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== Adverse effects == [[Adverse drug reaction]]s <!-- (ADRs) --> associated with the use of beta blockers include: [[nausea]], [[diarrhea]], [[bronchospasm]], [[dyspnea]], cold extremities, exacerbation of [[Raynaud's syndrome]], [[bradycardia]], [[hypotension]], [[heart failure]], [[heart block]], [[fatigue (medical)|fatigue]], [[dizziness]], [[alopecia]] (hair loss), abnormal vision, [[hallucinations]], [[insomnia]], [[nightmare]]s, [[sexual dysfunction]], [[erectile dysfunction]], alteration of [[glucose]] and [[lipid metabolism]].{{Medical citation needed|date=June 2023}} Mixed α<sub>1</sub>/β-antagonist therapy is also commonly associated with [[orthostatic hypotension]]. [[Carvedilol]] therapy is commonly associated with [[edema]].<ref name="Rossi"/>{{Page needed|date=June 2023}} Due to the high penetration across the [[blood–brain barrier]], lipophilic beta blockers, such as [[propranolol]] and [[metoprolol]], are more likely than other less lipophilic beta blockers to cause sleep disturbances, such as insomnia, vivid dreams and nightmares.<ref name="pmid21180298">{{cite journal | vauthors = Cruickshank JM | title = Beta-blockers and heart failure | journal = Indian Heart Journal | volume = 62 | issue = 2 | pages = 101–110 | year = 2010 | pmid = 21180298 }}</ref> Adverse effects associated with β<sub>2</sub>-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β<sub>1</sub>-selective (often termed "cardioselective") agents, but receptor selectivity diminishes at higher doses. Beta blockade, especially of the beta-1 receptor at the [[macula densa]], inhibits renin release, thus decreasing the release of [[aldosterone]]. This causes [[hyponatremia]] and [[hyperkalemia]].{{citation needed|date=October 2023}} [[Hypoglycemia]] can occur with beta blockade because β<sub>2</sub>-adrenoceptors normally stimulate [[glycogen]] breakdown (glycogenolysis) in the liver and pancreatic release of the [[hormone]] [[glucagon]], which work together to increase plasma glucose. Therefore, blocking β<sub>2</sub>-adrenoceptors lowers plasma glucose. β<sub>1</sub>-blockers have fewer metabolic side effects in diabetic patients; however, the fast heart rate that serves as a warning sign for insulin-induced low blood sugar may be masked, resulting in [[diabetic hypoglycemia#Unawareness|hypoglycemia unawareness]]. This is termed [[diabetic hypoglycemia#Beta blockers|beta blocker-induced hypoglycemia unawareness]]. Therefore, beta blockers are to be used cautiously in diabetics.<ref>Beta-Adrenoceptor Antagonists (Beta-Blockers); {{cite web |url=http://www.cvpharmacology.com/cardioinhibitory/beta-blockers.htm | work = CV Pharmacology | title = Beta-Adrenoceptor Antagonists (Beta-Blockers) |access-date=2011-08-08 |url-status=live |archive-url=https://web.archive.org/web/20110808021353/http://www.cvpharmacology.com/cardioinhibitory/beta-blockers.htm |archive-date=August 8, 2011 |df=mdy-all }}</ref> A 2007 study revealed diuretics and beta blockers used for hypertension increase a patient's risk of developing [[diabetes mellitus]], while [[ACE inhibitors]] and [[angiotensin II receptor antagonist]]s (angiotensin receptor blockers) actually decrease the risk of diabetes.<ref name="pmid17240286">{{cite journal | vauthors = Elliott WJ, Meyer PM | title = Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis | journal = Lancet | volume = 369 | issue = 9557 | pages = 201–207 | date = January 2007 | pmid = 17240286 | doi = 10.1016/S0140-6736(07)60108-1 | s2cid = 37044384 }}</ref> Clinical guidelines in Great Britain, but not in the United States, call for avoiding diuretics and beta blockers as first-line treatment of hypertension due to the risk of diabetes.<ref name="pmid16809680">{{cite journal | vauthors = Mayor S | title = NICE removes beta blockers as first line treatment for hypertension | journal = BMJ | volume = 333 | issue = 7557 | pages = 8 | date = July 2006 | pmid = 16809680 | pmc = 1488775 | doi = 10.1136/bmj.333.7557.8-a }}</ref> Beta blockers must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta receptors increases [[hypertension|blood pressure]], reduces coronary blood flow, left [[ventricular function]], and [[cardiac output]] and tissue perfusion by means of leaving the alpha-adrenergic system stimulation unopposed.{{medical citation needed|date=July 2015}} Beta blockers with lipophilic properties and CNS penetration such as [[metoprolol]] and [[labetalol]] may be useful for treating CNS and cardiovascular toxicity from a methamphetamine overdose.<ref name="Medscape meth toxicity">{{cite web | url = http://emedicine.medscape.com/article/820918-overview#showall | title = Methamphetamine Toxicity: Treatment & Management | vauthors = Richards JR, Derlet RW, Albertson TE | work = Medscape | publisher = WebMD | access-date = April 20, 2016 | url-status = live | archive-url = https://web.archive.org/web/20160409114830/http://emedicine.medscape.com/article/820918-overview#showall | archive-date = April 9, 2016 | df = mdy-all }}</ref> The mixed [[alpha blocker|alpha-]] and beta blocker labetalol is especially useful for treatment of concomitant tachycardia and hypertension induced by methamphetamine.<ref name="Richards 2015 review">{{cite journal | vauthors = Richards JR, Albertson TE, Derlet RW, Lange RA, Olson KR, Horowitz BZ | title = Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review | journal = Drug and Alcohol Dependence | volume = 150 | pages = 1–13 | date = May 2015 | pmid = 25724076 | doi = 10.1016/j.drugalcdep.2015.01.040 }}</ref> The phenomenon of "unopposed alpha stimulation" has not been reported with the use of beta blockers for treatment of methamphetamine toxicity.<ref name="Richards 2015 review" /> Other appropriate [[antihypertensive]] drugs to administer during hypertensive crisis resulting from stimulant overdose are [[vasodilators]] such as [[nitroglycerin (drug)|nitroglycerin]], [[diuretics]] such as [[furosemide]], and [[alpha blockers]] such as [[phentolamine]].<ref name="Toxicity, Amphetamine;eMedicine">{{cite web |url=http://www.emedicine.com/EMERG/topic23.htm |title=Toxicity, Amphetamine | vauthors = Handly M | work =Medscape |date=16 December 2016 |url-status=live |archive-url=https://web.archive.org/web/20071013053706/http://www.emedicine.com/emerg/topic23.htm |archive-date=October 13, 2007 |df=mdy-all }}</ref> === Contraindications and cautions === {{One source|section|date=November 2022}} {{div col|colwidth=30em}}Absolute contraindications: * [[Bradycardia]]<ref name="Wyeth Propranolol" /> * [[Hypotension]] * [[Hypersensitivity]] to beta blockers<ref name="Wyeth Propranolol" /> * [[Cardiogenic shock]]<ref name="Wyeth Propranolol" /> * Second or third degree AV block Relative contraindications, or contraindications specific to certain beta-blockers: * Long QT syndrome: sotalol is contraindicated * History of [[torsades de pointes]]: sotalol is contraindicated Cautions: * Abrupt discontinuations * Acute [[bronchospasm]]<ref name="Wyeth Propranolol">{{Cite web| author = Wyeth |title=Propranolol hydrochloride |url= https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/016418s078lbl.pdf |access-date=2020-09-03 }}{{dead link|date=May 2025|bot=medic}}{{cbignore|bot=medic}}</ref> * Acute [[heart failure]]<ref name="Wyeth Propranolol" /> * [[Asthma]]: see below * [[Bronchitis]]<ref name="Wyeth Propranolol" /> * [[Cerebrovascular disease]] * [[Chronic obstructive pulmonary disease|Chronic obstructive pulmonary disease (COPD)]] * [[Emphysema]]<ref name="Wyeth Propranolol" /> * [[Kidney failure]] * [[Liver disease|Hepatic disease]] * [[Myopathy]] * [[Pheochromocytoma]] * [[Psoriasis]] * Raynaud phenomenon * [[Stroke]] * [[Vasospastic angina]] * [[Wolff–Parkinson–White syndrome]]<ref name="Wyeth Propranolol" />{{div col end}} ==== Asthma ==== The 2007 National Heart, Lung, and Blood Institute ([[NHLBI]]) asthma guidelines recommend against the use of non-selective beta blockers in asthmatics, while allowing for the use of cardio selective beta blockers.<ref name="NHLBI Asthma 07">{{cite journal | vauthors = ((National Heart, Lung, and Blood Institute)) | author-link = National Heart, Lung, and Blood Institute | title = Expert Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Management of Asthma–Summary Report 2007 | journal = [[The Journal of Allergy and Clinical Immunology]] | volume = 120 | issue = 5 | pages = S94–S138 | year = 2007 | url = https://www.jacionline.org/article/S0091-6749(07)01823-4/fulltext | doi = 10.1016/j.jaci.2007.09.029 | access-date = 2017-12-09 | archive-url = https://web.archive.org/web/20210828002833/https://www.jacionline.org/article/S0091-6749%2807%2901823-4/fulltext | doi-access = free | archive-date = August 28, 2021 | url-access = subscription }}</ref>{{rp|182}} Cardio selective beta blocker (β<sub>1</sub> blockers) can be prescribed at the least possible dose to those with mild to moderate respiratory symptoms.<ref name="Morales Jackson Lipworth Donnan 2014 pp. 779–786"/><ref name="Salpeter Ormiston Salpeter p=715">{{cite journal | vauthors = Salpeter SR, Ormiston TM, Salpeter EE | title = Cardioselective beta-blockers in patients with reactive airway disease: a meta-analysis | journal = Annals of Internal Medicine | volume = 137 | issue = 9 | pages = 715–725 | date = November 2002 | pmid = 12416945 | doi = 10.7326/0003-4819-137-9-200211050-00035 | publisher = American College of Physicians | doi-access = free }}</ref> [[β2-agonist]]s can somewhat mitigate β-blocker-induced [[bronchospasm]] where it exerts greater efficacy on reversing ''selective'' β-blocker-induced bronchospasm than the ''nonselective'' β-blocker-induced worsening asthma and/or COPD.<ref name="Morales Jackson Lipworth Donnan 2014 pp. 779–786">{{cite journal | vauthors = Morales DR, Jackson C, Lipworth BJ, Donnan PT, Guthrie B | title = Adverse respiratory effect of acute β-blocker exposure in asthma: a systematic review and meta-analysis of randomized controlled trials | journal = Chest | volume = 145 | issue = 4 | pages = 779–786 | date = April 2014 | pmid = 24202435 | doi = 10.1378/chest.13-1235 | publisher = Elsevier BV }}</ref> ==== Diabetes mellitus ==== Epinephrine signals early warning of the upcoming [[hypoglycemia]].<ref name="Sprague Arbeláez 2011 pp. 463–475">{{cite journal | vauthors = Sprague JE, Arbeláez AM | title = Glucose counterregulatory responses to hypoglycemia | journal = Pediatric Endocrinology Reviews | volume = 9 | issue = 1 | pages = 463–475 | date = September 2011 | pmid = 22783644 | pmc = 3755377 }}</ref> Beta blockers' inhibition on epinephrine's effect can somewhat exacerbate hypoglycemia by interfering with [[glycogenolysis]] and mask signs of hypoglycemia such as tachycardia, palpitations, [[diaphoresis]], and tremors. Diligent blood glucose level monitoring is necessary for a patient with diabetes mellitus on beta blockers. ==== Hyperthyroidism ==== Abrupt withdrawal can result in a [[thyroid storm]].<ref name="Wyeth Propranolol" /> ==== Bradycardia or AV block ==== Unless a pacemaker is present, beta blockers can severely depress conduction in the AV node, resulting in a reduction of heart rate and cardiac output. One should be very cautious with the use of beta blockers in tachycardia patients with Wolff-Parkinson-White Syndrome, as it can result in life-threatening arrhythmia in certain patients. By slowing the conduction through the AV node, preferential conduction through the accessory pathway is favored. If the patient happens to develop atrial flutter, this could lead to a 1:1 conduction with very fast ventricular rate, or worse, ventricular fibrillation in the case of atrial fibrillation.{{citation needed|date=October 2023}} === Toxicity === [[Glucagon]], used in the treatment of overdose,<ref name="pmid2857542">{{cite journal | vauthors = Weinstein RS, Cole S, Knaster HB, Dahlbert T | title = Beta blocker overdose with propranolol and with atenolol | journal = Annals of Emergency Medicine | volume = 14 | issue = 2 | pages = 161–163 | date = February 1985 | pmid = 2857542 | doi = 10.1016/S0196-0644(85)81081-7 }}</ref><ref name="urlToxicity, Beta-blocker: Treatment & Medication - eMedicine Emergency Medicine">{{cite web |url=http://emedicine.medscape.com/article/813342-treatment |title=Toxicity, Beta-blocker: Treatment & Medication – eMedicine Emergency Medicine |access-date=2009-03-06 |url-status=live |archive-url=https://web.archive.org/web/20090317113942/http://emedicine.medscape.com/article/813342-treatment |archive-date=March 17, 2009 |df=mdy-all }}</ref> increases the strength of heart contractions, increases intracellular [[Cyclic adenosine monophosphate|cAMP]], and decreases renal [[vascular resistance]]. It is, therefore, useful in patients with beta blocker cardiotoxicity.<ref>{{cite web |url=http://www.courses.ahc.umn.edu/pharmacy/6124/handouts/Beta%20blockers.pdf |title=Beta-Adrenergic Blocker Poisoning |author=John Gualtier |website=Courses.ahc.umn.edu |access-date=2017-03-28 |url-status=dead |archive-url=https://web.archive.org/web/20160303210046/http://www.courses.ahc.umn.edu/pharmacy/6124/handouts/Beta%20blockers.pdf |archive-date=March 3, 2016 |df=mdy-all }}</ref><ref>USMLE WORLD 2009 Step1, Pharmacology, Q85</ref> [[Artificial cardiac pacemaker|Cardiac pacing]] is usually reserved for patients unresponsive to [[pharmacological therapy]]. People experiencing bronchospasm due to the β<sub>2</sub> receptor-blocking effects of nonselective beta blockers may be treated with [[anticholinergic]] drugs, such as [[ipratropium]], which are safer than [[Beta-adrenergic agonist|beta agonists]] in patients with [[cardiovascular disease]]. Other antidotes for beta blocker poisoning are [[salbutamol]] and [[isoprenaline]].
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