Clonidine
Catapres · Duraclon (epidural)
Central alpha-2 adrenergic agonist (antihypertensive / analgesic adjunct)
Central α2 agonism → ↓ sympathetic outflow → ↓ HR/BP; also spinal α2 analgesia + sedation.
Indications
- •Hypertension
- •Neuraxial/regional analgesic adjunct (prolongs blocks)
- •Opioid/alcohol/benzodiazepine withdrawal
- •Sympathetically-mediated pain
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Oral HTN / premed | 0.1–0.3 mg PO | — |
| Epidural adjunct | 1–2 mcg/kg (or per protocol) | — |
Pharmacokinetics
Oral onset 30–60 min; long duration. Renal + hepatic clearance.
Hemodynamic effects
↓ HR + ↓ BP; sedation. Blunts intraoperative catecholamine surges.
Respiratory effects
Minimal respiratory depression (α2 — like dexmedetomidine).
Side effects
- !Sedation, dry mouth
- !REBOUND HYPERTENSION on abrupt withdrawal (do not stop suddenly perioperatively)
- !Bradycardia
Contraindications
- ×Abrupt discontinuation (rebound HTN)
- ×Bradyarrhythmia (relative)
Clinical pearls
- ★REBOUND HYPERTENSION if stopped abruptly — continue perioperatively or use a patch.
- ★α2 mechanism (oral cousin of dexmedetomidine): sedation + analgesia + sympatholysis without respiratory depression; prolongs neuraxial/peripheral blocks.
Other drugs in Cardiac / BP
- Epinephrine
α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.
- Norepinephrine
Strong α1 → vasoconstriction. Mild β1 → modest inotropy. Minimal β2.
- Phenylephrine
Pure α1 agonist → vasoconstriction. No β activity.
- Dexmedetomidine
α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.
- Vasopressin
Endogenous nonapeptide hormone. V1 receptor agonist on vascular smooth muscle (Gq → IP3 → Ca²⁺ → vasoconstriction). V2 on renal collecting ducts (Gs → cAMP → aquaporin insertion → water reabsorption). At pressor doses (0.01–0.04 U/min), V1 effects dominate.
- Esmolol
Selective β1-adrenergic receptor antagonist. Decreases HR, contractility, conduction velocity, and AV node refractoriness. Selectivity for β1 over β2 reduces (does not eliminate) bronchospasm risk vs non-selective beta-blockers.
- Magnesium Sulfate
Multiple mechanisms: (1) NMDA receptor antagonism (anticonvulsant, analgesic); (2) Voltage-gated calcium channel blockade in vascular + uterine smooth muscle (vasodilation, tocolysis); (3) Decreased ACh release at neuromuscular junction (NMB potentiation); (4) Membrane stabilization (antiarrhythmic, especially torsades).
- Amiodarone
Multichannel blockade — primarily class III (K+ channel block → prolonged repolarization, increased refractory period), plus class I (Na+ block), class II (β-blocker), class IV (Ca²⁺ block) properties. Treats most supraventricular AND ventricular arrhythmias. Long elimination half-life (weeks–months) limits chronic use.
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Suggested reading
- •Stoelting & Hines, Pharmacology & Physiology in Anesthetic Practice, 6e
- •Miller's Anesthesia, 9e
- •FDA package insert
