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Monday, August 26, 2024

American Medical Association

From Wikipedia, the free encyclopedia
American Medical Association
FormationMay 7, 1847; 177 years ago
TypeProfessional association
36-0727175
Legal status501(c)(6)
Purpose"To Promote the art and science of medicine and the betterment of public health"
Headquarters330 North Wabash, Chicago, Illinois, United States
Region served
United States
Membership
271,660 as of 2022 
President
Jesse M. Ehrenfeld (MD, MPH)
Revenue (2022)
$493,147,829
Websiteama-assn.org

The American Medical Association (AMA) is an American professional association and lobbying group of physicians and medical students. Founded in 1847, it is headquartered in Chicago, Illinois. Membership was 271,660 in 2022.

The AMA's stated mission is "to promote the art and science of medicine and the betterment of public health." The organization was founded with the goal to raise the standards of medicine in the 19th century primarily through gaining control of education and licensing. In the 20th century, the AMA has frequently lobbied to restrict the supply of physicians, contributing to a doctor shortage in the United States. The organization has also lobbied against allowing physician assistants and other health care providers to perform basic forms of health care. The organization has historically lobbied against various forms of government-run health insurance.

The Association also publishes the Journal of the American Medical Association (JAMA). The AMA also publishes a list of Physician Specialty Codes which are the standard method in the U.S. for identifying physician and practice specialties.

The American Medical Association is governed by a House of Delegates as well as a board of trustees in addition to executive management. The organization maintains the AMA Code of Medical Ethics, and the AMA Physician Masterfile containing data on United States Physicians. The Current Procedural Terminology coding system was first published in 1966 and is maintained by the Association. It has also published works such as the Guides to Evaluation of Permanent Impairment and established the American Medical Association Foundation and the American Medical Political Action Committee. The current president is Jesse Ehrenfeld, an anesthesiologist affiliated with the Medical College of Wisconsin.

History

1847–1900

In 1846, the organization created a committee dedicated to analyzing the methodology of vital records registration. It urged state governments to adopt measures to register births, marriages and deaths within their populations. In 1847, the American Medical Association was founded in Philadelphia by Nathan Smith Davis as a national professional medical organization. The organization educated people about the dangers of patent medicines and called for legislation regulating their production and sale. One resulting legislation was the Drug Importation Act of 1848.

In 1848, the AMA began publishing Transactions of the American Medical Association, which included lists and reports of cases of physiological effects of ether and chloroform at the Massachusetts General Hospital in Boston, the New York Hospital and the clinics of the University of Pennsylvania and Jefferson Medical College.

At the organization's second meeting in 1849, Thomas Wood suggested a committee on medical science to establish a board to analyze quack remedies and nostrums to be published in order to inform the public about the dangers of such remedies. The AMA's attempts to expose quack remedies aided the passage of the first Pure Food and Drug Act in 1906.

The AMA Committee on Ethics advocated for recognition of qualified female physicians in 1869, and the AMA inducted its first female member, Sarah Hackett Stevenson, as an Illinois State Medical Society delegate in 1876.

In 1872, the AMA's book Nomenclature of Diseases was published. In 1883, the AMA launched the Journal of the American Medical Association. The organization's founder, Nathan Smith Davis, served as the first editor of the publication.

In 1897, the AMA was incorporated in the state of Illinois.

AMA pushed for laws requiring compulsory smallpox vaccinations in 1899. In 1899, the AMA appointed a committee to report on tuberculosis, including on its communicability and prevention. The Committee on Tuberculosis presented its report in October 1900.

1901–1920

In 1901, the AMA was reorganized with its central authority shifted to a House of Delegates, a board of trustees, and executive offices. The House of Delegates was modeled after the United States House of Representatives and included representatives from medical organizations across the United States as a formal, reform-minded legislative body. The organization's new president appointed a Committee on Medical Education in order to evaluate medical education in the United States and make recommendations for its improvement.

The AMA's Committee on National Legislation established the Committee on Medical Legislation in 1901.

AMA created the Council on Pharmacy and Chemistry in 1905 to set standards for drug manufacturing and advertising. That same year, the AMA began a voluntary program of drug approval, which would remain in effect until 1955. Drug companies were required to show proof of the effectiveness of their drugs to advertise them in AMA's journal.

In 1906, the AMA established a Physician Masterfile designed to contain data on physicians in the United States as well as graduates of American medical schools and international graduates who are in the United States. Each file is established when an individual either enters medical schools or enters the United States.

The AMA established the Council for the Defense of Medical Research in 1908. AMA's Council on Medical Education and Hospitals first published its annual list of hospitals approved for internships in 1914.

1921–1960

In May 1922, the Woman's Auxiliary to the AMA was organized. The following year, the AMA established standards for medical specialty training residency programs. The AMA later published its first list of hospitals approved for residency training in 1927.

In 1927, Congress passed the Caustic Poison Act, lobbied for by the AMA, which required product labels to include warnings if they included lye or 10 other caustic chemicals.

In 1933, the AMA's general medical guide the Standard Classified Nomenclature of Disease, (referred to as the Standard), was released. Along with the New York Academy of Medicine, the APA provided the psychiatric nomenclature subsection. A number of revisions were produced, with the last in 1961.

The Normal Diet, a comprehensive listing of what Americans should be eating, was published by the AMA in 1938.

A formal partnership between the AMA and the Association of American Medical Colleges formed the Liaison Committee on Medical Education in 1942 in order to establish requirements for certification of medical schools. In 1951, the Joint Commission on Accreditation of Hospitals was created through merging the Hospital Standardization Program with quality standards from the American College of Physicians, the American Hospital Association, and the American Medical Association. The commission, established for evaluation and accreditation of healthcare organizations in the United States, governed by a board of commissioners including physicians, consumers and administrators.

The AMA publicly endorsed the principle of fluoridation of community water supplies in 1951.

1961–1980

The AMA first published the Current Procedural Terminology (CPT) coding system in 1966. The system was created for uniform reporting of outpatient physician services. The first manual was 163 pages and contained only four-digit codes with descriptions of each. A second edition of the book was published in 1970 with a fifth digit added.

The AMA published the first Guides to the Evaluation of Permanent Impairment in 1971. The guides were later republished in 1977 before the AMA Council on Scientific Affairs created 12 committees to review the guides before the second edition was published in 1984.

In the 1970s, the AMA spoke out against gender discrimination in medical institutions. In 1975, the AMA adopted a policy stating that "discrimination based on sexual orientation is improper and unacceptable by any part of the federation of medicine." It adopted a resolution to repeal all state sodomy laws. In 1976, the AMA began encouraging all public facilities to have handicap access.

1981–2000

The AMA released a survey in 1981 that found two short-term effects of dioxin on humans and recommended further studies. By 1983, the AMA accused the news media of conducting a "witch hunt" against the toxic chemical and launched a public information campaign to counter media hysteria.

In May 1983, the Journal of the American Medical Association published a report that reviewed cases of childhood AIDS.

A Federal district judge ruled that the AMA had violated the Sherman Antitrust Act in 1987 by depriving chiropractors of access to the Association. The lawsuit, filed by four chiropractors, accused AMA of conspiring to prevent chiropractors from practicing in the United States.

The Journal of the American Medical Association first documented that Joe Camel cartoons reached more children than adults in December 1991. The Association called for the R. J. Reynolds Tobacco Company to stop using the Joe Camel character in its advertising because of its appeal to youth.

In 1995, Lonnie R. Bristow became the first African-American president of the American Medical Association. Before he became president, Bristow was the first African-American member of the board of trustees and first African-American chairman of the board.

In 1996, the AMA campaigned against health plan "gag clauses", which prohibited doctors from discussing with their patients treatments not covered by the plan, stating that the stipulations inhibit the communication of information and restrict the care doctors can give their patients. The clauses were removed from the contracts of five leading providers, and laws prohibiting such clauses were passed in 16 states.

In 1997, the AMA established the National Patient Safety Foundation as an independent, nonprofit research and education organization focused on patient safety.

Nancy W. Dickey was named president of the American Medical Association in June 1998. She was the first woman to head the organization and had been part of AMA's leadership since 1977.

2000–present

In 2002, the AMA released a report that found a medical liability insurance crisis in at least a dozen states was forcing physicians to either close practices or limit services. The association called for Congress to take action and campaigned for national reform.

In 2008, the AMA issued a formal apology for previous policies that excluded African-Americans from the organization and announced increased efforts to increase minority physician participation.

The AMA officially recognized obesity as a disease in 2013 in an attempt to change how the medical community approaches the issue.

In 2015, the AMA declared there is no medically valid reason to exclude transgender individuals from serving in the U.S. military. The Human Rights Campaign lauded the decision.

Patrice A. Harris became the AMA's 174th president in June 2019, the organization's first African-American woman to hold this position.

The AMA sponsors the Specialty Society Relative Value Scale Update Committee, which is an influential group of 29 physicians, mostly specialists, who help determine the value of different physicians' labor in Medicare prices.

Policy positions

The AMA has one of the largest political lobbying budgets of any organization in the United States. Its political positions throughout its history have often been controversial.

Lobbying

Between 1998 and 2020, the association has spent an average of $18 million annually on lobbying efforts. In the first quarter of 2021, they reported $6.36 million in lobbying expenses.

Restrictions on physician supply

The AMA has at various points in history advocated for restricting the supply of physicians. In the early 20th century, the AMA lobbied lawmakers to shut down medical schools on grounds that they were substandard, which in turn reduced the supply of doctors. The AMA lobbied for reductions in physician supply during the Great Depression. In 1997, the AMA lobbied Congress to restrict the number of doctors that could be trained in the United States, claiming that, "The United States is on the verge of a serious oversupply of physicians." The AMA successfully lobbied Congress to cap how much Medicare could reimburse hospitals for resident physicians, which reduced residency training. In the decades following these restrictions on physician supply, the United States has a shortage of doctors. The United States was forecasted to have a shortage of 46,900 to 121,900 physicians by 2032. As a consequence of the restrictions on medical training in the United States, a quarter of physicians in the United States were trained abroad by 2022.

In the 1930s, the AMA attempted to prohibit its members from working for the health maintenance organizations established during the Great Depression, which violated the Sherman Antitrust Act and resulted in a conviction ultimately affirmed by the US Supreme Court.

In 1982, the Supreme Court of the United States upheld a Federal Trade Commission order that allowed doctors and dentists to advertise without professional association interference. The order restrained the AMA from its power to obstruct agreements between physicians and health maintenance organizations.

The AMA has lobbied to restrict the ability of physician assistants to provide services with less oversight from doctors.

In 2007, the AMA called for state and federal agencies to investigate potential conflicts of interest between the retail clinics and pharmacy chains.

Opposition to expanded health care access

In 1917, the AMA endorsed compulsory health insurance, but the organization faced backlash from its state-level societies for this position. The AMA established a policy of opposition to compulsory health insurance by state or federal government in 1920.

A 1932 editorial in the Journal of the American Medical Society denounced a proposal for government-backed voluntary health insurance system.

In the 1940s, the AMA opposed President Harry Truman's proposed healthcare reforms, which would have expanded healthcare facilities in low-income and rural communities, bolstered public health services, increased investments in medical research and education, and provided a payroll-tax-financed, government-run health insurance plan to help relieve the burden of excessive healthcare bills from sick persons. The AMA condemned Truman's plan as "socialized medicine". The AMA charged each of its members an extra 25 dollars to finance a lobbying campaign against the Truman plan.

In 1961, the AMA opposed the King-Anderson bill proposing Medicare legislation and took out advertisements in newspapers, radio and television against government health insurance. The AMA established the American Medical Political Action Committee, which was separate from AMA though the Association nominated its board of directors. The AMA's efforts to defeat Medicare legislation was called Operation Coffee Cup. the AMA produced the LP, "Ronald Reagan Speaks Out Against Socialized Medicine". The AMA created an "Eldercare" proposal rather than hospital insurance through Social Security. Since the enactment of Medicare, the AMA reversed its position and now opposes any "cut to Medicare funding or shift [of] increased costs to beneficiaries at the expense of the quality or accessibility of care".

The AMA did not take a position on Bill Clinton's proposed health care reform.

The AMA supported the Barack Obama administration's health care reform. In 2009, the American Medical Association released a public letter to the United States Congress and President Barack Obama endorsing his proposed overhaul to the public health care system, including universal health coverage. The following year, it offered "qualified support" for the Patient Protection and Affordable Care Act.

The AMA supported the Medicare Access and CHIP Reauthorization Act of 2015, which introduced Medicare reforms and replaced the SGR formula with increased Medicare physician reimbursement.

The AMA opposed Republicans' proposed repeal of the Affordable Care Act in March 2017, saying millions of Americans would lose health care coverage.

The AMA has historically opposed single-payer health care.

Substance use and addiction

The AMA's Committee on Alcoholism issued a statement in 1956 calling alcoholism an illness and encouraging medical personnel and institutions to admit and treat alcoholic patients.

In 1972, the AMA launched a "war on smoking" and supported legislation that would prohibit tobacco sample disbursement.

In the early 1980s, the AMA advocated for raising the national legal drinking age to 21.

The AMA called for a ban on advertising and promotion of all tobacco products in any form of media. The AMA also proposed declaring snuff and chewing tobacco a health hazard, increasing the tax on cigarettes, prohibiting smoking on public transportation and urged medical facilities to ban smoking on their premises.

In 2014, the Association created the AMA Opioid Task Force to evaluate prescription opioid use and abuse.

Medical malpractice reform

The AMA has supported changes in medical malpractice law to limit damage awards, which, it contends, makes it difficult for patients to find appropriate medical care. In many states, high risk specialists have moved to other states that have enacted reform. For example, in 2004, all neurosurgeons had relocated out of the entire southern half of Illinois. The main legislative emphasis in multiple states has been to effect caps on the amount that patients can receive for pain and suffering. These costs for pain and suffering are only those that exceed the actual costs of healthcare and lost income. At the same time however, states without caps also experienced similar results, suggesting that other market factors may have contributed to the decreases. Some economic studies have found that caps have historically had an uncertain effect on premium rates. A recent report by the AMA found that, in a 12-month period, five percent of physicians had claims filed against them.

Structural racism controversy and outcomes

On a February 2021 JAMA podcast a Deputy Editor of the journal proposed that "structural racism is an unfortunate term to describe a very real problem," and that "taking racism out of the conversation would help" to ensure "all people who lived in disadvantaged circumstance have equal opportunities to become successful and have better qualities of life." In addition to the comments made during the podcast, JAMA then tweeted out the podcast with the caption "No physician is racist, so how can there be structural racism in health care" which further added to the controversy. The subsequent controversy led the Deputy Editor and the JAMA editor-in-chief Howard Bauchner to resign. Kirsten Bibbins-Domingo was chosen as Bauchner's replacement making her the first person of color and second woman to ever lead the journal.

After the podcast structural racism controversy in 2021, the AMA published a paper that included recommendations to help improve health equity and address structural racism which would encourage "explicit conversations about power, racism, gender and class oppression, forms of discrimination and exclusion." Its "Advancing Health Equity: A Guide to Language, Narrative and Concepts" document asked "questions about language and commonly used phrases and terms, with the goal of cultivating awareness about dominant narratives and offering equity-based, equity-explicit, and person-first alternatives."

Political donations

The association has donated between $1.6 million and $3.4 million in election cycles between 1990 and 2020. Their distributions have varied from near parity for both Democrats and Republicans to heavily favoring Republican candidates at 75% in the 1996 and 2004 elections.

Contributions by party of recipient (1990 to 2020)
Cycle Total Democrats % to Dems Republicans % to Repubs
1990 $2,846,407 $1,398,543 49.13% $1,447,864 50.87%
1992 $3,451,005 $1,696,551 49.23% $1,749,454 50.77%
1994 $2,838,629 $1,206,192 42.57% $1,627,437 57.43%
1996 $2,869,846 $695,525 24.23% $2,174,571 75.77%
1998 $2,712,032 $804,018 29.84% $1,890,514 70.16%
2000 $2,290,025 $1,081,268 47.27% $1,206,007 52.73%
2002 $2,704,238 $1,074,695 39.74% $1,629,543 60.26%
2004 $2,353,510 $564,375 24.24% $1,763,950 75.76%
2006 $2,261,629 $743,554 33.05% $1,506,410 66.95%
2008 $1,875,337 $1,044,987 55.74% $829,700 44.26%
2010 $1,624,409 $867,750 53.46% $755,409 46.54%
2012 $2,117,640 $880,062 41.66% $1,232,578 58.34%
2014 $2,062,906 $793,776 38.51% $1,267,640 61.49%
2016 $1,994,697 $739,187 37.12% $1,252,093 62.88%
2018 $1,470,984 $715,539 49.13% $740,805 50.87%
2020 $1,573,836 $830,438 54.14% $703,513 45.86%

Between 1990 and 2020, the majority of contributions came from PAC money.

Contributions by source of funds (1990 to 2020)
Cycle Individuals PACs Soft (Individuals) Soft (Organization)
1990 $19,321 $2,827,086 N/A N/A
1992 $31,425 $3,371,794 $0 $47,786
1994 $26,341 $2,742,156 $0 $70,132
1996 $46,633 $2,617,176 $0 $206,037
1998 $21,666 $2,609,991 $0 $80,375
2000 $41,056 $2,216,104 $350 $32,515
2002 $33,657 $2,656,131 $700 $13,750
2004 $81,800 $2,257,425 $35 $14,250
2006 $61,080 $2,188,884 $665 $11,000
2008 $124,869 $1,749,818 $0 $650
2010 $64,550 $1,538,859 $1,000 $20,000
2012 $70,062 $2,047,578 $0 $0
2014 $66,700 $1,985,716 $490 $10,000
2016 $101,903 $1,880,594 $2,200 $10,000
2018 $62,734 $1,400,190 $2,560 $5,500
2020 $171,963 $1,362,650 $4,223 $35,000

Criticism

During the Civil Rights Movement, the American Medical Association's policy of allowing its constituent groups to be racially segregated in areas with widespread prejudice faced opposition from doctors as well as other healthcare professionals. Pressure from organizations such as the Medical Committee for Human Rights (MCHR) resulted in changed policies by the late 1960s.

Nobel Memorial Prize-winning economist Milton Friedman, as well as his wife, Rose Friedman, have claimed that the organization acts as a guild and has attempted to increase physicians' wages and fees by influencing limitations on the supply of physicians and competition from non-physicians. In the book Free to Choose, the Friedmans stated that "the AMA has engaged in extensive litigation charging chiropractors and osteopathic physicians with the unlicensed practice of medicine, in an attempt to restrict them to as narrow an area as possible." The AMA was also criticized for holding up licensing of foreign-trained medical professionals who, after Adolf Hitler came to power, were fleeing to the U.S. from Nazi-controlled Germany and adjacent nations. Profession and Monopoly also criticized the AMA for limiting the supply of physicians and inflating the cost of medical care in the U.S. as well as its influence on hospital regulation. In a 1987 antitrust court case, a federal district judge called the AMA's behavior toward chiropractors "systematic, long-term wrongdoing". The AMA was accused of limiting the associations between physicians and chiropractors. In the 1960s and 1970s, the association's Committee on Quackery was said to have targeted the chiropractic profession, and for many years the AMA held that it was unethical for physicians to refer patients to chiropractors or to receive referrals from chiropractors.

In October 2020, the association used Twitter and Facebook to publicly oppose scope of practice creep, where non-physicians are permitted to provide healthcare services without physician oversight. The posts were removed the same day and the AMA commented that they were committed to "team-based healthcare guided by a physician" to "optimize patient outcomes." The American Academy of Physician Assistants published a letter expressing their frustration at the social media posts. Rebekah Bernard from the advocacy group Physicians for Patient Protection publicly criticized the AMA for retracting their social media posts.

Structure

The AMA is composed of policy discussion groups that meet twice a year for an annual meeting and an Interim meeting. Within the AMA, there are sections that include Medical Students, Resident and Fellows, Academic physicians, Medical School Deans and Faculty, Physicians in group practice setting, Retired and Senior Physicians, International Medical graduates, Woman physicians, Physician Diversity and Minority health, GLBT, USAN, AMA board of Trustees, Foundation and Council. External organizations, called AMA member organizations, come to these meetings by sending representatives. Representatives come from a state, specialty or the federal services/government service medical societies.

Beta blocker

From Wikipedia, the free encyclopedia
Beta blockers
Drug class
Propranolol
Skeletal formula of propranolol, the first clinically successful beta blocker.
Class identifiers
Synonymsbeta-blockers, β-blockers, beta-adrenergic blocking agents, beta antagonists, beta-adrenergic antagonists, beta-adrenoreceptor antagonists, beta adrenergic receptor antagonists, BB
UseHypertension, arrhythmia, etc.
ATC codeC07
Biological targetbeta receptors
Clinical data
Drugs.comDrug Classes
Consumer ReportsBest Buy Drugs
WebMDMedicineNet  RxList
External links
MeSHD000319
Legal status

Beta blockers, also spelled β-blockers, are a class of medications that are predominantly used to manage abnormal heart rhythms (arrhythmia), and to protect the heart from a second heart attack after a first heart attack (secondary prevention). They are also widely used to treat high blood pressure, although they are no longer the first choice for initial treatment of most patients.

Beta blockers are competitive antagonists that block the receptor sites for the endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response. Some block activation of all types of β-adrenergic receptors and others are selective for one of the three known types of beta receptors, designated β1, β2 and β3 receptors. β1-adrenergic receptors are located mainly in the heart and in the kidneys. β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β3-adrenergic receptors are located in fat cells.

Beta receptors are found on cells of the heart muscles, smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and lead to stress responses, especially when they are stimulated by epinephrine (adrenaline). Beta blockers interfere with the binding to the receptor of epinephrine and other stress hormones and weaken the effects of stress hormones.

In 1964, James Black synthesized the first clinically significant beta blockers—propranolol and pronethalol; it revolutionized the medical management of angina pectoris and is considered by many to be one of the most important contributions to clinical medicine and pharmacology of the 20th century.

For the treatment of primary hypertension, meta-analyses of studies which mostly used atenolol have shown that although beta blockers are more effective than placebo in preventing stroke and total cardiovascular events, they are not as effective as diuretics, medications inhibiting the renin–angiotensin system (e.g., ACE inhibitors), or calcium channel blockers.

Medical uses

Beta blockers are utilized in the treatment of various conditions related to the heart and vascular system, as well as several other medical conditions. Common heart-related conditions for which beta blockers are well-established include angina pectoris, acute coronary syndromes, hypertension, and arrhythmias such as atrial fibrillation and heart failure. They are also used in the management of other heart diseases, such as hypertrophic obstructive cardiomyopathy, mitral valve stenosis or prolapse, and dissecting aneurysm. Additionally, beta blockers find applications in vascular surgery, the treatment of anxiety states, cases of thyrotoxicosis, glaucoma, migraines, and esophageal varices.

Congestive heart failure

Although beta blockers were once contraindicated in congestive heart failure, as they have the potential to worsen the condition due to their effect of decreasing cardiac contractility, studies in the late 1990s showed their efficacy at reducing morbidity and mortality. Bisoprolol, carvedilol, and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive heart failure, although at doses typically much lower than those indicated for other conditions. Beta blockers are only indicated in cases of compensated, stable congestive heart failure; in cases of acute decompensated heart failure, beta blockers will cause a further decrease in ejection fraction, worsening the patient's current symptoms.

Beta blockers are known primarily for their reductive effect on heart rate, although this is not the only mechanism of action of importance in congestive heart failure. Beta blockers, in addition to their sympatholytic β1 activity in the heart, influence the renin–angiotensin system at the kidneys. Beta blockers cause a decrease in renin secretion, which in turn reduces the heart oxygen demand by lowering the extracellular volume and increasing the oxygen-carrying capacity of the blood. Heart failure characteristically involves increased catecholamine activity on the heart, which is responsible for several deleterious effects, including increased oxygen demand, propagation of inflammatory mediators, and abnormal cardiac tissue remodeling, all of which decrease the efficiency of cardiac contraction and contribute to the low ejection fraction. Beta blockers counter this inappropriately high sympathetic activity, eventually leading to an improved ejection fraction, despite an initial reduction in ejection fraction.

Trials have shown beta blockers reduce the absolute risk of death by 4.5% over a 13-month period. In addition to reducing the risk of mortality, the numbers of hospital visits and hospitalizations were also reduced in the trials. A 2020 Cochrane review found minimal evidence to support the use of beta blockers in congestive heart failure in children, however did identify that from the data available, that they may be of benefit.

Therapeutic administration of beta blockers for congestive heart failure ought to begin at very low doses (18 of target) with a gradual escalation of the dose. The heart of the patient must adjust to decreasing stimulation by catecholamines and find a new equilibrium at a lower adrenergic drive.

Acute myocardial infarction

Beta blockers are indicated for the treatment of acute myocardial infarctions. During a myocardial infarction, systemic stress causes an increase in circulating catecholamines. This results an increase in heart rate and blood pressure, therefore increasing myocardial oxygen demand. Beta blockers competitively inhibit catecholamines acting on the β1-adrenergic receptors, thus reducing these detrimental effects and resulting in reduced myocardial oxygen consumption and demand.

A 2019 Cochrane review compared beta blockers with placebo or no intervention, it found that beta blockers probably reduced the short-term risk of reinfarction and the long-term risk of all-cause mortality and cardiovascular mortality. The review identified that beta blockers likely had little to no impact on short-term all-cause mortality and cardiovascular mortality.

Hypertension

Beta blockers are widely used for the treatment of hypertension.

A 2014 Cochrane review found that in individuals with mild-to-moderate hypertension, non-selective beta blockers led to a reduction of -10/-7mmHg (systolic/diastolic) without increased rates of adverse events. At higher doses, it was found to increase the rate of adverse effects such as a reduction in heart rate, without a corresponding reduction in blood pressure.

A 2017 Cochrane review on the use of beta blockers in hypertension found a modest reduction in cardiovascular disease but little to no change in mortality It suggested that the effects of beta blockers are inferior to other anti-hypertensive medications.

Anxiety

Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug Administration. However, many controlled trials in the past 25 years indicate beta blockers are effective in anxiety disorders, though the mechanism of action is not known. The physiological symptoms of the fight-or-flight response (pounding heart, cold/clammy hands, increased respiration, sweating, etc.) are significantly reduced, thus enabling anxious individuals to concentrate on the task at hand.

Musicians, public speakers, actors, and professional dancers have been known to use beta blockers to avoid performance anxiety, stage fright, and tremor during both auditions and public performances. The application to stage fright was first recognized in The Lancet in 1976, and by 1987, a survey conducted by the International Conference of Symphony Orchestra Musicians, representing the 51 largest orchestras in the United States, revealed 27% of its musicians had used beta blockers and 70% obtained them from friends, not physicians. Beta blockers are inexpensive, said to be relatively safe, and on one hand, seem to improve musicians' performances on a technical level, while some, such as Barry Green, the author of "The Inner Game of Music" and Don Greene, a former Olympic diving coach who teaches Juilliard students to overcome their stage fright naturally, say the performances may be perceived as "soulless and inauthentic".

Surgery

Low certainty evidence indicates that the use of beta blockers around the time of cardiac surgery may decrease the risk of heart dysrhythmias and atrial fibrillation. Starting them around the time of other types of surgery, however, may worsen outcomes. For non-cardiac surgery, the use of beta blockers to prevent adverse effects may reduce the risk of atrial fibrillation and myocardial infarctions (very low certainty evidence), however, there is moderate certainty evidence that this approach may increase the risk of hypotension. Low-certainty evidence suggests that beta blockers used perioperatively in non-cardiac surgeries may increase the risk of bradycardia.

Other

A 2014 Cochrane review investigated the use of beta blockers in the maintenance of chronic type B thoracic aortic aneurysm in comparison to other anti hypertensive medications. The review found no suitable evidence to support the current guidelines recommending its use.

A 2017 Cochrane review on the use of beta blockers to prevent aortic dissections in people with Marfan syndrome was unable to draw definitive conclusions due to lack of evidence.

Medical uses

Adrenergic antagonists are mostly used for cardiovascular disease. The adrenergic antagonists are widely used for lowering blood pressure and relieving hypertension. These antagonists have a been proven to relieve the pain caused by myocardial infarction, and also the infarction size, which correlates with heart rate.

There are few non-cardiovascular uses for adrenergic antagonists. Alpha-adrenergic antagonists are also used for treatment of ureteric stones, pain and panic disorders, withdrawal, and anesthesia.

Beta blockers are used to treat acute cardiovascular toxicity (e.g. in overdose) caused by sympathomimetics, for instance caused by amphetamine, methamphetamine, cocaine, ephedrine, and other drugs. Combined α1 and beta blockers like labetalol and carvedilol may be more favorable for such purposes due to the possibility of "unopposed α-stimulation" with selective beta blockers.

Performance-enhancing use

Because they promote lower heart rates and reduce tremors, beta blockers have been used in professional sports where high accuracy is required, including archery, shooting, golf and snooker. Beta blockers are banned in some sports by the International Olympic Committee. In the 2008 Summer Olympics, 50-metre pistol silver medalist and 10-metre air pistol bronze medalist Kim Jong-su tested positive for propranolol and was stripped of his medals.

For similar reasons, beta blockers have also been used by surgeons.

Classical musicians have commonly used beta blockers since the 1970s to reduce stage fright.

Adverse effects

Adverse drug reactions 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, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction, alteration of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol therapy is commonly associated with edema. 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.

Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β1-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.

Hypoglycemia can occur with beta blockade because β2-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 β2-adrenoceptors lowers plasma glucose. β1-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 hypoglycemia unawareness. This is termed beta blocker-induced hypoglycemia unawareness. Therefore, beta blockers are to be used cautiously in diabetics.

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 antagonists (angiotensin receptor blockers) actually decrease the risk of diabetes. 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.

Beta blockers must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta receptors increases 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. 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. The mixed alpha- and beta blocker labetalol is especially useful for treatment of concomitant tachycardia and hypertension induced by methamphetamine. The phenomenon of "unopposed alpha stimulation" has not been reported with the use of beta blockers for treatment of methamphetamine toxicity. Other appropriate antihypertensive drugs to administer during hypertensive crisis resulting from stimulant overdose are vasodilators such as nitroglycerin, diuretics such as furosemide, and alpha blockers such as phentolamine.

Contraindications and cautions

Absolute contraindications:

Relative contraindications, or contraindications specific to certain beta-blockers:

  • Long QT syndrome: sotalol is contraindicated
  • History of torsades de pointes: sotalol is contraindicated

Cautions:

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.

Cardio selective beta blocker (β1 blockers) can be prescribed at the least possible dose to those with mild to moderate respiratory symptoms. β2-agonists 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.

Diabetes mellitus

Epinephrine signals early warning of the upcoming hypoglycemia.

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 blocker.

Hyperthyroidism

Abrupt withdrawal can result in a thyroid storm.

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.

Toxicity

Glucagon, used in the treatment of overdose, increases the strength of heart contractions, increases intracellular cAMP, and decreases renal vascular resistance. It is, therefore, useful in patients with beta blocker cardiotoxicity. Cardiac pacing is usually reserved for patients unresponsive to pharmacological therapy.

People experiencing bronchospasm due to the β2 receptor-blocking effects of nonselective beta blockers may be treated with anticholinergic drugs, such as ipratropium, which are safer than beta agonists in patients with cardiovascular disease. Other antidotes for beta blocker poisoning are salbutamol and isoprenaline.

Pharmacology

Intrinsic sympathomimetic activity

Also referred to as intrinsic sympathomimetic effect, this term is used particularly with beta blockers that can show both agonism and antagonism at a given beta receptor, depending on the concentration of the agent (beta blocker) and the concentration of the antagonized agent (usually an endogenous compound, such as norepinephrine). See partial agonist for a more general description.

Some beta blockers (e.g. oxprenolol, pindolol, penbutolol, labetalol and acebutolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low-level agonist activity at the β-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.

Agents with ISA should not be used for patients with any kind of angina as it can aggravate or after myocardial infarctions. They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia.

β-Adrenergic receptor antagonism

Stimulation of β1 receptors by epinephrine and norepinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β1 receptors on the kidney causes renin release. Stimulation of β2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle. Stimulation of β3 receptors induces lipolysis.

Beta blockers inhibit these normal epinephrine- and norepinephrine-mediated sympathetic actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement or physical exertion on heart rate and force of contraction, and also tremor, and breakdown of glycogen. Beta blockers can have a constricting effect on the bronchi of the lungs, possibly worsening or causing asthma symptoms.

Since β2 adrenergic receptors can cause vascular smooth muscle dilation, beta blockers may cause some vasoconstriction. However, this effect tends to be small because the activity of β2 receptors is overshadowed by the more dominant vasoconstricting α1 receptors. By far the greatest effect of beta blockers remains in the heart. Newer, third-generation beta blockers can cause vasodilation through blockade of alpha-adrenergic receptors.

Accordingly, nonselective beta blockers are expected to have antihypertensive effects. The primary antihypertensive mechanism of beta blockers is unclear, but may involve reduction in cardiac output (due to negative chronotropic and inotropic effects). It may also be due to reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity (for those beta blockers that do cross the blood–brain barrier, e.g. propranolol).

Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand. Negative chronotropic properties of beta blockers allow the lifesaving property of heart rate control. Beta blockers are readily titrated to optimal rate control in many pathologic states.

The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade—resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade.

Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin–angiotensin–aldosterone system, with a resultant decrease in blood pressure due to decreased sodium and water retention.

α1-Adrenergic receptor antagonism

Some beta blockers (e.g., labetalol and carvedilol) exhibit mixed antagonism of both β- and α1-adrenergic receptors, which provides additional arteriolar vasodilating action.

Blood–brain barrier permeability

Beta blockers vary in their lipophilicity (fat solubility) and in turn in their ability to cross the blood–brain barrier and exert effects in the central nervous system. Beta blockers with greater blood–brain barrier permeability can have both neuropsychiatric therapeutic benefits and side effects, as well as adverse cognitive effects. Central nervous system-related side effects and risks of beta blockers may include fatigue, depression, sleep disorders (namely insomnia) and nightmares, visual hallucinations, delirium, psychosis, Parkinson's disease, and falling. Conversely, central nervous system-related benefits of beta blockers may include prevention and treatment of migraine, essential tremor, akathisia, anxiety, post-traumatic stress disorder, aggression, and obsessive–compulsive disorder.

Most beta blockers are lipophilic and can cross into the brain, but there are a number of exceptions. Highly lipophilic beta blockers include penbutolol, pindolol, propranolol, and timolol, moderately lipophilic beta blockers include acebutolol, betaxolol, bisoprolol, carvedilol, metoprolol, and nebivolol, and low lipophilicity or hydrophilic beta blockers include atenolol, carteolol, esmolol, labetalol, nadolol, and sotalol. It is thought that highly lipophilic beta blockers are able to readily cross into the brain, moderately lipophilic beta blockers are able to cross to a lesser degree, and low lipophilicity or hydrophilic beta blockers are minimally able to cross. More lipophilic beta-blockers are known to suppress melatonin release by 50-80%. The preceding beta blockers also vary in their intrinsic sympathomimetic activity and β1-adrenergic receptor selectivity (or cardioselectivity), resulting in further differences in pharmacological profiles and suitability in different contexts between them.

Agents

Dichloroisoprenaline, the first beta blocker

Nonselective agents

Nonselective beta blockers display both β1 and β2 antagonism.

β1-selective agents

β1-selective beta blockers are also known as cardioselective beta blockers. Pharmacologically, the beta-blockade of the β1 receptors in the heart will act on cAMP. The function of cAMP as a second messenger in the cardiac cell is that it phosphorylates the LTCC and the ryanodine receptor to increase intracellular calcium levels and cause contraction. Beta-blockade of the β1 receptor will inhibit cAMP from phosphorylating, and it will decrease the ionotrophic and chronotropic effect. Note that drugs may be cardioselective, or act on β1 receptors in the heart only, but still have instrinsic sympathomimetic activity.

Nebivolol and bisoprolol are the most β1 cardioselective beta blockers.

β2-selective agents

β3-selective agents

β1 selective antagonist and β3 agonist agents

Comparative information

Pharmacological differences

  • Agents with intrinsic sympathomimetic action (ISA)
    • Acebutolol, pindolol, labetalol, mepindolol, oxprenolol, celiprolol, penbutolol
  • Agents organized by lipid solubility (lipophilicity)
    • High lipophilicity: propranolol, labetalol
    • Intermediate lipophilicity: metoprolol, bisoprolol, carvedilol, acebutolol, timolol, pindolol
    • Low lipophilicity (also known as hydrophilic beta blockers): atenolol, nadolol, and sotalol
  • Agents with membrane stabilizing effect
    • Carvedilol, propranolol > oxprenolol > labetalol, metoprolol, timolol

Indication differences

Propranolol is the only agent indicated for the control of tremor, portal hypertension, and esophageal variceal bleeding, and used in conjunction with α-blocker therapy in phaeochromocytoma.

Other effects

Beta blockers, due to their antagonism at beta-1 adrenergic receptors, inhibit both the synthesis of new melatonin and its secretion by the pineal gland. The neuropsychiatric side effects of some beta blockers (e.g. sleep disruption, insomnia) may be due to this effect.

Some pre-clinical and clinical research suggests that some beta blockers may be beneficial for cancer treatment. However, other studies do not show a correlation between cancer survival and beta blocker usage. Also, a 2017 meta-analysis failed to show any benefit for the use of beta blockers in breast cancer.

Beta blockers have also been used for the treatment of schizoid personality disorder. However, there is limited evidence supporting the efficacy of supplemental beta blocker use in addition to antipsychotic drugs for treating schizophrenia.

Contrast agents are not contraindicated in those receiving beta blockers.

Lie point symmetry

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