Midodrine

Oral
Orthostatic hypotension
Adult: Initially, 2.5 mg 2-3 times daily, adjusted gradually according to response at weekly intervals, up to 10 mg tid. Last dose of the day should not be taken after evening meal or <4 hr before bedtime to reduce potential for supine HTN.
Renal impairment: Initially, 2.5 mg 2-3 times daily, gradually increased as tolerated.

Severe organic heart disease (e.g. bradycardia, ischaemic heart disease, CHF), acute renal failure, urinary retention, phaeochromocytoma, thyrotoxicosis, persistent and excessive supine HTN.

Patient w/ DM, history of visual problems (esp when taken w/ fludrocortisone). Hepatic and renal impairment. Pregnancy and lactation. Monitoring Parameters Monitor supine and sitting BP; hepatic and renal function.

Supine and sitting HTN, bradycardia, paraesthesia, pilomotor reaction, chills, pruritus, rash; urinary urge, urinary retention, urinary frequency; headache, fullness in the head, vasodilation, flushing face, confusion, dry mouth, anxiety. Rarely, visual field defect, dizziness, skin hyperaesthesia, insomnia, somnolence, erythema multiforme, canker sore, dry skin; dysuria, impaired urination, asthenia, backache, pyrosis, GI distress, flatulence, leg cramps.

Symptoms: HTN, piloerection, coldness, urinary retention. Management: Induce emesis. Admin of α-sympatholytic drugs (e.g. phentolamine) may be beneficial.

Enhanced pressor effects w/ α-adrenergic agonists (e.g. phenylephrine, ephedrine, dihydroergotamine, phenylpropanolamine, pseudoephedrine). Reduced effect w/ α-adrenergic blockers (e.g. prazosin, terazosin, doxazosin). May precipitate bradycardia, AV block, or arrhythmia w/ cardiac glycosides.

Midodrine, a direct-acting sympathomimetic amine, is a prodrug which forms an active metabolite, desglymidodrine. It selectively activates the α₁-adrenergic receptors of the arteriolar and venous vasculature, producing peripheral vasoconstriction and elevation of BP.
Onset: Approx 1 hr.
Duration: 2-3 hr.
Absorption: Well absorbed from the GI tract. Bioavailability: 93% (desglymidodrine). Time to peak plasma concentration: 30 min (midodrine); 1-2 hr (desglymidodrine).
Distribution: Poorly crosses the blood brain barrier. Plasma protein binding: <30%.
Metabolism: Metabolised in the liver and other tissues. Undergoes rapid deglycination into its active metabolite, desglymidodrine.
Excretion: Via urine (80% as desglymidodrine). Elimination half-life: 25 min (midodrine); approx 3-4 hr (desglymidodrine).

Oral: Store between 20-25°C. Protect from light and moisture.

Vasoconstrictors

C01CA17 - midodrine ; Belongs to the class of adrenergic and dopaminergic cardiac stimulants excluding glycosides. Used in the treatment of heart failure.