oxygen is essential to life and the use of supplemental oxygen is the difference between life and death and many acute conditions in some cases the use of high levels of oxygen is actually required at these high levels there are risks with its use there are consequences to hyperoxia and subsequent oxygen toxicity which i'll discuss now [Music] all right you guys welcome back to another video lesson from icu advantage my name is eddie watson and my goal is to give you guys the confidence to succeed in the icu by making these complex critical care subjects easy to understand i truly hope that i'm able to do just that and if i am i do invite you to subscribe to the channel down below when you do make sure you hit that bell icon and select all notifications so you never miss out when i release a new lesson as always the notes for this lesson as well as all the previous videos are available exclusively to the youtube and patreon members you can find links to join both of those down in the lesson description below also don't forget to head over to icuadvantage.com or follow that link down in the lesson description to take a quiz on this lesson test your knowledge while also being entered into a weekly gift card as well as don't forget that you can help support this channel through the purchase of an icu advantage sticker again those are found at the website icuadvantage.com forward slash support link down in the description so in this lesson i'm going to talk about how the use of high oxygen can potentially be detrimental to our patients that being said there are things that increase the risk as well as times where in order to prevent life-threatening hypoxia the use of high levels are actually needed because of these negative consequences though this is why the ardsnet protocols that i did discuss in my lesson covering ard's diagnosis and management this is why they set out these protocols to have lower spo2 targets of that 88 to 95 percent this was to try and reduce the risk of these higher oxygen levels at the end of the day it's important to understand the risks that come with it and that high levels should really be avoided when possible unfortunately this is not always the case and the need for oxygen in the presence of hypoxia must be weighed against the risks of using such high levels all right so let's start things off here and talk a little bit about oxygen hyperoxia and oxygen toxicity so the concept of potential consequences of oxygen is really nothing new and it actually was first discovered all the way back in the 18th century there has been much debate around this topic though in that time so this has kind of led us to some of the perspectives that we have today now oxygen plays a critical role in our cellular respiration and the production of atp at the same time it has very strong oxidizing properties that can actually damage even biological material so one common example of oxidation that we're all familiar with is rust and while this is not a direct comparison to what's actually happening in the body it is helpful to remember when we're thinking about oxidizing damage so here as we can see in this picture here when metal reacts to oxygen and water rust is formed and corrosive damage all result from these two seemingly harmless molecules again while this is not what's actually happening inside of our bodies it is important to kind of relay and connect these two concepts of this oxidative damage taking place now the term hyperoxia is actually when we have tissue that's going to be exposed to high levels of oxygen above what is normal and this is really the result of breathing air that has a partial pressure of oxygen greater than normal atmospheric air and so when we breathe air with high levels of oxygen we can actually see the partial pressure of oxygen in the tissues rise and rise until it's in the hundreds or even thousands now hyperoxia if it's high enough can lead to oxygen toxicity and this is a result of the harmful effects of oxygen so this hyperoxia can actually lead to increased levels of reactive oxygen species which can interact with tissue damaging things like lipid membranes proteins and nucleic acid now i am going to discuss some of the pathophysiology here in a minute but the accumulation of changes from hyperoxia can lead to damage of alveolar epithelial as well as alveolar capillary endothelial cells this damage can lead to a cascade of changes such as the ones that i discussed in our discussion of arts in that first lesson and this includes increased capillary permeability and damage to the surfactant-producing type 2 cells all of these changes can lead to acute lung injury or ards depending on the severity of the damage and these changes are going to be directly related to the level of the partial pressure of oxygen so the quantity of oxygen that we're delivering the duration of our patient's exposure to that oxygen as well as the atmospheric pressure delivered all impact the total dose delivered and the potential damage all right so let's dive in a little bit into the pathophysiological changes that we see with the hyperoxia and oxygen toxicity so being in a state of hyperoxia as i mentioned leads to high levels of this reactive oxygen species and this disrupts the balance between oxidants and antioxidants in our body leading to the damage of cells and tissue so as you know oxygen is required for that atp production in the mitochondria via that electron transport chain as a result of this atp production oxidizing free radicals are naturally formed in the presence of hyperoxia we actually see an increase in the production of these free radicals and so free radicals are really just a type of unstable reactive and really short-lived chemical species and the key thing with these here is they actually have one or more unpaired electrons having the unpaired electron or electrons allows it to interact with surrounding molecules and it's this interaction with the tissue that damages those lipid membranes proteins and nucleic acids resulting in damage to that tissue these free radicals are also known as reactive oxygen species now in our lungs the pulmonary capillary endothelial cells as well as the alveolar epithelial cells really are susceptible to damage by reactive oxygen species while other parts of the body may also manifest issues as well for example we can actually see effects on the central nervous system with the most severe effects leading to seizure and coma but this is typically the result when we're delivering oxygen at higher atmospheric pressures such as in hyperbaric oxygen therapy or you can really think of it with scuba divers now oxygen toxicity results from reactive oxygen species so oxygen toxicity that's resulting from these reactive oxygen species can really be thought of in four progressive phases of severity so initially we have our initiation and here the reactive oxygen species depletes the antioxidant levels in the body and the lung is really unable to clear mucus at this point next and these phases can overlap with each other but next i want to talk about the inflammation and this is the result of damage of lung tissue and really the migration of leukocytes and the different inflammatory markers from there we have proliferation and here we see cellular hypertrophy as well as the increased presence of monocytes and then the last phase is actually going to be our fibrosis and here in this phase these changes are permanent and irreversible and so collagen is deposited and the interstitial space is thickened leading to fibrosis now the inflammation that i'm talking about here is damaging to those alveolar epithelial cells which really damages the alveolar capillary membrane and this leads to impaired gas exchange and edema this inflammation also causes these cells to release chemoattractants and cytokines that are going to mobilize those macrophages and monocytes to that area leading to additional reactive oxygen species and further exacerbating the damage that we have in addition to all that we can also see atelectasis that results from the administration of high levels of oxygen this is something that we actually call absorption atelectasis and this results from areas of the lungs that really are not well ventilated and so because we have the ease of oxygen to cross into the pulmonary circulation administration of these high levels of oxygen especially when we're doing 100 fio2 that this trapped air and those alveoli that aren't easily ventilated is readily absorbed into the blood thus leading to the collapse of those alveoli and this is something that's important to know as even pre-oxygenating patients for something like anesthesia or intubation can actually lead to this atelectasis as well so really kind of our two big things that we're worried about here are this atelectasis as well as the big and primary thing is this reactive oxygen species and ultimately the damage to the lungs so let's actually talk about some of the clinical implications of all this that i just talked about so as i mentioned before the total dose of oxygen is our biggest risk factor and here we consider if we have an fio2 being delivered that's greater than 60 for more than 24 hours at one atmospheric pressure that this is the level in which oxygen can become toxic now typically in the icu we're dealing with normal atmospheric pressure although we can have patients that are receiving hyperbaric oxygen therapy which increases atmospheric pressure while they're getting that therapy so thus this can actually lead to increases in risks as well as lower oxygen levels and shorter durations in order to get to some of those same risk levels now i know that i said 24 hours but in fact even 12 hours in sometimes we can see changes such as airway congestion pulmonary edema and atelectasis now if we do have patients at higher levels of fio2 so think 80 percent 100 for shorter durations that this can actually lead to again exposure levels and doses that can still become toxic so again remember that the higher the total dose the higher the risk and potential damage and so really when we're talking about this lung damage what we're talking about is acute lung injury and or ards and remember that acute lung injury and ards are really both acute inflammatory syndromes that are triggered by either that direct or indirect cause the only real difference between these two is the level of severity so with acute lung injury this is where our pf ratio is greater than 300 whereas ards are going to be those cases where we're under 300. now when it comes to our hyperoxic acute lung injury that this actually mimics our acute lung injury or are ards that's actually triggered by other conditions those same pathophysiologic changes that were seen in my discussion of ards are actually taking place here leading to that diffuse alveolar damage as a result of the inflammation damage so once again chest x-ray is going to be helpful in identifying the acute lung injury or the ards but it's not going to be diagnostically specific for our hyperoxic acute lung injury so again really just think about the precipitating cause of the acute lung injury or the ards in this case would be from the hyperoxia all right so that was basically my review and information sharing on hyperoxia and oxygen toxicity now remember that a lot of patients that we're going to come across in the icu are going to be in situations where no matter what we're going to have to deliver high levels of oxygen and sometimes for long periods of time in these cases this is just what's required in order to ensure that they don't have hypoxemia and that we can deliver throughout the body the proper amount of oxygen to the tissues that said there are risks there's potential damage that comes from it and more importantly the takeaway is going to be that if your patient is requiring high levels of oxygen but you've got very high spo2 that this is probably something that we need to be evaluating and looking to bring that down knowing that there are consequences to this so again there's a lot of different situations either in short term or long term for our patients where we're gonna have to use these high levels of oxygen or just make sense to do so but this is just something to always have on the back of your mind and be thinking about and if we certainly are able to reduce the amount of oxygen that's being delivered we want to do that because there are potential consequences to it so i hope that you guys found this information useful if you did please leave me a like on the video down below it really helps youtube know to show this video to other people out there as well as leave me a comment down below i love reading the comments that you guys leave and i try to respond to as many people as i can make sure you subscribe to this channel if you haven't already and a special 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