Editing Heart rate (section)

==Physiology==
[[File:Wiki Heart Antomy Ties van Brussel.jpg|thumb|alt=Anatomy of the Human Heart, made by Ties van Brussel|350px|The [[human heart]]]]
{{listen
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{{listen|filename=Emily's racing heartbeat.wav|title=Emily's racing heartbeat|description=Heart sounds of a 16 year old girl immediately after running, with a heart rate of 186 BPM. The S1 heart sound is intensified due to the increased cardiac output.|format=[[wav]]}}
While ''heart rhythm'' is regulated entirely by the [[sinoatrial node]] under normal conditions, ''heart rate'' is regulated by [[sympathetic nervous system|sympathetic]] and [[parasympathetic nervous system|parasympathetic]] input to the sinoatrial node. The [[accelerans nerve]] provides sympathetic input to the heart by releasing [[norepinephrine]] onto the cells of the sinoatrial node (SA node), and the [[vagus nerve]] provides parasympathetic input to the heart by releasing [[acetylcholine]] onto sinoatrial node cells. Therefore, stimulation of the [[accelerans nerve]] increases heart rate, while stimulation of the vagus nerve decreases it.<ref name="Schmidt-Nielsen 1997">{{cite book|last=Schmidt-Nielsen|first=Knut|title=Animal physiology: adaptation and environment|year=1997|publisher=Cambridge Univ. Press|location=Cambridge|isbn=978-0-521-57098-5|page=104|edition=5th}}</ref>

As water and blood are incompressible fluids, one of the physiological ways to deliver more blood to an organ is to increase heart rate.{{sfn|Fuster|Wayne|O'Rouke|2001|pp=78–79}} Normal resting heart rates range from 60 to 100 bpm.<ref name=":0">{{Cite journal|last1=Aladin|first1=Amer I.|last2=Whelton|first2=Seamus P.|last3=Al-Mallah|first3=Mouaz H.|last4=Blaha|first4=Michael J.|last5=Keteyian|first5=Steven J.|last6=Juraschek|first6=Stephen P.|last7=Rubin|first7=Jonathan|last8=Brawner|first8=Clinton A.|last9=Michos|first9=Erin D.|date=2014-12-01|title=Relation of resting heart rate to risk for all-cause mortality by gender after considering exercise capacity (the Henry Ford exercise testing project)|journal=The American Journal of Cardiology|volume=114|issue=11|pages=1701–06|doi=10.1016/j.amjcard.2014.08.042 |pmid=25439450}}</ref><ref name=":1">{{Cite journal|last1=Hjalmarson|first1=A.|last2=Gilpin|first2=E. A.|last3=Kjekshus|first3=J.|last4=Schieman|first4=G.|last5=Nicod|first5=P.|last6=Henning|first6=H.|last7=Ross|first7=J.|date=1990-03-01|title=Influence of heart rate on mortality after acute myocardial infarction|journal=The American Journal of Cardiology|volume=65|issue=9|pages=547–53 |pmid=1968702|doi=10.1016/0002-9149(90)91029-6}}</ref><ref name=":2">{{Cite journal|last1=Mason|first1=Jay W.|last2=Ramseth|first2=Douglas J.|last3=Chanter|first3=Dennis O.|last4=Moon|first4=Thomas E.|last5=Goodman|first5=Daniel B.|last6=Mendzelevski|first6=Boaz|date=2007-07-01|title=Electrocardiographic reference ranges derived from 79,743 ambulatory subjects|journal=[[Journal of Electrocardiology]]|volume=40|issue=3|pages=228–34|doi=10.1016/j.jelectrocard.2006.09.003 |pmid=17276451}}</ref><ref name=":3">{{Cite journal|last=Spodick|first=D. H.|date=1993-08-15|title=Survey of selected cardiologists for an operational definition of normal sinus heart rate|journal=The American Journal of Cardiology|volume=72|issue=5|pages=487–88 |pmid=8352202|doi=10.1016/0002-9149(93)91153-9}}</ref> [[Bradycardia]] is defined as a resting heart rate below 60 bpm. However, heart rates from 50 to 60 bpm are common among healthy people and do not necessarily require special attention.<ref name='aha_rest' /> [[Tachycardia]] is defined as a resting heart rate above 100 bpm, though persistent rest rates between 80 and 100 bpm, mainly if they are present during sleep, may be signs of hyperthyroidism or anemia (see below).{{sfn|Fuster|Wayne|O'Rouke|2001|pp=78–79}}
* [[Central nervous system]] [[stimulant]]s such as [[substituted amphetamine]]s increase heart rate.
* Central nervous system [[depressant]]s or [[sedative]]s decrease the heart rate (apart from some particularly strange ones with equally strange effects, such as [[ketamine]] which can cause – amongst many other things – stimulant-like effects such as [[tachycardia]]).
There are many ways in which the heart rate speeds up or slows down. Most involve stimulant-like [[endorphin]]s and [[hormone]]s being released in the brain, some of which are those that are 'forced'/'enticed' out by the ingestion and processing of drugs such as [[cocaine]] or [[atropine]].<ref>{{Cite web|last=PubChem|title=Atropine|url=https://pubchem.ncbi.nlm.nih.gov/compound/174174|access-date=2021-08-08|website=pubchem.ncbi.nlm.nih.gov|language=en}}</ref><ref>{{Cite journal|last1=Richards|first1=John R.|last2=Garber|first2=Dariush|last3=Laurin|first3=Erik G.|last4=Albertson|first4=Timothy E.|last5=Derlet|first5=Robert W.|last6=Amsterdam|first6=Ezra A.|last7=Olson|first7=Kent R.|last8=Ramoska|first8=Edward A.|last9=Lange|first9=Richard A.|date=June 2016|title=Treatment of cocaine cardiovascular toxicity: a systematic review|journal=Clinical Toxicology|volume=54|issue=5|pages=345–64|doi=10.3109/15563650.2016.1142090|issn=1556-9519|pmid=26919414|s2cid=5165666}}</ref><ref>{{Cite web|title=All About Heart Rate (Pulse)|url=https://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure/all-about-heart-rate-pulse|access-date=2021-08-08|website=www.heart.org|language=en}}</ref>

This section discusses target heart rates for healthy persons, which would be inappropriately high for most persons with coronary artery disease.<ref name="pmid1866953">{{cite journal | author = Anderson JM | title = Rehabilitating elderly cardiac patients | journal = West. J. Med. | volume = 154 | issue = 5 | pages = 573–78 | year = 1991 | pmid = 1866953 | pmc = 1002834 }}</ref>

===Influences from the central nervous system===

====Cardiovascular centres====
The heart rate is rhythmically generated by the [[sinoatrial node]]. It is also influenced by [[central nervous system|central]] factors through sympathetic and parasympathetic nerves.<ref name=GUYTONHALL2005>{{cite book |author=Arthur C. Guyton |author2=John E. Hall |title=Textbook of medical physiology|date=2005|publisher=W.B. Saunders|location=Philadelphia|isbn=978-0-7216-0240-0|pages=116–22|edition=11th}}</ref> Nervous influence over the heart rate is centralized within the two paired [[cardiovascular centre]]s of the [[medulla oblongata]]. The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the [[vagus nerve]]. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a [[sinus rhythm]] of approximately 100 bpm.<ref name="CNX2014">{{cite book|last1=Betts|first1=J. Gordon|title=Anatomy & physiology|date=2013|isbn=978-1-938168-13-0|url=http://cnx.org/content/m46676/latest/?collection=col11496/latest|access-date=11 August 2014|pages=787–846|publisher=OpenStax College, Rice University }}</ref>

Both sympathetic and parasympathetic stimuli flow through the paired [[cardiac plexus]] near the base of the heart. The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter [[norepinephrine]] (also known as [[noradrenaline]]) at the [[neuromuscular junction]] of the cardiac nerves. This shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increased heartrate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions.<ref name="CNX2014"/>

Norepinephrine binds to the beta–1 receptor. [[High blood pressure]] medications are used to block these receptors and so reduce the heart rate.<ref name="CNX2014"/>

[[File:2032 Automatic Innervation.jpg|thumb|left|Autonomic innervation of the heart: Cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in the medulla oblongata of the brain. They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus (parasympathetic) nerves that slow cardiac activity.<ref name="CNX2014"/>]]

Parasympathetic stimulation originates from the cardioinhibitory region of the brain<ref>{{cite journal |vauthors=Garcia A, Marquez MF, Fierro EF, Baez JJ, Rockbrand LP, Gomez-Flores J |title=Cardioinhibitory syncope: from pathophysiology to treatment-should we think on cardioneuroablation? |journal=J Interv Card Electrophysiol |date=May 2020 |volume=59 |issue=2 |pages=441–61 |pmid=32377918 |doi=10.1007/s10840-020-00758-2 |s2cid=218527702 }}</ref> with impulses traveling via the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization, which extends repolarization and increases the time before the next spontaneous depolarization occurs. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. This is similar to an individual driving a car with one foot on the brake pedal. To speed up, one need merely remove one's foot from the brake and let the engine increase speed. In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately 100 bpm. Any increases beyond this rate would require sympathetic stimulation.<ref name="CNX2014"/>
[[File:2033 Depolarization in Sinus Rhythm.jpg|thumb|Effects of parasympathetic and sympathetic stimulation on normal sinus rhythm: The wave of depolarization in a normal sinus rhythm shows a stable resting HR. Following parasympathetic stimulation, HR slows. Following sympathetic stimulation, HR increases.<ref name="CNX2014"/>]]

====Input to the cardiovascular centres====
The cardiovascular centre receive input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various [[proprioreceptor]]s, [[baroreceptor]]s, and [[chemoreceptor]]s, plus stimuli from the [[limbic system]] which normally enable the precise regulation of heart function, via cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. The cardiovascular centres monitor these increased rates of firing, suppressing parasympathetic stimulation or increasing sympathetic stimulation as needed in order to increase blood flow.<ref name="CNX2014"/>

Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.<ref name="CNX2014"/>

There is a similar reflex, called the atrial reflex or [[Bainbridge reflex]], associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The opposite is also true.<ref name="CNX2014"/>

Increased metabolic byproducts associated with increased activity, such as carbon dioxide, hydrogen ions, and lactic acid, plus falling oxygen levels, are detected by a suite of chemoreceptors innervated by the glossopharyngeal and vagus nerves. These chemoreceptors provide feedback to the cardiovascular centers about the need for increased or decreased blood flow, based on the relative levels of these substances.<ref name="CNX2014"/>

The limbic system can also significantly impact HR related to emotional state. During periods of stress, it is not unusual to identify higher than normal HRs, often accompanied by a surge in the stress hormone cortisol. Individuals experiencing extreme anxiety may manifest [[panic attack]]s with symptoms that resemble those of heart attacks. These events are typically transient and treatable. Meditation techniques have been developed to ease anxiety and have been shown to lower HR effectively.<ref name="pmid33728595">{{cite journal | vauthors = Morais P, Quaresma C, Vigário R, Quintão C| title=Electrophysiological effects of mindfulness meditation in a concentration test | journal= [[Medical & Biological Engineering & Computing]] | volume=59 | issue=4 | pages=759–773 | year=2021 | doi= 10.1007/s11517-021-02332-y | pmid=33728595  }}</ref> Doing simple deep and slow breathing exercises with one's eyes closed can also significantly reduce this anxiety and HR.<ref name="CNX2014"/>

===Factors influencing heart rate===
{{Factors influencing heart rate}}
{{Clear}}
Using a combination of autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control over the heart rate, but other factors can impact on this. These include hormones, notably epinephrine, norepinephrine, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance.<ref name="CNX2014"/>

====Epinephrine and norepinephrine====
The [[catecholamine]]s, epinephrine and norepinephrine, secreted by the [[adrenal medulla]] form one component of the extended fight-or-flight mechanism. The other component is sympathetic stimulation. Epinephrine and norepinephrine have similar effects: binding to the beta-1 [[adrenergic receptor]]s, and opening sodium and calcium ion chemical- or ligand-gated channels. The rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more quickly and the period of repolarization is shortened. However, massive releases of these hormones coupled with sympathetic stimulation may actually lead to arrhythmias. There is no parasympathetic stimulation to the adrenal medulla.<ref name="CNX2014"/>

====Thyroid hormones====
In general, increased levels of the [[thyroid hormones]] ([[thyroxine]](T4) and [[triiodothyronine]] (T3)), increase the heart rate; excessive levels can trigger [[tachycardia]]. The impact of thyroid hormones is typically of a much longer duration than that of the catecholamines. The physiologically active form of triiodothyronine, has been shown to directly enter [[cardiomyocytes]] and alter activity at the level of the genome.{{clarify|date=September 2014}} It also impacts the [[beta-adrenergic]] response similar to epinephrine and norepinephrine.<ref name="CNX2014"/>

====Calcium====
Calcium ion levels have a great impact on heart rate and [[myocardial contractility]]: increased calcium levels cause an increase in both. High levels of calcium ions result in [[hypercalcemia]] and excessive levels can induce [[cardiac arrest]]. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions.<ref name="CNX2014"/>

====Caffeine and nicotine====

[[Caffeine]] and [[nicotine]] are both stimulants of the nervous system and of the cardiac centres causing an increased heart rate. Caffeine works by increasing the rates of [[depolarization]] at the [[SA Node|SA node]], whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart.<ref name="CNX2014"/>

==== Effects of stress ====
Both surprise and stress induce physiological response: [[Tachycardia|elevate heart rate substantially]].<ref>{{cite journal|last1=Mustonen|first1=Veera|last2=Pantzar|first2=Mika|title=Tracking social rhythms of the heart|journal=Approaching Religion|date=2013|volume=3|issue=2|pages=16–21|doi=10.30664/ar.67512|doi-access=free}}</ref> In a study conducted on 8 female and male student actors ages 18 to 25, their reaction to an unforeseen occurrence (the cause of stress) during a performance was observed in terms of heart rate. In the data collected, there was a noticeable trend between the location of actors (onstage and offstage) and their elevation in heart rate in response to stress; the actors present offstage reacted to the stressor immediately, demonstrated by their immediate elevation in heart rate the minute the unexpected event occurred, but the actors present onstage at the time of the stressor reacted in the following 5 minute period (demonstrated by their increasingly elevated heart rate). This trend regarding stress and heart rate is supported by previous studies; [[negative emotion]]/stimulus has a prolonged effect on heart rate in individuals who are directly impacted.<ref>{{cite journal|last1=Brosschot|first1=J.F.|last2=Thayer|first2=J.F.|title=Heart rate response is longer after negative emotions than after positive emotions|journal=International Journal of Psychophysiology|date=2003|volume=50|issue=3|pages=181–87|doi=10.1016/s0167-8760(03)00146-6|pmid=14585487}}</ref>
In regard to the characters present onstage, a reduced startle response has been associated with a passive defense, and the diminished initial heart rate response has been predicted to have a greater tendency to dissociation.<ref>{{cite journal|last1=Chou|first1=C.Y.|last2=Marca|first2=R.L.|last3=Steptoe|first3=A.|last4=Brewin|first4=C.R.|title=Heart rate, startle response, and intrusive trauma memories|journal=Psychophysiology|date=2014|volume=51|issue=3|pages=236–46|doi=10.1111/psyp.12176|pmid=24397333|pmc=4283725}}</ref> Current evidence suggests that [[heart rate variability]] can be used as an accurate measure of [[psychological stress]] and may be used for an objective measurement of psychological stress.<ref>{{Cite journal|last1=Kim|first1=Hye-Geum|last2=Cheon|first2=Eun-Jin|last3=Bai|first3=Dai-Seg|last4=Lee|first4=Young Hwan|last5=Koo|first5=Bon-Hoon|date=March 2018|title=Stress and Heart Rate Variability: A Meta-Analysis and Review of the Literature|journal=Psychiatry Investigation|volume=15|issue=3|pages=235–45|doi=10.30773/pi.2017.08.17|issn=1738-3684|pmc=5900369|pmid=29486547}}</ref>

====Factors decreasing heart rate====
The heart rate can be slowed by altered sodium and potassium levels, [[hypoxia (medical)|hypoxia]], [[acidosis]], [[alkalosis]], and [[hypothermia]]. The relationship between electrolytes and HR is complex, but maintaining electrolyte balance is critical to the normal wave of depolarization. Of the two ions, potassium has the greater clinical significance. Initially, both [[hyponatremia]] (low sodium levels) and [[hypernatremia]] (high sodium levels) may lead to tachycardia. Severely high hypernatremia may lead to [[Fibrillation#Cardiology|fibrillation]], which may cause cardiac output to cease. Severe hyponatremia leads to both bradycardia and other arrhythmias. [[Hypokalemia]] (low potassium levels) also leads to arrhythmias, whereas [[hyperkalemia]] (high potassium levels) causes the heart to become weak and flaccid, and ultimately to fail.<ref name="CNX2014"/>

Heart muscle relies exclusively on [[Cellular respiration|aerobic metabolism]] for energy. Severe [[myocardial infarction]] (commonly called a heart attack) can lead to a [[Bradycardia|decreasing heart rate]], since metabolic reactions fueling heart contraction are restricted.<ref name="CNX2014"/>

[[Acidosis]] is a condition in which excess hydrogen ions are present, and the patient's blood expresses a low pH value. [[Alkalosis]] is a condition in which there are too few hydrogen ions, and the patient's blood has an elevated pH. [[Acid–base homeostasis|Normal blood pH]] falls in the range of 7.35–7.45, so a number lower than this range represents acidosis and a higher number represents alkalosis. Enzymes, being the regulators or catalysts of virtually all biochemical reactions – are sensitive to pH and will change shape slightly with values outside their normal range. These variations in pH and accompanying slight physical changes to the active site on the enzyme decrease the rate of formation of the enzyme-substrate complex, subsequently decreasing the rate of many enzymatic reactions, which can have complex effects on HR. Severe changes in pH will lead to denaturation of the enzyme.<ref name="CNX2014"/>

The last variable is body temperature. Elevated body temperature is called [[hyperthermia]], and suppressed body temperature is called [[hypothermia]]. Slight hyperthermia results in increasing HR and strength of contraction. Hypothermia slows the rate and strength of heart contractions. This distinct slowing of the heart is one component of the larger diving reflex that diverts blood to essential organs while submerged. If sufficiently chilled, the heart will stop beating, a technique that may be employed during open heart surgery. In this case, the patient's blood is normally diverted to an [[Cardiopulmonary bypass|artificial heart-lung machine]] to maintain the body's blood supply and [[gas exchange]] until the surgery is complete, and sinus rhythm can be restored. Excessive hyperthermia and hypothermia will both result in death, as enzymes drive the body systems to cease normal function, beginning with the central nervous system.<ref name="CNX2014"/>

==== Physiological control over heart rate ====
{{multiple image
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| image2            = Conditioned Variation in Heart Rate During Static Breath-Holds in the Bottlenose Dolphin (Tursiops truncatus) – examples of instantaneous heart rate (ifH) responses.jpg
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| alt2              = Conditioned Variation in Heart Rate During Static Breath-Holds in the Bottlenose Dolphin (Tursiops truncatus) – examples of instantaneous heart rate (ifH) responses
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A study shows that [[bottlenose dolphin]]s can learn – apparently via [[instrumental conditioning]] – to rapidly and selectively slow down their heart rate during diving for conserving oxygen depending on external signals. In humans regulating heart rate by methods such as listening to music, [[meditation]] or a [[vagal maneuver]] takes longer and only lowers the rate to a much smaller extent.<ref>{{cite journal |last1=Fahlman |first1=Andreas |last2=Cozzi |first2=Bruno |last3=Manley |first3=Mercy |last4=Jabas |first4=Sandra |last5=Malik |first5=Marek |last6=Blawas |first6=Ashley |last7=Janik |first7=Vincent M. |title=Conditioned Variation in Heart Rate During Static Breath-Holds in the Bottlenose Dolphin (Tursiops truncatus) |journal=[[Frontiers in Physiology]] |date=2020 |volume=11 |page=604018 |doi=10.3389/fphys.2020.604018 |pmid=33329056 |pmc=7732665 |s2cid=227128277 |doi-access=free }}
*{{lay source |template = cite web|url = https://phys.org/news/2020-11-dolphins-oxygen-dive-related-problems-consciously.html|title = Dolphins conserve oxygen and prevent dive-related problems by consciously decreasing their heart rates before diving|date = November 24, 2020 |website = Phys.org }}</ref>