ALS 05 ERC Guidelines 2005 Section4

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Resuscitation (2005) 67S1 , S39S86

European Resuscitation Council Guidelines forResuscitation 2005Section 4. Adult advanced life support

Jerry P. Nolan, Charles D. Deakin, Jasmeet Soar,Bernd W. B ottiger, Gary Smith

4a. Prevention of in-hospital cardiacarrest

The problem

This new section of the guidelines stresses theimportance of preventing in-hospital cardiac arrest.Fewer than 20% of patients suffering an in-hospitalcardiac arrest will survive to go home. 1,2 Most sur-vivors have a witnessed and monitored VF arrest,primary myocardial ischaemia as the cause, andreceive immediate debrillation.

Cardiac arrest in patients in unmonitored wardareas is not usually a sudden unpredictable event,nor is it usually caused by primary cardiac disease.These patients often have slow and progressivephysiological deterioration, involving hypoxia andhypotension, that is unnoticed by staff, or is recog-nised but poorly treated. 3,4 The underlying cardiacarrest rhythm in this group is usually non-shockable

and survival to hospital discharge is very poor.1,5

The records of patients who have a cardiacarrest or unanticipated intensive care unit (ICU)admission often contain evidence of unrecog-nised, or untreated, breathing and circulationproblems. 3,4,68 The ACADEMIA study showed

E-mail address: [email protected] (J.P. Nolan).

antecedents in 79% of cardiac arrests, 55% of deathsand 54% of unanticipated ICU admissions. 4 Early andeffective treatment of seriously ill patients mightprevent some cardiac arrests, deaths and unantici-pated ICU admissions. A third of patients who havea false cardiac arrest call die subsequently. 9

Nature of the deciencies in acute careThese often involve simple aspects of care includ-ing: the failure to treat abnormalities of thepatients airway, breathing and circulation, incor-rect use of oxygen therapy, failure to monitorpatients, failure to involve experienced seniorstaff, poor communication, lack of teamwork andinsufcient use of treatment limitation plans. 3,7

Several studies show that medical and nurs-ing staff lack knowledge and skills in acute care.For example, trainee doctors may lack knowl-edge about oxygen therapy, 10 uid and electrolyte

balance, 11 analgesia, 12 issues of consent, 13 pulseoximetry 14 and drug doses. 15 Medical studentsmay be unable to recognise abnormal breathingpatterns. 16 Medical school training provides poorpreparation for doctors early careers, and fails toteach them the essential aspects of applied physi-ology and acute care. 17 There is also little to sug-gest that the acute care training and knowledge of

0300-9572/$ see front matter 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.009


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S40 J.P. Nolan et al.

senior medical staff is better. 18,19 Staff often lackcondence when dealing with acute care problems,and rarely use a systematic approach to the assess-ment of critically ill patients. 20

Recognising the critically ill patient

In general, the clinical signs of acute illness aresimilar whatever the underlying process, as theyreect failing respiratory, cardiovascular and neu-rological systems. Abnormal physiology is com-mon on general wards, 21 yet the measurementand recording of important physiological observa-tions of sick patients occurs less frequently thanis desirable. 3,4,8 This is surprising, as respiratoryrate abnormalities may predict cardiorespiratoryarrest. 22 To assist in the early detection of criti-cal illness, many hospitals now use early warningscores (EWS) or calling criteria. 2325 Early warningscoring systems allocate points to routine vital signsmeasurements on the basis of their derangementfrom an arbitrarily agreed normal range. 2325 Theweighted score of one or more vital sign observa-tions, or the total EWS, may be used to suggestincreasing the frequency of vital signs monitoring tonurses, or to call ward doctors or critical care out-reach teams to the patient. Alternatively, systemsincorporating calling criteria are based on rou-tine observations, which activate a response whenone or more variables reach an extremely abnormalvalue. 23,26 There are no data to establish the supe-

riority of one system over another, but it may bepreferable to use an EWS system, which can trackchanges in physiology and warn of impending physi-ological collapse, rather than the calling criteriaapproach, which is triggered only when an extremevalue of physiology has been reached.

There is a clinical rationale to the use of EWSor calling criteria systems to identify sick patientsearly. However, their sensitivity, specicity andaccuracy in predicting clinical outcomes has yet tobe validated convincingly. 27,28 Several studies haveidentied abnormalities of heart rate, blood pres-sure, respiratory rate and conscious level as mark-ers of impending critical events. 22,23,29 The sugges-tion that their incidence has predictive value mustbe questioned, as not all important vital signs are,or can be, recorded continuously in general wardareas. Several studies show that charting of vitalsigns is poor, with gaps in data recording. 3,4,8,30Although the use of physiological systems canincrease the frequency of vital signs monitoring, 31they will be useful for outcome prediction onlyif widespread monitoring of hospitalised patientsbecomes available. Even when medical staff are

alerted to a patients abnormal physiology, thereis often delay in attending the patient or referringto higher levels of care. 3,4,7 Whereas the use of awarning score based on physiological abnormalitiesis attractive, it is possible that a more subjectiveapproach, based on staff experience and expertise,may also be effective. 32

Response to critical illness

The traditional response to cardiac arrest is areactive one in which hospital staff (the cardiacarrest team) attend the patient after the cardiacarrest has occurred. Cardiac arrest teams appearto improve survival after cardiac arrest in circum-stances where no team has previously existed. 33However, the role of the cardiac arrest team hasbeen questioned. In one study, only patients whohad return of spontaneous circulation before thecardiac arrest team arrived were discharged fromhospital alive. 34 When combined with the poorsurvival rate after in-hospital cardiac arrest, thisemphasises the importance of early recognition andtreatment of critically ill patients to prevent car-diac arrest. The name cardiac arrest team impliesthat the team will be called only after cardiacarrest has occurred.

In some hospitals the cardiac arrest team hasbeen replaced by a medical emergency team (MET)that responds, not only to patients in cardiacarrest, but also to those with acute physiologicaldeterioration. 26 The MET usually comprises medical

and nursing staff from intensive care and generalmedicine. and responds to specic calling crite-ria. Any member of the healthcare team can ini-tiate a MET call. Early involvement of the METmay reduce cardiac arrests, deaths and unantic-ipated ICU admissions. 35,36 The MET may also beuseful in detecting medical error, improving treat-ment limitation decisions and reducing postoper-ative ward deaths. 37,38 MET interventions ofteninvolve simple tasks such as starting oxygen ther-apy and intravenous uids. 39 Acircadian pattern ofMET activation has been reported, which may sug-gest that systems for identifying and responding tomedical emergencies may not be uniform through-out the 24-h period. 40 Studying the effect of theMET on patient outcomes is difcult. Many of thestudy ndings to date can be criticised becauseof poor study design. A recent, well-designed,cluster-randomised controlled trial of the MET sys-tem demonstrated that the introduction of a METincreased the calling incidence for the team. How-ever, it failed to show a reduction in the incidenceof cardiac arrest, unexpected death or unplannedICU admission.41


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in diagnosis of cardiac arrest and starting CPRwill adversely effect survival must be avoided.

If there is a pulse or signs of life, urgent medi-cal assessment is required. Depending on the localprotocols, this may take the form of a resusci-tation team. While awaiting this team, give thepatient oxygen, attach monitoring, and insert anintravenous cannula.

If there is no breathing, but there is a pulse (res-piratory arrest), ventilate the patients lungs andcheck for a circulation every 10 breaths.

Starting in-hospital CPR

One person starts CPR as others call the resusci-tation team and collect the resuscitation equip-ment and a debrillator. If only one memberof staff is present, this will mean leaving thepatient.

Give 30 chest compressions followed by 2 venti-lations.

Undertaking chest compressions properly is tir-ing; try to change the person doing chest com-pressions every 2 min.

Maintain the airway and ventilate the lungs withthe most appropriate equipment immediately tohand. A pocket mask, which may be supple-mented with an oral airway, is usually readilyavailable. Alternatively, use a laryngeal mask air-way (LMA) and self-inating bag, or bag-mask,according to local policy. Tracheal intubation

should be attempted only by those who aretrained, competent and experienced in this skill. Use an inspiratory time of 1 s and give enough

volume to produce a normal chest rise. Add sup-plemental oxygen as soon as possible.

Once the patients trachea has been intubated,continue chest compressions uninterrupted(except for debrillation or pulse checks whenindicated), at a rate of 100 min 1, and ventilatethe lungs at approximately 10 breaths min 1.Avoid hyperventilation.

If there is no airway and ventilation equipmentavailable, give mouth-to-mouth ventilation. Ifthere are clinical reasons to avoid mouth-to-mouth contact, or you are unwilling or unableto do this, do chest compressions until help orairway equipment arrives.

When the debrillator arrives, apply the pad-dles to the patient and analyse the rhythm. Ifself-adhesive debrillation pads are available,apply these without interrupting chest compres-sions. Pause briey to assess the heart rhythm. Ifindicated, attempt either manual or automatedexternal debrillation (AED).

Recommence chest compressions immediatelyafter the debrillation attempt. Minimise inter-ruptions to chest compressions.

Continue resuscitation until the resuscitationteam arrives or the patient shows signs of life.Follow the voice prompts if using an AED. If usinga manual debrillator, follow the universal algo-

rithm for advanced life support (Section 4c). Once resuscitation is underway, and if there aresufcient staff present, prepare intravenous can-nulae and drugs likely to be used by the resusci-tation team (e.g. adrenaline).

Identify one person to be responsible for han-dover to the resuscitation team leader. Locatethe patients records.

The quality of chest compressions during in-hospital CPR is frequently sub-optimal. 61,62 Theteam leader should monitor the quality of CPRand change CPR providers if the quality of CPRis poor. The person providing chest compressionsshould be changed every 2 min.

The monitored and witnessed cardiac arrest

If a patient has a monitored and witnessed cardiacarrest, act as follows.

Conrm cardiac arrest and shout for help. Consider a precordial thump if the rhythm is

VF/VT and a debrillator is not immediatelyavailable.

If the initial rhythm is VF/VT and a debrillatoris immediately available, give a shock rst. Theuse of adhesive electrode pads or a quick-lookpaddles technique will enable rapid assessmentof heart rhythm compared with attaching ECGelectrodes. 63

Training for healthcare professionals

The Immediate Life Support course trains health-care professionals in the skills required to startresuscitation, including debrillation, and to bemembers of a cardiac arrest team (see Section 9). 64The Advanced Life Support (ALS) course teaches theskills required for leading a resuscitation team. 65,66

4c. ALS treatment algorithm

Introduction

Heart rhythms associated with cardiac arrest aredivided into two groups: shockable rhythms (ven-tricular brillation/pulseless ventricular tachycar-dia (VF/VT)) and non-shockable rhythms (asystole


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If VF/VT is conrmed, charge the debrillatorand give one shock (150200-J biphasic or 360-J monophasic). Without reassessing the rhythm orfeeling for a pulse, resume CPR (CV ratio 30:2)immediately after the shock, starting with chestcompressions. Even if the debrillation attempt issuccessful in restoring a perfusing rhythm, it is very

rare for a pulse to be palpable immediately afterdebrillation, 68 and the delay in trying to palpatea pulse will further compromise the myocardiumif a perfusing rhythm has not been restored. 69 Ifa perfusing rhythm has been restored, giving chestcompressions does not increase the chance of VFrecurring. 70 In the presence of post-shock asystole,chest compressions may usefully induce VF. 70 Con-tinue CPR for 2 min, then pause briey to check themonitor: if there is still VF/VT, give a second shock(150360-J biphasic or 360-J monophasic). ResumeCPR immediately after the second shock.

Pause briey after 2min of CPR to check themonitor: if there is still VF/VT, give adrenalinefollowed immediately by a third shock (150360-J biphasic or 360-J monophasic) and resumptionof CPR (drug-shock-CPR-rhythm check sequence).Minimise the delay between stopping chest com-pressions and delivery of the shock. The adenalinethat is given immediately before the shock will becirculated by the CPR that immediately follows theshock. After drug delivery and 2 min of CPR, anal-yse the rhythm and be prepared to deliver anothershock immediately if indicated. If VF/VT persistsafter the third shock, give an intravenous bolus of

amiodarone 300 mg. Inject the amiodarone duringthe brief rhythm analysis before delivery of thefourth shock.

When the rhythm is checked 2 min after givinga shock, if a nonshockable rhythm is present andthe rhythm is organised (complexes appear regularor narrow), try to palpate a pulse. Rhythm checksmust be brief, and pulse checks undertaken onlyif an organised rhythm is observed. If an organ-ised rhythm is seen during a 2 min period of CPR,do not interrupt chest compressions to palpate apulse unless the patient shows signs of life suggest-ing ROSC. If there is any doubt about the presenceof a pulse in the presence of an organised rhythm,resume CPR. If the patient has ROSC, begin postre-suscitation care. If the patients rhythm changesto asystole or PEA, see non-shockable rhythmsbelow.

During treatment of VF/VT, healthcare providersmust practice efcient coordination between CPRand shock delivery. When VF is present for morethan a few minutes, the myocardium is depletedof oxygen and metabolic substrates. A briefperiod of chest compressions will deliver oxygen

and energy substrates and increase the probabil-ity of restoring a perfusing rhythm after shockdelivery. 71 Analyses of VF waveform character-istics predictive of shock success indicate thatthe shorter the time between chest compressionand shock delivery, the more likely the shockwill be successful. 71,72 Reduction in the interval

from compression to shock delivery by even afew seconds can increase the probability of shocksuccess. 73

Regardless of the arrest rhythm, give adrenaline1 mg every 35 min until ROSC is achieved; thiswill be once every two loops of the algorithm. Ifsigns of life return during CPR (movement, normalbreathing, or coughing), check the monitor: if anorganised rhythm is present, check for a pulse. If apulse is palpable, continue post-resuscitation careand/or treatment of peri-arrest arrhythmia. If nopulse is present, continue CPR. Providing CPR witha CV ratio of 30:2 is tiring; change the individualundertaking compressions every 2min.

Precordial thump

Consider giving a single precordial thump when car-diac arrest is conrmed rapidly after a witnessed,sudden collapse and a debrillator is not immedi-ately to hand (Section 3). 74 These circumstancesare most likely to occur when the patient is mon-itored. A precordial thump should be undertakenimmediately after conrmation of cardiac arrestand only by healthcare professionals trained in

the technique. Using the ulnar edge of a tightlyclenched st, deliver a sharp impact to the lowerhalf of the sternum from a height of about 20 cm,then retract the st immediately to create animpulse-like stimulus. A precordial thump is mostlikely to be successful in converting VT to sinusrhythm. Successful treatment of VF by precor-dial thump is much less likely: in all the reportedsuccessful cases, the precordial thump was givenwithin the rst 10s of VF. 75 There are very rarereports of a precordial thump converting a perfus-ing to a non-perfusing rhythm. 76

Airway and ventilation

During the treatment of persistent VF, ensure good-quality chest compressions between debrillationattempts. Consider reversible causes (4 Hs and 4Ts) and, if identied, correct them. Check theelectrode/debrillating paddle positions and con-tacts, and the adequacy of the coupling medium,e.g. gel pads. Tracheal intubation provides themost reliable airway, but should be attemptedonly if the healthcare provider is properly trained


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Figure 4.3 Causes of airway obstruction.

mon, but may arise from excessive bronchial secre-tions, mucosal oedema, bronchospasm, pulmonaryoedema or aspiration of gastric contents.

Recognition of airway obstruction

Airwayobstruction canbe subtle and is often missedby healthcare professionals, let alone by lay peo-ple. The look, listen and feel approach is a simple,systematic method of detecting airway obstruction.

Look for chest and abdominal movements. Listen and feel for airow at the mouth and nose.

In partial airway obstruction, air entry is dimin-

ished and usually noisy. Inspiratory stridor is causedby obstruction at the laryngeal level or above. Expi-ratory wheeze implies obstruction of the lower air-ways, which tend to collapse and obstruct duringexpiration. Other characteristic sounds include thefollowing:

Gurgling is caused by liquid or semisolid foreignmaterial in the main airways.

Snoring arises when the pharynx is partiallyoccluded by the soft palate or epiglottis.

Crowing is the sound of laryngeal spasm.

In a patient who is making respiratory efforts,complete airway obstruction causes paradoxicalchest and abdominal movement, often describedas see-saw breathing. As the patient attempts tobreathe in, the chest is drawn in and the abdomenexpands; the opposite occurs during expiration.This is in contrast to the normal breathing pattern

of synchronous movement upwards and outwardsof the abdomen (pushed down by the diaphragm)with the lifting of the chest wall. During airwayobstruction, other accessory muscles of respirationare used, with the neck and the shoulder mus-cles contracting to assist movement of the tho-racic cage. Full examination of the neck, chest andabdomen is required to differentiate the paradox-ical movements that may mimic normal respira-tion. The examination must include listening forthe absence of breath sounds in order to diagnosecomplete airway obstruction reliably; any noisybreathing indicates partial airway obstruction. Dur-ing apnoea, when spontaneous breathing move-ments are absent, complete airway obstruction isrecognised by failure to inate the lungs duringattempted positive pressure ventilation. Unless air-way patency can be re-established to enable ade-quate lung ventilation within a period of a very fewminutes, neurological and other vital organ injurymay occur, leading to cardiac arrest.

Basic airway management

Once any degree of obstruction is recognised,

immediate measures must be taken to create andmaintain a clear airway. There are three manoeu-vres that may improve the patency of an airwayobstructed by the tongue or other upper airwaystructures: head tilt, chin lift, and jaw thrust.

Head tilt and chin lift

The rescuers hand is placed on the patients fore-head and the head gently tilted back; the ngertipsof the other hand are placed under the point of thepatients chin, which is gently lifted to stretch theanterior neck structures ( Figure 4.4 ). 100105

Jaw thrust

Jaw thrust is an alternative manoeuvre for bringingthe mandible forward and relieving obstruction bythe soft palate and epiglottis. The rescuers indexand other ngers are placed behind the angle ofthe mandible, and pressure is applied upwards andforwards. Using the thumbs, the mouth is openedslightly by downward displacement of the chin(Figure 4.5 ).


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European Resuscitation Council Guidelines for Resuscitation 2005 S53

Figure 4.7 Mouth-to-mask ventilation. 2005 Euro-pean Resuscitation Council.

ciency virus (HIV) during provision of CPR hasnever been reported. Simple adjuncts are avail-able to enable direct person-to-person contact tobe avoided; some of these devices may reduce therisk of cross-infection between patient and res-cuer, although they are unlikely to offer signicantprotection from SARS. 123 The pocket resuscitationmask is used widely. It is similar to an anaestheticfacemask, and enables mouth-to-mask ventilation.It has a unidirectional valve, which directs thepatients expired air away from the rescuer. Themask is transparent so that vomit or blood from the

patient can be seen. Some masks have a connec-tor for the addition of oxygen. When using maskswithout a connector, supplemental oxygen can begiven by placing the tubing underneath one side andensuring an adequate seal. Use a two-hand tech-nique to maximise the seal with the patients face(Figure 4.7 ).

High airway pressures can be generated if thetidal volumes or inspiratory ows are excessive,predisposing to gastric ination and subsequent riskof regurgitation and pulmonary aspiration. The pos-sibility of gastric ination is increased by

malalignment of the head and neck, and anobstructed airway an incompetent oesophageal sphincter (present

in all patients with cardiac arrest) a high ination pressure

Conversely, if inspiratory ow is too low, inspi-ratory time will be prolonged and the time avail-able to give chest compressions is reduced. Delivereach breath over approximately 1 s and transfera volume that corresponds to normal chest move-ment; this represents a compromise between giving

an adequate volume, minimising the risk of gas-tric ination, and allowing adequate time for chestcompressions. During CPR with an unprotected air-way, give two ventilations after each sequence of30 chest compressions.

Self-inating bag

The self-inating bag can be connected to a face-mask, tracheal tube or alternative airway devicesuch as the LMA or Combitube. Without supple-mental oxygen, the self-inating bag ventilatesthe patients lungs with ambient air (21% oxygen).This can be increased to about 45% by attachingoxygen directly to the bag. If a reservoir systemis attached and the oxygen ow is increased toapproximately 10 l min 1, an inspired oxygen con-centration of approximately 85% can be achieved.

Although the bag-mask device enables ventila-tion with high concentrations of oxygen, its use by a

single personrequires considerable skill. When usedwith a face mask, it is often difcult to achieve agas-tight seal between the mask and the patientsface, and to maintain a patent airway with one handwhile squeezing the bag with the other. 124 Any sig-nicant leak will cause hypoventilation and, if theairway is not patent, gas may be forced into thestomach. 125,126 This will reduce ventilation furtherand greatly increase the risk of regurgitation andaspiration. 127 Cricoid pressure can reduce this riskbut requires the presence of a trained assistant.Poorly applied cricoid pressure may make it moredifcult to ventilate the patients lungs. 128

The two-person technique for bag-mask venti-lation is preferable ( Figure 4.8 ). One person holdsthe facemask in place using a jaw thrust with both

Figure 4.8 The two-person technique for bag-mask ven-tilation. 2005 European Resuscitation Council.


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is detected in cardiac arrest, it indicates reliablythat the tube is in the trachea or main bronchus but,when it is absent, tracheal tube placement is bestconrmed with an oesophageal detector device. Avariety of electronic as well as simple, inexpensive,colorimetric carbon dioxide detectors are availablefor both in-hospital and out-of-hospital use.

Cricoid pressure

During bag-mask ventilation and attempted intuba-tion, cricoid pressure applied by a trained assis-tant should prevent passive regurgitation of gas-tric contents and the consequent risk of pulmonaryaspiration. If the technique is applied impreciselyor with excessive force, ventilation and intubationcan be made more difcult. 128 If ventilation of thepatients lungs is not possible, reduce the pressureapplied to the cricoid cartilage or remove it com-pletely. If the patient vomits, release the cricoidimmediately.

Securing the tracheal tube

Accidental dislodgement of a tracheal tube canoccur at any time, but may be more likely duringresuscitation and during transport. The most effec-tive method for securing the tracheal tube has yetto be determined; use either conventional tapes orties, or purpose-made tracheal tube holders.

CricothyroidotomyOccasionally, it will be impossible to ventilate anapnoeic patient with a bag-mask, or to pass a tra-cheal tube or alternative airway device. This mayoccur in patients with extensive facial trauma orlaryngeal obstruction due to oedema or foreignmaterial. In these circumstances, delivery of oxy-gen through a needle or surgical cricothyroidotomymay be life-saving. A tracheostomy is contraindi-cated in an emergency, as it is time consuming,hazardous and requires considerable surgical skilland equipment.

Surgical cricothyroidotomy provides a deni-tive airway that can be used to ventilate thepatients lungs until semi-elective intubation or tra-cheostomy is performed. Needle cricothyroidotomyis a much more temporary procedure providingonly short-term oxygenation. It requires a wide-bore, non-kinking cannula, a high-pressure oxygensource, runs the risk of barotrauma and can be par-ticularly ineffective in patients with chest trauma.It is also prone to failure because of kinking of thecannula, and is unsuitable for patient transfer.

4e. Assisting the circulation

Drugs and uids for cardiac arrest

This topic is divided into: drugs used during themanagement of a cardiac arrest; anti-arrhythmicdrugs used in the peri-arrest period; other drugs

used in the peri-arrest period; uids; and routesfor drug delivery. Every effort has been made toprovide accurate information on the drugs in theseguidelines, but literature from the relevant phar-maceutical companies will provide the most up-to-date data.

Drugs used during the treatment of cardiacarrest

Only a few drugs are indicated during the imme-diate management of a cardiac arrest, and thereis limited scientic evidence supporting their use.Drugs should be considered only after initial shockshave been delivered (if indicated) and chest com-pressions and ventilation have been started.

There are three groups of drugs relevant to themanagement of cardiac arrest that were reviewedduring the 2005 Consensus Conference: vasopres-sors, anti-arrhythmics and other drugs. Routes ofdrug delivery other than the optimal intravenousroute were also reviewed and are discussed.

Vasopressors

There are currently no placebo-controlled studiesshowing that the routine use of any vasopressor atany stage during human cardiac arrest increasessurvival to hospital discharge. The primary goalof cardiopulmonary resuscitation is to re-establishblood ow to vital organs until the restoration ofspontaneous circulation. Despite the lack of datafrom cardiac arrest in humans, vasopressors con-tinue to be recommended as a means of increasingcerebral and coronary perfusion during CPR.

Adrenaline (epinephrine) versus vasopressin.Adrenaline has been the primary sympathomimeticagent for the management of cardiac arrest for40 years. 182 Its primary efcacy is due to itsalpha-adrenergic, vasoconstrictive effects caus-ing systemic vasoconstriction, which increasescoronary and cerebral perfusion pressures. Thebeta-adrenergic actions of adrenaline (inotropic,chronotropic) may increase coronary and cerebralblood ow, but concomitant increases in myocar-dial oxygen consumption, ectopic ventriculararrhythmias (particularly when the myocardiumis acidotic) and transient hypoxaemia due to


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pulmonary arteriovenous shunting may offset thesebenets.

The potentially deleterious beta-effects ofadrenaline have led to exploration of alternativevasopressors. Vasopressin is a naturally occurringantidiuretic hormone. In very high doses it is apowerful vasoconstrictor that acts by stimulation

of smooth muscle V1 receptors. The importance ofvasopressin in cardiac arrest was rst recognised instudies of out-of-hospital cardiac arrest patients,where vasopressin levels were found to be higher insuccessfully resuscitated patients. 183,184 Althoughclinical 185,186 and animal 187189 studies demon-strated improved haemodynamic variables whenusing vasopressin as an alternative to adrenalineduring resuscitation from cardiac arrest, some, 186but not all, demonstrated improved survival. 190,191

The rst clinical use of vasopressin during car-diac arrest was reported in 1996 and appearedpromising. In a study of cardiac arrest patientsrefractory to standard therapy with adrenaline,vasopressin restored a spontaneous circulation inall eight patients, three of whom were dischargedneurologically intact. 186 The following year, thesame group published a small randomised trialof out-of-hospital ventricular brillation, in whichthe rates of successful resuscitation and sur-vival for 24 h were signicantly higher in patientstreated with vasopressin than in those treated withadrenaline. 192 Following these two studies, theAmerican Heart Association (AHA) recommendedthat vasopressin could be used as an alternative

to adrenaline for the treatment of adult shock-refractory VF. 182 The success of these small stud-ies led to two large randomised studies compar-ing vasopressin with adrenaline for in-hospital 193and out-of-hospital 194 cardiac arrest. Both stud-ies randomised patients to receive vasopressin oradrenaline initially, and used adrenaline as a res-cue treatment in patients refractory to the initialdrug. Both studies were unable to demonstrate anoverall increase in the rates of ROSC or survivalfor vasopressin 40U, 193 with the dose repeatedin one study, 194 when compared with adrenaline(1 mg, repeated), as the initial vasopressor. In thelarge out-of-hospital cardiac arrest study, 194 post-hoc analysis suggested that the subset of patientswith asystole had signicant improvement in sur-vival to discharge, but survival neurologically intactwas no different.

A recent meta-analysis of ve randomisedtrials 195 showed no statistically signicant differ-ence between vasopressin and adrenaline for ROSC,death within 24h or death before hospital dis-charge. The subgroup analysis based on initial car-diac rhythm did not show any statistically signi-

cant difference in the rate of death before hospitaldischarge. 195

Participants at the 2005 Consensus Conferencedebated in depth the treatment recommendationsthat should follow from this evidence. Despite theabsence of placebo-controlled trials, adrenalinehas been the standard vasopressor in cardiac arrest.

It was agreed that there is currently insufcientevidence to support or refute the use of vaso-pressin as an alternative to, or in combination with,adrenaline in any cardiac arrest rhythm. Currentpractice still supports adrenaline as the primaryvasopressor for the treatment of cardiac arrest ofall rhythms.

AdrenalineIndications

Adrenaline is the rst drug used in cardiac arrestof any aetiology: it is included in the ALS algo-rithm for use every 35 min of CPR.

Adrenaline is preferred in the treatment of ana-phylaxis (Section 7g).

Adrenaline is second-line treatment for cardio-genic shock.

Dose . During cardiac arrest, the initial intra-venous dose of adrenaline is 1 mg. When intravascu-lar (intravenous or intra-osseous) access is delayedor cannot be achieved, give 23 mg, diluted to10 ml with sterile water, via the tracheal tube.Absorption via the tracheal route is highly variable.

There is no evidence supporting the use of higherdoses of adrenaline for patients in refractory car-diac arrest. In some cases, an adrenaline infusion isrequired in the post-resuscitation period.

Following return of spontaneous circulation,excessive ( 1 mg) doses of adrenaline may inducetachycardia, myocardial ischaemia, VT and VF.Once a perfusing rhythm is established, if furtheradrenaline is deemed necessary, titrate the dosecarefully to achieve an appropriate blood pressure.Intravenous doses of 50100 mcg are usually suf-cient for most hypotensive patients. Use adrenalinecautiously in patients with cardiac arrest associatedwith cocaine or other sympathomimetic drugs.

Use. Adrenaline is available most commonly intwo dilutions:

1 in 10,000 (10 ml of this solution contains 1 mgof adrenaline)

1 in 1000 (1 ml of this solution contains 1 mg ofadrenaline)

Both these dilutions are used routinely in Europeancountries.


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The recommended adult dose of atropine forasystole or PEA with a rate


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intrathoracic pressure as when used with a trachealtube. 297

In two randomised studies of out-of-hospitalcardiac arrest, ACD-CPR plus the ITD improvedROSC and 24-h survival compared with standardCPR alone. 296,298 When used during standard CPR,the ITD increased 24-h survival after PEA out-of-

hospital cardiac arrest.297

Mechanical piston CPR

Mechanical piston devices depress the sternumby means of a compressed gas-powered plungermounted on a backboard. In several studies inanimals, 299,300 mechanical piston CPR improvedend-tidal carbon dioxide, cardiac output, cerebralblood ow, MAP and short-term neurological out-come. Studies in humans also document improve-ment in end-tidal carbon dioxide and mean arterialpressure when using mechanical piston CPR com-pared with conventional CPR. 301303

Lund University cardiac arrest system (LUCAS)CPR

The Lund University cardiac arrest system (LUCAS)is a gas-driven sternal compression device thatincorporates a suction cup for active decompres-sion. There are no published randomised humanstudies comparing LUCAS-CPR with standard CPR.A study of pigs with VF showed that LUCAS-CPRimproves haemodynamic and short-term survivalcompared with standard CPR. 304 The LUCAS wasalso used in 20 patients, but incomplete outcomedata were reported. 304 In another pig study, in com-parison with standard CPR, LUCAS-CPR increasedcerebral blood ow and cardiac output. 305 TheLUCAS enables delivery of continuous compressionsduring transport and debrillation.

Mechanical piston CPR or LUCAS CPR may be par-ticularly useful when prolonged CPR is required;this might include during transport to hospital orafter cardiac arrest following hypothermia 306 orpoisoning.

Load-distributing band CPR or vest CPR

The load distributing band (LDB) is a cir-cumferential chest compression device compris-ing a pneumatically actuated constricting bandand backboard. The use of LDB CPR improveshaemodynamics. 307309 A casecontrol study docu-mented improvement in survival to the emergencydepartment when LDB-CPR was delivered after out-of-hospital cardiac arrest. 310

Phased thoracicabdominalcompressiondecompression CPR (PTACD-CPR)

Phased thoracicabdominal compressiondecom-pression CPR combines the concepts of IAC-CPRand ACD-CPR. It comprises a hand-held devicethat alternates chest compression and abdominaldecompression with chest decompression andabdominal compression. One randomised study ofadults in cardiac arrest documented no improve-ment in survival from use of PTACD-CPR. 311

Minimally invasive direct cardiac massage

Minimally invasive direct cardiac massage (MIDCM)is accomplished by insertion of a small plunger-likedevice through a 24-cm incision in the chest wall.In one clinical study the MIDCM generated improvedblood pressure over standard CPR, but the devicecaused cardiac rupture in one postoperative cardio-

vascular surgical patient. 312 The plunger device isno longer manufactured.

4f. Peri-arrest arrhythmias

Introduction

A successful strategy to reduce the mortalityand morbidity of cardiac arrest includes measuresto prevent other potentially serious arrhythmias,and optimal treatment should they occur. Cardiac

arrhythmias are well recognised complications ofmyocardial infarction. They may precede ventric-ular brillation or follow successful debrillation.The treatment algorithms described in this sectionhave been designed to enable the non-specialistALS provider to treat the patient effectively andsafely in an emergency; for this reason, they havebeen kept as simple as possible. If patients arenot acutely ill there may be several other treat-ment options, including the use of drugs (oral orparenteral), that will be less familiar to the non-expert. In this situation there will be time to seekadvice from cardiologists or other doctors with theappropriate expertise.

More comprehensive information on themanagement of arrhythmias can be found atwww.escardio.org .

Principles of treatment

In all cases, give oxygen and insert an intravenouscannula while thearrhythmia is assessed. Wheneverpossible, record a 12-lead ECG; this will help deter-mine the precise rhythm, either before treatment
http://www.escardio.org/


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Figure 4.11 Bradycardia algorithm.

Mobitz type II AV block complete (third-degree) heart block (espe-

cially with broad QRS or initial heart rate0.20s), and is usually benign. Second-degree AV block is divided into M obitz types I and II.In Mobitz type I, the block is at the AV node, is often

transient and may be asymptomatic. In M obitz typeII, the block is most often below the AV node atthe bundle of His or at the bundle branches, and isoften symptomatic, with the potential to progressto complete AV block. Third-degree heart block isdened by AV dissociation which may be permanentor transient, depending on the underlying cause.

Pacing is likely to be required if there is a riskof asystole, or if the patient is unstable and hasfailed to respond satisfactorily to atropine. Underthese circumstances, the denitive treatment istransvenous pacing. One or more of the followinginterventions can be used to improve the patientscondition while waiting for the appropriate person-nel and facilities:


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dia with adenosine suggests an atrial tachycardiasuch as atrial utter.

If adenosine is contraindicated or fails to ter-minate a regular narrow-complex tachycardiawithout demonstrating that it is atrial utter,give a calcium channel blocker (e.g., verapamil2.55mg intravenously over 2 min).

Irregular narrow-complex tachycardia

An irregular narrow-complex tachycardia is mostlikely to be AF with an uncontrolled ventricularresponse or, less commonly, atrial utter with vari-able AV block. Record a 12-lead ECG to identifythe rhythm. If the patient is unstable with adversefeatures caused by the arrhythmia, attempt syn-chronised electrical cardioversion.

If there are no adverse features, treatmentoptions include:

rate control by drug therapy rhythm control using drugs to encourage chemi-

cal cardioversion rhythm control by electrical cardioversion treatment to prevent complications (e.g., anti-

coagulation)

Obtain expert help to determine the most appro-priate treatment for the individual patient. Thelonger a patient remains in AF, the greater isthe likelihood of atrial clot developing. In gen-eral, patients who have been in AF for more than48 h should not be treated by cardioversion (elec-trical or chemical) until they have received fullanticoagulation or absence of atrial clot has beenshown by transoesophageal echocardiography. Ifthe aim is to control heart rate, options includea beta-blocker, 321,322 digoxin, diltiazem, 323,324magnesium 325,326 or combinations of these.

If the duration of AF is less than 48 h and rhythmcontrol is considered appropriate, this may beattempted using amiodarone (300 mg intravenouslyover 2060min followed by 900 mg over 24h). Ibu-

tilide or ecainide can also be given for rhythm con-trol, but expert advice should be obtained beforeusing these drugs for this purpose. Electrical car-dioversion remains an option in this setting and willrestore sinus rhythm in more patients than chemi-cal cardioversion.

Seek expert help if any patient with AF is knownor found to have ventricular pre-excitation (WPWsyndrome). Avoid using adenosine, diltiazem, vera-pamil or digoxin to patients with pre-excited AF oratrial utter, as these drugs block the AV node andcause a relative increase in pre-excitation.

Antiarrhythmic drugs

Adenosine

Adenosine is a naturally occurring purinenucleotide. It slows transmission across theAV node but has little effect on other myocardialcells or conduction pathways. It is highly effectivefor terminating paroxysmal SVT with re-entrantcircuits that include the AV node (AVNRT). Inother narrow-complex tachycardias, adenosine willreveal the underlying atrial rhythms by slowing theventricular response. It has an extremely short half-life of 1015s and, therefore, is given as a rapidbolus into a fast running intravenous infusion or fol-lowed by a saline ush. The smallest dose likely tobe effective is 6 mg (which is outside some currentlicences for an initial dose) and, if unsuccessfulthis can be followed with up to two doses each of12 mg every 12min. Patients should be warned

of transient unpleasant side effects, in particularnausea, ushing, and chest discomfort. 327 Adeno-sine is not available in some European countries,but adenosine triphosphate (ATP) is an alternative.In a few European countries neither preparationmay be available; verapamil is probably the nextbest choice. Theophylline and related compoundsblock the effect of adenosine. Patients receivingdipyridamole or carbamazepine, or with dener-vated (transplanted) hearts, display a markedlyexaggerated effect that may be hazardous. Inthese patients, or if injected into a central vein,reduce the initial dose of adenosine to 3 mg. In thepresence of WPW syndrome, blockage of conduc-tion across the AV node by adenosine may promoteconduction across an accessory pathway. In thepresence of supraventricular arrhythmias this maycause a dangerously rapid ventricular response. Inthe presence of WPW syndrome, rarely, adenosinemay precipitate atrial brillation associated with adangerously rapid ventricular response.

Amiodarone

Intravenous amiodarone has effects on sodium,

potassium and calcium channels as well as alpha-and beta-adrenergic blocking properties. Indica-tions for intravenous amiodarone include:

control of haemodynamically stable VT, polymor-phic VT and wide-complex tachycardia of uncer-tain origin

paroxysmal SVT uncontrolled by adenosine, vagalmanoeuvres or AV nodal blockade

to control rapid ventricular rate due to accessorypathway conduction in pre-excited atrial arrhyth-mias


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Give amiodarone, 300mg intravenously, over1060 min depending on the circumstances andhaemodynamic stability of the patient. This load-ing dose is followed by an infusion of 900 mg over24 h. Additional infusions of 150 mg can be repeatedas necessary for recurrent or resistant arrhyth-mias to a maximum manufacturer-recommended

total daily dose of 2 g (this maximum licensed dosevaries between countries). In patients known tohave severely impaired heart function, intravenousamiodarone is preferable to other anti-arrhythmicdrugs for atrial and ventricular arrhythmias. Majoradverse effects from amiodarone are hypotensionand bradycardia, which can be prevented by slow-ing the rate of drug infusion. The hypotension asso-ciated with amiodarone is caused by vasoactive sol-vents (Polysorbate 80 and benzyl alcohol). A newaqueous formulation of amiodarone does not con-tain these solvents and causes no more hypotensionthan lidocaine. 198 Whenever possible, intravenousamiodarone should be given via a central venouscatheter; it causes thrombophlebitis when infusedinto a peripheral vein. In an emergency it should beinjected into a large peripheral vein.

Calcium channel blockers: verapamil anddiltiazem

Verapamil and diltiazem are calcium channel block-ing drugs that slow conduction and increase refrac-toriness in the AV node. Intravenous diltiazem isnot available in some countries. These actions may

terminate re-entrant arrhythmias and control ven-tricular response rate in patients with a variety ofatrial tachycardias. Indications include:

stable regular narrow-complex tachycardiasuncontrolled or unconverted by adenosine orvagal manoeuvres

to control ventricular rate in patients with AF oratrial utter and preserved ventricular functionwhen the duration of the arrhythmia is less than48 h

The initial dose of verapamil is 2.55 mg intra-venously given over 2min. In the absence of a ther-apeutic response or drug-induced adverse event,give repeated doses of 510 mg every 1530 minto a maximum of 20 mg. Verapamil should be givenonly to patients with narrow-complex paroxysmalSVT or arrhythmias known with certainty to be ofsupraventricular origin.

Diltiazem at a dose of 250mcg kg 1, followed bya second dose of 350mcgkg 1, is as effective asverapamil. Verapamil and, to a lesser extent, dil-tiazem may decrease myocardial contractility andcritically reduce cardiac output in patients with

severe LV dysfunction. For the reasons stated underadenosine (above), calcium channel blockers areconsidered harmful when given to patients withAF or atrial utter associated with known pre-excitation (WPW) syndrome.

Beta-adrenergic blockers

Beta-blocking drugs (atenolol, metoprolol,labetalol (alpha- and beta-blocking effects),propranolol, esmolol) reduce the effects of cir-culating catecholamines and decrease heart rateand blood pressure. They also have cardiopro-tective effects for patients with acute coronarysyndromes. Beta-blockers are indicated for thefollowing tachycardias:

narrow-complex regular tachycardias uncon-trolled by vagal manoeuvres and adenosine in thepatient with preserved ventricular function

to control rate in AF and atrial utter when ven-tricular function is preserved

The intravenous dose of atenolol (beta 1) is5 mg given over 5 min, repeated if necessary after10 min. Metoprolol (beta 1) is given in doses of25 mg at 5-min intervals to a total of 15 mg. Pro-pranolol (beta 1 and beta 2 effects), 100mcg kg 1, isgiven slowly in three equal doses at 23-min inter-vals.

Intravenous esmolol is a short-acting (half-life of 29 min) beta 1-selective beta-blocker. Itis given as an intravenous loading dose of

500 mcg kg 1

over 1 min, followed by an infusion of50200mcg kg 1 min 1.Side effects of beta-blockade include bradycar-

dias, AV conduction delays and hypotension. Con-traindications to the use of beta-adrenergic block-ing agents include second- or third-degree heartblock, hypotension, severe congestive heart failureand lung disease associated with bronchospasm.

Magnesium

Magnesium can be given for control of ventricu-lar rate in atrial brillation. 326,328330 Give magne-sium sulphate 2 g (8 mmol) over 10min. This can berepeated once if necessary.

4g. Post-resuscitation care

Introduction

ROSC is the just the rst step toward the goalof complete recovery from cardiac arrest. Inter-ventions in the post-resuscitation period are likely


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maintain mean arterial pressure at the patientsnormal level.

Sedation

Although it has been common practice to sedateand ventilate patients for up to 24h after ROSC,

there are no data to support a dened period ofventilation, sedation and neuromuscular blockadeafter cardiac arrest. The duration of sedation andventilation may be inuenced by the use of thera-peutic hypothermia (see below). There are no datato indicate whether or not the choice of sedationinuences outcome, but short-acting drugs (e.g.,propofol, alfentanil, remifentanil) will enable ear-lier neurological assessment. There is an increasedincidence of pneumonia when sedation is prolongedbeyond 48 h after prehospital or in-hospital cardiacarrest. 342

Control of seizures

Seizures and/or myoclonus occur in 515% ofadult patients who achieve ROSC, and in approx-imately 40% of those who remain comatose. 343Seizures increase cerebral metabolism by up tofour-fold. Prolonged seizure activity may causecerebral injury, and should be controlled with ben-zodiazepines, phenytoin, propofol or a barbiturate.Each of these drugs can cause hypotension, andthis must be treated appropriately. Seizures andmyoclonus per se are not related signicantly to

outcome, but status epilepticus and, in particu-lar, status myoclonus are associated with a pooroutcome. 343,344

Temperature control

Treatment of hyperpyrexia. A period of hyper-thermia (hyperpyrexia) is common in the rst 48 hafter cardiac arrest. 345347 The risk of a poor neuro-logical outcome increases for each degree of bodytemperature >37 C.348 Antipyretics and/or phys-ical cooling methods decrease infarct volumes inanimal models of global ischaemia. 349,350 Treat anyhyperthermia occurring in the rst 72 h after car-diac arrest with antipyretics or active cooling.

Therapeutic hypothermia. Mild therapeutichypothermia is thought to suppress many ofthe chemical reactions associated with reperfu-sion injury. These reactions include free-radicalproduction, excitatory amino acid release, andcalcium shifts, which can in turn lead to mito-chondrial damage and apoptosis (programmedcell death). 351353 Two randomised clinical trials

showed improved outcome in adults remainingcomatose after initial resuscitation from out-of-hospital VF cardiac arrest, who were cooledwithin minutes to hours after ROSC. 354,355 Thesubjects were cooled to 3234 C for 1224 h. Onestudy documented improved metabolic endpoints(lactate and O 2 extraction) when comatose adult

patients were cooled after ROSC from out-of-hospital cardiac arrest in which the initial rhythmwas PEA/asystole. 356 A small study showed ben-et after therapeutic hypothermia in comatosesurvivors of non-VF arrest. 357

External and/or internal cooling techniques canbe used to initiate cooling. 354356,358361 An infu-sion of 30mgkg 1 of 4 C-saline decreases coretemperature by 1.5 C.358,359,361,362 Intravascularcooling enables more precise control of core tem-perature than external methods, but it is unknownwhether this improves outcome. 360,363365

Complications of mild therapeutic hypother-mia include increased infection, cardiovascularinstability, coagulopathy, hyperglycaemia and elec-trolyte abnormalities such as hypophosphataemiaand hypomagnesaemia. 366,367

Unconscious adult patients with spontaneous cir-culation after out-of-hospital VF cardiac arrestshould be cooled to 3234 C. Cooling should bestarted as soon as possible and continued for atleast 1224 h. 368374 Induced hypothermia mightalso benet unconscious adult patients with spon-taneous circulation after out-of-hospital cardiacarrest from a non-shockable rhythm, or cardiac

arrest in hospital. Treat shivering by ensuring ade-quate sedation and giving neuromuscular block-ing drugs. Bolus doses of neuromuscular block-ers are usually adequate, but infusions are nec-essary occasionally. Rewarm the patient slowly(0.250.5 C h 1) and avoid hyperthermia. Theoptimum target temperature, rate of cooling, dura-tion of hypothermia and rate of rewarming have yetto be determined; further studies are essential.

Blood glucose control

There is a strong association between high bloodglucose after resuscitation from cardiac arrestand poor neurological outcome. 237244 Persistenthyperglycaemia after stroke is also associatedwith a worse neurological outcome. 375378 Tightcontrol of blood glucose (4.46.1mmol l 1 or80110mgdl 1) using insulin reduces hospital mor-tality in critically ill adults, 379,380 but this has notbeen demonstrated in post-cardiac arrest patientsspecically. The benet is thought to result fromthe strict glycaemic control rather than the doseof insulin infused. 381 One rat study has shown


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91. Thel MC, Armstrong AL, McNulty SE, Califf RM, OConnorCM. Randomised trial of magnesium in in-hospital cardiacarrest. Lancet 1997;350:12726.

92. Allegra J, Lavery R, Cody R, et al. Magnesium sulfate inthe treatment of refractory ventricular brillation in theprehospital setting. Resuscitation 2001;49:2459.

93. Fatovich D, Prentice D, Dobb G. Magnesium in in-hospitalcardiac arrest. Lancet 1998;351:446.

94. Hassan TB, Jagger C, Barnett DB. A randomised trial toinvestigate the efcacy of magnesium sulphate for refrac-tory ventricular brillation. Emerg Med J 2002;19:5762.

95. Miller B, Craddock L, Hoffenberg S, et al. Pilot study ofintravenousmagnesiumsulfate in refractory cardiac arrest:safety data and recommendations for future studies. Resus-citation 1995;30:314.

96. Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Grif-fel MI. Difference in acidbase state between venous andarterial blood during cardiopulmonary resuscitation. N EnglJ Med 1986;315:1536.

97. Bottiger BW, Bode C, Kern S, et al. Efcacy and safety ofthrombolytic therapy after initially unsuccessful cardiopul-monary resuscitation: a prospective clinical trial. Lancet2001;357:15835.

98. Boidin MP. Airway patency in the unconscious patient. Br JAnaesth 1985;57:30610.

99. Nandi PR, Charlesworth CH, Taylor SJ, Nunn JF, Dore CJ.Effect of general anaesthesia on the pharynx. Br J Anaesth1991;66:15762.

100. Guildner CW. Resuscitation: opening the airway. A compar-ative study of techniques for opening an airway obstructedby the tongue. JACEP 1976;5:58890.

101. Safar P, Aguto-Escarraga L. Compliance in apneic anes-thetized adults. Anesthesiology 1959;20:2839.

102. Greene DG, Elam JO, Dobkin AB, Studley CL. Cineuoro-graphic study of hyperextension of the neck and upperairway patency. Jama 1961;176:5703.

103. Morikawa S, Safar P, Decarlo J. Inuence of the head-jaw position upon upper airway patency. Anesthesiology1961;22:26570.

104. Ruben HM, Elam JO, Ruben AM, Greene DG. Investigation ofupper airway problems in resuscitation. 1. Studies of pha-ryngeal X-rays and performance by laymen. Anesthesiology1961;22:2719.

105. Elam JO, Greene DG, Schneider MA, et al. Head-tilt methodof oral resuscitation. JAMA 1960;172:8125.

106. Aprahamian C, Thompson BM, Finger WA, Darin JC. Experi-mental cervical spine injury model: evaluation of airwaymanagement and splinting techniques. Ann Emerg Med1984;13:5847.

107. Donaldson 3rd WF, Heil BV, Donaldson VP, Silvaggio VJ. Theeffect of airwaymaneuvers on the unstable C1-C2 segment.A cadaver study. Spine 1997;22:12158.

108. Donaldson 3rd WF, Towers JD, Doctor A, Brand A, DonaldsonVP. A methodology to evaluate motion of the unstable spineduring intubation techniques. Spine 1993;18:20203.

109. Hauswald M, Sklar DP, Tandberg D, Garcia JF. Cervicalspine movement during airway management: cineuoro-scopic appraisal in human cadavers. Am J Emerg Med1991;9:5358.

110. Brimacombe J, Keller C, Kunzel KH, Gaber O, Boehler M,Puhringer F. Cervical spine motion during airway manage-ment: a cineuoroscopic study of the posteriorly destabi-lized third cervical vertebrae in human cadavers. AnesthAnalg 2000;91:12748.

111. Majernick TG, Bieniek R, Houston JB, Hughes HG. Cervicalspine movement during orotracheal intubation. Ann EmergMed 1986;15:41720.

112. Lennarson PJ, Smith DW, Sawin PD, Todd MM, Sato Y,Traynelis VC. Cervical spinal motion during intubation: ef-cacy of stabilization maneuvers in the setting of completesegmental instability. J Neurosurg Spine 2001;94:26570.

113. Marsh AM, Nunn JF, Taylor SJ, Charlesworth CH. Airwayobstruction associated with the use of the Guedel airway.Br J Anaesth 1991;67:51723.

114. Schade K, Borzotta A, Michaels A. Intracranial malpositionof nasopharyngeal airway. J Trauma 2000;49:9678.

115. Muzzi DA, Losasso TJ, Cucchiara RF. Complication from anasopharyngeal airway in a patient with a basilar skull frac-ture. Anesthesiology 1991;74:3668.

116. Roberts K, Porter K. How do you size a nasopharyngeal air-way. Resuscitation 2003;56:1923.

117. Stoneham MD. The nasopharyngeal airway. Assessmentof position by breoptic laryngoscopy. Anaesthesia1993;48:57580.

118. Moser DK, Dracup K, Doering LV. Effect of cardiopulmonaryresuscitation training for parents of high-risk neonateson perceived anxiety, control, and burden. Heart Lung1999;28:32633.

119. Kandakai T, King K. Perceived self-efcacy in perform-ing lifesaving skills: an assessment of the American RedCrosss Responding to Emergencies course. J Health Educ1999;30:23541.

120. Lester CA, Donnelly PD, Assar D. Lay CPR trainees: retrain-ing, condence and willingness to attempt resuscitation 4years after training. Resuscitation 2000;45:7782.

121. Pane GA, Salness KA. A survey of participants in a mass CPRtraining course. Ann Emerg Med 1987;16:11126.

122. Heilman KM, Muschenheim C. Primary cutaneous tubercu-losis resulting from mouth-to-mouth respiration. N Engl JMed 1965;273:10356.

123. Christian MD, Loutfy M, McDonald LC, et al. Possible SARScoronavirus transmission during cardiopulmonary resusci-tation. Emerg Infect Dis 2004;10:28793.

124. Alexander R, Hodgson P, Lomax D, Bullen C. A comparisonof the laryngeal mask airway and Guedel airway, bag andface mask for manual ventilation following formal training.Anaesthesia 1993;48:2314.

125. Dorges V, Sauer C, Ocker H, Wenzel V, Schmucker P.Smaller tidal volumes during cardiopulmonary resuscita-tion: comparison of adult and paediatric self-inatablebags with three different ventilatory devices. Resuscita-tion 1999;43:317.

126. Ocker H, Wenzel V, Schmucker P, Dorges V. Effective-ness of various airway management techniques in a benchmodel simulating a cardiac arrest patient. J Emerg Med2001;20:712.

127. Stone BJ,ChantlerPJ, Baskett PJ.The incidence of regurgi-tation during cardiopulmonary resuscitation: a comparisonbetween the bag valve mask and laryngeal mask airway.Resuscitation 1998;38:36.

128. Hartsilver EL, Vanner RG. Airway obstruction with cricoidpressure. Anaesthesia 2000;55:20811.

129. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al.Hyperventilation-induced hypotension during cardiopul-monary resuscitation. Circulation 2004;109:19605.

130. Stallinger A, Wenzel V, Wagner-Berger H, et al. Effects ofdecreasing inspiratory ow rate during simulated basic lifesupport ventilation of a cardiac arrest patient on lung andstomach tidal volumes. Resuscitation 2002;54:16773.

131. Noordergraaf GJ, van Dun PJ, Kramer BP, et al. Canrst responders achieve and maintain normocapnia whensequentially ventilating with a bag-valve device and twooxygen-driven resuscitators? A controlled clinical trial in104 patients. Eur J Anaesthesiol 2004;21:36772.


41/48


42/48


172. Gausche M, Lewis RJ, Stratton SJ, et al. Effect of out-of-hospital pediatric endotracheal intubation on survivaland neurological outcome: a controlled clinical trial. JAMA2000;283:783970.

173. Guly UM, Mitchell RG, Cook R, Steedman DJ, Robert-son CE. Paramedics and technicians are equally suc-cessful at managing cardiac arrest outside hospital. BMJ1995;310:10914.

174. Stiell IG, Wells GA, Field B, et al. Advanced cardiac lifesupport in out-of-hospital cardiac arrest. N Engl J Med2004;351:64756.

175. Garza AG, Gratton MC, Coontz D, Noble E, Ma OJ. Effectof paramedic experience on orotracheal intubation successrates. J Emerg Med 2003;25:2516.

176. Li J. Capnography alone is imperfect for endotracheal tubeplacement conrmation during emergency intubation. JEmerg Med 2001;20:2239.

177. Tanigawa K, Takeda T, Goto E, Tanaka K. Accuracy andrelia-bility of the self-inating bulb to verify tracheal intubationin out-of-hospital cardiac arrest patients. Anesthesiology2000;93:14326.

178. Takeda T, Tanigawa K, Tanaka H, Hayashi Y, Goto E, TanakaK. The assessment of three methods to verify trachealtube placement in the emergency setting. Resuscitation2003;56:1537.

179. Baraka A, Khoury PJ, Siddik SS, Salem MR, Joseph NJ. Ef-cacy of the self-inating bulb in differentiating esophagealfrom tracheal intubation in the parturient undergoingcesarean section. Anesth Analg 1997;84:5337.

180. Davis DP, Stephen KA, Vilke GM. Inaccuracy in endotra-cheal tube verication using a Toomey syringe. J EmergMed 1999;17:358.

181. Grmec S. Comparison of three different methods to conrmtracheal tube placement in emergency intubation. Inten-sive Care Med 2002;28:7014.

182. American Heart Association in collaboration with Interna-tional Liaison Committee on Resuscitation. Guidelines 2000for Cardiopulmonary Resuscitation and Emergency Cardio-vascular Care: International Consensus on Science. Part 6.Advanced Cardiovascular Life Support: Section 6. Pharma-cology II: Agents to Optimize Cardiac Output and BloodPressure. Circulation 2000;102(Suppl. I):I12935.

183. Lindner KH, Strohmenger HU, Ensinger H, Hetzel WD, Ahne-feld FW, Georgieff M. Stress hormone response duringand after cardiopulmonary resuscitation. Anesthesiology1992;77:6628.

184. Lindner KH, Haak T, Keller A, Bothner U, Lurie KG. Releaseof endogenous vasopressors during and after cardiopul-monary resuscitation. Heart 1996;75:14550.

185. Morris DC, Dereczyk BE, Grzybowski M, et al. Vaso-pressin can increase coronary perfusion pressure duringhuman cardiopulmonary resuscitation. Acad Emerg Med1997;4:87883.

186. Lindner KH, Prengel AW, Brinkmann A, Strohmenger HU,Lindner IM, Lurie KG. Vasopressin administration in refrac-tory cardiac arrest. Ann Intern Med 1996;124:10614.

187. Lindner KH, Brinkmann A, Pfenninger EG, Lurie KG, GoertzA, Lindner IM. Effect of vasopressin on hemodynamicvariables, organ blood ow, and acidbase status in apig model of cardiopulmonary resuscitation. Anesth Analg1993;77:42735.

188. Lindner KH, Prengel AW, Pfenninger EG, et al. Vaso-pressin improves vital organ blood ow during closed-chest cardiopulmonary resuscitation in pigs. Circulation1995;91:21521.

189. Wenzel V, Lindner KH, Prengel AW, et al. Vasopressinimproves vital organ blood ow after prolonged cardiac

arrest with postcountershock pulseless electrical activityin pigs. Crit Care Med 1999;27:48692.

190. Voelckel WG, Lurie KG, McKnite S, et al. Comparison ofepinephrine and vasopressin in a pediatric porcine model ofasphyxial cardiac arrest. Crit Care Med 2000;28:377783.

191. Babar SI, Berg RA, Hilwig RW, Kern KB, Ewy GA. Vaso-pressin versus epinephrine during cardiopulmonary resus-citation: a randomized swine outcome study. Resuscitation1999;41:18592.

192. Lindner KH, Dirks B, Strohmenger HU, Prengel AW, LindnerIM, Lurie KG. Randomised comparison of epinephrine andvasopressin in patients with out-of-hospital ventricular b-rillation. Lancet 1997;349:5357.

193. Stiell IG, Hebert PC, Wells GA, et al. Vasopressin versusepinephrine for inhospital cardiac arrest: a randomisedcontrolled trial. Lancet 2001;358:1059.

194. Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH,Lindner KH. A comparison of vasopressin and epinephrinefor out-of-hospital cardiopulmonary resuscitation. N Engl JMed 2004;350:10513.

195. Aung K, Htay T. Vasopressin for cardiac arrest: a sys-tematic review and meta-analysis. Arch Intern Med2005;165:1724.

196. Callaham M, Madsen C, Barton C, Saunders C, DaleyM, Pointer J. A randomized clinical trial of high-dose epinephrine and norepinephrine versus standard-dose epinephrine in prehospital cardiac arrest. JAMA1992;268:266772.

197. Masini E, Planchenault J, Pezziardi F, Gautier P, Gagnol JP.Histamine-releasing properties of Polysorbate 80 in vitroand in vivo: correlation with its hypotensive action in thedog. Agents Actions 1985;16:4707.

198. Somberg JC, Bailin SJ, Haffajee CI, et al. Intravenous lido-caine versus intravenous amiodarone (in a new aqueousformulation) for incessant ventricular tachycardia. Am JCardiol 2002;90:8539.

199. Somberg JC, Timar S, Bailin SJ, et al. Lack of a hypoten-sive effect with rapid administration of a new aque-ous formulation of intravenous amiodarone. Am J Cardiol2004;93:57681.

200. Skrifvars MB, Kuisma M, Boyd J, et al. The use of undilutedamiodarone in the management of out-of-hospital cardiacarrest. Acta Anaesthesiol Scand 2004;48:5827.

201. Petrovic T, Adnet F, Lapandry C. Successful resuscitationof ventricular brillation after low-dose amiodarone. AnnEmerg Med 1998;32:5189.

202. Levine JH, Massumi A, Scheinman MM, et al. Intravenousamiodarone for recurrent sustained hypotensive ventricu-lar tachyarrhythmias. Intravenous Amiodarone MulticenterTrial Group. J Am Coll Cardiol 1996;27:6775.

203. Matsusaka T, Hasebe N, Jin YT, Kawabe J, Kikuchi K.Magnesium reduces myocardial infarct size via enhance-ment of adenosine mechanism in rabbits. Cardiovasc Res2002;54:56875.

204. Longstreth Jr WT, Fahrenbruch CE, Olsufka M, Walsh TR,Copass MK, Cobb LA. Randomized clinical trial of mag-nesium, diazepam, or both after out-of-hospital cardiacarrest. Neurology 2002;59:50614.

205. Baraka A, Ayoub C, Kawkabani N. Magnesium therapyfor refractory ventricular brillation. J Cardiothorac VascAnesth 2000;14:1969.

206. Stiell IG, Wells GA, Hebert PC, Laupacis A, Weitzman BN.Association of drug therapy with survival in cardiac arrest:limited role of advanced cardiac life support drugs. AcadEmerg Med 1995;2:26473.

207. Engdahl J, Bang A, Lindqvist J, Herlitz J. Can we denepatients with no and those with some chance of sur-


43/48


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278. Chang MW, Coffeen P, Lurie KG, Shultz J, Bache RJ, WhiteCW. Active compressiondecompression CPR improvesvital organ perfusion in a dog model of ventricular bril-lation. Chest 1994;106:12509.

279. Orliaguet GA, Carli PA, Rozenberg A, Janniere D, SauvalP, Delpech P. End-tidal carbon dioxide during out-of-hospital cardiac arrest resuscitation: comparison of activecompressiondecompression and standard CPR. Ann EmergMed 1995;25:4851.

280. Tucker KJ, Galli F, Savitt MA, Kahsai D, Bresnahan L, Red-berg RF. Active compressiondecompression resuscitation:effect on resuscitation success after in-hospital cardiacarrest. J Am Coll Cardiol 1994;24:2019.

281. Malzer R, ZeinerA, Binder M, et al.Hemodynamiceffects ofactive compressiondecompression after prolonged CPR.Resuscitation 1996;31:24353.

282. Lurie KG, Shultz JJ, Callaham ML, et al. Evaluation ofactive compressiondecompression CPR in victims of out-of-hospital cardiac arrest. JAMA 1994;271:140511.

283. Cohen TJ, Goldner BG, Maccaro PC, et al. A comparisonof active compressiondecompression cardiopulmonaryresuscitation with standard cardiopulmonary resuscitationfor cardiac arrests occurring in the hospital. N Engl J Med1993;329:191821.

284. SchwabTM, Callaham ML,Madsen CD, UtechtTA. A random-ized clinical trial of active compressiondecompressionCPR vs standard CPR in out-of-hospital cardiac arrest intwo cities. JAMA 1995;273:12618.

285. Stiell I, Hebert P, Well G, et al. Tne Ontario trial of activecompressiondecompression cardiopulmonary resuscita-tion for in-hospital and prehospital cardiac arrest. JAMA1996;275:141723.

286. Mauer D, Schneider T, Dick W, Withelm A, Elich D, MauerM. Active compressiondecompression resuscitation: aprospective, randomized study in a two-tiered EMS systemwith physicians in the eld. Resuscitation 1996;33:12534.

287. Nolan J, Smith G, Evans R, et al. The United Kingdompre-hospital study of active compressiondecompressionresuscitation. Resuscitation 1998;37:11925.

288. Luiz T, Ellinger K, Denz C. Activecompressiondecompression cardiopulmonary resus-citation does not improve survival in patients withprehospital cardiac arrest in a physician-manned emer-gency medical system. J Cardiothorac Vasc Anesth1996;10:17886.

289. Plaisance P, Lurie KG, Vicaut E, et al. A compari-son of standard cardiopulmonary resuscitation andactive compressiondecompression resuscitationfor out-of-hospital cardiac arrest. French ActiveCompressionDecompression Cardiopulmonary Resuscita-tion Study Group. N Engl J Med 1999;341:56975.

290. Lafuente-Lafuente C, Melero-Bascones M. Active chestcompressiondecompression for cardiopulmonary resusci-tation. Cochrane Database Syst Rev 2004:CD002751.

291. Baubin M, Rabl W, Pfeiffer KP, Benzer A, Gilly H. Chestinjuries after active compressiondecompression car-diopulmonary resuscitation (ACD-CPR) in cadavers. Resus-citation 1999;43:915.

292. Rabl W, Baubin M, Broinger G, Scheithauer R. Serious com-plications from active compressiondecompressioncardiopulmonary resuscitation. Int J Legal Med1996;109:849.

293. Hoke RS, Chamberlain D. Skeletal chest injuries sec-ondary to cardiopulmonary resuscitation. Resuscitation2004;63:32738.

294. Plaisance P, Lurie KG, Payen D. Inspiratory impedance dur-ing active compressiondecompression cardiopulmonary

resuscitation: a randomized evaluation in patients in car-diac arrest. Circulation 2000;101:98994.

295. Plaisance P, Soleil C, Lurie KG, Vicaut E, Ducros L, PayenD. Use of an inspiratory impedance threshold device ona facemask and endotracheal tube to reduce intratho-racic pressures during the decompression phase of activecompressiondecompression cardiopulmonary resuscita-tion. Crit Care Med 2005;33:9904.

296. Wolcke BB, Mauer DK, Schoefmann MF, et al. Comparisonof standard cardiopulmonary resuscitation versus the com-bination of active compressiondecompression cardiopul-monary resuscitation and an inspiratory impedance thresh-old device for out-of-hospital cardiac arrest. Circulation2003;108:22015.

297. Aufderheide T, Pirrallo R, Provo T, Lurie K. Clini-cal evaluation of an inspiratory impedance thresholddevice during standard cardiopulmonary resuscitation inpatients with out-of-hospital cardiac arrest. Crit Care Med2005;33:73440.

298. Plaisance P, Lurie KG, Vicaut E, et al. Evaluation of animpedance threshold device in patients receiving activecompressiondecompression cardiopulmonary resuscita-tion for out of hospital cardiac arrest. Resuscitation2004;61:26571.

299. Sunde K, Wik L, Steen PA. Quality of mechanical, manualstandard and active compressiondecompression CPR onthe arrest site and during transport in a manikin model.Resuscitation 1997;34:23542.

300. Wik L, Bircher NG, Safar P. A comparison of prolongedmanual and mechanical external chest compression aftercardiac arrest in dogs. Resuscitation 1996;32:24150.

301. Dickinson ET, Verdile VP, Schneider RM, Salluzzo RF. Effec-tiveness of mechanical versus manual chest compressionsin out-of-hospital cardiac arrest resuscitation: a pilotstudy.Am J Emerg Med 1998;16:28992.

302. McDonald JL. Systolic and mean arterial pressures duringmanual and mechanical CPR in humans. Ann Emerg Med1982;11:2925.

303. WardKR, Menegazzi JJ,Zelenak RR, Sullivan RJ,McSwain JrN. A comparison of chest compressions between mechan-ical and manual CPR by monitoring end-tidal PCO 2 duringhuman cardiac arrest. Ann Emerg Med 1993;22:66974.

304. Steen S, Liao Q, Pierre L, Paskevicius A, Sjoberg T. Eval-uation of LUCAS, a new device for automatic mechani-cal compression and active decompression resuscitation.Resuscitation 2002;55:28599.

305. Rubertsson S, Karlsten R. Increased cortical cerebral bloodow with LUCAS; a new device for mechanical chest com-pressions compared to standard external compressions dur-ing experimental cardiopulmonary resuscitation. Resusci-tation 2005;65:35763.

306. Nielsen N, Sandhall L, Schersten F, Friberg H, Olsson SE.Successful resuscitation with mechanical CPR, therapeu-tic hypothermia and coronary intervention during man-ual CPR after out-of-hospital cardiac arrest. Resuscitation2005;65:1113.

307. Timerman S, Cardoso LF, Ramires JA, Halperin H. Improvedhemodynamic performance with a novel chest compres-sion device during treatment of in-hospital cardiac arrest.Resuscitation 2004;61:27380.

308. Halperin H, Berger R, Chandra N, et al. Cardiopulmonaryresuscitation with a hydraulic-pneumatic band. Crit CareMed 2000;28:N2036.

309. Halperin HR, Paradis N, Ornato JP, et al. Cardiopulmonaryresuscitation with a novel chest compression device in aporcine model of cardiac arrest: improved hemodynamicsand mechanisms. J Am Coll Cardiol 2004;44:221420.


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ALS 05 ERC Guidelines 2005 Section4