Endorsement af ERC´s afsnit om hjertestop hos gravide:

Endorsement af ERC´s afsnit om hjertestop hos gravide:

Truhlář A, Deakin CD, Soar J et al. European Resuscitation Council Guidelines for Resuscitation 2015:

Section 4. Cardiac arrest in special circumstances. Resuscitation. 2015 Oct; 95:148-201.

Af DASAIM´s Obstetrisk anæstesiudvalg maj 2020

Fysiologiske ændringer under graviditeten:

• Øget blodvolumen og cardiac output

• Øget minutventilation og ilt-forbrug

• Kompression af v. cava inferior kan medføre nedsat cardiac output og blodtryk

• Ødem af øvre luftveje

• Refluks

Hyppigste direkte årsager til død under graviditeten i I-lande:

• Blødning

• Emboli (trombotisk el amnion-)

• Hypertensive tilstande (herunder præeclampsi),

• Abort

• Sepsis

Tilgang til den kritisk syge gravide:

• Generel brug af ABCDE

• Venstre sideleje el. manuel displacering af uterus mod venstre

• Iltterapi vejledt af saturationsmåling

• Giv væskebolus ved hypotension eller tegn på hypovolæmi

• Reevaluer indikation for evt. medicin

• Tidligt tilsyn af pædiater og obstetriker

• Aggressiv behandling af til grundlæggende årsag

Basal hjerte-lungeredning ved hjertestop:

• Pædiater og obstetriker kaldes tidligt

• Kompressioner og ventilationer iflg. standard 30:2

• Høj kvalitet af hjertemassagen med minimale afbrydelser

• Evt. kompressioner højere på sternum sidst i graviditeten

• Cava-kompression aflastes med manuel displacering af uterus mod venstre

• Om muligt 15-30 graders venstre tilt

• Forbered perimortem sectio

Avanceret behandling af hjertestop modificeret hos gravide:

• Defibrillering efter gældende voksne retningslinjer

• Evt. tidlig intubation grundet aspirationsrisiko og øget intraabdominalt tryk

• Endotrachealtube 0,5-1 mm ID mindre end til ikke-gravid grundet luftvejsødemer

• Grundet risiko for vanskelig intubation kan opstå behov for ekspert-hjælp, nød- procedure og alternativt luftvejsudstyr

• Om muligt i.v. anlæggelse over v. cava inf.

• Reversible årsager: I tillæg til ”4 H´er og 4 T´er” overvejes:

o Blødning: Overvej infusionssystem til hurtig blodtransfusion og brug af auto- transfusion (cell salvage)

o AMI: Overvej reperfusionsbehandling med PCI el. trombolyse o Peripartum kardiomypati

o Lungeemboli: Overvej trombolyse. Amnion emboli behandles derimod understøttende

o Præeklampsi/ eklampsi: Magnesiumsulfat som krampeprofylakse og - behandling

• Perimortem sectio efter 20. graviditetsuge:

o Indiceret inden 5 minutters hjertestop mhp. maximal cavaaflastning o 20.-23.uge: Barnets overlevelse usandsynlig

o ≥ 24. uge: Barnets overlevelse mulig

Avanceret behandling efter hjertestop: Ingen modifikationer i forhold til ikke-gravide

Anbefalede organisatoriske tiltag:

• Planer for og udstyr til maternel og neonatal genoplivning

• Tidlig alarmering af obstetriske, pædiatriske og anæstesiologiske teams

• Regelmæssig træning i akutte obstetriske situationer

ContentslistsavailableatScienceDirect

Resuscitation

j o ur na l h o me p a g e:ww w . e l s e v i er . c o m / l o c a t e / r e s u s c i t a t i o n

European Resuscitation Council Guidelines for Resuscitation 2015 Section 4. Cardiac arrest in special circumstances

Anatolij Truhláˇr

, Charles D. Deakin

, Jasmeet Soar

, Gamal Eldin Abbas Khalifa

, Annette Alfonzo

, Joost J.L.M. Bierens

, Guttorm Brattebø

, Hermann Brugger

, Joel Dunning

, Silvija Hunyadi-Antiˇcevi ´c

, Rudolph W. Koster

, David J. Lockey

, Carsten Lott

, Peter Paal

, Gavin D. Perkins

, Claudio Sandroni

, Karl-Christian Thies

, David A. Zideman

, Jerry P. Nolan

, on behalf of the Cardiac arrest in special

circumstances section Collaborators

aEmergencyMedicalServicesoftheHradecKrálovéRegion,HradecKrálové,CzechRepublic

bDepartmentofAnaesthesiologyandIntensiveCareMedicine,UniversityHospitalHradecKrálové,HradecKrálové,CzechRepublic

cCardiacAnaesthesiaandCardiacIntensiveCare,NIHRSouthamptonRespiratoryBiomedicalResearchUnit,SouthamptonUniversityHospitalNHSTrust, Southampton,UK

dAnaesthesiaandIntensiveCareMedicine,SouthmeadHospital,NorthBristolNHSTrust,Bristol,UK

eEmergencyandDisasterMedicine,SixOctoberUniversityHospital,Cairo,Egypt

fDepartmentsofRenalandInternalMedicine,VictoriaHospital,Kirkcaldy,Fife,UK

gSocietytoRescuePeoplefromDrowning,Amsterdam,TheNetherlands

hBergenEmergencyMedicalServices,DepartmentofAnaesthesiaandIntensiveCare,HaukelandUniversityHospital,Bergen,Norway

iEURACInstituteofMountainEmergencyMedicine,Bozen,Italy

jDepartmentofCardiothoracicSurgery,JamesCookUniversityHospital,Middlesbrough,UK

kCenterforEmergencyMedicine,ClinicalHospitalCenterZagreb,Zagreb,Croatia

lDepartmentofCardiology,AcademicMedicalCenter,Amsterdam,TheNetherlands

mIntensiveCareMedicineandAnaesthesia,SouthmeadHospital,NorthBristolNHSTrust,Bristol,UK

nDepartmentofAnesthesiology,UniversityMedicalCenter,JohannesGutenberg-Universitaet,Mainz,Germany

oBartsHeartCentre,StBartholomew’sHospital,BartsHealthNHSTrust,QueenMaryUniversityofLondon,London,UK

pDepartmentofAnaesthesiologyandCriticalCareMedicine,UniversityHospitalInnsbruck,Austria

qWarwickMedicalSchool,UniversityofWarwick,Coventry,UK

rCriticalCareUnit,HeartofEnglandNHSFoundationTrust,Birmingham,UK

sDepartmentofAnaesthesiologyandIntensiveCare,CatholicUniversitySchoolofMedicine,Rome,Italy

tBirminghamChildren’sHospital,Birmingham,UK

uDepartmentofAnaesthetics,ImperialCollegeHealthcareNHSTrust,London,UK

vAnaesthesiaandIntensiveCareMedicine,RoyalUnitedHospital,Bath,UK

wSchoolofClinicalSciences,UniversityofBristol,UK

Introduction

Irrespectiveofthecauseofcardiacarrest,earlyrecognitionand callingforhelp,includingappropriatemanagementofthedeteri- oratingpatient,earlydefibrillation,high-qualitycardiopulmonary resuscitation(CPR)withminimalinterruptionofchestcompres- sionsandtreatmentofreversiblecauses,arethemostimportant interventions.

In certain conditions, however, advanced life support (ALS) guidelinesrequiremodification.Thefollowingguidelinesforresus- citation in special circumstances are divided into three parts:

∗Correspondingauthor.

E-mailaddress:anatolij.truhlar@gmail.com(A.Truhláˇr).

1 ThemembersoftheCardiacarrestinspecialcircumstancessectionCollaborators arelistedintheCollaboratorssection.

special causes, special environments and special patients. The firstpartcoverstreatmentofpotentiallyreversiblecausesofcar- diacarrest,forwhich specifictreatmentexists,andwhichmust beidentified orexcluded duringanyresuscitation. For improv- ingrecallduringALS,thesearedividedintotwogroupsoffour, based upon theirinitialletter –either H or T– and arecalled the‘4Hsand4Ts’:Hypoxia;Hypo-/hyperkalaemiaandotherelec- trolyte disorders; Hypo-/hyperthermia; Hypovolaemia; Tension pneumothorax;Tamponade(cardiac);Thrombosis(coronaryand pulmonary);Toxins(poisoning). Thesecondpartcoverscardiac arrestinspecial environments,whereuniversalguidelineshave tobemodifiedduetospecificlocationsorlocation-specificcauses ofcardiacarrest.Thethirdpartisfocusedonpatientswithspe- cificconditions,and thosewithcertainlong-termcomorbidities whereamodifiedapproachanddifferenttreatmentdecisionsmay benecessary.

http://dx.doi.org/10.1016/j.resuscitation.2015.07.017

0300-9572/©2015EuropeanResuscitationCouncil.PublishedbyElsevierIrelandLtd.Allrightsreserved.

Summaryofchangessince2010Guidelines

ThemainchangesintheERCGuidelines2015incomparison withtheGuidelines2010¹aresummarisedbelow:

Specialcauses

•Survivalafteranasphyxia-inducedcardiacarrestisrareandsur- vivorsoftenhavesevereneurologicalimpairment.DuringCPR, earlyeffectiveventilationofthelungswithsupplementaryoxy- genisessential.

•Ahighdegreeofclinicalsuspicionandaggressivetreatmentcan preventcardiacarrestfromelectrolyteabnormalities.Thenew algorithmprovidesclinicalguidancetoemergencytreatmentof life-threateninghyperkalaemia.

•Hypothermic patients without signs of cardiac instability (systolic blood pressure ≥90mmHg, absence of ventricular arrhythmiasorcoretemperature≥28^◦C)canberewarmedexter- nallyusingminimallyinvasivetechniques(e.g.withwarmforced airandwarmintravenousfluid).Patientswithsignsofcardiac instabilityshouldbetransferreddirectlytoacentrecapableof extracorporeallifesupport(ECLS).

•Earlyrecognitionandimmediatetreatmentwithintramuscular adrenalineremains the mainstayof emergency treatmentfor anaphylaxis.

•Themortalityfromtraumaticcardiacarrest(TCA)isveryhigh.

Themostcommoncauseofdeathishaemorrhage.Itisrecognised thatmostsurvivorsdonothavehypovolaemia,butinsteadhave otherreversiblecauses(hypoxia,tensionpneumothorax,cardiac tamponade)thatmustbeimmediatelytreated.Thenewtreat- mentalgorithmforTCAwasdevelopedtoprioritisethesequence oflife-savingmeasures.Chestcompressionsshouldnotdelaythe treatmentofreversiblecauses.Cardiacarrestsofnon-traumatic originleadingtoasecondarytraumaticeventshouldberecog- nisedandtreatedwithstandardalgorithms.

•Thereislimitedevidenceforrecommendingtheroutinetrans- portofpatientswithcontinuingCPRafterout-of-hospitalcardiac arrest(OHCA)ofsuspectedcardiacorigin.Transportmaybeben- eficialin selectedpatientswhere there is immediatehospital accessto thecatheterisation laboratoryand an infrastructure providing prehospital and in-hospital teams experienced in mechanicalorhaemodynamicsupportandpercutaneouscoro- naryintervention(PCI)withongoingCPR.

•Recommendationsforadministrationoffibrinolyticswhenpul- monaryembolismisthesuspectedcauseofcardiacarrestremain unchanged.Routineuseofsurgicalembolectomyormechani- calthrombectomywhenpulmonaryembolismisthesuspected cause of cardiac arrest is not recommended. Consider these methodsonlywhenthere isaknowndiagnosisofpulmonary embolism.

•Routineuseofgastriclavageforgastrointestinaldecontamina- tioninpoisoningisnolongerrecommended.Reducedemphasis isplacedonhyperbaricoxygentherapyincarbonmonoxidepoi- soning.

Specialenvironments

•Thespecialenvironmentssectionincludesrecommendationsfor treatmentofcardiacarrestoccurringinspecificlocations.These locationsarespecialisedhealthcarefacilities(e.g.operatingthe- atre,cardiac surgery, catheterisation laboratory, dialysis unit, dentalsurgery),commercialairplanesorairambulances,fieldof play,outsideenvironment(e.g.drowning,difficultterrain,high altitude,avalancheburial,lightningstrikeandelectricalinjuries) orthesceneofamasscasualtyincident.

•Patientsundergoingsurgicalproceduresinvolvinggeneralanaes- thesia,particularlyinemergencies,areatriskfromperioperative

cardiacarrest.Anewsectioncoversthecommoncausesandrel- evantmodificationtoresuscitativeproceduresinthisgroupof patients.

•Cardiacarrestfollowingmajorcardiacsurgeryisrelativelycom- monintheimmediatepost-operativephase.Keytosuccessful resuscitationisrecognitionoftheneedtoperformemergency resternotomy,especially inthecontext oftamponadeor hae- morrhage,whereexternalchestcompressionsmaybeineffective.

Resternotomyshouldbeperformedwithin5minifotherinter- ventionshavefailed.

•Cardiacarrestfromshockablerhythms(VentricularFibrillation (VF) or pulseless Ventricular Tachycardia (pVT)) during car- diaccatheterisationshouldimmediatelybetreatedwithupto three stacked shocks beforestarting chest compressions. Use ofmechanicalchestcompressiondevicesduringangiographyis recommendedtoensure high-qualitychestcompressionsand reducetheradiation burdentopersonnel duringangiography withongoingCPR.

•Indentalsurgery,donotmovethepatientfromthedentalchair inordertostartCPR.Quicklyreclinethedentalchairintoahor- izontalpositionandplaceastoolundertheheadofthechairto increaseitsstabilityduringCPR.

•Thein-flightuseofAEDsaboardcommercialairplanescanresult inupto50%survivaltohospitaldischarge.AEDsandappropriate CPRequipmentshouldbemandatoryonboardofallcommer- cialaircraftinEurope,includingregionalandlow-costcarriers.

Consideranover-the-headtechniqueofCPRifrestrictedaccess precludesaconventionalmethod,e.g.intheaisle.

•Theincidenceofcardiacarrestonboardhelicopteremergency medicalservices(HEMS)andairambulancesislow.Importance ofpre-flightpreparationanduseofmechanicalchestcompres- siondevicesareemphasised.

•Suddenandunexpectedcollapseofanathleteonthefieldofplay islikelytobecardiacinoriginandrequiresrapidrecognitionand earlydefibrillation.

•Theduration of submersionis a key determinantofoutcome fromdrowning.Submersionexceeding10minisassociatedwith pooroutcome.Bystandersplayacriticalroleinearlyrescueand resuscitation.Resuscitationstrategiesforthoseinrespiratoryor cardiacarrestcontinuetoprioritiseoxygenationandventilation.

•The chances of good outcome from cardiac arrest in diffi- cultterrainormountains maybereduced becauseof delayed access andprolonged transport. Thereis a recognisedrole of airrescueandavailabilityofAEDsinremotebutoften-visited locations.

•The cut-off criteria for prolonged CPR and extracorporeal rewarming of avalanche victims in cardiac arrest are more stringenttoreducethenumberoffutilecasestreatedwithextra- corpoereallifesupport(ECLS).ECLSisindicatediftheduration ofburialis >60min(instead of>35min),coretemperatureat extricationis <30^◦C (insteadof <32^◦C),and serumpotassium athospitaladmissionis≤8mmolL⁻¹(insteadof≤12mmolL⁻¹);

otherwisestandardguidelinesapply.

•SafetymeasuresareemphasisedwhenprovidingCPRtothevic- timofanelectricalinjury.

•Recommendationsformanagementofmultiplevictimsshould preventdelayoftreatmentavailableforsalvageablevictimsdur- ingmasscasualtyincidents(MCIs).Safetyatsceneisparamount.

Atriagesystemshouldbeusedtoprioritisetreatmentand,ifthe numberofcasualtiesoverwhelmshealthcareresources,withhold CPRforthosewithoutsignsoflife.

Specialpatients

•The section on special patients gives guidance for CPR in patientswithseverecomorbidities(asthma,heartfailurewith

ventricular assist devices, neurological disease, obesity) and thosewithspecificphysiologicalconditions(pregnancy,elderly people).

•Thefirstlinetreatmentforacuteasthmaisinhaledbeta-2ago- nistswhileintravenousbeta-2agonistsaresuggestedonlyfor thosepatientsinwhominhaledtherapycannotbeusedreliably.

Inhaledmagnesiumisnolongerrecommended.

•Inpatientswithventricularassistdevices(VADs),confirmation ofcardiacarrestmaybedifficult.Ifduringthefirst10daysafter surgery,cardiacarrestdoesnotrespondtodefibrillation,perform resternotomyimmediately.

•PatientswithsubarachnoidhaemorrhagemayhaveECGchanges thatsuggestanacutecoronarysyndrome(ACS).Whetheracom- putedtomography(CT)brainscanisdonebeforeoraftercoronary angiographywilldependonclinical judgementregarding the likelihoodofasubarachnoidhaemorrhageversusacutecoronary syndrome.

•Nochangestothesequenceofactionsarerecommendedinresus- citationofobesepatients,althoughdeliveryofeffectiveCPRmay bechallenging.Considerchangingrescuersmorefrequentlythan thestandard2-mininterval.Earlytrachealintubationbyanexpe- riencedproviderisrecommended.

•Forthepregnantwomanincardiacarrest,high-qualityCPRwith manualuterinedisplacement,earlyALSanddeliveryofthefetus ifearlyreturnofspontaneouscirculation(ROSC)isnotachieved remainkeyinterventions.

A–SPECIALCAUSES Hypoxia

Introduction

Cardiacarrestcausedbypurehypoxaemiaisuncommon.Itis seenmorecommonlyasaconsequenceofasphyxia,whichaccounts formostofthenon-cardiaccausesofcardiacarrest.Therearemany causesof asphyxialcardiacarrest(Table4.1); althoughthere is usuallya combinationof hypoxaemiaand hypercarbia,it isthe hypoxaemiathatultimatelycausescardiacarrest.²

Pathophysiologicalmechanisms

Ifbreathingiscompletelypreventedbyairwayobstructionor apnoea, consciousness will be lost when oxygen saturation in thearterial blood reachesabout 60%. The time taken toreach thisconcentrationisdifficulttopredict,butislikelytobeofthe order 1–2min.³ Based onanimal experiments of cardiac arrest causedbyasphyxia,pulselesselectricalactivity(PEA)willoccur in3–11min.Asystolewillensueseveralminuteslater.⁴Incompar- isonwithsimpleapnoea,theexaggeratedrespiratorymovements thatfrequentlyaccompanyairwayobstructionwillincreaseoxy- genconsumption resultingin morerapid arterialbloodoxygen desaturationand a shorter time tocardiac arrest. Accordingto Table4.1

Causesofasphyxialcardiacarrest

Airwayobstruction:softtissues(coma),laryngospasm,aspiration Anaemia

Asthma Avalancheburial

Centralhypoventilation–brainorspinalcordinjury Chronicobstructivepulmonarydisease

Drowning Hanging Highaltitude

Impairedalveolarventilationfromneuromusculardisease Pneumonia

Tensionpneumothorax Trauma

Traumaticasphyxiaorcompressionasphyxia(e.g.crowdcrush)

Safar,completeairwayobstructionafterbreathingairwillresult inPEAcardiacarrestin5–10min.²VFisrarelythefirstmonitored rhythmafterasphyxialcardiacarrest–inoneofthelargestseriesof hanging-associatedout-of-hospitalcardiacarrests(OHCAs),from Melbourne,Australia,just7(0.5%)of1321patientswereinVF.⁵ Treatment

Treatingthecauseoftheasphyxia/hypoxaemiaisthehighest prioritybecausethisisapotentiallyreversiblecauseofthecar- diacarrest.Effectiveventilationwithsupplementaryoxygenisa particularpriorityinthesepatients.ThebetteroutcomesforOHCA victimsreceivingcompression-onlyCPR⁶isnotthecaseforasphyx- ialcardiac arrests,which have much better survival rates with conventionalCPR.⁷FollowthestandardALSalgorithmwhenresus- citatingthesepatients.

Outcome

Survivalaftercardiacarrestfromasphyxiaisrareandmostsur- vivorssustainsevereneurologicalinjury.Offivepublishedseries thatincludedatotal of286patientswithcardiacarrest follow- ing hanging where CPR wasattempted (this wasattempted in onlyabout16%ofcases),therewerejustsix(2%)survivorswith afullrecovery;11othersurvivorsallhadseverepermanentbrain injury.^5,8–11Inonethird(89;31%)ofthese286patients,rescuers wereabletoachieveROSC–thuswhenCPRisattempted,ROSC is notuncommonbut subsequentneurologicallyintact survival israre.Thosewhoareunconsciousbuthavenotprogressedtoa cardiacarrestaremuchmorelikelytomakeagoodneurological recovery.^11,12

Hypo-/hyperkalaemiaandotherelectrolytedisorders

Introduction

Electrolyte abnormalities can cause cardiac arrhythmias or cardiacarrest.Life-threateningarrhythmias areassociatedmost commonlywithpotassiumdisorders,particularlyhyperkalaemia, and less commonly with disorders of serum calcium and magnesium.Consider electrolytedisturbancesin patientgroups atrisk–renalfailure,severeburns,cardiacfailureanddiabetes mellitus.

Theelectrolyte values for definitions havebeen chosenas a guidetoclinicaldecision-making.Theprecisevaluesthattrigger treatmentdecisionswilldependonthepatient’sclinicalcondition andrateofchangeofelectrolytevalues.Thereislittleornoevi- denceforthetreatmentofelectrolyteabnormalitiesduringcardiac arrest.Guidanceduringcardiacarrest isbasedonthestrategies usedinthenon-arrestpatient.

Preventionofelectrolytedisorders

Whenpossible,identifyandtreat life-threateningelectrolyte abnormalitiesbeforecardiacarrestoccurs.Monitorrenalfunction inpatientsatriskandavoidcombinationofdrugsthatmayexac- erbatehyperkalaemia.Preventrecurrenceofelectrolytedisorders byremovinganyprecipitatingfactors(e.g.drugs,diet).

Potassiumdisorders

Potassium homeostasis. Extracellularpotassium concentration is regulated tightly between 3.5 and 5.0mmolL⁻¹. A large con- centration gradient normally exists between intracellular and extracellularfluidcompartments.Thispotassiumgradientacross cellmembranescontributestotheexcitabilityofnerveandmuscle cells,includingthemyocardium.Evaluationofserumpotassium musttakeintoconsiderationtheeffectsofchangesinserumpH.

WhenserumpHdecreases(acidaemia),serumpotassiumincreases becausepotassiumshiftsfromthecellulartothevascularspace;a processthatisreversedwhenserumpHincreases(alkalaemia).

Hyperkalaemia. Thisisthemostcommonelectrolytedisorderasso- ciatedwithcardiacarrest.Itisusuallycausedbyimpairedexcretion bythekidneys,drugsorincreasedpotassiumrelease fromcells and metabolic acidosis. Hyperkalaemia occurs in up to 10% of hospitalisedpatients.^13–15 Chronickidneydisease(CKD)iscom- moninthegeneralpopulationandtheincidenceofhyperkalaemia increasesfrom2to42%asglomerularfiltrationrate(GFR)drops from60to20mLmin⁻¹.¹⁶ Patientswithend-stagerenaldisease areparticularlysusceptible,particularlyfollowinganOHCA.¹⁷Pro- longedhyperkalaemiaisanindependentriskfactorforin-hospital mortality.¹⁸ Acute hyperkalaemia is more likely than chronic hyperkalaemia tocause life-threatening cardiac arrhythmias or cardiacarrest.

Definition. Thereisnouniversaldefinition.Wehavedefined hyperkalaemiaasa serumpotassiumconcentrationhigherthan 5.5mmolL⁻¹; inpractice,hyperkalaemiais acontinuum.Asthe potassium concentration increases above this value the risk of adverse events increases and the need for urgent treatment increases.Severehyperkalaemiahasbeendefinedasaserumpotas- siumconcentrationhigherthan6.5mmolL⁻¹.

Causes. Themaincausesofhyperkalaemiaare:

•renalfailure(i.e.acutekidneyinjuryorchronickidneydisease);

•drugs (e.g. angiotensin converting enzyme inhibitors (ACE-I), angiotensin II receptor antagonists (ARB), potassium-sparing diuretics,non-steroidalanti-inflammatorydrugs,beta-blockers, trimethoprim);

•tissuebreakdown(e.g.rhabdomyolysis,tumourlysis,haemoly- sis);

•metabolicacidosis(e.g.renalfailure,diabeticketoacidosis);

•endocrinedisorders(e.g.Addison’sdisease);

•diet(maybesolecauseinpatientswithadvancedchronickidney disease)and

•spurious–pseudo-hyperkalaemia(suspectincaseswithnormal renalfunction,normalECGand/orhistoryofhaematologicaldis- order).Pseudo-hyperkalaemiadescribesthefindingofaraised serum (clotted blood) K⁺ value concurrently with a normal plasma(non-clottedblood)potassiumvalue.Theclottingprocess releasesK⁺fromcellsandplatelets,whichincreasestheserum K⁺concentrationbyanaverageof0.4mmol/L.Themostcommon causeofpseudo-hyperkalaemiaisaprolongedtransittimetothe laboratoryorpoorstorageconditions.^19,20

The risk of hyperkalaemia is even greater when there is a combinationoffactorssuchastheconcomitantuseofangiotensin- convertingenzymeinhibitorsorangiotensinIIreceptorblockers andpotassium-sparingdiuretics.

Recognition of hyperkalaemia. Exclude hyperkalaemia in all patientswithanarrhythmiaorcardiacarrest.Patientsmaypresent withweaknessprogressing toflaccid paralysis,paraesthesia,or depresseddeeptendonreflexes.Alternatively,theclinicalpicture can be overshadowed by the primary illness causing hyper- kalaemia.The firstindicator ofhyperkalaemia may alsobethe presenceofECGabnormalities,arrhythmias,orcardiacarrest.The useofabloodgasanalysertomeasurepotassiumcanreducedelays inrecognition.^21,22

TheeffectofhyperkalaemiaontheECGdependsontheabso- luteserumpotassiumaswellastherateofincrease.²³Thereported frequencyofECGchangesinseverehyperkalaemiaisvariable,but mostpatientsappeartoshowECGabnormalitiesataserumpotas- siumconcentrationhigherthan6.7mmolL⁻¹.^23,24Thepresenceof ECGchangesstronglycorrelateswithmortality.²⁵Insomecases, theECG maybenormal orshowatypical changes includingST elevation.

TheECG changes associated withhyperkalaemiaare usually progressiveandinclude:

•firstdegreeheartblock(prolongedPRinterval>0.2s);

•flattenedorabsentPwaves;

•tall,peaked(tented)Twaves(i.e.TwavelargerthanRwavein morethan1lead);

•ST-segmentdepression;

•S&Twavemerging(sinewavepattern);

•widenedQRS(>0.12s);

•ventriculartachycardia;

•bradycardia;

•cardiacarrest(PEA,VF/pVT,asystole).

Treatment of hyperkalaemia. There are five key treatment strategiesforhyperkalaemia²²:

•cardiacprotection;

•shiftingpotassiumintocells;

•removingpotassiumfromthebody;

•monitoringserumpotassiumandbloodglucose;

•preventionofrecurrence.

Whenhyperkalaemiaisstronglysuspected,e.g.inthepresence ofECGchanges,startlife-savingtreatmentevenbeforelaboratory resultsare available. The treatmentstrategy for hyperkalaemia hasbeenreviewedextensively.^13,22,26Followthehyperkalaemia emergency treatment algorithm (Fig. 4.1).²² Avoid salbutamol monotherapy,whichmaybeineffective.Thereisinsufficientevi- dencetosupporttheuseofsodiumbicarbonatetodecreaseserum potassium.Consider theneedforearlyspecialistorcriticalcare referral.

Themainrisksassociatedwithtreatmentofhyperkalaemiaare:

•Hypoglycaemia followinginsulin-glucose administration(usu- allyoccurswithin1–3hoftreatment,butmayoccurupto6h afterinfusion).²⁷Monitorbloodglucoseandtreathypoglycaemia promptly.

•Tissuenecrosissecondarytoextravasationofintravenouscal- ciumsalts.Ensuresecurevascularaccesspriortoadministration.

•Intestinal necrosis or obstruction following use of potassium exchangeresins.Avoidprolongeduseofresinsandgivelaxative.

•Reboundhyperkalaemiaaftertheeffectofdrugtreatmenthas wornoff(i.e.within4–6h).Continuetomonitorserumpotassium foraminimumof24hafteranepisode.

Patientnotincardiacarrest Assesspatient:

•UsesystematicABCDEapproachandcorrectanyabnormalities, obtainIVaccess.

•Checkserumpotassium.

•RecordanECG.

Monitorcardiacrhythminpatientswithseverehyperkalaemia.

Treatmentisdeterminedaccordingtoseverityofhyperkalaemia.

Approximate values are provided to guide treatment. Follow hyperkalaemiaemergencytreatmentalgorithm(Fig.4.1).

Mildelevation(5.5–5.9mmolL⁻¹).

•Addresscauseofhyperkalaemiatocorrectandavoidfurtherrise inserumpotassium(e.g.drugs,diet).

•If treatment is indicated, remove potassium from the body:

potassiumexchangeresins-calciumresonium15–30g,orsodium polystyrenesulfonate(Kayexalate)15–30g,giveneitherorallyor byretentionenema/PR(perrectum)(onsetin>4h).

Moderateelevation(6.0–6.4mmolL⁻¹)withoutECGchanges.

•Shift potassium intracellularly with glucose/insulin: 10 units short-actinginsulinand25gglucoseIVover15–30min(onset in15–30min;maximaleffectat30–60min;durationofaction 4–6h;monitorbloodglucose).

•Removepotassiumfromthebody(seeabove;considerdialysis guidedbyclinicalsetting).

Fig.4.1.Emergencytreatmentofhyperkalaemia.PRperrectum;ECGelectrocardiogram;VTventriculartachycardia.

ReproducedwithpermissionfromRenalAssociationandResuscitationCouncil(UK).

Severeelevation(≥6.5mmolL⁻¹)withoutECGchanges.

•Seekexperthelp.

•Giveglucose/insulin(seeabove).

•Givesalbutamol10–20mgnebulised(onsetin15–30min;dura- tionofaction4–6h).

•Removepotassiumfromthebody(considerdialysis).

Severeelevation(≥6.5mmolL⁻¹)withtoxicECGchanges.

•Seekexperthelp.

•Protect the heart with calcium chloride: 10mL 10% cal- cium chloride IV over 2–5min to antagonise the toxic effects of hyperkalaemia at the myocardial cell mem- brane. This protects the heart by reducing the risk of VF/pVT but does not lower serum potassium (onset in 1–3min).

•Useshiftingagents(glucose/insulinandsalbutamol).

•Removepotassiumfromthebody(considerdialysisatoutsetor ifrefractorytomedicaltreatment).

Modificationstocardiopulmonaryresuscitation. Thefollowing modificationstostandardALSguidelinesarerecommendedinthe presenceofseverehyperkalaemia:

•Confirmhyperkalaemiausingabloodgasanalyserifavailable.

•Protecttheheart:give10mLcalciumchloride10%IVbyrapid bolusinjection.

•Shiftpotassiumintocells:Giveglucose/insulin:10unitsshort- actinginsulin and 25gglucoseIV byrapid injection.Monitor bloodglucose.

•Givesodiumbicarbonate:50mmolIVbyrapidinjection(ifsevere acidosisorrenalfailure).

•Remove potassium from body: Consider dialysis for hyper- kalaemiccardiacarrestresistanttomedicaltreatment.Several dialysismodalitieshavebeenusedsafelyandeffectivelyincar- diacarrest,butthismayonlybeavailableinspecialistcentres.²⁸ Consideruseofamechanicalchestcompressiondeviceifpro- longedCPRisneeded.

Indications for dialysis. The main indications for dialysis in patientswithhyperkalaemiaare:

•severe life-threatening hyperkalaemia with or without ECG changesorarrhythmia;

•hyperkalaemiaresistanttomedicaltreatment;

•end-stagerenaldisease;

•oliguricacutekidneyinjury(<400mLday⁻¹urineoutput);

•markedtissuebreakdown(e.g.rhabdomyolysis).

Specialconsiderationsformanagement ofcardiacarrestin a dialysisunitareaddressedinthesectionSpecialenvironments(see cardiacarrestinadialysisunit).

Hypokalaemia. Hypokalaemiaisthemostcommonelectrolytedis- orderinclinicalpractice.²⁹Itisseeninupto20%ofhospitalised patients.³⁰Hypokalaemiaincreasestheincidenceofarrhythmias andsuddencardiacdeath(SCD).³¹Theriskisincreasedinpatients withpre-existingheartdiseaseandinthosetreatedwithdigoxin.

Definition. Hypokalaemiaisdefinedasaserumpotassiumlevel

<3.5mmolL⁻¹.Severehypokalaemiaisdefinedasaserumpotas- siumlevel<2.5mmolL⁻¹andmaybeassociatedwithsymptoms.

Causes. Themaincausesofhypokalaemiainclude:

•gastrointestinalloss(e.g.diarrhoea);

•drugs(e.g.diuretics,laxatives,steroids);

•renallosses(e.g.renaltubulardisorders,diabetesinsipidus,dial- ysis);

•endocrinedisorders (e.g.Cushing’s syndrome,hyperaldostero- nism);

•metabolicalkalosis;

•magnesiumdepletion;

•poordietaryintake.

Treatmentstrategiesusedforhyperkalaemiamayalsoinduce hypokalaemia.

Recognitionofhypokalaemia. Excludehypokalaemiainevery patientwithanarrhythmiaorcardiacarrest.Indialysispatients, hypokalaemiamayoccurattheendofahaemodialysissessionor duringtreatmentwithperitonealdialysis.

Asserumpotassium concentrationdecreases,thenervesand muscles are predominantly affected,causing fatigue, weakness, leg cramps, constipation. In severe cases (serum potassium

<2.5mmolL⁻¹),rhabdomyolysis,ascendingparalysisandrespira- torydifficultiesmayoccur.

ECGfeaturesofhypokalaemiaare:

•Uwaves;

•Twaveflattening;

•STsegmentchanges;

•arrhythmias,especiallyifpatientistakingdigoxin;

•cardiacarrest(PEA,VF/pVT,asystole).

Treatment. This depends on the severity of hypokalaemia and thepresenceof symptomsand ECG abnormalities.Gradual replacementofpotassiumispreferable,butinanemergency,intra- venous potassium is required. The maximumrecommended IV doseofpotassiumis 20mmolh⁻¹,but morerapidinfusion(e.g.

2mmolmin⁻¹for10min,followedby10mmolover5–10min)is indicatedforunstablearrhythmiaswhencardiacarrestisimmi- nent.ContinuousECGmonitoringisessentialduringIVinfusion andthedoseshouldbetitratedafterrepeatedsamplingofserum potassiumlevels.

Manypatientswhoarepotassiumdeficientarealsodeficient inmagnesium.Magnesiumisimportantforpotassiumuptakeand forthemaintenanceofintracellularpotassiumvalues,particularly inthemyocardium.Repletionofmagnesiumstoreswillfacilitate morerapid correctionofhypokalaemiaandis recommendedin severecasesofhypokalaemia.³²

Calciumandmagnesiumdisorders

Therecognitionandmanagementofcalciumandmagnesium disordersissummarisedinTable4.2.

Hypo-/hyperthermia

Accidentalhypothermia

Definition. Every year approximately 1500 people die of pri- maryaccidental hypothermia intheUnitedStates.³³ Accidental hypothermiaisdefinedasaninvoluntarydropofthebodycore temperature<35^◦C.TheSwissstagingsystemisusedtoestimate coretemperatureatthescene.Itsstagesarebasedonclinicalsigns, whichroughlycorrelatewiththecoretemperature:

•hypothermia I; mild hypothermia (conscious, shivering, core temperature35–32^◦C);

•hypothermiaII;moderatehypothermia(impairedconsciousness withoutshivering,coretemperature32–28^◦C);

•hypothermiaIII;severehypothermia(unconscious,vitalssigns present,coretemperature28–24^◦C);

•hypothermiaIV;cardiacarrestorlowflowstate(noorminimal vitalsigns,coretemperature<24^◦C);

•hypothermiaV;deathduetoirreversiblehypothermia(coretem- perature<13.7^◦C).³⁴

Diagnosis. Hypothermiaisdiagnosed inanypatientwitha core temperature<35^◦C,orwheremeasurementunavailable,ahistory of exposuretocold, orwhen thetrunkfeels cold.³³ Accidental hypothermiamaybeunder-diagnosedincountrieswithatemper- ateclimate.Whenthermoregulationisimpaired,forexample,in theelderlyandveryyoung,hypothermiamayfollowamildinsult.

Theriskofhypothermiaisincreasedbyalcoholordrugingestion, exhaustion, illness,injury or neglectespecially whenthere is a decreaseinthelevelofconsciousness.

Alow-readingthermometerisneededtomeasurethecoretem- peratureandconfirmthediagnosis.Thecoretemperatureinthe lower third of the oesophagus correlates wellwithheart tem- perature. Tympanic measurement usinga thermistor technique isareliablealternativebutmaybeconsiderablylowerthancore temperature if the environment is very cold, the probe is not wellinsulated,ortheexternalauditorycanalisfilledwithsnow orwater^35,36Widelyavailabletympanicthermometersbasedon infraredtechniquedonotsealtheearcanalandarenotdesignedfor lowcoretemperaturereadings.³⁷Thein-hospitalcoretemperature measurement site shouldbethesamethroughoutresuscitation andrewarming.Bladderandrectaltemperatureslagbehindcore temperature;^38,39 for this reason, measurement of bladder and

Table4.2

Calciumandmagnesiumdisorderswithassociatedclinicalpresentation,ECGmanifestationsandrecommendedtreatment

Disorder Causes Presentation ECG Treatment

Hypercalcaemia

Calcium>2.6mmolL⁻¹ Primaryortertiary hyperparathyroidism Malignancy Sarcoidosis Drugs

Confusion Weakness Abdominalpain Hypotension Arrhythmias Cardiacarrest

ShortQTinterval ProlongedQRSinterval FlatTwaves AVblock Cardiacarrest

FluidreplacementIV Furosemide1mgkg⁻¹IV Hydrocortisone200–300mgIV Pamidronate30–90mgIV Treatunderlyingcause

Hypocalcaemia

Calcium<2.1mmolL⁻¹ Chronicrenalfailure Acutepancreatitis Calciumchannelblocker overdose

Toxicshocksyndrome Rhabdomyolysis Tumourlysissyndrome

Paraesthesia Tetany Seizures AV-block Cardiacarrest

ProlongedQTinterval Twaveinversion Heartblock Cardiacarrest

Calciumchloride10%10–40mL Magnesiumsulphate50%

4–8mmol(ifnecessary)

Hypermagnesaemia

Magnesium>1.1mmolL⁻¹ Renalfailure Iatrogenic

Confusion Weakness

Respiratorydepression AV-block

Cardiacarrest

ProlongedPRandQT intervals

Twavepeaking AVblock Cardiacarrest

Considertreatmentwhen magnesium>1.75mmolL⁻¹ Calciumchloride10%5–10mL repeatedifnecessary Ventilatorysupportifnecessary Salinediuresis–0.9%salinewith furosemide1mgkg⁻¹IV Haemodialysis Hypomagnesaemia

Magnesium<0.6mmolL⁻¹ GIloss Polyuria Starvation Alcoholism Malabsorption

Tremor Ataxia Nystagmus Seizures

Arrhythmias–torsade depointes

Cardiacarrest

ProlongedPRandQT intervals

ST-segmentdepression T-waveinversion FlattenedPwaves IncreasedQRSduration Torsadedepointes

Severeorsymptomatic:2g50%

magnesiumsulphate(4mL;

8mmol)IVover15min Torsadedepointes:2g50%

magnesiumsulphate(4mL;

8mmol)IVover1–2min Seizure:2g50%magnesium sulphate(4mL;8mmol)IVover 10min

rectaltemperaturehasbeende-emphasisedinpatientswithsevere hypothermia.

Decisiontoresuscitate. Coolingofthehumanbodydecreasescel- lular oxygen consumption by about 6% per 1^◦C decrease in coretemperature.⁴⁰At28^◦C,oxygenconsumptionisreducedby approximately50%andat22^◦Cbyapproximately75%.At18^◦Cthe braincantoleratecardiacarrestforupto10timeslongerthanat 37^◦C.Thisresultsinhypothermiaexertingaprotectiveeffectonthe brainandheart,⁴¹andintactneurologicalrecoverymaybepossible evenafterprolongedcardiacarrestifdeephypothermiadevelops beforeasphyxia.

Bewareofdiagnosingdeathinahypothermicpatientbecause hypothermia itself may produce a very slow, small-volume, irregular pulse and unrecordable blood pressure. In a deeply hypothermicpatient(hypothermiaIV)signsoflifemaybesomini- malthatitiseasytooverlookthem.Therefore,lookforsignsoflife foratleast1minanduseanECGmonitortodetectanyelectrical cardiacactivity.Neurologicallyintactsurvivalhasbeenreported afterhypothermiccardiacarrestwithacoretemperatureaslowas 13.7^◦C⁴²andCPRforaslongassixandahalfhours.⁴³

IntermittentCPR,asrescueallows,mayalsobeofbenefit.⁴⁴If continuousCPRcannotbedelivered,apatientwithhypothermic cardiacarrestandacoretemperature<28^◦C(orunknown),should receive5minofCPR,alternatingwithperiods≤5minwithoutCPR.

Patientswithacoretemperature<20^◦C,shouldreceive5minof CPR,alternatingwithperiods≤10minwithoutCPR.⁴⁵

Intheprehospitalsetting,resuscitationshouldbewithheldin hypothermicpatientsonlyifthecauseofcardiacarrestisclearly attributabletoalethalinjury,fatalillness,prolongedasphyxia,or ifthechestisincompressible.⁴⁶Inallotherhypothermicpatients,

thetraditionalguidingprinciplethat‘nooneisdeaduntilwarm anddead’shouldbeconsidered.Inremoteareas,theimpracticali- tiesofachievingrewarminghavetobeconsidered.Inthehospital settinginvolveseniordoctorsanduseclinicaljudgementtodeter- minewhentostopresuscitatingahypothermicvictimincardiac arrest.

Modificationstocardiopulmonaryresuscitation

•Donotdelaycarefultrachealintubationwhenitisindicated.The advantagesofadequateoxygenationandprotectionfromaspi- rationoutweightheminimalriskoftriggeringVFbyperforming trachealintubation.⁴⁷

•Checkforsignsoflifeforupto1min.Palpateacentralarteryand assessthecardiacrhythm(ifECGmonitoravailable).Echocardi- ography,near-infraredspectroscopyorultrasoundwithDoppler maybeusedtoestablishwhetherthereis(anadequate)cardiac outputorperipheralbloodflow.^48,49Ifthereisanydoubt,start CPRimmediately.

•Hypothermiacancausestiffnessofthechestwall,makingven- tilationsand chestcompressionsdifficult.Considertheuseof mechanicalchestcompressiondevices.⁵⁰

•OnceCPRisunderway,confirmhypothermiawithalow-reading thermometer.

•The hypothermic heart may be unresponsive to cardioac- tivedrugs,attemptedelectricalpacinganddefibrillation.Drug metabolismisslowed,leadingtopotentiallytoxicplasmacon- centrationsofanydruggiven.⁵¹ Theevidencefor theefficacy of drugs in severe hypothermia is limited and based mainly onanimalstudies.Forinstance,inseverehypothermiccardiac arrest,theefficacyofamiodaroneisreduced.⁵²Adrenalinemay beeffectiveinincreasingcoronaryperfusionpressure,butnot

survival.^53,54Vasopressorsmayalsoincreasethechancesofsuc- cessfuldefibrillation,butwithacoretemperature<30^◦C,sinus rhythmoften degradesbackintoVF.Given that defibrillation andadrenalinemayinducemyocardialinjury, itisreasonable towithholdadrenaline,other CPRdrugs andshocksuntilthe patienthasbeenwarmedtoacoretemperature≥30^◦C.Once 30^◦Chasbeenreached,theintervalsbetweendrugdosesshould bedoubledwhen compared to normothermia(i.e.adrenaline every6–10min).Asnormothermia(≥35^◦C)isapproached,use standarddrugprotocols.

Treatmentof arrhythmias. As coretemperature decreases,sinus bradycardia tendstogive way toatrial fibrillationfollowed by VFand finallyasystole.^55,56 Arrhythmias otherthan VFtendto revertspontaneouslyascoretemperatureincreases,andusually donotrequireimmediatetreatment.Bradycardiaisphysiologicalin severehypothermia.Cardiacpacingisnotindicatedunlessbrady- cardiaassociatedwithhaemodynamiccompromisepersistsafter rewarming.Thetemperatureatwhichdefibrillationshouldfirstly beattempted,andhowoftenitshouldbeattemptedintheseverely hypothermicpatient,hasnotbeenestablished.IfVFisdetected, defibrillateaccordingtostandardprotocols.IfVFpersistsafterthree shocks,delayfurtherattemptsuntilcoretemperatureis≥30^◦C.⁵⁷ CPRandrewarmingmayhavetobecontinuedforseveralhoursto facilitatesuccessfuldefibrillation.

Insulation. Generalmeasuresforallvictimsincluderemovalfrom thecoldenvironment, preventionof furtherheatlossandrapid transfertohospital.⁵⁸Inthefield,apatientwithmoderateorsevere hypothermia(hypothermia≥II)shouldbeimmobilisedandhan- dledcarefully,oxygenatedadequately,monitored(includingECG andcoretemperature),andthewholebodydriedandinsulated.⁵¹ Removewetclotheswhileminimisingexcessivemovementof thevictim. Removalof wetclothing oruseof a vapour barrier seemstobeequallyeffectivetolimitheatloss.⁵⁹Consciousvic- tims(hypothermiaI)canmobiliseasexerciserewarmsaperson morerapidlythanshivering.⁶⁰Patientswillcontinuecoolingafter removalfromacoldenvironment(i.e.afterdrop),whichmayresult inalife-threateningdecreaseincoretemperaturetriggeringacar- diacarrestduringtransport(i.e.‘rescuedeath’).Prehospitally,avoid prolongedinvestigationsandtreatment,asfurtherheatlossisdiffi- culttoprevent.Patientswhostopshivering(e.g.hypothermiaII–IV, andsedatedoranaesthetisedpatients)willcoolfaster.

Prehospitalrewarming. Rewarmingmaybepassive,activeexternal, oractiveinternal.InhypothermiaIpassiverewarmingisappropri- ateaspatientsarestillabletoshiver.Passiverewarmingisbest achievedbyfullbodyinsulationwithwoolblankets,aluminium foil,capandawarmenvironment.InhypothermiaII–IVtheappli- cationofchemicalheatpackstothetrunkhasbeenrecommended.

Inconsciouspatientswhoareabletoshiver,thisimprovesthermal comfortbutdoesnotspeedrewarming.⁶¹Ifthepatientisuncon- sciousandtheairwayisnotsecured,arrangetheinsulationaround thepatientlyinginarecovery(lateraldecubitus)position.Rewarm- inginthefieldwithheatedintravenousfluidsandwarmhumidified gasesisnotfeasible.⁵¹Intensiveactiverewarmingmustnotdelay transport toa hospital where advanced rewarming techniques, continuousmonitoringandobservationareavailable.

Transport. Transport patients with hypothermia stage I to the nearesthospital.InhypothermiastageII–IV,signsofprehospital cardiacinstability(i.e.systolicbloodpressure<90mmHg,ventri- culararrhythmia,coretemperature<28^◦C)shoulddeterminethe choiceofadmittinghospital.Ifanysignsofcardiacinstabilityare present,transportthepatienttoanECLScentre,contactingthem wellinadvancetoensurethatthehospitalcanacceptthepatient

forextracorporealrewarming.InhypothermiaV,reasonsforwith- holdingorterminatingCPRshouldbeinvestigated(e.g.obvious signsofirreversibledeath,validDNAR,conditionsunsafeforres- cuer,avalancheburial≥60minandairwaypackedwithsnowand asystole).Intheabsenceofanyofthesesigns,startCPRandtransfer thepatienttoanECLScentre.

In-hospitalrewarming. Unless thepatient goesinto VF, rewarm using active external methods (i.e. with forced warm air) and minimallyinvasivelymethods(i.e.withwarmIVinfusions).With acoretemperature<32^◦C andpotassium <8mmolL⁻¹,consider ECLSrewarming.³³MostECLSrewarmingshavebeenperformed usingcardiopulmonarybypass, butmore recently,veno-arterial extracorporealmembraneoxygenation(VA-ECMO)hasbecomethe preferredmethodduetoitsrapidavailability,theneedforlessanti- coagulation,andthepotentialtoprolongcardiorespiratorysupport afterrewarming.

IfanECLScentreisnotavailable,rewarmingmaybeattempted inhospitalusingadedicatedteamandacombinationofexternal andinternalrewarming techniques(e.g.forcedwarmair,warm infusions,forcedperitoneallavage).⁶²

Continuous haemodynamic monitoring and warm IV fluids areessential.Patientswillrequirelargevolumesoffluidsduring rewarming,asvasodilationcausesexpansionoftheintravascular space.Avoidhyperthermiaduringandafterrewarming.OnceROSC hasbeenachievedusestandardpost-resuscitationcare.

Hyperthermia

Introduction. Hyperthermiaoccurswhenthebody’sabilitytother- moregulate fails and core temperature exceeds that normally maintainedby homeostaticmechanisms.Hyperthermiamay be exogenous,causedbyenvironmentalconditions,orsecondaryto endogenousheatproduction.

Environment-relatedhyperthermiaoccurswhereheat,usually intheformofradiantenergy,isabsorbedbythebodyataratefaster thancanbelostbythermoregulatorymechanisms.Hyperthermia isacontinuumofheat-relatedconditions,startingwithheatstress, progressingtoheatexhaustion,thentoheatstrokeandfinallyto multipleorgandysfunctionandcardiacarrest.⁶³

Malignant hyperthermia is a rare disorder of skeletal mus- clecalciumhomeostasischaracterisedbymusclecontractureand life-threateninghypermetaboliccrisisfollowingexposureofgenet- ically predisposed individuals to halogenated anaesthetics and depolarisingmusclerelaxants.^64,65

Heatexhaustion

Definition. Heatexhaustion isa non-life-threatening clinical syndromeofweakness,malaise,nausea,syncope,andothernon- specificsymptomscausedbyheatexposure.Thermoregulationis notimpaired.Heatexhaustioniscausedbywaterandelectrolyte imbalanceduetoheatexposure,withorwithoutexertion.Rarely, severeheatexhaustionafterphysicalexertionmaybecomplicated byrhabdomyolysis,myoglobinuria,acuterenalfailure,anddissem- inatedintravascularcoagulation(DIC).

Symptoms. Symptomsareoftenvague,andpatientsmaynot realisethatheatisthecause.Symptomsmayincludeweakness, dizziness,headache,nausea,andsometimesvomiting.Syncopedue tostandingforlongperiodsintheheat(heatsyncope)iscommon andmaymimiccardiovasculardisorders.Onexamination,patients appeartiredandareusuallysweatyandtachycardic.Mentalstatus istypicallynormal,unlikeinheatstroke.Temperatureisusually normaland,whenelevated,usuallydoesnotexceed40^◦C.

Diagnosis. Diagnosisisclinicalandrequiresexclusionofother possible causes (e.g. hypoglycaemia, acute coronary syndrome, infections).Laboratorytestingisrequiredonlyifneededtorule outotherdisorders.

Treatment

Fluidsandelectrolytereplacement. Treatmentinvolvesremov- ingpatientstoacoolenvironment,lyingthemflat,andgivingIV fluidsandelectrolytereplacementtherapy;oralrehydrationmay notbeeffectiveinrapidlyreplacingelectrolytes,butmaybeamore practicaltreatment.Rateandvolumeofrehydrationareguidedby age,underlyingdisorders, andclinicalresponse.Replacementof 1–2Lcrystalloidsat500mLh⁻¹ isoftenadequate.Externalcool- ingmeasuresareusuallynotrequired.Considerexternalcoolingin patientswithacoretemperatureof≥40^◦C.

Heatstroke

Definition. Heat stroke (HS) is defined as hyperthermia accompaniedbya systemic inflammatory response witha core temperature>40^◦C,accompaniedbymentalstatechangeandvary- inglevelsoforgandysfunction.⁶³

TherearetwoformsofHS:

1.Classic(non-exertional)heatstroke(CHS)occursduringhigh environmentaltemperaturesandofteneffectstheelderlyduring heatwaves.⁶⁶

2.Exertionalheat stroke (EHS) occurs during strenuous physi- calexercisein highenvironmentaltemperaturesand/orhigh humidityandusuallyeffectshealthyyoungadults.⁶⁷

Mortalityfromheatstrokerangesbetween10and50%.⁶⁸ Predisposing factors. The elderly are at increased risk for heat-related illness because of underlying illness, medication use, decliningthermoregulatorymechanisms and limited social support.Thereareseveralriskfactors:lackofacclimatisation,dehy- dration,obesity, alcohol,cardiovascular disease,skinconditions (psoriasis, eczema, scleroderma, burn, cystic fibrosis), hyper- thyroidism, phaeochromocytoma and drugs (anticholinergics, diamorphine, cocaine, amphetamine, phenothiazines, sympath- omimetics,calciumchannelblockers,beta-blockers).

Symptoms. Heat strokecan resembleseptic shockand may becausedby similarmechanisms.⁶⁹ Asinglecentre case series reported14ICUdeathsin22heatstrokepatientsadmittedtoICU withmultipleorganfailure.⁷⁰Featuresincluded:

•coretemperature≥40^◦C;

•hot,dryskin(sweatingpresentinabout50%ofcasesofexertional heatstroke);

•earlysignsandsymptoms(e.g.extremefatigue,headache,faint- ing,facialflushing,vomitinganddiarrhoea);

•cardiovascular dysfunction including arrhythmias and hypotension⁷¹;

•respiratorydysfunctionincludingacuterespiratorydistresssyn- drome(ARDS)⁷²;

•central nervous system dysfunction including seizures and coma⁷³;

•liverandrenalfailure⁷⁴;

•coagulopathy;

•rhabdomyolysis.⁷⁵

Otherclinicalconditionspresentingwithincreasedcoretem- perature need to be considered, including drug toxicity, drug withdrawalsyndrome,serotoninsyndrome,neurolepticmalignant syndrome,sepsis,centralnervoussysteminfection,endocrinedis- orders(e.g.thyroidstorm,phaeochromocytoma).

Treatment. Themainstayoftreatmentis supportivetherapy andrapidlycoolingthepatient.^76–78Startcoolingintheprehospi- talsettingifpossible.Aimtorapidlyreducethecoretemperature toapproximately39^◦C.Patientswithsevereheatstrokeneedto bemanagedinanICUenvironment.Largevolumesoffluidsand correctionofelectrolyteabnormalitiesmayberequired(seehypo- /hyperkalaemiaandotherelectrolytedisorders).

Cooling techniques. Several cooling methods have been described, but there are few formal trials to determine which isoptimal. Simple coolingtechniquesinclude drinkingcoldflu- ids,fanningthecompletelyundressedpatientandsprayingtepid wateronthepatient.Icepacksoverareaswheretherearelarge superficialbloodvessels(axillae,groins,neck)mayalsobeuseful.

Surfacecoolingmethodsmaycauseshivering.Incooperativesta- blepatients,immersionincoldwatercanbeeffective⁷⁹;however, thismaycauseperipheralvasoconstriction,shuntbloodawayfrom theperipheryandreduceheatdissipation.Immersionisalsonot practicalinthesickestpatients.

Furthertechniquestocoolpatientswithhyperthermiaaresim- ilar to those used for targeted temperature management after cardiacarrest(seepostresuscitationcare).⁸⁰Coldintravenousflu- idswilldecreasebodytemperature.Gastric,peritoneal,⁸¹pleural orbladderlavagewithcoldwaterwilllowerthecoretemperature.

IntravascularcoolingtechniquesincludetheuseofcoldIVfluids,⁸² intravascularcoolingcatheters^83,84andextracorporealcircuits,⁸⁵ e.g.continuousveno-venoushaemofiltrationorcardiopulmonary bypass.

Pharmacologicaltreatment. Therearenospecificdrugtherapies inheatstrokethatlowercoretemperature.Thereisnogoodevi- dencethatantipyretics(e.g.non-steroidalanti-inflammatorydrugs orparacetamol)areeffectiveinheatstroke.Diazepammaybeuse- fultotreatseizuresandfacilitatecooling.⁸⁶Dantrolenehasnotbeen showntobebeneficial.^87–89

Malignanthyperthermia

Malignanthyperthermiaisalife-threateninggeneticsensitivity ofskeletalmusclestohalogenatedvolatileanaestheticsanddepo- larisingneuromuscularblockingdrugs,occurringduringorafter anaesthesia.⁹⁰Stoptriggeringagents immediately;giveoxygen, correctacidosisandelectrolyteabnormalities.Startactivecooling andgivedantrolene.⁹¹

Other drugs such as 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’) and amphetamines also cause a condition similartomalignanthyperthermiaandtheuseofdantrolenemay bebeneficial.⁹²

Modifications to cardiopulmonary resuscitation. There are no specificstudiesofcardiacarrestinhyperthermia.Ifcardiacarrest occurs,followstandardguidelinesandcontinuecoolingthepatient.

Use the same cooling techniques as for targeted temperature managementaftercardiacarrest(seeSection5Post-resuscitation care).⁸⁰Attemptdefibrillationusingstandardenergylevels.Animal studiessuggesttheprognosisispoorcomparedwithnormothermic cardiacarrest.^93,94Theriskofunfavourableneurologicaloutcome increasesby2.26(oddsratio)foreachdegreeofbodytemperature

>37^◦C.⁹⁵ Hypovolaemia

Introduction

Hypovolaemiaisapotentiallytreatablecauseofcardiacarrest thatusuallyresultsfromareducedintravascularvolume(i.e.hae- morrhage),butrelativehypovolaemiamayalsooccurinpatients withseverevasodilation(e.g.anaphylaxis,sepsis).Hypovolaemia frommediator-activatedvasodilationandincreasedcapillaryper- meability is a major factor causing cardiac arrest in severe anaphylaxis.⁹⁶Hypovolaemiafrombloodloss,isa leadingcause ofdeathintraumaticcardiacarrest.⁹⁷Externalbloodlossisusually obvious,e.g.trauma,haematemesis,haemoptysis,butmaybemore challengingtodiagnosewhenoccult,e.g.gastrointestinalbleed- ingorruptureofanaorticaneurysm.Patientsundergoingmajor surgeryareathigh-riskfromhypovolaemiaduetopost-operative haemorrhageandmustbeappropriatelymonitored(seeperioper- ativecardiacarrest).

Dependingonthesuspectedcause,initiatevolumetherapywith warmedblood products and/orcrystalloids,in order to rapidly restoreintravascularvolume.Atthesametime,initiateimmedi- ateinterventiontocontrolhaemorrhage,e.g.surgery,endoscopy, endovasculartechniques,⁹⁸ortreattheprimarycause(e.g.anaphy- lacticshock).Intheinitialstagesofresuscitationuseanycrystalloid solutionthatisimmediatelyavailable.Ifthereisaqualifiedsono- grapherabletoperformultrasoundwithoutinterruptiontochest compressions,e.g.duringrhythmcheckorventilations,itmaybe consideredasanadditionaldiagnostictoolinhypovolaemiccardiac arrest.

Treatmentrecommendationsforcardiacarrestandperiarrest situationsin anaphylaxisandtraumaare addressedinseparate sectionsbecauseoftheneedforspecifictherapeuticapproaches.

Anaphylaxis

Definition. A precise definition of anaphylaxisis not important foritsemergencytreatment.⁹⁹TheEuropeanAcademyofAllergy and Clinical Immunology Nomenclature Committee proposed thefollowing broad definition:¹⁰⁰ anaphylaxisis a severe, life- threatening,generalisedorsystemichypersensitivityreaction.This is characterised by rapidly developing life-threatening airway and/orbreathingand/orcirculation problemsusuallyassociated withskinandmucosalchanges.1,96,101,102

Epidemiology. Anaphylaxisiscommonandaffectsabout1in300 oftheEuropeanpopulationatsomestageintheirlives,withan incidencefrom1.5 to7.9 per100,000person-years.¹⁰³ Anaphy- laxiscanbetriggeredbyanyofaverybroadrangeoftriggerswith food,drugs,stinginginsects,andlatexthemostcommonlyiden- tifiedtriggers.¹⁰³Foodisthecommonesttriggerinchildrenand drugsthecommonestinadults.¹⁰⁴Virtuallyanyfoodordrugcan beimplicated,butcertainfoods(nuts)anddrugs(musclerelax- ants,antibiotics,nonsteroidalanti-inflammatorydrugsandaspirin) causemostreactions.¹⁰⁵Asignificantnumberofcasesofanaphy- laxisareidiopathic.Between1992and2012intheUK,admission andfatalityratesfordrug-andinsectsting-inducedanaphylaxis werehighestinthegroupaged60years andolder.Incontrast, admissionsduetofood-triggeredanaphylaxisweremostcommon inyoungpeople,withamarkedpeakintheincidenceoffatalfood reactionsduringthesecondandthirddecadesoflife.¹⁰⁶

Theoverallprognosisofanaphylaxisisgood,withacasefatal- ityratiooflessthan1%reportedinmostpopulation-basedstudies.

TheEuropeanAnaphylaxisRegistryreportedthatonly2%of3333 caseswereassociatedwithcardiacarrest.¹⁰⁷Ifintensivecareunit admissionisrequired,survivaltodischargeisover90%.Overthe period2005–2009,therewere81paediatricand1269adultadmis- sionswithanaphylaxisadmittedtoUKcriticalcareunits.Survival todischargewas95%forchildren,and92%foradults.¹⁰⁸

Anaphylaxisandriskofdeathisincreasedinthosewithpre- existing asthma,particularlyifthe asthmais poorly controlled, severeorinasthmaticswhodelaytreatment.^109,110Whenanaphy- laxisisfatal,deathusuallyoccursverysoonaftercontactwiththe trigger.Fromacaseseries,fatalfoodreactionscauserespiratory arresttypicallywithin30–35min;insectstingscausecollapsefrom shockwithin10–15min;anddeathscausedbyintravenousmed- icationoccurmostcommonlywithin5min.Deathneveroccurred morethan6haftercontactwiththetrigger.^101,111

Recognition of an anaphylaxis. Anaphylaxis is the likely diagno- sisif a patient whois exposed to a trigger(allergen)develops asuddenillness(usuallywithinminutes)withrapidlydevelop- ing life-threatening airway and/or breathing and/or circulation problemsusuallyassociatedwithskinandmucosalchanges.The reactionisusuallyunexpected.

TheEuropeanAcademyofAllergyand ClinicalImmunology’s (EAACI)TaskforceonAnaphylaxisstatethatanaphylaxisishighly likelywhenanyoneofthefollowingthreecriteriaisfulfilled^96,112: 1.Acuteonsetofanillness(minutestoseveralhours)withinvolve- mentoftheskin,mucosaltissue,orboth(e.g.generalisedhives, pruritusorflushing,swollenlips–tongue–uvula)andatleastone ofthefollowing:

a.Respiratory compromise, e.g. dyspnoea, wheeze–

bronchospasm,stridor,reducedpeakexpiratoryflow(PEF), hypoxaemia.

b.Reducedbloodpressureorassociatedsymptomsofend-organ dysfunction,e.g.hypotonia(collapse),syncope,incontinence.

2.Twoormoreofthefollowingthatoccurrapidlyafterexposure toalikelyallergenforthatpatient(minutestoseveralhours):

a.Involvement of the skin–mucosal tissue, e.g. generalised hives,itch-flush,swollenlips–tongue–uvula.

b.Respiratory compromise, e.g. dyspnoea, wheeze–

bronchospasm,stridor,reducedPEF,hypoxaemia.

c.Reducedbloodpressureorassociatedsymptoms,e.g.hypoto- nia(collapse),syncope,incontinence.

d.Persistentgastrointestinalsymptoms,e.g.crampyabdominal pain,vomiting.

3.Reducedbloodpressureafterexposuretoknownallergenfor thatpatient(minutestoseveralhours):

a.Infantsandchildren:lowsystolicbloodpressure(<70mmHg from1monthto1year;<70mmHg+(2×age)from1yearto 10years;<90mmHgfrom11to17years)or>30%decreasein systolicbloodpressure.

b.Adults:systolicbloodpressureof<90mmHgor>30%decrease fromthatperson’sbaseline.

Treatment. The evidence supporting specific interventions for thetreatmentofanaphylaxisis limited.¹¹³ A systematicABCDE approach to recognise and treat anaphylaxis is recommended withimmediateadministrationofintramuscular(IM)adrenaline (Fig.4.2).Treatlife-threateningproblemsasyoufindthem.The basicprinciplesoftreatmentarethesameforallagegroups.Moni- torallpatientswhohavesuspectedanaphylaxisassoonaspossible (e.g.byambulancecrew,intheemergencydepartment,etc.).Min- imum monitoring includes pulse oximetry, non-invasive blood pressureanda3-leadECG.

Patientpositioning. Patientswithanaphylaxiscandeteriorate andareatriskofcardiacarrestifmadetosituporstandup.¹¹⁴All patientsshouldbeplacedinacomfortableposition.Patientswith airwayandbreathingproblemsmayprefertositup,asthiswill makebreathingeasier.Lyingflatwithorwithoutlegelevationis helpfulforpatientswithalowbloodpressure.

Remove the trigger(if possible). Stopany drugsuspected of causinganaphylaxis. Removethestingeraftera bee/waspsting.

Earlyremovalismoreimportantthanthemethodofremoval.¹¹⁵Do notdelaydefinitivetreatmentifremovingthetriggerisnotfeasible.

Cardiacarrestfollowinganaphylaxis. StartCPRimmediatelyand followcurrentguidelines.ProlongedCPRmaybenecessary.Rescu- ersshouldensurethathelpisonitswayasearlyALSisessential.

Airwayobstruction. Anaphylaxiscancauseairwayswellingand obstruction.Thiswillmakeairwayandventilationinterventions (e.g.bag-maskventilation,trachealintubation,cricothyroidotomy) difficult.Considerearlytrachealintubationbeforeairwayswelling makesthisdifficult.Callforexperthelpearly.

Adrenaline (first line treatment). Adrenaline is the most impor- tantdrugforthetreatmentofanaphylaxis.^116,117Althoughthere are no randomised controlled trials,¹¹⁸ adrenaline is a logical treatment and there is consistent anecdotal evidence suppor- tingitsusetoeasebronchospasmandcirculatorycollapse.Asan

Fig.4.2.Anaphylaxistreatmentalgorithm.¹⁰¹ ReproducedwithpermissionfromElsevierIrelandLtd.