Hydralazine
Apresoline
Direct arterial vasodilator (antihypertensive)
Direct arteriolar smooth-muscle relaxation (afterload reduction), minimal venodilation. Reflex tachycardia is common.
Indications
- •Acute HTN (incl. preeclampsia — long OB track record)
- •Chronic HF (with nitrates, esp. Black patients — A-HeFT)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Acute HTN | 5–10 mg IV q20–30 min, titrate | — |
| Preeclampsia | 5 mg IV, then 5–10 mg q20–40 min | — |
Pharmacokinetics
Onset 5–20 min IV; UNPREDICTABLE, DELAYED peak (up to 10–20 min) → don't re-dose too soon (stacking → hypotension). Hepatic acetylation (genetic).
Hemodynamic effects
↓ SVR/BP + reflex tachycardia (avoid in active ischemia unless β-blocked).
Side effects
- !Reflex tachycardia
- !Headache, flushing
- !Drug-induced lupus (chronic, slow acetylators)
- !Fluid retention
Contraindications
- ×Coronary ischemia/tachycardia-sensitive (relative)
- ×SLE
Clinical pearls
- ★DELAYED, variable onset — the classic error is stacking doses q5 min → delayed precipitous hypotension. Wait 20–30 min.
- ★Reflex tachycardia — pair with a β-blocker if ischemia is a concern.
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
