Editing Bradycardia

{{Short description|Heart rate below the normal range}}
{{Use dmy dates|date=August 2021}}
{{cs1 config|name-list-style=vanc|display-authors=3}}
{{Infobox medical condition (new)
| name          = Bradycardia
| synonyms      = Bradyarrhythmia, brachycardia
| image         = Sinus bradycardia lead2.svg
| caption       = [[Sinus bradycardia]] seen in lead II with a heart rate of about 50 BPM
| field         = [[Cardiology]]
| pronounce     = {{IPAc-en|ˌ|b|r|æ|d|ɪ|ˈ|k|ɑr|d|i|ə}}
| diagnosis     =  [[electrocardiogram]]
| alt           =
| treatment     =
| frequency     = 15% (males), 7% (females)
}}

'''Bradycardia''', also called '''bradyarrhythmia''', is a [[resting heart rate]] under 60 [[beats per minute]] (BPM).<ref name="hafeez222">{{Cite book |title=StatPearls [Internet] |vauthors=Hafeez Y, Grossman SA |date=2021-08-09 |publisher=StatPearls Publishing |location=Treasure Island (FL) |chapter=Sinus bradycardia |pmid=29630253 |access-date=2022-01-16 |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK493201/}}</ref> While bradycardia can result from various pathological processes, it is commonly a physiological response to cardiovascular conditioning or due to asymptomatic type 1 [[First-degree atrioventricular block|atrioventricular block]].<ref name="hafeez222" />

Resting heart rates of less than 50 BPM are often normal during sleep in young and healthy adults and [[Athletic heart syndrome|athletes]].<ref name="Patterson_2022">{{Cite book |title=Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine |vauthors=Patterson KK, Olgin JE |publisher=Elsevier |year=2022 |isbn=978-0-323-82467-5 |edition=12th |location=Philadelphia, PA |pages=1312–1320 |language=English |chapter=Bradyarrhythmias and Atrioventricular Block}}</ref> In large population studies of adults without underlying heart disease, resting heart rates of 45–50 BPM appear to be the lower limits of normal, dependent on age and sex.<ref>{{Cite journal |vauthors=Rijnbeek PR, van Herpen G, Bots ML, Man S, Verweij N, Hofman A, Hillege H, Numans ME, Swenne CA, Witteman JC, Kors JA |date=2014 |title=Normal values of the electrocardiogram for ages 16-90 years |journal=Journal of Electrocardiology |volume=47 |issue=6 |pages=914–921 |doi=10.1016/j.jelectrocard.2014.07.022 |pmid=25194872 |hdl-access=free |hdl=1887/117357}}</ref><ref>{{Cite web |date=2012 |title=Normal ECG values |url=http://www.normalecg.org/index.php/adult/standard |place=Rotterdam, The Netherlands |vauthors=Rijnbeek PR}}</ref> Bradycardia is most likely to be discovered in the elderly, as age and underlying cardiac disease progression contribute to its development.<ref name="KusumotoSchoenfeldBarrett2019">{{Cite journal |vauthors=Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD |date=August 2019 |title=2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society |journal=Circulation |volume=140 |issue=8 |pages=e382–e482 |doi=10.1161/CIR.0000000000000628 |pmid=30586772 |doi-access=free}}</ref>

Bradycardia may be associated with symptoms of [[fatigue]], [[Shortness of breath|dyspnea]], [[dizziness]], [[Altered level of consciousness|confusion]], and [[Syncope (medicine)|syncope]] due to reduced blood flow to the brain.<ref name="Sidhu-2020">{{Cite journal |vauthors=Sidhu S, Marine JE |date=July 2020 |title=Evaluating and managing bradycardia |journal=Trends in Cardiovascular Medicine |volume=30 |issue=5 |pages=265–272 |doi=10.1016/j.tcm.2019.07.001 |pmid=31311698 |doi-access=free}}</ref> The types of symptoms often depend on the [[Etiology (medicine)|etiology]] of the slow heart rate, classified by the anatomical location of a dysfunction within the [[cardiac conduction system]].<ref name="Patterson_2022" /> Generally, these classifications involve the broad categories of [[sinus node dysfunction]], atrioventricular block, and other conduction tissue diseases.<ref name="KusumotoSchoenfeldBarrett2019" /> However, bradycardia can also result without dysfunction of the conduction system, arising secondarily to medications, including [[beta blocker]]s, [[calcium channel blocker]]s, [[Antiarrhythmic agent|antiarrythmics]], and other [[Parasympathomimetic drug|cholinergic]] drugs. Excess [[vagus nerve]] activity or [[Carotid sinus|carotid sinus hypersensitivity]] are neurological causes of transient symptomatic bradycardia. Hypothyroidism and metabolic derangements are other common extrinsic causes of bradycardia.<ref name="Sidhu-2020" />

The management of bradycardia is generally reserved for people with symptoms, regardless of minimum heart rate during sleep or the presence of concomitant heart rhythm abnormalities (See: [[Sinus pause]]), which are common with this condition.<ref name="Sidhu-2020" /> Untreated sinus node dysfunction increases the risk of heart failure and syncope, sometimes warranting definitive treatment with an [[Artificial cardiac pacemaker|implanted pacemaker]].<ref>{{Cite journal |vauthors=Menozzi C, Brignole M, Alboni P, Boni L, Paparella N, Gaggioli G, Lolli G |date=November 1998 |title=The natural course of untreated sick sinus syndrome and identification of the variables predictive of unfavorable outcome |journal=The American Journal of Cardiology |volume=82 |issue=10 |pages=1205–1209 |doi=10.1016/s0002-9149(98)00605-5 |pmid=9832095}}</ref><ref name="KusumotoSchoenfeldBarrett2019" /> In atrioventricular causes of bradycardia, permanent pacemaker implantation is often required when no reversible causes of disease are found.<ref name="Sidhu-2020" /><ref name="Patterson_2022" /> In both SND and atrioventricular blocks, there is little role for medical therapy unless a person is [[Shock (circulatory)|hemodynamically unstable]], which may require the use of medications such as [[atropine]] and [[Isoprenaline|isoproterenol]] and interventions such as [[Transcutaneous pacing|transcutenous pacing]] until such time that an appropriate workup can be undertaken and long-term treatment selected.<ref name="Patterson_2022" /> While asymptomatic bradycardias rarely require treatment, consultation with a physician is recommended, especially in the elderly.{{Citation needed|date=December 2023}}

The term "relative bradycardia" can refer to a heart rate lower than expected in a particular disease state, often a febrile illness.<ref>{{Cite journal |vauthors=Ye F, Hatahet M, Youniss MA, Toklu HZ, Mazza JJ, Yale S |date=June 2018 |title=The Clinical Significance of Relative Bradycardia |url=https://pubmed.ncbi.nlm.nih.gov/30048576 |journal=WMJ |volume=117 |issue=2 |pages=73–78 |pmid=30048576}}</ref> [[Chronotropic incompetence]] (CI) refers to an inadequate rise in heart rate during periods of increased demand, often due to exercise, and is an important sign of SND and an indication for pacemaker implantation.<ref name="KusumotoSchoenfeldBarrett2019" /><ref name="Patterson_2022" />

The word "bradycardia" is from the [[Ancient Greek|Greek]] βραδύς ''bradys'' "slow", and καρδία ''kardia'' "heart".<ref>{{Cite book |last=Prutchi, David |url=https://books.google.com/books?id=Wtp5lg6UVygC&pg=PA371 |title=Design and Development of Medical Electronic Instrumentation |publisher=John Wiley & Sons |year=2005 |isbn=9780471681830 |pages=371}}</ref>

== Normal cardiac conduction ==
The heart is a specialized muscle containing repeating units of [[Cardiac muscle|cardiomyocytes]], or heart muscle cells. Like most cells, cardiomyocytes maintain a highly regulated negative voltage at rest and are capable of propagating [[action potential]]s, much like neurons.<ref name="Loscalzo-2022">{{Cite book |title=Harrison's Principles of Internal Medicine |vauthors=Loscalzo J, Keaney JF, MacRae CA |publisher=McGraw Hill |year=2022 |isbn=978-1-264-26850-4 |veditors=Loscalzo J, Fauci AS, Kasper DL, Hauser S, Longo D, Jameson JL |edition=21st |chapter=Basic Biology of the Cardiovascular System}}</ref> While at rest, the negative cellular voltage of a cardiomyocyte can be raised above a certain threshold (so-called [[depolarization]]) by an incoming action potential, causing the myocyte to [[Myocardial contractility|contract]]. When these contractions occur in a coordinated fashion, the atria and ventricles of the heart will pump, delivering blood to the rest of the body.<ref name="Loscalzo-2022" />

Normally, the origination of the action potential causing cardiomyocyte contraction originates from the [[sinoatrial node]] (SA node). This collection of specialized conduction tissue is located in the right atrium, near the entrance of the [[superior vena cava]].<ref name="Sauer-2022a">{{Cite book |title=Harrison's Principles of Internal Medicine |vauthors=Sauer WH, Koplan BA, Zei PC |publisher=McGraw Hill |year=2022 |isbn=978-1-264-26850-4 |veditors=Loscalzo J, Fauci AS, Kasper DL, Hauser S, Longo D, Jameson JL |edition=21st |chapter=Principles of Clinical Cardiac Electrophysiology}}</ref> The SA node contains pacemaker cells that demonstrate "automaticity" and can generate impulses that travel through the heart and create a steady heartbeat.<ref name="Sauer-2022a" />

At the beginning of the cardiac cycle, the SA node generates an electrical action potential that spreads across the right and left [[Atrium (heart)|atria]], causing the atrial contraction of the [[cardiac cycle]].<ref name="Sauer-2022a" /> This electrical impulse carries on to the [[atrioventricular node]] (AV node), another specialized grouping of cells located in the base of the right atrium, which is the only anatomically normal electrical connection between the atria and ventricles. Impulses coursing through the AV node are slowed before carrying on to the ventricles,<ref>{{Cite journal |vauthors=Kurian T, Ambrosi C, Hucker W, Fedorov VV, Efimov IR |date=June 2010 |title=Anatomy and electrophysiology of the human AV node |journal=Pacing and Clinical Electrophysiology |volume=33 |issue=6 |pages=754–762 |doi=10.1111/j.1540-8159.2010.02699.x |pmc=2889145 |pmid=20180918}}</ref> allowing for appropriate filling of the ventricles before contraction. The SA and AV nodes are both closely regulated by the autonomic nervous system's fibres, allowing for adjustment of cardiac output by the central nervous system in times of increased metabolic demand.{{cn|date=May 2025}}

Following slowed conduction through the atrioventricular node, the action potential produced initially at the SA node now flows through the His-Purkinje system. The [[bundle of His]] originates in the AV node and rapidly splits into a left and right branch, each destined for a different ventricle. Finally, these bundle branches terminate in the small [[Purkinje fibers]] that innervate myocardial tissue. The His-Purkinje system conducts action potentials much faster than can be propagated between myocardial cells, allowing the entire ventricular myocardium to contract in less time, improving pump function.<ref name="Sauer-2022a" />

==Classification==
[[File:Blausen 0099 bradycardia.png|thumb|Illustration comparing the ECGs of a healthy person (''top'') and a person with bradycardia (''bottom''): The points on the heart where the ECG signals are measured are also shown.]]

Most pathological causes of bradycardia result from damage to this normal cardiac conduction system at various levels: the sinoatrial node, the atrioventricular node, or damage to conduction tissue between or after these nodes.{{cn|date=May 2025}}

=== Sinus node ===
Bradycardia caused by the alterations of sinus node activity is divided into three types.{{cn|date=May 2025}}

==== Sinus bradycardia ====
[[Sinus bradycardia]] is a [[sinus rhythm]] of less than 50 BPM.<ref name="KusumotoSchoenfeldBarrett2019" /> Cardiac action potentials are generated from the SA node and propagated through an otherwise normal conduction system, but they occur at a slow rate. It is a common condition found in both healthy individuals and those considered well-conditioned athletes.<ref name="hafeez222" /> Studies have found that 50–85% of conditioned athletes have benign sinus bradycardia, as compared to 23% of the general population studied.<ref>{{Cite journal |vauthors=Bryan G, Ward A, Rippe JM |date=April 1992 |title=Athletic heart syndrome |journal=Clinics in Sports Medicine |publisher=Elsevier |volume=11 |issue=2 |pages=259–272 |doi=10.1016/S0278-5919(20)30529-9 |pmid=1591784}}</ref> The heart muscle of athletes has a higher [[stroke volume]], requiring fewer contractions to circulate the same volume of blood.<ref name="HN3">{{Cite book |title=Harwood-Nuss' Clinical Practice of Emergency Medicine |publisher=Lippincott Williams & Wilkins |year=2005 |isbn=978-0-7817-5125-4 |editor-last=Allan B. Wolfson |edition=4th |page=260}}</ref> Asymptomatic sinus bradycardia decreases in prevalence with age.{{cn|date=May 2025}}

==== Sinus arrhythmia ====
Sinus arrhythmias are heart rhythm abnormalities characterized by variations in the cardiac cycle length over 120 milliseconds (longest cycle - shortest cycle).<ref name="Patterson_2022" /> These are the most common type of arrhythmia in the general population and usually have no significant consequences. They typically occur in the young, athletes or after administration of medications such as morphine. The types of sinus arrhythmia are separated into the respiratory and non-respiratory categories.<ref name="Patterson_2022" />

===== Respiratory sinus arrhythmia =====
Respiratory sinus arrhythmia refers to the physiologically normal variation in heart rate due to breathing. During inspiration, vagus nerve activity decreases, reducing parasympathetic innervation of the sinoatrial node and  causing an increase in heart rate. During expiration, heart rates fall due to the converse occurring.<ref name="Patterson_2022" />

===== Non-respiratory sinus arrhythmia =====
Non-respiratory causes of sinus arrhythmia include sinus pause, [[Sinoatrial arrest|sinus arrest]], and [[Sinoatrial block|sinoatrial exit block]]. Sinus pause and arrest involve slowing or arresting of automatic impulse generation from the sinus node. This can lead to [[asystole]] or cardiac arrest if [[Ventricular escape beat|ventricular escape rhythms]] do not create backup sources of cardiac action potentials.<ref name="Patterson_2022" />

Sinoatrial exit block is a similar non-respiratory phenomenon of temporarily lost sinoatrial impulses. However, in contrast to a sinus pause, the action potential is still generated at the SA node but is either unable to leave or delayed from leaving the node, preventing or delaying atrial depolarization and subsequent ventricular systole. Therefore, the length of the pause in heartbeats is usually a multiple of the P-P interval, as seen on electrocardiography. Like a sinus pause, a sinoatrial exit block can be symptomatic, especially with prolonged pause length.<ref name="Patterson_2022" />

==== Sinus node dysfunction ====
A syndrome of intrinsic disease of the sinus node, referred to as sick sinus syndrome or [[sinus node dysfunction]], covers conditions that include symptomatic sinus bradycardia or persistent chronotropic incompetence, [[sinoatrial block]], [[sinus arrest]], and tachycardia-bradycardia syndrome.<ref name="Patterson_2022" /> These conditions can be caused by damage to the native sinus node itself and are frequently accompanied by damaged AV node conduction and reduced backup pacemaker activity.<ref>{{Cite journal |vauthors=John RM, Kumar S |date=May 2016 |title=Sinus Node and Atrial Arrhythmias |journal=Circulation |volume=133 |issue=19 |pages=1892–1900 |doi=10.1161/CIRCULATIONAHA.116.018011 |pmid=27166347 |doi-access=free}}</ref> The condition can also be caused by dysfunction of the autonomic nervous system that regulates the node and is commonly exacerbated by medications.<ref name="Patterson_2022" />

===Atrioventricular node===
Bradycardia can also result from the inhibition of the flow of action potentials through the atrioventricular (AV) node. While this can be normal in young people due to excessive vagus nerve tone, symptomatic bradycardia due to AV node dysfunction in older people is commonly due to structural heart disease, myocardial ischemia, or age-related fibrosis.<ref name="Sauer-2022b" />
[[File:Heart block.png|thumb|Characteristic ECGs of atrioventricular blocks, organized by degree.]]

==== Atrioventricular block ====
[[Atrioventricular block]]s are divided into three categories, ranked by severity. AV block is diagnosed via surface ECG, which is usually sufficient to locate the causal lesion of the block without the need for an invasive [[electrophysiology study]].<ref name="Patterson_2022" />

In [[First-degree atrioventricular block|1st degree AV block]], electrical impulses originating in the SA node (or other ectopic focus above the ventricles) are conducted with significant delay through the AV node. This condition is diagnosed via ECG, with [[PR interval]]s in excess of 200 milliseconds.<ref name="Patterson_2022" /> The PR interval represents the length of time between the start of atrial depolarization and the start of ventricular depolarization, representing the flow of electrical impulses between the SA and AV nodes. Despite the term "block," no impulses are fully lost in this conduction but are merely delayed. The location of the causal lesion can be anywhere between the AV node and the His-Purkinje system but is most commonly found in the AV node itself.<ref name="Clark-2021" /> Generally, isolated PR prolongation in 1st degree AV block is not associated with increased mortality or hospitalization.<ref>{{Cite journal |vauthors=Aro AL, Anttonen O, Kerola T, Junttila MJ, Tikkanen JT, Rissanen HA, Reunanen A, Huikuri HV |date=January 2014 |title=Prognostic significance of prolonged PR interval in the general population |journal=European Heart Journal |volume=35 |issue=2 |pages=123–129 |doi=10.1093/eurheartj/eht176 |pmid=23677846 |doi-access=free}}</ref>

[[Second-degree atrioventricular block|2nd degree AV block]] is characterized by intermittently lost conduction of impulses between the SA node and the ventricles. 2nd degree block is classified into two types. Mobitz type 1 block, otherwise known by the eponym [[Karel Frederik Wenckebach|Wenckebach]], classically demonstrates grouped patterns of heartbeats on ECG. Throughout the group, the PR interval gradually lengthens until a dropped conduction occurs, resulting in no QRS complex seen on surface ECG following the last P wave. After a delay, the grouping repeats, with the PR interval shortening again to baseline.<ref name="Clark-2021">{{Cite journal |vauthors=Clark BA, Prystowsky EN |date=December 2021 |title=Electrocardiography of Atrioventricular Block |journal=Cardiac Electrophysiology Clinics |volume=13 |issue=4 |pages=599–605 |doi=10.1016/j.ccep.2021.07.001 |pmid=34689889 |s2cid=239091592}}</ref> Type 1 2nd degree AV block due to disease in the AV node (as opposed to in the His-purkinje system) rarely needs intervention with pacemaker implantation.<ref name="Clark-2021" />

2nd degree, Mobitz type 2 AV block is another phenomenon of intermittently dropped QRS complexes after characteristic groupings of beats seen on surface ECG. The PR and RR intervals are consistent in this condition, followed by a sudden AV block and dropped QRS complex.<ref name="Clark-2021" /> Because type 2 blocks are typically due to lesions below the AV node, the ability for ventricular escape rhythms to maintain cardiac output is compromised. Permanent pacemaker implantation is often required.<ref name="Sauer-2022b">{{Cite book |title=Harrison's Principles of Internal Medicine |vauthors=Sauer WH, Koplan BA |publisher=McGraw Hill |year=2022 |isbn=978-1-264-26850-4 |veditors=Loscalzo J, Fauci AS, Kasper DL, Hauser S, Longo D, Jameson JL |edition=21st |chapter=The Bradyarrhythmias: Disorders of the Atrioventricular Node}}</ref>

==== Junctional rhythms ====
An [[AV-junctional rhythm]], or atrioventricular nodal bradycardia, is usually caused by the absence of the electrical impulse from the [[sinus node]]. This usually appears on an [[Electrocardiography|electrocardiogram]] with a normal [[QRS complex]] accompanied by an inverted [[P wave (electrocardiography)|P wave]] either before, during, or after the QRS complex.<ref name="HN3" />

An AV-junctional escape beat is a delayed heartbeat originating from an [[Ectopic beat|ectopic]] focus somewhere in the [[AV junction]]. It occurs when the rate of [[depolarization]] of the [[SA Node|SA node]] falls below the rate of the [[AV Node|AV node]].<ref name="HN3" /> This [[Cardiac dysrhythmia|dysrhythmia]] may also occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block.<ref name="AHA">{{Cite web |date=4 December 2008 |title=AV Junctional Rhythm Disturbances (for Professionals) |url=http://www.americanheart.org/presenter.jhtml?identifier=746 |access-date=15 December 2009 |publisher=American Heart Association}}</ref> This is a protective mechanism for the heart to compensate for an SA node that is no longer handling the pacemaking activity and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so. This would present with a longer [[PR interval]]. An AV-junctional escape complex is a normal response that may result from excessive vagal tone on the SA node. Pathological causes include sinus bradycardia, sinus arrest, sinus exit block, or AV block.<ref name="HN3" />

===Ventricular===
[[Idioventricular rhythm]], also known as atrioventricular bradycardia or ventricular escape rhythm, is a heart rate of less than 50 BPM. This is a safety mechanism when a lack of electrical impulse or stimuli from the [[Atrium (heart)|atrium]] occurs.<ref name="HN3" /> Impulses originating within or below the [[bundle of His]] in the AV node will produce a wide QRS complex with heart rates between 20 and 40 BPM. Those above the bundle of His, also known as junctional, will typically range between 40 and 60 BPM with a narrow QRS complex.<ref name="merck">{{Cite web |date=January 2008 |title=Arrhythmias and Conduction Disorders |url=http://www.merck.com/mmpe/sec07/ch075/ch075a.html |access-date=16 December 2009 |website=The Merck Manuals: Online Medical Library |publisher=Merck Sharp and Dohme Corp}}</ref><ref name=ajcc/> In a [[third-degree heart block]], about 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the bundle of His.<ref name="ajcc">{{Cite journal |vauthors=Adams MG, Pelter MM |date=September 2003 |title=Ventricular escape rhythms |journal=American Journal of Critical Care |volume=12 |issue=5 |pages=477–478 |doi=10.4037/ajcc2003.12.5.477 |pmid=14503433}}</ref> AV block may be ruled out with an ECG indicating "a 1:1 relationship between P waves and QRS complexes."<ref name="merck" /> Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block. Treatment often consists of the administration of [[atropine]] and [[cardiac pacing]].<ref name="HN3" />

===Infantile===
For infants, bradycardia is defined as a heart rate less than 100&nbsp;BPM (normal is around 120–160 BPM).<ref name=doyen/> Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood.<ref name=doyen/> The spells may be related to centers inside the brain that regulate breathing which may not be fully developed. Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate. The [[neonatal intensive-care unit]] standard practice is to electronically monitor the heart and lungs.<ref name="doyen">{{Cite journal |last=Doyen |first=Matthieu |last2=Hernández |first2=Alfredo I. |last3=Flamant |first3=Cyril |last4=Defontaine |first4=Antoine |last5=Favrais |first5=Géraldine |last6=Altuve |first6=Miguel |last7=Laviolle |first7=Bruno |last8=Beuchée |first8=Alain |last9=Carrault |first9=Guy |last10=Pladys |first10=Patrick |date=2021-05-18 |title=Early bradycardia detection and therapeutic interventions in preterm infant monitoring |journal=Scientific Reports |volume=11 |issue=1 |pages=10486 |doi=10.1038/s41598-021-89468-x |issn=2045-2322 |pmc=8131388 |pmid=34006917}}</ref>

==Causes==
Bradycardia [[arrhythmia]] may have many causes, both cardiac and non-cardiac.

Non-cardiac causes are usually secondary and can involve [[recreational drug use]] or [[drug abuse|abuse]], metabolic or endocrine issues, especially [[hypothyroidism]], an [[electrolyte imbalance]], neurological factors, [[autonomic nervous system|autonomic reflexes]], situational factors, such as prolonged [[bed rest]], and [[autoimmune|autoimmunity]].<ref>{{Cite journal |vauthors=Ye F, Hatahet M, Youniss MA, Toklu HZ, Mazza JJ, Yale S |date=June 2018 |title=The Clinical Significance of Relative Bradycardia |journal=WMJ |volume=117 |issue=2 |pages=73–78 |pmid=30048576}}</ref> At rest, although tachycardia is more commonly seen in [[Fatty-acid metabolism disorder|fatty acid oxidation disorders]], acute bradycardia can occur more rarely.<ref>{{Cite journal |vauthors=Bonnet D, Martin D, Villain E, Jouvet P, Rabier D, Brivet M, Saudubray JM |date=November 1999 |title=Arrhythmias and conduction defects as presenting symptoms of fatty acid oxidation disorders in children |journal=Circulation |volume=100 |issue=22 |pages=2248–2253 |doi=10.1161/01.cir.100.22.2248 |pmid=10577999 |doi-access=free}}</ref>

Cardiac causes include acute or chronic [[ischemic heart disease]], vascular heart disease, [[valvular heart disease]], or degenerative primary electrical disease. Ultimately, the causes act by three mechanisms: depressed automaticity of the heart, conduction block, or escape pacemakers and rhythms.<ref name="webmd.com">{{Cite web |title=What is Bradycardia? |url=https://www.webmd.com/heart-disease/atrial-fibrillation/bradycardia |access-date=5 July 2021 |website=WebMD}}</ref>

In general, two types of problems result in bradycardias: disorders of the SA node and disorders of the AV node.<ref>{{Cite web |title=Bradyarrhythmias |url=https://www.lecturio.com/concepts/bradyarrhythmias/ |access-date=5 July 2021 |website=The Lecturio Medical Concept Library}}</ref>

With SA node dysfunction (sometimes called sick sinus syndrome), there may be disordered automaticity or impaired conduction of the impulse from the SA node into the surrounding atrial tissue (an "exit block"). Second-degree sinoatrial blocks can be detected only by use of a 12-lead ECG.<ref name="NCBI">{{Cite journal |vauthors=Ufberg JW, Clark JS |date=February 2006 |title=Bradydysrhythmias and atrioventricular conduction blocks |journal=Emergency Medicine Clinics of North America |volume=24 |issue=1 |pages=1–9, v |doi=10.1016/j.emc.2005.08.006 |pmid=16308110}}</ref> It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia, but the underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent [[artificial pacemaker|pacemaker]].<ref name="webmd.com" />

AV conduction disturbances (AV block; [[First-degree AV block|primary AV block]], [[Second-degree AV block|secondary type I AV block]], [[Second-degree AV block|secondary type II AV block]], [[Third-degree AV block|tertiary AV block]]) may result from impaired conduction in the AV node or anywhere below it, such as in the bundle of His. The clinical relevance pertaining to AV blocks is greater than that of SA blocks.<ref name="NCBI" />

A variety of [[medication]]s can induce or exacerbate bradycardia.<ref name="KusumotoSchoenfeldBarrett2019" /> These include [[beta blocker]]s like [[propranolol]], [[calcium channel blocker]]s like [[verapamil]] and [[diltiazem]], [[cardiac glycoside]]s like [[digoxin]], [[Alpha-adrenergic agonist#α2 agonist|alpha-2 agonist]]s like [[clonidine]], and [[lithium]], among others.<ref name="KusumotoSchoenfeldBarrett2019" /><ref name="Miller1998">{{Cite journal |vauthors=Miller MB |date=May 1998 |title=Arrhythmias associated with drug toxicity |journal=Emerg Med Clin North Am |volume=16 |issue=2 |pages=405–417 |doi=10.1016/s0733-8627(05)70009-2 |pmid=9621850}}</ref> Beta blockers may slow the heart rate to a dangerous level if prescribed with calcium channel blockers.<ref name="webmd.com"/>

Chronic [[cocaine]] use has been associated with bradycardia.<ref name="DominicAhmadAwwab2022">{{Cite journal |vauthors=Dominic P, Ahmad J, Awwab H, Bhuiyan MS, Kevil CG, Goeders NE, Murnane KS, Patterson JC, Sandau KE, Gopinathannair R, Olshansky B |date=January 2022 |title=Stimulant Drugs of Abuse and Cardiac Arrhythmias |journal=Circulation: Arrhythmia and Electrophysiology |volume=15 |issue=1 |pages=e010273 |doi=10.1161/CIRCEP.121.010273 |pmc=8766923 |pmid=34961335}}</ref><ref name="SharmaRathnayakaGreen2016">{{Cite journal |vauthors=Sharma J, Rathnayaka N, Green C, Moeller FG, Schmitz JM, Shoham D, Dougherty AH |date=2016 |title=Bradycardia as a Marker of Chronic Cocaine Use: A Novel Cardiovascular Finding |journal=Behav Med |volume=42 |issue=1 |pages=1–8 |doi=10.1080/08964289.2014.897931 |pmc=4162850 |pmid=24621090}}</ref><ref name="FranklinThihalolipavanFontaine2017">{{Cite journal |vauthors=Franklin SM, Thihalolipavan S, Fontaine JM |date=May 2017 |title=Sinus Bradycardia in Habitual Cocaine Users |journal=Am J Cardiol |volume=119 |issue=10 |pages=1611–1615 |doi=10.1016/j.amjcard.2017.02.018 |pmid=28341362}}</ref> [[Downregulation and upregulation|Desensitization]] of [[β-adrenergic receptor]]s has been suggested as a possible cause of this.<ref name="DominicAhmadAwwab2022" /><ref name="FranklinThihalolipavanFontaine2017" /> In contrast to cocaine however, [[methamphetamine]] has not been associated with bradyarrhythmias.<ref name="DominicAhmadAwwab2022" />

Bradycardia is also part of the [[mammalian diving reflex]].<ref name="Michael Panneton2013">{{Cite journal |vauthors=Panneton WM |date=September 2013 |title=The mammalian diving response: an enigmatic reflex to preserve life? |journal=Physiology |volume=28 |issue=5 |pages=284–297 |doi=10.1152/physiol.00020.2013 |pmc=3768097 |pmid=23997188}}</ref>

[[COVID-19]] has been found to be a cause of bradycardia.<ref name="DouediMararenkoAlshami2021">{{Cite journal |vauthors=Douedi S, Mararenko A, Alshami A, Al-Azzawi M, Ajam F, Patel S, Douedi H, Calderon D |date=August 2021 |title=COVID-19 induced bradyarrhythmia and relative bradycardia: An overview |journal=J Arrhythm |volume=37 |issue=4 |pages=888–892 |doi=10.1002/joa3.12578 |pmc=8339085 |pmid=34386113}}</ref>

==Diagnosis==
A diagnosis of bradycardia in adults is based on a heart rate of less than 60 BPM,<ref name="hafeez222" /> although some studies use a heart rate of less than 50 BPM.<ref name="ACLS2010" /> This is usually determined either by palpation or ECG.<ref name="hafeez222" /> If symptoms occur, a determining electrolytes may help determine the underlying cause.<ref name="webmd.com" />

Many heathy young adults, and particularly well-trained athletes, have sinus bradycardia that is without symptoms.<ref name="KusumotoSchoenfeldBarrett2019" /> This can include heart rates of less than 50 or 60{{nbsp}}bpm or even less than 40{{nbsp}}bpm.<ref name="KusumotoSchoenfeldBarrett2019" /> Such individuals, without symptoms, do not require treatment.<ref name="KusumotoSchoenfeldBarrett2019" />

Temporal correlation of symptoms with bradycardia is necessary for diagnosis of symptomatic bradycardia.<ref name="KusumotoSchoenfeldBarrett2019" /> This can sometimes be difficult.<ref name="KusumotoSchoenfeldBarrett2019" /> Challenge with [[oral administration|oral]] [[theophylline]] can be used as a [[diagnostic agent]] in people with bradycardia caused by [[sinus node dysfunction]] (SND) to help correlate symptoms.<ref name="KusumotoSchoenfeldBarrett2019" /> Theophylline increases [[resting heart rate]] and improves subjective symptoms in most people with bradycardia due to SND.<ref name="KusumotoSchoenfeldBarrett2019" />

==Management==
The treatment of bradycardia depends on whether the person is stable or unstable.<ref name="hafeez222" /><ref name=ACLS2010/><ref name="KusumotoSchoenfeldBarrett2019" />

===Chronic or stable===
Emergency treatment is not needed if the person is asymptomatic or minimally symptomatic.<ref name="ACLS2010">{{Cite journal |vauthors=Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, Passman RS, White RD, Hess EP, Tang W, Davis D, Sinz E, Morrison LJ |date=November 2010 |title=Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=122 |issue=18 Suppl 3 |pages=S729-S767 |doi=10.1161/CIRCULATIONAHA.110.970988 |pmid=20956224 |doi-access=free}}</ref>

Treatment of chronic symptomatic bradycardia first necessitates correlation of symptoms.<ref name="KusumotoSchoenfeldBarrett2019" /> Once symptoms have been clearly linked to bradycardia, [[artificial cardiac pacemaker|permanent cardiac pacing]] can be provided to increase heart rate and symptoms will improve.<ref name="KusumotoSchoenfeldBarrett2019" />

In people who are unwilling to undergo pacemaker implantation or are not candidates for cardiac pacing, chronic [[oral administration|oral]] [[theophylline]], an [[adenosine receptor antagonist]], can be considered for treatment of symptomatic bradycardia.<ref name="KusumotoSchoenfeldBarrett2019" /><ref name="LingCrouch1998">{{Cite journal |vauthors=Ling CA, Crouch MA |date=1998 |title=Theophylline for chronic symptomatic bradycardia in the elderly |journal=Ann Pharmacother |volume=32 |issue=7-8 |pages=837–839 |doi=10.1345/aph.17463 |pmid=9681101}}</ref> Other [[Chronotropic#Positive chronotropes|positive chronotropes]] have also been used to treat bradycardia, including the [[vasodilator]] and [[antihypertensive agent]] [[hydralazine]], the [[alpha-1 blocker]] [[prazosin]], [[anticholinergic]]s, and [[sympathomimetic agent]]s like [[beta1-adrenergic agonist|beta-1 agonist]]s.<ref name="LingCrouch1998" /> However, [[side effect]]s, like [[orthostatic hypotension]] with hydralazine, prazosin, and anticholinergics and myocardial toxicity with sympathomimetics, as well as limited data for this indication, hinder their routine and long-term use.<ref name="LingCrouch1998" />

If [[hypothyroidism]] is present and is the cause of symptomatic bradycardia, symptoms respond well to [[hormone therapy|replacement therapy]] with [[thyroid hormone]].<ref name="KusumotoSchoenfeldBarrett2019" />

Discontinuation of [[medication]]s that induce or exacerbate bradycardia, such as [[beta blocker]]s, [[calcium channel blocker]]s, [[sodium channel blocker]]s, and [[potassium channel blocker]]s, can improve symptoms.<ref name="KusumotoSchoenfeldBarrett2019" /> If discontinuation of these medications is not possible due to clinical need, cardiac pacing can be considered with continuation of the medications.<ref name="KusumotoSchoenfeldBarrett2019" /> Beta blockers with [[intrinsic sympathomimetic activity]] (i.e., [[partial agonist]] activity), like [[pindolol]], have less risk of bradycardia and may be useful as replacements of pure beta blockers, like [[propranolol]], [[atenolol]], and [[metoprolol]].<ref name="Northcote1987">{{Cite journal |vauthors=Northcote RJ |date=May 1987 |title=The clinical significance of intrinsic sympathomimetic activity |journal=Int J Cardiol |volume=15 |issue=2 |pages=133–150 |doi=10.1016/0167-5273(87)90309-3 |pmid=2884187}}</ref><ref name="MangrumDiMarco2000">{{Cite journal |vauthors=Mangrum JM, DiMarco JP |date=March 2000 |title=The evaluation and management of bradycardia |url=https://www.researchgate.net/profile/John-Dimarco/publication/12608644_The_Evaluation_and_Management_of_Bradycardia/links/551c12490cf2fe6cbf764334/The-Evaluation-and-Management-of-Bradycardia.pdf |journal=N Engl J Med |volume=342 |issue=10 |pages=703–709 |doi=10.1056/NEJM200003093421006 |pmid=10706901}}</ref><ref name="Jaillon1990">{{Cite journal |vauthors=Jaillon P |date=September 1990 |title=Relevance of intrinsic sympathomimetic activity for beta blockers |journal=Am J Cardiol |volume=66 |issue=9 |pages=21C–23C |doi=10.1016/0002-9149(90)90758-s |pmid=1977302}}</ref>

===Acute or unstable===
If a person is unstable, the initial recommended treatment is intravenous [[atropine]].<ref name=ACLS2010/> Doses less than 0.5&nbsp;mg should not be used, which may further decrease the rate.<ref name=ACLS2010/> If this is ineffective, intravenous [[inotrope]] infusion ([[dopamine (medication)|dopamine]], [[epinephrine]]) or [[transcutaneous pacing]] should be used.<ref name=ACLS2010/> [[Transvenous pacing]] may be required if the cause of the bradycardia is not rapidly reversible.<ref name=ACLS2010/> [[Methylxanthine]]s like [[theophylline]] and [[aminophylline]] are also used in the treatment of acute bradycardia due to [[sinus node dysfunction]] (SND).<ref name="KusumotoSchoenfeldBarrett2019" />

In children, giving oxygen, supporting their breathing, and [[chest compressions]] are recommended.<ref>{{Cite journal |vauthors=de Caen AR, Berg MD, Chameides L, Gooden CK, Hickey RW, Scott HF, Sutton RM, Tijssen JA, Topjian A, van der Jagt ÉW, Schexnayder SM, Samson RA |date=November 2015 |title=Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=132 |issue=18 Suppl 2 |pages=S526-S542 |doi=10.1161/cir.0000000000000266 |pmc=6191296 |pmid=26473000}}</ref><ref>{{Cite journal |vauthors=Atkins DL, Berger S, Duff JP, Gonzales JC, Hunt EA, Joyner BL, Meaney PA, Niles DE, Samson RA, Schexnayder SM |date=November 2015 |title=Part 11: Pediatric Basic Life Support and Cardiopulmonary Resuscitation Quality: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=132 |issue=18 Suppl 2 |pages=S519-S525 |doi=10.1161/cir.0000000000000265 |pmid=26472999 |doi-access=free}}</ref>

==Epidemiology==
In clinical practice, elderly people over age 65 and young athletes of both sexes may have sinus bradycardia.<ref name="hafeez222" /> The US [[Centers for Disease Control and Prevention]] reported in 2011 that 15.2% of adult males and 6.9% of adult females had clinically defined bradycardia (a [[resting pulse rate]] below 60 BPM).<ref>{{Cite web |last=Yechiam Ostchega |display-authors=et al |date=24 August 2011 |title=Resting Pulse Rate Reference Data for Children, Adolescents, and Adults: United States, 1999–2008 |url=https://www.cdc.gov/nchs/data/nhsr/nhsr041.pdf |url-status=live |archive-url=https://ghostarchive.org/archive/20221010/https://www.cdc.gov/nchs/data/nhsr/nhsr041.pdf |archive-date=2022-10-10 |access-date=15 December 2018 |website=National Health Statistics Reports |publisher=Centers for Disease Control |number=41}}</ref>

==Society and culture==
===Records===
* Daniel Green holds the world record for the slowest heartbeat in a healthy human, with a heart rate measured in 2014 of 26 BPM.<ref>{{Cite web |date=29 November 2014 |title=Slowest heart rate: Daniel Green breaks Guinness World Records record |url=http://www.worldrecordacademy.com/medical/slowest_heart_rate_Daniel_Green_breaks_Guinness_World_Records_record_214157.html |access-date=5 August 2015 |website=World Record Academy}}</ref>
* Martin Brady holds the Guinness world record for the slowest heart rate, with a certified rate over a minute duration of 27 BPM.<ref>{{Cite web |date=11 August 2005 |title=Lowest heart rate |url=http://www.guinnessworldrecords.com/world-records/lowest-heart-rate |access-date=5 August 2015 |website=Guinness World Records}}</ref>
* During his career, professional cyclist [[Miguel Indurain]] had a resting heart rate of 28&nbsp;BPM.<ref>{{Cite web |date=20 August 2004 |title=Olympic Gold Begins With Good Genes, Experts Say |url=http://news.nationalgeographic.com/news/2004/08/0820_040820_olympics_athletes.html |url-status=dead |archive-url=https://web.archive.org/web/20040820230627/http://news.nationalgeographic.com/news/2004/08/0820_040820_olympics_athletes.html |archive-date=20 August 2004 |access-date=8 September 2014 |website=National Geographic News |vauthors=Lovgren S}}</ref>

== See also ==
* {{annotated link|Bezold–Jarisch reflex}}

== References ==
{{Reflist}}

{{Medical resources
 | DiseasesDB     =
 | ICD11          = {{ICD11|MC81.1}}
 | ICD10          = {{ICD10|R00.1}}
 | ICD9           = {{ICD9|427.81}}, {{ICD9|659.7}}, {{ICD9|785.9}}, {{ICD9|779.81}}
 | ICDO           =
 | OMIM           =
 | MedlinePlus    =
 | eMedicineSubj  =
 | eMedicineTopic =
 | MeshID         = D001919
}}

{{Heart diseases}}
{{Cardiovascular system symptoms and signs}}
{{Authority control}}

[[Category:Cardiac arrhythmia]]
[[Category:Symptoms and signs: Cardiac]]