EP39 – Cerebral Blood Flow, ICP & Spinal Cord Perfusion | Anaesthetic Primary Topic | Neurophysiology & Pain | CT10

Hello guys and welcome back to count to ten. My name is Arnie and on today's episode we're going to be talking about a topic that is very important and core to neurophysiology and pain. The topic we're going to talk about today has been asked multiple times as SCQs and in the Vibe setting and why it's an examinous favorite is really because it has a significant clinical implication and the topic we're going to talk about is cerebral blood flow, intercranial pressure and spinal cord perfusion. Now if you go through Mac95 this topic has eight learning objectives that are attached to it but really they're all interrelated and we're going to talk about the core principles that hopefully help to connect the dots when going through these eight learning objectives. As usual we'll touch on some past SCQs at the end both from the ANSCA and the Kikim exam and hopefully once we back this topic down into its core principles you'll start to see how everything is interconnected and this will then make answering those SCQs and Vibers a lot more easier. So with that said let's dive straight into it. The first learning objective we're going to cover today which has four components to it is discuss the determinants and control log firstly intercranial and intrasponal pressure secondly cerebral blood flow and order regulation thirdly cerebral perfusion pressure and fourthly spinal cord perfusion. Now this is a huge learning objective and it really covers a few of the other learning objectives that are listed on Mac95 but the way I'm breaking this down is in two sections. The first section we're going to really focus in on everything that's cerebrally related. The second section we'll focus in on everything that's spinal cord related. Now those two things are interconnected but we have to tackle them individually for them to make sense as a whole. So in my head when I think of this topic I just think a bit as two LOs. The first LO is looking at intracranial pressure and cerebral blood flow while the second LO is looking at intrasponal pressure and spinal cord perfusion. So to start off let's first look at intracranial pressure. Intracranial pressure can be described as the hydrostatic pressure within the cranial vault. Now this is normally quoted between 5 to 15 millimeters in mercury and it has a huge variation in neonates the normal ICP will be much lower because the suture lines haven't been formed yet and they have open fontanelles and in the elderly their ICP will also be lower because of the normal atrophy that occurs with the brain with aging. Now apart from aging ICP also varies due to some normal physiological behaviors and these involve the changes in respiration, changes in blood flow, changes with coughing or sneezing which can transiently lead to ICPs being above 50 millimeters of mercury and all of these can be seen if you display ICP in a graphical format. When you display ICP in a graphical form the ICP wave is slightly different to the normal arterial wave form. Instead of being a bifid wave form which the arterial wave form is with two peaks the ICP wave form is a trifid wave form it has three peaks and these peaks represent firstly the arterial pulsation secondly and what's distinct to the ICP wave form is a peak that's related to the intercranial compliance and then thirdly the last peak refers to the aortic valve closure or the insusura. The key characteristic with the ICP wave form is if you start to lose that intercranial compliance that second peak starts to raise up and can actually fuse with the first arterial pulse peak. That's really as technical as you need to be when looking at ICP wave forms and if you're getting asked this in a virus setting I guarantee you are doing really well. Now before we talk about ICP and its determinants we should briefly touch on how ICP can be measured. This is more important for part two of exam but it's a good thing to know clinically regardless of whether you're starting in the part one or the part two. When we're thinking about how we can measure ICP there's two overall ways you can measure it. There's the non-invasive method or the invasive method. When we look at the non-invasive method this involves clinical signs and radiological signs. Within clinical signs these would be the classical things of nausea, vomiting, headache, changes in vision, altered GCS and at the end stage these would be things like a cushing's reflex. While radiologically on a CT you might be looking for signs of cerebral edema which might be a midline shift, a loss of that ventricle space or sulcal effacement. On the flip side when you're looking at monitoring ICP invasively there's really two main ways you can do this. The gold standard is through an external ventricular drain which sits in the ventricle space in the lateral ventricle and this is a device that can both be diagnostic and therapeutic or the alternative is an intraparent chymal probe. Sometimes known as a codmin's probe because that's the brand name for it. This device cannot be therapeutic and the difference is that it's sitting in brain parent chimer so therefore it's only giving a local reflection of what the ICP is, not a general reflection of what the ICP is in the whole brain. i.e. it's a surrogate marker for estimating global ICP. There are other probes and devices that can also be used invasively but that is the general overview you need to know and like I said it's more important for the part two knowledge but it's good clinical knowledge to have now anyway. When we now move on and talk about the determinants of ICP this is the first core principle that you have to know. When you hear the term ICP automatically you should be thinking in your head the Monroe Kelly doctrine. This is something that you would have known and studied in med school but it's very important and makes the basis for your opening statement in your sq's and you're guaranteed to be asked this in the viber. The Monroe Kelly doctrine states that the brain is enclosed within a rigid bony skull of fixed volume. That fixed volume has contents within it that are incompressible therefore any change in those contents will cause an increase in the intercranial pressure. These contents that we refer to are firstly the brain parent chimer, secondly the CSF and thirdly the blood vessels. The brain parent chimer makes up 80% of the contents while the CSF and the blood vessels make up 10% each and if we apply this to the Monroe Kelly doctrine what this tells us is that if any of these contents increases then there needs to be a corresponding decrease with one of the other contents in order to keep the ICP the same otherwise the ICP will increase. The common things that can alter each one of these contents when we first look at the brain can be things like space occupying lesions, tumours or cerebral edema. When you look at CSF it can be any blockages in ducts that lead to an accumulation of CSF or hydrogethalis and then when you think about blood vessels this can either be an increase in cerebral perfusion pressure or an alteration in cerebral vascular resistance. Both of these things will touch on later when we look at cerebral blood flow. To describe the interrelationship between these three contents we can then use a graph which is very important and key and this is the intercranial elastins curve. Elastins is a reciprocal of compliance and it can be represented by the equation change in volume over change in pressure. This is the first key diagram you have to know when we're looking at the determinants of ICP. There are a few key important points on this diagram and how you draw this diagram on the y-axis you have ICP in millimeters of mercury and on the x-axis you have volume in mills. This graph shows an exponential increase in ICP as you increase volume. Between ICP zero to twenty millimetres of mercury you are in the flat part of that exponential curve. Therefore you have a lot of room to compensate and you have two compensatory mechanisms. You have early compensation that is mainly driven by translocation of CSF mainly from the brain into the spinal cord and if you remember me talked about functional anatomy we said that the overall volume of CSF was 150 mills which was equally divided between the brain and spinal cord. CSF production was cerebral perfusion dependent but CSF absorption was dependent on ventricular pressure. Therefore as pressure increased so did absorption up until a certain point. The key thing with CSF as a compensatory mechanism is that it's a slow compensatory mechanism but it has a huge buffering capacity comparatively to blood vessels. Blood vessels can compensate quickly but their buffering capacity is low. Therefore in the early phase blood vessel compensation is used up quickly until CSF compensation has the time to catch up. Once we get into the late phase of compensation this is when the ICP is approaching or close to twenty millimetres of mercury. This is when we're going to see the clinical signs on a patient and here we are reaching a critical point. The first critical point is when the ICP reaches 20 millimetres of mercury. At this point we say that focal ischemia is likely to occur in the brain and the reason is because that increase in ICP is leading to a decrease in cerebral blood flow which is leading to that focal ischemia. Once you reach that point you now reach the sharp part of the exponential curve where any small change or increase in the volume will lead to now a dramatic increase in ICP. So you go from an ICP of 20 millimetres of mercury up to 50 millimetres of mercury very quickly with very little change in volume. Once you reach 50 millimetres of mercury this is the point of decompensation i.e. the point of global ischemia where all the possible compensation mechanisms have been exhausted and now you're at risk of coning and getting the classical signs of cushings reflex. The physiology behind cushings reflex is really twofold. The first stage is that the increase in ICP leads to a decrease in blood supply to vasomoda areas. This leads to local hypoxia which creates a massive sympathetic surge. That leads to an increase in total peripheral resistance and an increase in mean arterial pressure and the second stage is that with this increase in mean arterial pressure you get the bar receptor reflex being activated. This leads to the vagus nerve being activated and you get the secondary bradycardia. So you classically see the bradycardia with that really high blood pressure and you might or might not see some altered respirations associated with this. The goal here if you get into this stage is to abruptly decrease ICP and again if you remember the monorachylic doctrine the only three things you can alter are brain-parent chimer, csf and blood volume. You can alter the brain-parent chimer and decrease cerebral edema by giving steroids so this might be the case if the increase in ICP is related to a chimer. You can decrease csf by what we spoke about earlier through an EVD. You can change blood volume through what we're going to talk about next which is manipulating cerebral blood flow and then pharmacological management through agents such as manitol or hypotonic saline. So that is ICP and a nutshell and like I said it takes us nicely into talking about the second component of this learning objective which is looking at cerebral blood flow. The normal cerebral blood flow is roughly 50 mils per 100 grams per minute of oxygen to brain tissue. This is equivalent in an adult to 750 mils per minute which is roughly 15% of the cardiac output. Out of this 15%, 80% goes to the grey matter while 20% goes to the white matter and this makes sense as the grey matter is more metabolically active. In terms of O2 consumption, the O2 consumption in the brain is roughly 3 to 5 mils per minute per 100 grams of brain tissue. This is equivalent to 50 mils per minute of oxygen consumption which makes up 20% of the total oxygen requirement of the body. Both cerebral blood flow and cerebral metabolic oxygen consumption are coupled together and this leads to our second important diagram. This is the diagram that depicts cerebral blood flow on the y-axis and CMRO2 on the x-axis. What is evident on this diagram is that it's a clear linear relationship as the CMRO2 increases so does the cerebral blood flow and the two reference points you can remember are those two important numbers that we spoke about with 50 mils per 100 grams of brain tissue being on the y-axis and 3 to 5 mils per 100 grams of brain tissue being on the x-axis for the CMRO2. If there's any deviation from this normal blood flow, you start to have impacts very quickly. At cerebral blood flows less than 50 mils per 100 grams, you start to get cellular acidosis. Less than 40 mils per 100 grams, you start to get impaired protein synthesis. At less than 30 mils per 100 grams, you get cellular edema and at less than 20 mils per 100 grams, you get failure of ion pumps. When you get to less than 10 mils per 100 grams, that's when you get cell death occurring. However, even small brief changes in blood flow can have a major impact. This is because the brain is the most sensitive to short periods of ischemia. And you see this clinically when patients have orthostatic hypotension or vaservagolds, a brief disruption of blood flow for even a few seconds leads to them being unconscious. And the reason why the brain is so sensitive to changes in blood flow is because cerebral function is totally dependent on oxidative phosphorylation of glucose to ATP. Glucose uptake is independent of insulin in the brain and it's independent using the glute 1 receptors. Glucose is the main substrate the brain uses and the brain extracts 10% of the glucose that's delivered to it. The brain has no ability to store oxygen or glucose, so once that glucose that's immediately available is used up, it is completely vulnerable to ischemia. This becomes more important in neonates that have a even higher CMRO2 requirement, but in these groups, key turns can be used as a secondary substrate for energy production. So remember this link between cerebral blood flow and CMRO2. From here, we can now take a deeper look at the factors that affect cerebral blood flow. To better understand these factors, there's two important equations you must know of. The first equation is that cerebral blood flow is equal to cerebral perfusion pressure divided by cerebral vascular resistance. The second equation is that cerebral perfusion pressure is equal to a map minus the ICP or the CVP depending on which one is higher. Knowing these two equations gives us the answer for how we can treat someone that has compromised cerebral blood flow. Looking at cerebral perfusion pressure first, the only three factors that you can change are map, CVP or ICP. We've already spoken about how map is under the control of the autonomic nervous system and the important reflexes such as the bar receptor reflexes in our cardiac physiology series. While CVP can be manipulated in a few ways, the easiest way to manipulate CVP is to decrease the CVP by changing the patient's position, i.e. positioning the head 30 degrees up, decreasing interterrastic pressure, decreasing peep and decreasing the right atrial pressure. All of these things are the reason why we say when someone has an acute brain injury, you want to implement these strategies to ensure that cerebral perfusion pressure is maintained. The third factor is ICP and this is how we link what we spoke about first at the start of learning objective with reference to Monrokele doctrine to talking about cerebral blood flow and cerebral perfusion pressure. The aim in someone that has a compromised brain is to try to keep the cerebral perfusion pressure above 60. 60 millimeters of mercury is the key number that you need to have in your head and it's the number that's referenced in guidelines that are really important like your brain foundation guidelines for patients that have traumatic brain injury. This is the key number that's referenced in these guidelines. Now going back and looking at the other equation, which is cerebral blood flow is equal to CPP divided by CVR, we can concentrate on the factors that alter cerebral vascular resistance. We know that these factors will be very important because this again relates to the Hagen-Persel equation and we know that the Hagen-Persel equation has a major impact on vascular resistance because radius is to the power of four. Within CVR there are five main factors that can have a dramatic change in the vascular resistance. The first one you need to know is metabolic auto-regulation. This is also known as flow metabolism coupling and it relates to auto-regulation principles that we've discussed across the body. Within the brain we've already said that cerebral blood flow is linked to cerebral metabolic oxygen consumption and these two things are linearly linked. The mechanism is straightforward, locally as oxygen requirement increases so does the production of metabolites such as hydrogen ions, potassium, adenosine, nitric oxide which all have vasodilating properties that relax the smooth muscle, decrease the cerebral vascular resistance and increase cerebral blood flow. Now when you're thinking about metabolic auto-regulation think of the brain in two different ways. Think of it firstly having local effects and then secondly having global effects. Locally this is where metabolic auto-regulation is having its major impact. It's changing that regional circulation and controlling that regional blood flow in areas that might be having specific increases in metabolic oxygen requirement. While globally this is more controlled by a second factor which is pressure auto-regulation. We've again discussed what pressure auto-regulation is in our cardiac physiology series. The principle is that the cerebral blood flow is kept constant across a wide range of map values. For the brain this map value range starts from 50 millimeters of mercury and goes all the way to 150 millimeters of mercury. Across this range cerebral blood flow is maintained at that 50 mils per minute per hundred grams of brain tissue. This range can importantly change both physiologically or pathologically. In neonates who have a lower cerebral blood flow this range is left shifted and in pathological states such as patients that might have chronic hypertension this range can be right shifted. This factor also has an associated diagram with it and it's another diagram that you must remember and for all these diagrams that we're talking about the easiest way to remember them is to look at the diagram or die resource that has all the diagrams in one PDF. Then the third factor altering cerebral vascular resistance are the chemical factors. The chemical factors involve the effect of carbon dioxide and oxygen. Both of these things you can pretty much predict what they're going to do to cerebral blood flow. In terms of carbon dioxide this again has a very linear relationship between a certain range. Between carbon dioxide pressures of 20 to 80 millimeters of mercury there is a linear response in the increase of cerebral blood flow and the increase is proportional to 2 to 4 percent increase in cerebral blood flow for every one millimeter change in the partial pressure of arterial carbon dioxide. Why we say this change is restricted to 20 to 80 millimeters of mercury of CO2 pressure is because at the extremes you reach the extremes of what the cerebral vascular resistance can do. The mechanism for this is at CO2 as we know from our very first podcast when we looked at the control of ventilation rapidly diffuses across the blood brain barrier. It leads to an increase in the hydrogen concentration of the extracellular fluid and this causes vasodilation. The effect isn't long lasting because the pH will eventually equalize and so therefore we say this effect is temporary for roughly four to 12 hours until that pH equalizes. To recap the diagrams we've touched on so far the first diagram was the intercranial elastens curve. The second diagram was the metabolic order regulation curve which linked cerebral blood flow to CMRO2. The third diagram was the pressure order regulation diagram where cerebral blood flow was constant across a pressure between 50 to 150 millimeters of mercury and now the fourth diagram is linking the arterial partial pressure of CO2 to changes in cerebral blood flow. This leads us on to our fifth and final diagram and our second chemical factor which is the effect of oxygen. On the x-axis for this diagram you have the partial pressure of oxygen and on the y-axis you have the cerebral blood flow. Across normal physiological oxygen levels there's very little change in cerebral blood flow. The key number to remember is when the partial pressure of oxygen drops below 50 millimeters of mercury that is when you get a sharp exponential increase in the cerebral blood flow. To the point when the partial pressure of oxygen is 30 millimeters of mercury cerebral blood flow has doubled from the value it was at when it was 50 millimeters of mercury. The reason why this curve is shaped this way is related to the oxygen dissociation curve and knowing that the steep part of the curve occurs when the partial pressure of oxygen drops below 60 millimeters of mercury. So like I said you might be able to find all of these five critical diagrams being superimposed on each other but just remember you might be asked to break each one of those apart and know what they're doing individually. The biggest issue I found with superimposing those graphs was that they didn't have a clear intersection point and I just found that if I was going to do an SUQ or be asked to draw one of these diagrams in a survivor I was just going to reference the individual diagram rather than remember how to superimpose all of these onto one diagram. Now there's two more factors to speak about when it comes to controlling cerebral vascular resistance. The fourth factor is temperature and this is again linked to cerebral metabolic oxygen consumption and makes sense when you think about decreasing the body temperature will lead to a decrease in CMRO2 which will therefore then lead to a decrease in cerebral blood flow. The key numbers here is that the change in temperature by one degree Celsius will lead to an alteration of CMRO2 by 7 percent and this is why you have the principle of a deep hypothermic cardiac arrest. At a temperature of 18 degrees you are significantly decreasing the CMRO2 of the brain and therefore you have a short period of time where you're quote unquote protecting the brain from mischemia while you're at these low temperatures. Then finally the fifth and last factor is nervous system control. This has very little implication on cerebral vascular resistance and more so a bigger implication on altering map but it's a factor that you must mention just to complete your list of factors that affect cerebral vascular resistance. To recap this list we started off by talking about metabolic order regulation then pressure order regulation followed by chemical factors which included carbon dioxide and oxygen followed by temperature and then finally nervous system control. To finish this section on cerebral blood flow we'll just quickly touch on the effects that anaesthetic drugs have on all the factors that we just mentioned. The key one that comes up all the time is the comparison between volatile anaesthetics versus proper fall. With volatile anaesthetics what is said is that above a MAC value of 1 you get an uncoupling of that metabolic order regulation which means that your cerebral blood flow increases despite your CMRO2 being low. Therefore you'll usually see in clinical practice most neurosurgery cases being done with a tibia anaesthetic but really this only applies if you use a MAC value that's greater than 1. Below 1 that order regulation is preserved. With proper fall based anaesthetics that order regulation is also preserved so you get the ongoing coupling of that metabolic order regulation so as CMRO2 decreases so does cerebral blood flow and this is a dose related effect so you can give someone birth suppression with a heavy dose of proper fall in an attempt to acutely decrease their CMRO2 and you know that that decrease in CMRO2 will lead to a corresponding decrease in cerebral blood flow and this can help to acutely decrease the patient's ICP. While in comparison you can't just crank up the Civo to a MAC of 2 or 3 hoping that your decrease in cerebral blood flow. At this level the cerebral blood flow will increase disproportionately to a decrease in CMRO2 and this will actually lead to an increase in ICP. And really this is the most important clinical implication depending on the choice of drugs we use that you need to know about for neuroanesthesia. Yes, drugs like ketamine can increase sympathetic nervous system output which also increase CMRO2 but the evidence for that is much lower compared to the evidence that we know of that exists with volatile anaesthetics. The same can be said with nitrous oxide which also increases sympathetic output and can also increase CMRO2. On the flip side opioids can help to decrease CMRO2 and are a good adjunct to use if you're trying to acutely decrease ICP. However if a patient is not intubated and ventilated opioids can lead to hyperventilation which will increase your CO2 which can therefore then lead to an increase in cerebral blood flow counteracting the effect that you're trying to have. Now those were some really core concepts that we went through in our first learning objective which was really looking at intracranial pressure and cerebral blood flow and now we'll move on and look at the second aspect of this learning objective which is looking at intraspinal pressure and spinal cord perfusion. Really hopefully by the end of this you'll be able to see how both of these two factors overlap and are essentially the same for if you're talking about the brain versus if you're talking about the spine. The thing we need to do before we talk about spinal cord perfusion and intraspinal pressure is just have a review quickly of the anatomy of the blood flow in both the brain and in the spinal cord. As we know the circulation of blood in the brain is through the circular willis and the circular willis is supplied by four main arteries. It's supplied by the left and right internal cord arteries and then the left and right vertebral arteries. The crotted arteries make up the anterior two-thirds of the circulation, the circular willis, while the vertebral arteries make up the posterior one-third. What does that mean? It means that the internal crotted arteries are supplying the arteries such as your anterior cerebral arteries, your middle cerebral arteries, and your posterior cerebral arteries and then the communicating arteries in between these. The bridge between the anterior and the posterior circulation appears to be where the bazilla artery sits. Above the bazilla artery you have your superior cerebral artery and below it you have your anterior inferior cerebral artery and this is normally considered part of the posterior circulation. The other artery that's part of the posterior circulation is then the posterior inferior cerebral artery. Why is this important to know? Apart from the obvious of knowing which areas of the brain are affected when a patient has a stroke, from our perspective it's important to know the origins of the circular willis so you know the origins of the spinal arteries. The spinal cord supply is a dual supply. It has an anterior spinal artery and two posterior spinal arteries. The single anterior spinal artery comes from the terminal branch of the vertebral arteries. While the dual posterior spinal arteries come from the posterior inferior cerebellar arteries. The clinical significance of this is that the anterior spinal cord is very vulnerable to any kind of ischemia if that single artery is damaged. While the posterior spinal cord has a dual supply, therefore it has a backup just in case any of the blood supplies damaged. The anterior spinal artery supplies 2/3 of the spinal cord while the posterior spinal artery only supplies 1/3 of the spinal cord. Clinically if there's damage to the anterior spinal artery this leads to anterior cord syndrome where the tracks in the anterior 2/3 of the spinal cord are damaged. These include the motor tracks and the spinal thelamic tracks. Therefore, clinically what you see is motor paralysis below the level of injury as well as a loss of pain and temperature. In opposition, if you get posterior cord syndrome, only the dorsal column is affected and the dorsal column is responsible for the sense of proprioception, vibration and touch. So if someone has a posterior cord syndrome, their ability to sense pain and temperature will be preserved as well as their motor function. Now with regards to the spinal cord, the anterior and posterior spinal arteries aren't the only ones that supply blood flow to the whole spinal cord. The unique thing with the spinal cord is that it gets multiple feeder arteries throughout your body. There's really feeder arteries at every level of the body, starting from the subclavian artery, then from the thyroid cervical artery, from the posterior cervical artery, from your thoracic region and then from your lumbar and sacral region. But the main feeder artery that we know clinically is very relevant to us is the artery of atom qubits. Now a may or may not be pronouncing that right, but it's the largest feeder artery in our whole body and this is very clinically significant when you're doing major procedures such as major vascular cases like t-vars, e-vars or any major surgery that involves a large portion of the thoracic and lumbar aorta. The origin for the atom qubits artery comes from the left posterior intercostal artery being a branch of the aorta. In 80% of the population, it sits normally between t8 to l3, but in 60%, it can sit between t9 to t12 and in 15%, it can start from as high as t5. The significance is that this variation can create a huge watershed area if that artery is damaged or is accidentally blocked off, which is what can happen when you're repairing someone's aneurysm and then this can lead to spinal cord ischemia and it's the reason why these patients may or may not have preoperatively a spinal drain put in to protect that spinal cord from ischemia. That is why from the anaesthetic perspective, it's important to know the blood vessel anatomy for both the circular willis but as well as the spinal cord supply. And this moves us on nicely to talking about the last part of our learning objective, which was looking at the intraspinal pressure factors and the spinal cord perfusion factors. This is where having a good understanding of intercranial pressure and cerebral blood flow really comes in handy, because you can think of the spinal cord as a continuum of the brain. What that means is that the same principles that apply in the cranial vault apply in the spinal cord and the spinal vault. So therefore in terms of intraspinal pressures, you have the same factors that apply as the monrokele doctrine. Instead of the brain-parent chimer, you have the spinal cord acting as a parent chimer. You have the same CSF because CSF is equally distributed between the brain and the spinal cord under normal conditions and you have the blood flow which we've just talked about. The two key things or more rightly, the two only things you can manipulate to protect the intraspinal pressure from increasing is either manipulation of the CSF which again can come through a spinal drain which is just mentioned that works to offload and remove CSF and really that's as much as you need to know about spinal drains for the part one exam, but you need to know a little bit more than that for the part two exam. And then the other way to manipulate intraspinal pressure is to manipulate the blood flow. But in this case, if the spinal cord is at risk of damage, instead of decreasing the blood flow, you want to increase the blood flow and maintain that supply to the spinal cord to limit spinal cord ischemia. So here we have some key parameters that then relate to the principles of spinal cord perfusion. The equation for spinal cord blood flow is the exact same equation you have for cerebral blood flow, where spinal cord blood flow is equal to spinal cord perfusion pressure divided by spinal cord vascular resistance. When we look at the numerator being spinal cord perfusion pressure, again, it's a derivative of map minus the higher of intraspinal pressure or CVP. Then when we look at spinal cord vascular resistance, it again encompasses the same five factors that encompassed cerebral vascular resistance. So this was pressure order regulation, metabolic order regulation, chemical factors, temperature and nervous system factors having a very minor effect. If you remember, when I spoke about cerebral perfusion pressure, I said that the key number there was trying to keep CPP above 60. The key number here for spinal cord is because we can't directly measure spinal cord perfusion pressure, we try to keep the map above a certain value, and usually we say we try to keep the map above 80 at least. Some guidelines will even push for a higher target trying to keep a map above 85 or 90, but when you think about this logically, what it's assuming is that the intraspinal pressure is probably around about 20, because 80 minus 20 means that your spinal cord perfusion pressure is 60. So again, you're trying to get to that magic number of trying to keep everything at least above 60 when you're thinking about perfusion pressure in either the brain or in the spinal cord. But with the spinal cord, because we can't directly measure perfusion pressure and the only thing we can measure is map, we just say to try to aim for a map above 80 and in some instances above 85 or even 90. There's not too much more to say about intraspinal pressure and spinal cord perfusion if you understand the initial principles that related to intracranial pressure and cerebral blood flow. What we will do is cover one of the SAQs that directly looks at this in our next section, which we're going to go through now, which is looking at the past SAQs. Before we look at the questions from Ansca, I just want to highlight how similar the questions are in the kicking exam. And really, they're just all the same question that's repeated in a different way. So in 2018, they were asked to describe the physiological regulation of intracranial pressure. Then in 2016, discuss the determinants of intracranial pressure and outline how it can be measured. Again, in 2016, describe the factors that influence intracranial pressure and then way back in 2010, describe the physiology of intracranial pressure and the physiological mechanisms that limit a rise in intracranial pressure. That same pattern of having that core information just asked in a different way is exactly what happens in the Ansca exam. And really, if you can fall back on the principles we've covered, these questions are really straightforward. The first question we're going to cover from 2023, second sitting, has three parts to it. And hopefully, you'll be able to see that this question is in that hard once you know the basic principles. The first part of this question asked, "List the intracranial contents which contribute to the intracranial pressure 10% of the mark." Then the second component was briefly outlined what is meant by the monoracally doctrine 10% of the mark. And then the third component was list the interventions that can be used to reduce ICP. For each intervention, outline the mechanism by which it works being 80% of the mark. The examiner report for this was really good and very succinct. It essentially broke down the answer into the three domains, starting off with the intracranial contents, being brain 80%, blood being 10% and CSF being 10%. And then they said variation was allowed for these percentages as an approximate. Then for the monoracally doctrine, only a simple definition was required. And then finally, for the interventions that can help to reduce ICP, some of the examples given were decreasing brain volume, such as hypertonic solutions like Manitol, which we haven't discussed in today's podcast because it moreso overlaps with pharmacology, decreasing arterial volume, which can be done by either targeting a low normal PACO2 or brief hyperventilation, decreasing CMRO2, correcting hypoxemia, correcting hypertension and preventing hypertension above the order regulation limit. Then you could decrease venous volume by elevating the head, decreasing peep, avoiding coughing or straining on the endotracheal tube, having no ties or cervical collars around the neck to allow venous drainage. And then for CSF, you could drain it by an EBD, and then for space occupying lesions, you could either remove the space occupying lesion or decrease the swelling around it through steroids. The key thing in this examiner report I think is that they specifically said a comprehensive list of interventions was not needed to pass, but it was expected that these would include some that are directed at manipulating arterial and venous cerebral blood volume. The key issues when people went wrong with this question was either spending too much time in part A or part B with the definitions, or a misinterpretation of what they thought would lead to a decrease in ICP. The key misinterpretation, they claim, was that hypertension would lead to a decreased ICP. But what the examiner said was that hypertension would actually increase ICP by cerebral vasodialation through myogenic order regulation. Furthermore, lowering the blood pressure will reduce cerebral perfusion pressure, resulting in brain ischemia and further vasodialation through metabolic order regulation, and that these points are illustrated in a diagram presented in the examiner report. And this diagram is one of our key diagrams that looks at that pressure order regulation graph between 50 to 150 millimetres of mercury. So if I was making a model answer for this question, I actually think the user-submitted answer in Mach 95 is very good for this. It succinctly answers this question in a one-page summary, starting off with the contents that relate to intracranial pressure. We've already said this is the brain, CSF, and blood, then talking about the monocleoductrin, and the key principle you have to know is that it's a fixed cranial vault. Therefore, you need to compensate for any changes in increase in ICP with a decrease in one of the contents. Then for part C, I would break this down into the components of the monocleoductrin. So this would include what can you do to the brain if the brain is the main issue leading to an increase in ICP? What can you do to the blood vessels if this is the main issue and relate this to the equation that leads to cerebral blood flow is equal to cerebral perfusion pressure divided by cerebral vascular resistance. And this gives you an automatic 5 factors that you can manipulate to therefore then decrease ICP. And then finally talk about CSF. Because I like to think about it as non-pharmacological and pharmacological management, I would put in pharmacological management at the end as its own subheading to then not miss out on drugs such as hypotonic saline, marital, all the drugs we talked about that can decrease CMRO2. So this would either be paralyzing the patient to avoid coughing, inducing burst suppression through prepofolbolicis and even thio pentone, which has really poor evidence and then steroids which aren't applicable in all situations but are useful in situations where there's edema, mainly associated with tumors or weird kind of infections. If you can answer this question, you can answer any of the variations we mentioned from the kick and exam as well. Then with regards to specifically cerebral blood flow, there's been a couple of questions that have been asked a few times and they both have pass rates below 50%. The last time this question was asked was back in 2021 second sitting and it was, describe the normal regulation of cerebral blood flow and outline the physiological factors which may alter it. Do not discuss the effects of medication or pathology. The key thing from the examiner report here is that people usually fell down by not reading the question accurately. All they wanted you to include was an understanding of normal cerebral blood flow and explanation of the major mechanisms that control it and then the physiological factors that alter it. And really my model answer for this question would just start off with some basic facts and equations starting off with what normal cerebral blood flow is and whether you remember it's 50 mils per minute per hundred grams of brain tissue or it's 750 mils per minute or it's 15% of cardiac output doesn't really matter you just put one of those in. Then you can talk about what normal oxygen requirement is so normal CMRO2 being between 3 to 5 mils per minute per hundred grams and the significance of that being that it's 20% of our oxygen consumption throughout our body. Then the next equation would be the equation for cerebral blood flow and this would have the two components of cerebral perfusion pressure and cerebral vascular resistance. You can then relate this to the Hagen-Persel equation when we talk about cerebral vascular resistance and then I would divide this question into specifically talking about the factors that affect cerebral perfusion pressure and that includes your map, your ICP or your CVP and when you're thinking about normal physiological factors that may alter those three things think about what you do on a day to day basis. From going from a sitting position to a standing position your map will change. From going from a supine position to a sitting position your CVP will change when you cough, when you sneeze your CVP and your ICP will change. So how does the cerebral perfusion pressure stay constant across a wide range? And really this is mainly due to the changes of cerebral vascular resistance that happen all the time in our cerebral blood flow. So those changes include the five factors that we spoke about, metabolic and pressure order regulation, chemical factors being oxygen and CO2, temperature and CMRO2 and the neural factors. And you guys at this stage should know what you put in with each one of these factors to then make it a broad answer. The final SQ I want to talk about is the last SQ that's been asked in this topic and it was asked back in 2024 first sitting which was outlined the anatomy of arterial blood supply to the spinal cord. This question had a sub 50% pass rate and because it's never been asked before the examiner report was very good for this. Again it broke down the answer into its domains. The main domains you needed to cover was talking about how there's one anterior spinal artery which arises from the vertebral arteries and supplies two thirds of the cord and there's two posterior spinal arteries that arise from the posterior inferior cerebellar arteries and supply the posterior one third of the spinal cord. For the examiners it was necessary to show the understanding that these arteries arise crannually and run down the whole length of the cord. It was anticipated that candidates would know that there are no anastomosis within the cord between the anterior and posterior artery territories and this is why you have this specific anterior cord syndrome and posterior cord syndrome because you don't have the ability for each of those arteries to compensate. Then the other key domain was understanding that reinforcement by radicular arteries was supplied at each vertebral level. It was necessary to show an understanding that one major branch in the lower thoracic or upper lumbar region being the artery of Adam Kuwitz arises from the intercostal or lumbar artery usually on the left side and contributes significantly to the supply of the lower cord. Usually by reinforcing the anterior spinal artery. The key thing here is to understand that disruption to this artery would lead to a huge watershed area. You could get additional credit in this answer by knowing more detail about the course of the anterior and posterior spinal arteries, the origins and the course of the radicular arteries, understand the vasocarona, which until I read the examiner report I didn't know what it was and it's really just a network of small blood vessels that surrounds the spinal cord providing its peripheral blood supply. It's formed by the peel and asthmosis between the anterior and posterior spinal arteries and the importance is that it helps to supply blood flow to the outer layer of the spinal cord. The other additional credits could be gained by understanding the potential vulnerability of the spinal cord blood supply with anatomical correlations to events such as clamping of the aorta or vertebral artery dissection and then understanding the track supplied by the anterior and posterior spinal arteries with clinical deficits resulting from the compromised supply, which is what we've already talked about when we said that in a posterior cord syndrome, the dorsal column is affected, which is a sensory column, while in an anterior cord syndrome, not only is the spinal thalamic track affected, but so is the motor pathway. However, that sensory pathway for fine touch, proprioception and vibration is preserved. And because this question was only an anatomy question, you didn't need to apply the spinal cord blood flow equation into here. You really needed a focus in on knowing the anatomy of the circulation, which is why I took time to explain that earlier, and it's not only relevant here for your part one exam, but it's also relevant in your part to exam, and trust me, everyone loves to ask about the artery of atom quits. So just know it, and if it's the only thing you know about spinal cord perfusion, you'll at least have a good starting point. So we've covered a lot today in a topic that was expected to be very heavy in terms of cerebral blood flow, intracranial pressure and spinal cord perfusion. Like I said, I haven't gone through all of the eight learning objectives individually, but I've just broken it down into the two learning objectives, one that looked at intracranial pressure and cerebral blood flow, and the other that looked at intracranial pressure and spinal cord perfusion. All the other learning objectives really encompassed everything we've spoken about. And if you have a good understanding of intracranial pressure and cerebral blood flow, you will have a good understanding of spinal cord perfusion and spinal cord pressure. So that will do it for me today guys. Thank you so much for listening. I'll be back with our last topic of this series, which is a huge one to end on, and it's pain physiology. I'm not going to make any terrible jokes about that. I'm just going to leave it there. I wish you guys the best of luck with your studying, and I'll catch you next time on count to 10. [Music]