ICU and You · Drugstore · Number 1
The drug you will reach for fastest, in the patient where the arithmetic is least forgiving
Drugstore is for drug profiles. Each one runs the same way: the few things that matter most, then the practical business of concentrations, routes and the errors that recur, and then the pharmacology proper — kinetics, dynamics, indications and adverse effects.
The intention is to serve two readers at once. The clinician who needs the drug at three in the morning, and the First Part candidate who has to be able to draw its dose–response curve. Those are different needs, and most drug references choose one. These pieces will try to do both, and will mark clearly which part is which.
Profiles will usually follow the fortnight's topic, but not always — some drugs belong to no particular age and will simply appear.
This one is adrenaline as it is used between one and five years: anaphylaxis, croup, arrest and shock. Not the whole drug — the whole drug is a textbook chapter — but the version of it that turns up in a small child, and the specific ways it goes wrong there.
| Situation | Dose | What that looks like |
|---|---|---|
| Anaphylaxis intramuscular |
10 microgram/kg maximum 500 microgram |
0.01 mL/kg of 1:1000, lateral thigh. Repeat at five minutes if not improving. Autoinjectors: 0.15 mg from about 15 kg, 0.3 mg from about 30 kg. |
| Cardiac arrest intravenous or intraosseous |
10 microgram/kg | 0.1 mL/kg of 1:10,000, every three to five minutes, flushed after. |
| Croup nebulised |
0.5 mL/kg of 1:1000 maximum 5 mL |
Buys time in moderate to severe disease. Wears off in a couple of hours, so the child is watched rather than sent home on the strength of it. |
| Shock infusion |
titrated from about 0.05 microgram/kg/min | Central line preferred. Peripheral is acceptable when the alternative is waiting, with the site watched and a plan for extravasation. |
Every one of those numbers must be checked against your own formulary and local guideline before use. They are here to be recognised, not copied.
The decimal point and the strength. A tenfold error in either direction is the recurring paediatric adrenaline incident. Say the concentration out loud, and have somebody else say it back.
The route. Intravenous adrenaline for anaphylaxis, given because a line happens to be in, is the wrong dose by the wrong route. Intramuscular is faster in practice, because the careful person giving it intravenously gives it slowly.
The autoinjector in a very small child. Below about 15 kg, an autoinjector into a small thigh can deliver past the muscle into bone — effectively an intraosseous dose, which is an intravenous dose. Draw it up instead.
The line it shares. Adrenaline is inactivated by alkali, so it does not go through a line running bicarbonate. And if it extravasates, treat it — phentolamine infiltration is the answer, and the site needs looking at rather than hoping.
What it is. An endogenous catecholamine from the adrenal medulla; a direct-acting, non-selective agonist at alpha-1, alpha-2, beta-1 and beta-2 receptors. It is given as the levorotatory isomer, which is far more potent than its mirror image.
What it does, and the reason dose matters. The receptor affinities differ, so the clinical effect shifts with concentration. At low doses beta effects dominate: increased rate and contractility through beta-1, bronchodilation and some vasodilation through beta-2, so the systemic resistance may actually fall. At higher doses alpha-1 vasoconstriction takes over and resistance rises. This is why the same drug can look like an inodilator at one rate and a vasoconstrictor at another, and why “a bit more adrenaline” is not a linear request.
In anaphylaxis, three actions at once. Alpha-1 constriction reverses the vasodilatation and reduces mucosal oedema. Beta-1 supports a failing output. Beta-2 relaxes bronchial smooth muscle and, importantly, stabilises mast cells and basophils, reducing further mediator release. No other single agent does all three, which is why antihistamines and steroids are adjuncts and not alternatives.
Kinetics. Not given orally: it is extensively conjugated in the gut wall and liver and would not survive first pass. Onset is within a minute or two intravenously, and around five to ten minutes after intramuscular injection into the thigh. Metabolism is by catechol-O-methyltransferase and monoamine oxidase to metanephrine and ultimately vanillylmandelic acid, with some uptake into sympathetic nerve endings.
The plasma elimination half-life of adrenaline is very short — of the order of a couple of minutes. What lasts longer after an intramuscular dose is absorption from the muscle, not elimination from the plasma.
That matters clinically. It is why the effect outlives the half-life, why repeating at five minutes is reasonable rather than reckless, and why an intravenous bolus behaves so differently from the same milligrams in a thigh. You will hear the intramuscular duration quoted as though it were the half-life. It is not.
Adverse effects, and the ones that mislead you. Tachyarrhythmia, hypertension and myocardial ischaemia are the feared ones. Tremor, pallor, anxiety and headache are common and frighten families who have just watched a child collapse. The metabolic effects are the ones that confuse monitoring: adrenaline raises glucose through glycogenolysis and gluconeogenesis, raises lactate through beta-2 stimulated aerobic glycolysis, and lowers potassium by driving it intracellularly. A rising lactate in a child on adrenaline is not automatically worsening perfusion, and reading it that way leads to more adrenaline.
One interaction worth knowing. In a patient on a non-selective beta-blocker, beta effects are blunted and alpha effects are unopposed — so the response may be hypertension without the expected bronchodilation. Glucagon is the classical rescue. Rare in a three-year-old, standard in a viva.
The predictable asks: draw the dose–response relationship and explain the shift from beta to alpha predominance. Explain why adrenaline is not given orally. Name the metabolic pathway and its end products. Explain the mechanism of its effect in anaphylaxis, by receptor. Account for the rise in lactate and glucose and the fall in potassium.
The structure that collects marks: classify it (endogenous catecholamine, direct-acting, non-selective), then pharmaceutics (presentations and the two strengths), then kinetics, then dynamics by receptor, then adverse effects, then the clinical turn — and give values with units wherever you can.
Which drug should the Drugstore cover next — and what do you actually want from a drug profile?
The balance in this first one is a guess: keynotes, then the practical, then the pharmacology. If you are a clinician and the pharmacology section is more than you need, say so. If you are sitting the First Part and it is nowhere near enough, say that too. I would rather build the format around what people use than around what I imagine they use.
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