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Part 8: Adult Advanced Cardiovascular Life Support: 2010 American HeartAssociation 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 2010122$23$4D!56 10.114175R8%95!N9-9.110.0::
irculation is *ublished by the 9merican -eart 9ssociation. 22 ;reen&ille 9&enue, Dallas,
o*yright ? 2010 9merican -eart 9ssociation. 9ll rights reser&ed. (rint 5$$N6 0003@22. !nline5$$N6 1=2>3>=@
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9
Part 8: Adult Advanced Cardiovascular Life Support2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and mer!ency Cardiovascular Care
Robert W. Neumar, hair 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 $in/ %aurie ). "orrison
d&anced cardio&ascular life su**ort B9%$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 ofbradyarrhythmias 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 IentilationJ :.26 H"anage3
ment of ardiac 9rrestJ and :.@6 H"anagement of
$ym*tomatic +radycardia and achycardia.J (ostG cardiac
arrest inter&entions are addressed in (art 6 H(ostGardiac
9rrest are.J
'ey changes from the 200= 9%$ ;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 anda&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 Controland %entilation
&vervie$ of Air$ay 'ana!ementhis section highlights recommendations for the su**ort of
&entilation and oEygenation during (R and the *eri3arrest
*eriod. he *ur*ose of &entilation during (R is to maintain
adeLuate oEygenation and sufficient elimination of carbon
dioEide. -owe&er, research has not identified the o*timal
tidal &olume, res*iratory rate, and ins*ired oEygen concen3
tration reLuired during resuscitation from cardiac arrest.
+oth &entilation and chest com*ressions are thought to be
im*ortant for &ictims of *rolonged &entricular fibrillation
BIFC cardiac arrest and for all &ictims with other *resentingrhythms. +ecause both systemic and *ulmonary *erfusion are
substantially reduced during (R, normal &entilation3
*erfusion relationshi*s can be maintained with a minute
&entilation that is much lower than normal. During (R with
an ad&anced airway in *lace, a lower rate of rescue breathing
is needed to a&oid hy*er&entilation.
%entilation and &(y!en Administration)urin! CPRDuring low blood flow states such as (R, oEygen deli&ery to
the heart and brain is limited by blood flow rather than by
arterial oEygen content.1,2 herefore, rescue breaths are less
im*ortant than chest com*ressions during the first few minutesof resus3 citation from witnessed IF cardiac arrest and could
reduce (R efficacy due to interru*tion in chest com*ressions
and the increase in intrathoracic *ressure that accom*anies
*ositi&e3 *ressure &entilation. hus, during the first few
minutes of witnessed cardiac arrest a lone rescuer should not
interru*t chest
he 9merican -eart 9ssociation reLuests that this document be cited as follows6 Neumar RW, !tto W, %in# "$, 'ronic# $%, $huster ", allawayW, 'udenchu# (), !rnato )(, "cNally +, $il&ers $", (assman R$, White RD, -ess (, ang W, Da&is D, $in/ , "orrison %). (art :6 adult ad&ancedcardio&ascular life su**ort6 2010 9merican -eart 9ssociation ;uidelines for ardio*ulmonary Resuscitation and mergency ardio&ascular are.
Circulation. 2010122Bsu**l @C6$2 G$4.*Circulation" 2010+122,suppl -.:S/2 S//"3? 2010 9merican -eart 9ssociation, 5nc.
Ci l i i il 4l 5 66 i 5 # l )&7 10 1116C7RCLA97&AHA 110 /088
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S218 Circulation ovem4er 2; 2010
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com*ressions for &entilation. 9d&anced airway *lacement in
cardiac arrest should not delay initial (R and defibrillation for
IF cardiac arrest Blass 5, %! C.
&(y!en )urin! CPR
Oxygen Administration During CPRhe o*timal ins*ired oEygen concentration during adult (R
has not been established in human or animal studies. 5n
addition, it is un#nown whether 100M ins*ired oEygen
BF5!2 1.0C is beneficial or whether titrated oEygen is better.
9lthough *rolonged eE*osure to 100M ins*ired oEygen
BF5!2 1.0C has *otential toEicity, there is insufficient e&i3
dence to indicate that this occurs during brief *eriods of adult
(R.@G= m*irical use of 100M ins*ired oEygen during (R
o*timi/es arterial oEyhemoglobin content and in turn oEygen
deli&ery therefore, use of 100M ins*ired oEygen BF 5!2 1.0C
as soon as it becomes a&ailable is reasonable during resusci3
tation from cardiac arrest Blass 55a, %! C. "anagement of
oEygen after R!$ is discussed in (art 6 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"$C *ersonnel was *art of a
*rotocol of bundled care inter&entions Bincluding continuous
chest com*ressionsC that resulted in im*ro&ed sur&i&al.4G :
When *assi&e oEygen deli&ery using a fenestrated tracheal
tube B+oussignac tubeC during uninterru*ted *hysician3managed (R was com*ared with standard (R, there was
no difference in oEygenation, R!$, or sur&i&al to hos*ital
admission.,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 ventila0,>1,=2,=@
5n one case seriesassessing >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*ture
for @ other
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*atients, &entilation was ineffecti&e because of massi&e
regurgitation and as*iration before laryngeal tube *lacement.
9nother out3of3hos*ital assessment of 1= attem*ts at laryn3
geal tube *lacement re&ealed a M 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 managementin cardiac arrest Blass 55b, %!
C.
Laryngeal Mask
Airwayhe laryngeal mas# airway *ro&ides a more secure andreliable
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>,== successful &entilation during (Rhas been re*orted in 2M to M of*atients.@4,@,>>,=4G=:
+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,=,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,@,>>,==,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*tablealternati&e to bag3 mas# &entilation Blass 55a, %! +C or
endotracheal intubation Blass 55a, %! C for airway
management in cardiac arrest.
#ndotraceal
$ntu%ationhe endotracheal tube was once considered the o*timal
method of managing the airway during cardiac arrest. -ow3
e&er, intubation attem*ts by uns#illed *ro&iders can *roduce
com*lications, such as trauma to the oro*harynE, interru*tion
of com*ressions and &entilations for unacce*tably long *eri3
ods, and hy*oEemia from *rolonged intubation attem*ts or
failure to recogni/e tube mis*lacement or dis*lacement. 5t is
now clear that the incidence of com*lications is unacce*tably
high when intubation is *erformed by ineE*erienced *ro&id3
ers or monitoring of tube *lacement is inadeLuate. he
o*timal method of managing the airway during cardiac arrest
will &ary based on *ro&ider eE*erience, characteristics of the
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"$ or healthcare system, and the *atients 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&als4 showed no
sur&i&al ad&antage for endotracheal intubation o&er bag3mas#
&entilation in children *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 thetube 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 tube 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: G2 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,4,0 es*ecially when the *atient is
mo&ed.@ 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 BDDC.>
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,
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no single confirmation techniLue is com*letely reliable.=,4
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 discussedbelow.
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 *assingthrough 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 arrest2, 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 andtrans3 *ort times.: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.2,,: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:G>
and nonwa&eform (!2 ca*nometers,:,0,= 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 !2C
in cardiac arrest, it is usually a reliable indicator of tube
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*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 arrest howe&er, the wa&eform
does not continue during subseLuent breaths.4
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.104,10 here is little e&i3
dence for the use of thoracic im*edance in diagnosing
adeLuacy of &entilation during (R. reatment decisionsshould 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 Management9fter 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 eEtension10: G110 and when the
airway obstruction Beg, status asthmaticusC and *ulmonary *atient is mo&ed from one location to another.111,112
edema.@,,: 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 !23detecting de&ices to determine the correct
*lacement of other ad&anced airways Beg, ombitube, laryn3
geal mas# airwayC has not been studied 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 tube
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, and
the self3inflating bulb DD: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 initialmethod 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,100,101because
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 eEhala3tion.102 9ir is a *oor electric conductor. (reliminary studies
suggest that changes in thoracic im*edance, as measured
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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 study11@ and 2 studies in an intensi&e3
care setting11>,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 PlacementEce*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.114,11 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=
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Automatic (ransport &entilators5n both out3of3hos*ital and in3hos*ital settings, automatic
trans*ort &entilators B9IsC 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 9Is attached to
ad&anced airways during ongoing resuscitati&e efforts.
During *rolonged resuscitati&e efforts the use of an 9I
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.124,12 (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 *haryngealti*s. $e&eral sterile suction catheters of &arious si/es
should be a&ailable for suctioning the lumen of the
ad&anced airway, along with a nonbrea#able collection
bottle and sterile water for cleaning tubes and catheters.
he installed suction unit should be *owerful enough to
*ro&ide an airflow of >0 %7min at the end of the deli&ery
tube and a &acuum of @00 mm -g when the tube is
clam*ed. he amount of suction should be adjustable for
use in children and intubated *atients.
Summary9ll basic and ad&anced healthcare *ro&iders should be able
to *ro&ide &entilation with a bag3mas# de&ice during (Ror when the *atient demonstrates cardiores*iratory com3
*romise. 9irway control with an ad&anced airway, which
may include an endotracheal tube or a su*raglottic airway
de&ice, is a fundamental 9%$ 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
airways 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 BIC, *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.
$ur&i&al from these cardiac arrest rhythms reLuires bothbasic life su**ort B+%$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 6 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 facilitat e learning and memori/ation of the
treatment recommendations discussed below. !&erall thesealgorithms 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 !2P(!2Q, arterial *ressure during the relaEation *hase of
chest com*ressions, or central &enous oEygen saturation
P$c&!2QC are encouraged Bsee H"onitoring During (RJ
belowC. 5n the absence of an ad&anced airway, a synchro3
ni/ed com*ressionG&entilation ratio of @062 is recom3
mended at a com*ression rate of at least 100 *er minute.
9fter *lacement of a su*raglottic airway or an endotra3
cheal tube, the *ro&ider *erforming chest com*ressions
should deli&er at least 100 com*ressions *er minute
continuously without *auses for &entilation. he *ro&ider
deli&ering &entilations should gi&e 1 breath e&ery 4 to :
seconds B: to 10 breaths *er minuteC and should be
*articularly careful to a&oid deli&ering an eEcessi&e num3
ber of &entilations Bsee (art :.16 H9djuncts for 9irwayontrol and IentilationJC.
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Figure 1.ACLS Cardiac Arrest Algorithm.
5n addition to high3Luality (R, the only rhythm3s*ecific
thera*y *ro&en to increase sur&i&al to hos*ital discharge is
defibrillation of IF7*ulseless I. herefore, this inter&entionis included as an integral *art of the (R cycle when the
rhythm chec# re&eals IF7*ulseless I. !ther 9%$ inter3
&entions during cardiac arrest may be associated with an
increased rate of R!$ but ha&e not yet been *ro&en toincrease sur&i&al to hos*ital discharge. herefore, they are
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Figure 2.ACLS Cardiac Arrest Circular Algorithm.
recommended as considerations and should be *erformed
without com*romising Luality of (R or timely defibril3lation. 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 -s and s to identify and
treat any factor that may ha&e caused the arrest or may be
com*licating the resuscitati&e effort Bable 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 anew cardiac arrest rhythm should necessarily be altered
based on the characteristics of the *re&ious rhythm. "ed3
ications administered during resuscitation should be mon3itored and total doses tabulated to a&oid *otential toEicity.
5f the *atient achie&es R!$, it is im*ortant to begin
*ostG cardiac arres t care immediately to a&oid rearrest and
o*timi/e the *atients chance of long3term sur&i&al with
good neurologic function Bsee (art C. Finally, the reality is
that the majority of resuscitati&e efforts do not result in
R!$. riteria for ending unsuccessful resuscitati&e ef3
forts are addressed briefly below Bsee HWhen $hould
Resuscitati&e fforts $to*JC and in more detail in (art @6
Hthics.J
R5yt5m
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in manual instead of automatic mode during cardiac arrest is
uncertain Blass 55b, %! C.
CP) *efore efibrillationDuring treatment of IF7*ulseless I healthcare *ro&iders
must ensure that coordination between (R and shoc#
deli&ery is efficient. When IF is *resent for more than a
few minutes, the myocardium is de*leted of oEygen and
metabolic substrates. 9 brief *eriod of chest com*ressions
can deli&er oEygen and energy substrates and HunloadJ the
&olume3o&erloaded right &entricle, increasing the li#eli3
hood that a *erfusing rhythm will return after shoc#
deli&ery.1>1
(erforming (R while a defibrillator is readied for use is
strongly recommended for all *atients in cardiac arrest Blass
5, %! +C. 9nalyses of IF wa&eform characteristics *redic3
ti&e of shoc# success ha&e documented that the shorter the
time inter&al between the last chest com*ression and shoc#
deli&ery, the more li#ely the shoc# will be successful. 1>1 9
reduction of e&en a few seconds in the inter&al from *ausing
com*ressions to shoc# deli&ery can increase the *robability
of shoc# success.1>2
he &alue of intentionally delaying defibrillation to *erform
(R is less clear. !ne randomi/ed controlled trial BRC1>@
and one clinical trial1>> in&ol&ing adults with out3of3hos*ital
cardiac arrest not witnessed by "$ *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 Rs1>=,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 unclearBlass 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>G144 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 *erfusingrhythm, then gi&ing a &aso*ressor soon after the shoc# will
o*timi/e
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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.@,14G1 -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 -s and s 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
$ituationsJC. 5n the case of refractory IF7*ulseless I, acute
coronary ischemia or myocardial infarction should be con3
sidered as a *otential etiology. Re*erfusion strategies such as
coronary angiogra*hy and (5 during (R or emergency
cardio*ulmonary by*ass ha&e been demonstrated to be fea3
sible in a number of case studies and case series but ha&e not
been e&aluated for their effecti&eness in Rs.1: G1: Fibrino3
lytic thera*y administered during (R for acute coronary
occlusion has not been shown to im*ro&e outcome.1::
ROSC A'ter &)*Pulseless &(5f the *atient has R!$, *ostG cardiac arrest care should be
started B(art C. !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.
PA6AsystoleWhen a rhythm chec# by an 9D 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 C. 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 *hysio3logic *arameters Bsee H"onitoring During (RJ belowC.
Drug (erapy 'or P#A*Asystole9 &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 betreated successfully if those conditions are identified andcorrected. During each 23minute *eriod of (R the *ro&ider
should recall the -s and s 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 embolismis *resumed or #nown to be the cause of cardiac arrest,
em*irical fibrinolytic thera*y can be considered Blass 55a,
%! + 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: $ee (art 12 for management of
toEicological causes of cardiac arrest.
9systole is commonly the end3stage rhythm that follows
*rolonged IF or (9, and for this reason the *rognosis isgenerally much worse.
ROSC A'ter P#A*Asystole5f the *atient has R!$, *ostG cardiac arrest care shouldbe
initiated Bsee (art C. !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
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non*hysi3
ologic techniLues that hel* the *ro&ider adhere to recom3
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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 $u**ortJ and (art 146
Hducation, 5m*lementation and eams.J
Pysiologic Parameters5n humans cardiac arrest is the most critically ill condition,
yet it is ty*ically monitored by rhythm assessment using
selected electocardiogra*hic B;C leads and *ulse chec#s
as the only *hysiologic *arameters to guide thera*y.
9nimal and human studies indicate that monitoring of
(!2, coronary *erfusion *ressure B((C, and central
&enous oEygen saturation B$c&!2C *ro&ides &aluable infor3mation on both the *atients condition and res*onse to
*ressed as a *artial *ressure in mm -g B(!2C. +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 thelungs. 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&ealso shown that (!2 correlates with (( and cerebral
thera*y. "ost im*ortantly, (!2, ((, and $c&!2 corre3*erfusion *ressure during (R.20,210 he correlation of
late with cardiac out*ut and myocardial blood flow during
(R, and threshold &alues below which R!$ is rarely
achie&ed ha&e been re*orted.14:,10 G1= 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.1,@,14G1=,1,14 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.
Pulselinicians 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.11,1@,1>,10,11,21=,214 $imilar data using Luantita3ti&e monitoring of (!2 are not a&ailable for *atients with
a su*raglottic airway or those recei&ing bag3mas# &entilation
during (R. !ne study using colorimetic end3tidal !2detection in nonintubated *atients during (R found that low
end3tidal !2 was not a reliable *redictor of failure to
achie&e R!$.21 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 thanmeasured (!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 *ausedis 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:,21 5n addition, an
abru*t sustained in3*ulse20@,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!$.1,1,14,1:G201 herefore, it is reasonable to consider
using Luantitati&e wa&eform ca*nogra*hy in intubated *a3
tients to monitor (R Luality, o*timi/e chest com*ressions,
and detect R!$ 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=,20
(!2 is 10 mm -g, it is reasonable to consider trying to
#nd-(idal CO2
nd3tidal !2 is the concentration of carbon dioEide ineEhaled air at the end of eE*iration. 5t is ty*ically eE3
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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
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&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 relaEationPHdiastolicJQ *ressure minus right atrial relaEation PHdia3
stolicJQ *ressureC during (R correlates with both
myocardial blood flow and R!$.14:,12,220 RelaEation *ressure
during (R is the trough of the *ressure wa&eform during the
relaEation *hase of chest com*ressions and is analogous to
diastolic *ressure when the heart is beating. 5ncreased ((
correlates with im*ro&ed 2>3hour sur&i&al rates in animal
studies1@ and is associated with im*ro&ed myocardial blood
flow and R!$ in animal studies of e*ine*hrine, &aso*ressin,
and angiotensin 55.1@G1= 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 1 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 considerusing 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, i t 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 SaturationWhen oEygen consum*tion, arterial oEygen saturation
B$a!2C, and hemoglobin are constant, changes in $c& !2reflect 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 $c&!2 of @0M during (R was associated with
failure to achie&e R!$.14 $c&!2
also hel*s to ra*idly detect
R!$ 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
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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 $c&!2 is @0M, it is
reasonable to consider trying to im*ro&e the Luality of (R
by o*timi/ing chest com*ression *arameters Blass 55b,
%! C.
Pulse OximetryDuring cardiac arrest, *ulse oEimetry ty*ically does not
*ro&ide a reliable signal because *ulsatile blood flow is
inadeLuate in *eri*heral tissue beds. +ut the *resence of a
*lethysmogra*h wa&eform on *ulse oEimetry is *otentially
&aluable in detecting R!$, and *ulse oEimetry is useful to
ensure a**ro*riate oEygenation after R!$.
Arterial .lood /ases9rterial 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 tissueacidosis.222 Routine measurement of arterial blood gases
during (R has uncertain &alue Blass 55b, %! C.
#cocardiograpyNo 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@G22
5n addition, @ *ros*ecti&e studies22: 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&eR!$6 of the @>1 *atients from the @ studies, 21: had no
detectable cardiac acti&ity and only 2 of these had R!$ 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 AccessDuring cardiac arrest, *ro&ision of high3Luality (R and
ra*id defibrillation are of *rimary im*ortance and drugadministration 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 studies1@>,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 study1@4 the inter&al from first shoc# to administration of
an antiarrhythmic drug was a significant *redictor ofsur&i&al.
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!ne animal study2@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 Delivery5f 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.
$O Drug Delivery5! cannulation *ro&ides access to a noncolla*sible &enous
*leEus, enabling drug deli&ery similar to that achie&ed by
*eri*heral &enous access at com*arable doses. wo *ros*ec3
ti&e trials in children2@> and adults2@= and 4 other studies2@4 G
2>2 suggest that 5! access can be established efficiently is
safe and effecti&e for fluid resuscitation, drug deli&ery, and
blood sam*ling for laboratory e&aluation and is attainable in
all age grou*s. -owe&er, many of these studies were con3
ducted during normal *erfusion states or hy*o&olemic shoc#
or in animal models of cardiac arrest. 9lthough &irtually all
9%$ 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 inclinical 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 Deliveryhe 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*h3eral 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:,14 -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>G2=1 and
multi*le animal studies2=2G2=> ha&e shown that lido3
caine,2>:,2==
e*ine*hrine,2=4
atro*ine,2=
naloEone, and &aso3*ressin2=> 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
studies2=:,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 &asodila3tion. hese effects can be detrimental, causing hy*otension,
lower (( and flow, and reduced *otential for R!$. hus,
although endotracheal administration of some resuscitation
drugs is *ossible, 5I or 5! drug administration is *referred
because it will *ro&ide more *redictable drug deli&ery and
*harmacologic effect.
5n one nonrandomi/ed cohort study of out3of3hos*ital
cardiac arrest in adults240 using a randomi/ed control, 5I
administration of atro*ine and e*ine*hrine was associated
with a higher rate of R!$ 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 21T2
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
$tudies with e*ine*hrine24@
andlidocaine2=1 showed that dilution with sterile water instead of
0.M saline may achie&e better drug absor*tion.
Advanced Air$ayhere 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 cardiacarrest in *atients with witnessed IF7I.
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9d&antages of ad&anced airway *lacement include elimi3
nation of the need for *auses in chest com*ressions for
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rates of R!$ with 9%$ medications to be translated into
increased long3term sur&i&al remains to be determined.
%asopressorso 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*ressoragents is associated with an increased rate of R!$.
#pineprin
e*ine*hrine hydrochloride *roduces beneficial effects in
*atients during cardiac arrest, *rimarily because of its
3adrenergic rece*tor3stimulating Bie, &asoconstrictorC *ro*3
erties.24> he 3adrenergic effects of e*ine*hrine can increase
(( and cerebral *erfusion *ressure during (R. 24= he
&alue and safety of the 3adrenergic effects of e*ine*hrine
are contro&ersial because they may increase myocardial
wor# and reduce subendocardial *erfusion.244
here are no Rs that adeLuately com*are e*ine*hrinewith *lacebo in treatment of and outcomes related to out3of3
hos*ital cardiac arrest. 9 retros*ecti&e study24 com*ared
e*ine*hrine to no e*ine*hrine for sustained IF and (97
asystole and found im*ro&ed R!$ 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!$,
but none ha&e demonstrated a sur&i&al benefit of high3dose
e*ine*hrine &ersus standard3dose e*ine*hrine in cardiac
arrest.1@=,24:G22
5t is reasonable to consider administering a 1 mg dose of
5I75! e*ine*hrine e&ery @ to = minutes during adult cardiac
arrest Blass 55b, %! 9C. -igher doses may be indicated to
treat s*ecific *roblems, such as a 3bloc#er or calcium
channel bloc#er o&erdose. -igher doses can also be consid3
ered if guided by hemodynamic monitoring such as arterial
relaEation HdiastolicJ *ressure or ((. 5f 5I75! access is
delayed or cannot be established, e*ine*hrine may be gi&en
endotracheally at a dose of 2 to 2.= mg.
&asopressinIaso*ressin is a nonadrenergic *eri*heral &asoconstrictor
that also causes coronary and renal &asoconstriction.2@
hree Rs and a meta3analysis of the trials2> G2 dem3
onstrated no difference in outcomes BR!$, sur&i&al to
discharge, or neurologic outcomeC with &aso*ressin B>0units 5IC &ersus e*ine*hrine B1 mgC as a first3line &aso3
*ressor in cardiac arrest. wo Rs2:,2 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.
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Oter &asopressorshere 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.
Amiodarone5I 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 *ara3medic administration of amiodarone B@00 mg1@> or = mg7#g1@4C
im*ro&ed hos*ital admission rates when com*ared with
administration of *lacebo1@> or 1.= mg7#g of lidocaine.1@4
9dditional studies2:@G2: 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 study2:: 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/ylalcoholC. 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 islimited eE*erience with amiodarone gi&en by this route.
0idocaine9 retros*ecti&e re&iew2: 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 I7IF, defined as I7IF 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
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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.= mg7#g 5I *ush may be administered at =3 to
103minute inter&als to a maEimum dose of @ mg7#g.
,agnesium Sul'atewo obser&ational studies20,21 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.21
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 $ym*tomatic +radycardia andachycardiaJ for additional information about management
of torsades de *ointes not associated with cardiac arrest.
hree Rs22G2> did not identify a significant benefit
from use of magnesium com*ared with *lacebo among
*atients with IF arrest in the *rehos*ital, intensi&e care unit,
and emergency de*artment setting, res*ecti&ely. hus, rou3
tine administration of magnesium sulfate in cardiac arrest is
not recommended Blass 555, %! 9C unless torsades de
*ointes is *resent.
7nterventions ot Recommended for Routine se)urin! Cardiac Arrest
Atropine9tro*ine sulfate re&erses cholinergic3mediated decreases in
heart rate and atrio&entricular nodal conduction. No *ros*ec3
ti&e controlled clinical trials ha&e eEamined the use of
atro*ine in asystole or bradycardic (9 cardiac arrest.
%ower3le&el clinical studies *ro&ide conflicting e&idence of
the benefit of routine use of atro*ine in cardiac arrest.@>,2=G@0>
here is no e&idence that atro*ine has detrimental effects
during bradycardic or asystolic cardiac arrest. 9&ailable
e&idence suggests that routine use of atro*ine during (9 or
asystole is unli#ely to ha&e a thera*eutic benefit Blass 55b,
%! +C. For this reason atro*ine has been remo&ed from the
cardiac arrest algorithm.
Sodium .icar%onateissue acidosis and resulting acidemia during cardiac arrest
and resuscitation are dynamic *rocesses resulting from no
blood flow during arrest and low blood flow during (R.
hese *rocesses are affected by the duration of cardiac arrest,
le&el of blood flow, and arterial oEygen content during (R.
Restoration of oEygen content with a**ro*riate &entilation
with oEygen, su**ort of some tissue *erfusion and some
cardiac out*ut with high3Luality chest com*ressions, then
ra*id R!$ are the mainstays of restoring acid3base balance
during cardiac arrest.
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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@0G@0 or found a relationshi*
with *oor outcome.@0>,@10G@12
here are few data to su**ort thera*y with buffers during
cardiac arrest. here is no e&idence that bicarbonate im*ro&esthe 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 $ituationsJC. -owe&er, routine use
of sodium bicarbonate is not recommended for *atients in
cardiac arrest Blass 555, %! +C. When bicarbonate is used
for s*ecial situations, an initial dose of 1 mL7#g is ty*ical.
Whene&er *ossible, bicarbonate thera*y should be guided by
the bicarbonate concentration or calculated base deficit ob3
tained from blood gas analysis or laboratory measurement. o
minimi/e the ris# of iatrogenically induced al#alosis, *ro&id3
ers should not attem*t com*lete correction of the calculated
base deficit. !ther nonG!23generating buffers such as car3
bicarb, -9", or tribonate ha&e shown *otential for mini3
mi/ing some ad&erse effects of sodium bicarbonate, including
!2 generation, hy*erosmolarity, hy*ernatremia, hy*oglyce3
mia, intracellular acidosis, myocardial acidosis, and Ho&er3
shootJ al#alosis.@1=G@1 +ut clinical eE*erience is greatly
limited and outcome studies are lac#ing.
Calcium$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 andout3of3hos*ital cardiac arrest is not recommended Blass 555,
%! +C.
)i%rinolysisFibrinolytic 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 standardthera*y. +ut 2 large clinical trials1::,@@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,
%! + see (art 12C.
$& )luidsNo *ublished human study directly com*ares the outcome of
routine 5I fluid administration to no fluid administration
during (R. "ost human and animal studies of fluid infusion
during (R did not ha&e a control grou*,@@2G@>@ and 2 animal
studies showed that normothermic fluid infusion during (R
caused a decrease in ((.@>> G@>4 5n addition to normothermic
fluid, hy*ertonic and chilled fluids ha&e been studied in
animal and small human studies without a sur&i&al bene3fit.@@2,@@>,@@4 G@@:,@>1G@>@ 5f cardiac arrest is associated with
eEtreme &olume losses, hy*o&olemic arrest should be sus3
*ected. hese *atients *resent with signs of circulatory shoc#
ad&ancing to (9. 5n these settings intra&ascular &olume
should be *rom*tly restored.
Pacin!lectric *acing is generally not effecti&e in cardiac arrest, and
no studies ha&e obser&ed a sur&i&al benefit from *acing in
cardiac arrest.@>G@=0 Eisting e&idence suggests that *acing
by transcutaneous, trans&enous, or transmyocardial means in
cardiac arrest does not im*ro&e the li#elihood of R!$ orsur&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 95umphe *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 *recordialthum* 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 thethum*.@=>,@=4G@41
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he *recordial thum* may be considered for termination
of witnessed monitored unstable &entricular tachyarrhyth3
mias when a defibrillator is not immediately r