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Nadolol

Medically reviewed on March 25, 2018

Pronunciation

(NAY doe lol)

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Tablet, Oral:

Corgard: 20 mg [DSC] [scored]

Corgard: 20 mg [scored; contains fd&c blue #2 (indigotine)]

Corgard: 40 mg [DSC] [scored]

Corgard: 40 mg [scored; contains fd&c blue #2 (indigotine)]

Corgard: 80 mg [DSC] [scored]

Corgard: 80 mg [scored; contains fd&c blue #2 (indigotine)]

Generic: 20 mg, 40 mg, 80 mg

Brand Names: U.S.

  • Corgard

Pharmacologic Category

  • Antianginal Agent
  • Antihypertensive
  • Beta-Blocker, Nonselective

Pharmacology

Competitively blocks response to beta1- and beta2-adrenergic stimulation; does not exhibit any membrane stabilizing or intrinsic sympathomimetic activity. Nonselective beta-adrenergic blockers (propranolol, nadolol) reduce portal pressure by producing splanchnic vasoconstriction (beta2 effect) thereby reducing portal blood flow.

Absorption

~30%

Distribution

Vd: ~2 L/kg

Metabolism

Not metabolized

Excretion

Urine (as unchanged drug)

Time to Peak

Serum: 3 to 4 hours

Duration of Action

17 to 24 hours

Half-Life Elimination

Infants 3 to 22 months (n=3): 3.2 to 4.3 hours (Mehta 1992)

Children 10 years (n=1): 15.7 hours (Mehta 1992)

Children ~15 years (n=1): 7.3 hours (Mehta 1992)

Adults: 20 to 24 hours; prolonged with renal impairment; (up to 45 hours in severe impairment) (Herrera 1979)

Protein Binding

30%

Use: Labeled Indications

Angina: Treatment of angina pectoris

Hypertension: Management of hypertension. Note: Beta-blockers are not recommended as first-line therapy (ACC/AHA [Whelton 2017]).

Off Label Uses

Atrial fibrillation (rate control)

Based on the American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guidelines for the management of patients with atrial fibrillation, the use of beta-blockers, including nadolol, for ventricular rate control in patients with paroxysmal, persistent, or permanent atrial fibrillation is effective and recommended for this condition.

Catecholaminergic polymorphic ventricular tachycardia (prevention)

In patients with catecholaminergic polymorphic ventricular tachycardia (CPVT), data from an observational study suggests that beta-blockers, especially nadolol, may be beneficial at reducing the risk of cardiac events [Hayashi 2009]. Additional data may be necessary to further define the role of nadolol in this condition.

Based on the American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for management of patients with ventricular arrhythmias and prevention of sudden cardiac death, beta-blockers are effective for control of CPVT.

Gastroesophageal variceal hemorrhage prophylaxis in patients with cirrhosis

Data from randomized controlled trials support the use of nadolol for primary prophylaxis against first variceal hemorrhage [Lo 2004], [Lo 2010] and secondary prophylaxis against recurrent variceal hemorrhage [de la Peña 2005]. Data from randomized controlled trials also supports the use of nadolol combined with isosorbide mononitrate for secondary prophylaxis against recurrent variceal hemorrhage [Lo 2009], [Lo 2012].

Based on the American Association for the Study of Liver Diseases and the American College of Gastroenterology guidelines for the prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis, nadolol among other non-selective beta-blockers (eg, propranolol) is an effective and recommended agent for primary and secondary prophylaxis of variceal hemorrhage.

Migraine prophylaxis

Based on the American Academy of Neurology and the American Headache Society evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults, the use of nadolol (among other beta-blockers) is probably effective and may be considered for migraine prevention. No specific dosing recommendations provided.

Supraventricular tachycardia (atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, atrial flutter, focal atrial tachycardia)

Based on the American College of Cardiology/American Heart Association/Heart Rhythm Society guidelines for the management of patients with supraventricular arrhythmias, the use of an oral beta-blocker, including nadolol, is effective and recommended for the ongoing management of a variety of symptomatic supraventricular tachycardias (atrioventricular nodal reentrant tachycardia [AVNRT], atrioventricular reentrant tachycardia [AVRT], focal atrial tachycardia [AT]) without pre-excitation in patients who are not candidates for, or prefer not to undergo catheter ablation. Oral beta-blockers, including nadolol, may also be useful for the ongoing management (rate control) in hemodynamically stable patients with atrial flutter.

Thyrotoxicosis

Based on the 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis, beta-blockers, including nadolol, are effective and recommended in the treatment symptomatic thyrotoxicosis. However, experience with nadolol is limited compared to other beta-blockers. Beta-blockers should also be considered in asymptomatic patients who are at increased risk of complications due to worsening hyperthyroidism [Ross 2016].

Ventricular arrhythmias due to congenital long QT syndrome (prevention)

In patients with congenital long QT syndrome (LQTS), data from observational studies suggest that beta-blockers may be beneficial at reducing the risk of cardiac events, including ventricular arrhythmias, especially in patients with congenital LQTS type 1 or type 2 [Chockalingam 2012], [Goldenberg 2010], [Moss 2000], [Sauer 2007]. Additional data may be necessary to further define the role of nadolol in this condition. Atenolol, nadolol, and propranolol may be preferred for patients with LQTS based on the currently available data.

Based on the American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for management of patients with ventricular arrhythmias and prevention of sudden cardiac death, beta-blockers are effective for control of ventricular arrhythmias in patients with congenital LQTS.

Ventricular premature beat (suppression)

Based on the American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for management of patients with ventricular arrhythmias and prevention of sudden cardiac death, beta-blockers are effective for control of ventricular premature beats.

Ventricular tachycardia (prevention)

Based on the American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for management of patients with ventricular arrhythmias and prevention of sudden cardiac death, beta-blockers are effective for prevention of ventricular tachycardia.

Contraindications

Bronchial asthma; sinus bradycardia; heart block greater than first degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac failure

Canadian labeling: Additional contraindications (not in US labeling): Hypersensitivity to nadolol or any component of the formulation; cor pulmonale; anesthesia with agents that produce myocardial depression; allergic rhinitis, bronchospasm, or severe chronic obstructive pulmonary disease (COPD)

Dosing: Adult

Angina: Oral: Initial: 40 mg once daily, increase dosage gradually by 40 to 80 mg increments at 3- to 7-day intervals until optimum clinical response is obtained usual dose: 40 to 80 mg daily; maximum dose: 240 mg daily

Atrial fibrillation (rate control) (off-label use): Oral: Usual maintenance dose: 10 to 240 mg once daily (AHA/ACC/HRS [January 2014])

Catecholaminergic polymorphic ventricular tachycardia (prevention) (off-label use): Oral: 40 to 320 mg once daily (AHA/ACC/HRS [Al-Khatib 2017]; Claudio 2018; Hyashi 2009)

Gastroesophageal variceal hemorrhage prophylaxis in patients with cirrhosis (off-label use): Oral: Initial: 40 mg once daily (de la Peña 2005; Garcia-Tsao 2017; Lo 2004; Lo 2009; Lo 2010; Lo 2012); consider starting with 20 mg once daily if concern for hypotension (Garcia-Tsao 2017; Sanyal 2018); adjust every 2 to 3 days to maximal tolerated dose or until heart rate is ~55 to 60 beats per minute (Garcia-Tsao 2017). If systolic blood pressure is <90 mm Hg, reduce dose or discontinue. Some experts recommend a maximum dose of 160 mg/day in patients without ascites and 80 mg/day in patients with ascites (Garcia-Tsao 2017). Note: May use for primary or secondary prophylaxis. Primary prophylaxis is indicated for patients with cirrhosis and medium/large varices, variceal red wale markings on endoscopy, or decompensation and small varices (Garcia-Tsao 2017).

Hypertension (alternative agent): Oral: Initial: 40 mg once daily; titrate as needed based on patient response by 40 to 80 mg increments; usual dosage range: 40 to 120 mg once daily (ACC/AHA [Whelton 2017]). Doses up to 320 mg once daily may be necessary.

Supraventricular tachycardia (off-label use): Oral: Initial: 40 mg once daily; maximum maintenance dose: 320 mg once daily (ACC/AHA/HRS [Page 2015])

Thyrotoxicosis (off-label use): Oral: 40 to 160 mg once daily (Ross 2016)

Ventricular arrhythmias due to congenital long QT syndrome (prevention) (off-label use): Oral: 40 to 320 mg daily (AHA/ACC/HRS [Al-Khatib 2017])

Ventricular premature beat (suppression) (off-label use): Oral: 40 to 320 mg daily (AHA/ACC/HRS [Al-Khatib 2017])

Ventricular tachycardia (prevention) (off-label use): Oral: 40 to 320 mg daily (AHA/ACC/HRS [Al-Khatib 2017])

Dosing: Geriatric

Refer to adult dosing. In the management of hypertension, consider lower initial doses (eg, 20 mg daily) and titrate to response (Aronow 2011).

Dosing: Renal Impairment

CrCl >50 mL/minute/1.73 m2: Administer every 24 hours

CrCl 31 to 50 mL/minute/1.73 m2: Administer every 24 to 36 hours

CrCl 10 to 30 mL/minute/1.73 m2: Administer every 24 to 48 hours

CrCl <10 mL/minute/1.73 m2: Administer every 40 to 60 hours

Dosage adjustments for dialysis are not provided in the manufacturer’s labeling; however, the following guidelines have been used by some clinicians (Aronoff, 2007):

ESRD requiring hemodialysis: Administer dose postdialysis.

Peritoneal dialysis: Administer every 40 to 60 hours

Dosing: Hepatic Impairment

There are no dosage adjustments provided in the manufacturer’s labeling.

Administration

Oral: May be administered without regard to meals.

Storage

Store at room temperature; avoid excessive heat. Protect from light.

Drug Interactions

Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Alpha1-Blockers: Beta-Blockers may enhance the orthostatic hypotensive effect of Alpha1-Blockers. The risk associated with ophthalmic products is probably less than systemic products. Monitor therapy

Alpha2-Agonists: May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Exceptions: Apraclonidine. Consider therapy modification

Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, blood pressure lowering medications should be withheld for 24 hours prior to amifostine administration. If blood pressure lowering therapy cannot be withheld, amifostine should not be administered. Consider therapy modification

Amiodarone: May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. Monitor therapy

Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Monitor therapy

Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Beta2-Agonists: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2-Agonists. Avoid combination

Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Monitor therapy

Bretylium: May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents. Monitor therapy

Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Monitor therapy

Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Avoid combination

Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Monitor therapy

Calcium Channel Blockers (Nondihydropyridine): May enhance the hypotensive effect of Beta-Blockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil. Monitor therapy

Cardiac Glycosides: Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. Monitor therapy

Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Avoid combination

Cholinergic Agonists: Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Management: Administer these agents in combination with caution, and monitor for conduction disturbances. Avoid methacholine with any beta blocker due to the potential for additive bronchoconstriction. Monitor therapy

Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. Monitor therapy

Dronedarone: May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Consider therapy modification

DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Monitor therapy

EPINEPHrine (Nasal): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Nasal). Monitor therapy

EPINEPHrine (Oral Inhalation): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Oral Inhalation). Monitor therapy

Epinephrine (Racemic): Beta-Blockers (Nonselective) may enhance the hypertensive effect of Epinephrine (Racemic). Monitor therapy

EPINEPHrine (Systemic): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Systemic). Monitor therapy

Ergot Derivatives: Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. Consider therapy modification

Fingolimod: Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. Consider therapy modification

Floctafenine: May enhance the adverse/toxic effect of Beta-Blockers. Avoid combination

Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Consider therapy modification

Green Tea: May decrease the serum concentration of Nadolol. Management: Advise patients to minimize green tea consumption during nadolol treatment. The impact of separating nadolol doses from green tea consumption has not been investigated. Consider therapy modification

Herbs (Hypertensive Properties): May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Herbs (Hypotensive Properties): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Monitor therapy

Insulins: Beta-Blockers may enhance the hypoglycemic effect of Insulins. Monitor therapy

Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Monitor therapy

Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Monitor therapy

Levodopa: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa. Monitor therapy

Lidocaine (Systemic): Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). Monitor therapy

Lidocaine (Topical): Beta-Blockers may increase the serum concentration of Lidocaine (Topical). Monitor therapy

Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Lumacaftor: May decrease the serum concentration of P-glycoprotein/ABCB1 Substrates. Lumacaftor may increase the serum concentration of P-glycoprotein/ABCB1 Substrates. Monitor therapy

Mepivacaine: Beta-Blockers may increase the serum concentration of Mepivacaine. Monitor therapy

Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Avoid combination

Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Midodrine: Beta-Blockers may enhance the bradycardic effect of Midodrine. Monitor therapy

Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Monitor therapy

Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Monitor therapy

Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Monitor therapy

Obinutuzumab: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Consider therapy modification

Opioids (Anilidopiperidine): May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

P-glycoprotein/ABCB1 Inducers: May decrease the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Monitor therapy

P-glycoprotein/ABCB1 Inhibitors: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Monitor therapy

Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Monitor therapy

Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Monitor therapy

Ranolazine: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. Monitor therapy

Regorafenib: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy

Reserpine: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Avoid combination

Ruxolitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. Monitor therapy

Sulfonylureas: Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents. Monitor therapy

Terlipressin: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Theophylline Derivatives: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. Consider therapy modification

Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Yohimbine: May diminish the antihypertensive effect of Antihypertensive Agents. Monitor therapy

Test Interactions

May lead to false-positive aldosterone/renin ratio (ARR) (Funder 2016)

Adverse Reactions

>10%: Central nervous system: Drowsiness, insomnia

1% to 10%:

Cardiovascular: Atrioventricular block, bradycardia, cardiac conduction disturbance, cardiac failure, cold extremities, edema, hypotension, palpitations, peripheral vascular insufficiency, Raynaud's phenomenon

Central nervous system: Depression, dizziness, fatigue, sedation

<1%, postmarketing, and/or case reports: Abdominal distress, anorexia, behavioral changes, bloating, blurred vision, bronchospasm, cardiac arrhythmia, chest pain, confusion (especially in the elderly), constipation, cough, decreased libido, diaphoresis, diarrhea, dyspepsia, dyspnea, facial edema, flatulence, hallucination, headache, impotence, nasal congestion, nausea, nervousness, paresthesia, pruritus, skin rash, slurred speech, thrombocytopenia, tinnitus, transient alopecia, vomiting, weight gain, xeroderma, xerophthalmia, xerostomia

ALERT: U.S. Boxed Warning

Exacerbation of ischemic heart disease following abrupt withdrawal:

Hypersensitivity to catecholamines has been observed in patients withdrawn from beta-blocker therapy; exacerbation of angina and, in some cases, myocardial infarction have occurred after abrupt discontinuation of such therapy. When discontinuing nadolol administered long term, particularly in patients with ischemic heart disease, gradually reduce the dosage over a period of 1 to 2 weeks and carefully monitor the patient. If angina markedly worsens or acute coronary insufficiency develops, reinstitute nadolol administration promptly, at least temporarily, and take other measures appropriate for the management of unstable angina. Warn patients against interruption or discontinuation of therapy without the health care provider's advice. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue nadolol therapy abruptly, even in patients treated only for hypertension.

Warnings/Precautions

Concerns related to adverse events:

• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.

Disease-related concerns:

• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring.

• Conduction abnormality: Consider preexisting conditions such as sick sinus syndrome before initiating.

• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.

• Heart failure (HF): Use with caution in patients with compensated heart failure and monitor for a worsening of the condition (efficacy of nadolol in HF has not been demonstrated).

• Myasthenia gravis: Use with caution in patients with myasthenia gravis.

• Peripheral vascular disease (PVD) and Raynaud disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud disease. Use with caution and monitor for progression of arterial obstruction.

• Pheochromocytoma (untreated): Adequate alpha-blockade is required prior to use of any beta-blocker.

• Prinzmetal variant angina: Beta-blockers without alpha1-adrenergic receptor blocking activity should be avoided in patients with Prinzmetal variant angina since unopposed alpha1-adrenergic receptors mediate coronary vasoconstriction and can worsen anginal symptoms (Mayer 1998).

• Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.

• Psychiatric disease: Use with caution in patients with a history of psychiatric illness; may cause or exacerbate CNS depression.

• Renal impairment: Use with caution in patients with renal impairment; dosage adjustments are required.

• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If hyperthyroidism is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.

Concurrent drug therapy issues:

• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.

Special populations:

• Elderly: Bradycardia may be observed more frequently in elderly patients (>65 years of age); dosage reductions may be necessary.

Other warnings/precautions:

• Abrupt withdrawal: [US Boxed Warning]: Beta-blocker therapy should not be withdrawn abruptly (particularly in patients with CAD), but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia. Severe exacerbation of angina, ventricular arrhythmias, and myocardial infarction (MI) have been reported following abrupt withdrawal of beta-blocker therapy. Temporary but prompt resumption of beta-blocker therapy may be indicated with worsening of angina or acute coronary insufficiency.

• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.

Monitoring Parameters

Heart rate, blood pressure, signs/symptom of angina exacerbation when discontinued

Hypertension: The 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults (ACC/AHA [Whelton 2017]):

Confirmed hypertension and known CVD or 10-year ASCVD risk ≥10%: Target blood pressure <130/80 mm Hg is recommended.

Confirmed hypertension without markers of increased ASCVD risk: Target blood pressure <130/80 mm Hg may be reasonable.

Pregnancy Risk Factor

C

Pregnancy Considerations

Adverse events were observed in some animal reproduction studies. Nadolol crosses the placenta and is measurable in infant serum after birth (Fox 1985). Bradycardia and hypoglycemia have been observed in neonates following maternal use of nadolol during pregnancy. Reduced birth weight has also been observed following in utero exposure to beta-blockers as a class. Adequate facilities for monitoring infants at birth is generally recommended.

Untreated chronic maternal hypertension and preeclampsia are also associated with adverse events in the fetus, infant, and mother (ACOG 2015; Magee 2014). Although beta-blockers may be used when treatment of hypertension in pregnancy is indicated, agents other than nadolol are preferred (ACOG 2013; Magee 2014).

Patient Education

• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)

• Have patient report immediately to prescriber severe dizziness, passing out, angina, sensation of cold, bradycardia, or signs of heart problems (cough or shortness of breath that is new or worse, swelling of the ankles or legs, abnormal heartbeat, weight gain of more than five pounds in 24 hours, dizziness, or passing out) (HCAHPS).

• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.

Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for health care professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

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