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lslect005

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<availability><p>The British Academic Spoken English (BASE) corpus was developed at the

Universities of Warwick and Reading, under the directorship of Hilary Nesi

(Centre for English Language Teacher Education, Warwick) and Paul Thompson

(Department of Applied Linguistics, Reading), with funding from BALEAP,

EURALEX, the British Academy and the Arts and Humanities Research Board. The

original recordings are held at the Universities of Warwick and Reading, and

at the Oxford Text Archive and may be consulted by bona fide researchers

upon written application to any of the holding bodies.

The BASE corpus is freely available to researchers who agree to the

following conditions:</p>

<p>1. The recordings and transcriptions should not be modified in any

way</p>

<p>2. The recordings and transcriptions should be used for research purposes

only; they should not be reproduced in teaching materials</p>

<p>3. The recordings and transcriptions should not be reproduced in full for

a wider audience/readership, although researchers are free to quote short

passages of text (up to 200 running words from any given speech event)</p>

<p>4. The corpus developers should be informed of all presentations or

publications arising from analysis of the corpus</p><p>

Researchers should acknowledge their use of the corpus using the following

form of words:

The recordings and transcriptions used in this study come from the British

Academic Spoken English (BASE) corpus, which was developed at the

Universities of Warwick and Reading under the directorship of Hilary Nesi

(Warwick) and Paul Thompson (Reading). Corpus development was assisted by

funding from the Universities of Warwick and Reading, BALEAP, EURALEX, the

British Academy and the Arts and Humanities Research Board. </p></availability>

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<date>24/02/2000</date><equipment><p>audio</p></equipment>

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<item n="speechevent">Lecture</item>

<item n="acaddept">Animal and Microbial Sciences</item>

<item n="acaddiv">ls</item>

<item n="partlevel">UG2</item>

<item n="module">Systems physiology</item>

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<u who="nm0228"><kinesic desc="overhead projector is on showing transparency" iterated="n"/> i said that # <pause dur="0.5"/> today was going to be <pause dur="0.3"/> # a short lecture # an hour and a bit i think <pause dur="0.5"/> next week will be normal length and the week after that will be a bit longer than usual <pause dur="0.3"/> # will will run about an extra quarter of an hour <pause dur="3.2"/> last week i was talking about <pause dur="0.6"/> fluid balance between plasma and tissue <pause dur="0.6"/> and i talked to you about # <pause dur="0.5"/> the fact that Starling had elucidated the factors governing this <pause dur="0.5"/> and that we therefore call it the Starling balance <pause dur="1.6"/> and i <pause dur="0.9"/> put up and explained <pause dur="1.3"/> an equation which defined the <pause dur="1.3"/> factors determining the flux of water J-V <pause dur="0.6"/> across a capillary wall <pause dur="0.8"/> and # for the first part of this lecture i'm going to carry on <pause dur="0.5"/> talking about that and in particular what happens when it goes wrong <pause dur="1.5"/> and # <pause dur="1.7"/> to start off with can anybody tell me <pause dur="0.7"/> what's missing <vocal desc="laughter" iterated="y" n="sl" dur="1"/> <pause dur="0.4"/> and so i'm not asking for the symbols but <pause dur="0.5"/> the <pause dur="0.2"/> principles what <pause dur="0.3"/> does the volume flux <pause dur="0.5"/> depend on what are the two gradients that drive <pause dur="0.6"/> the water flux can anybody remember that </u><pause dur="0.4"/> <u who="sf0233" trans="pause"> <gap reason="inaudible" extent="1 sec"/> </u><u who="nm0228" trans="latching"> what kind of pressure </u><pause dur="0.6"/> <u who="ss" trans="pause"> hydrostatic </u><pause dur="0.4"/> <u who="nm0228" trans="pause"> hydrostatic pressure is one of them and the

other </u><pause dur="0.5"/> <u who="sm0234" trans="pause"> oncotic </u><pause dur="0.2"/> <u who="nm0228" trans="pause"> oncotic <pause dur="0.2"/> plasma colloid osmotic or oncotic pressure <pause dur="0.5"/><kinesic desc="writes on transparency" iterated="y" dur="1:12"/> so we have the pressure in the capillary <pause dur="0.4"/> minus the pressure in the <trunc>c</trunc> <pause dur="0.2"/> in the interstitium <pause dur="1.4"/> the oncotic pressure in plasma minus the oncotic pressure <pause dur="0.7"/> in the interstitium <pause dur="1.3"/> what kind of sign do i have <pause dur="0.6"/> in the middle <pause dur="0.2"/> a minus sign <pause dur="0.4"/> because remember <pause dur="0.4"/> we define it's just the way we define these pressures <pause dur="0.5"/> that <pause dur="0.2"/> the high <pause dur="0.2"/> oncotic pressure <trunc>tren</trunc> tends to draw <pause dur="0.4"/> water towards it <pause dur="0.4"/> and a high hydrostatic pressure <pause dur="0.3"/> pushes water away from it so they work in opposite directions <pause dur="1.2"/> we have three membrane <pause dur="1.2"/> characteristics in this equation <pause dur="1.1"/> one of them </u><u who="sm0235" trans="overlap"> permeability </u><pause dur="0.3"/> <u who="nm0228" trans="pause"> <vocal desc="laughter" iterated="y" dur="1"/> <shift feature="voice" new="laugh"/>what <shift feature="voice" new="normal"/></u><pause dur="0.2"/> <u who="sm0235" trans="pause"> permeability </u><u who="nm0228" trans="latching"> yes which for water we call hydraulic conductivity <pause dur="0.9"/> multiplied by <pause dur="1.9"/> surface area <pause dur="0.4"/> if the surface area is low there's no exchange <pause dur="0.6"/> and then we have one more which shows how good <pause dur="0.5"/> a semi-permeable membrane <pause dur="0.3"/> the capillary wall is and that's called </u><pause dur="0.5"/> <u who="sf0236" trans="pause"> <gap reason="inaudible" extent="1 sec"/></u><u who="nm0228" trans="latching"> yeah what does that represent what's the technical term <pause dur="0.7"/> <vocal desc="laughter" iterated="y" dur="1"/> <pause dur="0.6"/> the reflection coefficient <pause dur="0.4"/> okay <pause dur="1.4"/> we're going to start off

today by talking about <pause dur="0.7"/> two normal conditions <pause dur="0.4"/> that occur <pause dur="0.5"/> which <pause dur="0.2"/> elevate <pause dur="0.4"/> P-C <pause dur="0.3"/> the hydrostatic pressure in the capillary <pause dur="0.6"/> and therefore <pause dur="0.4"/> you can see from this equation elevate <pause dur="0.5"/> the flux of water out of the blood into the tissue <pause dur="1.3"/> and the first one is one that you've studied <pause dur="0.5"/> in your practical class and that is standing up <pause dur="0.9"/> because when you stand up <pause dur="2.2"/> the <pause dur="0.2"/> pressure <pause dur="0.4"/> in your feet <pause dur="0.5"/> 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 <pause dur="0.4"/> when you stand up you have in addition <pause dur="0.4"/> the hydrostatic pressure <pause dur="0.4"/> from that column of water or column of blood more accurately <pause dur="0.3"/> between the heart and your foot so there's somewhere between <pause dur="0.4"/> a metre and two metres <pause dur="0.4"/> extra hydrostatic pressure of water there <pause dur="0.4"/> and that's a lot compared to the blood pressure <pause dur="1.1"/> and that's # in the arteries <pause dur="0.5"/> but # some of this pressure is transmitted through to the capillaries as well the pressure goes up <pause dur="0.5"/> in the capillaries <pause dur="1.4"/> so when you stand up <pause dur="0.6"/> there is an extra

flux of water out of the capillaries in your feet <pause dur="0.4"/> into the tissue <pause dur="0.5"/> in your feet <pause dur="1.4"/> and the question is what does the body do about this <pause dur="2.7"/> how do we prevent that from happening <pause dur="2.2"/> well <pause dur="0.3"/> 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 <pause dur="0.9"/> # <pause dur="1.1"/> <trunc>i</trunc> <pause dur="0.3"/> 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 <pause dur="0.6"/> # in an aeroplane for instance if you're on a eight hour aircraft ride you would definitely notice <pause dur="0.5"/> 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 <pause dur="0.4"/> you've been sitting immobile for many hours <pause dur="0.4"/> and <pause dur="0.3"/> although when you're sitting the hydrostatic pressure isn't <pause dur="0.4"/> as great as when you're standing it's still a lot more than when you're lying down <pause dur="0.4"/> and that forces fluid <pause dur="0.4"/> out of the capillaries <pause dur="0.4"/> into the tissue <pause dur="2.3"/> the <pause dur="0.2"/> body tries to compensate and what it does <pause dur="0.4"/> is to increase the

resistance of the arterioles <pause dur="4.7"/> so the arterioles constrict the <trunc>s</trunc> muscle cells in the arterioles constrict <pause dur="0.8"/> and this does <pause dur="0.3"/> three things <pause dur="3.2"/> first of all it reduces <pause dur="0.9"/> the pressure in the capillaries it reduces <pause dur="0.6"/> P-C <pause dur="1.4"/> remember that <pause dur="0.2"/> pressure <pause dur="0.4"/> is connected to the potential energy of a fluid <pause dur="0.6"/> and if we have to force that fluid through a higher resistance <pause dur="0.3"/> more energy is dissipated <pause dur="0.5"/> so if if the arterioles constrict <pause dur="0.4"/> more of that pressure the energy that's represented by that pressure <pause dur="0.4"/> will be used up forcing the fluid through the arterioles <pause dur="0.4"/> and the pressure in the capillaries <pause dur="0.3"/> will be lower so that's the first thing that happens <pause dur="0.4"/> and obviously we can't shut the arterioles down completely <pause dur="0.4"/> otherwise your feet wouldn't get <pause dur="0.4"/> the oxygen that they require <pause dur="3.7"/> so the <trunc>r</trunc> that <pause dur="0.3"/> also gives us a reduced flow <pause dur="0.3"/> in the capillary <pause dur="6.3"/> and because there's a reduced flow in the capillary <pause dur="0.5"/> we're getting <pause dur="0.4"/> the filtration <pause dur="0.4"/> that is the water is being removed <pause dur="0.4"/> from a smaller volume of blood than normal <pause dur="5.1"/> we're

reducing the amount of blood throwing flowing through the capillary <pause dur="0.3"/> and therefore all this water that's coming out of the blood is coming from a relatively small volume of it <pause dur="1.1"/> and that <pause dur="0.6"/> concentrates the blood we're losing water <pause dur="0.4"/> but we're not losing solutes <pause dur="0.4"/> and we get an increase <pause dur="0.4"/> in the oncotic pressure of the plasma <pause dur="0.5"/> so because we're losing a lot of fluid from a small volume of blood <pause dur="0.4"/> the oncotic pressure goes up the blood is becoming concentrated essentially <pause dur="0.7"/> and if you go back to the Starling equation <pause dur="0.4"/> you will see that having <pause dur="0.3"/> a high oncotic pressure in plasma <pause dur="1.0"/> opposes more water leaving it tends to pull water back into the plasma <pause dur="0.8"/> so that also helps <pause dur="9.2"/> the final thing <pause dur="0.4"/> is that we may <pause dur="0.8"/> shut down some capillaries <pause dur="7.0"/> remember that <pause dur="0.4"/> capillaries are opening and closing all the time well

that's not <pause dur="0.2"/> that's not strictly accurate <pause dur="0.4"/> it's the arterioles that are opening and closing all the time <pause dur="0.4"/> and allowing blood either to perfuse the capillary or not to <pause dur="0.2"/> perfuse it <pause dur="0.4"/> and i've mentioned that this is called vasomotion <pause dur="3.0"/> and if we <pause dur="0.3"/> increase the resistance of <pause dur="0.4"/> arterioles <pause dur="0.3"/> that means that more of the capillaries will be shut down more of the time <pause dur="0.7"/> so <pause dur="0.6"/> they have <pause dur="0.4"/> no flow going through them <pause dur="0.2"/> there's no there's no blood in them <pause dur="3.2"/> and then <trunc>he</trunc> <pause dur="0.4"/> and hence <pause dur="0.5"/> no filtration while they're <pause dur="0.3"/> closed down <pause dur="2.4"/> so those are three ways in which the body <pause dur="0.2"/> tries to combat this effect <pause dur="0.5"/> but as i've said <pause dur="0.3"/> the body can't <pause dur="0.5"/> prevent it completely and our our feet certainly do swell if we stand <pause dur="0.5"/> for a long period of time <pause dur="3.6"/> you

can see from this <pause dur="0.4"/> that <pause dur="0.3"/> exercise is also going to <pause dur="1.6"/> cause problems <pause dur="3.8"/> i've <pause dur="0.4"/> talked about the control of arteriole <unclear>return</unclear> <pause dur="0.5"/> and i've said that when our <pause dur="0.3"/> tissue is metabolizing more <pause dur="0.5"/> as it does during exercise <pause dur="0.4"/> that causes arterioles to dilate <pause dur="1.5"/> so during exercise <pause dur="0.4"/> our arterioles dilate <pause dur="0.8"/> and that is <pause dur="0.4"/> to provide the tissue with more blood <pause dur="2.7"/> but you can see from what i've just said <pause dur="0.4"/> i mean that that is of course <trunc>equiv</trunc> <pause dur="0.2"/> equivalent to a decreased resistance in the arterioles <pause dur="2.0"/> that this will have the opposite effect of all these <pause dur="0.8"/> protective mechanisms that i've just talked about <pause dur="0.7"/> for the <pause dur="0.3"/> effects of posture <pause dur="0.8"/> by <pause dur="0.2"/> when we exercise we decrease <pause dur="0.4"/> the resistance in our arteries <pause dur="0.3"/> and that will do the opposite of points one two and three <pause dur="0.8"/> so it will tend to increase <pause dur="0.2"/> filtration <pause dur="1.5"/> it's exactly the opposite effect <pause dur="9.1"/> and again <pause dur="0.6"/> you may very well have noticed that if <pause dur="0.3"/> you do exercise <pause dur="0.3"/> there is a lot of movement of water from the blood into tissue <pause dur="0.5"/> if you wear rings for instance and they come off easily <pause dur="0.4"/> if you do a

lot of exercise with your arms or hands you'll find that the rings won't come off <pause dur="0.6"/> and that's because <pause dur="0.5"/> the <pause dur="0.2"/> arterioles supplying blood to the arm muscles have dilated <pause dur="0.6"/> reduced the resistance and more fluid has filtered out into the tissue and swollen your fingers <pause dur="0.4"/> you can sometimes feel this if you exercise <pause dur="0.4"/> your skin will feel tight over the muscles compared to normal <pause dur="0.4"/> and that's due to this tissue swelling <pause dur="4.1"/> are there any questions about this so far <pause dur="2.7"/> okay <pause dur="0.4"/> well these are two cases <pause dur="0.3"/> where <pause dur="1.5"/> things <pause dur="0.5"/> go wrong for the Starling balance but there <pause dur="0.4"/> # we can cope with it the body can # # <pause dur="0.4"/> put up with this sort of level of increased filtration <pause dur="1.2"/><kinesic desc="changes transparency" iterated="y" dur="25"/> but it's not always the case <pause dur="1.4"/> and i said last week i apologize for leaving a <pause dur="0.5"/> a a figure behind that is <pause dur="0.5"/> an extreme clinical case of <pause dur="0.5"/> # <pause dur="0.6"/> movement of <pause dur="0.2"/> fluid from <pause dur="0.6"/> the blood vessels into the tissue it's affected <pause dur="0.4"/> one leg in this patient <pause dur="0.4"/> and not others and not the other <pause dur="4.8"/> and this <pause dur="0.4"/> inappropriate this pathological movement of water <pause dur="0.7"/> we call oedema <pause dur="0.9"/> and i'm going to

say <pause dur="0.5"/> quite a bit about oedema <pause dur="2.3"/> again if you're using American textbooks that will be spelled <pause dur="0.3"/> without the O <pause dur="0.3"/> spelled just E-D <pause dur="0.4"/> E-M-A <pause dur="8.0"/><kinesic desc="writes on transparency" iterated="y" dur="5"/> and <pause dur="1.0"/> oedema is <pause dur="0.4"/> # <pause dur="0.5"/> fluid accumulation <pause dur="0.4"/> in the interstitium <pause dur="0.7"/> pathological # accumulation of fluid in the interstitium <pause dur="0.6"/> and it occurs <pause dur="0.5"/> when this flux of water out of the blood that i've talked about <pause dur="0.4"/> is greater <pause dur="0.4"/> than the flow of lymph <pause dur="1.2"/> so this is the net <pause dur="1.6"/> flux of water out of the <pause dur="0.3"/> capillaries <pause dur="0.9"/> is greater than the lymph flow <pause dur="0.4"/> which returns <pause dur="0.3"/> water from the interstitium back to the blood system <pause dur="7.1"/><kinesic desc="changes transparency" iterated="y" dur="9"/> and if you go back to this <pause dur="2.7"/> to the Starling equation <pause dur="1.8"/> you can see <pause dur="0.3"/> the various factors that will cause this to be too high <pause dur="3.4"/> so i'm going to give you a list of <pause dur="0.6"/> factors that are of clinical importance that can cause <pause dur="0.4"/> oedema <pause dur="0.4"/> and the first one is the one we've just been talking about <pause dur="0.4"/> to do with posture and exercise <pause dur="0.3"/> that's when <pause dur="0.3"/> the pressure in the capillaries is too high <pause dur="0.5"/> so that's the first cause <pause dur="0.5"/> of oedema <pause dur="1.4"/> it's when P-C is too high <pause dur="7.3"/> and this tends to occur <pause dur="0.6"/>

if <pause dur="0.3"/> the <pause dur="1.0"/> if there's a problem with the veins <pause dur="0.4"/> and in particular <pause dur="0.4"/> if there's a high pressure in the veins <pause dur="3.0"/> because of course the capillaries empty into the venules and then thereby into the veins <pause dur="0.4"/> and if there's a high pressure <pause dur="0.4"/> in the veins <pause dur="0.4"/> that pressure will back up into the capillaries the capillaries won't be able to <pause dur="0.3"/> move fluid into the veins until their pressure also <pause dur="0.3"/> has become elevated <pause dur="0.6"/> so the main cause of having too high <pause dur="0.3"/> a capillary pressure <pause dur="0.4"/> is to have too high a venous pressure <pause dur="0.4"/> it prevents the fluid coming out of the capillaries <pause dur="0.5"/> and so it's venous problems <pause dur="0.3"/> that tend to <pause dur="0.7"/> to # <pause dur="0.6"/> cause this <pause dur="0.4"/> and particularly <pause dur="0.4"/> # thrombosis <pause dur="0.3"/> blood <trunc>co</trunc> clots <pause dur="0.2"/> forming <pause dur="0.3"/> inside the veins <pause dur="0.4"/> or other kinds of venous failure <pause dur="1.1"/> such as varicose veins <pause dur="0.4"/> when the valves in the veins <pause dur="0.2"/> # are reversed <pause dur="0.9"/> and i i'm sure you've seen <pause dur="0.6"/> # <pause dur="0.3"/> people <pause dur="0.5"/> it seems particularly to affect elderly women <pause dur="0.5"/> who've got <pause dur="0.4"/> # <pause dur="0.6"/> varicose veins or problems with the veins in their legs <pause dur="0.3"/> and also swollen <pause dur="0.2"/> legs swollen ankles and those two

go together <pause dur="0.5"/> it's because <pause dur="0.5"/> these venous problems are causing a high pressure in the veins <pause dur="0.4"/> that's causing a high <pause dur="0.2"/> <trunc>pro</trunc> pressure in the capillaries <pause dur="0.4"/> and the high pressure in the capillaries is forcing fluid out <pause dur="0.4"/> into the tissue <pause dur="11.0"/><kinesic desc="changes transparency" iterated="y" dur="10"/> again if we go back to this <pause dur="0.3"/> equation <pause dur="1.8"/> you can see that <pause dur="0.8"/> another <pause dur="0.3"/> cause of problems <pause dur="0.3"/> could be if we had something wrong with the oncotic <pause dur="0.4"/> pressure <pause dur="0.3"/> in plasma <pause dur="0.6"/> so i'll talk about that <pause dur="3.7"/> if the oncotic pressure in plasma is too low <pause dur="1.4"/> we will get <pause dur="0.4"/> problems <pause dur="0.4"/> <trunc>s</trunc> remember that these work in the opposite directions that's why <pause dur="0.6"/> the hydrostatic pressure has to be too high <pause dur="0.4"/> and the oncotic pressure has to be too low to cause problems <pause dur="0.4"/> if the oncotic pressure is too low <pause dur="0.5"/> that will stop water being attracted to the blood <pause dur="6.3"/> what is the <pause dur="0.3"/> oncotic pressure in blood caused by <pause dur="0.6"/> what is it <pause dur="0.2"/> that gives us the <pause dur="0.6"/> this osmotic pressure this oncotic pressure <pause dur="4.5"/> plasma proteins <pause dur="3.8"/> and particularly albumin <pause dur="2.9"/> which is made in the liver <pause dur="1.9"/> it's the plasma proteins <pause dur="0.6"/> that <pause dur="0.2"/> draw water towards

the blood <pause dur="0.8"/> and <pause dur="0.2"/> that's particularly the role of albumin which is about three-quarters of the total protein mass in the plasma <pause dur="3.9"/> so <pause dur="0.6"/> the first thing that will cause <pause dur="0.9"/> oedema <pause dur="0.4"/> is malnutrition <pause dur="0.7"/> because <pause dur="0.7"/> we need <pause dur="1.3"/> amino acids we need protein in our diet in order to manufacture <pause dur="0.6"/> proteins and if we don't <pause dur="0.5"/> have enough <pause dur="0.2"/> intake then we can't make the proteins <pause dur="0.7"/> and <pause dur="0.5"/> when you see these <pause dur="0.4"/> pictures of starving <pause dur="0.2"/> children <pause dur="0.7"/> in the developing countries <pause dur="0.3"/> with very swollen stomachs that's a form of oedema <pause dur="0.4"/> that's caused by <pause dur="0.5"/> malnutrition they're not able to make enough protein <pause dur="0.5"/> and that allows fluid to leak into the <pause dur="0.4"/> abdominal cavity <pause dur="6.1"/> we can also <pause dur="0.5"/> get <pause dur="0.2"/> oedema <pause dur="0.4"/> if we have poor <pause dur="0.6"/> gut absorption of protein <pause dur="2.1"/> even if you have a normal diet <pause dur="0.4"/> and your gut is not working properly it doesn't absorb the amino acids <pause dur="0.4"/> then again <pause dur="0.4"/> you will not be able to make <pause dur="0.2"/> enough plasma proteins <pause dur="0.4"/> to keep the water in the plasma <pause dur="6.3"/> even if you do synthesize the protein <pause dur="0.3"/> you can <pause dur="0.8"/> that that won't be enough if you lose it again so if you have some

condition <pause dur="0.5"/> that causes protein loss <pause dur="0.8"/> then again <pause dur="0.3"/> you can be <pause dur="0.2"/> prone to oedema <pause dur="0.4"/> and protein loss can occur <pause dur="0.7"/> # <pause dur="0.4"/> by the kidney <pause dur="0.4"/> this is a common complication of pregnancy <pause dur="0.4"/> for example <pause dur="0.6"/> # protein urea is when we get <pause dur="0.5"/> a large quantity of protein in the urine <pause dur="0.8"/> or again if <pause dur="0.3"/> one has problems with the gut <pause dur="0.3"/> then protein can be <pause dur="0.4"/> can be lost <pause dur="0.5"/><vocal desc="clears throat" iterated="n"/><pause dur="0.2"/> excuse me <pause dur="0.4"/> can be lost through the gut <pause dur="3.8"/> and finally <pause dur="0.3"/> if we have liver problems <pause dur="2.1"/> then we can <pause dur="0.3"/> have <pause dur="0.5"/> oedema <pause dur="0.3"/> because it's the liver that synthesizes the plasma proteins <pause dur="0.6"/> the albumen is synthesized in the liver <pause dur="0.4"/> and if you have <trunc>lime</trunc> liver damage <pause dur="0.5"/> # alcoholism for example <pause dur="0.6"/> causing cirrhosis of the liver <pause dur="0.6"/> # <pause dur="0.4"/> # <pause dur="0.3"/> protein production will be lowered <pause dur="0.7"/> and # <pause dur="1.6"/> oedema will result <pause dur="15.2"/><kinesic desc="changes transparency" iterated="y" dur="11"/>

another <pause dur="0.2"/> way in which we can get <pause dur="0.4"/> oedema <pause dur="0.8"/> is if <pause dur="0.6"/> the <pause dur="1.0"/> permeability of the capillary to water its hydraulic conductivity <pause dur="0.4"/> becomes too high <pause dur="24.0"/> so again <pause dur="2.2"/> if we get an increase in capillary permeability we will get a swelling <pause dur="0.3"/> because <pause dur="0.4"/> fluid leaks from the capillary <pause dur="0.7"/> into the <pause dur="0.4"/> tissue <pause dur="0.4"/> where did you see this in your practical </u><pause dur="4.9"/> <u who="sm0229" trans="pause"> when you scratch a little bit of you </u><u who="nm0228" trans="latching"> good <pause dur="0.3"/> scratching the skin <pause dur="0.4"/> you got a weal <pause dur="0.3"/> a raised <pause dur="0.2"/> area of redness <pause dur="0.5"/> because the capillaries had been damaged <pause dur="0.4"/> and leaked water into the tissue <pause dur="0.5"/> so this is a form <pause dur="0.4"/> of inflammation <pause dur="7.0"/> and of course any other kind of inflammation will do the same if you have a local <pause dur="0.4"/> infection <pause dur="0.7"/> or local tissue damage <pause dur="0.3"/> you get leaky capillaries <pause dur="0.3"/> and the area swells you know that from personal experience if you have a <pause dur="0.3"/> a local injury the tissue around it will swell up <pause dur="11.7"/><kinesic desc="changes transparency" iterated="y" dur="7"/> and the final point <pause dur="0.5"/> and i said at

the start <pause dur="0.4"/> that oedema occurred <pause dur="0.4"/> 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 <pause dur="0.3"/> so we're concerned with <pause dur="0.4"/> the net <pause dur="0.3"/> flux out of the capillaries <pause dur="0.6"/> if this is <pause dur="0.4"/> greater <pause dur="0.4"/> than lymph flow then we get accumulation in the tissues <pause dur="0.4"/> so <pause dur="0.3"/> even if this stays normal even if J-V stays normal <pause dur="0.3"/> we can still get oedema <pause dur="0.5"/> if something happens to the lymph <pause dur="0.6"/> if our lymph flow goes down for some reason <pause dur="0.4"/> so <pause dur="0.4"/> a final <pause dur="0.3"/> group of causes <pause dur="0.3"/> are concerned with lymphatic problems <pause dur="9.8"/> and <pause dur="0.7"/> we can have problems with our lymph <pause dur="0.5"/> # through developmental problems if the lymph vessels aren't <pause dur="0.2"/> formed properly <pause dur="4.3"/> through <pause dur="0.4"/> damage <pause dur="0.2"/> to lymph vessels and lymph nodes <pause dur="0.4"/> and that's the case in this # <pause dur="3.1"/><kinesic desc="changes transparency" iterated="y" dur="4"/> rather <pause dur="0.3"/> revolting picture what's happened here <pause dur="0.5"/> is that this is <pause dur="0.2"/> # <pause dur="0.7"/> a patient who's had surgery <pause dur="0.4"/> and the surgery has damaged the lymph nodes in the groin <pause dur="0.4"/> on one side <pause dur="0.4"/> and so this leg is being inadequately <pause dur="0.3"/> drained of lymph <pause dur="0.5"/> while this leg is being drained

properly so this is not a <pause dur="0.3"/> a problem with J-V <pause dur="0.3"/> this is a problem with <pause dur="0.4"/> lymphatic drainage </u><pause dur="0.3"/> <u who="sm0230" trans="pause"> all this water's coming out of your blood system does your blood become more viscous or </u><u who="nm0228" trans="overlap"> well it will become more concentrated but this tends to develop over a long period of time so your water intake will <pause dur="0.5"/> compensate for that <pause dur="2.0"/> and then # a final group of causes <pause dur="0.6"/> are <pause dur="0.3"/> # parasites <pause dur="0.4"/> which can block the lymphatic <pause dur="0.2"/> system and again i'm sure you've seen <pause dur="0.4"/> pictures of elephantiasis and similar conditions <pause dur="0.3"/> which look very similar to this <pause dur="0.3"/> patient that i've just shown you <pause dur="0.4"/> for the same reason <pause dur="0.3"/> that the lymph nodes are being blocked <pause dur="0.5"/> # in in most cases by nematode worms <pause dur="0.4"/> and that that # causes a poor <pause dur="0.2"/> drainage of fluid <pause dur="0.4"/> back from the tissue </u><pause dur="1.3"/> <u who="sf0231" trans="pause"> what was that called </u><pause dur="1.3"/> <u who="nm0228" trans="pause"> # well that particular one is called elephantiasis <pause dur="3.6"/><kinesic desc="writes on transparency" iterated="y" dur="6"/> i think that's how you spell it i wouldn't swear to it <pause dur="2.0"/> so called because the <pause dur="0.2"/> limbs swell to <pause dur="0.5"/> elephant-like # <pause dur="1.4"/> proportions <pause dur="0.9"/> # <pause dur="4.4"/> i think that's the technical <pause dur="0.4"/> term for it <pause dur="0.2"/> filariasis filariasis i'm not sure how you pronounce that either <pause dur="0.4"/> but it's a filarial <pause dur="0.4"/> worm a nematode worm <pause dur="0.4"/>

which is causing this blockage but there are many <pause dur="0.4"/> similar sorts of conditions that have the same effect <pause dur="5.4"/> so <pause dur="0.5"/> when we when we do have oedema when the <pause dur="0.3"/> # <pause dur="0.6"/> flux of water into the tissue overcomes the lymphatic flow <pause dur="0.8"/> then we get <pause dur="0.6"/> an <pause dur="0.3"/> accumulation of free water in the tissue <pause dur="0.8"/> and that's unusual <pause dur="0.5"/> i talked # <pause dur="2.1"/> last week i think it was last week <pause dur="0.4"/> about the fact that the <pause dur="0.7"/> # <pause dur="1.6"/> that the tissues filled with proteoglycans <pause dur="0.7"/> and have a high osmotic <pause dur="0.3"/> charge <pause dur="0.4"/> a high # a high charge density and hence a high osmotic pressure <pause dur="0.7"/> and that these tend to retain the water <pause dur="0.3"/> it's not strictly in chemical terms a gel <pause dur="0.4"/> but your interstitium acts like a gel the the water won't move through it easily <pause dur="0.4"/> and when you get <pause dur="0.3"/> # oedema <pause dur="0.7"/> the water is free water it's not trapped in this network of proteoglycans <pause dur="0.4"/> it's swishing around inside you free to move <pause dur="3.3"/> and the commonest place for it to <pause dur="0.5"/> to occur is under the skin <pause dur="1.4"/> which we call <pause dur="0.3"/> subcutaneous <pause dur="3.9"/> and you can actually feel that it's free water <pause dur="1.5"/> if <pause dur="0.3"/> if <pause dur="0.9"/> if you don't have oedema <pause dur="0.2"/> and you <pause dur="0.8"/>

# <pause dur="0.5"/> press your finger against your arm <pause dur="0.6"/> then <pause dur="1.3"/><kinesic desc="presses finger into arm" iterated="n"/> when you push the finger down the <pause dur="0.3"/> flesh is depressed the tissue is depressed but when you release the pressure <pause dur="0.5"/> the tissue bounces right back up again <pause dur="0.6"/> but <trunc>w</trunc> in oedema that's not the case <pause dur="0.3"/> if you push the <trunc>f</trunc> <pause dur="0.2"/> finger down you get a depression and when you take the finger up <pause dur="0.3"/> the depression stays there for a while <pause dur="0.4"/> because you've pushed this free water away it can actually flow <pause dur="0.3"/> and then it slowly <pause dur="0.3"/> flows back again <pause dur="0.5"/> and <pause dur="0.6"/> because of that we call this pitting oedema <pause dur="1.5"/> because <pause dur="0.7"/> you're able to make pits in it simply by pushing your finger in it <pause dur="5.7"/> <trunc>th</trunc> this is not a dangerous condition although the the pictures look horrific <pause dur="0.5"/> they are <pause dur="0.4"/> not life-threatening <pause dur="0.7"/> you can get <pause dur="0.3"/> local problems <pause dur="0.5"/> because this mass of water <pause dur="0.4"/> makes it hard for the cells to get nourished and to get rid of the their waste products it increases all these diffusion distances <pause dur="0.5"/> then individually cells can die <pause dur="0.4"/> so we get necrosis cell necrosis <pause dur="0.2"/> that's cell death <pause dur="3.1"/> and this can give rise to ulcers <pause dur="1.1"/>

and local tissue problems but it's <pause dur="0.2"/> unlikely to be <pause dur="0.2"/> a life-threatening <pause dur="0.6"/> # <pause dur="0.7"/> a life-threatening problem <pause dur="4.4"/> the second <pause dur="0.8"/> place in which you can have oedema though is very dangerous <pause dur="0.8"/> and that's when it's in the lungs <pause dur="7.3"/> which we call pulmonary oedema <pause dur="8.1"/> i've said <pause dur="0.5"/> that <pause dur="0.4"/> one of the causes <pause dur="0.4"/> of <pause dur="0.4"/> oedema <pause dur="0.3"/> is when we get a high <pause dur="1.4"/> pressure in the veins <pause dur="0.9"/> and that's the usually the case for pulmonary oedema <pause dur="0.4"/> and it occurs when we get a failure of the left ventricle <pause dur="5.1"/> remember that the <pause dur="0.3"/> blood from the lungs <pause dur="0.5"/> comes back to the heart <pause dur="0.2"/> through the pulmonary veins <pause dur="0.4"/> comes back into the left side of the heart first into the atrium <pause dur="0.5"/> and then into the left ventricle <pause dur="0.4"/> where it's pumped around the body <pause dur="2.2"/> if the left ventricle is damaged <pause dur="0.4"/> then it cannot pump the blood away around the body so effectively <pause dur="0.6"/> the the left ventricle if its pumping action is damaged <pause dur="0.4"/> tends to be filled with blood <pause dur="0.6"/> and that backs up into the left atrium <pause dur="0.3"/> and that backs up into the pulmonary veins <pause dur="0.2"/> and that backs up into the capillaries of the lungs

themselves <pause dur="0.3"/> so if the heart can't pump the blood away from the lungs <pause dur="0.4"/> the pressure <pause dur="0.4"/> in the lungs <pause dur="0.2"/> will increase <pause dur="0.4"/> so left ventricle damage <pause dur="1.6"/> gives us <pause dur="0.2"/> an increased <pause dur="0.2"/> P-C capillary pressure <pause dur="0.4"/> in the lungs <pause dur="0.4"/> and that's a common # effect of <pause dur="0.2"/> a heart attack <pause dur="0.7"/> because it's it's extremely common for heart attacks to damage <pause dur="0.5"/> the muscle of the <pause dur="0.4"/> left ventricle <pause dur="5.0"/> now when this happens <pause dur="0.5"/> the lung starts to <pause dur="0.3"/> # <pause dur="0.2"/> fill with water <pause dur="1.4"/> and initially <pause dur="0.3"/> that makes the lungs very stiff <pause dur="1.6"/> that would be the first thing <pause dur="0.4"/> that would be noticed it would be hard to breathe <pause dur="6.6"/> that would be the first step just a a stiffening of the lungs due to <pause dur="0.4"/> # <pause dur="0.8"/> to <pause dur="0.3"/> water accumulation <pause dur="1.4"/> but also <pause dur="0.3"/> the <pause dur="0.5"/> <trunc>w</trunc> extra water there increases the diffusion distances <pause dur="5.7"/> i've talked about <pause dur="0.3"/> how the lungs are very carefully designed to bring the gas as close as possible to the blood <pause dur="0.7"/> the gas in the blood is separated only by a fraction of a micron <pause dur="0.5"/> and diffusion takes place over that distance <pause dur="0.5"/> but if the lungs are filled with fluid <pause dur="0.4"/> then the gas has to diffuse through the fluid before it can get into the blood <pause dur="0.5"/> and so <pause dur="0.3"/> we get an increase in diffusion distances <pause dur="0.3"/> and that gives us <pause dur="0.4"/> poor gas exchange <pause dur="4.5"/>

so <pause dur="0.9"/> it seems unusual <pause dur="0.6"/> i mean it seems <pause dur="0.3"/> not unusual it seems <pause dur="0.7"/> strange that when somebody's had a heart attack <pause dur="0.4"/> they start to have problems with breathing and you often see people with <pause dur="0.3"/> chronic heart complaints they have to use <pause dur="0.3"/> oxygen masks they will have oxygen cylinders at home <pause dur="0.5"/> and it's not easy in your mind to see <pause dur="0.4"/> what the connection is between the breathing and the heart attack but it's this <pause dur="0.5"/> that if the heart can't pump the blood away <pause dur="0.4"/> then the lungs the <pause dur="0.2"/> capillary pressure goes up in the lungs <pause dur="0.3"/> lungs will fill with fluid <pause dur="0.3"/> and that makes it harder to breathe <pause dur="3.4"/> and this is a dangerous condition <pause dur="0.4"/> meaning that it can easily be <pause dur="0.4"/> fatal you can just have inadequate <pause dur="0.4"/> gas exchange <pause dur="0.6"/> and # <pause dur="0.6"/> this is the death rattle that's referred to in Victorian melodramas that <pause dur="0.2"/> the the death rattle was <pause dur="0.4"/> the gases in the lungs bubbling through the fluid that has accumulated in the lungs <pause dur="0.4"/> in pulmonary oedema <pause dur="9.1"/><kinesic desc="changes transparency" iterated="y" dur="38"/> are there any questions about <pause dur="0.5"/> what i've said so far <pause dur="2.3"/> no <pause dur="0.4"/> okay <pause dur="23.6"/> i'm going to finish up <pause dur="0.4"/> with two short

topics <pause dur="0.8"/> the the first is the return how how the <pause dur="0.6"/> water and solutes are returned to the heart <pause dur="0.7"/> and the second is <pause dur="0.2"/> on the control of blood pressure <pause dur="0.6"/> so let's start with <pause dur="1.1"/> the return of <pause dur="0.7"/> water and solutes <pause dur="0.8"/> to the heart <pause dur="17.2"/> and <pause dur="0.6"/> you know already from what i've said that there are two <trunc>rou</trunc> <pause dur="0.2"/> two routes back to the heart <pause dur="0.5"/> one through the blood system <pause dur="0.3"/> and one through the lymphatic system <pause dur="0.4"/> so let's start with the <pause dur="0.6"/> blood system <pause dur="0.6"/> and it's of course the veins <pause dur="0.3"/> the venous system <pause dur="0.6"/> which is involved in this <pause dur="5.3"/> and i've mentioned already <pause dur="0.7"/> that as the <pause dur="0.3"/> capillaries converge as they come out of tissue beds <pause dur="0.4"/> they converge to form vessels called venules <pause dur="1.0"/> and then the venules converge <pause dur="0.5"/> to form the veins <pause dur="0.5"/> and the veins also <pause dur="0.5"/> converge <pause dur="0.4"/> and the largest veins are called vena cavae <pause dur="4.2"/> and there are three of these <pause dur="0.4"/> which enter the <pause dur="0.5"/> right side of the heart <pause dur="13.3"/> and the veins <pause dur="0.4"/> have <pause dur="0.7"/> the <pause dur="0.3"/> function not only of <pause dur="0.4"/> moving the blood back to the heart <pause dur="0.4"/> but they are also where we store our blood <pause dur="0.7"/> they are the <pause dur="0.2"/> the body's reservoir for

blood <pause dur="0.5"/> and at any particular time about two-thirds of the blood <pause dur="0.4"/> will be in the venous system <pause dur="4.3"/> and <pause dur="0.2"/> i <trunc>th</trunc> i think i mentioned in the first lecture that we call <pause dur="0.4"/> veins capacitance vessels <pause dur="7.4"/> because they have this capacity to store blood <pause dur="0.4"/> and it's a variable capacity it's under control <pause dur="3.4"/> the veins are <pause dur="0.4"/> very <pause dur="0.7"/> stretchy <pause dur="1.1"/> they are very compliant <pause dur="4.0"/> that means that it doesn't take <pause dur="0.2"/> a big change in pressure to get a big change in volume even a little change in pressure <pause dur="0.4"/> will increase the volume substantially <pause dur="2.4"/> the reason for that <pause dur="0.4"/> is that the veins are very <pause dur="0.8"/> floppy <pause dur="0.3"/> structures and if you look at them in <trunc>c</trunc> <pause dur="0.2"/> cross-section <pause dur="0.4"/> they can collapse very easily <pause dur="0.4"/> so we might have a normal round vein <pause dur="0.4"/> but if we decrease the pressure in it it will become <pause dur="0.4"/> oval in cross-section <pause dur="0.3"/> and if we decrease the pressure even more <pause dur="0.3"/> it will collapse completely <pause dur="0.4"/> to look something like <pause dur="0.5"/> a dumbbell shape like that <pause dur="0.5"/> and obviously the amount of blood that can be stored has dropped dramatically <pause dur="0.4"/> as you go from the round shape to the dumb-bell

shape <pause dur="0.4"/> but it doesn't need much pressure <pause dur="0.5"/> to inflate the veins again so they're very compliant <pause dur="11.3"/> and the <pause dur="0.8"/> the veins <pause dur="0.3"/> have <pause dur="0.4"/> # <pause dur="0.3"/> smooth muscle cells in the walls <pause dur="0.4"/> and their smooth muscle cells are under nervous control <pause dur="0.5"/> so the the diameter of the veins <pause dur="2.0"/> is under nervous control and i'll come back to that when i talk about <pause dur="1.6"/> blood <pause dur="0.2"/> the control of blood pressure <pause dur="7.5"/> now the other peculiarity about the veins <pause dur="0.5"/> is that there isn't enough pressure <pause dur="0.4"/> to bring the blood back to the heart <pause dur="0.6"/> when the blood comes out of the capillaries it has a very low pressure <pause dur="0.6"/> certainly not enough <pause dur="0.4"/> to drive the blood <trunc>f</trunc> say from your feet <pause dur="0.4"/> back to your heart <pause dur="0.4"/> so there's a problem there the body has to work out some <pause dur="0.2"/> additional way <pause dur="0.4"/> of getting that blood to <pause dur="0.6"/> <trunc>t</trunc> <pause dur="0.3"/> to # <pause dur="1.4"/> to to elevate that blood though that metre or two metres <pause dur="1.5"/> and <pause dur="0.8"/> it does this by <pause dur="1.2"/> having valves the veins have valves in them <pause dur="2.4"/> and they get squeezed the veins <trunc>ge</trunc> get squeezed from the outside so supposing we have a vein like this <pause dur="2.2"/><kinesic desc="writes on transparency" iterated="y" dur="9"/> and it has two <pause dur="2.1"/>

valves in it <pause dur="3.5"/> so that's supposed to be a cross-section through a vein and there's <pause dur="0.6"/> # <pause dur="0.9"/> a <trunc>se</trunc> a segment of the vein enclosed <pause dur="0.5"/> by <pause dur="0.4"/><kinesic desc="writes on transparency" iterated="y" dur="32"/> valves and there's blood in here <pause dur="1.5"/> then if that vein gets squashed from the outside <pause dur="2.0"/> so if there's a pressure applied from the outside <pause dur="0.5"/> then the blood can only move in one direction <pause dur="0.6"/> it has to move back towards the heart <pause dur="0.4"/> so every time a vein gets squeezed from outside <pause dur="0.4"/> even though the blood pressure is normally low <pause dur="0.4"/> that <pause dur="0.2"/> is what moves the blood back towards the heart <pause dur="0.5"/> and this kind of squeezing <pause dur="0.7"/> can occur <pause dur="0.6"/> when you use your muscles <pause dur="1.1"/> and # <pause dur="1.2"/> this is a trick that's taught to soldiers when they stand on parade <pause dur="0.5"/> because if you stand completely still for a very long period of time <pause dur="0.4"/> there isn't any muscular action bringing the pressure back to the heart <pause dur="0.5"/> and you can easily faint because the blood pressure will drop <pause dur="0.5"/> as a result of there being a low <pause dur="0.3"/> cardiac output and i'm sure you've seen these pictures of a <pause dur="0.5"/> of a row of soldiers standing at attention and <pause dur="0.4"/> one of them was

lying on the ground horizontally because he's fainted <pause dur="0.6"/> and and soldiers on <pause dur="0.2"/> parade are taught to twitch their calf muscles <pause dur="0.4"/> and their feet <pause dur="0.3"/> from time to time <pause dur="0.3"/> to squeeze their veins <pause dur="0.9"/> and this <pause dur="0.3"/> pushes the blood back to the heart <pause dur="0.4"/> by the Frank Starling mechanism that we've talked about <pause dur="0.4"/> that will increase the cardiac output <pause dur="0.4"/> and hence keep the blood pressure up <pause dur="1.3"/> but it's not just this voluntary <pause dur="0.2"/> sort of muscle use that # <pause dur="0.2"/> does this <pause dur="0.4"/> it's also <pause dur="0.3"/> when you breathe <pause dur="2.0"/><kinesic desc="writes on transparency" iterated="y" dur="3"/> and also <pause dur="0.5"/> to a smaller extent the peristaltic movements of the gut <pause dur="0.3"/> so it's not just your voluntary muscles but also these # <pause dur="0.8"/> automatic things that are going on <pause dur="0.6"/> and in particular when you breathe <pause dur="0.7"/> when you <pause dur="0.3"/> inflate your chest you reduce the pressure <pause dur="0.4"/> in the thorax <pause dur="0.2"/> and also in the abdomen as well because they're connected via the diaphragm <pause dur="0.5"/> and as you <trunc>incr</trunc> <pause dur="0.3"/> # decrease the pressure when you inflate your chest <pause dur="0.3"/> that will tend to draw blood up <pause dur="0.8"/> the veins and towards the heart <pause dur="0.3"/> and if you look at a blood pressure recording which

shows the blood pressure beat by beat <pause dur="0.5"/> then # <pause dur="7.0"/><event desc="puts on transparency" iterated="n"/> you might expect a blood pressure trace <pause dur="2.8"/><kinesic desc="writes on transparency" iterated="y" dur="15"/> to look like this oscillating with each heartbeat but it doesn't look that it looks like this <pause dur="6.5"/> it has an extra longer wave superimposed on it and that's your breathing rhythm <pause dur="0.5"/> this is the heart beating <pause dur="0.4"/> and this slower wave <pause dur="0.5"/> is the breathing rhythm every time you breathe in <pause dur="0.4"/> more blood is drawn back towards the heart and the blood pressure goes up a little bit <pause dur="1.7"/> and conversely <pause dur="0.5"/> if you increase the pressure in your chest that reduces the blood flow back to the heart <pause dur="0.3"/> so if you cough <pause dur="0.2"/> for example <pause dur="0.4"/> that will reduce the the pressure during coughing <pause dur="0.4"/> in the chest gets extremely high <pause dur="0.4"/> and if you have a prolonged coughing fit <pause dur="0.5"/> that will stop the blood coming back to the heart long enough for you to faint <pause dur="0.5"/> so # babies that have whooping cough for instance one of the diagnostic features is that they lose consciousness <pause dur="0.4"/> during a coughing fit they go blue and lose consciousness <pause dur="0.5"/> and that's because <pause dur="0.4"/> the

increased pressure in the thorax <pause dur="0.5"/> # <pause dur="0.2"/> <trunc>s</trunc> <pause dur="0.6"/> prevents the blood from coming back up the veins <pause dur="0.5"/> and # <pause dur="0.6"/> therefore the cardiac output goes down and not enough blood gets to the head <pause dur="9.6"/>

so let's move on the other way of getting fluid <pause dur="0.3"/> and solutes back to the heart <pause dur="0.5"/> is through the lymphatic system <pause dur="4.4"/> and i introduced this system <pause dur="0.5"/> last week <pause dur="0.6"/> remember that i said that they were blind-ended capillaries this system lies parallel only to the venous side of the circulation <pause dur="0.5"/> there's a lymphatic equivalent to <pause dur="0.3"/> capillaries and venules and veins but not to <pause dur="0.3"/> arteries and arterioles so this is <pause dur="0.4"/> lying parallel just to the venous side <pause dur="0.6"/> and # remember that i said it has valves in it <pause dur="0.8"/> both at the <pause dur="0.2"/> capillary end where the endothelial cells act like flaps but also further up the lymphatic system it has <pause dur="0.3"/> proper valves <pause dur="0.4"/> and that it <trunc>ac</trunc> acts just like the venous system if it gets squeezed from outside <pause dur="0.4"/> that forces blood along the along the network of <trunc>lym</trunc> lymphatic vessels <pause dur="1.5"/> but the lymphatic system also <pause dur="0.3"/> has its

own pump <pause dur="1.8"/> there is smooth muscle in the walls of the larger lymph vessels <pause dur="0.4"/> and it contracts rhythmically it's rather like the sort of primitive heart that you get in <pause dur="0.4"/> worms <pause dur="0.4"/> in in lower invertebrates <pause dur="0.7"/> that <trunc>f</trunc> it forces blood back # <trunc>f</trunc> shouldn't say blood it forces lymph back along the lymphatic system <pause dur="0.4"/> and as i mentioned last week it can generate <pause dur="0.4"/> high pressures <pause dur="1.2"/><kinesic desc="changes transparency" iterated="y" dur="10"/> though what i didn't mention last week was where <pause dur="0.8"/> all that lymph ends up <pause dur="0.5"/> and this diagram is in your handout <pause dur="3.2"/> and it just shows the large scale anatomy <pause dur="0.4"/> of the lymphatic system <pause dur="0.7"/> and most of the lymph comes up this large vessel <pause dur="0.7"/> called <pause dur="0.2"/> the <pause dur="0.4"/> thoracic duct which i've underlined in green here <pause dur="0.5"/> and that lies very close to the aorta and the vena cava along the backbone <pause dur="0.4"/> so <pause dur="0.3"/> most of the lymph from your body <pause dur="0.4"/> tends to <pause dur="0.5"/> collect into this large thoracic duct <pause dur="0.7"/> and then it's # returned into the subclavian vein <pause dur="1.4"/> that duct joins onto the left <pause dur="0.3"/> subclavian <trunc>de</trunc> vein <pause dur="0.8"/> and that's how we return the lymph into the blood <pause dur="0.3"/> system the

water just simply pours into one of the veins <pause dur="0.9"/> that's about eighty per cent of the lymph about twenty per cent comes <pause dur="0.4"/> through <pause dur="0.2"/> another vessel on the right side of the body <pause dur="0.8"/> and this is lymph that's collected from the right <pause dur="0.3"/> thorax the right arm and the right side of the head <pause dur="0.7"/> it enters into <pause dur="0.4"/> another vessel which i've also lined in underlined in green here that's the right <pause dur="0.3"/> lymph duct <pause dur="0.4"/> that's about twenty per cent of the lymph comes in that <pause dur="0.4"/> route <pause dur="0.3"/> and that enters into the right subclavian vein <pause dur="0.3"/> instead of the left subclavian vein <pause dur="15.7"/><kinesic desc="changes transparency" iterated="y" dur="15"/> are there any questions about <pause dur="0.2"/> veins or <pause dur="0.2"/> the lymphatic system <pause dur="2.9"/> no <pause dur="0.2"/> good <pause dur="0.4"/> okay <pause dur="0.7"/> well i'll move on to the final topic <pause dur="0.2"/> a brief topic <pause dur="3.0"/> and that is <pause dur="0.4"/> the control of blood pressure <pause dur="20.7"/><kinesic desc="writes on transparency" iterated="y" dur="8"/> # the reason that i've had to leave this topic until the end we've i i <pause dur="0.3"/> hope you've noticed that i've gone around the circulation starting with the heart going around the arteries to the capillaries <pause dur="0.4"/> and then back to the heart <pause dur="0.8"/> and # <pause dur="0.2"/> the reason i've left the control of blood pressure

till the end <pause dur="0.4"/> is that it involves just about every aspect of the circulation so i couldn't introduce that until <pause dur="0.5"/> # <pause dur="1.5"/> # until i've discussed everything else <pause dur="2.4"/> and you should note that when people talk about <pause dur="0.2"/> blood pressure <pause dur="0.5"/> they are generally talking about arterial <pause dur="0.4"/> blood pressure when you go and have your <pause dur="0.5"/> blood pressure measured or as you measured it in the practicals <pause dur="0.5"/> that's the blood pressure in the large arteries near the heart <pause dur="0.5"/> usually the brachial artery <pause dur="8.0"/> as well as involving all the vessels that i've talked about <pause dur="0.8"/> this involves a specialized set of receptors <pause dur="1.1"/> that are called baroreceptors <pause dur="0.6"/> and you should have come across these when you <pause dur="0.7"/> wrote up your <pause dur="1.4"/> # <pause dur="1.4"/> wrote up your practical <pause dur="1.3"/> and the baroreceptors <pause dur="0.5"/> the <pause dur="0.2"/> prefix the baro here comes <pause dur="0.5"/> # means pressure <pause dur="0.3"/> in the in the same way as you find it in barometer for instance so these are pressure <pause dur="0.2"/> sensors <pause dur="1.0"/> and they're found in two locations in the arterial system <pause dur="0.9"/> one is the <pause dur="0.5"/> carotid sinus <pause dur="4.2"/> at <pause dur="0.3"/> two main locations i could say i should say there

there are other <pause dur="0.5"/> less important locations too <pause dur="0.5"/> the first one is in the carotid sinus the carotid artery's the large artery <pause dur="0.4"/> coming up either side of the neck <pause dur="0.4"/> and it splits into two <pause dur="0.4"/> one side helps to feed the brain and the other side <pause dur="0.3"/> feeds the face and the scalp <pause dur="0.7"/> and <pause dur="0.4"/> where the artery splits in two <pause dur="0.4"/> there's a kind of swelling at that bifurcation that's the carotid sinus <pause dur="1.6"/> and the other location <pause dur="0.4"/> is the aortic arch <pause dur="3.7"/> so that's as the <pause dur="0.5"/> # aorta is <pause dur="0.3"/> coming out of the heart it comes up and turns <pause dur="0.2"/> curves in two dimensions before it goes down <pause dur="0.3"/> along the backbone <pause dur="0.4"/> and at the <pause dur="0.2"/> top of the arch there are more of these receptors <pause dur="0.9"/> which are not to be confused with chemoreceptors <pause dur="0.5"/> remember that i talked to you about chemoreceptors when i was talking about the control of ventilation <pause dur="0.4"/> and the chemoreceptors are in the same place <pause dur="0.4"/> that's a separate system so don't get these two <pause dur="0.4"/> confused <pause dur="3.6"/> so if we have <pause dur="0.4"/> an increase in pressure <pause dur="0.6"/> or an increase <pause dur="0.2"/> in pulse pressure <pause dur="2.2"/> and by pulse pressure <pause dur="1.2"/> is meant the difference

between systolic blood pressure and diastolic blood pressure <pause dur="0.3"/> so it's how much the blood pressure <pause dur="0.3"/> jumps each heartbeat <pause dur="2.2"/> if these increase <pause dur="0.6"/> then we get <pause dur="0.3"/> an increase in firing <pause dur="0.5"/> of the baroreceptors <pause dur="8.0"/> and this is sent to the medulla <pause dur="6.1"/> where there's something that used to be called <pause dur="0.3"/> the cardiovascular centre <pause dur="0.4"/> but it's unfashionable to call it that these days <pause dur="0.6"/> it used to be thought that <pause dur="0.5"/> each <pause dur="0.3"/> physiological system had a centre in the brain there'd be a cardiovascular centre and a respiratory centre <pause dur="0.4"/> and that's now believed to be too simplistic but you'll probably still see that in textbooks <pause dur="0.5"/> it will be referred to as the medullary cardiovascular <pause dur="0.3"/> centre but it's in the brain stem a set of neurones in the brain stem that are <pause dur="0.5"/> concerned with regulating <pause dur="0.5"/> # blood pressure <pause dur="1.7"/> and <pause dur="1.0"/> the <trunc>m</trunc> medulla reacts <pause dur="0.4"/> by <pause dur="0.3"/> # changing the <pause dur="0.4"/> firing of the <pause dur="0.9"/> parasympathetic and the sympathetic nervous system <pause dur="0.4"/> so in this case we'd get an increase <pause dur="0.4"/> in the parasympathetic <pause dur="0.5"/> nervous system firing <pause dur="0.3"/> and a decrease in the

sympathetic <pause dur="0.4"/> nervous system firing <pause dur="1.5"/> these are the two components of the autonomic nervous system <pause dur="3.9"/> and these changes <pause dur="0.6"/> decrease pressure <pause dur="2.1"/> and we'll see how in a moment <pause dur="2.9"/> so we have a nice little negative feedback loop here a reflex <pause dur="0.5"/> and it's called the <trunc>baro</trunc> <pause dur="0.6"/> baroreceptor reflex <pause dur="0.4"/> or the baroreflex <pause dur="0.4"/> for short <pause dur="1.7"/> and i hope you've come across this when you wrote up your <pause dur="0.6"/> cardiovascular practical that's the baroreflex <pause dur="2.6"/> now before i say what this does <pause dur="0.3"/><kinesic desc="changes transparency" iterated="y" dur="9"/> i just want to say <pause dur="0.7"/> a few <pause dur="0.2"/> words about <pause dur="1.1"/> what <pause dur="0.5"/> blood pressure actually is <pause dur="1.8"/> and remember that we've got these variables <pause dur="1.5"/> blood flow <pause dur="0.7"/> blood pressure <pause dur="0.6"/> and <pause dur="0.5"/> resistance <pause dur="1.0"/> and who can tell me <pause dur="0.2"/> how i arrange those <pause dur="1.0"/> into an equation what's the relationship this is so important to remember this equation <pause dur="5.5"/><vocal desc="laughter" iterated="y" dur="1"/><pause dur="1.2"/> please learn this <pause dur="9.9"/> in fact it's it's more strictly written <pause dur="0.2"/> delta-P equals Q-R <pause dur="0.6"/> that is the difference in pressure that drives the flow <pause dur="0.3"/> to drive flow round a pipe we have to have a a higher pressure at one end <pause dur="0.4"/> than another please please <pause dur="0.4"/> do learn this <pause dur="0.6"/> and <pause dur="0.2"/>

as i've pointed out several times already it's the same <pause dur="0.4"/> as Ohm's law if you know Ohm's law you shouldn't have any trouble remembering this <pause dur="7.1"/> now <pause dur="0.7"/> in the circulation <pause dur="0.5"/> if we take apply this equation to the circulation as a whole <pause dur="0.7"/> we can say that this is the blood pressure <pause dur="0.6"/> coming out of the heart <pause dur="9.5"/> minus the blood pressure <pause dur="1.9"/> coming into the heart <pause dur="5.0"/> that's the pressure gradient that drives <pause dur="0.3"/> blood flow around the whole circulation <pause dur="0.3"/> the pressure generated by the heart <pause dur="0.3"/> minus the pressure of the blood when it returns to the heart <pause dur="1.6"/> and that equals <pause dur="0.5"/> the flow rate but the flow rate for the whole circulation <pause dur="0.3"/> is the same as the cardiac output <pause dur="5.1"/> that is the flow of blood around the circulation <pause dur="0.3"/> the flow of blood around the whole circulation is obviously the blood that's been pushed out by the heart <pause dur="0.4"/> so we can say that the flow rate is the cardiac output <pause dur="0.5"/> and cardiac output equals <pause dur="1.7"/><vocal desc="laugh" iterated="n"/><pause dur="1.2"/> come on guys <vocal desc="laughter" iterated="y" dur="1"/></u><pause dur="4.5"/> <u who="sm0232" trans="pause"> five litres </u><pause dur="0.4"/> <u who="nm0228" trans="pause"> sorry </u><pause dur="0.2"/> <u who="sm0232" trans="pause"> five litres per minute </u><pause dur="0.5"/> <u who="nm0228" trans="pause"> yes <pause dur="0.2"/> right <pause dur="0.5"/> five litres per minute but <trunc>w</trunc> <pause dur="4.0"/> what <pause dur="0.2"/> i said </u><pause dur="0.3"/> <u who="sm0232" trans="pause"> stroke volume times heart rate </u><u who="nm0228" trans="latching">

stroke volume times heart rate <pause dur="3.0"/> stroke volume <pause dur="0.8"/> times heart rate <pause dur="0.8"/> and then we have <pause dur="0.4"/> the resistance <pause dur="0.4"/> and where does the resistance of the circulation lie <pause dur="1.4"/> in the arterioles and we call it we have a <pause dur="0.3"/> a name for it <pause dur="1.4"/> total peripheral resistance <pause dur="0.3"/> T-P-R <pause dur="1.5"/> now <pause dur="0.4"/> the blood pressure coming into the heart i've just told you is very low <pause dur="0.3"/> there's almost no pressure in the blood <pause dur="0.5"/> by the time it gets to the heart it has to be sucked back up by our breathing muscles and something <pause dur="0.3"/> so i'm going to cross that out <pause dur="1.6"/><kinesic desc="writes on transparency" iterated="y" dur="1"/> and call that zero <pause dur="0.8"/> so the blood pressure coming into the heart is zero <pause dur="0.4"/> and the blood pressure coming out of the heart into the large arteries <pause dur="0.3"/> i've just told you is what we call <pause dur="0.3"/> blood pressure <pause dur="0.3"/> when you measure the blood pressure in a large artery <pause dur="0.3"/> that's effectively the pressure just outside the heart <pause dur="0.3"/> so we can simplify this whole thing <pause dur="0.4"/> as the blood pressure <pause dur="0.7"/><kinesic desc="writes on transparency" iterated="y" dur="16"/> yeah <pause dur="0.3"/> what we <pause dur="0.4"/> conventionally call blood pressure <pause dur="0.5"/> equals cardiac output <pause dur="0.6"/> that is <pause dur="0.3"/> stroke volume times heart rate <pause dur="1.6"/> multiplied by the resistance

in the arterioles <pause dur="0.4"/> which we call <pause dur="0.4"/> total peripheral resistance and please do <pause dur="0.5"/> learn how to arrive at that point <pause dur="2.9"/><kinesic desc="changes transparency" iterated="y" dur="11"/> and that's all i want to say <pause dur="0.4"/> about blood pressure except to show you on your <trunc>di</trunc> on your handout <pause dur="1.8"/> that you have <pause dur="0.2"/> the baroreflex here <pause dur="0.3"/><vocal desc="clears throat" iterated="n"/><pause dur="6.2"/> here you have <pause dur="0.3"/> at the top <pause dur="0.8"/> the <pause dur="0.2"/> arterial pressure <pause dur="2.3"/> and its being detected by the baroreceptors <pause dur="1.4"/> and the baroreceptors <pause dur="0.9"/> have to alter the blood pressure to bring it back to normal <pause dur="0.4"/> if if say <pause dur="0.3"/> this this example <pause dur="0.3"/> is given in the case of a fall in arterial <pause dur="0.2"/> pressure which would happen <pause dur="0.3"/> if you had a bad accident say and lost a lot of blood <pause dur="0.3"/> through haemorrhage <pause dur="0.7"/> or if you stood up quickly <pause dur="0.3"/> and a lot of your blood remained in your feet and didn't return to the heart <pause dur="0.4"/> then your blood pressure would drop <pause dur="0.4"/> and that would be picked up by the baroreceptors <pause dur="0.4"/> and the baroreceptors would have to do something about it <pause dur="0.5"/> and from this <pause dur="0.3"/> equation <pause dur="0.4"/> you can see exactly what they have to do <pause dur="0.4"/> if you want to increase blood pressure <pause dur="0.4"/> you have to increase

cardiac output <pause dur="0.4"/> that is you increase the stroke volume <pause dur="0.3"/> and the heart rate <pause dur="0.9"/> and you increase total peripheral resistance you constrict the arterioles <pause dur="0.4"/> so if you want to <pause dur="0.4"/> to raise blood pressure <pause dur="0.6"/> you have to make the heart beat faster <pause dur="0.5"/> make it beat stronger <pause dur="0.3"/> and constrict your blood vessels <pause dur="2.9"/> now i've asterisked <pause dur="0.2"/> here <pause dur="0.7"/> those three <pause dur="3.4"/> parts of the feedback loop <pause dur="0.3"/> the increase in heart rate <pause dur="0.3"/> the increase in stroke volume <pause dur="0.3"/> and the increase in peripheral resistance where did you see the increase in heart rate <pause dur="3.1"/> in the practical <pause dur="0.8"/> when you stood up you measured blood pressure <pause dur="0.5"/> which stayed more or less constant that's because the baroreflex was working <pause dur="1.2"/> but the heart rate went up <pause dur="0.6"/> went up a lot ten or fifteen beats per minute a big percentage increase <pause dur="0.5"/> that's this part of the loop the baroreflex increasing the heart rate <pause dur="0.4"/> to try and keep your blood pressure up <pause dur="2.8"/> # i just want to point out here <pause dur="0.4"/> that it's not just your arterioles that constrict <pause dur="0.5"/> but also your veins that constrict i've just

talked about your veins being under control <pause dur="0.5"/> here we have constriction of the veins <pause dur="0.3"/> and what that does is to squeeze blood towards the heart <pause dur="0.6"/> and <pause dur="1.1"/> makes the heart beat faster <pause dur="0.6"/> # <pause dur="0.2"/> beat stronger <pause dur="0.6"/> and what i want you to do <pause dur="0.8"/> some time between now and the exams <pause dur="0.4"/> is to go through this diagram we've covered all the bits individually <pause dur="0.3"/> in different lectures <pause dur="0.4"/> throughout the <pause dur="0.3"/> lecture course so far <pause dur="0.3"/> and i want you to make sure <pause dur="0.4"/> that you understand what's going on <pause dur="0.5"/> at each <pause dur="0.6"/> at each # step <pause dur="0.4"/> so if for instance if i point out to you here <pause dur="0.5"/> that an increase in end-diastolic volume <pause dur="0.4"/> makes the heart <pause dur="0.2"/> <trunc>pr</trunc> pump out more blood <pause dur="0.4"/> that's something we've already covered can anybody remember what that's called <pause dur="0.9"/> an increase in end-diastolic volume increase in <pause dur="0.3"/> the stroke volume <pause dur="1.7"/><vocal desc="laughter" iterated="y" dur="1"/><pause dur="0.8"/> i've obviously left a deep impression <pause dur="0.4"/> that's the

Frank Starling mechanism <pause dur="0.2"/> <unclear>at the out</unclear> <pause dur="0.3"/> the <pause dur="0.3"/> heart pumps out <pause dur="0.5"/> what is returned to it <pause dur="0.3"/> so i want you to go through this diagram and make sure that you can do that for each step in the diagram <pause dur="0.4"/> because we have covered all the individual bits <pause dur="2.7"/> okay <pause dur="0.9"/> the next two lectures the next two weeks will be on <pause dur="0.4"/> much broader topics next week i'm going to be talking about some specialized circulations which are rather interesting <pause dur="0.5"/> and the week after that i'm going to talk about how the <trunc>circuli</trunc> <pause dur="0.2"/> <trunc>s</trunc> how the circulation <pause dur="0.3"/> adapts to special <pause dur="0.2"/> conditions and i'm going to be <pause dur="0.4"/> taking the aviation world as an example of that <pause dur="0.8"/> # and i have <pause dur="0.2"/> # the marked practicals <pause dur="0.4"/> if you want to come and collect your practicals that were handed in last week i have them here

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