Please wait while the formulary information is being retrieved.
Drug overview for EPHEDRINE SULFATE (ephedrine sulfate):
Generic name: EPHEDRINE SULFATE
Drug class: Amphetamines/Anorexiants/Stimulants
Therapeutic class: Cardiovascular Therapy Agents
Ephedrine is a sympathomimetic agent that occurs naturally in plants of the genus Ephedra; ephedrine stimulates both alpha- and beta-adrenergic receptors.
No enhanced Uses information available for this drug.
Generic name: EPHEDRINE SULFATE
Drug class: Amphetamines/Anorexiants/Stimulants
Therapeutic class: Cardiovascular Therapy Agents
Ephedrine is a sympathomimetic agent that occurs naturally in plants of the genus Ephedra; ephedrine stimulates both alpha- and beta-adrenergic receptors.
No enhanced Uses information available for this drug.
DRUG IMAGES
No Image Available
The following indications for EPHEDRINE SULFATE (ephedrine sulfate) have been approved by the FDA:
Indications:
Acute hypotension
Hypotension secondary to spinal anesthesia
Professional Synonyms:
Acutely decreased blood pressure
Decreased blood pressure secondary to spinal anesthesia
Indications:
Acute hypotension
Hypotension secondary to spinal anesthesia
Professional Synonyms:
Acutely decreased blood pressure
Decreased blood pressure secondary to spinal anesthesia
The following dosing information is available for EPHEDRINE SULFATE (ephedrine sulfate):
Ephedrine is commercially available as ephedrine hydrochloride or ephedrine sulfate; dosage is expressed in terms of the salt.
When ephedrine hydrochloride or ephedrine sulfate is administered orally for self-medication as a bronchodilator (in fixed combination with guaifenesin) in adults and children 12 years of age and older, the usual oral dosage is 12.5-25 mg every 4 hours as needed, not to exceed 150 mg in 24 hours. Ephedrine should be used in children younger than 12 years of age only under the direction of a clinician.
When used as a pressor agent, ephedrine should be administered in the lowest effective dosage for the shortest possible time. The recommended initial adult dose of ephedrine sulfate for the treatment of clinically important hypotension during anesthesia is 5-10 mg by IV bolus injection; additional bolus doses should be administered as needed (up to a total dose of 50 mg) to achieve the desired blood pressure response. Other parenteral dosage regimens have been recommended in adults, including a dose of 5-25 mg by slow IV injection (repeated in 5-10 minutes if necessary) and an IM+ or subcutaneous+ dose of 25-50 mg.
In children+, parenteral ephedrine sulfate doses of 0.5 mg/kg or 16.7 mg/m2 have been administered every 4-6 hours by subcutaneous+ or IM+ injection; however, safety and efficacy of ephedrine sulfate injection have not been established in pediatric patients.
When used parenterally to relieve severe, acute bronchospasm, ephedrine sulfate doses of 12.5-25 mg usually have been given in adults.
When ephedrine hydrochloride or ephedrine sulfate is administered orally for self-medication as a bronchodilator (in fixed combination with guaifenesin) in adults and children 12 years of age and older, the usual oral dosage is 12.5-25 mg every 4 hours as needed, not to exceed 150 mg in 24 hours. Ephedrine should be used in children younger than 12 years of age only under the direction of a clinician.
When used as a pressor agent, ephedrine should be administered in the lowest effective dosage for the shortest possible time. The recommended initial adult dose of ephedrine sulfate for the treatment of clinically important hypotension during anesthesia is 5-10 mg by IV bolus injection; additional bolus doses should be administered as needed (up to a total dose of 50 mg) to achieve the desired blood pressure response. Other parenteral dosage regimens have been recommended in adults, including a dose of 5-25 mg by slow IV injection (repeated in 5-10 minutes if necessary) and an IM+ or subcutaneous+ dose of 25-50 mg.
In children+, parenteral ephedrine sulfate doses of 0.5 mg/kg or 16.7 mg/m2 have been administered every 4-6 hours by subcutaneous+ or IM+ injection; however, safety and efficacy of ephedrine sulfate injection have not been established in pediatric patients.
When used parenterally to relieve severe, acute bronchospasm, ephedrine sulfate doses of 12.5-25 mg usually have been given in adults.
No enhanced Administration information available for this drug.
No dosing information available.
No generic dosing information available.
The following drug interaction information is available for EPHEDRINE SULFATE (ephedrine sulfate):
There are 2 contraindications.
These drug combinations generally should not be dispensed or administered to the same patient. A manufacturer label warning that indicates the contraindication warrants inclusion of a drug combination in this category, regardless of clinical evidence or lack of clinical evidence to support the contraindication.
| Drug Interaction | Drug Names |
|---|---|
| Sympathomimetics (Indirect & Mixed Acting)/MAOIs 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: Catecholamine stores increased by MAOIs can be released by indirect acting sympathomimetics such as ephedrine and amphetamine. MAO inhibitors also interfere with gut and liver metabolism of direct acting sympathomimetics (e.g oral phenylephrine). CLINICAL EFFECTS: Concurrent use of MAOIs may result in potentiation of sympathomimetic effects, which may result in headaches, hypertensive crisis, toxic neurological effects, and malignant hyperpyrexia. Fatalities have occurred. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Concurrent use of monoamine oxidase inhibitors and sympathomimetics is contraindicated. The manufacturers of sympathomimetic agents recommend waiting 14 days after discontinuation of MAO inhibitors before initiating the sympathomimetic. DISCUSSION: Indirect acting sympathomimetic amines may cause abrupt elevation of blood pressure when administered to patients taking monoamine oxidase inhibitors, resulting in a potentially fatal hypertensive crisis. Mixed (direct and indirect) acting sympathomimetics have also been shown to interact with monoamine oxidase inhibitors depending on their degree of indirect action. The direct-acting sympathomimetics have not been reported to interact. Dopamine is metabolized by monoamine oxidase, and its pressor effect is enhanced by monoamine oxidase inhibitors. Since procarbazine, an antineoplastic agent, is a weak monoamine oxidase inhibitor, hypertensive reactions may result from its concurrent use with indirect and mixed acting sympathomimetics. Furazolidone, an antibacterial with monoamine oxidase inhibitor action, has also been shown to interact with indirect acting sympathomimetics. Linezolid is another antibacterial with monoamine oxidase inhibitor properties. Metaxalone is a weak inhibitor of MAO. Foods containing large amounts of tyramine have also been implicated in this interaction. Methylene blue, when administered intravenously, has been shown to reach sufficient concentrations to be a potent inhibitor of MAO-A. At recommended dosages, rasagiline, oral selegiline, and transdermal selegiline up to 6mg/day are selective for MAO-B; however, at higher dosages they have been shown to lose their selectivity. One or more of the drug pairs linked to this monograph have been included in a list of interactions that should be considered "high-priority" for inclusion and should not be inactivated in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
EMSAM, FURAZOLIDONE, MARPLAN, MATULANE, METAXALONE, METHYLENE BLUE, NARDIL, PARNATE, PHENELZINE SULFATE, PROCARBAZINE HCL, PROVAYBLUE, SELEGILINE HCL, TRANYLCYPROMINE SULFATE |
| Dihydroergotamine/Sympathomimetics 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. |
DIHYDROERGOTAMINE MESYLATE, MIGRANAL, TRUDHESA |
There are 7 severe interactions.
These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.
| Drug Interaction | Drug Names |
|---|---|
| Select Indirect-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 indirect-acting sympathomimetics would have decreased activity due to tricyclic blockage of their uptake into the adrenergic neuron. CLINICAL EFFECTS: Decreased effect of indirect acting sympathomimetics. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Use of tricyclic compounds and indirect-acting sympathomimetics should be approached with caution. Montior patients receiving concurrent therapy for decreased sympathomimetic efficacy. DISCUSSION: The pressor effects of the indirect-acting sympathomimetic amines (e.g., amphetamines, ephedrine, and methylphenidate) are antagonized by tricyclic antidepressants. |
AMITRIPTYLINE HCL, AMOXAPINE, ANAFRANIL, CHLORDIAZEPOXIDE-AMITRIPTYLINE, CLOMIPRAMINE HCL, DESIPRAMINE HCL, DOXEPIN HCL, IMIPRAMINE HCL, IMIPRAMINE PAMOATE, NORPRAMIN, NORTRIPTYLINE HCL, PAMELOR, PERPHENAZINE-AMITRIPTYLINE, PROTRIPTYLINE HCL, SILENOR, TRIMIPRAMINE MALEATE |
| Ergot Alkaloids/Sympathomimetics 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. |
ERGOLOID MESYLATES, ERGOMAR, ERGOTAMINE TARTRATE, ERGOTAMINE-CAFFEINE, METHYLERGONOVINE MALEATE, METHYSERGIDE MALEATE, MIGERGOT |
| Guanethidine/Sympathomimetics (Indirect Acting) SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Indirect-acting sympathomimetics may displace guanethidine from adrenergic neurons, thereby antagonizing the clinical effect. CLINICAL EFFECTS: Blood pressure may be increased. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: When possible, use an alternative antihypertensive agent or sympathomimetic. DISCUSSION: This interaction has been demonstrated with concomitant administration of anorexiant-type indirect-acting sympathomimetics and guanethidine. Increased blood pressure has been reported. |
GUANETHIDINE HEMISULFATE |
| Selected Inhalation Anesthetic Agents/Sympathomimetics 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. |
DESFLURANE, FORANE, ISOFLURANE, SEVOFLURANE, SUPRANE, TERRELL, ULTANE |
| Mixed;Indirect Sympathomimetics/Selected MAOIs SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Catecholamine stores increased by MAOIs can be released by indirect acting sympathomimetics such as ephedrine and amphetamine. MAO inhibitors also interfere with gut and liver metabolism of direct acting sympathomimetics (e.g oral phenylephrine). CLINICAL EFFECTS: Concurrent use of MAOIs may result in potentiation of sympathomimetic effects, which may result in headaches, hypertensive crisis, toxic neurological effects, and malignant hyperpyrexia. Fatalities have occurred with combinations of sympathomimetics and MAO-A inhibitors. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Concurrent use of MAO-A inhibitors and sympathomimetics is contraindicated. The manufacturers of sympathomimetic agents recommend waiting 14 days after discontinuation of MAO inhibitors before initiating the sympathomimetic. Patients receiving direct or indirect acting sympathomimetics should not receive linezolid unless they are monitored for potential increases in blood pressure. Initial dosages of dopamine and epinephrine should be reduced. At recommended dosages, oral selegiline and transdermal selegiline up to 6mg/day are selective for MAO-B; however, at higher dosages they have been shown to lose their selectivity. Patients receiving higher dosages of selegiline should be considered susceptive to this interaction. DISCUSSION: Indirect acting sympathomimetic amines may cause abrupt elevation of blood pressure when administered to patients taking monoamine oxidase inhibitors, resulting in a potentially fatal hypertensive crisis. Mixed (direct and indirect) acting sympathomimetics have also been shown to interact with monoamine oxidase inhibitors depending on their degree of indirect action. The direct-acting sympathomimetics have not been reported to interact. Dopamine is metabolized by monoamine oxidase, and its pressor effect is enhanced by monoamine oxidase inhibitors. Furazolidone, an antibacterial with monoamine oxidase inhibitor action, has also been shown to interact with indirect acting sympathomimetics. Foods containing large amounts of tyramine have also been implicated in this interaction. A significant pressor response was observed in normal subjects receiving linezolid and tyramine doses of more than 100 mg. Administration of linezolid (600 mg BID for 3 days) with pseudoephedrine (60 mg q 4 hours for 2 doses) increased blood pressure by 32 mmHg. Administration of linezolid (600 mg BID for 3 days) with phenylpropanolamine (25 mg q 4 hours for 2 doses) increased blood pressure by 38 mmHg. One or more of the drug pairs linked to this monograph have been included in a list of interactions that should be considered "high-priority" for inclusion and should not be inactivated in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
EMSAM, LINEZOLID, LINEZOLID-0.9% NACL, LINEZOLID-D5W, SELEGILINE HCL, XADAGO, ZELAPAR, ZYVOX |
| Iobenguane I 123/Agents that Affect Catecholamines 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) |
ADREVIEW |
| Mixed;Indirect Sympathomimetics/Rasagiline SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Catecholamine stores increased by MAOIs can be released by indirect acting sympathomimetics such as ephedrine and amphetamine. MAO inhibitors also interfere with gut and liver metabolism of direct acting sympathomimetics (e.g oral phenylephrine). CLINICAL EFFECTS: Concurrent use of MAOIs may result in potentiation of sympathomimetic effects, which may result in headaches, hypertensive crisis, toxic neurological effects, and malignant hyperpyrexia. Hypertensive crisis has been reported in patients taking recommended doses of rasagiline with sympathomimetic agents. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: At recommended dosages, rasagiline is selective for MAO-B; however, at higher dosages it has been shown to lose its selectivity. Patients receiving higher dosages of rasagiline should be considered susceptive to this interaction. Concurrent use should be approached with caution. DISCUSSION: Indirect acting sympathomimetic amines may cause abrupt elevation of blood pressure when administered to patients taking monoamine oxidase inhibitors, resulting in a potentially fatal hypertensive crisis. Mixed (direct and indirect) acting sympathomimetics have also been shown to interact with monoamine oxidase inhibitors depending on their degree of indirect action. The direct-acting sympathomimetics have not been reported to interact. Dopamine is metabolized by monoamine oxidase, and its pressor effect is enhanced by monoamine oxidase inhibitors. |
AZILECT, RASAGILINE MESYLATE |
There are 3 moderate interactions.
The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.
| Drug Interaction | Drug Names |
|---|---|
| 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. |
ACD SOLUTION A, ACD-A, ACETAZOLAMIDE, ACETAZOLAMIDE ER, ACETAZOLAMIDE SODIUM, CARDIOLITE, CITRIC ACID, DEXTROSE 5%-ELECTROLYTE #48, DICHLORPHENAMIDE, KEVEYIS, KONVOMEP, METHAZOLAMIDE, OMEPRAZOLE-SODIUM BICARBONATE, ORACIT, ORAL CITRATE, ORMALVI, POTASSIUM CITRATE, POTASSIUM CITRATE ER, SODIUM ACETATE, SODIUM BICARBONATE, SODIUM BICARBONATE-D5W, SODIUM BICARBONATE-WATER, SODIUM CITRATE, SODIUM LACTATE, TC99M SESTAMIBI PREP, THAM, TROMETHAMINE, TROMETHAMINE-STERILE WATER, UROCIT-K, VAXCHORA BUFFER COMPONENT |
| 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. |
RESERPINE |
| 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. |
METHYLDOPA, METHYLDOPA-HYDROCHLOROTHIAZIDE, METHYLDOPATE HCL |
The following contraindication information is available for EPHEDRINE SULFATE (ephedrine sulfate):
Drug contraindication overview.
No enhanced Contraindications information available for this drug.
No enhanced Contraindications information available for this drug.
There are 0 contraindications.
There are 1 severe contraindications.
Adequate patient monitoring is recommended for safer drug use.
| Severe List |
|---|
| Hypertension |
There are 1 moderate contraindications.
Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.
| Moderate List |
|---|
| Kidney disease with reduction in glomerular filtration rate (GFr) |
The following adverse reaction information is available for EPHEDRINE SULFATE (ephedrine sulfate):
Adverse reaction overview.
No enhanced Common Adverse Effects information available for this drug.
No enhanced Common Adverse Effects information available for this drug.
There are 8 severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
| None. | None. |
| Rare/Very Rare |
|---|
|
Bradycardia Cardiac arrhythmia Cerebrovascular accident Chest pain Drug-induced psychosis Paradoxical bronchospasm Seizure disorder Ventricular premature beats |
There are 20 less severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
|
Insomnia Nausea Nervousness Tachycardia Vomiting |
Anorexia Dizziness Dry throat Dysuria General weakness Headache disorder Hyperhidrosis Hypertension Pallor Palpitations Tremor Xerostomia |
| Rare/Very Rare |
|---|
|
Flushing Gastrointestinal irritation Symptoms of anxiety |
The following precautions are available for EPHEDRINE SULFATE (ephedrine sulfate):
No enhanced Pediatric Use information available for this drug.
Contraindicated
Severe Precaution
Management or Monitoring Precaution
Contraindicated
| None |
Severe Precaution
| None |
Management or Monitoring Precaution
| None |
Animal reproduction studies have not been performed to date with ephedrine sulfate injection; it is not known whether the drug can cause fetal harm or miscarriage when administered during pregnancy. However, ephedrine has been used in pregnant women for the treatment of hypotension during spinal anesthesia, and the available data support the efficacy and safety of ephedrine sulfate injection for such use. There is some evidence indicating that fetal acidosis is more likely to occur with maternal administration of ephedrine compared with phenylephrine.
Low umbilical artery pH (7.2 or less) has been reported at the time of delivery in neonates whose mothers were exposed to ephedrine. Newborn infants with such maternal exposure should be assessed for their acid-base status and monitored for signs and symptoms of metabolic acidosis.
Low umbilical artery pH (7.2 or less) has been reported at the time of delivery in neonates whose mothers were exposed to ephedrine. Newborn infants with such maternal exposure should be assessed for their acid-base status and monitored for signs and symptoms of metabolic acidosis.
Limited data indicate that ephedrine is distributed into human milk; however, there is no information regarding the effects of the drug on the breast-fed infant or on milk production. The known benefits of breast-feeding should be considered along with the mother's clinical need for ephedrine and any potential adverse effects of the drug or underlying maternal condition on the infant.
No enhanced Geriatric Use information available for this drug.
The following prioritized warning is available for EPHEDRINE SULFATE (ephedrine sulfate):
No warning message for this drug.
No warning message for this drug.
The following icd codes are available for EPHEDRINE SULFATE (ephedrine sulfate)'s list of indications:
| Acute hypotension | |
| I95 | Hypotension |
| I95.2 | Hypotension due to drugs |
| I95.3 | Hypotension of hemodialysis |
| I95.8 | Other hypotension |
| I95.81 | Postprocedural hypotension |
| I95.89 | Other hypotension |
| I95.9 | Hypotension, unspecified |
| Hypotension secondary to spinal anesthesia | |
| I95.2 | Hypotension due to drugs |
Formulary Reference Tool