 pulmonary edema is accumulation of fluid in the interstitial tissue and then in the alveoli in the lungs. Now this accumulation of fluid in the interstitial tissue and the alveoli depends on the balance of the starling's forces and these starling's forces operate everywhere in the body. So these starling's forces as you might be aware are the hydrostatic pressure and the oncotic pressure within the vessels and the hydrostatic pressure and oncotic pressure in the interstitial tissue and also the amount of the fluid movement depends on the capillary wall permeability. If it becomes more permeability then with the same balance of forces more fluid movement will occur. So with this let us see that what are the starling's forces which operate in the lungs. So here this diagram taken from Gaiden shows the starling's forces operating in the lungs and let us see that what are the forces which are promoting the fluid movement and what are the forces which are opposing the fluid movement. Now in pulmonary capillaries the hydrostatic pressure is quite less. Pulmonary capillary hydrostatic pressure is plus 7 millimeter mercury and as we know that the hydrostatic pressure is the push force which will cause the movement of fluid from the capillary towards the interstitial side. In the lung parankaima interstitial hydrostatic pressure you see it is negative. So normally everywhere else the interstitial hydrostatic pressure acts as a push force but here it is negative that means it will cause the fluid pull from the vessels towards the interstitial side and why it is negative that is because of the surface tension which is operating at the level of the alveoli. See surface tension is causing the collapse of the alveoli and all these tissues are interconnected the interstitial tissue and the alveolar wall are interconnected. So when the alveoli are collapsing they are pulling this interstitial tissue with them and this pull creates a negative hydrostatic pressure force within the interstitial tissue. So this interstitial hydrostatic pressure again is one of the forces which will cause the fluid movement towards the interstitial side. So we have to add all the forces which are causing the movement of fluid from the capillary towards the interstitial. So pulmonary capillary hydrostatic pressure interstitial tissue hydrostatic pressure then there is oncotic pressure of the interstitial tissue and that is also quite high that is 14 millimeter mercury. So these forces are trying to move the fluid from the capillary towards the interstitial side and let us add them up and see how much it comes it comes to 29 millimeter mercury. So this is the push force right coming to the pull force which will cause the fluid movement from the interstitial side towards the capillary that is the capillary oncotic pressure capillary oncotic pressure and here as it is shown it is 28 millimeter mercury. Now if we see the net balance of forces push force is 29 millimeter mercury and pull force is 28 millimeter mercury so we have to subtract these to get the net force and it comes to plus 1 millimeter mercury. So plus 1 millimeter mercury as shown here also it is the force which will drive the fluid from the capillary towards the interstitial lymphatics. However normally this interstitial tissue and the alveoli are kept dry because of the presence of the lymphatics and lymphatics by their expansion they will cause the movement of the fluid from the interstitial tissue into the lymphatics and these lymphatics will carry the excess fluid which has leaked out from the vessels. So that is the normal physiology. Now when will pulmonary edema developed? So if you get this concept that it is this is balance of forces which determines the fluid movement you can very well predict that when will pulmonary edema develop. So let us try to understand it in terms of where the disbalance will occur. Suppose if the pulmonary capillary hydrostatic pressure increases then this push force is going to increase so the force driving the fluid from the capillary to the interstitial tissue is going to increase so that is 1 here it is affected. Suppose this increases interstitial hydrostatic pressure it becomes more negative and when will it become more negative. See we are telling that interstitial hydrostatic pressure is negative because of the surface tension and you know that this surface tension is decreased because of the presence of surfactant. So if there is surfactant deficiency surface tension will be more so that pull force is going to be more and in this case interstitial hydrostatic pressure is going to increase. So that is why in surfactant deficiency that is acute respiratory distress syndrome that is a hyaline membrane disease we get pulmonary edema as well. Then obviously if this osmotic pressure becomes less then also there will be chances of developing the pulmonary edema and fourth as I told you before that it is the pulmonary permeability which also determines that how much fluid is going to move so with the presence of the same forces if the pulmonary permeability increases pulmonary capillary permeability increases then more fluid will move out of the pulmonary capillaries. So fundamentally these are the causes of pulmonary edema. Now based on this what are the cause pulmonary edema causes are broadly classified into two types one whether it is a cardiogenic origin cardiogenic edema and whether it is non-cardiogenic in origin so that is known as non-cardiogenic edema. Broadly we see in cardiogenic edema it is increased in the pulmonary capillary hydrostatic pressure so that is also known as high pressure edema high pressure pulmonary edema and non-cardiogenic pulmonary edema pressures are normal normal pressure pulmonary edema develops. So let us see that why this is happening you know that pulmonary vessels arise from the light ventricles so that is the pulmonary artery then goes into the lungs and divides into the pulmonary capillaries and from there again the blood is collected and the pulmonary veins drain into the left atrium and from there into the left ventricle. Now suppose if there is malfunction of the left ventricle or there is any problem in the valves which are between the left atrium and the left ventricle like mitral valves stenosis occurs, mitral valve regurgitation or aortic valve problems occurs suppose aortic stenosis is there then left ventricle has to generate more force ultimately left ventricular failure marker okay in that case basically if we classify in left heart failure conditions the blood will start accumulating in the pulmonary veins so back pressure will develop and this ultimately will lead to increase in the pulmonary capillary pressure and you have seen that how pulmonary capillary pressure if it increases there will be increase in the push force leading to the movement of fluid from the vessels into the interstitial site. Now before we proceed I want to here present a concept known as safety factor see we have seen that plus one millimeter mercury is the push force which is normally there and the the lymphatics are there which will take away the excess fluid now when this pulmonary capillary pressure starts rising actually it can rise up to 25 millimeter mercury before there we get the pulmonary edema so from plus seven millimeter mercury it can rise to plus 25 millimeter mercury and why is that because the lungs have capacity to carry that excess fluid that is the lymphatics are there so that excess fluid will be carried by lymphatics so even with the development of the left heart failure pulmonary edema will not develop till the pulmonary capillary pressure has risen to 25 millimeter mercury so that is known as safety factor and that is in acute cases if we go to chronic cases in which slowly the left atrial pressure and then the pulmonary capillary pressure is rising in that case the pulmonary capillary pressure can increase even up to 40 millimeter mercury without the development of pulmonary edema why again because of more expansion of the lymphatics it can carry approximately 10 times more fluid than in the normal physiological conditions so that is the safety factor now coming to the causes of non-cardiogenic pulmonary edema non-cardiogenic edema develops basically either directly there is injury to the lungs or there is injury to the lungs indirectly via blood stream so there might be certain systemic diseases which can lead to development of pulmonary edema and the injurative lungs say suppose as I spoke before about ARDS ARDS there will be surfactant deficiency so that is going to create the pull force so that will also lead to pulmonary edema then there can be infections like in case of pneumonia these infections will damage the alveolar walls so the fluid from the interstitium is going to enter into the alveoli so that can also lead to non-cardiogenic pulmonary edema and finally if there is increase in the pulmonary vessel permeability so any damage to the pulmonary vessel permeability that is going to increase the movement of the fluid and hence with the same forces that is going to lead to development of this pulmonary edema so I hope you got the concept of cardiogenic pulmonary edema and non-cardiogenic pulmonary edema coming to the signs and symptoms and what is their physiological basis so first thing you remember that if there is development of pulmonary edema that is accumulation of fluid here and in the alveoli ultimately because whenever you see accumulation of fluid will occur what will happen that these alveolar walls are very weak they will be damaged so ultimately the interstitial fluid is going to enter into the alveoli so when this occurs you see what will happen here oxygen is there the diffusion distance will increase so it will be very difficult for the oxygen to diffuse into the alveoli for this concept on diffusion of gases I have made another video you can have a look on that also so anyways this diffusion of oxygen will decrease and that will lead ultimately to hypoxia that is decrease in partial pressure of oxygen in the vessel so basically hypoxia hypoxia is going to occur and when this occurs ultimately it is going to stimulate the peripheral chemo receptors and when that happens you know the stimulation of the peripheral chemo receptors will lead to increase in respiratory rate and depth and that is known as tachypnea so one sign and symptom is tachypnea then peripheral chemo receptors not only affect the respiratory system they also cause increase in the sympathetic activity so stimulation of peripheral chemo receptors increases the sympathetic activity and this in turn is leading to tachycardia that is the increase in the heart rate so that is another symptom of pulmonary edema next there is development of orthopnea especially in case of cardiogenic pulmonary edema what is that orthopnea is breathlessness occurs in supine position why well in supine position because of now lack of the effect of the gravity there is increase in the venous return and this increased venous return what happens ultimately from right ventricle it will enter into the pulmonary vasculature but you see there is left heart failure which is not going to pump that extra blood forward isn't it so there will be accumulation of more blood into the pulmonary vasculature leading to increase in hydrostatic pressure right so further increase in pulmonary hydrostatic pressure is there and as in cardiogenic edema this is the main cause increase in pulmonary capillary hydrostatic pressure so this is going to further increase the fluid movement so that what is happening that more fluid accumulation is occurring when the person is in supine position so in supine position this hypoxia is increasing right so let me just put it in a flow chart supine position okay what happens increase in venous return increase pulmonary blood flow right so that is going to increase the pulmonary capillary hydrostatic pressure increased fluid movement and that is going to increase the hypoxia which further is going to stimulate the peripheral chemo receptors more and hence causing more tachypnea and once the tachypnea is much more the person will feel breathless so that is orthopnea so here I just have to use one more term that is the disnea more tachypnea ultimately results in disnea that is the subjective unpleasant sensation of breathlessness so that was all about the concept of pulmonary edema thanks for watching the video if you liked it do press the like button share the video with others and don't forget to subscribe to the channel Physiology Open thank you