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Good morning, everyone. My name is CJ. I'm here with you from the FT SS East Midlands and welcome to day one of our M Sra Prep series. Today, we're gonna have five sessions on clinical topics of respiratory cardiology, opt out ent and palliative care. Our first session will start in about five minutes uh which is respiratory commonly presented by Doctor Tau. Um For this session, we'll do questions at the end of the session. Uh You can put them on during, on the chat or at the end, but we'll read them out and they'll be answered at the end of the session. We hope you find the day useful. Um Our speakers today are kindly given up their Saturday time to come and uh help you. So please remember full feedback at the end of the day. Uh We put a poll on just out of interest to see which areas you're interested in. OK, I so just give people another five minutes to attend. Ok, good morning folks for anyone who's just joined us. Uh Welcome to the FDSs Emm Sra Prep series. It's day one. We'll be starting our first session in a minute, which is respiratory currently presented by doctor. Uh We'll do questions for the session at the end. Uh If you have any dear and you can put them on the chat, but we'll read out questions at the end and that's when they'll be answered. Uh We hope you find the whole day useful. Uh Please remember to fill feedback forms at the end. All right, I will hand over to doctor Dafu. All right. Thank you very much. Good morning, everyone. I'm happy to be with you all today. My name is uh Victor Epo and I am uh a specialty um doctor at uh the Sherwood Forest, uh NHS Foundation Trust in the East Midland. Uh I've been asked to talk about uh I have blood gas and uh at the end of it, uh I'll be talking briefly also about uh pulmonary embolism. I hope we have some time to discuss briefly about that. Um uh It's I II would like to make it more of a, an interactive session. Uh However, unfortunately, I can only see my slide right now. So, I mean, I don't know what is happening at the background. So just in case, I think uh I can hear you though, I can't see, you know, I can, can I see uh anything anyone is typing? So just in case. All right. So uh I'll be starting with uh arterial blood gas. Um arterial blood gas is uh well, our clinicians are very familiar with that. Uh, it's one of the very useful, uh, investigations that's, uh, as carried out in, uh, most acute case, uh, units of the hospital, virtually all departments depending on, um, what goes on there though. And, uh, it's very important because, uh, it just helps to give, uh, an idea about what's going on with our patients. It gives it, uh, some information about the clinical state of our patients and, uh it's also very uh easy to get the results done. You can have it within a few minutes. And so it's uh very, very helpful because uh especially in the emergency uh situations where you want to quickly know what's going on with the patients, even though clinical acumen is important or you want to have an idea of what's going on uh within it can also help you. And as such, you can get the result within a short time. So uh this is just uh a short uh a, a brief uh summary of uh some of the parameters that are contained in the blood gas um resort. So a blood gas and ABG arterial blood gas is very helpful because uh it tells us, first of all, it gives us an idea about the acid base balance. Uh you can uh get to know about what's happening with respect to uh any acid base disorder or disturbances. It also contains some other components that are involved in acid base uh with respect to uh acid base equilibrium. Now, it also gives us information on the body, the partial pressure of oxygen as well as carbon dioxide. And also we can also know the oxygen saturation was, we can also get to know about several other anions and cations which are often influenced by renal function. Now, uh because the uh process of obtaining uh arterial sample is quite painful and uh oftentimes it's also difficult. You see in most centers or Inoa department, we often tend to do more of venous blood gasses. Ok. Uh There's just a slight difference between both of them. Most of the parameters seem to be the same both for arterial sample and venous sample. However, arterial sample is more preferable when you want to know the level of oxygenation of your patients. So, uh in septic disease condition like COPD asthma, you want to be, you know how much uh oxygenation your patient is uh receiving. How are the tissues uh were, are the tissues were perfused? If you want to know more about that, it's often uh preferable to do an arterial blood gas or in all, in most cases, venous blood gas does give similar uh uh results to that of the arterial blood gas. So, uh if we can also get information about hemoglobin, most, it all depends on the type of analyzer you're using in your center. Some uh analyzers have ability to give uh tell you about the hemoglobin concentration hematocrit, carboxyhemoglobin. Some also talk about it uh contain glucose and lactate as well. So several of that also contain several. They have lots of electrolytes could get results about some electrolytes as well. So, uh these are the normal values. We are, we are familiar with this. A lot of us, we all know about the most. I'm not gonna dream so much on the pathophysiology and all of that about this. But we're just, we're gonna deal more with some uh clin care scenarios and then talk about how we can easily manage uh certain cases that's got to do with some acid base disorders. So, uh Ph oftentimes the the normal value is between 7.35 to 7.45 and the partial uh the partial uh pressure of the, of the CO2 in the arteria uh sample is often between 4.67 to 6.0. Some of these values don't vary. It all depends on other times the analyzer. So most times the result does come with um the normal values as well. So if there's other times where you getting, when you get your result, you are for seeing the normal values at the side of it. So we also have the arterial, the partial pressure of uh oxygen, which is 10 point, which is often 10, most times you told is 11 to uh 14, but sometimes of time. However, any patient who gets above 10, it's uh said to be well oxygenated. All right. Um And you know, this also uh matters the partial pressure of oxygen uh is important, especially for patients who have been oxygenated. So, uh oftentimes it is said that uh for every uh for every patient you should look at if the patient breathing in room a for a patient who is breathing in you room a it is expected that the uh partial pressure of oxygen should be greater than 10. Ok. Oftentimes you know, you know, uh in room A your 21% of uh is oxygen. So 1010 minus 21 gives you 11 so often. So it definitely means that if a patient is taking in room, uh the partial pressure of the oxygen in the arterial sample should be greater than 10. All right, 11 upwards should be taken as normal. So if you, if you or a patient is receiving uh supplemental oxygen, this it also depends on the uh the delivery method. So if your patient is receiving uh supplemental oxygen by from high flow uh meter, sorry, if, if probably you're using uh bug, uh your um no arial mask which delivers up to about 80 to 90% of uh I say 60 to 90% of oxygen. You will definitely expect your oxygen to start the partial pressure of your oxygen to be high. A lot higher than 11. All right. So even if you're getting 11 or for 12 or 13. For this patient, it does that is as much as that is taken to be a normal, the normal for a normal patient for this patient who is receiving 60 to 90% of oxygen, it is expected that the oxygen saturation should not be less than 50. All right, because I'm using a range of 62. So if a patient is receiving 60% oxygen, 10 minus 60 should therefore means that the partial uh pressure of the oxygen in the arterial sample should not be less than 50 often times in a better of you have the partial pressure of being less than that of the arterial sample. Uh Like I mentioned earlier, it's very, that's very important in certain patients, especially those who often tend to have some airway uh re restrictions. OK? Is uh some disease condition that has got to do with airway uh restriction? All right. So now the bicarbonate as well is 23 to 28. Uh Can you all hear me please? EMA Treta. Hello. Yes. Yes, we can hear you. All right. So like I said, I can, II don't know exactly what's happening on on the main page. So II can always see my slide at the moment. So I'm just gonna be checking just to be sure everything is going on. Well. All right. So, and uh please uh like I said, uh it's gonna be interactive at some point. So uh when we get there. I would like to get some feedback. OK. So the base ss the base is often uh important. Now, something that's important to mention here is that uh there is the respiratory component and the metabolic component to uh acid base uh balance. Now, uh the respiratory component also comes from the C two. So we all know we are taking uh CO2 is uh is, is produced as a product of uh uh metabolism. OK? And now it needs to be taken out of the body. All right, they are, of course they are the lungs. Now, the the CO2 partial pressure of CO2 is responsible for the respiratory component of the acid base uh balance. While the uh bicarbonate is responsible for the metabolic uh uh it takes care of the metabolic uh component is a metabolic component of acid base balance. Now, and that has to do with the kidneys. The uh kidneys are responsible for the, we all know it is is it ii don't want to go in deep into the physiology of acid base balance. But if you can remember very clearly, you remember that there are lots of uh in acid base balance, there are several components to it. OK. The kidneys play a role as well by um by the help of the bicarbonate. Ok. Now, the bicarbonate is uh takes care of that. And now we, when we talk about base SSS, oftentimes that has to do with the metabolic component. So base ss comes into place when whatever disturbances or the disorder we're dealing with has to do with a metabolic component. So if for example, you're having metabolic acidosis or alkalosis, then it definitely means that the base excess is gonna give you an idea of whether you are having an excess of the bicarbonate or you're having a deficit of that. And the anion gap also comes in, in uh in uh the metabolic component as well. Often times helping us to know whether you have helps to give an idea of, of what the possible cause of the acidosis is. Now, um Let me just quickly. OK. There he has a bad uh equation. I'm not going to ask so much about now, let's just really talk about how do you identify when you're faced with a question with the scenario? How are you able to identify whether you're dealing with uh uh a a metabolic disturbance or a respiratory disturbance? Oftentimes we all know that uh the ph the, like I said, the normal PH is 7.35 to 7.45. So when there's a decrease in the uh ph, we're talking about acidosis, all right. It simply means that we're dealing with acidosis. And then when there's an increase beyond 7.45 we're dealing with aosis. Now, how do you then know is this, what's responsible for this acidosis? Is it a respiratory component or it's a uh metabolic component that then depends on the bicarbonate uh uh concentration as well as the uh partial pressure of the C two. So I, when you have an increase in the uh partial pressure of uh carbon dioxide, well, you have an increase in the partial pressure of carbon dioxide and that automatically is gonna lead to a decrease in the Ph. And uh uh if you remember this uh equation, you know how that happens. Of course, when you have more of carbon dioxide, it's gonna the reaction is gonna shift forward and going to produce uh the uh weak acid like uh carbonic acid. All right. And so uh the PH is going to drop. OK. So you have your PH been less than 7.35. Now, that simply means that of course, because following this uh this uh equation is gonna lead to the production of more hydrogen ions. Of course. So we just all means that the concentration of the hydrogen ion is going to increase and that is going to give you respiratory acidosis. So, res respiratory acidosis, you have a low ph and you have a high uh partial pressure of uh CO2. In most cases, the bicarbonate may be normal. However, uh with respect to the uh uh in acid base balance, the bodies tries to normalize any change in the PH. So when there is an increase, when there is a decrease in the Ph, the body system tries to annul that change. And how does it do that? The, the kidney is a metabolic component could kick in. All right, the metabolic confident will kick in and try to uh eliminate that change. And how does that happen that often happens by an increase in the bicarbonate? But in this case, we have, when you have a normal bicarbonate, it simply means that there is no compensation. That's why compensation comes into play. So when there is compensation, it therefore means that the the increase in the, in the P CO2 causes an increase in the bicarbonates. All right, in a way to try to annul the change the increase in the uh CO2. And over time, this does happen, of course, you know, when uh if you remember the how respiration, the respiratory center is stimulated all times when there is an increase in the CO2, it does stimulate the respiratory center. Ok. And that tries to increase ventilation to try and uh expel the uh SS CO2 in the in the body. All right. And we also have the hypoxic drive. OK. Which often, in which case, the peripheral chemoreceptor help to also stimulate uh respiration. So all of that is in a way to try to balance the uh the ph of the body. So, in respiratory aosis, you have an increase in ph, you have an increase in ph and often times if the Respi the because we're talking about respiratory aosis, it means that that affects the respiratory components. And then you have the CO2 being low. So when you have low CO2, when you have the CO2 low, of course, that's going to translate to uh a lower concentration of the hydrogen ion. All right. And that oftentimes will lead to AKALS. The kidneys are also gonna try and compensate this. All right, the kidney is gonna try and compensate by helping to excrete more of the bicarbonate. Ok. Oftentimes this now, it is important to state here that metabolic compensation occurs over a period of time. All right, respiratory uh compensation happens quickly. All right. So that happens in the short term, it happens quite quickly. Meanwhile, for metabolic uh compensation, that takes a period of time, it takes several hours to days for uh metabolic compensation to uh take place. I'm just trying to run through all of this. So we can just go into some case uh scenarios. So we don't waste too much time. So now we're talking about metabolic acidosis. That's just a acidosis when it's acidosis. It simply means that the ph is low. You got low ph. And now we then determine what's causing it when we say it's metabolic. It simply means that we're dealing with the uh bicarbonate. So, bicarbonate therefore, will be sorry, bicarbonate would be low. All right. So we will have low bicarbonate and uh that translates to uh metabolic uh acidosis. The the lungs are going to try and compensate for this. Ok. So uh it's going to try and expel, it's going to try and also expel more of the C two. So as to balance up the uh the reduced ph. Ok. Well, if that's possible, then you can have its, it may succeed in bringing the PH back to normal. But when it's not possible, then it means what we have, there is just a partial compensation. Then we talk about the metabolic alkalosis in the same vein, we have a ph higher than normal, it higher than 7.45. And then um oftentimes because the meta one is metabolic, it means that the bicarbonates, there's an increase in the uh bicarbo concentration. All right, CO2 might be normal if it's normal. It means that it's uncompensated for. But when the CO2 also rises it in a way to compensate for the rise in bicarbonate. And if that succeeds, if it eventually corrects the uh a calloses, which therefore means that we brings in the ph to normal. It means that there is full compensation. It means that's a correct, it's a corrected P OO OK. Otherwise it becomes a partial compensation. So let's talk briefly about each of these conditions. Res respiratory acidosis, like we've mentioned earlier in respiratory acidosis, there has raised uh P CO2. OK. And there is low ph often times this is caused by an increased oxygen, oxygen demand. OK. Uh where you have uh uh increased oxygen demand in certain disease conditions. Ok. When there is increased oxygen demand, it means that it is not able to uh get rid of all the uh CO2, the body is unable to get rid of all the CO2. And as a result of that uh that respiratory failure uh results. Now uh remember that in respiratory failure, we have two types of respiratory failure and in respiratory failure, it is simply a failure of the uh the lung, the respiratory system to uh expel carbon uh dioxide. All right. And there are two types, oftentimes uh it may be due to hypoxia alone. In which case, there is a, there's not enough oxygenation. All right. And there is the body is able to be when there is not enough oxygenation and the body is is still able to get rid of enough uh carbon dioxide. That's uh type one respiratory failure occurs. Ok. And that occurs of cardiogenic or non cardiogenic pulmonary edema. It could also occur in pneumonia as well as pulmonary hemorrhage. All right. In this case, while you just have your have low uh oxygen saturation, ok. Partial pressure of oxygen is low, but the body is still able to expel the sss carbon dioxide that is produced. Ok. The body, there is an increase in ventilation uh which helps to expel the carbon dioxide when this continues. Uh If the if the uh level of hypoxia worsens, such that the body is unable to keep up with the uh the uh is able to increase ventilation such as to be able to expel dss carbon dioxide. Then type two respiratory failure cause. In which case, you have raised uh P CO2 and low CO2. OK. These are some of the disease condition where this is uh this often occurs. We have it in CO PD, we have it asthma often times there is uh airway uh restrictions. OK. That we have a neuromuscular disorders, drug overdose, chest wall abnormality like age, chest. All right, when there's uh inability of the body to uh to increase ventilation such as to be able to uh get rid of the SS uh carbon dioxide. Ok. That we now respiratory failure could be acute uh as well as or chronic. No. Uh like I said, I, when there is any change in ph the bodies tries to uh correct that and oftentimes the metabolic component kicks in. So, in acute respiratory failure, this occurs within uh minutes to hours. Ok? If the uh if there is no compensation from the kidneys where there is no renal compensation to uh arise to hypercapnia, then so hypoxia, then what you have there is acute respiratory failure. However, in the long term over this, when the kidneys are able to keep compensate for the change for the change, for the increase for the right uh drop in ph then what you have there is uh chronic respiratory failure. Now, for every rice for every rice in uh for every rise in the uh uh partial pressure of CO2. The kidney in the acute phase, the kidneys are able to, the bicarbonate level rises by about 1 to 2. OK. For every one rise in the CO2, the bicarbonate level rises by about 1 to 2 in the short term. Ok. In acute respiratory failure. However, a and as a result of that, you often have the ph uh very low in acute respiratory failure. So most times you have the PH being lower than 7.3. Meanwhile, in chronic respiratory failure, with the uh renal compensation, you often have uh the ph being higher than 7.3. So most cases you may have the PH of about 7.327 0.33. OK. In chronic respiratory fail, because over time, the uh kidneys are able to uh produce more of uh bicarbonate in order to uh bring, restore the ph OK. That often, of course. So uh that's for that. Now, um let's talk about respiratory callos, sorry, like respiratory alkalosis. Uh we have low uh bicarb um CO2 pressure pressure and often times this uh there is hyper ventilation when it's hyperventilation. Of course, the body gets rid of the SS uh CO2. Uh and then you have uh a, a deficit of CO2. OK. And then this could also cause this is could occur by uh some drug induced stimulation. So, when there's any medication that seems to uh increase ventilation, the rate of ventilation uh that could uh cause uh respiratory uh callos. So you have uh more co2 be uh released. And this of one very common um uh condition where this happens is anxiety and panic attacks. So, it is some patients coming to the hospital with um overcoming with chest pain. And at the end of the day, you do a blood gas, you can see that they've got, they've got uh respiratory callos that's quite common. Now, aci uh metabolic acidosis uh in metabolic acidosis, there is increased uh hydrogen concentration, all right, as well as increased bicarbonate loss. Now, I just, I'm just gonna run through all this. Let's just go, we need to go to uh the me now in in metabolic acidosis. Uh This is quite important, for example, uh purpose though that here with in uh metabolic acidosis, it is important to talk about anion gap. Now, the aio gap gives you an idea of what the possible cause of the uh metabolic acidosis is. Anion gap is often uh the difference between the uh anions and the CS. OK. Now, in most uh calculations, they tend to, to uh uh remove uh potassium. The reason is because the value of potassium is quite variable. So often times you have the difference just between the uh sodium ion and as well as the chloride and the bicarbonate ions. Now, we have high anion gap in which case that there is a higher than normal uh anion gap. And these are some of the conditions where this could occur. Now, this often occurs by due to a production of uh accumulation of organic acids. So if you look at all this, you find out that there are conditions that tend to lead to an increase in the concentration of acid. There is production of uh organic acid, different kinds of acid. Anything that uh leads to uh a breakdown of products that results in uh acid. An increase in the acid concentration of the blood would often lead to a high anion gap. OK. That's what happens in these conditions. Consider of them. A very important note is diabetic mellitus which case we have the keto acidosis in uh which is a complication of DM. All right. And in all the other uh condition and then you also have the lactic from tissue hypoxia. One very common condition is sepsis. All right, when you have uh uh decrease ation and the body is unable to uh come when there is anaerobic respiration of lactic acidosis occurs. And that's uh all of these lead to higher gap. There is often a an uh the C mode ps is often used to remember them using the uh the first word of each of the following courses. OK. So then we have the normal anion gap uh metabolic acidosis. Now, in this uh bicarbonate is lost from the gut or the kidneys. Now, when bicarbonate is lost, the body tries to correct this by raising uh the level of, of, of uh chloride to compensate for the extras that are there. And oftentimes this occurs in some of these conditions. So, this is often due to uh loss of bicarbonate from either the gut or the kidneys. So, these conditions will lead to uh metabolic acidosis. And uh talking about metabolic alkalosis here, you will have high ph uh raised uh bicarbonate or reduced hydrogen ions. This can also occur from that direct loss of hydrogen ions in gastric secretions. Uh for example, in vomiting and uh nasogastric suction. All right, this kind of even diarrhea as well. There is loss of hydrogen ion from the uh and then uh Kohn's syndrome. OK. Cohn's syndrome is another uh condition that could lead to that way. There is increase in aldosterone release, ok. That often consists uh hy uh as a result of that, there is uh increased in uh sodium uh reabsorption already and, and potassium uh excretion. OK. That causes hypokalemia which you often uh causes uh metabolic aal see hypokalemia as well. And in uh renal cirrhosis, OK. We also have can also occur from SS bicarbonate from uh probably administration of uh IV bicarbonate or ingestion of A AIDS. All of these can lead to metabolic alkalosis. All right. So let's uh do some discussions. Now, let's look at this uh case, I would like us to uh discuss this uh because I think it's uh we are preparing for example. So let's look at this condition. You have been asked to review a 65 year old man who presented with shortness of breath, which has been ongoing for three days. He is a non-diabetic hypertension and was recently diagnosed with COPD. His arterial blood gas shows the following. So, uh I'm just gonna explain quickly with this. Now, in looking at a question like this, the first thing you should look at is look at the ph, when you consider the ph what do you have? Is it acidosis or is it Akysis? So what do we have in this case, in this case? What do we have? II like us to interact. I'm not gonna, I'm not seeing anyone so I can't actually uh call any names. I like us to interact shortly. Let's, let's talk about uh let's see how we can get to answer questions like this. Hello? Can you hear me? Hello? Hello? I'm Ashley. Hello. Hello, Modera. Are you there? Hi. Yes, we are here. Uh Hi, everyone. You're happy to answer your questions in the chat and we'll pass it on to the, pass it on to Victor. Ok. 00, can they uh can you view, are they just viewing it? Can they have they got mics to talk? Uh I don't think they have mics but uh doctor if you will uh type on the chat box. OK. OK. Yeah, that's the challenge here. I've not got, if I have to go to chats, I have to stop sharing my screen. OK? I'm new to this. I'm new to this platform. So I really don't know. This is the first time I'm using it. So if I have to type it means that I have to stop sharing my screen and we can see the question. OK? I thought it was gonna be more uh we gonna be more of a discussion of this is all right. So I'll just continue then. OK. So, uh looking at this question, I really wish you could discuss because that's how I'm gonna be able to know that uh my audience are understanding what I'm saying. OK. Let me start share my screen a little bit and see if, but if there is any way I can do it such that I can see. OK. All right. Let me look at the chart. So shortly. So let me just look at the chart. OK. OK. OK. Sorry, I'm just trying to see what's going on. OK? You can't use your mics. OK. All right. OK. Uh So, so just give me a minute, let me just see if I can get into this with my phone and then we can cause I really like if we could be, if we could discoid, right? And just having to talk so I can get some feedbacks as well and know that will following. So just give me a minute, let me go ahead on my phone and then I can see what's going on here. All right. So, ok, we talk talking about that question. Ok. So unfortunately you can't see the question anymore. So just give me a minute please. I'll be here shortly. Ok. Ok. Ok. That's true. Ok, that's true. All right. So I think now I can, so I can interact with my phone. Look at your responses and then follow through. OK. So I'll share my screen now. All right. OK. Thank you. Uh So. All right. So I think I've seen some responses. Uh I tell everyone is saying it's uh respiratory acidosis. All right. That's fine. So uh what we have, what we've got here is uh you can see the ph the ph is uh 7.2 now, which is low and we definitely means that we're dealing with acidosis here. And then now look at the uh let's look at the oxygen uh uh PCO P CO2. You can see it's low, which means there's a problem with oxygenation in this patient. All right. And then uh if you look at the carbon uh CO2, it's 9.1 which is higher than normal, which therefore means that obviously this respiratory component is contributing to the acidosis. So, we've already established here that this is respiratory acidosis. Now, look at the bicarbonate. Is there compensation? Are we having any compensation here. What do you think? Are we having? Is there, is there any composition from the uh All right. No. Yeah, there is no compensation here. So uh we definitely miss that. Uh what we have here is uncompensated respiratory acidosis. Ok. We have uncompensated respiratory acidosis. Now uh now con remember in respiratory acidosis in this kind of patients, this is respiratory failure. Now, the question now is what are we having? Is it type one or type two? As long as there's hypoxia, sorry. As long as there there is hypoxia in this patient that's already respiratory failure. Now, what the question now is, are we having type one respiratory failure or type two? OK. Type two. So this is type two respiratory failure. Now, the next question is uh we have type two respiratory failure. Is this an acute respiratory failure or it's a chronic one other times, type two respiratory failure, most times it uh acute? Ok. So we see this is uh uh type two respiratory failure. OK. Now, so in this case, uh our base ss would not be uh necessary here as well as uh anion because this is not metabolic, the disorder is not a metabolic type. So this kind of patient. So what do you think we should do for this patient? This patient has got CO PD. All right, it's coming in with shortness of breath and it this has been ongoing for three days. Ok. And now it's got type two respiratory failure. Now, this kind of patient, what would we do? What do you think needs to be done for this patient? This patient you have, you have just received this patient probably in A&E and you've received this patient. What do you think should be the uh manage treatment of this patient? What would it be the first thing you would do? OK. N IV. OK, bipap, of course. OK. Do you, would you bother to try medical treatment at all or you go straight to N IV? Do you think this patient, you could try this patient on uh do you think you would try this patient on uh any nebulization or you go straight to an IV? Of course, of course. So you would rather want to try first and to see a give an hour to see if the patient responds to medical treatment. Well, in the hour when it doesn't respond to medical treatment often in the first one hour, then you, of course, you want to go straight to uh N I, all right. And bipap would be preferable for this patient. OK. That's fine. So I think uh we understand this. So this is uh type two respiratory failure. Now, let's look at this quickly, a 21 year old male presented to you in A&E with complaint of chest pain, which has been intermittent. He tells you that he believes that he is having a heart attack because his father had similar chest pain two years ago and died of a heart disease. His observations are normal and his ECG shows a sign of you decided to do a venous blood gas on him and the result is shown below. All right. So this is very common. You see a lot of young people, of course, fear several things causes them uh anxiety and then they come to the A&E often presenting with palpitations, chest pain, and sometimes shortness of breath. So this kind of, so let's look at this. What do you think? Now look at all the parameters here. What kind of acid base disturbance do we have here? Ok. Respiratory alkalosis, any contrary answer? All right. Respiratory A Akals. All right. That's fine. So first thing you look at the ph higher than uh no, which means that what we've got here is aosis. Now, this next thing to consider is what is contributing to the Akals. Is it a respiratory component or a uh metabolic component? So we'll look at the CO2 CO2 is low. OK CO2 is low, which therefore means that uh what you've got low CO2, that simply means that uh that's a respiratory uh uh the respiratory component is contributed to the Akals. All right. Now, let's also check the bicarbonate to see because remember you can also have mixed respiratory and uh metabolic uh acidosis. So the, the looking at the bicarbo, the bicarbonate is normal. OK. Which therefore means that uh firstly, it is not contributing to the Akals and also it is not compensating for the alkalosis. All right. So, in this case, uh what we have here is respiratory alkalosis. So we the base ss and the anion would not be contributing to this uh uh to this scenario. Ok. So, respiratory alkalosis. So what's the management for this patient coming in with him with chest pain and uh which has been intermittent and then he believes he's got heart attack and all of that. So what would you rather do for this patient? I think it's quite simple, but I want us to someone to tell it. Yeah, it's hyperventilation from stress. So what would you do? Your patient has come to you in A&E of course, you have to do something, breath in paper bag. Ok? Yeah, that's fine. I think Mary, reassurance would help this patient. I think Mary, if the patient is not in any form of distress at the moment, he says is what is just got chest pain all the time. Reassurance may just be fine. Ok? You may not necessarily need to. Ok, except if the patient has got all that. So I think this this kind of patient just need some reassurance that probably is as is worried because he believes he's having a heart attack. So reassuring this patient, I think will do uh good, good to the patient. All right. Now another question you are currently doing a rotational posting in the pediatric ward and a nine year old child have just been admitted into the ward on account of abdominal pain and persistent vomiting for three days. The registrar has asked you to do a venous blood gas for him and the result is as follows. So, um, what do we have here? What kind of disturbance have we got in this question? Ok. Metabolic alkalosis, metabolic alkalosis. That's fine. All right. Yes. So uh the PH is high and then uh we look at you, we'll look at to see which of the um what is contributing to, to the uh alkalosis. We look at it. Uh Co2 first CO2 is normal. So that's not. And then we look at the bicarbonate, bicarbonate is higher than normal. Now, often times you will also check uh it. Now it's uh with the that this is metabolic akos. Now you then check to see is there compensating, is the respiratory uh is there a respiratory compensation at all? There is none because the CO2 is still normal or oftentimes with AK calloses, you would expect an increase in the CO2 to correct for the increase in bicarbonate. So both of them, one easy way to know is uh increased increase or if there is uh an increase in in uh bicarbonate, the compensation would definitely mean that the uh CO2 would also increase. All right, when it's at a decrease in one of it compensation will mean also lead to a decrease as well. So if you have decreased CO2 for the bab to compensate, it has to also decrease, if you had a increase in C two for the bicarbonate to compensate, it has to also increase. All right, the same way, uh the opposite direction, the bicarbonate rises for the respiratory component to compensate for that. It also has to rise. Ok. Now, but in this case, we've got metabolic uh but we have got metabolic uh uh calloses. All right. So what would you do for this patient? This kind of patients coming in with uh history of uh abdominal pain and persistent vomiting come in with this. What are we gonna do? Yeah. Yeah. Oh I was all compensation. Exactly. That's very correct. OK. So what are we gonna do for this patient? What kind of, or what kind kind of conditions could cause this? Now, let's look at so now look in this kind of metabolic. Uh Now we've got me, OK. This is Akals. If you look at the base SSS, you can see we've got here plus three, which means that you've got SSS of the bicarbonate. All right, of course, you can see that there. So of course, you uh fluid electrolyte. OK. So you're gonna, of course, this patient has lost lots of uh electro. So you're gonna look at that and then, all right, look, think about what the underlying cause. Of course, you're gonna do your clinical examination and all of that, you're going to tell what the possible cost is and then manage accordingly. All right, obviously, where you correct the, the cost, the uh, the uh ph should be back to normal. All right. So we've got another case. You have just received a handover for a 65 year old woman who has been admitted to the medical assessment unit with chest pain and shortness of breath. She is a chronic smoker and is known to have type two diabetes and like two on examination, she has reduced breath, sound in the left axilla and dullness to precaution. Her heart rate is 104 BP is 145 of 71 restate is 28 and saturation. 92 on 2 L of bad minute of oxygen. You have just obtained a set of blood including an arterial blood gas with the patient on 2 L via nasal cannula. The result of the blood gas is shown below. Now, let's really talk about this. Now, for this patient who is on 2 L of oxygen via a nasal cannula. Now of time, nasal cannula, uh when you give deliver oxygen from via a nasal cannula, it also gives uh when it's 1 L per minute, it also gives 24 I think 24% it delivers 24% uh oxygen. So the F IO two is 24%. All right, at 1 L when it's 2 L, it means the patient is receiving about 28% oxygen. All right. And when it's 3 L, the patient is receiving about 32 and all of and then uh and so on. So it usually in uh you add four to each of them now. So for this patient who is receiving 28% of oxygen, you would definitely expect the, the O2 that is the uh partial pressure of oxygen to be at least 18. All right. But you can see in this patient, it is 12.9. As much as this is within the normal range. This patient, it tells you that this patient is not, no, what is happening to this patient is not normal. So it is an abnormality as much as the po pso two is normal here with respect to debate for this patient. It is not normal because this patient is receiving 28% oxygen. Is that right? So, so it's important to note that. So uh as you do not just treat the, your APG result in isolation, you also have to uh tie it with the clinical uh presentation of your patient. So in this case, let's look at it what we have here. So someone that you've already answered that uh OK, respiratory acidosis with metabolic compensation. So let's see, we have the ph our PH is 7.32. So let's see which of the components is contributing uh CO2 is 7.1 that's high. So which means that the respiratory component is responsible for this acidosis. So, we have respiratory acidosis. Let's see if the, if the bicarbonate is contributing, if for acidosis, if it's metabolic, if there's a metabolic component, you will expect a low CO2. But here we've got an increased CO2, which therefore means that the metabolic uh is not contributing to the acidosis rather, it is compensating for the acidosis. So, and you see that there is uh an increase in the bicarbonate. Now, however, unfortunately, the compensation does not correct the ph so what you have here is partial compensation. All right, the, the partial compensation of the uh respiratory acidosis. That's what we've got in this case. OK. And the patient is on this. So what do we think what could be causing this? Uh what could likely be the differential diagnosis for this patient? What are the differential diagnosis for this patient? Considering the uh the question, remember, this patient is a chronic smoker. He's known to have type two diabetes right now it's coming down with uh so now respiratory uh it's coming down with respiratory acidosis. Now, what kind of uh OK. We, we see this patient has not got hypoxia. So the CO2 is fine is normal. What we just got is just an increase in the uh uh in the uh partial pressure of carbon dioxide. So what are the differentials for this patient? What could this patient be having for the differentials? The what do you think this patient could be? What are the differential diagnosis for this patient? P EC O PD. OK. P EC O PD. So why do we think pe what in the question does suggest pe for this patient? What does suggest pe for this patient? We're just thinking about how we can reason any things. OK. What do suggests uh pe OK. What does suggests uh pe OK. Uh left pleural effusion. OK. Type one respiratory failure. However, uh we can see that our uh O2 is fine. Uh The patient is there is no problem with oxygenation for this patient, however, OK. OK. Chronic cause of metabolic compensation. OK. So I think this patient might be having COPD but it's chronic. All right, we can see this patient has been, I think this patient has COPD. I think that's be my, my guess for this patient, but it's chronic. So it's not really an acute pain. OK. So this kind of patient that has got chronic COPD, you will manage in a different way. OK. OK. So of course, first of all, you would usually want to uh try your medical treatment for this patient. So I think uh the best guess for this uh case would be COPD. All right. OK. So uh for P EI don't think uh uh except for the of course, the, the, if you follow the symptoms, the symptoms that's definitely one of the differential. You will not put that away considering the age and the, the comorbidities as well as the symptoms, the patient is coming with. He's also got a high heart rate. All right. So that's gonna be uh of the differentials. OK. Uh Well, I think uh considering the result of the bloggers, it is more in keeping with CO PD. All right, good. So let's look at the next question. A 79 year old man has just been brought to A I A by the AM crew with complaint of fever, shortness of breath, lethargy and vomiting. They have also noted that his heart rate is 113 base per minute and respiratory rate is 19. He is known to the urology team and is on long term urethral catheter. He is also known to have COPD left ventricular failure and type two DM. Your asked you to do an arterial blood gas as he suspects acute elation of COPD. Remember this, this reg has not seen this patient. All right. The result of the APG is as follows. So what do we have? What's is the um what's the acid base disorder in this patient? Metabolic acidosis? Ok. Any other, any other S OK. High gap. All right. Metabolic acidosis. All right. That's very accurate. Ok. Metabolic acidosis. That's fine. OK. All right. So let's look at it. Uh First of all, we've got uh a low ph here 7.29. So, uh so let's see which of the component is it respiratory or metabolic component that's contributing. Uh The RC two is normal, which is 5.5 and then bicarbonate, you see it is low. OK. So what we have here is metabolic acidosis and the metabolic acidosis one you have to find out is it, have you got what you've got? So, let's see. First of all, is the, have you got a respiratory compensation? There is no respiratory compensation RC two is normal. So it's not contributing. So it's not compensating. All right. So now we're res uh metabolic acidosis. It's important to know whether uh it is high anion uh gap, metabolic acidosis or what we've got is low. Uh It is a normal anion gap. So here you can see the anion gap is raised 32 higher than normal. So, what we've got here is high anion gap, respiratory acid uh sorry, metabolic acidosis. So, what is the differential for this patient? Consider the causes of the cat mod pies uh for as the, the possible causes of uh for these patients? What do you think? What do you think it could be DK A? OK. Has this patient? OK. This patient has got DM. So the DKA is one of it. Good. Yes, DKA. Yes, that's one of the possible uh diagnosis. All right, there's another very o there's another diagnosis which is also possible for this patient is also obvious from the question DK A. So which means that what did the register suspected wasn't co correct? Ok. So this register hasn't seen this patient, he's just been told and because of the history. Yes, sepsis. Yes, that's another very correct answer. Europs specifically, this patient has been on long term catheter. So he's at risk of eps. So I think these patients uh uh DK A is one important thing. But uh I would, but I think more likely this is more likely to be uh because considering your history of fever as well, it's more likely to be uh uh urosepsis, even though they are also setting uh things to features to suggest uh DK A as well. Of course, uh DKA, you would then need to check up what the uh the the glucose is as well as what the uh the uh the ketone is OK from the ketone and the glucose. You can then tell what it is. Ok. Even though bicarbonate is just borderline 15, which is often is, is the often cut off. So with the other ones, you can then tell. All. All right, let's look at the next one. A 22 year old female is broke A&E by ambulance with a five day history of vomiting and lethargy. When you begin to talk with the patient, you know that she appears disorientated and looks clinically dehydrated at present. You're unable to gain any further details, but the patient looks very unwell. From the end of the day, you gain IV acid, send off a routine panel of blood and come some fluids. You to check the patient's observation and she notes an increased respiratory rate, low BP and tachycardia. You perform an E PG on the advice of your registrar. The results are shown below. So, what do we have here? Uh We got in this patient. What's, what have we got? What's the metabolic disturbance in this patient? Waiting for answer. Metabolic acidosis with partial respiratory compensation. OK. Competitive metabolic acidosis. OK. So, OK, probably uh uh respiration, metabolic acidosis with compensation. All right. Metabolic acidosis with respiratory complication. OK. So let's look at it. So we have RPH is 7.3 which is acidosis and then we have OK, oxygen is often uh is fine. And now let's see which of the components is contributing. Now, we have what we have there here is we have uh uh C two to be 4.1. So this is not uh this would rather be a callos for it's that. So that's not. And then we have our C uh bon it to be 13. So which means that the bi the uh the bicarbonate is responsible for the acidosis. So, what we have here is what? Metabolic acidosis. All right. However, let's, so let's see if you look at the CO2, it's also there is a decrease. So when there is a decrease in CO2 and as well as a decrease in it means that there is a respiratory compensation. However, this compensation is not complete. All right. So, so it's partial compensation. That's if it's complete, it means that it would restore the PH to normal. All right, it is incomplete compensation of. However, the respiratory component, the respiratory component have tried to compensate for the uh low PH even though it wasn't complete. All right. So we have metabolic acidosis. All right. Which uh partial respiratory compensation here. Ok. So uh now let's look at uh the BS SS, what have we got here? We've got minus four, which is less. OK. Which means that we have deficit of, of bicarbonate. All right. And then let's look at the anion gap. The anion gap is normal. OK. So what what would then be the uh possible, what are the possible diagnosis for this patient? Right. With, well, now we are seeing metabolic acidosis. This is normal anion gap, metabolic acidosis. So what would likely considering the uh scenario? What are the options we've got? What are the possible diagnosis for this patient? Any possible diagnosis, possible diagnosis? Remember uh the uh remember the the uh the causes we explained earlier. So what would are the vomiting causes causing metabolic acidosis? Ok. So of time, like I said, uh for the patient, this patient has been vomiting. So now uh with vomiting, would you expect acidosis? What's the resistance of anion gap? Yeah. The relevance of anion gap is to give you an idea of what the cost of the uh of the acidosis is with high anion gap over time. The cost is due to a the production and increase in production of the of organic acids. Ok. So if you look at all the possible causes of, of, of, of higher ion gap, uh metabolic acid acids, you find out that all of them lead to the metabolism of some of them are due to the end products of, of all of them. That is if you look at the part of philology of all the condition that causes them, you find out that they all lead to the production of acids. All right, different organic acids. Some of them involve hyper acid, lactic acid, acetic acid. Uh OK. All of them lead to production of different organic acids in the bloodstream. All right. And all of these organic acids will lead to the high anion. Now, the reason why high anion uh production of acid leads to anion gap is that now for every acid that is produced in the body bicarbonate is used up. All right. So when you have an excess of acid, it means that you are going to have a deficit of bicarbonate because the the kidneys are going to try and balance up. Of course, the acid is gonna react with the bicarbonate such that it can eliminate, the body is gonna try and eliminate the acid. And in eliminating the acid, you are gonna have a shortfall of bicarbonate. That's what happens. OK. That's what happens with uh metabolic acidosis as more acids are being produced in the body. Because any organic acid irrespective of what kind of acid it is, any organic acid produced in the body will lead to the production of hydrogen ions. And this every hydrogen ions picks up a bicarbonate ions. OK? A bilateral ions neutralizes the acid. Therefore, you have a deficit of bicarbonate, which therefore leads to the metabolic acidosis. So, for high and metabolic acidosis, uh uh what you have done there is that you have organic acids produced. So if you look at all the causes all the cuts, mopi, all of them, you find out that they all lead to production of organic acids. All right. Meanwhile, in uh in uh in no and IG you rather have a loss, you have a loss of bicarbonate. OK? You have a loss of bicarbon, not necessarily that acid is being produced, but bicarbonate is being lost. OK. So that's the, the difference oftentimes it could be from like you have re uh rena tubular acid. All right, you have the type one. All right, where uh there is acid secretion and often times do you, if you look at the part of it also leads to bicarbonate loss? OK. And you have a type four as well. I think the type four has to do with aldosterone. Ok. Aldosterone. There is uh when there is uh uh a deficit, sorry, there is deficiency of aldosterone or resistance to the uh to uh the receptor become resistance to it. Ok. So, all of that. So that's actually the relevance of analoga. It does give you an idea of what could be the possible cause of the metabolic acidosis. OK. So, uh OK. We'll, we'll talked about this. All right. So let's look at the next one. Yes, as some time. OK. We're trying to wrap up on that. So, all right, a 53 year old man is seen in the respiratory clinic for chronic obstructive pulmonary disease. Follow up. He is known to have chronic CO2 retention and his oxygen saturation targets are 88 to 92% on examination. He chest sounds quiet throughout but with equal air entry or air expansion, the appearance of a hypa expanded chest and his oxygen saturations are 91% on air and arterial blood gas is performed in the clinic. All right. So what do we have here? What have we got in this question? He has a patient who is a chronic retainer. Ok. It's chronic. So you know what to expect. So what have we got in this patient? Type? Two respiratory acidosis? OK. OK. Anybody agrees with this. OK. So let's look at it. Uh If you see we've got uh ph 7.33 and then, OK, let's look at the Uh So, first of all, let's see what is contributing, we've got uh CO2 is high 6.1 which means the respiratory, there's respiratory acidosis. All right, how about the bicarbonate? Bicarbonate is not, is not uh low. So which means it is respiratory acidosis? Now, when you see these respiratory in, you look at the O2, OK. So the O2 is also low, it's less than 11 or less than 10 as well. So which means that uh that's OK. There's hypoxia there. So therefore, so what we have here is respiratory acidosis. Now, let's see if there's metabolic compensation. As you see, the bicarbonate uh uh concentration is also increased. So there is what there is some metabolic compensation. However, the compensation is not complete. All right. So there is partial compensation if, if that's what it is the acidosis. Ok. So we have uh metabolic uh we, so we have respiratory acidosis with partial uh metabolic compensation. Now, remember when there is metabolic compensation, it means that that is chronic when you have respiratory acidosis with metabolic compensation. That is definitely chronic because it takes days for the uh for the renal system to be able to compensate for uh respiratory acidosis. So which means that this has not occurred over a short period of time, this has been over a period. Ok. So, of course, you can see it from the question, you can already see that the patient has, is a chronic retina. So you see that that's the reason why there is some metabolic uh compensation in this patient. OK. So of course, it's over this patient. It is called CO PD. So uh you, the management would follow suit. OK. Let's look at this. We've got more. So, um a 37 year old male is brought to A&E following a house fire where he was trapped in his flat. He has no bone injuries, but he's drowsy with his G CS of 12. He is placed on high flow oxygen and his arterial blood gas analysis is shown below. All right. So what have we got here? I got here. What's the metabolic, uh what's the acid base disorder in this patient? Uncompressed acid respiratory acidosis. Ok. Ok. Metabolic acidosis. Ok. Metabolic acidosis and type one respiratory failure. All right. And look at it together. OK. So let's look at this. So firstly, we've got se uh the PH is low 7.13. So let's look at both to see which is uh contributing to the acidosis. All right, let's look at the CO2 AC two is normal. A CO2 is normal, which means it is not contributing to the acidosis. Ok. Now, let's look at our bicarbonate. We've got our low bicarbonate, bicarbonate is low, which means that what we got here is what? Metabolic acidosis. That's what I've got for this patient. OK. This is metabolic acidosis. So, let's see. Is there uh is there any uh respiratory uh compensation. No, there's no respiratory cause. The CO2 is normal. Ok. However, we can see that you see the O2 is low. OK. There is low O2. OK. This is low. So, of course, yeah, this patient is called hypoxia as well. Ok. So we can see that this patient just like someone has like listed type one respiratory failure. Yes, this patient has got type one respiratory failure, metabolic acidosis and type one respiratory failure. Ok. So what condition can this occur? So, what is the possible diagnosis for this patient was the possible diagnosis? This patient has been trapped in a house fire where he's been trapped in his flat. There was a house fire and he was trapped in his flat CO2 poisoning. All right, there's another one. What's the other one? What's your di di di differential diagnosis? How about sunnite poisoning? Isn't there a possibility as well? Rhabdomyolysis? OK. Why Abdom myolysis in this case? Um Why rhabdomyolysis? Why do we think there might be rhabdomyolysis could be even though it's possible. So, I'm not saying it's not, but what's, what's behind it? How can mid myolysis be contributing to this? Any other ques, any other contribution? OK. All right. So I think this is more of uh uh CO2 uh poisoning or C as well. OK. Now this, let's go to the last two. OK. It says muscle break the organic acid. OK. Uh oftentimes uh that would often cause, uh, anyway, rhabdomyolysis, most times will cause metabolic acidosis. More of metabolic acidosis. Yes. Yes. Exactly. That's actually what we've got here. Yes. That, so, that's correct. Yes. That's what, anyway, there was no bone injury. So that's why you would think less of metabolic acidosis, even though that's what we, what we've got here is you still have differential diagnosis. There may be other things to, uh, help. Of course, you could, you could do a CK uh creatinkinase to see if there's any, if you're suspecting that there's nothing wrong. If you choose to do that, it doesn't definitely rule it, rule that out entirely. All right. So let's look at this and I think this last two questions will lead to me to quickly talk briefly about pe and then we'll end. They. All right. So you have just received a cardiac arrest bleed for one of your patients in the ward. Your station team are in attendance and the reading on the monitor shows ap ea reading. One of the nurses have just handed you the result of bacterial blood gas for a sample from the patient. And it is as follows. So, what have we got here? This patient is in cardiac arrest. You have just walked in. I have meant that reation is currently ongoing by the resus team. However, as the, as the sho the nurse knows you very well, just hand your doctor. This is your uh this is the blood gas for this patient. And of course, you have to have a look at it and maybe just certify it before even if you have to hand to the team. So what have we got in this case? Mixed acidosis, mixed acidosis, definitely acidosis. Ok. So, let's see. So we've got a ph of 6.85. We've got uh oh, so what's contributing to the acid, the acidosis? Let's look at C two, we've got 12 very high. So that's respiratory acidosis. All right, let's also look at the bicarbonate. We can also see bicarbonate is also low, which means that the bicarbonate is also contributing to the acidosis. All right. And of course, if you look at the O2 O2 is also very low, which means we've got a combination of respiratory acid and, and what metabolic acidosis. So, this patient has got respiratory and um metabolic acidosis. Ok. Now, uh we would not say there is, there is no compensation. Actually, there is no metabolic compe for metabolic compensation. There would rather be an increase. All right. Yes. All right. So you're taking that out. So there is no metabolic compensation. When there is a metabolic a compensation for respiratory acidosis, there would rather be an increase in the bicarbonate component. All right. For um um the uh respiratory acidosis, you will have an increase in bicarbonate to correct that. So, what's the, what's are the differential diagnosis for this patient? What could this patient have the patient was in the ward and roughly uh he just had sudden cardiac arrest, no other details about the history. But just say, for instance, this patient had had surgery uh probably six days ago, had an abdominal surgery and then was in the surgical ward. And then this happened. What would be the most likely, what would you suspect? What would be the first thing that will come to your mind about discretion will be the first diagnosis that will come to your mind with this kind of result, it will come to your mind. Pe would come to your mind. Firstly, all right, cause especially for the this kind of patient. Yes, both sepsis and pe you could think about sepsis. Of course, we've not got more details about the uh other uh conditions. I I've just been, I've just rephrased the scenario to say that this patient has had surgery and has, ok. So you could still consider sepsis. Of course, you will check out other things. Ok. But one of time, the P ea uh pulmonary embolism often uh in cardiac arrest caused by pulmonary embolism uh is also in pless electrical activity, right? Patients often go to P So that's one thing that could uh capture that could easily make you suspect pe All right, somebody is asking a question at what range does it become missed when both uh bicarbonate and CO2 is low as opposed to compensated OK. Now, when, when back up on it is low, it is metabolic acidosis. OK. However, when CO2 is low, if it depends, it's this, this question would then depend on what the ph is. So if, for this question, you've asked the question at what range does it become missed when both bicarbonate and C two is low, as opposed to compensate. Now, when it depends on the PH, if the PH is acidosis and you've got low bicarbonate, it simply means that what you've got there is metabolic acidosis. All right. In that case, if CO2 is low, it means that there is respiratory compensation for the metabolic acidosis. Ok. Take note. So when you have both of them low, it will therefore, the, the first thing you to look at is to look at the, the Ph because if the Ph is alkalosis, then it definitely means that what you are having is respiratory alkalosis. If you are having bicarbonate low and CO2 low, it means that what you are having is Akals, right? But if the Ph is acidosis and you are having low bicarbonate and low CO2, it means that you're having metabolic acidosis with respiratory compensation. So that's, that's very important. All right, with M when you're having a missed, when you're having a missed acidosis, it therefore means that you would be having a low bicarbonate and a high CO2, there will be opposite. All right, for a mist, you will often have opposite. The, the bicarbonate would, could be rising and the uh the CO2 would be uh uh in uh decreasing. All right. Then, in that way, oftentimes you have uh missed, missed acidosis or missed uh Akals. All right. So, but when you have it, both of them low or both of them high check the ph, the ph will guide you as to what it is. So, the ph will give you an idea of whether it's an acidosis or an alkalosis first before you can then decide, check which of them is contributed to that. Uh And which of them is compensating. All right, let's look at the last question. OK. Oh, so we're talking about this patient. So what would you do in this case? So if this patient, this patient ha this happened in a war and this patient um uh in, in arrest is in arrest and you've just been informed and you've seen this is ap ea heart surgery and then this is the blood gas. What would be the, what would likely be the management plan for the exotic team? This is leading us to what we will talk about briefly. So what would you do in this case? Ok. CPR is still ongoing. All right, is still ongoing for this patient and you've got thrombolysis. Good. That's just what I want to hear. So you would need to quickly thrombolism this patient. All right, this patient will need thrombolysis immediately. OK? And that would be the Yeah, of course. Yes. First of all, this patient is in uh this patient is in arrest. So you, first of all need to achieve ro first before you think of moving to IC. So first of all, you have to uh first of all, get this patient out, out of uh this arrest, so immediately you trombol and often time when you tr like you need to continue CPR for at least 60 to 90 minutes. So in this kind of case, when you are suspecting pe you would need to trombol immediately and continue CPR for a longer time. All right, this is not the kind of patient you will want to stop CPR within 30 minutes. All right, you want to continue CPR for a longer time for this kind of patient. All right, of course, where you are eventually achieve risk, then you will need to move the patient to the uh intensive care unit. Of course. Right. And continue other management. Ok. So let's look at the last question. It, a two year old businessman presents to the emergency department, complaining of right-sided periodic chest pain and shortness of breath. He has recently returned from a business trip to China which involves 2 to 11 hour flights. His arterial blood gas on air is shown below. So what have we got here? So what I've got here, what have we got in this? What's what kind of uh disturbance is this. Yeah, I mean, what kind of disturbance, what acid base disturbance do we have here? Ok. OK. Complicated respiratory acidosis. OK. What else? What else we'll look at this shortly? Respiratory aosis. OK. Who has anyone? What is the answer? What have we got here? Fully compensated respiratory callos? Ok. Ok. Respiratory alkalosis. All right. OK. So let's look at it. So let's look at the ph first, what have we got? Uh PH is 7.45 which is higher than normal, which is Akals, all right. And this is normal. All right. And then, so let's look at the which of them is contributing to this. Uh So let's look at this. Look at the uh CO2 CO2 is less than normal. OK. So less than normal. However, now, yes, II brought this question for a reason. Now, if you look at this, OK, let's finish up with this. So your CO2 is, is less than normal. OK. Uh So if CO2 is less than normal, so we would normally then say that this is what respiratory alkalosis Co2 is less than normal. Now, let's look at, we can talk about that. Let's look at the bicarbonate. The bicarbonate is what is normal, bicarbonate is normal. But if you look at the CO2 CO2 is less than normal. And when you got low CO2, it does mean that there is a callos, however, the PH is normal. OK. Notwithstanding, notwithstanding, this is a case of respiratory alkalosis. However, you will say it is a fully compensated respiratory alkalosis, even though the bicarbonate is still normal. The reason is that of times when a ph is the, the 3.5 to 7.45 is usually the mid, the middle of both of that is often 7.4. So anything above 7.4 is tended towards a callos, anything less than 7.4 is tended towards uh towards acidosis. However, if you look at this, the, the CO2 is 3.5. OK, which is less than normal. OK. Which therefore means that of course, there is some Akals here even though the PH is normal. OK. So we would rather say this is a a even though there is no evidence of compensation cause the bicarbon is normal. So it's not doing any extra, it is just normal. OK. So this is uh a normal Ph, but there is some respiratory alkalosis. So it's a competitive respiratory alkalosis. All right. Now, considering the question, what do you think could be responsible for this uh gas? All right. I think someone already answered pe All right. So if you look at the question, this patient presented with le rightsided pru chest pain. So let's talk briefly about pe. So P EA uh what happens in pe is that in pulmonary embolism? Is that there is some occlusion, all right, of the vessels, uh the supply the lungs. Remember the like, OK. So, and often times there is a ventilation perfusion, mismatch. Ok. There's a ventilation, uh, fi mismatch. Remember for, uh, uh, air needs to come into the lungs. All right. And need to come into the lung, which is a ventilation and then it needs the, the blood needs to be carried to the alveoli where the blood in the oxygen in the, in the lung needs to get into the bloodstream and then carry it to the various tissues. All right. However, when there is a pulmonary em uh in pulmonary embolism, there is some occlusion. So you don't have enough blood getting to all the alveoli to take all the oxygen to the tissues. All right. So there is a problem with oxygenation. Ok. And one of the uh so it's important to mention here that in most cases, pulmonary embolism is one of the possible cause of respiratory alkalosis. Take note of that. All right. Uh pulmonary uh pulmonary embolism is cause, often causes respiratory alkalosis. Ok? It causes alkalosis. 11 of the reasons, the reasons why it causes alkalosis is that there is often reduced oxygenation. Ok. There is often reduced oxygenation. And as a result of the reduced oxygenation, uh the uh oxygen, the when when there is reduced oxidation, when you have low oxygen, uh partial pressure in the bloodstream, it is going to trigger the uh peripheral chemoreceptor which is going to try and help increase ventilation. So you have hyper ventilation because there is hyperventilation, you are supposed to have a buildup of, of CO2. Ok? Because you're not having enough oxygen to uh the there is the, the demand is there is less oxygen to meet up with the demand. So you would rather have more CO2. But as a result of the hyper ventilation, your body is able to get, get rid of the CO2. Ok. So you have, and that's going to lead to less CO2 in the bloodstream which will lead to the alkalosis. So, what you often have in pulmonary embolism is respiratory alkalosis. All right. So let's just really talk briefly about pulmonary edema. So, some of these symptoms just so let's discuss that. So what are the symptoms of the symptoms the patient will present with a patient come in with uh uh pulmonary embolism? What are the common symptoms this patient will come, come with? Uh of course, you have to take uh your history. All right. So if you see this, in this question, this patient has been on a long journey. All right, a long distance journey, 11 hours trip. All right. So uh that is one of the risk factors. So remember there are risk factors to pulmonary embodies. Ok. So the symptoms, somebody has mentioned sudden shortness of breath, uh chest pain. Ok. Yes, those are uh symptoms which patients could present with. All right, there may also be some uh nonspecific symptoms as well. Ok. So these are some of the symptoms patients uh, with, uh, could come with. All right, immobilization. That's a risk factor. Yeah, we talk about some risk factors. So you have risk factors that of this. So, uh previous surgery there are risk factors which could offer in most cases will lead to imma uh immobilization. Ok. So, so when you've got a patient who's coming with, uh, I've just brought it from the nice guideline. So when you're seeing a patient, so if, if a patient like this comes to your uh to see you, you see, you've got a patient is uh it is coming with right sided chest pain, shortness of breath. OK? And then of course, you're going to do your normal um examination, your clinical examination, you do your exa clinical examination and now you're suspecting that these patients got uh uh pe now, firstly, is this you have to talk about, are you dealing with a stable patient or are you dealing with an unstable patient? All right, the way you would approach a stable patient would be different where you are suspecting pe would be different from the way you would approach a unstable patient. OK. So let's look at this patient who is quite stable, this patient is quite stable. He just had got uh uh chest pain, shortness of breath and he's got a risk factor which is a long distance trip. OK. He's just had a long distance trip. So in this kind of question, what would you do? What would you then do say for instance, you are in A&E and you've received this, this patient, what would be the first thing you want to do for this patient? Having taken all the, the history? And let's say, for example, you've just done your, the nurses has done the observation and they've told you that this patient has got re uh p heart rate of uh of 115, 115. What would be the next thing you would do for this patient? Of course, the first thing you would do is to determine the two level uh well score, ok? Now you do the well score. Of course, you've got the we score here on the screen, on the right side of the screen, you do your, your two level uh pe well score and then see now if the patients got a well score greater than four, it means pe is more likely. However, if it's got a pe uh where score less than four points, pe is, is less likely. Now, there's something there, there's uh there is at this stage, there's uh the pe uh rule out criteria, the pe score. Uh it's, I think according to nice uh nice to of as much as they accepted, but they've not included it here because it's, yeah, there's still less evidence as to its uh to its uh its reliability. Ok? That's the reason why they have not included it here. However, if you've got uh there is also suggested that if you got a good clinical, you can use it in those patients who have got uh uh West score less than four. So you could use the P the pe score for patients who have got uh uh West score less than four. Ok? And with the pet score, you can actually tell uh those who are likely to the pe and that with that you can, that I think one of the things uh the P EO helps to do, it helps to reduce the, the level of uh use of uh uh of anticoagulation. It helps to reduce anticoagulation for our patients. So with that, you can actually tell those who have no risk who have no risk of uh pulmonary embolism. That's actually what it does. Ok. So someone has already suspected P eg vatic. Ok. So for this patient, so you've got a West score of if pe less than four, which means that it is quite unlikely. So for these patients, you will want to do ad diamant. All right, take notes that it is for those who have got pe less than four that you would do ad Dier for. You do not do D Dier. You do not need ad diamant for those who have got uh who have got a high risk of pe you go straight to uh if you can do CT pa immediately, you can go ahead and do it. However, if there is going to be some delay, then you are advised to start uh therapeutic anticoagulation while awaiting uh your CTP. OK. Now, uh uh for this patient anticoagulation. So what kind of anticoagulation would you do it usually uh used to be a lower molecular weight heparin. However, with the advent of do A, we often tend to use D these days. So you would either use Apixaban or revus depending on your trust policy. OK. So you would want to start these patients when you are not sure you can get your C TPA. If you're in a center where C TPA cannot be done immediately, you would rather want to uh to put this patient on start your therapeutic anticoagulation while uh awaiting C TPA. OK? And then for those who you have done ad dier form, if the D dimer is positive, in which case, now, if the in it, it depends on your, your laboratory for some lab over time, they tend to use a cut for 500. OK. Other times if your D dimer is more than 500 however, you have to correlate it with age, OK? For age greater than 65 you should correlate it with age. So if your, the age of the patient is uh we multiply the age by 10. So if the for example, for a 65 years old, for a 65 year old patient, you should have ad dimer greater than 650 for you to suspect uh pe or otherwise, if a 70 year, if a, if you've got an 80 years old woman with you and you've done ad Dier, the D diamond is 700 that does not uh increase the risk of pe. All right. So oftentimes you can do away with that result because for an 80 year old woman, the uh the, you would expect to have D dimer of 800 above. However, remember you can only use D dimer when you, when you have already used your well score to stage the uh that patient. So if your well score for that 80 year old woman already suggest that pe is likely you definitely will not do that. So if you are doing ad dimer, it means that you are going to correlate the result with uh the patient. So if the patient is 80 years old and DDA is 700 it simply means that that sense to rule out uh pe for that. All right. However, if you've got a significant D dimer, so if D dimer is positive, then you would need to then start anticoagulation if C TPA cannot be done immediately or have your C TPA done immediately. And it is also said, therefore, said that if your CDP CTP comes, becomes uh comes out to be positive or of course, with the diagnosis of pe, then you would offer to uh uh you will continue the treatment. Of course, you will continue that patient with. And I think currently you can put the treatment, the patient can continue dac, all right, can continue on or uh Atico over time for 6 to uh 3 to 6 months depending on uh whatever uh consider other risk factors. Ok. So you can then continue with treatment. However, if the C DPA is negative. All right, and you would then need to consider is DVT is suspected in, in this patient. If DVT is suspected, then you can proceed further to do a uh Doppler ultrasound of the uh leg. OK. All right. However, when you do not suspect any DVT for that patient, then you can simply stop uh any anticoagulation. OK. For that patient. So let's just talk about. So how do we, how about an unstable patient? What do you do for unstable patients? So what's the treatment of unstable patient? Let's just talk briefly about that. A patient who has come unstable and that's where you come. Uh We talk about massive pe. All right. Oftentimes you manage uh when you, when there's a high suspicion of pe in a patient who is unstable, oftentimes the treatment is different. So we've got treatment of uh uh the treatment for massive pe would be different for uh submassive P ei think I would like to stop at this point. So we don't go too far. I just wanted to just put a little bit of this. Ok. So I think that brings me to the end of my session. Yeah, I just wanna talk briefly about that. So, have you got any question so we can have some time for questions before the two hours elapses? Ok. We'll start with a ATL S. Oh, ok. A LSI guess you wanted to, right. We'll start with A S. All right. Most like A S, all right. Yes, you will start with A LS. Of course, Thrombolysis Embolectomy. Yeah. OK. You will want to, you would not want to go the route route. Even though some do suggest start, you will still want to that. Some do suggest that you still give anticoagulation. However, for that, for a patient who is unstable, you want to go straight to Trias to trolly the patients, there is some controversy about that. Anyway. All right. So any questions, any question from what we've talked about so far? Any question. So I don't know if I already have any questions I have not answered just in case probably in the previous charts. If there's any questions I'm here to answer any question. OK. No question. Hello, Morita. Hello. Thank you so much for that. It was right. Thank you. Thank you so much. Um It was great having you today. Thank you. Um We're just going to send the feedback on the chat, so please. All right. Yeah, that would be great. Yeah, that, yeah. And yeah, please do fill it up everyone. All right. Thank you very much. So I'll send you the slide up. Um Yes, please, please. That's great. Thank you. All right, have a great day. All right, bye everyone. Uh Please, everyone do fill up the feedback form because it will be really helpful for the presenters as well and we can improve on the sessions as well and we're planning on starting the next session which is cardiology at 1115. Um We're just waiting for the placenta to come online and we'll introduce you to them and we'll start off at 1115.