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CVS summary
The cardiovascular system is highly important in the transport of a plethora of substances around
the body, blood is capable of carrying many substances:
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Nutrients
Hormones
Oxygen
Carbon dioxide
Heat
Waste products

The cardiovascular system involves the heart and all the veins and arteries
that attach the heart to the rest of the body as well as the blood that is
pumped by the heart and through the many vessels
...

Veins always carry blood to the heart and arteries carry the blood away from
the heart, the left side of the heart always has oxygenated blood within it and
the right side is always deoxygenated blood
...

- Blood
Blood is a liquid with many cells and other substances in suspension and so it
has different properties depending on the level at which it is studied, at the macroscopic level it is a
fluid however at microscopic it is a suspension of solid particles (specialised cells)
...
They are highly resistant to distension, produced in the red bone marrow
...

Platelets, small cell fragments with organelles, contractile apparatus (to alter their shape)
and granules (for secretory purposes) that are important in clotting so have adhesive
properties
...
During clotting they secrete many mediators:
o Platelet activators – thromboxane, ADP
o Adhesive factors – Fibrinogen
o Coagulant factors – von Willebrand factor
o Vasoconstrictors – Serotonin
o Growth factors - PDGF
White blood cells which provide immunity and protection for the body
o Granulocytes (granular cytoplasm and segmented nucleus) – neutrophils (help fight
bacterial infection they change conformation and escape the blood), eosinophils
(combats allergic reactions, found in high numbers in asthmatic patients), basophils
o Mononuclear (single unsegmented nucleus) – lymphocytes and monocytes

The proportion of blood that is red blood cells is the haematocrit and it is calculated by centrifuging
blood into a small tube and we can measure the height of the blood including the plasma and then
divide that by the height of the RBC
...
However upon increasing the flow speed, the aggregate
breaks down and the red blood cells align with the flow and elongate, making themselves more
streamlined so the viscosity decreases
...
This also aids in the RBC ability to fit
through very small sinuses of the spleen to allow for old red blood cells to be removed
...

The resistance to flow is dependent on the vessels that the blood is flowing through and the flow
and deformation of the blood
...
Within a small vessel
however we have to take into account the rigidity of the RBC as well as the plasma viscosity
...

With a higher viscosity there is a greater resistance to flow so the flow rate decreases or the heart
has to work harder to increase the pressure to overcome the increased resistance
...
Conversely if there is a decrease in RBC whether that be due
to excessive RBC destruction or impaired synthesis it results in anaemia and a lack of oxygen
transport
...

The cardiac output is affected by the autonomic nervous system
...
The
noradrenaline binding to the beta 1 receptors on the nodes increases the cells permeability
to calcium and so there is a greater calcium ion influx at the action potential plateau
...


The many blood vessels within the body all have their own properties and their own pressures
within the body
...

Haemostasis:
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Local vasoconstriction, reducing the blood flow to the damaged area slightly so less blood is
lost
Platelet adhesion and activation, platelets adhere to the collagen in the wall of damaged
vessels as well as to other platelets which they activate and signal them to elongate
...
Immediately after there is damage to the vessel wall platelets passively undergo capture to
move along exposed collagen
2
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3
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GPIaIIa binds to the collagen strand and GPIIbIIIa binds to von
Willebrand factor on the surface of the collagen, both GP proteins are integrins
...
As more platelets arrive they adhere to one another by forming cross bridges with GPIIbIIIa
and fibrinogen, creating a platelet aggregate
5
...

Coagulation cascade:

1
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Tissue factor activates a series of proteases which
cleaves coagulation factor enzymes and activates
them, it is important to have the series of proteases
to implement control in the coagulation cascade
...
Eventually the series of coagulation factors amplifies
the generation of thrombin
4
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The fibrin filaments polymerise and form a protein
mesh which, together with the platelet aggregate
creates the clot
...
As well as this there are inhibitors of the
proteases and of thrombin within the plasma which further prevents activation
...
APC binds to endothelial cells along with protein S
in order to inactivate factor V and VII

Fibrin is broken down during fibrinolysis, this is carried out by plasmin
...

There are also substances that are capable of preventing the coagulation of fibrin to occur:
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Heparin – increases the action of antithrombinin III which is a protein that inactivates
proteases
Warfarin – inhibits the action of Vitamin K, and so the active form of coagulation factors
cannot be formed
Ca chelation (EDTA, citrate) – these are substances that make calcium ions unreactive which
prevents them from being used in activating thrombin so active fibrin cannot be made
...

Valves of the heart aid in the flow of blood throughout the heart, valves exist between the atria and
ventricles and the ventricles and the arteries that they lead into
...
When the valves close it means that there can be pressure
differences in each part of the heart
...
The ventricle wall then starts to contract in
isovolumetric systole, this is the increase of pressure
in the ventricles yet the volume of blood within the
ventricles remains the same
...
During this the pressure increase is the same
in both the aorta and the ventricle as the valve is
opened
After the blood has been ejected from the heart the
ventricular wall then relaxes so the pressure within
the ventricle decreases and allows the arterial valves to close, following this is a period of
isovolumetric relaxation within the ventricles as the pressure is decreasing yet the volume of
blood remains the same
...

In order to increase the heart rate, diastole is shortened which shifts the curve of the relative
pressures of the compartments of the heart to the left
...

There is some difference in the shapes of the two curves for each side of the heart as the right side is
smaller so the curve has a lower height, however the shape is the same
...
It is controlled by
electrical contractions that pass from the sinoatrial node through the cardiac muscle
...
Gap
junctions mean that the cells can exchange free ions and current, meaning that electrical activity can
move well
...
The electrical impulse originates in the sinoatrial node which is located within the right
atrium which has an intrinsic depolarising frequency of 100/minute, the intrinsic nature
means that the heart can beat without the need for extrinsic hormones or innervation
2
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3
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When the cell depolarises calcium
and sodium move in and during repolarisation potassium moves out
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1
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Once the funny current increases the membrane
potential to around -50mV the highly sensitive calcium
ion channels open and allow a calcium ion efflux
3
...
This
alters the pre-potential gradient and a similar thing can occur to
reduce the heart rate or the gradient can be increased to increase
the heart rate
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1
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The influx of
sodium ions raises the membrane potential of the cell
...
Calcium ion channels open and create the plateau of the membrane potential shown
3
...

- Electrocardiogram
The electrocardiogram works by measuring the transfer of electrical charge
through the body caused by the depolarisation of the heart tissue
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Electrodes are placed on each of the four
limbs, they are colour coded: Red on the right arm, Yellow on the left arm,
Black on the right leg, Green on the left leg
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The theory behind this is Einthoven’s triangle that the heart has three poles in the right arm
the left arm and left leg
...
This signal is proportional to the mass of tissue
that is creating the dipole
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If the depolarising current in the body is flowing to the positive node then it causes an
upwards deflection, if the depolarising current flows away from the positive nod then we can see a
downwards deflection on the electrocardiogram, if it is moving perpendicular to the lead (pair of
electrodes) then the deflection is small or in both directions
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- Regulation of Cardiac Output

The cardiac output is equal to the heart rate multiplied by the stroke volume and so by affecting
these two variables we can later the cardiac output
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Anxiety/stress: the sympathetic nervous system activates to produce a similar response to
exercise however it is usually less pronounced
Haemorrhage: the stroke volume is lower as blood is being lost however the heart rate
increases which, depending on the extent of the haemorrhage can create the same or lower
cardiac output
Heart failure: the death of some of the cardiac muscle means that there is a lower stroke
volume and the heart rate tends to remain the same so the cardiac output is lower than
usual
...
The
sympathetic nervous system increases the pre-potential gradient of the SAN by increasing the cells
permeability to calcium and sodium ions which means that it takes a shorter amount of time for the
threshold potential to be reached
...

The changes in stroke volume are affected by the end diastolic volume and the end systolic volume
...

Starling investigated the effects of the end diastolic volume on the force of ventricular
contraction and found the following results:
1
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2
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This was found to be due to the stretching of the heart muscle altering the cross bridge formation, at
low end diastolic volume the fibres are not stretched and so the actin strands cross over, limiting the
number of cross bridges that can form and so reducing the strength of contraction
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An increased heart rate means that the end diastolic volume decreases at very high heart rates due
to not enough blood returning, increased atrial contraction can solve this though
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However CVP can be affected by many
things:

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Increases or decreases in blood volume
Gravity causing venous pooling so more blood remains in the veins and is not returned to
the heart
The effects of the skeletal muscle pump can help return blood to the heart
Ventilation can draw blood up into the thorax
Venous tone can aid in increasing the CVP and helping more blood to return to the heart

Sterling’s laws are important in our bodies as they ensure that the end diastolic volume is
representative of the stroke volume to ensure equal quantities of blood are being pumped around
the body as are being returned
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We can change the end systolic volume by having different levels of sympathetic activity which
alternates the circulating adrenaline as well as the release of noradrenaline from the Vagus nerve
which stimulates the beta 1 adrenoceptors on the heart
...
This increases contractility of the ventricular
wall and means that more blood can be ejected
...
They have a large media layer which is composed of multiple
layers of elastin and some smooth muscle, only a small amount as the aorta
has limited capacity to dilate and constrict
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It is also the elastic arteries job to convert the intermittent flow of blood from the
ventricles into a continuous flow that reaches the tissues
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After this the pressure climbs
and then drops slightly until the aortic valve closes once again, where the pressure slowly decreases
once again
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The adventitia is the outermost layer of the elastic
artery and is highly collagenous and provides support to arteries to prevent excessive stretching so
the aorta doesn’t burst
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However as it is not distended as much it does not have as much elastic energy so the
pressure of the aorta drops faster
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When the pressure within the left ventricle exceeds that of the aorta, the aortic valve opens
and allows blood into the aorta
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In large arteries blood adopts a laminar flow, where the
blood flows fastest in the centre and is almost stationary at
the sides
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The blood cells move to the middle and so it is the
most efficient way to move blood around the body
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This movement is
inefficient and noisy and can be heard through a stethoscope
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Blood pressure is expressed by the systolic pressure of the aorta divided by the diastolic pressure, so
if the peak aortic pressure during systole was 120mmHg and the minimum aortic pressure at the
start of diastole was 80mmHg then the blood pressure would be 120/80
...
We use one third because the diastolic period is roughly twice the size of the
systolic period
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We can measure arterial blood pressure in the arm by putting a pump over the brachial artery, and
placing a stethoscope over the artery distally to the cuff
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To determine the pressure we increase
the pressure in the cuff and when the pressure exceeds the DP then turbulence can be heard as
blood velocity is increasing, when the pressure exceeds the SP then the turbulence ceases as blood is
no longer able to travel through
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Systolic pressure is increased by high
cardiac output
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Also if
the heart rate is raised then there is less time for aortic blood pressure to fall
between cardiac cycles so there is increased diastolic pressure
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If many of these arterioles constrict then the TPR increases which
increases the arterial blood pressure
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The flow decreases according to the equation:
Flow = ABP – VP
Resistance
The diameter of arterioles can be changed using a variety of methods:
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Endothelium influences – endothelial cells synthesise and secrete substances which
tonically dilate arterioles by acting on the smooth muscle which reduces the resistance
within the arterioles the greater the shear stress on the endothelium by the blood the
greater the release of these substances such as Nitrous oxide and prostaglandins
...

Myogenic tone – arterioles are also capable of constricting in response to stretch so the
greater the blood flow the more they contract however this is usually outweighed by the
tonic dilation, this response is stronger in the brain and kidneys
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This works at
high pressures which stretches the arterioles causing greater constriction raising the
resistance and reducing the flow
...
g
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The
dilation increases the blood flow and so increases the shear stress on the endothelial cells so
more NO and prostaglandins are released from them resulting in further dilation
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Neural influences –
o Acetyl choline – glandular tissues are controlled by the autonomic nervous system
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The activation of these cells increases the release of kallikrein
which converts kininogen to bradykinin and also causes arteriolar dilation
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o Noradrenaline – there are alpha adrenoceptors on the smooth muscle of arterioles
however less common in the brain which cause constriction when they are
activated
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This is important in
maintaining blood pressure as baroreceptors detect low pressure and create a reflex
to increase sympathetic activity causing vasoconstriction
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Hormones –
o Catecholamines – adrenaline and noradrenaline from the adrenal medulla circulate
in the blood and can act on alpha adreno receptors to cause vasoconstriction
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o

Angiotensin – this is produced by the action of renin from the kidney and can cause
arteriolar constriction at low arteriolar blood pressures
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Due to
the diameter of capillaries being smaller than the red blood cells, RBCs must fold to fit through the
capillary, it may take time for this to happen so RBC can occasionally block the capillary resulting in
intermittent flow
...
As no
blood is flowing through when there is blockage there is reduced surface for exchange
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Due to the vast number of capillaries there is a huge total cross sectional area of 600cm2 in addition
to this the blood flow through these capillaries is reduced to a very slow velocity which results in an
excellent environment for exchange so an equilibrium of solutes is always achieved
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Diffusion = Permeability of capillary endothelium x (difference in concentration) x cross
sectional Area
The permeability of the capillary varies, with fenestrated capillaries being the more
permeable, however all are impermeable to plasma proteins
...

An increase in permeability increases diffusion, however this only occurs in functional
hyperaemia and inflammatory responses
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Filtration
The movement of fluid across the capillary endothelium
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The osmotic pressure is
generated mostly by the presence of plasma proteins, creating oncotic pressure
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The hydrostatic pressure of the capillary
decreases towards the venous end
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However as the distance through the
capillary continues the pressure decreases and eventually falls below the oncotic pressure so
fluid returns
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The plasma protein levels can increase in the tissue fluid when there is a loss of
water from the circulatory system which increases the plasma oncotic pressure so more fluid
flows back
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Inflammation can lead to increase in the capillary’s permeability so plasma
proteins move out and results in increased movement of water out of the capillary
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- Venous vessels
Larger diameter
More branching
Larger cross sectional area
Larger proportion of the blood supply held within them
Lower resistance
More distensible – can fill with blood much more easily
… than arterial vessels (veins also have valves)
The pressure within venous vessels gradually falls and becomes about 2 or 3 mmHg in the
vena cava
...
However, once the adventitia of the vein is
fully stretched the pressure climbs rapidly
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Venous vessels have 3 major functions:
Helps to determine the level of filtration across capillaries
Act as a reservoir for blood by utilising the distensibility of venous vessels to hold more
blood
Determines the filling of the right ventricle by altering venous return

The pressure within veins is dependent on the volume of blood in them and the state of contraction
of the smooth muscle
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If lots of fluid is taken in then the blood volume increases which subsequently increases venous
pressure, thus stroke volume due to an increase in contraction strength, the increase in venous
pressure increases the capillary hydrostatic pressure and leads to increased outwards filtration of
the fluid
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Blood is returned through the veins to the heart with the help of several methods:
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Skeletal muscle pump
the sustained contraction of skeletal muscle when
standing squeezes the blood in the veins which limits
the extent to which the veins can distend so venous
pooling is decreased which results in higher venous
pressure so increased venous return
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Respiratory pump
the expansion of the thorax during inspiration increases the volume of the thorax and
decreases the pressure within it and the flattening of the diaphragm increases the pressure
within the abdomen, this increases the venous return to the right ventricle
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- Control of Cardiovascular system
The information that feeds to the central nervous system comes from receptors which are located
around the circulatory system and they relay afferent information along afferent neurones to the
central nervous system
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The hypothalamus
controls complex reflex patterns in discrete locations within the brainstem and the simple reflexes
are controlled in the medulla
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There is constant sympathetic activity which
causes tonic constriction of the vessels
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Baroreceptors are located at the
bifurcation of the common carotid arteries within
the wall of the internal carotid artery
...
Other
baroreceptors are located within the aortic arch
which relays stretch information to the Vagus
nerve and then to the brain
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When arterial blood
pressure is lowered there is:
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more vasopressin is secreted from the pituitary gland
Increased renin secretion from the kidney which is converted to angiotensin II

Vasopressin and angiotensin lead to vasoconstriction of the arterioles which increases the total
peripheral resistance as well as increasing sodium and water reabsorption in renal tubules which
increases blood volume
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When arterial blood
pressure falls the kidney undergoes myogenic dilation to regulate the pressure within the kidneys
...
There is
constant vasodilation within the brain to ensure sufficient blood flow to the brain and within the

cardiac muscle we can see functional hyperaemia which is brought about by adenosine release due
to increased metabolic action
...
At higher pressures the pressure on the wall the myogenic tone of
the arterioles constricts the walls to reduce the flow
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The results of stress include:
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Increased Ventilation, the inspiratory neurones inhibit the vagal parasympathetic nerves to
the heart during inspiration which results in less parasympathetic activity to the heart
...


All of these responses together result in raised arterial blood pressure due to higher heart rate and
greater contractility in addition to the increased total peripheral resistance in the organs of the
body
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During the alerting response the baroreceptor reflex is suppressed so ABP can be very high
...
It is characterised by:
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Sudden vagal activity resulting in parasympathetic responses within the heart and major
organs resulting in a lowering of the heart rate (bradycardia) and vasodilation in the major
organs
The sudden drop in heart rate and drop in total peripheral resistance drops the blood
pressure and causes the patient to faint

Vasovagal syncope is a very strong defence response induced by very strong negative emotions that
have led to greatly increased heart rate and contractility
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It can be observed that there are some important lacking veins however the reason for this is the
existence of portal systems where the blood from one organ drains into another before it reaches
the venous circulation, such as the hepatic portal system and the hypophyseal portal system
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They drain into the jugular vein
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Blood gas
levels leaving are determined by alveolar gasses
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This difference can be
affected by disease
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Bronchial circulation,
venous drainage from lungs goes straight to left atrium so no oxygenation, the blood going to
myocardium also drains straight into the left atrium through the thebesian veins, the blood that
doesn’t go through the lungs usually accounts for 2% of cardiac output
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Quickly after birth the hole very quickly
closes, so blood goes through the lungs
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If airflow and blood flow are equal then there is perfect gas exchange, some of these exist where
there is the same ventilation and perfusion and so V/Q =1
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However often there is uneven bloodflow or ventilation
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When the alveolus is blocked there is only limited exchange and the alveolar and blood gases
equilibrate so blood leaves hypoxic and hypercapnic so V/Q=0
If blood flow is blocked to an alveolus by an embolism so there is excessive ventilation and no
bloodflow so V/Q= infinity, therefore alveolar gasses now equilibrate with the air
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To alter the V/Q to get it as close to 1 as possible the lungs can alter bloodflow, in the lungs if there
is hypoxia vasoconstriction occurs to send blood to an area of ventilation instead of to the place of
poor ventilation
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Alveolar ventilation = 4L/min compared to 6L in total
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8
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As there is stretch on the lungs due to
gravity, resulting in more bloodflow and more airflow to the bottom of the lung when standing up,
resulting in more BF and AF to the posterior portion of the lungs when lying down
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Lung is like a balloon suspended from the top with more stretch at the top of the lung with bunching
at the bottom
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At apex the lung is less compliant as the lung is pulling with more force
against the pleural membrane which means that the lung sits at the top of the compliance curve as
the distending pressure is larger so smaller change in volume than at the base, more compliant =
more airflow
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The pressure inside = pulmonary
pressure, the outside pressure is alveolar pressure so if alveolar pressure is greater than the vessel
pressure
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Below the heart the blood pressure decreases to 1mmHg arteriole and 0mmHg venous so the
alveolar pressure can exceed the pressure in the vessels so flow is disturbed at the apex of the lung
...

Normal blood gas levels are Co2 40 and O2 100, anyone with emphysema or bronchitis than the V/q
will decrease so low O2 and high CO2 due to poor ventilation
...

- Hormonal control of breathing
Different receptors – Mechanoreceptors, peripheral and central chemoreptors
CO2 is very tightly controlled to maintain pH
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Alveolar ventilation ( that which is involved in gas exchange) is increased by low O2 and high CO2 the
levels are detected by chemoreceptors
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Peripheral chemoreceptors located at same place as baroreceptors in aortic bodies and carotid
arteries
...
Due to the branching of the blood system and each vascular bed gets
blood in parallel so is equal, venous levels are different depending on where it is measured as it can
alter depending on the O2 consumption of the organ
...
g cardiac muscle uses 80% of O2 so there is a
large a-vO2 difference
...
Nerve afferents connect to these cells, we have oxygen dependent K+ channels on the

cells, with high PO2 the channels are open so K+ leaves so it hyperpolarises the cell with the mP
being very negative
...
The cells respond to PaO2 and not to content, and so does not
take into account haemoglobin O2 concentration so the activation will not be affected by the effect
of carbon monoxide so we don’t sense the poisoning
...

Hypoxia:
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Hypoxaemia – low PaO2
Anaemic hypoxia – low total oxygen content, normal PaO2 but poor haemoglobin
content
Ischaemic hypoxia – low blood flow to an area
Histotoxic hypoxia – O2 cannot be used e
...
60mmHg is the point on the haemoglobin dissociation curve
where O2 starts to dissociate rapidly faster
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The central chemoreceptors are found in the ventrolateral section of the medulla,
however there are also chemoreceptors throughout the brain
...

We do not know if the chemoreceptors are neurones or not
...

It is a very steep slope with carbon dioxide levels rising and increasing ventilation, a few
mmHg increase will double ventilation rate
...

These responses are surpressed by sleep and blunted greatly by anaesthesia, narcotics,
alcohol and barbituates

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