Arc guideline 12.4 - medications & fluids in paediatric advanced life support

AUSTRALIAN
RESUSCITATION
GUIDELINE 12.4
MEDICATIONS & FLUIDS IN PAEDIATRIC ADVANCED LIFE

All intravenous (IV) and intraosseous (IO) drugs should be flushed with small boluses of
0.9% sodium chloride or 5% glucose (for amiodarone). This ensures that the drugs enter the
circulation and prevents precipitation or inactivation as occurs when sodium bicarbonate
mixes with calcium, or when sodium bicarbonate mixes with adrenaline. Medications used in
paediatric CPR are listed alphabetically. See guideline 12.5 for use in treatment of specific
dysrhythmias.
ADRENALINE
Both alpha and beta effects of adrenaline are useful in management of cardiopulmonary
resuscitation. Alpha vasoconstrictor effects diverts blood to the cerebral and coronary
circulation and can facilitate defibrillation while beta effects are chronotropic and inotropic.
The optimal dose and frequency of administration of adrenaline in children are unknown. The
initial and any subsequent dose by the intravenous or intraosseous route is 10mcg/kg, (10
micrograms/kg) with a maximum single dose of 1mg. 1 [Class A; Expert Consensus Opinion].
In special circumstances such as beta-blocker use or poisoning, larger doses may be used but
are otherwise not recommended.
Higher and excessive doses of adrenaline may have significant complications of severe
vasoconstriction, hypertension and tachydysrrhythmias. In the treatment of in-hospital
paediatric arrest, administration of 100 mcg/kg after an initial 10 mcg/kg was associated with
lower short-term survival than administration of first and subsequent doses of 10 mcg/kg
[LOE II] 1.
The systemic absorption of adrenaline from endotracheal tube (ETT) administration is
variable. Although unproven to be the optimal dose, 100mcg/kg is the accepted paediatric
endotracheal ETT dose 1 [Class A; Expert Consensus Opinion].
Adrenaline is used to treat asystole, severe bradycardia, ventricular fibrillation and
electromechanical dissociation. It should be given intravenously or intraosseously at intervals
of every second cycle (Guideline 12.3) [Class A, Expert Consensus Opinion]. Instead of
repeated bolus doses, a continuous infusion of approximately 0.1 – 0.2 mcg/kg/min or higher
doses may be given – preferably into a large vein to avoid extravasation necrosis.


AMIODARONE
Amiodarone
is an antiarrhythmic drug with complex pharmacokinetics and pharmacodynamics. It is effective for adult shock-resistant ventricular fibrillation and more
efficacious than lignocaine and has been used to treat paediatric life-threatening ventricular
arrhythmias 1 [LOE III-3]. The initial paediatric dose for shock-resistant ventricular
fibrillation and pulseless ventricular tachycardia is a bolus of 5 mg/kg, which may be
repeated. [Class A; Expert Consensus Opinion]. If amiodarone is not available, lignocaine
may be used but no data exists on its effectiveness in paediatrics 1. Acute adverse effects of
amiodarone which may be related to the rapidity of infusion include hypotension, bradycardia
and heart block, while long-term adverse effects include hypothyroidism and pulmonary
toxicity.
In children, amiodarone can be used to successfully treat a wide range of other
tachydysrhythmias, notably atrial tachycardias, (recurrent) supraventricular tachycardia,
pulsatile ventricular tachycardia junctional ectopic tachycardia [Class A; LOE III-3] and
wide QRS-complex tachycardia [Class A; Expert Consensus Opinion] (Refer Guideline
12.5).
ATROPINE
Parasympathetic cardiac blockade with atropine may be indicated if bradycardia is caused by
vagal stimulation or cholinergic drug toxicity 1.
The IV or IO dose is 20mcg/kg [Class A; Expert Consensus Opinion] and the ETT dose 30
mcg/kg 1 [Class A; LOE II].
Bradycardia caused by hypoxaemia should be treated with ventilation and oxygen but if
unresponsive, should be treated with adrenaline 1.
Severe bradycardia and or bradycardia with hypotension should be treated with adrenaline,
not atropine.
CALCIUM
Calcium may be used as an inotropic or vasopressor but it has no place in the management of
an arrhythmia unless it is caused by hyperkalaemia, hypocalcaemia, hypermagnesaemia or
calcium channel blocker 1. It should not be given routinely at cardiac arrest [Class A; Expert
Consensus Opinion] and is associated with worse outcome 1.
Calcium (0.15 mmol/kg) is the antidote to hypotension caused by a calcium channel blocker.
The intravenous or intraosseous dose is 0.2mL/kg of 10% calcium chloride or approximately
0.7mL/kg of 10% calcium gluconate (20 mg/kg). [Class A, Expert Consensus Opinion]
GLUCOSE
Hypoglycaemia may be present in paediatric critical illness [LOE IV], particularly in infants.
Hyperglycaemia also occurs in paediatric critical illness and is associated with increased
mortality [LOE IV] but it is not known if this is the cause. The normal level is 3-8 mmol/L.
The blood sugar level should be checked during CPR and after ROSC with the aim of
ensuring normoglycaemia 3 [Class A; Expert Consensus Opinion]. Hypoglycaemia may be
treated with 0.25g/kg glucose by IV or IO infusion with any hyperosmolar solution, for
example, 0.5ml/kg of 50% (only via a central venous line) or 2.5ml/kg of 10%. Avoid
extravasation, especially from peripheral veins, and avoid overdosage. The maintenance
requirement to avoid hypoglycaemia in infancy is approximately 5-8 mg/kg/min.
LIGNOCAINE
Although lignocaine has a membrane stabilizing effect and a potential to aid defibrillation, it
actually increases the defibrillation threshold. A benefit in the treatment of ventricular
fibrillation has never been demonstrated. Indeed, it is associated with worse outcome
compared with placebo when used as a prophylactic agent against dysrrhythmia after
myocardial infraction 10-12. [LOE I]. It is inferior to amiodarone for shock-resistant ventricular
fibrillation [LOE II] and has little if any place in management of this dysrrhythmia [Class A;
Expert Consensus Opinion]. It is inferior to amiodarone for the treatment of shock-resistant
ventricular tachycardia [LOE II]. Lignocaine is not recommended in paediatric cardiac arrest
unless amiodarone is not available (Class A, Expert Consensus Opinion) or when IV and IO
access are impossible as lignocaine may be given via endotracheal tube. The dose of
lignocaine is 1mg/kg IV or IO.
MAGNESIUM

Hypomagnesaemia may cause life-threatening ventricular tachyarrhythmia, particularly when
associated with hypokalaemia. Magnesium is the preferred antidysrrythmic treatment for
polymorphic ventricular tachycardia (Torsade de pointes – “Twisting of peaks”) due to
acquired or congenital prolonged QT interval syndromes 2 [Class A; LOE IV]. Neither
increased ROSC nor survival in adults has been demonstrated in treatment of VF with
magnesium 4 [LOE IV]. The intravenous or intraosseous bolus dose of magnesium sulphate is
0.1-0.2 mmol/kg followed by an infusion of 0.3mmol/kg over 4 hours.
POTASSIUM
Hypokalaemia may cause a life-threatening tachydysrhythmia. Emergency treatment is the
intravenous or intraosseous administration of 0.03 - 0.07 mmol/kg by slow injection [Class
A; Expert Consensus Opinion] over several minutes. If the situation is critical but not
immediately life-threatening severe hypokalaemia may be treated with an infusion of 0.2 -
0.5mmol/kg/hour to a maximum of 1mmol/kg.
Extreme caution in the use of concentrated solutions of potassium is advised. Infusions
should only be given by infusion pumps and frequent (half-hourly – hourly) serum
monitoring with continuous ECG display is required, preferably in an intensive care unit
setting. Mistakes in the calculation of potassium requirement and inadvertent administration
of potassium cause avoidable deaths. (Note that a small bolus injection may cause a
dangerous rise in serum potassium: a 1 mmol bolus of potassium in a 5 kg infant theoretically
raises the serum level approximately 4 mmol/L). Therapies which rapidly decrease serum
potassium level are intravenous glucose + insulin, inhaled or intravenous salbutamol +
intravenous glucose or a combination of these agents (insulin + glucose + salbutamol) with or
without sodium bicarbonate. Sodium bicarbonate alone is the least effective therapy [LOE
III-1].
PROCAINAMIDE
Numerous observational studies and small case series 3 suggest that procainamide can be
used to treat haemodynamically stable supraventricular tachycardia and ventricular
tachycardia in children [Class B; LOE IV]. The intravenous dose is 10-15 mg/kg infused over
30-60 minutes.
SODIUM BICARBONATE
Sodium bicarbonate has a limited and unproven place in the management of cardiorespiratory
arrest and routine administration is not recommended 1-3. Administration of IV or IO sodium
bicarbonate neutralizes hydrogen ions in the blood but in doing so produces carbon dioxide
which may re-enter cells to exacerbate intracellular acidosis.
Other deleterious effects include hypernatraemia and hyperosmolality which may depress
myocardial function. Nonetheless, administration of sodium bicarbonate may be useful in
severe metabolic acidosis (pH < 7.1) or prolonged arrest. The IV or IO dose is 0.5-1 mmol/kg
after adequate ventilation with oxygen and chest compression have been established [Class B;
Expert Consensus Opinion].
VASOPRESSIN

Vasopressin is an alternative vasopressor to adrenaline but a meta-analysis of trials
comparing vasopressin with adrenaline shows that vasopressin offers no advantages in the
treatment of adult ventricular fibrillation or tachycardia, pulseless electrical activity or
asystole [LOE I] 1.
Although vasopressin has been used in a series of paediatric case reports it has not been
investigated systematically in the paediatric age group and the optimal dose is unknown 1.
However, by extrapolation from adult experience a bolus dose would be approximately 0.5-
0.8 U/kg IV or IO [Class B; Expert Consensus Opinion].
FLUID THERAPY
If hypovolaemia is suspected as the cause of cardiorespiratory arrest, intravenous or
intraosseous crystalloid may be used initially for resuscitation 1 [Class A] as a bolus of
20mL/kg. Additional boluses or colloid solution should be titrated against the response.

REFERENCES
1.
de Caen AR, Kleinman ME, Chameides L, Atkins DL, Berg RA, Berg MD, Bhanji F, Biarent D, Bingham R, Coovadia AH, Hazinski MF, Hickey RW, Nadkarni VM, Reis AG, Rodriguez-Nunez A, Tibballs J, Zaritsky AL, Zideman D, On behalf of the Paediatric Basic and Advanced Life Support Chapter Collaborators. Part 10: Paediatric basic and advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2010;81:e213–e259. Consensus on Science and Treatment recommendations. Part 6: Paediatric basic and advanced life support. Resuscitation 2005; 67: 271-291. American Heart Association in collaboration with International Liaison Committee on Resuscitation. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: International Consensus on Science, Part 10: pediatric advanced life support. Resuscitation 2000; 46: 343-399. Advanced life support (Adult): 2010 International consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation 2010; 122: S345-S421. TABLE of DRUGS, FLUIDS, ENDOTRACHEAL TUBES and
DIRECT CURRENT SHOCK FOR PAEDIATRIC RESUSCITATION
Uncuffed size: Age/4 + 4 mm (2 years and above) Oral length: Age/2 + 12 cm (2 years and above) Nasal length: Age/2 + 14 cm (2 years and above) Direct Current shock (biphasic or monohasic) VF, pulseless VT, First Shock (4J/kg) and all subsequent shocks, Pulsatile VT, synchronized (approx 2J/kg): Joules SVT, synchronized (approx 1J/kg): Joules REFERENCE: Oakley P, Phillips B, Molyneux E, Mackway-Jones K. Updated standard reference chart. BMJ 1993; 306: 1613.

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Suzuki O, Yagi K : Formation of lipoperoxide in brain edema induced by cold injury. Experientia, 30: 248, 1974. Yagi K, Matsushima F, Suzuki O : Flavins in developing chick brain. J Nutr. Sci. Vitaminol., 21:65-67, 1975. Suzuki O, Nagase F, Yagi K : Tryptophan metabolism in developing chick brain. Brain Res., 93: 455-462, 1975. Suzuki O, Yagi K : 5-Hydroxytryptamine and monoamine oxidase in dev

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