476200fm rev.qxd 5/13/09 12:12 pm page iii - asnane.org facts.pdfand reviews and testing and...

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StaffExecutive PublisherJudith A. Schilling McCann, RN, MSN

Clinical DirectorJoan M. Robinson, RN, MSN

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Editorial AssistantsKaren J. Kirk, Jeri O’Shea, Linda K. Ruhf

The 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. Allrights 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.

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ECGMIQ2-010909

ISBN-13: 978-1-60547-476-2ISBN-10: 1-60547-476-2

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Most bedside monitoring systems allow for simultaneousmonitoring of two leads, such as lead II with V1 or MCL1.Lead II or the lead that clearly shows the P waves and QRS complex may be used for sinus node arrhythmias, PACs, and AV block. The precordial leads V1 and V6 or the bipolar leads MCL1 and MCL6 are the best leads for monitor-ing rhythms with wide QRS complexes and for differentiat-ing VT from SVT with aberrancy.

This table lists the best leads for monitoring challengingcardiac arrhythmias.

Best monitoring leads

Arrhythmia

PACsATPATAtrial flutterAtrial fibrillation

PJCsJunctional escape rhythmJunctional tachycardiaPVCsIdioventricular rhythmVTVFTorsades de pointesThird-degree AV block

Best monitoring leads

II or lead that shows best P wavesII, V1, V6, MCL1, MCL6II, V1, V6, MCL1, MCL6II, IIIII (or identified in most leads by fibrillatory waves and irregular R-R)IIIIII, V1, V6, MCL1, MCL6V1, V6, MCL1, MCL6V1, V6, MCL1, MCL6V1, V6, MCL1, MCL6AnyAnyII or lead that shows best P wavesand QRS complexes

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lHeart 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, SSSPACs, 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,ICD

SA

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

ACLS. . . . advanced cardiac life supportACS. . . . . acute coronary syndromesAED. . . . . automated external

defibrillatorAT . . . . . . atrial tachycardiaAV . . . . . . atrioventricularBBB . . . . bundle-branch blockBCLS. . . . basic cardiac life supportBP . . . . . . blood pressureCAD. . . . . coronary artery diseaseCI. . . . . . . cardiac indexCO . . . . . . cardiac outputCO2 . . . . . carbon dioxideCOPD . . . chronic obstructive

pulmonary diseaseCPR . . . . . cardiopulmonary

resuscitationCV . . . . . . cardiovascularDTR . . . . . deep tendon reflexECG . . . . . electrocardiogramEF . . . . . . ejection fractionEMS . . . . emergency medical serviceET . . . . . . endotrachealFIO2 . . . . . fraction of inspired oxygenGI. . . . . . . gastrointestinalGU . . . . . . genitourinaryHR . . . . . . heart rateIABP . . . . intra-aortic balloon pumpICD . . . . . implantable cardioverter-

defibrillatorICP . . . . . intracranial pressureICS . . . . . intercostal spaceICU . . . . . intensive care unitJVD . . . . . jugular vein distentionLBBB . . . left bundle-branch blockLVH . . . . . left ventricular hypertrophyMAP . . . . mean arterial pressureMAT . . . . multifocal atrial tachycardiaMCL . . . . modified chest lead

MI . . . . . . myocardial infarctionO2 . . . . . . oxygenPA . . . . . . pulmonary arteryPAC . . . . . premature atrial contractionPAD. . . . . pulmonary artery diastolicPAM . . . . pulmonary artery meanPAP . . . . . pulmonary artery pressurePAS . . . . . pulmonary artery systolicPAT . . . . . paroxysmal atrial

tachycardiaPAWP . . . pulmonary artery wedge

pressurePEA . . . . . pulseless electrical activityPJC . . . . . premature junctional

contractionPMI . . . . . point of maximal impulsePSVT. . . . paroxysmal supraventricular

tachycardiaPVC . . . . . premature ventricular

contractionRAP. . . . . right arterial pressureRBBB . . . right bundle-branch blockSA . . . . . . sinoatrial SaO2 . . . . arterial blood oxygen

saturationSB . . . . . . sinus bradycardiaSpO2 . . . . pulse oximetry blood oxygen

saturationSSS . . . . . sick sinus syndromeST . . . . . . sinus tachycardiaSV . . . . . . stroke volumeSVO2 . . . . mixed venous oxygen

saturationSVT . . . . . supraventricular tachycardiaVF . . . . . . ventricular fibrillationVT . . . . . . ventricular tachycardiaWPW . . . Wolff-Parkinson-White

(syndrome)

Common abbreviations

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This illustration shows exactly where the heart is located. Theheart 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

General

Where the heart lies

Base

Midline

Secondintercostalspace

Fifthintercostalspace

Apex

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2

General

Coronary vessels

Anterior view

LeftsubclavianarteryAortic arch

Pulmonarytrunk

Great cardiacvein

Circumflexbranch of leftcoronaryartery

Left commoncarotid artery

Brachiocephalicartery

Superior vena cava

Right atrium

Right coronary artery

Small cardiac vein

Anteriorinterventricular(descending)branch of leftmain coronary artery


3

General

Coronary vessels (continued)

Posterior view

Left common carotid artery

Left subclavian artery

Pulmonary artery

Left pulmonary veins

Left atriumGreat cardiac veinCircumflex branch of left coronary artery

Posterior vein of left ventricle

Middle cardiac vein

Brachiocephalicartery

Aortic arch

Superior venacava

Right pulmonaryveins

Right atrium

Inferior vena cava

Small cardiac vein

Right coronaryartery

Posteriorinterventricular(descending)branch of rightcoronary artery


4

General

Cardiac conduction system

SA node

Interatrial septum

AV node

AV bundle (bundle of His)

Right and leftbundle branches

Interventricularseptum

ECG gridThis ECG grid shows the horizontal axis and vertical axis andtheir respective measurement values.

1 mV

3 sec

0.04 sec

0.20 sec

Amplitudeor voltage

0.5 mV (5 mm)

0.1 mV (1 mm)

Time (in seconds)


The axes of the three bipolar limb leads (I, II, and III) form ashape known as Einthoven’s triangle. Because the electrodes forthese leads are about equidistant from the heart, the triangle isequilateral.

The axis of lead I extends from shoulder to shoulder, with theright-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 triangle

5

General

Lead I

Right arm Left arm

Left leg

Lead

IIILead II

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6

General

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

Augmented leads

� �

�

aVR aVL

aVF

Right arm Left arm

Left leg


7

General

Positioning cardiac monitoring leads

Lead I Lead IRA LA

C

RL LL

RA LA

LL

Lead II Lead IIRA LA

C

RL LL

RA LA

LL

Lead III Lead IIIRA LA

C

RL LL

RA LA

LL

LeadMCL1

LeadMCL1RA LA

C

RL LL

RA LA

LL

LeadMCL6

LeadMCL6RA LA

C

RL LL

RA LA

LL

Five-leadwire system Three-leadwire system


8

General

Normal ECG

0.12–0.20 sec

0.06–0.10 sec

0.36–0.44 sec


9

General

QTc 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 method1. 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)

405060708090100120150180200

QTc intervalnormal range(seconds)

0.41 – 0.510.38 – 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


10

General

Paper-and-pencil method• Position the straight edge ofa 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


Normal, regular (as in normal sinus rhythm)

Slow, regular (as in SB)

Fast, regular (as in ST)

Premature (as in a PVC)

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

Irregularly irregular (as in atrial fibrillation)

Paroxysm or burst (as in PAT)

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

General

Rhythm strip patterns


12

General

This table can helpmake 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 estimateThis rapid-rate cal-culation is also calledthe countdownmethod. Using thenumber 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

30025021418816715013612511510710094888379757168656360585654525048474544434241393837


13

General

In children, evaluate bradycardia and tachycardia in context.For example, bradycardia (less than 90 beats/minute) may occur in a healthy infant during sleep; tachycardia may be 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

Neonate1 wk-3 mo3 mo-2 yr2-10 yr> 10 yr

Awake(beats/min)

100-160100-22080-15070-11055-100

Asleep(beats/min)

80-14080-20070-12060-9050-90

Exercise orfever(beats/min)

< 220< 220< 200< 200< 200


14

General

ECG effects of electrolyte imbalances

Imbalance

Hypercalcemia

Hypocalcemia

Hyperkalemia

Hypokalemia

Key finding

Shortened QT interval

Prolonged QT interval

Tall, peaked T waves

Flat T wave; U wave appears

Other 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


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 beats

15

SA Node

Normal sinus rhythm

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16

SA 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 configuration

PR 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 quickening

Sinus arrhythmia

Expiration Inspiration Expiration


17

SA Node

Sinus 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


18

SA 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• Constant

QRS complex• Normal duration• Normal configuration


QT interval• Within normal limits• Possibly prolonged

Sinus bradycardia


19

SA Node

Sinus 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 compensatefor decreased CO

• No symptoms

If patient can’t compensate• Altered mental status• Blurred vision• Chest pain• Cool, clammy skin• Crackles• Dizziness• Dyspnea • Hypotension• S3 heart sound, indicatingheart 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


20

SA 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 identify

PR interval• Within normal limits• Constant

QRS complex• Normal duration • Normal configuration


QT interval• Within normal limits• Commonly shortened

Sinus tachycardia


21

SA Node

Sinus 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 compensatorymechanisms fail

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

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

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


22

SA 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 ispresent

QRS 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 pause

Sinus arrest


23

SA Node

Sinus arrest (continued)What causes it• Acute infection• Acute inferior-wall MI• Acute myocarditis• CAD• Cardioactive drugs

– Amiodarone– Beta-adrenergic blockers(bisoprolol, metoprolol, propranolol)– Calcium channel blockers(diltiazem, verapamil)– Digoxin– Procainamide– Quinidine

• Cardiomyopathy• Hypertensive heart disease• Increased vagal tone 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


24

SA Node

Rhythm• Regular except during apause (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 ispresent

QRS 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 interval

Sinoatrial exit block


25

SA Node

Sinoatrial 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


26

SA 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 changes

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


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

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

Sick sinus syndrome


27

SA Node

Sick sinus syndrome (continued)What causes it• Autonomic disturbances thataffect 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 cardiomyopathypresent

• Dilated and displaced leftventricular apical impulse• Possible crackles• S3 heart 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


28

Atrial

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 beat

QRS 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

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29

Atrial

Premature atrial contractions (continued)What causes them• Enhanced automaticity inatrial 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 heartdisease

What 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 withacute 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


30

Atrial

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 wave

QRS 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 waves

Atrial tachycardia


31

Atrial

Atrial tachycardia (continued)What causes it• Digoxin toxicity (most common)• Cardiomyopathy• COPD• Congenital anomalies• Cor pulmonale• Drugs

– Albuterol– Cocaine– Theophylline

• Electrolyte imbalances• Hyperthyroidism• Hypoxia• MI• Physical or psychological stress• Systemic hypertension• Triggers (alcohol, caffeine,nicotine)• Valvular heart disease• WPW syndrome

What to look for• Rapid HR• Sudden feeling of 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


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 appear

PR interval• Varies

QRS complex• Usually normal• May become aberrant if arrhythmia persists

T wave• Usually distorted

QT interval• May be indiscernible

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Atrial

Multifocal atrial tachycardia


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 wave

QRS 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 stopabruptly

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Atrial

Paroxysmal atrial tachycardia


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Atrial

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/minute

P 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 anirregular ventricular response• May be difficult to differentiateatrial flutter from atrial fibrillation

Atrial flutter


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Atrial

Atrial flutter (continued)What causes it• Cardiac surgery with acute MI• Conditions that enlarge atrial tissue and elevate atrialpressures• COPD• Digoxin toxicity• Hyperthyroidism• MI• 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– Syncope

What 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 before and aftercardioversion• 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


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Atrial

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 atrialdepolarizations

PR 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 MAT

Atrial fibrillation


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Atrial

Atrial 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 on

cardiac 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


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Atrial

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 pattern

T 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 cycle

Ashman’s phenomenon


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Atrial

Ashman’s phenomenon (continued)What causes it• Prolonged refractory periodin slower rhythm• Short cycle followed by longcycle because refractory periodvaries with length of cycle

What to look for• No signs or symptoms

What to do• Monitor heart rhythm.

How it’s treated• No interventions needed, butmay be needed for accom-panying arrhythmias


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Atrial

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 AVjunction

PR 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


Other• May be difficult to differentiatewandering pacemaker from PACs

Wandering pacemaker


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Atrial

Wandering 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


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Junc

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 aVF) (see shaded area onstrip)• May occur before, during, orafter QRS complex, dependingon initial direction of depolar-ization• 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 complex

QRS complex• Usually normal configurationand duration because ventriclesusually depolarize normally

T wave• Usually normal configuration


Other• Commonly accompanied by acompensatory pause reflectingretrograde atrial conduction

Premature junctional contractions

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What 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 enough

What 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 intake

Premature junctional contractions (continued)


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Junc



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


QRS complex• Duration: Usually within nor-mal limits• Configuration: Usually normal

T wave• Configuration: Usually normal


Other• Important to differentiatejunctional rhythm from idio-ventricular rhythm (a life-threatening arrhythmia)

Junctional rhythm


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 suppressed

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Junctional rhythm (continued)


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Junc



P wave• If present, inverted in leadsII, III, and aVF• May occur before, during, orafter QRS complex• May be hidden in QRS complex


QRS complex• Duration: Usually within nor-mal limits• Configuration: Usually normal

T wave• Usually within normal limits


Other• Need to differentiate acceler-ated junctional rhythm fromaccelerated idioventricularrhythm (a possibly life-threatening arrhythmia)

Accelerated junctional rhythm


What causes it• Digoxin toxicity (commoncause)• 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 pulses

What 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 digoxin

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Accelerated junctional rhythm (continued)


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Rhythm• Atrial: Usually regular butmay 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 aVF• May occur before, during, orafter QRS complex• May be hidden in 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


Other• May have gradual (non-paroxysmal) or sudden(paroxysmal) onset

Junctional tachycardia


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%): amiodarone

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Junctional tachycardia (continued)


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Rhythm• Atrial: Irregular during PVCs• Ventricular: Irregular duringPVCs• Underlying rhythm may beregular

Rate• Atrial: Reflects underlyingrhythm• 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 andwide but usually normal in underlying rhythm (see shaded areas 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 rhythm• Full compensatory pause absent with interpolated PVCs

Premature ventricular contractions

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What causes them• Enhanced automaticity (usualcause)• 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• MI• 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 frequent• 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 cause

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Premature ventricular contractions (continued)


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

Patterns of potentially dangerous PVCs

Two PVCs in a row, calledpaired PVCs or a ventricularcouplet (see shaded areas onstrip above), can produce VTbecause the second contrac-

tion usually meets refractorytissue. A burst, or salvo, ofthree or more PVCs in a row isconsidered a run of VT.

Paired PVCs

Multiform PVCs look differentfrom one another (see shadedareas on strip above) and ariseeither from different sites or

from the same site via abnor-mal conduction. MultiformPVCs may indicate severe heartdisease or digoxin toxicity.

Multiform PVCs


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Patterns of potentially dangerous PVCs(continued)

PVCs that occur every otherbeat (bigeminy) or every thirdbeat (trigeminy) can result in

VT or VF. The shaded areas onthe strip shown above illus-trate ventricular bigeminy.

Bigeminy and trigeminy

In R-on-T phenomenon, aPVC occurs so early that itfalls on the T wave of thepreceding beat (see shaded

area on strip above). Becausethe cells haven’t fully repolar-ized, VT or VF can result.

R-on-T phenomenon


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Rhythm• 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 wave

QRS 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 complex

Idioventricular rhythm


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• MI• 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 beats

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Idioventricular rhythm (continued)


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Rhythm• 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


QRS 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 complex

Accelerated idioventricular rhythm


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• MI• 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 beats

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Accelerated idioventricular rhythm (continued)


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Rhythm• 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


QRS 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


Other• Ventricular flutter: A variationof VT

Ventricular tachycardia


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• MI• Myocardial ischemia• Rewarming during hypothermia• Valvular heart disease

What to look for• Possibly only minor symptoms initially• Usually weak or absent pulses• Hypotension and decreasedlevel of consciousness, quicklyleading to unresponsiveness ifuntreated• Possible angina, heart failure,and substantial decrease in organ perfusion

What 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• ICD

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Ventricular tachycardia (continued)


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Rhythm• 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


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 suddenly

Torsades de pointes


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 respirations

What 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• ICD

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Torsades de pointes (continued)


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Rhythm• 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 determined

QRS complex• Can’t be determined

T wave• Can’t be determined


Other• Electrical defibrillation moresuccessful with coarse fibrilla-tory waves than with finewaves

Ventricular fibrillationCoarse

Fine


What causes it• Acid-base imbalance• CAD• Drug toxicity (digoxin,procainamide, quinidine)• Electric shock• Electrolyte imbalances (hypercalcemia, hyperkalemia,hypokalemia)• MI• 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 centralpulses

What 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 guidelines

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Ventricular fibrillation (continued)


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Rhythm• Atrial: Usually indiscernible• Ventricular: Not present

Rate• Atrial: Usually indiscernible• Ventricular: Not present

P wave• May be present


QRS complex• Absent or occasional escapebeats

T wave• Absent


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 response

Asystole


What causes it• Cardiac tamponade• Drug overdose• Hypothermia• Hypovolemia• Hypoxia• Massive pulmonary embolism• MI• 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 vitalorgans

What 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 resuscitation

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Asystole (continued)


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Rhythm• Atrial: Same as underlyingrhythm; 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 disappears

QRS 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 minutes

Pulseless electrical activity


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

Vent

Pulseless electrical activity (continued)


68

AV Block

Rhythm• Regular

Rate• Within normal limits orbradycardic• 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)• Constant

QRS 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

• MI• Myocardial ischemia• Myocarditis

What to look for• Normal or slow pulse rate• Regular rhythm• Usually no symptoms• Usually no significant effecton CO• Increased interval betweenS1 and S2 heard on cardiacauscultation if PR interval isextremely long

What 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 cause

69

AV Block

First-degree AV block (continued)


70

AV 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


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 repeats

Type I second-degree AV block


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 arrhythmiaresolves

71

AV Block

Type I second-degree AV block (continued)


72

AV 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 beat

QRS complex• Within normal limits or narrowif block occurs at bundle of His• Widened and similar to BBBif block occurs at bundlebranches• Periodically absent



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 occur

Type II second-degree AV block


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 placed

73

AV Block

Type II second-degree AV block (continued)


74

AV Block


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


QRS 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


Other• Atria and ventricles are depolarized from differentpacemaker sites and beat independently of each other• P waves occur without QRScomplexes

Third-degree AV block


What causes itAt 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 rate

What 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 pacemaker

75

AV Block

Third-degree AV block (continued)


76

General 12-Lead

Proper lead placement is critical for accurate recording of cardiacrhythms. 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 (�) indicates a positive pole, a minus sign (�) indicates a negative pole, and G indicates a ground. Below each drawing is a sample ECG strip for that lead.

RA(�)

RL(G)

LA(�)

� �

RA(�)

RL(G)

LL(�)

�

�

RL(G)

LA(�)

�

�

Limb lead placement

Lead IConnects the rightarm (negative pole)with the left arm(positive pole).

Lead IIConnects the rightarm (negative pole)with the left leg(positive pole).

Lead III Connects the leftarm (negative pole)with the left leg(positive pole).

LL(�)

12-Lead

476207-12LEAD_rev.qxd 5/13/09 12:13 PM Page 76

77

12-Lead

Limb lead placement (continued)Lead aVRConnects the rightarm (positive pole)with the heart(negative pole).

Lead aVLConnects the leftarm (positive pole)with the heart(negative pole).

Lead aVFConnects the leftleg (positive pole)with the heart(negative pole).

RA(�)

�

�

LA(�)

�

�

�

�

LL(�)


78

General 12-Lead

To record a 12-lead ECG, place electrodes on the patient’s armsand legs (with the ground lead on the patient’s right leg). Thethree standard limb leads (I, II, and III) and the three augmentedleads (aVR, aVL, and aVF) are recorded using these electrodes.Then, to record the precordial chest leads, place electrodes as follows:V1 . . . . . . . . . . . . Fourth ICS, right

sternal borderV2 . . . . . . . . . . . . Fourth ICS, left

sternal borderV3 . . . . . . . . . . . . Midway between

V2 and V4V4 . . . . . . . . . . . . Fifth ICS, left

midclavicular lineV5 . . . . . . . . . . . . Fifth ICS, left

anterior axillary lineV6 . . . . . . . . . . . . Fifth ICS, left

midaxillary line

Precordial lead placement

V1 V2

V3 V4V5

V6

V1 V4

V2 V5

V3 V6


79

12-Lead

To record the right precordial chest leads, place the electrodesas follows:V1R . . . . . Fourth ICS, left

sternal borderV2R . . . . . Fourth ICS,

right sternalborder

V3R . . . . . Halfway between V2Rand V4R

V4R . . . . . Fifth ICS, rightmidclavicularline

V5R . . . . . Fifth ICS, right anterior axil-lary line

V6R . . . . . Fifth ICS, right midaxillaryline

Right precordial lead placement

Posterior lead electrode placement

To ensure an accurate ECG reading, make sure the posteriorelectrodes V7, V8, and V9 areplaced at the same level horizon-tally as the V6 lead at the fifth in-tercostal space. Place lead V7 atthe posterior axillary line, lead V9at the paraspinal line, and lead V8halfway between leads V7 and V9.

Midaxillary linePosterior axillary line

Left paraspinal line

V8V7V6 V9

V1RV2R

V3RV4R

V5R

V6R

Midclavicular lineAnterior axillary line

Midaxillary line


80

General 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

aVR

aVL

I

aVF

V1V2 V3

V4

V5

V6

View of theLead heart

Limb leads (bipolar)I Lateral wall

II Inferior wall

III Inferior wall

Augmented limb leads (unipolar)aVR No specific view

aVL Lateral wall

aVF Inferior wall

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

V2 Septal wall

V3 Anterior wall

V4 Anterior wall

V5 Lateral wall

V6 Lateral wall

Views reflected on a 12-lead ECG

IIIII


81

12-Lead

This chart will help you quickly determine the direction of a patient’s electrical axis. Observe the deflections of the QRS complexes in leads I and aVF. Lead I indicates whether impulsesare moving to the right or left, and lead aVF indicates whetherthey’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 aVF points down.• Right axis deviation: Lead I points down and lead aVF is upright.• Extreme right axis deviation: Both waves point down.

Electrical axis determination: Quadrant method

180° 0°

–90°

�90°

Extreme rightaxis deviation

Right axisdeviation

Left axisdeviation

Normal

I

aVF

I

aVF

I

aVF

I

aVF

�–


82

General 12-Lead

The degree method provides a more precise measurement ofthe 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 aVF. To use thismethod, take these steps.

Electrical axis determination: Degree method

Step 1Identify 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 aVR Lead aVL Lead aVF

�180º I

�150º �

�120ºII

aVF III

�

�

�90º�60º

�30º

0º

�30ºNormal axis�150º

aVL

��

�

aVR

�120º�90º �60º

�180º I

�150º�

�120ºII

aVF III

�

�

�90º�60º

�30º

0º

�30º�150ºaVL

��

�

aVR

�120º�90º �60º

Step 2Locate the axis for lead III on thehexaxial diagram. Then find theaxis perpendicular to it, which isthe axis for lead aVR.

Step 3Examine the QRS complex in leadaVR, noting whether the deflectionis positive or negative. As you cansee, the QRS complex for this lead is negative, indicating that the current is moving toward thenegative pole of aVR, which is inthe right lower quadrant at +30 degrees on the hexaxial diagram.So the electrical axis here is normal at +30 degrees.


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 hypertrophypregnancy, tumors)• Left bundle-branch block• Left ventricular hypertrophy• Aging

12-Lead


84

12-Lead

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

ECG changes in angina

Peaked T wave

Flattened T wave

T-wave inversion

ST-segment depression with T-wave inversion

ST-segment depression without T-wave inversion


85

12-Lead

ECG 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, aVR, aVF,and V2 through V6.• Stage 2—As pericarditis resolves, the ST-segment elevationand accompanying T-wave inversion resolves in most leads.

Pericarditis

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6


86

General 12-Lead

IschemiaIschemia 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.

InjuryThe 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).

InfarctInfarct 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

Myocardialischemia• T-wave inversion• ST-depression

Myocardialinjury• ST-segmentelevation• T-wave inversion

Myocardialinfarction• Hyperacute T waves (earlieststage)

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


87

12-Lead

After 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

Wallaffected

Anterior

Anterolateral

Anteroseptal

Inferior

Lateral

Posterior

Right ventricular

Leads

V2, V3, V4

I, aVL, V3, V4,V5, V6

V1, V2, V3, V4

II, III, aVF

I, aVL, V5, V6

V8, V9

V4R, V5R, V6R

Artery involved

Left coronary artery, left anteriordescending (LAD)

LAD and diagonalbranches, circum-flex and marginalbranches

LAD

Right coronary artery (RCA)

Circumflex branchof left coronary artery

RCA or circumflex

RCA

Reciprocalchanges

II, III, aVF

II, III, aVF

None

I, aVL

II, III, aVF

V1, V2, V3, V4 (Rgreater than S in V1and V2, ST-segmentdepression, elevatedT wave)

None


88

General 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 V1 and a large R wave(shaded area in right strip) in V5. If the depth (in mm) of the S wave in V1 added to the height (in mm) of the R wave in V5exceeds 35 mm, then the patient has left ventricular hypertrophy.

Left ventricular hypertrophy

Lead V1 Lead V5


89

12-Lead

Electrical 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 accessorypathway — 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-Parkinson-White syndrome

Short PR interval Delta wave


1

2

3

Block

90

General 12-Lead

Understanding RBBB

In RBBB, the initial impulse activates the interventricular septumfrom 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 andhas a different configuration, sometimes resembling rabbit earsor the letter “M.” Septal depolarization isn’t affected in lead V1,so the initial small R wave remains.

The R wave is followed by an S wave, which represents leftventricular 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 bydepolarization of the left ventricle, which produces a tall R wave.Depolarization of the right ventricle then causes a broad S wave.In lead V6, the T wave should be positive.


91

12-Lead

This 12-lead ECG shows the characteristic changes of RBBB. Inlead V1, note the rsR� 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 aVR Lead V1 Lead V4

Lead II Lead aVL Lead V2 Lead V5

Lead III Lead aVF Lead V3 Lead V6


92

General 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 becausethe 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 V1 with a positive T wave.The S wave may be preceded by a Q wave or a small R wave.

In lead V6, no initial Q wave occurs. A tall, notched R wave, or aslurred 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

2

3

Block


93

12-Lead

This 12-lead ECG shows characteristic changes of LBBB. All leadshave prolonged QRS complexes. In lead V1, note the QS wavepattern. In lead V6, note the slurred R wave and T-wave inversion.The elevated ST segments and upright T waves in leads V1 and V4are also common in this condition.

Recognizing LBBB

Lead I Lead aVR Lead V1 Lead V4

Lead II Lead aVL Lead V2 Lead V5

Lead III Lead aVF Lead V3 Lead V6


Check rhythm. Shockable rhythm?2

VF/VT3 YES NO

Asystole/PEA

9

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

4

Pulseless 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

94

Treat


95

YES

Check 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

12Go to

box 4.

13


• 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

YESNO

Give 5 cycles of CPR*


NO


NO


Treat

Pulseless 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 forCardiopulmonary Resuscitation and Emergency Cardiovascular Care,” Circulation2005: 112 (suppl IV). © 2005, American Heart Association.


96

General

96

Tachycardia 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?

6Wide QRS*

Is rhythm regular?Expert consultation advised.

• Attempt vagalmaneuvers.• Give adeno-sine 6 mg rapidI.V. push. If noconversion, give12 mg rapid I.V. push; mayrepeat 12 mgdose once.

7Irregular Narrow-ComplexTachycardiaProbable 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).

11

Symptoms persist

Stable

Narrow (< 0.12 sec) Wide (> 0.12 sec)

Regular Irregular

Uns

tabl

e

Tachycardia with pulses1

12

3

Treat


97

Treat

Tachycardia algorithm (continued)

Does rhythm convert?Note: Consider expert consultation.

8

If rhythm con-verts, probablyreentry supra-ventriculartachycardia(SVT)• Observe forrecurrence.• Treatrecurrencewith adenosineor longer-acting AV nodalblockingagents (suchas diltiazem orbeta blockers).

9

If rhythm doesNOT convert,possible atrialflutter, ectopicatrial tachycardia,or junctionaltachycardia• Control rate(diltiazem, betablockers; use betablockers with caution in pulmonarydisease or CHF).• Treat underlyingcause.• Consider expertconsultation.

10Converts

If ventriculartachycardia oruncertainrhythm• Amiodarone150 mg I.V. over10 min. Repeatas needed tomaximum dose of 2.2 g/24 hours.• Prepare forelectivesynchronizedcardioversion.If SVT withaberrancy• Giveadenosine (goto box 7).

13 Regular

If atrial fibril-lation withaberrancy• See IrregularNarrow-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 recurrentpolymorphicVT• Seek expertconsultation.If torsades depointes• 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 HeartAssociation Guidelines for Cardiopulmonary Resuscitationand Emergency Cardiovascular Care,” Circulation 2005: 112(suppl IV). © 2005, American Heart Association.


98

General 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 forCardiopulmonary Resuscitation and Emergency Cardiovascular Care,” Circulation2005: 112 (suppl IV). © 2005, American Heart Association.

BradycardiaHeart rate < 60 beats/min and inadequate for clinical condition

Poor perfusionAdequate perfusion


99

Treat

Guide to antiarrhythmic drugs

This chart details the drugs most commonly used to managecardiac arrhythmias, including indications and special consider-ations for each.

Drugs

Disopyramide,procainamide,quinidine

Lidocaine, mexiletine

Flecainide,moricizine,propafenone

Indications

• VT• Atrial fibrillation• Atrial flutter• PAT

• VT• VT• VF

• VT• VF• Supraventriculararrhythmias

Special considerations

• Check apical pulse rate beforetherapy. 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 potentiatethe 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

100

Treat

Guide to antiarrhythmic drugs (continued)

Drugs

Acebutolol,atenolol, esmolol, propranolol

Amiodarone,dofetilide, ibutilide, sotalol

Diltiazem, verapamil

Indications

• Atrial flutter• Atrial fibrillation• PAT

• Life-threateningarrhythmias re-sistant to otherantiarrhythmicdrugs

• Supraventriculararrhythmias


• 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 andrhythm 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 andBP carefully when initiating therapyor increasing dosage.• Calcium supplements may reduceeffectiveness.

Class II antiarrhythmics

Class III antiarrhythmics

Class IV antiarrhythmics


101

Treat

Guide to antiarrhythmic drugs (continued)

Drugs

Adenosine

Atropine

Epinephrine

Vasopressin

Indications

• PSVT

• Symptomatic SB• AV block• Asystole• BradycardicPEA

• Pulseless VT• VF• Asystole• PEA

• VF that’s un-responsive to defibrillation


• Adenosine must be administeredover 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. Usethe 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 andBP 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. Usethe drug cautiously in patients withmyocardial ischemia.• Monitor for hypersensitivity reac-tions, especially urticaria, angio-edema, and bronchoconstriction.

Miscellaneous antiarrhythmics


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AnterolateralplacementPlace one paddle to theright 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 placementPlace 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


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Precautions must be taken when defibrillating a patient with anICD, a pacemaker, or a transdermal medication patch or a pa-tient who’s in contact with water.

Defibrillating a patient with an ICD or pacemakerAvoid 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 patchAvoid placing the defibrillator paddles or pads directly on topof 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 waterWater 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


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Monophasic defibrillatorsMonophasicdefibrillatorsdeliver 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 defibrillatorsBiphasic 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 efficientThe 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.

AdjustableThe 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 damageBecause 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

Currentflow

Currentflow

Currentflow


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How it worksIn synchronized cardioversion, an electric current is delivered tothe 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 cardioversionuses much lower energy levels and is synchronized to deliver an electric charge to the myocardium on the peak R wave.

What it doesThe 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 ensuresthat 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


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Transcutaneous pacing, also referred to as external or noninva-sive pacing, involves the delivery of electrical impulses throughexternally applied cutaneous electrodes. The electrical impulsesare 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 itTranscutaneous 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


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Implanting a pacemaker is a simple surgical procedure performedwith 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 placementFor 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 generatorWhen 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 insubcutaneouspocket

Right atrial lead

Rightventricular lead


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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.

Pacemaker spikes

Understanding pacemaker codesA permanent pacemaker’s three-letter (or sometimes five-letter)code simply refers to how it’s programmed.

First letter(chamber that’s paced)A atriumV ventricleD dual (both chambers)O not applicable

Secondletter(chamber that’s sensed)A atriumV ventricleD dual (both chambers)O not applicable

Third letter(pulsegenerator’sresponse)I inhibitedT triggeredD dual (inhibited andtriggered)O not applicable

Fourthletter(pacemaker’sprogrammability)P basic functions programmableM multiple programmableparametersC communi-cating func-tions such astelemetryR rate respon-sivenessN none

Fifth letter(pacemaker’sresponse totachycardia)P pacing abilityS shockD dual abilityto shock andpaceO none

QRS complexP wave

Atrial pacemaker spike

Ventricularpacemaker spike


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A biventricular pacemaker uses three leads: one to pace theright 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 atrium

Right ventricular lead

Right ventricle

Left ventricular lead (in coronary sinus vein)

Left ventricle


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The settings on a temporary pulse generator may be changed invarious 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 markingsidentify positive andnegative terminals.

Pace meterregisters every pacingstimulus delivered tothe heart.

Sensitivity controladjusts pacemakersensitivity (measuredin millivolts) to thepatient’s heart rate.Turning the dialcounterclockwise toASYNC fixes the rate.

Battery compartmentholds the alkalinebatteries.

Connector terminalshold the leads.

Sensing meterregisters every time anintrinsic depolarizationis recognized.

Rate controldirects the number ofpulses given eachminute.

Energy output controldetermines the amountof electricity (in milli-amperes) sent to theheart.

On-off switchactivates the pulsegenerator.

��


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Temporary pacemaker malfunctions

Failure to paceECG 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 captureECG 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.

Pacemakerspike shouldappear here

There’s a pacemakerspike but no responsefrom the heart

(continued)


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Failure to sense intrinsicbeats (undersensing)ECG shows pacemaker spikesanywhere 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 firesanywhere in the cycle

Temporary pacemaker malfunctions (continued)


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An ICD has a programmable pulse generator and lead systemthat monitors the heart’s activity, detects ventricular arrhyth-mias and other tachyarrhythmias, and responds with appro-priate therapies.

What it doesThe 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 ICDImplantation 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

Leadwire

Pulsegenerator


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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

Cardioversion

Defibrillation

Bradycardia pacing

Description

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) istimed to the R wave to terminate VT and returnthe heart to its normal rhythm.

A high-energy shock (up to 35 joules) to theheart is used to terminate VF and return theheart to its normal rhythm.

Electrical pacing pulses are used when theheart’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).


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Device• 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)


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• Multiple shocks indicate a medical emergency, and the patientmay 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)


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Notes


118

Notes


119

Notes


120

American Heart Association. Handbook of Emergency Cardio-vascular Care for Healthcare Providers. Dallas: American HeartAssociation, 2005.

Assessment Made Incredibly Easy, 4th ed. Philadelphia: LippincottWilliams & 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: LippincottWilliams & 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: LippincottWilliams & Wilkins, 2009.

Nursing Know-How: Interpreting ECGs. Philadelphia: LippincottWilliams & Wilkins, 2008.

Tsiperfal, A., et al. “What Is Drug-Induced Long QT and What Isa Potential Clinical Consequence?” Progress in CardiovascularNursing 21(2):104-5, Spring 2006.

Wysocki, L. “ST Segment Changes Clue You In to Injury Location,”RN 69(9):49, September 2006.

Selected references


121

IndexAbbreviations, viAccelerated junctional

rhythm, 46-47Accelerated idioventric-

ular rhythm, 56-57Angina, ECG changes in,

84Antiarrhythmic drugs,

99-101Ashman’s phenomenon,

38-39Asystole, 64-65Atrial fibrillation, 36-37Atrial flutter, 34-35Atrial tachycardia, 30-33Bradycardia

algorithm for, 98in children, 13

Cardiac conductionsystem, 4

Cardioversion, synchro-nized, 105

Coronary vessels, 2-3Defibrillators

paddle placement, 102

safety issues with, 103types of, 104

ECGevaluation, 9grid, 4normal, 8QTc interval normals, 9

Einthoven’s triangle, 5Electrical axis

determination of, 81-82

deviation of, 83Electrolyte imbalances,

ECG and, 14First-degree AV block,

68-69Heart location, 1

Heart ratecalculating, 12in children, 13

ICD, 113managing, 115-116therapies delivered

by, 114Idioventricular rhythm,

54-55Junctional rhythm, 44-45Junctional tachycardia,

48-49LBBB, 92-93Leads

augmented, 6best monitoring, iibiventricular, place-

ment of, 109cardiac monitoring,

positioning, 7limb, placement of,

76-77posterior, placement

of, 79precordial, placement

of, 78-79Left ventricular hyper-

trophy, 88Myocardial infarct, 86

locating damage in, 87Myocardial injury, 86Myocardial ischemia, 86Pacemaker

biventricular, 109codes, 108implanting, 107malfunctions, 111-112spikes, 108transcutaneous, 106

PACs, 28-29Pericarditis, ECG

changes in, 85PJCs, 42-43

Pulseless arrest algo-rithm, 94-95

Pulseless electricalactivity, 66-67

PVCs, 50-53QTc interval, normal, 9RBBB, 90-91Rhythm strips

interpreting, 9methods of measur-

ing, 10patterns of, 11

SA exit block, 24-25Sick sinus syndrome,

26-27Sinus 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-degreeAV block, 70-71

Type II second-degreeAV block, 72-73

Ventricular fibrillation,62-63

Ventricular tachycardia,58-59

Wandering pacemaker,40-41

WPW syndrome, 89


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