Fenoldopam
Corlopam
Selective dopamine-1 (D1) receptor agonist — antihypertensive
D1 agonist → arterial + renal/splanchnic/coronary vasodilation. Increases renal blood flow, natriuresis, and diuresis while lowering BP.
Indications
- •Severe HTN needing IV control, esp. with renal compromise (theoretical renal protection)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| IV infusion | 0.05–0.1 mcg/kg/min, titrate q15 min (up to ~1.6 mcg/kg/min) | — |
Pharmacokinetics
Onset ~5 min. Half-life ~5 min → titratable. No organ-specific dependence.
Hemodynamic effects
↓ BP + reflex tachycardia; increases renal perfusion.
Respiratory effects
None.
Side effects
- !Reflex tachycardia
- !Hypokalemia
- !↑ intraocular pressure (avoid in glaucoma)
- !Headache/flushing
Contraindications
- ×Glaucoma / ↑ IOP
- ×Sulfite allergy (formulation)
Clinical pearls
- ★Unique among IV antihypertensives for INCREASING renal blood flow — favored when renal protection is desired.
- ★Raises intraocular pressure — avoid in glaucoma.
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).
Suggested reading
- •Stoelting & Hines, Pharmacology & Physiology in Anesthetic Practice, 6e
- •Miller's Anesthesia, 9e
- •FDA package insert
