The Cardiovascular System:
Blood
Chapter 14
Function
• Transportation-hormones, gasses, nutrients,
ions, heat
• Regulation- pH, temperature, water balance
in cells
• Protection- clotting, white cells interferons,
complement
Composition
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Connective tissue-Two parts
Plasma = soluble materials (~55%)
Formed Elements = cells (~45%)
Percent occupied by red blood cells (RBC)
= hematocrit (Hct)
• White blood cells (WBC) ~1%
Figure 14.1a
Figure 14.1b
Plasma
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~91% water, 7% proteins, 1.5 % other solutes
Proteins: Albumin (54%)- osmosis and carriers;
Globulins (38%)- antibodies
Fibrinogen (7%)- clotting
Other: Electrolytes , nutrients, gases, hormones,
vitamins & waste products
Formed Elements
I. Red Blood Cells
II. White blood cells
–
A. granular Leukocytes
1. Neutrophils
2. Eosinophils
3. Basophils
–
B. Agranular leukocytes
1. T & B lymphocytes & natural Killer cells
2. monocytes
III Platelets
Formation of Blood Cells
• Called hemopoiesis
• Just before birth and throughout life occurs
in red bone marrow
• Contains pluripotent stem cells
• In response to specific hormones these
develop through a series of changes to form
all of the blood cells
Figure 14.2a
Figure 14.2b
Erythrocytes (RBCs)
• Hemoglobin package- carries oxygen
– Also carries some CO2
• Male has ~ 5.4 million cells/µl; Female has ~4.8
million
• membrane, no nucleus, flexible structure
• use glucose for ATP production to maintain ionic
composition
– No mitochondria
• Wear out fast- live ~120 days
RBC Cycling
• cleared by macrophages (liver & Spleen)
• Fe- recycled in bone marrow
– Carried in blood on transferrin
• Heme bilirubin and excreted (bile)
• Globin A.A. recycled.
Figure 14.3
RBC Synthesis
• called erythropoiesis
• From stem cells: hemocytoblasts
• Released as reticulocytes
– Mature to erythrocytes in 1-2 days
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Production & destruction is balanced
Low O2 delivery (hypoxia) 
erythropoietin release (EPO) from kidney
Stimulates erythropoiesis
Figure 14.4
White Blood Cells
• Defenses: phagocytes, antibody production and
antibacterial action
• Phagocytes:
– Neutrophil- first responders
– Monocytes macrophages (big eaters)
– Eosinophil- phagocitize antibody-antigen complexes Involved in
suppressing allergic responses
– Basophil- intensify allergic reactions
• Immune response:
– T-cells, B-cells& natural killer (NK) cells
WBC Life Span
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5000-10,00 WBC /µl blood
Limited number of bacteria can be eaten
Life span is a few days
During active infection may be hours
Leukocytosis= increased WBC numbers
response to stresses
• Leukopenia = decreased WBC numbers
Platelets
• Myeloid stem cells  megakaryocytes 
2000 -3000 fragments = platelets
• Plug damaged blood vessels
• Promote blood clotting
• Life span 5-9 days
Hemostasis
• Hemostasis = stationary blood
• 1. Vascular reactions (spasm)
– Response to damage
– Quick reduction of blood loss
• 2. platelet plug formation
– Become sticky when contact damaged vessel wall
• 3. blood clotting (coagulation)
– Series of chemical reactions involving clotting factors
• Clotting in unbroken vessel= thrombosis
Coagulation
• Extrinsic pathway common steps
– tissue factor(TF) from damaged cells 1
• Intrinsic Pathway  common steps
– Materials “intrinsic” to blood 1
• 1. prothrombinase which causes
• 2. prothrombin thrombin causes
• 3. fibrinogen  fibrin  clot
Clot Retraction & Vessel Repair
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Clot pugs ruptured area
Gradually contracts (retraction)
Pulls sides of wound together
Fibroblasts replace connective tissue
epithelial cells repair lining
Control Mechanisms
• Fibrinolysis: dissolving of clot by activated
plasmin enclosed in clot
• Clots can be triggered by roughness on
vessel wall = thrombosis
• Loose clot = embolus and can block a small
vessel = embolism
Figure 14.5
Blood Types
• Surface antigens- react with antibodies
• Divided into groups based on antigens
– > 24 blood groups and > 100 different antigens
• We will deal with ABO and Rh groups
ABO Group
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Two antigens = A & B
If have only A –type A
If have only B –type B
If neither then Type O
Blood usually has antibodies that can react with
antigens
– e.g. anti-A antibody or anti-B antibody
• You don’t react with your own antigens
– Thus: type A has anti-B and vice versa
Figure 14.6
Rh Blood Group
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Antigen discovered in rhesus monkey
If have antigen- Rh+
Normally don’t have antibodies
antibodies develop after the first exposure
from transfusion
Transfusions
• If mismatched blood given antibodies bind to it and
hemolyze cells
• Type AB has no AB antibodies so can receive any
ABO type blood called Universal recipients
• Type O have neither antigen so can donate to any
other ABO type called Universal donors
• Misleading because of many other blood groups
that must be matched
The Cardiovascular system:
Heart
Chapter 15
Location
• Thoracic cavity between two lungs
– ~2/3 to left of midline
• surrounded by pericardium:
• Fibrous pericardium– Inelastic and anchors heart in place
• Inside is serous pericardium- double layer around
heart
– Parietal layer fused to fibrous pericardium
– Inner visceral layer adheres tightly to heart
– Filled with pericardial fluid- reduces friction during beat.
Figure 15.1
Heart Wall
• Epicardium- outer layer
• Myocardium- cardiac muscle
– Two separate networks via gap junctions in
intercalated discs- atrial & ventricular
– Networks- contract as a unit
• Endocardium- Squamous epithelium
– lines inside of myocardium
Figure 15.2a
Figure 15.2b
Figure 15.2c
Chambers
• 4 chambers
• 2 upper chambers= Atria
– Between is interatrial septum
– Contains fossa ovalis- remnant of foramen ovalis
• 2 lower chambers = ventricles
– Between is interventricular septum
• Wall thickness depends on work load
– Atria thinnest
– Right ventricle pumps to lungs & thinner than left
Great Vessels Of Heart- Right
• Superior & inferior Vena Cavae
– Delivers deoxygenated blood to R. atrium from
body
– Coronary sinus drains heart muscle veins
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R. Atrium  R. Ventricle
pumps through Pulmonary Trunk
R & L pulmonary arteries
 lungs
Great Vessels Of Heart-Left
• Pulmonary Veins from lungs
– oxygenated blood
• L. atrium Left ventricle
• ascending aorta body
• Between pulmonary trunk & aortic arch is
ligamentum arteriosum
• fetal ductus arteriosum remnant
Figure 15.3a
Figure 15.3b
Figure 15.3c
Valves
• Designed to prevent back flow in response to
pressure changes
• Atrioventricular (AV) valves
– Between atria and ventricles
• Right = tricuspid valve (3 cusps)
• Left = bicuspid or mitral valve
• Semilunar valves near origin of aorta &
pulmonary trunk
• Aortic & pulmonary valves respectively
Figure 15.4ab
Figure 15.4c
Figure 15.4d
Figure 15.5a
Figure 15.5b
Blood Supply Of Heart
• Blood flow through vessels in myocardium
= coronary circulation
• L. & Right coronary arteries
– branch from aorta
– branch to carry blood throughout muscle
• Deoxygenated blood collected by Coronary
Sinus (posterior)
• Empties into R. Atrium
Conduction System
• 1% of cardiac muscle generate action
potentials= Pacemaker & Conduction system
• Normally begins at sinoatrial (SA) node
• Atria & atria contract
• AV node -slows
• AV bundle (Bundle of His)
• bundle branches Purkinje fibers
•  apex and up- then ventricles contract
Pacemaker
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Depolarize spontaneously
sinoatrial node ~100times /min
also AV node ~40-60 times/min
in ventricle ~20-35 /min
Fastest one run runs the heart = pacemaker
Normally the sinoatrial node
Figure 15.6
Electrocardiogram
• Recording of currents from cardiac conduction on
skin = electrocardiogram (EKG or ECG)
• P wave= atrial depolarization
– Contraction begins right after peak
– Repolarization is masked in QRS
• QRS complex= Ventricular depolarization
– Contraction of ventricle
• T-wave = ventricular repolarization
– Just after ventricles relax
Figure 15.7
Cardiac Cycle
• after T-wave ventricular diastole
– Ventricular pressure drops below atrial & AV valves open 
ventricular filling occurs
• After P-wave atrial systole
– Finishes filling ventricle (`25%)
• After QRS ventricular systole
– Pressure pushes AV valves closed
– Pushes semilunar valves open and ejection occurs
– Ejection until ventricle relaxes enough for arterial pressure to
close semilunar valves
Action Potential
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Review muscle
Heart has addition of External Ca2+
creates a plateau
prolonged depolarized period.
Can not go into tetanus.
Figure 15.8
Flow Terms
• Cardiac Output (CO) = liters/min pumped
• Heart Rate (HR) = beats/minute (bpm)
• Stroke volume (SV) = volume/beat
•
CO = HR x SV
Controls- Stroke Volume (S.V.)
• Degree of stretch = Frank-Starling law
– Increase diastolic Volume increases strength of
contraction increased S.V.
– Increased venous return  increased S.V.
• increased sympathetic activity
• High back pressure in artery  decreased S.V.
– Slows semilunar valve opening
Controls- Heart Rate
• Pacemaker adjusted by nerves
– Cardiovascular center in Medulla
• parasympathetic- ACh slows
– Via vagus nerve
• Sympathetic - norepinephrine speeds
• Sensory input for control:
– baroreceptors (aortic arch & carotid sinus)- B.P.
– Chemoreceptors- O2, CO2, pH
Other Controls
• Hormones:
– Epinephrine & norepinephrine increase H.R.
– Thyroid hormones stimulate H.R.
– Called tachycardia
• Ions
– Increased Na+ or K+ decrease H.R. & contraction force
– Increased Ca2+ increases H.R. & contraction force
Figure 15.9
Exercise
• Aerobic exercise (longer than 20 min)
strengthens cardiovascular system
• Well trained athlete doubles maximum
C.O.
• Resting C.O. about the same but resting
H.R. decreased
Figure 15.10
The Cardiovascular System:
Blood Vessels and Circulation
Chapter 16
Blood Vessels
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Arteries- from heart
1. Elastic => large
2. Muscular => distribution to organs
3. Arterioles => distribution to capillaries- mostly
muscle
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Capillaries- thin walled for diffusion
Veins- to heart
1. Venules => from capillaries
2. Veins from tissue to vena cavae to heart
Figure 16.1ab
Figure 16.1c
Blood Vessel Structure
• Three layers
• Arteries-> thicker tunica media
– Elastic tissue and/or muscle
– As they get smaller-> more muscle
– Arterioles-> very muscular- control
• Veins- bigger lumen and thinner walls
• Veins-> valves to prevent backflow
– Venules very thin, no valves
Vessel Functions
• Muscular arteries & arterioles regulate flow
• Sympathetic activity to smooth muscle
vasoconstriction (narrowing)
• Decreased sympathetic activity or NO causes
relaxation or dilation
• Arterioles adjust flow into capillaries
• Systemic veins & venules serve as blood
reservoirs (~64% total blood volume)
Capillary Details
• Capillaries only have endothelium
– Very thin cells & cell nuclei protrude into
lumen- easy diffusion
• Connected from arterioles to venules in
networks
– Sometimes direct route from arteriole to venule
• Filling controlled by small arterioles &
precapillary sphincters
Figure 16.2a
Figure 16.2b
Capillary Exchange
• Slow flow through capillaries
– Allows time for exchange through wall
• Blood pressure 
– filtration of fluid out of capillary
– Mostly in first ½ of vessel length
• Osmosis (protein concentration)
– Reabsorption of fluid from outside to inside
– Mostly in last ½ of vessel length
• Balance determines fluid in circulation
– Excess fluid returned via lymphatic system
– Local signals can adjust capillary flow
Figure 16.3
Venous Return
• Blood enters veins at very low pressure.
• Needs more pumping to get back to heart
• = action of heart; muscle pumps; respiratory
pump
• Some pressure from heart action
• Not enough to overcome gravity
Muscle & Respiratory Pumps
• Contracting skeletal muscles squeeze veins
emptying them
• Because of venous valves flow is toward heart
• Respiratory pump has similar action
• Inhalation decreased thoracic pressure &
increased abdominal pressure
– Blood flows toward heart
• Exhalation allows refilling of abdominal veins
Figure 16.4
Blood Flow
• from high pressure area to lower pressure area, i.e. down pressure
gradient
– Greater gradient greater flow
• Ventricular contraction blood pressure (BP)
– Highest in aorta and declines as flows through vessels
– 110-70 mmHg in aorta ~16 mmHg at venules
–  0 at R. Atrium
• Resistance= opposition to flow
• depends on lumen diameter & length & blood viscosity
– Smaller lumen  greater resistance
– Higher viscosity greater resistance
– viscosity of blood depends on Hct
Resistance
• Depends on vessel lumen diameter
– Smaller lumen  greater resistance
• And blood viscosity
– Higher viscosity greater resistance
– viscosity of blood depends on Hct
• And total vessel length
– Longer the length of flow the more friction with wall
– Total body resistance increases with growth and
addition of tissue
Anatomical Design
• Length and pressure
• Design and local flow control- central
pressure
Pressure Gradients
• Adult anatomy gives constant length
• If central blood pressure is controlled it is
constant
• Only variable is radius of the arterioles
• Each tissue can do it separately
• Review design in picture below
– All tissues have the same pressure gradient
Pressure Gradients (Cont.)
• Note pulse in aorta & large arteries
– MAP
• pressure fall related to resistance
– Note role of arterioles
• Note low venous pressures
– can’t get back to the heart!
Figure 16.5
Regulation of Blood Pressure & Flow
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Fast responses: e.g. standing up
Slower responses: e.g. blood volume
Distribution: e.g. to working muscles
Balance of CO with flow to body
Interacts with many other control systems
Cardiovascular (CV) Center major regulator
Inputs
• Higher centers:
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cerebral cortex,
limbic system,
hypothalamus
HR increases before race;
flow adjusted for body temperature
• Sensory receptor input:
– proprioceptors,
– baroreceptors
– chemoreceptors
Inputs (Cont.)
• Proprioceptors:
– Start HR change as activity starts
• Baroreceptors: in aorta & carotid
 pressure   parasympathetic &
  sympathetic stimulation  CO
• Chemoreceptors: in aorta & carotid
– Low O2, high H+, CO2   vasoconstriction
 BP
Figure 16.6
Output
• ANS to heart
–  Sympathetic  HR &  force of
contraction
–  Parasympathetic  HR
• Vasomotor
– to arterioles  vasomotor tone
– To veins move blood to heart  BP
Hormone regulation
• Renin-Angiotensin system
– Angiotensin II  vasoconstriction+ thirst
–  aldosterone   Na+ & water loss in urine on
• Epinephrine & Norepinephrine  CO
• ADH = Vasopressin
 constriction   BP
 Thirst & water retention in kidney BP
• ANP- from cells in atria
– Vasodilation & loss of salt & water in urine BP
Figure 16.7
Checking Circulation- Pulse
• Pulse in arteries = HR
– Use radial artery at wrist,
– carotid artery,
– brachial artery
• Tachycardia = rapid rest rate (>100 bpm)
• Bradycardia= slow rest rate (<50 bpm)
Blood Pressure
• Use sphygmomanometer
– Usually on brachial artery
• Raise pressure above systolic– stop flow
• Lower pressure in cuff until flow just starts
– first sound  Systolic Pressure
• Lower until sound suddenly gets faint
– Diastolic pressure
• Normal values <120 mmHg for systolic & < 80
mmHg for diastolic
Circulatory Routes
• Two parts: Systemic & Pulmonary
• Systemic circulation- throughout body
– Oxygenated blood deoxygenated as it goes
• All systemic arteries branch from aorta
• All systemic veins empty into Superior
Vena Cava, Inferior Vena Cava or the
Coronary Sinus
– Carry deoxygenated blood to heart
Figure 16.8
Figure 16.9
Figure 16.10a
Figure 16.10b
Figure 16.10c
Figure 16.11
Figure 16.12
Figure 16.13
Figure 16.14a
Figure 16.14b
Figure 16.14c
Figure 16.15
Pulmonary Circulation
• From right ventricle pulmonary trunk
• R. & L. pulmonary arteries
– Carry deoxygenated blood
•  R. & L. lungs
– Gas exchange occurs
•  2 R. & 2 L. pulmonary veins
– Carry oxygenated blood
•  L. atrium
Hepatic Petal Circulation
• Portal vein transports blood from one
capillary bed to another
• GI organs
•  Splenic & superior mesenteric veins
•  hepatic portal vein
• sinusoids in liver
– Mixes with oxygenated blood
•  hepatic vein inferior Vena Cava
Figure 16.16a
Figure 16.16b
Fetal Circulation
• Specialized for exchange of materials with maternal
blood and bypass of lungs
• Exchange in placenta umbilical vein
•  liver ductus venosus
•  inferior vena cava  R. atrium
– Mixes with deoxygenated blood from lower body
•  foramen ovale L. Atrium
• Or  R. Ventricle Pulmonary trunk  ductus
arteriosus  aorta
•  internal iliacs  umbilical arteries Placenta
Figure 16.17
At Birth
• Umbilical arteries medial umbilical
ligaments
• Umbilical vein  ligamentum teres
• Ductus venosus  ligamentum venosum
• Placenta expelled
• Foramen ovalis closes fossa ovale
• Ductus arteriosus  ligamentum
arteriosum
Aging
• Stiffening of aortae
• Loss of cardiac muscle strength
– Reduced CO & increased systolic pressure
• Coronary artery disease
• Congestive heart failure
• atherosclerosis