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CardiacArrestSupplement
GeneralCPRprinciples
DuringlowbloodflowstatessuchasCPR,oxygendeliverytotheheartandbrainis
limitedbybloodflowratherthanbyarterialoxygencontent.Therefore,rescue
breathsarelessimportantthanchestcompressionsduringthefirstfewminutesof
resuscitationfromwitnessedcardiacarrestandcouldreduceCPRefficacydueto
interruptioninchestcompressions.
ForeveryminutewithoutCPRanddefibrillation,survivalratesdecreasebyupto
10%.Therefore,itisimportanttoavoidinterruptionsinchestcompressionsfor
greaterthan10seconds.Continuouscompressionswhilethedefibrillatoris
chargingisencouraged.
Intheabsenceofanadvancedairway,asynchronizedcompression–ventilationratio
of30:2isrecommendedatacompressionrateof100-120compressionsperminute.
ThefoundationofsuccessfulACLSishighqualityCPR,and,forVF/pulselessVT,
attempteddefibrillationwithminutesofcollapse.OtherACLStherapiessuchas
somemedicationsandadvancedairways,althoughassociatedwithanincreased
rateofreturnofspontaneouscirculation(ROSC),havenotbeenshowntoincrease
therateofsurvivaltohospitaldischarge.
Vascularaccess,drugdelivery,andadvancedairwayplacementshouldnotcause
significantinterruptionsinchestcompressionordelaydefibrillation.
CPRreminders:
- Pushhard(atleast5cmor2inches)andfast(100-120/min)andallow
completechestrecoil
- Minimizeinterruptionsincompressions(e.g.<10seconds)
- Avoidexcessiveventilation(eachbreathover1second,justenoughforthe
chesttorise)
- Rotatecompressorevery2minutes,orsooneriffatigued
- Ifnoadvancedairway,30:2compression-ventilationratio
Reference:
ACLS2015ProviderManual.
Neumar,R.,etal.2010AmericanHeartAssociationGuidelinesforCardiopulmonary
ResuscitationandEmergencyCardiovascularCare.Circulation2010(122):S729–
S767.
OriginalbyNataliaJaworska(2015).ReviewedbyAnthonySeto(2016).
CardiacArrestSupplement
Ventricularfibrillation/pulselessventriculartachycardia
PerformingCPRwhileadefibrillatorisreadiedforuseisstronglyrecommendedfor
allpatientsincardiacarrestduetoVForpulselessVT.Theshorterthetimeinterval
betweenthelastchestcompressionandshockdelivery,themorelikelytheshock
willbesuccessful.Rapiddefibrillationistheonlyrhythmspecifictherapybeyond
CPRthatincreasessurvivalinVF/pulselessVT.
HighqualityCPRisimportantinVFandpulselessVT.WhenVF/pulselessVTis
presentformorethanafewminutes,themyocardiumisdepletedofoxygenand
metabolicsubstrates.Abriefperiodofchestcompressionscandeliveroxygenand
energysubstratesand“unload”thevolume-overloadedrightventricle,increasing
thelikelihoodthataperfusingrhythmwillreturnaftershockdelivery.
Vasopressormedications,particularlyepinephrine,areadjunctstoCPRand
defibrillation.Thedoseofepinephrineduringcardiacarrestis1mgof1:10:000
epinephrineIVq3-5minutes.Thepeakeffectofanintravenous(IV)/intraosseous
(IO)vasopressorgivenasabolusdoseduringCPRisdelayedforatleast1to2
minutes.
Itshouldbenotedthatifashockresultsinaperfusingrhythm,abolusdoseof
vasopressoratanytimeduringthesubsequent2-minuteperiodofCPR(before
rhythmcheck)couldtheoreticallyhavedetrimentaleffectsoncardiovascular
stability.
Otherwise,amiodaroneisthefirst-lineantiarrhythmicagentgivenduringcardiac
arrestbecauseithasbeenclinicallyshowntoimprovetherateofROSCandhospital
admissioninadultswithrefractoryVF/pulselessVT.Amiodaronemaybe
consideredwhenVF/VTisunresponsivetoCPR,defibrillation,andvasopressor
therapy.
Reference:
Neumar,R.,etal.2010AmericanHeartAssociationGuidelinesforCardiopulmonary
ResuscitationandEmergencyCardiovascularCare.Circulation2010(122):S729–
S767.
OriginalbyNataliaJaworska(2015).ReviewedbyAnthonySeto(2016).
CardiacArrestSupplement
Asystole/PEA
Pulselesselectricalactivity(PEA)referstoanynon-perfusingrhythmthatisnot
ventricularfibrillationorventriculartachycardia.PEAisoftencausedbyreversible
conditionsandcanbetreatedsuccessfullyifthoseconditionsareidentifiedand
corrected.The5HsandTsshouldbeparticularlyconsideredwiththisrhythm.
GiventhepotentialassociationofPEAwithhypoxemia,placementofanadvanced
airwayistheoreticallymoreimportantthanduringVF/pulselessVTandmaybe
necessarytoachieveadequateoxygenationorventilation.
PEAcanalsobecausedbysepsis,hypovolemia,cardiactamponade,andrightheart
strainandobstructionincludingpulmonaryembolismandtensionpneumothorax.
Allofthesepotentialetiologiesshouldbeconsideredwhentreatingapatientwith
PEAarrest.
ThetwomostcommoncausesofPEAarehypovolemiaandhypoxia.
Asystoleisdefinedasevidenceofnounderlyingcardiacrhythm.Asystoleis
commonlytheend-stagerhythmthatfollowsprolongedVForPEA,andforthis
reason,theprognosisisgenerallymuchworse.
TreatmentofPEA/asystoleisbasedoneffectiveCPR,identificationofanunderlying
etiology,andtheadministrationofavasopressoragent,typicallyepinephrine.A
vasopressorcanbegivenassoonasfeasiblewiththeprimarygoalofincreasing
myocardialandcerebralbloodflowduringCPRandachievingROSC.
Atropinehasbeenproventobeineffectiveandhasthereforebeenremovedfrom
theACLSalgorithm.
Reference:
ACLS2015ProviderManual.
Neumar,R.,etal.2010AmericanHeartAssociationGuidelinesforCardiopulmonary
ResuscitationandEmergencyCardiovascularCare.Circulation2010(122):S729–
S767.
OriginalbyNataliaJaworska(2015).ReviewedbyAnthonySeto(2016).
CardiacArrestSupplement
Primarysurvey
Assessresponsiveness(speakloudly,gentlyshakepatientifnotrauma)
Callforhelp/crashcartifunresponsive.
IV,O2,monitors!AssesstheABCs.IfyoufindsomethingatoneoftheABCs,stopand
completethenecessarytasktoresolvetheissuebeforecontinuingwiththeprimary
survey.
AssesstheABCs:
• Airway
o Checkforapatentairway.Ifthepatientistalking,theairwayis
patent.Assesstoensurethereisnostridororothersignsof
obstruction.
• Breathing
o Assesstheoxygensaturation,workofbreathing,trachealdeviation.
• Circulation
o Checkpulse.Ifpulseless,beginchestcompressionsat100-120/min,
30:2ratio.
SecondarySurvey
Atthistime,ifthepatientisstablethenyoucangetfurtherinformationusingthe
SAMPLEmnemonic(Signsandsymptoms,Allergies,Medications,Pastmedical
history,Lastmeal,andEventsprior)
Anotherpartofthesecondarysurveyisrecheckingthevitals,toensurethepatient
isstillstableandtoaddressanychanges.
Ifpatientisstable,continuewithahead-to-toeexam.
OriginalbyNataliaJaworska(2015).ReviewedbyAnthonySeto(2016).