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midodrine (ProAmatine, Gutron)

Tradename: ProAmantine. Indications: - symptomatic orthostatic hypotension (FDA-approved) - useful in the elderly with neurocardiogenic syncope [8] - symptomatic orthostatic hypotension (perhaps [5]) - treatment of vasovagal syncope in young, healthy persons with frequent episodes [7] - used in conjunction with octreotide for treatment of hepatorenal syndrome Contraindications: 1) severe heart disease 2) urinary retention 3) pheochromocytoma 4) thyrotoxicosis 5) persistent & severe supine hypertension 6) concurrent use of fludrocortisone Dosage: 1) 10 mg TID when patient is upright 2) do NOT administer after evening meal of < 4 hours before bedtime 3) dose may be given at 3-4 hours intervals 4) vasovagal syncope: start 2.5 mg BID; titrate to 10 mg TID (max) [7] Tabs: 2.5 mg, 5 mg. Dosage adjustment in renal failure: 1) start 2.5 mg PO BID 2) increase as necessary & tolerated Pharmacokinetics: 1) bioavailability of oral dose is 93% 2) midodrine is a prodrug 3) major active metabolite is desglymidodrine formed by deglycination of midodrine 4) plasma midodrine peaks 30 minutes after an oral dose with an elimination 1/2life of 25 minutes 5) desglymidodrine peaks in 1-2 hours 6) desglymidodrine elimination 1/2life of 3-4 hours 7) protein binding is minimal Monitor: renal function & hepatic function Adverse effects: 1) common (> 10%) - piloerection, pruritus, urinary urgency, urinary retention, polyuria, paresthesia 2) less common (1-10%) - supine hypertension, facial flushing, confusion, anxiety, dizziness, chills, rash, dry skin, xerostomia, nausea, abdominal pain, dysuria 3) uncommon (< 1%) - flushing, headache, insomnia, flatulence, leg cramps, visual changes Drug interactions: 1) concurrent use of fludrocortisone results in hypernatremia &/or an increase in intra-ocular pressure 2) bradycardia may accentuated by: a) digoxin b) psychotherapeutic agents c) beta blockers 3) alpha-adrenergic agonists may enhance hypertensive effects 4) alpha-adrenergic antagonists may antagonize effects of midodrine Mechanism of action: 1) enzymatic hydrolysis to active metabolite desglymidodrine 2) activates alpha-1 adrenergic receptors on arterioles & veins to increase peripheral vascular resistance 3) a 10 mg dose increases standing systolic BP 15-30 mm Hg 4) clinical benefit has not been demonstrated [5]

Interactions

drug adverse effects (more general classes)

Related

orthostatic hypotension; Bradbury-Eggleston Syndrome; postural orthostatic tachycardia syndrome (POTS)

General

alpha-1 adrenergic receptor agonist

Properties

AGONIST-FOR: alpha-1 adrenergic receptor MISC-INFO: elimination route LIVER pregnancy-category C safety in lactation ?

Database Correlations

PUBCHEM correlations

References

  1. Low et al JAMA 277:1046-51 1997
  2. Kaiser Permanente Northern California Regional Drug Formulary, 1998
  3. PDR 56th edition, 2002
  4. Department of Veterans Affairs, VA National Formulary
  5. FDA MedWatch [Posted 08/16/2010] Midodrine hydrochloride: FDA Proposes Withdrawal of Low Blood Pressure Drug http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm222640.htm
  6. Medical Knowledge Self Assessment Program (MKSAP) 18, American College of Physicians, Philadelphia 2018
  7. Sheldon R, Faris P, Tang A et al. Midodrine for the prevention of vasovagal syncope: A randomized clinical trial. Ann Intern Med 2021 Aug 3; [e-pub]. PMID: 34339231 https://www.acpjournals.org/doi/10.7326/M20-5415 - Brignole M. Establishing the efficacy of midodrine to prevent vasovagal syncope. Ann Intern Med 2021 Aug 3; [e-pub]. PMID: 34339220 https://www.acpjournals.org/doi/10.7326/M21-2859
  8. Geriatric Review Syllabus, 11th edition (GRS11) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2022