Main ECG Facts Made Incredibly Quick! (Incredibly Easy! Series) 2nd edition

ECG Facts Made Incredibly Quick! (Incredibly Easy! Series) 2nd edition

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Updated with new treatments and algorithms, ECG Facts Made Incredibly Quick! Second Edition provides instant access to information that every nurse needs for safe patient care. The book fits comfortably into a pocket, and the wipeable page surface allows nurses to write notes and remove them easily. Coverage includes basic electrocardiography including cardiac conduction, lead placement, and heart rate calculation; rhythm strip interpretation; causes, signs and symptoms, interventions, and treatment for arrhythmias; 12-lead and 15-lead ECG interpretation; ECG changes with angina, MI, pericarditis, and bundle branch block; and antiarrhythmic drugs, pacemakers, and ICDs. Scores of ECG waveforms, treatment algorithms, and charts are included. Distinctive-colored tabs identify each section.
Year:
2010
Edition:
Second
Publisher:
Lippincott Williams & Wilkins
Language:
english
Pages:
129
ISBN 10:
1605474762
ISBN 13:
9781605474762
File:
PDF, 1.30 MB

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Staff
Executive Publisher
Judith A. Schilling McCann, RN, MSN
Clinical Director
Joan M. Robinson, RN, MSN
Art Director
Elaine Kasmer
Editors
Margaret Eckman, Diane Labus
Illustrator
Bot Roda
Design Assistant
Kate Zulak
Associate Manufacturing Manager
Beth J. Welsh
Editorial Assistants
Karen J. Kirk, Jeri O’Shea,
Linda K. Ruhf

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The clinical treatments described and recommended in this publication are based on
research and consultation with nursing, medical, and legal authorities. To the best of our
knowledge, these procedures reflect currently
accepted practice. Nevertheless, they can’t be
considered absolute and universal recommendations. For individual applications, all recommendations must be considered in light of the
patient’s clinical condition and, before administration of new or infrequently used drugs, in
light of the latest package-insert information.
The authors and publisher disclaim any
responsibility for any adverse effects resulting
from the suggested procedures, from any
undetected errors, or from the reader’s
misunderstanding of the text.
© 2010 by Lippincott Williams & Wilkins. All
rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in
a retrieval system, or transmitted, in any form
or by any means—electronic, mechanical,
photocopy, recording, or otherwise—without
prior written permission of the publisher, except
for brief quotations embodied in critical articles
and reviews and testing and evaluation materials provided by publisher to instructors whose
schools have adopted its accompanying textbook. For information, write Lippincott Williams
& Wilkins, 323 Norristown Road, Suite 200,
Ambler, PA 19002-2756.
Printed in China.
ECGMIQ2-010909
ISBN-13: 978-1-60547-476-2
ISBN-10: 1-60547-476-2

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Best monitoring leads
Most bedside monitoring systems allow for simultaneous
monitoring of two leads, such as lea; d II with V1 or MCL1.
Lead II or the lead that clearly shows the P waves and
QRS complex may be used for sinus node arrhythmias,
PACs, and AV block. The precordial leads V1 and V6 or the
bipolar leads MCL1 and MCL6 are the best leads for monitoring rhythms with wide QRS complexes and for differentiating VT from SVT with aberrancy.
This table lists the best leads for monitoring challenging
cardiac arrhythmias.
Arrhythmia

Best monitoring leads

PACs
AT
PAT
Atrial flutter
Atrial fibrillation

II or lead that shows best P waves
II, V1, V6, MCL1, MCL6
II, V1, V6, MCL1, MCL6
II, III
II (or identified in most leads by
fibrillatory waves and irregular R-R)
II
II
II, V1, V6, MCL1, MCL6
V1, V6, MCL1, MCL6
V1, V6, MCL1, MCL6
V1, V6, MCL1, MCL6
Any
Any
II or lead that shows best P waves
and QRS complexes

PJCs
Junctional escape rhythm
Junctional tachycardia
PVCs
Idioventricular rhythm
VT
VF
Torsades de pointes
Third-degree AV block

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Heart anatomy, coronary vessels, cardiac conduction, ECG grid, Einthoven’s triangle, leads, normal ECG, QTc interval,
interpreting rhythm strips, measuring rhythm, rhythm strip patterns, calculating HR
Sinus rhythm, sinus arrhythmia, SB, ST, sinus arrest, SA exit block, SSS
PACs, AT, MAT, PAT, atrial flutter, atrial fibrillation, Ashman’s phenomenon,
wandering pacemaker
PJCs, junctional rhythm, accelerated junctional rhythm,
junctional tachycardia
PVCs, idioventricular rhythm, accelerated idioventricular
rhythm, VT, torsades de pointes, VF, asystole, PEA
First-degree AV block, second-degree AV
block, third-degree AV block
Lead placement, electrical
axis, angina, pericarditis,
MI, LVH, WPW, RBBB, LBBB

G
S
A
J
V
A
1
T

e n e r a l
A N o d e
t r i a l
u n c t i o n a l
e n t r i c u l a r
V B l o c k
2 - L e a d
r e a t m e n t

Algorithms,
drugs,
defibrillation,
pacemaker,
ICD

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Common abbreviations
ACLS. . . . advanced cardiac life support
ACS. . . . . acute coronary syndromes
AED. . . . . automated external
defibrillator
AT . . . . . . atrial tachycardia
AV . . . . . . atrioventricular
BBB . . . . bundle-branch block
BCLS. . . . basic cardiac life support
BP . . . . . . blood pressure
CAD. . . . . coronary artery disease
CI. . . . . . . cardiac index
CO . . . . . . cardiac output
CO2 . . . . . carbon dioxide
COPD . . . chronic obstructive
pulmonary disease
CPR . . . . . cardiopulmonary
resuscitation
CV . . . . . . cardiovascular
DTR . . . . . deep tendon reflex
ECG . . . . . electrocardiogram
EF . . . . . . ejection fraction
EMS . . . . emergency medical service
ET . . . . . . endotracheal
FIO2 . . . . . fraction of inspired oxygen
GI. . . . . . . gastrointestinal
GU . . . . . . genitourinary
HR . . . . . . heart rate
IABP . . . . intra-aortic balloon pump
ICD . . . . . implantable cardioverterdefibrillator
ICP . . . . . intracranial pressure
ICS . . . . . intercostal space
ICU . . . . . intensive care unit
JVD . . . . . jugular vein distention
LBBB . . . left bundle-branch block
LVH . . . . . left ventricular hypertrophy
MAP . . . . mean arterial pressure
MAT . . . . multifocal atrial tachycardia
MCL . . . . modified chest lead

MI . . . . . . myocardial infarction
O2 . . . . . . oxygen
PA . . . . . . pulmonary artery
PAC . . . . . premature atrial contraction
PAD. . . . . pulmonary artery diastolic
PAM . . . . pulmonary artery mean
PAP . . . . . pulmonary artery pressure
PAS . . . . . pulmonary artery systolic
PAT . . . . . paroxysmal atrial
tachycardia
PAWP . . . pulmonary artery wedge
pressure
PEA . . . . . pulseless electrical activity
PJC . . . . . premature junctional
contraction
PMI . . . . . point of maximal impulse
PSVT. . . . paroxysmal supraventricular
tachycardia
PVC . . . . . premature ventricular
contraction
RAP. . . . . right arterial pressure
RBBB . . . right bundle-branch block
SA . . . . . . sinoatrial
SaO2 . . . . arterial blood oxygen
saturation
SB . . . . . . sinus bradycardia
SpO2 . . . . pulse oximetry blood oxygen
saturation
SSS . . . . . sick sinus syndrome
ST . . . . . . sinus tachycardia
SV . . . . . . stroke volume
SVO2 . . . . mixed venous oxygen
saturation
SVT . . . . . supraventricular tachycardia
VF . . . . . . ventricular fibrillation
VT . . . . . . ventricular tachycardia
WPW . . . Wolff-Parkinson-White
(syndrome)

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1

Where the heart lies
This illustration shows exactly where the heart is located. The
heart lies within the mediastinum, a cavity that contains the
tissues and organs separating the two pleural sacs. In most
people, two-thirds of the heart extends to the left of the body’s
midline.

Base

Second
intercostal
space

Fifth
intercostal
space
Apex
Midline

General

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General

Coronary vessels
Anterior view
Left common
carotid artery
Brachiocephalic
artery

Left
subclavian
artery
Aortic arch

Superior vena
cava

Pulmonary
trunk

Right atrium
Right
coronary
artery

Great cardiac
vein

Small
cardiac
vein

Circumflex
branch of left
coronary
artery

Anterior
interventricular
(descending)
branch of left
main coronary
artery

2

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3

Coronary vessels

(continued)

Posterior view
Left common carotid artery
Left subclavian artery
Pulmonary
artery
Left
pulmonary
veins
Left atrium
Great
cardiac
vein
Circumflex
branch of
left
coronary
artery
Posterior
vein of
left
ventricle
Middle
cardiac vein

General

Brachiocephalic
artery
Aortic arch
Superior vena
cava
Right pulmonary
veins
Right atrium
Inferior vena
cava
Small cardiac
vein
Right coronary
artery
Posterior
interventricular
(descending)
branch of right
coronary artery

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General

Cardiac conduction system

SA node
Interatrial septum
AV node
AV bundle
(bundle of His)
Right and left
bundle branches
Interventricular
septum

ECG grid
This ECG grid shows the horizontal axis and vertical axis and
their respective measurement values.

Amplitude
or voltage

0.5 mV
(5 mm)

1 mV

0.1 mV
(1 mm)
0.20
sec

3 sec
Time (in seconds)

4

0.04
sec

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5

Einthoven’s triangle
The axes of the three bipolar limb leads (I, II, and III) form a
shape known as Einthoven’s triangle. Because the electrodes for
these leads are about equidistant from the heart, the triangle is
equilateral.
The axis of lead I extends from shoulder to shoulder, with the
right-arm lead being the negative electrode and the left-arm
lead being the positive electrode. The axis of lead II runs from
the negative right-arm lead electrode to the positive left-leg lead
electrode. The axis of lead III extends from the negative left-arm
lead electrode to the positive left-leg lead electrode.

Right arm

⫺

Left arm

⫺

Lea
d II
I

d II
Lea

⫹ ⫹
Left leg

General

⫹
⫺

Lead I

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General

Augmented leads
Leads aVR, aVL, and aVF are called augmented leads. They
measure electrical activity between one limb and a single
electrode. Lead aVR provides no specific view of the heart.
Lead aVL shows electrical activity coming from the heart’s
lateral wall. Lead aVF shows electrical activity coming from
the heart’s inferior wall.

Right arm

Left arm

aVR

aVL

⫹

⫹
⫹
aVF
Left leg

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Positioning cardiac monitoring leads
Five-leadwire system
Lead I

Three-leadwire system

RA

LA

Lead I

RA

LA

C
RL

Lead II

LL

LL

RA

LA

Lead II

RA

LA

C
RL

Lead III

LL

LL

RA

LA

Lead III

RA

LA

C
RL

Lead
MCL1

LL

LL

RA

LA

Lead
MCL1

LA

RA

C
LL
RL

Lead
MCL6

RA

LL

LA
C

RL

General

LL

Lead
MCL6

RA

LA
LL

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General

Normal ECG

0.12–0.20 sec
0.06–0.10 sec
0.36–0.44 sec

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9

QTc interval normals
Heart rate
(per minute)

QTc interval
normal range
(seconds)

40
50
60
70
80
90
100
120
150
180
200

0.41 – 0.51
0.38 – 0.46
0.35 – 0.43
0.33 – 0.41
0.32 – 0.39
0.30 – 0.36
0.28 – 0.34
0.26 – 0.32
0.23 – 0.28
0.21 – 0.25
0.20 – 0.24

Interpreting rhythm strips
Interpreting a rhythm strip is a skill developed through practice.
You can use several methods, as long as you’re consistent.
Rhythm strip analysis requires a sequential and systematic approach. The eight-step method outlined below provides just that.

Eight-step method
1.
2.
3.
4.
5.
6.
7.
8.

Determine the rhythm.
Determine the rate.
Evaluate the P wave.
Measure the PR interval.
Determine the QRS duration.
Examine the T waves.
Measure the QT interval.
Check for ectopic beats and other abnormalities.

General

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General

Methods of measuring rhythm
Paper-and-pencil method

Calipers method

• Position the straight edge of
a piece of paper along the
strip’s baseline.
• Move the paper up slightly
so the straight edge is near
the peak of the R wave.
• With a pencil, mark the paper
at the R waves of two consecutive QRS complexes, as shown
below. This is the R-R interval.
• Move the paper across the
strip lining up the two marks
with succeeding R-R intervals.
If the distance for each R-R interval is the same, the ventricular rhythm is regular. If the
distance varies, the rhythm is
irregular.
• Use the same method to
measure the distance between
P waves (the P-P interval) and
determine whether the atrial
rhythm is regular or irregular.

• With the ECG on a flat surface, place one point of the
calipers on the peak of the
first R wave of two consecutive QRS complexes.
• Adjust the calipers’ legs so
the other point is on the peak
of the next R wave, as shown
below. The distance is the R-R
interval.
• Pivot the first point of the
calipers toward the third R
wave and note whether it falls
on the peak of that wave.
• Check succeeding R-R intervals in the same way. If they’re
all the same, the ventricular
rhythm is regular. If they vary,
the rhythm is irregular.
• Using the same method,
measure the P-P intervals to
determine whether the atrial
rhythm is regular or irregular.

10

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11

Rhythm strip patterns
The more you look at rhythm strips, the more you’ll notice patterns. The symbols below represent some of the patterns you
might see as you study rhythm strips.

Normal, regular (as in normal sinus rhythm)

Slow, regular (as in SB)

Fast, regular (as in ST)

Premature (as in a PVC)

Grouped (as in type I second-degree AV block)

Irregularly irregular (as in atrial fibrillation)

Paroxysm or burst (as in PAT)

General

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General

Calculating heart rate
This table can help
make the sequencing
method of determining heart rate more
precise. After counting
the number of blocks
between R waves, use
this table to find the
rate. For example, if
you count 20 small
blocks or 4 large blocks
between R waves, the
heart rate is 75 beats/
minute. To calculate
the atrial rate, follow
the same method
using P waves.

Rapid estimate
This rapid-rate calculation is also called
the countdown
method. Using the
number of large
blocks between
R waves or P waves
as a guide, you can
rapidly estimate ventricular or atrial rates
by memorizing the
sequence “300, 150,
100, 75, 60, 50.”

Number of small blocks Heart rate
5 (1 large block)
6
7
8
9
10 (2 large blocks)
11
12
13
14
15 (3 large blocks)
16
17
18
19
20 (4 large blocks)
21
22
23
24
25 (5 large blocks)
26
27
28
29
30 (6 large blocks)
31
32
33
34
35 (7 large blocks)
36
37
38
39
40 (8 large blocks)

12

300
250
214
188
167
150
136
125
115
107
100
94
88
83
79
75
71
68
65
63
60
58
56
54
52
50
48
47
45
44
43
42
41
39
38
37

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13

Bradycardia and tachycardia in children
In children, evaluate bradycardia and tachycardia in context.
For example, bradycardia (less than 90 beats/minute) may
occur in a healthy infant during sleep; tachycardia may be a
normal response when a child is crying or otherwise upset.
Keep in mind that, because HR varies considerably from the
neonate to the adolescent, one definition of bradycardia or
tachycardia can’t fit all children.

Normal heart rates in children

Age

Awake
(beats/min)

Asleep
(beats/min)

Exercise or
fever
(beats/min)

Neonate
1 wk-3 mo
3 mo-2 yr
2-10 yr
> 10 yr

100-160
100-220
80-150
70-110
55-100

80-140
80-200
70-120
60-90
50-90

< 220
< 220
< 200
< 200
< 200

General

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General

ECG effects of electrolyte imbalances
Imbalance

Key finding

Other possible findings

Hypercalcemia

Shortened
QT interval

• Prolonged PR interval
• Prolonged QRS complex
• Depressed T wave

Hypocalcemia

Prolonged
QT interval

• Flat or inverted T wave
• Prolonged ST segment

Hyperkalemia

Tall, peaked
T waves

• Low amplitude P wave (mild
hyperkalemia)
• Wide, flattened P wave (moderate
hyperkalemia)
• Indiscernible P wave (severe
hyperkalemia)
• Widened QRS complex
• Shortened QT interval
• Intraventricular conduction
disturbances
• Elevated ST segment (severe
hyperkalemia)

Hypokalemia

Flat T wave;
U wave appears

• Peaked P wave (severe
hypokalemia)
• Prolonged QRS complex (severe
hypokalemia)
• Depressed ST segment

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15

Normal sinus rhythm

Rhythm

QRS complex

• Atrial: regular
• Ventricular: regular

• Within normal limits (0.06 to
0.10 second)

Rate

T wave

• 60 to 100 beats/minute (SA
node’s normal firing rate)

• Normal shape
• Upright and rounded in lead II

P Wave

QT interval

• Normal shape (round and
smooth)
• Upright in lead II
• One for every QRS complex
• All similar in size and shape

• Within normal limits (0.36 to
0.44 second)

PR Interval
• Within normal limits (0.12 to
0.20 second)

SA Node

Other
• Represents normal cardiac
conduction as the standard
against which all other
rhythms are compared
• No ectopic or aberrant beats

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SA Node

Sinus arrhythmia

Expiration

Inspiration

Expiration

Rhythm

PR interval

• Irregular
• Corresponds to the respiratory
cycle
• P-P interval and R-R interval
shorter during inspiration;
longer during expiration
• Difference between longest
and shortest P-P interval
exceeds 0.12 second

• May vary slightly
• Within normal limits

QRS complex
• Preceded by P wave

T wave
• Normal size
• Normal configuration

QT interval

Rate

• May vary slightly
• Usually within normal limits

• Usually within normal limits
(60 to 100 beats/minute)
• Varies with respiration
• Increases during inspiration
• Decreases during expiration

Other
• Phasic slowing and quickening

P wave
• Normal size
• Normal configuration

16

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17

Sinus arrhythmia (continued)
• Possible disappearance of
What causes it
• Drugs
– Digoxin
– Morphine
• Increased ICP
• Inferior-wall MI
• Inhibition of reflex vagal
activity (tone)

During inspiration
• Decreased vagal tone
• Increased HR
• Increased venous return

During expiration
• Decreased HR
• Decreased venous return
• Increased vagal tone

What to look for
• Possibly no symptoms (commonly insignificant)
• Increased peripheral pulse
rate during inspiration
• Decreased peripheral pulse
rate during expiration

SA Node

arrhythmia when HR increases, such as during exercise
• Signs and symptoms of
underlying condition, if
present
• Dizziness or syncope (with
marked sinus arrhythmia)

What to do
• Monitor heart rhythm.
• If sinus arrhythmia develops
suddenly in patient taking
digoxin, notify doctor.
• If induced by drugs (morphine or another sedative),
notify doctor, who will decide
whether to continue giving the
drug.

How it’s treated
• Usually no treatment if
patient asymptomatic
• If unrelated to respiration
(abnormal), treatment of
underlying cause

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SA Node

Sinus bradycardia

Rhythm

QRS complex

• Regular

• Normal duration
• Normal configuration

Rate
• Less than 60 beats/minute

T wave

P wave

• Normal size
• Normal configuration

• Normal size
• Normal configuration
• P wave before each QRS
complex

QT interval
• Within normal limits
• Possibly prolonged

PR interval
• Within normal limits
• Constant

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Sinus bradycardia (continued)
If patient can’t compensate
What causes it
• Cardiomyopathy
• Conditions that increase
vagal stimulation such as
vomiting
• Drugs
– Antiarrhythmics (amiodarone, propafenone, quinidine, sotalol)
– Beta-adrenergic blockers
(metoprolol, propanolol)
– Calcium channel blockers
(diltiazem, verapamil)
– Digoxin
– Lithium
• Glaucoma
• Hyperkalemia
• Hypothermia
• Hypothyroidism
• Increased ICP
• Inferior-wall MI
• Myocardial ischemia
• Myocarditis
• SA node disease

What to look for
• Pulse rate less than 60 beats/
minute
• Regular rhythm
• Possibly bradycardia-induced
syncope (known as a StokesAdams attack)

If patient can compensate
for decreased CO
• No symptoms

SA Node

• Altered mental status
• Blurred vision
• Chest pain
• Cool, clammy skin
• Crackles
• Dizziness
• Dyspnea
• Hypotension
• S3 heart sound, indicating
heart failure
• Syncope

What to do
• Observe patient and monitor
heart rhythm for bradycardia
progression.
• Evaluate patient’s tolerance
for rhythm at rest and with
activity.
• Prepare patient for treatments, as needed, such as
drug administration (atropine,
dopamine, epinephrine) or
temporary or permanent
pacemaker insertion.

How it’s treated
• No treatment if patient
asymptomatic
• If symptomatic, correction
of underlying cause
• Bradycardia algorithm
guidelines

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SA Node

Sinus tachycardia

Rhythm

PR interval

• Regular

• Within normal limits
• Constant

Rate
• Greater than 100 beats/minute

QRS complex

P wave

• Normal duration
• Normal configuration

• Normal size
• Normal configuration
• May increase in amplitude
• Precedes each QRS complex
• As HR increases, possibly
superimposed on preceding
T wave and difficult to identify

T wave
• Normal size
• Normal configuration

QT interval
• Within normal limits
• Commonly shortened

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Sinus tachycardia (continued)
If CO falls and compensatory
What causes it
• Anemia
• Cardiogenic shock
• Drugs
– Aminophylline
– Amphetamines
– Atropine
– Dobutamine
– Dopamine
– Epinephrine
– Isoproterenol
• Heart failure
• Hemorrhage
• Hyperthyroidism
• Hypovolemia
• Pericarditis
• Pulmonary embolism
• Respiratory distress
• Sepsis
• Triggers (alcohol, caffeine,
nicotine)
• Possibly normal response to
exercise, fever, stress, anxiety,
or pain

What to look for
• Peripheral pulse rate above
100 beats/minute
• Regular rhythm

SA Node

mechanisms fail
• Anxiety
• Blurred vision
• Chest pain
• Hypotension
• Nervousness
• Palpitations
• Syncope

If heart failure develops
• Crackles
• S3 heart sound
• Jugular vein distention

What to do
• Monitor heart rhythm.
• Notify doctor promptly if
sinus tachycardia arises
suddenly after MI.
• Provide calm environment and
teach relaxation techniques.

How it’s treated
• No treatment if patient
asymptomatic
• Correction of underlying
cause
• For cardiac ischemia: Betaadrenergic blockers (propranolol, atenolol) or calcium
channel blockers (verapamil,
diltiazem)
• Abstinence from triggers
(alcohol, caffeine, nicotine)

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SA Node

Sinus arrest

Rhythm

QRS complex

• Regular except during arrest
(irregular as result of missing
complexes)

• Normal duration
• Normal configuration
• Absent during arrest

Rate

T wave

• Usually within normal limits
(60 to 100 beats/minute) before
arrest
• Length or frequency of pause
may result in bradycardia

• Normal size
• Normal configuration
• Absent during arrest

QT interval
• Within normal limits
• Absent during arrest

P wave
• Periodically absent, with entire
PQRST complexes missing
• When present, normal size
and configuration
• Precedes each QRS complex

Other
• The pause isn’t a multiple of
the underlying P-P intervals
• Junctional escape beats may
occur at end of pause

PR interval
• Within normal limits when a
P wave is present
• Constant when a P wave is
present

22

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23

Sinus arrest (continued)
What causes it
• Acute infection
• Acute inferior-wall MI
• Acute myocarditis
• CAD
• Cardioactive drugs
– Amiodarone
– Beta-adrenergic blockers
(bisoprolol, metoprolol,
propranolol)
– Calcium channel blockers
(diltiazem, verapamil)
– Digoxin
– Procainamide
– Quinidine
• Cardiomyopathy
• Hypertensive heart disease
• Increased vagal tone or
carotid sinus sensitivity
• Salicylate toxicity
• Sinus node disease
• SSS

What to look for
• Absence of heart sounds and
pulse during arrest
• Absence of symptoms with
short pauses

SA Node

• Evidence of decreased CO
with recurrent or prolonged
pauses
– Altered mental status
– Blurred vision
– Dizziness
– Cool, clammy skin
– Low blood pressure
– Syncope or near-syncope

What to do
• Monitor heart rhythm.
• Protect patient from injury,
such as a fall, which may
result from syncopal or nearsyncopal episodes caused by
prolonged pause.

How it’s treated
• No treatment if patient
asymptomatic
• If symptoms, follow bradycardia algorithm
• As needed, discontinuation
of drugs affecting SA node
discharge or conduction, such
as beta-adrenergic blockers,
calcium channel blockers, and
digoxin

Page 23

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SA Node

Sinoatrial exit block

Rhythm

QRS complex

• Regular except during a
pause (irregular as result of a
pause)

• Normal duration
• Normal configuration
• Absent during a pause

Rate

T wave

• Usually within normal limits
(60 to 100 beats/minute) before
a pause
• Length or frequency of pause
may result in bradycardia

• Normal size
• Normal configuration
• Absent during a pause

QT interval
• Within normal limits
• Absent during a pause

P wave
• Periodically absent, with entire PQRST complex missing
• When present, normal size
and configuration and precedes each QRS complex

Other
• The pause is a multiple of
the underlying P-P interval

PR interval
• Within normal limits
• Constant when a P wave is
present

24

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25

Sinoatrial exit block (continued)
• Evidence of decreased CO
What causes it
• Acute infection
• Acute inferior-wall MI
• Acute myocarditis
• Cardioactive drugs
– Amiodarone
– Beta-adrenergic blockers
(bisoprolol, metoprolol, propranolol)
– Calcium channel blockers
(diltiazem, verapamil)
– Digoxin
– Procainamide
– Quinidine
• CAD
• Cardiomyopathy
• Hypertensive heart disease
• Increased vagal tone
• Salicylate toxicity
• Sinus node disease
• SSS

What to look for
• Absence of heart sounds and
pulse during SA exit block
• Absence of symptoms with
short pauses

SA Node

with recurrent or prolonged
pauses
– Altered mental status
– Blurred vision
– Cool, clammy skin
– Dizziness
– Low blood pressure
– Syncope or near-syncope

What to do
• Monitor heart rhythm.
• Protect patient from injury,
such as a fall, which may result from syncopal or nearsyncopal episodes caused by
prolonged pause.

How it’s treated
• No treatment if patient
asymptomatic
• If symptomatic, guidelines
for symptomatic bradycardia
response
• As needed, discontinuation
of drugs affecting SA node
discharge or conduction, such
as beta-adrenergic blockers,
calcium channel blockers, and
digoxin

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SA Node

Sick sinus syndrome

Rhythm

QRS complex

• Irregular
• Sinus pauses
• Abrupt rate changes

• Duration within normal limits
• Varies with rhythm changes
• Normal configuration

Rate

T wave

• Fast, slow, or alternating
• Interrupted by a long sinus
pause

• Normal size
• Normal configuration

P wave
• Varies with rhythm changes
• May be normal size and
configuration
• May be absent
• Usually precedes each QRS
complex

QT interval
• Usually within normal limits
• Varies with rhythm changes

Other
• Usually more than one
arrhythmia on a 6-second strip

PR interval
• Usually within normal limits
• Varies with rhythm changes

26

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27

Sick sinus syndrome (continued)
If underlying cardiomyopathy
What causes it
• Autonomic disturbances that
affect autonomic innervation
– Degeneration of autonomic
system
– Hypervagotonia
• Cardioactive drugs
– Beta-adrenergic blockers
– Calcium channel blockers
– Digoxin
• Conditions leading to fibrosis
of SA node
– Advanced age
– Atherosclerotic heart disease
– Cardiomyopathy
– Hypertension
• Inflammation of atrial wall
around SA node
• Trauma to SA node
– Open-heart surgery, especially valve surgery
– Pericarditis
– Rheumatic heart disease

What to look for
• Changes in heart rate and
rhythm
• Episodes of tachy-brady syndrome, atrial flutter, atrial fibrillation, SA block, or sinus arrest
• Syncope (Stokes-Adams
attacks)

SA Node

present
• Dilated and displaced left
ventricular apical impulse
• Possible crackles
• S3 heart sound

If thromboembolism present
• Acute chest pain
• Dyspnea or tachypnea
• Fatigue
• Hypotension
• Neurologic changes (confusion, vision disturbances,
weakness)

What to do
• Monitor for changes in heart
rhythm.
• Prepare patient for possible
treatment interventions.

How it’s treated
• No treatment if patient
asymptomatic
• If symptomatic, correction of
underlying cause
• Insertion of temporary pacemaker (transcutaneous or
transvenous)
• If arrhythmia due to chronic disorder: digoxin, beta-adrenergic
blocker, radio-frequency ablation, or permanent pacemaker
• Anticoagulant for atrial
fibrillation

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Atrial

Premature atrial contractions

Rhythm

QRS complex

• Atrial: Irregular
• Ventricular: Irregular
• Underlying: Possibly regular

• Conducted: Duration and
configuration usually normal
• Nonconducted: No QRS
complex follows PAC

Rate
• Atrial and ventricular: Vary
with underlying rhythm

P wave
• Premature
• Abnormal configuration
compared to a sinus P wave
• If varying configurations,
multiple ectopic sites
• May be hidden in preceding
T wave (see shaded area on
strip)

PR interval
• Usually within normal limits
• May be shortened or slightly
prolonged for the ectopic beat

T wave
• Usually normal
• May be distorted if P wave is
hidden in T wave

QT interval
• Usually within normal limits

Other
• May be a single beat
• May be bigeminal (every
other beat premature)
• May be trigeminal (every
third beat premature)
• May be quadrigeminal (every
fourth beat premature)
• May occur in couplets (pairs)
• Three or more PACs in a row
indicate atrial tachycardia

28

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29

Premature atrial contractions (continued)
What causes them
What to do
• Enhanced automaticity in
atrial tissue (most common
cause)
• Acute respiratory failure
• COPD
• Coronary heart disease
• Digoxin toxicity
• Drugs that prolong absolute
refractory period of SA node
– Procainamide
– Quinidine
• Electrolyte imbalances
• Endogenous catecholamine
release from pain or anxiety
• Fatigue
• Fever
• Heart failure
• Hyperthyroidism
• Hypoxia
• Infectious disease
• Triggers (alcohol, caffeine,
nicotine)
• Valvular heart disease

What to look for
• Pulse rhythm and rate that
reflect underlying rhythm
• Irregular peripheral or apical
pulse rhythm when PACs occur
• Evidence of decreased CO,
such as hypotension and
syncope, if patient has heart
disease

Atrial

• Monitor heart rhythm.
• If patient has ischemic or
valvular heart disease, watch
for evidence of heart failure,
electrolyte imbalances, and
more severe atrial arrhythmias. Note: In patients with
acute MI, PACs may be early
signs of heart failure or an
electrolyte imbalance.
• Teach patient to correct or
avoid underlying causes or
triggers such as caffeine.
• Demonstrate stress-reduction
techniques to lessen anxiety.

How they’re treated
• Usually no treatment if
patient asymptomatic
• If symptomatic, elimination
or control of triggers
• For frequent PACs: drugs
that prolong atrial refractory
period, such as beta-adrenergic
blockers and calcium channel
blockers

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Atrial

Atrial tachycardia

Rhythm

QRS complex

• Atrial: Usually regular
• Ventricular: Regular or irregular depending on AV conduction ratio and type of atrial
tachycardia

• Usually normal duration and
configuration
• May be abnormal if impulses
conducted abnormally
through ventricles

Rate

T wave

• Atrial: Three or more consecutive ectopic atrial beats at
150 to 250 beats/minute;
rarely exceeds 250 beats/
minute
• Ventricular: Varies, depending on AV conduction ratio

• Usually visible
• May be distorted by P wave
• May be inverted if ischemia
is present

P wave
• Deviates from normal
appearance
• May be hidden in preceding
T wave
• If visible, usually upright and
precedes each QRS complex

QT interval
• Usually within normal limits
• May be shorter because of
rapid rate

Other
• May be difficult to differentiate atrial tachycardia with
block from sinus arrhythmia
with U waves

PR interval
• May be difficult to measure if
P wave can’t be distinguished
from preceding T wave

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31

Atrial tachycardia (continued)
• Keep resuscitative equipWhat causes it
• Digoxin toxicity (most common)
• Cardiomyopathy
• COPD
• Congenital anomalies
• Cor pulmonale
• Drugs
– Albuterol
– Cocaine
– Theophylline
• Electrolyte imbalances
• Hyperthyroidism
• Hypoxia
• MI
• Physical or psychological stress
• Systemic hypertension
• Triggers (alcohol, caffeine,
nicotine)
• Valvular heart disease
• WPW syndrome

What to look for
• Rapid HR
• Sudden feeling of palpitations, especially with PAT
• Signs of decreased CO (hypotension, chest pain, syncope)

What to do
• Monitor heart rhythm.
• Assess patient for digoxin
toxicity; monitor digoxin
blood level.

Atrial

ment readily available if vagal
maneuvers are used.

How it’s treated
• Treatment dependent on
type of tachycardia and
symptom severity; directed
toward eliminating cause and
decreasing ventricular rate
• Possibly Valsalva’s maneuver
or carotid sinus massage to
treat PAT
• Drug therapy (pharmacologic
cardioversion): adenosine,
amiodarone, beta-adrenergic
blockers, calcium channel
blockers, digoxin
• If patient unstable, possible
synchronized electrical cardioversion
• Atrial overdrive pacing
• If arrhythmia related to WPW
syndrome, possible catheter
ablation
• In patient with COPD, correction of hypoxia and electrolyte
imbalances

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Atrial

Multifocal atrial tachycardia

Rhythm

PR interval

• Atrial: Irregular
• Ventricular: Irregular

• Varies

QRS complex

Rate

• Usually normal
• May become aberrant if
arrhythmia persists

• Atrial: 100 to 250 beats/
minute (usually less than
160 beats/minute)
• Ventricular: 100 to 250 beats/
minute

T wave
• Usually distorted

P wave

QT interval

• Configuration: Varies
• At least three different P wave
shapes must appear

• May be indiscernible

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33

Paroxysmal atrial tachycardia

Rhythm

QRS complex

• Atrial: Regular
• Ventricular: Regular

• Usually normal; may be
aberrantly conducted

Rate

T wave

• Atrial: 150 to 250 beats/minute
• Ventricular: 150 to 250 beats/
minute

• Usually indistinguishable

P wave
• May not be visible
• May be difficult to distinguish
from preceding T wave

PR interval
• May not be measurable if
P wave can’t be distinguished
from preceding T wave

Atrial

QT interval
• May be indistinguishable

Other
• Sudden onset, typically started
by PAC; may start and stop
abruptly

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Atrial

Atrial flutter

Rhythm

P wave

• Atrial: Regular
• Ventricular: Typically regular,
although cycles may alternate
(depends on AV conduction
pattern)

• Abnormal
• Sawtoothed appearance known
as flutter waves or F waves

PR interval
• Not measurable

Rate
• Atrial: 250 to 400 beats/minute
• Ventricular: Usually 60 to
150 beats/minute (one-half
to one-fourth of atrial rate),
depending on degree of AV block
• Usually expressed as a ratio
(2:1 or 4:1, for example)
• Commonly 300 beats/minute
atrial and 150 beats/minute
ventricular; known as 2:1 block
• Only every second, third, or
fourth impulse is conducted to
ventricles because the AV node
usually won’t accept more than
180 impulses/minute
• When atrial flutter is first recognized, ventricular rate typically
exceeds 100 beats/minute

QRS complex
• Duration: Usually within normal
limits
• May be widened if flutter waves
are buried within the complex

T wave
• Not identifiable

QT interval
• Not measurable because
T wave isn’t identifiable

Other
• Atrial rhythm may vary between
a fibrillatory line and flutter waves
(called atrial fib-flutter), with an
irregular ventricular response
• May be difficult to differentiate
atrial flutter from atrial fibrillation

34

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35

Atrial flutter (continued)
What causes it
• Cardiac surgery with acute MI
• Conditions that enlarge
atrial tissue and elevate atrial
pressures
• COPD
• Digoxin toxicity
• Hyperthyroidism
• MI
• Mitral or tricuspid valve disease
• Pericardial disease
• Systemic arterial hypoxia

What to look for
• Possibly no symptoms if
ventricular rate is normal
• Rapid HR if ventricular rate is
rapid (complaint of palpitations)
• Evidence of reduced CO if
ventricular rate is rapid
• Evidence of reduced ventricular filling time and coronary
perfusion from rapid ventricular rate
– Angina
– Heart failure
– Hypotension
– Pulmonary edema
– Syncope

Atrial

What to do
• Monitor heart rhythm.
• Keep resuscitative equipment
at bedside; be alert for bradycardia because cardioversion
can decrease HR.
• Be alert for effects of digoxin,
which depresses SA node.
• Monitor patient closely for
evidence of low CO.

How it’s treated
• If patient hemodynamically
unstable and with atrial flutter
of 48 hours or less, immediate
synchronized electrical cardioversion
• With atrial flutter of more
than 48 hours, anticoagulation therapy before and after
cardioversion
• With normal heart function:
beta-adrenergic blockers, such
as metoprolol, or calcium
channel blockers such as
diltiazem
• With impaired heart function
(heart failure or EF below
40%): digoxin or amiodarone
• Ablation therapy for recurrent
atrial flutter

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Atrial

Atrial fibrillation

Rhythm

PR interval

• Atrial: Irregularly irregular
• Ventricular: Irregularly irregular

• Indiscernible

Rate
• Atrial: Almost indiscernible,
usually above 400 beats/minute;
far exceeds ventricular rate
because most impulses aren’t
conducted through the AV
junction
• Ventricular: Usually 100 to
150 beats/minute but can be
below 100 beats/minute

P wave
• Absent
• Replaced by baseline fibrillatory waves that represent atrial
tetanization from rapid atrial
depolarizations

QRS complex
• Duration and configuration
usually normal

T wave
• Indiscernible

QT interval
• Not measurable

Other
• Atrial rhythm may vary between
fibrillatory line and flutter
waves (called atrial fib-flutter)
• May be difficult to differentiate atrial fibrillation from atrial
flutter and MAT

36

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37

Atrial fibrillation (continued)
cardiac monitor, be alert for
What causes it
• Acute MI
• Atrial septal defect
• CAD
• Cardiac surgery
• Cardiomyopathy
• COPD
• Digoxin toxicity
• Drugs such as aminophylline
• Endogenous catecholamine
released during exercise
• Hypertension
• Hyperthyroidism
• Pericarditis
• Rheumatic heart disease
• Triggers (alcohol, caffeine,
nicotine)
• Valvular heart disease (especially mitral valve disease)

What to look for
• Irregularly irregular pulse
rhythm with normal or
abnormal HR
• Radial pulse rate that’s slower
than apical pulse rate
• Evidence of decreased CO (lightheadedness, hypotension)
• Possibly no symptoms with
chronic atrial fibrillation

What to do
• Monitor heart rhythm.
• Monitor for evidence of
decreased cardiac output and
heart failure. If patient isn’t on

Atrial

irregular pulse and differences
in radial and apical pulse rates.
• If drug therapy is used, monitor serum drug levels; watch
for evidence of toxicity.
• Tell patient to report changes
in pulse rate, dizziness, faintness, chest pain, and signs of
heart failure, such as dyspnea
and peripheral edema.

How it’s treated
• Drug therapy to control ventricular response, or electrical
cardioversion with drug therapy
• If patient hemodynamically
unstable, immediate synchronized cardioversion (most successful if done within 48 hours
after atrial fibrillation onset)
• With atrial fibrillation of
more than 48 hours: anticoagulation before and after
cardioversion
• With otherwise normal heart
function: beta-adrenergic
blockers, such as metoprolol,
or calcium channel blockers
such as diltiazem
• With impaired heart function
(heart failure or EF below
40%): digoxin or amiodarone
• Radio-frequency ablation
therapy for unresponsive
symptomatic atrial fibrillation

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Atrial

Ashman’s phenomenon

Rhythm

T wave

• Atrial: Irregular
• Ventricular: Irregular

• Deflection opposite that of
QRS complex in most leads
because of RBBB

Rate
• Reflects the underlying
rhythm

P wave
• May be visible
• Abnormal configuration
• Unchanged if present in the
underlying rhythm

PR interval
• Commonly changes on the
premature beat, if measurable
at all

QT interval
• Usually changed because of
RBBB

Other
• No compensatory pause
after an aberrant beat
• Aberrancy may continue for
several beats and typically
ends a short cycle preceded
by a long cycle

QRS complex
• Altered configuration with
RBBB pattern

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39

Ashman’s phenomenon (continued)
What causes it
What to do
• Prolonged refractory period
in slower rhythm
• Short cycle followed by long
cycle because refractory period
varies with length of cycle

What to look for
• No signs or symptoms

Atrial

• Monitor heart rhythm.

How it’s treated
• No interventions needed, but
may be needed for accompanying arrhythmias

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Atrial

Wandering pacemaker

Rhythm

PR interval

• Atrial: Varies slightly, with
an irregular P-P interval
• Ventricular: Varies slightly,
with an irregular R-R interval

• Varies from beat to beat as
pacemaker site changes
• Usually less than 0.20 second
• Less than 0.12 second if the
impulse originates in the AV
junction

Rate
• Varies, but usually within
normal limits or less than
60 beats/minute

QRS complex

P wave
• Altered size and configuration from changing pacemaker
site with at least three different P-wave shapes visible
• May be absent or inverted
or occur after QRS complex if
impulse originates in the AV
junction

• Duration and configuration
usually normal because
ventricular depolarization
is normal

T wave
• Normal size and configuration

QT interval
• Usually within normal limits

Other
• May be difficult to differentiate
wandering pacemaker from PACs

40

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41

Wandering pacemaker (continued)
What causes it
What to do
• COPD
• Digoxin toxicity
• Increased parasympathetic
(vagal) influences on SA node
or AV junction
• Inflammation of atrial tissue
• Valvular heart disease

What to look for
• Usually no symptoms (patient
is unaware of arrhythmia)
• Pulse rate normal or less
than 60 beats/minute
• Rhythm regular or slightly
irregular
• At least three distinct P wave
configurations (distinguish
wandering pacemaker from
PACs)

Atrial

• Monitor heart rhythm.
• Watch for evidence of hemodynamic instability, such as
hypotension and changes in
mental status.

How it’s treated
• Usually no treatment if
patient asymptomatic
• If symptomatic, review of
medication regimen; investigation and treatment of underlying cause of arrhythmia

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Junc

Premature junctional contractions

Rhythm

PR interval

• Atrial: Irregular during PJCs
• Ventricular: Irregular during
PJCs
• Underlying rhythm possibly
regular

• Shortened (less than 0.12 second) if P wave precedes QRS
complex
• Not measurable if no P wave
precedes QRS complex

Rate

QRS complex

• Atrial: Reflects underlying
rhythm
• Ventricular: Reflects underlying rhythm

• Usually normal configuration
and duration because ventricles
usually depolarize normally

T wave

P wave

• Usually normal configuration

• Usually inverted (leads II, III,
and aVF) (see shaded area on
strip)
• May occur before, during, or
after QRS complex, depending
on initial direction of depolarization
• May be hidden in QRS complex

QT interval
• Usually within normal limits

Other
• Commonly accompanied by a
compensatory pause reflecting
retrograde atrial conduction

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43

Premature junctional contractions (continued)
What causes them
What to do
• CAD
• COPD
• Digoxin toxicity
• Electrolyte imbalances
• Heart failure
• Hyperthyroidism
• Inferior-wall MI
• Inflammatory changes in the
AV junction after heart surgery
• Myocardial ischemia
• Pericarditis
• Stress
• Triggers (alcohol, caffeine,
nicotine)
• Valvular heart disease

What to look for
• Usually no symptoms
• Possible feeling of palpitations
or skipped beats
• Hypotension if PJCs are
frequent enough

Junc

• Monitor cardiac rhythm
for frequent PJCs; may indicate junctional irritability
and can lead to more serious
arrhythmia such as junctional
tachycardia.
• Monitor patient for hemodynamic instability.

How they’re treated
• Usually no treatment if patient
asymptomatic
• If symptomatic, treatment of
underlying cause
• If digoxin toxicity, discontinuation of drug
• If ectopic beats frequent
because of caffeine, decrease
in or elimination of caffeine
intake

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Junc

Junctional rhythm

Rhythm

QRS complex

• Atrial: Regular
• Ventricular: Regular

• Duration: Usually within normal limits
• Configuration: Usually normal

Rate

T wave

• Atrial: 40 to 60 beats/minute
• Ventricular: 40 to 60 beats/
minute

• Configuration: Usually normal

QT interval

P wave

• Usually within normal limits

• Usually inverted (leads II, III,
and aVF)
• May occur before, during, or
after QRS complex
• May be hidden in QRS complex

PR interval

Other
• Important to differentiate
junctional rhythm from idioventricular rhythm (a lifethreatening arrhythmia)

• Shortened (less than 0.12 second) if P wave precedes QRS
complex
• Not measurable if no P wave
precedes QRS complex

44

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45

Junctional rhythm (continued)
What causes it
What to do
• Cardiomyopathy
• Conditions that disturb normal SA node function or impulse conduction
• Drugs
– Beta-adrenergic blockers
– Calcium channel blockers
– Digoxin
• Electrolyte imbalances
• Heart failure
• Hypoxia
• Increased parasympathetic
(vagal) tone
• Myocarditis
• SA node ischemia
• SSS
• Valvular heart disease

What to look for
• Possibly no symptoms
• Signs of decreased CO
(hypotension, syncope,
blurred vision)

Junc

• Monitor heart rhythm.
• Monitor digoxin and electrolyte levels.
• Watch for evidence of decreased CO.

How it’s treated
• Identification and correction
of underlying cause
• Atropine; temporary or permanent pacemaker
• Junctional rhythm can prevent ventricular standstill;
should never be suppressed

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Junc

Accelerated junctional rhythm

Rhythm

QRS complex

• Atrial: Regular
• Ventricular: Regular

• Duration: Usually within normal limits
• Configuration: Usually normal

Rate

T wave

• Atrial: 60 to 100 beats/minute
• Ventricular: 60 to 100 beats/
minute

• Usually within normal limits

QT interval

P wave

• Usually within normal limits

• If present, inverted in leads
II, III, and aVF
• May occur before, during, or
after QRS complex
• May be hidden in QRS complex

PR interval

Other
• Need to differentiate accelerated junctional rhythm from
accelerated idioventricular
rhythm (a possibly lifethreatening arrhythmia)

• Shortened (less than 0.12 second) if P wave precedes QRS
complex
• Not measurable if no P wave
precedes QRS complex

46

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47

Accelerated junctional rhythm (continued)
What causes it
What to do
• Digoxin toxicity (common
cause)
• Cardiac surgery
• Electrolyte disturbances
• Heart failure
• Inferior-wall MI
• Myocarditis
• Posterior-wall MI
• Rheumatic heart disease
• Valvular heart disease

What to look for
• Normal pulse rate and regular rhythm
• Possibly no symptoms
• Possibly symptoms of decreased CO (from loss of atrial
kick), such as hypotension,
changes in mental status,
weak peripheral pulses

Junc

• Monitor heart rhythm.
• Watch for evidence of decreased CO and hemodynamic
instability.
• Monitor serum digoxin and
electrolyte levels.

How it’s treated
• Identification and correction
of underlying cause
• Discontinuation of digoxin

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Junc

Junctional tachycardia

Rhythm

PR interval

• Atrial: Usually regular but
may be difficult to determine
if P wave is hidden in QRS
complex or preceding T wave
• Ventricular: Usually regular

• Shortened (less than 0.12 second) if P wave precedes QRS
complex
• Not measurable if no P wave
precedes QRS complex

Rate

QRS complex

• Atrial: Exceeds 100 beats/
minute (usually 100 to
200 beats/minute) but may
be difficult to determine if
P wave isn’t visible
• Ventricular: Exceeds 100 beats/
minute (usually 100 to 200 beats/
minute)

• Duration: Within normal limits
• Configuration: Usually normal

P wave
• Usually inverted in leads II,
III, and aVF
• May occur before, during, or
after QRS complex
• May be hidden in QRS complex

T wave
• Configuration: Usually normal
• May be abnormal if P wave
is hidden in T wave
• May be indiscernible because
of fast rate

QT interval
• Usually within normal limits

Other
• May have gradual (nonparoxysmal) or sudden
(paroxysmal) onset

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Junctional tachycardia (continued)
What causes it
How it’s treated
• Digoxin toxicity (most common)
• Electrolyte imbalances
• Heart failure
• Hypokalemia (may aggravate
condition)
• Inferior-wall MI
• Inferior-wall myocardial
ischemia
• Inflammation of AV junction
after heart surgery
• Posterior-wall MI
• Posterior-wall myocardial
ischemia
• Valvular heart disease

What to look for
• Pulse rate above 100 beats/
minute with regular rhythm
• Effects of decreased CO (loss
of atrial kick) and hemodynamic instability (hypotension) because of rapid HR

What to do
• Monitor heart rhythm.
• Watch for evidence of digoxin toxicity; monitor digoxin
blood level.

Junc

• Identification and treatment
of underlying cause
• If due to digoxin toxicity, discontinuation of digoxin; in
some cases, possibly digoxinbinding drug to reduce serum
digoxin level
• For recurrent junctional
tachycardia, possibly ablation
therapy followed by permanent pacemaker insertion
• If symptomatic with paroxysmal onset of junctional
tachycardia:
– vagal maneuvers and
drugs such as adenosine to
slow HR
– with otherwise normal heart
function: beta-adrenergic
blockers, calcium channel
blockers, or amiodarone
– with impaired heart function (heart failure or EF
below 40%): amiodarone

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Premature ventricular contractions

• Configuration: Bizarre and
wide but usually normal in
underlying rhythm (see
shaded areas on strip)

Rhythm
• Atrial: Irregular during PVCs
• Ventricular: Irregular during
PVCs
• Underlying rhythm may be
regular

T wave

• Atrial: Reflects underlying
rhythm
• Ventricular: Reflects underlying rhythm

• Opposite direction to QRS
complex
• May trigger more serious
rhythm disturbances when
PVC occurs on the downslope
of the preceding normal T
wave (R-on-T phenomenon)

P wave

QT interval

Rate

• Usually absent in ectopic beat
• May appear after QRS complex with retrograde conduction to atria
• Usually normal if present in
underlying rhythm

PR interval
• Not measurable except in
underlying rhythm

QRS complex
• Occurs earlier than expected
• Duration: Exceeds 0.12 second

• Not usually measured except
in underlying rhythm

Other
• PVC may be followed by full
or incomplete compensatory
pause
• Interpolated PVC: Occurs between two normally conducted
QRS complexes without great
disturbance to underlying rhythm
• Full compensatory pause
absent with interpolated PVCs

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Premature ventricular contractions (continued)
• Palpitations if PVCs are frequent
What causes them
• Enhanced automaticity (usual
cause)
• Drug intoxication (amphetamines, cocaine, digoxin,
phenothiazines, tricyclic antidepressants)
• Electrolyte imbalances (hyperkalemia, hypocalcemia, hypomagnesemia, hypokalemia)
• Enlargement of ventricular
chambers
• Hypoxia
• Increased sympathetic
stimulation
• Irritable focus
• Irritation of ventricles by pacemaker electrodes or PA catheter
• Metabolic acidosis
• MI
• Mitral valve prolapse
• Myocardial ischemia
• Myocarditis
• Sympathomimetic drugs
such as epinephrine
• Triggers (alcohol, caffeine,
nicotine)

What to look for
• Possibly no symptoms
• Normal pulse rate with
momentarily irregular pulse
rhythm when PVC occurs
• Abnormally early heart
sound with each PVC on
auscultation

• Evidence of decreased CO
(hypotension, syncope)

What to do
• Promptly assess patients
with recently developed PVCs,
especially those with underlying heart disease or complex
medical problems.
• Monitor heart rhythm of
patients with PVCs and serious symptoms.
• Observe closely for development of more frequent PVCs or
more dangerous PVC patterns.
• Teach family members how
to activate EMS and perform
CPR if the patient will be taking antiarrhythmic drugs after
discharge.

How they’re treated
• No treatment if patient
asymptomatic and has no evidence of heart disease
• If symptomatic, or dangerous form of PVC occurs, treatment dependent on cause
• For PVCs of purely cardiac
origin: drugs to suppress ventricular irritability, such as
amiodarone, lidocaine, procainamide
• For PVCs of noncardiac origin: treatment of cause

Vent

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Vent

Patterns of potentially dangerous PVCs
Some PVCs are more dangerous than others. Here are some
potentially dangerous ones.

Paired PVCs

Two PVCs in a row, called
paired PVCs or a ventricular
couplet (see shaded areas on
strip above), can produce VT
because the second contrac-

tion usually meets refractory
tissue. A burst, or salvo, of
three or more PVCs in a row is
considered a run of VT.

Multiform PVCs

Multiform PVCs look different
from one another (see shaded
areas on strip above) and arise
either from different sites or

from the same site via abnormal conduction. Multiform
PVCs may indicate severe heart
disease or digoxin toxicity.

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Patterns of potentially dangerous PVCs
(continued)

Bigeminy and trigeminy

PVCs that occur every other
beat (bigeminy) or every third
beat (trigeminy) can result in

VT or VF. The shaded areas on
the strip shown above illustrate ventricular bigeminy.

R-on-T phenomenon

In R-on-T phenomenon, a
PVC occurs so early that it
falls on the T wave of the
preceding beat (see shaded

area on strip above). Because
the cells haven’t fully repolarized, VT or VF can result.

Vent

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Vent

Idioventricular rhythm

Rhythm

QRS complex

• Atrial: Usually can’t be
determined
• Ventricular: Usually regular

• Duration: Exceeds 0.12 second because of abnormal
ventricular depolarization
• Configuration: Wide and bizarre

Rate
• Atrial: Usually can’t be
determined
• Ventricular: 20 to 40 beats/
minute

T wave
• Abnormal
• Usually deflects in opposite
direction from QRS complex

P wave

QT interval

• Usually absent

• Usually prolonged

PR interval

Other

• Not measurable because of
absent P wave

• Commonly occurs with thirddegree AV block
• If any P waves present, not
associated with QRS complex

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Idioventricular rhythm (continued)
• Enforce bed rest until effecWhat causes it
• Digoxin toxicity
• Drugs
– Beta-adrenergic blockers
– Calcium channel blockers
– Tricyclic antidepressants
• Failure of all of heart’s higher
pacemakers
• Failure of supraventricular
impulses to reach ventricles
because of block in conduction system
• Metabolic imbalance
• MI
• Myocardial ischemia
• Pacemaker failure
• SSS
• Third-degree AV block

What to look for
• Evidence of sharply decreased
CO (hypotension, dizziness,
feeling of faintness, syncope,
light-headedness)
• Difficult auscultation or
palpation of BP

What to do
• Monitor ECG continually;
periodically assess patient
until hemodynamic stability
has been restored.
• Keep atropine and pacemaker
equipment readily available.

tive HR has been maintained
and patient is stable.
• Tell patient and family about
the serious nature of this
arrhythmia and required
treatment.
• If patient needs a permanent
pacemaker, explain how it
works, how to recognize problems, when to contact doctor,
and how pacemaker function
will be monitored.

How it’s treated
• Suppression of arrhythmia
not goal of treatment; arrhythmia acts as safety mechanism
against ventricular standstill
• Possible atropine to increase
HR
• In emergency, transcutaneous
pacemaker until transvenous
pacemaker can be inserted
• Permanent pacemaker
• Antiarrhythmic drugs (such
as amiodarone, lidocaine)
contraindicated for idioventricular rhythm because of
possible suppression of
escape beats

Vent

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Vent

Accelerated idioventricular rhythm

Rhythm

QRS complex

• Atrial: Can’t be determined
• Ventricular: Usually regular

• Duration: Exceeds 0.12 second
• Configuration: Wide and bizarre

Rate

T wave

• Atrial: Usually can’t be
determined
• Ventricular: 40 to 100 beats/
minute

• Abnormal
• Usually deflects in opposite
direction from QRS complex

P wave
• Usually absent

PR interval
• Not measurable

QT interval
• Usually prolonged

Other
• If any P waves present, not
associated with QRS complex

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Accelerated idioventricular rhythm (continued)
• Enforce bed rest until effecWhat causes it
• Digoxin toxicity
• Drugs
– Beta-adrenergic blockers
– Calcium channel blockers
– Tricyclic antidepressants
• Failure of all of heart’s higher
pacemakers
• Failure of supraventricular
impulses to reach ventricles
because of block in conduction system
• Metabolic imbalance
• MI
• Myocardial ischemia
• Pacemaker failure
• SSS
• Third-degree AV block

What to look for
• Evidence of sharply decreased
CO (hypotension, dizziness,
light-headedness, syncope)
• Difficult auscultation or
palpation of BP

What to do
• Monitor ECG continually;
periodically assess patient
until hemodynamic stability
has been restored.
• Keep atropine and pacemaker
equipment readily available.

tive HR has been maintained
and patient is stable.
• Tell patient and family about
the serious nature of this
arrhythmia and required
treatment.
• If patient needs permanent
pacemaker, explain how it
works, how to recognize problems, when to contact physician, and how pacemaker
function will be monitored.

How it’s treated
• Suppression of arrhythmia
not goal of treatment; arrhythmia acts as safety mechanism
against ventricular standstill
• Possible atropine to increase
HR
• In emergency, transcutaneous pacemaker until transvenous pacemaker can be
inserted
• Permanent pacemaker
• Antiarrhythmic drugs (such
as amiodarone, lidocaine)
contraindicated for accelerated
idioventricular rhythm because
of possible suppression of
escape beats

Vent

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Vent

Ventricular tachycardia

Rhythm

QRS complex

• Atrial: Can’t be determined
• Ventricular: Usually regular
but may be slightly irregular

• Duration: Exceeds 0.12 second
• Configuration: Usually bizarre,
with increased amplitude
• Uniform in monomorphic VT
• Constantly changes shape in
polymorphic VT

Rate
• Atrial: Can’t be determined
• Ventricular: Usually rapid
(100 to 250 beats/minute)

P wave
• Usually absent
• If present, not associated
with QRS complex

T wave
• If visible, occurs opposite the
QRS complex

QT interval
• Not measurable

PR interval

Other

• Not measurable

• Ventricular flutter: A variation
of VT

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Ventricular tachycardia (continued)
What causes it
What to do
• Usually increased myocardial irritability, which may be
triggered by:
– enhanced automaticity
– PVCs during downstroke of
preceding T wave
– reentry in Purkinje system
• CAD
• Cardiomyopathy
• Drug toxicity (cocaine, procainamide, or quinidine)
• Electrolyte imbalances such
as hypokalemia
• Heart failure
• MI
• Myocardial ischemia
• Rewarming during hypothermia
• Valvular heart disease

What to look for
• Possibly only minor symptoms
initially
• Usually weak or absent pulses
• Hypotension and decreased
level of consciousness, quickly
leading to unresponsiveness if
untreated
• Possible angina, heart failure,
and substantial decrease in
organ perfusion

• Determine whether patient is
conscious and has spontaneous respirations and palpable carotid pulse.
• Monitor heart rhythm; rhythm
may rapidly progress to VF.
• Teach family members how
to activate EMS and perform
CPR if patient will have an ICD
or be on long-term antiarrhythmic therapy after discharge.
• Teach patient and family
about the serious nature of
arrhythmia and need for
prompt treatment.

How it’s treated
• For pulseless VT, cardiopulmonary resuscitation and
immediate defibrillation
• For unstable patient with
pulse, immediate synchronized cardioversion
• If no definitive diagnosis
of SVT or VT, amiodarone
and elective synchronized
cardioversion
• For stable patient with recurrent polymorphic VT, consultation with an expert
• Correction of electrolyte
imbalances
• ICD

Vent

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Torsades de pointes

Rhythm

QRS complex

• Atrial: Can’t be determined
• Ventricular: May be regular
or irregular

• Usually wide
• Usually a phasic variation
in electrical polarity, with
complexes that point downward for several beats and
then upward for several beats

Rate
• Atrial: Can’t be determined
• Ventricular: 150 to 300 beats/
minute

P wave
• Not identifiable

PR interval
• Not measurable

T wave
• Not discernible

QT interval
• Prolonged

Other
• May be paroxysmal, starting
and stopping suddenly

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Torsades de pointes (continued)
What causes it
What to do
• AV block
• Drug toxicity (sotalol,
procainamide, quinidine)
• Electrolyte imbalances
(hypocalcemia, hypokalemia,
hypomagnesemia)
• Hereditary QT prolongation
syndrome
• Myocardial ischemia
• Prinzmetal’s angina
• Psychotropic drugs (phenothiazines, tricyclic antidepressants)
• SA node disease resulting in
severe bradycardia

What to look for
• Palpitations, dizziness, chest
pain, and shortness of breath
if patient is conscious
• Hypotension and decreased
level of consciousness
• Loss of consciousness,
pulse, and respirations

• Monitor heart rhythm and
observe for QT prolongation
in patients receiving drugs
that may cause torsades de
pointes.
• Determine whether patient is
conscious and has spontaneous respirations and palpable carotid pulse.

How it’s treated
• Cardiopulmonary resuscitation
• Defibrillation
• Overdrive pacing
• Magnesium sulfate I.V.
• Discontinuation of offending
drug
• Correction of electrolyte
imbalances
• For unstable patient with
pulse, immediate synchronized
cardioversion
• ICD

Vent

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Vent

Ventricular fibrillation
Coarse

Fine

Rhythm

QRS complex

• Atrial: Can’t be determined
• Ventricular: No pattern or
regularity, just fibrillatory
waves

• Can’t be determined

Rate

QT interval

• Atrial: Can’t be determined
• Ventricular: Can’t be determined

• Not measurable

P wave
• Can’t be determined

PR interval

T wave
• Can’t be determined

Other
• Electrical defibrillation more
successful with coarse fibrillatory waves than with fine
waves

• Can’t be determined

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Ventricular fibrillation (continued)
What causes it
What to do
• Acid-base imbalance
• CAD
• Drug toxicity (digoxin,
procainamide, quinidine)
• Electric shock
• Electrolyte imbalances
(hypercalcemia, hyperkalemia,
hypokalemia)
• MI
• Myocardial ischemia
• Severe hypothermia
• Underlying heart disease such
as dilated cardiomyopathy
• Untreated VT

What to look for
• Full cardiac arrest
• Unresponsive patient with
no detectable BP or central
pulses

• Assess patient to determine
if rhythm is VF.
• Start CPR.
• Teach patient’s family about
the serious nature of this arrhythmia and how to activate
EMS and perform CPR.
• Teach patient and family
about the ICD if applicable or
antiarrhythmic therapy the patient will be taking after discharge.

How it’s treated
• Cardiopulmonary resuscitation
• Immediate defibrillation:
biphasic (120 to 200 joules),
monophasic (360 joules)
• Epinephrine or vasopressin
• Following pulseless arrest
algorithm guidelines

Vent

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Asystole

Rhythm

T wave

• Atrial: Usually indiscernible
• Ventricular: Not present

• Absent

Rate
• Atrial: Usually indiscernible
• Ventricular: Not present

P wave
• May be present

PR interval
• Not measurable

QRS complex

QT interval
• Not measurable

Other
• Looks like a nearly flat line on
a rhythm strip except during
chest compressions with CPR
• If the patient has a pacemaker,
pacer spikes may show on the
strip, but no P wave or QRS
complex occurs in response

• Absent or occasional escape
beats

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Asystole (continued)
What causes it
• Cardiac tamponade
• Drug overdose
• Hypothermia
• Hypovolemia
• Hypoxia
• Massive pulmonary
embolism
• MI
• Severe electrolyte disturbances, especially hyperkalemia and hypokalemia
• Severe, uncorrected acidbase disturbances, especially
metabolic acidosis
• Tension pneumothorax

What to look for
• Unresponsive patient
• Lack of spontaneous respirations, discernible pulse, and BP
• No CO or perfusion of vital
organs

What to do
• Verify lack of do-notresuscitate order.
• Verify asystole by checking
more than one ECG lead.
• Start CPR, supplemental
oxygen, and advanced
airway control with tracheal
intubation.

How it’s treated
• Cardiopulmonary resuscitation
• Identification and rapid treatment of potentially reversible
causes; otherwise, asystole
possibly irreversible
• Early transcutaneous pacing
• I.V. vasopressin, epinephrine,
and atropine
• For persistent asystole despite
appropriate management: possible end of resuscitation

Vent

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Pulseless electrical activity

Rhythm

QRS complex

• Atrial: Same as underlying
rhythm; becomes irregular as
rate slows
• Ventricular: Same as underlying rhythm; becomes irregular as rate slows

• Same as underlying rhythm;
becomes progressively wider

T wave
• Same as underlying rhythm;
eventually becomes indiscernible

Rate
• Atrial: Reflects underlying
rhythm
• Ventricular: Reflects underlying
rhythm; eventually decreases

P wave
• Same as underlying rhythm;
gradually flattens and then
disappears

PR interval
• Same as underlying rhythm;
eventually disappears as
P wave disappears

QT interval
• Same as underlying rhythm;
eventually becomes indiscernible

Other
• Also known as PEA
• Characterized by some electrical activity (may be any
rhythm) but no mechanical
activity or detectable pulse
• Usually becomes a flat line
indicating asystole within several minutes

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Pulseless electrical activity (continued)
What causes it
How it’s treated
• Acidosis
• Cardiac tamponade
• Drug overdoses (such as
tricyclic antidepressants)
• Hyperkalemia
• Hypokalemia
• Hypothermia
• Hypovolemia
• Hypoxia
• Massive acute MI
• Massive pulmonary embolism
• Tension pneumothorax

What to look for
• Apnea and sudden loss of
consciousness
• Lack of BP and pulse
• No CO or perfusion of vital
organs

What to do
• Start CPR immediately.

• Cardiopulmonary resuscitation
• Epinephrine, vasopressin,
and atropine according to
ACLS guidelines
• Identification and treatment
of cause including:
– pericardiocentesis for cardiac
tamponade
– volume infusion for hypovolemia from hemorrhage
– correction of electrolyte
imbalances
– ventilation for hypoxemia
– surgery or thrombolytic
therapy for massive pulmonary embolism
– needle decompression or
chest tube insertion for
tension pneumothorax
• Pacemaker therapy (rarely
effective)

Vent

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AV Block

First-degree AV block

Rhythm

QRS complex

• Regular

• Within normal limits
(0.08 second or less) if conduction delay occurs in AV
node
• If more than 0.12 second,
conduction delay may be in
His-Purkinje system

Rate
• Within normal limits or
bradycardic
• Atrial the same as ventricular

P wave
• Normal size
• Normal configuration
• Each followed by a QRS
complex

PR interval
• Prolonged
• More than 0.20 second (see
shaded area on strip)
• Constant

T wave
• Normal size
• Normal configuration
• May be abnormal if QRS
complex is prolonged

QT interval
• Within normal limits

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First-degree AV block (continued)
What causes it
What to do
• Degenerative (age-related)
changes in heart
• Drugs
– Beta-adrenergic blockers
– Calcium channel blockers
– Digoxin
• MI
• Myocardial ischemia
• Myocarditis

What to look for

• Monitor patient’s cardiac
rhythm to detect progression
to more serious heart block.
• Give digoxin, calcium channel
blockers, and beta-adrenergic
blockers cautiously.

How it’s treated
• Identification and correction
of underlying cause

• Normal or slow pulse rate
• Regular rhythm
• Usually no symptoms
• Usually no significant effect
on CO
• Increased interval between
S1 and S2 heard on cardiac
auscultation if PR interval is
extremely long

AV Block

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AV Block

Type I second-degree AV block

Rhythm

• After the nonconducted beat,
shorter than the interval preceding it

• Atrial: Regular
• Ventricular: Irregular

QRS complex

Rate

• Within normal limits
• Periodically absent

• Atrial rate exceeds ventricular rate because of nonconducted beats
• Both rates usually within
normal limits

T wave
• Normal size
• Normal configuration
• Deflection may be opposite
that of the QRS complex

P wave
• Normal size
• Normal configuration
• Each followed by a QRS complex except blocked P wave

QT interval
• Usually within normal limits

Other

PR interval

• Wenckebach pattern of
grouped beats (footprints of
Wenckebach)
• PR interval gets progressively
longer and R-R interval shortens until a P wave appears
without a QRS complex; cycle
then repeats

• Progressively longer (see
shaded areas on strip) with
each cycle until a P wave appears without a QRS complex
• Commonly described as
“long, longer, dropped”
• Slight variation in delay from
cycle to cycle

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Type I second-degree AV block (continued)
• Assess patient’s tolerance of
What causes it
• CAD
• Drugs
– Beta-adrenergic blockers
– Calcium channel blockers
– Digoxin
• Increased parasympathetic
tone
• Inferior-wall MI
• Rheumatic fever

What to look for
• Usually no symptoms
• Evidence of decreased CO
(hypotension, lightheadedness)
• Pronounced signs and symptoms if ventricular rate is slow

rhythm.
• Observe for signs and symptoms of decreased CO.
• Evaluate patient for possible
causes.
• Teach patient about temporary pacemaker, if indicated.

How it’s treated
• Identification and treatment
of underlying cause
• Atropine (use cautiously if
patient is having an MI; atropine can worsen ischemia)
• Transcutaneous pacing, if
needed, until the arrhythmia
resolves

What to do
• Monitor cardiac rhythm for
progression of degree of
block.

AV Block

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AV Block

Type II second-degree AV block

Rhythm

QRS complex

• Atrial: Regular
• Ventricular: Irregular
• Pauses correspond to
dropped beat
• Irregular when block is intermittent or conduction ratio is
variable
• Regular when conduction ratio
is constant, such as 2:1 or 3:1

• Within normal limits or narrow
if block occurs at bundle of His
• Widened and similar to BBB
if block occurs at bundle
branches
• Periodically absent

T wave
• Normal size
• Normal configuration

Rate

QT interval

• Atrial exceeds ventricular
• Both may be within normal
limits

• Within normal limits

Other

P wave

• PR and R-R intervals don’t
vary before a dropped beat
(see shaded area on strip), so
no warning occurs
• R-R interval that contains
nonconducted P wave equals
two normal R-R intervals
• Must be a complete block in
one bundle branch and intermittent interruption in conduction in the other bundle for a
dropped beat to occur

• Normal size
• Normal configuration
• Some not followed by a QRS
complex

PR interval
• Usually within normal limits
but may be prolonged
• Constant for conducted beats
• May be shortened after a
nonconducted beat

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Type II second-degree AV block (continued)
• Administer oxygen.
What causes it
• Anterior-wall MI
• Degenerative changes in
conduction system
• Organic heart disease
• Severe CAD

What to look for
• Usually no symptoms as
long as CO is adequate
• Evidence of decreased CO
(as dropped beats increase)
– Chest pain
– Dyspnea
– Fatigue
– Light-headedness
• Hypotension
• Slow pulse
• Regular or irregular rhythm

What to do
• Observe cardiac rhythm for
progression to more severe
block.
• Evaluate patient for correctable causes (such as
ischemia).

• Restrict patient to bedrest.
• If patient has no serious
signs and symptoms:
– monitor patient continuously, keeping transcutaneous pacemaker attached to
patient or in room.
– prepare patient for transvenous pacemaker insertion.
• Teach patient and family
about pacemakers, if indicated.

How it’s treated
• Transcutaneous pacing initiated quickly when indicated
and I.V. dopamine infusion,
epinephrine, or combination
of these drugs
• A transcutaneous pacemaker
(for serious signs and symptoms) until a permanent pacemaker is placed

AV Block

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AV Block

Third-degree AV block

Rhythm

QRS complex

• Atrial: Regular
• Ventricular: Regular

• Configuration depends on
location of escape mechanism and origin of ventricular
depolarization
• Appears normal if the block
is at the level of the AV node
or bundle of His
• Widened if the block is at the
level of the bundle branches

Rate
• Atrial: 60 to 100 beats/minute
(atria act independently under
control of SA node)
• Ventricular: Usually 40 to
60 beats/minute in an intranodal block (a junctional
escape rhythm)
• Ventricular: Usually less than
40 beats/minute in infranodal
block (a ventricular escape
rhythm)

T wave
• Normal size
• Normal configuration
• May be abnormal if QRS
complex originates in
ventricle

P wave

QT interval

• Normal size
• Normal configuration
• May be buried in QRS complex or T wave

• Within normal limits

Other
• Atria and ventricles are
depolarized from different
pacemaker sites and beat
independently of each other
• P waves occur without QRS
complexes

PR interval
• Not measurable

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Third-degree AV block (continued)
What causes it
What to do
At level of AV node
• AV node damage
• Increased parasympathetic
tone
• Inferior-wall MI
• Toxic effects of drugs (digoxin,
propranolol)

At infranodal level
• Extensive anterior MI

What to look for
• Possibly no symptoms except exercise intolerance and
unexplained fatigue
• Decreased CO from loss of
AV synchrony and resulting
loss of atrial kick
• Changes in level of consciousness and mental status
• Chest pain
• Diaphoresis
• Dyspnea
• Hypotension
• Light-headedness
• Pallor
• Severe fatigue
• Slow peripheral pulse rate

• Ensure patent I.V. line.
• Administer oxygen.
• Assess patient for correctable
causes of arrhythmia (drugs,
myocardial ischemia).
• Minimize patient’s activity
level.
• Restrict patient to bed rest.

How it’s treated
• For patient with serious
signs and symptoms, immediate treatment, including:
– transcutaneous pacing
(most effective)
– I.V. dopamine infusion,
epinephrine, or combination
(for short-term use in
emergencies)
• Atropine contraindicated,
especially when accompanied
by wide-complex ventricular
escape beats
• Permanent pacemaker

AV Block

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12:13 PM

12-Lead
12-Lead

Limb lead placement
Proper lead placement is critical for accurate recording of cardiac
rhythms. These drawings show correct electrode placement for
the six limb leads. RA stands for right arm; LA, left arm; RL, right
leg; and LL, left leg. A plus sign (⫹) indicates a positive pole,
a minus sign (⫺) indicates a negative pole, and G indicates
a ground. Below each drawing is a sample ECG strip for that lead.

Lead I

Lead II

Lead III

Connects the right
arm (negative pole)
with the left arm
(positive pole).

Connects the right
arm (negative pole)
with the left leg
(positive pole).

Connects the left
arm (negative pole)
with the left leg
(positive pole).

⫺

⫺
⫺

⫹

RA
(⫺)

LA
(⫹)

RL
(G)

RA
(⫺)

⫹

RL
(G)

LL
(⫹)

76

⫹

RL
(G)

LL
(⫹)

LA
(⫺)

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Limb lead placement
Lead aVR

Connects the right
arm (positive pole)
with the heart
(negative pole).

Connects the left
arm (positive pole)
with the heart
(negative pole).

⫹

Lead aVF

Connects the left
leg (positive pole)
with the heart
(negative pole).

⫹
⫺

RA
(⫹)

(continued)

Lead aVL

⫺

⫺

LA
(⫹)

LL
(⫹)

⫹

12-Lead

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12:13 PM

12-Lead

Precordial lead placement
To record a 12-lead ECG, place electrodes on the patient’s arms
and legs (with the ground lead on the patient’s right leg). The
three standard limb leads (I, II, and III) and the three augmented
leads (aVR, aVL, and aVF) are recorded using these electrodes.
Then, to record the precordial chest leads, place electrodes
as follows:
V1 . . . . . . . . . . . . Fourth ICS, right
sternal border
V2 . . . . . . . . . . . . Fourth ICS, left
sternal border
V3 . . . . . . . . . . . . Midway between
V1 V2
V6
V5
V3 V
V2 and V4
4
V4 . . . . . . . . . . . . Fifth ICS, left
midclavicular line
V5 . . . . . . . . . . . . Fifth ICS, left
anterior axillary line
V6 . . . . . . . . . . . . Fifth ICS, left
midaxillary line

V1

V4

V2

V5

V3

V6

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Right precordial lead placement
To record the right precordial chest leads, place the electrodes
as follows:
V1R . . . . . Fourth ICS, left
sternal border
V2R . . . . . Fourth ICS,
right sternal
border
V3R . . . . . Halfway
V2R
V1R
between V2R
V6R
and V4R
V5R V3R
V4R . . . . . Fifth ICS, right
V4R
midclavicular
line
V5R . . . . . Fifth ICS, right
anterior axillary line
Midclavicular line
V6R . . . . . Fifth ICS, right
Anterior axillary line
midaxillary
Midaxillary line
line

Posterior lead electrode placement
To ensure an accurate ECG
reading, make sure the posterior
electrodes V7, V8, and V9 are
placed at the same level horizontally as the V6 lead at the fifth intercostal space. Place lead V7 at
the posterior axillary line, lead V9
at the paraspinal line, and lead V8
halfway between leads V7 and V9.

Midaxillary line
Posterior axillary line
Left paraspinal line

V6 V7 V8

V9

12-Lead

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12:13 PM

12-Lead

Electrical activity and the 12-lead ECG
Each of the leads on a 12-lead ECG views the heart from a
different angle. These illustrations show the direction of electrical
activity (depolarization) monitored by each lead and the 12 views
of the heart.
Views reflected on a
12-lead ECG

Lead

View of the
heart

Limb leads (bipolar)
I
Lateral wall
aVL
aVR

II

Inferior wall

III

Inferior wall

I

Augmented limb leads (unipolar)
aVR
No specific view
III

II
aVF

aVL

Lateral wall

aVF

Inferior wall

Precordial, or chest, leads (unipolar)
V1
Septal wall

V1

V4
V2

V3

V2

Septal wall

V6

V3

Anterior wall

V5

V4

Anterior wall

V5

Lateral wall

V6

Lateral wall

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Electrical axis determination:
Quadrant method
This chart will help you quickly determine the direction of a
patient’s electrical axis. Observe the deflections of the QRS
complexes in leads I and aVF. Lead I indicates whether impulses
are moving to the right or left, and lead aVF indicates whether
they’re moving up or down. Then check the chart to determine
whether the patient’s axis is normal or has a left, right, or
extreme right deviation.
• Normal axis: QRS-complex deflection is positive or upright in
both leads.
• Left axis deviation: Lead I is upright and lead aVF points down.
• Right axis deviation: Lead I points down and lead aVF is upright.
• Extreme right axis deviation: Both waves point down.
–90°

Left axis
deviation

Extreme right
axis deviation
I

I

aVF

aVF

⫹180°
–

0°

I

I

aVF

aVF

Right axis
deviation

Normal

⫹90°

12-Lead

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General

12-Lead

Electrical axis determination:
Degree method
The degree method provides a more precise measurement of
the electrical axis. It allows you to identify a patient’s electrical
axis by degrees on the hexaxial system, not just by quadrant.
It also allows you to determine the axis even if the QRS complex
isn’t clearly positive or negative in leads I and aVF. To use this
method, take these steps.

Step 1
Identify the limb lead with the smallest QRS complex or the
equiphasic QRS complex. In this example, it’s lead III.

Lead I

Lead II

Lead III

Lead aVR

Lead aVL

⫺120º

Step 2
Locate the axis for lead III on the
hexaxial diagram. Then find the
axis perpendicular to it, which is
the axis for lead aVR.

Step 3

⫺150º ⫹
⫾180º

⫺90º
II

aVF

Lead aVF

⫺60º

III

⫺

⫺

I

⫹150º

⫺30º

aVL

0º

aVR
⫹

⫹120º

⫹

⫹

⫹60º

⫹30º

Examine the QRS complex in lead
⫹90º
aVR, noting whether the deflection
⫺90º
is positive or negative. As you can
⫺120º aVF ⫺60º
see, the QRS complex for this
III
II
⫺150º ⫹
⫺30º
lead is negative, indicating that
⫺
the current is moving toward the
⫺ 0º
⫾180º I
negative pole of aVR, which is in
the right lower quadrant at +30
aVR ⫹30º
aVL
degrees on the hexaxial diagram.
⫹150º
Normal axis
⫹
⫹
So the electrical axis here is
⫹
⫹120º
⫹60º
normal at +30 degrees.
⫹90º

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Causes of axis deviation
This list covers common causes of right and left axis deviation.

Left

Right

• Normal variation
• Inferior wall MI
• Left anterior hemiblock
• Wolff-Parkinson-White
syndrome
• Mechanical shifts (ascites,
pregnancy, tumors)
• Left bundle-branch block
• Left ventricular hypertrophy
• Aging

• Normal variation
• Lateral wall MI
• Left posterior hemiblock
• Right bundle-branch block
• Emphysema
• Right ventricular hypertrophy

12-Lead

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12-Lead

ECG changes in angina
These are some classic ECG changes involving the T wave and ST
segment that you may see when monitoring a patient with angina.

Peaked T wave

Flattened T wave

T-wave inversion

ST-segment depression with T-wave inversion

ST-segment depression without T-wave inversion

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85

Pericarditis
ECG changes in acute pericarditis evolve through two stages:
• Stage 1—Diffuse ST-segment elevations of 1 to 2 mm in most
limb leads and most precordial leads reflect the inflammatory
process. Upright T waves appear in most leads. The ST-segment
and T-wave changes are typically seen in leads I, II, III, aVR, aVF,
and V2 through V6.
• Stage 2—As pericarditis resolves, the ST-segment elevation
and accompanying T-wave inversion resolves in most leads.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

12-Lead

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12-Lead

Stages of myocardial ischemia, injury,
and infarct

Ischemia
Ischemia is the first stage and indicates that blood flow and oxygen demand are out of balance.
It can be resolved by improving
flow or reducing oxygen needs.
ECG changes indicate ST-segment
depression or T wave changes.

Injury
The second stage, injury, occurs
when the ischemia is prolonged
enough to damage the area of the
heart. ECG changes usually reveal
ST-segment elevation (usually in
two or more contiguous leads).

Infarct
Infarct is the third stage and occurs
with actual death of myocardial
cells. Scar tissue eventually replaces the dead tissue, and the
damage caused is irreversible.
In the earliest stage of an MI,
hyperacute or very tall T waves
may be seen on the ECG. Within
hours, the T waves become inverted and ST-segment elevation occurs in the leads facing the area of
damage. The pathologic Q wave
is the last change to occur in the
evolution of an MI and is the only
permanent ECG evidence of
myocardial necrosis.

86

Myocardial
ischemia

• T-wave inversion
• ST-depression

Myocardial
injury
• ST-segment
elevation
• T-wave inversion

Myocardial
infarction

• Hyperacute
T waves (earliest
stage)

• ST-segment
elevation
• T-wave inversion
• Pathologic
Q waves
– in 90% of
ST-segment
elevation MI
– in 25% non–
ST-segment
elevation MI

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87

Locating myocardial damage
After you’ve noted characteristic lead changes in an acute MI,
use this table to identify the areas of damage. Match the lead
changes (ST elevation, abnormal Q waves) in the second column
with the affected wall in the first column and the artery involved
in the third column. The fourth column shows reciprocal lead
changes.
Wall
affected

Leads

Artery
involved

Reciprocal
changes

Anterior

V2, V3, V4

Left coronary
artery, left anterior
descending (LAD)

II, III, aVF

Anterolateral

I, aVL, V3, V4,
V5, V6

LAD and diagonal
branches, circumflex and marginal
branches

II, III, aVF

Anteroseptal

V1, V2, V3, V4

LAD

None

Inferior

II, III, aVF

Right coronary
artery (RCA)

I, aVL

Lateral

I, aVL, V5, V6

Circumflex branch
of left coronary
artery

II, III, aVF

Posterior

V8, V9

RCA or circumflex

V1, V2, V3, V4 (R
greater than S in V1
and V2, ST-segment
depression, elevated
T wave)

Right
ventricular

V4R, V5R, V6R

RCA

None

12-Lead

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12-Lead

Left ventricular hypertrophy
Left ventricular hypertrophy can lead to heart failure or MI.
The rhythm strips shown here illustrate key ECG changes of
left ventricular hypertrophy as they occur in selected leads:
a large S wave (shaded area in left strip) in V1 and a large R wave
(shaded area in right strip) in V5. If the depth (in mm) of the
S wave in V1 added to the height (in mm) of the R wave in V5
exceeds 35 mm, then the patient has left ventricular hypertrophy.

Lead V1

Lead V5

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89

Wolff-Parkinson-White syndrome
Electrical impulses don’t always follow normal conduction pathways in the heart. In WPW syndrome, electrical impulses enter
the ventricles from the atria through an accessory pathway that
bypasses the AV junction.
WPW syndrome is clinically significant because the accessory
pathway — in this case, Kent’s bundle — may result in paroxysmal
tachyarrhythmias by reentry and rapid conduction mechanisms.

What happens
• A delta wave occurs at the beginning of the QRS complex,
usually causing a distinctive slurring or hump in its initial slope.
• On a 12-lead ECG, the delta wave will be most pronounced in
the leads looking at the part of the heart where the accessory
pathway is located.
• The delta wave shortens the PR interval in WPW syndrome.

Short PR interval

Delta wave

12-Lead

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12-Lead

Understanding RBBB
In RBBB, the initial impulse activates the interventricular septum
from left to right, just as in normal activation (arrow 1). Next,
the left bundle branch activates the left ventricle (arrow 2). The
impulse then crosses the interventricular septum to activate the
right ventricle (arrow 3).
In this disorder, the QRS complex exceeds 0.12 second and
has a different configuration, sometimes resembling rabbit ears
or the letter “M.” Septal depolarization isn’t affected in lead V1,
so the initial small R wave remains.
The R wave is followed by an S wave, which represents left
ventricular depolarization, and a tall R wave (called R prime,
or R’ ), which represents late right ventricular depolarization. The
T wave is negative in this lead; however, the negative deflection
is called a secondary T-wave change and isn’t clinically significant.
The opposite occurs in lead V6. A small Q wave is followed by
depolarization of the left ventricle, which produces a tall R wave.
Depolarization of the right ventricle then causes a broad S wave.
In lead V6, the T wave should be positive.
Block

1
2

3
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91

Recognizing RBBB
This 12-lead ECG shows the characteristic changes of RBBB. In
lead V1, note the rsR⬘ pattern and T-wave inversion. In lead V6,
note the widened S wave and the upright T wave. Also note the
prolonged QRS complexes.

Lead I

Lead aVR

Lead V1

Lead V4

Lead II

Lead aVL

Lead V2

Lead V5

Lead III

Lead aVF

Lead V3

Lead V6

12-Lead

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12:13 PM

12-Lead

Understanding LBBB
In LBBB, an impulse first travels down the right bundle branch
(arrow 1). Then it activates the interventricular septum from right
to left (arrow 2) ventricle, the opposite of normal activation.
Finally, the impulse activates the left ventricle (arrow 3).
On an ECG, the QRS complex exceeds 0.12 second because
the ventricles are activated sequentially, not simultaneously.
As the wave of depolarization spreads from the right ventricle to
the left, a wide S wave appears in lead V1 with a positive T wave.
The S wave may be preceded by a Q wave or a small R wave.
In lead V6, no initial Q wave occurs. A tall, notched R wave, or a
slurred one, appears as the impulse spreads from right to left. This
initial positive deflection is a sign of LBBB. The T wave is negative.
Block

3
1
2

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93

Recognizing LBBB
This 12-lead ECG shows characteristic changes of LBBB. All leads
have prolonged QRS complexes. In lead V1, note the QS wave
pattern. In lead V6, note the slurred R wave and T-wave inversion.
The elevated ST segments and upright T waves in leads V1 and V4
are also common in this condition.

Lead I

Lead aVR

Lead V1

Lead V4

Lead II

Lead aVL

Lead V2

Lead V5

Lead III

Lead aVF

Lead V3

Lead V6

12-Lead

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Treat

Pulseless arrest algorithm
1
Initiate BLS.

2
Check rhythm. Shockable rhythm?

3

YES

9
VF/VT

NO
Asystole/PEA

4

10
• Immediately resume CPR for
5 cycles.
• Give epinephrine 1 mg I.V. or I.O.
Repeat every 3 to 5 min OR give
1 dose of vasopressin 40 units I.V.
or I.O. to replace first or second
dose of epinephrine.
• Consider atropine 1 mg I.V. or I.O.
for asystole or slow PEA rate.
Repeat every 3 to 5 min (up to
3 doses).

• Give 1 shock (biphasic: 120 to
200 joules; monophasic: 360 joules).
• Immediately resume CPR.

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Pulseless arrest algorithm

(continued)

Give 5 cycles of CPR*

5

Check rhythm. Shockable rhythm?
YES

• Continue CPR while charging
defibrillator.
• Give 1 shock (biphasic: same as
first shock or higher dose;
monophasic: 360 joules).
• Immediately resume CPR.
• Epinephrine 1 mg I.V. or I.O.
Repeat every 3 to 5 min OR give
1 dose of vasopressin 40 units I.V.
or I.O. to replace first or second
dose of epinephrine.
Give 5 cycles of CPR*

7

Check rhythm. Shockable rhythm?

8

YES

Give 5 cycles of CPR*

11

Check rhythm. Shockable rhythm?

12

NO

6

NO

13 YES

• If asystole, go to box 10.
• If electrical activity,
check pulse. If no
pulse, go to box 10.
• If pulse present, begin
postresuscitation care.

Go
to
box 4.

NO
* After an advanced airway
is placed, give continuous
chest compressions without
pauses for breaths.

• Continue CPR while charging defibrillator.
• Give 1 shock (biphasic: same as first shock or higher
dose; monophasic: 360 joules).
• Immediately resume CPR.
• Consider antiarrhythmics; give during CPR.
• Consider magnesium, loading dose.
• After 5 cycles of CPR*, go to box 5.

Reprinted with permission. “2005 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care,” Circulation
2005: 112 (suppl IV). © 2005, American Heart Association.

Treat

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Treat

Tachycardia algorithm
1
Tachycardia with pulses
2
• Assess and support ABCs as needed.
• Give oxygen.
• Monitor ECG (identify rhythm), blood pressure,
oximetry.
• Identify and treat reversible causes.
Symptoms persist

Is patient stable?
Unstable signs include altered mental
status, ongoing chest pain, hypotension or other signs of shock.

Unstable

3

4
Perform immediate
synchronized cardioversion
• Establish I.V. access
and give sedation if
patient is conscious; do
not delay cardioversion.
• Consider expert
consultation.
• If pulseless arrest
develops, see pulseless
arrest algorithm.

Stable
5
• Establish I.V. access.
• Obtain 12-lead ECG (when available) or rhythm strip.
Is QRS narrow?
6

Narrow (< 0.12 sec)

12

Narrow QRS*
Is rhythm regular?
Regular
7
• Attempt vagal
maneuvers.
• Give adenosine 6 mg rapid
I.V. push. If no
conversion, give
12 mg rapid
I.V. push; may
repeat 12 mg
dose once.

Irregular
11
Irregular Narrow-Complex
Tachycardia
Probable atrial fibrillation
or possible atrial flutter or
multifocal atrial tachycardia
• Consider expert consultation.
• Control rate (diltiazem,
beta blockers; use beta
blockers with
96caution in
pulmonary disease or CHF).

96

Wide (> 0.12 sec)

Wide QRS*
Is rhythm regular?
Expert consultation advised.

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97

Tachycardia algorithm
8

13

Does rhythm convert?
Note: Consider expert consultation.
Converts

10 Does not convert

If rhythm converts, probably
reentry supraventricular
tachycardia
(SVT)
• Observe for
recurrence.
• Treat
recurrence
with adenosine
or longeracting AV nodal
blocking
agents (such
as diltiazem or
beta blockers).

If rhythm does
NOT convert,
possible atrial
flutter, ectopic
atrial tachycardia,
or junctional
tachycardia
• Control rate
(diltiazem, beta
blockers; use beta
blockers with
caution in pulmonary
disease or CHF).
• Treat underlying
cause.
• Consider expert
consultation.

9

(continued)
Regular

If ventricular
tachycardia or
uncertain
rhythm
• Amiodarone
150 mg I.V. over
10 min. Repeat
as needed to
maximum dose
of 2.2 g/24 hours.
• Prepare for
elective
synchronized
cardioversion.
If SVT with
aberrancy
• Give
adenosine (go
to box 7).

*Note: If patient becomes unstable, go to box 4.

Reprinted with permission. “2005 American Heart
Association Guidelines for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care,” Circulation 2005: 112
(suppl IV). © 2005, American Heart Association.

14

Irregular

If atrial fibrillation with
aberrancy
• See Irregular
NarrowComplex
Tachycardia
(box 11).
If pre-excited
atrial fibrillation
(AF + WPW)
• Expert consultation advised.
• Avoid AV
nodal blocking
agents (adenosine, digoxin,
diltiazem,
verapamil).
• Consider antiarrhythmics
(amiodarone
150 mg I.V.
over 10 min).
If recurrent
polymorphic
VT
• Seek expert
consultation.
If torsades de
pointes
• Give magnesium (load
with 1 to 2 g
over 5 to 60 min,
then infusion).

Treat

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Treat

Bradycardia algorithm
Bradycardia
Heart rate < 60 beats/min and inadequate for clinical condition

•
•
•
•

Maintain patent airway; assist breathing as needed.
Give oxygen.
Monitor ECG (identify rhythm), blood pressure, oximetry.
Establish I.V. access.

Signs or symptoms of poor perfusion caused by bradycardia?
(acute altered mental status, ongoing chest pain, hypotension, or other signs of shock)
Adequate perfusion
Observe/Monitor.

Poor perfusion
• Prepare for transcutaneous pacing; use without
delay for high-degree block (type II second-degree
block or third-degree AV block).
• Consider atropine while awaiting pacer. May repeat
to a total dose of 3 mg. If ineffective, begin pacing.
• Consider epinephrine or dopamine infusion while
awaiting pacer or if pacing ineffective.

• Prepare for transvenous pacing.
• Treat contributing causes.
• Consider expert consultation.

Reprinted with permission. “2005 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care,” Circulation
2005: 112 (suppl IV). © 2005, American Heart Association.

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Guide to antiarrhythmic drugs
This chart details the drugs most commonly used to manage
cardiac arrhythmias, including indications and special considerations for each.
Drugs

Indications

Class IA antiarrhythmics
Disopyramide,
• VT
procainamide,
• Atrial fibrillation
quinidine
• Atrial flutter
• PAT

Class IB antiarrhythmics
• VT
Lidocaine,
• VT
mexiletine
• VF

Class IC antiarrhythmics
Flecainide,
• VT
moricizine,
• VF
propafenone
• Supraventricular
arrhythmias

Special considerations
• Check apical pulse rate before
therapy. If you note extremes in
pulse rate, withhold the dose and
notify the prescriber.
• Use cautiously in patients with reactive airway disease such as asthma.
• Monitor for ECG changes (widening QRS complexes, prolonged QT
interval).
• IB antiarrhythmics may potentiate
the effects of other antiarrhythmics.
• Administer I.V. infusions using an
infusion pump.
• Correct electrolyte imbalances
before administration.
• Monitor the patient’s ECG before
and after dosage adjustments.
• Monitor for ECG changes (widening QRS complexes, prolonged QT
interval).

(continued)

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Guide to antiarrhythmic drugs (continued)
Drugs

Indications

Special considerations

Class II antiarrhythmics
Acebutolol,
• Atrial flutter
atenolol,
• Atrial fibrillation
esmolol,
• PAT
propranolol

• Monitor apical HR and BP.
• Abruptly stopping these drugs can exacerbate angina and precipitate MI.
• Monitor for ECG changes (prolonged PR interval).
• Drugs may mask common signs and
symptoms of shock and hypoglycemia.
• Use cautiously in patients with reactive airway disease such as asthma.

Class III antiarrhythmics
Amiodarone,
• Life-threatening
dofetilide,
arrhythmias reibutilide,
sistant to other
sotalol
antiarrhythmic
drugs

• Monitor BP and heart rate and
rhythm for changes.
• Amiodarone increases the risk of
digoxin toxicity in patients also taking
digoxin.
• Monitor for signs of pulmonary toxicity (nonproductive cough, dyspnea,
and pleuritic chest pain), thyroid dysfunction, and vision impairment in
patients taking amiodarone.
• Monitor for ECG changes (prolonged QT interval) in patients taking
dofetilide, ibutilide, and sotalol.

Class IV antiarrhythmics
Diltiazem,
• Supraventricular
verapamil
arrhythmias

• Monitor heart rate and rhythm and
BP carefully when initiating therapy
or increasing dosage.
• Calcium supplements may reduce
effectiveness.

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Guide to antiarrhythmic drugs (continued)
Drugs

Indications

Miscellaneous antiarrhythmics
• PSVT
Adenosine

Special considerations
• Adenosine must be administered
over 1 to 2 seconds, followed by a
20-ml flush of normal saline solution.
• Record rhythm strip during administration. Adenosine may cause
transient asystole or heart block.

Atropine

• Symptomatic SB
• AV block
• Asystole
• Bradycardic
PEA

• Monitor heart rate and rhythm. Use
the drug cautiously in patients with
myocardial ischemia.
• Atropine isn’t recommended for
third-degree AV block or infranodal
type II second-degree AV block.
• In adults, avoid doses less than
0.5 mg because of the risk of paradoxical slowing of the HR.

Epinephrine

• Pulseless VT
• VF
• Asystole
• PEA

• Monitor heart rate and rhythm and
BP carefully because the drug may
cause myocardial ischemia.
• Don’t mix an I.V. dose with alkaline
solutions.
• Give drug into a large vein to
prevent irritation or extravasation
at site.

Vasopressin

• VF that’s unresponsive to
defibrillation

• Monitor heart rate and rhythm. Use
the drug cautiously in patients with
myocardial ischemia.
• Monitor for hypersensitivity reactions, especially urticaria, angioedema, and bronchoconstriction.

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Defibrillator paddle placement
Anterolateral
placement
Place one paddle to the
right of the upper sternum, just below the right
clavicle, and the other
over the fifth or sixth intercostal space at the left
anterior axillary line.

Anteroposterior placement
Place the anterior paddle directly over the heart at the precordium, to the left of the lower sternal border. Place the flat posterior paddle under the patient’s body beneath the heart and just
below the left scapula (but not under the vertebral column).

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Safety issues with defibrillation
Precautions must be taken when defibrillating a patient with an
ICD, a pacemaker, or a transdermal medication patch or a patient who’s in contact with water.

Defibrillating a patient with an ICD or pacemaker
Avoid placing the defibrillator paddles or pads directly over the
implanted device. Place them at least 1” (2.5 cm) away from the
device.

Defibrillating a patient with a transdermal
medication patch
Avoid placing the defibrillator paddles or pads directly on top
of a transdermal medication patch, such as a nitroglycerin,
nicotine, analgesic, or hormone replacement patch. The patch
can block delivery of energy and cause a small burn to the
skin. Remove the medication patch and wipe the area clean
before defibrillation.

Defibrillating a patient near water
Water is a conductor of electricity and may provide a pathway
for energy from the defibrillator to the rescuers treating the victim. Remove the patient from freestanding water and dry his
chest before defibrillation.

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Monophasic and biphasic defibrillators
Monophasic defibrillators

Energy efficient

Monophasic
defibrillators
Current
deliver a sinflow
gle current
of electricity
that travels
in one direction between
the two pads
or paddles
on the patient’s chest. To be
effective, a large amount of
electrical current is required for
monophasic defibrillation.

Biphasic defibrillators
Biphasic
defibrillators
Current
have the
flow
same pad
or paddle
placement
as with the
Current
monophasic
flow
defibrillator.
The difference is that during biphasic
defibrillation, the electrical current discharged from the pads
or paddles travels in a positive
direction for a specified duration and then reverses and
flows in a negative direction
for the remaining time of the
electrical discharge.

The biphasic defibrillator delivers two currents of electricity
and lowers the defibrillation
threshold of the heart muscle,
making it possible to successfully defibrillate VF with smaller amounts of energy.

Adjustable
The biphasic defibrillator can
adjust for differences in impedance or resistance of the current through the chest. This
reduces the number of shocks
needed to terminate VF.

Less myocardial damage
Because