RESUSCITATION - Elsevier...also been observations that ‘cough CPR’ resulted in some blood flow....

1.1 Basic life support 2

1.2 Advanced life support 6

1.3 Advanced airway management 15

1.4 Cerebral resuscitation after cardiacarrest 20

1.5 Shock 23

1.6 Ethics of resuscitation 33

1

SECTION

1EDITED BY ANTHONY F.T. BROWN

RESUSCITATION

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application of a semi-automatic externaldefibrillator (SAED), if one is availableclose to the site of the cardiac arrest.

DEVELOPMENT OFPROTOCOLSIt is important that the guidelines forBLS be nationally consistent. To achievethis, many countries have establishednational expert committees to advise thecommunity, ambulance services andmedical profession on BLS guidelines.Table 1.1.1 shows the national associationsthat make up the International LiaisonCommittee on Resuscitation (ILCOR).This group meets every 6 years to reviewthe BLS guidelines and to consider changesto these guidelines. The most recentrevision of BLS guidelines occurred in2000.2 Subsequently, each nationalcommittee may determine regionalvariations to these guidelines to take intoaccount local practices.

One of the major considerations ofchanges to protocols for these commit-tees is the feasibility of these protocols tobe implemented by personnel with mini-mal training. The major handicap to con-sideration of the protocols is the relativepaucity of good scientific evidence forthe strategies that have been taught overmany years.

INITIAL EVALUATIONA flow chart for the initial evaluation of the collapsed patient is shown inFigure 1.1.1. This flow chart commenceswith the recognition that a patient hascollapsed. The initial steps are as follows:

Check for dangersAs the patient is approached, thebystander should immediately considerany dangers that may be associated with

2

INTRODUCTIONThe patient with sudden cardiac arrestrequires a bystander to initiate a numberof actions in rapid sequence for there tobe any hope of successful resuscitation.These steps are known as the ‘chain ofsurvival’.1 After the first step, a call toambulance, the bystander needs toinstitute basic life support (BLS) whilstawaiting the arrival of the emergencymedical services (EMS). The BLS proce-dures may be undertaken by personnelwith little or no medical training and areapplicable in the patient who has becomeunconscious as a result of airway obstruc-tion, respiratory arrest or cardiac arrest.In general, BLS includes interventionsthat involve minimal training in the useof equipment, but also now include the

1.1 BASIC LIFE SUPPORTSTEPHEN BERNARD

ESSENTIALS1 The patient with sudden cardiacarrest requires a bystander to institutethe ‘chain of survival’, includingimmediate call to emergency medicalservices and the performance ofbystander cardiopulmonaryresuscitation.

2 Current survival rates for pre-hospital cardiac arrest are low,however, strategies for improvementare increasingly being implemented.

3 Early defibrillation is life-savingand is now regarded as a part ofbasic life support.

4 Co-responders with ambulanceservices, such as fire fighters, mayprovide early defibrillation.

5 Early defibrillation may bedelivered by untrained bystanders orminimally trained security staff (public access defibrillation).

Table 1.1.1

American Heart Association

Australian Resuscitation Council

European Resuscitation Council

Heart and Stroke Foundation of Canada

Inter-American Heart Foundation

New Zealand Resuscitation Council

Resuscitation Council of Southern Africa

Jaw support

Jaw thrust

Jaw thrust

Fig. 1.1.1 Diagram of head tilt, jaw thrust(courtesy Australian Resuscitation Council).

1.1 BASIC LIFE SUPPORT

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the collapse of the patient. For example,the patient may have been electrocutedand there could be further casualties ifthe power source is not switched offprior to patient contact.

In the case of a motor-vehicle accidentwhere a patient is unconscious, there isthe risk of additional injury from furthercollisions involving passing vehicles andanother bystander should be tasked todirect traffic at the scene. There may alsobe a risk of fire if fuel has leaked onto hotengine parts or there is an electrical fault.Therefore, the ignition should be switchedoff, and it is advised that unconsciouspatients should be immediately removedfrom vehicles prior to the arrival ofemergency medical services, whist takingcare to minimize movement of the neck.It is considered that the risk of injuryfrom a sudden fire or explosion exceedsthat of moving an unconscious patientprior to immobilization of the cervicalspine with a hard collar.

In the case of a patient who hascollapsed in a confined space, the possibi-lity of poisoning with carbon monoxideor a similar toxic gas should be consid-ered, and the scene not entered until itcan be made safe by emergency services.

Check for responseThe patient who has collapsed must bequickly assessed to determine whetherthere is coma, indicating possible cardiacarrest or just a simple fall. This is assessedby a gentle ‘shake and shout’, followedby an examination of the motor andverbal response of the patient.

If the patient is unresponsive, cardiacarrest due to ventricular fibrillation shouldbe suspected and emergency medicalservices telephoned immediately (‘callfirst’). Alternatively, if the collapse is dueto suspected airway obstruction (choking)or inadequate ventilations (drowning,hanging, etc.), then resuscitation shouldbe commenced for approximately 1minute prior to the calling of emergencymedical services (‘call fast’).

AirwayIf the unconscious patient has collapsedin a prone position, then he/she shouldbe placed on his/her side in the coma

position (see Fig. 1.1.2) and an assess-ment of the airway should be made.Alternatively, if the patient has collapsedand is supine, the airway may be checkedin that position.

One exception to this initial step is if the unconscious patient has beenretrieved from near drowning. In thissetting, the initial step of rolling onto theside to allow assessment of airway andfacilitate airway clearance has beenpractised by surf life-savers for manyyears and is still recommended by someauthorities as the initial position forpatient assessment.

The airway is checked with visualinspection, careful forward movement ofthe jaw (‘jaw thrust’) and sweeping outany foreign material or vomitus with afinger. In general, ‘noisy breathing isobstructed breathing’, although anexception to this rule might include thepatient with severe asthma who has sucha low tidal volume that there are nosounds from the upper airway.

If the airway is obstructed with a foreignbody, there are a number of manoeuvresthat have been described as helpful inthis setting. In North America, theHeimlich manoeuvre is endorsed as thetechnique of choice. However, thistechnique is associated with some signi-

ficant complications, including intra-abdominal injuries. In Australia, therecommended technique for clearing anairway that is completely obstructed by aforeign body includes back blows andlateral chest thrusts.

In a study comparing standard chestcompressions and Heimlich manoeuvreon cadavers with a simulated completeairway obstruction, the mean peak airwaypressure was significantly lower with abdo-minal thrusts compared to chest com-pressions.3 This study concluded thatstandard chest compressions have thepotential of being more effective thanthe Heimlich manoeuvre for the manage-ment of complete airway obstruction bya foreign body in an unconscious patient.

BreathingAdequate respirations are assessed byvisually inspecting movement of the chestwall. In cases of cardiac arrest, infrequent,deep (agonal) respirations may continuefor some minutes.

If the patient is found to have in-adequate or absent breathing on initialassessment, then expired air resuscitation,mouth-to-mask or assisted ventilationwith a bag/valve/mask will be required.On the other hand, if the initial assess-ment of the unconscious patient reveals


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NADULT BASIC LIFE SUPPORT

Send or go for help as soon as possible according to guidelines

If breathing:Recovery position

Shake and shout

Head tilt/Chin lift

Look, listen and feel

2 effective breaths

Signs of a circulation

Check circulationevery minute 100 per minute

15:2 ratio

CHECK RESPONSIVENESS

OPEN AIRWAY

CHECK BREATHING

BREATHE

ASSESS10 seconds only

CIRCULATIONPRESENTContinue

Rescue Breathing

NO CIRCULATIONCompress Chest

Fig. 1.1.2 BLS algorithm (courtesy of ILCOR).

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adequate respirations, the victim shouldbe turned and maintained in a recoveryposition.

CirculationPreviously, it was recommended that abystander attempt to palpate a pulse inorder to diagnose cardiac arrest and, ifabsent, commence external cardiacmassage (ECM). However, it is nowrecognized that the pulse check is quiteinaccurate in this setting.4 Since cardiacarrest may be presumed if breathing isabsent and is very unlikely if breathing isadequate, this step has now been deletedfrom BLS assessment.

CARDIOPULMONARYRESUSCITATIONIf cardiac arrest is diagnosed, and theEMS has been summoned, the bystandershould now commence CPR, using bothexpired air resuscitation (EAR) andECM until a defibrillator arrives.

Expired air resuscitationSince first described in 1958, EAR hasbecome the standard in BLS for patientswho have absent or inadequate respira-tions. However, there is often consider-able reluctance for bystanders to performEAR due to the perceived difficulty andcontact with saliva resulting in thepossibility of cross-infection.

It has been demonstrated in animalmodels that some ventilation occurs duringchest compressions and it has been pro-posed that EAR may be withheld inpatients who have cardiac arrest. In astudy of 520 patients with pre-hospitalcardiac arrest, bystanders were giveninstructions by ambulance dispatchers toperform EAR plus ECM or ECM alone.5

There was a trend towards better survivalto hospital discharge in the ECM onlygroup compared with the EAR plusECM (14.6% vs. 10.4%), however, thisdifference was not statistically significant(P=0.18). In this study, response times forEMS were very short (mean 5 minutes),consequently, the role of EAR in EMSareas where response times are longerremains uncertain.

There are a number of simple pieces ofequipment that may be used as an alter-native to EAR. These include mouth-to-mask and bag/valve/mask, with orwithout an oral-pharyngeal airway. Thisequipment has the advantage that thereis no possible cross-infection risk, how-ever, some training in the use of thesedevices is required. Within BLS, Guide-lines 2000 recommends specific tidalvolumes in bag/valve mask ventilation.2

Whichever technique of assisted ventila-tion is used, adequate tidal volume isassessed by the rise of victim’s chest,whether there is any distension of thestomach, and by listening and feeling for air being exhaled from the patient’smouth.

The use of supplemental oxygen haspreviously not been considered as part ofBLS, however, some advisory committeeswithin ILCOR are now incorporatingoxygen use within BLS training. Althoughthere are little data on the effect onoutcome, it is intuitive that supplementaloxygen during CPR would increase theoxygen content of the blood and oxygendelivery to vital organs.

External cardiaccompressionsExternal cardiac massage was firstdescribed in 1960. Subsequently, ECMhas been adopted as the standard of carefor patients with cardiac arrest. However,there is debate as to whether ECM gen-erated blood flow via a ‘cardiac pump’mechanism or a ‘thoracic pump’. Thethoracic pump theory had been supportedby early transthoracic echocardiographicstudies during CPR showing that thecardiac valves remained open during therelaxation phase of ECM. There had also been observations that ‘cough CPR’resulted in some blood flow. It waspresumed that the changes in intra-thoracic pressure led to forward bloodflow and that valves in the venous systemprevented back flow.

However, more recent studies oftrans-oesophageal echocardiographyduring CPR in humans6 has found thatduring the compression phase, the leftventricle is compressed; the mitral valveremains closed and the aortic valve opens

only at the end of compression. Duringthe relaxation phase, the mitral valve opensand the left ventricle is filled. Thesefindings suggest that blood flow duringECM is a result of cardiac compression,at least early in the course of ECM.

Whatever the predominant mechanismof blood flow, ECM results in only 15%-20% of cardiac output in the adult, mainlyowing to the relative rigidity of the chestwall. Consequently, there is progressivemetabolic acidosis during CPR and veryfew adults survive when ECM has beengiven for more than 30 minutes.

The current recommended rate forECM is 100 per minute, to ensure thedelivery of a minimum of 60 compres-sions per minute. The sternum should bedepressed at least 4 cm in the adult withcompression being approximately 50% ofthe cycle. Pauses in chest compressionsresult in a prolonged decrease in meanarterial blood pressure, therefore, it isrecommended that two breaths for every15 compressions be delivered without apause in chest compressions if there aretwo rescuers.

DEFIBRILLATIONSemi-automatic external defibrillation(SAED) is now considered part of BLS.7

The SAED devices are extremely sensi-tive and specific for the correct diagnosisof ventricular fibrillation or ventriculartachycardia and are simple for bystandersto use with minimal training. Followingthe switching on of the device and theapplication of the pads, the SAED willrequest confirmation of coma and absentrespirations, and advise the bystander to‘stand clear’. The bystander is then advisedto press a button to deliver a shock.

There are four situations that havebeen proposed where non-medicalpersonnel could use a SAED. First, theSAED may be used by first responderssuch as fire services who co-respond withambulance services. For example, Ontario,Canada, has implemented an extensiveprogramme to introduce rapid defibrilla-tion across that state.8 The use of firedepartment first responders resulted in92.5% of cardiac arrest patients being de-


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fibrillated in under 8 minutes comparedwith 76.7% under the previous system(P<0.001). Survival to hospital dischargeimproved from 3.9% (183/4690 patients)to 5.2% (85/1614 patients) (P=0.03).This study demonstrated that an in-expensive, multifaceted system optimiza-tion approach to rapid defibrillation canlead to significant improvements in sur-vival after cardiac arrest in a large system.In Melbourne, Australia, a study of a fire-service first responder programme foundthat the mean time to defibrillation wasreduced from a mean of 7.1 minutes forambulance services to 6.0 minutes forthe combined approach.9 However, thisstudy did not have the power to assessthe impact on patient outcomes.

Second, the SAED may be placed in apublic area for use by designatedpersonnel such as security staff whoundergo a short training programme. Inplaces such as casinos10 and a largefootball stadium,11 this approach hasbeen shown to be effective.

Third, the SAED may be placed in apublic area for use by personnel with noprevious training at all in the use of anSAED. For example, at Chicago airport,there were defibrillators placed instrategic locations with signs advising ofthe correct use of the SAED.12 Over a 2-year period, there were 21 patients withcardiac arrests, of whom 18 had an initialrhythm of ventricular fibrillation. Adefibrillator was applied by a ‘goodSamaritan’ bystander in 14/18 patientswith ventricular fibrillation and 11 weresuccessfully resuscitated, with 10 patientsalive and well at 1 year.

However, most cardiac arrests occur in the home and it is estimated that the widespread implementation of thisapproach to all public areas would bevery costly and result in relatively fewlives saved.13

An SAED may be placed in the homeof a patient who is at increased risk ofsudden cardiac death for use by a partner

or relative who (hopefully) would witnessthe cardiac arrest. Clinical trials arerequired to assess the cost-effectivenessof this approach prior to widespreadimplementation.

SUMMARYBasic life support for the patient withsudden cardiac arrest has been describedas a ‘chain of survival’ and includesrecognition of cardiac arrest, a call toemergency medical services, the perform-ance of EAR and ECM, and early defib-rillation using a semi-automatic externaldefibrillator.

Current research explores the cost-effective means of delivering early defibril-lation using public access defibrillationby personnel with no previous training,first responders with minimal trainingsuch as security personnel, co-responders

with ambulance services (such as firefighters) or even defibrillators in thehomes of high-risk patients.

REFERENCES1. Cummins RO, Ornato JP, Thies WH, Pepe PE

1991 Improving survival from sudden cardiacarrest: The ‘chain of survival’ concept. A statementfor health professionals from the advanced cardiaclife-support subcommittee and the emergencycardiac care committee, American HeartAssociation. Circulation 83: 1832–47

2. American Heart Association in Collaboration withthe International Liaison Committee onResuscitation (ILCOR) 2000 Guidelines 2000 forcardiopulmonary resuscitation and emergencycardiovascular care. Resuscitation 46(1–3): 1–448

3. Langhelle A, Sunde K, Wik L, Steen PA 2001Airway pressure with chest compressions versusHeimlich manoeuvre in recently dead adults withcomplete airway obstruction. Resuscitation48: 185–7

4. Eberle B, Dick WF, Schneider T, Wisser G,Doetsch S, Tzanova I 1996 Checking the carotidpulse check: accuracy of first responders in patientswith and without a pulse. Resuscitation 33: 107–16

5. Hallstrom A, Cobb L, Johnson E, Copass M 2000Cardiopulmonary resuscitation by chestcompression alone or with mouth to mouthventilation. New England Journal of Medicine342: 1546–53

6. Mair P, Furtwaengler W, Baubin M 1993 Aorticvalve function during cardiopulmonaryresuscitation. New England Journal of Medicine329: 1965–6

7. Marenco JP, Wang PJ, Link MS, Homoud MK,Estes NA 2001 Improving survival from suddencardiac arrest: the role of the automated externaldefibrillator. Journal of the American MedicalAssociation 285: 1193–200

8. Stiell IG, Wells GA, Field BJ, et al 1999 Improvedout-of-hospital cardiac arrest survival through theinexpensive optimization of an existingdefibrillation program. Journal of the AmericanMedical Association 281: 1175–81.

9. Smith KL, McNeill JJ, Emergency MedicalResponse Steering Committee 2002 Cardiac arreststreated by ambulance paramedics and fire fighters.Medical Journal of Australia 177: 305–9

10. Valenzuela T, Roe TJ, Nichol G, et al 2000Outcomes of rapid defibrillation by security officersafter cardiac arrests in casinos. New EnglandJournal of Medicine 343: 1206–9

11. Wasserthiel J, Keane G, Fisher N, Leditschenke JF2000 Cardiac arrest at the Melbourne CricketGround and Shrine of Remembrance using a tieredresponse strategy – a forerunner to public accessdefibrillation. Resuscitation 44: 97–104

12. Caffrey SL, Willoughby PJ, Pepe PE, Becker LB2002 Public use of automated externaldefibrillators. New England Journal of Medicine347: 1242–7

13. Pell JP, Sirel JM, Marsden AK, Ford I, Walker NL,Cobbe SM 2002 Potential impact of public accessdefibrillators on survival after out of hospitalcardiopulmonary arrest: retrospective cohort study.British Medical Journal 325: 515–20


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CONTROVERSIES❶ The cost-effectiveness ofwidespread training programmes toteach bystanders to performcardiopulmonary resuscitation isuncertain.

❷ Expired air breathing may not berequired early in cardiopulmonaryresuscitation.

❸ The exact mechanism by whichexternal chest compressions generateblood flow is uncertain. In any case,external chest compressions areminimally effective, and few patientssurvive prolonged chestcompressions.

❹ Outcomes from public accessdefibrillation and first-responderprogrammes will need todemonstrate that these programmesare cost-effective.

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rate was the sum of the three coefficients,or 5.5% per minute.

The importance of rapid treatment ofcardiac arrest has led clinicians todevelop a systems management approach,represented by the concept of the ‘chainof survival’, which has become a widelyaccepted model for the emergencymedical services (EMS) systems.3 Thechain of survival idea maintains thatmore people survive sudden cardiacarrest when a sequence of events occursas rapidly as possible. This sequence is:

• early access to the EMS system• early BLS• early defibrillation• early advanced care.

A weakness in any link of the chain re-duces the probability of patient survival,and all of the links must be connected.By convention, ALS involves continua-tion of BLS as appropriate, with theaddition of defibrillation, invasive airwayand vascular access techniques, and theadministration of pharmacologic agents.

AETIOLOGY ANDINCIDENCE OFCARDIAC ARRESTThe commonest cause of adult suddencardiac arrest is ischaemic heart disease. 4,

5 Other causes of cardiac arrest includerespiratory failure, drug overdose, meta-bolic derangements, trauma, hypothermia,immersion and hypovolaemia. WhileALS guidelines are universally applicable,in these situations specific modificationsmay be appropriate. 4, 5

The incidence of sudden cardiac death(within 24 hours of the onset of symp-toms) in the USA has been estimated as1.24/1000/year.6 In western metropo-litan Melbourne, Australia, in 1995 theincidence of cardiac arrest notified toambulance was approximately 0.72/1000/year.7 In 20 communities fromdeveloped nations worldwide an average

of 0.62/1000/year received attemptedresuscitation after out-of-hospital cardiacarrest.6

ADVANCED LIFESUPPORT GUIDELINESAND ALGORITHMSIn 1997 the International LiaisonCommittee on Resuscitation (ILCOR),with delegates from Australia, Canada,Europe, South Africa and the USApublished an advisory statement on ALS,The Universal ALS Algorithm,1 basedlargely on the belief that valid scientificevidence supports only threeinterventions as unequivocally effectivein adult cardiac resuscitation:

• basic CPR• defibrillation if the dysrhythmia is

VF or pulseless VT• tracheal intubation.1

The algorithm (Fig. 1.2.1) recom-mends a specific sequence in which theabove interventions should be performed,and prompts consideration of othertherapies and potentially reversiblecauses of cardiac arrest. It is uncompli-cated, concise, easy to memorize andadapt into poster format and is readilyapplied to the clinical situation. Theguidelines and algorithm were ratified bythe European Resuscitation Council(ERC) in Copenhagen, in June 1998and published as The 1998 EuropeanResuscitation Council guidelines foradult advanced life support.8

In 2000, the American Heart Asso-ciation (AHA) convened the Interna-tional Guidelines 2000 Conference onCPR and Emergency Cardiac Care(ECC). Following this conference, theInternational Guidelines 2000 for CPRand ECC were developed andpublished.5 These guidelines represent aconsensus of expert individuals andresuscitation councils and similarorganizations from many countries,

6

INTRODUCTIONThe patient in cardiac arrest is the mosttime-critical medical crisis an emergencyphysician is likely to manage. The inter-ventions of basic life support (BLS) andadvanced life support (ALS) have thegreatest probability of success whenapplied immediately, but become lesseffective with the passing of time, andafter only a short interval without treat-ment are ineffectual.

In 1993, Larsen et al2 calculated thetime intervals from collapse to theinitiation of BLS, defibrillation and otherALS treatments, and analyzed their effectson survival from out-of-hospital cardiacarrest. When all three interventions wereimmediately available the survival was67%, and this figure declined by 2.3% perminute of delay to BLS, a further 1.1%per minute to defibrillation and 2.1% perminute to other ALS interventions.Without treatment the decline in survival

1.2 ADVANCED LIFE SUPPORTJOHN E. MAGUIRE

ESSENTIALS1

1 Follow international resuscitationguidelines.

2 Perform cardiopulmonaryresuscitation (CPR) without interruption for pulseless patients(except when analyzing the rhythm or applying defibrillation shocks).

3 Defibrillate ventricular fibrillation(VF) and pulseless ventriculartachycardia (VT) until reverted to astable, perfusing rhythm.

4 Obtain, maintain and protect an airway and provide adequateoxygenation and ventilation.

5 Give intravenous boluses ofadrenaline (epinephrine).

6 Correct reversible causes ofcardiac arrest.

1.2 ADVANCED LIFE SUPPORT

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cultures and disciplines. The underlyingprinciples that assisted decision-makingwhen developing the guidelines werethat additions to existing guidelines hadto pass a rigorous evidence-based review,and revisions or deletions occurredbecause of:

• lack of evidence to confirmeffectivenessand/or

• additional evidence to suggest harmor ineffectivenessand/or

• evidence that superior therapies hadbecome available.

The guidelines include a version of the Universal ALS Algorithm and severalother algorithms that expand on morespecific areas of ALS assessment andmanagement, and are a very valuable andclinically useful adjunct to the UniversalALS Algorithm.5

In 2002 the Australian ResuscitationCouncil published Protocols for AdultAdvanced Life Support, which aresuccinct and include a slightly modifiedversion of the Universal ALS Algorithm.9

The most exciting and clinicallyrelevant advances in ALS over the lastdecade have been the development ofguidelines and algorithms that are

becoming universal in both inclusion ofscientifically proven therapies and wide-spread acceptance, and have substantiallysimplified the management of cardiacarrest. Nevertheless, our resuscitationknowledge is still incomplete and manyof the ALS techniques that we currentlyuse are not supported by scientificallyrigorous evidence.10 Rigid adherence toguidelines is neither practical nor advis-able and they should be interpreted withcommon sense. Individuals with specialistknowledge should take the opportunityto modify them according to the level oftheir expertise and the specific clinicalsituation or environment in which theypractice.

CONFIRMATION OFCARDIAC ARRESTRHYTHM ANDINITIATION OF ALSBLS is only a temporary and inefficientsubstitute for normal cardiorespiratoryfunction. ALS is almost always necessaryto produce return of spontaneous circu-lation (ROSC) after circulatory arrest.The purpose of BLS is to maintain thepatient as effectively as possible untildrugs and equipment, particularly adefibrillator, are available.4, 5, 8

The point of entry to the ALS algo-rithm is dependent upon the circum-stances of the cardiac arrest. In manysituations, such as out-of-hospital cardiacarrest, BLS will already have beeninitiated and should continue while themonitor/defibrillator is being prepared.When the patient is being monitored atthe time of cardiac arrest, diagnosisshould be swift and the defibrillatorattached without delay.

For the rescuer with a manual defib-rillator the critical decision is whether ornot the rhythm present is VF/VT.4

Nearly 70% of patients with an out-of-hospital cardiac arrest are in VF at thetime of arrival of EMS personnel with amonitor/defibrillator.11 Most eventualsurvivors come from this group.3, 4

VF is a pulseless, chaotic, disorganizeddysrhythmia characterized by an undu-lating, irregular pattern that varies in


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Fig. 1.2.1 Algorithm for advanced life support management. BLS - Basic lifesupport. Reproduced with permission from British Journal of Anaesthesia 1997; 79:172–177.

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amplitude and morphology with aventricular waveform of more than 150/minute.1 Pulseless VT is characterized bybroad, bizarrely shaped ventricularcomplexes associated with no detectablecardiac output. By definition the rate isgreater than 100/minute and is usuallywell in excess of 150.

The absence of a detectable cardiacoutput in the presence of a coordinatedelectrical rhythm is called electro-mechanical dissociation (EMD) orpulseless electrical activity (PEA).9

Asystole is identified by the absence ofany cardiac electrical activity. Occasionallyasystole is incorrectly diagnosed because:

❶ ECG leads may be broken ordisconnected. The presence ofelectrical artifact during externalchest compression indicates that theleads are connected and probablyintact.

❷ Lead sensitivity may beinappropriate. The sensitivityshould be increased to maximum: anaccompanying increase in the size ofelectrical artifact will confirm that thesensitivity selection is functioning.

❸ On occasions VF has apredominant axis. If this is at rightangles to the selected monitor leadeven coarse VF may cause minimalundulation in the baseline andresemble asystole. At least two leadsshould be selected in successionbefore asystole is diagnosed,preferably leads at right angles, suchas II and aVL.

If there is any difficulty in diagnosingthe rhythm in a patient with cardiac arrestthe VF/VT protocol should be followed.5,8

DEFIBRILLATIONThe only proven effective treatment forVF is electrical defibrillation.1, 10, 12 Whena defibrillator is available, it should bebrought immediately to the side of theperson in cardiac arrest and, if the dys-rhythmia is VF/VT, defibrillation shouldbe attempted without delay.

The chances of defibrillation restoringa sustained, perfusing rhythm, and also

of a long-term favourable outcome areoptimal for as little as 90 seconds aftercardiac arrest and decline rapidly there-after as myocardial high-energy phosphatestores are consumed.4, 8, 9 BLS may beexpected only to slow further myocardialdeterioration, but is critical to themaintenance of cerebral circulation.Effective BLS will sustain the cerebralcirculation at viable levels for 5–10minutes or more. However, restorationof an effective spontaneous circulationprovides the only means of completelyreversing the effects of ischaemia andshould be achieved as rapidly aspossible.8 Defibrillation should only everbe delayed by the commencement orcontinuation of BLS if this can beexpected to improve the cellularbiochemistry of the myocardium or ifrestoration of some cerebral circulation isessential.1, 4, 8

All of the resuscitation guidelinesreferred to previously stress the impor-tance of minimum delay in the admin-istration of defibrillating shocks.1, 5, 8, 9

Furthermore, the ILCOR, ERC andARC guidelines and algorithms qualifythe commencement of BLS with thestatement – ‘if appropriate’.1, 8, 9 Thisapproach is justified because:

• the prospects of successfuldefibrillation decrease relativelyrapidly over a few minutes aftercardiac arrest

• BLS is unlikely to improve the oddsof successful defibrillation

• modern defibrillators have veryrapid charge times: three shocks ofappropriate energy levels can begiven within 30 seconds by a trainedand well-equipped team. 1, 8

TechniqueFor defibrillation to be successful, acritical myocardial mass must be depolar-ized synchronously to interrupt thefibrillation and allow recapture by asingle pacemaker. The technique usedmust minimize transthoracic impedancein order to maximize the probability ofsuccess.4, 11, 12, 13

Reducing transthoracic impedanceTransthoracic impedance is reduced by:

• paddles of 10–13 cm in diameter foradults. Smaller paddles allow tooconcentrated a discharge of energyand may cause focal myocardialdamage.11, 12 Larger paddles may notbe able to contact the chest overtheir entire area and/or may causemore current to be conductedthrough non-myocardial tissues.11, 13

• conductive electrode paste or padsreduce impedance by 30%.11 Careshould be taken to ensure that thereis no contact between the paddleseither directly or through electrodepaste or defibrillation pads, as thiswill result in current arcing acrossthe chest wall.11–13

• pressure of about 5 kg on eachpaddle.11

• defibrillation in expiration.13

• repeated countershocks with a shortinterval between.11, 13

Paddle placementThere are two widely accepted positionsfor the defibrillation paddles that opti-mize current delivery to the heart. Themost convenient is the antero-apicalposition, where one paddle is placed tothe right of the sternum just below theclavicle, and the other is centred lateralto the normal cardiac apex in the ante-rior or midaxillary line (V5-6 position).An alternative is the anteroposteriorposition with the anterior paddle placedover the precordium or apex and theposterior paddle on the back in the leftor right infrascapular region. Paddles areoften labelled sternum and apex, which isirrelevant for transthoracic defibrillation,but allows correct orientation of rhythmsdetected by the paddles for synchronizedcardioversion.4, 11, 12, 13

Defibrillation should not be attemptedover ECG electrodes or medicatedpatches, and placement of paddles overthe breast tissue in female patientsshould be avoided.4, 12 If the patient has an implanted pacemaker module orcardioverter defibrillator, the paddlesshould be placed at least 12–15 cm awayfrom the module and pulse generatorrespectively. Pacemaker function shouldbe checked as soon as practicable follow-ing successful defibrillation.11, 12


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Technical problemsIf attempted defibrillation is not accom-panied by skeletal muscle contraction,care should be taken to ensure goodcontact and that the defibrillator isturned on, charged, develops sufficientpower and is in asynchronous mode. Themajority of defibrillator problems are due to operator errors or faulty care andmaintenance.12 The operational status ofdefibrillators should be checked regularlyand a stand-by machine should beavailable when possible.

Timing and energy of shocksWhen using a conventional defibrillatorwith a damped monophasic sinusoidalwaveform (see below) the first shock isgiven with an energy level of 200 joules(J), which represents the best comprom-ise between the probability of successand the risk of myocardial damage.12 Ifthe first attempt at defibrillation is un-successful, a shock of the same energy isrepeated. If still unsuccessful a third shockis given, this time at 360 J.4,5,9,11,12 Thepaddles need not be removed from thechest while being recharged and CPRneed not be recommenced betweenthese initial shocks, unless there is a delayexceeding 20 seconds in recharging thedefibrillator.9 With modern defibrillatorsit is possible to administer three shockswithin 60 seconds.

The carotid pulse should be palpatedif, after a defibrillating shock, an ECGrhythm compatible with cardiac outputis obtained. However, if the monitorindicates persistent VF then additionalshocks in the sequence of three can beadministered without a further pulsecheck. After a defibrillating shock there is typically a delay of several secondsbefore an ECG trace of diagnosticquality is obtained. Additionally, evenwhen defibrillation is successful, there isoften a temporary impairment of cardiacfunction associated with a weak, or diffi-cult to palpate, central pulse for secondsto minutes. It is important to recognizethese phenomena and allow for themrather than hastily conclude that defibril-lation has been unsuccessful or thatEMD has developed.4, 12

COMPLICATIONS OFDEFIBRILLATION• Skin burns can occur; these are

usually superficial.• Skeletal muscle injury or thoracic

vertebral fractures are possible,though are uncommon.

• Myocardial injury and post-defibrillation dysrhythmias canhappen with cumulative high-energyshocks.11, 12

• Health-care providers can receiveelectrical injuries due to electricalcontact with the patient duringdefibrillation. These range fromparaesthesiae to deep partialthickness burns. Cardiac arrest is atheoretical possibility. The operatorshould ensure that all rescuepersonnel are clear of the patientbefore delivering a defibrillationshock. A particular concern shouldbe to ensure that the patient,rescuers and equipment are drybefore defibrillation is attempted,especially outdoors or around aswimming pool area.11, 12

DEVELOPMENTS INDEFIBRILLATIONAutomated externaldefibrillatorsAutomated external defibrillators (AEDs)were first introduced in 1979 and havebecome standard equipment in manyEMS systems primarily for use outside ofthe hospital. The AED is attached by twoconnecting cables to adhesive pads thatare placed on the patient’s chest in thestandard antero-apical positions for de-fibrillation. An internal microprocessoranalyses the ECG signal and, if VF/VTare detected, causes the AED to displayan alarm and either delivers a shock(automatic) or advises the operator to doso (semi-automatic).11, 12

AEDs are highly accurate with somemodels demonstrating 100% specificityand 90–92% sensitivity for coarse VF.12

Although their precision is less for fineVF and least for VT, their accuracy overallis comparable to that of experienced

cardiologists.11 Several EMS systemsequipped with AEDs have shown thatthey can deliver the first shock up to 1minute faster than when using conven-tional defibrillators and rates of survivalto hospital discharge are equivalent tothose achieved when first respondersused manual defibrillators.3

The major advantage of AEDs overconventional defibrillators is their sim-plicity, which has markedly reduced theskill required to defibrillate a patient in cardiac arrest. This decreases the time and expense of initial training andcontinuing education, and increases thenumber of persons who can operate thedevice.3, 11, 12 Members of the publichave been trained to use AEDs in avariety of community settings and havedemonstrated that they can retain skillsfor up to 1 year.3 Encouraging results havebeen produced when AEDs have beenplaced with community responders, suchas fire fighters, police officers, securityguards at large public assemblies andpublic transportation vehicle crews.3, 11

Current-based defibrillationConventional defibrillators are designedto deliver a specified number of joules(J). However, depolarization of myocar-dial tissue is accomplished by the passageof electrical current through the heart,and clinical studies have determined thatthe optimal current is 30–40 amperes(A).11, 13 At a fixed energy, the currentdelivered is inversely related to thetransthoracic impedance and a standardenergy dose of 200 J delivers about 30 Ato a patient with average transthoracicimpedance. In patients with greater thanaverage impedance, the current generatedmay be inadequate, whereas a patientwith smaller than average impedancemay sustain myocardial damage fromexcessive current flow.11, 12, 13

Some newer defibrillators automaticallymeasure transthoracic impedance and thenpredict and adjust the energy deliveredto avoid inappropriately high or lowtransmyocardial currents. These deviceshave defibrillation success rates compar-able to conventional defibrillators whilecumulatively delivering less energy. Thedecreased energy should result in less myo-


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cardial damage and may reduce post-defibrillation complications.4, 11, 12, 13

New defibrillator waveformsMost conventional defibrillators use adamped monophasic sinusoidal wave-form, which is a single pulse lasting for3–4 ms. Many studies over the last decadehave shown that biphasic (bidirectional)truncated transthoracic shocks are aseffective at lower energies as standarddamped sine wave shocks and result infewer post-defibrillation ECG abnormal-ities.4,11,12,13 In a recent review, thereviewers concluded that lower-energybiphasic shocks, delivered without anincrease in energy, achieved clinicaloutcomes equivalent to those of mono-phasic shocks with increasing energylevels, in out-of-hospital cardiac arrest.14

Defibrillators using biphasic waveformswith impedance compensation are nowavailable and will likely become thestandard in the near future. Research isstill needed to determine the optimalbiphasic waveform and energy levels for first and subsequent shocks, but thepotential advantages are equivalent ormore effective external defibrillationwith a reduction in myocardial injuryproduced by the defibrillatory shocks.5

FAILURE OFDEFIBRILLATION, EMDAND ASYSTOLEMost patients who will survive cardiacarrest are successfully defibrillated by oneof the first three shocks and even if thisfirst sequence is unsuccessful, the bestchance for restoring a perfusing rhythmis still defibrillation.4 However, at thisstage it is necessary to recommence BLSin an attempt to restore some myocardialand cerebral perfusion and maintaincellular viability. Additionally, effortsshould be made to secure advanced air-way management and ventilation, and toinstitute vascular access for administrationof drugs.

Potentially reversible causes oraggravating factors of cardiac arrest(Fig. 1.2.1) should be considered andspecific therapy commenced as indicated.

These interventions should occur duringthe 1 minute period of CPR, although itis unlikely that even a highly trainedteam will be able to complete all of theseaspects of management within thisinterval. Further opportunities will occurwith subsequent cycles.4

The ECG rhythm is then reassessedand if VF persists the next sequence ofthree defibrillating shocks is startedwithout delay. These shocks are all at360 J, or its equivalent if the defibrillatoris current-based or uses a biphasicwaveform.4, 11, 12, 13

If VF/VT is definitely excluded at thetime of initial or later rhythm analysis,defibrillation is not appropriate and maybe deleterious.4, 11, 12 These patients willhave EMD or asystole and the prognosisfor these rhythms is much less favourablethan for VF/VT. There are some situa-tions where EMD or asystole may havebeen provoked by conditions that aretreatable. The common causes are listedin Figure 1.2.1 and may be recalled underthe headings of the four Hs and four Ts.Apart from treating potentially remedi-able conditions the management of EMDand asystole is largely the application of other ALS therapies and thecontinuation of BLS.1, 4, 5, 8,

OTHER ALSINTERVENTIONSExcept for defibrillation, no single ALS intervention has been scientificallyproven to enhance patient outcome,10, 15

although the ILCOR considers that thereis valid scientific evidence to supporttracheal intubation as unequivocallyeffective.11 Many clinicians maintain thatALS has an incremental benefit comparedwith defibrillation alone.3, 15, 16 Whilethere are some data to support this con-tention, it remains impossible to prove.10

Advanced airwaymanagementNo randomized controlled studies existthat demonstrate the life-saving effect of endotracheal intubation compared tobasic airway management.15, 16 However,intuitively some benefit would be expected.

Direct expired air resuscitation and bag/valve-mask ventilation are less effectivethan ventilation via an endotracheal tubeand provide no protection against aspira-tion, which is found in 28% of patientsexamined by the coroner after failedresuscitation from cardiac arrest.16, 17 18

Also, EMS systems that use endotrachealintubation report higher survival ratesthan systems that do not.15, 17

Endotracheal intubation is the goldstandard for advanced management ofthe airway during cardiac arrest. It pro-vides a clear and secure airway, allowingventilation, oxygenation, suction andadministration of medications ifindicated.1,16,17,18 Attempts at intubationshould not interrupt BLS for longer than15–20 seconds. If intubation is notaccomplished within that time, addi-tional attempts should be delayed untilthe cycle of CPR following the nextsequence of three defibrillation shocks,or with EMD and asystole until after afurther 3 minutes of CPR.4, 8, 9

Ventilation and oxygenationDuring cardiac arrest, carbon dioxide(CO2) production and delivery to thepulmonary circulation is limited by therelatively low cardiac output achievedduring CPR. As a consequence, relativelylow minute volumes are sufficient toachieve adequate CO2 excretion andprevent hypercapnia. This situation maybe altered if CO2-producing buffers suchas sodium bicarbonate are administered,and relative increases in minute ventila-tion are required to prevent the develop-ment of respiratory acidosis.4

Several animal studies and evidencefrom humans in cardiac arrest indicatethat, when the airway is patent, spontan-eous gasping can provide sufficientventilation during CPR to maintainnormal arterial CO2 levels. Similarly,chest compression alone provides somepulmonary ventilation and gas exchange,which can approach normal values withactive compression–decompression CPR.Ventilation may actually be unnecessaryduring the first few minutes of CPR,although under conditions of prolongedcardiac arrest, it is essential for survi-val.10, 19 In most cardiac arrest situations,


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a tidal volume of 400–500 mL (5–6 mL/kg) is sufficient to clear CO2 during CPRand will cause a visible rise and fall of thepatient’s chest.18

Cardiac arrest and CPR cause anincrease in dead space and a reduction inlung compliance that may compromisegas exchange. As adequate oxygenationis of paramount importance in cardiacarrest, the aim should be to provide afractional inspired oxygen concentration(FIO2) of 1.0.4, 18

Tidal volumes of 400–500 mL andFIO2 approaching 1.0 are attainable usingself-inflating bag/valve/mask and intuba-tion devices, which remain the mainstayof ventilation in ALS.4, 8, 18

Drug therapyNo drug used in resuscitation has beenshown to improve long-term survival inhumans after cardiac arrest.10, 15, 20, 21

Despite this knowledge, a number ofpharmacotherapeutic agents continue tobe employed, largely for historical reasonsbased on theoretical, retrospective oranecdotal evidence of efficacy.10, 20

Adrenaline (epinephrine)

Actions The beneficial actions ofadrenaline (epinephrine) in cardiac arrestare due to its α-adrenergic effects,whereas the β-adrenergic activityappears, at best, to be unimportant andmay be detrimental. A series ofexperiments have demonstrated thatadrenaline (epinephrine) maintains tonein intrathoracic arteries, preventing theircollapse during external chest com-pression, and also increases resistance innon-cerebral and non-coronary arteries.These actions result in decreased bloodflow to non-cerebral and non-coronaryvessels, increased aortic blood pressureand increased perfusion of the cerebraland coronary vascular beds.22

Indications and dose Adrenaline(epinephrine) is recommended in VF/VTcardiac arrest if there is no ROSC afterthe first three attempts at defibrillation.It is recommended in EMD and asystoleafter commencement of CPR. Thestandard adult dose is 1 mg intrave-nously (IV) every 3 minutes.1, 4, 5, 8, 20, 21

For a number of years there has beenconsiderable interest in high-dose adre-naline, usually defined as amounts inexcess of 45 µg per kg every 5 minutes.However, no prospective randomizedclinical trials in humans have demon-strated a significant improvement insurvival to hospital discharge for adultpatients treated with either standard-dose or high-dose adrenaline.4, 10, 15, 16, 20

Potential complications Particularlyin higher doses adrenaline (epinephrine)may increase myocardial oxygen require-ments, induce myocardial contractionband necrosis and predispose to tachy-dysrhythmias. After ROSC it canproduce severe hypertension. Tissuenecrosis occurs commonly after extra-vasation.4, 18, 21, 22

Vasopressin

Actions Vasopressin is an endogenouspeptide hormone synthesized in thehypothalamus and secreted from theposterios pituitary in response to avariety of osmotic and non-osmoticstimuli. The principal physiologic effectsof vasopressin are direct vasoconstrictionof the systemic circulation, mediated byV1 receptors on vascular smooth muscleand renal water retention, mediated byrenal V2 receptors. During the lastdecade research has indicated that vaso-pressin may be an important hormoneduring cardiac arrest and levels ofvasopressin during CPR are significantlyhigher in eventual survivors than in thosewho do not survive. A possible advan-tage of vasopressin during cardiac arrestand CPR is that it produces vasoconstric-tion in non-vital tissues while preservingblood flow to the coronary and cerebralcirculations.23

Indications and dose The AHA inthe International Guidelines 2000recommend that vasopressin is aneffective vasopressor and can be used asan alternative to epinephrine for thetreatment of adult shock-refractory VF.5 The ERC and ARC do not includevasopressin in their recently publishedalgorithms.8, 21 Although there are stillinsufficient clinical data to support the

use of vasopressin as a first-line drug inthe management of cardiac arrest, reportsto date are promising and furtherresearch may well provide definitiveinformation in the near future.23 Thedose currently recommended by the AHAis an i.v. bolus of 40 U administered onceduring an episode of cardiac arrest.5

Potential complications The benefi-cial effect of vasopressin on the cerebralcirculation during CPR may increase therisk of cerebral oedema or haemorrhageafter ROSC. Vasopressin has a relativelylong half-life (10–20 minutes) and per-sistent vasoconstriction following ROSCmay exacerbate myocardial ischaemiaand interfere with left ventricular func-tion. Vasopressin also exerts a procoagu-lant effect on platelets.23

Lidocaine

Actions Lidocaine is a Vaughan–Williams class IB agent that depressesmyocardial excitability by blocking sodiumchannels without extending actionpotential duration. In animal models italso has an antifibrillatory action.

The role of lidocaine in assistingresuscitation from refractory VF iscontentious. Several experimental studiesin animals have shown that it increasesthe defibrillation threshold (the energyrequired for defibrillation).12, 18 Otherstudies have shown no effect, or a decreasein the defibrillation threshold.4, 24 Arecently reported retrospective observa-tional study of outcome from cardiacarrest with sustained VF, compared thesurvival of patients who received lido-caine with those who received no lido-caine. This study showed a significantincrease in ROSC in the lidocaine groupbut there was no difference in the rate ofhospital discharge between the twogroups.25 Controlled prospective trials oflidocaine and alternative antifibrillatorydrugs are still needed.4, 20

Indications and dose Lidocainecannot be recommended as first-linetherapy in cardiac arrest, but may beconsidered if multiple DC shocks andadrenaline have failed to revert VF/VT.


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It can also be used to help preventreversion to VF/VT after successfuldefibrillation.5, 12, 20, 21 The initial bolusdose is 1–1.5 mg/kg with an additionalbolus of 0.5 mg/kg after 5–10 minutes ifindicated.4, 5, 21

Potential complications Cardiovas-cular effects include hypotension, brady-dysrhythmias and asystole. Neurologicaltoxicity causes central nervous system(CNS) excitation with anxiety, tremorand convulsions followed by CNSdepression.4, 20, 21

Amiodarone

Actions Amiodarone is a class IIIagent that has some class I activity andweak non-competitive β-blocking effects.Amiodarone lowers the defibrillationthreshold and has a potent antifibrilla-tory effect. Its broad spectrum of anti-dysrhythmic activity and minimal adversehaemodynamic effects make it a poten-tially useful agent, but its value duringcardiac arrest has not been extensivelyexplored.20, 24

Indications and dose Amiodaronecannot be recommended as first-linetherapy in cardiac arrest, but may beconsidered if multiple DC shocks andadrenaline have failed to revert VF/VT.The initial dose is 5 mg/kg given as a slowintravenous infusion over 5–15 minutes.This may be repeated if indicated.

Potential complications Cardiovas-cular effects include hypotension andbradycardia.24

Atropine

Actions Atropine antagonizes para-sympathetic nervous effects on the heartby blocking cholinergic muscarinicreceptors, leading to increased sinoatrialand atrioventricular automaticity andrate of conduction.5, 20, 21 Atropine maybe effective when increased vagal toneresults in a haemodynamically significantbradyasystole but its effect on EMD orasystole caused by prolonged, widespreadmyocardial ischaemia is negligible.24

Indications and dose Atropine maybe considered in bradyasystolic cardiacarrest that does not respond to initialCPR and adrenaline (epinephrine). Thedose is 3 mg, which is considered to bethe vagolytic dose.4, 5, 8, 20

Potential complications Adverseeffects include tachycardia, CNS excite-ment and delirium, which are usuallyregarded as benign.21, 24

Magnesium

Actions Magnesium is an essentialelectrolyte that may be depleted bydiuretics, severe diarrhoea and alcoholabuse. Hypomagnesaemia may causecardiac dysrhythmias.5, 21 Several casereports and trials have yielded contra-dictory results concerning the effect ofmagnesium in cardiac arrest, and there is little to support its routine use atpresent.10, 20, 24

Indications and dose Magnesiummay be considered in refractory VF/VT,particularly if hypokalaemia is present,and is an agent of choice in torsades de pointes. The initial dose is 5 mmol(2.5 mL of 49.3% solution) given over 1 minute, which may be repeated ifindicated and followed by an infusion of20 mmol over 4 hours.5, 20, 21

Potential complications Adverseeffects include hypotension and heartblock. Muscle weakness and paralysismay occur if excessive quantities areadministered.5, 21

Calcium

Actions Calcium is a divalent cationessential to neuromuscular function.Human studies have shown that itspharmacotherapeutic effects in cardiacarrest are negligible and may beadverse.5, 20

Indications and dose Calcium shouldnot be administered unless there isevidence that cardiac arrest is caused orexacerbated by hyperkalaemia, hypocal-caemia or overdose of calcium-channel-blocking drugs.4, 5, 21 The dose is 5–10 mL

of 10% calcium chloride or three timesthat dose of 10% calcium gluconate.5, 21

Potential complications Calciummay increase the damage caused byprofound ischaemia of myocardial andcerebral cells.5, 20, 21 Extravasation causestissue necrosis.21

Sodium bicarbonate

Actions Sodium bicarbonate (NaHCO3)is an alkalinizing agent that, theoretically,reverses the metabolic acidosis associatedwith profound ischaemia. However,provided CPR is effective, acidosis doesnot develop rapidly or severely inotherwise healthy individuals duringcardiac arrest.4, 20, 21 There is no strongclinical evidence supporting the admin-istration of alkalinizing agents in cardiacarrest.4, 15, 20 Some benefits have beenreported, particularly when the dose can be titrated to avoid alkalosis and with concurrent use of adrenaline(epinephrine).16, 20 It is probably unwiseto completely abandon NaHCO3

therapy for all patients with cardiacarrest, and an objective reappraisal isneeded to define its role.10, 20

Indications and dose Sodium bicar-bonate is unnecessary in brief resuscita-tions when the patient has been previouslywell but can be considered if cardiac arrestexceeds 10–15 minutes duration.20, 21 Itshould also be considered when cardiacarrest occurs in a patient with a pre-existing profound acidosis or in specialcircumstances, such as tricyclic anti-depressant overdose and hyperkalaemia.5, 21

Potential complications Adverseeffects of NaHCO3 include alkalosis, hyper-osmolality and CO2 production, causingparadoxical intracellular acidosis.4, 5, 21

VASCULAR ACCESSAND DRUG DELIVERYDURING CARDIACARRESTThe ideal route of drug delivery com-bines rapid and easy vascular access withquick delivery to the central circulation.Central venous cannulae deliver drugs


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rapidly to the central circulation but re-quire considerable technical proficiencyto insert during CPR and some methodsof insertion interfere with defibrillationand CPR, which is unacceptable.4, 20 Themost appropriate method of vascularaccess will usually be via a peripheralvenous cannula. When drugs are admin-istered by this route the extremity shouldbe elevated and a 20 mL bolus of IVfluid should follow the agent to facilitatedelivery to the central circulation.4, 20

Intratracheal deposition is an alterna-tive route, and during cardiac arrest tra-cheal intubation often precedes venousaccess.4, 20 If there is a delay in achievingvascular access most ALS drugs, includ-ing adrenaline (epinephrine), lidocaineand atropine, may be safely administeredthrough the endotracheal tube.5, 20 Theideal dose and dilution of drugs given by this route is uncertain but currentrecommendations are to use two to threetimes the standard IV dose diluted in10 mL of normal saline. This solutionshould be delivered via a catheter placedbeyond the tip of the endotracheal tubeand followed by five ventilations to aiddispersion.4, 20, 26

Crystalloid solutions are preferred asthe standard vehicle of drug delivery asadministration of glucose-containingsolutions during CPR may contribute to post-arrest hyperglycaemia, which isdetrimental to cerebral recovery.26

HAEMODYNAMICMONITORING DURINGCPRResearchers and clinicians have proposedand measured numerous physiologicalparameters as a means of monitoring the effectiveness of resuscitation duringcardiac arrest. The techniques for mea-suring these parameters are usuallyinvasive, technically difficult and timeconsuming to establish and maintain,thereby limiting their utility in suddenand unexpected cardiac arrest.27

Numerous animal and clinical experi-ments indicate that measurement of end-tidal CO2 (ETCO2) may be an effectiveand informative method of determining

the progress of CPR.10, 27 The normalETCO2 is 4–5% and typically falls to lessthan 1% at the onset of cardiac arrest.With effective CPR, the ETCO2 rises tobetween one-quarter and one-third ofnormal and ROSC is associated with arise to normal or supranormal levels overthe next minute. These changes parallelproportionally similar alterations incardiac output.27

An ETCO2 of less than 1% duringattempted resuscitation from cardiacarrest is an indication of ineffective CPR.This may be due to inadequate ventila-tion due to airway obstruction or oesoph-ageal intubation, or due to the cardiacoutput being less than expected becauseof poor technique or causes such as hypo-volaemia, pulmonary embolism or peri-cardial tamponade. A sharp rise in ETCO2

may be the first indication of ROSC.27

End-tidal CO2 measured immediatelyafter commencement of CPR may alsohave a prognostic value in out-of-hospital cardiac arrests as it is higher inpatients who have had a short interval ofcardiac arrest, as compared with thosewho have had a longer period prior tothe initiation of resuscitation. There isalso evidence that patients who are even-tually resuscitated have a higher ETCO2

during CPR than those who will neverhave ROSC. Caution should be exercisedin interpreting ETCO2 following adrena-line (epinephrine), as this agent causes a decrease in ETCO2, which is notnecessarily a poor prognostic indicator.27

DISCONTINUING ALSWith the introduction of effective EMSsystems, initiation of ALS for patientswith out-of-hospital cardiac arrest movedfrom the institution into the community.Research indicates that the vast majorityof patients who survive out-of-hospitalcardiac arrest have ROSC before arrivalat the emergency department (ED). In18 papers published between 1981 and1995, only 33 (0.6%) of 5444 patientswho were transported to an ED still incardiac arrest after unsuccessful pre-hospital resuscitation, survived tohospital discharge.28 Twenty-four of the

surviving patients arrived in the ED inVF and 11 of these patients had theirinitial arrest in the ambulance en routeto the hospital or had temporary ROSCbefore arrival at the ED.

In 1993 a recommendation was madethat after out-of-hospital cardiac arrest inthe normothermic patient, resuscitationshould cease if there is no ROSC after 25minutes of ALS.29 The two exceptions to this practice are if the cardiac arrestoccurs in the presence of ambulancepersonnel, or the patient demonstratespersistent VF. These recommendationswere applied and considered to be validin a prospective study in the same year.30

Early in the resuscitation of patientswith in-hospital cardiac arrest there areno absolute predictors of futility but somevariables are associated with a greater orlesser chance of survival to discharge.Ventricular tachydysrhythmias, commence-ment of resuscitation within 5 minutesand ROSC within 15 minutes are alllinked to better outcomes. Pre-existingconditions such as metastatic cancer,renal failure, sepsis, acute cerebrovas-cular accident and cardiogenic shock areall linked to poor outcome. Age is not anindependent predictor of outcome andthis has also been confirmed in out-of-hospital cardiac arrest.31, 32 Resuscitationefforts lasting more than 30 minuteswithout ROSC appear to be so uniformlyunsuccessful that they should be aban-doned except in unusual circumstances.10, 32

PROGNOSIS AFTERCARDIAC ARRESTThe prognosis for survival after an out-of-hospital cardiac arrest fluctuates fromcommunity to community. Some of thevariation is due to differences in EMSsystems but much is also due to diverseresearch methodology and data report-ing. In King County, Washington, wherea sophisticated EMS system has been in place for over two decades, survival tohospital discharge was between 15% and20% from 1976 to 1987. These figuresare in contrast to US national rates of survival, which were estimated to befrom 1% to 3% in a 1991 report from the


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AHA.3 In 1987–88 in Perth, Australiasurvival was 22.7% of 231 cases of out-of-hospital cardiac arrest due to VF33 andin western metropolitan Melbourne in1995 the survival rate for all arrest dys-rhythmias was 3%.7 In a 1996 meta-analysis of 36 articles published between1973 and 1992 describing 41 EMSsystems in six countries, survival variedfrom 0% to 21% with an overall meansurvival of 8%.34

Prognosis for survival from in-hospitalcardiac arrest is only marginally better withsurvival to hospital discharge averaging13.8% of 12961 patients described inreports published between 1961 and1984.31 In a further seven reportspublished between 1978 and 1989, 11%of 1804 patients survived to hospitaldischarge.32

UNIFORM REPORTINGIN CARDIAC ARRESTRESEARCHCardiac arrest research and the inter-pretation of available data has often beenhampered by inconsistent methodologyand reporting. An important initiativehas been the recognition of the need foruniform, internationally recognized defi-nitions and guidelines for reporting ofcardiac arrest data. During the last fewyears a number of templates have beendeveloped to include the most relevantvariables for describing and comparingcardiac arrest research results. These arereferred to as Utstein style guidelines or templates after Utstein Abbey, nearStavanger, Norway, where expertresearchers and clinicians gathered in1990.35

REFERENCES1. Kloeck W, Cummins R, Chamberlain L 1997

The universal ALS algorithm. Resuscitation34: 109–11

2. Larsen MP, Eisenberg MS, Cummins RO,Hallstrom AP 1993 Predicting survival from out-of-hospital cardiac arrest: a graphic model. Annalsof Emergency Medicine 22: 1652–8

3. Cummins RO, Ornato JP, Thies WH, Pepe PE1991 Improving survival from sudden cardiacarrest: the ‘chain of survival’ concept: a statementfor health professionals from the Advanced CardiacLife Support Subcommittee and the EmergencyCardiac Care Committee, American HeartAssociation. Circulation 83: 1832–47

4. Robertson CE 1997 Advanced life supportguidelines. British Journal of Anaesthesia79: 172–7

5. The American Heart Association in collaborationwith the International Liaison Committee onResuscitation 2000 Guidelines 2000 forcardiopulmonary resuscitation and emergencycardiovascular care: a consensus on science.Circulation 102(Suppl. 8): I1–I384

6. Becker LB, Smith DW, Rhodes KV 1993 Incidenceof cardiac arrest: a neglected factor in evaluatingsurvival rates. Annals of Emergency Medicine22: 86–91

7. Bernard S 1998 Outcome from prehospital cardiacarrest in Melbourne Australia. EmergencyMedicine 10: 25–29

8. Advanced Life Support Working Group of theEuropean Resuscitation Council 1998 The 1998European Resuscitation Council guidelines foradult advanced life support. Resuscitation 37: 81–90

9. Australian Resuscitation Council February 2002Protocols for adult advanced life support. RevisedPolicy Statement P.S. 11.2.1

10. Maguire JE 1997 Advances in cardiac life support:sorting the science from the dogma. EmergencyMedicine 9(Suppl 4): 1–21

11. Truong JH, Rosen P 1997 Current concepts inelectrical defibrillation. Journal of EmergencyMedicine 15: 331–8

12. Bossaert LL 1997 Fibrillation and defibrillation ofthe heart. British Journal of Anaesthesia 79: 172–7

13. Kerber RE 1993 Electrical treatment of cardiacarrhythmias: defibrillation and cardioversion.Annals of Emergency Medicine 22: 296–301

14. Cummins RO, Hazinski MF, Kerber RE, et al1998 Low-energy biphasic waveform defibrillation:evidence-based review applied to emergencycardiovascular care guidelines: a statement for

healthcare professionals from the American HeartAssociation Committee on EmergencyCardiovascular Care and the subcommittees onBasic Life Support, Advanced Cardiac LifeSupport, and Pediatric Resuscitation. Circulation97: 1654–67

15. Pepe PE, Abramson NS, Brown CG 1994 ACLS-Does it really work? Annals of EmergencyMedicine 23: 1037–41

16. Ornato JP, Paradis N, Bircher N, et al 1996 Futuredirections for resuscitation research. III. Externalcardiopulmonary resuscitation advanced lifesupport. Resuscitation 32: 139–58

17. Pepe PE, Zachariah BS, Chandra NC 1993Invasive airway techniques in resuscitation. Annalsof Emergency Medicine 22: 393–403

18. Gabbott DA, Baskett PJF 1997 Management ofthe airway and ventilation during resuscitation.British Journal of Anaesthesia 79: 159–71

19. Idris AH 1996 Reassessing the need for ventilationduring CPR. Annals of Emergency Medicine27: 569–75

20. Vincent R 1997 Drugs in modern resuscitation.British Journal of Anaesthesia 79: 188–97

21. Australian Resuscitation Council February 2002Medications in adult cardiac arrest. Revised PolicyStatement P.S. 11.4

22. Paradis NA, Koscove EM 1990 Epinephrine incardiac arrest: a critical review. Annals ofEmergency Medicine 19: 1288–301

23. Barlow M 2002 Vasopressin. Emergency Medicine14: 304–14

24. Jaffe AS 1993 The use of antiarrhythmics inadvanced cardiac life support. Annals of EmergencyMedicine 22 (pt 2): 307–16

25. Herlitz J, Ekstrom L, Wennerblom B, et al 1997Lidocaine in out-of-hospital ventricular fibrillation.Does it improve outcome? Resuscitation 33: 199–205

26. Gonzalez ER 1993 Pharmacologic controversies inCPR. Annals of Emergency Medicine 22: 317–23

27. Ornato JP 1993 Hemodynamic monitoring duringCPR. Annals of Emergency Medicine 22: 289–95

28. Brennan RJ, Luke C 1995 Failed prehospitalresuscitation following out-of-hospital cardiacarrest: are further efforts in the emergencydepartment warranted? Emergency Medicine7: 131–8

29. Bonnin MJ, Pepe PE, Timball KT, et al 1993Distinct criteria for termination of resuscitation inthe out-of-hospital setting. Journal of the AmericanMedical Association 269: 1457–62

30. Pepe PE, Brown CG, Bonnin MJ, et al 1993Prospective validation of criteria for on-scenetermination of resuscitation efforts after out-of-hospital cardiac arrest. Annals of EmergencyMedicine 22: 884–5

31. McGrath RB 1987 In-house cardiopulmonaryresuscitation after a quarter of a century. Annals ofEmergency Medicine 16: 1365-8

32. Jastremski MS 1993. In-hospital cardiac arrest.Annals of Emergency Medicine 22: 113–7

33. Jacobs IG, Oxer HF 1990 A review of pre-hospitaldefibrillation by ambulance officers in Perth,Western Australia. Medical Journal of Australia153: 662–4

34. Nichol G, Destsky AS, Stiell IG, et al 1995Effectiveness of emergency medical services forvictims of out-of-hospital cardiac arrest: a meta-analysis. Annals of Emergency Medicine 27: 700–10

35. Dick WF 1997 Uniform reporting in resuscitation.British Journal of Anaesthesia 79: 241–52


14

CONTROVERSIES❶ Acceptance of universalguidelines and algorithms.

❷ The role of new technologies indefibrillation.

❸ The need for ventilation asinitial therapy in cardiac arrest.

❹ The role of vasopressors in ALS.

❺ When is CPR futile?

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and/or depression of the cough reflexmay require ETI for airway protection tominimize the risk of aspiration pneumo-nitis. In patients with severe head injury,ETI and controlled hyperventilation maybe required for the short-term treatmentof intracranial hypertension.3 Finally,ETI may be indicated as part of generalanaesthesia in combative patients whorequire investigations and/or procedures.

There are additional challenges tourgent intubation of the critically ill orinjured patient in the ED compared with elective intubation in the operatingroom. Details of current medications,previous anaesthetics and allergies maynot be available. There may be inade-quate time for a complete clinical assess-ment of the upper airway or thoroughconsultation with the patient and/orfamily. In patients with coma followingsevere head injury, the status of thecervical spine will be uncertain even ifinitial imaging is normal.

RAPID SEQUENCEINTUBATIONUnless the patient is deeply comatose orin cardiac arrest, ETI will require the useof sedative and neuro-muscular blockingdrugs to facilitate laryngoscopy and place-ment of the endotracheal tube. Rapidsequence intubation (RSI) is the tech-nique of choice when definitive airwaymanagement is required in the ED, tominimize hypoxaemia or the risk of aspi-ration of vomitus.4 Possible exceptionsinclude patients with upper airway obstruc-tion or severe facial trauma, wherealternate initial techniques, such asawake intubation or awake tracheos-tomy, may be preferred (see later).

Careful preparation for RSI isrequired. If time and patient conditionallow, a history should be sought ofcurrent medication, allergies and time of last meal. A careful examination of the upper airway is required, looking for

anatomical features that may predictdifficult intubation.5

The conscious, cooperative patientshould receive explanation and reassurance.Preoxygenation with 100% oxygen by maskis commenced using a non-rebreathingcircuit. Optimal pre-oxygenation requirestidal volume breathing for 3–5 minutesusing 10 litres/minute oxygen flow.6 Apillow under the head is essential, unlessthe patient has suspected spinal columninjury, in which case the neck must beimmobilized in an anatomically neutralposition.7 Reliable intravenous access isrequired, as well as equipment forsuctioning the airway.

Appropriate monitoring includescontinuous ECG and pulse oximetry.The blood pressure should be measured,either invasively using an intra-arterialcannula or non-invasively using anautomated blood-pressure monitoringdevice. Capnography must be preparedfor end-tidal CO2 (ETCO2) measurementfollowing intubation.

The required drugs should be chosenand will depend on operator preferenceand the clinical situation. In general, anarcotic and benzodiazepine are used incombination with a rapid-onset neuro-muscular blocking drug.8 Details of theindications, dosages and side effects ofthe commonly used drugs for rapidsequence intubation are shown in Table1.3.1. These must be drawn up, checkedand the syringes clearly labelled. A sparelaryngoscope must be available, in caseof failure of the first and the appropriatesize ETT opened, lubricated and the cuffchecked. Another ETT (one size smaller)should be immediately available. At least two assistants will be required, oneto assist the operator with the drugs andequipment, and another to providecricoid pressure following the inductionof sedation and muscle relaxation. Furtherequipment in case of difficult intubationshould be immediately available (seelater).

When all preparations are complete,

1.3 ADVANCED AIRWAY MANAGEMENT

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1.3 ADVANCED AIRWAY MANAGEMENTSTEPHEN BERNARD

ESSENTIALS1

1 Intubation of the trachea in theemergency department usuallyrequires the use of drugs for sedationand neuromuscular relaxation tofacilitate placement of anendotracheal tube.

2 Clinical checks for trachealplacement may be inaccurate, andcapnography or an air aspirationdevice should be used forconfirmation.

3 If visualization of the vocal cordsat laryngoscopy is difficult, a failedintubation drill should be followed toavoid patient hypoxaemia.

INTRODUCTIONAppropriate airway management is theinitial step in the resuscitation of thepatient with critical illness. Basic airwaymanoeuvres include jaw thrust, chin liftand finger sweeps to clear the airway,together with expired air or bag/valve/mask breathing for ventilation. Advancedairway management includes endotrachealintubation (ETI) to provide a secure air-way and allow assisted ventilation. Inmany emergency departments, advancedairway management is undertaken by anappropriately trained emergency physi-cian rather than an anaesthetist.1 Thischapter details the equipment, drugs andtechniques that may be used in advancedairway management in the emergencydepartment (ED).

Patients with respiratory arrest requireimmediate ETI and ventilation withoxygen. Although a trial of non-invasiveventilation may be used initially inconscious patients with severe hypo-xaemia or hypercapnoea,2 this may beunsuccessful and ETI will be required.Patients with a decreased conscious state

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premedication with adjunctive agentssuch as atropine, a benzodiazepine and/or a narcotic are administered as clini-cally indicated. The sedative drug is thengiven and, as consciousness is lost, themuscle relaxant (usually suxamethonium)is given with cricoid pressure applied.Following fasciculations and the loss ofmuscle tone, laryngoscopy is performedand the larynx sighted. The endotrachealtube is then placed through the vocalcords into the trachea, the cuff inflatedand the ETT is secured with tapes. Cri-coid pressure must be maintained untilthe ETT position is checked and secured.

Clinical methods of ensuring trachealposition include sighting the passage of the ETT through the vocal cords,misting of the ETT during exhalation,auscultation of breath sounds in the lungfields and palpation of the ETT cuff inthe suprasternal notch by the squeezetest.9 However, when visualization of the vocal cords has been difficult, theseclinical tests may be misleading andconfirmatory tests will be required.Although capnography is regarded as

the gold standard for confirmation oftracheal placement, during cardiac arrestthere may be inadequate delivery ofcarbon dioxide to the lungs and hence afalse-negative reading. In this setting, theuse of an oesophageal detector device(ODD) has been shown to be moreaccurate.10

After intubation, an orogastric ornasogastric tube should be inserted andchest X-ray taken to exclude right mainbronchus intubation and confirm place-ment of the orogastric or nasogastrictube in the stomach. As the drugs usedfor sedation and muscle relaxation wearoff, further drugs for the maintenance ofsedation and paralysis will be required.Appropriate monitoring of vital signs,pulse oximetry and capnography withvisual and audible alarms must be main-tained at all times. Humidification of theinspired oxygen is desirable using a dis-posable filter. If the patient is placed onmechanical ventilation, the PaCO2 shouldbe checked to ensure adequate ventilationand to confirm correlation with ETCO2.The unconscious patient requires eye care,

pressure area care, temperature controland catheterization of the urinarybladder.

Hypotension following intubationmust be treated promptly, especially inpatients with neurological injury.11 Thecauses include vasodilator and/ornegative inotropic effects of the sedativedrug(s) and/or positive pressure ventila-tion decreasing venous return and cardiacoutput. Treatment consists of a fluidchallenge and/or inotrope administration,depending on the clinical setting. Rarely,hypotension may be due to tension pneu-mothorax occurring after the commence-ment of positive-pressure ventilation.Hypertension usually indicates inadequatesedation and should be treated withsupplemental sedation.

In patients with severe head injury, thefollowing additional measures need to beconsidered. As there is the possibility ofcervical spine instability, an assistantmust hold the head in the neutralposition, which increases the difficulty invisualizing the larynx. Also, laryngoscopymay raise intracranial pressure, however,the benefit of lidocaine at 1.5 mg/kg aspremedication is uncertain.12 In hypo-tensive patients, thiopentone or propofolmust be used cautiously in small doses, if at all.

The technique of RSI is not advisedfor patients with upper airway pathologyand impending upper airway obstruc-tion. Following the administration of amuscle relaxant, the larynx may not bevisualized and ventilation of the apnoeicpatient may be impossible, the ‘can’tintubate, can’t ventilate’ situation. Inthese patients, an initial awake techniquemay be performed instead. Alternatively,an inhalational anaesthetic agent or intra-venous propofol is utilized, as their effectswill rapidly be reversed and spontaneousrespirations resume if intubation isimpossible.

DIFFICULT INTUBATIONThe intubation of the trachea underdirect vision may be easy or difficult,depending on the view of the larynxduring laryngoscopy. This has been


16

Table 1.3.1 Drugs commonly used in RSI

Drug Dose Action Onset (min) Duration (min)

Premedication agentsAtropine 0.02 mg/kg Vagal blockade 1 30Lidocaine 1.5 mg/kg Decreases ICP 1 30Fentanyl 1.5 µg/kg Analgesic 2 30Morphine 0.15 mg/kg Analgesic 4 120Midazolam 0.05 mg/kg Anxiolytic 2 30Vecuronium 0.01 mg/kg Defasciculation 2 10

Induction agentsThiopental 1–5 mg/kg Rapid-onset sedation

Decreases ICP 0.5 10Methohexital 1.0 mg/kg Rapid-onset sedation 0.5 5Midazolam 0.05–0.1 mg/kg Rapid-onset sedation 2 10Diazepam 0.1 mg/kg Rapid-onset sedation 2 20Ketamine 1 mg/kg Dissociative state 2 20Propofol 1–2 mg/kg Sedation 1 10Fentanyl 10–20 µg/kg Sedation, analgesic 1 20

Muscle relaxantsSuxamethonium 1.5 mg/kg Depolarizing MR 0.5 5Vecuronium 0.2 mg/kg Non-depolarizing MR 2 40Rocuronium 1.0 mg/kg Non-depolarizing MR 1 30Mivacurium 0.2 mg/kg Non-depolarizing MR 0.5 20Atracurium 0.5 mg/kg Non-depolarizing MR 3 30Pancuronium 0.1 mg/kg Non-depolarizing MR 3 40

ICP, intracranial pressureMR, muscle relaxantRSI, rapid sequence intubation

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classified into Grades 1-4 by Cormackand Lehane.13 In Grade 1 laryngoscopy,there is a clear view of the entire laryn-geal aperture. In Grade 2, only the poste-rior part of the larynx is visible. In Grade3, only the epiglottis is able to be visual-ized and in Grade 4 only the soft palateis seen. A difficult intubation is definedas a Grade 3 or 4 view at laryngoscopy.

Difficult intubation may be anticipatedin the presence of pathological disorderssuch as congenital facial and upper air-way disorders, maxillofacial and airwaytrauma, airway tumours and abscesses, orcervical spine immobility. There may also be anatomical reasons for Grade 3-4laryngoscopy and a range of clinical testshave been proposed that may predictdifficulty in visualization of the larynx,including relative tongue/pharyngealsize, atlanto-occipital joint mobility anda thyromental distance < 6 cm. However,these are unlikely to be clinically useful inthe emergency setting.14

When the larynx is not visualized,attempts at blind placement of the ETT into the trachea are unlikely to besuccessful and repeated attempts atintubation result in patient hypoxaemia.Failed intubation drills have beendescribed for use in the operatingtheatre15,16 and a failed intubation drillmore suitable for use in the ED is shownin Figure 1.3.1.

Initial simple manoeuvres to visualizethe larynx include the addition of pillowsto further flex the neck (unless cervicalspine injury is suspected), the use of astraight laryngoscope blade17 and back-ward/upward/rightward external pressure(BURP) on the thyroid cartilage.18 If the larynx is still unable to be visualized,blind placement of a gum elastic bougieand subsequent placement of the ETT byrail-roading the ETT over the bougieshould be attempted as the initial man-oeuvre.19 If resistance to ETT passage at the larynx occurs, rotation of the ETT through 90° in an anti-clockwisedirection may be helpful.20

If these initial steps are unsuccessful,oxygenation must be maintained using abag/valve/mask with a Guedel’s airwayand alternative equipment suitable foruse in the ED should be prepared for


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N

Fig. 1.3.1

FAILED INTUBATION DRILL:

Unable to see vocal cordsduring initial laryngoscopy?

Bag/mask/Oropharyngeal airway

Call for difficult intubation trayAdd introducer and additional pillow (unless contraindicated)

Immediate definitive check of position(ETCO2/Air aspiration test)

Immediate definitive check of position(ETCO2/Air aspiration test)

Retry using additional pillow/introducer/different laryngoscope blade

Trial of 'blind' placement of a gum-elastic bougie.Railroad lubricated ETT (One size smaller) over bougie

Trial of “blind” ETT placement

Able to oxygenate/ventilate,allow patient to awaken and/or

try alternative technique

Yes, now able to oxygenateand ventilate with LMA,

allow patient to awaken and/ortry alternative technique

ETT in trachea ETT in esophagus

Not able to oxygenate/ventilate

Remove ETT

Bag/mask/Guedel airway

Insert laryngeal mask airway

Still not able to oxygenate/ventilate

Cricothyroidotomy

LMA guided blind orotracheal intubationIntubating LMAFibreoptic assisted intubation via the LMAFibreoptic bronchoscope assisted nasotracheal intubationRetrograde wire guided intubationBlind nasotracheal intubationPercutaneous dilational tracheostomyTracheostomy

ETT = endotracheal tubeETCO2 = end-tidal CO2LMA = laryngeal mask airway

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use.21,22 A summary of these devices isgiven below. However, if oxygenationand ventilation is considered unsatisfactoryduring the failed intubation drill, imme-diate cricothyroidotomy is indicated.

THE LARYNGEAL MASKAIRWAYThe laryngeal mask airway (LMA) is nowused routinely for airway managementduring elective general anaesthesia.During a failed intubation drill, the LMAmay be superior to bag/mask and oralairway for oxygenation and ventilation ofthe patient.23 However, there has been alimited role for the LMA in the ED fortwo reasons. First, if pulmonary compli-ance is low or airway resistance is high,there will be a leak around the cuff of theLMA when peak inspiratory pressuresexceed 20–30 mmHg. Second, there is apotential risk of aspiration pneumonitis,since the airway remains unprotected. Tominimize the risk of aspiration pneumo-nitis, further developments of the LMAnow include a modified cuff to improvethe seal and a drainage tube to provideaccess to the gastrointestinal tract (theProSeal ™).24

THE INTUBATINGLARYNGEAL MASKAIRWAYThe LMA may be also used to assist inblind orotracheal intubation, either usinga 6 mm ETT passed through the LMA,or an intubating LMA that has beendeveloped for this purpose. Preliminaryreports of the intubating LMA indicate ahigh success rate in the prehospitalsetting,25 ED26 and operating theatre.27

THE OESOPHAGEALTRACHEAL COMBITUBE(COMBITUBE™)The oesophageal tracheal combitubecombines the functions of the oesoph-ageal obturator airway and a conven-tional ETT and may be useful in the

failed intubation algorithm. A 97% successrate for oxygenation and ventilation ofpatients undergoing elective anaesthesia28

and a 91% success rate for successfulinsertion and ventilation by paramedics incardiac arrest patients has been reported.29

However there are little data on emer-gency department use of this device.

THE LARYNGEAL TUBEAIRWAYThe laryngeal tube airway (AirwayManagement Device ™) combines thefunctions of the LMA and an oesoph-ageal obturator airway and consists of a tube placed in the oesophagus with aproximal cuff that inflates in theoropharynx to form a seal for ventilationand a distal cuff that inflates to seal theoesophagus and prevent aspiration ofvomitus and/or insufflation of thestomach. Evaluation of the laryngealtube airway in emergency medicine islimited to a manikin study, which foundthat adequate ventilation at the firstinsertion attempt was possible in 96%.30

BLIND NASOTRACHEALINTUBATIONBlind nasotracheal intubation (BNTI) isa technique that is now rarely used in theoperating theatre,31 but may occasionallybe useful in the ED, either as the initialtechnique of choice, or as part of a failedintubation drill. Requirements forsuccessful BNTI include spontaneousrespirations and depressed gag/coughreflexes. Contraindications include coa-gulopathy, fractured base of skull, maxil-lary fractures, upper airway obstructionor suspected laryngeal injury.

To perform BNTI, high-flow oxygenis administered by mask and the nareschecked to assess size and patency. Thenares are prepared with a pledget soakedin local anaesthetic and vasoconstrictorsuch as 5 ml of lidocaine 2% with adre-naline (epinephrine) 1:100 000. Afterseveral minutes, the pledget is removedand sterile lubricant applied. Localanaesthetic may also be applied by spray

to the pharynx and larynx. If requiredand clinically appropriate, sedation usingmidazolam 1–2 mg may be adminis-tered. An ETT of one size less than thepredicted oral size is passed via the noseto the pharynx and advanced slowly tothe larynx, with the operator listeningfor breath sounds. To facilitate entry intothe larynx, the head may need to beflexed, extended or rotated, the ETTrotated clockwise through 90°, and/or asuction catheter used to guide the ETT.When the ETT passes into the trachea,spontaneous respirations through theETT confirm placement. However, com-plications of BNTI including epistaxis,injuries to the turbinates, perforation ofthe posterior pharynx, laryngospasm andinjuries to the larynx currently limitenthusiasm for this technique.32

RETROGRADEINTUBATIONThe technique of retrograde intubationmay be useful in the ED when othertechniques fail and time allows.33 Thecricothyroid membrane is punctured bya needle/cannula and a guide wire ispassed through the cannula cephalad.This is brought out through the mouthusing Magill’s forceps. An ETT is placedover a special bougie that is passed overthe guide wire through the larynx. Resis-tance will be felt when the ETT reachesthe larynx. When the level of the crico-thyroid is reached, the guide-wire isremoved and the ETT passed furtherinto the trachea.

FIBRE-OPTICBRONCHOSCOPEASSISTED INTUBATIONThe fibre-optic bronchoscope may assistin the intubation of the patient whereRSI fails or is contraindicated.34 If thepatient is awake, the nasal passage andupper airway should have topical anaes-thetic applied as for BNTI. Initially, awell lubricated ETT is introduced nasallyand passed to the posterior pharynx. Thebronchoscope is then passed through the


18

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NETT and the vocal cords visualized. Thesuction port may be used to clear anysecretions. The bronchoscope is thenadvanced into the trachea and the ETT is railroaded over the bronchoscope.Following removal of the bronchoscope,the patient is ventilated with oxygen. If aLMA has been used during a failed intu-bation drill, this may be used to guidethe bronchoscope with the ETT alreadyplaced over it.

The use of the fibre-optic broncho-scope in the ED is limited by severalfactors. The bronchoscope and lightsource must be immediately available foruse during a failed intubation drill. Thelarynx may be difficult to visualize in thepresence of blood, vomitus or secretions.Finally, the equipment is expensive topurchase and maintain.

CRICOTHYROIDOTOMYCricothyroidotomy is an essential skillfor the emergency physician and must beconsidered immediately in cases of ‘can’tintubate-can’t ventilate’.

To perform cricothyroidotomy, a small vertical incision is made over thecricothyroid membrane and arteryforceps are used for blunt dissection tothe cricothyroid membrane. The arteryforceps are then passed into the tracheaand the cricothyroid membrane openedhorizontally. A size 6 mm ETT is passedthrough the opening into the trachea,the cuff is inflated and bag/valve ventila-tion commenced.

Alternatively, there are proprietary kits that allow a cricothyroidotomy tubeto be passed over a guide-wire using theSeldinger technique. In this approach,the cricothyroid membrane is puncturedwith a needle/cannula mounted on asyringe and free aspiration of air confirmsplacement in the airway. The cannula is advanced as the needle is withdrawnand a guidewire is passed through thecannula down the trachea. The cannulais removed and a dilator passed along theguide-wire. Finally, a 4.5–6 mm crico-thyroidotomy tube mounted on a dilatoris passed along the guide-wire and placedin the trachea. The position of the crico-

thyoidotomy tube must be carefullychecked, since misplacement in themediastinum, anterior to the trachea ispossible.

In children, puncture of the crico-thyroid membrane with a 14 gaugeneedle/cannula and insufflation withoxygen is preferred, as injury to thetracheal mucosa at the level of the crico-thyroid may lead to tracheal stenosis. Inadults, placement of a too large tube(>6 mm) through the cricothyroid mem-brane is also considered unsatisfactory inthe longer term because of possible stric-ture occurring at the level of the cricoid.Therefore, conversion of the cricothyroid-otomy to a sub-cricoid tracheostomy isgenerally undertaken at the earliest timeit is safe and convenient.

TRACHEOSTOMYCompared with cricothyroidotomy, asurgical tracheostomy is more time-consuming and difficult to perform inthe ED, although it is recommended insuspected direct laryngeal trauma whenan emergency airway is needed. Pre-tracheal dissection requires adequatelighting, instruments and diathermy.Percutaneous dilatational tracheostomymay be performed without these require-ments, however, there is little publishedexperience with this technique in the ED.

REFERENCES1. Nayyar P, Lisbon A 1997 Non-operating room

emergency airway management and endotrachealpractices: a survey of anaesthesiology programdirectors. Anesthesia and Analgesia 85: 62–8

2. Hillberg RE, Johnson DC 1997 Non-invasiveventilation. New England Journal of Medicine337: 1746–52

3. Fessler RD, Diaz FG 1993 The management ofcerebral perfusion pressure and intracranial pressureafter severe head injury. Annals of EmergencyMedicine 22: 998–1003

4. Sakles JC, Laurin EG, Rantapaa AA, Panacek EA1998 Airway management in the emergencydepartment: a one-year study of 610 trachealintubations. Annals of Emergency Medicine31: 325–32

5. Karkouti K, Rose DK, Ferris LE, et al 1996 Inter-observer reliability of ten tests used forpredicting difficult intubation. Canadian Journal ofAnaesthesia 43: 554–9

6. Nimmagadda U, Chiravuri SD, Salem R, JospehNJ, Wafai Y, Crystal GJ, El-Orbany MI 2001Preoxygenation with tidal volume and deepbreathing techniques: The impact of duration of

breathing and fresh gas flow. Anesthesia andAnalgesia 92: 1337–41

7. Suderman VS, Crosby ET, Lui A 1991 Electiveoral intubation in cervical spine-injured adults.Canadian Journal of Anaesthesia 38: 785–9

8. Morris J, Cook TM 2001 Rapid sequenceinduction: a national survey of practice. Anaesthesia56: 1090–7

9. Pollard RJ, Lobato EB 1995 Endotracheal tubelocation verified reliably by cuff palpation.Anesthesia and Analgesia 81: 135–8

10. Bozeman WP, Hexter D, Liang HK, Kelen GD1996 Esophageal detection device versus detectionof end tidal carbon dioxide levels in emergencyintubation. Annals of Emergency Medicine27: 595–9

11. Chesnut RM 1997 Avoidance of hypotension:conditio sine qua non of successful severe head-injury management. Journal of Trauma 42: S4–S9

12. Robinson N, Clancy M 2001 In patients with headinjury undergoing rapid sequence intubation, doespretreatment with intravenous lignocaine lead to animproved neurological outcome? A review of theliterature. Emergency Medicine 18: 453–7

13. Cormack RS, Lehane J 1984 Difficult intubation inobstetrics. Anaesthesia 39: 1105–11

14. Yentis SM 2002 Predicting difficult intubation-worthwhile exercise or pointless ritual? Anaesthesia57: 105–9

15. Practice Guidelines for the management of thedifficult airway 1993 A report by the AmericanSociety of Anesthesiologists Task Force onManagement of the Difficult AirwayAnesthesiology 78: 597–602

CONTROVERSIES/PITFALLS❶ A number of clinical signs havebeen described that may predictdifficult intubation, but none arecompletely accurate.

❷ When the larynx is unable to bevisualized, a failed intubation drillmust be followed to prevent patienthypoxaemia.

❸ The laryngeal mask airway,intubating laryngeal mask airway,Combitube™, retrograde intubationand fibre-optic-assisted intubationmay have a role when orotrachealintubation is difficult orcontraindicated.

❹ Capnography is recommendedfor confirmation of trachealplacement of the endotracheal tube.The air aspiration test is moreaccurate for patients in cardiac arrest.

❺ Cricothyroidotomy is anessential skill for the emergencyphysician and must be consideredimmediately in cases of ‘can’tintubate-can’t ventilate’.

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for aerobic metabolism. When cerebraloxygen delivery falls below 20 mL/100 gbrain/minute, anaerobic glycolysis pre-dominates with a marked decrease in thegeneration of adenosine triphosphate.After 3–6 minutes of complete cerebralischaemia, the supply of adenosine triphos-phate is exhausted and cellular metabo-lism ceases. The failure of the sodium/potassium transmembrane pump leads to persistant depolarization of the cellmembrane and allows the equilibrationof intracellular and extracellular ions, withthe shift of sodium and water leading tocell swelling.4 In addition, hydrogen ionswith lactate ions are generated and theresulting intracellular metabolic acidosisis toxic to intracellular enzyme systems.The pH shift is partly dependant on theconcentration of glucose, with hyper-glycaemia leading to an intracellularacidosis.

THE REPERFUSIONINJURYFollowing reperfusion, additional injuryoccurs.5 The intracellular levels of glu-

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20

16. Jansenns M, Harstein G 2001 Management ofdifficult intubation. European Journal ofAnaesthesiology 18: 3–12

17. Henderson JJ 1997 The use of paraglossal straightblade laryngoscopy in difficult tracheal intubation.Anaesthesia 52: 552–60

18. Knopp RK 2002 External laryngeal manipulation:A simple intervention for difficult intubations.Annals of Emergency Medicine 40: 38–40

19. Moscati R, Jehle D, Christiansen G, D’Aprix T,Radford J, Connery C, Billittier A 2000Endotracheal tube introducer for failed intubations:a variant of the gum elastic bougie. Annals ofEmergency Medicine 36: 52–6

20. Dogra S, Falconer R, Latto IP 1990 Successfuldifficult intubation. Tracheal tube placement over agum elastic bougie. Anaesthesia 45: 774–6

21. Levitan RM, Kush S, Hollander JE 1999 Devicesfor difficult airway management in academicemergency departments: Results of a nationalsurvey. Annals of Emergency Medicine 33: 694–8

22. Morton T, Brady S, Clancy M 2000 Difficult

airway equipment in English emergencydepartments. Anaesthesia 55: 485–88

23. Tobias J 1996 The laryngeal mask airway: A reviewfor the emergency physician. Pediatric EmergencyCare 12: 370–3

24. Keller C, Brimacombe J, Kleinsasse A, Brimacombe L 2002 The laryngeal mask airwayProSeal™ as a tempory ventilatory device in grosslyand morbidly obese patients before laryngoscope-guided tracheal intubation. Anesthesia andAnalgesia 94: 737–40

25. Mason AM 2001 Use of the intubating laryngealmask airway in pre-hospital care: a case report.Resuscitation 51: 91–95

26. Rosenblatt WH, Murphy M 1999 The intubatinglaryngeal mask: Use of a new ventilating-intubatingdevice in the emergency department. Annals ofEmergency Medicine 33: 234–8

27. Ferson DZ, Rosenblatt WH, Johansen MJ, et al2001 Use of the intubating LMA-Fastrach in 254patients with difficult to manage airways.Anaesthesiology 95: 1175–81

28. Gaitini LA, Vaida SJ, Mostafa S, et al 2001 The

Combitube in elective surgery. Anaesthesiology94: 79–82

29. Lefrancois DP, Dufour DG 2002 Use of theesophageal tracheal combitube by basic emergency medical technicians. Resuscitation52: 77–83

30. Genzwuerler HV, Hilker E, Hohner E, Kuhnert-Frey B 2000 The laryngeal tube: a newadjunct for airway management. PrehospitalEmergency Care 4: 168–72

31. Collins PD, Godkin RA 1992 Awake blind nasalintubation-A dying art. Anaesthesia and IntensiveCare 20: 225–7

32. Tintinalli JE, Claffey J 1981 Complications ofnasotracheal intubation. Annals of EmergencyMedicine 10: 142–4

33. Dhara SS 1992 Retrograde intubation: A facilitatedapproach. British Journal of Anaesthesia 69: 631–3

34. Mlinek EJ, Clinton JE, Plummer D, et al 1990Fibreoptic intubation in the emergencydepartment. Annals Emergency Medicine19: 359–62

INTRODUCTIONProlonged cardiac arrest causing globalcerebral ischaemia may lead to permanentneurological injury, despite effectivecardiopulmonary resuscitation. Manypatients who suffer out-of-hospitalcardiac arrest remain comatose in theemergency department (ED) and theneurological injury accounts for much of the disability and death followinghospital admission.1, 2 This chapterdetails the pathophysiology of anoxicneurological injury and current cerebralresuscitation treatment strategies.

DEFINITIONCerebral resuscitation involves the use ofpharmacological or other strategies tominimize injury to the brain following aprolonged ischaemic insult.3

PATHOPHYSIOLOGYThe brain is highly dependant on anadequate supply of oxygen and glucose

1.4 CEREBRAL RESUSCITATION AFTERCARDIAC ARREST

STEPHEN BERNARD

ESSENTIALS1

1 Brain injury following globalcerebral ischaemia is commonfollowing out-of-hospital cardiacarrest and is associated with highmorbidity and mortality rates.

2 Reperfusion of the ischaemic brain results in glutamate-mediatedcalcium influx into cells, withbiochemical cascades to cell death.

3 A number of pharmacologicalinterventions have failed to improveneurological outcome in humanrandomized controlled trials.

4 Prospective, controlled trialsindicate that induced hypothermia(33°C) for 12–24 hours afterresuscitation from cardiac arrest is an effective treatment for anoxicneurological injury.

5 There is some evidence thathypotension and/or hyperglycaemiaare deleterious to the injured brainand should be promptly treated.

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tamate, an excitatory neurotransmitterreleased from presynaptic terminals,increase dramatically during reperfusion.The glutamate activates ion channel com-plexes including N-methyl-D-aspartatereceptors and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acidreceptors. When activated, these ionchannels increase calcium conductancefrom the extracellular to intracellular fluid.In addition, glutamate activates G-proteinassociated metabotropic receptors,inducing changes in phospho-inositolmetabolism resulting in the productionof inositol triphosphate. This acts as asecond messenger, which releases furthercalcium from stores within mitochondriaand endoplasmic reticulum.

Multiple biochemical cascades are ini-tiated by calcium influx into cells, leadingto the production of oxygen free-radicalsand the activation of degradative enzymes,including proteases, endonucleases,phospholipases and xanthine oxidase.Phospholipase activation results in lipidperoxidation, which causes cell mem-brane destruction and neuronal death.Activated phospholipase A2 generatesarachidonic acid, which mediates injuryby several mechanisms, including the un-coupling of oxidative phosphorylation,inactivation of membrane Na/K-ATPaseand increased release of glutamate.Activated proteases (calpains) degradecytoskeletal and regulatory proteins.

Intracellular iron also plays an impor-tant role in free-radical production. Ironis usually maintained in a ferric state andis sequestered to intracellular proteins.During ischaemia, iron is reduced to the soluble ferrous form and reacts withperoxide, generating damaging hydroxylfree-radicals.

The generation of free-radicals activatesan upregulation of adhesion molecules inthe leucocytes, endothelium and pla-telets. These adhesion molecules mediateleucocyte adhesion and extravasationinto brain parenchyma, with increasedcerebral ischaemia by causing micro-vessel occlusion with leucocyte-plateletcomplexes. There is also experimentalevidence of marked activation of bloodcoagulation without endogenous fibrino-lysis and platelet activation during reper-

fusion after cardiac arrest.6 In addition,vasoconstriction may occur secondary tothe production of thromboxane A2 andprostaglandin F2α from arachidonic acid.

Ischaemia is also a stimulus for nitricoxide synthase activation. Nitric oxidesynthase converts L-arginine to nitricoxide, a potent mediator of excitotoxicinjury. The nitric oxide may combinewith superoxide to form peroxynitriteradicals, which are potent activators oflipid peroxidation. Other proposedactions of nitric oxide include DNAdamage, increased glutamate release andmicrovascular vasodilatation.

Finally, some neurones which survivethe initial anoxic insult proceed toprogrammed cell death (apoptosis).After reperfusion, this delayed neuronaldeath may occur at different rates,varying from 6 hours for neurones in thestriatum to 7 days for hippocampal CA1neurones. Apoptosis is characterized bycellular and nuclear shrinkage, chromatincondensation and DNA fragmentation.The complex bichemical pathways forthis phenomenon are currently underinvestigation.7

CEREBRALHAEMODYNAMICSAFTER REPERFUSIONAfter restoration of a spontaneous cir-culation, cerebral haemodynamics mayremain abnormal.8 Following an initialhyperaemia, cerebral blood flow decreases,despite normal mean arterial bloodpressure, whilst cerebral metabolic ratefor oxygen increases. Thus, there may becontinuing cerebral ischaemia for 12–24hours following resuscitation from pro-longed cardiac arrest. Cerebral oxygensupply/demand is also adversely affectedby systemic hypoxaemia, raised intra-cranial pressure and/or seizure activity.

PHARMACOLOGICALINTERVENTIONSAs much of the neurological injury seenfollowing ischaemic injury occurs afterreperfusion, there has been considerable

interest and research into pharmacolo-gical interventions that alter the abovemetabolic pathways and ameliorate thereperfusion injury.3,9

A number of drugs that have shownimproved neurological outcome in animalmodels of global cerebral ischaemia haveundergone large randomized controlledhuman trials, including thiopentone,10 acorticosteroid11 and the calcium anta-gonists, lidoflazine12 and nimodipine.13

However, none of these showed im-proved neurological or overall outcome.Magnesium has been shown to improveneurological outcome in patients resus-citated from in-hospital cardiac arrest;14

however a study of patients with anoxicneurological injury after resuscitationfrom out-of-hospital cardiac arrestshowed no benefit.15

Currently, there is some interest in thepossible role of thrombolytic drugsduring and after cardiac arrest with thegoal of decreasing cerebral microcircula-tory fibrin formation and improvingcerebral blood flow.6

INDUCEDHYPOTHERMIAInduced hypothermia is theoreticallybeneficial after cardiac arrest and resus-citation. Hypothermia decreases cerebraloxygen demand without decreasingcerebral oxygen supply and potentiallydecreases the reperfusion injury byreducing the production of oxygen free-radicals after reperfusion.

Two prospective, controlled humanstudies have suggested improvedoutcome using moderate hypothermia incomatose survivors of prehospital cardiacarrest.16,17 In one study, 43 patients wererandomized to induced hypothermia(IH) at 33°C for 12 hours and 34 patientswere maintained at normothermia.16

Hypothermia was induced in the EDusing ice-packs and neuromuscularblockade. At hospital discharge, 21/43(49%) in the IH group had a good out-come compared with 9/34 (26%) in thecontrol group (P=0.046). Followingmultivariate analysis for differences atbaseline, the odds ratio for good out-

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come in the hypothermic group was5.25 (95% confidence intervals 1.47 to18.76: P=0.011). There were no apparentadverse effects of IH such as sepsis, lacticacidosis or coagulopathy.

A second clinical trial of inducedhypothermia was conducted in Europe.17

This study enrolled 273 comatose sur-vivors of pre-hospital cardiac arrest, with136 patients undergoing IH (33°C for24 hours), and 137 patients maintainedat normothermia. Hypothermia wasinduced in the ED using a refrigeratedair mattress. At 6 months, 55% of the IHpatients had good outcome, comparedwith 39% of normothermic controls(odds ratio 1.4, 95% confidence interval1.08 to 1.81). The complication rate didnot differ between the two groups.

However, these two studies alsodemonstrated that surface cooling hadsignificant limitations. First, surfacecooling is a slow method of decreasingcore temperature, with 0.9°C/hourusing ice packs16 and 0.5°C/hour usingforced cold air cooling.17 Second, cover-ing the patient with ice packs or coolingblankets during resuscitation is inconve-nient and impractical for medical andnursing staff. Finally, the use of ice packsor refrigerated units (for forced aircooling) limit the use of these techniquesto the hospital environment.

Since there is evidence from animalstudies that outcome may be improved ifcooling is initiated during or immediatelyafter return of spontaneous circulation,3

current research focuses on the develop-ment of techniques for the induction ofhypothermia that may be feasible in theout-of-hospital setting.

One approach, which has beenrecently studied in 16 patients who wereresuscitated from out-of-hospital cardiacarrest, is the use of a cooling helmet.18

However, this technique is also a relativelyslow, with the target core temperature of34°C only reached after 180 minutes.

An alternative approach is the use oflarge volume, ice-cold (4°C) intravenousfluid.19 In a recent study of 22 patientswho had been resuscitated from out-of-hospital cardiac arrest, a rapid intravenousinfusion of large-volume (30 mL/kg)lactated Ringers solution at 4°C was

shown to be an effective and safe tech-nique for the induction of mild hypo-thermia. This therapy decreased coretemperature by 1.7°C over 25 minutesand there were improvements in meanarterial blood pressure, as well as acid-base and renal function. There were noapparent complications of this therapysuch as pulmonary oedema. If subsequentstudies confirm this finding, thisapproach may be applicable to the out-of-hospital environment.

OTHERINTERVENTIONSAnimal studies of anoxic brain injuryhave suggested that outcome may beimproved if elevated blood pressure ismaintained in the post-resuscitationperiod and it seems reasonable to provideelevated mean arterial blood pressureafter cardiac arrest.20 Hyperglycaemia isalso associated with worse outcomefollowing cerebral ischaemia and shouldalso be corrected.21

CEREBRALMONITORINGRecent developments in cerebral resus-citation include the use of invasive andnon-invasive neurological monitoring todetect persistant cerebral ischaemia.Currently, monitoring for neurologicaldeterioration after global or focalischaemic injury is largely clinical, withobservation of pupil reactivity, level ofconscious state and the development orprogression of focal neurologic signs.However, any change in clinical signsdue to an increase in cerebral ischaemiamay be delayed, with irreversible damageoccuring before appropriate intervention.Thus, there is considerable interest innewer methods of non-clinical monitor-ing of the central nervous system.

The monitoring of cerebral perfusionpressure equating to the mean arterialblood pressure (MAP) minus the intra-cranial pressure (ICP) may give anestimation of cerebral oxygen delivery.Although increased ICP may occur afterglobal ischaemia,22 there are little data

on ICP monitoring in adults followingprolonged cardiac arrest.

Cerebral oxygen delivery may also beestimated by the continuous or inter-mittent measurement of jugular venousoxygen saturation. However, this tech-nique does not appear to provide usefulinformation that alters management.23

Other neurological monitoring tech-niques that are currently being evaluatedinclude near infra-red spectroscopy, cereb-ral microdialysis and the direct continuousmeasurement of cerebral blood flowusing jugular venous thermodilution.

SUMMARYIn patients with prolonged cardiac arrestand global cerebral ischaemia, neurolo-gical injury is mainly related to the timeinterval between cardiac arrest and thereturn of spontaneous circulation.Comatose patients should be intubatedand have assisted ventilation with supple-mental oxygen to protect the airway andassure adequate oxygenation and ventila-tion. Following the return of spontan-eous circulation, a normal or elevatedmean arterial blood pressure should bemaintained using fluid and/or vasoactivedrug therapy. In addition, hyperglycae-mia should be promptly corrected withinsulin therapy. Since adult out-of-hospital cardiac arrest often occurs in the setting of an ischaemic coronarysyndrome, the usual cardiac care for this,such as the use of aspirin, heparin andthrombolysis, may be required.

There is now evidence that mild hypo-thermia for 12–24 hours following resus-citation is beneficial. The optimal techniquefor the induction of hypothermia is yetto be determined, however, preliminaryevidence suggests that the rapid infusionof large-volume (30 mL/kg), ice-cold(4°C) intravenous fluid has advantagescompared with surface cooling. Otherpharmacologic and non-pharmacologicinterventions are yet to be proven.

Admission to an intensive care unit willbe required for most patients with anoxicbrain injury following resuscitation forout-of-hospital cardiac arrest for furthersupportive care.

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REFERENCES1. Bernard SA 1998 Outcome from prehospital

cardiac arrest in Melbourne, Australia. EmergencyMedicine 10: 25–9

2. Edgren E, Hedstrand U, Kelsey S, et al 1994Assessment of neurological prognosis of comatosesurvivors of cardiac arrest. Lancet 343: 1055–9

3. Safar P, Behringer W, Bottinger BW, Stertz F 2002Cerebral resuscitation potentials for cardiac arrest.Critical Care Medicine 30: S140–S144

4. Ebmeyer U, Katz LM 2001 Brain energetics aftercardiopulmonary cerebral resuscitation. CurrentOpinion in Critical Care 7: 189–94

5. White BC, Grossman LI, ONeil BJ, et al 1996Global brain ischemia and reperfusion. Annals ofEmergency Medicine 27: 588–94

6. Bottinger BW, Martin E 2001 Thrombolytic therapyduring cardiopulmonary resuscitation and the roleof coagulation activation after cardiac arrest.Current Opinion in Critical Care 7: 176–83

7. Morita-Fujimura Y, Fujimura M, Yoshimoto T,Chan PH 2001 Superoxide during reperfusioncontributes to caspase-8 expression and apoptosisafter transient focal stroke. Stroke 32: 2356–61

8. Oku K, Kuboyama K, Safar P, et al 1994 Cerebraland systemic arteriovenous oxygen monitoringafter cardiac arrest: Inadequate cerebral oxygendelivery. Resuscitation 27: 141–52

9. Gisvold SE, Stertz F, Abramson NS, et al. 1996Cerebral resuscitation after cardiac arrest:Treatment potentials. Critical Care Medicine24: S69–S80.

10. The Brain Resuscitation Clinical Trial Study Group1986 Randomized clinical study of thiopentoneloading in comatose survivors of cardiac arrest.New England Journal of Medicine 314: 397–410

11. The Brain Resuscitation Clinical Trial Study Group1989 Glucocorticoid treatment does not improveneurologic recovery following cardiac arrest.Journal of the American Medical Association262: 3427–30

12. Brain Resuscitation Clinical Trial II Study Group1991 A randomized clinical study of a calcium-entry blocker (lidoflazine) in the treatment ofcomatose survivors of cardiac arrest. New EnglandJournal of Medicine 324: 1225–31

13. Roine RO, Kaste M, Kinnamen A, et al 1990Nimodipine after resuscitation from out-of-hospitalventricular fibrillation: A placebo-ciontrolleddouble-blind randomized trial. Journal of theAmerican Medical Association 264: 3171–7

14. Thel MC, Armstrong AL, McNulty SE, et al 1997Randomised trial of magnesium in in-hospitalcardiac arrest. Lancet 350: 1272–6

15. Fatovich DM, Prentice DA, Dobb GJ 1997Magnesium in cardiac arrest (the MAGIC trial).Resuscitation 35: 237–41

16. Bernard SA, Gray TW, Buist MD, Jones BM,Silvester W, Gutteridge GA, Smith K 2002 Arandomised, controlled trial of inducedhypothermia in comatose survivors of prehospitalcardiac arrest. New England Journal of Medicine346: 557–63

17. The Hypothermia after Cardiac Arrest StudyGroup 2002 Mild therapeutic hypothermia toimprove the neurological outcome after cardiacarrest. New England Journal of Medicine346: 549–56

18. Hachimi-Idrissi S, Corne L, Ebinger G, MichotteY, Huyghens L 2001 Mild hypothermia induced bya helmet device: a clinical feasibility study.Resuscitation 51: 275–81

19. Bernard SA, Buist M, Monteiro O, Smith K 2003Induced hypothermia using large volume, ice-coldintravenous fluid in comatose survivors of out-of-hospital cardiac arrest: A preliminary report.Resuscitation 56: 9–13

20. Safar P, Kochanek P 2000 Cerebral blood flowpromotion after prolonged cardiac arrest. CriticalCare Medicine 28: 3104–6

21. Longstreth WT, Inui TS 1984 High glucose levelson hospital admission and poor neurologicrecovery after cardiac arrest. Annals of Neurology15: 59–63

22. Morimoto Y, Kemmotsu O, Kitami K, MatsubaraI, Tedo I 1993 Acute brain swelling after out-of-hospital cardiac arrest: Pathogenesis and outcome.Critical Care Medicine 21: 104–9

23. Van der Hoeven JG, DeKoning J, Compier EA,Meinders AE 1995 Early jugular bulb monitoringin comatose patients after an out-of-hospitalcardiac arrest. Internal Care Medicine 21: 567–77

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CONTROVERSIES❶ The biochemical pathways ofneuronal death following ischaemiaand reperfusion are complex andrequire further study.

❷ Induced hypothermia is the onlyneuroprotective therapy that hasshown benefit in clinical studies ofglobal anoxic neurological injury.

❸ Future studies will focus ontechniques for the rapid induction ofhypothermia either in the ambulanceor the emergency department.

DEFINITIONShock is a clinical syndrome where tissueperfusion, and hence oxygenation, is in-adequate to maintain normal metabolicfunction.1 Insufficient ATP (adenosinetriphosphate) is generated intracellularlyto maintain the function and structuralintegrity of tissues. This causes a switchto anaerobic metabolism, resulting in anoxygen debt and tissue acidosis.2

The clinical recognition of shock maybe difficult, particularly at the extremesof age. Pre-existing disease and the useof medications modify the compensatorymechanisms that protect vital organperfusion. The emergency managementof shock requires a high clinical suspicionand early, aggressive resuscitation.

1.5 SHOCKROBERT A. SCOTT

ESSENTIALS1 The three broad categories of shock include disorders of cardiac rate or rhythm;volume or vascular resistance problems; and myocardial pump dysfunction.

2 Hypotension, although characteristic of shock, should be considered a latefinding.

3 Hypovolaemia, and hence volume resuscitation, should be carefully considered and excluded in every patient with undiagnosed shock.

4 The mortality following cardiogenic shock is improved by revascularizationstrategies, including angioplasty and coronary artery bypass grafting. Thrombolyis has no proven benefit but lysis may be supplemented with intra-aortic balloon counterpulsation where available.

5 Cyclo-oxygenase inhibitors, opioid antagonists and cytokine inhibitors conferlittle additional benefit in septic shock over fluid resuscitation, the use of inotropesand appropriate antibiotics or surgery. Activated protein C has been shown toimprove mortality in severe sepsis and severe organ dysfunction.

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SOURCES OF SHOCKShock is due to malfunction of the cardio-vascular system for which there may bemore than one contributing mechanism.A simple classification recognizes threebroad categories:

❶ Disorders of cardiac rate or rhythm❷ Volume or vascular resistance

problemsa. volume loss - ‘empty tank’ (Table

1.5.1)b. altered vascular resistance -

‘inappropriately sized tank’ (Table1.5.2)

❸ Myocardial pump dysfunction(Table 1.5.3).

This classification is not exhaustive andcontributing causes may feature in morethan one category.

PATHOPHYSIOLOGYThe consequences of shock are cellularinjury and death occurring by commonmechanisms.3 Shock and reperfusioncause intracellular calcium overload, pro-ducing ATP reduction, diastolic dysfunc-tion and decreased contractile forces inexcitable tissues. Calcium overload is alsorelated to free-radical oxidative damage,degradation of cell ionic pumps, and

the destruction of cytosol, nuclear andmitochondrial macromolecules.

The accumulation of hydrogen ionsdownregulates catecholamine receptors,resulting in a reduction in catecholamineeffectiveness and a decrease in intracellu-lar energy production. Shock also causesa catabolic state, with increased circulatingcatecholamines, angiotensins, glucagonand corticosteroids. Metabolism becomesglycolysis dependent, and circulatingglucose, lactic acid, free fatty acids andtriglycerides increase.

Oxygen consumption is defective insome tissues in shock. Many causes areresponsible, including physical barriers todiffusion such as dysfunctional endo-thelium, and interstitial and intracellularoedema, as well as metabolic dysfunc-tion. In humans, most shock states resultin flow-dependent oxygen uptake. How-ever, the role of supranormal oxygendelivery in therapy has yet to be resolved.

Prolonged shock results in myocardialdysfunction. An early compensatory in-crease in heart rate is common. Diastolicdysfunction has also been describedwhere active ventricular relaxation isimpaired through the disruption of ATP-dependent sarcoplasmic reticular calciumion uptake. Circulating catecholaminesare initially increased, but ultimately indecompensated shock the heart fails,owing partly to circulating myocardialdepressant factors described in haemor-rhagic and septic shock.

Organ blood flow changes are impor-tant in shock, as shock raises the thre-shold at which vital organ blood flowdecreases. These and other specific patho-physiologic changes are discussed later.

DIAGNOSIS OF SHOCK• Hypotension is a sentinel clinical

sign, defined as a systolic bloodpressure <90 mmHg or a reductionof >30 mmHg in a previouslyhypertensive patient. However, a lowblood pressure should be considereda late finding. Aggressivemanagement aims to prevent thedevelopment of hypotension.

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Table 1.5.2. Examples of shock resulting from altered vascular resistance:

Septic shock

Anaphylactic shock

Spinal neurogenic shock

Vasodilator drugs or toxins

Adrenal insufficiency (cortisol deficiency)

Central nervous system injury

Prolonged shock from any cause

Table 1.5.3. Examples of myocardial dysfunction resulting inshock:

Primary cause of myocardialdysfunction (cardiogenic shock)Acute myocardial infarctionCardiac contusionCardiomyopathyCongestive heart failureMyocarditisRuptured ventricular septum or free wallAcute valvular dysfunction– aortic insufficiency– chordae tendineae rupture– papillary muscle dysfunction– prosthetic valve thrombus/dysfunction– severe aortic stenosis

Secondary causes of myocardialdysfunctionObstructive causes– tension pneumothorax– pericardial disease (tamponade,

constriction)– pulmonary vascular disease

(thromboembolism,pulmonary hypertension)

– atrial myxoma– left atrial mural thrombus– obstructive valvular disease (aortic, mitral)DrugsSystemic toxins or myocardial depressantfactors

Table 1.5.1. Examples of volume loss contributing to shock:

Blood loss (haemorrhagic shock)External– trauma– gastrointestinal tract bleeding

Concealed– haemothorax– haemoperitoneum– ruptured abdominal aortic aneurysm– ruptured ectopic pregnancy

Loss of plasma– Burns– Exfoliative dermatitis

Loss of fluid and electrolytesExternal– vomiting– diarrhoea– excessive sweating– urinary losses– adrenal insufficiency (aldosterone

deficiency)– diabetes mellitus– diabetes insipidus– diuretics– renal disease

Concealed– pancreatitis– ascites– bowel obstruction– peritonitis– splanchnic ischaemia

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• Tachycardia is usually present, butmay be masked by drugs oradvanced age. The trend with serialobservation is more significant thanabsolute values. Bradycardia mayoccur, for instance, in catastrophichaemorrhage from a rupturedectopic pregnancy, or following aninferior myocardial infarction (MI).

• An abnormal respiratory rate of <10or >29 per minute depends on thecause, such as narcotic overdose orearly septicaemia, but may also bepart of the shock syndrome.

• Core temperature may be low,normal or elevated, and will beaffected by age, environment,volume status, coexisting disease anddrug therapy.

• SaO2 should be measured to detectearly hypoxaemia.

• The mental state reflects cerebralperfusion and may range fromnormal to confused or coma.

• The peripheral circulation usuallyreveals venoconstriction, decreasedperipheral temperature, diaphoresisand pallor. Capillary return may beprolonged beyond 4 seconds.Peripheral or central cyanosis is a latesign. However, spinal neurogenicshock and sepsis may lead to warm,dry skin as a consequence ofvasodilatation.

• Urine output is the most usefulbedside monitor of the adequacy ofend-organ perfusion. Levels below0.5 mL/kg/h indicateunderperfusion.

EMERGENCYDEPARTMENTMONITORINGThe presence and progress of shock may be monitored in the emergencydepartment (ED) by careful recording ofrepeated clinical assessment:

• vital signs, including temperature,pulse, respirations and bloodpressure

• ECG• pulse oximetry• urine output.

Invasive monitoring in the ED mayalso include:

• intra-arterial blood pressuremonitoring via the non-dominantradial artery

• central venous pressure (CVP)monitoring via the subclavian orinternal jugular veins. Trends in CVPmay be followed in response tovolume loading, but should beinterpreted in relation to the otherobserved parameters

• end-tidal CO2 in ventilated patients.

Pulmonary artery catheterization, gas-tric tonometry, Doppler cardiac outputstudies and other more sophisticatedinvestigations are best performed in anintegrated intensive care environment.

Lactate measurements are an objectivemarker of the presence and severity ofshock. Bedside lactate analysis is nowavailable. Normal levels are <2 mmol/L,and levels of >4 mmol/L are associatedwith increased mortality. Similarly, basedeficit (BD) is a useful indicator of hypo-perfusion and may be used to assess theadequacy of resuscitation. BD levelsreflect the volume of fluid required, thepresence and severity of intra-abdominalhaemorrhage and mortality. It may alsobe used to identify compensated shockand to predict transfusion requirements,the need for ICU and the length of stay.The incidence of adult respiratory distresssyndrome (ARDS), multiple organfailure, renal failure and coagulopathy allincrease with rising levels of BD.4,5

INITIAL EMERGENCYMANAGEMENT OF THESHOCKED PATIENT• The airway and ventilation are

assessed and supported.Supplemental high-flow oxygen isgiven. Tracheal intubation should beconsidered for the standardindications of airway protection,airway maintenance, airway creationand the need for ventilatory support(see Chapter 1.3).

• External haemorrhage should becontrolled with direct pressure while

intravenous access is obtained withlarge-bore peripheral cannulae.Cardiac rhythm and pulse oximetry(SaO2) should be monitored. A fluidchallenge may be given after drawingblood for investigations, including abedside glucose level, and arterialblood gases are measured.

• Vital signs are recorded and anyavailable history obtained, followedby a directed physical examination.Observations should be continuedregularly.

• A chest X-ray, ECG and otheremergency investigations areperformed, e.g. bedside ultrasoundto exclude pericardial tamponade,assess cardiac filling and ventricularfunction, or to seek intra-abdominalfree fluid.

MANAGEMENT OFSPECIFIC SHOCKSYNDROMESThe following shock syndromes arediscussed in detail.

• Hypovolaemic shock• Cardiogenic shock• Septic shock• Neurogenic shock.

Hypovolaemic shockTable 1.5.4 provides a guide to thepathophysiologic responses to acutehaemorrhage. They relate to sympathe-tically mediated vasoconstriction and the release of endogenous catabolichormones. Total peripheral resistanceincreases at the arteriolar level, venouscapacitance increases, and blood flow tothe brain and heart is maintained at theexpense of renal, splanchnic, skin andmuscle blood flow.1 Cerebral vascularautoregulation maintains cerebral bloodflow and oxygen transport down to amean blood pressure of 50–60 mmHg,below which acidosis and brain ischaemiadevelop, followed by a progressive fall incerebral perfusion pressure and coma.Lung parenchymal water increases withdecreasing surfactant and alveolar collapse.Pulmonary dysfunction develops through

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multiple insults at the microvascular andcellular level.4

Renal perfusion is decreased andglomerular filtration rate falls with intra-renal shunting of blood flow. Pancreaticblood flow may decrease to as little as15% of normal, which may persist postresuscitation.1 A myocardial depressantfactor has been isolated from the pancreas.Splanchnic blood flow is significantlyreduced, with some preservation ofmucosal circulation. Hypoperfusion maypersist after the hypotension is corrected,which contributes to a failure of gutbarrier function, leading to bacterialtranslocation and contributing to thedevelopment of multiple organ failure.1,4

Clinical presentation

Signs and symptoms: The pulse rate,blood pressure, pulse pressure, respira-tory rate, urine output and mental statuschange are detailed in Table 1.5.4. Neckveins will be flat as a consequence of lowcentral venous pressure, where cardiacfunction is normal. A specific cause forblood volume loss must be sought (seeTable 1.5.1).

Investigations:• Bedside glucose estimation, arterial

blood gases and serum lactate• Full blood examination, haematocrit,

coagulation profile, blood group andcross-match

• Urea, creatinine, electrolytes andliver function tests

• β-HCG in females of childbearingage

• Chest X-ray and 12-leadelectrocardiogram.

Additional studies will be indicated in specific situations, and all tests arerepeated serially according to the clinicalpicture.

Diagnosis Hypovolaemia, and hencevolume resuscitation, should be carefullyconsidered in every patient presentingwith undiagnosed shock.

Therapy• General supportive care is provided

as described previously, withsupplemental oxygen, cervical spineimmobilization in trauma, and earlyendotracheal intubation andmechanical ventilation for airway orrespiratory failure or progressiveshock.

• The Trendelenburg position providesno consistent effect on systemicvascular resistance or venous return.Passive leg raising is more effectivein increasing left ventricular end-diastolic volume, stroke volume and

cardiac output, but these effects aretransient.6

• Application of the pneumaticantishock garment (PASG or MASTsuit) results in a minimalautotransfusion effect. There is noevidence that it improves recovery inbleeding trauma patients and it hasno place in the management ofhypovolaemic shock.7

• External haemorrhage is controlledwith firm direct pressure.

• Intravenous access is gained withtwo 14 g cannulae, and fluidwarmers and infusers capable ofrapid delivery are employed.

• O-negative or type-specific bloodmust be transfused as soon aspossible in patients presenting withclass III or IV haemorrhage. Surgicalconsultation is also urgently required.

• Efforts to return blood pressure tonormal in bleeding trauma patientsmay be counter-productive andoccasionally harmful. Contemporaryresuscitation practice, in the absenceof evidence for the effectiveness ofcurrently recommended resuscitationprotocols, might best be regarded asexperimental.7 Patients with class Ior II haemorrhagic shock or non-haemorrhagic hypovolaemic shockshould continue to receive warmedcrystalloid. Timely restoration ofperfusion and oxygen deliveryshould be the primary objective inbleeding patients presenting in ruraland remote communities, in theelderly and in those with controlledhaemorrhage. In those patients withuncontrolled haemorrhage followingpenetrating truncal trauma, in closeproximity to facilities capable ofdefinitive care, less aggressive fluidresuscitation, pending promptsurgical intervention, may be used.8

• There is little evidence supportingthe continued use of colloids in theresuscitation of critically ill or injuredpatients.8

• A clinical role for hypertonic saline(HS) has yet to be defined assignificant advantages of HS overstandardized crystalloid solutions areunproven. HS may improve

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Table 1.5.4 Estimated volume losses in a 70 kg man at initial presentation

Class I Class II Class III Class IV

Blood loss (mL) Up to 750 750–1500 1500–2000 >2000

Blood loss as a % of Up to 15 15–30 30–40 >40blood vol.

Pulse rate per min <100 >100 >120 >140

Blood pressure (mmHg) Normal Normal Decreased Decreased

Pulse pressure Normal or Decreased Decreased Decreasedincreased

Respiratory rate per min 14–20 20–30 30–40 >35

Urine output (mL/h) >30 20–30 5–15 Negligible

Mental status Minimal Mildly Anxious, Confused,alteration anxious confused lethargic

Fluid replacement Crystalloid Crystalloid Crystalloid Crystalloidand blood and blood

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outcomes in a subgroup of patientswith shock and traumatic braininjury and has been recommended asthe initial fluid of choice inhaemorrhaging battlefield casualties.8

There are no current definitiverecommendations concerning theuse of modified haemoglobin orperfluorocarbon blood substitutes.8

• Tension pneumothorax, cardiactamponade and myocardialcontusion should always beconsidered in the hypotensive traumapatient, although such patientsshould be assumed to behypovolaemic until provenotherwise.

• Continuous monitoring andreassessment should take place in theED pending definitive care andadmission. Early ICU involvementshould be considered.

Cardiogenic shock

DefinitionCardiogenic shock is the inability of the heart to deliver sufficient blood tothe tissues to meet resting metabolicdemands,9 i.e. a systolic blood pressureof <90 mmHg or ≥30 mmHg below basallevels for at least 30 minutes; alterna-tively, a significant arteriovenous oxygendifference and a cardiac index of <2.2 L/min/m2 where pulmonary capillarywedge pressure is >15 mmHg are seen.There is clinical evidence of poor tissueperfusion in the form of oliguria,cyanosis and altered mentation. Failureto respond to correction of hypoxaemia,hypovolaemia, arrhythmias and acidosisis a requirement for the diagnosis.9

AetiologyThe commonest cause of cardiogenicshock is MI or ischaemia, resulting in atleast 40% dysfunctional myocardium (seeTable 1.5.3).

EpidemiologyCardiogenic shock complicates 6–20% ofpatients with acute myocardial infarction(AMI). The mortality rate exceeds 80%.It is the commonest cause of in-hospitalpost-infarct mortality, and there has been

no change in its incidence or prognosissince the early 1970s.9,10 Ten per cent ofpatients present already in establishedcardiogenic shock, while 90% develop itduring admission.11

Older patients with anterior AMI, pre-vious AMI, angina or congestive heartfailure are at greater risk. One-quarter ofpatients will have reinfarcted. There isalso a significant incidence of diabetesmellitus. There is a higher prevalence of patients with multivessel disease andpersistent occlusion of the infarct-relatedartery. Patients with an occluded leftanterior descending artery also have anincreased incidence, termed the ‘leftmain shock syndrome’, with a mortalityapproaching 100%.12 Only aggressiverevascularization within 12 hours ofsymptom onset makes any difference tothese patients.

In a series of 231 patients with cardio-genic shock, 214 presented with symp-toms and/or signs of left ventricularfailure: 42% received thrombolysis, 26%had percutaneous transcoronary angio-plasty (PTCA), and 8% had emergencycoronary artery bypass grafting (CABG).The overall mortality rate was 66%.Mortality in patients given intravenousthrombolytics was 61%, compared to71% in those not receiving lysis. This wasnot statistically significant. Over 53% of patients with inferior AMI died,compared to 67% of those with anteriorinfarctions.13

PathophysiologyThe clinical consequences of pumpdysfunction have been well described.9,14

The activation of the sympatheticnervous and renin-angiotensin systemscontributes to the failure to increase or afall in myocardial oxygen demand, whichcontributes to infarct expansion, andfurther decreases in contractility, coro-nary perfusion pressure and oxygenextraction. Systolic dysfunction results inan increase in end-systolic volumes andfalls in ejection fraction, stroke volumeand cardiac output. Diastolic dysfunc-tion is also well described. Systemichypoperfusion and selective vascularredistribution lead to organ failure andmetabolic acidosis.


Signs and symptoms These vary withthe cause. Non-specific findings aresimilar to those described under hypo-volaemic shock.

• Jugular venous pressure is frequentlyelevated, but is a non-specific findingas it is also seen in the followingconditions:– pericardial tamponade– constrictive pericarditis– pulmonary hypertension– right ventricular infarction– superior vena caval obstruction– tension pneumothorax– tricuspid valve insufficiency or

stenosis.• Blood pressure may be within

normal limits as a result ofcompensatory mechanisms, whichalso produce tachycardia and anarrowed pulse pressure.

• Signs of pulmonary venous congestionare common, but may be absent inpure right ventricular infarction.

• Precordial examination maydemonstrate a dyskinetic apex beator thrill. A fourth heart soundsuggests decreased ventricularcompliance, and third soundincreased ventricular diastolicpressure. Murmurs common insystole may be due to mitralregurgitation or, rarely, rupture ofthe ventricular septum.

Investigations• 12-lead ECG. Leads V4R and V7-9

are indicated in suspected rightventricular and posterior infarction,respectively

• Chest X-ray• Full blood examination and film• Bedside blood glucose, urea and

creatinine, electrolytes, liver-functiontests, calcium, magnesium andphosphorus levels

• Serial CK (creatine kinase), CKMB(creatine kinase, muscle-brain),myoglobin and troponin I or Tlevels, depending on local availability

• Blood-gas estimation, except incandidates for lysis orrevascularization.

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Bedside echocardiography should beavailable to all patients who present withundiagnosed shock, as an extension of thephysical examination. Pericardial effusionor tamponade may be excluded and globalsystolic function or wall motion abnormal-ities confirmed. The presence of hypo-volaemia with a hyperkinetic heart andsmall right-side chambers, or right ventricu-lar dysfunction may also be ascertained.15

Diagnosis Cardiogenic shock must beconsidered in any patient presenting witha primary or secondary cause for cardiacdysfunction (see Table 1.5.3) in thepresence of symptoms and signs of hypo-perfusion despite optimizing circulatingvolume following a fluid challenge.

Therapy• Initial care and monitoring should

be provided, as described earlier.• Tracheal intubation should be

considered for airway stabilizationand ventilatory support in thepresence of worsening hypoxia.

• Tension pneumothorax should beexcluded.

• Arrhythmias considered ascontributory to the presence ofcardiogenic shock should be treatedaccording to ACLS principles.

• Hypovolaemia must be sought andcorrected in all patients. A 250 mLaliquot of 0.9% saline should begiven cautiously as a bolus and theresponse assessed. Further bolusesmay be indicated. Volume loading tomaintain right atrial filling pressuresis essential in inferior MI with rightventricular (RV) involvement. CVPmonitoring may be indicated,although it is of limited value in thepresence of pulmonary oedema.

• Persistence of the shock statefollowing adequate fluid challenge inthe presence of end-organ dysfunctionis an indication for inotropic support.

• Dobutamine is a β1-adrenergicagonist with some β2 effects that,although weak, lead to increasedcontractility, cardiac output, strokevolume and heart rate (at the higherend of the dose range). Peripheralvasodilatation is also produced and

coronary and collateral blood flowaugmented.9,16 Dobutamine is indicatedat 2–20 µg/kg/min in patients withan SBP of 90–100 mmHg. It is thepreferred inotrope in RV infarctionand may be commenced by theperipheral route in the absence ofcentral venous access. Tachycardiamust be avoided, and obstructivecardiac lesions contraindicate itsuse.

• Dopamine is the endogenousprecursor of noradrenaline, with dose-dependent effects16 as listed below:– 1–2 µg/kg/min: Increases renal

plasma flow, glomerular filtrationrate (GFR) and sodium excretionvia dopamine-1and dopamine-2receptors. This effect is no longervalid.

– 2–10 µg/kg/min: Significantinotropic effects at the β-adrenoreceptor increase cardiacoutput.

– >10 µg/kg/min: Increasingperipheral vasoconstrictionthrough α-adrenergic stimulation.

Dopamine is useful as an inotropicagent when SBP is less than 90 mmHg in order to restore perfusion pressure tovital organs. It may increase the risk ofarrhythmias and cause tissue necrosisfollowing local extravasation. Its bene-ficial effects on renal blood flow in lowdosage are debatable.

• Adrenaline (epinephrine) is a potentα and β1 agonist and a moderate β2

agonist: 0.04–0.1 µg/kg/minproduces increased heart rate andcontractility with unchanged orlowered peripheral vascularresistance. Higher doses produce α-receptor mediated vasoconstriction.Adrenaline (epinephrine) is indicatedin profound hypotensionaccompanying cardiogenic shock,and in those unresponsive todobutamine and dopamine.

• Noradrenaline (norepinephrine) isthe main neurotransmitter atsympathetic postganglionic fibres,producing β1- and potent α1- andα2-agonist effects. It is indicated insevere cardiogenic shock to increaseperfusion pressure. Its peripheral

vasoconstricting effects may becounterbalanced by a vasodilator.The early use of noradrenaline(norepinephrine) in profoundundifferentiated shock helps restorevital organ perfusion while awaitingthe effects of fluid loading, andallows the introduction of otherinotropes or vasodilators. Thestarting dose is 0.5–10 µg/min.Myocardial oxygen consumption isincreased, with the risks ofmyocardial ischaemia andcompromised ventricular function.

• Systolic blood pressure shouldremain at least 100 mmHg. Aminimum value of 60 mmHg issuggested for mean arterial pressure(MAP). The use of pressors incardiogenic shock has not beenshown to improve survival.11

• Vasodilators are indicated whenperipheral and organ perfusion failsto respond to restoration of bloodpressure alone. Glyceryl trinitrate isthe vasodilator of choice inmyocardial ischaemia, in a doserange of 10–200 µg/min. Sodiumnitroprusside may be used whenpulmonary oedema occurs in theabsence of ischaemia. The doserange is 0.5–2.0 µg/kg/min, to amaximum of 10 µg/kg/min.

• MI must be sought and activemanagement pursued dependentprimarily on local facilities andexpertise. Thrombolytic therapy incardiogenic shock following AMIresults in inadequate exposure ofocclusive thrombus to thethrombolytic17. Intra-aortic ballooncounterpulsation increases aorticdiastolic pressure and cardiac outputwith no increase in oxygen demandand may be combined withthrombolytics, but when used aloneconfers no survival advantage unlessrevascularization is contemplated.Complications include leg ischaemia,dissection, thromboembolism andthrombocytopenia.11

Early transfer and revascularizationconfers a survival advantage in patientswith MI and cardiogenic shock.9,10,13,18

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Early revascularisation of the infarct-related artery by percutaneous trans-coronary angioplasty (PTCA) orcoronary artery bypass grafting (CABG)is the only intervention that decreasesmortality.11 The greatest benefit is inthose less than 75 years, with the optimalmanagement of those over this ageremaining unclear.17 If catheterizationfacilities are unavailable, thrombolyticsshould be given to eligible patients whileemergent transfer to an interventionalfacility is arranged.

Cardiac tamponade should be excludedby transthoracic echocardiography in thefollowing patient groups:

• Blunt or penetrating cardiac trauma• Pericarditis due to infection such as

TB or viral, radiation, connectivetissue disorders

• Uraemia• Anticoagulant use• Aortic dissection• Iatrogenic, e.g. CVP insertion• Pneumopericardium from

barotrauma, gas-forming infection,Valsalva, PEEP, cocaine.

Coexistent hypovolaemia may maskthe clinical signs of tamponade, such as afull JVP rising on inspiration (Kussmaul’ssign). Volume loading is indicated withinotropic support until pericardiocen-tesis under echo-control or surgicalpericardiotomy can be performed;

Aortic dissection should be consideredin patients with risk factors, e.g. Marfan’ssyndrome, Ehlers-Danlos syndrome,bicuspid aortic valve, aortic coarctation,Ebstein’s anomaly, hypertension inpregnancy and cocaine use.

Other causes of cardiogenic shockpresenting to the emergency physicianhave been reviewed extensively.14

In summary, those patients with largeinfarctions and a resting tachycardiashould be identified early and stabilizedwith inotropic and/or vasodilator agentswhen indicated. Intra-aortic ballooncounterpulsation should be institutedurgently while emergent revasculariz-ation is contemplated. Patients managedoutside centres with interventionalcapabilities should be considered forthrombolytics where eligible.19

DispositionPatients presenting with cardiogenicshock require admission to CCU orICU, depending on the requirement forventilation, invasive monitoring or activemanagement of myocardial ischaemia.Direct transfer from the ED to thecatheter laboratory or operating theatre,or transfer to a tertiary centre, may beindicated.

Septic shock

DefinitionsThe following definitions were formulatedat the consensus conference of theAmerican College of Chest Physiciansand Society of Critical Care Medicine(ACCP-SCCM) in 199220:

• Bacteraemia: the presence of viablebacteria in the blood, usuallyconfirmed by positive blood culture.

• Sepsis: clinical evidence of infection,accompanied by a systemic response,including two or more features fromthe following:– tachypnoea, RR >20/min or

PaCO2 <32 mmHg (4.3 kPa)– where the patient is mechanically

ventilated, minute ventilation>10 L/min

– tachycardia >90 beats/min– hyper- or hypothermia, core or

rectal temperature >38°C or<36°C and/or elevation orreduction in the leucocyte count>12000 cells/µL or <4000cells/µL, or 10% or more bands.

• Systemic inflammatory responsesyndrome (SIRS): the presence of asevere clinical insult accompanied bytwo or more of the systemicresponses outlined above.

• Severe sepsis: hypoperfusion (alteredmentation, lactic acidosis and/oroliguria), hypotension or organdysfunction associated with sepsis.

• Septic shock: sepsis accompanied byhypotension, systolic BP <90 mmHgor 40 mmHg or more below normalbaseline and perfusion abnormalitiesdespite adequate fluid resuscitation.Refractory septic shock is presentwhen hypotension lasts >1 hour,despite adequate volume

replacement and high-dosevasopressor use.

• Multiple organ dysfunctionsyndrome (MODS): a syndrome ofaltered organ function in an acutelyill patient requiring intervention tomaintain homoeostasis.

Debate surrounds these criteria,which, although still employed, shouldnot form the sole basis for the clinicaldiagnosis of sepsis. Symptoms and signsthat lead the clinician to suspect sepsisare as follows21:

Clinical signs:• Fever/hypothermia• Unexplained tachycardia• Unexplained tachypnoea• Signs of peripheral vasodilatation• Unexplained shock• Changes in mental state.

Laboratory parameters:• Leucocytosis/neutropenia• Unexplained lactic acidosis• Unexplained alteration in renal or

liver function tests• Thrombocytopenia/disseminated

intravascular coagulation• Increased procalcitonin levels• Increased cytokines, c-reactive

protein levels.

AetiologyInfection of bacterial, viral or fungalorigin is the precursor of septic shock,which may complicate up to 50% ofbacteraemic episodes.22 Typically inGram-negative sepsis, Escherichia coli,Klebsiella, Pseudomonas aeruginosa,Enterobacter, Acinetobacter, Proteus,Serratia, Aeromonas, Xanthomona,Citrobacter, Achronobacter, Salmonellaor Shigella species are responsible.

The pathogenic mechanisms in septicshock have been well reviewed.23,24 A nidusof infection is formed through multipli-cation of micro-organisms, which mayinvade the bloodstream or proliferatelocally, releasing various mediatorsconsisting of structural components andexotoxins into the circulation. Such media-tors in turn stimulate plasma precursorsor cells to release further endogenousmediators of sepsis. More than 100 me-

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diators have been identified, includingtumour necrosis factor-α (TNFα), inter-leukin-1 and interleukin-6, which are themost extensively studied. The effects ofmediator release include direct organinjury, hepatic failure, disseminated intra-vascular coagulation (DIC), vasodilata-tion, altered capillary permeability,myocardial depression, endothelial celldysfunction and leucocyte aggregation.

Circulatory changesNitric oxide overproduction in theperipheral vasculature causes the loss ofvascular control seen in septic shock.25

The vasodilatation and decreased syste-mic peripheral vascular resistance may be masked by hypovolaemia. Capillaryblood flow is reduced, and decreaseddeformability of red and white bloodcells underlies microvessel plugging,resulting in a potential trap for bacterialovergrowth in the microcirculation.26

Cardiac dysfunctionVentricular dilatation with decreasedejection fraction is the commonest find-ing in septic shock, associated with areduced stroke volume that is compen-sated for by an increase in heart rate tomaintain or increase cardiac index.27 Thisventricular dilatation is necessary, andusually reverses in 7–10 days in patientswho survive. Decreased right ventricular(RV) function and increased pulmonaryartery pressure are associated with a pooroutcome. As in decreased left ventricularfunction, circulating mediators havebeen implicated, as poor RV perform-ance is not entirely explained by raisedpulmonary vascular resistance.

MortalityReported mortality ranges from 20% to80%. Patients admitted to the ICU withhypotension associated with sepsis have amortality rate of over 50%.

High-risk groupsThese include the young and the old,those with burns, alcohol dependence,chronic renal failure, diabetes mellitus,immunosuppression, chronic cardiorespi-ratory disease, infection, malnutritionand the multiply injured.


Signs and symptoms

• Early: tachypnoea, tachycardia,temperature instability, oliguria,altered mental state, peripheralvasodilatation;

• Late: reduced capillary refill,hypotension, further altered mentalstatus and reduction in urine output,evidence of myocardial dysfunction,metabolic acidosis;

• Evidence of genitourinary,respiratory or gastrointestinalinfection. Many other sites arepossible, including iatrogenic sourcessuch as CVP lines and indwellingcatheters. A careful secondary surveyfollowing resuscitation is essential.

Investigations

• Full blood examination, urea,creatinine, electrolytes, bedsideglucose, coagulation profile, and β-HCG in females of reproductiveage.

• Arterial blood gases, arterial orvenous lactate.

• Two sets of blood cultures, includinga set through any indwellingcannulae or central venous lines.Consider arterial blood cultures inthe immunosuppressed, e.g.intravenous drug users, and culturesthrough a pre-existing arterial line.

• Urinalysis, microscopy, Gram stainand culture.

• Chest X-ray and 12-leadelectrocardiogram.

• Additional studies as indicated by theclinical situation, likely source ofsepsis and search for possible foci ofinfection.

Diagnosis This is made utilizingACCP-SCCM definitions. More thanone cause for shock may exist in the same patient. Volume depletion must betreated with an appropriate fluidchallenge.

Therapy• Initial care is provided as outlined

previously during the primary survey.

Early airway control with mechanicalventilation is necessary to optimizeoxygenation and ventilation.

• Volume replacement shouldcommence with 250 mL boluses of0.9% saline titrated against observedparameters, and frequent clinicalreassessment. CVP line insertionshould be performed rapidly in theED under strict asepsis if expertise isimmediately available. Trends inCVP response to fluid infusionshould be followed, rather thanabsolute values, in conjunction withother monitored parameters. CVP isof least value in the presence ofmyocardial dysfunction or elevatedpulmonary artery pressures. Anintra-arterial blood pressuremonitoring line should be insertedin addition.

• Persistent hypotension and/or signsof organ hypoperfusion areindications for inotropic support.Dopamine is used commonly inhigher doses, but is a weakvasoconstrictor in septic shock.28

There is no role for low-dosedopamine in improving renalfunction. The early use ofnoradrenaline is recommendedwhere hypotension is severe, SBP70 mmHg or less, and the responseto dopamine is suboptimal.Noradrenaline may preserve vitalorgan perfusion while volume isreplaced and hypoxaemia corrected.It may effectively optimize renalblood flow and renal vascularresistance.29

• Oxygen consumption is maintainedin haemorrhagic and cardiogenicshock by an ability to increaseoxygen extraction where oxygendelivery is extremely low.30 Thisability is impaired in septic shock.Thus, oxygen delivery aims toreverse hyperlacticacidaemia toincrease survival rates. The use ofdobutamine is only advocated inpatients with adequate centralpressures, in order to increase cardiacindex and hence oxygen delivery andconsumption. However, routinelymaintaining supranormal oxygen

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delivery is no longerrecommended.28

• The combination of noradrenalineand dobutamine appears to be moreappropriate to the goals of septicshock therapy and effects on thesplanchnic circulation.29 The effectsof vasopressin on the abnormalsympathetic function in sepsis issubject of further study.28

• The source of infection must beidentified where possible, collectionsof pus drained and intravenousantibiotic therapy instituted as soonas practicable. This may have toprecede complete specimencollection in life-threatening cases. Asuggested regimen, which can bemodified in the context of previousinfections where microbiologicalinformation is available in thepatient’s chart, or according to localrecommendations, may include31:

Immunocompetent adult:Di(flu)cloxacillin 2 g IV 4–6 hourly

PLUS gentamicin 4–6 mg/kg IVdaily (tailor dose to age and renalfunction of patient).

If hypersensitive to penicillin:cephalothin 2 g IV 6 hourly orcephazolin 2 g IV 8 hourly.

Neutropenic patients:<0.5×109/L or <1×109/L + predicted

decline to <0.5×109/L + fever> 38°C. Empirical regimes shouldcover Pseudomonas aeruginosa.

Gentamicin 4–6 mg/kg daily PLUSeither ceftazidime 1 g IV 8 hourlyOR ticarcillin+clavulanate 3.1 g IV6 hourly.

Cefpirome, cefepime or piperacillin +tazobactam may be substituted forceftazidime or ticarcillin+clavulanate.Altenatively monotherapy withceftazidime, cefpirome, cefepime,imipenem or meropenem inmaximal dosage is equally effective.

Vancomycin should not be used infebrile neutropenics unless thepatient is in shock, is known to becolonized with methicillin-resistantStaphylococcus aureus (MRSA) or hasclinical evidence of a catheter

infection from a unit with a highincidence of MRSA infection:vancomycin 1 g 12 hourly IV.

Appropriate antibiotic therapyconfirmed by in-vitro testingreduces mortality by 50%, andshould always be discussed withinfectious disease specialists andmicrobiologists. Further advice oncondition-specific antibiotic regimesis available elsewhere.31

• Sodium bicarbonate is notrecommended for the treatment oflactic acidosis.28

• Corticosteroids should only be givenfor adrenal insuffciency, or if thepatient is already receivingcorticosteroids.32 Corticosteroids inlow dosage have also been found tobe beneficial in a sub-set of patientswith refractory septic shock.28

• Cyclo-oxygenase inhibitors such asibuprofen have no significant effecton outcome.29 Opioid antagonists inhigh dosage reverse low SBP andmean arterial pressure, but have noeffect on survival.32 The use ofprostaglandins, pentoxifylline, N-acetylcysteine, selenium, anti-thrombin III, immunoglobulins,growth hormone and granulocytecolony stimulating factor in non-neutropenics is currentlyunsupported and is notrecommended.33

• The use of cytokine inhibitors hasnot been associated withimprovement in mortality rates insevere sepsis or septic shock.Inhibition of nitric oxide synthesis bymethylene blue and the use of opioidantagonists are subject of furtherstudy.28

• The use of activated protein C hasbeen associated with a relativereduction in the risk of death of20%. Despite a significantly increasedbleeding risk, this compound hasbeen approved by the US FDA foruse in those with severe sepsis athigh risk of death, with an APACHEscore of ≥25 or significant organdysfunction, especially refractorydysfunction or multiorgandysfunction.28

DispositionPatients presenting to the ED with septicshock will require ICU admission for in-tensive therapy and monitoring. Clinicalassessment, urine output and seriallactate levels are the best indicators ofthe effectiveness of therapy, whichshould see lactate levels decrease within24 hours.28

Neurogenic shock

DefinitionThe term spinal neurogenic shock hasbeen used to represent all phenomenasurrounding physiologic or anatomictransection of the spinal cord that resultsin temporary loss or depression of all ormost spinal reflex activity below the levelof the lesion. Arterial hypotension mayor may not be part of such phenomena.34

PathophysiologyLow thoracic lesions result in loss oflower extremity sympathetic tone andsubsequent venous pooling. Upperthoracic lesions result in venous poolingin the lower extremities and the abdo-minal viscera. Cervical lesions result inthe absence of intrinsic cardiovascularsympathetic tone, with loss of thoraco-lumbar vascular tone.

One in three patients with a completecervical-cord injury requires support fortheir hypotension. The presence of hypo-tension has no implications regarding thedegree of completeness of cord injury orprognosis.

Clinical features• This is a diagnosis of exclusion in the

injured patient. Hypotension shouldbe accompanied by flaccidity andareflexia distal to the suspected levelof the lesion. There should be nocompensatory tachycardia orperipheral pallor, sweating orvasoconstriction.

• Tension pneumothorax and cardiactamponade must always beconsidered, and hypovolaemic shock,which may be masked and should beexcluded by appropriate fluidchallenge and investigations, such asabdominal ultrasound or CT

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scanning for possible intra-abdominalor retroperitoneal blood loss.

Therapy• Supportive therapy should be

instituted to airway, ventilation andcirculation, as indicated.

• Atropine 0.5–1 mg is given tocounter unopposed parasympatheticvagal tone to a maximum dose of3 mg, if bradycardia and symptomatichypotension are present.

• Euvolaemia should be assessed witha fluid challenge: 250–1000 mLaliquots of 0.9% saline are given andthe clinical response followed.

• If the above measures fail to returnblood pressure and measurable signsof perfusion to normal, considerpharmacologic vasoconstriction.Ephedrine 5–10 mg IV, orphenylephrine 0.2–1 mg IV may beused. Noradrenaline(norepinephrine) at 2–5 µg/mintitrated to response is used inrefractory cases providing other causesof hypotension such as haemorrhage,tamponade, pneumothorax, etc.,have been excluded.

DispositionPatients should be cared for in an ICUor a dedicated spinal injury unit, depend-ing on other injuries and local facilities.

CONCLUSIONThe aetiology of shock in patients pres-enting to the emergency department isvaried. Hypovolaemia should be soughtin all cases, although specific manage-ment will depend on the underlyingcause.

REFERENCES1. Peitzman AB, Billiar TR, Harbrecht BG, Udekwu

AO, Kelly E, Simmons RL 1995 Haemorrhagicshock. Current Problems in Surgery 32: 925–1012

2. Fiddian-Green RG, Haglund U, Gutierrez G,Shoemaker WC 1993 Goals for the resuscitation ofshock. Critical Care 21: S25–S31

3. Kline JA. Shock. In: Rosen P, Barkin R (eds) 1998Emergency Medicine, Concepts and ClinicalPractice. Mosby Year Book Inc., St. Louis, pp 86–106

4. Britt LD, Weireter LJ Jr, Riblet JL, Asensio JA,Maull K 1996 Priorities in the management ofprofound shock. Surgical Clinics of North America76: 985–97

5. Davis JW, Parks JN, Kaups KL, Gladen HE,O’Donnell-Nicol S 1996 Admission base deficitpredicts transfusion requirements and risk ofcomplication. Journal of Trauma 41: 769–74

6. Terai C, Anada H, Matsushima S, Kawakami M,Okada Y 1996 Effects of Trendelenburg versuspassive leg-raising autotransfusion in humans.Intensive Care Medicine 22: 613–4

7. Roberts IA, Evans P, Bunn F, Kwan I, CrowhurstE 2001 Is the normalisation of blood pressure inbleeding trauma patients harmful? Lancet357: 385–7

8. Tremblay LN, Rizoli SB, Brennerman FD 2001Advances in fluid resuscitation of hemorrhagicshock. Journal Canadien de Chirurgerie 44: 172–9

9. Califf RM, Bengston JR 1994 Cardiogenic shock.Current concepts. New England Journal ofMedicine 330: 1724–30

10. Domanski MJ, Topol EJ 1994 Cardiogenic shock:current understandings and future researchdirections. American Journal of Cardiology74: 724–6

11. Prieto A, Eisenberg J, Thakar RK 2001 Non-arrhythmic complications of acute myocardial

infarction. Emergency Medical Clinics of NorthAmerica 19: 397–415

12. Quigley RL, Milano CA, Smith LR, White WD,Rankin JJ, Glover DD 1993 Prognosis andmanagement of anterolateral myocardial infarctionin patients with severe left main disease and shock:the left main shock syndrome. Circulation88: 1165–70

13. Whitman JJ, Boland J, Sleeper LA, et al 1995Current spectrum of cardiogenic shock and effectof early revascularisation on mortality. Circulation91: 873–81

14. Rodgers KG 1995 Cardiovascular shock.Emergency Medical Clinics of North America13: 793–810

15. Plummer D 1995 Other applications of ultrasound.In: Heller M, Jehle D (eds) Ultrasound inemergency medicine. WB Saunders, Philadelphia,pp 184–95

16. Barnard MJ, Linter SPK 1993 Acute circulatorysupport. British Medical Journal 307: 35–41

17. McPherson JA, Gibson RS 2001 Reperfusiontherapy for myocardial infarction. EmergencyMedical Clinics of North America 19: 433–49

18. Stomel RJ, Rasak M, Bates ER 1994 Treatmentstrategies for acute myocardial infarctioncomplicated by cardiogenic shock in a communityhospital. Chest 105: 997–1002

19. Brown M, D’Haem C, Berkompes D 1998Emergency Medical Clinics of North America16: 565–81

20. Bone RC, Balk RA, Cerra FB, et al 1992Definitions for sepsis and organ failure andguidelines for the use of innovative therapies insepsis. Chest 101: 1644–55

21. Matot I, Sprung CL 2001 Definition of sepsis inGuidelines for the Management of Severe Sepsisand Septic Shock. Intensive Care Medicine 27Suppl 1: S3–S9.

22. Dunn DL 1994 Gram-negative sepsis and sepsissyndrome. Surgical Clinics of North America74: 621–35

23. Baxter F 1997 Septic shock. Canadian Journal ofAnaesthesia 44: 59–72

24. Parrillo JE 1993 Pathogenetic mechanisms ofseptic shock. New England Journal of Medicine328: 1471–7

25. Brady AJB, Poole-Wilson PA 1993 Circulatoryfailure in septic shock. Nitric oxide: too much of agood thing? British Heart Journal 70: 103–10

26. Hinshaw LB 1996 Sepsis/septic shock:participation of the microcirculation: anabbreviated review. Critical Care Medicine24: 1073–8

27. Bunnell E, Parrillo JE 1996 Cardiac functionduring septic shock. Clinics in Chest Medicine17: 237–48

28. Fitch JJ Gossage JR 2002 Optimal management of septic shock. Postgraduate Medicine111: 53–66.

29. Vincent JL 2001 Haemodynamic support in septicshock. Intensive Care Medicine 27 Suppl 1: S80-S92.

30. Edwards JD 1993 Management of septic shock.British Medical Journal 306: 1661–4

31. Severe sepsis 2000 Therapeutic Guidelines:Antibiotic Version 11. Therapeutic GuidelinesLimited. State of Victoria: 159–68

32. Wessner WH, Casey LC, Zbilut JP 1995Treatment of sepsis and septic shock: a review.Heart and Lung 24: 380–92

33. Carlet J 2001 Immunological therapy in sepsis.Intensive Care Medicine 27 Suppl 1: S93–S103.

34. Pate Atkinson P, Atkinson JLD 1996 Spinal shock.Mayo Clinic Proceedings 71: 384–9

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CONTROVERSIES❶ There is currently no evidence tosupport the use of colloids overcrystalloids in shock management.

❷ The overall benefits of hypertonicfluids in shock are yet to be confirmedby prospective clinical studies.

❸ The use of fluid restriction untilearly surgery, although accepted inthe management of penetratingtruncal trauma, requires furtherevaluation in the blunt traumapatient.

❹ Corticosteroids have shown somebenefit in certain subgroups ofpatients with severe sepsis and septicshock

❺ Only activated protein C can becurrently recommended as adjunctivetherapy in severe sepsis associatedwith organ failure

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RESPECT FOR PATIENTAUTONOMYAutonomy is the patient’s moral right to determine his or her own destiny. It is a principle that has grown in stature in recent years. The realization of theimportance of informed consent is aconsequence of this.

Although the principle of respect forpatient autonomy remains sound, thereare many occasions in resuscitationmedicine where the patient’s compe-tence is impaired, as he or she is unableto receive information, undertake rationaldeliberation or express a decision free fromcoercion. Although we still endeavour to respect the patient’s autonomy, wewill struggle to define what the patient’sautonomous wishes would be, if he orshe was not impaired. This will bediscussed further later in the chapter.

BENEFICENCEBeneficence is the principle of acting in away that benefits the patient. Histori-cally, this and non-maleficence have beenthe overriding governing principles inmedical practice. When these principlesare enforced without due considerationof, or in contradiction to, the patient’sperceived or expressed wishes, the actionis termed paternalistic. When the prin-ciple of respect for patient autonomy isnot honoured, the patient is deprived ofa fundamental right and is treated as lessworthy by being reduced to a positionwhere he or she is considered incapableof self-governance. This harm to thepatient needs to be considered when therelative benefits and harms of any actionare considered.

INTRODUCTIONA working definition of ethics is thestudy of morality. It is reasonable todescribe moral behaviour as that which is‘the right thing to do’. Thus, medicalethical deliberation is the process ofdetermining what is the right thing to dowhen considering any of the dilemmasthat arise in medical practice.

The approach to these dilemmas mayvary according to the philosophicalperspective adopted.1 Although there area variety of models describing moraldecision making, only a pragmatic over-view will be given here. In general termsone may adopt a utilitarian approach,which values the positive balance ofgood over bad brought about by anyaction, or a deontological approach,which values actions that adhere tooverriding moral principles. However,moral philosophers have recognized that moral principles may competeagainst each other when specific actionsare considered. Moral principles shouldbe honoured, but when they are compet-ing, in a given circumstance, we shouldthen consider the relative balances ofgood and bad that ensue from theapplication of each principle. In otherwords, we have a composite philosophywherein the principles and the conse-quences of their application could bothbe considered.

Beauchamp and Childress2 haverecently developed this further into apractical framework for medical ethicaldeliberation. They describe four prin-ciples that should be honoured inmedical decision making. When theseprinciples compete, the relative balanceof good and bad should be considered.These principles are: respect for patientautonomy, beneficence, non-maleficenceand justice.

1.6 ETHICS OF RESUSCITATIONMICHAEL W. ARDAGH

ESSENTIALS1 Ethical deliberation may beaided by considering the fourprinciples of: respect for patientautonomy; beneficence; non-maleficence and justice.

2 During deliberation, if the ethicalprinciples seem to be competing therelative benefits and harms of theapplication of each should beconsidered.

3 During resuscitation, urgencyand impaired patient competenceconspire against adequateconsideration of these principles,especially non-maleficence andrespect for patient autonomy.

4 Resuscitation can be harmful ina number of ways. These should beconsidered when assessing thebalance of benefit and harm of anyresuscitation endeavour.

5 All medical interventions needsome form of consent, includingresuscitation, despite the urgencyand the impaired patientcompetence. Of the consent optionsavailable, presumed consent is theone most commonly employed.Presumed consent using professionalsubstituted judgement is a model thatbest respects patient autonomy.

6 The practice of resuscitationprocedures, particularly endotrachealintubation, on the newly dead iscommon and valuable. Some form ofconsent is required for this to occur,but currently there is no suitablemodel. Presumed consent would beappropriate if the practice wasexplicit and if the public was wellinformed. In so doing those whowould not consent are protected bythe opportunity to decline. Until then,practising on the newly dead isethically wrong.

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NON-MALEFICENCENon-maleficence, or the principle ofavoiding harm in therapeutic endeavours,is an established maxim attributed toHippocrates. Although this is an obviousand common sense principle, we willcommonly tolerate some harm, forexample when delivering chemotherapyfor cancer, or undertaking surgery that is known to have certain complications,because consideration of the otherprinciples tells us our actions are right.

The principles of beneficence and non-maleficence risk being poorly consideredbecause they ‘go without saying’. How-ever, we should be reasonably certain ofthe benefits and harms of our interven-tions before they may be considered right.For example, the performance of gastriclavage on a non-consenting patient aftera trivial overdose several hours earlier isethically unjustifiable as there is insuffi-cient benefit to override our principles ofrespect for autonomy and non-maleficence.In order to consider the benefits andharms, information is required regardingthe outcomes of our interventions, andto this end research becomes an ethicalnecessity to provide the evidence uponwhich to judge competing principles.

JUSTICEThe principle of justice is an essentialbalance to the first three principles, whichapply primarily to the individual. Justice,or the concept of fairness, is best addressedby questioning whether there are otherswho might be adversely affected by aparticular action. For example, in a masscasualty incident the performance of ahopeless resuscitation may be unjust (inaddition to harming the patient) as it de-prives another of resuscitation facilities.

APPLICATION OFTHESE PRINCIPLES TORESUSCITATIONMEDICINEThere are two components of resusci-tation medicine that conspire against

adequate consideration of the principlesoutlined by Beauchamp and Childress.The first of these is urgency and thesecond is the impaired ability of thepatient to make reasonable autonomousdecisions.

Urgency may be a barrier to the appli-cation of these principles in any givencase. It is often appropriate to performresuscitation assuming these delibera-tions might occur more fully when timepermits, rather than withhold resuscita-tion on the basis of limited deliberation.

The impaired competence of patientsundergoing resuscitation complicates theprinciple of respect for autonomy, as thepatient is commonly impaired in his orher ability to receive information, com-prehend it, consider it in context andmake a rational decision on the basis ofthis consideration. It is common practicenot to seek or to ignore the wishes of thepatient, and instead to presume thatresuscitation is the right thing to dobased on arguments of beneficence andnon-maleficence.

Thus, it is generally perceived thatconsent is not required for resuscitationbecause resuscitation brings benefit andprevents harm, and because the patient is not in a position to give or withholdconsent. Although this approach doesnot usually mean that bad things are done,from an ethical perspective it is funda-mentally flawed. Resuscitation may beharmful in a number of ways and someform of consent must be obtained, justas for any other medical intervention.

THE HARMS OFRESUSCITATION3

The benefits of resuscitation include theavoidance of death and the restoration ofgood health. The harms of resuscitation,may be of the following five types:

❶ The first is if resuscitation isunnecessary because the patient’scondition is insufficiently serious tojustify it. As a consequence, theharm includes pain and otherdiscomfort to the patient, iatrogenicillness and unnecessary use oflimited resources, thereby depriving

others in need of these resources. Inresuscitation medicine the extent ofovertreatment may be difficult topredict, as it is hard to knowwhether the patient would surviveintact without the treatment. Themost promising way of minimizingthis harm is to have senior staffpresent during a resuscitation todraw upon their experience.

❷ The second harm of resuscitation isif it is unsuccessful because thepatient’s condition is too faradvanced. When resuscitation willnot produce the desired effectsbecause the patient is too sick, thereis the potential for a great numberof harms. Harms to the patientinclude physical discomfort, loss ofdignity, a prolonged death, andsurvival with an unacceptable qualityof life. Harms to the family includethe psychological discomfort ofsurrogate pain and loss of dignity,unfulfilled hope, loss of control of aloved one’s destiny, the cost of lostearnings while at the bedside, andthe cost of supporting a disabledsurvivor. The harms to the healthworkers include frustration andsadness at lack of success, guilt atinflicting harm, and the cost ofbeing unable to treat others waitingfor resources. The harms to thecommunity include the loss ofresources to treat others, thedeception that resuscitation offeredhope, and the worry that deathmust be preceded by a loss ofdignity.

❸ The third harm of resuscitation is ifit is unkind because it brings aboutan outcome with which the patientor their family is unhappy.Resuscitation may condemn thepatient to a quality of life below thatconsidered acceptable. This ispotentially a tragic harm, with anongoing burden from which thepatient and their carers may have nomeans of escape.

❹ The fourth harm of resuscitation isif it is unwise because it divertsresources from alternative healthcareactivities that would bring more


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benefit to other patients.Resuscitation is a significant user ofresources: if it is futile and beneficialhealthcare activities cannot proceedfor lack of resources, thenresuscitation is causing significantharm.

❺ Finally, resuscitation is harmful if itis against the patient’s wishes. Apreconceived ‘do not resuscitate’order written by or negotiated withthe patient, or consent declined by acompetent patient, must behonoured, in keeping with theethical principle of respect forautonomy. However, preconceivedorders must be carefully consideredas they relate to the situation inwhich the patient finds him orherself. For example, a writtensigned and witnessed statement(often called an advance directive, orliving will) declining resuscitationfrom cardiac arrest means that thepatient should not be resuscitatedfrom cardiac arrest: it does notmean that the patient has declinedresuscitation from haemorrhagicshock. Similarly, a ‘no intensive care’directive does not mean the patienthas declined aggressive treatment forpulmonary oedema with a nitrateinfusion and continuous positiveairway pressure ventilation.Although such directives mayoccasionally apply specifically to thepatient’s illness, on other occasionsthey may not. In the setting of someform of an advance directive, threequestions should be considered: 1)Did the patient make this decisionbased on well informeddeliberation? 2) Is the context theyfind themselves in now what theyhad in mind when they made thedecision? If not, how closely does itrelate to what they had in mind? 3)Since they made this decision, isthere any indication they might havechanged their mind? If the answersto these questions suggest somedoubt as to how applicable theadvance directive is to thisresuscitation, at this time, then itshould be considered an indication

of the patient’s wishes, rather thanmorally binding.

These harms of resuscitation must beconsidered when weighing the relativemerits of the principles of respect forpatient autonomy, beneficence, non-maleficence and justice.

An ill-considered approach will lead tounderrepresentation of patient autonomyin these deliberations, and an inadequateappreciation of the extent of the harm thatmay ensue from resuscitation efforts.

FUTILITY4

The concept of futility has been widelydiscussed in the medical literature, withparticular emphasis on resuscitationmedicine. Regrettably, discussions of theharms of resuscitation have becomestalled by attempts to define futility. Theword is derived from the Latin futilis,meaning ‘that which easily pours ormelts’. The current usage stems from thestory in which the daughters of the Kingof Argos murdered their husbands andwere then condemned to collect waterfor eternity in leaking buckets. To arriveat your destination with an empty bucketwhen the intention of the journey was to bring water is undoubtedly a futileendeavour. However, futility in medicineis much more difficult to define. Someemphasize physiological futility, meaningthe inability to produce a physiologicalobjective, for example if CPR producesno pulse, or transfusion produces noblood pressure. The proponents of thisdefinition suggest that it has the least riskof unilaterally imposed physician valuejudgements. Others consider futility in terms of quantitative or qualitativemeasures. A quantitative estimate offutility is one in which an intervention isconsidered futile if it has failed in, forexample the last 100 times attempted.The qualitative component describesfutility if the patient’s resultant quality oflife falls below a threshold consideredminimal by general professional judge-ment. It is unlikely that there will ever be agreement as to what physiologicalmeasure or quality of outcome measuresare most appropriate, and what threshold

measure separates futility from benefit.Although these arguments are interest-ing, it is unfortunate that they have takenon more importance than they merit.Futility defines the absence of acceptablebenefit for any given intervention,whereas reasonable ethical deliberationdemands we consider the ratio of benefitand harm. If there is no benefit, anyharm at all would make the benefit-harmratio unfavourable. However, even if theendeavour is not futile and brings aboutmeasurable benefit, this does not neces-sarily mean that the endeavour is theright thing to do, as the amount of harmthat ensues, as defined above, mayoutweigh any benefit. It is the benefit-harm balance, as assessed by consideringthe four ethical principles and the fivetypes of harm described above, that hasthe most relevance in determiningwhether to start or stop resuscitation.

CONSENT,WITHHOLDING ANDWITHDRAWINGRESUSCITATIONConsent must be obtained for any med-ical intervention, including resuscitation.Informed consent, as is appropriate for elective surgery, may be inappropriateduring resuscitation owing to the urgencyof the treatment and impaired patientcompetence. However, if informedconsent is not relevant, other forms ofconsent still are. The two most commonforms of consent employed in resuscita-tion scenarios, where there is bothurgency and impaired patient compe-tence, are presumed consent and proxyconsent. Presumed consent uses theconcept that a reasonable patient undersimilar circumstances – or this patient ifhe or she were able to – would consent tothe resuscitation endeavours proposed.This form of consent has merit and iscommonly employed, but occasionallyattracts criticism as being a form ofmedical paternalism, in that it may beperceived to be respecting the principleof beneficence, as the resuscitators per-ceive it, while ignoring respect forpatient autonomy.


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Proxy consent involves obtainingconsent for resuscitation from a familymember or other person who isperceived to be able to speak on behalf ofthe patient. Proxy consent avoids thecriticism of medical paternalism as thedecision is taken out of the physician’shands, but it suffers as a model as thedecision maker may be unable to ade-quately receive information, understandit, and deliberate over it during a hurriedand rapidly evolving resuscitation. Inaddition, the proxy may not reflect the views of the patient. There may beoccasional circumstances where the proxydeclines resuscitation because of somefinancial or other benefit that wouldaccrue from the patient’s death. Morecommonly, proxies have a tendency todemand more resuscitation than thepatient would have wanted, for fear ofbecoming responsible for their death.When this form of consent is used thereis greater scope for the harms of resusci-tation. A modification of proxy consentthat better addresses the issue of respectfor patient autonomy is proxy consentwith substituted judgement. This involvesnot asking what the proxy would wantdone for the patient, but instead whatthe proxy thinks the patient would wantdone. In other words, it attempts to seethe resuscitation from the patient’sperspective as viewed by the proxy.

A modification of presumed consent ispresumed consent using professionalsubstituted judgement.5 This means theresuscitators gathering as much informa-tion about the patient as they possiblycan to attempt to understand how thepatient would view this decision. Thisusually involves speaking with thepatient’s loved ones. Then, with someknowledge of the likely outcome of theresuscitation proposed, based on previousexperience and a knowledge of themedical literature, they can exercise theirmoral imagination by asking ‘Would Iwant this treatment if I was this patient?’In this way the patient’s autonomy is asbest respected as it can be under difficultcircumstances, by combining a knowledgeof the harms and benefits of the resusci-tation with an appreciation of thisbalance from the patient’s perspective. If

presumed consent using professionalsubstituted judgement is employed andthe answer to the question is ‘No’, thenthe resuscitation cannot proceed. Toresuscitate without regard for thepatient’s explicit or perceived wishes is aharmful disrespect for their autonomy.Often, and appropriately, a decision toproceed will be made on the basis of aperceived marginal benefit over harm.This balance is made more appealing bythe alternative of certain death if resus-citation is not undertaken. However, thebalance is dynamic, with a clearer view ofthe likely benefits and harms emerging asthe patient responds to the resuscitation.If the treatment does not procure thehoped-for benefits, all concerned shouldbe willing to minimize the ongoing harmsof resuscitation by withdrawing treatmentas the balance becomes more unfavourable.

The concept of withholding andwithdrawing treatment is somewhatmisdirected in that it implies a need forpermission to stop the intervention,whereas the precedent in medicine is toobtain permission to proceed. It is wrongto withhold a resuscitation endeavourbecause of the concern that the life-saving treatment cannot be withdrawn ata later date if things are not going well.When resuscitation is withheld a smallbut significant number of patients maymiss out on an opportunity for a goodoutcome had the resuscitation beenoffered to them. Similarly, it is wrong tobe unable to withdraw treatment becauseof the ill-conceived concept that onceresuscitation has begun it must continue.

By employing professional substitutedjudgement, the resuscitators shouldrecognize when the balance of benefitand harm becomes unfavourable fromthe patient’s perspective. At this pointthey have a moral obligation to with-draw resuscitation as they can no longerpresume the patient’s consent. Byappreciating the benefits and harms ofresuscitation, the use of professionalsubstituted judgement to view thesefrom the patient’s perspective, and by acommitment to stop resuscitation whenwe cannot presume the patient’s consent,we will minimize the harms of resuscitationmedicine.

PRACTISINGRESUSCITATIONPROCEDURES ON THENEWLY DEAD6

Practising resuscitation procedures –most commonly endotracheal intubation– on patients who have died after anunsuccessful resuscitation is a commonpractice in many parts of the world. How-ever, some view this with a repugnancethat can be rationally argued. Otherswould propose that the benefit of thispractice to subsequent patients outweighsany repugnance felt by others who wit-ness it, or any harm done to the recentlydeceased. However, like all other inter-ventions in medicine, this procedurerequires permission before it mayproceed. Informed consent may beobtained from the terminally ill forpermission to perform procedures afterthey die, but this has limited relevance tothe practice as it occurs in many emer-gency departments. Implied consentargues that consent is implicit in the factthat the patient used the emergencyservices and, therefore, is agreeable to allthat this entails, including being used forteaching. Implied consent criteria arecommonly used for those who present oftheir own volition for non-invasivemedical care. However, patients who diein the emergency department most oftendo not present of their own volition, butinstead are brought in by others, usuallyambulance staff, in a state of impairedcompetence. Furthermore, impliedconsent confers the right to administertreatment that the patient would reason-ably expect at the time of presentation.Therefore, if a patient’s attendance isnon-voluntary with impaired compe-tence or with ignorance of the proce-dure, he or she cannot imply consent andwe cannot infer it.

Construed consent is a modification of implied consent, suggesting that ifconsent was obtained for a procedure itcan be construed for a related procedure.If we concede that a form of consent(presumed consent, as suggested above)is obtained to intubate a patient duringresuscitation, may we construe that


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Nconsent also applies to intubation afterdeath? There is a superficial logic to this,as to perform the same procedure on thesame patient with the same equipmentone minute before and one minute afterdeath seems a continuum of the sametherapeutic relationship. However, onclose analysis there is a difference suffi-ciently significant to render previousconsent null and void. The consent toresuscitate is based on a contract betweenmedical staff and patient dedicated tohelping the patient. When the objectiveis no longer to help the patient the pre-vious contract is irrelevant and a new onemust be entered. To proceed to intubatethe deceased under the old contract is aviolation of the trust inherent in thepreviously formed therapeutic relation-ship. An appreciation of this violationcontributes to the repugnance of theprocedure.

Presumed consent is appropriate when impaired competence renders thepatient unable to give informed consent.Although it is likely that most wouldconsent to postmortem procedures forthe benefit of medical staff and subse-quent patients, presumed consent doesdisadvantage the minority who wouldnot. Formal application of a presumedconsent rule for performing procedureson the recently dead mandates that thecommunity should be well informed, sothat individuals have the opportunity toexplicitly decline consent if they sodesire.

Proxy consent has also been argued inrelation to this procedure. However, whenproxy consent rules have been enforcedthe procedure tends not to occur,because staff are uncomfortable aboutobtaining consent in this way, or becauserelatives decline consent in an effort toprotect their loved one from furtherharm.

The value of practising endotrachealintubation and other procedures on thenewly dead is well argued and, therefore,there is a cost if it is disallowed. How-ever, the current pervading policy of ‘don’t

ask, don’t tell’ is ethically unjustifiable. Ifwe presume a patient’s consent and donot ask, we are obliged to tell. The signi-ficant minority that would not consentare thereby protected by an opportunityto decline. Therefore, to proceed withpresumed consent we must have a wellinformed public, and preferably a statuteto formalize consent. An extrapolation of this, which is the most convincingsolution, is called ‘mandated choice’,which proposes a process whereby, as amatter of public policy, individuals mustchoose on a variety of issues and thesechoices are recorded on, for example,their driving licence. This process informsand honours individual choice, gives thesignificant minority the opportunity todecline, and avoids deception. However,in the absence of a suitably informedpublic from whom we can presumeconsent, or a mandated choice, we donot have permission to proceed withpostmortem resuscitation practice.Therefore, to do so is ethically wrong.

CONCLUSIONEmergency medicine abounds with clin-ical dilemmas requiring ethical delibera-tion. Such deliberation may be influencedby theories regarding the consequencesof action, theories based on moralprinciples, or some combination of thesetwo. Beauchamp and Childress2 presenta model for deliberation based on theprinciples of respect for autonomy, non-maleficence, beneficence and justice.Although this model frequently will notprovide an answer beyond dispute, itdoes allow a rational examination of theimportant issues so that our consequentactions will at least be better directedthan they might otherwise have been.

Resuscitation medicine demands suchdeliberation despite the pressure ofurgency and the common impairment ofpatient competence. Patient autonomymust be respected by employing a suit-able consent process, such as the use

of presumed consent using professionalsubstituted judgement. In this way wecan attempt to honour the patient’s auto-nomy by viewing the benefits and harmsof resuscitation from their perspective.Often, particularly in the early stages of resuscitation, the relative benefits andharms may be difficult to establish andthe patient’s perspective may be difficultto formalize. It is appropriate to continuewith resuscitation until these variablesbecome more clear. However, as soon asthere is a negative answer to the question‘Would I want this done if I was thispatient, knowing what I know about thepatient and knowing what I know aboutthe likely outcome?’, the resuscitators havea moral obligation to stop resuscitation.

REFERENCES1. Beauchamp TL 1991 Philosophical Ethics. An

Introduction to Moral Philosophy, 2nd edn.McGraw-Hill, New York

2. Beauchamp TL, Childress JF 1994 Principles ofBiomedical Ethics, 4th edn. Oxford UniversityPress, New York

3. Ardagh M 1997 Preventing harm in resuscitationmedicine. New Zealand Medical Journal 110: 113–5

4. Ardagh MW 2000. Futility has no utility inresuscitation medicine. Journal of Medical Ethics26: 393–6

5. Ardagh MW. 1999 Resurrecting autonomy duringresuscitation - the concept of professionalsubstituted judgement. Journal of Medical Ethics25(5): 375–8

6. Ardagh M 1997 May we practise endotrachealintubation on the newly dead? Journal of MedicalEthics 23: 289–94

CONTROVERSIES❶ Performing resuscitationprocedures where a poor outcome isexpected or where there may bereasons to suspect that the patientmay not wish to be resuscitated.

❷ Withholding resuscitationprocedures on the basis of anargument of futility.

❸ Practising procedures on thenewly dead.

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