Angiotensin II
Giapreza
Synthetic vasopressor (renin-angiotensin system peptide)
Directly activates AT1 receptors → potent arterial + venous vasoconstriction; also aldosterone/ADH release. A vasopressor with a mechanism distinct from catecholamines/vasopressin.
Indications
- •Refractory distributive/vasodilatory shock (catecholamine-sparing add-on — ATHOS-3)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| IV infusion | Start 20 ng/kg/min, titrate (max 80 ng/kg/min first 3 h, then ≤40) | — |
Pharmacokinetics
Onset minutes. Very short half-life (<1 min) → titratable.
Hemodynamic effects
Raises MAP rapidly; catecholamine-sparing.
Side effects
- !THROMBOSIS (VTE) — give DVT prophylaxis
- !Digital/mesenteric ischemia (potent vasoconstriction)
Contraindications
- ×Untreated hypercoagulable/high VTE risk (relative — add prophylaxis)
Clinical pearls
- ★Third-mechanism vasopressor (alongside catecholamines + vasopressin) for refractory vasodilatory shock.
- ★Notable thrombosis risk — VTE prophylaxis is recommended.
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
