Control of Blood pressure is a cardinal vital sign that guides both acute and long-term clinical decision-making. Given its importance in directing care, it is essential to measure blood pressure accurately and consistently.
In general, two values are recorded during the measurement of blood pressure. The first, systolic pressure, represents the peak arterial pressure during systole. The second, diastolic pressure, represents the minimum arterial pressure during diastole. A third value, mean arterial pressure, can be calculated from the systolic and diastolic pressures.
The overall blood pressure as measured in the brachial artery is maintained by the cardiac output and the total peripheral resistance (TPR) to flow. The mean arterial pressure (MAP) is calculated by the formula:
where DBP and SBP are diastolic and systolic blood pressure, respectively. Mean arterial pressure is a useful concept because it can be used to calculate overall blood flow, and thus delivery of nutrients to the various organs. It is a good indicator of perfusion pressure (ΔP).
Blood flow is defined by Poiseuille’s law
where Q is the blood flow, ΔP is the pressure gradient, r is the radius of the vessel, N is the blood viscosity, and L is the length of the vessel. This formula is commonly restated in a more clinically useful expression:
Here CO is the cardiac output in liters/minute and is the clinical equivalent of blood flow (Q). MAP (in mm Hg) is used to approximate the pressure gradient (ΔP). TPR is the resistance to flow in dynes · sec · cm−5 and clinically represents 8 NL/πr4 The conversion factor 80 appears in the formula simply to allow the use of more conventional units.
Example 1: BP of 120/80 and normal cardiac output of 5 L/min:
In this example, the TPR demonstrated can be used as a standard in evaluating pathologic conditions.
Example 2: Normal cardiac output of 5.0 L/min and BP of 170/110:
In this example of a typical hypertensive, the cardiac output is normal and the elevated blood pressure is thought to occur as a direct result of increased TPR. The TPR is maintained by resistance vessels, small precapillary muscular arterioles that regulate the rate of diastolic runoff in the arterial tree. These resistance vessels regulate blood flow by changes in vascular tone that adjust the radius (r) of the vessel. Since radius appears in the formula to the fourth power (i.e., TPR = 8NL/πr4), small adjustments cause significant changes in TPR.
Example 3: BP of 80/60, TPR of 600:
This example is representative of septic shock. Lax vasomotor tone causes a low TPR, and blood pressure can be maintained only by a substantial rise in cardiac output.
Cardiac output is calculated by multiplying heart rate by stroke volume. In intrinsic cardiac disease, the stroke volume may be decreased, but the cardiac output can be maintained by a compensatory rise in heart rate. For a given TPR, the blood pressure is maintained unless there is relative bradycardia or a further fall in stroke volume.
During systole, the volume of blood ejected from the left ventricle must enter the aorta and major arterial branches. The distensibility of the arteries compensates for this volume and stores energy in order to perfuse the capillary beds during diastole. If, for example, the aorta is stiff from atherosclerotic disease, the left ventricle generates a higher pressure to eject a given quantity of blood, and so the systolic pressure is higher.
With each heartbeat, there are minor adjustments in these factors that are all intricately controlled to provide perfusion of the organs. Baroreceptors in the aorta and carotid body are stretched by the blood pressure and send feedback information to autonomic nervous system centers in the brainstem. Autonomic outflow then controls heart rate, vascular tone, and contractile state of the myocardium to adjust blood pressure accordingly.
Pulse pressure is the difference between systolic and diastolic blood pressures.[rx][rx][rx]
Pulse Pressure = Systolic Blood Pressure – Diastolic Blood Pressure
The systolic blood pressure is defined as the maximum pressure experienced in the aorta when the heart contracts and ejects blood into the aorta from the left ventricle (approximately 120 mmHg). The diastolic blood pressure is the minimum pressure experienced in the aorta when the heart is relaxing before ejecting blood into the aorta from the left ventricle (approximately 80 mmHg). Normal pulse pressure is, therefore, approximately 40 mmHg.
A change in pulse pressure (delta Pp) is proportional to volume change (delta-V) but inversely proportional to arterial compliance (C):
Delta Pp = Delta V/C
Because the change in volume is due to the stroke volume of blood ejected from the left ventricle (SV), we can approximate pulse pressure as:
Pp = SV/C
A normal young adult at rest has a stroke volume of approximately 80 mL. Arterial compliance is approximately 2 mL/mm Hg, which confirms that normal pulse pressure is approximately 40 mm Hg.
Arterial compliance is equal to the change in volume (Delta V) over a given change in pressure (Delta P):
C = Delta V/Delta P
Because the aorta is the most compliant portion of the human arterial system, the pulse pressure is the lowest. Compliance progressively decreases until it reaches a minimum in the femoral and saphenous arteries, and then it begins to increase again. This concept requires an understanding of the effect of pressure wave reflection on the amplification of aortic pressure and thus pulse pressure. The phenomenon mainly occurs in the lower body, especially the lower extremities where pressure waves reflect back due to vessel branching, and the vessels are less compliant (stiffer) When a reflected wave is in phase with a forward wave, it generates a wave with higher amplitude. An analogy here is waves bouncing off a seawall and interacting with an incoming wave. If they are in phase, the wave height is greater.
|Category||Subtype||Systolic BP (mmHg)||Diastolic BP (mmHg)|
|Office BP||NA||≥ 140||≥ 90|
|Ambulatory BP||Daytime (awake)||≥ 135||≥ 85|
|Nighttime (asleep)||≥ 120||≥ 70|
|24hr||≥ 130||≥ 80|
|Home BP||NA||≥ 135||≥ 85|
For the diagnosis of hypertension, systolic BP, diastolic BP or both have to exceed the reported values. NA, not applicable. Modified from Ref[rx].
|Guideline||Population||Goal BP (mmHg)|
|2010 Chinese Guidelines[rx]||Adults < 65 years||< 140/90|
|Adults 65 years and older||<150/90 (<140/90 if tolerated)|
|Adults with diabetes, CHD, or renal disease||<130/80|
|2013 ESH/ESC[rx]||Nonfrail adults < 80 years||< 140/90|
|Adults > 80 years||< 150/90|
|Adults with diabetes||< 140/85|
|Adults with CKD without proteinuria||< 140/90|
|Adults with CKD with overt proteinuria||< 130/90|
|Adults with CHD||< 140/90|
|2013 ASH/ISH[rx]||Adults 55–80 years||< 140/90|
|Young adults||< 130/80|
|Elderly > 80 years||< 150/90|
|2014 Hypertension guideline[rx]
(formerly known as JNC 8)
|Adults < 60 years||< 140/90|
|Adults ≥ 60 years||< 150/90|
|Adults with diabetes||< 140/90|
|Adults with CKD||< 140/90|
|2014 South African Guidelines[rx]||Most adults||< 140/90|
|Adults > 80 years||SBP 140–150|
|2014 Japanese Guidelines[rx]||Most adults||< 140/90|
|Late phase elderly patients||<150/90 (<140/90 if tolerated)|
|Adults with diabetes or CKD||< 130/80|
|Adults with CHD or CVD||< 140/90|
|CHEP 2016[rx]||Adults < 80 years||< 140/90|
|Adults ≥ 80 years||< 150|
|High-risk adults ≥ 50 years||≤ 120*|
|2016 Australian guidelines[rx]||Adults at high CV risk without diabetes mellitus, including CKD patients and those >75 years||< 120|
|Adults with diabetes in whom prevention of stroke is priority||< 120|
|ADA[rx]||Adults with diabetes||< 140/90|
|Adults with diabetes and high risk for CVD||< 130/80|
|Adults with known CVD or 10-year ASCVD event risk ≥ 10%||< 130/80|
|Adults without additional markers of increased CVD risk||< 130/80|
|Older adults ≥ 65 years of age,
|Older adults ≥ 65 years of age, with comorbidities and limited life expectancy||Individualized goal based on clinical judgment and patient preference|
Role of the Cardiovascular Center
The cardiovascular system plays a role in body maintenance by transporting hormones and nutrients and removing waste products.
- The cardiovascular center is a part of the human brain found in the medulla oblongata, responsible for the regulation of cardiac output.
- Numerous receptors in the circulatory system can detect changes in pH or stretch and signal these changes to the cardiovascular center.
- The cardiovascular center can alter heart rate and stroke volume to increase blood pressure and flow.
- cardiovascular center: A region of the brain responsible for nervous control of the cardiac output.
The cardiovascular center forms part of the autonomic nervous system and is responsible for the regulation of cardiac output. Located in the medulla oblongata, the cardiovascular center contains three distinct components: the cardio accelerator center, the cardioinhibitory center, and the vasomotor center.
The cardio accelerator center stimulates cardiac function by regulating heart rate and stroke volume via sympathetic stimulation from the cardiac accelerator nerve. The cardioinhibitory center slows cardiac function by decreasing heart rate and stroke volume via parasympathetic stimulation from the vagus nerve. The vasomotor center controls vessel tone or contraction of the smooth muscle in the tunica media. Changes in diameter affect peripheral resistance, pressure, and flow, which in turn affect cardiac output. The majority of these neurons act via the release of the neurotransmitter norepinephrine from sympathetic neurons. Although each center functions independently, they are not anatomically distinct.
The cardiovascular center can respond to numerous stimuli. Hormones such as epinephrine and norepinephrine or changes in pH such as acidification due to carbon dioxide accumulation in tissue during exercise are detected by chemoreceptors. Baroreceptors that detect stretch can also signal to the cardiovascular center to alter heart rate.
Short-Term Neural Control
Neural regulation of blood pressure is achieved through the role of cardiovascular centers and baroreceptor stimulation.
- The cardio accelerator center, the cardioinhibitory center, and the vasomotor center form the cardiovascular center, a cluster of neurons that function independently to regulate blood pressure and flow.
- The release of the neurotransmitter norepinephrine from sympathetic neurons directs the majority of neurons associated with the cardiovascular center.
- Baroreceptors respond to the degree of stretch caused by the presence of blood; this stimulates impulses to be sent to the cardiovascular center to regulate blood pressure to achieve homeostasis when needed.
- autonomic nervous system: The part of the nervous system that regulates the involuntary activity of the heart, intestines, and glands. These activities include digestion, respiration, perspiration, metabolism, and blood pressure modulation.
- norepinephrine: A catecholamine with multiple roles including as a hormone and neurotransmitter. Areas of the body that produce or are affected by this substance are described as noradrenergic.
- sympathetic: Of or related to the part of the autonomic nervous system that under stress raises blood pressure and heart rate, constricts blood vessels and dilates the pupils.
- baroreceptor: A nerve ending that is sensitive to changes in blood pressure.
- parasympathetic: Of or relating to the part of the autonomic nervous system that inhibits or opposes the effects of the sympathetic nervous system.
The autonomic nervous system plays a critical role in the regulation of vascular homeostasis. The primary regulatory sites include the cardiovascular centers in the brain that control both cardiac and vascular functions.
Neurological regulation of blood pressure and flow depends on the cardiovascular centers located in the medulla oblongata. This cluster of neurons responds to changes in blood pressure as well as blood concentrations of oxygen, carbon dioxide, and other factors such as pH.
Baroreceptors are specialized stretch receptors located within thin areas of blood vessels and heart chambers that respond to the degree of stretch caused by the presence of blood. They send impulses to the cardiovascular center to regulate blood pressure. Vascular baroreceptors are found primarily in sinuses (small cavities) within the aorta and carotid arteries. The aortic sinuses are found in the walls of the ascending aorta just superior to the aortic valve, whereas the carotid sinuses are located in the base of the internal carotid arteries. There are also low-pressure baroreceptors located in the walls of the venae cavae and right atrium.
When blood pressure increases, the baroreceptors are stretched more tightly and initiate action potentials at a higher rate. At lower blood pressures, the degree of stretch is lower and the rate of firing is slower. When the cardiovascular center in the medulla oblongata receives this input, it triggers a reflex that maintains homeostasis.
When blood pressure rises too high, baroreceptors fire at a higher rate and trigger parasympathetic stimulation of the heart. As a result, cardiac output falls. Sympathetic stimulation of the peripheral arterioles will also decrease, resulting in vasodilation. Combined, these activities cause blood pressure to fall.
When blood pressure drops too low, the rate of baroreceptor firing decreases. This triggers an increase in sympathetic stimulation of the heart, causing the cardiac output to increase. It also triggers sympathetic stimulation of the peripheral vessels, resulting in vasoconstriction. Combined, these activities cause blood pressure to rise.
The baroreceptors in the venae cavae and right atrium monitor blood pressure as the blood returns to the heart from the systemic circulation. Normally, blood flow into the aorta is the same as blood flow back into the right atrium. If blood is returning to the right atrium more rapidly than it is being ejected from the left ventricle, the atrial receptors will stimulate the cardiovascular centers to increase sympathetic firing and cardiac output until homeostasis is achieved. The opposite is also true. This mechanism is referred to as the atrial reflex.
Other neural mechanisms can also have a significant impact on cardiovascular function. These include the limbic system, which links physiological responses to psychological stimuli, chemoreceptor reflexes, generalized sympathetic stimulation, and parasympathetic stimulation.
Short-Term Chemical Control
Blood pressure is controlled chemically through dilation or constriction of the blood vessels by vasodilators and vasoconstrictors.
- Constriction or dilation of blood vessels alters resistance, increasing or decreasing blood pressure respectively.
- Generalized vasoconstriction usually results in an increase in systemic blood pressure, but it may also occur in specific tissues, causing a localized reduction in blood flow.
- Vasoconstriction results from increased concentration of calcium (Ca2+) ions within the vascular smooth muscle.
- When blood vessels dilate, the flow of blood is increased due to a decrease in vascular resistance. Therefore, dilation of arterial blood vessels (mainly the arterioles ) causes a decrease in blood pressure.
- Localized tissues increase blood flow in multiple ways, including releasing vasodilators, primarily adenosine, into the local interstitial fluid, which diffuses to capillary beds provoking local vasodilation.
- vasodilation: The dilation (widening) of a blood vessel.
- vasoconstriction: The constriction (narrowing) of a blood vessel.
Many physical factors influence arterial pressure. Each may in turn be influenced by physiological factors such as diet, exercise, disease, drugs or alcohol, stress, and obesity. In practice, each individual’s autonomic nervous system responds to and regulates all of these interacting factors so that the actual arterial pressure response varies widely because of both split-second and slow-moving responses of the nervous system and end organs. These responses are very effective in changing the variables and resulting blood pressure from moment to moment.
Vasoconstriction is the narrowing of blood vessels resulting from the contraction of the muscular wall of the vessels, particularly the large arteries and small arterioles. Generalized vasoconstriction usually results in an increase in systemic blood pressure, but may also occur in specific tissues, causing a localized reduction in blood flow.
The mechanism that leads to vasoconstriction results from the increased concentration of calcium (Ca2+ ions) and phosphorylated myosin within vascular smooth muscle cells. When stimulated, a signal transduction cascade leads to increased intracellular calcium from the sarcoplasmic reticulum through IP3 mediated calcium release, as well as enhanced calcium entry across the sarcolemma through calcium channels.
The rise in intracellular calcium interacts with calmodulin, which in turn activates myosin light chain kinase. This enzyme is responsible for phosphorylating the light chain of myosin to stimulate cross-bridge cycling. Once elevated, the intracellular calcium concentration is returned to its basal level through a variety of protein pumps and calcium exchanges located on the plasma membrane and sarcoplasmic reticulum. This reduction in calcium removes the stimulus necessary for contraction allowing for a return to baseline.
Endogenous vasoconstrictors include ATP, epinephrine, and angiotensin II.
Vasodilation is the widening of blood vessels resulting from the relaxation of smooth muscle cells within the vessel walls, particularly in the large veins, large arteries, and smaller arterioles. Generalized vasodilation usually results in a decrease in systemic blood pressure, but may also occur in specific tissues causing a localized increase in blood flow.
The primary function of vasodilation is to increase blood flow in the body to tissues that need it most. This is often in response to a localized need for oxygen but can occur when the tissue in question is not receiving enough glucose, lipids, or other nutrients. Localized tissues increase blood flow by several methods, including the release of vasodilators, primarily adenosine, into the local interstitial fluid, which diffuses to capillary beds provoking local vasodilation. Some physiologists have suggested the lack of oxygen itself causes capillary beds to vasodilate by the smooth muscle hypoxia of the vessels in the region.
As with vasoconstriction, vasodilation is modulated by calcium ion concentration and myosin phosphorylation within vascular smooth muscle cells. Dephosphorylation by myosin light-chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment both contribute to smooth muscle cell relaxation and therefore vasodilation. This is accomplished through the reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. Endogenous vasodilators include arginine and lactic acid.
Long-Term Renal Regulation
Consistent and long-term control of blood pressure is determined by the renin-angiotensin system.
- When blood volume is low, renin, excreted by the kidneys, stimulates the production of angiotensin I, which is converted into angiotensin II. This substance has many effects, including the increase in blood pressure due to its vasoconstrictive properties.
- The cells that excrete renin are called juxtaglomerular cells. When blood volume is low, juxtaglomerular cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I.
- Aldosterone secretion from the adrenal cortex is induced by angiotensin II and causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood, thereby increasing blood volume and blood pressure.
- juxtaglomerular cells: The juxtaglomerular cells (JG cells, or granular cells) are cells in the kidney that synthesize, store, and secrete the enzyme renin.
- aldosterone: A mineralocorticoid hormone secreted by the adrenal cortex that regulates the balance of sodium and potassium in the body.
- adrenal cortex: The outer portion of the adrenal glands that produce hormones essential to homeostasis.
Along with vessel morphology, blood viscosity is one of the key factors influencing resistance and hence blood pressure. A key modulator of blood viscosity is the renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS), a hormone system that regulates blood pressure and water balance.
When blood volume is low, juxtaglomerular cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I. Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme found in the lungs. Angiotensin II is a potent vasoactive peptide that causes blood vessels to constrict, resulting in increased blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex.
Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure. If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. Many drugs interrupt different steps in this system to lower blood pressure. These drugs are one of the main ways to control high blood pressure (hypertension), heart failure, kidney failure, and the harmful effects of diabetes.
It is believed that angiotensin I may have some minor activity, but angiotensin II is the major bioactive product. Angiotensin II has a variety of effects on the body: throughout the body, it is a potent vasoconstrictor of arterioles.
Checking circulation involves the measurement of blood pressure and pulse through a variety of invasive and noninvasive methods.
- Pulse rate is most commonly measured manually at the wrist by a trained medical professional.
- Arterial catheters and pulse oximetry allow for more accurate and long-term measurement of pulse rate.
- Heart rate can be measured directly by listening to the heart through the chest.
- Electrocardiography, which detects the electrical pattern of the heart muscle through the skin, can be used for more accurate or long-term measurements.
- Arterial pressure is most commonly measured via a sphygmomanometer.
- Blood pressure values are generally reported in millimeters of mercury (mmHg), though aneroid and electronic devices do not use mercury.
- The auscultatory method for determining blood pressure uses a stethoscope and a sphygmomanometer.
- electrocardiography: A measure of the electrical output of the heart detected through the skin.
- sphygmomanometer: A device used to measure blood pressure.
Circulatory health can be measured in a variety of ways as follows.
While a simple pulse rate measurement can be achieved by anyone, trained medical staff are capable of much more accurate measurements. The radial pulse is commonly measured using three fingers: the finger closest to the heart is used to occlude the pulse pressure, the middle finger is used to get a crude estimate of blood pressure, and the finger most distal to the heart is used to nullify the effect of the ulnar pulse as the two arteries are connected via the palmar arches.
Where more accurate or long-term measurements are required, pulse rate, pulse deficits, and much more physiologic data are readily visualized by the use of one or more arterial catheters connected to a transducer and oscilloscope. This invasive technique has been commonly used in intensive care since the 1970s. The rate of the pulse is observed and measured by tactile or visual means on the outside of an artery and recorded as beats per minute (BPM). The pulse may be further indirectly observed under light absorbencies of varying wavelengths with assigned and inexpensively reproduced mathematical ratios. Applied capture of variances of the light signal from the blood component hemoglobin under oxygenated vs. deoxygenated conditions allows the technology of pulse oximetry.
Heart rate can be measured by listening to the heart directly through the chest, traditionally using a stethoscope. For more accurate or long-term measurements, electrocardiography may be used.
During each heartbeat, a healthy heart has an orderly progression of depolarization that starts with pacemaker cells in the sinoatrial (SA) node, spreads out through the atrium, passes through the atrioventricular node down into the bundle of His and into the Purkinje fibers, and down and to the left throughout the ventricles. This organized pattern of depolarization can be detected through electrodes placed on the skin and recorded as the commonly seen ECG tracing. ECG provides a very accurate means to measure heart rate, rhythm, and other factors such as chamber sizing, as well as identifying possible regions of damage.
Arterial pressure is most commonly measured via a sphygmomanometer, which historically used the height of a column of mercury to reflect the circulating pressure. Blood pressure values are generally reported in millimeters of mercury (mmHg), though aneroid and electronic devices do not use mercury. For each heartbeat, blood pressure varies between systolic and diastolic pressures. Systolic pressure is peak pressure in the arteries, which occurs near the end of the cardiac cycle when the ventricles are contracting. Diastolic pressure is minimum pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are filled with blood. An example of normal measured values for a resting, healthy adult human is 120 mmHg systolic and 80 mmHg diastolic.
Hypertension refers to abnormally high arterial pressure, as opposed to hypotension, when it is abnormally low. Along with body temperature, respiratory rate, and pulse rate, blood pressure is one of the four main vital signs routinely monitored by medical professionals and healthcare providers.
Measuring pressure invasively by penetrating the arterial wall to take the measurement is much less common and usually restricted to a hospital setting. The noninvasive auscultatory and oscillometric measurements are simpler and faster than invasive measurements, require less expertise, have virtually no complications, are less unpleasant and painful for the patient. However, noninvasive methods may yield somewhat lower accuracy and small systematic differences in numerical results. Noninvasive measurement methods are more commonly used for routine examinations and monitoring.
The Auscultatory Method
The auscultatory method uses a stethoscope and a sphygmomanometer. This comprises an inflatable cuff placed around the upper arm at roughly the same vertical height as the heart, attached to a mercury or aneroid manometer. The mercury manometer, considered the gold standard, measures the height of a column of mercury, giving an absolute result without need for calibration.
A cuff of appropriate size is fitted smoothly and snugly, then inflated manually by repeatedly squeezing a rubber bulb until the artery is completely occluded. Listening with the stethoscope to the brachial artery at the elbow, the examiner slowly releases the pressure in the cuff. When blood just starts to flow in the artery, the turbulent flow creates a “whooshing” or pounding (first Korotkoff sound). The pressure at which this sound is first heard is the systolic blood pressure. The cuff pressure is further released until no sound can be heard (fifth Korotkoff sound), at the diastolic arterial pressure. The auscultatory method is the predominant method of clinical measurement.
Pulse is a measurement of heart rate by touching and counting beats at several body locations, typically at the wrist radial artery.
- Physiologically, pulse is the expansion of the artery due to pressure from the heartbeat, and thus is most closely correlated to systolic blood pressure.
- Sometimes the pulse cannot be taken at the wrist and may therefore be taken at the neck against the carotid artery (carotid pulse) or behind the knee ( popliteal artery ).
- The heart rate may be greater or less than the pulse rate depending upon physiologic demand. In this case, the heart rate is determined by auscultation or audible sounds at the heart apex, not the pulse.
- Pulse rate is recorded as beats per minute (bpm) and varies with age. A newborn or infant can have a heart rate of approximately 130-150 bpm, while an adult pulse rate is between 50 and 80 bpm.
- popliteal artery: The popliteal artery is defined as the extension of the superficial femoral artery after passing through the adductor canal and adductor hiatus above the knee.
- radial artery: The main artery that enters the wrist on the side of the thumb, it is the most common location for measuring pulse rate.
- heart rate: The number of heartbeats per unit of time, usually expressed as beats per minute.
- pulse rate: The physical expansion of an artery per unit of time, usually expressed as beats per minute.
- carotid artery: Either of a pair of arteries on each side of the neck that branch from the aorta and supply blood to the head.
The pulse is the physical expansion of an artery generated by the increase in pressure associated with systole of the heart. Pulse is often used as an equivalent of heart rate due to the relative ease of measurement; heart rate can be measured by listening to the heart directly through the chest, traditionally using a stethoscope.
Pulse rate or velocity is usually measured either at the wrist from the radial artery and is recorded as beats per minute (bpm). Other common measurement locations include the carotid artery in the neck and popliteal artery behind the knee
Pulse varies with age; a newborn or infant can have a heart rate of about 130-150 bpm. A toddler’s heart will beat about 100-120 times per minute, an older child’s heartbeat is around 60-100 bpm, adolescents around 80-100 bpm, and a healthy adults pulse rate is anywhere between 50 and 80 bpm.
The heart rate may be greater or less than the pulse rate depending upon physiologic demand. In this case, the heart rate is determined by auscultation or audible sounds at the heart apex, not the pulse. The pulse deficit (difference between heartbeats and pulsations at the periphery) is determined by simultaneous palpation at the radial artery and auscultation at the heart apex.
While a simple measurement of pulse rate is achievable by anyone, trained medical staff are capable of much more accurate measurements. Radial pulse is commonly measured using three fingers: the finger closest to the heart used to occlude the pulse pressure, the middle finger used get a crude estimate of blood pressure, and the finger most distal to the heart used to nullify the effect of the ulnar pulse as the two arteries are connected via the palmar arches.
Where more accurate or long-term measurements are required, pulse rate, pulse deficits, and more physiologic data are readily visualized by the use of one or more arterial catheters connected to a transducer and oscilloscope. This invasive technique has been commonly used in intensive care since the 1970’s. The rate of the pulse is observed and measured by tactile or visual means on the outside of an artery and is recorded as beats per minute. The pulse may be further indirectly observed under light absorbencies of varying wavelengths with assigned and inexpensively reproduced mathematical ratios. Applied capture of variances of light signal from the blood component hemoglobin under oxygenated vs. deoxygenated conditions allows the technology of pulse oximetry.
Measuring Blood Pressure
Measurement of blood pressure includes systolic pressure during cardiac contraction and diastolic pressure during cardiac relaxation.
- The difference between systolic and diastolic pressure is referred to as the pulse pressure. That difference can indicate hypertension or hypotension with a deviation from the norm.
- The measurement of these pressures is now usually done with an aneroid or electronic sphygmomanometer. The classic measurement device is a mercury sphygmomanometer, using a column of mercury measured in millimeters.
- Blood pressures are also taken at other portions of the extremities. These pressures are called segmental blood pressures and are used to evaluate blockage or arterial occlusion in a limb.
- pulse pressure: Blood pressure when feeling the pulse, measured by millimeters of mercury (mmHg).
- diastolic blood pressure: The lowest pressure within the bloodstream, occurring between heartbeats because of a diastole.
- systolic blood pressure: The highest pressure within the bloodstream, occurring during each heartbeat because of the systole.
Blood pressure is the pressure blood exerts on the arterial walls. It is recorded as two readings: the systolic blood pressure (the top number) occurs during cardiac contraction, and the diastolic blood pressure or resting pressure (the bottom number), occurs between heartbeats when the heart is not actively contracting.
Normal blood pressure is about 120 mmHg systolic over 80 mmHg diastolic. Usually, the blood pressure is read from the left arm, although blood pressures are also taken at other locations along the extremities. These pressures, called segmental blood pressures, are used to evaluate blockage or arterial occlusion in a limb (for example, the ankle-brachial pressure index). The difference between systolic and diastolic pressure is called pulse pressure.
The measurement of these pressures is usually performed with an aneroid or electronic sphygmomanometer. The classic measurement device is a mercury sphygmomanometer, using a column of mercury measured off in millimeters. In the United States and the UK, the common form is millimeters of mercury (mm Hg), while elsewhere SI units of pressure are used. There is no natural or normal value for blood pressure, but rather a range of values that are associated with increased risks for disease and health:
- Hypotension: under 90 mmHg systolic and under 60 mmHg diastolic.
- Normal: 90–119 mmHg systolic and 60–79 mmHg diastolic.
- Prehypertensive: 120–139 mmHg systolic and 80–89 mmHg diastolic.
- Hypertensive: 140 mmHg and above systolic and 90 mmHg and above diastolic.
The guidelines for acceptable readings also take into account other cofactors for disease, such as pre-existing health factors. Therefore, hypertension is indicated when the systolic number is persistently over 140–160 mmHg. Low blood pressure, or hypotension, is indicated when the systolic number is persistently below 90 mmHg.
Extremes in Blood Pressure
Chronically elevated blood pressure is called hypertension, while chronically low blood pressure is called hypotension.
- Hypertension, the unhealthy elevation of blood pressure, is a major risk factor for stroke, myocardial infarction ( heart attacks), heart failure, aneurysms of the arteries, and peripheral arterial disease and a cause of chronic kidney disease.
- Hypertension is classified as either primary or secondary hypertension. The majority of cases are primary hypertension, high blood pressure with no identified cause. The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the organs or endocrine system.
- Dietary and lifestyle changes can improve blood pressure control and decrease the risk of associated health complications, although drug treatment is often necessary in people for whom lifestyle changes prove ineffective or insufficient.
- Hypotension is an abnormally low blood pressure and often indicative of a short-term condition that is not necessarily linked to disease, but rather an altered physiological state.
- For some people who exercise and are in top physical condition, low blood pressure is a sign of good health and fitness.
- For many people, low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine, or neurological disorders.
- hypertension: High blood pressure, clinically diagnosed when above 140/90 mmHg.
- hypotension: Low blood pressure, clinically diagnosed when below 100/60 mmHg.
In healthy adults, physiological blood pressure should fall between the range of 100-140 mmHg systolic and 60-90 mmHg diastolic. Blood pressures above this are classed as hypertension and those below are hypotension, both considered medical conditions.
Hypertension or high blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated above 140/90 mmHg.
Hypertension is classified as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorized as “primary hypertension” which means high blood pressure with no obvious underlying medical cause. The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the kidneys, arteries, heart, or endocrine system.
Hypertension is a major risk factor for stroke, myocardial infarction (heart attacks), heart failure, aneurysms of the arteries (e.g. aortic aneurysm), peripheral arterial disease and a cause of chronic kidney disease. Even moderate elevation of arterial blood pressure is associated with a shortened life expectancy. Dietary and lifestyle changes can improve blood pressure control and decrease the risk of associated health complications, although drug treatment is often necessary in people for whom lifestyle changes prove ineffective or insufficient.
Hypotension is a medical condition in which the blood pressure in the arteries is reduced below 100/60 mmHg. Hypotension is best understood as a physiological state rather than a disease and is often associated with shock, though not necessarily indicative of it. However, blood pressure is considered too low only if noticeable symptoms are present.
For some people who exercise and are in top physical condition, hypotension is a sign of good health and fitness. For many people, low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine, or neurological disorders. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life-threatening condition called shock.
Lifestyle modification is a very important aspect of the treatment of diabetes and hypertension. It is generally agreed that lifestyle modification has a modest antihypertensive effect resulting in an effective blood pressure reduction of 5-10 mmHg. Changes to lifestyle which appear to have health benefits include:
Reducing salt intake to less than 1.5 g/day
Increasing consumption of fruits and vegetables (8-10 servings per day)
Increasing consumption of low-fat dairy products (2-3 servings per day)
Increasing activity levels/ engaging in regular aerobic physical activity (e.g. brisk walking 30 min/day)
Losing excess weight
Avoiding excessive alcohol consumption (less than 2 drinks (30 ml ethanol)/day for men and less than 1 drink/day for women)
Lifestyle modification may be used as a sole treatment modality in patients with blood pressure <140/80, but ideally should be combined with pharmacotherapy in patients with systolic blood pressure (SBP) ≥ 140 and or diastolic blood pressure (DBP) ≥ 80
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