The management of cardiac arrest
INTRODUCTION
Cardiac arrest has occurred when there are no palpable central pulses.
Before any specific therapy is started effective basic life support must be
established. Three cardiac arrest rhythms will be covered:
1.
2.
3.
Asystole
Ventricular fibrillation
Pulseless electrical activity (PEA)
PRE-HOSPITAL CONSIDERATIONS
Cardiac arrest in a child has a dismal prognosis. Every effort should therefore be made to prevent it occurring by early recognition of potentially
serious illness and appropriate management. Occasionally it is, however,
inevitable. It is particularly difficult to manage in the pre-hospital setting
because ideally a team of skilled, well equipped people are required to
provide optimum simultaneous management of the airway, breathing,
circulation (cardiac massage) and drug administration. This abundance of
resources is seldom, if ever, available outside hospital and therefore the
recommended guidelines and protocols may not be possible to implement in
full.
It must be remembered that, at the present time, the only factor known to
improve the outcome of paediatric arrest is the time from the arrest to the
arrival at hospital. This is regardless of the skill of the personnel or interventions performed. Thus the single most important “treatment”, likely to
improve the child’s chances of survival, is not to delay in transferring the
child to hospital. It is possible that if this is done, then other appropriate
procedures may also help the child’s outcome.
So when to move? This will depend on a number of issues, ranging from
the size of the child to equipment available. Points to bear in mind are:
.
.
THE MANAGEMENT OF CARDIAC ARREST
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If the child is small enough, remember, if possible, to “scoop and
run” into the ambulance, rather than wasting time bringing
equipment to the scene.
As in all resuscitation, airway and breathing come before circulation
and drugs.
Good basic life support is essential and should not be sacrificed at
the expense of performing advanced interventions such as
intraosseous cannulation and drug administration. However, some
advanced interventions may improve the quality of the basic life
support. A laryngeal mask airway of an appropriate size may be
inserted to facilitate ventilation during long transportation times.
Endotracheal intubation should only be undertaken exceptionally.
For example, such as in protecting the airway in children at high
risk of aspiration in near drowning.
If the child is in ventricular fibrillation, the most urgent treatment is
defibrillation, and this should not be delayed. As for an adult, the
sooner the child is defibrillated, the more likely the return to a
rhythm with an output.
It may be appropriate to perform one cycle of basic life support
before moving the child as a primed myocardium has been shown to
respond better to energy —particularly if the arrest is thought to be
due to hypoxia, as oxygenation is also crucial.
The remainder of this section deals with what is considered to be the optimum management of asystole and PEA (non shockable rhythms) (Figure 3.4)
and ventricular fibrillation and ventricular tachycardia without an output with
full facilities available (see Figures 3.5). It is, however, important to
appreciate that it will not always be possible to perform all the suggested
interventions and drug regimes outside hospital without compromising
transportation times and good basic life support with oxygen. Rapid
transportation is still the mainstay of the management of cardiac arrest in the
pre-hospital setting.
MANAGEMENT OF NON SHOCKABLE RHYTHMS (asystole or
PEA)
Good basic life support should be commenced and remain continuous and
the child ventilated with oxygen as soon as possible.
THE MANAGEMENT OF CARDIAC ARREST
Adrenaline 10 mcg /kg should be administered every 3-5 minutes.
Throughout management, possible underlying causes should be sought (see
figure 3.4). Hypovolaemia is the commonest cause in childhood and tension
pneumothorax and hypothermia should be considered. Other causes cannot
generally be managed before hospital.
Pulseless electrical activity (Figure 3.4 should usually be treated with rapid
volume expansion (20 ml/kg of crystalloid or colloid) because hypovolaemia
is the commonest cause.
SHOCKABLE RHYTHMS
Asynchronous electrical defibrillation should be carried out immediately at
a dose of 4 joules /kg. Paediatric paddles (4.5 cm) should be used for
children under 10 kg. One electrode is placed over the apex in the midaxillary line, while the other is put immediately below the clavicle just to the
right of the sternum. If only adult paddles are available for an infant under 10
kg, one may be placed on the infant’s back and one over the left lower part of
the chest at the front. See Practical Procedures (Part VII).
Refer to AED section for AED use.
Following the shock, CPR should be resumed immediately, commencing
with compressions. After 2 minutes, if the monitor still shows VF /Pulseless
VT, a second shock of 4 joules/kg. should be administered and, if the rhythm
remains shockable, a third shock of 4 J/kg after another 2 minutes, this time
giving adrenaline 10mcg/kg immediately before the shock. If the child
remains in VF/VT after 3 shocks, 5mg/kg amiodarone should be given and
the sequence of shock at 4J/kg – 2 minutes CPR continued until arrival at
hospital. Adrenaline 10mcg/kg should be given immediately before alternate
shocks.
The child should be transported as soon as possible, if necessary stopping
the ambulance to shock the child. Oxygen, and good basic life support must
be continued throughout.
During the resuscitation, the underlying cause of the arrhythmia should be
considered. If VF is due to hypothermia then defibrillation may be resistant
until core temperature is increased. Active rewarming should be commenced.
THE MANAGEMENT OF CARDIAC ARREST
If VF has been caused by drug overdose, then specific antiarrhythmic agents
may be needed, so urgent transfer to hospital is required.
POST-RESUSCITATION MANAGEMENT
Once spontaneous cardiac output has returned, frequent clinical reassessment must be carried out to detect deterioration or improvement until arrival
at hospital. All patients should have continuing assessment of:


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Pulse rate and rhythm
Oxygen saturation
The blood sugar should be measured and corrected if necessary
Often children who have been resuscitated from cardiac arrest die hours or
days later from multiple organ failure. In addition to the cellular and
homeostatic abnormalities that occur during the preceding illness, and during
the arrest itself, cellular damage continues after spontaneous circulation has
been restored. This is called reperfusion injury and is caused by the
following:
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
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Depletion of ATP
Entry of calcium into cells
Free fatty acid metabolism activation
Free oxygen radical production
Post-resuscitation management both before and after arrival at hospital aims
to achieve and maintain homeostasis in order to optimise the chances of
recovery.
WHEN TO STOP RESUSCITATION
If there have been no detectable signs of cardiac output, and there has been
no evidence of cerebral activity despite up to 30 minutes of cardiopulmonary
resuscitation, it is reasonable to stop resuscitation, and a suitably qualified
practitioner may elect to do so. Exceptions to this rule include the hypothermic child (in whom resuscitation must continue until the core temperature is
◦
at least 32 C or cannot be raised despite active measures) and children who
THE MANAGEMENT OF CARDIAC ARREST
have taken overdoses of drugs. In these cases prolonged resuscitation attempts will be necessary and should always be continued for the full journey
time to hospital.
The decision to stop resuscitation, in reality, is usually taken after the child
has arrived in hospital.
The teaching in this section is consistent with the ILCOR and
Resuscitation Council (UK), Resuscitation 2005. An enormous number of
references, have informed these guidelines which are available on the ALSG
Web site for those who are interested. See details on the “Contact Details and
Further Information” page.
THE MANAGEMENT OF CARDIAC ARREST
Asystole or PEA
Establish cardiac arrest
Ensure minimal interruptions in
CPR with 100% oxygen
IO or IV access
Check blood sugar
LMA, intubate for prolonged
transfer or failure to ventilate
only
This is the most common arrest rhythm in children,
because the response of the young heart to prolonged severe
hypoxia and acidosis is progressive bradycardia leading to
asystole.
The ECG will distinguish asystole from ventricular
fibrillation and electromechanical dissociation. The ECG
appearance of ventricular asystole is an almost straight line;
occasionally P waves are seen. Check that the appearance is not
caused by an artifact, eg a loose wire or disconnected electrode.
Turn up the gain on the ECG monitor, switch through leads.
Adrenaline (Epinephrine)
10 micrograms/kg
IO
Consider and Manage Reversible Causes
3 minutes CPR
Hypoxia
Adequate airway, 100% oxygen 02
manage respiratory problems then
transport.
Hypovolaemia
Fluid challenge 20ml/kg x1 then
transport
Hypo/hyperkalaemia
Rapid transport
Hypothermia
Passive warming, no more than 3o
shocks & no drugs until temp >30 C
(3 shocks then transport)
Tension pneumothorax
Needle decompression then
transport
Tamponade (cardiac)
Rapid transport
Toxins
Naloxone for opiates
Glucagon for betablockers
otherwise, rapid transport
Thromboembolism
Rapid transport
If hypoglycaemic give
5ml/kg 10% dextrose
Consider and correct
reversible causes.
Move to ambulance and
transport to hospital
Figure 3.4. Asystole and PEA algorithm
THE MANAGEMENT OF CARDIAC ARREST
Vascular access
Intraosseous access (IO) is the recommended route for vascular access in
cardiac arrest in young children.
Adrenaline (epinephrine)
Adrenaline (epinephrine) is the first line drug for asystole. The initial intravenous dose is 10 mcg/kg (0.1 ml/kg of 1:10 000 solution). This is given
through a peripheral or intraosseous line followed by a normal saline flush (2
– 5 ml). If there is no vascular access, the endotracheal tube can be used, but
absorption is erratic via this route. Ten times the intravenous dose (i.e. 100
mcg/kg) should be given via this route. The drug should be injected quickly
down a narrow-bore suction catheter beyond the tracheal end of the
endotracheal tube and then flushed in with 1 or 2 ml of normal saline. In
patients with pulmonary disease or prolonged asystole, pulmonary oedema
and intrapulmonary shunting may make the endotracheal route less effective.
If there has been no clinical effect, further doses should be given
intravenously or IO as soon as vascular access has been secured.
Fluids
In some situations, where the cardiac arrest has resulted from circulatory
failure, a standard (20 ml/kg) bolus of fluid should be given if there is no
response to the initial dose of adrenaline (epinephrine). The nature of the
fluid is less important than the volume - crystalloid such as normal (0.9%)
saline is suggested..
Alkalising agents
Children with asystole may be profoundly acidotic as their cardiac arrest
has usually been preceded by respiratory arrest or shock. However, the
routine use of alkalising agents has not been shown to be of benefit. and
these agents should be administered only in cases where alkalinisation may
be helpful such as tricyclic overdose or hyperkalaemia. Bicarbonate is the
most common alkalising agent currently available, the dose being 1 mmol/kg
(2 ml/kg of a 4.2% solution). The tracheal route must not be used, and
interactions with other drugs must be borne in mind.
Second adrenaline (epinephrine) dose
There is no convincing evidence that a tenfold increase in adrenaline
(epinephrine) dose is beneficial in children and it may even lead to a worse
THE MANAGEMENT OF CARDIAC ARREST
neurological outcome. It should only be used exceptionally for a specific
reason such as ß–blocker overdose. However, there are some anecdotal cases
of return of spontaneous circulation with large doses of adrenaline
(epinephrine) and therefore it can still be used for second and subsequent
doses (Figure 3.5) in patients where cardiac arrest is thought to have been
secondary to circulatory collapse. Adrenaline should be given every 3-5
minutes.
THE MANAGEMENT OF CARDIAC ARREST
Ventricular Fibrillation
CPR with 100% O2 and minimal
pauses until defibrillator ready
Check monitor
Ventilate with O2
LMA / Intubate
DC Shock 4J/kg
or AED (see note 2)
2 min CPR
Check monitor
Ventilate with O2
IO Access
Check blood sugar
Give 5ml/kg 10% dextrose if hypoglycaemic
DC Shock 4J/kg or AED
Consider and treat
reversible causes
2 min CPR
Check monitor
This arrhythmia is uncommon in children but is
commoner in those who are electrocuted, those with
from hypothermia, those poisoned by tricyclic
antidepressants, and those with cardiac disease.
Dose
Adrenaline (epinephrine) - 10 μg/kg
Amiodarone 5mg/kg - maximum 300mg
Lidocaine (Lignocaine): <12yrs – 500 μg/kg to 1 mg/kg
>12 yrs 50-100mg (see formulary)
Give drugs via IO route
Ventilations at
10 per minute.
Adrenaline then
DC Shock 4J/kg
or AED
Consider and Manage Reversible Causes
2 min CPR
Check monitor
Amiodarone then DC
Shock 4J/kg
or AED
If amiodarone is
unavailable then lidocaine
may be used (see below)
2 min CPR
Check monitor
Move to ambulance and
commence transportation
Hypoxia
Adequate airway, 100% oxygen 02
manage respiratory problems then
transport.
Hypovolaemia
Fluid challenge 20ml/kg x1 then
transport
Hypo/hyperkalaemia
Rapid transport
Hypothermia
Passive warming, no more than 3
shocks
& no drugs until temp
>30oC (3 shocks then transport)
Tension
pneumothorax
Needle decompression then
transport
Tamponade (cardiac)
Rapid transport
Toxins
Naloxone for opiates
Glucagon for betablockers
otherwise, rapid transport
Thromboembolism
Rapid transport
Adrenaline then
DC Shock 4J/kg
or AED
Notes
2 min CPR
Check monitor
DC Shock 4J/kg
or AED
i.e. Adrenaline
before every
other shock
1. Move as soon as is logistically reasonable
2. An adult AED may be used in children over the
age of 8 years. In children 1yr–8yrs an AED with
paediatric attenuation should be used if available.
In children under 1, nearly all had severe hypoxia
and the use of AEDs remains controversial.
2 min CPR
Check monitor
Figure 3.5. Ventricular fibrillation algorithm