Join us for this fantastic session to learn systematic approaches to interpreting common investigations, including formal bloods and ABGs!
Interpreting Investigations Part B
Summary
As part of this session, we will be teaching you useful systematic approaches to interpreting common investigations, including formal bloods and ABGs, and using examples from clinical cases to help you to apply these approaches to your real-life practice!
Description
Learning objectives
- To learn systematic approaches to interpreting formal blood results and ABGs.
- To use these systematic approaches to work through some examples and identify important pathological findings at each part of the system.
- To practise applying this learning to tackling common clinical scenarios.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.
Hi. Hi, everyone. Um, this is one of the committee members from Prepare for Practice. So if you guys don't know about us, but it's basically a national teaching program. Um, that our, our founder started a couple of years ago and it just basically helps fifth year medical students kinda ease into fy one, especially that it is a big step and, um, a lot of people struggle with it, including, to be honest, I struggled myself quite a lot in the beginning. So it's just making sure that we know the basics, um, and helping everyone kinda ease into that transition. And with that, can you just guys see my stories gonna confirm that before I start, you can just write in the chart? Perfect. And can you see a, a change as well while you guys are applying? But basically, um, oh, yeah, fine. Um, I'll try changing it but, um, I, as I said, I'm one of the fy ones in Musgrove Park Hospital. Um, I started my foundation yet in gi surgery, moved into geriatrics, which was quite different to surgery. Um, and currently I'm on endocrinology, which is basically just more general medicine. Um, and we've got a here. Um, hi, everyone. I, um, one of the fons too. I, um, started on a job on Gastro, which was, um, super busy and everyone had really deranged blood. So this would have been quite useful, I think before I started. Um, and then I went to psych, which was a super interesting, er, complete different pace though, to Gastro. And then now I'm back doing a surgery job and I'm doing urology, which once again, quite um, a different vibe from the other jobs. All right. So with that, let's make a start. I hope you guys can see the objective side. I changed it. Um But if you can't just let me know in the chart and we'll try and figure it out. But basically the aim of this session is just trying to start with simple things, trying to interpret form of blood results cause you're gonna see a lot of these and you're gonna need to know what's abnormal and why was it abnormal and act on it if needed? Uh We're also gonna discuss ABGS um cause also you're gonna see a lot of that during your F one. So we're gonna try and give you a systemic approach to interpreting both of these and what things to look for, um, and how to basically act upon them. So we're just gonna start with the blood. So, so as always, I'm not quite sure if you guys are 40 or 50 years. But um mainly with interpreting any investigation, especially acies, they like you to have a systematic approach and it's a bit different in real life. But you wanna first thing check the patient identity, you wanna check that um this is the right patient. You wanna check when the bloods were taken. What time is there any trends? Um what's changing with these bloods? Why were they taken? And then you wanna obviously check for any obvious abnormalities. Um And with that, you wanna go through review it systematically for the current C RPS using these and whatever blood that was sent. And lastly, you wanna consider the clinical question. So why did you even do these bloods? And what were you looking for? Because sometimes you ignore some of the buds because they're irrelevant to the clinical picture, right? So we're just gonna start with our first case. So you've got a 60 year old male who presented to Emmy you with chest pain, one of the consultant, he asked you to go clerk this patient and come to present to him. What questions would you like to ask? What would you like to know just prior to going to see this patient? What are you thinking and just right in the chart? Yeah, exactly. Absolutely. So when did it start? Have they ever had it before? Where is it? What type of pain is it? Yeah. Right. So you ask all these questions and you've taken a really good history and you've done your clinical assessment. So the patient tells you he's got central chest pain, it's not really radiating anywhere. And when you ask him about systemic symptoms, he tells you that he's got this bleeding from his back passage that's been ongoing for a while now, for a couple of days weeks. And he hasn't told anyone about it past his past medical history. He's got ischemic heart disease, diabetes and hypertension and he's quite well within himself. He tells you that he, he's quite well within himself. It's just that chest pain, um, which comes and goes in nature, he's new zero, he's not spiking at any temperature. You decide to do an ECG cause that's chest pain and you find that it's normal. So you've looked at the blood results, oh, you're already ahead of it all done. Um, so microcytic anemia. Yeah. Yeah. So just moving on. So the abnormal blood results is he's got anemia. The HB is quite low and the MCV is microcytic. And with that, even though you wanna rule out things like M I it's quite common that we see especially acute severe anemia. It's quite common that you see chest pain, which you initially think is an M I but it's not. Um, and that's mainly because obviously the body is not able to compensate cause there's not enough oxygen reaching the tissues. Um But also with any anemia, generally, you wanna see the trend cause some people are anemic all their lives and some people are, they, there's a trigger for that anemia. So you wanna see if it's an acute or chronic, if it's acute, you wanna double check. Is it true? Cause sometimes the patient is dehydrated and that's why they've got, it looks like they've got a HB drop but it's just dilutional. Um So you wanna do a VBG first thing just to make sure that this is the actual HB. And if you find that there is an acute job, an acute job I would say is around 2020 that would, I would consider that an acute job, then you wanna do group and safe because if they, in case they go for any procedure and that's quite an important thing cause a lot of the time, especially as med students, we don't think that you'd wanna take group and save that routinely, but sometimes you really need, especially if they need an intervention. Um And in our address, I'm not quite sure if it's the same, but in our address, the, the group and safe stays for 72 hours. So it's quite useful and I think you've already answered, but it is microcytic anemia. Um And just one thing you need to be quite aware of is an acute severe anemia. It can be a cause of unstable angina because if you think about it, the body's not having enough oxygen. So not enough oxygen reaching the heart muscle itself. So that causes ischemia and it can cause unstable angina, even unsteady. So you need to make sure that you're following up. If you're not transfusing or intervening quite rapidly within, within 24 hours to 48 hours, then you will need to make sure that this patient is getting serial EC GS and if needed to discuss with the cardiology and just moving on. Mm, I struggled a lot with anemia in my fourth year. Um I find them quite confusing. How do people figure out what type of anemia or what test to do? So, I kind of did this like flow chart um and how to classify it. So the most important thing is the M CV to look at it. Um As you guys already know, microcytic normocytic and microcytic microcytic, the most common cause is iron deficiency anemia. Um And in the UK, it's either lack of diet or um cause of menstruation having periods. But other things you need to consider is um inflammatory disease, chronic inflammatory disease. That could be also a cause of microcytic anemia. One thing to help differentiate. So once you've got a microcytic anemia, not quite sure if it's iron deficiency or not, you just wanna do um humans. So ferritin and transferrin usually in iron deficiency anemia, the ferritin is gonna be low because you haven't got enough storage of iron and the transferrin saturation is high because whatever iron you've got you want it to bind to the transferrin. Transferrin is the protein that um transports the Ferri the iron. And if you, if that come back normal and you're thinking, you know, they might have a history of SIA, then you wanna do the hemoglobinopathy screen. But to be honest, A as an F one, you don't wanna do that, you just escalate. Um and then they can figure out hematology, no cytic anemia, you wanna do a reticulocyte count. So with the reticulocyte count, if there is a low reticulocyte count, that means that the body is not producing enough. So that's a problem within the bone marrow. Um That's the main um cause of that. If you've got high reticulocyte count, that means that there's something happening in the body where the red blood cells are not aging, right? So the body has had to produce more red blood cells that are not mature. So, the most common thing for that is hemolytic anemia, uh or even sickle cell anemia. We see that quite a lot as well with macrocystic anemia, you mainly see them in B12 um and folate deficiencies and that's gonna be a megablastic anemia. So if you order blood film, it's gonna come back with um megablastic in the hypersegmented, that's like the B12 and FOLATE. If it's non megablastic, then you think about hypothyroidism, alcohol abuse and other syndromes, which are less likely. Ok. And always don't forget there's some um drugs especially antila drugs, they can cause anemia as well. So, if you can't find the cause of that anemia and it's concerning, you just make sure that to go through the medication list. So just moving on to the next case, if you guys got any questions, just put it in the chart and um I'll try to keep an eye on it just moving on to the next case. Right? So you've got this 72 year old male who was admitted to oncology. Your uncle, the nurse tells you that this patient looks quite unwell. He's got a new rash and he feels hot and cold. So, what are your thoughts at this point? And in the meanwhile, um he tell the nurses if he, they can run some bloods while you go and see them and these are the bloods and when you speak to him, um, he says that he's feeling quite weak, quite hot and cold. I look at his past medical history. He's got lung cancer. He had chemotherapy a week ago. Um, he's using one for tachycardia. His temperature, I forgot to that, but his temperature is 37.9 and you have a look at his arms and legs. You find a rash prefer rash, which has only come on over the last 24 hours and it's getting worse and you can't find any active bleeding and these are his bloods. What is happening? What do you guys think is happening? Yeah, pancytopenia. Well done. Mhm. All done. So look at his blood results. So, yeah. Neutropenic sepsis. Yeah, I see. That's quite a good shout. Right. So, just looking at his blood results. So you've got the white cells count, hb and platelets are all low. So, that's spine, cytopenia. And with patients who have got, they're taking chemotherapy, it's quite normal to see them pancytopenic. So don't be alerted if you find an oncology patient and all their bloods are low, um They're all abnormal, that's quite common. So you start to worry when they spike a temperature when they're tachycardic, when they're feeling quite unwell within themselves. Cause then you're thinking like I think some of you said neutropenic sepsis. Yeah, you're thinking an infection especially once you look at the nutr um neutrophils and you find them less than normal with neutropenic sepsis. Does anyone know what you need to give? What antibiotic you need to give? And how quickly that's why you say that. So D IC is a good shot, but it's unlikely in a patient like that. Um because we usually see it in patients who have had, for example, um in pregnancy or for example, p patients who were in ICU. So it's not the classic, classic history but definitely something to rule out as well. Yeah, well done you guys. So it is IV Tazocin. Um That's usually the first sign if they're using quite high if they're using less than five usually is Meriem. Um And you need to give it as soon as they spike a temperature. Obviously, you wanna take the blood culture, but it's quite essential. And usually, to be honest, if you're caring patients um with who are, are known to have cancer and taking chemotherapy, they carry a card, uh which tells you what antibiotic you need to give and how quickly. Um the other thing you wanna consider with that rash, obviously, that rash is due to the drop in platelets, it could have been an acute drop. Um So you wanna take a, a thorough history about when that did that rash start and you wanna look at their medication chart. So generally speaking, any platelet level, less than 50 wanna stop any antiplatelets, any blood thinners, basically, because they are very high risk of bleeding and with a platelet level of around 15 to 10, you wanna speak to the hematologist on call. Um Just to consider a platelet transfusion, especially if they are bleeding. And I know it might sound quite scary speaking to a consultant uncle, but generally this is an emergency. Um Any fever, to be honest with in any uh past orthopedic patient um who's on chemotherapy, that's an emergency and you wanna get seniors involved quite early on. Um So don't be afraid of that. Have you guys got any questions up until now? So she's gonna move on. Um So I think we already discussed that. So pit were quite common chemotherapy and you only really start to worry if they either had a significant drop that you're not expecting or if they start to spike a fever, get unwell um using um quite high because then it neutropenic sepsis. All right. Moving on. So, the next one is 82 year old woman presenting to AM U with a cough. You assess her, you find that she's confused. Um, she was recently started treatment for a chest infection for by her GP. And she's got a background of heart failure and asthma look her blood from today morning and that's what you find, what things strike you from these bloods. There's a couple of things. Yeah, definitely raise CRP should make you quite worried hypernatremia. Yeah, we always worry about hypernatremia and if it's especially if it's acute hyperkalemia. Mhm 3.1. All right. Thank you for everything and just looking at her creatinine that's also quite raised. No albumin, well done and lymphocytosis. Yeah. And the last thing is the AP is raised. So just going through with that systemic systematically. Um So the first thing, why do you think the white cells is raised and why do you think, what do you think we should do about it? Because bear in mind she is already on some antibiotics for that was started by her GP. Mhm. Yeah. Perfect. So probably either she acquired another infection. So it could be either chest infection, ear infection, skin infection, it could be something else. The dose is ineffective, right? It could be according to weight, whatever treatment the GP has given is not working or it could be that we're treating a bug that is resistant to this antibiotic. Um, so what would you want to do at this point? So usually at this point you wanna check what antibiotics they were on. How long have they been on for it? Have they ever had previous chest infections? And what did they take? Um cause usually whatever works for them would work for them again. Blood cultures well done. Um So blood cultures, you wanna send a urine sample. So basically, you're just doing another infectious. Yeah, basically you're doing another infection screen. Um So send the gene that well done cause we had a case which was quite recent, quite similar. And then when um he came to hospital, once we took more history, we found out that he was recently in China, stayed in a couple of hotels and he was V positive and that's why the antibiotics were not working with him. So it's always, especially with um a chest infection. You wanna ask, have they been anywhere else recently? Um And even though it's a low risk, it's always there. And once you've done all of that, you wanna either add another antibiotics, which is broad spectrum because you haven't got any blood cultures or increase the dose or speak to the oncom microbiology, especially with patients who's got, for example, background of bronchiectasis, background of CO PD, they've probably got previous cultures which you can um start antibiotics using that. Uh But you want to speak to the microblog just to make sure um moving on the C RP. So CRP is usually raise the infection. But as you guys know, CRP and AP are acute phase react reactants. Um And with CRP, sometimes it lacks with, it lasts about 24 to 48 hours. So if you find that the patient, your patient is getting better, the white cells are trending down, but the CRP is increasing or statin don't, don't get worried cause sometimes it just, that means that the CRP has been lagging. So you don't need to worry too much about it. The other thing in this patient is the creatinine. So with C you need to be quite careful to look at the trend because this could have been just his baseline. Um or this could have been an AK and um with AKI, you just need to make sure that you're looking at the creatinine rather than the urea cause sometimes, especially initially in a one, sometimes the urea is normal. So always remember to look at creatinine. Um And in his case, you'd ki or in her case, sorry, you'd kinda expect that um the Akis would be a prerenal ache. I just because she's been unwell, not drinking a lot and generally um, older patients are not a big fan of water so they do get achey quite easily. Um, other thing is hyponatremia. Why do you think? And you look at her previous trends and you find out this is a cute drop. So, usually she runs around 148 and now it's 127. Why do you think she's got hypernatremia? Any thoughts? Mhm. That's a good, that's a good thought. So, it could be si DH what else, what else can, could give you quite acute hyponatremia antibiotics. So, medication. So we're gonna speak a bit more about hypernatremia cause I think that's one of the things that I really um was confused about, especially during med school and when I started, I seen a lot of hypernatremia, especially acute ones and I started surgery. So as you guys know, and everyone knows surgeons are not the best when dealing with blood results, especially things like hyponatremia. So you have to deal with them quite a lot. Um So hyponatremia. So for her heart failure, yeah, it could be due to hydration or volume overload or things like antibiotics right side, we're gonna speak about it a bit later, but in this case, likely that it is dehydration just because looking at her creatinine that's raised as well. So you're kinda assuming that she has not been drinking enough causing an ache. I and that's a hypovolemic hyponatremia. Um you know, the potassium, the potassium is quite low as well. Main reason. So you're not with potassium, you don't get quite worried about them, you just replace them. Um, straight away you don't investigate why. It's so, because mainly it's, um, it comes from nutrition. So if you're not taking in enough potassium it's gonna be low. Um, I'll do it, do you know what I, in what cases we see? Low album. Mhm. Mhm. Well, then you guys, you guys are quite good. Mm Yeah. So I'll be in mainly we see it as an unwell patients, especially if they've been to I two their album really, really drops. So just the unwell patient, not eating, not drinking much. You're thinking about um low albumin and it's quite a good predictive value of prognosis. So the lower the albumin, the worse the prognosis is in patients um especially the elderly. So if you are treating this patient for quite a while, the keeps dropping, you can expect them to not have a good prognosis. Um but also things less common things to think about is nephrotic syndrome, liver disease as well. So if you've got liver disease that can cause low albumin overall. Um A LP that's an acute phase reaction. That's why it's quite raised here. Just gonna go through this. Yeah. So in this case, the confusion obviously is uh because of the infection. So the c is not resolving, it is causing patient delirium. Um and the hyponatremia, as we said, is likely due to dehydration. So another food chart cause you know why not. But um hyponatremia, the most important thing can hyponatremia is to check the fluid balance. So you need, if the patient, if you get um a beef saying that this patient is hypernatremic or you find that they drop their sodium, you wanna go and actually do a proper fluid review. Um If you find that you've got a negative fluid review, that's what we call hyperemic hyponatremia. So that's mainly from your eye losses. Um things like sepsis, per plate losses or um less commonly, but primary adrenal insufficiency because you are not um the body is not producing ADH and so um sodium is excreted if you find. So with hypervolemic, if you decide to do osmolalities, you're gonna find that you've got low serum osmolality because you've, you haven't got enough fluid in the body. Um You're gonna find that there is high urine as well and low urine sodium because you haven't got um enough urine to go through the kidneys as well. The other thing, the next thing that is um a bit less common than negative fluid. So, less common than hyperemic cartia is hypervolemic hyponatremia. And that's when the patient is very overloaded um to the point where the sodium is quite diluted and you see these in cases of congestive um heart failure, kidney disease and that common liver failure. So, in that case, you wanna start them on fura and initially, i it's quite scary because the patient would have an ache. I so usually they'd have an ache. I too, for example, low sodium and the treatment is not to give more fluids cause they're not dehydrated. But actually to give them furosemide an aggressive treatment of furosemide because the main reason why they get an A I is because of kidney hyperperfusion, not because they're dehydrated. Um So it is quite scary giving an AKI to patients like a hefty amount of fide. But this is the treatment. So always keep that in mind. The other thing, last thing is equal food. So if they're nogle, you wanna either think about si si DH or the other thing is drugs that's quite common. So you wanna pause any drugs with your eyes and psychotics. And the last thing you wanna do a CBG and take some lipid profile just because hyperglycemia um can cause hypernatremia as well cause it, it takes it out. So basically um the receptor, um basically more sodium is excreted in the urine with the glucose because um of the receptor and with S IH. So the bloods that you wanna take or consider is um obviously you're gonna send osmolalities for si DH. You wanna send the 9 a.m. Cortisol for add or any adrenal insufficiency. Um You wanna send the TSH, you wanna send the CBG as well for hyperglycemia. Um and that will aid also your diagnosis. Why has this patient got hypernatremia. And one thing is to be considered about is that severe loss of sodium can cause severe edema, which is a medical emergency. So you wanna escalate quite quickly and look for signs like headaches um and get unconscious all those G CS. And the other thing is if you're correcting sodium, either by giving other foods or by giving fide, you wanna correct it quite slowly. Um You wanna, you wanna correct it quite slowly. So, um we usually say that you aim for 8 to 10 millimoles per day and that mainly is to prevent central pontine um myelo um melanosis. All right. Any questions just let to speed up because I'm quite conscious of the time. Right? Next is NTS. So the one thing you wanna know is that, so LFT S, there are some LFT S that is related to the liver itself. Um So that's AST and A LT. And if they're doing sure thinking about things that affect the liver, like hepatitis, nonalcoholic, fatty liver disease, alcoholic liver disease. And the other thing to look at is the T and A LP. So that's more posthepatic. So mainly to do with the gallbladder. So the A LP is mainly to do with the gallbladder. If they got raised A LP, you think the colic cholecystitis depends on the symptoms. T is mainly related to alcohol. So, if you got a raised T you are thinking that they've got alkalis and with the liver, the matter of function is the first thing is the bilirubin and with the bilirubin, um you can divide it into conjugate and first it's nonconjugated, but you usually don't order these tests because they're very expensive to run. And usually hepatologists only um order them because it's gonna aid with diagnosis. But I as an F one, you do not need to really worry about them. The other thing is measuring the synthetic function is um clotting an albumin. So with albumin, it can drop quite quickly. Um as I said in malnutrition and all of that. But also if there is liver disease, that is quite a good um predictive val value or predictive test of how the liver disease is. If it's quite bad, then the other is gonna be low and so on and clotting. That's also a measure of synthetic function. And to be honest, you only see clotting abnormalities. Um once more than 70% of the liver function has been lost, which is quite a lot. So if you're starting to see closing abnormal, this patient is probably quite late in the liver disease, quite late stage of liver disease. So, um if you find any abnormal LT, especially AC and alt, you wanna check, you wanna do an ultrasound just to check for um hepatitis, you wanna check for enlarged liver. But also if you find there is a raised, you wanna check for gallbladder issues. So it's quite acceptable to do an ultrasound if you find any abnormal t especially if you've been repeating the test and it's not resolving. So just moving on to clotting. So the clotting cascade, um it's one of the easiest thing to forget honestly. Um It's quite difficult to remember, especially because there's so much going on. But basically, um the factors that are common, both extrinsic and intrinsic as factor five and 10. So these will get affected. Um if there is like things. So if things affect them, basically, you're gonna find prolonged PT and prolonged APTT, the other thing is you need to know the different agents affecting different factors and you need to differentiate between inr aptt and bleeding tongue cause these are three different things. So how I like to, to think about it. Basically, there's primary hemostasis, there's secondary hemostasis, primary hemostasis is basically the one where um you've got the factor V factor. Um And basically, it's just a temporary plug and then you've got the secondary hemostasis, that's the one involving all the clotting factors. Um And obviously, if you've got a liver disease that's gonna affect mainly the second secondary hemostasis. Um and any problems with clotting factors, even if you haven't got a clotting uh liver disease. So things like hemophilia a that's gonna affect mainly um either PT or a PTT. So one thing you need to know is Warfarin. So, Warfarin, as you know, is it causes a prolonged inr um because it affects um factor eight. The next thing is D IC. So D IC, uh basically, you've got a lack of lack of all clotting factors. So that's gonna affect both the inr and APT. But also you've got a lack of fibrinogen which what defines the IC. So you're gonna get a prolonged bleeding time. Um cause if you guys remember from um second or third year fibro is what holds the one fractures together. Um All the, basically the plug together. If you got Von Will brand disease, that's gonna be primary hemostasis. So you're gonna find that the bleeding time is prolonged if you got any hemophilia, um that's gonna affect um that I that's gonna affect the APTT just because the 89, that's mainly the um interesting pathway with early liver failure. Um That's gonna mainly affect the inr just because of the, the way the clotting factors are. Um APD is affected in late liver disease. So, if you find that the APD is prolonged, then you're thinking that's mainly um with progressing to endstage liver disease. Uh And with endstage liver disease, obviously, you're not gonna have enough as well. So that's the bleeding time is gonna be prolonged. Factor five and 10 deficiency. That's what is common between the tri and extrinsic um pathway. So, what you're gonna find is that the both inr and APTT is prolonged and the bleeding time is gonna be normal because the um fibrinogen is normal fibrinogen levels is normal with factor 12 because it's mainly affecting um the intrinsic pathway that's gonna be a PTT with aspirin. So, aspirin is an antiplatelet. So it stops the platelet sticking together for when the plug. So you're gonna find that the bleeding time is prolonged. Um And the IR and A PT are unaffected and lastly, heparin heparin mainly affects um the extrinsic pathway. Um So you're gonna find that the A PTT um, is, uh prolonged because it stops the thrombin. Um, from forming, uh, just put a little uh table down there. You can go through it. We're gonna send the side so you can, you can go through it on your own time. But basically which medication affects, um, which factors just because we're go running a bit late. Bye. Next case is 75 year old woman who presents to with shortness of breath. Um, so she tells you that the shortness of breath has come, come on suddenly she was climbing the stairs and then she felt hot, sweat clammy. Um, and she is progressively worse. Um, getting worse, especially that her breathing, she's not able to breathe quite properly. Um When you ask her if she's got any chest pain, she denies it chest pain. She does it collapse. And from a, from her history, you find out that she's a exsmoker for 20 years. So what can you find of these blood results? Yeah, we're just gonna, um, oh can you guys not see the slide? Can you guys see it now? OK. All right. Let me just try and figure out what's happening. What about now? But let me try that. Um Nope. Fine. It's so called and fine. Can you look? Nope. Right. II told. Do you wanna try sharing it? Yes, there we go. The perfect. We have been diluted. It's fine. Right. Um Right. If you guys can see the blood results now, what is um what's the abnormality in them? And what do you think is happening with this lady? Mhm Yeah. So I think someone got it. So it is pe so I think with this case it's quite confusing if it's a sty or a pe um I think obviously with a case like that you wanna rule out both but just be aware if the E CG is normal, it is likely to be a pe just because troponin is not specific. So even though it is specific to um cardio, it's, it is a cardiac mo uh marker but we often see it quite raised in P ES as well. So the is not specific um as well, but in P ES, we do see troponin rises. So if you find that the ECG is normal and you um you're less concerned if you find that the EKG is normal with ACR and a DDIMER R, you would wanna get a CTP just to make sure that this patient has not got a pe, especially with a symptom like this. So rapid onset of shortness of breath, feeling hot and sweaty, no chest pain. So you wanna just rule out, um, a pe as well and the cr um, can be normal in P ES but obviously in a patient like this, you wanna get an ECG testing before putting them through us counter, but just bear that in mind. Yeah. Right. I, yeah, so an end study would be likely to, that's why the first thing you wanna do is get an EKG. But the thing is if an ECG is normal and you're trying to figure out what you wanna do next, you'd wanna think the first thing is A, is A C TPA just because with P ES, we do in some cases, obviously, it's not the most obvious thing, but in some cases we do find AC rise which is very significant. Um But it's mainly because of the PE rather than an M I, but I'm not quite sure if we're gonna be able to go through these BGS just because I'm very aware of the time. Uh So we're gonna go through a BG straight away. Is that OK? Imat Yeah, perfect. Um So guys, we'll run through some ABG S just because um they'll be thrown you away quite often. Um And so just reminding you of the kind of the way to go through it because it can be a bit overwhelming when you've ordered an ABG and then a nurse is giving it to you and you're having to, to sign it off and interpret it. Um So yeah, we'll, we'll start. So, next slide, please. Um So once again, sys er systematic approach, it's what you guys have been taught. II know that you, if your final years, you would have done your final year of skiing if your fourth years. Um This is how they like you to do it. So you want to confirm patient identity really important. Um I've seen it on my ward where actually um we were panicking over the wrong patient. So it is worth doing. Um And in the end, it turned out it was OK because it was, we were already aware of that problem. So just make sure you check um patient identity, make sure you check whether it's an ABG or a VBG as well because that will affect how you're interpreting um the data. And then I think the most important thing and the thing that I didn't really think about when I was a med student is when you're looking at it, you really do need to think about the clinical context and think what, what are you looking for? Whereas before I'd be so used to just interpreting it, figuring out and then fitting it to the clinical context. So I think kind of in f one, what I've realized is changing the way you think about it um really helps. So the way that I like to do it is looking at the oxygen first with an ABG, then I look like to look at Ph, then I look at the CO2, then I look at the bicarb, I figure out if there's any compensation and then I look at the other results. Cool. Next slide, please. Um So yeah, other things to consider as well, which especially if you're on call and you're getting bleak to see a patient who you might not necessarily know cos you're covering all the medical wards is always worth flicking through and just checking the, the er obs charts to see how much oxygen the patient's on cos that can kind of give you an indicator to how severe you think it might be. And also if there's any previous ABG S or VV GS because you can, then once again it can, you can help figure out how severe it is and also allows you to think about just even before you see the ABG, like whether you need to escalate it or not. Next, please. Thank you. So case one. So Tom is a 65 year old man who was COVID positive. He's er, presented to Ed with shortness of breath, er, he's not on any oxygen. Um just starting off quite simple with looking at this um ABG. Does anyone want to chalk some interpretations in the chat? Perfect. Yeah, type one. Respiratory failure yeah, you guys have got it. So once again looking at the oxygen, you can see it's less than eight. So type one then looking at the ph is within range, uh looking at the CO2 er it's in range and the bicarb is fine as well. So yeah, type one respiratory failure. Um So what would you do? Um what would your management be? I track him on some oxygen. That's the first thing I would do um because you can see his oxygen is low. Perfect. Next slide, please. Perfect. Next one. Give him some oxygen. There you go. Uh Next one. So hypoxia, so kind of the causes you need to think about is kind of three broad categories. So not enough oxygen in the alveoli, you wanna think there could be increased effusion distance. Um So thinking of things that could be in the way. So like pulmonary edema past fibrosis and then uh lack of perfusion. So a pe emboli um and they're kind of your three broad categories. Next slide, please. Perfect case two. So um Nigel was admitted to hospital with shortness of breath and requiring 60% of oxygen via the TUI mask. So he's had an ABG done. That's his ABG on the side. Um What do we notice? Well, oh, sorry guys. Um it's, it's there. Um So no worries if you're not typing away, but the O2 is in range. But what you need to remember when interpreting this is that he is on oxygen. So of course, it would be. But um if you look at the rest of it, it's all looking. OK, if we could add the next slide, please. So later in the evening, Nigel is now on 15 L of oxygen via a non rebreath mask, he sat up in bed appears scared and has shortness of breath with a respirate of 40. Um So you, that's his ABG. Does anyone wanna give me a few interpretations? Tell me what they're thinking. So, would you, would you be worried if you got called to, to see this patient? Yeah, exactly. So um you can see that the o oxygen is low. So it's at eight. You're looking at the ph you've got alkalosis. Yeah. Um Do we think it's compensated panic? Yeah. So you would, you would feel quite worried cos he's on a non reb you can see that um there's not been any conversation um looking at the bicarb. Um So yes, you would panic at this point if I got shown that I would be escalating this to a senior. Um because you would be considering what would you be um considering you'd be considering N IV and kind of even potentially talking to itu So that is kind of beyond you. And I would at this point if I was um on and on call, I'd be talking to an sho or med reg. Um Next slide, please So an hour later, Nigel is still on 15 L of oxygen via a non rebreathe mask. But he's lying back in bed and appears more settled with a respirate of 25. So before his respirate was 40 now it's 25. And so the nurse has just bleeped you to let you know this. Uh, would you, would you be, uh, could we go back, could we go back slide? Um, would you be worried or would you feel more reassured? See, and this is where you need to have a think because if someone is, I would feel, you know, your gut instinct is to feel more reassured or more response is coming in, more worried. Exactly. Could be tiring. Exactly. So that's something to look out for, especially as well in patients with asthma. Um It's really important. So what you would do is go back and get an A VG which we have on the next slide and here you can see that the O2 is much lower. Um And he's tiring. So, yeah, everyone, you, you are right. Um You can see that because he's tiring, he's stopped hyperventilating and blowing off the carbon dioxide, which is what we had in the ABG before this. Um and his ph is normalizing, but actually this is where he, you should be most worried. And hopefully, before we've even got to this point, we would have all gone and seen the ABG and we would have escalated appropriately and this patient should be um wouldn't be on our kind of just on an F one level would be being looked after by a more senior team. Um Next side, please, so actively dying of respiratory failure. So this is just something to, to kind of keep in mind. Um Not to scare you guys. I actually have not come across that where uh a patient's actually dying from respiratory failure. Um because usually we'd everyone you would see that first ABG and you would escalate appropriately. But I think that this case is quite nice just to remember um to also look back and look at trends. Cool. Next case, please. So case three a morbidly obese, 70 year old woman with chronic back pain is admitted with a fall and an AK I she is on room air. So does anyone want to have a go at interpreting this? Yeah. So you've got respiratory acidosis. Yeah. Any other interpretations? Yeah. So there is some compensation. Yeah. So you can see that we uh they are acidotic. Um You know that it's a uh type. Exactly. There's um it's a type two respiratory failure. But one thing to always remember when looking at bicarb is that when there's metabolic compensation that takes a while. So that usually if you can see a bicarb that's changed so much that suggests that there's a chronic element to the case. Whereas when you're looking at uh respiratory compensation. That's more quick because we can change our breathing and regulate our co2 much quicker. Exactly. So, if we could have the next slide please, that's what we said. So, hypoxic, we've seen the acidosis, we know that it's respiratory. You've got the high bar uh bicarb partially compensated in the next slide, please. So it's acute on chronic type two respiratory failure. Um So um just up from the case vignette, does anyone have any guesses as to what could have caused this, if I say the back pain? Um is the hen O HS. What does that acronym stand for obesity, hyper fine. Um So the obesity, yes, when you're so big, it is more difficult to breathe, you're unable to expand your lungs as well. But what this Vignette was getting at is the chronic back pain. You, you are gonna have to take some leaps with me here. Uh But if we were to have taken a history, we would have found that she's really been struggling with this back pain for a while and has been using opiates to try and help deal with this. Um And that has caused um a bit of respiratory um depression with obesity, hyperventilation, which has caused this picture. So to treat uh we'd look at trust guidelines, we'd potentially need to use some naloxone to um reverse the opiate overdose. Um And she's got an AK I, so we'd like to give her some fluids, treat that um and support with ventilation if needed. Uh, which fab ok. Next slide, uh, respiratory acidosis. Sorry guys, I'm speaking so quick, but II appreciate that you've all probably got evenings to get to. Um, but important to think about as well and I think that bottom bit with anything that reduces ventilation will cause respiratory acidosis. So things like thinking about drugs, that's, I think most common thing to look for. Um, and it's something I think you get into the practice of uh in F one is often if you look at the drug chart, you can usually find um a course for what's going on. So if you're ever lost and you're thinking, I can't make sense of what's going on. Have a look at the drug chart um and see if that can help you C NS disturbances neuromuscular disease, chest wall problems, just things to, to consider next slide, please. So, um this is compensation. We've already kind of discussed this. Um So conversation will not er overcorrect at best. It will make the ph just within normal range. Uh restrictor conversations, fast, metabolic conversation is slow CO2 level above 7.5 will not be achieved by compensation. Next slide, please. And then I think this is my final ABG um slide. So in the last case, even so a 23 year old woman is admitted with abdominal pain and reduced consciousness. Um So this is her um ABG. Does anyone want to give some interpretations. Um And we'll just come to your child. You will come to your question at the, at the end. We'll just fly through these quickly if that's OK. OK. So we've got DK A, we've got metabolic metabolic acidosis. What's made you say? Um DK A Yeah. So this is Yeah. Yeah, exactly. Um So always consider uh DK A, it's the ABDO pain, the young lady. Um But yes, so the oxygen fine ph we can see uh acidotic. You've got the um low bicarb and you've then got the, the partial compensation um respiratory conversation going on as well. Next slide, please. Um And then here's just a little bit on a anion gap. Um So anion gap uses um oh it says Albumin there, the ano and gap equation I use is the sodium um potassium and then using chloride and bicarb ignore the albumin. Um And the way I remember it and I'm sure you guys will know it. Um I see the positive minus the negatives. Um So always worth sometimes calculating if you're a bit stuck and you're looking at an A VG or you want to impress your med reg. Um So if you've got a rose ano gap, it's from excess acid from somewhere. So, keto acids, Lactic acid. So in that last case, we'd have a raised anion gap. So if you're thinking it could be a DK A which we've got a L er someone with reduced consciousness. We'd wanna check their ketones for sure. But we can't get a um a history from them. So, always worth looking at and then um exogenous. So methanol poisoning, salicylate overdose. And then if you've got a normal gap, think loss of bicarb. So gi losses uh high output stomas on gastro, I saw a lot of that. Um Fischer's diarrhea could be renal, um renal losses of bicarb drugs and then inability to properly excrete acid renal acidosis. So, next slide please. And finally, um there are other bits of information that you get on an ABG as well to look at. So hemoglobin, um I know that mentioned it earlier when we were going through the first case, uh potassium, you want to look at glucose, you can look at and lactate as well is also quite important to look at. But also um the kind of ABG S usually are used more often when you're, when you need to look specifically at um oxygen. Um and next slide. Oh summary. So um just some key points. So if you wanna take it away and I'll have a look at the questions while you're speaking. Yeah, I think um just because of time constraints, shall we just answer the questions and the sides are gonna be sent out anyway. Um So what would rasp compensation l to a metabolic alkalosis look like God, that is taking me a second. So,