BBaarrbbaarraa AAeehhlleerrtt,, RN, BSPASouthwest EMS Education, Inc.Phoenix, Arizona/Pursley, Texas
Revised Second Edition
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RAPID ACLSRevised Second Edition
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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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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
lelin
eHe
elof
1ha
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
)sh
ortP
-Rw
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
PR intervalQRS duration
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
PR intervalQRS duration
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
lses
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
llati
on
.f,F
ibri
llato
ryw
ave.
32
44
Rate
Rhythm
P waves
PR intervalQRS duration
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
PR intervalQRS duration
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
PR intervalQRS duration
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
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
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.
70
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
72
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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74
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
79
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
Cap
ture
Cap
ture
Failu
reto
cap
ture
Cap
ture
Failu
reto
cap
ture
.49
82
100%
ven
tric
ula
rp
aced
rhyt
hm
.49
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.
87
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*
88
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
SpecialConsiderations
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
SpecialConsiderations
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
94
Mechanism ofAction
Indications
SpecialConsiderations
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
SpecialConsiderations
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
SpecialConsiderations
Hypotension and bradycardia a