The walls of all blood vessels except the smallest consist of three layers: the tunica intima, tunica media, and tunica externa.
The tunica intima reduces friction between the vessel walls and blood; the tunica media controls vasoconstriction and vasodilation of the vessel; and the tunica externa protects, reinforces, and anchors the vessel to surrounding structures.
Elastic, or conducting, arteries contain large amounts of elastin, which enables these vessels to withstand and smooth out pressure fluctuations due to heart action.
Muscular, or distributing, arteries deliver blood to specific body organs, and have the greatest proportion of tunica media of all vessels, making them more active in vasoconstriction.
Arterioles are the smallest arteries and regulate blood flow into capillary beds through vasoconstriction and vasodilation.
Capillaries are the smallest vessels and allow for exchange of substances between the blood and interstitial fluid.
Continuous capillaries are most common and allow passage of fluids and small solutes.
Fenestrated capillaries are more permeable to fluids and solutes than continuous capillaries.
Sinusoidal capillaries are leaky capillaries that allow large molecules to pass between the blood and surrounding tissues.
Capillary beds are microcirculatory networks consisting of a vascular shunt and true capillaries, which function as the exchange vessels.
A cuff of smooth muscle, called a precapillary sphincter, surrounds each capillary at the metarteriole and acts as a valve to regulate blood flow into the capillary.
Venules are formed where capillaries converge and allow fluid and white blood cells to move easily between the blood and tissues.
Venules join to form veins, which are relatively thin-walled vessels with large lumens containing about 65% of the total blood volume.
Vascular anastomoses form where vascular channels unite, allowing blood to be supplied to and drained from an area even if one channel is blocked .
Blood flow is the volume of blood flowing through a vessel, organ, or the entire circulation in a given period and may be expressed as ml/min (blood flow of the entire circulation is equal to cardiac output).
Blood pressure is the force per unit area exerted by the blood against a vessel wall and is expressed in millimeters of mercury (mm Hg).
Resistance is a measure of the friction between blood and the vessel wall, and arises from three sources: blood viscosity, blood vessel length, and blood vessel diameter. The variable with the greatest effect on resistance is the diameter (or radius, 1/2 the diameter) of a particular vessel - resistance drops exponentially as the radius increases.
TPR is total peripheral resistance - resistance throughout the entire systemic circulation.
Relationship Between Flow, Pressure, and Resistance
If blood pressure increases, blood flow increases; if peripheral resistance increases, blood flow decreases.
Peripheral resistance is the most important factor influencing local blood flow, because vasoconstriction or vasodilation can dramatically alter local resistance while systemic blood pressure remains unchanged (due to homeostatic mechanisms that maintain systemic BP at a constant value, see below).
The pumping action of the heart generates blood flow; pressure results when blood flow is opposed by resistance.
Systemic blood pressure is highest in the aorta, and declines throughout the pathway until it reaches 0 mm Hg in the right atrium.
Arterial blood pressure reflects how much the arteries close to the heart can be stretched (compliance, or distensibility), and the volume forced into them at a given time.
When the left ventricle contracts, blood is forced into the aorta, producing a peak in pressure called systolic pressure (120 mm Hg).
Diastolic pressure occurs when blood is prevented from flowing back into the ventricles by the closed semilunar valve, and the aorta recoils (70–80 mm Hg).
The difference between diastolic and systolic pressure is called the pulse presssure.
The mean arterial pressure (MAP) represents the pressure that propels blood to the tissues.
Capillary blood pressure is low, ranging from 40–20 mm Hg, which protects the capillaries from rupture, but is still adequate to ensure exchange between blood and tissues.
Venous blood pressure changes very little during the cardiac cycle, and is low, reflecting cumulative effects of peripheral resistance (17 mm Hg in venules dropping to almost 0 mm Hg at the termini of the venae cavae).
Venous return is aided by both structural modifications and functional adaptations.
Valves - present mostly in extremities, none in ventral body cavity
Smooth muscle layer under sympathetic control
Blood pressure varies with changes in blood volume, TPR, and cardiac output, which are determined primarily by venous return and neural and hormonal controls.
Short-term mechanisms include both (1) neural and (2) hormonal controls, which alter blood pressure by changing peripheral resistance and CO.
Long-term mechanisms alter blood pressure by using renal controls to alter blood volume.
Neural controls of peripheral resistance alter blood distribution to (1) meet specific tissue demands and (2) maintain adequate MAP by altering blood vessel diameter.
The vasomotor center is a cluster of sympathetic neurons in the medulla, lying close to the cardioacceleratory and cardioinhibitory centers, that controls changes in the diameter of blood vessels. It constantly sends impulses to vascular smooth muscle to maintain a state of partial contraction (remember "tone"?)
Most neural controls work through reflex arcs that send information on stretch to effectors (muscle) that respond accordingly.
Chemoreceptors and input from higher brain centers can also influence neural controls.
Baroreceptors in the carotid sinus and aortic arch detect stretch and send impulses to the vasomotor center, inhibiting its activity and promoting vasodilation of arterioles and veins. They also stimulate the cardioinhibitory center and stimulate the cardioacceleratory center when stretched.
Chemoreceptors located near the baroreceptors in the carotid sinus and aortic arch detect a rise in carbon dioxide levels, a drop in oxygen levels, and drops in pH of the blood, and stimulate the cardioacceleratory and vasomotor centers, which increases cardiac output and vasoconstriction.
The cortex and hypothalamus can modify arterial pressure by signaling the medullary centers.
Chemicals, both endocrine and paracrine, influence blood pressure by acting on vascular smooth muscle or the vasomotor center.
Norepinephrine and epinephrine promote an increase in cardiac output and generalized vasoconstriction when acting on alpha receptors (will promote vasodilation at beta receptors, which are present in skeletal and cardiac muscle).
Atrial natriuretic peptide acts as a vasodilator and an antagonist to aldosterone, resulting in a drop in blood volume.
Antidiuretic hormone promotes vasoconstriction and water conservation by the kidneys, resulting in an increase in blood volume.
Angiotensin II acts as a vasoconstrictor, as well as promoting the release of aldosterone and antidiuretic hormone.
Endothelium-derived factors promote vasoconstriction, and are released in response to low blood flow.
Nitric oxide is produced in response to high blood flow or other signaling molecules, and promotes systemic and localized vasodilation.
Inflammatory chemicals, such as histamine, prostacyclin, and kinins, are potent vasodilators.
Alcohol inhibits antidiuretic hormone release and the vasomotor center, resulting in vasodilation.
Long-Term Mechanisms: Renal Mechanisms
The direct renal mechanism counteracts changes in blood pressure or volume by altering blood volume independently of hormones. The direct mechanism works best to counteract an increase in blood pressure
Increased blood pressure or volume increases the rate of kidney filtration, causing filtrate to be formed faster than water can be reabsorbed back into circulation.
The result is an increased volume of dilute urine and a decrease in blood volume.
When faced with a decrease in blood pressure it does nothing to increase blood volume, it just decreases the amount of filtrate formed, increases reabsorption from filtrate to blood, and decreases the amount of water lost in urine.
The indirect renal mechanism is the renin-angiotensin mechanism, which counteracts a decline in arterial blood pressure by causing systemic vasoconstriction.
Monitoring circulatory efficiency is accomplished by measuring pulse and blood pressure; these values together with respiratory rate and body temperature are called vital signs.
A pulse is generated by the alternating stretch and recoil of elastic arteries during each cardiac cycle.
Systemic blood pressure is measured indirectly using the ascultatory method, which relies on the use of a blood pressure cuff to alternately stop and reopen blood flow into the brachial artery of the arm.
Alterations in blood pressure may result in hypotension (low blood pressure) or transient or persistent hypertension (high blood pressure).
Tissue perfusion is involved in delivery of oxygen and nutrients to, and removal of wastes from, tissue cells; gas exchange in the lungs; absorption of nutrients from the digestive tract; and urine formation in the kidneys.
Velocity of Blood Flow
Velocity or speed of blood flow changes as it passes through the systemic circulation; it is fastest in the aorta, and declines in velocity as vessel diameter decreases (and then increases on the venous side as vessel diameter increases again).
Autoregulation: Local Regulation of Blood Flow
Autoregulation is the automatic adjustment of blood flow to each tissue in proportion to its needs, and is controlled intrinsically by modifying the diameter of local arterioles. (Extrinsic influences control MAP.)
Metabolic controls of autoregulation are most strongly stimulated by a shortage of oxygen at the tissues.
Myogenic control involves the localized response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relaxation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.
Long-term autoregulation develops over weeks or months, and involves an increase in the size of existing blood vessels and an increase in the number of vessels in a specific area, a process called angiogenesis.
Blood Flow in Special Areas
Blood flow to skeletal muscles varies with level of activity and fiber type.
Muscular autoregulation occurs almost entirely in response to decreased oxygen concentrations.
Cerebral blood flow is tightly regulated to meet neuronal needs, since neurons cannot tolerate periods of ischemia, and increased blood carbon dioxide causes marked vasodilation.
In the skin, local autoregulatory events control oxygen and nutrient delivery to the cells, while neural mechanisms control the body temperature regulation function.
Autoregulatory controls of blood flow to the lungs are the opposite of what happens in most tissues: low pulmonary oxygen causes vasoconstriction, while higher oxygen causes vasodilation.
Movement of blood through the coronary circulation of the heart is influenced by aortic pressure and the pumping of the ventricles.
Blood Flow Through Capillaries and Capillary Dynamics
Vasomotion, the slow, intermittent flow of blood through the capillaries, reflects the action of the precapillary sphincters in response to local autoregulatory controls.
Capillary exchange of nutrients, gases, and metabolic wastes occurs between the blood and interstitial space through diffusion.
Through the phospholipid bilayer directly (lipid-soluble molecules)
Intercellular capillary clefts
Pinocytotic vesicles or caveolae
Fluid Movements: Bulk Flow (Starlings Law of the Capillary)
Hydrostatic pressure (HP) is the force of a fluid against a membrane.
Colloid osmotic pressure (OP), the force opposing hydrostatic pressure, is created by the presence of large, nondiffusible molecules that are prevented from moving through the capillary membrane.
Fluids will leave the capillaries if net HP exceeds net OP, but fluids will enter the capillaries if net OP exceeds net HP.
Circulatory shock is any condition in which blood volume is inadequate and cannot circulate normally, resulting in blood flow that cannot meet the needs of a tissue.
Hypovolemic shock results from a large-scale loss of blood, and may be characterized by an elevated heart rate and intense vasoconstriction.
Vascular shock is characterized by a normal blood volume, but extreme vasodilation, often related to a loss of vasomotor tone, resulting in poor circulation and a rapid drop in blood pressure.
Transient vascular shock is due to prolonged exposure to heat, such as while sunbathing, resulting in vasodilation of cutaneous blood vessels.
Cardiogenic shock occurs when the heart is too inefficient to sustain normal blood flow, and is usually related to myocardial damage, such as repeated myocardial infarcts.
Two distinct pathways travel to and from the heart: pulmonary circulation runs from the heart to the lungs and back to the heart; systemic circulation runs to all parts of the body before returning to the heart.
There are some important differences between arteries and veins.
There is one terminal systemic artery, the aorta, but two terminal systemic veins: the superior and inferior vena cava.
Arteries run deep and are well protected, but veins are both deep, which run parallel to the arteries, and superficial, which run just beneath the skin.
Arterial pathways tend to be clear, but there are often many interconnections in venous pathways, making them difficult to follow.
There are at least two areas where venous drainage does not parallel the arterial supply: the dural sinuses draining the brain, and the hepatic portal system draining from the digestive organs to the liver before entering the main systemic circulation.
Four paired arteries supply the head and neck. (Fig. 19.21; Table 19.5)
The upper limbs are supplied entirely by arteries arising from the subclavian arteries. Fig. 19.22; Table 19.6)
The arterial supply to the abdomen arises from the aorta. (Fig. 19.23; Table 19.7)
The internal iliac arteries serve mostly the pelvic region; the external iliacs supply blood to the lower limb and abdominal wall. Fig. 19.24; Table 19.8)
The venae cavae are the major tributaries of the venous circulation. (Fig. 19.25; Table 19.9)
Blood drained from the head and neck is collected by three pairs of veins. (Fig. 19.26; Table 19.10)
The deep veins of the upper limbs follow the paths of the companion arteries. (Fig. 19.27; Table 19.11)
Blood draining from the abdominopelvic viscera and abdominal walls is returned to the heart by the inferior vena cava. Fig. 19.28; Table 19.12)
Most deep veins of the lower limb have the same names as the arteries they accompany. (Fig. 19.29; Table 19.13)
The vascular endothelium is formed by mesodermal cells that collect throughout the embryo in blood islands, which give rise to extensions that form rudimentary vascular tubes.
By the fourth week of development, the rudimentary heart and vessels are circulating blood.
Fetal vascular modifications include shunts to bypass fetal lungs (the foramen ovale and ductus arteriosus), the ductus venosus that bypasses the liver, and the umbilical arteries and veins, which carry blood to and from the placenta.
At birth, the fetal shunts and bypasses close and become occluded.
Congenital vascular problems are rare, but the incidence of vascular disease increases with age, leading to varicose veins, tingling in fingers and toes, and muscle cramping.
Atherosclerosis begins in youth, but rarely causes problems until old age.
Blood pressure changes with age: the arterial pressure of infants is about 90/55, but rises steadily during childhood to an average 120/80, and tends to increase to somewhere around 150/90 in old age. Depending on how you live. It's an average but it's also a choice, so workout, eat right, and don't smoke and old age might look better than "young age".