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Chapter 13 Outline

Functions and Components of the Circulatory System

Composition of Blood

Structure of the Heart

Cardiac Cycle and Heart Sounds

Electrical Activity of the Heart and the ECG

Blood Vessels

Atherosclerosis and Cardiac Arrhythmias

Lymphatic System

13-2 13-2

Functions of Blood Transportation

O2, CO2, metabolic wastes, nutrients, &

hormones

Regulation

helps regulate pH

helps regulate body temperature

Vasodilatation/vasoconstriction

helps regulate water content of cells by

interactions with dissolved ions and proteins

Protection from disease & loss of blood

Plasma Proteins

Constitute 7-9% of plasma

3 types of plasma proteins: albumins, globulins, and fibrinogen

Albumin accounts for 60-80%

Creates colloid osmotic pressure that draws H2O from interstitial fluid into capillaries

Globulins:

Alpah & beta: prod. by liver - carry lipids (vitamins)

Gamma globulins: prod. by lymphocytes – are antibodies

Fibrinogen serves as clotting factor (vs. serum)

Plasma regulation: Osmoreceptors in hypothalamus 13-9 13-4

Hemoglobin

Globin protein consists of 4 polypeptide chains

1 Heme (non-protein, C-H-N ring)/polypeptide chain

Each heme has an iron ion (Fe) that can bond

(reversibly) with 1 O2 oxygen molecule

Each hemoglobin molecule can carry 4 O2

Each RBC ~ 280 million hemaglobin molecules

300 billion RBCs are produced each day

O2 O2

O2 O2

Leukocytes

Have a nucleus, mitochondria, amoeboid locomotion

Can squeeze through capillary walls (diapedesis)

Granular leukocytes: phaocytic, detoxify foreign

substances, release heparin

Agranular leukocytes: Provide immune response,

phagocytic

13-11

Platelets (thrombocytes)

lack nucleus

fragments of megakaryocytes from bone marrow

Constitute most of mass of blood clots

Release serotonin vasoconstricts vessels - reduce blood flow to clot area

Secrete growth factors to maintain integrity of blood vessel wall

Survive 5-9 days

Stored in Spleen

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13-7

Hematopoiesis (Erythropoiesis/Leukopoiesis)

Stimulate by

erythropietin

Stimulated by cytokines (autocrine regulators produced by immune system!!!!!)

Cytokines

8

• Terms to become familiar with:

• Agglutination – clumping of red blood cells in

response to a reaction between an antibody and an

antigen

• Antigens – a unique complex of self-molecules

on cell surfaces. Foreign antigens (non-self)

stimulate cells to produce antibodies

• Antibodies – proteins that react against a specific

foreign antigen

9

Type B blood

Type AB blood Type O blood

Red blood cell

Red blood cell Anti-B antibody

Antigen A

Anti-A antibody Anti-B antibody Red blood cell

Antigen A

Antigen B

Red blood cell Anti-A antibody

Antigen B

Type A blood

Transfusion Reactions

Type A blood (A antigens) make anti-B antigen antibodies

Type B blood (B antigens) make anti-A antigen antibodies

Type AB blood (A & B antigens) doesn’t have antibodies

Type O (no antigens) has both anti- A & B antigen antibodies

13-18

Anti B antigen antibody

Anti A antigen antibody

11

Rh Blood Group

•The group includes several Rh antigens or factors

• Rh positive – presence of antigen D (or other Rh

antigens)

• Rh negative – lack of these antigens

• erythroblastosis fetalis or hemolytic disease of the

newborn

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+ +

+ +

+ +

+

+

+

–

– –

–

– –

– – –

–

–

–

–

– –

–

– –

–

– –

–

–

– – –

– –

–

–

– – –

–

– –

– – –

– –

– – –

–

– –

– –

– – –

– –

+ +

+ +

+ +

+

+

+

–

– –

–

– –

– – –

–

–

–

–

– –

–

– –

–

– –

–

–

– – –

–

– – –

–

– –

– – –

–

– –

–

– –

– –

–

– – –

– –

– – –

–

–

–

– –

–

– – –

– – –

– – –

–

–

– –

– –

–

–

– –

– – –

– –

– –

– –

– –

– –

– – – – –

– –

– – –

– – +

+ +

+ +

+ +

+ +

+

Rh-negative

woman with

Rh-positive

fetus

Cells from

Rh-positive

fetus enter

woman’s

bloodstream

In the next

Rh-positive

pregnancy,

maternal

antibodies

attack fetal red

blood cells

Woman

becomes

sensitized—

Antibodies

form to fight

Rh-positive

blood cells

+

–

– – –

– –

– – –

–

–

–

– –

–

– – –

– – –

– – –

–

–

– – –

–

–

– –

– – –

– –

– –

– –

– –

– –

–

– –

– – –

– –

Anti-D antibodies not normally in blood – they form only in

Rh- who are exposed to Rh+ bloood

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Intact Blood Vessel Intact blood vessel:

- endothelium

- Connective tissue collegen

- Proteins (capable of activating

platelets)

1. Endothelium keeps blood away from

connective tissue (chemicals could

activate platelets)

2. Endothelium releases Prostoglandin

(PG1) & Nitric Oxide:

1. vasodialators

2. inhibit platelet aggregation

3. CD39 enzyme (endothelium) breaks

down ADP to AMP)

- ADP released by platelets

promotes platelet activation

3

2

1

Damage to

wall of

blood vessel

Tissue factor

exposed

Clot: reinforced

platelet plug

Collagen

exposed

Platelets aggregate

into platelet

plug

Temporary

hemostasis

Cell growth and

tissue repair

Vasoconstriction

Platelets

adhere and

release

platelet

factors

Thrombin

formation

Coagulation

cascade

Converts

fibrinogen

to fibrin

Overview of Hemostasis – 3 major steps

Vasocontriction – Step 1: endothelial cells of damaged vessel

Releases vasoconstrictive paracrines

Platelet Plug Formation – step 2

Figure 16-11

1

2

3

4

2

4

3

Prevents

platelet

adhesion

Lumen of

blood vessel

Intact

endothelium

Smooth

muscle cells

Collagen

subendothelial

layer

Exposed collagen

in damaged blood

vessel wall

1. Platelets adhere to collegen

2. Platelets bind to von willebrand factor

3. Platelets are activated

ECF

Releases

prostacyclin

and NO

Exposed collagen binds

and activates platelets.

Activated platelets release

platelet aggregating factors:

ADP, seratonin, PAF

Factors attract more platelets.

Platelets aggregate into

loose platelet plug.

1

enzyme breaks down

ADP in the blood

18-16

Coagulation – Step 3

Coagulation (clotting) – last and most effective defense against bleeding

Converts a platelet plug into a clot

insoluble network fibrin threads

18-17

Coagulation – Step 3

Coagulation (clotting) – last and most effective defense against bleeding

Converts platelet plug into a clot (insoluble network of fibrin threads)

2 pathways ways to make Fibrin – Both use a number of

Intrinsic (contact) pathway – exposure of plasma to collagen (or other negatively charged surface, e.g., test tube)

i.e., Damage to tissue exposes collagen

Activates plasma protein Factor XII (Protease)

Activates other Clotting Factors

Fibrinogen turns to Fibrin!!!!!!!!

Extrinsic pathway:

Tissue Factor III (aka tissue thromboblastin) released by damaged tissues begin cascade

Activates other clotting Factors

Fibrinogen turns to Fibrin!!!!!!!!

Coagulation Pathways

Inactive

Inactive

Inactive

Extrinsic mechanism Intrinsic mechanism

Factor V

Factor XII

Platelets degranualte

And release XII

Fibrin

Thrombin

Factor VII

Inactive

Ca2+

Damaged

tissues

Thromboplastin

(factor III)

Factor VIII

(active)

Ca2+, PF3

Factor IX

(active)

Factor XI

(active)

Factor X

(active)

Factor III

Factor V

Ca2+

PF3 Prothrombin

activator

Prothrombin

(factor II)

Fibrinogen

(factor I)

Fibrin

polymer

Factor XIII Ca2+

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3

2

1

Damage to

wall of

blood vessel

Tissue factor

exposed

Clot: reinforced

platelet plug

Fibrin slowly

dissolved by

plasmin

Collagen

exposed

Platelets aggregate

into loose platelet

plug

Temporary

hemostasis

Cell growth and

tissue repair

Vasoconstriction

Platelets

adhere and

release

platelet

factors

Thrombin

formation

Coagulation

cascade

Converts

fibrinogen

to fibrin

Overview of Hemostasis and Tissue Repair

Figure 16-10 (15 of 17)

Coagulation and Fibrinolysis

Figure 16-13

Thrombin Plasminogen

Fibrin

polymer

Plasmin

(enszyme)

tPA (tissue plasminogen

activator)

Fibrin

fragments

Coagulation Fibrinolysis

Fibrinogen

Clot

• clot retraction occurs within 30 minutes

• platelet-derived growth factor secreted by platelets and endothelial cells

- mitotic stimulant for fibroblasts and smooth muscle cells

Structure of Heart Heart has 4 chambers

2 atria receive blood from venous system

2 ventricles pump blood to arteries

Pulmonary and systemic systems

13-32

Cardiac Cycle

Is repeating pattern of contraction and relaxation of heart

Systole refers to contraction phase

Diastole refers to relaxation phase

Atria contract simultaneously; ventricles follow 0.1-0.2 sec later

Stroke volume : amount of blood ejected from 1 ventricles during systole (~ 70 mL)

EDV – ESV = Stroke Volume

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Electrical Activity of Heart

Myocardial cells are short, branched, and interconnected by gap junctions

Entire muscle that forms a chamber is called a myocardium

Remember action potentials originating in any cardiac cell are transmitted to all others:

Chambers separated by nonconductive tissue

13-52

SA Node Pacemaker

13-53

Conducting Tissues of Heart

SA node functions as pacemaker Depolarizes spontaneously

(autorythmic cells)

Pacemaker Potential

Wave of depolarization

moves into ventricles

13-58

Electrical Conduction in the Heart

Figure 14-18, steps 1–5

1

2

3

4

5

5

4

3

2

1

THE CONDUCTING SYSTEM

OF THE HEART

SA node

AV node

Purkinje

fibers

Bundle

branches

AV bundle

AV node

Internodal

pathways

SA node

SA node depolarizes.

Electrical activity goes

rapidly to AV node via

internodal pathways.

Depolarization spreads

more slowly across

atria. Conduction slows

through AV node.

Depolarization moves

rapidly through ventricular

conducting system to the

apex of the heart.

Depolarization wave

spreads upward from

the apex.

SA Node Pacemaker Potentials

+10

0

–10

–20

–30

–40

–50

–60

–70

0 .8 .4 1.2 1.6

Me

mb

ran

e p

ote

ntia

l (m

V)

Threshold

Fast K+

outflow Action

potential

Slow Na+

inflow

Pacemaker

potential

Time (sec)

Fast

Ca2+ inflow

(HCN channels)

HCN channels = hyperpolarization activated cyclic nucleotide channels – channels open in response to

hyperpolariztion!!!!! Na+ moves in

Cell

contracts

Slow Ca2+ inflow

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Action Potential in Myocardial Cells

Action potential of a cardiac contractile cell

Figure 14-13

4 4

0

0 100 200 300

Time (msec)

K+ out but Ca+ in (slow) +20

–20

–40

–60

–80

–100

Phase Membrane channels

Na+ channels open

Na+ channels close

Ca2+ channels open; fast K+ channels close

Ca2+ channels close; slow K+ channels open

Resting potential

Na+ in

0

0

1

2

3

4

1

2

3

Me

mb

ran

e p

ote

ntia

l (m

V)

Na+ Close

Ca+ close and More K+ open (out)

Excitation-Contraction Coupling

Depolarization of myocardial cells opens V-gated Ca2+

channels in sarcolemma

This depolarization opens V-gated and Ca2+ release

channels in SR (calcium-induced-calcium-release)

Ca2+ binds to troponin and stimulates contraction

(as in skeletal muscle)

During repolarization Ca2+ pumped out of cell and

into SR

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Cardiac Muscle (Myocardium)

12-77

Ca+ induced Ca+ release

Refractory Periods

13-62

Electrocardiogram (ECG or EKG) Composite of all action potentials/amplified/recorded

Recording of electrical activity of heart conducted thru ions

in body to surface

Electrocardiogram (ECG/EKG)

13-63

• P wave

– SA node fires, atria depolarize and contract

– atrial systole begins 100 msec after SA signal

• QRS complex

– ventricular depolarization

– complex shape of spike due to different thickness and shape of the two ventricles

• ST segment - ventricular systole

– plateau in myocardial action potential

• T wave

– ventricular repolarization and relaxation

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Electrical Activity of Cardiac Cycle

Figure 14-21 (9 of 9)

P

Q

R

T

S P

T wave:

ventricular

repolarization

PQ or PR segment:

conduction through

AV node and AV

bundle

P wave: atrial

depolarization

Repolarization

START

P

Q

P

Q

R

P

Q

R

T

S

R wave P

Q

R

S

S wave

Q

R

P

Q wave

Ventricles contract

ST segment

The end

P

Atria contract

S

13-72

Fenestrated & Discontinuous capillaries

Elastic - recoil

Muscular

Fenestrated &

Discontinuous capillaries

Veins

13-77

•Valves

•Skeletal muscular pumps

•Diaphragm

Cholesterol and Lipoproteins

Lipids & cholesterol carried in blood by plasma lipoproteins

LDLs: produced in liver

Many organs cells have receptors for lipoproteins

Cell engulfs it

Liver removes LDLs this way

HDLs take cholesterol to liver

Atherosclerosis

Plaques form in response to damage done to the

endothelium of a blood vessel.

Caused by:

Damage or ―insult‖ to endothelium

Smoking, high blood pressure, diabetes, high

cholesterol

LDL and Plaque

The development of

atherosclerotic

plaques

Figure 15-25

(a) Normal arterial wall

(b) Fatty streak

(c) Stable fibrous plaque

(d) Vulnerable plaque

Endothelial cells

Elastic connective tissue

Smooth muscle cells

Macrophages ingest Cholesterol and

become foam cells

Smooth muscle cells attracted by

Cytokines of macrophages take in

More cholesterol

A lipid core accumulates

Fibrous scar tissue accumulates

Smooth muscle cells

Calcifications are deposited

within the plaque.

Platelets

Macrophages

LDL cholesterol accumulates

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Ischemic Heart Disease

Ischemia = blood supply to tissue is deficient

Causes increased lactic acid from anaerobic metabolism

Is most commonly due to atherosclerosis in coronary arteries

Often accompanied by angina pectoris (chest pain)

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Arrhythmias Detected on ECG

Arrhythmias are abnormal heart rhythms

Heart rate <60/min is bradycardia; >100/min is tachycardia

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Arrhythmias Detected on ECG In flutter, contraction rates can be 200-300/min

In fibrillation, contraction of myocardial cells is uncoordinated and pumping ineffective

Ventricular fibrillation is life-threatening

Electrical defibrillation resynchronizes heart by depolarizing all cells at same time

13-88

Lymphatic System

3 basic functions:

1. Transports interstitial

fluid (lymph) back to

blood

2. Transports fat from small

intestine to blood

3. Provides immunological

defenses against

pathogens

Lymphatic capillaries

Very porous, absorb proteins, microorganisms, fat

13-95

Lymph nodes filter lymph

before returning it to R. &

L. subclavian veins via

thoracic duct or right

lymphatic duct

Nodes contain

lymphocytes and

phagocytic cells that

remove pathogens

Tonsils, spleen, thymus

(lymphoid organs)

Lymphatic System

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