Dexmedetomidine
Precedex
Selective α2-adrenergic agonist
α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.
Indications
- •ICU sedation
- •Awake fiberoptic intubation
- •Procedural sedation
- •Adjunct for emergence delirium prevention
- •Opioid-sparing analgesia
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Loading | 1 mcg/kg over 10 min (often skipped to avoid hypotension) | — |
| Maintenance | 0.2–0.7 mcg/kg/hr | — |
| Procedural | 0.5–1 mcg/kg load, 0.5–1 mcg/kg/hr | — |
Pharmacokinetics
Onset 5–10 min. Hepatic CYP. Half-life 2 h.
Hemodynamic effects
Biphasic: transient ↑BP at load (peripheral α2B vasoconstriction) → sustained ↓HR + ↓BP. Bradycardia frequent.
Respiratory effects
Minimal — preserved spontaneous ventilation, the key advantage.
Side effects
- !Bradycardia (sometimes profound, especially with vagotonic stimuli)
- !Hypotension
- !Withdrawal HTN if abrupt stop after long infusion
Contraindications
- ×Advanced heart block without pacer
- ×Severe LV dysfunction (relative)
Clinical pearls
- ★Skip the load if patient is already hypotensive.
- ★Lower MAC: dex 0.4 mcg/kg/hr lowers volatile MAC ~25%.
- ★Useful for awake intubation: patient cooperative, breathes spontaneously, less coughing.
📊 Related teaching panels
Standalone diagrams matched to this topic.
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.
- 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.
- Nicardipine
Selective L-type voltage-gated calcium channel blocker, dihydropyridine class (vascular >> cardiac selectivity). Vascular smooth muscle relaxation → arterial vasodilation → afterload reduction. Minimal direct cardiac inotropic or chronotropic effect at clinical doses (vs verapamil/diltiazem which are non-selective).
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