They vary in receptor specificity and are classified into five groups: nonselective adrenergic antagonists, nonselective alpha- and beta-adrenergic antagonists, and selective alpha1- and beta-adrenergic antagonists.
Adrenergic Antagonists: Generic and Brand Names
- Nonselective Adrenergic Blocking Agents
- amiodarone (Cordarone)
- carvedilol (Coreg)
- labetalol (Normodyne, Trandate)
- Nonselective Alpha-Adrenergic Blocking Agent
- phentolamine (Regitine)
- Alpha-1-Selective Adrenergic Blocking Agents
- alfuzosin (Uroxatral)
- doxazosin (Cardura)
- prazosin (Minipress)
- tamsulosin (Flomax)
- terazosin (Hytrin)
- Nonselective Beta-Adrenergic Blocking Agents
- bisoprolol (Zebeta)
- esmolol (Brevibloc)
- metoprolol (Lopressor, Toproxol XL)
Disease Spotlight: Cardiorespiratory Conditions, Benign Prostatic Hypertrophy
Nonselective adrenergic antagonists mainly treat cardiac conditions; by slowing rate and conduction they relieve the heart's workload, making them ideal for hypertension and heart failure. Of the nonselective alpha antagonists, only phentolamine (Regitine) is still used, since more specific drugs have replaced the class. Selective alpha1-receptor antagonists improve urine flow and treat benign prostatic hypertrophy (BPH) by blocking smooth muscle receptors in the genitourinary tract, relaxing the prostate and bladder. Nonselective beta-adrenergic antagonists treat CV problems and prevent reinfarction after MI. Selective beta1-receptor antagonists are preferred for smokers and patients with respiratory problems because they spare beta2-receptors, allowing bronchodilation; they also treat hypertension, angina, and cardiac arrhythmias.
Nonselective Adrenergic Blocking Agents
Nonselective adrenergic blocking agents block all alpha- and beta-receptors and are used mainly for cardiac conditions. Common examples are labetalol and carvedilol.
Therapeutic Action
They competitively block norepinephrine at both alpha and beta receptors throughout the SNS, lowering blood pressure, slowing pulse, and increasing renal perfusion with decreased renin levels.
Indications
Most nonselective adrenergic antagonists (labetalol, carvedilol) treat essential hypertension, alone or with diuretics. Others (amiodarone) are reserved for emergencies and used only as an antiarrhythmic.
By age group: children are at greater risk for bradycardia, difficulty breathing, and changes in glucose metabolism. Safety is not established in children younger than 18, though three drugs have established pediatric dosing, including prazosin (hypertension) and phentolamine (used during pheochromocytoma surgery). Adults with diabetes need close glucose monitoring because the drugs blunt sympathetic warning signs; those with CNS complications may do better on agents that are not centrally acting. Use in pregnancy or lactation is justified only when benefit clearly outweighs risk. Older adults need dose adjustment and reach toxic levels more easily with renal or hepatic impairment; bisoprolol is the drug of choice for hypertension in older patients because it causes fewer problems and allows regular dosing.
Pharmacokinetics
Here are the characteristic interactions of nonselective adrenergic antagonists and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| Oral | Varies | 1-2 h | 8-12 h |
| IM | Immediate | 5 min | 5.5 h |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 6-8 h | liver | urine |
Contraindications and Cautions
Contraindicated with allergy to any component. Use caution in bradycardia and heart block (worsened by slowed rate and conduction), hepatic impairment (altered metabolism), asthma (loss of norepinephrine's bronchodilation), shock or heart failure (worsened by loss of sympathetic reaction), and lactation (effects on neonates).
Adverse Effects
- CNS: dizziness, paresthesias, insomnia, depression, fatigue, vertigo
- CV: arrhythmias, hypotension, heart failure, pulmonary edema, CVA
- Respiratory: bronchospasm, cough, rhinitis, bronchial obstruction
- GI: nausea, vomiting, diarrhea, anorexia, flatulence
- GU: decreased libido, impotence, dysuria, Peyronie disease
- Others: decreased exercise tolerance, hypoglycemia, rash
Carvedilol has been associated with hepatic failure. Abrupt withdrawal can cause MI, stroke, and arrhythmias from the catecholamine hypersensitivity that develops once receptors have been blocked.
Interactions
Volatile liquid anesthetics (halothane, isoflurane) raise the risk of excessive hypotension. Antidiabetics have increased effect, so watch for hypoglycemia. Verapamil and diltiazem can cause dangerous conduction disturbances with carvedilol.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, heart block, asthma, pregnancy or lactation). Establish a baseline exam. Assess orientation and complaints of dizziness, paresthesias, or vertigo for CNS effects. Assess vital signs, especially pulse and blood pressure. Note respiratory rate and auscultate lungs. Monitor liver and renal function tests, serum electrolytes for fluid loss, and blood glucose for hyper- or hypoglycemia.
Nursing diagnoses. Decreased cardiac output related to CV effects; ineffective airway clearance related to lack of bronchodilation; risk for injury related to CNS effects; diarrhea related to increased parasympathetic activity.
Implementation. Do not stop abruptly after chronic therapy; taper slowly over 2 weeks while monitoring, since catecholamine hypersensitivity can trigger a severe reaction. Teach lifestyle changes (diet, exercise, smoking cessation) to help lower blood pressure. Assess heart rate for arrhythmia and blood pressure in various positions for orthostatic hypotension. Monitor GI function and arrange bathroom access and fluid intake for diarrhea. Provide comfort measures and patient education on drug effects and warning signs.
Evaluation. Monitor response (improved blood pressure and heart failure), watch for adverse effects (CV changes, headache, GI upset, liver failure), confirm the patient can name the drug, its indication, and adverse effects, and monitor compliance.
Nonselective Alpha-Adrenergic Blocking Agents
Nonselective alpha-adrenergic blocking agents have specific affinity for alpha-receptor sites. The class is limited because safer, more specific drugs exist, and only phentolamine is still used.
Therapeutic Action
Phentolamine blocks alpha1-adrenergic receptors, decreasing vascular sympathetic tone and causing vasodilation, which lowers blood pressure. It also blocks alpha2-receptors, removing the feedback control of norepinephrine release, which produces the reflex tachycardia that occurs when blood pressure falls.
Indications
Phentolamine is most often used to prevent cell death and tissue sloughing after extravasation of IV norepinephrine or dopamine, causing local vasodilation and restoring blood flow to the area. It also treats severe hypertensive reactions from pheochromocytoma manipulation before and during surgery and is used to diagnose pheochromocytoma.
Pharmacokinetics
Here are the characteristic interactions of nonselective alpha-adrenergic antagonists and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| IM | Rapid | 20 min | 30-45 min |
| IV | Immediate | 2 min | 15-30 min |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| Unknown | Unknown | Unknown |
Contraindications and Cautions
Contraindicated with allergy to any component. Use caution in coronary artery disease or MI (potential exacerbation) and pregnancy and lactation (effects on fetus or neonate).
Adverse Effects
- CNS: headache, weakness, dizziness
- CV: hypotension, orthostatic hypotension, angina, MI, cerebrovascular accident, flushing, tachycardia, arrhythmia
- GI: nausea, vomiting, diarrhea
Interactions
Ephedrine and epinephrine have decreased hypertensive and vasoconstrictive effects. Alcohol increases hypotension.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, CV disease, pregnancy or lactation). Establish a baseline exam. Assess orientation, affect, and reflexes for CNS changes. Monitor CV status (blood pressure, pulse, peripheral perfusion). Monitor urine output as a reflection of renal perfusion and cardiac function.
Nursing diagnoses. Decreased cardiac output related to blood pressure changes, arrhythmias, and vasodilation; risk for injury related to CNS and CV effects.
Implementation. Monitor heart rate and blood pressure closely so the drug can be stopped if reactions are severe. Inject phentolamine directly into the area of epinephrine or dopamine extravasation to prevent local cell death. Institute safety measures for weakness, dizziness, or orthostatic hypotension. Provide comfort measures and patient education on drug effects and warning signs.
Evaluation. Monitor response (improved pheochromocytoma signs, improved tissue condition after extravasation), watch for adverse effects (orthostatic hypotension, arrhythmias, CNS effects), confirm patient understanding, and monitor compliance.
Alpha1-Selective Adrenergic Blocking Agents
Alpha1-selective adrenergic blocking agents have specific affinity for alpha1-receptors. Common examples are prazosin, tamsulosin, and doxazosin.
Therapeutic Action
They block postsynaptic alpha1-receptor sites, decreasing vascular tone and causing vasodilation, which lowers blood pressure. Reflex tachycardia does not occur because they do not block presynaptic alpha2-receptors. They reduce total peripheral resistance through alpha blockade without affecting heart rate or cardiac output, increase high-density lipoproteins while lowering total cholesterol, and block smooth muscle receptors in the prostate, prostatic capsule, prostatic urethra, and bladder neck, relaxing the bladder and prostate and improving urine flow in male patients.
Indications
Treatment of benign prostatic hypertrophy (BPH) and of mild to moderate hypertension, as monotherapy or combined with other antihypertensives.
Pharmacokinetics
Here are the characteristic interactions of alpha 1 -selective adrenergic blocking agents and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| Oral | Varies | 2-3 h | Not known |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 22 hours | liver | bile, feces, urine |
Contraindications and Cautions
Contraindicated with allergy to any component. Use caution in lactation (drugs cross into breast milk), heart or renal failure (worsened by blood-pressure lowering), hepatic impairment (altered metabolism), and pregnancy (potential fetal effects).
Adverse Effects
- CNS: headache, weakness, dizziness, fatigue, drowsiness, depression
- CV: arrhythmia, hypotension, edema, HF, angina
- GI: nausea, vomiting, diarrhea, abdominal pain
- Vasodilation effects: flushing, rhinitis, reddened eyes, nasal congestion, priapism
Interactions
Nitrates, calcium-channel blockers, and angiotensin-converting-enzyme inhibitors increase hypotensive effects.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, heart or renal failure, pregnancy or lactation). Establish a baseline exam. Assess orientation, affect, and reflexes for CNS changes. Monitor CV status (blood pressure, pulse, peripheral perfusion). Assess renal function and urinary output, and assess BPH and its effect on urine flow. Monitor renal and hepatic function tests for dose adjustment.
Nursing diagnoses. Acute pain related to headache, GI upset, flushing, nasal congestion; decreased cardiac output related to blood pressure changes, arrhythmias, vasodilation; risk for injury related to CNS or CV effects.
Implementation. Monitor blood pressure, pulse, rhythm, and cardiac output regularly to adjust or stop the drug if CV effects are severe. Establish safety precautions for CNS effects or orthostatic hypotension. Arrange small, frequent meals for severe GI upset. Provide comfort measures and patient education on drug effects and warning signs.
Evaluation. Monitor response (lowered blood pressure, improved urine flow with BPH), watch for adverse effects (GI upset, CNS or CV changes), confirm patient understanding, and monitor compliance.
Nonselective Beta-Adrenergic Blocking Agents
Nonselective beta-adrenergic blocking agents block all beta-receptors within the SNS, which removes the reflex bronchodilation of sympathetic stimulation. Their use is limited in smokers and in patients with allergic or seasonal rhinitis, asthma, or COPD. Common examples are propranolol, nebivolol, and timolol.
Therapeutic Action
They competitively block beta-adrenergic receptors in the heart and juxtaglomerular apparatus and reduce vascular tone in the CNS.
Indications
These drugs treat a wide range of conditions, including hypertension, stage fright (situational anxiety), migraines, angina, and essential tremors. Timolol and carteolol in ophthalmic form reduce intraocular pressure in open-angle glaucoma.
Pharmacokinetics
Here are the characteristic interactions of nonselective beta-adrenergic blocking agents and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| Oral | 20-30 min | 60-90 min | 6-12 h |
| IV | Immediate | 1 min | 4-6 h |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 3-5 hours | liver | urine |
Contraindications and Cautions
Contraindicated with allergy to any component. Use caution in bradycardia, heart block, shock, and HF (worsened by cardiac suppression), bronchospasm, COPD, and acute asthma (worsened by blocked sympathetic bronchodilation), pregnancy (teratogenic effects occurred in animal studies with all these drugs except sotalol; neonatal apnea, bradycardia, and hypoglycemia can occur), lactation (neonatal slowed heart rate, hypotension, hypoglycemia), diabetes and hypoglycemia (the drugs mask the normal signs of hypo- and hyperglycemia), thyrotoxicosis (adrenergic blocking effects on the thyroid), and renal or hepatic dysfunction (altered metabolism and excretion).
Adverse Effects
- CNS: headache, fatigue, dizziness, depression, paresthesia, sleep disturbances, memory loss, disorientation
- CV: bradycardia, heart block, HF, hypotension, peripheral vascular insufficiency
- Respiratory: difficulty breathing, coughing, bronchospasm, severe pulmonary edema, severe bronchial obstruction
- GI: GI upset, nausea, vomiting, diarrhea, gastric pain, colitis
- GU: decreased libido, impotence, dysuria, Peyronie disease
- Other: decreased exercise tolerance, hypo- or hyperglycemia, liver changes
- Abrupt withdrawal: angina, MI, hypertension, stroke
Interactions
Clonidine can cause paradoxical hypertension, with increased rebound hypertension on clonidine withdrawal. NSAIDs decrease the antihypertensive effect. Epinephrine causes an initial hypertensive episode followed by bradycardia. Ergot alkaloids may cause peripheral ischemia. Insulin and other antidiabetic agents can produce changes in blood glucose.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, heart failure, pregnancy or lactation). Establish a baseline exam. Assess orientation, affect, and reflexes for CNS changes. Monitor CV status (blood pressure, pulse, peripheral perfusion). Assess the abdomen and auscultate bowel sounds for GI effects. Monitor renal and hepatic function tests and electrolytes for arrhythmia risk.
Nursing diagnoses. Acute pain related to CNS, GI, and systemic effects; decreased cardiac output related to CV effects; ineffective tissue perfusion related to CNS effects.
Implementation. Do not stop abruptly after chronic therapy; taper gradually over 2 weeks, because long-term use sensitizes the myocardium to catecholamines and severe reactions can occur. Continuously monitor any patient on an IV form to avert complications from rapid sympathetic blockade. Provide comfort measures and patient education on drug effects and warning signs.
Evaluation. Monitor response (lowered blood pressure, fewer angina episodes, improvement in the treated condition), watch for adverse effects (GI upset, CNS or CV changes), confirm patient understanding, and monitor compliance.
Beta1-Selective Adrenergic Blocking Agents
Beta1-selective adrenergic blocking agents do not block the beta2-receptors responsible for bronchodilation, which gives them an advantage over nonselective beta-blockers.. These drugs are preferred for patients who smoke or have asthma, other obstructive pulmonary disease, or seasonal or allergic rhinitis. Common examples are atenolol, metoprolol, and esmolol.
Therapeutic Action
They block beta1-adrenergic receptors, decreasing cardiac excitability, cardiac output, and oxygen consumption, and decrease renin release, which lowers blood pressure.
Indications
Treatment of cardiac arrhythmias, hypertension, and chronic angina; prevention of reinfarction after MI by decreasing cardiac workload and oxygen consumption; and, in oral form, decreasing intraocular pressure and treating open-angle glaucoma.
Pharmacokinetics
Here are the characteristic interactions of beta 1 -selective adrenergic blocking agents and the body in terms of absorption, distribution, metabolism, and excretion:
| Route | Onset | Peak | Duration |
|---|---|---|---|
| Oral | Varies | 2-4 h | 24 h |
| IV | Immediate | 5 min | 24 h |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 6-7 h | – | bile, urine, feces |
Contraindications and Cautions
Contraindicated with allergy to any component. Use caution in bradycardia, heart block, cardiogenic shock, and HF (worsened by cardiac suppression), pregnancy and lactation (effects on fetus or neonate), and diabetes, thyrotoxicosis, and COPD (adverse effects from sympathetic blockade).
Adverse Effects
- CNS: headache, fatigue, dizziness, depression, paresthesia, sleep disturbances, memory loss, disorientation
- CV: bradycardia, heart block, HF, hypotension, peripheral vascular insufficiency
- Respiratory: rhinitis, bronchospasm, dyspnea
- GI: GI upset, nausea, vomiting, diarrhea, gastric pain, colitis
- GU: decreased libido, impotence, dysuria, Peyronie disease
- Other: decreased exercise tolerance, hypo- or hyperglycemia, liver changes
- Abrupt withdrawal: angina, MI, hypertension, stroke
Interactions
Clonidine, NSAIDs, rifampin, and barbiturates decrease the hypertensive effect. Epinephrine causes an initial hypertensive episode followed by bradycardia. Lidocaine has increased serum levels and toxicity. Prazosin increases the risk of orthostatic hypotension. Verapamil, cimetidine, methimazole, and propylthiouracil increase the effects of selective beta1-blockers.
Nursing Considerations
Assessment. Screen for contraindications and cautions (allergy, bradycardia, pregnancy or lactation). Establish a baseline exam. Assess orientation, affect, and reflexes for CNS changes. Monitor CV status (blood pressure, pulse, peripheral perfusion). Assess the abdomen and auscultate bowel sounds for GI effects. Monitor renal and hepatic function tests and electrolytes for arrhythmia risk.
Nursing diagnoses. Acute pain related to CNS, GI, and systemic effects; decreased cardiac output related to CV effects; ineffective tissue perfusion related to CNS effects.
Implementation. Do not stop abruptly after chronic therapy; taper gradually over 2 weeks, because long-term use sensitizes the myocardium to catecholamines and severe reactions can occur. Continuously monitor any patient on an IV form to avert complications from rapid sympathetic blockade. Give oral metoprolol with food to aid absorption. Provide comfort measures and patient education on drug effects and warning signs.
Evaluation. Monitor response (lowered blood pressure, fewer angina episodes, lowered intraocular pressure), watch for adverse effects (GI upset, CNS or CV changes), confirm patient understanding, and monitor compliance.
Frequently Asked Questions
Why can't you stop a beta-blocker abruptly? Long-term blockade sensitizes the heart to catecholamines, so sudden withdrawal can trigger rebound hypertension, tachycardia, angina, MI, or arrhythmia. Taper the dose gradually, usually over about 2 weeks, while monitoring (StatPearls).
How do beta-blockers mask hypoglycemia? They blunt the adrenergic warning signs a diabetic normally feels, the rapid heartbeat and tremor, so a falling glucose can go unnoticed. Sweating is not blocked and may be the only clue, so teach diabetic patients to check glucose rather than rely on how they feel (AHA Hypertension).
What is the difference between a selective and a nonselective beta-blocker? Beta1-selective agents (atenolol, metoprolol, esmolol) act mainly on the heart and spare beta2 receptors, so they are preferred for patients who smoke or have asthma or COPD. Nonselective agents block beta2 as well, which can provoke bronchospasm.
Why are alpha1-blockers used for benign prostatic hyperplasia? Drugs like tamsulosin, prazosin, and doxazosin relax smooth muscle in the prostate, prostatic urethra, and bladder neck, improving urine flow. They also lower blood pressure, so watch for orthostatic hypotension and first-dose syncope.
Which patients need the closest monitoring on these drugs? Patients with bradycardia or heart block, asthma or COPD, decompensated heart failure, and diabetes, plus older adults with renal or hepatic impairment who reach toxic levels more easily. Check heart rate and blood pressure before dosing.
Why does phentolamine get injected into an extravasation site? It is an alpha-blocker that causes local vasodilation, which restores blood flow and prevents tissue death after IV norepinephrine or dopamine leaks into surrounding tissue.