document_title: Francium

question_text: in the alpha decay of francium-221 what daughter element is produced

text: Francium

text: Characteristics[edit]

text: Francium is one of the most unstable of the naturally occurring elements: its longest-lived isotope, francium-223, has a half-life of only 22 minutes. The only comparable element is astatine, whose most stable natural isotope, astatine-219 (the alpha daughter of francium-223), has a half-life of 56 seconds, although synthetic astatine-210 is much longer-lived with a half-life of 8.1 hours.[4] All isotopes of francium decay into astatine, radium, or radon.[4] Francium-223 also has a shorter half-life than the longest-lived isotope of each synthetic element up to and including element 105, dubnium.[5]

text: Francium is an alkali metal whose chemical properties mostly resemble those of caesium.[5] A heavy element with a single valence electron,[6] it has the highest equivalent weight of any element.[5] Liquid francium—if created—should have a surface tension of 0.05092 N/m at its melting point.[7] Francium's melting point was calculated to be around 27 °C (80 °F, 300 K).[8] The melting point is uncertain because of the element's extreme rarity and radioactivity. Thus, the estimated boiling point value of 677 °C (1250 °F, 950 K) is also uncertain.

text: Linus Pauling estimated the electronegativity of francium at 0.7 on the Pauling scale, the same as caesium;[9] the value for caesium has since been refined to 0.79, but there are no experimental data to allow a refinement of the value for francium.[10] Francium has a slightly higher ionization energy than caesium,[11] 392.811(4) kJ/mol as opposed to 375.7041(2) kJ/mol for caesium, as would be expected from relativistic effects, and this would imply that caesium is the less electronegative of the two. Francium should also have a higher electron affinity than caesium and the Fr− ion should be more polarizable than the Cs− ion.[12] The CsFr molecule is predicted to have francium at the negative end of the dipole, unlike all known heterodiatomic alkali metal molecules. Francium superoxide (FrO2) is expected to have a more covalent character than its lighter congeners; this is attributed to the 6p electrons in francium being more involved in the francium–oxygen bonding.[12]

text: Francium coprecipitates with several caesium salts, such as caesium perchlorate, which results in small amounts of francium perchlorate. This coprecipitation can be used to isolate francium, by adapting the radiocaesium coprecipitation method of Lawrence E. Glendenin and Nelson. It will additionally coprecipitate with many other caesium salts, including the iodate, the picrate, the tartrate (also rubidium tartrate), the chloroplatinate, and the silicotungstate. It also coprecipitates with silicotungstic acid, and with perchloric acid, without another alkali metal as a carrier, which provides other methods of separation.[13][14] Nearly all francium salts are water-soluble.[15]

text: Isotopes[edit]

text: There are 34 known isotopes of francium ranging in atomic mass from 199 to 232.[16] Francium has seven metastable nuclear isomers.[5] Francium-223 and francium-221 are the only isotopes that occur in nature, though the former is far more common.[17]

text: Francium-223 is the most stable isotope, with a half-life of 21.8 minutes,[5] and it is highly unlikely that an isotope of francium with a longer half-life will ever be discovered or synthesized.[18] Francium-223 is the fifth product of the actinium decay series as the daughter isotope of actinium-227.[19] Francium-223 then decays into radium-223 by beta decay (1149 keV decay energy), with a minor (0.006%) alpha decay path to astatine-219 (5.4 MeV decay energy).[20]

text: Francium-221 has a half-life of 4.8 minutes.[5] It is the ninth product of the neptunium decay series as a daughter isotope of actinium-225.[19] Francium-221 then decays into astatine-217 by alpha decay (6.457 MeV decay energy).[5]

text: The least stable ground state isotope is francium-215, with a half-life of 0.12 μs: it undergoes a 9.54 MeV alpha decay to astatine-211.[5] Its metastable isomer, francium-215m, is less stable still, with a half-life of only 3.5 ns.[21]

text: Applications[edit]

text:
Due to its instability and rarity, there are no commercial applications for francium.[22][23][24][19] It has been used for research purposes in the fields of chemistry[25]
and of atomic structure. Its use as a potential diagnostic aid for various cancers has also been explored,[4] but this application has been deemed impractical.[23]

text: Francium's ability to be synthesized, trapped, and cooled, along with its relatively simple atomic structure, has made it the subject of specialized spectroscopy experiments. These experiments have led to more specific information regarding energy levels and the coupling constants between subatomic particles.[26] Studies on the light emitted by laser-trapped francium-210 ions have provided accurate data on transitions between atomic energy levels which are fairly similar to those predicted by quantum theory.[27]

text: History[edit]

text: As early as 1870, chemists thought that there should be an alkali metal beyond caesium, with an atomic number of 87.[4] It was then referred to by the provisional name eka-caesium.[28] Research teams attempted to locate and isolate this missing element, and at least four false claims were made that the element had been found before an authentic discovery was made.

text: Erroneous and incomplete discoveries[edit]

text: Soviet chemist D. K. Dobroserdov was the first scientist to claim to have found eka-caesium, or francium. In 1925, he observed weak radioactivity in a sample of potassium, another alkali metal, and incorrectly concluded that eka-caesium was contaminating the sample (the radioactivity from the sample was from the naturally occurring potassium radioisotope, potassium-40).[29] He then published a thesis on his predictions of the properties of eka-caesium, in which he named the element russium after his home country.[30] Shortly thereafter, Dobroserdov began to focus on his teaching career at the Polytechnic Institute of Odessa, and he did not pursue the element further.[29]

text: The following year, English chemists Gerald J. F. Druce and Frederick H. Loring analyzed X-ray photographs of manganese(II) sulfate.[30] They observed spectral lines which they presumed to be of eka-caesium. They announced their discovery of element 87 and proposed the name alkalinium, as it would be the heaviest alkali metal.[29]

text: In 1930, Fred Allison of the Alabama Polytechnic Institute claimed to have discovered element 87 when analyzing pollucite and lepidolite using his magneto-optical machine. Allison requested that it be named virginium after his home state of Virginia, along with the symbols Vi and Vm.[30][31] In 1934, H.G. MacPherson of UC Berkeley disproved the effectiveness of Allison's device and the validity of his discovery.[32]

text: In 1936, Romanian physicist Horia Hulubei and his French colleague Yvette Cauchois also analyzed pollucite, this time using their high-resolution X-ray apparatus.[29] They observed several weak emission lines, which they presumed to be those of element 87. Hulubei and Cauchois reported their discovery and proposed the name moldavium, along with the symbol Ml, after Moldavia, the Romanian province where Hulubei was born.[30] In 1937, Hulubei's work was criticized by American physicist F. H. Hirsh Jr., who rejected Hulubei's research methods. Hirsh was certain that eka-caesium would not be found in nature, and that Hulubei had instead observed mercury or bismuth X-ray lines. Hulubei insisted that his X-ray apparatus and methods were too accurate to make such a mistake. Because of this, Jean Baptiste Perrin, Nobel Prize winner and Hulubei's mentor, endorsed moldavium as the true eka-caesium over Marguerite Perey's recently discovered francium. Perey took pains to be accurate and detailed in her criticism of Hulubei's work, and finally she was credited as the sole discoverer of element 87.[29] All other previous purported discoveries of element 87 were ruled out due to francium's very limited half-life.[30]

text: Perey's analysis[edit]

text: Eka-caesium was discovered in 1939 by Marguerite Perey of the Curie Institute in Paris, when she purified a sample of actinium-227 which had been reported to have a decay energy of 220 keV. Perey noticed decay particles with an energy level below 80 keV. Perey thought this decay activity might have been caused by a previously unidentified decay product, one which was separated during purification, but emerged again out of the pure actinium-227. Various tests eliminated the possibility of the unknown element being thorium, radium, lead, bismuth, or thallium. The new product exhibited chemical properties of an alkali metal (such as coprecipitating with caesium salts), which led Perey to believe that it was element 87, produced by the alpha decay of actinium-227.[28] Perey then attempted to determine the proportion of beta decay to alpha decay in actinium-227. Her first test put the alpha branching at 0.6%, a figure which she later revised to 1%.[18]

text: Perey named the new isotope actinium-K (it is now referred to as francium-223)[28] and in 1946, she proposed the name catium (Cm) for her newly discovered element, as she believed it to be the most electropositive cation of the elements. Irène Joliot-Curie, one of Perey's supervisors, opposed the name due to its connotation of cat rather than cation; furthermore, the symbol coincided with that which had since been assigned to curium.[28] Perey then suggested francium, after France. This name was officially adopted by the International Union of Pure and Applied Chemistry (IUPAC) in 1949,[4] becoming the second element after gallium to be named after France. It was assigned the symbol Fa, but this abbreviation was revised to the current Fr shortly thereafter.[33] Francium was the last element discovered in nature, rather than synthesized, following hafnium and rhenium.[28] Further research into francium's structure was carried out by, among others, Sylvain Lieberman and his team at CERN in the 1970s and 1980s.[34]

text: Occurrence[edit]

text: 223Fr is the result of the alpha decay of 227Ac and can be found in trace amounts in uranium minerals.[5] In a given sample of uranium, there is estimated to be only one francium atom for every 1 × 1018 uranium atoms.[23] It is also calculated that there is at most 30 g of francium in the Earth's crust at any given time.[35]

text: Production[edit]

text: Francium can be synthesized in the nuclear reaction:

text: This process, developed by Stony Brook Physics, yields francium isotopes with masses of 209, 210, and 211,[37] which are then isolated by the magneto-optical trap (MOT).[36] The production rate of a particular isotope depends on the energy of the oxygen beam. An 18O beam from the Stony Brook LINAC creates 210Fr in the gold target with the nuclear reaction 197Au + 18O → 210Fr + 5n. The production required some time to develop and understand. It was critical to operate the gold target very close to its melting point and to make sure that its surface was very clean. The nuclear reaction embeds the francium atoms deep in the gold target, and they must be removed efficiently. The atoms quickly diffuse to the surface of the gold target and are released as ions, but this does not happen every time. The francium ions are guided by electrostatic lenses until they land in a surface of hot yttrium and become neutral again. The francium is then injected into a glass bulb. A magnetic field and laser beams cool and confine the atoms. Although the atoms remain in the trap for only about 20 seconds before escaping (or decaying), a steady stream of fresh atoms replaces those lost, keeping the number of trapped atoms roughly constant for minutes or longer. Initially, about 1000 francium atoms were trapped in the experiment. This was gradually improved and the setup is capable of trapping over 300,000 neutral atoms of francium at a time.[3] These are neutral metallic atoms in a gaseous unconsolidated state. Enough francium is trapped that a video camera can capture the light given off by the atoms as they fluoresce. The atoms appear as a glowing sphere about 1 millimeter in diameter. This was the first time that anyone had ever seen francium. The researchers can now make extremely sensitive measurements of the light emitted and absorbed by the trapped atoms, providing the first experimental results on various transitions between atomic energy levels in francium. Initial measurements show very good agreement between experimental values and calculations based on quantum theory. Other synthesis methods include bombarding radium with neutrons, and bombarding thorium with protons, deuterons, or helium ions.[18] Francium has not been synthesized in amounts large enough to weigh.[4][8][23]

text: 223Fr can also be isolated from samples of its parent 227Ac, the francium being milked via elution with NH4Cl–CrO3 from an actinium-containing cation exchanger and purified by passing the solution through a silicon dioxide compound loaded with barium sulfate.[38]


document_title: MonsterVerse

question_text: when is the next kong movie coming out

question_tokens: when is the next kong movie coming out

root

text: MonsterVerse

text: Development[edit]

text: Legendary Entertainment confirmed at the July 2014 San Diego Comic-Con International that it had acquired the rights to Mothra, Rodan, and King Ghidorah from Toho and revealed concept footage with the closing title cards reading "Conflict: inevitable. Let them fight".[5] In September 2015, Legendary announced that the film Kong: Skull Island would not be developed with Universal Studios. Instead, it would be developed with Warner Bros., which sparked media speculation that Godzilla and King Kong would appear in a film together.[6][7]

tag: p

text: In October 2015, Legendary announced plans to unite Godzilla and King Kong in a film titled Godzilla vs. Kong, set for a 2020 release date. Legendary plans to create a shared cinematic franchise "centered around Monarch" (the secret government agency which debuted in 2014's Godzilla) and that "brings together Godzilla and Legendary’s King Kong in an ecosystem of other giant super-species, both classic and new".[8] Later in October, it was announced that Kong: Skull Island would have references to Monarch.[9]

text: In May 2016, Warner Bros. announced that Godzilla vs. Kong would be released on May 29, 2020, and that Godzilla: King of the Monsters would be pushed back from its original June 2018 release date to March 22, 2019,[10] however, the film was later pushed back again to May 31, 2019.[11] In October 2016, Legendary announced that Godzilla: King of the Monsters would be filmed at its parent company Wanda's Oriental Movie Metropolis facility in Qingdao, China, along with Pacific Rim Uprising.[12] That same month, it was revealed that Legendary was planning a writers room to create their Godzilla–Kong cinematic universe, with Alex Garcia overseeing the project for Legendary.[13]

text: In early January 2017, Thomas Tull, founder of Legendary, resigned from the company but will remain as producer for the Godzilla–Kong series, which was revealed as the "MonsterVerse".[14] In March 2017, Legendary assembled a writers room to develop the story for Godzilla vs. Kong.[15]

text: Films[edit]

text:
Film

U.S. release date

Director(s)

Story by

Screenplay by

Producer(s)

Status

Godzilla

May 16, 2014 (2014-05-16)

Gareth Edwards

David Callaham

Max Borenstein

Thomas Tull, Jon Jashni, Mary Parent and Brian Rogers

Released

Kong: Skull Island

March 10, 2017 (2017-03-10)

Jordan Vogt-Roberts

John Gatins

Dan Gilroy, Max Borenstein and Derek Connolly

Thomas Tull, Jon Jashni, Mary Parent, and Alex Garcia

Godzilla: King of the Monsters

May 31, 2019

Michael Dougherty

Max Borenstein, Michael Dougherty and Zach Shields

Thomas Tull, Jon Jashni, Mary Parent, Alex Garcia, and Brian Rogers

Post-Production

Godzilla vs. Kong

May 22, 2020

Adam Wingard

Terry Rossio, Patrick McKay, J.D. Payne, Lindsey Beer, Cat Vasko, T.S. Nowlin, Jack Paglen, J. Michael Straczynski

Terry Rossio[16]

Filming

tag: table

text: Godzilla (2014)[edit]

text: The film reimagines Godzilla's origins in contemporary times and is set 15 years after a nuclear meltdown in Japan which subsequently awakens two giant parasitic creatures, known as "MUTOs". As the MUTOs ravage the countryside in order to reproduce, they awaken a larger ancient alpha predator, known as "Godzilla", whose existence has been kept secret by the U.S. government since 1954. The film introduces Godzilla, the MUTOs, and the Monarch organization to the MonsterVerse.

text: In 2004, director Yoshimitsu Banno acquired permission from Toho to produce a short IMAX Godzilla film which was in development for several years until the project was eventually turned over to Legendary Pictures.[2][17] In March 2010, Legendary announced to have acquired the rights to Godzilla for a feature film reboot.[18] In January 2011, Gareth Edwards was announced as the director for the film.[19] The film was co-produced with Warner Bros. Pictures with filming completed in 2013 in Canada and the United States for release in 2014.[20] Godzilla was released on May 16, 2014 to positive reviews from critics[21][22] and was a box office success, grossing $200 million domestically and $529 million worldwide against its $160 million budget.[23]

text: Kong: Skull Island (2017)[edit]

text: The film is set in 1973 and follows a team of scientists and Vietnam War soldiers who travel to an uncharted island in the Pacific and encounter terrifying creatures and the mighty Kong. The film introduces King Kong, Mother Longlegs,[24] Sker Buffalos,[24] Mire Squid,[24] Leafwing,[24] Psychovulture,[24] Spore Mantis,[24] Ramarak,[25] and the Skullcrawlers to the MonsterVerse and a post-credits scene introduces Rodan, Mothra, and King Ghidorah to the MonsterVerse.[26]

text: In July 2014 at the San Diego Comic-Con, Legendary announced a King Kong origin story, initially titled Skull Island, with a release date of November 4, 2016, and Universal Pictures distributing.[27] In September 2014, Jordan Vogt-Roberts was announced as the film's director.[28] In September 2015, Legendary moved development of the film from Universal Pictures to Warner Bros. to create an expanded cinematic universe.[29] Principal photography began on October 19, 2015, in Hawaii and Vietnam. Kong: Skull Island was released on March 10, 2017 to positive reviews from critics[30][31] and was a box office success, grossing $168 million domestically and $566 million worldwide against its $185 million budget.[32] The film received a nomination for Best Visual Effects at the 90th Academy Awards.[33]

text: Godzilla: King of the Monsters (2019)[edit]

text: The Monarch agency struggles to ensure humanity's survival in an age of god-sized monsters. Three new monsters named Rodan, Mothra, and King Ghidorah rise to challenge Godzilla for supremacy.[34] The film retcons the monsters' designation from "MUTOs" to "Titans".[35]

text: Prior to announcing a shared cinematic universe between Godzilla and King Kong, Legendary originally intended to produce a Godzilla trilogy, with Gareth Edwards attached to direct all films.[36] However, Edwards left the sequel in May 2016 to work on smaller scale projects.[37] In January 2017, Michael Dougherty was announced as the director and co-writer for the film.[38] Principal photography began on June 19, 2017, in Atlanta, Georgia and wrapped on September 27, 2017.[39] The film is scheduled to be released on May 31, 2019, in 2D, 3D, and select IMAX by Warner Bros. Pictures, except in Japan where the film will be distributed by Toho.[11][34]

text: Godzilla vs. Kong (2020)[edit]

text: The project was announced in October 2015 when Legendary announced plans for a shared cinematic universe between Godzilla and King Kong. Adam Wingard was announced as the director in May 2017. Principal photography began in October 2018 in Atlanta, Hawaii and Australia and is expected to conclude in February 2019. Godzilla vs. Kong is scheduled to be released on May 22, 2020 by Warner Bros. Pictures.

text: Cast and characters[edit]

text:
A dark grey cell indicates the character was not in the film, or that the character's presence in the film has not yet been announced.
An M  indicates the character appears through use of motion capture.
A Y  indicates an appearance by an actor portraying a younger version of a character.

tag: ul

text:
Character

Released films

Upcoming films

Godzilla

Kong:Skull Island

Godzilla:King of the Monsters

Godzilla vs. Kong

2014

2017

2019

2020

Monsters

Godzilla

T.J. StormM

Silent cameo

TBA

King Kong

Terry NotaryM

TBA

Toby KebbellM

King Ghidorah

Silent cameo

Jason LilesM

Alan MaxsonM

Richard DortonM

Mothra

TBA

Rodan

Humans

Ford Brody

Aaron Taylor-Johnson

CJ AdamsY

Elle Brody

Elizabeth Olsen

Ishiro Serizawa

Ken Watanabe

Ken Watanabe

Joe Brody

Bryan Cranston

Sandra Brody

Juliette Binoche

Vivienne Graham

Sally Hawkins

Sally Hawkins

William Stentz

David Strathairn

James Conrad

Tom Hiddleston

Hank Marlow

John C. Reilly

Will BrittainY

Victor Nieves

John Ortiz

Preston Packard

Samuel L. Jackson

Bill Randa

John Goodman

San Lin

Jing Tian

Mason Weaver

Brie Larson

Mark Russell

Kyle Chandler

Emma Russell

Vera Farmiga

Madison Russell

Millie Bobby Brown

Stanton

Bradley Whitford

Sam Coleman

Thomas Middleditch

Barnes

O'Shea Jackson Jr.

Dr. Chen

Zhang Ziyi

text: Reception[edit]

text: Box office performance[edit]

text:
Film

Release date

Box office gross

Box office ranking

Budget

Ref(s)

North America

Other territories

Worldwide

North America

Worldwide

Godzilla

May 16, 2014

$200,676,069

$328,400,000

$529,076,069

183

165

$160 million

[23]

Kong: Skull Island

March 10, 2017

$168,052,812

$398,600,000

$566,652,812

268

144

$185 million

[32]

Total

$7008368728881000000♠368,728,881

$7008727000000000000♠727,000,000

$7009109572888100000♠1,095,728,881

$345 million

[4]

text: Critical and public response[edit]

text:
Film

Rotten Tomatoes

Metacritic

CinemaScore

Godzilla

74% (301 reviews) [40]

62 (48 critics) [41]

B+[42]

Kong: Skull Island

75% (335 reviews) [43]

62 (49 critics) [44]

B+[42]

text: Tie-in material[edit]

text: Books[edit]

text:
Title

Release date

Writer(s)

Note

Godzilla – The Official Movie Novelization

May 20, 2014

Greg Cox

Novelization of Godzilla

Kong: Skull Island – The Official Movie Novelization

March 14, 2017

Tim Lebbon

Novelization of Kong: Skull Island

text: Comics[edit]

text:
Title

Release date

Writer(s)

Illustrator(s)

Cover Artist(s)

Note

Godzilla: Awakening

May 7, 2014 (2014-05-07)

Max Borenstein and Greg Borenstein

Eric Battle, Yvel Guichet, Alan Quah, and Lee Loughridge

Arthur Adams

Tie-in prequel comic to Godzilla

Skull Island: The Birth of Kong

April 12, 2017

Arvid Nelson

Zid

Zid, Drew Johnson (issue #4)

Tie-in prequel/sequel comic to Kong: Skull Island

Godzilla: Aftershock

Spring 2019

Arvid Nelson

Drew Edward Johnson

Tie-in prequel comic to Godzilla: King of the Monsters

text: Video games[edit]

text: Legendary's Godzilla was featured as a playable character in Bandai Namco's 2014 video game Godzilla as "Hollywood Godzilla".[45][46]

text:
Title

Release date

Developer

Publisher

Note

Godzilla: Crisis Defense

May 7, 2014

Legendary

Legendary

Tie-in web game to Godzilla

Godzilla: Strike Zone[47]

May 15, 2014

Warner Bros. Entertainment

Warner Bros. International Enterprises

Tie-in mobile game to Godzilla

Godzilla: Smash 3[47]

May 16, 2014

Rogue Play

Pipeworks

Tie-in mobile game to Godzilla


document_title: Heart rate

question_text: what is the correct definition of target heart rate range

question_tokens: what is the correct definition of target heart rate range

text: Heart rate

text: Physiology[edit]

text:
Normal heart sounds

Normal heart sounds as heard with a stethoscope

Problems playing this file? See media help.

text: While heart rhythm is regulated entirely by the sinoatrial node under normal conditions, heart rate is regulated by sympathetic and 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.[8]

text: Due to individuals having a constant blood volume, one of the physiological ways to deliver more oxygen to an organ is to increase heart rate to permit blood to pass by the organ more often.[7] Normal resting heart rates range from 60–100 bpm. 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. Tachycardia is defined as a resting heart rate above 100 bpm, though persistent rest rates between 80–100 bpm, mainly if they are present during sleep, may be signs of hyperthyroidism or anemia (see below).[7]

text:
Central nervous system stimulants such as substituted amphetamines increase heart rate.
Central nervous system depressants or sedatives 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).

text: There are many ways in which the heart rate speeds up or slows down. Most involve stimulant-like endorphins and hormones being released in the brain, many of which are those that are 'forced'/'enticed' out by the ingestion and processing of drugs.

text: This section discusses target heart rates for healthy persons and are inappropriately high for most persons with coronary artery disease.[9]

text: Influences from the central nervous system[edit]

text: Cardiovascular centres[edit]

text: The heart rate is rhythmically generated by the sinoatrial node. It is also influenced by central factors through sympathetic and parasympathetic nerves.[10] Nervous influence over the heartrate is centralized within the two paired cardiovascular centres 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.[11]

text: 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.[11]

text: Norepinephrine binds to the beta–1 receptor. High blood pressure medications are used to block these receptors and so reduce the heart rate.[11]

text: Parasympathetic stimulation originates from the cardioinhibitory region 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.[11]

text: Input to the cardiovascular centres[edit]

text: The cardiovascular centres 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 proprioreceptors, baroreceptors, and chemoreceptors, 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.[11]

text: 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.[11]

text: 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.[11]

text: 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.[11]

text: 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 attacks 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. Doing simple deep and slow breathing exercises with one’s eyes closed can also significantly reduce this anxiety and HR.[11]

text: Factors influencing heart rate[edit]

text:
Table 1: Major factors increasing heart rate and force of contraction[11]

Factor
Effect

Cardioaccelerator nerves
Release of norepinephrine

Proprioreceptors
Increased rates of firing during exercise

Chemoreceptors
Decreased levels of O2; increased levels of H+, CO2, and lactic acid

Baroreceptors
Decreased rates of firing, indicating falling blood volume/pressure

Limbic system
Anticipation of physical exercise or strong emotions

Catecholamines
Increased epinephrine and norepinephrine

Thyroid hormones
Increased T3 and T4

Calcium
Increased Ca2+

Potassium
Decreased K+

Sodium
Decreased Na+

Body temperature
Increased body temperature

Nicotine and caffeine
Stimulants, increasing heart rate

Table 2: Factors decreasing heart rate and force of contraction[11]

Factor
Effect

Cardioinhibitor nerves (vagus)
Release of acetylcholine

Proprioreceptors
Decreased rates of firing following exercise

Chemoreceptors
Increased levels of O2; decreased levels of H+ and CO2

Baroreceptors
Increased rates of firing, indicating higher blood volume/pressure

Limbic system
Anticipation of relaxation

Catecholamines
Decreased epinephrine and norepinephrine

Thyroid hormones
Decreased T3 and T4

Calcium
Decreased Ca2+

Potassium
Increased K+

Sodium
Decreased Na+

Body temperature
Decrease in body temperature

text: 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.[11]

text: Epinephrine and norepinephrine[edit]

text: The catecholamines, 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 receptors, 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.[11]

text: Thyroid hormones[edit]

text: 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.[clarification needed] It also impacts the beta adrenergic response similar to epinephrine and norepinephrine.[11]

text: Calcium[edit]

text: Calcium ion levels greatly impact on heartrate and contractility; increased 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.[11]

text: Caffeine and nicotine[edit]

text: This section needs expansion. You can help by adding to it. (February 2015)

text: 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, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart.[11] Both stimulants are legal and unregulated, and are known to be very addictive.[11]

text: Effects of stress[edit]

text: Both surprise and stress induce physiological response: elevate heart rate substantially.[12] 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 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.[13] 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.[14] Further, note that heart rate is an accurate measure of stress and the startle response which can be easily observed to determine the effects of certain stressors.

text: Factors decreasing heart rate[edit]

text: The heart rate can be slowed by altered sodium and potassium levels, 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, which may cause CO 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.[11]

text: Heart muscle relies exclusively on aerobic metabolism for energy. Hypoxia (an insufficient supply of oxygen) leads to decreasing HRs, since metabolic reactions fueling heart contraction are restricted.[11]

text: 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. 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.[11]

text: 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 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.[11]

text: In different circumstances[edit]

text: Heart rate is not a stable value and it increases or decreases in response to the body's need in a way to maintain an equilibrium (basal metabolic rate) between requirement and delivery of oxygen and nutrients. The normal SA node firing rate is affected by autonomic nervous system activity: sympathetic stimulation increases and parasympathetic stimulation decreases the firing rate.[15] A number of different metrics are used to describe heart rate.

text: Resting heart rate[edit]

text: The basal or resting heart rate (HRrest) is defined as the heart rate when a person is awake, in a neutrally temperate environment, and has not been subject to any recent exertion or stimulation, such as stress or surprise. Most texts cite the typical resting heart rate in adults as 60–100 beats per minute (bpm). A large body of evidence indicates that the normal range is actually 50-90 beats per minute. For example, all-cause mortality is increased by 1.22 (hazard ratio) when heart rate exceeds 90 beats per minute.[3] The mortality rate of patients with myocardial infarction increased from 15% to 41% if their admission heart rate was greater than 90 beats per minute.[4] ECG of 46,129 individuals with low risk for cardiovascular disease revealed that 96% had resting heart rates ranging from 48-98 beats per minute.[6] Finally, expert consensus reveals that 98% of cardiologists believe that the "60 to 100" range is too high, with a vast majority of them agreeing that 50 to 90 beats per minute is more appropriate.[5] The normal resting heart rate is based on the at-rest firing rate of the heart's sinoatrial node, where the faster pacemaker cells driving the self-generated rhythmic firing and responsible for the heart's autorhythmicity are located.[16] For endurance athletes at the elite level, it is not unusual to have a resting heart rate between 33 and 50 bpm.[citation needed]

text: Maximum heart rate[edit]

text: The maximum heart rate (HRmax) is the highest heart rate an individual can achieve without severe problems through exercise stress,[17][unreliable medical source?][18] and generally decreases with age. Since HRmax varies by individual, the most accurate way of measuring any single person's HRmax is via a cardiac stress test. In this test, a person is subjected to controlled physiologic stress (generally by treadmill) while being monitored by an ECG. The intensity of exercise is periodically increased until certain changes in heart function are detected on the ECG monitor, at which point the subject is directed to stop. Typical duration of the test ranges ten to twenty minutes.

text: Adults who are beginning a new exercise regimen are often advised to perform this test only in the presence of medical staff due to risks associated with high heart rates. For general purposes, a formula is often employed to estimate a person's maximum heart rate. However, these predictive formulas have been criticized as inaccurate because they generalized population-averages and usually focus on a person's age. It is well-established that there is a "poor relationship between maximal heart rate and age" and large standard deviations relative to predicted heart rates.[19] (see Limitations of Estimation Formulas).

text: A number of formulas are used to estimate HRmax

text: Nes, et al.[edit]

text: Based on measurements of 3320 healthy men and women aged between 19 and 89, and including the potential modifying effect of gender, body composition, and physical activity, Nes et al found

text: HRmax = 211 − (0.64 × age)

text: This relationship was found to hold substantially regardless of gender, physical activity status, maximal oxygen uptake, smoking, or body mass index. However, a standard error of the estimate of 10.8 beats/min must be accounted for when applying the formula to clinical settings, and the researchers concluded that actual measurement via a maximal test may be preferable whenever possible.[20]

text: Tanaka, Monahan, & Seals[edit]

text: From Tanaka, Monahan, & Seals (2001):

text: HRmax = 208 − (0.7 × age)  [21]

text: Their meta-analysis (of 351 prior studies involving 492 groups and 18,712 subjects) and laboratory study (of 514 healthy subjects) concluded that, using this equation, HRmax was very strongly correlated to age (r = −0.90). The regression equation that was obtained in the laboratory-based study (209 − 0.7 x age), was virtually identical to that of the meta-study. The results showed HRmax to be independent of gender and independent of wide variations in habitual physical activity levels. This study found a standard deviation of ~10 beats per minute for individuals of any age, meaning the HRmax formula given has an accuracy of ±20 beats per minute.[21]

text: In 2007, researchers at the Oakland University analyzed maximum heart rates of 132 individuals recorded yearly over 25 years, and produced a linear equation very similar to the Tanaka formula, HRmax = 206.9 − (0.67 × age), and a nonlinear equation, HRmax = 191.5 − (0.007 × age2). The linear equation had a confidence interval of ±5–8 bpm and the nonlinear equation had a tighter range of ±2–5 bpm. Also a third nonlinear equation was produced: HRmax = 163 + (1.16 × age) − (0.018 × age2).[22][disputed (for: formulae conflict with source cited)  – discuss]

text: Haskell & Fox[edit]

text: Notwithstanding the research of Tanaka, Monahan, & Seals, the most widely cited formula for HRmax (which contains no reference to any standard deviation) is still:

text: Although attributed to various sources, it is widely thought to have been devised in 1970 by Dr. William Haskell and Dr. Samuel Fox.[23] Inquiry into the history of this formula reveals that it was not developed from original research, but resulted from observation based on data from approximately 11 references consisting of published research or unpublished scientific compilations.[24] It gained widespread use through being used by Polar Electro in its heart rate monitors,[23] which Dr. Haskell has "laughed about",[23] as the formula "was never supposed to be an absolute guide to rule people's training."[23]

text: While it is the most common (and easy to remember and calculate), this particular formula is not considered by reputable health and fitness professionals to be a good predictor of HRmax. Despite the widespread publication of this formula, research spanning two decades reveals its large inherent error, Sxy = 7–11 bpm. Consequently, the estimation calculated by   HRmax = 220 − age   has neither the accuracy nor the scientific merit for use in exercise physiology and related fields.[24]

text: Robergs & Landwehr[edit]

text: A 2002 study[24] of 43 different formulas for HRmax (including that of Haskell and Fox – see above) published in the Journal of Exercise Psychology concluded that:

text:
no "acceptable" formula currently existed (they used the term "acceptable" to mean acceptable for both prediction of VO2, and prescription of exercise training HR ranges)
the least objectionable formula was:

tag: ol

text: Gulati (for women)[edit]

text: Research conducted at Northwestern University by Martha Gulati, et al., in 2010[25] suggested a maximum heart rate formula for women:

text: Gellish[edit]

text: A 2008 study from Lund, Sweden gives reference values (obtained during bicycle ergometry) for men:

text: and for women:

text: Other formulae[edit]

text: HRmax = 206.3 − (0.711 × age)

text: HRmax = 217 − (0.85 × age)

text: Limitations[edit]

text: Maximum heart rates vary significantly between individuals.[23] Even within a single elite sports team, such as Olympic rowers in their 20s, maximum heart rates have been reported as varying from 160 to 220.[23] Such a variation would equate to a 60 or 90 year age gap in the linear equations above, and would seem to indicate the extreme variation about these average figures.

text: Figures are generally considered averages, and depend greatly on individual physiology and fitness. For example, an endurance runner's rates will typically be lower due to the increased size of the heart required to support the exercise, while a sprinter's rates will be higher due to the improved response time and short duration. While each may have predicted heart rates of 180 (= 220 − age), these two people could have actual HRmax 20 beats apart (e.g., 170-190).

text: Further, note that individuals of the same age, the same training, in the same sport, on the same team, can have actual HRmax 60 bpm apart (160–220):[23] the range is extremely broad, and some say "The heart rate is probably the least important variable in comparing athletes."[23]

text: Heart rate reserve[edit]

text: Heart rate reserve (HRreserve) is the difference between a person's measured or predicted maximum heart rate and resting heart rate. Some methods of measurement of exercise intensity measure percentage of heart rate reserve. Additionally, as a person increases their cardiovascular fitness, their HRrest will drop, and the heart rate reserve will increase. Percentage of HRreserve is equivalent to percentage of VO2 reserve.[28]

text: This is often used to gauge exercise intensity (first used in 1957 by Karvonen).[29]

text: Karvonen's study findings have been questioned, due to the following:

text:
The study did not use VO2 data to develop the equation.
Only six subjects were used, and the correlation between the percentages of HRreserve and VO2 max was not statistically significant.[30]

text: Target heart rate[edit]

text: For healthy people, the Target Heart Rate or Training Heart Rate (THR) is a desired range of heart rate reached during aerobic exercise which enables one's heart and lungs to receive the most benefit from a workout. This theoretical range varies based mostly on age; however, a person's physical condition, sex, and previous training also are used in the calculation. Below are two ways to calculate one's THR. In each of these methods, there is an element called "intensity" which is expressed as a percentage. The THR can be calculated as a range of 65–85% intensity. However, it is crucial to derive an accurate HRmax to ensure these calculations are meaningful.[citation needed]

text: Example for someone with a HRmax of 180 (age 40, estimating HRmax As 220 − age):

text: Karvonen method[edit]

text: The Karvonen method factors in resting heart rate (HRrest) to calculate target heart rate (THR), using a range of 50–85% intensity:[31]

text: Equivalently,

text: Example for someone with a HRmax of 180 and a HRrest of 70 (and therefore a HRreserve of 110):

text: Zoladz method[edit]

text: An alternative to the Karvonen method is the Zoladz method, which derives exercise zones by subtracting values from HRmax:

text: Example for someone with a HRmax of 180:

text: Heart rate recovery[edit]

text: Heart rate recovery (HRrecovery) is the reduction in heart rate at peak exercise and the rate as measured after a cool-down period of fixed duration.[32] A greater reduction in heart rate after exercise during the reference period is associated with a higher level of cardiac fitness.[33]

text: Heart rates that do not drop by more than 12 bpm one minute after stopping exercise are associated with an increased risk of death.[32] Investigators of the Lipid Research Clinics Prevalence Study, which included 5,000 subjects, found that patients with an abnormal HRrecovery (defined as a decrease of 42 beats per minutes or less at two minutes post-exercise) had a mortality rate 2.5 times greater than patients with a normal recovery.[33] Another study by Nishime et al. and featuring 9,454 patients followed for a median period of 5.2 years found a four-fold increase in mortality in subjects with an abnormal HRrecovery (≤12 bpm reduction one minute after the cessation of exercise).[33] Shetler et al. studied 2,193 patients for thirteen years and found that a HRrecovery of ≤22 bpm after two minutes "best identified high-risk patients".[33] They also found that while HRrecovery had significant prognostic value it had no diagnostic value.[33]

text: Development[edit]

text: The human heart beats more than 3.5 billion times in an average lifetime.

text: The heartbeat of a human embryo begins at approximately 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy in the medical community. The electrical depolarizations that trigger cardiac myocytes to contract arise spontaneously within the myocyte itself. The heartbeat is initiated in the pacemaker regions and spreads to the rest of the heart through a conduction pathway. Pacemaker cells develop in the primitive atrium and the sinus venosus to form the sinoatrial node and the atrioventricular node respectively. Conductive cells develop the bundle of His and carry the depolarization into the lower heart.

text: The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (BPM). The embryonic heart rate then accelerates linearly for the first month of beating, peaking at 165-185 BPM during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 BPM per day, or about 10 BPM every three days, an increase of 100 BPM in the first month.[34]

text: After peaking at about 9.2 weeks after the LMP, it decelerates to about 150 BPM (+/-25 BPM) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 BPM) BPM at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is:

text:
A
g
e

i
n

d
a
y
s

=

E
H
R

(
0.3
)
+
6

{\displaystyle \mathrm {Age\ in\ days} =\ \mathrm {EHR} (0.3)+6}

text: There is no difference in male and female heart rates before birth.[35]

text: Clinical significance[edit]

text: Measurement[edit]

text: Manual measurement[edit]

text: Heart rate is measured by finding the pulse of the heart. This pulse rate can be found at any point on the body where the artery's pulsation is transmitted to the surface by pressuring it with the index and middle fingers; often it is compressed against an underlying structure like bone. (A good area is on the neck, under the corner of the jaw.) The thumb should not be used for measuring another person's heart rate, as its strong pulse may interfere with the correct perception of the target pulse.

text: The radial artery is the easiest to use to check the heart rate. However, in emergency situations the most reliable arteries to measure heart rate are carotid arteries. This is important mainly in patients with atrial fibrillation, in whom heart beats are irregular and stroke volume is largely different from one beat to another. In those beats following a shorter diastolic interval left ventricle doesn't fill properly, stroke volume is lower and pulse wave is not strong enough to be detected by palpation on a distal artery like the radial artery. It can be detected, however, by doppler.[36][37]

text: Possible points for measuring the heart rate are:

text:
The ventral aspect of the wrist on the side of the thumb (radial artery).
The ulnar artery.
The neck (carotid artery).
The inside of the elbow, or under the biceps muscle (brachial artery).
The groin (femoral artery).
Behind the medial malleolus on the feet (posterior tibial artery).
Middle of dorsum of the foot (dorsalis pedis).
Behind the knee (popliteal artery).
Over the abdomen (abdominal aorta).
The chest (apex of the heart), which can be felt with one's hand or fingers. It is also possible to auscultate the heart using a stethoscope.
The temple (superficial temporal artery).
The lateral edge of the mandible (facial artery).
The side of the head near the ear (posterior auricular artery).

text: Electronic measurement[edit]

text: A more precise method of determining heart rate involves the use of an electrocardiograph, or ECG (also abbreviated EKG). An ECG generates a pattern based on electrical activity of the heart, which closely follows heart function. Continuous ECG monitoring is routinely done in many clinical settings, especially in critical care medicine. On the ECG, instantaneous heart rate is calculated using the R wave-to-R wave (RR) interval and multiplying/dividing in order to derive heart rate in heartbeats/min. Multiple methods exist:

text:
HR = 1,500/(RR interval in millimeters)
HR = 60/(RR interval in seconds)
HR = 300/number of "large" squares between successive R waves.
HR= 1,500 number of large blocks

text: Heart rate monitors allow measurements to be taken continuously and can be used during exercise when manual measurement would be difficult or impossible (such as when the hands are being used). Various commercial heart rate monitors are also available. Some monitors, used during sport, consist of a chest strap with electrodes. The signal is transmitted to a wrist receiver for display.

text: Alternative methods of measurement include pulse oximetry and seismocardiography.[38]

text: Tachycardia[edit]

text: Tachycardia is a resting heart rate more than 100 beats per minute. This number can vary as smaller people and children have faster heart rates than average adults.

text: Physiological conditions where tachycardia occurs:

text:
Exercise
Pregnancy
Emotional conditions such as anxiety or stress.

text: Pathological conditions where tachycardia occurs:

text:
Sepsis
Fever
Anemia
Hypoxia
Hyperthyroidism
Hypersecretion of catecholamines
Cardiomyopathy
Valvular heart diseases
Acute Radiation Syndrome

text: Bradycardia[edit]

text: Bradycardia was defined as a heart rate less than 60 beats per minute when textbooks asserted that the normal range for heart rates was 60–100 BPM. The normal range has since been revised in textbooks to 50–90 BPM for a human at total rest. Setting a lower threshold for bradycardia prevents misclassification of fit individuals as having a pathologic heart rate. The normal heart rate number can vary as children and adolescents tend to have faster heart rates than average adults. Bradycardia may be associated with medical conditions such as hypothyroidism.

text: Trained athletes tend to have slow resting heart rates, and resting bradycardia in athletes should not be considered abnormal if the individual has no symptoms associated with it. For example, Miguel Indurain, a Spanish cyclist and five time Tour de France winner, had a resting heart rate of 28 beats per minute,[39] one of the lowest ever recorded in a healthy human. Daniel Green achieved the world record for the slowest heartbeat in a healthy human with a heart rate of just 26 bpm in 2014.[40]

text: Arrhythmia[edit]

text: Arrhythmias are abnormalities of the heart rate and rhythm (sometimes felt as palpitations). They can be divided into two broad categories: fast and slow heart rates. Some cause few or minimal symptoms. Others produce more serious symptoms of lightheadedness, dizziness and fainting.

text: Correlation with cardiovascular mortality risk[edit]

text: This section needs more medical references for verification or relies too heavily on primary sources. Please review the contents of the section and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed. (July 2015)

text: A number of investigations indicate that faster resting heart rate has emerged as a new risk factor for mortality in homeothermic mammals, particularly cardiovascular mortality in human beings. Faster heart rate may accompany increased production of inflammation molecules and increased production of reactive oxygen species in cardiovascular system, in addition to increased mechanical stress to the heart. There is a correlation between increased resting rate and cardiovascular risk. This is not seen to be "using an allotment of heart beats" but rather an increased risk to the system from the increased rate.[41]

text: An Australian-led international study of patients with cardiovascular disease has shown that heart beat rate is a key indicator for the risk of heart attack. The study, published in The Lancet (September 2008) studied 11,000 people, across 33 countries, who were being treated for heart problems. Those patients whose heart rate was above 70 beats per minute had significantly higher incidence of heart attacks, hospital admissions and the need for surgery. Higher heart rate is thought to be correlated with an increase in heart attack and about a 46 percent increase in hospitalizations for non-fatal or fatal heart attack.[42]

text: Other studies have shown that a high resting heart rate is associated with an increase in cardiovascular and all-cause mortality in the general population and in patients with chronic disease.[43] A faster resting heart rate is associated with shorter life expectancy[44] and is considered a strong risk factor for heart disease and heart failure,[45] independent of level of physical fitness.[46] Specifically, a resting heart rate above 65 beats per minute has been shown to have a strong independent effect on premature mortality; every 10 beats per minute increase in resting heart rate has been shown to be associated with a 10–20% increase in risk of death.[47] In one study, men with no evidence of heart disease and a resting heart rate of more than 90 beats per minute had a five times higher risk of sudden cardiac death.[45] Similarly, another study found that men with resting heart rates of over 90 beats per minute had an almost two-fold increase in risk for cardiovascular disease mortality; in women it was associated with a three-fold increase.[44]

text: Given these data, heart rate should be considered in the assessment of cardiovascular risk, even in apparently healthy individuals.[48] Heart rate has many advantages as a clinical parameter: It is inexpensive and quick to measure and is easily understandable.[49] Although the accepted limits of heart rate are between 60 and 100 beats per minute, this was based for convenience on the scale of the squares on electrocardiogram paper; a better definition of normal sinus heart rate may be between 50 and 90 beats per minute.[50]

text: Standard textbooks of physiology and medicine mention that heart rate (HR) is readily calculated from the ECG as follows:

text: Lifestyle and pharmacological regimens may be beneficial to those with high resting heart rates.[47] Exercise is one possible measure to take when an individual's heart rate is higher than 80 beats per minute.[49][51] Diet has also been found to be beneficial in lowering resting heart rate: In studies of resting heart rate and risk of death and cardiac complications on patients with type 2 diabetes, legumes were found to lower resting heart rate.[52] This is thought to occur because in addition to the direct beneficial effects of legumes, they also displace animal proteins in the diet, which are higher in saturated fat and cholesterol.[52]

text: A very slow heart rate (bradycardia) may be associated with heart block.[medical citation needed] It may also arise from autonomous nervous system impairment.[medical citation needed]


document_title: The Better Angels of Our Nature

question_text: by the better angels of our nature meaning

text: The Better Angels of Our Nature

text: Thesis[edit]

text: The book's title was taken from the ending of U.S. President Abraham Lincoln's first inaugural address. Pinker uses the phrase as a metaphor for four human motivations — empathy, self-control, the "moral sense," and reason — that, he writes, can "orient us away from violence and towards cooperation and altruism."[3]:xxv

text: Pinker presents a large amount of data (and statistical analysis thereof) that, he argues, demonstrate that violence has been in decline over millennia and that the present is probably the most peaceful time in the history of the human species. The decline in violence, he argues, is enormous in magnitude, visible on both long and short time scales, and found in many domains, including military conflict, homicide, genocide, torture, criminal justice, and treatment of children, homosexuals, animals and racial and ethnic minorities. He stresses that "The decline, to be sure, has not been smooth; it has not brought violence down to zero; and it is not guaranteed to continue."[4]

text: Pinker argues that the radical declines in violent behavior that he documents do not result from major changes in human biology or cognition. He specifically rejects the view that humans are necessarily violent, and thus have to undergo radical change in order to become more peaceable. However, Pinker also rejects what he regards as the simplistic nature versus nurture argument, which would imply that the radical change must therefore have come purely from external ("nurture") sources. Instead, he argues: "The way to explain the decline of violence is to identify the changes in our cultural and material milieu that have given our peaceable motives the upper hand."[4]

text: Pinker identifies five "historical forces" that have favored "our peaceable motives" and "have driven the multiple declines in violence."[3] They are:

text:
The Leviathan – the rise of the modern nation-state and judiciary "with a monopoly on the legitimate use of force," which "can defuse the [individual] temptation of exploitative attack, inhibit the impulse for revenge, and circumvent ... self-serving biases."
Commerce – the rise of "technological progress [allowing] the exchange of goods and services over longer distances and larger groups of trading partners," so that "other people become more valuable alive than dead" and "are less likely to become targets of demonization and dehumanization."
Feminization – increasing respect for "the interests and values of women."
Cosmopolitanism – the rise of forces such as literacy, mobility, and mass media, which "can prompt people to take the perspectives of people unlike themselves and to expand their circle of sympathy to embrace them."
The Escalator of Reason – an "intensifying application of knowledge and rationality to human affairs," which "can force people to recognize the futility of cycles of violence, to ramp down the privileging of their own interests over others', and to reframe violence as a problem to be solved rather than a contest to be won."[3]:xxvi

text: Outline of the book[edit]

text: The first section of the book, chapters 2 through 7, seeks to demonstrate and to analyze historical trends related to declines of violence on different scales. Chapter 8 discusses five "inner demons" - psychological systems that can lead to violence. Chapter 9 examines four "better angels" or motives that can incline people away from violence. The last chapter examines the five historical forces listed above that have led to declines in violence.

text: Six trends of declining violence (Chapters 2 through 7)[edit]

text:
The Pacification Process: Pinker describes this as the transition from "the anarchy of hunting, gathering, and horticultural societies ... to the first agricultural civilizations with cities and governments, beginning around five thousand years ago" which brought "a reduction in the chronic raiding and feuding that characterized life in a state of nature and a more or less fivefold decrease in rates of violent death."[3]:xxiv
The Civilizing Process: Pinker argues that "between the late Middle Ages and the 20th century, European countries saw a tenfold-to-fiftyfold decline in their rates of homicide." He attributes the idea of the Civilizing Process to the sociologist Norbert Elias, who "attributed this surprising decline to the consolidation of a patchwork of feudal territories into large kingdoms with centralized authority and an infrastructure on commerce."[3]
The Humanitarian Revolution – Pinker attributes this term and concept to the historian Lynn Hunt. He says this revolution "unfolded on the [shorter] scale of centuries and took off around the time of the Age of Reason and the European Enlightenment in the 17th and 18th centuries." Although he also points to historical antecedents and to "parallels elsewhere in the world," he writes: "It saw the first organized movements to abolish slavery, dueling, judicial torture, superstitious killing, sadistic punishment, and cruelty to animals, together with the first stirrings of systematic pacifism."[3]
The Long Peace: a term he attributes to the historian John Lewis Gaddis's The Long Peace: Inquiries into the history of the Cold War. This fourth "major transition," Pinker says, "took place after the end of World War II." During it, he says, "the great powers, and the developed states in general, have stopped waging war on one another."[3]
The New Peace: Pinker calls this trend "more tenuous," but "since the end of the Cold War in 1989, organized conflicts of all kinds - civil wars, genocides, repression by autocratic governments, and terrorist attacks - have declined throughout the world."[3]
The Rights Revolutions: The postwar period has seen, Pinker argues, "a growing revulsion against aggression on smaller scales, including violence against ethnic minorities, women, children, homosexuals, and animals. These spin-offs from the concept of human rights—civil rights, women's rights, children's rights, gay rights, and animal rights—were asserted in a cascade of movements from the late 1950s to the present day."[3]:xxiv–xxv

text: Five inner demons (Chapter 8)[edit]

text: Pinker rejects what he calls the "Hydraulic Theory of Violence" – the idea "that humans harbor an inner drive toward aggression (a death instinct or thirst for blood), which builds up inside us and must periodically be discharged. Nothing could be further from contemporary scientific understanding of the psychology of violence." Instead, he argues, research suggests that "aggression is not a single motive, let alone a mounting urge. It is the output of several psychological systems that differ in their environmental triggers, their internal logic, their neurological basis, and their social distribution." He examines five such systems:

text:
Predatory or Practical Violence: violence "deployed as a practical means to an end"[3]:613
Dominance: the "urge for authority, prestige, glory, and power." Pinker argues that dominance motivations can occur within individuals and coalitions of "racial, ethnic, religious, or national groups"[3]:631
Revenge: the "moralistic urge toward retribution, punishment, and justice"[3]:639
Sadism: the "deliberate infliction of pain for no purpose but to enjoy a person's suffering..."[3]:660
Ideology: a "shared belief system, usually involving a vision of utopia, that justifies unlimited violence in pursuit of unlimited good."[3]

text: Four better angels (Chapter 9)[edit]

text: Pinker examines four motives that "can orient [humans] away from violence and towards cooperation and altruism." He identifies:

text:
Empathy: which "prompts us to feel the pain of others and to align their interests with our own."
Self-Control: which "allows us to anticipate the consequences of acting on our impulses and to inhibit them accordingly."
The Moral Sense: which "sanctifies a set of norms and taboos that govern the interactions among people in a culture." These sometimes decrease violence but can also increase it "when the norms are tribal, authoritarian, or puritanical."
Reason: which "allows us to extract ourselves from our parochial vantage points."

text: In this chapter Pinker also examines and partially rejects the idea that humans have evolved in the biological sense to become less violent.

text: Influences[edit]

text: Because of the interdisciplinary nature of the book Pinker uses a range of sources from different fields. Particular attention is paid to philosopher Thomas Hobbes who Pinker argues has been undervalued. Pinker's use of "un-orthodox" thinkers follows directly from his observation that the data on violence contradict our current expectations. In an earlier work Pinker characterized the general misunderstanding concerning Hobbes:

text: Hobbes is commonly interpreted as proposing that man in a state of nature was saddled with an irrational impulse for hatred and destruction. In fact his analysis is more subtle, and perhaps even more tragic for he showed how the dynamics of violence fall out of interactions among rational and self-interested agents.[3]:318

text: Pinker also references ideas from occasionally overlooked contemporary academics, for example the works of political scientist John Mueller and sociologist Norbert Elias, among others. The extent of Elias' influence on Pinker can be adduced from the title of Chapter 3, which is taken from the title of Elias' seminal The Civilizing Process.[5] Pinker also draws upon the work of international relations scholar Joshua Goldstein. They co-wrote a New York Times op-ed article titled 'War Really Is Going Out of Style' that summarizes many of their shared views,[6] and appeared together at Harvard's Institute of Politics to answer questions from academics and students concerning their similar thesis.[7]

text: Reception[edit]

text: Praise[edit]

text: Bill Gates considers the book one of the most important books he's ever read,[8] and on the BBC program Desert Island Discs he selected the book as the one he would take with him to a deserted island.[9] He has written that "Steven Pinker shows us ways we can make those positive trajectories a little more likely. That's a contribution, not just to historical scholarship, but to the world."[8] After Gates recommended the book as a graduate present in May 2017, the book re-entered the bestseller list.[10]

text: The philosopher Peter Singer gave the book a positive review in The New York Times. Singer concludes: "[It] is a supremely important book. To have command of so much research, spread across so many different fields, is a masterly achievement. Pinker convincingly demonstrates that there has been a dramatic decline in violence, and he is persuasive about the causes of that decline."[11]

text: Political scientist Robert Jervis, in a long review for The National Interest, states that Pinker "makes a case that will be hard to refute. The trends are not subtle – many of the changes involve an order of magnitude or more. Even when his explanations do not fully convince, they are serious and well-grounded."[12]

text: In a review for The American Scholar, Michael Shermer writes, "Pinker demonstrates that long-term data trumps anecdotes. The idea that we live in an exceptionally violent time is an illusion created by the media’s relentless coverage of violence, coupled with our brain’s evolved propensity to notice and remember recent and emotionally salient events. Pinker’s thesis is that violence of all kinds—from murder, rape, and genocide to the spanking of children to the mistreatment of blacks, women, gays, and animals—has been in decline for centuries as a result of the civilizing process... Picking up Pinker’s 832-page opus feels daunting, but it’s a page-turner from the start."[13]

text: In The Guardian, Cambridge University political scientist David Runciman writes, "I am one of those who like to believe that... the world is just as dangerous as it has always been. But Pinker shows that for most people in most ways it has become much less dangerous." Runciman concludes "everyone should read this astonishing book."[14]

text: In a later review for The Guardian, written when the book was shortlisted for the Royal Society Winton Prize for Science Books, Tim Radford wrote, "in its confidence and sweep, the vast timescale, its humane standpoint and its confident world-view, it is something more than a science book: it is an epic history by an optimist who can list his reasons to be cheerful and support them with persuasive instances.... I don't know if he's right, but I do think this book is a winner."[15]

text: Adam Lee writes, in a blog review for Big Think, that "even people who are inclined to reject Pinker's conclusions will sooner or later have to grapple with his arguments."[16]

text: In a long review in The Wilson Quarterly, psychologist Vaughan Bell calls it "an excellent exploration of how and why violence, aggression, and war have declined markedly, to the point where we live in humanity’s most peaceful age.... [P]owerful, mind changing, and important."[17]

text: In a long review for the Los Angeles Review of Books, anthropologist Christopher Boehm, Professor of Biological Sciences at the University of Southern California and co-director of the USC Jane Goodall Research Center, called the book "excellent and important."[18]

text: Political scientist James Q. Wilson, in the Wall Street Journal, called the book "a masterly effort to explain what Mr. Pinker regards as one of the biggest changes in human history: We kill one another less frequently than before. But to give this project its greatest possible effect, he has one more book to write: a briefer account that ties together an argument now presented in 800 pages and that avoids the few topics about which Mr. Pinker has not done careful research." Specifically, the assertions to which Wilson objected were Pinker's writing that (in Wilson's summation), "George W. Bush 'infamously' supported torture; John Kerry was right to think of terrorism as a 'nuisance"; 'Palestinian activist groups' have disavowed violence and now work at building a 'competent government.' Iran will never use its nuclear weapons... [and] Mr. Bush... is 'unintellectual.' " [19]

text: Brenda Maddox, in The Telegraph, called the book "utterly convincing" and "well-argued."[20]

text: Clive Cookson, reviewing it in the Financial Times, called it "a marvelous synthesis of science, history and storytelling, demonstrating how fortunate the vast majority of us are today to experience serious violence only through the mass media."[21]

text: The science journalist John Horgan called it "a monumental achievement" that "should make it much harder for pessimists to cling to their gloomy vision of the future" in a largely positive review in Slate.[22]

text: In The Huffington Post, Neil Boyd, Professor and Associate Director of the School of Criminology at Simon Fraser University, strongly defended the book against its critics, saying:

text: While there are a few mixed reviews (James Q. Wilson in the Wall Street Journal comes to mind), virtually everyone else either raves about the book or expresses something close to ad hominem contempt and loathing... At the heart of the disagreement are competing conceptions of research and scholarship, perhaps epistemology itself. How are we to study violence and to assess whether it has been increasing or decreasing? What analytic tools do we bring to the table? Pinker, sensibly enough chooses to look at the best available evidence regarding the rate of violent death over time, in pre-state societies, in medieval Europe, in the modern era, and always in a global context; he writes about inter-state conflicts, the two world wars, intrastate conflicts, civil wars, and homicides. In doing so, he takes a critical barometer of violence to be the rate of homicide deaths per 100,000 citizens... Pinker's is a remarkable book, extolling science as a mechanism for understanding issues that are all too often shrouded in unstated moralities, and highly questionable empirical assumptions. Whatever agreements or disagreements may spring from his specifics, the author deserves our respect, gratitude, and applause."[23]

text: The book also saw positive reviews from The Spectator,[24]  and The Independent.[25]

text: Criticism[edit]

text: R. Brian Ferguson, professor of Anthropology at Rutgers University–Newark, has challenged Pinker's archaeological evidence for the frequency of war in prehistoric societies, which he contends "consists of cherry-picked cases with high casualties, clearly unrepresentative of history in general."[26] Whereas "[b]y considering the total archaeological record of prehistoric populations of Europe and the Near East up to the Bronze Age, evidence clearly demonstrates that war began sporadically out of warless condition, and can be seen in varying trajectories in different areas, to develop over time as societies become larger, more sedentary, more complex, more bounded, more hierarchical, and in one critically important region, impacted by an expanding state." Ferguson's examination contradicts Pinker's claim that violence has declined under civilization, indicating the opposite is true.

text: Despite recommending the book as worth reading, the economist Tyler Cowen was skeptical of Pinker's analysis of the centralization of the use of violence in the hands of the modern nation state.[27]

text: In his review of the book in Scientific American, psychologist Robert Epstein criticizes Pinker's use of relative violent death rates, that is, of violent deaths per capita, as an appropriate metric for assessing the emergence of humanity's "better angels." Instead, Epstein believes that the correct metric is the absolute number of deaths at a given time. Epstein also accuses Pinker of an over-reliance on historical data, and argues that he has fallen prey to confirmation bias, leading him to focus on evidence that supports his thesis while ignoring research that does not.[28]

text: Several negative reviews have raised criticisms related to Pinker's humanism and atheism. John N. Gray, in a critical review of the book in Prospect, writes, "Pinker's attempt to ground the hope of peace in science is profoundly instructive, for it testifies to our enduring need for faith."[29]

text: New York Times columnist Ross Douthat, while "broadly convinced by the argument that our current era of relative peace reflects a longer term trend away from violence, and broadly impressed by the evidence that Pinker marshals to support this view," offered a list of criticisms and concludes Pinker assumes almost all the progress starts with "the Enlightenment, and all that came before was a long medieval dark."[30][31]

text: Theologian David Bentley Hart wrote that "one encounters [in Pinker's book] the ecstatic innocence of a faith unsullied by prudent doubt." Furthermore, he says, "it reaffirms the human spirit's lunatic and heroic capacity to believe a beautiful falsehood, not only in excess of the facts, but in resolute defiance of them." Hart continues:

text: In the end, what Pinker calls a "decline of violence" in modernity actually has been, in real body counts, a continual and extravagant increase in violence that has been outstripped by an even more exorbitant demographic explosion. Well, not to put too fine a point on it: So what? What on earth can he truly imagine that tells us about "progress" or "Enlightenment" or about the past, the present, or the future? By all means, praise the modern world for what is good about it, but spare us the mythology.[32]

text: Craig S. Lerner, a professor at George Mason University School of Law, in an appreciative but ultimately negative review in the Claremont Review of Books does not dismiss the claim of declining violence, writing, "let's grant that the 65 years since World War II really are among the most peaceful in human history, judged by the percentage of the globe wracked by violence and the percentage of the population dying by human hand," but disagrees with Pinker's explanations and concludes that "Pinker depicts a world in which human rights are unanchored by a sense of the sacredness and dignity of human life, but where peace and harmony nonetheless emerge. It is a future—mostly relieved of discord, and freed from an oppressive God—that some would regard as heaven on earth. He is not the first and certainly not the last to entertain hopes disappointed so resolutely by the history of actual human beings."[33] In a sharp exchange in the correspondence section of the Spring 2012 issue, Pinker attributes to Lerner a "theo-conservative agenda" and accuses him of misunderstanding a number of points, notably Pinker's repeated assertion that "historical declines of violence are 'not guaranteed to continue.'" Lerner, in his response, says Pinker's "misunderstanding of my review is evident from the first sentence of his letter" and questions Pinker's objectivity and refusal to "acknowledge the gravity" of issues he raises.[34]

text: Professor emeritus of finance and media analyst Edward S. Herman of the University of Pennsylvania, together with independent journalist David Peterson, wrote detailed negative reviews of the book for the International Socialist Review [35] and for The Public Intellectuals Project, concluding it "is a terrible book, both as a technical work of scholarship and as a moral tract and guide.  But it is extremely well-attuned to the demands of U.S. and Western elites at the start of the 21st century." Herman and Peterson take issue with Pinker's idea of a 'Long Peace' since World War Two: "Pinker contends not only that the 'democracies avoid disputes with each other,' but that they 'tend to stay out of disputes across the board...' This will surely come as a surprise to the many victims of US assassinations, sanctions, subversions, bombings, and invasions since 1945."[36]

text: Two critical reviews have been related to postmodern approaches. Elizabeth Kolbert wrote a critical review in The New Yorker,[37] to which Pinker posted a reply.[38] Kolbert states that "The scope of Pinker's attentions is almost entirely confined to Western Europe." Pinker replies that his book has sections on "Violence Around the World", "Violence in These United States", and the history of war in the Ottoman Empire, Russia, Japan, and China. Kolbert states that "Pinker is virtually silent about Europe’s bloody colonial adventures." Pinker replies that "a quick search would have turned up more than 25 places in which the book discusses colonial conquests, wars, enslavements, and genocides." Kolbert concludes, "Name a force, a trend, or a ‘better angel’ that has tended to reduce the threat, and someone else can name a force, a trend, or an ‘inner demon’ pushing back the other way." Pinker calls this "the postmodernist sophistry that The New Yorker so often indulges when reporting on science."

text: An explicitly postmodern critique—or more precisely, one based on perspectivism—is made at CTheory by Ben Laws, who argues that "if we take a 'perspectivist' stance in relation to matters of truth would it not be possible to argue the direct inverse of Pinker's historical narrative of violence? Have we in fact become even more violent over time? Each interpretation could invest a certain stake in 'truth' as something fixed and valid—and yet, each view could be considered misguided." Pinker argues in his FAQ page that economic inequality, like other forms of "metaphorical" violence, "may be deplorable, but to lump it together with rape and genocide is to confuse moralization with understanding. Ditto for underpaying workers, undermining cultural traditions, polluting the ecosystem, and other practices that moralists want to stigmatize by metaphorically extending the term violence to them. It's not that these aren't bad things, but you can't write a coherent book on the topic of 'bad things.' ... physical violence is a big enough topic for one book (as the length of Better Angels makes clear). Just as a book on cancer needn't have a chapter on metaphorical cancer, a coherent book on violence can't lump together genocide with catty remarks as if they were a single phenomenon." Quoting this, Laws argues that Pinker suffers from "a reductive vision of what it means to be violent."[39]

text: John Arquilla of the Naval Postgraduate School criticized the book in Foreign Policy for using statistics that he said did not accurately represent the threats of civilians dying in war:

text: The problem with the conclusions reached in these studies is their reliance on "battle death" statistics. The pattern of the past century—one recurring in history—is that the deaths of noncombatants due to war has risen, steadily and very dramatically. In World War I, perhaps only 10 percent of the 10 million-plus who died were civilians. The number of noncombatant deaths jumped to as much as 50 percent of the 50 million-plus lives lost in World War II, and the sad toll has kept on rising ever since".[40]

text: Stephen Corry, director of the charity Survival International, criticized the book from the perspective of indigenous people's rights. He asserts that Pinker's book "promotes a fictitious, colonialist image of a backward 'Brutal Savage', which pushes the debate on tribal peoples' rights back over a century and [which] is still used to justify their destruction."[41]

text: Anthropologist Rahul Oka has suggested that the apparent reduction in violence is just a scaling issue. Wars can be expected to kill larger percentages of smaller populations. As the population grows, fewer warriors are needed, proportionally.[42]

text: Sinisa Malesevic has argued that Pinker and other similar theorists, such as Azar Gat, articulate a false vision of human beings as being genetically predisposed to violence, while they focus on the last forty to fifty years.[43]

text: Statistician and philosophical essayist Nassim Taleb used the term "Pinker Problem" to describe errors in sampling under conditions of uncertainty after corresponding with Pinker regarding the theory of great moderation. "Pinker doesn’t have a clear idea of the difference between science and journalism, or the one between rigorous empiricism and anecdotal statements. Science is not about making claims about a sample, but using a sample to make general claims and discuss properties that apply outside the sample."[44] In a reply, Pinker denied that his arguments had any similarity to "great moderation" arguments about financial markets, and states that "Taleb’s article implies that Better Angels consists of 700 pages of fancy statistical extrapolations which lead to the conclusion that violent catastrophes have become impossible... [but] the statistics in the book are modest and almost completely descriptive" and "the book explicitly, adamantly, and repeatedly denies that major violent shocks cannot happen in the future."[45] Taleb with statistician and probabilist Pasquale Cirillo went on to publish a formal refutation in the journal Physica A: Statistical Mechanics and its Applications where they investigate the theses of “long peace” and drop in violence and find that these are statistically invalid and resulting from flawed and naive methodologies, incompatible with fat tails and non-robust to minor changes in data formatting and methodologies. They propose an alternative methodology to look at violence in particular, and other aspects of quantitative historiography in general in a way compatible with statistical inference, which needs to accommodate the fat-tailedness of the data and the unreliability of the reports of conflicts.[46][47]

text: In March of 2018, the academic journal Historical Reflections published the first issue of their 44th volume entirely devoted to responding to Pinker's book in light of its significant influence on the wider culture, such as its appraisal by Bill Gates. The issue contains essays by twelve historians on Pinker's thesis, and the editors of the issue Mark S. Micale, Professor of History at the University of Illinois, and Philip Dwyer, Professor of History at Newcastle University write in the introductory paper that "Not all of the scholars included in this journal agree on everything, but the overall verdict is that Pinker’s thesis, for all the stimulus it may have given to discussions around violence, is seriously, if not fatally, flawed. The problems that come up time and again are: the failure to genuinely engage with historical methodologies; the unquestioning use of dubious sources; the tendency to exaggerate the violence of the past in order to contrast it with the supposed peacefulness of the modern era; the creation of a number of straw men, which Pinker then goes on to debunk; and its extraordinarily Western-centric, not to say Whiggish, view of the world."[48]

text: Awards and honors[edit]

text:
2011 New York Times Notable Books of 2011[49]
2012 Samuel Johnson Prize, shortlist[50]
2012 Royal Society Winton Prize for Science Books, shortlist[51]
2012-2013 Gifford Lectures at the University of Edinburgh[52]
2015 Mark Zuckerberg book club selection, January[53]

text: Media[edit]

text:
"Prof. Steven Pinker - The Better Angels of Our Nature: A History of Violence and Humanity" on YouTube. The 2013 Gifford Lecture at the University of Edinburgh.
Pinker discusses The Better Angels of Our Nature with psychologist Paul Bloom on bloggingheads.tv, December 8, 2012.[54]
Pinker debates why violence has declined with Economist Judith Marquand, BHA Chief Executive Andrew Copson and BBC broadcaster Roger Bolton at the Institute of Art and Ideas.[55]