In a Blood Pressure Reading of 120/80, the 120 Is Measuring What Body Process?

Pressure exerted by circulating claret upon the walls of arteries

Blood pressure
A healthcare worker measuring blood force per unit area using a sphygmomanometer.
MeSH	D001795
MedlinePlus	007490
LOINC	35094-ii

Blood pressure level (BP) is the pressure of circulating claret confronting the walls of blood vessels. Most of this pressure level results from the center pumping blood through the circulatory arrangement. When used without qualification, the term "claret pressure" refers to the pressure level in the large arteries. Blood pressure is normally expressed in terms of the systolic pressure (maximum pressure level during one heartbeat) over diastolic pressure (minimum pressure between two heartbeats) in the cardiac bike. Information technology is measured in millimeters of mercury (mmHg) higher up the surrounding atmospheric pressure.

Blood pressure is i of the vital signs—together with respiratory rate, heart rate, oxygen saturation, and trunk temperature—that healthcare professionals utilise in evaluating a patient'due south wellness. Normal resting claret pressure level, in an adult is approximately 120 millimetres of mercury (sixteen kPa) systolic over fourscore millimetres of mercury (11 kPa) diastolic, denoted every bit "120/80 mmHg". Globally, the average blood pressure, age standardized, has remained near the aforementioned since 1975 to the present, at approx. 127/79 mmHg in men and 122/77 mmHg in women, although these boilerplate data mask significantly diverging regional trends.^[1]

Traditionally, a health-care worker measured blood pressure non-invasively by auscultation (listening) through a stethoscope for sounds in 1 arm's artery equally the avenue is squeezed, closer to the middle, by an aneroid estimate or a mercury-tube sphygmomanometer.^[2] Auscultation is still generally considered to be the gold standard of accuracy for non-invasive blood pressure level readings in clinic.^[3] However, semi-automated methods have become common, largely due to concerns nigh potential mercury toxicity,^[4] although price, ease of use and applicability to ambulatory blood pressure level or domicile blood pressure measurements have likewise influenced this tendency.^[5] Early automated alternatives to mercury-tube sphygmomanometers were ofttimes seriously inaccurate, but modernistic devices validated to international standards attain an average difference between two standardized reading methods of v mm Hg or less, and a standard divergence of less than 8 mm Hg.^[5] Almost of these semi-automated methods measure blood pressure level using oscillometry (measurement by a pressure transducer in the cuff of the device of pocket-size oscillations of intra-cuff pressure accompanying heartbeat-induced changes in the volume of each pulse).^[6]

Blood pressure is influenced by cardiac output, systemic vascular resistance and arterial stiffness and varies depending on situation, emotional land, activity, and relative health/disease states. In the short term, blood pressure level is regulated past 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 chosen hypertension, and normal pressure level is called normotension.^[seven] 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, middle illness, and kidney failure. Long-term hypertension is more common than long-term hypotension.

Classification, normal and abnormal values [edit]

Systemic arterial pressure level [edit]

The Task Force for the management of arterial hypertension of the European Society of Cardiology (ESC) and the European Lodge of Hypertension (ESH) classification of function blood pressure level (BP)^a and definitions of hypertension course^b.

Category	Systolic BP, mmHg	Diastolic BP, mmHg
Optimal	< 120	< eighty
Normal	120–129	fourscore–84
High normal	130–139	85–89
Grade 1 hypertension	140–159	90–99
Grade ii hypertension	160–179	100–109
Course 3 hypertension	≥ 180	≥ 110
Isolated systolic hypertensionb	≥ 140	< ninety
The aforementioned classification is used for all ages from xvi years. a BP category is defined according to seated clinic BP and past the highest level of BP, whether systolic or diastolic. b Isolated systolic hypertension is graded one, ii, or 3 co-ordinate to systolic BP values in the ranges indicated.

The risk of cardiovascular disease increases progressively in a higher place 115/75 mmHg,^[eight] below this level there is limited show.^[nine]

Observational studies demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long-term cardiovascular health. In that location 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.^[10]

The table shows the most recent classification (2018) of role (or clinic) claret pressure past The Task Forcefulness for the management of arterial hypertension of the European Society of Cardiology (ESC) and the European Guild of Hypertension (ESH).^[11] Similar thresholds had been adopted by the American Middle Clan for adults who are eighteen years and older,^[12] but in November 2022 the American Heart Clan announced revised definitions for blood pressure categories that increased the number of people considered to accept high claret pressure level.^[13]

Blood pressure fluctuates from minute to minute and normally shows a circadian rhythm over a 24-hour menses,^[14] with highest readings in the early morning and evenings and everyman readings at night.^{[15] [xvi]} Loss of the normal fall in blood pressure level at night is associated with a greater hereafter risk of cardiovascular disease and in that location is evidence that nighttime-time blood pressure is a stronger predictor of cardiovascular events than twenty-four hour period-time claret pressure.^[17] Blood pressure varies over longer time periods (months to years) and this variability predicts adverse outcomes.^[18] Blood pressure too changes in response to temperature, dissonance, emotional stress, consumption of nutrient or liquid, dietary factors, physical activity, changes in posture (such as standing-up), drugs, and disease.^[19] The variability in blood force per unit area and the better predictive value of ambulatory blood pressure measurements has led some authorities, such as the National Found for Health and Care Excellence (Prissy) in the U.k., to advocate for the use of convalescent blood pressure as the preferred method for diagnosis of hypertension.^[20]

A digital sphygmomanometer used for measuring blood pressure

Diverse other factors, such as age and sex, also influence a person'due south claret pressure. Differences between left-arm and right-arm blood pressure level measurements tend to exist minor. Still, occasionally there is a consequent divergence greater than 10 mmHg which may demand farther investigation, eastward.chiliad. for peripheral arterial disease or obstructive arterial disease.^{[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 force per unit area and age [edit]

Fetal claret pressure [edit]

In pregnancy, it is the fetal heart and not the female parent'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 boilerplate blood pressure for full-term infants:^[28]

• Systolic 65–95 mmHg
• Diastolic thirty–sixty mmHg

Babyhood [edit]

Reference ranges for blood force per unit area (BP) in children^[29]

Phase	Gauge age	Systolic BP, mmHg	Diastolic BP, mmHg
Infants	0 to 12 months	75–100	50–seventy
Toddlers and preschoolers	ane to 5 years	lxxx–110	50–80
School historic period	6 to 12 years	85–120	50–eighty
Adolescents	13 to 18 years	95–140	lx–xc

In children, the normal ranges for blood pressure are lower than for adults and depend on pinnacle.^[thirty] Reference blood force per unit area values take been developed for children in different countries, based on the distribution of claret pressure in children of these countries.^[31]

Aging adults [edit]

In adults in most societies, systolic blood pressure tends to rise from early on adulthood onward, upward to at to the lowest degree historic period 70;^{[32] [33]} diastolic pressure tends to begin to rise at the same time merely to showtime 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 later the age of forty. Consequently, in many older people, systolic blood pressure frequently exceeds the normal adult range,^[33] if the diastolic pressure level is in the normal range this is termed isolated systolic hypertension. The rising in pulse force per unit area with age is attributed to increased stiffness of the arteries.^[34] An age-related rise in claret pressure level is not considered salubrious and is non observed in some isolated unacculturated communities.^[35]

Systemic venous force per unit area [edit]

Site		Normal pressure range (in mmHg)[36]
Fundamental venous force per unit area		3–8
Right ventricular pressure	systolic	15–30
	diastolic	iii–8
Pulmonary artery force per unit area	systolic	15–30
	diastolic	4–12
Pulmonary vein/ Pulmonary capillary wedge pressure level		2–15
Left ventricular pressure level	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 organisation and the pulmonary vessels plays an of import role in intensive intendance medicine simply requires invasive measurement of pressure using a catheter.

Venous pressure is the vascular force per unit area in a vein or in the atria of the heart. It is much lower than arterial force per unit area, with common values of v mmHg in the right atrium and 8 mmHg in the left atrium.

Variants of venous pressure include:

• Central venous pressure, which is a skilful approximation of right atrial pressure,^[37] which is a major determinant of right ventricular end diastolic volume. (However, in that location tin can be exceptions in some cases.)^[38]
• The jugular venous force per unit area (JVP) is the indirectly observed pressure level over the venous arrangement. Information technology can be useful in the differentiation of different forms of heart and lung affliction.
• The portal venous pressure level is the claret pressure in the portal vein. It is ordinarily 5–ten mmHg^[39]

Pulmonary pressure [edit]

Normally, the pressure in the pulmonary artery is virtually 15 mmHg at rest.^[xl]

Increased blood pressure in the capillaries of the lung causes pulmonary hypertension, leading to interstitial edema if the pressure increases to to a higher place 20 mmHg, and to pulmonary edema at pressures above 25 mmHg.^[41]

Hateful systemic force per unit area [edit]

If the centre is stopped, blood pressure falls, just it does not autumn to nix. The remaining pressure measured after abeyance of the eye crush and redistribution of claret throughout the circulation is termed the mean systemic pressure or hateful circulatory filling pressure level;^[42] typically this is of the order of ~7mm Hg.^[42]

Disorders of blood pressure [edit]

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

Loftier blood pressure level [edit]

Overview of main complications of persistent high blood pressure

Arterial hypertension can be an indicator of other problems and may take long-term adverse effects. Sometimes it can be an acute problem, for example hypertensive emergency.

Levels of arterial pressure put mechanical stress on the arterial walls. College pressures increment eye workload and progression of unhealthy tissue growth (atheroma) that develops inside the walls of arteries. The higher the pressure level, the more stress that is nowadays and the more atheroma tend to progress and the heart muscle tends to thicken, enlarge and become weaker over time.

Persistent hypertension is 1 of the risk factors for strokes, middle attacks, middle failure, and arterial aneurysms, and is the leading cause of chronic kidney failure. Fifty-fifty moderate elevation of arterial pressure level leads to shortened life expectancy. At severely high pressures, hateful arterial pressures 50% or more to a higher place average, a person can wait to live no more than a few years unless appropriately treated.^[43]

In the past, most attention was paid to diastolic pressure; but nowadays information technology is recognized that both high systolic pressure and high pulse force per unit area (the numerical difference betwixt systolic and diastolic pressures) are likewise risk factors. In some cases, it appears that a subtract in excessive diastolic pressure can actually increase risk, due probably to the increased difference between systolic and diastolic pressures (encounter Pulse pressure). If systolic claret pressure is elevated (>140 mmHg) with a normal diastolic blood force per unit area (<90 mmHg), it is called "isolated systolic hypertension" and may nowadays a health concern.^{[44] [45]}

For those with middle valve regurgitation, a alter 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 claret pressure increased, whereas when diastolic blood force per unit area decreased, at that place was a decreased severity.^[46]

Low blood pressure [edit]

Blood pressure level 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 farthermost cases, circulatory shock.^[47]

Causes of low arterial pressure include:^[48]

• Sepsis
• Hemorrhage – blood loss
• Cardiogenic shock
• Neurally mediated hypotension (or reflex syncope)
• Toxins including toxic doses of blood force per unit area medicine
• Hormonal abnormalities, such as Addison's disease
• Eating disorders, particularly anorexia nervosa and bulimia

Orthostatic hypotension [edit]

A big fall in blood pressure upon standing (persistent systolic/diastolic blood pressure decrease of >20/ten mm Hg) is termed orthostatic hypotension (postural hypotension) and represents a failure of the body to compensate for the consequence of gravity on the circulation. Continuing results in an increased hydrostatic force per unit area in the blood vessels of the lower limbs. The consequent distension of the veins below the diaphragm (venous pooling) causes ~500 ml of claret to be relocated from the chest and upper body. This results in a rapid decrease in primal blood book and a reduction of ventricular preload which in turn reduces stroke volume, and mean arterial pressure level. Normally this is compensated for by multiple mechanisms, including activation of the autonomic nervous organisation which increases heart charge per unit, myocardial contractility and systemic arterial vasoconstriction to preserve blood pressure and elicits venous vasoconstriction to decrease venous compliance. Decreased venous compliance as well results from an intrinsic myogenic increment in venous smooth muscle tone in response to the elevated force per unit area in the veins of the lower body. Other compensatory mechanisms include the veno-arteriolar axon reflex, the 'skeletal musculus pump' and 'respiratory pump'. Together these mechanisms ordinarily stabilize blood pressure within a minute or less.^[49] If these compensatory mechanisms neglect and arterial pressure level and blood flow decrease beyond a certain indicate, the perfusion of the encephalon becomes critically compromised (i.east., the blood supply is not sufficient), causing lightheadedness, dizziness, weakness or fainting.^[50] Usually this failure of compensation is due to disease, or drugs that affect the sympathetic nervous system.^[49] A similar effect is observed following the feel of excessive gravitational forces (Chiliad-loading), such as routinely experienced by aerobatic or gainsay pilots 'pulling Gs' where the farthermost hydrostatic pressures exceed the ability of the torso's compensatory mechanisms.

Variable or fluctuating claret pressure [edit]

Some fluctuation or variation in blood pressure is normal. Variations in pressure level that are significantly greater than the norm are associated with increased risk of cardiovascular illness^[51] encephalon small vessel disease,^[52] and dementia^[53] independent of the average blood pressure level. Recent evidence from clinical trials has also linked variation in blood pressure to mortality,^{[54] [55]} stroke,^[56] centre failure,^[57] and cardiac changes that may give rise to heart failure.^[58] These data have prompted give-and-take of whether excessive variation in blood pressure should exist treated, even amid normotensive older adults.^[59] Older individuals and those who had received blood pressure medications are more likely to showroom larger fluctuations in pressure,^[60] and there is some testify that dissimilar antihypertensive agents have unlike effects on blood pressure variability;^[53] whether these differences translate to benefits in outcome is uncertain.^[53]

Physiology [edit]

Cardiac systole and diastole

Blood flow velocity waveforms in the fundamental retinal artery (red) and vein (blue), measured past laser Doppler imaging in the eye fundus of a healthy volunteer.

During each heartbeat, claret force per unit area varies betwixt a maximum (systolic) and a minimum (diastolic) pressure.^[61] The blood pressure in the circulation is principally due to the pumping action of the eye.^[62] Notwithstanding, blood pressure is also regulated by neural regulation from the encephalon (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 hateful blood menstruum depends on both blood pressure and the resistance to flow presented past the blood vessels. In the absence of hydrostatic furnishings (due east.g. standing), hateful blood pressure decreases as the circulating blood moves away from the centre through arteries and capillaries due to pasty losses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs forth the minor arteries and arterioles.^[63] Pulsatility also diminishes in the smaller elements of the arterial circulation, although some transmitted pulsatility is observed in capillaries.^[64]

Schematic of pressures in the circulation

Gravity affects claret pressure via hydrostatic forces (due east.g., during standing), and valves in veins, breathing, and pumping from contraction of skeletal muscles besides influence claret pressure, peculiarly in veins.^[62]

Hemodynamics [edit]

A simple view of the hemodynamics of systemic arterial pressure is based around mean arterial force per unit area (MAP) and pulse pressure. Most influences on blood force per unit area can be understood in terms of their effect on cardiac output,^[65] systemic vascular resistance, or arterial stiffness (the inverse of arterial compliance). Cardiac output is the production of stroke volume and heart rate. Stroke volume is influenced by 1) the end diastolic volume or filling pressure of the ventricle interim via the Frank Starling machinery - this is influenced past claret volume; ii) cardiac contractility; and three) afterload, the impedance to claret flow presented past the circulation.^[66] In the short-term, the greater the claret volume, the higher the cardiac output. This has been proposed every bit an explanation of the relationship between high dietary salt intake and increased claret pressure; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous arrangement responses and the renin–angiotensin arrangement,^{[67] [68] [69]} changes in plasma osmolarity may also be important.^[70] In the longer-term the relationship between volume and claret pressure is more complex.^[71] In simple terms, systemic vascular resistance is mainly determined by the caliber of modest arteries and arterioles. The resistance attributable to a blood vessel depends on its radius as described by the Hagen-Poiseuille'southward equation (resistance∝1/radius^four). 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)^[72] and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterial stenosis increases resistance to menstruum, however this increase in resistance rarely increases systemic claret pressure because its contribution to total systemic resistance is modest, although it may greatly decrease downstream catamenia.^[73] Substances chosen vasoconstrictors reduce the caliber of blood vessels, thereby increasing blood force per unit area. Vasodilators (such as nitroglycerin) increase the caliber of blood vessels, thereby decreasing arterial force per unit area. In the longer term a process termed remodeling too contributes to changing the quotient of small blood vessels and influencing resistance and reactivity to vasoactive agents.^{[74] [75]} Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances.^[76]

In exercise, each individual's autonomic nervous system and other systems regulating blood pressure, notably the kidney,^[77] respond to and regulate all these factors so that, although the higher up issues are important, they rarely human activity in isolation and the bodily arterial pressure response of a given individual can vary widely in the curt and long term.

Mean arterial pressure level [edit]

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)):^{[78] [79] [lxxx]}

${\displaystyle \!{\text{MAP}}=({\text{CO}}\cdot {\text{SVR}})+{\text{CVP}}}$

In practice, the contribution of CVP (which is pocket-sized) is by and large ignored and and so

${\displaystyle \!{\text{MAP}}={\text{CO}}\cdot {\text{SVR}}}$

MAP is ofttimes estimated from measurements of the systolic pressure, ${\displaystyle \!P_{\text{sys}}}$ and the diastolic pressure, ${\displaystyle \!P_{\text{dias}}}$ ^[lxxx] using the equation:

${\displaystyle \!{\text{MAP}}\approxeq P_{\text{dias}}+one thousand(P_{\text{sys}}-P_{\text{dias}})}$

where yard = 0.333 although other values for k have been advocated.^{[81] [82]}

Pulse pressure [edit]

A schematic representation of the arterial pressure waveform over one cardiac wheel. The notch in the curve is associated with closing of the aortic valve.

The pulse pressure is the departure between the measured systolic and diastolic pressures,^[83]

${\displaystyle \!P_{\text{pulse}}=P_{\text{sys}}-P_{\text{dias}}.}$

The pulse pressure level is a effect 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 book of the heart, the compliance (ability to expand) of the arterial system—largely attributable to the aorta and large rubberband arteries—and the resistance to catamenia in the arterial tree.^[83]

Regulation of blood pressure level [edit]

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

• Baroreceptor reflex: Baroreceptors in the high pressure level receptor zones detect changes in arterial pressure. These baroreceptors transport signals ultimately to the medulla of the brain stem, specifically to the rostral ventrolateral medulla (RVLM). The medulla, by fashion of the autonomic nervous system, adjusts the mean arterial pressure level 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 curvation.^[84]
• Renin–angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial force per unit area. This system allows the kidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known every bit 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 claret vessels past osmosis, aldosterone will increment fluid retention, and indirectly, arterial pressure.
• Baroreceptors in low force per unit area 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 claret volume results in an increased cardiac output by the Frank–Starling law of the heart, in plow increasing arterial blood force per unit area.

These different mechanisms are not necessarily independent of each other, every bit indicated by the link betwixt the RAS and aldosterone release. When blood pressure falls many physiological cascades commence in lodge to return the blood pressure to a more advisable level.

1. The claret pressure fall is detected by a subtract in blood catamenia and thus a decrease in glomerular filtration rate (GFR).
2. Decrease in GFR is sensed as a subtract in Na⁺ levels past 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 force per unit area 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 Two is a vasoconstrictor that will increase blood flow to the heart and subsequently the preload, ultimately increasing the cardiac output.
8. Angiotensin 2 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.

Currently, the RAS is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists, too known as angiotensin receptor blockers (ARBs). The aldosterone system is direct targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted past diuretics; the antihypertensive upshot of diuretics is due to its effect on claret book. Mostly, the baroreceptor reflex is not targeted in hypertension because if blocked, individuals may endure from orthostatic hypotension and fainting.

Taking blood pressure with a sphygmomanometer

Measurement [edit]

Arterial pressure is near commonly measured via a sphygmomanometer, which uses the elevation of a column of mercury, or an aneroid gauge, to reflect the blood pressure by auscultation.^[2] The nigh common automated claret pressure measurement technique is based on the oscillometric method.^[85] Fully automated oscillometric measurement has been available since 1981.^[86] This principle has recently been used to measure blood pressure with a smartphone.^[87] 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 whatsoever pressure level on patient'due south body are currently being explored.^[88] So-chosen cuffless measurements, these methods open up the door to more comfy and acceptable blood pressure level monitors. An example is a cuffless blood force per unit area monitor at the wrist that uses merely optical sensors^[89]

I mutual problem in office blood pressure measurement in the United States is final digit preference. 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 null"^[90] Therefore, addressing digit preference is a central issue for improving blood pressure measurement accuracy.

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 middle rates).^[91] The giraffe has a distinctly high arterial pressure of about 190 mm Hg, enabling blood perfusion through the two metres (six ft 7 in)-long neck to the caput.^[92] In other species subjected to orthostatic blood force per unit area, such equally arboreal snakes, claret force per unit area is higher than in non-arboreal snakes.^[93] A heart virtually to the head (short centre-to-head altitude) and a long tail with tight integument favor blood perfusion to the head.^{[94] [95]}

Every bit in humans, claret pressure in animals differs past age, sex activity, time of twenty-four hour period, and ecology circumstances:^{[96] [97]} measurements made in laboratories or under anesthesia may not exist representative of values nether free-living weather condition. Rats, mice, dogs and rabbits have been used extensively to study the regulation of blood pressure.^[98]

Blood force per unit area and heart charge per unit of diverse mammals^[96]

Species	Blood pressure mm Hg		Heart charge per unit beats per minute
	Systolic	Diastolic
Calves	140	70	75–146
Cats	155	68	100–259
Dogs	161	51	62–170
Goats	140	90	lxxx–120
Guinea-pigs	140	xc	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 claret pressure is greater than 160 mm Hg (systolic), although sight hounds have college blood pressures than most other dog breeds; a systolic pressure greater than 180 mmHg is considered abnormal in these dogs.^[99]

References [edit]

1. ^ NCD Risk Gene Collaboration (NCD-RisC) (January 2017). "Worldwide trends in blood pressure level from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19·1 million participants". The Lancet. 389 (10064): 37–55. doi:10.1016/S0140-6736(16)31919-5. PMC5220163. PMID 27863813.
2. ^ ^{a b} Booth J (November 1977). "A short history of blood force per unit area measurement". Proceedings of the Majestic Society of Medicine. 70 (11): 793–9. doi:10.1177/003591577707001112. PMC1543468. PMID 341169.
3. ^ Grim CE, Grim CM (March 2016). "Auscultatory BP: yet the gold standard". Journal of the American Society of Hypertension. 10 (3): 191–3. doi:10.1016/j.jash.2016.01.004. PMID 26839183.
4. ^ O'Brien East (January 2001). "Blood pressure measurement is irresolute!". Heart. 85 (ane): 3–5. doi:10.1136/eye.85.1.three. PMC1729570. PMID 11119446.
5. ^ ^{a b} Ogedegbe G, Pickering T (Nov 2010). "Principles and techniques of blood pressure measurement". Cardiology Clinics. 28 (4): 571–86. doi:x.1016/j.ccl.2010.07.006. PMC3639494. PMID 20937442.
6. ^ Alpert BS, Quinn D, Gallick D (December 2014). "Oscillometric blood pressure: a review for clinicians". Journal of the American Society of Hypertension. 8 (12): 930–8. doi:ten.1016/j.jash.2014.08.014. PMID 25492837.
7. ^ William Alexander Newman, ed. (2012). Dorland'south illustrated medical lexicon (32nd ed.). Philadelphia, PA: Saunders/Elsevier. ISBN978-1-4160-6257-viii. OCLC 706780870.
8. ^ Appel LJ, Brands MW, Daniels SR, Karanja N, Elmer PJ, Sacks FM (Feb 2006). "Dietary approaches to foreclose and treat hypertension: a scientific argument from the American Center Association". Hypertension. 47 (2): 296–308. CiteSeerX10.one.1.617.6244. doi:10.1161/01.HYP.0000202568.01167.B6. PMID 16434724. S2CID 1447853.
9. ^ Lewington S, Clarke R, Qizilbash Northward, Peto R, Collins R (December 2002). "Age-specific relevance of usual claret pressure to vascular bloodshed: a meta-analysis of individual data for ane million adults in 61 prospective studies". Lancet. 360 (9349): 1903–13. doi:10.1016/S0140-6736(02)11911-viii. PMID 12493255. S2CID 54363452.
10. ^ Yusuf S, Lonn Due east (November 2016). "The Sprint and the Promise-three Trial in the Context of Other Blood Pressure-Lowering Trials". JAMA Cardiology. 1 (8): 857–858. doi:10.1001/jamacardio.2016.2169. PMID 27602555.
11. ^ Williams B, Mancia Grand, Spiering W, Agabiti Rosei E, Azizi M, Burnier M, et al. (September 2018). "2018 ESC/ESH Guidelines for the management of arterial hypertension". European Centre Journal. 39 (33): 3021–3104. doi:x.1093/eurheartj/ehy339. PMID 30165516.
12. ^ "Understanding blood pressure readings". American Heart Clan. 11 Jan 2011. Retrieved 30 March 2011.
13. ^ "Nearly one-half of US adults could at present be classified with high claret force per unit area, under new definitions". American Heart Association. 13 Nov 2017. Retrieved 2019-07-28 .
14. ^ Smolensky MH, Hermida RC, Portaluppi F (June 2017). "Circadian mechanisms of 24-hour blood pressure regulation and patterning". Slumber Medicine Reviews. 33: 4–16. doi:10.1016/j.smrv.2016.02.003. PMID 27076261.
15. ^ van Berge-Landry HM, Bovbjerg DH, James GD (October 2008). "Relationship between waking-sleep claret pressure and catecholamine changes in African-American and European-American women". Blood Pressure Monitoring. 13 (v): 257–62. doi:ten.1097/MBP.0b013e3283078f45. PMC2655229. PMID 18799950. Table2: Comparison of ambulatory blood pressures and urinary norepinephrine and epinephrine excretion measured at work, home, and during sleep between European–American (n = 110) and African–American (north = 51) women
16. ^ van Berge-Landry HM, Bovbjerg DH, James GD (October 2008). "Relationship betwixt waking-sleep blood pressure and catecholamine changes in African-American and European-American women". Blood Pressure Monitoring. 13 (v): 257–62. doi:10.1097/MBP.0b013e3283078f45. PMC2655229. PMID 18799950. NIHMS90092.
17. ^ Hansen TW, Li Y, Boggia J, Thijs L, Richart T, Staessen JA (January 2011). "Predictive office of the nighttime blood pressure". Hypertension. 57 (i): 3–10. doi:10.1161/HYPERTENSIONAHA.109.133900. PMID 21079049.
18. ^ Rothwell PM (June 2011). "Does blood force per unit area variability modulate cardiovascular risk?". Current Hypertension Reports. thirteen (3): 177–86. doi:10.1007/s11906-011-0201-3. PMID 21465141. S2CID 207331784.
19. ^ Engel, Bernard T.; Blümchen, Gerhard, eds. (1992). Temporal Variations of the Cardiovascular System. Berlin, Heidelberg: Springer Berlin Heidelberg. ISBN9783662027486. OCLC 851391490.
20. ^ National Clinical Guideline Centre (Britain) (2011). Hypertension: The Clinical Management of Primary Hypertension in Adults: Update of Clinical Guidelines 18 and 34. National Plant for Wellness and Clinical Excellence: Guidance. London: Purple College of Physicians (United kingdom of great britain and northern ireland). PMID 22855971.
21. ^ Eguchi 1000, Yacoub Thousand, 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. doi:10.1001/archinte.167.4.388. PMID 17325301.
22. ^ Agarwal R, Bunaye Z, Bekele DM (March 2008). "Prognostic significance of between-arm claret pressure differences". Hypertension. 51 (3): 657–62. CiteSeerXx.i.1.540.5836. doi:ten.1161/HYPERTENSIONAHA.107.104943. PMID 18212263. S2CID 1101762.
23. ^ Clark, C. E.; Campbell, J. L.; Evans, P. H.; Millward, A. (December 2006). "Prevalence and clinical implications of the inter-arm blood pressure level difference: A systematic review". Journal of Homo Hypertension. 20 (12): 923–931. doi:ten.1038/sj.jhh.1002093. ISSN 0950-9240. PMID 17036043.
24. ^ Clark CE, et al. (December 2021). "Associations between systolic interarm differences in claret pressure and cardiovascular disease outcomes and mortality". Hypertension. 77 (2): 650–661. doi:x.1161/HYPERTENSIONAHA.120.15997. PMC7803446. PMID 33342236.
25. ^ Sharma South, Bhattacharya PT (2018). Hypotension. StatPearls. StatPearls Publishing. PMID 29763136. Retrieved 2018-12-23 .
26. ^ Mayo Dispensary staff (2009-05-23). "Low blood pressure (hypotension) – Causes". MayoClinic.com. Mayo Foundation for Medical Education and Research. Retrieved 2010-ten-nineteen .
27. ^ Struijk PC, Mathews VJ, Loupas T, Stewart PA, Clark EB, Steegers EA, Wladimiroff JW (October 2008). "Blood pressure level estimation in the human fetal descending aorta". Ultrasound Obstet Gynecol. 32 (five): 673–81. doi:10.1002/uog.6137. PMID 18816497. S2CID 23575926.
28. ^ Sharon SM, Emily SM (2006). Foundations of Maternal-Newborn Nursing (quaternary ed.). Philadelphia: Elsevier. p. 476.
29. ^ Pediatric Historic period Specific, p. six. Revised 6/ten. By Theresa Kirkpatrick and Kateri Tobias. UCLA Wellness System
30. ^ National Heart Lung and Blood Institute. "Blood pressure tables for children and adolescents". Archived from the original on 2014-06-xviii. Retrieved 2008-09-23 . (Note that the median blood force per unit area is given by the 50th percentile and hypertension is defined past the 95th percentile for a given age, height, and sex.)
31. ^ Chiolero A (Mar 2014). "The quest for blood pressure reference values in children". Journal of Hypertension. 32 (three): 477–79. doi:ten.1097/HJH.0000000000000109. PMID 24477093. S2CID 1949314.
32. ^ Wills AK, Lawlor DA, Matthews FE, Sayer AA, Bakra Eastward, Ben-Shlomo Y, Benzeval M, Brunner E, Cooper R, Kivimaki M, Kuh D, Muniz-Terrera Thou, Hardy R (June 2011). "Life grade trajectories of systolic blood pressure level using longitudinal data from 8 Uk cohorts". PLOS Medicine. 8 (half-dozen): e1000440. doi:x.1371/periodical.pmed.1000440. PMC3114857. PMID 21695075.
33. ^ ^{a b c} Franklin SS, Gustin Westward, Wong ND, Larson MG, Weber MA, Kannel WB, Levy D (July 1997). "Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study". Circulation. 96 (1): 308–15. doi:ten.1161/01.CIR.96.1.308. PMID 9236450. S2CID 40209177.
34. ^ Franklin SS (2008-05-01). "Across blood pressure: Arterial stiffness as a new biomarker of cardiovascular disease". Journal of the American Guild of Hypertension. two (3): 140–51. doi:10.1016/j.jash.2007.09.002. PMID 20409896.
35. ^ Gurven, Michael; Blackwell, Aaron D.; Rodríguez, Daniel Eid; Stieglitz, Jonathan; Kaplan, Hillard (July 2012). "Does blood pressure inevitably rise with age?: longitudinal bear witness among forager-horticulturalists". Hypertension. 60 (1): 25–33. doi:10.1161/HYPERTENSIONAHA.111.189100. ISSN 1524-4563. PMC3392307. PMID 22700319.
36. ^ Table 30-1 in: Trudie A Goers; Klingensmith, Mary E; Li Ern Chen; Sean C Glasgow (2008). The Washington manual of surgery. Philadelphia: Wolters Kluwer Wellness/Lippincott Williams & Wilkins. ISBN0-7817-7447-0.
37. ^ "Fundamental Venous Catheter Physiology". Archived from the original on 2008-08-21. Retrieved 2009-02-27 .
38. ^ Tkachenko BI, Evlakhov Six, Poyasov IZ (2002). "Independence of changes in right atrial pressure and central venous pressure". Bull. Exp. Biol. Med. 134 (4): 318–20. doi:x.1023/A:1021931508946. PMID 12533747. S2CID 23726657.
39. ^ "Esophageal Varices : Article Excerpt past: Samy A Azer". eMedicine. Retrieved 2011-08-22 .
40. ^ What Is Pulmonary Hypertension? From Diseases and Conditions Index (DCI). National Centre, Lung, and Blood Institute. Final updated September 2008. Retrieved on 6 April 2009.
41. ^ Chapter 41, p. 210 in: Cardiology secrets By Olivia Vynn Adair Edition: 2, illustrated Published by Elsevier Health Sciences, 2001 ISBN 1-56053-420-six, 978-1-56053-420-iv
42. ^ ^{a b} Rothe, C. F. (1993). "Mean circulatory filling pressure: its meaning and measurement". Journal of Applied Physiology. 74 (2): 499–509. doi:10.1152/jappl.1993.74.2.499. ISSN 8750-7587. PMID 8458763.
43. ^ Textbook of Medical Physiology, 7th Ed., Guyton & Hall, Elsevier-Saunders, ISBN 0-7216-0240-1, p. 220.
44. ^ "Isolated systolic hypertension: A health business organization?". MayoClinic.com . Retrieved 2018-01-25 .
45. ^ "Clinical Management of Isolated Systolic Hypertension". Archived from the original on September 29, 2011. Retrieved 2011-12-07 .
46. ^ Gottdiener JS, Panza JA, St John Sutton M, Bannon P, Kushner H, Weissman NJ (July 2002). "Testing the exam: The reliability of echocardiography in the sequential cess of valvular regurgitation". American Heart Journal. 144 (one): 115–21. doi:10.1067/mhj.2002.123139. PMID 12094197.
47. ^ "Diseases and conditions alphabetize – hypotension". National Heart Lung and Blood Establish. September 2008. Retrieved 2008-09-16 .
48. ^ Braunwald, Eugene; Bonow, Robert O. (2012). Braunwald's heart disease : a textbook of cardiovascular medicine (9th ed.). Philadelphia: Saunders. ISBN9781437703986. OCLC 671465395.
49. ^ ^{a b} Ricci, Fabrizio; De Caterina, Raffaele; Fedorowski, Artur (2015-08-18). "Orthostatic Hypotension: Epidemiology, Prognosis, and Handling". Journal of the American College of Cardiology. 66 (7): 848–860. doi:ten.1016/j.jacc.2015.06.1084. ISSN 0735-1097. PMID 26271068.
50. ^ Franco Folino A (2007). "Cerebral autoregulation and syncope". Prog Cardiovasc Dis. 50 (ane): 49–80. doi:10.1016/j.pcad.2007.01.001. PMID 17631437.
51. ^ Stevens, Sarah 50.; Forest, Sally; Koshiaris, Constantinos; Law, Kathryn; Glasziou, Paul; Stevens, Richard J.; McManus, Richard J. (2016-08-09). "Blood pressure variability and cardiovascular affliction: systematic review and meta-analysis". BMJ (Clinical Research Ed.). 354: i4098. doi:10.1136/bmj.i4098. ISSN 1756-1833. PMC4979357. PMID 27511067.
52. ^ Tully, Phillip J.; Yano, Yuichiro; Launer, Lenore J.; Kario, Kazuomi; Nagai, Michiaki; Mooijaart, Simon P.; Claassen, Jurgen A. H. R.; Lattanzi, Simona; Vincent, Andrew D.; Tzourio, Christophe; Variability in Blood Pressure and Brain Health Consortium † (2020-01-07). "Association Between Blood Pressure Variability and Cerebral Small-Vessel Disease: A Systematic Review and Meta-Analysis". Journal of the American Heart Clan. 9 (one): e013841. doi:10.1161/JAHA.119.013841. ISSN 2047-9980. PMC6988154. PMID 31870233.
53. ^ ^{a b c} Messerli, Franz H.; Hofstetter, Louis; Rimoldi, Stefano F.; Rexhaj, Emrush; Bangalore, Sripal (2019-05-28). "Risk Factor Variability and Cardiovascular Outcome: JACC Review Topic of the Calendar week". Journal of the American College of Cardiology. 73 (twenty): 2596–2603. doi:x.1016/j.jacc.2019.02.063. ISSN 0735-1097. PMID 31118154.
54. ^ Chiriaco Yard, et al. (2019). "Clan betwixt blood pressure variability, cardiovascular illness and mortality in type 2 diabetes: A systematic review and meta‐analysis". Diabetes, Obesity and Metabolism. 21 (12): 2587–2598. doi:x.1111/dom.13828. PMID 31282073. S2CID 195829708.
55. ^ Nuyujukian DS, Newell MS, Zhou JJ, Koska J, Reaven PD (2022). "Baseline claret pressure modifies the office of blood pressure variability in chance of mortality: results from Accordance". Diabetes, Obesity, and Metabolism. doi:x.1111/dom.14649. PMID 35014154. S2CID 245896131.
56. ^ Muntner, P (2015). "Visit-to-visit variability of blood pressure and coronary heart disease, stroke, heart failure and mortality: A cohort study". Register of Internal Medicine. 163 (5): 329–338. doi:ten.7326/M14-2803. PMC5021508. PMID 26215765.
57. ^ Nuyujukian, DS; Koska, J; Bahn, K; Reaven, PD; Zhou, JJ (2020). "Blood pressure variability and risk of middle failure in ACCORD and the VADT". Diabetes Care. 43 (7): 1471–1478. doi:x.2337/dc19-2540. hdl:10150/641980. PMC7305004. PMID 32327422.
58. ^ Nwabuo, CC (2020). "Association Betwixt Visit-to-Visit Blood Pressure Variability in Early Machismo and Myocardial Structure and Function in Later Life". JAMA Cardiology. v (7): 795–801. doi:x.1001/jamacardio.2020.0799. PMC7160747. PMID 32293640.
59. ^ Parati, Gianfranco; Ochoa, Juan E.; Lombardi, Carolina; Bilo, Grzegorz (March 2013). "Assessment and direction of claret-pressure variability". Nature Reviews. Cardiology. 10 (3): 143–155. doi:10.1038/nrcardio.2013.one. ISSN 1759-5010. PMID 23399972. S2CID 22425558.
60. ^ Brickman AM, Reitz C, Luchsinger JA, Manly JJ, Schupf Due north, Muraskin J, DeCarli C, Brown TR, Mayeux R (2010). "Long-term Blood Pressure Fluctuation and Cerebrovascular Illness in an Elderly Cohort". Archives of Neurology. 67 (v): 564–69. doi:ten.1001/archneurol.2010.70. PMC2917204. PMID 20457955.
61. ^ "Normal Blood Pressure level Range Adults". Health and Life. 2010-06-07. Archived from the original on 2016-03-xviii. Retrieved 2010-06-20 .
62. ^ ^{a b} Caro CG (1978). The Mechanics of The Circulation. Oxford [Oxfordshire]: Oxford Academy Press. ISBN978-0-19-263323-ane.
63. ^ Klabunde, Richard (2005). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins. pp. 93–94. ISBN978-0-7817-5030-i.
64. ^ Mahler, F.; Muheim, M. H.; Intaglietta, G.; Bollinger, A.; Anliker, 1000. (1979). "Blood pressure level fluctuations in human nailfold capillaries". The American Periodical of Physiology. 236 (6): H888–893. doi:10.1152/ajpheart.1979.236.half-dozen.H888. ISSN 0002-9513. PMID 443454.
65. ^ Guyton AC (December 1981). "The relationship of cardiac output and arterial pressure control". Circulation. 64 (6): 1079–88. doi:10.1161/01.cir.64.vi.1079. PMID 6794930.
66. ^ Milnor, W. R. (May 1975). "Arterial impedance as ventricular afterload". Circulation Research. 36 (v): 565–570. doi:10.1161/01.res.36.5.565. ISSN 0009-7330. PMID 1122568.
67. ^ Freis ED (April 1976). "Salt, volume and the prevention of hypertension". Circulation. 53 (four): 589–95. doi:x.1161/01.CIR.53.4.589. PMID 767020.
68. ^ Caplea A, Seachrist D, Dunphy G, Ely D (Apr 2001). "Sodium-induced rise in blood pressure is suppressed past androgen receptor blockade". American Periodical of Physiology. Center and Circulatory Physiology. 4. 280 (4): H1793–801. doi:10.1152/ajpheart.2001.280.4.H1793. PMID 11247793. S2CID 12069178.
69. ^ Houston MC (January 1986). "Sodium and hypertension. A review". Athenaeum of Internal Medicine. 1. 146 (1): 179–85. doi:10.1001/archinte.1986.00360130217028. PMID 3510595.
70. ^ Kanbay, Mehmet; Aslan, Gamze; Afsar, Baris; Dagel, Tuncay; Siriopol, Dimitrie; Kuwabara, Masanari; Incir, Said; Camkiran, Volkan; Rodriguez-Iturbe, Bernardo; Lanaspa, Miguel A.; Covic, Adrian (October 2018). "Astute effects of salt on blood force per unit area are mediated by serum osmolality". Journal of Clinical Hypertension (Greenwich, Conn.). 20 (10): 1447–1454. doi:10.1111/jch.13374. ISSN 1751-7176. PMC8030773. PMID 30232829.
71. ^ Titze, Jens; Luft, Friedrich C. (2017). "Speculations on table salt and the genesis of arterial hypertension". Kidney International. 91 (6): 1324–1335. doi:10.1016/j.kint.2017.02.034. ISSN 1523-1755. PMID 28501304.
72. ^ Lee AJ (December 1997). "The function of rheological and haemostatic factors in hypertension". Journal of Homo Hypertension. 11 (12): 767–76. doi:10.1038/sj.jhh.1000556. PMID 9468002.
73. ^ Coffman JD (December 1988). "Pathophysiology of obstructive arterial illness". Herz. 13 (half-dozen): 343–50. PMID 3061915.
74. ^ Korner, P. I.; Angus, J. A. (1992). "Structural determinants of vascular resistance properties in hypertension. Haemodynamic and model analysis". Journal of Vascular Research. 29 (4): 293–312. doi:10.1159/000158945. ISSN 1018-1172. PMID 1391553.
75. ^ Mulvany, Michael J. (2012). "Small artery remodelling in hypertension". Basic & Clinical Pharmacology & Toxicology. 110 (1): 49–55. doi:10.1111/j.1742-7843.2011.00758.x. ISSN 1742-7843. PMID 21733124.
76. ^ de Moraes, Roger; Tibirica, Eduardo (2017). "Early Functional and Structural Microvascular Changes in Hypertension Related to Aging". Current Hypertension Reviews. 13 (i): 24–32. doi:ten.2174/1573402113666170413095508. ISSN 1875-6506. PMID 28412915.
77. ^ Norman, Roger A.; Manning, R. Davis; Scheel, Konrad Westward.; Cowley, Allen West.; Coleman, Thomas G.; Guyton, Arthur C. (1972-05-01). "Arterial force per unit area regulation: Overriding dominance of the kidneys in long-term regulation and in hypertension". The American Journal of Medicine. 52 (five): 584–594. doi:10.1016/0002-9343(72)90050-ii. ISSN 1555-7162. PMID 4337474.
78. ^ Mayet, J; Hughes, A (2003). "Cardiac and vascular pathophysiology in hypertension". Heart. 89 (nine): 1104–9. doi:10.1136/heart.89.9.1104. ISSN 1355-6037. PMC1767863. PMID 12923045.
79. ^ Granger, Joey P.; Hall, John E. (2007). "Role of the Kidney in Hypertension". Comprehensive Hypertension. Elsevier. pp. 241–263. doi:10.1016/b978-0-323-03961-one.50026-x. ISBN978-0-323-03961-1.
80. ^ ^{a b} Klabunde RE (2007). "Cardiovascular Physiology Concepts – Mean Arterial Pressure". Archived from the original on 2009-10-02. Retrieved 2008-09-29 .
81. ^ Bos, Willem J. W.; Verrij, Elisabeth; Vincent, Hieronymus H.; Westerhof, Berend Due east.; Parati, Gianfranco; van Montfrans, Gert A. (April 2007). "How to assess mean blood pressure properly at the brachial artery level". Periodical of Hypertension. 25 (4): 751–755. doi:10.1097/HJH.0b013e32803fb621. ISSN 0263-6352. PMID 17351365. S2CID 23155959.
82. ^ Meaney, E.; Alva, F.; Moguel, R.; Meaney, A.; Alva, J.; Webel, R. (July 2000). "Formula and nomogram for the sphygmomanometric calculation of the mean arterial pressure level". Heart (British Cardiac Society). 84 (one): 64. doi:ten.1136/middle.84.1.64. ISSN 1468-201X. PMC1729401. PMID 10862592.
83. ^ ^{a b} Klabunde RE (2007). "Cardiovascular Physiology Concepts – Pulse Pressure". Archived from the original on 2009-x-18. Retrieved 2008-10-02 .
84. ^ Klabunde, RE (2007). "Cardiovascular Physiology Concepts – Arterial Baroreceptors". Retrieved 2008-09-09 . Archived version 2009-ten-03
85. ^ Forouzanfar M, Dajani HR, Groza VZ, Bolic One thousand, Rajan S, Batkin I (2015-01-01). "Oscillometric Blood Pressure Interpretation: Past, Present, and Futurity". IEEE Reviews in Biomedical Applied science. 8: 44–63. doi:10.1109/RBME.2015.2434215. PMID 25993705. S2CID 8940215.
86. ^ Google patents: Donald Nunn—Apparatus and method for measuring claret pressure level
87. ^ Chandrasekhar A, Kim CS, Naji M, Natarajan K, Hahn JO, Mukkamala R (March 2018). "Smartphone-based claret pressure monitoring via the oscillometric finger-pressing method". Science Translational Medicine. 10 (431): eaap8674. doi:10.1126/scitranslmed.aap8674. PMC6039119. PMID 29515001.
88. ^ Solà, Josep; Delgado-Gonzalo, Ricard (2019). The Handbook of Cuffless Blood Pressure Monitoring. Springer International Publishing. ISBN978-iii-030-24701-0.
89. ^ Sola J, Bertschi G, Krauss J (September 2018). "Measuring Pressure: Introducing oBPM, the Optical Revolution for Blood Pressure level Monitoring". IEEE Pulse. 9 (5): 31–33. doi:ten.1109/MPUL.2018.2856960. PMID 30273141. S2CID 52893219.
90. ^ Foti, Kathryn East; Appel, Lawrence J; Matsushita, Kunihiro; Coresh, Josef; Alexander, G Caleb; Selvin, Elizabeth (2020-xi-27). "Digit Preference in Office Blood Pressure Measurements, United States 2015–2019". American Periodical of Hypertension. 34 (hpaa196): 521–530. doi:ten.1093/ajh/hpaa196. ISSN 0895-7061. PMC8628654. PMID 33246327.
91. ^ Prothero JW (2015-10-22). The design of mammals : a scaling approach. Cambridge. ISBN9781107110472. OCLC 907295832.
92. ^ Brøndum, E.; Hasenkam, J. M.; Secher, N. H.; Bertelsen, K. F.; Grøndahl, C.; Petersen, Chiliad. Thousand.; Buhl, R.; Aalkjær, C.; Baandrup, U.; Nygaard, H.; Smerup, Thousand.; Stegmann, F.; Sloth, E.; Østergaard, K. H.; Nissen, P.; Runge, Grand.; Pitsillides, K.; Wang, T. (2009). "Jugular venous pooling during lowering of the head affects blood pressure level of the anesthetized giraffe". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 297 (4): R1058–R1065. doi:10.1152/ajpregu.90804.2008. ISSN 0363-6119. PMID 19657096.
93. ^ Seymore RS, Lillywhite HB (1976). "Claret pressure in snakes from different habitats". Nature. 264 (5587): 664–6. Bibcode:1976Natur.264..664S. doi:10.1038/264664a0. PMID 1004612. S2CID 555576.
94. ^ Nasoori, Alireza; Taghipour, Ali; Shahbazzadeh, Delavar; Aminirissehei, Abdolhossein; Moghaddam, Sharif (2014). "Heart identify and tail length evaluation in Naja oxiana, Macrovipera lebetina, and Montivipera latifii". Asian Pacific Periodical of Tropical Medicine. vii: S137–S142. doi:10.1016/s1995-7645(14)60220-0. ISSN 1995-7645. PMID 25312108.
95. ^ Seymour, RS (1987). "Scaling of cardiovascular physiology in snakes". American Zoologist. 27 (1): 97–109. doi:x.1093/icb/27.1.97. ISSN 0003-1569.
96. ^ ^{a b} Gross DR (2009). Brute Models in Cardiovascular Research (third ed.). Dordrecht: Springer. p. 5. ISBN9780387959627. OCLC 432709394.
97. ^ Brown S, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, Egner B, Elliott J, Henik R, Labato M, Littman G, Polzin D, Ross L, Snyder P, Stepien R (2007). "Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats". Journal of Veterinary Internal Medicine. 21 (three): 542–58. doi:10.1111/j.1939-1676.2007.tb03005.x. PMID 17552466.
98. ^ Lerman LO, Chade AR, Sica V, Napoli C (September 2005). "Animal models of hypertension: an overview". The Periodical of Laboratory and Clinical Medicine. 146 (3): 160–73. doi:10.1016/j.lab.2005.05.005. PMID 16131455.
99. ^ Acierno, Mark J.; Brown, Scott; Coleman, Amanda E.; Jepson, Rosanne Eastward.; Papich, Mark; Stepien, Rebecca L.; Syme, Harriet M. (2018). "ACVIM consensus argument: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats". Journal of Veterinary Internal Medicine. 32 (6): 1803–1822. doi:x.1111/jvim.15331. ISSN 0891-6640. PMC6271319. PMID 30353952.

Further reading [edit]

• Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, Jones DW, Kurtz T, Sheps SG, Roccella EJ (2005). Subcommittee of Professional person Public Didactics of the American Heart Association Quango on High Blood Pressure Enquiry. "Recommendations for claret pressure measurement in humans and experimental animals: Part 1: blood force per unit area measurement in humans: a statement for professionals from the Subcommittee of Professional person and Public Education of the American Heart Association Quango on Loftier Blood Pressure Inquiry". Hypertension. 45 (5): 142–61. doi:10.1161/01.HYP.0000150859.47929.8e. PMID 15611362.

External links [edit]

• Claret Pressure Association (Britain)
• Virtually High Blood Pressure, American Middle Association
• Control of Blood Pressure, Toronto General Infirmary
• Blood Pressure Chart, Vaughn's Summaries

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Source: https://en.wikipedia.org/wiki/Blood_pressure

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