View source for Blood pressure

{{short description|Pressure exerted by circulating blood upon the walls of arteries}}
{{Other uses|Blood pressure (disambiguation)}}
{{Infobox diagnostic
| name = Blood pressure
| image = Blood pressure monitoring.jpg
| alt = 
| caption = A healthcare worker measuring blood pressure using a [[sphygmomanometer]].
| DiseasesDB = 
| ICD10 = 
| ICD9 = 
| ICDO = 
| MedlinePlus = 007490
| eMedicine = 
| MeshID = D001794
| LOINC = {{LOINC|35094-2}}
| HCPCSlevel2 = 
| OPS301 = 
| reference_range = 
}}

'''Blood pressure''' ('''BP''') is the [[pressure]] of [[Circulatory system|circulating blood]] against the walls of [[blood vessel]]s. Most of this pressure results from the [[heart]] pumping blood through the [[circulatory system]]. When used without qualification, the term "blood pressure" refers to the pressure in a [[brachial artery]], where it is most commonly measured. Blood pressure is usually expressed in terms of the '''systolic pressure''' (maximum pressure during one [[Cardiac cycle|heartbeat]]) over '''diastolic pressure''' (minimum pressure between two heartbeats) in the [[cardiac cycle]]. It is measured in [[Millimetre of mercury|millimeters of mercury (mmHg)]] above the surrounding [[atmospheric pressure]], or in [[Pascal (unit)|kilopascals]] (kPa). The difference between the systolic and diastolic pressures is known as [[pulse pressure]],<ref name="Homan Cichowski 2019">{{cite book | vauthors = Homan TD, Bordes SJ, Cichowski E | chapter = Physiology, Pulse Pressure | date = 12 July 2022 | title = StatPearls [Internet]. | location = Treasure Island (FL) | publisher = StatPearls Publishing | pmid = 29494015 | chapter-url = https://www.ncbi.nlm.nih.gov/books/NBK482408/ | via = NCBI Bookshelf | access-date = 2019-07-21 }}</ref> while the average pressure during a cardiac cycle is known as [[mean arterial pressure]].<ref name="Mayet Hughes 2003 pp. 1104–9">{{cite journal | vauthors = Mayet J, Hughes A | title = Cardiac and vascular pathophysiology in hypertension | journal = Heart | volume = 89 | issue = 9 | pages = 1104–1109 | date = September 2003 | pmid = 12923045 | pmc = 1767863 | doi = 10.1136/heart.89.9.1104 }}</ref>

Blood pressure is one of the [[vital signs]]—together with [[respiratory rate]], [[heart rate]], [[Oxygen saturation (medicine)|oxygen saturation]], and [[body temperature]]—that healthcare professionals use in evaluating a patient's health. Normal resting blood pressure in an adult is approximately {{convert|120|mmHg}} systolic over {{convert|80|mmHg}} diastolic, denoted as "120/80&nbsp;mmHg". Globally, the average blood pressure, age standardized, has remained about the same since 1975 to the present,{{when?|date=January 2025}} at approximately 127/79 mmHg in men and 122/77 mmHg in women, although these average data mask significantly diverging regional trends.<ref>{{cite journal | title = Worldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19·1 million participants | journal = Lancet | volume = 389 | issue = 10064 | pages = 37–55 | date = January 2017 | pmid = 27863813 | pmc = 5220163 | doi = 10.1016/S0140-6736(16)31919-5 | vauthors = Zhou B, Bentham J, Di Cesare M, Bixby H, Danaei G, Cowan MJ, etal | collaboration = NCD Risk Factor Collaboration (NCD-RisC) }}</ref>

Traditionally, a health-care worker measured blood pressure non-invasively by [[auscultation]] (listening) through a [[stethoscope]] for sounds in one arm's [[artery]] as the artery is squeezed, closer to the heart, by an [[aneroid gauge]] or a [[mercury (element)|mercury-tube]] [[sphygmomanometer]].<ref name="Booth1977"/> Auscultation is still generally considered to be the gold standard of accuracy for non-invasive blood pressure readings in clinic.<ref>{{cite journal | vauthors = Grim CE, Grim CM | title = Auscultatory BP: still the gold standard | journal = Journal of the American Society of Hypertension | volume = 10 | issue = 3 | pages = 191–193 | date = March 2016 | pmid = 26839183 | doi = 10.1016/j.jash.2016.01.004 }}</ref> However, semi-automated methods have become common, largely due to concerns about potential mercury toxicity,<ref>{{cite journal | vauthors = O'Brien E | title = Blood pressure measurement is changing! | journal = Heart | volume = 85 | issue = 1 | pages = 3–5 | date = January 2001 | pmid = 11119446 | pmc = 1729570 | doi = 10.1136/heart.85.1.3 }}</ref> although cost, ease of use and applicability to [[ambulatory blood pressure]] or home blood pressure measurements have also influenced this trend.<ref name=":0">{{cite journal | vauthors = Ogedegbe G, Pickering T | title = Principles and techniques of blood pressure measurement | journal = Cardiology Clinics | volume = 28 | issue = 4 | pages = 571–586 | date = November 2010 | pmid = 20937442 | pmc = 3639494 | doi = 10.1016/j.ccl.2010.07.006 }}</ref> Early automated alternatives to mercury-tube sphygmomanometers were often seriously inaccurate, but modern devices validated to international standards achieve an average difference between two standardized reading methods of 5&nbsp;mm Hg or less, and a [[standard deviation]] of less than 8&nbsp;mm Hg.<ref name=":0" /> Most of these semi-automated methods measure blood pressure using oscillometry (measurement by a pressure transducer in the cuff of the device of small oscillations of intra-cuff pressure accompanying heartbeat-induced changes in the volume of each pulse).<ref>{{cite journal | vauthors = Alpert BS, Quinn D, Gallick D | title = Oscillometric blood pressure: a review for clinicians | journal = Journal of the American Society of Hypertension | volume = 8 | issue = 12 | pages = 930–938 | date = December 2014 | pmid = 25492837 | doi = 10.1016/j.jash.2014.08.014 }}</ref>

Blood pressure is influenced by [[cardiac output]], [[systemic vascular resistance]], blood volume and [[arterial stiffness]], and varies depending on person's situation, emotional state, activity and relative health or disease state. In the short term, blood pressure is [[Homeostasis#Arterial blood pressure|regulated]] by [[baroreceptor]]s, which act via the brain to influence the [[nervous system|nervous]] and the [[endocrine system|endocrine]] systems.

Blood pressure that is too low is called [[hypotension]], pressure that is consistently too high is called [[hypertension]], and normal pressure is called normotension.<ref>{{Cite book|title=Dorland's illustrated medical dictionary|date=2012|publisher=Saunders/Elsevier| veditors = Newman WA |isbn=978-1-4160-6257-8|edition=32nd|location=Philadelphia, PA|oclc=706780870}}</ref> Both hypertension and hypotension have many causes and may be of sudden onset or of long duration. Long-term hypertension is a risk factor for many diseases, including [[stroke]], [[heart disease]], and [[kidney failure]]. Long-term hypertension is more common than long-term hypotension.
{{TOC limit|3}}

==Classification, normal and abnormal values==
===Systemic arterial pressure===
Blood pressure measurements can be influenced by circumstances of measurement.<ref name=ESC2024/> Guidelines use different thresholds for office (also known as clinic), home (when the person measures their own blood pressure at home), and [[ambulatory blood pressure]] (using an automated device over a 24-hour period).<ref name=ESC2024/>
{| class="wikitable"
|+ Blood pressure classifications
|-
! Categories
! colspan="3" | Systolic blood pressure, [[mmHg]]
! rowspan=2 | and/or
! colspan="3" | Diastolic blood pressure, mmHg
|-
! Method
! Office
! Home
! 24h [[Ambulatory blood pressure|ambulatory]]
! Office
! Home
! 24h ambulatory
|-
! colspan="8" | [[American College of Cardiology]]/[[American Heart Association]] (2017)<ref name=Whelton2022>{{Cite journal |last1=Whelton |first1=Paul K |last2=Carey |first2=Robert M |last3=Mancia |first3=Giuseppe |last4=Kreutz |first4=Reinhold |last5=Bundy |first5=Joshua D |last6=Williams |first6=Bryan |date=2022-09-14 |title=Harmonization of the American College of Cardiology/American Heart Association and European Society of Cardiology/European Society of Hypertension Blood Pressure/Hypertension Guidelines |url=https://academic.oup.com/eurheartj/article/43/35/3302/6661233 |journal=European Heart Journal |language=en |volume=43 |issue=35 |pages=3302–3311 |doi=10.1093/eurheartj/ehac432 |issn=0195-668X |pmc=9470378 |pmid=36100239}}</ref>
|-
| Normal
| <120
| <120
| <115
| and
| <80
| <80
| <75
|-
| Elevated
| 120–129
| 120–129
| 115–124
| and
| <80
| <80
| <75
|-
| Hypertension, stage 1
| 130–139
| 130–134
| 125–129
| or
| 80–89
| 80–84
| 75–79
|-
| Hypertension, stage 2
| ≥140
| ≥135
| ≥130
| or
| ≥90
| ≥85
| ≥80
|-
! colspan="8" | [[European Society of Cardiology]] (2024)<ref name=ESC2024>{{Cite journal |last1=McEvoy |first1=John William |last2=McCarthy |first2=Cian P |last3=Bruno |first3=Rosa Maria |last4=Brouwers |first4=Sofie |last5=Canavan |first5=Michelle D |last6=Ceconi |first6=Claudio |last7=Christodorescu |first7=Ruxandra Maria |last8=Daskalopoulou |first8=Stella S |last9=Ferro |first9=Charles J |last10=Gerdts |first10=Eva |last11=Hanssen |first11=Henner |last12=Harris |first12=Julie |last13=Lauder |first13=Lucas |last14=McManus |first14=Richard J |last15=Molloy |first15=Gerard J |display-authors=5 |date=2024-08-30 |title=2024 ESC Guidelines for the management of elevated blood pressure and hypertension: Developed by the task force on the management of elevated blood pressure and hypertension of the European Society of Cardiology (ESC) and endorsed by the European Society of Endocrinology (ESE) and the European Stroke Organisation (ESO) |journal=European Heart Journal |volume=45 |issue=38 |pages=3912–4018 |language=en |doi=10.1093/eurheartj/ehae178 |doi-access=free |pmid=39210715 |issn=0195-668X}}</ref>
|-
| Non-elevated
| <120
| <120
| <115
| and
| <70
| <70
| <65
|-
| Elevated
| 120–139
| 120–134
| 115–129
| and
| 70–89
| 70–84
| 65–79
|-
| Hypertension
| ≥140
| ≥135
| ≥130
| or
| ≥90
| ≥85
| ≥80
|-
! colspan="8" | [[European Society of Hypertension]]/[[International Society of Hypertension]] (2023)<ref name=ESH2023>{{Cite journal |last1=Mancia |first1=Giuseppe |last2=Kreutz |first2=Reinhold |last3=Brunström |first3=Mattias |last4=Burnier |first4=Michel |last5=Grassi |first5=Guido |last6=Januszewicz |first6=Andrzej |last7=Muiesan |first7=Maria Lorenza |last8=Tsioufis |first8=Konstantinos |last9=Agabiti-Rosei |first9=Enrico |last10=Algharably |first10=Engi Abd Elhady |last11=Azizi |first11=Michel |last12=Benetos |first12=Athanase |last13=Borghi |first13=Claudio |last14=Hitij |first14=Jana Brguljan |last15=Cifkova |first15=Renata |display-authors = 5 |date=2023-12-01 |title=2023 ESH Guidelines for the management of arterial hypertension The Task Force for the management of arterial hypertension of the European Society of Hypertension: Endorsed by the International Society of Hypertension (ISH) and the European Renal Association (ERA) |journal=Journal of Hypertension |volume=41 |issue=12 |pages=1874–2071 |doi=10.1097/HJH.0000000000003480 |issn=1473-5598 |pmid=37345492|doi-access=free |hdl=11379/603005 |hdl-access=free }}</ref>
|-
| Optimal
| <120
| {{N/A}}
| {{N/A}}
| and
| <80
| {{N/A}}
| {{N/A}}
|-
| Normal
| 120–129
| {{N/A}}
| {{N/A}}
| and/or
| 80–84
| {{N/A}}
| {{N/A}}
|-
| High normal
| 130–139
| {{N/A}}
| {{N/A}}
| and/or
| 85–89
| {{N/A}}
| {{N/A}}
|-
| Hypertension, grade 1
| 140–159
| ≥135
| ≥130
| and/or
| 90–99
| ≥85
| ≥80
|-
| Hypertension, grade 2
| 160–179
| {{N/A}}
| {{N/A}}
| and/or
| 100–109
| {{N/A}}
| {{N/A}}
|-
| Hypertension, grade 3
| ≥180
| {{N/A}}
| {{N/A}}
| and/or
| ≥110
| {{N/A}}
| {{N/A}}
|}

The risk of cardiovascular disease increases progressively above 90&nbsp;mmHg, especially among women.<ref name=ESC2024/>

Observational studies demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long-term cardiovascular health. There is an ongoing medical debate over what is the optimal level of blood pressure to target when using drugs to lower blood pressure with hypertension, particularly in older people.<ref>{{cite journal | vauthors = Yusuf S, Lonn E | title = The SPRINT and the HOPE-3 Trial in the Context of Other Blood Pressure-Lowering Trials | journal = JAMA Cardiology | volume = 1 | issue = 8 | pages = 857–858 | date = November 2016 | pmid = 27602555 | doi = 10.1001/jamacardio.2016.2169 }}</ref>

Blood pressure fluctuates from minute to minute and normally shows a circadian rhythm over a 24-hour period,<ref>{{cite journal | vauthors = Smolensky MH, Hermida RC, Portaluppi F | title = Circadian mechanisms of 24-hour blood pressure regulation and patterning | journal = Sleep Medicine Reviews | volume = 33 | pages = 4–16 | date = June 2017 | pmid = 27076261 | doi = 10.1016/j.smrv.2016.02.003 }}</ref> with highest readings in the early morning and evenings and lowest readings at night.<ref>{{cite journal | vauthors = van Berge-Landry HM, Bovbjerg DH, James GD | title = Relationship between waking-sleep blood pressure and catecholamine changes in African-American and European-American women | journal = Blood Pressure Monitoring | volume = 13 | issue = 5 | pages = 257–262 | date = October 2008 | pmid = 18799950 | pmc = 2655229 | doi = 10.1097/MBP.0b013e3283078f45 | quote = Table2: Comparison of ambulatory blood pressures and urinary norepinephrine and epinephrine excretion measured at work, home, and during sleep between European–American (n = 110) and African–American (n = 51) women }}</ref><ref>{{cite journal | vauthors = van Berge-Landry HM, Bovbjerg DH, James GD | title = Relationship between waking-sleep blood pressure and catecholamine changes in African-American and European-American women | journal = Blood Pressure Monitoring | volume = 13 | issue = 5 | pages = 257–262 | date = October 2008 | pmid = 18799950 | pmc = 2655229 | doi = 10.1097/MBP.0b013e3283078f45 | id = NIHMS90092 }}</ref> Loss of the normal fall in blood pressure at night is associated with a greater future risk of cardiovascular disease and there is evidence that night-time blood pressure is a stronger predictor of cardiovascular events than day-time blood pressure.<ref name="HansenLi2010">{{cite journal | vauthors = Hansen TW, Li Y, Boggia J, Thijs L, Richart T, Staessen JA | title = Predictive role of the nighttime blood pressure | journal = Hypertension | volume = 57 | issue = 1 | pages = 3–10 | date = January 2011 | pmid = 21079049 | doi = 10.1161/HYPERTENSIONAHA.109.133900 | doi-access = free }}</ref> Blood pressure varies over longer time periods (months to years) and this variability predicts adverse outcomes.<ref>{{cite journal | vauthors = Rothwell PM | title = Does blood pressure variability modulate cardiovascular risk? | journal = Current Hypertension Reports | volume = 13 | issue = 3 | pages = 177–186 | date = June 2011 | pmid = 21465141 | doi = 10.1007/s11906-011-0201-3 | s2cid = 207331784 }}</ref> Blood pressure also changes in response to temperature, noise, emotional [[stress (medicine)|stress]], consumption of food or liquid, dietary factors, physical activity, changes in posture (such as [[orthostatic hypotension|standing-up]]), [[medication|drugs]], and disease.<ref>{{Cite book|title=Temporal Variations of the Cardiovascular System|date=1992|publisher=Springer Berlin Heidelberg | veditors = Engel BT, Blümchen G |isbn=978-3-662-02748-6 |location=Berlin, Heidelberg|oclc=851391490}}</ref> The variability in blood pressure and the better predictive value of ambulatory blood pressure measurements has led some authorities, such as the National Institute for Health and Care Excellence (NICE) in the UK, to advocate for the use of ambulatory blood pressure as the preferred method for diagnosis of hypertension.<ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK83274/|title=Hypertension: The Clinical Management of Primary Hypertension in Adults: Update of Clinical Guidelines 18 and 34|last=National Clinical Guideline Centre (UK)|date=2011|publisher=Royal College of Physicians (UK)|series=National Institute for Health and Clinical Excellence: Guidance|location=London|pmid=22855971|access-date=2019-01-28|archive-date=2022-08-12|archive-url=https://web.archive.org/web/20220812074204/https://www.ncbi.nlm.nih.gov/books/NBK83274/|url-status=live}}</ref>
[[File:Blutdruck.jpg|thumb|A digital [[sphygmomanometer]] used for measuring blood pressure]]
Various other factors, such as age and [[sex]], also influence a person's blood pressure. Differences between left-arm and right-arm blood pressure measurements tend to be small. However, occasionally there is a consistent difference greater than 10&nbsp;mmHg which may need further investigation, e.g. for [[Peripheral artery disease|peripheral arterial disease]], [[Cardiovascular disease|obstructive arterial disease]] or [[aortic dissection]].<ref>{{cite journal | vauthors = Eguchi K, Yacoub M, Jhalani J, Gerin W, Schwartz JE, Pickering TG | title = Consistency of blood pressure differences between the left and right arms | journal = Archives of Internal Medicine | volume = 167 | issue = 4 | pages = 388–393 | date = February 2007 | pmid = 17325301 | doi = 10.1001/archinte.167.4.388 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Agarwal R, Bunaye Z, Bekele DM | title = Prognostic significance of between-arm blood pressure differences | journal = Hypertension | volume = 51 | issue = 3 | pages = 657–662 | date = March 2008 | pmid = 18212263 | doi = 10.1161/HYPERTENSIONAHA.107.104943 | s2cid = 1101762 | citeseerx = 10.1.1.540.5836 }}</ref><ref>{{cite journal | vauthors = Clark CE, Campbell JL, Evans PH, Millward A | title = Prevalence and clinical implications of the inter-arm blood pressure difference: A systematic review | journal = Journal of Human Hypertension | volume = 20 | issue = 12 | pages = 923–931 | date = December 2006 | pmid = 17036043 | doi = 10.1038/sj.jhh.1002093 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Clark CE, Warren FC, Boddy K, McDonagh ST, Moore SF, Goddard J, Reed N, Turner M, Alzamora MT, Ramos Blanes R, Chuang SY, Criqui M, Dahl M, Engström G, Erbel R, Espeland M, Ferrucci L, Guerchet M, Hattersley A, Lahoz C, McClelland RL, McDermott MM, Price J, Stoffers HE, Wang JG, Westerink J, White J, Cloutier L, Taylor RS, Shore AC, McManus RJ, Aboyans V, Campbell JL | display-authors = 6 | title = Associations Between Systolic Interarm Differences in Blood Pressure and Cardiovascular Disease Outcomes and Mortality: Individual Participant Data Meta-Analysis, Development and Validation of a Prognostic Algorithm: The INTERPRESS-IPD Collaboration | journal = Hypertension | volume = 77 | issue = 2 | pages = 650–661 | date = February 2021 | pmid = 33342236 | pmc = 7803446 | doi = 10.1161/HYPERTENSIONAHA.120.15997 | doi-access = free }}</ref>

There is no accepted diagnostic standard for hypotension, although pressures less than 90/60 are commonly regarded as hypotensive.<ref>{{cite book|chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK499961/|chapter=Hypotension|vauthors=Sharma S, Bhattacharya PT|date=2018|title=StatPearls|publisher=StatPearls Publishing|pmid=29763136|name-list-style=vanc|access-date=2018-12-23|archive-date=2020-03-17|archive-url=https://web.archive.org/web/20200317233648/https://www.ncbi.nlm.nih.gov/books/NBK499961/|url-status=live}}</ref> In practice blood pressure is considered too low only if [[Hypotension#Signs and symptoms|symptoms]] are present.<ref name="Mayo2009causes">{{cite web|url=http://www.mayoclinic.com/health/low-blood-pressure/DS00590/DSECTION=causes|title=Low blood pressure (hypotension) – Causes|author=Mayo Clinic staff|date=2009-05-23|website=MayoClinic.com|publisher=Mayo Foundation for Medical Education and Research|access-date=2010-10-19|archive-date=2021-11-17|archive-url=https://web.archive.org/web/20211117175541/https://www.mayoclinic.org/diseases-conditions/low-blood-pressure/symptoms-causes/syc-20355465|url-status=live}}</ref>

===Systemic arterial pressure and age===
====Fetal blood pressure====
{{Further|Fetal circulation#Blood pressure}}
In [[pregnancy]], it is the fetal heart and not the mother's heart that builds up the fetal blood pressure to drive blood through the fetal circulation. The blood pressure in the fetal aorta is approximately 30&nbsp;mmHg at 20 weeks of gestation, and increases to approximately 45&nbsp;mmHg at 40 weeks of gestation.<ref name="Struijk">{{cite journal | vauthors = Struijk PC, Mathews VJ, Loupas T, Stewart PA, Clark EB, Steegers EA, Wladimiroff JW | title = Blood pressure estimation in the human fetal descending aorta | journal = Ultrasound in Obstetrics & Gynecology | volume = 32 | issue = 5 | pages = 673–681 | date = October 2008 | pmid = 18816497 | doi = 10.1002/uog.6137 | s2cid = 23575926 | doi-access = free }}</ref>

The average blood pressure for full-term infants:<ref name="SharonSmithMurray">{{cite book|title=Foundations of Maternal-Newborn Nursing|vauthors=Sharon SM, Emily SM|date=2006|publisher=Elsevier|edition= 4th|location=Philadelphia|page=476}}</ref>
* Systolic 65–95&nbsp;mmHg
* Diastolic 30–60&nbsp;mmHg

====Childhood====
{| class="wikitable" style = "float: right; margin-left: 15px; text-align: center;"
|+ [[Reference range]]s for blood pressure (BP) in children<ref name="ucla">[http://hr.uclahealth.org/workfiles/AgeSpecificSLM-Peds.pdf Pediatric Age Specific] {{Webarchive|url=https://web.archive.org/web/20170516204947/http://hr.uclahealth.org/workfiles/AgeSpecificSLM-Peds.pdf |date=2017-05-16 }}, p. 6. Revised 6/10. By Theresa Kirkpatrick and Kateri Tobias. UCLA Health System</ref>
|-
! scope="col" | Stage
! scope="col" | Approximate age
! scope="col" | Systolic BP,<br /> mmHg
! scope="col" | Diastolic BP,<br /> mmHg
|-
! scope="row" | Infants
| 0–12 months || 75–100 || 50–70
|-
! scope="row" | Toddlers and preschoolers
| 1–5 years || 80–110 || 50–80
|-
! scope="row" | School age
| 6–12 years || 85–120 || 50–80
|-
! scope="row" | Adolescents
| 13–18 years || 95–140 || 60–90
|}
In children the normal ranges for blood pressure are lower than for adults and depend on height.<ref>{{cite web|author=National Heart Lung and Blood Institute|title=Blood pressure tables for children and adolescents|url=http://www.nhlbi.nih.gov/guidelines/hypertension/child_tbl.htm|access-date=2008-09-23|archive-url=https://web.archive.org/web/20140618151357/http://www.nhlbi.nih.gov/guidelines/hypertension/child_tbl.htm|archive-date=2014-06-18|url-status=dead}} (The median blood pressure is given by the 50th percentile and hypertension is defined by the [[Percentile|95th percentile]] for a given age, height, and sex.)</ref> Reference blood pressure values have been developed for children in different countries, based on the distribution of blood pressure in children of these countries.<ref>{{cite journal | vauthors = Chiolero A | title = The quest for blood pressure reference values in children | journal = Journal of Hypertension | volume = 32 | issue = 3 | pages = 477–479 | date = March 2014 | pmid = 24477093 | doi = 10.1097/HJH.0000000000000109 | s2cid = 1949314 | doi-access = free }}</ref>

====Aging adults====
In adults in most societies, systolic blood pressure tends to rise from early adulthood onward, up to at least age 70;<ref>{{cite journal | vauthors = Wills AK, Lawlor DA, Matthews FE, Sayer AA, Bakra E, Ben-Shlomo Y, Benzeval M, Brunner E, Cooper R, Kivimaki M, Kuh D, Muniz-Terrera G, Hardy R | display-authors = 6 | title = Life course trajectories of systolic blood pressure using longitudinal data from eight UK cohorts | journal = PLOS Medicine | volume = 8 | issue = 6 | pages = e1000440 | date = June 2011 | pmid = 21695075 | pmc = 3114857 | doi = 10.1371/journal.pmed.1000440 | doi-access = free }}</ref><ref name=":3">{{cite journal | vauthors = Franklin SS, Gustin W, Wong ND, Larson MG, Weber MA, Kannel WB, Levy D | title = Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study | journal = Circulation | volume = 96 | issue = 1 | pages = 308–315 | date = July 1997 | pmid = 9236450 | doi = 10.1161/01.CIR.96.1.308 | s2cid = 40209177 }}</ref> diastolic pressure tends to begin to rise at the same time but start to fall earlier in mid-life, approximately age 55.<ref name=":3" />  Mean blood pressure rises from early adulthood, plateauing in mid-life, while pulse pressure rises quite markedly after the age of 40. Consequently, in many older people, systolic blood pressure often exceeds the normal adult range,<ref name=":3" /> if the diastolic pressure is in the normal range this is termed [[isolated systolic hypertension]]. The rise in pulse pressure with age is attributed to increased [[Arterial stiffness|stiffness of the arteries]].<ref>{{cite journal | vauthors = Franklin SS | title = Beyond blood pressure: Arterial stiffness as a new biomarker of cardiovascular disease | journal = Journal of the American Society of Hypertension | volume = 2 | issue = 3 | pages = 140–151 | date = 2008-05-01 | pmid = 20409896 | doi = 10.1016/j.jash.2007.09.002 }}</ref> An age-related rise in blood pressure is not considered healthy and is not observed in some isolated unacculturated communities.<ref>{{cite journal | vauthors = Gurven M, Blackwell AD, Rodríguez DE, Stieglitz J, Kaplan H | title = Does blood pressure inevitably rise with age?: longitudinal evidence among forager-horticulturalists | journal = Hypertension | volume = 60 | issue = 1 | pages = 25–33 | date = July 2012 | pmid = 22700319 | pmc = 3392307 | doi = 10.1161/HYPERTENSIONAHA.111.189100 }}</ref>

==Systemic venous pressure==
{{Non-systemic blood pressures}}
Blood pressure generally refers to the arterial pressure in the [[systemic circulation]]. However, measurement of pressures in the venous system and the [[Pulmonary circulation|pulmonary vessels]] plays an important role in [[intensive care medicine]] but requires invasive measurement of pressure using a [[catheter]].

Venous pressure is the vascular pressure in a [[vein]] or in the [[atrium (anatomy)|atria of the heart]]. It is much lower than arterial pressure, with common values of 5&nbsp;mmHg in the [[right atrium]] and 8&nbsp;mmHg in the left atrium.

Variants of venous pressure include:
* [[Central venous pressure]], which is a good approximation of right atrial pressure,<ref name="urlCentral Venous Catheter Physiology">{{cite web |url=http://www.healthsystem.virginia.edu/internet/anesthesiology-elective/cardiac/cvcphys.cfm |title=Central Venous Catheter Physiology |access-date=2009-02-27 |url-status=dead |archive-url=https://web.archive.org/web/20080821165806/http://www.healthsystem.virginia.edu/internet/anesthesiology-elective/cardiac/cvcphys.cfm |archive-date=2008-08-21 }}</ref> which is a major determinant of right ventricular end diastolic volume. (However, there can be exceptions in some cases.)<ref name="pmid12533747">{{cite journal | vauthors = Tkachenko BI, Evlakhov VI, Poyasov IZ | title = Independence of changes in right atrial pressure and central venous pressure | journal = Bulletin of Experimental Biology and Medicine | volume = 134 | issue = 4 | pages = 318–320 | date = October 2002 | pmid = 12533747 | doi = 10.1023/A:1021931508946 | s2cid = 23726657 }}</ref>
* The [[jugular venous pressure]] (JVP) is the indirectly observed pressure over the venous system. It can be useful in the differentiation of different forms of [[heart disease|heart]] and [[lung disease]].
* The [[portal venous pressure]] is the blood pressure in the [[portal vein]]. It is normally 5–10&nbsp;mmHg<ref>{{cite web |url=http://www.emedicine.com/med/byname/esophageal-varices.htm |title=Esophageal Varices : Article Excerpt by: Samy A Azer |publisher=eMedicine |access-date=2011-08-22 |archive-date=2008-10-07 |archive-url=https://web.archive.org/web/20081007113712/http://www.emedicine.com/med/byname/Esophageal-Varices.htm |url-status=live }}</ref>

==Pulmonary pressure==
{{Main|Pulmonary artery pressure}}
Normally, the pressure in the [[pulmonary artery]] is about 15&nbsp;mmHg at rest.<ref>{{cite web | url = http://www.nhlbi.nih.gov/health/dci/Diseases/pah/pah_what.html | title = What Is Pulmonary Hypertension? | work = From Diseases and Conditions Index (DCI) | publisher = National Heart, Lung, and Blood Institute. | date = September 2008 | access-date = 6 April 2009 | archive-date = 27 April 2012 | archive-url = https://web.archive.org/web/20120427144143/http://www.nhlbi.nih.gov/health/dci/Diseases/pah/pah_what.html | url-status = live }}</ref>

Increased blood pressure in the [[capillaries]] of the lung causes [[pulmonary hypertension]], leading to interstitial [[edema]] if the pressure increases to above 20&nbsp;mmHg, and to [[pulmonary edema]] at pressures above 25&nbsp;mmHg.<ref>{{cite book | vauthors = Adair OV | chapter = Chapter 41 |title=Cardiology secrets |date=2001 |publisher=Hanley & Belfus |location=Philadelphia |isbn=978-1-56053-420-4 |page=210 |edition=2nd | url = https://books.google.com/books?id=IYFAsxAUA_MC }}</ref>

==Aortic pressure==
{{Main|Aortic pressure}}
[[Aortic pressure]], also called central aortic blood pressure, or central blood pressure, is the blood pressure at the root of the [[aorta]]. Elevated aortic pressure has been found to be a more accurate predictor of both cardiovascular events and mortality, as well as structural changes in the heart, than has peripheral blood pressure (such as measured through the [[brachial artery]]).<ref name="Roman Devereux Kizer Lee 2007 pp. 197–203">{{cite journal | last1=Roman | first1=Mary J. | last2=Devereux | first2=Richard B. | last3=Kizer | first3=Jorge R. | last4=Lee | first4=Elisa T. | last5=Galloway | first5=James M. | last6=Ali | first6=Tauqeer | last7=Umans | first7=Jason G. | last8=Howard | first8=Barbara V. | title=Central Pressure More Strongly Relates to Vascular Disease and Outcome Than Does Brachial Pressure | journal=Hypertension | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=50 | issue=1 | year=2007 | issn=0194-911X | doi=10.1161/hypertensionaha.107.089078 | pages=197–203| pmid=17485598 }}</ref><ref name="Kesten Qasem Avolio 2022 pp. 128–139">{{cite journal | last1=Kesten | first1=Steven | last2=Qasem | first2=Ahmad | last3=Avolio | first3=Alberto | title=Viewpoint: The Case for Non-Invasive Central Aortic Pressure Monitoring in the Management of Hypertension | journal=Artery Research | volume=28 | issue=4 | date=2022-10-20 | issn=1876-4401 | doi=10.1007/s44200-022-00023-z | pages=128–139| doi-access=free }}</ref> Traditionally it involved an invasive procedure to measure aortic pressure, but now there are non-invasive methods of measuring it indirectly without a significant margin of error.<ref name="Avolio 2008 pp. 1470–1471">{{cite journal | last=Avolio | first=Alberto | title=Central Aortic Blood Pressure and Cardiovascular Risk: A Paradigm Shift? | journal=Hypertension | volume=51 | issue=6 | date=2008 | issn=0194-911X | doi=10.1161/HYPERTENSIONAHA.107.108910 | pages=1470–1471| pmid=18426994 }}</ref><ref name="Chen Nevo Fetics Pak 1997 pp. 1827–1836">{{cite journal | last1=Chen | first1=Chen-Huan | last2=Nevo | first2=Erez | last3=Fetics | first3=Barry | last4=Pak | first4=Peter H. | last5=Yin | first5=Frank C.P. | last6=Maughan | first6=W. Lowell | last7=Kass | first7=David A. | title=Estimation of Central Aortic Pressure Waveform by Mathematical Transformation of Radial Tonometry Pressure | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=95 | issue=7 | year=1997 | issn=0009-7322 | doi=10.1161/01.cir.95.7.1827 | pages=1827–1836| pmid=9107170 }}</ref>

Certain researchers have argued for physicians to begin using aortic pressure, as opposed to peripheral blood pressure, as a guide for clinical decisions.<ref name="McEniery Cockcroft Roman Franklin 2014 pp. 1719–1725">{{cite journal | last1=McEniery | first1=Carmel M. | last2=Cockcroft | first2=John R. | last3=Roman | first3=Mary J. | last4=Franklin | first4=Stanley S. | last5=Wilkinson | first5=Ian B. | title=Central blood pressure: current evidence and clinical importance | journal=European Heart Journal | publisher=Oxford University Press (OUP) | volume=35 | issue=26 | date=23 Jan 2014 | issn=1522-9645 | doi=10.1093/eurheartj/eht565 | pages=1719–1725| pmid=24459197 | pmc=4155427 }}</ref><ref name="Kesten Qasem Avolio 2022 pp. 128–139"/> The way antihypertensive drugs impact peripheral blood pressure can often be very different from the way they impact central aortic pressure.<ref name="The CAFE Investigators CAFE Steering Committee and Writing Committee Williams Lacy 2006 pp. 1213–1225">{{cite journal | author=The CAFE Investigators | author2=CAFE Steering Committee and Writing Committee | last3=Williams | first3=Bryan | last4=Lacy | first4=Peter S. | last5=Thom | first5=Simon M. | last6=Cruickshank | first6=Kennedy | last7=Stanton | first7=Alice | last8=Collier | first8=David | last9=Hughes | first9=Alun D. | last10=Thurston | first10=H. | last11=O’Rourke | first11=Michael | title=Differential Impact of Blood Pressure–Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study | journal=Circulation | volume=113 | issue=9 | date=2006-03-07 | issn=0009-7322 | doi=10.1161/CIRCULATIONAHA.105.595496 | pages=1213–1225| pmid=16476843 }}</ref>

==Mean systemic pressure==
{{Main|Mean systemic pressure}}
If the heart is stopped, blood pressure falls, but it does not fall to zero. The remaining pressure measured after cessation of the heart beat and redistribution of blood throughout the circulation is termed the mean systemic pressure or mean circulatory filling pressure;<ref name=":5">{{cite journal | vauthors = Rothe CF | title = Mean circulatory filling pressure: its meaning and measurement | journal = Journal of Applied Physiology | volume = 74 | issue = 2 | pages = 499–509 | date = February 1993 | pmid = 8458763 | doi = 10.1152/jappl.1993.74.2.499 }}</ref> typically this is proximally ~7&nbsp;mmHg.<ref name=":5"/>

==Disorders of blood pressure==
Disorders of blood pressure control include [[Hypertension|high blood pressure]], [[Hypotension|low blood pressure]], and blood pressure that shows excessive or maladaptive fluctuation.

===High blood pressure===
{{Main|Hypertension}}
[[File:Main complications of persistent high blood pressure.svg|thumb|right|300px|Overview of main complications of persistent high blood pressure.<ref name=aha23/>]]

[[Arterial hypertension]] can be an indicator of other problems and may have long-term adverse effects. Sometimes it can be an acute problem, such as in a [[hypertensive emergency]] when blood pressure is more than 180/120 mmHg.<ref name="aha23">{{cite web |title=The facts about high blood pressure |url=https://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure |publisher=American Heart Association |access-date=14 May 2023 |date=2023 |archive-date=14 May 2023 |archive-url=https://web.archive.org/web/20230514190952/https://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure |url-status=live }}</ref>

Levels of arterial pressure put mechanical stress on the arterial walls. Higher pressures increase heart workload and progression of unhealthy tissue growth ([[atheroma]]) that develops within the walls of arteries. The higher the pressure, the more stress that is present and the more atheroma tend to progress and the [[Myocardium|heart muscle]] tends to thicken, enlarge and become weaker over time.

Persistent [[hypertension]] is one of the risk factors for [[stroke]]s, [[myocardial infarction|heart attacks]], [[heart failure]], and [[arterial aneurysm]]s, and is the leading cause of [[chronic kidney failure]].<ref name=aha23/> Even moderate elevation of arterial pressure leads to shortened [[life expectancy]].<ref name=aha23/> At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.<ref>{{cite book | vauthors = Guyton AC |title=Textbook of Medical Physiology |date=2006 |publisher=Elsevier Saunders |location=Philadelphia |isbn=978-0-7216-0240-0 |edition=11th | page = 220 }}</ref> For people with high blood pressure, higher [[heart rate variability]] (HRV) is a risk factor for [[atrial fibrillation]].<ref name="pmid35260686">{{cite journal | vauthors = Kim SH, Lim KR, Chun KJ | title=Higher heart rate variability as a predictor of atrial fibrillation in patients with hypertensione | journal= [[Scientific Reports]] | volume=12 | issue=1 | pages=3702 | year=2022 | doi= 10.1038/s41598-022-07783-3 | pmc=8904557 | pmid=35260686 | bibcode=2022NatSR..12.3702K }}</ref>

Both high [[Systole (medicine)|systolic]] pressure and high [[pulse pressure]] (the numerical difference between systolic and diastolic pressures) are risk factors.<ref name=aha23/> Elevated pulse pressure has been found to be a stronger independent predictor of cardiovascular events, especially in older populations, than has systolic, diastolic, or mean arterial pressure.<ref name="Cleveland Clinic 2021"/><ref name="Mitchell Izzo Lacourcière Ouellet 2002 pp. 2955–2961"/><ref name="Benetos Safar Rudnichi Smulyan 1997 pp. 1410–1415"/><ref name="Franklin Khan Wong Larson 1999 pp. 354–360">{{cite journal | last1=Franklin | first1=Stanley S. | last2=Khan | first2=Shehzad A. | last3=Wong | first3=Nathan D. | last4=Larson | first4=Martin G. | last5=Levy | first5=Daniel | title=Is Pulse Pressure Useful in Predicting Risk for Coronary Heart Disease? | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=100 | issue=4 | date=27 Jul 1999 | issn=0009-7322 | doi=10.1161/01.cir.100.4.354 | pages=354–360| pmid=10421594 | doi-access=free }}</ref> In some cases, it appears that a decrease in excessive diastolic pressure can actually increase risk, probably due to the increased difference between systolic and diastolic pressures (ie. widened pulse pressure). If systolic blood pressure is elevated (>140&nbsp;mmHg) with a normal diastolic blood pressure (<90&nbsp;mmHg), it is called [[isolated systolic hypertension]] and may present a health concern.<ref name=aha23/><ref name="urlIsolated systolic hypertension: A health concern? – MayoClinic.com">{{cite web |url=https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/expert-answers/hypertension/faq-20058527 |title=Isolated systolic hypertension: A health concern? |website=MayoClinic.com |access-date=2018-01-25 |archive-date=2013-12-28 |archive-url=https://web.archive.org/web/20131228153711/http://www.mayoclinic.com/health/hypertension/AN01113 |url-status=live }}</ref> According to the 2017<ref>{{cite book | vauthors = Tan JL, Thakur K | chapter = Systolic Hypertension |date=2022 | chapter-url = http://www.ncbi.nlm.nih.gov/books/NBK482472/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29494079 |access-date=2022-10-03 }}</ref> American Heart Association blood pressure guidelines state that a systolic blood pressure of 130–139 mmHg with a diastolic pressure of 80–89 mmHg is "stage one hypertension".<ref name=aha23/>

For those with [[heart valve]] regurgitation, a change in its severity may be associated with a change in diastolic pressure.  In a study of people with heart valve regurgitation that compared measurements two weeks apart for each person, there was an increased severity of [[aortic insufficiency|aortic]] and [[mitral regurgitation]] when diastolic blood pressure increased, whereas when diastolic blood pressure decreased, there was a decreased severity.<ref name='Gottdiener2002'>{{cite journal | vauthors = Gottdiener JS, Panza JA, St John Sutton M, Bannon P, Kushner H, Weissman NJ | title = Testing the test: the reliability of echocardiography in the sequential assessment of valvular regurgitation | journal = American Heart Journal | volume = 144 | issue = 1 | pages = 115–121 | date = July 2002 | pmid = 12094197 | doi = 10.1067/mhj.2002.123139 }}</ref>

===Low blood pressure===
{{Main|Hypotension}}
Blood pressure that is too low is known as [[hypotension]]. This is a medical concern if it causes signs or symptoms, such as dizziness, fainting, or in extreme cases in medical emergencies, [[shock (circulatory)|circulatory shock]].<ref name="NHLBI2008">{{cite web|url=http://www.nhlbi.nih.gov/health/dci/Diseases/hyp/hyp_whatis.html|title=Diseases and conditions index – hypotension|date=September 2008|publisher=National Heart Lung and Blood Institute|access-date=2008-09-16|archive-date=2012-04-27|archive-url=https://web.archive.org/web/20120427145640/http://www.nhlbi.nih.gov/health/dci/Diseases/hyp/hyp_whatis.html|url-status=live}}</ref> Causes of low arterial pressure include [[sepsis]], [[hypovolemia]], [[bleeding]], [[cardiogenic shock]], [[reflex syncope]], [[hormone|hormonal]] abnormalities such as [[Addison's disease]], [[eating disorder]]s – particularly [[anorexia nervosa]] and [[bulimia]].<ref>{{Cite book|title=Braunwald's heart disease : a textbook of cardiovascular medicine|date=2012|publisher=Saunders| vauthors = Braunwald E, Bonow RO |isbn=978-1-4377-0398-6|edition= 9th |location=Philadelphia|oclc=671465395}}</ref>

====Orthostatic hypotension====
{{Main|Orthostatic hypotension}}
A large fall in blood pressure upon standing (typically a systolic/diastolic blood pressure decrease of >20/10&nbsp;mmHg) is termed [[orthostatic hypotension]] (postural hypotension) and represents a failure of the body to compensate for the effect of [[gravity]] on the circulation. Standing results in an increased [[Hydrostatics|hydrostatic]] pressure in the blood vessels of the lower limbs. The consequent distension of the veins below the [[Thoracic diaphragm|diaphragm]] (venous pooling) causes ~500 ml of blood to be relocated from the chest and upper body. This results in a rapid decrease in central blood volume and a reduction of ventricular [[Preload (cardiology)|preload]] which in turn reduces stroke volume, and mean arterial pressure. Normally this is compensated for by multiple mechanisms, including activation of the [[autonomic nervous system]] which increases [[heart rate]], [[myocardial contractility]] and systemic arterial [[vasoconstriction]] to preserve blood pressure and elicits [[Vein|venous]] vasoconstriction to decrease venous [[Compliance (physiology)|compliance]]. Decreased venous compliance also results from an intrinsic [[Myogenic mechanism|myogenic]] increase in venous [[smooth muscle]] tone in response to the elevated pressure in the veins of the lower body. 

Other compensatory mechanisms include the veno-arteriolar [[axon reflex]], the '[[Skeletal-muscle pump|skeletal muscle pump]]' and '[[respiratory pump]]'. Together these mechanisms normally stabilize blood pressure within a minute or less.<ref name=":4">{{cite journal | vauthors = Ricci F, De Caterina R, Fedorowski A | title = Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment | journal = Journal of the American College of Cardiology | volume = 66 | issue = 7 | pages = 848–860 | date = August 2015 | pmid = 26271068 | doi = 10.1016/j.jacc.2015.06.1084 | doi-access = free }}</ref> If these compensatory mechanisms fail and arterial pressure and blood [[rate of fluid flow|flow]] decrease beyond a certain point, the [[perfusion]] of the brain becomes critically compromised (i.e., the blood supply is not sufficient), causing [[lightheadedness]], [[dizziness]], weakness or [[Syncope (medicine)|fainting]].<ref>{{cite journal | vauthors = Franco Folino A | title = Cerebral autoregulation and syncope | journal = Progress in Cardiovascular Diseases | volume = 50 | issue = 1 | pages = 49–80 | year = 2007 | pmid = 17631437 | doi = 10.1016/j.pcad.2007.01.001 }}</ref> Usually this failure of compensation is due to disease, or drugs that affect the [[sympathetic nervous system]].<ref name=":4" /> A similar effect is observed following the experience of excessive gravitational forces (G-loading), such as routinely experienced by aerobatic or combat pilots '[[G-force|pulling Gs]]' where the extreme hydrostatic pressures exceed the ability of the body's compensatory mechanisms.

===Variable or fluctuating blood pressure===
{{Main|Labile hypertension}}
Some fluctuation or variation in blood pressure is normal. Variation in blood pressure that is significantly greater than the norm is known as [[labile hypertension]] and is associated with increased risk of cardiovascular disease<ref>{{cite journal | vauthors = Stevens SL, Wood S, Koshiaris C, Law K, Glasziou P, Stevens RJ, McManus RJ | title = Blood pressure variability and cardiovascular disease: systematic review and meta-analysis | journal = BMJ | volume = 354 | pages = i4098 | date = August 2016 | pmid = 27511067 | pmc = 4979357 | doi = 10.1136/bmj.i4098 }}</ref> brain small vessel disease,<ref>{{cite journal | vauthors = Tully PJ, Yano Y, Launer LJ, Kario K, Nagai M, Mooijaart SP, Claassen JA, Lattanzi S, Vincent AD, Tzourio C | display-authors = 6 | title = Association Between Blood Pressure Variability and Cerebral Small-Vessel Disease: A Systematic Review and Meta-Analysis | journal = Journal of the American Heart Association | volume = 9 | issue = 1 | pages = e013841 | date = January 2020 | pmid = 31870233 | pmc = 6988154 | doi = 10.1161/JAHA.119.013841 }}</ref> and dementia<ref name=":6"/> independent of the average blood pressure level.  Recent evidence from [[clinical trial]]s has also linked variation in blood pressure to mortality,<ref>{{cite journal | vauthors = Chiriacò M, Pateras K, Virdis A, Charakida M, Kyriakopoulou D, Nannipieri M, Emdin M, Tsioufis K, Taddei S, Masi S, Georgiopoulos G | display-authors = 6 | title = Association between blood pressure variability, cardiovascular disease and mortality in type 2 diabetes: A systematic review and meta-analysis | journal = Diabetes, Obesity & Metabolism | volume = 21 | issue = 12 | pages = 2587–2598 | date = December 2019 | pmid = 31282073 | doi = 10.1111/dom.13828 | s2cid = 195829708 | hdl = 11568/996646 }}</ref><ref>{{cite journal | vauthors = Nuyujukian DS, Newell MS, Zhou JJ, Koska J, Reaven PD | title = Baseline blood pressure modifies the role of blood pressure variability in mortality: Results from the ACCORD trial | journal = Diabetes, Obesity & Metabolism | volume = 24 | issue = 5 | pages = 951–955 | date = May 2022 | pmid = 35014154 | pmc = 8986598 | doi = 10.1111/dom.14649 | s2cid = 245896131 }}</ref> stroke,<ref>{{cite journal | vauthors = Muntner P, Whittle J, Lynch AI, Colantonio LD, Simpson LM, Einhorn PT, Levitan EB, Whelton PK, Cushman WC, Louis GT, Davis BR, Oparil S | display-authors = 6 | title = Visit-to-Visit Variability of Blood Pressure and Coronary Heart Disease, Stroke, Heart Failure, and Mortality: A Cohort Study | journal = Annals of Internal Medicine | volume = 163 | issue = 5 | pages = 329–338 | date = September 2015 | pmid = 26215765 | pmc = 5021508 | doi = 10.7326/M14-2803 }}</ref> heart failure,<ref>{{cite journal | vauthors = Nuyujukian DS, Koska J, Bahn G, Reaven PD, Zhou JJ | title = Blood Pressure Variability and Risk of Heart Failure in ACCORD and the VADT | journal = Diabetes Care | volume = 43 | issue = 7 | pages = 1471–1478 | date = July 2020 | pmid = 32327422 | pmc = 7305004 | doi = 10.2337/dc19-2540 | hdl-access = free | hdl = 10150/641980 }}</ref> and cardiac changes that may give rise to heart failure.<ref>{{cite journal | vauthors = Nwabuo CC, Yano Y, Moreira HT, Appiah D, Vasconcellos HD, Aghaji QN, Viera A, Rana JS, Shah RV, Murthy VL, Allen NB, Schreiner PJ, Lloyd-Jones DM, Lima JA | display-authors = 6 | title = Association Between Visit-to-Visit Blood Pressure Variability in Early Adulthood and Myocardial Structure and Function in Later Life | journal = JAMA Cardiology | volume = 5 | issue = 7 | pages = 795–801 | date = July 2020 | pmid = 32293640 | pmc = 7160747 | doi = 10.1001/jamacardio.2020.0799 }}</ref> These data have prompted discussion of whether excessive variation in blood pressure should be treated, even among normotensive older adults.<ref>{{cite journal | vauthors = Parati G, Ochoa JE, Lombardi C, Bilo G | title = Assessment and management of blood-pressure variability | journal = Nature Reviews. Cardiology | volume = 10 | issue = 3 | pages = 143–155 | date = March 2013 | pmid = 23399972 | doi = 10.1038/nrcardio.2013.1 | s2cid = 22425558 }}</ref> 

Older individuals and those who had received blood pressure medications are more likely to exhibit larger fluctuations in pressure,<ref name="ncbi.nlm.nih.gov">{{cite journal | vauthors = Brickman AM, Reitz C, Luchsinger JA, Manly JJ, Schupf N, Muraskin J, DeCarli C, Brown TR, Mayeux R | display-authors = 6 | title = Long-term blood pressure fluctuation and cerebrovascular disease in an elderly cohort | journal = Archives of Neurology | volume = 67 | issue = 5 | pages = 564–569 | date = May 2010 | pmid = 20457955 | pmc = 2917204 | doi = 10.1001/archneurol.2010.70 }}</ref> and there is some evidence that different antihypertensive agents have different effects on blood pressure variability;<ref name=":6">{{cite journal | vauthors = Messerli FH, Hofstetter L, Rimoldi SF, Rexhaj E, Bangalore S | title = Risk Factor Variability and Cardiovascular Outcome: JACC Review Topic of the Week | journal = Journal of the American College of Cardiology | volume = 73 | issue = 20 | pages = 2596–2603 | date = May 2019 | pmid = 31118154 | doi = 10.1016/j.jacc.2019.02.063 | doi-access = free }}</ref> whether these differences translate to benefits in outcome is uncertain.<ref name=":6" />

==Physiology==
[[File:Systolevs Diastole.png|thumb|Cardiac systole and diastole]]
[[File:VIM LDH.jpg|thumb|Blood flow velocity waveforms in the central retinal artery (red) and vein (blue), measured by [[laser Doppler imaging]] in the eye fundus of a healthy volunteer.|alt=]]
[[File:Circulation pressures v1.tif|thumb|Schematic of pressures in the circulation]]
During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastolic) pressure.<ref>{{cite web | title = Normal Blood Pressure Ranges in Adults | url = https://svollop.com/health/blood-pressure-ranges/ | website=svollop.com | date = 2023-03-16 | access-date = 2023-03-21 | archive-date = 2023-03-16 | archive-url = https://web.archive.org/web/20230316081326/https://svollop.com/health/blood-pressure-ranges/ | url-status = live }}</ref>{{Unreliable medical source|date=March 2023|sure=y}} The blood pressure in the circulation is principally due to the pumping action of the heart.<ref name = 'Caro'>{{cite book | vauthors = Caro CG |title=The Mechanics of The Circulation |publisher=Oxford University Press |location=Oxford [Oxfordshire] |year=1978 |isbn=978-0-19-263323-1}}</ref> However, blood pressure is also regulated by neural regulation from the brain (see [[Hypertension and the brain]]), as well as osmotic regulation from the kidney. Differences in mean blood pressure drive the flow of blood around the circulation. The rate of mean blood flow depends on both blood pressure and the resistance to flow presented by the blood vessels. In the absence of [[Fluid statics|hydrostatic]] effects (e.g. standing), mean blood pressure decreases as the [[Circulatory system|circulating blood]] moves away from the heart through arteries and [[capillaries]] due to [[Viscosity|viscous]] losses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries and [[arterioles]].<ref name='Klabunde2005p93-4'>{{cite book | vauthors = Klabunde R | title = Cardiovascular Physiology Concepts | publisher = Lippincott Williams & Wilkins | year = 2005 | pages = 93–94 | isbn = 978-0-7817-5030-1 }}</ref> Pulsatility also diminishes in the smaller elements of the arterial circulation, although some transmitted pulsatility is observed in capillaries.<ref>{{cite journal | vauthors = Mahler F, Muheim MH, Intaglietta M, Bollinger A, Anliker M | title = Blood pressure fluctuations in human nailfold capillaries | journal = The American Journal of Physiology | volume = 236 | issue = 6 | pages = H888–H893 | date = June 1979 | pmid = 443454 | doi = 10.1152/ajpheart.1979.236.6.H888 }}</ref> Gravity affects blood pressure via hydrostatic forces (e.g., during standing), and valves in veins, [[breathing]], and pumping from contraction of skeletal muscles also influence blood pressure, particularly in veins.<ref name = 'Caro'/>

===Hemodynamics===
{{main|Hemodynamics}}
A simple view of the [[hemodynamics]] of systemic arterial pressure is based around [[mean arterial pressure]] (MAP) and pulse pressure. Most influences on blood pressure can be understood in terms of their effect on [[cardiac output]],<ref>{{cite journal | vauthors = Guyton AC | title = The relationship of cardiac output and arterial pressure control | journal = Circulation | volume = 64 | issue = 6 | pages = 1079–1088 | date = December 1981 | pmid = 6794930 | doi = 10.1161/01.cir.64.6.1079 | doi-access = free }}</ref> [[Vascular resistance|systemic vascular resistance]], or [[arterial stiffness]] (the inverse of arterial compliance). Cardiac output is the product of stroke volume and heart rate. Stroke volume is influenced by 1) the [[end-diastolic volume]] or filling pressure of the ventricle acting via the [[Frank–Starling law|Frank–Starling mechanism]]—this is influenced by [[blood volume]]; 2) [[Myocardial contractility|cardiac contractility]]; and 3) [[afterload]], the impedance to blood flow presented by the circulation.<ref>{{cite journal | vauthors = Milnor WR | title = Arterial impedance as ventricular afterload | journal = Circulation Research | volume = 36 | issue = 5 | pages = 565–570 | date = May 1975 | pmid = 1122568 | doi = 10.1161/01.res.36.5.565 | doi-access = free }}</ref> In the short-term, the greater the blood volume, the higher the cardiac output. This has been proposed as an explanation of the relationship between high dietary salt intake and increased blood pressure; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous system responses and the [[renin–angiotensin system]],<ref>{{cite journal | vauthors = Freis ED | title = Salt, volume and the prevention of hypertension | journal = Circulation | volume = 53 | issue = 4 | pages = 589–595 | date = April 1976 | pmid = 767020 | doi = 10.1161/01.CIR.53.4.589 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Caplea A, Seachrist D, Dunphy G, Ely D | title = Sodium-induced rise in blood pressure is suppressed by androgen receptor blockade | journal = American Journal of Physiology. Heart and Circulatory Physiology | volume = 280 | issue = 4 | pages = H1793–H1801 | date = April 2001 | pmid = 11247793 | doi = 10.1152/ajpheart.2001.280.4.H1793 | series = 4 | s2cid = 12069178 }}</ref><ref>{{cite journal | vauthors = Houston MC | title = Sodium and hypertension. A review | journal = Archives of Internal Medicine | volume = 146 | issue = 1 | pages = 179–185 | date = January 1986 | pmid = 3510595 | doi = 10.1001/archinte.1986.00360130217028 | series = 1 }}</ref> changes in [[Plasma osmolality|plasma osmolarity]] may also be important.<ref>{{cite journal | vauthors = Kanbay M, Aslan G, Afsar B, Dagel T, Siriopol D, Kuwabara M, Incir S, Camkiran V, Rodriguez-Iturbe B, Lanaspa MA, Covic A, Johnson RJ | display-authors = 6 | title = Acute effects of salt on blood pressure are mediated by serum osmolality | journal = Journal of Clinical Hypertension | volume = 20 | issue = 10 | pages = 1447–1454 | date = October 2018 | pmid = 30232829 | pmc = 8030773 | doi = 10.1111/jch.13374 | doi-access = free }}</ref> In the longer-term the relationship between volume and blood pressure is more complex.<ref>{{cite journal | vauthors = Titze J, Luft FC | title = Speculations on salt and the genesis of arterial hypertension | journal = Kidney International | volume = 91 | issue = 6 | pages = 1324–1335 | date = June 2017 | pmid = 28501304 | doi = 10.1016/j.kint.2017.02.034 | doi-access = free }}</ref> In simple terms, systemic vascular resistance is mainly determined by the caliber of small arteries and arterioles. The resistance attributable to a blood vessel depends on its radius as described by the [[Hagen–Poiseuille equation|Hagen-Poiseuille's equation]]  (resistance∝1/radius<sup>4</sup>). Hence, the smaller the radius, the higher the resistance. Other physical factors that affect resistance include: vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance)<ref>{{cite journal | vauthors = Lee AJ | title = The role of rheological and haemostatic factors in hypertension | journal = Journal of Human Hypertension | volume = 11 | issue = 12 | pages = 767–776 | date = December 1997 | pmid = 9468002 | doi = 10.1038/sj.jhh.1000556 | doi-access = free }}</ref> and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterial [[stenosis]] increases resistance to flow, however this increase in resistance rarely increases systemic blood pressure because its contribution to total systemic resistance is small, although it may profoundly decrease downstream flow.<ref>{{cite journal | vauthors = Coffman JD | title = Pathophysiology of obstructive arterial disease | journal = Herz | volume = 13 | issue = 6 | pages = 343–350 | date = December 1988 | pmid = 3061915 }}</ref> Substances called [[vasoconstrictor]]s reduce the caliber of blood vessels, thereby increasing blood pressure. [[Vasodilator]]s (such as [[nitroglycerin]]) increase the caliber of blood vessels, thereby decreasing arterial pressure. In the longer term a process termed remodeling also contributes to changing the caliber of small blood vessels and influencing resistance and reactivity to vasoactive agents.<ref>{{cite journal | vauthors = Korner PI, Angus JA | title = Structural determinants of vascular resistance properties in hypertension. Haemodynamic and model analysis | journal = Journal of Vascular Research | volume = 29 | issue = 4 | pages = 293–312 | date = 1992 | pmid = 1391553 | doi = 10.1159/000158945 }}</ref><ref>{{cite journal | vauthors = Mulvany MJ | title = Small artery remodelling in hypertension | journal = Basic & Clinical Pharmacology & Toxicology | volume = 110 | issue = 1 | pages = 49–55 | date = January 2012 | pmid = 21733124 | doi = 10.1111/j.1742-7843.2011.00758.x | doi-access = free }}</ref> Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances.<ref>{{cite journal | vauthors = de Moraes R, Tibirica E | title = Early Functional and Structural Microvascular Changes in Hypertension Related to Aging | journal = Current Hypertension Reviews | volume = 13 | issue = 1 | pages = 24–32 | date = 2017 | pmid = 28412915 | doi = 10.2174/1573402113666170413095508 }}</ref>

In practice, each individual's autonomic nervous system and other systems regulating blood pressure, notably the kidney,<ref>{{cite journal | vauthors = Guyton AC, Coleman TG, Cowley AV, Scheel KW, Manning RD, Norman RA | title = Arterial pressure regulation. Overriding dominance of the kidneys in long-term regulation and in hypertension | journal = The American Journal of Medicine | volume = 52 | issue = 5 | pages = 584–594 | date = May 1972 | pmid = 4337474 | doi = 10.1016/0002-9343(72)90050-2 }}</ref> respond to and regulate all these factors so that, although the above issues are important, they rarely act in isolation and the actual arterial pressure response of a given individual can vary widely in the short and long term.

===Pulse pressure===
{{main|Pulse pressure}}
[[File:Arterial-blood-pressure-curve.svg|thumb|A schematic representation of the arterial pressure waveform over one cardiac cycle. The notch in the curve is associated with closing of the aortic valve.]]
The pulse pressure is the difference between the measured systolic and diastolic pressures,<ref name = KlabundePulse2007 />

:::::::::::<math>\! P_{\text{pulse}} = P_{\text{sys}} - P_{\text{dias}}.</math>

The pulse pressure is a consequence of the pulsatile nature of the [[cardiac output]], i.e. the heartbeat. The magnitude of the pulse pressure is usually attributed to the interaction of the [[stroke volume]] of the heart, the compliance (ability to expand) of the arterial system—largely attributable to the [[aorta]] and large elastic arteries—and the [[Drag (physics)|resistance]] to flow in the [[arterial tree]].<ref name=KlabundePulse2007>{{cite web |url=http://www.cvphysiology.com/Blood%20Pressure/BP003.htm |title=Cardiovascular Physiology Concepts – Pulse Pressure |access-date=2008-10-02 | vauthors = Klabunde RE |year=2007 |url-status=dead |archive-url=https://web.archive.org/web/20091018055524/http://www.cvphysiology.com/Blood%20Pressure/BP003.htm |archive-date=2009-10-18 }}</ref>

====Clinical significance of pulse pressure====
A healthy pulse pressure is around 40 mmHg.<ref name="Homan Cichowski 2019"/> A pulse pressure that is consistently 60 mmHg or greater is likely to be associated with disease, and a pulse pressure of 50 mmHg or more increases the risk of [[cardiovascular disease]] as well as other complications such as eye and kidney disease.<ref name="Cleveland Clinic 2021">{{cite web |url=https://my.clevelandclinic.org/health/symptoms/21629-pulse-pressure |title= Pulse pressure  |author=<!--Not stated--> |date=28 July 2021 |publisher=Cleveland Clinic |access-date=10 February 2023 }}</ref> Pulse pressure is considered low if it is less than 25% of the systolic. (For example, if the systolic pressure is 120 mmHg, then the pulse pressure would be considered low if it is less than 30 mmHg, since 30 is 25% of 120.)<ref name="pmid21848774">{{cite journal | vauthors = Liaw SY, Scherpbier A, Klainin-Yobas P, Rethans JJ | title = A review of educational strategies to improve nurses' roles in recognizing and responding to deteriorating patients | journal = International Nursing Review | volume = 58 | issue = 3 | pages = 296–303 | date = September 2011 | pmid = 21848774 | doi = 10.1111/j.1466-7657.2011.00915.x }}</ref> A very low pulse pressure can be a symptom of disorders such as [[congestive heart failure]].<ref name="Cleveland Clinic 2021"/>

Elevated pulse pressure has been found to be a stronger independent predictor of cardiovascular events, especially in older populations, than has systolic, diastolic, or mean arterial pressure.<ref name="Cleveland Clinic 2021"/><ref name="Mitchell Izzo Lacourcière Ouellet 2002 pp. 2955–2961">{{cite journal | last1=Mitchell | first1=Gary F. | last2=Izzo | first2=Joseph L. | last3=Lacourcière | first3=Yves | last4=Ouellet | first4=Jean-Pascal | last5=Neutel | first5=Joel | last6=Qian | first6=Chunlin | last7=Kerwin | first7=Linda J. | last8=Block | first8=Alan J. | last9=Pfeffer | first9=Marc A. | title=Omapatrilat Reduces Pulse Pressure and Proximal Aortic Stiffness in Patients With Systolic Hypertension | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=105 | issue=25 | date=25 Jun 2002 | issn=0009-7322 | doi=10.1161/01.cir.0000020500.77568.3c | pages=2955–2961| pmid=12081987 | s2cid=7092379 }}</ref> This increased risk exists for both men and women and even when no other cardiovascular risk factors are present. The increased risk also exists even in cases in which diastolic pressure decreases over time while systolic remains steady.<ref name="Franklin Khan Wong Larson 1999 pp. 354–360">{{cite journal | last1=Franklin | first1=Stanley S. | last2=Khan | first2=Shehzad A. | last3=Wong | first3=Nathan D. | last4=Larson | first4=Martin G. | last5=Levy | first5=Daniel | title=Is Pulse Pressure Useful in Predicting Risk for Coronary Heart Disease? | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=100 | issue=4 | date=27 Jul 1999 | issn=0009-7322 | doi=10.1161/01.cir.100.4.354 | pages=354–360| pmid=10421594 | doi-access=free }}</ref><ref name="Benetos Safar Rudnichi Smulyan 1997 pp. 1410–1415">{{cite journal | last1=Benetos | first1=Athanase | last2=Safar | first2=Michel | last3=Rudnichi | first3=Annie | last4=Smulyan | first4=Harold | last5=Richard | first5=Jacques-Lucien | last6=Ducimetière | first6=Pierre | last7=Guize | first7=Louis | title=Pulse Pressure | journal=Hypertension | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=30 | issue=6 | year=1997 | issn=0194-911X | doi=10.1161/01.hyp.30.6.1410 | pages=1410–1415| pmid=9403561 }}</ref>

A [[meta-analysis]] in 2000 showed that a 10&nbsp;mmHg increase in pulse pressure was associated with a 20% increased risk of cardiovascular mortality, and a 13% increase in risk for all coronary end points. The study authors also noted that, while risks of cardiovascular end points do increase with higher systolic pressures, at any given systolic blood pressure the risk of major cardiovascular end points increases, rather than decreases, with lower diastolic levels. This suggests that interventions that lower diastolic pressure without also lowering systolic pressure (and thus lowering pulse pressure) could actually be counterproductive.<ref name = "pulse pressure not mean">{{cite journal | vauthors = Blacher J, Staessen JA, Girerd X, Gasowski J, Thijs L, Liu L, Wang JG, Fagard RH, Safar ME | display-authors = 6 | title = Pulse pressure not mean pressure determines cardiovascular risk in older hypertensive patients | journal = Archives of Internal Medicine | volume = 160 | issue = 8 | pages = 1085–1089 | date = April 2000 | pmid = 10789600 | doi = 10.1001/archinte.160.8.1085 | doi-access = free }}</ref> There are no drugs currently approved to lower pulse pressure, although some antihypertensive drugs may modestly lower pulse pressure, while in some cases a drug that lowers overall blood pressure may actually have the counterproductive side effect of raising pulse pressure.<ref name="cushman">{{cite journal |last1=Cushman |first1=William C. |last2=Materson |first2=Barry J. |last3=Williams |first3=David W. |last4=Reda |first4=Domenic J. |date=1 Oct 2001 |title=Pulse Pressure Changes With Six Classes of Antihypertensive Agents in a Randomized, Controlled Trial |journal=Hypertension |volume=38 |issue=4 |pages=953–957 |doi=10.1161/hy1001.096212|pmid=11641316|doi-access=free }}</ref>

Pulse pressure can both widen or narrow in people with [[sepsis]] depending on the degree of [[hemodynamic]] compromise. A pulse pressure of over 70 mmHg in sepsis is correlated with an increased chance of survival and a more positive response to [[Fluid replacement#Intravenous|IV fluids]].<ref name=pedsepsis>{{cite journal |vauthors=Khilnani P, Singhi S, Lodha R, Santhanam I, Sachdev A, Chugh K, Jaishree M, Ranjit S, Ramachandran B, Ali U, Udani S, Uttam R, Deopujari S |date=January 2010 |title=Pediatric Sepsis Guidelines: Summary for resource-limited countries |journal=Indian J Crit Care Med |volume=14 |issue=1 |pages=41–52 |doi=10.4103/0972-5229.63029 |pmc=2888329 |pmid=20606908 |doi-access=free }}</ref><ref name=widesepsis>{{cite journal |vauthors=Al-Khalisy H, Nikiforov I, Jhajj M, Kodali N, Cheriyath P |date=11 December 2015 |title=A widened pulse pressure: a potential valuable prognostic indicator of mortality in patients with sepsis. J Community Hosp Intern Med Perspect |journal=J Community Hosp Intern Med Perspect |volume=5 |issue=6 |page=29426 |doi=10.3402/jchimp.v5.29426 |pmc=4677588 |pmid=26653692 }}</ref>

===Mean arterial pressure===
{{main|Mean arterial pressure}}
[[Mean arterial pressure]] (MAP) is the average of blood pressure over a [[cardiac cycle]] and is determined by the [[cardiac output]] (CO), [[systemic vascular resistance]] (SVR), and [[central venous pressure]] (CVP):<ref name="Mayet Hughes 2003 pp. 1104–9"/><ref name="Granger Hall 2007 pp. 241–263">{{cite book |  vauthors = Granger JP, Hall JE | title=Comprehensive Hypertension | chapter=Role of the Kidney in Hypertension | publisher=Elsevier | year=2007 | isbn=978-0-323-03961-1 | doi=10.1016/b978-0-323-03961-1.50026-x | pages=241–263}}</ref><ref name=KlabundeMAP2007>{{cite web |url=http://www.cvphysiology.com/Blood%20Pressure/BP006.htm |title=Cardiovascular Physiology Concepts – Mean Arterial Pressure |access-date=2008-09-29 | vauthors = Klabunde RE |year=2007 |url-status=dead |archive-url=https://web.archive.org/web/20091002040008/http://www.cvphysiology.com/Blood%20Pressure/BP006.htm |archive-date=2009-10-02 }}</ref>

:::::::::::<math>\! \text{MAP} = (\text{CO} \cdot \text{SVR}) + \text{CVP} </math>

In practice, the contribution of CVP (which is small) is generally ignored and so

:::::::::::<math>\! \text{MAP} = \text{CO} \cdot \text{SVR} </math>

MAP is often estimated from measurements of the systolic pressure,  <math> \! P_{\text{sys}}</math> and the diastolic pressure,  <math> \! P_{\text{dias}}</math>&nbsp;<ref name="KlabundeMAP2007" /> using the equation:

<math>\! \text{MAP} \approxeq P_{\text{dias}} + k (P_{\text{sys}} - P_{\text{dias}})</math>

where ''k'' = 0.333 although other values for ''k'' have been advocated.<ref>{{cite journal | vauthors = Bos WJ, Verrij E, Vincent HH, Westerhof BE, Parati G, van Montfrans GA | title = How to assess mean blood pressure properly at the brachial artery level | journal = Journal of Hypertension | volume = 25 | issue = 4 | pages = 751–755 | date = April 2007 | pmid = 17351365 | doi = 10.1097/HJH.0b013e32803fb621 | s2cid = 23155959 }}</ref><ref>{{cite journal | vauthors = Meaney E, Alva F, Moguel R, Meaney A, Alva J, Webel R | title = Formula and nomogram for the sphygmomanometric calculation of the mean arterial pressure | journal = Heart | volume = 84 | issue = 1 | pages = 64 | date = July 2000 | pmid = 10862592 | pmc = 1729401 | doi = 10.1136/heart.84.1.64 }}</ref>

===Regulation of blood pressure===
{{See also|Renin–angiotensin system}}
The [[endogenous]], [[Homeostasis|homeostatic]] regulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized:
* [[Baroreceptor reflex]]: [[Baroreceptor]]s in the [[high pressure receptor zones]] detect changes in arterial pressure. These baroreceptors send signals ultimately to the [[medulla oblongata|medulla of the brain stem]], specifically to the [[rostral ventrolateral medulla]] (RVLM). The medulla, by way of the [[autonomic nervous system]], adjusts the mean arterial pressure by altering both the force and speed of the heart's contractions, as well as the systemic vascular resistance. The most important arterial baroreceptors are located in the left and right [[carotid sinus]]es and in the [[aortic arch]].<ref name='KlabundeArtBar2007'>{{cite web |url=http://www.cvphysiology.com/Blood%20Pressure/BP012.htm |title=Cardiovascular Physiology Concepts – Arterial Baroreceptors |access-date=2008-09-09 |vauthors=Klabunde RE |year=2007 |archive-date=2009-12-23 |archive-url=https://web.archive.org/web/20091223020230/http://www.cvphysiology.com/Blood%20Pressure/BP012.htm |url-status=live }}</ref>
* [[Renin–angiotensin system]] (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows the [[kidney]] to compensate for loss in [[blood volume]] or drops in arterial pressure by activating an endogenous [[vasoconstrictor]] known as [[angiotensin II]].
* [[Aldosterone]] release: This [[steroid hormone]] is released from the [[adrenal cortex]] in response to activation of the renin-angiotensin system, high serum [[potassium]] levels, or elevated [[Adrenocorticotropic hormone|adrenocorticotropic hormone (ACTH)]]. Renin converts angiotensinogen to angiotensin I, which is converted by [[Angiotensin-converting enzyme|angiotensin converting enzyme]] to angiotensin II. Angiotensin II then signals to the adrenal cortex to release aldosterone.<ref>{{cite book |vauthors=Fountain J, Lappin SL |chapter=Physiology, Renin Angiotensin System. |date=January 2022 |title=StatPearls |publisher=StatPearls Publishing |location=Treasure Island, FL |pmid=29261862 |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK470410/ |access-date=18 November 2022 |archive-date=29 April 2019 |archive-url=https://web.archive.org/web/20190429200530/https://www.ncbi.nlm.nih.gov/books/NBK470410/ |url-status=live }}</ref> Aldosterone stimulates [[sodium]] retention and potassium excretion by the kidneys and the consequent salt and water retention increases plasma volume, and indirectly, arterial pressure. Aldosterone may also exert direct pressor effects on vascular smooth muscle and central effects on sympathetic nervous system activity.<ref>{{cite journal | vauthors = Feldman RD | title = Aldosterone and blood pressure regulation: recent milestones on the long and winding road from electrocortin to KCNJ5, GPER, and beyond | journal = Hypertension | volume = 63 | issue = 1 | pages = 19–21 | date = January 2014 | pmid = 24191283 | doi = 10.1161/HYPERTENSIONAHA.113.01251 | doi-access = free }}</ref>
* [[Baroreceptor]]s in [[low pressure receptor zones]] (mainly in the [[venae cavae]] and the [[pulmonary veins]], and in the [[atrium (heart)|atria]]) result in feedback by regulating the secretion of [[antidiuretic hormone]] (ADH/vasopressin), [[renin]] and [[aldosterone]]. The resultant increase in [[blood volume]] results in an increased [[cardiac output]] by the [[Frank–Starling law of the heart]], in turn increasing arterial blood pressure.

These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. When blood pressure falls many physiological cascades commence in order to return the blood pressure to a more appropriate level.

# The blood pressure fall is detected by a decrease in blood flow and thus a decrease in [[glomerular filtration rate]] (GFR).
# Decrease in GFR is sensed as a decrease in Na<sup>+</sup> levels by the [[macula densa]].
# The macula densa causes an increase in Na<sup>+</sup> reabsorption, which causes water to follow in via [[osmosis]] and leads to an ultimate increase in [[blood plasma|plasma]] volume. Further, the macula densa releases adenosine which causes constriction of the afferent arterioles.
# At the same time,  the [[juxtaglomerular cells]] sense the decrease in blood pressure and release [[renin]].
# Renin converts [[angiotensinogen]] (inactive form) to [[angiotensin I]] (active form).
# Angiotensin I flows in the bloodstream until it reaches the capillaries of the lungs where [[angiotensin-converting enzyme]] (ACE) acts on it to convert it into [[angiotensin II]].
# Angiotensin II is a vasoconstrictor that will increase blood flow to the heart and subsequently the preload, ultimately increasing the [[cardiac output]].
# Angiotensin II also causes an increase in the release of [[aldosterone]] from the [[adrenal gland]]s.
# Aldosterone further increases the Na<sup>+</sup> and H<sub>2</sub>O reabsorption in the [[distal convoluted tubule]] of the [[nephron]].

The RAS is targeted pharmacologically by [[ACE inhibitor]]s and [[angiotensin II receptor antagonist]]s (also known as angiotensin receptor blockers; ARB). The aldosterone system is directly targeted by [[aldosterone antagonist]]s. The fluid retention may be targeted by [[diuretic]]s; the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted in [[hypertension]] because if blocked, individuals may experience [[orthostatic hypotension]] and [[fainting]].

==Measurement==
{{Main|Blood pressure measurement}}
[[File:Blood Pressure - Take Another Person.png|thumb|Taking blood pressure with a sphygmomanometer]]
[[File:blood_pressure_measurement_principle.svg|thumb|Measuring systolic and diastolic blood pressure using a mercury sphygmomanometer]]
Arterial pressure is most commonly measured via a [[sphygmomanometer]], which uses the height of a column of mercury, or an [[aneroid gauge]], to reflect the blood pressure by auscultation.<ref name='Booth1977'>{{cite journal | vauthors = Booth J | title = A short history of blood pressure measurement | journal = Proceedings of the Royal Society of Medicine | volume = 70 | issue = 11 | pages = 793–799 | date = November 1977 | pmid = 341169 | pmc = 1543468 | doi = 10.1177/003591577707001112 }}</ref> The most common automated blood pressure measurement technique is based on the [[Blood pressure measurement#Oscillometric|oscillometric]] method.<ref name=For2015>{{cite journal | vauthors = Forouzanfar M, Dajani HR, Groza VZ, Bolic M, Rajan S, Batkin I | title = Oscillometric Blood Pressure Estimation: Past, Present, and Future | journal = IEEE Reviews in Biomedical Engineering | volume = 8 | pages = 44–63 | date = 2015-01-01 | pmid = 25993705 | doi = 10.1109/RBME.2015.2434215 | s2cid = 8940215 }}</ref> Fully automated oscillometric measurement has been available since 1981.<ref>{{Cite web|url=https://patents.google.com/patent/US4427013A/en?q=donald&q=nunn&oq=donald+nunn|title=Apparatus and method for measuring blood pressure|via=Google patents|access-date=2019-01-12|archive-date=2022-10-26|archive-url=https://web.archive.org/web/20221026151549/https://patents.google.com/patent/US4427013A/en?q=donald&q=nunn&oq=donald+nunn|url-status=live}}</ref> This principle has recently been used to measure blood pressure with a smartphone.<ref>{{cite journal | vauthors = Chandrasekhar A, Kim CS, Naji M, Natarajan K, Hahn JO, Mukkamala R | title = Smartphone-based blood pressure monitoring via the oscillometric finger-pressing method | journal = Science Translational Medicine | volume = 10 | issue = 431 | pages = eaap8674 | date = March 2018 | pmid = 29515001 | pmc = 6039119 | doi = 10.1126/scitranslmed.aap8674 }}</ref> Measuring pressure [[Invasive blood pressure|invasively]], by penetrating the arterial wall to take the measurement, is much less common and usually restricted to a hospital setting. Novel methods to measure blood pressure without penetrating the arterial wall, and without applying any pressure on patient's body are being explored,<ref>{{cite book |vauthors=Solà J, Delgado-Gonzalo R |title=The Handbook of Cuffless Blood Pressure Monitoring |date=2019 |publisher=Springer International Publishing |isbn=978-3-030-24701-0 |url=https://www.springer.com/gp/book/9783030247003 |access-date=2020-01-29 |archive-date=2021-06-17 |archive-url=https://web.archive.org/web/20210617182758/https://www.springer.com/gp/book/9783030247003 |url-status=live }}</ref> for example, cuffless measurements that uses only optical sensors.<ref>{{cite journal | vauthors = Sola J, Bertschi M, Krauss J | title = Measuring Pressure: Introducing oBPM, the Optical Revolution for Blood Pressure Monitoring | journal = IEEE Pulse | volume = 9 | issue = 5 | pages = 31–33 | date = September 2018 | pmid = 30273141 | doi = 10.1109/MPUL.2018.2856960 | s2cid = 52893219 }}</ref>

In office blood pressure measurement, [[terminal digit preference]] is common. According to one study, approximately 40% of recorded measurements ended with the digit zero, whereas "without bias, 10%–20% of measurements are expected to end in zero"<ref>{{cite journal | vauthors = Foti KE, Appel LJ, Matsushita K, Coresh J, Alexander GC, Selvin E | title = Digit Preference in Office Blood Pressure Measurements, United States 2015-2019 | journal = American Journal of Hypertension | volume = 34 | issue = 5 | pages = 521–530 | date = May 2021 | pmid = 33246327 | pmc = 8628654 | doi = 10.1093/ajh/hpaa196 | author-link4 = Josef Coresh }}</ref>

==In animals==
Blood pressure levels in non-human mammals may vary depending on the species. Heart rate differs markedly, largely depending on the size of the animal (larger animals have slower heart rates).<ref>{{Cite book|title=The Design of Mammals: A Scaling Approach | vauthors = Prothero JW |isbn=978-1-107-11047-2 |location=Cambridge |publisher=Cambridge University Press |oclc=907295832|date=2015-10-22}}</ref> The giraffe has a distinctly high arterial pressure of about 190&nbsp;mm Hg, enabling blood perfusion through the {{convert|2|m}}-long neck to the head.<ref name="brondum">{{cite journal | vauthors = Brøndum E, Hasenkam JM, Secher NH, Bertelsen MF, Grøndahl C, Petersen KK, Buhl R, Aalkjaer C, Baandrup U, Nygaard H, Smerup M, Stegmann F, Sloth E, Ostergaard KH, Nissen P, Runge M, Pitsillides K, Wang T | display-authors = 6 | title = Jugular venous pooling during lowering of the head affects blood pressure of the anesthetized giraffe | journal = American Journal of Physiology. Regulatory, Integrative and Comparative Physiology | volume = 297 | issue = 4 | pages = R1058–R1065 | date = October 2009 | pmid = 19657096 | doi = 10.1152/ajpregu.90804.2008 }}</ref> In other species subjected to orthostatic blood pressure, such as [[Arboreal locomotion|arboreal]] snakes, blood pressure is higher than in non-arboreal snakes.<ref>{{cite journal | vauthors = Seymour RS, Lillywhite HB | title = Blood pressure in snakes from different habitats | journal = Nature | volume = 264 | issue = 5587 | pages = 664–666 | date = December 1976 | pmid = 1004612 | doi = 10.1038/264664a0 | s2cid = 555576 | bibcode = 1976Natur.264..664S }}</ref> A heart near to the head (short heart-to-head distance) and a long tail with tight [[integument]] favor blood perfusion to the head.<ref>{{cite journal | vauthors = Nasoori A, Taghipour A, Shahbazzadeh D, Aminirissehei A, Moghaddam S | title = Heart place and tail length evaluation in Naja oxiana, Macrovipera lebetina, and Montivipera latifii | journal = Asian Pacific Journal of Tropical Medicine | volume = 7S1 | pages = S137–S142 | date = September 2014 | pmid = 25312108 | doi = 10.1016/s1995-7645(14)60220-0 | doi-access = free }}</ref><ref name="seymour">{{cite journal | vauthors = Seymour RS | title=Scaling of cardiovascular physiology in snakes | journal=American Zoologist| volume=27 | issue=1 | year=1987 | issn=0003-1569 | doi=10.1093/icb/27.1.97 | pages=97–109| doi-access=free }}</ref>

As in humans, blood pressure in animals differs by age, sex, time of day, and environmental circumstances:<ref name=":1">{{Cite book|title=Animal Models in Cardiovascular Research| vauthors = Gross DR |publisher=Springer |year=2009 |isbn=978-0-387-95962-7 |edition= 3rd |location=Dordrecht |pages=5 |oclc=432709394}}</ref><ref name=":2">{{cite journal | vauthors = Brown S, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, Egner B, Elliott J, Henik R, Labato M, Littman M, Polzin D, Ross L, Snyder P, Stepien R | display-authors = 6 | title = Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats | journal = Journal of Veterinary Internal Medicine | volume = 21 | issue = 3 | pages = 542–558 | date = 2007 | pmid = 17552466 | doi = 10.1111/j.1939-1676.2007.tb03005.x | doi-access = free }}</ref> measurements made in laboratories or under anesthesia may not be representative of values under free-living conditions. Rats, mice, dogs and rabbits have been used extensively to study the regulation of blood pressure.<ref>{{cite journal | vauthors = Lerman LO, Chade AR, Sica V, Napoli C | title = Animal models of hypertension: an overview | journal = The Journal of Laboratory and Clinical Medicine | volume = 146 | issue = 3 | pages = 160–173 | date = September 2005 | pmid = 16131455 | doi = 10.1016/j.lab.2005.05.005 }}</ref>
{| class="wikitable sortable"
|+Blood pressure and heart rate of various mammals<ref name=":1" />
!rowspan=2|Species
!colspan=2|Blood pressure<br />mm Hg

!rowspan=2|Heart rate<br />beats per minute
|-
!Systolic
!Diastolic
|-
|Calves
|140
|70
|75–146
|-
|Cats
|155
|68
|100–259
|-
|Dogs
|161
|51
|62–170
|-
|Goats
|140
|90
|80–120
|-
|Guinea-pigs
|140
|90
|240–300
|-
|Mice
|120
|75
|580–680
|-
|Pigs
|169
|55
|74–116
|-
|Rabbits
|118
|67
|205–306
|-
|Rats
|153
|51
|305–500
|-
|Rhesus monkeys
|160
|125
|180–210
|-
|Sheep
|140
|80
|63–210
|}

===Hypertension in cats and dogs===
Hypertension in cats and dogs is generally diagnosed if the blood pressure is greater than 150&nbsp;mm Hg (systolic),<ref>{{Cite web |title=AKC Canine Health Foundation {{!}} Hypertension in Dogs |url=https://www.akcchf.org/canine-health/your-dogs-health/caring-for-your-dog/hypertension-in-dogs.html |access-date=2022-10-03 |website=www.akcchf.org |archive-date=2022-10-03 |archive-url=https://web.archive.org/web/20221003215934/https://www.akcchf.org/canine-health/your-dogs-health/caring-for-your-dog/hypertension-in-dogs.html |url-status=live }}</ref> although [[Sighthound|sight hounds]] have higher blood pressures than most other dog breeds; a systolic pressure greater than 180 mmHg is considered abnormal in these dogs.<ref>{{cite journal | vauthors = Acierno MJ, Brown S, Coleman AE, Jepson RE, Papich M, Stepien RL, Syme HM | title = ACVIM consensus statement: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats | journal = Journal of Veterinary Internal Medicine | volume = 32 | issue = 6 | pages = 1803–1822 | date = November 2018 | pmid = 30353952 | pmc = 6271319 | doi = 10.1111/jvim.15331 }}</ref>

==See also==
* [[History of hypertension]]

== References ==
{{Reflist}}

== External links ==
* {{Commons category inline|Blood pressure}}

{{Cardiovascular physiology}}
{{Authority control}}
{{Interwiki extra|qid=Q9062560}}

{{DEFAULTSORT:Blood Pressure}}
[[Category:Blood pressure| ]]
[[Category:Articles containing video clips]]
[[Category:Cardiovascular physiology]]
[[Category:Mathematics in medicine]]