(MI doe dreen)
Orthostatic hypotension: Treatment of symptomatic orthostatic hypotension
Severe organic heart disease, acute renal disease, urinary retention, pheochromocytoma, thyrotoxicosis, persistent and excessive supine hypertension
Because midodrine can cause marked elevation of supine blood pressure, it should be used in patients whose lives are considerably impaired despite standard clinical care. The indication for use of midodrine in the treatment of symptomatic orthostatic hypotension is based primarily on a change in a surrogate marker of effectiveness, an increase in systolic blood pressure measured 1 minute after standing, a surrogate marker considered likely to correspond to a clinical benefit. At present, however, clinical benefits of midodrine, principally improved ability to carry out activities of daily living, have not been verified.
Orthostatic hypotension: Oral: 10 mg 3 times daily during daytime hours (every 3 to 4 hours) when patient is upright
Prevention of hemodialysis-induced hypotension (off-label use): Oral: 2.5 to 10 mg given 15 to 30 minutes prior to dialysis session (Cruz, 1998; KDOQI, 2005; Prakash, 2004)
Vasovagal syncope (off-label use): Oral: Initial: 5 mg 3 times/day during daytime hours (every 6 hours) increased up to 15 mg/dose if necessary (Perez-Lugones, 2001; Ward, 1998)
Refer to adult dosing.
Orthostatic hypotension: 2.5 mg 3 times daily; gradually increase as tolerated.
Hemodialysis: Dialyzable
No dosage adjustment provided in manufacturer 's labeling (has not been studied); use with caution.
Doses may be given in approximately 3- to 4-hour intervals (eg, shortly before or upon rising in the morning, at midday, in the late afternoon not later than 6 PM). Avoid dosing after the evening meal or within 4 hours of bedtime. Continue therapy only in patients who appear to attain symptomatic improvement during initial treatment. Standing systolic blood pressure may be elevated 15-30 mm Hg at 1 hour after a 10 mg dose. Some effect may persist for 2-3 hours.
Store at 20 ‚ °C to 25 ‚ °C (68 ‚ °F to 77 ‚ °F). Protect from light and moisture.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral, as hydrochloride:
Generic: 2.5 mg, 5 mg, 10 mg
Alpha1-Blockers: May diminish the vasoconstricting effect of Alpha1-Agonists. Similarly, Alpha1-Agonists may antagonize Alpha1-Blocker vasodilation. Monitor therapy
AtoMOXetine: May enhance the hypertensive effect of Sympathomimetics. AtoMOXetine may enhance the tachycardic effect of Sympathomimetics. Monitor therapy
Benzylpenicilloyl Polylysine: Alpha1-Agonists may diminish the diagnostic effect of Benzylpenicilloyl Polylysine. Management: Consider use of a histamine skin test as a positive control to assess a patients ability to mount a wheal and flare response. Consider therapy modification
Beta-Blockers: May enhance the bradycardic effect of Midodrine. Monitor therapy
Calcium Channel Blockers (Nondihydropyridine): May enhance the bradycardic effect of Midodrine. Monitor therapy
Cannabinoid-Containing Products: May enhance the tachycardic effect of Sympathomimetics. Exceptions: Cannabidiol. Monitor therapy
Cardiac Glycosides: May enhance the bradycardic effect of Midodrine. Monitor therapy
Doxofylline: Sympathomimetics may enhance the adverse/toxic effect of Doxofylline. Monitor therapy
Droxidopa: Midodrine may enhance the hypertensive effect of Droxidopa. Monitor therapy
Ergot Derivatives: May enhance the hypertensive effect of Alpha1-Agonists. Ergot Derivatives may enhance the vasoconstricting effect of Alpha1-Agonists. Exceptions: Ergoloid Mesylates; Nicergoline. Avoid combination
Iobenguane I 123: Sympathomimetics may diminish the therapeutic effect of Iobenguane I 123. Avoid combination
Linezolid: May enhance the hypertensive effect of Sympathomimetics. Management: Reduce initial doses of sympathomimetic agents, and closely monitor for enhanced pressor response, in patients receiving linezolid. Specific dose adjustment recommendations are not presently available. Consider therapy modification
MAO Inhibitors: May enhance the hypertensive effect of Alpha1-Agonists. While linezolid is expected to interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to linezolid specific monographs for details. Exceptions: Linezolid; Tedizolid. Avoid combination
Sympathomimetics: May enhance the adverse/toxic effect of other Sympathomimetics. Monitor therapy
Tedizolid: May enhance the hypertensive effect of Sympathomimetics. Tedizolid may enhance the tachycardic effect of Sympathomimetics. Monitor therapy
Tricyclic Antidepressants: May enhance the vasopressor effect of Alpha1-Agonists. Tricyclic Antidepressants may diminish the vasopressor effect of Alpha1-Agonists. Monitor therapy
Blood pressure; renal and hepatic function
>10%:
Cardiovascular: Supine hypertension (7% to 13%)
Dermatologic: Piloerection (13%), pruritus (12%)
Genitourinary: Urinary urgency, retention, or polyuria, dysuria (up to 13%)
Neuromuscular & skeletal: Paresthesia (18%)
1% to 10%:
Central nervous system: Chills (5%), pain (5%)
Dermatologic: Rash (2%)
Gastrointestinal: Abdominal pain
<1% (Limited to important or life-threatening): Anxiety, backache, canker sore, confusion, dizziness, dry skin, erythema multiforme, facial flushing, flatulence, flushing, GI distress, headache, heartburn, hyperesthesia, insomnia, ICP increased, leg cramps, nausea, somnolence, visual field defect, weakness, xerostomia
Concerns related to adverse effects:
- Bradycardia: May slow heart rate primarily due to vagal reflex. Use caution when administered concurrently with negative chronotropes (eg, digoxin, beta blockers). Discontinue use if signs or symptoms of bradycardia occur.
- Hypertension: May cause supine hypertension; discontinue use immediately if supine hypertension persists. Use with caution when administered concurrently with vasoconstrictors (eg, phenylephrine, ephedrine, dihydroergotamine, phenylpropanolamine, pseudoephedrine). Use is not recommended in patients with initial supine systolic pressure >180 mm Hg. Due to marked elevation of supine blood pressure (BP greater than 200 mm Hg systolic), use in patients whose lives are considerably impaired despite standard clinical care, including nonpharmacologic treatment (such as support stockings), fluid expansion, and lifestyle alterations. Supine and sitting blood pressure should be monitored.
Disease-related concerns:
- Diabetes: Use with caution in patients with diabetes mellitus.
- Hepatic impairment: Use with caution in patients with hepatic impairment; has not been studied.
- Renal impairment: Desglymidodrine, the active metabolite, is primarily renally excreted; assess renal function prior to initial dose; use with caution in patients with renal impairment (has not been studied) and initiate with a reduced dose; contraindicated in patients with acute renal failure.
- Visual problems: Use with caution in patients with visual problems, especially if receiving fludrocortisone.
Other warnings/precautions:
- Appropriate use: [U.S. Boxed Warning]: Indicated for patients for whom orthostatic hypotension significantly impairs their daily life despite standard clinical care. Use is not recommended with supine hypertension. Continue therapy only in patients who appear to attain symptomatic improvement during initial treatment.
C
Adverse events were observed in animal reproduction studies. Information related to the use of midodrine in pregnancy is limited (Glatter, 2005).
Midodrine forms an active metabolite, desglymidodrine, which is an alpha1-agonist. This agent increases arteriolar and venous tone resulting in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension.
Rapid
Poorly crosses blood-brain barrier
Hepatic and many other tissues; midodrine is a prodrug which undergoes rapid deglycination to desglymidodrine (active metabolite)
Urine (Midodrine: Insignificant; Desglymidodrine: 80% by active renal secretion)
~1 hour
Desglymidodrine: 1 to 2 hours; Midodrine: 30 minutes
2 to 3 hours
Desglymidodrine: ~3 to 4 hours; Midodrine: 25 minutes
Minimal
- Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
- Patient may experience, itching, goosebumps, chills, or polyuria. Have patient report immediately to prescriber bradycardia, severe dizziness, passing out, severe headache, vision changes, tinnitus, urinary retention, or burning or numbness feeling (HCAHPS).
- Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for healthcare professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience and judgment in diagnosing, treating and advising patients.