Midodrine (midodrine HCl)
Amphetamines/Anorexiants/Stimulants Oral Tablet
Last reviewed · Source: First Databank (FDB) drug data
Overview
Midodrine, a synthetic sympathomimetic amine, is a prodrug and has little pharmacologic activity until metabolized to desglymidodrine; desglymidodrine is a relatively long-acting alpha1-selective adrenergic agonist that acts almost exclusively by a direct effect on peripheral alpha-adrenergic receptors of the arterial and venous vasculature, increasing vascular tone.
Midodrine is a synthetic sympathomimetic amine that is structurally similar to methoxamine. Midodrine is a prodrug and has little pharmacologic activity until metabolized to desglymidodrine (St 1059).
Desglymidodrine is a relatively long-acting alpha1-selective adrenergic agonist that acts almost exclusively by a direct effect on peripheral alpha-adrenergic receptors of the arterial and venous vasculature, increasing vascular tone. Total peripheral resistance is increased, resulting in increased systolic and diastolic blood pressure. Standing blood pressure is increased by about 10-30 mm Hg 1 hour after a 10-mg dose of midodrine hydrochloride in patients with orthostatic hypotension, with some effect persisting for 2-3 hours; a 10-mg dose of the drug produces only modest elevations in supine and standing blood pressure in healthy individuals.
Some evidence suggests that midodrine's efficacy in improving standing blood pressure also may result in part from increased body weight during therapy with the drug, presumably secondary to expansion of extracellular fluid volume.
Unlike most vasopressors, midodrine has virtually no stimulant effect on beta-adrenergic receptors, including those of the heart. In addition, because desglymidodrine crosses the blood-brain barrier poorly, the drug generally does not appear to produce appreciable CNS stimulation. Because midodrine stimulates the trigone and sphincter of the urinary bladder, symptoms of urinary urgency can occur.
The drug also stimulates pilomotor muscles, resulting in pilomotor effects (e.g., goose bumps, sensation of hair standing on end), and contracts the radial muscle of the iris, resulting in pupillary dilation.
SumMon(R) (see Users Guide). For additional information on this drug until a more detailed monograph is developed and published, the manufacturer's labeling should be consulted. It is essential that the labeling be consulted for detailed information on the usual cautions, precautions, and contraindications.
USES: This medication is used for certain patients who have symptoms of low blood pressure when standing. This condition is also known as orthostatic hypotension. Midodrine is used in people whose daily activities are severely affected by this condition, even after other treatments are used (such as support stockings).
It is known as a sympathomimetic (alpha receptor agonist) that acts on the blood vessels to raise blood pressure.
Generic name: midodrine HCl
Pronunciation: (MY-doh-dreen)
Drug class: Amphetamines/Anorexiants/Stimulants
Therapeutic class: Cardiovascular Therapy Agents
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Midodrine
Indications
The following indications are listed for Midodrine:
- Symptomatic Orthostatic Hypotension
Also known as: Symptomatic Oh, Symptomatic Orthostatic Hypopiesis, Symptomatic Postural Hypotension.
Dosing
Safety and efficacy of midodrine hydrochloride in children younger than 18 years of age have not been established. The manufacturer states that midodrine hydrochloride dosage adjustment based solely on age is not necessary in geriatric patients. Dosage adjustment based solely on gender also is not necessary.
The manufacturer recommends that renal function be assessed prior to initiating midodrine therapy. Because the drug's active metabolite (desglymidodrine) is eliminated by renal excretion and because safety and efficacy have not been studied systematically in patients with renal impairment to date, the manufacturer states that midodrine should be dosed cautiously in patients with abnormal renal function. The manufacturer recommends that midodrine hydrochloride therapy be initiated with 2.5-mg doses in such adults. Desglymidodrine is dialyzable.
Midodrine has not been studied systematically in patients with hepatic impairment, and the effect of alterations in hepatic function on the disposition of the drug currently is not known. Therefore, while the manufacturer currently makes no specific recommendations for dosage adjustment in patients with hepatic impairment, midodrine should be used with caution in such patients.
Midodrine hydrochloride is administered orally, usually in 3 equally divided doses daily. Since food does not appear to affect GI absorption of midodrine hydrochloride, the drug generally can be administered without regard to meals.
| Drug label | Dosing type | Instructions |
|---|---|---|
| Midodrine Hcl 5 Mg Tablet | Maintenance | Take 2 tablets (10 mg) by oral route 3 times per day. |
| Drug label | Dosing type | Instructions |
|---|---|---|
| Midodrine Hcl 5 Mg Tablet | Maintenance | Take 2 tablets (10 mg) by oral route 3 times per day. |
Drug interactions
There is no enhanced messaging for this drug.
Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
Sympathomimetics/Dihydroergotamine
SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
MECHANISM OF ACTION: Concurrent use of dihydroergotamine and sympathomimetics may result in additive or synergistic effect on peripheral blood vessels.(1)
CLINICAL EFFECTS: Concurrent use of dihydroergotamine and sympathomimetics may result in increased blood pressure due to peripheral vasoconstriction.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Dihydroergotamine is contraindicated with sympathomimetics because the combination may result in additive or synergistic elevation of blood pressure.(1)
DISCUSSION: Significant elevation in blood pressure has been reported in patients treated with dihydroergotamine.(1) Sympathomimetics can be expected to have additional effects on blood pressure.
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Agents That Affect Catecholamines/Iobenguane I 123
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Many compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with iobenguane uptake into cells.(1)
CLINICAL EFFECTS: Compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with imaging completed with iobenguane.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discuss the use of agents that affect catecholamines. Discontinue drugs that reduce catecholamine uptake or deplete catecholamine stores prior to imaging with iobenguane. Before imaging with iobenguane, discontinue agents that affect catecholamines for at least 5 biological half-lives, as clinically tolerated.(1)
DISCUSSION: Many agents may reduce catecholamine uptake or deplete catecholamine stores.(1) Examples include: - CNS stimulants or amphetamines (e.g. cocaine, methylphenidate, dextroamphetamine) - norepinephrine and dopamine reuptake inhibitors (e.g. phentermine) - norepinephrine and serotonin reuptake inhibitors (e.g. tramadol) - monoamine oxidase inhibitors (e.g. phenelzine, linezolid) - central monoamine depleting drugs (e.g. reserpine) - non-select beta adrenergic blocking drugs (e.g. labetalol) - alpha agonists or alpha/beta agonists (e.g. pseudoephedrine, phenylephrine, ephedrine, phenylpropanolamine, naphazoline) - tricyclic antidepressants or norepinephrine reuptake inhibitors (e.g. amitriptyline, bupropion, duloxetine, mirtazapine, venlafaxine) - botanicals that may inhibit reuptake of norepinephrine, serotonin or dopamine (e.g. ephedra, ma huang, St. John's Wort, yohimbine)
Agents That Affect Catecholamines/Iobenguane I 131
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Many compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with iobenguane uptake into cells.(1)
CLINICAL EFFECTS: Compounds that reduce catecholamine uptake or that deplete catecholamine stores may impact the dosimetry calculations or effectiveness of iobenguane.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discuss the use of agents that affect catecholamines. Discontinue drugs that reduce catecholamine uptake or deplete catecholamine stores for at least 5 half-lives before administration of either the dosimetry or a therapeutic dose of iobenguane. Do not administer these drugs until at least 7 days after each iobenguane dose.(1)
DISCUSSION: Many agents may reduce catecholamine uptake or deplete catecholamine stores.(1) Examples include: - CNS stimulants or amphetamines (e.g. cocaine, methylphenidate, dextroamphetamine) - norepinephrine and dopamine reuptake inhibitors (e.g. phentermine) - norepinephrine and serotonin reuptake inhibitors (e.g. tramadol) - monoamine oxidase inhibitors (e.g. phenelzine, linezolid) - central monoamine depleting drugs (e.g. reserpine) - non-select beta adrenergic blocking drugs (e.g. labetalol) - alpha agonists or alpha/beta agonists (e.g. pseudoephedrine, phenylephrine, ephedrine, phenylpropanolamine, naphazoline) - tricyclic antidepressants or norepinephrine reuptake inhibitors (e.g. amitriptyline, bupropion, duloxetine, mirtazapine, venlafaxine) - botanicals that may inhibit reuptake of norepinephrine, serotonin or dopamine (e.g. ephedra, ma huang, St. John's Wort, yohimbine) - calcium channel blockers
Selected Direct-Acting Sympathomimetics/Tricyclic Compounds
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Unknown. However, it is speculated that direct-acting sympathomimetic amines have an enhanced effect due to tricyclic blockage of norepinephrine reuptake.
CLINICAL EFFECTS: Increased effect of direct acting sympathomimetics.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Consider avoiding the concurrent use of direct-acting sympathomimetics and tricyclic compounds. If concurrent use of direct-acting sympathomimetics and tricyclic compounds is warranted, the initial dose of the sympathomimetic should be lowered and the patient should be monitored for adverse cardiovascular effects. Use of tricyclic compounds and other sympathomimetics should be approached with caution.
DISCUSSION: Epinephrine and other direct-acting sympathomimetic amines exert enhanced cardiovascular effects (e.g., arrhythmias, hypertension, and tachycardia) in individuals concurrently receiving or previously treated with tricyclic antidepressants. Other direct and mixed acting sympathomimetic amines have also been reported to interact with tricyclic antidepressants. These include norepinephrine, phenylephrine, dopamine, and methoxamine. Protriptyline, amitriptyline, and desipramine have also been reported to interact with direct-acting sympathomimetics.
Sympathomimetics/Ergot Alkaloids
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Concurrent use of ergot alkaloids and sympathomimetics may result in additive or synergistic effect on peripheral blood vessels.
CLINICAL EFFECTS: Concurrent use of ergot alkaloids and sympathomimetics may result in increased blood pressure due to peripheral vasoconstriction.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: When possible, avoid the concurrent use of ergot alkaloids and sympathomimetics. If concurrent use is warranted, monitor blood pressure and for signs of vasoconstriction. Decreasing the dose of one or both drugs may be necessary.
DISCUSSION: There have been reports of severe vasoconstriction resulting in gangrene in patients receiving intravenous ergonovine with dopamine or norepinephrine.
Sympathomimetics/Selected Inhalation Anesthetic Agents
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The exact mechanism is unknown. The anesthetics produce conduction changes that increase impulse re-entry into the myocardial tissue.(1) The anesthetics' ability to precipitate arrhythmias is enhanced by elevated arterial blood pressure, tachycardia, hypercapnia, and/or hypoxia, events that stimulate the release of endogenous catecholamines.(1)
CLINICAL EFFECTS: Concurrent use of inhalation anesthetic agents and sympathomimetics may result in ventricular arrhythmias or sudden blood pressure and heart rate increase during surgery.(2)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Monitor blood pressure and avoid use of sympathomimetics in patients being treated with anesthetics on the day of surgery.(2) Intravenous use of epinephrine during surgery with halothane and related halogenated general anesthetics should be strongly discouraged. When intravenous epinephrine is necessary, nitrous oxide anesthesia supplemented with ether, muscle relaxants, or opioids should be used instead of halothane.(3,4) Epinephrine may safely be used subcutaneously with the following precautions: the patient is adequately ventilated to prevent hypoxia or respiratory acidosis; the total dose of epinephrine is limited to 100 mcg/10 minute period or 300 mcg/hour in adults, 3.5 mcg/Kg in infants, 2.5 mcg/Kg in children up to two years of age, and 1.45 mcg/Kg in children over two years of age; a minimum effective concentration of anesthetic is maintained; the drugs are not co-administered in patients with hypertension or other cardiovascular disorders; and the cardiac rhythm is continuously monitored during and after injection.(3-10) If arrhythmias occur after the administration of the epinephrine, the drugs of choice are lidocaine or propranolol, depending on the type of arrhythmia.(1)
DISCUSSION: Administration of epinephrine during halothane anesthesia may may lead to serious ventricular arrhythmias.(3-6,11-18) This has occurred when epinephrine was administered intravenously,(6) when it was administered with lidocaine as a dental block,(11,14) or when it was administered supraperiosteally.(5) Norepinephrine has been shown to interact with halothane in a manner similar to epinephrine.(1) In two case reports, patients were given terbutaline (0.25 to 0.35 mg) for wheezing following induction of anesthesia with halothane. One patient's heart rate increased from 68 to 100 beats/minute, and the ECG showed premature ventricular contractions and bigeminy, while the other patient developed multiple unifocal premature ventricular contractions and bigeminy. The arrhythmias resolved in both patients following lidocaine administration.(19) Although not documented, isoproterenol causes effects on the heart similar to terbutaline(20) and would probably interact with halothane in a similar manner. Other inhalation anesthetics that increase the incidence of arrhythmias with epinephrine include chloroform,(20) methoxyflurane,(20) and enflurane.(12) A similar interaction may be expected between the other inhalation anesthetics and sympathomimetics.
Moderate Interaction: Assess the risk to the patient and take action as needed.
Sympathomimetics (Direct, Mixed-Acting)/Guanethidine
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Direct or mixed-acting sympathomimetics may inhibit uptake of guanethidine at the adrenergic neuron.
CLINICAL EFFECTS: Decreased antihypertensive effectiveness. Effects may be seen for several days after discontinuation of the direct or mixed-acting sympathomimetic.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Avoid concomitant administration of these drugs. If both drugs are administered, adjust the guanethidine dose as needed based on blood pressure.
DISCUSSION: Documentation supports routine monitoring of this interaction. It should be noted that this interaction can occur quickly.
Sympathomimetics (Direct, Mixed-Acting)/Methyldopa
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Unknown.
CLINICAL EFFECTS: The pressor response to sympathomimetics may be increased.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Start with low doses of sympathomimetics and monitor blood pressure of patients during concurrent administration of sympathomimetics and methyldopa.
DISCUSSION: The pressor response to sympathomimetics has been reported to be increased during methyldopa administration. In addition to increased duration of pressor response, severe hypertension has been reported.
Sympathomimetics/Rauwolfia Alkaloids
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Reserpine depletes catecholamine stores within the peripheral vascular adrenergic nerve endings, thus indirect acting sympathomimetics are unable to trigger the release of catecholamines. The reserpine-induced catecholamine release increases sensitivity to the effects of direct acting sympathomimetics.
CLINICAL EFFECTS: Increased effects of direct acting sympathomimetics. Decreased effects of indirect acting sympathomimetics. Mixed acting sympathomimetics will show effects based on the predominance of either direct or indirect activity.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: If these agents are administered concurrently, monitor blood pressure. The dose of the sympathomimetic may need to be adjusted.
DISCUSSION: This interaction has been well documented in animal studies and human case reports have confirmed the interaction. Reserpine has been shown to decrease the response to epinephrine administered for hypotension. Reserpine has also been shown to decrease the effectiveness of ophthalmic epinephrine, a direct acting sympathomimetic. Ophthalmic phenylephrine has been shown to decrease the hypotensive effects of reserpine.
Sympathomimetics/Urinary Alkalinizers
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Unionized sympathomimetic amines will be reabsorbed into systemic circulation from the distal tubules of the kidneys.
CLINICAL EFFECTS: Enhanced sympathomimetic activity and increased risk of sympathomimetic toxicity.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Watch patient for enhanced sympathomimetic side effects when urinary alkalinizers are concomitantly used. A lower dose of certain sympathomimetics may be required.
DISCUSSION: Signs and symptoms of sympathomimetic toxicity include euphoria, confusion, delirium, hallucinations and nervousness.
Contraindications
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- Pheochromocytoma
- Thyrotoxicosis
- Urinary retention
- Acute renal failure
- Structural disorder of heart
- Supine hypertension
There are no moderate contraindications for this drug.
Adverse reactions
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More Frequent
- Hypertension
- Supine hypertension
Rare or Very Rare
- Bradycardia
- Erythema multiforme
More Frequent
- Chills
- Head sensation disturbance
- Increased urinary frequency
- Paresthesia
- Piloerection
- Pruritus of skin
- Urinary retention
- Urinary urgency
Less Frequent
- Acute cognitive impairment
- Flushing
- Headache disorder
- Nervousness
- Skin rash
- Symptoms of anxiety
- Vasodilation of blood vessels
- Xerostomia
Rare or Very Rare
- Aphthous stomatitis
- Back pain
- Cramps in legs
- Dizziness
- Drowsy
- Dry skin
- Dyspepsia
- Dysuria
- Flatulence
- General weakness
- Heartburn
- Insomnia
- Nausea
- Visual field defect
Precautions
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No enhanced messaging available.
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ICD codes
| Code | Type | Description |
|---|---|---|
| Symptomatic orthostatic hypotension | ||
| I95.1 | ICD10CM | Orthostatic hypotension |
ICD code information from First Databank (FDB).
Formulary status
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Last reviewed · Source: First Databank (FDB) drug data
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