Resuscitation 81 (2010) 14001433

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Resuscitation

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Europe ReSection cespoison hyanaphy cy,

Jasmeet AlfJoost J.L.M h, JoAnthony SanDavid A.a Anaesthesia ab University ofc Emergency Ded Queen Margae Intensive Caref Maxima Medig EURAC Institute of Mountain Emergency Medicine, Bozen, Italyh Cardiac Anaesthesia and Critical Care, Southampton University Hospital NHS Trust, Southampton, UKi Department of Cardiothoracic Surgery, James Cook University Hospital, Middlesbrough, UKj Nicosia General Hospital, Nicosia, Cyprusk Honorary Consultant Physician, Colchester, UKl Anaesthesia and Intensive Care Medicine, Frenchay Hospital, Bristol, UKm Departmentn Critical Care Mo Birmingham Cp Imperial Colleq Anaesthesia a

8a. Life-th

Overview

Electrolydiopulmonamost commkalaemia, amagnesiumdisorders sh

The elecguide to clitreatment dand rate of

There isabnormalitis based on

CorresponE-mail add

0300-9572/$ doi:10.1016/j.of Anesthesiology and Critical Care Medicine, University Hospital Innsbruck, Innsbruck, Austriaedicine at Policlinico Universitario Agostino Gemelli, Catholic University School of Medicine, Rome, Italyhildrens Hospital, Birmingham, UKge Healthcare NHS Trust, London, UKnd Intensive Care Medicine, Royal United Hospital, Bath, UK

reatening electrolyte disorders

te abnormalities can cause cardiac arrhythmias or car-ry arrest. Life-threatening arrhythmias are associatedonly with potassium disorders, particularly hyper-

nd less commonly with disorders of serum calcium and. In some cases therapy for life-threatening electrolyteould start before laboratory results become available.trolyte values for denitions have been chosen as anical decision-making. The precise values that triggerecisions will depend on the patients clinical conditionchange of electrolyte values.little or no evidence for the treatment of electrolyte

ies during cardiac arrest. Guidance during cardiac arrestthe strategies used in the non-arrest patient. There are

ding author.ress: jas.soar@btinternet.com (J. Soar).

no major changes in the treatment of these disorders since Guide-lines 2005.1

Prevention of electrolyte disorders

Identify and treat life-threatening electrolyte abnormalitiesbefore cardiac arrest occurs. Remove any precipitating factors (e.g.,drugs) and monitor electrolyte values to prevent recurrence of theabnormality. Monitor renal function in patients at risk of elec-trolyte disorders (e.g., chronic kidney disease, cardiac failure). Inhaemodialysis patients, review the dialysis prescription regularlyto avoid inappropriate electrolyte shifts during treatment.

Potassium disorders

Potassium homeostasis

Extracellular potassium concentration is regulated tightlybetween 3.5 and 5.0mmol l1. A large concentration gradientnormally exists between intracellular and extracellular uidcompartments. This potassium gradient across cell membranescontributes to the excitability of nerve and muscle cells, including

see front matter 2010 European Resuscitation Council. Published by Elsevier Ireland Ltd. All rights reserved.resuscitation.2010.08.015an Resuscitation Council Guidelines for8. Cardiac arrest in special circumstan

ing, drowning, accidental hypothermia,laxis, cardiac surgery, trauma, pregnan

Soara,, Gavin D. Perkinsb, Gamal Abbasc, Annette. Bierens f, Hermann Bruggerg, Charles D. Deakin

J. Handleyk, David J. Lockey l, Peter Paalm, ClaudioZidemanp, Jerry P. Nolanq

nd Intensive Care Medicine, Southmead Hospital, North Bristol NHS Trust, Bristol, UKWarwick, Warwick Medical School, Warwick, UKpartment, Al Rahba Hospital, Abu Dhabi, United Arab Emiratesret Hospital, Dunfermline, Fife, UKMedicine and Clinical Toxicology, Catholic University School of Medicine, Rome, Italy

cal Centre, Eindhoven, The Netherlandscate / resusc i ta t ion

suscitation 2010: Electrolyte abnormalities,perthermia, asthma,electrocution

onzod, Alessandro Barelli e,el Dunning i, Marios Georgiouj,dronin, Karl-Christian Thieso,

J. Soar et al. / Resuscitation 81 (2010) 14001433 1401

the myocardium. Evaluation of serum potassium must take intoconsideration the effects of changes in serum pH. When serumpH decreases (acidaemia), serum potassium increases becausepotassium shifts from the cellular to the vascular space. Whenserum pHbecause popH changesor hypokala

Hyperkalaem

This is tcardiopulmrelease frompotassium c

DenitionThere is

as a serumpractice, hycentrationincreases ahyperkalaetion higher

CausesThere ar

ing renal fa(ACE-I), aning diuretibeta-blocketumour lysi(Addisons dbe sole cauAbnormal ehigh potassgreaterwhetant use of A

RecognitionExclude

cardiac arring to accreexes. Alby the primof hyperkaties, arrhyteffect of hyppotassium aECG abnorm6.7mmol l

sium can reThe ECG

progressive

rst degre attened tall, peake

than 1 lea ST-segme S and T w widened ventricula bradycard

cardiac arrest (pulseless electrical activity [PEA], ventricular b-rillation/pulseless ventricular tachycardia [VF/VT], asystole).

Treatment of hyperkalaemiare are three key treatments for hyperkalaemia5:

iac pting povin

avene ofrt tonceted,ent ef hyp

ent ntionintr. Treia.roxi

d elev

oveumexalay or

ess crum

erat

pott-act0miove podithan

ere eld:

ultiose/itam

iredm bnt (oglucnjunemo

ere ehelp

ct thide Imiat by r

poincreases (alkalaemia), serum potassium decreasestassium shifts intracellularly. Anticipate the effects ofon serum potassium during therapy for hyperkalaemiaemia.

ia

he most common electrolyte disorder associated withonary arrest. It is usually causedby increasedpotassiumcells, impaired excretion by the kidneys or accidental

hloride administration.

nouniversal denition.Wehavedenedhyperkalaemiapotassium concentration higher than 5.5mmol l1; inperkalaemia is a continuum. As the potassium con-increases above this value the risk of adverse eventsnd the need for urgent treatment increases. Severemia has been dened as a serum potassium concentra-than 6.5mmol l1.

e several potential causes of hyperkalaemia, includ-ilure, drugs (angiotensin converting enzyme inhibitorsgiotensin II receptor antagonists, potassium spar-cs, non-steroidal anti-inammatory drugs (NSAIDs),rs, trimethoprim), tissue breakdown (rhabdomyolysis,s, haemolysis), metabolic acidosis, endocrine disordersisease), hyperkalaemic periodic paralysis, or diet (may

se in patients with advanced chronic kidney disease).rythrocytes or thrombocytosis may cause a spuriouslyium concentration.2 The risk of hyperkalaemia is evenn there is a combination of factors such as the concomi-CE-I and NSAIDs or potassium sparing diuretics.

of hyperkalaemiahyperkalaemia in patients with an arrhythmia or

est.3 Patients may present with weakness progress-id paralysis, paraesthesia, or depressed deep tendonternatively, the clinical picture can be overshadowedary illness causing hyperkalaemia. The rst indicator

laemia may also be the presence of ECG abnormali-hmias, cardiopulmonary arrest or sudden death. Theerkalaemia on the ECG depends on the absolute serums well as the rate of increase. Most patients will havealities at a serumpotassium concentration higher than

1.4 The use of a blood gas analyser that measures potas-duce delay in recognition.changes associated with hyperkalaemia are usuallyand include:

e heart block (prolonged PR interval) [>0.2 s];or absent P waves;d (tented) T waves [T wave larger than R wave in mored];nt depression;ave merging (sine wave pattern);QRS [>0.12 s];r tachycardia;ia;

The

1. card2. shif3. rem

Intrabsencbe alerecurresuspectreatmment o

PatiCirculaObtainan ECGkalaem

App

Mil

Remcalci(Kayorall6h).

Addrin se

Mod

Shiftshor153

Rem Haem

cient

Sevhelp an

Use m Gluc Salbu

requ Sodiu

presethanin co

Use r

Sevexpert

Protechlorkalaehearserumrotection;otassium into cells;

g potassium from the body.

ous calcium salts are not generally indicated in theECG changes. Monitor effectiveness of treatment,rebound hyperkalaemia and take steps to preventof hyperkalaemia. When hyperkalaemia is stronglye.g., in the presence of ECG changes, start life-savingven before laboratory results are available. The treat-erkalaemia has been the subject of a Cochrane review.6

ot in cardiac arrest. Assess ABCDE (Airway, Breathing,, Disability, Exposure) and correct any abnormalities.avenous access, check serum potassium and recordatment is determined according to severity of hyper-

mate values are provided to guide treatment.

ation (5.55.9mmol l1):

potassium from body: potassium exchange resins resonium 1530g OR sodium polystyrene sulfonatete) 1530g in 50100ml of 20% sorbitol, given eitherby retention enema (onset in 13h; maximal effect at

ause of hyperkalaemia to correct and avoid further risepotassium (e.g., drugs, diet).

e elevation (66.4mmol l1) without ECG changes:

assium intracellularly with glucose/insulin: 10 unitsing insulin and 25g glucose IV over 1530min (onset inn;maximal effect at 3060min;monitorbloodglucose).otassium from the body as described above.alysis: consider if oliguric; haemodialysis is more ef-peritoneal dialysis at removing potassium.

evation (6.5mmol l1) without ECG changes. Seek expert

ple shifting agents.nsulin (see above).ol 5mg nebulised. Several doses (1020mg) may be(onset in 1530min).icarbonate: 50mmol IV over 5min if metabolic acidosisnset in 1530min). Bicarbonate alone is less effective

ose plus insulin or nebulised salbutamol; it is best usedction with these medications.7,8

val strategies above.

levation (6.5mmol l1) WITH toxic ECG changes. Seekand:

e heart rst with calcium chloride: 10ml 10% calciumV over 25min to antagonise the toxic effects of hyper-at the myocardial cell membrane. This protects theeducing the risk of pulseless VT/VF but does not lowertassium (onset in 13min).

1402 J. Soar et al. / Resuscitation 81 (2010) 14001433

Use multiple shifting agents (see above). Use removal strategies. Prompt specialist referral is essential.

Patient imodicatioabnormalit

Modica

Follow thrapidly usrst: give

Shift pota Glucose

IV by ra Sodium

acidosis Remove p

diac arrestreatmeneffectivelspecialist

IndicationsHaemod

of potassiuis the diffuspotassium i1mmol l1

2h. The eftion can beconcentratidialysate bi

Considewith estab(

J. Soar et al. / Resuscitation 81 (2010) 14001433 1403

Table 8.1Calcium and magnesium disorders with associated clinical presentation, ECG manifestations and recommended treatment.

Disorder Causes Presentation ECG Treatment

Hypercalcaemia[Calcium]>2

Primary or tertiary Confusion Short QT interval Fluid replacement IV

Hypocalcaem[Calcium]1.1mmol l1

Renal failure Confusion

Iatrogenic WeaknessRespiratory depression

AV-block

Cardiac arrest

saemia] 1.75mmol l1

T wave peakingAV-block Calcium chloride 10% 510ml

repeated if necessaryCardiac arrest Ventilatory support if

necessarySaline diuresis 0.9% salinewith furosemide 1mgkg1 IVHaemodialysis

Prolonged PR and QTIntervals

Severe or symptomatic:

ST-segment depression 2g 50% magnesium sulphate(4ml; 8mmol) IV over 15min.

T-wave inversion Torsade de pointes:Flattened P waves 2g 50% magnesium sulphate

(4ml; 8mmol) IV over 12min.Increased QRS duration Seizure:Torsade de pointes 2 g 50% magnesium sulphate(4ml; 8mmol) IV over 10min.

f cardiac arrest

sing the ABCDE (Airway, Breathing, Circulation, Dis-osure) approach. Airway obstruction and respiratorydary to a decreased conscious level is a common causeter self-poisoning.23 Pulmonary aspiration of gastricn occur after poisoning with central nervous systems. Early tracheal intubation of unconscious patients byerson decreases the risk of aspiration. Drug-inducedn usually responds to uid infusion, but occasionallyr support (e.g., noradrenaline infusion) is required. Aof coma in a single position can cause pressure sores

omyolysis. Measure electrolytes (particularly potas-d glucose and arterial blood gases.Monitor temperatureermoregulation is impaired. Both hypothermia andia (hyperpyrexia) can occur after overdose of some

in samples of blood and urine for analysis. Patients withoning should be cared for in a critical-care setting.tions such as decontamination, enhanced elimina-ntidotes may be indicated and are usually secondntions.24 Alcohol excess is often associated with self-

s to BLS/ALS

gh index of personal safety where there is a suspiciousunexpected cardiac arrest. This is especially so whenn one casualty collapses simultaneously.

1404 J. Soar et al. / Resuscitation 81 (2010) 14001433

Avoid mouth-to-mouth ventilation in the presence of chemicalssuch as cyanide, hydrogen sulphide, corrosives and organophos-phates.

Treat life-threatening tachyarrhythmias with cardioversionaccordingAdvancedand acid-

Try to idecrews canmay reveabnormal

Measuremia may

Bepreparticularly iexcreted

Alternativsoned pastandard

Consult rtreatmenon Chemhttp://ww

Online dachemicals

Specic the

There arare useful im

Therapeactivated chantidotes. Mon expert apoisonings,

Gastrointest

Activateover time aactivated csingle dosepotentiallyvated charcan intact or

Multipleeliminationshown a reused followthe use of gingestion ofthen, clinicies. Gastricand if a hydsubstance h

Volunteability of inwhole-bowpatient. Basbe consideror enteric-cor packetsirrigation isperforation

Laxatives (cathartics) or emetics (e.g., ipecacuanha) have no rolein the management of the acutely poisoned patient and are notrecommended.26,32,33

ing e

ne asod

odert neow

inhloracid

icatiomodc lifeor mribut

oveg

c po

se gudue t

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ationre arby b

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s at reveradved vee of nrouteamuusedhavinan IV00ay

ratiotoryto the peri-arrest arrhythmia guidelines (see Section 4,Life Support).24a This includes correction of electrolyte

base abnormalities.ntify the poison(s). Relatives, friends and ambulanceprovide useful information. Examination of the patient

al diagnostic clues such as odours, needle marks, pupilities, and signs of corrosion in the mouth.the patients temperature because hypo- or hyperther-occur after drug overdose (see Sections 8d and 8e).ed to continue resuscitation for a prolongedperiod, par-n young patients, as the poison may be metabolized orduring extended life support measures.e approaches which may be effective in severely poi-tients include: higher doses of medication than inprotocols; non-standarddrug therapies; prolongedCPR.egional or national poisons centres for information ont of the poisoned patient. The International Programmeical Safety (IPCS) lists poison centres on its website:w.who.int/ipcs/poisons/centre/en/.tabases for information on toxicology and hazardous: (http://toxnet.nlm.nih.gov/).

rapeutic measures

e few specic therapeutic measures for poisoning thatmediately and improve outcomes.2529

utic measures include decontamination, multiple-dosearcoal, enhancing elimination and the use of specicany of these interventions should be used only based

dvice. For up-to-date guidance in severe or uncommonseek advice from a poisons centre.

inal decontamination

d charcoal adsorbs most drugs. Its benet decreasesfter ingestion. There is no evidence that treatment withharcoal improves clinical outcome. Consider giving aof activated charcoal to patients who have ingested atoxic amount of poison (known to be adsorbed by acti-oal) up to 1h previously.30 Give it only to patients withprotected airway.-dose activated charcoal signicantly increases drug, but no controlled study in poisoned patients hasduction in morbidity and mortality and should only being expert advice. There is little evidence to supportastric lavage. It should only be considered within 1h ofa potentially life-threatening amount of a poison. Even

al benet has not been conrmed in controlled stud-lavage is contraindicated if the airway is not protectedrocarbon with high aspiration potential or a corrosiveas been ingested.27,28

er studies show substantial decreases in the bioavail-gested drugs but no controlled clinical trials show thatel irrigation improves the outcome of the poisoneded on volunteer studies, whole-bowel irrigation mayed for potentially toxic ingestions of sustained-releaseoated drugs. Its use for the removal of iron, lead, zinc,of illicit drugs is a theoretical option. Whole-bowelcontraindicated in patients with bowel obstruction,

, ileus, and haemodynamic instability.31

Enhanc

Urivenousfor mdo nourinesidered2,4-dicpioniccompl

Haespecidrugsof distcan rembindin

Speci

Thearrest

Benzod

PatientOve

respirative anreversbenzodReversassociasion, adepentricyclcomat

ModicThe

caused

Opioid

Opipiratorof opio

PatientIn s

fewertion anThe usferredIV, intrcan bein notcult inIV,43 8doses mThe durespiralimination

lkalinisation (urine pH of 7.5 or higher) by intra-ium bicarbonate infusion is a rst line treatment

ate-to-severe salicylate poisoning in patients whoed haemodialysis.25 Urine alkalinisation with high

(approximately 600mlh1) should also be con-patients with severe poisoning by the herbicides

ophenoxyacetic acid and methylchlorophenoxypro-(mecoprop). Hypokalaemia is the most common

n of alkalaemia.ialysis or haemoperfusion should be considered in-threatening poisonings only. Haemodialysis removesetabolites that are water soluble, have a low volumeion and low plasma protein binding. Haemoperfusionsubstances that have a high degree of plasma protein

isonings

idelines address only some causes of cardiorespiratoryo acute poisoning.

ines

isk of cardiac arreste of benzodiazepines can cause loss of consciousness,depression and hypotension. Flumazenil, a competi-nist of benzodiazepines, should only be used only forsedation caused by a single ingestion of any of thepines and when there is no history or risk of seizures.benzodiazepine intoxication with umazenil can be

with signicant toxicity (seizure, arrhythmia, hypoten-ithdrawal syndrome) in patients with benzodiazepinee or co-ingestion of proconvulsant medications such astidepressants.3436 The routine use of umazenil in theverdose patient is not recommended.

s to BLS/ALSe no specic modications required for cardiac arrestenzodiazepines.3640

oisoning causes respiratory depression followedby res-ufciency or respiratory arrest. The respiratory effectsre reversed rapidly by the opiate antagonist naloxone.

isk of cardiac arreste respiratory depression caused by opioids, there arerse events when airway opening, oxygen administra-ntilation are carried out before giving naloxone.4147

aloxone can prevent the need for intubation. The pre-forgivingnaloxonedependson theskills of the rescuer:

scular (IM), subcutaneous (SC) and intranasal (IN) routes. The non-IV routes can be quicker because time is savedg to establish IV access, which can be extremely dif-drug abuser. The initial doses of naloxone are 400g

g IM, 800g SC,43 or 2mg IN.48,49 Large opioid over-require titration of naloxone to a total dose of 610mg.n of action of naloxone is approximately 4570min, butdepression can persist for 45h after opioid overdose.

J. Soar et al. / Resuscitation 81 (2010) 14001433 1405

Thus, the clinical effects of naloxone may not last as long as thoseof a signicant opioid overdose. Titrate the dose until the victim isbreathing adequately and has protective airway reexes.

Acute withdrawal from opioids produces a state of sympatheticexcess andventricularof opioid independence

ModicationThere ar

diac arrestarrest is uswith severeunlikely tostandard re

Tricyclic ant

This sedrugs (e.g.,doxepin, anpressants isand life-thranticholinewide compalpha-1 recasis, fever,retention. Mafter ingest

Patient at riA widen

indicates aate shouldventricularinvestigatedapy, a pH oreasonable.

Intraventoxicity havAnti-tricyclmodels of tprovided ev

ModicationThere ar

tional versutricyclic toxshowed imp

Cocaine

Sympathcan cause aand coronaangina.

Patients at rIn patien

(phentolamcalcium chlingual nitrhypertensioevidence foing those be

and labetolol).8587 is limited. The best choice of anti-arrhythmicdrug for the treatment of cocaine-induced tachyarrhythmias is notknown.

ationcardnes.8

naes

temis sycon

bradrrhytextrtingortent

s at rencdiac. Paattribent wdvanlipid

p tohe inum o

ationdard

accore incy.100,

locke

a-bloic ef

s at rencudie0godied in1

cha

iumof pctintainemia

ts areestiots, 1h fo

s at rnsive camay cause complications such as pulmonary oedema,arrhythmia and severe agitation. Use naloxone reversaltoxication with caution in patients suspected of opioid.

s for ALSe no studies supporting the use of naloxone once car-associated with opioid toxicity has occurred. Cardiacually secondary to a respiratory arrest and associatedbrain hypoxia. Prognosis is poor.42 Giving naloxone isbe harmful. Once cardiac arrest has occurred, followsuscitation protocols.

idepressants

ction addresses both tricyclic and related cyclicamitriptyline, desipramine, imipramine, nortriptyline,d clomipramine). Self-poisoning with tricyclic antide-common and can cause hypotension, seizures, comaeatening arrhythmias. Cardiac toxicity mediated byrgic and Na+ channel-blocking effects can produce alex tachycardia (VT). Hypotension is exacerbated byeptor blockade. Anticholinergic effects include mydri-dry skin, delirium, tachycardia, ileus, and urinaryost life-threatening problems occur within the rst 6h

ion.5052

sk of cardiac arresting QRS complex (>100ms) and right axis deviationgreater risk of arrhythmias.5355 Sodium bicarbon-be considered for the treatment of tricyclic-inducedconduction abnormalities.5663 While no study hasthe optimal target arterial pH with bicarbonate ther-

f 7.457.55 has been commonly accepted and seems

ous lipid infusions in experimental models of tricyclice suggested benet but there are few human data.64,65

ic antibodies have also been benecial in experimentalricyclic cardiotoxicity.6671 One small human study72

idence of safety but clinical benet has not been shown.

s to BLS/ALSe no randomised controlled trials evaluating conven-s alternative treatments for cardiac arrest caused byicity. One small case-series of cardiac arrest patients,rovement with the use of sodium bicarbonate.73

etic overstimulation associated with cocaine toxicitygitation, tachycardia, hypertensive crisis, hyperthermiary vasoconstriction causing myocardial ischaemia with

isk of cardiac arrestts with severe cardiovascular toxicity, alpha blockersine),74 benzodiazepines (lorazepam, diazepam),75,76

annel blockers (verapamil),77 morphine,78 and sub-oglycerine79,80 may be used as needed to controln, tachycardia,myocardial ischaemiaandagitation. Ther or against the use of beta-blocker drugs,8184 includ-ta-blockers with alpha blocking properties (carvedilol

ModicIf

guideli

Local a

Sysnervouloss ofsinustachyanancy,the setinadve

PatientEvid

ing carstudiesarresttreatmdard aof 20%Give utinue tmaxim

ModicStan

givenprovidtoxicit

Beta-b

Betinotroparrest.

PatientEvid

mal st(5015phosphreal ansalts.13

Calcium

Calccauseshort-aby susarrhythpatienthe ingproducand 24

PatientInte

massivs to BLS/ALSiac arrest occurs, follow standard resuscitation8

thetics

c toxicity of local anaesthetics involves the centralstem, the cardiovascular system. Severe agitation,sciousness, with or without tonicclonic convulsions,ycardia, conduction blocks, asystole and ventricularhmias can all occur. Toxicity can bepotentiated in preg-emes of age, or hypoxaemia. Toxicity typically occurs inf regional anaesthesia,whenabolusof local anaestheticly enters an artery or vein.

isk of cardiac arreste for specic treatment is limited to case reports involv-arrest and severe cardiovascular toxicity and animal

tients with both cardiovascular collapse and cardiacutable to local anaesthetic toxicity may benet fromith intravenous 20% lipid emulsion in addition to stan-

ced life support.89103 Give an initial intravenous bolusemulsion followed by an infusion at 15mlkg1 h1.

three bolus doses of lipid at 5-min intervals and con-fusion until the patient is stable or has received up to af 12mlkg1 of lipid emulsion.104

s to BLS/ALScardiac arrests drugs (e.g., adrenaline) should be

ding to standard guidelines, although animal studiesonsistent evidence for their role in local anaesthetic103,105107

rs

cker toxicity causes bradyarrhythmias and negativefects that are difcult to treat, and can lead to cardiac

isk of cardiac arreste for treatment is based on case reports and ani-s. Improvement has been reported with glucagonkg1),108121 high-dose insulin and glucose,122124

sterase inhibitors,125,126 calcium salts,127 extracorpo-tra-aortic balloon pump support,128130 and calcium

nnel blockers

channel blocker overdose is emerging as a commonrescription drug poisoning deaths.22,132 Overdose ofg drugs can rapidly progress to cardiac arrest. Overdosed-release formulations can result in delayed onset ofs, shock, and sudden cardiac collapse. Asymptomaticunlikely to develop symptoms if the interval betweenn and the call is greater than 6h for immediate-release8h for modied-release products other than verapamil,r modied-release verapamil.

isk of cardiac arreste cardiovascular support is needed for managing alcium channel blocker overdose. While calcium chlo-

1406 J. Soar et al. / Resuscitation 81 (2010) 14001433

ride in high doses can overcome some of the adverse effects, itrarely restores normal cardiovascular status. Haemodynamic insta-bility may respond to high doses of insulin given with glucosesupplementation and electrolyte monitoring in addition to stan-dard treatmpotentiallyphosphodie

Digoxin

Althouging calciumdigoxin isblockers andigoxin to rtricular hyparrhythmia

Patients at rStandard

with digoxiare arrhythAntibody-splants as wglycosides.1

with digoxitimation of

Cyanide

Cyanidesoning; howpatients wiIts main to(at cytochrophorylationof adequate(brain andpoisoning.

Patients at rPatients

diovascularcaused by kcyanide anincluding oenger (eithintravenousas soon asHydroxocobcobalamin mformation o

ModicationIn case o

ment will farespirationtion of cyto

Carbon mon

Carbon25,000 carbthe US in 2by carbon m

return of spontaneous circulation is achieved; however, hyper-baric oxygen therapy may be considered in these patients as itmay reduce the risk of developing persistent or delayed neuro-logical injury.177185 The risks inherent in transporting critically

-arreust be basmon

ity lamend

own

ew

wninrowrmin, aniateogicaion ostemen thch inrestguideoupsdrow

iolo

Wodrow

furearing18

-incfrom

itedd 1.ing if accith dvari

tions

r 30s ants.19

LCORtorym. Iment afromut wing inuid.ust bing thOR reno loing, sar-drents including uids and inotropic drugs.133148 Otheruseful treatments include glucagon, vasopressin andsterse inhibitors.139,149

h casesofdigoxinpoisoningare fewer than those involv-channel and beta-blockers, the mortality rate from

far greater. Other drugs including calcium channeld amiodarone can also cause plasma concentrations ofise. Atrioventricular conduction abnormalities and ven-erexcitability due to digoxin toxicity can lead to severes and cardiac arrest.

isk of cardiac arrestresuscitation measures and specic antidote therapy

n-specic antibody fragments should be used if theremias associated with haemodynamic instability.150163

pecic therapy may also be effective in poisoning fromell as Chinese herbal medications containing digitalis50,164,165 Digoxin-specic antibody fragments interferen immunoassay measurements and can lead to overes-plasma digoxin concentrations.

is generally considered to be a rare cause of acute poi-ever, cyanide exposure occurs relatively frequently in

th smoke inhalation from residential or industrial res.xicity results from inactivation of cytochrome oxidaseme a3), thus uncouplingmitochondrial oxidative phos-and inhibiting cellular respiration, even in thepresenceoxygen supply. Tissues with the highest oxygen needs

heart) are the most severely affected by acute cyanide

isk of cardiac arrestwith severe cardiovascular toxicity (cardiac arrest, car-instability,metabolic acidosis, or alteredmental status)nown or suspected cyanide poisoning should receivetidote therapy in addition to standard resuscitation,xygen. Initial therapy should include a cyanide scav-er intravenous hydroxocobalamin or a nitrite i.e.,sodium nitrite and/or inhaled amyl nitrite), followedpossible by intravenous sodium thiosulphate.166175

alamin and nitrites are equally effective but hydroxo-ay be safer because it does not cause methaemoglobin

r hypotension.

s to BLS/ALSf cardiac arrest caused by cyanide, standard ALS treat-il to restore spontaneous circulation as long as cellularis blocked. Antidote treatment is needed for reactiva-chrome oxidase.

oxide

monoxide poisoning is common. There were abouton monoxide related hospital admissions reported in005.176 Patients who develop cardiac arrest causedonoxide rarely survive to hospital discharge, even if

ill postand mby-cascarbonmortalrecom

8c. Dr

Overvi

DroAfter din detetilationImmedneurolprovisEMSsying whReseardiac arThesetain grof the

Epidem

Thewide,year. Aeach ydrownmiddledeathsthe Un0.56 androwncause oatedwabuse)

Deni

Oveprocesincidention (Irespiramediuis presvictimcess, bdrownother way minclud

ILCshoulddrownsus nest patients to a hyperbaric facility may be signicant,e weighed against the possibility of benet on a case-is. Patients who develop myocardial injury caused byoxide have an increased risk of cardiac and all-causesting at least 7 years after the event; it is reasonable tocardiology follow-up for these patients.186,187

ing

g is a common cause of accidental death in Europe.ning the duration of hypoxia is the most critical factoring the victims outcome; therefore, oxygenation, ven-d perfusion should be restored as rapidly as possible.resuscitation at the scene is essential for survival andl recovery after a drowning incident. This will requiref CPR by a bystander and immediate activation of the.Victimswhohavespontaneouscirculationandbreath-ey reach hospital usually recover with good outcomes.to drowning is limited in comparison with primary car-and there is a need for further research in this area.188

lines are intended for healthcare professionals and cer-of lay responders that have a special interest in the carening victim, e.g., lifeguards.

gy

rld Health Organization (WHO) estimates that, world-ning accounts for approximately 450,000 deaths eachther 1.3 million disability-adjusted life-years are lostas a result of premature death or disability from9; 97% of deaths from drowning occur in low- andome countries.189 In 2006 there were 312 accidental

drowning in the United Kingdom190 and 3582 inStates,191 yielding an annual incidence of drowning of2 per 100,000 population, respectively.192 Death froms more common in young males, and is the leadingidental death in Europe in this group.189 Factors associ-rowning (e.g., suicide, trafc accidents, alcohol and druges between countries.193

, classications and reporting

different terms have been used to describe thed outcome from submersion- and immersion-related4 The International Liaison Committee on Resuscita-) denes drowning as a process resulting in primaryimpairment from submersion/immersion in a liquidplicit in this denition is that a liquid/air interfacet the entrance of the victims airway, preventing thebreathing air. The victim may live or die after this pro-

hatever the outcome, he or she has been involved in acident.195 Immersion means to be covered in water orFor drowning to occur, usually at least the face and air-e immersed. Submersion implies that the entire body,e airway, is under the water or other uid.commends that the following terms, previously used,nger be used: dry andwet drowning, active andpassiveilent drowning, secondary drowning and drowned ver-owned.195 The Utstein drowning style should be used

J. Soar et al. / Resuscitation 81 (2010) 14001433 1407

when reporting outcomes from drowning incidents to improveconsistency in information between studies.195

Pathophysiology

The patdetail.195,19

holds beforfrequentlying/laryngoEventuallyinto their luand restorabefore sustpathophysisequence oobtaining a

Treatment

Treatmerelated phasupport, (iiiRescue andinvolves afrom the wawith a dutyators. Basicbefore arrivfrequentlyneous circuDrowninginvolving avictims. Theber of victimvictims outto determinsary. The rethe individuavailable.

Basic life sup

Aquatic rpersonal satim at all timvictim withing with aor buoyantland. Alternthe rescue.into the wadevice.197 ItNever divemay lose viinjury.

Removesafest meanincidence o(approximaperform inadequate recan also cauvical spineinjury are aof severe in

water-slide use, signs of trauma or signs of alcohol intoxication. Ifthe victim is pulseless and apnoeic remove them from the water asquickly as possible (even if a back support device is not available),while attempting to limit neck exion and extension.

cue bwnirescl.201

xygeible.cuebater pely tentilation.e vic

ntano. In-

edbrea

ot staue reromtim tilatio

st cobef

tivet breue Cing via. Inve an

omatavaie AE

urgitculted foairwtil ah co

itatio, tural usal injingompcont

d.211

ed li

ay agenpone vefailsxim

tionntrolmeashophysiology of drowning has been described in6 In brief, after submersion, the victim initially breathe developing laryngospasm. During this time the victimswallows large quantities of water. As breath hold-spasm continues, hypoxia and hypercapnia develops.these reexes abate and the victim aspirates waterngs leading to worsening hypoxaemia. Without rescuetion of ventilation the victim will become bradycardicaining a cardiac arrest. The key feature to note in theology of drowning is that cardiac arrest occurs as a con-f hypoxia and correction of hypoxaemia is critical toreturn of spontaneous circulation.

nt of a drowning victim involves four distinct but inter-ses. These comprise (i) aquatic rescue, (ii) basic life) advanced life support, and (iv) post-resuscitation care.resuscitation of the drowning victim almost always

multi-professional team approach. The initial rescueter is usually undertaken either by bystanders or thoseto respond such as trained lifeguards or lifeboat oper-life support is often provided by the initial respondersal of the emergency medical services. Resuscitationcontinues into hospital where, if return of sponta-lation is achieved, transfer to critical care often follows.incidents vary in their complexity from an incidentsingle victim to one that involves several or multipleemergency response will vary according to the num-s involved and available resources. If the number of

weighs the available resources then a system of triagee who to prioritise for treatment is likely to be neces-mainder of this sectionwill focus on themanagement ofal drowningvictimwhere there are sufcient resources

port

escue and recovery from the water. Always be aware offety and minimize the danger to yourself and the vic-es. Whenever possible, attempt to save the drowning

out entry into the water. Talking to the victim, reach-rescue aid (e.g., stick or clothing), or throwing a roperescue aid may be effective if the victim is close to dryatively, use a boat or other water vehicle to assist withAvoid entry into the water whenever possible. If entryter is essential, take a buoyant rescue aid or otationis safer to enter thewaterwith two rescuers thanalone.head rst in the water when attempting a rescue. Yousual contact with the victim and run the risk of a spinal

all drowning victims from the water by the fastest ands available and resuscitate as quickly as possible. Thef cervical spine injury in drowning victims is very lowtely 0.5%).198 Spinal immobilisation can be difcult tothe water and can delay removal from the water andsuscitation of the victim. Poorly applied cervical collarsse airway obstruction in unconscious patients.199 Cer-immobilisation is not indicated unless signs of severepparent or the history is consistent with the possibilityjury.200 These circumstances include a history of diving,

Resthe drotion ofsurvivawith oas poss

Reslow wIt is liknose vventila

If thno spoto do sperformrescuedoes ncontin5min fthe vicat vent

Chesurfaceineffecand noContindrownhypoxeffecti

AutAED isturn th

Regis difthe nein thetion unstomacresuscpletelymateriif spinlife-savchest cgastricbe use

Advanc

Airwan oxyof the sinvasivvictimpulse ocentraand coinitialreathing. The rst and most important treatment forng victim is alleviation of hypoxaemia. Prompt initia-ue breathing or positive pressure ventilation increases204 If possible supplement rescue breaths/ventilationsn.205 Give ve initial ventilations/rescue breaths as soon

reathing canbe initiatedwhilst thevictim is still in shal-rovided the safety of the rescuer is not compromised.o be difcult to pinch the victims nose, so mouth-to-tion may be used as an alternative to mouth-to-mouth

tim is in deep water, open their airway and if there iseous breathing start in-water rescuebreathing if trainedwater resuscitation is possible,206 but should ideally bewith the support of a buoyant rescue aid.207 Give 1015ths over approximately 1min.207 If normal breathingrt spontaneously, and the victim is

1408 J. Soar et al. / Resuscitation 81 (2010) 14001433

care to ensure optimal preoxygenation before intubation. Use arapid-sequence inductionwith cricoidpressure to reduce the riskofaspiration.213 Pulmonary oedema uid may pour from the airwayand may need suctioning to enable a view of the larynx.

After thinspired oxypositive enhowever hipatients is s

In the ethe victim etracheal tuinationpre

Circulaticardiac arrDelaying thcardiac arre

The typifrom the indrowning vpresence orable additioother moniechocardiog

If the vicsupport pro30 C, limituntil the co8d).

Duringvolaemic frGive IV uidcirculation,tation.

DiscontinuinMaking

victim of daccuratelyDecisions mincorrect.21

that such atmortis, putris not possiseveral victrare case reice-cold wa

Post-resusci

Salt verspast on diffExtensive dshown thatpredominansurfactant wsis, and intrdisturbancerequire trea

Lung injacute respiAlthough tspecicallyinclude stra

shown to improve survival in patients with ARDS.220 The severityof lung injury varies from a mild self-limiting illness to refractoryhypoxaemia. In severe cases extracorporeal membrane oxygena-tion has been used with some success.221,222 The clinical and cost

veneised

umoot beredage.p sub

othep prin iand

er, holdw

icatioatione reermactivducspitaidencch m34 CtheFede

er suogicantracntervcranal hye IC

ow-uess

carefs suge (wmptos oreartilityoveds unc

cide

tion

idenntionrily a8 C)usedconst shige Ve tracheal tube is conrmed in position, titrate thegen concentration to achieve an SaO2 of 9498%.205 Set

d-expiratory pressure (PEEP) to at least 510 cm H2O,gher PEEP levels (1520 cm H2O) may be required if theeverely hypoxaemic.214

vent of cardiopulmonary arrest protect the airway ofarly in the resuscitation attempt, ideally with a cuffedbe reduced pulmonary compliance requiring highssuresmay limit theuseof a supraglottic airwaydevice.

on and debrillation. Differentiating respiratory fromest is particularly important in the drowning victim.e initiation of chest compressions if the victim is inst will reduce survival.cal post-arrest gasping is very difcult to distinguishitial respiratory efforts of a spontaneous recoveringictim. Palpation of the pulse as the sole indicator of theabsence of cardiac arrest is unreliable.215 When avail-nal diagnostic information should be obtained from

toring modalities such as ECG trace, end-tidal CO2, andraphy to conrm the diagnosis of cardiac arrest.tim is in cardiac arrest, follow standard advanced lifetocols. If the victims core body temperature is less thandebrillation attempts to three, and withhold IV drugsre body temperature increases above 30 C (see Section

prolonged immersion, victims may become hypo-om the hydrostatic pressure of the water on the body.to correct hypovolaemia. After return of spontaneous

use haemodynamic monitoring to guide uid resusci-

g resuscitation effortsa decision to discontinue resuscitation efforts on arowning is notoriously difcult. No single factor canpredict good or poor survival with 100% certainty.ade in the eld frequently prove later to have been

6 Continue resuscitation unless there is clear evidencetempts are futile (e.g., massive traumatic injuries, rigorefaction etc), or timely evacuation to a medical facilityble. Neurologically intact survival has been reported inims submerged for greater than 60min however theseports almost invariably occur in children submerged inter.217,218

tation care

us fresh water. Much attention has focused in theerences between salt-water and fresh-water drowning.ata from animal studies and human case-series have, irrespective of the tonicity of the inhaled uid, thet pathophysiological process is hypoxaemia, driven byash-out and dysfunction, alveolar collapse, atelecta-

apulmonary shunting. Small differences in electrolyteare rarely of any clinical relevance and do not usuallytment.

ury. Victims of drowning are at risk of developingratory distress syndrome (ARDS) after submersion.219

here are no randomised controlled trials undertakenin this population of patients it seems reasonable totegies such as protective ventilation that have been

effectirandom

Pnehave nconsidas sewdevelo

Hypdevelooccursrapidlyhowevin ice-ccomplevapor

Cashypothsive orfrom inpre-hoing evapproaof 32duringSaving

Othneurolrates, ithese iof intrarologicalter th

FollsciousnTake afeaturesyncopmal syseizuretural hpossibhas prthere i

8d. Ac

Deni

Accunintearbitrathan 2can beclearlywithouand stass of these interventions has not been formally tested incontrolled trials.

nia is common after drowning. Prophylactic antibioticseen shown to be of benet,223 although they may beafter submersion in grossly contaminated water suchGive broad-spectrum antibiotics if signs of infectionsequently.200,224

rmia after drowning. Victims of submersion mayimary or secondary hypothermia. If the submersioncy water (37 C)subsequent period of intensive care (International Liferation, 2003).

pportive care. Attempts have been made to improvel outcome following drowning with the use of barbitu-ranial pressure (ICP) monitoring, and steroids. None ofentions has been shown to alter outcome. In fact, signsial hypertension serve as a symptom of signicant neu-poxic injury, and there is no evidence that attempts toP will affect outcome.200

p. Cardiac arrhythmias may cause rapid loss of con-leading to drowning if the victim is in water at the time.ul history in survivors of a drowning incident to identifygestive of arrhythmic syncope. Symptoms may includehilst supine position, during exercise,with brief prodro-ms, repetitive episodesor associatedwithpalpitations),a family history of sudden death. The absence of struc-disease at post-mortem examination does not rule theof sudden cardiac death. Post-mortem genetic analysishelpful in these situations and should be considered ifertainty over the cause of a drowning death.227229

ntal hypothermia

tal hypothermia existswhen the body core temperatureally drops below 35 C. Hypothermia can be classieds mild (3532 C), moderate (3228 C) or severe (less

.230 The Swiss staging system231 based on clinical signsby rescuers at the scene to describe victims: stage I cious and shivering; stage II impaired consciousnessvering; stage III unconscious; stage IV no breathing; death due to irreversible hypothermia.

J. Soar et al. / Resuscitation 81 (2010) 14001433 1409

Diagnosis

Accidental hypothermia may be under-diagnosed in countrieswith a temperate climate. In persons with normal thermoreg-ulation, hyenvironmenwho have bWhen thermand very yohypothermtion, illnessin the levelthe clinicalpatient. A lotemperatursured in thetemperatur using a thbe lower thtemperaturnal auditoryno ow in tmometers barenotdesital setting, tsame throubladder, rec

Decision to

Coolingtion by 6oxygen conIn some cabrain and vbe possiblemia develohypothermsmall-voluma hypotherIV) alone istolerate per37 C. Dilatenot be regareported aftimmersiona severely hsix and a ha

In the ponly if the cinjury, fatapressible. Inno one isremotewilding have todoctors andcitating a h

Resuscitati

All the papply to thchest compmia can cauchest compsuch as ins

advantages of adequate oxygenation and protection from aspira-tion outweigh the minimal risk of triggering VF by performingtracheal intubation.240

Clear the airway and, if there is no spontaneous respiratoryventinsidanceECGconcultras a cabouPR ismethy

drugolisms ofy of dmaladrere, bud.244

untilpprotweethermstaner ps ap

hmi

theto givle.245

rresthmiaraturradypac

dynatem

tedermse pasett

llatioED it. CPRto fac

ming

eralvirohospermrefure temothesive mrcisen inccoldreshpothermia may develop during exposure to coldts, particularly wet or windy conditions, and in people

een immobilised, or following immersion in cold water.oregulation is impaired, for example, in the elderly

ung, hypothermia may follow a mild insult. The risk ofia is also increased by drug or alcohol ingestion, exhaus-, injury or neglect especially when there is a decreaseof consciousness. Hypothermia may be suspected fromhistory or a brief external examination of a collapsedw-reading thermometer is needed to measure the coree and conrm thediagnosis. The core temperaturemea-lower third of the oesophagus correlates well with thee of the heart. Epitympanic (tympanic) measurementermistor technique is a reliable alternative but mayan the oesophageal temperature if the environmentale is very cold, the probe is not well insulated, the exter-canal is blocked or during cardiac arrest when there is

he carotid artery.232 Widely available tympanic ther-ased on infrared technique donot seal the ear canal andgned for lowcore temperature readings.233 In thehospi-he method of temperature measurement should be theghout resuscitation and rewarming. Use oesophageal,tal or tympanic temperature measurements.234,235

resuscitate

of the human body decreases cellular oxygen consump-% per 1 C decrease in core temperature.236 At 28 Csumption is reduced by 50% and at 22 C by 75%.ses, hypothermia can exert a protective effect on theital organs237 and intact neurological recovery mayeven after prolonged cardiac arrest if deep hypother-ps before asphyxia. Beware of diagnosing death in aic patient because cold alone may produce a very slow,e, irregular pulse and unrecordable blood pressure. In

mic patient, no signs of life (Swiss hypothermia stageunreliable for declaring death. At 18 C the brain caniods of circulatory arrest for ten times longer than atd pupils can be caused by a variety of insults and mustrded as a sign of death. Good quality survival has beener cardiac arrest and a core temperature of 13.7 C afterin cold water with prolonged CPR.238 In another case,ypothermic patient was resuscitated successfully afterlf hours of CPR.239

re-hospital setting, resuscitation should be withheldause of a cardiac arrest is clearly attributable to a lethall illness, prolonged asphyxia, or if the chest is incom-all other patients the traditional guiding principle that

dead until warm and dead should be considered. Inerness areas, the impracticalities of achieving rewarm-be considered. In the hospital setting involve senioruse clinical judgment to determinewhen to stop resus-

ypothermic arrest victim.

on

rinciples of prevention, basic and advanced life supporte hypothermic patient. Use the same ventilation andression rates as for a normothermic patient. Hypother-se stiffness of the chest wall, making ventilation and

ressions more difcult. Do not delay urgent procedures,erting vascular catheters and tracheal intubation. The

effort,gen. Coto advat thebeforephy orthere idoubtOnce Cthermo

Theactivemetabtrationefcacon aniarrest,pressureducedrugsthan avals benormo35 C),out othand 4 T

Arrhyt

Astendsasystodiac aArrhyttempement. Bcardiachaemo

Theattemphypothon theenergydebriIf an Apatienhours

Rewar

Gencold enfer tohypothdled caand coWet clexcessas execise cafrom alow thlate the patients lungswithhigh concentrations of oxy-er careful tracheal intubationwhen indicated accordingd life support guidelines. Palpate a central artery, look(if available), and look for signs of life for up to 1minluding that there is no cardiac output. Echocardiogra-sound with Doppler may be used to establish whetherardiac output or peripheral blood ow. If there is anyt whether a pulse is present, start CPR immediately.under way, conrm hypothermia with a low-reading

er.pothermic heart may be unresponsive to cardio-s, attempted electrical pacing and debrillation. Drugis slowed, leading to potentially toxic plasma concen-any drugs given repeatedly.241 The evidence for therugs in severe hypothermia is limited and basedmainlystudies. For instance, in severe hypothermic cardiacnalinemaybe effective in increasing coronary perfusiont not survival.242,243 The efcacy of amiodarone is alsoFor these reasons, withhold adrenaline and other CPRthe patient has been warmed to a temperature higherximately 30 C. Once 30 C has been reached, the inter-n drug doses should be doubled when compared withia intervals. As normothermia is approached (over

dard drug protocols should be used. Remember to rulerimary causes of cardiorespiratory arrest using the 4 Hsproach (e.g., drug overdose, hypothyroidism, trauma).

as

body core temperature decreases, sinus bradycardiae way to atrial brillation followed by VF and nallyOnce in hospital, severely hypothermic victims in car-should be rewarmed with active internal methods.s other thanVF tend to revert spontaneously as the coree increases, andusually donot require immediate treat-cardiamaybephysiological in severehypothermia, anding is not indicated unless bradycardia associated withmic compromise persists after rewarming.perature at which debrillation should rst beand how often it should be tried in the severelyic patient has not been established. AEDs may be usedtients. If VF is detected, give a shock at the maximuming; if VF/VT persists after three shocks, delay furthern attempts until the core temperature is above 30 C.246

s used, follow the AED prompts while rewarming theand rewarming may have to be continued for several

ilitate successful debrillation.246

measures for all victims include removal from thenment, prevention of further heat loss and rapid trans-ital. In the eld, a patient with moderate or severeia (Swiss stages II) should be immobilised and han-lly, oxygenated adequately, monitored (including ECGperature), and the whole body dried and insulated.241

shouldbecutoff rather than strippedoff; thiswill avoidovement of the victim. Conscious victims can mobiliserewarms a person more rapidly than shivering. Exer-rease any after-drop, i.e., further cooling after removalenvironment. Somnolent or comatose victims have a

old for developing VF or pulseless VT and should be

1410 J. Soar et al. / Resuscitation 81 (2010) 14001433

immobilised and kept horizontal to avoid an after-drop or cardio-vascular collapse. Adequate oxygenation is essential to stabilise themyocardiumandall victims should receive supplemental oxygen. Ifthe patient is unconscious, the airway should be protected. Pre hos-pital, prolonfurther hea

RewarmPassive rewhypothermfull body inwarm envirtrunk is parto prevent fis unconscibe arrangedposition. Rewarmhumiuid to a 7only abouttransport tcontinuousalert hypotmay be tranand observness shouldinternal rew

Severaldescribed, anique hasrewarming(up to 42

(rewarmingand a perfunicant afteRewarmingmented by crewarmingperitoneal,and extraco

In a hyextracorpornal rewarmoxygenatio812 Ch1

65min of cwhich undefacilities fora combinatis advisableof arrival textracorpor(ECMO) redcommonlyextracorpor

During ras vasodilatuous haemoAvoid hypeare no formstrategies foif appropria

Avalanche

In Euroavalanche d

skiers, snowboarders and snowmobilers. Death from avalanchesis due to asphyxia, trauma and hypothermia. Avalanches occur inareas that are difcult to access by rescuers in a timelymanner, andburials frequently involve multiple victims. The decision to initiate

uscits andood othey

d >3tricad intricad ini

m po

l resuhen at evi

per

tion

erthils an

eosby e

roduironorman bcurseat sd n

ces.25

lignacalc

e-thrcallypolakeye inc

trok

t strraturryingnonntal260; Ted innal hhigeffebetw

osin

eldeerlyechactorsrdioged investigation and treatments should be avoided, ast loss is difcult to prevent.ing may be passive, active external, or active internal.arming is appropriate in conscious victims with mildia who are still able to shiver. This is best achieved bysulation with wool blankets, aluminium foil, cap andonment. The application of chemical heat packs to theticularly helpful in moderate and severe hypothermiaurther heat loss in the pre hospital setting. If the patientous and the airway is not secured, insulation shouldaround the patient in the recovery (lateral decubitus)

warming in theeldwith heated intravenous uids anddiedgases isnot efcient. Infusinga litreof 40 Cwarm0kg patient at 28 C elevates the core temperature by0.3 C.241 Intensive active rewarming must not delayo a hospital where advanced rewarming techniques,monitoring and observation are available. In general,hermic and shivering victims without an arrhythmiasported to the nearest hospital for passive rewarming

ation. Hypothermic victims with an altered conscious-be taken to a hospital capable of active external andarming.active in-hospital rewarming techniques have beenlthough in a patient with stable circulation no tech-shown better survival over others. Active externaltechniques include forced air rewarming and warmedC) intravenous uids. These techniques are effectiverate 11.5 Ch1) in patients with severe hypothermia

sing rhythm.247,248 Even in severe hypothermia no sig-r-drop or malignant arrhythmias have been reported.with forced air and warm uid has been widely imple-linicians because it is easy and effective. Active internaltechniques include warm humidied gases; gastric,

pleural or bladder lavage with warmed uids (at 40 C),rporeal rewarming.237,249253

pothermic patient with apnoea and cardiac arrest,eal rewarming is the preferred method of active inter-ing because it provides sufcient circulation and

n while the core body temperature is increased by.253 Survivors in one case-series had an average ofonventional CPR before cardiopulmonary bypass,254

rlines that continuous CPR is essential. Unfortunately,extracorporeal rewarming arenot always available andion of rewarming techniques may have to be used. Itto contact the destination hospital well in advance

o make sure that the unit can accept the patient foreal rewarming. Extracorporealmembrane oxygenationuces the risk of intractable cardiorespiratory failureobserved after rewarming and may be a preferableeal rewarming procedure.255

ewarming, patients will require large volumes of uidsion causes expansionof the intravascular space. Contin-dynamic monitoring and warm IV uids are essential.rthermia during and after rewarming. Although thereal studies, once ROSC has been achieved use standardr post-resuscitation care, including mild hypothermiate (Section 4g).24a

burial

pe and North America, there are about 150 snoweaths each year. Most are sports-related and involve

full resvictimlikelihwhen

burieon ex

burieon ex

burieseru

Fuling, wwithou

8e. Hy

Deni

Hyplate faby homcausedheat p

Envin the fthan cmia ocwith h(HS) aninstan

Mamuscleand lifgenetiand de

Thetion ar

Heat s

Heatempeand vaclassicronmewavesincreasExertiocise inusuallyranges

Predisp

Theof undtory mrisk fahol, caative measures should be determined by the number ofthe resources available, and should be informed by thef survival.256 Avalanche victims are not likely to surviveare:

5min and in cardiac arrest with an obstructed airwaytion;itially and in cardiac arrest with an obstructed airwaytion, and an initial core temperature of 12mmol.

scitative measures, including extracorporeal rewarm-vailable, are indicated for all other avalanche victimsdence of an unsurvivable injury.

thermia

ermia occurs when the bodys ability to thermoregu-d core temperature exceeds that normally maintainedtatic mechanisms. Hyperthermia may be exogenous,nvironmental conditions, or secondary to endogenousction.ment-related hyperthermia occurs where heat, usuallyof radiant energy, is absorbedby the body at a rate fastere lost by thermoregulatory mechanisms. Hyperther-along a continuum of heat-related conditions, startingtress, progressing to heat exhaustion, to heat strokeally multiorgan dysfunction and cardiac arrest in some7

nt hyperthermia (MH) is a rare disorder of skeletalium homeostasis characterised by muscle contractureeatening hypermetabolic crisis following exposure ofpredisposed individuals to halogenated anaesthetics

rizing muscle relaxants.258,259

features and treatment of heat stress and heat exhaus-luded in Table 8.2.

e

oke is a systemic inammatory response with a coree above 40.6 C, accompanied by mental state changelevels of organ dysfunction. There are two forms of HS:

-exertional heat stroke (CHS) occurs during high envi-temperatures and often effects the elderly during heathe 2003 heatwave in France was associated with ancidence of cardiac arrests in those over 60-years old.261

eat stroke (EHS) occurs during strenuousphysical exer-h environmental temperatures and/or high humiditycts healthy young adults.262 Mortality from heat strokeeen 10 and 50%.263

g factors

rly are at increased risk for heat-related illness becauseing illness, medication use, declining thermoregula-nisms and limited social support. There are several: lack of acclimatization, dehydration, obesity, alco-vascular disease, skin conditions (psoriasis, eczema,

J. Soar et al. / Resuscitation 81 (2010) 14001433 1411

Table 8.2Heat stress and heat exhaustion.

Condition Features Treatment

Heat stress Normal or mild temperature elevation Rest

Heat exhaus

sclerodermmocytomaamphetaminel blockers

Clinical pres

Heat strsimilar mecdeaths in 2organ failur

core temp hot, dry s

tional hea early sign

ing, facial cardiovas

hypotens respirator central n

coma268; liver and coagulopa rhabdomy

Other cl

drug toxic drug with serotonin neurolept sepsis275; central ne endocrine

Managemen

The maimizing thecooling befothe core temheat strokehaemodynaof uid madescribed in

tech

eral ctrial

quessedover, grouseatersocoheatientstherthoseectioraturaterquesheteeno

erap

re arratural anrokeolingial.2

ant

lignaetalmlar bHeat oedema: swelling of feet and anklesHeat syncope: vasodilation causing hypotensionHeat cramps: sodium depletion causing cramps

tion Systemic reaction to prolonged heat exposure(hours to days)Temperature >37 C and

1412 J. Soar et al. / Resuscitation 81 (2010) 14001433

and advanced life support and cool the patient. Cooling techniquessimilar to those used to induce therapeutic hypothermia shouldbe used (see Section 4g).24a There are no data on the effects ofhyperthermia on debrillation threshold; therefore, attempt deb-rillation accthe patient.with normoneurologicature >37 C.guidelines.

8f. Asthm

Introductio

Worldwethnic backasthma syma high prevIreland andsymptom pespecially iestimated tlost annualburden. Anmated at 25with asthmfor the manfocuses oncardiac arre

Patients at

The riskto asthma s

a historyical ventil

a hospitayear300;

low or no an increa anxiety,

therapy.3

Causes of c

Cardiacafter a periodiac arrest i

severe br(this condeaths);

cardiac arcause of acaused byphylline)

dynamicsure (autoics. Auto-entering tof pressur

tension p

Diagnosis

Wheezing is a common physical nding, but severity doesnot correlate with the degree of airway obstruction. The absence

eezing may indicate critical airway obstruction, whereased wheezing may indicate a positive response to bron-

ator therapy. SaO2 may not reect progressive alveolarentilation, particularly if oxygen is being given. The SaO2itially decrease during therapy because beta-agonists causeronchodilation and vasodilation and may initially increaselmonary shunting.er causes of wheezing include: pulmonary oedema,c obstructive pulmonary disease (COPD), pneumonia,ylaxis,305 pneumonia, foreign bodies, pulmonary embolism,iectasis and subglottic mass.306

severity of an asthma attack is dened in Table 8.3.

terventions to prevent arrest

patient with severe asthma requires aggressive medicalement to prevent deterioration. Base assessment and treat-on an ABCDE approach. Patients with SaO2 40%diurnal variation for >50% of thetime over a period >150 days)despite intense therapyType 2: sudden severe attacks on abackground of apparently wellcontrolled asthma

ratory ow.

J. Soar et al. / Resuscitation 81 (2010) 14001433 1413

Nebulised beta-2 agonists

Salbutamol, 5mg nebulised, is the cornerstone of therapyfor acute asthma in most of the world. Repeated doses every1520mintinuous nebby high-oassociatedtive deliveravailable brepeating aspacer devitional beneasthma.308

Intravenous

Early usemergencyrates, especticosteroideffects betwIV route is pvomit or be

Nebulised an

Nebulisemay produthose who d

Nebulised m

Results oulised isotovolume of 2it is associatests and aadmission iare needed

Intravenous

Nebulisesevere andlack of debronchodilataneously bexacerbatiolife-threatevenous brounresponsitherapy is nlation).

IntravenousStudies o

life-threateMagnesiumindependeneffects (usside effectsuse intravewith life-thticentre ran

to report in 2012 and should provide denitive evidence on the roleof magnesium in acute severe asthma.

hyllochrce ocardier amentts aning sphyll

on00gntain

agonochrebulevideent.3

g IV

rienere artagons ofevidont

aneo

enalsubcuf subin in

rdial(eve

alineeateddrenthemlinesiderincreinguiircu

aphy

nous

ere olaementsce ots anted w

iox i. Amox inare often needed. Severe asthma may necessitate con-ulised salbutamol. Nebuliser units that can be drivenw oxygen should be available. The hypoventilationwith severe or near-fatal asthma may prevent effec-y of nebulised drugs. If a nebuliser is not immediatelyeta-2 agonists can be temporarily administered byctivations of a metered dose inhaler via a large volumece.298,307 Nebulised adrenaline does not provide addi-t over and above nebulised beta-2 agonists in acute

corticosteroids

e of systemic corticosteroids for acute asthma in thedepartment signicantly reduces hospital admissionially for those patients not receiving concomitant cor-therapy.309 Although there is no difference in clinicaleen oral and IV formulations of corticosteroids,310 thereferable because patients with near-fatal asthma mayunable to swallow.

ticholinergics

d anticholinergics (ipratropium, 0.5mg 46 hourly)ce additional bronchodilation in severe asthma or ino not respond to beta-agonists.311,312

agnesium sulphate

f small randomised controlled trials showed that a neb-nic solution of magnesium sulphate (250mmol l1) in a.55ml in combination with beta-2 agonists is safe andted with both an improvement of pulmonary functionnon-signicant trend towards lower rates of hospitaln patients with acute severe asthma.313 Further studiesto conrm those ndings.

bronchodilators

d bronchodilators are the rst line treatment for acutelife-threatening exacerbations of asthma. There is anitive evidence for or against the use of intravenoustors in this setting. Trials haveprimarily included spon-reathing patients with moderate to life-threateningns of asthma, evidence in ventilated patients withning asthma or cardiac arrest is sparse. The use of intra-nchodilators should generally be restricted to patientsve to nebulised therapy or where nebulised/inhaledot possible (e.g., a patient receiving bag-mask venti-

magnesium sulphatef intravenous magnesium sulphate in acute severe and

ning asthma have produced conicting results.314,315

sulphate causes bronchial smooth muscle relaxationt of the serummagnesium level andhas onlyminor sidehing, light-headedness). Given the low risk of seriousfrom magnesium sulphate it would seem reasonable tonous magnesium sulphate (1.22g IV slowly) in adultsreatening unresponsive to nebulised therapy. The mul-domised controlled trial 3Mg (ISRCTN04417063) is due

AminopA C

eviden(tachyWhethtreatmagonisobtainamino(unless5007be mai

Beta-2A C

with nsometreatm(250

LeukotThe

tor anndingstratedLRTA m

Subcut

Adrgivendose oat 20-mmyocaits useTerbutbe repto chilshownterbutabe conare atto distthese cthe an

Intrave

Sevhypovoin patievidenagoniscorrec

Heliox

Hel70:30)of heliineane review of intravenous aminophylline found nof benet and a higher incidence of adverse effectsa, vomiting) compared with standard care alone.316,317

inophylline has a place as an additional therapy afterwith established medications such as inhaled beta-d systemic corticosteroids remains uncertain. If afterenior advice the decision is taken to administer IVine a loading dose of 5mgkg1 is given over 2030minmaintenance therapy), followed by an infusion ofkg1 h1. Serum theophylline concentrations shoulded below 20gml1 to avoid toxicity.

istsane review on intravenous beta-2 agonists comparedised beta-2 agonists found no evidence of benet andnce of increased side effects compared with inhaled18 Salbutamolmay be given as either a slow IV injectionslowly) or continuous infusion of 320gmin1.

receptor antagonistse few data on the use of intravenous leukotriene recep-ists.319 Further studies are required to conrm thea recent randomised controlled trial which demon-ence of additional bronchodilation when intravenous

elukast was used as a rescue therapy.320

us or intramuscular adrenaline and terbutaline

ine and terbutaline are adrenergic agents that may betaneously to patients with acute severe asthma. The

cutaneous adrenaline is 300g up to a total of 3 dosestervals. Adrenalinemay cause an increase in heart rate,irritability and increased oxygen demand; however,n in patients over 35-years old) is well tolerated.321

is given in a dose of 250g subcutaneously, which canin 3060min. These drugs are more commonly givenwith acute asthma and, although most studies haveto be equally effective,322 one study concluded that

was superior.323 These alternative routes may need toed when IV access is impossible. Patients with asthmaased risk of anaphylaxis. Sometimes it may be difcultsh severe life-threatening asthma from anaphylaxis. Inmstances intramuscular adrenaline given according tolaxis guidelines may be appropriate (Section 8g).

uids and electrolytes

r near-fatal asthma is associated with dehydration andia, and this will further compromise the circulationwith dynamic hyperination of the lungs. If there isf hypovolaemia or dehydration, give IV uids. Beta-2d steroids may induce hypokalaemia, which should beith electrolyte supplements.

s a mixture of helium and oxygen (usually 80:20 oreta-analysis of four clinical trials did not support theusethe initial treatment of patients with acute asthma.324

1414 J. Soar et al. / Resuscitation 81 (2010) 14001433

Referral to intensive care

Patients that fail to respond to initial treatment, or develop signsof life-threatening asthma, should be assessed by an intensive carespecialist. Adiac arrestif cardiac ar

Rapid seconsideredhas:

a decreas persisting deteriora ndings o

oxygen m progressi respirator

Elevatiocheal intub

Non-invasiv

Non-invtality in COasthma is uits routine u

Treatment

Basic life sup

Give baslation will bto avoid gas

Advanced li

Modicathe need forecorded du67.811.1the normal20 cm H2O)hypoventilaasthmatic weven highersubstantiall

Respiratrequired fodynamic hydepends ondepends oncally ventil(achieved bgains in terless than 10

There isin patientsdisconnectepected duriof apnoea (ping if dynasupported botherwise d

Dynamic hyperination increases transthoracic impedance.337

Consider higher shock energies for debrillation if initial debril-lation attempts fail.338

There is no good evidence for the use of open-chest cardiacessiong thible crax cicatetrached htectio

aira larg, in ththe lal pnracorion ay ana-reled340

maECLSavai

aph

tion

recisencyropeomeion34

temidevtions.305

phylromtingted oine

for tabilit

iolo

ovees belifeti0 pea ver, andthe clicatntibiantoverf lesylaxig asor inanapdmission to intensive care after asthma-related car-is associated with signicantly poorer outcomes thanrest does not occur.325

quence induction and tracheal intubation should beif, despite efforts to optimize drug therapy, the patient

ing conscious level, coma;or worsening hypoxaemia;

ting respiratory acidosis despite intensive therapy;f severe agitation, confusion and ghting against theask (clinical signs of hypoxaemia);ve exhaustion;y or cardiac arrest.

n of the PaCO2 alone does not indicate the need for tra-ation.326 Treat the patient, not the numbers.

e ventilation

asive ventilationdecreases the intubation rate andmor-PD327; however, its role in patients with severe acutencertain. There is insufcient evidence to recommendse in asthma.328

of cardiac arrest

port

ic life support according to standard guidelines. Venti-e difcult because of increased airway resistance; trytric ination.

fe support

tions to standard ALS guidelines include consideringr early tracheal intubation. The peak airway pressuresring ventilation of patients with severe asthma (mean

cm H2O in 12 patients) are signicantly higher thanlower oesophageal sphincter pressure (approximately.329 There is a signicant risk of gastric ination andtion of the lungs when attempting to ventilate a severeithout a tracheal tube. During cardiac arrest this risk is, because the lower oesophageal sphincter pressure isy less than normal.330

ory rates of 810 breathsmin1 and tidal volumer a normal chest rise during CPR should not causeperination of the lungs (gas trapping). Tidal volumeinspiratory time and inspiratory ow. Lung emptyingexpiratory time and expiratory ow. In mechani-

ated severe asthmatics, increasing the expiratory timey reducing the respiratory rate) provides onlymoderatems of reduced gas trapping when a minute volume oflmin1 is used.329

limited evidence from case reports of unexpected ROSCwith suspected gas trapping when the tracheal tube isd.331335 If dynamic hyperination of the lungs is sus-ng CPR, compression of the chest wall and/or a perioddisconnection of tracheal tube) may relieve gas trap-mic hyperination occurs. Although this procedure isy limited evidence, it is unlikely to be harmful in anesperate situation.336

comprWorkireversmothobe indof thein skillthe dereleaseInsertthe ribture ofbilater

Extperfuspiratorasthmreportby asthuse ofnot be

8g. An

Deni

A pemergThe Euogy Ndenitor sysrapidlycirculachange

Anaators finteracmediaHistamsibleperme

Epidem

Thedata liand a100,00any ofinsectsdrugsbe impants, asignic

Theratio oAnaphexistinsevereWhenns in patients with asthma-associated cardiac arrest.rough the 4 Hs and 4 Ts will identify potentiallyauses of asthma-related cardiac arrest. Tension pneu-an be difcult to diagnose in cardiac arrest; it mayd by unilateral expansion of the chest wall, shiftingea and subcutaneous emphysema. Pleural ultrasoundands is faster and more sensitive than chest X-ray forn of pneumothorax.339 If pneumothorax is suspected,from the pleural space with needle decompression.e-gauge cannula in the second intercostal space, aboveemid-clavicular line, being careful to avoiddirect punc-ung. If air is emitted, insert a chest tube. Always considereumothoraces in asthma-related cardiac arrest.poreal life support (ECLS) can ensure both organnd gas exchange in case of otherwise untreatable res-d circulatory failure. Cases of successful treatment ofated cardiac arrest in adults using ECLS have been,341; however, the role of ECLS in cardiac arrest causedhas never been investigated in controlled studies. Therequires appropriate skills and equipment which may

lable everywhere.

ylaxis

of anaphylaxis

e denition of anaphylaxis is not important for itstreatment. There is no universally agreed denition.an Academy of Allergology and Clinical Immunol-

nclature Committee proposed the following broad2: Anaphylaxis is a severe, life-threatening, generalisedc hypersensitivity reaction. This is characterised byeloping life-threatening airway and/or breathing and/orproblems usually associated with skin and mucosal,343

axis usually involves the release of inammatory medi-mast cells and, or basophils triggered by an allergenwith cell-bound immunoglobulin E (IgE). Non-IgE-r non-immune release of mediators can also occur.and other inammatory mediator release are respon-he vasodilatation, oedema and increased capillaryy.

gy

rall frequency of episodes of anaphylaxis using currenttween 30 and 950 cases per 100,000 persons per yearme prevalence of between 50 and 2000 episodes perrsons or 0.052.0%.344 Anaphylaxis can be triggered byy broad range of triggers including foods, drugs, stinginglatex. Food is the commonest trigger in children and

ommonest in adults.345 Virtually any food or drug caned, but certain foods (nuts) and drugs (muscle relax-otics, NSAIDs and aspirin) cause most reactions.346 Anumber of cases of anaphylaxis are idiopathic.all prognosis of anaphylaxis is good, with a case fatalitys than 1% reported in most population-based studies.s and risk of death is increased in those with pre-thma, particularly if the asthma is poorly controlled,asthmaticswhodelay treatmentwithadrenaline.347,348

hylaxis is fatal, death usually occurs very soon after

J. Soar et al. / Resuscitation 81 (2010) 14001433 1415

contact with the trigger. From a case-series, fatal food reactionscause respiratory arrest typically after 3035min; insect stingscause collapse from shock after 1015min; and deaths causedby intravenous medication occur most commonly within 5min.Death neveger.

Recognitio

Anaphylto a triggerminutes) wbreathing aand mucosa

Many prect treatmsystemic allalised urticaanaphylaxisAnaphylaxiinevitable dsafety. Patiecirculation

Airway prob

Airway sgeal/laryn

Hoarse vo Stridor.

Breathing pr

Shortness Wheeze. Confusion Respirato Life-threa

triggered

Circulation p

Pale, clam Tachycard Hypotens Decreased Myocardi

even in in Cardiac ar

Circulatican be causcapillary leausually a la

Skin and, or

These shthe ABCDE

They arephylaxis c

They can There ma

changes a

There may be erythema, urticaria (also called hives, nettle rash,weals or welts), or angioedema (eyelids, lips, and sometimes inthe mouth and throat).

st pao de

ent

anife-thtreausperew,al mre an

posi

ientsrestin ablemat wlood

e the

p anyafte

d of rtrig

respir

t carrrentensus ess

obst

phylke a, trahelp

nd t

line (enallaxi

58 adtal e

probt, it ra-recce ofrienehat ierityk beis noe efuscuenals. Ifr occurred more than 6h after contact with the trig-

n of an anaphylaxis

axis is the likely diagnosis if a patient who is exposed(allergen) develops a sudden illness (usually within

ith rapidly developing life-threatening airway and/ornd/or circulation problems usually associated with skinl changes. The reaction is usually unexpected.atients with anaphylaxis are not given the cor-ent.349 Confusion arises because some patients haveergic reactions that are less severe. For example, gener-ria, angioedema, and rhinitiswould not be described as, because the life-threatening features are not present.s guidelines must therefore take into account someiagnostic errors, with an emphasis on the need fornts can have either an airway and/or breathing and/orproblem:

lems

welling, e.g., throat and tongue swelling (pharyn-geal oedema).ice.

oblems

of breath.

caused by hypoxia.ry arrest.tening asthma with no features of anaphylaxis can beby food allergy.350

roblems

my.ia.ion.conscious level.

al ischaemia and electrocardiograph (ECG) changesdividuals with normal coronary arteries.351

rest.

on problems (often referred to as anaphylactic shock)ed by direct myocardial depression, vasodilation andk, and loss of uid from the circulation. Bradycardia is

te feature, often preceding cardiac arrest.352

mucosal changes

ould be assessed as part of the exposure when usingapproach.

often the rst feature and present in over 80% of ana-ases.353

be subtle or dramatic.y be just skin, just mucosal, or both skin and mucosalny where on the body.

Mogo on t

Treatm

UseTreat lples ofhave slance cMinimpressu

Patient

Patdiac arplaceding proLying a low b

Remov

Stostingermethoing the

Cardio

Starlow cushould(ALS) i

Airway

Anawillmatilationexpert

Drugs a

AdrenaAdr

anaphytrials,3

anecdolationagonisIts betthe forleukotcells tthe sevto worbut itAdversintram

Adrfeaturetients who have skin changes caused by allergy do notvelop anaphylaxis.

of an anaphylaxis

ABCDE approach to recognise and treat anaphylaxis.reatening problems as you nd them. The basic princi-tment are the same for all age groups. All patients whocted anaphylaxis should be monitored (e.g., by ambu-in the emergency department etc,) as soon as possible.onitoring includes pulse oximetry, non-invasive bloodd 3-lead ECG.

tioning

with anaphylaxis can deteriorate and are at risk of car-if made to sit up or stand up.354 All patients should becomfortable position. Patients with airway and breath-smayprefer to sit up as thiswillmake breathing easier.ith or without leg elevation is helpful for patients withpressure (circulation problem).

trigger if possible

drug suspected of causing anaphylaxis. Remove ther a bee sting. Early removal is more important than theemoval.355 Do not delay denitive treatment if remov-ger is not feasible.

atory arrest following an anaphylaxis

diopulmonary resuscitation (CPR) immediately and fol-guidelines. Prolonged CPR may be necessary. Rescuersre that help is on its way as early advanced life support

ential.

ruction

axis can cause airway swelling and obstruction. Thisirwayandventilation interventions (e.g., bag-maskven-cheal intubation, cricothyroidotomy) difcult. Call forearly.

heir delivery

epinephrine)ine is the most important drug for the treatment ofs.356,357 Although there are no randomised controlledrenaline is a logical treatment and there is consistentvidence supporting its use to ease breathing and circu-lems associated with anaphylaxis. As an alpha-receptoreverses peripheral vasodilation and reduces oedema.eptor activity dilates the bronchial airways, increasesmyocardial contraction, and suppresses histamine andrelease. There are beta-2 adrenergic receptors on mastnhibit activation, and so early adrenaline attenuatesof IgE-mediated allergic reactions. Adrenaline seems

st when given early after the onset of the reaction359

t without risk, particularly when given intravenously.fects are extremely rare with correct doses injectedlarly (IM).ine should be given to all patients with life-threateningthese features are absent but there are other features of

1416 J. Soar et al. / Resuscitation 81 (2010) 14001433

a systemic allergic reaction, the patient needs careful observationand symptomatic treatment using the ABCDE approach.

Intramuscular (IM) adrenaline. The intramuscular (IM) routeis the besttreat anaphblood pressthe respons

There is a It does no The IM ro

The bestmiddle thirenough toThe subcutamended foeffective th

Adrenaliweak.Doseto draw up

(The eqbrackets)

>12 years>612 ye>6 month

J. Soar et al. / Resuscitation 81 (2010) 14001433 1417

Mast cell tryptase

The specic test to help conrm a diagnosis of anaphylaxis ismeasurement of mast cell tryptase. Tryptase is the major proteincomponentcell degranucentrationssignicantlypeak 12himately 2h68h, so timof onset ofnoticed.

(a) Minimu(b) Ideally:

Initial samdo not de

Second sa Third sam

follow-upsome indi

Serial sagle measure

Discharge a

Patientsbreathing othen observthreateningtreatment srence of syunder obseunknown. Aclear whethphylaxis anThere is noreaction. Itare made fo

Before d

Reviewed Given clea Considere

3 days. Ththe chanc

Considerereplacem

Have a plgeneral p

An adrepatients atat continuestings and finjector isdrug-inducIdeally, all phave a treat

Individuhospital muto use it. En

patients general practitioner. All patients presenting with anaphy-laxis should be referred to an allergy clinic to identify the cause,and thereby reduce the risk of future reactions and prepare thepatient to manage future episodes themselves. Patients need to

the able tn sutionencedecr

rdia

diacon ince odete

ts.398

ponarax, oed phigh

ter ca99 toto t

ts isally ial ch

cati

ientso beperfunaryind

g CP

t exollapia cneumlaempactherapumd byloodty toothomergngedakerF.

illati

re isl disry ICUted illatioof mast cell secretory granules. In anaphylaxis, mastlation leads to markedly increased blood tryptase con-

. Tryptase concentrations in the blood may not increaseuntil 30min or more after the onset of symptoms, and

after onset.385 The half-life of tryptase is short (approx-), and concentrations may be back to normal withining of any blood samples is very important. The time

the anaphylaxis is the time when symptoms were rst

m: one sample at 12h after the start of symptoms.three timed samples:

ple as soon as feasible after resuscitation has started lay resuscitation to take sample.mple at 12h after the start of symptomsple either at 24h or in convalescence (for example in aallergy clinic). This provides baseline tryptase levels viduals have an elevated baseline level.

mples have better specicity and sensitivity than a sin-ment in the conrmation of anaphylaxis.386

nd follow-up

who have had suspected anaphylaxis (i.e., an airway,r circulation (ABC) problem) should be treated anded in a clinical area with facilities for treating life-ABC problems. Patients with a good response to initialhould be warned of the possibility of an early recur-mptoms and in some circumstances should be keptrvation. The exact incidence of biphasic reactions islthough studies quote an incidence of 120%, it is noter all the patients in these studies actually had an ana-d whether the initial treatment was appropriate.387

reliable way of predicting who will have a biphasicis therefore important that decisions about discharger each patient by an experienced clinician.ischarge from hospital all patients must be:

by a senior clinician.r instructions to return to hospital if symptoms return.d for antihistamines and oral steroids therapy for up tois is helpful for treatment of urticaria and may decreasee of further reaction.d for an adrenaline auto-injector, or given aent.388390

an for follow-up, including contact with the patientsractitioner.

naline auto-injector is an appropriate treatment forincreased risk of idiopathic anaphylaxis, or for anyoned high risk of reaction, e.g., to triggers such as venomood-induced reactions (unless easy to avoid). An auto-not usually necessary for patients who have suffereded anaphylaxis, unless it is difcult to avoid the drug.atients should be assessed by an allergy specialist andment plan based on their individual risk.als provided with an auto-injector on discharge fromst be given instructions and training on when and howsure appropriate follow-up including contact with the

knowto be athey camedicais evidshould

8h. Ca

Carcommincidenlogicalpatienas tammothoif treatatively24h afis 54%3

Keypatienespeciextern

Identi

Patlikely ttionorpulmocient topulse.

Startin

Starwho chypoxsion phypovocardiaclong asnectedmaximverietolic bInabilipneumitate ebe chapacemlying V

Debr

Thesternasurgerbe treadebrillergen responsible and how to avoid it. Patients needo recognise the early symptoms of anaphylaxis, so thatmmon help quickly and prepare to use their emergency. Although there are no randomised clinical trials, therethat individualised action plans for self-managementease the risk of recurrence.391

c arrest following cardiac surgery

arrest following major cardiac surgery is relativelythe immediate post-operative phase, with a reportedf 0.72.9%.392400 It is usually preceded by physio-rioration,401 although it can occur suddenly in stableThere are usually specic causes of cardiac arrest, suchde, hypovolaemia,myocardial ischaemia, tensionpneu-r pacing failure. These are all potentially reversible andromptly cardiac arrest after cardiac surgery has a rel-survival rate. If cardiac arrest occurs during the rstrdiac surgery, the rate of survival to hospital discharge79%398,402 in adults and 41% in children.401

he successful resuscitation of cardiac arrest in thesethe need to perform emergency resternotomy early,n the context of tamponade or haemorrhage, whereest compressions may be ineffective.

on of cardiac arrest

in the ICU are highly monitored and an arrest is mostsignalled bymonitoring alarmswhere absence of pulsa-singpressureon thearterial line, lossofpulseoximeter,artery (PA) trace, or end-tidal CO2 trace can be suf-icate cardiac arrestwithout the need to palpate a central

R

ternal chest compressions immediately in all patientsse without an output. Consider reversible causes:heck tube position, ventilate with 100% oxygen; ten-othorax clinical examination, thoracic ultrasound;ia, pacing failure. In asystole, secondary to a loss of

ing, external massage may be delayed mo