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Chapter: Clinical Anesthesiology: Clinical Pharmacology: Adjuncts to Anesthesia


Clonidine (Catapres, Duraclon) is an imidazoline derivative with predominantly α2-adrenergic ago-nist activity.


Mechanism of Action

Clonidine (Catapres, Duraclon) is an imidazoline derivative with predominantly α2-adrenergic ago-nist activity. It is highly lipid soluble and readily penetrates the blood–brain barrier and the placenta. Studies indicate that binding of clonidine to recep-tors is highest in the rostral ventrolateral medulla in the brainstem (the final common pathway for sym-pathetic outflow) where it activates inhibitory neu-rons. The overall effect is to decrease sympathetic activity, enhance parasympathetic tone, and reduce circulating catecholamines. There is also evidence that much of clonidine’s antihypertensive action occurs via binding to a nonadrenergic (imidazo-line) receptor. In contrast, its analgesic effects, par-ticularly in the spinal cord, are mediated entirely via pre- and possibly postsynaptic α2-adrenergic recep-tors that block nociceptive transmission. Clonidine also has local anesthetic effects when applied to peripheral nerves and is frequently added to local anesthetic solutions.

Clinical Uses

Clonidine is a commonly used antihyper-tensive agent that reduces sympathetic tone,decreasing systemic vascular resistance, heart rate, and blood pressure. In anesthesia, clonidine is used as an adjunct for epidural, caudal, and peripheral nerve block anesthesia and analgesia. It is often used in the management of patients with chronic neuro-pathic pain to increase the efficacy of epidural opioid infusions. When given epidurally, the analgesic effect of clonidine is segmental, being localized to the level at which it is injected or infused. When added to local anesthetics of intermediate duration (eg, mepi-vacaine or lidocaine) administered for epidural or peripheral nerve block, clonidine will markedly pro-long both the anesthetic and analgesic effects.

Unlabeled/investigational uses of clonidine include serving as an adjunct in premedication, control of withdrawal syndromes (nicotine, opioids, alcohol, and vasomotor symptoms of menopause), and treatment of glaucoma as well as various psychi-atric disorders.

Side Eects

Sedation, dizziness, bradycardia, and dry mouth are common side effects. Less commonly, bradycardia, orthostatic hypotension, nausea, and diarrhea may be observed. Abrupt discontinuation of clonidine following long-term administration (>1 mo) can produce a withdrawal phenomenon characterized by rebound hypertension, agitation, and sympa-thetic overactivity.


Epidural clonidine is usually started at 30 mcg/h in a mixture with an opioid or a local anesthetic. Oral clonidine is readily absorbed, has a 30–60 min onset, and lasts 6–12 h. In the treatment of acute hyperten-sion, 0.1 mg can be given orally every hour until the blood pressure is controlled, or up to a maximum of 0.6 mg; the maintenance dose is 0.1–0.3 mg twice daily. Transdermal preparations of clonidine can also be used for maintenance therapy. They are available as 0.1, 0.2, and 0.3 mg/d patches that are replacedevery 7 days. Clonidine is metabolized by the liver and excreted renally. Dosages should be reduced for patients with renal insufficiency.

Drug Interactions

Clonidine enhances and prolongs sensory and motor blockade from local anesthetics. Additive effects with hypnotic agents, general anesthetics, and sedatives can potentiate sedation, hypotension, and bradycardia. The drug should be used cautiously, if at all, in patients who take β-adrenergic blockers and in those with significant cardiac conduction system abnormalities. Lastly, clonidine can mask the symp-toms of hypoglycemia in diabetic patients.

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