Edema | Types | Causes and Symptoms👨‍⚕️

today we are going to talk about the core concepts related with the edema right now ah before I really give the lecture I would love to ask you a few questions how do you define what is edema yes please right uh she's saying that edema is accumulation of interstitial fluid interstitial fluid is normally there interstitial fluid is normally there but normally we are not edematers someone can improve on this definition yes it's really we can say you are saying that it is accumulation of abnormal fluid in interstitium still not good yes is us you can make it a better okay he's saying that edema means accumulation of excessive fluid in interstation right this is right definition but it's not the complete because by this definition you miss a big part of Edema anyone can improve it further definition of Edema yes abnormal accumulation of fluid in the interstitium yet not yes okay anyone else excellent very good uh he is saying excess fluid in the body there is excessive fluid either inside the cells which is intracellular edema or in the interstitium and body cavities which is called extracellular edema so my dear friend at least you should know what is edema let me tell you edema is just edema is excessive fluid excess fluid in body tissues that's it what is the edema a demise excess fluid yes in body tissues that's it it may be intracellular or edema may be extra cellular right when you say edema mean fluid in interstitium that is wrong because normally there is fluid in interstitium and if you say edema is excessive fluid in interstitium then you miss intracellular edema right so what is the edema edema simply means excessive amount of fluid present in the body tissues but let's refine it further why because its excessive fluid not in all body tissues for example if their excessive fluid in the blood if there is excessive fluid in the blood is it called edema no if there is excessive fluid in the blood that is not called edema it means that when Whenever there is excessive fluid in the vascular compartment that is not considered edema so we can further improve our definition that edema is excessive fluid in body tissues extra vascularly extra vascular ly right now let me draw a diagram to make it more clear let's suppose from your body I remove a piece of tissue right this is a piece of tissue a typical tissue from your body and naturally the tissue is having arterial Supply right let's suppose here is your left heart all right systemic circulation and this is hypothetically we make that there is arterial Supply coming to this tissue right arterial input in the same way this tissue must have some outflow mechanism that is venous right and that will be going to which side of the heart yes please right heart very good that would be going to the right heart and of course all of you know that blood from the right heart yes blood from the right Hearts the pulmonary what arteries go to lungs and through the microvasculature of the lungs blood is eventually being brain to the left side so pulmonary veins which have oxygenated blood right now what have what what I am showing in this diagram from the left heart blood is going to the tissues right and we have taken a sample tissue here and this is the arteriolar input and here I have shown the venous output is that right now let's see in detail in this tissue right arterial system of course arteries come they divide into arterioles and eventually they divide into Capital rays right uh there's some going draw micro circulation this is your micro circulation this one right and there is arterial input here is Venous output here are your cells cells in the tissue right parenchymal cells and let's suppose this is representing body cavities right body cavities these are parenchymal cells in the body and this area this area this is interstitial tissue what is this interstitial tissue so we can say interstitial tissues between the parenchymal cells and the vasculature is that right this is interstitial tissue now let's divide our body weight and see what are the normal fluid compartment because when we Define edema as excessive fluid we Define edema as excess amount of fluid in body tissues but extra vascularly right when we Define like this we must know what is the normal amount of fluid in different body compartment right because when fluid is Success then it is edema but as a good doctor you must know what is the normal amount of fluid in different body compartments let's suppose here you are your beautiful picture right yes let's suppose you are adult and your weight is 72 kg right if you are 72 kg how much water will be there in your body yes five liter water I think I will die immediately five liter water is too low water you know if you are 72 kg and if you have only 5 liter bottle five liter of water in total body you must be dead already uh foreign how did you calculate it excellent very good actually when we say total body weight total body weight right 72 kg is the total body weight of this person total body weight is divided into two total body water and lean body mass lean body mass and total body water if we remove that for example if this diagram is representing all the body weight right if it is representing all the body weight then in this person this hole should represent 42 kg out of that total body weight divided into lean body mass which is about 40 percent and total body water is about 60 percent this is very important to understand whatever our weight approximately sixty percent we are just water when we say if I say I'm falling in love with a girl actually sixty percent water of Dr najib is and plus 40 percent of lean body mass is falling in love with the girls how much water sixty percent of the water and forty percent off lean body mass so you need to remember this that all of us consist of six to about 60 percent of water about 60 percent of water is that right children have a little more percentage anyway so sixty percent of water it means if my weight is 72 kg then okay this whole system has 72 kg weight how much water 60 percent about 42 liters so if my weight is 72 kg I will have how much water 42 letters don't sell 42 kgs and if my weight is 100 kg then how much water I have 60 liters so is that clear right and out of this 42 this 42 liter is divided into very important fluid compartments in the body right for example out of this 42 one third is in the intra cellular fluid it means one third fluid is present inside the cells these are cells so all your if my weight is 42 yes 40 72 kg total water I have is 42 out of that intracellular is two thirds and extra cellular fluid is one third extracellular is one third intracellular is two third and what is the extracellular fluid extracellular fluid mean outside the cell outside the salmon fluid in the interstitium including body cavities and fluid in the blood your understanding so if I have 72 kg weight the 42 liter of water in my body out of that 28 liter is present inside the cells because 42 3 is 28 letters and one third is 14 letters so it means I will write it here how much I have 28 28 liters here and how much is left then 14 so 14 letters here outside the cells out of this 14 inside the plasma is about 3.5 liters 3.5 liters and outside is about 10.5 liters approximately of course the degree of hydration changes percent to person and time to time but approximately now we come back so what we have decided that extra solar fluid is divided into interstitial fluid which is here and what is this intravascular fluid normally how much blood you have how much blood you have five letters you are answering this thing you are saying five letter five letters the amount of blood in a person but we have fluid outside the blood secondly in the blood even five liter is not the whole fluid there are cells too we are talking about let's suppose this is vascular system these are red blood cells now which is the fluid inside the red blood cell that is intravascular not only intravascular that is intra cellular to in the blood vessels you have five liter of the blood but in the blood there are cells right and there are red blood cells the white blood cells and there are platelets all of them have fluid inside but that fluid is considered part of the intra cellular compartment that is considered part of the intra cellular compartment so plasma which is left that is considered extra cellular so plasma is about three and a half liter out of five liter blood one and a half liter you can see is your cells cells my friend you are having five letter blood right out of that blood approximately one and a half liter is yourself and whatever fluid is present inside the cells that is considered intra cellular fluid is that right but other than cells blood has plasma so five liter of the blood one half liter is cells and three and a half liter is plasma that three and a half liter plasma is considered part of the extracellular fluid that is considered part of the extracellular fluid that is why extracellular fluid I write three and a half liter here and remaining within the interstitium and very little into body cavities right so into three some approximately 10.5 liters right so this is the normal distribution of fluid why I am teaching you normal distribution because in edema there is abnormal abnormal distribution or excessive accumulation of fluid in extracellular or intracellular is component right now let me repeat if I'm having 72 kg weight right lean body masses 40 percent and total body water is 60 out of that sixty percent total body right okay let me put it that we are having this is total body mass right forty percent we remove what was that laneward now what is the remaining 60 is water now out of that water intracellular will be two thirds and extracellular will be one third is that right so intracellular out of 42 will be 28 liters and extra solo will be 14 letters right and this extracellular fluid further divided into interstitial fluid and plasma is it clear any question up to this now why we were studying let's suppose interstitial fluid in total body rather than 10.5 liter it become 20 later then it is generalized edema or in a specific tissue in a local area interstitial fluid is excessive now before we go into further detail let's go to the very basic right and we have talked about that again I will repeat that edema is excessive fluid in the body tissues extra vascularly right so this is the definition of edema and edema can be divided into now two types of Edema intracellular edema intracellular edema which is this edema if there is over excessive accumulation of fluid inside the cells that is considered intra cellular edema and if there is excessive accumulation of fluid outside the cells what is that extra cellular edema extracellular edema and here it is intracellular edema right so today onward when you talk about edema please clear that are you talking about intracellular edema or extra cellular edema but in medical literature and during medical discussions generally generally speaking when we say edema usually we mean excessive fluid in interstitial area right so if excessive fluid is here what is this what type of Edema extra cellular edema or in general discussions non-specifically speaking we call it just edema we just call it edema right excessive fluid intracellular edema excessive fluid here and in body cavities and in body cavity both are called extracellular edema amiclet now what are these body cavities Excel solar edema is either in the interstitium enter station here or it is in serous body cavities serous body cavities are yes pericardium when there is excessive fluid in pericardium we call it just a minute when there is excessive fluid in the pericardium we call it we call it pericardial effusion OK we can call it pericardial effusion very good or we can call it hydropericardium very good Hydro Perry cardium when there is excessive fluid in the pericardium what we call it hydropericardium or we call it as you said pericardial effusion someone said pericardial tamponade someone said it who was that raise your hand raise your both hands you are absolutely wrong what is cardiac tamponade it means you do not have the concept of cardiac tamponade listen let me tell you if there is normal fluid here then we say this is normal pericardial fluid of course but when there is excessive fluid we call there is cardiac pericardial effusion and now listen carefully and if due to excessive fluid if due to accumulation of excessive fluid cardiac filling is significantly compromised then that is called cardiac tamponade you understand it whenever you have extra fluid here in the pericardium that is not cardiac tamponade having more fluid here is just pericardial effusion but when a fusion is able to compress the heart and does not allow the Heart during dastly to fill and compromise compromises cardiac function then we say there is cardiac tamponade so please yes now in acute case if there is cardiac pericardial Fusion if it rapidly develop a smaller fume can produce tamponade but if pericardial effusion is developing very gradually very slowly over the months and years then too much fluid can accumulate in pericardium and still it doesn't compress hard so we say there is Big pericardial effusion there is no cardiac tamponade am I clear so next time in your life before you speak about tamponade remember tamponade is only there when a fusion is able to compromise cardiac function right now let's move forward so hydropericardium what else pleural cavity may have extra fluid normally there is fluid if floral cavity has extra fluid we call it we can call it plural efficient we can also call it Hydro thorax in the same way if there is excess fluid excess fluid in the peritoneal cavity we can call it peritoneal effusion Which is less commonly used term more commonly we can say Hydro Hydro peritoneum but very commonly we use the word very good cities excellent who said site is first very good so when the scientists become symptomatic house how large and Society sciatic fluid should be to detect it clinically just a minute just a minute First Let Me Clear My question when there is normally peritoneal cavity in abdomen do does have a little fluid okay if there is excessive fluid there we call it Hydro peritoneum or we call it a site is very good my question is that if a person is having ascites it start developing maybe in the very beginning a slight increase in fluid cannot be detected clinically how much fluid extra fluid or how much total amount of fluid should be present in my peritoneal cavity to be detected by a stute clinician a sharp doctor yes no you are not understanding my question 2.5 liter absolutely wrong if some doctor can guess that I have developed 2.5 liter of water and only then he can guess he is a very pathetic clinical method that is listen if you are able to detect the societies when I have developed 2.5 liter of fluid in my abdomen that is not a great physician a very sharp physician should have so good clinical methods that he should be able to detect even a small amount of fluid in the abdomen free fluid how small can be usually detected by a good doctor I'm not talking about doctor with yes yes half letter a good doctor should be able to detect presence of ascites when it is about half letter and if someone only detect a site is when there is two and a half liter water oh that's a very sad and bad situation for that doctor okay and for patient too anyway so we were talking about extrasolar edema mean edema fluid excessive fluid in interstitial area and and or serous body cavities I'm saying serious body cavities not everybody can they have a nasal cavity it doesn't have edema there I just got nasal secretions there are other cavities I will not commence there right so what I'm talking about serous body cavities especially pericardial cavity return cavity and pleural cavity right so this is a basic concept of edema right but here I would love to mention one more thing that as we mentioned a fluid is more here intracellular edema fluid is more here excessive fluid here and here extracellular edema but if there is flu excessive fluid here what is that if we take a tissue let's suppose you take a small tissue here and there is excessive amount of blood present in micro circulation excessive amount of blood or fluid present in micro circulation of course we know we do not call it edema we don't call it edema what do we call it yes anyone raise your hand all of you know it but you don't know you know it yes hyperbolemia is a simple term yes you can call it simply hyperbolemia but the hyperbolemia is usually used when all body has total blood volume more than normal what I'm talking about is specific tissue if there is a small amount of tissue right and due to some reason uh in this tissue amount of blood in micro circulation is more than normal right okay talk about my finger in in my finger due to some reason total amount of blood is more than the normal of don't call it edema because edema will be called if there is excessive fluid either intracellularly in the finger or excessive fluid in the interstitium of the finger then it is edema but if there is excessive fluid in the vascular compartment of the fin of the finger we will call it very good we'll call it high premium or congestion we'll call it very no we can call it hyperemia hyperemia or congestion now a good doctor will tell me what is the difference in hybrid listen if I have excessive amount of fluid or blood in my circulatory compartment of this finger one finger or some small tissue we say either tissue is hyperemic or tissue is can just having circulation which is congested what is the real difference between hyperemia and congestion she is very shy she doesn't want to reveal her knowledge yes but she's shy otherwise she knows hyperemia is that excessive amount of blood is because more blood is entering here because more blood is entering here is that right if there is arterial or dilation here an excessive amount of blood is entering here and total amount of blood here is more because of more arrival of blood into tissue we say tissue is hyperamic and if you look a little reddish we call it there is erythema what we call it there is erythema classically this is seen in inflammation but why to go for inflammation do a little exercise and to show us more blood but don't tell that my tissue develop edema you say that is a there's increased blood flow in the tissue and we can call what is there hyperemia right but if there is due to some reason blood flow out of the tissue is reduced if there is some obstruction to the outflow or due to any reason outflow for example if there's a thrombosier and outflow of the blood is reduced then excessive fluid is accumulated here this situation is called congestion so again if there is excessive fluid present in intracellular compartment intracellular edema if there is excessive fluid in interstitium and body cavities or body cavities this is called extracellular edema but generally speaking in medical literature and generally in discussions medical community call edema if not specified only for extracellular edema but please don't say that excess fluid in body tissues is edema because blood is also body tissue right but if blood if there's excessive fluid here it is either High premium when there is more inflow of the blood or it is congestion if there is decreased outflow of the blood any question up to this oh my God you are the thinking of our God things he's asking what is vascular and gorged meant right so many things coming in my mind but I will stay simple engagement is that when blood vessels dilate and more blood coming to tissue and venous outflow from a particular organ is reduced just imagine an organ it's up to your wild imagination and more blood is coming in due to arteriologation and less blood is going out due to venous compression we say there is engorgement of the tissue is that right and in this case hyperemia is there as well as congestion is there we can use the word engorgement a very dangerous word am I right so anyway let's come back to edema any question up to this yes no no no no no he's saying that hyperemia can occur only in arteries no I'm talking about this accumulation of fluid is in the micro circulation which may be arterial and capillaries of meta capillaries or whatever types of is and venules and veins excessive blood here is simply excessive blood thank God doctor didn't put any name or maybe he is trying to put a name here that we say micro circulation is engorged if microcirculation here is in God then this engorgement is due to excessive fluid input then it will be in government engorgement and hyperemia right but if engagement is due to decreased fluid going out excessive flu blood here then we say there is congestion right classically when we say a specific tissues on God and there is usually there is arteriologation so hyperemia is occurring and venous compression so the degree of congestion there too right so in government both components can be there right but let's go back to edema okay before I really go into very big detail of extra cellular edema right I will mention few words about intracellular edema which is also called cellular swelling right so few words about intracellular edema and then we go into detail of extracellular Edema which is called just edema also intra yes cellular edema now when we talk about intracellular edema it means there is excessive fluid in the intracellular compartment it means healthar swollen is that right in what condition it can happen why excessive fluid will enter into cells what could be the reason anyone from the last row no from the last row anyone okay you are saying hyper or small Clarity where extra cellularly or intracellular intracellularly very good that inside the cell if inside the cell is hyperosmolar if there is more solute in the cells actually let me tell you he is right if Whenever there are more solute in the cells or the left solutes outside the cells water will shift to the intracellular compartment right now what could be the reasons of why the cells become hyper or smaller okay you are saying that intracellular edema may be due to increased osmolarity of intracellular fluid why this fluid become hyper or smaller raise your hand just to remind everyone has two hands yes okay he's trying to impress me he has read something which he doesn't remember clearly but he has read something let me explain what he is trying to say let me explain what he is trying to say all of you know that every cell has special type of pump which is called sodium potassium 80 pays the sodium potassium pump sodium potassium pump is all the time taking three ions of sodium three ions of sodium outside and always actively pushing two ions of potassium inside it is taking two potassium in and it is taken three sodiums out is that right this is sodium potassium pump which is always pumping the sodium out of the cells and taking the potassium in is that right now due to some reason if this pump is not working well due to some reason if this pump is not working well then it is not bringing two potassium in but it is keeping the three sodium in and gradually sodium will accumulate in the cell and then cell will become hyperosmotic and pull the extra cellular water in pull the extracellular water in so whenever sodium potassium pumps which are present in every cell sodium potassium pumps are present on every cell more accurately they should be called sodium potassium ET phases what we call sodium potassium 80 Pages because this pump has special enzyme which break down the ATP uses the energy of ATP to operate and do its function right we call it sodium potassium 80 phases if due to any reason sodium potassium 80 pages are not working then sodium is no more expelled from the cells the sodium which is retained in the cell that pulls the water with it and cell become swollen and intracellular edema develop but can you tell me a condition in which sodium potassium 80 pages will not be working any pathological disease condition s conditions in which sodium potassium body phases are not working is right but he should explain more elaborately simple as that I mentioned so just a minute now my turn sodium potassium metal phase is using ATP ATP is the energy in the cell if cells become hypoxic it's very simple if any tissue becomes ischemic if any tissue become ischemic the less blood flow going there less oxygen going there less glucose than other nutrients going there if the tissue is ischemic or cell is ischemic cancel make without oxygen without glucose or other nutrients can it make ATP no if it cannot make energy how it will operate the pump and if this pump is not working how it will throw the sodium out sodium love to go in it is like I must say I will not say what kind of iron what kind of behavior but it loves to go in right so we have to push it out all the time out of the cell why you are smiling very naughty smile on your face all boys very bad okay sodium is just sodium ion okay so it loves to go in and we keep on pushing it out but whenever the tissue is the skimmick or hypoxic less oxygen energy producing Pathways collapse ATP deficiency develop sodium potassium 80 phases are not working sodium start accumulating in the cells and sodium will pull the water with it and cell will swollen up is that right these are like unhappy cells like making unhappy phase is that clear so these are swollen cells no energy if you don't have money how is your face a big one in the same way when cells don't have ATP no energy they also make a big face right so hypoxia ischemia can make the cells admit a swollen this is one of the feature of cell injury then due to any other toxin if mitochondria are damaged still ATP is not produced because ATP is mainly produced through the help of mitochondria and if mitochondrial Machinery fail the ATP is not produced sodium potassium battery phases are not working again cells will undergo swelling right then any type of injury direct to the membrane remember outside the cells there is a lot of let me make a cell here a typical Cellar normally normally sell them more potassium or sodium think and then answer yes yes normally myself have more sodium or more potassium wow that's very good cells are just bags of potassium they have a lot of potassium that is why when Crush injury is there when there is Crash injury a lot of cell rupture and potassium come out in the blood and hyperkalemia develops right but anyway come back cells are the bags of potassium and cells love to keep the sodium outside cells love to keep the sodium outside extracellularly sodium bind a lot of water with it so sodium cannot enter into cell through the simple cell membranes sodium can only enter in the cells so special transport mechanisms or channels right but whatever sodium enter into cell we must get it out we must get it out now so outside there is higher concentration of sodium and inside there is high concentration of potassium and also there's one more iron which has extracellularly in high concentration outside as compared to the inside very important okay color right but more important than chloride calcium calcium it's very important so extracellular environment is rich in sodium and calcium and many other things of course but right now it's relevant that extracellular environment is rich in sodium and calcium intracellular environment is rich in potassium and other things now a cell normally cell membrane is not freely permeable to these sodium and calcium normally cell membranes are not freely permeable to sodium and calcium so normally sodium are trying to go in but they are repelled in the same way calcium loves to go in but it is not allowed only under special physiological functions sodium and calcium go in like sodium goes in during action potentials depolarization or calcium go in when there is some security functions but remember normally extracellular fluid is rich in sodium and calcium intercellular fluid is rich in potassium and if there is membrane damage due to any reason whatever the reason if cell membranes are damaged in any way what will go in sodium and calcium and the sodium and calcium when when it will go in not only in toxic concentration it will hurt the intracellular Machinery but it will do one more thing it will drag the water with it and cell will start swelling so intracellular edema it may be due to impairment of sodium potassium 80 pages which fail to keep the sodium out and sodium starter being retained inside or intracellular edema may occur when generally cell membranes are damaged whatever the mechanism whatever the cause whatever etiology right then one more condition let's suppose in the cell sodium potassium 80 phases are working fine sodium potassium atps are working fine and generally cell membrane is also okay cell membrane is also ok right in this cell but due to some reason outside the cell hyponatremia develops what is the difference of sodium concentration in the blood in the plasma and interstitial fluid some very good doctor can answer everyone cannot my question is what is the sodium concentration difference between the blood concentration of sodium and interstitial concentration of sodium here I've told you intracellular fluid very poor in sodium extracellular fluid very rich in sodium but now I'm asking a tricky question that sodium concentration difference in Blood and interstitution fluid yes ma'am uh not a normal person healthy person you think interstitial fluid is more yes ma'am you also agree with her but remember medical facts are not decided by democracy the 10 people are wrong then right become wrong Yes Man G iven same why you think it should be the same in the vasflow compartment and here because capillaries are freely permeable to sodium he is right oh my God you don't know this sodium chloride and many ions concentration in the plasma and interstitial fluid is same because sodium is freely permeable here here it cannot freely go sodium is like men it can be on the road or it can be on the side of the road but men are not allowed to enter in every house you understand and you know why and if they have entered in under special circumstances a sodium Channel open like Windows when someone call at midnight or every day time when doorbell and special Channel sodium goes in right but if sodium goes inappropriately who throws it out sodium potassium 80 phase it comes it is kicked out is that right but sodium concentration in the cell extra in extrasal of fluid everywhere is same in the blood and interstitial fluid is same you are understanding am I clear okay but here now I was saying due to any reason if you develop hyponatremia hyponatremia mean in the blood sodium level is less it means it's pertaining to blood so when I say the person has hyponatremia what does it mean sodium concentration in the blood is less what is the normal concentration of sodium in the blood yes only this man ah yeah he's smiling but not telling normal concentration of sodium in the blood oh no no I know you know the ions too much you are in love of electrolytes electrophilic boy 142 watt machine guns equivalent per liter okay all of you are right that when we say normal amount of sodium in the blood is 142 ml equivalent per liter but please be a good doctor tell me the range don't tell me your phone 42 the way you are telling me that normal sodium is 142 it means if I have 41 or 43 it is abnormal it is not abnormal so what is the range oh my God you I don't know you are very consistent to be wrong today sodium is sodium is 135 to 145 Milli equivalent yes equivalents per liter or millimole per liter so why it's so important to know that lower limit is 135 upper limit is 145 because when sodium becomes less than 135 we say that patient is going to hyponatremia because hyponatremia is basically defined as amount of sodium a concentration of sodium in the blood less than 135 Milli equivalent per literally mole per liter right even though clinical problems start appearing at lower level of sodium but what I'm saying whatever sodium level is here the same level is here let's suppose someone has severe hyponatremia rapidly developing severe hypo nutrimia sodium level drop very rapidly in the blood of course they will also drop here and sodium become less sodium love to hold water if sodium is very less here inside the cell normally normally total osmolarity inside the cell and outside the cell normally it is equal or different equal equal normally it is equal so what happens even though there are different type of ions here and there are other different type of ions here but two in total extracellular osmolarity and intracellular osmolality in physiological condition is and most of the tissue is equal but if from outside we remove the sodium so it become a hyponatremic situation right and it become hyper hyposmolar loss molality what will happen to the cells they will absorb water because cells will be hyperspolar as compared to interstitium and blood again I will repeat it if I develop rapidly hyponatremia whatever the mechanism if myosodium level in the blood is going down of course it will also go down in interstitium interstitial fluid is surrounding all the cells so all the cells have around them less than normal sodium so around the cell there's hypoosmolality and when the hyposmolarity of course then normal similarity of the cell will be more than the surrounding fluid and it will pull the water in and cells will again swell so cellular edema cellular edema can be due to three mechanisms I told you number one I just told you now cellular edema can be due to low sodium hypo natremia or cellular swelling may be due to cell membrane damage cell membrane damage when cell membrane is damaged right sodium and calcium will jump in and water will follow and then I told you those conditions in which sodium potassium 80 phases are impaired where sodium potassium 80 pages are impaired it may be hypoxia or is chemical or whatever right so these are the conditions in which there can be intracellular adhima now we forget about the intracellular edema now we come to the real edema which most of the doctors talk about that is extra cellular edema because when in your Wards or generally when you speak with each other you say patient as edema usually it is meant extracellular edema because if patient has intracellular edema we always mention there is intracellular edema right so now our lecture will go towards what are the causes and mechanism of extracellular Edema why excessive fluid accumulate an interstitution and or body cavities let's have a break and then we'll continue with this discussion right in previous lecture we were talking about edema right and we defined edema as how the edema was defined yes please edema was defined as excessive fluid in body tissues excessive fluid in the body tissue and then we divided edema in two types of Edema intracellular edema and extra solar edema and we discussed intracellular admires in excessive fluid inside the cells where cells are swollen especially after atps pump failure or hypoxia ischemia cell membrane injury right and then we were talking about extra cellular edema and there we discussed Excelsior edema is actually excessive amount of fluid present in interstitium and or body serous cavities right now today we'll go into detail that of the specially extracellular edema we will talk about extracellular edema now onward in this series of lectures when I use the word edema you you should pre-assume that I am talking about extra smaller edema right so let's go for that as let's suppose here is your arterial system here was your left heart right and you know left heart is pumping in the body it's left heart not anything else right with the aorta and let's suppose here is an arterial system coming out this is representing let me make a piece of tissue here let's suppose this is a piece of tissue and this is the arterial input into this tissue right you know our artery is divided into arterials and then met arterial then eventually into capillary Network and here is the venous output from that specific tissue which we have put it over here and here is your guess micro circulation I'm going to make micro circulation here in between the arterial end and the when ascent okay so in this specific tissue this is arterial end of the micro circulation and here is the venous end of the micro circulation and here is your micro circulation and let's suppose here are your parenchymal cells right these are parenchymal cells and these are of course what are these cells endo thelial cells right along with the basement membrane and the capillaries and venules and the blood which is draining from the tissues eventually going to Major veins which will eventually drain into right heart right they will drain into right heart which will itself eventually drain into lungs right and now this is pulmonary dishes tell me pulmonary artery and here is the pulmonary veins and in between them there is pulmonary micro circulation right you shouldn't go out of the lung now as we were discussing yesterday that when we talk about interstitial edema this is the area which is interstitium is basically area which is outside the circulation and also outside the parenchymal functional cells right when we say that there is an interstitial edema it means a demise in this area right and as we Define that there is excessive fluid in the interstitution when there's edema but normally there is some fluid in the interstitium in a man with 72 kg weight usually how much interstitial fluid is there yesterday we discussed that is around 10 to 11 letters right but if interstitial fluid become excessive in all over the body or in a localized area we say there is edema now what is the function of interstitial edema or sorry what is the function of the interstitution and what is the relationship of interstitial fluid with the plasma fluid or blood fluid that is first thing to understand because let's suppose we say that there should be 10 liter fluid present in this area but do you think this fluid is static or dynamic is it always there or it keep on changing yes ma'am just keep on changing what normally happen that all the time okay I am dividing this micro circulation and venous side of the micro circulation now what normally happens all over your body from arterial side of the micro circulation fluid is coming out constantly fluid is coming out and this fluid is bringing the oxygen and in glucose and other nutrients and this fluid is serving these cells that's why they are so happy oxygen is coming glucose is coming amino acids are coming and many other things and then this fluid goes back from this area right it's coming serving these cells right washing these cells providing them the nutrients and removing their waste product and then this fluid let's suppose come here comes here and then goes back right all your capillaries in all your tissues a small amount of fluid is coming out serving the cells and removing the waste product and going back this is what is a normal mechanism right Plus sometimes usually a very small amount of protein leak out not much a very small amount of protein also leak out which cannot be pulled back here that small amount of protein along with some small amount of fluid is drained by an other pathway and that is called lymphatics it means that most of the fluid about 80 to 90 fluid which comes out from arterial side of micro circulation adds to interstitium and constantly being sucked back into innocent of the micro circulation and about 10 to 15 percent fluid along with proteins these are proteins it is being drained into lymphatics it is being drained into lymphatics but remember all lymph fluid eventually drains back into yes venous system you know all the lymph of the body eventually drain through the thoracic duct system into subclavian internal jugular Venus system so in a way hypo we can say that in a typical tissue the fluid input is by arterial site and fluid output is mainly by the venous side and also there is an accessory pathway an additional pathway for fluid draining through the lymphatics but both of these eventually go back to the winner system is that clear now how the edema will fall how the edema can be made how this fluid suddenly become too much it's very easy to understand I don't know why they teach in medical Sciences it's so easy it's very simple either too much fluid is coming from here some if more than normal fluid is too much fluid come here and then edema will occur or this refused to take the fluid back it is not sucking the fluid back again fluid will accumulate or lymphatic system is not working again fluid will accumulate these are three basic mechanisms even though for edema there are more mechanisms too but let me tell you three basic mechanisms we will get other four basic mechanisms first of all when fluid is trying to come out it has to pass through what is this capillary capillary membrane which is semi-permeable membrane a fluid has to come out it has to pass through capillary membrane now how much fluid will be coming here how much fluid will be coming here it depends on multiple factors including the capillary membrane features if capillary membrane is damaged too much fluid will come if this membrane is damaged from inside too much fluid will come so we can say that in a general concept why edema should be their interstitial edema very simple either more fluid is coming to this tissue or less fluid is draining on the venous end of the micro circulation or less fluid draining into in fact they are so simple or there is increased permeability of micro circulation right so how many things I mentioned either more fluid coming out through micro circulation number one mechanism number two or there is decreased reabsorption of fluid number two mechanism number three or there is decreased lymphatic drainage number three mechanism or overall in the body salt and water is too much I will explain the mechanism later if body retains excessive salt and water not only excessive fluid will be here it will also come here so that will also add to the edema and eventually if permeability of this membrane is increased pathologically then excessive fluid will also leak out any question up to this everyone is clear so now first of all I will talk about why in some disease condition fluid is excessively coming out but before really we go into that condition we will talk about normal physiological mechanisms I will tell you how in a normal healthy person and a healthy tissue how this fluid movement out and back is regulated what are the factors which push the fluid out and what are the factors which reabsorb the fluid because when those factors are Disturbed edema will occur you are understanding now what are the factors normally first of all when heart is pumping left ventricle it is pushing the blood into whole body circulation with pressure the pressure which is generated by pumping of the heart that pressure is called hydrostatic pressure normally you call it blood pressure right and of course as blood is moving forward and it divides into different arterial tree and arterioles and smaller hydrostatic pressure will keep on dropping is that right from here the blood is pumped with pressure heart is pumping the blood in the tissues with pressure but as it is moving forward pressure will drop is that right but in a typical tissue in a classical tissue for example we are taking this example the hydrostatic pressure is let's suppose 35 millimeter of Mercury so I will just write it here this is hydrostatic pressure what is this in the normal tissue this hypothetical tissue which I am showing here it has pressure of 35 millimeter of mercury now if fluid is under pressure here and heart is pushing Under Pressure it will love to go out it will love to go out so it means outward pressures is how much 35 millimeter of mercury it is trying to push the fluid on both directions outside but there is something which holds the fluid in normally hydrostatic pressure is trying to push the fluid outward but there is something which is not Pusher you can say hydrostatic pressure in the vascular system right hydrostatic pressure is little here but hydrostatic pressure here and osmotic pressure here I will ignore in this discussion because there are minor factors major factor here which are mentioning hydrostatic pressure inside the micro circulation on the arterial side of the vessels now to 35 millimeter mercury and with this 35 millimeter mercury it is trying to push the fluid outward but there is something which is not Pusher this pressure we can say is Pusher it is pushing the fluid outward Whenever there is a pusher there must be a sucker or at least holder why you laugh at sucker I'm not talking about that sucker which is coming to your mind sucker means suck the fluid back okay so what we are talking about there's a hole okay I will not use the word holder uh sucker I will use the word holder plasma proteins you know plasma proteins in this plasma there are certain proteins which are globulins and albumins and fibrinogen but classically albumin that plasma protein has a power to retain the fluid plasma protein is the power to hold the fluid they hold the water hydrostatic pressure is trying to get the water out and osmotic pressure osmotic pressure which is exerted by the plant presence of plasma protein especially albumin that is trying to hold the water Within circulatory compartment and osmotic pressure which is determined by the plasma protein that is usually 25 millimeter of mercury that is trying to hold the fluid and what it is doing it is trying to keep the water inward it is trying to keep the water inward now we can see that hydrodynamic forces which will eventually determine the movement of the fluid here is determined by the balance between do these two forces this is acting as a pusher and this is acting as a holder or sucker so power outward is 35 power invert is 25 so fluid will move outward or inward outward so net pressure the difference is net outward pressure is 35 minus 25 so this is the pressure with which fluid will be coming out right and this is 10 millimeter of mercury so we can say in a normal tissue on arterial end of the micro circulation with the net filter out pressure what we can say filtration pressure what is this filtration pressure forces out the fluid along with its dissolved components through the semi-permeable membrane from the intravascular compartment to the interstitial compartment with the net filtration pressure of 10 millimeter of mercury I will repeat it that usually tissue to tissues to tissues these values little vary we are taking a typical tissue and a typical tissue on the arterial side of the micro circulation hydrostatic pressure is about 35 millimeter of mercury and Collide osmotic pressure is 25 millimeter of mercury okay we call Collide osmotic pressure or some books right on cortic pressure what is the difference in Collide osmotic pressure and oncotic pressure just please they are the same okay just a minute collide collide osmotic pressure right this is one term versus oncortic pressure on cortic pressure what is the difference in them before you tell me any difference there is no difference they are one and the same thing ah Collide osmotic pressure Collide osmotic pressure which is determined by the plasma proteins that is also called just on cortex pressure but if there is Collide osmotic pressure due to proteins in the interstitial tissue that is not called oncotic pressure actually when colloidal molecules like plasma proteins because when fluid is going out plasma proteins cannot go out so what plasma proteins will do try to hold the water for example if husband is going to the other country if wife cannot go she will try to hold the husband don't go that is an example of collide osmotic pressure but maybe Financial pressures are there he has to go do you get it now what I'm trying to say that could Collide osmotic pressure simply mean that osmotic pressure determined by the colloidal molecules but when we use the term on cortic pressure when we use the term oncortic pressure it means Collide osmotic pressure produced due to plasma proteins interstitial proteins also exert some Collide osmotic pressure but that is not called oncotic pressure am I clear so now onwards in our discussion I may use the term Collide osmotic pressure or may use the term only osmotic pressure or I may use the term oncotic pressure so it is one of the same thing in our discussion forward so we decided that on this side fluid will gradually come out slowly and will come to the tissue circuit but what really happens as some fluid has lost but intravascular fluid is moving to the venous end it is moving forward hydrostatic pressure will drop why it will drop because micro circulation as it moves from arterial and to the pill venous end it becomes white bore diameter its total cross-sectional area increases right so naturally pressures will drop if there is some pipe if suddenly you expand it pressure inside will decrease so here pressure decreases and on this side this on hydrostatic pressure usually become only 15 millimeter of Mercury and but plasma protein osmotic pressure or oncotic pressure remains almost same because proteins did not leak the amount of protein which was here and amount of protein which is here is almost same so osmotic pressure Remain the same is that right but hydrostatic pressure here it was 35 and here it is 15 so it means now hydrodynamic mechanisms shift a little point actually when a some amount of fluids seep out filter out plasma protein become a little concentrated and when plasma proteins become little concentrated on cortic pressure become little more rather than 25 it may become 27 or 28 but for our discussion we will not go into that detail we just assume as fluid is moving in micro circulation on arterial and it is losing the fluid is that right cells especially red blood cells and what platelets they are not coming out only leukocyte under certain circumstances they come out and plasma proteins are not mainly going out most of the plasma proteins are retained here very little plasma proteins leak out which will be taken back through lymphatic system is that clear now look at the Bella hydrodynamic forces balances here these forces are also called Starling forces right what is the balance here now 25 is the polar 25 is the puller or we can say sucker it is trying to suck the fluid and Pusher is very weak it is only 15. so what will be the net effect it will pull the fluid from here backward because net difference 25 is pulling in 15 is just like 25 men pulling a person Inward and 15 pushing it outward still this man will move inward so fluids slowly start going back right and net filtration pressure is now inward here net filtration pressure was outward so under the 10 millimeter of mercury diff right fluid was filtering out on our arterial side of micro circulation and here at almost 10 millimeter mercury fluid was being sucked back or reabsorbed back right but a small amount of protein which was leaking from here a very small amount of protein which leaked from here it cannot be sucked back they are larger molecules and some cellular debris or even microbe so they will be drained through this pathway this is our secret pathway lymphatic is a additional or secret Pathway to drain the protein-rich fluid is that clear this is very important that don't allow these small amount of proteins which are leaking here to stay here it should not stay here it should be taken back because if this proteins keep on coming here and they are not drained they accumulate here those proteins will increase the osmotic pressure here and they will start holding the water and produce edema now these are the normal basic mechanisms right so what are the factors which determine the pre amount of fluid in interstitial tissue interstitial area number one hydrostatic pressure it determines how much fluid will go out on this side osmotic pressure or oncotic pressure which determines how it will be pulled back and then lymphatic drainage is that another way to look at it that this side of circulatory system we can say for fluid intravascular fluid it is pusher and this side of the circulation at other reabsorb ping mechanism or suckers here's The Pusher and here is the sucker right in every tissue you have a pusher and you have a sucker I hope you'll remember that there is a pushing mechanism and there is a suction mechanism not sucking mechanism right now let's suppose we disturb these mechanisms let's suppose we disturb these mechanisms and see how a remarker I will go in detail later but just I will mention the mechanisms let's suppose due to any reason hydrostatic pressure increases here due to any reason hydrostatic pressure increases here if there is increased hydrostatic pressure in the micro circulation what will happen just imagine just imagine due to in one person there is sphere arterial or dilation arteries dilate and too much fluid enter here this pressure will be 35 or it will go up it will go up or it is normal but this venous outflow is reduced due to any mechanism which we close this or due to any reason blood cannot go back to venous system easily right if for example there is a thrombus here if blood cannot go out easily and some of it is not going out what will happen to hydrostatic pressures here increase so if due to any reason if there is increased hydrostatic pressure in micro circulation let's see what happen let's suppose hydrostatic pressure has addition of 20 what millimeter of mercury here and of course 20 millimeter of mercury here now rather than 35 how much is it 50 okay don't do that much let's put it only 10. we increase the pressure of 10 here and we increase the pressure of 10 here now it is how much 45 and it is still 25 so pressure outward filtration out pressure will decrease or increase it will become double and it will become 20 millimeter of mercury when hydrostatic pressure increases here either due to arteriologation or due to venous increase the resistance to the venous outflow when hydrostatic pressure increases here right the result will be yes filtration out will be more and on this side look at it if this is also rather than 15 10 is added 25 now osmotic is 25 and it is also 25 do you think it can act as a sucker can it suck no so what will happen excessive amount of fluid is coming into interstitium on the but venous side is unable to reabsorb the fluid properly so too much fluid is coming out but not going back so there is excessive fluid arriving here is that right if excessive fluid is arriving here what will happen then yes before the edema develop let me tell you something very important lymphatics they increase their capacity to drain lymphatics can increase their capacity to drain the fluid so as pressure keep on increasing here filtration pressure net filtration out pressure increases net filtration out fluid increases reabsorption fluid decreases whatever extra fluid is coming it will not produce edema immediately first initial fluid that will be drained through this this will increase its power to drain but it is a limitation when fluid coming out becomes so much that lymphatics are overwhelmed when fluid coming out due to increase hydrostatic pressure becomes so much that lymphatic in spite of increasing their draining capacity they still cannot drain all additional fluid if they cannot drain all additional fluid then fluids start accumulating here and edema develops and what develops interstitial edema develop so first mechanism of interstitial edema I told you that when there is increased hydrostatic pressure increased hydrostatic pressure now the second mechanism of Edema I will go into detail later what are the diseases and condition in which hydrostatic pressure goes up but right now just Basics now we imagine another person let's suppose hydrostatic pressure is normal how much it should be here 35 yes normal and if it is normal how much it should be 15 millimeter of mercury let's suppose due to some reason those reasons we'll talk later due to some reason concentration of plasma proteins drop what is the normal uh uh yes what is the normal concentration of plasma proteins anyone from this row yes yes please what is the normal concentration of plasma proteins yes 8.5 watt tanks tank for what we can mention plasma protein levels in two ways total plasma proteins you can say it is 6 to 6.02 8.0 uh grams per decilator or we can say six to eight grams per 100 ml deciliters 100 mm or we can say 60 to 80 grams per liter your understanding because 10 deciliter is equal to one letter so in some books because I don't want you to be confused some books mentioned it is six to eight grams per deciliter or other books mentioned 60 to 80 grams per liter what but it's one and the same thing total plasma protein but out of total plasma protein as you know that there are three types there are many types of plasma proteins but three are very important number one albumin albumin number two very good globulin number three fibrinogen right and there are many others but I will not go into detail albumin normal level are how much yes albumin three point three to five point 5 or maximum 5 grams per DL or per 100 ml globulins are 1.5 to 2.5 grams per Dr fibrinogen is 0.252 point five grams per deal but right now what I want to tell you out of these proteins if you take the total proteins present here right they are usually six to eight grams per 100 ml of the plasma right is clear out of this most abundant protein is albumin it's the maximum less than albumin there is globulin and less than globulin there is fibrinogen now because the albumin is most abundant in the blood and number of molecules of albumin are smaller so albumin is the main protein which determines the osmotic pressure so who is the main sucker or a holder of the water I must use holder of the water I'll be a man even though uh holding power of water here is determined mainly by the women and to some extent by the other proteins now normal person normal healthy person must have six to eight grams proteins in the blood or 60 to 80 grams per liter proteins now if someone has due to any disease condition in his blood proteins level go down if someone has a problem we'll talk later either proteins cannot be synthesized or they are lost out of the body excessively we'll discuss it later but for a while we just imagine that I'm suffering with the disease in which plasma level of proteins go dangerously down right a women become very low if albumin concentration become very low what do you think this osmotic pressure will remain same or it will become less less so let's suppose due to low osmotic pressure become only 15. now hydrostatic pressure is normal but osmotic pressure of the protein they have gone down or on Plasma on cortic pressure has gone down due to hypoproteinemia low protein level or to be more specifically we can say hypo album anemia so those diseases in which in the blood albumin level goes down or the severe hypovolevinemia proteinemia then plasma proteins ability to hold the water in circulatory system is less osmotic pressure is less than what will happen now in this case even though hydrostatic pressure is 35 but it is not 25 it is 15. so filter out pressure is again double so in this patient previously we had a patient in which hydrostatic pressure here was high but also oncotic pressure was normal previously and still extra fluid was coming and less fluid was absorbing and extra which was draining full lymphatic if it couldn't be drained fully then it will accumulate and produce edema now we discuss another condition that that group of patients in which what is happening the plasma protein levels go down osmotic pressures of circulatory system become less than throughout the capability in the body more fluid will leak out and less fluid will reabsorb back so here on arterial side it acts as a poor holder it is not a very good holder and or venous side of the capillary it acts as a poor sucker your understanding so what happened under these circumstances excessive amount of fluid is leaking out in the interstitution but can it pull back no so what will happen edema what will happen edema right again in this condition also here edema is due to low oncotic pressures right due to loss of due to low protein levels in the blood so all those diseases which produce dangerously low proteins in the blood right they will result into edema right generalize the edema remember when edema is all over the body right we call it Anna sarka we call it Anna sarka Anna sarka it is generalized edema all over the body especially in subcutaneous tissue Anyway come back so now we have learned another mechanism what is that second mechanism of production of a demise reduced colloid osmotic pressure or reduce oncotic uncortic pressures right this is the second mechanism so here what we have seen we have only seen that normally it is the balance of hydrostatic and the osmotic pressures right they determine the fluid which is being filtered out and fluid which is being filtered back reabsorbed right if these forces are Disturbed these are called Starling forces if these forces are dearranged or we call them hydrodynamic forces if these hydrodynamic forces balance is Disturbed either hydrostatic pressure is high or osmotic pressure is less than normal that will result into edema formation any question after this then another mechanism of Edema that is very simple due to any reason if blood cannot sorry lymphatic system cannot drain well for example if a person has a female has breast cancer then breast cancer cells enter into lymph node and then from the arm lymph cannot drain well lymph cannot drain well or due to some radiotherapy lymphatics are damaged or lymph nodes are damaged or some infection like finally releases hilarious is a nematode right this parasite multiplies or stays in the lymphatics this parasite stays into lymphatics damages them and produces fibrosis of the lymphatic in the lymph node so due to any reason either due to file areases due to any infection lymphatic system is damaged or due to surgery you remove the lymphatics and lymph node in some area or due to irradiation lymphatic system is damaged right so due to any reason if an lymphatic system is damaged can fluid go out of the system can fluid go out of the system no now even if these hydrodynamic forces are absolutely normal normal amount of fluid is filtering out normal amount of fluid is being reabsorbed but if this back door is closed what will happen small amount of proteins which are leaking out over the months and years over that time they will accumulate here because they are not being drained so these proteins when they will accumulate here they will increase the colloidal osmotic pressure in interstitium and that will hold the water at and this area will swell up and that will lead to edema such kind of Edema is called lymphedema will have a full lecture on lymphedimulator here I want to mention one thing a edema let's suppose just imagine in my right arm edema developed due to some compression of the vein right and on this arm edema developed because my lymph nodes are blocked due to some pathological process is that right this side will develop edema as well as this again imagine if my this arm has compressed veins then blood is going through the arterial system but it cannot go back through veins so all capillaries in the arm will have high hydrostatic pressure and fluid will come out and fluid will accumulate in the arm and my arm will be edematous is that right this is one situation other situation we talk about that here the lymph nodes due to some disease process are blocked if this lymph nodes are blocked blood is going in the arm through the arterial system draining well through the venous system but because lymphatics are not draining small amount of proteins which are left there are not drained they are not getting back though the retained proteins will reabsorb they will hold the water and this will also get edema this will also get edema and these plasma these proteins which are leaking out these proteins which were accumulating here these proteins it may have fibrinogen which will clot the produce semi-clot situation right rather not really clot clot is really here I must say coagulation process right or we can say this fibrinogen will try to make fibrin and make a little fibrillar proteins which will hold the water plus other proteins which are holding here those proteins are retaining water held with them again I will repeat here only water was there but were there any proteins here no here there was originally proteins accumulated along with water is that right now what will be the real difference both armor swollen both arms are swollen but if you press the one point for example if this arm is swollen you press it with thumb firmly right and remove the thumb for few seconds there will be a little depression there again I will repeat on this side where fluid was accumulated but without proteins when you press with the finger when you press with the finger with pressure you push the fluid on the side you push the fluid on the side with pressure and you remove your thumb what will happen that that depression point or indentation will be left there and it will take few seconds fluid come back and again that depression is finished is that right we say with finger pressure we can produce a pit here p i t pit what we can produce pit here and this type of a demand called pitting edema what we call it pitting edema but if you come over here and you press it here now you know that even though there is excessive fluid here and this is edema but this fluid is held with proteins and maybe some fibrinogen maybe those proteins which were accumulated here for a long time they have activated the fibroblast and some collagen is deposit so that water is water which is here edema water that is trapped in the proteins and that is held with the proteins now if you produce pressure with pressure you can displace the water but you cannot displace the proteins and if you cannot displace the protein if you put a pressure you remove your finger will there be a pit there there will be no depression this type of Edema is called non-pitting edema so what is the difference in pitting edema and non-pitting edema again listen pitting edema is that when you find there is edema you put a pressure there you displace the water there is displaceable water there is that right and when water is displaced right you remove your finger water will take some time to come back and for short transient time for short time there will be indentation produced or depression produced and such kind of a demise fitting edema actually when when edema is due to increased hydrostatic pressure or due to reduced osmotic pressure it is pitting edema why because if this increases extra fluid which come here it is without much proteins is that right or if this decreases still extra fluid combat without much protein so when fluid is held in the tissues but not with excessive proteins and not fibrinogen right then this fluid can be displaced and there can be cutting edema so all those diseases in which hydrostatic pressure is increased or on cortic pressures decrease in all those group of diseases edema which is produced is called peten edema but if edema is due to impaired lymphatic drainage when edema is due to reduced lymphatic drainage then what is happening fluid is retained along with proteins and fibrinogen and all this will produce such kind of Edema plus proteins which are retained here for long term those proteins some of those proteins stimulate the growth of fibroblasts to produce collagen right so what what is there fibrinogen is their collagen is there other extra proteins are there all of them are holding the water and when they are holding the water then if you press this if you press this you could as you cannot displace the collagen as you cannot displace the fibrinogen as you cannot displace with little pressure other proteins so proteins stay there when proteins stay there and trapped water is also staying there so you cannot produce a pet so we call this non-preting edema Mi clear any question up to this here I want to yes you have a question so when there is increase uh amount of blood flow in this microvasculature there will be accumulation of blood and there will be the raised hydrostatic pressure but increased amount of blood in the microvasculature wouldn't that bring more amount of protein as in the oncotic pressure also listen he's saying uh when there is let's suppose this arterial or dilation he is saying when hydrostatic pressure increases here not only hydrostatic pressure come with an extra amount of blood there is also increased protein so edema should not be formed I agree with him when you do exercise when you do exercise you develop more blood going to muscles but muscles don't become animators they only become hyperemic they don't become animators edema will only develop when these balance between these two hydrodynamic forces is significantly Disturbed your understanding so in only increased arterial blood flow up to a limit up to a limit cannot produce edema is that right even when blood when hydrostatic pressure becomes so much that fluid which is going to become slightly increase still not edema as safety Factor by the lymphatics actually edema will form when so much fluid is so much balance is Disturbed that too much fluid is coming here and that extra fluid cannot be drained well by lymphatics only then edema will develop is that right Claire now we go back so we were talking about between the demand non-preting edema right so when hydrostatic forces are more and edema develop or osmotic pressure is less and edema develop this kind of Edema is really and classically if there is a long term obstruction of lymphatics then what kind of Edema will be there non-peting edema am I clear to everyone no issue at all why this is so important to know that a person has edema is it pitting or non-pitting answer is very simple the pitting edema if generalized edema is there if it is spitting edema it can be managed by diuretics if you give the person diuretic he will push more water out through the kidneys if you produce more water out of the kidneys what will happen if through the kidneys you are getting more water out eventually this water will suck back from here but if they're spitting at non-pitting edema if a patient if I have okay I'm the patient here I have petting edema and here I have non-preting edema if you give me diuretics pitting edema will be reduced but non-pitting edema well not reduced because you can pull the water back into circulation and get the water out through kidneys by the diuretic drugs is that right but in non-pitting edema you you don't have a drug to suck back the proteins and get them out into urine so what we what did we learn that pitting edemas better respond to diuretic and non-protein edema do not respond well to the diuretics here I want to highlight one more Factor that is about dependent edema another term is dependent edema what is dependent edema yes anyone from this line dependent edema what is dependent have you heard of dependent edema very good he is saying that as edema or swelling due to interstitial fluid increases in the dependent part of the body let's suppose if I have a Divine my arm right if arm is like this then my hand hand and lower part of the arm edema will gravitate towards that there will be more fluid here but if I make it up then edema will become less now classically we say if someone has generalized edema all over the body right all over the body the hydrostatic pressure is increased later on I will tell you it happens in a heart failure right now ah if I have generalized edema and if I stand for long time then there will be more edema in my legs ankles that is called dependent edema but if it with edema if I keep on sitting then more edema will be seen on my sacrum and that is also another example dependent edema dependent edema is actually that edema where edema fluid distribution is affected by the gravitational forces is the right lower part of the body gets more fluid why it's very simple let's suppose all over my body hydrostatic pressure is high in all my veins from lying down position if I suddenly stand up then it will be difficult for the blood to come back to the heart so already there is increased hydrostatic pressure little more increase will listen let's suppose my arm is all 30 meters and my leg is all 30 meters but both of them are edemators due to congestive cardiac failure so due to increased hydrostatic pressure now do you think my arm is like this and leg is straight down there will be more edema in the leg why because from here fluid can easily come to the heart right so hydrostatic pressures will be still not so much but from the leg hydrostatic pressure will be lower part of the body too much because gravity is trying to pull the fluid down right and body is trying to bring the fluid back to the heart right and that will gravitate the edema fluid to the leg now to make the concept more clear about the dependent edema to make the concept more clear I will ask a question yes this question is to our very brilliant student is us normally when you are lying down you suddenly stand up does you do it does water redistribute and too much fluid go into interstitial fluids of leg normally yes normally when you are lying down suddenly when you stand up too much fluid gravitate in the legs no if my arm is like this do you think does it happen if I do like this interstitial fluid will empty too much or if I go down then arm size become double why why it doesn't happen first you understand this thing why it does not happen it means in normal body fluid distribution is not dependent normal body fluid distribution is not gravitational dependent thanks God otherwise the standing position lower part of the body will be heavy I mean on lying down position it depends on your turn on this side the sound will be double and this will be half it doesn't happen thanks God why it doesn't happen how come that in a normal person with normal fluid in all body interstitution is not significantly affected by the gravity yes there is a reflex mechanism no I will not go for that he's I know he's going to talk about when we stand up there is Venus pulling in lower part of the body I know what you are going to talk I'm not talking about venous blood I'm talking about interstitial fluid I'm talking about interstitial fluid from lying down position when you stand up I agree there is a tendency for the blood to pull in the lower part of the body and when blood is pulling into lower part of venous vasculature Venus return to the heart decreases cardiac output decreases construct and maintain the blood going back I'm not talking about this my friend I'm talking a different question I'm not talking about Venus blood I'm talking about interstitial fluid this fluid normal person from lying down position this is my head from lying down to the okay let's take it like this red is the head this person is lying down it suddenly stand up does all interstitial fluid tend to go down in the body no why not okay before you guys tell me very new theories which are your personal theories let me tell you the truth it's the very basic concept our interstitial fluid this interstitial fluid or interstitial tissue has lot of fluid holders they have lot of fluid holders those are glycoproteins suppose this is a one glycoprotein molecule it has lot of this is one glycoprotein molecule this is another glycoprotein molecule glycoprotein molecules have what these are brush piles what are these brush piles normally what happens all your body interstitium is very very rich in glyco proteins you can say Combs like this this is one molecule of glycoproteins you know every tissue they are trillions and trillions of glycoprotein molecules you know what is the purpose of these molecules have lot of functions one of the function is the small amount of fluid that 11 liter of the fluid which is the interstitium that is held at its place by this brush piled off glycoproteins am I clear so what happened that when I raise my arm all interstitial fluid will not drain because the glycoprotein in interstitium which hold the water they absorb the water and they don't allow too much movement of the water your understanding this is the real reason that when you from lying down position from lying down position if you suddenly stand up the glycoprotein in interstitium they will hold the water and don't allow to gravitate it even though when air air travel your legs get swollen or if you're sitting for a long time it only happens when for long time hydrostatic pressure becomes so much it fills the glycoprotein mechanism is that clear what holds the holds the water in the interstitial flow tissue normally that interstitial fluid is held in the interstitial tissue at its places by the glycoproteins so small amount of water is coming passing through the glycoproteins very small amount of water given Services here removing the waste going back or draining from here most of the water here is held with the glycoproteins am I clear any question up to this now imagine another thing normally okay let me show you here is a glycoprotein molecule and these are its brush piles right now water very small very very small bubbles of water not bubbles really very very small amounts of water are held with this this water which is held with these points this is not free water it is no free water an interstitial space mostly water is held with glyco protein brush piles what we call it glyco proteins brush brush always disturbs me you know don't look at my head brush pile yes these glycoprotein brush piles very bad you are still looking at my head okay no problem anyone who laughed at me sooner or later they tend to lose the hair yes yes you will see inshallah in coming years okay now what I'm saying that brush pile of glycoproteins holding the water right so very little water is coming passing through it percolating through giving the services going back clear now you imagine either hydrostatic pressure is too much or oncortic pressure is too less too much fluid is coming here if too much fluid is coming here it is another Hydro what is this molecule now if excessive amount of fluid is coming here it will separate the glycoprotein molecules and produce produce very small free water channels listen carefully normal person in the intersection the amount of water small amount of water which is called interstitial fluid that is held along the brush pile of glycoprotein and the very small normally very small pockets of fluid and fluid is not freely moving normally but if there's too much fluid coming here if there's too much fluid coming here then what will happen that extra some of the extra fluid will make a free Channel it will separate the glycoprotein molecules in between a free channel will form it is just like that that you have sponge you know what is sponge yes sponge the sponge is holding the water but if there's too much water can sponge hold it free water will come so these are the you can say interstitial tissue sponges these are normally there they hold the water but when either there is suppose cardiac failure right ventricular failure especially all over the body hydrostatic pressure in every capillary goes up and too much fluid come here or there is severe decrease in plasma albumin in that case also too much water here in such kind of edemas and such type of edemas which has produced you through the arrangement of Starling forces or which is produced due to the arrangement of hydrodynamic forces or such a Dimas which are produced due to either increase the hydrostatic pressure or decrease osmotic pressure such edema fluid can become so excessive excessive that it produces free water channels when this free water channel is there then gravity can play a role if I hear edema due to increased hydrostatic pressure or edema due to decreased osmotic pressure is that right if my arm is like this then edema will be in this area more and upper area less because through the free what is this free water channels gravity will affect and fluid will move but if I take it down then what will happen edema will again gravitate so what happens that in a normal person fluid in the interstitial spaces is held adsorbed along with the brush piled of glycoproteins right but in a person where there is excessive fluid in interstitial tissue especially due to increased hydrostatic pressure or decreases osmotic pressure this fluid separates the glycoprotein molecules and produces free channels of fluid water free water channels in such patients if patient from lying down position suddenly stand up more fluid into lower part of the body this is called dependent edema or a such patient is sitting for a long time more fluid in the sacrament that is dependent edema so what is the mechanism of dependent edema mechanism of dependent edema average doctor will say simply when there's the edema and gravity redistribute the edema fluid and those part of the body which are exerted more by the gravitational forces they have more edema fluid that is the right answer but a very good answer should be because in lymphedema there may not be much dependent tendency but in case of congestive cardiac failure or in nephrotic syndrome which we'll discuss later where plasma proteins are very low edema become very dependent it means distribution of Edema fluid in such patient is very much determined by the gravitational effect why because free fluid is producing free fluid channels and water can rapidly rapidly gravitate on the dependent part of the body any question up to this but we will continue let's go back I was talking about why the edema should be produced One mechanism was increased hydrostatic pressure other mechanism I told you decrease on cortic pressure third mechanism I told you reduced foreign reduced lymphatic drainage reduced lymphatic drainage or lymphatic obstruction then there can be other mechanisms too yes anyone will tell me another mechanism increase fluid coming here or decrease fluid sucked back or lymphatic obstruction then there can be if there is increased increased permeability is it classically occurs in inflammation increase permeability of micro of micro circulation of micro circulation classically in inflammation you know when there is inflammation if there is injury right in any tissue inflammation develops during inflammation what happened chemical mediators are produced which will lead to which will increase the permeability of this and when permeability of micro circulation is increased even at normal pressure it will allow more fluid to go out but actually in inflammation hydrostatic pressures also increase right but I will not talk about that simply I am saying any pathological condition which will increase damage the what micro circulation wall or increase more enter endothelial gaps if endothelial cells which are holding with each other they shrink their ends then enter endothelial gaps will develop so whenever there is increased permeability of micro circulation there is a tendency to develop edema Mi clear we'll discuss that again later into detail and then another cause of Edema is salt and water retention salt and water retention in the body due to any condition like someone has a high level of circulating aldosterone which will reabsorb excessive salt from the kidneys if too much salt and water is retained in the body my question is if too much salt whenever salt is retained water tend to retain with it if salt and water is retained in the body it will produce interstitial edema or it will produce intracellular edema who will tell me my question is okay I'll give you a simple example if you overload me I'm a healthy person if you too much overload me with normal saline salt and water more than what I can get out of my urine if you are giving me that too many changes will occur in the body one of the change in the long run will occur that I will start developing certain type of Edema now if salt and water is retained in the body excessively this will lead to edema you will tell me it will lead to intra cellular edema or interstitial edema or what why not intracellular both you are wrong let me tell you actually in this case if retention there is excessive retention of salt and water this usually leads to interstitial edema not intracellular but someone has to explain why not intracellular yes remember remember actually sodium who loves to follow sodium water and negatively charged ions right now we'll talk about water wherever sodium goes water follows you understand few things in life like that wherever she goes many follow right so what happens sodium is always followed by water if there is more sodium let's suppose I inject lot of sodium here now sodium will come into circulatory system but sodium cannot retain in circulatory system because capillary membranes are fully permeable to sodium so if you give the sodium here inject the sodium here right whatever sodium is coming here some of it will be strain circulated system some of it will go out but sodium cannot enter into cells so what I'm saying when you add the sodium to the blood sodium will first enter into circulatory system and it can easily go from circulatory system to interstitial fluid but sodium cannot enter into cell because cell membranes are not freely permeable to sodium so barrier between the interstitial barrier between the cell membrane is a barrier between the interstitium and cells sodium cannot cross it easily but barrier between vascular compartment and interstitial compartment it allows sodium movement freely so what happens if someone is getting too much sodium it will hold the water and wherever sodium goes what will follow water so sodium will come from here to here so water will come here and if it is not drained well it will lead to edema so it will lead to extra cellular edema not interested your understanding so when you give lot of normal saline to a person normal saline is being added to circulatory system if you are giving through intravenous and then it is redistributing into interstitial fluid but it is not entering into self that is why when normalcy line or extra salt and water when it is entering into interstitial tissue it is producing edema and when it is retained in circulatory system it produces hypertension high blood pressure your understanding so what did we learn we learn this thing that excessive salt and water retention in the body all those diseases will retain too much salt and water in the body they have a tendency to produce edema also but in such conditions there may be hypertension too right so let's come back hydrostatic pressure can producer Dima by increasing the increasing by increasing the filtration pressures and decreasing the reabsorption pressure less osmotic pressure if this is also smaller again filtration is more and Resurrection is less or lymphatic drainage again this drainage is impaired and fluid accumulate here but here we have to remember edema due to increase hydrostatic pressure or due to decreased oncortic pressure the fluid which is retained here it is without proteins without additional proteins so this redeem is pitting edema and this edema is dependent edema 2. and in lymphatic obstruction especially at Advanced stage produces non-preting edema because here fluid is held along with the extra amount of proteins and fibrinogen and some growth of fibroblasts and collagen then we are talking about in inflammatory conditions if permeability of this membrane is this membrane becomes too much leaky although edema can occur and then salt and water retention I told you if body is holding salt and water all this salt and water cannot be held in circulated system as salt can freely move from circulatory system to interstitial system the salt will bring additional water and may produce edema now in next lectures I will go in detail of what are the causes and mechanism of hydrostatic edema and I will go in full detail of a demand patient with congestive cardiac failure after that we'll have another lecture we'll talk about what are the diseases which produce oncotic reduced from cortic pressure and edema and specially we will go into detail of a demon nephrotic syndrome and edema and cirrhosis then of course inflammation will discuss and eventually mechanisms which detain salt and water any question up to this what happens if we inject rather than normalcy line some hypertonic solution hypotonic solution okay if you inject some hypotonic solution it depends on that solute which is there can it go out of vascular system or not basic rule is this whenever you inject the fluid water follows the solute let me give you an example if you give dextrose water the glucose molecule which are coming into blood some of them will stain blood some will come into interstitial area but most of them will enter into cells in that case the water which came with the dextrose that will distribute little hair more hair and mostly here if you inject the salt and water then salt will distribute into two compartments is that right so when you give glucose that will distribute in how many compartment vascular interstitial and intracellular but because intracellular compartment is too big and this is smaller and this is smallest so water with glucose mostly will go intracellular and interstitial and very little in blood your understanding but if you inject normal saline salt then salt will distribute in the body in vascular compartment and interstitial and will not enter here so water which went with the salt will be retained in vascular system and interstitial system but let's suppose you inject plasma proteins with water if you inject plasma proteins they will remain mostly in the circulatory system so water which will go with the plasma proteins that will be also mostly in the circulatory system so basic concept I think one day I need to teach you surgery and the fluids on the surgical floors but anyway ah basic concept is that whenever we are injecting some body fluids in large amount right how the fluid will distribute it depends on many factors one of the factor is the movement of the solute if solute can go to all compart fluid compartment then water along with the solute will go to the r fluid compartment right classical example is dextrose water right then a fluid is going only to two compartments like normal saline if solute is going only to distribute into two compartment water will also go there let me tell you if you give one later off one liter of dextrose water now glucose will go into intracellular compartment interstitial compartment and Vascular compartment so that one liter fluid will be diluted into all these compartment so dextrose water cannot stay much in circulation so it's not very good to support the circulatory system say line is better when you give normal saline one liter of normal saline what will happen two thirds will come here one third will go here because normal saline whatever salt water it has they will distribute in these two is that right so what will happen in this case normal say line may be out of 1000 ml 600 mL will come here or 700 mL will come here and 300 ml will support circulatory system but if you give one liter of fluid with plasma proteins as plasma proteins will stay here they will not go out immediately so naturally then water will be staying here that is why in a person when person is going into shock after hemorrhage dextrose water is not good saline is better but plasma proteins are very good and if you can get the blood human blood Cross Match that is excellent because when you give the human blood mostly the cells and proteins and other components stay in the circulation so hold the water with it any more question be compromised okay here the question that if we give normal saline the it fluid will be distributed in vascular compartment and interstitial compartment then he came with some hypothetical situation that in some disease if sodium potassium pumps in the body are not working at all what will happen answer is someone whose sodium and potassium pumps are not working at all will not take birth we'll never have a patient like this until we give some toxic substance like ubane or some other substances which can really pump a paralyze all the sodium potassium pump that would be a very big poison life is not possible without sodium potassium pump sodium potassium pumps are present and functional in every cell including your cell and dog cells and rabbit cells and monkey cells right cluster space thank you today we are going to talk about that what is the role of increased hydrostatic pressure in the capillaries in Genesis of Edema right let's go back and look at our basic diagram that let's suppose here is your left heart and here is aorta right was arterial tree and here lies your yes right heart systems pose it is a functional diagram not anatomical and here is cable system or venous system and let's make a micros yes micro circulation of a part of a yes this is arterial side this is arterial side this is Peanut size and from an isolated tissue I have taken a piece of tissue let's suppose I make this tissue okay here this is that tissue right and this was the arterial input into that tissue and here is the venous drainage from that tissue right and of course here should be lymphatics right which also drain the fluid back eventually to the venous system from these tissues now we start getting the basic concept as we discussed in the previous video that let's suppose for understanding purpose we say that micro circulation as an arterial end and micro circulation has an Venus and right micro circulation has arterial and right this side and this part of the micro circulation is on the yes Venus and now what is the hydrostatic pressure in a typical tissue hydrostatic pressure in in micro circulation let's suppose here hydrostatic pressure is 35 millimeter of Mercury and it is pushing the fluid outward and here on cortic pressure which is due to plasma proteins especially albumin oncortic pressure as 25 millimeter of mercury which is trying to hold the fluid in so balance of these Starling forces on the arterial end is that one arterial end of the capillaries hydrostatic is pressure is more hydrostatic pressure is also called hydraulic pressure hydrostatic pressure is more an oncotic pressure is less oncotic pressure is the colloidal osmotic pressure exerted by the plasma proteins especially albumin in the micro circulation so oncotic pressure is less so net filtration pressure is outward net filtration pressure is outward right this is our tissue these are yourself very happy because they're also listening to the lecture now so we can say on the arterial end of micro circulation fluid is extra visiting with approximately under the pressure of 10 millimeter of mercury and so and constantly adding to the interstitial fluid and on the venous side Hydro oncotic pressure remain almost same almost same but as fluid moves through the micro circulation towards the venous side right hydrostatic pressure drop and it is about let's suppose 15 millimeter mercury so hydrostatic pressure is now less and on this side balance has become in the favor of inward so net pressure across the semi-permeable capillary membrane is inward we can say this is filter out pressure this is reabsorption pressure this is extravagation pressure this is reabsorption pressure of about 10 millimeter of mercury plus we know that some proteins which which may leak they will be drained through lymphatic back to the circulatory system is that clear now I am going to put a question to you guys that this hydrostatic pressure depends it is how it is generated in the capillaries my question is now how normal hydrostatic pressure in a typical tissue is created what is the Genesis of normal hydrostatic pressure right ah yes doctor blood pressure very right cardiac output and total peripheral resistance determine what is the pressure in arterial tree what is the pressure in arterial tree this pressure is transmitted in the micro circulation so actually this is the cardiac output along with total peripheral resistance which determines the blood pressure cardiac output into total peripheral resistance is equal to blood pressure so blood pressure arterial blood pressure here is what arterial blood pressure this arterial blood pressure the pressure in the arterial tree transmits the pressure into microcirculation and produces what is this is that right yes after knowing this thing now we come to another situation that let's suppose a person's blood pressure goes up a person whose blood pressure was 1 20 by 80 millimeter of mercury this is a blood pressure of a person 120 by 80 millimeter of mercury and due to some reason just for a short duration of time for a short duration of time maybe that person got excited maybe that person got angry maybe that person was under some kind of stress pressure goes up and let's pause this blood pressure become 170 by 1 10. so this person blood pressure goes up if this blood pressure goes up what will happen to the hydrostatic pressure in the kipple is right yes what will happen to the hydrostatic pressure in the Excel is just doctor yes you are saying that if blood pressure goes up as blood pressure is the major determinant of hydrostatic pressure in kipple Rays so when blood pressure goes up I'm not saying he is saying that hydrostatic pressure should also go up and if hydrostatic pressure goes up the hydrostatic pressure goes up what will happen let's suppose hydrostatic pressure goes up 20 degree so 35 plus 20 35 plus 20 units right and also here 20 unit we are hypothetically talking that is someone's blood pressure goes up my friend is saying that if blood pressure goes up then hydrostatic pressure incapillas should also go up and if hydrostatic pressure in capillaries goes up then what will happen that force is moving the fluid outward will be stronger stronger so you feel filter out a little bit more and filter back will be less and edema will be produced but actually edema does not produce but in fact in clinical practice if someone has blood pressure going up without cardiac failure I'm talking about just an episode of high blood pressure a simple episode of high blood pressure does not lead to edema is that right if cardiac function is the question is that why it does not leads to edema answer is just please question is to you my question is very clear listen my question is that in day to day life even in a normal healthy person blood pressure fluctuates if whenever blood pressure goes up if with rising blood pressure immediately if there is rise in the micro circulation pressure that will favor the edema but in real life thanks God it does not happen why it does not happen no you are trying to confuse me anyone who is yes you understand what I'm saying my question is very very simple when blood pressure goes up right why edema does not occur because in all people who have clinical practice they know that blood pressure goes up if cardiac function is okay edema does not result answer is this now listen very carefully answer is this wow just before the what is this capillaries there are special type of group of smooth muscles here this is called precapillary what are these pre-capillaries sphincters before every micro circulation there's a regulator what is this there's a regulator it's very important to understand all micro circulatory beds have a regulator at the input level on the arterial side these are called pre-capillaries factors so filters just before the capillary Network and these are wonderful filters you know what did they do when blood pressure goes up they construct they become tight and don't allow the excessive blood to come into capillaries and produce increased hydrostatic pressure and don't allow the edema listen carefully in all our body if right there are three capillary sphincters just before micro circulation these are The Regulators these are The Regulators whenever blood pressure goes up they become tight so that too much blood does not enter here too much pressure does not come to microcirculation and fluid exchanges between the vascular compartment and interstitial copper compartment is kept is kept stable is that right this is the right answer that whenever there is transient fluctuations in the blood pressure Whenever there is transient fluctuation of the blood pressure with every episode of blood pressure going up does not produce increase hydrostatic pressure so this is not going to be there blood pressure is there but it will become tight and it will not allow extra hydrostatic pressure here is that right and this is what prevents the edema in day to day life that minute to minute sometimes our blood pressure is going up and down but we are not repeatedly developing edema is that clear now another thing when blood pressure goes down splinters relax when blood pressure goes down this fingers relax so the increase more pressure to come here to stabilize the fluid exchanges so what is there that on the arterial side of the micro circulation there are very powerful regulators these Regulators are pre capillary blood pressure goes up they become tight and don't pre and don't allow in micro circulation hydrostatic pressure to jump too much and when blood pressure goes down they become relaxed and don't allow the hydrostatic pressure in micro circulation to fall too much is that clear to everyone yeah uh doctors have is asking who tells this that when blood pressure is high to constrict right the reason these all the smooth muscles are connected with each other right number one number two neuro humoral mechanisms number three local waste metabolic products so the multiple reasons how they are regulated the simplest explanation is myogenic response myogenic responses as soon as pressure goes up that will stretch the Splinter now listen carefully he is asking who tells filter that blood pressure is high and they should construct now I'm going to answer this simple there are multiple answers that because of multiple mechanism but one of the important mechanism is myogenic responses what is myogenic response as soon as high pressure come this will be stretched when they stretch let's suppose this is a smooth muscle there is out of this circle this is the sphincter and there is a smooth muscle in this what is this there are smooth muscles in there agreed yeah when more pressure will come smooth muscle will stretch then smooth muscle will become from this size they will stretch they have calcium channels they have calcium channels calcium channels will also stretch and there will be there will be more calcium influx and this this calcium which goes in will lead to the smooth muscle construction is that clear to everyone so what is what happens this is a great just a minute this I know I'm giving too much detail but this is important for doctors and Medicals to understand that blood pressure day-to-day fluctuations especially when it goes up does not lead to edema because microcirculation in the beginning has pre-cupless filters and whenever pressure is more these smooth muscles in the preciplinary sphinctures are stretched their calcium channels open more and more calcium influx lead to construction and that construction regulates the input of blood volume and pressure in micro circulation yes you have a question we'll talk about that later he's asking that how these sphincters are affected in the cardiac failure later on we are going to have a full lecture today that what is the Genesis of edemine cardiac failure now we come to another thing that if there is now you understand if there is extra pressure coming from this side if there is extra pressure coming from this side it will not produce edema is that right it's clear to everyone now let's suppose if right heart fails right heart fails or there is some compression here then pressure will come backward central venous pressure will go up again I will tell you what is the function of right heart to pump the blood into lungs micro circulation of lungs that is pulmonary circulation right heart pumps into lungs and from the lungs blood get oxygenated and goes to the left heart is the right pulmonary circulation let's suppose that due to some reason right heart is not pumping well blood is coming to the right heart from the body blood is going to the right heart but this pump is failing it is unable to pump due to any reason it cannot pump forward so what will happen to the pressure in this area it will go down or up it will go up of course there will be bad pressure it will go up if this pressure goes up in central Venus pressure goes up what will happen to hydrostatic pressure in micro circulation just here my question is due to any reason first I talked about if arterial blood pressure goes up it does not lead to edema and we talked about precapillary sphincter which are the regulator here now we are talking about venuside that due to any reason if pressure in the venous side goes up for example right heart is not pumping well due to any reason if right heart is not pumping well blood is coming to right heart but it cannot move forward properly the pressure in the central venous system will increase will that increase the hydrostatic pressure in micro circulation or not okay what about you okay he thought he thinks uh one of my very good student decent loving person but always saying something unusual he's saying that if central venous pressure goes up central venous pressure goes up then of course back pressure will come chances are hydrostatic pressure will go up then my friend told that there should be foreign there should be post capillary surfingers to this is his idea not mine he he thinks that there should be post capillaries finters there and they will constrict and don't allow this pressure to go back you are wrong there are very powerful pre-capillary sphincters but post triple sphincters are not very efficient and really not there I should say or if they are there physiologically they are very weak so we can say that micro circulation on arterial end micro circulation on arterial end is having strong regulators but Micro on the Venus is poorly regulated the point to remember is micro circulation on the venous and is poorly regulated I will give you an example every tube every tube in the body does not have sphincters on both sides look at your mouth you don't have sphincter here you can open whenever you want but other end has sphincter right so what I am saying that every tube in the body does not have Splinter on both sides and micro circulation has sphincters tight on one side one side arterial side but not on the venous side that is why when central venous pressure goes up bad pressure will come and hydrostatic pressure in micro circulations go up and that produces edema that's produces edema so today's up to now what did we learn listen carefully what did we learn that hydrostatic pressure If hydrostatic pressure in the micro circulation goes up then more fluid will come out and less fluid will go back to the circulation so edema will be produced but we need to remember that if pressure goes up in arterial tree does not produces edema because of pre-cupalis spinters due to sphincters pressure going up on our arterial side does not take the micro circulatory pressure significantly up so thanks God there's no edema but when pressure goes up in the venous system then back pressure will come back pressure will come as venous end of micro circulations do not have very good Regulators they don't have specially designed pre post capillary spinters not as powerful as pre-crepancy filter so whenever central venous pressure goes up right that will transmit the pressure backward and definitely increase hydrostatic pressure and when hydrostatic pressure will go up that will favor the movement of fluid from vascular compartment to interstitial compartment and that can initiate the process of Edema formation am I clear any question up to this done ok now I have another question in the very beginning of the uh one more question if someone is standing like this let's suppose I'm standing like this and suddenly I undergo massive massive myocardial infarction Global myocardial infarction and my ventricles fail to pump all right do you think I will immediately develop edema or not question goes to that lady yes yes I will not why okay this is right she's right in this thing that if I'm standing here I go into cardiogenic shock of course after that I will not be standing but anyway if I'm going to cardiogenic shock if I go into cardiogenic shock will I develop edema or not I will not why I will not develop edema because the strong breakability sphincters are not involved you have your own Theory anyone else you have super yes wow that is the answer if there's cardiogenic shock whole circulatory system if pumps are not pumping throughout the circulation pressures will fall from where edema will come if throughout the pressure fall on the arterial side and in capillaries edema cannot come right how edema develops in heart failure we'll discuss after some time in detail now we come back once you have had these basic concepts now we start talking about that what could be the causes of increased hydrostatic pressure what could be the causes of increased hydrostatic pressure I'm going to make this diagram again this is arterial side yes and here it is venous side and there is Venus outflow and Central Venus system going to and here is your which heart right heart now edema I'm going to contradict what I said in previously but I will explain why edema will occur whenever hydrostatic pressure goes up significantly right now I'll go back due to any reason if hydrostatic pressure become rather than 35 due to any reason it has 20 units added and here rather than 15 it has also 20 units added so hydrostatic pressure in the micro circulation has gone gone up and let's suppose that oncotic pressure is the same as normal right now in this person okay first I add 10 first I add 10 units here and 10 units here so hydrostatic pressure rather than 35 has become 45 now pressure the fluid will extravagate more or less more and fluid will reabsorb more or less listen 25 is on cortic pressure and hydrostatic pressure on this side is also 25 can it pull the fluid back no so actually reabsorption is reduced so we have done that is mild increase mild increase in hydrostatic pressure in this capillary circulation now extra position of fluid is more and reabsorption of fluid is less will edema develop or not yes or not okay people who believe edema will develop raise your hands I want to see their beautiful faces yes okay and people who believe edema will not dwell up raise their hands it really depends on it may develop a may not develop it depends on one more player that is the lymphatics lymphatic now listen carefully when more fluid is moving out and less fluid is being reabsorbed then fluid in this area become less or more more right if this fluid become more and all additional fluid there is normal fluid which is coming in and reabsorbing but if all additional fluid can be successfully drained by lymphatic edema will not develop this is a very important concept what I'm saying if there is increased hydrostatic pressure due to that reason extravization of fluid is more reabsorption of fluid by micro circulation is less than additional fluid which is here will it produce edema or not it really depends on the performance of lymphatic drainage it depends on performance of local lymphatics if additional fluid is well drained well lymphatics and you know lymphatic lymphatis can increase their flu fluid drainage capacity 5 to 10 times if a lymphatic system is working well in a tissue it can drain extra fluid if all the extra fluid which is coming due to this excessive Hydro hydraulic hydrostatic pressure if this fluid is drained by the lymphatic successfully then edema well not develop it means that in micro circulation now listen with your both ears everyone should should have to ear functional listen now carefully edema will develop only when hydrostatic pressure becomes so high that extravaged fluid is so much extra that lymphatic drainage is overwhelmed only then edema will develop I will rephrase it in another word in simple words increase hydrostatic pressure brings more fluid into interstitial area but hydrostatic pressure should be so much high that so much fluid should come that all extra fluid cannot be drained by lymphatics only then edema will develop is that clear so simple little rise in hydrostatic pressure does not lead to edema is it clear now we come to the causes of Edema causes of edema due to raised hydrostatic pressure number one increase hydrostatic pressure due to arteriolo dilatation RT Riolo dilation I told you that there were three capillary yes Spencer here I told you there are pre-capillary sphincter if we fail these printers now listen carefully if we fail these filters then extra blood will come here and extra pressure will come here then edema can be produced classical example of this is ah if one part of the body is overheated if heat is applied for a little bit long time part of the body then that heat will dilate pre-cupal respect us and extra fluid will come and extra pressure will come and local edema will form because edema will only form into that micro circulation and around that micro circulation where heat was applied where heat was applied so this is an example that if there is too much arteriola dilation that may lead to edema formation classical example is application of heat on some part of the body right but don't burn I'm saying simply Heat oh yes erythema yes he's right that when there is too much heat that area will become red hot swollen it will become red due to increased inflow of the blood erythema it will become hot the cereal become hot because it is receiving heat heat externally and internally also increase blood flow bring more temperature there heat thirdly it will become swollen because pre capillary sphincters fails and excessive fluid and pressure come here and so much fluid may come that local lymphatids cannot drain well the accumulated fluid will lead to swelling of the tissue is that right yes then I will not go into detail but I will just mention that arterial or dilation once I mentioned heat and other I am going to mention uh yes neuro humoral dysfunction neurohumeral dysfunction May logically digest it and produce localized edema in some part of the body classical example is in angioedema where if there's pathological dilation of what is this particularly sphincters but angiodynamic multiple mechanism because there is increased permeability too both of them lead to the edema but you know these printers are very tightly regulated by a sympathetic nervous system these precapillas filters are also regulated by sympathetic input norepinephrine and epinephrine dependent splinters if those humoral mechanisms they are also controlled by potential two and there are other factors too so if those neuro humoral mechanism which control these sphincters if in some part of the body those neuro humoral mechanisms which control the regulator those controllers fail then Regulators fail that may produce localized edema right but this these are less common situations that there are many drugs which can fail the sphincter like hydralazine right there are many drugs which can fill the specters that is why as a side effect of hydralazine you may have edema ankle or Demar there are many drugs which which are very strong you can say relaxer of the prepared sphincters right they can also produce localized edema some part of the body as a side effect now we come to Venus and most of the time most of the time edema is produced due to raised pressure raise pressure on the venous side now if due to any reason this venous outflow is reduced blocked pressure will go up excessive fluid will come out and if it cannot be drained well by the lymphatic edema will reside now some local causes local causes of what could be the local causes first of all external pressure on a vein if vein is pressed from outside as sometimes children put a rubber band on the hand you put a rubber band this will compress the veins but not compress the arteries which are high pressure system if veins are compressed arterial blood will move into hand but cannot drain back properly and capabilities of the hand will have high pressure and when capillaries of the hand will have high pressure more fluid will extra visit and that will lead to a demoral swelling of the hand so this is one example yes yes another on the clinical side doctor is mentioning that if someone applies a knee pad very tightly right if it is applied tight then arterial blood is going to the lower part of the lower limb but venous blood cannot drain well then pressure in the micro circulation of lower lower leg will increase and that will lead to edema so external pressure on the venous system can produce localized edema isn't that clear then another another example is ah yes if there is thrombosis if there is thrombosis right if a vein is blocked due to thrombosis or thromboembolism if a vein is blocked can fluid drain properly out no no if fluid cannot drain out again pressure will go up and chances of producing edema so edema can be produced by increasing the venous pressure venous pressure can be increased locally by external pressure or can be increased locally in some micro circulation due to formation of thrombus the classical example here is deep Venous Thrombosis in lower limb deep ities deep to Venus thrombosis that actually blood clots intravascularly within the veins of the leg right in that case arterial side is taking the blood to the leg but venous side is not draining well and that may lead to swelling of the limb is that right so by the way what is the difference in thrombus there are three four terms I want you to declare number one what is platelet adhere what is platelet aggregation what is platelet plug and what is thrombus yes these are the terms what is platelet adhian what is play I'm asking four questions to you rather I should ask five questions from bus trigger me to that side what is platelet at hand what is platelet aggregation what is platelet primary platelet plug and what is thrombus and what is coagulation someone should be able to differentiate these five terms raise your hands okay one person has one hand anyone else has hands yes I should remind you everyone has two hands raise your hands who really knows very clearly the difference in plateleted here platelet aggregation platelet plug primary plug coagulation and thrombus yes ma'am have you heard of these terms but do you know how they are different at least tell me they are different in spellings yes yes but any other concept better than this adhesion very good let me explain what she is saying let's suppose this is your endothelial cells right these are endothelial cells which are injured these are endothelial cells which are injured when platelet first time come and stick here these platelets are sticking to they are starting to not to the platelet this first layer of platelet is sticking to non-platelet surface when platelets stick to non-platelet surface we say there is platelet adhere right what is happening what is platelet adherence that if this is Bored whiteboard if four boys come and stand here this is wired here right this is wired here in the same way when platelet boils are like platelets when platelets stick to the non-platelet surface they are called platelet adhere okay you come here three boys I need here rapidly rapidly let's suppose this white board is white board is what endothelial injured endothelium now this platelet come and stick here yes another platelet come come come two platelets now now these three platelets which are sticking with the endothelium or sub endothelial exposed collagen injured these platelets are sticking to this surface we say this is a process of platelet and here now another boy come yes you come no no you stick to this boy oh okay you face there so no risk yes yes one more point you did just please come I'm not going to call girls relax okay now the second layer is platelet aggregation because platelets are now sticking to the platelets right so when first layer when platelets stick to the non-platelet surface plateleted here but when when platelet in him stick with each other when platelets stick with each other this is platelet aggregation and then become more platelets yes just just just come yes more platelets if too many platelets come and stick with each other and why more platelets are coming because the first platelet when they arrive and stick those platelets are activated and they release the substances which call more platelets so more and more platelets are coming and these platelets are getting attached over here when too many platelets are collected right we say this is primary platelet plug right but when this primary platelet plug convert into thrombus yes anyone just stops up when we say that this primary platelet plug become a thrombus no idea okay listen um collagen doesn't come here just a minute now one platelet plugs are attached here you activate your hands like this yes activate your hands like this these are activated platelets activated platelets what comes the coagulation factors come touch them and coagulation factors become activated coagulation factors are basically proteins and the final result of that coagulation factor is that activated coagulation Factor eventually converts soluble protein hibernogen and two vibrant and fibrin strength will come over here what will come fibrin stains all these boys are tied together with ropes chains so what happened in the blood there were proteins going coagulation proteins I will not go into detail when they they are caught by the activated platelets and those proteins start converting fibrinogen into fibrin fibrins are the strands their strengths and those fibrant deposition will help these platelets to stick with each other in a way over all these wires we throw the network of net of fibrance this process conversion of soluble fibrinogen the process of converting soluble fibrinogen into insoluble fibrin that process is called coagulation that process is called coagulation so what happened first plateleted here then platelet aggregation and activation then coagulation and when platelet plug plus coagulation that is called thrombosis so what is thrombus thrombus is when within the circulatory system somewhere platelets undergo process of adhian aggregation activation and make a platelet plug and once this plug is formed on the top of that plug if fibrin deposits we say platelet plug has which process coagulation process and this platelet plug plus coagulated fibrin these together make a thrombus please thank you go back to your seats so anyway I will not go into detail further you know the difference plateleted here platelets sticking to non platelet surface platelet aggregation platelet speaking to each other platelet plug when lot of platelets are sticking together activated and then undergoes certain morphological changes and making a unified mass that is primary platelet plug at the top of that blood plug if coagulation process deposits the fiber in that is coagulation then plug lateral plug plus coagulation together make the thrombus and if that thrombus which is formed here it detaches detaches from here it's Breakaway and start moving here then this thrombus is called ambulance when thrombus break away and moves like a MLS then it is called embolus and because this end this thrombus keep on moving and goes in some other part of the vascular system and plugs that for example if this thrombus detached from here it kept on moving moving and blocked this area we say this part of the vascular system has undergone the process of thrombos embolism so you understand thrombuses until it is attached and if it is freely moving it is ambulous and when it reaches to new place and block we say a thrombus which become ambuli has blocked when blockage occur then we say there is thrombo embolism let's go back so we were talking about the raised pressure in micro circulation may lead to increase hydrostatic pressure excessive oozing of the fluid right and this excessive fluid if it cannot be successfully drained completely extra fluid staying here will produce edema and local local causes of Fatima were on the venous side external pressure or thrombus formation right then local pressure can be can you tell me some other cause of the local pressure especially lower limb inactivity lower limb inactivity and prolonged dependency for example when you have 12 hours flight if you are sitting keep sitting in a long haul flight you keep sitting sitting sitting then what happened that veins the Venus return from the lower lens to the upper part of the body become less because when you are sitting you are not moving your muscles usually lower part of the body around the veins there are muscles like Soleus and other and muscles in the limbs contract and help the veins to push the blood back to the central veins but when lower limbs are inactive they are inactive and they are dependent for long time then what happens two things happen number one hydrostatic pressure independent veins of the lower limb increases right there are no post capability sphincters which are very effective right so that will lead to edema and prolonged sitting may also predispose the person for thrombus formation is that right so these were local causes of Edema these were the causes of localized edema due to increased hydrostatic pressure or arterial side local heat or neurohumeral dysfunction on venous side local causes are what yes external pressure or thrombus or prolonged inactivity of lower limb and dependency of lower limb as it happens and very long flights there actually you are advised to that you stand up in the plane and little will walk after some time right after this we come to causes of increase hydrostatic pressure in the capillaries generally not local which will produce generalized edema for example in cardiac failure in cardiac failure if someone has heart failure let's suppose someone has right ventricular failure right blood is not going forward pressure is accumulating here from here blood is coming into circulation but from here it is not going back if right ventricular failure occur what will happen central venous pressure will increase and all the capillary beds pressure will be increased increased your understanding not localized all the capillary bad number one bad number two bed number three so it means multiple capability beds in the body when central venous pressure goes up I'm talking about Central previously I was talking about local venous pressure going up now I'm talking about central venous pressure goes up due to any reason if it goes up especially in cardiac failure or constructive pericarditis or in splanchnic circulation portal hypertension and cirrhosis when central venous pressure goes up that produces generalized edema and we will discuss that after the break after the break I will specially discuss the Genesis of Edema in cardiac failure right let's have a break

Channel: Dr. Najeeb Lectures

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Id: fwlso8c0FSg

Length: 170min 27sec (10227 seconds)

Published: Mon Oct 03 2022