Aortic Diseases | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about aortic diseases that includes aortic dissections and aortic aneurisms again this is going to be a part of our clinical medicine section for those students preparing for their step two their pants their nurse practitioner exam so please continue to watch this series if you guys do like it please hit that like button comment down in the comment section and please subscribe also highly suggest you guys go down in the description box below click on the link to go to our website on there

we have notes we have illustrations a lot of great things there also some merchandise and we're developing courses for your exams such as those preparing for the step two the pants and the nurse practitioner exam so please go check those out all right first things first aortic dissection when we talk about an aor dissection it's actually pretty straightforward there is a tear within the intimal layer so you know based upon the anatomy of a blood vessel you have the tuna intimar or the tuna interna then you have the tuna media and the tuna externa there's

a tear within that tuna intima or the tuna interna when you have that intimal tear we're going to call it what happens is blood can actually easily dissect easily dissect in between the tuna intima and the tuna media so blood will naturally go you know normally should go left ventrical it should go into the aorta it should move down the true Lumen of the aorta but sometimes it can rip right through this tuna intima and cause blood to kind of accumulate and propagate inside of this false Lumen if you will so now we have blood

kind of getting trapped into this little area here and this is the problematic issue where you can kind of form this thing called a false Lumen which you'll also have blood kind of moving down through this true Lumen and that's some of the things that you can notice in patients who develop aord dissections is you have what's called an intimal tear this will cause blood to rip into to what's called it'll create a false lumen and then we will talk later why this is a problematic issue because these actual false lumens what can happen is

blood can continue to propagate down them and pinch off let's say for example we'll talk about this a little bit later let's say that there is actually a branch off of the aorta here this is going to start kind of accumulating here sagging where all that blood will start accumulate and compress that branch and now no blood flow is going to come off of that branch and we'll talk about that a little bit later okay so again big thing to remember here is that you create these things called an intimal tear that can create a

false Lumen and we'll talk about the complications of the false Lumin a little bit later all right that's aortic dissections with aortic dissection we have to ask ourselves the question what's causing this intimal tear why is the actual blood vessel linting ripping and causing blood to rip into this false Lumen two reasons one is the pressure the order is just way too dang High all right now what would cause aortic pressures to be so high that literally blood could rip through the intimal lining and start accumulating in this like little space here this false loom

in space you see how again it's in between the tuna the red here is the tuna intima and this maroon is the tunic media that's all going to be blood sitting here in this area here what is the reason why the aortic pressure would be too high it's not that hard to imagine hypertension so chronic hypertension is by far going to be one of the most common causes of aortic dissections another one would be something that's causing damage to the actual or something that's causing breakdown of the actual vessel wall so what do I mean

here so let's say that there's actually some type of connective tissue destruction that would be one way that we could actually really weaken the blood vessel wall what's diseases that cause connective tissue destruction vasculitis so if you have a vasculitis these are relatively rare but things like syphilis and takayasu another one is is where you not necessarily have destruction but you have mutations where you don't form proper connective tissue these are rare but things like ell's donlo syndrome and morphon syndrome are also going to be particular disorders where you can notice this as well the

other thing that I would want you guys to realize is that there can be just natural kind of like just what's called proteolytic destruction here as well and you can see this sometimes where some sometimes you can have like weakness of the vessel wall where it kind of dilates and so another potential scenario where you can see this is another disease called aneurysms which we're going to talk about in a little bit so if you have a weak aorta or a weak vessel wall that thing causes this vessel wall to be weak out here and

it's going to be much more easy for you to kind of Pop through the intima and spill blood right in between the tuna media and the tuna intima creating that false Lumin if you will so again High pressures or connected tissue destruction causing a weak aorta all right the next concept that I want you guys to understand here is when we talk about dissections aortic dissections there is two types all right so we have to be able to classify them so we know it's usually an intimal tear creating a false Lumen we know that there

is going to be potentially due to high blood pressure or connective tissue destruction but we also have to be able to classify this based upon where it occurs so Stanford a dissections they have to involve the ascending aorta they have to so you have to have an intimal tear here and what we're going to do is we're going to show now all the results here's the intimal tear and look how the actual dissection continues to propagate so blood will flow left ventricle up here go into the false Lumen and all this blood will kind of

propagate into this kind of false Lumin here and it may continue kind of like far but all that that matters is is that it originates the actual dissection originates at the ascending aorta that has to be the big defining factor is it has to involve the ascending aorta that's it okay standord B is it doesn't have to start at the ascending aorta it has to become be it has to begin beyond the left subclavian artery so I want you to remember Beyond the left sub caving artery so it would start somewhere like right here maybe

so here I'm going to have my intimal tear and then I'm going to have all that blood ripping in through that area here so we go left ventricle up through the ascending aorta aortic Arch oh there's a little tear here boom and blood's going to start creating this false Lumen at this point here okay so it has to be after the left side subclavian artery and that is kind of how we defined these particular types of aortic dissections okay so we got aortic dissection done for the most part kind of introducing it talking about the

pathophys the causes and then the classification we're going to do the same thing with aortic anisms aortic anisms is just the dilation of the aortic vessel wall so this is usually going to be some type of dilation of the aortic vessel so you're going to notice this as the potential cause here so look look at this monster dilation here and we'll talk about the degrees of dilation depending upon the location often times anything greater than 3 cm usually within the abdominal aorta is considered to be pretty pretty large and at least abnormally large so we

have to ask ourselves the question we have dilation of the atic vessels why is there the dilation of the TIC vessels and it's actually a combination of what weal talked about in patients who have abdominal I'm sorry aortic dissections they have to have a combination of a weak aorta and usually High aortic pressures so what happens is and these patients they have some type of proteolytic destruction of the smooth muscle and the connective tissue so what we're going to say is is you're going to say there's going to be vessel wall destruction it's not just

the connective tissue it's going to be the smooth muscle a bunch of different tissue what's causing this vessel wall destruction so there's here's going to be this vessel wall destruction what is causing this it's going to be all the things that we just mentioned vasculitis would be one particular thing another one would be any kind of connective tissue disease we'll put ERS Dono syndrome and we'll put Maron syndrome it could also be what else this one's interesting for these patients you really want to think about smoking smoking is a really really strong risk factor because

it can cause proteolytic activation and lead to a lot of destruction of this tissue in the vessel wall so smoking is a really bad one and there's one more and this is atherosclerosis this may be kind of a double fold one is it may create inflammation within the vessel wall but it may actually knock out some of the blood vessels that supply the outer part of the vessel like the What's called the vas of vasorum and so this can cause a lot of destruction of the vessel wall so now the vessel wall is weak because

of this vessel wall destruction all of a sudden you decide to increase so we're going to have increased vessel wall destruction and then on top of that you're going to increase the ortic pressure what diseases do this hypertension so if I have a patient who has hypertension they're going to cause the pressure that's being exerted on this weak vessel wall to increase and what do you think is going to happen it's going to cause vessel dilation so you're going to have a weak weak vessel wall that will then progress to become a dilated this will

cause a excessive dilation of the aortic vessel so this will precipitate as dilation of the aortic vessel so often times what you want to think about in a patient who has aortic aneurysms is look for smoking atherosclerosis these happen to be for the most part very common and very common in combination with having a very high blood pressure aortic dissections you're going to notice that high blood pressure is going to be by far the most common cause but it could be connective tissue destruction all right aortic anisms we know it's a dilation of the vessel

we know it's because of vessel wall destruction in combination with high BP that's leading to the dilation of the aortic vessel but we have to Define aortic aneurysms and the same way that we Define aortic dissections so there's what's called thoracic aortic aneurysms or we're going to abbreviate TAA and abdominal aortic anisms which will abbreviate AAA okay now with TAA you have to have dilation which we're going to Mark here with this blue kind of like Arrow here this is going to be the vessel wall dilation for the AAA this is going to be the

vessel wall dilation really the pro the actual determination of where it's a thoracic aortic anism versus abdominal is very straightforward where is it with respect to the diaphragm thoracic aortic above the diaphragm abdominal aortic below the diaphragm but it's more particular than that and so what we have to say is usually with thoracic aortic aneurysms they most commonly involve ascending aorta because there's a lot of space between the ascending aorta all the way to the diaphragm whereas it most common It's usually the descending aorta same situation an aortic andm in the abdomen can form anywhere

from below the diaphragm down but where's it most common it's most common to involve just below the the kidneys and we call that the infrarenal so it most commonly involves the infra renal aorta so often times we call this an infrarenal abdominal aortic aneurysm all right so at this point we Now understand what is an aortic dissection what is an aortic aneurysm what is the pathophysiology behind them what's the causes and then we understand some of the classifications now what I want to do is we have a patient who has an atic dissection what are

the complications we have a patient with an aortic aneurysm what are the complications all right my friends on to the complications things that you can see in patients who have aortic diseases such as dissections and aneurysms so when a patient comes in who has an aortic dissection often times the classic finding like you look for this in your boards is that ripping tearing chest pain that's honestly the classic sign of an aortic dissection that's really the thing that you're you should already know it should be ingrained into your brain ripping tearing ing chest pain I

don't even have to write that up you should know that for aortic dissections what you can see is aortic dissections as they continue to propagate along that false Lumen you see a lot of scary complications associated with this that'll also cue you up on your clinical vignette one of those is shock and this can happen in two ways one is let's say that blood is traveling through the left ventricle into the aorta it's moving through the true Lumen oh there's an intimal tear why because of high blood pressure right high aor pressure or because of

a weak vessel wall from connective tissue destruction and from there it just rips right in there and creates this false Lum in and then what can happen is blood can kind of settle in this area but what else could it do if it's possible enough it could rip right out of the vessel so blood that's running through this highpressure system could spill right out of your vascular system this will quickly lead to blood loss and if you lose blood what do you think is going to going to happen to the patient's blood pressure it is

going to become very low and they can progress to where the actual blood pressure is so low that multiple organ systems start becoming dysfunctional and this patient starts requiring vasopressor support this is a very specific type of shock which we call hypovolemic shock but it's more of a hypovolemic shock from blood loss so sometimes you may also hear the term um hemorrhagic shock it's just the type of hypmic so one of the scary complic associated with aortic dissections is it rips through and causes what we refer to as a rupture if you will so if

this puppy ruptures then you can start seeing blood loss the other one this is actually really interesting if you guys remember from the pericardial disease lecture in cardiac tamponade one of the causes of cardiac tanod is hemopericardium so if blood moves from the left ventricle through the aorta and here at the ascending aorta it rips right through the Tima and then from there it rips right through the wall into the paracardial sack now this patient can start developing what blood that can accumulate directly into their pericardium what is this called a hemo pericardium this hemopericardium

is terrifying because if it accumulates rapidly enough blood it will then cause the patient to develop what's called cardiac tamponade and if that pressure Rises up it compresses the actual heart and prevents it from filling which can progress to shock except this type of shock is not a hypovolemic shock this type of shock is usually what we refer to as a obstructive shock so we call this obstructive shock so you can see two different types of shock potentially based upon the complications that can arise from an aortic dissection all right so the next component here

is if we come down here we're going to have Mal perfusion syndromes so what do I mean here well remember I told you that as blood leaves the left ventricle and it rips out of the left ventricle and it goes into the aorta let's say that it rips right here right into the actual ascending order rips right through the Tima The Blood starts kind of sitting and creating what this kind of problem within the false Lum in here now what happens is is if this Blood kind of accumulates here it can really start to even

retrogradely work backwards and then start to compress the aortic valve if it compresses the aortic valve it can lead to aortic valve dysfunction so what you may see here is you may see what's called aortic valve damage which then then can lead to acute aortic regurgitation which can lead to acute CHF acute heart failure this is the problem because if you damage the aortic valve now blood can easily just rip right back in right and so that's the problem here is now we have blood that rips right into this area creates a false Lumen compresses

the TIC valve and now blood can easily pop back into the left ventricle and cause a q CHF okay the next concept here is that if blood does move from the left ventricle into the aorta and then from here it goes into this ascending part here this order where there's a dissection now blood can actually track into this in the same way that it tracked into this causing aortic regurgitation it can track in and cause blood to settle here where it starts to compress or narrow the coronary artery and if I develop coronary artery compression

then I'm going to lead to a myocardial esea or myocardial infarction so look at that you're compressing the coronary vessels and this can lead to an MI so so far from the Mal profusions ripped in damaged the valve ripped in narrowed the coronary artery what if it rips in here same thing runs from the left ventricle into the ordera rips here and then it starts to compress here at the brachio falic well now it's going to be really hard to get blood out into the right subclavian artery and it'll be easy to get blood into

the left subclavian artery so that means that the pressure on this side will be normal but the pressure and pulse on this side will be lower and so what you'll notice out of this scenario for these patients is you will notice a decrease in the systolic blood pressure and a decrease in the pulse so you'll notice asymmetric blood pressures generally we say that this should at least be greater than a 20 mm Mercury difference 20 mm Mercury difference here it'll be low so here you'll have decreased flow and here you'll have normal flow so here

you'll have normal blood flow here you'll have decreased flow and the reason why you'll have decreased flow is because this is actually being narrowed because as the blood rips through this part it creates this like false Lumin which Narrows the brachio calic trunk okay so noticing asymmetric blood pressures and asymmetrically decreased pulses in a patient with ripping tearing chest pain is classic for eortic dissection I don't want you to forget this one with that being said we're kind of working our way up right so we started with the ascending aorta then we're up to the

brachos falic trunk what's the next Parts the kateed so what if the blood goes from the left ventricle into the sending aorta passes the brachio calic but then rips right here and starts compressing and narrowing the cids if you narrow the cors now you're going to reduce the blood flow to the cerebrum and if you reduce the blood flow to the cerebrum you can lead to a TIA worst case scenario you cause a stroke like a c CVA the other thing is it can compress what's called your sympathetic plexus and if it compresses so here

you have what's called your sympathetic plexus if that puppy gets compressed what it'll do is it'll decrease the actual function of that sympathetic nerve and it'll lead to something which we call horners syndrome now you have compression here this leads to Horner syndrome that begs the question what are the classic features of horer syndrome one is tosis so the eyelid will kind of droop the other one is meiosis the pupil on that same side will be constricted in anhydrosis you won't sweat on that side of the actual forehead so when we have ascending aortic dissection

you can have aortic regurgitation coordin AR compression with Mi brachio calic compression you develop asymmetric blood pressures and pulses cored common cored artery compression you can develop Tia CVA because you don't profuse the brain or you can compress the sympathetic plexus causing horer syndrome now we're going to keep going down into the descending aoic dissection so now we're getting into these parts we're now blood is actually past the entire aortic Arch it's moving down and what it does is it dissects through a part here Blood starts accumulating here in this false Lumen and compresses the

renal artery now you're getting very little blood flow to the kidney and if you get very reduced cor uh reduced uh renal profusion what can that lead to an acute kidney injury and so you'll see these patients maybe having an increase in the creatin and a decrease in their urine output the other thing is if it continues maybe it's running down here and then it dissects into this one and dissects through the actual descending aort here blood pulls up in this false Lum and and compresses here maybe this is an inferior mezan terar AR or

a suzan teric artery supplying the bowel now the bowel is going to get reduced perfusion and if you get reduced perfusion to the bowel this can lead to bowel esema so you want to watch out for things like bowel eskia and usually the big one is going to be acute mesenteric esia all right so that was kind of in the descending aorta now let's come all the way down to the distort so we started ascending aortic Arch descending a aorta and then all the way at the distal aorta blood's kind of flowing down the distal

aorta it hasn't ripped through an intima but here it gets to this part here right at like the bifurcation and whoop what does it do it rips in here and sometimes you can have the same thing let's say it happens on both sides here here you have another scenario where again same kind of concept happen blood kind of rips through here and accumulates in these false lumens Blood starts settling here if Blood starts settling here what can happen is it can really narrow this Lumen and it can make it almost impossible for blood flow to

go to the distal extremities and these patients May develop something called an acute Limb esea and sometimes what you can see with this is they can develop something called larich syndrome where they have decreased pulses in the lower extremities they have erectile dysfunction and hip and buttock pain and this is something that's very very terrifying if you have a patient with a cold leg very decreased pulses they have less pain or they have intense pain then you want to start thinking about an acute Lim memia from potentially an aortic dissection in the differential all right

so with aortic dissections we have covered the classic finding is usually that ripping tering chest pain but we covered the most terrifying complications which is shock and then the ones that you really want to watch out for your on your boards the Mal profusion Syndrome from The dissection creating a false Lumen and knocking the blood are narrowing the actual blood vessels off that Branch off of that aorta and we've talked about these here we come over the aortic aneurysm with aortic aneurysms again it's that vessel dilation if you will when that puppy dilates man it's

a thin wall it's already been destroyed the actual vessel wall is super weak that's why it's dilated pressure shoots up and when it does shoot up these can literally cause them to pop when this happens these patients can literally cause so if it ruptures you will have these patients with a massive blood loss and they will Ex sanguinate and when they BL have this massive blood loss they will drop their pressure and develop shock right usually hypovolemic or that subtype which we call it hemorrhagic shock now one of the other things that you want to

be able to pick up so when if the patient comes in shocky their blood pressure is really really low they're requiring vasil pressure support or fluid support or whatever it may be one of the things that usually is a Telltale sign to help you on your exam is that whenever this ruptures it usually produces like a sentinel sign so usually like if you ever heard the term that subarachnoid hemorrhage is that Thunderclap headache that terrible worst headache you've ever had of your life that's usually a sign that the vessel is ruptured in the same way

where is the abdominal orta in the belly so usually at the same time that you precipitate with this rupture these patients may also present with back pain or belly pain so look for back or abdomen pain the other thing is is when this thing ruptures and how big this thing is it may cause a pulsatile mass so you also want to watch out for any evidence of a pulsatile a pulsatile abdominal mass and the last thing here is sometimes as this Blood starts leaking out here we'll draw it over here let's see that this puppy

ruptures the abdominal aort is usually retrop paranal so when blood kind of leaks into that retr parital space it'll cause this flank kind of ecosis sign and so look for any any evidence of like flank ecosis with all of that being said you have a patient who comes in low blood pressure belly back pain pulsatile mass and maybe flank ecosis think about shock potentially due to an aortic aneurysm that's ruptured now we have a couple complications here that you can see with a thoracic aortic aneurysm now thoracic aortic aneurisms they can generally be like asymptomatic

and the way that they present was with complications right or they may cause mild chest pain but some of the biggest complications associated with a thoracic aortic aneurism is usually a thrombo emoli so think about this you have this dilated area that's stasis right there my friends if there is at any point this dilation that causes stasis of blood flow what is stasis of blood flow going to do create an opportunity for a clot to form a thrombus that thrombus will then break pieces off and these are called emili and these emies will just float

and when they go and Float where can they float to they can float to the brain they can float to the belly and they can float to the legs and they may cause a stroke a acute mesenteric esea or an acute limb esea so they may have a neurod deficit belly pain pain or leg pain and decreased pulses in a cold limb these are terrifying events another one here is that look at this look look at this son of a gun this thing's so dilated look at the space between the aortic valves they can't even

co-a together and because of that blood will easily rush back into the heart and cause aortic regurgitation so with this you may also see a Aortic regurgitation which can cause massive amounts of blood to accumulate within the heart and very little blood to go out so you have a low cardiac output and the heart's filled with blood what can that lead to acute heart failure so watch out for acute CHF that can develop as a result of aortic regurgitation due to an ascending aortic aneurysm all right the last one I'd say it's not as high

yield but it's something to think about that sometimes they can mess with you on the vignette when this aorta is so dang big all right big as a mother stinka it starts compressing on nearby structures it'll compress on the esophagus which is this blue tube here it may get big enough that it compresses the esophagus so it compresses the trachea sorry in the blue here compresses the brown here which is the esophagus compresses the super vnea and there's even nerves nearby like the recurrent lenial nerve compresses that puppy think about all the nasty effects if

we come down here for a second think about this you compress the blue here the super prena you can develop something called SVC syndrome you compress the trachea what do you think is going to happen it's going to be hard to get air in so sometimes these patients develop something called a Strider or sometimes even a disia you're compressing the esophagus and that can lead to something we refer to as uh dysphasia and lastly you may even compress like the recurrent lenial nerve so the recurrent lenial nerve we're going to put put R Ln can

be compressed and this may lead to like a horseness of the voice all right so think about that because of these puppies being compressed if you will we'll kind of put like a little thing here these are all being compressed this could be some of the compressive symptoms that you may see with the thoracic yism all right on to the last one here so AAA obviously the most concerning signs and the most common feature is what we talked about above with shock and the kind of the abdominal pain back pain pulsatile Mass Etc but other

things that again when you got this big dileted area blood kind of like circulates and stays in this area a little bit more so that's called stasis with stasis this creates an opportunity for a thrombus that can break off a piece and form a embolis that can then embolize via the superior mesenteric inferior mesenteric artery or it can embolize down the lower extremity and this could lead to acute limb esmia so pain in leg decreased pulses cold limb or to the belly where may cause acute mesentericus gemia belly pain right that's going to be out

of proportion so these are other complications you can see with the AA scary scary one is what's called an upper GI bleed this usually just as a quick note this is actually called an a orto inic fistula now with this being said it can happen with aaa's but I'm going to put a little note here it's usually in patients who have AAA that have had recently have some type of surgery where they've had a graft that's done and what can happen is that graft that's usually around that AAA starts fusing with the small bowel and

you create a fistula a little connection and blood that's in this high pressure aorta right here into the small bowel you'll start peeing out blood faster than you can imagine and so these patients will definitely develop sometimes a Melina but if it's fast enough if it's a really brisk GI bleed sometimes it can be pretty bright and so sometimes you may even see what we call Hamato and we'll write this out over here so you can have Melena but you can also have something called hemato kesia all right and so these are some of the

features that you may see Melena or hesia now that may sound kind of like wait I thought upper GI bleeds is always kind of going to be Molina it definitely will most likely be Molen but if it is a very very brisk upper G I believe which is what this one will be sometimes it can be so fast it doesn't have enough time to kind of like oxidize it all and it can cause this kind of hmates this bright red kind of blood appearance all right so with all of this being said a patient who

comes in with an aortic disease such as an aortic dissection and aortic aneurysm we know the causes the pathophys the classification the comp lications in the classic findings now we got to diagnose and treat these babes we move on to the next component here we have a patient who has an aortic dissection are we at least suspected they're coming in with them ripping tearing chest pain jaw scapular pain asymmetric blood pressures decreased pulses maybe decrease kind of like pulses at the lower extremities claudication featuring of acute lisia whatever it may be I think they have

an aortic dissection what's the first thing that I need to do okay what's their blood pressure again the most common cause is hypertension do they have that tearing chest pain do they have asymmetric blood pressure differences do they have any features of Mal perfusion syndromes if they do get an ECG and a chest x-ray you're getting the ECG because you don't want to miss an MI and you don't want to actually miss anything else in the chest that could be causing this chest pain so if you do that chest x-ray is actually somewhat helpful for

roric dissections if it's a really kind of wide media at least greater than equal to 8 centimeters you can say for some kind of reason there may be some type of disease within the medyum and guess what's involved in that the or and so you should take a further look if you have any of these features above the question that comes up as to determine the next test is if they are hemodynamically unstable or not there is also this other question of the risk of contrast induced nephropathy I'll let my pet peeve go aside of

this one but again if you're going to give somebody contrast there is the risk of kidney injury so if they do have instage renal disease you should also be very very cautious with giving them more contrast but that should never delay the need for a test that is life-saving or at least identifying of a cause that could be completely killing the patient so in this scenario if they are hemodynamically unstable or they have a risk of contrast and du nephropathy what do we do well if they do have this then we probably shouldn't take the

time to send them to the CT scanner because it's going to give them contrast and there is risk of decompensation in transport so instead I should do a bedside transesophageal echocardiogram and that'll help me to see if there is any false Lumin and true Lumin and thus an intimal flap that would be supportive of an aortic dissection if they're not unstable and they don't have a risk of cin then I have time to go to the CT scanner and they have no risk of causing contrast induc nephropathy so therefore I'm going to get the best

possible test which is a CT angiogram and if they don't have the ability to go to a CT angiogram you can also do Mr so it's an MRI with an angiography as well they're both the same and this is going to give you a really good look because it's going to give you all these different dimensions the severity of it and so this is a really really good test for determining the cause or determining if they have an aortic dissection all right now with that being said that gives us our nice beautiful approach to an

aortic dissection question then comes how do we treat it it really depends upon the type I told you before Stanford A's are really dangerous because of the risk of aortic gation myocardial infarction and cardiac tamponade and rupture therefore the yes I will medically temporize them so if they are hypertensive I don't want that dissection to get worse and so I'll control their blood pressure with different medications Nitro proside is the drug that will get to vasod dilate and reduce their blood pressure and then we'll try to get their heart rate a little bit lower by

using beta blockers if they are in Frank shock so hemorrhagic shock so they have ruptured then I will use pressors an IV fluid or blood but the m main thing for Stanford a and if they ask you any question on the exam what's the the definitive treatment for Stanford a it is always surgical intervention temporize them if you need to but get them to surgery as soon as possible and usually with this one we're going to do a graft so we'll take where the disease kind of dissection is and we'll cut that out and put

in this graft the other thing that you could potentially do is if you have a Stanford B you would medically temporize them all right you would treat their hypertension treat their their tacac cardia and if for whatever reason they develop scary complications so what would be Stanford B ones there'd be acute kidney injury mesenteric eskee acute Lim esmia rupture that would cause hemodynamic compromise in those scenarios you take them to surgery and you can do a graft or you can do a stin all right also known as a endovascular kind of aortic repair here or

an Evar but only if complications arise every patient for stand for day so now we have a patient who comes in we think that they have an aortic aneurysm you want to think about something if they have signs of aortic aneurysms we're going to go through that but remember I told you for aortic aneurysms which was the AAA the most common right what did I say was the most common cause hypertension high cholesterol and smoking the other thing is Advanced age as people get older their we their vessel actually gets super weak you really want

to be able to know when to screen a patient for AAA cuz not all patients will present with any symptoms and so you have to be able to help them out surveillance is key if they are greater than 65 years old a male with a history of smoking they need to be screened for a AAA and then from there monitor it throughout if they have those three things male greater than 65 and smoking you screen them how do you do that you get an abdominal ultrasound what they'll do is they'll measure the abdominally order and

see the width of it if this poppy is less than three they have no AAA and don't really need any further ma like monitoring if it's greater than three that's big and we can't miss that so from there we will take the next step in Ultras sign them again in 6 to 12 months but here's the big thing that you can't forget if the size of it is greater than or equal to 5.5 CM or it grew greater than 0.5 cm in 6 months these patients need to be evaluated for surgery so you need to

consult surgical service for them to get an elective surgical procedure okay that's that's for surveilling them making sure that you don't miss it what about the patients who you think are actually having these things okay we'll talk about that in a second but TAA screening is a little bit less common the only reason you would be doing this is if a patient has a bicus aortic valve or 's donow syndrome Maran synd because they are at high risk in these scenario you'll get a CT angiogram and look at that and see hey do they have

a thoracic eortic anism hey we can't miss this we should probably keep track of it see if it gets bigger and then if need be contact surgery for patients who are symptomatic so they're presenting with any of the features of the thoracic aortic aneurism or abdominal aortic aneurism you have to ask the question are they stable or not if they are not then you have to do something different if they are stable you want to do something at the bedside where that doesn't require transport abdominal ultrasound or te is usually pretty good and you'll be

able to see here off the E Echo look at this sucker look how huge the aortic kind of root is that's massive and then the other thing here is look at your abdominal ultrasound to see hey what's the size of that b bad boy and that's going to be super helpful as well if they are not hemodynamically unstable then you have time go get a CT angiogram take a look here at the aort oh it doesn't look too big but oh my gosh there is a huge goom boach here in their abdomen that's actually ruptured

so that's going to be super helpful for being able to identify for surgical planning and to determine the actual size of the aneurysm okay and that would be the big things for a TAA or a AAA that is presenting with symptoms okay from there what do we do we now got to treat these bad boys so with these it's always going to be medical management all right smoking sensation is going to be really important for anybody who smokes Statin therapy for hyper lipidemia because again I told you smoking is a big risk factor hyper lipidemia

is the big reactive factor and then what do you think is the last one hypertension so control their blood pressure beta blockers a Inhibitors or an ARB but make sure that's properly controlled surgical management is indicated and I already talked about this before but I want to remind you again the reason we would do surgery is if a patient has greater than or equal to 5.5 CM on their aorta scan right or it's gotten bigger and very quickly greater than 0.5 cm in 6 months those are the primary reasons we would do that the other

one is that they're symptomatic in other words they're coming in with hemodynamic instability that are showing potential signs of rupture or really scary complications in that scenario we need to go to surgery so it's usually elective under these scenarios or it's urgent or emergent because they're developing complications or they in shock and those would be the indications that I want you guys to think about again we can do this with a graft or we can do this with this stent called the Evar all right my friends we covered aortic diseases I hope that made sense

I hope that you guys enjoyed it and as always until next time [Music]