECG Strip 27
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 28

193

ECG Test Strip 29

STRIPS
TEST
 ECG Test Strip 30

194
ECG Strip 28 ECG Strip 29 ECG Strip 30
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 31

195

ECG Test Strip 32

STRIPS
TEST
 ECG Test Strip 33

196
ECG Strip 31 ECG Strip 32 ECG Strip 33
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 34

197

ECG Test Strip 35

STRIPS
TEST
 ECG Test Strip 36

198
ECG Strip 34 ECG Strip 35 ECG Strip 36
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 37

199

ECG Test Strip 38

STRIPS
TEST
 ECG Test Strip 39

200
ECG Strip 37 Interpretation:
ECG Strip 38 Interpretation:
ECG Strip 39 Interpretation:
STRIPS
TEST
 ECG Test Strip 40

201

ECG Test Strip 41

STRIPS
TEST
 ECG Test Strip 42

202
ECG Strip 40 ECG Strip 41 ECG Strip 42
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 43

203

ECG Test Strip 44

STRIPS
TEST
 ECG Test Strip 45

204
ECG Strip 43 ECG Strip 44 ECG Strip 45
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 46

205

ECG Test Strip 47

STRIPS
TEST
 ECG Test Strip 48

206
ECG Strip 46 ECG Strip 47 ECG Strip 48
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 ECG Test Strip 49

207

ECG Test Strip 50

STRIPS
TEST
 ECG Test Strip 51

208
ECG Strip 49 ECG Strip 50 ECG Strip 51
Rate: Rate: Rate:
Rhythm: Rhythm: Rhythm:
P Waves: P Waves: P Waves:
PR Interval: PR Interval: PR Interval:
QRS: QRS: QRS:
Interpretation: Interpretation: Interpretation:
STRIPS
TEST
 Answers to ECG Test Strips

ECG Strip 1 ECG Strip 2 ECG Strip 3

Rate: 35 bpm Rate: 34 bpm Rate: Ventricular 150 bpm, atrial 280 bpm
Rhythm: Regular Rhythm: Regular Rhythm: Regular
P Waves: Normal P Waves: None P Waves: Flutter waves
PR Interval: 0.16 sec PR Interval: None PR Interval: Variable
QRS: 0.10 sec QRS: 0.20 sec QRS: 0.08 sec
Interpretation: Sinus Interpretation: Idioventricular Interpretation: Atrial flutter with 2:1
bradycardia rhythm conduction
209

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

ECG Strip 7 ECG Strip 8 ECG Strip 9

Rate: 115 bpm Rate: None Rate: 115 bpm
Rhythm: Regular Rhythm: None Rhythm: Regular
P Waves: Normal P Waves: None P Waves: None
PR Interval: 0.12 sec PR Interval: None PR Interval: None
QRS: 0.10 sec QRS: None QRS: Wide (<0.12 sec), bizarre

STRIPS
TEST
Interpretation: Sinus Interpretation: Asystole Interpretation: Ventricular
tachycardia tachycardia––monomorphic
 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

ECG Strip 13 ECG Strip 14 ECG Strip 15

Rate: 41 bpm Rate: Basic rate 79 bpm Rate: 58 bpm
Rhythm: Regular Rhythm: Irregular Rhythm: Regular
P Waves: Normal P Waves: Normal P Waves: Normal
PR Interval: 0.20 sec PR Interval: 0.16 sec PR Interval: 0.32 sec
QRS: 0.24 sec QRS: 0.08 sec QRS: 0.08 sec

210
Interpretation: Sinus bradycardia Interpretation: Sinus rhythm Interpretation: Sinus bradycardia
with a bundle branch block with sinus pause/arrest with first-degree AV block

ECG Strip 16 ECG Strip 17 ECG Strip 18

Rate: Atrial <350 bpm, Rate: Atrial 60 bpm Rate: Basic rate 68 bpm
ventricular 88–115 bpm
Rhythm: Irregular Rhythm: Atrial regular Rhythm: Irregular
P Waves: None P Waves: Normal P Waves: Normal
PR Interval: None PR Interval: None PR Interval: 0.16 sec
QRS: 0.12 sec QRS: None QRS: 0.08 sec
Interpretation: Atrial fibrillation Interpretation: P Wave Interpretation: Sinus rhythm
STRIPS

asystole with premature ventricular

TEST

contractions—triplets
 ECG Strip 19 ECG Strip 20 ECG Strip 21
Rate: 65 bpm Rate: 214 bpm Rate: Basic rate 35 bpm
Rhythm: Regular Rhythm: Regular Rhythm: Regular
P Waves: Normal P Waves: None P Waves: Normal
PR Interval: 0.20 sec PR Interval: None PR Interval: 0.16 sec
QRS: 0.08 sec QRS: Wide (<0.12 sec), bizarre QRS: 0.08 sec
Interpretation: Normal sinus Interpretation: VT— Interpretation: Sinus bradycardia
rhythm with U wave monomorphic with ventricular bigeminy

ECG Strip 22 Interpretation: VT—monomorphic

ECG Strip 23 Interpretation: VT—monomorphic with cardioversion converting to same rhythm
211

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

65 bpm

ECG Strip 25 ECG Strip 26 ECG Strip 27

Rate: Pacing spikes 68 bpm Rate: Atrial 125 bpm, Rate: 200–250 bpm
ventricular 44 bpm
Rhythm: Regular pacing spikes Rhythm: Regular Rhythm: Irregular
P Waves: None P Waves: Normal P Waves: None
PR Interval: None PR Interval: 0.16 sec PR Interval: None
QRS: None QRS: 0.10 sec QRS: Wide (<0.12 sec), bizarre
Interpretation: Pacemaker— Interpretation: Second- Interpretation: VT—torsade

STRIPS
TEST
100% failure to capture, degree AV block type II de pointes
underlying rhythm asystole with 3:1 conduction
 ECG Strip 28 ECG Strip 29 ECG Strip 30
Rate: 50–75 bpm Rate: None Rate: Basic rate 68 bpm
Rhythm: Irregular Rhythm: None Rhythm: Irregular
P Waves: Normal P Waves: None P Waves: Normal
PR Interval: 0.12–0.28 sec PR Interval: None PR Interval: 0.16 sec
QRS: 0.08 sec QRS: None QRS: 0.10 sec
Interpretation: Second-degree Interpretation: Loose Interpretation: Sinus rhythm with
AV block type I electrodes multiform PVCs—couplets

ECG Strip 31 ECG Strip 32 ECG Strip 33

Rate: 68 bpm Rate: Atrial 75 bpm, Rate: Indeterminate

212
ventricular 48 bpm
Rhythm: Regular Rhythm: Regular Rhythm: Irregular
P Waves: Upright with pacing P Waves: Normal, P Waves: None
spikes superimposed on QRS
and T waves
PR Interval: 0.16 sec PR Interval: Varies PR Interval: None
QRS: 0.10 sec QRS: 0.16 sec QRS: None
Interpretation: Atrial pacemaker Interpretation: Third-degree Interpretation: VF
with 100% capture AV block
STRIPS
TEST
 ECG Strip 34 ECG Strip 35 ECG Strip 36
Rate: 48 bpm Rate: 250 bpm Rate: Atrial ≥350 bpm, ventricular
94–167 bpm
Rhythm: Regular Rhythm: Irregular Rhythm: Irregular
P Waves: Inverted P Waves: None P Waves: None
PR Interval: 0.12 sec PR Interval: None PR Interval: None
QRS: 0.08 sec QRS: Wide (<0.12 sec), bizarre QRS: 0.10 sec
Interpretation: Junctional Interpretation: VT—polymorphic Interpretation: A-fib
rhythm

ECG Strip 37 Interpretation: Agonal rhythm at 22 bpm

ECG Strip 38 Interpretation: Pacemaker failure to capture. When the pacemaker voltage is increased,
213

there is capture at pacemaker spike 4.

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

ECG Strip 40 ECG Strip 41 ECG Strip 42

Rate: 75 bpm Rate: Basic rate 79 bpm Rate: Basic rate 68 bpm
Rhythm: Regular Rhythm: Irregular Rhythm: Irregular
P Waves: Normal P Waves: Normal P Waves: Normal; none associated
with premature junctional contraction
PR Interval: 0.16 sec PR Interval: 0.20 sec PR Interval: 0.16 sec
QRS: 0.08 sec QRS: 0.10 sec QRS: 0.10 sec

STRIPS
Interpretation: Normal Interpretation: Sinus rhythm Interpretation: Sinus rhythm with

TEST
sinus rhythm with ventricular trigeminy PJCs at beats 4 and 6
 ECG Strip 43 ECG Strip 44 ECG Strip 45
Rate: 75 bpm Rate: 75 bpm Rate: 68 bpm
Rhythm: Regular Rhythm: Regular Rhythm: Irregular
P Waves: Upright with pacing spike P Waves: Not visible P Waves: Normal
PR Interval: 0.20 sec PR Interval: Not measurable PR Interval: 0.16 sec
QRS: 0.16 sec QRS: Not measurable QRS: 0.10 sec
Interpretation: Atrial-ventricular Interpretation: Sinus rhythm Interpretation: Sinus rhythm
pacemaker with muscle artifact with two premature atrial
contractions (beats 2 and 7)

ECG Strip 46 ECG Strip 47 ECG Strip 48

214
Rate: 88 bpm Rate: 250 bpm Rate: 136 bpm
Rhythm: Regular Rhythm: Regular Rhythm: Regular
P Waves: Normal P Waves: Buried in T waves P Waves: Not visible
PR Interval: 0.12 sec PR Interval: Not measurable PR Interval: Not measurable
QRS: 0.12 sec QRS: 0.08 sec QRS: 0.10 sec
Interpretation: Sinus rhythm with Interpretation: SVT Interpretation: Sinus
ST segment elevation tachycardia with muscle
artifact
STRIPS
TEST
 ECG Strip 49 ECG Strip 50 ECG Strip 51
Rate: 71 bpm Rate: Basic rate 79 bpm Rate: 107 bpm
Rhythm: Regular Rhythm: Irregular Rhythm: Regular
P Waves: Normal P Waves: Normal P Waves: Notched (P prime)
PR Interval: 0.16 sec PR Interval: 0.16 sec PR Interval: 0.20 sec
QRS: 0.10 sec QRS: 0.10 sec QRS: 0.12 sec
Interpretation: Sinus rhythm Interpretation: Sinus rhythm Interpretation: Sinus tachycardia
with ST segment depression with two SA blocks with P prime wave
215

STRIPS
TEST
 TEST
STRIPS

Notes:
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216
 217
Troubleshooting ECG Problems
Without proper assessment and treatment, a patient with an abnormal
ECG could have a potentially fatal outcome. An accurate and properly
monitored ECG is extremely important, so remember the following trou-
bleshooting tips:
■ 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.
The most accurate tracings are obtained through the smallest 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 the 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 whether you are using an American or a
European cable for ECG monitoring. The colors of the wires differ,
as shown below.

Monitoring Cable Connections

U.S. Connect to Europe

White Right arm Red
Black Left arm Yellow
Red Left leg Green
Green Right leg Black
Brown Chest White

TOOLS
 TOOLS

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.

Patient ECG Record

Patient Name: ____________________________________________

Sex: Female Male

Heart Rate: _______ bpm

■ Normal (60–100 bpm): Y N
■ Bradycardia (<60 bpm): Y N
■ Tachycardia (>100 bpm): Y N
Rhythm
■ Regular: Y N
■ Irregular: Y N
■ P waves: Y N
P waves
■ Normal (upright and uniform): Y N
■ Inverted: Y N
■ P wave associated with QRS complex: Y N
■ PR interval normal (0.12–0.20 sec): Y N
■ P waves and QRS complexes associated with one another: Y N
QRS complex
■ Normal (0.06–0.10 sec): Y N
■ Wide (>0.10 sec): Y N

218
 219
Are the QRS complexes grouped or not grouped?
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Are there any dropped beats?
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Is there a compensatory or noncompensatory pause?
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QT interval: __________________________________________________________
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Interpretation: _______________________________________________________
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TOOLS
TOOLS

Heart Sounds

QRS QRS

P T P T

S1 S2 S1 S2

Aortic
valve
Pulmonic
valve

S1 Mitral
S2
valve
S2

S1

Tricuspid
valve

220
 150 100 75 60 50 40 25 20 16
125 80 65 55 45 35 30 27 23 21 19 18 17
HEART RATE 1 Cycle from reference arrow (25 mm/s)
221

TOOLS
HEART RATE 2 Cycles from reference arrow (25 mm/s)
300 75
30 35 40 45 50 400 200 150 125 100 90 80 70 65 60 55
 400 200 150 125 100 90 80 75 70 65 60 55 50 45
300
HEART RATE 3 Cycles from reference arrow (25 mm/s)

222
TOOLS 4 3 2 1 Inches
 223
Abbreviations
ACE . . . . . .angiotensin-converting enzyme
ACLS . . . . .advanced cardiac life support
ACS . . . . . .acute coronary syndrome
AED . . . . . .automatic external defibrillator
A-fib . . . . . .atrial fibrillation
A-flutter . . .atrial flutter
AV . . . . . . . .atrioventricular
BBB . . . . . .bundle branch block
BP . . . . . . . .blood pressure
bpm . . . . . .beats per minute
BUN . . . . . .blood urea nitrogen
CHF . . . . . . .congestive heart failure
CO . . . . . . .cardiac output
COPD . . . . .chronic obstructive pulmonary disease
CPR . . . . . . .cardiopulmonary resuscitation
CT . . . . . . . .computed tomography
ECG . . . . . .electrocardiogram
EMD . . . . . .electromechanical dissociation
ET . . . . . . . .endotracheal
FAB . . . . . . .fragment antigen binding
gtt . . . . . . . .drops
HR . . . . . . . .heart rate
HTN . . . . . .hypertension
IHSS . . . . . .idiopathic hypertrophic subaortic stenosis
IM . . . . . . . .intramuscular
IO . . . . . . . .intraosseous
IV . . . . . . . .intravenous
LA . . . . . . . .left arm
LL . . . . . . . .left leg
LMA . . . . . .laryngeal mask airway
LOC . . . . . .level of consciousness
MAT . . . . . .multifocal atrial tachycardia
MCL . . . . . .modified chest lead
MI . . . . . . . .myocardial infarction
NSR . . . . . .normal sinus rhythm
PAC . . . . . . .premature atrial contraction
PALS . . . . . .pediatric advanced life support
PAT . . . . . . .paroxysmal atrial tachycardia

TOOLS
 TOOLS

PEA . . . . . . .pulseless electrical activity

PJC . . . . . . .premature junctional contraction
PO . . . . . . . .by mouth
PSVT . . . . .paroxysmal supraventricular tachycardia
PVC . . . . . . .premature ventricular contraction
QTc . . . . . . .QT interval corrected for heart rate
RA . . . . . . . .right arm
RL . . . . . . . .right leg
SA . . . . . . . .sinoatrial
SV . . . . . . . .stroke volume
SVT . . . . . . .supraventricular tachycardia
TKO . . . . . .to keep open
VF . . . . . . . .ventricular fibrillation
VT . . . . . . . .ventricular tachycardia
WAP . . . . . .wandering atrial pacemaker
WPW . . . . .Wolff-Parkinson-White (syndrome)
Selected References
1. American Heart Association: Basic Life Support for Healthcare Providers
(Student Manual). American Heart Association, Dallas, TX, 2015.
2. American Heart Association: Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Supplement to
Circulation 132 (18), November 3, 2015.
3. Deglin, JH, Vallerand, AH: Davis’s Drug Guide for Nurses, ed 13.
F. A. Davis, Philadelphia, 2013.
4. Jones, SA: Author’s personal collection.
5. Jones, SA: ECG Notes, ed 1. F. A. Davis, Philadelphia, 2005.
6. Jones, SA: ECG Success. F. A. Davis, Philadelphia, 2008.
7. Myers, E: RNotes, ed 3. F. A. Davis, Philadelphia, 2010.
8. Hopkins, T: MedSurg Notes, ed 3. F. A. Davis, Philadelphia, 2011.
9. Scanlon, VC, Sanders, T: Essentials of Anatomy and Physiology, ed 6.
F. A. Davis, Philadelphia, 2011.

224
 225
Illustration Credits
ECG strips on pages 28, 32–70, 73–78, 152–185 from Jones, SA: Author’s
personal collection.
Pages 10, 12, 13 from Jones, SA: ECG Success. F. A. Davis, Philadelphia,
2008.
Pages 14, 109, 123 from Myers, E: RNotes, ed 2. F. A. Davis, Philadelphia,
2006.
Pages 19, 81, 112, 127, 197 from Myers, E, Hopkins, T: MedSurg Notes.
F. A. Davis, Philadelphia, 2004.
Pages 11, 22 adapted from Myers, E, Hopkins, T: MedSurg Notes. F. A. Davis,
Philadelphia, 2004.
Pages 2, 3, 4, 5, 6, 7, 8 from Scanlon, VC, Sanders, T: Essentials of Anatomy
and Physiology, ed 4. F. A. Davis, Philadelphia, 2003.

TOOLS
 INDEX

Index
Abbreviations, 223–224 Arteries
Accelerated idioventricular coronary, 7
rhythm, 56 cross-section of, 8
Accelerated junctional rhythm, 51 major, 9
ACE inhibitors, 101 Artifacts
Acetylsalicylic acid. See Aspirin baseline varies with respiration, 83
ACLS (advanced cardiovascular life loose electrodes, 82
support) muscle, 84
acute coronary syndrome, 60-cycle interference, 83
149–150 Artificial cardiac pacemakers, 74
asystole, 148–149 codes, 75
bradycardia, 151–152 failure to capture, 80
pulseless electrical activity, failure to sense, 80
147–148 malfunctions, 79
tachycardia modes, 75
narrow-complex-stable regular oversensing, 81
rhythm, 154 rhythms, 76
pulseless ventricular, 145–146 Aspirin (acetylsalicylic acid, ASA),
unstable, 152–153 104–105
wide-complex-stable regular Asystole, 68
rhythm, 155 ACLS, 148–149
ventricular fibrillation, 145–146 PALS, 165–167
Acute coronary syndrome (ACS), Atrial arrhythmias, 41–49
ACLS, 149–150 Atrial fibrillation (A-fib), 48
Adenosine (Adenocard), 101–102 Atrial flutter (A-flutter), 47
Adenosine diphosphate (ADP) Atrial tachycardia, 44
antagonists, 102–103 Atrioventricular (AV) blocks, 69–73
Airway obstruction. See Obstructed Atropine sulfate, 105
airway Automated external defibrillation
Albuterol (ProAir, Proventil, (AED), 124–126
Ventolin), 103 AV blocks. See Atrioventricular
Amiodarone (Cordarone, Pacerone), blocks
104
Arixtra. See Fondaparinux Beta blockers, 105–106
Arrhythmias Bradycardia, 36
classification of, 34 ACLS, 151–152
See also specific types PALS, 168

226
 227
Bundle branch block (BBB), 73 Depolarization
left, 99 process of, 15
right, 100 progression through heart, 16
and repolarization, correlation
Calan. See Verapamil with ECG, 17
Cardiac arrest. See Post-cardiac Digoxin immune fab (fragment
arrest, immediate care antigen binding, DigiFab), 107
Cardiovascular system, anatomy of, Digoxin (Lanoxin), 106–107
8–10 Diltiazem (Cardizem), 107–108
Cardioversion (synchronized), Dobutamine, 108
126–127 Dopamine (Intropin), 108–109
Cardizem. See Diltiazem Dual-chamber pacemaker, 74
Carotid sinus massage (vagal atrial/ventricular rhythms, 78
maneuver), 128–129
Chest leads, 22 Electrical axis deviation, 88
electrode placement with 3-/5-wire Electrocardiogram (ECG), 18
cable, 23 cable connections, 217–218
elements of, 22 electrical activity/components, 28
15-lead ECG, 26 15-lead, 26
location of myocardial infarction heart sounds and, 220
by, 89 patient record, 218–219
modified, 24 recording of, 27
right-sided 12-lead ECG, 25 test strips, 175–208
12-lead ECG, 86 interpretations, 209–215
Cincinnati prehospital stroke tracing components, 27
scale, 160 troubleshooting, 217
Cordarone. See Amiodarone 12-lead, 86
Corvert. See Ibutilide normal tracing, 93
CPR right-sided, 25
age of puberty or older, 131–132 Epinephrine (adrenalin), 109–110
guidelines for, 130
and obstructed airway, Fibrinolytic agents, 110
positions, 144 15-lead ECG, 26
under one year, 134–135 First-degree AV block, 69
one year to age of puberty, Fondaparinux (Arixtra), 110–111
132–133 Furosemide (Lasix), 111

Defibrillation, 123 Glasgow coma scale, 160

automated external, 124–126 Glycoprotein IIB/IIIA inhibitors,
manual, 124 111–112

INDEX
 INDEX

Heart Limb leads

anatomy of, 1 augmented, 21
anterior section, 5 electrode placement, 19
anterior surface, 3 elements of, 20
arteries/veins, 7
posterior surface, 4 Magnesium sulfate, 115
valves, 6 Medication(s)
wall, 2 common formulas, 121
electrical conduction system of, emergency, 101–120
13–17 IV fluid drip rates, 121
physiology of, 10–12 universal formula for drip
systolic/diastolic phases, 12 rates/drug amounts, 122
Heart rates Morphine sulfate, 115–116
methods for calculating, 29–30, Multifocal atrial tachycardia
32, 221–222 (MAT), 42
normal values, 34 Myocardial infarction
Heart sounds, 220 anterior, 94
Heparin (unfractionated heparin, inferior, 95
UFH), 112–113 lateral, 96
location of, by ECG leads, 89
Ibutilide (Corvert), 113 posterior, 98
Idioventricular rhythm, 55 progression of, 90
Infarction, 89, 90 septal, 97
Intropin. See Dopamine
Ischemia, 89, 90 Naloxone (Narcan), 116
Isoproterenol (Isuprel), 113–114 Nitroglycerin (Nitrostat,
Isoptin. See Verapamil Nitrolingual), 116–117
Isuprel. See Isoproterenol Norepinephrine (Levophed), 117–118
Normal sinus rhythm (NSR), 35
Junctional arrhythmias, 50–54
Junctional escape beat, 53 Obstructed airway
Junctional rhythm, 50 conscious adult/child over one
Junctional tachycardia, 52 year, 135–136
conscious infant, 136–137
Lanoxin. See Digoxin positions, 144
Lasix. See Furosemide unconscious adult, 137–138
Levophed. See Norepinephrine unconscious child, 139–140
Lidocaine (Xylocaine), 114 unconscious infant, 140–141

228
 229
Opioid-associated life-threatening same form, 58
emergency, 142–143 ventricular bigeminy (PVC every
Oxygen, 118 2nd beat), 59
ventricular quadrigeminy (PVC
Pacemakers. See Artificial cardiac every 4th beat), 60
pacemakers ventricular trigeminy (PVC every
Pacerone. See Amiodarone 3rd beat), 59
PALS (pediatric advanced life support) Premature ventricular contraction
asystole, 165–167 (R-on-T phenomenon), 61
bradycardia, 168 ProAir. See Albuterol
immediate post-cardiac arrest Procainamide (Pronestyl), 118–119
care, 173–174 Pronestyl. See Procainamide
pulseless electrical activity, Proventil. See Albuterol
164–165 Pulseless electrical activity (PEA), 67
tachycardia ACLS, 147–148
narrow-complex with adequate PALS, 164–165
perfusion, 169
narrow-complex with poor R wave progression, 87
perfusion, 171–172 Rhythm(s)
wide-complex with adequate analysis of, 33–34
perfusion, 170 artificial pacemaker, 76
wide-complex with poor
perfusion, 173 Second-degree AV block
ventricular fibrillation/pulseless type I (Mobitz I, Wenckebach), 70
ventricular tachycardia, 161–163 type II (Mobitz II), 71
Paroxysmal supraventricular Single-chamber pacemaker rhythm,
tachycardia (PSVT), 46 atrial/ventricular rhythms, 77
Permanent pacemaker, 74 Sinoatrial (SA) block, 40
Pitressin. See Vasopressin Sinoatrial (SA) node arrhythmias,
Post-cardiac arrest, immediate care, 35–40
156–157 Sinus arrhythmia, 38
PALS, 173–174 Sinus bradycardia, 36
Premature atrial contraction Sinus pause (sinus arrest), 39
(PAC), 43 Sinus tachycardia, 37
Premature junctional contraction Sodium bicarbonate, 119
(PJC), 54 ST segment elevation/depression, 91
Premature ventricular contraction Stroke, 157–159
(PVC), 57 Cincinnati prehospital stroke
couplets (paired PVCs), 60 scale, 160
different forms, 58 general care, 159
interpolated, 62 Supraventricular tachycardia (SVT), 45

INDEX
 INDEX

Tachycardia Vasopressin (Pitressin), 120

narrow-complex-stable regular Veins
rhythm, ACLS, 154 coronary, 7
narrow-complex with adequate cross-section of, 8
perfusion, PALS, 169 major, 10
narrow-complex with poor Ventolin. See Albuterol
perfusion, PALS, 171–172 Ventricular arrhythmias, 55–68
unstable, ACLS, 152–153 Ventricular fibrillation (VF), 66
wide-complex-stable regular ACLS, 145–146
rhythm, ACLS, 155 Ventricular tachycardia (VT)
wide-complex with adequate monomorphic, 63
perfusion, PALS, 170 polymorphic, 64
wide-complex with poor pulseless
perfusion, PALS, 173 ACLS, 145–146
See also specific types PALS, 161–163
Temporary pacemaker, 74 Verapamil (Calan, Isoptin), 120
Third-degree AV block, 72
Torsade de pointes, 65 Wandering atrial pacemaker
Transcutaneous pacing, 127–128 (WAP), 41
12-lead ECG, 86 Wolff-Parkinson-White (WPW)
normal tracing, 93 syndrome, 49
right-sided, 25
Xylocaine. See Lidocaine
Vagal maneuver (carotid sinus
massage), 128–129

230