Pulmonary Embolism | Etiology, Pathophysiology, Clinical Features, Diagnosis, Treatment | Retired

what's up ninja nerds in this video we're going to be talking about pulmonary embolism but before we get started if you guys want to follow along with some really comprehensive notes some great illustrations drawings before the board's actually been filled out drawings after so they can just help you to truly understand and kind of really follow along with this topic please go down below in the description box we have links to our website you guys can get all of that stuff go check that out also if you guys like this video you benefit from it it helps you please hit that like button comment down in the comment section and please subscribe alright let's get into it all right ninjas let's talk about pulmonary embolism so causes of pulmonary embolism before we start talking about that what is a pulmonary embolus it's a clot a blood clot that develops within the pulmonary arterial circulation now the question is how did that clot actually develop that's a great question engineers let's talk about those the most common cause if you guys remember don't remember all these other ones i'm going to talk about please remember this one it's the most important one the most common cause for someone developing a pulmonary embolus is they develop a clot what's called a thrombus that develops within a deep vein within usually a lower extremity most commonly so what do we call that thrombus within a deep vein of the lower extremity we call it a dvt so usually a dvt deep vein thrombosis is going to be one of the most common causes of a pulmonary embolus now how does that actually cause an imbalance there's a clot in the leg how does it get to the lung generally what happens is this clot is usually what's called a thrombus so a thrombus is a blood clot that's kind of situated it stays still in the vessel wall but whenever that actual thrombus breaks off breaks off and gives a piece of the imblus that now this embolus can freely circulate up through the ivc into the right side of the heart go flooding through the pulmonary arterial circulation it can get stuck in a pulmonary artery you got yourself a pulmonary embolus okay so a big thing to remember by far the most common cause of someone developing a pulmonary embolus is they have a dvt that broke off and then went through the pulmonary circulation all right what's another potential cause or etiology that i want you guys to think about for pulmonary embolism another one to potentially think about here is if someone is actually scuba diving right when they're scuba diving they're usually under higher pressure as they go deeper and deeper and deeper but whenever they rise back up quicker sometimes what can happen is some of that nitrogen oxygen because of the pressure changes and the solubility changes within those gases can form these air bubbles okay whenever you arise too quickly they call it the bends and it can form emboli that develop within the pulmonary circulation leading to a pulmonary embolus and so another potential thing that you can think about here is what's called a air embolus and the best classic case to think about this is when someone's usually they're scuba diving and then they arise too quickly called the bends other potential causes is whenever somebody breaks a really big bone usually a long bone you know within the long bones they have a medullary cavity that's usually filled with fat and so what happens is if you get really good long bone fractures so long bone fractures within the center the medullary cavity you have all of this fat tissue and so what happens is you can actually break off fat globules and those fat globules have the ability to get stuck in some of the pulmonary circulation and cause a fat embolus so that is another thing to potentially think about so we got dvt being by far the most common air embolus from scuba diving and quickly arising the bends very big long bone fractures where you open up that medullary cavity and some of the fat globules get out into the circulation aggregate and cause a fat embolus what else not as common but something to think about whenever somebody has they're pregnant and what happens is whenever you're pregnant you have this amniotic cavity right and sometimes in patients maybe for some reason maybe a premature birth they have an opening okay of their amniotic fluid that leaks into the actual circulation and some of the proteins with inside of the amniotic fluid are very immunogenic and can lead to clots that actually little emboli that can form and so sometimes you can get what's called a amniotic embolus so that is another thing to potentially think about especially in patients who are pregnant usually there's some type of like premature complication associated with it okay so we've got dbt most common air embolus long bone fractures that cause fat emboli and amniotic embolism that are usually during pregnancy the other one is if someone is an iv drug abuser okay an iv drug abuser and whenever they have this iv drug abuse there's a easy way for them to carry bacteria staphylococcus aureus different types of staphylococcus species straight from the skin into the actual blood and you know what those little nasty staphylococcus species love to go especially staphylococcus aureus it loves to go and kind of lay up its house on the tricuspid valve okay especially in ib drug abuse or staphylococcus aureus it takes up residence on the actual tricuspid valve and leads to these really nasty vegetations these little vegetations can then break off and guess where they can go right into the right ventricle from the right ventricle they can go into the pulmonary circulation and then they can get stuck or dislodged somewhere downstream within the pulmonary artery and so these are called bacterial or septic emboli so another one to potentially think about here is what's called bacterial or what's called septic emboli okay or embolus okay so these are the big things that i want you guys to think about okay as potential causes of someone developing a pulmonary embolus dvt most common air embolus long bone fractures causing a fat imbolus pregnancy rupturing of the amniotic membrane leading to an amniotic embolus or some type of iv drug abuser which has vegetations that form in the tricuspid valve leading to infective endocarditis vegetations that break off causing bacterial or septic emboli now once all of these emboli floated through the pulmonary circulation the problematic issue that arises here is that they get stuck in one of these pulmonary arteries or arterials depending upon how big the clot is and that obstructs the blood flow distal to that occlusion and in the lungs what's what's this responsible for putting oxygen into the blood and getting rid of co2 and so as a result what we're going to see a little bit later here is that you significantly affect the gas exchange process okay and we'll talk about the negative ramifications of that okay so we have an idea of the basic causes but what i really want us to focus on for the roast of this kind of like causes portion is dvt since it is the most common okay so first thing that we need to know is dvt is a deep vein thrombosis what are the deep veins that i should be aware of that i should know because those are the ones that whenever i'm doing an ultrasound or i'm checking i'm trying to look at the reports i know which vessels are most commonly affected let's talk about that so here we have this like nice little anatomical diagram here just to get the point across here you have here your ivc right so this is your inferior vena cava and then from the inferior vena cava this branches off right into your iliacs okay so let's say that this is the common iliac and let's say off the common iliac is your internal iliac so this is your external iliac right so this right here is your external iliac then coming down off the external iliac you'll have the femoral generally we call it like a common femoral vein and then off of that you have what's called a deep femoral vein that comes off of that common femoral vein and then generally you'll have the continuation of the femoral vein and that'll eventually go near the knee and produce what's called the popliteal vein and then the popliteal vein will usually bifurcate and give way to what's called the anterior tibial vein it'll give way to what's called the posterior tibial vein air give way to what's called the peroneal or fibular vein okay now these are deep veins and so there's particular things particular risk factors particular causes that can increase the risk of clots that form within these vessels so if you form a clot within any of these particular vessels they have the possibility the potential to break off embolize up through the one of these vessels upstream go from the ivc right into the right atrium right ventricle pulmonary trunk and then produce a pulmonary embolus so the question is what in the heck can lead to clots that form within either the external iliac that form within the femoral that form within the deep femoral that form within the popliteal that form within the anterior tibial posterior tibial or peroneal let's talk about that so the first one that i want you guys to think about here there's this guy okay he came up with a triad you guys might see where i'm going here with this he came up with this triad and it's called vert goes or virtuo's triad okay and what he said you see these there's three particular things that increase the risk of forming blood clots three particular things the first one here is there is a increased stasis of blood flow okay there's an increased stasis blood isn't really moving very quickly it's staying within a particular area and i've found that whenever there's stasis of blood flow there's an increased risk of blood clot the second thing he said is you know what i also noticed is that if somebody has what's called a hypercoagulable condition meaning they have an increase in maybe like different types of uh pro coagulant enzymes so enzymes that want to induce clots or they have a decrease in anticoagulant enzymes enzymes that are supposed to break down clots there's less of them and i know that whenever that happens there's an increased risk of forming blood clots and the last thing he said is i noticed that whenever you damage or injure the endothelium there's also an increased risk of forming blood clots and the the mechanism of this is actually relatively simple you guys know our hemostasis video that we have within our hematology playlist if you guys don't you don't understand all of this stuff we're not going to go into great detail go check out that video it'll give you way more understanding about blood clots and how we form them but generally what happens is blood should kind of have a nice laminar flow through a blood vessel okay if blood is kind of really stagnant in a particular area you know what happens platelets love to stick to the actual endothelial vessels and so what platelets will do is they'll come and stick to the endothelial vessels and start causing aggregation of other platelets okay so whenever there's a stasis of blood flow there's always going to be an increased opportunity for platelets to be able to stick to the actual blood vessels if there's endothelial injury platelets will come and stick to the blood vessels and if you have tons of pro-coagulant enzymes or a decrease in anticoagulant enzymes that's also going to increase the risk of blood clots okay so we have the three aspects of vircose triad we have an increased stages of blood flow hypercoagulability or endothelial injury now let's talk about each one of these particularly the first one that i want to focus on as a potential cause is stasis of blood flow okay so with stasis of blood flow what are potential things that you have to think about what would cause someone to have a localized kind of slow flow through a particular venous structure here the first one is like anything where the person is not utilizing you know there's what's called the muscular milking activity i know it sounds it sounds it doesn't sound real but there's what's called a muscular pump or a muscular milking activity on the sides of your uh your deep veins you have muscles in your calves right and they're supposed to be every time you're kind of contracting or walking around you're utilizing those muscles maybe doing some calf raises you're getting your gains or maybe you're walking around and utilizing those muscles those muscles are squeezing and helping to push blood up through the venous structures and so there really isn't much stasis of blood flow but what if someone isn't ambulating they aren't moving a lot they're staying still for some reason and they're not able to engage that muscular milking activity what kind of conditions would do that maybe if someone is post-operative so they're post-operative and they're on bed rest okay so they're immobilized because they are post-op and so they need to be on bed rest or maybe they're just immobilized for some other reason okay maybe they just had like a fracture of their leg and they're stuck because they aren't able to move now because they have to rest their leg or they can't actually walk around on a cast or whatever it may be okay so it could be post-op you know another particular potential thing is when somebody is had a stroke so generally after a stroke what happens if you have a good enough stroke what happens maybe to like one of the lower extremities you can't utilize that muscle if you can't utilize the muscles in this area you aren't able to ambulate properly and so sometimes paralysis after a stroke can also be a potential cause so paralysis post cva cerebrovascular accident right the next thing to think about here is airplanes so long travel so if someone's on an airplane for a long period of time they're not moving okay and so generally whenever there's like long airplane rides usually greater than or equal to like eight hours there's not much movement within those lower extremities and so there's an increased risk of stasis of blood flow and therefore blood clots same thing not just airplanes but also uh car rides okay where there's just these long car rides with not much uh time between to be able to ambulate get some muscular milking activity going on okay you guys will never forget that the muscular milking activity so we got stasis of blood flow they're immobilized for some reason post-operative maybe they're paralysis after a stroke they're kind of sitting in their car for long drives or they're an airplane for very long periods of time what's another potential cause believe it or not you know you have these valves within our veins okay they're basically kind of like your endothelial lining is extensions of the endothelial lining they form these things called venous valves you know in patients who develop what's called varicose veins what's called varicose veins varicose veins is basically when they have these incompetent or leaky valves normally what valves do is if blood would come from this segment it would come up and it's very slow what would happen is we would want to prevent blood flow because it's not under a lot of pressure from back flowing okay into the you know the segments just proximal and so what happens is let's say that it goes up and then the pressure is enough it starts going back down we don't want it to go all the way back down so what happens is we have these like little valves these little venous valves that basically kind of trap and say okay blood's going to stay here for now but what happens if i have an incompetent valve and so i push blood up here and maybe the valve on this side helps to block it but this valve's all jacked up and because it's all jacked up it allows the blood to kind of flow again proximal to that area there and so blood can kind of stagnate and if it stagnates there's an increased risk of clots so varicose veins is another potential thing okay the other thing that i want you guys to think about is what if there's some type of compression of a vessel and wherever there's compression the stasis actually develops proximal to wherever that compression is so blood's supposed to come here and then exit up here but if there's something that's compressing where very little blood is able to pass through and stasis occurs at this area proximal to wherever that compression is that could be a potential trigger what are things that could compress on these actual deep veins you know someone's pregnant and their uterus is just smashing up against their iliac vein that could be a potential reason so it could be something like pregnancy and pregnancy could have the uterus compressing up against the iliac vein you know there's another one it's a very weird one but it's an important one to remember for your exams there's a condition called may thurner syndrome may thurner syndrome and in may thurner syndrome what happens is you have what's called the right iliac artery and then you have what's called the lumbar vertebrae what happens is between these two the lumbar verter and the right iliac artery they squeeze and compress onto the iliac vein and decrease the actual blood flow up through the iliac vein and that can again cause the increased risk of stasis of blood flow and one more what if you don't have a baby in there you just got a little fat baby like you know i got a little bit of a fat baby but obesity obesity is another potential thing here that can cause compression of of these actual deep veins because of the large amount of adipose or you know kind of like centrally located kind of uh abdominal tissue that may be compressing on some of those actual venous structures that could be another potential reason for stasis so stasis big things to think about post-op when a person's immobilized they're on bed rest they got paralysis after a stroke or they're you know sitting in a particular location without having the ability to ambulate for long periods of times like air pains and car rides varicose veins or any compression of vessels like pregnancy may thurner syndrome and obesity all right let's talk about the second component of virgo's triad all right so the second thing that virko says okay let's think about things that can cause an increase in hypercoagulable states where there's a problem with the coagulation system there isn't an issue with like the stasis of blood flow blood is kind of flowing normally but there's a problem where my coagulation system is either hyperactive i don't have enough enzymes to counteract that uh the normal kind of like a pro coagulant function so what am i talking about okay generally let's say here we want to form a clot right whenever you want to form a blood clot you need very particular types of coagulant enzymes pro coagulant enzymes so within our coagulation cascade that would include things like thrombin factor 12 factor 10 factor 5 factor 7. there's many different types of factors that generally want to cause a pro-coagulant type of activity right and you know there's particular cases in which there is uh very very specific cases uh you know there's a condition that's one of the most common hypercological conditions called factor 5 lyden and what happens is there is an increase in pro-coagulant enzymes okay i mentioned a bunch but you know not all of those do you actually see so increase of pro-coagulant enzymes which ones would i want you guys to remember the particular one is what's called factor five liden and this condition you have an increase in factor five factor five is a pro coagulant enzyme if you have increased factor five you're going to want to be able to stimulate thrombus formation if you have a lot of it another one is what's called a pro-thrombin gene mutation you know what this pro-thrombin enzyme does generally prothrombin is a precursor for thrombin so you have this mutation where you have an increase in the prothrombin actual like activator system and increasing prothrombine to thrombin so you have an increase in thrombin thrombin is a very strong pro-coagulant enzyme so you have an increase in thrombin indirectly you're going to increase the formation of these blood clots okay so increase in factor 5 and factor 5 leiden or an increase in thrombin via the the pro-thrombin gene mutation what is other things so these are the two big ones for increase in pro coagulant but what if there's actually you know there's particular enzymes that want to break down the clots they're supposed to be able to break down the clots protein c protein s antithrombin three beautiful enzymes that help us with this process but what if we inhibit the anticoagulant enzymes we decrease their ability to function or we don't have enough of them that would be a potential issue right so there's a decrease in anti coagu enzymes what are potential conditions that you want to think about here these are usually something like what's called protein c and s deficiency and another one is called anti thrombin iii deficiency these are two potential conditions that i want you guys to think about so two conditions for pro coagulant activity factor v leiden prothrombin gene mutation two particular conditions that can cause and decrease in anticoagulant enzymes is protein cs deficiency and antithrombin iii deficiency big thing to remember are these are genetic causes so these are something wrong with the actual individual's genetics where they have an issue with these particular types of mutations so please don't forget that these are genetic causes of hypercoagulability these are required causes of hypercoagulability that we also have to talk about let's talk about that so it's a potential acquired cause you know whenever somebody's pregnant okay they prego or something that kind of like can mimic pregnancy is potential oral contraceptives that contain estrogen so ocps but again i'm going to put here e for estrogen the ocps have to contain estrogen so in pregnancy or when someone's taking oral contraceptives containing estrogen there's an increase in estrogen activity estrogen actually does like to have a increase in pro-coagulant activity and a decrease in anti-coagulant activity what is that similar of hypercoagulable conditions so please don't forget that whenever somebody is having high estrogen from pregnancy or ocps that increases the pro coagulant activity and that increases the risk of forming clots okay other conditions is usually malignancies cancers certain cancers have the ability to produce hypercoagulant activity the mechanisms aren't completely known but it may be certain factors that are released from the actual cancers the particular cancers that i really want you guys to remember are lung cancers and pancreatic cancers these are definitely associated with a high incidence of hypercoagulable activity and what they think is that it may particularly induce an increase in pro-coagulant activity maybe through certain factors that are released from these actual cancers okay so we have an idea now about certain acquired cases of hypercoagulability what are some other ones some other ones that i really want you guys to remember that will definitely probably show up on your exam this is a big one so don't forget this one in someone who has what's called nephrotic syndrome you know nephrotic syndrome is where they kind of have issues with their glomerulus they have a problem being able to kind of keep that glomerulus as you know selectively permeable as possible so there's injury to the glomerulus and whenever this injury to the glomerulus the glomerulus is responsible for filtering out specific types of proteins and things like that generally you don't want proteins to get filtered across the glomerulus whenever there's injury to the actual glomerulus or particularly the basement membrane in conditions like nephrotic syndrome they lose the ability to be able to block proteins from being excreted into the urine and one of those proteins that get excreted into the urine unfortunately nephrotic syndrome is called anti thrombin iii what do we just say antithrombin 3 is it's an anticoagulant enzyme if i'm excreting antithrombin 3 what am i doing i'm decreasing the functional antithrombin 3 anticoagulant enzyme in my blood and that is going to increase risk of clots okay what else you know there's another condition really unfortunate condition it's an autoimmune disease it's you potentially can see this associated with somebody who has sle or lupus systemic lupus erythromytosis it's called anti-phospholipid syndrome anti-phospholipid syndrome is basically a an acquired but also may have some type of genetic susceptibility genes that are involved where antibodies attack potentially phospholipids but you know what else they can attack they can attack particular types of anticoagulant enzymes i have their names right there for you protein c and protein s these are anticoagulant enzymes if you act if you actually have antibodies directed against them you decrease the activity of the anticoagulant enzymes if you decrease the activity of the anticoagulant enzymes you increase the risk for clots the last one that i want you guys to think about is really important as well you know someone let's say they have a potential issue where they have a pe this is a great example they have a pe and the treatment for pe sometimes is heparin you give them heparin and all of a sudden they develop more clots what the heck happened this is a condition called heparin induced thrombocytopenia also known as hit and what happens isn't in hit is their immune system develops antibodies that are kind of like directed against the heparin but instead of interacting with the heparin they interact with particular types of molecules present on the platelets called platelet factor four and when it sticks with these it causes the platelets to want to stick with one another and when they stick with one another it causes an increased risk of platelet kind of aggregation and whenever these platelets stick to one another and they aggregate it increases the risk of clots forming and then therefore you develop some clots you potentially develop a pe as a result of a dvt okay so that covers the hyperquad global conditions let's finish up with the last part of vertical stride which is endothelial injury all right last but not least endothelial injury right it's this is actually probably the easiest one all right it's the easiest one because you got to cut you got an injury you got to damage the endothelium surgery it's obvious right someone goes and does like some type of surgical procedure there's definitely going to be some type of vascular endothelial injury so certain types of like c-sections or certain types of orthopedic surgeries those are potential risks there right the other one is smoking believe it or not smoking which contains the nicotine some of the other chemicals within side of the actual cigarettes the tobacco have the ability to cause direct cytotoxic injury to the endothelial cells so that's another particular thing the other one is obesity believe it or not obesity is a son of a gun it can actually cause hypercoagulable conditions as well and not only can it cause compression causing stasis not only can it cause hypercoagulability via cytokine release but also endothelial injury this can happen because it releases something called interleukin-6 and what's called crp c-reactive peptide and these can actually cause endothelial injury but also they can cause an increase in kind of a pro-coagulant enzyme activity and so they can also cause clots too so they can be related in hyper-coagulable conditions but obesity is a big trigger for endothelial injury as well and last but not least what if i use particular catheters so i'm using a vascular catheter and i'm inserting it into a vessel these vascular catheters are definitely high risk for developing particular clots especially around that vicinity of where the actual catheter is okay so that's a big thing to remember for endothelial injury is surgery smoking obesity which can be involved in all three of these particular aspects of virtuostriad and vascular catheters now we've covered the causes let's start talking about how these causes leads to the pathophysiological mechanisms which explains the clinical features of a patient who develops a pe all right so let's talk about the pathophys right so we have an understanding now about how dvts which are the most common cause of someone developing a pe can develop via the three mechanisms of virco's triad now when someone comes in you have to be able to tie the causes the risk factors to their clinical features via the pathophys right so if someone comes in and you have a high suspicion of a pe based upon the other things that we'll talk about one of the things to think about is what was the common cause dvts how do dvts generally present it's actually relatively simple right so let's say here you have a clot that develops with inside of a deep vein right maybe it's the popliteal vein maybe it's an anterior tibial posterior tibia whatever but whenever there's this clot there usually blood is going to want to flow up through this vessel obviously right but there's an occlusion there and so what happens is there's some extravasation of plasma into the surrounding area right and that can cause some swelling okay also you can also lead to some redness okay because of the actual potential not just extravasation of plasma but blood kind of staying localized within that area so there can be not only just extravasation causing edema but there can also be a little bit of redness there as well and because of all that swelling and starting to cause kind of a little bit of a compartment type of syndrome kind of thing it can cause pain as well and so before you know it this could potentially progress to this where you have a patient who presents with swelling of a lower extremity they present with pain they present with redness but here's a big one to think about they love to ask this on the exam you shouldn't do it because sometimes it can actually be problematic but if you suspect that someone has an asymmetric swelling pain redness of an actual lower extremity you can take and dorsiflex their foot and it should produce a very intense pain and this is called a positive homan sign so this is another thing to think about for a patient that you suspect a dvt okay so they have swelling pain redness of an actual uh asymmetrically of lower extremity and positive homan's sign think about a potential dvt now the problem is is that if that actual dvt breaks off embolizes gets stuck in the pulmonary circulation what is the complications of this well come on in baby let's see let's say that that sucker breaks off here's the little clot coming up from one of these actual deep veins it comes up through the inferior vena cava into the right atrium from the right atrium it goes into the right ventricle from the right ventricle goes up through the pulmonary tract and then from the pulmonary trunk it then can bifurcate and go to the right pulmonary artery or left pulmonary artery right and then from there what can happen it may get stuck in a vessel with inside of the pulmonary circulation sometimes even worse sometimes it can actually form a clot right within a big pulmonary artery one of the right ones maybe one of the left ones the worst case scenario is you form a clot right in the center where it actually bifurcates causing a saddle embolus we'll talk about those in a little bit but either way you're developing a clot somewhere within the pulmonary circulation how does that affect the ventilation perfusion processes let's say that here we have an alveoli that we're going to take and zoom in on and look at if we look at that where there's a pulmonary capillary and alveolar interface this is what we get and generally what happens is whenever you take a breath in you're bringing oxygen into the alveoli right and then that gives you a particular like partial pressure of oxygen within the alveoli you guys remember generally like the partial pressure of oxygen is generally somewhere around like 100 104 millimeters of mercury right and then generally the oxygen that's in within the pulmonary capillary blood usually the pulmonary arterial oxygen is usually somewhere around like 40 millimeters of mercury right and so you have like 140 like generally like gradient here where oxygen easily should move from the alveoli into the blood right but you have a clot that's occurring right here blood is supposed to flow through here pick up oxygen drop off co2 and then exit out as oxygenated blood but i have a clot now that's blocking the profusion to this area so if i'm blocking the profusion to this alveoli my ventilation is normal because i can breathe and bring as much oxygen into this alveoli so this could be normal but the perfusion is significantly affected and i'm not actually bringing enough blood to this area to be able to put oxygen into the blood so effectively what happens to the oxygen that leaves this alveolar capillary interface is it going to be normal oxygen or is it going to be low oxygen it's going to be low because i didn't have enough blood that was actually traveling through here to pick up oxygen so not many red blood cells are going to get through here so the amount of red blood cells that are picking up the oxygen are going to be very very low and so generally this is called what whenever you have low oxygen in the actual arterial blood this is called high poxemia and so this hypoxemia that we have is actually a result of what it's a result of not ventilation right so the ventilation it's important to realize this the ventilation is normal so that's not the problem the ventilation is definitely normal the problem is the profusion yeah so the profusion this aspect is abnormal and this leads us to this thing called the vq ratio right you guys probably remember that right so the vq ratio you usually want this to be like less than 0.8 the ventilation is up it's normal but the perfusion is down so what happens to the overall ventilation perfusion ratio does it go up or does it go down well the numerator is big and the denominator is small our ticket goes off yeah so it does so this causes a increase in the ventilation perfusion ratio we translate that into what's called an increase in this they're going to ask you this probably on your exam and increase alveolar arterial gradient okay meaning that there's more oxygen within the alveoli and very little oxygen within the arterial blood okay so we have an understanding of this okay results hypoxemia why is the hypoxemia problematic well hypoxemia is going to cause low oxygen saturation so whenever you actually look at this person's o2 sat it'll be low potentially the problem with hypoxemia is that hypoxemia can potentially activate very specialized receptors that are located within our aortic bodies and carotid bodies you know there's like these little chemoreceptors located here and then they're also located over here they're called carotid bodies they're little chemoreceptors and they pick up the concentration of oxygen whenever the oxygen concentration is low hypoxemia it stimulates these chemoreceptors what are these called they're called chemoreceptors if you really want to be special which types of chemoreceptors are they the peripheral are central they're peripheral chemoreceptors right and these are called they're within the carotid bodies and the aortic bodies what happens is when they're stimulated they're connected to particular cranial nerves do you guys know what cranial nerves these are connected to these are connected to cranial nerve nine which is going to be your glossopharyngeal nerve and they're also connected with cranial nerve 10 which is your vagus nerve and what happens is these guys will pick up any kind of sensation of altered oxygen and send that to your brain stem it'll activate particular breathing centers within the brain and say hey oxygen is low buddy we i think we need to try to breathe faster or something so that we can bring more oxygen into other alveolar that are working well and are perfusing well and so i can try to get my oxygen up and so what it does it tells the actual medulla say hey start increasing the breathing rate and so what happens is as a result you're going to increase the stimulation of your intercostal nerves your diaphragm and what happens as a result you increase your respiratory rate and depth as you increase your respiratory rate and depth you're trying to breathe faster the whole goal is that you'll bring more oxygen into the alveoli and then the whole thought is is that if you bring more oxygen into the alveoli into the ones that are perfusing properly you'll get oxygen into the blood and fix the actual hypoxemia but you know what actually ends up happening as an unfortunate result because there may be a very significant perfusion deficit and you can ventilate all you want it may not fix the hypoxemia instead what it may do is if you breathe faster and deeper not only are you bringing in more oxygen but guess what else you're getting rid of co2 and so you're starting to exhale out lots and lots of co2 so what happens to the concentration of co2 within the blood so what does this call whenever you have an increase in respiratory rate and depth it's tachypnea right so this is going to produce what's called tachypnea which is an increase in the respiratory rate you're going to try to bring more oxygen to offset the hypoxemia but unfortunately as a result you actually blow off more co2 so what happens is if you get rid of more co2 what happens at the co2 levels in the blood the co2 levels in the blood go down what does that call when the co2 levels on the blood go down hypocapnia what happens to the ph you guys remember ph and co2 what's the kind of relationship between these if co2 goes down it should be inverse for ph right ph should go up so as a result you can develop what's called a respiratory alkalosis that's a result of their tachypnea them breathing faster and deeper okay and this is again usually because of what's called hypo capnia you're breathing off all that co2 dropping the amount of co2 within the blood now that's one of the mechanisms here right that we're going to try so first and foremost a person will have hypoxemia may present with a low pulse ox on their actual pulse oximetry they may also have signs and symptoms of a dvt then they may breathe faster they may have tachypnea you know what else is interesting is not only does this sympathetic mechanism increase to cause increase in respiratory and depth but you may also from this hypoxemia you may also get an increase in heart rate and the whole reason why is whenever you're hypoxemic the thought is is that okay there's less oxygen maybe that's either not being ventilated i'm going to fix that by breathing faster but i'm going to increase my heart rate which should increase the cardiac output i should push more blood to the alveoli and hopefully that will increase my oxygen as well so that's kind of the whole process by which that that would occur so they may have tachycardia tachypnea respiratory alkalosis in their abg hypoxemia presenting as a low pulse ox what's another clinical manifestation of hypoxemia please don't forget this let's write this down i actually should have told you guys this a second ago but if a person maybe has a normal pulse ox or they have hypoxemia in general this can present as dyspnea so shortness of breath okay so remember for a person p presents with symptoms of dyspnea hypoxemia tachycardia tachypnea respiratory alkalosis you start having some ideas of a pulmonary embolus okay what else is potential clinical features of this all right let's say here you have a going back to this pulmonary vessel we're just zooming in on it okay we're zooming in on this portion right here okay so here's our clot within that pulmonary vessel okay and within this clot you have a bunch of platelets you know platelets whenever they're sticking and they're forming a clot they're sometimes a little bit mean but they're smart sometimes it's just it's a mean reaction they start saying hey guys let's start see creating a bunch of different enzymes so there's the clot right containing lots of platelets they release three particular chemicals adp thromboxane a2 and what's called 5-hydroxytryptamine also known as serotonin these three chemicals do a couple things the first thing that they do is they act on the bronchial smooth muscle stimulate the bronchial smooth muscle to undergo contraction whenever the bronchial smooth muscle undergoes contraction what is this called it contracts and narrows the airway it's called bronchoconstriction so this can induce what's called broncho constriction which can worsen their already present dyspnea okay the other thing is that these chemicals also induce vasoconstriction of the pulmonary vasculature so what else is going to happen it's going to cause pulmonary vaso constriction and the problem with this is when you cause this pulmonary vasoconstriction why are we trying to pulmonary vasoconstrict these vessels it's very interesting it's an interesting mechanism the whole thought behind this is this here you have this alveoli that's ventilating properly it's getting oxygen but the issue is that the blood vessel that you're actually trying to send to this alveoli has a clot in it and so this alveoli is unfortunately a waste of time so what i actually want to do is is clamp down on this vessel and send blood to a nearby alveoli that actually would be able to participate in the gas exchange process and so what happens is it undergoes a pulmonary vasoconstriction mechanism here and the attempts to shunt blood through the other pulmonary vessels where gas exchange will actually occur okay so it's trying to enable the alveoli to particularly allow for gas exchange to occur with an alveoli where the gas exchange is actually going to be efficient and not having this issue because of a pulmonary embolus or clot the problem with this is is that if you pulmonary vasoconstrict vessels that can put stress on the heart and we'll talk about how that does that in a second but the other thing that this pulmonary vasoconstriction can do is it can decrease oxygen supply to the lungs now the lungs has a dual blood supply is the bronchial blood supply and then it also has the pulmonary artery supply sometimes if a patient develops a severe kind of like pulmonary vasoconstriction and you decrease oxygen supply to the lungs it could lead to an infarction of the of the actual lungs and if that occurs sometimes it can cause a rupture within the alveolar capillary membrane blood can leak into it and then whenever you cough you start coughing up not just material within the airways but the actual bloody material that occurred from the rupture and this can present with what's called hemoptysis so they can present with respiratory alkalosis tachypnea tachycardia dyspnea representative their hypoxemia bronchoconstriction which can worsen dyspnea pulmonary vasoconstriction which can put stress on the right side of the heart also can decrease oxygen supply to the lungs you usually have a dual blood supply so this doesn't happen too often but if there's a significant amount of oxygen deprivation to the lung tissue they can undergo infarction they can disrupt the alveolar capillary membrane blood cells can actually start leaking in and then whenever you cough you can develop the hemothesis process okay all right here's another thing that we got to talk about one more you know whenever somebody has this kind of clot okay with inside of the the uh the pulmonary capillary system it causes a lot of pain okay and this pain is very intense sometimes but the pain is very specific and it's very important to remember this the pain that these patients usually develop is what's called sometimes like a pleuritic chest pain so sometimes the pain that they get is another big thing to remember is what's called a pluritic chest pain meaning it's pain that occurs particularly whenever they're breathing so another potential clinical manifestation of these patients is not just dyspnea hypoxemia tachypnea tachycardia as well as potential hemoptysis but also pleuritic chest pain here's the usually the most devastating aspect of the condition if you get one of these saddle emboli okay or a very proximal like pulmonary artery embolus that is going to put a lot of stress on the right side of the heart so here's the clot right and it's restricting blood flow right so now i have very little blood that's actually moving through this vessel what happens to the what's called the systemic vascular resistance in this vessel it goes up because it has a very small diameter with small diameter there's more resistance to blood flow so what happens is you get an increase in the systemic vascular resistance when you increase systemic vascular resistance you increase afterload but you also increase the blood pressure but in what system the pulmonary system so now the pressure inside of this pulmonary system here is much higher the pulmonary system isn't usually very high it's a very low system but as you have this increased systemic vascular resistance increase afterload and higher pressure now this poor little right ventricle's got to work so hard against that high afterload against that high blood pressure and so you know what happens is the right ventricle starts really getting stressed out and it just geeks out unfortunately it's going to become so difficult so what happens is the right ventricle undergoes dilation then it undergoes right ventricular dysfunction where it's having to work so hard to be able to pump blood against this high pressure that the stroke volume and the cardiac output just goes down unfortunately so you know what happens as a result because of this right ventricular dilation and right ventricular dysfunction there is a decrease in stroke volume therefore there is a decrease in cardiac output you know the problem with that is the blood that goes from the right ventricle where else does it go the blood from the right ventricle will go to the pulmonary circulation and then come back through the pulmonary veins to the left side of the heart so if i have a decreased stroke volume and decreased cardiac output from the right side that's going to lead to a decreased preload to the left ventricle and so now the left ventricle focusing on the left ventricle will have a decrease preload and a decrease stroke volume a decreased cardiac output and therefore a decrease in blood pressure hypotension systemic hypotension that's a problematic issue there we'll talk about the reflex of events there but here's another thing if the pressure in the right system is so high and blood isn't able to get out you're having less blood get out where is the blood going to start backing up into the right atrium and when it backs up into the right atrium guess where it can go up the right atrium up through the superior vena cava and you know what that leads to whenever it goes back up the superior vena cava it goes up via the jugular vein and the jugular vein starts getting all puffy what is that called jugular venous distension so they may have what's called jvd one more thing if the pressure with inside of the right ventricle is so high and it starts getting dilated it might start shifting and encroaching that interventricular septum into the actual cavity of the left ventricle and if you start kind of obstructing the left ventricular cavity what happens to the left ventricular outflow tract it gets obstructed and so the left ventricle can't pump as much blood out so another thing here that can happen as a result is not just a decrease in cardiac output because of a decrease in stroke volume that's affecting the left heart but another thing is that the interventricular septum may be kind of bowing in and occluding into the lumen of the left ventricle and that's kind of increasing left ventricular afterload as well so another effect that you may get here that causes hypotension is a left ventricular afterload effect that increases okay we got jvd we got a right ventricular dysfunction right ventricular dilation high stress hypotension from the left side of the heart okay next thing hypotension is a problematic issue right that's not a good thing what your body tries to do in response to this is you have little receptors similar to the chemoreceptors they're here in the carotid area and they're in the aortic area and they're here in the carotid area these are called your carotid sinuses and your aortic sinuses these are barrel receptors and these baroreceptors they pick up changes in particular pressure so whenever the pressure is low it's going to tell these baroreceptors the bare receptors will send that information of low pressure via cranial nerve 9 and cranial nerve 10 to the medulla let the medulla know hey blood pressure be low homie you got to do something about this and you know what the medulla says he says don't worry i got you i'm going to try to do a couple things to try to get the blood pressure up i'm going to try to increase my sympathetic system and increase the heart rate and so what happens is they develop what's called tachycardia the whole goal behind that is that if you increase heart rate you should increase cardiac output it should increase blood pressure to fix that issue right the other thing it says i'm going to increase contractility okay and that hopefully the increase in contractility will increase the blood pressure it's not going to do too good though because it's got very little blood coming from that right side of the heart and it's got that right ventricle kind of bowing in so that might not help and the last thing it does is it tries to undergo vasoconstriction of like peripheral vessels and so the vasoconstriction of peripheral vessels try to increase your systemic vascular resistance and increase your blood pressure that way and that might help a little bit so again to summate everything we talked about with the clinical features associated with the pathophysiology you can see a patient coming in with symptoms of dvt right so you want to think about potentially any kind of swelling any kind of pain any kind of redness any positive home and sign associated with a dvt right we also want to say okay do they have any pleuritic chest pain do they have any signs of dyspnea or any hypoxemia that we see on their pulse ox okay do they have an increase in respiratory work or depth that's in the sign of tachypnea are they trying to compensate for that with an increase in their heart rate as well on their abg do we see signs of early respiratory alkalosis maybe a little bit later as they start to tuck her out from having to breathe this fast they may develop respiratory acidosis the other thing is is there any signs of coughing or coughing up of blood from significant pulmonary infarction from a decreased blood supply and hemorrhage of particular alveolar capillary membrane in the form of hemoptysis is there any signs of jvd due to right ventricular stress like in dilation and dysfunction is there any other signs of right ventricular stress in the form of decreased blood flow to the left ventricle causing hypotension because of a drop in their preload and then them creating a reflexive tachycardia and response to that so these are some of the big things that i want you guys to think about now that we've covered that let's start getting into the diagnostics all right engineer so now let's talk about the diagnostics we're not going to go too crazy on like all these different things uh like unnecessary like lab testing we're gonna get down to like the the most important things that you really need to know for your exams and clinically on the wards so what kind of labs could we order you could really do a lot of labs you can always get a cbc you can get a cmp you know but and all those are great things you can get an abg we kind of have an idea of what it's going to tell us right so if we were let's say get some labs you can get a cbc the cbc may help you to kind of look at underlying etiologies like maybe they have hit right maybe they have heparin induced thrombocytopenia maybe they'll see that with low red blood cells and low platelets that's fine you can get a a bmp i think a bmp is is good the reason why is if you give contrast to a person potentially if they have a significant like renal dysfunction like a very very very low gfr there is risk of worsening that overview of what's called a contrast induced nephropathy so getting a bmp if you're going to do some of these studies may be a good idea to get a good idea of what their renal function is the other thing we can get is what's called an abg and we already have an idea of why we can get an abg the abg will tell us what the early stages of the pe and they're trying to breathe off their co2 by increasing their ventilation to try to bring more oxygen in they have a respiratory alkalosis if it's a little bit later as they're starting to tuck her out eventually because they've been breathing so fast and their muscles are getting weak they may start developing what's called a respiratory acidosis so again we might see them in two different stages there the other test that i want you guys to realize we're going to talk about this one here is called a d-dimer okay it's an okay test i think it's a good test if you have a very very low pre-test probability you can do this test and we'll talk about the algorithm that i really want you guys to remember out of this is what the big important thing for diagnostics is is the approach but really really quickly let me talk to you about d-dimers d-dimers what they're helpful for is telling us an activity of fibrinolysis right so it tells us about somewhat of a clot burden also kind of inflammatory activity in general so let's say here we have a clot right generally in this clot we have natural enzymes you know there's an enzyme called plasmin plasmin naturally wants to break down the actual fibrin within the blood clot you know fibrin is made up of fibrinogen and fibrinogen contains these little d segments these little d structures within it okay and whenever you break down fibrin you can break it down into what's called these fibrin degradation products and one of them are called d-dimers now imagine you have a big clot here you're going to have more plasma activity trying to break down that clot you're going to be breaking down more fiber and making more fibrinogen degradation products and more d dimers so the thought behind checking a d dimer is telling us that there is a big clot burden and that there's a lot of plasmid enzyme activity that's trying to naturally trying to break that down and dissolve the clot that's kind of the indication so you can say oh big old clot burden is the d-dimer elevated greater than 500 maybe there's a potential for a clot somewhere like a dvt or a pe okay now that we understand that you can get a cbc you can get a bmp you can get an abg you can get your d-dimer when do we get the d-dimer you shouldn't always get a d-dimer let's talk about when you get a d-dimer and when that's not even going to matter and there's more particular tests that you should be utilizing for diagnostic diagnosis and then a junctive test which may help you but also you just got to know it for your exam so the first thing is let's say that you have a high suspicion of a pe right so we're thinking that you got a pe all right let's say that you just have a pe you have a suspicion of a pe you're not quite sure if you have a high suspicion or a low suspicion yet right so you just think oh maybe a pe all right so don't don't bother you know memorizing every single aspect of the wells criteria you have these things called like md calc which you can kind of just utilize to get yourself a score i'd rather you just know that this score exists for determining your pre-test probability for pe so if you have a high wells criteria score you have a high suspicion of a pe if you have a low for wells criteria score then you have a low pretest probability or suspicion of a pe it just helps you in that sense don't memorize every single component of it so once you've gotten your wells criteria which you can get on like mdcalc you get scores out of this right then the newest one the most recent like modified well score is we go based upon a number that if it's less than four or greater than or equal to four okay so less than four are greater than or equal to four if it's less than four a p e is unlikely and we say this another way is that you have a low pre-test probability it's not a very very high chance that they have a pe but to be on the safe side let's see if they have some a high clock burden they have a lot of fiber analysis going on naturally so how do i do that i check a d dimer if the d dimer is very low generally we say like less than 500 so here we'll put less than 500 you can say that a pe is excluded okay so some type of vte or pe is excluded now if it's greater than 500 greater than or equal to 500 then there's somewhat of a higher suspicion and so we may do another test now if you're we'll get to what that test is in just a second because we're going to move down that way right so again wells criteria score less than 4p unlikely low pre-test probability just check a d-dimer see if there's a high cloud burden that's going on if it's not you can exclude a pe if there is you have to be compelled to potentially order another test now if the wells criteria score is greater than or equal to four now your pre-test probability is higher and so the pe is more on the likely side so because of that we don't waste our time with the d dimer we go straight to the definitive diagnostic test which is a ctpa which is a ct pulmonary angiogram it's just basically give them contrast and that's why you maybe want to get a bmp to check their kidney function you're giving them contrast because it's going to light up those pulmonary vessels and look to see if there's any kind of like filling defect or clot in that circulation a big thing to remember let's do this one in pink so that you guys don't forget is that ctpa sometimes let's say you can't get this done okay so there's let's call it let's say there's a contraindication to it for whatever reason unless you have a very severe like you get contrast allergies you go into like full-blown anaphylaxis or you have just severe ckd with a very low gfr and you're at high risk for a contrast induced nephropathy okay those kinds of situations you might not be able to get a ctpa and those scenarios what they usually go with an alternative is you do what's called a vq scan and we'll talk about that a little bit later okay so an alternative to a ctpa and those circumstances may warrant a vq scan now pe likely based upon the score you get a ctpa or p unlikely based upon the score d dime or elevated you get a ctpa ctpa is done if it is normal should be in red if it is normal then what does that tell us that means that there's no clot there's no kind of like blockage within the pulmonary circulation so if there's no blockage within the pulmonary circulation what can we say then it's unlikely that there is a pe so a pe can be excluded okay now what if you get a ctpa and it's indeterminate you can't really it's not conclusive enough you don't have a clear enough idea whether or not they truly have a clot within the pulmonary circulation so this is referred to as indeterminate okay in determinant now in that kind of situation when it's an indeterminate study you have no idea if there's truly a pe the next thing which is a very invasive test what you can do it is you can get what's called a a pulmonary angiogram where they actually put a catheter that runs down into the right atrium right ventricle and you throw contrast into the pulmonary circulation and light it up okay another option is they do what's called a lower extremity venous ultrasound because again what is the most common cause of someone developing a pe a dvt so if you find a positive dvt within the lower extremity you can also say a good chance it's a p and they can anticoagulate now if it's positive if they definitely have a clot then you go and you treat a pe as the diagnosis okay so we have a good i think idea here of how to approach a patient that we have a suspicion of a pe based upon all the things that we talked about now that we've done that let us take a look here at the different tests what they would look like what are some of the things that i want you guys to be keen on through some of these actual images let's go ahead and take a look at these hi ninja so let's go ahead and take a look at the gold standard diagnostic test it's the biggest one that i want you guys to be able to recognize for pulmonary embolism and that is a ctpa so here we're going to take a ct and we're just looking at the pulmonary arteries when they're getting filled with iv contrast okay so let's go ahead and take a look here we're in the abdomen right now so let's come up into the thorax a big quick orientation of a ct is that you're looking at the ct from the feet towards the head so this is actually the right side of the patient's thorax and this is the left side of the hemithorax and then here we have the heart right and the heart always points towards like the left side all right now as we continue to kind of scroll through here we're going to move our way up we want to focus our attention on the pulmonary trunk so as you can see here the pulmonary trunk is where we're going to have this bifurcation so look right there is our pulmonary trunk so this is going to be coming from the right ventricle pulmonary trunk right here and then as we move this way we're going to be moving right pulmonary artery and as we divert this way left pulmonary artery it should all be white but look what i'm seeing here i'm seeing some kind of like darkness darkness right here in that right pulmonary artery that's a clot that's actually an embolus and then look over here in the left pulmonary artery boom another embolus in the left pulmonary artery this patient is all jacked up they got bilateral pulmonary emboli that we can see on their ctpa so this gives you an idea of what it would look like so to kind of summa what we have here for this patient boom we have this patient showing signs of a bilateral right and left pulmonary emboli on evidence of the ctpa now let's take a look at the alternative test that we can utilize called a vq scan all right ninjas let's take a look here at a vq scan so a ventilation perfusion scan we utilize kind of a an element called technetium and it helps us to light up on this actual ventilation perfusion scan so here on the right this shows ventilation so you're seeing the technetium getting inhaled and ventilating all of the alveoli in the right and left lung but then we get to see what happens for the perfusion image here on the left so as you can see there's perfusion deficits here in this aspect of the lower part of the right lung and even here in kind of the middle and lower part of the left lung so we know that there's potentially some pulmonary emboli that's occluding perfusion to these segments of the lung so we see a ventilation perfusion deficit particularly here more particularly on the end of the perfusion deficit so again what does this vq scan tell us but bam ventilation is normal in this patient but we have some perfusion deficits that are occurring here in these two lobes along on our vq scan all right now let's take a look at our pulmonary angiogram all right engineers let's take a look here at a pulmonary angiogram this is a very invasive test it is actually the most definitive diagnostic test but it shouldn't be done because if it has you know a lot of risk because it is an invasive study but you're basically taking a catheter and filling contrast with the pulmonary arteries and when you do that you should see it kind of light up nice and black where all the contrast is filling you can see it pretty well here on that right lung but you notice how there's kind of like a deficit or kind of like a filling defect at this point where they fill the contrast there isn't any contrast coming down into these lower dependent segments so we can potentially say that there may be a filling defect here in this left kind of lower segment here where this pulmonary artery may have an emboli so let's go ahead and take a look at what we would see as our label here but boom there is a filling defect here in that left lung potentially secondary to an emboli that's kind of within this portion of that left pulmonary artery all right so that takes care of our pulmonary angiogram let's take a look now at an ekg of someone with a pulmonary embolism all right ninjas let's take a look here an ekg for someone who has a pulmonary embolism again one of the most common findings we're not going to look at it here on this one but the one of the most common findings on an ekg for a person with a pulmonary embolism is sinus tachycardia but on your exam what are some things that you really need to be thinking about so this was called an s1q3t3 pattern so you look at lead one if they have a very deep s wave that's the s1 component all right then you look at lead three they have an inverted t wave here in lead three and then a q wave a deep q wave in lead three so there's an s1 q3 t3 the other thing is your axis sometimes they may have what's called a right axis deviation use your thumbs your left is going to be for lead 1 and your right thumb is going to be for avf which one's actually going to be doing here right so lead 1 is pointing down avf is pointing up so my right thumb is pointing up so it's a right axis deviation the other thing is look here in v1 v2 v3 it has that bundle branch kind of pattern right rsr prime pattern so there's a bright bundle branch block here so s1q3 t3 right axis deviation and a right bundle branch block that is going to be what we would see so take a look here at our ekg boom s1 q3 t3 classic sine right bundle branch block and then we also have right axis deviation all right that's our ekg now let's take a look here at the next which is the echo all right ninjas let's take a look here at an echo this is actually one of my favorite tests that i love to do on patients who i suspect as a pulmonary embolism it's something that you can do with ease at this bedside so what i want us to do is to actually point out some of the structures get a little bit of orientation down here so let's actually kind of scroll through this nice and slowly here a couple of things that i want you guys to see here on this side right here this is actually the left ventricle this is your left atrium so you have some valves here this would actually be your mitral valve over here this is actually going to be your right atrium and this is your right ventricle and then over here you'll see kind of a dark anechoic structure that'll be the inferior vena cava now what i want us to notice here is that in someone who has a pe the right ventricle will be dilated and it'll be dysfunctional won't be contracting very well and it actually the right ventricle can be bigger than the left ventricle and on top of that the inferior vena cava may be a little bit plumpier than usual so let's take a look here and actually scroll through look at the left ventricle for a second look at how well it squeezes it squeezes super well now compare that to the right ventricle as i'm scrolling here it's not really making much of a really good squeeze so there's little squeeze there in comparison between the left ventricle and compared to the right ventricle and if you look up towards that left side you see that big anechoic structure is the inferior vena cava it's relatively dilated and the right atrium is also a lot bigger too so there's a lot of right sided pressure and again this is a classic signs of a pulmonary embolism so dilated right ventricle very decreased hypokinesis of the right ventricle bigger than the left ventricle and a dilated right atrium with a dilated ivc these can be signs of a pulmonary embolism on echo now let's take a look at the lower extremity venous ultrasounds all right engineers let's take a look here at seeing if there's any kind of signs of dvt which may be kind of a prelude to why the person has a pulmonary embolism so i just took and did a quick ultrasound on one of rob's legs to kind of show you what a compressible vein should look like because that's one of the big signs sometimes you can see a fresh clot within the vein but one of the big things is compressibility of the vein so if i play this video here you can see i'm going to push down on the probe on his leg and you see that it actually collapses the vein so that is a good sign that means that there is no kind of evidence of a thrombus that's actually blocking the compressibility now let's take a look at someone who actually has an abnormal kind of compression ultrasound sign and that it doesn't actually collapse this vein here so here's the vein on this patient right and this would be one of the arteries so this is actually going to be the femoral vein and this is the femoral artery and what we're going to do is we're going to look here watch as this does not actually show any signs of compression ready boom it should have compressed it did not compress so again if we look here we're going to squeeze no compression there you actually don't see any signs of a fresh clot but again there is no compression of that femoral vein it should collapse when you compress down on it so that's a common sign of a dvt or a clot with inside of this actual deep vein all right that covers our imaging let's go ahead and take a look at a chester x-ray back on the whiteboard all right so the last thing i wanted to talk about now that we've taken a look at all these images is another thing to be thinking about a really big thing a big clue okay is that if a patient comes in you have a high suspicion of a pe they're having some symptoms of shortness of breath you get a chest x-ray because you want to rule out other kinds of causes a big clue to think about someone having a pe is if you obtain a chest x-ray the most common finding is that it's normal and that should cue you in if a person has some of the symptoms that we talked about above and they have a normal chest x-ray be having a high suspicion about pe now on your exams there's these classic findings that you don't really see but you should know about them sometimes what happens is if you get a clot within the pulmonary circulation like a pulmonary vessel the tissue that it's supposed to supply maybe start undergoing a vascular necrosis and can show a dark hyperlucent area that dark hyperloosened area that's actually distal to wherever there was a clot was is called westermark's sign okay so it's a sign of where there is a cutoff of a pulmonary vessel causing a hyperlucency on the actual chest x-ray the other one is sometimes you can get this wedge-shaped opacification and that's due to pulmonary infarction and so if there's a wedge-shaped kind of opacity and there's what's called a wedge-shaped infarction that can be called a hamptons hump these are things that you really don't classically see but they're things that you should know for your exam okay now that we've covered the diagnostics let's talk about the treatment of pe all right so let's talk about the treatment of pe so it's actually not that bad believe it or not so treating a pe okay first thing you have to do is determine their hemodynamic status because then once you determine their hemodynamic status it takes you down the algorithmic pathway of what to do all right so first things first you have a pe that you have diagnosed the next thing you say is okay what's their hemodynamic status if they are hemodynamically stable what do i mean by that well if you guys remember the pathophysiology is that they could be very very tachycardic they could be severely hypoxemic and they could even have hypotension jugular venous distension so those are signs of hemodynamic instability right if that happens okay or they're not actually perfusing the brain so they develop like an altered mental status that's also another thing or it's a very very severe pleuritic chest pain in those kinds of situations where they're very very hemodynamically stable more specifically significant hypotension significant tachycardia significant hypoxemia those are things to think about and this person they don't have that so we don't have to go with the very aggressive therapies we can go with a little bit of the less aggressive therapy we have two options the first one is that we can do what's called anti-coagulation and there's different types of anticoagulants that we will discuss in great detail now if they have a contraindication two anticoagulations we'll put ac then we do what's called an ivc filter okay simple as that hemodynamically stable diagnosed with a pe you can do what anticoagulation if they have a contraindication anticoagulation or for some reason anticoagulation is unsuccessful you do an ivc filter right done if they have a pe and they are hemodynamically unstable now what do i mean they're severely hypotensive they're severely tachycardic they have very bad hypoxemia these are potential signs of hemodynamic instability that leads us to the next question which you may actually see in your exams let's quickly discuss it is there is definitions of pes and the degrading of their severity so we have what's called a sub massive pe a submassive pe is you have a pe within the pulmonary circulation but they're hemodynamically stable they don't have any severe hypotension they don't have any severe tachycardia but they have right ventricular dysfunction and this kind of scenario you might lean more to the anticoagulation of the ivc filter if someone has the other end of the spectrum which is a massive pe usually this is what's called a saddle embolus and again remember i told you satellite imbulous is it's basically when there's a clot in the pulmonary trunk i'll show you that when we get down to this other diagram but in this situation they are hemodynamically unstable they're hypotensive severely tachycardic severely hypoxemic and they have right ventricular dysfunction and again usually this is a saddle emblem so they have evidence of a very significant kind of clot burden within the pulmonary circulation so in these kinds of scenarios your massive p's where they're more hemodynamically unstable you might opt to these treatments what are those treatments the options that you have here is that generally you can give something called tpa tissue plasminogen activator to help to bust open that clot but if they have a contra indication look look how easy it is it was just the same thing for this one if they have a contraindication to tpa then you go with something called a mbolectomy done so now we know a person has a pe we determine their hemodynamic status if they're hemodynamically stable they got right ventricular dysfunction they got a decent clot burden we might have a submassive pe i might lean more towards the area of giving them anticoagulation of contraindication ibc filter if they have a massive pe they're hemodynamically unstable they get a saddle endless they've got a very heavy clot burden and they have right ventricular dysfunction i might lean more towards my thrombolytics or contraindicated and black to me now that we know those things let's talk very briefly about what type of agents that we would use and like other potential things that you need to know that are high yield all right so anticoagulation i don't want us to talk too much about this we already have a video if you guys want to discussing each one of these in great detail but heparin okay heparin is a really good kind of drug that we can use to treat patients who have pes now there's two different types that i do want you guys to know there's called unfractionated heparin and then there's what's called low molecular weight heparin what i really want you to know about these is unfractionated heparin is going to be more for like your hospitalized patients okay because this is the one that you do like a drip okay you do an infusion and then when you infuse this you titrate the infusion okay per what's called their ptt their partial thromboplastin time which is a measure of the activity of unfractionated heparin to determine if the ptt is too high there's too much heparin you've got to lower the dosage if there's low ptt then you're not actually having enough of the unfracturing heparin and you got to increase the dosage so this is ease of titration you have to have ptt monitoring though to give this and there is a risk of hit heparin induced thrombocytopenia with this and compared to low molecular weight heparin with low molecular weight heparin this is good for outpatient use so you can use this as an outpatient medication and it's usually a bridge so you give this as a subcutaneous injection okay as it compared to an infusion with unfat fractionated heparin you get this as a subcutaneous injection it usually has a bridge for like a couple days and then you start them on one of these two agents over here for a long term for like three to six months okay the only thing to think about with low molecular weight heparin is there's no ptt monitoring and you don't even need the anti what's called xa activity the only thing to be wary of with this one is if someone has renal failure so if they have severe chronic kidney disease you may have to either renally dose this magic medication or potentially opt for another medication so just be cautious in that scenario doax your direct oral acting anticoagulants okay these are great again kind of that you'll do these okay these are generally kind of like outpatient like long-term kind of things that you'll do for about three to six months okay and again we're not going to go through all of these but you have your 10a inhibitors which consists of rivaroxaban apixaban a doxaband and then you have your two a inhibitors which is your debigatran okay again these are good drugs they're actually preferred over warfarin because of a less risk of hemorrhage and also you don't have to have as much monitoring with uh doax as compared to warfarin there's less drug interaction so a little bit superior when it comes to those okay warfarin the other thing is same thing you can continue this outpatient and you can do this for about three to six months and again usually you're bridging them with some type of heparin heparin into the douak or heparin into the warfarin especially for the first five days when someone's on warfarin warfarin is actually hypercoagulable in the first couple days so you definitely want to bridge them with some low like of the weight heparin or unfractionated heparin and then continue this the only big thing that you have to remember is with warfarin you have to keep monitoring their inr okay because if you have too much warfarin their inr can be super therapeutic and they have an increased risk of bleeding okay so that's our anticoagulation we have a good idea now right what's the next thing okay if we have a contraindication anticoagulation then we got to come down here now and talk about the ivc filters so if they have a contraindication they can't get that anticoagulation then what we have to do is we take and put this little like it's like a sieve basically right it's like a sieve and so what happens is like blood plasma and small like solute particles we'll be able to pass up through this structure uh this like a little ivc filter via the inferior vena cava and into what's called the right atrium right into the right side of the heart because effectively this this inferior vena cava ivc will then pass blood where it's effectively kind of doing like one of these things coming up from the ibc into the right atrium right ventricle pulmonary circulation right so if we give them this ivc filter it's designed to be able to block any kind of clots coming up from a dvt and propagating into the actual pulmonary circulation so again generally this is if there's a contraindication to anticoagulation or anticoagulation failed this brings me to one other thing that i really want to make sure that we understand actually so let's come up for just a second because i really want to make sure that we understand this sometimes it might be misconstrued anticoagulation these medications are not busting open this clot they're not breaking open the clot they're preventing the further development of the clot the propagation or enlargement of the clot they are not breaking down the clot that is the job of thrombolysis or the job of an embolectomy so when you compare these two ivc filter it's not breaking up a clot it's preventing the further development of pulmonary emboli from a dvt same thing with the anticoagulation with hepa and doax warfarin all they're doing is they're basically augmenting our coagulation cascade in a particular way that it prevents the activity of hypercoagulable states are forming clots and therefore preventing further development or propagation of the clots okay now that we've got that done we've covered the hemodynamic stable side now we've got to cover the unstable side it's really simple thrombolysis if they're hemodynamically unstable you give them the tpas baby the tpas tpa generally you give them what's called alteplase okay there's different types of thrombolytics like particularly tpa types but ultraplace is kind of the most common one that you'll give here now generally whenever you give someone all the place you can give them like some sometimes like 50 to 100 milligrams the big thing to remember with this one is that again how is it working this one is busting up the clot because what it does is it stimulates an enzyme called so this is basically what's called a tissue plasminogen activator right it's going to stimulate plasminogen and convert it into plasmin and plasmin did what again it broke down the actual clot the fibrin into the fiber degradation products and the d dimers okay so this will bust the clot open okay in comparison to the anticoagulation okay now they have a contraindication i run into this a lot into the neural eye sinus icu a patient maybe has a pe or they have like some other issue and they can't get tpa because they have a bleed in their brain what do i do and uh an optor tune kind of situation here is to do what's called an envolectomy a catheter driven suction or aspiration of that clot so come down here for embolectomy so for embolectomy all you do is you take like a catheter you thread it down through like the svc you thread it down through the right atrium into the right ventricle you thread it through the pulmonary trunk and this leads to that one quick thing that i was talking about with the saddle imbulance satellite are really dangerous because what they do is they literally like they straddle right in this area here they straddle between the actual pulmonary trunk as it bifurcates and if you get a big clot there you almost get no blood going into both of the actual pulmonary circulations and so imagine the significant effect that you can have on the right ventricle and the significant hypoxemia that you develop either way the catheter then runs up through the pulmonary trunk and then what you do is it may actually help to suck up some of this actual clot it may bust up some of the clot and then suck up the clot so an imbilectomy is good if there is a contraindication to tpa and they're hemodynamically unstable okay beautiful now another thing that you have to be thinking about is what if a patient what are the other things i can do to help them besides fixing the issue sometimes if a person is really hypotensive what can i give them to augment their blood pressure well supportive care measures i can give them iv fluids effectively if i give them iv fluids you got to be very careful okay they don't want to overload their rights out of the heart but if you give them iv fluids it should hopefully increase their preload it should increase their stroke volume their cardiac output their blood pressure it should increase their effective arterial blood volume if that doesn't work the next option is to go with things called vasopressors okay so these can augment particularly the hypotension that you see related with this condition for the hypoxemia you may have to progress with oxygen support right and this may come in the form of just a simple kind of non-rebreather it may be nasal cannula it may be optical you may even have to intubate the person it kind of varies depending upon the scenario but generally there's some form of oxygen support so we've got fluids and pressures to augment the blood pressure and we got oxygen support for the hypoxemia and then busting up the clot as the definitive treatment the last thing that i wanted to discuss here is what are ways that we can prevent these things from actually forming how can we prevent clots from actually forming because this is a big deal especially people with a lot of those risk factors that we talked about for vircos sometimes these patients especially when in the hospital they may need to be what's called subcutaneous low molecular weight heparin little doses like 5000 units maybe twice a day and it just helps to give them a little bit of the heparin to reduce the risk of forming clots this is very important especially in the hospital because if a person's laying in the bed all day and they're not moving around and ambulating that's a problematic issue you may have to give them heparin the other thing is ambulating getting around and walking if you can get around a walk you reduce that risk of stasis and you keep pushing the blood flow up the other thing is if they can't ambulate they can't be on subcutaneous heparin because they have a contraindication with it putting on what's called some type of compression okay some some type of compression device and this may be compression stockings this may be these little things called pneumatic compression devices and what they do is they kind of inflate and then squeeze down kind of basically replicating you trying to contract your your calf muscles to be able to induce some contraction and push some of the blood flow up so that's kind of another way that we can do this is utilizing compression devices and pneumatic compression devices as well so that covers everything that we need to know about pe all right ninjas in this video we talk about pulmonary embolism i hope it made sense i hope that you guys enjoyed it as always ninja nerds until next time [Music] you

Channel: Ninja Nerd

Views: 313,972

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: cmmINOpIVuY

Length: 89min 21sec (5361 seconds)

Published: Mon Nov 01 2021