Circulatory System

William Harvey
 Researched and discovered the circulation of blood
 He demonstrated:
o Blood flow through the larger vessels is unidirectional, with valves to prevent back flow
o Rate of flow through major vessels was far too high for blood to be consumed as it was believed
o Predicted the existence of fine vessels that connected arteries and veins

SYSTEMIC CIRCULATION: moves blood to the body

and back
PULMONARY CIRCULATION: moves blood to the
lungs and back

Left Ventricle is much thicker and stronger because it

has to generate enough pressure to move blood
through the whole body

1. Deoxygenated blood returns from the body to the

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heart through the vena cava to the right atrium
2. Blood is pumped to the right ventricle through the atrio-ventricular valve
3. Right ventricle contracts, the blood is sent through the semilunar pulmonary valve, to the pulmonary artery
4. Blood is taken to the lungs, and picks up oxygen
5. Oxygenated blood returns to the left atrium through the pulmonary veins
6. Blood gets pumped to the left ventricle across the atrioventricular valve
7. Left ventricle contracts, and the blood exits through the semilunar aortic valve, to the aorta, and travels
through the whole body

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 8. When blood reaches the desired location, the oxygen is dropped off, and the blood becomes deoxygenated
9. Returns to the vena cava, and the whole process begins again

ARTERIES CAPILLARIES VEINS

PRESSURE High Low Low

Collect blood from the

Carry blood from heart to Exchange of materials
FUNCTION body and take it to the
the body between cells & blood
heart

FROM – TO Heart to body tissues Tissues to blood Body to heart

Yes (tissue pocket which

VALVES No No prevents backflow of
blood)

MUSCLES Many None Small amounts

Elastic fibres
 They store the energy
that stretches them, at
the peak of every
FIBERS None Few elastic ones
pumping cycle)
 Their recoil helps propel
the blood on down the
artery

Narrow (thin in relation to Just thick enough for an Wide in relation to the
LUMEN DIAMETER
the muscle) RBC to squeeze through wall

3 tunicas

TUNICAS [EXTERNA,
1 layer (intima) 3 tunicas
MEDIA, INTIMA]

 The blood progress along major arteries is pulsatile

TUNICA EXTERNA: tough outer layer of connective tissue

TUNICA MEDIA: a thick layer containing smooth muscle and elastic fibres made of the protein elastin
TUNICA INTIMA: smooth endothelium forming the lining of the artery

SYSTOLIC PRESSURE: peak pressure reached in an artery

 Pushes the wall of the artery outwards  widens the lumen and stretches elastic fibres = storing potential
energy

DIASTOLIC PRESSURE: minimum pressure inside the artery

 At the end of each heartbeat the pressure in the arteries falls sufficiently for the stretched elastic fibres to
squeeze the blood in the lumen = saves energy & prevents diastolic pressure from becoming too low

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VASCONTRICTION: contraction of the circular muscles in the wall of the artery
 In vasocontraction blood pressure is increased in the arteries, circumference is reduced, and the lumen is
narrowed

ARTERIOLES: branches of arteries

 Have high density of muscle cells that respond to various hormones and neural signals to control blood flow
to downstream tissues

Vasoconstriction of arterioles restrict blood flow to the part of the body that they supply, whilst VASOLIDATION increases it

Blood
 PLASMA
o H20 (70% - 80%)
o Vitamins
o Heat (from cell respiration)
o 02/ CO2
o Plasma Protein
o Hormones
o Urea (from decomposition of nitrogen)
o Antibodies (immunoglobulins)

 CELL COMPONENTS
o Red Blood Cells (Erythrocytes)  Haemoglobin for transport of O2 and CO2)
o White blood cells (lymphocytes)  B-Cells, T-Cells & macrophagocytes
o Platelets (cell debris)

Sinoatrial Node
 Contraction in heart is generated by the muscle itself  MYOGENIC
 Membrane of a heart muscle cell depolarizes when the cell contracts  activates adjacent cells, so they also
contract
 SINOATRIAL NODE: muscle cells in the wall of the right atrium, and region of the heart with the fastest
spontaneous beating / Patch of cardiac cells (tissue) with electrical (movement of ions) activity
 Signals from SAN (which cause atrial contraction/systole) cannot pass directly from the atria to ventricles. It
passes through the Atrioventricular node (2nd pacemaker)
o This signal from the SAN reaches the AVN
o From the AVN  signal spreads through the heart via Purkinje fibers
o This signal  ventricle systole
o Closing of the atrioventricular valves
o After ventricles are emptied  semilunar valves close
o Ventricles begin diastole
o Atrioventricular valves open  ventricles start filling with blood
o Four chambers in diastole and filling
o Atria filled, ventricles 70% filled  the cycle has ended
o Cells in the AVN take longer than the ones in the SAN to become excited

1. Waves send electrical impulses

2. Helps in the propagation of the impulse  happens 0,12s later (delay between the arrival of the stimulus
from the SAN and the initiation of contraction of ventricles by the AVN)
Features of the AVN that lead to a delayed initiation of contraction of ventricles:
 AVN cell  smaller diameter  don not conduct as quickly
 Small amounts of Na+ channels in the membrane of the AVN  more negative resting potential

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  Fewer gap junctions between cells of the AVN
 More non-conductive connective tissue
oDelay allows time for atrial systole before the atrioventricular valves close
 Ensures that the atria contract and empty the blood they contain into the ventricles before they
contract
 Contraction of ventricles  causes AVN valves to shut because early contraction of ventricles
would lead to a small volume of blood entering the ventricles
3. Conducting fibers  also help in the propagation of the impulse

Coordination of contraction
 Conducting fibers  coordinated contraction of the entire
ventricle wall
 Once through the AV bundle  signal must be conducted
rapidly to ensure coordinated contraction of ventricle
 AV bundle  receives impulse from the AVN and conducts
the signal to a point where it splits into right and left bundle
branches
o Bundle branches  conduct impulses through the wall
between the two ventricles
 Base of the heart  bundle branches connect to the Purkinje
fibers which conduct the signal more quickly to the ventricles
 Adaptations of Purkinje fibers to facilitate and increase the
speed in the conduction of signals:
o Have a bigger diameter
o Higher densities of voltage gated sodium channels
o High numbers of mitochondria and high glycogen
stores
 Contraction of the ventricle begins at the apex of the heart Scanned with CamScanner

Cardiac cycle
 Heartbeats per minute  BPM
o ‘lub’  closing of the atrioventricular valves
o ‘dub’  closing of the semilunar valves
 Circuit of events between one heartbeat to another (difference of pressure excreted by the blood between
the chambers)
1. SAN sends a wave of electrical impulse
2. Atria relax (diastole)  fill up with blood
a. Atrioventricular valves close
3. Atria contraction (systole)  blood goes into ventricles (0.0 – 0.1s)
a. Atrioventricular valves open
b. Ventricles  relaxed (diastole)
c. Semilunar valves close
4. Ventricles contraction (systole) (0.1 – 0.15s)
a. Semilunar valves open (0.15 – 0.4s)
b. Atrioventricular valves close (0.4 – 0.45s)
5. Diastole of heart before the cycle begins again

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ATHEROSCLEROSIS: hardening of the arteries caused by the formation of plaques, or atheromas, on the inner
lining of arteries

1. LDL = Low Density Lipoprotein  containing fats and cholesterol (‘bad’ cholesterol) accumulate and
phagocytes are attracted by signals from endothelium cells and smooth muscle.
2. Phagocytes engulf the fats and cholesterol by endocytosis, and grow
3. Smooth muscle cells migrate to form a tough cap over the atheroma
4. Artery wall bulges into the lumen = narrows it and impedes blood flow

WHAT MAY CAUSE ATHEROSCLEROSIS:

 High blood concentrations of LDL
 Chronic high blood glucose concentrations due to overeating, obesity or diabetes
 Chronic high blood pressure due to smoking, stress or any other cause
 Consumption of trans fats, which damage the endothelium of the artery

Recent theories that include microbes:

 Infection of the artery wall with chlamydia pneumoniae
 Production of trimethylamine N-oxide (TMAO) by microbes in the intestine

CORONARY OCCUSION: narrowing of the arteries that supply blood containing oxygen and nutrients to the heart
muscle

1. Lack of oxygen (anoxia) causes pain (angina), and impairs the muscles ability to contract  heart beats
faster to try to maintain blood circulation with some of its muscle out of action
2. SOMETIMES: fibrous cap covering atheroma’s rupture  stimulates the formation of blood clots that
can block arteries supplying blood to the heart and cause acute heart problems

Changing the heart rate

 Can be decreased or increased by impulses brought to the heart through two nerves from the medulla of the
brain called the cardiovascular centre

CARDIAC NERVE: signal that causes the pacemaker to increase the frequency of heartbeats (accelerator)

VAGUS NERVE: signal that decreases the rate of heart beats (inhibitor)

 Cardiovascular centre  receives inputs from receptors which monitor blood pressure and its pH and
oxygen concentration (pH of blood reflects CO2 concentrations)

o Low blood pressure, oxygen concentration and pH: suggest that the heart rate needs to speed
up, to increase the blood flow to the tissues, deliver more oxygen and remove more carbon
dioxide
o High blood pressure, oxygen concentration and pH: indicators that the heart rate may need to
slow down.

Epinephrine
Increases heart rate to prepare for vigorous physical activity
 Sinoatrial node responds to epinephrine in the blood, by increasing the heart rate
 Epinephrine (adrenalin): produced by adrenal glands
 SECRETION: controlled by the brain and rises when vigorous physical activity may be necessary because of a
threat or opportunity (fight or flight)
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Hypertension and thrombosis
HYPERTENSION: abnormally high blood pressure on the walls of the arteries
 Clots can block the blood flow through the artery and deny the tissue access to oxygen  can cause a
MYOCARDIAL INFARCTION (heart attack
 Greater resistance to the flow of blood can slow the flow of blood = hypertension

CONSEQUENCES OF HYPERTENSION:
 Damage to the cells that line arteries, and cause a cascade of events that lead to the arteries becoming
narrower and stiff
 Constant high blood pressure  weaken the artery causing a section of the wall to enlarge and form and
ANEURYSM. If the aneurysm bursts, it causes internal bleeding
 Chronic high blood pressure  can lead to stroke by weakening blood vessels in the brain causing them to
narrow, leak or rupture
 Chronic high blood pressure can cause kidney failure as it damages both the arteries leading to the kidney and
the capillaries within the glomerulus

CAUSES:
 Genetic precondition
 Old age  less flexible blood vessels
 Menopause  correlated with the fall of oestrogen levels
 Smoking  raises blood pressure, because nicotine causes vasoconstriction
 High salt diet, excessive amount of alcohol, stress
 Eating too much fat and cholesterol  plaque formation
 Sedentary lifestyle
 Height  affects blood pressure

Artificial Pacemakers
 An artificial pacemaker is a medical device that delivers
electrical impulses to the heart in order to regulate a
malfunctioning sinoatrial node
 Modern pacemakers are externally programmable, allowing
cardiologists to make adjustments as required

Artificial pacemakers are typically used to treat one of two

conditions:
 Abnormally slow heart rates (bradycardia)
 Arrhythmias arising from blockages within the heart’s
electrical conduction system

Defibrillators
FIBRILLATION: rapid, irregular and unsynchronised contraction of the heart muscle fibres
 Cardiac arrest (when blood supply to the heart is reduced and the heart tissues are deprived from oxygen),
causes heart muscle to convulse spasmodically rather than beat in concert, preventing the optimal flow of
blood (ventricular fibrillation)
 Fibrillation is treated by applying a controlled electrical current to the heart via a device called a defibrillator
 This functions to depolarise the heart tissue in an effort to terminate unsynchronised contractions

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 Once heart tissue is depolarised, normal sinus rhythm should hopefully be re-established by the sinoatrial node

Defence against infectious diseases

PATHOGENS: any agent (organism or virus) causing a disease

IMMUNITY: the science that is going to study the way our bodies defend from pathogens

ANTIGEN: any chemical that stimulates an immune response

PLASMA CELLS: large clone of lymphocytes

ANTIBODIES: large proteins that have two functional regions:

 Hypervariable region: binds to a specific antigen
 Another region: helps the body to fight the pathogen by making it more recognizable to phagocytes,
and by preventing viruses from docking to host cells so that they can’t enter the cells

Physical Barrier Chemical Barrier

Skin contains sebaceous glands  sebum

Skin is thick; thus, it is hard for
Skin (made out of lactic acid and fatty acids), the
pathogens to go through it
FIRST LINE pH is acidic, thus killing bacteria’s) barrier
OF
DEFENCE
Mucous
Membranes (nose,
Contains lysozyme, which helps kill pathogens
trachea, vagina,
urethra)

1. Squeeze through pores in

the walls of capillaries and
SECOND move to sites of infection
Phagocytes: non-
LINE OF specific response
DEFENCE 2. Engulf pathogens by
endocytosis and digest
them with enzymes from
lysosomes

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 3. When wounds become
infected, large number of
phagocytes are attracted,
resulting in the formation
of pus (white liquid)
Production of antibodies in response to a
pathogen (antibodies bind to an antigen on
that pathogen)

 Each lymphocyte produces just one type of

antibody (many types of lymphocytes)
 There are too few lymphocytes to initially
produce enough antibodies to control a
pathogen that hasn’t infected the body
before.
 But, antigens in the pathogen stimulate
cell division of the small group of
lymphocytes that produce the appropriate
type of antibody
 Plasma cells are produced within days and
they secrete large enough quantities of the
antibody to control the pathogen and clear
Lymphocytes: the infection
specific response
- Antibodies only persist for a few weeks or
months, and plasma cells (that produce
them) are gradually lost after the infection
has been overcome.
- But some lymphocytes produced during
an infection are not active plasma cells but
become memory cells
- These memory cells remain inactive unless
the same pathogen infects the body again
(in which case they become active and
divide to produce plasma cells very rapidly

T-cells (helper t-cells or Th)

B-cells
Immunity to an infectious disease involves either having antibodies against the pathogen, or memory cells
that allow rapid production of the antibody

Cuts and clots

 When the skin is cut  blood vessels in it are severed and start to bleed. This bleeding is stopped by clotting
 CLOTTING: Blood emerging from cut changes from being liquid to a semi-solid gel  seals up the wound and
prevents loss of blood and blood pressure
 Clotting is important because cuts breach the barrier to infection provided by the skin, and clots prevent entry
of pathogens until new tissue has grown to heal the cut

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Platelets and blood clotting
 Blood clotting: involves a cascade of reaction, each of which produces a catalyst for the next reaction = blood
clots very rapidly
 Blood clotting has to be under rigorous control because if it occurs inside blood vessels the resulting clots can
cause blockages
 Clotting only occurs if platelets release clotting factors

PLATELETS: cellular fragments that circulate in the blood (are smaller than red or white cells)

 In an injury:
1. Platelets aggregate at the site forming a temporary plug
2. Platelets release clotting factors that trigger off the clotting process
3. Cascade of reactions that occur after the release of clotting factors, quickly results in the production
of the enzyme THROMBIN
4. Thrombin converts the soluble protein fibrinogen in to the insoluble fibrin
5. Fibrin  forms a mesh in cuts that traps more platelets and also blood cells
6. Resulting clot is initially a gel, but if it is exposed to the air it dries to form a hard scab

Coronary Thrombosis
CORONARY ARTERIES: carry blood to the wall of the heart, supplying oxygen and glucose (nutrients), needed by
cardiac muscle fibres for cell respiration

CORONARY THROMBOSIS: formation of a clot within the blood vessels that supply and sustain the heart tissue
(coronary arteries)

THROMBUS: blood clot

 Coronary artery is blocked by a thrombus, part of the heart is deprived of oxygen and nutrients:
1. Cardiac muscle cells are then unable to produce sufficient ATP by aerobic respiration 
contractions become irregular and uncoordinated
2. Wall of the heart makes quivering movements (FIBRILLATIONS), that don’t pump blood effectively

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  This condition can be fatal unless it resolves naturally or through medical intervention
 Atherosclerosis causes occlusion in the coronary arteries  where the atheroma develops, the endothelium of
the arteries tends to become damaged and roughened (especially if the artery wall is hardened by deposition
of calcium salts
 Patches of atheroma sometimes rupture causing a lesion
 Coronary occlusion, damage to the capillary epithelium, hardening of arteries and rupture of atheroma all
increase the risk of coronary thrombosis

What causes coronary thrombosis and heart attacks:

 Smoking
 High blood cholesterol concentration
 High blood pressure
 Diabetes
 Obesity
 Lack of exercise

Antibiotics
ANTIBIOTIC: chemical that inhibits the growth of microorganisms (most of them are anti-bacterial)

 They block processes that occur inn prokaryotes, but not in eukaryotes  can be used to kill bacteria inside
the body without causing harm to human cells
 Antibiotics target bacterial:
o DNA replication
o Transcription
o Ribosome function
o Cell wall formation
 Bacteria resistant to ATB: happening randomly, because of a random mutation
 If a bacterium with a random mutation survives ATB, then reproduces, eventually al the cells are going to be
resistant

 To be used only when you have an infection caused by a bacterium  Viral diseases can’t be treated using
antibiotic because they lack metabolism
 VIRUSES ARE NON-LVING AND CAN ONLY REPRODUCE WHEN THEY ARE INSIDE LIVING CELLS
 They use the chemical processes of a living host cell
 They rely on the host cell’s enzymes for ATP synthesis and other metabolic pathways  cannot be targeted
by drugs as the host cell would also be damaged
 If antibiotics are prescribed for a viral infection  it contributes to overuse of antibiotics and increases
antibiotic resistance in bacteria

 There are few viral enzymes which can be used as targets for drugs to control viruses without damaging the
host cell - ANTIVIRALS

 Strains of bacteria with resistance are usually discovered soon after the introduction of the antibiotic 
NOT A CONCERN unless strain develops multiple resistance.
 This is avoided by:
o Doctors prescribing antibiotics only for serious bacterial infections
o Patients completing courses of antibiotics to eliminate infections completely
o Hospital staff maintain high standards of hygiene to prevent cross-infection
o Farmers not using antibiotics in animal feeds to stimulate growth
o Pharmaceutical companies developing new types of antibiotics
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Gas Exchange
GAS EXCHANGE: The movement of gases between the alveoli and bloodstream (via passive diffusion), inside the
lungs

VENTILATION: The exchange of air between the atmosphere and the lungs – achieved by the physical act of
breathing, based on the concept of partial pressure

CELL RESPIRATION: The control release of energy coming from the breaking down of glucose, can be aerobic or
anaerobic

DIFFUSION: The net movement of molecules from a region of high concentration to a region of low concentration,
following a concentration gradient

PARTIAL PRESSURE: The concentration of a particular gas, in a mixture of gases

Components of the System

 NOSE/MOUTH: Tiny hairs which clean the air / mucus function is to catch dust / more blood capillaries
(heat from cell respiration  warmer air)
 LARYNX: Place of the vocal chords / tissue that vibrates with air
 TRACHEA: to let the air pass through / rings of cartilage to prevent it from collapsing when empty
 BRONCHI (Left and Right): transport air  to left and right lung (through bronchus)
 BRONCHIOLE: guide the air to the alveoli
 ALVEOLI: Place for gas exchange with diffusion, based Inside the lungs
on differences between partial pressure

 EXTERNAL AND INTERNAL INTERCOSTAL MUSCLE (pleural membranes: connection between lungs and
ribs)
 ABDOMINAL MUSCLES
 RIB CAGE
 DIAPHRAGM

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Adaptations of Alveoli
 Many and small  ASA
 Wall one cell thick  very thin
 Network of capillaries  more exchange
 A moist ure:
o to prevent it from collapsing
o and to speed up diffusion

Type I pneumocytes
 Very thin alveolar cells that are adapted to carry out gas exchange
 The wall of each alveolus consists of a single layer of cells called the epithelium  most cells in this
epithelium are TYPE I PNEUMOCYTES
 The wall of the adjacent capillaries also
consists of a single layer of very thin cells
 The air in the alveolus and the blood in the
alveolar capillaries is less than 0.5M distance
over which oxygen and CO2 has to diffuse 
is very small  increases the rate of gas
exchange

Type II pneumocytes
 Secrete a solution containing surfactant
that creates a moist surface inside the
alveoli to prevent the sides of the alveolus
adhering to each other by reducing
surface tension
 Rounded cells, and occupy 5% of the alveolar
surface area
 Moisture:
o allows oxygen in the alveolus to
dissolve and the diffuse to the blood
in the alveolar capillaries
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 o provides an area from which CO2 can evaporate into the air and be exhaled

 Fluid secreted by type II pneumocytes contains a pulmonary surfactant

  They form a monolayer on the surface of the moisture lining in the alveoli, hydrophobic heads facing the
air, hydrophilic tails facing the water
 Reduces
o surface tension
o prevents the sides of the alveoli to stick together when air is exhaled (helps to prevent collapse of
the lung)

Pressure changes during

ventilation
 During ventilation, muscle contractions cause the pressure inside the thorax to drop below atmospheric
pressure  air is drawn into the lungs from the
atmosphere (inspiration), until the lung
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pressure has risen to atmospheric pressure
 Muscle contractions then cause pressure inside
the thorax to rise above atmospheric, so air is
forced out form the lungs to the atmosphere
(expiration)

Antagonistic Muscles
 Muscles do work when they contract by
exerting a tension that causes a particular
movement  they become shorter when they
do this
 Muscles lengthen when they are relaxing
(happens passively)

ANTAGONISTIC MUSCLES: when one muscles

contracts and causes a movement, and the second muscle relaxes and is elongated by the first, and vice versa
Ex.: external and intercostal, and diaphragm and abdominal muscles

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 INHALATION EXHALATION

DIAPHRAGM Contraction = down & flattens Relaxation = up and domes

ABDOMINAL MUSCLES relax Contracts

EXTERNAL INTERCOSTAL
contracts Relax
MUSCLES
INTERNAL INTERCOSTAL
Relax contracts
MUSCLES

RIB CAGE Up & outwards Down & inwards

LUNGS VOLUME Increases (less partial pressure) Decreases (more partial pressure)

Epidemiology
 The study of the incidence and causes of a disease
 To obtain evidence  survey data is collected that allows the association between the disease and its
theoretical cause to be tested
 Confounding factors also have an effect on the incidence  can cause false or incorrect associations
between a disease and a factor that does not cause it
 To try to compensate for this  necessary to collect data on many factors apart from the one being
investigated  allows statistical procedures which identify the confounding factors and try to isolate the
effect of single factors

Lung Cancer
CAUSES:
87% of cases
SMOKING Tobacco smoke contains mutagenic chemicals
3% of cases
PASSIVE SMOKING When non-smokers inhale tobacco smoke exhaled by
smokers
5% of cases
Sources of air pollution that are the most significant
AIR POLLUTION are diesel exhaust fumes, nitrogen oxides, and smoke
from burning coal, Wood, etc

Radioactive gas that leaks out of certain rocks like

granite
RADON GAS It accumulates in badly ventilated buildings and people
inhale it

Can cause cancer if dust of them are inhaled

ASBESTOS, SILICA, ETC (SOLIDS) (construction sites, etc)

Symptoms:
 Difficulties breathing


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  Persistent coughing
 Coughing blood
 Chest pain
 Loss of appetite
 Weight loss
 General fatigue

Emphysema
 The large amounts of thinned walled alveoli become less and with more thick walls
o Total surface area for gas exchange  reduced
o Distance over which diffusion of gases occur  increased
o Gas exchange  less effective
o Lungs become less elastic  ventilation is more difficult

 Phagocytes inside alveoli prevent lung infections by engulfing the bacteria and producing elastase (protein
digesting enzyme to kill bacteria inside the vesicles formed by endocytosis)
 Enzyme inhibitor (alpha 1-antitrypsin) prevents elastase from digesting the lung tissue (smokers  +
phagocytes in lungs  + elastase)
 Genetic factors  affect quality and quantity of A1AT produced in the lungs
 About 30% of smokers  digestion of proteins in the alveolus wall by the increased quantity of proteases is
not prevented and alveolus walls are weakened and destroyed

 Chronic disease  damage to the alveoli is irreversible

 Emphysemas cause:
o Low oxygen saturation in the blood
o Higher carbon dioxide concentrations than normal

 Symptom: Patient may lack energy

 Mild cases  shortness of breath during vigorous exercise, ventilation is difficult and tends to be more rapid
than normal.

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