nm0228: i said that er today was going to be er a short lecture er an hour and 
a bit i think next week will be normal length and the week after that will be a 
bit longer than usual er will will run about an extra quarter of an hour last 
week i was talking about fluid balance between plasma and tissue and i talked 
to you about er the fact that Starling had elucidated the factors governing 
this and that we therefore call it the Starling balance and i put up and 
explained an equation which defined the factors determining the flux of water J-
V across a capillary wall and er for the first part of this lecture i'm going 
to carry on talking about that and in particular what happens when it goes 
wrong and er to start off with can anybody tell me what's missing [laughter] 
and so i'm not asking for the symbols but the principles what does the volume 
flux depend on what are the two gradients that drive the water flux can anybody 
remember that 
sf0233: 
nm0228: what kind of pressure 
ss: hydrostatic 
nm0228: hydrostatic pressure is one of them and the 
other 
sm0234: oncotic 
nm0228: oncotic plasma colloid osmotic or oncotic pressure so we have the 
pressure in the capillary minus the pressure in the c-, in the interstitium the 
oncotic pressure in plasma minus the oncotic pressure in the interstitium what 
kind of sign do i have in the middle a minus sign because remember we define 
it's just the way we define these pressures that the high oncotic pressure tren-
, tends to draw water towards it and a high hydrostatic pressure pushes water 
away from it so they work in opposite directions we have three membrane 
characteristics in this equation one of them 
sm0235: permeability 
nm0228: [laughter] what 
sm0235: permeability 
nm0228: yes which for water we call hydraulic conductivity multiplied by 
surface area if the surface area is low there's no exchange and then we have 
one more which shows how good a semi-permeable membrane the capillary wall is 
and that's called 
sf0236: 
nm0228: yeah what does that represent what's the technical term [laughter] the 
reflection coefficient okay we're going to start off 
today by talking about two normal conditions that occur which elevate P-C the 
hydrostatic pressure in the capillary and therefore you can see from this 
equation elevate the flux of water out of the blood into the tissue and the 
first one is one that you've studied in your practical class and that is 
standing up because when you stand up the pressure in your feet is much higher 
than it is when you're lying down we have the normal blood pressure that's 
being provided by the heart all the time when you stand up you have in addition 
the hydrostatic pressure from that column of water or column of blood more 
accurately between the heart and your foot so there's somewhere between a metre 
and two metres extra hydrostatic pressure of water there and that's a lot 
compared to the blood pressure and that's er in the arteries but er some of 
this pressure is transmitted through to the capillaries as well the pressure 
goes up in the capillaries so when you stand up there is an extra 
flux of water out of the capillaries in your feet into the tissue in your feet 
and the question is what does the body do about this how do we prevent that 
from happening well to a certain extent we can't do anything about it and if 
you do stand up for a long time your feet will swell er i-, it's not often that 
you do stand still for very long periods of time but you sit still for very 
long periods of time er in an aeroplane for instance if you're on a eight hour 
aircraft ride you would definitely notice that your feet swell if you take your 
shoes off at the beginning of the flight it's difficult to get them back on at 
the end and that is because you've been sitting immobile for many hours and 
although when you're sitting the hydrostatic pressure isn't as great as when 
you're standing it's still a lot more than when you're lying down and that 
forces fluid out of the capillaries into the tissue the body tries to 
compensate and what it does is to increase the 
resistance of the arterioles so the arterioles constrict the s-, muscle cells 
in the arterioles constrict and this does three things first of all it reduces 
the pressure in the capillaries it reduces P-C remember that pressure is 
connected to the potential energy of a fluid and if we have to force that fluid 
through a higher resistance more energy is dissipated so if if the arterioles 
constrict more of that pressure the energy that's represented by that pressure 
will be used up forcing the fluid through the arterioles and the pressure in 
the capillaries will be lower so that's the first thing that happens and 
obviously we can't shut the arterioles down completely otherwise your feet 
wouldn't get the oxygen that they require so the r-, that also gives us a 
reduced flow in the capillary and because there's a reduced flow in the 
capillary we're getting the filtration that is the water is being removed from 
a smaller volume of blood than normal we're 
reducing the amount of blood throwing flowing through the capillary and 
therefore all this water that's coming out of the blood is coming from a 
relatively small volume of it and that concentrates the blood we're losing 
water but we're not losing solutes and we get an increase in the oncotic 
pressure of the plasma so because we're losing a lot of fluid from a small 
volume of blood the oncotic pressure goes up the blood is becoming concentrated 
essentially and if you go back to the Starling equation you will see that 
having a high oncotic pressure in plasma opposes more water leaving it tends to 
pull water back into the plasma so that also helps the final thing is that we 
may shut down some capillaries remember that capillaries are opening and 
closing all the time well 
that's not that's not strictly accurate it's the arterioles that are opening 
and closing all the time and allowing blood either to perfuse the capillary or 
not to perfuse it and i've mentioned that this is called vasomotion and if we 
increase the resistance of arterioles that means that more of the capillaries 
will be shut down more of the time so they have no flow going through them 
there's no there's no blood in them and then he-, and hence no filtration while 
they're closed down so those are three ways in which the body tries to combat 
this effect but as i've said the body can't prevent it completely and our our 
feet certainly do swell if we stand for a long period of time you 
can see from this that exercise is also going to cause problems i've talked 
about the control of arteriole return and i've said that when our tissue is 
metabolizing more as it does during exercise that causes arterioles to dilate 
so during exercise our arterioles dilate and that is to provide the tissue with 
more blood but you can see from what i've just said i mean that that is of 
course equiv-, equivalent to a decreased resistance in the arterioles that this 
will have the opposite effect of all these protective mechanisms that i've just 
talked about for the effects of posture by when we exercise we decrease the 
resistance in our arteries and that will do the opposite of points one two and 
three so it will tend to increase filtration it's exactly the opposite effect 
and again you may very well have noticed that if you do exercise there is a lot 
of movement of water from the blood into tissue if you wear rings for instance 
and they come off easily if you do a 
lot of exercise with your arms or hands you'll find that the rings won't come 
off and that's because the arterioles supplying blood to the arm muscles have 
dilated reduced the resistance and more fluid has filtered out into the tissue 
and swollen your fingers you can sometimes feel this if you exercise your skin 
will feel tight over the muscles compared to normal and that's due to this 
tissue swelling are there any questions about this so far okay well these are 
two cases where things go wrong for the Starling balance but there er we can 
cope with it the body can er er put up with this sort of level of increased 
filtration but it's not always the case and i said last week i apologize for 
leaving a a a figure behind that is an extreme clinical case of er movement of 
fluid from the blood vessels into the tissue it's affected one leg in this 
patient and not others and not the other and this inappropriate this 
pathological movement of water we call oedema and i'm going to 
say quite a bit about oedema again if you're using American textbooks that will 
be spelled without the O spelled just E-D E-M-A and oedema is er fluid 
accumulation in the interstitium pathological er accumulation of fluid in the 
interstitium and it occurs when this flux of water out of the blood that i've 
talked about is greater than the flow of lymph so this is the net flux of water 
out of the capillaries is greater than the lymph flow which returns water from 
the interstitium back to the blood system and if you go back to this to the 
Starling equation you can see the various factors that will cause this to be 
too high so i'm going to give you a list of factors that are of clinical 
importance that can cause oedema and the first one is the one we've just been 
talking about to do with posture and exercise that's when the pressure in the 
capillaries is too high so that's the first cause of oedema it's when P-C is 
too high and this tends to occur 
if the if there's a problem with the veins and in particular if there's a high 
pressure in the veins because of course the capillaries empty into the venules 
and then thereby into the veins and if there's a high pressure in the veins 
that pressure will back up into the capillaries the capillaries won't be able 
to move fluid into the veins until their pressure also has become elevated so 
the main cause of having too high a capillary pressure is to have too high a 
venous pressure it prevents the fluid coming out of the capillaries and so it's 
venous problems that tend to to er cause this and particularly er thrombosis 
blood co-, clots forming inside the veins or other kinds of venous failure such 
as varicose veins when the valves in the veins er are reversed and i i'm sure 
you've seen er people it seems particularly to affect elderly women who've got 
er varicose veins or problems with the veins in their legs and also swollen 
legs swollen ankles and those two 
go together it's because these venous problems are causing a high pressure in 
the veins that's causing a high pro-, pressure in the capillaries and the high 
pressure in the capillaries is forcing fluid out into the tissue again if we go 
back to this equation you can see that another cause of problems could be if we 
had something wrong with the oncotic pressure in plasma so i'll talk about that 
if the oncotic pressure in plasma is too low we will get problems s-, remember 
that these work in the opposite directions that's why the hydrostatic pressure 
has to be too high and the oncotic pressure has to be too low to cause problems 
if the oncotic pressure is too low that will stop water being attracted to the 
blood what is the oncotic pressure in blood caused by what is it that gives us 
the this osmotic pressure this oncotic pressure plasma proteins and 
particularly albumin which is made in the liver it's the plasma proteins that 
draw water towards 
the blood and that's particularly the role of albumin which is about three-
quarters of the total protein mass in the plasma so the first thing that will 
cause oedema is malnutrition because we need amino acids we need protein in our 
diet in order to manufacture proteins and if we don't have enough intake then 
we can't make the proteins and when you see these pictures of starving children 
in the developing countries with very swollen stomachs that's a form of oedema 
that's caused by malnutrition they're not able to make enough protein and that 
allows fluid to leak into the abdominal cavity we can also get oedema if we 
have poor gut absorption of protein even if you have a normal diet and your gut 
is not working properly it doesn't absorb the amino acids then again you will 
not be able to make enough plasma proteins to keep the water in the plasma even 
if you do synthesize the protein you can that that won't be enough if you lose 
it again so if you have some 
condition that causes protein loss then again you can be prone to oedema and 
protein loss can occur er by the kidney this is a common complication of 
pregnancy for example er protein urea is when we get a large quantity of 
protein in the urine or again if one has problems with the gut then protein can 
be can be lost excuse me can be lost through the gut and finally if we have 
liver problems then we can have oedema because it's the liver that synthesizes 
the plasma proteins the albumen is synthesized in the liver and if you have 
lime-, liver damage er alcoholism for example causing cirrhosis of the liver er 
er protein production will be lowered and er oedema will result 
another way in which we can get oedema is if the permeability of the capillary 
to water its hydraulic conductivity becomes too high so again if we get an 
increase in capillary permeability we will get a swelling because fluid leaks 
from the capillary into the tissue where did you see this in your practical 
sm0229: when you scratch a little bit of you 
nm0228: good scratching the skin you got a weal a raised area of redness 
because the capillaries had been damaged and leaked water into the tissue so 
this is a form of inflammation and of course any other kind of inflammation 
will do the same if you have a local infection or local tissue damage you get 
leaky capillaries and the area swells you know that from personal experience if 
you have a a local injury the tissue around it will swell up and the final 
point and i said at 
the start that oedema occurred if the movement of fluid out the net movement i 
say net movement here because there's water moving backwards and forwards into 
the capillaries so we're concerned with the net flux out of the capillaries if 
this is greater than lymph flow then we get accumulation in the tissues so even 
if this stays normal even if J-V stays normal we can still get oedema if 
something happens to the lymph if our lymph flow goes down for some reason so a 
final group of causes are concerned with lymphatic problems and we can have 
problems with our lymph er through developmental problems if the lymph vessels 
aren't formed properly through damage to lymph vessels and lymph nodes and 
that's the case in this er rather revolting picture what's happened here is 
that this is er a patient who's had surgery and the surgery has damaged the 
lymph nodes in the groin on one side and so this leg is being inadequately 
drained of lymph while this leg is being drained 
properly so this is not a a problem with J-V this is a problem with lymphatic 
drainage 
sm0230: all this water's coming out of your blood system does your blood become 
more viscous or 
nm0228: well it will become more concentrated but this tends to develop over a 
long period of time so your water intake will compensate for that and then er a 
final group of causes are er parasites which can block the lymphatic system and 
again i'm sure you've seen pictures of elephantiasis and similar conditions 
which look very similar to this patient that i've just shown you for the same 
reason that the lymph nodes are being blocked er in in most cases by nematode 
worms and that that er causes a poor drainage of fluid back from the tissue 
sf0231: what was that called 
nm0228: er well that particular one is called elephantiasis i think that's how 
you spell it i wouldn't swear to it so called because the limbs swell to 
elephant-like er proportions er i think that's the technical term for it 
filariasis filariasis i'm not sure how you pronounce that either but it's a 
filarial worm a nematode worm 
which is causing this blockage but there are many similar sorts of conditions 
that have the same effect so when we when we do have oedema when the er flux of 
water into the tissue overcomes the lymphatic flow then we get an accumulation 
of free water in the tissue and that's unusual i talked er last week i think it 
was last week about the fact that the er that the tissues filled with 
proteoglycans and have a high osmotic charge a high er a high charge density 
and hence a high osmotic pressure and that these tend to retain the water it's 
not strictly in chemical terms a gel but your interstitium acts like a gel the 
the water won't move through it easily and when you get er oedema the water is 
free water it's not trapped in this network of proteoglycans it's swishing 
around inside you free to move and the commonest place for it to to occur is 
under the skin which we call subcutaneous and you can actually feel that it's 
free water if if if you don't have oedema and you 
er press your finger against your arm then when you push the finger down the 
flesh is depressed the tissue is depressed but when you release the pressure 
the tissue bounces right back up again but w-, in oedema that's not the case if 
you push the f-, finger down you get a depression and when you take the finger 
up the depression stays there for a while because you've pushed this free water 
away it can actually flow and then it slowly flows back again and because of 
that we call this pitting oedema because you're able to make pits in it simply 
by pushing your finger in it th-, this is not a dangerous condition although 
the the pictures look horrific they are not life-threatening you can get local 
problems because this mass of water makes it hard for the cells to get 
nourished and to get rid of the their waste products it increases all these 
diffusion distances then individually cells can die so we get necrosis cell 
necrosis that's cell death and this can give rise to ulcers 
and local tissue problems but it's unlikely to be a life-threatening er a life-
threatening problem the second place in which you can have oedema though is 
very dangerous and that's when it's in the lungs which we call pulmonary oedema 
i've said that one of the causes of oedema is when we get a high pressure in 
the veins and that's the usually the case for pulmonary oedema and it occurs 
when we get a failure of the left ventricle remember that the blood from the 
lungs comes back to the heart through the pulmonary veins comes back into the 
left side of the heart first into the atrium and then into the left ventricle 
where it's pumped around the body if the left ventricle is damaged then it 
cannot pump the blood away around the body so effectively the the left 
ventricle if its pumping action is damaged tends to be filled with blood and 
that backs up into the left atrium and that backs up into the pulmonary veins 
and that backs up into the capillaries of the lungs 
themselves so if the heart can't pump the blood away from the lungs the 
pressure in the lungs will increase so left ventricle damage gives us an 
increased P-C capillary pressure in the lungs and that's a common er effect of 
a heart attack because it's it's extremely common for heart attacks to damage 
the muscle of the left ventricle now when this happens the lung starts to er 
fill with water and initially that makes the lungs very stiff that would be the 
first thing that would be noticed it would be hard to breathe that would be the 
first step just a a stiffening of the lungs due to er to water accumulation but 
also the w-, extra water there increases the diffusion distances i've talked 
about how the lungs are very carefully designed to bring the gas as close as 
possible to the blood the gas in the blood is separated only by a fraction of a 
micron and diffusion takes place over that distance but if the lungs are filled 
with fluid then the gas has to diffuse through the fluid before it can get into 
the blood and so we get an increase in diffusion distances and that gives us 
poor gas exchange 
so it seems unusual i mean it seems not unusual it seems strange that when 
somebody's had a heart attack they start to have problems with breathing and 
you often see people with chronic heart complaints they have to use oxygen 
masks they will have oxygen cylinders at home and it's not easy in your mind to 
see what the connection is between the breathing and the heart attack but it's 
this that if the heart can't pump the blood away then the lungs the capillary 
pressure goes up in the lungs lungs will fill with fluid and that makes it 
harder to breathe and this is a dangerous condition meaning that it can easily 
be fatal you can just have inadequate gas exchange and er this is the death 
rattle that's referred to in Victorian melodramas that the the death rattle was 
the gases in the lungs bubbling through the fluid that has accumulated in the 
lungs in pulmonary oedema are there any questions about what i've said so far 
no okay i'm going to finish up with two short 
topics the the first is the return how how the water and solutes are returned 
to the heart and the second is on the control of blood pressure so let's start 
with the return of water and solutes to the heart and you know already from 
what i've said that there are two rou-, two routes back to the heart one 
through the blood system and one through the lymphatic system so let's start 
with the blood system and it's of course the veins the venous system which is 
involved in this and i've mentioned already that as the capillaries converge as 
they come out of tissue beds they converge to form vessels called venules and 
then the venules converge to form the veins and the veins also converge and the 
largest veins are called vena cavae and there are three of these which enter 
the right side of the heart and the veins have the function not only of moving 
the blood back to the heart but they are also where we store our blood they are 
the the body's reservoir for 
blood and at any particular time about two-thirds of the blood will be in the 
venous system and i th-, i think i mentioned in the first lecture that we call 
veins capacitance vessels because they have this capacity to store blood and 
it's a variable capacity it's under control the veins are very stretchy they 
are very compliant that means that it doesn't take a big change in pressure to 
get a big change in volume even a little change in pressure will increase the 
volume substantially the reason for that is that the veins are very floppy 
structures and if you look at them in c-, cross-section they can collapse very 
easily so we might have a normal round vein but if we decrease the pressure in 
it it will become oval in cross-section and if we decrease the pressure even 
more it will collapse completely to look something like a dumbbell shape like 
that and obviously the amount of blood that can be stored has dropped 
dramatically as you go from the round shape to the dumb-bell 
shape but it doesn't need much pressure to inflate the veins again so they're 
very compliant and the the veins have er smooth muscle cells in the walls and 
their smooth muscle cells are under nervous control so the the diameter of the 
veins is under nervous control and i'll come back to that when i talk about 
blood the control of blood pressure now the other peculiarity about the veins 
is that there isn't enough pressure to bring the blood back to the heart when 
the blood comes out of the capillaries it has a very low pressure certainly not 
enough to drive the blood f-, say from your feet back to your heart so there's 
a problem there the body has to work out some additional way of getting that 
blood to t-, to er to to elevate that blood though that metre or two metres and 
it does this by having valves the veins have valves in them and they get 
squeezed the veins ge-, get squeezed from the outside so supposing we have a 
vein like this and it has two 
valves in it so that's supposed to be a cross-section through a vein and 
there's er a se-, a segment of the vein enclosed by valves and there's blood in 
here then if that vein gets squashed from the outside so if there's a pressure 
applied from the outside then the blood can only move in one direction it has 
to move back towards the heart so every time a vein gets squeezed from outside 
even though the blood pressure is normally low that is what moves the blood 
back towards the heart and this kind of squeezing can occur when you use your 
muscles and er this is a trick that's taught to soldiers when they stand on 
parade because if you stand completely still for a very long period of time 
there isn't any muscular action bringing the pressure back to the heart and you 
can easily faint because the blood pressure will drop as a result of there 
being a low cardiac output and i'm sure you've seen these pictures of a of a 
row of soldiers standing at attention and one of them was 
lying on the ground horizontally because he's fainted and and soldiers on 
parade are taught to twitch their calf muscles and their feet from time to time 
to squeeze their veins and this pushes the blood back to the heart by the Frank 
Starling mechanism that we've talked about that will increase the cardiac 
output and hence keep the blood pressure up but it's not just this voluntary 
sort of muscle use that er does this it's also when you breathe and also to a 
smaller extent the peristaltic movements of the gut so it's not just your 
voluntary muscles but also these er automatic things that are going on and in 
particular when you breathe when you inflate your chest you reduce the pressure 
in the thorax and also in the abdomen as well because they're connected via the 
diaphragm and as you incr-, er decrease the pressure when you inflate your 
chest that will tend to draw blood up the veins and towards the heart and if 
you look at a blood pressure recording which 
shows the blood pressure beat by beat then er you might expect a blood pressure 
trace to look like this oscillating with each heartbeat but it doesn't look 
that it looks like this it has an extra longer wave superimposed on it and 
that's your breathing rhythm this is the heart beating and this slower wave is 
the breathing rhythm every time you breathe in more blood is drawn back towards 
the heart and the blood pressure goes up a little bit and conversely if you 
increase the pressure in your chest that reduces the blood flow back to the 
heart so if you cough for example that will reduce the the pressure during 
coughing in the chest gets extremely high and if you have a prolonged coughing 
fit that will stop the blood coming back to the heart long enough for you to 
faint so er babies that have whooping cough for instance one of the diagnostic 
features is that they lose consciousness during a coughing fit they go blue and 
lose consciousness and that's because the 
increased pressure in the thorax er s-, prevents the blood from coming back up 
the veins and er therefore the cardiac output goes down and not enough blood 
gets to the head 
so let's move on the other way of getting fluid and solutes back to the heart 
is through the lymphatic system and i introduced this system last week remember 
that i said that they were blind-ended capillaries this system lies parallel 
only to the venous side of the circulation there's a lymphatic equivalent to 
capillaries and venules and veins but not to arteries and arterioles so this is 
lying parallel just to the venous side and er remember that i said it has 
valves in it both at the capillary end where the endothelial cells act like 
flaps but also further up the lymphatic system it has proper valves and that it 
ac-, acts just like the venous system if it gets squeezed from outside that 
forces blood along the along the network of lym-, lymphatic vessels but the 
lymphatic system also has its 
own pump there is smooth muscle in the walls of the larger lymph vessels and it 
contracts rhythmically it's rather like the sort of primitive heart that you 
get in worms in in lower invertebrates that f-, it forces blood back er f-, 
shouldn't say blood it forces lymph back along the lymphatic system and as i 
mentioned last week it can generate high pressures though what i didn't mention 
last week was where all that lymph ends up and this diagram is in your handout 
and it just shows the large scale anatomy of the lymphatic system and most of 
the lymph comes up this large vessel called the thoracic duct which i've 
underlined in green here and that lies very close to the aorta and the vena 
cava along the backbone so most of the lymph from your body tends to collect 
into this large thoracic duct and then it's er returned into the subclavian 
vein that duct joins onto the left subclavian de-, vein and that's how we 
return the lymph into the blood system the 
water just simply pours into one of the veins that's about eighty per cent of 
the lymph about twenty per cent comes through another vessel on the right side 
of the body and this is lymph that's collected from the right thorax the right 
arm and the right side of the head it enters into another vessel which i've 
also lined in underlined in green here that's the right lymph duct that's about 
twenty per cent of the lymph comes in that route and that enters into the right 
subclavian vein instead of the left subclavian vein are there any questions 
about veins or the lymphatic system no good okay well i'll move on to the final 
topic a brief topic and that is the control of blood pressure er the reason 
that i've had to leave this topic until the end we've i i hope you've noticed 
that i've gone around the circulation starting with the heart going around the 
arteries to the capillaries and then back to the heart and er the reason i've 
left the control of blood pressure 
till the end is that it involves just about every aspect of the circulation so 
i couldn't introduce that until er er until i've discussed everything else and 
you should note that when people talk about blood pressure they are generally 
talking about arterial blood pressure when you go and have your blood pressure 
measured or as you measured it in the practicals that's the blood pressure in 
the large arteries near the heart usually the brachial artery as well as 
involving all the vessels that i've talked about this involves a specialized 
set of receptors that are called baroreceptors and you should have come across 
these when you wrote up your er wrote up your practical and the baroreceptors 
the prefix the baro here comes er means pressure in the in the same way as you 
find it in barometer for instance so these are pressure sensors and they're 
found in two locations in the arterial system one is the carotid sinus at two 
main locations i could say i should say there 
there are other less important locations too the first one is in the carotid 
sinus the carotid artery's the large artery coming up either side of the neck 
and it splits into two one side helps to feed the brain and the other side 
feeds the face and the scalp and where the artery splits in two there's a kind 
of swelling at that bifurcation that's the carotid sinus and the other location 
is the aortic arch so that's as the er aorta is coming out of the heart it 
comes up and turns curves in two dimensions before it goes down along the 
backbone and at the top of the arch there are more of these receptors which are 
not to be confused with chemoreceptors remember that i talked to you about 
chemoreceptors when i was talking about the control of ventilation and the 
chemoreceptors are in the same place that's a separate system so don't get 
these two confused so if we have an increase in pressure or an increase in 
pulse pressure and by pulse pressure is meant the difference 
between systolic blood pressure and diastolic blood pressure so it's how much 
the blood pressure jumps each heartbeat if these increase then we get an 
increase in firing of the baroreceptors and this is sent to the medulla where 
there's something that used to be called the cardiovascular centre but it's 
unfashionable to call it that these days it used to be thought that each 
physiological system had a centre in the brain there'd be a cardiovascular 
centre and a respiratory centre and that's now believed to be too simplistic 
but you'll probably still see that in textbooks it will be referred to as the 
medullary cardiovascular centre but it's in the brain stem a set of neurones in 
the brain stem that are concerned with regulating er blood pressure and the m-, 
medulla reacts by er changing the firing of the parasympathetic and the 
sympathetic nervous system so in this case we'd get an increase in the 
parasympathetic nervous system firing and a decrease in the 
sympathetic nervous system firing these are the two components of the autonomic 
nervous system and these changes decrease pressure and we'll see how in a 
moment so we have a nice little negative feedback loop here a reflex and it's 
called the baro-, baroreceptor reflex or the baroreflex for short and i hope 
you've come across this when you wrote up your cardiovascular practical that's 
the baroreflex now before i say what this does i just want to say a few words 
about what blood pressure actually is and remember that we've got these 
variables blood flow blood pressure and resistance and who can tell me how i 
arrange those into an equation what's the relationship this is so important to 
remember this equation [laughter] please learn this in fact it's it's more 
strictly written delta-P equals Q-R that is the difference in pressure that 
drives the flow to drive flow round a pipe we have to have a a higher pressure 
at one end than another please please do learn this and 
as i've pointed out several times already it's the same as Ohm's law if you 
know Ohm's law you shouldn't have any trouble remembering this now in the 
circulation if we take apply this equation to the circulation as a whole we can 
say that this is the blood pressure coming out of the heart minus the blood 
pressure coming into the heart that's the pressure gradient that drives blood 
flow around the whole circulation the pressure generated by the heart minus the 
pressure of the blood when it returns to the heart and that equals the flow 
rate but the flow rate for the whole circulation is the same as the cardiac 
output that is the flow of blood around the circulation the flow of blood 
around the whole circulation is obviously the blood that's been pushed out by 
the heart so we can say that the flow rate is the cardiac output and cardiac 
output equals [laugh] come on guys [laughter] 
sm0232: five litres 
nm0228: sorry 
sm0232: five litres per minute 
nm0228: yes right five litres per minute but w-, what i said 
sm0232: stroke volume times heart rate 
nm0228: 
stroke volume times heart rate stroke volume times heart rate and then we have 
the resistance and where does the resistance of the circulation lie in the 
arterioles and we call it we have a a name for it total peripheral resistance T-
P-R now the blood pressure coming into the heart i've just told you is very low 
there's almost no pressure in the blood by the time it gets to the heart it has 
to be sucked back up by our breathing muscles and something so i'm going to 
cross that out and call that zero so the blood pressure coming into the heart 
is zero and the blood pressure coming out of the heart into the large arteries 
i've just told you is what we call blood pressure when you measure the blood 
pressure in a large artery that's effectively the pressure just outside the 
heart so we can simplify this whole thing as the blood pressure yeah what we 
conventionally call blood pressure equals cardiac output that is stroke volume 
times heart rate multiplied by the resistance 
in the arterioles which we call total peripheral resistance and please do learn 
how to arrive at that point and that's all i want to say about blood pressure 
except to show you on your di-, on your handout that you have the baroreflex 
here here you have at the top the arterial pressure and its being detected by 
the baroreceptors and the baroreceptors have to alter the blood pressure to 
bring it back to normal if if say this this example is given in the case of a 
fall in arterial pressure which would happen if you had a bad accident say and 
lost a lot of blood through haemorrhage or if you stood up quickly and a lot of 
your blood remained in your feet and didn't return to the heart then your blood 
pressure would drop and that would be picked up by the baroreceptors and the 
baroreceptors would have to do something about it and from this equation you 
can see exactly what they have to do if you want to increase blood pressure you 
have to increase 
cardiac output that is you increase the stroke volume and the heart rate and 
you increase total peripheral resistance you constrict the arterioles so if you 
want to to raise blood pressure you have to make the heart beat faster make it 
beat stronger and constrict your blood vessels now i've asterisked here those 
three parts of the feedback loop the increase in heart rate the increase in 
stroke volume and the increase in peripheral resistance where did you see the 
increase in heart rate in the practical when you stood up you measured blood 
pressure which stayed more or less constant that's because the baroreflex was 
working but the heart rate went up went up a lot ten or fifteen beats per 
minute a big percentage increase that's this part of the loop the baroreflex 
increasing the heart rate to try and keep your blood pressure up er i just want 
to point out here that it's not just your arterioles that constrict but also 
your veins that constrict i've just 
talked about your veins being under control here we have constriction of the 
veins and what that does is to squeeze blood towards the heart and makes the 
heart beat faster er beat stronger and what i want you to do some time between 
now and the exams is to go through this diagram we've covered all the bits 
individually in different lectures throughout the lecture course so far and i 
want you to make sure that you understand what's going on at each at each er 
step so if for instance if i point out to you here that an increase in end-
diastolic volume makes the heart pr-, pump out more blood that's something 
we've already covered can anybody remember what that's called an increase in 
end-diastolic volume increase in the stroke volume [laughter] i've obviously 
left a deep impression that's the 
Frank Starling mechanism at the out the heart pumps out what is returned to it 
so i want you to go through this diagram and make sure that you can do that for 
each step in the diagram because we have covered all the individual bits okay 
the next two lectures the next two weeks will be on much broader topics next 
week i'm going to be talking about some specialized circulations which are 
rather interesting and the week after that i'm going to talk about how the 
circuli-, s-, how the circulation adapts to special conditions and i'm going to 
be taking the aviation world as an example of that er and i have er the marked 
practicals if you want to come and collect your practicals that were handed in 
last week i have them here