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CARDIOVASCULAR
SYSTEM
The blood, heart and blood vessels
Blood
 The heart beats by the third week after
conception.
 Blood allows transport of oxygen, nutrients and
waste
 Hemopoeisisblood cell formation,
occurs in the bone
marrow
Blood Functions
 Transports dissolved gases
 Distributes nutrients
 Transports wastes
 Transports enzymes and hormones
 Regulates pH and electrolyte composition of
interstitial fluids
 Clotting prevents fluid loss
 Defends against toxins and pathogens
(WBCs)
 Regulates body temperature
Blood Composition
(blood is connective tissue)
 Plasma-ground substance-watery with dissolved

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proteins, is sticky and resists flow
Formed elements--RBCs, WBCs, Platelets
Plasma + formed elements = whole blood
Blood Volume:
5-6 L adult male
4-5 L adult female
hypovolemic
hypervolemic
normovolemic
Plasma = 55% of blood
volume
Formed elements = 45% of
blood volume
Red Blood Cells/RBCs/Erythrocytes
 Function-Transport oxygen and carbon dioxide
 Structure- flat, circular, no nucleus. Can’t repair
or reproduce. Breaks down in 120 days. Made in
red bone marrow
 Hematocrit (hct)= percentage of whole blood
taken up by formed elements
 Hemoglobin (hgb)= Oxygen
carrying protein in RBCs,
makes RBCs red, contains
iron
Anemias
 O2 carrying ability of blood is decreased.

Signs and symptoms: weakness, lethargy,
pale skin and mucous membranes
 Iron Deficiency Anemia- too little
iron coming in or too much lost
(bleeding). RBCs can’t make
functional hemoglobin, therefore blood can
carry less oxygen.
Iron Rich Foods
 Red meats
 Liver
 Dark green leafy vegetable
 Whole grains
 Dried fruits (raisins, prunes)
Sickle Cell Anemia
 Sickle Cell Anemia-affects a small proportion
of the African-American population. (1 out of
every 500 births). Caused by defective
hemoglobin.
 Lots of O2- the RBCs look normal but, when
O2 is given up RBCs get stiff and curved and
are easily damaged. The ‘sickled’ RBCs get
stuck in the small capillaries leading to pain
and organ damage.
 Treatment: blood transfusion, drugs – no cure
Anemias
 Hemorrhagic Anemia- caused by severe
bleeding-leads to low blood volume with low
hemoglobin and hematocrit
 Aplastic Anemia- bone marrow doesn’t make
new RBCs. Fatal without bone marrow
transplant
 Pernicious Anemia- RBCs don’t mature
because of lack of vitamin B12. Requires
supplementation by injection- B12 not
absorbed well through digestive system.
Blood Types
 Agglutinogens-antigens (substances that can
make the body produce antibodies) on the
surface of RBCs
 3 important agglutinogens:
 A, B, Rh
Blood Types
 ABO Types
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Type A- has agglutinogen A-40% of American
population
Type B –has agglutinogen B-10% of American
population
Type O-has NO agglutinogens- 46% of the
American population
Type AB- has both agglutinogens-4% of the
American population
Blood Types
 If the wrong type of blood is given to a person, the
agglutinogens in the person's blood will attack the
donor blood and cause agglutination (clumping) and
hemolysis (breakdown of RBCs) which causes
transfusion reaction and death!
 Type A can take Type A or Type O blood
 Type B can take Type B or Type O blood
 Type AB can take Type A, B,or O blood(universal
recipient)
 Type O can only take Type O blood (universal
donor)
Rh Factor
 Rh agglutinogen (Rh factor)
 Rh+ has the RH agglutinogen
 Rh- does not have the Rh agglutinogen
 75% of U.S. population is Rh+
 Hemolytic disease of the newborn (Rh
compatibility)- erythroblastosis fetalis.
Rhogam given to Rh- moms to protect future
Rh positive babies
White Blood Cells/WBCs/Leukocytes
 2 Classes
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Granulocytes—(look like granules in
cytoplasm) neutrophils, eosinophils, basophils
Agranulocytes— (have no
granules)monocytes, lymphocytes
Typical WBC count is 5,000-10,000 leukocytes
per microliter of blood
Leukemia
 Usually WBC count is > 100,000
 Abnormal WBCs will proliferate. Immature and
abnormal WBCs get into blood stream in large
numbers, can invade tissues and organs
 These cells use LOTS of energy and replace normal
cells in the bone marrow
 RBCs decrease (resulting in anemia), platelets
decrease (resulting in decreased clotting ability,)
untreated leads to death!
 Can be acute (short and severe) or chronic (lasts a
long time)
Leukemia (cont.)
 Acute can be caused by radiation exposure or virus.
 Chronic can be caused by chromosomal abnormalities or
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immune system malfunction
There are very effective treatments for some types, but
not for others.
Acute lymphoid leukemia if detected early and treated85-90% of patients in remission more than 5 years. Acute
myeloid leukemia- only 10-14% are in remission five
years
Treatments include bone marrow transplants, radiation,
chemotherapy
Need to isolate patient to protect them from infection
Platelets/Thrombocytes or
Megakaryocytes
 Thrombocytes (clotting cells) or
megakaryocytes (big nucleus cells)—
 found in bone marrow—make platelets
 Platelets are really cell fragments—packets of
enzymes, not cells
 New platelets constantly replace old platelets
 Too few platelets = thrombocytopenia
 Too many platelets = thrombocytosis
Platelets/Thrombocytes or
Megakaryocytes
 Functions

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Transport chemicals needed for clotting
Plug holes in damaged blood vessels
Shrink clots so healing can take place
Hemostasis
 (hemo=blood, stasis=halt) stops blood flow so
healing can start
 5 steps
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1. Vascular phase-local vasoconstriction
makes vessels smaller at site of injuryhappens immediately and lasts for 30 min.
2. Platelet phase-platelets attach to site and
plug the hole (within seconds of injury)
3. Coagulation phase- starts 30 sec. to several
min. after injury. Coagulation = blood clotting
Hemostasis
 4. Clot retraction- platelets contraction and
cause clot to get smaller
 5. Fibrinolysis- (lysis=destruction) clot
dissolves
Clotting Abnormalities
 Hemophilia- inherited disorder causing
excessive bleeding- inadequate production of
clotting factors. 80-90% of victims are male.
Usually a clotting factor VIII is lacking.
Transfusions of Factor VIII come from the
pooled blood of many donors.
 Sometimes blood clots within the vessels
when it shouldn’t:
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Thrombus =stationary clot
Embolus=clot moving through circulation
The Heart
 Heart = pump
 Beats about 100,000 times
daily
 Circulatory system: heart, hollow blood
vessels and blood
 Arteries: efferent—carry blood away
from heart
 Veins: afferent—return blood to heart
The Heart
 Capillaries-tiny blood vessels
that connect the smallest veins
Pulmonary Circuit- takes blood to and from the
lungs
Systemic Circuit-takes blood to and from the
rest of the body (except the lungs)
Heart Chambers
 2 Atria(atrium is
singular)
(atrium =chamber)
function of atria
is to collect
blood
 2 Ventricles-function of ventricles is to pump
the blood
Heart Chambers
 Right atrium- takes blood away
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from the body (systemic
circulation) and pumps it into the right
ventricle
Right Ventricle- pumps blood
into the pulmonary circuit
Left atrium-takes blood from the lungs (pulmonary circuit) then
pumps blood into the left ventricle
Left ventricle-pumps blood out to the body(systemic)
Every time the heart beats, both ventricles contract pumping out
equal amounts of blood
Superficial Anatomy of the Heart
 Size- size of one’s fist about the
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center of the thoracic cavity,
enclosed by mediastinum
(divider between the 2 plueral
cavities wt. about 11 oz. (300g)
Pericardial cavity-encases the
heart (lined by pericardium)
Base- (top) connected to the
great vessels
Apex- tip of heart
Valve=tissue folds allow blood to
flow only one way through heart
Right pulmonary artery
Aorta
Left pulmonary artery
Superior vena cava
Left pulmonary veins
Right pulmonary veins
Inferior vena cava
Apex
Deoxygenated blood
Oxygenated blood
Left atrium
Pulmonary valve
Right atrium
Tricuspid valve
Right ventricle
Aortic valve
Bicuspid/ Mitral valve
Left ventricle
Blood Flow
Heart Wall
 3 layers
 Epicardium /
Pericardium
 Myocardium
 Endocardium
Epicardium (Pericardium)
 Outer, protective covering
 Double layer membrane (or sac) that helps
decrease friction during heart beats- prevents
tissue damage
Myocardium
 Muscle layer, layers that wrap around atria
and ventricles
Endocardium
 Inner layer- lines chambers of heart
 Smooth layer of cells that line inside of the
heart.
 Allows blood to flow
smoothly
Diseases and Disorders
 Carditis—general term for inflammation of the
Heart

Endocarditis-inflammation of the endocardium20-30% mortality rate-usually caused by blood
clots that break away from the inner surface
and go into the circulation as emboli leading to
stroke, heart attack, kidney failure
Diseases and Disorders
 Myocarditis- inflammation of the myocardium
caused by bacteria, viruses or fungi. Usually
results in increased heart rate leading to
abnormal contraction of the heart
Diseases and Disorders
 Pericarditis-inflammation of the pericardium. Can be
caused by a variety of pathogens. Layers of the
pericardium (epicardium) rub together leading to an
increase in fluid which can restrict heart movement
resulting in cardiac tamponade (excess fluid in
pericardium leading to decreased effectiveness of
heartbeat)
Diseases an Disorders
 Coronary Artery Disease (CAD)-
causes a decrease in coronary
circulation leading to decreased oxygen in the
heart muscle.
Decreased circulatory supply=coronary
ischemia(usually caused by partial or complete
blockage of blood flow through the coronary arteries)
CAD is progressive
Primary Symptom=angina pectoris (angina=pain,
pectoris=chest)
Exertion or emotional stress can bring on pain
Diseases and Disorders
 CAD treatment
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Reduce stress or find positive ways to deal
with stress
Decrease dietary fat
Drugs-beta blockers (prevent sympathetic
nervous system from stimulating heart
muscle), nitroglycerin (vasodilator-transdermal
patch or sublingual pill)
Diseases and Disorders
 CAD treatment

Cardiac Catheterization- catheter inserted until
blocked place is reached and imaged
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Options: tool inserted to ream out artery and plaque
suctioned out OR
Balloon angioplasty- balloon in catheter is inflated
pushing plaque against vessel walls OR
Stent inserted to hold plaque against artery walls
Coronary Bypass surgery- Part of a blood
vessel (usually a vein) taken from another
part of the body (chest or leg), grafted on to
bypass blocked artery
Myocardial Infarction
 Heart Attack!
 What happens?
 Treatment
 Risk factors
Myocardial Infarction (heart attack)
 Cardiac muscle cells die from decreased oxygen.
Tissue degenerates so there is an area of the heart
that doesn’t function (infarct)
 Often caused by severe CAD- scar tissue that forms
in damaged area causes heart to beat inefficiently.
Heart beat can become irregular, blood vessels may
constrict
 Most dangerous time after MI is the first hour after
the attack (golden hour) -25% die before Medical
help arrives. 65% of MI deaths in those under age 50
happen in the first hour
Myocardial Infarction (heart attack)
 Treatment goals
limit size of infarct
 Prevent further complications
 Increase circulation with vasodilators
 Increase Oxygen
 Decrease cardiac workload
 Eliminate source of blockage
 Risk Factors- Smoking, increased blood pressure,
increased cholesterol, diabetes, obesity, sedentary
life style, high stress, hereditary factors
 If a person has 2 of these, MI risk doubles

The Heartbeat
 Normal heart rate 60- 100 beats per
minute
 Bradycardia- slow heart rate, <60
bpm

Treat with artificial pacemaker
 Tachycardia- fast heart rate, >100
bpm,
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Heart works too hard
Ventricles don’t have time to fill with
blood
The Heartbeat
 Cardiac cycle- time of the start of one heart
beat to the start of the next heart beat
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Systole- contraction phase. Heart is
pumping/beating
Diastole- relaxation phase, between beats
 Heart Sounds

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Stethoscope- instrument used to listen to heart
sounds
Auscultation- act of listening to sound with an
instrument
Electrocardiogram/ECG/EKG
 Record of electrical activity
of heart.

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Gives info on the
performance of different
areas of the heart.
The tracing looks different
when the electrodes are
placed in different areas
Cardiac Arrhythmias
 Cardiac Arrhythmias—abnormal patterns of heart
activity
 Heart block—damage to conductive pathways.
Can cause skipped beats
 PVC—premature ventricular contractions
 Ventricular tachycardia (V-tach)—

very rapid heart beat—can lead to Ventricular
fibrillation (V-fib)

(V-fib) heart quivering, not pumping blood—rapidly fatal
unless defibrillation occurs
Cardiac Arrhythmias
 Defibrillator—electric shock depolarizes entire
myocardium at the same time—gives
ventricles a chance to respond to normal
electrical impulses within heart
Blood Vessels
 Arteries
 Veins
 Capillaries
 Heart, arteries and capillaries
have 30-35% of all body’s blood
(~1.5L)
 Venous system has 65-70% of
all body’s blood (~3.5L)
Arteries
common carotid
subclavian
brachiocephalic
 Carry blood
away from heart
 Branch into
arterioles
 Thicker,
muscular walls
axillary
brachial
renal
abdominal aorta
ulnar
radial
common iliac
femoral
popliteal
Veins
jugular
subclavian
brachiocephalic
 Carry blood
toward heart
Branch into venules
 Venous system
has less pressure
than arterial sys.
 Thinner walls
axillary
superior vena cava
brachial
hepatic portal
inferior vena cava
renal
ulnar
radial
common iliac
great saphenous
femoral
popliteal
Capillaries
 The smallest blood vessels (10 billion in
body) connect arterioles and venules
 The only vessels allowing gas, nutrient and
waste exchange.
 Work together in capillary beds
Diseases and Disorders
 Aneurysm-bulge in the weakened wall of a vessel (often an
artery)-like a bubble in a tire. Can lead to catastrophic blow
out. In the brain it can lead to stroke. In the aorta-the
person can bleed out in seconds. Cause: usually chronic
high blood pressure, can be linked to hereditary disorders
(Marfan’s syndrome)
 Painless, often undetected
 Diagnosis: ultrasound, often found when having tests done
for another condition
 Treatment: Decrease blood pressure with vasodilators,
beta blockers or surgery if aneurysm is accessible
Disease and Disorders
 Arteriosclerosis- artery walls get thick
and tough. Leads to about ½ of all U.S.
deaths each year. CAD (coronary artery
disease) is a form of arteriosclerosis.
 Atherosclerosis
Disease and Disorders
 Atherosclerosis- fatty plaque builds
up on artery walls.
 Most common in elderly, especially males. Estrogen
has a negative effect on plaque build up.
 Other factors- high blood pressure, high cholesterol,
cigarette smoking, diabetes mellitus, obesity and
stress.
 Treatment: decrease fat and cholesterol, stop
smoking, check BP and lower if needed, check blood
cholesterol, control weight, exercise, for severe
cases; cardiac catherization and balloon angioplasty
or stents
Disease and Disorders
 Thrombus- stationary clot
 Embolus clot moving through circulation
Blood Pressure
 Blood pressure=arterial pressure-force of blood against vessel
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walls
Systolic pressure= peak pressure, pressure during ventricular
systole. Pressure while heart is contracting
Diastolic pressure=minimum pressure, pressure during
ventricular diastole. Pressure between heart beats
Measure using a Stethoscope and a Sphygmomanometer
Hypertension-high blood pressure
Hypotension- low blood pressure
Normal-100-140/60-90
Treatment-quit smoking, exercise, decrease
sodium, fat and calories in diet, medication
Exercise and Cardiovascular System
 Benefits of regular exercise to cardiovascular
system
Increase heart size and cardiac output
Decrease heart rate
Decrease blood cholesterol
Decrease blood pressure
Helps decrease consequences of stress
Could reduce heart attack chance by 1/2
Blood Loss and Shock
 Blood Loss:
Immediate problemmaintain adequate BP
and blood flow to
peripheral tissues
 Long term problemrestore normal blood
volume

Blood Loss
 Shock
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Acute crisis situation – life threatening
Low and falling blood pressure leads to too little
blood flow. Therefore, tissues are starved for
oxygen and nutrients
Causes; hemorrhage, heart damage, external
pressure on the heart, extensive peripheral
vasodilatation
Signs and symptoms- hypotension, cool and
clammy skin, rapid and weak pulse, confusion, no
urination and metabolic acidosis(lactic acid made
in oxygen deprived tissues
Aging and the Cardiovascular
System
 Changes to the Blood-
Hematocrit decreases
 Increased likelihood of venous thrombosis(usually in the
legs)
Changes to the HeartDecreased cardiac output
decreased maximum heart rate and arrhythmias
Increased atherosclerosis->decreased circulation
Increased scar tissue
Changes to the Vessels
Some arteriosclerosis, arteries lose some elasticity
Increase risk of stroke and heart attack
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