Blood pressure(Redirected from Diastolic blood pressure)
Blood pressure (BP) is the pressure of circulating blood on the walls of blood vessels. When used without further specification, "blood pressure" usually refers to the pressure in large arteries of the systemic circulation. Blood pressure is usually expressed in terms of the systolic pressure (maximum during one heart beat) over diastolic pressure (minimum in between two heart beats) and is measured in millimeters of mercury (mmHg), above the surrounding atmospheric pressure (considered to be zero for convenience).
A sphygmomanometer, a device used for measuring arterial pressure
It is one of the vital signs, along with respiratory rate, heart rate, oxygen saturation, and body temperature. Normal resting blood pressure in an adult is approximately 120 millimetres of mercury (16 kPa) systolic, and 80 millimetres of mercury (11 kPa) diastolic, abbreviated "120/80 mmHg".
Traditionally, blood pressure was measured non-invasively using a mercury manometer and this is still generally considered the gold standard. More recently other semi-automated methods have become common, largely due to concerns about potential mercury toxicity, although cost and ease of use have also influenced this trend. Early alternatives to mercury sphygmomanometers were often inaccurate, but more modern validated devices have similar accuracy to mercury devices.
Blood pressure is influenced by cardiac output, total peripheral resistance and arterial stiffness and varies depending on situation, emotional state, activity, and relative health/disease states. In the short term it is regulated by baroreceptors which act via the brain to influence nervous and endocrine systems.
Blood pressure that is low due to a disease state is called hypotension, and pressure that is consistently high is hypertension. Both have many causes and may be of sudden onset or of long duration. Long term hypertension is a risk factor for many diseases, including heart disease, stroke and kidney failure. Long term hypertension is more common than long term hypotension. Long term hypertension often goes undetected because of infrequent monitoring and the absence of symptoms.
Systemic arterial pressureEdit
|Category||systolic, mmHg||diastolic, mmHg|
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.
The table shows the classification of blood pressure adopted by the American Heart Association for adults who are 18 years and older. It assumes the values are a result of averaging resting blood pressure readings measured at two or more visits to the doctor.
Blood pressure fluctuates from minute to minute and normally shows a circadian rhythm over a 24-hour period, with highest readings in the early morning and evenings and lowest readings at night. 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. Also, an individual's blood pressure varies with exercise, emotional reactions, sleep, digestion and time of day (circadian rhythm).
Various other factors, such as age and sex, also influence a person's blood pressure. In children, the normal ranges are lower than for adults and depend on height. Reference blood pressure values have been developed for children in different countries, based on the distribution of blood pressure in children of these countries. As adults age, systolic pressure tends to rise and diastolic pressure tends to fall. Consequently, in the elderly, systolic blood pressure often exceeds the normal adult range, this is thought to be due to increased stiffness of the arteries.
Differences between left and right arm blood pressure measurements tend to be small. However, occasionally there is a consistent difference greater than 10 mmHg which may need further investigation, e.g. for obstructive arterial disease.
|Infants||1 to 12 months||75–100||50–70|
|Toddlers and preschoolers||1 to 5 years||80–110||50–80|
|School age||6 to 12 years||85–120||50–80|
|Adolescents||13 to 18 years||95–140||60–90|
Mean arterial pressureEdit
In practice the contribution of CVP (which is small) is generally ignored and so
MAP can be estimated from measurements of the systolic pressure and the diastolic pressure 
The up and down fluctuation of the arterial pressure results from the pulsatile nature of the cardiac output, i.e. the heartbeat. Pulse pressure is determined by 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 resistance to flow in the arterial tree. By expanding under pressure, the aorta absorbs some of the force of the blood surge from the heart during a heartbeat. In this way, the pulse pressure is reduced from what it would be if the aorta were not compliant. The loss of arterial compliance that occurs with aging explains the elevated pulse pressures found in elderly patients.
Systemic venous pressureEdit
|Central venous pressure||3–8|
|Right ventricular pressure||systolic||15–30|
|Pulmonary artery pressure||systolic||15–30|
|Left ventricular pressure||systolic||100–140|
Blood pressure generally refers to the arterial pressure in the systemic circulation. However, measurement of pressures in the venous system and the 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 atria of the heart. It is much less than arterial pressure, with common values of 5 mmHg in the right atrium and 8 mmHg in the left atrium.
Variants of venous pressure include:
- Central venous pressure, which is a good approximation of right atrial pressure, which is a major determinant of right ventricular end diastolic volume. (However, there can be exceptions in some cases.)
- 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 and lung disease.
- The portal venous pressure is the blood pressure in the portal vein. It is normally 5–10 mmHg
Increased blood pressure in the capillaries of the lung causes pulmonary hypertension, leading to interstitial edema if the pressure increases to above 20 mmHg, and to pulmonary edema at pressures above 25 mmHg.
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 heart muscle tends to thicken, enlarge and become weaker over time.
Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysms, and is the leading cause of chronic kidney failure. Even moderate elevation of arterial pressure leads to shortened life expectancy. 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.
In the past, most attention was paid to diastolic pressure; but nowadays it is recognised that both high systolic pressure and high pulse pressure (the numerical difference between systolic and diastolic pressures) are also risk factors. In some cases, it appears that a decrease in excessive diastolic pressure can actually increase risk, due probably to the increased difference between systolic and diastolic pressures (see the article on pulse pressure). If systolic blood pressure is elevated (>140 mmHg) with a normal diastolic blood pressure (<90 mmHg), it is called "isolated systolic hypertension" and may present a health concern.
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 2 weeks apart for each person, there was an increased severity of aortic and mitral regurgitation when diastolic blood pressure increased, whereas when diastolic blood pressure decreased, there was a decreased severity.
When arterial pressure and blood flow decrease beyond a certain point, the perfusion of the brain becomes critically decreased (i.e., the blood supply is not sufficient), causing lightheadedness, dizziness, weakness or fainting.
Sometimes the arterial pressure drops significantly when a patient stands up from sitting. This is known as orthostatic hypotension (postural hypotension); gravity reduces the rate of blood return from the body veins below the heart back to the heart, thus reducing stroke volume and cardiac output.
When people are healthy, the veins below their heart quickly constrict and the heart rate increases to minimize and compensate for the gravity effect. This is carried out involuntarily by the autonomic nervous system. The system usually requires a few seconds to fully adjust and if the compensations are too slow or inadequate, the individual will suffer reduced blood flow to the brain, dizziness and potential blackout. Increases in G-loading, such as routinely experienced by aerobatic or combat pilots 'pulling Gs', greatly increases this effect. Repositioning the body horizontally largely eliminates the problem.
Other causes of low arterial pressure include:
- Hemorrhage – blood loss
- Toxins including toxic doses of blood pressure medicine
- Hormonal abnormalities, such as Addison's disease
- Eating disorders, particularly anorexia nervosa and bulimia
Shock is a complex condition which leads to critically decreased perfusion. The usual mechanisms are loss of blood volume, pooling of blood within the veins reducing adequate return to the heart and/or low effective heart pumping. Low arterial pressure, especially low pulse pressure, is a sign of shock and contributes to and reflects decreased perfusion.
If there is a significant difference in the pressure from one arm to the other, that may indicate a narrowing (for example, due to aortic coarctation, aortic dissection, thrombosis or embolism) of an artery.
Fluctuating blood pressureEdit
Normal fluctuation in blood pressure is adaptive and necessary. Fluctuations in pressure that are significantly greater than the norm are associated with greater white matter hyperintensity, a finding consistent with reduced local cerebral blood flow and a heightened risk of cerebrovascular disease. Within both high and low blood pressure groups, a greater degree of fluctuation was found to correlate with an increase in cerebrovascular disease compared to those with less variability, suggesting the consideration of the clinical management of blood pressure fluctuations, even among normotensive older adults. Older individuals and those who had received blood pressure medications were more likely to exhibit larger fluctuations in pressure.
During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastolic) pressure. The blood pressure in the circulation is principally due to the pumping action of the heart. Differences in mean blood pressure are responsible for blood flow from one location to another in the circulation. The rate of mean blood flow depends on both blood pressure and the resistance to flow presented by the blood vessels. Mean blood pressure decreases as the circulating blood moves away from the heart through arteries and capillaries due to viscous losses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries and arterioles. 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 in veins.
Most influences on blood pressure can be understood in terms of their effect on cardiac output and resistance (the determinants of mean arterial pressure).
Some factors are:
- Blood volume: the greater the blood volume, the higher the cardiac output. There is some relationship between dietary salt intake and increased blood volume, potentially resulting in higher arterial pressure, though this varies with the individual and is highly dependent on autonomic nervous system response and the renin–angiotensin system.
- Cardiac output: the pumping action of the heart is ultimately responsible for blood pressure. Increases or decreases in cardiac output can result in increases or decreases respectively in blood pressure.
- Systemic vascular resistance: the higher the resistance to blood flow, the higher the arterial pressure upstream needs to be to maintain flow. In simple terms, resistance is related to vessel radius by the Hagen-Poiseuille's equation (resistance∝1/radius4, so the smaller the radius, the very much 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) and the presence of an arterial stenosis (a narrow stenosis increases resistance to flow, however this increase in resistance rarely if ever increases systemic blood pressure, it decreases downstream flow). Substances called vasoconstrictors can reduce the calibre of blood vessels, thereby increasing blood pressure. Vasodilators (such as nitroglycerin) increase the calibre of blood vessels, thereby decreasing arterial pressure.
In practice, each individual's autonomic nervous system and other systems regulating blood pressure 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.
The endogenous regulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized:
- Baroreceptor reflex: Baroreceptors in the high pressure receptor zones detect changes in arterial pressure. These baroreceptors send signals ultimately to the 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 sinuses and in the aortic arch.
- 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 angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.
- Baroreceptors in low pressure receptor zones (mainly in the venae cavae and the pulmonary veins, and in the 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+ levels by the macula densa.
- The macula densa cause an increase in Na+ reabsorption, which causes water to follow in via osmosis and leads to an ultimate increase in 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 which will increase bloodflow 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 glands.
- Aldosterone further increases the Na+ and H2O reabsorption in the distal convoluted tubule of the nephron.
Currently, the RAS is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists. The aldosterone system is directly targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted by diuretics; 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 suffer from orthostatic hypotension and fainting.
Arterial pressure is most commonly measured via a sphygmomanometer, which historically used the height of a column of mercury to reflect the circulating pressure. The most common automated blood pressure measurement technique is based on the so-called "oscillometric" method. Blood pressure values are generally reported in millimetres of mercury (mmHg), though aneroid and electronic devices do not contain mercury.
For each heartbeat, blood pressure varies between systolic and diastolic pressures. Systolic pressure is peak pressure in the arteries, which occurs near the end of the cardiac cycle when the ventricles are contracting. Diastolic pressure is minimum pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are filled with blood. An example of normal measured values for a resting, healthy adult human is 120 mmHg systolic and 80 mmHg diastolic (written as 120/80 mmHg, and spoken as "one-twenty over eighty").
Systolic and diastolic arterial blood pressures are not static but undergo natural variations from one heartbeat to another and throughout the day (in a circadian rhythm). They also change in response to stress, nutritional factors, drugs, disease, exercise, and momentarily from standing up. Sometimes the variations are large. Hypertension refers to arterial pressure being abnormally high, as opposed to hypotension, when it is abnormally low. Along with body temperature, respiratory rate, and pulse rate, blood pressure is one of the four main vital signs routinely monitored by medical professionals and healthcare providers.
Measuring pressure invasively, by penetrating the arterial wall to take the measurement, is much less common and usually restricted to a hospital setting.
Fetal blood pressureEdit
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 mmHg at 20 weeks of gestation, and increases to approximately 45 mmHg at 40 weeks of gestation.
The average blood pressure for full-term infants:
- Systolic 65–95 mmHg
- Diastolic 30–60 mmHg
- Ogedegbe, Gbenga; Pickering, Thomas (2010-11-01). "Principles and techniques of blood pressure measurement". Cardiology Clinics. 28 (4): 571–586. ISSN 1558-2264. PMC . PMID 20937442. doi:10.1016/j.ccl.2010.07.006.
- O'brien, Eoin (2001-01-01). "Blood pressure measurement is changing!". Heart. 85 (1): 3–5. ISSN 1468-201X. PMC . PMID 11119446. doi:10.1136/heart.85.1.3.
- "Understanding blood pressure readings". American Heart Association. 11 January 2011. Retrieved 30 March 2011.
- Mayo Clinic staff (2009-05-23). "Low blood pressure (hypotension) – Causes". MayoClinic.com. Mayo Foundation for Medical Education and Research. Retrieved 2010-10-19.
- "Guideline for the diagnosis and management of hypertension in adults" (PDF). Heart Foundation. 2016. p. 12. Retrieved 12 January 2017.
- Appel LJ, Brands MW, Daniels SR, Karanja N, Elmer PJ, Sacks FM (February 2006). "Dietary approaches to prevent and treat hypertension: a scientific statement from the American Heart Association". Hypertension. 47 (2): 296–308. PMID 16434724. doi:10.1161/01.HYP.0000202568.01167.B6.
- Yusuf, Salim; Lonn, Eva (2016-11-01). "The SPRINT and the HOPE-3 Trial in the Context of Other Blood Pressure-Lowering Trials". JAMA cardiology. 1 (8): 857–858. ISSN 2380-6591. PMID 27602555. doi:10.1001/jamacardio.2016.2169.
- Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT, Roccella EJ (December 2003). "Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure". Hypertension. 42 (6): 1206–52. PMID 14656957. doi:10.1161/01.HYP.0000107251.49515.c2.
- "Diseases and conditions index – hypotension". National Heart Lung and Blood Institute. September 2008. Retrieved 2008-09-16.
- NHS choices: What is blood pressure? Retrieved 2012-03-27
- NHS choices: High blood pressure (hypertension) Retrieved 2012-03-27
- Table: 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
- van Berge-Landry HM, Bovbjerg DH, James GD (October 2008). "Relationship between waking-sleep blood pressure and catecholamine changes in African-American and European-American women". Blood Press Monit. 13 (5): 257–62. PMC . PMID 18799950. doi:10.1097/MBP.0b013e3283078f45. NIHMS90092.
- Hansen, T. W.; Li, Y.; Boggia, J.; Thijs, L.; Richart, T.; Staessen, J. A. (2010). "Predictive Role of the Nighttime Blood Pressure". Hypertension. 57 (1): 3–10. ISSN 0194-911X. doi:10.1161/HYPERTENSIONAHA.109.133900.
- National Heart, Lung and Blood Institute. "Blood pressure tables for children and adolescents". (Note that the median blood pressure is given by the 50th percentile and hypertension is defined by the 95th percentile for a given age, height, and sex.)
- Chiolero A (Mar 2014). "The quest for blood pressure reference values in children.". Journal of Hypertension. 32 (3): 477–79. PMID 24477093. doi:10.1097/HJH.0000000000000109.
- (Pickering et al. 2005, p. 145) See Isolated Systolic Hypertension.
- "...more than half of all Americans aged 65 or older have hypertension." (Pickering et al. 2005, p. 144)
- Franklin, Stanley S. (2008-05-01). "Beyond blood pressure: Arterial stiffness as a new biomarker of cardiovascular disease". Journal of the American Society of Hypertension: JASH. 2 (3): 140–151. ISSN 1933-1711. PMID 20409896. doi:10.1016/j.jash.2007.09.002.
- Eguchi K, Yacoub M, Jhalani J, Gerin W, Schwartz JE, Pickering TG (February 2007). "Consistency of blood pressure differences between the left and right arms". Arch Intern Med. 167 (4): 388–93. PMID 17325301. doi:10.1001/archinte.167.4.388.
- Agarwal R, Bunaye Z, Bekele DM (March 2008). "Prognostic significance of between-arm blood pressure differences". Hypertension. 51 (3): 657–62. PMID 18212263. doi:10.1161/HYPERTENSIONAHA.107.104943.
- PEDIATRIC AGE SPECIFIC, p. 6. Revised 6/10. By Theresa Kirkpatrick and Kateri Tobias. UCLA Health System
- Klabunde, RE (2007). "Cardiovascular Physiology Concepts – Mean Arterial Pressure". Archived from the original on 2009-10-04. Retrieved 2008-09-29.
- Klabunde, RE (2007). "Cardiovascular Physiology Concepts – Pulse Pressure". Archived from the original on 2009-10-04. Retrieved 2008-10-02.
- Table 30-1 in: Trudie A Goers; Washington University School of Medicine Department of Surgery; Klingensmith, Mary E; Li Ern Chen; Sean C Glasgow (2008). The Washington manual of surgery. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 0-7817-7447-0.
- "Central Venous Catheter Physiology". Archived from the original on 2008-08-21. Retrieved 2009-02-27.
- Tkachenko BI, Evlakhov VI, Poyasov IZ (2002). "Independence of changes in right atrial pressure and central venous pressure". Bull. Exp. Biol. Med. 134 (4): 318–20. PMID 12533747. doi:10.1023/A:1021931508946.
- "Esophageal Varices : Article Excerpt by: Samy A Azer". eMedicine. Retrieved 2011-08-22.
- What Is Pulmonary Hypertension? From Diseases and Conditions Index (DCI). National Heart, Lung, and Blood Institute. Last updated September 2008. Retrieved on 6 April 2009.
- Chapter 41, p. 210 in: Cardiology secrets By Olivia Vynn Adair Edition: 2, illustrated Published by Elsevier Health Sciences, 2001 ISBN 1-56053-420-6, ISBN 978-1-56053-420-4
- Textbook of Medical Physiology, 7th Ed., Guyton & Hall, Elsevier-Saunders, ISBN 0-7216-0240-1, p. 220.
- "Isolated systolic hypertension: A health concern? – MayoClinic.com". Retrieved 2011-12-07.
- "Clinical Management of Isolated Systolic Hypertension". Archived from the original on September 29, 2011. Retrieved 2011-12-07.
- Gottdiener JS, Panza JA, St John Sutton M, Bannon P, Kushner H, Weissman NJ (July 2002). "Testing the test: The reliability of echocardiography in the sequential assessment of valvular regurgitation". American Heart Journal. 144 (1): 115–21. PMID 12094197. doi:10.1067/mhj.2002.123139. Retrieved 2010-06-30.
- Franco Folino A (2007). "Cerebral autoregulation and syncope". Prog Cardiovasc Dis. 50 (1): 49–80. PMID 17631437. doi:10.1016/j.pcad.2007.01.001.
- Thomas AJ, Perry R, Barber R, Kalaria RN, O'Brien JT (2002). "Pathologies and Pathological Mechanisms for White Matter Hyperintensities in Depression". Annals of the New York Academy of Sciences. 977: 333–339. PMID 12480770. doi:10.1111/j.1749-6632.2002.tb04835.x.
- Brickman AM, Reitz C, Luchsinger JA, Manly JJ, Schupf N, Muraskin J, DeCarli C, Brown TR, Mayeux R (2010). "Long-term Blood Pressure Fluctuation and Cerebrovascular Disease in an Elderly Cohort". Archives of Neurology. 67 (5): 564–569. PMC . PMID 20457955. doi:10.1001/archneurol.2010.70.
- "Normal Blood Pressure Range Adults". Health and Life.
- Caro, Colin G. (1978). The Mechanics of The Circulation. Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-263323-6.
- Klabunde, Richard (2005). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins. pp. 93–4. ISBN 978-0-7817-5030-1.
-  Archived April 15, 2011, at the Wayback Machine.
- Freis ED (1976). "Salt, volume and the prevention of hypertension". Circulation. 53 (4): 589–95. PMID 767020. doi:10.1161/01.CIR.53.4.589. Retrieved 4 April 2012.
- Caplea A, Seachrist D, Dunphy G, Ely D (April 2001). "Sodium-induced rise in blood pressure is suppressed by androgen receptor blockade". AJP: Heart. 4. 280 (4): H1793–801. PMID 11247793. Retrieved 4 April 2012.
- Houston, Mark (January 1986). "Sodium and Hypertension: A Review". Archives of Intern Medicine. 1. 146 (1): 179–85. doi:10.1001/archinte.1986.00360130217028. Retrieved 4 April 2012.
- Guyton, A. C. (1981-12-01). "The relationship of cardiac output and arterial pressure control". Circulation. 64 (6): 1079–1088. ISSN 0009-7322. PMID 6794930. doi:10.1161/01.cir.64.6.1079.
- Lee, A. J. (1997-12-01). "The role of rheological and haemostatic factors in hypertension". Journal of Human Hypertension. 11 (12): 767–776. ISSN 0950-9240. PMID 9468002. doi:10.1038/sj.jhh.1000556.
- Coffman, J. D. (1988-12-01). "Pathophysiology of obstructive arterial disease". Herz. 13 (6): 343–350. ISSN 0340-9937. PMID 3061915.
- Klabunde, RE (2007). "Cardiovascular Physiology Concepts – Arterial Baroreceptors". Retrieved 2008-09-09. Archived version 2009-10-03
- Booth J (1977). "A short history of blood pressure measurement". Proceedings of the Royal Society of Medicine. 70 (11): 793–9. PMC . PMID 341169.
- Forouzanfar, M.; Dajani, H. R.; Groza, V. Z.; Bolic, M.; Rajan, S.; Batkin, I. (2015-01-01). "Oscillometric Blood Pressure Estimation: Past, Present, and Future". IEEE Reviews in Biomedical Engineering. 8: 44–63. ISSN 1937-3333. doi:10.1109/RBME.2015.2434215.
- "Vital Signs (Body Temperature, Pulse Rate, Respiration Rate, Blood Pressure)". OHSU Health Information. Oregon Health & Science University. Retrieved 2014-04-16.
- Struijk PC, Mathews VJ, Loupas T, Stewart PA, Clark EB, Steegers EA, Wladimiroff JW (October 2008). "Blood pressure estimation in the human fetal descending aorta". Ultrasound Obstet Gynecol. 32 (5): 673–81. PMID 18816497. doi:10.1002/uog.6137.
- Sharon, S. M. & Emily, S. M. (2006). Foundations of Maternal-Newborn Nursing. (4th ed p.476). Philadelphia:Elsevier.
- Pickering TG, Hall JE, Appel LJ, et al. (2005). Subcommittee of Professional Public Education of the American Heart Association Council on High Blood Pressure Research. "Recommendations for blood pressure measurement in humans and experimental animals: Part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research". Hypertension. 45 (5): 142–61. PMID 15611362. doi:10.1161/01.HYP.0000150859.47929.8e. Retrieved 2009-10-01.