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Resuscitation (2005) 67S1, S1—S2

Preface

This supplement of Resuscitation contains the Euro- co-chairman, for thanks and praise. He is univer-
pean Resuscitation Council (ERC) Guidelines for sally respected and popular, and has proved to be
Resuscitation 2005. It is derived from the 2005 a wonderful ambassador for Europe. His scientific
International Consensus Conference on Cardiopul- credibility and understanding are beyond doubt and
monary Resuscitation and Emergency Cardiovascu- his integrity, dedication, sheer hard work, patience
lar Care Science with Treatment Recommendations and meticulous attention to detail and sensitivities
produced by the International Liaison Committee have won the admiration of all. He has led the Con-
on Resuscitation (ILCOR) published simultaneously sensus on Science process on our behalf, and has
in an issue of Resuscitation. been the lead co-ordinator in producing the Euro-
The European representatives at that Confer- pean Guidelines.
ence, held in Dallas in January 2005, more than Finally we thank our publishers, Elsevier, through
pulled their weight in the process of producing the the Publishing Editor for Resuscitation, Anne Lloyd
Consensus on Science conclusions arising as a result and her colleagues, for their professionalism, tol-
of presentations and debate. Their names are listed erance and patience in these endeavours.
at the end of this Foreword, and the resuscitation
community in Europe and beyond is most grateful
to them for their talent, dedication and selfless
hard work. In addition, they, and many others from Representatives from Europe at the
Europe, also produced worksheets addressing the International Consensus Conference
evidence for and against every conceivable detail held in Dallas, USA, in January 2005
of resuscitation theory and practice.
The ERC Guidelines contain recommendations Hans-Richard Arntz (Germany), Dennis Azzopardi
that, by consensus of the European representatives, (UK), Jan Bahr (Germany), Gad Bar-Joseph (Israel),
are suitable for European practice in the light of Peter Baskett (UK), Michael Baubin (Austria),
today’s conclusions agreed in the Consensus on Sci- Dominique Biarent (Belgium), Bob Bingham (UK),
ence. As with the Consensus on Science document, Bernd Böttiger (Germany), Leo Bossaert (Belgium),
they represent an enormous amount of work by Steven Byrne (UK), Pierre Carli (France), Pascal
many people who have worked against the clock Cassan (France), Sian Davies (UK), Charles Deakin
to produce the Guidelines for Europe. Each section (UK), Burkhard Dirks (Germany), Volker Doerges
of the Guidelines has been masterminded and coor- (Germany), Hans Domanovits (Austria), Christoph
dinated by the leaders of the ERC working groups Eich (Germany), Lars Ekstrom (Sweden), Peter
and areas of special interest. Fenici (Italy), F. Javier Garcia-Vega (Spain), Hen-
Such ventures do not happen without leader- rik Gervais (Germany) Anthony Handley (UK), Johan
ship, and we are grateful to Vinay Nadkarni, Bill Herlitz (Sweden), Fulvio Kette (Italy), Rudolph
Montgomery, Peter Morley, Mary Fran Hazinski, Arno Koster (Netherlands), Kristian Lexow (Norway),
Zaritsky, and Jerry Nolan for guiding the Consensus Perttu Lindsberg (Finland), Freddy Lippert (Den-
on Science process through to completion. It would mark), Vit Marecek (Czech Republic), Koenraad
not be invidious to single out Jerry Nolan, the ILCOR Monsieurs (Belgium), Jerry Nolan (UK), Narcisco

0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.
doi:10.1016/j.resuscitation.2005.10.001
S2 Preface

Perales (Spain), Gavin Perkins (UK), Sam Rich- bach (Germany), Christian Torp Pederson (Den-
mond (UK), Antonio Rodriquez Nunez (Spain), Sten mark), Volker Wenzel (Austria), Lars Wik (Norway),
Rubertsson (Sweden), Sebastian Russo (Germany), Benno Wolke (Germany), Jonathan Wyllie (UK),
Jas Soar (UK), Eldar Soreide (Norway), Petter Steen David Zideman (UK).
(Norway), Benjamin Stenson (UK), Kjetil Sunde Peter Baskett
(Norway), Caroline Telion (France), Andreas Thier- David Zideman
Resuscitation (2005) 67S1, S7—S23

European Resuscitation Council Guidelines for


Resuscitation 2005
Section 2. Adult basic life support and use of
automated external defibrillators
Anthony J. Handley, Rudolph Koster, Koen Monsieurs, Gavin D. Perkins,
Sian Davies, Leo Bossaert

Basic life support (BLS) refers to maintaining airway effectively.9 Many victims of SCA can survive if
patency and supporting breathing and the circula- bystanders act immediately while VF is still present,
tion, without the use of equipment other than a but successful resuscitation is unlikely once the
protective device.1 This section contains the guide- rhythm has deteriorated to asystole.10 The opti-
lines for adult BLS by lay rescuers and for the use mum treatment for VF cardiac arrest is immediate
of an automated external defibrillator (AED). It bystander CPR (combined chest compression and
also includes recognition of sudden cardiac arrest, rescue breathing) plus electrical defibrillation. The
the recovery position and management of choking predominant mechanism of cardiac arrest in victims
(foreign-body airway obstruction). Guidelines for of trauma, drug overdose, drowning, and in many
in-hospital BLS and the use of manual defibrillators children is asphyxia; rescue breaths are critical for
may be found in Sections 3 and 4b. resuscitation of these victims.
The following concept of the Chain of Survival
summarises the vital steps needed for success-
ful resuscitation (Figure 1.1). Most of these links
Introduction
are relevant for victims of both VF and asphyxial
arrest.11
Sudden cardiac arrest (SCA) is a leading cause of
death in Europe, affecting about 700,000 individ- 1. Early recognition of the emergency and call-
uals a year.2 At the time of the first heart rhythm ing for help: activate the emergency medical
analysis, about 40% of SCA victims have ventricular services (EMS) or local emergency response sys-
fibrillation (VF).3—6 It is likely that many more vic- tem, e.g. ‘‘phone 112’’.12,13 An early, effective
tims have VF or rapid ventricular tachycardia (VT) response may prevent cardiac arrest.
at the time of collapse but, by the time the first 2. Early bystander CPR: immediate CPR can double
ECG is recorded, their rhythm has deteriorated to or triple survival from VF SCA.10,14—17
asystole.7,8 VF is characterized by chaotic, rapid 3. Early defibrillation: CPR plus defibrillation
depolarisation and repolarisation. The heart loses within 3—5 min of collapse can produce survival
its coordinated function and stops pumping blood rates as high as 49—75%.18—25 Each minute of

0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.
doi:10.1016/j.resuscitation.2005.10.007
S8 A.J. Handley et al.

delay in defibrillation reduces the probability of


survival to discharge by 10—15%.14,17
4. Early advanced life support and post-
resuscitation care: the quality of treatment
during the post-resuscitation phase affects
outcome.26

In most communities, the time from EMS call to


EMS arrival (response interval) is 8 min or longer.27
During this time the victim’s survival is dependent
on early initiation by bystanders of the first three
of the links of the Chain of Survival.
Victims of cardiac arrest need immediate CPR.
This provides a small but critical blood flow to the
heart and brain. It also increases the likelihood
that a defibrillatory shock will terminate VF and
enable the heart to resume an effective rhythm and
effective systemic perfusion. Chest compression is
especially important if a shock cannot be delivered
sooner than 4 or 5 min after collapse.28,29 Defibril-
lation interrupts the uncoordinated depolarisation-
repolarisation process that occurs during VF. If
the heart is still viable, its normal pacemakers
then resume their function and produce an effec-
tive rhythm and resumption of circulation. In the
first few minutes after successful defibrillation, the Figure 2.1 Adult basic life support algorithm.
rhythm may be slow and ineffective; chest com-
pressions may be needed until adequate cardiac • gently shake his shoulders and ask loudly:
function returns.30 ‘‘Are you all right?’’
Lay rescuers can be trained to use an automated 3a If he responds
external defibrillator (AED) to analyse the victim’s • leave him in the position in which you find him
cardiac rhythm and deliver a shock if VF is present. provided there is no further danger
An AED uses voice prompts to guide the rescuer. It • try to find out what is wrong with him and get
analyses the ECG rhythm and informs the rescuer help if needed
if a shock is needed. AEDs are extremely accurate • reassess him regularly
and will deliver a shock only when VF (or its precur-
sor, rapid ventricular tachycardia) is present.31 AED
function and operation are discussed in Section 3.
Several studies have shown the benefit on sur-
vival of immediate CPR, and the detrimental effect
of delay before defibrillation. For every minute
without CPR, survival from witnessed VF decreases
by 7—10%.10 When bystander CPR is provided, the
decline in survival is more gradual and averages
3—4% min−1 .10,14,17 Overall, bystander CPR dou-
bles or triples survival from witnessed cardiac
arrest.10,14,32

Adult BLS sequence

BLS consists of the following sequence of actions


(Figure 2.1).

1 Make sure you, the victim and any bystanders


are safe. Figure 2.2 Check the victim for a response. © 2005
2 Check the victim for a response (Figure 2.2). European Resuscitation Council.
European Resuscitation Council Guidelines for Resuscitation 2005 S9

Figure 2.3 Shout for help. © 2005 European Resuscita-


tion Council.

3b If he does not respond Figure 2.5 Head tilt and chin lift in detail. © 2005 Euro-
pean Resuscitation Council.
• shout for help (Figure 2.3)
• turn the victim onto his back and then
index finger free to close his nose if rescue
open the airway using head tilt and chin lift
breathing is required (Figure 2.5)
(Figure 2.4)
◦ with your fingertips under the point of the
◦ place your hand on his forehead and gently
victim’s chin, lift the chin to open the air-
tilt his head back keeping your thumb and
way
4 Keeping the airway open, look, listen and feel
for normal breathing (Figure 2.6).
• Look for chest movement.
• Listen at the victim’s mouth for breath
sounds.
• Feel for air on your cheek.
In the first few minutes after cardiac arrest, a
victim may be barely breathing, or taking infre-
quent, noisy gasps. Do not confuse this with
normal breathing. Look, listen, and feel for no

Figure 2.4 Head tilt and chin lift. © 2005 European Figure 2.6 Look listen and feel for normal breathing.
Resuscitation Council. © 2005 European Resuscitation Council.
S10 A.J. Handley et al.

Figure 2.7 The recovery position. © 2005 European Resuscitation Council.

more than 10 s to determine whether the vic- press down on the sternum 4—5 cm
tim is breathing normally. If you have any doubt (Figure 2.11)
whether breathing is normal, act as if it is not ◦ after each compression, release all the
normal. pressure on the chest without losing con-
5a If he is breathing normally tact between your hands and the sternum;
• turn him into the recovery position (see repeat at a rate of about 100 min−1 (a little
below) (Figure 2.7) less than 2 compressions s−1 )
• send or go for help/call for an ambulance ◦ compression and release should take equal
• check for continued breathing amounts of time
5b If he is not breathing normally 6a Combine chest compression with rescue
• send someone for help or, if you are on your breaths.
own, leave the victim and alert the ambu- • After 30 compressions open the airway again
lance service; return and start chest compres- using head tilt and chin lift (Figure 2.12).
sion as follows: • Pinch the soft part of the nose closed, using
◦ kneel by the side of the victim the index finger and thumb of your hand on
◦ place the heel of one hand in the centre of the forehead.
the victim’s chest (Figure 2.8) • Allow the mouth to open, but maintain chin
◦ place the heel of your other hand on top of lift.
the first hand (Figure 2.9) • Take a normal breath and place your lips
◦ interlock the fingers of your hands and around his the mouth, making sure that you
ensure that pressure is not applied over the have a good seal.
victim’s ribs (Figure 2.10). Do not apply any • Blow steadily into the mouth while watch-
pressure over the upper abdomen or the ing for the chest to rise (Figure 2.13), taking
bottom end of the bony sternum (breast- about 1 s as in normal breathing; this is an
bone) effective rescue breath.
◦ position yourself vertically above the vic- • Maintaining head tilt and chin lift, take your
tim’s chest and, with your arms straight, mouth away from the victim and watch for the
chest to fall as air passes out (Figure 2.14).

Figure 2.8 Place the heel of one hand in the centre of


the victim’s chest. © 2005 European Resuscitation Coun- Figure 2.9 Place the heel of your other hand on top of
cil. the first hand. © 2005 European Resuscitation Council.
European Resuscitation Council Guidelines for Resuscitation 2005 S11

Figure 2.10 Interlock the fingers of your hands. © 2005 Figure 2.11 Press down on the sternum 4—5 cm. © 2005
European Resuscitation Council. European Resuscitation Council.

• Take another normal breath and blow into the


victim’s mouth once more, to achieve a total
of two effective rescue breaths. Then return
your hands without delay to the correct posi-
tion on the sternum and give a further 30
chest compressions.
• Continue with chest compressions and rescue
breaths in a ratio of 30:2.
• Stop to recheck the victim only if he starts
breathing normally; otherwise do not inter-
rupt resuscitation.
If your initial rescue breath does not make the
chest rise as in normal breathing, then before
your next attempt:
• check the victim’s mouth and remove any
obstruction
• recheck that there is adequate head tilt and Figure 2.12 After 30 compressions open the airway
chin lift again using head tilt and chin lift. © 2005 European Resus-
• do not attempt more than two breaths each citation Council.
time before returning to chest compressions
If there is more than one rescuer present, 6b Chest-compression-only CPR may be used as fol-
another should take over CPR every 1—2 min to lows.
prevent fatigue. Ensure the minimum of delay • If you are not able or are unwilling to give
during the changeover of rescuers. rescue breaths, give chest compressions only.
S12 A.J. Handley et al.

adverse effects from undertaking CPR, with only


isolated reports of infections such as tuberculosis
(TB)33 and severe acute respiratory distress syn-
drome (SARS).34 Transmission of HIV during CPR
has never been reported. There have been no
human studies to address the effectiveness of bar-
rier devices during CPR; however, laboratory stud-
ies have shown that certain filters, or barrier
devices with one-way valves, prevent oral bacterial
transmission from the victim to the rescuer during
mouth-to-mouth ventilation.35,36 Rescuers should
take appropriate safety precautions where feasi-
ble, especially if the victim is known to have a
serious infection, such as TB or SARS. During an
outbreak of a highly infectious condition such as
SARS, full protective precautions for the rescuer are
essential.
Figure 2.13 Blow steadily into his mouth whilst watch-
ing for his chest to rise. © 2005 European Resuscitation
Council. Opening the airway

• If chest compressions only are given, these The jaw thrust is not recommended for lay res-
should be continuous, at a rate of 100 min−1 . cuers because it is difficult to learn and perform
• Stop to recheck the victim only if he starts and may itself cause spinal movement.37 Therefore,
breathing normally; otherwise do not inter- the lay rescuer should open the airway using a head
rupt resuscitation. tilt-chin lift manoeuvre for both injured and non-
7 Continue resuscitation until injured victims.
• qualified help arrives and takes over
• the victim starts breathing normally Recognition of cardiorespiratory arrest
• you become exhausted
Checking the carotid pulse is an inaccurate
method of confirming the presence or absence
Risk to the rescuer
of circulation.38 However, there is no evidence
The safety of both rescuer and victim are that checking for movement, breathing or cough-
paramount during a resuscitation attempt. There ing (‘signs of a circulation’) is diagnostically supe-
have been few incidents of rescuers suffering rior. Healthcare professionals as well as lay rescuers
have difficulty determining the presence or absence
of adequate or normal breathing in unresponsive
victims.39,40 This may be because the airway is
not open41 or because the victim is making occa-
sional (agonal) gasps. When bystanders are asked
by ambulance dispatchers over the telephone if
breathing is present, they often misinterpret agonal
gasps as normal breathing. This erroneous informa-
tion can result in the bystander withholding CPR
from a cardiac arrest victim.42 Agonal gasps are
present in up to 40% of cardiac arrest victims.
Bystanders describe agonal gasps as barely breath-
ing, heavy or laboured breathing, or noisy or gasp-
ing breathing.43
Laypeople should, therefore, be taught to begin
CPR if the victim is unconscious (unresponsive) and
not breathing normally. It should be emphasised
during training that agonal gasps occur commonly
Figure 2.14 Take your mouth away from the victim and in the first few minutes after SCA. They are an indi-
watch for his chest to fall as air comes out. © 2005 Euro- cation for starting CPR immediately and should not
pean Resuscitation Council. be confused with normal breathing.
European Resuscitation Council Guidelines for Resuscitation 2005 S13

Initial rescue breaths rise, but to avoid rapid or forceful breaths This
recommendation applies to all forms of ventilation
During the first few min after non-asphyxial cardiac during CPR, including mouth-to-mouth and bag-
arrest the blood oxygen content remains high, and valve-mask (BVM) with and without supplementary
myocardial and cerebral oxygen delivery is limited oxygen.
more by the diminished cardiac output than a lack Mouth-to-nose ventilation is an effective alter-
of oxygen in the lungs. Ventilation is, therefore, native to mouth-to-mouth ventilation.57 It may be
initially less important than chest compression.44 considered if the victim’s mouth is seriously injured
It is well recognised that skill acquisition and or cannot be opened, the rescuer is assisting a vic-
retention is aided by simplification of the BLS tim in the water, or a mouth-to-mouth seal is diffi-
sequence of actions.45 It is also recognized that cult to achieve.
rescuers are frequently unwilling to carry out There is no published evidence on the
mouth-to-mouth ventilation for a variety of rea- safety, effectiveness or feasibility of mouth-
sons, including fear of infection and distaste for the to-tracheostomy ventilation, but it may be used
procedure.46—48 For these reasons, and to empha- for a victim with a tracheostomy tube or tracheal
sise the priority of chest compressions, it is recom- stoma who requires rescue breathing.
mended that in adults CPR should start with chest To use bag-mask ventilation requires consider-
compression rather than initial ventilation. able practice and skill.58,59 The lone rescuer has
to be able to open the airway with a jaw thrust
Ventilation while simultaneously holding the mask to the vic-
tim’s face. It is a technique that is appropriate
During CPR the purpose of ventilation is to maintain only for lay rescuers who work in highly specialised
adequate oxygenation. The optimal tidal volume, areas, such as where there is a risk of cyanide poi-
respiratory rate and inspired oxygen concentration soning or exposure to other toxic agents. There
to achieve this, however, are not fully known. The are other specific circumstances in which non-
current recommendations are based on the follow- healthcare providers receive extended training in
ing evidence: first aid which could include training, and retrain-
1. During CPR, blood flow to the lungs is sub- ing, in the use of bag-mask ventilation. The same
stantially reduced, so an adequate ventilation- strict training that applies to healthcare profession-
perfusion ratio can be maintained with lower als should be followed.
tidal volumes and respiratory rates than Chest compression
normal.49
2. Not only is hyperventilation (too many breaths Chest compressions produce blood flow by increas-
or too large a volume) unnecessary, but it is ing the intrathoracic pressure and by directly com-
harmful because it increases intrathoracic pres- pressing the heart. Although chest compressions
sure, thus decreasing venous return to the heart performed properly can produce systolic arterial
and diminishing cardiac output. Survival is con- pressure peaks of 60—80 mmHg, diastolic pressure
sequently reduced.50 remains low and mean arterial pressure in the
3. When the airway is unprotected, a tidal volume carotid artery seldom exceeds 40 mmHg.60 Chest
of 1 l produces significantly more gastric disten- compressions generate a small but critical amount
tion than a tidal volume of 500 ml.51 of blood flow to the brain and myocardium and
4. Low minute-ventilation (lower than normal tidal increase the likelihood that defibrillation will be
volume and respiratory rate) can maintain successful. They are especially important if the first
effective oxygenation and ventilation during shock is delivered more than 5 min after collapse.61
CPR.52—55 During adult CPR, tidal volumes of Much of the information about the physiology of
approximately 500—600 ml (6—7 ml kg−1 ) should chest compression and the effects of varying the
be adequate. compression rate, compression-to-ventilation ratio
5. Interruptions in chest compression (for exam- and duty cycle (ratio of time chest is compressed
ple to give rescue breaths) have a detrimental to total time from one compression to the next) is
effect on survival.56 Giving rescue breaths over derived from animal models. However, the conclu-
a shorter time will help to reduce the duration sions of the 2005 Consensus Conference62 included
of essential interruptions. the following:
The current recommendation is, therefore, for (1) Each time compressions are resumed, the res-
rescuers to give each rescue breath over about 1 s, cuer should place his hands without delay ‘‘in
with enough volume to make the victim’s chest the centre of the chest’’.63
S14 A.J. Handley et al.

(2) Compress the chest at a rate of about mouth ventilation in unknown victims of cardiac
100 min−1 .64—66 arrest.46,48 Animal studies have shown that chest
(3) Pay attention to achieving the full compression compression-only CPR may be as effective as com-
depth of 4—5 cm (for an adult).67,68 bined ventilation and compression in the first few
(4) Allow the chest to recoil completely after each minutes after non-asphyxial arrest.44,79 In adults,
compression.69,70 the outcome of chest compression without venti-
(5) Take approximately the same amount of time lation is significantly better than the outcome of
for compression and relaxation. giving no CPR.80 If the airway is open, occasional
(6) Minimise interruptions in chest compression. gasps and passive chest recoil may provide some air
(7) Do not rely on a palpable carotid or femoral exchange.81,82 A low minute-ventilation may be all
pulse as a gauge of effective arterial flow.38,71 that is necessary to maintain a normal ventilation-
perfusion ratio during CPR.
There is insufficient evidence to support a spe- Laypeople should, therefore, be encouraged to
cific hand position for chest compression during CPR perform compression-only CPR if they are unable
in adults. Previous guidelines have recommended a or unwilling to provide rescue breaths, although
method of finding the middle of the lower half of combined chest compression and ventilation is the
the sternum by placing one finger on the lower end better method of CPR.
of the sternum and sliding the other hand down to
it.72 It has been shown that for healthcare profes-
sionals the same hand position can be found more CPR in confined spaces
quickly if rescuers are taught to ‘‘place the heel
of your hand in the centre of the chest with the Over-the-head CPR for single rescuers and straddle
other hand on top’’, provided the teaching includes CPR for two rescuers may be considered for resus-
a demonstration of placing the hands in the middle citation in confined spaces.83,84
of the lower half of the sternum.63 It is reasonable
to extend this to laypeople.
Compression rate refers to the speed at which Recovery position
compressions are given, not the total number deliv-
There are several variations of the recovery posi-
ered in each minute. The number delivered is
tion, each with its own advantages. No single posi-
determined by the rate, but also by the number
tion is perfect for all victims.85,86 The position
of interruptions to open the airway, deliver res-
should be stable, near a true lateral position with
cue breaths and allow AED analysis. In one out-
the head dependent, and with no pressure on the
of-hospital study rescuers recorded compression
chest to impair breathing.87
rates of 100—120 min−1 but, the mean number of
The ERC recommends the following sequence
compressions was reduced to 64 min−1 by frequent
of actions to place a victim in the recovery
interruptions.68
position:
Compression—ventilation ratio
• Remove the victim’s spectacles.
Insufficient evidence from human outcome studies • Kneel beside the victim and make sure that both
exists to support any given compression:ventilation legs are straight.
ratio. Animal data support an increase in the ratio • Place the arm nearest to you out at right angles to
above 15:2.73—75 A mathematical model suggests the body, elbow bent with the hand palm upper-
that a ratio of 30:2 would provide the best compro- most (Figure 2.15).
mise between blood flow and oxygen delivery.76,77 • Bring the far arm across the chest, and hold the
A ratio of 30 compressions to two ventilations is back of the hand against the victim’s cheek near-
recommended for the single rescuer attempting est to you (Figure 2.16).
resuscitation on an adult or child out of hospi- • With your other hand, grasp the far leg just above
tal. This should decrease the number of inter- the knee and pull it up, keeping the foot on the
ruptions in compression, reduce the likelihood ground (Figure 2.17).
of hyperventilation,50,78 simplify instruction for • Keeping his hand pressed against his cheek, pull
teaching and improve skill retention. on the far leg to roll the victim towards you onto
his side.
Compression-only CPR • Adjust the upper leg so that both hip and knee
are bent at right angles.
Healthcare professionals as well as lay rescuers • Tilt the head back to make sure the airway
admit to being reluctant to perform mouth-to- remains open.
European Resuscitation Council Guidelines for Resuscitation 2005 S15

Figure 2.15 Place the arm nearest to you out at right


angles to his body, elbow bent with the hand palm upper-
most. © 2005 European Resuscitation Council.

Figure 2.18 The recovery position. © 2005 European


Resuscitation Council.

• Adjust the hand under the cheek, if necessary, to


keep the head tilted (Figure 2.18).
• Check breathing regularly.

If the victim has to be kept in the recovery posi-


Figure 2.16 Bring the far arm across the chest, and hold
the back of the hand against the victim’s cheek nearest tion for more than 30 min turn him to the opposite
to you. © 2005 European Resuscitation Council. side to relieve the pressure on the lower arm.

Foreign-body airway obstruction (choking)

Foreign-body airway obstruction (FBAO) is an


uncommon but potentially treatable cause of acci-
dental death.88 Each year approximately 16,000
adults and children in the UK receive treatment in
an emergency department for FBAO. Fortunately,
less than 1% of these incidents are fatal.89 The
commonest cause of choking in adults is airway
obstruction caused by food such as fish, meat or
poultry.89 In infants and children, half the reported
episodes of choking occur while eating (mostly con-
fectionery), and the remaining choking episodes
occur with non-food items such as coins or toys.90
Deaths from choking are rare in infants and chil-
Figure 2.17 With your other hand, grasp the far leg just dren; 24 deaths a year on average were reported
above the knee and pull it up, keeping the foot on the in the UK between 1986 and 1995, and over half of
ground. © 2005 European Resuscitation Council. these children were under 1 year.90
S16 A.J. Handley et al.

Table 2.1 Differentiation between mild and severe foreign body airway obstruction (FBAO)a
Sign Mild obstruction Severe obstruction
‘‘Are you choking?’’ ‘‘Yes’’ Unable to speak, may nod
Other signs Can speak, cough, breathe Cannot breathe/wheezy breathing/silent
attempts to cough/unconsciousness
a General signs of FBAO: attack occurs while eating; victim may clutch at neck.

As most choking events are associated with eat- • Apply up to five back blows as follows.
ing, they are commonly witnessed. Thus, there is ◦ Stand to the side and slightly behind the vic-
often the opportunity for early intervention while tim.
the victim is still responsive. ◦ Support the chest with one hand and lean
the victim well forwards so that when the
obstructing object is dislodged it comes out
Recognition
of the mouth rather than goes further down
Because recognition of airway obstruction is the key the airway.
to successful outcome, it is important not to con- ◦ Give up to five sharp blows between the
fuse this emergency with fainting, heart attack, shoulder blades with the heel of your other
seizure or other conditions that may cause sud- hand
den respiratory distress, cyanosis or loss of con- • Check to see if each back blow has relieved the
sciousness. Foreign bodies may cause either mild or airway obstruction. The aim is to relieve the
severe airway obstruction. The signs and symptoms obstruction with each slap rather than neces-
enabling differentiation between mild and severe sarily to give all five.
airway obstruction are summarised in Table 2.1. It • If five back blows fail to relieve the airway
is important to ask the conscious victim ‘Are you obstruction, give up to five abdominal thrusts
choking?’ as follows:
◦ Stand behind the victim and put both arms
round the upper part of his abdomen.
Adult FBAO (choking) sequence ◦ Lean the victim forwards.
◦ Clench your fist and place it between the
(This sequence is also suitable for use in children umbilicus and xiphisternum.
over the age of 1 year) (Figure 2.19). ◦ Grasp this hand with your other hand and
1 If the victim shows signs of mild airway obstruc- pull sharply inwards and upwards.
tion ◦ Repeat up to five times.
• Encourage him to continue coughing but do • If the obstruction is still not relieved, continue
nothing else alternating five back blows with five abdominal
2 If the victim shows signs of severe airway obstruc- thrusts.
tion and is conscious 3 If the victim at any time becomes unconscious.

Figure 2.19 Adult foreign body airway obstruction treatment algorithm.


European Resuscitation Council Guidelines for Resuscitation 2005 S17

• Support the victim carefully to the ground. documented harm to the victim96,99 or rescuer.91
• Immediately activate EMS. Therefore, avoid use of a blind finger sweep and
• Begin CPR (from 5b of the adult BLS sequence). manually remove solid material in the airway only
Healthcare providers, trained and experienced if it can be seen.
in feeling for a carotid pulse, should initiate
chest compressions, even if a pulse is present
Aftercare and referral for medical review
in the unconscious choking victim.
Following successful treatment for FBAO, foreign
material may nevertheless remain in the upper or
FBAO causing mild airway obstruction
lower respiratory tract and cause complications
Coughing generates high and sustained airway pres- later. Victims with a persistent cough, difficulty
sures and may expel the foreign body. Aggressive swallowing or the sensation of an object being still
treatment, with back blows, abdominal thrusts and stuck in the throat, should therefore be referred for
chest compression, may cause potentially serious a medical opinion.
complications and could worsen the airway obstruc- Abdominal thrusts can cause serious internal
tion. It should be reserved for victims who have injuries, and all victims treated with abdomi-
signs of severe airway obstruction. Victims with nal thrusts should be examined for injury by a
mild airway obstruction should remain under con- doctor.91
tinuous observation until they improve, as severe
airway obstruction may develop.
Resuscitation of children (see also
FBAO with severe airway obstruction
Section 6) and victims of drowning (see
also Section 7c)
The clinical data on choking are largely retrospec-
tive and anecdotal. For conscious adults and chil- Both ventilation and compression are important
dren over 1 year with a complete FBAO, case reports for victims of cardiac arrest when the oxygen
demonstrate the effectiveness of back blows or stores become depleted—–about 4—6 min after col-
‘slaps’, abdominal thrusts and chest thrusts.91 lapse from VF and immediately after collapse
Approximately 50% of episodes of airway obstruc- from asphyxial arrest. Previous guidelines tried to
tion are not relieved by a single technique.92 The take into account the difference in pathophysiol-
likelihood of success is increased when combina- ogy, and recommended that victims of identifiable
tions of back blows or slaps, and abdominal and asphyxia (drowning; trauma; intoxication) and chil-
chest thrusts are used.91 dren should receive 1 min of CPR before the lone
A randomised trial in cadavers93 and two rescuer left the victim to get help. The majority
prospective studies in anaesthetised volunteers94,95 of cases of SCA out of hospital, however, occur in
showed that higher airway pressures can be gener- adults, and are of cardiac origin due to VF. These
ated using chest thrusts compared with abdominal additional recommendations, therefore, added to
thrusts. Since chest thrusts are virtually identical the complexity of the guidelines while affecting
to chest compressions, rescuers should be taught only a minority of victims.
to start CPR if a victim of known or suspected It is important to be aware that many children
FBAO becomes unconscious. During CPR, each time do not receive resuscitation because potential res-
the airway is opened the victim’s mouth should be cuers fear causing harm. This fear is unfounded;
quickly checked for any foreign body that has been it is far better to use the adult BLS sequence for
partly expelled. The incidence of unsuspected resuscitation of a child than to do nothing. For
choking as a cause of unconsciousness or cardiac ease of teaching and retention, therefore, laypeo-
arrest is low; therefore, during CPR routinely ple should be taught that the adult sequence may
checking the mouth for foreign bodies is not also be used for children who are not responsive
necessary. and not breathing.
The following minor modifications to the adult
sequence will, however, make it even more suitable
The finger sweep for use in children.

No studies have evaluated the routine use of a finger • Give five initial rescue breaths before starting
sweep to clear the airway in the absence of visible chest compressions (adult sequence of actions,
airway obstruction,96—98 and four case reports have 5b).
S18 A.J. Handley et al.

• A lone rescuer should perform CPR for approxi- • push shock button as directed (fully auto-
mately 1 min before going for help. matic AEDs will deliver the shock automat-
• Compress the chest by approximately one third ically)
of its depth; use two fingers for an infant under • continue as directed by the voice/visual
1 year; use one or two hands for a child over 1 prompts
year as needed to achieve an adequate depth of 5b If no shock indicated
compression. • immediately resume CPR, using a ratio of 30
compressions to 2 rescue breaths
The same modifications of five initial breaths, and • continue as directed by the voice/visual
1 min of CPR by the lone rescuer before getting prompts
help, may improve outcome for victims of drown- 6 Continue to follow the AED prompts until
ing. This modification should be taught only to • qualified help arrives and takes over
those who have a specific duty of care to poten- • the victim starts to breathe normally
tial drowning victims (e.g. lifeguards). Drowning is • you become exhausted
easily identified. It can be difficult, on the other
hand, for a layperson to determine whether car-
diorespiratory arrest is a direct result of trauma CPR before defibrillation
or intoxication. These victims should, therefore, be
managed according to the standard protocol. Immediate defibrillation, as soon as an AED
becomes available, has always been a key ele-
ment in guidelines and teaching, and considered of
Use of an automated external paramount importance for survival from ventricu-
defibrillator lar fibrillation. This concept has been challenged
because evidence suggests that a period of chest
Section 3 discusses the guidelines for defibrillation compression before defibrillation may improve sur-
using both automated external defibrillators (AEDs) vival when the time between calling for the ambu-
and manual defibrillators. However, there are some lance and its arrival exceeds 5 min.28,61,100 One
special considerations when an AED is to be used by study101 did not confirm this benefit, but the weight
lay or non-healthcare rescuers. of evidence supports a period of CPR for victims of
Standard AEDs are suitable for use in children prolonged cardiac arrest before defibrillation.
older than 8 years. For children between 1 and 8 In all of these studies CPR was performed by
years use paediatric pads or a paediatric mode if paramedics, who protected the airway by intuba-
available; if these are not available, use the AED as tion and delivered 100% oxygen. Such high-quality
it is. Use of AEDs is not recommended for children ventilation cannot be expected from lay rescuers
less than 1 year. giving mouth-to-mouth ventilation. Secondly, the
benefit from CPR occurred only when the delay from
Sequence for use of an AED call to the availability of a defibrillator was greater
than 5 min; the delay from collapse to arrival of the
See Figure 2.20. rescuer with an AED will rarely be known with cer-
tainty. Thirdly, if good bystander CPR is already in
(1) Make sure you, the victim, and any bystanders progress when the AED arrives, it does not seem
are safe. logical to continue it any further. For these reasons
(2) If the victim is unresponsive and not breathing these guidelines recommend an immediate shock,
normally, send someone for the AED and to call as soon as the AED is available. The importance of
for an ambulance. early uninterrupted external chest compression is
(3) Start CPR according to the guidelines for BLS. emphasised.
(4) As soon as the defibrillator arrives
• switch on the defibrillator and attach the
electrode pads. If more than one rescuer is Voice prompts
present, CPR should be continued while this
is carried out In several places, the sequence of actions states
• follow the spoken/visual directions ‘follow the voice/visual prompts’. The prompts are
• ensure that nobody touches the victim while usually programmable, and it is recommended that
the AED is analysing the rhythm they be set in accordance with the sequence of
5a If a shock is indicated shocks and timings for CPR given in Section 2. These
• ensure that nobody touches the victim should include at least:
European Resuscitation Council Guidelines for Resuscitation 2005 S19

Figure 2.20 Algorithm for use of an automated external defibrillator.

(1) a single shock only, when a shockable rhythm is input from the rescuer. One manikin study showed
detected that untrained nursing students committed fewer
(2) no rhythm check, or check for breathing or a safety errors using a fully-automatic AED rather
pulse, after the shock than a semi-automatic AED.102 There are no human
(3) a voice prompt for immediate resumption of data to determine whether these findings can be
CPR after the shock (giving chest compressions applied to clinical use.
in the presence of a spontaneous circulation is
not harmful)
Public access defibrillation programmes
(4) two minutes for CPR before a prompt to assess
the rhythm, breathing or a pulse is given Public access defibrillation (PAD) and first responder
AED programmes may increase the number of vic-
The shock sequence and energy levels are dis-
tims who receive bystander CPR and early defibril-
cussed in Section 3.
lation, thus improving survival from out-of-hospital
SCA.103 These programmes require an organised
Fully-automatic AEDs and practised response with rescuers trained and
equipped to recognise emergencies, activate the
Having detected a shockable rhythm, a fully- EMS system, provide CPR and use the AED.104,105 Lay
automatic AED will deliver a shock without further rescuer AED programmes with very rapid response
S20 A.J. Handley et al.

times in airports,22 on aircraft23 or in casinos,25 and tality and Morbidity Statistics in Europe. Eur Heart J
1997;18:1231—48.
uncontrolled studies using police officers as first
3. Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK. Chang-
responders,106,107 have achieved reported survival ing incidence of out-of-hospital ventricular fibrillation,
rates as high as 49—74%. 1980—2000. JAMA 2002;288:3008—13.
The logistic problem for first responder pro- 4. Rea TD, Eisenberg MS, Sinibaldi G, White RD. Incidence of
grammes is that the rescuer needs to arrive not EMS-treated out-of-hospital cardiac arrest in the United
States. Resuscitation 2004;63:17—24.
just earlier than the traditional EMS, but within
5. Vaillancourt C, Stiell IG. Cardiac arrest care and
5—6 min of the initial call, to enable attempted emergency medical services in Canada. Can J Cardiol
defibrillation in the electrical or circulatory phase 2004;20:1081—90.
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curve flattens;10,17 a few minutes’ gain in time will diac arrests in Amsterdam and its surrounding areas:
results from the Amsterdam resuscitation study (ARREST)
have little impact when the first responder arrives
in ‘Utstein’ style. Resuscitation 1998;38:157—67.
more than 10 min after the call27,109 or when a first 7. Cummins R, Thies W. Automated external defibrillators and
responder does not improve on an already short the Advanced Cardiac Life Support Program: a new initia-
EMS response time.110 However, small reductions tive from the American Heart Association. Am J Emerg Med
in response intervals achieved by first-responder 1991;9:91—3.
8. Waalewijn RA, Nijpels MA, Tijssen JG, Koster RW. Preven-
programmes that have an impact on many residen-
tion of deterioration of ventricular fibrillation by basic life
tial victims may be more cost effective than the support during out-of-hospital cardiac arrest. Resuscitation
larger reductions in response interval achieved by 2002;54:31—6.
PAD programmes that have an impact on fewer car- 9. Page S, Meerabeau L. Achieving change through reflec-
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2000;20:365—72.
Recommended elements for PAD programmes
10. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP.
include: Predicting survival from out-of-hospital cardiac arrest: a
graphic model. Ann Emerg Med 1993;22:1652—8.
• a planned and practised response 11. Cummins RO, Ornato JP, Thies WH, Pepe PE. Improving
• training of anticipated rescuers in CPR and use of survival from sudden cardiac arrest: the ‘‘chain of sur-
the AED vival’’ concept. A statement for health professionals from
• link with the local EMS system the Advanced Cardiac Life Support Subcommittee and the
• programme of continuous audit (quality improve- Emergency Cardiac Care Committee, American Heart Asso-
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of an out-of-hospital cardiac arrest benefit from a training
Public access defibrillation programmes are most
program for emergency medical dispatchers? Resuscitation
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14. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, Larsen
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MP. Estimating effectiveness of cardiac arrest interven-
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facilities).103 Approximately 80% of out-of-hospital 1997;96:3308—13.
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vival in out-of-hospital cardiac arrest patients in Sweden.
impact that PAD programmes can have on survival
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97. Elam JO, Ruben AM, Greene DG. Resuscitation of drowning 107. Mosesso Jr VN, Davis EA, Auble TE, Paris PM, Yealy DM. Use
victims. JAMA 1960;174:13—6. of automated external defibrillators by police officers for
98. Ruben HM, Elam JO, Ruben AM, Greene DG. Investigation of treatment of out-of-hospital cardiac arrest. Ann Emerg Med
upper airway problems in resuscitation. 1. Studies of pha- 1998;32:200—7.
ryngeal X-rays and performance by laymen. Anesthesiology 108. Weisfeldt M, Becker L. Resuscitation after cardiac arrest.
1961;22:271—9. A 3-phase time-sensitive model. JAMA 2002;288:3035—8.
99. Kabbani M, Goodwin SR. Traumatic epiglottis following 109. Groh WJ, Newman MM, Beal PE, Fineberg NS, Zipes DP. Lim-
blind finger sweep to remove a pharyngeal foreign body. ited response to cardiac arrest by police equipped with
Clin Pediatr (Phila) 1995;34:495—7. automated external defibrillators: lack of survival bene-
100. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopul- fit in suburban and rural Indiana—–the police as responder
monary resuscitation on predictors of ventricular fibrilla- automated defibrillation evaluation (PARADE). Acad Emerg
tion defibrillation success during out-of-hospital cardiac Med 2001;8:324—30.
arrest. Circulation 2004;110:10—5. 110. Sayre M, Evans J, White L, Brennan T. Providing automated
101. Jacobs IG, Finn JC, Oxer HF, Jelinek GA. CPR before defibril- external defibrillators to urban police officers in addition
lation in out-of-hospital cardiac arrest: a randomized trial. to fire department rapid defibrillation program is not effec-
Emerg Med Australas 2005;17:39—45. tive. Resuscitation 2005;66:189—96.
102. Monsieurs KG, Vogels C, Bossaert LL, Meert P, Calle PA. 111. Nichol G, Hallstrom AP, Ornato JP, et al. Potential cost-
A study comparing the usability of fully automatic ver- effectiveness of public access defibrillation in the United
sus semi-automatic defibrillation by untrained nursing stu- States. Circulation 1998;97:1315—20.
dents. Resuscitation 2005;64:41—7. 112. Nichol G, Valenzuela T, Roe D, Clark L, Huszti E, Wells GA.
103. The Public Access Defibrillation Trial Investigators. Cost effectiveness of defibrillation by targeted responders
Public-access defibrillation and survival after out-of- in public settings. Circulation 2003;108:697—703.
hospital cardiac arrest. N Engl J Med 2004;351:637— 113. Becker L, Eisenberg M, Fahrenbruch C, Cobb L. Public loca-
46. tions of cardiac arrest: implications for public access defib-
104. Priori SBL, Chamberlain D, Napolitano C, Arntz HR, Koster rillation. Circulation 1998;97:2106—9.
R, Monsieurs K, Capucci A, Wellens H. Policy Statement: 114. Becker DE. Assessment and management of cardiovascular
ESC-ERC recommendations for the use of AEDs in Europe. urgencies and emergencies: cognitive and technical con-
Eur Heart J 2004;25:437—45. siderations. Anesth Progress 1988;35:212—7.
Resuscitation (2005) 67S1, S3—S6

European Resuscitation Council Guidelines for


Resuscitation 2005
Section 1. Introduction
Jerry Nolan

It is five years since publication of the Guide- sus on treatment recommendations. The process
lines 2000 for Cardiopulmonary Resuscitation (CPR) for the latest resuscitation guideline update began
and Emergency Cardiovascular Care (ECC).1 The in 2003, when ILCOR representatives established
European Resuscitation Council (ERC) based its six task forces: basic life support; advanced car-
own resuscitation guidelines on this document, diac life support; acute coronary syndromes; pae-
and these were published as a series of papers diatric life support; neonatal life support; and an
in 2001.2—7 Resuscitation science continues to interdisciplinary task force to address overlapping
advance, and clinical guidelines must be updated topics, such as educational issues. Each task force
regularly to reflect these developments and advise identified topics requiring evidence evaluation, and
healthcare providers on best practice. In between appointed international experts to review them.
major guideline updates (about every five years), To ensure a consistent and thorough approach, a
interim advisory statements can inform the health- worksheet template was created containing step-
care provider about new therapies that might influ- by-step directions to help the experts document
ence outcome significantly;8 we anticipate that their literature review, evaluate studies, determine
further advisory statements will be published in levels of evidence and develop recommendations.10
response to important research findings. A total of 281 experts completed 403 worksheets on
The guidelines that follow do not define the 276 topics; 380 people from 18 countries attended
only way that resuscitation should be achieved; the 2005 International Consensus Conference on
they merely represent a widely accepted view of ECC and CPR Science with Treatment Recommen-
how resuscitation can be undertaken both safely dations (C2005), which took place in Dallas in
and effectively. The publication of new and revised January 2005.11 Worksheet authors presented the
treatment recommendations does not imply that results of their evidence evaluations and pro-
current clinical care is either unsafe or ineffective. posed summary scientific statements. After discus-
sion among all participants, these statements were
refined and, whenever possible, supported by treat-
Consensus on science ment recommendations. These summary science
statements and treatment recommendations have
The International Liaison Committee on Resuscita- been published in the 2005 International Consensus
tion (ILCOR) was formed in 1993.9 Its mission is on Cardiopulmonary Resuscitation and Emergency
to identify and review international science and Cardiovascular Care Science with Treatment Rec-
knowledge relevant to CPR, and to offer consen- ommendations (CoSTR).12

0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.
doi:10.1016/j.resuscitation.2005.10.002
S4 Jerry Nolan

From science to guidelines Table 1.1 Out-of-hospital cardiopulmonary arrests


(21,175) by aetiology.19
The resuscitation organisations forming ILCOR will
Aetiology Number (%)
publish individual resuscitation guidelines that are
consistent with the science in the consensus docu- Presumed cardiac disease 17451 (82.4)
ment, but will also consider geographic, economic Non-cardiac internal aetiologies 1814 (8.6)
and system differences in practice, and the avail- Lung disease 901 (4.3)
ability of medical devices and drugs. These 2005 Cerebrovascular disease 457 (2.2)
ERC Resuscitation Guidelines are derived from the Cancer 190 (0.9)
CoSTR document but represent consensus among Gastrointestinal haemorrhage 71 (0.3)
members of the ERC Executive Committee. The Obstetric/paediatric 50 (0.2)
Pulmonary embolism 38 (0.2)
ERC Executive Committee considers these new rec-
Epilepsy 36 (0.2)
ommendations to be the most effective and eas-
Diabetes mellitus 30 (0.1)
ily learned interventions that can be supported Renal disease 23 (0.1)
by current knowledge, research and experience.
Inevitably, even within Europe, differences in the Non-cardiac external aetiologies 1910 (9.0)
Trauma 657 (3.1)
availability of drugs, equipment, and personnel will
Asphyxia 465 (2.2)
necessitate local, regional and national adaptation
Drug overdose 411 (1.9)
of these guidelines. Drowning 105 (0.5)
Other suicide 194 (0.9)
Other external 50 (0.2)
Demographics Electric shock/lightning 28 (0.1)

Ischaemic heart disease is the leading cause of


death in the world.13—17 Sudden cardiac arrest is
responsible for more than 60% of adult deaths
includes prevention of conditions leading to the
from coronary heart disease.18 Based on data from
cardiopulmonary arrest, early CPR, early activa-
Scotland and from five cities in other parts of
tion of the emergency services and early advanced
Europe, the annual incidence of resuscitation for
life support. In hospital, the importance of early
out-of-hospital cardiopulmonary arrest of cardiac
recognition of the critically ill patient and activa-
aetiology is 49.5—66 per 100,000 population.19,20
tion of a medical emergency team (MET) is now well
The Scottish study includes data on 21,175 out-
accepted.23 Previous resuscitation guidelines have
of-hospital cardiac arrests, and provides valuable
provided relatively little information on treatment
information on aetiology (Table 1.1). The incidence
of the patient during the post-resuscitation care
of in-hospital cardiac arrest is difficult to assess
phase. There is substantial variability in the way
because it is influenced heavily by factors such as
comatose survivors of cardiac arrest are treated
the criteria for hospital admission and implementa-
in the initial hours and first few days after return
tion of a do-not-attempt-resuscitation (DNAR) pol-
of spontaneous circulation (ROSC). Differences in
icy. In a general hospital in the UK, the incidence
treatment at this stage may account for some of
of primary cardiac arrest (excluding those with
the interhospital variability in outcome after car-
DNAR and those arresting in the emergency depart-
diac arrest.24 The importance of recognising crit-
ment) was 3.3/1000 admissions;21 using the same
ical illness and/or angina and preventing cardiac
exclusion criteria, the incidence of cardiac arrest
arrest (in- or out-of-hospital), and post resuscita-
in a Norwegian University hospital was 1.5/1000
tion care has been highlighted by the inclusion of
admissions.22
these elements in a new four-ring Chain of Sur-
vival. The first link indicates the importance of
recognising those at risk of cardiac arrest and call-
The Chain of Survival ing for help in the hope that early treatment can
prevent arrest. The central links in this new chain
The actions linking the victim of sudden cardiac depict the integration of CPR and defibrillation as
arrest with survival are called the Chain of Sur- the fundamental components of early resuscitation
vival. They include early recognition of the emer- in an attempt to restore life. The final link, effec-
gency and activation of the emergency services, tive post resuscitation care, is targeted at preserv-
early CPR, early defibrillation and early advanced ing function, particularly of the brain and heart
life support. The infant-and-child Chain of Survival (Figure 1.1).25,26
European Resuscitation Council Guidelines for Resuscitation 2005 S5

Figure 1.1 ERC Chain of Survival.

The universal algorithm occur frequently both in and out of hospital.28—31


Resuscitation instructors must emphasise the
The adult basic, adult advanced and paediatric importance of minimising interruptions to chest
resuscitation algorithms have been updated to compressions.
reflect changes in the ERC Guidelines. Every effort
has been made to keep these algorithms simple
yet applicable to cardiac arrest victims in most Summary
circumstances. Rescuers begin CPR if the victim
is unconscious or unresponsive, and not breath- It is intended that these new guidelines will
ing normally (ignoring occasional gasps). A single improve the practice of resuscitation and, ulti-
compression—ventilation (CV) ratio of 30:2 is used mately, the outcome from cardiac arrest. The
for the single rescuer of an adult or child (exclud- universal ratio of 30 compressions to two ventila-
ing neonates) out of hospital, and for all adult CPR. tions should decrease the number of interruptions
This single ratio is designed to simplify teaching, in compression, reduce the likelihood of hyper-
promote skill retention, increase the number of ventilation, simplify instruction for teaching and
compressions given and decrease interruption to improve skill retention. The single-shock strat-
compressions. Once a defibrillator is attached, if egy should minimise ‘no-flow’ time. Resuscitation
a shockable rhythm is confirmed, a single shock course materials are being updated to reflect these
is delivered. Irrespective of the resultant rhythm, new guidelines.
chest compressions and ventilations (2 min with a
CV ratio of 30:2) are resumed immediately after the
shock to minimise the ‘no-flow’ time. Advanced life
support interventions are outlined in a box at the References
centre of the ALS algorithm (see Section 4). Once
1. American Heart Association, In collaboration with Interna-
the airway is secured with a tracheal tube, laryn- tional Liaison Committee on Resuscitation. Guidelines for
geal mask airway (LMA) or Combitube, the lungs cardiopulmonary resuscitation and emergency cardiovascu-
are ventilated at a rate of 10 min−1 without pausing lar care—–an international consensus on science. Resuscita-
during chest compressions. tion 2000;46:3—430.
2. Handley AJ, Monsieurs KG, Bossaert LL, European Resus-
citation Council Guidelines 2000 for Adult Basic Life Sup-
port. A statement from the Basic Life Support and Auto-
mated External Defibrillation Working Group. Resuscitation
Quality of CPR 2001;48:199—205.
3. Monsieurs KG, Handley AJ, Bossaert LL, European Resuscita-
Interruptions to chest compressions must be min- tion Council Guidelines 2000 for Automated External Defib-
imised. On stopping chest compressions, the coro- rillation. A statement from the Basic Life Support and Auto-
nary flow decreases substantially; on resuming mated External Defibrillation Working Group. Resuscitation
2001;48:207—9.
chest compressions, several compressions are nec-
4. de Latorre F, Nolan J, Robertson C, Chamberlain D, Baskett
essary before the coronary flow recovers to its P, European Resuscitation Council Guidelines 2000 for Adult
previous level.27 Recent evidence indicates that Advanced Life Support. A statement from the Advanced Life
unnecessary interruptions to chest compressions Support Working Group. Resuscitation 2001;48:211—21.
S6 Jerry Nolan

5. Phillips B, Zideman D, Garcia-Castrillo L, Felix M, Shwarz- 17. Levi F, Lucchini F, Negri E, La Vecchia C. Trends in mor-
Schwierin U, European Resuscitation Council Guidelines tality from cardiovascular and cerebrovascular diseases in
2000 for Basic Paediatric Life Support. A statement from Europe and other areas of the world. Heart 2002;88:119—
the Paediatric Life Support Working Group. Resuscitation 24.
2001;48:223—9. 18. Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden car-
6. Phillips B, Zideman D, Garcia-Castrillo L, Felix M, Shwarz- diac death in the United States, 1989 to 1998. Circulation
Schwierin V, European Resuscitation Council Guidelines 2001;104:2158—63.
2000 for Advanced Paediatric Life Support. A statement 19. Pell JP, Sirel JM, Marsden AK, Ford I, Walker NL, Cobbe SM.
from Paediatric Life Support Working Group. Resuscitation Presentation, management, and outcome of out of hospital
2001;48:231—4. cardiopulmonary arrest: comparison by underlying aetiology.
7. Phillips B, Zideman D, Wyllie J, Richmond S, van Reempts Heart 2003;89:839—42.
P, European Resuscitation Council Guidelines 2000 for Newly 20. Herlitz J, Bahr J, Fischer M, Kuisma M, Lexow K, Thorgeirsson
Born Life Support. A statement from the Paediatric Life Sup- G. Resuscitation in Europe: a tale of five European regions.
port Working Group. Resuscitation 2001;48:235—9. Resuscitation 1999;41:121—31.
8. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW. Therapeu- 21. Hodgetts TJ, Kenward G, Vlackonikolis I, et al. Incidence,
tic hypothermia after cardiac arrest. An advisory statement location and reasons for avoidable in-hospital cardiac arrest
by the Advancement Life support Task Force of the Inter- in a district general hospital. Resuscitation 2002;54:115—23.
national Liaison committee on Resuscitation. Resuscitation 22. Skogvoll E, Isern E, Sangolt GK, Gisvold SE. In-hospital car-
2003;57:231—5. diopulmonary resuscitation. 5 years’ incidence and survival
9. The Founding Members of the International Liaison Commit- according to the Utstein template. Acta Anaesthesiol Scand
tee on Resuscitation. The International Liaison Committee 1999;43:177—84.
on Resuscitation (ILCOR)—–past, present and future. Resus- 23. The MERIT study investigators. Introduction of the medical
citation 2005;67:157—61. emergency team (MET) system: a cluster-randomised con-
10. Morley P, Zaritsky A. The evidence evaluation process for the trolled trial. Lancet 2005;365:2091—7.
2005 International Consensus on Cardiopulmonary Resuscita- 24. Langhelle A, Tyvold SS, Lexow K, Hapnes SA, Sunde K, Steen
tion and Emergency Cardiovascular Care Science With Treat- PA. In-hospital factors associated with improved outcome
ment Recommendations. Resuscitation 2005;67:167—70. after out-of-hospital cardiac arrest. A comparison between
11. Nolan JP, Hazinski MF, Steen PA, Becker LB. Controversial four regions in Norway. Resuscitation 2003;56:247—63.
topics from the 2005 International Consensus Conference on 25. Langhelle A, Nolan J, Herlitz J, et al. Recommended guide-
Cardiopulmonary Resuscitation and Emergency Cardiovascu- lines for reviewing, reporting, and conducting research on
lar Care Science with treatment recommendations. Resusci- post-resuscitation care: The Utstein style. Resuscitation
tation 2005;67:175—9. 2005;66:271—83.
12. International Liaison Committee on Resuscitation. 2005 26. Perkins GD, Soar J. In hospital cardiac arrest: missing links
International Consensus on Cardiopulmonary Resuscitation in the chain of survival. Resuscitation 2005;66:253—5.
and Emergency Cardiovascular Care Science with Treatment 27. Kern KB, Hilwig RW, Berg RA, Ewy GA. Efficacy of chest
Recommendations. Resuscitation 2005;67:157—341. compression-only BLS CPR in the presence of an occluded
13. Murray CJ, Lopez AD. Mortality by cause for eight regions airway. Resuscitation 1998;39:179—88.
of the world: global burden of disease study. Lancet 28. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality of
1997;349:1269—76. cardiopulmonary resuscitation during out-of-hospital cardiac
14. Sans S, Kesteloot H, Kromhout D. The burden of cardiovas- arrest. JAMA 2005;293:299—304.
cular diseases mortality in Europe. Task Force of the Euro- 29. Abella BS, Alvarado JP, Myklebust H, et al. Quality of car-
pean Society of Cardiology on Cardiovascular Mortality and diopulmonary resuscitation during in-hospital cardiac arrest.
Morbidity Statistics in Europe. Eur Heart J 1997;18:1231— JAMA 2005;293:305—10.
48. 30. Abella BS, Sandbo N, Vassilatos P, et al. Chest compression
15. Kesteloot H, Sans S, Kromhout D. Evolution of all-causes rates during cardiopulmonary resuscitation are suboptimal:
and cardiovascular mortality in the age-group 75—84 years a prospective study during in-hospital cardiac arrest. Circu-
in Europe during the period 1970—1996; a comparison with lation 2005;111:428—34.
worldwide changes. Eur Heart J 2002;23:384—98. 31. Valenzuela TD, Kern KB, Clark LL, et al. Interruptions of chest
16. Fox R. Trends in cardiovascular mortality in Europe. Circula- compressions during emergency medical systems resuscita-
tion 1997;96:3817. tion. Circulation 2005;112:1259—65.
Resuscitation (2005) 67S1, S25—S37

European Resuscitation Council Guidelines for


Resuscitation 2005
Section 3. Electrical therapies: Automated
external defibrillators, defibrillation,
cardioversion and pacing
Charles D. Deakin, Jerry P. Nolan

Introduction the rhythm while CPR is in progress is required to


prevent unnecessary delays in CPR. Waveform anal-
This section presents guidelines for defibrillation ysis may also enable the defibrillator to calculate
using both automated external defibrillators (AEDs) the optimal time at which to give a shock.
and manual defibrillators. All healthcare providers
and lay responders can use AEDs as an integral com-
ponent of basic life support. Manual defibrillation is A vital link in the chain of survival
used as part of advanced life support (ALS) therapy.
In addition, synchronised cardioversion and pacing Defibrillation is a key link in the Chain of Survival
are ALS functions of many defibrillators and are also and is one of the few interventions that have been
discussed in this section. shown to improve outcome from VF/VT cardiac
Defibrillation is the passage across the myocard- arrest. The previous guidelines, published in 2000,
ium of an electrical current of sufficient magnitude rightly emphasised the importance of early defib-
to depolarise a critical mass of myocardium and rillation with minimum delay.1
enable restoration of coordinated electrical activ- The probability of successful defibrillation and
ity. Defibrillation is defined as the termination of subsequent survival to hospital discharge declines
fibrillation or, more precisely, the absence of ven- rapidly with time2,3 and the ability to deliver
tricular fibrillation/ventricular tachycardia (VF/VT) early defibrillation is one of the most important
at 5 s after shock delivery; however, the goal of factors in determining survival from cardiac
attempted defibrillation is to restore spontaneous arrest. For every minute that passes following
circulation. collapse and defibrillation, mortality increases
Defibrillator technology is advancing rapidly. AED 7%—10% in the absence of bystander CPR.2—4 EMS
interaction with the rescuer through voice prompts systems do not generally have the capability to
is now established, and future technology may deliver defibrillation through traditional paramedic
enable more specific instructions to be given by responders within the first few minutes of a call,
voice prompt. The ability of defibrillators to assess and the alternative use of trained lay responders

0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.
doi:10.1016/j.resuscitation.2005.10.008
S26 C.D. Deakin, J.P. Nolan

to deliver prompt defibrillation using AEDs is now Automated external defibrillators have been
widespread. EMS systems that have reduced time to tested extensively against libraries of recorded
defibrillation following cardiac arrest using trained cardiac rhythms and in many trials in adults18,19
lay responders have reported greatly improved and children.20,21 They are extremely accurate in
survival-to-discharge rates,5—7 some as high as rhythm analysis. Although AEDs are not designed to
75% if defibrillation is performed within 3 min of deliver synchronised shocks, all AEDs will recom-
collapse.8 This concept has also been extended to mend shocks for VT if the rate and R-wave mor-
in-hospital cardiac arrests where staff, other than phology exceed preset values.
doctors, are also being trained to defibrillate using
an AED before arrival of the cardiac arrest team.
When bystander CPR is provided, the reduction in In-hospital use of AEDs
survival rate is more gradual and averages 3%—4%
At the time of the 2005 Consensus Confer-
per minute from collapse to defibrillation;2—4
ence, there were no published randomised trials
bystander CPR can double2,3,9 or treble10 sur-
comparing in-hospital use of AEDs with manual
vival from witnessed out-of-hospital cardiac
defibrillators. Two lower level studies of adults
arrest.
with in-hospital cardiac arrest from shockable
All healthcare providers with a duty to perform
rhythms showed higher survival-to-hospital dis-
CPR should be trained, equipped, and encouraged
charge rates when defibrillation was provided
to perform defibrillation and CPR. Early defibrilla-
through an AED programme than with manual defib-
tion should be available throughout all hospitals,
rillation alone.22,23 A manikin study showed that
outpatient medical facilities and public areas of
use of an AED significantly increased the likelihood
mass gathering (see Section 2). Those trained in
of delivering three shocks, but increased the time
AED use should also be trained to deliver at least
to deliver the shocks when compared with manual
external chest compressions before the arrival of
defibrillators.24 In contrast, a study of mock arrests
ALS providers, to optimise the effectiveness of early
in simulated patients showed that use of monitor-
defibrillation.
ing leads and fully automated defibrillators reduced
time to defibrillation when compared with manual
defibrillators.25
Automated external defibrillators
Delayed defibrillation may occur when patients
sustain cardiac arrest in unmonitored hospital beds
Automated external defibrillators are sophisti-
and in outpatient departments. In these areas sev-
cated, reliable computerised devices that use voice
eral minutes may elapse before resuscitation teams
and visual prompts to guide lay rescuers and health-
arrive with a defibrillator and deliver shocks.26
care professionals to safely attempt defibrillation
Despite limited evidence, AEDs should be consid-
in cardiac arrest victims. Automated defibrillators
ered for the hospital setting as a way to facilitate
have been described as ‘‘. . . the single greatest
early defibrillation (a goal of <3 min from collapse),
advance in the treatment of VF cardiac arrest since
especially in areas where staff have no rhythm
the development of CPR.’’11 Advances in technol-
recognition skills or where they use defibrillators
ogy, particularly with respect to battery capacity,
infrequently. An effective system for training and
and software arrhythmia analysis have enabled the
retraining should be in place. Adequate numbers of
mass production of relatively cheap, reliable and
staff should be trained to enable achievement of
easily operated portable defibrillators.12—15 Use of
the goal of providing the first shock within 3 min of
AEDs by lay or non-healthcare rescuers is covered
collapse anywhere in the hospital. Hospitals should
in Section 2.
monitor collapse-to-first-shock intervals and resus-
citation outcomes.
Automated rhythm analysis
Automated external defibrillators have micropro-
cessors that analyse several features of the ECG, Strategies before defibrillation
including frequency and amplitude. Some AEDs are
programmed to detect spontaneous movement by Safe use of oxygen during defibrillation
the patient or others. Developing technology should
soon enable AEDs to provide information about In an oxygen-enriched atmosphere, sparking from
frequency and depth of chest compressions dur- poorly applied defibrillator paddles can cause a
ing CPR that may improve BLS performance by all fire.27—32 There are several reports of fires being
rescuers.16,17 caused in this way, and most have resulted in
European Resuscitation Council Guidelines for Resuscitation 2005 S27

significant burns to the patient. The risk of fire dur- Shaving the chest
ing attempted defibrillation can be minimised by
taking the following precautions. Patients with a hairy chest have air trapping
beneath the electrode and poor electrode-to-skin
• Take off any oxygen mask or nasal cannulae and electrical contact. This causes high impedance,
place them at least 1 m away from the patient’s reduced defibrillation efficacy, risk of arcing
chest. (sparks) from electrode to skin and electrode
• Leave the ventilation bag connected to the tra- to electrode and is more likely to cause burns
cheal tube or other airway adjunct. Alterna- to the patient’s chest. Rapid shaving of the
tively, disconnect any bag-valve device from the area of intended electrode placement may be
tracheal tube (or other airway adjunct such as necessary, but do not delay defibrillation if a
the laryngeal mask airway, combitube or laryn- shaver is not immediately available. Shaving the
geal tube), and remove it at least 1 m from the chest per se may reduce transthoracic impedance
patient’s chest during defibrillation. slightly and has been recommended for elective DC
• If the patient is connected to a ventilator, for cardioversion.35
example in the operating room or critical care
unit, leave the ventilator tubing (breathing cir-
Paddle force
cuit) connected to the tracheal tube unless chest
compressions prevent the ventilator from deliv- If using paddles, apply them firmly to the chest
ering adequate tidal volumes. In this case, the wall. This reduces transthoracic impedance by
ventilator is usually substituted for a ventila- improving electrical contact at the electrode—skin
tion bag, which can itself be left connected or interface and reducing thoracic volume.36 The
detached and removed to a distance of at least defibrillator operator should always press firmly
1 m. If the ventilator tubing is disconnected, on handheld electrode paddles, the optimal force
ensure it is kept at least 1 m from the patient being 8 kg in adults37 and 5 kg in children aged
or, better still, switch the ventilator off; mod- 1—8 years when using adult paddles38 ; 8-kg force
ern ventilators generate massive oxygen flows may be attainable only by the strongest mem-
when disconnected. During normal use, when bers of the cardiac arrest team, and therefore it
connected to a tracheal tube, oxygen from a ven- is recommended that these individuals apply the
tilator in the critical care unit will be vented from paddles during defibrillation. Unlike self-adhesive
the main ventilator housing well away from the pads, manual paddles have a bare metal plate that
defibrillation zone. Patients in the critical care requires a conductive material placed between the
unit may be dependent on positive end expiratory metal and patient’s skin to improve electrical con-
pressure (PEEP) to maintain adequate oxygena- tact. Use of bare metal paddles alone creates high
tion; during cardioversion, when the spontaneous transthoracic impedance and is likely to increase
circulation potentially enables blood to remain the risk of arcing and to worsen cutaneous burns
well oxygenated, it is particularly appropriate to from defibrillation.
leave the critically ill patient connected to the
ventilator during shock delivery.
Electrode position
• Minimise the risk of sparks during defibrillation.
Theoretically, self-adhesive defibrillation pads No human studies have evaluated the electrode
are less likely to cause sparks than manual pad- position as a determinant of return of spontaneous
dles. circulation (ROSC) or survival from VF/VT cardiac
arrest. Transmyocardial current during defibrilla-
The technique for electrode contact with tion is likely to be maximal when the electrodes
the chest are placed so that the area of the heart that is fib-
rillating lies directly between them, i.e., ventricles
Optimal defibrillation technique aims to deliver in VF/VT, atria in atrial fibrillation (AF). Therefore,
current across the fibrillating myocardium in the the optimal electrode position may not be the same
presence of minimal transthoracic impedance. for ventricular and atrial arrhythmias.
Transthoracic impedance varies considerably with More patients are presenting with implantable
body mass, but is approximately 70—80  in medical devices (e.g., permanent pacemaker,
adults.33,34 The techniques described below aim to automatic implantable cardioverter defibrillator
place external electrodes (paddles or self-adhesive (AICD)). MedicAlert bracelets are recommended for
pads) in an optimal position using techniques that such patients. These devices may be damaged dur-
minimise transthoracic impedance. ing defibrillation if current is discharged through
S28 C.D. Deakin, J.P. Nolan

electrodes placed directly over the device. Place fibrillation.43 Most,44,45 but not all,46,47 studies
the electrode away from the device or use an alter- have shown that anteroposterior electrode place-
native electrode position as described below. On ment is more effective than the traditional antero-
detecting VF/VT, AICD devices will discharge no apical position in elective cardioversion of atrial
more than six times. Further discharges will occur fibrillation. Efficacy of cardioversion may be less
only if a new episode of VF/VT is detected. Rarely, dependent on electrode position when using bipha-
a faulty device or broken lead may cause repeated sic impedance-compensated waveforms.48 Either
firing; in these circumstances, the patient is likely position is safe and effective for cardioversion of
to be conscious, with the ECG showing a relatively atrial arrhythmias.
normal rate. A magnet placed over the AICD will
disable the defibrillation function in these circum- Respiratory phase
stances. AICD discharge may cause pectoral muscle
contraction, but an attendant touching the patient Transthoracic impedance varies during respiration,
will not receive an electric shock. AICD and pacing being minimal at end expiration. If possible, defib-
function should always be re-evaluated following rillation should be attempted at this phase of
external defibrillation, both to check the device the respiratory cycle. Positive end-expiratory pres-
itself and to check pacing/defibrillation thresholds sure (PEEP) increases transthoracic impedance and
of the device leads. should be minimised during defibrillation. Auto-
Transdermal drug patches may prevent good PEEP (gas trapping) may be particularly high in
electrode contact, causing arcing and burns if the asthmatics and may necessitate higher than usual
electrode is placed directly over the patch during energy levels for defibrillation.49
defibrillation.39,40 Remove medication patches and
wipe the area before applying the electrode. Electrode size
For ventricular arrhythmias, place electrodes
(either pads or paddles) in the conventional The Association for the Advancement of Medi-
sternal—apical position. The right (sternal) elec- cal Instrumentation recommends a minimum elec-
trode is placed to the right of the sternum, below trode size of for individual electrodes and the
the clavicle. The apical paddle is placed in the mid- sum of the electrode areas should be a mini-
axillary line, approximately level with the V6 ECG mum of 150 cm2 .50 Larger electrodes have lower
electrode or female breast. This position should impedance, but excessively large electrodes may
be clear of any breast tissue. It is important that result in less transmyocardial current flow.51 For
this electrode is placed sufficiently laterally. Other adult defibrillation, both handheld paddle elec-
acceptable pad positions include: trodes and self-adhesive pad electrodes 8—12 cm
in diameter are used and function well. Defib-
• each electrode on the lateral chest wall, one
rillation success may be higher with electrodes
on the right and the other on the left side (bi-
of 12-cm diameter compared with those of 8-cm
axillary);
diameter.34,52
• one electrode in the standard apical position and
Standard AEDs are suitable for use in children
the other on the right or left upper back;
over the age of 8 years. In children between 1 and
• one electrode anteriorly, over the left pre-
8 years, use paediatric pads with an attenuator
cordium, and the other electrode posterior to the
to reduce delivered energy, or a paediatric mode,
heart just inferior to the left scapula.
if they are available; if not, use the unmodified
It does not matter which electrode (apex/ machine, taking care to ensure that the adult pads
sternum) is placed in either position. do not overlap. Use of AEDs is not recommended in
Transthoracic impedance has been shown to be children less than 1 year.
minimised when the apical electrode is not placed
over the female breast.41 Asymmetrically shaped Coupling agents
apical electrodes have a lower impedance when
placed longitudinally rather than transversely.42 If using manual paddles, gel pads are preferable
The long axis of the apical paddle should therefore to electrode pastes and gels because the latter
be orientated in a craniocaudal direction. can spread between the two paddles, creating the
Atrial fibrillation is maintained by functional potential for a spark. Do not use bare electrodes
re-entry circuits anchored in the left atrium. As without a coupling material, because this causes
the left atrium is located posteriorly in the tho- high transthoracic impedance and may increase the
rax, an anteroposterior electrode position may be severity of any cutaneous burns. Do not use med-
more efficient for external cardioversion of atrial ical gels or pastes of poor electrical conductivity
European Resuscitation Council Guidelines for Resuscitation 2005 S29

(e.g., ultrasound gel). Electrode pads are preferred with immediate defibrillation. In contrast, a sin-
to electrode gel because they avoid the risk of gle randomised study in adults with out-of-hospital
smearing gel between the two paddles and the sub- VF or VT failed to show improvements in ROSC or
sequent risk of arcing and ineffective defibrillation. survival following 1.5 min of paramedic CPR.80 In
animal studies of VF lasting at least 5 min, CPR
Pads versus paddles before defibrillation improved haemodynamics and
survival.81—83 It may not be possible to extrapo-
Self-adhesive defibrillation pads are safe and effec- late the outcomes achieved by paramedic-provided
tive and are preferable to standard defibrillation CPR, which includes intubation and delivery of 100%
paddles.52 Consideration should be given to use oxygen,79 to those that may be achieved by laypeo-
of self-adhesive pads in peri-arrest situations and ple providing relative poor-quality CPR with mouth-
in clinical situations where patient access is diffi- to-mouth ventilation.
cult. They have a similar transthoracic impedance51 It is reasonable for EMS personnel to give a period
(and therefore efficacy)53,54 to manual paddles, of about 2 min of CPR (i.e., about five cycles at
and enable the operator to defibrillate the patient 30:2) before defibrillation in patients with pro-
from a safe distance rather than leaning over the longed collapse (>5 min). The duration of collapse
patient (as occurs with paddles). When used for ini- is frequently difficult to estimate accurately, and it
tial monitoring of a rhythm, both pads and paddles may be simplest if EMS personnel are instructed to
enable quicker delivery of the first shock compared provide this period of CPR before attempted defib-
with standard ECG electrodes, but pads are quicker rillation in any cardiac arrest they have not wit-
than paddles.55 nessed. Given the relatively weak evidence avail-
When gel pads are used with paddles, the elec- able, individual EMS directors should determine
trolyte gel becomes polarised and thus is a poor whether to implement a CPR-before-defibrillation
conductor after defibrillation. This can cause spu- strategy; inevitably, protocols will vary depending
rious asystole that may persist for 3—4 min when on the local circumstances.
used to monitor the rhythm; a phenomenon not Laypeople and first responders using AEDS should
reported with self-adhesive pads.56,57 When using deliver the shock as soon as possible.
a gel pad/paddle combination, confirm a diagnosis There is no evidence to support or refute CPR
of asystole with independent ECG electrodes rather before defibrillation for in-hospital cardiac arrest.
than the paddles. We recommend shock delivery as soon as possible
following in-hospital cardiac arrest (see Section 4b
Fibrillation waveform analysis and c).
The importance of early uninterrupted external
It is possible to predict, with varying reliability, chest compression is emphasised throughout these
the success of defibrillation from the fibrillation guidelines. In practice, it is often difficult to ascer-
waveform.58—77 If optimal defibrillation waveforms tain the exact time of collapse and, in any case,
and the optimal timing of shock delivery can be CPR should be started as soon as possible. The res-
determined in prospective studies, it should be pos- cuer providing chest compressions should interrupt
sible to prevent the delivery of unsuccessful high- chest compressions only for rhythm analysis and
energy shocks and minimise myocardial injury. This shock delivery, and should be prepared to resume
technology is under active development and inves- chest compressions as soon as a shock is delivered.
tigation. When two rescuers are present, the rescuer operat-
ing the AED should apply the electrodes while CPR
CPR versus defibrillation as the initial is in progress. Interrupt CPR only when it is nec-
treatment essary to assess the rhythm and deliver a shock.
The AED operator should be prepared to deliver a
Although the previous guidelines have recom- shock as soon as analysis is complete and the shock
mended immediate defibrillation for all shockable is advised, ensuring all rescuers are not in contact
rhythms, recent evidence has suggested that a with the victim. The single rescuer should practice
period of CPR before defibrillation may be bene- coordination of CPR with efficient AED operation.
ficial after prolonged collapse. In clinical studies
where response times exceeded 4—5 min, a period
of 1.5—3 min of CPR by paramedics or EMS physi- One-shock versus three-shock sequence
cians before shock delivery improved ROSC, sur-
vival to hospital discharge78,79 and 1-year survival79 There are no published human or animal studies
for adults with out-of-hospital VF or VT, compared comparing a single-shock protocol with a three-
S30 C.D. Deakin, J.P. Nolan

stacked-shock protocol for treatment of VF car-


diac arrest. Animal studies show that relatively
short interruptions in external chest compression
to deliver rescue breaths84,85 or perform rhythm
analysis86 are associated with post-resuscitation
myocardial dysfunction and reduced survival.
Interruptions in external chest compression also
reduce the chances of converting VF to another
rhythm.87 Analysis of CPR performance during out-
of-hospital16,88 and in-hospital17 cardiac arrest has
shown that significant interruptions are common,
with external chest compressions comprising no
more than 51%16 to 76%17 of total CPR time.
In the context of a three-shock protocol being
recommended in the 2000 guidelines, interruptions
in CPR to enable rhythm analysis by AEDs were
Figure 3.1 Monophasic damped sinusoidal waveform
significant. Delays of up to 37 s between delivery
(MDS).
of shocks and recommencing chest compressions
have been reported.89 With first shock efficacy of of repetitive shocks, which in turn limits myocardial
biphasic waveforms exceeding 90%,90—93 failure to damage.95
cardiovert VF successfully is more likely to suggest After a cautious introduction a decade ago,
the need for a period of CPR rather than a fur- defibrillators delivering a shock with a biphasic
ther shock. Thus, immediately after giving a single waveform are now preferred. Monophasic defibril-
shock, and without reassessing the rhythm or feel- lators are no longer manufactured, although many
ing for a pulse, resume CPR (30 compressions:2 ven- remain in use. Monophasic defibrillators deliver cur-
tilations) for 2 min before delivering another shock rent that is unipolar (i.e., one direction of cur-
(if indicated) (see Section 4c). Even if the defibril- rent flow). There are two main types of monopha-
lation attempt is successful in restoring a perfusing sic waveform. The commonest waveform is the
rhythm, it is very rare for a pulse to be palpable monophasic damped sinusoidal (MDS) waveform
immediately after defibrillation, and the delay in (Figure 3.1) which gradually returns to zero current
trying to palpate a pulse will further compromise flow. The monophasic truncated exponential (MTE)
the myocardium if a perfusing rhythm has not been waveform is electronically terminated before cur-
restored.89 In one study of AEDs in out-of-hospital rent flow reaches zero (Figure 3.2). Biphasic defib-
VF cardiac arrest, a pulse was detected in only 2.5% rillators, in contrast, deliver current that flows in
(12/481) of patients with the initial post shock pulse a positive direction for a specified duration before
check, though a pulse was detected sometime after reversing and flowing in a negative direction for the
the initial shock sequence (and before a second remaining milliseconds of the electrical discharge.
shock sequence) in 24.5% (118/481) of patients.93 If There are two main types of biphasic waveform: the
a perfusing rhythm has been restored, giving chest biphasic truncated exponential (BTE) (Figure 3.3)
compressions does not increase the chance of VF and rectilinear biphasic (RLB) (Figure 3.4). Bipha-
recurring.94 In the presence of post-shock asystole sic defibrillators compensate for the wide varia-
chest compressions may induce VF.94 tions in transthoracic impedance by electronically
This single shock strategy is applicable to both
monophasic and biphasic defibrillators.

Waveforms and energy levels

Defibrillation requires the delivery of sufficient


electrical energy to defibrillate a critical mass of
myocardium, abolish the wavefronts of VF and
enable restoration of spontaneous synchronised
electrical activity in the form of an organised
rhythm. The optimal energy for defibrillation is
that which achieves defibrillation while causing the
minimum of myocardial damage.33 Selection of an Figure 3.2 Monophasic truncated exponential wave-
appropriate energy level also reduces the number form (MTE).
European Resuscitation Council Guidelines for Resuscitation 2005 S31

The optimal current for defibrillation using a


monophasic waveform is in the range of 30—40 A.
Indirect evidence from measurements during car-
dioversion for atrial fibrillation suggest that the cur-
rent during defibrillation using biphasic waveforms
is in the range of 15—20 A.100 Future technology
may enable defibrillators to discharge according to
transthoracic current: a strategy that may lead to
greater consistency in shock success. Peak current
amplitude, average current and phase duration all
need to be studied to determine optimal values,
Figure 3.3 Biphasic truncated exponential waveform and manufacturers are encouraged to explore fur-
(BTE). ther this move from energy-based to current-based
defibrillation.
adjusting the waveform magnitude and duration.
The optimal ratio of first-phase to second-phase First shock
duration and leading-edge amplitude has not been
First-shock efficacy for long-duration cardiac arrest
established. Whether different waveforms have dif-
using monophasic defibrillation has been reported
fering efficacy for VF of differing durations is also
as 54%—63% for a 200-J monophasic truncated
unknown.
exponential (MTE) waveform97,101 and 77%—91%
All manual defibrillators and AEDs that allow
using a 200-J monophasic damped sinusoidal (MDS)
manual override of energy levels should be labelled
waveform.96—98,101 Because of the lower efficacy
to indicate their waveform (monophasic or bipha-
of this waveform, the recommended initial energy
sic) and recommended energy levels for attempted
level for the first shock using a monophasic defib-
defibrillation of VF/VT. First-shock efficacy for
rillator is 360 J. Although higher energy levels risk
long-duration VF/VT is greater with biphasic than
a greater degree of myocardial injury, the bene-
monophasic waveforms,96—98 and therefore use of
fits of earlier conversion to a perfusing rhythm are
the former is recommended whenever possible.
paramount. Atrioventricular block is more common
Optimal energy levels for both monophasic and
with higher monophasic energy levels, but is gen-
biphasic waveforms are unknown. The recommen-
erally transient and has been shown not to affect
dations for energy levels are based on a consensus
survival to hospital discharge.102 Only 1 of 27 animal
following careful review of the current literature.
studies demonstrated harm caused by attempted
Although energy levels are selected for defibril-
defibrillation using high-energy shocks.103
lation, it is the transmyocardial current flow that
There is no evidence that one biphasic wave-
achieves defibrillation. Current correlates well with
form or device is more effective than another. First-
the successful defibrillation and cardioversion.99
shock efficacy of the BTE waveform using 150—200 J
has been reported as 86%—98%.96,97,101,104,105 First-
shock efficacy of the RLB waveform using 120 J is up
to 85% (data not published in the paper but sup-
plied by personnel communication).98 The initial
biphasic shock should be no lower than 120 J for
RLB waveforms and 150 J for BTE waveforms. Ide-
ally, the initial biphasic shock energy should be at
least 150 J for all waveforms.
Manufacturers should display the effective wave-
form dose range on the face of the biphasic device.
If the provider is unaware of the effective dose
range of the device, use a dose of 200 J for the
first shock. This 200 J default energy has been cho-
sen because it falls within the reported range of
selected doses that are effective for first and subse-
quent biphasic shocks and can be provided by every
biphasic manual defibrillator available today. It is
a consensus default dose and not a recommended
Figure 3.4 Rectilinear biphasic waveform (RLB). ideal dose. If biphasic devices are clearly labelled
S32 C.D. Deakin, J.P. Nolan

and providers are familiar with the devices they use Blind defibrillation
in clinical care, there will be no need for the default
200 J dose. Ongoing research is necessary to firmly Delivery of shocks without a monitor or an ECG
establish the most appropriate initial settings for rhythm diagnosis is referred to as ‘‘blind’’ defibril-
both monophasic and biphasic defibrillators. lation. Blind defibrillation is unnecessary. Handheld
paddles with ‘‘quick-look’’ monitoring capabilities
Second and subsequent shocks on modern manually operated defibrillators are
widely available. AEDs use reliable and proven deci-
With monophasic defibrillators, if the initial shock sion algorithms to identify VF.
has been unsuccessful at 360 J, second and sub-
sequent shocks should all be delivered at 360 J. Spurious asystole and occult ventricular
With biphasic defibrillators there is no evidence to fibrillation
support either a fixed or escalating energy proto-
col. Both strategies are acceptable; however, if the Rarely, coarse VF can be present in some leads, with
first shock is not successful and the defibrillator is very small undulations seen in the orthogonal leads,
capable of delivering shocks of higher energy, it which is called occult VF. A flat line that may resem-
is rational to increase the energy for subsequent ble asystole is displayed; examine the rhythm in
shocks. If the provider is unaware of the effective two leads to obtain the correct diagnosis. Of more
dose range of the biphasic device and has used the importance, one study noted that spurious asystole,
default 200 J dose for the first shock, use either a flat line produced by technical errors (e.g., no
an equal or higher dose for second or subsequent power, leads unconnected, gain set to low, incor-
shocks, depending on the capabilities of the device. rect lead selection, or polarisation of electrolyte
If a shockable rhythm (recurrent ventricular fib- gel (see above)), was far more frequent than occult
rillation) recurs after successful defibrillation (with VF.120
or without ROSC), give the next shock with the There is no evidence that attempting to defib-
energy level that had previously been successful. rillate true asystole is beneficial. Studies in
children121 and adults122 have failed to show bene-
fit from defibrillation of asystole. On the contrary,
Other related defibrillation topics repeated shocks will cause myocardial injury.

Defibrillation of children Precordial thump


Cardiac arrest is less common in children. Aetiology There are no prospective studies that evaluate
is generally related to hypoxia and trauma.106—108 use of precordial (chest) thump. The rationale for
VF is relatively rare compared with adult cardiac giving a thump is that the mechanical energy of
arrest, occurring in 7%—15% of paediatric and ado- the thump is converted to electrical energy, which
lescent arrests.108—112 Common causes of VF in may be sufficient to achieve cardioversion.123
children include trauma, congenital heart disease, The electrical threshold of successful defibrillation
long QT interval, drug overdose and hypothermia. increases rapidly after the onset of the arrhythmia,
Rapid defibrillation of these patients may improve and the amount of electrical energy generated falls
outcome.112,113 below this threshold within seconds. A precordial
The optimal energy level, waveform and shock thump is most likely to be successful in convert-
sequence are unknown but, as with adults, bipha- ing VT to sinus rhythm. Successful treatment of
sic shocks appear to be at least as effective as, VF by precordial thump is much less likely: in all
and less harmful than, monophasic shocks.114—116 the reported successful cases, the precordial thump
The upper limit for safe defibrillation is unknown, was given within the first 10 s of VF.123 Although
but doses in excess of the previously recommended three case series124—126 reported that VF or pulse-
maximum of 4 J kg−1 (as high as 9 J kg−1 ) have less VT was converted to a perfusing rhythm by
defibrillated children effectively without signifi- a precordial thump, there are occasional reports
cant adverse effects.20,117,118 The recommended of thump causing deterioration in cardiac rhythm,
energy level for manual monophasic defibrillation such as rate acceleration of VT, conversion of VT
is 4 J kg−1 for the initial shock and for subsequent into VF, complete heart block or asystole.125,127—132
shocks. The same energy level is recommended for Consider giving a single precordial thump when
manual biphasic defibrillation.119 As with adults, if cardiac arrest is confirmed rapidly after a wit-
a shockable rhythm recurs, use the energy level for nessed, sudden collapse and a defibrillator is not
defibrillation that had previously been successful. immediately to hand. These circumstances are
European Resuscitation Council Guidelines for Resuscitation 2005 S33

most likely to occur when the patient is monitored. randomised study comparing escalating monophasic
Precordial thump should be undertaken immedi- energy levels to 360 J and biphasic energy levels to
ately after confirmation of cardiac arrest and only 200 J found no difference in efficacy between the
by healthcare professionals trained in the tech- two waveforms.137 An initial shock of 120—150 J,
nique. Using the ulnar edge of a tightly clenched escalating if necessary, is a reasonable strategy
fist, a sharp impact is delivered to the lower half of based on current data.
the sternum from a height of about 20 cm, followed
by immediate retraction of the fist, which creates Atrial flutter and paroxysmal
an impulse-like stimulus. supraventricular tachycardia

Atrial flutter and paroxysmal SVT generally


Cardioversion require less energy than atrial fibrillation for
cardioversion.138 Give an initial shock of 100-J
If electrical cardioversion is used to convert atrial monophasic or 70—120 J biphasic waveform. Give
or ventricular tachyarrhythmias, the shock must be subsequent shocks using stepwise increases in
synchronised to occur with the R wave of the elec- energy.99
trocardiogram rather than with the T wave: VF can
be induced if a shock is delivered during the rel- Ventricular tachycardia
ative refractory portion of the cardiac cycle.133
Synchronisation can be difficult in VT because of The energy required for cardioversion of VT
the wide-complex and variable forms of ventricular depends on the morphological characteristics and
arrhythmia. If synchronisation fails, give unsynchro- rate of the arrhythmia.139 Ventricular tachycardia
nised shocks to the unstable patient in VT to avoid with a pulse responds well to cardioversion using
prolonged delay in restoring sinus rhythm. Ventric- initial monophasic energies of 200 J. Use biphasic
ular fibrillation or pulseless VT requires unsynchro- energy levels of 120—150 J for the initial shock.
nised shocks. Conscious patients must be anaes- Give stepwise increases if the first shock fails to
thetised or sedated before attempting synchronised achieve sinus rhythm.139
cardioversion.
Pacing
Atrial fibrillation
Consider pacing in patients with symptomatic
Biphasic waveforms are more effective than bradycardia refractory to anticholinergic drugs or
monophasic waveforms for cardioversion of other second-line therapy (see Section 4f). Immedi-
AF100,134,135 ; when available, use a biphasic defib- ate pacing is indicated, especially when the block is
rillator in preference to a monophasic defibrillator. at or below the His—Purkinje level. If transthoracic
pacing is ineffective, consider transvenous pacing.
Monophasic waveforms Whenever a diagnosis of asystole is made, check the
ECG carefully for the presence of P waves, because
A study of electrical cardioversion for atrial fib-
this may respond to cardiac pacing. Do not attempt
rillation indicated that 360-J MDS shocks were
pacing for asystole; it does not increase short-term
more effective than 100-J or 200-J MDS shocks.136
or long-term survival in or out of hospital.140—148
Although a first shock of 360-J reduces overall
energy requirements for cardioversion, 360 J may
cause greater myocardial damage than occurs with References
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S36 C.D. Deakin, J.P. Nolan

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89. van Alem AP, Sanou BT, Koster RW. Interruption of car- cardiac arrest treated with a non-escalating biphasic wave-
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115. Tang W, Weil MH, Jorgenson D, et al. Fixed-energy bipha- 135. Page RL, Kerber RE, Russell JK, et al. Biphasic versus
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116. Clark CB, Zhang Y, Davies LR, Karlsson G, Kerber RE. Pedi- blind multicenter trial. J Am Coll Cardiol 2002;39:1956—63.
atric transthoracic defibrillation: biphasic versus monopha- 136. Joglar JA, Hamdan MH, Ramaswamy K, et al. Initial energy
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2001;51:159—63. rillation. Am J Cardiol 2000;86:348—50.
117. Gurnett CA, Atkins DL. Successful use of a biphasic wave- 137. Alatawi F, Gurevitz O, White R. Prospective, randomized
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Am J Cardiol 2000;86:1051—3. safety of transthoracic biphasic cardioversion of atrial fib-
118. Atkins DL, Jorgenson DB. Attenuated pediatric electrode rillation. Heart Rhythm 2005;2:382—7.
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119. Gutgesell HP, Tacker WA, Geddes LA, Davis S, Lie JT, McNa- of atrial flutter. Am Heart J 1999;137:439—42.
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Resuscitation (2005) 67S1, S39—S86

European Resuscitation Council Guidelines for


Resuscitation 2005
Section 4. Adult advanced life support
Jerry P. Nolan, Charles D. Deakin, Jasmeet Soar,
Bernd W. Böttiger, Gary Smith

4a. Prevention of in-hospital cardiac antecedents in 79% of cardiac arrests, 55% of deaths
arrest and 54% of unanticipated ICU admissions.4 Early and
effective treatment of seriously ill patients might
The problem prevent some cardiac arrests, deaths and unantici-
pated ICU admissions. A third of patients who have
This new section of the guidelines stresses the a false cardiac arrest call die subsequently.9
importance of preventing in-hospital cardiac arrest.
Fewer than 20% of patients suffering an in-hospital Nature of the deficiencies in acute care
cardiac arrest will survive to go home.1,2 Most sur-
vivors have a witnessed and monitored VF arrest, These often involve simple aspects of care includ-
primary myocardial ischaemia as the cause, and ing: the failure to treat abnormalities of the
receive immediate defibrillation. patient’s airway, breathing and circulation, incor-
Cardiac arrest in patients in unmonitored ward rect use of oxygen therapy, failure to monitor
areas is not usually a sudden unpredictable event, patients, failure to involve experienced senior
nor is it usually caused by primary cardiac disease. staff, poor communication, lack of teamwork and
These patients often have slow and progressive insufficient use of treatment limitation plans.3,7
physiological deterioration, involving hypoxia and Several studies show that medical and nurs-
hypotension, that is unnoticed by staff, or is recog- ing staff lack knowledge and skills in acute care.
nised but poorly treated.3,4 The underlying cardiac For example, trainee doctors may lack knowl-
arrest rhythm in this group is usually non-shockable edge about oxygen therapy,10 fluid and electrolyte
and survival to hospital discharge is very poor.1,5 balance,11 analgesia,12 issues of consent,13 pulse
The records of patients who have a cardiac oximetry14 and drug doses.15 Medical students
arrest or unanticipated intensive care unit (ICU) may be unable to recognise abnormal breathing
admission often contain evidence of unrecog- patterns.16 Medical school training provides poor
nised, or untreated, breathing and circulation preparation for doctors’ early careers, and fails to
problems.3,4,6—8 The ACADEMIA study showed teach them the essential aspects of applied physi-
ology and acute care.17 There is also little to sug-
E-mail address: jerry.nolan@ukgateway.net (J.P. Nolan). 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
S40 J.P. Nolan et al.

senior medical staff is better.18,19 Staff often lack alerted to a patient’s abnormal physiology, there
confidence when dealing with acute care problems, is often delay in attending the patient or referring
and rarely use a systematic approach to the assess- to higher levels of care.3,4,7 Whereas the use of a
ment of critically ill patients.20 warning score based on physiological abnormalities
is attractive, it is possible that a more subjective
approach, based on staff experience and expertise,
Recognising the critically ill patient may also be effective.32

In general, the clinical signs of acute illness are Response to critical illness
similar whatever the underlying process, as they
reflect failing respiratory, cardiovascular and neu- The traditional response to cardiac arrest is a
rological systems. Abnormal physiology is com- reactive one in which hospital staff (‘the cardiac
mon on general wards,21 yet the measurement arrest team’) attend the patient after the cardiac
and recording of important physiological observa- arrest has occurred. Cardiac arrest teams appear
tions of sick patients occurs less frequently than to improve survival after cardiac arrest in circum-
is desirable.3,4,8 This is surprising, as respiratory stances where no team has previously existed.33
rate abnormalities may predict cardiorespiratory However, the role of the cardiac arrest team has
arrest.22 To assist in the early detection of criti- been questioned. In one study, only patients who
cal illness, many hospitals now use early warning had return of spontaneous circulation before the
scores (EWS) or calling criteria.23—25 Early warning cardiac arrest team arrived were discharged from
scoring systems allocate points to routine vital signs hospital alive.34 When combined with the poor
measurements on the basis of their derangement survival rate after in-hospital cardiac arrest, this
from an arbitrarily agreed ‘normal’ range.23—25 The emphasises the importance of early recognition and
weighted score of one or more vital sign observa- treatment of critically ill patients to prevent car-
tions, or the total EWS, may be used to suggest diac arrest. The name ‘cardiac arrest team’ implies
increasing the frequency of vital signs monitoring to that the team will be called only after cardiac
nurses, or to call ward doctors or critical care out- arrest has occurred.
reach teams to the patient. Alternatively, systems In some hospitals the cardiac arrest team has
incorporating ‘calling criteria’ are based on rou- been replaced by a medical emergency team (MET)
tine observations, which activate a response when that responds, not only to patients in cardiac
one or more variables reach an extremely abnormal arrest, but also to those with acute physiological
value.23,26 There are no data to establish the supe- deterioration.26 The MET usually comprises medical
riority of one system over another, but it may be and nursing staff from intensive care and general
preferable to use an EWS system, which can track medicine. and responds to specific calling crite-
changes in physiology and warn of impending physi- ria. Any member of the healthcare team can ini-
ological collapse, rather than the ‘‘calling criteria’’ tiate a MET call. Early involvement of the MET
approach, which is triggered only when an extreme may reduce cardiac arrests, deaths and unantic-
value of physiology has been reached. ipated ICU admissions.35,36 The MET may also be
There is a clinical rationale to the use of EWS useful in detecting medical error, improving treat-
or calling criteria systems to identify sick patients ment limitation decisions and reducing postoper-
early. However, their sensitivity, specificity and ative ward deaths.37,38 MET interventions often
accuracy in predicting clinical outcomes has yet to involve simple tasks such as starting oxygen ther-
be validated convincingly.27,28 Several studies have apy and intravenous fluids.39 A circadian pattern of
identified abnormalities of heart rate, blood pres- MET activation has been reported, which may sug-
sure, respiratory rate and conscious level as mark- gest that systems for identifying and responding to
ers of impending critical events.22,23,29 The sugges- medical emergencies may not be uniform through-
tion that their incidence has predictive value must out the 24-h period.40 Studying the effect of the
be questioned, as not all important vital signs are, MET on patient outcomes is difficult. Many of the
or can be, recorded continuously in general ward study findings to date can be criticised because
areas. Several studies show that charting of vital of poor study design. A recent, well-designed,
signs is poor, with gaps in data recording.3,4,8,30 cluster-randomised controlled trial of the MET sys-
Although the use of physiological systems can tem demonstrated that the introduction of a MET
increase the frequency of vital signs monitoring,31 increased the calling incidence for the team. How-
they will be useful for outcome prediction only ever, it failed to show a reduction in the incidence
if widespread monitoring of hospitalised patients of cardiac arrest, unexpected death or unplanned
becomes available. Even when medical staff are ICU admission.41
European Resuscitation Council Guidelines for Resuscitation 2005 S41

In the UK, a system of pre-emptive ward study shows that higher nurse staffing is associated
care, based predominantly on individual or teams with reduction in cardiac arrest rates, as well as
of nurses known as critical care outreach, has rates of pneumonia, shock and death.55
developed.42 Outreach services exist in many
forms, ranging from a single nurse to a 24-h, 7 days Resuscitation decisions
per week multiprofessional team. An outreach team
or system may reduce ward deaths, postoperative Consider ‘do not attempt resuscitation’ (DNAR)
adverse events, ICU admissions and readmissions, when the patient:
and increase survival.43—45
Other attempts to improve the general ward • does not wish to have CPR
care of patients and prevent physiological deteri- • will not survive cardiac arrest even if CPR is
oration and cardiac arrest include new admission attempted
processes, early physiological monitoring and clini- Hospital staff often fail to consider whether
cal intervention in the emergency department (ED), resuscitation attempts are appropriate and resus-
and the appointment of new grades of emergency citation attempts in futile cases are common.37
physicians. Many of these models attempt to sup- Even when there is clear evidence that cardiac
port the primary admitting team with the skills arrest or death is likely, ward staff rarely make
of ‘resuscitation’ specialists.46 Medical and surgi- decisions about the patient’s resuscitation status.4
cal assessment units act as a single location for all Many European countries have no formal policy for
acute admissions until their required level of care recording DNAR decisions and the practice of con-
is evaluated. Patients are monitored and observed sulting patients about the decision is variable.56
for periods of up to 72 h, and there is usually Improved knowledge, training and DNAR decision-
rapid access to senior medical staff, diagnostics and making should improve patient care and prevent
urgent treatment.47 The single location provides a futile CPR attempts (see Section 8).
central focus for on-call medical, nursing and phys-
iotherapy staff, in contrast to the traditional system
Guidelines for prevention of in-hospital
in which staff and patients are dispersed through-
out the hospital. cardiac arrest
Many acutely ill patients present to hospital via
The following strategies may prevent avoidable in-
the ED and are obviously in need of immediate
hospital cardiac arrests.
ICU-type interventions. Early goal-directed therapy
in the ED reverses physiological derangement and 1. Provide care for patients who are critically ill
appears to improve patient survival.48 or at risk of clinical deterioration in appropriate
areas, with the level of care provided matched
Appropriate placement of patients to the level of patient sickness.
2. Critically ill patients need regular observations:
Ideally, the sickest patients should be admitted match the frequency and type of observations to
to an area that can provide the greatest super- the severity of illness or the likelihood of clinical
vision and the highest level of organ support and deterioration and cardiopulmonary arrest. Often
nursing care. This often occurs, but some patients only simple vital sign observations (pulse, blood
are placed incorrectly.49 International organisa- pressure, respiratory rate) are needed.
tions have offered definitions of levels of care and 3. Use an EWS system to identify patients who are
produced admission and discharge criteria for high critically ill and or at risk of clinical deteriora-
dependency units (HDUs) and ICUs.50,51 tion and cardiopulmonary arrest.
4. Use a patient charting system that enables the
Staffing levels regular measurement and recording of EWS.
5. Have a clear and specific policy that requires
Hospital staffing tends to be at its lowest during the a clinical response to EWS systems. This should
night and at weekends. This may influence patient include advice on the further clinical manage-
monitoring, treatment and outcomes. Admission to ment of the patient and the specific responsibil-
a general medical ward after 17:00 h52 or to hos- ities of medical and nursing staff.
pital at weekends53 is associated with increased 6. The hospital should have a clearly identified
mortality. Patients who are discharged from ICUs response to critical illness. This may include
to general wards at night have an increased risk of a designated outreach service or resuscitation
in-hospital death compared with those discharged team (e.g. MET) capable of responding to acute
during the day and those discharged to HDUs.54 One clinical crises identified by clinical triggers or
S42 J.P. Nolan et al.

other indicators. This service must be available risk of cardiac arrest should be cared for in a mon-
24 h per day. itored area where facilities for immediate resusci-
7. Train all clinical staff in the recognition, mon- tation are available.
itoring and management of the critically ill
patient. Include advice on clinical management Training of first responders
while awaiting the arrival of more experienced
staff. All healthcare professionals should be able to
8. Identify patients for whom cardiopulmonary recognise cardiac arrest, call for help and start CPR.
arrest is an anticipated terminal event and in Staff should do what they have been trained to do.
whom CPR is inappropriate, and patients who For example, staff in critical care and emergency
do not wish to be treated with CPR. Hospitals medicine will have more advanced resuscitation
should have a DNAR policy, based on national skills than staff who are not involved regularly in
guidance, which is understood by all clinical resuscitation in their normal clinical role. Hospital
staff. staff who attend a cardiac arrest may have differ-
9. Ensure accurate audit of cardiac arrest, ‘false ent levels of skill to manage the airway, breathing
arrest’, unexpected deaths and unanticipated and circulation. Rescuers must undertake the skills
ICU admissions using common datasets. Audit in which they are trained and competent.
also the antecedents and clinical response to
these events.
Number of responders

The single responder must ensure that help is com-


4b. In-hospital resuscitation ing. If other staff are nearby, several actions can be
undertaken simultaneously.
After in-hospital cardiac arrest, the division
between basic life support and advanced life sup-
port is arbitrary; in practice, the resuscitation pro- Equipment available
cess is a continuum and is based on common sense.
All clinical areas should have immediate access
The public expect that clinical staff can under-
to resuscitation equipment and drugs to facilitate
take cardiopulmonary resuscitation (CPR). For all
rapid resuscitation of the patient in cardiopul-
in-hospital cardiac arrests, ensure that:
monary arrest. Ideally, the equipment used for CPR
• cardiorespiratory arrest is recognised immedi- (including defibrillators) and the layout of equip-
ately ment and drugs should be standardised throughout
• help is summoned using a standard telephone the hospital.57
number
• CPR is started immediately using airway Resuscitation team
adjuncts, e.g. a pocket mask and, if indicated,
defibrillation attempted within 3 min The resuscitation team may take the form of a tra-
The exact sequence of actions after in-hospital ditional cardiac arrest team, which is called only
cardiac arrest will depend on many factors, includ- when cardiac arrest is recognised. Alternatively,
ing: hospitals may have strategies to recognise patients
at risk of cardiac arrest and summon a team (e.g.,
• location (clinical/non-clinical area; moni- MET) before cardiac arrest occurs.35,36,39,41,58 The
tored/unmonitored area) term ‘resuscitation team’ reflects the range of
• training of the first responders response teams. In hospital cardiac arrests are
• number of responders rarely sudden or unexpected. A strategy of recog-
• equipment available nising patients at risk of cardiac arrest may enable
• hospital response system to cardiac arrest and some of these arrests to be prevented, or may pre-
medical emergencies, (e.g. MET) cardiac arrest vent futile resuscitation attempts in those who are
team unlikely to benefit from CPR.
Location
Immediate actions for a collapsed patient in
Patients who have monitored arrests are usu- a hospital
ally diagnosed rapidly. Ward patients may have
had a period of deterioration and an unwitnessed An algorithm for the initial management of in-
arrest.3,4,6—8 Ideally, all patients who are at high hospital cardiac arrest is shown in Figure 4.1.
European Resuscitation Council Guidelines for Resuscitation 2005 S43

Figure 4.1 Algorithm for the treatment of in-hospital cardiac arrest.

• Ensure personal safety. ◦ Open the airway using a head tilt chin lift
• Check the victim for a response. ◦ Look in the mouth. If a foreign body or debris
• When healthcare professionals see a patient col- is visible attempt to remove with forceps or
lapse or find a patient apparently unconscious in suction as appropriate
a clinical area, they should first shout for help, ◦ If you suspect that there may have been an
then assess if the patient is responsive. Gently injury to the neck, try to open the airway using
shake the shoulders and ask loudly: ‘‘Are you all a jaw thrust. Remember that maintaining an
right?’’ airway and adequate ventilation is the overrid-
• If other members of staff are nearby, it will be ing priority in managing a patient with a sus-
possible to undertake actions simultaneously. pected spinal injury. If this is unsuccessful, use
just enough head tilt to clear the airway. Use
The responsive patient manual in-line stabilisation to minimise head
movement if sufficient rescuers are available.
Urgent medical assessment is required. Depending
on the local protocols, this may take the form of a Keeping the airway open, look, listen, and feel
resuscitation team (e.g., MET). While awaiting this for normal breathing (an occasional gasp, slow,
team, give the patient oxygen, attach monitoring laboured or noisy breathing is not normal):
and insert an intravenous cannula. • Look for chest movement
• Listen at the victim’s mouth for breath sounds
The unresponsive patient • Feel for air on your cheek
The exact sequence will depend on the training Look, listen, and feel for no more than 10 s to
of staff and experience in assessment of breath- determine if the victim is breathing normally
ing and circulation. Trained healthcare staff cannot
assess the breathing and pulse sufficiently reliably • Check for signs of a circulation:
to confirm cardiac arrest.16,59,60 Agonal breathing ◦ It may be difficult to be certain that there is no
(occasional gasps, slow, laboured or noisy breath- pulse. If the patient has no signs of life (lack
ing) is common in the early stages of cardiac arrest of movement, normal breathing, or coughing),
and is a sign of cardiac arrest and should not be start CPR until more experience help arrives or
confused as a sign of life/circulation. the patient shows signs of life.
◦ Those experienced in clinical assessment
• Shout for help (if not already) should assess the carotid pulse whilst simulta-
Turn the victim on to his back and then open the neously looking for signs of life for not more
airway: than 10 s.
◦ If the patient appears to have no signs of life, or
• Open Airway and check breathing: if there is doubt, start CPR immediately. Delays
S44 J.P. Nolan et al.

in diagnosis of cardiac arrest and starting CPR • Recommence chest compressions immediately
will adversely effect survival must be avoided. after the defibrillation attempt. Minimise inter-
ruptions to chest compressions.
If there is a pulse or signs of life, urgent medi- • Continue resuscitation until the resuscitation
cal assessment is required. Depending on the local team arrives or the patient shows signs of life.
protocols, this may take the form of a resusci- Follow the voice prompts if using an AED. If using
tation team. While awaiting this team, give the a manual defibrillator, follow the universal algo-
patient oxygen, attach monitoring, and insert an rithm for advanced life support (Section 4c).
intravenous cannula. • Once resuscitation is underway, and if there are
If there is no breathing, but there is a pulse (res- sufficient staff present, prepare intravenous can-
piratory arrest), ventilate the patient’s lungs and nulae and drugs likely to be used by the resusci-
check for a circulation every 10 breaths. tation team (e.g. adrenaline).
• Identify one person to be responsible for han-
Starting in-hospital CPR dover to the resuscitation team leader. Locate
the patient’s records.
• One person starts CPR as others call the resusci- • The quality of chest compressions during in-
tation team and collect the resuscitation equip- hospital CPR is frequently sub-optimal.61,62 The
ment and a defibrillator. If only one member team leader should monitor the quality of CPR
of staff is present, this will mean leaving the and change CPR providers if the quality of CPR
patient. is poor. The person providing chest compressions
• Give 30 chest compressions followed by 2 venti- should be changed every 2 min.
lations.
• Undertaking chest compressions properly is tir- The monitored and witnessed cardiac arrest
ing; try to change the person doing chest com-
pressions every 2 min. If a patient has a monitored and witnessed cardiac
• Maintain the airway and ventilate the lungs with arrest, act as follows.
the most appropriate equipment immediately to
hand. A pocket mask, which may be supple- • Confirm cardiac arrest and shout for help.
mented with an oral airway, is usually readily • Consider a precordial thump if the rhythm is
available. Alternatively, use a laryngeal mask air- VF/VT and a defibrillator is not immediately
way (LMA) and self-inflating bag, or bag-mask, available.
according to local policy. Tracheal intubation • If the initial rhythm is VF/VT and a defibrillator
should be attempted only by those who are is immediately available, give a shock first. The
trained, competent and experienced in this skill. use of adhesive electrode pads or a ‘quick-look’
• Use an inspiratory time of 1 s and give enough paddles technique will enable rapid assessment
volume to produce a normal chest rise. Add sup- of heart rhythm compared with attaching ECG
plemental oxygen as soon as possible. electrodes.63
• Once the patient’s trachea has been intubated,
continue chest compressions uninterrupted Training for healthcare professionals
(except for defibrillation or pulse checks when
indicated), at a rate of 100 min−1 , and ventilate The Immediate Life Support course trains health-
the lungs at approximately 10 breaths min−1 . care professionals in the skills required to start
Avoid hyperventilation. resuscitation, including defibrillation, and to be
• If there is no airway and ventilation equipment members of a cardiac arrest team (see Section 9).64
available, give mouth-to-mouth ventilation. If The Advanced Life Support (ALS) course teaches the
there are clinical reasons to avoid mouth-to- skills required for leading a resuscitation team.65,66
mouth contact, or you are unwilling or unable
to do this, do chest compressions until help or
airway equipment arrives. 4c. ALS treatment algorithm
• When the defibrillator arrives, apply the pad-
dles to the patient and analyse the rhythm. If Introduction
self-adhesive defibrillation pads are available,
apply these without interrupting chest compres- Heart rhythms associated with cardiac arrest are
sions. Pause briefly to assess the heart rhythm. If divided into two groups: shockable rhythms (ven-
indicated, attempt either manual or automated tricular fibrillation/pulseless ventricular tachycar-
external defibrillation (AED). dia (VF/VT)) and non-shockable rhythms (asystole
European Resuscitation Council Guidelines for Resuscitation 2005 S45

Figure 4.2 Advanced life support cardiac arrest algorithm.

and pulseless electrical activity (PEA)). The prin- discharge after cardiac arrest, although they are
cipal difference in the management of these two still included among ALS interventions. Thus, during
groups of arrhythmias is the need for attempted advanced life support, attention must be focused
defibrillation in those patients with VF/VT. Subse- on early defibrillation and high-quality, uninter-
quent actions, including chest compressions, air- rupted BLS.
way management and ventilation, venous access,
administration of adrenaline and the identification Shockable rhythms (ventricular
and correction of reversible factors, are common to
fibrillation/pulseless ventricular
both groups.
tachycardia)
Although the ALS cardiac arrest algorithm
(Figure 4.2) is applicable to all cardiac arrests, In adults, the commonest rhythm at the time of
additional interventions may be indicated for car- cardiac arrest is VF, which may be preceded by a
diac arrest caused by special circumstances (Sec- period of VT or even supraventricular tachycardia
tion 7). (SVT).67 Having confirmed cardiac arrest, summon
The interventions that unquestionably con- help (including the request for a defibrillator) and
tribute to improved survival after cardiac arrest are start CPR, beginning with external chest compres-
early defibrillation for VF/VT and prompt and effec- sion, with a compression:ventilation (CV) ratio of
tive bystander basic life support (BLS). Advanced 30:2. As soon as the defibrillator arrives, diagnose
airway intervention and the delivery of drugs have the rhythm by applying paddles or self-adhesive
not been shown to increase survival to hospital pads to the chest.
S46 J.P. Nolan et al.

If VF/VT is confirmed, charge the defibrillator and energy substrates and increase the probabil-
and give one shock (150—200-J biphasic or 360- ity of restoring a perfusing rhythm after shock
J monophasic). Without reassessing the rhythm or delivery.71 Analyses of VF waveform character-
feeling for a pulse, resume CPR (CV ratio 30:2) istics predictive of shock success indicate that
immediately after the shock, starting with chest the shorter the time between chest compression
compressions. Even if the defibrillation attempt is and shock delivery, the more likely the shock
successful in restoring a perfusing rhythm, it is very will be successful.71,72 Reduction in the interval
rare for a pulse to be palpable immediately after from compression to shock delivery by even a
defibrillation,68 and the delay in trying to palpate few seconds can increase the probability of shock
a pulse will further compromise the myocardium success.73
if a perfusing rhythm has not been restored.69 If Regardless of the arrest rhythm, give adrenaline
a perfusing rhythm has been restored, giving chest 1 mg every 3—5 min until ROSC is achieved; this
compressions does not increase the chance of VF will be once every two loops of the algorithm. If
recurring.70 In the presence of post-shock asystole, signs of life return during CPR (movement, normal
chest compressions may usefully induce VF.70 Con- breathing, or coughing), check the monitor: if an
tinue CPR for 2 min, then pause briefly to check the organised rhythm is present, check for a pulse. If a
monitor: if there is still VF/VT, give a second shock pulse is palpable, continue post-resuscitation care
(150—360-J biphasic or 360-J monophasic). Resume and/or treatment of peri-arrest arrhythmia. If no
CPR immediately after the second shock. pulse is present, continue CPR. Providing CPR with
Pause briefly after 2 min of CPR to check the a CV ratio of 30:2 is tiring; change the individual
monitor: if there is still VF/VT, give adrenaline undertaking compressions every 2 min.
followed immediately by a third shock (150—360-
J biphasic or 360-J monophasic) and resumption Precordial thump
of CPR (drug-shock-CPR-rhythm check sequence).
Minimise the delay between stopping chest com- Consider giving a single precordial thump when car-
pressions and delivery of the shock. The adenaline diac arrest is confirmed rapidly after a witnessed,
that is given immediately before the shock will be sudden collapse and a defibrillator is not immedi-
circulated by the CPR that immediately follows the ately to hand (Section 3).74 These circumstances
shock. After drug delivery and 2 min of CPR, anal- are most likely to occur when the patient is mon-
yse the rhythm and be prepared to deliver another itored. A precordial thump should be undertaken
shock immediately if indicated. If VF/VT persists immediately after confirmation of cardiac arrest
after the third shock, give an intravenous bolus of and only by healthcare professionals trained in
amiodarone 300 mg. Inject the amiodarone during the technique. Using the ulnar edge of a tightly
the brief rhythm analysis before delivery of the clenched fist, deliver a sharp impact to the lower
fourth shock. half of the sternum from a height of about 20 cm,
When the rhythm is checked 2 min after giving then retract the fist immediately to create an
a shock, if a nonshockable rhythm is present and impulse-like stimulus. A precordial thump is most
the rhythm is organised (complexes appear regular likely to be successful in converting VT to sinus
or narrow), try to palpate a pulse. Rhythm checks rhythm. Successful treatment of VF by precor-
must be brief, and pulse checks undertaken only dial thump is much less likely: in all the reported
if an organised rhythm is observed. If an organ- successful cases, the precordial thump was given
ised rhythm is seen during a 2 min period of CPR, within the first 10 s of VF.75 There are very rare
do not interrupt chest compressions to palpate a reports of a precordial thump converting a perfus-
pulse unless the patient shows signs of life suggest- ing to a non-perfusing rhythm.76
ing ROSC. If there is any doubt about the presence
of a pulse in the presence of an organised rhythm, Airway and ventilation
resume CPR. If the patient has ROSC, begin postre-
suscitation care. If the patient’s rhythm changes During the treatment of persistent VF, ensure good-
to asystole or PEA, see non-shockable rhythms quality chest compressions between defibrillation
below. attempts. Consider reversible causes (4 H’s and 4
During treatment of VF/VT, healthcare providers T’s) and, if identified, correct them. Check the
must practice efficient coordination between CPR electrode/defibrillating paddle positions and con-
and shock delivery. When VF is present for more tacts, and the adequacy of the coupling medium,
than a few minutes, the myocardium is depleted e.g. gel pads. Tracheal intubation provides the
of oxygen and metabolic substrates. A brief most reliable airway, but should be attempted
period of chest compressions will deliver oxygen only if the healthcare provider is properly trained
European Resuscitation Council Guidelines for Resuscitation 2005 S47

and has adequate ongoing experience with the route for vascular access in children, it can also be
technique. Personnel skilled in advanced airway effective in adults.78 Intraosseous injection of drugs
management should attempt laryngoscopy with- achieves adequate plasma concentrations in a time
out stopping chest compressions; a brief pause in comparable with injection through a central venous
chest compressions may be required as the tube catheter. The intraosseous route also enables with-
is passed through the vocal cords. Alternatively, to drawal of marrow for venous blood gas analysis and
avoid any interruptions in chest compressions, the measurement of electrolytes and haemoglobin con-
intubation attempt may be deferred until return centration.
of spontaneous circulation. No intubation attempt
should take longer than 30 s: if intubation has not Tracheal route. If neither intravenous nor
been achieved after this time, recommence bag- intraosseous access can be established, some
mask ventilation. After intubation, confirm cor- drugs can be given by the tracheal route. How-
rect tube position and secure it adequately. Once ever, unpredictable plasma concentrations are
the patient’s trachea has been intubated, con- achieved when drugs are given via a tracheal tube,
tinue chest compressions, at a rate of 100 min−1 , and the optimal tracheal dose of most drugs is
without pausing during ventilation. Ventilate the unknown. During CPR, the equipotent dose of
lungs at 10 breaths min−1 ; do not hyperventilate adrenaline given via the trachea is three to ten
the patient. A pause in the chest compressions times higher than the intravenous dose.79,80 Some
allows the coronary perfusion pressure to fall sub- animal studies suggest that the lower adrenaline
stantially. On resuming compressions there is some concentrations achieved when the drug is given via
delay before the original coronary perfusion pres- the trachea may produce transient beta-adrenergic
sure is restored, thus chest compressions that are effects, which will cause hypotension and lower
not interrupted for ventilation result in a substan- coronary artery perfusion pressure.81—84 If given
tially higher mean coronary perfusion pressure. via the trachea, the dose of adrenaline is 3 mg
In the absence of personnel skilled in tracheal diluted to at least 10 ml with sterile water. Dilution
intubation, acceptable alternatives are the Com- with water instead of 0.9% saline may achieve
bitube, laryngeal mask airway (LMA), ProSeal LMA, better drug absorption.85 The solutions in prefilled
or Laryngeal Tube (Section 4d). Once one of these syringes are acceptable for this purpose.
airways has been inserted, attempt to deliver con- Adrenaline. Despite the widespread use of
tinuous chest compressions, uninterrupted during adrenaline during resuscitation, and several
ventilation. If excessive gas leakage causes inade- studies involving vasopressin, there is no placebo-
quate ventilation of the patient’s lungs, chest com- controlled study that shows that the routine use of
pressions will have to be interrupted to enable ven- any vasopressor at any stage during human cardiac
tilation (using a CV ratio of 30:2). arrest increases survival to hospital discharge. Cur-
During continuous chest compressions, ventilate rent evidence is insufficient to support or refute
the lungs at 10 breaths min−1 . the routine use of any particular drug or sequence
of drugs. Despite the lack of human data, the use
Intravenous access and drugs of adrenaline is still recommended, based largely
on animal data. The alpha-adrenergic actions of
Peripheral versus central venous drug delivery. adrenaline cause vasoconstriction, which increases
Establish intravenous access if this has not already myocardial and cerebral perfusion pressure. The
been achieved. Although peak drug concentrations higher coronary blood flow increases the frequency
are higher and circulation times are shorter when of the VF waveform and should improve the chance
drugs are injected into a central venous catheter of restoring a circulation when defibrillation is
compared with a peripheral cannula,77 insertion of attempted.86—88 The optimal duration of CPR and
a central venous catheter requires interruption of number of shocks that should be given before
CPR and is associated with several complications. giving drugs is unknown. On the basis of expert
Peripheral venous cannulation is quicker, easier to consensus, if VF/VT persists after two shocks,
perform and safer. Drugs injected peripherally must give adrenaline and repeat every 3—5 min during
be followed by a flush of at least 20 ml of fluid and cardiac arrest. Do not interrupt CPR to give drugs.
elevation of the extremity for 10—20 s to facilitate
drug delivery to the central circulation. Anti-arrhythmic drugs. There is no evidence that
giving any anti-arrhythmic drug routinely dur-
Intraosseous route. If intravenous access is diffi- ing human cardiac arrest increases survival to
cult or impossible, consider the intraosseous route. hospital discharge. In comparison with placebo89
Although normally considered as an alternative and lidocaine,90 the use of amiodarone in shock-
S48 J.P. Nolan et al.

refractory VF improves the short-term outcome of Non-shockable rhythms (PEA and asystole)
survival to hospital admission. In these studies,
the anti-arrhythmic therapy was given if VF/VT Pulseless electrical activity (PEA) is defined as
persisted after at least three shocks; however, cardiac electrical activity in the absence of any
these were delivered using the conventional three- palpable pulses. These patients often have some
stacked shocks strategy. There are no data on the mechanical myocardial contractions, but these are
use of amiodarone for shock-refractory VF/VT when too weak to produce a detectable pulse or blood
single shocks are used. On the basis of expert con- pressure. PEA is often caused by reversible condi-
sensus, if VF/VT persists after three shocks, give tions, and can be treated if those conditions are
300 mg amiodarone by bolus injection. A further identified and corrected (see below). Survival fol-
dose of 150 mg may be given for recurrent or refrac- lowing cardiac arrest with asystole or PEA is unlikely
tory VF/VT, followed by an infusion of 900 mg over unless a reversible cause can be found and treated
24. Lidocaine 1 mg kg−1 may be used as an alterna- effectively.
tive if amiodarone is not available, but do not give If the initial monitored rhythm is PEA or asys-
lidocaine if amiodarone has been given already. tole, start CPR 30:2 and give adrenaline 1 mg as
soon as intravascular access is achieved. If asystole
Magnesium. Although the routine use of mag- is displayed, check without stopping CPR that the
nesium in cardiac arrest does not increase leads are attached correctly. Asystole is a condi-
survival,91—95 give magnesium (8 mmol = 4 ml 50% tion that could be exacerbated or precipitated by
magnesium sulphate or 2 g) for refractory VF if excessive vagal tone and, theoretically, this could
there is any suspicion of hypomagnesaemia (e.g., be reversed by a vagolytic drug; therefore, despite
patients on potassium-losing diuretics). the lack of evidence that routine atropine for asys-
Bicarbonate. Administering sodium bicarbonate tolic cardiac arrest increases survival, give atropine
routinely during cardiac arrest and CPR (especially 3 mg (the dose that will provide maximum vagal
in out-of-hospital cardiac arrests) or after return of blockade) if there is asystole or the rhythm is slow
spontaneous circulation is not recommended. Give PEA (rate <60 min−1 ). Secure the airway as soon
sodium bicarbonate (50 mmol) if cardiac arrest is as possible, to enable chest compressions to be
associated with hyperkalaemia or tricyclic antide- delivered without pausing during ventilation. After
pressant overdose; repeat the dose according to the 2 min of CPR, recheck the rhythm. If no rhythm is
clinical condition and result of repeated blood gas present (asystole), or if there is no change in the
analysis. Some experts give bicarbonate if the arte- ECG appearance, resume CPR immediately. If an
rial pH is less than 7.1, but this is controversial. organised rhythm is present, attempt to palpate a
During cardiac arrest, arterial blood gas values do pulse. If no pulse is present (or if there is any doubt
not reflect the acid—base state of the tissues96 ; the about the presence of a pulse), continue CPR. If a
tissue pH will be lower than that in arterial blood. pulse is present, begin post-resuscitation care. If
Mixed venous blood values give a more accurate signs of life return during CPR, check the rhythm
estimate of the pH in the tissues,96 but it is rare and attempt to palpate a pulse.
for a pulmonary artery catheter to be in situ at the Whenever a diagnosis of asystole is made, check
time of cardiac arrest. If a central venous catheter the ECG carefully for the presence of P waves,
is in situ, central venous blood gas analysis will pro- because this may respond to cardiac pacing. There
vide a closer estimate of tissue acid/base state than is no benefit in attempting to pace true asystole.
that provided by arterial blood. If there is doubt about whether the rhythm is
asystole or fine VF, do not attempt defibrillation;
Persistent ventricular fibrillation instead, continue chest compressions and ventila-
tion. Fine VF that is difficult to distinguish from
In VF persists, consider changing the position of asystole will not be shocked successfully into a per-
the paddles (Section 3). Review all potentially fusing rhythm. Continuing good-quality CPR may
reversible causes (see below) and treat any that improve the amplitude and frequency of the VF and
are identified. improve the chance of successful defibrillation to a
The duration of any individual resuscitation perfusing rhythm. Delivering repeated shocks in an
attempt is a matter of clinical judgement, taking attempt to defibrillate what is thought to be fine VF
into consideration the circumstances and the per- will increase myocardial injury, both directly from
ceived prospect of a successful outcome. If it was the electricity and indirectly from the interruptions
considered appropriate to start resuscitation, it is in coronary blood flow.
usually considered worthwhile continuing as long as During the treatment of asystole or PEA, if
the patient remains in VF/VT. the rhythm changes to VF, follow the left side of
European Resuscitation Council Guidelines for Resuscitation 2005 S49

the algorithm. Otherwise, continue CPR and give In the absence of a specific history, the acci-
adrenaline every 3—5 min (every other loop of the dental or deliberate ingestion of therapeutic or
algorithm). toxic substances may be revealed only by labora-
tory investigations (Section 7b). Where available,
the appropriate antidotes should be used, but most
Potentially reversible causes often treatment is supportive.
The commonest cause of thromboembolic or
Potential causes or aggravating factors for which
mechanical circulatory obstruction is massive pul-
specific treatment exists must be considered during
monary embolus. If cardiac arrest is thought to be
any cardiac arrest. For ease of memory, these are
caused by pulmonary embolism, consider giving a
divided into two groups of four based upon their
thrombolytic drug immediately (Section 4e).97
initial letter: either H or T. More details on many of
these conditions are covered in Section 7.

4d. Airway management and ventilation


The four Hs

Minimise the risk of hypoxia by ensuring that the


Introduction
patient’s lungs are ventilated adequately with 100% Patients requiring resuscitation often have an
oxygen. Make sure there is adequate chest rise obstructed airway, usually secondary to loss of con-
and bilateral breath sounds. Using the techniques sciousness, but occasionally it may be the primary
described in Section 4d, check carefully that the cause of cardiorespiratory arrest. Prompt assess-
tracheal tube is not misplaced in a bronchus or the ment, with control of the airway and ventilation of
oesophagus. the lungs, is essential. This will help to prevent sec-
Pulseless electrical activity caused by hypo- ondary hypoxic damage to the brain and other vital
volaemia is due usually to severe haemorrhage. organs. Without adequate oxygenation it may be
This may be precipitated by trauma (Section 7i), impossible to restore a spontaneous cardiac output.
gastrointestinal bleeding or rupture of an aortic These principles may not apply to the witnessed pri-
aneurysm. Intravascular volume should be restored mary cardiac arrest in the vicinity of a defibrillator;
rapidly with fluid, coupled with urgent surgery to in this case, the priority is immediate attempted
stop the haemorrhage. defibrillation.
Hyperkalaemia, hypokalaemia, hypocalcaemia,
acidaemia and other metabolic disorders are
detected by biochemical tests or suggested by the Airway obstruction
patient’s medical history, e.g. renal failure (Sec-
Causes of airway obstruction
tion 7a). A 12-lead ECG may be diagnostic. Intra-
venous calcium chloride is indicated in the pres- Obstruction of the airway may be partial or com-
ence of hyperkalaemia, hypocalcaemia and calcium plete. It may occur at any level, from the nose
channel-blocker overdose. and mouth down to the trachea (Figure 4.3). In
Suspect hypothermia in any drowning incident the unconscious patient, the commonest site of
(Sections 7c and d); use a low-reading thermome- airway obstruction is at the level of the pharynx.
ter. Until recently this obstruction had been attributed
to posterior displacement of the tongue caused by
The four Ts decreased muscle tone; with the tongue ultimately
touching the posterior pharyngeal wall. The pre-
A tension pneumothorax may be the primary cause cise cause of airway obstruction in the unconscious
of PEA and may follow attempts at central venous state has been identified by studying patients under
catheter insertion. The diagnosis is made clinically. general anaesthesia.98,99 These studies of anaes-
Decompress rapidly by needle thoracocentesis, and thetised patients have shown that the site of air-
then insert a chest drain. way obstruction is at the soft palate and epiglottis
Cardiac tamponade is difficult to diagnose and not the tongue. Obstruction may be caused
because the typical signs of distended neck veins also by vomit or blood (regurgitation of gastric
and hypotension are usually obscured by the contents or trauma), or by foreign bodies. Laryn-
arrest itself. Cardiac arrest after penetrating chest geal obstruction may be caused by oedema from
trauma is highly suggestive of tamponade and is an burns, inflammation or anaphylaxis. Upper airway
indication for needle pericardiocentesis or resusci- stimulation may cause laryngeal spasm. Obstruc-
tative thoracotomy (see Section 7i). tion of the airway below the larynx is less com-
S50 J.P. Nolan et al.

In a patient who is making respiratory efforts,


complete airway obstruction causes paradoxical
chest and abdominal movement, often described
as ‘see-saw breathing’. As the patient attempts to
breathe in, the chest is drawn in and the abdomen
expands; the opposite occurs during expiration.
This is in contrast to the normal breathing pattern
of synchronous movement upwards and outwards
of the abdomen (pushed down by the diaphragm)
with the lifting of the chest wall. During airway
obstruction, other accessory muscles of respiration
are used, with the neck and the shoulder mus-
cles contracting to assist movement of the tho-
racic cage. Full examination of the neck, chest and
abdomen is required to differentiate the paradox-
ical movements that may mimic normal respira-
tion. The examination must include listening for
the absence of breath sounds in order to diagnose
complete airway obstruction reliably; any noisy
breathing indicates partial airway obstruction. Dur-
ing apnoea, when spontaneous breathing move-
ments are absent, complete airway obstruction is
recognised by failure to inflate the lungs during
attempted positive pressure ventilation. Unless air-
way patency can be re-established to enable ade-
quate lung ventilation within a period of a very few
minutes, neurological and other vital organ injury
may occur, leading to cardiac arrest.

Figure 4.3 Causes of airway obstruction.


Basic airway management
mon, but may arise from excessive bronchial secre-
tions, mucosal oedema, bronchospasm, pulmonary Once any degree of obstruction is recognised,
oedema or aspiration of gastric contents. immediate measures must be taken to create and
maintain a clear airway. There are three manoeu-
Recognition of airway obstruction vres that may improve the patency of an airway
obstructed by the tongue or other upper airway
Airway obstruction can be subtle and is often missed structures: head tilt, chin lift, and jaw thrust.
by healthcare professionals, let alone by lay peo-
ple. The ‘look, listen and feel’ approach is a simple, Head tilt and chin lift
systematic method of detecting airway obstruction.
The rescuer’s hand is placed on the patient’s fore-
• Look for chest and abdominal movements. head and the head gently tilted back; the fingertips
• Listen and feel for airflow at the mouth and nose. of the other hand are placed under the point of the
In partial airway obstruction, air entry is dimin- patient’s chin, which is gently lifted to stretch the
ished and usually noisy. Inspiratory stridor is caused anterior neck structures (Figure 4.4).100—105
by obstruction at the laryngeal level or above. Expi-
ratory wheeze implies obstruction of the lower air- Jaw thrust
ways, which tend to collapse and obstruct during
expiration. Other characteristic sounds include the Jaw thrust is an alternative manoeuvre for bringing
following: the mandible forward and relieving obstruction by
the soft palate and epiglottis. The rescuer’s index
• Gurgling is caused by liquid or semisolid foreign and other fingers are placed behind the angle of
material in the main airways. the mandible, and pressure is applied upwards and
• Snoring arises when the pharynx is partially forwards. Using the thumbs, the mouth is opened
occluded by the soft palate or epiglottis. slightly by downward displacement of the chin
• Crowing is the sound of laryngeal spasm. (Figure 4.5).
European Resuscitation Council Guidelines for Resuscitation 2005 S51

Airway management in patients with suspected


cervical spine injury

If spinal injury is suspected (e.g., if the victim has


fallen, been struck on the head or neck, or has been
rescued after diving into shallow water), maintain
the head, neck, chest and lumbar region in the neu-
tral position during resuscitation. Excessive head
tilt could aggravate the injury and damage the cer-
vical spinal cord106—110 ; however, this complication
has not been documented and the relative risk is
unknown. When there is a risk of cervical spine
injury, establish a clear upper airway by using jaw
thrust or chin lift in combination with manual in-
line stabilisation (MILS) of the head and neck by an
assistant.111,112 If life-threatening airway obstruc-
tion persists despite effective application of jaw
thrust or chin lift, add head tilt a small amount
at a time until the airway is open; establishing a
patent airway takes priority over concerns about a
potential cervical spine injury.

Adjuncts to basic airway techniques

Simple airway adjuncts are often helpful, and


sometimes essential, to maintain an open airway,
Figure 4.4 Head tilt and chin lift. © 2005 European particularly when resuscitation is prolonged. The
Resuscitation Council.
position of the head and neck must be maintained
to keep the airway aligned. Oropharyngeal and
nasopharyngeal airways overcome backward dis-
These simple positional methods are successful placement of the soft palate and tongue in an
in most cases where airway obstruction results from unconscious patient, but head tilt and jaw thrust
relaxation of the soft tissues. If a clear airway can- may also be required.
not be achieved, look for other causes of airway
obstruction. Use a finger sweep to remove any solid Oropharyngeal airways. Oropharyngeal airways
foreign body seen in the mouth. Remove broken or are available in sizes suitable for the newborn
displaced dentures, but leave well-fitting dentures to large adults. An estimate of the size required
as they help to maintain the contours of the mouth, is obtained by selecting an airway with a length
facilitating a good seal for ventilation. corresponding to the vertical distance between

Figure 4.5 Jaw thrust. © 2005 European Resuscitation Council.


S52 J.P. Nolan et al.

Figure 4.6 Insertion of oropharyngeal airway. © 2005 European Resuscitation Council.


the patient’s incisors and the angle of the jaw Oxygen
(Figure 4.6). The most common sizes are 2, 3 and 4
for small, medium and large adults, respectively. Give oxygen whenever it is available. A stan-
If the glossopharyngeal and laryngeal reflexes dard oxygen mask will deliver up to 50% oxy-
are present, vomiting or laryngospasm may be gen concentration, providing the flow of oxygen
caused by inserting an oropharyngeal airway; thus, is high enough. A mask with a reservoir bag (non-
insertion should be attempted only in comatose rebreathing mask), can deliver an inspired oxygen
patients. The oropharyngeal airway can become concentration of 85% at flows of 10—15 l min−1 . Ini-
obstructed at three possible sites:113 part of the tially, give the highest possible oxygen concentra-
tongue can occlude the end of the airway; the air- tion, which can then be titrated to the oxygen sat-
way can lodge in the vallecula; and the airway can uration by pulse oximeter (SpO2 ) or arterial blood
be obstructed by the epiglottis. gases.

Nasopharyngeal airways. In patients who are not Suction


deeply unconscious, a nasopharyngeal airway is
tolerated better than an oropharyngeal airway. Use a wide-bore rigid sucker (Yankauer) to remove
The nasopharyngeal airway may be life saving in liquid (blood, saliva and gastric contents) from
patients with clenched jaws, trismus or maxillofa- the upper airway. Use the sucker cautiously if the
cial injuries, when insertion of an oral airway is patient has an intact gag reflex; the sucker can pro-
impossible. Inadvertent insertion of a nasopharyn- voke vomiting.
geal airway through a fracture of the skull base
and into the cranial vault is possible, but extremely Ventilation
rare.114,115 In the presence of a known or suspected
basal skull fracture an oral airway is preferred but, Provide artificial ventilation as soon as possible
if this is not possible and the airway is obstructed, for any patient in whom spontaneous ventilation
gentle insertion of a nasopharyngeal airway may be is inadequate or absent. Expired air ventilation
life saving (i.e., the benefits may far outweigh the (rescue breathing) is effective, but the rescuer’s
risks). expired oxygen concentration is only 16—17%, so
The tubes are sized in millimetres according to it must be replaced as soon as possible by venti-
their internal diameter, and the length increases lation with oxygen-enriched air. Although mouth-
with diameter. The traditional methods of siz- to-mouth ventilation has the benefit of not requir-
ing a nasopharyngeal airway (measurement against ing any equipment, the technique is aestheti-
the patient’s little finger or anterior nares) do cally unpleasant, particularly when vomit or blood
not correlate with the airway anatomy and are is present, and rescuers may be reluctant to
unreliable.116 Sizes of 6—7 mm are suitable for place themselves in intimate contact with a vic-
adults. Insertion can cause damage to the mucosal tim who may be unknown to them.118—121 There
lining of the nasal airway, with bleeding in up to are only isolated reports of individuals acquiring
30% of cases.117 If the tube is too long it may stim- infections after providing CPR, e.g. tuberculosis122
ulate the laryngeal or glossopharyngeal reflexes to and severe acute respiratory distress syndrome
produce laryngospasm or vomiting. (SARS).123 Transmission of human immunodefi-
European Resuscitation Council Guidelines for Resuscitation 2005 S53

an adequate volume, minimising the risk of gas-


tric inflation, and allowing adequate time for chest
compressions. During CPR with an unprotected air-
way, give two ventilations after each sequence of
30 chest compressions.

Self-inflating bag

The self-inflating bag can be connected to a face-


mask, tracheal tube or alternative airway device
such as the LMA or Combitube. Without supple-
mental oxygen, the self-inflating bag ventilates
the patient’s lungs with ambient air (21% oxygen).
This can be increased to about 45% by attaching
oxygen directly to the bag. If a reservoir system
is attached and the oxygen flow is increased to
approximately 10 l min−1 , an inspired oxygen con-
centration of approximately 85% can be achieved.
Figure 4.7 Mouth-to-mask ventilation. © 2005 Euro-
pean Resuscitation Council. Although the bag-mask device enables ventila-
tion with high concentrations of oxygen, its use by a
ciency virus (HIV) during provision of CPR has single person requires considerable skill. When used
never been reported. Simple adjuncts are avail- with a face mask, it is often difficult to achieve a
able to enable direct person-to-person contact to gas-tight seal between the mask and the patient’s
be avoided; some of these devices may reduce the face, and to maintain a patent airway with one hand
risk of cross-infection between patient and res- while squeezing the bag with the other.124 Any sig-
cuer, although they are unlikely to offer significant nificant leak will cause hypoventilation and, if the
protection from SARS.123 The pocket resuscitation airway is not patent, gas may be forced into the
mask is used widely. It is similar to an anaesthetic stomach.125,126 This will reduce ventilation further
facemask, and enables mouth-to-mask ventilation. and greatly increase the risk of regurgitation and
It has a unidirectional valve, which directs the aspiration.127 Cricoid pressure can reduce this risk
patient’s expired air away from the rescuer. The but requires the presence of a trained assistant.
mask is transparent so that vomit or blood from the Poorly applied cricoid pressure may make it more
patient can be seen. Some masks have a connec- difficult to ventilate the patient’s lungs.128
tor for the addition of oxygen. When using masks The two-person technique for bag-mask venti-
without a connector, supplemental oxygen can be lation is preferable (Figure 4.8). One person holds
given by placing the tubing underneath one side and the facemask in place using a jaw thrust with both
ensuring an adequate seal. Use a two-hand tech-
nique to maximise the seal with the patient’s face
(Figure 4.7).
High airway pressures can be generated if the
tidal volumes or inspiratory flows are excessive,
predisposing to gastric inflation and subsequent risk
of regurgitation and pulmonary aspiration. The pos-
sibility of gastric inflation is increased by
• malalignment of the head and neck, and an
obstructed airway
• an incompetent oesophageal sphincter (present
in all patients with cardiac arrest)
• a high inflation pressure
Conversely, if inspiratory flow is too low, inspi-
ratory time will be prolonged and the time avail-
able to give chest compressions is reduced. Deliver
each breath over approximately 1 s and transfer
a volume that corresponds to normal chest move- Figure 4.8 The two-person technique for bag-mask ven-
ment; this represents a compromise between giving tilation. © 2005 European Resuscitation Council.
S54 J.P. Nolan et al.

hands, and an assistant squeezes the bag. In this A manikin study of simulated cardiac arrest and
way, a better seal can be achieved and the patient’s a study involving fire-fighters ventilating the lungs
lungs can be ventilated more effectively and safely. of anaesthetised patients both showed a signifi-
Once a tracheal tube, Combitube or supraglottic cant decrease in gastric inflation with manually-
airway device has been inserted, ventilate the lungs triggered flow-limited oxygen-powered resuscita-
at a rate of 10 breaths min−1 and continue chest tors and mask compared with a bag-mask.130,131
compressions without pausing during ventilations. However, the effect of automatic resuscitators on
The seal of the LMA around the larynx is unlikely gastric inflation in humans in cardiac arrest has not
to be good enough to prevent at least some gas been studied, and there are no data demonstrating
leaking when inspiration coincides with chest com- clear benefit over bag-valve-mask devices.
pressions. Moderate gas leakage is acceptable, par-
ticularly as most of this gas will pass up through the Alternative airway devices
patient’s mouth; if excessive gas leakage results in
inadequate ventilation of the patient’s lungs, chest The tracheal tube has generally been considered
compressions will have to be interrupted to enable the optimal method of managing the airway dur-
ventilation, using a compression—ventilation ratio ing cardiac arrest. There is evidence that, without
of 30:2. adequate training and experience, the incidence of
complications, such as unrecognised oesophageal
Automatic ventilators intubation (6—14% in some studies)132—135 and
dislodgement, is unacceptably high.136 Prolonged
Very few studies address specific aspects of ventila- attempts at tracheal intubation are harmful; the
tion during advanced life support. There are some cessation of chest compressions during this time
data indicating that the ventilation rates delivered will compromise coronary and cerebral perfusion.
by healthcare personnel during cardiac arrest are Several alternative airway devices have been con-
excessive.61,129 Automatic ventilators or resuscita- sidered for airway management during CPR. The
tors provide a constant flow of gas to the patient Combitube, the LMA, and the Laryngeal Tube
during inspiration; the volume delivered is depen- (LT) are the only alternative devices to be stud-
dent on the inspiratory time (a longer time provides ied during CPR, but none of these studies have
a greater tidal volume). Because pressure in the air- been powered adequately to enable survival to
way rises during inspiration, these devices are often be studied as a primary endpoint; instead, most
pressure limited to protect the lungs against baro- researchers have studied insertion and ventilation
trauma. An automatic ventilator can be used with success rates. There are no data supporting the
either a facemask or other airway device (e.g., tra- routine use of any specific approach to airway
cheal tube, LMA). management during cardiac arrest. The best tech-
An automatic resuscitator should be set ini- nique is dependent on the precise circumstances
tially to deliver a tidal volume of 6—7 ml kg−1 at of the cardiac arrest and the competence of the
10 breaths min−1 . Some ventilators have coordi- rescuer.
nated markings on the controls to facilitate easy
and rapid adjustment for patients of different sizes, Laryngeal mask airway (LMA)
and others are capable of sophisticated variation in
respiratory pattern. In the presence of a sponta- The laryngeal mask airway comprises a wide-bore
neous circulation, the correct setting will be deter- tube with an elliptical inflated cuff designed to seal
mined by analysis of the patient’s arterial blood around the laryngeal opening (Figure 4.9). It is eas-
gases. ier to insert than a tracheal tube.137—143 The LMA
Automatic resuscitators provide many advan- has been studied during CPR, but none of these
tages over alternative methods of ventilation. studies has compared it directly with the tracheal
tube. During CPR, successful ventilation is achieved
• In unintubated patients, the rescuer has both with the LMA in 72—98% of cases.144—150
hands free for mask and airway alignment. Ventilation using the LMA is more efficient and
• Cricoid pressure can be applied with one hand easier than with a bag-mask.124 When an LMA can be
while the other seals the mask on the face. inserted without delay it is preferable to avoid bag-
• In intubated patients they free the rescuer for mask ventilation altogether. When used for inter-
other tasks. mittent positive pressure ventilation, provided high
• Once set, they provide a constant tidal volume, inflation pressures (>20 cm H2 O) are avoided, gas-
respiratory rate and minute ventilation; thus, tric inflation can be minimised. In comparison with
they may help to avoid excessive ventilation. bag-mask ventilation, use of a self-inflating bag and
European Resuscitation Council Guidelines for Resuscitation 2005 S55

Figure 4.9 Insertion of a laryngeal mask airway. © 2005 European Resuscitation Council.

LMA during cardiac arrest reduces the incidence of may be one of the main benefits of a tracheal tube.
regurgitation.127 There are remarkably few cases of pulmonary aspi-
In comparison with tracheal intubation, the per- ration reported in the studies of the LMA during
ceived disadvantages of the LMA are the increased CPR.
risk of aspiration and inability to provide adequate
ventilation in patients with low lung and/or chest- The Combitube
wall compliance. There are no data demonstrating
whether or not it is possible to provide adequate The Combitube is a double-lumen tube intro-
ventilation via an LMA without interruption of chest duced blindly over the tongue, and provides a
compressions. The ability to ventilate the lungs route for ventilation whether the tube has passed
adequately while continuing to compress the chest into the oesophagus (Figure 4.10a) or the tra-

Figure 4.10 (a) Combitube in the oesophageal position. (b) Combitube in the tracheal position. © 2005 European
Resuscitation Council.
S56 J.P. Nolan et al.

chea (Figure 4.10b). There are many studies of version appeared to function slightly better.167 The
the Combitube in CPR and successful ventilation pharyngeal airway express (PAX) also performed
was achieved in 79—98% of patients.146,151—157 All poorly in one study of anaesthetised patients.168
except one151 of these studies involved out-of- There are no data on the use of either of these
hospital cardiac arrest, which reflects the infre- devices during CPR.
quency with which the Combitube is used in hospi-
tals. On the basis of these studies, the Combitube Intubating LMA. The intubating LMA (ILMA) is
appears as safe and effective as tracheal intubation valuable for managing the difficult airway during
for airway management during cardiac arrest; how- anaesthesia, but it has not been studied during
ever, there are inadequate survival data to be able CPR. Although it is relatively easy to insert the
to comment with certainty on the impact on out- ILMA,169,170 reliable, blind insertion of a tracheal
come. It is possible to attempt to ventilate the lungs tube requires considerable training171 and, for this
through the wrong port of the Combitube (2.2% in reason, it is not an ideal technique for the inexpe-
one study)152 : This is equivalent to unrecognised rienced provider.
oesophageal intubation with a standard tracheal
tube.
Tracheal intubation
Other airway devices
There is insufficient evidence to support or refute
Laryngeal Tube. The LT is a relatively new air- the use of any specific technique to maintain an
way device; its function in anaesthetised patients airway and provide ventilation in adults with car-
has been reported in several studies. The per- diopulmonary arrest. Despite this, tracheal intuba-
formance of the LT is favourable in comparison tion is perceived as the optimal method of providing
with the classic LMA and LMA,158,159 and success- and maintaining a clear and secure airway. It should
ful insertion rates have been reported even in be used only when trained personnel are available
studies of paramedics.160 There are sporadic case to carry out the procedure with a high level of skill
reports relating to use of the laryngeal tube during and confidence. The only randomised controlled
CPR.161,162 In a recent study, the LT was placed in trial comparing tracheal intubation with bag-mask
30 patients in cardiac arrest out of hospital by mini- ventilation was undertaken in children requir-
mally trained nurses.163 LT insertion was successful ing airway management out-of-hospital.172 In this
within two attempts in 90% of patients, and ventila- investigation there was no difference in survival to
tion was adequate in 80% of cases. No regurgitation discharge, but it is unclear how applicable this pae-
occurred in any patient. diatric study is to adult resuscitation. Two reports
compared outcomes from out-of-hospital cardiac
ProSeal LMA. The ProSeal LMA has been studied arrest in adults when treated by either emer-
extensively in anaesthetised patients, but there are gency medical technicians or paramedics.173,174
no studies of its function and performance during The skills provided by the paramedics, including
CPR. It has several attributes that, in theory, make intubation and intravenous cannulation and drug
it more suitable than the classic LMA for use dur- administration,174 made no difference to survival
ing CPR: improved seal with the larynx enabling to hospital discharge.
ventilation at higher airway pressures,164,165 the The perceived advantages of tracheal intubation
inclusion of a gastric drain tube enabling venting of over bag-mask ventilation include: maintenance of
liquid regurgitated gastric contents from the upper a patent airway, which is protected from aspiration
oesophagus and passage of a gastric tube to drain of gastric contents or blood from the oropharynx;
liquid gastric contents, and the inclusion of a bite ability to provide an adequate tidal volume reliably
block. The Proseal LMA has potential weaknesses as even when chest compressions are uninterrupted;
an airway device for CPR: it is slightly more difficult the potential to free the rescuer’s hands for other
to insert than a classic LMA, it is not available in dis- tasks; the ability to suction airway secretions; and
posable form and is relatively expensive, and solid the provision of a route for giving drugs. Use of the
regurgitated gastric contents will block the gastric bag-mask is more likely to cause gastric distension
drainage tube. Data are awaited on its performance which, theoretically, is more likely to cause regur-
during CPR. gitation with risk of aspiration. However, there are
no reliable data to indicate that the incidence of
Airway management device. In anaesthetised aspiration is any more in cardiac arrest patients
patients, the airway management device (AMD) ventilated with bag-mask versus those that are ven-
performed poorly in one study,166 but a modified tilated via tracheal tube.
European Resuscitation Council Guidelines for Resuscitation 2005 S57

The perceived disadvantages of tracheal intu- niques to confirm correct placement of the tra-
bation over bag-mask ventilation include: the risk cheal tube should reduce this risk. Primary assess-
of an unrecognised misplaced tracheal tube, which ment includes observation of chest expansion bilat-
in patients with out-of-hospital cardiac arrest in erally, auscultation over the lung fields bilater-
some studies ranges from 6%132—134 to 14%135 ; a ally in the axillae (breath sounds should be equal
prolonged period without chest compressions while and adequate) and over the epigastrium (breath
intubation is attempted; and a comparatively high sounds should not be heard). Clinical signs of cor-
failure rate. Intubation success rates correlate with rect tube placement (condensation in the tube,
the intubation experience attained by individual chest rise, breath sounds on auscultation of lungs,
paramedics.175 Rates for failure to intubate are and inability to hear gas entering the stomach) are
as high as 50% in prehospital systems with a low not completely reliable. Secondary confirmation of
patient volume and providers who do not perform tracheal tube placement by an exhaled carbon diox-
intubation frequently.134 The cost of training pre- ide or oesophageal detection device should reduce
hospital staff to undertake intubation should also the risk of unrecognised oesophageal intubation. If
be considered. Healthcare personnel who under- there is doubt about correct tube placement, use
take prehospital intubation should do so only within the laryngoscope and look directly to see if the tube
a structured, monitored programme, which should passes through the vocal cords.
include comprehensive competency-based training None of the secondary confirmation techniques
and regular opportunities to refresh skills. will differentiate between a tube placed in a main
In some cases, laryngoscopy and attempted bronchus and one placed correctly in the trachea.
intubation may prove impossible or cause life- There are inadequate data to identify the optimal
threatening deterioration in the patient’s condi- method of confirming tube placement during car-
tion. Such circumstances include acute epiglot- diac arrest, and all devices should be considered
tal conditions, pharyngeal pathology, head injury as adjuncts to other confirmatory techniques.176
(where straining may occur further rise in intracra- There are no data quantifying their ability to mon-
nial pressure) or cervical spine injury. In these itor tube position after initial placement.
circumstances, specialist skills such as the use of The oesophageal detector device creates a suc-
anaesthetic drugs or fibreoptic laryngoscopy may tion force at the tracheal end of the tracheal
be required. These techniques require a high level tube, either by pulling back the plunger on a large
of skill and training. syringe or releasing a compressed flexible bulb. Air
Rescuers must weigh the risks and benefits of is aspirated easily from the lower airways through
intubation against the need to provide effective a tracheal tube placed in the cartilage-supported
chest compressions. The intubation attempt will rigid trachea. When the tube is in the oesopha-
require interruption of chest compressions but, gus, air cannot be aspirated because the oesoph-
once an advanced airway is in place, ventilation agus collapses when aspiration is attempted. The
will not require interruption of chest compressions. oesophageal detector device is generally reliable in
Personnel skilled in advanced airway management patients with both a perfusing and a non-perfusing
should be able to undertake laryngoscopy with- rhythm, but it may be misleading in patients with
out stopping chest compressions; a brief pause in morbid obesity, late pregnancy or severe asthma
chest compressions will be required only as the or when there are copious tracheal secretions; in
tube is passed through the vocal cords. Alterna- these conditions the trachea may collapse when
tively, to avoid any interruptions in chest compres- aspiration is attempted.133,177—180
sions, the intubation attempt may be deferred until Carbon dioxide detector devices measure the
return of spontaneous circulation. No intubation concentration of exhaled carbon dioxide from the
attempt should take longer than 30 s; if intubation lungs. The persistence of exhaled carbon dioxide
has not been achieved after this time, recommence after six ventilations indicates placement of the
bag-mask ventilation. After intubation, tube place- tracheal tube in the trachea or a main bronchus.181
ment must be confirmed and the tube secured ade- Confirmation of correct placement above the carina
quately. will require auscultation of the chest bilaterally in
the mid-axillary lines. In patients with a sponta-
Confirmation of correct placement of the neous circulation, a lack of exhaled carbon dioxide
tracheal tube indicates that the tube is in the oesophagus. Dur-
ing cardiac arrest, pulmonary blood flow may be so
Unrecognised oesophageal intubation is the most low that there is insufficient exhaled carbon diox-
serious complication of attempted tracheal intuba- ide, so the detector does not identify a correctly
tion. Routine use of primary and secondary tech- placed tracheal tube. When exhaled carbon dioxide
S58 J.P. Nolan et al.

is detected in cardiac arrest, it indicates reliably 4e. Assisting the circulation


that the tube is in the trachea or main bronchus but,
when it is absent, tracheal tube placement is best Drugs and fluids for cardiac arrest
confirmed with an oesophageal detector device. A
variety of electronic as well as simple, inexpensive, This topic is divided into: drugs used during the
colorimetric carbon dioxide detectors are available management of a cardiac arrest; anti-arrhythmic
for both in-hospital and out-of-hospital use. drugs used in the peri-arrest period; other drugs
used in the peri-arrest period; fluids; and routes
for drug delivery. Every effort has been made to
Cricoid pressure
provide accurate information on the drugs in these
During bag-mask ventilation and attempted intuba- guidelines, but literature from the relevant phar-
tion, cricoid pressure applied by a trained assis- maceutical companies will provide the most up-to-
tant should prevent passive regurgitation of gas- date data.
tric contents and the consequent risk of pulmonary
aspiration. If the technique is applied imprecisely Drugs used during the treatment of cardiac
or with excessive force, ventilation and intubation arrest
can be made more difficult.128 If ventilation of the
patient’s lungs is not possible, reduce the pressure Only a few drugs are indicated during the imme-
applied to the cricoid cartilage or remove it com- diate management of a cardiac arrest, and there
pletely. If the patient vomits, release the cricoid is limited scientific evidence supporting their use.
immediately. Drugs should be considered only after initial shocks
have been delivered (if indicated) and chest com-
pressions and ventilation have been started.
Securing the tracheal tube There are three groups of drugs relevant to the
management of cardiac arrest that were reviewed
Accidental dislodgement of a tracheal tube can
during the 2005 Consensus Conference: vasopres-
occur at any time, but may be more likely during
sors, anti-arrhythmics and other drugs. Routes of
resuscitation and during transport. The most effec-
drug delivery other than the optimal intravenous
tive method for securing the tracheal tube has yet
route were also reviewed and are discussed.
to be determined; use either conventional tapes or
ties, or purpose-made tracheal tube holders.
Vasopressors
Cricothyroidotomy There are currently no placebo-controlled studies
showing that the routine use of any vasopressor at
Occasionally, it will be impossible to ventilate an any stage during human cardiac arrest increases
apnoeic patient with a bag-mask, or to pass a tra- survival to hospital discharge. The primary goal
cheal tube or alternative airway device. This may of cardiopulmonary resuscitation is to re-establish
occur in patients with extensive facial trauma or blood flow to vital organs until the restoration of
laryngeal obstruction due to oedema or foreign spontaneous circulation. Despite the lack of data
material. In these circumstances, delivery of oxy- from cardiac arrest in humans, vasopressors con-
gen through a needle or surgical cricothyroidotomy tinue to be recommended as a means of increasing
may be life-saving. A tracheostomy is contraindi- cerebral and coronary perfusion during CPR.
cated in an emergency, as it is time consuming,
hazardous and requires considerable surgical skill Adrenaline (epinephrine) versus vasopressin.
and equipment. Adrenaline has been the primary sympathomimetic
Surgical cricothyroidotomy provides a defini- agent for the management of cardiac arrest for
tive airway that can be used to ventilate the 40 years.182 Its primary efficacy is due to its
patient’s lungs until semi-elective intubation or tra- alpha-adrenergic, vasoconstrictive effects caus-
cheostomy is performed. Needle cricothyroidotomy ing systemic vasoconstriction, which increases
is a much more temporary procedure providing coronary and cerebral perfusion pressures. The
only short-term oxygenation. It requires a wide- beta-adrenergic actions of adrenaline (inotropic,
bore, non-kinking cannula, a high-pressure oxygen chronotropic) may increase coronary and cerebral
source, runs the risk of barotrauma and can be par- blood flow, but concomitant increases in myocar-
ticularly ineffective in patients with chest trauma. dial oxygen consumption, ectopic ventricular
It is also prone to failure because of kinking of the arrhythmias (particularly when the myocardium
cannula, and is unsuitable for patient transfer. is acidotic) and transient hypoxaemia due to
European Resuscitation Council Guidelines for Resuscitation 2005 S59

pulmonary arteriovenous shunting may offset these cant difference in the rate of death before hospital
benefits. discharge.195
The potentially deleterious beta-effects of Participants at the 2005 Consensus Conference
adrenaline have led to exploration of alternative debated in depth the treatment recommendations
vasopressors. Vasopressin is a naturally occurring that should follow from this evidence. Despite the
antidiuretic hormone. In very high doses it is a absence of placebo-controlled trials, adrenaline
powerful vasoconstrictor that acts by stimulation has been the standard vasopressor in cardiac arrest.
of smooth muscle V1 receptors. The importance of It was agreed that there is currently insufficient
vasopressin in cardiac arrest was first recognised in evidence to support or refute the use of vaso-
studies of out-of-hospital cardiac arrest patients, pressin as an alternative to, or in combination with,
where vasopressin levels were found to be higher in adrenaline in any cardiac arrest rhythm. Current
successfully resuscitated patients.183,184 Although practice still supports adrenaline as the primary
clinical185,186 and animal187—189 studies demon- vasopressor for the treatment of cardiac arrest of
strated improved haemodynamic variables when all rhythms.
using vasopressin as an alternative to adrenaline
during resuscitation from cardiac arrest, some,186 Adrenaline
but not all, demonstrated improved survival.190,191 Indications
The first clinical use of vasopressin during car-
diac arrest was reported in 1996 and appeared • Adrenaline is the first drug used in cardiac arrest
promising. In a study of cardiac arrest patients of any aetiology: it is included in the ALS algo-
refractory to standard therapy with adrenaline, rithm for use every 3—5 min of CPR.
vasopressin restored a spontaneous circulation in • Adrenaline is preferred in the treatment of ana-
all eight patients, three of whom were discharged phylaxis (Section 7g).
neurologically intact.186 The following year, the • Adrenaline is second-line treatment for cardio-
same group published a small randomised trial genic shock.
of out-of-hospital ventricular fibrillation, in which
the rates of successful resuscitation and sur- Dose. During cardiac arrest, the initial intra-
vival for 24 h were significantly higher in patients venous dose of adrenaline is 1 mg. When intravascu-
treated with vasopressin than in those treated with lar (intravenous or intra-osseous) access is delayed
adrenaline.192 Following these two studies, the or cannot be achieved, give 2—3 mg, diluted to
American Heart Association (AHA) recommended 10 ml with sterile water, via the tracheal tube.
that vasopressin could be used as an alternative Absorption via the tracheal route is highly variable.
to adrenaline for the treatment of adult shock- There is no evidence supporting the use of higher
refractory VF.182 The success of these small stud- doses of adrenaline for patients in refractory car-
ies led to two large randomised studies compar- diac arrest. In some cases, an adrenaline infusion is
ing vasopressin with adrenaline for in-hospital193 required in the post-resuscitation period.
and out-of-hospital194 cardiac arrest. Both stud- Following return of spontaneous circulation,
ies randomised patients to receive vasopressin or excessive (≥1 mg) doses of adrenaline may induce
adrenaline initially, and used adrenaline as a res- tachycardia, myocardial ischaemia, VT and VF.
cue treatment in patients refractory to the initial Once a perfusing rhythm is established, if further
drug. Both studies were unable to demonstrate an adrenaline is deemed necessary, titrate the dose
overall increase in the rates of ROSC or survival carefully to achieve an appropriate blood pressure.
for vasopressin 40 U,193 with the dose repeated Intravenous doses of 50—100 mcg are usually suffi-
in one study,194 when compared with adrenaline cient for most hypotensive patients. Use adrenaline
(1 mg, repeated), as the initial vasopressor. In the cautiously in patients with cardiac arrest associated
large out-of-hospital cardiac arrest study,194 post- with cocaine or other sympathomimetic drugs.
hoc analysis suggested that the subset of patients Use. Adrenaline is available most commonly in
with asystole had significant improvement in sur- two dilutions:
vival to discharge, but survival neurologically intact
was no different. • 1 in 10,000 (10 ml of this solution contains 1 mg
A recent meta-analysis of five randomised of adrenaline)
trials195 showed no statistically significant differ- • 1 in 1000 (1 ml of this solution contains 1 mg of
ence between vasopressin and adrenaline for ROSC, adrenaline)
death within 24 h or death before hospital dis-
charge. The subgroup analysis based on initial car- Both these dilutions are used routinely in European
diac rhythm did not show any statistically signifi- countries.
S60 J.P. Nolan et al.

Various other pressor drugs (e.g., volume of 20 ml (or from a pre-filled syringe), if
noradrenaline)196 have been used experimen- VF/VT persists after the third shock. Amiodarone
tally as an alternative to adrenaline for the can cause thrombophlebitis when injected into a
treatment of cardiac arrest. peripheral vein; use a central venous catheter if
one is in situ but,if not, use a large peripheral vein
Anti-arrhythmics and a generous flush. Details about the use of amio-
As with vasopressors, the evidence that anti- darone for the treatment of other arrhythmias are
arrhythmic drugs are of benefit in cardiac arrest given in Section 4f.
is limited. No anti-arrhythmic drug given during Clinical aspects of use. Amiodarone may para-
human cardiac arrest has been shown to increase doxically be arrhythmogenic, especially if given
survival to hospital discharge, although amiodarone concurrently with drugs that prolong the QT
has been shown to increase survival to hospital interval. However, it has a lower incidence of
admission.89,90 Despite the lack of human long-term pro-arrhythmic effects than other anti-arrhythmic
outcome data, the balance of evidence is in favour drugs under similar circumstances. The major acute
of the use anti-arrhythmic drugs for the manage- adverse effects from amiodarone are hypotension
ment of arrhythmias in cardiac arrest. and bradycardia, which can be prevented by slow-
Amiodarone. Amiodarone is a membrane- ing the rate of drug infusion, or can be treated with
stabilising anti-arrhythmic drug that increases the fluids and/or inotropic drugs. The side effects asso-
duration of the action potential and refractory ciated with prolonged oral use (abnormalities of
period in atrial and ventricular myocardium. Atri- thyroid function, corneal microdeposits, peripheral
oventricular conduction is slowed, and a similar neuropathy, and pulmonary/hepatic infiltrates) are
effect is seen with accessory pathways. Amiodarone not relevant in the acute setting.
has a mild negative inotropic action and causes
peripheral vasodilation through non-competitive Lidocaine. Until the publication of the 2000 ILCOR
alpha-blocking effects. The hypotension that guidelines, lidocaine was the antiarrhythmic drug
occurs with intravenous amiodarone is related to of choice. Comparative studies with amiodarone90
the rate of delivery and is due more to the solvent have displaced it from this position, and lidocaine
(Polysorbate 80), which causes histamine release, is now recommended only when amiodarone is
rather than the drug itself.197 The use of an unavailable. Amiodarone should be available at all
aqueous amiodarone preparation that is relatively hospital arrests and to all out-of-hospital arrests
free from these side effects is encouraged but is attended by ambulance crew.
not yet widely available 198,199 . Lidocaine is a membrane-stabilising anti-
Following three initial shocks, amiodarone in arrhythmic drug that acts by increasing the
shock-refractory VF improves the short-term out- myocyte refractory period. It decreases ventricular
come of survival to hospital admission com- automaticity, and its local anaesthetic action
pared with placebo89 or lignocaine.90 Amio- suppresses ventricular ectopic activity. Lidocaine
darone also appears to improve the response to suppresses activity of depolarised, arrhythmogenic
defibrillation when given to humans or animals tissues while interfering minimally with the elec-
with VF or haemodynamically unstable ventricular trical activity of normal tissues. Therefore, it is
tachycardia.198—202 There is no evidence to indi- effective in suppressing arrhythmias associated
cate the time at which amiodarone should be given with depolarisation (e.g. ischaemia, digitalis toxic-
when using a single shock strategy. In the clini- ity) but is relatively ineffective against arrhythmias
cal studies to date, the amiodarone was given if occurring in normally polarised cells (e.g., atrial
VF/VT persisted after at least three shocks. For this fibrillation/flutter). Lidocaine raises the threshold
reason, and in the absence of any other data, amio- for ventricular fibrillation.
darone 300 mg is recommended if VF/VT persists Lidocaine toxicity causes paraesthesia, drowsi-
after three shocks. ness, confusion and muscular twitching progressing
Indications. Amiodarone is indicated in to convulsions. It is considered generally that a safe
dose of lidocaine must not exceed 3 mg kg−1 over
• refractory VF/VT
the first hour. If there are signs of toxicity, stop the
• haemodynamically stable ventricular tachycardia
infusion immediately; treat seizures if they occur.
(VT) and other resistant tachyarrhythmias (Sec-
Lidocaine depresses myocardial function, but to a
tion 4f)
much lesser extent than amiodarone. The myocar-
Dose. Consider an initial intravenous dose of dial depression is usually transient and can be
300 mg amiodarone, diluted in 5% dextrose to a treated with intravenous fluids or vasopressors.
European Resuscitation Council Guidelines for Resuscitation 2005 S61

Indications. Lidocaine is indicated in refractory Indications. Magnesium sulphate is indicated in


VF/VT (when amiodarone is unavailable).
• shock-refractory VF in the presence of possible
Dose. When amiodarone is unavailable, con- hypomagnesaemia
sider an initial dose of 100 mg (1—1.5 mg kg−1 ) of • ventricular tachyarrhythmias in the presence of
lidocaine for VF/pulseless VT refractory to three possible hypomagnesaemia
shocks. Give an additional bolus of 50 mg if neces- • torsades de pointes
sary. The total dose should not exceed 3 mg kg−1 • digoxin toxicity
during the first hour. Dose. In shock-refractory VF, give an initial intra-
Clinical aspects of use. Lidocaine is metabolised venous dose of 2 g (4 ml (8 mmol)) of 50% magne-
by the liver, and its half-life is prolonged if the sium sulphate) peripherally over 1—2 min; it may
hepatic blood flow is reduced, e.g. in the pres- be repeated after 10—15 min. Preparations of mag-
ence of reduced cardiac output, liver disease nesium sulphate solutions differ among European
or in the elderly. During cardiac arrest normal countries.
clearance mechanisms do not function, thus high Clinical aspects of use. Hypokalaemic patients
plasma concentrations may be achieved after a are often hypomagnesaemic. If ventricular tach-
single dose. After 24 h of continuous infusion, the yarrhythmias arise, intravenous magnesium is a
plasma half-life increases significantly. Reduce the safe, effective treatment. The role of magnesium
dose in these circumstances, and regularly review in acute myocardial infarction is still in doubt. Mag-
the indication for continued therapy. Lidocaine is nesium is excreted by the kidneys, but side effects
less effective in the presence of hypokalaemia associated with hypermagnesaemia are rare, even
and hypomagnesaemia, which should be corrected in renal failure. Magnesium inhibits smooth mus-
immediately. cle contraction, causing vasodilation and a dose-
related hypotension, which is usually transient and
Magnesium sulphate. Magnesium is an important responds to intravenous fluids and vasopressors.
constituent of many enzyme systems, especially
Other drugs
those involved with ATP generation in muscle.
It plays a major role in neurochemical transmis- The evidence for the benefits of other drugs, includ-
sion, where it decreases acetylcholine release and ing atropine, aminophylline and calcium, given
reduces the sensitivity of the motor endplate. routinely during human cardiac arrest, is limited.
Magnesium also improves the contractile response Recommendations for the use of these drugs are
of the stunned myocardium, and limits infarct based on our understanding of their pharmacody-
size by a mechanism that has yet to be fully namic properties and the pathophysiology of car-
elucidated.203 The normal plasma range of magne- diac arrest.
sium is 0.8—1.0 mmol l−1 .
Hypomagnesaemia is often associated with Atropine. Atropine antagonises the action of the
hypokalaemia, and may contribute to arrhythmias parasympathetic neurotransmitter acetylcholine at
and cardiac arrest. Hypomagnesaemia increases muscarinic receptors. Therefore, it blocks the
myocardial digoxin uptake and decreases cellular effect of the vagus nerve on both the sinoatrial (SA)
Na+ /K+ -ATP-ase activity. Patients with hypomagne- node and the atrioventricular (AV) node, increasing
saemia, hypokalaemia, or both may become car- sinus automaticity and facilitating AV node conduc-
diotoxic even with therapeutic digitalis levels. Mag- tion.
nesium deficiency is not uncommon in hospitalised Side effects of atropine are dose-related
patients and frequently coexists with other elec- (blurred vision, dry mouth and urinary retention);
trolyte disturbances, particularly hypokalaemia, they are not relevant during a cardiac arrest.
hypophosphataemia, hyponatraemia and hypocal- Acute confusional states may occur after intra-
caemia. venous injection, particularly in elderly patients.
Although the benefits of giving magnesium in After cardiac arrest, dilated pupils should not be
known hypomagnesaemic states are recognised, the attributed solely to atropine.
benefit of giving magnesium routinely during car- Atropine is indicated in:
diac arrest is unproven. Studies in adults in and out • asystole
of hospital91—95,204 have failed to demonstrate any • pulseless electrical activity (PEA) with a rate
increase in the rate of ROSC when magnesium is <60 min−1
given routinely during CPR. There is some evidence • sinus, atrial, or nodal bradycardia when the
that magnesium may be beneficial in refractory haemodynamic condition of the patient is unsta-
VF.205 ble
S62 J.P. Nolan et al.

The recommended adult dose of atropine for not give calcium solutions and sodium bicarbonate
asystole or PEA with a rate <60 min−1 is 3 mg intra- simultaneously by the same route.
venously in a single bolus. Its use in the treatment
of bradycardia is covered in Section 4f. Several Buffers. Cardiac arrest results in combined res-
recent studies have failed to demonstrate any ben- piratory and metabolic acidosis caused by cessa-
efit from atropine in out-of-hospital or in-hospital tion of pulmonary gas exchange and the devel-
cardiac arrests174,206—210 ; however, asystole carries opment of anaerobic cellular metabolism, respec-
a grave prognosis and there are anecdotal accounts tively. The best treatment of acidaemia in cardiac
of success after giving atropine. It is unlikely to be arrest is chest compression; some additional ben-
harmful in this situation. efit is gained by ventilation. If the arterial blood
pH is less than 7.1 (or base excess more negative
Theophylline (aminophylline). Theophylline is a than −10 mmol l−1 ) during or following resuscita-
phosphodiesterase inhibitor that increases tissue tion from cardiac arrest, consider giving small doses
concentrations of cAMP and releases adrenaline of sodium bicarbonate (50 ml of an 8.4% solution).
from the adrenal medulla. It has chronotropic and During cardiac arrest, arterial gas values may be
inotropic actions. The limited studies of amino- misleading and bear little relationship to the tissue
phylline in bradyasystolic cardiac arrest have failed acid—base state96 ; analysis of central venous blood
to demonstrate an increase in ROSC or survival to may provide a better estimation of tissue pH (see
hospital discharge211—214 ; the same studies have Section 4c). Bicarbonate causes generation of car-
not shown that harm is caused by aminophylline. bon dioxide, which diffuses rapidly into cells. This
Aminophylline is indicated in: has the following effects.
• asystolic cardiac arrest • It exacerbates intracellular acidosis.
• peri-arrest bradycardia refractory to atropine • It produces a negative inotropic effect on
ischaemic myocardium.
Theophylline is given as aminophylline, a mix- • It presents a large, osmotically active, sodium
ture of theophylline with ethylenediamine, which is load to an already compromised circulation and
20 times more soluble than theophylline alone. The brain.
recommended adult dose is 250—500 mg (5 mg kg−1 ) • It produces a shift to the left in the oxygen disso-
given by slow intravenous injection. ciation curve, further inhibiting release of oxygen
Theophylline has a narrow therapeutic win- to the tissues.
dow with an optimal plasma concentration of
10—20 mg l−1 (55—110 mmol l−1 ). Above this con- Mild acidaemia causes vasodilation and can
centration, side effects such as arrhythmias and increase cerebral blood flow. Therefore, full cor-
convulsions may occur, especially when given rection of the arterial blood pH may theoretically
rapidly by intravenous injection. reduce cerebral blood flow at a particularly critical
time. As the bicarbonate ion is excreted as car-
Calcium. Calcium plays a vital role in the cellu- bon dioxide via the lungs, ventilation needs to be
lar mechanisms underlying myocardial contraction. increased. For all these reasons, metabolic acidosis
There are very few data supporting any benefi- must be severe to justify giving sodium bicarbon-
cial action for calcium after most cases of car- ate.
diac arrest. High plasma concentrations achieved Several animal and clinical studies have exam-
after injection may be harmful to the ischaemic ined the use of buffers during cardiac arrest. Clin-
myocardium and may impair cerebral recovery. ical studies using Tribonate®215 or sodium bicar-
Give calcium during resuscitation only when indi- bonate as buffers have failed to demonstrate any
cated specifically, i.e. in pulseless electrical activ- advantage.216—220 Only one study has found clinical
ity caused by benefit, suggesting that EMS systems using sodium
• hyperkalaemia bicarbonate earlier and more frequently had sig-
• hypocalcaemia nificantly higher ROSC and hospital discharge rates
• overdose of calcium channel-blocking drugs and better long-term neurological outcome.221 Ani-
mal studies have generally been inconclusive, but
The initial dose of 10 ml 10% calcium chloride some have shown benefit in giving sodium bicarbon-
(6.8 mmol Ca2+ ) may be repeated if necessary. ate to treat cardiovascular toxicity (hypotension,
Calcium can slow the heart rate and precipitate cardiac arrhythmias) caused by tricyclic antidepres-
arrhythmias. In cardiac arrest, calcium may be sants and other fast sodium channel blockers (Sec-
given by rapid intravenous injection. In the pres- tion 7b).222 Giving sodium bicarbonate routinely
ence of a spontaneous circulation give it slowly. Do during cardiac arrest and CPR (especially in out-
European Resuscitation Council Guidelines for Resuscitation 2005 S63

of-hospital cardiac arrests) or after return of spon- to proven or suspected acute pulmonary embolus.
taneous circulation is not recommended. Consider Thrombolysis may be considered in adult cardiac
sodium bicarbonate for life-threatening hyper- arrest on a case by case basis following initial fail-
kalaemia or cardiac arrest associated with hyper- ure of standard resuscitation in patients in whom
kalaemia, severe metabolic acidosis, or tricyclic an acute thrombotic aetiology for the arrest is sus-
overdose. Give 50 mmol (50 ml of an 8.4% solu- pected. Ongoing CPR is not a contraindication to
tion) of sodium bicarbonate intravenously. Repeat thrombolysis.
the dose as necessary, but use acid/base analysis Following thrombolysis during CPR for acute pul-
(either arterial or central venous) to guide therapy. monary embolism, survival and good neurological
Severe tissue damage may be caused by subcuta- outcome have been reported in cases requiring in
neous extravasation of concentrated sodium bicar- excess of 60 min of CPR. If a thrombolytic drug is
bonate. The solution is incompatible with calcium given in these circumstances, consider performing
salts as it causes the precipitation of calcium car- CPR for at least 60—90 min before termination of
bonate. resuscitation attempts.235,236

Thrombolysis during CPR. Adult cardiac arrest Intravenous fluids


is usually caused by acute myocardial ischaemia
following coronary artery occlusion by thrombus. Hypovolaemia is a potentially reversible cause of
There are several reports on the successful use cardiac arrest. Infuse fluids rapidly if hypovolaemia
of thrombolytics during cardiac arrest, particu- is suspected. In the initial stages of resuscitation
larly when the arrest was caused by pulmonary there are no clear advantages to using colloid, so
embolism. The use of thrombolytic drugs to break use saline or Hartmann’s solution. Avoid dextrose,
down coronary artery and pulmonary artery throm- which is redistributed away from the intravascu-
bus has been the subject of several studies. Throm- lar space rapidly and causes hyperglycaemia, which
bolytics have also been demonstrated in animal may worsen neurological outcome after cardiac
studies to have beneficial effects on cerebral blood arrest.237—244
flow during cardiopulmonary resuscitation,223,224 Whether fluids should be infused routinely during
and a clinical study has reported less anoxic cardiac arrest is controversial. There are no pub-
encephalopathy after thrombolytic therapy during lished human studies of routine fluid use compared
CPR.225 to no fluids during normovolaemic cardiac arrest.
Several studies have examined the use of throm- Four animal studies245—248 of experimental ventric-
bolytic therapy given during non-traumatic cardiac ular fibrillation neither support nor refute the use
arrest refractory to standard therapy. Two stud- of intravenous fluids routinely. In the absence of
ies have shown an increase in ROSC with non- hypovolaemia, infusion of an excessive volume of
significant improvements in survival to hospital fluid is likely to be harmful. Use intravenous fluid
discharge,97,226 and a further study demonstrated to flush peripherally injected drugs into the central
greater ICU survival.225 A small series of case circulation.
reports has also reported survival to discharge in
three cases refractory to standard therapy with VF Alternative routes for drug delivery
or PEA treated with thrombolytics227 ; conversely,
one large clinical trial228 failed to show any signif- Intraosseous route
icant benefit for thrombolytics in cases of undif-
ferentiated PEA out-of-hospital cardiac arrest unre- If intravenous access cannot be established,
sponsive to initial interventions. intraosseous delivery of resuscitation drugs will
When given to cardiac arrest patients with achieve adequate plasma concentrations. Several
suspected or proven pulmonary embolus, two studies indicate that intraosseous access is safe
studies have demonstrated possible benefits229,230 ; and effective for fluid resuscitation, drug delivery
one found an improvement in 24-h survival.229 and laboratory evaluation.78,249—255 Traditionally,
Several clinical studies97,226,229,231 and case the intraosseous route is used mainly for children,
series227,230,232—234 have not demonstrated any but it is also effective in adults.
increase in bleeding complications with thrombol-
ysis during CPR in non-traumatic cardiac arrest. Drugs given via the tracheal tube
There are insufficient clinical data to recom-
mend the routine use of thrombolysis during non- Resuscitation drugs can also be given via the tra-
traumatic cardiac arrest. Consider thrombolytic cheal tube, but the plasma concentrations achieved
therapy when cardiac arrest is thought to be due using this route are variable and substantially
S64 J.P. Nolan et al.

lower than those achieved by the intravenous or Interposed abdominal compression (IAC-CPR)
intraosseous routes.
Doses of adrenaline 3—10 times higher than when The IAC-CPR technique involves compression of
given intravenously are required to achieve sim- the abdomen during the relaxation phase of
ilar plasma concentrations.79,80 During CPR, lung chest compression.269,270 This enhances venous
perfusion is only 10—30% of the normal value, return during CPR271,272 and improves ROSC
resulting in a pulmonary adrenaline depot. When and short-term survival.273,274 One study showed
cardiac output is restored after a high dose of improved survival to hospital discharge with IAC-
endobronchial adrenaline, prolonged reabsorption CPR compared with standard CPR for out-of-
of adrenaline from the lungs into the pulmonary hospital cardiac arrest,274 but another showed no
circulation may occur, causing arterial hyperten- survival advantage.275 CPR devices include the
sion, malignant arrhythmias and recurrence of VF.80 following.
Lidocaine and atropine can also be given via a tra-
cheal tube, but the plasma concentrations achieved Active compression-decompression CPR
are also variable.256—258 If intravenous access is (ACD-CPR)
delayed or cannot be achieved, consider obtain-
ing intraosseous access. Give drugs via the tracheal ACD-CPR is achieved with a hand-held device
tube if intravascular (intravenous or intraosseous) equipped with a suction cup to lift the ante-
access is delayed or cannot be achieved. There are rior chest actively during decompression. Decreas-
no benefits from endobronchial injection compared ing intrathoracic pressure during the decompres-
with injection of the drug directly into the tracheal sion phase increases venous return to the heart
tube.256 Dilution with water instead of 0.9% saline and increases cardiac output and subsequent coro-
may achieve better drug absorption and cause less nary and cerebral perfusion pressures during the
reduction in PaO2 .85,259 compression phase.276—279 Results of ACD-CPR have
been mixed. In some clinical studies ACD-CPR
improved haemodynamics compared with stan-
CPR techniques and devices dard CPR,173,277,279,280 but in another study it
did not.281 In three randomised studies,280,282,283
At best, standard manual CPR produces coronary ACD-CPR improved long-term survival after out-of-
and cerebral perfusion that is just 30% of normal.260 hospital cardiac arrest; however, in five other ran-
Several CPR techniques and devices may improve domised studies, ACD-CPR made no difference to
haemodynamics or short-term survival when used outcome.284—288 The efficacy of ACD-CPR may be
by well-trained providers in selected cases. To date, highly dependent on the quality and duration of
no adjunct has consistently been shown to be supe- training.289
rior to conventional manual CPR. CPR techniques A meta-analysis of 10 trials of out-of-hospital
include the following. cardiac arrest and two of in-hospital cardiac arrest
showed no early or late survival benefit to ACD-CPR
over conventional CPR.290 Two post-mortem stud-
High-frequency chest compressions (HFCC) ies have shown more rib and sternal fractures after
ACD-CPR compared with conventional CPR,291,292
High-frequency (>100 compressions min−1 ) manual but another found no difference.293
or mechanical chest compressions improve haemo-
dynamics but have not been shown to improve long- Impedance threshold device (ITD)
term outcome.261—265
The impedance threshold device (ITD) is a valve
that limits air entry into the lungs during chest
Open-chest CPR recoil between chest compressions; this decreases
intrathoracic pressure and increases venous return
Open-chest CPR produces better coronary perfusion to the heart. When used with a cuffed tra-
coronary pressure than standard CPR266 and may cheal tube and active compression-decompression
be indicated for patients with cardiac arrest due to (ACD),294—296 the ITD is thought to act synergis-
trauma (see Section 7i), in the early postoperative tically to enhance venous return during active
phase after cardiothoracic surgery267,268 (see Sec- decompression. The ITD has also been used dur-
tion 7h) or when the chest or abdomen is already ing conventional CPR with a tracheal tube or
open (transdiaphragmatic approach), for example, facemask.297 If rescuers can maintain a tight face-
in trauma surgery. mask seal, the ITD may create the same negative
European Resuscitation Council Guidelines for Resuscitation 2005 S65

intrathoracic pressure as when used with a tracheal Phased thoracic—abdominal


tube.297 compression—decompression CPR (PTACD-CPR)
In two randomised studies of out-of-hospital
cardiac arrest, ACD-CPR plus the ITD improved Phased thoracic—abdominal compression—decom-
ROSC and 24-h survival compared with standard pression CPR combines the concepts of IAC-CPR
CPR alone.296,298 When used during standard CPR, and ACD-CPR. It comprises a hand-held device
the ITD increased 24-h survival after PEA out-of- that alternates chest compression and abdominal
hospital cardiac arrest.297 decompression with chest decompression and
abdominal compression. One randomised study of
adults in cardiac arrest documented no improve-
Mechanical piston CPR ment in survival from use of PTACD-CPR.311
Mechanical piston devices depress the sternum
by means of a compressed gas-powered plunger Minimally invasive direct cardiac massage
mounted on a backboard. In several studies in
Minimally invasive direct cardiac massage (MIDCM)
animals,299,300 mechanical piston CPR improved
is accomplished by insertion of a small plunger-like
end-tidal carbon dioxide, cardiac output, cerebral
device through a 2—4-cm incision in the chest wall.
blood flow, MAP and short-term neurological out-
In one clinical study the MIDCM generated improved
come. Studies in humans also document improve-
blood pressure over standard CPR, but the device
ment in end-tidal carbon dioxide and mean arterial
caused cardiac rupture in one postoperative cardio-
pressure when using mechanical piston CPR com-
vascular surgical patient.312 The plunger device is
pared with conventional CPR.301—303
no longer manufactured.

Lund University cardiac arrest system (LUCAS)


CPR 4f. Peri-arrest arrhythmias
The Lund University cardiac arrest system (LUCAS)
Introduction
is a gas-driven sternal compression device that
incorporates a suction cup for active decompres- A successful strategy to reduce the mortality
sion. There are no published randomised human and morbidity of cardiac arrest includes measures
studies comparing LUCAS-CPR with standard CPR. to prevent other potentially serious arrhythmias,
A study of pigs with VF showed that LUCAS-CPR and optimal treatment should they occur. Cardiac
improves haemodynamic and short-term survival arrhythmias are well recognised complications of
compared with standard CPR.304 The LUCAS was myocardial infarction. They may precede ventric-
also used in 20 patients, but incomplete outcome ular fibrillation or follow successful defibrillation.
data were reported.304 In another pig study, in com- The treatment algorithms described in this section
parison with standard CPR, LUCAS-CPR increased have been designed to enable the non-specialist
cerebral blood flow and cardiac output.305 The ALS provider to treat the patient effectively and
LUCAS enables delivery of continuous compressions safely in an emergency; for this reason, they have
during transport and defibrillation. been kept as simple as possible. If patients are
Mechanical piston CPR or LUCAS CPR may be par- not acutely ill there may be several other treat-
ticularly useful when prolonged CPR is required; ment options, including the use of drugs (oral or
this might include during transport to hospital or parenteral), that will be less familiar to the non-
after cardiac arrest following hypothermia306 or expert. In this situation there will be time to seek
poisoning. advice from cardiologists or other doctors with the
appropriate expertise.
Load-distributing band CPR or vest CPR More comprehensive information on the
management of arrhythmias can be found at
The load distributing band (LDB) is a cir- www.escardio.org.
cumferential chest compression device compris-
ing a pneumatically actuated constricting band Principles of treatment
and backboard. The use of LDB CPR improves
haemodynamics.307—309 A case—control study docu- In all cases, give oxygen and insert an intravenous
mented improvement in survival to the emergency cannula while the arrhythmia is assessed. Whenever
department when LDB-CPR was delivered after out- possible, record a 12-lead ECG; this will help deter-
of-hospital cardiac arrest.310 mine the precise rhythm, either before treatment
S66 J.P. Nolan et al.

or retrospectively, if necessary with the help of an 1. anti-arrhythmic (and other) drugs


expert. Correct any electrolyte abnormalities (e.g., 2. attempted electrical cardioversion
K+ , Mg2+ , Ca2+ ) (Section 7a). 3. cardiac pacing
The assessment and treatment of all arrhyth-
mias addresses two factors: the condition of the All anti-arrhythmic treatments—–physical man-
patient (stable versus unstable), and the nature of oeuvres, drugs, or electrical treatment—–can also
the arrhythmia. be pro-arrhythmic, so that clinical deterioration
may be caused by the treatment rather than
lack of effect. Furthermore, the use of multiple
Adverse signs anti-arrhythmic drugs or high doses of a single drug
can cause myocardial depression and hypotension.
The presence or absence of adverse signs or symp-
This may cause a deterioration of the cardiac
toms will dictate the appropriate treatment for
rhythm. Anti-arrhythmic drugs are slower in effect
most arrhythmias. The following adverse factors
and less reliable than electrical cardioversion in
indicate a patient who is unstable because of the
converting a tachycardia to sinus rhythm; thus,
arrhythmia.
drugs tend to be reserved for stable patients
1. Clinical evidence of low cardiac output. This without adverse signs, and electrical cardioversion
is seen as pallor, sweating, cold and clammy is usually the preferred treatment for the unstable
extremities (increased sympathetic activity), patient displaying adverse signs.
impaired consciousness (reduced cerebral blood Once the arrhythmia has been treated success-
flow), and hypotension (e.g., systolic blood pres- fully, repeat the 12-lead ECG to enable detection
sure <90 mmHg). of any underlying abnormalities that may require
2. Excessive tachycardia. Coronary blood flow long-term therapy.
occurs predominantly during diastole. Very high
heart rates (e.g., >150 min−1 ) reduce diastole Bradycardia
critically, decreasing coronary blood flow and
causing myocardial ischaemia. Broad, complex A bradycardia is defined strictly as a heart rate
tachycardias are tolerated less well by the heart of <60 beats min−1 . However, it is more helpful to
than narrow, complex tachycardias. classify a bradycardia as absolute (<40 beats min−1 )
3. Excessive bradycardia. This is defined as a or relative, when the heart rate is inappropriately
heart rate of <40 beats min−1 , but rates of slow for the haemodynamic state of the patient.
<60 beats min−1 may not be tolerated by The first step in the assessment of bradycar-
patients with poor cardiac reserve. Even a higher dia is to determine if the patient is unstable
heart rate may be inappropriately slow for a (Figure 4.11). The following adverse signs may indi-
patient with a low stroke-volume. cate instability:
4. Heart failure. By reducing coronary artery blood
flow, arrhythmias compromise myocardial per- • systolic blood pressure <90 mmHg
formance. In acute situations this is manifested • heart rate <40 beats min−1
by pulmonary oedema (failure of the left ven- • ventricular arrhythmias requiring suppression
tricle) or raised jugular venous pressure, and • heart failure
hepatic engorgement (failure of the right ven-
If adverse signs are present, give atropine,
tricle).
500 mcg, intravenously and, if necessary, repeat
5. Chest pain. The presence of chest pain implies
every 3—5 min to a total of 3 mg. Doses of atropine
that the arrhythmia (particularly a tach-
of less than 500 mcg paradoxically may cause fur-
yarrhythmia) is causing myocardial ischaemia.
ther slowing of the heart rate.313 In healthy vol-
This is especially important if there is underly-
unteers a dose of 3 mg produces the maximum
ing coronary artery disease or structural heart
achievable increase in resting heart rate.314 Use
disease in which myocardial ischaemia is likely
atropine cautiously in the presence of acute coro-
to lead to further life-threatening complications
nary ischaemia or myocardial infarction; increased
including cardiac arrest.
heart rate may worsen ischaemia or increase the
zone of infarction. If a satisfactory response is
Treatment options achieved with atropine, or the patient is stable,
next determine the risk of asystole, which is indi-
Having determined the rhythm and the presence or cated by:
absence of adverse signs, there are broadly three
options for immediate treatment: • recent asystole
European Resuscitation Council Guidelines for Resuscitation 2005 S67

Figure 4.11 Bradycardia algorithm.

• Möbitz type II AV block transient and may be asymptomatic. In Möbitz type


• complete (third-degree) heart block (espe- II, the block is most often below the AV node at
cially with broad QRS or initial heart rate the bundle of His or at the bundle branches, and is
<40 beats min−1 ) often symptomatic, with the potential to progress
• ventricular standstill of more than 3 s to complete AV block. Third-degree heart block is
defined by AV dissociation which may be permanent
Atrioventricular (AV) blocks are divided into first, or transient, depending on the underlying cause.
second, and third degrees and may be associ- Pacing is likely to be required if there is a risk
ated with multiple medications or electrolyte dis- of asystole, or if the patient is unstable and has
turbances, as well as structural problems caused failed to respond satisfactorily to atropine. Under
by acute myocardial infarction and myocarditis. A these circumstances, the definitive treatment is
first-degree AV block is defined by a prolonged P—R transvenous pacing. One or more of the following
interval (>0.20 s), and is usually benign. Second- interventions can be used to improve the patient’s
degree AV block is divided into Möbitz types I and II. condition while waiting for the appropriate person-
In Möbitz type I, the block is at the AV node, is often nel and facilities:
S68 J.P. Nolan et al.

• transcutaneous pacing third-degree block). Transcutaneous pacing can be


• adrenaline infusion in the range of painful and may fail to produce effective mechani-
2—10 mcg min−1 titrated to response cal capture. Verify mechanical capture and reassess
the patient’s condition. Use analgesia and sedation
Other drugs that can be given for symptomatic to control pain, and attempt to identify the cause
bradycardia include dopamine, isoprenaline and of the bradyarrhythmia.
theophylline. Consider giving intravenous glucagon
if beta-blockers or calcium channel blockers are Fist pacing. If atropine is ineffective and transcu-
a potential cause of the bradycardia. Do not give taneous pacing is not immediately available, fist
atropine to patients with cardiac transplants—– pacing can be attempted while waiting for pacing
paradoxically, it can cause a high-degree AV block equipment316—318 : give serial rhythmic blows with
or even sinus arrest.315 the closed fist over the left lower edge of the ster-
Complete heart block with a narrow QRS is not num to pace the heart at a physiological rate of
an absolute indication for pacing, because AV junc- 50—70 beats min−1 .
tional ectopic pacemakers (with a narrow QRS) may
provide a reasonable and stable heart rate. Tachycardias

Pacing Previous ERC guidelines have included three sepa-


rate tachycardia algorithms: broad-complex tachy-
Transcutaneous pacing. Initiate transcutaneous cardia, narrow-complex tachycardia and atrial fib-
pacing immediately if there is no response to rillation. In the peri-arrest setting, many treatment
atropine, if atropine is unlikely to be effective or if principles are common to all the tachycardias; for
the patient is severely symptomatic, particularly if this reason, they have been combined into a single
there is high-degree block (Möbitz Type II second- or tachycardia algorithm (Figure 4.12).

Figure 4.12 Tachycardia algorithm.


European Resuscitation Council Guidelines for Resuscitation 2005 S69

If the patient is unstable and deteriorating, Broad-complex tachycardia


with signs and symptoms caused by the tachycar-
dia (e.g., impaired conscious level, chest pain, In broad-complex tachycardias the QRS complexes
heart failure, hypotension or other signs of shock), are >0.12 s and are usually ventricular in ori-
attempt synchronised cardioversion immediately. gin. Although broad-complex tachycardias may be
In patients with otherwise normal hearts, serious caused by supraventricular rhythms with aberrant
signs and symptoms are uncommon if the ventricu- conduction, in the unstable patient in the peri-
lar rate is <150 beats min−1 . Patients with impaired arrest context assume they are ventricular in origin.
cardiac function or significant comorbidity may be In the stable patient with broad-complex tachycar-
symptomatic and unstable at lower heart rates. If dia, the next step is to determine if the rhythm is
cardioversion fails to restore sinus rhythm and the regular or irregular.
patient remains unstable, give amiodarone 300 mg
intravenously over 10—20 min and re-attempt elec- Regular broad complex tachycardia. A regular
trical cardioversion. The loading dose of amio- broad-complex tachycardia is likely to be ventric-
darone can be followed by an infusion of 900 mg ular tachycardia or SVT with bundle branch block.
over 24 h. Serial DC shocks are not appropriate for Stable ventricular tachycardia can be treated with
recurrent (within hours or days) paroxysms (self- amiodarone 300 mg intravenously over 20—60 min
terminating episodes) of atrial fibrillation. This is followed by an infusion of 900 mg over 24 h. If the
relatively common in critically ill patients who broad-complex regular tachycardia is thought to be
may have ongoing precipitating factors causing the SVT with bundle branch block, give adenosine, using
arrhythmia (e.g., metabolic disturbance, sepsis). the strategy indicated for narrow-complex tachy-
Cardioversion does not prevent subsequent arrhyth- cardia (below).
mias. If there are recurrent episodes, treat them
with drugs. Irregular broad complex tachycardia. Irregular
broad complex tachycardia is most likely to
Synchronised electrical cardioversion be AF with bundle branch block, but careful
examination of a 12-lead ECG (if necessary by
If electrical cardioversion is used to convert atrial an expert) may enable confident identification
or ventricular tachyarrhythmias, the shock must be of the rhythm. Another possible cause is AF
synchronised with the R wave of the ECG rather with ventricular pre-excitation (in patients with
than with the T wave. By avoiding the relative Wolff—Parkinson—White (WPW) syndrome). There
refractory period in this way, the risk of induc- is more variation in the appearance and width of the
ing ventricular fibrillation is minimised. Conscious QRS complexes than in AF with bundle branch block.
patients must be anaesthetised or sedated before A third possible cause is polymorphic VT (e.g., tor-
synchronised cardioversion is attempted. For a sade de pointes), but polymorphic VT is relatively
broad-complex tachycardia and AF, start with 200-J unlikely to be present without adverse features.
monophasic or 120—150 J biphasic and increase in Seek expert help with the assessment and treat-
increments if this fails (see Section 3). Atrial flutter ment of irregular broad-complex tachyarrhythmia.
and paroxysmal SVT will often convert with lower If treating AF with bundle branch block, treat as for
energies: start with 100-J monophasic or 70—120-J AF (see below). If pre-excited AF (or atrial flutter) is
biphasic. suspected, avoid adenosine, digoxin, verapamil and
If the patient with tachycardia is stable (no seri- diltiazem. These drugs block the AV node and cause
ous signs or symptoms caused by the tachycardia) a relative increase in pre-excitation. Electrical car-
and is not deteriorating, there is time to evaluate dioversion is usually the safest treatment option.
the rhythm using the 12-lead ECG and determine Treat torsades de pointes VT immediately by
treatment options. The ALS provider may not have stopping all drugs known to prolong QT inter-
the expertise to diagnose the tachycardia precisely, val. Correct electrolyte abnormalities, especially
but should be capable of differentiating between hypokalaemia. Give magnesium sulphate, 2 g, intra-
sinus tachycardia, narrow-complex SVT and broad- venously over 10 min.319,320 Obtain expert help, as
complex tachycardia. If the patient is stable there other treatment (e.g., overdrive pacing) may be
is normally time to consult an expert. If the patient indicated to prevent relapse once the arrhythmia
becomes unstable, proceed immediately to syn- has been corrected. If adverse features develop
chronised electrical cardioversion. Management of (which is usual), arrange immediate synchronised
patients with significant comorbid conditions and cardioversion. If the patient becomes pulseless,
symptomatic tachycardia requires treatment of the attempt defibrillation immediately (cardiac arrest
comorbid conditions. algorithm).
S70 J.P. Nolan et al.

Narrow-complex tachycardia or will slow the ventricular response enabling iden-


tification of the rhythm. Most typical atrial flutter
Regular narrow-complex tachycardias include: has an atrial rate of about 300 beats min−1 , so atrial
flutter with 2:1 block tends to produce a tachy-
• sinus tachycardia
cardia of about 150 beats min−1 . Much faster rates
• AV nodal re-entry tachycardia (AVNRT, the com-
(170 beats min−1 or more) are unlikely to be due to
monest type of SVT)
atrial flutter with 2:1 block.
• AV re-entry tachycardia (AVRT (due to WPW syn-
drome)) Treatment of regular narrow complex tachycar-
• atrial flutter with regular AV conduction (usually dia. If the patient is unstable with adverse fea-
2:1) tures caused by the arrhythmia, attempt synchro-
nised electrical cardioversion. It is reasonable to
Irregular narrow-complex tachycardia is most give adenosine to an unstable patient with a regu-
commonly AF or sometimes atrial flutter with vari- lar narrow-complex tachycardia while preparations
able AV conduction (‘variable block’). are made for synchronised cardioversion; however,
do not delay electrical cardioversion if the adeno-
Regular narrow-complex tachycardia
sine fails to restore sinus rhythm. In the absence of
Sinus tachycardia. Sinus tachycardia is a com-
adverse features, proceed as follows.
mon physiological response to a stimulus such as
exercise or anxiety. In a sick patient it may be seen • Start with vagal manoeuvres. Carotid sinus mas-
in response to many stimuli, such as pain, fever, sage or the Valsalva manoeuvre will terminate
anaemia, blood loss and heart failure. Treatment up to a quarter of episodes of paroxysmal SVT.
is almost always directed at the underlying cause; A Valsalva manoeuvre (forced expiration against
trying to slow sinus tachycardia that has occurred a closed glottis) in the supine position may be
in response to most of these situations will make the most effective technique. A practical way
the situation worse. of achieving this without protracted explana-
tion is to ask the patient to blow into a 20-
AVNRT and AVRT (paroxysmal SVT). AVNRT is the
ml syringe with enough force to push back the
commonest type of paroxysmal SVT, often seen in
plunger. Avoid carotid massage if a carotid bruit
people without any other form of heart disease
is present; rupture of an atheromatous plaque
and is relatively uncommon in a peri-arrest setting.
could cause cerebral embolism and stroke. In the
It causes a regular narrow-complex tachycardia,
context of acute ischaemia or digitalis toxicity,
often with no clearly visible atrial activity on the
sudden bradycardia may trigger VF. Record an
ECG, with heart rates usually well above the typical
ECG (preferably multi-lead) during each manoeu-
range of sinus rates at rest (60—120 beats min−1 ).
vre. If the rhythm is atrial flutter, slowing of the
It is usually benign, unless there is additional co-
ventricular response will often occur and demon-
incidental structural heart disease or coronary dis-
strate flutter waves.
ease, but may cause symptoms that the patient
• If the arrhythmia persists and is not atrial flutter,
finds frightening.
use adenosine. Give 6 mg as a rapid intravenous
AV re-entry tachycardia (AVRT) is seen in patients
bolus. Record an ECG (preferably multi-lead) dur-
with the WPW syndrome and is also usually benign
ing each injection. If the ventricular rate slows
unless there happens to be additional structural
transiently but the arrhythmia then persists, look
heart disease. The common type of AVRT is a regu-
for atrial activity such as atrial flutter or other
lar narrow-complex tachycardia, also often having
atrial tachycardia and treat accordingly. If there
no visible atrial activity on the ECG.
is no response to adenosine 6 mg, give a 12-mg
Atrial flutter with regular AV conduction (often bolus; if there is no response, give one further
2:1 block). Atrial flutter with regular AV conduc- 12 mg-bolus.
tion (often 2:1 block) produces a regular narrow- • Successful termination of a tachyarrhythmia by
complex tachycardia in which it may be difficult vagal manoeuvres or adenosine indicates that
to see atrial activity and identify flutter waves it was almost certainly AVNRT or AVRT. Monitor
with confidence, so it may be indistinguishable ini- the patients for further rhythm abnormalities.
tially from AVNRT and AVRT. When atrial flutter Treat recurrence either with further adenosine or
with 2:1 block or even 1:1 conduction is accompa- with a longer-acting drug with AV nodal-blocking
nied by bundle branch block, it produces a regular action (e.g., diltiazem or beta-blocker).
broad-complex tachycardia that will usually be very • Vagal manoeuvres or adenosine will terminate
difficult to distinguish from VT; treatment of this almost all AVNRT or AVRT within seconds. Failure
rhythm as if it were VT will usually be effective, to terminate a regular narrow-complex tachycar-
European Resuscitation Council Guidelines for Resuscitation 2005 S71

dia with adenosine suggests an atrial tachycardia Antiarrhythmic drugs


such as atrial flutter.
• If adenosine is contraindicated or fails to ter- Adenosine
minate a regular narrow-complex tachycardia
Adenosine is a naturally occurring purine
without demonstrating that it is atrial flutter,
nucleotide. It slows transmission across the
give a calcium channel blocker (e.g., verapamil
AV node but has little effect on other myocardial
2.5—5 mg intravenously over 2 min).
cells or conduction pathways. It is highly effective
for terminating paroxysmal SVT with re-entrant
circuits that include the AV node (AVNRT). In
Irregular narrow-complex tachycardia
other narrow-complex tachycardias, adenosine will
An irregular narrow-complex tachycardia is most reveal the underlying atrial rhythms by slowing the
likely to be AF with an uncontrolled ventricular ventricular response. It has an extremely short half-
response or, less commonly, atrial flutter with vari- life of 10—15 s and, therefore, is given as a rapid
able AV block. Record a 12-lead ECG to identify bolus into a fast running intravenous infusion or fol-
the rhythm. If the patient is unstable with adverse lowed by a saline flush. The smallest dose likely to
features caused by the arrhythmia, attempt syn- be effective is 6 mg (which is outside some current
chronised electrical cardioversion. licences for an initial dose) and, if unsuccessful
If there are no adverse features, treatment this can be followed with up to two doses each of
options include: 12 mg every 1—2 min. Patients should be warned
of transient unpleasant side effects, in particular
nausea, flushing, and chest discomfort.327 Adeno-
• rate control by drug therapy sine is not available in some European countries,
• rhythm control using drugs to encourage chemi- but adenosine triphosphate (ATP) is an alternative.
cal cardioversion In a few European countries neither preparation
• rhythm control by electrical cardioversion may be available; verapamil is probably the next
• treatment to prevent complications (e.g., anti- best choice. Theophylline and related compounds
coagulation) block the effect of adenosine. Patients receiving
dipyridamole or carbamazepine, or with dener-
Obtain expert help to determine the most appro- vated (transplanted) hearts, display a markedly
priate treatment for the individual patient. The exaggerated effect that may be hazardous. In
longer a patient remains in AF, the greater is these patients, or if injected into a central vein,
the likelihood of atrial clot developing. In gen- reduce the initial dose of adenosine to 3 mg. In the
eral, patients who have been in AF for more than presence of WPW syndrome, blockage of conduc-
48 h should not be treated by cardioversion (elec- tion across the AV node by adenosine may promote
trical or chemical) until they have received full conduction across an accessory pathway. In the
anticoagulation or absence of atrial clot has been presence of supraventricular arrhythmias this may
shown by transoesophageal echocardiography. If cause a dangerously rapid ventricular response. In
the aim is to control heart rate, options include the presence of WPW syndrome, rarely, adenosine
a beta-blocker,321,322 digoxin, diltiazem,323,324 may precipitate atrial fibrillation associated with a
magnesium325,326 or combinations of these. dangerously rapid ventricular response.
If the duration of AF is less than 48 h and rhythm
control is considered appropriate, this may be Amiodarone
attempted using amiodarone (300 mg intravenously
over 20—60 min followed by 900 mg over 24 h). Ibu- Intravenous amiodarone has effects on sodium,
tilide or flecainide can also be given for rhythm con- potassium and calcium channels as well as alpha-
trol, but expert advice should be obtained before and beta-adrenergic blocking properties. Indica-
using these drugs for this purpose. Electrical car- tions for intravenous amiodarone include:
dioversion remains an option in this setting and will
• control of haemodynamically stable VT, polymor-
restore sinus rhythm in more patients than chemi-
phic VT and wide-complex tachycardia of uncer-
cal cardioversion.
tain origin
Seek expert help if any patient with AF is known
• paroxysmal SVT uncontrolled by adenosine, vagal
or found to have ventricular pre-excitation (WPW
manoeuvres or AV nodal blockade
syndrome). Avoid using adenosine, diltiazem, vera-
• to control rapid ventricular rate due to accessory
pamil or digoxin to patients with pre-excited AF or
pathway conduction in pre-excited atrial arrhyth-
atrial flutter, as these drugs block the AV node and
mias
cause a relative increase in pre-excitation.
S72 J.P. Nolan et al.

Give amiodarone, 300 mg intravenously, over severe LV dysfunction. For the reasons stated under
10—60 min depending on the circumstances and adenosine (above), calcium channel blockers are
haemodynamic stability of the patient. This load- considered harmful when given to patients with
ing dose is followed by an infusion of 900 mg over AF or atrial flutter associated with known pre-
24 h. Additional infusions of 150 mg can be repeated excitation (WPW) syndrome.
as necessary for recurrent or resistant arrhyth-
mias to a maximum manufacturer-recommended Beta-adrenergic blockers
total daily dose of 2 g (this maximum licensed dose
varies between countries). In patients known to Beta-blocking drugs (atenolol, metoprolol,
have severely impaired heart function, intravenous labetalol (alpha- and beta-blocking effects),
amiodarone is preferable to other anti-arrhythmic propranolol, esmolol) reduce the effects of cir-
drugs for atrial and ventricular arrhythmias. Major culating catecholamines and decrease heart rate
adverse effects from amiodarone are hypotension and blood pressure. They also have cardiopro-
and bradycardia, which can be prevented by slow- tective effects for patients with acute coronary
ing the rate of drug infusion. The hypotension asso- syndromes. Beta-blockers are indicated for the
ciated with amiodarone is caused by vasoactive sol- following tachycardias:
vents (Polysorbate 80 and benzyl alcohol). A new
• narrow-complex regular tachycardias uncon-
aqueous formulation of amiodarone does not con-
trolled by vagal manoeuvres and adenosine in the
tain these solvents and causes no more hypotension
patient with preserved ventricular function
than lidocaine.198 Whenever possible, intravenous
• to control rate in AF and atrial flutter when ven-
amiodarone should be given via a central venous
tricular function is preserved
catheter; it causes thrombophlebitis when infused
into a peripheral vein. In an emergency it should be The intravenous dose of atenolol (beta1 ) is
injected into a large peripheral vein. 5 mg given over 5 min, repeated if necessary after
10 min. Metoprolol (beta1 ) is given in doses of
Calcium channel blockers: verapamil and 2—5 mg at 5-min intervals to a total of 15 mg. Pro-
diltiazem pranolol (beta1 and beta2 effects), 100 mcg kg−1 , is
given slowly in three equal doses at 2—3-min inter-
Verapamil and diltiazem are calcium channel block- vals.
ing drugs that slow conduction and increase refrac- Intravenous esmolol is a short-acting (half-
toriness in the AV node. Intravenous diltiazem is life of 2—9 min) beta1 -selective beta-blocker. It
not available in some countries. These actions may is given as an intravenous loading dose of
terminate re-entrant arrhythmias and control ven- 500 mcg kg−1 over 1 min, followed by an infusion of
tricular response rate in patients with a variety of 50—200 mcg kg−1 min−1 .
atrial tachycardias. Indications include: Side effects of beta-blockade include bradycar-
dias, AV conduction delays and hypotension. Con-
• stable regular narrow-complex tachycardias
traindications to the use of beta-adrenergic block-
uncontrolled or unconverted by adenosine or
ing agents include second- or third-degree heart
vagal manoeuvres
block, hypotension, severe congestive heart failure
• to control ventricular rate in patients with AF or
and lung disease associated with bronchospasm.
atrial flutter and preserved ventricular function
when the duration of the arrhythmia is less than
Magnesium
48 h
The initial dose of verapamil is 2.5—5 mg intra- Magnesium can be given for control of ventricu-
venously given over 2 min. In the absence of a ther- lar rate in atrial fibrillation.326,328—330 Give magne-
apeutic response or drug-induced adverse event, sium sulphate 2 g (8 mmol) over 10 min. This can be
give repeated doses of 5—10 mg every 15—30 min repeated once if necessary.
to a maximum of 20 mg. Verapamil should be given
only to patients with narrow-complex paroxysmal
SVT or arrhythmias known with certainty to be of 4g. Post-resuscitation care
supraventricular origin.
Diltiazem at a dose of 250 mcg kg−1 , followed by Introduction
a second dose of 350 mcg kg−1 , is as effective as
verapamil. Verapamil and, to a lesser extent, dil- ROSC is the just the first step toward the goal
tiazem may decrease myocardial contractility and of complete recovery from cardiac arrest. Inter-
critically reduce cardiac output in patients with ventions in the post-resuscitation period are likely
European Resuscitation Council Guidelines for Resuscitation 2005 S73

to influence the final outcome significantly,237,331 Circulation


yet there are relatively few data relating to this
phase. Of 22,105 patients admitted to intensive If there is evidence of coronary occlusion, consider
care units in the UK after cardiac arrest, 9974 (45%) the need for immediate revascularisation by throm-
survived to leave intensive care and 6353 (30%) bolysis or percutaneous coronary intervention (see
survived to hospital discharge (data from Intensive acute coronary syndromes).
Care National Audit and Research Centre (ICNARC), Haemodynamic instability is common after car-
London, December 1995 to October 2004). To return diac arrest and manifests as hypotension, low
the patient to a state of normal cerebral func- cardiac index and arrhythmias.337 This post-
tion with no neurological deficit, a stable cardiac resuscitation myocardial dysfunction (or myocar-
rhythm and normal haemodynamic function, fur- dial stunning) is usually transient and often reverses
ther resuscitation tailored to each patient’s individ- within 24—48 h.338 The post-resuscitation period
ual needs is required. The post-resuscitation phase is associated with marked elevations in plasma
starts at the location where ROSC is achieved but, cytokine concentrations, manifesting as a sepsis-
once stabilised, the patient is transferred to the like syndrome and multiple organ dysfunction.339
most appropriate high-care area (e.g., intensive Infusion of fluids may be required to increase
care unit, coronary care unit) for continued mon- right heart filling pressures or, conversely, diuretics
itoring and treatment. and vasodilators may be needed to treat left ven-
tricular failure. In the ICU an arterial line for contin-
Airway and breathing uous blood pressure monitoring is essential, and the
use of a non-invasive or invasive (pulmonary artery
Patients who have had a brief period of car- catheter) cardiac output monitor may be helpful.
diac arrest responding immediately to appropri- There are very few randomised trials evaluating the
ate treatment may achieve an immediate return role of blood pressure on the outcome after car-
of normal cerebral function. These patients do diac arrest. One randomised study demonstrated
not require tracheal intubation and ventilation but no difference in the neurological outcome among
should be given oxygen via a facemask. Hypoxia patients randomised to a mean arterial blood pres-
and hypercarbia both increase the likelihood of a sure of >100 mmHg versus ≤100 mmHg 5 min after
further cardiac arrest and may contribute to sec- ROSC; however, good functional recovery was asso-
ondary brain injury. Consider tracheal intubation, ciated with a higher blood pressure during the first
sedation and controlled ventilation in any patient 2 h after ROSC.340 In the absence of definitive data,
with obtunded cerebral function. Ensure the tra- target the mean arterial blood pressure to achieve
cheal tube is positioned correctly well above the an adequate urine output, taking into consideration
carina. Hypocarbia causes cerebral vasoconstric- the patient’s normal blood pressure.
tion and a decreased cerebral blood flow.332 After Immediately after a cardiac arrest there is
cardiac arrest, hypocapnia induced by hyperventi- typically a period of hyperkalaemia. Subse-
lation causes cerebral ischaemia.333—336 There are quent endogenous catecholamine release promotes
no data to support the targeting of a specific arte- intracellular transportation of potassium, causing
rial PCO2 after resuscitation from cardiac arrest, hypokalaemia. Hypokalaemia may predispose to
but it is reasonable to adjust ventilation to achieve ventricular arrhythmias. Give potassium to main-
normocarbia and to monitor this using the end- tain the serum potassium concentration between
tidal PCO2 and arterial blood gas values. Adjust 4.0 and 4.5 mmol l−1 .
the inspired oxygen concentrations to achieve ade-
quate arterial oxygen saturation. Disability (optimising neurological recovery)
Insert a gastric tube to decompress the stom-
ach; gastric distension caused by mouth-to-mouth Cerebral perfusion
or bag-mask-valve ventilation will splint the
diaphragm and impair ventilation. Avoid coughing; Immediately after ROSC there is a period of cere-
this will increase intracranial pressure and may bral hyperaemia.341 After 15—30 min of reperfu-
cause transient hypoxaemia. Give adequate doses sion, however, global cerebral blood flow decreases
of sedative and, if absolutely necessary, give a neu- and there is generalised hypoperfusion. Normal
romuscular blocking drug. Obtain a chest radio- cerebral autoregulation is lost, leaving cerebral
graph to check the position of the tracheal tube perfusion dependent on mean arterial pressure.
and central venous lines, etc., assess for pulmonary Under these circumstances, hypotension will com-
oedema and to detect complications from CPR such promise cerebral blood flow severely and will com-
as a pneumothorax associated with rib fractures. pound any neurological injury. Thus, after ROSC,
S74 J.P. Nolan et al.

maintain mean arterial pressure at the patient’s showed improved outcome in adults remaining
normal level. comatose after initial resuscitation from out-
of-hospital VF cardiac arrest, who were cooled
Sedation within minutes to hours after ROSC.354,355 The
subjects were cooled to 32—34 ◦ C for 12—24 h. One
Although it has been common practice to sedate study documented improved metabolic endpoints
and ventilate patients for up to 24 h after ROSC, (lactate and O2 extraction) when comatose adult
there are no data to support a defined period of patients were cooled after ROSC from out-of-
ventilation, sedation and neuromuscular blockade hospital cardiac arrest in which the initial rhythm
after cardiac arrest. The duration of sedation and was PEA/asystole.356 A small study showed ben-
ventilation may be influenced by the use of thera- efit after therapeutic hypothermia in comatose
peutic hypothermia (see below). There are no data survivors of non-VF arrest.357
to indicate whether or not the choice of sedation External and/or internal cooling techniques can
influences outcome, but short-acting drugs (e.g., be used to initiate cooling.354—356,358—361 An infu-
propofol, alfentanil, remifentanil) will enable ear- sion of 30 mg kg−1 of 4 ◦ C-saline decreases core
lier neurological assessment. There is an increased temperature by 1.5 ◦ C.358,359,361,362 Intravascular
incidence of pneumonia when sedation is prolonged cooling enables more precise control of core tem-
beyond 48 h after prehospital or in-hospital cardiac perature than external methods, but it is unknown
arrest.342 whether this improves outcome.360,363—365
Complications of mild therapeutic hypother-
Control of seizures mia include increased infection, cardiovascular
instability, coagulopathy, hyperglycaemia and elec-
Seizures and/or myoclonus occur in 5—15% of trolyte abnormalities such as hypophosphataemia
adult patients who achieve ROSC, and in approx- and hypomagnesaemia.366,367
imately 40% of those who remain comatose.343 Unconscious adult patients with spontaneous cir-
Seizures increase cerebral metabolism by up to culation after out-of-hospital VF cardiac arrest
four-fold. Prolonged seizure activity may cause should be cooled to 32—34 ◦ C. Cooling should be
cerebral injury, and should be controlled with ben- started as soon as possible and continued for at
zodiazepines, phenytoin, propofol or a barbiturate. least 12—24 h.368—374 Induced hypothermia might
Each of these drugs can cause hypotension, and also benefit unconscious adult patients with spon-
this must be treated appropriately. Seizures and taneous circulation after out-of-hospital cardiac
myoclonus per se are not related significantly to arrest from a non-shockable rhythm, or cardiac
outcome, but status epilepticus and, in particu- arrest in hospital. Treat shivering by ensuring ade-
lar, status myoclonus are associated with a poor quate sedation and giving neuromuscular block-
outcome.343,344 ing drugs. Bolus doses of neuromuscular block-
ers are usually adequate, but infusions are nec-
Temperature control essary occasionally. Rewarm the patient slowly
(0.25—0.5 ◦ C h−1 ) and avoid hyperthermia. The
Treatment of hyperpyrexia. A period of hyper- optimum target temperature, rate of cooling, dura-
thermia (hyperpyrexia) is common in the first 48 h tion of hypothermia and rate of rewarming have yet
after cardiac arrest.345—347 The risk of a poor neuro- to be determined; further studies are essential.
logical outcome increases for each degree of body
temperature >37 ◦ C.348 Antipyretics and/or phys- Blood glucose control
ical cooling methods decrease infarct volumes in
animal models of global ischaemia.349,350 Treat any There is a strong association between high blood
hyperthermia occurring in the first 72 h after car- glucose after resuscitation from cardiac arrest
diac arrest with antipyretics or active cooling. and poor neurological outcome.237—244 Persistent
hyperglycaemia after stroke is also associated
Therapeutic hypothermia. Mild therapeutic with a worse neurological outcome.375—378 Tight
hypothermia is thought to suppress many of control of blood glucose (4.4—6.1 mmol l−1 or
the chemical reactions associated with reperfu- 80—110 mg dl−1 ) using insulin reduces hospital mor-
sion injury. These reactions include free-radical tality in critically ill adults,379,380 but this has not
production, excitatory amino acid release, and been demonstrated in post-cardiac arrest patients
calcium shifts, which can in turn lead to mito- specifically. The benefit is thought to result from
chondrial damage and apoptosis (programmed the strict glycaemic control rather than the dose
cell death).351—353 Two randomised clinical trials of insulin infused.381 One rat study has shown
European Resuscitation Council Guidelines for Resuscitation 2005 S75

that glucose plus insulin improves cerebral out- only meta-analysis to look at this topic estimated
come after asphyxial cardiac arrest.382 There are that to obtain 95% CI with 5% false-positive rate
no randomised controlled human trials of glucose would require a study population of approximately
control after cardiac arrest. The optimal blood glu- 600 patients.400 No study this large has been
cose target in critically ill patients has not been conducted, and these biochemical tests remain
determined. Comatose patients are at particular unreliable for predicting outcome in individual
risk from unrecognised hypoglycaemia, and the risk cases.
of this complication occurring increases as the tar-
get blood glucose concentration is lowered. Electrophysiological tests
In common with all critically ill patients, patients
admitted to a critical care environment after car- Median nerve somatosensory evoked potentials in
diac arrest should have their blood glucose moni- normothermic patients, comatose for at least 72 h
tored frequently and hyperglycaemia treated with after cardiac arrest, predict poor outcome with
an insulin infusion. The blood glucose concentration 100% specificity.384 Bilateral absence of the N20
that triggers insulin therapy, and the target range component of the evoked potentials in comatose
of blood glucose concentrations, should be deter- patients with coma of hypoxic-anoxic origin is uni-
mined by local policy. There is a need for studies of formly fatal. When recorded at least 24—48 h after
glucose control after cardiac arrest. ROSC, the electroencephalogram (EEG), provides
limited prognostic information.401—413 A normal or
grossly abnormal EEG predicts outcome reliably, but
Prognostication
an EEG between these extremes is unreliable for
Once a heart has been resuscitated to a stable prognostication.
rhythm and cardiac output, the organ that influ-
ences an individual’s survival most significantly is
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Crit Care Med 2004;32:1489—95. ill: insulin dose versus glycemic control. Crit Care Med
365. Keller E, Imhof HG, Gasser S, Terzic A, Yonekawa Y. 2003;31:359—66.
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method to induce and maintain hypothermia. Intensive cose plus insulin infusion improves cerebral outcome after
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366. Polderman KH, Peerdeman SM, Girbes AR. Hypophos- 383. Laver S, Farrow C, Turner D, Nolan J. Mode of death after
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in patients with severe head injury. J Neurosurg Intensive Care Med 2004;30:2126—8.
2001;94:697—705. 384. Zandbergen EG, de Haan RJ, Stoutenbeek CP, Koel-
367. Polderman KH. Application of therapeutic hypothermia man JH, Hijdra A. Systematic review of early predic-
in the intensive care unit. Opportunities and pitfalls tion of poor outcome in anoxic-ischaemic coma. Lancet
of a promising treatment modality—–Part 2. Practical 1998;352:1808—12.
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757—69. dead, vegetative, or severely neurologically impaired?
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Assessing outcome for comatose survivors of cardiac arrest. diopulmonary resuscitation: a multimodal approach com-
Jama 2004;291:870—9. bining neurobiochemical and electrophysiological investi-
386. Edgren E, Hedstrand U, Kelsey S, Sutton-Tyrrell K, Safar gations may provide high prognostic certainty in patients
P. Assessment of neurological prognosis in comatose sur- after cardiac arrest. Eur Neurol 2003;49:79—84.
vivors of cardiac arrest. BRCT I Study Group. Lancet 400. Zandbergen EG, de Haan RJ, Hijdra A. Systematic review of
1994;343:1055—9. prediction of poor outcome in anoxic-ischaemic coma with
387. Tiainen M, Roine RO, Pettila V, Takkunen O. Serum biochemical markers of brain damage. Intensive Care Med
neuron-specific enolase and S-100B protein in car- 2001;27:1661—7.
diac arrest patients treated with hypothermia. Stroke 401. Synek VM. Validity of a revised EEG coma scale for pre-
2003;34:2881—6. dicting survival in anoxic encephalopathy. Clin Exp Neurol
388. Fogel W, Krieger D, Veith M, et al. Serum neuron-specific 1989;26:119—27.
enolase as early predictor of outcome after cardiac arrest. 402. Moller M, Holm B, Sindrup E, Nielsen BL. Electroencephalo-
Crit Care Med 1997;25:1133—8. graphic prediction of anoxic brain damage after resuscita-
389. Mussack T, Biberthaler P, Kanz KG, et al. Serum S-100B tion from cardiac arrest in patients with acute myocardial
and interleukin-8 as predictive markers for comparative infarction. Acta Med Scand 1978;203:31—7.
neurologic outcome analysis of patients after cardiac 403. Scollo-Lavizzari G, Bassetti C. Prognostic value of EEG
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2002;30:2669—74. 1987;26:161—70.
390. Mussack T, Biberthaler P, Kanz KG, Wiedemann E, Gippner- 404. Bassetti C, Karbowski K. Prognostic value of electroen-
Steppert C, Jochum M. S-100b, sE-selectin, and sP-selectin cephalography in non-traumatic comas. Schweiz Med
for evaluation of hypoxic brain damage in patients after Wochenschr 1990;120:1425—34.
cardiopulmonary resuscitation: pilot study. World J Surg 405. Bassetti C, Bomio F, Mathis J, Hess CW. Early prognosis
2001;25:539—43 [discussion 44]. in coma after cardiac arrest: a prospective clinical, elec-
391. Rosen H, Karlsson JE, Rosengren L. CSF levels of neurofil- trophysiological, and biochemical study of 60 patients. J
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cardiac arrest. J Neurol Sci 2004;221:19—24. 406. Rothstein TL. Recovery from near death following cerebral
392. Rosen H, Rosengren L, Herlitz J, Blomstrand C. Increased anoxia: a case report demonstrating superiority of median
serum levels of the S-100 protein are associated with somatosensory evoked potentials over EEG in predicting
hypoxic brain damage after cardiac arrest. Stroke a favorable outcome after cardiopulmonary resuscitation.
1998;29:473—7. Resuscitation 2004;60:335—41.
393. Meynaar IA, Straaten HM, van der Wetering J, et al. Serum 407. Berkhoff M, Donati F, Bassetti C. Postanoxic alpha (theta)
neuron-specific enolase predicts outcome in post-anoxic coma: a reappraisal of its prognostic significance. Clin Neu-
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2003;29:189—95. 408. Kaplan PW, Genoud D, Ho TW, Jallon P. Etiology, neurologic
394. Rosen H, Sunnerhagen KS, Herlitz J, Blomstrand C, Rosen- correlations, and prognosis in alpha coma. Clin Neurophys-
gren L. Serum levels of the brain-derived proteins S-100 iol 1999;110:205—13.
and NSE predict long-term outcome after cardiac arrest. 409. Yamashita S, Morinaga T, Ohgo S, et al. Prognostic value
Resuscitation 2001;49:183—91. of electroencephalogram (EEG) in anoxic encephalopathy
395. Schreiber W, Herkner H, Koreny M, et al. Predictors of sur- after cardiopulmonary resuscitation: relationship among
vival in unselected patients with acute myocardial infarc- anoxic period, EEG grading and outcome. Intern Med
tion requiring continuous catecholamine support. Resusci- 1995;34:71—6.
tation 2002;55:269—76. 410. Ajisaka H. Early electroencephalographic findings in
396. Schoerkhuber W, Kittler H, Sterz F, et al. Time course of patients with anoxic encephalopathy after cardiopul-
serum neuron-specific enolase. A predictor of neurologi- monary arrest and successful resusitation. J Clin Neurosci
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Stroke 1999;30:1598—603. 411. Rothstein TL, Thomas EM, Sumi SM. Predicting outcome in
397. Bottiger BW, Mobes S, Glatzer R, et al. Astroglial protein hypoxic-ischemic coma. A prospective clinical and elec-
S-100 is an early and sensitive marker of hypoxic brain trophysiologic study. Electroencephalogr Clin Neurophysiol
damage and outcome after cardiac arrest in humans. Cir- 1991;79:101—7.
culation 2001;103:2694—8. 412. Edgren E, Hedstrand U, Nordin M, Rydin E, Ronquist G.
398. Martens P, Raabe A, Johnsson P, Serum. S-100 and neuron- Prediction of outcome after cardiac arrest. Crit Care Med
specific enolase for prediction of regaining consciousness 1987;15:820—5.
after global cerebral ischemia. Stroke 1998;29:2363—6. 413. Sorensen K, Thomassen A, Wernberg M. Prognostic signifi-
399. Zingler VC, Krumm B, Bertsch T, Fassbender K, Pohlmann- cance of alpha frequency EEG rhythm in coma after cardiac
Eden B. Early prediction of neurological outcome after car- arrest. J Neurol Neurosurg Psychiatry 1978;41:840—2.
Resuscitation (2005) 67S1, S87—S96

European Resuscitation Council Guidelines for


Resuscitation 2005
Section 5. Initial management of acute
coronary syndromes
Hans-Richard Arntz, Leo Bossaert, Gerasimos S. Filippatos

Introduction Acute coronary syndromes are the commonest


cause of malignant arrhythmias leading to sudden
The incidence of acute myocardial infarction cardiac death. The therapeutic goals are to treat
(AMI) is decreasing in many European countries.1 acute life-threatening conditions, such as ventricu-
Although in-hospital mortality from AMI has been lar fibrillation (VF) or extreme bradycardias, and to
reduced significantly by modern reperfusion ther- preserve left ventricular function and prevent heart
apy and improved secondary prophylaxis,1 the over- failure by minimising the extent of any myocar-
all 28-day mortality is virtually unchanged because dial infarction. These guidelines address the first
about two thirds of those that die do so before hours after onset of symptoms. Out-of-hospital
arrival at hospital.2 Thus, the best chance of treatment and initial therapy in the emergency
improving survival after AMI is by improving treat- department may vary according to local capabili-
ment in the early, and particularly the out-of hos- ties, resources and regulations. The data supporting
pital, phase of the disease. out-of-hospital treatment are usually extrapolated
The term acute coronary syndrome (ACS) encom- from studies of initial treatment early after hospital
passes three different entities within the acute admission; there are only few high-quality out-of-
manifestation of coronary heart disease: ST eleva- hospital studies. Comprehensive guidelines for the
tion myocardial infarction (STEMI), non-ST eleva- diagnosis and treatment of ACS with and without
tion myocardial infarction (NSTEMI) and unstable ST elevation have been published by the European
angina pectoris (UAP) (Figure 5.1). The common Society of Cardiology and the American College of
pathophysiology of ACS is a ruptured or eroded Cardiology/American Heart Association.4,5 The cur-
atherosclerotic plaque.3 Electrocardiographic char- rent recommendations are in line with these guide-
acteristics (absence or presence of ST elevation) lines.
differentiate STEMI from the other forms of ACS.
A NSTEMI or UAP may present with ST segment
depression or non-specific ST segment wave abnor- Diagnostic tests in acute coronary
malities, or even a normal ECG. In the absence of syndromes
ST elevation, an increase in the plasma concentra-
tion of cardiac markers, particularly troponin T or Since early treatment offers the greatest benefits,
I as the most specific markers of myocardial cell and myocardial ischaemia is the leading precipitant
necrosis, indicates NSTEMI. of sudden cardiac death, it is essential that the

0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.
doi:10.1016/j.resuscitation.2005.10.003
S88 H.-R. Arntz et al.

Figure 5.1 Classification of acute coronary syndromes.

public are aware of the typical symptoms associ- presentations may occur in the elderly, in females,
ated with ACS. Patients at risk, and their families, and in people with diabetes.6,7
should be able to recognise characteristic symp-
toms such as chest pain, which may radiate into 12-lead ECG
other areas of the upper body, often accompanied
by other symptoms including dyspnoea, sweating, A 12-lead ECG is the key investigation for assess-
nausea or vomiting and syncope. They should under- ment of an ACS. In case of STEMI, a 12-lead ECG can
stand the importance of early activation of the indicate the need for immediate reperfusion ther-
emergency medical service (EMS) system and, ide- apy (e.g., primary percutaneous coronary interven-
ally, should be trained in basic life support (BLS). tion (PCI) or prehospital thrombolysis). Recording
EMS dispatchers must be trained to recognize of a 12-lead ECG out-of-hospital enables advanced
ACS symptoms and to ask targeted questions. When notification to the receiving facility and expe-
an ACS is suspected, an EMS crew trained in dites treatment decisions after hospital arrival;
advanced life support (ALS) and capable of mak- in many studies, the time from hospital admis-
ing the diagnosis and starting treatment should sion to initiating reperfusion therapy is reduced by
be alerted. The sensitivity, specificity and clinical 10—60 min.8—10 Recording and transmission of diag-
impact of various diagnostic strategies have been nostic quality ECGs to the hospital takes usually
evaluated for ACS/AMI. These include signs and less than 5 min. Trained EMS personnel (emergency
symptoms, the 12-lead electrocardiogram (ECG) physicians, paramedics and nurses) can identify
and biochemical markers of cardiac risk. STEMI, defined by ST elevation of ≥0.1 mV eleva-
tion in at least two adjacent limb leads or >0.2 mV in
Signs and symptoms of ACS/AMI two adjacent precordial leads, with high specificity
and sensitivity comparable to diagnostic accuracy
Even though typical symptoms such as radiating in the hospital.11—13
chest pain, shortness of breath or sweating may be
more intense and generally last longer in patients Biomarkers
with AMI, they are not adequately specific for a
reliable diagnosis of AMI. A 12-lead ECG, cardiac In the presence of a suggestive history, the absence
biomarkers and other diagnostic tests are required of ST elevation on the ECG, and elevated concen-
before ACS or AMI can be ruled out in the presence trations of biomarkers (troponin T and troponin
of a typical history. Atypical symptoms or unusual I, CK, CK-MB, myoglobin) characterise non-STEMI
European Resuscitation Council Guidelines for Resuscitation 2005 S89

and distinguish it from STEMI and unstable angina, Morphine


respectively.3 Elevated concentrations of troponin
are particularly helpful in identifying patients at Morphine is the analgesic of choice for nitrate-
increased risk of adverse outcome.14 However, refractory pain. Being a dilator of venous capac-
the delay in release of biomarkers from dam- itance vessels, it may have additional benefit in
aged myocardium prevents their use in diagnosing patients with pulmonary congestion. Give morphine
myocardial infarction in the first 4—6 h after the in initial doses of 3—5 mg intravenously and repeat
onset of symptoms.15 every few minutes until the patient is pain free.

Principles of acute treatment for ACS Oxygen

Give supplementary oxygen (4—8 l min−1 ) to all


Nitrates patients with arterial oxygen saturation <90%
and/or pulmonary congestion. Despite lack of proof
Glyceryl trinitrate is an effective treatment for
for long-term benefit of supplementary oxygen,16
ischaemic chest pain (Figure 5.2) and has some
give it to all patients with uncomplicated STEMI; it
beneficial haemodynamic effects, e.g., dilation of
will benefit patients with unrecognised hypoxia.
the venous capacitance vessels, coronary arteries
and, to a minor degree, peripheral arteries. Glyc-
eryl trinitrate may be considered if the systolic Acetylsalicylic acid
blood pressure is higher than 90 mmHg and the
patient has ongoing ischaemic chest pain. Glyc- Several large randomised controlled trials indi-
eryl trinitrate can be useful in the treatment of cate decreased mortality when acetylsalicylic acid
acute pulmonary congestion. Do not use nitrates in (ASA), 75—325 mg, is given to patients in hospital
patients with hypotension (systolic blood pressure with ACS.17,18 A few studies have suggested reduced
≤90 mmHg), particularly if combined with brady- mortality if ASA is given earlier.19 Therefore, give
cardia, nor in patients with inferior infarction and ASA as soon as possible to all patients with sus-
suspected right ventricular involvement. Use of pected ACS unless the patient has a known true
nitrates under these circumstances may cause a allergy to ASA. The initial dose of ASA to be chewed
precipitous decrease in blood pressure and cardiac is 160—325 mg. Other forms of ASA (soluble, IV) may
output. be as effective as chewed tablets.20

Figure 5.2 Early treatment of patients with signs/symptoms of ACS.


S90 H.-R. Arntz et al.

Reperfusion therapy Table 5.1 Contraindications for thrombolysisa .

Reperfusion therapy is the most important advance Absolute contraindications


in the treatment of AMI in the last 20 years. Haemorrhagic stroke or stroke of unknown origin
Large clinical trials have proven that fibrinolytic at any time
therapy in ACS patients with STEMI or new or Ischaemic stroke in the preceding 6 months
Central nervous system damage or neoplasms
presumed new LBBB, who present within 12 h of
Recent major trauma/surgery/head injury (within
onset of symptoms, reduces short- and long-term
the preceding 3 weeks)
mortality.17,21—23 The benefit achieved with fibri- Gastro-intestinal bleeding within the last month
nolytic therapy is profoundly time dependent; it Known bleeding disorder
is particularly effective if given within the first 3 h Aortic dissection
of the onset of symptoms.17,21,22,24 The efficacy of
primary PCI is also time-sensitive but less so than Relative contraindications
fibrinolysis.25 Transient ischaemic attack in preceding 6 months
Oral anticoagulant therapy
Pregnancy within 1 week post partum
Out-of-hospital fibrinolysis
Non-compressible punctures
Traumatic resuscitation
A meta-analysis of six trials involving 6434 patients
Refractory hypertension (systolic blood pressure
documented a 17% decrease in the mortality among >180 mmHg
patients treated with out-of-hospital fibrinolysis Advanced liver disease
compared with in-hospital fibrinolysis.26 The aver- Infective endocarditis
age time gained by out-of-hospital fibrinolysis was Active peptic ulcer
60 min, and the results were independent of the a According to the guidelines of the European Society of
experience of the provider. Thus, giving fibrinolyt- Cardiology.
ics out-of-hospital to patients with STEMI or signs
and symptoms of an ACS with presumed new LBBB is
beneficial. Fibrinolytic therapy can be given safely risk of intracranial bleeding from fibrinolysis; thus,
by trained paramedics, nurses or physicians using the absolute benefit of thrombolysis is reduced by
an established protocol.27—29 The efficacy is great- this complication.30 The risk of intracranial bleed-
est within the first 3 h of the onset of symptoms. ing in patients with a systolic blood pressure of over
An effective and safe system for out-of-hospital 180 mmHg is increased; this degree of hypertension
thrombolytic therapy requires adequate facilities is a relative contraindication to fibrinolytic therapy.
for the diagnosis and treatment of STEMI and its The intracranial bleeding risk also depends in part
complications. Ideally, there should be a capability on which fibrinolytic drug is used; the total mor-
to communicate with experienced hospital doctors tality is lower with the more fibrin-specific throm-
(e.g., emergency physicians or cardiologists). bolytics (alteplase, tenecteplase, reteplase), but
Patients with symptoms of ACS and ECG evidence the intracranial bleeding risk is lower with strep-
of STEMI (or presumably new LBBB or true posterior tokinase. The risk of intracranial bleeding is also
infarction) presenting directly to the emergency increased by the use of antithrombotic therapy,
department should be given fibrinolytic therapy as particularly heparin.
soon as possible unless there is immediate access
to primary PCI within 90 min. Primary percutaneous intervention

Risks of fibrinolytic therapy Coronary angioplasty with or without stent place-


ment has become the first-line treatment for
Healthcare professionals who give fibrinolytic patients with STEMI, because it has been shown
therapy must be aware of its contraindications to be superior to fibrinolysis in the combined end-
(Table 5.1) and risks. Patients with large AMIs (e.g., points of death, stroke and reinfarction in sev-
indicated by extensive ECG changes) are likely to eral studies and meta-analyses.31,32 This improve-
derive the greatest benefit from fibrinolytic ther- ment was found when primary PCI was undertaken
apy. Benefits of fibrinolytic therapy are less impres- by a skilled person in a high-volume centre (i.e.,
sive in inferior wall infarctions than in anterior >75 procedures per operator per year), with a
infarctions. Older patients have an absolute higher delay of balloon inflation of not more than 90 min
risk of death, but the absolute benefit of fibrinolytic after first contact. In the randomised studies com-
therapy is similar to that of younger patients. paring primary PCI and fibrinolytic therapy, the
Patients over 75 years of age have an increased typical delay from decision to the beginning of
European Resuscitation Council Guidelines for Resuscitation 2005 S91

treatment with either primary PCI or fibrinolytic or have persistent ischaemic symptoms after fibri-
therapy was less than 60 min; however, in registries nolytic therapy.
that reflect standard practice more realistically,
the delay was often longer. One study33 and one Cardiogenic shock
post hoc analysis34 comparing fibrinolytic therapy
with primary PCI showed no difference in survival Cardiogenic shock (and to some extent, severe left
if fibrinolytic therapy was initiated within 2 or 3 h ventricular failure) is one of the complications of
of onset of symptoms. ACS and has a mortality rate of more than 50%.
All patients presenting with STEMI and symptoms Cardiogenic shock in STEMI is not a contraindica-
of ACS and presumably new LBBB presenting within tion to fibrinolytic therapy, but PCI is preferable.
12 h after onset of symptoms should be evaluated Early revascularisation (i.e., primary or facilitated
for reperfusion therapy (fibrinolytic therapy or PCI). PCI or surgery) is indicated for those patients who
Primary PCI is preferred in patients with symptom develop shock within 36 h after symptom onset of
duration of over 3 h, if a skilled team can under- AMI and are suitable for revascularisation.38,39
take it within 90 min after first patient contact, and Suspect right ventricular infarction in patients
in all patients who have contraindications to fibri- with inferior infarction, clinical shock and clear
nolytic therapy. If the duration of symptoms is less lung fields. ST segment elevation ≥1 mm in lead
than 3 h, treatment is more time-sensitive and the V4R is a useful indicator of right ventricular infarc-
superiority of out-of-hospital fibrinolytic therapy, tion. These patients have an in-hospital mortality of
immediate in-hospital fibrinolytic therapy or trans- up to 30%, and many benefit greatly from reperfu-
fer for primary PCI is not yet established clearly. sion therapy (fibrinolytic therapy and/or PCI). Avoid
nitrates and other vasodilators, and treat hypoten-
Triage and interfacility transfer for primary PCI. sion with intravenous fluid.
The risk of death, reinfarction or stroke is reduced
if patients with STEMI are transferred promptly Adjunctive treatment in reperfusion
from community hospitals to tertiary care facilities
therapy in ACS
for primary PCI.35 It is unclear whether immedi-
ate fibrinolytic therapy (in- or out-of-hospital) or Heparin
transfer for primary PCI is superior for patients
presenting with STEMI with a symptom duration of Heparin is an indirect inhibitor of thrombin, which
<2—3 h.33,34 Transfer of STEMI patients for primary in combination with ASA is used as an adjunct
PCI is reasonable for those presenting later than 3 h with fibrinolytic therapy or primary PCI and as an
but less than 12 h after onset of symptoms, pro- important part of treatment of unstable angina
vided that the transfer can be achieved rapidly. and STEMI. Limitations of unfractionated heparin
Optimally, primary PCI should occur within 90 min include its unpredictable anticoagulant effect in
from the first contact with the healthcare provider individual patients, the need for it to be given
deciding to treat or transfer. intravenously and the need to monitor aPTT. More-
over, heparin can induce thrombocytopenia. Low-
Interfacility transfer for early PCI after fibrinolytic molecular-weight heparin has a more predictable
therapy. Older studies, that did not include mod- anticoagulant effect with lower rates of thrombocy-
ern adjunctive drugs and PCI techniques with stent- topenia. It can be given subcutaneously in a weight-
ing, do not support a strategy of fibrinolytic therapy adjusted dose and does not require laboratory mon-
combined with early PCI. In contrast, several recent itoring. Low-molecular-weight heparins may accu-
smaller studies support a strategy of in-hospital mulate in patients with impaired renal function.
fibrinolytic therapy in a peripheral hospital fol-
lowed by transfer for PCI within 24 h of fibrinolytic Unfractionated heparin versus
therapy.36,37 The timing of PCI after fibrinolytic low-molecular-weight heparin in NSTEMI
therapy, the use of coronary stents and control-
group interventions differ widely among these tri- In comparison with unfractionated heparin (UFH),
als. low-molecular-weight heparin (LMWH) (enoxa-
There is insufficient evidence to recommend rou- parin) reduces the combined endpoint of mortal-
tine transfer of patients for early PCI after suc- ity, myocardial infarction and the need for urgent
cessful fibrinolytic therapy. Transfer for early PCI revascularisation, if given within the first 24—36 h
after is recommended for patients in cardiogenic of onset of symptoms of NSTEMI/UAP.40—42 Although
shock, particularly for those younger than 75 years LMWH increases the incidence of minor bleed-
and for those who are haemodynamically unstable ing, in comparison with UFH, the incidence of
S92 H.-R. Arntz et al.

serious bleeding is not increased. Early treatment rent ischaemia in patients with UA/NSTEMI with-
with LMWH (enoxaparin) is the preferred therapy out mechanical perfusion, but showed a reduc-
for patients with NSTEMI/UAP in addition to ASA, tion in 30-day mortality in a later meta-analysis.46
whenever a non-interventional strategy is planned. In patients with UA/NSTEMI, abciximab, given in
Consider UFH if reperfusion is planned in the addition to standard therapy without mechanical
first 24—36 h after symptom onset. Optimal target intervention, resulted in a trend towards a worse
value of aPPT is 50—70 s. Avoid switching between outcome.47 Therefore, in high-risk patients, give
UFH and LMWH, because it may increase bleeding Gp IIb/IIIa inhibitors in addition to standard ther-
complications.43 apy in patients for whom revascularisation ther-
apy is planned. If revascularisation therapy is not
Unfractionated heparin versus planned, tirofiban and eptifibatide can be given to
low-molecular-weight heparin in STEMI high-risk NSTEMI/UAP patients in conjunction with
ASA and LMWH. Do not give abciximab if PCI is not
Two large randomised controlled thrombolysis stud- planned.
ies comparing LMWH with UFH demonstrated a Gp IIb/IIIa inhibitors in STEMI. Gp IIb/IIIa receptor
reduced frequency of ischaemic complications blockers in combination with a reduced dose of fib-
when given to patients with STEMI within 6 h of rinolytics do not reduce mortality in patients with
the onset of symptoms.44,45 This must be balanced STEMI, but increase bleeding risk in patients over
against the increase in intracranial haemorrhage in 75 years of age.44,48 Abciximab reduces mortality
patients over 75 years of age who receive LMWH.45 when given to patients with STEMI and planned
There is no evidence to support giving LMWH to primary PCI, but is not beneficial in patients not
patients with STEMI proceeding to an invasive strat- proceeding to primary PCI.46 Prehospital use of
egy. Thus, LMWH is an acceptable alternative to abciximab may improve the patency of the infarct-
UFH as an ancillary therapy for patients younger related artery with regard to PCI.49 There is no
than 75 years without significant renal dysfunction benefit in giving tirofiban in addition to stan-
who are treated with fibrinolytic therapy. UFH is dard therapy out of hospital or in the emergency
recommended as an ancillary therapy to fibrinolytic department.50 Abciximab may be helpful in reduc-
therapy in elderly patients and any STEMI patient ing short-term mortality and short-term reinfarc-
for whom revascularisation is planned. The optimal tion in patients treated with PCI without fibrinolytic
target value of aPPT is 50—70 s. The use of hep- therapy. Abciximab is not recommended in combi-
arin (preferably LMWH) depends partly on which nation with fibrinolytics in patients with STEMI.
fibrinolytic drug is used. Heparin is needed after
shorter-acting drugs because of the rebound hyper- Clopidogrel
coagulable state that occurs after a few hours,
but not after streptokinase because the fibrinolytic Clopidogrel inhibits the platelet ADP receptor irre-
effect of streptokinase lasts for about 48 h. versibly, which further reduces platelet aggregation
in addition to that produced by ASA. Compared
Glycoprotein IIb/IIIa inhibitors with ASA, there is no increased risk of bleeding
with clopidogrel.51 If given in addition to hep-
The platelet glycoprotein (Gp) IIb/IIIa receptor is arin and ASA within 4 h of presentation, clopi-
the final common pathway to platelet aggregation. dogrel improves outcome in patients with high-
The synthetic substances eptifibatide and tirofiban risk ACS.52,53 There is a significant reduction in
modulate this receptor activity reversibly, whereas adverse ischaemic events at 28 days after elective
the receptor antibody abciximab blocks it irre- PCI when clopidogrel is given at least 6 h before
versibly. intervention.54 A recent trial documented a signif-
icant reduction in the composite endpoint of an
Gp IIb/IIIa inhibitors in NSTEMI/unstable angina. occluded infarct-related artery (TIMI flow grade 0
The incidences of death and recurrent ischaemia or 1) on angiography or death or recurrent myocar-
are reduced when Gp IIb/IIIa inhibitors are added dial infarction before angiography, when clopido-
to standard therapy including ASA and heparin grel (300 mg loading dose, followed by 75 mg daily
in high-risk patients with UAP/NSTEMI treated dose up to 8 days in hospital) is given to patients up
with mechanical reperfusion.46 High-risk features to 75 years of age with STEMI who are treated with
include persistent pain, haemodynamic or rhythm fibrinolytic therapy, ASA and heparin.55
instability, diabetes, acute or dynamic ECG changes Give a 300-mg oral loading dose of clopidogrel
and any elevation in cardiac troponins. Tirofiban early, as well as standard care, to patients with
or eptifibatide failed to reduce death or recur- ACS if they have an increase in serum cardiac
European Resuscitation Council Guidelines for Resuscitation 2005 S93

biomarkers and/or new ECG changes consistent hours after onset of symptoms.59,60 This explains
with ischaemia when a medical approach or PCI is why numerous studies have been performed with
planned. Give clopidogrel to patients with STEMI the aim of demonstrating the prophylactic effect
up to 75 years of age receiving fibrinolytic therapy, of anti-arrhythmic therapy. The effects of anti-
ASA and heparin. Clopidogrel, 300 mg, can be given arrhythmic drugs (lidocaine, magnesium, disopy-
instead of ASA to patients with a suspected ACS who ramide, mexiletine, verapamil) given prophylacti-
have a true allergy to or gastrointestinal intoler- cally to patients with ACS have been studied.61—63
ance of ASA. Prophylaxis with lidocaine reduces the incidence
of VF but may increase mortality.58 Routine treat-
ment with magnesium in patients with AMI does
Primary and secondary prevention not improve mortality.64 Arrhythmia prophylaxis
interventions using disopyramide, mexiletine or verapamil, given
within the first hours of an ACS, does not improve
Start preventive interventions, at the latest, at the mortality.63 In contrast, intravenous beta-blockers
initial admission with a confirmed diagnosis of ACS. reduced the incidence of VF when given to patients
Give a beta-blocker as soon as possible unless con- with ACS.56,57
traindicated or poorly tolerated. Treat all patients
with a statin (HRG co-enzyme A reductase inhibitor) Angiotensin-converting enzyme inhibitors
unless contraindicated or poorly tolerated. Start an and angiotensin-II receptor blockers
ACE inhibitor in all patients with STEMI, all patients
with STEMI and left ventricular systolic impair- Oral angiotensin-converting inhibitors (ACE) inhibi-
ment, and consider it in all other patients with tors reduce mortality when given to patients with
STEMI unless contraindicated or poorly tolerated. acute myocardial infarction with or without early
In patients unable to tolerate an ACE inhibitor, an reperfusion therapy.65,66 The beneficial effects are
angiotensin receptor blocker may be used as a sub- most pronounced in patients presenting with ante-
stitute in those patients with left ventricular sys- rior infarction, pulmonary congestion or left ven-
tolic impairment. tricular ejection fraction <40%.66 Do not give ACE
inhibitors if the systolic blood pressure is less than
Beta-blockers 100 mmHg at admission or if there is a known con-
traindication to these drugs.66 A trend towards
Several studies, undertaken mainly in the pre- higher mortality has been documented if an intra-
reperfusion era, indicate decreased mortality and venous ACE inhibitor is started within the first 24 h
incidence of reinfarction and cardiac rupture as after onset of symptoms.67 Therefore, give an oral
well as a lower incidence of VF and supraventric- ACE inhibitor within 24 h after symptom onset in
ular arrhythmia in patients treated early with a patients with AMI regardless of whether early reper-
beta-blocker.56,57 Intravenous beta-blockade may fusion therapy is planned, particularly in those
also reduce mortality in patients undergoing pri- patients with anterior infarction, pulmonary con-
mary PCI who are not on oral beta-blockers.58 gestion or left ventricular ejection fraction below
Haemodynamically stable patients presenting 40%. Do not give intravenous ACE inhibitors within
with an ACS should be given intravenous beta- 24 h of onset of symptoms. Give an angiotensin
blockers promptly, followed by regular oral therapy receptor blocker (ARB) to patients intolerant of ACE
unless contraindicated or poorly tolerated. Con- inhibitors.
traindications to beta-blockers include hypoten-
sion, bradycardia, second- or third-degree AV block, Statins
moderate to severe congestive heart failure and
severe reactive airway disease. Give a beta-blocker Statins reduce the incidence of major adverse car-
irrespective of the need for early revascularisation diovascular events when given within a few days
therapy. after onset of ACS. Start statin therapy within 24 h
of onset of symptoms of ACS. If patients are already
Anti-arrhythmics receiving statin therapy, do not stop it.68

Apart from the use of a beta-blocker as recom-


mended above, there is no evidence to support References
the use of anti-arrhythmic prophylaxis after ACS.
VF accounts for most of the early deaths from 1. Tunstall-Pedoe H, Vanuzzo D, Hobbs M, et al. Estimation
ACS; the incidence of VF is highest in the first of contribution of changes in coronary care to improving
S94 H.-R. Arntz et al.

survival, event rates, and coronary heart disease mortal- 17. Randomised trial of intravenous streptokinase, oral aspirin,
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Resuscitation (2005) 67S1, S97—S133

European Resuscitation Council Guidelines for


Resuscitation 2005
Section 6. Paediatric life support
Dominique Biarent, Robert Bingham, Sam Richmond, Ian Maconochie,
Jonathan Wyllie, Sheila Simpson, Antonio Rodriguez Nunez,
David Zideman

Introduction Guidelines changes

The process The approach to changes has been to alter the


guidelines in response to convincing new scientific
The European Resuscitation Council (ERC) issued evidence and, where possible, to simplify them in
guidelines for paediatric life support (PLS) in 1994, order to assist teaching and retention. As before,
1998 and 2000.1—4 The last edition was based on there remains a paucity of good-quality evidence on
the International Consensus on Science published paediatric resuscitation specifically and some con-
by the American Heart Association in collaboration clusions have had to be drawn from animal work
with the International Liaison Committee on Resus- and extrapolated adult data.
citation (ILCOR), undertaking a series of evidence- The current guidelines have a strong focus on
based evaluations of the science of resuscitation simplification based on the knowledge that many
which culminated in the publication of the Guide- children receive no resuscitation at all because res-
lines 2000 for Cardiopulmonary Resuscitation and cuers fear doing harm. This fear is fuelled by the
Emergency Cardiovascular Care in August 2000.5,6 knowledge that resuscitation guidelines for chil-
This process was repeated in 2004/2005, and the dren are different. Consequently, a major area of
resulting Consensus on Science and Treatment Rec- study was the feasibility of applying the same guid-
ommendations were published simultaneously in ance for all adults and children. Bystander resusci-
Resuscitation, Circulation and Pediatrics in Novem- tation improves outcome significantly,9,10 and there
ber 2005.7,8 The PLS Working Party of the ERC has is good evidence from paediatric animal models
considered this document and the supporting sci- that even doing chest compressions or expired air
entific literature, and has recommended changes ventilation alone may be better than doing noth-
to the ERC PLS Guidelines. These are presented in ing at all.11 It follows that outcomes could be
this paper. improved if bystanders, who would otherwise do
nothing, were encouraged to begin resuscitation,
even if they do not follow an algorithm targeted
specifically at children. There are, however, dis-

0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.
doi:10.1016/j.resuscitation.2005.10.010
S98 D. Biarent et al.

tinct differences between the predominantly adult ondary cardiac arrest. The onset of puberty, which
arrest of cardiac origin and asphyxial arrest, which is the physiological end of childhood, is the most
is most common in children,12 so a separate paedi- logical landmark for the upper age limit for use
atric algorithm is justified for those with a duty to of paediatric guidance. This has the advantage of
respond to paediatric emergencies (usually health- being simple to determine, in contrast to an age
care professionals), who are also in a position to limit in years, as age may be unknown at the start of
receive enhanced training. resuscitation. Clearly, it is inappropriate and unnec-
essary to establish the onset of puberty formally; if
Compression:ventilation ratios rescuers believe the victim to be a child they should
use the paediatric guidelines. If a misjudgement is
The ILCOR treatment recommendation was that made and the victim turns out to be a young adult,
the compression:ventilation ratio should be based little harm will accrue, as studies of aetiology have
on whether one or more than one rescuers were shown that the paediatric pattern of arrest contin-
present. ILCOR recommends that lay rescuers, ues into early adulthood.19 An infant is a child under
who usually learn only single rescuer techniques, 1 year of age; a child is between 1 year and puberty.
should be taught to use a ratio of 30 compres- It is necessary to differentiate between infants and
sions to 2 ventilations, which is the same as the older children, as there are some important differ-
adult guidelines and enables anyone trained in ences between these two groups.
BLS techniques to resuscitate children with mini-
mal additional information. Two or more rescuers Chest compression technique
with a duty to respond should learn a different
ratio (15:2), as this has been validated by animal The modification to age definitions enables a sim-
and manikin studies.13—17 This latter group, who plification of the advice on chest compression.
would normally be healthcare professionals, should Advice for determining the landmarks for infant
receive enhanced training targeted specifically at compression is now the same as for older chil-
the resuscitation of children. Although there are dren, as there is evidence that the previous rec-
no data to support the superiority of any partic- ommendation could result in compression over the
ular ratio in children, ratios of between 5:1 and upper abdomen.20 Infant compression technique
15:2 have been studied in manikins, and animal remains the same: two-finger compression for sin-
and mathematical models, and there is increasing gle rescuers and two-thumb, encircling technique
evidence that the 5:1 ratio delivers an inadequate for two or more rescuers,21—25 but for older children
number of compressions.14,18 There is certainly no there is no division between the one- or two-hand
justification for having two separate ratios for chil- technique.26 The emphasis is on achieving an ade-
dren aged greater or less than 8 years, so a single quate depth of compression with minimal interrup-
ratio of 15:2 for multiple rescuers with a duty to tions, using one or two hands according to rescuer
respond is a logical simplification. preference.
It would certainly negate any benefit of simplic-
ity if lay rescuers were taught a different ratio for Automated external defibrillators
use if there were two of them, but those with a duty
to respond can use the 30:2 ratio if they are alone, Case reports published since International Guide-
particularly if they are not achieving an adequate lines 2000 have reported safe and successful use of
number of compressions because of difficulty in the AEDs in children less than 8 years of age.27,28 Fur-
transition between ventilation and compression. thermore, recent studies have shown that AEDs are
capable of identifying arrhythmias in children accu-
Age definitions rately and that, in particular, they are extremely
unlikely to advise a shock inappropriately.29,30 Con-
The adoption of single compression:ventilation sequently, advice on the use of AEDs has been
ratios for children of all ages, together with the revised to include all children aged greater than 1
change in advice on the lower age limit for the year.31 Nevertheless, if there is any possibility that
use of automated external defibrillators (AEDs), an AED may need to be used in children, the pur-
renders the previous guideline division between chaser should check that the performance of the
children above and below 8 years of age unneces- particular model has been tested against paediatric
sary. The differences between adult and paediatric arrhythmias.
resuscitation are based largely on differing aeti- Many manufacturers now supply purpose-made
ology, as primary cardiac arrest is more common paediatric pads or programmes, which typically
in adults whereas children usually suffer from sec- attenuate the output of the machine to 50—75 J.32
European Resuscitation Council Guidelines for Resuscitation 2005 S99

These devices are recommended for children aged


1—8 years.33,34 If no such system or manually
adjustable machine is available, an unmodified
adult AED may be used in children older than 1
year.35 There is currently insufficient evidence to
support a recommendation for or against the use of
AEDs in children aged less than 1 year.

Manual defibrillators

The 2005 Consensus Conference treatment rec-


ommendation for paediatric ventricular fibrillation
(VF) or paediatric pulseless ventricular tachycar-
dia (VT) is to defibrillate promptly. In adult ALS,
the recommendation is to give a single shock and
then resume CPR immediately without checking for
a pulse or reassessing the rhythm (see Section 3). As
a consequence of this single-shock strategy, when
using a monophasic defibrillator in adults a higher Figure 6.1 Paediatric basic life support algorithm.
initial energy dose than used previously is recom-
mended (360 J versus 200 J) (see Section 3). The
ideal energy dose for safe and effective defibril-
The following sequence is to be observed by
lation in children is unknown, but animal models
those with a duty to respond to paediatric emer-
and small paediatric series show that doses larger
gencies (usually health professionals).
than 4 J kg−1 defibrillate effectively with negligible
side effects.27,34,36,37 Biphasic shocks are at least 1. Ensure the safety of rescuer and child.
as effective and produce less post-shock myocardial 2. Check the child’s responsiveness.
dysfunction than monophasic shocks.33,34,37—40 For • Gently stimulate the child and ask loudly:
simplicity of sequence and consistency with adult ‘‘Are you all right?’’
BLS and ALS, we recommend a single-shock strategy • Do not shake infants or children with sus-
using a non-escalating dose of 4 J kg−1 (monophasic pected cervical spinal injuries.
or biphasic) for defibrillation in children.
3a If the child responds by answering or moving
• leave the child in the position in which you
Foreign-body airway obstruction sequence find him (provided he is not in further danger)
• check his condition and get help if needed
The guidance for managing foreign-body airway
• reassess him regularly
obstruction (FBAO) in children has been simpli-
fied and brought into closer alignment to the adult 3b If the child does not respond
sequence. These changes are discussed in detail at • shout for help;
the end of this section. • open the child’s airway by tilting the head and
In the following text the masculine includes the lifting the chin, as follows:
feminine and ‘child’ refers to both infants and chil- o initially with the child in the position in
dren unless noted otherwise. which you find him, place your hand on his
forehead and gently tilt his head back;
o at the same time, with your fingertip(s)
6a Paediatric basic life support under the point of the child’s chin, lift the
chin. Do not push on the soft tissues under
Sequence of action the chin as this may block the airway;
o if you still have difficulty in opening the air-
Rescuers who have been taught adult BLS and have way, try the jaw thrust method. Place the
no specific knowledge of paediatric resuscitation first two fingers of each hand behind each
may use the adult sequence, with the exception side of the child’s mandible and push the
that they should perform 5 initial breaths followed jaw forward;
by approximately 1 min of CPR before they go for o both methods may be easier if the child is
help (Figure 6.1; also see adult BLS guideline). turned carefully onto his back.
S100 D. Biarent et al.

If you suspect that there may have been an injury • Pinch the soft part of the nose closed with the
to the neck, try to open the airway using chin lift or index finger and thumb of your hand on his fore-
jaw thrust alone. If this is unsuccessful, add head head.
tilt a small amount at a time until the airway is • Open his mouth a little, but maintain the chin
open. upwards.
• Take a breath and place your lips around the
4. Keeping the airway open, look, listen and feel mouth, making sure that you have a good seal.
for normal breathing by putting your face close • Blow steadily into the mouth over about 1—1.5 s,
to the child’s face and looking along the chest. watching for chest rise.
• Look for chest movements. • Maintain head tilt and chin lift, take your mouth
• Listen at the child’s nose and mouth for breath away from the victim and watch for his chest to
sounds. fall as air is expelled.
• Feel for air movement on your cheek. • Take another breath and repeat this sequence
five times. Identify effectiveness by seeing that
Look, listen and feel for no more than 10 s before the child’s chest has risen and fallen in a similar
deciding. fashion to the movement produced by a normal
breath.
5a If the child is breathing normally
• turn the child on his side into the recovery Rescue breaths for an infant are performed as
position (see below) follows (Figure 6.3).
• check for continued breathing
• Ensure a neutral position of the head and a chin
5b If the child is not breathing or is making agonal lift.
gasps (infrequent, irregular breaths) • Take a breath and cover the mouth and nasal
• carefully remove any obvious airway obstruc- apertures of the infant with your mouth, making
tion; sure you have a good seal. If the nose and mouth
• give five initial rescue breaths; cannot be covered in the older infant, the res-
• while performing the rescue breaths, note cuer may attempt to seal only the infant’s nose
any gag or cough response to your action. or mouth with his mouth (if the nose is used, close
These responses or their absence will form the lips to prevent air escape).
part of your assessment of signs of a circu- • Blow steadily into the infant’s mouth and nose
lation, which will be described later. over 1—1.5 s, sufficient to make the chest visibly
rise.
Rescue breaths for a child over 1 year are per-
• Maintain head tilt and chin lift, take your mouth
formed as follows (Figure 6.2).
away from the victim and watch for his chest to
• Ensure head tilt and chin lift. fall as air is expelled.
• Take another breath and repeat this sequence
five times.

Figure 6.2 Mouth-to-mouth ventilation— child. © 2005 Figure 6.3 Mouth-to-mouth and nose ventilation—
ERC. infant. © 2005 ERC.
European Resuscitation Council Guidelines for Resuscitation 2005 S101

If you have difficulty achieving an effective breath,


the airway may be obstructed.
• Open the child’s mouth and remove any visible
obstruction. Do not perform a blind finger sweep.
• Ensure that there is adequate head tilt and chin
lift but also that the neck is not over-extended.
• If head tilt and chin lift have not opened the air-
way, try the jaw thrust method.
• Make up to five attempts to achieve effective
breaths; if still unsuccessful, move on to chest
compressions.
6. Assess the child’s circulation. Take no more than
10 s to
Figure 6.4 Chest compression — infant. © 2005 ERC.
• look for signs of a circulation. This includes
any movement, coughing or normal breathing
(not agonal gasps, which are infrequent, irreg- rate of compressions will be 100 min−1 , the actual
ular breaths); number delivered per minute will be less than 100
• check the pulse (if you are a health care because of pauses to give breaths. The best method
provider) but ensure you take no more than for compression varies slightly between infants and
10 s. children.
To perform chest compression in infants, the lone
If the child is aged over 1 year, feel for the rescuer compresses the sternum with the tips of
carotid pulse in the neck. two fingers (Figure 6.4). If there are two or more
In an infant, feel for the brachial pulse on the rescuers, use the encircling technique. Place both
inner aspect of the upper arm. thumbs flat side by side on the lower third of the
sternum (as above) with the tips pointing towards
7a If you are confident that you can detect signs of the infant’s head. Spread the rest of both hands
a circulation within 10 s with the fingers together to encircle the lower part
• continue rescue breathing, if necessary, until of the infant’s rib cage with the tips of the fin-
the child starts breathing effectively on his gers supporting the infant’s back. Press down on the
own lower sternum with the two thumbs to depress it
• turn the child onto his side (into the recovery approximately one third of the depth of the infant’s
position) if he remains unconscious chest.
• re-assess the child frequently To perform chest compression in children over
7b If there are no signs of a circulation, or no pulse 1 year of age, place the heel of one hand
or a slow pulse (less than 60 min−1 with poor over the lower third of the sternum (as above)
perfusion), or you are not sure (Figures 6.5 and 6.6). Lift the fingers to ensure that
• start chest compressions pressure is not applied over the child’s ribs. Position
• combine rescue breathing and chest compres- yourself vertically above the victim’s chest and,
sions with your arm straight, compress the sternum to
Chest compressions are performed as follows. depress it by approximately one third of the depth
For all children, compress the lower third of the of the chest. In larger children or for small rescuers,
sternum. To avoid compressing the upper abdomen, this is achieved most easily by using both hands with
locate the xiphisternum by finding the angle where the fingers interlocked.
the lowest ribs join in the middle. Compress the 8. Continue resuscitation until
sternum one finger’s breadth above this; the com- • the child shows signs of life (spontaneous res-
pression should be sufficient to depress the ster- piration, pulse, movement)
num by approximately one third of the depth of • qualified help arrives
the chest. Release the pressure and repeat at a • you become exhausted
rate of about 100 min−1 . After 15 compressions,
tilt the head, lift the chin, and give two effective
breaths. Continue compressions and breaths in a When to call for assistance
ratio of 15:2. Lone rescuers may use a ratio of 30:2,
particularly if having difficulty with the transition It is vital for rescuers to get help as quickly as pos-
between compression and ventilation. Although the sible when a child collapses.
S102 D. Biarent et al.

• When more than one rescuer is available, one recovery positions; each has its advocates. There
starts resuscitation while another rescuer goes are important principles to be followed.
for assistance. • Place the child in as near true lateral position
• If only one rescuer is present, undertake resus- as possible, with his mouth dependent to enable
citation for about 1 min before going for assis- free drainage of fluid.
tance. To minimise interruption in CPR, it may • The position should be stable. In an infant this
be possible to carry an infant or small child while may require the support of a small pillow or
summoning help. a rolled-up blanket placed behind the back to
• The only exception to performing 1 min of CPR maintain the position.
before going for help is in the case of a child with • Avoid any pressure on the chest that impairs
a witnessed, sudden collapse when the rescuer is breathing.
alone. In this case cardiac arrest is likely to be • It should be possible to turn the child onto his side
arrhythmogenic in origin and the child will need and to return him back easily and safely, taking
defibrillation. Seek help immediately if there is into consideration the possibility of cervical spine
no one to go for you. injury.
• Ensure the airway can be observed and accessed
easily.
Recovery position • The adult recovery position is suitable for use in
children.
An unconscious child whose airway is clear, and who
is breathing spontaneously, should be turned on his
side into the recovery position. There are several
Foreign-body airway obstruction (FBAO)
No new evidence on this subject was presented dur-
ing the 2005 Consensus Conference. Back blows,
chest thrusts and abdominal thrusts all increase
intrathoracic pressure and can expel foreign bod-
ies from the airway. In half of the episodes,
more than one technique is needed to relieve the
obstruction.41 There are no data to indicate which
measure should be used first or in which order they
should be applied. If one is unsuccessful, try the
others in rotation until the object is cleared.
The International Guidelines 2000 algorithm is
difficult to teach and knowledge retention poor.
The FBAO algorithm for children has been simpli-
fied and aligned with the adult version (Figure 6.7).
Figure 6.5 Chest compression with one hand — child. This should improve skill retention and encourage
© 2005 ERC. people, who might otherwise have been reluctant,
to perform FBAO manoeuvres on children.

Figure 6.6 Chest compression with two hands — child. Figure 6.7 Paediatric foreign body airway obstruction
© 2005 ERC. algorithm.
European Resuscitation Council Guidelines for Resuscitation 2005 S103

The most significant difference from the adult treatment of the choking child.
algorithm is that abdominal thrusts should not be
used to treat choking infants. Although abdominal • If the child is coughing effectively, no external
thrusts have caused injuries in all age groups, the manoeuvre is necessary. Encourage the child to
risk is particularly high in infants and very young cough, and monitor continually.
children. This is because of the horizontal position • If the child’s coughing is (or is becoming) ineffec-
of the ribs, which leaves the upper abdominal vis- tive, shout for help immediately and determine
cera much more exposed to trauma. For this reason, the child’s conscious level.
the guidelines for the treatment of FBAO are differ-
ent between infants and children.
2. Conscious child with FBAO
Recognition of FBAO
• If the child is still conscious but has absent or
When a foreign body enters the airway, the child ineffective coughing, give back blows.
reacts immediately by coughing in an attempt to • If back blows do not relieve the FBAO, give
expel it. A spontaneous cough is likely to be more chest thrusts to infants or abdominal thrusts to
effective and safer than any manoeuvre a rescuer children. These manoeuvres create an ‘artificial
might perform. However, if coughing is absent or cough’ to increase intrathoracic pressure and dis-
ineffective and the object completely obstructs the lodge the foreign body.
airway, the child will rapidly become asphyxiated.
Active interventions to relieve FBAO are therefore Back blows. Back blows in the infant are per-
required only when coughing becomes ineffective, formed as follows.
but they then need to be commenced rapidly and
confidently. • Support the infant in a head downwards, prone
The majority of choking events in infants and position, to enable gravity to assist removal of
children occur during play or eating episodes when the foreign body.
a carer is usually present; thus, the events are fre- • A seated or kneeling rescuer should be able to
quently witnessed and interventions are usually ini- support the infant safely across their lap.
tiated when the child is conscious. • Support the infant’s head by placing the thumb of
Foreign-body airway obstruction is characterized one hand at the angle of the lower jaw, and one
by the sudden onset of respiratory distress associ- or two fingers from the same hand at the same
ated with coughing, gagging or stridor. Similar signs point on the other side of the jaw.
and symptoms may be associated with other causes • Do not compress the soft tissues under the
of airway obstruction, such as laryngitis or epiglot- infant’s jaw, as this will exacerbate the airway
titis, which require different management. Suspect obstruction.
FBAO if the onset was very sudden and there are no • Deliver up to five sharp back blows with the heel
other signs of illness and if there are clues to alert of one hand in the middle of the back between
the rescuer, e.g. a history of eating or playing with the shoulder blades.
small items immediately before the onset of symp- • The aim is to relieve the obstruction with each
toms. blow rather than to give all five blows.

Back blows in the child over 1 year of age are


performed as follows.

• Back blows are more effective if the child is posi-


tioned head down.
• A small child may be placed across the rescuer’s
lap, as with the infant.
• If this is not possible, support the child in a
forward-leaning position and deliver the back
blows from behind.
Relief of FBAO
If back blows fail to dislodge the object, and
1. Safety and summoning assistance the child is still conscious, use chest thrusts for
infants or abdominal thrusts for children. Do not
Safety is paramount: rescuers must not place them- use abdominal thrusts (Heimlich manoeuvre) in
selves in danger and should consider the safest infants.
S104 D. Biarent et al.

Chest thrusts for infants. object more deeply into the pharynx and cause
injury.
• Turn the infant into a head-downwards supine • Open the airway using a head tilt and/or chin
position. This is achieved safely by placing the lift and attempt five rescue breaths. Assess the
free arm along the infant’s back and encircling effectiveness of each breath; if a breath does not
the occiput with the hand. make the chest rise, reposition the head before
• Support the infant down your arm, which is making the next attempt.
placed down (or across) your thigh. • Attempt five rescue breaths and, if there is
• Identify the landmark for chest compressions no response (moving, coughing, spontaneous
(lower sternum approximately a finger’s breadth breaths), proceed to chest compressions without
above the xiphisternum). further assessment of the circulation.
• Give five chest thrusts; these are similar to chest • Follow the sequence for single-rescuer CPR (step
compressions but sharper and delivered at a 7b above) for approximately 1 min before sum-
slower rate. moning the EMS (if this has not already been done
by someone else).
Abdominal thrusts for children over 1 year. • When the airway is opened for attempted deliv-
ery of rescue breaths, look to see if the foreign
• Stand or kneel behind the child; place your arms body can be seen in the mouth.
under the child’s arms and encircle his torso. • If an object is seen, attempt to remove it with a
• Clench your fist and place it between the umbili- single finger sweep.
cus and xiphisternum. • If it appears the obstruction has been relieved,
• Grasp this hand with the other hand and pull open and check the airway as above; deliver res-
sharply inwards and upwards. cue breaths if the child is not breathing.
• Repeat up to five times. • If the child regains consciousness and exhibits
• Ensure that pressure is not applied to the xiphoid spontaneous effective breathing, place him in a
process or the lower rib cage; this might cause safe position lying on his side and monitor breath-
abdominal trauma. ing and conscious level while awaiting the arrival
of the EMS.
Following the chest or abdominal thrusts,
reassess the child. If the object has not been
expelled and the victim is still conscious, continue
the sequence of back blows and chest (for infant) or 6b Paediatric advanced life support
abdominal (for children) thrusts. Call out, or send,
for help if it is still not available. Do not leave the Prevention of cardiopulmonary arrest
child at this stage.
If the object is expelled successfully, assess In children, secondary cardiopulmonary arrests,
the child’s clinical condition. It is possible that caused by either circulatory or respiratory fail-
part of the object may remain in the respira- ure, are more frequent than primary arrests
tory tract and cause complications. If there is caused by arrhythmias.9,12,43—46 So-called ‘asphyx-
any doubt, seek medical assistance. Abdominal ial arrests’ or respiratory arrests are also more
thrusts may cause internal injuries, and all vic- common in young adulthood (e.g., trauma, drown-
tims so treated should be examined by a medical ing, poisoning).47,48 The outcome from cardiopul-
practitioner.42 monary arrests in children is poor; identification of
the antecedent stages of cardiac or respiratory fail-
ure is a priority, as effective early intervention may
3. Unconscious child with FBAO be life saving.
The order of assessment and intervention for any
If the child with FBAO is, or becomes, uncon- seriously ill or injured child follows the ABC princi-
scious, place him on a firm, flat surface. Call ples.
out, or send, for help if it is still not available.
Do not leave the child at this stage; proceed as • A indicates airway (Ac for airway and cervical
follows. spine stabilisation for the injured child).
• B indicates breathing.
• Open the mouth and look for any obvious object. • C indicates circulation.
If an object is seen, make an attempt to remove it
with a single finger sweep. Do not attempt blind Interventions are made at each step of the
or repeated finger sweeps; these can impact the assessment as abnormalities are identified; the next
European Resuscitation Council Guidelines for Resuscitation 2005 S105

step of the assessment is not started until the • level of consciousness may decrease because of
preceding abnormality has been managed and cor- poor cerebral perfusion
rected if possible.
Diagnosing cardiopulmonary arrest
Diagnosing respiratory failure: assessment
Signs of cardiopulmonary arrest include
of A and B
• unresponsiveness
The first steps in the assessment of the seriously ill • apnoea or gasping respiratory pattern
or injured child are the management of the airway • absent circulation
and breathing. Abnormalities in airway patency and • pallor or deep cyanosis
breathing lead to respiratory failure. Signs of res-
piratory failure are In the absence of ‘signs of life’, search for a
central pulse or cardiac sounds (by direct chest aus-
• respiratory rate outside the normal range for the cultation) for a maximum of 10 s, before starting
child’s age—–either too fast or too slow CPR. If there is any doubt, start CPR.50—53
• initially increasing work of breathing which
may progress to inadequate/decreased work
of breathing, additional noises such as stridor, Management of respiratory and
wheeze or grunting, or the loss of breath sounds circulatory failure
• cyanosis (without/with supplemental oxygen)

There may be associated signs in other organ sys- A and B


tems affected by inadequate ventilation and oxy-
genation; these are detectable in the C steps of Open the airway and ensure adequate ventilation
assessment, such as and oxygenation.
• Deliver high-flow oxygen.
• increasing tachycardia progressing to bradycar-
• Achieving adequate ventilation and oxygenation
dia (this latter sign being an ominous indicator of
may include the use of airway adjuncts, bag-mask
the loss of compensatory mechanisms)
ventilation (BMV), use of a laryngeal mask airway
• alteration in the level of consciousness
(LMA), securing a definitive airway by tracheal
intubation and positive pressure ventilation.
Diagnosing circulatory failure: assessment • In rare, extreme circumstances, a surgical airway
of C may be required.

Shock is characterised by a mismatch between C


metabolic tissue demand and delivery of oxy-
gen and nutrients by the circulation.49 Physiolog- Establish cardiac monitoring.
ical compensatory mechanisms lead to changes
in the heart rate, in the systemic vascular resis- • Secure vascular access to the circulation. This
tance (which commonly increases as an adaptive may be via peripheral or central intravenous (IV)
response) and in tissue and organ perfusion. Signs or by intraosseous (IO) cannulation.
of circulatory failure are • Give a fluid bolus and/or inotropes as required.
Assess and re-assess the child continuously, each
• increased heart rate (bradycardia is an ominous
time commencing at Airway before Breathing,
sign, heralding physiological decompensation)
thereafter moving onto the Circulation
• decreased systemic blood pressure
• decreased peripheral perfusion (prolonged capil-
lary refill time, decreased skin temperature, pale Airway
or mottled skin)
Open the airway using basic life support tech-
• weak or absent peripheral pulses
niques. Oropharyngeal and nasopharyngeal airways
• decreased or increased preload
adjuncts can help maintain the airway. Use the
• decreased urine output and metabolic acidosis
oropharyngeal airway only in the unconscious child,
Other systems may be affected, for example in whom there is no gag reflex. Use the appro-
priate size, to avoid pushing the tongue back-
• respiratory rate may be increased initially, be- ward and obstructing the epiglottis, or directly
coming bradypnoeic with decompensated shock compressing the glottic area. The soft palate in
S106 D. Biarent et al.

the child can be damaged by insertion of the tor must be experienced and familiar with rapid-
oropharygneal airway; avoid this by inserting the sequence induction drugs.
oropharygneal airway under direct vision and pass-
ing it over a tongue depressor or laryngoscope. Tracheal tube sizes. The tracheal tube internal
The nasopharyngeal airway is tolerated better in diameters (ID) for different ages are
the conscious child (who has an effective gag • for neonates, 2.5—3.5 mm according to the for-
reflex), but should not be used if there is a basal mula (gestational age in weeks 10)
skull fracture or a coagulopathy. These simple • for infants, 4 or 4.5 mm
airway adjuncts do not protect the airway from • for children older than 1 year, according to the
aspiration of secretions, blood or stomach con- formula [(age in years/4) + 4]
tents.
Tracheal tube size estimation according the
Laryngeal mask airway length of the child’s body as measured by resusci-
tation tapes is more accurate than using the above
The LMA is an acceptable initial airway device for formulae.67
providers experienced in its use. It may be particu-
Cuffed versus uncuffed tracheal tubes. In the pre-
larly helpful in airway obstruction caused by upper
hospital setting, an uncuffed tracheal tube may be
airway abnormalities. The LMA does not, however,
preferable when using sizes of up to 5.5 mm ID (i.e.,
protect the airway from aspiration of secretions,
for children up to 8 years). In hospital, a cuffed tra-
blood or stomach contents, and therefore close
cheal tube may be useful in certain circumstances,
observation is required. LMA use is associated with
e.g. in cases of poor lung compliance, high air-
a higher incidence of complications in small chil-
way resistance or large glottic air leak.68—70 The
dren compared with adults.54
correctly sized cuffed tracheal tube is as safe as
an uncuffed tube for infants and children (not for
Tracheal intubation neonates), provided attention is paid to its place-
ment, size and cuff inflation pressure; excessive
Tracheal intubation is the most secure and effective
cuff pressure can lead to ischaemic necrosis of
way to establish and maintain the airway, prevent
the surrounding laryngeal tissue and stenosis. Main-
gastric distension, protect the lungs against pul-
tain the cuff inflation pressure below 20 cmH2 O and
monary aspiration, enable optimal control of the
check it regularly.71
airway pressure and provide positive end expiratory
pressure (PEEP). The oral route is preferable during Confirmation of correct tracheal tube placement.
resuscitation. Oral intubation is usually quicker and Displaced, misplaced or obstructed tubes occur
is associated with fewer complications than nasal frequently in the intubated child and are asso-
placement. The judicious use of anaesthetics, seda- ciated with increased risk of death.72,73 No sin-
tives and neuromuscular blocking drugs is indicated gle technique is 100% reliable for distinguishing
in the conscious child to avoid multiple intubation oesophageal from tracheal intubation.74—76 Assess-
attempts or intubation failure.55—65 The anatomy ment of the correct tracheal tube position is made
of a child’s airway differs significantly from that of by
an adult; hence, intubation of a child requires spe-
cial training and experience. Check that tracheal • observation of the tube passing beyond the vocal
tube placement is correct by clinical examination cords
and end-tidal capnography. The tracheal tube must • observation of symmetrical chest wall movement
be secured, and monitoring of the vital signs is during positive pressure ventilation
essential.66 • observation of mist in the tube during the expi-
It is also essential to plan an alternative airway ratory phase of ventilation
management technique in case the trachea cannot • absence of gastric distension
be intubated. • equal air entry heard on bilateral auscultation of
both axillae and apices of the chest
Rapid sequence induction and intubation. The • absence of air entry into the stomach on auscul-
child who is in cardiopulmonary arrest and deep tation
coma does not require sedation or analgesia to be • detection of end-tidal CO2 if the child has a per-
intubated; otherwise, intubation must be preceded fusing rhythm (this may be seen with effective
by oxygenation, rapid sedation, analgesia and the CPR)
use of neuromuscular blocking drugs to minimise • improvement or stabilisation of SpO2 to the
intubation complications and failure.63 The intuba- expected range
European Resuscitation Council Guidelines for Resuscitation 2005 S107

• improvement of heart rate towards the age- tion is adequate during chest compressions. When
expected value (or remaining within the normal circulation is restored, or if the child still has a per-
range) fusing rhythm, ventilate at 12—20 breaths min−1 to
achieve a normal pCO2 . Hyperventilation is harm-
If the child is in cardiopulmonary arrest and
ful.
exhaled CO2 is not detected, or if there is any
doubt, confirm tracheal tube position by direct Bag-mask ventilation. BMV is effective and safe
laryngoscopy. After correct placement and confir- for a child requiring assisted ventilation for a short
mation, secure the tracheal tube and reassess its period, i.e. in the prehospital setting or in an emer-
position. Maintain the child’s head in neutral posi- gency department.73,90—92 Assess the effectiveness
tion; flexion of the head drives the tube further into of BMV by observing adequate chest rise, monitor-
the trachea whereas extension may pull it out of the ing heart rate, auscultating for breath sounds and
airway.77 Confirm the position of the tracheal tube measuring peripheral oxygen saturation (SpO2 ). Any
at mid trachea by plain chest radiograph; the tra- healthcare provider dealing with children must be
cheal tube tip should be at the level of the 2nd or able to deliver BMV effectively.
3rd thoracic vertebra.
DOPES is a useful acronym for the causes of sud- Prolonged ventilation. If prolonged ventilation is
den deterioration in an intubated child required, the benefits of a secured airway prob-
ably outweigh the potential risks associated with
• D: displacement of the tracheal tube tracheal intubation.
• O: obstruction of the tracheal tube
• P: pneumothorax Monitoring of breathing and ventilation
• E: equipment failure (source of gas, BMV, venti-
lator, etc.) End tidal CO2 . Monitoring end-tidal CO2 with a
• S: stomach (gastric distension may alter dia- colorimetric detector or capnometer confirms tra-
phragm mechanics) cheal tube placement in the child weighing more
than 2 kg, and may be used in pre- and in-hospital
Breathing settings, as well as during any transportation of the
child.93—97 A colour change or the presence of a
Oxygenation capnographic waveform indicates that the tube is
in the tracheobronchial tree, both in the presence
Use oxygen at the highest concentration (i.e., 100%) of a perfusing rhythm and during cardiopulmonary
during resuscitation. Once circulation is restored, arrest. Capnography does not rule out intubation
give sufficient oxygen to maintain peripheral oxy- of the right mainstem bronchus. The absence of
gen saturation at or above 95%.78,79 exhaled CO2 during cardiopulmonary arrest may not
Studies in neonates suggest some advantages to be caused by tube misplacement, since a low or
using room air during resuscitation, but the evi- absent end-tidal CO2 may reflect low or absent pul-
dence as yet is inconclusive (see Section 6c).80—83 monary blood flow.98—101
In the older child, there is no evidence for any such
advantages, so use 100% oxygen for resuscitation. Oesophageal detector devices. The self-inflating
bulb or aspirating syringe (oesophageal detector
Ventilation device, ODD) may be used for the secondary confir-
mation of tracheal tube placement in children with
Healthcare providers commonly provide excessive a perfusing rhythm.102,103 There are no studies on
ventilation to victims of cardiopulmonary or res- the use of ODD in children who are in cardiopul-
piratory arrest, and this may be detrimental. monary arrest.
Hyperventilation causes increased thoracic pres-
sure, decreased cerebral and coronary perfusion, Pulse oximetry. Clinical evaluation of the oxygen
and poorer survival rates in animals and adults.84—89 level is unreliable; therefore monitor the child’s
The ideal tidal volume should achieve modest chest peripheral oxygen saturation continuously by pulse
wall rise. Use a ratio of 15 chest compressions to 2 oximetry. Pulse oximetry can be unreliable under
ventilations (a lone rescuer may use 30:2); the cor- certain conditions, e.g. if the child is in shock, in
rect compression rate is 100 min−1 . cardiopulmonary arrest or has poor peripheral per-
Once the airway is protected by tracheal intu- fusion. Although pulse oximetry is relatively simple,
bation, continue positive pressure ventilation at it is a poor guide to tracheal tube displacement;
12—20 breaths min−1 without interrupting chest capnography detects tracheal tube dislodgement
compressions. Take care to ensure that lung infla- more rapidly than pulse oximetry.104
S108 D. Biarent et al.

Circulation Fluids and drugs

Vascular access Volume expansion is indicated when a child shows


signs of shock in the absence of volume overload.135
Vascular access is essential to give drugs and fluids If systemic perfusion is inadequate, give a bolus
and obtain blood samples. Venous access can be dif- of 20 ml kg−1 of an isotonic crystalloid, even if the
ficult to establish during resuscitation of an infant systemic blood pressure is normal. Following every
or child.105 Limit the maximum number of attempts bolus, re-assess the child’s clinical state using ABC,
to obtain IV access to three; thereafter, insert an IO to decide whether a further bolus or other treat-
needle.106 ment is required.
There are insufficient data to make recommen-
Intraosseous access. IO access is a rapid, safe, dations about the use of hypertonic saline for shock
and effective route to give drugs, fluids and blood associated with head injuries or hypovolaemia.136
products.107—113 The onset of action and time There are also insufficient data to recommend
to achieve adequate plasma drug concentrations delayed fluid resuscitation in the hypotensive child
are similar to those provided by central venous with blunt trauma.137 Avoid dextrose-containing
access.114,115 Bone marrow samples can be used to solutions unless there is hypoglycaemia.138—141
cross-match for blood type or group,116 for chem- However, hypoglycaemia must actively be sought
ical analysis,117,118 and for blood gas measure- and avoided, particularly in the small child or
ment (the values are comparable to central venous infant.
blood gases).117,119,120 Flush each drug with a bolus
of normal saline to ensure dispersal beyond the
Adenosine
marrow cavity and to achieve faster distribution
to the central circulation. Inject large boluses of Adenosine is an endogenous nucleotide which
fluid using manual pressure. Intraosseous access can causes a brief atrioventricular (AV) block and
be maintained until definitive IV access has been impairs accessory bundle re-entry at the level of the
established. AV node. Adenosine is recommended for the treat-
ment of supraventricular tachycardia (SVT).142 It is
Intravenous access. Peripheral IV access pro-
safe to use, as it has a short half-life (10 s); give
vides plasma concentrations of drugs and clinical
it intravenously via upper limb or central veins, to
responses equivalent to central or IO access.121—125
minimise the time taken to reach the heart. Give
Central lines provide more secure long-term
adenosine rapidly, followed by a flush of 3—5 ml of
access121,122,124,125 but offer no advantages during
normal saline.143
resuscitation, compared with IO or peripheral IV
access.
Adrenaline (epinephrine)
Tracheal tube access Adrenaline is an endogenous catecholamine with
potent alpha, beta-1 and beta-1 adrenergic actions.
IV and IO access are better than the tracheal route
It is the essential medication in cardiopulmonary
for giving drugs.126 Lipid-soluble drugs, such as
arrest, and is placed prominently in the treat-
lidocaine, atropine, adrenaline and naloxone are
ment algorithms for non-shockable and shock-
absorbed via the lower airway.127—131 Optimal tra-
able rhythms. Adrenaline induces vasoconstriction,
cheal tube drug doses are unknown because of the
increases diastolic pressure and thereby improves
great variability of alveolar drug absorption, but
coronary artery perfusion pressure, enhances
the following dosages have been recommended as
myocardial contractility, stimulates spontaneous
guidance
contractions and increases the amplitude and fre-
• adrenaline, 100 mcg kg−1 quency of VF, so increasing the likelihood of suc-
• lidocaine, 2—3 mg kg−1 cessful defibrillation. The recommended IV/IO dose
• atropine, 30 mcg kg−1 of adrenaline in children is 10 mcg kg−1 . The dose of
adrenaline given via the tracheal tube is ten times
The optimal dose of naloxone is not known. this (100 mcg kg−1 ).127,144—146 If needed, give fur-
Dilute the drug in 5 ml of normal saline and fol- ther doses of adrenaline every 3—5 min. The use of
low administration with five ventilations.132—134 Do higher doses of adrenaline via the IV or IO route is
not give non-lipid soluble medications (e.g., glu- not recommended routinely, as it does not improve
cose, bicarbonate, calcium) via the tracheal tube survival or neurological outcome after cardiopul-
because they will damage the airway mucosa. monary arrest.147—150
European Resuscitation Council Guidelines for Resuscitation 2005 S109

Once spontaneous circulation is restored, a con- and hypoglycaemia following return of spontaneous
tinuous infusion of adrenaline may be required. Its circulation (ROSC).
haemodynamic effects are dose related; there is
also considerable variability between children in Magnesium
response, therefore, titrate the infusion dose to
the desired effect. High infusion rates may cause There is no evidence for giving magnesium rou-
excessive vasoconstriction, compromising extrem- tinely during cardiopulmonary arrest.165 Magne-
ity, mesenteric, and renal blood flow. High-dose sium treatment is indicated in the child with doc-
adrenaline may cause severe hypertension and umented hypomagnesaemia or with torsades de
tachyarrhythmias.151 pointes VF, regardless of the cause.166
To avoid tissue damage it is essential to give
adrenaline through a secure intravascular line (IV or Sodium bicarbonate
IO). Adrenaline and other catecholamines are inac-
tivated by alkaline solutions and should never be Giving sodium bicarbonate routinely during car-
mixed with sodium bicarbonate.152 diopulmonary arrest and CPR or after ROSC is
not recommended.167,168 After effective ventila-
Amiodarone tion and chest compressions have been achieved
and adrenaline given, sodium bicarbonate may be
Amiodarone is a non-competitive inhibitor of adren- considered for the child who has had a prolonged
ergic receptors; it depresses conduction in myocar- cardiopulmonary arrest and severe metabolic aci-
dial tissue and therefore slows AV conduction and dosis. Sodium bicarbonate may also be consid-
prolongs the QT interval and the refractory period. ered in the case of haemodynamic instability
Except when given for the treatment of refrac- and co-existing hyperkalaemia, or in the man-
tory VF/pulseless VT, amiodarone must be injected agement of tricyclic overdose. Excessive quan-
slowly (over 10—20 min) with systemic blood pres- tities of sodium bicarbonate may impair tissue
sure and ECG monitoring to avoid fast-infusion- oxygen delivery, produce hypokalaemia, hyper-
related hypotension. This side effect is less common natraemia and hyperosmolality and inactivate
with the aqueous solution.153 Other rare but signif- catecholamines.
icant adverse effects are bradycardia and polymor-
phic VT.154 Lidocaine

Atropine Lidocaine is less effective than amiodarone for


defibrillation-resistant VF/VT in adults,169 and
Atropine accelerates sinus and atrial pacemakers therefore is not the first-line treatment in
by blocking the parasympathetic response. It may defibrillation-resistant VF/VT in children.
also increase AV conduction. Small doses (<100 mcg)
may cause paradoxical bradycardia.155 Procainamide

Calcium Procainamide slows intra-atrial conduction and pro-


longs the QRS and QT intervals; it can be used in
Calcium is essential for myocardial con- SVT170,171 or VT172 resistant to other medications,
traction156,157 but routine use of calcium does in the haemodynamically stable child. However,
not improve the outcome from cardiopulmonary paediatric data are sparse and procainamide should
arrest.158—160 be used cautiously.173,174 Procainamide is a potent
vasodilator and can cause hypotension; infuse it
Glucose slowly with careful monitoring.170,175,176

Neonatal, child and adult data show that both Vasopressin


hyperglycaemia and hypoglycaemia are associ-
ated with poor outcome after cardiopulmonary Vasopressin is an endogenous hormone that acts
arrest,161—163 but it is uncertain if this is causative at specific receptors, mediating systemic vasocon-
or merely an association.164 Check blood or plasma striction (via V1 receptor) and the reabsorption of
glucose concentration and monitor closely in any ill water in the renal tubule (by the V2 receptor).177
or injured child, including after cardiac arrest. Do The use of vasopressin for the treatment of cardiac
not give glucose-containing fluids during CPR unless arrest in adults is discussed in detail in Section 4e.
hypoglycaemia is present. Avoid hyperglycaemia There is currently insufficient evidence to support
S110 D. Biarent et al.

or refute the use of vasopressin as an alternative to,


or in combination with, adrenaline in any cardiac
arrest rhythm in adults. Thus, there is currently
insufficient evidence to recommend the routine use
of vasopressin in the child with cardiopulmonary
arrest.178—180

Defibrillators

Defibrillators are either automatically (such as the


AED) or manually operated, and may be capable
of delivering either monophasic or biphasic shocks.
Manual defibrillators capable of delivering the full
energy requirements from neonates upwards must Figure 6.8 Paddle positions for defibrillation — child.
be available within hospitals and in other health- © 2005 ERC.
care facilities caring for children at risk of car-
diopulmonary arrest. Automated external defibril- Biphasic shocks are at least as effective and pro-
lators are preset for all variables, including the duce less post-shock myocardial dysfunction than
energy dose. monophasic shocks.33,34,37—40 Animal models show
better results with paediatric doses of 3—4 J kg−1
Pad/paddle size for defibrillation. The largest than with lower doses,34,37 or adult doses.35 Doses
possible available paddles should be chosen to pro- larger than 4 J kg−1 (as much as 9 J kg−1 ) have defib-
vide good contact with the chest wall. The ideal rillated children effectively with negligible side
size is unknown, but there should be good separa- effects.27,36 When using a manual defibrillator, use
tion between the pads.181,182 Recommended sizes 4 J kg−1 (biphasic or monophasic waveform) for the
are first and subsequent shocks.
• 4.5 cm diameter for infants and children weighing If no manual defibrillator is available, use
<10 kg an AED that can recognise paediatric shockable
• 8—12 cm diameter for children >10 kg (older than rhythms.29,30,185 This AED should be equipped with
1 year) a dose attenuator which decreases the delivered
energy to a lower dose more suitable for children
To decrease skin and thoracic impedance, aged 1—8 years (50—75 J).31 If such an AED in not
an electrically conducting interface is required available, in an emergency use a standard AED and
between the skin and the paddles. Preformed gel the preset adult energy levels. For children weigh-
pads or self-adhesive defibrillation electrodes are ing more than 25 kg (above 8 years), use a standard
effective. Do not use ultrasound gel, saline-soaked AED with standard paddles. There is currently insuf-
gauze, alcohol-soaked gauze/pads or ultrasound ficient evidence to support a recommendation for
gel. or against the use of AEDs in children less than 1
year.
Position of the paddles. Apply the paddles firmly
to the bare chest in the anterolateral position, one
paddle placed below the right clavicle and the other Management of cardiopulmonary arrest
in the left axilla (Figure 6.8). If the paddles are too
large, and there is a danger of charge arcing across ABC
the paddles, one should be placed on the upper
back, below the left scapula, and the other on the Commence and continue with basic life support
front, to the left of the sternum. This is known as (Figure 6.9).
the anteroposterior position.
A and B
Optimal paddle force. To decrease transthoracic
impedance during defibrillation, apply a force of Oxygenate and ventilate with BMV.
3 kg for children weighing <10 kg, and 5 kg for larger
children.183,184 • Provide positive pressure ventilation with a high
inspired oxygen concentration.
Energy dose in children. The ideal energy dose • Give five rescue breaths followed by external
for safe and effective defibrillation is unknown. chest compression and positive pressure ventila-
European Resuscitation Council Guidelines for Resuscitation 2005 S111

Figure 6.9 Paediatric advanced life support algorithm.

tion in the ratio of 15:2 (lone rescuer may use • If no vascular access is available and a tracheal
30:2). tube is in situ, give adrenaline, 100 mcg kg−1 , via
• Avoid rescuer fatigue by changing the rescuer this route until IV/IO access is obtained.
performing chest compressions frequently. • Identify and treat any reversible causes (4Hs &
• Establish cardiac monitoring. 4Ts).

C
VF/pulseless VT—–shockable
Assess cardiac rhythm and signs of circulation
(±check for a central pulse for no more than 10 s). • Attempt defibrillation immediately (4 J kg−1 for
all shocks).
Asystole, pulseless electrical activity • Resume CPR as soon as possible.
(PEA)—–non-shockable • After 2 min, check the cardiac rhythm on the
monitor.
• Give adrenaline, 10 mcg kg−1 IV or IO, and repeat • Give second shock if still in VF/pulseless
every 3—5 min. VT.
S112 D. Biarent et al.

• Immediately resume CPR for 2 min and check tion between a shockable and a non-shockable car-
monitor; if no change, give adrenaline followed diac rhythm. Invasive monitoring of systemic blood
immediately by a 3rd shock. pressure may help to improve effectiveness of chest
• CPR for 2 min. compression,186 but must not delay the provision of
• Give amiodarone if still in VF/pulseless VT fol- basic or advanced resuscitation.
lowed immediately by a 4th shock. Shockable rhythms comprise pulseless VT and
• Give adrenaline every 3—5 min during CPR. VF. These rhythms are more likely in the child
• If the child remains in VF/pulseless VT, continue who presents with sudden collapse. Non-shockable
to alternate shocks with 2 min of CPR. rhythms comprise PEA, bradycardia (<60 beats
• If signs of life become evident, check the monitor min−1 with no signs of circulation) and asystole. PEA
for an organised rhythm; if this is present, check and bradycardia often have wide QRS complexes.
for a central pulse.
• Identify and treat any reversible causes (4Hs & Non-shockable rhythms
4Ts).
• If defibrillation was successful but VF/pulseless Most cardiopulmonary arrests in children and ado-
VT recurs, resume CPR, give amiodarone and lescents are of respiratory origin.19,44,187—189 A
defibrillate again at the dose that was effective period of immediate CPR is therefore mandatory
previously. Start a continuous infusion of amio- in this age group, before searching for an AED
darone. or manual defibrillator, as their immediate avail-
ability will not improve the outcome of a res-
Reversible causes of cardiac arrest (4 Hs piratory arrest.11,13 Bystander CPR is associated
and 4 Ts) with a better neurological outcome in adults and
children.9,10,190 The most common ECG patterns in
infants, children and adolescents with cardiopul-
• Hypoxia monary arrest are asystole and PEA. PEA is charac-
• Hypovolaemia terised by organised, wide complex electrical activ-
• Hyper/hypokalaemia ity, usually at a slow rate, and absent pulses. PEA
• Hypothermia commonly follows a period of hypoxia or myocardial
• Tension pneumothorax ischaemia, but occasionally can have a reversible
• Tamponade (coronary or pulmonary) cause (i.e., one of the 4 H’s and 4 T’S) that led to
• Toxic/therapeutic disturbances a sudden impairment of cardiac output.
• Thrombosis (coronary or pulmonary)
Shockable rhythms
Sequence of events in cardiopulmonary
arrest VF occurs in 3.8—19% of cardiopulmonary arrests
in children9,45,188,189 ; the incidence of VF/pulseless
• When a child becomes unresponsive, with- VT increases with age.185,191 The primary deter-
out signs of life (no breathing, cough or any minant of survival from VF/pulseless VT cardiopul-
detectable movement), start CPR immediately. monary arrest is the time to defibrillation. Prehospi-
• Provide BMV with 100% oxygen. tal defibrillation within the first 3 min of witnessed
• Commence monitoring. Send for a manual or adult VF arrest results in >50% survival. However,
automatic external defibrillator (AED) to identify the success of defibrillation decreases dramatically
and treat shockable rhythms as quickly as possi- as the time to defibrillation increases; for every
ble. minute delay in defibrillation (without any CPR),
survival decreases by 7—10%. Survival after more
In the less common circumstance of a witnessed than 12 min of VF in adult victims is <5%.192 Car-
sudden collapse, early activation of emergency ser- diopulmonary resuscitation provided before defib-
vices and getting an AED may be more appropriate; rillation for response intervals longer than 5 min
start CPR as soon as possible. improved outcome in some studies,193,194 but not
Rescuers must perform CPR with minimal inter- in others.195
ruption until attempted defibrillation.
Drugs in shockable rhythms
Cardiac monitoring
Adrenaline is given every 3—5 min by the IV or IO
Position the cardiac monitor leads or defibrillation route in preference to the tracheal tube route.
paddles as soon as possible, to enable differentia- Amiodarone is indicated in defibrillation-resistant
European Resuscitation Council Guidelines for Resuscitation 2005 S113

VF/pulseless VT. Experimental and clinical experi- Tachycardia


ence with amiodarone in children is scarce; evi-
dence from adult studies169,196,197 demonstrates Narrow complex tachycardia. If supraventricu-
increased survival to hospital admission, but not lar tachycardia (SVT) is the likely rhythm, vagal
to hospital discharge. One paediatric case series manoeuvres (Valsalva or diving reflex) may be used
demonstrates the effectiveness of amiodarone for in haemodynamically stable children. The manoeu-
life-threatening ventricular arrhythmias.198 There- vres can be used in unstable children if they do
fore, IV amiodarone has a role in the treatment of not delay chemical or electrical cardioversion.200 If
defibrillation refractory or recurrent VF/pulseless the child is haemodynamically unstable, omit vagal
VT in children. manoeuvres and attempt electrical cardioversion
immediately. Adenosine is usually effective in con-
verting SVT into sinus rhythm. Adenosine is given
by rapid IV injection as closely as practical to the
Arrhythmias
heart (see above), followed immediately by a bolus
of normal saline.
Unstable arrhythmias Electrical cardioversion (synchronised with R
Check the central pulse of any child with an wave) is indicated in the haemodynamically com-
arrhythmia; if the pulse is absent, proceed to promised child, in whom vascular access is not
treating the child as being in cardiopulmonary available, or in whom adenosine has failed to con-
arrest. If the child has a central pulse, evaluate vert the rhythm. The first energy dose for electrical
his haemodynamic status. Whenever the haemody- cardioversion of SVT is 0.5—1 J kg−1 and the second
namic status is compromised, the first steps are as dose is 2 J kg−1 . If unsuccessful, give amiodarone
follows. or procainamide under guidance from a paediatric
cardiologist or intensivist before the third attempt.
• Open the airway. Amiodarone has been shown to be effective
• Assist ventilation and give oxygen. in the treatment of SVT in several paediatric
• Attach ECG monitor or defibrillator and assess the studies.198,201—207 However, since most studies of
cardiac rhythm. the use of amiodarone in narrow-complex tachy-
• Evaluate if the rhythm is slow or fast for the cardias have been for junctional ectopic tachycar-
child’s age. dia in postoperative children, the applicability of
• Evaluate if the rhythm is regular or irregular. its use in all cases of SVT may be limited. If the
• Measure QRS complex (narrow complexes, <0.08 s child is haemodynamically stable, early consulta-
duration; large complexes, >0.08 s). tion with an expert is recommended before giving
• The treatment options are dependent on the amiodarone.
child’s haemodynamic stability.
Wide complex tachycardia. In children, wide-
Bradycardia QRS-complex tachycardia is more likely to be
supraventricular than ventricular in origin.208
Bradycardia is caused commonly by hypoxia, acido- However, wide-QRS-complex tachycardia, although
sis and severe hypotension; it may progress to car- uncommon, must be considered to be VT in haemo-
diopulmonary arrest. Give 100% oxygen, and posi- dynamically unstable children until proven other-
tive pressure ventilation if required, to any child wise. VT occurs most often in the child with under-
presenting with bradyarrhythmia and circulatory lying heart disease (e.g., after cardiac surgery,
failure. cardiomyopathy, myocarditis, electrolyte disor-
If a poorly perfused child has a heart rate <60 ders, prolonged QT interval, central intracardiac
beats min−1 , and does not respond rapidly to ven- catheter). Synchronised cardioversion is the treat-
tilation with oxygen, start chest compressions and ment of choice for unstable VT with a pulse. Con-
give adrenaline. If the bradycardia is caused by sider antiarrhythmic therapy if a second cardiover-
vagal stimulation, provide ventilation with 100% sion dose is unsuccessful or if VT recurs. Amio-
oxygen and give atropine, before giving adrenaline. darone has been shown to be safe and effective in
A cardiac pacemaker is useful only in cases of treating paediatric arrhythmias.198,202,203,209
AV block or sinus node dysfunction unresponsive to
oxygenation, ventilation, chest compressions and Stable arrhythmias
other medications; the pacemaker is not effective
in asystole or arrhythmias caused by hypoxia or Contact an expert before initiating therapy, while
ischaemia.199 maintaining the child’s ABC. Depending on the
S114 D. Biarent et al.

child’s clinical history, presentation and ECG diag- Fever is common following cardiopulmonary
nosis, a child with stable, wide-QRS-complex tachy- resuscitation; it is associated with a poor neuro-
cardia may be treated for SVT and be given vagal logical outcome,230—232 the risk of which increases
manoeuvres or adenosine. Otherwise, consider with each degree of body temperature greater
amiodarone as a treatment option; similarly, con- than 37 ◦ C.230 There are limited experimental
sider amiodarone if the diagnosis of VT is confirmed data suggesting that the treatment of fever with
by ECG. Procainamide may also be considered in antipyretics and/or physical cooling reduces neu-
stable SVT refractory to vagal manoeuvres and ronal damage.233,234 Antipyretics and accepted
adenosine210—212 as well as in stable VT.172,213,214 drugs to treat fever are safe; therefore, use them
Do not give procainamide with amiodarone. to treat fever aggressively.

Post-arrest management Prognosis of cardiopulmonary arrest

Myocardial dysfunction is common after cardiopul- There are no simple guidelines to determine when
monary resuscitation.215,216 Vasoactive drugs may resuscitative efforts become futile. After 20 min
improve the child’s post-arrest haemodynamic val- of resuscitation, the team leader of the resus-
ues, but the drugs must be titrated according to the citation team should consider whether or not
clinical condition. They must be given continuously to stop.187,235—239 The relevant considerations in
through an IV line. the decision to continue the resuscitation include
the cause of arrest,45,240 pre-existing conditions,
whether the arrest was witnessed, the duration
Temperature control and management of untreated cardiopulmonary arrest (‘‘no flow’’),
the effectiveness and duration of CPR (‘‘low
Hypothermia is common in the child following car- flow’’), the promptness of extracorporeal life sup-
diopulmonary resuscitation.217 Central hypother- port for a reversible disease process241—243 and
mia (32—34 ◦ C) may be beneficial, whereas fever associated special circumstances (e.g, icy water
may be detrimental to the injured brain of sur- drowning,9,244 exposure to toxic drugs).
vivors. Although there are no paediatric studies,
mild hypothermia has an acceptable safety pro-
file in adults218,219 and neonates;220—224 it could
increase the number of neurologically intact sur- Parental presence
vivors.
A child who regains a spontaneous circulation The majority of parents would like to be present
but remains comatose after cardiopulmonary arrest during resuscitation and when any procedure is car-
may benefit from being cooled to a core tem- ried out on their child.245—255 . Parents witnessing
perature of 32—34 ◦ C for 12—24 h. The success- their child’s resuscitation can see that everything
fully resuscitated child with hypothermia and ROSC possible has been attempted.256—260 Furthermore,
should not be actively rewarmed unless the core they may have the opportunity to say goodbye to
temperature is below 32 ◦ C. Following a period their child; allowing parents to be at the side of
of mild hypothermia, rewarm the child slowly at their child has been shown to help them gain a
0.25—0.5 ◦ C h−1 . realistic view of the attempted resuscitation and
There are several methods to induce, moni- the child’s death.261 Families who were present at
tor and maintain body temperature in children. their child’s death showed less anxiety and depres-
External and/or internal cooling techniques can sion, better adjustment and had an improved griev-
be used to initiate cooling.225—227 Shivering can ing process when assessed several months later.260
be prevented by deep sedation and neuromuscular Parental presence in the resuscitation room may
blockade. Complications can occur and include an help healthcare providers maintain their profes-
increased risk of infection, cardiovascular instabil- sional behaviour while also helping them to see the
ity, coagulopathy, hyperglycaemia and electrolyte child as a human being and a family member.261
abnormalities.228,229
The optimum target temperature, rate of cool- Family presence guidelines
ing, duration of hypothermia and rate of re-
warming after deliberate cooling have yet to be A dedicated member of the resuscitation team
determined; currently, no specific protocol for chil- should be present with the parents to explain the
dren can be recommended. process in an empathetic manner, ensuring that
European Resuscitation Council Guidelines for Resuscitation 2005 S115

the parents do not interfere with or distract the (0.2%) appeared to need resuscitation at delivery.
resuscitation. If the presence of the parents is Of these, 90% responded to mask inflation alone,
impeding the progress of the resuscitation, they whereas the remaining 10% appeared not to respond
should be sensitively asked to leave. When appro- to mask inflation and therefore were intubated at
priate, physical contact with the child should be birth.
allowed and, wherever possible, the parents should Resuscitation or specialist help at birth is more
be allowed to be with their dying child at the final likely to be needed by babies with intrapartum evi-
moment.256,261—264 dence of significant fetal compromise, babies deliv-
The leader of the resuscitation team, not the ering before 35 weeks’ gestation, babies delivering
parents, will decide when to stop the resuscita- vaginally by the breech and multiple pregnancies.
tion; this should be expressed with sensitivity and Although it is often possible to predict the need
understanding. After the event the team should be for resuscitation before a baby is born, this is not
debriefed, to enable any concerns to be expressed always the case. Therefore, personnel trained in
and for the team to reflect on their clinical practice newborn life support should be easily available at
in a supportive environment. every delivery and, should there be any need for
resuscitation, the care of the baby should be their
sole responsibility. One person experienced in tra-
cheal intubation of the newborn should also be
6c Resuscitation of babies at birth
easily available for normal low-risk deliveries and,
ideally, in attendance for deliveries associated with
Introduction a high risk for neonatal resuscitation. Local guide-
lines indicating who should attend deliveries should
The following guidelines for resuscitation at birth be developed based on current practice and clinical
have been developed during the process that cul- audit.
minated in the 2005 International Consensus Con- An organised programme educating in the stan-
ference on Emergency Cardiovascular Care (ECC) dards and skills required for resuscitation of the
and Cardiopulmonary Resuscitation (CPR) Science newborn is therefore essential for any institution
with Treatment Recommendations.265 They are an in which deliveries occur.
extension of the guidelines already published by
the ERC,2 and take into account recommenda-
tions made by other national266 and international Planned home deliveries
organisations.267
The recommendations for those who should attend
The guidelines that follow do not define the only
a planned home delivery vary from country to coun-
way that resuscitation at birth should be achieved;
try, but the decision to undergo a planned home
they merely represent a widely accepted view of
delivery, once agreed by the medical and midwifery
how resuscitation at birth can be carried out both
staff, should not compromise the standard of ini-
safely and effectively.
tial resuscitation at birth. There will inevitably
be some limitations to resuscitation of a newborn
baby in the home because of the distance from
Preparation further assistance, and this must be made clear
to the mother at the time plans for home delivery
Relatively few babies need any resuscitation at are made. Ideally, two trained professionals should
birth. Of those that do need help, the overwhelm- be present at all home deliveries;269 one of these
ing majority will require only assisted lung aera- must be fully trained and experienced in providing
tion. A small minority may need a brief period of mask ventilation and chest compressions in the
chest compressions in addition to lung aeration. newborn.
Of 100,000 babies born in Sweden in 1 year, only
10 per 1000 (1%) babies weighing 2.5 kg or more Equipment and environment
appeared to need resuscitation at delivery.268 Of
those babies receiving resuscitation, 8 per 1000 Resuscitation at birth is often a predictable event.
responded to mask inflation and only 2 per 1000 It is therefore simpler to prepare the environment
appeared to need intubation.268 The same study and the equipment before delivery of the baby
tried to assess the unexpected need for resuscita- than is the case in adult resuscitation. Resuscita-
tion at birth, and found that for low-risk babies, i.e. tion should ideally take place in a warm, well-lit,
those born after 32 weeks’ gestation and follow- draught-free area with a flat resuscitation surface
ing an apparently normal labour, about 2 per 1000 placed below a radiant heater and other resusci-
S116 D. Biarent et al.

tation equipment immediately available. All equip- Respiratory activity


ment must be checked daily.
When a birth takes place in a non-designated Check whether the baby is breathing. If so, eval-
delivery area, the recommended minimum set of uate the rate, depth and symmetry of respiration,
equipment includes a device for safe, assisted lung together with any abnormal breathing pattern such
aeration of an appropriate size for the newborn, as gasping or grunting.
warm dry towels and blankets, a clean (sterile)
instrument for cutting the umbilical cord and clean
gloves for the attendant. It may also be helpful to Heart rate
have a suction device with a suitably sized suction
catheter and a tongue depressor (or laryngoscope), This is best evaluated by listening to the apex beat
to enable the oropharynx to be examined. with a stethoscope. Feeling the pulse in the base
of the umbilical cord is often effective but can be
misleading; cord pulsation is only reliable if found
to be more than 100 beats min−1 .276
Temperature control
Naked, wet, newborn babies cannot maintain their Colour
body temperature in a room that feels comfortably
warm for adults. Compromised babies are partic- A healthy baby is born blue but becomes pink within
ularly vulnerable.270 Exposure of the newborn to 30 s of the onset of effective breathing. Observe
cold stress will lower arterial oxygen tension271 and whether the baby is centrally pink, cyanosed or
increase metabolic acidosis.272 Prevent heat loss by pale. Peripheral cyanosis is common and does not,
by itself, indicate hypoxaemia.
• protecting the baby from draughts
• keeping the delivery room warm
• drying the term baby immediately after delivery. Tone
Cover the head and body of the baby, apart from
the face, with a warm towel to prevent further A very floppy baby is likely to be unconscious and is
heat loss. Alternatively, place the baby skin to likely to need respiratory support.
skin with the mother and cover both with a towel
• placing the baby on a warm surface under a pre-
heated radiant warmer if resuscitation is needed Tactile stimulation

In very preterm babies (especially below 28 Drying the baby usually produces enough stimula-
weeks’ gestation), drying and wrapping may not be tion to induce effective respiration. Avoid more
sufficiently effective. A more effective method of vigorous methods of stimulation. If the baby fails
keeping these babies warm is to cover the head and to establish spontaneous and effective respirations
body of the baby (apart from the face) with plas- following a brief period of stimulation, further sup-
tic wrapping, without drying the baby beforehand, port will be required.
and then to place the baby so covered under radiant
heat.
Classification according to initial assessment
On the basis of the initial assessment, the babies
Initial assessment can usually be divided into four groups.

The Apgar scoring system was not designed to iden- Group 1: vigorous breathing or crying
tify prospectively babies needing resuscitation.273 good tone
Several studies have also suggested that it is rapidly becoming pink
heart rate higher than 100 beats min−1
highly subjective.274 However, components of the
score, namely respiratory rate, heart rate and This baby requires no intervention other than
colour, if assessed rapidly, can identify babies need- drying, wrapping in a warm towel and, where
ing resuscitation.275 Furthermore, repeated assess- appropriate, handing to the mother. The baby will
ment of these components can indicate whether the remain warm through skin-to-skin contact with
baby is responding or whether further efforts are mother under a cover, and may be put to the breast
needed. at this stage.
European Resuscitation Council Guidelines for Resuscitation 2005 S117

Group 2: breathing inadequately or apnoeic bradycardia.277 The presence of thick meconium in


remaining centrally blue a non-vigorous baby is the only indication for con-
normal or reduced tone sidering immediate suction. If suction is required,
heart rate less than 100 beats min−1 it is best done under direct vision. Connect a 12—14
This baby may respond to tactile stimulation FG suction catheter, or a Yankauer sucker, to a suc-
and/or facial oxygen, but may need mask inflation. tion source not exceeding −100 mmHg.

Group 3: breathing inadequately or apnoeic Breathing


blue or pale
floppy There is currently insufficient evidence to specify
heart rate less than 100 beats min−1
the concentration of oxygen to be used when start-
This baby may improve with mask inflation but ing resuscitation. After initial steps at birth, if res-
may also require chest compressions. piratory efforts are absent or inadequate, lung aer-
ation is the priority (Figure 6.12). The primary mea-
Group 4: breathing inadequately or apnoeic sure of adequate initial lung inflation is a prompt
pale improvement in heart rate; assess chest wall move-
floppy ment if the heart rate does not improve.
no detectable heart rate
For the first few breaths maintain the initial
This baby will require immediate airway control, inflation pressure for 2—3 s. This will help lung
lung inflation and ventilation. Once this has been expansion. Most babies needing resuscitation at
successfully accomplished, the baby may also need birth will respond with a rapid increase in heart
chest compressions and perhaps drugs. rate within 30 s of lung inflation. If the heart rate
There remains a very rare group of babies who, increases but the baby is not breathing adequately,
though breathing adequately and with a good heart continue ventilation at a rate of about 30 breaths
rate, remain blue. This group includes a range of min−1 , allowing approximately 1 s for each infla-
possible diagnoses such as diaphragmatic hernia, tion, until there is adequate spontaneous breath-
surfactant deficiency, congenital pneumonia, pneu- ing.
mothorax or cyanotic congenital heart disease. Adequate passive ventilation is usually indicated
by either a rapidly increasing heart rate or a heart
rate that is maintained faster than 100 beats min−1 .
If the baby does not respond in this way, the
Newborn life support most likely reason is inadequate airway control or
ventilation. Look for passive chest movement in
Commence newborn life support (Figure 6.10) if time with inflation efforts; if these are present,
assessment demonstrates that the baby has failed then lung aeration has been achieved. If these
to establish adequate regular normal breathing, or are absent, then airway control and lung aeration
has a heart rate of less than 100 beats min−1 . Open- have not been confirmed. Without adequate lung
ing the airway and aerating the lungs is usually aeration chest compressions will be ineffective;
all that is necessary. Furthermore, more complex therefore, confirm lung aeration before progress-
interventions will be futile unless these two first ing to circulatory support. Some practitioners will
steps have been successfully completed. ensure lung aeration by tracheal intubation, but
this requires training and experience to be achieved
Airway effectively. If this skill is not available and the heart
rate is decreasing, re-evaluate airway position and
The baby should be on his or her back with the deliver aeration breaths while summoning a col-
head in a neutral position (Figure 6.11). A 2-cm league with intubation skills.
thickness of the blanket or towel placed under Continue ventilatory support until the baby has
the baby’s shoulder may be helpful in maintaining established normal regular breathing.
proper head position. In floppy babies, application
of jaw thrust or the use of an appropriately sized Circulatory support
oropharyngeal airway may be helpful in opening the
airway. Circulatory support with chest compressions is
Suction is needed only if there is particulate mat- effective only if the lungs have first been success-
ter or blood obstructing the airway. Aggressive pha- fully inflated. Give chest compressions if the heart
ryngeal suction can delay the onset of spontaneous rate is less than 60 beats min−1 despite adequate
breathing and cause laryngeal spasm and vagal ventilation. The optimal technique is to place the
S118 D. Biarent et al.

Figure 6.10 Newborn life support algorithm.

two thumbs side by side over the lower third of depth of approximately one third of the anterior-
the sternum, with the fingers encircling the torso posterior diameter of the chest. A compression to
and supporting the back (Figure 6.13).21,22,25,278,279 relaxation ratio with a slightly shorter compres-
The lower third of the sternum is compressed to a sion than relaxation phase offers theoretical advan-
tages for blood flow in the very young infant.280
Do not lift the thumbs off the sternum during
the relaxation phase, but allow the chest wall to
return to its relaxed position between compres-
sions. Use a 3:1 ratio of compressions to ventila-
tions, aiming to achieve approximately 120 events
min−1 , i.e. approximately 90 compressions and 30
breaths. However, the quality of the compressions
and breaths are more important than the rate.281
Check the heart rate after about 30 s and peri-
odically thereafter. Discontinue chest compressions
Figure 6.11 Newborn head in neutral position. © 2005 when the spontaneous heart rate is faster then 60
Resuscitation Council (UK). beats min−1 .
European Resuscitation Council Guidelines for Resuscitation 2005 S119

Figure 6.14 Newborn umbilical cord showing the arter-


ies and veins. © 2005 Resuscitation Council (UK).
Figure 6.12 Airway and ventilation — newborn. © 2005
Resuscitation Council (UK).
it is used, it is highly likely that doses of 30 mcg kg−1
Drugs or less are ineffective. Try a higher dose (up to
100 mcg kg−1 ). The safety of these higher tracheal
Drugs are rarely indicated in resuscitation of the doses has not been studied. Do not give high IV
newborn infant. Bradycardia in the newborn infant doses.
is usually caused by inadequate lung inflation or
profound hypoxia, and establishing adequate ven-
tilation is the most important step to correct it. Bicarbonate
However, if the heart rate remains less than 60
beats min−1 despite adequate ventilation and chest If effective spontaneous cardiac output is not
compressions, drugs may be needed. These drugs restored despite adequate ventilation and ade-
are presumed to exert their effect by their action quate chest compressions, reversing intracar-
on the heart and are being given because cardiac diac acidosis may improve myocardial function
function is inadequate. It is therefore necessary to and achieve a spontaneous circulation. Give
give them as close to the heart as possible, ide- 1—2 mmol kg−1 IV.
ally via a rapidly inserted umbilical venous catheter
(Figure 6.14).
Fluids
Adrenaline
Consider volume expansion when there has been
Despite the lack of human data, it is reasonable to suspected blood loss or the infant appears to be
continue to use adrenaline when adequate ventila- in shock (pale, poor perfusion, weak pulse) and
tion and chest compressions have failed to increase has not responded adequately to other resuscita-
the heart rate above 60 beats min−1 . Use the IV tive measures. In the absence of suitable blood
route as soon as venous access is established. The (i.e., irradiated and leucocyte-depleted group O
recommended IV dose is 10—30 mcg kg−1 . The tra- Rh-negative blood) isotonic crystalloid rather than
cheal route is not recommended (see below) but, if albumin is the solution of choice for restoring
intravascular volume in the delivery room. Give a
bolus of 10—20 ml kg−1 .

Stopping resuscitation

Local and national committees will determine the


indications for stopping resuscitation. However,
data from infants without signs of life from birth
lasting at least 10 min or longer show either high
mortality or severe neurodevelopmental disability.
After 10 min of continuous and adequate resusci-
Figure 6.13 Ventilation and chest compression — new- tation efforts, discontinuation of resuscitation may
born. © 2005 Resuscitation Council (UK). be justified if there are no signs of life.
S120 D. Biarent et al.

Communication with the parents Meconium

It is vitally important that the team caring for Five years ago, a large randomised controlled study
the newborn baby informs the parents of the showed that attempting to intubate and aspirate
baby’s progress. At delivery adhere to the routine inhaled meconium from the tracheas of vigorous
local plan and, if possible, hand the baby to the infants at birth was not beneficial.290 A more recent
mother at the earliest opportunity. If resuscitation large multicentre randomised controlled study has
is required, inform the parents of the procedures now shown that suctioning meconium from the
being undertaken and why they are required. baby’s nose and mouth before delivery of the baby’s
Decisions to discontinue resuscitation ideally chest (intrapartum suctioning) does not reduce
should involve senior paediatric staff. Whenever the incidence or severity of meconium aspiration
possible, the decision to attempt resuscitation of syndrome.291 Intrapartum suctioning is therefore
an extremely preterm baby should be taken in close no longer recommended. Intubation and suction of
consultation with the parents and senior paediatric meconium from the trachea of non-vigorous infants
and obstetric staff. Where a difficulty has been born through meconium-stained liquor is still rec-
foreseen, for example in the case of severe con- ommended.
genital malformation, the options and prognosis
should be discussed with the parents, midwives, Air or 100% oxygen
obstetricians and birth attendants before deliv-
ery. Several studies in recent years have raised concerns
All discussions and decisions should be carefully about the potential adverse effects of 100% oxygen
recorded in the mother’s notes before delivery and on respiratory physiology and cerebral circulation,
also in the baby’s records after birth. and the potential tissue damage from oxygen free
radicals. There are also concerns about tissue dam-
age from oxygen deprivation during and following
asphyxia. Studies examining blood pressure, cere-
Specific questions addressed at the bral perfusion, and various biochemical measures
2005 Consensus Conference of cell damage in asphyxiated animals resuscitated
with 100% versus 21% oxygen, have shown conflict-
Maintaining normal temperature in preterm ing results.292—296 One study of preterm infants
infants (below 33 weeks’ gestation) exposed to 80% oxy-
gen found lower cerebral blood flow when com-
Significantly, preterm babies are likely to become pared with those stabilised with 21% oxygen.297
hypothermic despite careful application of the tra- Some animal data indicate the opposite effect,
ditional techniques for keeping them warm (dry- i.e. reduced blood pressure and cerebral perfu-
ing, wrapping and placing under radiant heat).282 sion with air versus 100% oxygen.292 Meta-analysis
Several randomised controlled trials and observa- of four human studies demonstrated a reduction
tional studies have shown that placing preterm in mortality and no evidence of harm in infants
babies under radiant heat and then covering the resuscitated with air versus those resuscitated with
babies with food-grade plastic wrapping, without 100% oxygen. However, there are several signifi-
drying them, significantly improves temperature on cant concerns about the methodology of these stud-
admission to intensive care compared with tra- ies, and these results should be interpreted with
ditional techniques.283—285 The baby’s tempera- caution.80,298
ture must be monitored closely because of the At present, the standard approach to resuscita-
small but described risk of hyperthermia with this tion is to use 100% oxygen. Some clinicians may
technique.286 All resuscitation procedures, includ- elect to start resuscitation with an oxygen con-
ing intubation, chest compression and insertion of centration less than 100%, including some who
lines, can be achieved with the plastic cover in may start with air. Evidence suggests that this
place. approach may be reasonable. However, where pos-
Infants born to febrile mothers have been sible, ensure supplemental oxygen is available
reported to have a higher incidence of perina- for use if there is no rapid improvement follow-
tal respiratory depression, neonatal seizures, early ing successful lung aeration. If supplemental oxy-
mortality and cerebral palsy.286—288 Animal stud- gen is not readily available, ventilate the lungs
ies indicate that hyperthermia during or following with air. Supplemental oxygen is recommended
ischaemia is associated with a progression of cere- for babies who are breathing but have central
bral injury.233,289 Hyperthermia should be avoided. cyanosis.
European Resuscitation Council Guidelines for Resuscitation 2005 S121

Monitoring the oxygen saturation of babies of 20—25 cmH2 O, though some infants appear to
undergoing resuscitation may be useful, but stud- require a higher pressure.313,314
ies have shown that term healthy newborns may When ventilating preterm infants, very obvious
take more than 10 min to achieve a preductal oxy- passive chest wall movement may indicate exces-
gen saturation above 95% and nearly an hour to sive tidal volumes and should be avoided. Monitor-
achieve this post-ductally.299—301 Giving a variable ing of pressure may help to provide consistent infla-
concentration of oxygen guided by pulse oximetry tions and avoid high pressures. If positive-pressure
may improve the ability to achieve ‘normal’ oxy- ventilation is required, an initial inflation pres-
gen saturation values while more quickly avoiding sure of 20—25 cmH2 O is adequate for most preterm
‘hyperoxia’, but the definition of these two terms infants. If a prompt increase in heart rate or chest
in the baby at birth are undetermined. Oxygen is a movement is not obtained, higher pressures may
drug, and oxidant injury is theoretically more likely be needed. If continued positive-pressure ventila-
in preterm infants. tion is required, PEEP may be beneficial. Continuous
positive airway pressure (CPAP) in spontaneously
Initial breaths and assisted ventilation breathing preterm infants following resuscitation
may also be beneficial.314
In term infants, spontaneous or assisted initial
inflations create a functional residual capacity Devices
(FRC).302—309 The optimum pressure, inflation time
and flow required to establish an effective FRC have Effective ventilation can be achieved with either
not been determined. Average initial peak inflat- a flow-inflating or self-inflating bag or with a
ing pressures of 30—40 cmH2 O (inflation time unde- T-piece mechanical device designed to regu-
fined) usually ventilate unresponsive term infants late pressure.315—317 The blow-off valves of self-
successfully.305—307,309 Assisted ventilation rates of inflating bags are flow dependent, and pressures
30—60 breaths min−1 are used commonly, but the generated may exceed the value specified by the
relative efficacy of various rates has not been inves- manufacturer.318 Target inflation pressures and long
tigated. inspiratory times are achieved more consistently in
The primary measure of adequate initial ven- mechanical models when using T-piece devices than
tilation is prompt increase in heart rate; assess when using bags,319 although the clinical implica-
passive chest wall movement if the heart rate tions are not clear. More training is required to
does not increase. The initial peak inflating pres- provide an appropriate pressure using flow-inflating
sures needed are variable and unpredictable, and bags compared with self-inflating bags.320 A self-
should be individualised to achieve an increase in inflating bag, a flow-inflating bag or a T-piece
heart rate or movement of the chest with each mechanical device, all designed to regulate pres-
breath. Where pressure is being monitored, an ini- sure or limit pressure applied to the airway, can be
tial inflation pressure of 20 cmH2 O may be effec- used to ventilate a newborn.
tive, but 30—40 cmH2 O or higher may be required Laryngeal mask airways (LMAs) are effective
in some term babies. If pressure is not being moni- for ventilating newborn near-term and full-term
tored but merely limited by a non-adjustable ‘blow- infants.321,322 There are few data on the use of
off’ valve, use the minimum inflation required to these devices in small preterm infants.323,324 Three
achieve an increase in heart rate. There is insuffi- case series show that the LMA can provide effective
cient evidence to recommend an optimum inflation ventilation in a time frame consistent with current
time. In summary, provide artificial ventilation at resuscitation guidelines, although the babies being
30—60 breaths min−1 to achieve or maintain a heart studied were not being resuscitated.322,325,326 A
rate higher than 100 beats min−1 promptly. randomised controlled trial found no clinically
significant difference between the LMA and tra-
Assisted ventilation of preterm infants cheal intubation when bag-mask ventilation was
unsuccessful.321 It is unclear whether the conclu-
Animal studies show that preterm lungs are eas- sions of this study can be generalized, since the
ily damaged by large volume inflations immediately LMA was inserted by experienced providers. Case
after birth,310 and that maintaining a positive end- reports suggest that when bag-mask ventilation has
expiratory pressure (PEEP) immediately after birth been unsuccessful and tracheal intubation is unfea-
protects against lung damage. PEEP also improves sible or unsuccessful, the LMA may provide effec-
lung compliance and gas exchange.311,312 Human tive ventilation.327—329 There is insufficient evi-
case series show that most apnoeic preterm infants dence to support the routine use of the LMA as the
can be ventilated with an initial inflation pressure primary airway device for resuscitation at birth.
S122 D. Biarent et al.

Table 6.1 Calculation of tracheal tube size and depth of insertiona


Child’s weight (kg) Gestation (weeks) Tube size (mm ID) Depth of insertion (cm)a
<1 <28 2.5 6.5—7
1—2 28—34 3.0 7—8
2—3 34—38 3.0/3.5 8—9
>3 >38 3.5/4.0 >9
a Depth of insertion from the upper lip can be estimated as insertion depth at lip (cm) = weight in kg + 6 cm.

There are also reservations concerning its effec- Tracheal tube placement (Table 6.1) must be
tiveness in the following situations assessed visually during intubation and, in most
cases, will be confirmed by a rapid increase in heart
• when chest compressions are required
rate on ventilating via the tracheal tube. If the
• for very low birth weight (VLBW) babies
heart rate remains slow, incorrect tube placement
• when the amniotic fluid is meconium stained
is the most likely cause. Check tube place-
ment either visually or by detection of exhaled
Confirming tracheal tube placement CO2 .
Tracheal intubation may be considered at several
points during neonatal resuscitation Route and dose of adrenaline
• when suctioning to remove meconium or other There are no placebo-controlled studies that have
tracheal blockage is required evaluated the use of adrenaline at any stage
• if bag-mask ventilation is ineffective or pro- in human neonatal resuscitation. A paediatric
longed study148 and newborn animal studies335,336 showed
• when chest compressions are performed no benefit and a trend toward reduced sur-
• in special circumstances (e.g., congenital vival and worse neurological status after high-
diaphragmatic hernia or birth weight below dose IV adrenaline (100 mcg kg−1 ) during resusci-
1000 g) tation. Animal and adult human studies demon-
The use and timing of tracheal intubation will strate that, when given via the trachea, consid-
depend on the skill and experience of the available erably higher doses of adrenaline than currently
resuscitators. recommended are required to achieve adequate
Following tracheal intubation and intermittent plasma concentrations.337—339 One neonatal ani-
positive pressure, a prompt increase in heart rate mal study using the currently recommended dose
is the best indicator that the tube is in the tracheo- of tracheal adrenaline (10 mcg kg−1 ) showed no
bronchial tree.330 Exhaled CO2 detection is effec- benefit.126 One neonatal cohort study of nine
tive for confirmation of tracheal tube placement preterm babies requiring resuscitation showed
in infants, including VLBW infants.331—334 Detection that tracheal adrenaline was absorbed, but these
of exhaled CO2 in patients with adequate cardiac workers used 7—25 times the dose recommended
output confirms placement of the tube within the currently.340
trachea, whereas failure to detect exhaled CO2
strongly suggests oesophageal intubation.331,333 Post-resuscitation care
Poor or absent pulmonary blood flow or tracheal
obstruction may prevent detection of exhaled CO2 Babies who have required resuscitation may dete-
despite correct tracheal tube placement. Tracheal riorate. Once adequate ventilation and circulation
tube placement is identified correctly in nearly all are established, the infant should be maintained
patients who are not in cardiac arrest99 ; however, in in or transferred to an environment in which close
critically ill infants with poor cardiac output, inabil- monitoring and anticipatory care can be provided.
ity to detect exhaled CO2 despite correct place-
ment may lead to unnecessary extubation. Other Glucose
clinical indicators of correct tracheal tube place-
ment include evaluation of condensed humidified Hypoglycaemia was associated with adverse neu-
gas during exhalation and presence or absence of rological outcome in a neonatal animal model
chest movement, but these have not been evalu- of asphyxia and resuscitation.341 Newborn ani-
ated systematically in newborn babies. mals which were hypoglycaemic at the time of
European Resuscitation Council Guidelines for Resuscitation 2005 S123

an anoxic or hypoxic-ischaemic insult had larger continue life support in severely compromised
areas of cerebral infarction and/or decreased sur- babies.350 There is considerable variability among
vival compared with controls.342,343 One clinical providers about the benefits and disadvantages of
study demonstrated an association between hypo- aggressive therapies in such babies.351,352
glycaemia and poor neurological outcome following
perinatal asphyxia.344 No clinical neonatal studies Withholding resuscitation
have investigated the relationship between hyper-
glycaemia and neurological outcome, although in It is possible to identify conditions associated with
adults hyperglycaemia is associated with a worse high mortality and poor outcome, where withhold-
outcome.345 The range of blood glucose concentra- ing resuscitation may be considered reasonable,
tion that is associated with the least brain injury particularly when there has been the opportunity
following asphyxia and resuscitation cannot be for discussion with parents.282,353 A consistent and
defined on available evidence. Infants who require coordinated approach to individual cases by the
significant resuscitation should be monitored and obstetric and neonatal teams and the parents is an
treated to maintain blood glucose within the nor- important goal. Withholding resuscitation and dis-
mal range. continuation of life-sustaining treatment during or
following resuscitation are considered by many to
Induced hypothermia be ethically equivalent, and clinicians should not
be hesitant to withdraw support when the possi-
In a multicentre trial involving newborns with bility of functional survival is highly unlikely. The
suspected asphyxia (indicated by need for resus- following guidelines must be interpreted according
citation at birth, metabolic acidosis and early to current regional outcomes.
encephalopathy), selective head cooling (34.5 ◦ C)
was associated with a non-significant reduction in • Where gestation, birth weight and/or congeni-
the number of survivors with severe disability at tal anomalies are associated with almost certain
18 months, but a significant benefit in the sub- early death, and unacceptably high morbidity is
group with moderate encephalopathy as judged likely among the rare survivors, resuscitation is
by amplitude-integrated electroencephalogram.220 not indicated. Examples from the published liter-
Infants with severe electroencephalographic sup- ature include extreme prematurity (gestational
pression and seizures did not benefit from age <23 weeks and/or birthweight <400 g), and
treatment.346 A second, small, controlled pilot anomalies such as anencephaly and confirmed tri-
study in asphyxiated infants with early induced somy 13 or 18.
systemic hypothermia resulted in fewer deaths • Resuscitation is nearly always indicated in con-
and disabilities at 12 months. Modest hypother- ditions associated with a high survival rate and
mia is associated with bradycardia and ele- acceptable morbidity. This will generally include
vated blood pressure that do not usually require babies with gestational age of 25 weeks or
treatment, but a rapid increase in body tem- above (unless there is evidence of fetal compro-
perature may cause hypotension.347 Profound mise such as intrauterine infection or hypoxia-
hypothermia (core temperature below 33 ◦ C) may ischaemia) and those with most congenital mal-
cause arrhythmia, bleeding, thrombosis and sep- formations.
sis, but studies so far have not reported these • In conditions associated with uncertain progno-
complications in infants treated with modest sis, where there is borderline survival and a rel-
hypothermia.220,348 atively high rate of morbidity, and where the
There are insufficient data to recommend rou- anticipated burden to the child is high, parental
tine use of modest systemic or selective cere- desires regarding resuscitation should be sup-
bral hypothermia following resuscitation of infants ported.
with suspected asphyxia. Further clinical trials are
needed to determine which infants benefit most Withdrawing resuscitation efforts
and which method of cooling is most effective.
Data from infants without signs of life from
Withholding or discontinuing resuscitation birth, lasting at least 10 min or longer, show
either high mortality or severe neurodevelopmental
Mortality and morbidity for newborns varies accord- disability.354,355 After 10 min of uninterrupted and
ing to region and to availability of resources.349 adequate resuscitation efforts, discontinuation of
Social science studies indicate that parents desire resuscitation may be justified if there are no signs
a larger role in decisions to resuscitate and to of life.
S124 D. Biarent et al.

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320. Kanter RK. Evaluation of mask-bag ventilation in resuscita- 340. Schwab KO, von Stockhausen HB. Plasma catecholamines
tion of infants. Am J Dis Child 1987;141:761—3. after endotracheal administration of adrenaline during
321. Esmail N, Saleh M, et al. Laryngeal mask airway ver- postnatal resuscitation. Arch Dis Child Fetal Neonatal Ed
sus endotracheal intubation for Apgar score improve- 1994;70:F213—7.
ment in neonatal resuscitation. Egypt J Anesthesiol 341. Brambrink AM, Ichord RN, Martin LJ, Koehler RC, Trayst-
2002;18:115—21. man RJ. Poor outcome after hypoxia-ischemia in newborns
322. Gandini D, Brimacombe JR. Neonatal resuscitation with is associated with physiological abnormalities during early
the laryngeal mask airway in normal and low birth weight recovery. Possible relevance to secondary brain injury after
infants. Anesth Analg 1999;89:642—3. head trauma in infants. Exp Toxicol Pathol 1999;51:151—62.
323. Brimacombe J, Gandini D. Airway rescue and drug delivery 342. Vannucci RC, Vannucci SJ. Cerebral carbohydrate
in an 800 g neonate with the laryngeal mask airway. Paedi- metabolism during hypoglycemia and anoxia in newborn
atr Anaesth 1999;9:178. rats. Ann Neurol 1978;4:73—9.
324. Lonnqvist PA. Successful use of laryngeal mask airway in 343. Yager JY, Heitjan DF, Towfighi J, Vannucci RC. Effect
low-weight expremature infants with bronchopulmonary of insulin-induced and fasting hypoglycemia on peri-
European Resuscitation Council Guidelines for Resuscitation 2005 S133

natal hypoxic-ischemic brain damage. Pediatr Res 350. Lee SK, Penner PL, Cox M. Comparison of the attitudes
1992;31:138—42. of health care professionals and parents toward active
344. Salhab WA, Wyckoff MH, Laptook AR, Perlman JM. Initial treatment of very low birth weight infants. Pediatrics
hypoglycemia and neonatal brain injury in term infants with 1991;88:110—4.
severe fetal acidemia. Pediatrics 2004;114:361—6. 351. Kopelman LM, Irons TG, Kopelman AE. Neonatologists
345. Kent TA, Soukup VM, Fabian RH. Heterogeneity affecting judge the ‘‘Baby Doe’’ regulations. N Engl J Med
outcome from acute stroke therapy: making reperfusion 1988;318:677—83.
worse. Stroke 2001;32:2318—27. 352. Sanders MR, Donohue PK, Oberdorf MA, Rosenkrantz TS,
346. Eicher DJ, Wagner CL, Katikaneni LP, et al. Moderate Allen MC. Perceptions of the limit of viability: neonatolo-
hypothermia in neonatal encephalopathy: efficacy out- gists’ attitudes toward extremely preterm infants. J Peri-
comes. Pediatr Neurol 2005;32:11—7. natol 1995;15:494—502.
347. Thoresen M, Whitelaw A. Cardiovascular changes dur- 353. Draper ES, Manktelow B, Field DJ, James D. Tables for
ing mild therapeutic hypothermia and rewarming in predicting survival for preterm births are updated. BMJ
infants with hypoxic-ischemic encephalopathy. Pediatrics 2003;327:872.
2000;106:92—9. 354. Jain L, Ferre C, Vidyasagar D, Nath S, Sheftel D. Car-
348. Shankaran S, Laptook A, Wright LL, et al. Whole-body diopulmonary resuscitation of apparently stillborn infants:
hypothermia for neonatal encephalopathy: animal obser- survival and long-term outcome. J Pediatr 1991;118:778—
vations as a basis for a randomized, controlled pilot study 82.
in term infants. Pediatrics 2002;110:377—85. 355. Haddad B, Mercer BM, Livingston JC, Talati A, Sibai BM.
349. De Leeuw R, Cuttini M, Nadai M, et al. Treatment choices Outcome after successful resuscitation of babies born with
for extremely preterm infants: an international perspec- apgar scores of 0 at both 1 and 5 minutes. Am J Obstet
tive. J Pediatr 2000;137:608—16. Gynecol 2000;182:1210—4.
Resuscitation (2005) 67S1, S135—S170

European Resuscitation Council Guidelines for


Resuscitation 2005
Section 7. Cardiac arrest in special circumstances
Jasmeet Soar, Charles D. Deakin, Jerry P. Nolan, Gamal Abbas,
Annette Alfonzo, Anthony J. Handley, David Lockey,
Gavin D. Perkins, Karl Thies

7a. Life-threatening electrolyte Prevention of electrolyte disorders


disorders
• Treat life-threatening electrolyte abnormalities
before cardiac arrest occurs.
Overview
• After initial treatment, remove any precipitating
Electrolyte abnormalities can cause cardiac factors (e.g., drugs) and monitor electrolyte lev-
arrhythmias or cardiopulmonary arrest. Life- els to prevent recurrence of the abnormality.
threatening arrhythmias are associated commonly • Monitor renal function in patients at risk of elec-
with potassium disorders, particularly hyper- trolyte disorders.
kalaemia, and less commonly with disorders of • In haemodialysis patients, review the dialy-
serum calcium and magnesium. In some cases sis prescription regularly to avoid inappropriate
therapy for life-threatening electrolyte disorders electrolyte shifts during treatment.
should start before the laboratory results become
available. Potassium disorders
The electrolyte values for definitions have been
chosen as a guide to clinical decision-making. Potassium homeostasis
The precise values that trigger treatment deci-
sions will depend on the patient’s clinical con- Extracellular potassium concentration is regulated
dition and the rate of change of the electrolyte tightly between 3.5—5.0 mmol l−1 . A large con-
values. centration gradient normally exists between the
There is little or no evidence base for the treat- intracellular and extracellular fluid compartments.
ment of electrolyte abnormalities during cardiac This potassium gradient across the cell membranes
arrest. Guidance during cardiac arrest is based contributes to the excitability of nerve and mus-
on the strategies used in the non-arrest patient. cle cells, including the myocardium. Evaluation
There are no major changes in the treatment of of serum potassium must take into consideration
these disorders since the International Guidelines the effects of changes in serum pH. When serum
2000.1 pH decreases, serum potassium increases because

0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.
doi:10.1016/j.resuscitation.2005.10.004
S136 J. Soar et al.

potassium shifts from the cellular to the vascular • first-degree heart block (prolonged PR interval)
space. When serum pH increases, serum potassium >0.2 s;
decreases because potassium shifts intracellularly. • flattened or absent P waves;
We therefore anticipate the effects of pH changes • tall, peaked (tented) T waves, larger than R wave
on serum potassium during the therapy for hyper- in more than one lead;
kalaemia or hypokalaemia. • ST segment depression;
• S and T waves merging;
Hyperkalaemia • widened QRS >0.12 s;
• ventricular tachycardia (VT);
This is the most common electrolyte disorder asso- • bradycardia;
ciated with cardiopulmonary arrest. It is usually • cardiac arrest, i.e., pulseless electrical activity
caused by increased potassium release from the (PEA), ventricular fibrillation (VF), asystole.
cells or impaired excretion by the kidneys.
Treatment of hyperkalaemia. The five key steps
Definition. There is no universal definition, in treating hyperkalaemia are:
although we have defined hyperkalaemia as a serum
potassium concentration higher than 5.5 mmol l−1 ; 1. cardiac protection by antagonising the effects of
in practice, hyperkalaemia is a continuum. As hyperkalaemia;
the potassium concentration increases above this 2. shifting potassium into cells;
value, the risk of adverse events increases and the 3. removing potassium from the body;
need for urgent treatment increases. Severe hyper- 4. monitoring serum potassium for rebound hyper-
kalaemia has been defined as a serum potassium kalaemia;
concentration higher than 6.5 mmol l−1 . 5. prevention of recurrence of hyperkalaemia.

When hyperkalaemia is strongly suspected, e.g.,


Causes. There are several potential causes of in the presence of ECG changes, start life-saving
hyperkalaemia, including renal failure, drugs treatment even before laboratory results are avail-
(angiotensin converting enzyme inhibitors (ACEI), able. The management of hyperkalaemia is the sub-
angiotensin II receptor blockers (ARB), potassium- ject of a recent Cochrane review.4
sparing diuretics, non-steroidal anti-inflammatory
drugs (NSAIDs), beta-blockers, trimethoprim, tis- Patient not in cardiac arrest. If the patient
sue breakdown (rhabdomyolysis, tumour lysis, is not in cardiac arrest, assess fluid status;
haemolysis), metabolic acidosis, endocrine disor- if hypovolaemic, give fluid to enhance urinary
ders (Addison’s disease), hyperkalaemic periodic potassium excretion. The values for classification
paralysis, or diet, which may be the sole cause are an approximate guide. For mild elevation
in patients with established renal failure. Abnor- (5.5—6 mmol l−1 ), remove potassium from the body
mal erythrocytes or thrombocytosis may cause a with:
spuriously high potassium concentration. The risk
• potassium exchange resins, i.e., calcium reso-
of hyperkalaemia is even greater when there is
nium 15—30 g or sodium polystyrene sulfonate
a combination of factors, such as the concomi-
(Kayexalate® ) 15—30 g in 50—100 ml of 20% sor-
tant use of ACEI and NSAIDs or potassium-sparing
bitol, given either orally or by retention enema
diuretics.
(onset in 1—3 h, maximal effect at 6 h);
Recognition of hyperkalaemia. Exclude hyper- • diuretics, i.e., furosemide 1 mg kg−1 IV slowly
kalaemia in patients with an arrhythmia or car- (onset with the diuresis);
diac arrest.2 Patients may present with weakness • dialysis; haemodialysis is more efficient than
progressing to flaccid paralysis, paraesthesia or peritoneal dialysis at removing potassium (imme-
depressed deep tendon reflexes. The first indica- diate onset, 25—30 mmol potassium h−1 removed
tor of hyperkalaemia may also be the presence of with haemodialysis).
ECG abnormalities, arrhythmias, cardiopulmonary For moderate elevation (6—6.5 mmol l−1 ) with-
arrest or sudden death. The effect of hyper- out ECG changes, shift potassium into cells with:
kalaemia on the ECG depends on the absolute serum
potassium as well as the rate of increase. Most • dextrose/insulin: 10 units short-acting insulin
patients will have ECG abnormalities at a serum and 50 g glucose IV over 15—30 min (onset in
potassium concentration higher than 6.7 mmol l−1 .3 15—30 min, maximal effect at 30—60 min; mon-
The ECG manifestations of hyperkalaemia are usu- itor blood glucose). Use in addition to removal
ally progressive and include: strategies above.
European Resuscitation Council Guidelines for Resuscitation 2005 S137

For severe elevation (≥6.5 mmol l−1 ) without breakdown. Dialysis is also indicated when hyper-
ECG changes, shift potassium into cells with: kalaemia is resistant to medical management.
Serum potassium frequently rebounds after ini-
• salbutamol, 5 mg nebulised. Several doses may tial treatment. In unstable patients, continuous
be required (onset in 15—30 min); veno-venous haemofiltration (CVVH) is less likely
• sodium bicarbonate, 50 mmol IV over 5 min if to compromise cardiac output than intermittent
metabolic acidosis present (onset in 15—30 min). haemodialysis.
Bicarbonate alone is less effective than glucose
plus insulin or nebulised salbutamol; it is best Hypokalaemia
used in conjunction with these medications;5,6
• use multiple shifting agents in addition to Hypokalaemia is common in hospital patients.7
removal strategies above. Hypokalaemia increases the incidence of arrhyth-
mias, particularly in patients with pre-existing
For severe elevation (≥6.5 mmol l−1 ) with toxic heart disease and in those treated with digoxin.
ECG changes, protect the heart first with:
Definition. Hypokalaemia is defined as a serum
• calcium chloride, i.e., 10 ml 10% calcium chloride
potassium <3.5 mmol l−1 . Severe hypokalaemia is
IV over 2—5 min to antagonise the toxic effects of
defined as a K+ < 2.5 mmol l−1 and may be associ-
hyperkalaemia at the myocardial cell membrane.
ated with symptoms.
This protects the heart by reducing the risk of
VF, but does not lower serum potassium (onset in Causes. Causes of hypokalaemia include gas-
1—3 min). Use in addition to potassium removal trointestinal loss (diarrhoea), drugs (diuretics,
and shifting strategies stated above. laxatives, steroids), renal losses (renal tubular
disorders, diabetes insipidus, dialysis), endocrine
Patient in cardiac arrest. If the patient is in
disorders (Cushing’s syndrome, hyperaldostero-
cardiac arrest, there are no modifications to BLS
nism), metabolic alkalosis, magnesium depletion
in the presence of electrolyte abnormalities. For
and poor dietary intake. Treatment strategies used
ALS, follow the universal algorithm. The general
for hyperkalaemia may also induce hypokalaemia.
approach to treatment depends on the degree of
hyperkalaemia, rate of rise of serum potassium and Recognition of hypokalaemia. Exclude hypoka-
the patient’s clinical condition. laemia in every patient with an arrhythmia or
In cardiopulmonary arrest, protect the heart cardiac arrest. In dialysis patients, hypokalaemia
first, then apply shifting and removal strategies occurs commonly at the end of a haemodialysis
using: session or during treatment with continuous ambu-
latory peritoneal dialysis (CAPD).
• calcium chloride: 10 ml of 10% calcium chloride
As serum potassium concentration decreases,
IV by rapid bolus injection to antagonise the toxic
the nerves and muscles are predominantly
effects of hyperkalaemia at the myocardial cell
affected, causing fatigue, weakness, leg
membrane;
cramps and constipation. In severe cases
• sodium bicarbonate: 50 mmol IV by rapid injec-
(K+ < 2.5 mmol l−1 ), rhabdomyolysis, ascending
tion (if severe acidosis or renal failure);
paralysis and respiratory difficulties may occur.
• dextrose/insulin: 10 units short-acting insulin and
ECG features of hypokalaemia comprise:
50 g glucose IV by rapid injection;
• haemodialysis: consider this for cardiac arrest • U waves;
induced by hyperkalaemia, which is resistant to • T-wave flattening;
medical treatment. • ST segment changes;
• arrhythmias, especially if patient is taking
Indications for dialysis. Haemodialysis is the digoxin;
most effective method of removal of potassium • cardiopulmonary arrest (PEA, VF, asystole).
from the body. The principal mechanism of action
is the diffusion of potassium ions across the Treatment. Treatment depends on the severity of
transmembrane potassium ion gradient. The typ- hypokalaemia and the presence of symptoms and
ical decline in serum potassium is 1 mmol l−1 in ECG abnormalities. Gradual replacement of potas-
the first 60 min, followed by 1 mmol l−1 over the sium is preferable but in emergency intravenous
next 2 h. Consider haemodialysis early for hyper- potassium is required. The maximum recommended
kalaemia associated with established renal fail- IV dose of potassium is 20 mmol h−1 , but more rapid
ure, oliguric acute renal failure (<400 ml day−1 infusion, e.g., 2 mmol min−1 for 10 min followed by
urine output) or when there is marked tissue 10 mmol over 5—10 min is indicated for unstable
S138 J. Soar et al.

arrhythmias when cardiac arrest is imminent. Con- arrest secondary to a decreased conscious level is
tinuous ECG monitoring is essential during IV infu- a common cause of death. Alcohol excess is often
sion, and the dose should be titrated after repeated associated with self-poisoning.
sampling of serum potassium levels.
Many patients who are potassium deficient are • After opening and clearing the airway, check for
also deficient in magnesium. Magnesium is impor- breathing and a pulse. Avoid mouth-to-mouth
tant for potassium uptake and for the mainte- resuscitation in the presence of toxins, such
nance of intracellular potassium levels, partic- as cyanide, hydrogen sulphide, corrosives and
ularly in the myocardium. Repletion of magne- organophosphates. Ventilate the patient’s lungs
sium stores will facilitate more rapid correction of using a pocket- or bag-mask and the highest
hypokalaemia and is recommended in severe cases possible concentration of oxygen. Be careful in
of hypokalaemia.8 paraquat poisoning as pulmonary injury may be
exacerbated by high concentrations of oxygen.14
• There is a high incidence of pulmonary aspira-
Calcium and magnesium disorders tion of gastric contents after poisoning. Intubate
unconscious patients who cannot protect their
The recognition and management of calcium and
airway early, using a rapid-sequence induction
magnesium disorders is summarised in Table 7.1.
with cricoid pressure to decrease the risk of aspi-
ration (see section 4d). This must be undertaken
Summary by persons trained in the technique.
• In the event of cardiac arrest, provide standard
Electrolyte abnormalities are among the most com- basic and advanced life support.
mon causes of cardiac arrhythmias. Of all the • With the exception of torsades de pointes
electrolyte abnormalities, hyperkalaemia is most (see below), cardioversion is indicated for life-
rapidly fatal. A high degree of clinical suspicion and threatening tachyarrhythmias (see section 4f).
immediate treatment of the underlying electrolyte • Drug-induced hypotension is common after self-
abnormalities can prevent many patients from pro- poisoning. This usually responds to fluid therapy,
gressing to cardiac arrest. but occasionally inotropic support is required.
• Once resuscitation is under way, try to identify
the poison(s). Relatives, friends and ambulance
7b. Poisoning crews can usually provide useful information.
Examination of the patient may reveal diagnos-
General considerations tic clues, such as odours, needle puncture marks,
pinpoint pupils, tablet residues, signs of corro-
Poisoning is an infrequent cause of cardiac arrest, sion in the mouth or blisters associated with pro-
but remains a leading cause in victims younger than longed coma.
40 years.9—12 Most research on this topic consists • Measure the patient’s temperature; hypo- or
primarily of small case series, animal studies and hyperthermia may occur after drug overdose (see
case reports. sections 7d and 7e).
Self-poisoning with therapeutic or recreational • Consult regional or national poisons centres
drugs is the main reason for hospital admission. for information on treatment of the poi-
Drug toxicity can also be caused by inappropriate soned patient.15,16 The World Health Orga-
dosing and drug interactions. Accidental poisoning nization lists poison centres on its website:
is commonest in children. Homicidal poisoning is http://www.who.int/ipcs/poisons/centre/en/.
uncommon. Industrial accidents, warfare or ter-
rorism may cause extensive chemical or radiation Specific therapeutic measures
exposure. Decontamination and safe management
for mass casualty incidents is not part of these There are few specific therapeutic measures for
guidelines. poisons that are useful immediately. The emphasis
is on intensive supportive therapy, with correction
Resuscitation of hypoxia, hypotension and acid/base and elec-
trolyte disorders.
Treatment of the self-poisoning (‘overdose’) Therapeutic measures include limiting absorp-
patient is based on an ABCDE approach to pre- tion of ingested poisons, enhancing elimination,
vent cardiorespiratory arrest whilst awaiting drug or the use of specific antidotes. For up-to-date
elimination.13 Airway obstruction and respiratory guidance in severe or uncommon poisonings, seek
European Resuscitation Council Guidelines for Resuscitation 2005
Table 7.1 Calcium (Ca2+ ) and magnesium (Mg2+ ) disorders with associated clinical presentation, ECG manifestations and recommended treatment
Disorder Causes Presentation ECG Treatment
2+
Hypercalcaemia (Ca Primary or tertiary Confusion Short QT interval Fluid replacement IV
>2.6 mmol l−1 hyperparathyroidism Weakness Prolonged QRS interval Furosemide, 1 mg kg−1 IV
Malignancy Abdominal pain Flat T waves Hydrocortisone, 200—300 mg IV
Sarcoidosis Hypotension AV-block Pamidronate, 60—90 mg IV
Drugs Arrhythmias Cardiac arrest Calcitonin, 4—8 units kg−1 8 h−1 IM
Cardiac arrest Review medication
Haemodialysis
Hypocalcaemia (Ca2+ Chronic renal failure Paraesthesia Prolonged QT interval Calcium chloride 10%, 10—40 ml
<2.1 mmol l−1 Acute pancreatitis Tetany T-wave inversion Magnesium sulphate 50%, 4—8 mmol (if
Calcium channel blocker Seizures Heart block necessary)
overdose AV-block Cardiac arrest
Toxic shock syndrome Cardiac arrest
Rhabdomyolysis
Tumour lysis syndrome
Hypermagnesaemia Renal failure Confusion Prolonged PR and QT Calcium chloride 10%, 5—10 ml,
(Mg2+ > 1.1 mmol l−1 ) Iatrogenic Weakness intervals repeated if necessary
Respiratory depression T-wave peaking Ventilatory support if necessary
AV-block AV-block Saline diuresis: 0.9% saline with
Cardiac arrest Cardiac arrest furosemide 1 mg kg−1 IV
Haemodialysis

Hypomagnesaemia Gastrointestinal loss Tremor Prolonged PR and QT Severe or symptomatic: 2 g 50%


(Mg2+ <0.6 mmol l−1 ) Polyuria Ataxia Intervals magnesium sulphate (4 ml = 8 mmol) IV
Starvation Nystagmus ST-segment depression over 15 min
Alcoholism Seizures Torsades de pointes Torsade de pointes: 2 g 50%
Malabsorption Arrhythmias: torsades T-wave inversion magnesium sulphate (4 ml = 8 mmol) IV
de pointes Flattened P waves over 1—2 min
Cardiac arrest Increased QRS duration Seizure: 2 g 50% magnesium sulphate
(4 ml = 8 mmol) IV over 10 min

S139
S140 J. Soar et al.

advice from a poisons centre. or dicobalt edetate for cyanides; digoxin-specific


Fab antibodies for digoxin; flumazenil for ben-
• Activated charcoal is known to adsorb certain zodiazepines; and naloxone for opioids. Reversal
drugs. Its value decreases over time after inges- of benzodiazepine intoxication with flumazenil
tion. There is no evidence that ingestion of char- is associated with significant toxicity in patients
coal improves clinical outcome. According to evi- with benzodiazepine dependence or co-ingestion
dence from volunteer studies, consider giving a of proconvulsant medications, such as tricyclic
single dose of activated charcoal to patients who antidepressants.24 The routine use of flumazenil
have ingested a potentially toxic amount of poi- in the comatose patient with an overdose is not
son (known to be adsorbed by activated charcoal) recommended.
up to 1 h previously.17 Give it only to patients
with an intact or protected airway. Multiple doses Specific antidotes
of activated charcoal can be beneficial in life-
threatening poisoning with carbemazepine, dap- These guidelines will address only some causes of
sone, phenobarbital, quinine and theophylline. cardiorespiratory arrest due to poisoning.
• Gastric lavage followed by activated charcoal
therapy is useful only within 1 h of ingesting the Opioid poisoning
poison.17 Generally this should be carried out
after tracheal intubation. Delayed gastric lavage Opioid poisoning commonly causes respiratory
has very little effect on drug absorption and may depression followed by respiratory insufficiency or
propel drugs further along the gastrointestinal respiratory arrest. The respiratory effects of opi-
tract.18 Do not give ipecacuanha syrup to induce oids are reversed rapidly by the opiate antago-
vomiting; there is little evidence of benefit.19 nist naloxone. In severe respiratory depression, the
• There is little evidence for the use of laxatives, evidence shows fewer adverse events when air-
e.g., lactulose or magnesium citrate, to enhance way opening, oxygen administration and ventila-
drug elimination from the gut.20 tion are carried out before giving naloxone in cases
• Whole-bowel irrigation by enteral administra- of opioid-induced respiratory depression;25—30 how-
tion of a polyethylene glycol solution can reduce ever, the use of naloxone can prevent the need for
drug absorption by cleansing the gastrointesti- intubation. The preferred route for giving naloxone
nal tract. It can be useful in cases of potentially depends on the skills of the rescuer: IV, intramus-
toxic ingestion of sustained release or enteric- cular (IM), subcutaneous (SC), endotracheal (ET)
coated drugs, oral iron poisoning and the removal and intranasal (IN) routes can be used. The non-
of ingested packets of illicit drugs.21 IV routes can be quicker because time is saved in
• Urine alkalinisation (pH 7.5) by giving IV sodium not having to establish IV access, which can be
bicarbonate can be useful in moderate-to-severe extremely difficult in an IV drug abuser. The ini-
salicylate poisoning in patients who do not need tial doses of naloxone are 400 mcg IV,27 800 mcg
haemodialysis.22 Urine alkalinisation can also be IM, 800 mcg SC,27 2 mg IN31 or 1—2 mg ET. Large
useful in tricyclic overdose (see below). opioid overdoses may require titration to a total
• Haemodialysis or haemoperfusion can be use- naloxone dose of 6—10 mg. The duration of action
ful for elimination of specific life-threatening of naloxone is approximately 45—70 min, but respi-
toxins. Haemodialysis removes drugs or metabo- ratory depression can persist for 4—5 h after opioid
lites that are water soluble, have a low vol- overdose. Thus, the clinical effects of naloxone may
ume of distribution and low plasma protein not last as long as those of a significant opioid over-
binding.23 It may be considered for poison- dose. Titrate the dose until the victim is breathing
ing with methanol, ethylene glycol, salicylates adequately and has protective airway reflexes.
and lithium. Haemoperfusion involves passing Acute withdrawal from opioids produces a state
blood through an absorptive-containing cartridge of sympathetic excess and may cause compli-
(usually charcoal). This technique removes sub- cations, such as pulmonary oedema, ventricular
stances that have a high degree of plasma pro- arrhythmia and severe agitation. Use naloxone
tein binding. Charcoal haemoperfusion may be reversal of opiate intoxication with caution in
indicated for intoxications with carbamazepine, patients suspected of opioid dependence.
phenobarbital, phenytoin and theophylline. There is no good evidence that naloxone
• Specific antidotes (see below) which may be improves outcome once cardiac arrest associated
effective include: N-acetylcysteine for parac- with opioid toxicity has occurred. Cardiac arrest is
etamol; high-dose atropine for organophosphate usually secondary to a respiratory arrest and associ-
insecticides; sodium nitrite, sodium thiosulphate ated with severe brain hypoxia. Prognosis is poor.26
European Resuscitation Council Guidelines for Resuscitation 2005 S141

Giving naloxone is unlikely to be harmful. Once car- tively with digoxin-specific antibody fragments.53
diac arrest has occurred, follow the standard resus- Antibody-specific therapy may also be effective in
citation protocols. poisoning from plants as well as Chinese herbal
medications containing digitalis glycosides.53—55
Tricyclic antidepressants Vasopressors, inotropes, calcium, glucagon,
phosphodiesterase inhibitors and insulin-glucose
Self-poisoning with tricyclic antidepressants is com- may all be useful in beta-blocker and calcium chan-
mon and can cause hypotension, seizures and nel blocker overdose.56—58 Transcutaneous pacing
arrhythmias. Anticholinergic effects include mydri- may be effective for severe bradycardia caused by
asis, fever, dry skin, delirium, tachycardia, ileus poisoning and overdose (see section 3).
and urinary retention. Most life-threatening prob-
lems occur within the first 6 h after ingestion. A Further treatment and prognosis
widening QRS complex indicates a greater risk of
arrhythmias. There is evidence to support the use of A long period of coma in a single position can cause
sodium bicarbonate to treat arrhythmias induced by pressure sores and rhabdomyolysis. Measure elec-
tricyclic antidepressants and/or hypotension.32—47 trolytes (particularly potassium), blood glucose and
The exact threshold for starting treatment based arterial blood gases. Monitor temperature because
on QRS duration has not been established. No study thermoregulation is impaired. Both hypothermia
has investigated the optimal target arterial or uri- and hyperthermia (hyperpyrexia) can occur after
nary pH with bicarbonate therapy, but an arterial the overdose of some drugs. Retain samples of blood
pH of 7.45—7.55 has been commonly accepted and and urine for analysis.
seems reasonable. Hypertonic saline may also be Be prepared to continue resuscitation for a pro-
effective in treating cardiac toxicity.48 longed period, particularly in young patients as
the poison may be metabolised or excreted during
Cocaine toxicity extended life support measures.
Alternative approaches which may be effective
Sympathetic overstimulation associated with in severely poisoned patients include:
cocaine toxicity may cause agitation, symptomatic
tachycardia, hypertensive crisis, hyperthermia and • higher doses of medication than in standard pro-
myocardial ischaemia with angina. Glyceryl trini- tocols;
trate and phentolamine reverse cocaine-induced • non-standard drug therapies;
coronary vasoconstriction, labetalol has no signifi- • prolonged CPR.
cant effect, and propranolol makes it worse.49—52
Small doses of IV benzodiazepines (midazolam,
diazepam, lorazepam) are effective first-line 7c. Drowning
drugs. Use nitrates only as second-line therapy for
myocardial ischaemia. Labetalol (alpha- and beta- Overview
blocker) is useful for the treatment of tachycardia
and hypertensive emergencies due to cocaine Drowning is a common cause of accidental death in
toxicity. Europe. The most important and detrimental con-
sequence of drowning is hypoxia. The duration of
Drug-induced severe bradycardia hypoxia is the critical factor in determining the
victim’s outcome. Therefore, oxygenation, venti-
Severe bradycardia from poisoning or drug over- lation and perfusion should be restored as rapidly
dose may be refractory to standard ALS protocols as possible. Immediate resuscitation at the scene
because of prolonged receptor binding or direct is essential for survival and neurological recovery
cellular toxicity. Atropine may be life saving in after drowning. This will require bystander provi-
organophosphate, carbamate or nerve agent poi- sion of CPR plus immediate activation of the EMS
soning. Give atropine for bradycardia caused by system. Victims who have spontaneous circulation
acetylcholinesterase-inhibiting substances. Large and breathing when they reach hospital usually
(2—4 mg) and repeated doses may be required to recover with good outcomes.
achieve a clinical effect. Isoprenaline may be useful
at high doses in refractory bradycardia induced by Epidemiology
beta-antagonist receptor blockade. Heart block and
ventricular arrhythmias associated with digoxin or The World Health Organization (WHO) esti-
digitalis glycoside poisoning may be treated effec- mates that, worldwide, drowning accounts for
S142 J. Soar et al.

approximately 450,000 deaths each year. A further tim, reaching with a rescue aid (e.g., stick or cloth-
1.3 million disability-adjusted life-years are lost ing), or throwing a rope or buoyant rescue aid may
each year as a result of premature death or disabil- be effective if the victim is close to dry land. Alter-
ity from drowning;59 97% of deaths from drowning natively, use a boat or other water vehicle to assist
occur in low- and middle-income countries.59 In with the rescue. Avoid entry into the water when-
2002, there were 427 deaths from drowning in the ever possible. If entry into the water is essential,
United Kingdom (Royal Society for the Prevention take a buoyant rescue aid or flotation device.
of Accidents 2002) and 4073 in the United States Remove all the drowning victims from the water
(National Center for Injury Prevention 2002), by the fastest and safest means available and resus-
yielding an annual incidence of drowning of 0.8 citate as quickly as possible. The incidence of
and 1.45 per 100,000 population, respectively. cervical spine injury in drowning victims is low
Death from drowning is more common in young (approximately 0.5%).63 Spinal immobilisation can
males and is the leading cause of accidental death be difficult to perform in the water and can delay
in Europe in this group.59 Alcohol consumption is a removal from the water and adequate resuscita-
contributory factor in up to 70% of drownings.60 tion of the victim. Poorly applied cervical collars
The guidelines in this chapter focus on the treat- can also cause airway obstruction in unconscious
ment of the individual drowning victim rather than patients.64 Despite potential spinal injury, victims
the management of mass casualty aquatic inci- who are pulseless and apnoeic should be removed
dents. from water as quickly as possible (even if a back
support device is not available), while attempt-
Definitions, classifications and reporting ing to limit neck flexion and extension. Cervical
spine immobilisation is not indicated unless signs of
Over 30 different terms have been used to describe severe injury are apparent or the history is consis-
the process and outcome from submersion- and tent with the possibility of severe injury.65 These
immersion-related incidents.61 To improve clarity circumstances include a history of diving, water-
and to help comparability of future scientific and slide use, signs of trauma or signs of alcohol intoxi-
epidemiological reports, the International Liaison cation. Whenever possible, remove the victim from
Committee on Resuscitation (ILCOR) has proposed the water in a horizontal position to minimise the
new definitions related to drowning.62 Drowning risks of post-immersion hypotension and cardiovas-
itself is defined as a process resulting in primary res- cular collapse.66
piratory impairment from submersion/immersion in
a liquid medium. Implicit in this definition is that Rescue breathing
a liquid/air interface is present at the entrance
of the victim’s airway, preventing the victim from The first and most important treatment for the
breathing air. The victim may live or die after this drowning victim is alleviation of hypoxaemia.
process, but whatever the outcome, he or she has Prompt initiation of rescue breathing or positive
been involved in a drowning incident. Immersion pressure ventilation increases the survival.67,68 In
means to be covered in water or other fluid. For the apnoeic victim, start rescue breathing as soon
drowning to occur, usually at least the face and as the victim’s airway is opened and the rescuer’s
airway must be immersed. Submersion implies that safety ensured. This can sometimes be achieved
the entire body, including the airway, is under the when the victim is still in shallow water. It is likely
water or other fluid. to be difficult to pinch the victim’s nose, so mouth-
ILCOR recommends that the following terms, to-nose ventilation may be used as an alternative to
previously used, should no longer be used: dry and mouth-to-mouth ventilation. If the victim is in deep
wet drowning, active and passive drowning, silent water, start in-water rescue breathing if trained to
drowning, secondary drowning and drowned versus do so, ideally with the support of a buoyant rescue
near-drowned.62 aid,69 although in-water, unsupported resuscitation
may also be possible.70 Untrained rescuers should
Basic life support not attempt to perform any form of resuscitation
with a victim in deep water.
Aquatic rescue and recovery from the water If there is no spontaneous breathing after open-
ing the airway, give rescue breaths for approxi-
Always be aware of personal safety and minimise mately 1 min.69 If the victim does not start breath-
the danger to yourself and the victim at all times. ing spontaneously, further management depends on
Whenever possible, attempt to save the drowning the distance from land. If the victim can be brought
victim without entry into water. Talking to the vic- to land in <5 min of rescue time, continue rescue
European Resuscitation Council Guidelines for Resuscitation 2005 S143

breaths while towing. If more than an estimated Advanced life support


5 min from land, give further rescue breaths over
1 min, then bring the victim to land as quickly as Airway and breathing
possible without further attempts at ventilation.69
There is no need to clear the airway of aspi- Give high-flow oxygen during the initial assess-
rated water. The majority of drowning victims aspi- ment of the spontaneously breathing drowning
rate only a modest amount of water, and this is victim. Consider non-invasive ventilation or contin-
absorbed rapidly into the central circulation. An uous positive airway pressure if the victim fails to
attempt to remove water from the air passages respond to treatment with high-flow oxygen.76 Use
by any means other than suction is unnecessary pulse oximetry and arterial blood gas analysis to
and dangerous. Abdominal thrusts cause regurgi- titrate the concentration of inspired oxygen and
tation of gastric contents and subsequent aspira- to provide an indicator of the adequacy of ven-
tion. They have been associated with other life- tilation. Consider early intubation and controlled
threatening injuries and should not be performed ventilation for victims who fail to respond to these
unless there are clear signs of foreign-body airway initial measures or who have a reduced level of
obstruction.71 consciousness. Take care to ensure optimal preoxy-
genation before intubation. Use a rapid-sequence
induction with cricoid pressure to reduce the high
Chest compression risk of aspiration.77 Protect the airway of the victim
in cardiopulmonary arrest early in the resuscita-
As soon as the victim is removed from water,
tion attempt, ideally with a tracheal tube. Reduced
check for breathing. A healthcare professional who
pulmonary compliance requiring high inflation pres-
is trained in pulse checking may also check for
sures may limit the use of adjuncts, such as the
pulse, but this may be even more difficult to find
laryngeal mask airway. Initiate ventilation with a
in a drowning victim, particularly if cold. If the
high-inspired oxygen concentration as soon as pos-
victim is not breathing, start chest compressions
sible, to treat the severe hypoxaemia that is likely
immediately. Chest compression is ineffective in
to be present.
water.72,73

Circulation and defibrillation


Defibrillation
Follow standard advanced life support protocols. If
If the victim is unresponsive and not breathing and severe hypothermia is present (core body temper-
an AED is available, attach it to the victim and ature ≤30 ◦ C or 86 ◦ F), limit defibrillation attempts
turn it on. Before attaching the AED pads, dry to three, and withhold IV drugs until the core
the victim’s chest to enable adherence. Deliver body temperature increases above these levels. If
shocks according to the AED prompts. If the vic- moderate hypothermia is present, give IV drugs at
tim is hypothermic with a core body temperature longer than standard intervals (see section 7d).
≤30 ◦ C (86 ◦ F), limit defibrillation to a total of three During prolonged immersion, victims may
attempts until the core body temperature rises become hypovolaemic from the hydrostatic pres-
above 30 ◦ C (86 ◦ F).74 sure of water on the body. Give IV fluid to correct
the hypovolaemia but avoid excessive volumes,
Regurgitation during resuscitation which may cause pulmonary oedema. After return
of spontaneous circulation, use haemodynamic
Regurgitation of stomach contents is common fol- monitoring to guide fluid resuscitation.
lowing resuscitation from drowning and will com-
plicate efforts to maintain a patent airway. In one Discontinuing resuscitation efforts
study, regurgitation occurred in two-thirds of vic-
tims who received rescue breathing and 86% of vic- Making a decision to discontinue resuscitation
tims who required compression and ventilation.75 efforts on a victim of drowning is notoriously dif-
If regurgitation occurs, turn the victim’s mouth to ficult. No single factor can accurately predict good
the side and remove the regurgitated material using or poor survival with 100% certainty. Decisions made
directed suction if possible. If spinal cord injury is in the field frequently prove later to have been
suspected, log-roll the victim, keeping the head, incorrect.78 Continue resuscitation unless there
neck and torso aligned, before aspirating the regur- is clear evidence that resuscitation attempts are
gitated material. Log-rolling will require several futile (e.g., massive traumatic injuries, rigor mor-
rescuers. tis, putrefaction etc.), or timely evacuation to
S144 J. Soar et al.

a medical facility is not possible. Neurologically In contrast, there is evidence of benefit from
intact survival has been reported in several victims induced hypothermia for comatose victims resus-
submerged for greater than 60 min.79,80 citated from prehospital cardiac arrests.83 To date,
there is no convincing evidence to guide therapy
Post-resuscitation care in this patient group. A pragmatic approach might
be to consider instituting active rewarming until a
Salt versus fresh water core temperature of 32—34 ◦ C is achieved, and then
actively to avoid hyperthermia (>37 ◦ C) during the
Much attention has been focused in the past on dif- subsequent period of intensive care (International
ferences between salt- and fresh-water drowning. Life Saving Federation, 2003).
Extensive data from animal studies and human case
series have shown that, irrespective of the tonicity Other supportive care
of the inhaled fluid, the predominant pathophys-
iological process is hypoxaemia, driven by surfac- Attempts have been made to improve neurologi-
tant wash-out and dysfunction, alveolar collapse, cal outcome following drowning with the use of
atelectasis and intrapulmonary shunting. Small dif- barbiturates, intracranial pressure (ICP) monitoring
ferences in electrolyte disturbance are rarely of any and steroids. None of these interventions has been
clinical relevance and do not usually require treat- shown to alter the outcome. In fact, signs of high
ment. ICP serve as a symptom of significant neurological
hypoxic injury, and no evidence that attempts to
Lung injury alter the ICP will affect the outcome.65
Victims of drowning are at high risk of develop-
ing acute respiratory distress syndrome (ARDS) for
upto 72 h after submersion. Protective ventilation 7d. Hypothermia
strategies improve survival in patients with ARDS.81
The propensity towards alveolar collapse may Definition
require the use of PEEP or other alveolar recruit-
Hypothermia exists when the body core tempera-
ment manoeuvres to reverse severe hypoxaemia.82
ture is below 35 ◦ C and is classified arbitrarily as
Extracorporeal membrane oxygenation and nitric
mild (35—32 ◦ C), moderate (32—30 ◦ C) or severe
oxide administration have been used in some cen-
(less than 30 ◦ C). Hypothermia can occur in peo-
tres for refractory hypoxaemia in drowning victims
ple with normal thermoregulation who are exposed
but the efficacy of these treatments is unproven.65
to cold environments, particularly wet or windy
Pneumonia is common after drowning. Prophy-
conditions, or following immersion in cold water.
lactic antibiotics have not been shown to be of
When thermoregulation is impaired, for example,
benefit, although they may be considered after
in the elderly and very young, hypothermia may
submersion in grossly contaminated water such as
follow a mild cold insult. The risk of hypother-
sewage. Give broad-spectrum antibiotics if signs of
mia is also increased by drug or alcohol ingestion,
infection develop subsequently.65
illness, injury or neglect. Hypothermia may be sus-
Hypothermia pected from the clinical history or a brief external
examination of a collapsed patient. A low-reading
Victims of submersion may develop primary or thermometer is needed to measure the core tem-
secondary hypothermia. If the submersion occurs perature and confirm diagnosis.
in icy water (<5 ◦ C or 41 ◦ F), hypothermia may In some cases, hypothermia may exert a protec-
develop rapidly and provide some protection tive effect on the brain after cardiac arrest.84,85
against hypoxia. Such effects, however, have typ- Intact neurological recovery may be possible after
ically been reported after submersion of children hypothermic cardiac arrest, although those with
in icy water.59 Hypothermia may also develop as non-asphyxial arrest have a better prognosis than
a secondary complication of the submersion, and those with asphyxial hypothermic arrest.86—88 Life-
subsequent heat loss through evaporation dur- saving procedures should not be withheld on the
ing attempted resuscitation. In these victims the basis of clinical presentation alone.87
hypothermia is not protective (see section 7d).
Several small clinical studies in patients with Decision to resuscitate
accidental hypothermia have shown that survival
may be improved by either passive or active warm- Beware of pronouncing death in a hypothermic
ing out of hospital or in the emergency room.65 patient, as cold alone may produce a very slow,
European Resuscitation Council Guidelines for Resuscitation 2005 S145

small-volume, irregular pulse and an unrecordable Use the same ventilation and chest compression
blood pressure. Hypothermia protects the brain and rates as for a normothermic patient. Hypothermia
vital organs, and associated arrhythmias are poten- can cause stiffness of the chest wall, making venti-
tially reversible either before or during rewarming. lation and chest compression difficult.
At 18 ◦ C the brain can tolerate periods of circula- The hypothermic heart may be unresponsive
tory arrest for 10 times longer than at 37 ◦ C. Dilated to cardioactive drugs, attempted electrical pac-
pupils can be caused by a variety of insults and must ing and attempted defibrillation. Drug metabolism
not be taken as a sign of death. is slowed, leading to potentially toxic plasma
On discovering a hypothermic cardiac arrest concentrations of any drug given repeatedly.90
victim in cold environment, it is not always easy The evidence for the efficacy of drugs in severe
to distinguish between primary and secondary hypothermia is limited and based mainly on animal
hypothermia. Cardiac arrest could be caused pri- studies. Adrenaline may be effective in increas-
marily by hypothermia, or hypothermia could fol- ing coronary perfusion pressure, but not survival,
low a normothermic cardiac arrest (e.g., cardiac in severe hypothermic cardiac arrest.93,94 The effi-
arrest caused by myocardial ischaemia in a person cacy of amiodarone is also reduced.95 For these
in cold environment). reasons, withhold adrenaline and other drugs until
Do not confirm death until the patient has been the patient has been warmed to a temperature
rewarmed or until attempts to raise the core tem- greater than 30 ◦ C. Once 30 ◦ C has been reached,
perature have failed; prolonged resuscitation may the intervals between doses should be doubled. As
be necessary. In the prehospital setting, resusci- the patient’s temperature returns towards normal,
tation should be withheld only if the patient has the standard drug protocols should be used.
obvious lethal injuries or if the body is completely Remember to rule out other primary causes of
frozen making resuscitation attempts impossible.89 cardiorespiratory arrest using the four Hs and four
In the hospital setting, use clinical judgment to Ts approach (e.g., drug overdose, hypothyroidism,
determine when to stop resuscitating a hypother- trauma).
mic arrest victim.
Arrhythmias
Resuscitation
As the body core temperature decreases, sinus
All the principles of prevention, basic and advanced bradycardia tends to give way to atrial fibrillation
life support apply to the hypothermic patient. Do (AF) followed by ventricular fibrillation (VF) and
not delay the urgent procedures, such as intu- finally asystole.96 Follow the standard treatment
bation and insertion of vascular catheters. Intu- protocols.
bation can provoke VF in a patient with severe Severely hypothermic victims (core tempera-
hypothermia.87,90 ture <30 ◦ C) in cardiac arrest in hospital must be
rapidly rewarmed using internal methods. Arrhyth-
• Clear the airway and, if there is no spontaneous mias other than VF tend to revert spontaneously
respiratory effort, ventilate the patient’s lungs as the core temperature increases, and usually do
with high concentrations of oxygen. If possible, not require immediate treatment. Bradycardia may
use warmed (40—46 ◦ C) and humidified oxygen. be physiological in severe hypothermia, and cardiac
Consider careful tracheal intubation when indi- pacing is not indicated unless bradycardia persists
cated according to the ALS algorithm. after rewarming.
• Palpate a major artery and, if available, look at The temperature at which defibrillation should
the ECG for up to 1 min and look for signs of life first be attempted and how often it should be tried
before concluding that there is no cardiac out- in the severely hypothermic patient has not been
put. If a Doppler ultrasound probe is available, established. AEDs may be used on these patients. If
use it to establish whether there is peripheral VF is detected, give a shock; if VF/VT persists after
blood flow. If the victim is pulseless, start chest three shocks, delay further defibrillation attempts
compressions immediately. If there is any doubt until the core temperature is above 30 ◦ C.97,98 If an
about whether a pulse is present, start CPR. AED is used, follow the AED prompts while rewarm-
• Once resuscitation is under way, confirm ing the patient.
hypothermia with a low-reading thermometer.
The method of temperature measurement Rewarming
should be the same throughout resuscitation and
rewarming. Use oesophageal, bladder, rectal or General measures for all casualties include removal
tympanic temperature measurements.91,92 from the cold environment, prevention of further
S146 J. Soar et al.

heat loss and rapid transfer to the hospital. Remove tions, or secondary to endogenous heat produc-
cold or wet clothing as soon as possible. Cover the tion.
dry casualties with blankets and keep them out of Environment-related hyperthermia occurs where
the wind. heat, usually in the form of radiant energy, is
Rewarming may be passive external, active absorbed by the body at a rate faster than that can
external, or active internal. Passive warming is be lost by thermoregulatory mechanisms. Hyper-
achieved with blankets and a warm room, and is thermia occurs along a continuum of heat-related
suitable for conscious victims with mild hypother- conditions, starting with heat stress, progressing
mia. In severe hypothermia or cardiac arrest, to heat exhaustion, to heat stroke (HS) and finally
active warming is required, but this must not multiorgan dysfunction and cardiac arrest in some
delay transport to a hospital where more advanced instances.108
rewarming techniques are available. Several tech- Malignant hyperthermia (MH) is a rare disorder of
niques have been described, although there are no skeletal muscle calcium homeostasis characterised
clinical trials of outcome to determine the best by muscle contracture and life-threatening hyper-
rewarming method. Studies show that forced air metabolic crisis following exposure of genetically
rewarming and warm IV fluids are effective in predisposed individuals to halogenated anaesthet-
patients with severe hypothermia and a perfus- ics and depolarising muscle relaxants.109,110
ing rhythm.99,100 Other warming techniques include The key features and treatment of heat stress
the use of warm humidified gases, gastric, peri- and heat exhaustion are included in Table 7.2.
toneal, pleural or bladder lavage with warm fluids
(at 40 ◦ C), and extracorporeal blood warming with Heat stroke (HS)
partial bypass.87,90,101—103
In the patient with cardiac arrest and hypother- HS is a systemic inflammatory response with a
mia, cardiopulmonary bypass is the preferred core temperature above 40.6 ◦ C, accompanied by
method of active internal rewarming because it mental state change and varying levels of organ
also provides circulation, oxygenation and ventila- dysfunction. There are two forms of HS: clas-
tion, while the core body temperature is increased sic non-exertion heat stroke (CHS) occuring dur-
gradually.104,105 Survivors in one case series had an ing high environmental temperatures and often
average of 65 min of conventional CPR before car- effecting the elderly during heat waves;111 exer-
diopulmonary bypass.105 Unfortunately, facilities tion heat stroke (EHS) occuring during strenu-
for cardiopulmonary bypass are not always avail- ous physical exercise in high environmental tem-
able and a combination of methods may have to be peratures and/or high humidity usually effecting
used. healthy young adults.112 Mortality from HS ranges
During rewarming, patients will require large between 10 and 50%.113
volumes of fluids as their vascular space expands
with vasodilation. Warm all the IV fluids. Use con- Predisposing factors
tinuous haemodynamic monitoring and, if possi-
ble, treat the patient in a critical care unit. Avoid The elderly are at an increased risk for heat-related
hyperthermia during and after the warming period. illness because of underlying illness, medication
Although there are no formal studies, once ROSC use, declining thermoregulatory mechanisms and
has been achieved use standard strategies for post- limited social support. There are several risk fac-
resuscitation care, including mild hypothermia if tors: lack of acclimatisation, dehydration, obe-
appropriate (section 4g). There is no evidence sity, alcohol, cardiovascular disease, skin condi-
for the routine use of steroids, barbiturates or tions (psoriasis, eczema, scleroderma, burn, cys-
antibiotics.106,107 tic fibrosis), hyperthyroidism, phaeochromocytoma
and drugs (anticholinergics, diamorphine, cocaine,
amphetamine, phenothiazines, sympathomimetics,
7e. Hyperthermia calcium channel blockers, beta-blockers).

Definition Clinical presentation

Hyperthermia occurs when the body’s ability Heat stroke can resemble septic shock and may be
to thermoregulate fails, and core temperature caused by similar mechanisms.114 Features include:
exceeds the one that is normally maintained • core temperature 40.6 ◦ C or more;
by homeostatic mechanisms. Hyperthermia may • hot, dry skin (sweating is present in about 50% of
be exogenous, caused by environmental condi- cases of exertional heat stroke);
European Resuscitation Council Guidelines for Resuscitation 2005 S147

Table 7.2 Heat stress and heat exhaustion


Condition Features Treatment
Heat stress Normal or mild temperature elevation Rest
Heat oedema: swelling of feet and ankles Elevation of oedematous limbs
Heat syncope: vasodilation causing hypotension Cooling
Heat cramps: sodium depletion causing cramps Oral rehydration
Salt replacement
Heat exhaustion Systemic reaction to prolonged heat exposure As above
(hours to days)
Temperature >37 ◦ C and <40 ◦ C Consider IV fluids and ice packs
for severe cases
Headache, dizziness, nausea, vomiting, tachycar-
dia, hypotension, sweating muscle pain, weak-
ness and cramps
Haemoconcentration
Hyponatraemia or hypernatraemia
May progress rapidly to heat stroke

• early signs and symptoms, e.g., extreme fatigue, Cooling techniques


headache, fainting, facial flushing, vomiting and
diarrhoea; Several cooling methods have been described,
• cardiovascular dysfunction including arrhyth- but there are few formal trials to determine
mias115 and hypotension; which method is best. Simple cooling techniques
• respiratory dysfunction including ARDS;116 include drinking cool fluids, fanning the completely
• central nervous system dysfunction including undressed patient and spraying tepid water on the
seizures and coma;117 patient. Ice packs over areas where there are large
• liver and renal failure;118 superficial blood vessels (axillae, groins, neck) may
• coagulopathy;116 also be useful. Surface cooling methods may cause
• rhabdomyolysis.119 shivering. In cooperative stable patients, immer-
sion in cold water can be effective;128 however, this
Other clinical conditions need to be considered, may cause peripheral vasoconstriction, shunt blood
including: away from the periphery and reduce heat dissipa-
tion. Immersion is also not practical in the most sick
• drug toxicity;120,121
patients.
• drug withdrawal syndrome;
Further techniques to cool patients with hyper-
• serotonin syndrome;122
thermia are similar to those used for therapeu-
• neuroleptic malignant syndrome123
tic hypothermia after cardiac arrest (see section
• sepsis;124
4g). Gastric, peritoneal,129 pleural or bladder
• central nervous system infection;
lavage with cold water lowers the core tem-
• endocrine disorders, e.g., thyroid storm, phaeo-
perature. Intravascular cooling techniques include
chromocytoma.125
the use of cold IV fluids,130 intravascular cool-
ing catheters131,132 and extracorporeal circuits,133
Management e.g., continuous veno-venous haemofiltration or
cardiopulmonary bypass.
The mainstay of treatment is supportive ther-
apy based on optimising the ABCDEs and cool-
ing the patient.126,127 Start cooling before the Drug therapy in heat stroke
patient reaches the hospital. Aim to reduce the core
temperature to approximately 39 ◦ C. Patients with There are no specific drug therapies in heat stroke
severe heat stroke need to be managed in a criti- to lower the core temperature. There is no good
cal care setting. Use haemodynamic monitoring to evidence that antipyretics (e.g., non-steroidal anti-
guide fluid therapy. Large volumes of fluid may be inflammatory drugs or paracetamol) are effective in
required. Correct the electrolyte abnormalities as heat stroke. Dantrolene (see below) has not been
described in Section 7a. shown to be beneficial.134
S148 J. Soar et al.

Malignant hyperthermia (MH) (e.g., beta-adrenergic agonists, aminophylline)


or electrolyte abnormalities;
MH is a life-threatening genetic sensitivity of skele- • dynamic hyperinflation, i.e., autopositive end-
tal muscles to volatile anaesthetics and depolaris- expiratory pressure (auto-PEEP), can occur in
ing neuromuscular blocking drugs, occurring during mechanically ventilated asthmatics. Auto-PEEP
or after anaesthesia. Stop triggering agents imme- is caused by air trapping and ‘breath stack-
diately; give oxygen, correct acidosis and elec- ing’ (breathed air entering and being unable to
trolyte abnormalities. Start active cooling and give escape). Gradual build-up of pressure occurs and
dantrolene.135 reduces blood flow and blood pressure;
• tension pneumothorax (often bilateral).
Modifications to cardiopulmonary The four Hs and four Ts approach to reversible
resuscitation and post-resuscitation care causes helps identify these causes in cardiac arrest.
There are no specific studies on cardiac arrest in
hyperthermia. If cardiac arrest occurs, follow stan- Diagnosis
dard procedures for basic and advanced life sup-
Wheezing is a common physical finding, but sever-
port and cool the patient. There are no data on
ity does not correlate with the degree of airway
the effects of hyperthermia on defibrillation thresh-
obstruction. The absence of wheezing may indi-
old; therefore, attempt defibrillation according to
cate critical airway obstruction, whereas increased
current guidelines, while continuing to cool the
wheezing may indicate a positive response to bron-
patient. Animal studies suggest that the progno-
chodilator therapy. SaO2 may not reflect progres-
sis is poor compared with normothermic cardiac
sive alveolar hypoventilation, particularly if oxygen
arrest.136,137 The risk of unfavourable neurological
is being given. The SaO2 may initially decrease dur-
outcome increases for each degree of body tem-
ing the therapy because beta-agonists cause both
perature >37 ◦ C.138 Provide post-resuscitation care
bronchodilation and vasodilation and may increase
according to the normal guidelines.
intrapulmonary shunting initially.
Other causes of wheezing include: pulmonary
oedema, chronic obstructive pulmonary disease
7f. Asthma (COPD), pneumonia, anaphylaxis,141 pneumonia,
foreign bodies, pulmonary embolism, bronchiecta-
Introduction sis and subglottic mass.142
The severity of an asthma attack is defined in
Approximately 300 million people of all ages Table 7.3.
and ethnic backgrounds suffer from asthma
worldwide.139 Asthma still causes many deaths in
Key interventions to prevent arrest
young adults, mostly among those with chronic
severe asthma, adverse psychosocial circumstances The patient with severe asthma requires aggres-
and poor medical management. National and inter- sive medical management to prevent deteriora-
national guidance for the management of asthma tion. Base assessment and treatment on an ABCDE
already exists.139,140 The following guidelines focus approach. Experienced clinicians should treat these
on the treatment of patients with near-fatal asthma high-risk patients in a critical care area. The spe-
and cardiac arrest. cific drugs and the treatment sequence will vary
according to local practice.
Causes of cardiac arrest
Oxygen
Cardiac arrest in the asthmatic person is often a
terminal event after a period of hypoxaemia; occa- Use a concentration of inspired oxygen that will
sionally, it may be sudden. Cardiac arrest in asth- achieve an SaO2 ≥92%. High-flow oxygen by mask
matics has been linked to: is sometimes necessary. Consider rapid-sequence
induction and tracheal intubation if, despite efforts
• severe bronchospasm and mucous plugging lead-
to optimise drug therapy, the patient has:
ing to asphyxia (this condition causes the vast
majority of asthma-related deaths); • decreased conscious level, coma;
• cardiac arrhythmias caused by hypoxia, which is • profuse sweating;
the common cause of asthma-related arrhythmia. • reduced muscle tone (clinical signs of hypercar-
Arrhythmias can be caused by stimulant drugs bia);
European Resuscitation Council Guidelines for Resuscitation 2005 S149

Table 7.3 The severity of asthma140


Asthma Features
Near-fatal Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures
Life-threatening Any one of:
PEF <33% best or predicted
Bradycardia
SpO2 <92%, dysrhythmia
PaO2 <8 kPa, hypotension
Normal PaCO2 (4.6—6.0 kPa (35—45 mmHg)), exhaustion
Silent chest, confusion
Cyanosis, coma
Feeble respiratory effort
Acute severe Any one of:
PEF 33-50% best or predicted
Respiratory rate >25/min
Heart rate >110/min
Inability to complete sentences in one breath
Moderate exacerbation Increasing symptoms
PEF >50—75% best or predicted
No features of acute severe asthma
Brittle Type 1: wide PEF variability (>40% diurnal variation for >50% of the time over a period
>150 days) despite intense therapy
Type 2: sudden severe attacks on a background of apparently well controlled asthma
PEF, peak expiratory flow.

• findings of severe agitation, confusion and fight- Nebulised anticholinergics


ing against the oxygen mask (clinical signs of
hypoxemia). Nebulised anticholinergics (ipratropium, 0.5 mg
4—6 h) may produce additional bronchodilation in
Elevation of the PaCO2 alone does not indicate severe asthma or in those who do not respond to
the need for tracheal intubation. Treat the patient, beta-agonists.144,145
not the numbers.
Intravenous salbutamol
Nebulised beta2 -agonists
Several studies have shown intravenous salbuta-
Salbutamol, 5 mg nebulised, is the cornerstone of mol (250 mcg IV slowly) to provide additional ben-
therapy for acute asthma in most of the world. efit in severe asthmatics who are already receiv-
Repeated doses every 15—20 min are often needed. ing nebulised salbutamol.146 Give an infusion of
Severe asthma may necessitate continuous neb- 3—20 mcg min−1 .
ulised salbutamol. Nebuliser units that can be
driven by high-flow oxygen should be available. Intravenous magnesium sulphate
The hypoventilation associated with severe or near-
Magnesium sulphate (2 g, IV slowly) may be useful as
fatal asthma may prevent effective delivery of neb-
a bronchodilator in severe or near-fatal asthma. A
ulised drugs.
Cochrane meta-analysis of seven studies concluded
that magnesium is beneficial, particularly for those
Intravenous corticosteroids with the most severe exacerbations.147 Magnesium
causes bronchial smooth muscle relaxation inde-
Oxygen and beta-agonists are the most important pendent of the serum magnesium level and has only
therapies initially, but give corticosteroids (hydro- minor side effects (flushing, light-headedness).
cortisone, 200 mg IV,) early. Although there is no
difference in clinical effects between oral and IV Intravenous theophylline
formulations of corticosteroids,143 the IV route is
preferable because patients with near-fatal asthma Theophylline is given IV as aminophylline, a
may vomit or be unable to swallow. mixture of theophylline with ethylenediamine,
S150 J. Soar et al.

which is 20 times more soluble than theophylline Non-invasive ventilation


alone. Aminophylline should only be considered
in severe or near-fatal asthma. A loading dose Non-invasive ventilation decreases the intubation
of 5 mg kg−1 is given over 20—30 min (unless on rate and mortality in COPD;154 however, its role
maintenance therapy), followed by an infusion of in patients with severe acute asthma is uncertain.
500—700 mcg kg−1 h−1 . Addition of this drug to high Although promising, a recent Cochrane review sug-
doses of beta-agonists increases side effects more gests that more studies are needed.155
than it increases bronchodilation. Check levels to
avoid toxicity. Management of cardiac arrest

Subcutaneous or intramuscular adrenaline and Basic life support


terbutaline
Give basic life support according to the standard
Adrenaline and terbutaline are adrenergic agents guidelines. Ventilation will be difficult because of
that may be given subcutaneously to patients increased airway resistance; try to prevent gastric
with acute severe asthma. The dose of subcuta- inflation.
neous adrenaline is 300 mcg up to a total of three
doses at 20-min intervals. Adrenaline may cause an Advanced life support
increase in heart rate, myocardial irritability and
increased oxygen demand; however, its use (even Modifications to standard ALS guidelines. Con-
in patients over 35 years old) is well tolerated.148 sider the need for intubation early. The peak
Terbutaline is given in a dose of 250 mcg subcu- airway pressures recorded during the ventila-
taneously, which can be repeated in 30—60 min. tion of patients with severe asthma (mean
These drugs are more commonly given to children 67.8 ± 11.1 cmH2 0 in 12 patients) are significantly
with acute asthma and, although most studies have higher than the normal lower oesophageal sphinc-
shown them to be equally effective,149 one study ter pressure (approximately 20 cmH2 0).156 There is
concluded that terbutaline was superior.150 These a significant risk of gastric inflation and hypoven-
alternative routes may need to be considered when tilation of the lungs when attempting to ventilate
IV access is impossible. a severe asthmatic without a tracheal tube. Dur-
ing cardiac arrest this risk is even higher because
the lower oesophageal sphincter pressure is sub-
Intravenous fluids stantially less than normal.157
The new recommended respiratory rate
Severe or near-fatal asthma is associated with
(10 breaths min−1 ) and tidal volume required
dehydration and hypovolaemia, and this will fur-
for a normal chest rise during CPR should not
ther compromise the circulation in patients with
cause dynamic hyperinflation of the lungs (gas
dynamic hyperinflation of the lungs. If there is evi-
trapping). Tidal volume depends on the inspiratory
dence of hypovolaemia or dehydration, give IV flu-
time and inspiratory flow, while lung emptying
ids.
depends on the expiratory time and expiratory
flow. In mechanically ventilated severe asth-
Heliox matics, increasing the expiratory time (achieved
by reducing the respiratory rate) provides only
Heliox is a mixture of helium and oxygen (usually moderate gains in terms of reduced gas trapping
80:20 or 70:30). A recent meta-analysis of four when a minute volume of less than 10 l min−1 is
clinical trials did not support the use of heliox used.156
in the initial treatment of patients with acute There is limited evidence from the case
asthma.151 reports of unexpected ROSC in patients with
suspected gas trapping when the tracheal tube is
Ketamine disconnected.158—161 If dynamic hyperinflation of
the lungs is suspected during CPR, compression of
Ketamine is a parenteral dissociative anaesthetic the chest wall and/or a period of apnoea (discon-
with bronchodilatory properties. One case series nection of tracheal tube) may relieve gas trapping
suggested substantial effectiveness,152 but the sin- if dynamic hyperinflation occurs. Although this
gle randomised trial published to date showed procedure is supported by limited evidence, it is
no benefit to ketamine compared with standard unlikely to be harmful in an otherwise desperate
care.153 situation.
European Resuscitation Council Guidelines for Resuscitation 2005 S151

Dynamic hyperinflation increases transthoracic Anaphylaxis is a severe life-threatening, gen-


impedance.162 Consider the higher shock energies eralised or systemic hypersensitivity reaction.
for defibrillation if initial defibrillation attempts Investigations will show whether the reaction
fail. is allergic (immunoglobulin E (IgE) or non IgE
There is no good evidence for the use of open- mediated) or non-allergic anaphylaxis. The term
chest cardiac compressions in patients with asthma- anaphylactoid reaction is no longer used. An ana-
associated cardiac arrest. Working through the four phylactic reaction is generally defined as a severe,
Hs and four Ts will identify potentially reversible systemic allergic reaction characterized by multi-
courses of asthma related cardiac arrest. Tension system involvement, including the airway, vascular
pneumothorax can be difficult to diagnose in car- system, gastrointestinal tract and skin. Severe
diac arrest; it may be indicated by unilateral expan- cases may cause complete airway obstruction
sion of the chest wall, shifting of the trachea and secondary to laryngeal oedema, bronchospasm,
subcutaneous emphysema. Release air from the hypotension, cardiovascular collapse and death.
pleural space with needle decompression. Insert a Other symptoms include rhinitis, conjunctivitis,
large-gauge cannula in the second intercostal space abdominal pain, vomiting, diarrhoea and a sense
in the mid clavicular line, being careful to avoid of impending doom. There is also usually a colour
direct puncture of the lung. If air is emitted, insert change; the patient may appear either flushed or
a chest tube. Always consider bilateral pneumoth- pale. Anaphylactic reactions vary in severity, and
oraces in asthma-related cardiac arrest. progress may be rapid, slow or (unusually) biphasic.
Rarely, manifestations may be delayed (this may
occur with latex allergy), or persist for more than
Post-resuscitation care 24 h.
The following should be added to usual manage-
ment after ROSC: Pathophysiology

• Optimise the medical management of bron- Initial exposure to an allergen may trigger an
chospasm. immune response that sensitises the body to sub-
• Use permissive hypercapnia; it may not be pos- sequent exposure. This sensitisation results in
sible to achieve normal oxygenation and venti- antigen-specific IgE bound to the cell membrane of
lation in a patient with severe bronchospasm. basophils and mast cells. On repeat exposure, the
Efforts to achieve normal arterial blood gas val- antigen is bound by the IgE, triggering release of
ues may worsen lung injury. Mild hypoventilation a series of inflammatory mediators including his-
reduces the risk of barotraumas, and hypercap- tamines, leukotrienes, prostaglandins, thrombox-
noea is typically well-tolerated.163 Target lower anes and bradykinins. These mediators act system-
arterial blood oxygen saturations (e.g., 90%). ically to cause increased mucous membrane secre-
• Provide sedation (neuromuscular paralysis if tion, increased capillary permeability and markedly
needed) and controlled ventilation. Despite the reduced vascular smooth muscle tone. This causes
absence of formal studies, ketamine and inhala- the clinical symptoms of angioedema and airway
tional anaesthetics have bronchodilator proper- swelling, bronchospasm, hypotension and cardio-
ties that may be useful in the asthmatic patient vascular collapse.
who is difficult to ventilate. Anaphylaxis is caused by a hypersensitivity reac-
• Involve a senior critical care doctor early. tion in which histamine, serotonin and other
vasoactive substances are released from basophils
and mast cells in response to an IgE-mediated reac-
tion. Antigen-specific immunoglobulins are pro-
7g. Anaphylaxis duced after initial exposure to an allergen. Sub-
sequent re-exposure to this allergen provokes an
Introduction anaphylactic reaction, although many anaphylactic
reactions occur without known previous exposure.
Anaphylaxis is a rare, but potentially reversible,
cause of cardiac arrest. Although the management Aetiology
of cardiac arrest secondary to anaphylaxis follows
the general principles described elsewhere in these Although anaphylaxis is relatively common, pro-
guidelines, the pathophysiological processes occur- gression to a severe life-threatening reaction is
ring during anaphylaxis may require additional spe- rare. Any antigen capable of activating IgE can the-
cific therapy. oretically be a trigger for anaphylaxis. The com-
S152 J. Soar et al.

monest causes of life-threatening reactions are Signs and symptoms


drugs, stinging insects and food. In as many as 5%
of the cases, the antigen triggering the anaphylaxis Anaphylaxis should be considered when two or
cannot be identified. more body systems are affected (cutaneous, res-
piratory, cardiovascular, neurological or gastroin-
testinal), with or without cardiovascular or air-
Drugs way involvement. Symptoms may be particularly
severe in patients with asthma, those taking beta-
Neuromuscular blocking drugs (particularly suxam- adrenoceptor blockers and during neuraxial anaes-
ethonium) and antibiotics are the most common thesia: states associated with reduced endogenous
triggers for drug-induced anaphylaxis.164 Aspirin, catecholamine response. The speed of the onset of
non-steroidal anti-inflammatory drugs and IV con- signs and symptoms is related to the likely severity
trast agents are also common causes of life- of the ensuing anaphylaxis.
threatening anaphylaxis. Early signs and symptoms include urticaria, rhini-
tis, conjunctivitis, abdominal pain, vomiting and
Latex diarrhoea. Flushing is common but pallor may also
occur. Marked upper airway (laryngeal) oedema
Latex, or natural rubber, is a significant trigger of and bronchospasm may develop, causing stridor
anaphylaxis among hospitalised patients because of and wheezing (or high airway pressures in venti-
frequent instrumentation and operations in which lated patients). In asthmatics, this may be par-
latex products are used. Avoidance is the only ticularly severe and difficult to treat. Cardiovas-
effective therapy, and the availability of latex-free cular collapse is the most common peri-arrest
clinic and hospital environments, including patient manifestation. Vasodilation causes relative hypo-
and operating rooms, is now a priority.165 Life- volaemia, exacerbated by true volume loss as
threatening anaphylactic reactions to latex are very increased capillary permeability results in extrava-
rare166,167 with a decade-long registry of anaphy- sation of intravascular fluid. Additional cardiac dys-
lactic deaths in England not registering any latex- function may follow from underlying disease or
associated deaths.168,169 from the development of myocardial ischaemia
from adrenaline administration.168,169,171

Stinging insects
Differential diagnosis
The prevalence of IgE-mediated systemic reac-
tions to insect stings is 2.8% in temperate The lack of any consistent clinical manifestation
climates, although higher in countries, such as and a wide range of possible presentations may
Australia where exposure to insect stings is more cause diagnostic difficulty. In each case, take as
common.170 The stinging insects belong to the full a history and examination as possible. The his-
Hymenoptera order and include hornets, wasps, tory of previous allergic reactions, as well as that
honeybees and fire ants. Most stings cause local of the recent incident is important. Pay particular
reactions with pain and swelling at the site but attention to the condition of the skin, the pulse
progress to anaphylaxis in susceptible persons. rate, the blood pressure and the upper airways,
Fatal anaphylaxis occurs in people who are re-stung and auscultate the chest. Measure and record the
after a previous sting has induced IgE antibodies. peak flow where possible. Consider the diagnosis
Fatal reactions occur within 10—15 min, with car- of other conditions only after anaphylaxis has been
diovascular collapse being the commonest cause of excluded; failure to identify and treat anaphylaxis
death.168,169,171 can be fatal:173,174

• ACE inhibitors may cause angioedema with


Foods marked swelling of the upper airway. This reac-
tion may occur at any time and is not related to an
Life-threatening allergic reactions to food are initial exposure to the drug. The best treatment
increasing. Peanuts, seafood (in particular prawns for this form of angioedema is unclear, but early
and shellfish) and wheat are the foods asso- recognition and appropriate airway management
ciated most frequently with life-threatening are critical.175
anaphylaxis.172 Bronchospasm, angioedema, air- • Hereditary angioedema is familial and indistin-
way obstruction and asphyxia comprise the most guishable from the early angioedema of anaphy-
common fatal mechanism.168,169,171 laxis or drug-related angioedema. An important
European Resuscitation Council Guidelines for Resuscitation 2005 S153

distinguishing feature is the absence of urticaria tion can develop rapidly due to soft tissue swelling.
with hereditary angioedema. This is treated with Consider early tracheal intubation; delay may make
C1 esterase inhibitor, either as a specific concen- intubation extremely difficult.
trate or contained within fresh frozen plasma.
• Severe asthma may present with bronchospasm Oxygen
and stridor, which are also common features of
severe anaphylaxis. However, asthma attacks do Give high-flow oxygen (10—15 l min−1 ).
not usually present with urticaria or angioedema.
• Rarely, panic attacks may be associated with
functional stridor as a result of forced adduction Adrenaline
of the vocal cords. As with asthma, there is no
Give adrenaline intramuscularly to all patients with
urticaria, angioedema, hypoxia or hypotension.
clinical signs of shock, airway swelling or definite
• Vasovagal reactions cause sudden collapse and
breathing difficulty; adrenaline will be absorbed
extreme bradycardia that may be mistaken for
rapidly. Inspiratory stridor, wheeze, cyanosis, pro-
absence of a pulse. Recovery is usually rela-
nounced tachycardia and decreased capillary fill-
tively rapid, and is not associated with urticaria,
ing indicate a severe reaction. For adults, give
angioedema or bronchospasm.
an IM dose of adrenaline, 0.5 ml of 1:1000 solu-
tion (500 mcg). If the patient’s condition fails to
Considerations in relation to treatment improve, repeat the dose after about 5 min. In some
cases several doses may be needed, particularly if
Wide variations in aetiology, severity and organ
improvement is transient. The IM route is prefer-
involvement preclude standardised treatment rec-
able to SC administration because absorption is
ommendations. The lack of clinical trials necessi-
more rapid in shock.177,178
tates guidelines based on consensus opinion.
IV adrenaline (in a dilution of at least 1:10,000;
Adrenaline is generally agreed to be the most
never 1:1000) is hazardous and must be reserved
important drug for any severe anaphylactic reac-
for patients with profound shock that is immedi-
tion. As an alpha-agonist, it reverses peripheral
ately life threatening and for special indications,
vasodilation and reduces oedema. Its beta-agonist
for example during anaesthesia. A further 10-fold
properties dilate the airways, increase the force of
dilution to 1:100,000 adrenaline enables finer titra-
myocardial contraction and suppress histamine and
tion of the dose and increases its safety by reducing
leukotriene release.
the risk of unwanted adverse effects. This should
Adrenaline is most effective when given early
be carried out with a minimum of electrocardio-
after the onset of the reaction, but it is not without
graphic monitoring. Doctors experienced in the use
risk, particularly when given IV. When given intra-
of IV adrenaline may prefer to use the IV route in
muscularly, adrenaline is very safe. Adverse effects
any patient with signs of severe anaphylaxis.
are extremely rare, and the only patient reported
to have had a myocardial infarction after intra-
muscular injection had numerous risk factors for Antihistamine
coronary disease. Sometimes there has been uncer-
tainty as to whether complications (e.g., myocar- Give an H1 -antihistamine (e.g., chlorphenamine
dial ischaemia) have been due to the effects of the 10—20 mg) by slow IV injection. Consider also an
allergen itself or to adrenaline given as treatment H2 -blocker, e.g., ranitidine, 50 mg IV.179
for it.168,176
Rarely, adrenaline may fail to reverse the clinical Hydrocortisone
manifestations of anaphylaxis, particularly in late
reactions or in patients treated with beta-blockers. Give hydrocortisone by slow IV injection after
Other measures then assume greater importance, severe attacks to help avert late sequelae. This is
particularly volume replacement. particularly important for asthmatics (who are at an
increased risk of severe or fatal anaphylaxis) if they
General resuscitation measures have been treated with corticosteroids previously.
Corticosteroids are considered as slow-acting drugs
All victims should recline in a position of comfort. and may take up to 4—6 h to have an effect, even if
Remove the likely allergen (i.e., stop drug infusion given IV. However, they may help in the emergency
or blood transfusion). Lying flat, with or without leg treatment of an acute attack, and they also have
elevation, may be helpful for hypotension but not a role in preventing or shortening the protracted
helpful for breathing difficulties. Airway obstruc- reactions.
S154 J. Soar et al.

Inhaled bronchodilators Antihistamines

An inhaled beta2 agonist, such as salbutamol Give an antihistamine IV if antihistamine has not
(5 mg, repeated if necessary), may help reverse already been given before the arrest.179
the refractory bronchospasm. Inhaled ipratropium
(500 mcg, repeated as necessary) may be partic-
ularly useful for the treatment of bronchospasm Steroids
in patients on beta-blockers. Some cases of near-
fatal asthma may really be anaphylaxis, resulting Steroids given during a cardiac arrest will have little
in mistaken overtreatment with conventional bron- immediate effect but, if ROSC is restored, they may
chodilators rather than more specific treatment be effective in the post-resuscitation period.
with adrenaline.141
Prolonged CPR
Intravenous fluids
Patients with anaphylaxis are often young, with
If severe hypotension does not respond rapidly to
healthy hearts and cardiovascular systems. Effec-
drug treatment, give fluid; a rapid infusion of 1—2 l
tive CPR may maintain sufficient oxygen delivery
may be required. Further fluid is likely to be nec-
until the catastrophic effects of the anaphylactic
essary.
reaction resolve.
Potential therapies

Vasopressin. There are case reports that Airway obstruction


vasopressin may benefit severely hypotensive
Airway obstruction may occur rapidly in severe ana-
patients.180,181
phylaxis, particularly in patients with angioedema.
Atropine. Case reports also suggest that, when Warning signs are lingual and labial swelling,
relative or severe bradycardia is present, there may hoarseness and oropharyngeal swelling. Consider
be a role for atropine.174 early, elective intubation. As airway obstruction
progresses, both LMAs and Combitubes are likely
Glucagon. For patients unresponsive to to be difficult to insert. Tracheal intubation and
adrenaline, especially those receiving beta- cricothyroidotomy will also become increasingly
blockers, glucagon may be effective. This agent difficult. Attempts at tracheal intubation may exac-
is short-acting (1—2 mg every 5 min IM, or IV). erbate laryngeal oedema. Early involvement of a
Nausea, vomiting and hyperglycaemia are common senior anaesthetist is mandatory when managing
side effects. these patients.

Envenomation
Observation
Rarely, insect envenomation by bees, but not
wasps, leaves a venom sac. Immediately scrape Warn patients with even moderate attacks of the
away any insect parts at the site of the sting.182 possibility of an early recurrence of symptoms and,
Squeezing may increase envenomation. in some circumstances, keep them under observa-
tion for 8—24 h. This caution is particularly applica-
Cardiac arrest ble to:

In addition to the ALS drugs, consider the following • severe reactions with slow onset due to idio-
therapies. pathic anaphylaxis;
• reactions in severe asthmatics or with a severe
Rapid fluid resuscitation asthmatic component;
• reactions with the possibility of continuing
Near-fatal anaphylaxis produces profound vasodila- absorption of allergen;
tion and a relative hypovolaemia. Massive volume • patients with a previous history of biphasic
replacement is essential. Use at least two large- reactions.179,183—187
bore cannulae with pressure bags to give large vol-
umes (as much as 4—8 l IV fluid may be necessary in A patient who remains symptom-free for 4 h after
the immediate resuscitation period). treatment may be discharged.188
European Resuscitation Council Guidelines for Resuscitation 2005 S155

Investigations and further management Diagnosis

Measurement of mast cell tryptase may help with An immediate decision on the likely cause of car-
retrospective diagnosis of anaphylaxis.189,190 Take diac arrest must be made to enable rapid interven-
three 10-ml clotted blood samples: tion and successful resuscitation. Auscultation of
the chest, examination of the ECG and chest radio-
• immediately after the reaction has been treated; graph, transoesophageal/transthoracic echocardio-
• about 1 h after reaction; graphy and measurement of blood loss from chest
• about 6 h and up to 24 h after reaction. drains will aid in identifying the cause of the arrest.
Actively seek and exclude reversible causes of car-
It is important to identify the allergen after suc-
diac arrest: the four Hs and four Ts. Myocardial
cessful resuscitation from anaphylaxis, to prevent
ischaemia often causes myocardial irritability and
recurrence. Refer the patient to a specialist clinic.
progressive hypotension before an arrest. A tension
Patients at very high risk of anaphylaxis may carry
pneumothorax and cardiac tamponade will cause
their own adrenaline syringe for self-administration
progressive hypotension and an increasing central
and wear a ‘MedicAlert’ type bracelet. Report reac-
venous pressure. Increasing airway pressures and
tions to drugs to the appropriate monitoring agency.
poor air entry in the affected lung will differenti-
ate between the two conditions. Lack of drainage of
blood from the chest drains does not exclude haem-
7h. Cardiac arrest following cardiac orrhage or tamponade, because drains may block
surgery with clot.

Cardiac arrest following major cardiac surgery Treatment


(both on and off bypass) is relatively common in the
immediate postoperative phase, with a reported Treatment of cardiac arrest following cardiac
incidence of 0.7% in the first 24 h191 and 1.4% surgery follows the same principles of BLS and
within the first 8 days.192 Cardiac arrest is usu- ALS that have already been described in these
ally caused by specific pathology that is reversible guidelines. Seek assistance from experienced clin-
if treated promptly and appropriately, and there- icians without delay. Exclude immediately cor-
fore, has a relatively high survival rate. Car- rectable causes, such as pacing-lead disconnection
diac arrest is usually preceded by physiological and tension pneumothorax. Extreme bradycardia or
deterioration,193 although it may occur suddenly asystole may respond to pacing via internal pacing-
in stable patients.191 Continuous monitoring on the wires (if present) connected to an external pace-
intensive care unit (ICU) enables immediate inter- maker. Ensure correction of hypo/hyperkalaemia
vention at the time of arrest. Survival to hospi- and hypomagnesaemia. Rapid restoration of an ade-
tal discharge of patients suffering from cardiac quate blood volume is important, ensuring that
arrest during the first 24 h after adult cardiac haemoglobin levels are maintained no lower than
surgery is reported as 54%192 —79%191,194 and 41% 8.0 g dl−1 . Be careful when giving IV adrenaline, as
in children.193 the resulting hypertension may cause catastrophic
failure of anastomoses.
Aetiology
External chest compressions
Perioperative myocardial infarction is the common-
est cause of sudden cardiac arrest and is often sec- External chest compressions may be necessary but
ondary to graft occlusion.191,192 may cause sternal subluxation, fractured ribs and
The main causes of cardiac arrest in the initial damage to grafts. Continuous observation of the
postoperative period include: invasive blood pressure will enable the force of
compression to be optimised. Effective external
• myocardial ischaemia; chest compressions should take precedence over
• tension pneumothorax; the concerns of damage to grafts.
• haemorrhage causing hypovolaemic shock;
• cardiac tamponade; Internal cardiac massage
• disconnection of pacing system in pacing-
dependent patient; Mechanical factors (e.g., haemorrhage, tampon-
• electrolyte disturbances (particularly hypo/ ade, graft occlusion) account for a substantial
hyperkalaemia). proportion of causes of sudden cardiac arrest
S156 J. Soar et al.

occurring in haemodynamically stable patients dur- Internal defibrillation


ing the immediate postoperative period.191 Correc-
tion of this pathology may require chest reopen- Internal defibrillation using paddles applied directly
ing and therefore internal cardiac massage. Up across the ventricles requires considerably less
to 10% of patients may need chest reopening fol- energy than that used for external defibrillation.
lowing cardiac surgery.195 Overall survival to dis- Biphasic shocks are substantially more effective
charge the following internal cardiac massage is than the monophasic shocks for direct defibrilla-
17%196 —25%.195 Cardiac arrest on the ICU, arrest tion. For biphasic shocks, starting at 5 J creates
within 24 h of surgery, and reopening within 10 min the optimum conditions for lowest threshold and
of arrest are independent predictors of survival.195 cumulative energy, whereas 10 or 20 J offers opti-
The high incidence of potentially correctable mum conditions for more rapid defibrillation and
mechanical causes of arrest, in conjunction with fewer shocks.200 Monophasic shocks require approx-
the high survival rate achieved by open CPR, sup- imately double these energy levels.200
ports an early approach to open-chest CPR in these
patients.191,197 Reopen the patient’s chest imme-
diately if there is no output with external chest 7i. Traumatic cardiorespiratory arrest
compressions or if there is a shockable rhythm
refractory to cardioversion. Management of asys- Introduction
tole usually requires prompt chest opening. Open-
ing of the chest is relatively straightforward and, Cardiac arrest secondary to traumatic injury has
if indicated, should be undertaken within 10 min of a very high mortality, with an overall survival of
cardiac arrest. Consider training the non-surgical just 2.2% (range, 0—3.7%) (Table 7.4).201—207 In
medical staff to open the wound and remove ster- those who survive, neurological disability is com-
nal wires, while a surgeon is summoned. Make sure mon, being absent in only 0.8% of those suffering
that a chest opening kit is immediately available on from traumatic cardiorespiratory arrest (TCRA).
the ICU. The invasive blood pressure will guide the
effectiveness of internal cardiac massage Remove Diagnosis of traumatic cardiorespiratory
the blood clot carefully, either manually or by suc- arrest
tioning, to avoid damaging the grafts. Early iden-
tification and treatment of underlying pathology is The diagnosis of TCRA is made clinically: the trauma
challenging under these circumstances and requires patient is unresponsive, apnoeic and pulseless. Both
an experienced surgeon. asystole and organised cardiac activity without car-
diac output are regarded as TCRA.
Reinstitution of emergency cardiopulmonary
bypass Commotio cordis
The need for emergency cardiopulmonary bypass Commotio cordis is actual or near cardiac arrest
(CPB) may occur in approximately 0.8% patients, caused by a blunt impact to the chest wall over
occurring at a mean of 7 h postoperatively,198 and the heart.208—211 A blow on the chest during the
is usually indicated to correct surgical bleeding or vulnerable phase of the cardiac cycle may cause
graft occlusion and rest an exhausted myocardium. malignant arrhythmias (usually VF). Syncope after
Emergency institution of CPB should be available chest wall impact may be caused by non-sustained
on all units undertaking cardiac surgery. Survival to arrhythmic events. Commotio cordis occurs mostly
discharge the rates of 32%,195 42%198 and 56.3%199 during sports (most commonly baseball) and recre-
have been reported when CPB is reinstituted on the ational activities, and victims are usually young
ICU. Survival rates decline rapidly when this pro- males (mean age 14 years). The Commotio Cordis
cedure is undertaken more than 24 h after surgery Registry in Minneapolis is accruing 5—15 cases of
and when performed on the ward rather than the commotio cordis each year. The overall survival rate
ICU. Emergency CPB should probably be restricted from commotio cordis is 15%, but reaches 25% if
to patients who arrest within 72 h of surgery, as resuscitation is started within 3 min.211
surgically remediable problems are unlikely after
this time.195 Ensuring adequate re-anticoagulation Trauma secondary to medical events
before commencing CPB, or the use of a heparin-
bonded CPB circuit, is important. The need for a A cardiorespiratory arrest caused by a medi-
further period of aortic cross-clamping does not cal pathology (e.g., cardiac arrhythmia, hypo-
preclude a favourable outcome.198 glycaemia, seizure) may precipitate a secondary
European Resuscitation Council Guidelines for Resuscitation 2005 S157

traumatic event (e.g., fall, road traffic accident, but treatment on scene should focus on good qual-
etc.). Traumatic injuries may not be the primary ity BLS and ALS and exclusion of reversible causes.
cause of a cardiorespiratory arrest. Look for and treat any medical condition that may
have precipitated the trauma event. Undertake
only the essential lifesaving interventions on scene
Mechanism of injury
and, if the patient has signs of life, transfer rapidly
Blunt trauma to the nearest appropriate hospital. Consider on-
scene thoracostomy for appropriate patients.227,228
Of 1242 patients with cardiac arrest after blunt Do not delay for unproven interventions, such as
trauma, 19 (1.5%) survived, but only 2 (0.16%) had spinal immobilisation.229
a good neurological outcome (Table 7.4).
Resuscitative thoracotomy
Penetrating trauma
Prehospital. Resuscitative thoracotomy has been
Of 839 patients with cardiac arrest after pene- reported as futile if out-of-hospital time has
trating injury, there were 16 (1.9%) survivors, of exceeded 30 min;225 others consider thoracotomy
whom 12 (1.4%) had a good neurological outcome to be futile in patients with blunt trauma requiring
(Table 7.4). more than 5 min of prehospital CPR and in patients
with penetrating trauma requiring more than 15 min
Signs of life and initial ECG activity of CPR.226 With these time limits in mind, one UK
service recommends that, if surgical intervention
There are no reliable predictors of survival for cannot be accomplished within 10 min after loss
TCRA. One study reported that the presence of of pulse in patients with penetrating chest injury,
reactive pupils and sinus rhythm correlated signif- on-scene thoracotomy should be considered.227
icantly with survival.217 In a study of penetrating Following this approach, of 39 patients who
trauma, pupil reactivity, respiratory activity and underwent thoracotomy at scene, 4 patients sur-
sinus rhythm were correlated with survival but were vived and 3 of these made a good neurological
unreliable.207 Three studies reported no survivors recovery.
among patients presenting with asystole or agonal
rhythms.202,207,218 Another reported no survivors in Hospital. A relatively simple technique for
PEA after blunt trauma.219 Based on these studies, resuscitative thoracotomy has been described
the American College of Surgeons and the National recently.228,230 The American College of Surgeons
Association of EMS Physicians produced prehospi- has published practice guidelines for emergency
tal guidelines on withholding resuscitation.220 They department thoracotomy (EDT) based on a meta-
recommend withholding resuscitation in: analysis of 42 outcome studies including 7035
EDTs.231 The overall survival rate was 7.8%, and
• blunt trauma victims presenting apnoeic and of 226 survivors (5%), only 34 (15%) exhibited a
pulseless, and without organised ECG activity; neurological deficit. The investigators concluded
• penetrating trauma victims found apnoeic and the following:
pulseless after rapid assessment for signs of life,
such as pupillary reflexes, spontaneous move- • After blunt trauma, EDT should be limited to
ment or organised ECG activity. those with vital signs on arrival and a witnessed
cardiac arrest (estimated survival rate 1.6%).
A recent retrospective study questions these • Emergency department thoracotomy is best
recommendations: in a series of 184 TCRA vic- applied to patients with penetrating cardiac
tims, several survivors met the criteria for non- injuries, who arrive at the trauma centre after
resuscitation.221 short on-scene and transport times, with wit-
nessed signs of life or ECG activity (estimated
Treatment survival rate 31%).
• Emergency department thoracotomy should be
Survival from TCRA is correlated with duration of undertaken in penetrating non-cardiac thoracic
CPR and prehospital time.205,222—226 Prolonged CPR injuries even though survival rates are low.
is associated with a poor outcome; the maximum • Emergency department thoracotomy should be
CPR time associated with a favourable outcome is undertaken in patients with exsanguinating
16 min.205,222—224 The level of prehospital interven- abdominal vascular injury even though survival
tion will depend on the skills of local EMS providers, rates are low. This procedure should be used as
S158 J. Soar et al.

Table 7.4 Survival after traumatic cardiac arrest


Source Entry criteria Number of survivors Number of survivors of Number of survivors
neurologically intact penetrating trauma of blunt trauma
neurologically intact neurologically intact
Bouillon212 Pulseless, requiring 224
CPR at scene 4
3
Battistella202 Pulseless, requiring 604 300 304
CPR at scene, en route 16 12 4
or in ED 9 9 0
Pasquale206 CPR before or on 106 21 85
hospital admission 3 1 2
Fisher213 Children requiring CPR 65 38
before or on admission 1 1
after blunt trauma 0 0
Hazinski214 Children requiring CPR 38 65
or being severely 1 1
hypotensive on 0 0
admission after blunt
trauma
Shimazu203 TCRA on admission 267
7
4

Calkins215 Children requiring CPR 25 25


after blunt trauma 2 2
2 2
Yanagawa216 OHCA in blunt trauma 332 332
6 6
0 0
Rosemurgy201 CPR before admission 138 42 96
0 0 0
0 0 0
Stratton207 Unconscious, pulseless 879 497 382
at scene 9 4 5
3 3 0
Cera217 CPR on admission 161
15
?
For each study, the first number indicates the number of patients in cardiac arrest, the second indicates the numbers of sur-
vivors and the third indicates the number of survivors with a good neurological outcome. CPR = cardiopulmonary resuscitation;
ED = emergency department; TCRA = traumatic cardiorespiratory arrest; OHCA = out-of-hospital cardiac arrest.

an adjunct to definitive repair of abdominal vas- vivors who were intubated in the field was 9.1 min
cular injury. versus 4.2 min for those who were not intubated.224
Tracheal intubation of trauma victims is a dif-
Airway management ficult procedure with a high failure rate if car-
ried out by less experienced care providers.232—235
Effective airway management is essential to main- Use the basic airway management manoeuvres and
tain oxygenation of the severely compromised alternative airways to maintain oxygenation if tra-
trauma victim. In one study, tracheal intubation on- cheal intubation cannot be accomplished immedi-
scene of patients with TCRA doubled the tolerated ately. If these measures fail, a surgical airway is
period of CPR, i.e., the mean time of CPR for sur- indicated.
European Resuscitation Council Guidelines for Resuscitation 2005 S159

Ventilation servative approach to IV fluid infusion, with per-


missive hypotension until surgical haemostasis is
In low cardiac output states positive pressure ven- achieved.241,242 In the UK, the National Institute for
tilation causes further circulatory depression, or Clinical Excellence (NICE) has published guidelines
even cardiac arrest, by impeding venous return to on prehospital fluid replacement in trauma.243 The
the heart.236 Monitor ventilation with capnome- recommendations include giving 250 ml boluses of
try and adjust to achieve normocapnia. This may crystalloid solution until a radial pulse is achieved,
enable slow respiratory rates and low tidal volumes, and not delaying rapid transport of trauma victims
and the corresponding decrease in transpulmonary for fluid infusion in the field. Prehospital fluid ther-
pressure may increase venous return and cardiac apy may have a role in prolonged entrapments, but
output. there is no reliable evidence for this.244,245

Chest decompression
Ultrasound
Effective decompression of a tension pneumothorax
can be achieved quickly by lateral thoracostomy, Ultrasound is a valuable tool in the evaluation of the
which is likely to be more effective than needle compromised trauma victim. Haemoperitoneum,
thoracostomy and quicker than inserting a chest haemo- or pneumothorax and cardiac tamponade
tube.237 can be diagnosed reliably in minutes even in the
prehospital phase.246 Diagnostic peritoneal lavage
Effectiveness of chest compressions in TCRA and needle pericardiocentesis have virtually disap-
peared from clinical practice since the introduction
In hypovolaemic cardiac arrest or cardiac tam- of sonography in trauma care. Prehospital ultra-
ponade, chest compressions are unlikely to be as sound is now available, although its benefits are yet
effective as in cardiac arrest from other causes;238 to be proven.
nonetheless, return of spontaneous circulation with
ALS in patients with TCRA is well described. Chest
compressions are still the standard of care in Vasopressors
patients with cardiac arrest, irrespective of aeti-
The possible role of vasopressors (e.g., vasopressin)
ology.
in trauma resuscitation is unclear and is based
mainly on case reports.247
Haemorrhage control

Early haemorrhage control is vital. Handle the


patient gently at all times, to prevent clot disrup-
tion. Apply external compression and pelvic and
7j. Cardiac arrest associated with
limb splints when appropriate. Delays in surgical pregnancy
haemostasis are disastrous for patients with exsan-
guinating trauma. Overview

Pericardiocentesis Mortality related to pregnancy in developed coun-


tries is rare, occurring in an estimated 1:30,000
In patients with suspected trauma-related cardiac deliveries.248 The fetus must always be considered
tamponade, needle pericardiocentesis is probably when an adverse cardiovascular event occurs in a
not a useful procedure.239 There is no evidence pregnant woman. Resuscitation guidelines for preg-
of benefit in the literature. It may increase scene nancy are based largely on case series and scientific
time, cause myocardial injury and delay effective rationale. Most reports address the causes in devel-
therapeutic measures, such as emergency thoraco- oped countries, whereas the majority of pregnancy-
tomy. related deaths occur in the developing world.
Significant physiological changes occur during
Fluids and blood transfusion on scene pregnancy, e.g., cardiac output, blood volume,
minute ventilation and oxygen consumption all
Fluid resuscitation of trauma victims before haem- increase. Furthermore, the gravid uterus may cause
orrhage is controlled is controversial, and there is significant compression of iliac and abdominal ves-
no clear consensus on when it should be started sels when the mother is in the supine position,
and what fluids should be given.240 Limited evi- resulting in reduced cardiac output and hypoten-
dence and general consensus support a more con- sion.
S160 J. Soar et al.

Causes of the diaphragm and abdominal contents caused


by the gravid uterus. Attempt defibrillation using
There are many causes of cardiac arrest in pregnant standard energy doses.252 There is no evidence
women. A review of nearly 2 million pregnancies in that shocks from a direct current defibrillator have
the UK248 showed that maternal death was associ- adverse effects on the fetal heart. Left lateral tilt
ated with: and large breasts will make it difficult to place an
apical defibrillator paddle. Adhesive defibrillator
• pre-existing cardiac disease;
pads are preferable to paddles in pregnancy.
• thromboembolism;
• suicide;
• hypertensive disorders of pregnancy; Modifications to advanced life support
• sepsis;
There is a greater potential for gastro-oesophageal
• ectopic pregnancy;
sphincter insufficiency and risk of pulmonary aspi-
• haemorrhage;
ration of gastric contents. Early tracheal intubation
• amniotic fluid embolism;
with correctly applied cricoid pressure decreases
Pregnant women can also suffer the same causes this risk. Tracheal intubation will make ventilation
of cardiac arrest as women of the same age of the lungs easier in the presence of increased
group. intra-abdominal pressure.
A tracheal tube 0.5—1 mm internal diameter (ID)
Key interventions to prevent cardiac arrest smaller than that used for a non-pregnant woman
of similar size may be necessary because of mater-
In an emergency, use an ABCDE approach. Many nal airway narrowing from oedema and swelling.253
cardiovascular problems associated with pregnancy Tracheal intubation may be more difficult in the
are caused by caval compression. Treat a distressed pregnant patient.254 Expert help, a failed intuba-
or compromised pregnant patient as follows: tion drill and the use of alternative airway devices
may be needed (see section 4d).255
• Place the patient in the left lateral position or
manually and gently displace the uterus to the
Reversible causes
left.
• Give 100% oxygen. Rescuers should attempt to identify common and
• Give a fluid bolus. reversible causes of cardiac arrest in pregnancy
• Immediately re-evaluate the need for any drugs during resuscitation attempts. The 4 Hs and 4 Ts
being given. approach helps to identify all the common causes of
• Seek expert help early. cardiac arrest in pregnancy. Pregnant patients are
at risk of all the other causes of cardiac arrest for
Modifications to BLS guidelines for cardiac their age group (e.g., anaphylaxis, drug overdose,
arrest trauma). Consider the use of abdominal ultrasound
by a skilled operator to detect pregnancy and possi-
After 20 weeks’ gestation, the pregnant woman’s ble causes during cardiac arrest in pregnancy; how-
uterus can press down against the inferior vena cava ever, do not delay other treatments. Specific causes
and the aorta, impeding venous return and cardiac of cardiac arrest in pregnancy include the follow-
output. Uterine obstruction of venous return can ing:
cause