Chapter 6.

Advanced Life Support algorithm

LEARNING OUTCOMES
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To understand:
• the function of the advanced life support (ALS) algorithm
• the importance of minimally interrupted high-quality chest compressions
• the treatment of shockable and non-shockable rhythms
• when and how to give drugs during cardiac arrest
• the potentially reversible causes of cardiac arrest

1. Introduction
Heart rhythms associated with cardiac arrest are divided into two groups: shockable
rhythms (ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT)) and non-
shockable rhythms (asystole and pulseless electrical activity (PEA)). The principle
difference in the management of these two groups of arrhythmias is the need for
attempted defibrillation in patients with VF/pVT. Subsequent actions, including chest
compressions, airway management and ventilation, venous access, injection of adrenaline
and the identification and correction of reversible factors, are common to both groups.

The ALS algorithm (figure 6.1) is a standardised approach to cardiac arrest management.
This has the advantage of enabling treatment to be delivered expediently, without
protracted discussion. It enables each member of the resuscitation team to predict and
prepare for the next stage in the patient’s treatment, further enhancing efficiency of
the team. Although the ALS algorithm is applicable to most cardiac arrests, additional
interventions may be indicated for cardiac arrest caused by special circumstances (see
chapter 12).

The interventions that unquestionably contribute to improved survival after cardiac arrest
are prompt and effective bystander cardiopulmonary resuscitation (CPR), uninterrupted,
high-quality chest compressions, and early defibrillation for VF/pVT. The use of adrenaline

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has been shown to increase return of spontaneous circulation (ROSC), but no resuscitation
drugs or advanced airway interventions have been shown to increase survival to hospital
discharge after cardiac arrest. Thus, although drugs and advanced airways are still
included among ALS interventions, they are of secondary importance to high-quality,
uninterrupted chest compressions and early defibrillation.

2. Shockable rhythms (VF/pVT)

The first monitored rhythm is VF/pVT in approximately 20 % of cardiac arrests, both in-
and out-of-hospital. VF/pVT will also occur at some stage during resuscitation in about
25 % of cardiac arrests with an initial documented rhythm of asystole or PEA.

2.1. Treatment of shockable rhythms (VF/pVT)

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1. Confirm cardiac arrest - check for signs of life or if trained to do so, breathing and
pulse simultaneously.
2. Call resuscitation team.
3. Perform uninterrupted chest compressions while applying self-adhesive
defibrillation/monitoring pads - one below the right clavicle and the other in the V6
position in the midaxillary line.
4. Plan actions before pausing CPR for rhythm analysis and communicate these to the
team.
5. Stop chest compressions not longer than 2 seconds to check rhythm, Resume chest
compressions immediately.
6. Confirm VF/pVT, if in doubt use a print out rhythm strip; the designated person
selects the appropriate energy on the defibrillator (150-200 J biphasic for the
first shock and 150-360 J biphasic for subsequent shocks) and presses the
charge button.
7. While the defibrillator is charging, warn all rescuers other than the individual
performing the chest compressions to “stand clear” and remove any oxygen
delivery device as appropriate. Ensure that the rescuer giving the compressions is
the only person touching the patient.
8. Once the defibrillator is charged, tell the rescuer doing the chest compressions to
”stand clear”; when clear, give the shock.
9. Without reassessing the rhythm or feeling for a pulse, restart CPR using a ratio of
30:2, starting with chest compressions.
10. Continue CPR for 2 min; the team leader prepares the team for the next pause in
CPR.
11. Pause briefly to check the monitor.
12. If VF/pVT, repeat steps 6-11 above and deliver a second shock.

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 13. If VF/pVT persists repeat steps 6-8 above and deliver a third shock. Without
reassessing the rhythm or feeling for a pulse, resume CPR (30:2) immediately after
the shock, starting with chest compressions.
14. If IV/IO access has been obtained, during the next 2 minutes of CPR give adrenaline
1 mg and amiodarone 300 mg.
15. The use of waveform capnography may enable ROSC to be detected without
pausing chest compressions and may be used as a way of avoiding a bolus
injection of adrenaline after ROSC has been achieved. If ROSC is suspected during
CPR withhold adrenaline. Give adrenaline if cardiac arrest is confirmed at the next
rhythm check.
16. Give further adrenaline 1 mg IV after alternate shocks (i.e., in practice, this will be
about once every two cycles of the algorithm).
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Figure 6.1
Shock delivery

If signs of life return during CPR (purposeful movement, normal breathing or coughing),
or there is a significant increase in ETCO2, check the monitor.

If organised electrical activity compatible with a cardiac output is seen during a

rhythm check, seek evidence of ROSC:
• Check a central pulse and end-tidal (ETCO2) trace if available.
• If there is evidence of ROSC, start post-resuscitation care.
• If no signs of ROSC, continue CPR and switch to the non-shockable algorithm.

If asystole is confirmed during a rhythm check continue CPR and switch to the non-
shockable algorithm.

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Chapter 6
Advanced Life Support algorithm

Figure 6.2
Adult advanced life support algorithm

Unresponsive and
not breathing normally?

Call Resuscitation Team

CPR 30:2
Attach defibrillator/monitor
Minimise interruptions

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Assess rhythm

Shockable Non-shockable
(VF/Pulseless VT) (PEA/Asystole)

1 Shock Return of
Minimise spontaneous
interruptions circulation

Immediately resume IMMEDIATE POST CARDIAC Immediately resume

CPR for 2 min ARREST TREATMENT CPR for 2 min
Minimise interruptions n Use ABCDE approach Minimise interruptions
n Aim for SaO of 94-98 %
2
n Aim for normal PaCO
2
n 12 Lead ECG

n Treat precipitating cause

n  Targeted temperature

management

DURING CPR TREAT REVERSIBLE CAUSES

Hypoxia Thrombosis – coronary or pulmonary
n E  nsure high-quality chest compressions
Hypovolaemia Tension pneumothorax
n  Minimise interruptions to compressions
Hypo-/hyperkalaemia/metabolic Tamponade – cardiac
n  Give oxygen
Hypothermia/hyperthermia Toxins
n  Use waveform capnography

n C  ontinuous compressions when advanced airway CONSIDER

in place  ltrasound imaging
n U
n V ascular access (intravenous or intraosseous) n 
Mechanical chest compressions to facilitate transfer/treatment
n G ive adrenaline every 3-5 min n Coronary angiography and percutaneous coronary intervention
n Give amiodarone after 3 shocks n E xtracorporeal CPR

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 The interval between stopping compressions and delivering a shock must be minimised
and, ideally, should not exceed 5 s. Longer interruptions in chest compressions reduce the
chance of a shock restoring spontaneous circulation.

Chest compressions are resumed immediately after a shock without checking the rhythm
or a pulse because even if the defibrillation attempt is successful in restoring a perfusing
rhythm. It is very rare for a pulse to be palpable immediately after defibrillation and the
delay in trying to palpate a pulse will further compromise the myocardium if a perfusing
rhythm has not been restored. If a perfusing rhythm has been restored, giving chest
compressions does not increase the chance of VF recurring. In the presence of post-shock
asystole chest compressions may usefully induce VF.

If ROSC has not been achieved with this 3rd shock, the adrenaline may improve myocardial
blood flow and increase the chance of successful defibrillation with the next shock. Despite
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the widespread use of adrenaline during resuscitation, there is no placebo-controlled

study that shows that the routine use of any vasopressor at any stage during human cardiac
arrest increases neurologically intact survival to hospital discharge. Current evidence is
insufficient to support or refute the routine use of any particular drug or sequence of
drugs. Despite the lack of human data, the use of adrenaline is still recommended, based
largely on animal data and increased short-term survival in humans.

Timing of adrenaline dosing can cause confusion amongst ALS providers and this aspect
needs to be emphasised during training. Training should emphasise that giving drugs
must not lead to interruptions in CPR and delay interventions such as defibrillation. The
first dose of adrenaline is given during the 2 minutes period following delivery of the third
shock; amiodarone 300 mg may also be given after the third shock. Do not stop CPR to
check the rhythm before giving drugs unless there are clear signs of ROSC.

Figure 6.3
Shock delivery

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Subsequent doses of adrenaline are given after alternate 2-minute cycles of CPR (which
equates to every 3-5 min) for as long as cardiac arrest persists. If VF/pVT persists, or
recurs, give a further dose of 150 mg amiodarone. Lidocaine, 1 mg kg-1, may be used as an
alternative if amiodarone is not available, but do not give lidocaine if amiodarone has been
given already.

When the rhythm is checked 2 min after giving a shock, if a non-shockable rhythm is
present and the rhythm is organised (complexes appear regular or narrow), try to palpate
a central pulse and look for other evidence of ROSC (e.g. sudden increase in ETCO2 or
evidence of cardiac output on any invasive monitoring equipment). Rhythm checks
must be brief, and pulse checks undertaken only if an organised rhythm is observed.
If an organised rhythm is seen during a 2-minute period of CPR, do not interrupt chest
compressions to palpate a pulse unless the patient shows signs of life suggesting ROSC. If
there is any doubt about the presence of a pulse in the presence of an organised rhythm,

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resume CPR. If the patient has ROSC, begin post-resuscitation care. If the patient’s rhythm
changes to asystole or PEA, see non-shockable rhythms below.

It is important in shock-refractory VF/pVT to check the position and contact of the

defibrillation pads. The duration of any individual resuscitation attempt is a matter of
clinical judgement, and should take into account the perceived prospect of a successful
outcome. If it was considered appropriate to start resuscitation, it is usually considered
worthwhile continuing as long as the patient remains in identifiable VF/pVT.

If there is doubt about whether the rhythm is asystole or very fine VF, do not attempt
defibrillation; instead, continue chest compressions and ventilation. Very fine VF that is
difficult to distinguish from asystole is unlikely to be shocked successfully into a perfusing
rhythm. Continuing high-quality CPR may improve the amplitude and frequency of the
VF and improve the chance of subsequent successful defibrillation to a perfusing rhythm.
Delivering repeated shocks in an attempt to defibrillate what is thought to be very fine VF
will increase myocardial injury both directly from the electric current and indirectly from
the interruptions in coronary blood flow. If the rhythm is clearly VF, attempt defibrillation.

2.1.1. Precordial thump

A single precordial thump has a very low success rate for cardioversion of a shockable
rhythm. Its routine use is therefore not recommended. It may be appropriate therapy only
when used without delay whilst awaiting the arrival of a defibrillator in a monitored VF/
pVT arrest. Using the ulnar edge of a tightly clenched fist, deliver a sharp impact to the
lower half of the sternum from a height of about 20 cm, then retract the fist immediately
to create an impulse-like stimulus. There are rare reports of a precordial thump converting
a perfusing to a non-perfusing rhythm.

2.1.2. Witnessed, monitored VF/pVT in specific settings

If a patient has a monitored and witnessed cardiac arrest in the catheter laboratory,
coronary care unit, a critical care area or whilst monitored after cardiac surgery, and a
manual defibrillator is rapidly available:

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 • 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 two minutes if the third shock is
unsuccessful. With respect to the ALS algorithm, these three quick, successive
shocks are regarded as the first shock. Only exception is that 300 mg Amiodarone
should be given before the next shock, if already available, and, if the next shock
remains unsuccessful, repeated once with a dose of 150 mg.
This three-shock strategy may also be considered for an initial, witnessed VF/pVT cardiac
arrest if the patient is already connected to a manual defibrillator - these circumstances are
rare. There are no data supporting a three-shock strategy in any of these circumstances,
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but 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.

2.2. Non-shockable rhythms (PEA and asystole)

Pulseless electrical activity (PEA) is defined as organised cardiac electrical activity in the
absence of any palpable pulses. These patients often have some mechanical myocardial
contractions but they are too weak to produce a detectable pulse or blood pressure. PEA
may be caused by reversible conditions that can be treated (see below). Survival following
cardiac arrest with asystole or PEA is unlikely unless a reversible cause can be found and
treated quickly and effectively.

Asystole is the absence of electrical activity on the ECG trace. During CPR, ensure the
ECG pads are attached to the chest and the correct monitoring mode is selected. Ensure
the gain setting is appropriate. Whenever a diagnosis of asystole is made, check the ECG
carefully for the presence of P waves because in this situation ventricular standstill may
be treated effectively by cardiac pacing. Attempts to pace true asystole are unlikely to be
successful.

Treatment for PEA and asystole

1. Start CPR 30:2.
2. If asystole is displayed, without stopping CPR, check that the leads are attached
correctly.
3. Once an advanced airway has been sited, continue chest compressions without
pausing during ventilation.
4. Give adrenaline 1 mg as soon as venous or intraosseous access is achieved, and
repeat every alternate CPR cycle (i.e. about every 3-5 minutes).
5. After 2 minutes of CPR, recheck the rhythm. If asystole is present, resume CPR
immediately.

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6. If an organised rhythm is present, attempt to palpate a pulse.

7. If a pulse and/or signs of life are present, start post resuscitation care.
8. If no pulse and/or no signs of life are present (PEA):
-- Continue CPR.
-- Recheck the rhythm after 2 min and proceed accordingly.
-- Give further adrenaline 1 mg IV every 3-5 min (during alternate 2-min cycles
of CPR).
-- If VF/pVT at rhythm check, change to shockable side of algorithm.
9. If asystole or an agonal rhythm is seen at rhythm check:
-- Continue CPR.

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-- Recheck the rhythm after 2 min and proceed accordingly.
-- Give further adrenaline 1 mg IV every 3-5 min (during alternate 2-min cycles
of CPR).
Whenever a diagnosis of asystole is made, check the ECG carefully for the presence of P
waves, because this may respond to cardiac pacing. There is no benefit in attempting to
pace true asystole.

3. During CPR
During the treatment of persistent VF/pVT or PEA/asystole, emphasis is placed on high-
quality chest compressions between defibrillation attempts, recognising and treating
reversible causes (4 Hs and 4 Ts), obtaining a secure airway, and vascular access.

During CPR with a 30:2 ratio, the underlying rhythm may be seen clearly on the monitor
as compressions are paused to enable ventilation. If VF is seen during this brief pause
(whether on the shockable or non-shockable side of the algorithm), do not attempt
defibrillation at this stage; instead, continue with CPR until the 2-minute period is
completed. Knowing that the rhythm is VF, the team should be fully prepared to deliver
a shock with minimal delay at the end of the 2-minute period of CPR.

3.1. Maintain high-quality, uninterrupted chest compressions

The quality of chest compressions and ventilations are important determinants of
outcome, yet are frequently performed poorly by healthcare professionals. Avoid
interruptions in chest compressions because pauses cause coronary perfusion pressure
to decrease substantially. Ensure compressions are of adequate depth (approximately 5
cm but not more than 6 cm) and rate (100-120 min-1), and release pressure from the chest
completely between compressions.

As soon as the airway is secured, continue chest compressions without pausing during
ventilation. To reduce fatigue, change the individual undertaking compressions every

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 2 min or earlier if necessary. Use CPR feedback/prompt devices when available. Be aware
that some devices may fail to compensate for compression of the underlying mattress
during CPR on a bed when providing feedback.

3.2. Airway and ventilation

Tracheal intubation provides the most reliable airway, but should be attempted only if
the healthcare provider is properly trained and has regular, ongoing experience with the
technique. Tracheal intubation must not delay defibrillation attempts. Personnel skilled
in advanced airway management should attempt laryngoscopy and intubation without
stopping chest compressions; a brief pause in chest compressions may be required as
the tube is passed through the vocal cords, but this pause should be less than 5 seconds.
Alternatively, to avoid any interruptions in chest compressions, the intubation attempt
may be deferred until ROSC.
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No studies have shown that tracheal intubation increases survival after cardiac arrest. After
intubation, confirm correct tube position, ideally with waveform capnography and secure
it adequately. Ventilate the lungs at 10 breaths min-1; do not hyperventilate the patient.
Once the patient’s trachea has been intubated, continue chest compressions, at a rate
of 100-120 min-1 without pausing during ventilation. A pause in the chest compressions
causes the coronary perfusion pressure to fall substantially. On resuming compressions,
there is some delay before the original coronary perfusion pressure is restored, thus
chest compressions that are not interrupted for ventilation (or any reason) result in a
substantially higher mean coronary perfusion pressure.

In the absence of personnel skilled in tracheal intubation, a supraglottic airway (SGA) (e.g.
laryngeal mask airway, laryngeal tube or i-gel) is an acceptable alternative. Once a SGA
has been inserted, attempt to deliver continuous chest compressions, uninterrupted by
ventilation. If excessive gas leakage causes inadequate ventilation of the patient’s lungs,
chest compressions will have to be interrupted to enable ventilation (using a ratio of 30:2).

3.3. Vascular access

Obtain intravenous access if this has not been done already. Although peak drug
concentrations are higher and circulation times are shorter when drugs are injected into a
central venous catheter compared with a peripheral cannula, insertion of a central venous
catheter requires interruption of CPR and is associated with several potential complications.
Peripheral venous cannulation is quicker, easier, and safer. Drugs injected peripherally
must be followed by a flush of at least 20 ml of fluid and elevation of the extremity for
10-20 s to facilitate drug delivery to the central circulation. If intravenous access cannot
be established within the first 2 min of resuscitation, consider gaining intraosseous (IO)
access (figure 6.4). Tibial and humeral sites are readily accessible and provide equal flows
for fluids. Intraosseous delivery of resuscitation drugs will achieve adequate plasma
concentrations. Several studies indicate that IO access is safe and effective for fluid
resuscitation and drug delivery.

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4. 
Use of Intraosseous (IO) access during cardiac arrest

4.1. Introduction
Intraosseous (IO) infusion as a means of vascular access has been recognised for close to
a century and has seen a resurgence in the last decade particularly for use in resuscitation
in adults (figure 1). This is due in part to the publication of a number of studies that
suggest it is a viable alternative to intravenous (IV) access but also the development of
powered devices for inserting the needle, a technique recently supported by the findings
of a systematic review. Intraosseous access is also quicker than central venous access
in patients in whom peripheral venous access is not possible. Furthermore, the use of
central venous catheters (CVC) during resuscitation requires considerable skill and can
lead to prolonged interruptions to chest compressions. Current recommendations are
to establish IO access if IV access is not possible or associated with a delay in the first 2

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minutes of resuscitation.

4.1.1. Practical considerations

There are 3 main insertion sites recommended for use in adults:
• proximal tibia
• distal tibia
• proximal humerus

The patient should be assessed for the presence of contraindications for the use of IO
access. These are:
• fracture or prosthesis in the targeted bone
• recent IO (past 24-48 hrs) in the same limb including previous failed attempt
• signs of infection at insertion site
• inability to locate landmarks

4.1.2. Insertion
Training in the specific device to be used in clinical practice is essential. Site of insertion,
identification of landmarks and technique for insertion will differ depending on the device
being used. Errors in identification of landmarks or in insertion technique increase the risk
of failure and complications.
1. Once inserted, correct placement must be confirmed before delivery of drugs or
infusion of fluids. The needle should be aspirated; presence of IO blood indicates
correct placement, absence of aspirate does not necessarily imply a failed attempt.
There are reports of IO blood being used for laboratory analysis including glucose,
haemogolobin and electrolytes. Samples must be labeled as bone marrow aspirate
before being sent to the laboratory.

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 2. The needle should be flushed to ensure patency and observed for leakage or
extravasation. This is best achieved using an extension set flushed with 0.9 % saline
attached to the hub of the needle before use.
3. Once IO access has been confirmed resuscitation drugs including adrenaline and
amiodarone can be infused. Fluids and blood products can also be delivered but
pressure will be needed to achieve reasonable flow rates using either a pressure
bag or a 50 ml syringe.
4. Manufacturer’s guidance should be followed both for securing the needle and the
maximum length of time it can be left in place.
Complications associated with IO access/use are:
• extravasations into the soft tissues surrounding the insertion site
• dislodgement of the needle
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• embolism
• compartment syndrome due to extravasation
• fracture or chipping of the bone during insertion
• pain related to the infusion of drugs/fluids
• infection/osteomyelitis

Figures 6.4
Examples of intraosseous devices

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Advanced Life Support algorithm

5. Reversible causes
Potential causes or aggravating factors for which specific treatment exists must be
considered during any cardiac arrest. For ease of memory, these are divided into two
groups of four based upon their initial letter - either H or T (figure 6.5). More details on
many of these conditions are covered in chapter 12.
• Hypoxia
• Hypovolaemia
• Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and
other metabolic disorders
• Hypothermia
• Tension pneumothorax

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• Tamponade
• Toxins
• Thrombosis (pulmonary embolism or coronary thrombosis)

Figure 6.5
The four Hs and four Ts

Hypoxia Hypothermia

Hyperkalaemia Hypovolaemia

Tamponade

T
Tension Thrombosis
Pneumothorax

Toxins

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 • The four Hs
Minimise the risk of hypoxia by ensuring that the patient’s lungs are ventilated adequately
with 100 % oxygen. Make sure there is adequate chest rise and bilateral breath sounds.
Using the techniques described in chapter 7, check carefully that the tracheal tube is not
misplaced in a bronchus or the oesophagus.

Pulseless electrical activity caused by hypovolaemia is due usually to severe haemorrhage.

Evidence of haemorrhage may be obvious, e.g. trauma (chapter 12), or occult e.g.
gastrointestinal bleeding, or rupture of an aortic aneurysm. Intravascular volume should be
restored rapidly with fluid and blood, coupled with urgent surgery to stop the haemorrhage.

Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other

metabolic disorders are detected by biochemical tests or suggested by the patient’s
medical history e.g. renal failure (chapter 12).
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A 12-lead ECG may show suggestive features. Intravenous calcium chloride is indicated in
the presence of hyperkalaemia, hypocalcaemia, and calcium channel-blocker overdose.

Suspect hypothermia in any drowning incident (chapter 12); use a low reading thermometer.

• The four Ts
A tension pneumothorax may be the primary cause of PEA and may follow attempts at
central venous catheter insertion. The diagnosis is made clinically. Decompress rapidly by
thoracostomy or needle thoracocentesis and then insert a chest drain.

Cardiac tamponade is difficult to diagnose because the typical signs of distended

neck veins and hypotension cannot be assessed during cardiac arrest. Cardiac arrest
after penetrating chest trauma or after cardiac surgery should raise strong suspicion of
tamponade - the need for needle pericardiocentesis or resuscitative thoracotomy should
be considered in this setting (chapter 12).

In the absence of a specific history of accidental or deliberate ingestion, poisoning by

therapeutic or toxic substances may be difficult to detect but in some cases may be
revealed later by laboratory investigations (chapter 12). Where available, the appropriate
antidotes should be used but most often the required treatment is supportive.

The commonest cause of thromboembolic or mechanical circulatory obstruction

is massive pulmonary embolism. If pulmonary embolism is thought to be the
cause cardiac arrest consider giving a thrombolytic drug immediately. Following
fibrinolysis during CPR for acute pulmonary embolism, survival and good neurological
outcome have been reported in cases requiring in excess of 60 min of CPR. If a
fibrinolytic drug is given in these circumstances, consider performing CPR for at least
60-90 min before termination of resuscitation attempts.

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6. Use of ultrasound during advanced life support

Although no studies have shown that use of this imaging modality improves outcome,
there is no doubt that echocardiography has the potential to detect reversible causes
of cardiac arrest. Specific protocols for ultrasound evaluation during CPR may help to
identify potentially reversible causes (e.g. cardiac tamponade, pulmonary embolism,
hypovolaemia, pneumothorax) and identify pseudo-PEA (organised myocardial
contractions without palpable pulses). When available for use by trained clinicians,
ultrasound may be of use in assisting with diagnosis and treatment of potentially reversible
causes of cardiac arrest. The integration of ultrasound into advanced life support requires
considerable training if interruptions to chest compressions are to be minimised. A sub-
xiphoid probe position has been recommended. Placement of the probe just before
chest compressions are paused for a planned rhythm assessment enables a well-trained
operator to obtain views within 5 seconds. Absence of cardiac motion on sonography

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during resuscitation of patients in cardiac arrest is highly predictive of death although
sensitivity and specificity has not been reported.

7. Signs of life
If signs of life (such as regular respiratory effort, movement) or readings from patient
monitors compatible with ROSC (e.g. sudden increase in exhaled carbon dioxide or arterial
blood pressure waveform) appear during CPR, stop CPR briefly and check the monitor. If
an organised rhythm is present, check for a pulse. If a pulse is palpable, continue post-
resuscitation care and/or treatment of peri-arrest arrhythmias if appropriate. If no pulse is
present, continue CPR.

The use of waveform capnography may enable ROSC to be detected without pausing
chest compressions. A significant increase in ETCO2 during CPR may be seen when ROSC
occurs.

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 8. 
Waveform Capnography during advanced life sup-
port

8.1. Introduction
Carbon dioxide (CO2) is a waste product of metabolism; approximately 400 L are produced
each day. It is carried in the blood to the lungs where it is exhaled. The concentration in the
blood is measured as the partial pressure of CO2 (PCO2) and in arterial blood (PaCO2) is normally
5.3 kPa (4.7-6.0 kPa) = 40 mmHg (35-45 mmHg). The concentration of CO2 can also be
measured in expired air and is expressed as either percentage by volume or as a partial
pressure, both of which are very similar numerically. The concentration varies throughout
expiration, being maximal at the end and it is this value, the end-tidal CO2 (ETCO2) that is
most useful. Figure 6.6 shows CO2 curves during resuscitation starting with low quality chest
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compression, increase in CO2 indicates good quality chest compressions with immediate
sustained increase at ROSC.

Figure 6.6
Waveform capnography

8.2. Nomenclature
The terms describing the measurement of carbon dioxide are derived from the Greek
‘capnos’, which means smoke. A capnometer is a device used to measure the concentration
of CO2 and gives a numerical value of the % or partial pressure (kPa) of the concentration
of CO2. A capnograph is a device that displays a waveform of the concentration of CO2 as
it varies during expiration and a numerical value. This is usually referred to as waveform
capnography and is the most useful display for clinical use.

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Advanced Life Support algorithm

Figure 6.7
Waveform Capnography
“A: Start Expiration; B: End Expiration = ETCO2 “

CO2
B
5

A
0
Time

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Figure 6.8
Spontaneous breathing

CO2 WAVEFORM

0
CO2 TREND

Figure 6.9
Ventilated patient

8 etCO2 RR

5.3 11
7 30
4 3 8

Figure 6.10
High-quality CPR
8 etCO2 RR

2.3 11
7 30
4 3 8

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 Figure 6.11
Chest compression provider tiring

8 etCO2 RR

1.3 11
7 30
4 3 8

Figure 6.12
ETCO2 with ROSC

8 etCO2 RR

5.6 11
7 30

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4 3 8

Figure 6.13
Persistently low ETCO2 - associated with poor prognosis

8 etCO2 RR

1.3 11
7 30
4 3 8

Figure 6.14
Disconnection

8 etCO2 RR

5 11
7 30
4 3 8

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Advanced Life Support algorithm

8.3. Equipment
In order to analyse the concentration of CO2 in expired gas, most capnographs employ
side-stream sampling. A connector (T-piece) is placed in the breathing system, usually
on the end of the tracheal tube or supraglottic airway device (SAD). This has a small port
on the side to which is attached a fine bore sampling tube. A continuous sample of gas is
aspirated (about 50 ml min-1) and analysed by using the property of absorption of infra-
red light. The amount absorbed is proportional to the concentration of the absorbing
molecule (in this case CO2) and this is compared to a known standard, enabling the CO2
concentration to be determined. An alternative system is main-stream sampling in which
the infrared source and detector are contained within a cell or cuvette which is placed
directly in the breathing system, usually between the tracheal tube or SAD and circuit. Gas
is analysed as it passes through the sensor and none is removed from the system. Both
systems are used in fixed or portable monitors.

Osobní kopie Anne Le Roy (ID: 720345)

• What factors affect the end-tidal CO2?
There are 3 determinants of the ETCO2:
• production by cellular metabolism
• transport to the lungs – the cardiac output
• elimination by ventilation

In health, the greatest variation is the result of changes in metabolism, usually increasing
CO2 production. This causes compensatory changes in transport, an increase in cardiac
output, and elimination, an increase in ventilation to prevent accumulation of carbon
dioxide.

In critically ill patients it is usually a failure in transportation (reduced cardiac output),

elimination (inadequate ventilation) or a combination of both that causes changes in the
arterial concentration of CO2 and hence changes in the end-tidal CO2. During a cardiac
arrest, blood flow to the lungs ceases and despite continued production, if ventilation
is maintained, ETCO2 falls to zero. Once chest compressions are started, blood flow to
the lungs will be partially restored and if the patient is ventilated, the end-tidal CO2 will
increase, proportionately to the cardiac output generated.

• W
 hat information can be gained from monitoring ETCO2 during
cardiopulmonary resuscitation?
1. Tube placement
Capnography has a high sensitivity and specificity for confirming placement of a
tracheal tube in the airway.

2. Quality of CPR
The more efficient the chest compression, the greater the cardiac output which
delivers more CO2 to the lungs from where it is exhaled thus generating a higher
end-tidal concentration. High-quality chest compressions will result in typical
ETCO2 values of 2.0-2.5 kPa.

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 3. Return of Spontaneous Circulation (ROSC)
With ROSC, there is an immediate, sustained increase in ETCO2. This is often the
first indicator of ROSC. This often precedes other indicators such as the presence of
a palpable pulse. It is a result of the circulation transporting accumulated carbon
dioxide from the tissues to the lungs and often results in an initial raised ETCO2.

4. Guide to rate of ventilation

Hyperventilation of the patient’s lungs by rescuers is common during cardiac
arrest, and usually the result of increased rate rather than tidal volume. Excessive
ventilation reduces coronary perfusion and survival. Waveform capnography
provides a measure of ventilation rate during CPR and may therefore reduce the
incidence of hyperventilation.

5. Prognostication
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Osobní kopie Anne Le Roy (ID: 720345)

A higher ETCO2 during resuscitation is associated with an increased likelihood

of ROSC and chance of survival to discharge. In one study, an ETCO2 of < 1.9 kPa
(14 mmHg) during resuscitation had a sensitivity and specificity of 100 % in
predicting non-survivors. After cardiac arrest and CPR for more than 30 minutes,
exhaled carbon dioxide values decrease and may become zero. The inter-individual
differences and influence of cause of cardiac arrest, the problem with self-fulfilling
prophecy in studies, our lack of confidence in the accuracy of measurement during
CPR, and the need for an advanced airway to measure end-tidal CO2 reliably limits
our confidence in its use for prognostication. Thus, we recommend that a specific
end-tidal CO2 value at any time during CPR should not be used alone to stop CPR
efforts. End-tidal CO2 values should be considered only as part of a multi-modal
approach to decision-making for prognostication during CPR.

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Advanced Life Support algorithm

9. Discontinuing resuscitation and diagnosing death

If attempts at obtaining ROSC are unsuccessful the cardiac arrest team leader should
discuss stopping CPR with the resuscitation team. The decision to stop CPR requires
clinical judgement and a careful assessment of the likelihood of achieving ROSC.

After stopping CPR, observe the patient for a minimum of 5 min before confirming death.
The absence of mechanical cardiac function is normally confirmed using a combination
of the following:
• absence of a central pulse on palpation
• absence of heart sounds on auscultation

One or more of the following can supplement these criteria:

Osobní kopie Anne Le Roy (ID: 720345)

• asystole on a continuous ECG display
• absence of pulsatile flow using direct intra-arterial pressure monitoring
• absence of contractile activity using echocardiography

Any return of cardiac or respiratory activity during this period of observation should
prompt a further 5 min observation from the next point of cardiorespiratory arrest. After 5
min of continued cardiorespiratory arrest, the absence of the pupillary responses to light,
of the corneal reflexes, and of any motor response to supra-orbital pressure should be
confirmed. The time of death is recorded as the time at which these criteria are fulfilled.

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 FURTHER READING
• Soar J, et al. European Resuscitation Council Guidelines for Resuscitation 2015. Section 3. Adult
Advanced Life Support. 10.1016/j.resuscitation.2015.07.016; p99 - p146
• Soar J, Callaway CW, Aibiki M, et al. Part 4: Advanced life support: 2015 International Consensus
on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment
Recommendations. 10.1016/j.resuscitation.2015.07.042; e71 - e122
• Truhlar A, Deakin CD, Soar J, et al. European Resuscitation Council Guidelines for Resuscitation
2015 Section 4 Cardiac Arrest in Special Circumstances. 10.1016/j.resuscitation.2015.07.017; p147 -
p200
• Weiser G, Hoffmann Y, Galbraith R, Shavit I 2012 Current advances in intraosseous infusion – A
systematic review. Resuscitation 83 (2012) 20– 26
• Reades R, Studnek JR, Vandeventer S, Garrett J. 2011 Intraosseous versus intravenous vascular access
during out-of-hospital cardiac arrest: a randomized controlled trial. Ann Emerg Med. Dec;58(6):509-
16.
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Osobní kopie Anne Le Roy (ID: 720345)

• Kolar M, Krizmaric M, Klemen P, Grmec S. Partial pressure of end-tidal carbon dioxide successful
predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care.
2008;12(5):R115. doi:10.1186/cc7009
• Heradstveit BE, Sunde K, Sunde GA, Wentzel-Larsen T, Heltne JK. Factors complicating interpreta-
tion of capnography during advanced life support in cardiac arrest—a clinical retrospective study
in 575 patients. Resuscitation. 2012 Jul;83(7):813-8.
• Cook TM, Woodall N, Harper J, Benger J; Fourth National Audit Project. Major complications of
airway management in the UK: results of the Fourth National Audit Project of the Royal College of
Anaesthetists and the Difficult Airway Society. Part 2: intensive care and emergency departments.
Br J Anaesth. 2011 May;106(5):632-42.

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Advanced Life Support algorithm

Osobní kopie Anne Le Roy (ID: 720345)

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