chapter 19
Chapter 19: Vascular System.
1. Describe the general structure of a blood vessel; include the tunics.
Blood vessels generally have three tunics (“coverings”) surrounding a blood-filled lumen. Tunica intima is innermost and is in direct contact with blood in lumen. Tunica intima contains endothelium, simple squamous epithelium which provides smooth surface for blood flow. Middle layer is tunica media, which contains circular smooth muscle and sheets of elastin. Contraction or relaxation of smooth muscle has profound effect on blood pressure by changing diameter of vessel lumen. Outermost layer is tunica externa, composed of collagen fibers that reinforce the vessels and anchor them to surrounding structures. Tunica externa also has extensive nerve fibers, lymphatic vessels, and a network of elastic fibers in large veins. Larger vessels contain “vasa vasorum”, “vessels of the vessels”, that supply nourishment to most external tissues of blood vessel wall.
2. Compare and contrast the structural and functional differences between arteries, arterioles, capillaries (complete, fenestrated and sinusoids), veins, and venules.
Arteries are either elastic, muscular, or arterioles. Elastic arteries are thick-walled arteries near heart (aorta and branches). Largest in diameter and most elastic (due to most elastin). Even though elastic arteries have extensive smooth muscle, they are relatively inactive in vasoconstriction. Elastic arteries are pressure reservoirs that expand and recoil as the heart pumps blood.
Elastic arteries (conducting arteries) deliver blood to muscular arteries, which deliver blood to specific body organs. These arteries have thickest tunica media; relatively more smooth muscle, and less elastic tissue than elastic arteries. Therefore, play greater role in vasoconstriction, and less distensible than elastic arteries.
Muscular arteries flow into arterioles, which are major resistance vessels. Arteriole diameter controls blood flow into capillary beds, so mostly smooth muscle with relatively few elastic fibers.
Capillaries are smallest blood vessels, with thin vessel wall consisting of tunica intima only. Some capillaries have pericytes (smooth muscle-like cells) on outer surface that regulate capillary permeability and stabilize capillary wall. Only thin layer of endothelium, capillaries are ideally suited for exchange of materials (gases, nutrients, hormones etc.) between blood and interstitial fluid. Capillaries form interweaving network called capillary beds. Blood can flow from terminal arteriole directly through metarteriole to postcapillary venule, thereby bypassing the capillary bed, OR can flow through metarteriole to true capillaries of the capillary bed. Entrance to true capillaries is guarded by precapillary sphincters. When open, blood flow through capillary bed to exchange nutrients, as in true capillaries of GI tract after eating a meal. Between meals, however, the same precapillary sphincters are closed.
3 types of capillaries:
1. Continuous capillaries are abundant in skin and muscles, and are most common, but least permeable. Called continuous because tight junctions between endothelial cells provide uninterrupted lining. Limited passage of fluids and solutes is allowed by intercellular clefts. Brain capillaries have no interruptions and form structural basis for blood-brain barrier.
2. Fenestrated capillaries are similar to continuous, but endothelium is littered with holes (fenestrae, “windows”) These fenestrations greatly increase permeability and are found where there is active capillary absorption or filtration (e.g. kidney, small intestine). For example, fenestrated capillaries in small intestine receive nutrients from ingested food.
3. Sinusoid capillaries (Sinusoids)-Most permeable capillaries with incomplete basement membrane. Found only in liver, spleen, bone marrow, and adrenal medulla. Capillary walls have large fenestrations, fewer tight junctions, and larger intercellular clefts than continuous capillaries. Allows for passage of large solutes and blood cells. Phagocytes in liver and spleen sit just outside sinusoids and protect blood by attacking bacteria or other foreign pathogens.
Capillaries converge to form venules, of which postcapillary venules are smallest. Postcapillary venules are entirely endothelium and are extremely permeable to fluid and white bed cells. Larger venules have a few layers of smooth muscle cells and thin tunica externa as well.
Venules converge to form veins, which have all three tunics, but thinner walls and larger lumens than corresponding arteries. Veins have relatively little smooth muscle or elastin in tunica media, while tunica externa is thickest. Large lumens and thin walls make veins capacitance vessels and blood reservoirs that can hold up to 65% of blood supply. Large lumen creates low resistance in veins. Additionally, venous valves, prevent backflow, particularly in veins of lower limbs where gravity opposes return of blood to heart.
3. Define atherosclerosis, arteriosclerosis, aneurysm, varicose vein, phlebitis.
Arteriosclerosis is hardening, thickening, and loss of elasticity in walls of arteries. Typically occurs in small arteries and arterioles. Results in reduced tissue blood perfusion and hypertension. Atherosclerosis is a particular type of arteriosclerosis in which there is a buildup of fatty plaques (atheromas) in the vessel wall which reduces the lumen size. Typically affects large and medium-sized arteries.
Atherosclerosis pathophysiology-Endothelial damage (hypertension, cigarette smoke, bacteria etc.) leading to inflammation. Damaged endothelium releases chemotactic factors and begin to pick up low-density lipoproteins (LDL’s) that transport cholesterol in the blood. LDL’s are oxidized in the immediate environment, damaging neighboring cells and attracting macrophages. Macrophages ingest oxidized LDL’s and transform into foam cells. Foam cells form the core of the fatty streak, the initial stage of the developing atheroma. Smooth muscle cells migrate over fatty streak secreting collagen and creating a fibrous cap over the foam cells. At this point, the lesion is called a fibrous or atherosclerotic plaque. Plaque can become unstable, and prone to rupture.
Aneurysm-balloon like outpocketing of artery wall that is at risk for rupture. Most commonly develops in abdominal aorta and arteries feeding brain and kidneys.
Varicose veins, are dilated veins due to incompetent venous valves. This may be caused by heredity, or conditions that hinder venous return, such as obesity or pregnancy. In either case, enlarged uterus or potbelly, downward pressure is exerted on vessels of groin, hindering venous return. Blood pools in lower limbs, valves weaken and venous walls stretch. Superficial veins with little support from surrounding tissues are particularly vulnerable.
Phlebitis-Inflammation of a vein accompanied by painful throbbing and redness of the skin over the inflamed vessel. Most often caused by bacterial infection or local physical trauma.
4. Define blood pressure (BP); include systolic, diastolic, pulse and mean arterial pressures.
Arterial blood pressure is pulsatile, reflecting the pressure when ventricle contracts (systole) and pressure when ventricle relaxes (diastole). Blood moves forward because pressure generated by heart exceeds that in distal arteries. When ventricle relaxes, elastic recoil of arteries maintains some blood pressure but is lower than systole. Difference between systolic and diastolic pressure is pulse pressure. In normal healthy adults, this value is about 40 mmHg (120 mmHg - 80 mm Hg). In atherosclerosis, vessels become less stretchy, and pulse pressure rises.
Most important pressure figure to consider is mean arterial pressure (MAP), the pressure that propels blood to the tissues. Since diastole lasts longer than systole (1/3 of time of cardiac cycle is systole; 2/3 of time is diastole), MAP = SBP(*1/3) + DBP(*2/3). In healthy human, MAP = 120/3 + 80(2/3) = 93 mm Hg. Both MAP and pulse pressure decrease as you move farther away from heart.
5. Briefly describe the theory behind the measurement of BP using a sphygmomanometer.
Sphygmomanometer is the blood pressure cuff. Typically wrapped around arm, proximal to elbow, superior to brachial artery pressure point. Cuff is inflated until pressure exceeds systolic pressure. This is achieved when blood flow to brachial artery is stopped and brachial pulse cannot be heard. Then reduce cuff pressure gradually and listen (auscultate) with a stethoscope for sounds in brachial artery. The pressure read when soft tapping sounds first come through brachial artery is systolic BP. Continue to reduce cuff pressure until no sounds (sounds of Korotkoff) are heard. The pressure at which sounds are no longer heard is diastolic pressure.
6. Describe, and explain the reasons for, the pressure changes that occur as blood flows from the left ventricle to the body and back to the right atrium.
Pressure is down to 35 mm Hg by the time blood reaches the capillaries, and 17 mm Hg by end of capillary beds. The primary factor in the drop in blood pressure along the vascular system is the cumulative effect of resistance as blood moves through the vascular tree. The biggest drop in pressure occurs across the arterioles, as they have small lumen, vasoconstrict to regulate bloodflow into the capillaries. Moreover, they have few elastic fibers, so pulse pressure is dampened out. Capillaries are delicate, so don’t need high pressure or flow, which would damage the vessels. Venous blood pressure is not pulsatile, but fairly steady, and goes from about 15 mm Hg, down to 0 mm Hg in blood returning to right atrium.
Blood pressure drops because of endless friction along vessel walls and low elasticity in arterioles, capillaries, and venous system.
7. Describe the physiology of capillary hemodynamics; include the factors that control the movement of fluids between capillaries and tissues in terms of hydrostatic and osmotic pressures, etc.
Gases and nutrients, and wastes pass between blood and interstitial space via diffusion, from area of high concentration to area of low concentration. Fluid moves via filtration. Lipid-soluble molecules (e.g. O2 and CO2) pass directly through endothelium. Small water-soluble substances (e.g. amino acids) diffuse through fenestrations or intercellular clefts. Large substances (e.g. proteins) pass via active transport across endothelium (transcytosis).
Filtration is determined by Starling forces (hydrostatic and oncotic pressures). Capillary hydrostatic pressure (HPc) is pressure exerted on interior of vessel wall by blood flowing through capillary, and is same as capillary blood pressure. HPc tends to push fluid out of the vessel into the interstitial space. Typically 35 mm Hg on arterial side and 17 mm Hg on venous side. Interstitial fluid hydrostatic pressure (HPif) acts on outside of capillary wall and tends to push fluid back into vessel. It is negligible and is typically considered to be zero. Colloid osmotic pressure, or oncotic pressure (OPc) is due to nondiffusable proteins (e.g. albumin) in the blood that draw fluid towards them. The OPc is typically about 26 mm Hg and opposes fluid leakage from vessel. Protein is minimal in interstitial space, so interstitial oncotic pressure (OPif) is 0.1-5 mm Hg and attracts fluid from vessel. Since the oncotic pressure is due to nondiffusable proteins, these forces do not vary significantly from one end of the capillary bed to the other.
Net filtration pressure (NFP) takes into account these 4 forces to determine whther there will be filtration (movement of fluid out of capillary) or reabsorption (movement of fluid into capillary). Filtration occurs at arterial side and reabsorption at venous side.
NFP = (HPc + OPif) - (OPc + HPif)
8. Discuss the factors that influence BP and blood flow; include peripheral resistance, vessel length & diameter & viscosity.
Blood flow is volume of blood flowing through vessel in a given time period (e.g. ml/min). For entire system, blood flow equals cardiac output. Blood pressure is force per unit area exerted on vessel wall by blood (mmHg). Blood flow = Pressure gradient/resistance
Resistance is opposition to blood flow, a measure of friction blood encounters as it travels through vessels. Since most is encountered outside heart, the term peripheral resistance is used. Three important components of resistance:
1. Blood viscosity, is internal resistance to flow of the liquid itself. Blood viscosity is increased by polycythemia (increase in RBCs), thus increasing resistance.
2. Total blood vessel length, is directly proportional to resistance. For example, as an infant grows, blood vessels lengthen and blood pressure rises.
3. Blood vessel diameter, is the most significant factor in blood pressure, because vessel length and blood viscosity are relatively constant. As blood vessel diameter narrows, more blood is in contact with wall, increasing resistance. Resistance varies inversely with the radius of the vessel raised to the 4th power. For example, doubling of vessel radius decreases resistance to 1/16 (2x2x2x2 = 16). Since large arteries don’t constrict much, major determinant of peripheral resistance in arterioles.
9. Discuss the homeostasis of BP; include the role of the cardiac and vasomotor centers of the medulla oblongata, baroreceptors, chemoreceptors and hormonal control. Define chronotropic and inotropic effects; cite examples. Discuss hypertension.
BP = CO x TPR, so TPR and CO vary directly with BP. Practically speaking, changes in BP are compensated for in order to maintain homeostasis. At rest, heart rate controlled by cardioinhibitory center in medulla oblongata, though PNS innervation of heart nodal tissue. In times of stress, cardioacceleratory center takes over, increasing heart rate and contractility via SNS innervation of nodal tissue and cardiac myocardium. Increased HR and SV increase CO and therefore, BP.
Short Term Regulation of BP: Neural Control
Short term regulation of heart rate is through modulation of peripheral resistance and blood volume. Cardiovascular center in medulla oblongata consists of cardiac center (cardioacceleratory and cardioinhibitory) and vasomotor center which control blood vessel diameter. Vasomotor center sends SNS efferent impulses mainly to arterioles. Generally, arterioles of skin and and digestive viscera receive vasomotor impulses more frequently and are more constricted than vessels serving skeletal muscle.
Cardiovascular center activity modified by:
1. Baroreceptor Reflexes: Baroreceptors, located in carotid sinuses, aortic arch, and walls of nearly every large artery in neck and thorax, are stretch receptors that respond to changes in blood pressure. When stretched, send impulses to inhibit cardioacceleratory and vasomotor centers, and stimulating the cardioinhibitory center. BP is reduced by arteriolar vasodilation, venodilation, and decreased CO by reducing SNS stimulation of heart. In this way, rapidly responding baroreceptors protect the circulation against acute BP changes.
2. Chemoreceptor Reflexes: Rise in CO2 or drop in pH or O2 content of blood stimulates chemoreceptors in aortic body (in aortic arch) or carotid bodies (in carotid sinus) to stimulate cardioacceleratory center to increase cardiac output. Chemoreceptors play much larger role in regulating respiratory rate.
3. Higher brain centers: Hypothalamus in particular can regulate cardiac centers through fight or flight response, and trough responses to exercise or changes in body temperature.
Short Term Regulation of BP: Hormonal Control
Catecholamines from adrenal medulla enhance SNS response by increasing cardiac output and causing generalized vasoconstriction.
Angiotensin II- in response to low blood pressure or blood volume, kidneys release renin, ultimately producing Ang II, which vasoconstricts, and which stimulates ADH and aldosterone release, which raise blood volume.
ANP- Produced by cardiac atria, ANP antagonizes aldosterone and promotes sodium and water excretion, reducing blood volume. Also promotes vasodilation.
ADH-Produced by hypothalamus, causes water reabsorption and at high concentration, stimulates blood vessel constriction to raise blood pressure.
Long Term Regulation of Blood Pressure
Long term regulation of BP is through renal modulation of blood volume either directly or indirectly. Direct renal mechanism is independent of hormones. As BP rises, the rate of glomerular filtration rises and cannot reabsorb all of fluid, so more water lost in urine. Conversely, as blood pressure falls, filtration goes down, more fluid is reabsorbed and blood volume is restored. Indirect mechanism involves renin-angiotensin-aldosterone system. When blood pressure goes down, juxtaglomerular cells of kidney release renin, which cleaves angiotensinogen to Ang I. Ang I is converted by ACE to Ang II and Ang II raises blood pressure by:
1. stimulating release of aldosterone from adrenal cortex.
2. directly stimulating sodium reabsorption by kidneys.
3. stimulating release of ADH from posterior pituitary.
4. activating hypothalamic thirst center, increasing fluid intake.
5. acting as potent vasoconstrictor
Hypertension: Chronically elevated blood pressure of systolic >140 mm Hg or diastolic > 90 mm Hg. Typically a “silent killer”, patients are asymptomatic for 10-20 years, chronically elevated BP strains heart, arteries, and kidneys, causing renal failure, heart failure, stroke, and vascular disease. 90% of patients have primary hypertension in which no underlying cause is identified. Multifactorial contributions from heredity, diet (high salt, saturated fat, and cholesterol), obesity, age, diabetes mellitus, stress, smoking. Secondary hypertension due to renal disease or hyperthyroidism, for example.
10. Describe venous blood flow; include factors which aid in venous return.
Venous pressure is normally too low to promote adequate blood return to heart. 3 adaptations in venous circulation address this:
1. Muscular pump-When skeletal muscle contract, they compress veins, opening upstream venous valves and closing downstream valves.
2. Respiratory pump- When we inhale, pressure in thoracic cavity goes down, allowing thoracic veins to expand and deliver blood to right atrium. At the same time, abdominal pressure increases, forcing blood towards the heart.
3. SNS innervation of veins causes vasoconstriction, increasing venous return.
11. Describe circulatory shock; distinguish between the major types.
Circulatory shock occurs when blood vessels are inadequately filled and blood cannot circulate sufficiently to meet tissue needs. There are three major types.
1. Hypovolemic shock is most common type, and results from large-scale fluid loss (e.g. burns) or blood loss (e.g. hemorrhage). Blood volume drops, so HR increases and vasoconstriction occurs to raise BP and shift blood from reservoirs to major circulatory channels.
2. In vascular shock, blood volume is normal, but circulation is compromised due to extreme vasodilation. Peripheral resistance and BP drop rapidly. Can occur in anaphylactic shock (severe allergic reaction), neurogenic shock (failure of ANS), or sepsis (bacterial infection).
3. Cardiogenic shock occurs when heart muscle is damaged, so can’t sustain adequate pumping of blood. Usual cause is multiple heart attacks.
12. Identify on a diagram and vascular model the major arteries and veins listed on the "Vascular System" handout. For each, know the function/area served.
13. Describe the fetal circulatory system; discuss the general reasons for this system and include the general path of blood flow and the functions of the umbilical vein, ductus venosus, foramen ovale, ductus arteriosus, and umbilical arteries.
Umbilical artery goes out from fetus and picks up oxygen from placenta and carries it back to fetus via umbilical vein. Maternal liver metabolizes nutrients so blood in fetus largely bypasses the liver (ductus venosus) in order to deliver oxygenated blood to the fatal brain quicker. Foramen ovale is shunt between right atrium and left atrium. Ductus arteriosus is shunt between pulmonary trunk and aorta. Both of these shunts allow blood to largely bypass the fetal lungs where gas exchange does not occur.