An adrenergic agonist (sympathomimetic) stimulates the adrenergic receptors of the sympathetic nervous system (SNS) either directly, by binding receptor sites, or indirectly, by raising norepinephrine levels. They fall into three groups: alpha- and beta-adrenergic agonists, alpha-specific agonists, and beta-specific agonists.
Adrenergic Agonists: Generic and Brand Names
- Alpha and Beta Adrenergic Drugs
- dobutamine (Dobutrex)
- dopamine (Intropin)
- ephedrine
- epinephrine (Adrenalin, Sus-Phrine)
- norepinephrine (Levophed)
- Alpha-specific Adrenergic Agonists
- clonidine (Catapres)
- phenylephrine (Neo-synephrine)
- Beta-specific Adrenergic Agonists
- albuterol (Proventil, Ventolin)
- arformoterol (Brovana)
- isoproterenol (Isuprel)
- levalbuterol (Xopenex)
- metaproterenol (Alupent)
- pirbuterol (Maxair Autohaler)
- salmeterol (Serevent Diskus)
- terbutaline (Brethine)
Disease Spotlight: Glaucoma, Shock, and Asthma
These agents treat glaucoma, asthma, and shock or shock-like states. In glaucoma (raised intraocular pressure), alpha agonists dilate the pupil, decrease aqueous humor secretion, and increase uveoscleral outflow, relieving pressure. In shock (most often from acute blood loss), they raise pressure, cause vasoconstriction, and increase blood flow to muscle. In asthma (a hypersensitivity reaction with inflammation and bronchospasm), beta agonists relieve bronchospasm and other obstructive respiratory conditions.
Alpha- and Beta-Adrenergic Agonists
Alpha- and beta-agonists stimulate all adrenergic receptors, hitting both alpha- and beta-sites. Common examples are dopamine, dobutamine, and epinephrine.
Therapeutic Action
They act on adrenergic receptors of target organs: increased heart rate and myocardial contractility in the heart, bronchodilation in the lungs, decreased intraocular pressure in the eyes. They also cause sweating, pupil dilation, and increased rate and depth of respiration, and they drive glycogenolysis to free glucose for energy.
Indications
Dopamine, a naturally occurring catecholamine, acts in a dose-dependent way on dopaminergic, alpha, and beta receptors, so low doses favor renal and splanchnic arteriolar dilation while higher doses raise cardiac contractility and vasoconstriction. Besides increasing the rate and force of cardiac contraction, it raises blood flow to the kidneys. Dobutamine and ephedrine are synthetic catecholamines for heart failure, increasing cardiac contractility without raising oxygen demand. Ephedrine stimulates norepinephrine release from nerve endings; its use is declining in favor of drugs with more predictable onset and action, though many OTC cold products still contain it.
By age group: children are at greater risk for GI and CV complications, so dosing must be exact and validated. Phenylephrine is common in OTC allergy and cold products, so caregivers must check labels and avoid combining drugs with the same ingredients. Adults in shock need constant dose adjustment by response, especially those at risk for cardiac complications; most of these are emergency drugs and may be used in pregnancy or lactation when benefit clearly outweighs risk. Older adults need dose adjustment, are more prone to side effects, and reach toxic levels more easily with renal or hepatic impairment. Caution all adults against OTC drugs and complementary therapies.
Pharmacokinetics
Here are the characteristic interactions of alpha- and beta-adrenergic agonists and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| IV | 1-2 min | 10 min | Length of infusion |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 2 min | liver | urine |
Contraindications and Cautions
Contraindicated with allergy to any component. Use with extreme caution in pheochromocytoma (a systemic catecholamine overload could be fatal), pulmonary hypertension (worsened by the drug), tachyarrhythmias and ventricular fibrillation (increased rate and oxygen consumption worsens them), hypovolemia (fluid replacement is the preferred treatment for the hypotension), halogenated hydrocarbon general anesthetics (these sensitize the myocardium to catecholamines and can cause serious cardiac effects), and peripheral cardiovascular disease (worsened by systemic vasoconstriction).
Adverse Effects
- Sympathetic stimulation: headache, sweating, tension or anxiety, piloerection
- CV: arrhythmias, hypertension, palpitations, angina, dyspnea
- GI: nausea, vomiting, constipation
WARNING: Because of vasoconstriction, prevent extravasation of any infused drug. Vasoconstriction at the extravasation site causes necrosis and cell death.
Interactions
Tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) increase these drugs' effects through higher norepinephrine levels or receptor stimulation; TCAs increase the sympathomimetic effect of phenylephrine but decrease the antihypertensive effect of clonidine. Ma huang, guarana, and caffeine raise the risk of hypertension, especially with alpha agonists. Propranolol causes paradoxical hypertension with clonidine. Any adrenergic antagonist causes loss of effectiveness.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, pheochromocytoma, fatal arrhythmias). Establish a baseline physical exam. Assess vital signs, especially pulse and blood pressure, for cardiac overstimulation. Note respiratory rate and auscultate lungs for adventitious sounds. Monitor urine output for renal perfusion and therapeutic effect. Monitor liver and renal function tests for dose adjustment and serum electrolytes for fluid loss.
Nursing diagnoses. Decreased cardiac output related to CV effects; ineffective tissue perfusion related to CV effects.
Implementation. Calculate and prepare doses with extreme care, since small errors have serious effects. Use aseptic technique for ophthalmic or nasal agents. Monitor response closely (vital signs, ECG, urine output) for maximum benefit with least toxicity. Keep phentolamine on standby for extravasation; save the area by infiltrating 10 mL of saline containing 5-10 mg of phentolamine. Provide comfort measures (light control, encouragement to void, bowel monitoring, support and relaxation) and patient education on drug effects and warning signs.
Evaluation. Monitor response (improved blood pressure, ocular pressure, bronchial airflow), watch for adverse effects (CV changes, decreased urine output, headache, GI upset), confirm the patient can name the drug, its indication, and adverse effects, and monitor compliance.
Alpha-Specific Adrenergic Agonists
Alpha-agonists bind primarily to alpha-receptors rather than beta-receptors. Common examples are clonidine, midodrine, and phenylephrine.
Therapeutic Action
They act as powerful postsynaptic alpha-adrenergic stimulants, causing vasoconstriction and raising systolic and diastolic blood pressure with little effect on the heart's beta-receptors.
Indications
Phenylephrine is a potent vasoconstrictor and alpha1-agonist with little or no effect on the heart or bronchi, used in many combination cold and allergy products. Parenterally it treats shock or shock-like states and paroxysmal supraventricular tachycardia, prolongs local anesthesia, and maintains blood pressure during spinal anesthesia; topically it treats allergic rhinitis and otitis media symptoms. Midodrine is an oral drug for orthostatic hypotension unresponsive to traditional therapy; it activates alpha1-adrenergic receptors, causing peripheral vasoconstriction and raising vascular tone and blood pressure. Clonidine stimulates alpha2-receptors of the CNS, decreasing CNS norepinephrine outflow; oral and transdermal forms control hypertension, and the injection is used for epidural infusion to control cancer pain.
Pharmacokinetics
Here are the characteristic interactions of alpha-agonists and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| IV | Immediate | – | 15-20 min |
| IM, subcutaneous | 10-15 min | – | 30-120 min |
| Topically | Very little systemic absorption occurs | – | – |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 47-100 hours | tissues | urine and bile |
Contraindications and Cautions
Contraindicated with allergy to any component. Use caution in severe hypertension or tachycardia (additive effects), narrow-angle glaucoma (worsened by arterial constriction), pregnancy and lactation (reserve for when maternal benefit outweighs fetal or neonatal risk), CV disease and vasospasm (aggravated by vascular effects), thyrotoxicosis and diabetes (sympathetic stimulation is thyroid-stimulating and glucose-elevating), and renal or hepatic impairment (alters metabolism and excretion).
Adverse Effects
- CNS: anxiety, restlessness, depression, fatigue, strange dreams, personality changes
- Sympathetic stimulation: blurred vision, photosensitivity
- CV: arrhythmias, ECG changes, blood pressure changes, peripheral vascular problems
- GI: nausea, vomiting, anorexia
- GU: decreased urinary output, difficulty urinating, dysuria, changes in sexual function
WARNING: Sudden withdrawal can cause tachycardia, hypertension, arrhythmias, flushing, and even death. Taper drugs over 2-4 days.
Interactions
MAOIs cause severe hypertension, headache, and hyperpyrexia with phenylephrine. TCAs increase the sympathomimetic effect of phenylephrine and decrease the antihypertensive effect of clonidine. Digoxin, beta-blockers, and antipsychotics increase drug effects with midodrine. Adrenergic antagonists cause loss of effectiveness.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, CV disease, thyrotoxicosis, diabetes). Establish a baseline exam. Assess orientation, affect, reflexes, and vision for CNS changes. Monitor blood pressure and pulse, assess peripheral perfusion, and obtain an ECG if indicated. Monitor urine output for renal perfusion. Evaluate for nausea and constipation. Monitor liver and renal function tests for dose adjustment.
Nursing diagnoses. Decreased cardiac output related to blood pressure changes, arrhythmias, or vasoconstriction; disturbed sensory perception related to CNS effects; risk for injury related to CNS or CV effects.
Implementation. Do not discontinue abruptly; taper to prevent rebound hypertension. Monitor blood pressure, orthostatic blood pressure, pulse, rhythm, and cardiac output regularly to adjust or stop the drug if CV effects are severe. Keep phentolamine on standby when giving phenylephrine; save the area by infiltrating 10 mL of saline containing 5-10 mg of phentolamine within 12 hours after extravasation to preserve tissue. Provide comfort measures (rest, environmental control) and patient education on drug effects and warning signs.
Evaluation. Monitor response (improvement in the treated condition), watch for adverse effects (GI upset, CNS and CV changes), confirm the patient can name the drug, its indication, and adverse effects, and monitor compliance.
Beta-Specific Adrenergic Agonists
Beta-agonists bind primarily to beta-receptors rather than alpha-receptors. Common examples are albuterol, salmeterol, and terbutaline.
Therapeutic Action
They act on beta-adrenergic receptors to increase heart rate, produce a positive inotropic effect, and cause bronchodilation and vasodilation.
Indications
Treatment of bronchial spasm, asthma, and other obstructive pulmonary conditions.
Pharmacokinetics
Here are the characteristic interactions of beta-agonists and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| IV | Immediate | – | 1-2 min |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| Unknown | tissues | – |
Contraindications and Cautions
Contraindicated with allergy to any component. Use caution in pulmonary hypertension (worsened by the drug), anesthesia with halogenated hydrocarbons (sensitizes the myocardium to catecholamines, risking a severe reaction), eclampsia, uterine hemorrhage, and intrauterine death (complicated by uterine relaxation or raised blood pressure), thyrotoxicosis and diabetes (thyroid-stimulating and glucose-elevating effects), and severe renal impairment (alters excretion).
Adverse Effects
- CNS: anxiety, restlessness, fatigue, fear, tremor, headache
- CV: tachycardia, angina, myocardial infarction, palpitations
- Respiratory: difficulty breathing, bronchospasm, severe pulmonary edema
- GI: nausea, vomiting, anorexia, GI upset
- Others: sweating, pupil dilation, rash, muscle cramps
Interactions
Other sympathomimetic drugs increase sympathomimetic effects. Beta-blockers decrease therapeutic effects.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, uterine hemorrhage, thyrotoxicosis, diabetes). Establish a baseline exam. Assess CV status (pulse and blood pressure) for SNS stimulation effects. Assess respiratory status for drug effects and adverse respiratory effects. Monitor urine output for renal perfusion. Monitor liver and renal function tests for dose adjustment.
Nursing diagnoses. Acute pain related to CV and systemic effects; decreased cardiac output related to CV effects; ineffective tissue perfusion related to CV effects.
Implementation. Monitor pulse and blood pressure carefully during administration so the drug can be stopped at any sign of toxicity. Keep a beta-blocker readily available when giving parenteral isoproterenol in case of severe reaction. Use the minimal effective dose of isoproterenol to limit adverse effects. Provide comfort measures and patient education on drug effects and warning signs.
Evaluation. Monitor response (improvement in the treated condition, stable blood pressure, prevention of preterm labor), watch for adverse effects (GI upset, respiratory and CV changes), confirm the patient can name the drug, its indication, and adverse effects, and monitor compliance.
Frequently Asked Questions
What do adrenergic agonists do? They stimulate the sympathetic nervous system, producing fight-or-flight effects: faster and stronger heartbeat, bronchodilation, vasoconstriction, and raised blood pressure. That makes them central to treating shock, asthma, and some forms of glaucoma.
What is the difference between alpha and beta agonists? Alpha agonists like phenylephrine mainly cause vasoconstriction and raise blood pressure with little direct cardiac effect. Beta agonists act on the heart (beta-1) and airways (beta-2) to increase heart rate, contractility, and bronchodilation. Drugs like epinephrine and dopamine hit both families.
Why is dopamine used in shock? Dopamine works in a dose-dependent way across dopaminergic, alpha, and beta receptors, supporting blood pressure and cardiac output. Modern practice often favors norepinephrine as a first-line vasopressor, and the agent is chosen by the type of shock and the patient's response.
What is the most dangerous bedside complication of the vasoconstrictors? Extravasation. Leakage of a vasoconstrictor into surrounding tissue causes intense local vasoconstriction, tissue necrosis, and cell death. Protect the IV site, monitor it closely, and keep phentolamine available to infiltrate the area if extravasation occurs.
Why can you not stop clonidine abruptly? Sudden withdrawal of clonidine and similar alpha-2 agonists can cause rebound tachycardia, severe hypertension, arrhythmias, and flushing. Taper the drug over several days rather than stopping it at once.
Which patients need extra caution with these drugs? Use extreme caution in pheochromocytoma, tachyarrhythmias, pulmonary hypertension, uncontrolled hyperthyroidism, and severe cardiovascular disease, since the sympathetic stimulation can be dangerous. Older adults and patients with renal or hepatic impairment reach toxic levels more easily and need dose adjustment.