116 Control of Blood Pressure

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 forms part of the autonomic nervous system and is responsible for regulation of cardiac output. Located in the medulla oblongata, the cardiovascular center  contains three distinct components: the cardioaccelerator center, the cardioinhibitor center, and the vasomotor center.

The cardioaccelerator center stimulates cardiac function by regulating heart rate and stroke volume via sympathetic stimulation from the cardiac accelerator nerve. The cardioinhibitor 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 a 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 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.

Baroreceptor Function

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.

Baroreceptor Reflexes

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 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 vasocontrictors.

Many physical factors that 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.

Chemical Vasoconstriction

Vasoconstriction is the narrowing of blood vessels resulting from 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.

Chemical Vasodilation

Vasodilation is the widening of blood vessels resulting from 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 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.

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 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

Checking circulation involves measurement of blood pressure and pulse through a variety of invasive and noninvasive methods.

Circulatory health can be measured in a variety of ways as follows.

Pulse

While a simple pulse rate measurement can be achieved 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 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 1970’s. 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 light signal from the blood component hemoglobin under oxygenated vs. deoxygenated conditions allows the technology of pulse oximetry.

Heart Rate

Heart rate can be measured by listening to the heart directly though 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.

Blood Pressure

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

Pulse is a measurement of heart rate by touching and counting beats at several body locations, typically at the wrist radial artery.

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.

Measurement Techniques

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.

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.

A 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 the systolic and diastolic pressure is called the 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 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.

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

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

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.