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Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart
Association Guidelines for Cardiopulmonary Resuscitation and mer!ency
Cardiovascular Care
Robert W. Neumar, harles W. !tto, "ar# $. %in#, $te&en %. 'ronic#, "ichael
$huster, lifton W. allaway, (eter ). 'udenchu#, )ose*h (. !rnato, +ryan "cNally,
$cott ". $il&ers, Rod $. (assman, Roger D. White, ,ri# (. -ess, Wanchun .ang,
Daniel Da&is, ,li/abeth $in/ and %aurie ). "orrison
Circulation 201001220$1223$141
D!56 10.114175R8%9.5!N9-9.110.2102::
irculation is *ublished by the 9merican -eart 9ssociation. 1212 ;reen&ille 9&enue, Dallas, .<
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o*yright ? 2010 9merican -eart 9ssociation. 9ll rights reser&ed. (rint 5$$N6 000231@22. !nline
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9
Part 8: Adult Advanced Cardiovascular Life Support
2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and mer!ency Cardiovascular Care
Robert W. Neumar, hair0 harles W. !tto0 "ar# $. %in#0 $te&en %. 'ronic#0
"ichael $huster0 lifton W. allaway0 (eter ). 'udenchu#0 )ose*h (. !rnato0 +ryan "cNally0
$cott ". $il&ers0 Rod $. (assman0 Roger D. White0 ,ri# (. -ess0 Wanchun .ang0
Daniel Da&is0 ,li/abeth $in/0 %aurie ). "orrison
d&anced cardio&ascular life su**ort B9%$C im*acts mul3
ti*le #ey lin#s in the chain of sur&i&al that include
inter&entions to *re&ent cardiac arrest, treat cardiac arrest, and
im*ro&e outcomes of *atients who achie&e return of s*ontane3
ous circulation BR!$C after cardiac arrest. 9%$
inter&entions aimed at *re&enting cardiac arrest include airway
management, &entilation su**ort, and treatment of
bradyarrhythmias and tachyarrhythmias. For the treatment of
cardiac arrest, 9%$ inter&entions build on the basic life
su**ort B+%$C foundation of immediate recognition and
acti&ation of the emergency res*onse system, early (R, and
ra*id defibrillation to further increase the li#elihood of R!$
with drug thera*y, ad&anced airway man3 agement, and
*hysiologic monitoring. Following R!$, sur3 &i&al and
neurologic outcome can be im*ro&ed with integrated
*ostG cardiac arrest care.
(art : *resents the 2010 9dult 9%$ ;uidelines6 :.16
H9djuncts for 9irway ontrol and IentilationJ0 :.26 H"anage3
ment of ardiac 9rrestJ0 and :.@6 H"anagement of
$ym*tomatic +radycardia and .achycardia.J (ostG cardiac
arrest inter&entions are addressed in (art 26 H(ostGardiac
9rrest are.J
'ey changes from the 200= 9%$ ;uidelines include
K
ontinuous Luantitati&e wa&eform ca*nogra*hy is rec3
ommended for confirmation and monitoring of endotra3
cheal tube *lacement.
K
ardiac arrest algorithms are sim*lified and redesigned
to em*hasi/e the im*ortance of high3Luality (R Bin3
cluding chest com*ressions of adeLuate rate and de*th,
allowing com*lete chest recoil after each com*ression,
minimi/ing interru*tions in chest com*ressions and
a&oiding eEcessi&e &entilationC.
K
9tro*ine is no longer recommended for routine use in the
management of *ulseless electrical acti&ity B(,9C7asystole.
K
.here is an increased em*hasis on *hysiologic monitoring
to o*timi/e (R Luality and detect R!$.
K
hronotro*ic drug infusions are recommended as an alter3
nati&e to *acing in sym*tomatic and unstable bradycardia.
K
9denosine is recommended as a safe and *otentially
effecti&e thera*y in the initial management of stable
undifferentiated regular monomor*hic wide3com*leE
tachycardia.
Part 8"1: Ad#uncts for Air$ay Control
and %entilation
&vervie$ of Air$ay 'ana!ement
.his section highlights recommendations for the su**ort of
&entilation and oEygenation during (R and the *eri3arrest
*eriod. .he *ur*ose of &entilation during (R is to maintain
adeLuate oEygenation and sufficient elimination of carbon
dioEide. -owe&er, research has not identified the o*timal
tidal &olume, res*iratory rate, and ins*ired oEygen concen3
tration reLuired during resuscitation from cardiac arrest.
+oth &entilation and chest com*ressions are thought to be
im*ortant for &ictims of *rolonged &entricular fibrillation
BIFC cardiac arrest and for all &ictims with other *resenting
rhythms. +ecause both systemic and *ulmonary *erfusion are
substantially reduced during (R, normal &entilation3
*erfusion relationshi*s can be maintained with a minute
&entilation that is much lower than normal. During (R with
an ad&anced airway in *lace, a lower rate of rescue breathing
is needed to a&oid hy*er&entilation.
%entilation and &(y!en Administration
)urin! CPR
During low blood flow states such as (R, oEygen deli&ery to
the heart and brain is limited by blood flow rather than by
arterial oEygen content.
1,2
.herefore, rescue breaths are less
im*ortant than chest com*ressions during the first few minutes
of resus3 citation from witnessed IF cardiac arrest and could
reduce (R efficacy due to interru*tion in chest com*ressions
and the increase in intrathoracic *ressure that accom*anies
*ositi&e3 *ressure &entilation. .hus, during the first few
minutes of witnessed cardiac arrest a lone rescuer should not
interru*t chest
.he 9merican -eart 9ssociation reLuests that this document be cited as follows6 Neumar RW, !tto W, %in# "$, 'ronic# $%, $huster ", allaway
W, 'udenchu# (), !rnato )(, "cNally +, $il&ers $", (assman R$, White RD, -ess ,(, .ang W, Da&is D, $in/ ,, "orrison %). (art :6 adult ad&anced
cardio&ascular life su**ort6 2010 9merican -eart 9ssociation ;uidelines for ardio*ulmonary Resuscitation and ,mergency ardio&ascular are.
Circulation. 20100122Bsu**l @C6$122 G$141.
*Circulation" 2010+122,suppl -.:S/20 1S/2/"3
? 2010 9merican -eart 9ssociation, 5nc.
Circulation is availa4le at 5ttp:66circ"a5a#ournals"or! )&7: 10"11216C7RC8LA97&:AHA"110"0/0088
Downloaded from circ.ahajouSr7n2a9ls.org by on February 1,
2011
S218 Circulation :ovem4er 2; 2010
Downloaded from circ.ahajournals.org by on February 1, 2011
com*ressions for &entilation. 9d&anced airway *lacement in
cardiac arrest should not delay initial (R and defibrillation for
IF cardiac arrest Blass 5, %!, C.
&(y!en )urin! CPR
Oxygen Administration During CPR
.he o*timal ins*ired oEygen concentration during adult (R
has not been established in human or animal studies. 5n
addition, it is un#nown whether 100M ins*ired oEygen
BF5!
2
1.0C is beneficial or whether titrated oEygen is better.
9lthough *rolonged eE*osure to 100M ins*ired oEygen
BF5!
2
1.0C has *otential toEicity, there is insufficient e&i3
dence to indicate that this occurs during brief *eriods of adult
(R.
@G=
,m*irical use of 100M ins*ired oEygen during (R
o*timi/es arterial oEyhemoglobin content and in turn oEygen
deli&ery0 therefore, use of 100M ins*ired oEygen BF5!
2
1.0C
as soon as it becomes a&ailable is reasonable during resusci3
tation from cardiac arrest Blass 55a, %!, C. "anagement of
oEygen after R!$ is discussed in (art 26 H(ost3ardiac
9rrest are.J
Passive Oxygen Delivery During CPR
(ositi&e3*ressure &entilation has been a mainstay of (R but
recently has come under scrutiny because of the *otential for
increased intrathoracic *ressure to interfere with circulation
due to reduced &enous return to the heart. 5n the out3of3
hos*ital setting, *assi&e oEygen deli&ery &ia mas# with an
o*ened airway during the first 4 minutes of (R *ro&ided by
emergency medical ser&ices B,"$C *ersonnel was *art of a
*rotocol of bundled care inter&entions Bincluding continuous
chest com*ressionsC that resulted in im*ro&ed sur&i&al.
4G:
When *assi&e oEygen deli&ery using a fenestrated tracheal
tube B+oussignac tubeC during uninterru*ted *hysician3
managed (R was com*ared with standard (R, there was
no difference in oEygenation, R!$, or sur&i&al to hos*ital
admission.
2,10
hest com*ressions cause air to be eE*elled
from the chest and oEygen to be drawn into the chest
*assi&ely due to the elastic recoil of the chest. 5n theory,
because &entilation reLuirements are lower than normal
during cardiac arrest, oEygen su**lied by *assi&e deli&ery is
li#ely to be sufficient for se&eral minutes after onset of
cardiac arrest with a *atent u**er airway.
2
At t5is time t5ere
is insufficient evidence to support t5e removal of ventila<
tions from CPR performed 4y ACLS providers"
=a!<'as> %entilation
+ag3mas# &entilation is an acce*table method of *ro&iding
&entilation and oEygenation during (R but is a challenging
s#ill that reLuires *ractice for continuing com*etency. 9ll
healthcare *ro&iders should be familiar with the use of the
bag3mas# de&ice.
11,12
8se of bag3mas# &entilation is not
recom3 mended for a lone *ro&ider. When &entilations are
*erformed by a lone *ro&ider, mouth3to3mouth or mouth3to3
mas# are more efficient. When a second *ro&ider is a&ailable,
bag3mas# &enti3 lation may be used by a trained and
eE*erienced *ro&ider. +ut bag3mas# &entilation is most
effecti&e when *erformed by 2 trained and eE*erienced
*ro&iders. !ne *ro&ider o*ens the airway and seals the mas# to
the face while the other sLuee/es the bag. +ag3mas#
&entilation is *articularly hel*ful when
*lacement of an ad&anced airway is delayed or unsuccessful.
.he desirable com*onents of a bag3mas# de&ice are listed in
(art
=6 H9dult +asic %ife $u**ort.J
.he *ro&ider should use an adult B1 to 2 %C bag and the
*ro&ider should deli&er a**roEimately 400 m% of tidal &olume
sufficient to *roduce chest rise o&er 1 second.
1@
.his &olume of
&entilation is adeLuate for oEygenation and minimi/es the ris#
of gastric inflation. .he *ro&ider should be sure to o*en the
airway adeLuately with a head tiltG chin lift, lifting the jaw
against the mas# and holding the mas# against the face,
creating a tight seal. During (R gi&e 2 breaths Beach 1
secondC during a brief Babout
@ to > secondsC *ause after e&ery @0 chest com*ressions.
+ag3mas# &entilation can *roduce gastric inflation with
com*lications, including regurgitation, as*iration, and *neu3
monia. ;astric inflation can ele&ate the dia*hragm, restrict
lung mo&ement, and decrease res*iratory system
com*liance.
1> G14
Air$ay Ad#uncts
Cricoid Pressure
ricoid *ressure in nonarrest *atients may offer some measure
of *rotection to the airway from as*iration and gastric insuffla3
tion during bag3mas# &entilation.
11G20
-owe&er, it also may
im*ede &entilation and interfere with *lacement of a
su*raglottic airway or intubation.
21G21
.he role of cricoid
*ressure during out3of3hos*ital cardiac arrest and in3hos*ital
cardiac arrest has not been studied. 5f cricoid *ressure is used
in s*ecial circum3 stances during cardiac arrest, the *ressure
should be adjusted, relaEed, or released if it im*edes &entilation
or ad&anced airway *lacement. .he routine use of cricoid
*ressure in cardiac arrest is not recommended Blass 555, %!,
C.
Oroparyngeal Air!ays
9lthough studies ha&e not s*ecifically considered the use of
oro*haryngeal airways in *atients with cardiac arrest, airways
may aid in the deli&ery of adeLuate &entilation with a
bag3mas# de&ice by *re&enting the tongue from occluding
the airway. 5ncorrect insertion of an oro*haryngeal airway
can dis*lace the tongue into the hy*o*harynE, causing airway
obstruction. .o facilitate deli&ery of &entilations with a
bag3mas# de&ice, oro*haryngeal airways can be used in
unconscious Bunres*onsi&eC *atients with no cough or gag
refleE and should be inserted only by *ersons trained in their
use Blass 55a, %!, C.
"asoparyngeal Air!ays
Naso*haryngeal airways are useful in *atients with airway
obstruction or those at ris# for de&elo*ing airway obstruction,
*articularly when conditions such as a clenched jaw *re&ent
*lacement of an oral airway. Naso*haryngeal airways are
better tolerated than oral airways in *atients who are not
dee*ly unconscious. 9irway bleeding can occur in u* to @0M
of *atients following insertion of a naso*haryngeal airway.
2:
.wo case re*orts of inad&ertent intracranial *lacement of a
naso*haryngeal airway in *atients with basilar s#ull frac3
tures
22,@0
suggest that naso*haryngeal airways should be used
with caution in *atients with se&ere craniofacial injury.
9s with all adjuncti&e eLui*ment, safe use of the naso*ha3
:eumar et al Part 8: Adult Advanced Cardiovascular Life Support S219
Downloaded from circ.ahajournals.org by on February 1, 2011
ryngeal airway reLuires adeLuate training, *ractice, and
retraining. No studies ha&e s*ecifically eEamined the use of
naso*haryngeal airways in cardiac arrest *atients. .o facili3
tate deli&ery of &entilations with a bag3mas# de&ice, the
naso*haryngeal airway can be used in *atients with an
obstructed airway. 5n the *resence of #nown or sus*ected
basal s#ull fracture or se&ere coagulo*athy, an oral airway is
*referred Blass 55a, %!, C.
Advanced Air$ays
Ientilation with a bag and mas# or with a bag through an
ad&anced airway Beg, endotracheal tube or su*raglottic air3
wayC is acce*table during (R. 9ll healthcare *ro&iders
should be trained in deli&ering effecti&e oEygenation and
&entilation with a bag and mas#. +ecause there are times
when &entilation with a bag3mas# de&ice is inadeLuate,
ideally 9%$ *ro&iders also should be trained and eE*eri3
enced in insertion of an ad&anced airway.
(ro&iders must be aware of the ris#s and benefits of
insertion of an ad&anced airway during a resuscitation at3
tem*t. $uch ris#s are affected by the *atientNs condition and
the *ro&iderNs eE*ertise in airway control. .here are no
studies directly addressing the timing of ad&anced airway
*lacement and outcome during resuscitation from cardiac
arrest. 9lthough insertion of an endotracheal tube can be
accom*lished during ongoing chest com*ressions, intubation
freLuently is associated with interru*tion of com*ressions for
many seconds. (lacement of a su*raglottic airway is a
reasonable alternati&e to endotracheal intubation and can be
done successfully without interru*ting chest com*ressions.
.he *ro&ider should weigh the need for minimally inter3
ru*ted com*ressions against the need for insertion of an
endotracheal tube or su*raglottic airway. .here is inadeLuate
e&idence to define the o*timal timing of ad&anced airway
*lacement in relation to other inter&entions during resuscita3
tion from cardiac arrest. 5n a registry study of 2= 004
in3hos*ital cardiac arrests, earlier time to in&asi&e airway B
= minutesC was not associated with im*ro&ed R!$ but was
associated with im*ro&ed 2>3hour sur&i&al.
@1
5n an urban
out3of3hos*ital setting, intubation that was achie&ed in 12
minutes was associated with better sur&i&al than intubation
achie&ed in 1@ minutes.
@2
5n out3of3hos*ital urban and rural settings, *atients intu3
bated during resuscitation had a better sur&i&al rate than
*atients who were not intubated,
@@
whereas in an in3hos*ital
setting, *atients who reLuired intubation during (R had a
worse sur&i&al rate.
@>
9 recent study
:
found that delayed
endotracheal intubation combined with *assi&e oEygen deli&3
ery and minimally interru*ted chest com*ressions was asso3
ciated with im*ro&ed neurologically intact sur&i&al after
out3of3hos*ital cardiac arrest in *atients with adult witnessed
IF7*ulseless I.. 5f ad&anced airway *lacement will interru*t
chest com*ressions, *ro&iders may consider deferring inser3
tion of the airway until the *atient fails to res*ond to initial
(R and defibrillation attem*ts or demonstrates R!$
Blass 55b, %!, C.
For a *atient with *erfusing rhythm who reLuires intuba3
tion, *ulse oEimetry and electrocardiogra*hic B,;C status
should be monitored continuously during airway *lacement.
5ntubation attem*ts should be interru*ted to *ro&ide oEygen3
ation and &entilation as needed.
.o use ad&anced airways effecti&ely, healthcare *ro&iders
must maintain their #nowledge and s#ills through freLuent
*ractice. 5t may be hel*ful for *ro&iders to master one
*rimary method of airway control. (ro&iders should ha&e a
second Bbac#u*C strategy for airway management and &enti3
lation if they are unable to establish the first3choice airway
adjunct. +ag3mas# &entilation may ser&e as that bac#u*
strategy.
!nce an ad&anced airway is inserted, *ro&iders should
immediately *erform a thorough assessment to ensure that it
is *ro*erly *ositioned. .his assessment should not interru*t
chest com*ressions. 9ssessment by *hysical eEamination
consists of &isuali/ing chest eE*ansion bilaterally and listen3
ing o&er the e*igastrium Bbreath sounds should not be heardC
and the lung fields bilaterally Bbreath sounds should be eLual
and adeLuateC. 9 de&ice also should be used to confirm
correct *lacement Bsee the section H,ndotracheal 5ntubationJ
belowC.
ontinuous wa&eform ca*nogra*hy is recommended in
addition to clinical assessment as the most reliable method of
confirming and monitoring correct *lacement of an endotra3
cheal tube Blass 5, %!, 9C. (ro&iders should obser&e a
*ersistent ca*nogra*hic wa&eform with &entilation to confirm
and monitor endotracheal tube *lacement in the field, in the
trans*ort &ehicle, on arri&al at the hos*ital, and after any
*atient transfer to reduce the ris# of unrecogni/ed tube
mis*lacement or dis*lacement.
.he use of ca*nogra*hy to confirm and monitor correct
*lacement of su*raglottic airways has not been studied, and
its utility will de*end on airway design. -owe&er, effecti&e
&entilation through a su*raglottic airway de&ice should result
in a ca*nogra*h wa&eform during (R and after R!$.
!nce an ad&anced airway is in *lace, the 2 *ro&iders
should no longer deli&er cycles of (R Bie, com*ressions
interru*ted by *auses for &entilationC unless &entilation is
inadeLuate when com*ressions are not *aused. 5nstead the
com*ressing *ro&ider should gi&e continuous chest com*res3
sions at a rate of at least 100 *er minute, without *auses for
&entilation. .he *ro&ider deli&ering &entilation should *ro3
&ide 1 breath e&ery 4 to : seconds B: to 10 breaths *er
minuteC. (ro&iders should a&oid deli&ering an eEcessi&e
&entilation rate because doing so can com*romise &enous
return and cardiac out*ut during (R. .he 2 *ro&iders should
change com*ressor and &entilator roles a**roEimately e&ery
2 minutes to *re&ent com*ressor fatigue and deterioration in
Luality and rate of chest com*ressions. When multi*le
*ro&iders are *resent, they should rotate the com*ressor role
about e&ery 2 minutes.
Supraglottic Air!ays
$u*raglottic airways are de&ices designed to maintain an o*en
airway and facilitate &entilation. 8nli#e endotracheal
intubation, intubation with a su*raglottic airway does not
reLuire &isuali/a3 tion of the glottis, so both initial training and
maintenance of s#ills are easier. 9lso, because direct
&isuali/ation is not neces3 sary, a su*raglottic airway is inserted
without interru*ting com*ressions. $u*raglottic airways that
ha&e been studied in cardiac arrest are the laryngeal mas#
airway B%"9C, the eso*hageal3tracheal tube BombitubeC and
the laryngeal tube
B%aryngeal .ube or 'ing %.C. When *rehos*ital *ro&iders are
trained in the use of ad&anced su*raglottic airways such as the
eso*hageal3tracheal tube, laryngeal tube, and the laryngeal
mas# airway, they a**ear to be able to use these de&ices safely
and can *ro&ide &entilation that is as effecti&e as that *ro&ided
with a bag and mas# or an endotracheal tube.
12,@=G >1
9d&anced airway inter&entions are technically com*li3
cated. Failure can occur0 thus maintenance of s#ills through
freLuent eE*erience or *ractice is essential.
>2
5t is im*ortant
to remember that there is no e&idence that ad&anced airway
measures im*ro&e sur&i&al rates in the setting of out3of3
hos*ital cardiac arrest. During (R *erformed by *ro&iders
trained in its use, the su*raglottic airway is a reasonable
alternati&e to bag3mas# &entilation Blass 55a, %!, +C and
endotracheal intubation Blass 55a, %!, 9C.
Esophageal-Tracheal Tube
.he ad&antages of the eso*hageal3tracheal tube BombitubeC
are
similar to the ad&antages of the endotracheal tube when either is
com*ared with bag3mas# &entilation6 isolation of the airway,
reduced ris# of as*iration, and more reliable &entilation. .he
ad&antages of the eso*hageal3tracheal tube o&er the
endotracheal tube are related chiefly to ease of training.
12,>@
Ientilation and oEygenation with the eso*hageal3tracheal tube
com*are fa&or3 ably with those achie&ed with the endotracheal
tube.
>>
5n se&eral controlled clinical trials in&ol&ing both in3
hos*ital and out3of3hos*ital resuscitation of adults, *ro&iders
with all le&els of eE*erience were able to insert the
eso*hageal3tracheal tube and deli&er &entilation com*arable
to that achie&ed with endotracheal intubation.
@=,>=G >:
5n a
retros*ecti&e study no difference in outcome was obser&ed in
*atients treated with the eso*hageal3tracheal tube com*ared
with those treated with endotracheal intubation.
@:
.he
eso*hageal3tracheal tube is re*orted to *ro&ide successful
&entilation during (R in 42M to 100M of *atients.
@=,>=G >2
For healthcare *rofessionals trained in its use, the
eso*hageal3 tracheal tube is an acce*table alternati&e to
both bag3mas# &entilation Blass 55a, %!, C or
endotracheal intubation Blass 55a, %!, 9C for airway
management in cardiac arrest. Fatal com*lications may occur
with use of the eso*hageal3 tracheal tube if the *osition
of the distal lumen of the eso*hageal3tracheal tube in the
eso*hagus or trachea is identified incorrectly. For this reason,
confirmation of tube *lacement is essential. !ther *ossible
com*lications related to the use of the eso*hageal3tracheal
tube are eso*hageal trauma, including lac3
erations, bruising, and subcutaneous em*hysema.
>=,=0,=1
Laryngeal Tube
.he ad&antages of the laryngeal tube B%aryngeal .ube or
'ing %.C are similar to those of the eso*hageal3tracheal tube0
howe&er, the laryngeal tube is more com*act and less
com*licated to insert Bunli#e the eso*hageal3tracheal tube,
the laryngeal tube can only go into the eso*hagusC. 9t this
time there are limited data *ublished on the use of the
laryngeal tube in cardiac arrest.
>0,>1,=2,=@
5n one case series
assessing >0 out3of3hos*ital cardiac arrest *atients, insertion
of the laryn3 geal tube by trained *aramedics was successful
and &entila3 tion was effecti&e in :=M of *atients.
>1
For @
*atients, &entilation was ineffecti&e because of cuff ru*ture0
for @ other
*atients, &entilation was ineffecti&e because of massi&e
regurgitation and as*iration before laryngeal tube *lacement.
9nother out3of3hos*ital assessment of 1=1 attem*ts at laryn3
geal tube *lacement re&ealed a 21M success rate in a
miEed *o*ulation of cardiac arrest and noncardiac arrest
*atients.
>0
For healthcare *rofessionals trained in its use, the
laryngeal tube may be considered as an alternati&e to bag3
mas# &entilation Blass 55b, %!, C or endotracheal intubation
for airway management
in cardiac arrest Blass 55b, %!,
C.
Laryngeal Mask
Airway
.he laryngeal mas# airway *ro&ides a more secure and
reliable
means of &entilation than the face mas#.
=>,==
9lthough the
laryngeal mas# airway does not ensure absolute *rotection
against as*iration, studies ha&e shown that regurgitation is less
li#ely with the laryngeal mas# airway than with the bag3mas#
de&ice and that as*iration is uncommon. When com*ared with
the endotracheal tube, the laryngeal mas# airway *ro&ides
eLui&alent &entilation
>2,==
0 successful &entilation during (R
has been re*orted in 12M to 21M of *atients.
@4,@1,>>,=4 G=:
+ecause insertion of the laryngeal mas# airway does not
reLuire laryngosco*y and &isuali/ation of the &ocal cords,
training in its *lacement and use is sim*ler than that for
endotracheal intubation. .he laryngeal mas# airway also may
ha&e ad&antages o&er the endotracheal tube when access to
the *atient is limited,
=2,40
there is a *ossibility of unstable
nec# injury,
41
or a**ro*riate *ositioning of the *atient for
endotracheal intubation is im*ossible.
Results from studies in anestheti/ed *atients com*aring
the laryngeal mas# airway with endotracheal intubation, as
well as additional studies com*aring it with other airways or
&entilation techniLues su**ort the use of the laryngeal mas#
airway for airway control in a &ariety of settings by nurses,
res*iratory thera*ists, and ,"$ *ersonnel, many of whom
had not *re&iously used this de&ice.
12,@2,>>,==,42G 4=
9fter successful insertion, a small *ro*ortion of *atients
cannot be &entilated with the laryngeal mas# airway.
12,>>,==
With this in mind, it is im*ortant for *ro&iders to ha&e an
alternati&e strategy for airway management. (ro&iders who
insert the laryngeal mas# airway should recei&e adeLuate initial
training and then should *ractice insertion of the de&ice
regularly. $uccess rates and the occurrence of com*lications
should be monitored closely. For healthcare *rofessionals
trained in its use, the laryngeal mas# airway is an acce*table
alternati&e to bag3 mas# &entilation Blass 55a, %!, +C or
endotracheal intubation Blass 55a, %!, C for airway
management in cardiac arrest.
#ndotraceal
$ntu%ation
.he endotracheal tube was once considered the o*timal
method of managing the airway during cardiac arrest. -ow3
e&er, intubation attem*ts by uns#illed *ro&iders can *roduce
com*lications, such as trauma to the oro*harynE, interru*tion
of com*ressions and &entilations for unacce*tably long *eri3
ods, and hy*oEemia from *rolonged intubation attem*ts or
failure to recogni/e tube mis*lacement or dis*lacement. 5t is
now clear that the incidence of com*lications is unacce*tably
high when intubation is *erformed by ineE*erienced *ro&id3
ers or monitoring of tube *lacement is inadeLuate. .he
o*timal method of managing the airway during cardiac arrest
will &ary based on *ro&ider eE*erience, characteristics of the
,"$ or healthcare system, and the *atientNs condition.
FreLuent eE*erience or freLuent retraining is recommended
for *ro&iders who *erform endotracheal intubation Blass 5,
%!, +C.
@1,44
,"$ systems that *erform *rehos*ital intuba3
tion should *ro&ide a *rogram of ongoing Luality im*ro&e3
ment to minimi/e com*lications Blass 55a, %!, +C.
No *ros*ecti&e randomi/ed clinical trials ha&e *erformed a
direct com*arison of bag3mas# &entilation &ersus endotra3
cheal intubation in adult &ictims of cardiac arrest. !ne
*ros*ecti&e, randomi/ed controlled trial in an ,"$ system
with short out3of3hos*ital trans*ort inter&als
41
showed no
sur&i&al ad&antage for endotracheal intubation o&er bag3mas#
&entilation in children0 *ro&iders in this study had limited
training and eE*erience in intubation.
.he endotracheal tube #ee*s the airway *atent, *ermits
suctioning of airway secretions, enables deli&ery of a high
concentration of oEygen, *ro&ides an alternati&e route for the
administration of some drugs, facilitates deli&ery of a selected
tidal &olume, and, with use of a cuff, may *rotect the airway
from as*iration.
5ndications for emergency endotracheal intubation are B1C
the inability of the *ro&ider to &entilate the unconscious
*atient adeLuately with a bag and mas# and B2C the absence
of airway *rotecti&e refleEes Bcoma or cardiac arrestC. .he
*ro&ider must ha&e a**ro*riate training and eE*erience in
endotracheal intubation.
During (R *ro&iders should minimi/e the number and
duration of interru*tions in chest com*ressions, with a goal to
limit interru*tions to no more than 10 seconds. 5nterru*tions for
su*raglottic airway *lacement should not be necessary at all,
whereas interru*tions for endotracheal intubation can be mini3
mi/ed if the intubating *ro&ider is *re*ared to begin the
intubation attem*tOie, insert the laryngosco*e blade with the
tube ready at handOas soon as the com*ressing *ro&ider
*auses com*ressions. om*ressions should be interru*ted only
for the time reLuired by the intubating *ro&ider to &isuali/e the
&ocal cords and insert the tube0 this is ideally less than 10
seconds. .he com*ressing *ro&ider should be *re*ared to
resume chest com*ressions immediately after the tube is *assed
through the &ocal cords. 5f the initial intubation attem*t is
unsuccessful, a second attem*t may be reasonable, but early
consideration should be gi&en to using a su*raglottic airway.
5n retros*ecti&e studies, endotracheal intubation has been
associated with a 4M to 2=M incidence of unrecogni/ed tube
mis*lacement or dis*lacement.
4: G12
.his may reflect inade3
Luate initial training or lac# of eE*erience on the *art of the
*ro&ider who *erformed intubation, or it may ha&e resulted
from dis*lacement of a correctly *ositioned tube when the
*atient was mo&ed. .he ris# of tube mis*lacement, dis*lace3
ment, or obstruction is high,
41,10
es*ecially when the *atient is
mo&ed.
1@
.hus, e&en when the endotracheal tube is seen to
*ass through the &ocal cords and tube *osition is &erified by
chest eE*ansion and auscultation during *ositi&e3*ressure
&entilation, *ro&iders should obtain additional confirmation
of *lacement using wa&eform ca*nogra*hy or an eEhaled
!
2
or eso*hageal detector de&ice B,DDC.
1>
.he *ro&ider should use both clinical assessment and
confirmation de&ices to &erify tube *lacement immediately
after insertion and again when the *atient is mo&ed.
-owe&er,
no single confirmation techniLue is com*letely reliable.
1=,14
ontinuous wa&eform ca*nogra*hy is recommended in addi3
tion to clinical assessment as the most reliable method of
confirming and monitoring correct *lacement of an endotra3
cheal tube Blass 5, %!, 9C.
5f wa&eform ca*nogra*hy is not a&ailable, an ,DD or
nonwa&eform eEhaled !
2
monitor in addition to clinical
assessment is reasonable Blass 55a, %!, +C. .echniLues to
confirm endotracheal tube *lacement are further discussed
below.
Clinical Assessment to Confirm Tube Placement
(ro&iders should *erform a thorough assessment of endotra3
cheal tube *osition immediately after *lacement. .his assess3
ment should not reLuire interru*tion of chest com*ressions.
9ssessment by *hysical eEamination consists of &isuali/ing
chest eE*ansion bilaterally and listening o&er the e*igastrium
Bbreath sounds should not be heardC and the lung fields
bilaterally Bbreath sounds should be eLual and adeLuateC. 9
de&ice should also be used to confirm correct *lacement in
the trachea Bsee belowC. 5f there is doubt about correct tube
*lacement, use the laryngosco*e to &isuali/e the tube *assing
through the &ocal cords. 5f still in doubt, remo&e the tube and
*ro&ide bag3mas# &entilation until the tube can be re*laced.
Use of e!ices to Confirm Tube Placement
(ro&iders should always use both clinical assessment and
de&ices to confirm endotracheal tube location immediately
after *lacement and throughout the resuscitation. .wo studies
of *atients in cardiac arrest
12,11
demonstrated 100M sensiti&3
ity and 100M s*ecificity for wa&eform ca*nogra*hy in
identifying correct endotracheal tube *lacement in &ictims of
cardiac arrest. -owe&er, @ studies demonstrated 4>M sensi3
ti&ity and 100M s*ecificity when wa&eform ca*nogra*hy
was first used for &ictims with *rolonged resuscitation and
trans3 *ort times.
1: G:0
9ll confirmation de&ices should be
consid3 ered adjuncts to other confirmation techniLues.
E"hale# C$
%
etectors. Detection of eEhaled !
2
is one of
se&eral inde*endent methods of confirming endotracheal tube
*osition. $tudies of wa&eform ca*nogra*hy to &erify endo3
tracheal tube *osition in &ictims of cardiac arrest ha&e shown
100M sensiti&ity and 100M s*ecificity in identifying correct
endotracheal tube *lacement.
12,11,:1G ::
ontinuous wa&eform
ca*nogra*hy is recommended in addition to clinical assess3
ment as the most reliable method of confirming and moni3
toring correct *lacement of an endotracheal tube Blass 5,
%!, 9C.
;i&en the sim*licity of colorimetric and nonwa&eform
eEhaled !
2
detectors, these methods can be used in addition
to clinical assessment as the initial method for confirming
correct tube *lacement in a *atient in cardiac arrest when
wa&eform ca*nogra*hy is not a&ailable Blass 55a, %!, +C.
-owe&er, studies of colorimetric eEhaled !
2
detectors
:2 G2>
and nonwa&eform (,.!
2
ca*nometers
11,:2,20,2=
indicate that
the accuracy of these de&ices does not eEceed that of ausculta3
tion and direct &isuali/ation for confirming the tracheal *osition
of an endotracheal tube in &ictims of cardiac arrest.
When eEhaled !
2
is detected B*ositi&e reading for !
2
C
in cardiac arrest, it is usually a reliable indicator of tube
*osition in the trachea. False3*ositi&e readings Bie, !
2
is
detected but the tube is located in the eso*hagusC ha&e been
obser&ed in animals after ingestion of large amounts of
carbonated liLuids before the arrest0 howe&er, the wa&eform
does not continue during subseLuent breaths.
24
False3negati&e readings Bdefined in this conteEt as failure
to detect !
2
des*ite tube *lacement in the tracheaC may be
*resent during cardiac arrest for se&eral reasons. .he most
common is that blood flow and deli&ery of !
2
to the lungs
is low. False3negati&e results also ha&e been re*orted in
association with *ulmonary embolus because *ulmonary
blood flow and deli&ery of !
2
to the lungs are reduced. 5f
the detector is contaminated with gastric contents or acidic
drugs Beg, endotracheally administered e*ine*hrineC, a color3
imetric de&ice may dis*lay a constant color rather than
breath3to3breath color change. 5n addition, elimination and
through standard defibrillation *ads, may distinguish tracheal
from eso*hageal intubations.
10@G10=
.here are 2 *ublished re*orts in&ol&ing 4 *atients where
&entilation3induced changes in thoracic im*edance disa*3
*eared after eso*hageal intubation.
104,101
.here is little e&i3
dence for the use of thoracic im*edance in diagnosing
adeLuacy of &entilation during (R. .reatment decisions
should not be based solely on thoracic im*edance measure3
ments until further study has confirmed its utility and accu3
racy in this *o*ulation.
Postintubation Airway Management
9fter inserting and confirming correct *lacement of an
endotracheal tube, the *ro&ider should record the de*th of
the tube as mar#ed at the front teeth or gums and secure it.
.here is significant *otential for endotracheal tube mo&e3
detection of !
2
can be drastically reduced with se&ere
ment with head fleEion and eEtension
10: G110
and when the
airway obstruction Beg, status asthmaticusC and *ulmonary
*atient is mo&ed from one location to another.
111,112
edema.
2@,21,2:
For these reasons, if !
2
is not detected, we
recommend that a second method be used to confirm endo3
tracheal tube *lacement, such as direct &isuali/ation or the
eso*hageal detector de&ice.
8se of !
2
3detecting de&ices to determine the correct
*lacement of other ad&anced airways Beg, ombitube, laryn3
geal mas# airwayC has not been studied0 their utility will
de*end on airway design. -owe&er, effecti&e &entilation
through a su*raglottic airway de&ice should result in ca*no3
gra*h wa&eform during (R and after R!$.
Esophageal etector e!ices. .he ,DD consists of a bulb
that is com*ressed and attached to the endotracheal tube. 5f the
tube is in the eso*hagus B*ositi&e result for an ,DDC, the
suction created by the ,DD will colla*se the lumen of the
eso*hagus or *ull the eso*hageal tissue against the ti* of the
tube, and the bulb will not re3eE*and. .he ,DD may also
consist of a syringe that is attached to the endotracheal tube0
the *ro&ider attem*ts to *ull the barrel of the syringe. 5f the
tube is in the eso*hagus, it will not be *ossible to *ull the
barrel Bas*irate airC with the syringe.
-owe&er, studies of the syringe as*iration ,DD
12,22
and
the self3inflating bulb ,DD
1: G :0
indicate that the accuracy
of these de&ices does not eEceed that of auscultation and
direct &isuali/ation for confirming the tracheal *osition of
an endotracheal tube in &ictims of cardiac arrest. ;i&en the
sim*licity of the ,DD, it can be used as the initial
method for confirming correct tube *lacement in addition
to clinical assessment in the &ictim of cardiac arrest when
wa&eform ca*nogra*hy is not a&ailable Blass 55a, %!,
+C.
.he ,DD may yield misleading results in *atients with
morbid obesity, late *regnancy, or status asthmaticus, or
when there are co*ious endotracheal secretions,
100,101
because
the trachea tends to colla*se in the *resence of these condi3
tions. .here is no e&idence that the ,DD is accurate for the
continued monitoring of endotracheal tube *lacement.
Thoracic &mpe#ance. .ransthoracic im*edance is slightly but
significantly higher during ins*iration than during eEhala3
tion.
102
9ir is a *oor electric conductor. (reliminary studies
suggest that changes in thoracic im*edance, as measured
ontinuous monitoring of endotracheal tube *lacement
with wa&eform ca*nogra*hy is recommended as discussed
abo&e. .he endotracheal tube should be secured with ta*e
or a commercial de&ice Blass 5, %!, C. De&ices and ta*e
should be a**lied in a manner that a&oids com*ression of
the front and sides of the nec#, which may im*air &enous
return from the brain.
!ne out3of3hos*ital study
11@
and 2 studies in an intensi&e3
care setting
11>,11=
indicate that bac#boards, commercial de3
&ices for securing the endotracheal tube, and other strategies
*ro&ide eLui&alent methods for *re&enting inad&ertent tube
dis*lacement when com*ared with traditional methods of
securing the tube Bta*eC. .hese de&ices may be considered
during *atient trans*ort Blass 55b, %!, C. 9fter tube
confirmation and fiEation, obtain a chest E3ray Bwhen feasi3
bleC to confirm that the end of the endotracheal tube is
*ro*erly *ositioned abo&e the carina.
&entilation A'ter Advanced Air!ay Placement
,Ece*t for res*iratory rate, it is un#nown whether monitoring
&entilatory *arameters Beg, minute &entilation, *ea# *ressureC
during (R will influence outcome. -owe&er, *ositi&e3
*ressure &entilation increases intrathoracic *ressure and may
reduce &enous return and cardiac out*ut, es*ecially in *a3
tients with hy*o&olemia or obstructi&e airway disease. Ien3
tilation at high res*iratory rates B 2= breaths *er minuteC is
common during resuscitation from cardiac arrest.
114,111
5n
animal models, slower &entilation rates B4 to 12 breaths *er
minuteC are associated with im*ro&ed hemodynamic *aram3
eters and short3term sur&i&al.
114,11: G12>
+ecause cardiac out*ut is lower than normal during
cardiac arrest, the need for &entilation is reduced. Follow3
ing *lacement of an ad&anced airway, the *ro&ider deli&3
ering &entilations should *erform 1 breath e&ery 4 to :
seconds B: to 10 breaths *er minuteC without *ausing in
a**lying chest com*ressions Bunless &entilation is inade3
Luate when com*ressions are not *ausedC Blass 55b, %!,
C. "onitoring res*iratory rate cou*led with real3time
feedbac# during (R may result in better com*liance with
&entilation guidelines.
12=
Automatic (ransport &entilators
5n both out3of3hos*ital and in3hos*ital settings, automatic
trans*ort &entilators B9.IsC can be useful for &entilation
of adult *atients in noncardiac arrest who ha&e an ad3
&anced airway in *lace Blass 55b, %!, C. .here are &ery
few studies e&aluating the use of 9.Is attached to
ad&anced airways during ongoing resuscitati&e efforts.
During *rolonged resuscitati&e efforts the use of an 9.I
B*neumatically *owered and time3 or *ressure3cycledC may
allow the ,"$ team to *erform other tas#s while *ro&id3
ing adeLuate &entilation and oEygenation Blass 55b, %!,
C.
124,121
(ro&iders should always ha&e a bag3mas# de&ice
a&ailable for bac#u*.
Suction )evices
+oth *ortable and installed suction de&ices should be
a&ailable for resuscitation emergencies. (ortable units
should *ro&ide adeLuate &acuum and flow for *haryngeal
suction. .he suction de&ice should be fitted with large3
bore, non#in#ing suction tubing and semirigid *haryngeal
ti*s. $e&eral sterile suction catheters of &arious si/es
should be a&ailable for suctioning the lumen of the
ad&anced airway, along with a nonbrea#able collection
bottle and sterile water for cleaning tubes and catheters.
.he installed suction unit should be *owerful enough to
*ro&ide an airflow of >0 %7min at the end of the deli&ery
tube and a &acuum of @00 mm -g when the tube is
clam*ed. .he amount of suction should be adjustable for
use in children and intubated *atients.
Summary
9ll basic and ad&anced healthcare *ro&iders should be able
to *ro&ide &entilation with a bag3mas# de&ice during (R
or when the *atient demonstrates cardiores*iratory com3
*romise. 9irway control with an ad&anced airway, which
may include an endotracheal tube or a su*raglottic airway
de&ice, is a fundamental 9%$ s#ill. (rolonged interru*3
tions in chest com*ressions should be a&oided during
ad&anced airway *lacement. 9ll *ro&iders should be able
to confirm and monitor correct *lacement of ad&anced
airways0 this #ey s#ill is reLuired to ensure the safe and
effecti&e use of these de&ices. .raining, freLuency of use,
and monitoring of success and com*lications are more
im*ortant than the choice of a s*ecific ad&anced airway
de&ice for use during (R.
Part 8"2: 'ana!ement of Cardiac Arrest
&vervie$
.his section details the general care of a *atient in cardiac
arrest and *ro&ides an o&er&iew of the 2010 9%$ 9dult
ardiac 9rrest 9lgorithms BFigures 1 and 2C. ardiac
arrest can be caused by > rhythms6 &entricular fibrillation
BIFC, *ulseless &entricular tachycardia BI.C, *ulseless
electric acti&ity B(,9C, and asystole. IF re*resents disor3
gani/ed electric acti&ity, whereas *ulseless I. re*resents
organi/ed electric acti&ity of the &entricular myocardium.
Neither of these rhythms generates significant forward
blood flow. (,9 encom*asses a heterogeneous grou* of
organi/ed electric rhythms that are associated with either
absence of mechanical &entricular acti&ity or mechanical
&entricular acti&ity that is insufficient to generate a clini3
cally detectable *ulse. 9systole B*erha*s better described
as &entricular asystoleC re*resents absence of detectable
&entricular electric acti&ity with or without atrial electric
acti&ity.
$ur&i&al from these cardiac arrest rhythms reLuires both
basic life su**ort B+%$C and a system of ad&anced cardio3
&ascular life su**ort B9%$C with integrated *ostG cardiac
arrest care. .he foundation of successful 9%$ is high3
Luality (R, and, for IF7*ulseless I., attem*ted defibrillation
within minutes of colla*se. For &ictims of witnessed IF arrest,
early (R and ra*id defibrillation can significantly increase the
chance for sur&i&al to hos*ital discharge.
12: G1@@
5n com*arison,
other 9%$ thera*ies such as some medications and ad&anced
airways, although associated with an increased rate of R!$,
ha&e not been shown to increase the rate of sur&i&al to hos*ital
discharge.
@1,@@,1@> G1@:
.he majority of clinical trials testing these
9%$ inter&entions, howe&er, *receded the recently renewed
em*hasis on high3Luality (R and ad&ances in *ostG cardiac
arrest care Bsee (art 26 H(ostGardiac 9rrest areJC. .here3
fore, it remains to be determined if im*ro&ed rates of R!$
achie&ed with 9%$ inter&entions might better translate into
im*ro&ed long3term outcomes when combined with higher3
Luality (R and *ostG cardiac arrest inter&entions such as
thera*eutic hy*othermia and early *ercutaneous coronary
inter&ention B(5C.
.he 2010 9%$ 9dult ardiac 9rrest 9lgorithms BFig3
ures 1 and 2C are *resented in the traditional boE3and3line
format and a new circular format. .he 2 formats are
*ro&ided to facilitate learning and memori/ation of the
treatment recommendations discussed below. !&erall these
algorithms ha&e been sim*lified and redesigned to em*ha3
si/e the im*ortance of high3Luality (R that is fundamen3
tal to the management of all cardiac arrest rhythms.
(eriodic *auses in (R should be as brief as *ossible and
only as necessary to assess rhythm, shoc# IF7I., *erform
a *ulse chec# when an organi/ed rhythm is detected, or
*lace an ad&anced airway. "onitoring and o*timi/ing
Luality of (R on the basis of either mechanical *arame3
ters Bchest com*ression rate and de*th, adeLuacy of
relaEation, and minimi/ation of *ausesC or, when feasible,
*hysiologic *arameters B*artial *ressure of end3tidal !
2
P(,.!
2
Q, arterial *ressure during the relaEation *hase of
chest com*ressions, or central &enous oEygen saturation
P$c&!
2
QC are encouraged Bsee H"onitoring During (RJ
belowC. 5n the absence of an ad&anced airway, a synchro3
ni/ed com*ressionG&entilation ratio of @062 is recom3
mended at a com*ression rate of at least 100 *er minute.
9fter *lacement of a su*raglottic airway or an endotra3
cheal tube, the *ro&ider *erforming chest com*ressions
should deli&er at least 100 com*ressions *er minute
continuously without *auses for &entilation. .he *ro&ider
deli&ering &entilations should gi&e 1 breath e&ery 4 to :
seconds B: to 10 breaths *er minuteC and should be
*articularly careful to a&oid deli&ering an eEcessi&e num3
ber of &entilations Bsee (art :.16 H9djuncts for 9irway
ontrol and IentilationJC.
Figure 1. ACLS Cardiac Arrest Algorithm.
5n addition to high3Luality (R, the only rhythm3s*ecific
thera*y *ro&en to increase sur&i&al to hos*ital discharge is
defibrillation of IF7*ulseless I.. .herefore, this inter&ention
is included as an integral *art of the (R cycle when the
rhythm chec# re&eals IF7*ulseless I.. !ther 9%$ inter3
&entions during cardiac arrest may be associated with an
increased rate of R!$ but ha&e not yet been *ro&en to
increase sur&i&al to hos*ital discharge. .herefore, they are
Figure 2. ACLS Cardiac Arrest Circular Algorithm.
recommended as considerations and should be *erformed
without com*romising Luality of (R or timely defibril3
lation. 5n other words, &ascular access, drug deli&ery, and
ad&anced airway *lacement should not cause significant
interru*tions in chest com*ression or delay defibrillation.
.here is insufficient e&idence to recommend a s*ecific
timing or seLuence BorderC of drug administration and
ad&anced airway *lacement during cardiac arrest. 5n most
cases the timing and seLuence of these secondary inter3
&entions will de*end on the number of *ro&iders *artici3
*ating in the resuscitation and their s#ill le&els. .iming
and seLuence will also be affected by whether &ascular
access has been established or an ad&anced airway *laced
before cardiac arrest.
8nderstanding the im*ortance of diagnosing and treating
the underlying cause is fundamental to management of all
cardiac arrest rhythms. During management of cardiac arrest
the *ro&ider should consider the -Ns and .Ns to identify and
treat any factor that may ha&e caused the arrest or may be
com*licating the resuscitati&e effort B.able 1C.
5t is common for the arrest rhythm to e&ol&e during the
course of resuscitation. 5n such cases management should
shift smoothly to the a**ro*riate rhythm3based strategy. 5n
*articular, *ro&iders should be *re*ared to deli&er a timely
shoc# when a *atient who *resented with asystole or (,9
is found to be in IF7*ulseless I. during a rhythm chec#.
.here is no e&idence that the resuscitation strategy for a
new cardiac arrest rhythm should necessarily be altered
based on the characteristics of the *re&ious rhythm. "ed3
ications administered during resuscitation should be mon3
itored and total doses tabulated to a&oid *otential toEicity.
5f the *atient achie&es R!$, it is im*ortant to begin
*ostG cardiac arrest care immediately to a&oid rearrest and
o*timi/e the *atientNs chance of long3term sur&i&al with
good neurologic function Bsee (art 2C. Finally, the reality is
that the majority of resuscitati&e efforts do not result in
R!$. riteria for ending unsuccessful resuscitati&e ef3
forts are addressed briefly below Bsee HWhen $hould
Resuscitati&e ,fforts $to*RJC and in more detail in (art @6
H,thics.J
R5yt5m<=ased 'ana!ement of Cardiac Arrest
5n most cases of witnessed and unwitnessed cardiac arrest the
first *ro&ider should start (R with chest com*ressions and
the second *ro&ider should get or turn on the defibrillator,
Table 1. Treatable Causes of Cardiac Arrest: The Hs and Ts
Hs Ts Hypoxia
Toxins Hypovolemia Tamponade
(cardiac) Hydrogen ion (acidosis) Tension
pneumothorax Hypo-hyper!alemia
Throm"osis# pulmonary Hypothermia
Throm"osis# coronary
$or %urther explanation o% the Hs and Ts# see &art '() *Special +esusci-
tation Situations.,
*lace the adhesi&e *ads or *addles, and chec# the rhythm.
(addles and electrode *ads should be *laced on the eE*osed
chest in an anterior3lateral *osition. 9cce*table alternati&e
*ositions are anterior3*osterior, anterior3left infrasca*ular,
and anterior3right infrasca*ular. Rhythm chec#s should be
brief, and if an organi/ed rhythm is obser&ed, a *ulse chec#
should be *erformed. 5f there is any doubt about the *resence
of a *ulse, chest com*ressions should be resumed immedi3
ately. 5f a cardiac monitor is attached to the *atient at the time
of arrest, the rhythm can be diagnosed before (R is
initiated.
&)*Pulseless &(
When a rhythm chec# by an automated eEternal defibrillator
B9,DC re&eals IF7I., the 9,D will ty*ically *rom*t to
charge, HclearJ the &ictim for shoc# deli&ery, and then deli&er
a shoc#, all of which should be *erformed as Luic#ly as
*ossible. (R should be resumed immediately after shoc#
deli&ery Bwithout a rhythm or *ulse chec# and beginning with
chest com*ressionsC and continue for 2 minutes before the
neEt rhythm chec#.
When a rhythm chec# by a manual defibrillator re&eals
IF7I., the first *ro&ider should resume (R while the
second *ro&ider charges the defibrillator. !nce the defibril3
lator is charged, (R is *aused to HclearJ the *atient for
shoc# deli&ery. 9fter the *atient is Hclear,J the second
*ro&ider gi&es a single shoc# as Luic#ly as *ossible to
minimi/e the interru*tion in chest com*ressions BHhands3off
inter&alJC. .he first *ro&ider resumes (R immediately after
shoc# deli&ery Bwithout a rhythm or *ulse chec# and begin3
ning with chest com*ressionsC and continues for 2 minutes.
9fter 2 minutes of (R the seLuence is re*eated, beginning
with a rhythm chec#.
.he *ro&ider gi&ing chest com*ressions should switch at
e&ery 23minute cycle to minimi/e fatigue. (R Luality
should be monitored based on mechanical or *hysiologic
*arameters Bsee H"onitoring During (RJ belowC.
De'i%rillation Strategies
'a!eform an# Energy
5f a bi*hasic defibrillator is a&ailable, *ro&iders should use
the manufacturerNs recommended energy dose Beg, initial
dose of 120 to 200 )C for terminating IF Blass 5, %!, +C. 5f
the *ro&ider is unaware of the effecti&e dose range, the
*ro&ider may use the maEimal dose Blass 55b, %!, C.
$econd and subseLuent energy le&els should be at least
eLui&alent, and higher energy le&els may be considered if
a&ailable Blass 55b, %!, +C. 5f a mono*hasic defibrillator is
used, *ro&iders should deli&er an initial shoc# of @40 ) and
use that dose for all subseLuent shoc#s. 5f IF is terminated
by a shoc# but then recurs later in the arrest, deli&er
subseLuent shoc#s at the *re&iously successful energy le&el.
Automatic (ersus Manual Mo#es for
Multimo#al efibrillators
8se of a multimodal defibrillator in manual mode may
reduce
the duration of interru*tion of (R reLuired for rhythm
analysis com*ared with automatic mode but could increase
the freLuency of ina**ro*riate shoc#.
1@2,1>0
urrent e&idence
indicates that the benefit of using a multimodal defibrillator
in manual instead of automatic mode during cardiac arrest is
uncertain Blass 55b, %!, C.
CP) *efore efibrillation
During treatment of IF7*ulseless I. healthcare *ro&iders
must ensure that coordination between (R and shoc#
deli&ery is efficient. When IF is *resent for more than a
few minutes, the myocardium is de*leted of oEygen and
metabolic substrates. 9 brief *eriod of chest com*ressions
can deli&er oEygen and energy substrates and HunloadJ the
&olume3o&erloaded right &entricle, increasing the li#eli3
hood that a *erfusing rhythm will return after shoc#
deli&ery.
1>1
(erforming (R while a defibrillator is readied for use is
strongly recommended for all *atients in cardiac arrest Blass
5, %!, +C. 9nalyses of IF wa&eform characteristics *redic3
ti&e of shoc# success ha&e documented that the shorter the
time inter&al between the last chest com*ression and shoc#
deli&ery, the more li#ely the shoc# will be successful.
1>1
9
reduction of e&en a few seconds in the inter&al from *ausing
com*ressions to shoc# deli&ery can increase the *robability
of shoc# success.
1>2
.he &alue of intentionally delaying defibrillation to *erform
(R is less clear. !ne randomi/ed controlled trial BR.C
1>@
and one clinical trial
1>>
in&ol&ing adults with out3of3hos*ital
cardiac arrest not witnessed by ,"$ *ersonnel showed that
sur&i&al was im*ro&ed by a *eriod of (R *erformed before
the first defibrillation shoc# when the ,"$ res*onse inter&al
was > to
= minutes. +ut 2 R.s
1>=,1>4
demonstrated no im*ro&ement in
R!$ or sur&i&al to hos*ital discharge in *atients with out3of3
hos*ital IF or *ulseless I. who recei&ed (R from ,"$
*ersonnel for 1.= to @ minutes before defibrillation, regardless
of ,"$ res*onse inter&al. 9t this time the benefit of delaying
defibrillation to *erform (R before defibrillation is unclear
Blass 55b, %!, +C.
(+ 'a!eform Analysis to Pre#ict efibrillation ,uccess
Retros*ecti&e analysis of IF wa&eforms in multi*le clinical
studies suggests that it is *ossible to *redict the success of
defibrillation from the fibrillation wa&eform with &arying
reliability.
1>1,1>1G144
No *ros*ecti&e human studies ha&e s*e3
cifically e&aluated whether treatment altered by *redicting
success of defibrillation can im*ro&e successful defibrilla3
tion, rate of R!$, or sur&i&al from cardiac arrest. .he &alue
of IF wa&eform analysis to guide management of defibril3
lation in adults with in3hos*ital and out3of3hos*ital cardiac
arrest is uncertain Blass 55b, %!, C.
Drug (erapy in &)*Pulseless
&(
When IF7*ulseless I. *ersists after at least 1 shoc# and a
23minute (R *eriod, a &aso*ressor can be gi&en with the
*rimary goal of increasing myocardial blood flow during
(R and achie&ing R!$ Bsee H"edications for 9rrest
RhythmsJ below for dosingC Blass 55b, %!, 9C. .he *ea#
effect of an intra&enous B5IC7intraosseous B5!C &aso*ressor
gi&en as a bolus dose during (R is delayed for at least 1 to
2 minutes. .he o*timal timing of &aso*ressor administration
during the 23minute *eriod of uninterru*ted (R has not
been established. 5f a shoc# fails to generate a *erfusing
rhythm, then gi&ing a &aso*ressor soon after the shoc# will
o*timi/e
the *otential im*act of increased myocardial blood flow
before the neEt shoc#. -owe&er, if a shoc# results in a
*erfusing rhythm, a bolus dose of &aso*ressor at any time
during the subseLuent 23minute *eriod of (R Bbefore
rhythm chec#C could theoretically ha&e detrimental effects on
cardio&ascular stability. .his may be a&oided by using
*hysiologic monitoring such as Luantitati&e wa&eform ca*3
nogra*hy, intra3arterial *ressure monitoring, and continuous
central &enous oEygen saturation monitoring to detect R!$
during chest com*ressions.
2@,141G111
-owe&er, adding an ad3
ditional *ause for rhythm and *ulse chec# after shoc#
deli&ery but before &aso*ressor thera*y will decrease myo3
cardial *erfusion during the critical *ostshoc# *eriod and
could reduce the chance of achie&ing R!$.
9miodarone is the first3line antiarrhythmic agent gi&en
during cardiac arrest because it has been clinically demon3
strated to im*ro&e the rate of R!$ and hos*ital admission
in adults with refractory IF7*ulseless I.. 9miodarone may
be considered when IF7I. is unres*onsi&e to (R,
defibrilla3 tion, and &aso*ressor thera*y Blass 55b, %!, 9C.
5f amiod3 arone is una&ailable, lidocaine may be considered,
but in clinical studies lidocaine has not been demonstrated to
im*ro&e rates of R!$ and hos*ital admission com*ared
with amiodarone Blass 55b, %!, +C. "agnesium sulfate
should be considered only for torsades de *ointes associated
with a long S. inter&al Blass 55b, %!, +C.
(reating Potentially Reversi%le Causes o'
&)*Pulseless &(
.he im*ortance of diagnosing and treating the underlying
cause of IF7*ulseless I. is fundamental to the management
of all cardiac arrest rhythms. 9s always, the *ro&ider should
recall the -Ns and .Ns to identify a factor that may ha&e
caused the arrest or may be com*licating the resuscitati&e
effort Bsee .able 1 and (art 126 H$*ecial Resuscitation
$ituationsJC. 5n the case of refractory IF7*ulseless I., acute
coronary ischemia or myocardial infarction should be con3
sidered as a *otential etiology. Re*erfusion strategies such as
coronary angiogra*hy and (5 during (R or emergency
cardio*ulmonary by*ass ha&e been demonstrated to be fea3
sible in a number of case studies and case series but ha&e not
been e&aluated for their effecti&eness in R.s.
11: G1:1
Fibrino3
lytic thera*y administered during (R for acute coronary
occlusion has not been shown to im*ro&e outcome.
1::
ROSC A'ter &)*Pulseless &(
5f the *atient has R!$, *ostG cardiac arrest care should be
started B(art 2C. !f *articular im*ortance are treatment of
hy*oEemia and hy*otension, early diagnosis and treatment of
$.3ele&ation myocardial infarction B$.,"5C Blass 5, %!,
+C and thera*eutic hy*othermia in comatose *atients Blass 5,
%!, +C.
PA6Asystole
When a rhythm chec# by an 9,D re&eals a nonshoc#able
rhythm, (R should be resumed immediately, beginning with
chest com*ressions, and should continue for 2 minutes before
the rhythm chec# is re*eated. When a rhythm chec# using a
manual defibrillator or cardiac monitor re&eals an organi+ed
rytm, a *ulse chec# is *erformed. 5f a *ulse is detected,
*ostG cardiac arrest care should be initiated immediately Bsee
(art 2C. 5f the rhythm is asystole or the *ulse is absent Beg,
(,9C, (R should be resumed immediately, beginning with
chest com*ressions, and should continue for 2 minutes before
the rhythm chec# is re*eated. .he *ro&ider *erforming chest
com*ressions should switch e&ery 2 minutes. (R Luality
should be monitored on the basis of mechanical or *hysio3
logic *arameters Bsee H"onitoring During (RJ belowC.
Drug (erapy 'or P#A*Asystole
9 &aso*ressor can be gi&en as soon as feasible with the
*rimary goal of increasing myocardial and cerebral blood
flow during (R and achie&ing R!$ Bsee HIaso*ressorsJ
below for dosingC Blass 55b, %!, 9C. 9&ailable e&idence
suggests that the routine use of atro*ine during (,9 or
asystole is unli#ely to ha&e a thera*eutic benefit Blass 55b,
%!, +C. For this reason atro*ine has been remo&ed from the
cardiac arrest algorithm.
(reating Potentially Reversi%le Causes o' P#A*Asystole
(,9 is often caused by re&ersible conditions and can be
treated successfully if those conditions are identified and
corrected. During each 23minute *eriod of (R the *ro&ider
should recall the -Ns and .Ns to identify factors that may ha&e
caused the arrest or may be com*licating the resuscitati&e
effort Bsee .able 1 and (art 126 H$*ecial Resuscitation
$ituationsJC. ;i&en the *otential association of (,9 with
hy*oEemia, *lacement of an ad&anced airway is theoretically
more im*ortant than during IF7*ulseless I. and might be
necessary to achie&e adeLuate oEygenation or &entilation.
(,9 caused by se&ere &olume loss or se*sis will *otentially
benefit from administration of em*irical 5I75! crystalloid. 9
*atient with (,9 caused by se&ere blood loss will *otentially
benefit from a blood transfusion. When *ulmonary embolism
is *resumed or #nown to be the cause of cardiac arrest,
em*irical fibrinolytic thera*y can be considered Blass 55a,
%!, +0 see (art 12C. Finally, if tension *neumothoraE is
clinically sus*ected as the cause of (,9, initial management
includes needle decom*ression. 5f a&ailable, echocardiogra3
*hy can be used to guide management of (,9 because it
*ro&ides useful information about intra&ascular &olume status
Bassessing &entricular &olumeC, cardiac tam*onade, mass
lesions Btumor, clotC, left &entricular contractility, and re3
gional wall motion.
1:2
$ee (art 12 for management of
toEicological causes of cardiac arrest.
9systole is commonly the end3stage rhythm that follows
*rolonged IF or (,9, and for this reason the *rognosis is
generally much worse.
ROSC A'ter P#A*Asystole
5f the *atient has R!$, *ostG cardiac arrest care should
be
initiated Bsee (art 2C. !f *articular im*ortance is treatment of
hy*oEemia and hy*otension and early diagnosis and treat3
ment of the underlying cause of cardiac arrest. .hera*eutic
hy*othermia may be considered when the *atient is comatose
Blass 55b, %!, C.
'onitorin! )urin! CPR
,ecanical Parameters
(R Luality can be im*ro&ed by using a number of
non*hysi3
ologic techniLues that hel* the *ro&ider adhere to recom3
mended (R *arameters such as rate and de*th of com*res3
sion and rate of &entilation. .he most sim*le are auditory or
&isual metronomes to guide *ro&iders in *erforming the
recommended rate of chest com*ressions or &entilations.
"ore so*histicated de&ices actually monitor chest com*res3
sion rate, de*th, relaEation, and *auses in real time and
*ro&ide &isual and auditory feedbac#. When recorded, this
information can also be useful in *ro&iding feedbac# to the
entire team of *ro&iders after the resuscitation has ended.
.his ty*e of (R Luality monitoring is discussed in more
detail in (art =6 H9dult +asic %ife $u**ortJ and (art 146
H,ducation, 5m*lementation and .eams.J
Pysiologic Parameters
5n humans cardiac arrest is the most critically ill condition,
yet it is ty*ically monitored by rhythm assessment using
selected electocardiogra*hic B,;C leads and *ulse chec#s
as the only *hysiologic *arameters to guide thera*y.
9nimal and human studies indicate that monitoring of
(,.!
2
, coronary *erfusion *ressure B((C, and central
&enous oEygen saturation B$c&!
2
C *ro&ides &aluable infor3
mation on both the *atientNs condition and res*onse to
*ressed as a *artial *ressure in mm -g B(,.!
2
C. +ecause
!
2
is a trace gas in atmos*heric air, !
2
detected by
ca*nogra*hy in eEhaled air is *roduced in the body and
deli&ered to the lungs by circulating blood. 8nder normal
conditions (,.!
2
is in the range of @= to >0 mm -g.
During untreated cardiac arrest !
2
continues to be
*roduced in the body, but there is no !
2
deli&ery to the
lungs. 8nder these conditions (,.!
2
will a**roach /ero
with continued &entilation. With initiation of (R, cardiac
out*ut is the major determinant of !
2
deli&ery to the
lungs. 5f &entilation is relati&ely constant, (,.!
2
corre3
lates well with cardiac out*ut during (R. .he correlation
between (,.!
2
and cardiac out*ut during (R can be
transiently altered by gi&ing 5I sodium bicarbonate.
20:
.his is eE*lained by the fact that the bicarbonate is
con&erted to water and !
2
, causing a transient increase in
deli&ery of !
2
to the lungs. .herefore, a transient rise in
(,.!
2
after sodium bicarbonate thera*y is eE*ected and
should not be misinter*reted as an im*ro&ement in Luality
of (R or a sign of R!$. 9nimal and human studies ha&e
also shown that (,.!
2
correlates with (( and cerebral
thera*y. "ost im*ortantly, (,.!
2
, ((, and $c&!
2
corre3
*erfusion *ressure during (R.
202,210
.he correlation of
late with cardiac out*ut and myocardial blood flow during
(R, and threshold &alues below which R!$ is rarely
achie&ed ha&e been re*orted.
14:,120 G12=
Furthermore, an
abru*t increase in any of these *arameters is a sensiti&e
indicator of R!$ that can be monitored without interru*ting
chest com*ressions.
21,2@,141G11=,111,124 G201
9lthough no clinical
study has eEamined whether titrating resuscitati&e efforts to
these or other *hysiologic *arameters im*ro&es outcome, it is
reasonable to consider using these *arameters when feasible
to o*timi/e chest com*ressions and guide &aso*ressor ther3
a*y during cardiac arrest Blass 55b, %!, C.
Pulse
linicians freLuently try to *al*ate arterial *ulses during chest
com*ressions to assess the effecti&eness of com*ressions. No
studies ha&e shown the &alidity or clinical utility of chec#ing
*ulses during ongoing (R. +ecause there are no &al&es in the
inferior &ena ca&a, retrograde blood flow into the &enous
system
(,.!
2
with (( during (R can be altered by &aso*res3
sor thera*y, es*ecially at high doses Bie, 1 mg of
e*ine*hrineC.
211G21>
Iaso*ressors cause increased after3
load, which will increase blood *ressure and myocardial
blood flow during (R but will also decrease cardiac
out*ut. .herefore, a small decrease in (,.!
2
after &aso3
*ressor thera*y may occur but should not be misinter*reted
as a decrease in (R Luality.
(ersistently low (,.!
2
&alues B 10 mm -gC during
(R in intubated *atients suggest that R!$ is
unli#ely.
111,11@,11>,120,121,21=,214
$imilar data using Luantita3
ti&e monitoring of (,.!
2
are not a&ailable for *atients with
a su*raglottic airway or those recei&ing bag3mas# &entilation
during (R. !ne study using colorimetic end3tidal !
2
detection in nonintubated *atients during (R found that low
end3tidal !
2
was not a reliable *redictor of failure to
achie&e R!$.
211
9n air lea# during bag3mas# &entilation or
&entilation with a su*raglottic airway could result in lower
may *roduce femoral &ein *ulsations.
202
.hus, *al*ation of a
*ulse in the femoral triangle may indicate &enous rather than
measured (,.!
2
&alues. 9lthough a (,.!
2
&alue of
arterial blood flow. arotid *ulsations during (R do not
indicate the efficacy of myocardial or cerebral *erfusion during
(R. (al*ation of a *ulse when chest com*ressions are *aused
is a reliable indicator of R!$ but is *otentially less sensiti&e
than other *hysiologic measures discussed below.
-ealthcare *ro&iders also may ta#e too long to chec# for a
10 mm -g in intubated *atients indicates that cardiac
out*ut is inadeLuate to achie&e R!$, a s*ecific target
(,.!
2
&alue that o*timi/es the chance of R!$ has not
been established. "onitoring (,.!
2
trends during (R
has the *otential to guide indi&idual o*timi/ation of
com*ression de*th and rate and to detect fatigue in the
*ro&ider *erforming com*ressions.
201,21:,212
5n addition, an
abru*t sustained in3
*ulse
20@,20>
and ha&e difficulty determining if a *ulse is
crease in (,.!
2
during (R is an indicator of
*resent or absent.
20@G20=
.here is no e&idence, howe&er, that
chec#ing for breathing, coughing, or mo&ement is su*erior
for detection of circulation.
204
+ecause delays in chest com3
*ressions should be minimi/ed, the healthcare *ro&ider
should ta#e no more than 10 seconds to chec# for a *ulse,
and
R!$.
21,111,124,12: G201
.herefore, it is reasonable to consider
using Luantitati&e wa&eform ca*nogra*hy in intubated *a3
tients to monitor (R Luality, o*timi/e chest com*ressions,
and detect R!$ during chest com*ressions or when rhythm
chec# re&eals an organi/ed rhythm Blass 55b, %!, C. 5f
if it is not felt within that time *eriod chest com*ressions
should be started.
20=,201
(,.!
2
is 10 mm -g, it is reasonable to consider trying to
#nd-(idal CO
2
,nd3tidal !
2
is the concentration of carbon dioEide in
eEhaled air at the end of eE*iration. 5t is ty*ically eE3
im*ro&e (R Luality by o*timi/ing chest com*ression *a3
rameters Blass 55b, %!, C. 5f (,.!
2
abru*tly increases to
a normal &alue B@= to >0 mm -gC, it is reasonable to consider
that this is an indicator of R!$ Blass 55a, %!, +C. .he
&alue of using Luantitati&e wa&eform ca*nogra*hy in nonin3
tubated *atients to monitor and o*timi/e (R Luality and
detect R!$ is uncertain Blass 55b, %!, C.
Coronary Per'usion Pressure and Arterial
Relaxation Pressure
(( Bcoronary *erfusion *ressure aortic relaEation
PHdiastolicJQ *ressure minus right atrial relaEation PHdia3
stolicJQ *ressureC during (R correlates with both
myocardial blood flow and R!$.
14:,122,220
RelaEation *ressure
during (R is the trough of the *ressure wa&eform during the
relaEation *hase of chest com*ressions and is analogous to
diastolic *ressure when the heart is beating. 5ncreased ((
correlates with im*ro&ed 2>3hour sur&i&al rates in animal
studies
12@
and is associated with im*ro&ed myocardial blood
flow and R!$ in animal studies of e*ine*hrine, &aso*ressin,
and angiotensin 55.
12@G12=
5n one human study R!$ did not
occur unless a ((
1= mm -g was achie&ed during (R.
14:
-owe&er,
monitoring of (( during (R is rarely a&ailable clinically
because measurement and calculation reLuire simultaneous
recording of aortic and central &enous *ressure.
9 reasonable surrogate for (( during (R is arterial
relaEation BHdiastolicJC *ressure, which can be measured
using a radial, brachial, or femoral artery catheter. .hese
closely a**roEimate aortic relaEation *ressures during (R
in humans.
211,221
.he same study that identified a ((
threshold of 1= mm -g for R!$ also re*orted that R!$
was not achie&ed if aortic relaEation HdiastolicJ *ressure
did not eEceed 11 mm -g during (R.
14:
9 s*ecific target
arterial relaEation *ressure that o*timi/es the chance of
R!$ has not been established. 5t is reasonable to consider
using arterial relaEation HdiastolicJ *ressure to monitor
(R Luality, o*timi/e chest com*ressions, and guide
&aso*ressor thera*y. Blass 55b, %!, C. 5f the arterial
relaEation HdiastolicJ *ressure is 20 mm -g, it is
reasonable to consider trying to im*ro&e Luality of (R by
o*timi/ing chest com*ression *arameters or gi&ing a
&aso*ressor or both Blass 55b, %!, C. 9rterial *ressure
monitoring can also be used to detect R!$ during chest
com*ressions or when a rhythm chec# re&eals an organi/ed
rhythm Blass 55b, %!, C.
Central &enous Oxygen Saturation
When oEygen consum*tion, arterial oEygen saturation
B$a!
2
C, and hemoglobin are constant, changes in $c&!
2
reflect changes in oEygen deli&ery by means of changes in
cardiac out*ut. $c&!
2
can be measured continuously using
oEimetric ti**ed central &enous catheters *laced in the
su*erior &ena ca&a. $c&!
2
&alues normally range from 40M
to
:0M. During cardiac arrest and (R these &alues range from
2=M to @=M, indicating the inadeLuacy of blood flow
*roduced during (R. 5n one clinical study the failure to
achie&e $c&!
2
of @0M during (R was associated with
failure to achie&e R!$.
142
$c&!
2
also hel*s to ra*idly detect
R!$ without interru*ting chest com*ressions to chec#
rhythm and *ulse. When a&ailable, continuous $c&!
2
moni3
toring is a *otentially useful indicator of cardiac out*ut and
oEygen deli&ery during (R. .herefore, when in *lace
before cardiac arrest, it is reasonable to consider using
continuous $c&!
2
measurement to monitor Luality of
(R, o*timi/e chest com*ressions, and detect R!$ during
chest com*res3 sions or when rhythm chec# re&eals an
organi/ed rhythm Blass 55b, %!, C. 5f $c&!
2
is @0M, it is
reasonable to consider trying to im*ro&e the Luality of (R
by o*timi/ing chest com*ression *arameters Blass 55b,
%!, C.
Pulse Oximetry
During cardiac arrest, *ulse oEimetry ty*ically does not
*ro&ide a reliable signal because *ulsatile blood flow is
inadeLuate in *eri*heral tissue beds. +ut the *resence of a
*lethysmogra*h wa&eform on *ulse oEimetry is *otentially
&aluable in detecting R!$, and *ulse oEimetry is useful to
ensure a**ro*riate oEygenation after R!$.
Arterial .lood /ases
9rterial blood gas monitoring during (R is not a reliable
indicator of the se&erity of tissue hy*oEemia, hy*ercarbia
Band therefore adeLuacy of &entilation during (RC, or tissue
acidosis.
222
Routine measurement of arterial blood gases
during (R has uncertain &alue Blass 55b, %!, C.
#cocardiograpy
No studies s*ecifically eEamine the im*act of echocardiog3
ra*hy on *atient outcomes in cardiac arrest. -owe&er, a
number of studies suggest that transthoracic and transeso*h3
ageal echocardiogra*hy ha&e *otential utility in diagnosing
treatable causes of cardiac arrest such as cardiac tam*onade,
*ulmonary embolism, ischemia, and aortic dissection.
22@G221
5n addition, @ *ros*ecti&e studies
22: G2@0
found that absence of
cardiac motion on sonogra*hy during resuscitation of *atients
in cardiac arrest was highly *redicti&e of inability to achie&e
R!$6 of the @>1 *atients from the @ studies, 21: had no
detectable cardiac acti&ity and only 2 of these had R!$ Bno
data on sur&i&al3to3hos*ital discharge were re*ortedC. .rans3
thoracic or transeso*hageal echocardiogra*hy may be con3
sidered to diagnose treatable causes of cardiac arrest and
guide treatment decisions Blass 55b, %!, C.
Access for Parenteral 'edications )urin!
Cardiac Arrest
(iming o' $&*$O Access
During cardiac arrest, *ro&ision of high3Luality (R and
ra*id defibrillation are of *rimary im*ortance and drug
administration is of secondary im*ortance. 9fter beginning
(R and attem*ting defibrillation for identified IF or *ulse3
less I., *ro&iders can establish 5I or 5! access. .his should
be *erformed without interru*ting chest com*ressions. .he
*rimary *ur*ose of 5I75! access during cardiac arrest is to
*ro&ide drug thera*y. .wo clinical studies
1@>,1@4
re*orted data
suggesting worsened sur&i&al for e&ery minute that antiar3
rhythmic drug deli&ery was delayed Bmeasured from time of
dis*atchC. -owe&er, this finding was *otentially biased by a
concomitant delay in onset of other 9%$ inter&entions. 5n
one study
1@4
the inter&al from first shoc# to administration of
an antiarrhythmic drug was a significant *redictor of
sur&i&al.
!ne animal study
2@1
re*orted lower (( when deli&ery of a
&aso*ressor was delayed. .ime to drug administration was
also a *redictor of R!$ in a retros*ecti&e analysis of swine
cardiac arrest.
2@2
.hus, although time to drug treatment
a**ears to ha&e im*ortance, there is insufficient e&idence to
s*ecify eEact time *arameters or the *recise seLuence with
which drugs should be administered during cardiac arrest.
Periperal $& Drug Delivery
5f a resuscitation drug is administered by a *eri*heral &enous
route, it should be administered by bolus injection and
followed with a 203m% bolus of 5I fluid to facilitate the drug
flow from the eEtremity into the central circulation.
2@@
+riefly
ele&ating the eEtremity during and after drug administration
theoretically may also recruit the benefit of gra&ity to
facilitate deli&ery to the central circulation but has not been
systematically studied.
$O Drug Delivery
5! cannulation *ro&ides access to a noncolla*sible &enous
*leEus, enabling drug deli&ery similar to that achie&ed by
*eri*heral &enous access at com*arable doses. .wo *ros*ec3
ti&e trials in children
2@>
and adults
2@=
and 4 other studies
2@4 G
2>2 suggest that 5! access can be established efficiently0 is
safe and effecti&e for fluid resuscitation, drug deli&ery, and
blood sam*ling for laboratory e&aluation0 and is attainable in
all age grou*s. -owe&er, many of these studies were con3
ducted during normal *erfusion states or hy*o&olemic shoc#
or in animal models of cardiac arrest. 9lthough &irtually all
9%$ drugs ha&e been gi&en intraosseously in the clinical
setting without #nown ill effects, there is little information on
the efficacy and effecti&eness of such administration in
clinical cardiac arrest during ongoing (R. 5t is reasonable
for *ro&iders to establish 5! access if 5I access is not readily
a&ailable Blass 55a, %!, C. ommercially a&ailable #its
can facilitate 5! access in adults.
Central $& Drug Delivery
.he a**ro*riately trained *ro&ider may consider *lacement
of a central line Binternal jugular or subcla&ianC during
cardiac arrest, unless there are contraindications Blass 55b,
%!, C. .he *rimary ad&antage of a central line is that *ea#
drug concentrations are higher and drug circulation times
shorter com*ared with drugs administered through a *eri*h3
eral 5I catheter.
2>@G2>=
5n addition, a central line eEtending
into the su*erior &ena ca&a can be used to monitor $c&!
2
and
estimate (( during (R, both of which are *redicti&e of
R!$.
14:,142
-owe&er, central line *lacement can interru*t
(R. entral &enous catheteri/ation is a relati&e Bbut not
absoluteC contraindication for fibrinolytic thera*y in *atients
with acute coronary syndromes.
#ndotraceal Drug Delivery
!ne study in children,
2>4
= studies in adults,
2>1G2=1
and
multi*le animal studies
2=2G2=>
ha&e shown that lido3
caine,
2>:,2==
e*ine*hrine,
2=4
atro*ine,
2=1
naloEone, and &aso3
*ressin
2=>
are absorbed &ia the trachea. .here are no data
regarding endotracheal administration of amiodarone. 9d3
ministration of resuscitation drugs into the trachea results in
lower blood concentrations than when the same dose is gi&en
intra&ascularly. Furthermore, the results of recent animal
studies
2=:,2=2
suggest that the lower e*ine*hrine concentra3
tions achie&ed when the drug is deli&ered endotracheally may
*roduce transient 3adrenergic effects, resulting in &asodila3
tion. .hese effects can be detrimental, causing hy*otension,
lower (( and flow, and reduced *otential for R!$. .hus,
although endotracheal administration of some resuscitation
drugs is *ossible, 5I or 5! drug administration is *referred
because it will *ro&ide more *redictable drug deli&ery and
*harmacologic effect.
5n one nonrandomi/ed cohort study of out3of3hos*ital
cardiac arrest in adults
240
using a randomi/ed control, 5I
administration of atro*ine and e*ine*hrine was associated
with a higher rate of R!$ and sur&i&al to hos*ital
admission than administration by the endotracheal route. Fi&e
*ercent of those who recei&ed 5I drugs sur&i&ed to hos*ital
discharge, but no *atient sur&i&ed in the grou* recei&ing
drugs by the endotracheal route.
5f 5I or 5! access cannot be established, e*ine*hrine,
&aso*ressin, and lidocaine may be administered by the
endotracheal route during cardiac arrest Blass 55b, %!, +C.
.he o*timal endotracheal dose of most drugs is un#nown, but
ty*ically the dose gi&en by the endotracheal route is 2 to 2
1
T2
times the recommended 5I dose. 5n 2 animal (R studies the
eLui*otent e*ine*hrine dose gi&en endotracheally was a*3
*roEimately @ to 10 times higher than the 5I dose.
241,242
(ro&iders should dilute the recommended dose in = to 10 m%
of sterile water or normal saline and inject the drug directly
into the endotracheal tube.
2=4
$tudies with e*ine*hrine
24@
and
lidocaine
2=1
showed that dilution with sterile water instead of
0.2M saline may achie&e better drug absor*tion.
Advanced Air$ay
.here is inadeLuate e&idence to define the o*timal timing of
ad&anced airway *lacement in relation to other inter&entions
during resuscitation from cardiac arrest. .here are no *ro3
s*ecti&e studies that directly address the relationshi* between
timing or ty*e of ad&anced airway *lacement during (R
and outcomes. 5n an urban out3of3hos*ital setting,
intubation in
12 minutes has been associated with a better rate of
sur&i&al than intubation in 1@ minutes.
@2
5n a registry
study of
2= 004 in3hos*ital cardiac arrests, earlier time to ad&anced
airway B = minutesC was not associated with increased
R!$ but was associated with im*ro&ed 2>3hour sur&i&al.
@1
5n out3of3hos*ital urban and rural settings, *atients intubated
during resuscitation had better sur&i&al rates than *atients
who were not intubated.
@@
5n an in3hos*ital setting *atients
reLuiring intubation during (R had worse sur&i&al rates.
@>
9
recent study
:
found that delayed endotracheal intubation
combined with *assi&e oEygen deli&ery and minimally inter3
ru*ted chest com*ressions was associated with im*ro&ed
neurologically intact sur&i&al after out3of3hos*ital cardiac
arrest in *atients with witnessed IF7I..
9d&antages of ad&anced airway *lacement include elimi3
nation of the need for *auses in chest com*ressions for
&entilation, *otentially im*ro&ed &entilation and oEygena3
tion, reduction in the ris# of as*iration, and ability to use
Luantitati&e wa&eform ca*nogra*hy to monitor Luality of
(R, o*timi/e chest com*ressions, and detect R!$ during
chest com*ressions or when a rhythm chec# re&eals an
organi/ed rhythm. .he *rimary disad&antages are interru*3
tions in chest com*ression during *lacement and the ris# of
unrecogni/ed eso*hageal intubation.
When an ad&anced airway Beg, endotracheal tube or su*ra3
glottic airwayC is *laced, 2 *ro&iders no longer deli&er cycles
of com*ressions interru*ted with *auses for &entilation.
5nstead, the *ro&ider *erforming com*ressions should deli&er
at least 100 com*ressions *er minute continuously without
*auses for &entilation. .he *ro&ider deli&ering &entilations
should gi&e 1 breath e&ery 4 to : seconds B: to 10 breaths *er
minuteC and should be careful to a&oid deli&ering an eEces3
si&e number of &entilations.
?5en S5ould Resuscitative fforts Stop@
.he final decision to sto* can ne&er rest on a single
*arameter, such as duration of resuscitati&e efforts. Rather,
clinical judgment and res*ect for human dignity must enter
into decision ma#ing. 5n the out3of3hos*ital setting, cessation
of resuscitati&e efforts in adults should follow system3
s*ecific criteria under direct medical control. .here are
limited clinical data to guide this decision in neonatal and
*ediatric out3of3hos*ital or in3hos*ital cardiac arrest. 9 more
detailed discussion is *ro&ided in (art @6 H,thics.J
'edications for Arrest R5yt5ms
.he *rimary goal of *harmacologic thera*y during cardiac
arrest is to facilitate restoration and maintenance of a *erfus3
ing s*ontaneous rhythm. .oward this goal, 9%$ drug
thera*y during (R is often associated with increased rates
of R!$ and hos*ital admission but not increased rates
of long3term sur&i&al with good neurologic outcome. !ne
study
1@:
randomi/ed *atients to 5I or no 5I medications
during management of adult out3of3hos*ital cardiac arrest.
.he study demonstrated higher rates of R!$ in the 5I
grou* B>0M 5I &ersus 2=M no 5I Podds ratio B!RC 1.220 2=M
confidence inter&al B5C 1.>: to 2.41QC, but there was no
statistical difference in sur&i&al to hos*ital discharge B10.=M
5I &ersus 2.2M no 5I P!R 1.140 2=M 5 0.1> to 1.:2QC or
sur&i&al with fa&orable neurologic outcome B2.:M 5I &ersus
:.1M no 5I P!R 1.2>0 2=M 5 0.11 to 1.2:QC. .his study was
not adeLuately *owered to detect clinically im*ortant differ3
ences in long3term outcomes. ,&idence from one nonrandom3
i/ed trial
1@1
found that the addition of 9%$ inter&entions
including 5I drugs in a *re&iously o*timi/ed +%$ system
with ra*id defibrillation resulted in an increased rate of
R!$ B1:.0M with 9%$ &ersus 12.2M before 9%$,
P 0.001C and hos*ital admission B1>.4M with 9%$ &ersus
10.2M before 9%$, P 0.001C but no statistical difference
in sur&i&al to hos*ital discharge B=.1M with 9%$ &ersus
=.0M before 9%$C. Whether o*timi/ed high3Luality (R
and ad&ances in *ostG cardiac arrest care will enable the
increased
rates of R!$ with 9%$ medications to be translated into
increased long3term sur&i&al remains to be determined.
%asopressors
.o date no *lacebo3controlled trials ha&e shown that admin3
istration of any &aso*ressor agent at any stage during man3
agement of IF, *ulseless I., (,9, or asystole increases the
rate of neurologically intact sur&i&al to hos*ital discharge.
.here is e&idence, howe&er, that the use of &aso*ressor
agents is associated with an increased rate of R!$.
#pineprin
e
,*ine*hrine hydrochloride *roduces beneficial effects in
*atients during cardiac arrest, *rimarily because of its
3adrenergic rece*tor3stimulating Bie, &asoconstrictorC *ro*3
erties.
24>
.he 3adrenergic effects of e*ine*hrine can increase
(( and cerebral *erfusion *ressure during (R.
24=
.he
&alue and safety of the 3adrenergic effects of e*ine*hrine
are contro&ersial because they may increase myocardial
wor# and reduce subendocardial *erfusion.
244
.here are no R.s that adeLuately com*are e*ine*hrine
with *lacebo in treatment of and outcomes related to out3of3
hos*ital cardiac arrest. 9 retros*ecti&e study
241
com*ared
e*ine*hrine to no e*ine*hrine for sustained IF and (,97
asystole and found im*ro&ed R!$ with e*ine*hrine but no
difference in sur&i&al between the treatment grou*s. 9
meta3analysis and other studies ha&e found im*ro&ed R!$,
but none ha&e demonstrated a sur&i&al benefit of high3dose
e*ine*hrine &ersus standard3dose e*ine*hrine in cardiac
arrest.
1@=,24: G212
5t is reasonable to consider administering a 1 mg dose of
5I75! e*ine*hrine e&ery @ to = minutes during adult cardiac
arrest Blass 55b, %!, 9C. -igher doses may be indicated to
treat s*ecific *roblems, such as a 3bloc#er or calcium
channel bloc#er o&erdose. -igher doses can also be consid3
ered if guided by hemodynamic monitoring such as arterial
relaEation HdiastolicJ *ressure or ((. 5f 5I75! access is
delayed or cannot be established, e*ine*hrine may be gi&en
endotracheally at a dose of 2 to 2.= mg.
&asopressin
Iaso*ressin is a nonadrenergic *eri*heral &asoconstrictor
that also causes coronary and renal &asoconstriction.
21@
.hree R.s and a meta3analysis of the trials
21> G211
dem3
onstrated no difference in outcomes BR!$, sur&i&al to
discharge, or neurologic outcomeC with &aso*ressin B>0
units 5IC &ersus e*ine*hrine B1 mgC as a first3line &aso3
*ressor in cardiac arrest. .wo R.s
21:,212
demonstrated no
difference in outcomes BR!$, sur&i&al to discharge, or
neurologicC when com*aring e*ine*hrine in combination
with &aso*ressin &ersus e*ine*hrine alone in cardiac
arrest. !ne R. found that re*eated doses of &aso*ressin
during cardiac arrest did not im*ro&e sur&i&al rates com3
*ared with re*eated doses of e*ine*hrine.
2:0
+ecause the effects of &aso*ressin ha&e not been shown to
differ from those of e*ine*hrine in cardiac arrest, 1 dose of
&aso*ressin >0 units 5I75! may re*lace either the first or
second dose of e*ine*hrine in the treatment of cardiac arrest
Blass 55b, %!, 9C.
Oter &asopressors
.here are no alternati&e &aso*ressors Bnore*ine*hrine,
*henyle*hrineC with *ro&en sur&i&al benefit com*ared
with e*ine*hrine.
24:,2:1,2:2
Antiarr5yt5mics
.here is no e&idence that any antiarrhythmic drug gi&en
routinely during human cardiac arrest increases sur&i&al to
hos*ital discharge. 9miodarone, howe&er, has been shown to
increase short3term sur&i&al to hos*ital admission when
com*ared with *lacebo or lidocaine.
Amiodarone
5I amiodarone affects sodium, *otassium, and calcium chan3
nels and has 3 and 3adrenergic bloc#ing *ro*erties. 5t can
be considered for treatment of IF or *ulseless I. unres*on3
si&e to shoc# deli&ery, (R, and a &aso*ressor. 5n blinded
randomi/ed controlled clinical trials in adults with refractory
IF7*ulseless I. in the out3of3hos*ital setting,
1@>,1@4
*ara3
medic administration of amiodarone B@00 mg
1@>
or = mg7#g
1@4
C
im*ro&ed hos*ital admission rates when com*ared with
administration of *lacebo
1@>
or 1.= mg7#g of lidocaine.
1@4
9dditional studies
2:@G2:1
documented consistent im*ro&ement
in termination of arrhythmias when amiodarone was gi&en to
humans or animals with IF or hemodynamically unstable
I.. 9 higher incidence of bradycardia and hy*otension was
re*orted for amiodarone in one out3of3hos*ital study.
1@>
9
canine study
2::
noted that administration of a &asoconstrictor
before amiodarone *re&ented hy*otension. .he ad&erse he3
modynamic effects of the 5I formulation of amiodarone are
attributed to &asoacti&e sol&ents B*olysorbate :0 and ben/yl
alcoholC. When administered in the absence of these sol&ents,
an analysis of the combined data of > *ros*ecti&e clinical
trials of *atients with I. Bsome hemodynamically unstableC
showed that amiodarone *roduced no more hy*otension than
lidocaine.
2:4
9 formulation of 5I amiodarone without these
&asoacti&e sol&ents was a**ro&ed for use in the 8nited
$tates. 9miodarone may be considered for IF or *ulseless
I. unres*onsi&e to (R, defibrillation, and a &aso*ressor
ther3 a*y Blass 55b, %!, +C. 9n initial dose of @00 mg
5I75! can be followed by 1 dose of 1=0 mg 5I75!.
9lthough anecdot3 ally administered 5! without #nown
ad&erse effects, there is
limited eE*erience with amiodarone gi&en by this route.
0idocaine
9 retros*ecti&e re&iew
2:2
demonstrated an association
between im*ro&ed hos*ital admission rates and use of
lidocaine Bcom*ared with standard treatmentC in *atients
with out3of3hos*ital IF cardiac arrest. +ut there is inade3
Luate e&idence to recommend the use of lidocaine in
*atients who ha&e refractory I.7IF, defined as I.7IF not
terminated by defibrillation or that continues to recur after
defibrillation during out3of3hos*ital cardiac arrest or in3
hos*ital cardiac arrest.
%idocaine is an alternati&e antiarrhythmic of long3standing
and wides*read familiarity with fewer immediate side effects
than may be encountered with other antiarrhythmics. %ido3
caine, howe&er, has no *ro&en short3 or long3term efficacy in
cardiac arrest. %idocaine may be considered if amiodarone is
not a&ailable Blass 55b, %!, +C. .he initial dose is 1 to 1.=
mg7#g 5I. 5f IF7*ulseless I. *ersists, additional doses of 0.=
to 0.1= mg7#g 5I *ush may be administered at =3 to
103minute inter&als to a maEimum dose of @ mg7#g.
,agnesium Sul'ate
.wo obser&ational studies
220,221
showed that 5I magnesium
sulfate can facilitate termination of torsades de *ointes
Birregular7*olymor*hic I. associated with *rolonged S.
inter&alC. "agnesium sulfate is not li#ely to be effecti&e in
terminating irregular7*olymor*hic I. in *atients with a
normal S. inter&al.
221
9 number of doses of magnesium sulfate ha&e been used
clinically, and an o*timal dosing regimen has not been
established. When IF7*ulseless I. cardiac arrest is associ3
ated with torsades de *ointes, *ro&iders may administer an
5I75! bolus of magnesium sulfate at a dose of 1 to 2 g
diluted in 10 m% D
=
W Blass 55b, %!, C. $ee (art :.@6
H"anage3 ment of $ym*tomatic +radycardia and
.achycardiaJ for additional information about management
of torsades de *ointes not associated with cardiac arrest.
.hree R.s
222G22>
did not identify a significant benefit
from use of magnesium com*ared with *lacebo among
*atients with IF arrest in the *rehos*ital, intensi&e care unit,
and emergency de*artment setting, res*ecti&ely. .hus, rou3
tine administration of magnesium sulfate in cardiac arrest is
not recommended Blass 555, %!, 9C unless torsades de
*ointes is *resent.
7nterventions :ot Recommended for Routine 8se
)urin! Cardiac Arrest
Atropine
9tro*ine sulfate re&erses cholinergic3mediated decreases in
heart rate and atrio&entricular nodal conduction. No *ros*ec3
ti&e controlled clinical trials ha&e eEamined the use of
atro*ine in asystole or bradycardic (,9 cardiac arrest.
%ower3le&el clinical studies *ro&ide conflicting e&idence of
the benefit of routine use of atro*ine in cardiac arrest.
@>,22=G@0>
.here is no e&idence that atro*ine has detrimental effects
during bradycardic or asystolic cardiac arrest. 9&ailable
e&idence suggests that routine use of atro*ine during (,9 or
asystole is unli#ely to ha&e a thera*eutic benefit Blass 55b,
%!, +C. For this reason atro*ine has been remo&ed from the
cardiac arrest algorithm.
Sodium .icar%onate
.issue acidosis and resulting acidemia during cardiac arrest
and resuscitation are dynamic *rocesses resulting from no
blood flow during arrest and low blood flow during (R.
.hese *rocesses are affected by the duration of cardiac arrest,
le&el of blood flow, and arterial oEygen content during (R.
Restoration of oEygen content with a**ro*riate &entilation
with oEygen, su**ort of some tissue *erfusion and some
cardiac out*ut with high3Luality chest com*ressions, then
ra*id R!$ are the mainstays of restoring acid3base balance
during cardiac arrest.
.wo studies demonstrated
@0=,@04
increased R!$, hos3
*ital admission, and sur&i&al to hos*ital discharge associ3
ated with use of bicarbonate. -owe&er, the majority of
studies showed no benefit
@01G@02
or found a relationshi*
with *oor outcome.
@0>,@10 G@12
.here are few data to su**ort thera*y with buffers during
cardiac arrest. .here is no e&idence that bicarbonate im*ro&es
the li#elihood of defibrillation or sur&i&al rates in animals
with IF cardiac arrest. 9 wide &ariety of ad&erse effects ha&e
been lin#ed to administration of bicarbonate during cardiac
arrest. +icarbonate may com*romise (( by reducing sys3
temic &ascular resistance.
@1@
5t can create eEtracellular al#a3
losis that will shift the oEyhemoglobin saturation cur&e and
inhibit oEygen release. 5t can *roduce hy*ernatremia and
therefore hy*erosmolarity. 5t *roduces eEcess !
2
, which
freely diffuses into myocardial and cerebral cells and may
*aradoEically contribute to intracellular acidosis.
@1>
5t can
eEacerbate central &enous acidosis and may inacti&ate simul3
taneously administered catecholamines.
5n some s*ecial resuscitation situations, such as *reeEisting
metabolic acidosis, hy*er#alemia, or tricyclic antide*ressant
o&erdose, bicarbonate can be beneficial Bsee (art 126
Hardiac 9rrest in $*ecial $ituationsJC. -owe&er, routine use
of sodium bicarbonate is not recommended for *atients in
cardiac arrest Blass 555, %!, +C. When bicarbonate is used
for s*ecial situations, an initial dose of 1 m,L7#g is ty*ical.
Whene&er *ossible, bicarbonate thera*y should be guided by
the bicarbonate concentration or calculated base deficit ob3
tained from blood gas analysis or laboratory measurement. .o
minimi/e the ris# of iatrogenically induced al#alosis, *ro&id3
ers should not attem*t com*lete correction of the calculated
base deficit. !ther nonG!
2
3generating buffers such as car3
bicarb, .-9", or tribonate ha&e shown *otential for mini3
mi/ing some ad&erse effects of sodium bicarbonate, including
!
2
generation, hy*erosmolarity, hy*ernatremia, hy*oglyce3
mia, intracellular acidosis, myocardial acidosis, and Ho&er3
shootJ al#alosis.
@1=G@11
+ut clinical eE*erience is greatly
limited and outcome studies are lac#ing.
Calcium
$tudies of calcium during cardiac arrest ha&e found &ariable
results on R!$, and no trial has found a beneficial effect on
sur&i&al either in or out of hos*ital.
@01,@0>,@1: G@2@
Routine
administration of calcium for treatment of in3hos*ital and
out3of3hos*ital cardiac arrest is not recommended Blass 555,
%!, +C.
)i%rinolysis
Fibrinolytic thera*y was *ro*osed for use during cardiac
arrest to treat both coronary thrombosis Bacute coronary
syndromeC with *resumably com*lete occlusion of a *roEi3
mal coronary artery and major life3threatening *ulmonary
embolism. !ngoing (R is not an absolute contraindication
to fibrinolysis. 5nitial studies were *romising
@2> G@@0
and sug3
gested benefit from fibrinolytic thera*y in the treatment of
&ictims of cardio*ulmonary arrest unres*onsi&e to standard
thera*y. +ut 2 large clinical trials
1::,@@1
failed to show any
im*ro&ement in outcome with fibrinolytic thera*y during
(R. !ne of these showed an increased ris# of intracranial
bleeding associated with the routine use of fibrinolytics
during cardiac arrest.
1::
Fibrinolytic thera*y should not be routinely used in cardiac
arrest Blass 555, %!, +C. When *ulmonary embolism is
*resumed or #nown to be the cause of cardiac arrest,
em*irical fibrinolytic thera*y can be considered Blass 55a,
%!, +0 see (art 12C.
$& )luids
No *ublished human study directly com*ares the outcome of
routine 5I fluid administration to no fluid administration
during (R. "ost human and animal studies of fluid infusion
during (R did not ha&e a control grou*,
@@2G@>@
and 2 animal
studies showed that normothermic fluid infusion during (R
caused a decrease in ((.
@>> G@>4
5n addition to normothermic
fluid, hy*ertonic and chilled fluids ha&e been studied in
animal and small human studies without a sur&i&al bene3
fit.
@@2,@@>,@@4 G@@:,@>1G@>@
5f cardiac arrest is associated with
eEtreme &olume losses, hy*o&olemic arrest should be sus3
*ected. .hese *atients *resent with signs of circulatory shoc#
ad&ancing to (,9. 5n these settings intra&ascular &olume
should be *rom*tly restored.
Pacin!
,lectric *acing is generally not effecti&e in cardiac arrest, and
no studies ha&e obser&ed a sur&i&al benefit from *acing in
cardiac arrest.
@>1G@=0
,Eisting e&idence suggests that *acing
by transcutaneous, trans&enous, or transmyocardial means in
cardiac arrest does not im*ro&e the li#elihood of R!$ or
sur&i&al outcome regardless of the timing of *acing admin3
istration Bearly or delayed in established asystoleC, location of
arrest Bin3hos*ital or out3of3hos*italC, or *rimary cardiac
rhythm Basystole, (,9C targeted for treatment. ,lectric *ac3
ing is not recommended for routine use in cardiac arrest
Blass 555, %!, +C.
Precordial 95ump
.he *otential utility of *recordial thum* in cardiac arrest has
not been well studied. When hemodynamically unstable
&entricular tachyarrhythmias were induced during electro3
*hysiological testing, initial administration of a *recordial
thum* a**eared to be safe but rarely effecti&e in terminating
&entricular arrhythmias.
@=1
5n a *ros*ecti&e obser&ational
study of *atients with out3of3hos*ital cardiac arrest, *rec3
ordial thum* was associated with R!$ when administered
*rom*tly to *atients with res*onder3witnessed asystolic ar3
rest. When administered for IF7I. or (,9 arrest it was
ineffecti&e but resulted in no a**arent harm.
@=2
5n @ case
series
@=@G@==
IF or *ulseless I. was con&erted to a *erfusing
rhythm by a *recordial thum*. on&ersely, other case series
documented deterioration in cardiac rhythm, such as rate
acceleration of I., con&ersion of I. to IF, or de&elo*ment
of com*lete 9I bloc# or asystole following the
thum*.
@=>,@=4 G@41
.he *recordial thum* may be considered for termination
of witnessed monitored unstable &entricular tachyarrhyth3
mias when a defibrillator is not immediately ready for use
Blass 55b, %!, +C, but should not delay (R and shoc#
deli&ery. .here is insufficient e&idence to recommend for
or against the use of the *recordial thum* for witnessed
onset of asystole, and there is insufficient e&idence to
recommend *ercussion *acing during ty*ical attem*ted
resuscitation from cardiac arrest.
Summary
5nter&ention to *re&ent cardiac arrest in critically ill
*atients is ideal. When cardiac arrest occurs, high3Luality
(R is fundamental to the success of any subseLuent
9%$ inter&ention. During resuscitation healthcare *ro3
&iders must *erform chest com*ressions of adeLuate rate
and de*th, allow com*lete recoil of the chest after each
com*ression, minimi/e interru*tions in chest com*res3
sions, and a&oid eEcessi&e &entilation, es*ecially with an
ad&anced airway. Suality of (R should be continuously
monitored. (hysiologic monitoring may *ro&e useful to
o*timi/e resuscitati&e efforts. For *atients in IF7*ulseless
I., shoc#s should be deli&ered *rom*tly with minimal
interru*tions in chest com*ressions. .he increased rates of
R!$ associated with 9%$ drug thera*y ha&e yet to be
translated into long3term sur&i&al benefits. -owe&er, im3
*ro&ed Luality of (R, ad&ances in *ostG cardiac arrest
care, and im*ro&ed o&erall im*lementation through com3
*rehensi&e systems of care may *ro&ide a *athway to
o*timi/e the outcomes of cardiac arrest *atients treated
with 9%$ inter&entions.
Part 8"-: 'ana!ement of Symptomatic
=radycardia and 9ac5ycardia
&vervie$
.his section highlights recommendations for management
of *atients with acute sym*tomatic arrhythmias. ,lectro3
cardiogra*hic B,;C and rhythm information should be
inter*reted within the conteEt of total *atient assessment.
,rrors in diagnosis and treatment are li#ely to occur if
ad&anced cardio&ascular life su**ort B9%$C *ro&iders
base treatment decisions solely on rhythm inter*retation
and neglect clinical e&aluation. (ro&iders must e&aluate
the *atientNs sym*toms and clinical signs, including &en3
tilation, oEygenation, heart rate, blood *ressure, le&el of
consciousness, and signs of inadeLuate organ *erfusion.
Unstable and symptomatic are terms ty*ically used to
describe the condition of *atients with arrhythmias. ;en3
erally, unstable refers to a condition in which &ital organ
function is acutely im*aired or cardiac arrest is ongoing or
imminent. When an arrhythmia causes a *atient to be
unstable, immediate inter&ention is indicated. ,ymptomatic
im*lies that an arrhythmia is causing sym*toms, such as
*al*itations, lightheadedness, or dys*nea, but the *atient is
stable and not in imminent danger. 5n such cases more time
is a&ailable to decide on the most a**ro*riate inter&ention.
5n both unstable and sym*tomatic cases the *ro&ider must
ma#e an assessment as to whether it is the arrhythmia that
is causing the *atient to be unstable or sym*tomatic. For
eEam*le, a *atient in se*tic shoc# with sinus tachycardia of
1>0 beats *er minute is unstable0 howe&er, the arrhythmia
is a *hysiologic com*ensation rather than the cause of
instability. .herefore, electric cardio&ersion will not im3
*ro&e this *atientNs condition. 9dditionally, if a *atient
with res*iratory failure and se&ere hy*oEemia becomes
hy*otensi&e and de&elo*s a bradycardia, the bradycardia is
not the *rimary cause of instability. .reating the bradycar3
dia without treating the hy*oEemia is unli#ely to im*ro&e
the *atientNs condition. 5t is critically im*ortant to deter3
mine the cause of the *atientNs instability in order to
*ro*erly direct treatment. 5n general, sinus tachycardia is a
res*onse to other factors and, thus, it rarely Bif e&erC is the
cause of instability in and of itself.
.he %-.- A/A 0ui#lines for CP) an# ECC em*hasi/e
the im*ortance of clinical e&aluation and highlight *rinci3
*les of thera*y with algorithms that ha&e been refined and
streamlined since *ublication of the %--1 A/A 0ui#elines
for CP) an# ECC.
@42
.he #ey *rinci*les of arrhythmia
recognition and management in adults are as follows6
5f bradycardia *roduces signs and sym*toms of instabil3
ity Beg, acutely altered mental status, ischemic chest
discomfort, acute heart failure, hy*otension, or other signs
of shoc# that *ersist des*ite adeLuate airway and breath3
ingC, the initial treatment is atro*ine Blass 55a, %!, +C. 5f
bradycardia is unres*onsi&e to atro*ine, intra&enous B5IC
infusion of 3adrenergic agonists with rate3accelerating
effects Bdo*amine, e*ine*hrineC or transcutaneous *acing
B.(C can be effecti&e Blass 55a, %!, +C while the *atient
is *re*ared for emergent trans&enous tem*orary *acing if
reLuired.
5f the tachycardic *atient is unstable with se&ere signs and
sym*toms related to a sus*ected arrhythmia Beg, acute altered
mental status, ischemic chest discomfort, acute heart failure,
hy*otension, or other signs of shoc#C, immediate cardio&er3
sion should be *erformed Bwith *rior sedation in the con3
scious *atientC Blass 5, %!, +C. 5n select cases of regular
narrow3com*leE tachycardia with unstable signs or sym*3
toms, a trial of adenosine before cardio&ersion is reasonable
to consider Blass 55b, %!, C.
5f the *atient with tachycardia is stable, determine if the
*atient has a narrow3com*leE or wide3com*leE tachycardia,
whether the rhythm is regular or irregular, and for wide
com*leEes whether the SR$ mor*hology is monomor*hic or
*olymor*hic. .hera*y is then tailored accordingly B.able 2C.
'now when to call for eE*ert consultation regarding
com*licated rhythm inter*retation, drugs, or management
decisions.
9 com*rehensi&e *resentation of the e&aluation and man3
agement of bradyarrhythmias and tachyarrhythmias is beyond
the sco*e of the %-.- A/A 0ui#elines for CP) an# ECC.
.he following selected rhythm scenarios are meant to aid
with the management of *eriarrest rhythm disorders. 5f
cardiac arrest de&elo*s at any time, see the 9%$ ardiac
9rrest 9lgo3 rithms in (art :.26 H"anagement of ardiac
9rrest.J
Table 2. IV Drugs Used for Tachcardia
-rug Characteristics .ndication(s) -osing Side /%%ects
&recautions or Special
Considerations
.ntravenous -rugs
0sed to Treat
Supraventricular
Tachyarrhythmias
Adenosine /ndogenous purine
nucleoside1 "rie%ly
depresses sinus
K Sta"le# narro2-complex regular tachycardias
K 0nsta"le narro2-complex regular tachycardias
2hile preparations are made %or electrical
3 mg .4 as a rapid .4 push
%ollo2ed "y a (5 mL saline %lush1
repeat i% re6uired as '( mg .4
Hypotension#
"ronchospasm#
chest discom%ort
Contraindicated in
patients 2ith asthma1
may precipitate atrial
node rate and A4 cardioversion push %i"rillation# 2hich may "e
node conduction1
vasodilator
K Sta"le# regular# monomorphic# 2ide complex
tachycardia as a therapeutic and diagnostic
very rapid in patients
2ith 7&71 thus a
maneuver de%i"rillator should "e
readily availa"le1 reduce
dose in post8cardiac
transplant patients# those
ta!ing dipyridamole or
car"ama9epine and
2hen administered via a
central vein
-iltia9em# :on-dihydropyridine K Sta"le# narro2-complex tachycardias i% rhythm -iltia9em) .nitial dose '; to (5 Hypotension# Should only "e given to
4erapamil calcium channel remains uncontrolled or unconverted "y mg (5.(; mg!g) .4 over ( "radycardia# patients 2ith
"loc!ers1 slo2 A4 adenosine or vagal maneuvers or i% S4T is minutes1 additional (5 to (; mg precipitation o% narro2-complex
node conduction and recurrent (5.<; mg!g) .4 in '; minutes i% heart %ailure tachycardias (regular or
increase A4 node
re%ractoriness1
K Control ventricular rate in patients 2ith atrial
%i"rillation or atrial %lutter
needed1 ; to '; mgh .4
maintenance in%usion (titrated to
irregular). Avoid in
patients 2ith heart
vasodilators# A$ heart rate i% given %or rate %ailure and pre-excited
negative inotropes control) A$ or %lutter or rhythms
4erapamil) .nitial dose (.; to ; consistent 2ith 4T
mg .4 given over ( minutes1 may
repeat as ; to '5 mg every '; to
<5 minutes to total dose o% (5 to
<5 mg
Atenolol# -=loc!ers1 reduce K Sta"le# narro2-complex tachycardias i% rhythm Atenolol ( ' speci%ic "loc!er) ; Hypotension# Avoid in patients 2ith
/smolol# e%%ects o% circulating remains uncontrolled or unconverted "y mg .4 over ; minutes1 repeat ; "radycardia# asthma# o"structive
>etoprolol# catecholamines1 adenosine or vagal maneuvers or i% S4T is mg in '5 minutes i% arrhythmia precipitation o% air2ay disease#
&ropranolol reduce heart rate# recurrent persists or recurs heart %ailure decompensated heart
A4 node conduction
and "lood pressure1
K Control ventricular rate in patients 2ith atrial
%i"rillation or atrial %lutter
/smolol ( ' speci%ic "loc!er 2ith
(- to ?-minute hal%-li%e) .4
%ailure and pre-excited
artrial %i"rillation or
negative inotropes K Certain %orms o% polymorphic 4T (associated
2ith acute ischemia# %amilial L@TS#
loading dose ;55 mcg!g (5.;
mg!g) over ' minute# %ollo2ed
%lutter
catecholaminergic) "y an in%usion o% ;5 mcg!g per
minute (5.5; mg!g per minute)1
i% response is inade6uate# in%use
second loading "olus o% 5.;
mg!g over ' minute and
increase maintenance in%usion to
'55 mcg!g (5.' mg!g) per
minute1 increment1 increase in
this manner i% re6uired to
maximum in%usion rate o% <55
mcg!g 5.< mg!g per minute
>etoprolol ( ' speci%ic "loc!er) ;
mg over ' to ( minutes repeated
as re6uired every ; minutes to
maximum dose o% '; mg
&ropranolol (nonselective
-"loc!er) 5.; to ' mg over '
minute# repeated up to a total
dose o% 5.' mg!g i% re6uired
&rocainamide Sodium and
potassium channel
K &re-excited atrial %i"rillation (5 to ;5 mgmin until
arrhythmia suppressed#
hypotension ensues#
=radycardia#
hypotension#
Avoid in patients 2ith @T
prolongation and CH$
"loc!er or @+S prolonged "y ;5A# or torsades de
total cumulative dose o% 'B pointes
mg!g1 or '55 mg every ;
minutes until arrhythmia is
controlled or other conditions
descri"ed a"ove are met
(Continued)
Table 2. Continued
-rug Characteristics .ndication(s) -osing Side /%%ects
&recautions or Special
Considerations
Amiodarone >ultichannel "loc!er
(sodium# potassium#
K Sta"le irregular narro2 complex tachycardia
(atrial %i"rillation)
';5 mg given over '5 minutes
and repeated i% necessary#
=radycardia#
hypotension#
calcium channel#
and noncompetitive
-"loc!er)
K Sta"le regular narro2-complex tachycardia
K To control rapid ventricular rate due to
accessory path2ay conduction in pre-excited
%ollo2ed "y a ' mgmin in%usion
%or 3 hours# %ollo2ed "y 5.;
mgmin. Total dose over (C
phle"itis
atrial arrhythmias hours should not exceed (.( g.
-igoxin Cardiac glycoside
2ith positive
K Sta"le# narro2-complex regular tachycardias i%
rhythm remains uncontrolled or unconverted
D to '( mcg!g total loading
dose# hal% o% 2hich is
=radycardia Slo2 onset o% action and
relative lo2 potency
inotropic e%%ects1 "y adenosine or vagal maneuvers or i% S4T is administered initially over ; renders it less use%ul %or
slo2s A4 node recurrent minutes# and remaining portion treatment o% acute
conduction "y
enhancing
K Control ventricular rate in patients 2ith atrial
%i"rillation or atrial %lutter
as (;A %ractions at C- to D- hour
intervals
arrhythmias
.ntravenous -rugs
0sed to Treat
4entricular
Tachyarrhythmias
parasympathetic
tone1 slo2 onset o%
action
&rocainamide Sodium and
potassium channel
"loc!er
K Hemodynamically sta"le monomorphic 4T (5 to ;5 mgmin until
arrhythmia suppressed#
hypotension ensues# or @+S
prolonged "y ;5A# or
total cumulative dose o% 'B
mg!g1 or '55 mg every ;
minutes until arrhythmia is
controlled or other conditions
descri"ed a"ove are met
=radycardia#
hypotension#
torsades de
pointes
Avoid in patients 2ith @T
prolongation and CH$
Amiodarone >ultichannel "loc!er
(sodium# potassium#
calcium channel#
- and noncompetitive
-"loc!er)
K Hemodynamically sta"le monomorphic 4T
K &olymorphic 4T 2ith normal @T interval
';5 mg given over '5 minutes
and repeated i% necessary#
%ollo2ed "y a ' mgmin in%usion
%or 3 hours# %ollo2ed "y 5.;
mgmin. Total dose over (C
hours should not exceed (.( g.
=radycardia#
hypotension#
phle"itis
Sotalol &otassium channel
"loc!er and
nonselective
-"loc!er
Lidocaine +elatively 2ea!
sodium channel
"loc!er
K Hemodynamically sta"le monomorphic 4T .n clinical studies '.; mg!g
in%used over ; minutes1 ho2ever#
0S pac!age la"eling recommends
any dose o% the drug should "e
in%used slo2ly over a period o% ;
hours
K Hemodynamically sta"le monomorphic 4T .nitial dose range %rom ' to '.;
mg!g .41 repeated i% re6uired at
5.; to 5.B; mg!g .4 every ; to
'5 minutes up to maximum
cumulative dose o% < mg!g1 '
to
C mgmin (<5 to ;5 mcg!g per
minute) maintenance in%usion
=radycardia#
hypotension#
torsades de
pointes
Slurred speech#
altered
consciousness#
sei9ures#
"radycardia
Avoid in patients 2ith @T
prolongation and CH$
>agnesium Co%actor in variety o%
cell processes
including control o%
sodium and
potassium transport
K &olymorphic 4T associated 2ith @T
prolongation (torsades de pointes)
' to ( g .4 over '; minutes Hypotension#
C:S toxicity#
respiratory
depression
$ollo2 magnesium levels
i% %re6uent or prolonged
dosing re6uired#
particularly in patients
2ith impaired renal
%unction
=radycardia
.his section summari/es the management of bradyarrhyth3
mias. Following the o&er&iew of bradyarrhythmias and sum3
mary of the initial e&aluation and treatment of bradycardia,
drugs used in the treatment of bradycardia are *resented. $ee
the +radycardia 9lgorithm, Figure @. +oE numbers in the teEt
refer to the numbered boEes in the algorithm.
#valuation
+radycardia is defined as a heart rate of 40 beats *er
minute. -owe&er, when bradycardia is the cause of sym*3
toms, the rate is generally =0 beats *er minute, which is
the
wor#ing definition of bradycardia used here BFigure @, =o(
1C. 9 slow heart rate may be *hysiologically normal for some
*atients, whereas a heart rate of =0 beats *er minute may be
inadeLuate for others. .he +radycardia 9lgorithm focuses on
management of clinically significant bradycardia Bie, brady3
cardia that is ina**ro*riate for the clinical conditionC.
+ecause hy*oEemia is a common cause of bradycardia,
initial e&aluation of any *atient with bradycardia should focus
on signs of increased wor# of breathing Btachy*nea, intercos3
tal retractions, su*rasternal retractions, *aradoEical abdomi3
nal breathingC and oEyhemoglobin saturation as determined
by *ulse oEimetry BFigure @, =o( 2C. 5f oEygenation is
Figure !. =radycardia Algorithm.
inadeLuate or the *atient shows signs of increased wor# of
breathing, *ro&ide su**lementary oEygen. 9ttach a monitor
to the *atient, e&aluate blood *ressure, and establish 5I
access. 5f *ossible, obtain a 123lead ,; to better define the
rhythm. While initiating treatment, e&aluate the *atientNs
clinical status and identify *otentially re&ersible causes.
.he *ro&ider must identify signs and sym*toms of *oor
*erfusion and determine if those signs are li#ely to be caused
by the bradycardia BFigure @, =o( -C. 5f the signs and
sym*toms are not due to bradycardia, the *ro&ider should
reassess the underlying cause of the *atientNs sym*toms.
Remember that signs and sym*toms of bradycardia may be
mild0 asym*tomatic or minimally sym*tomatic *atients do
not necessarily reLuire treatment BFigure @, =o( AC unless
there is sus*icion that the rhythm is li#ely to *rogress to
sym*toms or become life3threatening Beg, "obit/ ty*e 55
second3degree 9I bloc# in the setting of acute myocardial
infarction P9"5QC. 5f the bradycardia is sus*ected to be the
cause of acute altered mental status, ischemic chest discom3
fort, acute heart failure, hy*otension, or other signs of shoc#,
the *atient should recei&e immediate treatment.
9trio&entricular B9IC bloc#s are classified as first3, second3,
and third3degree. +loc#s may be caused by medications or
electrolyte disturbances, as well as structural *roblems resulting
from 9"5 or other myocardial diseases. 9 first3degree 9I
bloc# is defined by a *rolonged (R inter&al B 0.20 secondC
and is generally benign. $econd3degree 9I bloc# is di&ided
into "obit/ ty*es 5 and 55. 5n "obit/ ty*e 5 bloc#, the bloc# is
at the 9I node0 the bloc# is often transient and
asym*tomatic. 5n
"obit/ ty*e 55 bloc#, the bloc# is usually below the 9I node
within the -is3(ur#inje system0 this bloc# is often
sym*tomatic, with the *otential to *rogress to com*lete Bthird3
degreeC 9I bloc#. .hird3degree 9I bloc# may occur at the
9I node, bundle of -is, or bundle branches. When third3
degree 9I bloc# is *resent, no im*ulses *ass between the atria
and &entricles. .hird3degree 9I bloc# can be *ermanent or
transient, de*end3 ing on the underlying cause.
(erapy 1)igure 23 .ox
45
Atropine
9tro*ine remains the first3line drug for acute sym*tomatic
bradycardia Blass 55a, %!, +C. linical trials in adults
@4@G@41
showed that 5I atro*ine im*ro&ed heart rate, sym*toms, and
signs associated with bradycardia. 9tro*ine sulfate re&erses
cholinergic3mediated decreases in heart rate and should be
considered a tem*ori/ing measure while awaiting a transcu3
taneous or trans&enous *acema#er for *atients with sym*3
tomatic sinus bradycardia, conduction bloc# at the le&el of
the 9I node, or sinus arrest.
@41
.he recommended atro*ine dose for bradycardia is 0.= mg
5I e&ery @ to = minutes to a maEimum total dose of @ mg.
Doses of atro*ine sulfate of 0.= mg may *aradoEically
result in further slowing of the heart rate.
@4:
9tro*ine admin3
istration should not delay im*lementation of eEternal *acing
for *atients with *oor *erfusion.
8se atro*ine cautiously in the *resence of acute coronary
ischemia or "50 increased heart rate may worsen ischemia or
increase infarction si/e. 9tro*ine will li#ely be ineffecti&e in
*atients who ha&e undergone cardiac trans*lantation because
the trans*lanted heart lac#s &agal inner&ation. !ne small
uncontrolled study documented *aradoEical slowing of the
heart rate and high3degree 9I bloc# when atro*ine was
administered to *atients after cardiac trans*lantation.
@42
9&oid relying on atro*ine in ty*e 55 second3degree or third3
degree 9I bloc# or in *atients with third3degree 9I bloc# with
a new wide3SR$ com*leE where the location of bloc# is li#ely
to be in non3nodal tissue Bsuch as in the bundle of -is or more
distal conduction systemC. .hese bradyarrhythmias are not
li#ely to be res*onsi&e to re&ersal of cholinergic effects by
atro*ine and are *referably treated with .( or
3adrenergic su**ort as tem*ori/ing measures while the *atient
is *re*ared for trans3 &enous *acing BFigure @, =o( 2C.
Pacing
.( may be useful for the treatment of sym*tomatic bradycar3
dias. .here are limited studies com*aring .( with drug
thera*y for the treatment of sym*tomatic bradycardia. 9
randomi/ed controlled trial in which atro*ine and
glyco*yrrolate were com*ared with .( showed few
differences in outcome and sur&i&al, although the .( grou*
obtained a more consistent heart rate.
@4@
5n a study e&aluating
the feasibility of treatment with do*amine as com*ared with
.(, no differences were obser&ed between treatment grou*s
in sur&i&al to hos*ital discharge.
@10
.( is, at best, a
tem*ori/ing measure. .( is *ainful in conscious *atients, and,
whether effecti&e or not Bachie&ing inconsistent ca*tureC, the
*atient should be *re*ared for trans&enous *acing and eE*ert
consultation should be ob3 tained. 5t is reasonable for healthcare
*ro&iders to initiate .( in unstable *atients who do not
res*ond to atro*ine Blass 55a, %!, +C. 5mmediate *acing
might be considered in unstable *atients with high3degree 9I
bloc# when 5I access is not a&ailable Blass 55b, %!, C. 5f
the *atient does not res*ond to drugs or .(, trans&enous
*acing is *robably indicated Blass 55a, %!, C BFigure @, =o(
2C.
Alternati!e rugs to Consi#er
9lthough not first3line agents for treatment of sym*tomatic
bradycardia, do*amine, e*ine*hrine, and iso*roterenol are
alternati&es when a bradyarrhythmia is unres*onsi&e to or
ina**ro*riate for treatment with atro*ine, or as a tem*ori/ing
measure while awaiting the a&ailability of a *acema#er.
9lternati&e drugs may also be a**ro*riate in s*ecial circum3
stances such as the o&erdose of a 3bloc#er or calcium
channel bloc#er.
opamine. Do*amine hydrochloride is a catecholamine with
both 3 and 3adrenergic actions. 5t can be titrated to more
selecti&ely target heart rate or &asoconstriction. 9t lower
doses do*amine has a more selecti&e effect on inotro*y and
heart rate0 at higher doses B 10 mcg7#g *er minuteC, it also
has &asoconstricti&e effects. Do*amine infusion may be used
for *atients with sym*tomatic bradycardia, *articularly if
associated with hy*otension, in whom atro*ine may be
ina**ro*riate or after atro*ine fails Blass 55b, %!, +C. +egin
do*amine infusion at 2 to 10 mcg7#g *er minute and titrate to
*atient res*onse.
@10
8se of &asoconstrictors reLuires that the
reci*ient be assessed for adeLuate intra&ascular &olume and
&olume status su**orted as needed.
Epinephrine. ,*ine*hrine is a catecholamine with 3 and
3adrenergic actions. ,*ine*hrine infusion may be used for
*atients with sym*tomatic bradycardia, *articularly if
associated with hy*otension, for whom atro*ine may be
ina**ro*riate or after atro*ine fails Blass 55b, %!, +C. +egin
the infusion at 2 to
10 mcg7min and titrate to *atient res*onse. 8se of
&asoconstric3 tors reLuires that the reci*ient be assessed for
adeLuate intra&as3 cular &olume and &olume status su**orted
as needed.
&soproterenol. 5so*roterenol is a 3adrenergic agent with 31
and 32 effects, resulting in an increase in heart rate and
&asodilation. .he recommended adult dose is 2 to 10 mcg7
min by 5I infusion, titrated according to heart rate and
rhythm res*onse.
9ac5ycardia
.his section summari/es the management of a wide &ariety
of
tachyarrhythmias. Following the o&er&iew of tachyarrhythmias
and summary of the initial e&aluation and treatment of
tachycardia, common antiarrhythmic drugs used in the
treatment of tachycardia are *resented. $ee the .achycardia
9lgorithm, Figure >. +oE numbers in the teEt refer to the
numbered boEes in the algorithm.
Classi'ication o' (acyarrytmias
.achycardias can be classified in se&eral ways, based on the
a**earance of the SR$ com*leE, heart rate, and regularity.
9%$ *rofessionals should be able to recogni/e and differ3
entiate between sinus tachycardia, narrow3com*leE su*ra&en3
tricular tachycardia B$I.C, and wide3com*leE tachycardia.
+ecause 9%$ *ro&iders may be unable to distinguish
between su*ra&entricular and &entricular rhythms, they
should be aware that most wide3com*leE Bbroad3com*leEC
tachycardias are !entricular in origin.
K
NarrowGSR$3com*leE B$I.C tachycardias BSR$ 0.12
secondC, in order of freLuency
K
$inus tachycardia
K
9trial fibrillation
K
9trial flutter
K
9I nodal reentry
K
9ccessory *athwayGmediated tachycardia
K
9trial tachycardia Bincluding automatic and reentry
formsC
K
"ultifocal atrial tachycardia B"9.C
K
)unctional tachycardia Brare in adultsC
K
WideGSR$3com*leE tachycardias BSR$ 0.12 secondC
K
Ientricular tachycardia BI.C and &entricular fibrillation
BIFC
K
$I. with aberrancy
K
(re3eEcited tachycardias BWolff3(ar#inson3White
PW(WQ syndromeC
K
Ientricular *aced rhythms
5rregular narrow3com*leE tachycardias are li#ely atrial
fibrillation or "9.0 occasionally atrial flutter is irregular.
.he management of atrial fibrillation and flutter is discussed
in the section H5rregular .achycardiasJ below.
$nitial #valuation and (reatment o' (acyarrytmias
.achycardia is defined as an arrhythmia with a rate of 100
beats *er minute, although, as with defining bradycardia, the
Figure ". Tachycardia Algorithm.
rate of a tachycardia ta#es on clinical significance at its
greater eEtremes and is more li#ely attributable to an arrhyth3
mia rate of 1=0 beats *er minute BFigure >, =o( 1C. 9 ra*id
heart rate is an a**ro*riate res*onse to a *hysiologic stress
Beg, fe&er, dehydrationC or other underlying conditions. When
encountering *atients with tachycardia, efforts should be
made to determine whether the tachycardia is the *rimary
cause of the *resenting sym*toms or secondary to an under3
lying condition that is causing both the *resenting sym*toms
and the faster heart rate. "any eE*erts suggest that when a
heart rate is 1=0 beats *er minute, it is unli#ely that
sym*toms of instability are caused *rimarily by the
tachycardia unless there is im*aired &entricular function.
.he e&aluation and management of tachyarrhythmias is
de*icted in the 9%$ .achycardia With (ulse 9lgorithm
BFigure >C. +oE numbers in the teEt refer to numbered boEes
in this algorithm. 5f cardiac arrest de&elo*s at any time, see
the 9%$ ardiac 9rrest 9lgorithms in (art :.26 H"anage3
ment of ardiac 9rrest.J
+ecause hy*oEemia is a common cause of tachycardia,
initial e&aluation of any *atient with tachycardia should focus
on signs of increased wor# of breathing Btachy*nea, intercos3
tal retractions, su*rasternal retractions, *aradoEical abdomi3
nal breathingC and oEyhemoglobin saturation as determined
by *ulse oEimetry BFigure >, =o( 2C. 5f oEygenation is
inadeLuate or the *atient shows signs of increased wor# of
breathing, *ro&ide su**lementary oEygen. 9ttach a monitor
to the *atient, e&aluate blood *ressure, and establish 5I
access. 5f a&ailable, obtain a 123lead ,; to better define the
rhythm, but this should not delay immediate cardio&ersion if
the *atient is unstable. While initiating treatment, e&aluate
the *atientNs clinical status and identify *otential
re&ersible causes of the tachycardia.
5f signs and sym*toms *ersist des*ite *ro&ision of su**le3
mentary oEygen and su**ort of airway and &entilation, the
*ro&ider should assess the *atientNs degree of instability and
determine if the instability is related to the tachycardia
BFigure >, =o( -C. 5f the *atient demonstrates rate3related
cardio&ascular com*romise with signs and sym*toms such as
acute altered mental status, ischemic chest discomfort, acute
heart failure, hy*otension, or other signs of shoc# sus*ected
to be due to a tachyarrhythmia, *roceed to immediate syn3
chroni/ed cardio&ersion BFigure >, =o( AC. -owe&er, with
&entricular rates 1=0 beats *er minute in the absence of
&entricular dysfunction, it is more li#ely that the tachycardia
is secondary to the underlying condition rather than the cause
of the instability. 5f not hy*otensi&e, the *atient with a regular
narrow3com*leE $I. Bli#ely due to sus*ected reentry, *ar3
oEysmal su*ra&entricular tachycardia, as described belowC
may be treated with adenosine while *re*arations are made
for synchroni/ed cardio&ersion Blass 55b, %!, C.
5f the *atient with tachycardia is stable Bie, no serious signs
related to the tachycardiaC, the *ro&ider has time to obtain a
123lead ,;, e&aluate the rhythm, determine if the width of
the SR$ com*leE is 0.12 second BFigure >, =o( BC, and
determine treatment o*tions. $table *atients may await eE*ert
consultation because treatment has the *otential for harm.
Cardioversion
5f *ossible, establish 5I access before cardio&ersion and
administer sedation if the *atient is conscious. Do not delay
cardio&ersion if the *atient is eEtremely unstable. For further
information about defibrillation and cardio&ersion, see (art 46
H,lectrical .hera*ies.J
,ynchroni2e# Car#io!ersion an# Unsynchroni2e# ,hocks
3+igure 45 *o" 46
$ynchroni/ed cardio&ersion is shoc# deli&ery that is timed
Bsynchroni/edC with the SR$ com*leE. .his synchroni/ation
a&oids shoc# deli&ery during the relati&e refractory *eriod of
the cardiac cycle when a shoc# could *roduce IF.
@11
5f
cardio&ersion is needed and it is im*ossible to synchroni/e a
shoc#, use high3energy unsynchroni/ed shoc#s Bdefibrillation
dosesC.
$ynchroni/ed cardio&ersion is recommended to treat B1C
unstable $I., B2C unstable atrial fibrillation, B@C unstable
atrial flutter, and B>C unstable monomor*hic BregularC I..
$hoc# can terminate these tachyarrhythmias by interru*ting
the underlying reentrant *athway that is res*onsible for them.
'a!eform an# Energy
.he recommended initial bi*hasic energy dose for cardio&er3
sion of atrial fibrillation is 120 to 200 ) Blass 55a, %!,
9C.
@12G@14
5f the initial shoc# fails, *ro&iders should increase
the dose in a ste*wise fashion.
ardio&ersion of atrial flutter and other $I.s generally
reLuires less energy0 an initial energy of =0 ) to 100 ) is often
sufficient.
@14
5f the initial =03) shoc# fails, the *ro&ider
should increase the dose in a ste*wise fashion.
@11
ardio&ersion with mono*hasic wa&eforms should begin at
200 ) and increase in ste*wise fashion if not successful
Blass 55a, %!, +C.
@12G@1>
"onomor*hic I. Bregular form and rateC with a *ulse
res*onds well to mono*hasic or bi*hasic wa&eform cardio&er3
sion Bsynchroni/edC shoc#s at initial energies of 100 ). 5f there
is no res*onse to the first shoc#, it may be reasonable to
increase the dose in a ste*wise fashion. No studies were
identified that addressed this issue. .hus, this recommendation
re*resents eE*ert o*inion Blass 55b, %!, C.
9rrhythmias with a *olymor*hic SR$ a**earance Bsuch as
torsades de *ointesC will usually not *ermit synchroni/ation.
.hus, if a *atient has *olymor*hic I., treat the rhythm as IF
and deli&er high3energy unsynchroni2e# shoc#s Bie, defibril3
lation dosesC. 5f there is any doubt whether monomor*hic or
*olymor*hic I. is *resent in the unstable *atient, do not
delay shoc# deli&ery to *erform detailed rhythm analysis6
*ro&ide high3energy unsynchroni/ed shoc#s Bie, defibrillation
dosesC. 8se the 9%$ ardiac 9rrest 9lgorithm Bsee (art
:.26 H"anagement of ardiac 9rrestJC.
Regular "arro!-Complex (acycardia
,inus Tachycar#ia
$inus tachycardia is common and usually results from a
*hysi3
ologic stimulus, such as fe&er, anemia, or hy*otension7shoc#.
$inus tachycardia is defined as a heart rate 100 beats
*er minute. .he u**er rate of sinus tachycardia is age3related
Bcalculated as a**roEimately 220 beats *er minute, minus the
*atientNs age in yearsC and may be useful in judging whether
an a**arent sinus tachycardia falls within the eE*ected range
for a *atientNs age. 5f judged to be sinus tachycardia, no
s*ecific drug treatment is reLuired. 5nstead, thera*y is directed
toward identi3 fication and treatment of the underlying cause.
When cardiac function is *oor, cardiac out*ut can be
de*endent on a ra*id heart rate. 5n such com*ensatory
tachycardias, stro#e &olume is limited, so Hnormali/ingJ the
heart rate can be detrimental.
,upra!entricular Tachycar#ia 3)eentry ,(T6
E!aluation. "ost $I.s are regular tachycardias that are
caused by reentry, an abnormal rhythm circuit that allows a
wa&e of de*olari/ation to re*eatedly tra&el in a circle in
cardiac tissue. .he rhythm is considered to be of su*ra&en3
tricular origin if the SR$ com*leE is narrow B 120 millisec3
onds or 0.12 secondC or if the SR$ com*leE is wide
BbroadC and *reeEisting bundle branch bloc# or rate3
de*endent aber3 rancy is known to be *resent. Reentry
circuits resulting in $I. can occur in atrial myocardium
Bresulting in atrial fibrillation, atrial flutter, and some
forms of atrial tachycardiaC. .he reentry circuit may also
reside in whole or in *art in the 9I node itself. .his results in
9I nodal reentry tachycardia B9INR.C if both limbs of the
reentry circuit in&ol&e 9I nodal tissue. 9lternati&ely, it may
result in 9I reentry tachycardia B9IR.C if one limb of the
reentry circuit in&ol&es an accessory *athway and the other
in&ol&es the 9I node. .he characteristic abru*t onset and
termination of each of the latter grou*s of reentrant
tachyarrhythmias B9INR. and 9IR.C led to the original
name, *aroEysmal su*ra&en3 tricular tachycardia B($I.C.
.his subgrou* of reentry ar3 rhythmias, due to either 9INR.
or 9IR., is characteri/ed by abru*t onset and termination
and a regular rate that eEceeds the ty*ical u**er limits of
sinus tachycardia at rest Busually 1=0 beats *er minuteC
and, in the case of an 9INR., often *resents without
readily identifiable ( wa&es on the ,;.
Distinguishing the forms of reentrant $I.s that are based in
atrial myocardium Bsuch as atrial fibrillationC &ersus those with
a reentry circuit *artly or wholly based in the 9I node itself
B($I.C is im*ortant because each will res*ond differently to
thera*ies aimed at im*eding conduction through the 9I node.
.he &entricular rate of reentry arrhythmias based in atrial
myocardium will be slowed but not terminated by drugs that
slow conduction through the 9I node. on&ersely, reentry
arrhythmias for which at least one limb of the circuit resides in
the 9I node B($I. attributable to 9INR. or 9IR.C can be
terminated by such drugs.
Uet another grou* of $I.s is referred to as automatic
tachycardias. .hese arrhythmias are not due to a circulat3
ing circuit but to an eEcited automatic focus. 8nli#e the
abru*t *attern of reentry, the characteristic onset and
termination of these tachyarrhythmias are more gradual
and analogous to how the sinus node beha&es in gradually
accelerating and slowing heart rate. .hese automatic ar3
rhythmias include ecto*ic atrial tachycardia, "9., and
junctional tachycardia. .hese arrhythmias can be difficult
to treat, are not res*onsi&e to cardio&ersion, and are
usually controlled acutely with drugs that slow conduction
through the 9I node and thereby slow &entricular rate.
Therapy
%a!al 'aneuvers" Iagal maneu&ers and adenosine are the
*referred initial thera*eutic choices for the termination of
stable ($I. BFigure >, =o( /C. Iagal maneu&ers alone
BIalsal&a maneu&er or carotid sinus massageC will terminate
u* to 2=M of ($I.s.
@1: G@:0
For other $I.s, &agal maneu&ers
and adenosine may transiently slow the &entricular rate and
*otentially assist rhythm diagnosis but will not usually
terminate such arrhythmias.
Adenosine" 5f ($I. does not res*ond to &agal maneu&ers,
gi&e 4 mg of 5I adenosine as a ra*id 5I *ush through a large
Beg, antecubitalC &ein followed by a 20 m% saline flush Blass
5, %!, +C. 5f the rhythm does not con&ert within 1 to 2
minutes, gi&e a 12 mg ra*id 5I *ush using the method abo&e.
+ecause of the *ossibility of initiating atrial fibrillation with
ra*id &entricular rates in a *atient with W(W, a defibrillator
should be a&ailable when adenosine is administered to any
*atient in whom W(W is a consideration. 9s with &agal
maneu&ers, the effect of adenosine on other $I.s Bsuch as
atrial fibrillation or flutterC is to transiently slow &entricular
rate Bwhich may be useful diagnosticallyC but not afford their
termination or meaningful lasting rate control.
9 number of studies
@:1G@2:
su**ort the use of adenosine in
the treatment of stable ($I.. 9lthough 2 randomi/ed clinical
trials
@:@,@:4
documented a similar ($I. con&ersion rate be3
tween adenosine and calcium channel bloc#ers, adenosine
was more ra*id and had fewer se&ere side effects than
&era*amil. 9miodarone as well as other antiarrhythmic
agents can be useful in the termination of ($I., but the onset
of action of amiodarone is slower than that of adenosine,
@22
and the *otential *roarrhythmic ris#s of these agents fa&or
the use of safer treatment alternati&es.
9denosine is safe and effecti&e in *regnancy.
>00
-owe&er,
adenosine does ha&e se&eral im*ortant drug interactions.
%arger doses may be reLuired for *atients with a significant
blood le&el of theo*hylline, caffeine, or theobromine. .he
initial dose should be reduced to @ mg in *atients ta#ing
di*yridamole or carbama/e*ine, those with trans*lanted
hearts, or if gi&en by central &enous access. $ide effects with
adenosine are common but transient0 flushing, dys*nea, and
chest discomfort are the most freLuently obser&ed.
>01
9den3
osine should not be gi&en to *atients with asthma.
9fter con&ersion, monitor the *atient for recurrence and
treat any recurrence of ($I. with adenosine or a longer3
acting 9I nodal bloc#ing agent Beg, diltia/em or 3bloc#erC.
5f adenosine or &agal maneu&ers disclose another form of
$I. Bsuch as atrial fibrillation or flutterC, treatment with a
longer3acting 9I nodal bloc#ing agent should be considered
to afford more lasting control of &entricular rate.
Calcium C5annel =loc>ers and <=loc>ers" 5f adenosine
or &agal maneu&ers fail to con&ert ($I. BFigure >, =o( /C,
($I. recurs after such treatment, or these treatments disclose a
different form of $I. Bsuch as atrial fibrillation or flutterC, it is
reasonable to use longer3acting 9I nodal bloc#ing agents, such
as the nondihydro*yridine calcium channel bloc#ers B&era*amil
and diltia/emC Blass 55a, %!, +C or 3bloc#ers Blass 55a,
%!, C. .hese drugs act *rimarily on nodal tissue either to
terminate the reentry ($I.s that de*end on conduction
through the 9I node or to slow the &entricular res*onse to
other $I.s by bloc#ing conduction through the 9I node. .he
alternate mech3 anism of action and longer duration of these
drugs may result in more sustained termination of ($I. or
afford more sustained rate control of atrial arrhythmias Bsuch as
atrial fibrillation or flutterC. 9 number of studies ha&e
established the effecti&eness
of &era*amil
@:1,@:@,@:>,@:4,@2>, @2:,>02G
>0=
and diltia/em
>02,>04,>01
in
con&erting ($I. to normal sinus
rhythm.
For &era*amil, gi&e a 2.= mg to = mg 5I bolus o&er 2
minutes
Bo&er @ minutes in older *atientsC. 5f there is no thera*eutic
res*onse and no drug3induced ad&erse e&ent, re*eated doses of
= mg to 10 mg may be administered e&ery 1= to @0 minutes
to a total dose of 20 mg. 9n alternati&e dosing regimen is to
gi&e a = mg bolus e&ery 1= minutes to a total dose of @0 mg.
Iera*amil should be gi&en only to *atients with narrow3
com*leE reentry $I. or arrhythmias #nown with certainty to
be of su*ra&entricular origin. Iera*amil should not be gi&en to
*atients with wide3com*leE tachycardias. 5t should not be
gi&en to *atients with im*aired &entricular function or heart
failure.
For diltia/em, gi&e a dose of 1= mg to 20 mg B0.2= mg7#gC
5I o&er 2 minutes0 if needed, in 1= minutes gi&e an additional
5I dose of 20 mg to 2= mg B0.@= mg7#gC. .he maintenance
infusion dose is = mg7hour to 1= mg7hour, titrated to heart
rate.
9 wide &ariety of 5I 3bloc#ers are a&ailable for treatment
of su*ra&entricular tachyarrhythmias. .hese include meto*rolol,
atenolol, *ro*ranolol, esmolol, and labetolol Bthe latter more
commonly used for acute management of hy*ertension than for
arrhythmiasC. 5n *rinci*le these agents eEert their effect by
antagoni/ing sym*athetic tone in nodal tissue, resulting in
slowing of conduction. %i#e calcium channel bloc#ers, they
also ha&e negati&e inotro*ic effects and further reduce cardiac
out*ut in *atients with heart failure. "ore detailed information
is *ro&ided below. $ide effects of 3bloc#ers can include
brady3 cardias, 9I conduction delays, and hy*otension.
3bloc#ers should be used with caution in *atients with
obstructi&e *ulmo3 nary disease or congesti&e heart failure.
aution is ad&ised when encountering *re3eEcited atrial
fibril3 lation or flutter that conducts to the &entricles &ia both
the 9I node and an accessory *athway. .reatment with an 9I
nodal bloc#ing agent Bincluding adenosine, calcium
bloc#ers,
3bloc#ers, or digoEinC is unli#ely to slow the &entricular
rate and in some instances may accelerate the &entricular
res*onse. .herefore, 9I nodal bloc#ing drugs should not
be used for *re3eEcited atrial fibrillation or flutter Blass 555,
%!, C.
aution is also ad&ised to a&oid the combination of 9I
nodal bloc#ing agents that ha&e a longer duration of action. For
eEam*le, the short elimination half3life of adenosine affords
follow3u* treatment, if reLuired, with a calcium channel
bloc#er or 3bloc#er. on&ersely the longer half3life of a
calcium channel or 3bloc#er means their effects will o&erla*0
*rofound bradycardia can de&elo* if they are gi&en serially.
9lthough antiarrhythmic medications Beg, amiodarone, *ro3
cainamide, or sotalolC can also be used to treat $I.s, the
higher toEicity and ris# for *roarrhythmia ma#e these
medications less desirable alternati&es to the described 9I
nodal bloc#ing agents. 9 *ossible eEce*tion is in *atients with
*re3eEcited atrial arrhythmias0 the ty*ical 9I nodal bloc#ing
drugs are contrain3 dicated in these *atients and rate control
may be achie&ed with antiarrhythmic medications. 5m*ortantly,
use of these agents for atrial3based $I.s, such as atrial
fibrillation and flutter can result in their termination, which may
be undesirable in the absence of *recautions to *re&ent the
thromboembolic com*lications that may result from such
con&ersion.
6ide-Complex (acycardia 1)igure 73 .oxes 43 83 and 75
E!aluation
.he first ste* in the management of any tachycardia is
to
determine if the *atientNs condition is stable or unstable
BFigure
>, =o( -C. 9n unstable *atient with a wide3com*leE
tachycardia should be *resumed to ha&e I. and immediate
cardio&ersion should be *erformed BFigure >, =o( A and see
abo&eC. (recordial thum* may be considered for *atients with
witnessed, moni3 tored, unstable &entricular tachycardia if a
defibrillator is not immediately ready for use Blass 55b, %!,
C.
5f the *atient is stable, the second ste* in management is to
obtain a 123lead ,; BFigure >, =o(es 2 and /C to e&aluate
the rhythm. 9t this *oint the *ro&ider should consider the
need to obtain eE*ert consultation. 5f the *atient becomes
unstable at any time, *roceed with synchroni/ed cardio&er3
sion or unsynchroni/ed defibrillation should the arrhythmia
deteriorate to IF or be due to a *olymor*hic I..
Wide3com*leE tachycardias are defined as those with a
SR$ 0.12 second. .he most common forms of wide3
com*leE tachycardia are
K
I. or IF
K
$I. with aberrancy
K
(re3eEcited tachycardias Bassociated with or mediated by
an accessory *athwayC
K
Ientricular *aced rhythms
.he third ste* in management of a tachycardia is to
determine if the rhythm is regular or irregular. 9 regular
wide3com*leE tachycardia is li#ely to be I. or $I. with
aberrancy. 9n irregular wide3com*leE tachycardia may be
atrial fibrillation with aberrancy, *re3eEcited atrial fibrillation
Bie, atrial fibrillation using an accessory *athway for ante3
grade conductionC, or *olymor*hic I.7torsades de *ointes.
(ro&iders should consider the need for eE*ert consultation
when treating wide3com*leE tachycardias.
Therapy for )egular 'i#e-Comple" Tachycar#ias
5n *atients with stable undifferentiated wide3SR$ com*leE
tachycardia, a reasonable a**roach is to try to identify the
wide3com*leE tachycardia as $I. or I. and treat based on
the algorithm for that rhythm.
5f the etiology of the rhythm cannot be determined, the rate
is regular, and the SR$ is monomor*hic, recent e&idence
suggests that 5I adenosine is relati&ely safe for both treatment
and diagnosis
>1
Blass 55b, %!, +C. -owe&er, adenosine should
not be gi&en for unstable or for irregular or polymorpic
wide3
com*leE tachycardias, as it may cause degeneration of the
arrhythmia to IF Blass 555, %!, C. 5f the wide3com*leE
tachycardia *ro&es to be $I. with aberrancy, it will li#ely be
transiently slowed or con&erted by adenosine to sinus rhythm0
if due to I. there will be no effect on rhythm BeEce*t in rare
cases of idio*athic I.C, and the bre&ity of the transient
adenosine effect should be reasonably tolerated
hemodynamically. +ecause close attention to these &arying
res*onses may hel* to diagnose the underlying rhythm,
whene&er *ossible, continuous ,; recording is strongly
encouraged to *ro&ide such written docu3 mentation. .his
documentation can be in&aluable in hel*ing to establish a firm
rhythm diagnosis e&en if after the fact. .y*i3 cally, adenosine is
administered in a manner similar to treatment of ($I.6 as a 4
mg ra*id 5I *ush0 *ro&iders may follow the first dose with a
12 mg bolus and a second 12 mg bolus if the rate fails to
con&ert. When adenosine is gi&en for undifferentiated wide3
com*leE tachycardia, a defibrillator should be a&ailable.
De*ending on the underlying rhythm, the res*onse to adeno3
sine challenge can be &ariable. $ome studies
>0: G >12
showed
that adenosine con&erted an undifferentiated wide3com*leE
tachycardia to sinus rhythm. 9nother study
>1@
showed *oor
rates of con&ersion to sinus rhythm in *atients #nown to ha&e
I.. .he following ad&erse effects were re*orted in *atients
with *re3 eEcited atrial fibrillation treated with adenosine6
con&ersion to atrial fibrillation with a ra*id &entricular res*onse
in one *atient later found to ha&e *reeEcitation, con&ersion to
IF in one *atient with #nown W(W,
>1>
con&ersion to IF
in > *atients with *re3eEcited atrial fibrillation,
>1=
con&ersion
to IF in 2 *atients with W(W,
>14
and a single case of IF in a
*atient with I..
>11
Iera*amil is contraindicated for wide3com*leE
tachycardias unless #nown to be of su*ra&entricular origin
Blass 555, %!, +C. 9d&erse effects when the rhythm was due
to I. were shown in = small case series.
>1> G >1:
(rofound
hy*otension was re*orted in 11 of 2= *atients #nown to ha&e
I. treated with &era*amil.
>1:
For *atients who are stable with li#ely I., 5I
antiarrhythmic drugs or electi&e cardio&ersion is the *referred
treatment strat3 egy. 5f 5I antiarrhythmics are administered,
*rocainamide Blass 55a, %!, +C, amiodarone Blass 55b, %!,
+C, or sotalol Blass 55b, %!, +C can be considered.
(rocainamide and sotalol should be a&oided in *atients with
*rolonged S.. 5f one of these antiarrhythmic agents is gi&en, a
second agent should not be gi&en without eE*ert consultation
Blass 555, %!, +C. 5f antiar3 rhythmic thera*y is unsuccessful,
cardio&ersion or eE*ert con3 sultation should be considered
Blass 55a, %!, C.
!ne randomi/ed com*arison found *rocainamide B10
mg7#gC to be su*erior to lidocaine B1.= mg7#gC for termination
of hemodynamically stable monomor*hic I..
>12
(rocainamide
can be administered at a rate of 20 to =0 mg7min until the
arrhythmia is su**ressed, hy*otension ensues, SR$
duration increases
=0M, or the maEimum dose of 11 mg7#g is gi&en.
"aintenance infusion is 1 to > mg7min. (rocainamide should be
a&oided in *atients with *rolonged S. and congesti&e heart
failure.
5I sotalol B100 mg 5I o&er = minutesC was found to be
more effecti&e than lidocaine B100 mg 5I o&er = minutesC
when administered to *atients with s*ontaneous
hemodynamically stable sustained monomor*hic I. in a
double3blind randomi/ed trial within a hos*ital setting.
>20
5n
a se*arate study of 102 *atients with a history of
s*ontaneous and inducible sustained
&entricular tachyarrhythmias, infusing 1.= mg7#g of sotalol
o&er
= minutes was found to be relati&ely safe and effecti&e,
causing hy*otension in only 2 *atients, both of whom
res*onded to 5I fluid.
>21
(ac#age insert recommends slow
infusion, but the literature su**orts more ra*id infusion of 1.=
mg7#g o&er = minutes or less. $otalol should be a&oided in
*atients with a *rolonged S. inter&al.
9miodarone is also effecti&e in *re&enting recurrent
monomor*hic I. or treating refractory &entricular
arrhythmias
2:4,>22G >2>
in *atients with coronary artery disease
and *oor &entricular function. 5t is gi&en 1=0 mg 5I o&er 10
minutes0 dosing should be re*eated as needed to a maEimum
dose of 2.2 g 5I *er 2> hours. -igher doses B@00 mgC were
associated with an increased freLuency of hy*otension, al3
though some re*orts
>22,>2>
attributed the hy*otension to the
&asoacti&e sol&ents that are not *resent in a new form of the
drug recently a**ro&ed for use in the 8$.
+y com*arison, lidocaine is less effecti&e in terminating I.
than *rocainamide, sotalol, and amiodarone,
2:4,>12,>20
and when
gi&en to *atients with or without a history of "5 with s*onta3
neous sustained stable I. in the hos*ital setting.
>1@,>2=,>24
%ido3
caine has been re*orted to &ariably terminate I. when admin3
istered intramuscularly to *atients with 9"5 and I. in
the out3of3hos*ital setting.
>21,>2:
.hus, while occasionally
effecti&e, lidocaine should be considered second3line
antiarrhythmic ther3 a*y for monomor*hic I.. %idocaine can
be administered at a dose of 1 to 1.= mg7#g 5I bolus.
"aintenance infusion is 1 to > mg7min B@0 to =0 mcg7#g *er
minuteC.
7rre!ular 9ac5ycardias
Atrial )i%rillation and )lutter
E!aluation
9n irregular narrow3com*leE or wide3com*leE tachycardia is
most li#ely atrial fibrillation Bwith or without aberrant conduc3
tionC with an uncontrolled &entricular res*onse. !ther
diagnostic *ossibilities include "9. or sinus
rhythm7tachycardia with freLuent atrial *remature beats. When
there is doubt about the rhythm diagnosis and the *atient is
stable, a 123lead ,; with eE*ert consultation is
recommended.
Therapy
;eneral management of atrial fibrillation should focus
on
control of the ra*id &entricular rate Brate controlC, con&ersion of
hemodynamically unstable atrial fibrillation to sinus rhythm
Brhythm controlC, or both. (atients with an atrial fibrillation
duration of >: hours are at increased ris# for
cardioembolic e&ents, although shorter durations of atrial
fibrillation do not eEclude the *ossibility of such e&ents.
,lectric or *harmacologic cardio&ersion Bcon&ersion to normal
sinus rhythmC should not be attempte# in these *atients unless
the *atient is unstable. 9n alternati&e strategy is to *erform
cardio&ersion following anti3 coagulation with he*arin an#
*erformance of transeso*hageal echocardiogra*hy to ensure the
absence of a left atrial thrombus0 see the 979-9 ;uidelines
for "anagement of (atients with 9trial Fibrillation.
>22
)ate Control
(atients who are hemodynamically unstable should recei&e
*rom*t electric cardio&ersion. "ore stable *atients reLuire
&entricular rate control as directed by *atient sym*toms
and hemodynamics. 5I 3bloc#ers and nondihydro*yri3
dine calcium channel bloc#ers such as diltia/em
>@0 G >@@
are
the drugs of choice for acute rate control in most indi&id3
uals with atrial fibrillation and ra*id &entricular res*onse
Blass 55a, %!, 9C. DigoEin
>@> G >@4
and amiodarone
>@1,>@:
may be used for rate control in *atients with congesti&e
heart failure0 howe&er, the *otential ris# of con&ersion to
sinus rhythm with amiodarone should be considered before
treating with this agent.
9 wide3com*leE irregular rhythm should be considered *re3
eEcited atrial fibrillation. ,E*ert consultation is ad&ised. 9&oid
9I nodal bloc#ing agents such as adenosine, calcium channel
bloc#ers, digoEin, and *ossibly 3bloc#ers in *atients
with *re3eEcitation atrial fibrillation because these drugs may
cause a *aradoEical increase in the &entricular res*onse.
.y*ically, *atients with *re3eEcited atrial fibrillation *resent
with &ery ra*id heart rates and reLuire emergent electric
cardio&ersion. When electric cardio&ersion is not feasible or
effecti&e, or atrial fibrillation is recurrent, use of rhythm control
agents Bdiscussed belowC may be useful for both rate control
and stabili/ation of the rhythm.
)hythm Control
9 &ariety of agents ha&e been shown to be effecti&e in
terminating atrial fibrillation B*harmacologic or chemical
cardio&ersionC, although success between them &aries and not
all are a&ailable as *arenteral formulations. ,E*ert consulta3
tion is recommended.
Polymorpic 1$rregular5 &(
(olymor*hic BirregularC I. reLuires immediate defibrillation
with the same strategy used for IF.
(harmacologic treatment to *re&ent recurrent *olymor*hic
I. should be directed by the underlying cause of I. and the
*resence or absence of a long S. inter&al during sinus
rhythm.
5f a long S. inter&al is obser&ed during sinus rhythm Bie,
the I. is torsades de *ointesC, the first ste* is to sto*
medications #nown to *rolong the S. inter&al. orrect
electrolyte imbalance and other acute *reci*itants Beg, drug
o&erdose or *oisoning6 see (art 12.16 Hardiac 9rrest
9ssociated With .oEic 5ngestionsJC. 9lthough magnesium is
commonly used to treat torsades de *ointes I. B*olymor*hic
I. associated with long S. inter&alC, it is su**orted by only 2
obser&ational studies
101,110
that showed effecti&eness in *atients
with *rolonged S. inter&al. !ne adult case series
>@2
showed
that iso*roterenol or &entricular *acing can be effecti&e in
terminating torsades de *ointes associated with bradycardia and
drug3induced S. *rolongation. (olymor*hic I. associated
with familial long S. syndrome may be treated with 5I
magnesium, *acing, and7or 3bloc#ers0 iso*roterenol should
be a&oided. (olymor*hic I. associated with acLuired long S.
syndrome may be treated with 5I magnesium. .he addition of
*acing or 5I iso*roterenol may be considered when
*olymor*hic I. is accom*anied by bradycardia or a**ears to
be *reci*itated by *auses in rhythm.
5n the absence of a *rolonged S. inter&al, the most
common cause of *olymor*hic I. is myocardial ischemia. 5n
this situation 5I amiodarone and 3bloc#ers may reduce the
fre3 Luency of arrhythmia recurrence Blass 55b, %!, C.
"yocar3
dial ischemia should be treated with 3bloc#ers and consider3
ation be gi&en to eE*editious cardiac catheteri/ation with
re&asculari/ation. "agnesium is unli#ely to be effecti&e in
*re&enting *olymor*hic I. in *atients with a normal S.
inter&al Blass 55b, %!, C,
101
but amiodarone may be
effecti&e Blass 55b, %!, C.
>>0
!ther causes of *olymor*hic I. a*art from ischemia and
long S. syndrome are catecholaminergic I. Bwhich may be
res*onsi&e to 3bloc#ersC and +rugada syndrome Bwhich may
be res*onsi&e to iso*roterenolC.
Summary
.he goal of thera*y for bradycardia or tachycardia is to
ra*idly identify and treat *atients who are hemodynamically
unstable or sym*tomatic due to the arrhythmia. Drugs or,
when a**ro*riate, *acing may be used to control unstable or
sym*tomatic bradycardia. ardio&ersion or drugs or both
may be used to control unstable or sym*tomatic tachycardia.
9%$ *ro&iders should closely monitor stable *atients *end3
ing eE*ert consultation and should be *re*ared to aggres3
si&ely treat those with e&idence of decom*ensation.
)isclosures
#uidelines $art %: AC&' (riting #rou) Disclosures
7riting
Eroup
>em"er /mployment +esearch Erant
Fther +esearch
Support
Spea!ers =ureau
Honoraria
F2nership
.nterest
Consultant
Advisory =oard Fther
+o"ert 7. 0niversity o% :one :one :one :one :one :one
:eumar &ennsylvania-Associate
&ro%essor o%
/mergency >edicine
Charles 7. 0niversity o% Ari9ona8 :one :one :one :one :one :one
Ftto &ro%essor
>ar! S. Tu%ts >edical Center8 :one :one :one :one :one :one
Lin! &hysician
Steven L. 0niversity o% :one :one :one :one :one :one
Gronic! >ichigan8Assistant
&ro%essor
>ichael Sel%-employed8 :one :one :one :one :one :one
Shuster emergency physician
Cli%ton 7. 0niversity o% &itts"urgh HErants to ILoan o% an :one HCo-inventor on :one :one
Calla2ay School o% 0niversity o% Arctic Sun patent a"out
>edicine8Associate &itts"urgh) cooling device ventricular
&ro%essor1 0&>C :HL=.- (2ithout %i"rillation
Health +esuscitation disposa"les) to 2ave%orm
SystemJ&hysician Futcomes human analysis#
IAmerican Heart Consortium physiology licensed "y
Association-7or! Sheet H+SA--evelopment la"oratory %or 0niversity o%
/ditor %or (5'5 and -issemination experiments on &itts"urgh to
Euidelines. >y e%%ort o% &rogram Tools hypothermia "y >edtronic /+S#
on this proKect is paid %or 0ncontrolled >edivance# .nc. .nc.
to 0niversity o% -onation A%ter
&itts"urgh as a Cardiac -eath
contracted services
agreement# and not
paid directly to me
(0-C-)
&eter L. 0niversity o% H+esuscitation :one :et2or! %or Continuing Sano%i-Aventis# :one :one
Gudenchu! 7ashington8 Futcomes >edical /ducation# :ovartis
&ro%essor o% >edicine Consortium Academy %or
(:.H:HL=.) Healthcare /ducation#
Sano%i-Aventis# 2ith
honoraria
Loseph &. +ichmond Am"ulance HConsultant and :one IHospital grand rounds :one IMFLL Circulation :one
Frnato Authority8>edical Cardiac Co-Chairman# presentations %unded Science Advisory
-irector1 4irginia :.H +esuscitation "y MFLL Circulation =oard (0:&A.-#
Common2ealth Futcomes IFccasional hospital only receive
0niversity-&ro% N Consortium &rincipal grand rounds travel
Chmn# /mergency .nvestigator# 4C0 site supported "y reim"ursement)
>edicine %or :.H :eurological unrestricted
/mergency educational grants
Treatment Trials %rom S6ui""Sano%i#
:et2or! MFLL
(Continued)
#uidelines $art %: AC&' (riting #rou) Disclosures* Continued
7riting
Eroup
>em"er /mployment +esearch Erant
Fther +esearch
Support
Spea!ers =ureau
Honoraria
F2nership
.nterest
Consultant
Advisory =oard Fther
=ryan
>c:ally
/mory 0niversity8
Assistant &ro%essor o%
/mergency >edicine
HCenter %or -isease
Control and
&revention#
CA+/S-Cardiac Arrest
+egistry to /nhance
Survival# >oney
comes to /mory
0niversity School o%
>edicine as part o% a
cooperative
agreement through
American Association
o% >edical Colleges
:one :one :one :one :one
Scott >.
Silvers
>ayo Clinic8Chair#
-epartment o%
/mergency >edicine
:one :one :one :one :one :one
+od S.
&assman
:orth2estern
0niversity8Associate
&ro%essor
:one :one :one :one ISteering
Committee
mem"er %or
>edtronic Crystal
A$ study
:one
+oger -.
7hite
>ayo Clinic8sta%%
physician
:one :one :one :one :one :one
/ri! &.
Hess
>ayo Clinic8Senior
Associate Consultant
:one :one :one :one :one :one
7anchun
Tang
7eil .nstitute o% Critical
Care >edicine8
&ro%essor and president
:one :one ICBth 7eil Critical
Care Symposium)
O'#;55
:one :one :one
-aniel 0C San -iego8$aculty HMoll >edical (Air I=ispectral //E IContinuous +enal :one HCardinal Health I-ere!
-avis physician >edical Advanced
>onitoring
Strategies)
Analy9er (Moll
>edical)
+eplacement Therapy
Con%erence (55?
Hospital >edicine
:ational and +egional
>eeting (55? Erand
+ounds +edding
>edical Center
(-evelopment o%
a &rehospital
4entilator)
7hite La2
$irm Lohn
Anderson
La2 $irm
Ftoro2s!i
Lohnston
-iamond
N Eolden
La2 $irm
/li9a"eth
Sin9
&enn State Hershey
>edical Center8
&ro%essor o%
Anesthesiology and
:eurosurgery1 AHA)
&aid Consultant
Associate Science
/ditor
:one :one :one :one :one :one
Laurie L.
>orrison
St >ichaels Hosp.
Clinician Scientist
:one :one :one :one :one :one
This ta"le represents the relationships o% 2riting group mem"ers that may "e perceived as actual or reasona"ly perceived con%licts o% interest as reported on the
-isclosure @uestionnaire# 2hich all mem"ers o% the 2riting group are re6uired to complete and su"mit. A relationship is considered to "e *signi%icant, i% (a) the person
receives O'5 555 or more during any '(-month period# or ;A or more o% the persons gross income1 or (") the person o2ns ;A or more o% the voting stoc! or share o%
the entity# or o2ns
O'5 555 or more o% the %air mar!et value o% the entity. A relationship is considered to "e *modest, i% it is less than *signi%icant, under the preceding de%inition.
I>odest.
HSigni%icant.
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',U W!RD$6 arrhythmia

cardiac arrest

drugs

&entricular arrhythmia

&entricular fibrillation
Correction
5n the article by Neumar, et al, H(art :6 9dult 9d&anced ardio&ascular %ife $u**ort6 2010
9merican -eart 9ssociation ;uidelines for ardio*ulmonary Resuscitation and ,mergency
ardio&ascular are,J which *ublished ahead of *rint on !ctober 1:, 2010, and a**eared with
the No&ember 2, 2010, issue of the journal BCirculation. 20100122Psu**l @Q0$122G$141C, se&eral
corrections were needed.
1. !n *age $1@4, in Figure 1, in gray teEt boE on the right, under H$hoc# ,nergy,J the bullet for
H+i*hasicJ read, H=ip5asic: "anufacturer recommendation B1203200 )C0 if un#nown, use
maEimum a&ailable. $econd and subseLuent doses should be eLui&alent, and higher doses
may be considered.J 5t has been u*dated to read, H=ip5asic: "anufacturer recommendation
Beg, initial dose of 1203200 )C0 if un#nown, use maEimum a&ailable. $econd and subseLuent
doses should be eLui&alent, and higher doses may be considered.J
2. !n *age $1@1, in Figure 2, in gray teEt boE on the right, under H$hoc# ,nergy,J the bullet for
H+i*hasicJ read, H=ip5asic: "anufacturer recommendation B1203200 )C0 if un#nown, use
maEimum a&ailable. $econd and subseLuent doses should be eLui&alent, and higher doses
may be considered.J 5t has been u*dated to read, H=ip5asic: "anufacturer recommendation
Beg, initial dose of 1203200 )C0 if un#nown, use maEimum a&ailable. $econd and subseLuent
doses should be eLui&alent, and higher doses may be considered.J
@. !n *age $1@:, in the left column, the first *aragra*h under HWa&eform and ,nergy,J the first
sentence read, H5f a bi*hasic defibrillator is a&ailable, *ro&iders should use the
manufacturerNs recommended energy dose B120 to 200 )C for terminating IF Blass 5, %!,
+C.J 5t has been u*dated to read, H5f a bi*hasic defibrillator is a&ailable, *ro&iders should use
the manufacturerNs recommended energy dose Beg, initial dose of 120 to 200 )C for
terminating IF Blass 5, %!, +C.J
.hese corrections ha&e been made to the current online &ersion of the article, which is a&ailable
at htt*677circ.ahajournals.or g 7cgi7content7full712271:Asu**lA@7$122.
? 2011 9merican -eart 9ssociation, 5nc.
Circulation is a&ailable at htt*677 c irc .ahajour n als .org
)&7:10"11216C7R"0401-e-1820ffB11
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