European Resuscitation Council

Guidelines for Resuscitation

October 2015
Adina Blejuşcă
Alexandru Caragea
Cristian Pristavu

Coordonatori: Prof. Dr. Ioana Grigoraş

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 3–11 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 5–10 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
V1–V4, 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 60–90 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 patient’s 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 50–100 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 0.4–2 mg IV, IO, IM or SC, and may be
repeated every 2–3 min. Additional doses may be needed every 20–60 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 (50–150 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 2–5 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 0.5–2.0 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
patient’s 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 1–5 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 (4.7–5.4 kPa/35–40 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 94–98%.
• Inhaled beta-2 agonists are first line drugs in patients with an
acute asthma attack – Salbutamol 5 mg nebulised, repeated doses
every 15–20 min are often needed; high-flow oxygen (at least 6 L
min−1). 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 3–20 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 20–30 min (unless on maintenance
therapy), followed by an infusion of 500–700 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 8–10 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 36◦C instead of the previously recommended
32–34◦C.

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 following B. Percutaneous coronary intervention following
ROSC with ST-elevation 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 32◦C and 36◦C 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 (32–34◦C) or higher (36◦C) 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., 33◦C) 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