all right so what I want to talk about is this blood edge trivia stuff how this is tested it's confusing it's scary people feel intimidated by it it's not well understood most of the time even by people who are teaching it I've got a couple of different ways to remember it in my books and you know I sort of blow off the idea of trying to reason your way through it but I'm gonna change my tune on that slightly because I think it's valuable if you can't understand it for a couple of reasons one it makes it harder for you to be tricked on a multiple-choice question - it helps review some other adjacent topics that the better you understand them again the harder it will be to trick you now these questions are almost always shown with brain MRI the reason is the the physics and stuff for this like aging blood doesn't really follow the same rules other places in the body and you don't really need to understand why just know that blood age stuff is almost it's for the purpose of multiple-choice it's only going to be shown in the brain and the only two sequences you need to worry about are T 1 and T 2 so this right here is probably the most common phraseology for the question now I gonna go into detail understanding this stuff and then I'll come back to this question so don't like try to figure it out right now but I just want to point out a couple of things on how this can be asked so this is probably the most common is this terminology of like hyper acute acute subacute late sub acute chronic those are words that people who write multiple-choice questions like to use those are words that are all over the radiology literature some other ways they could do it is by giving specific time frames and hours or days and then you saw you have to know well which one of those is hyper acute or subacute the other way that they can do it is they can actually ask what the change with the red blood cell is is this oxyhemoglobin giving the signal or deoxyhemoglobin etc etc and the last way which is probably the least common would be to ask a specific real specific physics question like is this because of t2 star effect or something along those lines so as we go through this material sort of the four things that you need to know five you need to know what the color changes are as the blood edges you need to be familiar with this terminology the hyper acute subacute late sub acute stuff you need to know the hours / days that correlate with that and you need to know the changes in the actual red blood cell like the actual like physiology portion and then you need to know a little bit of the physics the more you know the better because it sort of translates into other stuff so this is the way this topic is typically taught in residency sort of you've got a PhD in kind that comes out and he says I'm gonna make I'm gonna break this down and make it simple and then you know and then starts to do that I'm gonna try not to do that I'm gonna try to sort of use general concepts to sort of make it so it's a little bit easier to understand maths not necessary all right and to get there we're gonna have to review a couple of topics here first I'm gonna introduce some fancy physics vocab words and then we're gonna go back in time and review what susceptibility is related to T 2 and T 2 star why stuff is T 1 dark I'm gonna use water as an example and then we're gonna talk about blood physiologically and then we're gonna go back through all of the different physics and title together and hopefully it is my goal that you won't have to make baby noises or anything like that anymore that you can actually understand it so let's start out with the fancy physics vocab now the first word that I want to introduce is susceptibility what does that actually mean so susceptibility is a measure of the extent to which a substance becomes magnetized when it's placed in an external magnetic field so something like that so maybe a better way to think about susceptibility is this magnetized ability like that would be a synonym for susceptibility so as a review in the absence of an applied magnetic field the magnetic movements of hydrogen nuclei are going to be randomly oriented and then when you apply the field to be zero you're gonna have them align or majority of them align in a specific direction you know with with the magnetic field so let's imagine that in this sea of protons that you've got the magnetic field applied against this tissue that you've got a specific kind tissue that is susceptible to being magnetized so that could be a piece of metal like a gallbladder clip or maybe the surgery resin left a wrench inside the patient so let's imagine that we've applied this mech rb0 right which is always on right the magnets always on well through this particular tissue within that wrench the an internal magnetization or polarization is going to be created and it's going to have a choice it can either oppose the direction of the main magnetic field or can augment it so here's the vocabulary if the polarization opposes the applied magnetic field the effective field within the object is reduced a little bit and the lines that they'll draw like in the dive diagrams for this kind of stuff they sort of squish out they're dispersed this is called diamagnetism now that so that is when the stuff lines up against the field now when it lines up with the field in the same direction augmenting it there's a couple of different vocabulary words that you'll see para super para and ferrimagnetism and and the reason you would use one versus the other is how strong that opposition is so just sort of to put that in relative perspective para if you thought a pair is like a one superoes like a thousand and Faris like a 5000 so there's a big step up there and it's all along the spectrum now most things in the body biological tissues are actually weakly diamagnetic it's on and it's on a spectrum you know water fat calcium is actually you be strongest diamagnetic substance in the body sort of way see signal drop out like along the cortex of bone etc now that's most of stuff in the body now there is a minority of tissues in the body that contain accumulations of metal copper manganese iron a little bit of iron right like maybe some red blood cells gadolinium actually works by being paramagnetic air why would it air be oxygen actually acts weakly paramagnetic and then you've got some other things in the body where we're going to talk about also Feridun hemosiderin that are having even stronger augmentation of the magnetic field and they were considered superparamagnetic and then there are foreign bodies like iron and steel like the the gallbladder clips and stuff like that that you know will show up in a scan and they are extremely ferromagnetic so like those the effects that we're going to talk about related to this will be exaggerated to an even more extreme so those are our fancy vocab boards now let's pivot back to this idea of T 2 and T 2 star so just as a refresher we've got our tissue it's in the magnet the magnet is always on it's aligned the the net vector is aligned with the main magnetic field and then we strike it with an RF pulse here and that knocks it down and we're talking about t2 we're talking about the transverse dimension this one here and when it first gets knocked down all of the you know this is like a some ear right the arrow is not just one arrow it's a it's an it's a bunch of little arrows sort of added up in that direction they're lined up for some period of time so look at it like this little bit easier and then over a certain period of time they start to get out of order they D phase back to randomness here and that is that's t2 decay so you often see it sort of diagrammed out like this right more and more and more and more and more sort of out of sync with each other what causes this T to signal to like what actually causes them to get out of sync like that why does that happen so there's two main reasons you've got an in homogeneity within the external field and then you've got in homogeneity within the local magnetic field within the tissue themselves so you may remember this here also were like this is like the hypothetical t2 decay but then you you know you've got this t2 star which is sort of like random causes plus your fix causes so it's not just the the tissue spin interactions what you think about with the the pure t2 like one being a little bit different than the other it's it's that plus field inhomogeneity that actually causes the t2 star to be more rapid than the actual like just signal and signal crime so maybe a better way to think about t2 is like this so imagine that we've got a attract team here and these guys are from I don't know Jamaica or Kenya or something like that and there are three twin brothers here identical in every way and they're gonna start on the starting line together and they're gonna they're gonna go around well they're gonna stay right next to each other right these guys are identical they're gonna be staying right next to each other for a while and then maybe one of them just happens to train a little harder than other and the other guy he had you know he had Taco Bell for for breakfast and that but that was just a bad idea and so he starts to lag behind the other guy starts to pull ahead and other guys in the metal and then so even though they're pretty similar eventually they they begin to deface but that happens more slowly when things are very homogeneous now if you've got three different guys from three different teams and backgrounds etc and they all start on the starting line together they're going to separate out from each other really fast so the point of this is to sort of help you remember that things that are heterogeneous are going to lose that t2 signal faster than things that are homogeneous so maybe make it an attempt to bring this together with the prior topic here's our b0 will have to be zeros here and one of them is total home totally homogeneous it doesn't have any local tissue that's creating susceptibility versus the other one that has like speckles of tissue that are capable of being magnetized and then either opposing or augmenting the magnetic field in this case augmenting it so were these guys for homogeneous this is heterogeneous right so if we look at our diagram here the homogeneous ones are going to be like the yellow here like the regular t2 and the heterogeneous stuff that's got augmentation focally different little tiny spots is going to be the orange that's going to be like and the more heterogeneous it would be the stronger that t2 star effect would be so when you've got something that is homogeneous you're gonna see something you know a homogeneous slow or D phasing more signal t2 bright and then the opposite is true heterogeneous faster D phasing less signal t2 dark so where I'm going with this is if you've got a lot of susceptibility you're gonna augment that t2 star effect because it's more heterogeneous and then you're going to have you're gonna become t2 dark all right now let's move on to review the topic of t1 so again quick review here we're lined up with the field we get struck with our RF pulse we get knocked down in opposition to it and then we're gonna build back up so for the longitudinal signal which is the t1 right to recover we've got to take protons that are in our spins or whatever that are in a high energy state and put them in a low energy State what do I mean by that high energy state is the state where they're opposing the main magnetic field that's considered a high energy how do they get high energy they got energy transferred to them from that RF pulse now remember you can't create or destroy energy right that's one of those like basic scientific laws so you gotta do something with it you got to give it back to somebody you can't just throw it away you got to give it back to somebody so somebody handed you the gift you can't just pitch it in the dumpster you got to hand it back to somebody what are you going to give it to well usually what happens is that it's a transfer of heat now it's not a lot of heat you're not cooking people on the magnet right but that is how you know it's this energy transfer into the lattice it gives off that energy and heat and as it does that you start to turn them more and more and more from that high energy state into the low energy state and that is considered recovery that's t1 recovering and you'll see you know it graphed out like this typically right so you know and again you know if you've got something here and that's from that's how we define t1 signal as the recovery to 63 percent of its potential if you get something that does that quicker like that it's considered a short it did it quicker so it did it shorter shorter amount of time to do it it got t1 shortened that's brighter so when people say and there's intrinsic t1 shortening of the pancreas it's a bright means it's bright it's bright it's bright on its own you know gadolinium works by shortening t1 effect right so that term shortening for t1 if you look at that out backed up more signal gets to the 63% faster and that that that's what that means so why would one type of tissue be better than another type of tissue at doing that well remember I said it's all about giving heat back so tissues that are efficient at transferring energy as heat have really short t1 times and tissues that suck at sharing their t1 Heat have very long t1 times so like large stationary things have low vibrations and therefore they are very efficient at giving their energy back whereas something like water has a high vibration and therefore it is terrible at giving back its energy and we're gonna talk about why in a second but I want to drive home this idea of sort of movement and heat being the same thing think back to whenever basic chemistry or science or whatever when you learned about like what heat actually was remember it's how fast stuff is moving is what makes it hot right so like a theoretical absolute zero like nothing's like complete stopping that's why there there is an absolute zero because you can't slow down any more than being stopped whereas you can just get hotter and hotter and hotter and hotter and hotter because things can move faster and faster and faster and faster faster so it's just how fast things are is how hot they are and for them to become cool they have to slow down their movement which means for them to slow down they have to make something up else speed up a little bit because you can't destroy energy it's always just being transferred so I guess another way to look at it would be water is bad at sharing it doesn't want to share and it's because it's you know it's gone it's moving it has a high vibrational frequency well what if what does that mean so let's look at the molecule of water remember that that's two hydrogen's and an oxygen and I like to think about the oxygen is like a jealous lover and it's got a pull on these on its when it's two wives the hydrogen's here in that pole creates like a like a little polarization here it's polar and the the pole on the hydrogen electrons supposedly it's you know I think about I guess there's a couple ways to think about it one would be to think about it like a top that's uneven spinning how easy it would be to spend that kind of thing another way to think about it is that when it pulls the electrons like towards it it's exposing the hydrogen nuclei so when they get hit with the pulse it really spins them it was highly susceptible to that so they spin it spins very fast and remember because of that and this is gonna I'm gonna make this matter later the this spinning is is the reason that it's not good at transferring its energy and therefore it has a long t1 time and therefore it's darker on t1 alright so rapid review here the stuff we talked about so remember that susceptibility basically just means you're gonna either oppose or line with the field less homogeneous things create a loss of t2 signal amplifying at t2 star effect and the pole of oxygen on hydrogen sets it up to hold on to its heat longer in that water molecule and therefore recover the t1 signal slower alright so the last thing here we did it almost is to just sort of review the physiology of blood and then bring all this physics together in a way that it makes sense alright so we first need to talk about what blood is now remember that blood is made up of liquid and cellular components the liquid part is the plasma that's just pretty much can be thought his water it's like quite water but he just pretty much think about it as water and then the cellular portions is all the other crap that's in there but you know you can think about it as basically red blood cells for the purpose of blood changing obviously there's platelets and white blood cells and all that other stuff in there too all right so let's talk about the red blood cell for a second so the whole point of the red blood cells to do what the carries oxygen right and the way that it does that is by using a glue hemoglobin now sort of in the life cycle here it changes right so we've got this would be oxygenated hemoglobin and then you know it's going to shed its oxygen and then it becomes deoxygenated hemoglobin and then after a period of time breaking down like in the clot it's gonna become met hemoglobin and we'll talk about the difference what that means in a second and then eventually the hemoglobin gets broken down into fragments or chunks of iron proteins called Feridun and hemosiderin sort of like that and the difference between these two things I sort of mentioned earlier but I'll just recap it is that the Feridun and hemosiderin is super paramagnetic as opposed to the met hemoglobin which is pretty strongly paramagnetic so how strong how super is super now you may remember it's like a thousand times more so it's it's a big difference all right so here's our brain and we're gonna get a bleed now so schematically here now when arterial blood extry novice eights and this like hyper acute setting over 95% of the hemoglobin is still in an oxygenated state and because of this it's like most tissues in the body it's very very weakly diamagnetic and you can think about the structure of the the clot at this point it's probably easiest to think about it is basically just being in water and because it's water it has signal that's sort of predictable where it's gonna be T to bright a little bit and it's gonna be a little bit on the darker and 41 maybe I so it's not quite water right but it's it's like I said there's other stuff floating in there but I start my brain sort of thinking about it like it's water ish a little bit on the t2 bright in a little bit on the t1 you know it's not dark dark dark but it's it's I so did on the dark around so this here is our oxygenated hemoglobin and within a few hours that oxygen is going to begin to dissociate from the clots hemoglobin and when it does that we've make a change from being oxyhemoglobin to deoxyhemoglobin in the main thing that's going to change there is now we have four unpaired electrons and that is going to result in a change from being diamagnetic to paramagnetic actually pretty strongly paramagnetic I'll just sort of as a review here remember now we've got some heterogeneity within that local field right there's a little bit of speckles of susceptibility augmenting that local magnetic field and because in this state that it's still concentrated within the red blood cell sort of like it's strong enough there to actually create a signal change so just reviewing here instead of having that normal t2 curve we're now dropping into the the more exaggerated t2 star effect which is going to result in a heterogeneous field and therefore faster D phasing less signal and darkening of the t2 star so at this point we're going to change from being t2 bright to t2 dark now the t1 signal is going to be the same in both hypercute and acute stages so this is what he considered the acute stage now the next thing that's gonna happen is there's going to be a continued breakdown of the blood product so we're going to change from the oxygenated hemoglobin to met hemoglobin now met hemoglobin has five on electrons and that is gonna mean that it's even more strongly paramagnetic I sort of like drew the color-changing here but let's take a more in-depth look okay so we've got a more detailed look here and we've got oxygenated hemoglobin here their oxygen here and that that'll leave right now or in our deoxygenated hemoglobin State and I want you to notice that we've got our iron here and it's in a +2 state and then when we make our change over to meki McLovin it's now in a +3 state and you may remember this thing like methemoglobinemia the chocolate colored blood was like the step 1 buzzword well the reason that was a thing that was bad was because this can't bind oxygen instead it binds it binds water so white who cares right well that close proximity of that oxygen molecule remember we said he was he was the jealous lover to this iron it's gonna alter the way he operates and does business because now he's sort of like he's around a real alpha dog now and so it D masculinize is him he's now going to act like a beta male and we're gonna talk about why that why that matters here in a bit oh sorry that histamine needs a needs an extra hydrogen there all right okay there we go so remember I said that oxygen is like the jealous lover and it pulls the electrons of hydrogen close to it well when it gets in close to the iron like that something magical happens and you know people who pretend to understand this stuff call this an inner sphere relaxation basically what happens is it chills that oxygen out that interaction right there makes it so that it's not doing that pole thing as much as it was before and it doesn't just happen there there's like a cascading effect where it sort of spreads to all the local water right there so they all sort of chill and now they lose that fast spinning that they were doing it not doing that anymore they spin slower because they're not top-heavy and they therefore transfer their heat better and therefore their t1 time is faster then they become t1 bright and that is the reason why at this stage which is now the sub acute stage that blood becomes t1 bright it's because of that interaction of the water molecule with that net haemoglobin as opposed to the interaction that it has with the deoxygenated hemoglobin that's the change and that's why it matters so late in the first week you're going to have lysis of the red blood cell and as that occurs the met hemoglobin is going to spill out into the extracellular space so everything that we've been talking about before this happening has been intracellular but now that red blood cells getting older older and older and older it's been living in a clot for a week and it starts to crack and leak now the significance of that is that that met hemoglobin that was strongly paramagnetic that was creating that TT star fact is now gonna leak out and it instead of thinking and then it's gonna I think about it sort of like oozing and spreading around something like like this and now it's less concentrated so it's more homogeneous and therefore there's less T to star fact so you're going to start to see the signal become brighter on T 2 again now the molecule itself is intact still with those five unpaired electrons still allowing that Inner Sphere bonding of water so you're still having that bright T one signal but you changed your t2 signal because you lost that you went from being a real focal e heterogeneous clumped within the cell to more homogeneous spread around so T one stays bright T two becomes bright again it's not it's being more the T two and less of the T two star so in the final stages of hemoglobin degradation we're going to end up getting that breakdown of met hemoglobin completely into basically fragments of iron hemosiderin and Feridun and these guys are no longer paramagnetic they are super pair of magnetic so whereas before I said that the signal was sort of diluted and we lost that T 2 star effect now we're going to get it back because remember the difference between paramagnetic and superparamagnetic is like a thousand times so we're really gonna ramp up that heterogeneity in the field and we're gonna really amplify that T 2 star effect the other thing that's going to happen is that we lost that met hemoglobin that was allowing the water you know to be nice about giving off its energy so with that gone we're gonna make a change back from being tea one bright 2t1 dark so at the very end here we're gonna go dark dark so let's do let's do a quick rapid review here we've got we've got our hematoma and we've got our hemoglobins in its oxygenated state and because of that it's basically the same as other biologic tissues it's weakly diamagnetic so we're gonna think about it is basically just the plasma of just the water so that's going to be t2 bright and then slightly I so on the you know it's a slightly dark on the t1 end and then after that we're gonna have our oxygen dissociate away and now we're in the deoxygenated state which remember makes the change from being weakly diamagnetic same as sort of a lot of the other tissue to paramagnetic and now we're going to generate some heterogeneity right and because of that it's going to amplify that t2 star effect and that's gonna have us lose our t2 signal and drop out t1 is going to stay the same because we don't have that that behavior that water molecule is the same right now after a little bit of time we're gonna have the change to that +3 state which is gonna let the water molecule bind and that's this this is our met hemoglobin situation we're still intracellular now and that's very strongly paramagnetic which is still going to give us a t2 star effect it's still going to give us a dark thing on t2 but it's gonna do something different with the water right it's gonna mess with the water so that it spins in a way that it gives off its energy in a more fish way and then instead of being t1 dark it becomes t1 bright and then after about a week or so the cell is gonna start to break down and rupture and that all that intracellular met hemoglobin is gonna bust out and sort of dissolve around and get diluted and become homogeneous again and as that happens we're going to have a more homogeneous field so we've got all the runners that are sort of identical twins now so that's gonna bring us back to a regular t2 instead of that t2 star and then we've still got the functioning net hemoglobin molecule it's just extracellular remember I said that that thing sort of diffuses around so the water effect is gonna stay the same so it's still t1 bright and then lastly right it's gonna break down and be changed into Feridun and hemosiderin and that's going to create that really strong paramagnetic effect super pair of magnetic effect which is going to bring back it's going to revive our t2 star effect and drop our signal back out and we also because the hemoglobin broke down we lost our met hemoglobin which was the thing that was making the water protons be bright instead of their usual darker or ISO configuration so now we're on a dark dark situation now the one thing that I left out here for completeness is that in the center of a chronic hematoma you usually have some water contact and that will often make the center bright also so sort of it becomes this pattern that we're describing in the chronic state is more of a rim pattern all right so here's a chart that you have to memorize this as promised you know here the hours and days remember we said that it takes about a week or so for that red blood cell to break down remember that's the difference between when we have your intracellular met hemoglobin to your extracellular met hemoglobin chronic you know it takes and it's a gradual process that takes about two months so chronic is just going to be the one that's the longest one possible and the difference between hyper acute and acute you know you sort of go half a day one day two days maybe would be one way to remember it but regardless you have to memorize this chart memorize the vocab words memorize times and memorize the colors now there are certain people probably most academic centers still teach the stupid mnemonic with the bit IB itty bitty baby doodoo it's it's embarrassing so don't do that don't don't do that if you have to sort of draw it out I like this thing this is the thing that's in my book and you know just sort of taking this like coiled approach if you can draw this diagram just draw it out once or twice that makes sense I actually think it's easier to sort of remember the mechanism now remember that things sort of that the middle so let's take a look at this question again so remember the first way the first thing you have to do when you're solving this is which one's d1 which one's t2 so t1 right white matter is white on t1 and then t2 if you can get a little bit of fluid signal that's nice if you can't see that then you know you're what the white matter to be dark take a look at this thing we're looking right there and so what we've got is bright on t1 and dark on T - all right so I can look back at this good think there it's right there so knowing that it's bright on t1 right away makes you know that it's in that subacute slash late subacute face because it's bright on t 1 because of the met hemoglobin right that's it mess with that water molecule and then we look at the T 2 and we say okay it's dark that means there's T 2 star fact that means that it's still really concentrated within the red blood so it hasn't been diluted out so it's still intracellular it's not extracellular yet so now we're in the sub acute phase all right I hope that was helpful that's my best effort teaching it it's a complex topic and ok