Clevidipine
Cleviprex
Ultra-short-acting dihydropyridine calcium channel blocker
Arterial-selective L-type Ca²⁺ blockade → ↓ SVR with little effect on venous capacitance/preload or myocardial contractility. Ester-metabolized (like esmolol/remifentanil).
Indications
- •Acute perioperative hypertension (titratable IV BP control)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| IV infusion | 1–2 mg/hr, double q90 sec toward effect (typical 4–6 mg/hr; max 32 mg/hr) | — |
Pharmacokinetics
Onset 2–4 min. Half-life ~1 min (blood/tissue esterases) — very fast on/off, organ-independent.
Hemodynamic effects
Smooth ↓ BP with reflex tachycardia possible; preserves preload/contractility.
Respiratory effects
None.
Side effects
- !Reflex tachycardia
- !Lipid emulsion vehicle (like propofol — egg/soy allergy, caloric load, avoid in lipid disorders)
- !Rebound HTN after abrupt stop
Contraindications
- ×Egg/soy allergy
- ×Defective lipid metabolism / severe hyperlipidemia
- ×Severe aortic stenosis
Clinical pearls
- ★Lipid emulsion formulation (like propofol) — egg/soy allergy caution + counts as calories.
- ★Ultra-short half-life → nicardipine-like control but far more titratable; great for tight OR BP swings.
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.
Browse all classes: /reference/drugs
Suggested reading
- •Stoelting & Hines, Pharmacology & Physiology in Anesthetic Practice, 6e
- •Miller's Anesthesia, 9e
- •FDA package insert
