Enalaprilat (IV Enalapril)
Vasotec IV
IV ACE inhibitor (antihypertensive)
Enalaprilat is the active de-esterified ACE inhibitor → blocks angiotensin I→II conversion → ↓ SVR without reflex tachycardia; the only IV ACE inhibitor.
Indications
- •Hypertension when oral route unavailable
- •HTN with heart failure
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| IV | 1.25 mg IV q6h over 5 min (0.625 mg if on diuretics/renal impairment) | — |
Pharmacokinetics
Onset ~15 min. Duration ~6 h. Renally cleared.
Hemodynamic effects
↓ BP without reflex tachycardia; response variable (renin-dependent).
Side effects
- !Angioedema
- !Hyperkalemia
- !Acute kidney injury (bilateral RAS)
- !First-dose hypotension (high-renin/volume-depleted)
Contraindications
- ×Pregnancy
- ×History of ACE-inhibitor angioedema
- ×Bilateral renal artery stenosis
- ×Hyperkalemia
Clinical pearls
- ★Only IV ACE inhibitor. Response is unpredictable (renin-dependent) — not ideal for tight titration.
- ★Angioedema + hyperkalemia + AKI are the class watch-outs; contraindicated in pregnancy.
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
