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Available online at www.sciencedirect.com

Resuscitation
journal homepage: www.elsevier.com/locate/resuscitation

European Resuscitation Council Guidelines 2021:
Adult advanced life support
Jasmeet Soar a, *, Bernd W. Böttiger b , Pierre Carli c , Keith Couper d,Charles D. Deakin e , Therese Djärv f , Carsten Lott g , Theresa Olasveengen h ,Peter Paal i , Tommaso Pellis j , Gavin D. Perkins k , Claudio Sandroni l,m , Jerry P. Nolan naSouthmead Hospital, North Bristol NHS Trust, Bristol, UK
Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Cologne, Germanyc
SAMU de Paris, Centre Hospitalier Universitaire Necker Enfants Malades, Assistance Publique Hôpitaux de Paris, and Université Paris
Descartes, Paris, FrancedCritical Care Unit, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK; Warwick Medical School, University of Warwick,
Coventry,UKe
University Hospital Southampton NHS Foundation Trust, Southampton, UK; South Central Ambulance Service NHS Foundation Trust,Otterbourne,UKf
Dept of Acute and Reparative Medicine, Karolinska University Hospital, Stockholm, Sweden, Department of Medicine Solna, Karolinska Institutet,
Stockholm, Swedeng
Department of Anesthesiology, University Medical Center, Johannes Gutenberg-Universitaet Mainz, GermanyhDepartment of Anesthesiology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Norwayi
Department of Anaesthesiology and Intensive Care Medicine, Hospitallers Brothers Hospital, Paracelsus Medical University, Salzburg, AustriajDepartment of Anaesthesia and Intensive Care, Azienda Sanitaria Friuli Occidentale, Italyk
University of Warwick, Warwick Medical School and University Hospitals Birmingham NHS Foundation Trust, Coventry, UKl
Department of Intensive Care, Emergency Medicine and Anaesthesiology, Fondazione Policlinico Universitario A. Gemelli-IRCCS, Rome, Italym
Institute of Anaesthesiology and Intensive Care Medicine, Università Cattolica del Sacro Cuore, Rome, Italyn
University of Warwick, Warwick Medical School, Coventry, CV4 7AL; Royal United Hospital, Bath, UKb

Abstract
These European Resuscitation Council Advanced Life Support guidelines, are based on the 2020 International Consensus on Cardiopulmonary
Resuscitation Science with Treatment Recommendations. This section provides guidelines on the prevention of and ALS treatments for both in-hospital
cardiac arrest and out-of-hospital cardiac arrest.

Introduction
Adult advanced life support (ALS) includes the advanced interventions that follow basic life support (BLS) and use of an automatedexternal defibrillator (AED). Basic life support continues during andoverlaps with ALS interventions.

This ALS section includes the prevention and treatment of both inhospital cardiac arrest (IHCA) and out-of-hospital cardiac arrest cardiac
arrest (OHCA), the ALS algorithm, manual defibrillation, airway
management during cardiopulmonary resuscitation (CPR), drugs andtheir delivery during CPR, and the treatment of peri-arrest arrhythmias.
These Guidelines are based on the International Liaison
Committee on Resuscitation (ILCOR) 2020 Consensus on Scienceand Treatment Recommendations (CoSTR) for ALS.1 For these ERC* Corresponding author.
E-mail address: jasmeet.soar@nbt.nhs.uk (J. Soar).
https://doi.org/10.1016/j.resuscitation.2021.02.010
0300-9572/© 2021 European Resuscitation Council. Published by Elsevier B.V. All rights reserved

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Guidelines the ILCOR recommendations were supplemented byfocused literature reviews undertaken by the ERC ALS Writing Groupfor those topics not reviewed in the 2020 ILCOR CoSTR. Whenrequired, the guidelines were informed by the expert consensus of thewriting group membership.
The ERC has also produced guidance on cardiac arrest for patientswith coronavirus disease 2019 (COVID-19),2 which is based on an
ILCOR CoSTR and systematic review.3,4 Our understanding of the
optimal treatment of patients with COVID-19 and the risk of virustransmission and infection of rescuers is poorly understood andevolving. Please check ERC and national guidelines for the latest
guidance and local policies for both treatment and rescuer precautions.
Guidelines were drafted and agreed by the ALS Writing Group
members before posting for public comment between 21 October and5 November 2020. Twenty-five individuals from 11 countries made109 comments. Review of these comments led to 46 changes. The
Guideline was presented to and approved by the ERC General
Assembly on 10th December 2020. The methodology used for
guideline development is presented in the Executive summary.4a

Summary of key changes

151

prevent inadvertent deprivation of other indicated treatments,
besides CPR. These plans should be recorded in a consistentmanner (See Ethics section).
 Hospitals should use a track and trigger early warning scoresystem for the early identification of patients who are critically ill or
at risk of clinical deterioration.
 Hospitals should train staff in the recognition, monitoring and
immediate care of the acutely-ill patient.
 Hospitals should empower all staff to call for help when they identify
a patient at risk of physiological deterioration. This includes calls
based on clinical concern, rather than solely on vital signs.
 Hospitals should have a clear policy for the clinical response toabnormal vital signs and critical illness. This may include a criticalcare outreach service and, or emergency team (e.g. medical
emergency team, rapid response team).
 Hospital staff should use structured communication tools toensure effective handover of information.
 Patients should receive care in a clinical area that has theappropriate staffing, skills, and facilities for their severity of illness.
 Hospitals should review cardiac arrest events to identify
opportunities for system improvement and share key learning
points with hospital staff.

 There are no major changes in the 2020 Adult ALS Guidelines.
 There is a greater recognition that patients with both in- and out-ofhospital cardiac arrest have premonitory signs, and that many ofthese arrests may be preventable.
 High quality chest compressions with minimal interruption andearly defibrillation remain priorities.
 During CPR, start with basic airway techniques and progress
stepwise according to the skills of the rescuer until effective
ventilation is achieved. If an advanced airway is required, rescuerswith a high tracheal intubation success rate should use tracheal
intubation. The expert consensus is that a high success rate isover 95% within two attempts at intubation.
 When adrenaline is used it should be used as soon as possible
when the cardiac arrest rhythm is non-shockable cardiac arrest, andafter 3 defibrillation attempts for a shockable cardiac arrest rhythm.
 The guideline recognises the increasing role of point-of-careultrasound (POCUS) in peri-arrest care for diagnosis, butemphasise that it requires a skilled operator, and the need tominimise interruptions during chest compression.
 The guideline reflects the increasing evidence for extracorporeal
CPR (eCPR) as a rescue therapy for selected patients with cardiac
arrest when conventional ALS measures are failing or to facilitate
specific interventions (e.g. coronary angiography and percutaneous coronary intervention (PCI), pulmonary thrombectomy for
massive pulmonary embolism, rewarming after hypothermic
cardiac arrest) in settings in which it can be implemented.
 These ERC guidelines have followed European and internationalguidelines for the treatment of peri-arrest arrhythmias.
Key messages from this section are presented in Fig. 1.

Concise guidelines for clinical practicePrevention of in-hospital cardiac arrest
 The ERC supports shared decision making and advanced careplanning which integrates resuscitation decisions with emergency
care treatment plans to increase clarity of treatment goals and also

Prevention of out-of-hospital cardiac arrest
 Symptoms such as syncope (especially during exercise, while
sitting or supine), palpitations, dizziness and sudden shortness ofbreath that are consistent with an arrhythmia should be
investigated.
 Apparently healthy young adults who suffer sudden cardiac death(SCD) can also have signs and symptoms (e.g. syncope/presyncope, chest pain and palpitations) that should alert healthcare
professionals to seek expert help to prevent cardiac arrest.
 Young adults presenting with characteristic symptoms ofarrhythmic syncope should have a specialist cardiology assessment, which should include an electrocardiogram (ECG) and in
most cases echocardiography and an exercise test.
 Systematic evaluation in a clinic specialising in the care of those atrisk for SCD is recommended in family members of young victimsof SCD or those with a known cardiac disorder resulting in an
increased risk of SCD.
 Identification of individuals with inherited conditions and screeningof family members can help prevent deaths in young people with
inherited heart disorders.
 Follow current European Society of Cardiology (ESC) guidelines
for the diagnosis and management of syncope.

Treatment of in-hospital cardiac arrest Hospital systems should aim to recognise cardiac arrest, start
CPR immediately, and defibrillate rapidly (<3 min) whenappropriate.
 All hospital staff should be able to rapidly recognise cardiac arrest,
call for help, start CPR and defibrillate (attach an AED and follow
the AED prompts, or use a manual defibrillator).
 European hospitals should adopt a standard “Cardiac Arrest Call”
telephone number (2222).
 Hospitals should have a resuscitation team that immediately
responds to IHCAs.

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Fig. 1 – ALS summary The hospital resuscitation team should include team members
who have completed an accredited adult ALS course.
 Resuscitation team members should have the key skills andknowledge to manage a cardiac arrest including manual
defibrillation, advanced airway management, intravenous access,intra-osseous access, and identification and treatment of reversible causes.
 The resuscitation team should meet at the beginning of each shift
for introductions and allocation of team roles.
 Hospitals should standardise resuscitation equipment.

 Start ALS as early as possible.
 Emergency medical systems (EMS) should consider implementing criteria for the withholding and termination of resuscitation(TOR) taking in to consideration specific local legal, organizationaland cultural context (see Ethics section)
 Systems should define criteria for the withholding and termination of
CPR, and ensure criteria are validated locally (see the Ethics section).
 Emergency medical systems (EMS) should monitor staff exposure
to resuscitation and low exposure should be addressed toincrease EMS team experience in resuscitation.

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 Adult patients with non-traumatic OHCA should be considered fortransport to a cardiac arrest centre according to local protocols(see Systems saving lives)151 For refractory VF, consider using an alternative defibrillation pad
position (e.g. anterior- posterior) Do not use dual (double) sequential defibrillation for refractory VF
outside of a research setting.

Manual defibrillation
Airway and ventilation
Defibrillation strategy
 Continue CPR while a defibrillator is retrieved and pads applied.
 Give a shock as early as possible when appropriate.
 Deliver shocks with minimal interruption to chest compression, andminimise the pre-shock and post-shock pause. This is achieved bycontinuing chest compressions during defibrillator charging, delivering defibrillation with an interruption in chest compressions of lessthan 5 s and then immediately resuming chest compressions.
 Immediately resume chest compressions after shock delivery. If
there is a combination of clinical and physiological signs of returnof spontaneous circulation (ROSC) such as waking, purposeful
movement, arterial waveform or a sharp rise in end-tidal carbon
dioxide (ETCO2), consider stopping chest compressions forrhythm analysis, and if appropriate a pulse check.

Safe and effective defibrillation
 Minimise the risk of fire by taking off any oxygen mask or nasal
cannulae and place them at least 1 m away from the patient’s
chest. Ventilator circuits should remain attached.
 Antero-lateral pad position is the position of choice for initial pad
placement. Ensure that the apical (lateral) pad is positioned
correctly (mid-axillary line, level with the V6 pad position) i.e. below
the armpit.
 In patients with an implantable device, place the pad > 8 cm awayfrom the device, or use an alternative pad position. Also consider
an alternate pad position when the patient is in the prone position(bi-axillary), or in a refractory shockable rhythm (see below).
 A shock can be safely delivered without interrupting mechanicalchest compression.
 During manual chest compressions, ‘hands-on’ defibrillation, evenwhen wearing clinical gloves, is a risk to the rescuer.

Energy levels and number of shocks
 Use single shocks where indicated, followed by a 2 min cycle ofchest compressions.
 The use of up to three-stacked shocks may be considered only
if initial ventricular fibrillation/pulseless ventricular tachycardia(VF/pVT) occurs during a witnessed, monitored cardiac arrest witha defibrillator immediately available e.g. during cardiac catheterisation or in a high dependency area.
 Defibrillation shock energy levels are unchanged from the 2015
guidelines:
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, deliver the first shock at
120 150 J.
 If the rescuer is unaware of the recommended energy settings ofthe defibrillator, for an adult use the highest energy setting for all
shocks.

Recurrent or refractory VF
 Consider escalating the shock energy, after a failed shock and forpatients where refibrillation occurs.

 During CPR, start with basic airway techniques and progress
stepwise according to the skills of the rescuer until effective
ventilation is achieved.
 If an advanced airway is required, rescuers with a high tracheal
intubation success rate should use tracheal intubation. The expert
consensus is that a high success rate is over 95% within two
attempts at intubation.
 Aim for less than a 5 s interruption in chest compression fortracheal intubation.
 Use direct or video laryngoscopy for tracheal intubation according
to local protocols and rescuer experience Use waveform capnography to confirm tracheal tube position.
 Give the highest feasible inspired oxygen during CPR.
 Give each breath over 1 s to achieve a visible chest rise.
 Once a tracheal tube or a supraglottic airway (SGA) has been
inserted, ventilate the lungs at a rate of 10 min 1 and continue
chest compressions without pausing during ventilations. With a
SGA, if gas leakage results in inadequate ventilation, pause
compressions for ventilation using a compression-ventilation ratioof 30:2.

Drugs and fluids
Vascular access Attempt intravenous (IV) access first to enable drug delivery inadults in cardiac arrest.
 Consider intraosseous (IO) access if attempts at IV access are
unsuccessful or IV access is not feasible

Vasopressor drugs
 Give adrenaline 1 mg IV (IO) as soon as possible for adult patientsin cardiac arrest with a non-shockable rhythm.
 Give adrenaline 1 mg IV (IO) after the 3rd shock for adult patients in
cardiac arrest with a shockable rhythm.
 Repeat adrenaline 1 mg IV (IO) every 3 5 min whilst ALS
continues.

Antiarrhythmic drugs
 Give amiodarone 300 mg IV(IO) for adult patients in cardiac arrest
who are in VF/pVT after three shocks have been administered.
 Give a further dose of amiodarone 150 mg IV (IO) for adult patientsin cardiac arrest who are in VF/pVT after five shocks have been
administered.
 Lidocaine 100 mg IV (IO) may be used as an alternative if
amiodarone is not available or a local decision has been made touse lidocaine instead of amiodarone. An additional bolus oflidocaine 50 mg can also be given after five defibrillation attempts.

Thrombolytic drugs
 Consider thrombolytic drug therapy when pulmonary embolus is
the suspected or confirmed cause of cardiac arrest.
 Consider CPR for 60 90 min after administration of thrombolytic
drugs.

RESUSCITATION 161 (2021) 115

Fluids Give IV (IO) fluids only where the cardiac arrest is caused by or
possibly caused by hypovolaemia.

Waveform capnography during advanced life support
 Use waveform capnography to confirm correct tracheal tube
placement during CPR.
 Use waveform capnography to monitor the quality of CPR.
 An increase in ETCO2 during CPR may indicate that ROSC has
occurred. However, chest compression should not be interrupted
based on this sign alone.
 Although high and increasing ETCO2 values are associated withincreased rates of ROSC and survival after CPR, do not use a low
ETCO2 value alone to decide if a resuscitation attempt should be
stopped.

Use of ultrasound imaging during advanced life support
 Only skilled operators should use intra-arrest point-of-careultrasound (POCUS).
 POCUS must not cause additional or prolonged interruptions inchest compressions.
 POCUS may be useful to diagnose treatable causes of cardiac
arrest such as cardiac tamponade and pneumothorax.
 Right ventricular dilation in isolation during cardiac arrest should
not be used to diagnose massive pulmonary embolism.
 Do not use POCUS for assessing contractility of the myocardium
as a sole indicator for terminating CPR.

Mechanical chest compression devices
 Consider mechanical chest compressions only if high-quality
manual chest compression is not practical or compromises
provider safety.
 When a mechanical chest compression device is used, minimise
interruptions to chest compression during device use by using only
trained teams familiar with the device.

Extracorporeal CPR Consider extracorporeal CPR (eCPR) as a rescue therapy forselected patients with cardiac arrest when conventional ALS
measures are failing or to facilitate specific interventions (e.g.
coronary angiography and percutaneous coronary intervention(PCI), pulmonary thrombectomy for massive pulmonary embolism, rewarming after hypothermic cardiac arrest) in settings inwhich it can be implemented.

Peri-arrest arrhythmias
 The assessment and treatment of all arrhythmias addresses thecondition of the patient (stable versus unstable) and the nature of
the arrhythmia. Life-threatening features in an unstable patient
include:Shockappreciated as hypotension (e.g. systolic bloodpressure < 90 mmHg) and symptoms of increased sympathetic
activity and reduced cerebral blood flow.
Syncope as a consequence of reduced cerebral blood flow.

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119

Severe heart failure
manifested by pulmonary oedema(failure of the left ventricle) and/or raised jugular venous
pressure (failure of the right ventricle).
Myocardial ischaemia may present with chest pain (angina) or
may occur without pain as an isolated finding on the 12-lead
ECG (silent ischaemia).

Tachycardias
 Electrical cardioversion is the preferred treatment for tachyarrhythmia in the unstable patient displaying potentially lifethreatening adverse signs.
 Conscious patients require anaesthesia or sedation, before
attempting synchronised cardioversion.
 To convert atrial or ventricular tachyarrhythmias, the shock must
be synchronised to occur with the R wave of the electrocardiogram(ECG).
 For atrial fibrillation:
An initial synchronised shock at maximum defibrillator output
rather than an escalating approach is a reasonable strategy
based on current data.
 For atrial flutter and paroxysmal supraventricular tachycardia:
Give an initial shock of 70 120 J.
Give subsequent shocks using stepwise increases in energy.
 For ventricular tachycardia with a pulse:
Use energy levels of 120 150 J for the initial shock.
Consider stepwise increases if the first shock fails to achievesinus rhythm.
 If cardioversion fails to restore sinus rhythm and the patient
remains unstable, give amiodarone 300 mg intravenously over
10 20 min (or procainamide 10 15 mg/kg over 20 min) and reattempt electrical cardioversion. The loading dose of amiodarone
can be followed by an infusion of 900 mg over 24 h.
 If the patient with tachycardia is stable (no adverse signs or
symptoms) and is not deteriorating, pharmacological treatment
may be possible.
 Consider amiodarone for acute heart rate control in AF patientswith haemodynamic instability and severely reduced left ventricular ejection fraction (LVEF). For patients with LVEF < 40%consider the smallest dose of beta-blocker to achieve a heart
rate less than 110 min-1 . Add digoxin if necessary.

Bradycardia
 If bradycardia is accompanied by adverse signs, give atropine
500 mg IV (IO) and, if necessary, repeat every 3 5 min to a total of
3 mg.
 If treatment with atropine is ineffective, consider second line drugs.
These include isoprenaline (5 mg min 1 starting dose), andadrenaline (2 10 mg min 1).
 For bradycardia caused by inferior myocardial infarction, cardiac
transplant or spinal cord injury, consider giving aminophylline(100 200 mg slow intravenous injection).
 Consider giving 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 cancause a high-degree AV block or even sinus arrest
useaminophylline.
 Consider pacing in patients who are unstable, with symptomatic
bradycardia refractory to drug therapies.
 If transthoracic pacing is ineffective, consider transvenous pacing.

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 Whenever a diagnosis of asystole is made, check the ECG
carefully for the presence of P waves because unlike true asystole,
this is more likely to respond to cardiac pacing.
 If atropine is ineffective and transcutaneous pacing is not
immediately available, fist pacing can be attempted while waitingfor pacing equipment.

Uncontrolled organ donation after circulatory death When there is no ROSC, consider uncontrolled organ donation
after circulatory death in settings where there is an establishedprogramme, and in accordance with local protocols andlegislation.

Debriefing Use data-driven, performance-focused debriefing of rescuers to
improve CPR quality and patient outcomes.

151

Monitoring
Most cases of IHCA have an initial non-shockable rhythm andpreceding signs of respiratory depression or shock are common.5,6,17
To help detect deterioration and critical illness early, all patientsshould have a documented plan for vital sign monitoring that includes
which physiological measurements should be recorded and how
frequently. This can be addressed by using a standardised early
warning score (EWS) system for all patients. The choice of systemdepends on local circumstances and should align with nationalguidelines. For example in the UK the National Early Warning Score 2(NEWS2) is endorsed by the National Institute for Health and Care
Excellence (NICE) guidelines.14,15 Higher trained nurse staffing levels
are associated with lower rates of failure-to-respond to abnormal vital
signs, and the quality of patient care.18,19 There is a lack ofrandomised controlled trials (RCTs) or consensus on which patientsshould undergo continuous ECG monitoring. In a registry-based
study, settings where patients are closely monitored are associatedwith improved survival irrespective of initial rhythm.20

Recognition

Evidence informing the guidelines
Prevention of in-hospital cardiac arrest (IHCA)
In-hospital cardiac arrest (IHCA) occurs in about 1.5 patients per 1000
admitted to hospital.5,6 There are two main strategies to prevent
cardiac arrest and the need for attempted CPR: Patient-focussed decision-making to determine if CPR isappropriate.
 Identifying and treating physiological deterioration early to prevent
cardiac arrest.

Strategies to simplify and standardise tracking of a patient's condition,and recognising acute illness or deterioration, and triggering a
response include early warning score (EWS) systems.
These systems have a predefined graded and escalating response
according to the patient’s EWS. The EWS is used to identify ward
patients needing escalation of care, increasing vital sign monitoring,and may improve identification of deterioration, and reduce time toemergency team activation.21 Clinical concern from nurses and othermembers of the multidisciplinary team can also indicate patient
deterioration.22,23

The call for help
Emergency care treatment and CPR decisions
Most patients who die in hospital do not have a resuscitation attempt.7 10
The ERC Ethics guidelines promote shared decision making andadvanced care planning which integrates resuscitation decisions withemergency care treatment plans to increase clarity of treatment goals
and also prevent inadvertent deprivation of other indicated treatments,
besides CPR. Further information is provided in the Ethics section.

Physiological deterioration
In-hospital cardiac arrest is often preceded by physiological deterioration.11,12 This provides an opportunity to recognise deterioration andprevent the cardiac arrest. The 5 key steps have been conceptualised
as the in-hospital chain of survival: 'staff education', 'monitoring','recognition', the 'call for help' and the 'response'.13 This ERC
guidance is based on an ILCOR COSTR and systematic review ofadult rapid response systems, and UK guidance for early warningscores and recognising and responding to deterioration of acutely-ill
adults in hospital.14 16

Staff education
Education should include measurement of vital signs, a structured
ABCDE-type approach that includes assessment and initial
treatment interventions, use of structured communication tools
such as Situation-Background-Assessment-Recommendation(SBAR), and how to call for help and escalate care.15 Staff should
also know how to implement local policies about do-not-attempt
CPR (DNACPR) decisions, treatment escalation plans, and starting
end-of-life care.

All staff should be empowered to call for help and also trained to use
structured communication tools such as SBAR (situation-background-assessment-recommendation) to ensure effective communication.24 26 The response to patients who are critically ill or who are at
risk of becoming critically ill is often provided by a medical emergency
team (MET), rapid response team (RRT), or critical care outreachteam (CCOT). Any member of the health-care 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.27 29

Response
The response to patients who are or at risk of being critically ill is often
provided by a MET/RRT/CCOT. These teams usually comprise criticalcare medical and nursing staff who respond to specific calling criteria.
They replace or coexist with traditional cardiac arrest teams, which
typically only respond to patients already in cardiac arrest. Systematic
reviews, meta-analyses and multicentre studies suggest that RRT/
MET/CCOT systems reduce the rate of IHCA and hospital mortality.30,31 These data led ILCOR to suggest that hospitals consider the
introduction of rapid response systems (rapid response team/medical
emergency team) to reduce the incidence of IHCA and in-hospitalmortality (weak recommendation, low-quality evidence).16 Team
interventions often involve simple tasks such as starting oxygentherapy and intravenous fluids, as well as more complex decisionmaking such as transferring the patient to the intensive care unit (ICU)
or initiating discussions regarding DNACPR, treatment escalation or
end-of-life care plans (See Ethics section). An important part of the
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deteriorating patient, in an appropriate setting. Patients should betreated in a clinical area that is equipped and staffed to meet thepatient’s needs.

Prevention of out-of-hospital cardiac arrest (OHCA)
In industrialised countries, sudden cardiac death (SCD) is the third
leading cause of death. Survival following out-of-hospital cardiac
arrest (OHCA) is only 10% or less,32 34 which makes prevention of
OHCA important.35 Apparently healthy young adults who sustain SCD
can also have signs and symptoms (e.g. syncope/pre-syncope, chest
pain and palpitations) that should alert healthcare professionals toseek expert help to prevent cardiac arrest.36 45
There is no systematic review on this topic. A search on 26
February 2020 using the terms “out-of-hospital cardiac arrest” AND“prevention” limited to clinical trials and reviews since 1 January 2015
identified 65 articles. The references of these articles were also
reviewed. Existing guidelines of the European Society of Cardiology(ESC), the American Heart Association (AHA) and European
Resuscitation Council (ERC) were considered.

Epidemiology and pathophysiology of sudden cardiac death
Coronary heart disease (CHD) accounts for 80% of SCD, especially inolder patients, and non-ischaemic cardiomyopathies account foranother 10 15%.46 In the young, inherited diseases, congenital heartdisease, myocarditis and substance abuse are predominant causes.
Knowledge of the causes of SCD will assist in early treatment and theprevention of OHCA (Table 1).

Coronary heart disease (CHD)
Arrhythmias triggered by acute myocardial infarction (AMI) or
subsequent myocardial scarring can result in SCD.48 About twothirds of SCDs occur as the first CHD event or in individuals
considered to be at low risk.46 During the last 50 years primaryprevention and secondary revascularisation have reduced CHD ageadjusted mortality.46 The percentage of SCDs associated with CHD
remains unchanged suggesting that there are interactions between
CHD and triggering events such as autonomic nervous systemdysfunction, electrolyte disturbances, drug toxicity and individual
genetic profiles.46 Cardiac electrophysiology studies can identify
patients with CHD at high versus low risk of SCD.49 Additional factors
such as heart failure (HF) and left ventricular hypertrophy (LVH)
predispose to ventricular arrhythmias (polymorphic ventriculartachycardia [VT] and VF]). How to identify patients at high risk of
SCD with HF and LVH is uncertain.50 Changes in left ventriculargeometry affect the likelihood of developing VT and VF. High bloodlevels of B-type natriuretic peptide (BNP) and its N-terminal fragment(NT-proBNP) are associated with higher rates of appropriate
implantable cardioverter defibrillator (ICD) placement and mortality.51,52 The only indicator that has been identified to be consistently
associated with an increased risk of SCD in the setting of CHD and left
ventricular (LV) dysfunction is LV ejection fraction (LVEF).48 LVEF is
used to indicate the need for an implantable cardioverter defibrillator(ICD) for the primary and secondary prevention of SCD.53 Despite
considerable progress, the ability to recognise the risk of SCD before
the event remains very limited.48

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Table 1 – Causes of sudden cardiac arrest (SCD).
Adapted from Kandala46 and Winkel.47.
Coronary heart disease
ST-segment elevation
Other myocardial infarction
Unstable angina
Silent ischaemia
Electrical heart disease, often associated with SCD in the young
Long QT-syndrome (LQTS)
Short QT syndrome
Brugada syndrome
Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
Triadin knock-out syndrome (TKOS)
Arrhythmogenic bi-leaflet mitral valve prolapse (ABiMVPS))
Drug or medication induced
Non-atherosclerotic coronary artery anomalies
Congenital heart disease
Hypertrophic cardiomyopathy (HCM)
Dilated cardiomyopathy (DCM)
Valvular heart diseaseadolescent SCD, 50% of patients had misinterpreted symptoms
before death.44 CHD is the most frequent cause of explained SCDY;
25 31% of the cases remain unexplained after post mortem
examination (Sudden Arrhythmic Death Syndrome- SADS).47 The
majority of inherited cardiac diseases can be treated if diagnosed, yetmost young SCD victims are not diagnosed.42 Premonitory signs of
SCDY were present in only 29% in one study, and thus lower than inolder patients.55 QT-prolonging and psychotropic drugs, alone or in
combination, increase the risk of SCD.56 Post mortem examination is
crucial to identify inherited cardiac disease in unexplained cases of
SCD; this should result in a cardiac investigation of first-degree
relatives. This screening resulted in a diagnosis of an inherited cardiac
disease in over half of the families.57 In a large retrospective SCDY
study, a cause was identified in 113/180 patients (62.8%), the rest
were classified as idiopathic VF.58 With improvements in diagnosis(e.g. provocation drug testing for cardiac channelopathies andcoronary vasospasm, genetical testing), the number of unexplained
SCDs should decrease.58 (See the Epidemiology section).35

Non-atherosclerotic coronary artery anomalies
Coronary artery embolism, coronary arteritis (e.g. Kawasaki disease,polyarteritis nodosa), spasm and myocardial bridging have all been
described with SCD.

Congenital heart disease
Congenital coronary anomalies are present in 1% of all patients. SCD
because of congenital coronary anomalies is exercise-related andaccounts for 17% of SCD in young athletes.46,55

Hypertrophic cardiomyopathy (HCM)
Hypertrophic cardiomyopathy is the most common genetic disorder ofthe heart, with 1 in 200 500 cases, and it is the most frequent cause of
SCDY.59 It often remains clinically silent until SCD presents as the firstcardiac event. The incidence of SCD in families with HCM may be 24% a year and 4-6% in children and adolescents.46

Premonitory signs
SCD in the young
SCD in the young (SCDY, 5 35 years of age) accounts for 7% of all
SCDs;47 the incidence is 1 8/100 000 fatalities per year.54 In

Approximately 50% of cardiac arrests occur in individuals with
undiagnosed CHD. 48,60 Many SCD victims have a history of cardiac
disease and warning signs before cardiac arrest, most commonly

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chest or upper abdominal pain or dyspnoea that has not been acted onby the patient or health care professionals.61,62 Approximately one
third of elderly patients will have symptoms in the days or hours before
cardiac arrest; primarily chest pain, dyspnoea, syncope and/or cold
sweats.62,63 In 1960 OHCA patients, 9.4% had been assessed by an
ambulance crew within the preceding 48 h.64 Emergency care inpatients with symptoms is associated with improved survival.61 Early
recognition of acute coronary syndrome (ACS) by emergency medical
system (EMS) teams with 12-lead ECG capabilities and reduction oftime to reperfusion may prevent SCD.65 The most effective approachto prevent SCD in the general population remains the quantification of
the individual risk of developing CHD followed by control of risk
factors.65 Syncope can be an important premonitory sign of SCD.

Syncope
Syncope occurring during strenuous exercise, while sitting or in thesupine position should always raise the suspicion of a cardiac cause;in other situations it is more likely to be vasovagal syncope or postural
hypotension.65 In patients with known cardiac disease, syncope (withor without prodrome particularly recent or recurrent) is an independent151

risk factor for increased risk of death.53,59,66 76 High-risk (suggestinga serious condition) and low-risk features (suggesting a benign
condition) of patients with syncope at initial evaluation in theemergency department have been published by the ESC (Table 2).53
Early EMS acquisition of a 12 lead-ECG may be helpful.
Screening programs for athletes may be helpful but vary between
countries.88,89 In one study from the United Kingdom between 1996
and 2016 11,168 athletes received cardiovascular screening anddiseases associated with SCD were identified in 0.38% (n = 42).90

Preventive measures against SCD
Prevention of SCD is focused on the associated medical conditions
that may contribute to or exacerbate arrhythmia, the risk posed byarrhythmia and the risk-benefit of a given therapy. Interventions
include anti-arrhythmic drugs, implantable cardioverter defibrillators(ICD), and ablation or surgery.53,91 Noninvasive telemetry or
implantable devices transmitting the ECG are currently used inselected group of patients to detect high risk arrhythmias and prevent
SCD. More recently, connected devices with arrhythmia detection
capabilities (smartwatch, smartphone applications) have been

Table 2 – High risk features suggesting a serious condition in patients with syncope at initial evaluation in theemergency department. Adapted from Brignole 2018.53 ECG electrocardiogram; ICD implantable cardioverter defibrillator; LVEF left
ventricular ejection fraction; SCD sudden cardiac death; VT ventricular tachycardia.
Syncopal event features
Major
New onset of chest discomfort, breathlessness, abdominal pain or headache77 79
Syncope during exertion or when supine80
Sudden onset palpitation immediately followed by syncope80
Minor
No warning symptoms or short (<10 s) prodrome 80 83
Family history of SCD at young age84
Syncope in the sitting position85
Past medical history
Major
Severe structural or coronary artery disease (heart failure, low LVEF or previous myocardial infarction)77,79
Physical examination
Major
Unexplained systolic blood pressure <90 mmHg77,79
Persistent bradycardia (<40 min 1) in awake state in absence of physical training
Undiagnosed systolic murmur
ECG
Major
ECG changes consistent with acute ischaemia
Mobitz II second- and third-degree atrioventricular (AV) block
Slow atrial fibrillation (AF) (<40 min 1)
Persistent sinus bradycardia (<40 min 1) or repetitive sinoatrial block or sinus pauses >3 s in awake state in absence of physical training
Bundle branch block, intraventricular conduction disturbance, ventricular hypertrophy or Q waves consistent with ischaemic heart disease or cardiomyopathy78,83
Sustained and non-sustained VT
Dysfunction of an implantable cardiac device (pacemaker or ICD)
Type 1 Brugada pattern
ST-segment elevation with type 1 morphology in leads V1-V3 (Brugada pattern)
QTc >460 ms in repeated 12-lead ECGs indicating long QT syndrome (LQTS)86
Minor (high-risk only if history consistent with arrhythmic syncope)
Mobitz I second-degree AV block and 1st degree AV block with markedly prolonged PR interval
Asymptomatic inappropriate mild sinus bradycardia (40 50 bpm.)83
Paroxysmal supraventricular (SVT) or atrial fibrillation87
Pre-excited QRS complex
Short QTc interval (< = 340 ms)86
Atypical Brugada patterns86
Negative T waves in right precordial leads, epsilon waves suggestive of arrhythmogenic right ventricular cardiomyopathy (ARVC)86

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introduced and may be helpful in detecting asymptomatic AF, however
their potential role in the general population to detect SCD arrhythmias
is unknown.92,93 Public education to report on symptoms before SCD
and to help a persons in cardiac arrest are important.61

Treatment of in-hospital cardiac arrest (IHCA)
Cardiac arrest treatment principles, such as rapid defibrillation anddelivery of high-quality CPR, are consistent across both the IHCA and
OHCA settings. In the hospital setting, the immediate availability of
trained clinical staff and equipment provides an opportunity for the
rapid identification of cardiac arrest and initiation of treatment. An
IHCA can be defined as any cardiac arrest that occurs on the hospital
premises. This can include a cardiac arrest in patients, hospital visitors
or staff, in a variety of hospital settings. For IHCA, BLS and ALS
interventions can often start and take place at the same time (seeFig. 2). These guidelines are based on the ILCOR CoSTR,1 the 2015
ERC ALS Guidelines21 and ERC Quality Standards for CPR Practiceand Training.94
ILCOR undertook a systematic review of accredited training in
adult ALS. The review included eight observational studies andidentified benefits of ALS for ROSC and survival to hospital discharge
or 30-days.16 ILCOR also undertook a systematic review on team andleadership training including sixteen RCTs and three observational
studies identifying a benefit for patient survival as well as skill
performance.16

First responders
The clinical skill of a first responder may range from a non-clinicalmember of staff trained in BLS to an ALS provider. Irrespective of skill
level, the initial action of the first responder is to recognise cardiac
arrest, immediately start CPR, call for help and facilitate rapid
defibrillation. Delays in starting treatment reduce the likelihood of a
successful outcome.95,96
The process for calling for help may differ between hospitals or
locations within a hospital. If the responder is alone, they may need toleave the patient to call for help. Where a telephone system is used toactivate the emergency team, the standard European number (2222)
should be used.97
Following the completion of initial actions and provided sufficient
staff are available, staff should collect ALS equipment and prepare tohandover to the resuscitation team using either the SBAR (Situation,
Background, Assessment, Recommendation) or RSVP (Reason,
Story, Vital Signs, Plan) systems.24,98,99 Each clinical area in a
hospital should consider patient acuity, risk of cardiac arrest, andgeographical location (i.e. distance for the resuscitation team to travel)
in determining the specific training needs of staff.

Resuscitation teamThe resuscitation team may take the form of a traditional cardiac arrest
team that responds only to cardiac arrest events or a MET/RRT(medical emergency team/ rapid response team) that responds toboth cardiac arrests and critically unwell patients. The ILCOR
recommends accredited ALS level training for healthcare staff (weakrecommendation based on very low certainty evidence) as ALS
training is associated with increased ROSC and patient survival.16
ILCOR also recommends team and leadership training (weakrecommendation based on very low certainty evidence) because it
is associated with improved patient and process-outcomes.16
Resuscitation teams often form on an ad hoc basis depending on

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hospital work rosters and include individuals from a range of
specialities (e.g. acute medicine, cardiology, critical care). Lack ofknowledge of team member roles, including who is acting as teamleader can lead to errors during CPR for IHCA.100,101 A team meetingat the beginning of each shift for introductions and allocation of roles
may support effective team-working during resuscitation.

Equipment
Hospitals should ensure that clinical areas should have immediate
access to resuscitation equipment and drugs to facilitate rapid
resuscitation of the patient in cardiac arrest. Missing or malfunctioning
equipment contributes to treatment delays.100,102 Equipment should
be standardised throughout the hospital and equipment checked
regularly.

Treatment of out-of-hospital cardiac arrest
This section provides an overview of specific ALS issues related to
CPR for OHCA. Further information is available in the sections Basiclife support (BLS), Cardiac Arrest in Special Circumstances, Systemsof Care, Epidemiology, Post-resuscitation care, and Ethics. The aim of
ALS for OHCA is to provide the same interventions as available inhospital as early as possible, and to rapidly transfer the patient tohospital for those interventions that are not feasible out-of-hospital.
Three ILCOR systematic reviews were identified.103,103a108 A
focused search on 13 March limited to clinical trials and reviews since
1 January 2015 identified 612 articles. The titles and abstracts werescreened and pertaining articles included.

Initial ALS treatment of OHCA
Several patient and CPR factors affect outcome from OHCA (Table 3).
Community programs of lay bystander CPR and AED use improveoutcome from OHCA.104 Chest compressions and early defibrillation
are the cornerstones of CPR in OHCA. The only definitive treatment
for VF remains prompt defibrillation.105

EMS personnel and interventions
ILCOR performed a systematic review of EMS exposure to andexperience of OHCA on outcome.103 The largest study in this review
linked exposure of paramedics to OHCA, defined as the number oftimes a paramedic had attended an OHCA, to patient survival tohospital discharge.106 Increasing exposure in the preceding three
years was associated with increased survival to discharge:  6
exposure (control group), >6-11 exposures (adjusted odds ratio(aOR) 1.26, 95% CI 1.04 1.54), 11 17 exposures (aOR 1.29, 95%CI
1.04 1.59), >17 exposures (aOR 1.50, 95%CI 1.22 1.86).106
Another large observational study reported that increased exposureof the treating paramedic was associated with increased ROSC(<15 exposures, control group vs.  15 exposures (aOR 1.22, 95%CI
1.11 1.36).107 The ILCOR CoSTR concluded that EMS should
monitor exposure of their clinical personnel to resuscitation andimplement strategies to address low exposure or ensure that treatingteams have members with recent exposure (weak recommendation,very-low certainty of evidence).

Termination of CPR rules
Termination of resuscitation (TOR) rules are used by many EMS. An
ILCOR systematic review on the use of TOR rules found that
implementing the currently studied TOR rules would result in somemissed survivors.103a ILCOR recommended the use of TOR rules to124

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151

Fig. 2 – In-hospital resuscitation algorithm. AED automated external defibrillator; ALS advanced life support; CPR cardiopulmonary
resuscitation; SBAR situation, background, assessment, recommendation.

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Table 3 – Patient and CPR factors affecting outcome
from OHCA. Adapted from Kandala 2017.46 AED automatedexternal defibrillation; CPR cardiopulmonary resuscitation.
Patient
Age
Sex
Comorbidities
Cardiac function
Pulmonary function
Renal function
TraumaSpecial circumstances
Cardiopulmonary resuscitation
Location (private vs. public)
Witnessed vs. unwitnessed cardiac arrest
Bystander CPR
Type of bystander CPR (compression only vs. standard)First cardiac arrest rhythm
Use of AED by bystander
Time to return of spontaneous circulation

assist clinicians in deciding whether to discontinue resuscitation
efforts at the scene or to transport the patient to the hospital withongoing CPR (weak recommendation, very-low certainty evidence).
Decisions to terminate resuscitation should also take into account the
local legal, organizational, and cultural context. EMS personnel
working in systems where TOR by non-physicians is not legal orculturally acceptable should transport patients with ongoing CPR tohospital. The Ethics section provides more specific guidance on theuse of termination of resuscitation rules.

Care at cardiac arrest centres
An ILCOR systematic review assessed the benefits of care at a
dedicated cardiac arrest centre (CAC).16,108 The resulting ILCOR
treatment recommendations included:
 We suggest adult non-traumatic OHCA cardiac arrest patients becared for in cardiac arrest centres rather than in non-cardiac arrest
centres (weak recommendation, very low certainty of evidence).
 We cannot make a recommendation for or against regional triage
of OHCA patients to a cardiac arrest centre by primary EMS
transport (bypass protocols) or secondary interfacility transfer.
For further information about cardiac arrest centres see sections
on Systems Saving Lives and Post Resuscitation Care.

ALS treatment algorithm
Cardiac arrest is associated with either shockable rhythms (ventricularfibrillation/pulseless ventricular tachycardia (VF/pVT)) or non-shockable rhythms (asystole and pulseless electrical activity (PEA)). The
main difference in the treatment of shockable rhythms is the need forattempted defibrillation. Other interventions, including high-quality
chest compressions with minimal interruption, airway management
and ventilation, venous access, administration of adrenaline and theidentification and treatment of reversible causes, are common for allarrests. The ALS algorithm (Fig. 3) provides an overview of these key
interventions. These are based on the expert consensus of the writing
group. The ALS cardiac arrest algorithm is applicable to all cardiac
arrests. Additional interventions may be indicated for cardiac arrest
caused by special circumstances.

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Manual defibrillation
Defibrillation is a vital component of CPR as it has the potential toterminate VF/pVT and achieve ROSC. Defibrillation is indicated inapproximately 20% of cardiac arrests. As its effectiveness decreases
with time and VF duration, defibrillation attempts must be timely, whilst
remaining efficient and safe. Knowledge of how to use a defibrillator(manual or AED) is key for rescuers performing advanced life support.
Rescuers who use a manual defibrillator should aim to take less than 5 s
to recognise a shockable cardiac arrest rhythm and make the decision
to give a shock in order to minimise interruption to chest compressions.
Since 2015, ERC defibrillation guidelines have referred solely tobiphasic energy waveforms and in these 2020 guidelines we refer only
to the use of defibrillation pads (rather than paddles).21
The evidence for this section is based on ILCOR 2020 CoSTRs,
the ERC 2015 ALS Guidelines, and expert consensus.1,21,104

Strategies for minimising the peri-shock pause
The delay between stopping chest compressions and shock delivery (thepre-shock pause) must be kept to an absolute minimum; even a 5 10 sdelay will reduce the chances of the shock being successful.109 114 The
pre-shock pause can be reduced to less than 5 s by continuing
compressions during charging of the defibrillator and by having anefficient team coordinated by a leader who communicates effectively.115,116 The safety check to avoid rescuer contact with the patient at the
moment of defibrillation should be undertaken rapidly but efficiently. The
delay between shock delivery and recommencing chest compressions(the post-shock pause) is minimised by immediately resuming chest
compressions after shock delivery.1 If there are clinical and physiologicalsigns of ROSC (e.g. arterial waveform, increase in ETCO2), chest
compressions can be paused briefly for rhythm analysis. The entire
process of manual defibrillation should be achievable with less than a 5 s
interruption to chest compressions.

CPR versus defibrillation as the initial treatment
A 2020 ILCOR systematic review addressed whether a specified period(typically 1.5 3 min) of chest compressions before shock delivery
compared with a short period of chest compressions before shock
delivery affected resuscitation outcomes. Outcomes were no different
when CPR was provided for up to 180 s before attempted defibrillation,compared with rhythm analysis and attempted defibrillation first.104
Therefore, the routine delivery of a pre-specified period of CPR (e.g. 2
3 min) before rhythm analysis and a shock is delivered is notrecommended. Rescuers should provide a short period of CPR until thedefibrillator is ready for rhythm analysis in unmonitored cardiac arrest(weak recommendation, low-certainty evidence). Defibrillation should
then be delivered as indicated, without delay. Immediate defibrillation of
VF of any amplitude should be attempted at the end of each 2 min cycle.
The 2015 ERC ALS Guideline stated that if there is doubt about
whether the rhythm is asystole or extremely fine VF, do not attempt
defibrillation; instead, continue chest compressions and ventilation.21
We wish to clarify that when the rhythm is clearly judged to be VF ashock should be given.

Anticipatory defibrillator charging
Using this method, the defibrillator is charged as the end of acompression cycle is approached, but before the rhythm is checked.
When compressions are paused briefly to check rhythm, a shock can
be delivered immediately (if indicated) from a defibrillator that isalready charged, avoiding a period of further chest compressions

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151

Fig. 3 – Advanced Life Support algorithm. ABCDE airway, breathing, circulation, disability, exposure CPR cardiopulmonary resuscitation;
ECG electrocardiogram; EMS emergency medical system; PEA pulseless electrical activity; PaCO2 arterial partial pressure of carbon dioxide;
ROSC return of spontaneous circulation; SpO2 arterial oxygen saturation; VF ventricular fibrillation; VT ventricular tachycardia.

while the defibrillator is charged. This method was reviewed by ILCOR
in 2020 as the technique is already in use as an alternative to theconventional sequence.117 Manikin studies show anticipatory charging is feasible, can reduce the overall interruption to chest
compression, but increases pre- post, and peri-shock pause duration.
This technique may be a reasonable alternative for use by well-drilled
teams that can minimise pre- post, and peri-shock pause duration.
Clinical studies are required to determine the best technique formanual defibrillation.

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 thepatient.118 123 Although defibrillation pads may be safer than paddles
with regards to arcing and spark generation, recommendations for thesafe use of oxygen during defibrillation remain unchanged in theseguidelines. 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 atleast 1 m away from the patient’s chest.
 Leave the ventilation bag or ventilation circuit connected to thetracheal tube or supraglottic airway, any oxygen exhaust is
directed away from the chest.

 If the patient is connected to a ventilator, for example in theoperating room or critical care unit, leave the ventilator tubing(breathing circuit) connected to the tracheal tube.

Pad contact with the chest and anatomical position
There is no new evidence since the 2015 guidelines regarding optimal
defibrillation pad position.21 The techniques described below aim toplace external defibrillation pads (self-adhesive pads) in an optimal
position to maximise transmyocardial current density and minimisetransthoracic impedance. No human studies have evaluated the padposition as a determinant of ROSC or survival from VF/pVT.104
Transmyocardial current during defibrillation is likely to be maximal
when pads 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 pad position may not be the same forventricular and atrial arrhythmias.

Pad placement for ventricular arrhythmias and cardiac arrest
Place pads in the conventional antero-lateral (sternal-apical) position.
The right (sternal) pad is placed to the right of the sternum, below theclavicle. The apical pad is placed in the left mid-axillary line,
approximately level with the V6 ECG electrode. This position should
be clear of any breast tissue.124 It is important that this pad is placed

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sufficiently laterally (Fig. 4) and in practical terms, the pad should beplaced just below the armpit.125 Other acceptable pad positions
include: Placement of each pad on the lateral chest walls, one on the rightand the other on the left side (bi-axillary).
 One pad in the standard apical position and the other on the rightupper back.
 One pad anteriorly, over the left precordium, and the other pad
posteriorly to the heart just inferior to the left scapula.
Either pad can be placed in either position (apex or sternal). An
observational study in patients undergoing elective cardioversion withexternal defibrillator paddles showed that transthoracic impedance
was lower when the paddle was orientated in a cranio-caudal
direction.126 Consider shaving the chest if it is very hairy and theelectrodes will not stick firmly. Do not delay shock delivery, andconsider alternative pad positions if necessary.

Pad placement for atrial arrhythmias
Atrial fibrillation is usually maintained by functional re-entry circuits inthe left atrium. As the left atrium is located posteriorly in the thorax, padpositions that result in a more posterior current pathway may
theoretically be more effective for atrial arrhythmias. Although somestudies have shown that antero-posterior pad placement is more
effective than the traditional antero-apical position in elective
cardioversion of atrial fibrillation,127,128 the majority have failed toshow any clear advantage of any specific pad position.129 132 Efficacy
of cardioversion may be less dependent on pad position when using
biphasic impedance-compensated waveforms.131 133 The following
pad positions are safe and effective for cardioversion of atrial
arrhythmias:

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127

 Traditional sternal-apical position.
 Antero-posterior position (one pad anteriorly, over the left
precordium, and the other pad posteriorly to the heart just inferior
to the left scapula).

Pad placement to avoid implantable medical devices
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 pads placed directly over the device.134,135 Place the padaway from the device (at least 8 cm) or use an alternative pad position(anterior-lateral, anterior-posterior).134,136

Hands-on defibrillation
By allowing continuous chest compressions during the delivery of thedefibrillation shock, hands-on defibrillation can minimise peri-shockpause and allow continuation of chest compressions during
defibrillation. The benefits of this approach are unproven and further
studies are required to assess the safety and efficacy of this technique.
A post-hoc analysis of a multi-centre trial did not observe any benefit
when shocks were delivered without pausing manual or mechanicalchest compressions.137 Only Class 1 electrical safety gloves, but notstandard clinical examination gloves (or bare hands) provide a safe
level of electrical insulation for hands-on defibrillation.138 There havebeen no new studies since the 2015 guidelines and the recommendation therefore remain unchanged.21

Respiratory phase
Positive end expiratory pressure (PEEP) increases transthoracic
impedance and should be minimised where possible during

Fig. 4 – Correct pad placement for defibrillation (© Charles Deakin).

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defibrillation. Auto-PEEP (gas trapping) may be particularly high inpatients with asthma and may necessitate higher than usual energy
values for defibrillation.139

151

since the 2010 guidelines review 140,141 have shown promise andsome improvements in this technology, there remains insufficientevidence to support routine use of VF waveform analysis to guide theoptimal timing for a shock attempt.1,104

One shock versus three stacked shock sequence
In 2010, it was recommended that when defibrillation was required, asingle shock should be provided with immediate resumption of chest
compressions after the shock.140,141 This recommendation was madefor two reasons. Firstly, to minimise peri-shock interruptions to chest
compressions and secondly, given the greater efficacy of biphasic
shocks, if a biphasic shock failed to defibrillate, a further period of chest
compressions could be beneficial. Studies have not shown that any
specific shock strategy is of benefit for any survival end-point.142,143
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 byminimising interruptions to chest compressions, we continue in 2020 torecommend single shocks for most situations (see below).
When defibrillation is warranted, give a single shock and resume
chest compressions immediately following the shock.104 Do not delay
CPR for rhythm reanalysis or a pulse check immediately after a shock.
Continue CPR for 2 min until rhythm reanalysis is undertaken andanother shock given (if indicated). Even if the defibrillation attempt is
successful, it takes time until the post shock circulation is establishedand it is very rare for a pulse to be palpable immediately after
defibrillation.144,145 Patients can remain pulseless for over 2 min andthe duration of asystole before ROSC can be longer than 2 min in as
many as 25% of successful shocks.146 In patients where defibrillationachieves a perfusing rhythm, the effect of chest compressions on reinducing VF is not clear.147
If a patient has a monitored and witnessed cardiac arrest (e.g. in
the catheter laboratory, coronary care unit, or other monitored criticalcare setting in or out-of-hospital) 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 toa manual defibrillator. Although there are no data supporting a threeshock 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/pVT (expert opinion).

Fibrillation waveform analysis
It is possible to predict, with varying reliability, the success ofdefibrillation from the fibrillation waveform.148 170 If optimal defibrillation waveforms and the optimal timing of shock delivery can be
determined in prospective studies, it should be possible to prevent thedelivery of unsuccessful high energy shocks and minimise myocardial
injury. This technology is under active development and investigation,
but current sensitivity and specificity are insufficient to enable
introduction of VF waveform analysis into clinical practice. Although
one large RCT,171 and 20 observational studies172 191 published

Waveforms
Biphasic waveforms are now well established as a safe and effective
waveform for defibrillation. Biphasic defibrillators compensate for thewide 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, inwhich the current rapidly oscillates between baseline and a positive
value before inverting in a negative pattern.21

Energy levels
Defibrillation requires the delivery of sufficient electrical energy todefibrillate 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 defibrillationis that which achieves defibrillation whilst causing the minimum of
myocardial damage.192 Selection of an appropriate energy level also
reduces the number of repetitive shocks, which in turn limits
myocardial damage.193
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 transmyocardialcurrent flow that achieves defibrillation; the electrical current
correlates well with successful defibrillation and cardioversion.194
Defibrillation shock energy levels are unchanged from the 2015
guidelines.21

First shock
Relatively few studies have been published with which to refine thecurrent defibrillation energy levels set in the 2010 guidelines.195
There is no evidence that one biphasic waveform or device is more
effective than another. First shock efficacy of the BTE waveformusing 150 200 J has been reported as 86-98%.196 200 First shock
efficacy of the RLB waveform using 120 J has been reported as
85%.201 Four studies have suggested equivalence with lower andhigher starting energy biphasic defibrillation.202 205 although one
has suggested that initial low energy (150 J) defibrillation isassociated with better survival.206 Although human studies havenot shown harm (raised biomarkers, ECG changes, ejection
fraction) from any biphasic waveform up to 360 J,202,207 several
animal studies have suggested the potential for harm with higher
energy levels.208 211
The initial biphasic shock should be no lower than 120 J for RLB
waveforms and at least 150 J for BTE waveforms. For pulsed biphasic
waveforms, begin at 120 150 J. Ideally, the initial biphasic shock
energy should be at least 150 J for all biphasic waveforms in order tosimplify energy levels across all defibrillators, particularly because thetype of waveform delivered by a defibrillator is not marked.
Manufacturers should display the effective waveform dose range
on the face of the biphasic defibrillator. If the rescuer is unaware of therecommended energy settings of the defibrillator, for an adult use thehighest energy setting for all shocks (expert opinion).

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Second and subsequent shocks
The 2010 guidelines recommended either a fixed or escalating energy
strategy for defibrillation. Several studies show that although anescalating strategy reduces the number of shocks required to restore
an organised rhythm compared with fixed-dose biphasic defibrillation,and may be needed for successful defibrillation,212,213 rates of ROSC
or survival to hospital discharge are not significantly different between
strategies.202 204 Conversely, a biphasic protocol using a fixedenergy level showed high cardioversion rates (>90%) but significantly
lower ROSC rate for recurrent VF could not be excluded.214 Several
in-hospital studies using an escalating shock energy strategy haveshown improvement in cardioversion rates (compared with fixed dose
protocols) in non-arrest rhythms.215 220
In 2020, there remains no evidence to support either a fixed or
escalating energy protocol. Both strategies are acceptable; however,if the first shock is not successful and the defibrillator is capable ofdelivering shocks of higher energy it is reasonable to increase theenergy for subsequent shocks.

Recurrent ventricular fibrillation (refibrillation)
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 sameproviders (usually out-of-hospital).’ Refibrillation is common andoccurs in >50% of patients following initial first-shock termination of
VF.212 Two studies showed termination rates of subsequent
refibrillation were unchanged when using fixed 120 J or 150 J shock
protocols respectively,214,221 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.212 In a
retrospective analysis, conversion of VF to an organised rhythm washigher if the VF had first appeared after a perfusing rhythm, than after
PEA or asystole.222
In view of the larger study suggesting benefit from higher
subsequent energy levels for refibrillation,212 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.

Refractory ventricular fibrillation
Refractory VF is defined as fibrillation that persists after three or more
shocks and occurs in approximately 20% of patients who present in
VF.212 Duration of VF correlates negatively with good outcome.
Actively search for and correct any reversible causes (Fig. 3 ALS
algorithm). Ensure that the defibrillation energy output is on the
maximum setting an escalating protocol may be more effective intreating refractory VF. Check that the defibrillation pads are placedcorrectly (particularly the apical pad, when using the antero-lateral pad
position). Consider using an alternative defibrillation pad orientation(e.g. antero-posterior).

Dual/double sequential defibrillation
Patients in refractory VF have significantly lower rates of survival
than patients who respond to standard resuscitation treatments.
Double sequential defibrillation is the use of two defibrillators todeliver two overlapping shocks or two rapid sequential shocks, onewith standard pad placement and the other with either anteriorposterior or additional antero-lateral pad placement. The technique has been suggested as a possible means of increasing VF
termination rates. With numerous case reports and some

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observational studies,223 230 ILCOR reviewed the efficacy ofthis technique and based on very low certainty evidence made aweak recommendation against the routine use of a double
sequential defibrillation strategy in comparison with standard
defibrillation strategy for cardiac arrest with a refractory shockablerhythm.1,231

Analysis of rhythm during chest compression
New software technology in some defibrillators enables removal of
ECG motion artefact generated during chest compressions in orderto show the real-time underlying waveform during CPR. An ILCOR
systematic review found no studies in humans evaluating thistechnology leading to a weak recommendation based on very low
certainty evidence to suggest against the routine use of artifactfiltering algorithms for analysis of electrocardiographic rhythm
during CPR.104 In making its recommendation, ILCOR placed apriority on avoiding the costs of a new technology where
effectiveness remains to be determined. The ILCOR task force
acknowledged that some EMS already use artifact-filtering algorithms for rhythm analysis during CPR, and strongly encouraged
EMS to report their experience to build the evidence base regardingthese technologies in clinical practice.

Implantable cardioverter defibrillators
Implantable cardioverter defibrillators (ICDs) are becoming increasingly common as they are implanted more frequently in an aging
population. They are implanted because a patient is at risk from, or has
had, a life-threatening shockable arrhythmia. They are usuallyembedded under the pectoral muscle below the left clavicle (in asimilar 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 leadrunning parallel to the left of the sternum.232 In a recent randomised
controlled trial the subcutaneous ICD was non-inferior to thetransvenous ICD with respect to device-related complications andinappropriate shocks.233
On sensing a shockable rhythm, an ICD will discharge approximately 40 J (approximately 80 J for subcutaneous devices) through aninternal 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, thepatient 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.136
Discharge of an ICD may cause pectoral muscle contraction in thepatient, and shocks to the rescuer have been documented.234 In viewof the low energy values discharged by conventional ICDs, it is unlikelythat any harm will come to the rescuer, but minimising contact with thepatient whilst the device is discharging is prudent. Surface current
from subcutaneous ICDs is significant and may cause a perceptible
shock to the rescuer.235,236 Cardioverter and pacing function should
always be re-evaluated following external defibrillation, both to checkthe device itself and to check pacing/defibrillation thresholds of thedevice leads.
Pacemaker spikes generated by devices programmed to unipolarpacing may confuse AED software and emergency personnel, andmay prevent the detection of VF.237 The diagnostic algorithms ofmodern AEDs can be insensitive to such spikes.

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Airway and ventilation
In 2015 the ERC recommended a stepwise approach to airway
management during CPR.21 Three large RCTs of airway management for OHCA have been published since 2015.238 240 Check thelatest ERC guidelines for COVID-19 precautions required during
airway management.
An ILCOR systematic review addressed whether a specificadvanced airway management strategy improved outcome fromcardiac arrest (CA) in comparison with an alternative airway
management strategy.241,242 Seventy-eight observational studies
were included; nine of these addressed the question of timing ofadvanced airway management. Eleven controlled trials were
included but only three of these were RCTs.238 240 The first ofthese RCTs compared early tracheal intubation (TI) with bag-mask
ventilation (TI delayed until after ROSC) in a physician-staffed EMS
system.239 The result of this non-inferiority trial that recruited over2000 patients was inconclusive (4.3% versus 4.2% for 28-day
survival with favourable functional outcome (CPC 1 2), no
significant difference). Notably, the TI success rate was 98% and
146 patients in the bag-mask ventilation group underwent ‘rescue
intubation’ (i.e. crossed over); 100 of these were because of
regurgitation. In a comparison of initial laryngeal tube (LT) insertion
with TI in 3000 OHCAs by paramedics in the United States, 72-h
survival (primary outcome) was higher in the LT group (18.2%
versus 15.3%; p = 0.04).240 However, the overall TI success rate
was just 51% making it possible that the lower survival rate in the TI
group was a reflection of the poor TI success rate. The third of these
RCTs was a comparison of the initial insertion of an i-gel supraglottic
airway (SGA) with TI in OHCA treated by paramedics in the United
Kingdom (UK).238 Among the more than 9000 patients enrolled,there was no difference in the primary outcome of favourable
functional survival (mRS  3; 6.4% versus 6.8%; P = 0.33).
A large observational cohort study of IHCA from the American
Heart Association (AHA) Get with the Guidelines-Resuscitation(GWTG-R) registry matched patients intubated at any given minutewithin the first 15 min after cardiac arrest onset, with patients still
receiving CPR at risk of being intubated within the same minute.243
The matching was based on a time-dependent propensity score andmatched 43,314 intubated patients with patients with same propensity
for intubation but who were not intubated in the same minute.
Compared with not intubating, TI was associated with a lower rate of
ROSC (risk ratio [RR] = 0.97; 95% CI 0.96 0.99; p < 0.001), lower
survival to hospital discharge (RR = 0.84; 95% CI 0.81 0.87;
p < 0.001), and worse neurological outcome (RR = 0.78; 95% CI
0.75 0.81; p < 0.001).
After reviewing the evidence for airway management during
cardiac arrest, the ILCOR ALS Task Force made the following
treatment recommendations:244
 We suggest using bag-mask ventilation or an advanced airway
strategy during CPR for adult cardiac arrest in any setting (weakrecommendation, low to moderate certainty of evidence).
 If an advanced airway is used, we suggest a SGA for adults with
OHCA in settings with a low TI success rate (weak recommendation, low certainty of evidence).
 If an advanced airway is used, we suggest an SGA or TI for adults
with OHCA in settings with a high TI success rate (weakrecommendation, very low certainty of evidence).
 If an advanced airway is used, we suggest an SGA or TI for adults
with IHCA (weak recommendation, very low certainty of evidence).

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Patients often have more than one type of airway intervention,
typically starting with basic and advancing to more complex
techniques that are inevitably applied later during cardiac arrest
the stepwise approach.238,245 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. If basic airway techniques enable effective ventilation, there
may be no need to progress to advanced techniques until after ROSC.
One potential advantage of inserting an advanced airway is that it
enables chest compressions to be delivered continuously withoutpausing during ventilation. Most patients with ROSC remain comatose
and will need tracheal intubation (TI) and mechanical ventilation (SeePost-resuscitation Care).246

Airway obstruction
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 othervital organs. Without adequate oxygenation it may be impossible toachieve ROSC. These principles may not apply to the witnessedprimary cardiac arrest in the vicinity of a defibrillator; in this case, thepriority is immediate defibrillation.

Basic airway management and adjuncts
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. Despite a total lack of published dataon the use of nasopharyngeal and oropharyngeal airways during
CPR, they are often helpful, and sometimes essential, to maintain an
open airway, particularly when CPR is prolonged.

Oxygen during CPR
During cardiac arrest the blood flow and oxygen reaching the brain is
low even with effective CPR. Based on the physiological rationale andexpert opinion, ILCOR recommends giving the highest feasible
inspired oxygen concentration during cardiac arrest to maximise
oxygen delivery to the brain thereby minimising hypoxic-ischaemic
injury.1 Immediately after ROSC, as soon as arterial blood oxygen
saturation can be monitored reliably (by pulse oximetry or arterial
blood gas analysis), titrate the inspired oxygen concentration tomaintain the arterial blood oxygen saturation between 94 98% orarterial partial pressure of oxygen (PaO2) of 10 13 kPa or
75 100 mmHg. (See Post Resuscitation Care).246

Choking
The initial management of foreign body airway obstruction (choking) isaddressed in the BLS section.247,248 In an unconscious patient withsuspected 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.104

Ventilation
Advanced life support providers should give artificial ventilation assoon as possible for any patient in whom spontaneous ventilation isinadequate or absent. This is usually achieved with a self-inflating bag
attached to a facemask or an advanced airway. Deliver each breathover approximately 1 s, giving a volume that corresponds to normal
chest movement (expert opinion). The chest should visibly rise; this

RESUSCITATION 161 (2021) 115

represents a compromise between giving an adequate volume,
minimizing the risk of gastric inflation, and allowing adequate time forchest compressions. Although the delivery of continuous chest
compressions during face-mask ventilation was previously thought toincrease the risk of regurgitation, a trial of continuous versus
interrupted chest compressions during CPR (CCC Trial) that enrolled
more than 23,000 patients showed no statistically significant
difference in survival to discharge.249 ILCOR has subsequently
recommended that when using bag mask, EMS providers perform
CPR either using a 30:2 compression-ventilation ratio (pausing chest
compressions for ventilation) or continuous chest compressions
without pausing while delivering positive pressure ventilation (strong
recommendation, high-quality evidence).250 In Europe, the mostcommon approach during CPR with an unprotected airway is to givetwo ventilations after each sequence of 30 chest compressions.
Once a tracheal tube (TT) or an SGA has been inserted, ventilate
the lungs at a rate of 10 min 1 and continue chest compressions
without pausing during ventilations (expert opinion).251 The laryngeal
seal achieved with an SGA may not be good enough to prevent at least
some gas leaking when inspiration coincides with chest compressions. Moderate gas leakage is acceptable (unless there is asignificant risk of infection, e.g. see ERC COVID-19 Guidelines),
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 toenable 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.252 Oxygen can be delivered
passively, either via an adapted TT (Boussignac tube),253,254 or withthe combination of an oropharyngeal airway and standard oxygenmask with non-rebreather reservoir.255 In theory, an 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) comparedwith bag-mask ventilation after VF OHCA, but this was a retrospective
analysis and is subject to numerous confounders.255 The CCC Trial
included a subgroup of patients who were treated with passive
oxygenation but until further data are available, passive oxygen
delivery without ventilation is not recommended for routine use during
CPR.249

Choice of airway devices
Disadvantages of TI over bag-mask ventilation include: The risk of an unrecognised misplaced TT; in patients with OHCA
the reliably documented incidence ranges from 0.5% to 17%:
0.5%;256 paramedics - 2.4%,257
emergency physicians
258,259
260
261
6%,
9%,
17%.
 A prolonged period without chest compressions while TI is
attempted. In a study of prehospital TI by paramedics during 100
CA the total duration of the interruptions in CPR associated with TI
attempts was 110 s (IQR 54 - 198 s; range 13 446 s) and in 25%
the interruptions were more than 3 min.262 Tracheal intubation
attempts accounted for almost 25% of all CPR interruptions.
 A comparatively high failure rate. Intubation success rates
correlate with the TI experience attained by individual paramedics.263 The high failure rate of 51% documented in the PART
trial240 is similar to those documented in some prehospitalsystems more than 20 years ago.264,265

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 Tracheal intubation is a difficult skill to acquire and maintain. In one
study, anaesthesia residents required about 125 intubations in theoperating room setting before they were able to achieve a TI
success rate of 95% under such optimal conditions.266
Healthcare personnel who undertake prehospital TI should do soonly within a structured, monitored program, which should include
comprehensive competency-based training and regular opportunities
to refresh skills (expert opinion).
The ILCOR recommendation is that only systems that achieve hightracheal intubation success rates should use this technique.242 ILCOR
did not recommend a particular success rate but suggested it should
be similar to that achieved in the RCT comparing early tracheal
intubation with bag-mask ventilation (TI delayed until after ROSC) in aphysician-staffed EMS system.239 The TI success rate in this study
was 98%. The expert consensus of this writing group is that a highsuccess rate is greater than 95% with up to 2 intubation attempts.
Rescuers must weigh the risks and benefits of intubation against theneed to provide effective chest compressions. To avoid any interruptions
in chest compressions, unless alternative airway management techniques are ineffective, it is reasonable to defer TI until after ROSC. In
settings with personnel skilled in advanced airway management
laryngoscopy should be undertaken without stopping chest compressions; a brief pause in chest compressions will be required only as thetube is passed through the vocal cords. The TI attempt should interrupt
chest compressions for less than 5 s (expert opinion); if intubation is notachievable within these constraints, recommence bag-mask ventilation.
After TI, tube placement must be confirmed immediately (see below) andthe tube must be secured adequately.

Videolaryngoscopy
Videolaryngoscopy is being used increasingly in anaesthetic andcritical care practice.267,268 Preliminary studies indicate that compared with direct laryngoscopy, videolaryngoscopy during CPR
improves laryngeal view and TI success rates,269,270 reduces therisk of oesophageal intubation271 and reduces interruptions to chest
compressions.272 One systematic review concluded that in theprehospital setting, videolaryngoscopy decreased the first-attempt TI
success rate (RR, 0.57; P < 0.01; high-quality evidence) and overall
success rate (RR, 0.58; 95% CI, 0.48 0.69; moderate-quality
evidence) by experienced operators.273 Several different videolaryngoscopy systems are available and they do not all perform in thesame way. The expert consensus of the writing group is that the
rescuer’s choice of direct laryngoscopy or videolaryngoscopy should
be guided by local protocols and rescuer experience.

Confirmation of correct placement of the tracheal tube
Unrecognised oesophageal intubation is the most serious complication of attempted tracheal intubation. The evidence supporting theguideline is summarised in longstanding ILCOR recommendations.1,274,275 Routine use of clinical assessment and immediate
capnography reduces this risk significantly.275,276 Initial assessment
includes observation of bilateral chest expansion, bilateral lungauscultation in the axillae (breath sounds should be equal andadequate) and over the epigastrium (breath sounds should beabsent). Clinical signs of correct TT placement (condensation in thetube, chest rise, breath sounds on auscultation of lungs, and inability tohear gas entering the stomach) are not reliable. The reported
sensitivity (proportion of TI correctly identified) and specificity(proportion of oesophageal intubations correctly identified) of132

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clinical assessment varies: sensitivity 74
100%; specificity
66 100%.256,277 279
The ILCOR ALS Task Force recommends using waveform
capnography to immediately confirm and continuously monitor the
position of a TT during CPR in addition to clinical assessment (strong
recommendation, low quality evidence).275 Waveform capnography isgiven a strong recommendation because it has other potential uses
during CPR (see below). The persistence of exhaled CO2 after six
ventilations indicates placement of the TT in the trachea or a main
bronchus.256 The ‘No Trace = Wrong Place’ campaign by the UK
Royal College of Anaesthetists emphasises that immediately after TI(even during CA) the absence of exhaled CO2 strongly suggests
oesophageal intubation.280
Waveform capnography is the most sensitive and specific way toconfirm and continuously monitor the position of a TT in victims ofcardiac arrest and must supplement clinical assessment (visualizationof TT through cords and auscultation). Existing portable monitors
make capnographic initial confirmation and continuous monitoring of
TT position feasible in all out- and in-of-hospital settings where TI is
performed.
Ultrasonography of the neck or visualisation with a fibreoptic scopeby skilled operators can also be used to identify the presence of atracheal tube in the trachea. This requires additional equipment andskills. These techniques were not formally reviewed for this guideline.

Cricoid pressure
The use of cricoid pressure in CA is not recommended (expert
consensus). Cricoid pressure can impair ventilation, laryngoscopy, TT
and SGA insertion, and may even cause complete airway obstruction.281

Securing the tracheal tube and supraglottic device
Accidental dislodgement of a TT can occur at any time but may be
more likely during CPR and during transport. An SGA is more prone tobeing dislodged than a TT.238 The most effective method for securing
the TT or a SGA has yet to be determined. Use either conventional
tapes or ties, or purpose-made holders (Expert opinion).

Cricothyroidotomy
Occasionally it will be impossible to ventilate an apnoeic patient with abag-mask, or to pass a TT or SGA. This may occur in patients withextensive facial trauma or laryngeal obstruction caused by oedema,
tumour or foreign material. In these circumstances, delivery of oxygen
through a surgical cricothyroidotomy may be lifesaving.282 A
tracheostomy is contraindicated in an emergency because it is time
consuming, hazardous and requires considerable surgical skill andequipment.
Surgical cricothyroidotomy provides a definitive airway that can beused to ventilate the patient’s lungs until semi-elective intubation ortracheostomy is performed. Needle cricothyroidotomy is a much more
temporary procedure providing only short-term oxygenation andminimal if any pulmonary CO2 removal.

Drugs and fluids
Vascular access
ILCOR suggests the intravenous route as opposed to the intraosseous route is used as the first attempt for drug administration
during adult cardiac arrest.1,283 This weak recommendation is basedon very low-certainty evidence drawn from three retrospective
observational studies which included 34,686 adult out-of-hospital

151

cardiac arrests which suggests worse outcomes when the IO route
was used.284 286 Since the ILCOR review, secondary analyses of the
PARAMEDIC2.287 and ALPS randomised trials288 suggested nosignificant effect modification by drug administration route although
the studies were underpowered to assess for differences between the
IV and IO routes.
Consistent with ILCOR, the ERC suggests attempting IV accessfirst to enable drug delivery in adults in cardiac arrest. IO access may
be considered if unable to obtain IV access in adults in cardiac arrest.

Vasopressors
ILCOR reviewed the use of vasopressors in cardiac arrest
following the publication of the PARAMEDIC2 trial.242,289 Systematic reviews and meta-analyses examined standard dose adrenaline (1 mg) versus placebo, high dose (5 10 mg) versus standard
dose (1 mg) adrenaline, adrenaline versus vasopressin andadrenaline and vasopressin versus adrenaline alone.290,291 The
reviews reported evidence that adrenaline (1 mg) improved therate of survival to hospital admission and long-term survival (to 3months) but did not improve favourable neurological outcome. By
contrast, the use of high-dose adrenaline or vasopressin (with orwithout adrenaline) did not improve long term survival or
favourable neurological outcome.
These data led to ILCOR upgrading the strength of recommendation to strong recommendation in favour of the use of adrenaline during
CPR (strong recommendation, low to moderate certainty ofevidence).242 The justification and evidence to decision framework
highlights that the Task Force placed a very high value on the apparent
life-preserving benefit of adrenaline, even if the absolute effect size islikely to be small and the effect on survival with favourable neurologicaloutcome is uncertain.
The PARAMEDIC2 trial followed the ERC ALS 2015 Guidelines,
which recommended that adrenaline was given as soon as vascularaccess is obtained for non-shockable rhythms and for shockablerhythms, refractory to 3 attempts at defibrillation.21 Meta-analysis of
the two placebo-controlled trials (PACA and PARAMEDIC2) foundthat the effects of adrenaline on ROSC relative to placebo weregreater for patients with an initially non-shockable rhythm than thosewith a shockable rhythms.292 Similar patterns were observed for
longer term survival and favourable neurological outcomes, although
the differences in effects were less pronounced.292 A secondary
analysis which examined the time to drug administration in the
PARAMEDIC2 trial found that whilst the relative treatment effects ofadrenaline did not change over time, survival rates and favourable
neurological outcomes decreased over time, suggesting earlyintervention would lead to the best outcomes.293
These findings led ILCOR to recommend that adrenaline isadministered as soon as feasible for non-shockable rhythms (PEA/
asystole) (strong recommendation, very low-certainty evidence). For
shockable rhythms (VF/pVT), ILCOR suggests administration ofadrenaline after initial defibrillation attempts are unsuccessful during
CPR (weak recommendation, very low-certainty evidence).
Consistent with the ILCOR Treatment Recommendations, the
ERC recommends adrenaline 1 mg IV (IO) is administered as soon as
possible for adult patients in cardiac arrest with a non-shockablerhythm. For patients with a shockable rhythm persisting after 3 initialshocks, give adrenaline 1 mg IV (IO). Repeat adrenaline 1 mg IV (IO)
every 3 5 min whilst ALS continues.
If 3 stacked shocks have been given for a witnessed and monitored
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considered as the first shock with regards to timing of the first dose of
adrenaline.
Consistent with the ILCOR treatment recommendation, the ERC
does not support the use of vasopressin during cardiac arrest.

Antiarrhythmic drugs
ILCOR updated the Consensus on Science and Treatment Recommendation for antiarrhythmic drugs in 2018.294 No further relevant
studies were identified upon searching the literature to 10 February
2020.
The ILCOR systematic review identified evidence from 14
randomised controlled trials and 17 observational studies which
evaluated lidocaine, amiodarone, magnesium, bretylium, nifekalantand procainamide.295 Meta-analysis of randomised trials in adults,
found that none of the anti-arrhythmic drugs improved survival or
favourable neurological outcome compared to placebo. Metaanalysis showed that lidocaine compared to placebo improved ROSC(RR = 1.16; 95% CI, 1.03 1.29, p = 0.01).
The largest and most recent randomised trial compared
amiodarone, lidocaine or placebo in patients with VF/pVT refractory
after at least one defibrillation attempt. Compared with placebo,
amiodarone and lidocaine increased survival to hospital admission.
However, there was no difference in survival to discharge orfavourable neurological survival at discharge between groups.296 In
the pre-defined sub-group of bystander witnessed cardiac arrests,
amiodarone and lidocaine increased survival to hospital discharge
compared with placebo. Survival was also higher with amiodarone
than with placebo after EMS-witnessed arrest.
These data led ILCOR to suggest that amiodarone or lidocaine
could be used in adults with shock refractory VF/pVT (weakrecommendation, low quality evidence).294 The values and preferences analysis indicates that the Task Force prioritised the predefined and reported sub-group analysis from the ALPS study, whichshowed greater survival with amiodarone and lidocaine in patientswith a witnessed cardiac arrest. ILCOR did not support the use ofmagnesium, bretylium, nifekalant or procainamide.
The ERC updated its guidelines in 2018 to 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.297 The initialrecommended dose is amiodarone 300 mg; a further dose of 150 mg
may be given after five defibrillation attempts. The recommendation infavour of amiodarone was based on 21 of 24 National Resuscitation
Councils of Europe reporting that amiodarone was the main drug usedduring CPR.297 Lidocaine 100 mg may be used as an alternative if
amiodarone is not available, or a local decision has been made to use
lidocaine instead of amiodarone. An additional bolus of lidocaine
50 mg can also be given after five defibrillation attempts.297

Thrombolytic therapy
The 2020 ILCOR Consensus on Science with Treatment Recommendations pooled evidence from a sub-group analysis of the
TROICA trial298 and 4 observational studies299 302 which examined
the use of thrombolytic drugs in cardiac arrest caused by suspected orconfirmed pulmonary embolus (PE). The studies did not find evidence
that thrombolytic drugs improved neurological outcome.298,301 By
contrast, in one study, 30-day survival was higher in the intervention
group (16% vs 6%; P = 0.005)302 but not in 3 other studies which
examined survival to discharge.299 301 ROSC also improved in one
study300 but not two others.299,301 In making a weak recommendation

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for the use of thrombolytic drugs for suspected or confirmed PE andcardiac arrest based on very low certainty evidence, the ILCOR Task
Force considered the potential benefits outweighed the potential harmfrom bleeding.1
The ERC endorses the recommendation from ILCOR, which aligns
with the ERC guidelines in 2015.21 The ERC does not support theroutine use of thrombolytic drugs in cardiac arrest, unless the cause issuspected or confirmed PE. When thrombolytic drugs have been
administered, consider continuing CPR attempts for at least 60
90 min before termination of resuscitation attempts.303 305

Fluid therapy
No randomised controlled trials have evaluated the routine administration of fluids versus no fluids as a treatment strategy for cardiac
arrest. Two large randomised trials provide indirect evidence fromtreatment strategies designed to induce hypothermia which included
administration of up to 2 L ice cold intravenous fluids during OHCA306
or immediately after ROSC.307 The studies found no improvement inshort306,307 or long-term outcomes.308 The studies reported evidenceof reduced ROSC in patients with VF,306 increased rate of re-arrest,307
and higher rates of pulmonary oedema.306,307 It is not possible todetermine from these studies whether the harmful effects were related
to fluid volume per se or the temperature of the infused fluids.309
Nevertheless, based on expert consensus, the ERC maintains its
recommendation to avoid the routine infusion of large volume fluids inthe absence of evidence of suspicion of a hypovolaemic cause of the
cardiac arrest.

Waveform capnography during advanced life support
This guideline is based on an ILCOR evidence update and scoping
review,1 a recent systematic review,276 a narrative review310 and theprevious 2015 ERC ALS Guidelines.21 End-tidal carbon dioxide is thepartial pressure of carbon dioxide (PCO2) measured at the end of
expiration. It reflects cardiac output, tissue perfusion and pulmonary
blood flow, as well as the ventilation minute volume. Carbon dioxide is
produced in perfused tissues by aerobic metabolism, transported by
the venous system to the right side of the heart and pumped to thelungs by the right ventricle, where it is removed by alveolar ventilation.
Waveform capnography enables a continuous, non-invasive
measurement of PCO2 in the exhaled air during CPR. In the typicalcapnogram, the ETCO2 recorded at the end of the plateau phase bestreflects the alveolar PCO2. End-tidal CO2 is most reliable when thepatient’s trachea is intubated, but it can also be used with a SGA or bag
mask.311
The aims of monitoring waveform capnography during CPR
include:21,310
 Confirming correct tracheal tube placement (see airway
section).
 Monitoring the quality of CPR (ventilation rate and chest
compressions). Monitoring ventilation rate helps avoiding hyperventilation during CPR. In a paediatric resuscitation model agreater depth of chest compression was associated with higher
end-tidal CO2 values.312 Whether this can be used to guide careand improve outcome requires further study.313
 Detecting ROSC during CPR. When ROSC occurs, end-tidal
CO2 may increase up to three times above the values during
CPR.314 Capnography may therefore help detect ROSC duringresuscitation and avoid unnecessary chest compression or
adrenaline in a patient with ROSC. However, no specific threshold

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for the increase in end-tidal CO2 has been identified for reliablediagnosis of ROSC. The increase in ETCO2 can start several
minutes before a palpable pulse is detected.315 317
 Prognostication during CPR. Failure to achieve an ETCO2
value >1.33 kPa (10 mmHg) during CPR is associated with apoor outcome in observational studies276,318,319 This thresholdhas also been suggested as a criterion to withhold e-CPR inrefractory cardiac arrest.320 However values of ETCO2 during
CPR depend on several factors including the timing of
measurement (initial vs. final,321,322 cause of cardiac arrest,
323,324chest compression quality,312 ventilation rate and325
presence of airway closure during CPR326 and thevolume,use of adrenaline.327,328 In general, ETCO2 tends to decreaseduring CPR in patients in whom resuscitation is unsuccessful
and tends to increase in those who go on to achieve
ROSC.318,329 For this reason, ETCO2 trends might be more
appropriate than point values for predicting ROSC during
CPR.276 However, evidence on this is still limited.329 Studies
assessing the prognostic value of ETCO2 have not been blinded,
which may have caused a self-fulfilling prophecy. For thisreason, although an ETCO2 > 1.33 kPa (10 mmHg) measured
after tracheal intubation or after 20 min of CPR may be a
predictor of ROSC or survival to discharge, using ETCO2
threshold values alone as a mortality predictor or for thedecision to stop a resuscitation attempt is not recommended.1 In
selected patients, continue CPR to facilitate the implementationof other technologies such as E-CPR, that buy time fortreatments that address a reversible cause of the cardiac arrest(e.g. re-warming following accidental hypothermia, intra-arrest
primary percutaneous coronary intervention for acute myocardial ischaemia).

Use of ultrasound imaging during advanced life support
Point-of-care ultrasound (POCUS) imaging is already commonly usedin emergency care settings. Its use during CPR is also increasing.
Previous and current guidance emphasises the need for skilled
POCUS operators.21
An ILCOR systematic review assessed the role of POCUS during
cardiac arrest as a prognostic tool.330 The review identified several
limitations such as inconsistent definitions and terminology aroundsonographic evidence of cardiac motion, low inter-rater reliability offindings, low sensitivity and specificity for outcomes, confounding fromself-fulfilling prophecy when terminating resuscitation in unblindedsettings as well as unspecified timing of POCUS.330 The review
concluded that no sonographic finding had sufficiently or consistently
high sensitivity to support its use as a sole criterion to terminate CPR.
The authors of the ILCOR systematic review advised that clinicians
should be cautious about introducing additional interruptions in chest
compressions with a transthoracic approach to POCUS during cardiac
arrest.1,331,332
POCUS can be used to diagnose treatable causes of cardiac
arrest such as cardiac tamponade or pneumothorax. The ERC ALS
2015 guidelines recommended a sub-xiphoid probe position placed
just before chest compressions are paused for a planned rhythm
assessment.21 [Soar 2015 100] These applications were not coveredin the ILCOR systematic review; however, the review stressed theissue of over-interpreting the finding of right ventricular dilation in
isolation as a diagnostic indicator of massive pulmonary embolism.
Right ventricular dilation begins a few minutes after onset of cardiac

151

arrest as blood shifts from the systemic circulation to the right heart
along its pressure gradient.333 335 Right ventricular dilation wasconsistently observed in a porcine model of cardiac arrest caused byhypovolaemia, hyperkalaemia, and primary arrhythmia,336 and is acommon finding regardless of the cause of OHCA during transoesophageal echocardiography performed in the emergency department.337 At present, there is limited knowledge about the use POCUS
during CPR to assess deep vein thrombosis to help diagnose
pulmonary embolism, to assess for pleural effusion and FAST
(Focussed Assessment with Sonography for Trauma) assessment of
the abdomen and aorta.

Mechanical chest compression devices
Informed by evidence from 8 RCTs338 345 the ILCOR 2015 CoSTR
and ERC Guidelines did not recommend the routine use of automatedmechanical chest compression devices but did suggest that they are areasonable alternative when sustained high-quality manual chest
compressions are impractical or compromise provider safety.21,275
This evidence update focused on randomised controlled trials andsystematic reviews.
Two new randomised trials were identified.346,347 One study
examined the use of the Autopulse applied in the emergency
department following OHCA (n = 133). The trial found the rate ofsurvival to hospital discharge was higher in the Autopulse group(18.8% versus 6.3%, p = 0.03) but no difference in favourable
neurological outcome (16.2% versus 13.4%). A randomized noninferiority safety study, involving 374 patients, reported that LUCAS
device did not cause significantly more serious or life-threatening
visceral damage than manual chest compressions. For the Autopulse
device, significantly more serious or life-threatening visceral damage
than manual compressions cannot be excluded.346
Six systematic reviews and meta-analyses were published since
the ILCOR review, including a Cochrane review.348 353 Significant
methodological errors in one systematic review and meta-analysis led
to its exclusion.354 Four reviews drew conclusions similar to the
ILCOR 2015 review, that mechanical CPR did not improve critical orimportant outcomes.348 351 A review focusing solely on mechanical
CPR in the in-hospital setting, reported very low-certainty evidence
that mechanical chest compressions improved patient outcomes inthat setting.352 A Bayesian network meta-analysis reported thatmanual CPR was more effective than Autopulse mechanical chest
compression device and comparable to LUCAS mechanical chest
compression device.353
The writing group considered that the new data did not materiallyalter the previous ERC guidelines on the use of mechanical chest
compression devices in cardiac arrest.21

Circumstances to consider mechanical chest compression
devices
A review identified several specific circumstances where it is difficult todeliver high-quality manual CPR where mechanical CPR can beconsidered as an alternative.355 Examples include transporting tohospital in an ambulance or helicopter, during percutaneous coronary
intervention, diagnostic imaging such as a CT scan, as a bridge toestablishing extra-corporeal CPR or maintaining circulation prior toorgan retrieval when resuscitation is unsuccessful. The expert
consensus is that mechanical devices should be considered whenhigh-quality manual compressions are not practical or pose a risk to
rescuer safety.

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Device deployment

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135

The role of eCPR for specific causes of cardiac arrest is addressed.
Cardiac Arrest in Special Circumstances. Establishing an eCPR
programme requires a whole system approach (in- and out-of
hospital) and considerable resources to implement effectively, andnot all healthcare systems will have sufficient resources.371 373

American College of Cardiology (ACC) and the Heart Rhythm Society(HRS).86,91,374 377 Table 4 summarises the supporting evidence forvagal manoeuvres and some of the more commonly used drugs for thetreatment of arrhythmias.
Pharmacological cardioversion restores sinus rhythm in approximately 50% of patients with recent-onset AF. Among the several
drugs for pharmacological conversion suggested by the ESC,378
beta-blockers and diltiazem/verapamil are preferred over digoxin
because of their rapid onset of action and effectiveness at highsympathetic tone. For patients with LVEF < 40%, consider thesmallest dose of beta-blocker to achieve a heart rate less than 110
min 1 and add digoxin if necessary. Amiodarone is the drug most
likely to be familiar to non-specialists and can be considered for
acute heart rate control in atrial fibrillation (AF) patients withhaemodynamic instability and severely reduced left ventricularejection fraction (LVEF).
The ESC has published recent guidelines for the acute management of regular tachycardias in the absence of an establisheddiagnosis.91 The guidelines for treating regular narrow QRS (120 ms) and wide QRS (> 120 ms) tachycardias have been
incorporated into the tachycardia algorithm. The ESC Guidelines
provide more detailed recommendations and evidence for treating
rhythms once a specific diagnosis of the rhythm has been made.
In a randomised trial involving haemodynamically stable patientswith wide QRS-complex tachycardia of unknown aetiology, procainamide was associated with fewer major adverse cardiac events anda higher proportion of tachycardia termination within 40 min comparedwith amiodarone.379 However, in many countries procainamide iseither unavailable and/or unlicensed.
Evidence for the treatment of patients with bradycardia wasincluded in ACC/AHA/HRS guidelines published in 2019 (Fig. 6
Bradycardia algorithm).377 If bradycardia is accompanied by adverse
signs, atropine remains the first choice drug.21 When atropine isineffective, second line drugs include isoprenaline (5 mg min starting
dose) and adrenaline (2 10 mg min). For bradycardia caused byinferior myocardial infarction, heart transplant or spinal cord injury,
consider giving aminophylline (100 200 mg slow intravenous injection). Atropine can cause a high-degree atrioventricular (AV) block oreven sinus arrest in heart transplant patients.380 Consider giving
intravenous glucagon if beta-blockers or calcium channel blockers area potential cause of the bradycardia. Consider pacing in patients who
are unstable, with symptomatic bradycardia refractory to drug therapy(see below).

Peri-arrest arrhythmias

Cardioversion

Prompt identification and treatment of life-threatening arrhythmias
may prevent cardiac arrest or its recurrence. This section offers
guidance and treatment algorithms for the non-specialist ALS
provider. The scope is to focus on peri-arrest arrhythmias that cause
life-threatening instability. If patients are stable there is time to seek
advice from a specialist or more experienced physician. Other
international organisations have produced comprehensive evidencebased arrhythmia guidelines.86,91,374 377 Electrical cardioversion isrequired in the peri-arrest patient with a clinical unstable arrhythmia
while pacing is used in refractory bradycardia. The key interventions
are summarised in Fig. 5 and 6.
These guidelines follow recommendations published by international cardiology societies including the European Society ofCardiology (ESC), the American Heart Association (AHA), theElectrical cardioversion is the preferred treatment for tachycardia inthe unstable patient displaying potentially life-threatening adverse
signs (Fig. 5. Tachycardia algorithm).381 383 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.384 Synchronisation
can be difficult in VT because of the wide-complex and variable formsof ventricular arrhythmia. Inspect the synchronisation marker carefully
for consistent recognition of the R wave. If needed, choose anotherlead and/or adjust the amplitude. If synchronisation fails, giveunsynchronised shocks to the unstable patient in VT to avoid
prolonged delay in restoring sinus rhythm. Ventricular fibrillation or
pulseless VT require unsynchronised shocks. Conscious patientsrequire anaesthesia or sedation, before attempting synchronised
cardioversion.

Observational studies show that interruptions in chest compressions,particularly immediately before or around the time of attempted
defibrillation are harmful.111,356 Some studies report long pauses inchest compressions associated with mechanical chest compression
device deployment.357 359 Training those responsible for mechanicaldevice deployment can reduce interruptions to less than 15 s.358,360
The expert consensus is that mechanical devices should be used only
in settings where teams are trained in their deployment.

Extracorporeal CPR
Extracorporeal CPR (eCPR) is defined by the ELSO (Extracorporeal
Life Support Organization) as the application of rapid-deploymentveno-arterial extracorporeal membrane oxygenation (VA-ECMO) to
provide circulatory support in patients in whom conventional CPR is
unsuccessful in achieving sustained ROSC.361 The use of eCPR has
increased for both IHCA and OHCA in recent years.362 365
The 2019 ILCOR CoSTR informed by a systematic review madethe following recommendation:242,244,366
 We suggest that eCPR may be considered as a rescue therapy forselected patients with cardiac arrest when conventional CPR isfailing in settings in which it can be implemented (weakrecommendation, very low certainty of evidence).
There is one recent small randomised controlled trial of eCPR for
OHCA refractory VF cardiac arrest,367 and several others in progress.
There are no universally agreed indications for eCPR regarding which
patients and the optimum time-point during conventional ALS. There
are guidelines on when to start eCPR.320,363,368 370 Inclusion criteria
have not been used consistently or prospectively tested in trials.365
Commonly used criteria include: Witnessed cardiac arrest with bystander CPR.
 Time to establishing eCPR is less than 60 min from starting CPR.
 Younger patients (e.g. less than 65 70 years) and no major
comorbidities precluding a return to independent life.
 Known or suspected treatable underlying cause of cardiac arrest.

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151

Fig. 5 – Tachycardia algorithm. ABCDE airway, breathing, circulation, disability, exposure BP blood pressure; DC direct current; ECG
electrocardiogram; IV intravenous; SpO2 arterial oxygen saturation; VT ventricular tachycardia.

Cardioversion for atrial fibrillation

Cardioversion for pulsatile ventricular tachycardia

Some studies,127,128 but not all,130,133 have suggested that anteroposterior pad position is more effective than antero-lateral pad
position, but both are acceptable positions.131 More data are needed
before specific recommendations can be made for optimal biphasicenergy levels and different biphasic waveforms. Biphasic rectilinear
and biphasic truncated exponential (BTE) waveform show similar highefficacy in the elective cardioversion of atrial fibrillation.385 A recent
RCT showed that maximum fixed energy electrical cardioversion(360 J BTE in this study) was more effective in achieving sinus rhythm
one minute after cardioversion than an energy-escalating strategy.386
There was no increase in adverse events. An initial synchronised
shock at maximum defibrillator output rather than an escalating
approach is a reasonable strategy based on current data. In stablepatients, follow appropriate guidelines on the need for anticoagulation
before cardioversion to minimise stroke risk.378

The energy required for cardioversion of VT depends on themorphological characteristics and rate of the arrhythmia.388 Ventricular tachycardia with a pulse responds well using energy levels of
120 150 J for the initial shock. Consider stepwise increases if the firstshock fails to achieve sinus rhythm.388

Cardioversion for atrial flutter and paroxysmal supraventricular tachycardia
Atrial flutter and paroxysmal supraventricular tachycardia (SVT)
generally require less energy than atrial fibrillation for cardioversion.387 Give an initial shock of 70 120 J. Give subsequent shocks
using stepwise increases in energy.194

PacingConsider pacing in patients who are unstable, with symptomatic
bradycardia refractory to drug therapy. Immediate pacing is indicatedespecially when the block is at or below the His-Purkinje level. If
transthoracic (transcutaneous) 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 arepresent; it does not increase short or long-term survival in- or out-ofhospital.389 397 For haemodynamically unstable, conscious patientswith bradyarrhythmia, percussion pacing as a bridge to electrical
pacing may be attempted, although its effectiveness has not been
established.104,398,399 Give serial rhythmic blows with the closed fist
over the left lower edge of the sternum to pace the heart at a

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151

137

Fig. 6 – Bradycardia algorithm. ABCDE airway, breathing, circulation, disability, exposure BP blood pressure; ECG electrocardiogram; IV
intravenous; SpO2 arterial oxygen saturation.

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151

Table 4 – Recommendations for the acute management of narrow and wide QRS tachycardia (Drugs may be
administered via peripheral IV in an emergency. HF heart failure; LV left ventricular).
Drug /procedure

Indication

Vagal Manoeuvre

Narrow QRS tachycardia
Wide QRS tachycardia

Adenosine

Narrow QRS tachycardia
Wide QRS tachycardia

Verapamil or diltiazem

Timing

Dose/delivery

Notes

Blow into a 10 mL syringe with
sufficient force to move the plunger

Preferably in the supine position with leg elevation400 403

Recommended if vagal
manoeuvres fail

Incremental, starting at 6 mg, followed by 12 mg IV.
An 18 mg dose should then beconsidered

If no evidence of pre-excitation
on resting ECG404 406
When using an 18 mg dose,take into account the tolerability/side effects in the individual
patient.

Narrow QRS tachycardia

Consider if vagal manoeuvres and adenosine fail

Verapamil (0.075 0.15 mg/kg IV[average 5 10 mg] over 2 min)Diltiazem [0.25 mg/kg IV(average
20 mg) over 2 min].

Should be avoided in patientswith haemodynamic instability,
HF with reduced LV ejection
fraction (<40%).404,406 411

Beta-blockers(IV esmolol or metoprolol)

Narrow QRS tachycardia

Consider if vagal manoeuvres and adenosine failEsmolol (0.5 mg/kg IV bolus or
0.05 0.3 mg/kg/min infusion)
Metoprolol (2.5 15 mg given IV in
2.5 mg boluses),More effective in reducing theheart rate than in terminatingtachycardia.410,412 414

Procainamide

Wide QRS tachycardia

Consider if vagal manoeuvres and adenosine fail10 15 mg/kg IV over 20 min

379,415

Amiodarone

Narrow and wide
QRS tachycardia

Consider if vagal manoeuvres and adenosine fail300 mg IV over 10 60 min according to circumstances followed by infusion of 900 mg in 24h

416,417

Magnesium

Polymorphic wide
QRS tachycardia(torsades de pointes -TdP)

2 g IV over 10 min. Can be repeatedonce if necessary.

Magnesium can suppress episodes of TdP without necessarily shortening QT, evenwhen serum magnesium concentration is normal361,418

physiological rate of 50 70 min 1. Transthoracic and percussion
pacing can cause discomfort Consider giving analgesic or sedative
drugs in conscious patients

Uncontrolled organ donation after circulatory death
Following cardiac arrest, less than a half of patients achieve
ROSC.17,34 When standard ALS fails to achieve ROSC, there arethree broad treatment strategies:419
 Stop resuscitation and declare death.
 In selected patients, continue CPR to facilitate the implementationof other technologies such as E-CPR, that buy time for treatmentsthat address a reversible cause of the cardiac arrest (e.g. rewarming following accidental hypothermia, intra-arrest primarypercutaneous coronary intervention for acute myocardialischaemia).
 Continue CPR to maintain organ perfusion and transfer to a
hospital with an uncontrolled donation after circulatory death(uDCD) pathway.
This guideline focuses on uDCD (Maastricht category I/II
donors).420 The post-resuscitation care guidelines includes guidancefor organ donation pathways following brain death or controlled
donation after circulatory death (Maastricht category III donors) inpatients who achieve ROSC or are treated with eCPR.246,420 We

acknowledge the ethical, cultural and legislative issues that lead tovariation in the use of uDCD.
Across Europe, demand for transplanted organs continues tooutstrip supply. Uncontrolled donation after circulatory death (uDCD)
provides an opportunity for cardiac arrest victims in whom ROSC
cannot be achieved, to donate their organs. In Europe, uDCD iscurrently undertaken in regions of Spain, France, The Netherlands,
Belgium, and Italy.421 430 Organs that can be recovered include
kidneys, liver, pancreas and lungs. Observational data show that longterm uDCD graft success is comparable to other organ recovery
approaches.428,430 432
There is no universal consensus on selection criteria for uDCD,
and the identification of a potential donor currently follows regional/
national protocols. These generally include: age above 18 year (foradults) and not over 55 or 65 years, a no-flow time (the interval
between cardiac arrest and CPR start) within 15 30 min, and a total
warm ischaemia time (the interval between cardiac arrest and the startof organ preservation) not longer than 150 min.433 Exclusion criteria
generally include trauma, homicide, or suicide as a cause of arrest,and comorbidities such as cancer, sepsis, and, according to local
programme and the targeted organ to transplant, kidney and liverdisease.433
Uncontrolled donation after circulatory death is a time-critical,
resource-intensive, complex and ethically challenging process.434,435
Following completion of aggressive resuscitation efforts andRESUSCITATION 161 (2021) 115

confirmation of death, a ‘no-touch’ period is observed to rule-out thepossibility of auto-resuscitation.436 Organ preservation procedures
are then immediately started and continued whilst family consent fororgan recovery is sought, and organs are assessed for suitability for
donation. 437 439 For abdominal organs, organ preservation typicallyuses an extracorporeal circulation with membrane oxygenation via afemoro-femoral bypass.434 Catheters with balloons are used to limit
circulation to the abdominal cavity.440 Following consent andcompletion of practical arrangements, the patient is transferred tothe operating theatre for organ recovery.
Consent to organ donation is obtained as soon as possible during
the process from a surrogate decision maker (e.g., a family member)or by retrieving previous consent registered on a donor card or in a
public registry, if available. The urgency and nature of the processcreates several ethical challenges that are unique to uDCD,
highlighting the importance of clear local protocols, and legislativeand societal acceptance of the process.434 These issues are
discussed in the ethics section of the guidelines.441

151

139

BB declared speakers honorarium from Baxalta, ZOLL, FomF,
Bard, Stemple, Novartis Pharma, Philips Market DACH, Bioscience
Valuation BSV.
TP declares Speakers honorarium from BARD.

Acknowledgements
The authors acknowledge the following individuals who contributed to
the 2015 version of this guideline:, Markus B. Skrifvars, Gary B. Smith,Kjetil Sunde, Rudolph W. Koster, Koenraad G. Monsieurs, Nikolaos I.
Nikolaou. GDP is supported by the National Institute for HealthResearch (NIHR) Applied Research Collaboration (ARC) West
Midlands. The views expressed are those of the author(s) and notnecessarily those of the NIHR or the Department of Health and Social
Care.

REFERENCES

Debriefing
ILCOR undertook a systematic review of debriefing following cardiac
arrest in 2020.16 The review included four observational studies andidentified that debriefing was associated with improvements in
hospital survival, ROSC and CPR quality.442 445 These studies all
described use of a cold debrief that incorporated data on CPR quality
downloaded from defibrillators.446 Based on these data, ILCOR
continues to make a weak recommendation based on very low
certainty evidence supporting the use of data-driven performancefocused debriefing. The justification and evidence to decisionframework noted the substantial heterogeneity in debriefing intervention between studies. ILCOR also noted that the intervention is highly
likely to be acceptable to stakeholders and cost of implementation
may be modest. A potential harm of debriefing is the psychologicaleffect on rescuers of discussing challenging clinical events. The
ILCOR summary recorded no evidence of harm from included studies
but highlighted the need to consider this effect when implementing
debriefing interventions.

Conflict of interest
JS declares his role of Co-editor Resuscitation; he declares
institutional research funding for the NAP7 project from the Royal
College of Anaesthetists.
GDP reports funding from Elsevier for his role as an editor of thejournal Resuscitation. He reports research funding from the National
Institute for Health Research in relation to the PARAMEDIC2 trial andthe RESPECT project.
JN reports funding from Elsevier for his role as Editor in Chief of thejournals Resuscitation and Resuscitation Plus. He reports researchfunding from the National Institute for Health Research in relation to
the PARAMEDIC2 trial and the AIRWAYS2 trial.
CD declares research grants from RCUK and funding from the
National Institute for Health Research in relation to the PARAMEDIC2
trial and the AIRWAYS2 trial.
TO declares research grants from Swedish Heart and Lung
Foundation, Laerdal Foundation and Lof -Swedish patient insurance
and Swedish state under the agreement between the Swedish
government and the county councils, the ALF-agreement.

1. Soar J, Berg KM, Andersen LW, et al. Adult Advanced Life
Support: 2020 International Consensus on Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care Science
with Treatment Recommendations. Resuscitation 2020;156:
A80 A119.
2. Nolan JP, Monsieurs KG, Bossaert L, et al. European Resuscitation
Council COVID-19 guidelines executive summary. Resuscitation
2020;153:45 55.
3. Perkins GD, Morley PT, Nolan JP, et al. International Liaison
Committee on Resuscitation: COVID-19 consensus on science,treatment recommendations and task force insights. Resuscitation
2020;151:145 7.
4. Couper K, Taylor-Phillips S, Grove A, et al. COVID-19 in cardiac
arrest and infection risk to rescuers: A systematic review.
Resuscitation 2020;151:59 66.
4a. Perkins GD, Graesner JT, Semeraro F, et al. European
resuscitation council guidelines 2021 executive summary.
Resuscitation 2021;161.
5. Andersen LW, Holmberg MJ, Berg KM, Donnino MW, Granfeldt A.
In-Hospital Cardiac Arrest: A Review. JAMA 2019;321:
1200 10.
6. Hessulf F, Karlsson T, Lundgren P, et al. Factors of importance to30-day survival after in-hospital cardiac arrest in Sweden - A
population-based register study of more than 18,000 cases.
International Journal of Cardiology 2018;255:237 42.
7. Aune S, Herlitz J, Bang A. Characteristics of patients who die in
hospital with no attempt at resuscitation. Resuscitation 2005;65:
291 9.
8. Skrifvars MB, Hilden HM, Finne P, Rosenberg PH, Castren M.
Prevalence of’ do not attempt resuscitation’ orders and living wills
among patients suffering cardiac arrest in four secondary hospitals.
Resuscitation 2003;58:65 71.
9. Fritz ZB, Heywood RM, Moffat SC, Bradshaw LE, Fuld JP.
Characteristics and outcome of patients with DNACPR orders in anacute hospital; an observational study. Resuscitation 2014;85:
104 8.
10. Perkins GD, Griffiths F, Slowther AM, et al. Do-not-attemptcardiopulmonary-resuscitation decisions: an evidence synthesis.
Southampton (UK). 2016.
11. Moskowitz A, Berg KM, Cocchi MN, et al. Cardiac arrest in theintensive care unit: An assessment of preventability. Resuscitation
2019;145:15 20.
12. Roberts D, Djarv T. Preceding national early warnings scoresamong in-hospital cardiac arrests and their impact on survival. Am J
Emerg Med 2017;35:1601 6.

140

RESUSCITATION 161 (2021) 115

13. Smith GB. In-hospital cardiac arrest: is it time for an in-hospital’chain of prevention’? Resuscitation 2010;81:1209 11.
14. Physicians RCo. National Early Warning Score (NEWS) 2:
Standardising the assessment of acute-illness severity in the NHS.
Updated report of a working party. London: RCP; 2017.
15. National Institute for Health and Clinical Excellence. NICE clinicalguideline 50 Acutely ill patients in hospital: recognition of andresponse to acute illness in adults in hospital. London: National
Institute for Health and Clinical Excellence. 2007.
16. Greif R. Education, Implementation, and Teams 2020 International
Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science With Treatment Recommendations.
Resuscitation 2020.
17. Nolan JP, Soar J, Smith GB, et al. Incidence and outcome of inhospital cardiac arrest in the United Kingdom National Cardiac
Arrest Audit. Resuscitation 2014;85:987 92.
18. Smith GB, Redfern O, Maruotti A, Recio-Saucedo A, Griffiths P. The
Missed Care Study G. The association between nurse staffing
levels and a failure to respond to patients with deranged physiology:
A retrospective observational study in the UK. Resuscitation
2020;149:202 8.
19. Griffiths P, Recio-Saucedo A, Dall’Ora C, et al. The association
between nurse staffing and omissions in nursing care: A systematic
review. J Adv Nurs 2018;74:1474 87.
20. Thoren A, Rawshani A, Herlitz J, et al. ECG-monitoring of in-hospital
cardiac arrest and factors associated with survival. Resuscitation
2020;150:130 8.
21. Soar J, Nolan JP, Bottiger BW, et al. European Resuscitation
Council Guidelines for Resuscitation 2015: Section 3. Adult
advanced life support. Resuscitation 2015;95:100 47.
22. Douw G, Schoonhoven L, Holwerda T, et al. Nurses’ worry orconcern and early recognition of deteriorating patients on generalwards in acute care hospitals: a systematic review. Crit Care
2015;19:230.
23. Douw G, Huisman-de Waal G, van Zanten ARH, van der Hoeven
JG, Schoonhoven L. Capturing early signs of deterioration: thedutch-early-nurse-worry-indicator-score and its value in the Rapid
Response System. Journal of clinical nursing 2017;26:2605 13.
24. Marshall S, Harrison J, Flanagan B. The teaching of a structured tool
improves the clarity and content of interprofessional clinicalcommunication. Qual Saf Health Care 2009;18:137 40.
25. Buljac-Samardzic M, Doekhie KD, van Wijngaarden JDH.
Interventions to improve team effectiveness within health care: asystematic review of the past decade. Hum Resour Health2020;18:2.
26. Muller M, Jurgens J, Redaelli M, Klingberg K, Hautz We, Stock S.
Impact of the communication and patient hand-off tool SBAR on
patient safety: a systematic review. BMJ Open 2018;8:e022202.
27. Brady PW, Zix J, Brilli R, et al. Developing and evaluating the
success of a family activated medical emergency team: a quality
improvement report. BMJ Qual Saf 2015;24:203 11.
28. Albutt AK, O’Hara JK, Conner MT, Fletcher SJ, Lawton RJ. Is there arole for patients and their relatives in escalating clinical deterioration
in hospital? A systematic review. Health Expect 2017;20:818 25.
29. McKinney A, Fitzsimons D, Blackwood B, McGaughey J. Patientand family-initiated escalation of care: a qualitative systematic
review protocol. Syst Rev 2019;8:91.
30. Subbe CP, Bannard-Smith J, Bunch J, et al. Quality metrics for theevaluation of Rapid Response Systems: Proceedings from the thirdinternational consensus conference on Rapid Response Systems.
Resuscitation 2019;141:1 12.
31. Winters Bd, Weaver Sj, Pfoh Er, Yang T, Pham Jc, Dy Sm. Rapidresponse systems as a patient safety strategy: a systematic review.
Ann Intern Med 2013;158:417 25.
32. Virani SS, Alonso A, Benjamin EJ, et al. Heart Disease and Stroke
Statistics-2020 Update: A Report From the American Heart
Association. Circulation 2020;141:e139 596.
33. Kiguchi T, Okubo M, Nishiyama C, et al. Out-of-hospital cardiac
arrest across the World: First report from the International Liaison

151

Committee on Resuscitation (ILCOR). Resuscitation 2020;152:
39 49.
34. Grasner JT, Wnent J, Herlitz J, et al. Survival after out-of-hospital
cardiac arrest in Europe - Results of the EuReCa TWO study.
Resuscitation 2020;148:218 26.
35. Grasner JT. Epidemiology of cardiac arrest in Europe.
Resuscitation 2021.
36. Basso C, Carturan E, Pilichou K, Rizzo S, Corrado D, Thiene G.
Sudden cardiac death with normal heart: molecular autopsy.
Cardiovasc Pathol 2010;19:321 5.
37. Goldberger JJ, Basu A, Boineau R, et al. Risk stratification for
sudden cardiac death: a plan for the future. Circulation
2014;129:516 26.
38. Harmon KG, Drezner JA, Wilson MG, Sharma S. Incidence ofsudden cardiac death in athletes: a state-of-the-art review. Heart
2014;100:1227 34.
39. Kramer MR, Drori Y, Lev B. Sudden death in young soldiers. Highincidence of syncope prior to death. Chest 1988;93:345 7.
40. Mazzanti A, O’Rourke S, Ng K, et al. The usual suspects in sudden
cardiac death of the young: a focus on inherited arrhythmogenic
diseases. Expert Rev Cardiovasc Ther 2014;12:499 519.
41. Quigley F, Greene M, O’Connor D, Kelly F. A survey of the causes ofsudden cardiac death in the under 35-year-age group. Ir Med J
2005;98:232 5.
42. Winkel BG, Risgaard B, Sadjadieh G, Bundgaard H, Haunso S,
Tfelt-Hansen J. Sudden cardiac death in children (1-18 years):
symptoms and causes of death in a nationwide setting. Eur Heart J
2014;35:868 75.
43. Wisten A, Forsberg H, Krantz P, Messner T. Sudden cardiac deathin 15-35-year olds in Sweden during 1992-99. J Intern Med
2002;252:529 36.
44. Wisten A, Messner T. Symptoms preceding sudden cardiac death in
the young are common but often misinterpreted. Scandinavian
Cardiovascular Journal 2005;39:143 9.
45. Wisten A, Messner T. Young Swedish patients with sudden cardiac
death have a lifestyle very similar to a control population.
Scandinavian Cardiovascular Journal 2005;39:137 42.
46. Kandala J, Oommen C, Kern KB. Sudden cardiac death. Br Med Bull
2017;122:5 15.
47. Winkel BG, Jabbari R, Tfelt-Hansen J. How to prevent SCD in theyoung? International Journal of Cardiology 2017;237:6 9.
48. Wellens HJ, Schwartz PJ, Lindemans FW, et al. Risk stratification
for sudden cardiac death: current status and challenges for the
future. Eur Heart J 2014;35:1642 51.
49. Buxton AE, Lee KL, DiCarlo L, et al. Electrophysiologic testing to
identify patients with coronary artery disease who are at risk forsudden death. Multicenter Unsustained Tachycardia Trial
Investigators. N Engl J Med 2000;342:1937 45.
50. Buxton AE. Sudden death in ischemic heart disease - 2017.
International Journal of Cardiology 2017;237:64 6.
51. Levine YC, Rosenberg MA, Mittleman M, et al. B-type natriuretic
peptide is a major predictor of ventricular tachyarrhythmias. Heart
Rhythm 2014;11:1109 16.
52. Levine YC, Matos J, Rosenberg MA, Manning WJ, Josephson ME,
Buxton AE. Left ventricular sphericity independently predicts
appropriate implantable cardioverter-defibrillator therapy. Heart
Rhythm 2016;13:490 7.
53. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the
diagnosis and management of syncope. Eur Heart J 2018;39:1883
948.
54. Stecker EC, Reinier K, Marijon E, et al. Public health burden of
sudden cardiac death in the United States. Circ Arrhythm
Electrophysiol 2014;7:212 7.
55. Jayaraman R, Reinier K, Nair S, et al. Risk Factors of Sudden
Cardiac Death in the Young: Multiple-Year Community-WideAssessment. Circulation 2018;137:1561 70.
56. Bjune T, Risgaard B, Kruckow L, et al. Post-mortem toxicology inyoung sudden cardiac death victims: a nationwide cohort study.
Europace 2018;20:614 21.

RESUSCITATION 161 (2021) 115

57. Behr ER, Dalageorgou C, Christiansen M, et al. Sudden arrhythmic
death syndrome: familial evaluation identifies inheritable heartdisease in the majority of families. Eur Heart J 2008;29:1670 80.
58. Giudicessi JR, Ackerman MJ. Role of genetic heart disease insentinel sudden cardiac arrest survivors across the age spectrum.
International Journal of Cardiology 2018;270:214 20.
59. Maron BJ. Clinical Course and Management of Hypertrophic
Cardiomyopathy. N Engl J Med 2018;379:655 68.
60. Stecker EC, Vickers C, Waltz J, et al. Population-based analysis ofsudden cardiac death with and without left ventricular systolic
dysfunction: two-year findings from the Oregon Sudden
Unexpected Death Study. J Am Coll Cardiol 2006;47:1161 6.
61. Marijon E, Uy-Evanado A, Dumas F, et al. Warning Symptoms Are
Associated With Survival From Sudden Cardiac Arrest. Ann Intern
Med 2016;164:23 9.
62. Muller D, Agrawal R, Arntz HR. How sudden is sudden cardiac
death? Circulation 2006;114:1146 50.
63. Nishiyama C, Iwami T, Kawamura T, et al. Prodromal symptoms ofout-of-hospital cardiac arrests: a report from a large-scale
population-based cohort study. Resuscitation 2013;84:558 63.
64. Deakin CD, Quartermain A, Ellery J. Do patients suffering an out-ofhospital cardiac arrest present to the ambulance service withsymptoms in the preceding 48 h? Eur Heart J Qual Care Clin
Outcomes 2020;6:308 14.
65. Priori SG, Blomstrom-Lundqvist C. 2015 European Society ofCardiology Guidelines for the management of patients withventricular arrhythmias and the prevention of sudden cardiac deathsummarized by co-chairs. Eur Heart J 2015;36:2757 9.
66. Authors/Task Force m, Elliott PM, Anastasakis A, et al. 2014 ESC
Guidelines on diagnosis and management of hypertrophic
cardiomyopathy: the Task Force for the Diagnosis andManagement of Hypertrophic Cardiomyopathy of the European
Society of Cardiology (ESC). Eur Heart J 2014;35:2733 79.
67. Brugada J, Brugada R, Brugada P. Determinants of sudden cardiac
death in individuals with the electrocardiographic pattern of Brugada
syndrome and no previous cardiac arrest. Circulation
2003;108:3092 6.
68. Jons C, Moss AJ, Goldenberg I, et al. Risk of fatal arrhythmic eventsin long QT syndrome patients after syncope. J Am Coll Cardiol
2010;55:783 8.
69. Krahn AD, Healey JS, Simpson CS, et al. Sentinel symptoms inpatients with unexplained cardiac arrest: from the cardiac arrest
survivors with preserved ejection fraction registry (CASPER). J
Cardiovasc Electrophysiol 2012;23:60 6.
70. Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis ofarrhythmogenic right ventricular cardiomyopathy/dysplasia:
proposed modification of the Task Force Criteria. Eur Heart J
2010;31:806 14.
71. Marjamaa A, Hiippala A, Arrhenius B, et al. Intravenous epinephrine
infusion test in diagnosis of catecholaminergic polymorphic ventriculartachycardia. J Cardiovasc Electrophysiol 2012;23:194 9.
72. Nava A, Bauce B, Basso C, et al. Clinical profile and long-term
follow-up of 37 families with arrhythmogenic right ventricularcardiomyopathy. J Am Coll Cardiol 2000;36:2226 33.
73. Priori SG, Napolitano C, Gasparini M, et al. Natural history of
Brugada syndrome: insights for risk stratification and management.
Circulation 2002;105:1342 7.
74. Schinkel Af. Implantable cardioverter defibrillators inarrhythmogenic right ventricular dysplasia/cardiomyopathy: patient
outcomes, incidence of appropriate and inappropriate
interventions, and complications. Circ Arrhythm Electrophysiol
2013;6:562 8.
75. Schwartz PJ, Spazzolini C, Priori SG, et al. Who are the long-QT
syndrome patients who receive an implantable cardioverterdefibrillator and what happens to them?: data from the European
Long-QT Syndrome Implantable Cardioverter-Defibrillator (LQTS
ICD) Registry. Circulation 2010;122:1272 82.
76. Spirito P, Autore C, Rapezzi C, et al. Syncope and risk of sudden deathin hypertrophic cardiomyopathy. Circulation 2009;119:1703 10.

151

141

77. Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective
validation of the San Francisco Syncope Rule to predict patientswith serious outcomes. Ann Emerg Med 2006;47:448 54.
78. Reed MJ, Newby DE, Coull AJ, Prescott RJ, Jacques KG, Gray AJ.
The ROSE (risk stratification of syncope in the emergency
department) study. J Am Coll Cardiol 2010;55:713 21.
79. Quinn JV, Stiell IG, McDermott DA, Sellers KL, Kohn MA, Wells GA.
Derivation of the San Francisco Syncope Rule to predict patients withshort-term serious outcomes. Ann Emerg Med 2004;43:224 32.
80. Del Rosso A, Ungar A, Maggi R, et al. Clinical predictors of cardiac
syncope at initial evaluation in patients referred urgently to a general
hospital: the EGSYS score. Heart 2008;94:1620 6.
81. Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history inpatients with syncope with or without heart disease. J Am Coll
Cardiol 2001;37:1921 8.
82. Calkins H, Shyr Y, Frumin H, Schork A, Morady F. The value of theclinical history in the differentiation of syncope due to ventriculartachycardia, atrioventricular block, and neurocardiogenic syncope.
Am J Med 1995;98:365 73.
83. Costantino G, Perego F, Dipaola F, et al. Short- and long-term
prognosis of syncope, risk factors, and role of hospital admission:
results from the STePS (Short-Term Prognosis of Syncope) study. J
Am Coll Cardiol 2008;51:276 83.
84. Colman N, Bakker A, Linzer M, Reitsma JB, Wieling W, Wilde AA.
Value of history-taking in syncope patients: in whom to suspect long
QT syndrome? Europace 2009;11:937 43.
85. Jamjoom AA, Nikkar-Esfahani A, Fitzgerald JE. Operating theatre
related syncope in medical students: a cross sectional study. BMC
Med Educ 2009;9:14.
86. Priori SG, Blomstrom-Lundqvist C, Mazzanti A, et al. 2015 ESC
Guidelines for the management of patients with ventricular arrhythmias
and the prevention of sudden cardiac death: The Task Force for theManagement of Patients with Ventricular Arrhythmias and the Preventionof Sudden Cardiac Death of the European Society of Cardiology (ESC).
Endorsed by: Association for European Paediatric and Congenital
Cardiology (AEPC). Eur Heart J 2015;36:2793 867.
87. Sheldon R, Rose S, Connolly S, Ritchie D, Koshman ML, Frenneaux
M. Diagnostic criteria for vasovagal syncope based on a quantitative
history. Eur Heart J 2006;27:344 50.
88. Mahmood S, Lim L, Akram Y, Alford-Morales S, Sherin K,
Committee APP. Screening for sudden cardiac death before
participation in high school and collegiate sports: American College
of Preventive Medicine position statement on preventive practice.
Am J Prev Med 2013;45:130 3.
89. Hainline B, Drezner J, Baggish A, et al. Interassociation consensus
statement on cardiovascular care of college student-athletes. Br J
Sports Med 2017;51:74 85.
90. Malhotra A, Dhutia H, Finocchiaro G, et al. Outcomes of Cardiac
Screening in Adolescent Soccer Players. N Engl J Med
2018;379:524 34.
91. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the
management of patients with supraventricular tachycardiaThe Task
Force for the management of patients with supraventriculartachycardia of the European Society of Cardiology (ESC). Eur HeartJ 2020;41:655 720.
92. Perez MV, Mahaffey KW, Hedlin H, et al. Large-Scale Assessmentof a Smartwatch to Identify Atrial Fibrillation. N Engl J Med
2019;381:1909 17.
93. Guo Y, Wang H, Zhang H, et al. Mobile Photoplethysmographic
Technology to Detect Atrial Fibrillation. J Am Coll Cardiol
2019;74:2365 75.
94. ERC Quality standards for cardiopulmonary resuscitation practiceand training. 2019. (Accessed 05 October 2020, 2020, at https://www.erc.edu/sites/5714e77d5e615861f00f7d18/assets/5dedf6
664c84860818e4d3c0/CPR_quality_standards_In_hosp_
accute_ERC_V3_Final_1_.pdf.).
95. Chan PS, Krumholz HM, Nichol G, Nallamothu BK. Delayed time to
defibrillation after in-hospital cardiac arrest. N Engl J Med
2008;358:9 17.

142

RESUSCITATION 161 (2021) 115

96. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP. Predicting
survival from out-of-hospital cardiac arrest: a graphic model. Ann
Emerg Med 1993;22:1652 8.
97. Whitaker DK, Nolan JP, Castren M, Abela C, Goldik Z. Implementing
a standard internal telephone number 2222 for cardiac arrest calls inall hospitals in Europe. Resuscitation 2017;115:A14-A5.
98. Featherstone P, Chalmers T, Smith GB. RSVP: a system forcommunication of deterioration in hospital patients. Br J Nurs
2008;17:860 4.
99. De Meester K, Verspuy M, Monsieurs KG, Van Bogaert P. SBAR
improves nurse-physician communication and reduces unexpected
death: a pre and post intervention study. Resuscitation
2013;84:1192 6.
100. Ornato JP, Peberdy MA, Reid RD, Feeser VR, Dhindsa HS. Impactof resuscitation system errors on survival from in-hospital cardiac
arrest. Resuscitation 2012;83:63 9.
101. Weng TI, Huang CH, Ma MH, et al. Improving the rate of return ofspontaneous circulation for out-of-hospital cardiac arrests with aformal, structured emergency resuscitation team. Resuscitation
2004;60:137 42.
102. Panesar Ss, Ignatowicz Am, Donaldson Lj. Errors in the
management of cardiac arrests: an observational study of patient
safety incidents in England. Resuscitation 2014;85:1759 63.
103. Bray J, Nehme Z, Nguyen A, Lockey A, Finn J. Education
Implementation Teams Task Force of the International Liaison
Committee on R. A systematic review of the impact of emergency
medical service practitioner experience and exposure to out of
hospital cardiac arrest on patient outcomes. Resuscitation
2020;155:134 42.
103a. Smyth M, Perkins G, Coppola A, et al. - on behalf of the International
Liaison Committee on Resuscitation Education, Implementation
and Teams Task Force. Prehospital termination of resuscitation(TOR) rules Draft Consensus on Science with Treatment
Recommendations. International Liaison Committee on
Resuscitation (ILCOR) Education, Implementation and Teams
Task Force, 2020, January 6. Available from: http://ilcor.org.
104. Olasveengen TM, Mancini ME, Perkins GD, et al. Adult Basic Life
Support: 2020 International Consensus on Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care Science With
Treatment Recommendations. Circulation 2020;142:S41 91.
105. Nichol G, Sayre MR, Guerra F, Poole J. Defibrillation for VentricularFibrillation: A Shocking Update. J Am Coll Cardiol 2017;70:1496 509.
106. Dyson K, Bray Je, Smith K, Bernard S, Straney L, Finn J. Paramedic
Exposure to Out-of-Hospital Cardiac Arrest Resuscitation Is
Associated With Patient Survival. Circ Cardiovasc Qual Outcomes
2016;9:154 60.
107. Tuttle JE, Hubble MW. Paramedic Out-of-hospital Cardiac Arrest
Case Volume Is a Predictor of Return of Spontaneous Circulation.
West J Emerg Med 2018;19:654 9.
108. Yeung J, Matsuyama T, Bray J, Reynolds J, Skrifvars MB. Does care
at a cardiac arrest centre improve outcome after out-of-hospital cardiac
arrest? - A systematic review. Resuscitation 2019;137:102 15.
109. Edelson DP, Abella BS, Kramer-Johansen J, et al. Effects ofcompression depth and pre-shock pauses predict defibrillation
failure during cardiac arrest. Resuscitation 2006;71:137 45.
110. Eftestol T, Sunde K, Steen PA. Effects of interrupting precordial
compressions on the calculated probability of defibrillation successduring out-of-hospital cardiac arrest. Circulation 2002;105:2270 3.
111. Cheskes S, Schmicker RH, Christenson J, et al. Perishock pause:
an independent predictor of survival from out-of-hospital shockablecardiac arrest. Circulation 2011;124:58 66.
112. Cheskes S, Schmicker RH, Verbeek PR, et al. The impact of perishock pause on survival from out-of-hospital shockable cardiac
arrest during the Resuscitation Outcomes Consortium PRIMED
trial. Resuscitation 2014;85:336 42.
113. Gundersen K, Kvaloy JT, Kramer-Johansen J, Steen PA, Eftestol T.
Development of the probability of return of spontaneous circulation

151

in intervals without chest compressions during out-of-hospital
cardiac arrest: an observational study. BMC Med 2009;7:6.
114. Sell RE, Sarno R, Lawrence B, et al. Minimizing pre- and postdefibrillation pauses increases the likelihood of return ofspontaneous circulation (ROSC). Resuscitation 2010;81:822 5.
115. Edelson DP, Robertson-Dick BJ, Yuen TC, et al. Safety and efficacy
of defibrillator charging during ongoing chest compressions: a multicenter study. Resuscitation 2010;81:1521 6.
116. Perkins GD, Davies RP, Soar J, Thickett DR. The impact of manual
defibrillation technique on no-flow time during simulated
cardiopulmonary resuscitation. Resuscitation 2007;73:109 14.
117. Otto Q, Musiol S, Deakin CD, Morley P, Soar J. Anticipatory manual
defibrillator charging during advanced life support: A scoping
review. Resuscitation Plus 2020 1 2:100004.
118. Miller PH. Potential fire hazard in defibrillation. JAMA 1972;221:192.
119. Hummel 3rd RS, Ornato JP, Weinberg SM, Clarke AM. Sparkgenerating properties of electrode gels used during defibrillation. A
potential fire hazard. JAMA 1988;260:3021 4.
120. ECRI. Defibrillation in oxygen-enriched environments [hazard].
Health Devices 1987;16:113 4.
121. Lefever J, Smith A. Risk of fire when using defibrillation in an oxygen
enriched atmosphere. Medical Devices Agency Safety Notices
1995;3:1 3.
122. Ward ME. Risk of fires when using defibrillators in an oxygen
enriched atmosphere. Resuscitation 1996;31:173.
123. Theodorou AA, Gutierrez JA, Berg RA. Fire attributable to adefibrillation attempt in a neonate. Pediatrics 2003;112:677 9.
124. Pagan-Carlo LA, Spencer KT, Robertson CE, Dengler A, Birkett C,
Kerber RE. Transthoracic defibrillation: importance of avoiding
electrode placement directly on the female breast. J Am Coll Cardiol
1996;27:449 52.
125. Foster AG, Deakin CD. Accuracy of instructional diagrams forautomated external defibrillator pad positioning. Resuscitation
2019;139:282 8.
126. Deakin CD, Sado DM, Petley GW, Clewlow F. Is the orientation of
the apical defibrillation paddle of importance during manual external
defibrillation? Resuscitation 2003;56:15 8.
127. Kirchhof P, Eckardt L, Loh P, et al. Anterior-posterior versus
anterior-lateral electrode positions for external cardioversion of
atrial fibrillation: a randomised trial. Lancet 2002;360:1275 9.
128. Botto GL, Politi A, Bonini W, Broffoni T, Bonatti R. External
cardioversion of atrial fibrillation: role of paddle position on technicalefficacy and energy requirements. Heart 1999;82:726 30.
129. Alp NJ, Rahman S, Bell JA, Shahi M. Randomised comparison ofantero-lateral versus antero-posterior paddle positions for DC
cardioversion of persistent atrial fibrillation. International Journal of
Cardiology 2000;75:211 6.
130. Mathew TP, Moore A, McIntyre M, et al. Randomised comparison ofelectrode positions for cardioversion of atrial fibrillation. Heart
1999;81:576 9.
131. Kirkland S, Stiell I, AlShawabkeh T, Campbell S, Dickinson G, Rowe
BH. The efficacy of pad placement for electrical cardioversion of
atrial fibrillation/flutter: a systematic review. Acad Emerg Med
2014;21:717 26.
132. Zhang B, Li X, Shen D, Zhen Y, Tao A, Zhang G. Anterior-posteriorversus anterior-lateral electrode position for external electrical
cardioversion of atrial fibrillation: a meta-analysis of randomized
controlled trials. Arch Cardiovasc Dis 2014;107:280 90.
133. Walsh SJ, McCarty D, McClelland AJ, et al. Impedancecompensated biphasic waveforms for transthoracic cardioversion
of atrial fibrillation: a multi-centre comparison of antero-apicaland antero-posterior pad positions. Eur Heart J 2005;26:
1298 302.
134. Manegold JC, Israel CW, Ehrlich JR, et al. External cardioversion of
atrial fibrillation in patients with implanted pacemaker or
cardioverter-defibrillator systems: a randomized comparison ofmonophasic and biphasic shock energy application. Eur Heart J
2007;28:1731 8.

RESUSCITATION 161 (2021) 115

135. Alferness CA. Pacemaker damage due to external countershock inpatients with implanted cardiac pacemakers. Pacing Clin
Electrophysiol 1982;5:457 8.
136. Pitcher D, Soar J, Hogg K, et al. Cardiovascular implanted electronic
devices in people towards the end of life, during cardiopulmonary
resuscitation and after death: guidance from the Resuscitation
Council (UK), British Cardiovascular Society and National Council
for Palliative Care. Heart 2016;102(Suppl 7):A1 A17.
137. Olsen JA, Brunborg C, Steinberg M, et al. Pre-shock chest
compression pause effects on termination of ventricular fibrillation/tachycardia and return of organized rhythm within mechanical andmanual cardiopulmonary resuscitation. Resuscitation 2015;93:158
63.
138. Deakin CD, Lee-Shrewsbury V, Hogg K, Petley GW. Do clinicalexamination gloves provide adequate electrical insulation for safe
hands-on defibrillation? I: Resistive properties of nitrile gloves.
Resuscitation 2013;84:895 9.
139. Deakin CD, McLaren RM, Petley GW, Clewlow F, Dalrymple-Hay
MJ. Effects of positive end-expiratory pressure on transthoracic
impedance– implications for defibrillation. Resuscitation 1998;37:9
12.
140. Jacobs I, Sunde K, Deakin CD, et al. Part 6: Defibrillation: 2010
International Consensus on Cardiopulmonary Resuscitation andEmergency Cardiovascular Care Science With Treatment
Recommendations. Circulation 2010;122:S325 37.
141. Sunde K, Jacobs I, Deakin CD, et al. Part 6: Defibrillation: 2010
international consensus on cardiopulmonary resuscitation andemergency cardiovascular care science with treatment
recommendations. Resuscitation 2010;81(Suppl 1):e71 85.
142. Jost D, Degrange H, Verret C, et al. DEFI 2005: a randomized
controlled trial of the effect of automated external defibrillator
cardiopulmonary resuscitation protocol on outcome from out-ofhospital cardiac arrest. Circulation 2010;121:1614 22.
143. Berdowski J, Schulten RJ. Tijssen JG, van Alem AP, Koster RW.
Delaying a shock after takeover from the automated external
defibrillator by paramedics is associated with decreased survival.
Resuscitation 2010;81:287 92.
144. Sunde K, Eftestol T, Askenberg C, Steen PA. Quality assessment ofdefibrillation and advanced life support using data from the medical
control module of the defibrillator. Resuscitation 1999;41:237 47.
145. Rea TD, Shah S, Kudenchuk PJ, Copass MK, Cobb LA. Automatedexternal defibrillators: to what extent does the algorithm delay CPR?
Ann Emerg Med 2005;46:132 41.
146. Pierce AE, Roppolo LP, Owens PC, Pepe PE, Idris AH. The need toresume chest compressions immediately after defibrillation
attempts: an analysis of post-shock rhythms and duration ofpulselessness following out-of-hospital cardiac arrest.
Resuscitation 2015;89:162 8.
147. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult Advanced
Cardiovascular Life Support: 2015 American Heart Association
Guidelines Update for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care. Circulation 2015;(132):
S444 64.
148. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonary
resuscitation on predictors of ventricular fibrillation defibrillation
success during out-of-hospital cardiac arrest. Circulation
2004;110:10 5.
149. Eftestol T, Sunde K, Aase SO, Husoy JH, Steen PA. Predicting
outcome of defibrillation by spectral characterization andnonparametric classification of ventricular fibrillation in patients with
out-of-hospital cardiac arrest. Circulation 2000;102:1523 9.
150. Callaway CW, Sherman LD, Mosesso Jr. VN, Dietrich TJ, Holt E,
Clarkson MC. Scaling exponent predicts defibrillation success forout-of-hospital ventricular fibrillation cardiac arrest. Circulation
2001;103:1656 61.
151. Weaver WD, Cobb LA, Dennis D, Ray R, Hallstrom AP, Copass MK.
Amplitude of ventricular fibrillation waveform and outcome after
cardiac arrest. Ann Intern Med 1985;102:53 5.

151

143

152. Brown CG, Dzwonczyk R. Signal analysis of the human
electrocardiogram during ventricular fibrillation: frequency andamplitude parameters as predictors of successful countershock.
Ann Emerg Med 1996;27:184 8.
153. Callaham M, Braun O, Valentine W, Clark Dm, Zegans C.
Prehospital cardiac arrest treated by urban first-responders: profile
of patient response and prediction of outcome by ventricularfibrillation waveform. Ann Emerg Med 1993;22:1664 77.
154. Strohmenger HU, Lindner KH, Brown CG. Analysis of the ventricularfibrillation ECG signal amplitude and frequency parameters as
predictors of countershock success in humans. Chest
1997;111:584 9.
155. Strohmenger HU, Eftestol T, Sunde K, et al. The predictive value ofventricular fibrillation electrocardiogram signal frequency andamplitude variables in patients with out-of-hospital cardiac arrest.
Anesth Analg 2001;93:1428 33.
156. Podbregar M, Kovacic M, Podbregar-Mars A, Brezocnik M.
Predicting defibrillation success by’ genetic’ programming inpatients with out-of-hospital cardiac arrest. Resuscitation
2003;57:153 9.
157. Menegazzi JJ, Callaway CW, Sherman LD, et al. Ventricularfibrillation scaling exponent can guide timing of defibrillation andother therapies. Circulation 2004;109:926 31.
158. Povoas HP, Weil MH, Tang W, Bisera J, Klouche K, Barbatsis A.
Predicting the success of defibrillation by electrocardiographic
analysis. Resuscitation 2002;53:77 82.
159. Noc M, Weil MH, Tang W, Sun S, Pernat A, Bisera J.
Electrocardiographic prediction of the success of cardiac
resuscitation. Crit Care Med 1999;27:708 14.
160. Strohmenger HU, Lindner KH, Keller A, Lindner IM, Pfenninger EG.
Spectral analysis of ventricular fibrillation and closed-chest
cardiopulmonary resuscitation. Resuscitation 1996;33:155 61.
161. Noc M, Weil MH, Gazmuri RJ, Sun S, Biscera J, Tang W. Ventricularfibrillation voltage as a monitor of the effectiveness of
cardiopulmonary resuscitation. Journal of Laboratory and Clinical
Medicine 1994;124:421 6.
162. Lightfoot CB, Nremt P, Callaway CW, et al. Dynamic nature ofelectrocardiographic waveform predicts rescue shockoutcome in porcine ventricular fibrillation. Ann Emerg Med
2003;42:230 41.
163. Marn-Pernat A, Weil MH, Tang W, Pernat A, Bisera J. Optimizing
timing of ventricular defibrillation. Crit Care Med 2001;29:2360 5.
164. Hamprecht FA, Achleitner U, Krismer AC, et al. Fibrillation power, analternative method of ECG spectral analysis for prediction ofcountershock success in a porcine model of ventricular fibrillation.
Resuscitation 2001;50:287 96.
165. Amann A, Achleitner U, Antretter H, et al. Analysing ventricularfibrillation ECG-signals and predicting defibrillation success during
cardiopulmonary resuscitation employing N(alpha)-histograms.
Resuscitation 2001;50:77 85.
166. Brown CG, Griffith RF, Van Ligten P, et al. Median frequency–a newparameter for predicting defibrillation success rate. Ann Emerg Med
1991;20:787 9.
167. Amann A, Rheinberger K, Achleitner U, et al. The prediction of
defibrillation outcome using a new combination of mean frequency
and amplitude in porcine models of cardiac arrest. Anesth Analg
2002;95:716 22.
168. Firoozabadi R, Nakagawa M, Helfenbein ED, Babaeizadeh S.
Predicting defibrillation success in sudden cardiac arrest patients. J
Electrocardiol 2013;46:473 9.
169. Ristagno G, Li Y, Fumagalli F, Finzi A, Quan W. Amplitude spectrum
area to guide resuscitation-a retrospective analysis during out-ofhospital cardiopulmonary resuscitation in 609 patients withventricular fibrillation cardiac arrest. Resuscitation 2013;84:1697
703.
170. Ristagno G, Mauri T, Cesana G, et al. Amplitude spectrum area toguide defibrillation: a validation on 1617 patients with ventricularfibrillation. Circulation 2015;131:478 87.

144

RESUSCITATION 161 (2021) 115

171. Freese JP, Jorgenson DB, Liu PY, et al. Waveform analysis-guided
treatment versus a standard shock-first protocol for the treatment ofout-of-hospital cardiac arrest presenting in ventricular fibrillation:
results of an international randomized, controlled trial. Circulation
2013;128:995 1002.
172. Coult J, Blackwood J, Sherman L, Rea TD, Kudenchuk PJ, Kwok H.
Ventricular Fibrillation Waveform Analysis During Chest
Compressions to Predict Survival From Cardiac Arrest. Circ
Arrhythm Electrophysiol 2019;12:e006924.
173. Aiello S, Perez M, Cogan C, et al. Real-Time Ventricular Fibrillation
Amplitude-Spectral Area Analysis to Guide Timing of Shock
Delivery Improves Defibrillation Efficacy During Cardiopulmonary
Resuscitation in Swine. Journal of the American Heart Association
2017;6.
174. Nakagawa Y, Amino M, Inokuchi S, Hayashi S, Wakabayashi T,
Noda T. Novel CPR system that predicts return of spontaneous
circulation from amplitude spectral area before electric shock inventricular fibrillation. Resuscitation 2017;113:8 12.
175. He M, Lu Y, Zhang L, Zhang H, Gong Y, Li Y. Combining Amplitude
Spectrum Area with Previous Shock Information Using Neural
Networks Improves Prediction Performance of Defibrillation
Outcome for Subsequent Shocks in Out-Of-Hospital Cardiac Arrest
Patients. PLoS One 2016;11:e0149115.
176. Shandilya S, Ward K, Kurz M, Najarian K. Non-linear dynamicalsignal characterization for prediction of defibrillation successthrough machine learning. BMC Med Inform Decis Mak
2012;12:116.
177. Nakagawa Y, Sato Y, Kojima T, et al. Electrical defibrillation
outcome prediction by waveform analysis of ventricular fibrillation in
cardiac arrest out of hospital patients. Tokai J Exp Clin Med
2012;37:1 5.
178. Lin LY, Lo MT, Ko PC, et al. Detrended fluctuation analysis predicts
successful defibrillation for out-of-hospital ventricular fibrillation
cardiac arrest. Resuscitation 2010;81:297 301.
179. Balderston JR, Gertz ZM, Ellenbogen KA, Schaaf KP, Ornato JP.
Association between ventricular fibrillation amplitude immediately
prior to defibrillation and defibrillation success in out-of-hospital
cardiac arrest. Am Heart J 2018;201:72 6.
180. Agerskov M, Hansen MB, Nielsen AM, Moller TP, Wissenberg M,
Rasmussen LS. Return of spontaneous circulation and long-term
survival according to feedback provided by automated external
defibrillators. Acta Anaesthesiol Scand 2017;61:1345 53.
181. Coult J, Kwok H, Sherman L, Blackwood J, Kudenchuk PJ, Rea TD.
Ventricular fibrillation waveform measures combined with priorshock outcome predict defibrillation success during
cardiopulmonary resuscitation. J Electrocardiol 2018;51:99 106.
182. Hulleman M, Salcido DD, Menegazzi JJ, et al. Predictive value of
amplitude spectrum area of ventricular fibrillation waveform inpatients with acute or previous myocardial infarction in out-ofhospital cardiac arrest. Resuscitation 2017;120:125 31.
183. Jin D, Dai C, Gong Y, et al. Does the choice of definition fordefibrillation and CPR success impact the predictability ofventricular fibrillation waveform analysis? Resuscitation
2017;111:48 54.
184. Hidano D, Coult J, Blackwood J, et al. Ventricular fibrillation
waveform measures and the etiology of cardiac arrest.
Resuscitation 2016;109:71 5.
185. Coult J, Sherman L, Kwok H, Blackwood J, Kudenchuk PJ, Rea TD.
Short ECG segments predict defibrillation outcome using
quantitative waveform measures. Resuscitation 2016;109:16 20.
186. Indik JH, Conover Z, McGovern M, et al. Association of amplitude
spectral area of the ventricular fibrillation waveform with survival of
out-of-hospital ventricular fibrillation cardiac arrest. J Am Coll
Cardiol 2014;64:1362 9.
187. Howe A, Escalona OJ, Di Maio R, et al. A support vector machine forpredicting defibrillation outcomes from waveform metrics.
Resuscitation 2014;85:343 9.
188. Wu X, Bisera J, Tang W. Signal integral for optimizing the timing of
defibrillation. Resuscitation 2013;84:1704 7.

151

189. Hall M, Phelps R, Fahrenbruch C, Sherman L, Blackwood J, Rea
TD. Myocardial substrate in secondary ventricular fibrillation:
insights from quantitative waveform measures. Prehosp Emerg
Care 2011;15:388 92.
190. Foomany FH, Umapathy K, Sugavaneswaran L, et al. Waveletbased markers of ventricular fibrillation in optimizing human cardiac
resuscitation. Annu Int Conf IEEE Eng Med Biol Soc
2010;2010:2001 4.
191. Endoh H, Hida S, Oohashi S, Hayashi Y, Kinoshita H, Honda T.
Prompt prediction of successful defibrillation from 1-s ventricularfibrillation waveform in patients with out-of-hospital sudden cardiac
arrest. Journal of Anesthesia 2011;25:34 41.
192. Kerber RE. External defibrillation: new technologies. Ann Emerg
Med 1984;13:794 7.
193. Joglar JA, Kessler DJ, Welch PJ, et al. Effects of repeated electricaldefibrillations on cardiac troponin I levels. Am J Cardiol 199983:
270-2, A6.
194. Kerber RE, Martins JB, Kienzle MG, et al. Energy, current, andsuccess in defibrillation and cardioversion: clinical studies using an
automated impedance-based method of energy adjustment.
Circulation 1988;77:1038 46.
195. Deakin CD, Nolan JP, Soar J, et al. European Resuscitation Council
Guidelines for Resuscitation 2010 Section 4. Adult advanced life
support. Resuscitation 2010;(81):1305 52.
196. van Alem AP, Chapman FW, Lank P, Hart AA, Koster RW. A
prospective, randomised and blinded comparison of first shock
success of monophasic and biphasic waveforms in out-of-hospital
cardiac arrest. Resuscitation 2003;58:17 24.
197. Martens PR, Russell JK, Wolcke B, et al. Optimal Response to
Cardiac Arrest study: defibrillation waveform effects. Resuscitation
2001;49:233 43.
198. Carpenter J, Rea TD, Murray JA, Kudenchuk PJ, Eisenberg MS.
Defibrillation waveform and post-shock rhythm in out-of-hospital
ventricular fibrillation cardiac arrest. Resuscitation 2003;59:
189 96.
199. Gliner BE, Jorgenson DB, Poole JE, et al. Treatment of out-ofhospital cardiac arrest with a low-energy impedance-compensating
biphasic waveform automatic external defibrillator. The LIFE
Investigators. Biomed Instrum Technol 1998;32:631 44.
200. White RD, Blackwell TH, Russell JK, Snyder DE, Jorgenson DB.
Transthoracic impedance does not affect defibrillation,
resuscitation or survival in patients with out-of-hospital cardiac
arrest treated with a non-escalating biphasic waveform defibrillator.
Resuscitation 2005;64:63 9.
201. Morrison LJ, Henry RM, Ku V, Nolan JP, Morley P, Deakin CD.
Single-shock defibrillation success in adult cardiac arrest: asystematic review. Resuscitation 2013;84:1480 6.
202. Stiell IG, Walker RG, Nesbitt LP, et al. BIPHASIC Trial: arandomized comparison of fixed lower versus escalating higher
energy levels for defibrillation in out-of-hospital cardiac arrest.
Circulation 2007;115:1511 7.
203. Walsh SJ, McClelland AJ, Owens CG, et al. Efficacy of distinct
energy delivery protocols comparing two biphasic defibrillators for
cardiac arrest. Am J Cardiol 2004;94:378 80.
204. Olsen JA, Brunborg C, Steinberg M, et al. Survival to hospitaldischarge with biphasic fixed 360 joules versus 200 escalating
to 360 joules defibrillation strategies in out-of-hospital cardiac
arrest of presumed cardiac etiology. Resuscitation 2019;136:
112 8.
205. Anantharaman V, Tay SY, Manning PG, et al. A multicenterprospective randomized study comparing the efficacy of escalating
higher biphasic versus low biphasic energy defibrillations in patients
presenting with cardiac arrest in the in-hospital environment. Open
Access Emerg Med 2017;9:9 17.
206. Schneider T, Martens PR, Paschen H, et al. Multicenter,randomized, controlled trial of 150-J biphasic shocks compared with
200- to 360-J monophasic shocks in the resuscitation of out-ofhospital cardiac arrest victims. Optimized Response to Cardiac
Arrest (ORCA) Investigators. Circulation 2000;102:1780 7.

RESUSCITATION 161 (2021) 115

207. Higgins SL, Herre JM, Epstein AE, et al. A comparison of biphasic
and monophasic shocks for external defibrillation. Physio-Control
Biphasic Investigators. Prehosp Emerg Care 2000;4:305 13.
208. Berg RA, Samson RA, Berg MD, et al. Better outcome after pediatricdefibrillation dosage than adult dosage in a swine model of pediatricventricular fibrillation. J Am Coll Cardiol 2005;45:786 9.
209. Killingsworth CR, Melnick SB, Chapman FW, et al. Defibrillationthreshold and cardiac responses using an external biphasic
defibrillator with pediatric and adult adhesive patches in pediatricsized piglets. Resuscitation 2002;55:177 85.
210. Tang W, Weil MH, Sun S, et al. The effects of biphasic waveform
design on post-resuscitation myocardial function. J Am Coll Cardiol
2004;43:1228 35.
211. Xie J, Weil MH, Sun S, et al. High-energy defibrillation increases theseverity of postresuscitation myocardial dysfunction. Circulation
1997;96:683 8.
212. Koster RW, Walker RG, Chapman FW. Recurrent ventricularfibrillation during advanced life support care of patients withprehospital cardiac arrest. Resuscitation 2008;78:252 7.
213. Walker RG, Koster RW, Sun C, et al. Defibrillation probability and
impedance change between shocks during resuscitation from outof-hospital cardiac arrest. Resuscitation 2009;80:773 7.
214. Hess EP, Russell JK, Liu PY, White RD. A high peak current 150-J
fixed-energy defibrillation protocol treats recurrent ventricularfibrillation (VF) as effectively as initial VF. Resuscitation 2008;79:
28 33.
215. Deakin CD, Ambler JJ. Post-shock myocardial stunning: aprospective randomised double-blind comparison of monophasic
and biphasic waveforms. Resuscitation 2006;68:329 33.
216. Khaykin Y, Newman D, Kowalewski M, Korley V, Dorian P. Biphasic
versus monophasic cardioversion in shock-resistant atrial
fibrillation. J Cardiovasc Electrophysiol 2003;14:868 72.
217. Koster RW, Dorian P, Chapman FW, Schmitt PW, O’Grady SG,
Walker RG. A randomized trial comparing monophasic and biphasic
waveform shocks for external cardioversion of atrial fibrillation. Am
Heart J 2004;147:e20.
218. Mittal S, Ayati S, Stein KM, et al. Transthoracic cardioversion of
atrial fibrillation: comparison of rectilinear biphasic versus damped
sine wave monophasic shocks. Circulation 2000;101:1282 7.
219. Kmec J. Comparison the effectiveness of damped sine wave
monophasic and rectilinear biphasic shocks in patients withpersistent atrial fibrillation. Kardiologia 2006;15:265 78.
220. Kosior DA, Szulec M, Torbicki A, Opolski G, Rabczenko D. A
decrease of enlarged left atrium following cardioversion of atrial
fibrillationpredicts the long-term maintenance of sinus rhythm.
Kardiologia Polska 2005;62:428 37.
221. Hess EP, Agarwal D, Myers LA, Atkinson EJ, White RD.
Performance of a rectilinear biphasic waveform in defibrillation ofpresenting and recurrent ventricular fibrillation: a prospective
multicenter study. Resuscitation 2011;82:685 9.
222. Eilevstjonn J, Kramer-Johansen J, Sunde K. Shock outcome isrelated to prior rhythm and duration of ventricular fibrillation.
Resuscitation 2007;75:60 7.
223. Mapp JG, Hans AJ, Darrington AM, et al. Prehospital Double
Sequential Defibrillation: A Matched Case-Control Study. Acad
Emerg Med 2019;26:994 1001.
224. Ross EM, Redman TT, Harper SA, Mapp JG, Wampler DA,
Miramontes DA. Dual defibrillation in out-of-hospital cardiac arrest:
A retrospective cohort analysis. Resuscitation 2016;106:14 7.
225. Cortez E, Krebs W, Davis J, Keseg DP, Panchal AR. Use of double
sequential external defibrillation for refractory ventricular fibrillation during
out-of-hospital cardiac arrest. Resuscitation 2016;108:82 6.
226. Beck LR, Ostermayer DG, Ponce JN, Srinivasan S, Wang HE.
Effectiveness of Prehospital Dual Sequential Defibrillation for
Refractory Ventricular Fibrillation and Ventricular Tachycardia
Cardiac Arrest. Prehosp Emerg Care 2019;23:597 602.
227. Emmerson AC, Whitbread M, Fothergill RT. Double sequential
defibrillation therapy for out-of-hospital cardiac arrests: The London
experience. Resuscitation 2017;117:97 101.

151

145

228. Cabanas JG, Myers JB, Williams JG, De Maio VJ, Bachman MW.
Double Sequential External Defibrillation in Out-of-Hospital
Refractory Ventricular Fibrillation: A Report of Ten Cases. Prehosp
Emerg Care 2015;19:126 30.
229. Cheskes S, Wudwud A, Turner L, et al. The impact of double
sequential external defibrillation on termination of refractory
ventricular fibrillation during out-of-hospital cardiac arrest.
Resuscitation 2019;139:275 81.
230. Cheskes S, Dorian P, Feldman M, et al. Double sequential external
defibrillation for refractory ventricular fibrillation: The DOSE VF pilot
randomized controlled trial. Resuscitation 2020;150:178 84.
231. Deakin CD, Morley P, Soar J, Drennan IR. Double (dual) sequential
defibrillation for refractory ventricular fibrillation cardiac arrest: A
systematic review. Resuscitation 2020;155:24 31.
232. Friedman DJ, Parzynski CS, Varosy PD, et al. Trends and InHospital Outcomes Associated With Adoption of the Subcutaneous
Implantable Cardioverter Defibrillator in the United States. JAMA
Cardiol 2016;1:900 11.
233. Knops RE, Olde Nordkamp LRA, Delnoy PHM, et al. Subcutaneousor Transvenous Defibrillator Therapy. N Engl J Med 2020;383:
526 36.
234. Stockwell B, Bellis G, Morton G, et al. Electrical injury during "handson" defibrillation-A potential risk of internal cardioverter
defibrillators? Resuscitation 2009;80:832 4.
235. Peran D, Cmorej PC, Pekara J. Bystander hit by leakage current
from S-ICD. Resuscitation 2019;138:297 8.
236. Petley GW, Albon B, Banks P, Roberts PR, Deakin CD. Leakage
current from transvenous and subcutaneous implantablecardioverter defibrillators (ICDs): A risk to the rescuer?
Resuscitation 2019;137:148 53.
237. Monsieurs KG, Conraads VM, Goethals MP, Snoeck JP, Bossaert
LL. Semi-automatic external defibrillation and implanted cardiac
pacemakers: understanding the interactions during resuscitation.
Resuscitation 1995;30:127 31.
238. Benger JR, Kirby K, Black S, et al. Effect of a Strategy of a
Supraglottic Airway Device vs Tracheal Intubation During Out-ofHospital Cardiac Arrest on Functional Outcome: The AIRWAYS-2
Randomized Clinical Trial. JAMA 2018;320:779 91.
239. Jabre P, Penaloza A, Pinero D, et al. Effect of Bag-Mask Ventilation
vs Endotracheal Intubation During Cardiopulmonary Resuscitation
on Neurological Outcome After Out-of-Hospital Cardiorespiratory
Arrest: A Randomized Clinical Trial. JAMA 2018;319:779 87.
240. Wang HE, Schmicker RH, Daya MR, et al. Effect of a Strategy of
Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72Hour Survival in Adults With Out-of-Hospital Cardiac Arrest: A
Randomized Clinical Trial. JAMA 2018;320:769 78.
241. Granfeldt A, Avis SR, Nicholson TC, et al. Advanced airway
management during adult cardiac arrest: A systematic review.
Resuscitation 2019;139:133 43.
242. Soar J, Maconochie I, Wyckoff MH, et al. 2019 International
Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science With Treatment Recommendations.
Resuscitation 2019;145:95 150.
243. Andersen LW, Granfeldt A, Callaway CW, et al. Association
Between Tracheal Intubation During Adult In-Hospital Cardiac
Arrest and Survival. JAMA 2017;317:494 506.
244. Soar J, Maconochie I, Wyckoff MH, et al. 2019 International
Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science With Treatment Recommendations:
Summary From the Basic Life Support; Advanced Life Support;
Pediatric Life Support; Neonatal Life Support; Education,
Implementation, and Teams; and First Aid Task Forces. Circulation
2019;140:e826-e80.
245. Voss S, Rhys M, Coates D, et al. How do paramedics manage theairway during out of hospital cardiac arrest? Resuscitation
2014;85:1662 6.
246. Nolan JP. European Resuscitation Council and European Society of
Intensive Care Medicine Guidelines for Post-resuscitation Care
2020. Resuscitation 2021.

146

RESUSCITATION 161 (2021) 115

247. Olasveengen TM, Semeraro F, Ristagno G, et al. European
Resuscitation Council Guidelines for Basic Life Support.
Resuscitation 2021.
248. Couper K, Abu Hassan A, Ohri V, et al. Removal of foreign body
airway obstruction: A systematic review of interventions.
Resuscitation 2020;156:174 81.
249. Nichol G, Leroux B, Wang H, et al. Trial of Continuous or Interrupted
Chest Compressions during CPR. N Engl J Med 2015;373:2203
14.
250. Olasveengen TM, de Caen AR, Mancini ME, et al. 2017
International Consensus on Cardiopulmonary Resuscitation andEmergency Cardiovascular Care Science With Treatment
Recommendations Summary. Resuscitation 2017;121:201 14.
251. Vissers G, Soar J, Monsieurs KG. Ventilation rate in adults with atracheal tube during cardiopulmonary resuscitation: A systematic
review. Resuscitation 2017;119:5 12.
252. Deakin CD, O’Neill JF, Tabor T. Does compression-only
cardiopulmonary resuscitation generate adequate passive
ventilation during cardiac arrest? Resuscitation 2007;75:53 9.
253. Saissy JM, Boussignac G, Cheptel E, et al. Efficacy of continuous
insufflation of oxygen combined with active cardiac compressiondecompression during out-of-hospital cardiorespiratory arrest.
Anesthesiology 2000;92:1523 30.
254. Bertrand C, Hemery F, Carli P, et al. Constant flow insufflation ofoxygen as the sole mode of ventilation during out-of-hospital cardiac
arrest. Intensive Care Med 2006;32:843 51.
255. Bobrow BJ, Ewy GA, Clark L, et al. Passive oxygen insufflation issuperior to bag-valve-mask ventilation for witnessed ventricularfibrillation out-of-hospital cardiac arrest. Ann Emerg Med 200954:
656-62 e1.
256. Grmec S. Comparison of three different methods to confirm tracheal
tube placement in emergency intubation. Intensive Care Med
2002;28:701 4.
257. Lyon RM, Ferris JD, Young DM, McKeown DW, Oglesby AJ,
Robertson C. Field intubation of cardiac arrest patients: a dying art?
Emergency Medicine 2010;27:321 3.
258. Jones JH, Murphy MP, Dickson RL, Somerville GG, Brizendine EJ.
Emergency physician-verified out-of-hospital intubation: miss rates
by paramedics. Acad Emerg Med 2004;11:707 9.
259. Pelucio M, Halligan L, Dhindsa H. Out-of-hospital experience withthe syringe esophageal detector device. Acad Emerg Med
1997;4:563 8.
260. Jemmett ME, Kendal KM, Fourre MW, Burton JH. Unrecognizedmisplacement of endotracheal tubes in a mixed urban to rural
emergency medical services setting. Acad Emerg Med 2003;10:
961 5.
261. Katz SH, Falk JL. Misplaced endotracheal tubes by paramedics inan urban emergency medical services system. Ann Emerg Med
2001;37:32 7.
262. Wang HE, Simeone SJ, Weaver MD, Callaway CW. Interruptions in
cardiopulmonary resuscitation from paramedic endotracheal
intubation. Ann Emerg Med 200954: 645-52 e1.
263. Garza AG, Gratton MC, Coontz D, Noble E, Ma OJ. Effect ofparamedic experience on orotracheal intubation success rates. J
Emerg Med 2003;25:251 6.
264. Bradley JS, Billows GL, Olinger ML, Boha SP, Cordell WH, Nelson
DR. Prehospital oral endotracheal intubation by rural basic
emergency medical technicians. Ann Emerg Med 1998;32:
26 32.
265. Sayre MR, Sakles JC, Mistler AF, Evans JL, Kramer AT, Pancioli
AM. Field trial of endotracheal intubation by basic EMTs. Ann Emerg
Med 1998;31:228 33.
266. Bernhard M, Mohr S, Weigand MA, Martin E, Walther A. Developing
the skill of endotracheal intubation: implication for emergency
medicine. Acta Anaesthesiol Scand 2012;56:164 71.
267. Cook TM, Boniface NJ, Seller C, et al. Universal videolaryngoscopy:
a structured approach to conversion to videolaryngoscopy for all
intubations in an anaesthetic and intensive care department. Br J
Anaesth 2018;120:173 80.

151268. Goto Y, Goto T, Hagiwara Y, et al. Techniques and outcomes of
emergency airway management in Japan: An analysis of two
multicentre prospective observational studies, 2010-2016.
Resuscitation 2017;114:14 20.
269. Lee DH, Han M, An JY, et al. Video laryngoscopy versus direct
laryngoscopy for tracheal intubation during in-hospital
cardiopulmonary resuscitation. Resuscitation 2015;89:195 9.
270. Park SO, Kim JW, Na JH, et al. Video laryngoscopy improves thefirst-attempt success in endotracheal intubation during
cardiopulmonary resuscitation among novice physicians.
Resuscitation 2015;89:188 94.
271. Jiang J, Kang N, Li B, Wu AS, Xue FS. Comparison of adverse
events between video and direct laryngoscopes for tracheal
intubations in emergency department and ICU patients-a
systematic review and meta-analysis. Scand J Trauma Resusc
Emerg Med 2020;28:10.
272. Kim JW, Park SO, Lee KR, et al. Video laryngoscopy vs. direct
laryngoscopy: Which should be chosen for endotracheal intubation
during cardiopulmonary resuscitation? A prospective randomized
controlled study of experienced intubators. Resuscitation
2016;105:196 202.
273. Jiang J, Ma D, Li B, Yue Y, Xue F. Video laryngoscopy does not
improve the intubation outcomes in emergency and critical patients a systematic review and meta-analysis of randomized controlled
trials. Crit Care 2017;21:288.
274. Deakin CD, Morrison LJ, Morley PT, et al. Part 8: Advanced life
support: 2010 International Consensus on Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care Science with
Treatment Recommendations. Resuscitation 201081(Suppl 1)e93-e174.
275. Soar J, Callaway CW, Aibiki M, et al. Part 4: Advanced life support:
2015 International Consensus on Cardiopulmonary Resuscitationand Emergency Cardiovascular Care Science with Treatment
Recommendations. Resuscitation 2015;95:e71 120.
276. Paiva EF, Paxton JH, O’Neil BJ. The use of end-tidal carbon dioxide(ETCO2) measurement to guide management of cardiac arrest: A
systematic review. Resuscitation 2018;123:1 7.
277. Grmec S, Mally S. Prehospital determination of tracheal tube
placement in severe head injury. Emergency Medicine 2004;21:518 20.
278. Knapp S, Kofler J, Stoiser B, et al. The assessment of four different
methods to verify tracheal tube placement in the critical care setting.
Anesth Analg 1999;88:766 70.
279. Takeda T, Tanigawa K, Tanaka H, Hayashi Y, Goto E, Tanaka K.
The assessment of three methods to verify tracheal tube placementin the emergency setting. Resuscitation 2003;56:153 7.
280. Cook TM, Harrop-Griffiths AW, Whitaker DK, McNarry AF, Patel A,
McGuire B. The’ No Trace=Wrong Place’ campaign. Br J Anaesth
2019;122:e68-e9.
281. Salem MR, Khorasani A, Zeidan A. Crystal GJ. Cricoid Pressure
Controversies: Narrative Review. Anesthesiology 2017;126:738 52.
282. Higgs A, McGrath BA, Goddard C, et al. Guidelines for the
management of tracheal intubation in critically ill adults. Br J
Anaesth 2018;120:323 52.
283. Granfeldt A, Avis SR, Lind PC, et al. Intravenous vs. intraosseousadministration of drugs during cardiac arrest: A systematic review.
Resuscitation 2020;149:150 7.
284. Feinstein BA, Stubbs BA, Rea T, Kudenchuk PJ. Intraosseouscompared to intravenous drug resuscitation in out-of-hospital
cardiac arrest. Resuscitation 2017;117:91 6.
285. Kawano T, Grunau B, Scheuermeyer FX, et al. Intraosseous
Vascular Access Is Associated With Lower Survival and Neurologic
Recovery Among Patients With Out-of-Hospital Cardiac Arrest. Ann
Emerg Med 2018;71:588 96.
286. Mody P, Brown SP, Kudenchuk PJ, et al. Intraosseous versus
intravenous access in patients with out-of-hospital cardiac arrest:
Insights from the resuscitation outcomes consortium continuouschest compression trial. Resuscitation 2019;134:69 75.

RESUSCITATION 161 (2021) 115

287. Nolan JP, Deakin CD, Ji C, et al. Intraosseous versus intravenous
administration of adrenaline in patients with out-of-hospital cardiac
arrest: a secondary analysis of the PARAMEDIC2 placebocontrolled trial. Intensive Care Med 2020;46:954 62.
288. Daya MR, Leroux BG, Dorian P, et al. Survival After Intravenous
Versus Intraosseous Amiodarone, Lidocaine, or Placebo in Out-ofHospital Shock-Refractory Cardiac Arrest. Circulation
2020;141:188 98.
289. Perkins GD, Ji C, Deakin CD, et al. A Randomized Trial of
Epinephrine in Out-of-Hospital Cardiac Arrest. N Engl J Med
2018;379:711 21.
290. Finn J, Jacobs I, Williams TA, Gates S, Perkins GD. Adrenaline andvasopressin for cardiac arrest. Cochrane Database Syst Rev
2019;1:CD003179.
291. Holmberg MJ, Issa MS, Moskowitz A, et al. Vasopressors during
adult cardiac arrest: A systematic review and meta-analysis.
Resuscitation 2019;139:106 21.
292. Perkins GD, Kenna C, Ji C, et al. The effects of adrenaline in out of
hospital cardiac arrest with shockable and non-shockable rhythms:
Findings from the PACA and PARAMEDIC-2 randomised controlled
trials. Resuscitation 2019;140:55 63.
293. Perkins GD, Kenna C, Ji C, et al. The influence of time to adrenaline
administration in the Paramedic 2 randomised controlled trial.
Intensive Care Med 2020;46:426 36.
294. Soar J, Donnino MW, Maconochie I, et al. 2018 International
Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science With Treatment Recommendations
Summary. Resuscitation 2018;133:194 206.
295. Ali MU, Fitzpatrick-Lewis D, Kenny M, et al. Effectiveness ofantiarrhythmic drugs for shockable cardiac arrest: A systematic
review. Resuscitation 2018;132:63 72.
296. Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, Lidocaine, orPlacebo in Out-of-Hospital Cardiac Arrest. N Engl J Med
2016;374:1711 22.
297. Soar J, Perkins GD, Maconochie I, et al. European Resuscitation
Council Guidelines for Resuscitation: 2018 Update - Antiarrhythmic
drugs for cardiac arrest. Resuscitation 2019;134:99 103.
298. Bottiger BW, Arntz HR, Chamberlain DA, et al. Thrombolysis duringresuscitation for out-of-hospital cardiac arrest. N Engl J Med
2008;359:2651 62.
299. Yousuf T, Brinton T, Ahmed K, et al. Tissue Plasminogen Activator
Use in Cardiac Arrest Secondary to Fulminant Pulmonary
Embolism. J Clin Med Res 2016;8:190 5.
300. Kurkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as acause of cardiac arrest: presentation and outcome. Arch Intern Med
2000;160:1529 35.
301. Janata K, Holzer M, Kurkciyan I, et al. Major bleeding complications
in cardiopulmonary resuscitation: the place of thrombolytic therapy
in cardiac arrest due to massive pulmonary embolism.
Resuscitation 2003;57:49 55.
302. Javaudin F, Lascarrou JB, Le Bastard Q, et al. Thrombolysis During
Resuscitation for Out-of-Hospital Cardiac Arrest Caused by
Pulmonary Embolism Increases 30-Day Survival: Findings From
the French National Cardiac Arrest Registry. Chest 2019;156:
1167 75.
303. Böttiger BW, Böhrer H, Bach A, Motsch J, Martin E. Bolus injectionof thrombolytic agents during cardiopulmonary resuscitation for
massive pulmonary embolism. Resuscitation 1994;28:45 54.
304. Wu JP, Gu DY, Wang S, Zhang ZJ, Zhou JC, Zhang RF. Good
neurological recovery after rescue thrombolysis of presumed
pulmonary embolism despite prior 100 minutes CPR. J Thorac Dis
2014;6:E289 93.
305. Summers K, Schultheis J, Raiff D, Dahhan T. Evaluation of Rescue
Thrombolysis in Cardiac Arrest Secondary to Suspected orConfirmed Pulmonary Embolism. Ann Pharmacother 2019;53:
711 5.
306. Bernard SA, Smith K, Finn J, et al. Induction of Therapeutic
Hypothermia During Out-of-Hospital Cardiac Arrest Using a Rapid

151

147

Infusion of Cold Saline: The RINSE Trial (Rapid Infusion of Cold
Normal Saline). Circulation 2016;134:797 805.
307. Kim F, Nichol G, Maynard C, et al. Effect of prehospital induction ofmild hypothermia on survival and neurological status among adults
with cardiac arrest: a randomized clinical trial. JAMA 2014;311:
45 52.
308. Maynard C, Longstreth Jr. WT, Nichol G, et al. Effect of prehospitalinduction of mild hypothermia on 3-month neurological status and 1year survival among adults with cardiac arrest: long-term follow-up
of a randomized, clinical trial. Journal of the American Heart
Association 2015;4:e001693.
309. Soar J, Foster J, Breitkreutz R. Fluid infusion during CPR and after
ROSC–is it safe? Resuscitation 2009;80:1221 2.
310. Sandroni C, De Santis P, D’Arrigo S. Capnography during cardiac
arrest. Resuscitation 2018;132:73 7.
311. Gutierrez JJ, Ruiz JM, Ruiz de Gauna S, et al. Modeling the impactof ventilations on the capnogram in out-of-hospital cardiac arrest.
PLoS One 2020;15:e0228395.
312. Hamrick JL, Hamrick JLT, Lee JK, Lee BH, Koehler RC, Shaffner
DH. Efficacy of chest compressions directed by end-tidal CO2
feedback in a pediatric resuscitation model of basic life support.
Journal of the American Heart Association 2014;3:e000450.
313. Sheak KR, Wiebe DJ, Leary M, et al. Quantitative relationshipbetween end-tidal carbon dioxide and CPR quality during both inhospital and out-of-hospital cardiac arrest. Resuscitation
2015;89:149 54.
314. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal
carbon dioxide monitoring during cardiopulmonary resuscitation.
JAMA 1987;257:512 5.
315. Pokorna M, Necas E, Kratochvil J, Skripsky R, Andrlik M, Franek O.
A sudden increase in partial pressure end-tidal carbon dioxide(P(ET)CO(2)) at the moment of return of spontaneous circulation. J
Emerg Med 2010;38:614 21.
316. Lui Ct, Poon Km, Tsui Kl. Abrupt rise of end tidal carbon dioxide level
was a specific but non-sensitive marker of return of spontaneous
circulation in patient with out-of-hospital cardiac arrest.
Resuscitation 2016;104:53 8.
317. Sandroni C, Ristagno G. End-tidal CO2 to detect recovery of
spontaneous circulation during cardiopulmonary resuscitation: We
are not ready yet. Resuscitation 2016;104:A5 6.
318. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide andoutcome of out-of-hospital cardiac arrest. N Engl J Med
1997;337:301 6.
319. Sutton RM, French B, Meaney PA, et al. Physiologic monitoring of
CPR quality during adult cardiac arrest: A propensity-matchedcohort study. Resuscitation 2016;106:76 82.
320. Conseil francais de reanimation c, Societe francaise d’anesthesie
et de r, Societe francaise de c, et al. Guidelines for indications forthe use of extracorporeal life support in refractory cardiac arrest.
French Ministry of Health. Ann Fr Anesth Reanim 2009;28:
182 90.
321. Kolar M, Krizmaric M, Klemen P, Grmec S. Partial pressure of endtidal carbon dioxide successful predicts cardiopulmonary
resuscitation in the field: a prospective observational study. Crit
Care 2008;12:R115.
322. Poppe M, Stratil P, Clodi C, et al. Initial end-tidal carbon dioxide as apredictive factor for return of spontaneous circulation innonshockable out-of-hospital cardiac arrest patients: A
retrospective observational study. European Journal of
Anaesthesiology 2019;36:524 30.
323. Grmec S, Lah K, Tusek-Bunc K. Difference in end-tidal CO2
between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospitalsetting. Crit Care 2003;7:R139-R44.
324. Heradstveit BE, Sunde K, Sunde GA, Wentzel-Larsen T, Heltne JK.
Factors complicating interpretation of capnography during
advanced life support in cardiac arrest-A clinical retrospective study
in 575 patients. Resuscitation 2012;83:813 8.

148

RESUSCITATION 161 (2021) 115

325. Gazmuri RJ, Ayoub IM, Radhakrishnan J, Motl J, Upadhyaya MP.
Clinically plausible hyperventilation does not exert adverse
hemodynamic effects during CPR but markedly reduces end-tidal
PCO(2). Resuscitation 2012;83:259 64.
326. Grieco DL, L JB, Drouet A, et al. Intrathoracic Airway Closure
Impacts CO2 Signal and Delivered Ventilation during
Cardiopulmonary Resuscitation. Am J Respir Crit Care Med
2019;199:728 37.
327. Callaham M, Barton C, Matthay M. Effect of epinephrine on theability of end-tidal carbon dioxide readings to predict initialresuscitation from cardiac arrest. Crit Care Med 1992;20:337 43.
328. Hardig BM, Gotberg M, Rundgren M, et al. Physiologic effect of
repeated adrenaline (epinephrine) doses during cardiopulmonary
resuscitation in the cath lab setting: A randomised porcine study.
Resuscitation 2016;101:77 83.
329. Brinkrolf P, Borowski M, Metelmann C, Lukas RP, Pidde-Kullenberg
L, Bohn A. Predicting ROSC in out-of-hospital cardiac arrest using
expiratory carbon dioxide concentration: Is trend-detection insteadof absolute threshold values the key? Resuscitation 2018;122:
19 24.
330. Reynolds JC, Issa MS, T CN, et al. Prognostication with point-ofcare echocardiography during cardiac arrest: A systematic review.
Resuscitation 2020;152:56 68.
331. Huis In’ t Veld MA, Allison MG, Bostick DS, et al. Ultrasound use
during cardiopulmonary resuscitation is associated with delays inchest compressions. Resuscitation 2017;119:95-98.
332. Clattenburg EJ, Wroe P, Brown S, et al. Point-of-care ultrasounduse in patients with cardiac arrest is associated prolonged
cardiopulmonary resuscitation pauses: A prospective cohort study.
Resuscitation 2018;122:65 8.
333. Berg RA, Sorrell VL, Kern KB, et al. Magnetic resonance imaging
during untreated ventricular fibrillation reveals prompt rightventricular overdistention without left ventricular volume loss.
Circulation 2005;111:1136 40.
334. Querellou E, Leyral J, Brun C, et al. [In and out-of-hospital cardiac
arrest and echography: a review]. Ann Fr Anesth Reanim
2009;28:769 78.
335. Blanco P, Volpicelli G. Common pitfalls in point-of-care ultrasound:a practical guide for emergency and critical care physicians. Crit
Ultrasound J 2016;8:15.
336. Aagaard R, Granfeldt A, Botker MT, Mygind-Klausen T, Kirkegaard
H, Lofgren B. The Right Ventricle Is Dilated During Resuscitation
From Cardiac Arrest Caused by Hypovolemia: A Porcine
Ultrasound Study. Crit Care Med 2017;45:e963-e70.
337. Teran F. Resuscitative Cardiopulmonary Ultrasound andTransesophageal Echocardiography in the Emergency
Department. Emerg Med Clin North Am 2019;37:409 30.
338. Perkins GD, Lall R, Quinn T, et al. Mechanical versus manual chest
compression for out-of-hospital cardiac arrest (PARAMEDIC): a
pragmatic, cluster randomised controlled trial. Lancet
2015;385:947 55.
339. Rubertsson S, Lindgren E, Smekal D, et al. Mechanical chest
compressions and simultaneous defibrillation vs conventional
cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the
LINC randomized trial. JAMA 2014;311:53 61.
340. Hallstrom A, Rea TD, Sayre MR, et al. Manual chest compression vsuse of an automated chest compression device during resuscitation
following out-of-hospital cardiac arrest: a randomized trial. JAMA
2006;295:2620 8.
341. Wik L, Olsen JA, Persse D, et al. Manual vs. integrated automatic
load-distributing band CPR with equal survival after out of hospital
cardiac arrest. The randomized CIRC trial. Resuscitation
2014;85:741 8.
342. Lu XG, Kang X, Gong DB. [The clinical efficacy of Thumper modal
1007 cardiopulmonary resuscitation: a prospective randomized
control trial]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 2010;22:496 7.
343. Smekal D, Johansson J, Huzevka T, Rubertsson S. A pilot study ofmechanical chest compressions with the LUCAS device in
cardiopulmonary resuscitation. Resuscitation 2011;82:702 6.

151344. Dickinson ET, Verdile VP, Schneider RM, Salluzzo RF.
Effectiveness of mechanical versus manual chest compressions in
out-of-hospital cardiac arrest resuscitation: a pilot study. Am J
Emerg Med 1998;16:289 92.
345. Halperin HR, Tsitlik JE, Gelfand M, et al. A preliminary study ofcardiopulmonary resuscitation by circumferential compression of
the chest with use of a pneumatic vest. N Engl J Med 1993;329:
762 8.
346. Koster RW, Beenen LF, van der Boom EB, et al. Safety ofmechanical chest compression devices AutoPulse and LUCAS in
cardiac arrest: a randomized clinical trial for non-inferiority. Eur
Heart J 2017;38:3006 13.
347. Gao C, Chen Y, Peng H, Chen Y, Zhuang Y, Zhou S. Clinicalevaluation of the AutoPulse automated chest compression devicefor out-of-hospital cardiac arrest in the northern district of Shanghai.
China. Arch Med Sci 2016;12:563 70.
348. Liu M, Shuai Z, Ai J, et al. Mechanical chest compression with
LUCAS device does not improve clinical outcome in out-of-hospital
cardiac arrest patients: A systematic review and meta-analysis.
Medicine (Baltimore) 2019;98:e17550.
349. Zhu N, Chen Q, Jiang Z, et al. A meta-analysis of the resuscitative
effects of mechanical and manual chest compression in out-ofhospital cardiac arrest patients. Crit Care 2019;23:100.
350. Wang PL, Brooks SC. Mechanical versus manual chest
compressions for cardiac arrest. Cochrane Database Syst Rev
2018;8:CD007260.
351. Gates S, Quinn T, Deakin CD, Blair L, Couper K, Perkins GD.
Mechanical chest compression for out of hospital cardiac arrest:
Systematic review and meta-analysis. Resuscitation 2015;94:91 7.
352. Couper K, Yeung J, Nicholson T, Quinn T, Lall R, Perkins GD.
Mechanical chest compression devices at in-hospital cardiac arrest:
A systematic review and meta-analysis. Resuscitation 2016;103:24
31.
353. Khan SU, Lone AN, Talluri S, Khan MZ, Khan MZU, Kaluski E.
Efficacy and safety of mechanical versus manual compression in
cardiac arrest - A Bayesian network meta-analysis. Resuscitation
2018;130:182 8.
354. Li H, Wang D, Yu Y, Zhao X, Jing X. Mechanical versus manual
chest compressions for cardiac arrest: a systematic review andmeta-analysis. Scand J Trauma Resusc Emerg Med 2016;24:10.
355. Poole K, Couper K, Smyth MA, Yeung J, Perkins GD. Mechanical
CPR: Who? When? How?. Crit Care 2018;22:140.
356. Brouwer TF, Walker RG, Chapman FW, Koster RW. Association
Between Chest Compression Interruptions and Clinical Outcomesof Ventricular Fibrillation Out-of-Hospital Cardiac Arrest. Circulation
2015;132:1030 7.
357. Yost D, Phillips RH, Gonzales L, et al. Assessment of CPRinterruptions from transthoracic impedance during use of the
LUCAS mechanical chest compression system. Resuscitation
2012;83:961 5.
358. Levy M, Yost D, Walker RG, Scheunemann E, Mendive SR. A
quality improvement initiative to optimize use of a mechanical chest
compression device within a high-performance CPR approach toout-of-hospital cardiac arrest resuscitation. Resuscitation
2015;92:32 7.
359. Esibov A, Banville I, Chapman FW, Boomars R, Box M, Rubertsson
S. Mechanical chest compressions improved aspects of CPR in the
LINC trial. Resuscitation 2015;91:116 21.
360. Couper K, Velho RM, Quinn T, et al. Training approaches for the
deployment of a mechanical chest compression device: arandomised controlled manikin study. BMJ Open 2018;8:e019009.
361. Richardson ASC, Tonna JE, Nanjayya V, et al. Extracorporeal
cardiopulmonary resuscitation in adults. Interim guideline
consensus statement from the extracorporeal life support
organization. ASAIO J 2021;67(3):221 8, doi:http://dx.doi.org/
10.1097/MAT.0000000000001344.
362. Richardson AS, Schmidt M, Bailey M, Pellegrino VA, Rycus PT,
Pilcher DV. ECMO Cardio-Pulmonary Resuscitation (ECPR),RESUSCITATION 161 (2021) 115

trends in survival from an international multicentre cohort study over
12-years. Resuscitation 2017;112:34 40.
363. Hutin A, Abu-Habsa M, Burns B, et al. Early ECPR for out-of-hospital
cardiac arrest: Best practice in 2018. Resuscitation 2018;130:44 8.
364. Swol J, Belohlavek J, Brodie D, et al. Extracorporeal life support in
the emergency department: A narrative review for the emergency
physician. Resuscitation 2018;133:108 17.
365. Dennis M, Lal S, Forrest P, et al. In-Depth Extracorporeal
Cardiopulmonary Resuscitation in Adult Out-of-Hospital Cardiac
Arrest. Journal of the American Heart Association 2020;9:e016521.
366. Holmberg MJ, Geri G, Wiberg S, et al. Extracorporeal
cardiopulmonary resuscitation for cardiac arrest: A systematic
review. Resuscitation 2018;131:91 100.
367. Yannopoulos D, Bartos J, Raveendran G, et al. Advanced
reperfusion strategies for patients with out-of-hospital cardiac arrest
and refractory ventricular fibrillation (ARREST): a phase 2, single
centre, open-label, randomised controlled trial. Lancet
2020;396:1807 16.
368. Guglin M, Zucker MJ, Bazan VM, et al. Venoarterial ECMO for
Adults: JACC Scientific Expert Panel. J Am Coll Cardiol
2019;73:698 716.
369. Debaty G, Babaz V, Durand M, et al. Prognostic factors for
extracorporeal cardiopulmonary resuscitation recipients following
out-of-hospital refractory cardiac arrest. A systematic review andmeta-analysis. Resuscitation 2017;112:1 10.
370. Yu HY, Wang CH, Chi NH, et al. Effect of interplay between age andlow-flow duration on neurologic outcomes of extracorporeal
cardiopulmonary resuscitation. Intensive Care Med 2019;45:
44 54.
371. Dennis M, Zmudzki F, Burns B, et al. Cost effectiveness and qualityof life analysis of extracorporeal cardiopulmonary resuscitation(ECPR) for refractory cardiac arrest. Resuscitation 2019;139:
49 56.
372. Kawashima T, Uehara H, Miyagi N, et al. Impact of first documented
rhythm on cost-effectiveness of extracorporeal cardiopulmonary
resuscitation. Resuscitation 2019;140:74 80.
373. Bharmal MI, Venturini JM, Chua RFM, et al. Cost-utility of
extracorporeal cardiopulmonary resuscitation in patients withcardiac arrest. Resuscitation 2019;136:126 30.
374. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS
Guideline for the Management of Adult Patients With
Supraventricular Tachycardia: A Report of the American College of
Cardiology/American Heart Association Task Force on Clinical
Practice Guidelines and the Heart Rhythm Society. J Am Coll
Cardiol 2016;67:e27-e115.
375. Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC Guidelines for the
management of atrial fibrillation developed in collaboration with
EACTS. Eur Heart J 2016;37:2893 962.
376. January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS
Focused Update of the 2014 AHA/ACC/HRS Guideline for theManagement of Patients With Atrial Fibrillation: A Report of theAmerican College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines and the Heart Rhythm
Society. J Am Coll Cardiol 2019;74:104 32.
377. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With
Bradycardia and Cardiac Conduction Delay: A Report of theAmerican College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines and the Heart Rhythm
Society. J Am Coll Cardiol 2019;74:e51-e156.
378. Hindricks G, Potpara T, Dagres N, et al. 2020 ESC Guidelines for the
diagnosis and management of atrial fibrillation developed incollaboration with the European Association of Cardio-Thoracic
Surgery (EACTS). Eur Heart J 2020.
379. Ortiz M, Martin A, Arribas F, et al. Randomized comparison of
intravenous procainamide vs. intravenous amiodarone for the acutetreatment of tolerated wide QRS tachycardia: the PROCAMIO
study. Eur Heart J 2017;38:1329 35.

151

149

380. Bernheim A, Fatio R, Kiowski W, Weilenmann D, Rickli H, Rocca
HP. Atropine often results in complete atrioventricular block
or sinus arrest after cardiac transplantation: an unpredictable anddose-independent phenomenon. Transplantation 2004;77:
1181 5.
381. Roth A, Elkayam I, Shapira I, et al. Effectiveness of prehospitalsynchronous direct-current cardioversion for supraventriculartachyarrhythmias causing unstable hemodynamic states. Am J
Cardiol 2003;91:489 91.
382. Wittwer MR, Rajendran S, Kealley J, Arstall MA. A South Australianregistry of biphasic cardioversions of atrial arrhythmias: efficacy andpredictors of success. Heart Lung Circ 2015;24:342 7.
383. Reisinger J, Gstrein C, Winter T, et al. Optimization of initial energy
for cardioversion of atrial tachyarrhythmias with biphasic shocks.
Am J Emerg Med 2010;28:159 65.
384. Lown B. Electrical reversion of cardiac arrhythmias. Br Heart J
1967;29:469 89.
385. Deakin CD, Connelly S, Wharton R, Yuen HM. A comparison ofrectilinear and truncated exponential biphasic waveforms in elective
cardioversion of atrial fibrillation: a prospective randomized
controlled trial. Resuscitation 2013;84:286 91.
386. Schmidt AS, Lauridsen KG, Torp P, Bach LF, Rickers H, Lofgren B.
Maximum-fixed energy shocks for cardioverting atrial fibrillation.
Eur Heart J 2020;41:626 31.
387. Pinski SL, Sgarbossa EB, Ching E, Trohman RG. A comparison of
50-J versus 100-J shocks for direct-current cardioversion of atrial
flutter. Am Heart J 1999;137:439 42.
388. Kerber RE, Kienzle MG, Olshansky B, et al. Ventricular tachycardia
rate and morphology determine energy and current requirements
for transthoracic cardioversion. Circulation 1992;85:158 63.
389. Hedges JR, Syverud SA, Dalsey WC, Feero S, Easter R, Shultz B.
Prehospital trial of emergency transcutaneous cardiac pacing.
Circulation 1987;76:1337 43.
390. Barthell E, Troiano P, Olson D, Stueven HA, Hendley G. Prehospital
external cardiac pacing: a prospective, controlled clinical trial. Ann
Emerg Med 1988;17:1221 6.
391. Cummins RO, Graves JR, Larsen MP, et al. Out-of-hospitaltranscutaneous pacing by emergency medical technicians inpatients with asystolic cardiac arrest. N Engl J Med 1993;328:
1377 82.
392. Ornato JP, Peberdy MA. The mystery of bradyasystole during
cardiac arrest. Ann Emerg Med 1996;27:576 87.
393. Niemann JT, Adomian GE, Garner D, Rosborough JP. Endocardial
and transcutaneous cardiac pacing, calcium chloride, andepinephrine in postcountershock asystole and bradycardias. Crit
Care Med 1985;13:699 704.
394. Quan L, Graves JR, Kinder DR, Horan S, Cummins RO.
Transcutaneous cardiac pacing in the treatment of out-of-hospital
pediatric cardiac arrests. Ann Emerg Med 1992;21:905 9.
395. Dalsey WC, Syverud SA, Hedges JR. Emergency department useof transcutaneous pacing for cardiac arrests. Crit Care Med
1985;13:399 401.
396. Knowlton AA, Falk RH. External cardiac pacing during in-hospital
cardiac arrest. Am J Cardiol 1986;57:1295 8.
397. Ornato JP, Carveth WL, Windle JR. Pacemaker insertion forprehospital bradyasystolic cardiac arrest. Ann Emerg Med
1984;13:101 3.
398. Chan L, Reid C, Taylor B. Effect of three emergency pacing
modalities on cardiac output in cardiac arrest due to ventricular
asystole. Resuscitation 2002;52:117 9.
399. Eich C, Bleckmann A, Schwarz SK. Percussion pacing–an almost
forgotten procedure for haemodynamically unstable bradycardias?
A report of three case studies and review of the literature. Br J
Anaesth 2007;98:429 33.
400. Appelboam A, Reuben A, Mann C, et al. Postural modification to thestandard Valsalva manoeuvre for emergency treatment ofsupraventricular tachycardias (REVERT): a randomised controlled
trial. Lancet 2015;386:1747 53.

150

RESUSCITATION 161 (2021) 115

401. Smith GD, Fry MM, Taylor D, Morgans A, Cantwell K. Effectivenessof the Valsalva Manoeuvre for reversion of supraventriculartachycardia. Cochrane Database Syst Rev 2015;CD009502.
402. Smith G, Morgans A, Boyle M. Use of the Valsalva manoeuvre in theprehospital setting: a review of the literature. Emergency Medicine
2009;26:8 10.
403. Lim SH, Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison oftreatment of supraventricular tachycardia by Valsalva maneuverand carotid sinus massage. Ann Emerg Med 1998;31:30 5.
404. Brady Jr. WJ, DeBehnke DJ, Wickman LL, Lindbeck G. Treatment ofout-of-hospital supraventricular tachycardia: adenosine vsverapamil. Acad Emerg Med 1996;3:574 85.
405. Glatter K, Cheng JPD, et al. Electrophysiologic effects of adenosine
in patients with supraventricular tachycardia. Circulation
1999;99:1034 40.
406. Delaney B, Loy J, Kelly AM. The relative efficacy of adenosine
versus verapamil for the treatment of stable paroxysmal
supraventricular tachycardia in adults: a meta-analysis. Eur J
Emerg Med 2011;18:148 52.
407. Van Gelder IC, Rienstra M, Crijns HJ, Olshansky B. Rate control inatrial fibrillation. Lancet 2016;388:818 28.
408. Dougherty AH, Jackman WM, Naccarelli GV, Friday KJ, Dias VC.
Acute conversion of paroxysmal supraventricular tachycardia withintravenous diltiazem: IV Diltiazem Study Group. Am J Cardiol
1992;70:587 92.
409. Hood MA, Smith WM. Adenosine versus verapamil in the treatmentof supraventricular tachycardia: a randomized double-crossover
trial. Am Heart J 1992;123:1543 9.
410. Gupta A, Naik A, Vora A, Lokhandwala Y. Comparison of efficacy of
intravenous diltiazem and esmolol in terminating supraventriculartachycardia. J Assoc Physicians India 1999;47:969 72.
411. Lim SH, Anantharaman V, Teo WS, Chan YH. Slow infusion of
calcium channel blockers compared with intravenous adenosine in
the emergency treatment of supraventricular tachycardia.
Resuscitation 2009;80:523 8.
412. Das G, Tschida V, Gray R, et al. Efficacy of esmolol in the treatment
and transfer of patients with supraventricular tachyarrhythmias toalternate oral antiarrhythmic agents. J Clin Pharmacol 1988;28:
746 50.
413. Amsterdam EA, Kulcyski J, Ridgeway MG. Efficacy of
cardioselective beta-adrenergic blockade with intravenously
administered metoprolol in the treatment of supraventriculartachyarrhythmias. J Clin Pharmacol 1991;31:714 8.
414. Brubaker S, Long B, Koyfman A. Alternative Treatment Options for
Atrioventricular-Nodal-Reentry Tachycardia: An Emergency
Medicine Review. J Emerg Med 2018;54:198 206.
415. Gorgels AP, van den Dool A, Hofs A, et al. Comparison ofprocainamide and lidocaine in terminating sustained monomorphic
ventricular tachycardia. Am J Cardiol 1996;78:43 6.
416. Scheinman MM, Levine JH, Cannom DS, et al. Dose-ranging
study of intravenous amiodarone in patients with life- threatening
ventricular tachyarrhythmias. The Intravenous Amiodarone
Multicenter
Investigators
Group.
Circulation
1995;92:
3264 72.
417. Levine JH, Massumi A, Scheinman MM, et al. Intravenous
amiodarone for recurrent sustained hypotensive ventriculartachyarrhythmias. Intravenous Amiodarone Multicenter Trial
Group. J Am Coll Cardiol 1996;27:67 75.
418. Tzivoni D, Banai S, Schuger C, et al. Treatment of torsade depointes with magnesium sulfate. Circulation 1988;77:392 7.
419. Manara AR, Dominguez-Gil B, Perez-Villares JM, Soar J. Whatfollows refractory cardiac arrest: Death, extra-corporeal
cardiopulmonary resuscitation (E-CPR), or uncontrolled donation
after circulatory death? Resuscitation 2016;108:A3 5.
420. Thuong M, Ruiz A, Evrard P, et al. New classification of donation
after circulatory death donors definitions and terminology. Transpl
Int 2016;29:749 59.

151421. Champigneulle B, Fieux F, Cheisson G, et al. French survey of thefirst three-years of liver transplantation activity from uncontrolled
donors deceased after cardiac death. Anaesth Crit Care Pain Med
2015;34:35 9.
422. Dupriez F, De Pauw L, Darius T, et al. Fourteen years of experiencein uncontrolled organ donation after cardio-circulatory death.
Transplantation Proceedings 2014;46:3134 7.
423. Fieux F, Losser MR, Bourgeois E, et al. Kidney retrieval after sudden
out of hospital refractory cardiac arrest: a cohort of uncontrolled nonheart beating donors. Crit Care 2009;13:R141.
424. Fondevila C, Hessheimer AJ, Flores E, et al. Applicability andresults of Maastricht type 2 donation after cardiac death livertransplantation. Am J Transplant 2012;12:162 70.
425. Gamez P, Cordoba M, Ussetti P, et al. Lung transplantation fromout-of-hospital non-heart-beating lung donors. one-year experienceand results. J Heart Lung Transplant 2005;24:1098 102.
426. Mateos-Rodriguez AA, Navalpotro-Pascual JM, Del Rio Gallegos F,
Andres-Belmonte A. Out-hospital donors after cardiac death in
Madrid, Spain: a 5-year review. Australasian emergency nursing
journal : AENJ 2012;15:164 9.
427. Ortega-Deballon I, Hornby L, Shemie SD. Protocols for uncontrolled
donation after circulatory death: a systematic review of internationalguidelines, practices and transplant outcomes. Crit Care
2015;19:268.
428. Peters-Sengers H, Homan van der Heide JJ, Heemskerk MBA, et al.
Similar 5-Year Estimated Glomerular Filtration Rate Between
Kidney Transplants From Uncontrolled and Controlled Donors After
Circulatory Death-A Dutch Cohort Study. Transplantation
2017;101:1144 51.
429. Mateos-Rodríguez A, Pardillos-Ferrer L, Navalpotro-Pascual JM,
Barba-Alonso C, Martin-Maldonado ME, Andrés-Belmonte A.
Kidney transplant function using organs from non-heart-beating
donors maintained by mechanical chest compressions.
Resuscitation 2010;81:904 7.
430. Sanchez-Fructuoso AI, Marques M, Prats D, et al. Victims of cardiac
arrest occurring outside the hospital: a source of transplantable
kidneys. Ann Intern Med 2006;145:157 64.
431. Minambres E, Rubio JJ, Coll E, Dominguez-Gil B. Donation after
circulatory death and its expansion in Spain. Curr Opin Organ
Transplant 2018;23:120 9.
432. West S, Soar J, Callaway CW. The viability of transplanting organs
from donors who underwent cardiopulmonary resuscitation: A
systematic review. Resuscitation 2016;108:27 33.
433. Dominguez-Gil B, Duranteau J, Mateos A, et al. Uncontrolled
donation after circulatory death: European practices andrecommendations for the development and optimization of aneffective programme. Transpl Int 2016;29:842 59.
434. Dalle Ave AL, Bernat JL. Uncontrolled Donation After Circulatory
Determination of Death: A Systematic Ethical Analysis. J Intensive
Care Med 2018;33:624 34.
435. Molina M, Dominguez-Gil B, Perez-Villares JM, Andres A.
Uncontrolled donation after circulatory death: ethics ofimplementation. Curr Opin Organ Transplant 2019;24:358 63.
436. Gordon L, Pasquier M, Brugger H, Paal P. Autoresuscitation(Lazarus phenomenon) after termination of cardiopulmonary
resuscitation - a scoping review. Scand J Trauma Resusc Emerg
Med 2020;28:14.
437. Bruce CM, Reed MJ, MacDougall M. Are the public ready for organ
donation after out of hospital cardiac arrest? Emergency Medicine
2013;30:226 31.
438. Joffe AR, Carcillo J, Anton N, et al. Donation after cardiocirculatory
death: a call for a moratorium pending full public disclosure and fully
informed consent. Philos Ethics Humanit Med 2011;6:17.
439. Rodriguez-Arias D, Tortosa JC, Burant CJ, Aubert P, Aulisio MP,
Youngner SJ. One or two types of death? Attitudes of healthprofessionals towards brain death and donation after circulatory
death in three countries. Med Health Care Philos 2013;16:457 67.

RESUSCITATION 161 (2021) 115

440. Manara A, Shemie SD, Large S, et al. Maintaining the permanence
principle for death during in situ normothermic regional perfusion for
donation after circulatory death organ recovery: A United Kingdom
and Canadian proposal. Am J Transplant 2020;20:2017 25.
441. Mentzelopoulos SD, Couper K, Van de Voorde P, et al. Ethics ofresuscitation and end of life decisions. Resuscitation 2021.
442. Bleijenberg E, Koster RW, de Vries H, Beesems SG. The impact of
post-resuscitation feedback for paramedics on the quality ofcardiopulmonary resuscitation. Resuscitation 2017;110:1 5.
443. Couper K, Kimani PK, Davies RP, et al. An evaluation of threemethods of in-hospital cardiac arrest educational debriefing: The

151

151

cardiopulmonary resuscitation debriefing study. Resuscitation
2016;105:130 7.
444. Edelson DP, Litzinger B, Arora V, et al. Improving in-hospital cardiac
arrest process and outcomes with performance debriefing. Arch
Intern Med 2008;168:1063 9.
445. Wolfe H, Zebuhr C, Topjian AA, et al. Interdisciplinary ICU cardiac
arrest debriefing improves survival outcomes*. Crit Care Med
2014;42:1688 95.
446. Couper K, Perkins GD. Debriefing after resuscitation. Curr Opin Crit
Care 2013;19:188 94.