Milrinone
Primacor
Phosphodiesterase-3 inhibitor (inodilator)
Selective PDE3 inhibitor in cardiac + vascular smooth muscle. Increases intracellular cAMP → ↑contractility (positive inotropy) + ↓SVR + ↓PVR (vasodilation). 'INODILATOR' — distinct from pure inotropes (dobutamine) and pure vasodilators. Particularly effective for RV failure and pulmonary hypertension.
Indications
- •Acute decompensated heart failure (low cardiac output)
- •RV failure / pulmonary hypertension (lowers PVR more than other inotropes)
- •Post-cardiopulmonary bypass low cardiac output syndrome
- •Bridge to LVAD or transplant
- •Pediatric cardiac surgery
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Loading dose (often skipped to avoid hypotension) | 50 mcg/kg IV over 10-20 min | — |
| Maintenance infusion | 0.25-0.75 mcg/kg/min IV titrated | — |
| Pediatric cardiac | (weight-based) | 0.25-0.75 mcg/kg/min IV |
Pharmacokinetics
Onset 5-15 min IV. Half-life 2-3 h (much longer than dobutamine ~2 min). Renal excretion ~85% — accumulates in renal failure (reduce dose).
Hemodynamic effects
↑Contractility, ↓SVR, ↓PVR, modest ↑HR. Particularly valuable for RV failure: reduces PVR while supporting contractility.
Side effects
- !HYPOTENSION (vasodilation often dominates inotropy at low doses) — pre-load fluid, cautious in already hypotensive
- !Tachyarrhythmia + ventricular arrhythmia (less than dobutamine)
- !Thrombocytopenia (rare, prolonged use)
- !Increased mortality in chronic outpatient use (OPTIME-CHF) — restricted to acute settings
Contraindications
- ×Severe hypotension without pre-treatment
- ×Severe hypovolemia
- ×Severe renal impairment (relative)
Clinical pearls
- ★PRIMARY USE in cardiac anesthesia: post-CPB low cardiac output syndrome with pulmonary HTN.
- ★Often added to NOREPINEPHRINE: norepi for SVR, milrinone for inotropy/PVR — synergistic.
- ★SKIP THE LOADING DOSE in unstable patients — go straight to 0.25-0.5 mcg/kg/min infusion.
- ★Long half-life (2-3 h): wash-out takes hours. Plan accordingly.
- ★RENAL FAILURE: reduce to 0.1-0.3 mcg/kg/min if CrCl <30.
📊 Related teaching panels
Standalone diagrams matched to this topic.
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