European Resuscitation Council

Guidelines for Resuscitation

October 2015
Adina Blejuc
Alexandru Caragea
Cristian Pristavu

Coordonatori: Prof. Dr. Ioana Grigora

Dr. Irina Ristescu
 Prevention of in-hospital cardiac arrest
Provide care for patients who are critically ill or at risk of clinical deterioration in
appropriate areas, with the level of care provided matched to the level of patient sickness
Critically ill patients need regular observations: each patient should have a documented
plan for vital signs monitoring that identifies which variables need to be measured and the
frequency of measurement
Use a track and trigger system (early warning scores) Call for help

Traditional CA Teams
Medical emergency team
Training of first responders
All healthcare professionals should be able to recognise cardiac arrest, call for help
and start CPR. Staff should do what they have been trained to do.

Hospital staff who attend a cardiac arrest may have different levels of skill to manage
the airway, breathing and circulation. Rescuers must undertake only the skills in
which they are trained and competent.

Continued emphasis on minimally interrupted high-quality chest compressions

throughout any ALS intervention: chest compressions are paused briefly only to
enable specific interventions. This includes minimising interruptions in chest
compressions for less than 5 s to attempt defibrillation

The routine use of mechanical chest compression devices is not recommended, but
they are a reasonable alternative in situations where sustained high-quality manual
chest compressions are impractical or compromise provider safety.
There is a new section on monitoring during ALS with an increased emphasis on the
use of waveform capnography to confirm and continually monitor tracheal tube
placement, quality of CPR and to provide an early indication of return of
spontaneous circulation (ROSC)

When available for use by trained clinicians, ultrasound may be of use in assisting
with diagnosis and treatment of potentially reversible causes of cardiac arrest

Absence of cardiac motion on sonography during resuscitation of patients in

cardiac arrest is highly predictive of death although sensitivity and specificity has not
been reported

Cerebral oximetry using near-infrared spectroscopy measures regional cerebral

oxygen saturation (rSO2) non-invasively. This remains an emerging technology that
is feasible during CPR. Its role in guiding CPR interventions including
prognostication during and after CPR is yet to be established
Keeping the focus on the use of self-adhesive pads for defibrillation and a
defibrillation strategy to minimise the preshock pause, although we recognise that
defibrillator paddles are used in some settings.

There are a variety of approaches to airway management during CPR and a stepwise
approach based on patient factors and the skills of the rescuer is recommended

No RCTs have shown that tracheal intubation increases survival after cardiac arrest.
To avoid any interruptions in chest compressions, the intubation attempt may be
deferred until ROSC

In one observational study of patients receiving 100% inspired oxygen via a

trachealtube during CPR, a higher measured PaO2 value during CPR was associated
with ROSC and hospital admission
Several recent observational studies and a meta-analysis have documented better
outcomes with use of bag-mask ventilation compared with more advanced airways
(SGA or tracheal tube). However, these observation studies are subject to
significant bias caused by confounders such as advanced airways not being required
in those patients who achieve ROSC and awaken early.

Until further data are available, passive oxygen delivery without ventilation is not
recommended for routine use during CPR.

The recommendations for drug therapy during CPR have not changed, but there is
greater equipoise concerning the role of drugs in improving outcomes from cardiac
arrest.

The use of adrenaline has been shown to increase ROSC but not survival to
discharge. Furthermore there is a possibility that it causes worse long-term
neurological survival
Our current recommendation is to continue the use of adrenaline during CPR as
for Guidelines 2010. We have considered the benefit in short-term outcomes
(ROSC and admission to hospital) and our uncertainty about the benefit or harm
on survival to discharge and neurological outcome given the limitations of the
observational studies. We have decided not to change current practice until there
is high-quality data on longterm outcomes.

We suggest vasopressin should not be used in cardiac arrest instead of adrenaline.

Those healthcare professionals working in systems that already use vasopressin
may continue to do so because there is no evidence of harm from using
vasopressin when compared to adrenaline.

No anti-arrhythmic drug given during human cardiac arrest has been shown to
increase survival to hospital discharge, although amiodarone has been shown to
increase survival to hospital admission
The best treatment of acidaemia in cardiac arrest is CPR. Consider sodium
bicarbonate for:
life-threatening hyperkalaemia
cardiac arrest associated with hyperkalaemia
tricyclic overdose.

The interventions that unquestionably contribute to improved survival after

cardiac arrest are prompt and effective bystander basic life support (BLS),
uninterrupted, high-quality chest compressions and early defibrillation for
VF/pVT

It is generally accepted that asystole for more than 20 min in the absence of a
reversible cause and with ongoing ALS constitutes a reasonable ground for
stopping further resuscitation attempts
Cardiac arrest in special
circumstances
 The following guidelines for resuscitation in
special circumstances are divided into three
parts:
1. Special causes - potentially reversible causes of cardiac
arrest called the 4Hs and 4Ts:
Hypoxia;
Hypo-/hyperkalaemia and other electrolyte disorders;
Hypo-/hyperthermia;
Hypovolaemia;
Tension pneumothorax;
Tamponade (cardiac);
Thrombosis (coronary and pulmonary);
Toxins (poisoning)
2. Special environments
3. Special patients with specific conditions and those with
certain long-term comorbidities
 A SPECIAL CAUSES
Hypoxia
If breathing is completely prevented by airway
obstruction or apnoea, consciousness will be lost when
SaO2 reaches about 60% - 1-2 min
PEA will occur in 311 min
Asystole will ensue several minutes later
Effective ventilation with supplementary oxygen, not
just CPR
Survival after cardiac arrest from asphyxia is rare and
most survivors sustain severe neurological injury
 Hyperkalaemia - serum potassium concentration higher
than 5.5 mmol/L
impaired excretion by the kidneys, drugs or increased
potassium release from cells and metabolic acidosis
weakness progressing to flaccid paralysis, paraesthesia, or
depressed deep tendon reflexes
most patients appear to show ECG abnormalities at a
serum potassium concentration higher than 6.7 mmol/L
five key treatment strategies
cardiac protection;
shifting potassium into cells;
removing potassium from the body;
monitoring serum potassium and blood glucose;
prevention of recurrence
modifications to cardiopulmonary resuscitation
Confirm hyperkalaemia
Protect the heart
Shift potassium into cells
Give sodium bicarbonate 50 mmol IV by rapid
injection (if severe acidosis or renal failure)
Remove potassium from body
 Hypokalaemia - serum potassium level <3.5
mmol/L
fatigue, weakness, leg cramps, constipation
gradual replacement of potassium
in an emergency, intravenous potassium is required; the
maximum recommended IV dose of potassium is 20
mmol/h, but more rapid infusion (e.g. 2 mmol/min for 10
min, followed by 10 mmol over 510 min) is indicated for
unstable arrhythmias when cardiac arrest is imminent
continuous ECG monitoring; repeated sampling of serum
potassium levels.
magnesium is important for potassium uptake and for
the maintenance of intracellular potassium values,
particularly in the myocardium. Repletion of magnesium
stores will facilitate more rapid correction of
hypokalaemia and is recommended in severe cases of
hypokalaemia
 Hypovolaemia usually results from a reduced
intravascular volume (i.e. haemorrhage), but
relative hypovolaemia may also occur in patients
with severe vasodilation (e.g. anaphylaxis, sepsis)

Hypovolaemia from mediator-activated

vasodilation and increased capillary permeability is
a major factor causing cardiac arrest in severe
anaphylaxis
Hypovolaemia from blood loss, is a leading cause
of death in traumatic cardiac arrest
 Tension pneumothorax
trauma, asthma and other respiratory disease, but can also
be iatrogenic following invasive procedures, e.g. attempts
at central venous catheter insertion
haemodynamic compromise (hypotension or cardiac
arrest) in conjunction with signs suggestive of a
pneumothorax (preceding respiratory distress, hypoxia,
absent unilateral breath sounds on auscultation,
subcutaneous emphysema) and mediastinal shift (tracheal
deviation and jugular venous distention)
Needle decompression
Thoracostomy
Tamponade
Thoracotomy
Ultrasound-guided pericardiocentesis
 Thrombosis
Pulmonary embolism
Cardiac arrest from acute pulmonary embolism is the most serious
clinical presentation of venous thromboembolism, in most cases
originating from a deep venous thrombosis
Sudden onset of dyspnoea, pleuritic or substernal chest pain, cough,
haemoptysis, syncope and signs of DVT in particular (unilateral low
extremity swelling)
Previous pulmonary embolism or DVT, surgery or immobilisation
within the past four weeks, active cancer
If a 12-lead ECG can be obtained before onset of cardiac arrest,
changes indicative of right ventricular strain may be found: inversion
of T waves in leads V1V4, QR pattern in V1, S1 Q3 T3 pattern,
incomplete or complete RBBB
Cardiac arrest commonly presents as PEA
Low ETCO2 readings while performing high quality chest
compressions
Emergency echocardiography: enlarged right ventricle with a
flattened interventricular septum
Consider administration of fibrinolytic therapy when acute
pulmonary embolism is a known or suspected cause of cardiac arrest;
ongoing CPR is not a contraindication to fibrinolysis; continue CPR
for at least 6090 min before terminating resuscitation attempts
 Toxins
Prevention of cardiac arrest
Early tracheal intubation of unconscious patients may decrease the risk of aspiration
Drug-induced hypotension usually responds to IV fluids, but occasionally vasopressor
support is required
Measure electrolytes (particularly potassium), blood glucose and arterial blood gases

Modifications to resuscitation
Avoid mouth-to-mouth breathing
Treat life-threatening tachyarrhythmias with cardioversion, this includes correction of
electrolyte and acid-base abnormalities
Measure the patients temperature because hypo- or hyperthermia may occur after drug
overdose
Be prepared to continue resuscitation for a prolonged period, particularly in young
patients, as the poison may be metabolised or excreted during extended resuscitation
measures.

Specific therapeutic measures

Decontamination: routine use of gastric lavage for gastrointestinal decontamination is
no longer recommended; the preferred method is activated charcoal it is most
effective if given within 1 h of the time of the ingestion; avoid routine administration
of laxatives (cathartics) and do not use emetics (e.g. ipecac syrup)
Enhanced elimination: multiple-dose activated charcoal - initial dose of 50100 g;
urinary alkalinisation (urine pH 7.5) involves an IV sodium bicarbonate infusion;
haemodialysis - in case of hypotension, use continuous veno-venous hemofiltration
(CVVH) or continuous veno-venous haemodialysis (CVVHD) alternatively
Benzodiazepines
Flumazenil, a competitive antagonist of benzodiazepines, may be
used for reversal of benzodiazepine sedation when there is no
history or risk of seizures - not recommended the routine use of
flumazenil in the comatose overdose patient
Opioids
In severe respiratory depression there are fewer adverse events when
airway opening, oxygen administration and ventilation are carried
out before giving naloxone
The initial doses of naloxone are 0.42 mg IV, IO, IM or SC, and
may be repeated every 23 min. Additional doses may be needed
every 2060 min
Acute withdrawal from opioids produces a state of sympathetic
excess and may cause complications such as pulmonary oedema,
ventricular arrhythmias and severe agitation
In respiratory arrest there is good evidence for the use of naloxone
Local anaesthetics
Severe agitation, loss of consciousness, seizures, bradycardia,
asystole or ventricular tachyarrhythmias
Initial intravenous bolus injection of 20% lipid emulsion 1.5 mL/kg
over 1 min followed by an infusion at 15 mL/kg/h. Give up to a
maximum of two repeat boluses at 5-min intervals and continue
until the patient is stable or has received up to a maximum
cumulative dose of 12 mL/kg of lipid emulsion
Beta-blockers
Glucagon (50150 mcg/kg), high-dose insulin and glucose, lipid
emulsions, phosphodiesterase inhibitors, extracorporeal and
intra-aortic balloon pump support and calcium salts
Calcium channel blockers
calcium chloride 10% in boluses of 20 mL or equivalent dose of
calcium gluconate every 25 min in severe bradycardia or
hypotension followed by an infusion if needed
Haemodynamic instability may respond to high doses of insulin
(1 unit/kg followed by an infusion of 0.52.0 units/kg/h) given
with glucose supplementation and electrolyte monitoring in
addition to standard treatments including fluids and vasopressors
Digoxin
Specific antidote therapy with digoxin-specific antibody
fragments (digoxin-Fab) should be used if there are arrhythmias
associated with haemodynamic instability
In a cardiac arrest, consider administration of 2 up to 10 vials IV
over 30 min
 B SPECIAL ENVIRONMENTS
Perioperative cardiac arrest
May be caused by the underlying condition being treated,
physiological effects of the surgery, anaesthetic drugs and fluids,
complications relating to existing comorbidities, or adverse events
The incidence of perioperative cardiac arrest during general
anaesthesia (GA) is higher than that of regional anaesthesia (RA)
Overall causes of cardiac arrest: hypovolaemia (e.g. bleeding), cardiac-
related, drug-induced (e.g. muscle relaxants), anaesthesia related,
airway loss, ventilation failure, anaphylaxis (drugs, blood products).
Management: if cardiac arrest is a strong possibility, apply self-
adhesive defibrillation electrodes before induction of anaesthesia,
ensure adequate venous access and prepare resuscitation drugs and
fluids. Use fluid warmers and forced air warmers to limit
perioperative hypothermia and monitor the patients temperature.
Adjust the position and height of the operating table or trolley to
optimise delivery of chest compressions. CPR is optimal in the supine
position, but is possible in patients who are prone and where
immediate turning to a supine position is not possible
 Anaphylaxis - Neuromuscular blocking drugs are the commonest
cause; Adrenaline is the most effective drug
Systemic toxicity of local anaesthetics following inadvertent
intravascular injection: cardiovascular collapse, usually within 15 min
of injection, but onset may range from 30 s to as long as 60 min -
significant hypotension, dysrhythmias, and seizures.
IV lipid therapy
Stop injecting the LA
Secure and maintain the airway and, if necessary, intubate.
Give 100% oxygen and ensure adequate ventilation (hyperventilation may
help by increasing plasma pH in the presence of metabolic acidosis).
Control seizures using a benzodiazepine, propofol
Ventricular fibrillation
call for a defibrillator
if one is not immediately available, apply a precordial thump. If that is
unsuccessful, give chest compressions and ventilation until the
defibrillator arrives
most common reversible causes: hypoxaemia and hypovolaemia
Asystole/extreme bradycardia.
Stop any surgical activity likely to be causing excessive vagal activity
give 0.5 mg atropine IV
Start CPR
Exclude a completely straight line
 Pulseless electrical activity the onset might not be so obvious loss
of the pulse oximeter signal and very low end-tidal CO2-values
Start CPR
Give fluid unless you are certain that the intravascular volume is
adequate
Stop administration of the anaesthetic
Give a smaller dose (e.g. 1 mcg/kg) of adrenaline, or another
vasopressor initially; if this fails to restore the cardiac output, increase
the dose while continuing to perform chest compressions and
ventilation.
in patients with invasive arterial monitoring, aim for a diastolic blood
pressure >25 mmHg titrating it to this level (after chest
compressions are optimised) by administration of a vasopressor, if
necessary.
An end-tidal carbon dioxide (ETCO2) value<1.4 kPa/10 mmHg
suggests a low cardiac output and rescuers may be able to adjust their
technique to optimise this variable. An abrupt sustained increase to a
normal value (4.75.4 kPa/3540 mmHg) or even higher may be an
indicator of ROSC. Optimise CPR to achieve an ETCO2 >2.7
kPa/20 mmHg, while ventilating the lungs at about 10 breaths/min,
with only minimal chest rise
Stop operative surgery unless it is addressing a reversible cause of the
cardiac arrest
 C SPECIAL PATIENTS
Asthma
Cardiac arrest in a person with asthma is often a terminal
event after a period of hypoxaemia
severe bronchospasm and mucous plugging
leading to asphyxia
cardiac arrhythmias caused by hypoxia or
stimulant drugs (e.g. beta-adrenergic agonists,
aminophylline) or electrolyte abnormalities
dynamic hyperinflation - auto-PEEP can occur in
mechanically ventilated asthmatics
tension pneumothorax (often bilateral).
 Prevention of cardiac arrest
Patients with SpO2< 92% or with features of life-threatening
asthma are at risk of hypercapnia and require arterial blood gas
measurement
Use a concentration of inspired oxygen that will achieve an
SpO2 9498%.
Inhaled beta-2 agonists are first line drugs in patients with an
acute asthma attack Salbutamol 5 mg nebulised, repeated doses
every 1520 min are often needed; high-flow oxygen (at least 6 L
min1). Nebulised adrenaline does not provide additional
benefit over and above nebulised beta-2 agonists in acute asthma
Inhaled magnesium sulphate is currently not recommended for
the treatment of acute asthma
Give a single dose of IV magnesium sulphate to patients with
acute severe asthma (PEF < 50% best or predicted) who have
not had a good initial response to inhaled bronchodilator therapy
Early use of systemic corticosteroids for acute asthma in the
emergency department significantly reduces hospital admission
rates
 Intravenous beta-2 agonists should be reserved for those
patients in who inhaled therapy cannot be used reliably . A
Cochrane review of intravenous beta-2 agonists compared with
nebulised beta-2 agonists found no evidence of benefit and some
evidence of increased side effects compared with inhaled
treatment. Salbutamol may be given as either a slow IV injection
(250 mcg IV slowly) or continuous infusion of 320 mcg/min.
A Cochrane review of intravenous aminophylline found no
evidence of benefit and a higher incidence of adverse effects
(tachycardia, vomiting) compared with standard care alone
loading dose of 5 mg/kg over 2030 min (unless on maintenance
therapy), followed by an infusion of 500700 mcg/kg/h
If there is evidence of hypovolaemia or dehydration, give IV
crystalloids. Beta-2 agonists and steroids may induce
hypokalaemia, which should be monitored and corrected with
electrolyte supplements as required
Sometimes it may be difficult to distinguish severe life-threatening
asthma from anaphylaxis. Treat patients presenting with severe
asthma-like symptoms, but without pre-existing pulmonary
disease (asthma, COPD), as if the cause was anaphylaxis. In these
circumstances, administration of adrenaline 0.5 mg IM
 Consider rapid sequence induction and tracheal
intubation if, despite efforts to optimise drug therapy, the
patient has:
a decreasing conscious level, or coma
persisting or worsening hypoxaemia
deteriorating respiratory acidosis, despite intensive therapy
severe agitation, confusion and fighting against the oxygen
mask(clinical signs of hypoxaemia)
progressive exhaustion
respiratory or cardiac arrest
Elevation of the PCO2 alone does not indicate the need
for tracheal intubation
Non-invasive ventilation (NIV) role in patients with
severe acute asthma is uncertain. There is insufficient
evidence to recommend its routine use in asthma
Modifications to standard ALS guidelines include
considering the need for early tracheal intubation
 Respiratory rates of 810 breaths per minute and a tidal
volume required for a normal chest rise during CPR should
minimise dynamic hyperinflation of the lungs (air trapping)
In mechanically ventilated severe asthmatics, increasing the
expiratory time (achieved by reducing the respiratory rate)
provides only moderate gains in terms of reduced gas trapping
when a minute volume of less than 10 L/min is used
If dynamic hyperinflation of the lungs is suspected during
CPR, compression of the chest while disconnecting tracheal
tube may relieve air trapping
Dynamic hyperinflation increases transthoracic impedance, but
modern impedance-compensated biphasic defibrillation wave-
forms are no less effective in patients with a higher impedance;
consider increasing defibrillation energy if the first shock is
unsuccessful and a manual defibrillator is available
Post-resuscitation Care
 Post-cardiac arrest syndrome

brain injury cause of death in: - 2/3 of OHCA

- 25% of IHCA
myocardial dysfunction the major cause of death in the first 3
days
systemic ischaemia/reperfusion response - activates immune
and coagulation pathways - multiple organ failure
persistent precipitating pathology

- intravascular volume depletion

- vasodilation
Many features in common with sepsis: - endothelial injury
- abnormalities of the microcirculation
 Changes in post-resuscitation care since 2010

1. A greater emphasis on the need for urgent coronary catheterisation and

percutaneous coronary intervention (PCI) following out-of-hospital cardiac
arrest of likely cardiac cause.

2. Targeted temperature management remains important but there is now an

option to target a temperature of 36C instead of the previously recommended
3234C.

3. Prognostication using a multimodal strategy and allowing sufficient time

for neurological recovery and to enable sedatives to be cleared

4. A novel section has been added which addresses rehabilitation after survival
from a cardiac arrest.
 1. Coronary reperfusion
- Prevalence of an acute coronary artery lesion: 59% to 71% in OHCA
patients without an obvious non-cardiac aetiology.
- The invasive management of these patients is controversial because of the
lack of specific evidence and significant implications on use of resources.
A. Percutaneous coronary intervention B. Percutaneous coronary intervention
following ROSC with ST-elevation following ROSC without ST-elevation
The absence of STE may also be
- ST segment elevation (STE) associated with ACS
- left bundle branch block (LBBB)
PCI should be considered as soon as
possible (less than 2 h) in non-STE patients
if they are haemodynamically unstable and
80% will have an acute coronary considering:
lesion!!!

- patient age
emergent cardiac catheterisation - duration of CPR
laboratory evaluation - cardiac rhythm
(and immediate PCI if required) - neurological status upon hospital arrival
- perceived likelihood of cardiac aetiology
 2. Targeted Temperature Management (TTM)
- treatment recommendations -
Maintain a constant, target temperature between 32C and 36C for those
patients in whom temperature control is used (strong recommendation,
moderate-quality evidence)
Whether certain subpopulations of cardiac arrest patients may benefit from
lower (3234C) or higher (36C) temperatures remains unknown
TTM is recommended for adults after OHCA with an initial shockable
rhythm who remain unresponsive after ROSC (strong recommendation, low-
quality evidence)
TTM is suggested for adults after OHCA with an initial non-shockable
rhythm who remain unresponsive after ROSC (weak recommendation, very
low-quality evidence)
TTM is suggested for adults after IHCA with any initial rhythm who
remain unresponsive after ROSC (weak recommendation,very low-quality
evidence)
If TTM is used, it is suggested that the duration is at least 24(weak
recommendation, very low-quality evidence)
 2. Targeted Temperature Management (TTM)
a. When?
- prehospital cooling using a rapid infusion of large volumes of cold
intravenous fluid immediately after ROSC is not recommended
- infuse cold intravenous fluid when patients are well monitored and a
lower target temperature (e.g., 33C) is the goal

b. How?
- in three phases: induction, maintenance and rewarming
- external and/or internal cooling techniques: simple ice packs, cooling
blankets, transnasal evaporative cooling, intravascular heat exchanger, extracorporeal
circulation.

c. Contraindications
- severe systemic infection
- pre-existing medical coagulopathy
- fibrinolytic therapy is not a contraindication to mild induced hypothermia
 3. Prognostication

1. Why?

Withdrawal of life sustaining therapy (WLST) is the most frequent cause of

death (approximately 50%) in patients with a prognosticated poor
neurological outcome

Ideally, when predicting a poor outcome the false positive rate (FPR)
should be zero.

TTM and sedatives or neuromuscular blocking drugs may potentially

interfere with prognostication indices, especially those based on clinical
examination.
 3. Prognostication
2. How?
Clinical examination poor outcome if:
Bilateral absence of pupillary light reflex at 72 h from ROSC.
Bilateral absence of corneal reflex at 72 h from ROSC.
Absence or extensor motor response to pain at 72 h from ROSC in non-TTM
treated patients.
Presence of a status myoclonus starting within 48 h from ROSC.

Electrophysiology - short-latency somatosensory evoked potentials (SSEPs)

In TTM-treated patients, bilateral absence of the SSEP wave is very accurate in
predicting poor outcome both during mild induced hypothermia and after
rewarming criterion for WLST.

Electroencephalography - absence of EEG reactivity

Biomarkers - NSE and S-100B are protein biomarkers released following injury to
neurons and glial cells, respectively.

Imaging Brain CT and MRI

3. Prognostication
 4. Rehabilitation

Screening for cognitive impairments:

- Memory
- Attention
- Executive functioning

Screening for emotional problems:

- depression
- anxiety
- posttraumatic stress

Provision of information
Initial management of acute
coronary syndromes
Definitions of acute coronary syndromes (ACS)
 Diagnostic Interventions in ACS
- new views and changes in recommendations -

Pre-hospital recording of a 12-lead electrocardiogram

(ECG) is recommended in patients with suspected STEMI.

Non-physician ECG STEMI interpretation with or without

the aid of computer ECG STEMI interpretation.

Pre-hospital STEMI activation of the catheterisation

laboratory

The use of negative high-sensitivity cardiac troponins (hs-

cTn) during initial patient evaluation cannot be used as a
standalone measure to exclude an ACS, but in patients with
very low risk scores may justify early discharge.
Therapeutic Interventions in ACS
- new views and changes in recommendations -
 Therapeutic Interventions in ACS
- new views and changes in recommendations -

Adenosine diphosphate (ADP) receptor antagonists (clopidogrel,

ticagrelor, or prasugrel) may be given either pre-hospital or in the ED
for STEMI patients planned for primary PCI.

Unfractionated heparin (UFH) can be administered either in the pre-

hospital or in-hospital setting in patients with STEMI and a planned
primary PCI approach.

Pre-hospital enoxaparin may be used as an alternative to pre-hospital

UFH for STEMI.

Patients with acute chest pain with presumed ACS do not need
supplemental oxygen unless they present with signs of hypoxia,
dyspnoea, or heart failure.
 Reperfusion decisions in STEMI
- new views and changes in recommendations -

Pre-hospital fibrinolysis vs in-hospital fibrinolysis for STEMI where

transport times are > 30 min.

Direct triage and transport for PCI is preferred to pre-hospital

fibrinolysis for STEMI.

Patients presenting with STEMI in the ED of a non-PCI capable

hospital should be transported immediately to a PCI centre if
treatment delays for PPCI are less than 120 min, otherwise patients
should receive first fibrinolysis.

PCI in less than 3 h following administration of fibrinolytics is not

recommended and can be performed only in case of failed fibrinolysis
 Take home messages
Continued emphasis on the use of rapid response systems for care of the
deteriorating patient and prevention of in-hospital cardiac arrest.

The interventions that unquestionably contribute to improved survival after

cardiac arrest are prompt and effective bystander basic life support (BLS),
uninterrupted, high-quality chest compressions and early defibrillation for
VF/pVT

Pay attention to all the reversible causes of cardiac arrest

There is a greater emphasis on the need for urgent coronary catheterisation

and PCI following out-of-hospital cardiac arrest of likely cardiac cause.

Prognostication is now undertaken using a multimodal strategy and allowing

sufficient time for neurological recovery and to enable sedatives to be cleared.

Asystole for more than 20 min in the absence of a reversible cause and with
ongoing ALS constitutes a reasonable ground for stopping further
resuscitation attempts