3/21/2012
Functions of Blood
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
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

13-2
13-2
Hemoglobin
Plasma Proteins
Constitute
7-9% of plasma
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)
3
Plasma
regulation: Osmoreceptors in hypothalamus
13-9
O2
O2
O2
O2
Globin protein
consists of 4 polypeptide chains
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
1
13-4
Leukocytes
Platelets (thrombocytes)
lack
nucleus
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
Have
a nucleus, mitochondria, amoeboid locomotion
squeeze through capillary walls (diapedesis)
Granular leukocytes: phaocytic, detoxify foreign
substances, release heparin
Agranular leukocytes: Provide immune response,
phagocytic
fragments
Can
13-11
13-13
1
3/21/2012
Hematopoiesis (Erythropoiesis/Leukopoiesis)
Cytokines
• Terms to become familiar with:
• Agglutination – clumping of red blood cells in
response to a reaction between an antibody and an
antigen
Stimulate by
erythropietin
• Antigens – a unique complex of self-molecules
on cell surfaces. Foreign antigens (non-self)
stimulate cells to produce antibodies
Stimulated by cytokines (autocrine regulators produced by immune system!!!!!)
• Antibodies – proteins that react against a specific
foreign antigen
13-7
8
Transfusion Reactions
Red blood cell
Red blood cell
Anti-B antibody
Anti-A antibody
 Type
Antigen A
Antigen B
Type B blood
Type A blood
Red blood cell
Anti-A antibody
Anti-B antibody
Antigen A
Antigen B
Red blood cell
Type AB blood
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
Anti B antigen antibody
Anti A antigen antibody
Type O blood
9
13-18
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
11
–– –
– – –
– – –
– ––
–
–
– –– –
–
– –
–
–
– – –– – –
– – – – –
–
–
–
–
– –
–
+
– –
–
–
+
+
– –
+ + +
–
+
–
+
–
+
– –
–
–
–– –
– – –
– – –
– ––
–
–
– –– –
–
– –
–
–
–– –– – –
– – +– +– –
–
+
–
++
–
+
–
+
+
+
– +
+ + +
+
+
–
+
–
+ +
– +
–
–
Rh-negative
woman with
Rh-positive
fetus
Cells from
Rh-positive
fetus enter
woman’s
bloodstream
– –
– – –– –
–
– –
– –
–
–
–
– ––
–
– ––
–– – –
––
–– –
––– –
– – –
–
–
–
–
–
– –+
–
–
–
– –
–
–
–
–
–
–
–
–
–
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
– –
– – –– –
–
– –
– –
–
–
–
– ––
–
– ––
–– – –
––
–– –
– –– –
– –
–
–
–
–
–
– –
–
–
–
–
–
–
–
–
–
–
In the next
Rh-positive
pregnancy,
maternal
antibodies
attack fetal red
blood cells
12
2
3/21/2012
Intact Blood Vessel
Overview of Hemostasis – 3 major steps
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
Damage to
wall of
blood vessel
1
Vasoconstriction
Releases
prostacyclin
and NO
Thrombin
formation
3
Temporary
hemostasis
Converts
fibrinogen
to fibrin
Clot: reinforced
platelet plug
Cell growth and
tissue repair
Vasocontriction – Step 1: endothelial cells of damaged vessel
Releases vasoconstrictive paracrines
3
Prevents
platelet
adhesion
Coagulation
cascade
Platelets aggregate
into platelet
plug
1
Intact
endothelium
Tissue factor
exposed
Platelets
adhere and
release
platelet
factors
2
Coagulation – Step 3
Platelet Plug Formation – step 2
Lumen of
blood vessel
Collagen
exposed
Exposed collagen binds
and activates platelets.
Activated platelets release
2 platelet aggregating factors:
ADP, seratonin, PAF
3
4

Coagulation (clotting) – last and most effective defense against
bleeding

Converts a platelet plug into a clot

insoluble network fibrin threads
Factors attract more platelets.
2
4
enzyme breaks down
ADP in the blood
Platelets aggregate into
loose platelet plug.
1
Smooth
muscle cells
Collagen
subendothelial
layer
2.
Exposed collagen
in damaged blood
vessel wall
1. Platelets adhere to collegen
Platelets bind to von willebrand factor
3. Platelets are activated
ECF
Figure 16-11
18-16
Coagulation – Step 3
Coagulation (clotting) – last and most effective defense against
bleeding
 Converts platelet plug into a clot (insoluble network of fibrin threads)
Coagulation Pathways
Extrinsic mechanism
Intrinsic mechanism
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!!!!!!!!
Platelets degranualte
And release XII
Factor XII
Factor XI
(active)
Damaged
tissues
Factor IX
(active)
Thromboplastin
(factor III)
Inactive
Inactive
Ca2+, PF3
Factor VII
Factor VIII
(active)
Inactive
Ca2+
Factor X
(active)
Prothrombin
activator
Prothrombin
(factor II)
Inactive
Factor III
Factor V
Ca2+
PF3
Factor V
Factor XIII
Ca2+
Thrombin
Fibrinogen
(factor I)
Fibrin
Fibrin
polymer
18-17
3
3/21/2012
Overview of Hemostasis and Tissue Repair
Coagulation and Fibrinolysis
Damage to
wall of
blood vessel
1
Vasoconstriction
Collagen
exposed
Tissue factor
exposed
Platelets
adhere and
release
platelet
factors
Coagulation
cascade
2
Cell growth and
tissue repair
3
Clot: reinforced
platelet plug
Fibrinolysis
Clot
Thrombin
Thrombin
formation
Platelets aggregate
into loose platelet
plug
Temporary
hemostasis
Coagulation
Plasminogen
tPA
Fibrinogen
Converts
fibrinogen
to fibrin
(tissue plasminogen
activator)
Fibrin
polymer
Plasmin
(enszyme)
Fibrin
fragments
Fibrin slowly
dissolved by
plasmin
• clot retraction occurs within 30 minutes
• platelet-derived growth factor secreted by platelets and endothelial cells
- mitotic stimulant for fibroblasts and smooth muscle cells
Figure 16-10 (15 of 17)
Figure 16-13
Cardiac Cycle
Structure of Heart
 Heart has
4 chambers
 2 atria receive blood from venous system
 2 ventricles pump blood to arteries
 Pulmonary and systemic systems
Is
repeating pattern of contraction and relaxation of
heart
Systole refers to contraction phase
Diastole refers to relaxation phase
Atria contract simultaneously; ventricles follow 0.10.2 sec later
Stroke
volume : amount of blood ejected from 1
ventricles during systole (~ 70 mL)
EDV – ESV = Stroke Volume
13-32
13-43
13-46
4
3/21/2012
Electrical Activity of Heart
SA Node Pacemaker
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
13-53
Electrical Conduction in the Heart
Conducting Tissues of Heart
1
1 SA node depolarizes.
SA node
SA
node functions as
pacemaker

Depolarizes spontaneously

(autorythmic cells)
Pacemaker Potential
AV node
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
2
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
3
Internodal
pathways
 Wave of
depolarization
moves into ventricles
5
Depolarization wave
spreads upward from
the apex.
AV node
4
AV bundle
Bundle
branches
Purkinje
fibers
5
13-58
Figure 14-18, steps 1–5
SA Node Pacemaker Potentials
Membrane potential (mV)
+10
0
Cell
contracts
–10
Fast
Ca2+ inflow
–20
Fast K+
outflow
–30
Action
potential
Threshold
–40
Slow Ca2+ inflow
–50
Pacemaker
potential
(HCN channels)
Slow Na+
inflow
–60
–70
0
.4
.8
1.2
1.6
Time (sec)
HCN channels = hyperpolarization activated cyclic nucleotide channels – channels open in response to
hyperpolariztion!!!!! Na+ moves in
5
3/21/2012
Action Potential in Myocardial Cells
Action
Excitation-Contraction Coupling
potential of a cardiac contractile cell
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
Depolarization
Membrane potential (mV)
1 Na+ Close
+20
2
K+ out but Ca+ in (slow)
0
–20
–40
3 Ca+ close and More K+ open (out)
0
–60 Na+ in
–80
4
4
–100
0
100
200
Time (msec)
Phase
300
Membrane channels
0
Na+ channels open
1
Na+ channels close
2
Ca2+ channels open; fast K+ channels close
3
Ca2+ channels close; slow K+ channels open
4
Resting potential
13-61
Figure 14-13
Cardiac Muscle (Myocardium)
 Ca+
Refractory Periods
induced Ca+ release
12-77
13-62
Electrocardiogram (ECG/EKG)
Electrocardiogram (ECG or EKG)
 Composite of
all action potentials/amplified/recorded
electrical activity of heart conducted thru ions
in body to surface
 Recording of
•
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
13-63
6
3/21/2012
Electrical Activity of Cardiac Cycle
START
P wave: atrial
depolarization
P
The end
R
P
Elastic - recoil
PQ or PR segment:
conduction through
AV node and AV
bundle
T
P
QS
Atria contract
T wave:
ventricular
repolarization
R
Muscular
Repolarization
T
P
QS
P
ST segment
R
Q wave
Q
R wave
R
P
QS
R
Ventricles contract
P
Q
P
Fenestrated &
Discontinuous capillaries
S wave
QS
Fenestrated & Discontinuous capillaries
13-72
Figure 14-21 (9 of 9)
Cholesterol and Lipoproteins
Veins
 Lipids
& cholesterol
carried in blood by
plasma lipoproteins
•Valves
•Skeletal muscular pumps
•Diaphragm
 LDLs: produced in
liver
 Many
organs cells
have receptors for
lipoproteins
 Cell engulfs it
 Liver removes LDLs
this way
 HDLs take cholesterol
to liver
13-77
LDL and Plaque
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
The
development of
atherosclerotic
plaques
Endothelial cells
Elastic connective tissue
Smooth muscle cells
(a) Normal arterial wall
LDL cholesterol accumulates
Macrophages ingest Cholesterol and
become foam cells
(b) Fatty streak
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.
(c) Stable fibrous plaque
Platelets
Macrophages
(d) Vulnerable plaque
Figure 15-25
7
3/21/2012
Arrhythmias Detected on ECG
Ischemic Heart Disease
Arrhythmias
are abnormal heart rhythms
rate <60/min is bradycardia; >100/min is
tachycardia
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)
Heart
13-84
13-87
Arrhythmias Detected on ECG
Lymphatic System
 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
3
basic functions:
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
1.
13-88
13-95
Lymphatic System

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)
13-97
8