Rapid ACLS Revised 2nd Ed

BBaarrbbaarraa AAeehhlleerrtt,, RN, BSPASouthwest EMS Education, Inc.Phoenix, Arizona/Pursley, Texas

Revised Second Edition

11830Westline Industrial DriveSt. Louis, Missouri 63146

RAPID ACLSRevised Second Edition

Copyright 2012, 2007, 2003 by Mosby, Inc., an affiliate ofElsevier Inc.

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NoticeKnowledge and best practice in this field are constantlychanging. As new research and experience broaden ourknowledge, changes in practice, treatment and drug therapymay become necessary or appropriate. Readers are advised tocheck the most current information provided (i) on proceduresfeatured or (ii) by the manufacturer of each product to beadministered, to verify the recommended dose or formula, themethod and duration of administration, and contraindications.It is the responsibility of the practitioners, relying on their ownexperience and knowledge of the patient, to make diagnoses,to determine dosages and the best treatment for eachindividual patient, and to take all appropriate safetyprecautions.To the fullest extent of the law, neither thePublisher nor the Author assumes any liability for any injuryand/or damage to persons or property arising out or related toany use of the material contained in this book.

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Last digit is the print number: 9 8 7 6 5 4 3 2 1

ISBN-13: 978-0-323-08320-1

ABCDs OF EMERGENCY CARDIAC CARE

Risk Factors for Coronary Artery Disease . . . . .1 Sudden Cardiac Death . . . . . . . . . . . . . . . . . . . . .2

Cardiac Arrest Rhythms . . . . . . . . . . . . . . . . . .4Chain of Survival . . . . . . . . . . . . . . . . . . . . . . . . .4Basic Life Support . . . . . . . . . . . . . . . . . . . . . . . .4Phases of CPR . . . . . . . . . . . . . . . . . . . . . . . . . . . .5

Components of Advanced Cardiac Care . . . . .5Initial Goals of Post-Cardiac

Arrest Care . . . . . . . . . . . . . . . . . . . . . . . . . . .8Possible Treatable Causes of Cardiac

Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . .9

RISK FACTORS FOR CORONARYARTERY DISEASE

Non-modifiable(Fixed) Factors

Heredity

Race

Gender

Age

ModifiableFactors

High bloodpressure

Elevated serumcholesterollevels

Tobacco use

Diabetes Physical

inactivity Obesity Metabolic

syndrome

ContributingFactors

Stress

Inflammatorymarkers

Psychosocialfactors

Alcohol intake

Cardiovascular Disease Risk Factors

2

SUDDEN CARDIAC DEATH Cardiopulmonary (cardiac) arrest is the

absence of cardiac mechanical activity,confirmed by the absence of a detectablepulse, unresponsiveness, and apnea oragonal, gasping breathing.

Sudden cardiac death (SCD) is an unex-pected death due to a cardiac cause thatoccurs either immediately or within 1 hourof the onset of symptoms. Some victims of SCD have no warning

signs of the impending event. For others,warning signs may be present up to 1hour before the actual arrest.

Because of irreversible brain damage anddependence upon life support, somepatients may live days to weeks after thecardiac arrest before biological deathoccurs.These factors influence interpreta-tion of the 1 hour definition of suddencardiac death.1

CategoryNormalPrehypertensionStage 1 highblood pressure

Stage 2 highblood pressure

Systolicblood pressure

(in mm Hg)Less than 120120 to 139

140 to 159

160 or higher

Diastolicblood pressure

(in mm Hg)Less than 8080 to 89

90 to 99

100 or higher

From the National Heart Lung and Blood Institute:High blood pressure,www.nhlbi.nih.gov/health/dci/Diseases/Hbp/HBP_WhatIs.html. Accessed 5/15/2005.

* For adults 18 and older who: Are not on medicine for high bloodpressure Are not having a short-term serious illness Do not have other conditions such as diabetes and

kidney disease

Blood Pressure Values in Adults*

Upto1hour

TimeReferencesinSuddenCardiacDeath

Days-to-months

Prodromes

Cardiacarrest

Onsetofterminal

event

Biological

death

Minutes-to-weeks

Newor

worsening

cardiovascular

symptoms

Chestpain

Palpitations

Dyspnea

Fatigability

Abruptchangein

clinicalstatus

Arrhythmia

Hypotension

Chestpain

Dyspnea

Lightheadedness

Suddencollapse

Lossofeffective

circulation

Lossof

consciousness

Failureof

resuscitation

OR

Failureofelectrical,

mechanical,or

CNSfunction

afterinitial

resuscitation

3

14

4

CARDIAC ARREST RHYTHMS

Shockable rhythms Ventricular tachycardia (VT) Ventricular fibrillation (VF)

Nonshockable rhythms Asystole Pulseless electrical activity (PEA)

CHAIN OF SURVIVALThe Chain of Survival represents the idealseries of events that should take place imme-diately after the recognition of the onset ofsudden illness. The chain consists of five keysteps that are interrelated. Following thesesteps gives the victim the best chance of sur-viving a heart attack or sudden cardiac arrest.The links in the chain of survival for adultsinclude early recognition and activation, earlyCPR, early defibrillation, early advanced lifesupport (ALS), and integrated post-cardiacarrest care.

BASIC LIFE SUPPORTCOMPONENTS OF BASIC LIFE SUPPORT

Recognition of signs of: Cardiac arrest Heart attack Stroke Foreign-body airway obstruction (FBAO)

Relief of FBAOCardiopulmonary resuscitation (CPR)Defibrillation with an automated externaldefibrillator (AED)

5

COMPONENTS OF ADVANCEDCARDIAC CARE

Basic life support Advanced airway management Ventilation support ECG/dysrhythmia recognition 12-lead ECG interpretation Vascular access and fluid resuscitation Electrical therapy including defibrillation,

synchronized cardioversion, and pacing Giving medications Coronary artery bypass, stent insertion,

angioplasty, intraaortic balloon pump therapy

Phase 1

2

3

Phase NameElectrical phase

Circulatory(hemodynamic)phase

Metabolicphase

Time from VFarrest

From time of arrestto about the first 5min after arrest

About 5 min to 15min after arrest

After about 15 min

Importantintervention

Electrical therapy

CPR beforeelectrical therapy

Therapeutichypothermia

Phases of CPR

6

Infa

ntUn

der1

year

Child

1to

abou

t12

to14

year

sAd

ult/O

lder

Child

Mor

eth

an12

to14

year

sCP

R/Re

scue

Brea

thin

gAg

eLe

velo

fRes

pons

iven

ess

Chec

kfo

rbre

athi

ng

C=

Circ

ulat

ion

Chec

kpu

lse

Chec

kla

ndm

arks

Com

pres

sch

estw

ith

Com

pres

sion

dept

h

Com

pres

sion

rate

Com

pres

sion

/ven

tilat

ion

ratio

Esta

blis

hun

resp

onsi

vene

ss,t

apan

das

klo

udly,

Are

you

okay

?If

norm

albr

eath

ing

ispr

esen

t,CP

Ris

notn

eede

d.If

the

vict

imis

unre

spon

sive

and

notb

reat

hing

(oro

nly

gasp

ing)

,ask

som

eone

toac

tivat

eth

eem

erge

ncy

resp

onse

syst

eman

dge

tade

fibril

lato

r.*Br

achi

alPu

lse

pres

ent,

supp

ort

airw

ayan

dbr

eath

ing.

No

puls

e,st

artc

ompr

essi

ons

Just

belo

wni

pple

line

2fin

gers

(1re

scue

r)or

2th

umbs

enci

rclin

gch

est(

2re

scue

rs)

Atle

ast1

/3th

ean

terio

r-po

ster

iord

iam

eter

ofth

ech

est(

abou

t1.5

in[4

cm])

Atle

ast1

00/m

in1

resc

uer=

30:2

2re

scue

rs=

15:2

Caro

tidPu

lse

pres

ent,

supp

orta

irway

and

brea

thin

g.N

opu

lse,

star

tco

mpr

essi

ons,

call

forA

EDJu

stbe

low

nipp

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elof

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ndor

asfo

radu

lt

Atle

ast1

/3th

ean

terio

r-pos

terio

rdi

amet

erof

the

ches

t(a

bout

2in

[5cm

])At

leas

t100

/min

1re

scue

r=30

:22

resc

uers

=15

:2

Caro

tidPu

lse

pres

ent,

supp

orta

irway

and

brea

thin

g.N

opu

lse,

star

tco

mpr

essi

ons,

call

forA

EDJu

stbe

low

nipp

lelin

eHe

elof

1ha

nd,o

ther

hand

onto

p

Atle

ast2

in(5

cm)

Atle

ast1

00/m

in1

or2

resc

uers

=30

:2

Su

mm

ary

ofT

reat

men

tfo

rA

du

lt,C

hild

,In

fan

tC

ho

kin

g,a

nd

CP

R

7

Infa

nt

CPR

for5

cycl

es,r

eche

ckpu

lse.

Ifno

puls

e,co

ntin

ueCP

R.Re

chec

kpu

lse

ever

y5

cycl

es(a

bout

ever

y2

min

utes

).M

anua

ldef

ibril

lato

rpre

-fe

rred

.Ifa

man

uald

efib

ril-

lato

ris

nota

vaila

ble,

anAE

Deq

uipp

edw

itha

pedi

-at

ricat

tenu

ator

isde

sir-

able

.Ifn

eith

eris

avai

labl

e,us

ea

stan

dard

AED.

Child

Ifw

itnes

sed

arre

st,u

seAE

D.Po

wer

onAE

D,ap

ply

pads

.An

alyz

erh

thym

,sho

ckif

indi

cate

dus

ing

pedi

atric

pads

/cab

lesy

stem

.Us

eAE

Deq

uipp

edw

itha

pedi

atric

atte

nuat

or,i

fava

ilabl

e.If

unav

aila

ble,

use

stan

dard

AED.

Adul

t/Old

erCh

ild

Ifw

itnes

sed

arre

st,u

seAE

D.Po

wer

onAE

D,ap

ply

pads

.An

alyz

erh

thym

,sho

ckif

indi

cate

d

Use

stan

dard

AED.

CPR/

Resc

ueBr

eath

ing

A=

Airw

ayB

=Br

eath

ing

D=

Defib

rilla

tion,

ifne

cess

ary

Deliv

er2

brea

ths;

each

brea

thsh

ould

take

abou

t1se

c.M

ake

sure

the

brea

ths

are

effe

ctiv

e(th

ech

estr

ises

).If

the

ches

tdoe

sno

tris

e,re

posi

tion

the

head

,mak

ea

bette

rsea

l,an

dtry

agai

n.Av

oid

exce

ssiv

eve

ntila

tion

(too

man

ybr

eath

s,to

ola

rge

avo

lum

e).

Ifsho

ckad

vised

,clea

rvict

im,g

ive1s

hock

,imm

ediat

elyre

sum

eCPR

for5

cycle

s,th

enre

analy

zerh

ythm

.Sho

ckde

liver

ysho

uldide

allyo

ccur

asso

onas

poss

iblea

fterc

ompr

essio

ns.If

nosh

ocka

dvise

d,im

med

iately

resu

meC

PR.

*Alo

ne

resc

uer

sho

uld

per

form

5cy

cles

of

CP

R(a

bo

ut

30co

mp

ress

ion

san

d2

bre

ath

sfo

rab

ou

t2

min

)b

efo

rele

avin

gan

infa

nt

or

child

vict

im(o

rad

ult

vict

imo

fp

resu

med

asp

hyxi

alar

rest

,su

chas

dro

wn

ing

)to

acti

vate

the

emer

gen

cyre

spo

nse

syst

eman

do

bta

inan

AE

D.

8

INITIAL GOALS OFPOST-CARDIAC ARREST CARE*

Provide cardiorespiratory support tooptimize tissue perfusionespecially tothe heart, brain, and lungs (the organsmost affected by cardiac arrest).

Transport of the out-of-hospital post-cardiac arrest patient to an appropriatefacility capable of providing comprehen-sive postcardiac arrest care includingacute coronary interventions, neurologicalcare, goal-directed critical care, andhypothermia.

Transport of the in-hospital post-cardiacarrest patient to a critical care unit capableof providing comprehensive postcardiacarrest care.

Attempt to identify the precipitating cause of the arrest, start specific treatmentif necessary, and take actions to preventrecurrence.

*Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: postcardiac arrest care: 2010 American Heart AssociationGuidelines for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care. Circulation. 2010;122(suppl3):S768 S786.

9

POSSIBLE TREATABLE CAUSESOF CARDIAC EMERGENCIES

PATCH-4-MD

Pulmonary embolism anticoagulants? surgery?Acidosis ventilation, correct acid-base disturbancesTension pneumothorax needle decompressionCardiac tamponade pericardiocentesisHypovolemia replace volumeHypoxia ensure adequate oxygenation and ventilationHeat / cold (hyperthermia/hypothermia) cooling/warming methodsHypo-/hyperkalemia (and other electrolytes) monitor serum glucose levels closely, cor-rect electrolyte disturbances Myocardial infarction reperfusion therapyDrug overdose / accidents antidote/specifictherapy

10

POSSIBLE TREATABLE CAUSESOF CARDIAC EMERGENCIES

Five Hs and Five Ts

Hypovolemia Tamponade, cardiac

Hypoxia Tension pneumothorax

Hypothermia Thrombosis: lungs(massive pulmonary embolism)

Hypo-/Hyperkalemia Thrombosis: heart(acute coronary syndromes)

Hydrogen ion Tablets/toxins: drug overdose(acidosis)

AIRWAY MANAGEMENT ANDVENTILATION

Oxygen Percentage Delivery by Device . . . . . .11Manual Airway Maneuvers . . . . . . . . . . . . . . . .12Mouth-to-Mask Ventilation . . . . . . . . . . . . . . . .13Oral and Nasal Airways . . . . . . . . . . . . . . . . . . .14Bag-Mask Ventilation . . . . . . . . . . . . . . . . . . . . .16Combitube . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17Laryngeal Mask Airway . . . . . . . . . . . . . . . . . . .20Tracheal Intubation . . . . . . . . . . . . . . . . . . . . . . .24Confirming Tracheal Tube Placement . . . . . . . . .26

DeviceNasal CannulaSimple Face MaskPartial Rebreather

Mask

Nonrebreather Mask

ApproximateInspired OxygenConcentration

22% to 45%35% to 60%35% to 60%

60% to 80%

Liter Flow(Liters/Minute)

0.25 to 85 to 10 Typically 6 to 10

to prevent bagcollapse

Typically 10 toprevent bag collapse

Oxygen Percentage Delivery by Device

12

Indi

catio

ns

Cont

rain

dica

tions

Adva

ntag

es

Disa

dvan

tage

s

Head

-tilt/

chin

-lift

Unre

spon

sive

patie

ntN

om

echa

nism

forc

ervi

cals

pine

inju

ryU

nabl

eto

prot

ecto

wn

airw

ayA

wak

epa

tient

Pos

sibl

ece

rvic

alsp

ine

inju

ryS

impl

eto

pref

orm

No

equi

pmen

treq

uire

dN

onin

vasi

veD

oes

notp

rote

ctlo

wer

airw

ayfro

mas

pira

tion

May

caus

esp

inal

mov

emen

t

Jaw

thru

stw

ithou

thea

d-til

tUn

resp

onsi

vepa

tient

Pos

sibl

ece

rvic

alsp

ine

inju

ryU

nabl

eto

prot

ecto

wn

airw

ayA

wak

epa

tient

No

equi

pmen

treq

uire

dN

onin

vasi

ve

Diff

icul

tto

mai

ntai

nS

econ

dre

scue

rnee

ded

forb

ag-

valv

e-m

ask

vent

ilatio

nD

oes

notp

rote

ctlo

wer

airw

ayfro

mas

pira

tion

May

caus

esp

inal

mov

emen

t

Man

ual

Air

way

Man

euve

rs

13

Inspired Oxygen Concentration

Advantages

Disadvantages

Without supplemental oxygen equalsabout 16% to 17% (exhaled air)

Mouth-to-mask breathing combined withsupplemental oxygen at a minimum flowrate of 10 L/min equals about 50%

Aesthetically more acceptable thanmouth-to-mouth ventilation

Easy to teach and learn Physical barrier between the rescuer

and the patient's nose, mouth, andsecretions

Reduces (but does not prevent) the riskof exposure to infectious disease

Use of a one-way valve at the ventilationport decreases exposure to patientsexhaled air

If the patient resumes spontaneousbreathing, the mask can be used as asimple face mask to deliver 40% to 60%oxygen by giving supplemental oxygenthrough the oxygen inlet on the mask (ifso equipped).

Can deliver a greater tidal volume withmouth-to-mask ventilation than with abag-mask device

Rescuer can feel the compliance of thepatients lungs (Compliance refers to theresistance of the patients lung tissue toventilation)

Rescuer fatigue Possible gastric distention

Mouth-to-Mask Ventilation

14

Indi

catio

ns

Cont

rain

dica

tions

Sizin

gAd

vant

ages

Oral

Airw

ayH

elp

mai

ntai

nan

open

airw

ayin

anun

resp

onsi

vepa

tient

who

isno

tint

ubat

edH

elp

mai

ntai

nan

open

airw

ayin

anun

resp

onsi

vepa

tient

with

noga

gre

flex

who

isbe

ing

vent

ilate

dw

itha

bag-

mas

kor

othe

rpos

itive

-pre

ssur

ede

vice

May

beus

edas

abi

tebl

ock

afte

rins

ertio

nof

atra

chea

ltub

eor

orog

astri

ctu

beR

espo

nsiv

epa

tient

Cor

nero

fmou

thto

tipof

earlo

beor

angl

eof

jaw

Pos

ition

sth

eto

ngue

forw

ard

and

away

from

the

back

ofth

eth

roat

Eas

ilypl

aced

Nas

alAi

rway

To

aid

inm

aint

aini

ngan

open

airw

ayw

hen

use

ofan

oral

airw

ayis

cont

rain

dica

ted

orim

poss

ible

Tris

mus

(spa

smof

the

mus

cles

used

togr

ind,

crus

h,an

dch

ewfo

od)

Biti

ngC

lenc

hed

jaw

sor

teet

h

Sev

ere

cran

iofa

cial

traum

aP

atie

ntin

tole

ranc

eT

ipof

nose

toan

gle

ofth

eja

wor

the

tipof

the

ear

Pro

vide

san

open

airw

ayT

oler

ated

byre

spon

sive

patie

nts

Doe

sno

treq

uire

mou

thto

beop

en

Ora

lan

dN

asal

Air

way

s

15

Disa

dvan

tage

s

Prec

autio

ns

Doe

sno

tpro

tect

the

low

erai

rway

from

aspi

ratio

nM

aypr

oduc

evo

miti

ngif

used

ina

resp

onsi

veor

sem

i-res

pons

ive

patie

ntw

itha

gag

refle

x

Use

ofth

ede

vice

does

note

limin

ate

the

need

for

mai

ntai

ning

prop

erhe

adpo

sitio

n

Doe

sno

tpro

tect

the

low

erai

rway

from

aspi

ratio

nI

mpr

oper

tech

niqu

em

ayre

sult

inse

vere

blee

ding

Res

ultin

gep

ista

xis

may

bedi

fficu

ltto

cont

rol

Suc

tioni

ngth

roug

hth

ede

vice

isdi

fficu

ltA

lthou

ghto

lera

ted

bym

ostr

espo

nsiv

ean

dse

mi-

resp

onsi

vepa

tient

s,ca

nst

imul

ate

the

gag

refle

xin

sens

itive

patie

nts,

prec

ipita

ting

lary

ngos

pasm

and

vom

iting

Use

ofth

ede

vice

does

note

limin

ate

the

need

for

mai

ntai

ning

prop

erhe

adpo

sitio

n

16

Advantages

Disadvantages

Provides a means for delivery of an oxy-gen enriched mixture to the patient

Conveys a sense of compliance ofpatients lungs to the bag-mask operator

Provides a means for immediate ventila-tory support

Can be used with the spontaneouslybreathing patient as well as the non-breathing patient

Requires practice to use effectively Delivery of inadequate tidal volume Rescuer fatigue Possible gastric distention

Bag-Mask Ventilation

17

Air

Esophageal tube

Tracheal tube

Cuff inflationports

Pharyngeal cuff

Tracheal oresophageal cuff

Air

A

B

A,The Combitube inserted into the esophagus.16B,The Combitube inserted into the trachea.16

18

Indications

Contraindications

Advantages

Difficult face mask fit (beards, absenceof teeth)

Patient in whom intubation has beenunsuccessful and ventilation is difficult

Patient in whom airway management isnecessary but the healthcare provideris untrained in the technique of visual-ized orotracheal intubation

Patient with an intact gag reflex Patient with known or suspected

esophageal disease Patient known to have ingested a caus-

tic substance Suspected upper airway obstruction due

to laryngeal foreign body or pathology Patient less than 4 feet tall Minimal training and retraining

requiredVisualization of the upper airway or useof special equipment not required forinsertion

Reasonable technique for use in sus-pected neck injury since the head doesnot need to be hyperextended

Because of the oropharyngeal balloon,the need for a face mask is eliminated

Can provide an open airway with eitheresophageal or tracheal placement

If placed in the esophagus, allows suc-tioning of gastric contents withoutinterruption of ventilation

Reduces risk of aspiration of gastriccontents

Combitube

19

Disadvantages Proximal port may be occluded withsecretions

Proper identification of tube location maybe difficult, leading to ventilation throughthe wrong lumen

Soft tissue trauma due to rigidity of tube Impossible to suction the trachea when

the tube is in the esophagus Esophageal or tracheal trauma due to

poor insertion technique or use of wrongsize device

Damage to the cuffs by the patientsteeth during insertion

Inability to insert due to limited mouthopening

Combitubecontd

20

Indications

Contraindications

Advantages

Difficult face mask fit (beards, absenceof teeth)

Patient in whom intubation has beenunsuccessful and ventilation is difficult

Patient in whom airway management isnecessary but the healthcare provideris untrained in the technique ofvisualized orotracheal intubation

Many elective surgical procedures(i.e., minimal soft tissue trauma withless patient discomfort and relativelyshort periods of anesthesia)

Healthcare provider untrained in use ofLaryngeal Mask Airway (LMA)

Contraindicated if a risk of aspirationexists (i.e., patients with full stomachs)

Can be quickly inserted to provideventilation when bag-mask ventilationis not sufficient and tracheal intubationcannot be readily accomplished

Tidal volume delivered may be greaterwhen using the LMA than with facemask ventilation

Less gastric insufflation than withbag-mask ventilation

Provides ventilation equivalent to thetracheal tube

Training simpler than with trachealintubation

Unaffected by anatomic factors (e.g.,beard, absence of teeth)

No risk of esophageal or bronchialintubation

When compared to tracheal intubation,less potential for trauma from directlaryngoscopy and tracheal intubation

Less coughing, laryngeal spasm, sorethroat, and voice changes than withtracheal intubation

Laryngeal Mask Airway

21

Disadvantages Does not provide protection against aspiration

Cannot be used if the mouth cannot beopened more than 0.6 in (1.5 cm)

May not be effective when respiratoryanatomy is abnormal (i.e., abnormaloropharyngeal anatomy or the presenceof pathology is likely to result in a poormask fit)

May be difficult to provide adequateventilation if high airway pressures arerequired

Laryngeal Mask Airwaycontd

22

The laryngeal mask airway (LMA). A, An LMA withthe cuff inflated. B, LMA placement into the pharynx.C, LMA placement using the index finger as a guide.D, LMA in place with cuff overlying pharynx.17

B

A

23

C

D

24

Indications

Contraindications

Advantages

Disadvantages

Inability of the patient to protect his orher own airway due to the absence ofprotective reflexes (e.g., coma,respiratory and/or cardiac arrest)

Inability of the rescuer to ventilate theunresponsive patient with less invasivemethods

Present or impending airway obstruc-tion/respiratory failure (e.g., inhalationinjury, severe asthma, exacerbation ofchronic obstructive pulmonary disease,severe pulmonary edema, severe flailchest or pulmonary contusion)

When prolonged ventilatory support isrequired

Healthcare provider untrained intracheal intubation

Isolates the airway Keeps the airway open Reduces the risk of aspiration Ensures delivery of a high

concentration of oxygen Permits suctioning of the trachea Provides a route for administration of

some medications (see IV/Meds chapter)

Ensures delivery of a selected tidalvolume to maintain lung inflation

Considerable training and experiencerequired; retraining may be needed toensure competency

Special equipment needed Bypasses physiologic function of upper

airway (e.g., warming, filtering,humidifying of inhaled air)

Requires direct visualization of vocalcords

Tracheal Intubation

25Esophageal detector device. A, Syringe. B, Bulb.18

A

B

26

CONFIRMING TRACHEAL TUBE PLACEMENT

Methods used to verify proper placement ofa tracheal tube include the following: Visualizing the passage of the tracheal

tube between the vocal cords Auscultating the presence of bilateral

breath sounds Confirming the absence of sounds over

the epigastrium during ventilation Adequate chest rise with each ventilation Absence of vocal sounds after placement

of the tracheal tube End-tidal carbon dioxide measurement

(waveform capnography preferred) Verification of tube placement by an

esophageal detector device Chest radiograph

RHYTHM RECOGNITION

Too Fast RhythmsNarrow-QRS Tachycardias . . . . . . . . . . . . . .32Wide-QRS Tachycardias . . . . . . . . . . . . . . . .38Irregular Tachycardias . . . . . . . . . . . . . . . . .40

Too Slow RhythmsSinus Bradycardia . . . . . . . . . . . . . . . . . . . .46Junctional Rhythm . . . . . . . . . . . . . . . . . . . .48Ventricular Escape Rhythm . . . . . . . . . . . . .49First-Degree AV Block . . . . . . . . . . . . . . . . .51Second-Degree AV BlockType I . . . . . . . .52Second-Degree AV BlockType II . . . . . . .53Second-Degree AV Block, 2:1

Conduction . . . . . . . . . . . . . . . . . . . . . . .55Third-Degree AV Block . . . . . . . . . . . . . . . . .58

Absent/Pulseless RhythmsVentricular Fibrillation (VF) . . . . . . . . . . . . .59Ventricular Tachycardia (VT) . . . . . . . . . . . .61Asystole (Cardiac Standstill) . . . . . . . . . . . .62Pulseless Electrical Activity . . . . . . . . . . . . .65

28

Lead Positive Electrode PositionRight side of sternum, 4thintercostal space

Left side of sternum, 4th inter-costal space

Midway between V2 and V4Left midclavicular line, 5thintercostal space

Left anterior axillary line atsame level as V4

Left midaxillary line at samelevel as V4

Heart SurfaceViewed

Septum

Septum

AnteriorAnterior

Lateral

Lateral

Summary of Standard Limb Leads

Positive ElectrodeRight armLeft armLeft leg

Heart Surface ViewedNoneLateralInferior

Summary of Augmented Leads

LeadLead ILead IILead III

PositiveElectrodeLeft armLeft legLeft leg

NegativeElectrode

Right armRight armLeft arm

Heart SurfaceViewed

LateralInferiorInferior

Summary of Standard Limb Leads

Lead

Lead aVRLead aVLLead aVF

Lead V1

Lead V2

Lead V3Lead V4

Lead V5

Lead V6

29

V6V5V4V3V2(V2R)(V1R)

V3 R

V4 R

V5 R

V6 R

V1

V9R

Posterior view

Left Right

V8R V7RV7 V8 V9

Placement of the left and right chest leads.19

Posterior chest lead placement.20

30

PT

Atrial depolarization

Q S

Ventricular depolarization(and atrial repolarization)

Ventricular repolarizationTime

ECG deflections

Volta

geR

PS-T

segment T

P-R interval Q R S

0.12-0.20 sec. 0.11 sec.or less

Q-Tintervalunder

0.38 sec.Time

ECG intervals

Volta

ge

ECG waveformsP, QRS, and T.21

ECG segments and intervalsPR interval, QRS duration,ST-segment, QT interval.21

31

P

R QS

PR

-seg

men

t

T TP

-seg

men

t

P

AB

C

Th

eT

P-se

gm

ent.

A,T

he

TP-

seg

men

tis

use

das

the

bas

elin

efr

om

wh

ich

tod

eter

min

eth

ep

rese

nce

of

ST-

seg

men

tel

evat

ion

or

dep

ress

ion

.B,S

T-se

gm

ent

elev

atio

n.C

,ST-

seg

men

td

epre

ssio

n.2

2

32

TOO FAST RHYTHMSNARROW-QRS TACHYCARDIAS

Sinus Tachycardia

1 2 3

Impulsebeginsin the SA node

Sinus rhythm continues at 60 to 100 beats per minute

Sinus bradycardia continues at less than 60 beats per minute

Sinus tachycardia continues faster than 100 beats per minute

QRS

QRS

QRS

P

P

P

T

T

T

Refractory periods. 1,The absolute refractory period,2, Relative refractory period. 3,The supernormalperiod.23

Sinus rhythm, sinus bradycardia, and sinus tachycardia.24

SA SA

AV AV

X

II II

Atrial Tachycardia

33

RateRhythmP waves

PR interval

QRS duration

101 to 180 bpmRegularUniform in appearance, positive (upright) inlead II, one precedes each QRS complex; atvery fast rates it may be difficult to distin-guish a P wave from a T wave

0.12-0.20 second and constant from beat tobeat

0.11 second or less unless an intraventricularconduction delay exists

Sinus Tachycardia

SA SABT

AV AV

II II

Supraventricular tachycardias. A, Normal sinus rhythm.B, Atrial tachycardia. C, AV nodal reentrant tachycardia(AVNRT). D, AV reentrant tachycardia (AVRT).25

C D

A B

34

RateRhythmP waves

PR interval

QRS duration

150 to 250 bpmRegular One positive P wave precedes each QRScomplex in lead II but the P waves differ inshape from sinus P waves. With rapid rates,it is difficult to distinguish P waves from Twaves.

May be shorter or longer than normal andmay be difficult to measure because Pwaves may be hidden in T waves

0.11 second or less unless an intraventricularconduction delay exists

Atrial Tachycardia (AT)

RateRhythmP waves

PR interval

QRS duration

150 to 250 bpm; typically 170 to 250 bpmVentricular rhythm is usually very regularP waves are often hidden in the QRS com-plex. If the ventricles are stimulated firstand then the atria, a negative (inverted) Pwave will appear after the QRS in leads II,III, and aVF. When the atria are depolarizedafter the ventricles, the P wave typicallydistorts the end of the QRS complex.

P waves are not seen before the QRScomplex, therefore the PR interval is notmeasurable

0.11 second or less unless an intraventricu-lar conduction delay exists

AV Nodal Reentrant Tachycardia(AVNRT)

Kent

(W-P

-W)

shor

tP-R

with

wav

e

Jam

es(L

-G-L

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ortP

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ithou

t

wav

e

Mahaim

normal

P-R

with

wav

e

AV

Ree

ntr

antT

achy

card

ia(A

VR

T)

35

Th

eth

ree

maj

or

form

so

fp

reex

cita

tio

n.L

oca

tio

no

fth

eac

cess

ory

pat

hw

ays

and

corr

esp

on

din

gE

CG

char

acte

rist

ics.

26

36

V3

Rate

Rhythm

P waves

PR interval

QRS duration

Usually 60-100 bpm, if the underlying rhythmis sinus in origin

Regular, unless associated with atrialfibrillation

Upright in lead II unless WPW is associatedwith atrial fibrillation

If P waves are observed, less than 0.12 sec-ond because the impulse travels veryquickly across the accessory pathway,bypassing the normal delay in the AV node

Usually greater than 0.12 second. Slurredupstroke of the QRS complex (delta wave)may be seen in one or more leads.

Wolff-Parkinson-White (WPW)Syndrome

Lead V3.Typical WPW pattern showing the short PRinterval, delta wave, wide QRS complex and secondaryST, and T-wave changes.27

Jun

ctio

nal

Tach

ycar

dia

28

37

J-point

J-point

WIDE-QRS TACHYCARDIAS

Intraventricular Conduction Defects

38

RateRhythmP waves

PR interval

QRS duration

101-180 bpmVery regular May occur before, during, or after the QRS.If visible, the P wave is inverted in leads II,III, and aVF

If a P wave occurs before the QRS, the PRinterval will usually be less than or equal to0.12 second. If no P wave occurs before theQRS, there will be no PR interval.

0.11 second or less unless an intraventricu-lar conduction delay exists.

Junctional Tachycardia

Move from the J-point back into the QRS complex anddetermine whether the terminal portion (last 0.04 sec-ond) of the QRS complex is a positive (upright) or nega-tive (downward) deflection. If the two criteria for bundlebranch block are met and the terminal portion of theQRS is positive, a right bundle branch block (BBB) ismost likely present. If the terminal portion of the QRS isnegative, a left BBB is most likely present.29

Differentiatingright versus leftBBB. The turnsignal theoryright is up, left isdown.29

39

Mo

no

mo

rph

icV

T

Su

stai

ned

ven

tric

ula

rta

chyc

ard

ia.W

hen

the

QR

Sco

mp

lexe

so

fve

ntr

icu

lar

tach

ycar

dia

(VT

)ar

eo

fth

esa

me

shap

ean

dam

plit

ud

e,th

erh

yth

mis

calle

dm

on

om

orp

hic

VT.

30

IRREGULAR TACHYCARDIAS

40

RateRhythmP waves

PR intervalQRS duration

101-250 bpmEssentially regular Usually not seen; if present, they have no setrelationship to the QRS complexes appear-ing between them at a rate different fromthat of the VT

NoneGreater than 0.12 second; often difficult todifferentiate between the QRS and T wave

Monomorphic Ventricular Tachycardia

RateRhythm

P waves


Ventricular rate is greater than 100 bpmMay be irregular as the pacemaker siteshifts from the SA node to ectopic atriallocations and the AV junction

Size, shape, and direction may change frombeat to beat; at least three different P waveconfigurations (seen in the same lead) arerequired for a diagnosis of wandering atrialpacemaker or multifocal atrial tachycardia

Variable0.11 second or less unless an intraventricu-lar conduction delay exists

Multifocal Atrial Tachycardia

41

Mu

ltifo

calA

tria

lTac

hyca

rdia

(MA

T)3

1

Atrial Flutter

42

In artrial flutter, theatrial rate canrange from 250 to450/min.

Notconducted

Conducted

QRS

TF F

Rate

Rhythm

P waves


In type I atrial flutter (also called typicalrapid atrial flutter), the atrial rate rangesfrom 250 to 350 bpm. In type II atrial flutter(also called atypical or very rapid atrial flut-ter), the atrial rate ranges from 350 to 450bpm.

Atrial regular, ventricular regular or irregulardepending on AV conduction/blockade

No identifiable P waves; saw-toothed flut-ter waves are present

Not measurableUsually less than 0.11 second but may bewidened if flutter waves are buried in theQRS complex or an intraventricular conduc-tion delay exists

Atrial Flutter

Atrial flutter. F, Flutter wave.32

43

Onl

yso

me

ofth

eat

rial

impu

lses

are

cond

ucte

dth

roug

hth

eA

Vno

de.

Atr

iali

mpu

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prod

uce

aner

ratic

wav

yba

selin

ebe

fore

the

QR

Sco

mpl

exes

.

Ect

opic

site

sin

the

atria

fire

ata

rate

of40

0-60

0/m

in.

QR

STf

ff

Not

cond

ucte

d

Con

duct

ed

Atr

ialF

ibri

llati

on

Atr

ialf

ibri

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on

.f,F

ibri

llato

ryw

ave.

32

44

Rate

Rhythm

P waves


Atrial rate usually greater than 400-600 bpm;ventricular rate variable

Ventricular rhythm usually irregularlyirregular

No identifiable P waves; fibrillatory wavespresent. Erratic, wavy baseline.

Not measurableUsually less than 0.11 second but may bewidened if an intraventricular conductiondelay exists

Atrial Fibrillation

RateRhythmP wavesPR intervalQRS duration

150 to 300 bpm, typically 200-250 bpmMay be regular or irregularNoneNoneGreater than 0.12 sec; gradual alteration inamplitude and direction of the QRS com-plexes; a typical cycle consists of 5 to 20QRS complexes

Polymorphic Ventricular Tachycardia

45

Poly

mo

rph

icV

entr

icu

larT

achy

card

ia

Wh

enth

eQ

RS

com

ple

xes

of

ven

tric

ula

rta

chyc

ard

ia(V

T)

vary

insh

ape

and

amp

litu

de,

the

rhyt

hm

iste

rmed

po

lym

orp

hic

VT.

33

TOO SLOW RHYTHMSSINUS BRADYCARDIA

46

RateRhythmP waves

PR interval

QRS duration

Less than 60 bpmRegularUniform in appearance, positive (upright) inlead II, one precedes each QRS complex

0.12-0.20 second and constant from beat tobeat

0.11 second or less unless an intraventri-cular conduction delay exists

Sinus Bradycardia

47

Sin

us

Bra

dyc

ard

ia34

48

RateRhythmP waves

PR interval

QRS duration

40 to 60 bpmVery regular May occur before, during, or after the QRS.If visible, the P wave is inverted in leads II,III, and aVF

If a P wave occurs before the QRS, the PRinterval will usually be less than or equal to0.12 second. If no P wave occurs before theQRS, there will be no PR interval.

0.11 second or less unless an intraventricu-lar conduction delay exists.

Junctional Escape Rhythm

Impulse begins in the AV junction.

Junctional escape continues at 40 to 60 beats per minute.

Accelerated junctional rhythm continues at 60 to 100 beats per minute.

Junctional tachycardia continues at 100 to 180 beats per minute.

QRS

QRS

QRS

T

T

T

P

P

P

JUNCTIONAL RHYTHM

Junctional rhythms.35

49

Ven

tric

ula

rE

scap

eR

hyth

m36

50

RateRhythmP waves


20 to 40 bpmEssentially regular Usually absent or, with retrograde conduc-tion to the atria, may appear after the QRS(usually upright in the ST-segment orT wave)

NoneGreater than 0.12 second, T wave frequentlyin opposite direction of the QRS complex

Ventricular Escape(Idioventricular) Rhythm

51

FIRST-DEGREE AV BLOCK

mpulse eginsSA

ode

delay

delay

delay

delay

delay

QRS QRSQRS QRSQRS QRSQRS

PP PP PP PPTT TT TT TT

Rate

RhythmP waves

PR interval

QRS duration

Usually within normal range, but depends onunderlying rhythm

RegularNormal in size and shape, one positive(upright) P wave before each QRS in leadsII, III, and aVF

Prolonged (greater than 0.20 second) butconstant

0.11 second or less unless an intraventricu-lar conduction delay exists

First-Degree AV Block

First-degree atrioventricular (AV) block.37

52

SECOND-DEGREE AV BLOCKTYPE I(WENCKEBACH, MOBITZ TYPE I)37

Impu

lse

begi

nsin

SA

node

PP

PP

PP

PP

QR

SQ

RS

QR

SQ

RS

QR

SQ

RS

QR

S

TT

TT

TT

cond

ucts

with

mor

ede

lay

cond

ucts

with

mor

ede

lay

mor

e de

lay

cond

ucts

with

dela

y

cond

ucts

with

dela

y

with

del

ay

fails

to

cond

uct

fails

to

fails

to

cond

uct

cond

uct

SECOND-DEGREE AV BLOCKTYPE II(MOBITZ TYPE II)

53

RateRhythm

P waves

PR interval

QRS duration

Atrial rate is greater than the ventricular rateAtrial regular (Ps plot through on time), ven-tricular irregular

Normal in size and shape. Some P wavesare not followed by a QRS complex (morePs than QRSs).

Lengthens with each cycle (although length-ening may be very slight), until a P waveappears without a QRS complex. The PRIafter the nonconducted beat is shorter thanthe interval preceding the nonconductedbeat.

Usually 0.11 second or less but is periodically dropped.

Second-Degree AV BlockType I

Rate

Rhythm

P waves

PR interval

QRS duration

Atrial rate is greater than the ventricularrate. Ventricular rate is often slow.

Atrial regular (Ps plot through on time), ven-tricular irregular.

Normal in size and shape. Some P wavesare not followed by a QRS complex (morePs than QRSs).

Within normal limits or slightly prolonged butccoonnssttaanntt for the conducted beats. Theremay be some shortening of the PR intervalthat follows a nonconducted P wave.

Usually 0.11 second or greater, periodicallyabsent after P waves.

Second-Degree AV BlockType II

54

Sec

on

d D

egre

e A

V B

lock

Typ

e II

38

55

RateRhythm

P waves


Atrial rate is twice the ventricular rateAtrial regular (Ps plot through). Ventricularregular.

Normal in size and shape; every other Pwave is followed by a QRS complex (morePs than QRSs)

ConstantWithin normal limits, if the block occursabove the bundle of His (probably type I);wide if the block occurs below the bundleof His (probably type II); absent after everyother P wave.

Second-Degree AV Block 2:1Conduction (2:1 AV Block)

56

Lea

d II

Lea

d II

A B

57

Lea

d II

C

Typ

es o

f se

con

d-d

egre

e A

V b

lock

. A, S

eco

nd

-deg

ree

AV

blo

ck t

ype

I; B

, sec

on

d-d

egre

eA

V b

lock

typ

e II;

C, 2

:1 A

V b

lock

.39

THIRD-DEGREE AV BLOCK

58

Impulse begins in SA node Escape

impulse originatesin the AVnode or below

P P P P P P P P P P PP

P

QRS QRS QRS QRS QRS

T T T TT

comp

lete b

lock

comp

lete b

lock

comp

lete b

lock

Rate

Rhythm

P wavesPR interval

QRS duration

Atrial rate is greater than the ventricularrate. The ventricular rate is determined bythe origin of the escape rhythm.

Atrial regular (Ps plot through). Ventricularregular. There is no relationship betweenthe atrial and ventricular rhythms.

Normal in size and shape.Nonethe atria and ventricles beat inde-pendently of each other, thus there is notrue PR interval.

Narrow or wide depending on the location ofthe escape pacemaker and the condition ofthe intraventricular conduction system.

Narrow = junctional pacemaker, wide = ven-tricular pacemaker.

Third-degree AV Block

Third-degree AV block.40

59

ABSENT/PULSELESS RHYTHMS

Rate

Rhythm

P wavesPR intervalQRS duration

Cannot be determined because there are nodiscernible waves or complexes to measure

Rapid and chaotic with no pattern orregularity

Not discernibleNot discernibleNot discernible

Ventricular Fibrillation (VF)

60

Coa

rse

VF

Fin

e V

FC

oars

e V

F

Ven

tric

ula

r Fi

bri

llati

on

(V

F)41

Co

arse

an

d f

ine

ven

tric

ula

r fi

bri

llati

on

.

61

Ven

tric

ula

r Tac

hyca

rdia

(V

T)4

2

ASYSTOLE (CARDIAC STANDSTILL)

62

RateRhythmP waves


101-250 bpmEssentially regular Usually not seen; if present, they have no setrelationship to the QRS complexes appear-ing between them at a rate different fromthat of the VT

NoneGreater than 0.12 second; often difficult todifferentiate between the QRS and T wave

Ventricular Tachycardia

Rate

Rhythm

P wavesPR intervalQRS duration

Ventricular usually not discernible but atrialactivity may be observed (P waveasystole)

Ventricular not discernible, atrial may bediscernible

Usually not discernibleNot measurableAbsent

Asystole

63

Asy

sto

le43

64

P-W

ave

Asy

sto

le44

65

Pulseless electrical activity (PEA) is a clinicalsituation, not a specific dysrhythmia. PEAexists when organized electrical activity(other than VT) is observed on the cardiacmonitor but the patient is unresponsive, notbreathing, and a pulse cannot be felt.

PULSELESS ELECTRICAL ACTIVITY

66

Th

e rh

yth

m s

ho

wn

is a

sin

us

tach

ycar

dia

; ho

wev

er, i

f n

o p

uls

e is

ass

oci

ated

wit

h t

he

rhyt

hm

, th

e cl

inic

al s

itu

atio

n is

ter

med

pu

lsel

ess

elec

tric

al a

ctiv

ity

(PE

A).

44

ELECTRICAL THERAPY

Defibrillation . . . . . . . . . . . . . . . . . . . . . . . . . . . .67Transthoracic Resistance . . . . . . . . . . . . . . . .68Monophasic Defibrillation . . . . . . . . . . . . . . .68Biphasic Defibrillation . . . . . . . . . . . . . . . . . . .69Automated External Defibrillators . . . . . . . . .70

Synchronized Cardioversion . . . . . . . . . . . . . . .73Special Considerations . . . . . . . . . . . . . . . . . . . .75Transcutaneous Pacing . . . . . . . . . . . . . . . . . . . .76

DEFIBRILLATION Defibrillation is delivery of an electrical cur-rent across the heart muscle over a very briefperiod to terminate an abnormal heartrhythm. Defibrillation is also called unsyn-chronized countershock, or asynchronouscountershock, because the delivery of currenthas no relationship to the cardiac cycle.Indications for defibrillation include sustainedpolymorphic VT, pulseless VT, and VF.

Defibrillation does not jump start the heart.The shock attempts to deliver a uniform elec-trical current of sufficient intensity to depolar-ize ventricular cells (including fibrillatingcells) at the same time, briefly stunning theheart. This provides an opportunity for thehearts natural pacemakers to resume normalactivity. When the cells repolarize, the pace-maker with the highest degree of automatici-ty should assume responsibility for pacingthe heart.

Manual defibrillation refers to the placementof paddles or pads on a patients chest, inter-pretation of the patients cardiac rhythm by atrained healthcare professional, and thehealthcare professionals decision to deliver ashock (if indicated). Automated externaldefibrillation refers to the placement of pad-dles or pads on a patients chest and interpre-

tation of the patients cardiac rhythm by thedefibrillators computerized analysis system.Depending on the type of automated externaldefibrillator (AED) used, the machine willdeliver a shock (if a shockable rhythm isdetected) or instruct the operator to deliver ashock.

TRANSTHORACIC RESISTANCE

Although the energy selected for defibrilla-tion or cardioversion is expressed in joules, itis current that delivers energy to the patientand depolarizes the myocardium. Impedancerefers to the resistance to the flow of currentand is measured in ohms. Transthoracicimpedance (resistance) refers to the naturalresistance of the chest wall to the flow of cur-rent. Transthoracic resistance varies greatly.Factors known to affect transthoracic resist-ance include the following: Paddle/electrode size Paddle/electrode position Use of conductive material (when using

handheld paddles) Paddle pressure (when using handheld

paddles) Selected energy

MONOPHASIC DEFIBRILLATION

Pressing the charge button on a defibrillatorcharges the capacitor. Once the capacitor ischarged and the shock control is pressed,voltage pushes a flow of electrons (current)to the patient by means of handheld paddlesor combination pads. Current passes throughthe heart in waveforms that travel fromone paddle/pad, through the chest, and backto the other paddle/pad over a brief period.

68

BIPHASIC DEFIBRILLATION

69

When a monophasic waveform is used, current passesthrough the heart in one direction.45

With biphasic waveforms, energy is delivered intwo phases. The current moves in one direction for aspecified period, stops, and then passes through theheart a second time in the opposite direction.45

AUTOMATED EXTERNAL DEFIBRILLATORS(AEDs)

An AED is an external defibrillator that has acomputerized cardiac rhythm analysis sys-tem. AEDs are easy to use. Voice promptsand visual indicators guide the user througha series of steps that may includedefibrillation.

When the adhesive electrodes are attached tothe patients chest, the AED examines andanalyzes the patients cardiac rhythm. SomeAEDs require the operator to press an ana-lyze control to initiate rhythm analysiswhereas others automatically begin analyz-ing the patients cardiac rhythm when theelectrode pads are attached to the patientschest. Safety filters check for false signals(e.g., radio transmissions, poor electrodecontact, 60-cycle interference, looseelectrodes).

When the AED analyzes the patients cardiacrhythm, it looks at multiple features of therhythm, including the QRS width, rate, andamplitude. If the AED detects a shockablerhythm, it charges the capacitors. In additionto VF, AEDs will recommend a shock formonomorphic VT and polymorphic VT. Thepreset rate for shockable VT varies depend-ing on the AED. For instance, some manufac-turers set the shockable VT rate (for adults) atgreater than 150 beats/minute. Others set therate at greater than 120 beats/minute.

If a shockable rhythm is detected by a fullyautomated AED, it will signal everyone tostand clear of the patient and then delivers ashock by means of the adhesive pads thatwere applied to the patients chest.

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If a shockable rhythm is detected by a semi-automated AED, it will instruct the AED oper-ator (by means of voice prompts and visualsignals) to press the shock control to delivera shock.

Some AEDs: Can be configured to allow advanced life

support personnel to switch to a manualmode, allowing more decision-makingcontrol

Have CPR pads available that are equippedwith a sensor. The sensor detects thedepth of chest compressions. If the depthof chest compressions is inadequate, themachine provides voice prompts to therescuer.

Provide voice instructions in adult andinfant-child CPR at the users option. Ametronome function encourages rescuersto perform chest compressions at the rec-ommended rate of 100 compressions perminute.

Are programmed to detect spontaneousmovement by the patient or others.

Have adapters available for many popularmanual defibrillators, enabling the AEDpads to remain on the patient whenpatient care is transferred

Are equipped with a pediatric attenuator(pad-cable system or key). When the atten-uator is attached to the AED, the machinerecognizes the pediatric cable connectionand automatically adjusts its defibrillationenergy accordingly.

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Use a standard AED for a patient who isunresponsive, apneic, pulseless, and 8 yearsof age or older. If the patient is between 1and 8 years of age and a pediatric attenuatoris unavailable for the AED, use a standard

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A, Automated external defibrillator (AED).B,This defib-rillation pad and cable system reduces the energy deliv-ered by a standard AED to that appropriate for a child.46

A

B

AED. In infants, defibrillation with a manualdefibrillator is preferred. If a manual defibril-lator is not available, an AED equipped with apediatric attenuator is desirable. If neither isavailable, use a standard AED.

Some AEDs can detect the patients transtho-racic resistance through the adhesive padsapplied to the patients chest. The AED auto-matically adjusts the voltage and length ofthe shock, thus customizing how the energyis delivered to that patient. AED OperationTo operate an AED: Turn on the power. Attach the device. Analyze the rhythm. Deliver a shock if indicated and safe.

SYNCHRONIZED CARDIOVERSIONSynchronized cardioversion is a type of elec-trical therapy in which a shock is timed orprogrammed for delivery during the QRScomplex. A synchronizing circuit in themachine searches for the highest (R wavedeflection) or deepest (QS deflection) part ofthe QRS complex and delivers the shock afew milliseconds after this portion of theQRS. Delivery of a shock during this portionof the cardiac cycle reduces the potential forthe delivery of current during the vulnerableperiod of the T wave (relative refractoryperiod).

Synchronized cardioversion is used to treatrhythms that have a clearly identifiable QRScomplex and a rapid ventricular rate (such as some narrow-QRS tachycardias andmonomorphic VT).

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RecommendedEnergy

Levels

Variesdependingondeviceused

Biphasicdefibrillatoreffectivedosetypically120Jto200J

Ifeffectivedoserangeofdefibrillatorisunknown,considerusing

atthemaximaldose

Ifusingmonophasicdefibrillator,360Jforallshocks

50Jto100Jinitially,increaseinstepwisefashionifinitialshockfails

50Jto100Jinitially,increaseinstepwisefashionifinitialshockfails

120Jto200Jinitially(biphasic),increaseinstepwisefashionifinitial

shockfails;beginwith200Jifusingmonophasicenergyand

increaseifunsuccessful

100Jinitially,reasonabletoincreaseinstepwisefashionifinitial

shockfails

Rhythm

Pulselessventriculartachycardia

(VT)/ventricularfibrillation(VF)

SustainedpolymorphicVT

Unstablenarrow-QRStachycardia

Unstableatrialflutter

Unstableatrialfibrillation

UnstablemonomorphicVT

Type

ofSh

ock

Defibrillation

Cardioversion

Def

ibri

llati

on

and

Car

dio

vers

ion

Su

mm

ary

Synchronized cardioversion is not used totreat disorganized rhythms (such as polymor-phic VT) or those that do not have a clearlyidentifiable QRS complex (such as VF).

DEFIBRILLATION ANDSYNCHRONIZED CARDIOVERSION

SPECIAL CONSIDERATIONS Remove supplemental oxygen sources

from the area of the patients bed beforedefibrillation and cardioversion attemptsand place them at least 31/2 to 4 feet fromthe patients chest. Examples of supple-mental oxygen sources include masks,nasal cannulae, resuscitation bags, andventilator tubing. Case reports describeinstances of fires ignited by sparks frompoorly applied defibrillator paddles/pads inan oxygen-enriched atmosphere. Severefires have resulted when ventilator tubingwas disconnected from an endotrachealtube and then left next to the patientshead while defibrillation was attempted.

To prevent fires during defibrillationattempts: Be sure to use defibrillator paddles/pads

of the appropriate size. Adultpaddles/pads should be used for patientsgreater than 10 kg. Use pediatric pad-dles/pads for patients less than 10 kg.

Make sure there are no air pocketsbetween the paddle/pads and thepatients skin. When applying combina-tion pads to a patients bare chest, pressfrom one edge of the pad across theentire surface to remove all air.

When using handheld paddles, useappropriate conductive gel or disposablegel pads and apply firm, even pressureduring defibrillation attempts.

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Keep monitoring electrodes and wiresaway from the area where defibrillatorpads or combination pads will be placed.Contact may cause electrical arcing andpatient skin burns during defibrillation orcardioversion.

Remove transdermal patches, bandages,necklaces, or other materials from the sitesused for paddle placementdo notattempt to defibrillate through them. Wiperesidue from a medication patch or oint-ment from the patients chest. Do not usealcohol or alcohol-based cleansers.

If an unresponsive patient is lying in wateror the patients chest is covered withwater, it may be reasonable to remove thevictim from the water and quickly wipe thechest before applying the AED pads andattempting defibrillation.

If the patient has a pacemaker or ICD, anAED may be used; but the AED padsshould be placed at least 3 inches (8 cm)from the implanted device. If an ICD is inthe process of delivering shocks to thepatient, allow it about 30 to 60 seconds tocomplete its cycle.

TRANSCUTANEOUS PACING A pacemaker is an artificial pulse genera-

tor that delivers an electrical current to theheart to stimulate depolarization.Transcutaneous pacing (TCP) delivers pac-ing impulses to the heart using electrodesplaced on the patients chest. TCP is alsocalled temporary external pacing, or non-invasive pacing.

TCP is indicated for symptomatic brady-cardias unresponsive to atropine therapy

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or when atropine is not immediately avail-able or indicated. It may also be used as abridge until transvenous pacing can beaccomplished or the cause of the brady-cardia is reversed (as in cases of drugoverdose or hyperkalemia).

Although TCP is a type of electrical thera-py, the current delivered is considerablyless than that used for cardioversion ordefibrillation. The energy levels selectedfor cardioversion or defibrillation are indi-cated in joules. The stimulating currentselected for TCP is indicated in mil-liamperes (mA). The range of output cur-rent of a transcutaneous pacemaker variesdepending on the manufacturer.

PROCEDURE Pacing may be performed in either

demand or nondemand (asynchronous)mode. The demand mode is used for mostpatients. When the pacemaker is indemand mode, pacing is inhibited whenthe pacemaker senses the patients own(intrinsic) beats. To detect the patients own beats (QRS

complexes), the pacemaker must be con-nected to ECG electrodes and an ECGcable. In addition, the QRS complexesmust be of adequate size to be sensed bythe pacemaker.

If the gain (ECG size) on the monitor isset too low to detect the patients beats(or an ECG lead is off), the pacemakerproduces pacing stimuli asynchronously.In other words, the pacemaker generatesa pacing stimulus at the selected rateregardless of the patients own rhythm.

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78

A

B

CTranscutaneous pacing. A and B, Anterior-posteriorpacing pad placement. C, Anterior-lateral pacingpad placement.47

Place adhesive pacing pads on thepatients bare chest according to themanufacturers instructions. The padsshould fit completely on the patientschest with a minimum of 1 inch of spacebetween them. The pads should not over-lap the sternum, spine, or scapula. Inwomen, the anterior pacer pad is posi-tioned under (not on) the left breast.

Connect the patient to an ECG monitor,obtain a rhythm strip, and verify the pres-ence of a paceable rhythm. Connect thepacing cable to the adhesive electrodes onthe patient and the pulse generator.

Turn the power on to the pacemaker andset the pacing rate. When TCP is used totreat a symptomatic bradycardia, the rateis set at a nonbradycardic rate, generallybetween 60 and 80 pulses per minute(ppm).

After the rate has been regulated, set thestimulating current. This control is usuallylabeled CURRENT, PACER OUTPUT, and/or

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Transcutaneous pacemaker controls.48

mA. Increase the current slowly but steadi-ly until capture is achieved. Sedationand/or analgesia may be needed to mini-mize the discomfort associated with thisprocedure (common with currents of 50mA or more).

Watch the cardiac monitor closely for elec-trical capture. This is usually evidenced bya wide QRS and a T wave that appears in adirection opposite the QRS. In somepatients, electrical capture is not as obvi-ous and appears only as a change in theshape of the QRS.

Assess mechanical capture by checking thepatients right upper extremity or femoralpulses. Avoid assessment of pulses in thepatients neck or on the patients left side.This minimizes confusion between thepresence of an actual pulse and skeletalmuscle contractions caused by the pace-maker.

Once capture is achieved, continue pacingat an output level slightly higher (about 2mA) than the threshold of initial electricalcapture. For example, if capture isachieved at 90 mA, set the output level at92 mA.

Assess the patients BP and level ofresponsiveness. Monitor the patient close-ly and record the ECG rhythm.

Documentation should include the dateand time pacing was initiated (includingbaseline and pacing rhythm strips), thecurrent required to obtain capture, the pac-ing rate selected, the patients responsesto electrical and mechanical capture, med-ications administered during the proce-dure, and the date and time pacing wasterminated.

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81

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Cap

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VASCULAR ACCESS ANDMEDICATIONS

IV Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .83Intraosseous Infusion . . . . . . . . . . . . . . . . . . . .85Drugs Used in Acute

Coronary Syndromes . . . . . . . . . . . . . . . . .87Drugs Used for Control of Heart Rhythm

and Rate . . . . . . . . . . . . . . . . . . . . . . . . . . . .96Drugs Used to Improve Cardiac Output

and Blood Pressure . . . . . . . . . . . . . . . . . .114Vasodilators . . . . . . . . . . . . . . . . . . . . . . . . . . .121Other Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . .122

IV THERAPYIV cannulation is the placement of a catheterinto a vein to gain access to the bodysvenous circulation. IV access may beachieved by cannulating a peripheral or cen-tral vein. During circulatory collapse or car-diac arrest, the preferred vascular access siteis the largest, most accessible vein that doesnot require the interruption of resuscitationefforts. If no IV is in place before the arrest,establish IV access using a peripheral vein,preferably the antecubital or external jugularvein. During cardiac arrest, give IV drugs rap-idly by bolus injection. Follow each drug witha 20-mL bolus of IV fluid and raise theextremity for 10 to 20 seconds to aid deliveryof the drug(s) to the central circulation.

INDICATIONS

Maintain hydration Restore fluid and electrolyte balance Provide fluids for resuscitation Administer medications, blood and blood

components, nutrient solutions Obtain venous blood specimens for labo-

ratory analysis

84

PERIPHERAL VENOUS ACCESSAdvantages Effective route for medications during CPR Does not require interruption of CPR Easier to learn than central venous access Easily compressible site to reduce bleed-

ing if an IV attempt is unsuccessful Results in fewer complications than central

venous accessDisadvantages In circulatory collapse the vein may be dif-

ficult to access. Phlebitis is common with saphenous vein

use. Should be used only for administration of

isotonic solutions; hypertonic or irritatingsolutions may cause pain and phlebitis.

In cardiac arrest, drugs given from aperipheral vein require 1 to 2 minutes toreach the central circulation.

CENTRAL VENOUS ACCESS

To access the central circulation, a centralvenous catheter (also called a central line) isinserted into the vena cava from the subcla-vian, jugular, or femoral vein. If peripheral IVaccess is unsuccessful during cardiac arrest,consider an intraosseous infusion beforeplacing a central line.Indications Emergency access to venous circulation

when peripheral sites are not readily avail-able

Need for long-term IV therapy Administration of large volume of fluid Administration of hypertonic solutions,

85

caustic medications, or parenteral feedingsolutions

Placement of transvenous pacemakerelectrodes

Placement of central venous pressure orright heart catheters

Advantages Peak medication concentrations are higher

and circulation times shorter when med-ications are administered via a centralroute compared with peripheral sites.

Disadvantages Special equipment (syringe, catheter, nee-

dle) required Excessive time (5-10 minutes) for

placement High complication rate Skill deterioration (frequent practice

required to maintain proficiency) Inability to initiate procedure while other

patient care activities in progress

INTRAOSSEOUS INFUSIONWhen IV cannulation is unsuccessful or istaking too long, an intraosseous (IO) infusionis an alternative method of gaining access tothe vascular system. An IO infusion is theprocess of infusing medications, fluids, andblood products into the bone marrow cavityfor subsequent delivery to the venous circu-lation. Any medication or fluid that can beadministered IV can be administered IO.

INDICATIONS Emergency administration of fluids and/or

medications, especially in the setting ofcirculatory collapse where rapid vascularaccess is essential

86

Difficult, delayed, or impossible IV access Burns or other injuries preventing venous

access at other sites

TRACHEAL DRUG ADMINISTRATION

If IV or IO access cannot be achieved to givedrugs during a cardiac arrest, the trachealroute can be used to give selected medica-tions.

Studies have shown that naloxone, atropine,vasopressin, epinephrine, and lidocaine aremedications that are absorbed via the tra-chea. The tracheal route of drug administra-tion is not preferred because multiple studieshave shown that giving resuscitation drugstracheally results in lower blood concentra-tions than the same dose given IV.

The recommended dose of some drugs thatcan be given via the tracheal route is general-ly 2 to 2.5 times the IV dose, although theoptimum tracheal dose of most drugs isunknown.

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Mechanismof Action

Indications

Dosing

Precautions

Increases oxygen tension Increases hemoglobin saturation if ventila-

tion is supported Improves tissue oxygenation when circula-

tion is maintained Cardiac or respiratory arrest Suspected hypoxemia of any cause Any suspected cardiopulmonary emergency,

especially complaints of shortness of breathand/or suspected ischemic chest pain

Spontaneously breathing patientbest guidedby pulse oximetry*, blood gases, and patienttolerance to oxygen delivery device.

Nasal cannula (0.25 to 8 L/min) Simple face mask (5 to 10 L/min) Partial rebreather mask (6 to 10 L/min) Nonrebreather mask (10 L/min)Cardiac arrestpositive-pressure ventilationwith 100% oxygen

Toxicity possible with prolonged administra-tion of high flow oxygen

*Pulse oximetry is inaccurate in low cardiac output states orwith vasoconstriction.

Oxygen

DRUGS USED IN ACUTE CORONARY SYNDROMES

Mechanism ofAction

Indications

Dosing (Adult)

Relaxes vascular smooth muscle;including dilation of the coronary arter-ies (particularly in the area of plaquedisruption), the peripheral arterial bed,and venous capacitance vessels

Dilation of postcapillary vessels peripheral pooling of blood decreas-es venous return to the heart decreases preload

Arteriolar relaxation reduces systemicvascular resistance and arterial pres-sure (afterload)

Sublingual tablets or spray: Ongoing ischemic chest discomfortSublingual or spray Give a nitroglycerin tablet (or spray)

every 5 minutes up to 3 doses if thepatients SBP remains > 90 mm Hg or nomore than 30 mm Hg below baseline andthe heart rate remains between 50 and100 bpm*

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Nitroglycerin

LV, Left ventricular.

OConnor RE, Brady W, Brooks SC, et al. Part 10: acute coronary syndromes: 2010 American Heart AssociationGuidelines for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care. Circulation. 2010;122(suppl 3):S787S817.

SBP, Systolic blood pressure; SL, sublingual; IV, intravenous;MI, myocardial infarction.

89

Precautions

Contraindications

SpecialConsiderations

Primary side effect is hypotension. Otherside effects include tachycardia, brady-cardia, headache, palpitations, syncope

Use of a phosphodiesterase inhibitorsuch as sildenafil (Viagra) within 24hours or tadalafil (Cialis) within 48 hoursbefore NTG administration

Suspected inferior wall MI with possibleright ventricular MI

Hypotension (SBP < 90 mm Hg or< 30 mm Hg below baseline)

Extreme bradycardia (100 bpm) in the absence

of heart failure Uncorrected hypovolemia Inadequate cerebral circulation Hypotension may worsen myocardial

ischemia. Hypotension usually respondsto administration of IV fluids.Establishing an IV before giving SLnitroglycerin is strongly recommended.

Significant hypotension may occurin the presence of right ventricularinfarction.

Nitroglycerincontd

90

Mechanism ofAction

Indications

Dosing (Adult)

Precautions

Contraindications


Reduces pain of ischemia Reduces anxiety Increases venous capacitance (venous

pooling) and decreases venous return(preload)

Decreases systemic vascular resistance(afterload)

Decreases myocardial oxygen demandUnstable angina (UA)/non-ST-elevation MI

(NSTEMI): Reasonable for patientswhose symptoms are not relieveddespite NTG or whose symptoms recurdespite adequate anti-ischemic therapy*

ST-elevation MI (STEMI): Analgesic ofchoice for patients with STEMI whoexperience persistent chest discomfortunresponsive to nitrates

UA/NSTEMI: 1 to 5 mg IVSTEMI: 2 to 4 mg IV with increments of

2 to 8 mg IV repeated at 5- to 15-minintervals

Watch closely for: Bradycardia CNS depression Nausea/vomiting Respiratory depression Hypotension Hypersensitivity to morphine/opiates Respiratory depression CNS depression due to head injury,

overdose, poisoning, etc. Increased intracranial pressure Asthma (relative) Undiagnosed abdominal pain Hypovolemia HypotensionEnsure a narcotic antogonist and airway

equipment is within reach before giving

* and : For reference see next page.

Morphine Sulfate

91

Mechanism ofAction

Indications

Dosing (Adult)

While the mechanism of action of nalox-one is not fully understood, evidencesuggests naloxone antagonizes theeffects of opiates by competing for thesame receptor sites, thereby preventingor reversing the effects of narcoticsincluding respiratory depression, seda-tion, and hypotension.

Complete or partial reversal of narcoticdepression, including respiratorydepression, induced by opioids includingnatural and synthetic narcotics,propoxyphene, methadone and the nar-cotic-antagonist analgesics: nalbuphine,pentazocine and butorphanol.

Diagnosis of suspected acute opioidoverdosage

IV, IM, SubQknown or suspected nar-cotic overdose

Initial dose 0.4 mg to 2 mg. If the desireddegree of counteraction and improve-ment in respiratory function is notobtained, it may be repeated at 2 to 3minute intervals.*

If no response is observed after 10 mg ofnaloxone have been given, reevaluatediagnosis. IM or SubQ administrationmay be necessary if IV route is notavailable.

Continued.

Naloxone

IV, Intravenous; IM, intramuscular; SubQ, subcutaneous.

*Mosby's Drug Consult, St Louis, 2006, Mosby.

Morphine Sulfate: *Anderson JL, Adams CD, Antman EM, et al.ACC/AHA 2007 guidelines for the management of patients with unstableangina/nonST-elevation myocardial infarction: a report of the AmericanCollege of Cardiology/American Heart Association Task Force on PracticeGuidelines (Writing Committee to Revise the 2002 Guidelines for theManagement of Patients With Unstable Angina/NonST-ElevationMyocardial Infarction): developed in collaboration with the AmericanCollege of Emergency Physicians, American College of Physicians,Society for Academic Emergency Medicine, Society for CardiovascularAngiography and Interventions, and Society of Thoracic Surgeons, J AmColl Cardiol 50: e1e157, 2007.

OConnor RE, Brady W, Brooks SC, et al. Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines forCardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(suppl 3):S787S817.

92

CNS, Central nervous system.

2005 American Heart Association guidelines for cardiopul-monary resuscitation and emergency cardiovascular care,part 10.2, toxicology in ECC, Circulation 112(suppl IV):IV-129,2005.

Precautions

ContraindicationsSpecialConsiderations

Abrupt reversal of narcotic depressionmay result in nausea, vomiting,sweating, tachycardia,increased blood pressure,tremulousness, seizures, cardiac arrest

Known hypersensitivity to the medication Ineffective if respiratory depression due

to hypnotics, sedatives, anesthetics, or other nonnarcotic CNS depressants

Effects of narcotics are usually longer than those of naloxone thus, respiratory depression may return when naloxone has worn off. Monitor the patientclosely.

Naloxone can also be given by the intranasal or endotracheal routes. The IV, IM, or SubQ routes are preferred over the tracheal route.

Naloxonecontd

93

Mechanism ofActionIndications

Dosing (Adult)

Precautions

Contraindications


Blocks synthesis of thromboxane A2,inhibiting platelet aggregation.

Chest discomfort or other signs/symp-toms suggestive of an acute coronarysyndrome (unless hypersensitive toaspirin)

ECG changes suggestive of acute MI 162 to 325 mg ,chewed, if no history of

aspirin allergy or signs of active orrecent gastrointestinal bleeding*

Asthma (relative contraindication) Active ulcer disease (relative

contraindication) Hypersensitivity to aspirin and/or non-

steroidal anti-inflammatory agents Recent history of GI bleeding Bleeding disorders (hemophilia) Use with caution in the patient with a

history of asthma, nasal polyps, or nasalallergies. Anaphylactic reactions in sen-sitive patients have occurred.

Consider ticlopidine, or clopidogrel ifaspirin allergy, intolerant, or ineffective

Rectal suppository may be used forpatients who cannot take aspirin orally

*OConnor RE, Brady W, Brooks SC, et al. Part 10: acutecoronary syndromes: 2010 American Heart AssociationGuidelines for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care. Circulation. 2010;122(suppl 3):S787S817.

Aspirin

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Mechanism ofAction

Indications


Fibrinolytics work by altering plasmin inthe body, which then breaks down fib-rinogen and fibrin clots

Improvement of ventricular function fol-lowing ST-elevation MI (STEMI) withonset of symptoms of 12 hours andECG findings consistent with STEMI

tPA may be used in acute ischemicstroke, after intracranial hemorrhagehas been excluded by CT scan or otherdiagnostic imaging

Acute pulmonary thromboembolism Pay careful attention to all potential

bleeding sites (including catheter inser-tion sites, arterial and venous puncturesites, cutdown sites, and needle punc-ture sites).

Some fibrinolytics are associated withan increased risk of bleeding or hemor-rhage if used with heparin, oral antico-agulants, vitamin K antagonists, aspirin,or dipyridamole

Fibrinolytics

95

AbsoluteContraindications

Cautions andRelativeContraindications

Any prior intracranial hemorrhage Known structural cerebrovascular

lesion (e.g., AVM) Known malignant intracranial neoplasm

(primary or metastatic) Ischemic stroke within 3 months

EXCEPT acute ischemic stroke within 3 hours

Suspected aortic dissection Active bleeding or bleeding diathesis

(excluding menses) Significant closed head trauma or facial

trauma within 3 months1. History of chronic, severe, poorly con-

trolled hypertension2. Severe uncontrolled hypertension on

presentation (SBP > 180 mm Hg or DBP > 110 mm Hg) (could be an absolute contraindication in low-risk patients with myocardial infarction)

3. History of prior ischemic stroke within 3 months, dementia, or intracranialpathology not contraindicated

4. Traumatic or prolonged (10 minutes) CPR or major surgery (

96

Mechanism ofAction

Indications*

Dosing (Adult)*

Found naturally in all body cells Rapidly metabolized in the blood vessels Slows sinus rate Slows conduction time through AV node Can interrupt reentry pathways through

AV node Can restore sinus rhythm in reentry SVT,

including SVT associated with Wolff-Parkinson-White Syndrome

Stable narrow-QRS regular tachycardias Unstable narrow-QRS regular tachycar-

dia while preparations are made for syn-chronized cardioversion

Stable, regular, wide-QRS tachycardia 6 mg rapid IV push over 1-3 seconds.

Decrease the dose to 3 mg in patientson dipyridamole (Persantine), carba-mazepine (Tegretol), those with trans-planted hearts, or if given via a centralIV line. Consider increasing the dose inpatients on theophylline, caffeine, ortheobromine.

If no response within 1-2 minutes, give12 mg. May repeat 12 mg dose once in1-2 minutes.

*Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advancedcardiovascular life support: 2010 American Heart AssociationGuidelines for Cardiopulmonary Resuscitation and EmergencyCardiovascular Care. Circulation. 2010;122(suppl 3):S729 S767.

Adenosine

DRUGS USED FOR CONTROL OFHEART RHYTHM AND RATE

97

Precautions

Contraindications


Side effects common but transient andusually resolve within 1-2 minutes

Cardiovascular: Facial flushing (com-mon), chest pain (common), headache,sweating, palpitations, hypotension

Respiratory: Shortness of breath/dysp-nea (common), chest pressure,hyperventilation

Central nervous system: Lightheadedness,dizziness, tingling in arms, numbness,apprehension, blurred vision, burning sen-sation, heaviness in arms, neck and backpain

Gastrointestinal: Nausea, metallic taste,tightness in throat, pressure in groin

Use with caution with obstructive lungdisease not associated with bronchocon-striction (emphysema, bronchitis)

Poison/drug-induced tachycardia Bronchoconstriction or bronchospasm

(asthma) Second- or third-degree AV block Sick sinus syndrome (except in patients

with a functioning artificial pacemaker) Recommended IV site is the antecubital

fossa. Follow each dose immediatelywith a 20-mL normal saline flush andraise the arm for 10-20 seconds. Use theinjection port nearest the hub of the IVcatheter. Constant ECG monitoring isessential.

Must be injected into the IV tubing asfast as possible (over a period of sec-onds). Failure may result in medicationbreakdown while still in the IV tubing.

Discontinue in any patient who developssevere respiratory difficulty

Adenosinecontd

98

Mechanism ofAction

Indications

Dosing (Adult)

Slows conduction in the His-Purkinjesystem and in accessory pathway ofpatients with Wolff-Parkinson-Whitesyndrome

Inhibits alpha- and beta-receptorsand possesses both vagolytic and calci-um-channel blocking properties

Lengthens action potential duration andincreases refractory period in all car-diac tissues including the SA node, AVnode, atrial cells, Purkinje fibers, and inthe ventricular myocardium

Pulseless VT/VF (after CPR, defibrilla-tion, and a vasopressor)

Stable narrow-QRS tachycardias if therhythm persists despite vagal maneu-vers or adenosine or the tachycardia isrecurrent

To control ventricular rate in atrial fibril-lation

To control ventricular rate in pre-excitedatrial dysrhythmias with conduction overan accessory pathway

Stable monomorphic VT Polymorphic VT with normal QT intervalCardiac arrestPulseless VT/VF Initial bolus300 mg IV/IO bolus.* Other indications: Loading dose150 mg IV bolus over 10

minutes (15 mg/min). May repeat every10 min as needed. After conversion, fol-low with a 1 mg/min infusion for 6 hoursand then a 0.5 mg/min maintenance infu-sion over 18 hours.

Maximum cumulative dose 2.2 g IV/24hours.

Amiodarone

*Neumar RW, Otto CW, Link MS, et al. Part 8: Adultadvanced cardiovascular life support: 2010 American HeartAssociation Guidelines for Cardiopulmonary Resuscitationand Emergency Cardiovascular Care. Circulation.2010;122(suppl 3):S729 S767.

Neumar RW, Otto CW, Link MS, et al. Part 8: Adultadvanced cardiovascular life support: 2010 American HeartAssociation Guidelines for Cardiopulmonary Resuscitationand Emergency Cardiovascular Care. Circulation.2010;122(suppl 3):S729 S767.

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Precautions

Contraindications


Hypotension and bradycardia a

Documents

Rapid ACLS Revised 2nd Ed