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Blood pressure
A healthcare worker measuring blood pressure using a sphygmomanometer.
MeSHD001794
MedlinePlus007490
LOINC35094-2

Blood pressure (BP) is the pressure of circulating blood against the walls of blood vessels. 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 heartbeat) over diastolic pressure (minimum pressure between two heartbeats) in the cardiac cycle. It is measured in millimetres of mercury (mmHg) above the surrounding atmospheric pressure, or in kilopascals (kPa). The difference between the systolic and diastolic pressures is known as pulse pressure,[1] while the average pressure during a cardiac cycle is known as mean arterial pressure.[2]

Blood pressure is one of the vital signs—together with respiratory rate, heart rate, oxygen saturation, and body temperature—that healthcare professionals use in evaluating a patient's health. Normal resting blood pressure in an adult is approximately 120 millimetres of mercury (16 kPa) systolic over 80 millimetres of mercury (11 kPa) diastolic, denoted as "120/80 mmHg". Globally, the average blood pressure, age standardized, has remained about the same since 1975 to the present,[when?] at approximately 127/79 mmHg in men and 122/77 mmHg in women, although these average data mask significantly diverging regional trends.[3]

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-tube sphygmomanometer.[4] Auscultation is still generally considered to be the gold standard of accuracy for non-invasive blood pressure readings in clinic.[5] However, semi-automated methods have become common, largely due to concerns about potential mercury toxicity,[6] although cost, ease of use and applicability to ambulatory blood pressure or home blood pressure measurements have also influenced this trend.[7] 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 mm Hg or less, and a standard deviation of less than 8 mm Hg.[7] 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).[8]

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 regulated by baroreceptors, which act via the brain to influence the nervous and the 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.[9] 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.

Classification, normal and abnormal values

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Systemic arterial pressure

[edit]

Blood pressure measurements can be influenced by circumstances of measurement.[10] 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).[10]

Blood pressure classifications
Categories Systolic blood pressure, mmHg and/or Diastolic blood pressure, mmHg
Method Office Home 24h ambulatory Office Home 24h ambulatory
American College of Cardiology/American Heart Association (2017)[11]
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
European Society of Cardiology (2024)[10]
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
European Society of Hypertension/International Society of Hypertension (2023)[12]
Optimal <120 — — and <80 — —
Normal 120–129 — — and/or 80–84 — —
High normal 130–139 — — and/or 85–89 — —
Hypertension, grade 1 140–159 ≥135 ≥130 and/or 90–99 ≥85 ≥80
Hypertension, grade 2 160–179 — — and/or 100–109 — —
Hypertension, grade 3 ≥180 — — and/or ≥110 — —

The risk of cardiovascular disease increases progressively above 90 mmHg, especially among women.[10]

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.[13]

Blood pressure fluctuates from minute to minute and normally shows a circadian rhythm over a 24-hour period,[14] with highest readings in the early morning and evenings and lowest readings at night.[15][16] 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.[17] Blood pressure varies over longer time periods (months to years) and this variability predicts adverse outcomes.[18] Blood pressure also changes in response to temperature, noise, emotional stress, consumption of food or liquid, dietary factors, physical activity, changes in posture (such as standing-up), drugs, and disease.[19] 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.[20]

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 mmHg which may need further investigation, e.g. for peripheral arterial disease, obstructive arterial disease or aortic dissection.[21][22][23][24]

There is no accepted diagnostic standard for hypotension, although pressures less than 90/60 are commonly regarded as hypotensive.[25] In practice blood pressure is considered too low only if symptoms are present.[26]

Systemic arterial pressure and age

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Fetal blood pressure

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Further information: 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 mmHg at 20 weeks of gestation, and increases to approximately 45 mmHg at 40 weeks of gestation.[27]

The average blood pressure for full-term infants:[28]

  • Systolic 65–95 mmHg
  • Diastolic 30–60 mmHg

Childhood

[edit]
Reference ranges for blood pressure (BP) in children[29]
Stage Approximate age Systolic BP,
mmHg 		Diastolic BP,
mmHg
Infants 0–12 months 75–100 50–70
Toddlers and preschoolers 1–5 years 80–110 50–80
School age 6–12 years 85–120 50–80
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.[30] Reference blood pressure values have been developed for children in different countries, based on the distribution of blood pressure in children of these countries.[31]

Aging adults

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In adults in most societies, systolic blood pressure tends to rise from early adulthood onward, up to at least age 70;[32][33] diastolic pressure tends to begin to rise at the same time but start to fall earlier in mid-life, approximately age 55.[33] 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,[33] 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 stiffness of the arteries.[34] An age-related rise in blood pressure is not considered healthy and is not observed in some isolated unacculturated communities.[35]

Systemic venous pressure

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Site Normal
pressure range
(in mmHg)[36]
Central venous pressure 3–8
Right ventricular pressure systolic 15–30
diastolic 3–8
Pulmonary artery pressure systolic 15–30
diastolic 4–12
Pulmonary vein/

Pulmonary capillary wedge pressure

2–15
Left ventricular pressure systolic 100–140
diastolic 3–12

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 lower 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:

Pulmonary pressure

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Main article: Pulmonary artery pressure

Normally, the pressure in the pulmonary artery is about 15 mmHg at rest.[40]

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.[41]

Aortic pressure

[edit]
Main article: 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).[42][43] 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.[44][45]

Certain researchers have argued for physicians to begin using aortic pressure, as opposed to peripheral blood pressure, as a guide for clinical decisions.[46][43] The way antihypertensive drugs impact peripheral blood pressure can often be very different from the way they impact central aortic pressure.[47]

Mean systemic pressure

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Main article: 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;[48] typically this is proximally ~7 mmHg.[48]

Disorders of blood pressure

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Disorders of blood pressure control include high blood pressure, low blood pressure, and blood pressure that shows excessive or maladaptive fluctuation.

High blood pressure

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Main article: Hypertension
Overview of main complications of persistent high blood pressure.[49]

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.[49]

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.[49] Even moderate elevation of arterial pressure leads to shortened life expectancy.[49] 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.[50] For people with high blood pressure, higher heart rate variability (HRV) is a risk factor for atrial fibrillation.[51]

Both high systolic pressure and high pulse pressure (the numerical difference between systolic and diastolic pressures) are risk factors.[49] 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.[52][53][54][55] 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 mmHg) with a normal diastolic blood pressure (<90 mmHg), it is called isolated systolic hypertension and may present a health concern.[49][56] According to the 2017[57] 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".[49]

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 and mitral regurgitation when diastolic blood pressure increased, whereas when diastolic blood pressure decreased, there was a decreased severity.[58]

Low blood pressure

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Main article: 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, circulatory shock.[59] Causes of low arterial pressure include sepsis, hypovolemia, bleeding, cardiogenic shock, reflex syncope, hormonal abnormalities such as Addison's disease, and eating disorders – particularly anorexia nervosa and bulimia.[60]

Orthostatic hypotension

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Main article: Orthostatic hypotension

A large fall in blood pressure upon standing (typically a systolic/diastolic blood pressure decrease of >20/10 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 hydrostatic pressure in the blood vessels of the lower limbs. The consequent distension of the veins below the 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 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 venous vasoconstriction to decrease venous compliance. Decreased venous compliance also results from an intrinsic 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' and 'respiratory pump'. Together these mechanisms normally stabilize blood pressure within a minute or less.[61] If these compensatory mechanisms fail and arterial pressure and blood 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 fainting.[62] Usually this failure of compensation is due to disease, or drugs that affect the sympathetic nervous system.[61] A similar effect is observed following the experience of excessive gravitational forces (G-loading), such as routinely experienced by aerobatic or combat pilots 'pulling Gs' where the extreme hydrostatic pressures exceed the ability of the body's compensatory mechanisms.

Variable or fluctuating blood pressure

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Main article: 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[63] brain small vessel disease,[64] and dementia[65] independent of the average blood pressure level. Recent evidence from clinical trials has also linked variation in blood pressure to mortality,[66][67] stroke,[68] heart failure,[69] and cardiac changes that may give rise to heart failure.[70] These data have prompted discussion of whether excessive variation in blood pressure should be treated, even among normotensive older adults.[71]

Older individuals and those who had received blood pressure medications are more likely to exhibit larger fluctuations in pressure,[72] and there is some evidence that different antihypertensive agents have different effects on blood pressure variability;[65] whether these differences translate to benefits in outcome is uncertain.[65]

Physiology

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Cardiac systole and diastole
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.
Schematic of pressures in the circulation

During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastolic) pressure.[73][unreliable medical source] The blood pressure in the circulation is principally due to the pumping action of the heart.[74] 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 hydrostatic effects (e.g. standing), 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.[75] Pulsatility also diminishes in the smaller elements of the arterial circulation, although some transmitted pulsatility is observed in capillaries.[76] 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.[74]

Hemodynamics

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Main article: 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,[77] 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 mechanism—this is influenced by blood volume; 2) cardiac contractility; and 3) afterload, the impedance to blood flow presented by the circulation.[78] 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,[79][80][81] changes in plasma osmolarity may also be important.[82] In the longer-term the relationship between volume and blood pressure is more complex.[83] 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's equation (resistance∝1/radius4). 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)[84] 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.[85] Substances called vasoconstrictors reduce the caliber of blood vessels, thereby increasing blood pressure. Vasodilators (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.[86][87] Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances.[88]

In practice, each individual's autonomic nervous system and other systems regulating blood pressure, notably the kidney,[89] 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

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Main article: Pulse pressure
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,[90]

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 resistance to flow in the arterial tree.[90]

Clinical significance of pulse pressure

[edit]

A healthy pulse pressure is around 40 mmHg.[1] 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.[52] 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.)[91] A very low pulse pressure can be a symptom of disorders such as congestive heart failure.[52]

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.[52][53] 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.[55][54]

A meta-analysis in 2000 showed that a 10 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.[92] 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.[93]

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 IV fluids.[94][95]

Mean arterial pressure

[edit]
Main article: 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):[2][96][97]

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

MAP is often estimated from measurements of the systolic pressure, and the diastolic pressure,  [97] using the equation:

where k = 0.333 although other values for k have been advocated.[98][99]

Regulation of blood pressure

[edit]
See also: Renin–angiotensin system

The endogenous, homeostatic regulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized:

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.

  1. The blood pressure fall is detected by a decrease in blood flow and thus a decrease in glomerular filtration rate (GFR).
  2. Decrease in GFR is sensed as a decrease in Na+ levels by the macula densa.
  3. The macula densa causes 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.
  4. At the same time, the juxtaglomerular cells sense the decrease in blood pressure and release renin.
  5. Renin converts angiotensinogen (inactive form) to angiotensin I (active form).
  6. 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.
  7. Angiotensin II is a vasoconstrictor that will increase blood flow to the heart and subsequently the preload, ultimately increasing the cardiac output.
  8. Angiotensin II also causes an increase in the release of aldosterone from the adrenal glands.
  9. Aldosterone further increases the Na+ and H2O reabsorption in the distal convoluted tubule of the nephron.

The RAS is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists (also known as angiotensin receptor blockers; ARB). The aldosterone system is directly targeted by aldosterone antagonists. 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 experience orthostatic hypotension and fainting.

Measurement

[edit]
Main article: Blood pressure measurement
Taking blood pressure with a sphygmomanometer
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.[4] The most common automated blood pressure measurement technique is based on the oscillometric method.[103] Fully automated oscillometric measurement has been available since 1981.[104] This principle has recently been used to measure blood pressure with a smartphone.[105] Measuring 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,[106] for example, cuffless measurements that uses only optical sensors.[107]

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"[108]

In animals

[edit]

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).[109] The giraffe has a distinctly high arterial pressure of about 190 mm Hg, enabling blood perfusion through the 2 metres (6 ft 7 in)-long neck to the head.[110] In other species subjected to orthostatic blood pressure, such as arboreal snakes, blood pressure is higher than in non-arboreal snakes.[111] A heart near to the head (short heart-to-head distance) and a long tail with tight integument favor blood perfusion to the head.[112][113]

As in humans, blood pressure in animals differs by age, sex, time of day, and environmental circumstances:[114][115] 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.[116]

Blood pressure and heart rate of various mammals[114]
Species Blood pressure
mm Hg 		Heart rate
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

[edit]

Hypertension in cats and dogs is generally diagnosed if the blood pressure is greater than 150 mm Hg (systolic),[117] although sight hounds have higher blood pressures than most other dog breeds; a systolic pressure greater than 180 mmHg is considered abnormal in these dogs.[118]

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Blood pressure

View on Grokipedia
from Grokipedia
Blood pressure is the force exerted by circulating blood against the walls of arteries as the heart pumps it through the body to deliver oxygen and nutrients to tissues. It is typically measured in millimeters of mercury (mmHg) and expressed as two values: the higher systolic pressure, which occurs when the heart contracts to eject blood, and the lower diastolic pressure, which reflects the pressure in arteries when the heart relaxes between beats. A normal blood pressure reading is less than 120/80 mmHg. Readings with systolic pressure of 120-129 mmHg and diastolic less than 80 mmHg are considered elevated per American Heart Association guidelines, not normal, and indicate a need for monitoring and lifestyle adjustments to prevent progression to hypertension. Readings at or above 130/80 mmHg indicate hypertension, a condition that affects nearly half of adults in the United States and increases risks for heart disease, stroke, and kidney damage if unmanaged. The physiological regulation of blood pressure maintains adequate perfusion of organs while preventing vascular damage, primarily through the interplay of cardiac output—the volume of blood pumped by the heart per minute—and total peripheral resistance, which is influenced by the diameter of arterioles. Key mechanisms include the baroreceptor reflex, where sensors in the carotid arteries and aorta detect pressure changes and signal the autonomic nervous system to adjust heart rate and vessel tone; the renin-angiotensin-aldosterone system (RAAS), which promotes vasoconstriction and fluid retention to raise pressure when it falls; and antidiuretic hormone (ADH), which similarly increases blood volume and resistance. These short-term and long-term controls ensure blood pressure remains stable under varying conditions, such as exercise or stress, with deviations often linked to factors like age, genetics, diet, and lifestyle. Clinically, blood pressure is measured using a , often with an automated cuff on the upper arm, and regular monitoring is essential since is frequently , earning it the moniker "silent killer." Elevated pressure can lead to —plaque buildup in arteries—and heighten the likelihood of cardiovascular events, while low blood pressure () may cause or fainting due to insufficient organ perfusion. Management typically involves lifestyle modifications, such as reducing salt intake and increasing , alongside medications like ACE inhibitors that target RAAS pathways when necessary.

Fundamentals

Definition and Types

Blood pressure is the force exerted by circulating blood against the walls of arteries as the heart pumps it through the body, primarily reflecting the hydrostatic pressure within the major arterial system. This pressure is measured in millimeters of mercury (mmHg) and arises mainly from the mechanical action of the heart ejecting blood into the compliant arterial tree. The hydrostatic component represents the physical force generated by cardiac output and vascular resistance, driving blood flow throughout the circulation. Additionally, osmotic pressure—particularly the oncotic pressure exerted by plasma proteins like albumin—contributes by counteracting fluid leakage from vessels, thereby helping to sustain intravascular volume and indirectly supporting overall blood pressure levels. The primary types of arterial blood pressure are systolic, diastolic, and mean arterial pressure, each characterizing different phases of the cardiac cycle. Systolic pressure denotes the maximum pressure attained in large arteries during ventricular contraction (systole), when blood is forcefully ejected from the heart. Diastolic pressure, in contrast, is the minimum pressure occurring during ventricular relaxation (diastole), when the heart refills between beats. Mean arterial pressure (MAP) provides an average value over the entire cardiac cycle, calculated as the integral of arterial pressure across systole and diastole, and serves as a key indicator of perfusion adequacy to organs. Blood pressure is distinguished into systemic and pulmonary types based on the circulatory pathway. Systemic blood pressure refers to the higher pressures in the arteries distributing oxygenated blood to the body's tissues via the left ventricle. Pulmonary blood pressure, driven by the right ventricle, involves lower pressures in the pulmonary arteries that carry deoxygenated blood to the lungs for , typically about one-sixth of systemic levels to accommodate the lung's delicate vasculature. The concept of blood pressure measurement originated in the early 18th century, with English clergyman and scientist Stephen Hales conducting the first direct recording in 1733 by inserting a brass tube into a horse's carotid artery and observing the blood's rise in a vertical glass tube connected to it.

Basic Physiology

Blood pressure is fundamentally generated and maintained by the cardiovascular system, which consists of the heart acting as the central pump and the network of blood vessels serving as conduits for blood flow. The heart propels blood through rhythmic contractions, producing a cardiac output that represents the volume of blood ejected per minute, typically around 5 liters in a resting adult. Arteries carry oxygenated blood away from the heart under high pressure, veins return deoxygenated blood to the heart under lower pressure, and capillaries facilitate exchange of nutrients, gases, and wastes between blood and tissues. This closed system ensures continuous circulation, with blood pressure arising from the force exerted by the heart against vascular resistance. Hemodynamics describes the physical principles governing blood flow and pressure, analogous to Ohm's law in electricity, where mean arterial pressure (MAP) equals cardiac output (CO) multiplied by total peripheral resistance (TPR): MAP = CO × TPR. Cardiac output is the product of heart rate and stroke volume, while TPR arises primarily from the arterioles due to their narrow lumens and smooth muscle control, though the entire vascular tree contributes. This relationship highlights how pressure gradients drive flow from high-pressure regions (aorta) to low-pressure areas (right atrium), with blood viscosity and vessel geometry influencing overall dynamics. Blood flow in vessels is predominantly laminar, characterized by smooth, layered movement parallel to the vessel walls, which minimizes energy loss and on endothelial cells. In contrast, turbulent flow involves chaotic eddies and mixing, occurring rarely in normal such as during peak in the or at vessel bifurcations, and is quantified by the (Re = ρVD/μ, where ρ is blood density, V is velocity, D is , and μ is ); prevails when Re < 2000. Resistance to flow in individual vessels follows Poiseuille's law for laminar conditions in rigid tubes: R=8ηLπr4R = \frac{8 \eta L}{\pi r^4}, where η is blood , L is vessel length, and r is radius, emphasizing that resistance is inversely proportional to the fourth power of the radius—thus, small changes in vessel profoundly affect pressure. Arteries exhibit vascular compliance and elasticity due to their layered structure, including elastin fibers in the media, allowing them to distend during systole and recoil during diastole, thereby buffering the intermittent pressure pulses from the heart to maintain steady downstream flow. This transforms pulsatile cardiac ejection into more continuous perfusion of capillaries and tissues, with arterial compliance defined as the change in volume per change in pressure (C = ΔV/ΔP). Large elastic arteries like the aorta are particularly adept at this buffering, absorbing up to 50% of stroke volume during contraction.

Pressure Parameters

Arterial Pressure

Systemic arterial pressure is the force exerted by circulating blood on the walls of the arteries in the systemic circulation, which delivers oxygenated blood from the left ventricle to the body's tissues. It consists of two primary components: systolic pressure, the maximum pressure occurring during ventricular contraction, and diastolic pressure, the minimum pressure during ventricular relaxation. In healthy adults, systolic arterial pressure typically ranges from 90 to 120 mmHg, while diastolic pressure ranges from 60 to 80 mmHg, with values below 90/60 mmHg indicating hypotension and above 120/80 mmHg suggesting elevated pressure. Aortic pressure, measured in the proximal aorta near the heart, represents the central arterial pressure where blood is ejected directly from the left ventricle. Due to this proximity, the mean arterial pressure is highest in the aorta, calculated as approximately one-third systolic plus two-thirds diastolic, and it declines gradually toward the peripheral arteries owing to frictional losses and increasing vascular resistance along the arterial tree. Although systolic pressure can exhibit amplification in peripheral sites due to wave reflections, the overall pressure profile ensures adequate perfusion while minimizing cardiac workload. Pulse pressure, defined as the difference between systolic and diastolic pressures, normally ranges from 30 to 50 mmHg in adults and reflects arterial compliance and stroke volume. It is computed simply as systolic pressure minus diastolic pressure, providing insight into vascular health; for instance, a pulse pressure of 40 mmHg is typical for a reading of 120/80 mmHg. A widened pulse pressure exceeding 60 mmHg often signifies arterial stiffness, where reduced elasticity leads to higher systolic peaks and lower diastolic troughs, increasing cardiovascular risk.

Venous and Pulmonary Pressure

Venous pressure in the systemic circulation is significantly lower than arterial pressure, reflecting the role of veins as capacitance vessels that store and return blood to the heart. Central venous pressure (CVP), measured at the junction of the superior vena cava and right atrium, typically ranges from 0 to 8 mmHg in healthy individuals. This low pressure serves as the primary determinant of venous return, acting as the back pressure that opposes the flow of blood from peripheral veins toward the heart; higher CVP reduces venous return, while lower values facilitate it. In the pulmonary circulation, pressures are also low to accommodate the thin-walled alveoli and minimize the work of breathing. Normal pulmonary artery pressure includes a systolic value of 15 to 30 mmHg, diastolic of 4 to 12 mmHg, and mean of 9 to 18 mmHg. These values are substantially lower than systemic arterial pressures due to the pulmonary vasculature's high compliance and low resistance, which prevent excessive strain on the lung tissue during gas exchange. Mean systemic filling pressure (MSFP) represents the equilibrium pressure throughout the systemic circulation in the absence of blood flow, such as during cardiac arrest, and is approximately 7 mmHg in normovolemic humans. This pressure arises primarily from the elastic recoil of the vascular walls and the volume of blood within the system, serving as a key indicator of circulatory filling status and the driving force for venous return under static conditions. Compared to the arterial system, both venous and pulmonary circulations exhibit lower resistance and higher volume compliance, allowing them to handle larger blood volumes with minimal pressure changes. The venous system's compliance is about 30 times greater than that of arteries, enabling it to store up to 60-70% of total blood volume while maintaining low pressures. Similarly, the pulmonary circuit's low resistance (about one-tenth of systemic) ensures efficient perfusion without compromising oxygenation.

Specialized Pressures

In the fetal circulation, systemic arterial blood pressure at term averages approximately 70/45 mmHg, with a mean of 55 mmHg, reflecting the underdeveloped vascular system and reliance on placental gas exchange. Prior to birth, pulmonary vascular resistance remains elevated—approximately 8 to 10 times higher than systemic vascular resistance—due to factors such as fluid-filled lungs, low oxygen tension, and vasoconstrictive mediators, which minimizes pulmonary blood flow and directs most right ventricular output through the ductus arteriosus to the systemic circulation. This high resistance ensures oxygenation via the placenta but requires a dramatic drop in pulmonary pressure postnatally for effective lung perfusion. Portal venous pressure, which governs blood flow through the liver's portal system, normally ranges from 5 to 10 mmHg in healthy adults, exceeding inferior vena caval pressure by about 4 to 5 mmHg to facilitate nutrient-rich blood delivery from the splanchnic organs. This low-pressure system supports sinusoidal filtration without excessive resistance, but elevations beyond 10 mmHg indicate portal hypertension, often linked to liver cirrhosis or thrombosis. Intracranial pressure (ICP) interacts closely with systemic to determine cerebral perfusion pressure (CPP), calculated as CPP = mean arterial pressure (MAP) minus ICP, ensuring adequate oxygen delivery to brain tissue. In adults, normal ICP ranges from 7 to 15 mmHg in the supine position, maintained by cerebrospinal fluid dynamics and cerebral blood volume; when ICP rises above 20 mmHg, it can compress cerebral vessels, reducing CPP and risking ischemia unless compensated by elevated MAP. This relationship underscores the brain's autoregulation, where CPP is typically kept between 60 and 150 mmHg to match metabolic demands. In the microcirculation, capillary hydrostatic pressure drives fluid exchange across vessel walls and varies along the capillary length, typically ranging from 10 to 25 mmHg at heart level, with higher values (around 30-35 mmHg) at the arterial end and lower (10-15 mmHg) at the venous end. This gradient, influenced by precapillary sphincter tone and interstitial forces, balances filtration and reabsorption per Starling's principle, preventing edema while nourishing tissues; for instance, in skin capillaries, pressures measured at the apex fall within 10.5 to 22.5 mmHg under normal conditions.

Normal Values and Variations

Norms by Age and Population

Blood pressure norms vary significantly across life stages, reflecting developmental changes in cardiovascular physiology. In the fetal period, blood pressure is low, with mean arterial pressure around 30-50 mmHg near term, but it rises rapidly postnatally as the circulatory system adapts to independent oxygenation. For newborns, average systolic blood pressure is approximately 60-80 mmHg, with values typically ranging from 60-90 mmHg in the first days of life, increasing to 70-100 mmHg by one month. Diastolic pressures follow a similar pattern, averaging 40-50 mmHg initially. These early norms are established through population-based studies of term infants, emphasizing the need for age-specific reference ranges to avoid misdiagnosis. During childhood, blood pressure increases gradually with growth and body size, necessitating norms adjusted for age, sex, and height percentiles rather than fixed values. For example, in a 10-year-old child, normal systolic blood pressure falls between 100-120 mmHg and diastolic between 60-80 mmHg at the 50th-90th percentiles, with hypertension defined above the 95th percentile (e.g., >122/78 mmHg for boys of average height). These percentile-based standards, derived from large cohorts like the and Nutrition Examination Survey, account for the linear upward trend in both systolic and diastolic pressures from infancy through , reaching near-adult levels by late teens. In adulthood, normal blood pressure is generally defined as less than 120/80 mmHg for both sexes. According to ACC/AHA guidelines, blood pressure categories are classified as normal (systolic <120 mmHg and diastolic <80 mmHg), elevated (systolic 120-129 mmHg and diastolic <80 mmHg), stage 1 hypertension (systolic 130-139 mmHg or diastolic 80-89 mmHg), and stage 2 hypertension (systolic ≥140 mmHg or diastolic ≥90 mmHg). Examples include normal readings such as 115/75 mmHg or 118/76 mmHg, elevated at 125/78 mmHg, stage 1 hypertension at 135/85 mmHg, and stage 2 hypertension at 145/92 mmHg. For example, a blood pressure reading of 122/73 mmHg is classified as elevated (systolic 120-129 mmHg and diastolic <80 mmHg), not normal (<120/80 mmHg), and not hypertensive. It indicates a need for monitoring and lifestyle adjustments to prevent progression to hypertension. Conversely, a blood pressure reading of 110/70 mmHg is classified as normal (healthy) for a 59-year-old woman, according to American Heart Association and Mayo Clinic guidelines. Normal is defined as less than 120 mmHg systolic and less than 80 mmHg diastolic. Classification categories do not differ by age or gender for adults. This reading is below the average for women aged 40-59 (around 122/74 mmHg) but remains within the healthy range. A concurrent pulse rate of 64 bpm is normal and good for adults, within the typical resting heart rate range of 60-100 bpm. In student physiology labs, resting readings for healthy young adults are commonly in the normal range, such as 110–130 mmHg systolic over 70–85 mmHg diastolic. The Japanese Society of Hypertension guidelines define normal blood pressure as systolic <130 mmHg and diastolic <85 mmHg, with optimal <120/80 mmHg. Though mean values rise with age, peaking in before a potential decline in extreme due to reduced vascular compliance. For adults aged 18-39, systolic is around 115-120 mmHg and diastolic 75-80 mmHg; by ages 60-79, systolic averages 130-140 mmHg while diastolic stabilizes or slightly decreases to 70-80 mmHg. Women often exhibit lower pressures than men until , after which differences narrow. Ethnic variations are notable, with individuals of African descent showing higher systolic pressures (e.g., 5-10 mmHg above ) and earlier onset of elevated readings across adulthood. In the elderly (aged 80+), systolic values often reach 130-150 mmHg due to reduced vascular compliance, but normal blood pressure is still defined as less than 120/80 mmHg, with thresholds applying at 130/80 mmHg. Recent ACC/AHA guidelines, updated in 2025, maintain the threshold for onset at 130/80 mmHg for adults, including older populations, while emphasizing individualized targets below 130/80 mmHg for most to reduce cardiovascular events, with considerations for frailty and limited life expectancy in those over 80 to ensure benefits outweigh harms. The 2025 guidelines incorporate the PREVENT equations for risk stratification to inform treatment initiation in those with stage 1 . These standards, informed by trials like SPRINT, underscore the importance of accurate measurement to interpret norms reliably.
Age GroupTypical Average Systolic (mmHg)Typical Average Diastolic (mmHg)Key Notes
Newborn (0-1 day)60-9040-50Rapid postnatal rise; averages 64/41. Normal BP defined as <120/<80 mmHg for adults; age-specific for children.
Child (10 years)100-12060-8050th-90th percentiles; height-adjusted.
Adult (18-39 years)<120<80Lower in women pre-menopause. Normal BP defined as <120/<80 mmHg.
Elderly (60+ years)120-14070-80Systolic peaks mid-life, higher in African descent. Normal BP defined as <120/<80 mmHg.

Factors Influencing Baseline Pressure

Lifestyle factors play a significant role in determining baseline blood pressure levels. High dietary sodium intake promotes fluid retention, thereby elevating blood pressure, while reducing sodium consumption can lower systolic blood pressure by 2-8 mmHg in normotensive individuals and up to 8-14 mmHg in those with hypertension. Regular aerobic exercise, such as brisk walking or cycling for at least 150 minutes per week, contributes to a modest reduction in baseline blood pressure, typically by 4-9 mmHg systolic, through improvements in vascular function and weight management. Obesity, defined by a body mass index greater than 30 kg/m², is associated with higher baseline blood pressure due to increased cardiac output and sympathetic activation; intentional weight loss of 5-10 kg can decrease systolic blood pressure by 5-20 mmHg. The Dietary Approaches to Stop Hypertension (DASH) diet, which emphasizes fruits, vegetables, whole grains, and low-fat dairy while limiting saturated fats and sodium, has been shown to reduce systolic blood pressure by 5-11 mmHg in diverse populations. Genetic factors account for 30-50% of the variability in baseline blood pressure, with heritability estimates derived from twin and family studies indicating polygenic influences on vascular tone and renal sodium handling. Ethnic variations contribute to differences in baseline levels; for instance, non-Hispanic Black adults in the United States exhibit higher average systolic blood pressure (approximately 4-7 mmHg greater) compared to non-Hispanic White adults, potentially due to interactions between genetic predispositions and environmental exposures. Similarly, South Asian and African Caribbean populations often display elevated baselines relative to European-descended groups, with prevalence rates of hypertension 1.5-2 times higher. Environmental influences also modulate baseline blood pressure. Residence at high altitudes, where chronic hypoxia prevails due to lower atmospheric oxygen partial pressure, is linked to reduced baseline blood pressure in long-term inhabitants; studies of populations above 3,000 meters report systolic values 5-10 mmHg lower than at sea level, attributed to adaptations in erythropoiesis and vasodilation. Circadian rhythms impose a daily pattern, with blood pressure typically dipping 10-20% during nighttime sleep compared to daytime averages, reflecting sympathetic nervous system withdrawal and renal mechanisms that promote this nocturnal decline. Gender differences emerge prominently in baseline blood pressure profiles. In premenopausal women, estrogen-mediated vasodilation results in lower average systolic blood pressure (about 5-10 mmHg less) than in age-matched men, who exhibit higher levels due to androgen influences on vascular resistance. This disparity reverses post-menopause, when women's systolic blood pressure rises to exceed men's by 3-5 mmHg on average, coinciding with estrogen decline and accelerated arterial stiffening.

Short-term and Daily Variations

In healthy individuals, blood pressure exhibits short-term and daily fluctuations in addition to circadian patterns and longer-term influences. Systolic blood pressure commonly varies by 10-20 mmHg or more throughout the day due to everyday factors such as physical activity, stress or anxiety, caffeine consumption, talking, posture changes, time of day (often higher in the morning), and the body's natural circadian rhythm. Such fluctuations can temporarily shift readings from normal (<120 mmHg) to elevated (120-129 mmHg) or borderline stage 1 hypertension levels without signifying chronic hypertension. Variations of this magnitude are typical in healthy individuals. While these fluctuations are normal physiological responses, frequent, extreme (>40 mmHg), symptomatic, or persistent variations may indicate underlying issues such as labile hypertension, obstructive sleep apnea, kidney disease, or adrenal problems, and warrant medical evaluation.

Measurement Techniques

Non-Invasive Methods

Non-invasive methods for measuring blood pressure primarily involve external devices that detect pressure changes in the arteries without penetrating the skin, making them suitable for routine clinical and home use. These techniques rely on occlusion of arterial blood flow using an inflatable cuff placed around the upper arm, followed by gradual deflation to assess systolic and diastolic pressures. The two most common approaches are the auscultatory and oscillometric methods, both of which have been standardized in clinical guidelines for accuracy and reproducibility. The auscultatory method, considered the gold standard for manual blood pressure measurement, uses a sphygmomanometer—an inflatable cuff connected to a pressure gauge—and a stethoscope placed over the brachial artery in the antecubital fossa. As the cuff is inflated to a pressure exceeding the systolic value (typically 20-30 mm Hg above estimated systolic pressure), it occludes arterial flow; during controlled deflation at 2-3 mm Hg per second, the observer listens for Korotkoff sounds, which are turbulent blood flow noises produced as the artery reopens. Systolic blood pressure is recorded at the onset of the first of at least two consecutive clear tapping sounds (Korotkoff phase I), while diastolic pressure is noted at the disappearance of sounds (Korotkoff phase V), though phase IV (muffling) may be used in certain cases like pregnancy. This method requires a trained observer to minimize errors, such as avoiding the auscultatory gap—a period of silence between systolic and diastolic sounds that can lead to underestimation if not anticipated. Proper cuff sizing is essential, with the bladder length covering 80% of the arm circumference to ensure accurate readings within ±5 mm Hg of intra-arterial values. The oscillometric method, widely used in automated devices, detects pressure oscillations in the cuff caused by arterial pulsations during deflation, eliminating the need for auditory detection. The cuff is inflated similarly to the auscultatory technique, then deflated automatically while a sensor measures the magnitude of oscillations; the mean arterial pressure (MAP) is identified at the point of maximum oscillation amplitude, with systolic and diastolic values back-calculated using proprietary algorithms based on ratios of oscillation peaks (typically 0.5-0.6 for systolic and 0.7-0.8 for diastolic relative to MAP). These devices are validated against auscultatory standards and are recommended for office and home use due to reduced observer bias, though they may be less accurate in conditions like arrhythmias or obesity. Validation protocols, such as those from the Association for the Advancement of Medical Instrumentation, ensure devices meet criteria for mean differences of ≤5 mm Hg compared to mercury sphygmomanometry. Ambulatory blood pressure monitoring (ABPM) extends non-invasive techniques to provide continuous, real-world assessments over 24 hours using portable, wearable oscillometric devices that automatically inflate the cuff at programmed intervals. Typically, measurements occur every 15-30 minutes during daytime hours and every 30-60 minutes at night, yielding an average of 50-100 readings to calculate 24-hour, daytime, and nighttime means, which better predict cardiovascular risk than single office readings by accounting for diurnal variations and white-coat hypertension. Devices must be validated for comfort and accuracy, with guidelines recommending at least 70% successful readings for a valid profile; ABPM is particularly useful for diagnosing masked hypertension and guiding therapy adjustments. The 2025 American College of Cardiology/American Heart Association guidelines endorse ABPM for confirming hypertension in adults with elevated office readings. Home blood pressure monitoring (HBPM) guidelines emphasize validated automated oscillometric devices to empower patients in self-management, with readings taken under standardized conditions to avoid errors exceeding 5-10 mm Hg. Patients should select a sized to their mid-arm circumference—such as small adult (≤26 cm), regular (>26 to ≤34 cm), or large (>34 to ≤44 cm)—ensuring the bladder encircles 80-100% of the arm for accuracy; improper sizing, like using a too small, can overestimate systolic by up to 10 mm Hg. The must be positioned on bare skin with the lower edge 2-3 cm above the antecubital fossa, the arm supported at heart level, and the patient seated quietly for 5 minutes, avoiding , exercise, or talking beforehand; duplicate readings, 1-2 minutes apart, should be averaged, taken twice daily (morning and evening) for a week to establish baselines. The recommends validated devices listed on organizations like Educational Trust for reliability in detecting , as reaffirmed in the 2025 guidelines.

Invasive and Advanced Methods

Invasive blood pressure monitoring involves direct access to the vascular system, typically in critical care environments, to provide real-time, high-fidelity essential for managing hemodynamically unstable patients. Arterial catheterization, often performed via a inserted into the radial, femoral, or , enables continuous waveform analysis for systolic, diastolic, and mean arterial pressures, surpassing the limitations of intermittent methods in detecting rapid changes during or shock. This technique, commonly used in intensive care units (ICUs), requires sterile insertion and leveling at the phlebostatic axis to ensure accuracy, with complications such as or occurring in less than 5% of cases when protocols are followed. Central venous pressure (CVP) measurement assesses right atrial filling pressures through a placed in the internal jugular, subclavian, or , guiding in ICU settings where preload optimization is critical. The procedure involves advancing a to the or right atrium, connected to a for monitoring, with normal CVP values ranging from 2 to 6 mmHg in spontaneously patients. Recent guidelines emphasize its utility in mechanically ventilated patients but caution against over-reliance due to variability influenced by intrathoracic , recommending integration with other hemodynamic parameters for decisions. Advanced non-catheter-based methods enhance precision in specialized contexts. estimates pulmonary artery systolic noninvasively by measuring tricuspid regurgitant jet velocity via Doppler, adding an estimate of right atrial to derive values, which is vital for screening without invasive right heart catheterization. This approach, validated against invasive measurements, shows correlation coefficients exceeding 0.8 in multiple studies, though it underestimates pressures in severe cases. Wearable optical sensors utilizing photoplethysmography (PPG) enable cuffless monitoring by analyzing propagation from absorption changes in peripheral tissues, offering continuous assessment with accuracies within 5-10 mmHg of reference standards in controlled trials. Waveforms from these invasive and advanced techniques also allow derivation of pulse pressure, reflecting arterial stiffness and stroke volume. Emerging developments from 2024-2025 integrate artificial intelligence into wearables for real-time blood pressure variability detection, processing PPG signals to identify patterns indicative of autonomic dysfunction or early hypertension with improved sensitivity over 85% compared to traditional metrics. These AI-enhanced devices, such as smartwatches with machine learning algorithms, facilitate long-term monitoring in outpatient settings, reducing calibration needs and enhancing predictive analytics for cardiovascular risk.

Regulation Mechanisms

Short-Term Control

Short-term control of blood pressure involves rapid neural and hormonal mechanisms that respond to acute changes, maintaining on a timescale of seconds to minutes. These mechanisms primarily act through feedback loops that detect deviations in arterial pressure and adjust and accordingly. The primary is the baroreceptor reflex, supplemented by inputs and catecholamine release, which collectively buffer against sudden perturbations such as postural changes or respiratory alterations. The reflex serves as the cornerstone of immediate blood pressure regulation. , located in the and , are stretch-sensitive mechanoreceptors embedded in arterial walls that continuously monitor distending pressure. An increase in blood pressure stretches these receptors, elevating their firing rate and sending afferent signals via the (from carotid baroreceptors) and (from aortic baroreceptors) to the nucleus tractus solitarius in the . This input activates parasympathetic outflow and inhibits sympathetic activity, resulting in (reduced ) and to lower pressure. Conversely, a decrease in pressure reduces baroreceptor firing, disinhibiting sympathetic outflow, which promotes (increased ) and to elevate pressure. This loop operates beat-to-beat, providing precise, short-term stabilization. Chemoreceptors contribute to short-term blood pressure adjustments, particularly during conditions of altered blood gases. Peripheral chemoreceptors in the carotid and aortic bodies detect hypoxia (low oxygen) and (high ), triggering increases in sympathetic nerve activity. In response to hypoxia, these sensors stimulate the medulla to enhance and , raising blood pressure to improve oxygen delivery to tissues. similarly augments sympathetic outflow, often in concert with hypoxic stimuli, leading to elevated arterial pressure as part of the chemoreflex. This mechanism is especially prominent during acute respiratory challenges, where it overrides baseline tone to prioritize systemic . Hormonal responses from the provide an additional layer of short-term control through catecholamine release. In acute stress or pressure drops, preganglionic sympathetic fibers innervating the trigger secretion of adrenaline (epinephrine) and noradrenaline (norepinephrine) into the bloodstream. Noradrenaline primarily induces via α1-adrenergic receptors on vascular , increasing peripheral resistance and blood pressure. Adrenaline complements this by stimulating β1-adrenergic receptors in the heart, enhancing contractility, , and , while also promoting mild in beds. These effects occur within seconds, amplifying neural reflexes during "fight-or-flight" scenarios. The rapidity of these mechanisms is evident in responses to orthostatic stress, such as standing from a , where blood pressure transiently drops due to venous pooling in the lower body. The baroreceptor reflex counters this within a few heartbeats (typically 2–5 seconds), increasing by 10–20 beats per minute and restoring pressure through . Overall, short-term controls operate over seconds to minutes, preventing syncope and ensuring continuous organ without relying on slower renal or endocrine adjustments.

Long-Term Control

Long-term blood pressure regulation primarily involves hormonal and renal mechanisms that adjust , vascular tone, and electrolyte balance over extended periods, from days to years, to maintain in response to chronic changes in physiological demands. These processes integrate signals from the cardiovascular, renal, and endocrine systems, ensuring that deviations in pressure are corrected through sustained alterations in retention or excretion and . Unlike rapid neural adjustments, these mechanisms operate on slower timescales, often through feedback loops involving circulating peptides and organ-specific responses. The renin-angiotensin-aldosterone system (RAAS) is a central hormonal pathway for long-term blood pressure control, activated when renal perfusion pressure decreases. Low pressure in the juxtaglomerular cells of the kidney triggers the release of renin, an that cleaves angiotensinogen from the liver into I; this is then converted to II by (ACE) primarily in the lungs. II exerts vasoconstrictive effects on arterioles, increasing systemic and thereby elevating blood pressure, while also stimulating the to secrete aldosterone. Aldosterone promotes sodium reabsorption in the distal tubules of the kidney, leading to water retention and expansion of volume, which further supports pressure maintenance. This cascade ensures that chronic or is counteracted, with RAAS activity modulated by factors such as levels and sympathetic input to fine-tune long-term pressure stability. Antidiuretic hormone (ADH), also known as , contributes to long-term blood pressure regulation by responding to increases in or decreases in . Secreted by the gland upon detection by hypothalamic osmoreceptors or low-pressure in the atria and great vessels, ADH primarily acts on V2 receptors in the renal collecting ducts to increase aquaporin-2 insertion, enhancing water and thereby expanding plasma . At higher concentrations, ADH binds to V1 receptors on vascular , inducing that raises peripheral resistance. These actions integrate with RAAS to counteract , such as during or hemorrhage, helping sustain blood pressure over extended periods. In contrast, (ANP), secreted by atrial myocytes in response to high or stretch, serves as a counter-regulatory to RAAS during states of volume expansion. Elevated atrial wall tension, often due to increased , prompts ANP release, which binds to receptors on vascular and renal cells. This binding induces by relaxing arterioles and venules, reducing preload and to lower blood pressure, while also inhibiting renin and aldosterone secretion to dampen RAAS activity. In the kidneys, ANP enhances and suppresses sodium in the collecting ducts, promoting and to reduce plasma volume over time. Chronic elevation of ANP, as seen in conditions like , helps mitigate sustained by maintaining and vascular compliance. Renal pressure natriuresis represents an intrinsic mechanism that directly links arterial to sodium and water , providing a key long-term buffer against . As renal rises, it inhibits sodium primarily in the and medullary thick ascending limb through physical forces that alter tubular flow and peritubular capillary dynamics, without requiring hormonal intermediaries. This results in increased urinary sodium output, which decreases volume and thereby reduces and blood until equilibrium is restored. The slope of the pressure-natriuresis curve—reflecting the kidney's sensitivity to pressure changes—determines the chronic pressure level needed for adequate sodium balance, with blunted responses contributing to sustained in various pathologies. Over days to weeks, this mechanism integrates with dietary salt intake to stabilize blood , ensuring that higher pressures lead to proportional fluid loss. Endothelial cells lining the vasculature contribute to long-term pressure regulation through the balanced release of vasoactive factors, notably (NO) and . NO, synthesized from L-arginine by endothelial in response to or agonists like , diffuses to cells to activate , increasing cyclic GMP and promoting sustained that lowers peripheral resistance. This chronic vasodilatory tone prevents excessive pressure elevation and supports endothelial integrity over time. Conversely, , particularly endothelin-1 produced by endothelial cells under hypoxic or inflammatory conditions, binds to endothelin receptors on to induce potent , aiding in pressure maintenance during volume depletion by enhancing vascular tone and sodium retention. The interplay between NO and ensures adaptive vascular remodeling, with NO often counteracting endothelin's effects to preserve long-term hemodynamic stability.

Clinical Disorders

Hypertension

Hypertension, also known as high blood pressure, is defined as a sustained elevation in blood pressure with systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥80 mmHg, according to the 2017 / (ACC/AHA) guidelines, a threshold that remains unchanged in the 2025 update. This condition is classified into stage 1 (130–139/80–89 mmHg) and stage 2 (≥140/90 mmHg), with defined as ≥180/120 mmHg, with diagnosis requiring multiple office readings or ambulatory monitoring to confirm persistence beyond temporary fluctuations. Globally, affects approximately 1.4 billion adults aged 30-79 years as of 2024, representing about 33% of this population, with prevalence having more than doubled since 1990 due to aging demographics and lifestyle factors. Hypertension is classified into primary (essential) and secondary forms. Primary hypertension accounts for 90-95% of cases and lacks a single identifiable cause, arising instead from a complex interplay of genetic predispositions, such as variations in genes regulating sodium handling and vascular tone, and modifiable lifestyle factors including high-sodium diet, physical inactivity, , and excessive alcohol intake. In contrast, secondary hypertension, comprising 5-10% of cases, stems from an underlying medical condition, most commonly renal disorders like or renovascular stenosis (accounting for up to 5% of secondary cases), and endocrine abnormalities such as or . Other causes include and , often presenting with abrupt onset, severe readings, or in younger patients, prompting targeted diagnostic evaluation. Uncontrolled hypertension significantly elevates the risk of cardiovascular diseases and stroke, serving as a primary modifiable risk factor for these leading causes of global mortality. It promotes atherosclerosis by inducing endothelial dysfunction and arterial stiffening, increasing the likelihood of coronary heart disease by 2-3 times and stroke by up to 7 times compared to normotensive individuals. Additionally, prolonged exposure—such as hypertension persisting for over five years—amplifies stroke risk by 31% or more, while contributing to heart failure, aortic aneurysm, and chronic kidney disease through sustained vascular damage. In 2023, high blood pressure was implicated in over 700,000 U.S. deaths from heart disease and stroke, underscoring its public health impact. Management of hypertension emphasizes a combination of modifications and to achieve a target blood pressure below 130/80 mmHg for most adults, as recommended in the 2025 ACC/AHA guidelines. interventions form the cornerstone, including adoption of the DASH (Dietary Approaches to Stop Hypertension) diet rich in fruits, vegetables, and low-fat dairy; sodium restriction to under 1,500 mg daily; of 5-10% body weight in individuals; and at least 150 minutes of moderate weekly, which can lower systolic pressure by 5-8 mmHg. For those requiring medication, initial therapy often involves two agents in a single pill for better adherence, with first-line options including (ACE) inhibitors or angiotensin receptor blockers (ARBs) for their renoprotective effects, for , and thiazide diuretics for volume control; beta-blockers are reserved for patients with comorbid or post-myocardial infarction. Regular monitoring and individualized adjustments are essential, as only about 1 in 5 affected individuals worldwide achieve control, highlighting the need for sustained efforts. Hypotension is generally defined as a systolic blood pressure below 90 mmHg or a drop of more than 20 mmHg from baseline, which can impair organ and lead to symptoms such as , , fainting, , , , and . A systolic blood pressure of 112 mmHg falls within the normal range (typically <120 mmHg systolic and <80 mmHg diastolic per international guidelines like AHA/ACC) and is not considered too low absent symptoms of inadequate perfusion; hypotension is generally defined as below 90/60 mmHg (example: 85/55 mmHg) or symptomatic. Lower values may be beneficial if well-tolerated, as hypertension treatment targets are <140/90 mmHg generally or <130/80 mmHg for high-risk patients. This condition often arises from failures in short-term blood pressure regulation mechanisms, resulting in inadequate compensatory responses to maintain . Orthostatic hypotension, a common subtype, is characterized by a sustained drop of at least 20 mmHg in systolic blood pressure or 10 mmHg in diastolic blood pressure within of standing from a or sitting position. It typically results from dysfunction, leading to impaired and reduced venous return, and is particularly prevalent in older adults due to age-related declines in sensitivity, as well as in individuals with , certain medications, or neurodegenerative disorders. The prevalence of increases with age, affecting approximately 6.9% of the general population but rising to 18.5% or more in those aged 80 and older, and up to 20% in community-dwelling individuals over 60. Other forms of hypotension include cardiogenic hypotension, which stems from or impaired , such as in or , leading to reduced pumping efficiency. Hypovolemic hypotension occurs due to significant blood or fluid loss, as seen in hemorrhage, severe , or burns, which decreases circulating volume and preload. Septic shock, a distributive type, involves profound and capillary leakage from systemic , often causing refractory hypotension despite initial fluid . Management of hypotension focuses on addressing the underlying cause and restoring , with intravenous fluids as a primary intervention for hypovolemic and distributive forms to expand volume and support hemodynamic stability. For , nonpharmacologic strategies include , which apply graduated pressure to the lower extremities to prevent venous pooling and enhance venous return, thereby reducing postural drops. Additional measures, such as slow positional changes and adequate hydration, are recommended, particularly in the 5-10% of older adults where contributes to falls and syncope. In severe cases like cardiogenic or , vasopressors or inotropes may be required alongside fluids to maintain pressure.

Pressure Variability

Blood pressure variability refers to fluctuations in blood pressure levels over short or extended periods, distinct from sustained elevations or reductions, and can manifest in patterns that influence cardiovascular health. These variations are quantified through metrics such as standard deviation of readings or visit-to-visit differences, providing insights into dynamic physiological responses beyond average values. Key types of blood pressure variability include , characterized by rapid and unpredictable swings between normal and high levels, often exceeding typical daily fluctuations. White-coat hypertension involves elevated readings in clinical settings due to anxiety or environmental factors, while readings outside the clinic remain normal. In contrast, masked hypertension presents normal clinic measurements but higher pressures in daily life, potentially leading to underdiagnosis of risks. Causes of such variability often stem from autonomic nervous system dysfunction, which impairs the body's ability to regulate vascular tone and dynamically. Obstructive sleep apnea contributes by inducing intermittent hypoxia and sympathetic activation, exacerbating nighttime fluctuations. A normal physiological pattern is nocturnal dipping, where blood pressure decreases by 10-20% during compared to levels, reflecting healthy circadian rhythms; disruptions to this, such as non-dipping, amplify variability. Clinically, increased blood pressure variability is associated with heightened risks of and cardiovascular events, independent of mean levels, as it promotes vascular damage and . monitoring is the preferred method for detecting these patterns, capturing 24-hour profiles to assess variability more accurately than office measurements. As of 2025, advancements in enable enhanced analysis of blood pressure variability from wearable and ambulatory data, improving early prediction of by identifying subtle patterns linked to adverse outcomes. These AI models integrate variability metrics with other biomarkers to forecast risks more precisely than traditional methods.

Applications in Animals

Comparative Physiology

Blood pressure in mammals is remarkably consistent across species, typically ranging from 100 to 150 mmHg systolic and 60 to 100 mmHg diastolic, similar to norms of around 120/80 mmHg, reflecting evolutionary adaptations for maintaining in closed circulatory systems with high metabolic demands. This uniformity supports efficient oxygen delivery to tissues in endothermic animals, where larger species like exhibit mean arterial pressures of approximately 100 mmHg under resting conditions, with systolic pressures often around 120 mmHg and diastolic around 80 mmHg, scaled to their substantial body mass for gravitational and circulatory efficiency. In birds and reptiles, systemic blood pressures are adapted for varying levels of activity and metabolic efficiency, often higher than in many other vertebrates to facilitate rapid circulation despite environmental challenges. Birds, with their fully separated pulmonary and systemic circuits, maintain elevated systemic pressures ranging from 108 to 250 mmHg systolic to support the high cardiac outputs required for flight and endothermy, preventing through specialized vascular barriers. Reptiles generally exhibit lower pressures, around 50 to 100 mmHg systolic, but active species such as varanid and pythons can achieve mammalian-like levels (60 to 100 mmHg ) during exertion, enabling bursts of efficient circulation in ectothermic lifestyles. Invertebrates, such as , possess open circulatory systems where —the equivalent of —circulates under much lower pressures, typically 1 to 5 mmHg or equivalent to 2 to 7 cm H₂O, driven by a simple dorsal vessel rather than a high-pressure . This low-pressure design suffices for distribution and removal in small-bodied organisms with diffuse oxygen delivery via tracheae, minimizing energy costs compared to closed systems. Evolutionarily, blood pressure across animal species scales allometrically with body mass and metabolic rate, allowing larger animals to maintain adequate without excessive cardiac workload. This scaling reflects adaptations to body size, where higher pressures in endotherms like mammals and birds support elevated , while lower pressures in and many ectotherms align with reduced oxygen demands and simpler circulatory architectures.

Common Pathologies

In companion animals, systemic is a prevalent condition, particularly in older cats and dogs, defined as a systolic blood pressure exceeding 160 mmHg on repeated measurements. This disorder is most commonly secondary to underlying diseases, with accounting for approximately 90% of cases in cats, where it exacerbates renal and leads to target organ such as or . In cats, additionally, hypertension develops in up to 87% of cats with , often presenting concurrently with cardiac or . Dogs experience similar , primarily linked to , though idiopathic forms occur less commonly than in cats. Hypotension, characterized by below 60 mmHg, is a critical in hospitalized companion animals, often arising in contexts of shock or and affecting 20-30% of such patients during or intensive care. In these scenarios, from leads to and hypoperfusion, while from fluid losses compounds the issue, potentially causing if untreated. Initial management focuses on rapid fluid resuscitation with crystalloids at shock doses (45-60 mL/kg in cats, 70-90 mL/kg in dogs) to restore , though persistent cases may require vasopressors like norepinephrine. Accurate blood pressure assessment in pets presents challenges, particularly with noninvasive methods using versus limb cuffs, as improper cuff sizing (ideally 30-40% of limb or ) or positioning can yield readings 10-20 mmHg higher or lower than direct arterial measurements. cuffs are preferred in cats for reduced stress but may overestimate systolic values in agitated animals compared to forelimb placements in dogs; the American College of Veterinary Internal Medicine (ACVIM) guidelines emphasize multiple readings in a calm environment to mitigate white-coat effects and validate results against target organ damage. Management of hypertension prioritizes treating underlying causes alongside antihypertensive therapy, with (ACE) inhibitors such as benazepril or enalapril serving as first-line agents in dogs at doses of 0.5-2.0 mg/kg orally every 12-24 hours to reduce and . In cats, ACE inhibitors are often adjunctive to like amlodipine, but they effectively lower pressure in renal-associated cases. Monitoring protocols involve rechecking blood pressure 7-14 days post-initiation, then every 3-6 months once controlled (target systolic <160 mmHg), alongside serial and to detect progression.

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