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Autonomic pharmacology in anaesthesia
In theatre heart rate and blood pressure are controlled with a small group of drugs: antimuscarinics (atropine, glycopyrrolate), beta-blockers (esmolol, labetalol), alpha-2 agonists and vasodilators (nitroglycerin, nitroprusside, hydralazine) — and each is known for its own special effect.
Why it matters in the exam
The exam asks how atropine differs from glycopyrrolate (passage into the brain), what central anticholinergic syndrome is and what treats it (physostigmine), why esmolol suits tachycardia during surgery (a half-life of about 9 minutes), the alpha-to-beta ratio of labetalol, and what cyanide toxicity from nitroprusside is — metabolic acidosis and a high mixed venous saturation. It also asks about abrupt withdrawal of clonidine.
Atropine is a tertiary amine and enters the brain — in older patients it may cause confusion, and at high doses central anticholinergic syndrome: fever, dry flushed skin, dilated pupils, tachycardia and confusion. Glycopyrrolate is a quaternary amine, does not cross into the brain or the placenta, dries secretions well and raises heart rate less. Physostigmine, which enters the brain, reverses the central syndrome, and neostigmine does not.
Esmolol is broken down by red cell esterases and acts for a few minutes — it suits the response to laryngoscopy and transient tachycardia. Labetalol blocks alpha-1 and beta, at a ratio of about 1 to 7 when given intravenously, and suits hypertension in pregnancy. Nitroglycerin dilates mainly veins and lowers preload; nitroprusside dilates arteries and veins and acts fast, but at a high or prolonged dose cyanide is released — treated with hydroxocobalamin and sodium thiosulfate. Abrupt withdrawal of clonidine may cause severe rebound hypertension.
Key points
- Atropine enters the brain; glycopyrrolate does not.
- Central anticholinergic syndrome — physostigmine.
- Esmolol very short; labetalol blocks alpha and beta.
- Nitroprusside — cyanide: acidosis and high venous saturation.
- Clonidine is not stopped abruptly.
Summary table
| Drug | Mechanism | Use | Special feature |
|---|---|---|---|
| Atropine | Antimuscarinic, enters the brain | Bradycardia | Central anticholinergic syndrome |
| Glycopyrrolate | Antimuscarinic, does not enter the brain or placenta | Drying secretions; with neostigmine | Less tachycardia and confusion |
| Esmolol / labetalol | Short beta-1 blocker / alpha-1 and beta | Tachycardia and hypertension in surgery | Esmolol about 9 minutes; labetalol in pregnancy |
| Clonidine / dexmedetomidine | Alpha-2 agonists | Sedation, opioid sparing | Rebound hypertension on abrupt withdrawal |
| Nitroglycerin / nitroprusside | Venodilator / arterial and venous dilator | Ischaemia, hypertension | Cyanide with nitroprusside: acidosis and high venous saturation |
In the full version for subscribers
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Sources
- Miller's Anesthesia, 9th edition (2020) — Autonomic Nervous System: Physiology and Pharmacology; Cardiovascular Pharmacology
- Morgan & Mikhail's Clinical Anesthesiology, 7th edition (2022) — Anticholinergic Drugs; Adrenergic Agonists and Antagonists; Hypotensive Agents
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-02. The text may contain errors; when in doubt, check the source.