Blood pressure

For other uses, see Blood pressure (disambiguation).

Blood pressure (BP) is the pressure exerted by circulat-ing blood upon the walls of blood vessels. When usedwithout further specification, “blood pressure” usuallyrefers to the arterial pressure in the systemic circulation.It is usually measured at a person’s upper arm. Bloodpressure is usually expressed in terms of the systolic(maximum) pressure over diastolic (minimum) pressureand is measured in millimeters of mercury (mm Hg). Itis one of the vital signs along with respiratory rate, heartrate, oxygen saturation, and body temperature. Normalresting blood pressure in an adult is approximately 120/80mm Hg.Blood pressure varies depending on situation, activity,and disease states. It is regulated by the nervous andendocrine systems. Blood pressure that is low due to adisease state is called hypotension, and pressure that isconsistently high is hypertension. Both have many causeswhich can range from mild to severe. Both may be ofsudden onset or of long duration. Long term hypertensionis a risk factor for many diseases, including kidney fail-ure, heart disease, and stroke. Long term hypertensionis more common than long term hypotension in West-ern countries. Long term hypertension often goes unde-tected because of infrequent monitoring and the absenceof symptoms.

1 Classification

1.1 Systemic arterial pressure

The table presented here shows the classification of bloodpressure adopted by the American Heart Association foradults who are 18 years and older.[1] It assumes the valuesare a result of averaging resting blood pressure readingsmeasured at two or more visits to the doctor.[3][4]

In the UK, clinic blood pressures are usually categorisedinto three groups; low (90/60 or lower), normal (between90/60 and 139/89), and high (140/90 or higher).[5][6]

Blood pressure fluctuates fromminute to minute and nor-mally shows a circadian rhythm over a 24-hour period,with highest readings in the early morning and eveningsand lowest readings at night.[7][8] Loss of the normal fallin blood pressure at night is associated with a greater fu-ture risk of cardiovascular disease and there is evidencethat night-time blood pressure is a stronger predictor of

cardiovascular events than day-time blood pressure.[9]

Various factors, such as age and sex, influence a person’sblood pressure and variations in it. In children, the normalranges are lower than for adults and depend on height.[10]Reference blood pressure values have been developedfor children in different countries, based on the distribu-tion of blood pressure in children of these countries.[11]As adults age, systolic pressure tends to rise and dias-tolic tends to fall.[12] In the elderly, systolic blood pres-sure tends to be above the normal adult range,[13] thoughtto be largely because of reduced flexibility of the arter-ies. Also, an individual’s blood pressure varies with ex-ercise, emotional reactions, sleep, digestion and time ofday (circadian rhythm).Differences between left and right arm blood pressuremeasurements tend to be random and average to nearlyzero if enough measurements are taken. However, in asmall percentage of cases there is a consistent differencegreater than 10 mm Hg which may need further investi-gation, e.g. for obstructive arterial disease.[14][15]

The risk of cardiovascular disease increases progressivelyabove 115/75 mm Hg.[16] In the past, hypertension wasonly diagnosed if secondary signs of high arterial pres-sure were present, along with a prolonged high systolicpressure reading over several visits. Regarding hypoten-sion, in practice blood pressure is considered too low onlyif noticeable symptoms are present.[2]

Clinical trials demonstrate that people who maintain ar-terial pressures at the low end of these pressure rangeshave much better long term cardiovascular health. Theprincipal medical debate concerns the aggressiveness andrelative value of methods used to lower pressures into thisrange for thosewho do notmaintain such pressure on theirown. Elevations, more commonly seen in older people,though often considered normal, are associated with in-creased morbidity and mortality.

1.2 Mean arterial pressure

The mean arterial pressure (MAP) is the average overa cardiac cycle and is determined by the cardiac output(CO), systemic vascular resistance (SVR), and central ve-nous pressure (CVP),[18]

MAP = (CO · SVR) + CVP.

1

2 2 DISORDERS

MAP can be approximately determined from measure-ments of the systolic pressurePsys and the diastolic pres-surePdias [18]

MAP ≊ Pdias +1

3(Psys − Pdias).

1.3 Pulse pressure

120

80

Curve of the arterial pressure during one cardiac cycle. The clos-ing of the aortic valve causes the notch in the curve.

The pulse pressure is the difference between themeasuredsystolic and diastolic pressures,[19]

Ppulse = Psys − Pdias.

The up and down fluctuation of the arterial pressure re-sults from the pulsatile nature of the cardiac output, i.e.the heartbeat. Pulse pressure is determined by the in-teraction of the stroke volume of the heart, the compli-ance (ability to expand) of the arterial system—largelyattributable to the aorta and large elastic arteries—andthe resistance to flow in the arterial tree. By expandingunder pressure, the aorta absorbs some of the force ofthe blood surge from the heart during a heartbeat. In thisway, the pulse pressure is reduced from what it would beif the aorta were not compliant.[19] The loss of arterialcompliance that occurs with aging explains the elevatedpulse pressures found in elderly patients.

1.4 Systemic venous pressure

Blood pressure generally refers to the arterial pressurein the systemic circulation. However, measurement ofpressures in the venous system and the pulmonary vesselsplays an important role in intensive care medicine but re-quires invasive measurement of pressure using a catheter.Venous pressure is the vascular pressure in a vein or in theatria of the heart. It is much less than arterial pressure,

with common values of 5 mm Hg in the right atrium and8 mm Hg in the left atrium.Variants of venous pressure include:

• Central venous pressure, which is a good approxi-mation of right atrial pressure,[21] which is a majordeterminant of right ventricular end diastolic vol-ume. (However, there can be exceptions in somecases.)[22]

• The jugular venous pressure (JVP) is the indirectlyobserved pressure over the venous system. It canbe useful in the differentiation of different forms ofheart and lung disease.

• The portal venous pressure is the blood pressure inthe portal vein. It is normally 5–10 mm Hg[23]

1.5 Pulmonary pressure

Main article: Pulmonary artery pressure

Normally, the pressure in the pulmonary artery is about15 mm Hg at rest.[24]

Increased blood pressure in the capillaries of the lungcause pulmonary hypertension, leading to interstitialedema if the pressure increases to above 20 mm Hg, andto pulmonary edema at pressures above 25 mm Hg.[25]

2 Disorders

Disorders of blood pressure control include: high bloodpressure, low blood pressure, and blood pressure thatshows excessive or maladaptive fluctuation.

2.1 High

Main article: HypertensionArterial hypertension can be an indicator of other prob-lems and may have long-term adverse effects. Sometimesit can be an acute problem, for example hypertensiveemergency.Levels of arterial pressure put mechanical stress on thearterial walls. Higher pressures increase heart workloadand progression of unhealthy tissue growth (atheroma)that develops within the walls of arteries. The higherthe pressure, the more stress that is present and the moreatheroma tend to progress and the heart muscle tends tothicken, enlarge and become weaker over time.Persistent hypertension is one of the risk factorsfor strokes, heart attacks, heart failure and arterialaneurysms, and is the leading cause of chronic kidney fail-ure. Even moderate elevation of arterial pressure leadsto shortened life expectancy. At severely high pressures,

2.3 Fluctuating blood pressure 3

Main complications of persistent

High blood pressure

Kidneys: - Hypertensive nephropathy: chronic renal failure

Blood: - Elevated sugar levels

Retina of eye: - Hypertensive retinopathy

Heart: - Myocardial infarction (heart attack) - Hypertensive cardiomyopathy: heart failure

Brain: - Cerebrovascular accident (strokes) - Hypertensive encephalopathy: -confusion -headache -convulsion

Overview of main complications of persistent high blood pres-sure.

mean arterial pressures 50% or more above average, aperson can expect to live no more than a few years unlessappropriately treated.[26]

In the past, most attention was paid to diastolic pressure;but nowadays it is recognised that both high systolic pres-sure and high pulse pressure (the numerical differencebetween systolic and diastolic pressures) are also risk fac-tors. In some cases, it appears that a decrease in excessivediastolic pressure can actually increase risk, due probablyto the increased difference between systolic and diastolicpressures (see the article on pulse pressure). If systolicblood pressure is elevated (>140) with a normal diastolicblood pressure (<90), it is called “isolated systolic hyper-tension” and may present a health concern.[27][28]

For those with heart valve regurgitation, a change in itsseverity may be associated with a change in diastolic pres-sure. In a study of people with heart valve regurgitationthat compared measurements 2 weeks apart for each per-son, there was an increased severity of aortic and mitralregurgitation when diastolic blood pressure increased,whereas when diastolic blood pressure decreased, therewas a decreased severity.[29]

2.2 Low

Main article: Hypotension

Blood pressure that is too low is known as hypotension.Hypotension is a medical concern if it causes signs orsymptoms, such as dizziness, fainting, or in extremecases, shock.[4]

When arterial pressure and blood flow decrease beyond acertain point, the perfusion of the brain becomes criticallydecreased (i.e., the blood supply is not sufficient), causinglightheadedness, dizziness, weakness or fainting.[30]

Sometimes the arterial pressure drops significantly whena patient stands up from sitting. This is known asorthostatic hypotension (postural hypotension); gravityreduces the rate of blood return from the body veins be-low the heart back to the heart, thus reducing stroke vol-ume and cardiac output.When people are healthy, the veins below their heartquickly constrict and the heart rate increases to minimizeand compensate for the gravity effect. This is carried outinvoluntarily by the autonomic nervous system. The sys-tem usually requires a few seconds to fully adjust and ifthe compensations are too slow or inadequate, the indi-vidual will suffer reduced blood flow to the brain, dizzi-ness and potential blackout. Increases in G-loading, suchas routinely experienced by aerobatic or combat pilots'pulling Gs', greatly increases this effect. Repositioningthe body perpendicular to gravity largely eliminates theproblem.Other causes of low arterial pressure include:

• Sepsis

• Hemorrhage – blood loss

• Toxins including toxic doses of blood pressuremedicine

• Hormonal abnormalities, such as Addison’s disease

• Eating disorders, particularly anorexia nervosa andbulimia

Shock is a complex condition which leads to criticallydecreased perfusion. The usual mechanisms are loss ofblood volume, pooling of blood within the veins reduc-ing adequate return to the heart and/or low effective heartpumping. Low arterial pressure, especially low pulsepressure, is a sign of shock and contributes to and reflectsdecreased perfusion.If there is a significant difference in the pressure fromone arm to the other, that may indicate a narrowing(for example, due to aortic coarctation, aortic dissection,thrombosis or embolism) of an artery.

2.3 Fluctuating blood pressure

Normal fluctuation in blood pressure is adaptive and nec-essary. Fluctuations in pressure that are significantlygreater than the norm are associated with greater whitematter hyperintensity, a finding consistent with reducedlocal cerebral blood flow[31] and a heightened risk ofcerebrovascular disease.[32] Within both high and lowblood pressure groups, a greater degree of fluctuationwas found to correlate with an increase in cerebrovascu-lar disease compared to those with less variability, sug-gesting the consideration of the clinical management ofblood pressure fluctuations, even among normotensive

4 3 PHYSIOLOGY

older adults.[32] Older individuals and those who had re-ceived blood pressure medications weremore likely to ex-hibit larger fluctuations in pressure.[32]

3 Physiology

Systole on the left and diastole on the right

During each heartbeat, blood pressure varies betweena maximum (systolic) and a minimum (diastolic)pressure.[33] The blood pressure in the circulation isprincipally due to the pumping action of the heart.[34]Differences in mean blood pressure are responsible forblood flow from one location to another in the circu-lation. The rate of mean blood flow depends on bothblood pressure and the resistance to flow presented bythe blood vessels. Mean blood pressure decreases asthe circulating blood moves away from the heart througharteries 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 arter-ies and arterioles.[35] Gravity affects blood pressure viahydrostatic forces (e.g., during standing), and valves inveins, breathing, and pumping from contraction of skele-tal muscles also influence blood pressure in veins.[34]

3.1 Hemodynamics

Main article: Hemodynamics

There are many physical factors that influence arterialpressure. Each of these may in turn be influenced byphysiological factors, such as: diet, exercise, disease,drugs or alcohol, stress, and obesity.[36]

Some physical factors are:

• Volume of fluid or blood volume, the amount ofblood that is present in the body. The more bloodpresent in the body, the higher the rate of blood re-turn to the heart and the resulting cardiac output.

There is some relationship between dietary salt in-take and increased blood volume, potentially result-ing in higher arterial pressure, though this varieswith the individual and is highly dependent on au-tonomic nervous system response and the renin–angiotensin system.[37][38][39]

• Resistance. In the circulatory system, this is the re-sistance of the blood vessels. The higher the resis-tance, the higher the arterial pressure upstream fromthe resistance to blood flow. Resistance is relatedto vessel radius (the larger the radius, the lower theresistance), vessel length (the longer the vessel, thehigher the resistance), blood viscosity, as well as thesmoothness of the blood vessel walls. Smoothnessis reduced by the buildup of fatty deposits on the ar-terial walls. Substances called vasoconstrictors canreduce the size of blood vessels, thereby increasingblood pressure. Vasodilators (such as nitroglycerin)increase the size of blood vessels, thereby decreas-ing arterial pressure. Resistance, and its relationto volumetric flow rate (Q) and pressure differencebetween the two ends of a vessel are described byPoiseuille’s Law.

• Viscosity, or thickness of the fluid. If the blood getsthicker, the result is an increase in arterial pressure.Certain medical conditions can change the viscosityof the blood. For instance, anemia (low red bloodcell concentration), reduces viscosity, whereas in-creased red blood cell concentration increases vis-cosity. It had been thought that aspirin and re-lated "blood thinner" drugs decreased the viscosityof blood, but instead studies found[40] that they actby reducing the tendency of the blood to clot.

In practice, each individual’s autonomic nervous systemresponds to and regulates all these interacting factors sothat, although the above issues are important, the ac-tual arterial pressure response of a given individual varieswidely because of both split-second and slow-moving re-sponses of the nervous system and end organs. These re-sponses are very effective in changing the variables andresulting blood pressure from moment to moment.Moreover, blood pressure is the result of cardiac out-put increased by peripheral resistance: blood pressure =cardiac output X peripheral resistance. As a result, an ab-normal change in blood pressure is often an indication ofa problem affecting the heart’s output, the blood vessels’resistance, or both. Thus, knowing the patient’s bloodpressure is critical to assess any pathology related to out-put and resistance.

3.2 Regulation

The endogenous regulation of arterial pressure is notcompletely understood, but the following mechanisms ofregulating arterial pressure have been well-characterized:

5

• Baroreceptor reflex: Baroreceptors in the high pres-sure receptor zones detect changes in arterial pres-sure. These baroreceptors send signals ultimatelyto the medulla of the brain stem, specifically to therostral ventrolateral medulla (RVLM). Themedulla,by way of the autonomic nervous system, adjusts themean arterial pressure by altering both the force andspeed of the heart’s contractions, as well as the totalperipheral resistance. The most important arterialbaroreceptors are located in the left and right carotidsinuses and in the aortic arch.[41]

• Renin-angiotensin system (RAS): This system isgenerally known for its long-term adjustment ofarterial pressure. This system allows the kidneyto compensate for loss in blood volume or dropsin arterial pressure by activating an endogenousvasoconstrictor known as angiotensin II.

• Aldosterone release: This steroid hormone is re-leased from the adrenal cortex in response to an-giotensin II or high serum potassium levels. Aldos-terone stimulates sodium retention and potassiumexcretion by the kidneys. Since sodium is the mainion that determines the amount of fluid in the bloodvessels by osmosis, aldosterone will increase fluid re-tention, and indirectly, arterial pressure.

• Baroreceptors in low pressure receptor zones(mainly in the venae cavae and the pulmonaryveins, and in the atria) result in feedback byregulating the secretion of antidiuretic hormone(ADH/Vasopressin), renin and aldosterone. The re-sultant increase in blood volume results in an in-creased cardiac output by the Frank–Starling law ofthe heart, in turn increasing arterial blood pressure.

These different mechanisms are not necessarily indepen-dent of each other, as indicated by the link between theRAS and aldosterone release. When blood pressure fallsmany physiological cascades commence in order to returnthe blood pressure to a more appropriate level.

1. The blood pressure fall is detected by a decrease inblood flow and thus a decrease in Glomerular filtra-tion rate (GFR).

2. Decrease in GFR is sensed as a decrease in Na+ lev-els by the macula densa.

3. The macula densa cause an increase in Na+ reab-sorption, which causes water to follow in via osmosisand leads to an ultimate increase in plasma volume.Further, the macula densa releases adenosine whichcauses constriction of the afferent arterioles.

4. At the same time, the juxtaglomerular cells sense thedecrease in blood pressure and release renin.

5. Renin converts angiotensinogen (inactive form) toangiotensin I (active form).

6. Angiotensin I flows in the bloodstream untilit reaches the capillaries of the lungs whereangiotensin converting enzyme (ACE) acts on it toconvert it into angiotensin II.

7. Angiotensin II is a vasoconstrictor which will in-crease bloodflow to the heart and subsequently thepreload, ultimately increasing the cardiac output.

8. Angiotensin II also causes an increase in the releaseof aldosterone from the adrenal glands.

9. Aldosterone further increases the Na+ and H2O re-absorption in the distal convoluted tubule of thenephron.

Currently, the RAS is targeted pharmacologically byACE inhibitors and angiotensin II receptor antago-nists. The aldosterone system is directly targeted byspironolactone, an aldosterone antagonist. The fluid re-tention may be targeted by diuretics; the antihyperten-sive effect of diuretics is due to its effect on blood vol-ume. Generally, the baroreceptor reflex is not targeted inhypertension because if blocked, individuals may sufferfrom orthostatic hypotension and fainting.

4 Measurement

A medical student checking blood pressure using a sphygmo-manometer and stethoscope.

Arterial pressure is most commonly measured via asphygmomanometer, which historically used the heightof a column of mercury to reflect the circulatingpressure.[42] Blood pressure values are generally reportedin millimetres of mercury (mm Hg), though aneroid andelectronic devices do not contain mercury.For each heartbeat, blood pressure varies between systolicand diastolic pressures. Systolic pressure is peak pressurein the arteries, which occurs near the end of the cardiaccycle when the ventricles are contracting. Diastolic pres-sure is minimum pressure in the arteries, which occurs

6 4 MEASUREMENT

Right position for taking blood pressure

near the beginning of the cardiac cycle when the ventri-cles are filled with blood. An example of normal mea-sured values for a resting, healthy adult human is 120 mmHg systolic and 80 mm Hg diastolic (written as 120/80mm Hg, and spoken as “one-twenty over eighty”).Systolic and diastolic arterial blood pressures are notstatic but undergo natural variations from one heartbeat toanother and throughout the day (in a circadian rhythm).They also change in response to stress, nutritional factors,drugs, disease, exercise, and momentarily from standingup. Sometimes the variations are large. Hypertensionrefers to arterial pressure being abnormally high, as op-posed to hypotension, when it is abnormally low. Alongwith body temperature, respiratory rate, and pulse rate,blood pressure is one of the four main vital signs rou-tinely monitored by medical professionals and healthcareproviders.[43]

Measuring pressure invasively, by penetrating the arterialwall to take the measurement, is much less common andusually restricted to a hospital setting.

4.1 Noninvasive

The noninvasive auscultatory and oscillometric measure-ments are simpler and quicker than invasive measure-ments, require less expertise, have virtually no compli-cations, are less unpleasant and less painful for the pa-tient. However, noninvasive methods may yield some-what lower accuracy and small systematic differences innumerical results. Noninvasive measurement methodsare more commonly used for routine examinations andmonitoring.

4.1.1 Palpation

A minimum systolic value can be roughly estimated bypalpation, most often used in emergency situations, butshould be usedwith caution.[44] It has been estimated that,using 50% percentiles, carotid, femoral and radial pulsesare present in patients with a systolic blood pressure >70 mm Hg, carotid and femoral pulses alone in patientswith systolic blood pressure of > 50 mm Hg, and only a

carotid pulse in patients with a systolic blood pressure of> 40 mm Hg.[44]

A more accurate value of systolic blood pressure can beobtained with a sphygmomanometer and palpating the ra-dial pulse.[45] The diastolic blood pressure cannot be esti-mated by this method. The American Heart Associationrecommends that palpation be used to get an estimate be-fore using the auscultatory method.

4.1.2 Auscultatory

Auscultatory method aneroid sphygmomanometer with stetho-scope

Mercury manometer

The auscultatory method (from the Latin word for “listen-ing”) uses a stethoscope and a sphygmomanometer. Thiscomprises an inflatable (Riva-Rocci) cuff placed aroundthe upper arm at roughly the same vertical height as theheart, attached to a mercury or aneroid manometer. Themercury manometer, considered the gold standard, mea-sures the height of a column of mercury, giving an abso-

4.1 Noninvasive 7

lute result without need for calibration and, consequently,not subject to the errors and drift of calibration which af-fect other methods. The use of mercury manometers isoften required in clinical trials and for the clinical mea-surement of hypertension in high-risk patients, such aspregnant women.A cuff of appropriate size[46] is fitted smoothly and alsosnugly, then inflated manually by repeatedly squeezing arubber bulb until the artery is completely occluded. It isimportant that the cuff size is correct: undersized cuffsrecord too high a pressure; oversized cuffs may yield toolow a pressure.[47] Usually three or four cuff sizes shouldbe available to allow measurements in arms of differ-ent size.[47] Listening with the stethoscope to the brachialartery at the antecubital area of the elbow, the examinerslowly releases the pressure in the cuff. When blood juststarts to flow in the artery, the turbulent flow creates a“whooshing” or pounding (first Korotkoff sound). Thepressure at which this sound is first heard is the systolicblood pressure. The cuff pressure is further released un-til no sound can be heard (fifth Korotkoff sound), at thediastolic arterial pressure.The auscultatory method is the predominant method ofclinical measurement.[48]

4.1.3 Oscillometric

The oscillometric method was first demonstrated in 1876and involves the observation of oscillations in the sphyg-momanometer cuff pressure[49] which are caused by theoscillations of blood flow, i.e., the pulse.[50] The elec-tronic version of this method is sometimes used in long-term measurements and general practice. It uses a sphyg-momanometer cuff, like the auscultatory method, butwith an electronic pressure sensor (transducer) to observecuff pressure oscillations, electronics to automatically in-terpret them, and automatic inflation and deflation of thecuff. The pressure sensor should be calibrated periodi-cally to maintain accuracy.Oscillometric measurement requires less skill than theauscultatory technique and may be suitable for use by un-trained staff and for automated patient home monitoring.As for the auscultatory technique it is important that thecuff size is appropriate for the arm. There are some singlecuff devices that may be used for arms of differing sizes,although experience with these is limited.[47]

The cuff is inflated to a pressure initially in excess of thesystolic arterial pressure and then reduced to below dias-tolic pressure over a period of about 30 seconds. Whenblood flow is nil (cuff pressure exceeding systolic pres-sure) or unimpeded (cuff pressure below diastolic pres-sure), cuff pressure will be essentially constant. Whenblood flow is present, but restricted, the cuff pressure,which is monitored by the pressure sensor, will vary peri-odically in synchrony with the cyclic expansion and con-traction of the brachial artery, i.e., it will oscillate.

Over the deflation period, the recorded pressure wave-form forms a signal known as the cuff deflation curve.A bandpass filter is utilized to extract the oscillometricpulses from the cuff deflation curve. Over the deflationperiod, the extracted oscillometric pulses form a signalknown as the oscillometric waveform (OMW). The am-plitude of the oscillometric pulses increases to a maxi-mum and then decreases with further deflation. A varietyof analysis algorithms can be employed in order to esti-mate the systolic, diastolic, and mean arterial pressure.Oscillometric monitors may produce inaccurate readingsin patients with heart and circulation problems, which in-clude arteriosclerosis, arrhythmia, preeclampsia, pulsusalternans, and pulsus paradoxus.[47][51]

In practice the different methods do not give identical re-sults; an algorithm and experimentally obtained coeffi-cients are used to adjust the oscillometric results to givereadings which match the auscultatory results as well aspossible. Some equipment uses computer-aided analy-sis of the instantaneous arterial pressure waveform to de-termine the systolic, mean, and diastolic points. Sincemany oscillometric devices have not been validated, cau-tion must be given as most are not suitable in clinical andacute care settings.Recently, several coefficient-free oscillometric algo-rithms have developed for estimation of blood pressure.These algorithms do not rely on experimentally obtainedcoefficients and have been shown to provide more accu-rate and robust estimation of blood pressure. These al-gorithms are based on finding the fundamental relation-ship between the oscillometric waveform and the BP us-ing modeling [52][53] and learning [54] approaches.The term NIBP, for non-invasive blood pressure, is oftenused to describe oscillometric monitoring equipment.

4.1.4 Continuous noninvasive techniques (CNAP)

Continuous Noninvasive Arterial Pressure (CNAP) is themethod of measuring arterial blood pressure in real-timewithout any interruptions and without cannulating the hu-man body. CNAP combines the advantages of the follow-ing two clinical “gold standards”: it measures blood pres-sure continuously in real-time like the invasive arterialcatheter system and it is noninvasive like the standard up-per arm sphygmomanometer. Latest developments in thisfield show promising results in terms of accuracy, ease ofuse and clinical acceptance.

4.1.5 Non-occlusive techniques: The Pulse WaveVelocity (PWV) principle

Since the 1990s a novel family of techniques based onthe so-called pulse wave velocity (PWV) principle havebeen developed. These techniques rely on the fact thatthe velocity at which an arterial pressure pulse travels

8 4 MEASUREMENT

along the arterial tree depends, among others, on theunderlying blood pressure.[55] Accordingly, after a cali-bration maneuver, these techniques provide indirect esti-mates of blood pressure by translating PWV values intoblood pressure values.[56]

The main advantage of these techniques is that it is pos-sible to measure PWV values of a subject continuously(beat-by-beat), without medical supervision, and withoutthe need of inflating brachial cuffs. PWV-based tech-niques are still in the research domain and are not adaptedto clinical settings.

4.1.6 Ambulatory and home monitoring

Ambulatory blood pressure devices take readings reg-ularly (e.g. every half hour throughout the day andnight). They have been used to exclude measurementproblems like white-coat hypertension and provide morereliable estimates of usual blood pressure and cardiovas-cular risk. Blood pressure readings outside of a clini-cal setting are usually slightly lower in the majority ofpeople; however studies that quantified the risks fromhypertension and the benefits of lowering blood pres-sure have mostly been based on readings in a clinicalenvironment. Use of ambulatory measurements is notwidespread but guidelines developed by the UK NationalInstitute for Health and Care Excellence and the BritishHypertension Society recommended that 24-hour ambu-latory blood pressure monitoring should be used for diag-nosis of hypertension.[57] Health economic analysis sug-gested that this approach would be cost effective com-pared with repeated clinic measurements.[58]

Home monitoring is a cheap and simple alternative toambulatory blood pressure monitoring, although it doesnot usually allow assessment of blood pressure duringsleepwhichmay be a disadvantage.[59][60] Automatic self-contained blood pressure monitors are available at rea-sonable prices, however measurements may not be accu-rate in patients with atrial fibrillation or other arrhyth-mias such as frequent ectopic beats.[59][60] Home mon-itoring may be used to improve hypertension manage-ment and to monitor the effects of lifestyle changes andmedication related to blood pressure.[3] Compared to am-bulatory blood pressure measurements, home monitor-ing has been found to be an effective and lower costalternative,[59][61][62] but ambulatory monitoring is moreaccurate than both clinic and home monitoring in diag-nosing hypertension.When measuring blood pressure in the home, an accu-rate reading requires that one not drink coffee, smokecigarettes, or engage in strenuous exercise for 30 minutesbefore taking the reading. A full bladdermay have a smalleffect on blood pressure readings; if the urge to urinatearises, one should do so before the reading. For 5 minutesbefore the reading, one should sit upright in a chair withone’s feet flat on the floor and with limbs uncrossed. The

blood pressure cuff should always be against bare skin, asreadings taken over a shirt sleeve are less accurate. Thesame arm should be used for all measurements. Duringthe reading, the arm that is used should be relaxed andkept at heart level, for example by resting it on a table.[63]

Since blood pressure varies throughout the day, homemeasurements should be taken at the same time of day.A Joint Scientific Statement From the American HeartAssociation, American Society of Hypertension, andPreventive Cardiovascular Nurses Association on homemonitoring in 2008[60] recommended that 2 to 3 readingsshould be taken in the morning (after awakening, beforewashing/dressing, taking breakfast/drink or taking med-ication) and another 2 to 3 readings at night, each dayover a period of 1 week. It was also recommended thatthe readings from the first day should be discarded andthat a total of ≥12 readings (i.e. at least two readings perday for the remaining 6 days of the week) should be usedfor making clinical decisions.

4.1.7 White-coat hypertension

For some patients, blood pressure measurements taken ina doctor’s office may not correctly characterize their typ-ical blood pressure.[64] In up to 25% of patients, the of-fice measurement is higher than their typical blood pres-sure. This type of error is called white-coat hypertension(WCH) and can result from anxiety related to an exam-ination by a health care professional.[65] White coat hy-pertension can also occur because, in a clinical setting,patients are seldom given the opportunity to rest for fiveminutes before blood pressure readings are taken. Themisdiagnosis of hypertension for these patients can re-sult in needless and possibly harmful medication. WCHcan be reduced (but not eliminated) with automated bloodpressure measurements over 15 to 20 minutes in a quietpart of the office or clinic.[66] In some cases a lower bloodpressure reading occurs at the doctor’s - this has beentermed 'masked hypertension'.[67]

• Blood Pressure - Take another person.

• Blood Pressure - Take your own.

4.2 Invasive

Arterial blood pressure (BP) is most accurately measuredinvasively through an arterial line. Invasive arterial pres-sure measurement with intravascular cannulae involvesdirect measurement of arterial pressure by placing a can-nula needle in an artery (usually radial, femoral, dorsalispedis or brachial).The cannula must be connected to a sterile, fluid-filledsystem, which is connected to an electronic pressuretransducer. The advantage of this system is that pressureis constantly monitored beat-by-beat, and a waveform (a

9

graph of pressure against time) can be displayed. This in-vasive technique is regularly employed in human and vet-erinary intensive care medicine, anesthesiology, and forresearch purposes.Cannulation for invasive vascular pressure monitoringis infrequently associated with complications such asthrombosis, infection, and bleeding. Patients with inva-sive arterial monitoring require very close supervision, asthere is a danger of severe bleeding if the line becomesdisconnected. It is generally reserved for patients whererapid variations in arterial pressure are anticipated.Invasive vascular pressure monitors are pressure monitor-ing systems designed to acquire pressure information fordisplay and processing. There are a variety of invasivevascular pressure monitors for trauma, critical care, andoperating room applications. These include single pres-sure, dual pressure, and multi-parameter (i.e. pressure/ temperature). The monitors can be used for measure-ment and follow-up of arterial, central venous, pulmonaryarterial, left atrial, right atrial, femoral arterial, umbilicalvenous, umbilical arterial, and intracranial pressures.

5 Fetal blood pressure

Further information: Fetal circulation § Blood pressure

In pregnancy, it is the fetal heart and not the mother’sheart that builds up the fetal blood pressure to drive itsblood through the fetal circulation.The blood pressure in the fetal aorta is approximately 30mmHg at 20 weeks of gestation, and increases to approx-imately 45 mm Hg at 40 weeks of gestation.[68]The average blood pressure for full-term infants:Systolic 65–95 mm HgDiastolic 30–60 mm Hg[69]

6 References

[1] “Understanding blood pressure readings”. AmericanHeart Association. 11 January 2011. Retrieved 30 March2011.

[2] Mayo Clinic staff (2009-05-23). “Low blood pressure(hypotension) — Causes”. MayoClinic.com. Mayo Foun-dation for Medical Education and Research. Retrieved2010-10-19.

[3] Chobanian AV, Bakris GL, Black HR, CushmanWC, Green LA, Izzo JL, Jones DW, Materson BJ,Oparil S, Wright JT, Roccella EJ (December 2003).“Seventh report of the Joint National Committee onPrevention, Detection, Evaluation, and Treatment ofHigh Blood Pressure”. Hypertension 42 (6): 1206–52.doi:10.1161/01.HYP.0000107251.49515.c2. PMID14656957.

[4] “Diseases and conditions index – hypotension”. NationalHeart Lung and Blood Institute. September 2008. Re-trieved 2008-09-16.

[5] NHS choices: What is blood pressure? Retrieved 2012-03-27

[6] NHS choices: High blood pressure (hypertension) Re-trieved 2012-03-27

[7] Table: Comparison of ambulatory blood pressures andurinary norepinephrine and epinephrine excretion mea-sured at work, home, and during sleep between European–American (n = 110) and African–American (n = 51)women

[8] van Berge-Landry HM, Bovbjerg DH, James GD;Bovbjerg; James (October 2008). “Relationshipbetween waking-sleep blood pressure and cate-cholamine changes in African-American and European-American women”. Blood Press Monit 13 (5): 257–62.doi:10.1097/MBP.0b013e3283078f45. PMC 2655229.PMID 18799950. NIHMS90092.

[9] Hansen, T. W.; Li, Y.; Boggia, J.; Thijs, L.; Richart,T.; Staessen, J. A. (2010). “Predictive Role of theNighttime Blood Pressure”. Hypertension 57 (1): 3–10.doi:10.1161/HYPERTENSIONAHA.109.133900. ISSN0194-911X.

[10] National Heart, Lung and Blood Institute. “Blood pres-sure tables for children and adolescents”. (Note that themedian blood pressure is given by the 50th percentile andhypertension is defined by the 95th percentile for a givenage, height, and gender.)

[11] Chiolero A (Mar 2014). “The quest for blood pressurereference values in children.”. Journal of Hypertension32 (3): 477–9. doi:10.1097/HJH.0000000000000109.PMID 24477093.

[12] (Pickering et al. 2005, p. 145) See Isolated Systolic Hy-pertension.

[13] "...more than half of all Americans aged 65 or older havehypertension.” (Pickering et al. 2005, p. 144)

[14] Eguchi K, Yacoub M, Jhalani J, Gerin W, SchwartzJE, Pickering TG (February 2007). “Consistencyof blood pressure differences between the left andright arms”. Arch Intern Med 167 (4): 388–93.doi:10.1001/archinte.167.4.388. PMID 17325301.

[15] Agarwal R, Bunaye Z, Bekele DM (March 2008).“Prognostic significance of between-arm blood pres-sure differences”. Hypertension 51 (3): 657–62.doi:10.1161/HYPERTENSIONAHA.107.104943.PMID 18212263.

[16] Appel LJ, Brands MW, Daniels SR, Karanja N, Elmer PJ,Sacks FM (February 2006). “Dietary approaches to pre-vent and treat hypertension: a scientific statement fromthe American Heart Association”. Hypertension 47 (2):296–308. doi:10.1161/01.HYP.0000202568.01167.B6.PMID 16434724.

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[48] (Pickering et al. 2005, p. 146) See Blood Pressure Mea-surement Methods.

[49] (Pickering et al. 2005, p. 147) See The OscillometricTechnique.

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JM, Manolis AJ, Nilsson PM, O'Brien E, Ponikowski P,Redon J, Ruschitzka F, Tamargo J, van Zwieten P, Vi-igimaa M, Waeber B, Williams B, Zamorano JL (June2007). “2007 Guidelines for the management of ar-terial hypertension: The Task Force for the Manage-ment of Arterial Hypertension of the European Societyof Hypertension (ESH) and of the European Society ofCardiology (ESC)". Eur Heart J 28 (12): 1462–536.doi:10.1093/eurheartj/ehm236. PMID 17562668.

[60] Pickering TG, Miller NH, Ogedegbe G, Krakoff LR,Artinian NT, Goff D (2008). “Call to action onuse and reimbursement for home blood pressure mon-itoring: executive summary: a joint scientific state-ment from the American Heart Association, Ameri-can Society Of Hypertension, and Preventive Cardio-vascular Nurses Association”. Hypertension 52 (1):1–9. doi:10.1161/HYPERTENSIONAHA.107.189011.PMID 18497371.

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[62] Shimbo D, Pickering TG, Spruill TM, Abraham D,Schwartz JE, Gerin W (2007). “The Relative Utilityof Home, Ambulatory, and Office Blood Pressures inthe Prediction of End-Organ Damage”. Am J Hypertens20 (5): 476–82. doi:10.1016/j.amjhyper.2006.12.011.PMC 1931502. PMID 17485006. Archived from theoriginal on May 25, 2014.

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[66] (Pickering et al. 2005, p. 145) SeeWhite Coat Hyperten-sion or Isolated Office Hypertension.

[67] (Pickering et al. 2005, p. 146) See Masked Hypertensionor Isolated Ambulatory Hypertension.

[68] Struijk PC, Mathews VJ, Loupas T, Stewart PA, ClarkEB, Steegers EA, Wladimiroff JW; Mathews; Loupas;Stewart; Clark; Steegers; Wladimiroff (October 2008).“Blood pressure estimation in the human fetal descend-ing aorta”. Ultrasound Obstet Gynecol 32 (5): 673–81.doi:10.1002/uog.6137. PMID 18816497.

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12 8 EXTERNAL LINKS

7 Further reading• Pickering TG, Hall JE, Appel LJ, Falkner BE,Graves J, Hill MN, Jones DW, Kurtz T, ShepsSG, Roccella EJ; Hall; Appel; et al. (2005).“Recommendations for blood pressure measure-ment in humans and experimental animals: Part 1:blood pressure measurement in humans: a state-ment for professionals from the Subcommittee ofProfessional and Public Education of the Amer-ican Heart Association Council on High BloodPressure Research”. Hypertension 45 (5): 142–61. doi:10.1161/01.HYP.0000150859.47929.8e.PMID 15611362. Retrieved 2009-10-01.

8 External links• Blood Pressure Association (UK)

• About High Blood Pressure, American Heart Asso-ciation

• Control of Blood Pressure, Toronto General Hospi-tal

• Blood Pressure Chart, Vaughn’s Summaries

13

9 Text and image sources, contributors, and licenses

9.1 Text• Blood pressure Source: https://en.wikipedia.org/wiki/Blood_pressure?oldid=709644159 Contributors: AxelBoldt, Dreamyshade, Tarquin,

Alex.tan, Andre Engels, Fnielsen, Heron, Ryguasu, Someone else, Patrick, Dominus, Gabbe, Ixfd64, Kosebamse, Ronz, Docu, Statkit1,Darkwind, LittleDan, Lupinoid, Kylet, AugPi, Rob Hooft, Emperorbma, Bemoeial, Selket, Tpbradbury, Toreau, Renato Caniatti~enwiki,Jeffq, Robbot, Fredrik, Romanm, Hadal, Wikibot, Diberri, Rsduhamel, Sho Uemura, Giftlite, Nmg20, Ksheka, Peruvianllama, Gro-Tsen,Bensaccount, Jfdwolff, Isidore, Chowbok, Pgan002, HorsePunchKid, Doops, Rdsmith4, Icairns, JulieADriver, Joyous!, Sonett72, Fabrí-cio Kury, Eliazar, M1ss1ontomars2k4, N-k, Mike Rosoft, Rich Farmbrough, Westendgirl, MAlvis, Tsujigiri~enwiki, Bender235, RobertP. O'Shea, Lankiveil, Shanes, RoyBoy, Bobo192, Smalljim, Keron Cyst, Davidruben, Wisdom89, PeteThePill, Arcadian, Phansen, Ra-jah, Haham hanuka, Mpulier, Jonathunder, Hooperbloob, Nsaa, Jjron, Tom Yates, Jumbuck, Yoweigh, Gary, Uncle Bill, Wouterstomp,Ekko, Water Bottle, Stack, David Henderson, Wtshymanski, Knowledge Seeker, Cburnett, Harej, Gene Nygaard, Stephen, Jackhynes,Lkinkade, Woohookitty, Gccwang, TigerShark, BillC, Holdspa, Pol098, WadeSimMiser, MONGO, Julo, BlaiseFEgan, Macaddct1984,Tkessler, Wayward, Prashanthns, Dovid, Palica, RichardWeiss, FreplySpang, Sjakkalle, Rjwilmsi, Vary, Hiberniantears, Bruce1ee, SMC,ElKevbo, Brighterorange, Bensin, DoubleBlue, Sango123, Yamamoto Ichiro, RexNL, RobyWayne, BrendanMoody, Jeremygbyrne, Steven-fruitsmaak, King of Hearts, Colenso, Mfranck, Nastajus, The Rambling Man, YurikBot, Wavelength, TexasAndroid, Phil Wardle, An-gus Lepper, Todd Vierling, Jimp, Charles Gaudette, Polacrilex, Gravecat, Grubber, Nfu-peng, Okedem, Eleassar, Pseudomonas, Wimt,Sesquiannual, Brandon, E rulez, Moe Epsilon, Wap, Nick C, Supten, Natkeeran, BOT-Superzerocool, Zephalis, DeadEyeArrow, DRosen-bach, Phgao, Zzuuzz, Closedmouth, E Wing, Rlove, Jecowa, CWenger, Jacqui M, Thomas Blomberg, Jeff Silvers, DVD R W, CIreland,Tom Morris, AndrewWTaylor, Luk, Crystallina, SmackBot, Justinstroud, Prodego, Olorin28, Kimon, Delldot, Edgar181, Eiler7, Gilliam,Ohnoitsjamie, Skizzik, SportWagon, Master Jay, Bluebot, RDBrown, Algumacoisaqq~enwiki, Thumperward, Kilbosh, Roscelese, Deli nk,Uthbrian, Sadads, Jfsamper, Darth Panda, Enigma55, Can't sleep, clown will eat me, Jorvik, Frap, KaiserbBot, Snowmanradio, Yidish-eryid, Addshore, Celarnor, Dreadstar, Sljaxon, Puffball, DMacks, Just plain Bill, Daniel.Cardenas, Kukini, Lexicontra, John, Mike1901,Dog Eat Dog World, JohnCub, Piplicus, Osbus, Jkgray, MarkSutton, Uknowme imbehindu, Utopianheaven, Beetstra, Kyoko, Larrymcp,Spiff666, TastyPoutine, DanConnolly, Hu12, Dan Gluck, Nehrams2020, Iridescent, Dionysia, JHP, J Di, CapitalR, Tawkerbot2, Dlo-hcierekim, Emote, JForget, Ale jrb, Myadav, Van helsing, Scohoust, Xlegiofalco, 5-HT8, Zureks, FlyingToaster, AndrewHowse, Abeg92,Founders4, Gogo Dodo, Anthonyhcole, JuliaHavey, UISKuwait, LordRae, Roberta F., Surturz, Kansas Sam, TSoprano, Biyer, JamesAM,Thickycat, Thijs!bot, Epbr123, Qwyrxian, Jasonkodat, HappyInGeneral, Headbomb, Marek69, James086, Jonny-mt, Klausness, Visik,Mentifisto, AntiVandalBot, Yuanchosaan, Davidoff, Blue Tie, Jared Hunt, Tpaba, Kelliel@iinet.net.au, Notepadpage, BigNate37, Djgre-gory, DavidSmith8888, Fulkkari~enwiki, Gizz, Jprey~enwiki, DrMacrophage, Res2216firestar, JAnDbot, HTGuru, Barek, MER-C, Archdude, Hut 8.5, Bradtaylor, Bencherlite, Magioladitis, Unused0029, Karlhahn, Michael V Hayes, Bongwarrior, VoABot II, Nyq, Kuyabribri,Lheydon, Bubba hotep, WhatamIdoing, 28421u2232nfenfcenc, DerHexer, GermanX, Matt povey, PEBill, Ashishbhatnagar72, B. Wol-terding, FisherQueen, Yobol, MartinBot, CliffC, Arjun01, Bfesser, Anaxial, TheEgyptian, Tgeairn, J.delanoy, Bitbotbotbot, Ali, Boghog,Xris0, 5Q5, Shawn in Montreal, Naniwako, Mikael Häggström, Johnduffell, Adh30, NewEnglandYankee, SJP, MKoltnow, Cometstyles,Zuff, Vanished user 39948282, Adam Zivner, TheNewPhobia, Muchclag, Idioma-bot, Burlywood, Remi0o, Deor, VolkovBot, PreThinker,Butwhatdoiknow, Lear’s Fool, VasilievVV, Philip Trueman, TXiKiBoT, Oshwah, Red Act, Miranda, Ann Stouter, CoJaBo, Pandaas-sassin7, Charlesdrakew, Anna Lincoln, Martin451, Dawaegel, BwDraco, Jackfork, LeaveSleaves, Nutcrakerr, Csdorman, Oguk, Mad-hero88, Anfieldroad, Falcon8765, Lmuenchen, Waimate01, Doc James, AlleborgoBot, Bakerstmd, CMBJ, Wraithdart, Bear and Dragon,SieBot, Tresiden, 4wajzkd02, Scarian, Ymaziar, PatronSaintOfEntropy, Mrdocjb, Yintan, G0dsweed, LeadSongDog, Mzcrazybitch, Bj-keefe, Strasburger, Oxymoron83, Antonio Lopez, Faradayplank, Avnjay, Assume5, Steven Crossin, Correogsk, Muszek, Sean.hoyland, Me,GordonMarjory, Troop350, Maderchoudsala44, Buchskj, Dig deeper, Ocdcntx, ClueBot, LAX, Wayunga, GorillaWarfare, Wikievil666,The Thing That Should Not Be, Maderchoud334, Helenabella, Abhinav, ImperfectlyInformed, Arakunem, John Kaduwanema, WDM27,Nikzbitz, Sinkker, SstrykerR, Excirial, Alexbot, Abdmy011, Seuwin, Abrech, BobKawanaka, Ice Cold Beer, EhJJ, Septine, Arjayay, Nicnicm, Jack-A-Roe, TruthIsStrangerThanFiction, Aitias, Wyferltd, Dank, Djk3, Canihaveacookie, Bücherwürmlein, DumZiBoT, XLinkBot,Mjharrison, Mike Magowan, Blood Pressure Association Publications Officer, Svadhisthana, Facts707, Skarebo, Alexius08, Freestyle-69,Quaint and curious, Addbot, Mortense, Willking1979, Aceofhearts1968, DOI bot, Jojhutton, Kitty bean, Fyrael, Mootros, Cst17, Mo-hamad398, Healy24, MrOllie, Morning277, Chamal N, Ccacsmss, DFS454, AndersBot, User38934, Wikiperson0202, Quercus solaris,Bob K31416, Brainmachine, Tide rolls, Krano, Frmatt, Rojypala, Yobot, OrgasGirl, Kartano, Ptbotgourou, Fraggle81, Ajh16, Kamikaze-Bot, IW.HG, عالم ,محبوب Eric-Wester, Tempodivalse, AnomieBOT, Byeitical, DemocraticLuntz, Housecarl, Jim1138, Neptune5000,Piano non troppo, Merube 89, Ulric1313, Flewis, Materialscientist, Citation bot, Masterchiefthespartan117, Jmarchn, LilHelpa, Xqbot, Tin-ucherianBot II, RNchoo, TracyMcClark, Srich32977, J04n, GrouchoBot, Orangedwarf, Mig174, TonyHagale, Amaury, Jmor7, Losmog,Miyagawa, Erik9, ArielGenesis, Imveracious, Spongefrog, FrescoBot, CanuckViking, Paine Ellsworth, Kwiki, Lactotripeptide, Citation bot1, Pinethicket, A8UDI, V.narsikar, PRONIZ,Mtynerod, December21st2012Freak, Chuckmoran7, Anim8cme, TobeBot, Zvn, Paiamshadi,Defender of torch, MrGoulash, Minimac, DifuWu, Pilarian, JimmyAndRobert!, Ripchip Bot, Dwinner, LimpThis, EmausBot, Eastchester,John of Reading, WikitanvirBot, Eekerz, Heimoma, GoingBatty, RenamedUser01302013, Uploadvirus, MeVsAll, Wikipelli, Kevino62,Josve05a, Bollyjeff, Traxs7, Kiwi128, Vanished user sh304hjsj3hsl43, Anaselshamy, Donner60, Puffin, Carmichael, Rishigupta02445,Tefomaste, Mjbmrbot, Ashraf khan99, Fenggegecn, Petrb, Will Beback Auto, ClueBot NG, BOMBINI, Postmeta, Adville, Mattsnow81,Frietjes, Mesoderm, CopperSquare, Weeksgo, Helpful Pixie Bot, HMSSolent, Braksb, Calabe1992, DBigXray, Vjhamilton, BG19bot,Ckdsiteckd, Amoooorlin, MusikAnimal, Chafe66, Silvrous, Iggydawn, MrBill3, Zedshort, Glacialfox, Bffsrliars, Dr Bilal Alshareef, Batty-Bot, Lalchand91, Terrytibbs1983, Vgviz1001, Sixtythirdy, Pratyya Ghosh, Cyberbot II, Mansoornbangash, Leništudent, Garamond Lethe,TylerDurden8823, Ujongbakuto, Josep sola, Fycafterpro, ProfBondi, Tentinator, Wuerzele, Carlydan, Avi8tor, BallenaBlanca, Traw187,Whubsch, Ginsuloft, BruceBlaus, Attila v m, JMW1044, Monkbot, BillionApps, Mcgillcanada, Poiuytrewqvtaatv123321, KH-1, Santos33,Ah91086, CherryCoke027, KasparBot, Malv0isin, Shrirangab123, Hot Pork Pie, BSGTeam, Bronzudex and Anonymous: 907

9.2 Images• File:Arterial-blood-pressure-curve.svg Source: https://upload.wikimedia.org/wikipedia/commons/8/85/

Arterial-blood-pressure-curve.svg License: Public domain Contributors: Benutzer:Lupino sein Kopf Original artist: Benutzer:Lupino• File:Commons-logo.svg Source: https://upload.wikimedia.org/wikipedia/en/4/4a/Commons-logo.svg License: CC-BY-SA-3.0 Contribu-tors: ? Original artist: ?

14 9 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

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