Resuscitation 95 (2015) 100–147
Contents lists available at ScienceDirect
Resuscitation
journal homepage: www.elsevier.com/locate/resuscitation
European Resuscitation Council Guidelines for Resuscitation 2015
Section 3. Adult advanced life support
Jasmeet Soara,∗
, Jerry P. Nolanb,c
, Bernd W. Böttigerd
, Gavin D. Perkinse,f
, Carsten Lottg
,
Pierre Carlih
, Tommaso Pellisi
, Claudio Sandronij
, Markus B. Skrifvarsk
, Gary B. Smithl
,
Kjetil Sundem,n
, Charles D. Deakino
, on behalf of the Adult advanced life support section
Collaborators1
a
Anaesthesia and Intensive Care Medicine, Southmead Hospital, Bristol, UK
b
Anaesthesia and Intensive Care Medicine, Royal United Hospital, Bath, UK
c
School of Clinical Sciences, University of Bristol, UK
d
Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Germany
e
Warwick Medical School, University of Warwick, Coventry, UK
f
Heart of England NHS Foundation Trust, Birmingham, UK
g
Department of Anesthesiology, University Medical Center, Johannes Gutenberg-University, Mainz, Germany
h
SAMU de Paris, Department of Anaesthesiology and Intensive Care, Necker University Hospital, Paris, France
i
Anaesthesia, Intensive Care and Emergency Medical Service, Santa Maria degli Angeli Hospital, Pordenone, Italy
j
Department of Anaesthesiology and Intensive Care, Catholic University School of Medicine, Rome, Italy
k
Division of Intensive Care, Department of Anaesthesiology, Intensive Care and Pain Medicine, Helsinki University Hospital and Helsinki University,
Helsinki, Finland
l
Centre of Postgraduate Medical Research & Education, Bournemouth University, Bournemouth, UK
m
Department of Anaesthesiology, Division of Emergencies and Critical Care, Oslo University Hospital, Oslo, Norway
n
Institute of Clinical Medicine, University of Oslo, Oslo, Norway
o
Cardiac Anaesthesia and Cardiac Intensive Care, NIHR Southampton Respiratory Biomedical Research Unit, University Hospital Southampton,
Southampton, UK
Introduction
Adult advanced life support (ALS) includes advanced interventions
after basic life support has started and when appropriate an
automated external defibrillator (AED) has been used. Adult basic
life support (BLS) and use of AEDs is addressed in Section 2. The
transition between basic and advanced life support should be seamless
as BLS will continue during and overlap with ALS interventions.
This section on ALS includes the prevention of cardiac arrest, specific
aspects of prehospital ALS, starting in-hospital resuscitation,
the ALS algorithm, manual defibrillation, airway management during
CPR, drugs and their delivery during CPR, and the treatment
of peri-arrest arrhythmias. There are two changes in the presentation
of these guidelines since European Resuscitation Council (ERC)
Guidelines 2010.1 There is no longer a separate section on electrical
therapies2 and the ALS aspects are now part of this section.
Post-resuscitation care guidelines are presented in a new section
(Section 5) that recognises the importance of the final link in the
Chain of Survival.3
∗ Corresponding author.
E-mail address: jasmeet.soar@nbt.nhs.uk (J. Soar).
1
The members of the Adult advanced life support section Collaborators are listed
in the Collaborators section.
These Guidelines are based on the International Liaison Committee
on Resuscitation (ILCOR) 2015 Consensus on Science and
Treatment Recommendations (CoSTR) for ALS.4 The 2015 ILCOR
review focused on 42 topics organised in the approximate sequence
of ALS interventions: defibrillation, airway, oxygenation and ventilation,
circulatory support, monitoring during CPR, and drugs
during CPR. For these Guidelines the ILCOR recommendations were
supplemented by focused literature reviews undertaken by the ERC
ALS Writing Group for those topics not reviewed in the 2015 ILCOR
CoSTR. Guidelines were drafted and agreed by the ALS Writing
Group members before final approval by the ERC General Assembly
and ERC Board.
Summary of changes since 2010 Guidelines
The 2015 ERC ALS Guidelines have a change in emphasis aimed
at improved care and implementation of these guidelines in order
to improve patient focused outcomes.5 The 2015 ERC ALS Guidelines
do not include any major changes in core ALS interventions
since the previous ERC guidelines published in 2010.1,2 The key
changes since 2010 are:
• Continuing emphasis on the use of rapid response systems for
care of the deteriorating patient and prevention of in-hospital
cardiac arrest.
• Continued emphasis on minimally interrupted high-quality
chest compressions throughout any ALS intervention: chest
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J. Soar et al. / Resuscitation 95 (2015) 100–147 101
compressions are paused briefly only to enable specific interventions.
This includes minimising interruptions in chest
compressions to attempt defibrillation.
• Keeping the focus on the use of self-adhesive pads for defibrillation
and a defibrillation strategy to minimise the preshock pause,
although we recognise that defibrillator paddles are used in some
settings.
• There is a new section on monitoring during ALS with an
increased emphasis on the use of waveform capnography to confirm
and continually monitor tracheal tube placement, quality of
CPR and to provide an early indication of return of spontaneous
circulation (ROSC).
• There are a variety of approaches to airway management during
CPR and a stepwise approach based on patient factors and the
skills of the rescuer is recommended.
• The recommendations for drug therapy during CPR have not
changed, but there is greater equipoise concerning the role of
drugs in improving outcomes from cardiac arrest.
• The routine use of mechanical chest compression devices is not
recommended, but they are a reasonable alternative in situations
where sustained high-quality manual chest compressions
are impractical or compromise provider safety.
• Peri-arrest ultrasound may have a role in identifying reversible
causes of cardiac arrest.
• Extracorporeal life support techniques may have a role as a rescue
therapy in selected patients where standard ALS measures are not
successful.
3a – Prevention of in-hospital cardiac arrest
Early recognition of the deteriorating patient and prevention of
cardiac arrest is the first link in the chain of survival.3 Once cardiac
arrest occurs, only about 20% of patients who have an in-hospital
cardiac arrest will survive to go home.6,7
The key recommendations for the prevention of in-hospital cardiac
arrest are unchanged since the previous guidance in 2010.1
We suggest an approach to prevention of in-hospital cardiac arrest
that includes staff education, monitoring of patients, recognition
of patient deterioration, a system to call for help and an effective
response – the chain of prevention.8
The problem
Cardiac arrest in patients in unmonitored ward areas is not
usually a sudden unpredictable event.9 Patients often have slow
and progressive physiological deterioration, involving hypoxaemia
and hypotension that is unnoticed or poorly managed
by ward staff.10–12 The initial cardiac arrest rhythm is usually
non-shockable6,7 and survival to hospital discharge is poor, particularly
in patients with preceding signs of respiratory depression
or shock.7,13 Early and effective treatment might prevent some
cardiac arrests, deaths and unanticipated ICU admissions. Studies
conducted in hospitals with traditional cardiac arrest teams have
shown that patients attended by the team but who were found not
to have a cardiac arrest, have a high morbidity and mortality.14–16
Registry data from the US suggests that hospitals with lowest incidence
of IHCA also have the highest CA survival.17
Nature of the deficiencies in the recognition and response to
patient deterioration
These include infrequent, late or incomplete vital signs assessments;
lack of knowledge of normal vital signs values; poor design
of vital signs charts; poor sensitivity and specificity of ‘track and
trigger’ systems; failure of staff to increase monitoring or escalate
care, and staff workload.18–26 Problems with assessing and
treating airway, breathing and circulation abnormalities as well
organisational problems such as poor communication, lack of teamwork
and insufficient use of treatment limitation plans are not
infrequent.10,27,28
Education in acute care
Several studies show that medical and nursing staff lack knowledge
and skills in acute care,29–37 e.g. oxygen therapy,30 fluid
and electrolyte balance,31 analgesia,32 issues of consent,33 pulse
oximetry,30,34,35 and drug doses.36 Staff education is an essential
part of implementing a system to prevent cardiac arrest but to date,
randomised controlled studies addressing the impact of specific
educational interventions are lacking.37
In one study, virtually all the improvement in the hospital
cardiac arrest rate occurred during the educational phase of implementation
of a medical emergency team (MET) system.38,39 Rapid
response teams, such as METs, play a role in educating and improving
acute care skills of ward personnel.37,40 The introduction of
specific, objective calling criteria,41 referral tools42 and feedback
to caregivers43 has resulted in improved MET use and a significant
reduction in cardiac arrests. Another study found that the number
of cardiac arrest calls decreased while pre-arrest calls increased
after implementing a standardised educational programme44 in
two hospitals45; this was associated with a decrease in CA incidence
and improved CA survival. Other research suggests that multiprofessional
education did not alter the rate of mortality or staff
awareness of patients at risk on general wards.46
Monitoring and recognition of the critically ill patient
Clinical signs of acute illness are similar whatever the underlying
process, as they reflect failing respiratory, cardiovascular and
neurological systems. Alterations in physiological variables, singly
or in combination are associated with, or can be used to predict
the occurrence of cardiac arrest,12,47–50 hospital death20,21,51–68
and unplanned ICU admission,47,66,69,70 and with increasing magnitude
and number of derangements the likelihood of death is
increased.18,47,48,63,71–79 Even though abnormal physiology is common
on general wards,80 the measurement and documentation of
vital signs is suboptimal.9,11,22,49,81–83 To assist in the early detection
of critical illness, each patient should have a documented plan
for vital signs monitoring including which physiological measurements
needs no be undertaken and frequency.24,84
Many hospitals use early warning scores (EWS) or calling criteria
to identify ward patients needing escalation of care,22,49,82,85–89
and this increases vital signs monitoring.82,88,89 These calling criteria
or ‘track and trigger’ systems include single-parameter systems,
multiple-parameter systems, aggregate weighted scoring systems
or combination systems.90 Aggregate weighted track and trigger
systems offer a graded escalation of care, whereas single parameter
track and trigger systems provide an all-or-nothing response. Simpler
systems may have advantages over more complex ones.91,92
Nurse concern may also be an important predictor of patient
deterioration.93–95
The use of an aggregate score based on a number of vital
sign abnormalities appears more important than abnormalities
in a single criteria.96,97 Aggregate-weighted scoring systems vary
in their performance and in which endpoint they predict.20,70,98
In older (>65 year) patients, who represent the largest group of
IHCA patients,99 signs of deterioration before cardiac arrest are
often blunted, and the predictive value of the Modified Early Warning
Score (MEWS) progressively decreases with increasing patient
age.100
The design of vital signs charts19,101 or the use of
technology102–104 may have an important role in the detection of
102 J. Soar et al. / Resuscitation 95 (2015) 100–147
deterioration and the escalation of care, but these require further
study. Possible benefits include increased vital signs recording,105
improved identification of signs of deterioration,19,101,104 reduced
time to team activation103 and improved patient outcomes.103,106
Calling for help and the response to critical illness
Nursing staff and junior doctors often find it difficult to ask for
help or escalate treatment as they feel their clinical judgement
may be criticised.107–110 In addition, there is a common belief,
especially amongst younger staff, that the patient’s primary team
should be capable of dealing with problems close to their area of
specialty.110 It is logical that hospitals should ensure all staff are
empowered to call for help and also trained to use structured communication
tools such as RSVP (reason-story-vital signs-plan)111
or SBAR (situation-background-assessment-recommendation)112
tools to ensure effective inter-professional communication. However,
recent research suggests that structured communication tools
are rarely used in clinical practice.113
The response to patients who are critically ill or who are
at risk of becoming critically ill is now usually provided by a
medical emergency team (MET), rapid response team (RRT), or
critical care outreach team (CCOT).114–117 These replace or coexist
with traditional cardiac arrest teams, which typically respond to
patients already in cardiac arrest. MET/RRT usually comprise medical
and nursing staff from intensive care and general medicine,
who respond to specific calling criteria. Any member of the healthcare
team can initiate a MET/RRT/CCOT call. In some hospitals,
the patient, and their family and friends, are also encouraged
to activate the team.118–120 Team interventions often involve
simple tasks such as starting oxygen therapy and intravenous
fluids.121–125 However, post-hoc analysis of the MERIT study data
suggests that nearly all MET calls required ‘critical care-type’
interventions.126 The MET, RRT or CCOT is often also involved in
discussions regarding ‘do not attempt cardiopulmonary resuscitation’
(DNACPR) or end-of-life plans.127–133 Recently, attempts have
been made to develop a screening tool to identify patients at the end
of life and quantify the risk of death in order to minimise prognostic
uncertainty and avoid potentially harmful and futile treatments.134
Studying the effect of the MET/RRT/CCOT systems on patient
outcomes is difficult because of the complex nature of the intervention.
During the period of most studies of rapid response teams,
there has been a major international focus on improving other
aspects of patient safety, e.g. hospital acquired infections, earlier
treatment of sepsis and better medication management, all of
which have the potential to influence patient deterioration and may
have a beneficial impact on reducing cardiac arrests and hospital
deaths. Most studies on RRT/MET systems to date originate from
the USA and Australia and the systems effectiveness in other health
care systems in not clear.135
A well-designed, cluster-randomised controlled trial of the MET
system (MERIT study) involving 23 hospitals22 did not show a
reduction in cardiac arrest rate after introduction of a MET when
analysed on an intention-to-treat basis. Both the control and MET
groups demonstrated improved outcome compared to baseline.
Post hoc analysis of the MERIT study showed there was a decrease in
cardiac arrest and unexpected mortality rate with increased activation
of the MET system.136 The evidence from predominantly
single centre observational studies is inconclusive, with some studies
showing reduced numbers of cardiac arrests after MET/RRT
implementation38,41,123,137–159 and some studies failing to show a
reduction121,122,124,125,160–163. However, systematic reviews, metaanalyses
and multicentre studies do suggest that RRT/MET systems
reduce rates of cardiopulmonary arrest and lower hospital mortality
rates.164–166 Concern has been expressed about MET activity
leading to potential adverse events resulting from staff leaving
normal duties to attend MET calls. Research suggests that although
MET calls may cause disruption to normal hospital routines and
inconvenience to staff, no major patient harm follows.167
Appropriate placement of patients
Ideally, the sickest patients should be admitted to an area that
can provide the greatest supervision and the highest level of organ
support and nursing care. International organisations have offered
definitions of levels of care and produced admission and discharge
criteria for high dependency units (HDUs) and ICUs.168,169
Staffing levels
Hospital staffing tends to be at its lowest during the night and at
weekends, which may influence patient monitoring, treatment and
outcome. Data from the US National Registry of CPR Investigators
shows that survival rates from in-hospital cardiac arrest are lower
during nights and weekends.170 Outcomes for patients admitted to
hospital and those discharged from the ICU are worse after hours
and at weekends.171–174 Studies show that higher nurse staffing is
associated with lower rates of failure-to-rescue, and reductions in
rates of cardiac arrest rates, pneumonia, shock and death.23,175–177
Resuscitation decisions
The decision to start, continue and terminate resuscitation
efforts is based on the balance between the risks, benefits and burdens
these interventions place on patients, family members and
healthcare providers. There are circumstances where resuscitation
is inappropriate and should not be provided. Consider a ‘do not
attempt cardiopulmonary resuscitation’ (DNACPR) decision when
the patient:
• does not wish to have CPR
• is very unlikely to survive cardiac arrest even if CPR is attempted.
There is wide variation in DNACPR decision-making practice
throughout Europe particularly with respect to involvement of
patients in decision-making.178–181 Improved knowledge, training
and DNACPR decision-making should improve patient care and prevent
futile CPR attempts.182,183 The section on ethics in the ERC
Guidelines provides further information.184
Guidelines for prevention of in-hospital cardiac arrest
Hospitals should provide a system of care that includes: (a) staff
education regarding the signs of patient deterioration and the rationale
for rapid response to illness, (b) appropriate, and frequent
monitoring of patients’ vital signs, (c) clear guidance (e.g. via calling
criteria or early warning scores) to assist staff in the early detection
of patient deterioration, (d) a clear, uniform system of calling
for assistance, and (e) an appropriate and timely clinical response
to calls for help.8 The following strategies may prevent avoidable
in-hospital cardiac arrests:
(1) Provide care for patients who are critically ill or at risk of clinical
deterioration in appropriate areas, with the level of care
provided matched to the level of patient sickness.
(2) Critically ill patients need regular observations: each patient
should have a documented plan for vital signs monitoring
that identifies which variables need to be measured and
the frequency of measurement. Frequency of measurement
should relate to the patient’s severity of illness, and the likelihood
of clinical deterioration and cardiopulmonary arrest.
J. Soar et al. / Resuscitation 95 (2015) 100–147 103
Recent guidance suggests monitoring of simple physiological
variables including pulse, blood pressure, respiratory rate,
conscious level, temperature and SpO2.24,84
(3) Use a track and trigger system (either ‘calling criteria’ or early
warning system) to identify patients who are critically ill and,
or at risk of clinical deterioration and cardiopulmonary arrest.
(4) Use a patient charting system that enables the regular measurement
and recording of vital signs and, where used, early
warning scores. The charting system should facilitate easy
identification of signs of deterioration.
(5) Have a clear and specific policy that requires a clinical
response to abnormal physiology, based on the track and trigger
system used. This should include advice on the further
clinical management of the patient and the specific responsibilities
of medical and nursing staff.
(6) The hospital should have a clearly identified response to critical
illness. This may include a designated outreach service or
resuscitation team (e.g. MET, RRT system) capable of responding
in a timely fashion to acute clinical crises identified by
the track and trigger system or other indicators. This service
must be available 24 h/day and seven days per week. The team
must include staff with the appropriate skills. The patient’s
primary clinical team should also be involved at an early stage
in decision-making.
(7) Train all clinical staff in the recognition, monitoring and management
of the critically ill patient. Include advice on clinical
management while awaiting the arrival of more experienced
staff. Ensure that staff know their role(s) in the rapid response
system.
(8) Hospitals must empower staff of all disciplines to call for help
when they identify a patient at risk of deterioration or cardiac
arrest. Staff should be trained in the use of structured communication
tools to ensure effective handover of information
between doctors, nurses and other healthcare professions.
(9) Identify patients for whom cardiopulmonary arrest is an anticipated
terminal event and in whom CPR is inappropriate, and
patients who do not wish to be treated with CPR. Hospitals
should have a DNACPR policy, based on national guidance,
which is understood by all clinical staff.
(10) Ensure accurate audit of cardiac arrest, deteriorating patients,
unexpected deaths and unanticipated ICU admissions using
common datasets. Also audit the antecedents and clinical
response to these events.
Prevention of sudden cardiac death (SCD) out-of-hospital
Coronary artery disease is the commonest cause of SCD. Nonischaemic
cardiomyopathy and valvular disease account for most
other SCD events in older people. Inherited abnormalities (e.g. Brugada
syndrome, hypertrophic cardiomyopathy), congenital heart
disease, myocarditis and substance abuse are predominant causes
in the young.
Most SCD victims have a history of cardiac disease and warning
signs, most commonly chest pain, in the hour before cardiac
arrest.185 In patients with a known diagnosis of cardiac disease,
syncope (with or without prodrome – particularly recent or recurrent)
is an independent risk factor for increased risk of death.186–196
Chest pain on exertion only, and palpitations associated with
syncope only, are associated with hypertrophic cardiomyopathy,
coronary abnormalities, Wolff–Parkinson–White, and arrhythmogenic
right ventricular cardiomyopathy.
Apparently healthy children and young adults who suffer SCD
can also have signs and symptoms (e.g. syncope/pre-syncope, chest
pain and palpitations) that should alert healthcare professionals to
seek expert help to prevent cardiac arrest.197–206
Children and young adults presenting with characteristic symptoms
of arrhythmic syncope should have a specialist cardiology
assessment, which should include an ECG and in most cases an
echocardiogram and exercise test. Characteristics of arrhythmic
syncope include: syncope in the supine position, occurring during
or after exercise, with no or only brief prodromal symptoms,
repetitive episodes, or in individuals with a family history of
sudden death. In addition, non-pleuritic chest pain, palpitations
associated with syncope, seizures (when resistant to treatment,
occurring at night or precipitated by exercise, syncope, or loud
noise) and drowning in a competent swimmer should raise suspicion
of increased risk. Systematic evaluation in a clinic specialising
in the care of those at risk for SCD is recommended in family members
of young victims of SCD or those with a known cardiac disorder
resulting in an increased risk of SCD.186,207–211 A family history of
syncope or SCD, palpitations as a symptom, supine syncope and
syncope associated with exercise and emotional stress are more
common in patients with long QT syndrome (LQTS).212 In older
adults213,214 the absence of nausea and vomiting before syncope
and ECG abnormalities is an independent predictor of arrhythmic
syncope.
Inexplicable drowning and drowning in a strong swimmer
may be due to LQTS or catecholaminergic polymorphic ventricular
tachycardia (CPVT).215 There is an association between LQTS and
presentation with seizure phenotype.216,217
Guidance has been published for the screening of those at risk
of sudden death including the screening of athletes. Screening programmes
for athletes vary between countries.218,219 Identification
of individuals with inherited conditions and screening of family
members can help prevent deaths in young people with inherited
heart disorders.220–222
3b – Prehospital resuscitation
This section provides an overview of prehospital resuscitation.
Many of the specific issues about prehospital resuscitation are
addressed in sections covering ALS interventions, or are generic
for both resuscitation for in-hospital and out-of-hospital cardiac
arrest.223 Adult BLS and automated external defibrillation contains
guidance on the techniques used during the initial resuscitation
of an adult cardiac arrest victim. In addition, many of the specific
situations associated with cardiac arrest that are encountered in
prehospital resuscitation are addressed in Section 4 – cardiac arrest
in special circumstances.224
EMS personnel and interventions
There is considerable variation across Europe in the structure
and process of emergency medical services (EMS) systems. Some
countries have adopted almost exclusively paramedic/emergency
medical technician (EMT)-based systems while other incorporate
prehospital physicians to a greater or lesser extent. Although some
studies have documented higher survival rates after cardiac arrest
in EMS systems that include experienced physicians,225–232 compared
with those that rely on non-physician providers,225,226,233,234
some other comparisons have found no difference in survival
between systems using paramedics or physicians as part of
the response.235–237 Well-organised non-physician systems with
highly trained paramedics have also reported high survival rates.238
Given the inconsistent evidence, the inclusion or exclusion of physicians
among prehospital personnel responding to cardiac arrests
will depend largely on existing local policy.
Whether ALS interventions by EMS improve outcomes is also
uncertain. A meta-analysis suggested that ALS care can increase
survival in non-traumatic OHCA.239 However, a recent large
104 J. Soar et al. / Resuscitation 95 (2015) 100–147
observational study using propensity matching showed survival to
hospital discharge and 90 day survival was greater among patients
receiving BLS.240 It is not possible to say whether this is a true
difference or the result of unmeasured confounders.
CPR versus defibrillation first for out-of-hospital cardiac arrest
There is evidence that performing chest compressions while
retrieving and charging a defibrillator improves the probability
of survival.241 One randomised controlled trial (RCT)242 found
increased ROSC, discharge- and one-year survival in patients with
longer arrest times (>5 min). However, we have to keep in mind
that this, and a large before-after study from Seattle243 that showed
better outcomes with 90 s of CPR before a shock when the response
interval was >4 min), are from a time when 3 stacked-shocks were
used and shorter periods of CPR between shocks (1 min). Evidence
from five RCTs242,244–247 and another study248 suggests that among
unmonitored patients with OHCA and an initial rhythm of VF/pVT,
there is no benefit in a period of CPR of 90–180 s before defibrillation
when compared with immediate defibrillation with CPR being
performed while the defibrillator equipment is being applied.
A sub-analysis in one RCT245 showed no difference in survival
to hospital discharge with a prolonged period of CPR (180 s) and
delayed defibrillation in patients with a shockable initial rhythm
who received bystander CPR. Yet, for those EMS agencies with a
higher baseline survival to hospital discharge (defined as >20% for
an initial shockable rhythm), 180 s of CPR prior to defibrillation was
more beneficial compared with a shorter period of CPR (30–60 s).
EMS personnel should provide high-quality CPR while a defibrillator
is retrieved, applied and charged. Defibrillation should not be
delayed longer than needed to establish the need for defibrillation
and charging. The routine delivery of a pre-specified period of CPR
(e.g. 2 or 3 min) before rhythm analysis and a shock is delivered is
not recommended.
Termination of resuscitation rules
The ‘basic life support termination of resuscitation rule’ is predictive
of death when applied by defibrillation-only emergency
medical technicians.249 The rule recommends termination when
there is no ROSC, no shocks are administered and EMS personnel
do not witness the arrest. Several studies have shown external
generalisability of this rule.250–256 More recent studies show that
EMS systems providing ALS interventions can also use this BLS rule
and therefore termed it the ‘universal’ termination of resuscitation
rule.251,257,258
Additional studies have shown associations with futility of certain
variables such as no ROSC at scene; non-shockable rhythm;
unwitnessed arrest; no bystander CPR, call response time and
patient demographics.259–267
Termination of resuscitation rules for in-hospital cardiac arrest
are less reliable although EMS rules may be useful for those with
out-of-hospital cardiac arrest who have ongoing resuscitation in
the emergency department.268–271
Prospectively validated termination of resuscitation rules can
be used to guide termination of prehospital CPR in adults; however,
these must be validated in an EMS system similar to the one
in which implementation is proposed. Termination of resuscitation
rules may require integration with guidance on suitability for
extracorporeal CPR (eCPR) or organ donation.272 Organ donation is
specifically addressed in Section 5 – Post-resuscitation care.273,274
3c – In-hospital resuscitation
After in-hospital cardiac arrest, the division between BLS
and ALS is arbitrary; in practice, the resuscitation process is a
continuum and is based on common sense. The public expect that
clinical staff can undertake cardiopulmonary resuscitation (CPR).
For all in-hospital cardiac arrests, ensure that:
• cardiorespiratory arrest is recognised immediately;
• help is summoned using a standard telephone number;
• CPR is started immediately using airway adjuncts, e.g. a bag mask
and, if indicated, defibrillation attempted as rapidly as possible
and certainly within 3 min.
The exact sequence of actions after in-hospital cardiac arrest
will depend on many factors, including:
• location (clinical/non-clinical area; monitored/unmonitored
area);
• training of the first responders;
• number of responders;
• equipment available;
• hospital response system to cardiac arrest and medical emergencies,
(e.g. MET, RRT).
Location
Patients who have monitored arrests are usually diagnosed
rapidly. Ward patients may have had a period of deterioration and
an unwitnessed arrest.9,11 Ideally, all patients who are at high risk
of cardiac arrest should be cared for in a monitored area where
facilities for immediate resuscitation are available.
Training of first responders
All healthcare professionals should be able to recognise cardiac
arrest, call for help and start CPR. Staff should do what they have
been trained to do. For example, staff in critical care and emergency
medicine will have more advanced resuscitation skills than
staff who are not involved regularly in resuscitation in their normal
clinical role. Hospital staff who attend a cardiac arrest may
have different levels of skill to manage the airway, breathing and
circulation. Rescuers must undertake only the skills in which they
are trained and competent.
Number of responders
The single responder must ensure that help is coming. If other
staff are nearby, several actions can be undertaken simultaneously.
Equipment available
All clinical areas should have immediate access to resuscitation
equipment and drugs to facilitate rapid resuscitation of the patient
in cardiopulmonary arrest. Ideally, the equipment used for CPR
(including defibrillators) and the layout of equipment and drugs
should be standardised throughout the hospital.275–277 Equipment
should be checked regularly, e.g. daily, to ensure its readiness for
use in an emergency.
Resuscitation team
The resuscitation team may take the form of a traditional cardiac
arrest team, which is called only when cardiac arrest is recognised.
Alternatively, hospitals may have strategies to recognise patients
at risk of cardiac arrest and summon a team (e.g. MET or RRT)
before cardiac arrest occurs. The term ‘resuscitation team’ reflects
the range of response teams. In hospital cardiac arrests are rarely
sudden or unexpected. A strategy of recognising patients at risk of
cardiac arrest may enable some of these arrests to be prevented, or
J. Soar et al. / Resuscitation 95 (2015) 100–147 105
Fig. 3.1. In-hospital resuscitation algorithm. ABCDE – Airway, Breathing Circulation, Disability, Exposure; IV – intravenous; CPR – cardiopulmonary resuscitation
may prevent futile resuscitation attempts in those who are unlikely
to benefit from CPR.
Immediate actions for a collapsed patient in a hospital
An algorithm for the initial management of in-hospital cardiac
arrest is shown in Fig. 3.1.
• Ensure personal safety.
• When healthcare professionals see a patient collapse or find a
patient apparently unconscious in a clinical area, they should
first summon help (e.g. emergency bell, shout), then assess if the
patient is responsive. Gently shake the shoulders and ask loudly:
‘Are you all right?’
• If other members of staff are nearby, it will be possible to undertake
actions simultaneously.
The responsive patient
Urgent medical assessment is required. Depending on the local
protocols, this may take the form of a resuscitation team (e.g. MET,
RRT). While awaiting this team, give oxygen, attach monitoring and
insert an intravenous cannula.
The unresponsive patient
The exact sequence will depend on the training of staff and
experience in assessment of breathing and circulation. Trained
healthcare staff cannot assess the breathing and pulse sufficiently
reliably to confirm cardiac arrest.278–287
Agonal breathing (occasional gasps, slow, laboured or noisy
breathing) is common in the early stages of cardiac arrest and is
a sign of cardiac arrest and should not be confused as a sign of
life.288–291 Agonal breathing can also occur during chest compressions
as cerebral perfusion improves, but is not indicative of ROSC.
Cardiac arrest can cause an initial short seizure-like episode that
can be confused with epilepsy.292,293 Finally changes in skin colour,
notably pallor and bluish changes associated with cyanosis are not
diagnostic of cardiac arrest.292
• Shout for help (if not already)
• Turn the victim on to his back and then open the airway:
• Open airway and check breathing:
• Open the airway using a head tilt chin lift
• Keeping the airway open, look, listen and feel for normal
breathing (an occasional gasp, slow, laboured or noisy breathing
is not normal):
• Look for chest movement
• Listen at the victim’s mouth for breath sounds
• Feel for air on your cheek
• Look, listen and feel for no more than 10 s to determine if the
victim is breathing normally.
• Check for signs of a circulation:
• It may be difficult to be certain that there is no pulse. If
the patient has no signs of life (consciousness, purposeful
106 J. Soar et al. / Resuscitation 95 (2015) 100–147
movement, normal breathing, or coughing), or if there is doubt,
start CPR immediately until more experienced help arrives or
the patient shows signs of life.
• Delivering chest compressions to a patient with a beating heart
is unlikely to cause harm.294 However, delays in diagnosing cardiac
arrest and starting CPR will adversely effect survival and
must be avoided.
• Only those experienced in ALS should try to assess the carotid
pulse whilst simultaneously looking for signs of life. This rapid
assessment should take no more than 10 s. Start CPR if there is
any doubt about the presence or absence of a pulse.
• If there are signs of life, urgent medical assessment is required.
Depending on the local protocols, this may take the form of a
resuscitation team. While awaiting this team, give the patient
oxygen, attach monitoring and insert an intravenous cannula.
When a reliable measurement of oxygen saturation of arterial
blood (e.g. pulse oximetry (SpO2)) can be achieved, titrate the
inspired oxygen concentration to achieve a SpO2 of 94–98%.
• If there is no breathing, but there is a pulse (respiratory arrest),
ventilate the patient’s lungs and check for a circulation every 10
breaths. Start CPR if there is any doubt about the presence or
absence of a pulse.
Starting in-hospital CPR
The key steps are listed here. Supporting evidence can be found
in the sections on specific interventions that follow.
• One person starts CPR as others call the resuscitation team and
collect the resuscitation equipment and a defibrillator. If only one
member of staff is present, this will mean leaving the patient.
• Give 30 chest compressions followed by 2 ventilations.
• Compress to a depth of at least 5 cm but not more than 6 cm.
• Perform chest compressions should be performed at a rate of
100–120 min−1.
• Allow the chest to recoil completely after each compression; do
not lean on the chest.
• Minimise interruptions and ensure high-quality compressions.
• Undertaking high-quality chest compressions for a prolonged
time is tiring; with minimal interruption, try to change the person
doing chest compressions every 2 min.
• Maintain the airway and ventilate the lungs with the most appropriate
equipment immediately to hand. Pocket mask ventilation
or two-rescuer bag-mask ventilation, which can be supplemented
with an oral airway, should be started. Alternatively, use
a supraglottic airway device (SGA) and self-inflating bag. Tracheal
intubation should be attempted only by those who are trained,
competent and experienced in this skill.
• Waveform capnography must be used for confirming tracheal
tube placement and monitoring ventilation rate. Waveform
capnography can also be used with a bag-mask device and SGA.
The further use of waveform capnography to monitor CPR quality
and potentially identify ROSC during CPR is discussed later in this
section.295
• Use an inspiratory time of 1 s and give enough volume to produce
a normal chest rise. Add supplemental oxygen to give the highest
feasible inspired oxygen as soon as possible.4
• Once the patient’s trachea has been intubated or a SGA has been
inserted, continue uninterrupted chest compressions (except
for defibrillation or pulse checks when indicated) at a rate
of 100–120 min−1 and ventilate the lungs at approximately
10 breaths min−1. Avoid hyperventilation (both excessive rate
and tidal volume).
• If there is no airway and ventilation equipment available, consider
giving mouth-to-mouth ventilation. If there are clinical
reasons to avoid mouth-to-mouth contact, or you are unable to
do this, do chest compressions until help or airway equipment
arrives. The ALS Writing Group recognises that there can be good
clinical reasons to avoid mouth-to-mouth ventilation in clinical
settings, and it is not commonly used in clinical settings, but there
will be situations where giving mouth-to-mouth breaths could be
life-saving.
• When the defibrillator arrives, apply self-adhesive defibrillation
pads to the patient whilst chest compressions continue and then
briefly analyse the rhythm. If self-adhesive defibrillation pads
are not available, use paddles. The use of self-adhesive electrode
pads or a ‘quick-look’ paddles technique will enable rapid
assessment of the heart rhythm compared with attaching ECG
electrodes.296 Pause briefly to assess the heart rhythm. With a
manual defibrillator, if the rhythm is VF/pVT charge the defibrillator
while another rescuer continues chest compressions. Once the
defibrillator is charged, pause the chest compressions and then
give one shock, and immediately resume chest compressions.
Ensure no one is touching the patient during shock delivery. Plan
and ensure safe defibrillation before the planned pause in chest
compressions.
• If using an automated external defibrillator (AED) follow the
AED’s audio-visual prompts, and similarly aim to minimise
pauses in chest compressions by rapidly following prompts.
• The ALS Writing Group recognises that in some settings where
self-adhesive defibrillation pads are not available, alternative
defibrillation strategies using paddles are used to minimise the
preshock pause.
• The ALS writing group is aware that in some countries a defibrillation
strategy that involves charging the defibrillator towards
the end of every 2 min cycle of CPR in preparation for the pulse
check is used.297,298 If the rhythm is VF/pVT a shock is given and
CPR resumed. Whether this leads to any benefit is unknown,
but it does lead to defibrillator charging for non-shockable
rhythms.
• Restart chest compressions immediately after the defibrillation
attempt. Minimise interruptions to chest compressions. When
using a manual defibrillator it is possible to reduce the pause
between stopping and restarting of chest compressions to less
than 5 s.
• Continue resuscitation until the resuscitation team arrives or the
patient shows signs of life. Follow the voice prompts if using an
AED.
• Once resuscitation is underway, and if there are sufficient staff
present, prepare intravenous cannulae and drugs likely to be used
by the resuscitation team (e.g. adrenaline).
• Identify one person to be responsible for handover to the resuscitation
team leader. Use a structured communication tool for
handover (e.g. SBAR, RSVP).111,112 Locate the patient’s records.
• The quality of chest compressions during in-hospital CPR is
frequently sub-optimal.299,300 The importance of uninterrupted
chest compressions cannot be over emphasised. Even short interruptions
to chest compressions are disastrous for outcome and
every effort must be made to ensure that continuous, effective
chest compression is maintained throughout the resuscitation
attempt. Chest compressions should commence at the beginning
of a resuscitation attempt and continue uninterrupted unless
they are paused briefly for a specific intervention (e.g. rhythm
check). Most interventions can be performed without interruptions
to chest compressions. The team leader should monitor the
quality of CPR and alternate CPR providers if the quality of CPR is
poor.
• Continuous ETCO2 monitoring during CPR can be used to indicate
the quality of CPR, and a rise in ETCO2 can be an indicator of ROSC
during chest compressions.295,301–303
• If possible, the person providing chest compressions should be
changed every 2 min, but without pauses in chest compressions.
J. Soar et al. / Resuscitation 95 (2015) 100–147 107
3d – ALS treatment algorithm
Introduction
Heart rhythms associated with cardiac arrest are divided into
two groups: shockable rhythms (ventricular fibrillation/pulseless
ventricular tachycardia (VF/pVT)) and non-shockable rhythms
(asystole and pulseless electrical activity (PEA)). The principal difference
in the treatment of these two groups of arrhythmias is the
need for attempted defibrillation in those patients with VF/pVT.
Other interventions, including high-quality chest compressions
with minimal interruptions, airway management and ventilation,
venous access, administration of adrenaline and the identification
and correction of reversible causes, are common to both groups.
Although the ALS cardiac arrest algorithm (Fig. 3.2) is applicable
to all cardiac arrests, additional interventions may be indicated for
cardiac arrest caused by special circumstances (see Section 4).224
The interventions that unquestionably contribute to improved
survival after cardiac arrest are prompt and effective bystander
basic life support (BLS), uninterrupted, high-quality chest compressions
and early defibrillation for VF/pVT. The use of adrenaline
has been shown to increase ROSC but not survival to discharge.
Furthermore there is a possibility that it causes worse long-term
neurological survival. Similarly, the evidence to support the use of
advanced airway interventions during ALS remains limited.4,304–311
Thus, although drugs and advanced airways are still included
among ALS interventions, they are of secondary importance to
early defibrillation and high-quality, uninterrupted chest compressions.
As an indicator of equipoise for many ALS interventions at
the time of writing these guidelines, three large RCTs (adrenaline
versus placebo [ISRCTN73485024], amiodarone versus lidocaine
versus placebo312 [NCT01401647] and SGA versus tracheal intubation
[ISRCTN No: 08256118]) are currently ongoing.
As with previous guidelines, the ALS algorithm distinguishes
between shockable and non-shockable rhythms. Each cycle is
broadly similar, with a total of 2 min of CPR being given before
assessing the rhythm and where indicated, feeling for a pulse.
Adrenaline 1 mg is injected every 3–5 min until ROSC is achieved
– the timing of the initial dose of adrenaline is described below.
In VF/pVT, a single dose of amiodarone 300 mg is indicated after a
total of three shocks and a further dose of 150 mg can be considered
after five shocks. The optimal CPR cycle time is not known and
algorithms for longer cycles (3 min) exist which include different
timings for adrenaline doses.313
Duration of resuscitation attempt
The duration of any individual resuscitation attempt should be
based on the individual circumstances of the case and is a matter
of clinical judgement, taking into consideration the circumstances
and the perceived prospect of a successful outcome. If it was considered
appropriate to start resuscitation, it is usually considered
worthwhile continuing, as long as the patient remains in VF/pVT,
or there is a potentially reversible cause than can be treated. The
use of mechanical compression devices and extracorporeal CPR
techniques make prolonged attempts at resuscitation feasible in
selected patients.
In a large observational study of patients with IHCA, the median
duration of resuscitation was 12 min (IQR 6–21 min) in those with
ROSC compared with 20 min (IQR 14–30 min) for those with no
ROSC.314 Hospitals with the longest resuscitation attempts (median
25 min [IQR 25–28 min]) had a higher risk-adjusted rate of ROSC
and survival to discharge compared with a shorter median duration
of resuscitation attempt.314,315 It is generally accepted that
asystole for more than 20 min in the absence of a reversible cause
and with ongoing ALS constitutes a reasonable ground for stopping
further resuscitation attempts.316 The ethical principles of starting
and stopping CPR are addressed in Section 11, the Ethics of
resuscitation and end-of-life decisions.184
Shockable rhythms (ventricular fibrillation/pulseless ventricular
tachycardia)
The first monitored rhythm is VF/pVT in approximately 20% both
for in-hospital317,7,318,319 and out-of-hospital cardiac arrests.320
The incidence of VF/pVT may be decreasing,321–324 and can vary
according to bystander CPR rates. Ventricular fibrillation/pulseless
ventricular tachycardia will also occur at some stage during resuscitation
in about 25% of cardiac arrests with an initial documented
rhythm of asystole or PEA.317,325 Having confirmed cardiac arrest,
summon help (including the request for a defibrillator) and start
CPR, beginning with chest compressions, with a compression: ventilation
(CV) ratio of 30:2. When the defibrillator arrives, continue
chest compressions while applying the defibrillation electrodes.
Identify the rhythm and treat according to the ALS algorithm.
• If VF/pVT is confirmed, charge the defibrillator while another
rescuer continues chest compressions. Once the defibrillator is
charged, pause the chest compressions, quickly ensure that all
rescuers are clear of the patient and then give one shock.
• Defibrillation shock energy levels are unchanged from the 2010
guidelines.2 For biphasic waveforms (rectilinear biphasic or
biphasic truncated exponential), use an initial shock energy of
at least 150 J. For pulsed biphasic waveforms, begin at 120–150 J.
The shock energy for a particular defibrillator should be based
on the manufacturer’s guidance. It is important that those using
manual defibrillators are aware of the appropriate energy settings
for the type of device used. Manufacturers should consider
labelling their manual defibrillators with energy level instructions,
but in the absence of this and if appropriate energy levels
are unknown, for adults use the highest available shock energy
for all shocks. With manual defibrillators it is appropriate to consider
escalating the shock energy if feasible, after a failed shock
and for patients where refibrillation occurs.326,327
• Minimise the delay between stopping chest compressions and
delivery of the shock (the preshock pause); even a 5–10 s delay
will reduce the chances of the shock being successful.328–331
• Without pausing to reassess the rhythm or feel for a pulse, resume
CPR (CV ratio 30:2) immediately after the shock, starting with
chest compressions to limit the post-shock pause and the total
peri-shock pause.330,331 Even if the defibrillation attempt is successful
in restoring a perfusing rhythm, it takes time to establish
a post shock circulation332 and it is very rare for a pulse to
be palpable immediately after defibrillation.333 In one study,
after defibrillation attempts, most patients having ALS remained
pulseless for over 2 min and the duration of asystole before ROSC
was longer than 2 min beyond the shock in as many as 25%.334
If a shock has been successful immediate resumption of chest
compressions does not increase the risk of VF recurrence.335
Furthermore, the delay in trying to palpate a pulse will further
compromise the myocardium if a perfusing rhythm has not been
restored.336
• Continue CPR for 2 min, then pause briefly to assess the rhythm;
if still VF/pVT, give a second shock (150–360 J biphasic). Without
pausing to reassess the rhythm or feel for a pulse, resume CPR
(CV ratio 30:2) immediately after the shock, starting with chest
compressions.
• Continue CPR for 2 min, then pause briefly to assess the rhythm;
if still VF/pVT, give a third shock (150–360 J biphasic). Without
reassessing the rhythm or feeling for a pulse, resume CPR (CV
108 J. Soar et al. / Resuscitation 95 (2015) 100–147
Fig. 3.2. Advanced life support algorithm. CPR – cardiopulmonary resuscitation; VF/Pulseless VT – ventricular fibrillation/pulseless ventricular tachycardia; PEA – pulseless
electrical activity; ABCDE – Airway, Breathing Circulation, Disability, Exposure; SaO2 – oxygen saturation; PaCO2 – partial pressure carbon dioxide in arterial blood; ECG –
electrocardiogram.
J. Soar et al. / Resuscitation 95 (2015) 100–147 109
ratio 30:2) immediately after the shock, starting with chest com-
pressions.
• If IV/IO access has been obtained, during the next 2 min of CPR
give adrenaline 1 mg and amiodarone 300 mg.337
• The use of waveform capnography may enable ROSC to be
detected without pausing chest compressions and may be used
as a way of avoiding a bolus injection of adrenaline after ROSC
has been achieved. Several human studies have shown that
there is a significant increase in end-tidal CO2 when ROSC
occurs.295,301–303,338,339 If ROSC is suspected during CPR withhold
adrenaline. Give adrenaline if cardiac arrest is confirmed at the
next rhythm check.
• If ROSC has not been achieved with this 3rd shock, the adrenaline
may improve myocardial blood flow and increase the chance of
successful defibrillation with the next shock. In animal studies,
peak plasma concentrations of adrenaline occur at about 90 s
after a peripheral injection and the maximum effect on coronary
perfusion pressure is achieved around the same time (70 s).340
Importantly, high-quality chest compressions are needed to circulate
the drug to achieve these times.
• Timing of adrenaline dosing can cause confusion amongst
ALS providers and this aspect needs to be emphasised during
training.341 Training should emphasise that giving drugs must
not lead to interruptions in CPR and delay interventions such as
defibrillation. Human data suggests drugs can be given without
affecting the quality of CPR.305
• After each 2-min cycle of CPR, if the rhythm changes to asystole
or PEA, see ‘non-shockable rhythms’ below. If a non-shockable
rhythm is present and the rhythm is organised (complexes appear
regular or narrow), try to feel a pulse. Ensure that rhythm checks
are brief, and pulse checks are undertaken only if an organised
rhythm is observed. If there is any doubt about the presence
of a pulse in the presence of an organised rhythm, immediately
resume CPR. If ROSC has been achieved, begin post-resuscitation
care.
During treatment of VF/pVT, healthcare providers must practice
efficient coordination between CPR and shock delivery whether
using a manual defibrillator or an AED. When VF is present for
more than a few minutes, the myocardium is depleted of oxygen
and metabolic substrates. A brief period of chest compressions will
deliver oxygen and energy substrates and increase the probability
of restoring a perfusing rhythm after shock delivery.342 Analyses
of VF waveform characteristics predictive of shock success indicate
that the shorter the time between chest compression and
shock delivery, the more likely the shock will be successful.342,343
Reduction in the peri-shock pause (the interval between stopping
compressions to resuming compressions after shock delivery)
by even a few seconds can increase the probability of shock
success.328–331 Moreover, continuing high-quality CPR however
may improve the amplitude and frequency of the VF and improve
the chance of successful defibrillation to a perfusing rhythm.344–346
Regardless of the arrest rhythm, after the initial adrenaline dose
has been given, give further doses of adrenaline 1 mg every 3–5 min
until ROSC is achieved; in practice, this will be about once every two
cycles of the algorithm. If signs of life return during CPR (purposeful
movement, normal breathing or coughing), or there is an increase in
ETCO2, check the monitor; if an organised rhythm is present, check
for a pulse. If a pulse is palpable, start post-resuscitation care. If no
pulse is present, continue CPR.
Witnessed, monitored VF/pVT
If a patient has a monitored and witnessed cardiac arrest in
the catheter laboratory, coronary care unit, a critical care area or
whilst monitored after cardiac surgery, and a manual defibrillator
is rapidly available:
• Confirm cardiac arrest and shout for help.
• If the initial rhythm is VF/pVT, give up to three quick successive
(stacked) shocks.
• Rapidly check for a rhythm change and, if appropriate, ROSC after
each defibrillation attempt.
• Start chest compressions and continue CPR for 2 min if the third
shock is unsuccessful.
This three-shock strategy may also be considered for an initial,
witnessed VF/pVT cardiac arrest if the patient is already connected
to a manual defibrillator. Although there are no data supporting a
three-shock strategy in any of these circumstances, it is unlikely
that chest compressions will improve the already very high chance
of ROSC when defibrillation occurs early in the electrical phase,
immediately after onset of VF.
If this initial three-shock strategy is unsuccessful for a monitored
VF/pVT cardiac arrest, the ALS algorithm should be followed
and these three-shocks treated as if only the first single shock has
been given.
The first dose of adrenaline should be given after another 2
shock attempts if VF persists, i.e. Give 3 shocks, then 2 min CPR,
then shock attempt, then 2 min CPR, then shock attempt, and then
consider adrenaline during this 2 min of CPR. We recommend amiodarone
is given after three defibrillation attempts irrespective of
whether they are consecutive shocks, or interrupted by CPR and
non-shockable rhythms.
Specific guidance concerning the need for resternotomy, and
drug timing if the initial stacked shocks are unsuccessful when cardiac
arrest occurs after cardiac surgery is addressed in Section 4 –
cardiac arrest in special circumstances.224
Persistent ventricular fibrillation/pulseless ventricular tachycardia
In VF/pVT persists, consider changing the position of the
pads/paddles.2 Review all potentially reversible causes using the
4 H and 4 T approach (see below) and treat any that are identified.
Persistent VF/pVT may be an indication for percutaneous
coronary intervention (PCI) – in these cases, a mechanical chest
compression device can be used to maintain high-quality chest
compressions for transport and PCI.347 The use of extracorporeal
CPR (see below) should also be considered to support the circulation
whilst a reversible cause it treated.
Precordial thump
A single precordial thump has a very low success rate for cardioversion
of a shockable rhythm.348–352 Its routine use is therefore
not recommended. It may be appropriate therapy only when used
without delay whilst awaiting the arrival of a defibrillator in a monitored
VF/pVT arrest.353 Using the ulnar edge of a tightly clenched
fist, deliver a sharp impact to the lower half of the sternum from a
height of about 20 cm, then retract the fist immediately to create an
impulse-like stimulus. There are rare reports of a precordial thump
converting a perfusing to a non-perfusing rhythm.354
Airway and ventilation
During the treatment of persistent VF, ensure good-quality chest
compressions between defibrillation attempts. Consider reversible
causes (4 Hs and 4 Ts) and, if identified, correct them. Tracheal intubation
provides the most reliable airway, but should be attempted
only if the healthcare provider is properly trained and has regular,
ongoing experience with the technique. Tracheal intubation must
not delay defibrillation attempts. Personnel skilled in advanced
airway management should attempt laryngoscopy and intubation
without stopping chest compressions; a brief pause in chest compressions
may be required as the tube is passed through the vocal
cords, but this pause should be less than 5 s. Alternatively, to avoid
any interruptions in chest compressions, the intubation attempt
110 J. Soar et al. / Resuscitation 95 (2015) 100–147
may be deferred until ROSC. No RCTs have shown that tracheal
intubation increases survival after cardiac arrest. After intubation,
confirm correct tube position and secure it adequately. Ventilate
the lungs at 10 breaths min−1; do not hyperventilate the patient.
Once the patient’s trachea has been intubated, continue chest
compressions, at a rate of 100–120 min−1 without pausing during
ventilation. A pause in the chest compressions causes the coronary
perfusion pressure to fall substantially. On resuming compressions,
there is some delay before the original coronary perfusion pressure
is restored, thus chest compressions that are not interrupted for
ventilation (or any reason) result in a substantially higher mean
coronary perfusion pressure.
In the absence of personnel skilled in tracheal intubation,
a supraglottic airway (SGA) (e.g. laryngeal mask airway, laryngeal
tube or i-gel) is an acceptable alternative. Once a SGA has
been inserted, attempt to deliver continuous chest compressions,
uninterrupted by ventilation.355 If excessive gas leakage causes
inadequate ventilation of the patient’s lungs, chest compressions
will have to be interrupted to enable ventilation (using a CV ratio
of 30:2). Airway interventions for cardiac arrest and the evidence
supporting them are described in Section 3f.
Intravenous access and drugs
Peripheral versus central venous drug delivery. Establish intravenous
access if this has not already been achieved. Although peak drug
concentrations are higher and circulation times are shorter when
drugs are injected into a central venous catheter compared with
a peripheral cannula,356 insertion of a central venous catheter
requires interruption of CPR and can be technically challenging
and associated with complications. Peripheral venous cannulation
is quicker, easier to perform and safer. Drugs injected peripherally
must be followed by a flush of at least 20 ml of fluid and elevation
of the extremity for 10–20 s to facilitate drug delivery to the central
circulation.
Intraosseous route. If intravenous access is difficult or impossible,
consider the IO route. This is now established as an effective route
in adults.357–365 Intraosseous injection of drugs achieves adequate
plasma concentrations in a time comparable with injection through
a vein.366,367 Animal studies suggest that adrenaline reaches a
higher concentration and more quickly when it is given intravenously
as compared with the intraosseous route, and that the
sternal intraosseous route more closely approaches the pharmacokinetic
of IV adrenaline.368 The recent availability of mechanical
IO devices has increased the ease of performing this technique.369
There are a number of intraosseous devices available as well as a
choice of insertion sites including the humerus, proximal or distal
tibia, and sternum. We have not done a formal review of devices
or insertion sites as part of the 2015 Guidelines process. The decision
concerning choice of device and insertion site should be made
locally and staff adequately trained in its use.
Adrenaline for initial VF/pVT arrest. On the basis of expert consensus,
for VF/pVT give adrenaline after the third shock once chest
compressions have resumed, and then repeat every 3–5 min during
cardiac arrest (alternate cycles). Do not interrupt CPR to give
drugs. The use of waveform capnography may enable ROSC to be
detected without pausing chest compressions and may be used as a
way of avoiding a bolus injection of adrenaline after ROSC has been
achieved. If ROSC is suspected during CPR, withhold adrenaline and
continue CPR. Give adrenaline if cardiac arrest is confirmed at the
next rhythm check.
Despite the widespread use of adrenaline during resuscitation,
there is no placebo-controlled study that shows that the routine
use of any vasopressor at any stage during human cardiac
arrest increases neurologically intact survival to hospital discharge.
Further information concerning the role of adrenaline in cardiac
arrest is addressed in Section 3g – drugs and fluids during CPR.
Anti-arrhythmic drugs. We recommend that amiodarone should be
given after three defibrillation attempts irrespective of whether
they are consecutive shocks, or interrupted by CPR, or for recurrent
VF/pVT during cardiac arrest. Give amiodarone 300 mg intravenously;
a further dose of 150 mg may be given after five
defibrillation attempts. Lidocaine 1 mg kg−1 may be used as an
alternative if amiodarone is not available but do not give lidocaine if
amiodarone has been given already. Further information concerning
the role of amiodarone in cardiac arrest is addressed in Section
3g – drugs and fluid during CPR.
Non-shockable rhythms (PEA and asystole)
Pulseless electrical activity (PEA) is defined as cardiac arrest
in the presence of electrical activity (other than ventricular tachyarrhythmia)
that would normally be associated with a palpable
pulse.370 These patients often have some mechanical myocardial
contractions, but these are too weak to produce a detectable pulse
or blood pressure – this is sometimes described as ‘pseudo-PEA’
(see below). PEA is often caused by reversible conditions, and can
be treated if those conditions are identified and corrected. Survival
following cardiac arrest with asystole or PEA is unlikely unless a
reversible cause can be found and treated effectively.
If the initial monitored rhythm is PEA or asystole, start CPR
30:2. If asystole is displayed, without stopping CPR, check that
the leads are attached correctly. Once an advanced airway has
been sited, continue chest compressions without pausing during
ventilation. After 2 min of CPR, recheck the rhythm. If asystole
is present, resume CPR immediately. If an organised rhythm is
present, attempt to palpate a pulse. If no pulse is present (or if there
is any doubt about the presence of a pulse), continue CPR.
Give adrenaline 1 mg as soon as venous or intraosseous access
is achieved, and repeat every alternate CPR cycle (i.e. about every
3–5 min). If a pulse is present, begin post-resuscitation care. If signs
of life return during CPR, check the rhythm and check for a pulse.
If ROSC is suspected during CPR withhold adrenaline and continue
CPR. Give adrenaline if cardiac arrest is confirmed at the next
rhythm check.
Whenever a diagnosis of asystole is made, check the ECG carefully
for the presence of P waves, because this may respond to
cardiac pacing. There is no benefit in attempting to pace true asystole.
In addition, if there is doubt about whether the rhythm is
asystole or extremely fine VF, do not attempt defibrillation; instead,
continue chest compressions and ventilation. Continuing highquality
CPR however may improve the amplitude and frequency
of the VF and improve the chance of successful defibrillation to a
perfusing rhythm.344–346
The optimal CPR time between rhythm checks may vary according
to the cardiac arrest rhythm and whether it is the first or
subsequent loop.371 Based on expert consensus, for the treatment
of asystole or PEA, following a 2-min cycle of CPR, if the rhythm has
changed to VF, follow the algorithm for shockable rhythms. Otherwise,
continue CPR and give adrenaline every 3–5 min following
the failure to detect a palpable pulse with the pulse check. If VF
is identified on the monitor midway through a 2-min cycle of CPR,
complete the cycle of CPR before formal rhythm and shock delivery
if appropriate – this strategy will minimise interruptions in chest
compressions.
Potentially reversible causes
Potential causes or aggravating factors for which specific treatment
exists must be considered during any cardiac arrest. For ease
J. Soar et al. / Resuscitation 95 (2015) 100–147 111
of memory, these are divided into two groups of four, based upon
their initial letter: either H or T. More details on many of these
conditions are covered in Section 4 – special circumstances.224
The four ‘Hs’
Minimise the risk of hypoxia by ensuring that the patient’s lungs
are ventilated adequately with the maximal possible inspired oxygen
during CPR. Make sure there is adequate chest rise and bilateral
breath sounds. Using the techniques described in Section 3f, check
carefully that the tracheal tube is not misplaced in a bronchus or
the oesophagus.
Pulseless electrical activity caused by hypovolaemia is due usually
to severe haemorrhage. This may be precipitated by trauma
(Section 4),224 gastrointestinal bleeding or rupture of an aortic
aneurysm. Intravascular volume should be restored rapidly with
warmed fluid, coupled with urgent surgery to stop the haemorr-
hage.
Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia and
other metabolic disorders are detected by biochemical tests (usually
by using a blood gas analyser) or suggested by the patient’s
medical history, e.g. renal failure (Section 4).224 Intravenous calcium
chloride is indicated in the presence of hyperkalaemia,
hypocalcaemia and calcium channel-blocker overdose.
Hypothermia should be suspected based on the history such as
cardiac arrest associated with drowning (Section 4).224
The four ‘Ts’
Coronary thrombosis associated with an acute coronary syndrome
or ischaemic heart disease is the most common cause of
sudden cardiac arrest. An acute coronary syndrome is usually diagnosed
and treated after ROSC is achieved. If an acute coronary
syndrome is suspected, and ROSC has not been achieved, urgent
coronary angiography should be considered when feasible and if
required percutaneous coronary intervention. Mechanical chest
compression devices and extracorporeal CPR can help facilitate this.
The commonest cause of thromboembolic or mechanical circulatory
obstruction is massive pulmonary embolism. The treatment
of cardiac arrest with known or suspected pulmonary embolism is
addressed in Section 4 including the role of fibrinolysis, surgical or
mechanical thrombectomy and extracorporeal CPR.224
A tension pneumothorax may be the primary cause of PEA and
may be associated with trauma or follow attempts at central venous
catheter insertion. The diagnosis is made clinically or by ultrasound.
Decompress rapidly by thoracostomy or needle thoracocentesis,
and then insert a chest drain. In the context of cardiac arrest from
major trauma, consider bilateral thoracostomies for decompression
of a suspected tension pneumothorax (Section 4).224
Cardiac tamponade is difficult to diagnose because the typical
signs of distended neck veins and hypotension are usually obscured
by the arrest itself. Cardiac arrest after penetrating chest trauma is
highly suggestive of tamponade and is an indication for resuscitative
thoracotomy (Section 4).224 The use of ultrasound will make
the diagnosis of cardiac tamponade much more reliable.
In the absence of a specific history, the accidental or deliberate
ingestion of therapeutic or toxic substances may be revealed only
by laboratory investigations (Section 4).224 Where available, the
appropriate antidotes should be used, but most often treatment is
supportive and standard ALS protocols should be followed.
Use of ultrasound imaging during advanced life support
Several studies have examined the use of ultrasound during cardiac
arrest to detect potentially reversible causes.372–374 Although
no studies have shown that use of this imaging modality improves
outcome, there is no doubt that echocardiography has the potential
to detect reversible causes of cardiac arrest. Specific protocols for
ultrasound evaluation during CPR may help to identify potentially
reversible causes (e.g. cardiac tamponade, pulmonary embolism,
hypovolaemia, pneumothorax) and identify pseudo-PEA.373,375–382
When available for use by trained clinicians, ultrasound may be
of use in assisting with diagnosis and treatment of potentially
reversible causes of cardiac arrest. The integration of ultrasound
into advanced life support requires considerable training if interruptions
to chest compressions are to be minimised. A sub-xiphoid
probe position has been recommended.375,381,383 Placement of the
probe just before chest compressions are paused for a planned
rhythm assessment enables a well-trained operator to obtain views
within 10 s.
Absence of cardiac motion on sonography during resuscitation
of patients in cardiac arrest is highly predictive of death although
sensitivity and specificity has not been reported.384–387
Monitoring during advanced life support
There are a number of methods and emerging technologies to
monitor the patient during CPR and potentially help guide ALS
interventions. These include:
• Clinical signs such as breathing efforts, movements and eye opening
can occur during CPR. These can indicate ROSC and require
verification by a rhythm and pulse check, but can also occur
because CPR can generate a sufficient circulation to restore signs
of life including consciousness.388
• The use of CPR feedback or prompt devices during CPR is
addressed in Section 2 – basic life support.223 The use of CPR feedback
or prompt devices during CPR should only be considered as
part of a broader system of care that should include comprehensive
CPR quality improvement initiatives 389,390 rather than an
isolated intervention.
• Pulse checks when there is an ECG rhythm compatible with an
output can be used to identify ROSC, but may not detect pulses in
those with low cardiac output states and a low blood pressure.391
The value of attempting to feel arterial pulses during chest compressions
to assess the effectiveness of chest compressions is
unclear. A pulse that is felt in the femoral triangle may indicate
venous rather than arterial blood flow. There are no valves in the
inferior vena cava and retrograde blood flow into the venous system
can produce femoral vein pulsations.392 Carotid pulsation
during CPR does not necessarily indicate adequate myocardial or
cerebral perfusion.
• ECG monitoring of heart rhythm. Monitoring heart rhythm
through pads, paddles or ECG electrodes is a standard part of
ALS. Motion artefacts prevent reliable heart rhythm assessment
during chest compressions forcing rescuers to stop chest compressions
to assess the rhythm, and preventing early recognition
of recurrent VF/pVT. Some modern defibrillators have filters that
remove artefact from compressions but there are no human studies
showing improvements in patient outcomes from their use.
We suggest against the routine use of artefact-filtering algorithms
for analysis of ECG rhythm during CPR unless as part of
a research programme.393
• End-tidal carbon dioxide with waveform capnography. The use
of waveform capnography during CPR has a greater emphasis in
Guidelines 2015 and is addressed in more detail below.
• Blood sampling and analysis during CPR can be used to identify
potentially reversible causes of cardiac arrest. Avoid finger
prick samples in critical illness because they may not be reliable;
instead, use samples from veins or arteries.
• Blood gas values are difficult to interpret during CPR. During
cardiac arrest, arterial gas values may be misleading and bear
little relationship to the tissue acid-base state.394 Analysis of central
venous blood may provide a better estimation of tissue pH.
112 J. Soar et al. / Resuscitation 95 (2015) 100–147
Central venous oxygen saturation monitoring during ALS is feasible
but its role in guiding CPR is not clear.
• Invasive cardiovascular monitoring in critical care settings, e.g.
continuous arterial blood pressure and central venous pressure
monitoring. Invasive arterial pressure monitoring will enable the
detection of low blood pressure values when ROSC is achieved.
Consider aiming for an aortic diastolic pressure of greater than
25 mmHg during CPR by optimising chest compressions.395
In practice this would mean measuring an arterial diastolic
pressure. Although haemodynamic-directed CPR showed some
benefit in experimental studies396–399 there is currently no evidence
of improvement in survival with this approach in humans.4
• Ultrasound assessment is addressed above to identify and
treat reversible causes of cardiac arrest, and identify low cardiac
output states (‘pseudo-PEA’). Its use has been discussed
above.
• Cerebral oximetry using near-infrared spectroscopy measures
regional cerebral oxygen saturation (rSO2) non-invasively.400–402
This remains an emerging technology that is feasible during CPR.
Its role in guiding CPR interventions including prognostication
during and after CPR is yet to be established.403
Waveform capnography during advanced life support
End-tidal carbon dioxide is the partial pressure of carbon dioxide
(CO2) at the end of an exhaled breath. It reflects cardiac output and
pulmonary blood flow, as CO2 is transported by the venous system
to the right side of the heart and then pumped to the lungs by the
right ventricle, as well as the ventilation minute volume. During
CPR, end-tidal CO2 values are low, reflecting the low cardiac output
generated by chest compression. Waveform capnography enables
continuous real time end-tidal CO2 to be monitored during CPR. It
works most reliably in patients who have a tracheal tube, but can
also be used with a supraglottic airway device or bag mask. There
is currently no evidence that use of waveform capnography during
CPR results in improved patient outcomes, although the prevention
of unrecognised oesophageal intubation is clearly beneficial. The
role of waveform capnography during CPR includes:
• Ensuring tracheal tube placement in the trachea (see below for
further details).
• Monitoring ventilation rate during CPR and avoiding hyperven-
tilation.
• Monitoring the quality of chest compressions during CPR. Endtidal
CO2 values are associated with compression depth and
ventilation rate and a greater depth of chest compression will
increase the value.404 Whether this can be used to guide care and
improve outcome requires further study.295 (Fig. 3.3)
• Identifying ROSC during CPR. An increase in end-tidal CO2 during
CPR may indicate ROSC and prevent unnecessary and potentially
harmful dosing of adrenaline in a patient with ROSC.295,301,338,339
If ROSC is suspected during CPR withhold adrenaline. Give
adrenaline if cardiac arrest is confirmed at the next rhythm check.
• Prognostication during CPR. Lower end-tidal CO2 values may
indicate a poor prognosis and less chance of ROSC.4 Precise values
of end-tidal CO2 depend on several factors including the cause of
cardiac arrest, bystander CPR, chest compression quality, ventilation
rate and volume, time from cardiac arrest and the use of
adrenaline. Values are higher after an initial asphyxial arrest, with
bystander CPR and decline over time after cardiac arrest.295,302,405
Low end-tidal CO2 values during CPR have been associated with
lower ROSC rates and increased mortality, and high values with
better ROSC and survival.295,406,407 Failure to achieve an end-tidal
CO2 value >1.33 kPa (10 mmHg) after 20 min of CPR is associated
with a poor outcome in observational studies.4 In addition
it has been used as a criterion for withholding extracorporeal life
support in patients with refractory cardiac arrest.408 The interindividual
differences and influence of cause of cardiac arrest,
the problem with self-fulfilling prophecy in studies, our lack of
Fig. 3.3. Waveform capnography showing changes in the end-tidal carbon dioxide during CPR and after ROSC. The boxes show examples of monitor displays at the times
indicated. In this example the patient’s trachea is intubated at zero minutes. The patient is then ventilated at 10 breaths min−1
and given chest compressions (indicated
by CPR) at about two per second. A minute after tracheal intubation, there is pause in chest compressions and ventilation followed by a defibrillation attempt, and chest
compressions and ventilation then continue. Higher-quality chest compressions lead to an increased end-tidal carbon dioxide value. There is a further defibrillation attempt
after two minutes of chest compressions. There are then further chest compressions and ventilation. There is a significant increase in the end-tidal carbon dioxide value during
chest compressions and the patient starts moving and eye opening. Chest compressions are stopped briefly and there is a pulse indicating ROSC. Ventilation continues at
10 breaths min−1
. CPR – cardiopulmonary resuscitation; ROSC – return of spontaneous circulation; End tidal CO2 – end-tidal carbon dioxide; HR – heart rate; RR – respiratory
rate.
J. Soar et al. / Resuscitation 95 (2015) 100–147 113
confidence in the accuracy of measurement during CPR, and the
need for an advanced airway to measure end-tidal CO2 reliably
limits our confidence in its use for prognostication. Thus, we
recommend that a specific end-tidal CO2 value at any time during
CPR should not be used alone to stop CPR efforts. End-tidal
CO2 values should be considered only as part of a multi-modal
approach to decision-making for prognostication during CPR.
Extracorporeal cardiopulmonary resuscitation (eCPR)
Extracorporeal CPR (eCPR) should be considered as a rescue
therapy for those patients in whom initial ALS measures are unsuccessful
and, or to facilitate specific interventions (e.g. coronary
angiography and percutaneous coronary intervention (PCI) or pulmonary
thrombectomy for massive pulmonary embolism).409,410
There is an urgent need for randomised studies of eCPR and large
eCPR registries to identify the circumstances in which it works best,
establish guidelines for its use and identify the benefits, costs and
risks of eCPR.411,412
Extracorporeal techniques require vascular access and a circuit
with a pump and oxygenator and can provide a circulation of oxygenated
blood to restore tissue perfusion. This has the potential
to buy time for restoration of an adequate spontaneous circulation,
and treatment of reversible underlying conditions. This is
commonly called extracorporeal life support (ECLS), and more
specifically extracorporeal CPR (eCPR) when used during cardiac
arrest. These techniques are becoming more commonplace and
have been used for both in-hospital and out-of-hospital despite
limited observational data in select patient groups. Observational
studies suggest eCPR for cardiac arrest is associated with improved
survival when there is a reversible cause for cardiac arrest (e.g.
myocardial infarction, pulmonary embolism, severe hypothermia,
poisoning), there is little comorbidity, the cardiac arrest is witnessed,
the individual receives immediate high-quality CPR, and
eCPR is implemented early (e.g. within 1 h of collapse) including
when instituted by emergency physicians and intensivists.413–419
The implementation of eCPR requires considerable resource and
training. When compared with manual or mechanical CPR, eCPR
has been associated with improve survival after IHCA in selected
patients.413,415 After OHCA outcomes with both standard and
eCPR are less favourable.420 The duration of standard CPR before
eCPR is established and patient selection are important factors for
success.409,413,417,419,421–423
3e – Defibrillation
This section predominantly addresses the use of manual
defibrillators. Guidelines concerning the use of an automated
external defibrillator (AED) are addressed in Section 2 – Basic
Life Support.223 The defibrillation strategy for the 2015 European
Resuscitation Council (ERC) guidelines has changed little from the
former guidelines:
• The importance of early, uninterrupted chest compressions
remains emphasised throughout these guidelines, together with
minimising the duration of pre-shock and post-shock pauses.
• Continue chest compressions during defibrillator charging,
deliver defibrillation with an interruption in chest compressions
of no more than 5 s and immediately resume chest compressions
following defibrillation.
• Self-adhesive defibrillation pads have a number of advantages
over manual paddles and should always be used in preference
when they are available.
• CPR should be continued while a defibrillator or automated external
defibrillator (AED) is retrieved and applied but defibrillation
should not be delayed longer than needed to establish the need
for defibrillation and charging.
• The use of up to three-stacked shocks may be considered if initial
VF/pVT occurs during a witnessed, monitored arrest with a
defibrillator immediately available e.g. cardiac catheterisation.
• Although it is recognised that some geographic areas continue
to use the older monophasic waveforms, they are not considered
in this chapter. When possible, biphasic waveforms should
be used in preference to the older monophasic waveform for
the treatment of both atrial and ventricular arrhythmias. Defibrillation
recommendations in these guidelines apply only to
biphasic waveforms. For those using monophasic defibrillators,
please refer to Guidelines 2010.2
• Defibrillation shock energy levels are unchanged from the 2010
guidelines.2 For biphasic waveforms (rectilinear biphasic or
biphasic truncated exponential), deliver the first shock with an
energy of at least 150 J. For pulsed biphasic waveforms, begin at
120–150 J. The shock energy for a particular defibrillator should
be based on the manufacturer’s guidance. It is important that
those using manual defibrillators are aware of the appropriate
energy settings for the type of device used. Manufacturers should
consider labelling their manual defibrillators with energy level
instructions, but in the absence of this and if appropriate energy
levels are unknown, for adults use the highest available shock
energy for all shocks. With manual defibrillators it is appropriate
to consider escalating the shock energy if feasible, after a failed
shock and for patients where refibrillation occurs.326,327
There are no high-quality clinical studies to indicate the optimal
strategies within any given waveform and between different
waveforms.4 Knowledge gaps include the minimal acceptable firstshock
energy level; the characteristics of the optimal biphasic
waveform; the optimal energy levels for specific waveforms; and
the best shock strategy (fixed versus escalating). It is becoming
increasingly clear that selected energy is a poor comparator with
which to assess different waveforms as impedance-compensation
and subtleties in waveform shape result in significantly different
transmyocardial current between devices for any given selected
energy. The optimal energy levels may ultimately vary between
different manufacturers and associated waveforms. Manufacturers
are encouraged to undertake high-quality clinical trials to support
their defibrillation strategy recommendations.
Strategies for minimising the pre-shock pause
The delay between stopping chest compressions and delivery
of the shock (the pre-shock pause) must be kept to an absolute
minimum; even 5–10 s delay will reduce the chances of the shock
being successful.328–331,424,425 The pre-shock pause can be reduced
to less than 5 s by continuing compressions during charging of
the defibrillator and by having an efficient team coordinated by
a leader who communicates effectively.297,426 The safety check to
avoid rescuer contact with the patient at the moment of defibrillation
should be undertaken rapidly but efficiently. The post shock
pause is minimised by resuming chest compressions immediately
after shock delivery (see below). The entire process of manual defibrillation
should be achievable with less than a 5 s interruption to
chest compressions.
Hands-on defibrillation
By allowing continuous chest compressions during the delivery
of the defibrillation shock, hands-on defibrillation can minimise
peri-shock pause and allow continuation of chest compressions
during defibrillation. The benefits of this approach are not proven
and further studies are required to assess the safety and efficacy
of this technique. A recent study did not observe a benefit when
114 J. Soar et al. / Resuscitation 95 (2015) 100–147
shocks were delivered without pausing manual or mechanical chest
compressions.427 Standard clinical examination gloves (or bare
hands) do not provide a safe level of electrical insulation for handson
defibrillation.428
Safe use of oxygen during defibrillation
In an oxygen-enriched atmosphere, sparking from poorly
applied defibrillator paddles can cause a fire and significant burns
to a patient.429–434 The absence of case reports of fires caused by
sparking where defibrillation was delivered using self-adhesive
defibrillation pads suggests that the latter minimise the risk of
electrical arcing and should always be used when possible.
• The risk of fire during attempted defibrillation can be minimised
by taking the following precautions:
• Take off any oxygen mask or nasal cannulae and place them at
least 1 m away from the patient’s chest.
• Leave the ventilation bag connected to the tracheal tube or supraglottic
airway, ensuring that there is no residual PEEP remaining
in the circuit.
• If the patient is connected to a ventilator, for example in the
operating room or critical care unit, leave the ventilator tubing
(breathing circuit) connected to the tracheal tube unless chest
compressions prevent the ventilator from delivering adequate
tidal volumes. In this case, the ventilator is usually substituted
by a ventilation bag, which can itself be left connected. If not in
use, switch off the ventilator to prevent venting large volumes of
oxygen into the room or alternatively connect it to a test lung.
During normal use, when connected to a tracheal tube, oxygen
from a ventilator in the critical care unit will be vented from the
main ventilator housing well away from the defibrillation zone.
Patients in the critical care unit may be dependent on positive end
expiratory pressure (PEEP) to maintain adequate oxygenation;
during cardioversion, when the spontaneous circulation potentially
enables blood to remain well oxygenated, it is particularly
appropriate to leave the critically ill patient connected to the
ventilator during shock delivery.
The technique for electrode contact with the chest
The techniques described below aim to place external defibrillation
electrodes (self-adhesive pads) in an optimal position using
techniques that minimise transthoracic impedance.
Electrode position
No human studies have evaluated the electrode position as a
determinant of ROSC or survival from VF/pVT. Transmyocardial
current during defibrillation is likely to be maximal when the electrodes
are placed so that the area of the heart that is fibrillating
lies directly between them (i.e. ventricles in VF/pVT, atria in AF).
Therefore, the optimal electrode position may not be the same for
ventricular and atrial arrhythmias.
More patients are presenting with implantable medical devices
(e.g. permanent pacemaker, implantable cardioverter defibrillator
(ICD)). Medic alert bracelets are recommended for these
patients. These devices may be damaged during defibrillation if
current is discharged through electrodes placed directly over the
device.435,436 Place the electrode away from the device (at least
8 cm) or use an alternative electrode position (anterior–lateral,
anterior–posterior) as described below.435
Placement for ventricular arrhythmias and cardiac arrest. Place electrodes
(either pads or paddles) in the conventional sternal–apical
position. The right (sternal) electrode is placed to the right of the
sternum, below the clavicle. The apical paddle is placed in the left
mid-axillary line, approximately level with the V6 ECG electrode.
This position should be clear of any breast tissue.437 It is important
that this electrode is placed sufficiently laterally. Other acceptable
pad positions include
• Placement of each electrode on the lateral chest walls, one on the
right and the other on the left side (bi-axillary).
• One electrode in the standard apical position and the other on the
right upper back.
• One electrode anteriorly, over the left precordium, and the other
electrode posteriorly to the heart just inferior to the left scapula.
It does not matter which electrode (apex/sternum) is placed
in either position. The long axis of the apical paddle should be
orientated in a cranio-caudal direction to minimise transthoracic
impedance.438
Placement for atrial arrhythmias. Atrial fibrillation is maintained by
functional re-entry circuits anchored in the left atrium. As the left
atrium is located posteriorly in the thorax, electrode positions that
result in a more posterior current pathway may theoretically be
more effective for atrial arrhythmias. Although some studies have
shown that antero-posterior electrode placement is more effective
than the traditional antero-apical position in elective cardioversion
of atrial fibrillation,439,440 the majority have failed to demonstrate
any clear advantage of any specific electrode position.441–444 Efficacy
of cardioversion may be less dependent on electrode position
when using biphasic impedance-compensated waveforms.443–445
The following electrode positions all appear safe and effective for
cardioversion of atrial arrhythmias:
• Traditional antero-apical position.
• Antero-posterior position (one electrode anteriorly, over the left
precordium, and the other electrode posteriorly to the heart just
inferior to the left scapula).
Respiratory phase
Transthoracic impedance varies during respiration, being minimal
at end-expiration. If possible, defibrillation should be
attempted at this phase of the respiratory cycle. Positive end expiratory
pressure (PEEP) increases transthoracic impedance and should
be minimised during defibrillation. Auto-PEEP (gas trapping) may
be particularly high in asthmatics and may necessitate higher than
usual energy levels for defibrillation.446
Fibrillation waveform analysis
It is possible to predict, with varying reliability, the success of
defibrillation from the fibrillation waveform.342,343,447–467 If optimal
defibrillation waveforms and the optimal timing of shock
delivery can be determined in prospective studies, it should be possible
to prevent the delivery of unsuccessful high energy shocks and
minimise myocardial injury. This technology is under active development
and investigation but current sensitivity and specificity is
insufficient to enable introduction of VF waveform analysis into
clinical practice.
CPR versus defibrillation as the initial treatment
This aspect has been dealt with in detail above in 4b – prehospital
resuscitation. Rescuers should provide high-quality CPR while
a defibrillator is retrieved, applied and charged. Do not delay defibrillation
longer than needed to establish the need for defibrillation
and charging. The routine delivery of a pre-specified period of CPR
(e.g. 2 or 3 min) before rhythm analysis and a shock is delivered is
not recommended.
J. Soar et al. / Resuscitation 95 (2015) 100–147 115
One shock versus three stacked shock sequence
In 2010, it was recommended that when defibrillation was
required, a single shock should be provided with immediate
resumption of chest compressions after the shock.468,469 This recommendation
was made for two reasons. Firstly in an attempt to
minimise peri-shock interruptions to chest compressions and secondly
because it was felt that with the greater efficacy of biphasic
shocks, if a biphasic shock failed to defibrillate, a further period of
chest compressions could be beneficial.
Studies since 2010 have not shown that any specific shock
strategy is of benefit for any survival end-point.470,471 There is no
conclusive evidence that a single shock strategy is of benefit for
ROSC or recurrence of VF compared with three stacked shocks, but
in view of the evidence suggesting that outcome is improved by
minimising interruptions to chest compressions, we continue to
recommend single shocks for most situations.
When defibrillation is warranted, give a single shock and resume
chest compressions immediately following the shock. Do not delay
CPR for rhythm reanalysis or a pulse check immediately after a
shock. Continue CPR (30 compressions: 2 ventilations) for 2 min
until rhythm reanalysis is undertaken and another shock given (if
indicated). Even if the defibrillation attempt is successful, it takes
time until the post shock circulation is established332 and it is very
rare for a pulse to be palpable immediately after defibrillation.333
Patients can remain pulseless for over 2 min and the duration of
asystole before ROSC can be longer than 2 min in as many as 25% of
successful shocks.334
If a patient has a monitored and witnessed cardiac arrest in
the catheter laboratory, coronary care unit, a critical care area or
whilst monitored after cardiac surgery, and a manual defibrillator
is rapidly available:
• Confirm cardiac arrest and shout for help.
• If the initial rhythm is VF/pVT, give up to three quick successive
(stacked) shocks.
• Rapidly check for a rhythm change and if appropriate ROSC after
each defibrillation attempt.
• Start chest compressions and continue CPR for 2 min if the third
shock is unsuccessful.
This three-shock strategy may also be considered for an initial,
witnessed VF/pVT cardiac arrest if the patient is already connected
to a manual defibrillator. Although there are no data supporting a
three-shock strategy in any of these circumstances, it is unlikely
that chest compressions will improve the already very high chance
of ROSC when defibrillation occurs early in the electrical phase,
immediately after onset of VF.
Waveforms
Biphasic waveforms, are now well established as a safe and
effective waveform for defibrillation. Biphasic defibrillators compensate
for the wide variations in transthoracic impedance by
electronically adjusting the waveform magnitude and duration to
ensure optimal current delivery to the myocardium, irrespective of
the patient’s size (impedance compensation). There are two main
types of biphasic waveform: the biphasic truncated exponential
(BTE) and rectilinear biphasic (RLB). A pulsed biphasic waveform is
also in clinical use, in which the current rapidly oscillates between
baseline and a positive value before inverting in a negative pattern.
It may have a similar efficacy as other biphasic waveforms,
but the single clinical study of this waveform was not performed
with an impedance compensating waveform, which is used in the
commercially available product.472,473
We recommend that a biphasic waveform is used for cardioversion
of both atrial and ventricular arrhythmias in preference to
a monophasic waveform. We place a high value on the reported
higher first shock success rate for termination of fibrillation with
a biphasic waveform, the potential for less post shock myocardial
dysfunction and the existing 2010 Guidelines.1,2,468,469 We
acknowledge that many emergency medical services (EMS) systems
and hospitals continue to use older monophasic devices. For
those using monophasic defibrillators, please refer to Guidelines
2010.2
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 whilst causing
the minimum of myocardial damage.474 Selection of an appropriate
energy level also reduces the number of repetitive shocks, which
in turn limits myocardial damage.475
Optimal energy levels for defibrillation are unknown. The recommendations
for energy levels are based on a consensus following
careful review of the current literature. Although delivered energy
levels are selected for defibrillation, it is the transmyocardial current
flow that achieves defibrillation. Current correlates well with
successful defibrillation and cardioversion.476 Defibrillation shock
energy levels are unchanged from the 2010 guidelines.2
First shock
Relatively few studies have been published in the past five
years on which to refine the 2010 guidelines. There is no evidence
that one biphasic waveform or device is more effective than
another. First shock efficacy of the BTE waveform using 150–200 J
has been reported as 86–98%.477–481 First shock efficacy of the
RLB waveform using 120 J is up to 85%.327 First shock efficacy of
a new pulsed biphasic waveform at 130 J showed a first shock
success rate of 90%.472 Two studies have suggested equivalence
with lower and higher starting energy biphasic defibrillation.482,483
Although human studies have not shown harm (raised biomarkers,
ECG changes, ejection fraction) from any biphasic waveform up to
360 J,482,484 several animal studies have suggested the potential for
harm with higher energy levels.485–488
The initial biphasic shock should be no lower than 120 J for RLB
waveforms and at least 150 J for BTE waveforms. Ideally, the initial
biphasic shock energy should be at least 150 J for all waveforms.
Manufacturers should display the effective waveform dose range
on the face of the biphasic defibrillator. If the rescuer is unaware
of the recommended energy settings of the defibrillator, use the
highest setting for all shocks.
Second and subsequent shocks
The 2010 guidelines recommended either a fixed or escalating
energy strategy for defibrillation. Several studies demonstrated
that although an escalating strategy reduces the number of shocks
required to restore an organised rhythm compared with fixeddose
biphasic defibrillation, and may be needed for successful
defibrillation,326,489 rates of ROSC or survival to hospital discharge
are not significantly different between strategies.482,483 Conversely,
a fixed-dose biphasic protocol demonstrated high cardioversion
rates (>90%) with a three-shock fixed dose protocol but the small
number of cases did not exclude a significant lower ROSC rate
for recurrent VF.490 Several in-hospital studies using an escalating
shock energy strategy have demonstrated improvement in cardioversion
rates (compared with fixed dose protocols) in non-arrest
116 J. Soar et al. / Resuscitation 95 (2015) 100–147
rhythms with the same level of energy selected for both biphasic
and monophasic waveforms.491–496
Animal studies, case reports and small case series have documented
the use of two defibrillators to deliver a pair of shocks at the
same time (‘dual sequential defibrillation’) to patients in refractory
shockable states.497–501 Given the very limited evidence, the routine
use of dual sequential defibrillation’ cannot be recommended.
There remains no evidence to support either a fixed or escalating
energy protocol, although an escalating protocol may be associated
with a lower incidence of refibrillation (see below). Both strategies
are acceptable; however, if the first shock is not successful and the
defibrillator is capable of delivering shocks of higher energy it is
reasonable to increase the energy for subsequent shocks.
Recurrent ventricular fibrillation (refibrillation). Refibrillation is
common and occurs in the majority of patients following initial
first-shock termination of VF. Refibrillation was not specifically
addressed in 2010 guidelines. Distinct from refractory VF, defined
as ‘fibrillation that persists after one or more shocks’, recurrence
of fibrillation is usually defined as ‘recurrence of VF during a documented
cardiac arrest episode, occurring after initial termination of
VF while the patient remains under the care of the same providers
(usually out-of-hospital).’ Two studies showed termination rates
of subsequent refibrillation were unchanged when using fixed
120 J or 150 J shock protocols respectively,490,502 but a larger study
showed termination rates of refibrillation declined when using
repeated 200 J shocks, unless an increased energy level (360 J) was
selected.326 In a retrospective analysis, termination rate of VF into
a pulse generating rhythm was higher if the VF appeared after a
pulse generating rhythm, than after PEA or asystole.503
In view of the larger study suggesting benefit from higher subsequent
energy levels for refibrillation,326 we recommend that if a
shockable rhythm recurs after successful defibrillation with ROSC,
and the defibrillator is capable of delivering shocks of higher energy
it is reasonable to increase the energy for subsequent shocks.
Other related defibrillation topics
Cardioversion
If electrical cardioversion is used to convert atrial or ventricular
tachyarrhythmias, the shock must be synchronised to occur
with the R wave of the electrocardiogram rather than with the T
wave: VF can be induced if a shock is delivered during the relative
refractory portion of the cardiac cycle.504 Synchronisation can be
difficult in VT because of the wide-complex and variable forms of
ventricular arrhythmia. Inspect the synchronisation marker carefully
for consistent recognition of the R wave. If needed, choose
another lead and/or adjust the amplitude. If synchronisation fails,
give unsynchronised shocks to the unstable patient in VT to avoid
prolonged delay in restoring sinus rhythm. Ventricular fibrillation
or pulseless VT requires unsynchronised shocks. Conscious patients
require anaesthesia or sedation, and analgesia before attempting
synchronised cardioversion.
Atrial fibrillation. Optimal electrode position has been discussed
previously, but anterolateral and anteroposterior are both acceptable
positions.443 Biphasic waveforms are more effective than
monophasic waveforms for cardioversion of AF493,494,505,506; and
cause less severe skin burns.507 More data are needed before
specific recommendations can be made for optimal biphasic
energy levels and different biphasic waveforms. Biphasic rectilinear
and biphasic truncated exponential waveform show similar
high efficacy in the elective cardioversion of atrial fibrillation.508
Commencing at high energy levels has not shown to result in
more successful cardioversion rates compared to lower energy
levels.494,509–514 An initial synchronised shock of 120–150 J, escalating
if necessary is a reasonable strategy based on current data.
Atrial flutter and paroxysmal supraventricular tachycardia. Atrial
flutter and paroxysmal SVT generally require less energy than
atrial fibrillation for cardioversion.513 Give an initial shock of
70–120 J biphasic. Give subsequent shocks using stepwise increases
in energy.476
Ventricular tachycardia. The energy required for cardioversion of
VT depends on the morphological characteristics and rate of the
arrhythmia.515 Ventricular tachycardia with a pulse responds well
using biphasic energy levels of 120–150 J for the initial shock. Consider
stepwise increases if the first shock fails to achieve sinus
rhythm.515
Pacing
Consider pacing in patients with symptomatic bradycardia
refractory to anti-cholinergic drugs or other second line therapy.
Immediate pacing is indicated especially when the block is at or
below the His-Purkinje level. If transthoracic pacing is ineffective,
consider transvenous pacing. Whenever a diagnosis of asystole is
made, check the ECG carefully for the presence of P waves because
this will likely respond to cardiac pacing. The use of epicardial wires
to pace the myocardium following cardiac surgery is effective and
discussed elsewhere. Do not attempt pacing for asystole unless P
waves are present; it does not increase short or long-term survival
in- or out-of-hospital.516–524 For haemodynamically unstable,
conscious patients with bradyarrhythmias, percussion pacing as a
bridge to electrical pacing may be attempted, although its effectiveness
has not been established.525,526
Implantable cardioverter defibrillators
Implantable cardioverter defibrillators (ICDs) are becoming
increasingly common as the devices are implanted more frequently
as the population ages. They are implanted because a patient is considered
to be at risk from, or has had, a life-threatening shockable
arrhythmia and are usually embedded under the pectoral muscle
below the left clavicle (in a similar position to pacemakers, from
which they cannot be immediately distinguished). More recently,
extravascular devices can be implanted subcutaneously in the left
chest wall, with a lead running to the left of the sternum.
On sensing a shockable rhythm, an ICD will discharge approximately
40 J (approximately 80 J for subcutaneous devices) through
an internal pacing wire embedded in the right ventricle. On detecting
VF/pVT, ICD devices will discharge no more than eight times,
but may reset if they detect a new period of VF/pVT. Patients with
fractured ICD leads may suffer repeated internal defibrillation as
the electrical noise is mistaken for a shockable rhythm; in these
circumstances, the patient is likely to be conscious, with the ECG
showing a relatively normal rate. A magnet placed over the ICD will
disable the defibrillation function in these circumstances.
Discharge of an ICD may cause pectoral muscle contraction in
the patient, and shocks to the rescuer have been documented.527
In view of the low energy levels discharged by conventional ICDs, it
is unlikely that any harm will come to the rescuer, but minimising
contact with the patient whilst the device is discharging is prudent.
Surface current from subcutaneous ICDs is currently under
investigation. Cardioverter and pacing function should always be
re-evaluated following external defibrillation, both to check the
device itself and to check pacing/defibrillation thresholds of the
device leads.
Pacemaker spikes generated by devices programmed to unipolar
pacing may confuse AED software and emergency personnel,
J. Soar et al. / Resuscitation 95 (2015) 100–147 117
and may prevent the detection of VF.528 The diagnostic algorithms
of modern AEDs can be insensitive to such spikes.
3f – Airway management and ventilation
Introduction
The optimal strategy for managing the airway has yet to be
determined. Several observational studies have challenged the
premise that advanced airway interventions (tracheal intubation
or supraglottic airways) improve outcomes.529 Options for airway
management and ventilation during CPR include: no airway and no
ventilation (compression-only CPR), compression-only CPR with
the airway held open (with or without supplementary oxygen),
mouth-to-mouth breaths, mouth-to-mask, bag-mask ventilation
with simple airway adjuncts, supraglottic airways (SGAs), and
tracheal intubation (inserted with the aid of direct laryngoscopy
or videolaryngoscopy, or via a SGA). In practice a combination
of airway techniques will be used stepwise during a resuscitation
attempt.530 The best airway, or combination of airway
techniques will vary according to patient factors, the phase of the
resuscitation attempt (during CPR, after ROSC), and the skills of
rescuers.311 A stepwise approach to airway and ventilation management
using a combination of techniques is therefore suggested.
Compression-only CPR and use of ventilation during basic life support
is addressed in Section 2 – Basic Life Support.223
Patients requiring resuscitation often have an obstructed airway,
usually secondary to loss of consciousness, but occasionally
it may be the primary cause of cardiorespiratory arrest. Prompt
assessment, with control of the airway and ventilation of the lungs,
is essential. This will help to prevent secondary hypoxic damage
to the brain and other vital organs. Without adequate oxygenation
it may be impossible to achieve ROSC. These principles may not
apply to the witnessed primary cardiac arrest in the vicinity of a
defibrillator; in this case, the priority is immediate defibrillation.
Airway obstruction
Causes of airway obstruction
Obstruction of the airway may be partial or complete. It may
occur at any level, from the nose and mouth down to the trachea.
In the unconscious patient, the commonest site of airway obstruction
is at the soft palate and epiglottis.531,532 Obstruction may also
be caused by vomit or blood (regurgitation of gastric contents or
trauma), or by foreign bodies. Laryngeal obstruction may be caused
by oedema from burns, inflammation or anaphylaxis. Upper airway
stimulation may cause laryngeal spasm. Obstruction of the airway
below the larynx is less common, but may arise from excessive
bronchial secretions, mucosal oedema, bronchospasm, pulmonary
oedema or aspiration of gastric contents.
Recognition of airway obstruction
Airway obstruction can be subtle and is often missed by healthcare
professionals, let alone by laypeople. The ‘look, listen and
feel’ approach is a simple, systematic method of detecting airway
obstruction.
• Look for chest and abdominal movements.
• Listen and feel for airflow at the mouth and nose.
In partial airway obstruction, air entry is diminished and usually
noisy. Inspiratory stridor is caused by obstruction at the laryngeal
level or above. Expiratory wheeze implies obstruction of the lower
airways, which tend to collapse and obstruct during expiration.
In a patient who is making respiratory efforts, complete airway
obstruction causes paradoxical chest and abdominal movement,
often described as ‘see-saw’ breathing. During airway obstruction,
other accessory muscles of respiration are used, with the neck and
the shoulder muscles contracting to assist movement of the thoracic
cage.
Basic airway management
There are three manoeuvres that may improve the patency of an
airway obstructed by the tongue or other upper airway structures:
head tilt, chin lift, and jaw thrust.
Head tilt and chin lift
The rescuer’s hand is placed on the patient’s forehead and the
head gently tilted back; the fingertips of the other hand are placed
under the point of the patient’s chin, which is lifted gently to stretch
the anterior neck structures.533–538
Jaw thrust
Jaw thrust is an alternative manoeuvre for bringing the
mandible forward and relieving obstruction by the soft palate and
epiglottis. The rescuer’s index and other fingers are placed behind
the angle of the mandible, and pressure is applied upwards and
forwards. Using the thumbs, the mouth is opened slightly by downward
displacement of the chin.
Airway management in patients with suspected cervical spine
injury
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.539,540 If life-threatening airway obstruction persists
despite effective application of jaw thrust or chin lift, add head tilt
in small increments until the airway is open; establishing a patent
airway takes priority over concerns about a potential cervical spine
injury.
Adjuncts to basic airway techniques
Despite a total lack of published data on the use of nasopharyngeal
and oropharyngeal airways during CPR, they are often helpful,
and sometimes essential, to maintain an open airway, particularly
when resuscitation is prolonged. The position of the head and
neck is maintained to keep the airway aligned. Oropharyngeal and
nasopharyngeal airways overcome backward displacement of the
soft palate and tongue in an unconscious patient, but head tilt and
jaw thrust may also be required.
Oropharyngeal airways. Oropharyngeal airways are available in
sizes suitable for the newborn to large adults. An estimate of the
size required is obtained by selecting an airway with a length corresponding
to the vertical distance between the patient’s incisors
and the angle of the jaw. The most common sizes are 2, 3 and 4 for
small, medium and large adults, respectively.
Nasopharyngeal airways. In patients who are not deeply unconscious,
a nasopharyngeal airway is tolerated better than an
oropharyngeal airway. The nasopharyngeal airway may be life saving
in patients with clenched jaws, trismus or maxillofacial injuries,
when insertion of an oral airway is impossible. The tubes are sized
in millimetres according to their internal diameter and the length
increases with diameter. Sizes of 6–7 mm are suitable for adults.
Oxygen during CPR
During CPR, give the maximal feasible inspired oxygen concentration.
A self-inflating bag can be connected to a facemask, tracheal
tube or supraglottic airway (SGA). Without supplementary oxygen,
118 J. Soar et al. / Resuscitation 95 (2015) 100–147
the self-inflating bag ventilates the patient’s lungs with ambient air
(21% oxygen). The delivered oxygen concentration can be increased
to about 85% by using a reservoir system and attaching oxygen at
a flow 10 l min−1. There are no data to indicate the optimal arterial
blood oxygen saturation (SaO2) during CPR, and no trials comparing
different inspired oxygen concentrations. In one observational
study of patients receiving 100% inspired oxygen via a tracheal tube
during CPR, a higher measured PaO2 value during CPR was associated
with ROSC and hospital admission.541 The worse outcomes
associated with a low PaO2 during CPR could however be an indication
of illness severity. Animal data and observational clinical data
indicate an association between high SaO2 after ROSC and worse
outcome (Section 5 – Post-resuscitation care).273,542–544
After ROSC, as soon as arterial blood oxygen saturation can be
monitored reliably (by blood gas analysis and/or pulse oximetry),
titrate the inspired oxygen concentration to maintain the arterial
blood oxygen saturation in the range of 94–98%. Avoid hypoxaemia,
which is also harmful – ensure reliable measurement of
arterial oxygen saturation before reducing the inspired oxygen concentration.
This is addressed in further detail in Section 5 – post
resuscitation care.273
Suction
Use a wide-bore rigid sucker (Yankauer) to remove liquid (blood,
saliva and gastric contents) from the upper airway. Use the sucker
cautiously if the patient has an intact gag reflex; pharyngeal stimulation
can provoke vomiting.
Choking
The initial management of foreign body airway obstruction
(choking) is addressed in Section 2 – basic life support.223 In an
unconscious patient with suspected foreign body airway obstruction
if initial basic measures are unsuccessful use laryngoscopy and
forceps to remove the foreign body under direct vision. To do this
effectively requires training.
Ventilation
Advanced Life Support providers should give artificial ventilation
as soon as possible for any patient in whom spontaneous
ventilation is inadequate or absent. Expired air ventilation (rescue
breathing) is effective, but the rescuer’s expired oxygen concentration
is only 16–17%, so it must be replaced as soon as possible
by ventilation with oxygen-enriched air. The pocket resuscitation
mask is similar to an anaesthetic facemask, and enables mouthto-mask
ventilation. It has a unidirectional valve, which directs the
patient’s expired air away from the rescuer. The mask is transparent
so that vomit or blood from the patient can be seen. Some masks
have a connector for the addition of oxygen. When using masks
without a connector, supplemental oxygen can be given by placing
the tubing underneath one side and ensuring an adequate seal. Use
a two-hand technique to maximise the seal with the patient’s face.
High airway pressures can be generated if the tidal volume or
inspiratory flow is excessive, predisposing to gastric inflation and
subsequent risk of regurgitation and pulmonary aspiration. The risk
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 airway inflation pressure.
Conversely, if inspiratory flow is too low, inspiratory time will
be prolonged and the time available to give chest compressions is
reduced. Deliver each breath over approximately 1 s, giving a volume
that corresponds to normal chest movement; this represents
a compromise between giving an adequate volume, minimising
the risk of gastric inflation, and allowing adequate time for chest
compressions. During CPR with an unprotected airway, give two
ventilations after each sequence of 30 chest compressions.
Inadvertent hyperventilation during CPR is common. While this
increased intrathoracic pressure545 and peak airway pressures546
in small case series in humans, a carefully controlled animal experiment
revealed no adverse effects.547 We suggest a ventilation
rate of 10 min−1 during continuous chest compressions with an
advanced airway based on very limited evidence.4
Self-inflating bag
The self-inflating bag can be connected to a facemask, tracheal
tube or supraglottic airway (SGA). Without supplementary oxygen,
the self-inflating bag ventilates the patient’s lungs with ambient air
(21% oxygen). The delivered oxygen concentration can be increased
to about 85% by using a reservoir system and attaching oxygen at a
flow 10 l min−1.
Although a bag-mask enables ventilation with high concentrations
of oxygen, its use by a single person requires considerable
skill. When used with a face mask, it is often difficult to achieve a
gas-tight seal between the mask and the patient’s face, and to maintain
a patent airway with one hand while squeezing the bag with
the other. Any significant leak will cause hypoventilation and, if
the airway is not patent, gas may be forced into the stomach.548,549
This will reduce ventilation further and greatly increase the risk of
regurgitation and aspiration.550 The two-person technique for bagmask
ventilation is preferable. Several recent observational studies
and a meta-analysis have documented better outcomes with use of
bag-mask ventilation compared with more advanced airways (SGA
or tracheal tube).529,551–554 However, these observation studies are
subject to significant bias caused by confounders such as advanced
airways not being required in those patients who achieve ROSC and
awaken early.
Once a tracheal tube or a SGA has been inserted, ventilate the
lungs at a rate of 10 breaths min−1 and continue chest compressions
without pausing during ventilations. The laryngeal seal achieved
with a SGA may not be good enough to prevent at least some
gas leaking when inspiration coincides with chest compressions.
Moderate gas leakage is acceptable, particularly as most of this gas
will pass up through the patient’s mouth. If excessive gas leakage
results in inadequate ventilation of the patient’s lungs, chest compressions
will have to be interrupted to enable ventilation, using a
compression–ventilation ratio of 30:2.
Passive oxygen delivery
In the presence of a patent airway, chest compressions alone
may result in some ventilation of the lungs.555 Oxygen can be delivered
passively, either via an adapted tracheal tube (Boussignac
tube),556,557 or with the combination of an oropharyngeal airway
and standard oxygen mask with non-rebreather reservoir.558 In
theory, a SGA can also be used to deliver oxygen passively but
this has yet to be studied. One study has shown higher neurologically
favourable survival with passive oxygen delivery (oral airway
and oxygen mask) compared with bag-mask ventilation after outof-hospital
VF cardiac arrest, but this was a retrospective analysis
and is subject to numerous confounders.558 Until further data are
available, passive oxygen delivery without ventilation is not recommended
for routine use during CPR.
Alternative airway devices
The tracheal tube has generally been considered the optimal
method of managing the airway during cardiac arrest.309
There is evidence that, without adequate training and experience,
the incidence of complications, such as unrecognised
J. Soar et al. / Resuscitation 95 (2015) 100–147 119
oesophageal intubation (2.4–17% in several studies involving
paramedics)559–563 and dislodgement, is unacceptably high.564
Prolonged attempts at tracheal intubation are harmful; the cessation
of chest compressions during this time will compromise
coronary and cerebral perfusion. Several alternative airway devices
have been used for airway management during CPR. There are
published studies on the use during CPR of the Combitube, the
classic laryngeal mask airway (cLMA), the laryngeal tube (LT), the
i-gel, and the LMA Supreme (LMAS) but none of these studies have
been powered adequately to enable survival to be studied as a primary
endpoint; instead, most researchers have studied insertion
and ventilation success rates. The SGAs are easier to insert than a
tracheal tube and,565 unlike tracheal intubation, can generally be
inserted without interrupting chest compressions.566
There are no data supporting the routine use of any specific
approach to airway management during cardiac arrest. The best
technique is dependent on the precise circumstances of the cardiac
arrest and the competence of the rescuer. It is recognised that during
cardiac arrest a stepwise approach to airway management is
commonly used, which implies that multiple devices may be used
during a single resuscitation attempt.
Laryngeal mask airway (LMA)
The original LMA (classic LMA [cLMA]), which is reusable, has
been studied during CPR, but none of these studies has compared
it directly with the tracheal tube. Although the cLMA
remains in common use in elective anaesthetic practice, it has
been superseded by several 2nd generation SGAs that have more
favourable characteristics, particularly when used for emergency
airway management.567 Most of these SGAs are single use and
achieve higher oropharyngeal seal pressures than the cLMA, and
some incorporate gastric drain tubes.
Combitube
The Combitube is a double-lumen tube introduced blindly over
the tongue, and provides a route for ventilation whether the tube
has passed into the oesophagus. There are many studies of the Combitube
in CPR and successful ventilation was achieved in 79–98% of
patients.568–576 Two RCTs of the Combitube versus tracheal intubation
for out-of-hospital cardiac arrest showed no difference in
survival.575,576 Use of the Combitube is waning and in many parts
of the world it is being replaced by other devices such as the LT.
Laryngeal tube
The laryngeal tube (LT) was introduced in 2001; it is known as
the King LT airway in the United States. After just 2 h of training,
nurses successfully inserted a laryngeal tube and achieved ventilation
in 24 of 30 (80%) of OHCAs.577 In five observational studies, a
disposable version of the laryngeal tube (LT-D) was inserted successfully
by prehospital personnel in 85–100% of OHCAs (number
of cases ranged from 92 to 347).578–582 Although some studies are
supportive of the use of the LT during cardiac arrest several other
studies have reported that insertion problems are common; these
include problems with positioning and leakage.580,583
i-gel
The cuff of the i-gel is made of thermoplastic elastomer gel and
does not require inflation; the stem of the i-gel incorporates a bite
block and a narrow oesophageal drain tube. It is very easy to insert,
requiring only minimal training and a laryngeal seal pressure of
20–24 cmH2O can be achieved.584,585 The ease of insertion of the
i-gel and its favourable leak pressure make it theoretically very
attractive as a resuscitation airway device for those inexperienced
in tracheal intubation. In observational studies insertion success
rates for the i-gel were 93% (n = 98) when used by paramedics for
OHCA586 and 99% (n = 100) when used by doctors and nurses for
IHCA.587
LMA supreme (LMAS). The LMAS is a disposable version of the Proseal
LMA, which is used in anaesthetic practice. In an observational
study, paramedics inserted the LMAS successfully and were able to
ventilate the lungs of 33 (100%) cases of OHCA.588
Tracheal intubation
There is insufficient evidence to support or refute the use of
any specific technique to maintain an airway and provide ventilation
in adults with cardiopulmonary arrest. Despite this, tracheal
intubation is perceived as the optimal method of providing and
maintaining a clear and secure airway.309 It should be used only
when trained personnel are available to carry out the procedure
with a high level of skill and confidence. A systematic review of
randomised controlled trials (RCTs) of tracheal intubation versus
alternative airway management in acutely ill and injured patients
identified just three trials589: two were RCTs of the Combitube
versus tracheal intubation for out-of-hospital cardiac arrest,575,576
which showed no difference in survival. The third study was a
RCT of prehospital tracheal intubation versus management of the
airway with a bag-mask in children requiring airway management
for cardiac arrest, primary respiratory disorders and severe
injuries.590 There was no overall benefit for tracheal intubation; on
the contrary, of the children requiring airway management for a
respiratory problem, those randomised to intubation had a lower
survival rate that those in the bag-mask group.
The perceived advantages of tracheal intubation over bag-mask
ventilation include: enabling ventilation without interrupting
chest compressions591; enabling effective ventilation, particularly
when lung and/or chest compliance is poor; minimising gastric
inflation and therefore the risk of regurgitation; protection against
pulmonary aspiration of gastric contents; and the potential to free
the rescuer’s hands for other tasks. Use of the bag-mask is more
likely to cause gastric distension that, theoretically, is more likely
to cause regurgitation with risk of aspiration. However, there are
no reliable data to indicate that the incidence of aspiration is any
more in cardiac arrest patients ventilated with bag-mask versus
those that are ventilated via tracheal tube.
The perceived disadvantages of tracheal intubation over bagvalve-mask
ventilation include:
• The risk of an unrecognised misplaced tracheal tube – in patients
with out-of-hospital cardiac arrest the reliably documented incidence
ranges from 0.5% to 17%: emergency physicians–0.5%;592
paramedics – 2.4%,559 6%,560,561 9%,562 17%.563
• A prolonged period without chest compressions while intubation
is attempted – in a study of prehospital intubation by paramedics
during 100 cardiac arrests the total duration of the interruptions
in CPR associated with tracheal intubation attempts was 110 s
(IQR 54–198 s; range 13–446 s) and in 25% the interruptions were
more than 3 min.593 Tracheal intubation attempts accounted for
almost 25% of all CPR interruptions.
• A comparatively high failure rate. Intubation success rates correlate
with the intubation experience attained by individual
paramedics.594 Rates for failure to intubate are as high as 50%
in prehospital systems with a low patient volume and providers
who do not perform intubation frequently.595,596
• Tracheal intubation is a difficult skill to acquire and maintain. In
one study, anaesthesia residents required about 125 intubations
in the operating room setting before they were able to achieve
and intubation success rate of 95%.597
120 J. Soar et al. / Resuscitation 95 (2015) 100–147
Only one study has prospectively compared tracheal intubation
with insertion of a SGA in OHCA and this was a feasibility
study that is not powered to show differences in survival.530 A
secondary analysis of the North American Resuscitation Outcomes
Consortium (ROC) PRIMED study that compared tracheal intubation
(n = 8487) with SGAs (LT, Combitube, or LMA; n = 1968)
showed that successful tracheal intubation was associated with
increased neurologically favourable survival to hospital discharge
(adjusted OR 1.40, 95% CI 1.04–1.89) when compared with successful
SGA insertion.598 In a Japanese OHCA study, tracheal intubation
(n = 16,054) was compared with the LMA (n = 34,125) and the
oesophageal obturator airway (n = 88,069) over a 3-year period.599
Adjusted ORs for favourable one-month survival were lower for
the LMA (0.77, 95% CI 0.64–0.94) and the oesophageal obturator
airway (0.81, 95% CI 0.68–0.96) in comparison with tracheal intubation.
Even though the data from these two observational studies
are risk-adjusted, it is likely that hidden confounders account for
the findings.
Healthcare personnel who undertake prehospital intubation
should do so only within a structured, monitored programme,
which should include comprehensive competency-based training
and regular opportunities to refresh skills. Rescuers must weigh the
risks and benefits of intubation against the need to provide effective
chest compressions. The intubation attempt may require some
interruption of chest compressions but, once an advanced airway is
in place, ventilation will not require interruption of chest compressions.
Personnel skilled in advanced airway management should be
able to undertake laryngoscopy without stopping chest compressions;
a brief pause in chest compressions will be required only as
the tube is passed through the vocal cords. Alternatively, to avoid
any interruptions in chest compressions, the intubation attempt
may be deferred until ROSC558,600; this strategy is being studied
in a large prehospital randomised trial.601 The intubation attempt
should interrupt chest compressions for less than 5 s; if intubation
is not achievable within these constraints, recommence bag-mask
ventilation. After intubation, tube placement must be confirmed
and the tube secured adequately.
Videolaryngoscopy
Videolaryngoscopes are being used increasingly in anaesthetic
and critical care practice.602,603 In comparison with direct laryngoscopy,
they enable a better view of the larynx and improve the
success rate of intubation. Preliminary studies indicate that use of
videolaryngoscopes improve laryngeal view and intubation success
rates during CPR604–606 but further data are required before
recommendations can be made for wider use during CPR.
Confirmation of correct placement of the tracheal tube
Unrecognised oesophageal intubation is the most serious complication
of attempted tracheal intubation. Routine use of primary
and secondary techniques to confirm correct placement of the tracheal
tube should reduce this risk.
Clinical assessment. Primary assessment includes observation of
chest expansion bilaterally, auscultation over the lung fields bilaterally
in the axillae (breath sounds should be equal and adequate)
and over the epigastrium (breath sounds should not be heard).
Clinical signs of correct tube placement (condensation in the tube,
chest rise, breath sounds on auscultation of lungs, and inability to
hear gas entering the stomach) are not reliable. The reported sensitivity
(proportion of tracheal intubations correctly identified) and
specificity (proportion of oesophageal intubations correctly identified)
of clinical assessment varies: sensitivity 74–100%; specificity
66–100%.592,607–610
Secondary confirmation of tracheal tube placement by an
exhaled carbon dioxide or oesophageal detection device should
reduce the risk of unrecognised oesophageal intubation but the performance
of the available devices varies considerably. Furthermore,
none of the secondary confirmation techniques will differentiate
between a tube placed in a main bronchus and one placed correctly
in the trachea.
Oesophageal detector device. The oesophageal detector device creates
a suction force at the tracheal end of the tracheal tube,
either by pulling back the plunger on a large syringe or releasing
a compressed flexible bulb. Air is aspirated easily from the
lower airways through a tracheal tube placed in the cartilagesupported
rigid trachea. When the tube is in the oesophagus,
air cannot be aspirated because the oesophagus collapses when
aspiration is attempted. The oesophageal detector device may
be misleading in patients with morbid obesity, late pregnancy
or severe asthma or when there are copious tracheal secretions;
in these conditions the trachea may collapse when aspiration is
attempted. Detection of correct placement of a tracheal tube during
CPR has been documented in five observational studies561,611–614
that included 396 patients, and in one randomised study615 that
included 48 patients.4 The pooled specificity was 92% (95% CI
84–96%), the pooled sensitivity was 88% (95% CI 84–192%), and
the false positive rate was 0.2% (95% CI, 0–0.6%). One observational
study showed no statistically significant difference between
the performance of a bulb (sensitivity 71%, specificity 100%) and a
syringe (sensitivity 73%, specificity 100%) type oesophageal detection
devices in the detection of tracheal placement of a tracheal
tube.615
Thoracic impedance. There are smaller changes in thoracic
impedance with oesophageal ventilations than with ventilation of
the lungs.616–618 Changes in thoracic impedance may be used to
detect ventilation619 and oesophageal intubation591,620 during cardiac
arrest. It is possible that this technology can be used to measure
tidal volume during CPR. The role of thoracic impedance as a tool
to detect tracheal tube position and adequate ventilation during
CPR is undergoing further research but is not yet ready for routine
clinical use.
Ultrasound for tracheal tube detection. Three observational studies
including 254 patients in cardiac arrest have documented the use
of ultrasound to detect tracheal tube placement.621–623 The pooled
specificity was 90% (95% CI 68–98%), the sensitivity was 100% (95%
CI 98–100%), and the FPR was 0.8% (95% CI 0.2–2.6%).
Carbon dioxide detectors. Carbon dioxide (CO2) detector devices
measure the concentration of exhaled carbon dioxide from the
lungs. The persistence of exhaled CO2 after six ventilations indicates
placement of the tracheal tube in the trachea or a main
bronchus.592 Confirmation of correct placement above the carina
will require auscultation of the chest bilaterally in the mid-axillary
lines. Broadly, there three types of carbon dioxide detector device:
(1) Disposable colorimetric end-tidal carbon dioxide (ETCO2)
detectors use a litmus paper to detect CO2, and these devices
generally give readings of purple (ETCO2 < 0.5%), tan (ETCO2
0.5–2%) and yellow (ETCO2 > 2%). In most studies, tracheal
placement of the tube is considered verified if the tan
colour persists after a few ventilations. Seven observational
studies592,614,624–628 including 1119 patients have evaluated
the diagnostic accuracy of colorimetric CO2 devices in cardiac
arrest patients.4 The specificity was 97% (95% CI 84–99%), the
sensitivity was 87% (95% CI 85–89%), and the FPR was 0.3%
(0–1%). Although colorimetric CO2 detectors identify placement
in patients with good perfusion quite well, these devices are
less accurate than clinical assessment in cardiac arrest patients
J. Soar et al. / Resuscitation 95 (2015) 100–147 121
because pulmonary blood flow may be so low that there is
insufficient exhaled carbon dioxide. Furthermore, if the tracheal
tube is in the oesophagus, six ventilations may lead to gastric
distension, vomiting and aspiration.
(2) Non-waveform electronic digital ETCO2 devices generally measure
ETCO2 using an infrared spectrometer and display the
results with a number; they do not provide a waveform graphical
display of the respiratory cycle on a capnograph. Five
studies of these devices for identification of tracheal tube position
in cardiac arrest document 70–100% sensitivity and 100%
specificity.592,609,614,627,629,630
(3) End-tidal CO2 detectors that include a waveform graphical display
(capnographs) are the most reliable for verification of
tracheal tube position during cardiac arrest. Two studies of
waveform capnography to verify tracheal tube position in victims
of cardiac arrest demonstrate 100% sensitivity and 100%
specificity in identifying correct tracheal tube placement.592,631
One observational study showed that the use of waveform
capnography compared with no waveform capnography in
153 critically-ill patients (51 with cardiac arrest) decreased
the occurrence of unrecognised oesophageal intubation on
hospital arrival from 23% to 0% (OR 29; 95% CI 4–122).631
Three observational studies with 401 patients592,607,613 and
one randomised study615 including 48 patients showed that
the specificity for waveform capnography to detect correct tracheal
placement was 100% (95% CI 87–100%). The sensitivity
was 100% in one study when waveform capnography was used
in the pre-hospital setting immediately after intubation, and
oesophageal intubation was less common than the average
(1.5%).592,607 The sensitivity was between 65% to 68% in the
other three studies when the device was used in OHCA patients
after intubation in the emergency department (ED).607,613,615
The difference may be related to prolonged resuscitation with
compromised or non-existent pulmonary blood flow. Based
on the pooled sensitivity/specificity from these studies and
assumed oesophageal intubation prevalence of 4.5%, the false
positive rate (FPR) of waveform capnography was 0% (95% CI
0–0.6%).
Based on the available data, the accuracy of colorimetric CO2
detectors, oesophageal detector devices and non-waveform capnometers
does not exceed the accuracy of auscultation and direct
visualisation for confirming the tracheal position of a tube in victims
of cardiac arrest. Waveform capnography is the most sensitive
and specific way to confirm and continuously monitor the position
of a tracheal tube in victims of cardiac arrest and must supplement
clinical assessment (auscultation and visualisation of tube through
cords). Waveform capnography will not discriminate between tracheal
and bronchial placement of the tube – careful auscultation
is essential. Existing portable monitors make capnographic initial
confirmation and continuous monitoring of tracheal tube position
feasible in almost all settings, including out-of-hospital, emergency
department and in-hospital locations where intubation is
performed.
The ILCOR ALS Task Force recommends using waveform capnography
to confirm and continuously monitor the position of a
tracheal tube during CPR in addition to clinical assessment (strong
recommendation, low quality evidence). Waveform capnography
is given a strong recommendation as it may have other potential
uses during CPR (e.g. monitoring ventilation rate, assessing
quality of CPR). The ILCOR ALS Task Force recommends that if waveform
capnography is not available, a non-waveform carbon dioxide
detector, oesophageal detector device or ultrasound in addition to
clinical assessment is an alternative (strong recommendation, low
quality evidence).
Cricoid pressure
The routine use of cricoid pressure in cardiac arrest is not recommended.
If cricoid pressure is used during cardiac arrest, the
pressure should be adjusted, relaxed or released if it impedes ventilation
or intubation.
In non-arrest patients cricoid pressure may offer some measure
of protection to the airway from aspiration but it may also
impede ventilation or interfere with intubation. The role of cricoid
pressure during cardiac arrest has not been studied. Application
of cricoid pressure during bag-mask ventilation reduces gastric
inflation.632–635
Studies in anaesthetised patients show that cricoid pressure
impairs ventilation in many patients, increases peak inspiratory
pressures and causes complete obstruction in up to 50% of patients
depending on the amount of cricoid pressure (in the range of recommended
effective pressure) that is applied.632,633,636–641
Securing the tracheal tube
Accidental dislodgement of a tracheal tube can occur at any time,
but may be more likely during resuscitation and during transport.
The most effective method for securing the tracheal tube has yet to
be determined; use either conventional tapes or ties, or purposemade
tracheal tube holders.
Cricothyroidotomy
Occasionally it will be impossible to ventilate an apnoeic patient
with a bag-mask, or to pass a tracheal tube or alternative airway
device. This may occur in patients with extensive facial trauma
or laryngeal obstruction caused by oedema or foreign material.
In these circumstances, delivery of oxygen through a needle or
surgical cricothyroidotomy may be life-saving. A tracheostomy is
contraindicated in an emergency, as it is time consuming, hazardous
and requires considerable surgical skill and equipment.
Surgical cricothyroidotomy provides a definitive airway that can
be used to ventilate the patient’s lungs until semi-elective intubation
or tracheostomy is performed. Needle cricothyroidotomy
is a much more temporary procedure providing only short-term
oxygenation. It requires a wide-bore, non-kinking cannula, a highpressure
oxygen source, runs the risk of barotrauma and can be
particularly ineffective in patients with chest trauma. It is also
prone to failure because of kinking of the cannula, and is unsuitable
for patient transfer. In the 4th National Audit Project of the UK Royal
College of Anaesthetists and the Difficult Airway Society NAP4, 60%
of needle cricothyroidotomies attempted in the intensive care unit
(ICU), and elsewhere, failed.642 In contrast, all surgical cricothyroidotomies
achieved access to the trachea. While there may be
several underlying causes, these results indicate a need for more
training in surgical cricothyroidotomy and this should include regular
manikin-based training using locally available equipment.643
Summary of airway management for cardiac arrest
The ILCOR ALS Task Force has suggested using either an
advanced airway (tracheal intubation or SGA) or a bag-mask for
airway management during CPR.4 This very broad recommendation
is made because of the total absence of high quality data to
indicate which airway strategy is best.
The type of airway used may depend on the skills and training of
the healthcare provider. In comparison with bag-mask ventilation
and use of a SGA, tracheal intubation requires considerably more
training and practice and may result in unrecognised oesophageal
intubation and increased hands-off time. A bag-mask, a SGA and
a tracheal tube are frequently used in the same patient as part
of a stepwise approach to airway management but this has not
been formally assessed. Patients who remain comatose after initial
122 J. Soar et al. / Resuscitation 95 (2015) 100–147
resuscitation from cardiac arrest will ultimately require tracheal
intubation regardless of the airway technique used during cardiac
arrest. Anyone attempting tracheal intubation must be well trained
and equipped with waveform capnography. In the absence of these
prerequisites, consider use of bag-mask ventilation and/or an SGA
until appropriately experience and equipped personnel are present.
There are very few data relating to airway management during
in-hospital cardiac arrest and it is necessary to extrapolate
from data derived from out-of-hospital cardiac arrest. On this basis,
the principles discussed above apply equally to in-hospital cardiac
arrest.
3g – Drugs and fluids for cardiac arrest
This topic is divided into: drugs used during the management
of a cardiac arrest; anti-arrhythmic drugs used in the peri-arrest
period; other drugs used in the peri-arrest period; and fluids. Every
effort has been made to provide accurate information on the drugs
in these guidelines, but literature from the relevant pharmaceutical
companies will provide the most up-to-date data.
There are three groups of drugs relevant to the management
of cardiac arrest that were reviewed during the 2015 Consensus
Conference: vasopressors, anti-arrhythmics and other drugs.4
The systematic reviews found insufficient evidence to comment
on critical outcomes such as survival to discharge and survival to
discharge with good neurological outcome with either vasopressors
or anti-arrhythmic drugs. There was also insufficient evidence
to comment on the best time to give drugs to optimise outcome.
Thus, although drugs are still included among ALS interventions,
they are of secondary importance to high-quality uninterrupted
chest compressions and early defibrillation. As an indicator of
equipoise regarding the use of drugs during ALS, two large RCTs
(adrenaline versus placebo [ISRCTN73485024], and amiodarone
versus lidocaine versus placebo312 [NCT01401647] are currently
ongoing.
Vasopressors
Despite the continued widespread use of adrenaline and the use
of vasopressin during resuscitation in some countries, there is no
placebo-controlled study that shows that the routine use of any
vasopressor during human cardiac arrest increases survival to hospital
discharge, although improved short-term survival has been
documented.305,306,308 The primary goal of CPR is to re-establish
blood flow to vital organs until the restoration of spontaneous circulation.
Despite the lack of data from cardiac arrest in humans,
vasopressors continue to be recommended as a means of increasing
cerebral and coronary perfusion pressure during CPR.
Adrenaline (epinephrine) versus no adrenaline
One randomised, placebo-controlled trial on patients with
out-of-hospital cardiac arrest from all rhythms showed that
administration of standard-dose adrenaline was associated with
significantly higher rates of prehospital ROSC (relative risk [RR]
2.80 [95% CI 1.78–4.41], p < 0.00001) and survival to hospital admission
(RR 1.95 [95% CI 1.34–2.84], p = 0.0004) when compared to
placebo.308 Therewasnodifferenceinsurvivaltohospitaldischarge
(RR 2.12 [95% CI 0.75–6.02], p = 0.16) or good neurological outcome,
defined as Cerebral Performance Categories (CPC) 1 or 2 (RR 1.73,
[95% CI 0.59–5.11], p = 0.32). The trial, however, was stopped early
and included only 534 subjects.
Another trial randomised 851 patients with out-of-hospital
cardiac arrest to receive advanced life support with or without
intravenous drug administration. Results of this trial showed that
administration of intravenous drugs was associated with significantly
higher rates of prehospital ROSC (40% vs. 25%; p < 0.001) and
admission to hospital (43% vs. 29%; p < 0.001).305 However, the rates
of survival to hospital discharge did not differ (10.5 vs.9.2; p = 0.61).
The effect on ROSC was most prominent and only significant in the
non-shockable group.305 In a post-hoc analysis comparing patients
who were given adrenaline vs. not given adrenaline, the OR of being
admitted to hospital was higher with adrenaline, but the likelihood
of being discharged from hospital alive and surviving with
favourable neurological outcome was reduced [OR for adrenaline
vs. no-adrenaline were 2.5 (95% CI 1.9–3.4), 0.5 (95% CI 0.3–0.8) and
0.4 (95% CI 0.2–0.7) respectively].644
A series of observational studies on large cohorts of out-ofhospital
cardiac arrest patients have compared the outcomes of
patients who were administered adrenaline with those of patients
who did not receive adrenaline. Adjustments were made using
logistic regression and propensity matching. A study conducted
in Japan which included a total of 417,188 patients (13,401 of
whom were propensity-matched) showed that use of prehospital
adrenaline was significantly associated with increased odds of
ROSC before hospital arrival (adjusted OR 2.36 [95% CI 2.22–2.50])
but decreased chance of survival (0.46 [95%CI 0.42–0.51]) and good
functional outcome (0.31 [95% CI 0.26–0.36]) at one month after
the arrest.645 Conversely, another Japanese study conducted on
11,048 propensity-matched, bystander-witnessed arrests showed
that prehospital administration of adrenaline was associated with
significantly higher rates of overall survival and, for patients with
non-shockable rhythms, it was also associated with significantly
higher odds of neurologically intact survival (adjusted OR 1.57 [95%
CI 1.04–2.37]).646 However, the absolute increase of neurologically
intact survival in this last group of patients was minimal (0.7% vs.
0.4%). Finally, in a recent study in France on 1556 cardiac arrest
patients who achieved ROSC and were admitted to hospital, administration
of adrenaline was associated with significantly lower odds
of neurologically intact survival.647
There is an increasing concern about the potential detrimental
effects of adrenaline. While its alpha-adrenergic, vasoconstrictive
effects cause systemic vasoconstriction, which increases
macrovascular coronary and cerebral perfusion pressures, its betaadrenergic
actions (inotropic, chronotropic) may increase coronary
and cerebral blood flow, but with concomitant increases in myocardial
oxygen consumption, ectopic ventricular arrhythmias (particularly
when the myocardium is acidotic), transient hypoxaemia from
pulmonary arteriovenous shunting, impaired microcirculation,648
and worse post-cardiac arrest myocardial dysfunction.649,650
Experimental evidence suggests that epinephrine also impairs
cerebral microcirculation.651 In retrospective secondary analyses,
adrenaline use is associated with more rhythm transitions during
ALS, both during VF652 and PEA.325
Two systematic reviews of adrenaline for OHCA indicate rates
of ROSC are increased with adrenaline but good long-term survival
(survival to discharge and neurological outcome) is either no better,
or worse.653,654
The optimal dose of adrenaline is not known, and there are no
human data supporting the use of repeated doses. In fact, increasing
cumulative dose of epinephrine during resuscitation of patients
with asystole and PEA is an independent risk factor for unfavourable
functional outcome and in-hospital mortality.655
Our current recommendation is to continue the use of
adrenaline during CPR as for Guidelines 2010. We have considered
the benefit in short-term outcomes (ROSC and admission
to hospital) and our uncertainty about the benefit or harm on
survival to discharge and neurological outcome given the limitations
of the observational studies.4,653,654 We have decided not to
change current practice until there is high-quality data on longterm
outcomes. Dose response and placebo-controlled efficacy
trials are needed to evaluate the use of adrenaline in cardiac arrest.
We are aware of an ongoing randomised study of adrenaline vs.
J. Soar et al. / Resuscitation 95 (2015) 100–147 123
placebo for OHCA in the UK (PARAMEDIC 2: The Adrenaline Trial,
ISRCTN73485024).
Adrenaline (epinephrine) versus vasopressin
The potentially deleterious beta-effects of adrenaline have led to
exploration of alternative vasopressors. Vasopressin is a naturally
occurring antidiuretic hormone. In very high doses it is a powerful
vasoconstrictor that acts by stimulation of smooth muscle
V1 receptors. Vasopressin has neither chronotropic nor inotropic
effects on the heart. In comparison with adrenaline it has a longer
half-life (10–20 min vs. 4 min) and it is potentially more effective
during acidosis.656,657 Vasopressin has been proposed as an alternative
to adrenaline in cardiac arrest, based on the finding that its
levels were significantly higher in successfully resuscitated patients
than in patients who died.658 However, a trial comparing up to four
doses of either 40 IU vasopressin or 1 mg adrenaline every 5–10 min
in patients with out of hospital cardiac arrest did not demonstrate
any significant difference in terms of survival to hospital discharge
or neurological outcome between the two study arms.659 This trial
had serious methodological issues and included a small number of
patients.
A series of randomised controlled trials660–664 demonstrated no
difference in outcomes (ROSC, survival to discharge, or neurological
outcome) with vasopressin versus adrenaline as a first line vasopressor
in cardiac arrest. Other studies comparing adrenaline alone
or in combination with vasopressin also demonstrated no difference
in ROSC, survival to discharge or neurological outcome.665–667
There are no alternative vasopressors that provide survival benefit
during cardiac arrest resuscitation when compared with
adrenaline.
We suggest vasopressin should not be used in cardiac arrest
instead of adrenaline. Those healthcare professionals working in
systems that already use vasopressin may continue to do so because
there is no evidence of harm from using vasopressin when compared
to adrenaline.4
Steroids
Two studies suggest that a bundled regimen of adrenaline,
vasopressin and methylprednisolone improved survival after
in-hospital cardiac arrest. In a single-centre randomised, placebocontrolled
trial in patients with in-hospital cardiac arrest, a
combination of vasopressin 20 IU and adrenaline 1 mg per CPR cycle
for the first 5 CPR cycles plus methylprednisolone 40 mg at the first
CPR cycle plus hydrocortisone 300 mg in case of post-resuscitation
shock was associated with significantly higher rates of ROSC (39/48
[81%] vs. 27 of 52 [52%]; p = 0.003) and survival to hospital discharge
(9 [19%] vs. 2 [4%]; p = 0.02) than conventional treatment.668 These
results were confirmed by a subsequent three-centre trial including
a total of 300 patients from the same group of investigators.669
This last trial also showed significantly higher odds of survival with
good neurological outcome (CPC = 1–2) (OR 3.28, 95% CI 1.17–9.20;
p = 0.02).
The population in these studies had very rapid advanced life support,
a high incidence of asystolic cardiac arrest and low baseline
survival compared to other in-hospital studies. Thus the findings
of these studies are not generalisable to all cardiac arrests
and we suggest that steroids are not used routinely for cardiac
arrest.4
Adrenaline
Indications. Adrenaline is:
• the first drug used in cardiac arrest of any cause: it is included in
the ALS algorithm for use every 3–5 min of CPR (alternate cycles).
• preferred in the treatment of anaphylaxis (Section 4).224
• a second-line treatment for cardiogenic shock.
Dose during CPR. During cardiac arrest, the initial IV/IO dose of
adrenaline is 1 mg. There are no studies showing improvement in
survival or neurological outcomes with higher doses of adrenaline
for patients in refractory cardiac arrest.4
Following ROSC, even small doses of adrenaline (50–100 ␮g)
may induce tachycardia, myocardial ischaemia, VT and VF. Once
a perfusing rhythm is established, if further adrenaline is deemed
necessary, titrate the dose carefully to achieve an appropriate blood
pressure. Intravenous doses of 50 ␮g are usually sufficient for most
hypotensive patients.
Use. Adrenaline is available most commonly in two dilutions:
• 1 in 10,000 (10 ml of this solution contains 1 mg of adrenaline)
• 1 in 1000 (1 ml of this solution contains 1 mg of adrenaline).
Both these dilutions are used routinely in Europe.
Anti-arrhythmics
As with vasopressors, the evidence that anti-arrhythmic drugs
are of benefit in cardiac arrest is limited. No anti-arrhythmic drug
given during human cardiac arrest has been shown to increase survival
to hospital discharge, although amiodarone has been shown
to increase survival to hospital admission.670,671 Despite the lack
of human long-term outcome data, the balance of evidence is in
favour of the use anti-arrhythmic drugs for the management of
arrhythmias in cardiac arrest. There is an ongoing trial comparing
amiodarone to lidocaine and to placebo designed and powered to
evaluate for functional survival.312
Amiodarone
Amiodarone is a membrane-stabilising anti-arrhythmic drug
that increases the duration of the action potential and refractory
period in atrial and ventricular myocardium. Atrioventricular
conduction is slowed, and a similar effect is seen with accessory
pathways. Amiodarone has a mild negative inotropic action and
causes peripheral vasodilation through non-competitive alphablocking
effects. The hypotension that occurs with intravenous
amiodarone is related to the rate of delivery and is due more
to the solvent (Polysorbate 80 and benzyl alcohol), which causes
histamine release, rather than the drug itself.672 A premixed
formulation of intravenous amiodarone (PM101) that does not
contain Polysorbate 80 and uses a cyclodextrin to maintain
amiodarone in the aqueous phase is available in the United
States.673
Following three initial shocks, amiodarone in shock-refractory
VF improves the short-term outcome of survival to hospital admission
compared with placebo670 or lidocaine.671 Amiodarone also
appears to improve the response to defibrillation when given to
humans or animals with VF or haemodynamically unstable ventricular
tachycardia.674–678 There is no evidence to indicate the
optimal time at which amiodarone should be given when using
a single-shock strategy. In the clinical studies to date, the amiodarone
was given if VF/pVT persisted after at least three shocks.
For this reason, and in the absence of any other data, amiodarone
300 mg is recommended if VF/pVT persists after three
shocks.
Indications. Amiodarone is indicated in:
• refractory VF/pVT
• haemodynamically stable ventricular tachycardia (VT) and other
resistant tachyarrhythmias (Section 11).
Dose during CPR. We recommend that an initial intravenous dose
of 300 mg amiodarone, diluted in 5% glucose (or other suitable solvent)
to a volume of 20 ml (or from a pre-filled syringe) should
124 J. Soar et al. / Resuscitation 95 (2015) 100–147
be given after three defibrillation attempts irrespective of whether
they are consecutive shocks, or interrupted by CPR, or for recurrent
VF/pVT during cardiac arrest. A further dose of 150 mg may
be given after five defibrillation attempts. Amiodarone can cause
thrombophlebitis when injected into a peripheral vein; use a central
vein if a central venous catheter is in situ but, if not, use a large
peripheral vein or the IO route followed by a generous flush.
Clinical aspects of use. Amiodarone may paradoxically be arrhythmogenic,
especially if given concurrently with drugs that prolong
the QT interval. However, it has a lower incidence of pro-arrhythmic
effects than other anti-arrhythmic drugs under similar circumstances.
The major acute adverse effects from amiodarone are
hypotension and bradycardia in patients with ROSC, and can
be treated with fluids and/or inotropic drugs. The side effects
associated with prolonged oral use (abnormalities of thyroid
function, corneal microdeposits, peripheral neuropathy, and pulmonary/hepatic
infiltrates) are not relevant in the acute setting.
Lidocaine
Lidocaine is recommended for use during ALS when amiodarone
is unavailable.671 Lidocaine is a membrane-stabilising
anti-arrhythmic drug that acts by increasing the myocyte refractory
period. It decreases ventricular automaticity, and its local
anaesthetic action suppresses ventricular ectopic activity. Lidocaine
suppresses activity of depolarised, arrhythmogenic tissues
while interfering minimally with the electrical activity of normal
tissues. Therefore, it is effective in suppressing arrhythmias associated
with depolarisation (e.g. ischaemia, digitalis toxicity) but
is relatively ineffective against arrhythmias occurring in normally
polarised cells (e.g. atrial fibrillation/flutter). Lidocaine raises the
threshold for VF.
Lidocaine toxicity causes paraesthesia, drowsiness, confusion
and muscular twitching progressing to convulsions. It is considered
generally that a safe dose of lidocaine must not exceed 3 mg kg−1
over the first hour. If there are signs of toxicity, stop the infusion
immediately; treat seizures if they occur. Lidocaine depresses
myocardial function, but to a much lesser extent than amiodarone.
The myocardial depression is usually transient and can be treated
with intravenous fluids or vasopressors.
Indications. Lidocaine is indicated in refractory VF/pVT (when
amiodarone is unavailable).
Dose. When amiodarone is unavailable, consider an initial dose of
100 mg (1–1.5 mg kg−1) of lidocaine for VF/pVT refractory to three
shocks. Give an additional bolus of 50 mg if necessary. The total
dose should not exceed 3 mg kg−1 during the first hour.
Clinical aspects of use. Lidocaine is metabolised by the liver, and
its half-life is prolonged if the hepatic blood flow is reduced, e.g.
in the presence of reduced cardiac output, liver disease or in the
elderly. During cardiac arrest normal clearance mechanisms do not
function, thus high plasma concentrations may be achieved after a
single dose. After 24 h of continuous infusion, the plasma half-life
increases significantly. Reduce the dose in these circumstances, and
regularly review the indication for continued therapy. Lidocaine is
less effective in the presence of hypokalaemia and hypomagnesaemia,
which should be corrected immediately.
Magnesium
We recommend magnesium is not routinely used for the treatment
of cardiac arrest. Studies in adults in and out of hospital have
failed to demonstrate any increase in the rate of ROSC when magnesium
is given routinely during CPR.679–684
Magnesium is an important constituent of many enzyme systems,
especially those involved with ATP generation in muscle.
It plays a major role in neurochemical transmission, where it
decreases acetylcholine release and reduces the sensitivity of the
motor endplate. Magnesium also improves the contractile response
of the stunned myocardium, and limits infarct size by a mechanism
that has yet to be fully elucidated.685 The normal plasma range of
magnesium is 0.8–1.0 mmol l−1.
Hypomagnesaemia is often associated with hypokalaemia, and
may contribute to arrhythmias and cardiac arrest. Hypomagnesaemia
increases myocardial digoxin uptake and decreases
cellular Na+/K+-ATP-ase activity. In patients with hypomagnesaemia,
hypokalaemia, or both digitalis may become cardiotoxic
even with therapeutic digitalis levels. Magnesium deficiency is
not uncommon in hospitalised patients and frequently coexists
with other electrolyte disturbances, particularly hypokalaemia,
hypophosphataemia, hyponatraemia and hypocalcaemia.
Give an initial intravenous dose of 2 g (4 ml (8 mmol)) of 50%
magnesium sulphate); it may be repeated after 10–15 min. Preparations
of magnesium sulphate solutions differ among European
countries.
Clinical aspects of use. Hypokalaemic patients are often hypomagnesaemic.
If ventricular tachyarrhythmias arise, intravenous
magnesium is a safe, effective treatment. Magnesium is excreted
by the kidneys, but side effects associated with hypermagnesaemia
are rare, even in renal failure. Magnesium inhibits smooth muscle
contraction, causing vasodilation and a dose-related hypotension,
which is usually transient and responds to intravenous fluids and
vasopressors.
Calcium
Calcium plays a vital role in the cellular mechanisms underlying
myocardial contraction. There is no data supporting any beneficial
action for calcium after most cases of cardiac arrest686–691;
conversely, other studies have suggested a possible adverse effect
when given routinely during cardiac arrest (all rhythms).692,693
High plasma concentrations achieved after injection may be harmful
to the ischaemic myocardium and may impair cerebral recovery.
Give calcium during resuscitation only when indicated specifically,
i.e. in pulseless electrical activity caused by:
• hyperkalaemia
• hypocalcaemia
• overdose of calcium channel-blocking drugs.
The initial dose of 10 ml 10% calcium chloride (6.8 mmol Ca2+)
may be repeated if necessary. Calcium can slow the heart rate and
precipitate arrhythmias. In cardiac arrest, calcium may be given by
rapid intravenous injection. In the presence of a spontaneous circulation
give it slowly. Do not give calcium solutions and sodium
bicarbonate simultaneously by the same route to avoid precipita-
tion.
Buffers
Cardiac arrest results in combined respiratory and metabolic
acidosis because pulmonary gas exchange ceases and cellular
metabolism becomes anaerobic. The best treatment of acidaemia
in cardiac arrest is CPR. During cardiac arrest, arterial gas values
may be misleading and bear little relationship to the tissue
acid-base state394; analysis of central venous blood may provide
a better estimation of tissue pH. Bicarbonate causes generation of
carbon dioxide, which diffuses rapidly into cells. It has the following
effects.
J. Soar et al. / Resuscitation 95 (2015) 100–147 125
• It exacerbates intracellular acidosis.
• It produces a negative inotropic effect on ischaemic myocardium.
• It presents a large, osmotically active, sodium load to an already
compromised circulation and brain.
• It produces a shift to the left in the oxygen dissociation curve,
further inhibiting release of oxygen to the tissues.
Mild acidaemia causes vasodilation and can increase cerebral
blood flow. Therefore, full correction of the arterial blood pH may
theoretically reduce cerebral blood flow at a particularly critical
time. As the bicarbonate ion is excreted as carbon dioxide via the
lungs, ventilation needs to be increased.
Several animal and clinical studies have examined the use of
buffers during cardiac arrest. Clinical studies using Tribonate®
694 or sodium bicarbonate as buffers have failed to demonstrate
any advantage.694–701 Two studies have found that EMS
systems using sodium bicarbonate earlier and more frequently
had significantly higher ROSC and hospital discharge rates and
better long-term neurological outcome.702,703. Animal studies
have generally been inconclusive, but some have shown benefit
in giving sodium bicarbonate to treat cardiovascular toxicity
(hypotension, cardiac arrhythmias) caused by tricyclic antidepressants
and other fast sodium channel blockers (Section
4).224,704,705 Giving sodium bicarbonate routinely during cardiac
arrest and CPR or after ROSC is not recommended. Consider sodium
bicarbonate for:
• life-threatening hyperkalaemia
• cardiac arrest associated with hyperkalaemia
• tricyclic overdose.
Give 50 mmol (50 ml of an 8.4% solution) or 1 mmol kg−1 of
sodium bicarbonate intravenously. Repeat the dose as necessary,
but use acid/base analysis (either arterial, central venous or marrow
aspirate from IO needle) to guide therapy. Severe tissue damage
may be caused by subcutaneous extravasation of concentrated
sodium bicarbonate. The solution is incompatible with calcium
salts as it causes the precipitation of calcium carbonate.
Fibrinolysis during CPR
Fibrinolytic drugs may be used when pulmonary embolism is
the suspected or known cause of cardiac arrest. Thrombus formation
is a common cause of cardiac arrest, most commonly due to
acute myocardial ischaemia following coronary artery occlusion
by thrombus, but occasionally due to a dislodged venous thrombus
causing a pulmonary embolism. The use of fibrinolytic drugs
to break down coronary artery and pulmonary artery thrombus
has been the subject of several studies. Fibrinolytics have also been
demonstrated in animal studies to have beneficial effects on cerebral
blood flow during cardiopulmonary resuscitation,706,707 and a
clinical study has reported less anoxic encephalopathy after fibrinolytic
therapy during CPR.708
Several studies have examined the use of fibrinolytic therapy
given during non-traumatic cardiac arrest unresponsive to
standard therapy.709–715 and some have shown non-significant
improvements in survival to hospital discharge,709,712 and greater
ICU survival.708 A small series of case reports also reported survival
to discharge in three cases refractory to standard therapy with VF
or PEA treated with fibrinolytics.716 Conversely, two large clinical
trials717,718 failed to show any significant benefit for fibrinolytics in
out-of-hospital cardiac arrest unresponsive to initial interventions.
Results from the use of fibrinolytics in patients suffering
cardiac arrest from suspected pulmonary embolism have been variable.
A meta-analysis, which included patients with pulmonary
embolism as a cause of the arrest, concluded that fibrinolytics
increased the rate of ROSC, survival to discharge and long-term
neurological function.719 Several other studies have demonstrated
an improvement in ROSC and admission to hospital or the intensive
care unit, but not in survival to neurologically intact hospital
discharge.709–712,714,715,720–723
Although several relatively small clinical studies709,710,712,721
and case series708,716,724–726 have not demonstrated any increase
in bleeding complications with thrombolysis during CPR in
non-traumatic cardiac arrest, a recent large study718 and
meta-analysis719 have shown an increased risk of intracranial
bleeding associated with the routine use of fibrinolytics during
non-traumatic cardiac arrest. Successful fibrinolysis during
cardiopulmonary resuscitation is usually associated with good neurological
outcome.719,721,722
Fibrinolytic therapy should not be used routinely in cardiac
arrest. Consider fibrinolytic therapy when cardiac arrest is caused
by proven or suspected acute pulmonary embolism. Following fibrinolysis
during CPR for acute pulmonary embolism, survival and
good neurological outcome have been reported in cases requiring
in excess of 60 min of CPR. If a fibrinolytic drug is given in these circumstances,
consider performing CPR for at least 60–90 min before
termination of resuscitation attempts.727–729 Ongoing CPR is not a
contraindication to fibrinolysis. Treatment of pulmonary embolism
is addressed in Section 4 including the role of extracorporeal CPR,
and surgical or mechanical thrombectomy.224
Intravenous fluids
Hypovolaemia is a potentially reversible cause of cardiac arrest.
Infuse fluids rapidly if hypovolaemia is suspected. In the initial
stages of resuscitation there are no clear advantages to using colloid,
so use balanced crystalloid solutions, Hartmann’s solution
or 0.9% sodium chloride. Avoid glucose, which is redistributed
away from the intravascular space rapidly and causes hyperglycaemia,
and may worsen neurological outcome after cardiac
arrest.730–738
Whether fluids should be infused routinely during cardiac arrest
is controversial. There are no published human studies specifically
aimed to evaluate the advantages of routine fluid use compared
to no fluids during normovolaemic cardiac arrest. Three animal
studies show that the increase in right atrial pressure produced
by infusion of fluids during CPR decreases coronary perfusion
pressure,739–741 and another animal study742 shows that the coronary
perfusion pressure rise with adrenaline during CPR is not
improved with the addition of a fluid infusion. In a clinical trial
which randomised patients to rapid prehospital cooling, accomplished
by infusing up to 2 L of 4 ◦C normal saline immediately
after ROSC, the incidence of re-arrest and pulmonary oedema
on first chest X-ray was significantly higher in the intervention
group.743 This was not confirmed by a similar study in which
patients received a median of 1 L of cold saline before hospital
admission.744 Results of a further study on rapid prehospitalcooling
(NCT01173393) are awaited.
One animal study shows that hypertonic saline improves cerebral
blood flow during CPR.745 However, one small clinical study746
and one randomised trial747 have not shown any benefit with
hypertonic fluid during CPR. One retrospective matched pair analysis
of a German OHCA registry showed that use of hypertonic saline
with 6% hydroxyethyl starch was associated with increased rates
of survival to hospital admission.748 However there are concerns
regarding the use of colloids and starch solutions in particular in
critically ill patients.749
Ensure normovolaemia, but in the absence of hypovolaemia,
infusion of an excessive volume of fluid is likely to be harmful.750
Use intravenous fluid to flush peripherally injected drugs into the
central circulation.
126 J. Soar et al. / Resuscitation 95 (2015) 100–147
3h – CPR techniques and devices
At best, standard manual CPR produces coronary and cerebral
perfusion that is just 30% of normal.751 Several CPR techniques and
devices aim to improve haemodynamics and survival when used
by trained providers in selected cases. However, the success of any
technique or device depends on the education and training of the
rescuers and on resources (including personnel). In the hands of
some groups, novel techniques and adjuncts may be better than
standard CPR. However, a device or technique which provides good
quality CPR when used by a highly trained team or in a test setting
may show poor quality and frequent interruptions when used in an
uncontrolled clinical setting.752 It is prudent that rescuers are welltrained
and that if a circulatory adjunct is used, a programme of
continuous surveillance be in place to ensure that use of the adjunct
does not adversely affect survival. Although manual chest compressions
are often performed very poorly,753–755 no adjunct has consistently
been shown to be superior to conventional manual CPR.
Mechanical chest compression devices
Providing high-quality manual chest compressions can be
challenging and there is evidence that CPR quality deteriorates
with time. Automated mechanical chest compression devices may
enable the delivery of high quality compressions especially in
circumstances where this may not be possible with manual compressions
– CPR in a moving ambulance where safety is at risk,
prolonged CPR (e.g. hypothermic arrest), and CPR during certain
procedures (e.g. coronary angiography or preparation for extracorporeal
CPR).347,390,414,756–761 Data from the US American CARES
(Cardiac Arrest Registry to Enhance Survival) registry shows that
45% of participating EMS services use mechanical devices.762
Since Guidelines 2010 there have been three large RCTs
enrolling 7582 patients that have shown no clear advantage
from the routine use of automated mechanical chest compression
devices for OHCA.763–765 Ensuring high-quality chest compressions
with adequate depth, rate and minimal interruptions, regardless
of whether they are delivered by machine or human is
important.766,767 In addition mechanical compressions usually
follow a period of manual compressions.768 The transition from
manual compressions to mechanical compressions whilst minimising
interruptions to chest compression and avoiding delays in defibrillation
is therefore an important aspect of using these devices.
We suggest that automated mechanical chest compression
devices are not used routinely to replace manual chest compressions.
We suggest that automated mechanical chest compression
devices are a reasonable alternative to high-quality manual chest
compressions in situations where sustained high-quality manual
chest compressions are impractical or compromise provider
safety.4 Interruptions to CPR during device deployment should be
avoided. Healthcare personnel who use mechanical CPR should do
so only within a structured, monitored programme, which should
include comprehensive competency-based training and regular
opportunities to refresh skills.
The experience from the three large RCTs suggests that use
of mechanical devices requires initial and on-going training and
quality assurance to minimise interruptions in chest compression
when transitioning from manual to mechanical compressions and
preventing delays in defibrillation. The use of training drills and
‘pit-crew’ techniques for device deployment are suggested to help
minimise interruptions in chest compression.769–771
Our recommendation is generic for automated chest compression
devices. Although there may be some device specific
differences, they have not been directly compared in RCTs, and
the three large RCTs763–765 did not suggest a difference between
the two most studied devices [the AutoPulse (Zoll Circulation,
Chelmsford, Massachusetts, USA) and LUCAS-2 (Physio-Control
Inc/Jolife AB, Lund, Sweden)] for critical and important patient outcomes
when compared with the use of manual chest compressions
alone.4
Information concerning the routine use of mechanical devices
for IHCA is limited.772 One small RCT of 150 IHCA patients showed
improved survival with mechanical chest compressions delivered
by a piston device [Thumper 1007 CCV device (Michigan
Instruments, Grand Rapids, Michigan, USA)] when compared with
manual compressions (OR 2.81, 95% CI 1.26–6.24).773
Lund University cardiac arrest system (LUCAS) CPR
The LUCAS delivers chest compression and active decompression
through a piston system with suction cup. The current model
is a battery driven device that delivers 100 compressions min−1 to
a depth of 40–50 mm. There have been two large RCTs of the LUCAS
device since the 2010 Guidelines.764,765
The LINC (LUCAS in cardiac arrest) RCT included 2589 adult
OHCA patients and compared a modified CPR algorithm, which
included mechanical chest compressions with a standard resuscitation
algorithm which included manual chest compressions.764
In the intention to treat analysis, there was no improvement in the
primary outcome of 4-h survival (mechanical CPR 23.6% vs. manual
CPR 23.7%, treatment difference −0.05%, 95% CI 3.3–3.2%; p > 0.99),
1 month survival (survival: 8.6% vs. 8.5%, treatment difference
0.16%, 95% CI 2.0–2.3%) and favourable neurological survival (8.1%
vs. 7.3%, treatment difference 0.78%, 95% CI 1.3–2.8%). A follow-up
study reported that patients who received LUCAS CPR were more
likely to sustain injury (OR 3.4, 95% CI 1.55–7.31%), including rib
fractures (OR 2.0, 95% CI 1.11–3.75%).774
The PaRAMeDIC trial (Prehospital Randomised Assessment of
a Mechanical Compression Device) trial was cluster RCT that randomised
ambulance vehicles to LUCAS or control and included 4471
patients (1652 LUCAS, 2819 manual chest compressions).765 The
intention-to-treat analysis found no improvement in the primary
outcome of 30-day survival (LUCAS CPR 6% vs. manual CPR 7%,
adjusted OR 0.86, 95% CI 0.64–1.15). Survival with a favourable
neurological outcome at three months was lower amongst patients
randomised to LUCAS CPR (5% vs. 6%, adjusted OR 0.72, 95% CI
0.52–0.99). In addition, in patients with VF/pVT, there was a lower
30-day survival with LUCAS CPR (OR 0.71, 95% CI 0.52–0.98). Delays
in attempted defibrillation caused by device deployment may have
caused this.
A meta-analysis of the three LUCAS RCTs that included
7178 patients with OHCA was included in the PARAMEDIC
publication.764,765,775 and reported similar initial and long-term
survival (survived event OR 1.00, 95% CI 0.90–1.11; survival to
discharge/30-days OR 0.96, 95% CI 0.80–1.15). Meta-analysis from
the two larger RCTs noted significant heterogeneity (I2 = 69%) but
no overall difference in neurological outcomes between LUCAS and
manual chest compressions (random effects model OR 0.93, 95% CI
0.64–1.33).764,765
Load-distributing band CPR (AutoPulse)
The load-distributing band (LDB) is a battery-powered device
consisting of a large backboard and a band that encircles the
patient’s chest. Compressions are delivered at a rate of 80 min−1
by tightening of the band. The evidence from clinical trials considered
for the LDB in 2010 was conflicting. Evidence from one
OHCA multi-centre RCT showed no improvement in 4-h survival
and worse neurological outcome with LDB-CPR.776 A further study
showed lower odds of 30-day survival (OR 0.4) but subgroup
analysis showed an increased rate of ROSC in LDB-CPR treated
patients.777 Non-randomised trials reported increased rates of
sustained ROSC,778,779 increased survival to discharge following
J. Soar et al. / Resuscitation 95 (2015) 100–147 127
OHCA779 and improved haemodynamics following failed resuscitation
from in-hospital cardiac arrest.780
A recent large RCT showed similar outcomes for LDB and manual
CPR.763 The CIRC (Circulation Improving Resuscitation Care) trial,
an equivalence RCT, randomised 4753 adult OHCA patients to the
LDB or manual chest compressions. After a predefined adjustment
for covariates and multiple interim analyses the adjusted OR was
1.06 (95% CI 0.83–1.37) and within the pre-defined region of equivalence
for the primary outcome of survival to discharge (manual
CPR vs. LDB CPR 11.0% vs. 9.4%). Good neurological survival to hospital
discharge was similar (mechanical CPR 44.4% vs. manual CPR
48.1%, adjusted OR 0.80, 95% CI 0.47–1.37).
Open-chest CPR
Open-chest CPR produces better coronary perfusion coronary
pressure than standard CPR and may be indicated for patients
with cardiac arrest caused by trauma,781 in the early postoperative
phase after cardiothoracic surgery782,783 (see Section 4 –
special circumstances224) or when the chest or abdomen is already
open (transdiaphragmatic approach), for example, in trauma
surgery.784
Active compression-decompression CPR (ACD-CPR)
ACD-CPR is achieved with a hand-held device equipped with a
suction cup to lift the anterior chest actively during decompression.
Decreasing intrathoracic pressure during the decompression phase
increases venous return to the heart and increases cardiac output
and subsequent coronary and cerebral perfusion pressures during
the compression phase.785–788 Results of ACD-CPR have been
mixed. In some clinical studies ACD-CPR improved haemodynamics
compared with standard CPR,786,788–790 but in another study it did
not.791 In three randomised studies,790,792,793 ACD-CPR improved
long-term survival after out-of-hospital cardiac arrest; however,
in five other randomised studies, ACD-CPR made no difference to
outcome.794–798 The efficacy of ACD-CPR may be highly dependent
on the quality and duration of training.799
A meta-analysis of 10 trials of out-of-hospital cardiac arrest
and two of in-hospital cardiac arrest showed no early or late survival
benefit to ACD-CPR over conventional CPR234,800 and this is
confirmed by another recent meta-analysis.801 Two post-mortem
studies have shown more rib and sternal fractures after ACDCPR
compared with conventional CPR,802,803 but another found no
difference.804
Impedance threshold device (ITD)
The impedance threshold device (ITD) is a valve that limits
air entry into the lungs during chest recoil between chest
compressions; this decreases intrathoracic pressure and increases
venous return to the heart. When used with a cuffed tracheal tube
and active compression–decompression (ACD),805–807 the ITD is
thought to act synergistically to enhance venous return during
active decompression. The ITD has also been used during conventional
CPR with a tracheal tube or facemask.808 If rescuers can
maintain a tight face-mask seal, the ITD may create the same
negative intrathoracic pressure as when used with a tracheal
tube.808
An RCT of the ITD with standard CPR compared to standard CPR
alone with 8718 OHCA patients failed to show any benefit with ITD
use in terms of survival and neurological outcome.809 We therefore
recommend that the ITD is not used routinely with standard CPR.
Two RCTs did not show a benefit in terms of survival to hospital
discharge of the ITD with active compression decompression
CPR when compared with active compression decompression CPR
alone.805,810
Results of a large trial of a combination of ITD with active compression
decompression CPR (ACD CPR) compared to standard CPR
was reported in two publications. The primary publication reported
the results from 2470 patients with OHCA811 whereas the secondary
publication reported results from those with non-traumatic
cardiac arrest (n = 27380).812 This study did detect a statistically
significant difference in neurologically favourable survival at discharge,
and survival at 12 months but no difference for survival
to discharge and neurologically favourable survival at 12 months.4
After consideration of the number needed to treat a decision was
made not to recommend the routine use of the ITD and ACD.4
3i – Peri-arrest arrhythmias
The correct identification and treatment of arrhythmias in the
critically ill patient may prevent cardiac arrest from occurring
or reoccurring after successful initial resuscitation. The treatment
algorithms described in this section have been designed to enable
the non-specialist ALS provider to treat the patient effectively and
safely in an emergency; for this reason, they have been kept as
simple as possible. If patients are not acutely ill there may be several
other treatment options, including the use of drugs (oral or
parenteral) that will be less familiar to the non-expert. In this situation
there will be time to seek advice from cardiologists or other
senior doctors with the appropriate expertise.
More comprehensive information on the management of
arrhythmias can be found at www.escardio.org.
Principles of treatment
The initial assessment and treatment of a patient with an
arrhythmia should follow the ABCDE approach. Key elements in this
process include assessing for adverse signs; oxygen if indicated and
guided by pulse oximetry; obtaining intravenous access, and establishing
monitoring (ECG, blood pressure, SpO2). Whenever possible,
record a 12-lead ECG; this will help determine the precise rhythm,
either before treatment or retrospectively. Correct any electrolyte
abnormalities (e.g. K+, Mg2+, Ca2+). Consider the cause and context
of arrhythmias when planning treatment.
The assessment and treatment of all arrhythmias addresses two
factors: the condition of the patient (stable versus unstable), and
the nature of the arrhythmia. Anti-arrhythmic drugs are slower in
onset and less reliable than electrical cardioversion in converting a
tachycardia to sinus rhythm; thus, drugs tend to be reserved for stable
patients without adverse signs, and electrical cardioversion is
usually the preferred treatment for the unstable patient displaying
adverse signs.
Adverse signs
The presence or absence of adverse signs or symptoms will dictate
the appropriate treatment for most arrhythmias. The following
adverse factors indicate a patient who is unstable because of the
arrhythmia.
1. Shock – this is seen as pallor, sweating, cold and clammy extremities
(increased sympathetic activity), impaired consciousness
(reduced cerebral blood flow), and hypotension (e.g. systolic
blood pressure < 90 mmHg).
2. Syncope – loss of consciousness, which occurs as a consequence
of reduced cerebral blood flow
3. Heart failure – arrhythmias compromise myocardial performance
by reducing coronary artery blood flow. In acute
situations this is manifested by pulmonary oedema (failure of the
128 J. Soar et al. / Resuscitation 95 (2015) 100–147
left ventricle) and/or raised jugular venous pressure, and hepatic
engorgement (failure of the right ventricle).
4. Myocardial ischaemia – this occurs when myocardial oxygen
consumption exceeds delivery. Myocardial ischaemia may
present with chest pain (angina) or may occur without pain as
an isolated finding on the 12-lead ECG (silent ischaemia). The
presence of myocardial ischaemia is especially important if there
is underlying coronary artery disease or structural heart disease
because it may cause further life-threatening complications
including cardiac arrest.
Treatment options
Having determined the rhythm and the presence or absence of
adverse signs, the options for immediate treatment are categorised
as:
1. Electrical (cardioversion, pacing).
2. Pharmacological (anti-arrhythmic (and other) drugs).
Tachycardias
If the patient is unstable
If the patient is unstable and deteriorating, with any of the
adverse signs and symptoms described above being caused by
the tachycardia, attempt synchronised cardioversion immediately
(Fig. 3.4). In patients with otherwise normal hearts, serious
signs and symptoms are uncommon if the ventricular rate is
<150 beats min−1. Patients with impaired cardiac function or significant
comorbidity may be symptomatic and unstable at lower
heart rates. If cardioversion fails to restore sinus rhythm and
the patient remains unstable, give amiodarone 300 mg intravenously
over 10–20 min and re-attempt electrical cardioversion.
Fig. 3.4. Tachycardia algorithm. ABCDE – Airway, Breathing Circulation, Disability, Exposure; IV – intravenous; SpO2 – oxygen saturation measured by pulse oximetry; BP –
blood pressure; ECG – electrocardiogram; DC – direct current; AF – atrial fibrillation; VT – ventricular tachycardia; SVT – supraventricular tachycardia; PSVT – paroxysmal
supraventricular tachycardia.
J. Soar et al. / Resuscitation 95 (2015) 100–147 129
The loading dose of amiodarone can be followed by an infusion of
900 mg over 24 h.
Repeated attempts at electrical cardioversion are not appropriate
for recurrent (within hours or days) paroxysms (selfterminating
episodes) of atrial fibrillation. This is relatively
common in critically ill patients who may have ongoing precipitating
factors causing the arrhythmia (e.g. metabolic disturbance,
sepsis). Cardioversion does not prevent subsequent arrhythmias. If
there are recurrent episodes, treat them with drugs.
Synchronised electrical cardioversion. If electrical cardioversion is
used to convert atrial or ventricular tachyarrhythmias, the shock
must be synchronised with the R wave of the ECG rather than with
the T wave.813 By avoiding the relative refractory period in this way,
the risk of inducing ventricular fibrillation is minimised. Conscious
patients must be anaesthetised or sedated before synchronised cardioversion
is attempted. For a broad-complex tachycardia and AF,
start with 120–150 J biphasic and increase in increments if this
fails. Atrial flutter and paroxysmal supraventricular tachycardia
(SVT) will often convert with lower energies: start with 70–120-J
biphasic.
If the patient is stable
If the patient with tachycardia is stable (no adverse signs or
symptoms) and is not deteriorating, pharmacological treatment
may be possible. Evaluate the rhythm using a 12-lead ECG and
assess the QRS duration. If the QRS duration is greater than 0.12 s
(3 small squares on standard ECG paper) it is classified as a broad
complex tachycardia. If the QRS duration is less than 0.12 s it is a
narrow complex tachycardia.
All anti-arrhythmic treatments – physical manoeuvres, drugs, or
electrical treatment – can also be pro-arrhythmic, so that clinical
deterioration may be caused by the treatment rather than lack of
effect. The use of multiple anti-arrhythmic drugs or high doses of
a single drug can cause myocardial depression and hypotension.
This may cause a deterioration of the cardiac rhythm. Expert help
should be sought before using repeated doses or combinations of
anti-arrhythmic drugs.
Broad-complex tachycardia
Broad-complex tachycardias are usually ventricular in origin.
Although broad-complex tachycardias may be caused by supraventricular
rhythms with aberrant conduction, in the unstable patient
in the peri-arrest context assume they are ventricular in origin. In
the stable patient with broad-complex tachycardia, the next step
is to determine if the rhythm is regular or irregular.
Regular broad complex tachycardia. A regular broad-complex tachycardia
is likely to be ventricular tachycardia or SVT with bundle
branch block. If there is uncertainty about the source of the arrhythmia,
give intravenous adenosine (using the strategy described
below) as it may convert the rhythm to sinus and help diagnose
the underlying rhythm.
Stable ventricular tachycardia can be treated with amiodarone
300 mg intravenously over 20–60 min followed by an infusion of
900 mg over 24 h. Specialist advice should be sought before considering
alternatives treatments such as procainamide, nifekalant or
sotalol.
Irregular broad complex tachycardia. Irregular broad complex
tachycardia is most likely to be AF with bundle branch block.
Another possible cause is AF with ventricular pre-excitation
(Wolff–Parkinson–White (WPW) syndrome). In this case there is
more variation in the appearance and width of the QRS complexes
than in AF with bundle branch block. A third possible cause is
polymorphic VT (e.g. torsade de pointes), although this rhythm is
relatively unlikely to be present without adverse features.
Seek expert help with the assessment and treatment of irregular
broad-complex tachyarrhythmia. If treating AF with bundle branch
block, treat as for AF (see below). If pre-excited AF (or atrial flutter)
is suspected, avoid adenosine, digoxin, verapamil and diltiazem.
These drugs block the AV node and cause a relative increase in
pre-excitation – this can provoke severe tachycardias. Electrical
cardioversion is usually the safest treatment option.
Treat torsades de pointes VT immediately by stopping all drugs
known to prolong the QT interval. Correct electrolyte abnormalities,
especially hypokalaemia. Give magnesium sulphate 2 g,
intravenously over 10 min. Obtain expert help, as other treatment
(e.g. overdrive pacing) may be indicated to prevent relapse once
the arrhythmia has been corrected. If adverse features develop
(which is usual), arrange immediate synchronised cardioversion. If
the patient becomes pulseless, attempt defibrillation immediately
(cardiac arrest algorithm).
Narrow-complex tachycardia
The first step in the assessment of a narrow complex tachycardia
is to determine if it is regular or irregular.
The commonest regular narrow-complex tachycardias include:
• sinus tachycardia;
• AV nodal re-entry tachycardia (AVNRT, the commonest type of
SVT);
• AV re-entry tachycardia (AVRT), which is associated with
Wolff–Parkinson–White (WPW) syndrome;
• atrial flutter with regular AV conduction (usually 2:1).
Irregular narrow-complex tachycardia is most commonly AF
or sometimes atrial flutter with variable AV conduction (‘variable
block’).
Regular narrow-complex tachycardia.
Sinus tachycardia. Sinus tachycardia is a common physiological
response to a stimulus such as exercise or anxiety. In a sick patient
it may be seen in response to many stimuli, such as pain, fever,
anaemia, blood loss and heart failure. Treatment is almost always
directed at the underlying cause; trying to slow sinus tachycardia
will make the situation worse.
AVNRT and AVRT (paroxysmal SVT). AVNRT is the commonest
type of paroxysmal SVT, often seen in people without any other
form of heart disease and is relatively uncommon in a periarrest
setting.814 It causes a regular narrow-complex tachycardia,
often with no clearly visible atrial activity on the ECG. Heart
rates are usually well above the typical range of sinus rates
at rest (60–120 beats min−1). It is usually benign, unless there
is additional co-incidental structural heart disease or coronary
disease.
AV re-entry tachycardia (AVRT) is seen in patients with the
WPW syndrome and is also usually benign unless there happens to
be additional structural heart disease. The common type of AVRT is
a regular narrow-complex tachycardia, also often having no visible
atrial activity on the ECG.
Atrial flutter with regular AV conduction (often 2:1 block). Atrial
flutter with regular AV conduction (often 2:1 block) produces a
regular narrow-complex tachycardia in which it may be difficult
to see atrial activity and identify flutter waves with confidence, so
it may be indistinguishable initially from AVNRT and AVRT. When
atrial flutter with 2:1 block or even 1:1 conduction is accompanied
by bundle branch block, it produces a regular broad-complex
tachycardia that will usually be very difficult to distinguish from VT.
Treatment of this rhythm as if it were VT will usually be effective,
or will lead to slowing of the ventricular response and identification
of the rhythm. Most typical atrial flutter has an atrial rate of
130 J. Soar et al. / Resuscitation 95 (2015) 100–147
about 300 beats min−1, so atrial flutter with 2:1 block tends to produce
a tachycardia of about 150 beats min−1. Much faster rates are
unlikely to be due to atrial flutter with 2:1 block.
Treatment of regular narrow complex tachycardia. If the patient
is unstable with adverse features caused by the arrhythmia,
attempt synchronised electrical cardioversion. It is reasonable to
give adenosine to an unstable patient with a regular narrowcomplex
tachycardia while preparations are made for synchronised
cardioversion; however, do not delay electrical cardioversion if the
adenosine fails to restore sinus rhythm. In the absence of adverse
features, proceed as follows.
• Start with vagal manoeuvres814: carotid sinus massage or the
Valsalva manoeuvre will terminate up to a quarter of episodes
of paroxysmal SVT. Carotid sinus massage stimulates baroreceptors,
which increase vagal tone and reduces sympathetic drive,
which slows conduction via the AV node. Carotid sinus massage
is given by applying pressure over the carotid artery at the
level of the cricoid cartilage. Massage the area with firm circular
movements for about 5 s. If this does not terminate the
arrhythmia, repeat on the opposite side. Avoid carotid massage
if a carotid bruit is present: rupture of an atheromatous plaque
could cause cerebral embolism and stroke. A Valsalva manoeuvre
(forced expiration against a closed glottis) in the supine
position may be the most effective technique. A practical way
of achieving this without protracted explanation is to ask the
patient to blow into a 20 ml syringe with enough force to push
back the plunger. Record an ECG (preferably multi-lead) during
each manoeuvre. If the rhythm is atrial flutter, slowing of
the ventricular response will often occur and demonstrate flutter
waves.
• If the arrhythmia persists and is not atrial flutter, use adenosine.
Give 6 mg as a rapid intravenous bolus. Record an ECG
(preferably multi-lead) during each injection. If the ventricular
rate slows transiently but the arrhythmia then persists, look for
atrial activity such as atrial flutter or other atrial tachycardia and
treat accordingly. If there is no response to adenosine 6 mg, give
a 12 mg bolus; if there is no response, give one further 12 mgbolus.
This strategy will terminate 90–95% of supraventricular
arrhythmias.
• Successful termination of a tachyarrhythmia by vagal manoeuvres
or adenosine indicates that it was almost certainly AVNRT
or AVRT. Monitor the patients for further rhythm abnormalities.
Treat recurrence either with further adenosine or with a
longer-acting drug with AV nodal-blocking action (e.g. diltiazem
or verapamil).
• If adenosine is contraindicated or fails to terminate a regular
narrow-complex tachycardia without demonstrating that it is
atrial flutter, give a calcium channel blocker (e.g. verapamil or
diltiazem).
Irregular narrow-complex tachycardia
An irregular narrow-complex tachycardia is most likely to be AF
with an uncontrolled ventricular response or, less commonly, atrial
flutter with variable AV block. Record a 12-lead ECG to identify
the rhythm. If the patient is unstable with adverse features caused
by the arrhythmia, attempt synchronised electrical cardioversion
as described above. The European Society of Cardiology provides
detailed guidelines on the management of AF: www.escardio.org.
If there are no adverse features, treatment options include:
• rate control by drug therapy
• rhythm control using drugs to encourage chemical cardioversion
• rhythm control by electrical cardioversion
• treatment to prevent complications (e.g. anticoagulation).
Obtain expert help to determine the most appropriate treatment
for the individual patient. The longer a patient remains in AF, the
greater is the likelihood of atrial clot developing. In general, patients
who have been in AF for more than 48 h should not be treated by
cardioversion (electrical or chemical) until they have received full
anticoagulation or absence of atrial clot has been shown by transoesophageal
echocardiography. If the clinical scenario dictates that
cardioversion is required and the duration of AF is greater than
48 h (or the duration is unknown) discuss anticoagulation, choice
of agent, and duration with a cardiologist.
If the aim is to control heart rate, the drugs of choice are betablockers
and diltiazem. Digoxin and amiodarone may be used in
patients with heart failure.
If the duration of AF is less than 48 h and rhythm control is
considered appropriate, chemical cardioversion may be attempted.
Seek expert help and consider, flecainide, propafenone, or ibutilide.
Amiodarone (300 mg intravenously over 20–60 min followed by
900 mg over 24 h) may also be used but is less effective. Electrical
cardioversion remains an option in this setting and will restore
sinus rhythm in more patients than chemical cardioversion.
Seek expert help if any patient with AF is known or found to have
ventricular pre-excitation (WPW syndrome). Avoid using adenosine,
diltiazem, verapamil or digoxin in patients with pre-excited
AF or atrial flutter, as these drugs block the AV node and cause a
relative increase in pre-excitation.
Bradycardia
A bradycardia is defined as a heart rate of <60 beats min−1.
Bradycardia can have cardiac causes (e.g. myocardial infarction;
myocardial ischaemia; sick sinus syndrome), non-cardiac causes
(e.g. vasovagal response, hypothermia; hypoglycaemia; hypothyroidism,
raised intracranial pressure) or be caused by drug toxicity
(e.g. digoxin; beta blockers; calcium channel blockers).
Bradycardias are caused by reduced sinoatrial node firing or
failure of the atrial–ventricular conduction system. Reduced sinoatrial
node firing is seen in sinus bradycardia (caused by excess
vagal tone), sinus arrest, and sick sinus syndrome. Atrioventricular
(AV) blocks are divided into first, second, and third degrees and
may be associated with multiple medications or electrolyte disturbances,
as well as structural problems caused by acute myocardial
infarction and myocarditis. A first-degree AV block is defined by
a prolonged P-R interval (>0.20 s), and is usually benign. Seconddegree
AV block is divided into Mobitz types I and II. In Mobitz
type I, the block is at the AV node, is often transient and may be
asymptomatic. In Mobitz type II, the block is most often below the
AV node at the bundle of His or at the bundle branches, and is often
symptomatic, with the potential to progress to complete AV block.
Third-degree heart block is defined by AV dissociation, which may
be permanent or transient, depending on the underlying cause.
Initial assessment
Assess the patient with bradycardia using the ABCDE approach.
Consider the potential cause of the bradycardia and look for the
adverse signs. Treat any reversible causes of bradycardia identified
in the initial assessment. If adverse signs are present start to treat
the bradycardia. Initial treatments are pharmacological, with pacing
being reserved for patients unresponsive to pharmacological
treatments or with risks factors for asystole (Fig. 3.5).
Pharmacological treatment
If adverse signs are present, give atropine 500 ␮g, intravenously
and, if necessary, repeat every 3–5 min to a total of 3 mg. Doses
of atropine of less than 500 ␮g, paradoxically, may cause further
slowing of the heart rate.815 In healthy volunteers a dose of
3 mg produces the maximum achievable increase in resting heart
J. Soar et al. / Resuscitation 95 (2015) 100–147 131
Fig. 3.5. Bradycardia algorithm. ABCDE – Airway, Breathing Circulation, Disability, Exposure; IV – intravenous; SpO2 – oxygen saturation measured by pulse oximetry; BP –
blood pressure; ECG – electrocardiogram; AV – atrioventricular.
132 J. Soar et al. / Resuscitation 95 (2015) 100–147
rate.816 Use atropine cautiously in the presence of acute coronary
ischaemia or myocardial infarction; increased heart rate may
worsen ischaemia or increase the zone of infarction.
If treatment with atropine is ineffective, consider second
line drugs. These include isoprenaline (5 ␮g min−1 starting dose),
adrenaline (2–10 ␮g min−1) and dopamine (2–10 ␮g kg−1 min−1).
Theophylline (100–200 mg slow intravenous injection) should be
considered if the bradycardia is caused by inferior myocardial
infarction, cardiac transplant or spinal cord injury. Consider giving
intravenous glucagon if beta-blockers or calcium channel blockers
are a potential cause of the bradycardia. Do not give atropine to
patients with cardiac transplants – it can cause a high-degree AV
block or even sinus arrest.817
Pacing
Initiate transcutaneous pacing immediately if there is no
response to atropine, or if atropine is unlikely to be effective.
Transcutaneous pacing can be painful and may fail to produce
effective mechanical capture. Verify mechanical capture and
reassess the patient’s condition. Use analgesia and sedation to control
pain, and attempt to identify the cause of the bradyarrhythmia.
If atropine is ineffective and transcutaneous pacing is not immediately
available, fist pacing can be attempted while waiting for
pacing equipment. Give serial rhythmic blows with the closed fist
over the left lower edge of the sternum to pace the heart at a physiological
rate of 50–70 beats min−1.
Seek expert help to assess the need for temporary transvenous
pacing. Temporary transvenous pacing should be considered
if there are is a history of recent asystole; Mobitz type II AV block;
complete (third-degree) heart block (especially with broad QRS or
initial heart rate < 40 beats min−1) or evidence of ventricular standstill
of more than 3 s.
Antiarrhythmic drugs
Adenosine
Adenosine is a naturally occurring purine nucleotide. It slows
transmission across the AV node but has little effect on other
myocardial cells or conduction pathways. It is highly effective for
terminating paroxysmal SVT with re-entrant circuits that include
the AV node (AVNRT). In other narrow-complex tachycardias,
adenosine will reveal the underlying atrial rhythms by slowing
the ventricular response. It has an extremely short half-life of
10–15 s and, therefore, is given as a rapid bolus into a fast running
intravenous infusion or followed by a saline flush. The smallest
dose likely to be effective is 6 mg (which is outside some current
licences for an initial dose) and, if unsuccessful this can be followed
with up to two doses each of 12 mg every 1–2 min. Patients
should be warned of transient unpleasant side effects, in particular
nausea, flushing, and chest discomfort. Adenosine is not available
in some European countries, but adenosine triphosphate (ATP) is
an alternative. In a few European countries neither preparation
may be available; verapamil is probably the next best choice. Theophylline
and related compounds block the effect of adenosine.
Patients receiving dipyridamole or carbamazepine, or with denervated
(transplanted) hearts, display a markedly exaggerated effect
that may be hazardous. In these patients, or if injected into a central
vein, reduce the initial dose of adenosine to 3 mg. In the presence
of WPW syndrome, blockage of conduction across the AV node by
adenosine may promote conduction across an accessory pathway.
In the presence of supraventricular arrhythmias this may cause a
dangerously rapid ventricular response. In the presence of WPW
syndrome, rarely, adenosine may precipitate atrial fibrillation associated
with a dangerously rapid ventricular response.
Amiodarone
Intravenous amiodarone has effects on sodium, potassium and
calcium channels as well as alpha- and beta-adrenergic blocking
properties. Indications for intravenous amiodarone include:
• Control of haemodynamically stable monomorphic VT, polymorphic
VT and wide-complex tachycardia of uncertain origin.
• Paroxysmal SVT uncontrolled by adenosine, vagal manoeuvres or
AV nodal blockade;
• to control rapid ventricular rate due to accessory pathway
conduction in pre-excited atrial arrhythmias. In patients with
pre-excitation and AF, digoxin, non-dihydropyridine calcium
channel antagonists, or intravenous amiodarone should not be
administered as they may increase the ventricular response and
may result in VF.818,819
• Unsuccessful electrical cardioversion.
Give amiodarone, 300 mg intravenously, over 10–60 min
depending on the circumstances and haemodynamic stability of
the patient. This loading dose is followed by an infusion of 900 mg
over 24 h. Additional infusions of 150 mg can be repeated as
necessary for recurrent or resistant arrhythmias to a maximum
manufacturer-recommended total daily dose of 2 g (this maximum
licensed dose varies between different countries). In patients
with severely impaired heart function, intravenous amiodarone is
preferable to other anti-arrhythmic drugs for atrial and ventricular
arrhythmias. Major adverse effects from amiodarone are hypotension
and bradycardia, which can be prevented by slowing the rate
of drug infusion. The hypotension associated with amiodarone is
caused by vasoactive solvents (Polysorbate 80 and benzyl alcohol).
An aqueous formulation of amiodarone does not contain these
solvents and causes no more hypotension than lidocaine.677 Whenever
possible, intravenous amiodarone should be given via a central
venous catheter; it causes thrombophlebitis when infused into a
peripheral vein. In an emergency it can be injected into a large
peripheral vein.
Calcium channel blockers: verapamil and diltiazem
Verapamil and diltiazem are calcium channel blocking drugs
that slow conduction and increase refractoriness in the AV node.
Intravenous diltiazem is not available in some countries. These
actions may terminate re-entrant arrhythmias and control ventricular
response rate in patients with a variety of atrial tachycardias.
Indications include:
• stable regular narrow-complex tachycardias uncontrolled or
unconverted by adenosine or vagal manoeuvres;
• to control ventricular rate in patients with AF or atrial flutter and
preserved ventricular function.
The initial dose of verapamil is 2.5–5 mg intravenously given
over 2 min. In the absence of a therapeutic response or druginduced
adverse event, give repeated doses of 5–10 mg every
15–30 min 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 supraventricular origin. The administration
of calcium channel blockers to a patient with ventricular
tachycardia may cause cardiovascular collapse.
Diltiazem at a dose of 250 ␮g kg−1 intravenously, followed by a
second dose of 350 ␮g kg−1, is as effective as verapamil. Verapamil
and, to a lesser extent, diltiazem may decrease myocardial contractility
and critically reduce cardiac output in patients with severe
LV dysfunction. For the reasons stated under adenosine (above),
calcium channel blockers are considered harmful when given to
patients with AF or atrial flutter associated with pre-excitation
(WPW) syndrome.
J. Soar et al. / Resuscitation 95 (2015) 100–147 133
Beta-adrenergic blockers
Beta-blocking drugs (atenolol, metoprolol, labetalol (alpha- and
beta-blocking effects), propranolol, esmolol) reduce the effects of
circulating catecholamines and decrease heart rate and blood pressure.
They also have cardioprotective effects for patients with acute
coronary syndromes. Beta-blockers are indicated for the following
tachycardias:
• narrow-complex regular tachycardias uncontrolled by vagal
manoeuvres and adenosine in the patient with preserved ventricular
function;
• to control rate in AF and atrial flutter when ventricular function
is preserved.
The intravenous dose of atenolol (beta1) is 5 mg given over
5 min, repeated if necessary after 10 min. Metoprolol (beta1) is
given in doses of 2–5 mg at 5-min intervals to a total of 15 mg.
Propranolol (beta1 and beta2 effects), 100 ␮g kg−1, is given slowly
in three equal doses at 2–3-min intervals.
Intravenous esmolol is a short-acting (half-life of 2–9 min)
beta1-selective beta-blocker. It is given as an intravenous loading
dose of 500 ␮g kg−1 over 1 min, followed by an infusion of
50–200 ␮g kg−1 min−1.
Side effects of beta-blockade include bradycardia, AV conduction
delay and hypotension. Contraindications to the use of
beta-adrenergic blocking drugs include second- or third-degree
heart block, hypotension, severe congestive heart failure and lung
disease associated with bronchospasm.
Magnesium
Magnesium is the first line treatment for polymorphic ventricular
tachycardia (torsades de pointes) and ventricular or
supraventricular tachycardia associated with hypomagnesaemia.
It may also reduce ventricular rate in atrial fibrillation. Give magnesium
sulphate 2 g (8 mmol) over 10 min. This can be repeated
once if necessary.
Collaborators
Rudolph W. Koster, Department of Cardiology, Academic Medical
Center, Amsterdam, The Netherlands
Koenraad G. Monsieurs, Emergency Medicine, Faculty of Medicine
and Health Sciences, University of Antwerp, Antwerp, Belgium; Faculty
of Medicine and Health Sciences, University of Ghent, Ghent,
Belgium
Nikolaos I. Nikolaou, Cardiology Department, Konstantopouleio
General Hospital, Athens, Greece
Conflicts of interest
Jasmeet Soar Editor Resuscitation
Bernd W. Böttiger No conflict of interest reported
Carsten Lott No conflict of interest reported
Charles D. Deakin Director Prometheus Medical Ltd
Claudio Sandroni No conflict of interest reported
Gavin D. Perkins Editor Resuscitation
Jerry P. Nolan Editor-in-Chief Resuscitation
Kjetil Sunde No conflict of interest reported
Markus B. Skrifvars No conflict of interest reported
Pierre Carli No conflict of interest reported
Thomas Pellis Speakers honorarium BARD Medica
Gary B. Smith The Learning Clinic company (VitalPAC): research
advisor, family shareholder
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