476200FM_rev.qxd 51309 12:12 PM Page iii [604200]

476200FM_rev.qxd 5/13/09 12:12 PM Page iii

Staff
Executive Publisher
Judith A. Schilling McCann, RN, MSN
Clinical DirectorJoan M. Robinson,
RN, MSN
Art DirectorElaine 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. RuhfThe clinical treatments described and recom-
mended in this publication are based onresearch and consultation with nursing, med-ical, and legal authorities. To the best of ourknowledge, these procedures reflect currentlyaccepted practice. Nevertheless, they can’t beconsidered absolute and universal recommen-dations. For individual applications, all recom-mendations must be considered in light of thepatient’s clinical condition and, before adminis-tration of new or infrequently used drugs, inlight of the latest package-insert information.The authors and publisher disclaim anyresponsibility for any adverse effects resultingfrom the suggested procedures, from anyundetected errors, or from the reader’s misunderstanding of the text.
© 2010 by Lippincott Williams & Wilkins. All
rights reserved. This book is protected by copy-right. No part of it may be reproduced, stored ina retrieval system, or transmitted, in any form or by any means—electronic, mechanical, photocopy, recording, or otherwise—withoutprior written permission of the publisher, exceptfor brief quotations embodied in critical articlesand reviews and testing and evaluation materi-als provided by publisher to instructors whoseschools have adopted its accompanying text-book. For information, write Lippincott Williams& Wilkins, 323 Norristown Road, Suite 200,Ambler, PA 19002-2756.
Printed in China.ECGMIQ2-010909ISBN-13: 978-1-60547-476-2
ISBN-10: 1-60547-476-2 476200FM_rev.qxd 5/13/09 12:12 PM Page iv

Most bedside monitoring systems allow for simultaneous
monitoring of two leads, such as lead II with V1or 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 V
1and V6or the
bipolar leads MCL1and MCL6are the best leads for monitor-
ing rhythms with wide QRS complexes and for differentiat-ing VT from SVT with aberrancy.
This table lists the best leads for monitoring challenging
cardiac arrhythmias.Best monitoring leads
Arrhythmia
PACs
AT
PAT
Atrial flutter
Atrial fibrillation
PJCs
Junctional escape rhythm
Junctional tachycardia
PVCs
Idioventricular rhythm
VT
VF
Torsades de pointes
Third-degree AV blockBest monitoring leads
II or lead that shows best P waves
II, V1, V6, MCL1, MCL6
II, V1, V6, MCL1, MCL6
II, IIIII (or identified in most leads by fibrillatory waves and irregular R-R)IIIIII, V
1, V6, MCL1, MCL6
V1, V6, MCL1, MCL6
V1, V6, MCL1, MCL6
V1, V6, MCL1, MCL6
AnyAnyII or lead that shows best P wavesand QRS complexes 476200FM_rev.qxd 5/13/09 12:12 PM Page ii

GeneralHeart 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 idioventricularrhythm, VT, torsades de pointes, VF, asystole, PEA
First-degree AV block, second-degree AVblock, third-degree AV block
Lead placement, electricalaxis, angina, pericarditis,MI, LVH, WPW, RBBB, LBBB
Algorithms,drugs, defibrillation,pacemaker,ICDSA Node
AtrialJunctionalVentricularAV Block12-LeadTreatment 476200FM_rev.qxd 5/13/09 12:12 PM Page v

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 cardioverter-
defibrillator
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 leadMI. . . . . . 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)Common abbreviations 476200FM_rev.qxd 5/13/09 12:12 PM Page vi

LWBK942-FM.qxd 6/25/11 8:45 AM Page x

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’smidline.1
GeneralWhere the heart lies
Base
MidlineSecond
intercostalspace
Fifth
intercostalspace
Apex 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 1

2General
Coronary vessels
Anterior view
Left
subclavianartery
Aortic arch
Pulmonary
trunk
Great cardiac
vein
Circumflex
branch of leftcoronaryarteryLeft commoncarotid artery
Brachiocephalic
artery
Superior vena
cava
Right atrium
Right
coronary artery
Small
cardiac vein
Anterior
interventricular(descending)branch of leftmain coronary artery 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 2

3
GeneralCoronary vessels (continued)
P osterior 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 veinBrachiocephalicartery
Aortic arch
Superior vena
cava
Right pulmonary
veins
Right atrium
Inferior vena
cava
Small cardiac vein
Right coronary
artery
Posterior
interventricular(descending)branch of rightcoronary artery 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 3

4General
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.
1 mV
3 sec0.04
sec0.20
secAmplitude
or voltage0.5 mV
(5 mm)0.1 mV
(1 mm)
Time (in seconds) 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 4

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 isequilateral.
The axis of lead I extends from shoulder to shoulder, with the
right-arm lead being the negative electrode and the left-armlead being the positive electrode. The axis of lead II runs fromthe negative right-arm lead electrode to the positive left-leg leadelectrode. The axis of lead III extends from the negative left-armlead electrode to the positive left-leg lead electrode.Einthoven’s triangle5
General
Lead IRight arm Left arm
Left legLead IIILead II/H11001 /H11002
/H11002 /H11002
/H11001/H11001 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 5

6General
Leads aVR, aVL, and aVFare called augmented leads. They
measure electrical activity between one limb and a single
electrode. Lead aVRprovides no specific view of the heart.
Lead aVLshows electrical activity coming from the heart’s
lateral wall. Lead aVFshows electrical activity coming from
the heart’s inferior wall.Augmented leads
/H11001 /H11001
/H11001aVR aVL
aVFRight arm Left arm
Left leg 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 6

7
GeneralP ositioning cardiac monitoring leads
Lead I Lead I
RA LA
C
RLLLRA LA
LL
Lead II Lead II
RA LA
C
RLLLRA LA
LL
Lead III Lead III
RA LA
C
RLLLRA LA
LL
Lead
MCL1LeadMCL
1RA LA
C
RLLLRA LA
LL
Lead
MCL6LeadMCL
6 RA LA
C
RLLLRA LA
LLFive-leadwire system Three-leadwire system 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 7

8General
Normal ECG
0.12–0.20 sec
0.06–0.10 sec
0.36–0.44 sec 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 8

9
GeneralQTc interval normals
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 ap-proach. The eight-step method outlined below provides just that.
Eight-step method
1.Determine the rhythm.
2.Determine the rate.
3.Evaluate the P wave.
4.Measure the PR interval.
5.Determine the QRS duration.
6.Examine the T waves.
7.Measure the QT interval.
8.Check for ectopic beats and other abnormalities.Heart rate
(per minute)
40
5060708090100120150180200QTc intervalnormal range(seconds)
0.41 – 0.51
0.38 – 0.460.35 – 0.430.33 – 0.410.32 – 0.390.30 – 0.360.28 – 0.340.26 – 0.320.23 – 0.280.21 – 0.250.20 – 0.24 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 9

10General
P aper-and-pencil method
• Position the straight edge of
a piece of paper along thestrip’s baseline.• Move the paper up slightlyso the straight edge is nearthe peak of the R wave.• With a pencil, mark the paperat the R waves of two consecu-tive QRS complexes, as shownbelow. This is the R-R interval.• Move the paper across thestrip lining up the two markswith succeeding R-R intervals.If the distance for each R-R in-terval is the same, the ventric-ular rhythm is regular. If thedistance varies, the rhythm isirregular.• Use the same method tomeasure the distance betweenP waves (the P-P interval) anddetermine whether the atrialrhythm is regular or irregular. Calipers method
• With the ECG on a flat sur-face, place one point of thecalipers on the peak of thefirst R wave of two consecu-tive QRS complexes.• Adjust the calipers’ legs sothe other point is on the peakof the next R wave, as shownbelow. The distance is the R-Rinterval.• Pivot the first point of thecalipers toward the third Rwave and note whether it fallson the peak of that wave.• Check succeeding R-R inter-vals in the same way. If they’reall the same, the ventricularrhythm is regular. If they vary,the rhythm is irregular.• Using the same method,measure the P-P intervals todetermine whether the atrialrhythm is regular or irregular.Methods of measuring rhythm
476201BASIC_rev.qxd 5/13/09 12:14 PM Page 10

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)P aroxysm or burst (as in PAT)The more you look at rhythm strips, the more you’ll notice pat-
terns. The symbols below represent some of the patterns youmight see as you study rhythm strips.11
GeneralRhythm strip patterns
476201BASIC_rev.qxd 5/13/09 12:14 PM Page 11

12General
This table can help
make the sequencingmethod of determin-ing heart rate moreprecise. After countingthe number of blocksbetween R waves, usethis table to find therate. For example, ifyou count 20 smallblocks or 4 large blocksbetween R waves, theheart rate is 75 beats/minute. To calculatethe atrial rate, followthe same method using P waves.
Rapid estimate
This rapid-rate cal-culation is also calledthe
countdown
method. Using the
number of largeblocks between R waves or P waves as a guide, you canrapidly estimate ven-tricular or atrial ratesby memorizing the sequence “300, 150,100, 75, 60, 50.”Calculating heart rate
Number of small blocks
5 (1 large block)
678910 (2 large blocks)1112131415 (3 large blocks)1617181920 (4 large blocks)2122232425 (5 large blocks)2627282930 (6 large blocks)3132333435 (7 large blocks)3637383940 (8 large blocks)Heart rate
300
25021418816715013612511510710094888379757168656360585654525048474544434241393837
476201BASIC_rev.qxd 5/13/09 12:14 PM Page 12

13
GeneralIn 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 anormal response when a child is crying or otherwise upset.Keep in mind that, because HR varies considerably from theneonate to the adolescent, one definition of bradycardia ortachycardia can’t fit all children.Bradycardia and tachycardia in children
Normal heart rates in children
Age
Neonate
1 wk-3 mo3 mo-2 yr2-10 yr> 10 yrAwake
(beats/min)
100-160
100-22080-15070-11055-100Asleep
(beats/min)
80-140
80-20070-12060-9050-90Exercise or
fever(beats/min)
< 220
< 220< 200< 200< 200 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 13

14General
ECG effects of electrolyte imbalances
Imbalance
Hypercalcemia
Hypocalcemia
Hyperkalemia
HypokalemiaKey finding
Shortened
QT interval
Prolonged
QT interval
Tall, peaked
T waves
Flat T wave;
U wave appearsOther possible findings
• Prolonged PR interval
• Prolonged QRS complex• Depressed T wave
• Flat or inverted T wave
• Prolonged ST segment
• Low amplitude P wave (mild
hyperkalemia)• Wide, flattened P wave (moderatehyperkalemia)• Indiscernible P wave (severe hyperkalemia)• Widened QRS complex• Shortened QT interval• Intraventricular conduction disturbances• Elevated ST segment (severe hyperkalemia)
• Peaked P wave (severe
hypokalemia)• Prolonged QRS complex (severehypokalemia)• Depressed ST segment 476201BASIC_rev.qxd 5/13/09 12:14 PM Page 14

Rhythm
• Atrial: regular
• Ventricular: regular
Rate
• 60 to 100 beats/minute (SAnode’s normal firing rate)
P Wave
• Normal shape (round andsmooth)• Upright in lead II• One for every QRS complex• All similar in size and shape
PR Interval
• Within normal limits (0.12 to0.20 second)QRS complex
• Within normal limits (0.06 to0.10 second)
T wave
• Normal shape• Upright and rounded in lead II
QT interval
• Within normal limits (0.36 to0.44 second)
Other
• Represents normal cardiacconduction as the standardagainst which all otherrhythms are compared• No ectopic or aberrant beats15
SA NodeNormal sinus rhythm
476202SANODE_rev.qxd 5/13/09 12:15 PM Page 15

16SA Node
Rhythm
• Irregular
• Corresponds to the respiratorycycle• P-P interval and R-R intervalshorter during inspiration;longer during expiration• Difference between longestand shortest P-P interval exceeds 0.12 second
Rate
• Usually within normal limits(60 to 100 beats/minute)• Varies with respiration• Increases during inspiration• Decreases during expiration
P wave
• Normal size• Normal configurationPR interval
• May vary slightly• Within normal limits
QRS complex
• Preceded by P wave
T wave
• Normal size• Normal configuration
QT interval
• May vary slightly• Usually within normal limits
Other
• Phasic slowing and quickeningSinus arrhythmia
Expiration Inspiration Expiration 476202SANODE_rev.qxd 5/13/09 12:15 PM Page 16

17
SA NodeSinus arrhythmia (continued)
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 (com-monly insignificant)• Increased peripheral pulserate during inspiration• Decreased peripheral pulserate during expiration• Possible disappearance of arrhythmia when HR increas-es, such as during exercise• Signs and symptoms of underlying condition, if present• Dizziness or syncope (withmarked sinus arrhythmia)
What to do
• Monitor heart rhythm.• If sinus arrhythmia developssuddenly in patient takingdigoxin, notify doctor.• If induced by drugs (mor-phine or another sedative),notify doctor, who will decidewhether to continue giving thedrug.
How it’s treated
• Usually no treatment if patient asymptomatic• If unrelated to respiration(abnormal), treatment of underlying cause 476202SANODE_rev.qxd 5/13/09 12:15 PM Page 17

18SA Node
Rhythm
• Regular
Rate
• Less than 60 beats/minute
P wave
• Normal size
• Normal configuration• P wave before each QRScomplex
PR interval
• Within normal limits• ConstantQRS complex
• Normal duration• Normal configuration
T wave
• Normal size• Normal configuration
QT interval
• Within normal limits• Possibly prolongedSinus bradycardia
476202SANODE_rev.qxd 5/13/09 12:15 PM Page 18

19
SA NodeSinus bradycardia (continued)
What causes it
• Cardiomyopathy
• Conditions that increase vagal stimulation such asvomiting• Drugs
– Antiarrhythmics (amio-darone, propafenone, quini-dine, 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-inducedsyncope (known as a
Stokes-
Adams attack )
If patient can compensate
for decreased CO
• No symptomsIf patient can’t compensate
• Altered mental status
• Blurred vision• Chest pain• Cool, clammy skin• Crackles• Dizziness• Dyspnea • Hypotension•S
3heart sound, indicating
heart failure• Syncope
What to do
• Observe patient and monitorheart rhythm for bradycardiaprogression.• Evaluate patient’s tolerancefor rhythm at rest and with activity.• Prepare patient for treat-ments, as needed, such asdrug administration (atropine,dopamine, epinephrine) ortemporary or permanent pacemaker insertion.
How it’s treated
• No treatment if patientasymptomatic• If symptomatic, correction of underlying cause • Bradycardia algorithm guidelines 476202SANODE_rev.qxd 5/13/09 12:15 PM Page 19

20SA Node
Rhythm
• Regular
Rate
• Greater than 100 beats/minute
P wave
• Normal size
• Normal configuration• May increase in amplitude• Precedes each QRS complex• As HR increases, possibly superimposed on precedingT wave and difficult to identifyPR interval
• Within normal limits• Constant
QRS complex
• Normal duration • Normal configuration
T wave
• Normal size• Normal configuration
QT interval
• Within normal limits• Commonly shortenedSinus tachycardia
476202SANODE_rev.qxd 5/13/09 12:15 PM Page 20

21
SA NodeSinus tachycardia (continued)
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 toexercise, fever, stress, anxiety,or pain
What to look for
• Peripheral pulse rate above100 beats/minute• Regular rhythm If CO falls and compensatory
mechanisms fail
• Anxiety• Blurred vision• Chest pain• Hypotension• Nervousness• Palpitations• Syncope
If heart failure develops
• Crackles•S
3heart sound
• Jugular vein distention
What to do
• Monitor heart rhythm.• Notify doctor promptly if sinus tachycardia arises suddenly after MI. • Provide calm environment andteach relaxation techniques.
How it’s treated
• No treatment if patientasymptomatic• Correction of underlyingcause• For cardiac ischemia: Beta-adrenergic blockers (propran-olol, atenolol) or calciumchannel blockers (verapamil,diltiazem)• Abstinence from triggers (alcohol, caffeine, nicotine) 476202SANODE_rev.qxd 5/13/09 12:15 PM Page 21

22SA Node
Rhythm
• Regular except during arrest
(irregular as result of missingcomplexes)
Rate
• Usually within normal limits(60 to 100 beats/minute) beforearrest• Length or frequency of pausemay result in bradycardia
P wave
• Periodically absent, with entirePQRST complexes missing• When present, normal sizeand configuration• Precedes each QRS complex
PR interval
• Within normal limits when aP wave is present• Constant when a P wave ispresentQRS complex
• Normal duration• Normal configuration• Absent during arrest
T wave
• Normal size• Normal configuration• Absent during arrest
QT interval
• Within normal limits• Absent during arrest
Other
• The pause isn’t a multiple ofthe underlying P-P intervals• Junctional escape beats mayoccur at end of pauseSinus arrest
476202SANODE_rev.qxd 5/13/09 12:15 PM Page 22

23
SA NodeSinus 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 orcarotid sinus sensitivity• Salicylate toxicity• Sinus node disease• SSS
What to look for
• Absence of heart sounds andpulse during arrest• Absence of symptoms withshort pauses• Evidence of decreased COwith recurrent or prolongedpauses
– 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 near-syncopal episodes caused byprolonged pause.
How it’s treated
• No treatment if patientasymptomatic• If symptoms, follow brady-cardia algorithm• As needed, discontinuationof drugs affecting SA nodedischarge or conduction, suchas beta-adrenergic blockers,calcium channel blockers, anddigoxin 476202SANODE_rev.qxd 5/13/09 12:15 PM Page 23

24SA Node
Rhythm
• Regular except during a
pause (irregular as result of apause)
Rate
• Usually within normal limits(60 to 100 beats/minute) beforea pause• Length or frequency of pausemay result in bradycardia
P wave
• Periodically absent, with en-tire PQRST complex missing• When present, normal sizeand configuration and pre-cedes each QRS complex
PR interval
• Within normal limits• Constant when a P wave ispresentQRS complex
• Normal duration• Normal configuration• Absent during a pause
T wave
• Normal size• Normal configuration• Absent during a pause
QT interval
• Within normal limits• Absent during a pause
Other
• The pause is a multiple ofthe underlying P-P intervalSinoatrial exit block
476202SANODE_rev.qxd 5/13/09 12:15 PM Page 24

25
SA NodeSinoatrial exit block (continued)
What causes it
• Acute infection
• Acute inferior-wall MI• Acute myocarditis• Cardioactive drugs
– Amiodarone– Beta-adrenergic blockers(bisoprolol, metoprolol, pro-pranolol)– 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 andpulse during SA exit block• Absence of symptoms withshort pauses• Evidence of decreased COwith recurrent or prolongedpauses
– 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 re-sult from syncopal or near-syncopal episodes caused byprolonged pause.
How it’s treated
• No treatment if patientasymptomatic• If symptomatic, guidelinesfor symptomatic bradycardiaresponse• As needed, discontinuationof drugs affecting SA nodedischarge or conduction, suchas beta-adrenergic blockers,calcium channel blockers, anddigoxin 476202SANODE_rev.qxd 5/13/09 12:15 PM Page 25

26SA Node
Rhythm
• Irregular
• Sinus pauses• Abrupt rate changes
Rate
• Fast, slow, or alternating• Interrupted by a long sinuspause
P wave
• Varies with rhythm changes• May be normal size and configuration• May be absent• Usually precedes each QRScomplex
PR interval
• Usually within normal limits• Varies with rhythm changesQRS complex
• Duration within normal limits• Varies with rhythm changes• Normal configuration
T wave
• Normal size• Normal configuration
QT interval
• Usually within normal limits• Varies with rhythm changes
Other
• Usually more than one arrhythmia on a 6-second stripSick sinus syndrome
476202SANODE_rev.qxd 5/13/09 12:15 PM Page 26

27
SA NodeSick sinus syndrome (continued)
What causes it
• Autonomic disturbances that
affect autonomic innervation
– Degeneration of autonomicsystem– Hypervagotonia
• Cardioactive drugs
– Beta-adrenergic blockers– Calcium channel blockers– Digoxin
• Conditions leading to fibrosisof SA node
– Advanced age– Atherosclerotic heart disease– Cardiomyopathy– Hypertension
• Inflammation of atrial wallaround SA node • Trauma to SA node
– Open-heart surgery, espe-cially valve surgery– Pericarditis– Rheumatic heart disease
What to look for
• Changes in heart rate andrhythm• Episodes of tachy-brady syn-drome, atrial flutter, atrial fibril-lation, SA block, or sinus arrest• Syncope (Stokes-Adams attacks)If underlying cardiomyopathy
present
• Dilated and displaced left
ventricular apical impulse• Possible crackles•S
3heart sound
If thromboembolism present
• Acute chest pain• Dyspnea or tachypnea• Fatigue• Hypotension• Neurologic changes (confu-sion, vision disturbances,weakness)
What to do
• Monitor for changes in heartrhythm.• Prepare patient for possibletreatment interventions.
How it’s treated
• No treatment if patientasymptomatic• If symptomatic, correction ofunderlying cause• Insertion of temporary pace-maker (transcutaneous ortransvenous)• If arrhythmia due to chronic dis-order: digoxin, beta-adrenergicblocker, radio-frequency abla-tion, or permanent pacemaker • Anticoagulant for atrial fibrillation 476202SANODE_rev.qxd 5/13/09 12:15 PM Page 27

28Atrial
Rhythm
• Atrial: Irregular
• Ventricular: Irregular• Underlying: Possibly regular
Rate
• Atrial and ventricular: Varywith underlying rhythm
P wave
• Premature• Abnormal configurationcompared to a sinus P wave• If varying configurations,multiple ectopic sites• May be hidden in precedingT wave (see shaded area onstrip)
PR interval
• Usually within normal limits• May be shortened or slightlyprolonged for the ectopic beatQRS complex
• Conducted: Duration andconfiguration usually normal• Nonconducted: No QRScomplex follows PAC
T wave
• Usually normal• May be distorted if P wave ishidden 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 (everythird beat premature)• May be quadrigeminal (everyfourth beat premature)• May occur in couplets (pairs)• Three or more PACs in a rowindicate atrial tachycardia
Premature atrial contractions 476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 28

29
AtrialPremature atrial contractions (continued)
What causes them
• Enhanced automaticity in
atrial tissue (most commoncause)• Acute respiratory failure• COPD• Coronary heart disease• Digoxin toxicity• Drugs that prolong absoluterefractory period of SA node
– Procainamide– Quinidine
• Electrolyte imbalances• Endogenous catecholaminerelease 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 thatreflect underlying rhythm• Irregular peripheral or apicalpulse rhythm when PACs occur• Evidence of decreased CO,such as hypotension and syncope, if patient has heartdiseaseWhat to do
• Monitor heart rhythm.• If patient has ischemic orvalvular heart disease, watchfor evidence of heart failure,electrolyte imbalances, andmore severe atrial arrhyth-mias.
Note: In patients with
acute MI, PACs may be earlysigns of heart failure or anelectrolyte imbalance.• Teach patient to correct oravoid underlying causes ortriggers such as caffeine. • Demonstrate stress-reductiontechniques to lessen anxiety.
How they’re treated
• Usually no treatment if patient asymptomatic • If symptomatic, eliminationor control of triggers• For frequent PACs: drugsthat prolong atrial refractoryperiod, such as beta-adrenergicblockers and calcium channelblockers 476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 29

30Atrial
Rhythm
• Atrial: Usually regular
• Ventricular: Regular or irreg-ular depending on AV conduc-tion ratio and type of atrialtachycardia
Rate
• Atrial: Three or more consec-utive ectopic atrial beats at150 to 250 beats/minute;rarely exceeds 250 beats/minute• Ventricular: Varies, depend-ing on AV conduction ratio
P wave
• Deviates from normal appearance• May be hidden in precedingT wave• If visible, usually upright andprecedes each QRS complex
PR interval
• May be difficult to measure ifP wave can’t be distinguishedfrom preceding T waveQRS complex
• Usually normal duration andconfiguration• May be abnormal if impulsesconducted abnormallythrough ventricles
T wave
• Usually visible• May be distorted by P wave• May be inverted if ischemiais present
QT interval
• Usually within normal limits• May be shorter because ofrapid rate
Other
• May be difficult to differenti-ate atrial tachycardia withblock from sinus arrhythmiawith U wavesAtrial tachycardia
476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 30

31
AtrialAtrial tachycardia (continued)
What causes it
• Digoxin toxicity (most common)
• Cardiomyopathy• COPD• Congenital anomalies• Cor pulmonale• Drugs
– Albuterol– Cocaine– Theophylline
• Electrolyte imbalances• Hyperthyroidism• Hypoxia•M I• Physical or psychological stress• Systemic hypertension• Triggers (alcohol, caffeine,nicotine)• Valvular heart disease• WPW syndrome
What to look for
• Rapid HR• Sudden feeling of palpita-tions, especially with PAT• Signs of decreased CO (hypo-tension, chest pain, syncope)
What to do
• Monitor heart rhythm.• Assess patient for digoxintoxicity; monitor digoxinblood level.• Keep resuscitative equip-ment readily available if vagalmaneuvers are used.
How it’s treated
• Treatment dependent ontype of tachycardia and symptom severity; directed toward eliminating cause anddecreasing ventricular rate• Possibly Valsalva’s maneuveror carotid sinus massage totreat PAT• Drug therapy (pharmacologiccardioversion): adenosine,amiodarone, beta-adrenergicblockers, calcium channelblockers, digoxin• If patient unstable, possiblesynchronized electrical cardio-version• Atrial overdrive pacing • If arrhythmia related to WPWsyndrome, possible catheterablation• In patient with COPD, correc-tion of hypoxia and electrolyteimbalances 476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 31

Rhythm
• Atrial: Irregular
• Ventricular: Irregular
Rate
• Atrial: 100 to 250 beats/minute (usually less than160 beats/minute)• Ventricular: 100 to 250 beats/minute
P wave
• Configuration: Varies• At least three different P waveshapes must appearPR interval
• Varies
QRS complex
• Usually normal• May become aberrant if arrhythmia persists
T wave
• Usually distorted
QT interval
• May be indiscernible
32Atrial
Multifocal atrial tachycardia
476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 32

Rhythm
• Atrial: Regular
• Ventricular: Regular
Rate
• Atrial: 150 to 250 beats/minute• Ventricular: 150 to 250 beats/minute
P wave
• May not be visible• May be difficult to distinguishfrom preceding T wave
PR interval
• May not be measurable ifP wave can’t be distinguishedfrom preceding T waveQRS complex
• Usually normal; may beaberrantly conducted
T wave
• Usually indistinguishable
QT interval
• May be indistinguishable
Other
• Sudden onset, typically started by PAC; may start and stopabruptly33
AtrialP aroxysmal atrial tachycardia
476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 33

34Atrial
Rhythm
• Atrial: Regular
• Ventricular: Typically regular,although cycles may alternate(depends on AV conductionpattern)
Rate
• Atrial: 250 to 400 beats/minute• Ventricular: Usually 60 to150 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/minuteatrial and 150 beats/minuteventricular; known as
2:1 block
• Only every second, third, orfourth impulse is conducted toventricles because the AV nodeusually won’t accept more than180 impulses/minute• When atrial flutter is first rec-ognized, ventricular rate typicallyexceeds 100 beats/minuteP wave
• Abnormal• Sawtoothed appearance knownas
flutter waves or F waves
PR interval
• Not measurable
QRS complex
• Duration: Usually within normallimits• May be widened if flutter wavesare buried within the complex
T wave
• Not identifiable
QT interval
• Not measurable because T wave isn’t identifiable
Other
• Atrial rhythm may vary betweena fibrillatory line and flutter waves (called
atrial fib-flutter ), with an
irregular ventricular response• May be difficult to differentiateatrial flutter from atrial fibrillationAtrial flutter
476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 34

35
AtrialAtrial flutter (continued)
What causes it
• Cardiac surgery with acute MI
• Conditions that enlarge atrial tissue and elevate atrialpressures• COPD• Digoxin toxicity• Hyperthyroidism•M I• Mitral or tricuspid valve disease• Pericardial disease• Systemic arterial hypoxia
What to look for
• Possibly no symptoms ifventricular rate is normal• Rapid HR if ventricular rate israpid (complaint of palpitations)• Evidence of reduced CO ifventricular rate is rapid• Evidence of reduced ventric-ular filling time and coronaryperfusion from rapid ventricu-lar rate
– Angina– Heart failure– Hypotension– Pulmonary edema– SyncopeWhat to do
• Monitor heart rhythm.• Keep resuscitative equipmentat bedside; be alert for brady-cardia because cardioversioncan decrease HR.• Be alert for effects of digoxin,which depresses SA node.• Monitor patient closely forevidence of low CO.
How it’s treated
• If patient hemodynamicallyunstable and with atrial flutterof 48 hours or less, immediatesynchronized electrical cardio-version• With atrial flutter of morethan 48 hours, anticoagula-tion therapy bef ore and after
cardioversion• With normal heart function:beta-adrenergic blockers, suchas metoprolol, or calciumchannel blockers such as diltiazem• With impaired heart function(heart failure or EF below40%): digoxin or amiodarone• Ablation therapy for recurrentatrial flutter 476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 35

36Atrial
Rhythm
• Atrial: Irregularly irregular
• Ventricular: Irregularly irregular
Rate
• Atrial: Almost indiscernible,usually above 400 beats/minute; far exceeds ventricular ratebecause most impulses aren’tconducted through the AVjunction• Ventricular: Usually 100 to150 beats/minute but can bebelow 100 beats/minute
P wave
• Absent• Replaced by baseline fibrilla-tory waves that represent atrialtetanization from rapid atrialdepolarizationsPR interval
• Indiscernible
QRS complex
• Duration and configurationusually normal
T wave
• Indiscernible
QT interval
• Not measurable
Other
• Atrial rhythm may vary between fibrillatory line and flutterwaves (called
atrial fib-flutter )
• May be difficult to differenti-ate atrial fibrillation from atrialflutter and MATAtrial fibrillation
476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 36

37
AtrialAtrial fibrillation (continued)
What causes it
• Acute MI
• Atrial septal defect• CAD• Cardiac surgery • Cardiomyopathy• COPD• Digoxin toxicity• Drugs such as aminophylline• Endogenous catecholaminereleased during exercise• Hypertension• Hyperthyroidism• Pericarditis• Rheumatic heart disease• Triggers (alcohol, caffeine,nicotine)• Valvular heart disease (espe-cially mitral valve disease)
What to look for
• Irregularly irregular pulserhythm with normal or abnormal HR• Radial pulse rate that’s slowerthan apical pulse rate• Evidence of decreased CO (light-headedness, hypotension)• Possibly no symptoms withchronic atrial fibrillation
What to do
• Monitor heart rhythm.• Monitor for evidence of decreased cardiac output andheart failure. If patient isn’t oncardiac monitor, be alert for irregular pulse and differencesin radial and apical pulse rates.• If drug therapy is used, mon-itor serum drug levels; watchfor evidence of toxicity. • Tell patient to report changesin pulse rate, dizziness, faint-ness, chest pain, and signs ofheart failure, such as dyspneaand peripheral edema.
How it’s treated
• Drug therapy to control ven-tricular response, or electrical cardioversion with drug therapy• If patient hemodynamicallyunstable, immediate synchro-nized cardioversion (most suc-cessful if done within 48 hoursafter atrial fibrillation onset) • With atrial fibrillation ofmore than 48 hours: anti-coagulation before and aftercardioversion • With otherwise normal heartfunction: beta-adrenergicblockers, such as metoprolol,or calcium channel blockerssuch as diltiazem• With impaired heart function(heart failure or EF below40%): digoxin or amiodarone• Radio-frequency ablationtherapy for unresponsivesymptomatic atrial fibrillation 476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 37

38Atrial
Rhythm
• Atrial: Irregular
• Ventricular: Irregular
Rate
• Reflects the underlyingrhythm
P wave
• May be visible• Abnormal configuration• Unchanged if present in theunderlying rhythm
PR interval
• Commonly changes on thepremature beat, if measurableat all
QRS complex
• Altered configuration withRBBB patternT wave
• Deflection opposite that ofQRS complex in most leadsbecause of RBBB
QT interval
• Usually changed because ofRBBB
Other
• No compensatory pause after an aberrant beat• Aberrancy may continue forseveral beats and typicallyends a short cycle precededby a long cycleAshman’s phenomenon
476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 38

39
AtrialAshman’s phenomenon (continued)
What causes it
• Prolonged refractory period
in slower rhythm• Short cycle followed by longcycle because refractory periodvaries with length of cycle
What to look for
• No signs or symptomsWhat to do
• Monitor heart rhythm.
How it’s treated
• No interventions needed, butmay be needed for accom-panying arrhythmias 476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 39

40Atrial
Rhythm
• Atrial: Varies slightly, with
an irregular P-P interval• Ventricular: Varies slightly,with an irregular R-R interval
Rate
• Varies, but usually withinnormal limits or less than 60 beats/minute
P wave
• Altered size and configura-tion from changing pacemakersite with at least three differ-ent P-wave shapes visible• May be absent or inverted or occur after QRS complex ifimpulse originates in the AVjunctionPR interval
• Varies from beat to beat aspacemaker site changes• Usually less than 0.20 second• Less than 0.12 second if theimpulse originates in the AVjunction
QRS complex
• Duration and configurationusually normal because ventricular depolarization is normal
T wave
• Normal size and configuration
QT interval
• Usually within normal limits
Other
• May be difficult to differentiatewandering pacemaker from PACsWandering pacemaker
476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 40

41
AtrialWandering pacemaker (continued)
What causes it
• COPD
• Digoxin toxicity• Increased parasympathetic(vagal) influences on SA nodeor AV junction• Inflammation of atrial tissue• Valvular heart disease
What to look for
• Usually no symptoms (patientis unaware of arrhythmia)• Pulse rate normal or lessthan 60 beats/minute• Rhythm regular or slightly irregular• At least three distinct P waveconfigurations (distinguishwandering pacemaker fromPACs)What to do
• Monitor heart rhythm.• Watch for evidence of hemo-dynamic instability, such ashypotension and changes inmental status.
How it’s treated
• Usually no treatment if patient asymptomatic • If symptomatic, review ofmedication regimen; investiga-tion and treatment of under-lying cause of arrhythmia 476203ATRIAL_rev.qxd 5/13/09 12:12 PM Page 41

42Junc
Rhythm
• Atrial: Irregular during PJCs
• Ventricular: Irregular duringPJCs• Underlying rhythm possiblyregular
Rate
• Atrial: Reflects underlyingrhythm• Ventricular: Reflects under-lying rhythm
P wave
• Usually inverted (leads II, III,and aV
F) (see shaded area on
strip)• May occur before, during, orafter QRS complex, dependingon initial direction of depolar-ization• May be hidden in QRS complexPR interval
• Shortened (less than 0.12 sec-ond) if P wave precedes QRScomplex• Not measurable if no P waveprecedes QRS complex
QRS complex
• Usually normal configurationand duration because ventriclesusually depolarize normally
T wave
• Usually normal configuration
QT interval
• Usually within normal limits
Other
• Commonly accompanied by acompensatory pause reflectingretrograde atrial conduction
Premature junctional contractions 476204JUNC_rev.qxd 5/13/09 1:13 PM Page 42

43
JuncWhat causes them
• CAD
• COPD• Digoxin toxicity• Electrolyte imbalances• Heart failure• Hyperthyroidism• Inferior-wall MI• Inflammatory changes in theAV 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 palpitationsor skipped beats• Hypotension if PJCs are frequent enoughWhat to do
• Monitor cardiac rhythm for frequent PJCs; may indi-cate junctional irritability and can lead to more seriousarrhythmia such as junctionaltachycardia. • Monitor patient for hemo-dynamic instability.
How they’re treated
• Usually no treatment if patientasymptomatic• If symptomatic, treatment ofunderlying cause• If digoxin toxicity, discontin-uation of drug • If ectopic beats frequent because of caffeine, decreasein or elimination of caffeine intakePremature junctional contractions (continued) 476204JUNC_rev.qxd 5/13/09 12:16 PM Page 43

44Junc
Rhythm
• Atrial: Regular
• Ventricular: Regular
Rate
• Atrial: 40 to 60 beats/minute• Ventricular: 40 to 60 beats/minute
P wave
• Usually inverted (leads II, III,and aV
F)
• May occur before, during, orafter QRS complex• May be hidden in QRS complex
PR interval
• Shortened (less than 0.12 sec-ond) if P wave precedes QRScomplex• Not measurable if no P waveprecedes QRS complexQRS complex
• Duration: Usually within nor-mal limits• Configuration: Usually normal
T wave
• Configuration: Usually normal
QT interval
• Usually within normal limits
Other
• Important to differentiatejunctional rhythm from idio-ventricular rhythm (a life-threatening arrhythmia)Junctional rhythm
476204JUNC_rev.qxd 5/13/09 12:16 PM Page 44

What causes it
• Cardiomyopathy
• Conditions that disturb nor-mal SA node function or im-pulse 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)What to do
• Monitor heart rhythm.• Monitor digoxin and elec-trolyte levels.• Watch for evidence of de-creased CO.
How it’s treated
• Identification and correctionof underlying cause• Atropine; temporary or per-manent pacemaker • Junctional rhythm can pre-vent ventricular standstill;should never be suppressed45
JuncJunctional rhythm (continued) 476204JUNC_rev.qxd 5/13/09 12:16 PM Page 45

46Junc
Rhythm
• Atrial: Regular
• Ventricular: Regular
Rate
• Atrial: 60 to 100 beats/minute• Ventricular: 60 to 100 beats/minute
P wave
• If present, inverted in leadsII, III, and aV
F
• May occur before, during, orafter QRS complex• May be hidden in QRS complex
PR interval
• Shortened (less than 0.12 sec-ond) if P wave precedes QRScomplex• Not measurable if no P waveprecedes QRS complexQRS complex
• Duration: Usually within nor-mal limits• Configuration: Usually normal
T wave
• Usually within normal limits
QT interval
• Usually within normal limits
Other
• Need to differentiate acceler-ated junctional rhythm fromaccelerated idioventricularrhythm (a possibly life-threatening arrhythmia)Accelerated junctional rhythm
476204JUNC_rev.qxd 5/13/09 12:16 PM Page 46

What causes it
• 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 regu-lar rhythm• Possibly no symptoms • Possibly symptoms of de-creased CO (from loss of atrialkick), such as hypotension,changes in mental status,weak peripheral pulsesWhat to do
• Monitor heart rhythm.• Watch for evidence of de-creased CO and hemodynamicinstability.• Monitor serum digoxin andelectrolyte levels.
How it’s treated
• Identification and correctionof underlying cause• Discontinuation of digoxin47
JuncAccelerated junctional rhythm (continued) 476204JUNC_rev.qxd 5/13/09 12:16 PM Page 47

48Junc
Rhythm
• Atrial: Usually regular but
may be difficult to determineif P wave is hidden in QRScomplex or preceding T wave• Ventricular: Usually regular
Rate
• 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)
P wave
• Usually inverted in leads II,III, and aV
F
• May occur before, during, orafter QRS complex• May be hidden in QRS complexPR interval
• Shortened (less than 0.12 sec-ond) if P wave precedes QRScomplex• Not measurable if no P waveprecedes QRS complex
QRS complex
• Duration: Within normal lim-its• Configuration: Usually normal
T wave
• Configuration: Usually normal• May be abnormal if P waveis hidden in T wave• May be indiscernible becauseof fast rate
QT interval
• Usually within normal limits
Other
• May have gradual (non-paroxysmal) or sudden(paroxysmal) onsetJunctional tachycardia
476204JUNC_rev.qxd 5/13/09 12:16 PM Page 48

What causes it
• Digoxin toxicity (most com-
mon) • Electrolyte imbalances• Heart failure• Hypokalemia (may aggravatecondition)• Inferior-wall MI• Inferior-wall myocardial ischemia• Inflammation of AV junctionafter 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 (lossof atrial kick) and hemody-namic instability (hypoten-sion) because of rapid HR
What to do
• Monitor heart rhythm.• Watch for evidence of digox-in toxicity; monitor digoxinblood level.How it’s treated
• Identification and treatmentof underlying cause• If due to digoxin toxicity, dis-continuation of digoxin; insome cases, possibly digoxin-binding drug to reduce serumdigoxin level• For recurrent junctionaltachycardia, possibly ablationtherapy followed by perma-nent pacemaker insertion• If symptomatic with parox-ysmal onset of junctionaltachycardia:
– vagal maneuvers anddrugs such as adenosine toslow HR – with otherwise normal heartfunction: beta-adrenergicblockers, calcium channelblockers, or amiodarone– with impaired heart func-tion (heart failure or EF below 40%): amiodarone49
JuncJunctional tachycardia (continued) 476204JUNC_rev.qxd 5/13/09 12:16 PM Page 49

Vent
50Rhythm
• Atrial: Irregular during PVCs
• Ventricular: Irregular duringPVCs• Underlying rhythm may beregular
Rate
• Atrial: Reflects underlying
rhythm• Ventricular: Reflects underly-ing rhythm
P wave
• Usually absent in ectopic beat
• May appear after QRS com-plex with retrograde conduc-tion to atria• Usually normal if present inunderlying rhythm
PR interval
• Not measurable except inunderlying rhythm
QRS complex
• Occurs earlier than expected
• Duration: Exceeds 0.12 second• Configuration: Bizarre and
wide but usually normal in underlying rhythm (see shaded ar eas on strip)
T wave
• Opposite direction to QRScomplex• May trigger more seriousrhythm disturbances whenPVC occurs on the downslopeof the preceding normal Twave (R-on-T phenomenon)
QT interval
• Not usually measured exceptin underlying rhythm
Other
• PVC may be followed by fullor incomplete compensatorypause• Interpolated PVC: Occurs be-tween two normally conductedQRS complexes without great disturbance to underlying r hythm
• Full compensatory pause absent with interpolated PVCs
Premature ventricular contractions 476205VENT_rev.qxd 5/13/09 12:17 PM Page 50

What causes them
• Enhanced automaticity (usual
cause)• Drug intoxication (amphet-amines, cocaine, digoxin,phenothiazines, tricyclic anti-depressants)• Electrolyte imbalances (hyper-kalemia, hypocalcemia, hypo-magnesemia, hypokalemia)• Enlargement of ventricularchambers• Hypoxia• Increased sympathetic stimulation• Irritable focus • Irritation of ventricles by pace-maker electrodes or PA catheter• Metabolic acidosis•M I• Mitral valve prolapse• Myocardial ischemia• Myocarditis• Sympathomimetic drugssuch as epinephrine• Triggers (alcohol, caffeine,nicotine)
What to look for
• Possibly no symptoms• Normal pulse rate with momentarily irregular pulserhythm when PVC occurs• Abnormally early heartsound with each PVC on auscultation• Palpitations if PVCs are fre quent
• Evidence of decreased CO(hypotension, syncope)
What to do
• Promptly assess patientswith recently developed PVCs,especially those with underly-ing heart disease or complexmedical problems.• Monitor heart rhythm of patients with PVCs and seri-ous symptoms. • Observe closely for develop-ment of more frequent PVCs ormore dangerous PVC patterns.• Teach family members howto activate EMS and performCPR if the patient will be tak-ing antiarrhythmic drugs afterdischarge.
How they’re treated
• No treatment if patientasymptomatic and has no evi-dence of heart disease• If symptomatic, or danger-ous form of PVC occurs, treat-ment dependent on cause • For PVCs of purely cardiac origin: drugs to suppress ven-tricular irritability, such asamiodarone, lidocaine, pro-cainamide• For PVCs of noncardiac ori-gin: treatment of cause51
VentPremature ventricular contractions (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 51

Vent
52Some PVCs are more dangerous than others. Here are some
potentially dangerous ones.P atterns of potentially dangerous 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 refractorytissue. A burst, or
salvo, of
three or more PVCs in a row isconsidered a run of VT.P aired PVCs
Multiform PVCs look different
from one another (see shadedareas on strip above) and ariseeither from different sites orfrom the same site via abnor-mal conduction. MultiformPVCs may indicate severe heartdisease or digoxin toxicity.Multiform PVCs 476205VENT_rev.qxd 5/13/09 12:17 PM Page 52

53
VentP atterns of potentially dangerous PVCs
(continued)
PVCs that occur every other
beat (bigeminy) or every thirdbeat (trigeminy) can result inVT or VF. The shaded areas onthe strip shown above illus-trate ventricular bigeminy.Bigeminy and trigeminy
In R-on-T phenomenon, a
PVC occurs so early that itfalls on the T wave of thepreceding beat (see shadedarea on strip above). Becausethe cells haven’t fully repolar-ized, VT or VF can result.R-on-T phenomenon 476205VENT_rev.qxd 5/13/09 12:17 PM Page 53

Vent
54Rhythm
• Atrial: Usually can’t be
determined• Ventricular: Usually regular
Rate
• Atrial: Usually can’t be determined• Ventricular: 20 to 40 beats/minute
P wave
• Usually absent
PR interval
• Not measurable because ofabsent P waveQRS complex
• Duration: Exceeds 0.12 sec-ond because of abnormal ventricular depolarization• Configuration: Wide and bizarre
T wave
• Abnormal• Usually deflects in oppositedirection from QRS complex
QT interval
• Usually prolonged
Other
• Commonly occurs with third-degree AV block• If any P waves present, notassociated with QRS complexIdioventricular rhythm
476205VENT_rev.qxd 5/13/09 12:17 PM Page 54

What causes it
• Digoxin toxicity
• Drugs
– Beta-adrenergic blockers– Calcium channel blockers– Tricyclic antidepressants
• Failure of all of heart’s higherpacemakers• Failure of supraventricularimpulses to reach ventriclesbecause of block in conduc-tion system• Metabolic imbalance•M I• Myocardial ischemia• Pacemaker failure• SSS• Third-degree AV block
What to look for
• Evidence of sharply decreasedCO (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 stabilityhas been restored.• Keep atropine and pacemakerequipment readily available.• Enforce bed rest until effec-tive HR has been maintainedand patient is stable.• Tell patient and family aboutthe serious nature of this arrhythmia and requiredtreatment.• If patient needs a permanentpacemaker, explain how itworks, how to recognize prob-lems, when to contact doctor,and how pacemaker functionwill be monitored.
How it’s treated
• Suppression of arrhythmianot goal of treatment; arrhyth-mia acts as safety mechanismagainst ventricular standstill• Possible atropine to increaseHR• In emergency, transcutaneouspacemaker until transvenouspacemaker can be inserted• Permanent pacemaker• Antiarrhythmic drugs (suchas amiodarone, lidocaine)contraindicated for idioven-tricular rhythm because ofpossible suppression of escape beats55
VentIdioventricular rhythm (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 55

Vent
56Rhythm
• Atrial: Can’t be determined
• Ventricular: Usually regular
Rate
• Atrial: Usually can’t be determined• Ventricular: 40 to 100 beats/minute
P wave
• Usually absent
PR interval
• Not measurableQRS complex
• Duration: Exceeds 0.12 second• Configuration: Wide and bizarre
T wave
• Abnormal• Usually deflects in oppositedirection from QRS complex
QT interval
• Usually prolonged
Other
• If any P waves present, notassociated with QRS complexAccelerated idioventricular rhythm
476205VENT_rev.qxd 5/13/09 12:17 PM Page 56

What causes it
• Digoxin toxicity
• Drugs
– Beta-adrenergic blockers– Calcium channel blockers– Tricyclic antidepressants
• Failure of all of heart’s higherpacemakers• Failure of supraventricularimpulses to reach ventriclesbecause of block in conduc-tion system• Metabolic imbalance•M I• Myocardial ischemia• Pacemaker failure• SSS• Third-degree AV block
What to look for
• Evidence of sharply decreasedCO (hypotension, dizziness,light-headedness, syncope)• Difficult auscultation or palpation of BP
What to do
• Monitor ECG continually; periodically assess patient until hemodynamic stabilityhas been restored.• Keep atropine and pacemakerequipment readily available.• Enforce bed rest until effec-tive HR has been maintainedand patient is stable.• Tell patient and family aboutthe serious nature of this arrhythmia and requiredtreatment.• If patient needs permanentpacemaker, explain how itworks, how to recognize prob-lems, when to contact physi-cian, and how pacemakerfunction will be monitored.
How it’s treated
• Suppression of arrhythmianot goal of treatment; arrhyth-mia acts as safety mechanismagainst ventricular standstill• Possible atropine to increaseHR• In emergency, transcuta-neous pacemaker until trans-venous pacemaker can be inserted• Permanent pacemaker• Antiarrhythmic drugs (suchas amiodarone, lidocaine)contraindicated for acceleratedidioventricular rhythm becauseof possible suppression of escape beats57
VentAccelerated idioventricular rhythm (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 57

Vent
58Rhythm
• Atrial: Can’t be determined
• Ventricular: Usually regularbut may be slightly irregular
Rate
• Atrial: Can’t be determined• Ventricular: Usually rapid(100 to 250 beats/minute)
P wave
• Usually absent• If present, not associatedwith QRS complex
PR interval
• Not measurableQRS complex
• Duration: Exceeds 0.12 second• Configuration: Usually bizarre,with increased amplitude• Uniform in monomorphic VT• Constantly changes shape inpolymorphic VT
T wave
• If visible, occurs opposite theQRS complex
QT interval
• Not measurable
Other
• Ventricular flutter: A variationof VTVentricular tachycardia
476205VENT_rev.qxd 5/13/09 12:17 PM Page 58

What causes it
• Usually increased myocar-
dial irritability, which may betriggered by:
– enhanced automaticity– PVCs during downstroke of preceding T wave– reentry in Purkinje system
• CAD• Cardiomyopathy• Drug toxicity (cocaine, procain-amide, or quinidine)• Electrolyte imbalances suchas hypokalemia• Heart failure•M I• Myocardial ischemia• Rewarming during hypothermia• Valvular heart disease
What to look for
• Possibly only minor symptoms initially• Usually weak or absent pulses• Hypotension and decreasedlevel of consciousness, quicklyleading to unresponsiveness ifuntreated• Possible angina, heart failure,and substantial decrease in organ perfusionWhat to do
• Determine whether patient isconscious and has sponta-neous respirations and palpa-ble carotid pulse.
• Monitor heart rhythm; rhythmmay rapidly progress to VF.• Teach family members howto activate EMS and performCPR if patient will have an ICDor be on long-term antiarrhyth-mic therapy after discharge. • Teach patient and familyabout the serious nature ofarrhythmia and need forprompt treatment.
How it’s treated
• For pulseless VT, cardio-pulmonary resuscitation and immediate defibrillation • For unstable patient withpulse, immediate synchro-nized cardioversion • If no definitive diagnosis of SVT or VT, amiodarone and elective synchronized cardioversion • For stable patient with re-current polymorphic VT, con-sultation with an expert• Correction of electrolyte imbalances• ICD59
VentVentricular tachycardia (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 59

Vent
60Rhythm
• Atrial: Can’t be determined
• Ventricular: May be regularor irregular
Rate
• Atrial: Can’t be determined• Ventricular: 150 to 300 beats/minute
P wave
• Not identifiable
PR interval
• Not measurable QRS complex
• Usually wide• Usually a phasic variation in electrical polarity, with complexes that point down-ward for several beats andthen upward for several beats
T wave
• Not discernible
QT interval
• Prolonged
Other
• May be paroxysmal, startingand stopping suddenlyTorsades de pointes
476205VENT_rev.qxd 5/13/09 12:17 PM Page 60

What causes it
• AV block
• Drug toxicity (sotalol,procainamide, quinidine)• Electrolyte imbalances(hypocalcemia, hypokalemia,hypomagnesemia)• Hereditary QT prolongationsyndrome• Myocardial ischemia• Prinzmetal’s angina• Psychotropic drugs (pheno-thiazines, tricyclic anti-depressants)• SA node disease resulting insevere bradycardia
What to look for
• Palpitations, dizziness, chestpain, and shortness of breathif patient is conscious• Hypotension and decreasedlevel of consciousness• Loss of consciousness,pulse, and respirationsWhat to do
• Monitor heart rhythm andobserve for QT prolongationin patients receiving drugsthat may cause torsades depointes.• Determine whether patient isconscious and has sponta-neous respirations and palpa-ble carotid pulse.
How it’s treated
• Cardiopulmonary resuscitation• Defibrillation• Overdrive pacing• Magnesium sulfate I.V.• Discontinuation of offendingdrug• Correction of electrolyte imbalances• For unstable patient withpulse, immediate synchronizedcardioversion• ICD61
VentTorsades de pointes (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 61

Vent
62Rhythm
• Atrial: Can’t be determined
• Ventricular: No pattern orregularity, just fibrillatorywaves
Rate
• Atrial: Can’t be determined• Ventricular: Can’t be deter-mined
P wave
• Can’t be determined
PR interval
• Can’t be determinedQRS complex
• Can’t be determined
T wave
• Can’t be determined
QT interval
• Not measurable
Other
• Electrical defibrillation moresuccessful with coarse fibrilla-tory waves than with finewavesVentricular fibrillation
Coarse
Fine 476205VENT_rev.qxd 5/13/09 12:17 PM Page 62

What causes it
• Acid-base imbalance
• CAD• Drug toxicity (digoxin,procainamide, quinidine)• Electric shock• Electrolyte imbalances (hypercalcemia, hyperkalemia,hypokalemia)•M I• Myocardial ischemia• Severe hypothermia• Underlying heart disease suchas dilated cardiomyopathy• Untreated VT
What to look for
• Full cardiac arrest• Unresponsive patient withno detectable BP or centralpulsesWhat to do
• Assess patient to determineif rhythm is VF.• Start CPR.• Teach patient’s family aboutthe serious nature of this ar-rhythmia and how to activateEMS and perform CPR.• Teach patient and familyabout the ICD if applicable orantiarrhythmic therapy the pa-tient will be taking after dis-charge.
How it’s treated
• Cardiopulmonary resuscitation• Immediate defibrillation:biphasic (120 to 200 joules),monophasic (360 joules)• Epinephrine or vasopressin• Following pulseless arrest algorithm guidelines63
VentVentricular fibrillation (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 63

Vent
64Rhythm
• Atrial: Usually indiscernible
• Ventricular: Not present
Rate
• Atrial: Usually indiscernible• Ventricular: Not present
P wave
• May be present
PR interval
• Not measurable
QRS complex
• Absent or occasional escapebeatsT wave
• Absent
QT interval
• Not measurable
Other
• Looks like a nearly flat line ona rhythm strip except duringchest compressions with CPR• If the patient has a pacemaker,pacer spikes may show on thestrip, but no P wave or QRScomplex occurs in responseAsystole
476205VENT_rev.qxd 5/13/09 12:17 PM Page 64

What causes it
• Cardiac tamponade
• Drug overdose• Hypothermia• Hypovolemia• Hypoxia• Massive pulmonary embolism•M I• Severe electrolyte distur-bances, especially hyper-kalemia and hypokalemia• Severe, uncorrected acid-base disturbances, especiallymetabolic acidosis• Tension pneumothorax
What to look for
• Unresponsive patient• Lack of spontaneous respira-tions, discernible pulse, and BP• No CO or perfusion of vitalorgansWhat to do
• Verify lack of do-not-resuscitate order. • Verify asystole by checkingmore than one ECG lead.• Start CPR, supplemental oxygen, and advanced airway control with trachealintubation.
How it’s treated
• Cardiopulmonary resus-citation• Identification and rapid treat-ment of potentially reversiblecauses; otherwise, asystolepossibly irreversible• Early transcutaneous pacing • I.V. vasopressin, epinephrine,and atropine • For persistent asystole despiteappropriate management: pos-sible end of resuscitation65
VentAsystole (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 65

Vent
66Rhythm
• Atrial: Same as underlying
rhythm; becomes irregular asrate slows• Ventricular: Same as under-lying rhythm; becomes irregu-lar as rate slows
Rate
• Atrial: Reflects underlyingrhythm• Ventricular: Reflects underlyingrhythm; eventually decreases
P wave
• Same as underlying rhythm;gradually flattens and thendisappears
PR interval
• Same as underlying rhythm;eventually disappears as P wave disappearsQRS complex
• Same as underlying rhythm;becomes progressively wider
T wave
• Same as underlying rhythm;eventually becomes indis-cernible
QT interval
• Same as underlying rhythm;eventually becomes indiscernible
Other
• Also known as PEA
• Characterized by some elec-trical activity (may be anyrhythm) but no mechanical activity or detectable pulse• Usually becomes a flat lineindicating asystole within sev-eral minutesPulseless electrical activity
476205VENT_rev.qxd 5/13/09 12:17 PM Page 66

What causes it
• 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 ofconsciousness• Lack of BP and pulse• No CO or perfusion of vitalorgans
What to do
• Start CPR immediately.How it’s treated
• Cardiopulmonary resuscitation• Epinephrine, vasopressin,and atropine according toACLS guidelines• Identification and treatmentof cause including:
– pericardiocentesis for cardiactamponade– volume infusion for hypo-volemia from hemorrhage– correction of electrolyte imbalances– ventilation for hypoxemia– surgery or thrombolytictherapy for massive pul-monary embolism– needle decompression orchest tube insertion for tension pneumothorax
• Pacemaker therapy (rarely effective)67
VentPulseless electrical activity (continued) 476205VENT_rev.qxd 5/13/09 12:17 PM Page 67

68AV Block
Rhythm
• Regular
Rate
• Within normal limits or
bradycardic• Atrial the same as ventricular
P wave
• Normal size• Normal configuration• Each followed by a QRScomplex
PR interval
• Prolonged• More than 0.20 second (seeshaded area on strip)• ConstantQRS complex
• Within normal limits (0.08 second or less) if con-duction delay occurs in AVnode• If more than 0.12 second,conduction delay may be inHis-Purkinje system
T wave
• Normal size• Normal configuration• May be abnormal if QRScomplex is prolonged
QT interval
• Within normal limits
First-degree AV block 476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 68

What causes it
• Degenerative (age-related)
changes in heart• Drugs
– Beta-adrenergic blockers– Calcium channel blockers– Digoxin
•M I• Myocardial ischemia• Myocarditis
What to look for
• Normal or slow pulse rate• Regular rhythm• Usually no symptoms• Usually no significant effecton CO• Increased interval betweenS
1and S2heard on cardiac
auscultation if PR interval isextremely longWhat to do
• Monitor patient’s cardiacrhythm to detect progressionto more serious heart block.• Give digoxin, calcium channelblockers, and beta-adrenergicblockers cautiously.
How it’s treated
• Identification and correctionof underlying cause69
AV BlockFirst-degree AV block (continued) 476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 69

70AV Block
Rhythm
• Atrial: Regular
• Ventricular: Irregular
Rate
• Atrial rate exceeds ventricu-lar rate because of noncon-ducted beats• Both rates usually withinnormal limits
P wave
• Normal size• Normal configuration• Each followed by a QRS com-plex except blocked P wave
PR interval
• Progressively longer (seeshaded areas on strip) witheach cycle until a P wave ap-pears without a QRS complex• Commonly described as“long, longer, dropped”• Slight variation in delay fromcycle to cycle• After the nonconducted beat,shorter than the interval pre-ceding it
QRS complex
• Within normal limits• Periodically absent
T wave
• Normal size• Normal configuration• Deflection may be oppositethat of the QRS complex
QT interval
• Usually within normal limits
Other
• Wenckebach pattern ofgrouped beats (footprints ofWenckebach)• PR interval gets progressivelylonger and R-R interval short-ens until a P wave appearswithout a QRS complex; cyclethen repeatsType I second-degree AV block
476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 70

What causes it
• CAD
• Drugs
– Beta-adrenergic blockers– Calcium channel blockers– Digoxin
• Increased parasympathetictone• Inferior-wall MI• Rheumatic fever
What to look for
• Usually no symptoms• Evidence of decreased CO(hypotension, light-headedness)• Pronounced signs and symp-toms if ventricular rate is slow
What to do
• Monitor cardiac rhythm forprogression of degree ofblock.• Assess patient’s tolerance ofrhythm.• Observe for signs and symp-toms of decreased CO.• Evaluate patient for possiblecauses.• Teach patient about tempo-rary pacemaker, if indicated.
How it’s treated
• Identification and treatmentof underlying cause• Atropine (use cautiously ifpatient is having an MI; at-ropine can worsen ischemia)• Transcutaneous pacing, ifneeded, until the arrhythmiaresolves71
AV BlockType I second-degree AV block (continued) 476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 71

72AV Block
Rhythm
• Atrial: Regular
• Ventricular: Irregular• Pauses correspond todropped beat• Irregular when block is inter-mittent or conduction ratio isvariable• Regular when conduction ratiois constant, such as 2:1 or 3:1
Rate
• Atrial exceeds ventricular• Both may be within normallimits
P wave
• Normal size• Normal configuration• Some not followed by a QRScomplex
PR interval
• Usually within normal limitsbut may be prolonged• Constant for conducted beats• May be shortened after anonconducted beatQRS complex
• Within normal limits or narrowif block occurs at bundle of His• Widened and similar to BBBif block occurs at bundlebranches• Periodically absent
T wave
• Normal size• Normal configuration
QT interval
• Within normal limits
Other
• PR and R-R intervals don’tvary before a dropped beat(see shaded area on strip), sono warning occurs• R-R interval that containsnonconducted P wave equalstwo normal R-R intervals• Must be a complete block inone bundle branch and inter-mittent interruption in conduc-tion in the other bundle for adropped beat to occurType II second-degree AV block
476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 72

What causes it
• Anterior-wall MI
• Degenerative changes inconduction system• Organic heart disease• Severe CAD
What to look for
• Usually no symptoms aslong 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 forprogression to more severeblock.• Evaluate patient for cor-rectable causes (such as ischemia).• Administer oxygen.• Restrict patient to bedrest.• If patient has no serioussigns and symptoms:
– monitor patient continu-ously, keeping transcuta-neous pacemaker attached topatient or in room.– prepare patient for transve-nous pacemaker insertion.
• Teach patient and familyabout pacemakers, if indicated.
How it’s treated
• Transcutaneous pacing initi-ated quickly when indicatedand I.V. dopamine infusion,epinephrine, or combinationof these drugs• A transcutaneous pacemaker(for serious signs and symp-toms) until a permanent pace-maker is placed73
AV BlockType II second-degree AV block (continued) 476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 73

74AV Block
Rhythm
• Atrial: Regular
• Ventricular: Regular
Rate
• Atrial: 60 to 100 beats/minute(atria act independently undercontrol of SA node)• Ventricular: Usually 40 to60 beats/minute in an intra-nodal block (a junctional escape rhythm)• Ventricular: Usually less than40 beats/minute in infranodalblock (a ventricular escaperhythm)
P wave
• Normal size• Normal configuration• May be buried in QRS com-plex or T wave
PR interval
• Not measurableQRS complex
• Configuration depends on location of escape mecha-nism and origin of ventriculardepolarization• Appears normal if the blockis at the level of the AV nodeor bundle of His• Widened if the block is at thelevel of the bundle branches
T wave
• Normal size• Normal configuration• May be abnormal if QRScomplex originates in ventricle
QT interval
• Within normal limits
Other
• Atria and ventricles are depolarized from differentpacemaker sites and beat independently of each other• P waves occur without QRScomplexesThird-degree AV block
476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 74

What causes it
At level of AV node
• AV node damage
• Increased parasympathetictone• Inferior-wall MI• Toxic effects of drugs (digoxin,propranolol)
At infranodal level
• Extensive anterior MI
What to look for
• Possibly no symptoms ex-cept exercise intolerance andunexplained fatigue• Decreased CO from loss ofAV synchrony and resultingloss of atrial kick• Changes in level of conscious-ness and mental status• Chest pain• Diaphoresis• Dyspnea• Hypotension• Light-headedness• Pallor• Severe fatigue• Slow peripheral pulse rateWhat to do
• Ensure patent I.V. line.• Administer oxygen.• Assess patient for correctablecauses of arrhythmia (drugs,myocardial ischemia).• Minimize patient’s activitylevel.• Restrict patient to bed rest.
How it’s treated
• For patient with serioussigns and symptoms, immedi-ate treatment, including:
– transcutaneous pacing(most effective)– I.V. dopamine infusion, epinephrine, or combination(for short-term use in emergencies)
• Atropine contraindicated, especially when accompaniedby wide-complex ventricularescape beats• Permanent pacemaker75
AV BlockThird-degree AV block (continued) 476206AV-BLOCK_rev.qxd 5/13/09 12:16 PM Page 75

76General 12-Lead
Proper lead placement is critical for accurate recording of cardiac
rhythms. These drawings show correct electrode placement forthe six limb leads. RA stands for right arm; LA, left arm; RL, rightleg; and LL, left leg. A plus sign ( /H11001) indicates a positive pole,
a minus sign (/H11002 ) indicates a negative pole, and G indicates
a ground. Below each drawing is a sample ECG strip for that lead.
RA
(/H11002)
RL
(G)LA
(/H11001)/H11002 /H11001
RA
(/H11002)
RL
(G)LL
(/H11001)/H11002
/H11001
RL
(G)LA
(/H11002)/H11001/H11002Limb lead placement
Lead I
Connects the right
arm (negative pole)with the left arm(positive pole).Lead II
Connects the rightarm (negative pole)with the left leg(positive pole).Lead III
Connects the leftarm (negative pole)with the left leg(positive pole).
LL
(/H11001)12-Lead 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 76

77
12-LeadLimb lead placement (continued)
Lead aVR
Connects the right
arm (positive pole)with the heart(negative pole).Lead aVL
Connects the leftarm (positive pole)with the heart(negative pole).Lead aVF
Connects the leftleg (positive pole)with the heart(negative pole).
RA
(/H11001)/H11002/H11001
LA
(/H11001)/H11002/H11001
/H11001/H11002
LL
(/H11001) 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 77

78General 12-Lead
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). Thethree standard limb leads (I, II, and III) and the three augmentedleads (aV
R, aVL, and aVF) are recorded using these electrodes.
Then, to record the precordial chest leads, place electrodes as follows:
V
1. . . . . . . . . . . . Fourth ICS, right
sternal border
V2. . . . . . . . . . . . Fourth ICS, left
sternal border
V3. . . . . . . . . . . . Midway between
V2and V4
V4. . . . . . . . . . . . Fifth ICS, left
midclavicular line
V5. . . . . . . . . . . . Fifth ICS, left
anterior axillary line
V6. . . . . . . . . . . . Fifth ICS, left
midaxillary linePrecordial lead placement
V1V2
V3V4V5V6
V1
V4
V2
V5
V3
V6
476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 78

79
12-LeadTo 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
between V2R
and V4R
V4R. . . . . Fifth ICS, right
midclavicularline
V
5R. . . . . Fifth ICS, right
anterior axil-lary line
V
6R. . . . . Fifth ICS, right
midaxillarylineRight precordial lead placement
P osterior lead electrode placement
To ensure an accurate ECG reading, make sure the posteriorelectrodes V
7, V8, and V9are
placed at the same level horizon-tally as the V
6lead at the fifth in-
tercostal space. Place lead V7at
the posterior axillary line, lead V9
at the paraspinal line, and lead V8
halfway between leads V7and V9.
Midaxillary line
Posterior axillary line
Left paraspinal line
V8V7V6V9
V1RV2R
V3RV4RV5RV6R
Midclavicular line
Anterior axillary line
Midaxillary line 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 79

80General 12-Lead
Each of the leads on a 12-lead ECG views the heart from a
different angle. These illustrations show the direction of electricalactivity (depolarization) monitored by each lead and the 12 viewsof the heart.Electrical activity and the 12-lead ECG
aVRaVL
I
aVF
V1V2V3V4V5V6View of the
Lead heart
Limb leads (bipolar)
I Lateral wall
II Inferior wall
III Inferior wall
Augmented limb leads (unipolar)
aVRNo specific view
aVLLateral wall
aVFInferior wall
Precordial, or chest, leads (unipolar)
V1Septal wall
V2Septal wall
V3Anterior wall
V4Anterior wall
V5Lateral wall
V6Lateral wallViews reflected on a
12-lead ECG
II III 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 80

81
12-LeadThis 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 aV
F. Lead I indicates whether impulses
are moving to the right or left, and lead aVFindicates whether
they’re moving up or down. Then check the chart to determinewhether the patient’s axis is normal or has a left, right, or extreme right deviation.• Normal axis: QRS-complex deflection is positive or upright inboth leads.• Left axis deviation: Lead I is upright and lead aV
Fpoints down.
• Right axis deviation: Lead I points down and lead aVFis upright.
• Extreme right axis deviation: Both waves point down.Electrical axis determination:
Quadrant method
180° 0°–90°
/H1100190°Extreme right
axis deviation
Right axis
deviationLeft axisdeviation
Normal
I
aVF
I
aVFI
aVF
I
aVF/H11001– 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 81

82General 12-Lead
The degree method provides a more precise measurement of
the electrical axis. It allows you to identify a patient’s electricalaxis by degrees on the hexaxial system, not just by quadrant. It also allows you to determine the axis even if the QRS complexisn’t clearly positive or negative in leads I and aV
F. To use this
method, take these steps.Electrical axis determination:
Degree method
Step 1
Identify the limb lead with the smallest QRS complex or theequiphasic QRS complex. In this example, it’s lead III.
Lead I Lead II Lead III
Lead aVRLead aVLLead aVF
/H11006180ș I/H11002150ș/H11001/H11002120ș
IIaVFIII
/H11002
/H11002/H1100290ș
/H1100260ș
/H1100230ș
0ș
/H1100130ș
Normal axis/H11001150șaVL
/H11001/H11001/H11001aVR
/H11001120ș/H1100190ș/H1100160ș/H11006180ș I/H11002150ș/H11001/H11002120ș
IIaVFIII
/H11002
/H11002/H1100290ș
/H1100260ș
/H1100230ș
0ș
/H1100130ș /H11001150șaVL
/H11001/H11001/H11001aVR
/H11001120ș/H1100190ș/H1100160șStep 2
Locate the axis for lead III on the
hexaxial diagram. Then find theaxis perpendicular to it, which isthe axis for lead aV
R.
Step 3
Examine the QRS complex in leadaV
R, noting whether the deflection
is positive or negative. As you cansee, the QRS complex for this lead is negative, indicating that the current is moving toward thenegative pole of aV
R, which is in
the right lower quadrant at +30 degrees on the hexaxial diagram.So the electrical axis here is normal at +30 degrees. 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 82

83
Causes of axis deviation
This list covers common causes of right and left axis deviation.
Left Right
• Normal variation • Normal variation
• Inferior wall MI • Lateral wall MI
• Left anterior hemiblock • Left posterior hemiblock
• Wolff-Parkinson-White • Right bundle-branch blocksyndrome • Emphysema
• Mechanical shifts (ascites, • Right ventricular hypertrophy
pregnancy, tumors)• Left bundle-branch block• Left ventricular hypertrophy• Aging
12-Lead 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 83

8412-Lead
These are some classic ECG changes involving the T wave and ST
segment that you may see when monitoring a patient with angina.ECG changes in angina
P eaked T wave
Flattened T wave
T-wave inversion
ST-segment depression with T-wave inversion
ST-segment depression without T-wave inversion
476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 84

85
12-LeadECG changes in acute pericarditis evolve through two stages:
• Stage 1—Diffuse ST-segment elevations of 1 to 2 mm in mostlimb leads and most precordial leads reflect the inflammatoryprocess. Upright T waves appear in most leads. The ST-segmentand T-wave changes are typically seen in leads I, II, III, aV
R, aVF,
and V2 through V6.
• Stage 2—As pericarditis resolves, the ST-segment elevationand accompanying T-wave inversion resolves in most leads.P ericarditis
Ia VRV1V4
II aVLV2V5
III aVFV3V6 476207-12LEAD_rev.qxd 6/2/09 5:50 PM Page 85

86General 12-Lead
Ischemia
Ischemia is the first stage and in-
dicates that blood flow and oxy-gen demand are out of balance. It can be resolved by improvingflow or reducing oxygen needs.ECG changes indicate ST-segment depression or T wave changes.
Injury
The second stage, injury, occurswhen the ischemia is prolongedenough to damage the area of theheart. ECG changes usually revealST-segment elevation (usually intwo or more contiguous leads).
Infarct
Infarct is the third stage and occurswith actual death of myocardialcells. Scar tissue eventually re-places the dead tissue, and thedamage caused is irreversible.
In the earliest stage of an MI,
hyperacute or very tall T wavesmay be seen on the ECG. Withinhours, the T waves become invert-ed and ST-segment elevation oc-curs in the leads facing the area ofdamage. The pathologic Q wave is the last change to occur in theevolution of an MI and is the only permanent ECG evidence of myocardial necrosis.Stages of myocardial ischemia, injury,
and infarct
Myocardial
ischemia
• T-wave inversion
• ST-depression
Myocardial
injury
• ST-segment
elevation• T-wave inversion
Myocardial
infarction
• Hyperacute
T waves (earlieststage)
• ST-segment
elevation• T-wave inversion• Pathologic Q waves– in 90% of ST-segmentelevation MI– in 25% non–ST-segmentelevation MI
476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 86

87
12-LeadAfter you’ve noted characteristic lead changes in an acute MI,
use this table to identify the areas of damage. Match the leadchanges (ST elevation, abnormal Q waves) in the second columnwith the affected wall in the first column and the artery involvedin the third column. The fourth column shows reciprocal leadchanges.Locating myocardial damage
Wall
affected
Anterior
Anterolateral
Anteroseptal
Inferior
Lateral
Posterior
Right
ventricularLeads
V2, V3, V4
I, aVL, V3, V4,
V5, V6
V1, V2, V3, V4
II, III, aVF
I, aVL, V5, V6
V8, V9
V4R, V5R, V6RArtery
involved
Left coronary
artery, left anteriordescending (LAD)
LAD and diagonal
branches, circum-flex and marginalbranches
LADRight coronary
artery (RCA)
Circumflex branch
of left coronary artery
RCA or circumflex
RCAReciprocal
changes
II, III, aV
F
II, III, aVF
NoneI, aV
L
II, III, aVF
V1, V2, V3, V4(R
greater than S in V1and V2, ST-segment
depression, elevated
T wave)
None 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 87

88General 12-Lead
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 V
1and a large R wave
(shaded area in right strip) in V5. If the depth (in mm) of the
S wave in V1added to the height (in mm) of the R wave in V5
exceeds 35 mm, then the patient has left ventricular hypertrophy.Left ventricular hypertrophy
Lead V1Lead V5
476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 88

89
12-LeadElectrical impulses don’t always follow normal conduction path-
ways in the heart. In WPW syndrome, electrical impulses enterthe ventricles from the atria through an accessory pathway thatbypasses the AV junction.
WPW syndrome is clinically significant because the accessory
pathway — in this case, Kent’s bundle — may result in paroxysmaltachyarrhythmias 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 inthe leads looking at the part of the heart where the accessorypathway is located.• The delta wave shortens the PR interval in WPW syndrome.Wolff-P arkinson-White syndrome
Short PR interval Delta wave 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 89

1
2
3Block
90General 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). Theimpulse then crosses the interventricular septum to activate theright ventricle (arrow 3).
In this disorder, the QRS complex exceeds 0.12 second and
has a different configuration, sometimes resembling rabbit earsor the letter “M.” Septal depolarization isn’t affected in lead V
1,
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 deflectionis called a
secondary T-wave change and isn’t clinically signifi-
cant.
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 V
6, the T wave should be positive. 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 90

91
12-LeadThis 12-lead ECG shows the characteristic changes of RBBB. In
lead V1, note the rsR/H11032 pattern and T-wave inversion. In lead V6,
note the widened S wave and the upright T wave. Also note theprolonged QRS complexes.Recognizing RBBB
Lead I Lead aVRLead V1Lead V4
Lead II Lead aVLLead V2Lead V5
Lead III Lead aVFLead V3Lead V6
476207-12LEAD_rev.qxd 6/2/09 5:51 PM Page 91

92General 12-Lead
In LBBB, an impulse first travels down the right bundle branch
(arrow 1). Then it activates the interventricular septum from rightto 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 tothe left, a wide S wave appears in lead V
1with 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. Thisinitial positive deflection is a sign of LBBB. The T wave is negative.Understanding LBBB
1
23Block 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 92

93
12-LeadThis 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.Recognizing LBBB
Lead I Lead aVRLead V1Lead V4
Lead II Lead aVLLead V2Lead V5
Lead III Lead aVFLead V3Lead V6
476207-12LEAD_rev.qxd 6/2/09 5:51 PM Page 93

Check rhythm. Shockable rhythm?2
VF/VT3YES NO
Asystole/PEA9
• Give 1 shock (biphasic: 120 to
200 joules; monophasic: 360 joules).• Immediately resume CPR.4Pulseless arrest algorithm
Initiate BLS.1
• 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 seconddose 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).10
94Treat 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 94

95
YESCheck rhythm. Shockable rhythm?
• If asystole, go to box 10.
• If electrical activity,check pulse. If nopulse, go to box 10.• If pulse present, beginpostresuscitation care.11
12
Go
to
box 4.13Check rhythm. Shockable rhythm?5
• Continue CPR while chargingdefibrillator.• Give 1 shock (biphasic: same asfirst 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 seconddose of epinephrine.6
* After an advanced airwayis placed, give continuouschest compressions withoutpauses for breaths.YES
YES NO
Give 5 cycles of CPR*Give 5 cycles of CPR*NO
Check rhythm. Shockable rhythm?7NOGive 5 cycles of CPR*
TreatPulseless arrest algorithm (continued)
• Continue CPR while charging defibrillator.
• Give 1 shock (biphasic: same as first shock or higherdose; monophasic: 360 joules).• Immediately resume CPR.• Consider antiarrhythmics; give during CPR.• Consider magnesium, loading dose.• After 5 cycles of CPR*, go to box 5.8
Reprinted with permission. “2005 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care,” Circulation
2005: 112 (suppl IV). © 2005, American Heart Association. 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 95

96General
96Tachycardia algorithm
• Assess and support ABCs as needed.
• Give oxygen.• Monitor ECG (identify rhythm), blood pressure,oximetry.• Identify and treat reversible causes.2
Is patient stable?
Unstable signs include altered mental
status, ongoing chest pain, hypo-
tension or other signs of shock.Perform immediate
synchronized cardio-version• Establish I.V. accessand give sedation ifpatient is conscious; donot delay cardioversion.• Consider expert consultation.• If pulseless arrestdevelops, see pulselessarrest algorithm.4
• Establish I.V. access.• Obtain 12-lead ECG (when available) or rhythm strip.
Is QRS narrow?5
Narrow QRS*
Is rhythm regular?6
Wide QRS*
Is rhythm regular?
Expert consultation advised.
• Attempt vagal
maneuvers.• Give adeno-sine 6 mg rapidI.V. push. If noconversion, give12 mg rapid I.V. push; mayrepeat 12 mgdose once.7
Irregular Narrow-Complex
TachycardiaProbable atrial fibrillation or possible atrial flutter ormultifocal atrial tachycardia• Consider expert consultation.• Control rate (diltiazem,beta blockers; use betablockers with caution inpulmonary disease or CHF).11Symptoms persist
Stable
Narrow (< 0.12 sec) Wide (> 0.12 sec)
Regular Irregular
UnstableTachycardia with pulses1
123Treat 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 96

97
TreatTachycardia algorithm (continued)
Does rhythm convert?
Note: Consider expert consultation.8
If rhythm con-
verts, probably
reentry supra-
ventricular
tachycardia
(SVT)
• Observe for
recurrence.• Treatrecurrencewith adenosineor longer-acting AV nodalblockingagents (suchas diltiazem orbeta blockers).9
If rhythm does
NOT convert,
possible atrial
flutter, ectopic
atrial tachycardia,
or junctional
tachycardia
• Control rate(diltiazem, betablockers; use betablockers with caution in pulmonarydisease or CHF).• Treat underlyingcause.• Consider expertconsultation.10 ConvertsIf ventricular
tachycardia or
uncertain
rhythm
• Amiodarone
150 mg I.V. over10 min. Repeatas needed tomaximum dose of 2.2 g/24 hours.• Prepare forelectivesynchronizedcardioversion.
If SVT with
aberrancy
• Giveadenosine (goto box 7).13 Regular
If atrial fibril-
lation with
aberrancy
• See Irregular
Narrow-ComplexTachycardia(box 11).
If pre-excited
atrial fibrillation
(AF + WPW)
• Expert consul-tation advised.• Avoid AVnodal blockingagents (adeno-sine, digoxin,diltiazem,verapamil).• Consider anti-arrhythmics(amiodarone150 mg I.V. over 10 min).
If recurrent
polymorphic
VT
• Seek expertconsultation.
If torsades de
pointes
• Give mag-nesium (loadwith 1 to 2 gover 5 to 60 min,then infusion).14 Irregular
Does not convert
*Note: If patient becomes unstable, go to box 4.
Reprinted with permission. “2005 American Heart
Association Guidelines for Cardiopulmonary Resuscitationand Emergency Cardiovascular Care,”
Circulation 2005: 112
(suppl IV). © 2005, American Heart Association. 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 97

98General Treat
Bradycardia algorithm
• 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)
Observe/Monitor. • Prepare for transcutaneous pacing; use withoutdelay for high-degree block (type II second-degreeblock or third-degree AV block).• Consider atropine while awaiting pacer. May repeatto a total dose of 3 mg. If ineffective, begin pacing.• Consider epinephrine or dopamine infusion whileawaiting 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.Bradycardia
Heart rate < 60 beats/min and inadequate for clinical condition
Poor perfusion Adequate perfusion 476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 98

99
TreatGuide to antiarrhythmic drugs
This chart details the drugs most commonly used to manage
cardiac arrhythmias, including indications and special consider-ations for each.
Drugs
Disopyramide,
procainamide,quinidine
Lidocaine,
mexiletine
Flecainide,
moricizine,propafenoneIndications
•V T
• Atrial fibrillation• Atrial flutter•P A T
•V T
•V T
•V F
•V T
•V F• SupraventriculararrhythmiasSpecial considerations
• Check apical pulse rate before
therapy. If you note extremes inpulse rate, withhold the dose andnotify the prescriber.• Use cautiously in patients with reac-tive airway disease such as asthma.• Monitor for ECG changes (widen-ing QRS complexes, prolonged QTinterval).
• IB antiarrhythmics may potentiate
the effects of other antiarrhythmics.• Administer I.V. infusions using aninfusion pump.
• Correct electrolyte imbalances
before administration.• Monitor the patient’s ECG beforeand after dosage adjustments.• Monitor for ECG changes (widen-ing QRS complexes, prolonged QTinterval).Class IA antiarrhythmics
Class IB antiarrhythmics
Class IC antiarrhythmics
(continued) 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 99

100Treat
Guide to antiarrhythmic drugs (continued)
Drugs
Acebutolol,
atenolol, esmolol, propranolol
Amiodarone,
dofetilide, ibutilide, sotalol
Diltiazem,
verapamilIndications
• Atrial flutter
• Atrial fibrillation•P A T
• Life-threatening
arrhythmias re-sistant to otherantiarrhythmicdrugs
• Supraventricular
arrhythmiasSpecial considerations
• Monitor apical HR and BP .
• Abruptly stopping these drugs can ex-acerbate angina and precipitate MI.• Monitor for ECG changes (pro-longed PR interval).• Drugs may mask common signs andsymptoms of shock and hypoglycemia.• Use cautiously in patients with reac-tive airway disease such as asthma.
• Monitor BP and heart rate and
rhythm for changes.• Amiodarone increases the risk ofdigoxin toxicity in patients also takingdigoxin.• Monitor for signs of pulmonary tox-icity (nonproductive cough, dyspnea,and pleuritic chest pain), thyroid dys-function, and vision impairment inpatients taking amiodarone.• Monitor for ECG changes (pro-longed QT interval) in patients takingdofetilide, ibutilide, and sotalol.
• Monitor heart rate and rhythm and
BP carefully when initiating therapyor increasing dosage.• Calcium supplements may reduceeffectiveness.Class II antiarrhythmics
Class III antiarrhythmics
Class IV antiarrhythmics 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 100

101
TreatGuide to antiarrhythmic drugs (continued)
Drugs
Adenosine
Atropine
Epinephrine
VasopressinIndications
• PSVT
• Symptomatic SB
• AV block• Asystole• BradycardicPEA
• Pulseless VT
•V F• Asystole• PEA
• VF that’s un-
responsive to defibrillationSpecial considerations
• Adenosine must be administered
over 1 to 2 seconds, followed by a20-ml flush of normal saline solution.• Record rhythm strip during admin-istration. Adenosine may causetransient asystole or heart block.
• Monitor heart rate and rhythm. Use
the drug cautiously in patients withmyocardial ischemia.• Atropine isn’t recommended forthird-degree AV block or infranodaltype II second-degree AV block.• In adults, avoid doses less than 0.5 mg because of the risk of para-doxical slowing of the HR.
• Monitor heart rate and rhythm and
BP carefully because the drug maycause myocardial ischemia.• Don’t mix an I.V. dose with alkalinesolutions.• Give drug into a large vein to prevent irritation or extravasation at site.
• Monitor heart rate and rhythm. Use
the drug cautiously in patients withmyocardial ischemia.• Monitor for hypersensitivity reac-tions, especially urticaria, angio-edema, and bronchoconstriction.Miscellaneous antiarrhythmics 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 101

102Treat
Anterolateral
placement
Place one paddle to the
right of the upper ster-num, just below the rightclavicle, and the otherover the fifth or sixth in-tercostal space at the leftanterior axillary line.
Anteroposterior placement
Place the anterior paddle directly over the heart at the precordi-um, to the left of the lower sternal border. Place the flat posteri-or paddle under the patient’s body beneath the heart and justbelow the left scapula (but not under the vertebral column).
Defibrillator paddle placement 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 102

103
TreatPrecautions must be taken when defibrillating a patient with an
ICD, a pacemaker, or a transdermal medication patch or a pa-tient who’s in contact with water.
Defibrillating a patient with an ICD or pacemaker
Avoid placing the defibrillator paddles or pads directly over theimplanted device. Place them at least 1” (2.5 cm) away from thedevice.
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 patchcan block delivery of energy and cause a small burn to theskin. 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 pathwayfor energy from the defibrillator to the rescuers treating the vic-tim. Remove the patient from freestanding water and dry hischest before defibrillation.Safety issues with defibrillation 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 103

104Treat
Monophasic defibrillators
Monophasic
defibrillatorsdeliver a sin-gle currentof electricitythat travelsin one direc-tion betweenthe two padsor paddleson the patient’s chest. To beeffective, a large amount ofelectrical current is required formonophasic defibrillation.
Biphasic defibrillators
Biphasic defibrillatorshave thesame pad or paddleplacementas with themonophasicdefibrillator.The differ-ence is that during biphasic defibrillation, the electrical cur-rent discharged from the padsor paddles travels in a positivedirection for a specified dura-tion and then reverses andflows in a negative directionfor the remaining time of theelectrical discharge.Energy efficient
The biphasic defibrillator deliv-ers two currents of electricityand lowers the defibrillationthreshold of the heart muscle,making it possible to success-fully defibrillate VF with small-er amounts of energy.
Adjustable
The biphasic defibrillator canadjust for differences in imped-ance or resistance of the cur-rent through the chest. This reduces the number of shocksneeded to terminate VF.
Less myocardial damage
Because the biphasic defibrilla-tor requires lower energy lev-els and fewer shocks, damageto the myocardial muscle is re-duced. Biphasic defibrillatorsused at the clinically appropri-ate energy level may be usedfor defibrillation and, in thesynchronized mode, for syn-chronized cardioversion.Monophasic and biphasic defibrillators
Current
flow
Current
flow
Currentflow 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 104

105
TreatHow it works
In synchronized cardioversion, an electric current is delivered to
the heart to correct an arrhythmia. This procedure may be doneelectively in a stable patient with recurrent atrial fibrillation orurgently in an unstable patient with such arrhythmias as PSVT,atrial flutter, atrial fibrillation, and VT with a pulse.
Compared with defibrillation, synchronized cardioversion
uses much lower energy levels and is synchronized to deliver an electric charge to the myocardium on the peak R wave.
What it does
The procedure causes immediate depolarization, interruptingreentry circuits (abnormal impulse conduction that occurs whencardiac tissue is activated two or more times, causing reentryarrhythmias) and allowing the SA node to resume control.
Synchronizing the electric charge with the R wave ensures
that the current won’t be delivered on the vulnerable T waveand disrupts repolarization. This reduces the risk that the cur-rent will strike during the relative refractory period of a cardiaccycle and induce VF.Synchronized cardioversion 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 105

106Treat
Transcutaneous pacing, also referred to as external or noninva-
sive pacing, involves the delivery of electrical impulses through
externally applied cutaneous electrodes. The electrical impulses
are conducted through an intact chest wall using skin electrodesplaced in either anterior-posterior or sternal-apex positions. (Ananterior-posterior placement is shown here.)
When to use it
Transcutaneous pacing is the pacing method of choice in emer-gency situations because it’s the least invasive technique and itcan be instituted quickly.Transcutaneous pacemaker
Electrode Electrode 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 106

107
TreatImplanting a pacemaker is a simple surgical procedure performed
with local anesthesia and moderate sedation. To implant an endo-cardial pacemaker, the surgeon usually selects a transvenousroute and begins lead placement by inserting a catheter percuta-neously or by venous cutdown. Using fluoroscopic guidance, thesurgeon then threads the catheter through the vein until the tipreaches the endocardium.
Lead placement
For lead placement in the atrium, the tip must lodge in the rightatrium or coronary sinus, as shown below. For placement in theventricle, it must lodge in the right ventricular apex in one of theinterior muscular ridges, or trabeculae (as shown below).
Implanting the generator
When the lead is in proper position, the surgeon secures thepulse generator in a subcutaneous pocket of tissue just below thepatient’s clavicle. Changing the generator’s battery or microchipcircuitry requires only a shallow incision over the site and a quickexchange of components.Placing a permanent pacemaker
Subclavian vein
Generator in
subcutaneouspocket
Right atrial lead
Right
ventricular lead 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 107

108Treat
Pacemaker impulses—
the stimuli that travelfrom the pacemakerto the heart—appearas spikes on an ECGtracing. Whetherlarge or small, pace-maker spikes appearabove or below theisoelectric line. This illustration shows an atrial pacemakerspike and a ventricu-lar pacemaker spike.P acemaker spikes
Understanding pacemaker codes
A permanent pacemaker’s three-letter (or sometimes five-letter)
code simply refers to how it’s programmed.
First letter
(chamber
that’s paced)
Aatrium
Vventricle
Ddual (both
chambers)
Onot
applicableSecondletter
(chamber
that’s sensed)
Aatrium
Vventricle
Ddual (both
chambers)Onot
applicableThird letter
(pulse
generator’s
response)
Iinhibited
Ttriggered
Ddual
(inhibited andtriggered)Onot
applicableFourthletter
(pacemaker’s
programmability)
Pbasic
functions programmableMmultiple
programmableparametersCcommuni-
cating func-tions such astelemetryRrate respon-
sivenessNnoneFifth letter
(pacemaker’s
response to
tachycardia)
Ppacing
abilitySshock
Ddual ability
to shock andpaceOnoneQRS complex
P wave
Atrial
pacemaker spike
Ventricular
pacemaker spike 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 108

109
TreatA biventricular pacemaker uses three leads: one to pace the
right atrium, one to pace the right ventricle, and one to pace theleft ventricle. The left ventricular lead is placed in the coronarysinus. Both ventricles are paced at the same time, causing themto contract simultaneously, which improves CO.Biventricular lead placement
Subclavian vein
Generator
Right atrial lead
Right atriumRight ventricular leadRight ventricleLeft ventricular lead
(in coronary sinus vein)
Left ventricle 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 109

110Treat
The settings on a temporary pulse generator may be changed in
various ways to meet the patient’s specific needs. This illustra-tion shows a single-chamber temporary pulse generator andgives brief descriptions of its various parts.Temporary pulse generator
Polar markings
identify positive andnegative terminals.
Pace meter
registers every pacingstimulus delivered tothe heart.
Sensitivity control
adjusts pacemakersensitivity (measuredin millivolts) to thepatient’s heart rate.Turning the dialcounterclockwise to
ASYNC fixes the rate.
Battery compartmentholds the alkalinebatteries.Connector terminalshold the leads.
Sensing meter
registers every time anintrinsic depolarizationis recognized.
Rate control
directs the number ofpulses given eachminute.
Energy output control
determines the amountof electricity (in milli-amperes) sent to theheart.
On-off switch
activates the pulsegenerator./H11002 /H11001 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 110

111
TreatTemporary pacemaker malfunctions
Failure to pace
ECG shows no pacemaker
activity when activity shouldbe present.
Nursing interventions
• Check connections to cableand position of pacing elec-trode in patient (by X-ray).• If pulse generator is on butindicators aren’t flashing,change battery. If that doesn’thelp, change pulse generator.• Adjust the sensitivity setting.Failure to capture
ECG shows pacemaker spikesbut the heart isn’t responding.
Nursing interventions
• If patient’s condition haschanged, notify doctor andask for new settings.• If pacemaker settings are altered, return them to theircorrect positions.• If heart isn’t responding,check all connections; increasemilliamperes slowly (accordingto policy or doctor’s order);turn patient on his left side,then on his right; and sched-ule an anteroposterior or later-al chest X-ray to determineposition of electrode.
Pacemaker
spike shouldappear hereThere’s a pacemakerspike but no responsefrom the heart
(continued) 476208TREAT_rev.qxd 6/2/09 5:54 PM Page 111

112Treat
Failure to sense intrinsic
beats (undersensing)
ECG shows pacemaker spikes
anywhere in the cycle (thepacemaker fires, but at thewrong times or for the wrongreasons).Nursing interventions
• If the pacemaker is under-sensing, turn the sensitivitycontrol completely to the right.• If the pacemaker isn’t func-tioning correctly, change thebattery or pulse generator.• Remove items in room caus-ing electromechanical interfer-ence (such as electric razors,radios, and cautery devices).Check ground wires on thebed and other equipment fordamage. Unplug each pieceand see if interference stops.When you locate the cause,ask a staff engineer to check it.• If the pacemaker is still firingon the T wave, notify the doc-tor and turn off the pacemaker.Have atropine available in caseHR drops. Call a code and insti-tute CPR if needed.
The pacemaker fires
anywhere in the cycleTemporary pacemaker malfunctions (continued) 476208TREAT_rev.qxd 6/2/09 5:54 PM Page 112

113
TreatAn ICD has a programmable pulse generator and lead system
that monitors the heart’s activity, detects ventricular arrhyth-mias and other tachyarrhythmias, and responds with appro-priate therapies.
What it does
The range of therapies includes antitachycardia and antibrady-cardia pacing, cardioversion, and defibrillation. The ICD can alsopace both the right atrium and right ventricle. Some can performbiventricular pacing. ICDs that provide therapy for atrial arrhyth-mias, such as atrial fibrillation, are also available.
Implanting the ICD
Implantation of an ICD is similar to that of a permanent pacemak-er. The cardiologist positions the lead (or leads) transvenously inthe endocardium of the right ventricle (and the right atrium, ifboth chambers need pacing). The lead connects to a generatorbox implanted in the right or left upper chest near the clavicle.ICD review
LeadwirePulse
generator 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 113

114Treat
ICDs can deliver a range of therapies depending on the arrhyth-
mia detected and how the device is programmed. Some ICDscan also detect and treat atrial arrhythmias or provide biventric-ular pacing. Therapies include antitachycardia pacing, cardio-version, defibrillation, and bradycardia pacing.Types of ICD therapies
Therapy
Antitachycardia pacing
CardioversionDefibrillationBradycardia pacingDescription
A series of small, rapid, electrical pacing puls-
es are used to interrupt VT and return the heartto its normal rhythm.
A low- or high-energy shock (up to 35 joules) is
timed to the R wave to terminate VT and returnthe heart to its normal rhythm.
A high-energy shock (up to 35 joules) to the
heart is used to terminate VF and return theheart to its normal rhythm.
Electrical pacing pulses are used when the
heart’s natural electrical signals are too slow.ICD systems can pace one chamber (VVI pac-ing) of the heart at a preset rate or sense andpace both chambers (DDD pacing). 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 114

115
TreatDevice
• Know the device and how it’s programmed, including:
– type and model of ICD
– status of the device (on or off)– detection rates– types of therapies that will be delivered and when.
Appropriateness
• Evaluate the appropriateness of ICD shocks, including:
– number of isolated and multiple shocks– situation and activity related to shocks– patient symptoms– ECG rhythm– drugs taken.
Shocks
• Shocks may not occur despite VT or VF under certain circum-
stances, such as:
– if the HR is less than the detection rate– if there’s a lead or circuitry problem– if therapy is suspended or turned off– if the battery is depleted.
• Shocks can occur without VT or VF under certain circum-stances, such as:
– when the rate in ST ventures into the VT zone– when noise is detected on the sensing lead (from electro-magnetic interference or lead dysfunction)– when the patient develops atrial fibrillation.
• Multiple shocks may occur in certain circumstances, such as:
– when the patient has persistent or recurrent VT or VF– when the device malfunctions.Managing an ICD
(continued) 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 115

116Treat
• Multiple shocks indicate a medical emergency, and the patient
may require adjunct treatment, such as:
– CPR– external defibrillation
– drugs, such as amiodarone, lidocaine, procainamide– suspension of tachyarrhythmia therapy by magnet applica-tion or reprogramming of device.
Problems
• If cardiac arrest occurs in a patient with an ICD, CPR and ACLSshould be used immediately.• If the patient needs external defibrillation, take these steps:
– Position the paddles as far from the device as possible or use anterior-posterior position.– Anticipate that defibrillation will result in “power on reset”and reversion to nominal settings.– Programming of the device should be verified with the programmer.
• Look for evidence of problems, including:
– decreased CO (hypotension, chest pain, dyspnea, syncope)– infection– pneumothorax– misplaced electrode (abnormal electrical stimulation occur-ring in synchrony with the pacemaker, such as pectoral muscletwitching)– stimulation of diaphragm (hiccups)– cardiac tamponade.Managing an ICD (continued) 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 116

117
Notes 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 117

118Notes 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 118

119
Notes 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 119

120American Heart Association. Handbook of Emergency Cardio-
vascular Care for Healthcare Providers. Dallas: American Heart
Association, 2005.
Assessment Made Incredibly Easy, 4th ed. Philadelphia: Lippincott
Williams & Wilkins, 2008.
Cardiovascular Care Made Incredibly Visual. Philadelphia:
Lippincott Williams & Wilkins, 2007.
ECG Interpretation Made Incredibly Easy, 4th ed. Philadelphia:
Lippincott Williams & Wilkins, 2008.
Fugate, J.H. “Pharmacologic Management of Cardiac Emergen-
cies,” Journal of Infusion Nursing 29(3):147-50, May-June 2006.
Lippincott’s Nursing Procedures, 5th ed. Philadelphia: Lippincott
Williams & Wilkins, 2009.
Moses, H.W., and Mullin, J.C. A Practical Guide to Cardiac Pacing,
6th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.
Nursing2009 Drug Handbook, 29th ed. Philadelphia: Lippincott
Williams & Wilkins, 2009.
Nursing Know-How: Interpreting ECGs. Philadelphia: Lippincott
Williams & Wilkins, 2008.
Tsiperfal, A., et al. “What Is Drug-Induced Long QT and What Is
a Potential Clinical Consequence?” Progress in Cardiovascular
Nursing 21(2):104-5, Spring 2006.
Wysocki, L. “ST Segment Changes Clue You In to Injury Location,”
RN69(9):49, September 2006.Selected references 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 120

121
Index
Abbreviations, vi
Accelerated junctional
rhythm, 46-47
Accelerated idioventric-
ular rhythm, 56-57
Angina, ECG changes in,
84
Antiarrhythmic drugs,
99-101
Ashman’s phenomenon,
38-39
Asystole, 64-65Atrial fibrillation, 36-37Atrial flutter, 34-35Atrial tachycardia, 30-33Bradycardia
algorithm for, 98in children, 13
Cardiac conduction
system, 4
Cardioversion, synchro-
nized, 105
Coronary vessels, 2-3Defibrillators
paddle placement,
102
safety issues with, 103types of, 104
ECG
evaluation, 9grid, 4normal, 8QTc interval normals, 9
Einthoven’s triangle, 5Electrical axis
determination of,
81-82
deviation of, 83
Electrolyte imbalances,
ECG and, 14
First-degree AV block,
68-69
Heart location, 1Heart rate
calculating, 12in children, 13
ICD, 113
managing, 115-116therapies delivered
by, 114
Idioventricular rhythm,
54-55
Junctional rhythm, 44-45Junctional tachycardia,
48-49
LBBB, 92-93Leads
augmented, 6best monitoring, iibiventricular, place-
ment of, 109
cardiac monitoring,
positioning, 7
limb, placement of,
76-77
posterior, placement
of, 79
precordial, placement
of, 78-79
Left ventricular hyper-
trophy, 88
Myocardial infarct, 86
locating damage in, 87
Myocardial injury, 86Myocardial ischemia, 86Pacemaker
biventricular, 109codes, 108implanting, 107malfunctions, 111-112spikes, 108transcutaneous, 106
PACs, 28-29Pericarditis, ECG
changes in, 85
PJCs, 42-43Pulseless arrest algo-
rithm, 94-95
Pulseless electrical
activity, 66-67
PVCs, 50-53QTc interval, normal, 9RBBB, 90-91Rhythm strips
interpreting, 9methods of measur-
ing, 10
patterns of, 11
SA exit block, 24-25Sick sinus syndrome,
26-27
Sinus arrest, 22-23Sinus arrhythmia, 16-17Sinus bradycardia, 18-19Sinus rhythm, normal, 15Sinus tachycardia, 20-21Tachycardia
algorithm, 96-97in children, 13
Temporary pulse gener-
ator, 110
Third-degree AV block,
74-75
Torsades de pointes,
60-61
12-lead, electrical activ-
ity and, 80
Type I second-degree
AV block, 70-71
Type II second-degree
AV block, 72-73
Ventricular fibrillation,
62-63
Ventricular tachycardia,
58-59
Wandering pacemaker,
40-41
WPW syndrome, 89 476208TREAT_rev.qxd 5/13/09 12:13 PM Page 121