Inamrinone (Amrinone)
Inocor
Phosphodiesterase-3 inhibitor inodilator
Inhibits cardiac PDE3 → ↑ cAMP → inotropy + vasodilation (inodilator); mechanism identical to milrinone (milrinone has largely replaced it).
Indications
- •Acute decompensated heart failure / low-output states (historical; milrinone preferred)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Load + infusion | 0.75 mg/kg IV over 2–3 min, then 5–10 mcg/kg/min | — |
Pharmacokinetics
Onset ~5 min. Half-life ~3–6 h. Renal + hepatic.
Hemodynamic effects
↑ CO + ↓ SVR/PVR (afterload reduction); can cause hypotension.
Side effects
- !THROMBOCYTOPENIA (more than milrinone — a key reason it fell out of favor)
- !Hypotension, arrhythmia
Contraindications
- ×Severe aortic/pulmonic valvular disease
- ×Thrombocytopenia (relative)
Clinical pearls
- ★Same inodilator mechanism as milrinone but causes dose-dependent thrombocytopenia → milrinone replaced it.
- ★Like all PDE3 inhibitors: inotropy + vasodilation; watch for hypotension.
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
