Phenylephrine
Synthetic α1-agonist
Pure α1 agonist → vasoconstriction. No β activity.
Indications
- •Anesthesia-induced hypotension
- •OB spinal hypotension (preferred over ephedrine for fetal pH)
- •Mydriasis (ophthalmic)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Bolus | 50–200 mcg IV | — |
| Infusion (general OR) | 0.15–1.5 mcg/kg/min | — |
| OB spinal prophylaxis (SOAP 2018) | 25–50 mcg/min infusion at spinal placement; titrate to baseline SBP; OR variable-rate 50 mcg bolus PRN | — |
Pharmacokinetics
Onset 1 min. Duration 10–20 min.
Hemodynamic effects
↑SVR, ↑BP. Reflex bradycardia (often ↓CO).
Side effects
- !Bradycardia + ↓CO (relevant in poor LV function)
- !Reduced uteroplacental flow at high dose
Contraindications
- ×Severe LV dysfunction (relative — reduced CO with vasoconstriction)
Clinical pearls
- ★OB spinal: phenylephrine maintains umbilical artery pH better than ephedrine.
- ★Cardiac surgery off-pump: phenyl preferred for systemic pressure during graft anastomoses.
- ★Watch for reflex bradycardia in LVH/HOCM patients.
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.
- 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
- •FDA package insert
- •SOAP guidance on spinal hypotension management
