Chapter 19
Cardiovascular System:
The Blood
AP2 Chap. 19: Cardiovascular Syst
1
Cardiovascular System: The Blood
I. Functions of the Blood
II. Plasma
III. Formed Elements
IV. Hemostasis
V. Blood Grouping
VI. Diagnostic Blood Tests
AP2 Chap. 19: Cardiovascular Syst
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Cardiovascular System
• Cells req. constant nutrition &
waste removal b/c they are
metabolically active
Fig. 1.3 pg 8
• This system made up of the heart,
the blood vessels, & the blood:
connects the various tissues of
the body. The heart pumps blood
thru the blood vessels & the blood
delivers nutrients & picks up
waste products.
AP2 Chap. 19: Cardiovascular Syst
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Blood: Facts & Figures
• Blood: Type of CT
– Formed Elements:
• 45% make-up
• Cells
• Cell Fragments
– Plasma
• 55% bld vol.
• Liquid Matrix
• Total Bld Vol.
Figure 19.1 pg 651
– ♀ 4-5 Liters
– ♂ 5-6 Liters
• 8% of total body Weight
AP2 Chap. 19: Cardiovascular Syst
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I. Fxns of the blood
AP2 Chap. 19: Cardiovascular Syst
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I. Fxns of the blood
The blood helps maintain homeostasis in several ways:
1. Transport of gases, nutrients, & waste products.
2. Transport of processed molecules
3. Transport of regulatory molecules
4. Regulation of pH & Osmosis
5. Maintenance of Body Temperature
6. Protection against foreign substances
7. Clot formation
AP2 Chap. 19: Cardiovascular Syst
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I. Fxns of the blood
The blood helps maintain homeostasis in several ways:
1. Transport of gases,
nutrients, & waste products.
2. Transport of processed
molecules
• O2:
– lungs cells
• CO2:
– cells  lungs for exhalation
• Ingested nutrients, ions, & H2O:
– Digestive system  cells
• Waste products:
– Cells  kidneys for elimination
• Many things are made in one place
in the body. They are then carried
via the blood to another part for
modification & finalization.
• Ex\
– Skin prod’s Vit D
– Transferred to liver & kidney to
modify into its active form
– Finalized form travels to the
small intestine to promote
Ca2+ uptake
3. Transport of regulatory molecules
• Carries hormones & enz’s that regulate body processes from 1 body part
to another
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I. Fxns of the blood
The blood helps maintain homeostasis in several ways:
4. Regulation of pH & Osmosis
6. Protection against foreign
substances
• Buffers maintain blood pH
• Homeostasis=7.35-7.45
• Osmotic composition:
– Bld is critical for maintaining
normal fluid &ion balance
• An important part of the immune
system is located w/in the blood
& helps fight foreign substances
such as toxins or
microorganisms
5. Maintenance of Body Temp.
7. Clot formation
• Warm bld is transferred from
the body core to the body
surface where heat is released
• Protects against XSV bld loss
when bld vessels are damaged
• 1st step in tissue repair & return
to fxn when tissues are
damaged
8
AP2 Chap. 19: Cardiovascular Syst
II. Plasma
AP2 Chap. 19: Cardiovascular Syst
9
II. Plasma
• 91% water & 9% other
– Proteins, ions, nutrients,
gases, wastes
– Colloid
Figure 19.1 pg 651
• Plasma Proteins:
 Pro’d by liver or bld cells
1. Globulins
2. Albumins
3. Fibrinogen
•
Ions: Na, K, Ca, Mg, Cl,
Fe, PO4, H, OH-, HCO3Nutrients:
• Waste: Urea, Uric Acid,
•
Creatinine, Ammonia
– Vitamins
Salts, Bilirubin, & lactic
– Glucose, AA’s, Cholesterol,
acid
& triglycerides (aka triacylglycerol )
• Gases: O2, CO2, & N2
• Regulatory Substances
10
• Water:
– Acts as a solvent & suspending medium
– Involved in osmosis, membrane potential, & acidbase balance
• Nutrients:
– Vitamins: promote enz activity
– Rest: energy & building blocks
• Regulatory Substances:
– Enz’s catalyze chem rxns
– Hormones stimulate/inhibit body fxns
• Gases
– O2
• Req’d for aerobic respiration
II. Plasma
Functions in the plasma:
• Ions:
– CO2
• Waste product of aerobic respiration that can be used as
bicarbonate helping buffer bld
– N2
• Inert
11
II. Plasma
Fxn of plasma proteins
1. Globulins:
–a
• Protects tissues via
inflammation
• Fxns as a transport protein
• Converts Fe2+ to Fe3+ for
transport in transferrin
• Transports hemoglobin from
damaged RBC’s
–b
• Acts as a transport protein
• Involved in immunity
• Prevents blood loss
2. Albumin:
– Partly responsible for
bld viscosity & osmotic
pressure
– Acts as a buffer
– Acts as a transport
protein
3. Fibrinogen
– Fxns in bld clotting
–g
• Most antibodies are g
globulins involved in immunity
12
II. Plasma
Composition
Waste:
• Urea, Uric Acid, Creatinine, Ammonia Salts:
– Byproducts of protein metabolism that are
excreted by the kidneys
• Bilirubin
– Byproduct of RBC breakdown that is excreted by
the liver as part of the bile into the intestine
• Lactic Acid
– Byproduct of anaerobic respiration that is
converted into glucose by the liver
AP2 Chap. 19: Cardiovascular Syst
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III. Formed Elements
A.
B.
C.
D.
Production of Formed Elements
Red Blood Cells
White Blood Cells
Platelets
AP2 Chap. 19: Cardiovascular Syst
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III. Formed Elements:
3 major classes
Red Blood Cells
(Erythrocytes)
RBC’s
700X more than WBC
17X more than platelets
White Blood Cells
(Leukocytes)
WBC’s
Granulocytes
Basophil
Platelets
(Thrombocytes)
Agranulocytes
Monocyte
Eosinophil
Lymphocyte
Neutrophil
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Hematopoiesis
(Hemopoiesis)
III. Formed Elements
Prod’n of formed elements
• Embryo:
– Tissues like the yoke
sac, liver, thymus,
spleen, lymph nodes,
& red bone marrow
(RBM)
• After Birth:
– Confined to RBM with
some lymphoid tissue
aiding in prod’n of
lymphocytes
– Young children
almost all bone marrow
is RBM
– Adults RBM confined
to ribs, sternum,
vertebrae, pelvis,
proximal femur &
humerus (rest replaced
by Yellow bone
marrow)
Figure 19.2 pg 655
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III. Formed Elements
RBC’s: Structure
• Biconcave disk with thicker
edges than in the center
– Allows for greater surface area &
makes movement of gases into the
cell more rapid
– Allows for easier bending & folding
’ing its size to allow it to pass
more easily thru small bld vessels
• Original cell looses its nucleus &
almost all organelles when
mature.
• Main Component w/in RBC:
– Hemoglobin red pigmented
protein filling 1/3 of the RBC vol.
• Minor Components:
– Lipids, ATP & the enz: carbonic
anhydrase
AP2 Chap. 19: Cardiovascular Syst
Figure 19.3 pg 656
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III. Formed Elements
RBC’s: FXN
Primary Fxn O2 transport
– Take O2 from the lungs to
the body tissues
– 98.5% of O2 in bld linked to
hemoglobin
– 1.5% dissolved in plasma
– Take CO2 from body tissues
to the lungs
• CO2 Transport in blood
– 3 major ways:
1. 7% dissolved in plasma
2. 23% attached to
Hemoglobin
3. 70% transported as
bicarbonate ion (HCO3-)
•
• RBC rupturehemolysis
• Hemoglobin must be in
cell if not denatures & no
longer fxnal
AP2 Chap. 19: Cardiovascular Syst
Carbonic anhydrase is the
enzyme responsible for
converting CO2 & H2O into
Carbonic Acid
wh/dissociates into a H+ &
HCO318
III. Formed Elements
RBC’s: Hemoglobin
Figure 19.4 pg 656
• 4 PP-Chain + 4 Heme-groups
• Each polypeptide chain (globin) is bound to 1 heme.
– 9 hemoglobin types based on aa sequence (a, b, g, d &
embryonic)
– Most adult is a combo of 2 a and 2 b
• Heme is a red pigment molecule containing an iron atom
• 3 types of Hemoglobin exist w/ diff’s in their affinity for O2
1. Embryonic: pro’d up to 3rd mo. of development
2. Fetal: @ 3rd mo fetal replaces embryonic hemoglobin
3. Adult: by birth 60-90% is adult by 2 to 4 almost nothing but
adult
AP2 Chap. 19: Cardiovascular Syst
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III. Formed Elements
RBC’s: Hemoglobin Iron (Fe)
• Fe is req’d for normal
hemoglobin fxn b/c O2
binds to the Fe molecule
w/in the heme
• It is usually ingested in
diet.
• Exposure to O2, binds 1 O2
to each Heme
(oxyhemoglobin) w/o
(deoxyhemoglobin)
• AA’s of the globin bind to
CO2 :
• Also bind to NO, which
fxns as a chemical
signal in the body
(hormone) & induces
the relaxation of
smooth muscle
• Thus Hemoglobin may
play a role in blood
pressure via NO
involvement.
– Carbaminohemoglobin
AP2 Chap. 19: Cardiovascular Syst
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III. Formed Elements: RBC’s
Life History of RBC’s
RBC Production
• Lowered bld O2 induced
the kidney to release
erythropoietin wh/goes to
bone marrow & increases
RBC prod’n thus
increasing bld O2 levels
Figure 19.5 pg 659
AP2 Chap. 19: Cardiovascular Syst
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III. Formed Elements: RBC’s
Life History of RBC’s
• RBC’s only live for 110(♀)120(♂) days
• W/O nuclei they have no way
to prod. new proteins or divide
thus existing proteins, enz’s,
PM components & other
structures begin to degenerate
& the RBC becomes less able
to transport O2 & the PM b/c’s
more fragile over time. They
can rupture releasing
hemoglobin.
• What to do????
Figure 19.6 pg 660
RBC death and Hemoglobin recycling
Aged, damaged, or abnormal
RBC’s are taken to the spleen,
liver & other lymphatic tissue.
Here macrophages isolate
hemoglobin.
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III. Formed Elements: RBC’s: Life History of RBC’s
RBC death and Hemoglobin recycling
• Hemoglobin is separated into
Heme & Globin
• Globin is broken down into it’s
component AA’s that can be
used to make new proteins or
metabolized.
• Heme - Fe is released and the
rest is converted 1st into
biliverdin then to bilirubin
– Bilirubin via bld goes to the liver
& excreted w/in bile to the small
intestine (colors both feces &
urine & reabsorbed bilirubin
derivatives)
– Fe: bound to transferrin & carried
in bld to:
• Various tissues for storage
• Bone marrow to be used in the
production of new hemoglobin.
Figure 19.6 pg 660
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III. Formed Elements: WBC’s
Figure 19.3 pg 656
Figure 19.7 pg 661
Figure 19.8 pg 662
AP2 Chap. 19: Cardiovascular Syst
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III. Formed Elements: WBC’s
• Lack hemoglobin
• Have a nucleus
• Protect the body
against invading
microorganisms &
remove dead cells &
debris from the body
• Most are motile
exhibiting ameboid
movement.
• Leave the bld stream
& enter the tissue via
diapedesis
– b/c thin & elongated &
slip btwn or thru the
cells of the blood
vessel walls
• Chemotaxis: WBC
attraction to foreign
materials or dead
cells w/in the tissue
• At the site of infections WBC’s accumulate &
phagocytize bacteria, dirt, & dead cells; then they die:
• Pus buildup of dead WBC’s+ bacteria + fluid + cell
debris
AP2 Chap. 19: Cardiovascular Syst
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III. Formed Elements: WBC’s
3 major classes
Red Blood Cells
(Erythrocytes)
RBC’s
700X more than WBC
17X more than platelets
White Blood Cells
(Leukocytes)
WBC’s
Granulocytes
Basophil
Platelets
(Thrombocytes)
Agranulocytes
Monocyte
Eosinophil
Lymphocyte
Neutrophil
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III. Formed Elements: WBC’s
Granulocytes
Eosinophil
Basophil
•
Nucleus w/ 2 indistinct
lobes; cytoplasmic
granules stain bluepurple; 10-12 mm in
diameter
• Fxn:
•
Neutrophil
Nucleus often bilobed;
cytoplasmic granules
stain orange-red to
bright red; 11-14 mm
diameter
• Fxn:
– Releases:
– Histamine
promotes
inflammation
– Heparin
prevents clot
formation
•
•
0.5-1%
WBC
•
Nucleus has 2 to 4 lobes
connected by thin
filaments; cytoplasmic
granules stain light pink
to reddish purple; 10-12
mm diameter
• Fxn
Releases
chemicals that
reduce
inflammation
Attacks certain
worm parasites
2-4%
WBC
AP2 Chap. 19: Cardiovascular Syst
•
•
Phagocytizes
microorganisms,
Ag-Ab complexes
& other
substances
Lysozyme
60-70%
WBC
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III. Formed Elements: WBC’s
Agranulocytes
Lymphocytes
Monocytes
• Round nucleus; cytoplasm
forms a halo around the
nucleus; 6-14 mm diameter
• Produces antibodies (Ab’s)
& other chemicals
responsible for destroying
microorganisms; contributes
to allergic rxns, graft
rejection, tumor control, &
reg’n of the immune system
• Nucleus can be round,
kidney shaped, or horse
shoe shaped; contains more
cytoplasm than lymphocyte;
12-20mm diameter
• Phagocytic cell in the bld;
leaves the bld & becomes a
macrophage, wh/
phagocytizes bacteria, dead
cells, cell fragments, & other
debris w/in tissue
20-25%
WBC
AP2 Chap. 19: Cardiovascular Syst
3-8%
WBC
28
III. Formed Elements: Platelets
• Cell fragments
surrounded by plasma
membrane & containing
granules
• ~ 3mm diameter
• Surface displays proteins
that allow platelets to
stick to other molecules
(glycoproteins)
• These surface molecules
& internal granules help
control bld loss
• Also contains actin &
myosin to cause platelet
contraction
• Life 5-7 days
• Essential Functional
Roles:
1. Forming platelet plugs,
which seal holes in
small vessels
2. Promoting the formation
& contraction of clots;
wh/help seal off larger
wounds in bld vessels
AP2 Chap. 19: Cardiovascular Syst
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IV. Hemostasis
A.
B.
C.
D.
E.
Vascular Spasm
Platelet plug formation
Coagulation
Control of Clot formation
Clot retraction & Dissolution
AP2 Chap. 19: Cardiovascular Syst
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IV. Hemostasis
• The stoppage of bleeding
to maintain homeostasis.
• 3 major steps to
achieve hemostasis 
1. Vascular
Spasm
2. Platelet plug
formation
3. Coagulation
AP2 Chap. 19: Cardiovascular Syst
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IV. Hemostasis:
1. Vascular Spasm
• Immediate but temporary constriction of
blood vessel resultant from vessel wall
smooth muscle contraction.
• Can close small vessels completely to stop
bleeding
• Produced by:
1. Nervous System Reflexes

Damage can cause reflexive contraction
2. Chemical Signals

Ex/ platelets release thromboxanes & damaged
endothelial cells release endothelian both of wh/
induce contraction
AP2 Chap. 19: Cardiovascular Syst
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IV. Hemostasis:
2. Platelet Plug Formation
• Accumulation of platelets that
can seal-up small breaks in
blood vessels
• Described in steps that
actually occur simultaneously
Figure 19.9
pg 663
• Platelet Adhesion:
• von Willebrand factor (vWF)
binds platelets to collagen in
damaged tissue attaching
platelets to damaged surface
• Platelet release rxn:
• Bound platelets release ADP,
thromboxanes, & other
chemicals that activate other
platelets
• Platelet aggregation
• Activated platelets express
fibrinogen receptors that bind
fibrinogen (a plasma protein)
wh/ is used to link platelet to
platelet with an interlinking
fibrinogen.
• Activated platelets also express
platelet factor III & coagulation
factor V wh/ are imp. to clot
formation
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IV. Hemostasis: Coagulation
• When a bld vessel is severely
damaged blood clotting
(coagulation) results in the
formation of a clot.
• Blood clot network of threadlike
protein fibers called fibrin that trap
blood cells, platelets, & fluid.
• Formation of a blood clot depends
on a number of proteins called
coagulation factors.
– These factors only fxn after
activation wh/is a complex process
involving multiple chemical rxns.
– Activation begins with 1. Extrinsic &
2. Intrinsic pathways that converge
into the Common Pathway
AP2 Chap. 19: Cardiovascular Syst
Figure 19.10
pg 664
34
IV. Hemostasis: Coagulation: Clot
Extrinsic Pathway
formation
For simplicity Factor will be abbreviated as F
and roman numerals will be numbers
• Extrinsic is so called b/c
chemicals being released
come from damaged
tissue and not w/in the
blood.
• Tissues release
thromboplastin/tissue
factor(TF)/F3 (combo of
lipoproteins &
phospholipids)
• TF in the presence of Ca2+
forms a complex with F7

• This complex activates
F10
• This is the beginning of
the common pathway
AP2 Chap. 19: Cardiovascular Syst
Figure 19.11
pg 665
35
IV. Hemostasis: Coagulation: Clot
formation
Intrinsic Pathway
• Intrinsic is so called b/c
chemicals being
released come directly
from the blood.
• Plasma F12 contacts
collagen from damaged
tissue  F12 activation
• Active F12 stimulation
F11 activates F9
• Activated F9 joins with
F13, platelet
phospholipids & Ca2+ to
activate F10
• This is the beginning of
the common pathway
AP2 Chap. 19: Cardiovascular Syst
Figure 19.11
pg 665
36
IV. Hemostasis: Coagulation: Clot
formation
Common Pathway
• Extrinsic pathway may influence
the fxn of the intrinsic thus they
are not exclusive
• On the platelet surface activated
F10, F5, platelet phospholipids,
& Ca2+ complex to form
Prothrombinase (PT).
• PT converts soluble plasma
protein prothrombin into the enz
 Thrombin (Tn)
• Tn:
– Converts soluble plasma protein
fibrinogen into insoluble fibrin wh/
forms the fibrous network of the
clot
– Stimulate F13 activation
necessary to stabilize the clot
– Also part of + fdbk that stimulates
the production of more Tn &
platelet activation
AP2 Chap. 19: Cardiovascular Syst
Figure 19.11
pg 665
37
IV.Hemostasis:Control of clot formation
• If clotting got out of control…homeostasis wouldn’t be
maintained and it would lead to death.
• Bld has several anticoagulants to prevent unwanted
clotting via inhibition of clotting factors.
• Examples:
• @ site of injury
– Antithrombin
anticoagulants are
• Plasma protein from liver that
outnumbered and thus
slowly inactivates thrombin
– Heparin
unable to prevent
• w/antithrombin inactivates
clotting
thrombin
– Prostacyclin
• Away from site of injury
• Counteracts prothrombin by
clotting factors are so
causing vasodilatation & inhibiting
coagulation factor release from
dilute that anticoagulants
platelets
can fxn properly.
38
IV. Hemostasis: Clot Retraction & Dissolution
• Clot retraction: formed clot begins condenses
into denser compact structure.
– Actin & myosin w/in platelets are like smooth
muscle & begin to contract causing retraction
– Serum will also be squeezed out of the clot.
• Plasma minus fibrinogen & clotting factors
• Consolidation of the clot pulls edges of
damaged bld vessel together helps stop
bld flw, reduces infection, & enhances
healing.
AP2 Chap. 19: Cardiovascular Syst
39
IV. Hemostasis: Clot Retraction & Dissolution
• Fibrinolysis: process by which a clot is dissolved w/in a
few days of its formation.
• Norm bld protein plasminogen is converted into
plasmin: once active it is an enz that hydrolyzes fibrin.
• It b/c part of the clot as it is forming.
• Activated by: thrombin, F12, tissue plasminogen
activator, urokinase, & lysosomal enz’s released from
damaged tissues
Figure 19.12
pg 667
AP2 Chap. 19: Cardiovascular Syst
40
V. Blood Grouping
ABO Blood Group
Rh Blood Group
AP2 Chap. 19: Cardiovascular Syst
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V. Blood Grouping
• Transfusion: transfer of blood or blood
components from one individual to another
• Infusion: introduction of fluid other than blood
(Saline/Glucose sol’n) into the blood.
– Used in cases when bld vol needs to be restored to
prevent shock.
• Antigen (Ag): Surface protein
• Antibody (Ab): protein from the blood plasma
that binds to an antigen and marks that cell for
death.
– Ab’s are specific to a certain Ag. When Ab’s bind
Ag’s on RBC’s they form molecular bridges
attaching multiple RBC’s together. This “clumping”
is called Agglutination.
– This complex may also cause hemolysis.
42
V. Blood Grouping
43
Red Blood Cell
Antigen (Ag)
Antibody (Ab)
In the human there have been 35 blood groups identified,
but there are 2 primary groups of antigens that are
displayed on RBC’s
ABO-Blood Group Variants on Chromosome 9
Type A
Surface displays
A-Ag’s only
Type B
Surface displays
B-Ag’s only
Type AB
Type O
Surface displays Surface displays
No Ags
A & B-Ag’s
Codominance
Rh-Factor Blood Group on Chromosome 1
Rh+
RhSurface displays
Surface displays
Rh-Fator
No antigens
44
Most common blood types that exist
Type A-
Type B-
Type AB-
Type O-
Type A+
Type B+
Type AB+
Type O+
45
Issues w/blood donation & necessity of blood typing:
• Ab’s do not develop unless they are exposed to
a foreign Ag. Thus:
 Frank
A-type Blood
Shot 

Needs a blood transfusion
• Transfused with Type A
blood…lives happily
every after

• Transfused with Type B
blood…his body makes Ab’s
against the B-Ag and his
blood agglutinates &
hemolysis and Frank dies
from massive clot formation


46
Figure 19.13
pg 668
V. Blood Grouping: Ag’s & Ab’s
What would happen to the type AB if an A-Ab was introduced??
AP2 Chap. 19: Cardiovascular Syst
47
Agglutination reaction
Figure 19.14
pg 669
AP2 Chap. 19: Cardiovascular Syst
48
Hemolytic Disease of a Newborn
(HDN)
• Rh- mother gives birth to
an Rh+ fetus
• 1st birth:
– Everything is okay. Baby is
born with out incident.
– During birth mother is exposed
to babies blood and can form
antibodies…
• 2nd birth:
– Antibodies in the mothers body
attack the baby as a foreign
object and can kill it.
• Prevention:
– Injection of mother with
RhoGAM soon after each birth.
– It takes care of babies blood
before the immune system can
respond.