1. Vessels and Circulation
Chapter 19.
Vessels and Circulation

2. Quiz Thurs On Chap 18 Heart
Exam next Thurs on 18, 19 (more about this next time)

3. Overview Classes of blood vessels and their structures
Cardiovascular physiology
Circulatory pressures
Capillary exchange
Cardiovascular regulation
Vascular diseases
Vessels to know (repeat from lab)

4. Blood Vessels Closed system of tubes that starts and ends at the heart
Arteries: large vessels that carry blood away from heart
Arterioles: smallest branches of arteries
Capillaries: smallest blood vessels with a small diameter and thin walls; location of exchange between blood and interstitial fluid (exchange vessels)
Venules: smaller branches of veins collect blood from capillaries
Veins: Larger vessels that return blood to heart

5. Structure of Vessel Walls
Figure 21-1

6. Generalized Structure of Blood Vessels
Arteries and veins are composed of three tunics – tunica interna, tunica media, and tunica externa
Lumen – central blood-containing space surrounded by tunics
Capillaries are composed of endothelium with sparse basal lamina

7. Artery and Vein Walls – 3 layers
Tunica Interna (Intima): innermost layer
endothelial lining of all vessels
In vessels larger than 1 mm, a subendothelial connective tissue basement membrane is present
In arteries only the internal elastic membrane is a layer of elastic fibers in outer margin
Tunica Media: middle layer
concentric sheets of smooth muscle in loose connective tissue
regulated by sympathetic nervous system
Controls vasoconstriction/vasodilation of vessels
External elastic membrane (arteries only) separates tunica media from tunica externa
Thickest layer in a small artery

8. Artery and Vein Walls – 3 Layers
Tunica Externa (adventitia): outer layer
Connective tissue sheath with collagen fibers
Anchors vessel to adjacent tissues
Thick in veins
Larger vessels contain vasa vasorum
In arteries:
collagen fibers
elastic fibers
In veins:
smooth muscle cells

9. Vasa Vasorum
Small arteries and veins found in the walls of large arteries and veins
These are the blood supply for the large vessels
Supply cells of tunica media and tunica externa with oxygen and nutrients
Why don’t you need these in capillaries?

10. Arteries vs. Veins at a glance
Arteries and veins run side-by-side
Arteries have thicker walls and higher blood pressures
Collapsed artery has small, round lumen
Vein has a large, flat lumen
Vein lining contracts, artery lining does not
Artery lining folds
Arteries more elastic
Veins have valves
Arteries thick t. media, veins thick t.externa

11. Vessel Composition

12. Arteries
Elasticity allows arteries to absorb pressure waves that come with each heartbeat
Contractility: arteries change diameter, controlled by sympathetic division of ANS
Vasoconstriction: contraction of arterial smooth muscle by the ANS, shrinking lumen
Vasodilation: The relaxation of arterial smooth muscle, enlarging lumen

13. Vasoconstriction and Vasodilation
Active processes that affect:
afterload on heart (how?)
peripheral blood pressure (how?)
capillary blood flow
Note: elasticity of the arteries also allows them to expand and contract passively in response to changes in blood pressure

14. Structure of Blood Vessels
Figure 21-2

15. Vascular Components

16. Artery Characteristics
From heart to capillaries, arteries change characteristics (along a continuum):
Elastic arteries (conducting arteries)
Large vessels (e.g. and aorta) dmax = 2.5cm, lumen allow low-resistance conduction of blood
Contain elastin in all three tunics
Withstand and even out large blood pressure fluctuations
Serve as pressure reservoirs
Tunica media has many elastic fibers and few muscle cells
Muscular arteries (distribution arteries)
Medium-sized davg =0.4cm
Account for most arteries
Thick tunica media has many muscle cells
Active in vasoconstiction
Arterioles (resistance vessels)
Smallest arteries (d ≤ 30micons)
Have little or no tunica externa, thin or incomplete media
Contol blood flow into capillaries by change diameter in response to ANS, local conditions

17. Artery Diameter and Resistance
Small muscular arteries and arterioles changes diameter with sympathetic or endocrine stimulation (vasomotor response)
Decreasing diameter increases resistance, the force opposing blood flow
Arterioles also called resistance vessels

18. Aneurysm Bulge in an arterial wall
Caused by weak spot in elastic fibers
Pressure may rupture vessel

19. Capillaries Are smallest vessels with thin walls (davg = 8 microns)
We have about 10 billion or 25,000 miles
Have only a tunica interna, one cell thick
Pericytes on the outer surface stabilize their walls
Microscopic capillary networks permeate all active tissues
Blood flow through caps is slow
Exchange occurs here: materials diffuse between blood and interstitial fluid
All living cells no more than 125um from a cap

20. 3 Types of Capillaries Continuous Fenestrated Sinusoids
Abundant in skin and muscles
Have complete endothelial lining, connected by tight junctions
Small clefts permit diffusion of water, small solutes, and lipid soluble material (but NOT blood cells or plasma proteins)
thymus and brain have specialized continuous capillaries (barriers)
Fenestrated
Have pores in endothelial lining (not gaps between cells)
Permit more rapid exchange of water and larger solutes between plasma and interstitial fluid
Found in: choroid plexus, kidneys, intestinal tract, and?
Sinusoids
Modified fenestrated capillaries
Very leaky, with large gaps between adjacent endothelial cells that allow large molecules (plasma proteins) and cells through
Found only in: Liver, spleen, bone marrow, other lymphoid tissues, used for phagocyte monitoring, plasma protein entry from liver

21. Capillary Structure
Figure 21-4

22. Capillary Networks One arteriole gives rise to several capillary beds
Each Capillary bed connects 1 arteriole to 1 venule
Each capillary entrance guarded by precapillary sphincter

23. Capillary Bed – key parts
Capillaries
10 to 100 capillaries per capillary bed, they branch off the metarteriole and return to the thoroughfare channel at the distal end of the bed
Thoroughfare Channels
Are direct capillary connections between arterioles and venules
Controlled by smooth muscle segments called metarterioles found at channel entrance
Collaterals
Multiple arteries contribute to one capillary bed and allow circulation if one artery is blocked
Arterial anastomosis = fusion of two collateral arteries
Arteriovenous Anastomoses
direct connections between arterioles and venules allow blood to bypass the capillary bed

24. Capillary Networks
Figure 21-5

25. Precapillary Sphincters
Guards entrance to each capillary
Open and close, causing capillary blood to flow in pulses
Vasomotion:
Contraction and relaxation cycle of capillary sphincters
Causes blood flow in capillary beds to constantly change routes
Contract/relax on the order of 10 times/min
Causes capillary flow to pulse
Controlled by autoregulation (see later)

26. Closed precapillary sphincters

27. Capillary Volume
At rest, blood is flowing in about 25% of your capillaries
When you begin to exercise, vessels must redistribute blood within the capillary network (you can’t just open up more capillaries)
If all your capillaries open at once: shock

28. Veins
Collect blood from capillaries in all tissues and organs and return it to heart
Larger in diameter than arteries, but have thinner walls and much lower blood pressures
Tunica externa is usually thickest layer
Capacitance vessels (blood reservoirs) that contain 65% of the blood supply
Classified on the basis of size

29. Vein Characteristics Venules Medium Sized Veins
Collect blood from capillaries
Average diameter of 20um, resemble capillaries in structure
Allow fluids and WBCs to pass from the bloodstream to tissues
Medium Sized Veins
thin tunica media and few smooth muscle cells
Thickest part is tunica externa with longitudinal bundles of elastic fibers and collagen
Size ranges from 2-9mm
Large Veins (e.g. sup/inf vena cava)
have all 3 tunica layers
thick tunica externa with thin tunica media

30. Vein Valves Valves are folds of tunica interna
Resemble semilunar heart valves
Prevent blood from flowing backward
Compression from muscular contractions (even rotation in isometric contractions) pushes blood toward heart
Not so important when laying down
Compartmentalize blood flow: blood return from below heart is like a boat traversing several locks to get up a hill

31. Valves in the Venous System
Figure 21-6

32. Blood Distribution
Figure 21-7

33. Blood Distribution Heart, arteries, and capillaries: Venous system:
30–35% of blood volume
Venous system:
60–65%
Fully 1/3 of venous blood is in the large venous networks of the liver, bone marrow, and skin (some of this is part of the venous reserve)

34. Capacitance
The ability to stretch or the relationship between blood volume and blood pressure
Veins (capacitance vessels) stretch more than arteries (8x as much as arteries)
Lower resistance = higher capacitance = expands easily at low pressures
Means veins can accommodate large changes in blood volume

35. Veins Response to Blood Loss
Vasomotor centers (medulla) stimulate sympathetic nerves
Venoconstriction = smooth muscles in systemic medium sized veins constrict
Affects blood pressure in venous system but major effect is to cause veins in liver, skin and lungs to redistribute venous reserve back to arterial system (about 20% of total blood)

36. Cardiovascular Physiology
Figure 21-8

37. Cardiovascular Physiology
Cardiac output = blood flow
Determined by pressure and resistance in the cardiovascular system
Force is proportional to pressure gradient
Pressure (P)= force the heart generates to overcome resistance
Absolute pressure is less important than pressure gradient
Pressure Gradient (P) = the difference between pressure at the heart and pressure at peripheral capillary beds
resistance

38. Blood Flow, Pressure, and Resistance
Blood flow (F) is directly proportional to the difference in blood pressure (P) between two points in the circulation
If P increases, blood flow speeds up; if P decreases, blood flow declines
Blood flow is inversely proportional to resistance (R)
If R increases, blood flow decreases
R is more important than P in influencing local blood pressure
The differences in pressure within the vascular system provide the driving force that keeps blood moving, always from higher to lower pressure area

39. Measuring Pressure Blood pressure (BP):
arterial pressure (mm Hg)
Pressure required to move blood
Capillary hydrostatic pressure (CHP):
pressure within the capillary beds
pressure where diffusion and osmosis occur
Venous pressure:
pressure in the venous system
Circulatory Pressure: ∆P across the systemic circuit (about 100 mm Hg)

40. Resistance Resistance – opposition to flow
Measure of the amount of friction blood encounters
Generally encountered in the systemic circulation
Referred to as peripheral resistance (PR)
Circulatory pressure must overcome total peripheral resistance of entire cardiovascular system which comes from 3 sources:
Vascular resistance (length and diameter)
Blood viscosity
Turbulence

41. Peripheral Resistance: vascular resistance
Vascular resistance (= major factor): R of blood vessels due to friction between blood and vessel walls depends on vessel length and vessel diameter
Adult vessel length is constant
Vessel diameter varies by vasodilation and vasoconstriction
R increases exponentially (4th power!) as vessel diameter decreases (double the radius, decrease resistance by 16x)

42. Peripheral Resistance: viscosity and Turbulence
Viscosity also increases resistance
Normal whole blood viscosity is about 4-5 times that of water, changes with hematocrit
Turbulence: swirling action that disturbs smooth flow of liquid
Occurs in heart chambers and great vessels
Atherosclerotic plaques cause abnormal turbulence

43. Overview of Circulatory Pressures: Arteries
Largest pressure gradient is between aorta and proximal end of capillary beds (100  35mmHg so gradient = 65)
This part of the system also has the highest resistance.
Both the pressure (CO) and the resistance (vasomotor tone) can be regulated, determining the rate of flow in the capillaries

44. Overview of Circulatory Pressures: Capillaries
Blood at the proximal (arterial) side of cap beds has pressure of 35mmHg
At distal end, where blood enters venules, pressure is 18mmHg
Low capillary pressure is desirable because high BP would rupture fragile, thin-walled capillaries
Low BP is sufficient to force filtrate out into interstitial space and distribute nutrients, gases, and hormones between blood and tissues

45. Overview of Circulatory Pressures: Veins
Blood entering venules is 18mmHg, enters right atrium at 0 - 2mmHg so gradient = 18mmHg (pretty small)
However, veins provide very low resistance and so they don’t require great pressures for blood to move
As blood gets closer to heart, veins get larger and larger, decreasing resistance. This doesn’t increase the pressure but it does increase the velocity of blood flow

46. Systemic Blood Pressure
Figure 19.5

47. Vessel Diameter Cross-Sectional Area Average Systemic Blood Pressure
Systemic Blood Velocity

48. What the graphs show Arteries  caps (divergence)
Caps veins (convergence)
Blood pressure and velocity are proportional to the TOTAL cross sectional area of all vessels
As total cross-sectional area increases, avg. blood pressures and velocities decline
Velocity continues to decline until the veins, where cross sectional areas increase (reducing friction)
Velocity is slowest at capillaries and flow allows adequate time for exchange between blood and tissues

49. Pressures in the Systemic Circuit
Systolic pressure:
peak arterial pressure during ventricular systole
Diastolic pressure:
minimum arterial pressure during diastole
Pulse pressure:
difference between systolic pressure and diastolic pressure
Mean arterial pressure (MAP):
MAP = diastolic pressure + 1/3 pulse pressure

50. Pressure and Distance
MAP and pulse pressure decrease with distance from heart
Blood pressure decreases with friction
Pulse pressure decreases due to elastic rebound
Near the heart, BP pulses
By the arterioles, pulsing is gone (if you cut a vein it will bleed continuously; an artery spurts)

51. Elastic Rebound
Elastic rebound = Ability of arteries to expand and recoil
Arterial walls:
stretch during systole
rebound during diastole
keeps blood moving during diastole
Dampens the effect of the pulse:
By the time the blood reaches the arterioles, flow is continuous

52. Abnormal Blood Pressure
Hypertension:
abnormally high blood pressure, greater than 140/90
High diastolic can be very dangerous
Hypotension:
abnormally low blood pressure

53. Venous Return Amount of blood arriving at right atrium each minute
Both pressure and resistance are low in venous system
Venous BP alone is too low to promote adequate blood return and is aided by
the respiratory pump: pressure changes created during breathing suck blood toward the heart by squeezing local veins. Becomes a larger factor as breathing rate increases.
compression of skeletal muscles, pushes blood toward heart (one-way valves)

54. Capillary Diffusion Routes
Oxygen and nutrients pass from the blood to tissues
Carbon dioxide and metabolic wastes pass from tissues to the blood
Water-soluble solutes pass through clefts and fenestrations
Lipid-soluble molecules diffuse directly through endothelial membranes
Plasma proteins cross endothelial lining in sinusoids only

55. Capillary Exchange
Capillary Exchange is fluid movement between capillaries and interstitial space
Capillary pressure normally forces water and solutes OUT into the tissues
vital to homeostasis, creates and circulates interstitial fluid
moves materials across capillary walls by:
Filtration
Reabsorption (diffusion)

56. Filtration
Filtration: the removal of solutes through a porous membrane, driven by hydrostatic pressure
Hydrostatic pressure = pressure exerted by a fluid (at rest or while flowing)
Capillary filtration: water and small solutes forced through capillary wall, leaving behind larger solutes in bloodstream

57. Capillary Filtration
Figure 21-11

58. Reabsorption
Occurs via osmosis, where water enters the solute compartment with higher osmotic pressure
Solutes in a solvent generate a pressure = Osmotic pressure:
equals pressure required to prevent osmosis
is a pulling force generated by solutes in a solution that cannot cross the membrane

59. Overview: Osmotic and Hydrostatic Pressures
forces water out of a solution compartment
Osmotic pressure:
forces water into a solution compartment
Balance between them controls filtration and reabsorption through capillaries

60. Forces Across Capillary Walls
Figure 21-12

61. Hydrostatic Pressures
Capillary hydrostatic pressure (HPc): pressure within the capillary beds generated by heart pumping
Ranges from 35 at arterial end to 18 at venous end
Interstitial fluid hydrostatic pressure (HPif): pressure generated by mechanical force pushing fluid back into the blood
Different in different tissues but overall average is 0
Net Hydrostatic Pressure (NHP): The difference between HPc and HPif
HPc is higher, so net pushes water and solutes out of capillaries into interstitial fluid (this is filtration)

62. Osmotic Pressures
Capillary Colloid Osmotic Pressure (OPc) = 25 mmHg normally because suspended plasma proteins are too large to cross capillary walls thus they exert an osmotic pressure that pulls water back into the capillary
Also called oncotic pressure
Interstitial Fluid Colloid Osmotic Pressure (OPif) = effectively zero under normal conditions because there is no pressure exerted by suspended proteins outside cells
Net Colloid Osmotic Pressure (NCOP): The difference between OPc and OPif
OPc is higher and so it pulls water and solutes into capillary from interstitial fluid (this is reabsorption)

63. Net Filtration Pressure (NFP)
NFP – all the forces acting on a capillary bed
The difference between net hydrostatic pressure and net osmotic pressure
NFP = (NHP) – (NCOP)
NFP = (HPc – HPif) – (OPc – OPif)
NFPArt = (35 – 0) – (25 – 0) = +10 mmHg (out)
NFPVen = (18 – 0) – (25 – 0) = -7 mmHg (in)

64. Capillary Exchange
At arterial end of capillary bed hydrostatic forces dominate:
fluid moves out of capillary into interstitial fluid = filtration
At venous end of capillary osmotic forces dominate:
fluid moves into capillary out of interstitial fluid = reabsorption
But what about in between?
Transition Point = point along cap bed where filtration switches to reabsorption.
If this were right in the middle, what would the net result be (filtration, reabsorption?)

65. Capillary Exchange
Since we know which one dominates (right?) the question is, where is the transition point?
Closer to the arterial end or to the venous end?

66. Forces Across Capillary Walls
Figure 21-12

67. Summary: Forces in the capillary bed
Hydrostatic pressure tends to push water and solutes OUT OF blood, into interstitial fluid
Colloid osmotic pressure tends to pull water and solutes INTO capillary
Net filtration pressure is the difference between the NHP and NCOP
At proximal end, NHP is higher
At distal end, NCOP is higher

68. The Transition Point
Transition occurs closer to distal (venous) end, thus capillaries filter more than reabsorb so more fluids enter the tissue beds than return to the blood,
Excess fluid enters interstitial space, becomes interstitial fluid (net 3.6L/day)
Eventually, fluid will enter lymphatic vessels, become lymph
Then what?

69. Changes in Capillary Dynamics
Hemorrhaging:
reduces HPc and thus NFP
increases reabsorption of interstitial fluid (called recall of fluids)
Dehydration:
increases OPc, decreases NFP
Also accelerates reabsorption (recalls fluids)
Increase in HPc or decline in OPc :
Happens in starvation, heart failure
fluid moves out of blood
builds up in peripheral tissues (edema)

70. Cardiovascular Regulation
Goal is to maintain adequate Tissue Perfusion, blood flow through the tissues
Carries O2 and nutrients to tissues and organs, carries CO2 and wastes away
Is affected by:
cardiac output (HR, stroke volume)
peripheral resistance (vessel diameter)
blood volume
Blood pressure = CO x PR

71. Cardiovascular Regulation
Changes blood flow to a specific area at an appropriate time, without changing blood flow to vital organs

72. 3 Regulatory Mechanisms
Control of cardiac output and blood pressure:
1. Autoregulation:
causes immediate, localized homeostatic adjustments
2. Neural mechanisms:
respond quickly to changes at specific sites
3. Endocrine mechanisms:
direct long-term changes
Short-term controls counteract moment-to-moment fluctuations in blood pressure by altering peripheral resistance
Long-term controls regulate blood volume

73. Cardiovascular Responses
Figure 21-13

74. 1. Autoregulation
Local blood flow within tissues is adjusted by peripheral resistance while cardiac output stays the same (no effect on heart)
Vasodilators: dilate precapillary sphincters
Local vasodilators: accelerate blood flow at tissue level:
Low O2 or high CO2 levels
Low pH (acids)
Nitric oxide (NO)
High K+ or H+ concentrations
Chemicals released by inflammation (histamine)
Elevated local temperature

75. Autoregulation Local Vasoconstrictors
e.g. prostaglandins and thromboxanes released by damaged tissues
constrict precapillary sphincters
affect a single capillary bed
At high concentrations, both local vasodilators and vasoconstrictors may also affect arterioles (which would affect many capillary beds)

76. 2. Neural Mechanisms
Cardiovascular (CV) centers: vasomotor center plus the cardiac centers of medulla oblongata that integrate blood pressure control by altering cardiac output and blood vessel diameter (adjusts cardiac output and peripheral resistance)
Vasomotor center: adjust size of arterioles
Cardioacceleratory center: increases cardiac output
Cardioinhibitory center: reduces cardiac output
All are part of sympathetic nervous system
Neural controls of peripheral resistance:
Alter blood distribution in response to demands
Maintain MAP by altering blood vessel diameter

77. Neural: Vessels Vasomotor Center
Vasomotor center – a cluster of sympathetic neurons in the medulla that oversees changes in blood vessel diameter
Maintains blood vessel tone by innervating smooth muscles of blood vessels, especially arterioles
Vasoconstriction
controlled by adrenergic nerves (NE)
stimulates smooth muscle contraction in arteriole walls
neurons innervate peripheral blood vessels throughout body
Vasodilation:
controlled by special sympathetic nerves
relaxes smooth muscle
neurons found only in skeletal muscles and heart

78. Vasomotor Center
Vasomotor tone: constant action of sympathetic vasoconstrictor nerves keep arterioles constricted to a point about halfway between fully dilated and fully constricted
Modest adjustments can make huge changes in peripheral resistance, and thus in arterial blood pressure
Extreme widespread sympathetic stimulation causes venoconstriction too, a narrowing of systemic veins to mobilize the venous reserve

79. Vasomotor Control
For most peripheral tissues the sympathetic nervous system affects the state of the arterioles: at rest, sympathetic tone keeps them in the middle of their possible openness.
If BP drops, sympathetic activity increases and vasoconstriciton occurs
If too high, sympathetic activity declines and vasodilation occurs
Parasympathetic NS does not play a role

80. Cardiovascular centers
Baroreceptors and chemoreceptors monitor arterial blood composition and pressure and signal the cardiovascular centers to change

81. Baroreceptor Reflexes
Baroreceptor reflexes: stretch receptors in walls of the carotid sinuses, aortic sinuses, and right atrium respond to changes in blood pressure:
When blood pressure rises, increased stimulation to cardiovascular centers causes them to:
decrease cardiac output
cause peripheral vasodilation
When blood pressure falls, less stimulation to cardiovascular centers causes them to:
increase cardiac output
cause peripheral vasoconstriction

82. Baroreceptor Reflexes
Impulse traveling along
afferent nerves from
baroreceptors:
Stimulate cardio-
inhibitory center
(and inhibit cardio-
acceleratory center)
Sympathetic
impulses to
heart
( HR and contractility)
Baroreceptors
in carotid
sinuses and
aortic arch
stimulated
Inhibit
vasomotor center CO R
Rate of vasomotor
impulses allows
vasodilation
( vessel diameter)
Arterial
blood pressure
rises above
normal range
CO and R
return blood
pressure to
Homeostatic
range
Stimulus:
Rising blood
pressure
Imbalance
Homeostasis: Blood pressure in normal range
Stimulus:
Declining
blood pressure
Imbalance
CO and R
return blood
pressure to
homeostatic
range
Impulses from
baroreceptors:
Stimulate cardio-
acceleratory center
(and inhibit cardio-
inhibitory center)
Arterial blood pressure
falls below normal range
Cardiac
output
(CO)
Baroreceptors in
carotid sinuses
and aortic arch
inhibited
Sympathetic
impulses to heart
( HR and contractility)
Peripheral
resistance (R)
Vasomotor
fibers
stimulate
vasoconstriction
Stimulate
vasomotor
center
Figure 21-14

83. Chemoreceptor Reflexes
Chemoreceptors in carotid bodies and aortic bodies
monitor blood for changes in pH, O2, and CO2 concentrations
Reflexes produced by coordinating cardiovascular and respiratory activities

84. 3. Hormonal Regulation
Hormones have short-term and long-term effects on cardiovascular regulation
E and NE, hormones produced by adrenal medullae (neuroendocrine) increase BP
Antidiuretic hormone (ADH) – causes intense vasoconstriction in cases of extremely low BP
Angiotensin II – kidney release of renin generates angiotensin II, which causes vasoconstriction
Erythropoietin (EPO) increases blood volume and pressure
Natriuretic peptides (ANP, BNP) decrease blood volume and pressure

85. Antidiuretic Hormone (ADH)
Released by posterior lobe of pituitary in response to reduced blood volume, an increase in blood oncotic pressure, or to Angoiotensin II release
Elevates blood pressure (mild vasoconstrictor)
Reduces water loss at kidneys to increase blood volume

86. Angiotensin II Responds to fall in renal blood pressure
Renin – angiotensin system results in its production by ACE in lung capillaries
Increases aldosterone
Increases ADH
Induces thirst
Increases cardiac output
Vasoconstritor (arterioles)
Effect on BP is times greater than NE
Think about what that means for blood pressure drugs (ACE inhibitors versus Beta blockers)

87. Erythropoietin (EPO) Released at kidneys
Responds to low blood pressure, low O2 content
Stimulates red blood cell production

88. ANP and BNP Atrial natriuretic peptide (ANP):
produced by cells in right atrium
Brain natriuretic peptide (BNP):
produced by ventricular muscle cells
Respond to excessive diastolic stretching
Lower blood volume and blood pressure by:
blocking ADH, aldosterone, E and NE and stimulating peripheral vasodilation
Reduces stress on heart

89. Hormonal Regulation
Figure 21-16

90. CV Response to: Light Exercise
Local vasodilation (capillaries): local changes in oxygen cause release of local vasodilators
Increased venous return from increased skeletal muscle contractions and increased respiratory rate (resp. pump)
Cardiac output rises to 2 times resting levels due to increased venous return (Frank-Starling principle) and atrial reflex
A little sympathetic activation

91. CV Response to: Heavy Exercise
General sympathetic activation
Major redistribution of blood to muscles due to dilation there and constriction everywhere else
Cardioaccelaratory centers increase HR, increase CO, so blood moves through the system more quickly

92. Vascular pathology

93. Hemorrhage Short term problem: maintain blood pressure and flow
Long term problem: restore normal blood volume

94. Responses to Blood Loss
Figure 21-17

95. Short-Term Responses to Hemorrhage
To prevent drop in blood pressure baroreceptor reflexes:
increase cardiac output (increasing heart rate)
cause peripheral vasoconstriction
Sympathetic nervous system:
further vasoconstriciton constricts arterioles
venoconstriction improves venous return if necessary
Hormonal effects:
increase cardiac output
increase peripheral vasoconstriction (E, NE, ADH, angiotensin II)
Kidneys filter less, make less urine

96. Long-Term Responses to Hemorrhage
Restoration of blood volume can take several days:
Recall of fluids from interstitial spaces (caused by decline in CHP)
2. Aldosterone and ADH promote fluid retention and reabsorption
3. Thirst increases, replaces “borrowed” fluid
4. Erythropoietin stimulates red blood cell production

97. Kidney and blood pressure

98. Shock Short-term responses compensate up to 20% loss of blood volume
Failure to restore blood pressure results in circulatory shock
Certain after 30-35% blood loss

99. Circulatory collapse
When arterioles and precapillary sphincters can no longer vasoconstrict despite the vasomotor stimulation to elevate blood pressure
Widespread peripheral vasodilation
Leads to fatal decline in BP
This is the endpoint of all types of shock if untreated

100. Newborn Heart Before Birth At Birth Fetal lungs are collapsed
O2 provided by placental circulation
At Birth
Newborn breathes air
Lungs expand
Pulmonary circulation provides O2

101. The Neonatal Heart
Figure 21-33b

102. Cardiovascular Changes at Birth
Pulmonary vessels expand
Reduced resistance allows blood flow to pulmonry circuit
Rising O2 causes ductus arteriosus constriction
short vessel that connects pulmonary and aortic trunks in fetus
Rising left atrium pressure closes foramen ovale

103. Congenital Cardiovascular Problems
Figure 21-34

104. Congenital Cardiovascular Problems
PFO – Left to right shunt
Patent ductus arteriosus – right to left shunt, can lead to cyanosis
Ventricular septal defects (common) – causes mixing of ventricular blood similar to PFO
Tetralogy of Fallot – narrow pulmonary trunk, incomplete IV septum, aorta originates in middle of defective septum, RV is enlarged
Transposition of great vessels

105. Arteriosclerosis
Thickening of arterial walls, leads to coronary artery disease (CAD), peripherial artery disease, and stroke
Calcification: t. media smooth muscle replaced by calcium
Atherosclerosis: lipid deposits form in t. media
High levels of lipids in blood lead to phagocytosis of lipid particles plaques clot formation
Common in familial hypercholesterolemia
How do plaques increase vascular resistance (and thus afterload) in in two ways?

106. Antihypertensive medications
Calcium channel blockers – negative inotropic effect, may slow conduction
Beta blockers – blocks sympathetic effects on heart, vessels
Diuretics – lower blood volume
Vasodilators – lower BP
ACE inhibitors

107. Edema
Tissue swelling
Caused by disruptions in balance of hydrostatic and oncotic forces
Cap damage: OPif increases as plasma proteins leak out, reduces reabsorbtion  swelling at injury site
Starvation: decreased plasma protein synthesis, reduced OPc, edema in abdominopelvic cavity (ascites)
Most common in US: increase in HPc due to high afterload (CHF, atherosclerosis, etc.)

108. Vessels

109. Vessels - Generalities
Peripheral distributions are the same on the left and right side of the body except near the heart.
Most arteries and veins follow similar paths and are often similarly named
One vessel can have several names (like a street)
Many tissues are serviced by several arteries and veins

110. Veins - Generalities
Veins are far more variable from person ot person than arteries
Several veins, especially in the limbs, have superficial and deep routes. Superficial route usually only caries 10-15% of blood at a maximum and serves to aid in thermoregulation

111. Vessels to know
Be able to identify the following arteries/veins on a model: inferior and superior vena cava, left and right pulmonary arteries and veins,, common carotid, subclavian, brachiocephalic, coronary
thoracic and abdominal aorta, celiac, renal, axillary, brachial, radial, ulnar, mesenteric, iliac, peroneal, femoral, popliteal, tibial, jugular, celiac, splenic, gastric, hepatic and saphenous.

113. Major Systemic Arteries
Figure 21-20

114. Branches of the Aortic Arch
Deliver blood to head and neck:
brachiocephalic trunk
right subclavian artery
right common carotid artery
left common carotid artery
left subclavian artery

115. Arteries of Upper Limbs
Subclavian  axial  brachial  splits into radial, ulnar
3D Peel Away

116. Descending aorta thoracic aorta  abdominal aorta  common illiac  to be continued
renal

117. 3 Unpaired Branches of the Abdominal Aorta
Celiac trunk, divides into:
left gastric artery
splenic artery
common hepatic artery
Superior mesenteric artery
Left mesenteric artery

118. celiac
gastric
hepatic
splenic
mesenteric
iliac

119. Illiac  femoral  popliteal Posterior and anterior tibial.
Posteror tibial gives rise to peroneal (fibular)

120. Veins Know the veins with the same names as arteries Exceptions:
saphenous (leg) no comparable artery
jugular (neck) like carotid arteries