midodrine (ProAmatine, Gutron)
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Introduction
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
- severe heart disease
- urinary retention
- pheochromocytoma
- thyrotoxicosis
- persistent & severe supine hypertension
- concurrent use of fludrocortisone
Dosage
- 10 mg TID when patient is upright
- do NOT administer after evening meal of < 4 hours before bedtime
- dose may be given at 3-4 hours intervals
- 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
Pharmacokinetics
- bioavailability of oral dose is 93%
- midodrine is a prodrug
- major active metabolite is desglymidodrine formed by deglycination of midodrine
- plasma midodrine peaks 30 minutes after an oral dose with an elimination 1/2life of 25 minutes
- desglymidodrine peaks in 1-2 hours
- desglymidodrine elimination 1/2life of 3-4 hours
- protein binding is minimal
elimination via liver
Monitor
renal function & hepatic function
Adverse effects
- common (> 10%)
- less common (1-10%)
- supine hypertension, facial flushing, confusion, anxiety, dizziness, chills, rash, dry skin, xerostomia, nausea, abdominal pain, dysuria
- uncommon (< 1%)
- drug adverse effects of adrenergic receptor agonists
- drug adverse effects of alpha-adrenergic receptor agonists
- drug adverse effects of sympathomimetic(s)
Drug interactions
- concurrent use of fludrocortisone results in hypernatremia &/or an increase in intra-ocular pressure
- bradycardia may accentuated by:
- digoxin
- psychotherapeutic agents
- beta blockers
- alpha-adrenergic agonists may enhance hypertensive effects
- alpha-adrenergic antagonists may antagonize effects of midodrine
Mechanism of action
- enzymatic hydrolysis to active metabolite desglymidodrine
- activates alpha-1 adrenergic receptors on arterioles & veins to increase peripheral vascular resistance
- a 10 mg dose increases standing systolic BP 15-30 mm Hg
- clinical benefit has not been demonstrated[5]
More general terms
Additional terms
References
- ↑ Low et al JAMA 277:1046-51 1997
- ↑ Kaiser Permanente Northern California Regional Drug Formulary, 1998
- ↑ PDR 56th edition, 2002
- ↑ Department of Veterans Affairs, VA National Formulary
- ↑ 5.0 5.1 5.2 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
- ↑ Medical Knowledge Self Assessment Program (MKSAP) 18, American College of Physicians, Philadelphia 2018
- ↑ 7.0 7.1 7.2 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: https://www.ncbi.nlm.nih.gov/pubmed/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: https://www.ncbi.nlm.nih.gov/pubmed/34339220 https://www.acpjournals.org/doi/10.7326/M21-2859 - ↑ 8.0 8.1 Geriatric Review Syllabus, 11th edition (GRS11) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2022