The Oral Ward Vasopressor
Second-line oral vasopressor for HRS-AKI, always combined with Octreotide. Use only as bridge to ICU or when ICU admission is inappropriate.
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Mechanism: Prodrug converted to active metabolite (desglymidodrine). Selective -adrenergic agonist (peripheral vasoconstriction). Increases SVR and MAP without cardiac effects (no activity). Synergistic with Octreotide: Midodrine provides systemic vasoconstriction; Octreotide reduces splanchnic vasodilation.
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Dosing: HRS: PO q8h (titrate to maximum tolerated BP). Target: MAP increase of or MAP .
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PK: Onset: 30–60 minutes (oral). Peak Effect: 1–2 hours. Half-life: ~3–4 hours. Metabolism: Hepatic (prodrug activation). Elimination: Renal.
indications
- Hepatorenal Syndrome (HRS-AKI) – Second-line therapy. Ward-based therapy when ICU admission is inappropriate or as bridge to ICU.
- Off-label: Orthostatic hypotension, autonomic dysfunction.
evidence & efficacy
- HRS Efficacy: Significantly inferior to Terlipressin and Norepinephrine for HRS reversal.
- Response Rate: Lower than vasopressin analogs (~20–30% vs 40–50%).
- Limitation: No large RCTs; evidence primarily from small studies and case series.
cautions
- Severe bradycardia or heart block
- Severe peripheral vascular disease
- Urinary retention (prostatic hypertrophy)
- Supine hypertension (monitor closely)
- Coronary artery disease
- Thyrotoxicosis
- Adverse Effects: Supine hypertension (must monitor BP in supine position), piloerection, pruritus, urinary retention, bradycardia (rare, due to baroreceptor reflex).
special considerations
- Role: Used as a bridge to ICU or when ICU admission is deemed inappropriate (Goals of Care discussions).
- Combination Therapy in HRS: Synergistic effect when used with Octreotide.
- Limitation: Significantly inferior efficacy compared to IV vasoconstrictors; not recommended as first-line.
exam pearl
Midodrine + Octreotide is the “ward therapy” option when ICU/Norepinephrine is not available or appropriate.
related pages: Hepatorenal syndrome (HRS-AKI)