Note: Original PowerPoint slides by Lee Ann Frederick (Univ. Texas Arlington) were extensively modified by Drs. Kwast and Brown for use in MCB 244 & 246, University of Illinois, 2014 - 2015

Chapter 21 Blood Vessels and

Circulation

2015 Pearson Education, Inc.

1. Describe the different types of blood vessels based on structure/function.

2. Describe mechanisms that regulate blood flow through vessels. 3. Describe control mechanisms for regulating blood flow and

pressure. 4. Describe how homeostasis is maintained in the cardiovascular

system in response to exercise and hemorrhaging. 5. Be able to identify major arteries and veins in the pulmonary &

systemic systems. 6. Describe differences among fetal and adult circulatory systems. 7. Describe the effects of aging on the cardiovascular system.

Chapter 21 Learning Objectives

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21-1 5 Classes of Blood Vessels 1. Arteries carry blood away from heart 2. Arterioles the smallest branches of arteries 3. Capillaries smallest blood vessels; location of exchange between blood and interstitial fluid 4. Venules Collect blood from capillaries 5. Veins Return blood to heart The pulmonary trunk and aorta (originating from rt. & lt. ventricles, respectively) are the largest blood vessels (2.5 cm diameter) Capillaries are the smallest blood vessels (4 m diameter)

form an extensive network of ~10 billion covering ~25,000 miles! thin-walled to aid in diffusion of gases and nutrients most cells are no further than one or 2 cell-diameters away from a

capillary (Why? Diffusion is very limiting) 3

1. Tunica intima innermost; endothelial lining and underlying connective tissue with elastic membrane (called internal elastic membrane in arteries)

2. Tunica media middle; concentric sheets of smooth muscle in loose connective tissue with external elastic membrane (arteries only); contains smooth muscle responsible for dilation/constriction

3. Tunica externa outermost; connective tissue sheath; anchors vessel to adjacent tissues; contains collagen & elastic fibers + in veins smooth muscle

Fig 211

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21-1 Blood Vessel Wall Structure: 3 Layers

21-1 Comparison of Artery & Vein Gross Morphology

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Veins Thinner walls Less elastin and smooth muscle Thickest = tunica externa Open lumen, no recoil Collapse flat in cross section Valves of tunica intima prevent backflow Smooth endothelium No elastic membranes

Arteries Thicker walls More elastin and smooth muscle in tunica media Thickest tunic = tunica media Elastic walls recoil constricting lumen without BP Circular in cross section No valves Pleated endothelium Internal and external elastic membranes

Fig 211

21-1 Structure/Function of Arteries Arteries and Pressure

Elasticity allows arteries to absorb pressure waves from heartbeat Contractility - change vessel diameter via sympathetic division of ANS

Vasoconstriction: contraction of arterial smooth muscle; shrink lumen Vasodilatation: relaxation of arterial smooth muscle; enlarging the lumen

These affect afterload on heart, peripheral blood pressure, and capillary blood flow

Changes in elasticity & musculature from heart to capillaries From elastic arteries (also called conducting arteries)

Large vessels (e.g., pulmonary trunk and aorta) Tunica media has many elastic fibers and few muscle cells; evens out pulse

To muscular arteries (distribution arteries) Medium sized (most arteries); tunica media has many muscle cells

To arterioles (small) no longer a pulse, rather even flow Have little or no tunica externa; thin or incomplete tunica media 6

21-1 Histological Structures of Blood Vessels Fig 212

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also sinusoidal capillaries

21-1 Health Problems with Arteries Aneurysm: bulge in weakened artery wall produced when pressure of

blood exceeds elastic capacity of wall prone to rupture, caused by chronic high BP or arteriosclerosis

Stroke = cerebrovascular accident (CVA): interruption of arterial supply to portion of brain (embolism, athero-sclerosis) tissue death & dysfunction

Clinical Note pp. 728-729

8

Arteriosclerosis: thickening or toughening of the arterial walls ( elasticity) caused by a variety of pathological conditions; 2 types: Focal calcification: deposition of calcium salts

followed by degeneration of smooth muscle in tunica media

Atherosclerosis (athero = fatty degeneration): lipid deposits in tunica media; can form plaque

21-1 Structure and Function of Capillaries Capillary Function

Location of all exchange functions of cardiovascular system Materials diffuse between blood and interstitial fluid

Capillary Structure Endothelial tube inside thin basal lamina No tunica media OR tunica externa (only tunica intima) Avg. diameter = 8 m 2 major types:

1. Continuous 2. Fenestrated Fig. 213 9

21-1 Structure and Function of Capillaries Continuous Capillaries

Have complete endothelial lining (fenestrated do not)

Found in all tissues except epithelia and cartilage

Function: Permit diffusion of water, small

solutes, and lipid-soluble materials Block blood cells and plasma

proteins

Specialized Continuous Capillaries Found in CNS and thymus Have very restricted permeability For example, the bloodbrain barrier

Fig. 213a

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21-1 Structure and Function of Capillaries Fenestrated Capillaries

Have pores in endothelial lining Permit rapid exchange of water and

larger solutes between plasma and interstitial fluid

Found in choroid plexus, endocrine organs, kidneys, intestinal tract

Sinusoids (Sinusoidal Capillaries) Have gaps between adjacent endothelial cells

Found in liver, spleen, bone marrow, endocrine organs Permit free exchange of water and large plasma proteins between

blood and interstitial fluid

Fig. 213

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21-1 Structure and Function of Capillaries

Thoroughfare channels Direct capillary connections: arterioles to venules Controlled by smooth muscle segments

(metarterioles)

Capillary Beds (capillary plexus) One arteriole gives rise to dozens of capillaries

that empty into several venules Collaterals

Multiple arteries that contribute to one capillary bed Allow circulation if one artery is blocked

Arteriovenous Anastomoses Capillary bed bypass 12

Precapillary Sphincter Guards entrance to each capillary

Vasomotion Contraction & relaxation cycle of capillary sphincters Blood volume not sufficient to fill all capillaries at any

given time

Fig. 21-5

21-1 Structure and Function of Veins Collect blood from capillaries and return to heart Are larger in diameter than arteries, have thinner walls and lower blood pressure

Vein Classification Venules (internal diameter 20 - 50m)

Very small veins Collect blood from capillaries Small ones (9mm) Thick tunica externa Thin tunica media

Fig. 21-2

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21-1 Structure and Function of Veins While pressure from cardiac pumping drives

blood flow in arteries, pressure in veins often too low to oppose gravity

Rely on skeletal muscle movement and valves in tunica intima to ensure 1-way movement

Health problems with veins: resistance to flow (gravity, obesity) causes

pooling above valves, veins stretch out: e.g., varicose veins and hemorrhoids

Blood Reservoir: venous system contains 65-70% total blood

volume can constrict during hemorrhage to keep volume

in capillaries & arteries near normal

Fig. 21-5

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21-1 Distribution of Blood Among Vessels Heart, arteries & capillaries

3035% of blood volume Venous system

6570% of blood volume 1/3 of venous blood is in the

large venous networks of the liver, bone marrow, and skin

Blood Vessel Capacitance The ability to stretch Relationship between blood

volume and blood pressure Veins (capacitance vessels)

stretch more than arteries (8x) Thus, veins can accommodate

large changes in blood volume

Fig 21-6

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21-1 Response to Severe Hemorrhaging Vasomotor centers in the medulla oblongata stimulate

sympathetic nerves

Systemic veins constrict (venoconstriction) - reduces the amount of blood in venous system

Veins in liver, skin, and lungs redistribute venous reserve (= amount that can be shifted [~20% total volume]) to more critical organs (e.g., brain, heart)

Net result: keep blood volume in arteries and capillaries at near-normal levels

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21-2 Pressure and Resistance Determine Blood Flow Blood Flow = volume of blood flowing

through a vessel in given period (total body flow = cardiac output [CO])

Blood Pressure = force per unit area exerted on vessel by blood (mmHg)

Blood pressure greatest in arteries leaving heart, lowest in veins returning to heart; absolute pressure not as important as differential pressure (P) in determining flow

Resistance = opposition to blood flow blood viscosity resistance vessel length resistance vessel diameter resistance Vasoconstriction flow, BP, resistance Vasodilation flow, BP, resistance

Neural & hormonal activities influence cardiac output, peripheral resistance, & venous pressure. Capillary pressure drives exchange.

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21-2 Pressure and Resistance Blood pressure (BP)

Arterial pressure (mm Hg) BP at arteries near heart: Systolic Pressure / Diastolic

Pressure; normal = 120/80 mm Hg Capillary hydrostatic pressure (CHP)

Pressure within the capillary beds (35 - 18 mm Hg) Venous pressure

Pressure in the venous system (18 mm Hg) Circulatory pressure

P across entire systemic circuit (~100 mm Hg) Total peripheral resistance

Resistance (R) of entire cardiovascular system 18

21-2 Total Peripheral Resistance Total peripheral resistance is a combination of vascular resistance,

blood viscosity and turbulence

Vascular Resistance Due to friction between blood and vessel walls Depends on vessel length (constant) & vessel diameter:

vessel diameter varies by vasodilation and vasoconstriction: R increases exponentially as vessel radius (r) decreases (R 1/r 4)

Viscosity R caused by molecules and suspended materials in a liquid Whole blood viscosity is about 4 - 5 times that of water

Turbulence Swirling action that disturbs smooth flow of liquid Occurs in heart chambers and great vessels Arteriosclerotic plaques cause abnormal turbulence 19

21-2 Pressure, Resistance, Vessel Diameter, and Turbulence

20

Fig 21-7

21-2 Pressure and Resistance

21

21-2 Pressure and Flow

Fig. 219

Pulse pressure Difference between systolic pressure and

diastolic pressure

Mean arterial pressure (MAP) MAP = diastolic pressure + 1/3 pulse pressure (MAP = 80 mm Hg + 1/3 x 40 93 mm Hg)

Fig. 218

Arterial BP Systolic pressure Peak arterial pressure

during ventricular systole

Diastolic pressure Minimum arterial

pressure during diastole

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21-2 Pressure and Resistance Normal BP = 120/80

Hypertension Abnormally high blood pressure

Greater than 140/90 Hypotension

Abnormally low blood pressure

Elastic Rebound Arterial walls

Stretch during systole and rebound during diastole Keep blood moving during diastole

MAP and pulse pressure decrease with distance from heart Blood pressure decreases with friction Pulse pressure decreases due to elastic rebound

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21-2 Capillary Pressure and Resistance Capillary Exchange

Vital to homeostasis Moves materials across

capillary walls by Diffusion Filtration Reabsorption

Diffusion (movement from high concentration to low)

Diffusion Routes Vary: Plasma proteins

Cross endothelial lining in sinusoids

Water, ions, and small molecules such as glucose

Diffuse between adjacent endothelial cells or through fenestrated capillaries

Some ions (Na+, K+, Ca2+, Cl-) Diffuse through channels in plasma

membranes

Large, water-soluble compounds Pass through fenestrated capillaries

Lipids and lipid-soluble materials such as O2 and CO2

Diffuse through endothelial plasma membranes

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21-2 Capillary Pressure and Resistance Fig 21-10

Equals the pressure required to prevent osmosis

Filtration Driven by hydrostatic pressure (i.e.,

blood pressure via heart activity) Water and small solutes forced through

capillary wall Leaves larger solutes, amino acids,

proteins, etc. in bloodstream Reabsorption

The result of osmosis (water moving down its concentration gradient)

In capillaries, it is the result of blood colloid osmotic pressure Caused by suspended blood proteins

that are too large to cross capillary walls

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21-2 Pressure and Resistance: Putting it all together Capillary Exchange

Interplay between Filtration and Reabsorption can be summarized by:

Hydrostatic pressure forces water out of capillaries and into interstitial fluid

Colloid Osmotic pressure forces water into capillaries from interstitial fluid

Key Concept: Hydrostatic pressure and osmotic pressure oppose one another

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21-2 Pressure and Resistance: Putting it all together Capillary Exchange

Net Hydrostatic Pressure Is the difference between the capillary

hydrostatic pressure (CHP) and the interstitial fluid hydrostatic pressure (IHP)

Pushes water and solutes out of capillaries and into interstitial fluid

Net Colloid Osmotic Pressure Is the difference between the blood

colloid osmotic pressure (BCOP) and the interstitial fluid colloid osmotic pressure (ICOP)

Pulls water and solutes into the capillary from the interstitial fluid

NFP = (CHP IHP) (BCOP ICOP) NFP = Net HP Net COP

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Fig 21-11 Net Filtration Pressure (NFP) Is the difference between the net

hydrostatic pressure and the net colloid osmotic pressure

At ARTERIAL end of the capillary

Net hydrostatic pressure (35 mmHg) > Net colloid osmotic pressure (25 mmHg)

Result = Fluid moves out of capillary and into interstitial fluid (filtration)

21-2 Capillary Exchange Fig 21-11

At VENOUS end of capillary Net hydrostatic pressure (18

mmHg) < Net colloid osmotic pressure (25 mmHg)

Result = Fluid moves out of interstitial fluid and into capillary

Somewhere between the arterial and venous end of capillary

Net hydrostatic pressure (25 mmHg) = Net colloid osmotic pressure (25 mmHg)

Result = NO fluid movement 28

21-2 Capillary Exchange: Lymphatic system Fluid Recycling

IF the maximum filtration pressure at the arterial end were exactly the same as the maximum reabsorption pressure at the venous end, then there would be no NET fluid loss or gain.

BUT the filtration forces are greater than reabsorption forces, which results in an imbalance in fluid movement.

Balance is restore by lymphatic system, which returns the excess interstitial fluid to venous circulation)

If fluid lost to interstial fluid is NOT returned to circulatory system, edema results

Person suffering from elephantiasis (infection of the lymphatic system)

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21-2 Pressure and Resistance Capillary Dynamics

Hemorrhaging Reduces capillary hydrostatic pressure (CHP) and net filtration

pressure (NFP) Increases reabsorption of interstitial fluid (recall of fluids) in blood

Dehydration Increases blood colloid osmotic pressure (BCOP) Accelerates reabsorption

Conversely, if CHP increases or BCOP decreases Fluid moves out of blood into interstitial fluid Builds up in peripheral tissues (edema)

30

21-3 Cardiovascular Regulation Tissue Perfusion Regulated by Homeostatic Cardiovascular

Activities Carries O2 and nutrients to tissues and organs and CO2 and

wastes away Affected by

Cardiac output Peripheral resistance Blood pressure

Cardiovascular regulation changes blood flow to a specific area At an appropriate time In the right area Without changing blood pressure & flow to vital organs

31

21-3 Cardiovascular Regulation How is cardiovascular activity (cardiac output, blood pressure and blood flow) regulated? Three basic mechanisms:

1. Autoregulation Causes immediate,

localized homeostatic adjustments

2. Neural Mechanisms Respond quickly to

changes at specific sites

3. Endocrine Mechanisms Direct long-term changes Fig 21-12 32

21-3 Cardiovascular Regulation Autoregulation of Blood Flow within Tissues

Adjustments to peripheral resistance; cardiac output stays the same

Fig 21-12

Local Vasoconstrictors: Reduce blood flow at capillary by causing contraction of smooth muscle cells of the precapillary sphincters examples include prostaglandins and thromboxanes

(by platelets & WBCs) endothelins released by damaged tissues

33

Local Vasodilators: Accelerate blood flow at capillary beds by relaxing smooth muscle cells of the precapillary sphincters low O2 or high CO2 levels low pH nitric oxide (NO) from endothelial cells high K+ or H+ concentrations chemicals released by inflammation (histamine) elevated local temperature

all constrict precapillary sphincters

21-3 Cardiovascular Regulation *Vasomotor Tone

Produced by constant action (even at rest) of sympathetic vasoconstrictor nerves

Fig 21-12

Neural Mechanisms: Cardiovascular (CV) centers of the Medulla Oblongata

Cardiac Centers: cardioacceleratory center: CO cardioinhibitory center: CO

Vasomotor Center: Vasoconstriction (sympathetic*)

controlled by adrenergic nerves (NE) stimulates smooth muscle contraction in

arteriole walls Vasodilation: (parasympathetic)

controlled by cholinergic nerves (ACh) that cause the release of NO

relaxes vascular smooth muscle 34

21-3 Reflex Control of Cardiovascular Function Baroreceptor Reflexes: monitor blood pressure Stretch receptors

(mechanoreceptors) in walls of Carotid sinuses: maintain

blood flow to brain Aortic sinuses: monitor start of

systemic circuit Right atrium: monitors end of

systemic circuit

Fig 21-13

When BP rises, CV centers: Decrease CO and cause

peripheral vasodilation

When BP falls, CV centers: Increase CO and cause 35 peripheral vasoconstriction

Chemoreceptors Monitor changes in pH, O2, and/or

CO2 and modulate activity of cardiovascular, vasomotor & respiratory centers

Peripheral: located in carotid & aortic

bodies

monitor arterial blood O2, and/or CO2

modulate cardiovascular & vasomotor centers

Central: located in medulla

oblongata

21-3 Cardiovascular Regulation Fig 21-14

monitor cerebrospinal fluid pH (indirectly pCO2) primarily modulates respiration but also local

vasomotor control (brain blood flow) 36

21-3 Cardiovascular Regulation CNS Activities and the

Cardiovascular Centers Higher brain centers involved

in thought and emotions can also dramatically affect cardiovascular and vasomotor centers

Strong emotions such as fear, anxiety and rage can strongly affect cardiac output and blood pressure

37

21-3 Hormones & Cardiovascular Regulation Fig 21-15

Hormones can have both short-term and long-term effects on cardiovascular regulation

For example, E and NE from suprarenal medullae stimulate cardiac output and peripheral vasoconstriction 38

21-3 Hormones & Cardiovascular Regulation Fig 21-15 Antidiuretic Hormone (ADH)

Released by pituitary to elevate BP in response high plasma osmotic concentration or low BP

Angiotensin II Responds to fall in renal blood pressure

and ultimately results in an increase in BP and CO

Erythropoietin (EPO) Responds to fall in renal blood pressure or

O2 concentration thus stimulating RBC production

Natriuretic Peptides Atrial & Brain Produced by atrial and ventricular muscle

cells, respectively, in response to stretch, thereby lowering blood volume & press. 39

21-4 Cardiovascular Adaptation to Exercise The cardiovascular system operates as an integrated unit in its

response to physical and physiological changes (e.g., exercise, blood loss, etc.) in order to maintain homeostasis

In response to exercise: Light Exercise

Extensive vasodilation occurs: increasing circulation

Venous return increases: with muscle contractions

Cardiac output rises: due to rise in venous return

(FrankStarling principle) and atrial stretching

Heavy Exercise Activates sympathetic nervous

system Cardiac output increases to

maximum: about four times resting level

Restricts blood flow to nonessential organs (e.g., digestive system)

Redirects blood flow to skeletal muscles, lungs, and heart

Blood supply to brain is unaffected 40

21-4 Cardiovascular Adaptation to Exercise

Bottom Line: A well-trained heart pumps more efficiently 41

21-4 Cardiovascular Adaptation to Hemorrhaging Goal is to maintain blood pressure and restore volume

42

Fig 21-16

21-4 Cardiovascular Adaptation to Hemorrhaging Short-Term Elevation of Blood Pressure

Carotid and aortic reflexes Increase cardiac output (HR) and cause peripheral vasoconstriction

Sympathetic nervous system Stress & anxiety trigger hypothalamus to increase vasomotor tone;

causes further constriction to arterioles to raise BP while venoconstriction quickly improves venous return

Hormonal effects Increased E, NE, ADH, angiotensin II causes increased cardiac

output and peripheral vasoconstriction

In combination, these mechanisms elevate BP, improve peripheral blood flow, and restore arterial pressures for blood losses up to 20%.

43

21-4 Cardiovascular Adaptation to Hemorrhaging

Long-Term (Days) Restoration of Blood Volume Recall of fluids from interstitial spaces Aldosterone and ADH promote fluid retention and

reabsorption at kidneys Thirst increases additional H2O uptake in GI tract Erythropoietin stimulates red blood cell production

Vascular Supply to Special Regions Brain, Heart and Lungs have separate mechanisms to

control blood flow 44

Blood Flow to Brain Blood Flow to Heart (cont.) No. 1 priority! Brain has high O2 demand and

receives 12% cardiac output When peripheral vessels constrict,

cerebral vessels dilate, normalizing blood flow

If system fails cerebrovascular accident (CVA) 4 major arteries form cranial

anastomoses

Low O2 levels and lactic acid: Dilate coronary vessels & increase

coronary blood flow Epinephrine

Dilates coronary vessels & has positive chrono- and ino-tropic effects

Blood Flow to Heart With increased work load, O2

demand increases

Blood Flow in Lungs Locally regulated by alveolar O2

levels High O2 content vessel dilation

(ensures O2 uptake) Low O2 content vessels

constrict (damage/blocked) 45

21-4 Cardiovascular Adaptation to Hemorrhaging

21-5 Pulmonary and Systemic Patterns Three General Functional Patterns

1. Peripheral artery and vein distribution is the same on right and left, except near the heart

2. The same vessel may have different names in different locations

3. Tissues and organs usually have multiple arteries and veins Vessels may be interconnected with

anastomoses

Figure 21-17 A Schematic Overview of the Pattern of Circulation 46

Figure 21-18 A Schematic Overview of the Pattern of Circulation 47

21-6 The Pulmonary Circuit

47

21-6 The Pulmonary Circuit Deoxygenated Blood Arrives at Heart

from Systemic Circuit Passes through right atrium and

right ventricle Enters pulmonary trunk At the lungs

CO2 is removed O2 is added

Oxygenated blood Returns to the heart Is distributed to systemic circuit

Pulmonary Vessels Pulmonary Arteries

Carry deoxygenated blood Pulmonary trunk

Branches to left and right

pulmonary arteries Pulmonary arteries

Branch into pulmonary arterioles Pulmonary arterioles

Branch into capillary networks that surround alveoli

Pulmonary Veins Carry oxygenated blood Capillary networks around alveoli

Join to form venules Venules

Join to form four pulmonary veins Pulmonary veins

Empty into left atrium 48

21-7 The Systemic Circuit The ascending aorta

Rises from the left ventricle Curves to form aortic arch Turns downward to

become descending aorta

From Fig 21-21

Aortic arch Ascending aorta

Branches of the Aortic Arch Deliver blood to head and neck

Brachiocephalic trunk Left common carotid artery Left subclavian artery

Brachiocephalic trunk

Left subclavian

Left common carotid

49

Brachial

Basilic

Cephalic Radial

Basilic Ulnar

Palmar venous arches Digital veins

21-7 The Systemic Circuit: Upper Extremities The Brachial Artery

Divides at coronoid fossa of humerus into radial artery and ulnar artery:

fuse at wrist to form superficial and deep palmar arches, which supply digital arteries

Brachial

Radial

Ulnar

Palmar arches

From Fig 21-20

Veins of the Arm & Hand Digital veins

Empty into superficial & deep palmar veins

Which interconnect to form palmar venous arches

Superficial arch empties into: cephalic vein median antebrachial vein basilic vein median cubital vein

Deep palmar veins drain into: radial and ulnar veins which fuse above elbow to

form brachial vein From Fig 21-28

50

21-7 The Systemic Circuit: Head and Neck The Common Carotid Arteries

Each common carotid divides into External carotid artery -

supplies blood to structures of the neck, lower jaw, and face (supplies occipital and facial arteries)

Internal carotid artery - enters skull and delivers blood to brain: Divides into 3 branches:

Internal carotid External carotid

Carotid sinus Common carotid

Brachiocephalic trunk

Occipital Facial

From Fig 21-21

ophthalmic artery anterior cerebral artery middle cerebral artery

Middle cerebral

Ophthalmic

Anterior cerebral

51

21-7 The Systemic Circuit: Head and Neck The Vertebral Arteries

Also supply brain with blood supply Left and right vertebral arteries

Arise from subclavian arteries Enter cranium through foramen

magnum

Fuse to form basilar artery: branches to form posterior

cerebral arteries

posterior cerebral arteries: become posterior

communicating arteries

Posterior cerebral

Basilar

Vertebral

Subclavian

From Fig 21-21

52

21-7 The Systemic Circuit: Head and Neck

Middle cerebral

Basilar

Vertebral

Posterior cerebral

Posterior communicating

Cerebral arterial circle

Anterior cerebral

Anterior communicating

Comprised of: Anterior & posterior

communicating arteries Anterior & posterior

cerebral arteries Internal carotid artery

From Fig 21-22

Anastomoses The cerebral arterial

circle (Circle of Willis) interconnects The internal carotid

arteries And the basilar artery

Internal carotid

(cut)

53

21-7 The Systemic Circuit: Head & Neck

Occipital Vertebral

External jugular

Axillary

Clavicle

Right subclavian

Internal jugular

Right brachiocephalic Superior vena cava

Facial

From Fig 21-27

Superficial Veins of the Head Converge to form Temporal, facial, and

maxillary veins: temporal and maxillary

veins: drain to external

jugular vein facial vein: drains to internal

jugular vein

Temporal

Maxillary

54

21-7 The Systemic Circuit: Trunk

Brachiocephalic trunk Thyrocervical trunk

Internal thoracic Esophageal arteries

Pericardial arteries

Lumbar

Internal iliac Median sacral

Terminal segment of the aorta

Gonadal

Left gastric

Axillary

Vertebral

Aortic arch

THORACIC AORTA

Superior phrenic

Inferior phrenic

Diaphragm Common

hepatic

Suprarenal Renal

External iliac common iliac Inferior mesenteric

ABDOMINAL AORTA

Superior mesenteric

Splenic

Celiac trunk

Intercostal arteries

Left subclavian

Common carotid arteries

From Fig 21-23

The Descending Aorta Thoracic aorta

Supply organs of the chest: Supply chest wall:

intercostal arteries superior phrenic arteries

Abdominal Aorta Divides at terminal segment

of the aorta into: left common iliac artery right common iliac artery

Unpaired branches: major branches to visceral organs

Paired branches: to body wall kidneys urinary bladder structures outside abdominopelvic

cavity 55

21-7 The Systemic Circuit: Trunk Major Tributaries of the Abdominal

Inferior Vena Cava

Hepatic veins Renal veins Suprarenal veins Phrenic veins Iliac veins

Brachiocephalic SUPERIOR VENA CAVA

INFERIOR VENA CAVA

Hepatic veins

Renal veins

Common iliac Internal iliac External iliac

Supraneal veins

From Fig 21-28

56

21-7 The Systemic Circuit: Lower Limb

Arteries & Veins of the Pelvis and Lower Limbs

Femoral artery (v) deep femoral artery

Becomes popliteal artery Posterior to knee Branches to form:

posterior and anterior tibial arteries (v)

posterior gives rise to fibular artery (v)

Common iliac

External iliac

Fibular

Posterior tibial

Anterior tibial

Popliteal

Femoral

External iliac Common iliac Internal iliac

Femoral

Femoral

Popliteal

Anterior tibial

Posterior tibial Fibular

From Fig 21-30

From Fig 21-25 Plantar Arteries

57

21-8 Fetal and Maternal Circulation Fetal and Maternal Cardiovascular Systems Promote the Exchange

of Materials Embryonic lungs and digestive tract nonfunctional Respiratory functions and nutrition provided by placenta

Placental Blood Supply Deoxygenated blood flows from the fetus to the placenta

Through a pair of umbilical arteries that arise from internal iliac arteries Enters umbilical cord

Oxygenated blood returns from placenta In a single umbilical vein that drains into ductus venosus

Ductus venosus Empties into inferior vena cava

58

21-8 Fetal and Maternal Circulation Before birth, O2 provided by placental circulation Fetal Pulmonary Circulation Bypasses

Foramen ovale Interatrial opening; directs blood from right to left atrium Covered by valve-like flap

Ductus arteriosus Short vessel that connects pulmonary and aortic trunks

Cardiovascular Changes at Birth Newborn breathes air thereby expanding lungs Pulmonary vessels expand reducing resistance and allowing for blood flow Rising O2 causes ductus arteriosus to constrict and close Rising left atrium pressure closes foramen ovale Pulmonary circulation now provides O2

59

21-8 Fetal and Maternal Circulation

Figure 21-32 Fetal Circulation

60

(Fossa ovalis)

(Ligamentum arteriosum)

21-8 Fetal and Maternal Circulation Patent Foramen Ovale and Patent Ductus Arteriosus

In patent (open) foramen ovale, blood recirculates through pulmonary circuit instead of entering left ventricle

Fairly common (up to 25% population); not dangerous A patent ductus arteriosus creates a right-to-left shunt

Very dangerous; needs to be surgically corrected

Figure 21-33 Congenital Heart Problems

Patent Foramen Ovale and Patent Ductus Arteriosus If the foramen ovale remains open, or patent, blood recirculates through the pulmonary circuit instead of entering the left ventricle. The movement, driven by the relatively high systemic pressure, is called a left-to-right shunt. Arterial oxygen content is normal, but the left ventricle must work much harder than usual to provide adequate blood flow through

the systemic circuit. Hence, pressures rise in the pulmonary circuit. If the pulmonary pressures rise enough, they may force blood into the systemic circuit through the ductus arteriosus. This conditiona patent ductus arteriosus creates a right-to-left shunt. Because the circulating blood is not adequately oxygenated, it develops a deep red color. The skin then develops the blue tones typical of cyanosis and the infant is known as a blue baby.

Patent ductus arteriosus

Patent foramen

ovale

61

21-9 Effects of Aging on the Cardiovascular System Age-Related Changes in Blood

1. Decreased hematocrit 2. Peripheral blockage by blood clot (thrombus) 3. Pooling of blood in legs (due to venous valve deterioration)

Age-Related Changes in the Heart 1. Reduced maximum cardiac output 2. Changes in nodal and conducting cells 3. Reduced elasticity of cardiac (fibrous) skeleton 4. Progressive atherosclerosis 5. Replacement of damaged cardiac muscle cells by scar tissue

Age-Related Changes in Blood Vessels 1. Arteries become less elastic (can lead to aneurysms) 2. Calcium deposits on vessel walls (can lead to stroke or infarct) 3. Thrombi can form at atherosclerotic plaques 62