Anaes · Anaesthetic adjuncts
Adrenaline
Also known as Epinephrine · Direct-acting catecholamine · Alpha and beta adrenergic agonist · Adrenal medullary hormone
Adrenaline (epinephrine) is the physiological HORMONE of the adrenal medulla and a DIRECT-ACTING catecholamine that is a potent agonist at the ALPHA-1, ALPHA-2, BETA-1 and BETA-2 adrenergic receptors, making it the only endogenous catecholamine with significant BETA-2 activity. Its exam-defining feature is dose-dependent receptor selectivity: at LOW infusion doses (0.01 to 0.05 mcg per kg per min) beta-2 effects dominate (bronchodilation, vasodilation), at MODERATE doses beta-1 and beta-2 effects combine (increased cardiac output with bronchodilation), and at HIGH doses (above 0.5 mcg per kg per min) alpha-1 vasoconstriction dominates (raised systemic vascular resistance) (Dong 2026, Yahya 2026). These three receptor tiers underpin the three great clinical uses: ANAPHYLAXIS (first-line, intramuscular 500 micrograms, where alpha-1 reverses oedema and hypotension, beta-2 bronchodilates and beta-1 supports the circulation — Najem 2026), CARDIAC ARREST (1 mg intravenously every 3 to 5 minutes on the advanced life support algorithm, where alpha-1 vasoconstriction raises aortic diastolic pressure and improves coronary and cerebral perfusion), and SEVERE ASTHMA (beta-2 bronchodilation). Adrenaline is also an inotropic infusion for cardiogenic shock, a local anaesthetic additive (vasoconstriction), and a nebulised agent for croup (Chirumamilla 2026). It has a very short half-life of about 2 to 3 minutes (continuous infusion for sustained effect; metabolised by COMT and MAO), and it is the most arrhythmogenic catecholamine — tachyarrhythmias (ventricular tachycardia, ventricular fibrillation) plus hypertension, myocardial ischaemia, HYPERGLYCAEMIA (beta-2 glycogenolysis), HYPOKALAEMIA (beta-2 cellular potassium uptake) and a LACTATE RISE (beta-2 glycolysis, NOT lactic acidosis) dominate the adverse-effect profile; extravasation causes necrosis reversed by phentolamine. Against noradrenaline, adrenaline uniquely adds beta-2 (bronchodilation, more tachycardia, hyperglycaemia, lactate); against phenylephrine, adrenaline is a broad alpha-plus-beta agonist where phenylephrine is pure alpha-1. The NAP6 audit confirmed neuromuscular blocking agents as the leading cause of perioperative anaphylaxis and adrenaline (intramuscular 500 micrograms) as first-line treatment. Built on the anaphylaxis-in-schools epinephrine law study (Najem 2026), the neonatal septic shock first-line vasopressor trial (Yahya 2026), the refractory malignant upper GI bleeding case report (Chirumamilla 2026), the vasopressor selection and postoperative delirium in older adults study (Dong 2026), the cost and environmental comparison of anaesthetic emergency vasopressors (Parkinson 2026).
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Red flags
- Adrenaline is the first-line treatment for ANAPHYLAXIS and must be given EARLY by the INTRAMUSCULAR route — 500 micrograms (0.5 mL of 1 in 1000) into the anterolateral thigh. Delay or inappropriate intravenous dosing in anaphylaxis increases mortality. The NAP6 audit confirmed neuromuscular blocking agents as the leading cause of perioperative anaphylaxis and intramuscular adrenaline as first-line treatment (Najem 2026).
- Adrenaline is the MOST ARRHYTHMOGENIC catecholamine. Beta-1 stimulation precipitates ventricular tachycardia and ventricular fibrillation, particularly at high infusion doses and in the ischaemic or digitalised heart. This is the single most important safety distinction from noradrenaline, which lacks beta-2 activity and causes less tachyarrhythmia.
- Adrenaline causes a LACTATE RISE through beta-2-driven aerobic glycolysis — this is NOT lactic acidosis and does NOT by itself indicate tissue hypoperfusion. Confusing the two leads to inappropriate escalation of resuscitation. Beta-2 also causes HYPERGLYCAEMIA (glycogenolysis) and HYPOKALAEMIA (cellular potassium uptake), both relevant in the diabetic patient and during prolonged infusion.
- Extravasation of concentrated adrenaline causes tissue NECROSIS through intense alpha-1 vasoconstriction. A running infusion above moderate dose should go through a CENTRAL line where practical, and any extravasation must be promptly treated with INTRADERMAL PHENTOLAMINE (an alpha-1 antagonist) to prevent skin loss.
- Dose-dependent receptor selectivity must be applied at the bedside: a LOW dose adrenaline infusion (0.01 to 0.05 mcg per kg per min) can produce beta-2 VASODILATION and worsen hypotension rather than raise it — escalating a septic-shock patient from a low to a higher dose changes the dominant receptor from beta-2 to alpha-1 (Yahya 2026, Dong 2026).
Meet the patient
A patient in the anaesthetic room becomes hypotensive, flushed, and wheezy within a minute of receiving rocuronium — textbook perioperative anaphylaxis. The single most important action in the next 60 seconds is 500 micrograms of intramuscular adrenaline into the anterolateral thigh, not a fluid debate or an intravenous fumble. Everything else follows that.[1]
Hold the two ideas that hold the whole drug together: adrenaline's clinical effect changes with the dose because the four receptor subtypes have different affinities (beta-2 is most sensitive, alpha-1 least), and the drug is mandatory and non-substitutable in anaphylaxis and cardiac arrest but too arrhythmogenic and metabolic to be a routine perioperative vasopressor.[1]
References6ShowHide
- [1]Najem J, et al. Effectiveness of a Provincial Law to Improve Epinephrine Use for Anaphylaxis in Schools in Alberta, Canada: A Pre-Post Study Int Arch Allergy Immunol, 2026.PMID 42360928
- [2]Yahya R, et al. First-line vasopressor therapy in neonates with fluid-refractory septic shock: A systematic review and meta-analysis of randomized controlled trials Am J Emerg Med, 2026.PMID 42361705
- [3]Chirumamilla L, et al. Multidisciplinary management of refractory malignant upper gastrointestinal bleeding in metastatic gastric adenocarcinoma BMJ Case Rep, 2026.PMID 42362336
- [4]Dong T, et al. Vasopressor Selection and Postoperative Delirium in Older Adults: A Propensity-Matched Database Analysis Semin Cardiothorac Vasc Anesth, 2026.PMID 42359892
- [5]Parkinson EA, et al. The Financial and Environmental Cost of Anaesthetic Emergency Drugs: Comparing Ampoules With Prefilled Syringes. Cureus, 2026.PMID 42005180
- [7]Shyu D, et al. Overview of Peripheral Vasopressor Use in an Academic Health System. Ann Am Thorac Soc, 2025.PMID 40126143