Chapter 21: Blood Vessels and Circulation

1. Chapter 21: Blood Vessels and Circulation BIO 211 Lecture Instructor: Dr. Gollwitzer

2. Today in class we will discuss: • The relationship between blood flow and • Cardiac output • Pressure and resistance • Pressure differences in various vessels in the CVS • Blood pressure , mean arterial pressure, and pulse • The basis for systolic pressure and diastolic pressure • Total peripheral resistance and its major components

3. Cardiovascular Physiology • Goal of cardiovascular physiology • To maintain adequate blood flow through peripheral tissues and organs • Cardiovascular system (CVS) continuously adjusted to maintain homeostasis • Contracting ventricle must produce enough tension to force open the semilunar valve and eject blood • Determined by interplay between pressure and resistance in cardiovascular network • If no resistance to blood flow, heart would not have to generate pressure to force blood through pulmonary and systemic circuits

4. Cardiovascular Physiology Figure 21-8

5. Cardiovascular Physiology • Cardiac output (CO) • Normally = blood flow • When CO goes up, blood flow through the capillary beds goes up; and vice versa • Blood (arterial) pressure (BP) • Responsible for maintaining blood flow within capillaries • Peripheral resistance controls: • Blood flow • Capillary pressure • Drives exchange via diffusion and osmosis between blood and interstitial fluid • Venous pressure • Due to venoconstriction • Aided by valves, skeletal muscle contraction • Venous return • Brings blood back to heart

6. Cardiovascular Pressures • General concepts • Liquids, including blood, cannot be compressed • Force exerted against an enclosed liquid (blood in CVS) generates hydrostatic pressure • If pressure gradient exists, hydrostatic pressure will push liquid from an area of higher pressure to an area of lower pressure

7. Cardiovascular Pressures • Pressure gradient of systemic circuit = circulatory pressure (approx 100 mm Hg) • Difference between pressure at base of ascending aorta (100 mm Hg) and entrance to R atrium (2 mm Hg) • This pressure needed to force blood through arterioles (resistance vessels) and into peripheral capillaries

8. Cardiovascular Pressures • 3 components • Blood pressure (BP) • = force exerted against vessel walls by blood in vessels in systemic arterial system • Ranges from 100 at heart to 35 mm Hg at start of capillary network • Capillary blood flow is directly proportional to BP • Capillary hydrostatic pressure • = Pressure in capillary beds • Declines from 35 to 18 mm Hg along length of capillary • Venous pressure • = Pressure in venous system • Pressure gradient from venules to R atrium approx. 18 mm Hg (ranges from 18 to 2 mm Hg)

9. Figure 20–1

10. Pressures in the Systemic Circuit Figure 21-10

11. Arterial Blood Pressure • Important because it maintains blood flow through capillary beds • Must be high enough to overcome peripheral resistance • Not stable • Rises during ventricular systole and falls during ventricular diastole • Systolic pressure (SP) = peak arterial pressure during ventricular systole • Diastolic pressure (DP) = minimum arterial pressure during diastole

12. Arterial Blood Pressure • Measure with sphygmomanometer • Compress brachial artery • Place stethoscope over artery, distal to compress • Inflate cuff until pressure is great enough to collapse artery and blood flow stops, pulse is eliminated • Let air out slowly • When pressure is less than SP = blood enters, pulse appears • When pressure is less than DP = pulse disappears and flow is continuous • Record by separating systolic and diastolic pressures by a slash mark (e.g., 120/80) • Normal = 120/80

13. Arterial Blood Pressure • Pulse • = Rhythmic pressure oscillation that accompanies each heart beat • Common site: inner wrist (radial artery pressed against radius) • Pulse pressure (PP) • = Difference between systolic and diastolic pressure (i.e., SP-DP) • Mean arterial pressure (MAP) • = Diastolic pressure + (pulse pressure/3), e.g., • If SP = 120, DP = 80 • MAP = 80 + ((120-80)/3) = 80 + 13 = 93 mm Hg

14. Resistance • Any force that opposes movement of fluid • Resistance of CVS • Due to friction between blood and vessel walls • Opposes movement of blood • The greater the resistance, the slower the movement of blood • For circulation to occur, pressure gradient must be great enough to overcome total peripheral resistance = resistance of the entire CVS (mostly arterial resistance b/c venous resistance so low)

15. Peripheral Resistance • = Resistance of the arterial system • For blood to flow into peripheral capillaries the pressure gradient must be great enough to overcome peripheral resistance • 3 sources of peripheral resistance • Vascular resistance (resistance of blood vessels) • Viscosity • Turbulence

16. Peripheral Resistance:Vascular Resistance • = Resistance of blood vessels • Largest component of peripheral resistance • Due to friction between blood and vessel wall • Depends on: • Vessel length • Vessel diameter

17. Peripheral Resistance:Vascular Resistance • Vessel length • Resistance directly proportional to length, i.e., pulmonary vs. systemic circuit • Constant in adults • Vessel diameter • Much greater effect on resistance • Effects of friction occur in zone close to vessel wall • In large diameter vessel, blood near center does not encounter resistance • In small diameter vessel, nearly all blood is slowed by friction with walls • Increases exponentially as vessel diameter decreases • ½ diameter = 16 X resistance • Mechanisms that alter diameter of arterioles provide control over peripheral resistance and blood flow • Vessel diameter varies by vasodilation (bigger) and vasoconstriction (smaller) • Most resistance occurs in arterioles (smallest diameter) = resistance vessels

18. Figure 21-10 a, c

19. Peripheral Resistance: Viscosity • = Resistance to flow caused by interactions among molecules in a liquid • Low viscosity liquids (water) flow at low pressure • Blood is 4X as viscous as water due to presence of plasma proteins and blood cells • Viscosity remains stable except in anemia, polycythemia (elevated hematocrit) and other disorders that affect hematocrit

20. Peripheral Resistance: Turbulence • = Swirling action disturbs smooth flow of blood • Created by: • High flow rates • Between atria and ventricles • Between ventricles and trunks • In aorta • Irregular surfaces, e.g., • Scar tissue • Atherosclerotic plaques • Sudden changes in vessel diameter, e.g., • Vasoconstriction • Slows flow and increases resistance • Does not develop in small vessels except when damaged

21. Figure 21-10 b, c

22. Figure 21-10 b, d

23. Vascular Pathology • Arteriosclerosis • = Thickening and toughening of arterial walls; hardening of the arteries • Complications account for half of all deaths in US • CAD (coronary artery disease) = arteriosclerosis of coronary vessels • Stroke = result of arteriosclerosis of arteries supplying brain

24. Vascular Pathology • Arteriosclerosis (Cont.) • 2 Forms of arteriosclerosis • Focal calcification • = Gradual degeneration of smooth muscle in tunica media and deposition of Ca2+ salts • Typically involves arteries of limbs and genitals • Rapid and severe calcification may occur as complication of diabetes mellitus • Atherosclerosis • Aka: Fatty degeneration • = Damage to endothelial lining and formation of lipid deposits (plaque) in tunica media • Most common form of arteriosclerosis

25. Vascular Pathology • Arteriosclerosis (Cont.) • Factors involved in development • Lipid levels; high cholesterol • High lipids in blood for an extended period of time • Monocytes begin removing them and become filled with lipid droplets (foam cells) • Attach to endothelial walls, release growth factors that stimulate smooth muscle to divide near the tunica interna, thickening the vessel wall, decreasing diameter • Other monocytes migrate resulting in a fatty mass of tissue (plaque) that projects into lumen • Because cells swollen with lipids, gaps appear in endothelial lining • Platelets appear to repair, clot forms which further restricts blood flow • High blood pressure, smoking, diabetes mellitus, obesity, stress, chronic bacterial infection, chronic inflammation

26. Vascular Pathology • Hypertension • = Abnormally high BP (>140/90) • Increases workload on heart, L ventricle gradually enlarges, more muscle mass • Greater O2 demand, coronary circulation can’t keep pace, eventually coronary ischemia (inadequate blood supply) • Increases stress on walls of blood vessels, accelerates development of arteriosclerosis and aneurysms • Hypotension • Abnormally low BP (SP < 90 mm Hg)

27. Today in class we will discuss: • The importance of maintaining adequate blood flow through the capillaries and the mechanisms involved in capillary exchange • Venous return and its role in moving blood • How autoregulatory, neural, and hormonal mechanisms compensate for a reduction in blood flow and blood pressure • How the cardiovascular system responds to hemorrhage

28. Capillary Exchange • As blood flows through peripheral tissues, BP forces water and solutes out of plasma, across capillary walls • Most of water is reabsorbed by capillaries • A portion (approx. 3.6 L) enters the lymphatic system and eventually re-enters bloodstream

29. Blood-lymph Cycle • = Continuous movement of water out of the capillaries, through peripheral walls, to lymphatics, then back to bloodstream • Has 4 important functions • Ensures plasma and interstitial fluid are in constant communication • Accelerates distribution of nutrients, hormones, dissolved gases through tissues • Transports insoluble lipids and tissue proteins that can’t cross capillary walls • Flushes bacterial toxins and chemicals into immune system tissues

30. Capillary Exchange • 3 processes involved in moving materials across capillary walls • Filtration • Diffusion • Reabsorption

31. Forces Across Capillary Walls Figure 21-13

32. Capillary Exchange • Filtration • Driving force is hydrostatic pressure • Forces water out of a solution from high to low pressure area (35 mm Hg in capillaries vs. 25 mm Hg in tissues) • When water is forced out of capillary walls, small solute particles travel with the water • Larger molecules and protein stay in bloodstream • Because BP drops from 35 to 18 mm Hg in capillaries, filtration occurs mostly at the arterial end

33. Capillary Exchange • Diffusion • = Movement of ions or molecules from high to low concentration • Does not involve pressure effects • Primary route for capillary exchange

34. Capillary Exchange • Capillary diffusion occurs by 5 routes • Between endothelial cells, e.g., water, ions, small organic compounds (glucose, amino acids, urea) • Through channels in cell membrane, e.g., water, Na+, K+, Ca2+, Cl- ions • At fenestrated capillaries, e.g., above and large water-soluble compounds otherwise unable to leave bloodstream • Found in hypothalamus, kidneys, endocrine organs, intestinal tract • Through endothelial cell membranes, e.g., lipids (FAs, steroids), lipid-soluble materials including gases (O2 and CO2 • In sinusoids, e.g., where plasma proteins are produced and enter bloodstream in liver

35. Capillary Exchange • Reabsorption • Result of osmosis = diffusion of water across membrane toward higher solute concentration, e.g, blood + plasma proteins • From arterial to venous ends of capillaries, rates of filtration and reabsorption change at about 25 mm Hg • Filtration higher at beginning and reabsorption higher at end • Of the 24 L of fluid that moves out of capillaries every day, 85% is reabsorbed • Remainder enters lymphatic vessels and eventually venous system

36. Capillary Exchange • Summary • Hydrostatic pressure • Forces water and solutes out of capillaries • Into interstitial fluid • At arterial end of capillary • Osmotic pressure • Pulls water and solutes into capillaries • Out of interstitial fluid • At venous end of capillary

37. Edema • = Abnormal accumulation of interstitial fluid (ECF) • Filtration out > reabsorption in • Results from a disturbance between hydrostatic and osmotic forces at capillary level • Causes • Damage to capillary, increase BP from heart problems, blockage of lymphatic vessels, kidney failure

38. Venous Pressure and Venous Return • BP very low at venules (18 mm Hg), but they provide very little resistance • As blood approaches heart • Veins become larger • Resistance drops even more • Velocity of blood increases • When individual stands, venous blood entering IVC must overcome gravity

39. Venous Pressure and Venous Return • 2 factors help venous blood overcome gravity • Muscular compression • Muscular contraction near vein push blood toward heart because of 1-way valves • Is why standing still for long time results in little blood flow to the brain and person faints • Respiratory pump • When inhale: • Thoracic cavity expands • Pressure in pleural cavities drops • Pulls air into lungs • Also pulls blood into IVC and R atrium from smaller veins in abdominal cavity • When exhale: • Pressure in pleural cavities rises • Pushes blood into R atrium • Important during heavy exercise

40. Cardiovascular Regulation • 3 Regulatory mechanisms control cardiovascular function, i.e, CO and BP • Autoregulation • Local factors at tissue level cause immediate, localized adjustments • Neural mechanisms • Respond quickly to changes at specific sitesflex control • Endocrine mechanisms • Direct long-term changes

41. Cardiovascular Responses Figure 21-13, 8th edition

42. Cardiovascular Regulation:Autoregulation • Local factors change pattern of blood flow in capillary bed in response to chemical changes in interstitial fluid • Affect precapillary sphincters • Local vasodilators – dilate sphincters • Accelerate blood flow through tissues brings O2, other nutrients to restore homeostasis • e.g., low O2 or high CO2, lactic or other acid, NO, high K+ or H+, histamine, high temperatures • Local vasoconstrictors – constrict sphincters • e.g., compounds produced by platelets and damaged tissues (antihemorrhage prostaglandins and thromboxanes from platelets and WBCs) • Cause immediate, localized hemostatic adjustments • If this fails, then neural and endocrine factors activated

43. Cardiovascular Regulation:Neural Mechanisms • Reflexes regulated through negative feedback loop • 2 types of reflex control • Baroreceptor reflexes • Chemoreceptor reflexes

44. Cardiovascular Regulation • Special cardiovascular receptors monitor conditions • Baroreceptors • Monitor and respond to stretch in blood vessels and atrium • Chemoreceptors • Monitor composition of arterial blood and CSF • Respond to changes in CO2, O2, or pH in blood • Found near carotid sinus (carotid bodies) and aortic arch (aortic bodies) • Receptors trigger neural reflex arcs to neurons in cardiovascular centers in medulla oblongata

45. Cardiovascular Regulation:Neural Mechanisms • Baroreceptor reflexes • Stretch receptors respond to changes in BP • Found in vessel walls and heart (carotid sinuses, R atrium, aortic sinuses) • Controlled by ANS • When BP increases, CV centers • Dec HR • Cause peripheral vasodilation  dec BP • When BP decreases, CV centers • Inc HR and stroke volume • Cause peripheral vasoconstriction  inc BP • Maintains normal/adequate arterial pressure

46. Baroreceptor Reflexes Figure 21-14, 8th edition

47. Cardiovascular Regulation:Neural Mechanisms • Chemoreceptor reflexes • Receptors respond to changes in O2, CO2 levels and pH in blood and CSF • Found in aortic bodies, carotid bodies, and medulla oblongata • Lead to increased HR and BP by sympathetic activation or decreased by parasympathetic activation

48. Chemoreceptor Reflexes Figure 21–15

49. Cardiovascular Regulation:Endocrine Mechanisms • Short-term regulation • Of cardiac output and peripheral vasoconstriction (resistance) • With E and NE • Long-term regulation • Of BP and/or volume • With: • ADH – increases BP and volume • Angiotensin II – increases BP and volume • Erythropoietin – increases volume • Atrial natriuretic peptide (ANP) - decreases volume

50. Cardiovascular Regulation:Endocrine Mechanisms • ADH • Released from post pit in response to: • Low blood volume • High plasma Na+ • Angiotensin II • Immediate result is vasoconstriction that increases BP • Stimulates conservation of water at kidneys which prevents further drop in blood volume