"Understand the pharmacology, indications and contraindications, dose calculation and routes of administration of drugs used in resuscitation and the stabilisation of children in cardiac arrest."
Where better to start looking for resources on this kind of thing than in the anaesthetic literature?
Adrenaline
There is an anaesthetic FRCA tutorial here, which probably covers everything we need to know. It tells us similar things to LITFL. LITFL have a good summary here and here.
- Naturally occurring catecholamine
- Hormone and a neurotransmitter
- Broken down by monoamine oxidase (MAO) and catechol-O -methyltransferase (COMT).
- Comes in 1:1000 strength (in vials) or 1:10000 (mini-jets)
- Acts non selectively at all the adrenergic receptors (α1, α2, β1, β2, β 3)
- At low doses the beta effects predominate - increase heart rate
- At high doses the alpha effects predominate
- Produces the flight or fight response (sympathomimetic)
- Causes
- increased heart rate
- increased contractility
- vasoconstriction and vasodilation
- bronchodilation
- glycogenolysis
- smooth muscle relaxation
- Side effects are normally because of overdose or inappropriate use.
- Dizziness
- Palpitations
- Tremour
- Arrhythmias
- Hypertension
- Cerebral haemorrhage
- Acute pulmonary oedema
- Lactic acidosis
- Hyperlactaemia - with long term use
- Hyperglycaemia - with long term use
- Caution
- At all times: big effects on the cardiovascular symptoms
- In patients with arrhythmias, hypertension or ischaemic heart disease
- Care in patients taking Mono-Amine Oxidase Inhibitors
- Uses
- Cardiac Arrest: 1mg every 3-5 minutes, after 3rd shock. 10mcg/kg in children
This is in the guidelines, but its use is still controversial. - ROSC use 1: 100 000 to support BP if needed
- Anaphylaxis: Adult or > 12 500mcg IM or 50mcg IV titrated to effect if experienced in use.
6- 12 years: 300mcg IM or 1mcg/kg IV titrated to effect
<6: 150mcg IM or 1mcg/kg titrated to effect - Inotropic support: continuous infusion via central line with invasive BP monitoring
- 4mg adrenaline diluted to 50ml in saline or glucose
- Severe croup:
- 0.5 ml/kg of a 1:1000 solution (maximum of 5 ml)
- Topical or local vasoconstrictionRemember:
1ml of 1:1000 = 1 mg
1ml of 1:10 000 = 0.1 mg = 100 mcg
1ml of 1:100 000 = 0.01 mg = 10 mcg
CV pharmacology has a good summary with some pretty pictures. LITFL has a good summary and a more pharmacology focused tutorial - they do state that efficacy of amiodarone in paediatric children hasn't been established.
- Membrane stabilising anti-arrhythmic drug
- Increases the duration of the action potential
- Slows AV conduction
- Mild negative inotropic effect
- Causes peripheral vasodilation because of alpha-blocking effects
- The solvent with it causes histamine release.
- 25 - 60 days half life
- Class I, II, III & IV actions
- Generally considered a Class III arrhythmic drug
- Dose:
- 5mg/kg after third shock in shockable rhythms
- Repeat the dose after the fifth shock
- Central vein if possible - causes thrombophlebitis
- Side effects
- Pulmonary fibrosis
- Thyroid problems
- Can cause hypotension
- Can cause Bradycardia and AV Block
- Can cause liver enzyme elevations
- May be arrhythmogenic
There aren't so many summaries on atropine - probably because it's been taken out of the resus algorithm. There's something on CV pharmacology, LITFL summary and a page on the non resuscitation uses- Death Rattle.
- Atropine is a muscarinic receptor antagonist and bind to muscarinic receptors.
- Stops ACh from binding
- So stops the effects of vagal nerve activity on the heart
- Administration of less than 500mcg in adults and less than 100mcg in children can produce a paradoxical
bradycardia because of the central or peripheral parasympathomimatic
effects of low dose.
- Atropine rapidly crosses the placenta
- Atropine crosses the blood-brain barrier
- Side effects:
- tachycardia
- pupil dilation
- dry mouth
- urinary retention inhibition of sweating
- blurred vision
- constipation
- Contraindicated in patients with:
- glaucoma,
- pyloric stenosis and
- prostatic hypertrophy
- Uses
- Dose
- 10mcg/kg
Magnesium is a panacea for everything at the moment. There is a summary article here, BNF entry here and a LIFFL summary. There are some good flashcards for Paramedics here. AAFP has got an interesting simply written article about magnesium.
- Extracellular cation
- Depressant effect on the release of catecholamines
- Uses
- Eclampsia
- Torsades
- Asthma
- Contraindications
- Heart block
- Shock
- Persistent hypertension
- Hypocalcaemia
- Myocardial damage
- Cautions
- Renal damage
- Patients on digoxin
- Use of CNS depressants or neuromuscular blocking agents
- Side Effects
- Hypotension
- Sedation
- Confusion
- Bradycardia
- Pruritis
- Arrhythmias
- Decreased deep tendon reflexes
- Respiratory depression/paralysis
- Drowsiness
- Muscle weakness
- Complete heart block
- Dose
- Torsade de Pointe
- By intravenous injection over 10–15 minutes
- Child 1 month–18 years 0.1–0.2 mmol/kg (25–50 mg/kg magnesium sulfate heptahydrate); max. 8 mmol (2 g magnesium sulfate heptahydrate); dose repeated once if necessary
- Asthma
- Children over 2 years with severe acute asthma may be helped by intravenous infusion of magnesium sulfate injection 40 mg/kg (max. 2 g) over 20 minutes
- Used for: hyperkalaemia, hypocalcaemia, and over-dose of calcium-channel-blocking drugs
- Dose for urgent calcium correction
- By slow intravenous injection over 5–10 minutes
- Neonate 0.11 mmol/kg (0.5 mL/kg of calcium gluconate 10%) as a single dose. [Some units use a dose of 0.46 mmol/kg (2 mL/kg calcium gluconate 10%) for hypocalcaemia in line with US practice]
- Child 1 month–18 years 0.11 mmol/kg (0.5 mL/kg calcium gluconate 10%), max 4.5 mmol (20 mL calcium gluconate 10%)
From the PALS algorithm:
"The best treatment for acidaemia in cardiac arrest is a combination of effective chest compression and ventilation (good quality CPR). Administration of sodium bicarbonate generates carbon dioxide, which diffuses rapidly into the cells, exacerbating intracellular acidosis if it is not rapidly cleared via the lungs.
It also has the following detrimental effects:
- It produces a negative inotropic effect on an ischaemic myocardium.
- It presents a large, osmotically active, sodium load to an already compromised circulation and brain.
- It produces a shift to the left in the oxygen dissociation curve further inhibiting release of oxygen to the tissues.
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