SPOT IT
Rising EtCO₂ that won't fall with ventilation, tachycardia, rigidity
MH
Anaphylaxis is this type of reaction and this cause
Type B — immune (mast-cell degranulation)
First-line in anaphylaxis; works via α1, β1, β2
Adrenaline
1:1,000 adrenaline in mg/mL
1 mg/mL
A drug has a half-life of 2 hours. Approximately how long until it is largely cleared from the body?
8-10 HRS
Tingling lips, metallic taste, tinnitus are the early warning
LAST
The faulty calcium-release channel in MH.
Ryanodine receptor (RyR1)
Blocks the ryanodine receptor to stop MH
Dantrolene
mg in 20 mL of 0.5% bupivacaine
100 mg (5 mg/mL × 20)
For many drugs the oral dose is much larger than the intravenous dose. The best explanation is:
First-pass metabolism reduces the amount of oral drug reaching the circulation
Stridor and see-saw breathing at a light plane
Laryngospasm
Local anaesthetics block these
Voltage-gated sodium channels
The "lipid sink" antidote for LAST.
Lipid emulsion 20%
1 mL of 10 mg/mL metaraminol diluted to 20 mL
0.5 mg/mL
A drug has a narrow therapeutic window, what does this mean?
The range between the minimum effective dose (the amount needed to make the drug work) and the toxic dose (the amount that causes harmful side effects) is very small.
Collapse + bronchospasm + skin signs, all at once after a drug
Anaphylaxis
Opioids depress breathing by acting on these
μ-opioid receptors
Competitive μ-opioid antagonist, short half-life
Naloxone
Volume of sux for 1 mg/kg, 70 kg, stock 50 mg/mL
1.4 mL (70 ÷ 50)
A synergistic effect
When two drugs work together to create a result that is much greater than their individual roles
In MH, the sign that moves before the temperature
Rising EtCO₂ (earliest sign)
Sux apnoea is caused by a deficiency of this enzyme
Plasma (pseudo)cholinesterase
Deepens via GABA-A; also MH-safe for TIVA
Propofol
1% propofol
10mg/ml
Why can a tiny dose of a drug trigger anaphylaxis, when a Type A reaction needs a large dose?
Anaphylaxis is an immune reaction, not the drug's own pharmacology