Transcript for:
Respiratory Concepts and Assessment

welcome to unit two uh respiratory part one so in respiratory uh we can notice a lot of things just from across the room so in your books you'll kind of notice um just that across the room assessment and those of you who are you know work in EMS or who are currently respiratory therapists know how important this is and we do this for all of our patients we are constantly assessing whether we realize it or not and so as nursing students we really want you guys to kind of start paying attention and being more intentional when you first walk into a room like what do you notice uh is the room a mess um but more importantly what does the patient look like how are they breathing what does their skin color look like are they struggling to breathe are they sleeping are they alert there's a lot of things that we can gain knowledge from just by looking at our patients and it tells us a lot of information so what's their mentation are they anxious are they sitting forward are they tripoding can they speak to you um you know what does their skin color look like are they pale are they cyanatic um are they obese there's a lot of things that we can gain just from looking at our patients across the room so take that into account before you even touch your patient that you are constantly assessing them so when we talk about the lungs uh we are always going to t kind of tie in some cardiac concepts and throughout these next uh few units so really throughout the next four units units 2 3 four and five when we talk about respiratory and cardiac we're going to bring all of these things together you're going to hear me say a lot that the heart and the lungs are married to each other so you can't have one without the other and an an effect in one is going to affect the other you know with each heartbeat your heart pumps blood and then of course that blood pumps to the lungs where it gets oxygenated so oxygen moves across that o alvoli into the bloodstream and CO2 moves off it's a very intricate process and these two organs are very much tied together and because the heart and lungs are so connected a problem in one can often cause issues in the other so if your heart or lungs aren't working properly it can lead to very very serious complications for both systems so moving on to the respiratory assessment and kind of adding on to that um shortness of breath is often a sign of lung or heart problems so knowing when symptoms start can actually help you figure out what's causing them and how long they've been happening so for instance um you know do when you walk in the room are they tripoding and leaning forward um does it happen more when they're lying flat what sort of medical uh you know background do they have do they have COPD or do they have heart failure these things are going to help you as the nurse anticipate what to expect in your patients what that kind of classic myriad of symptoms are going to be based on their their history uh and presentation you know does it wake you up at night suddenly um does it only happen during physical activity so what makes it worse how long does it um last you know and what relieves it does you know when you're up walking around and you become short of breath when you sit down does that help uh these are all very very important uh assessment findings um and things to ask our uh patients when we are conducting that respiratory assessment so ventilation and older adults and we're going to talk more about uh alvoli and things like that this is just kind of a brief kind of taking you back to that respiratory assessment some things to consider in an older adult is you know older adults have poor muscle tone right so compliance is decreased um maybe their lungs are a little bit more fibroatic these patients have a lot more comorbidities that are going to affect not just how their lungs function but also that blood flow to the lungs uh again because the heart and lungs are married to each other so that blood flow to the lungs and how CO2 and oxygen are exchanged so there's a lot of things that can occur uh also positional changes just regular physiological functional changes so the alvolar elasticity is decreased um the number of alvoli is actually reduced uh resulting in decreased surface area for diffusion um our respiratory muscle strength uh posture issues with these patients um blood oxygen levels are usually decreased um many of these patients have coorbidities uh that cause them to be anemic which reduces their oxygen carrying capacity which we talked a little bit about last unit so all of these things uh really contribute to how our patients present and then of course respiratory issues that involve uh these patients so when we talk about lung compliance um lung compliance is a measure of how easily the lungs can expand when you breathe in so when I personally think about lung compliance I think about how stiff my patients lungs are and again there's going to be a lot of different disease processes that can make our patients lungs stiffer and of course the first one that always comes to mind is COPD so COPD is basically just a kind of umbrella term for these um bronchial uh disease processes right so when our alvoli get stiff and we'll talk more about COPD uh here later in this lecture but basically it takes more effort because our lungs are stiffer one they don't blow up very nice so if you think about our alvoli as like a little balloon um you know when you first take that lovely little balloon out of the package um it's all nice and kind of soft it might take a couple you know good breaths to blow it up real good but once you have blown it up it actually blows up very nicely over and over and over again right i know you guys have all had kid parties or whatever where you've blown up balloons multiple times but now think about that balloon that's been sitting in the package maybe for the last five years you take it out because maybe the colors match your kids birthday party five years later and it's not what it once was maybe it's stiff it doesn't they're all kind of stuck together uh they don't really blow up very nicely and because of that they're more prone to pop right um other disease processes that can affect lung compliance uh is like that fibrodic tissue that surrounds the alvoli um also any sort of you know fluid that either surrounds the lung or that is even inside the lung all of these things are going to affect how well when we talk about lung compliance how well those balloons can inflate our alvoli can inflate because when those inflate it increases the surface area and improves um gas exchange so also because if these things um are more stiff or just can't blow up very nicely it increases our work of breathing so patients have to work harder in order to fill their lung sacks with air and and get that oxygen and gas exchange to occur so airway resistance is a little bit different um so when I think of airway resistance I think more of my asthmatics yes your COPDers and other sort of lung disease processes are going to have decreased airway resistance um but when we think about airway resistance I think about really any inflammatory process um that is going to occur in the airway so this can occur either in the upper airway like in the you know kind of upper bronchioles or trachea or it can occur down here most oftentimes it's going to occur kind of in your bronchioles uh and then of course in your lower airways like your um alvoli and things like that so what can occur here is it it's affected by how much resistance uh the air meets as it moves through the airways so things that are going to affect this is inflammation is going to be huge so you think about your asthmatics or your patients with you know really terrible allergies anything that's going to trigger these bronco constrictive diseases um is going to really uh impair our really the movement of air down into the alvoli so airway resistance um obviously in a beautiful healthy airway we're going to have this nice big open straw that we can easily suck air in and blow air back out when we have a patient who has airway resistance um or some sort of inflammation or thickening that's impeding airway or sorry air into the lungs basically what happens is it restricts uh this this opening so we can't get air in very well so these are the patients where uh they are leaning forward they're kind of um you know they're they're having trouble part of tripoding or that leaning forward that positioning is to open up the airway so then what happens is they lean forward and these patients actually need longer exhalation times because they can usually get air in um halfway decent but think about sucking air in through this little narrow opening and maybe the actual muscle of the airway is inflamed maybe there's some mucus in there too so think about what the air would sound like when your uh when your patient is trying to suck air in and then of course blow air back out so these are the patients where you're going to hear severe wheezing um in asthmatic patients which we'll talk about asthma here a little bit later but in asthma patients um you know these airways can actually close off and create such tight airway resistance that they do they sound tight um when our patients are no longer wheezing but their work of breathing is so extensive and they're not moving much air at all you don't hear much airway movement these patients get in really big trouble and this is where we need to use our bronco dilators in order to increase um the size and diameter of that airway so all of these things help with diffusion um so diffusion is basically gas exchange within the alvoli so after you breathe in air oxygen moves from that alvoli into your blood vessels while carbon dioxide moves out of the blood into the airway so we can then be uh so then it can then be exhaled this happens passively so it's passive diffusion and it goes from areas of high concentration to areas of low concentration um so definitely get familiar with this concept because this concept is going to come back um when we talk about electrolytes and sodium and all of these other things because a lot of things in our body happen uh passively you know our bodies don't like to have to work too hard and expend too much energy doing basic processes like this which is why it goes from areas of high concentration to low concentration so essentially uh CO2 is a byproduct of metabolism so then it gets carried on the blood back to the lungs where it can get exhaled out whereas when we breathe in oxygen fills the alvoli and then because the oxygen content inside the alvoli is higher now than it is on the blood so CO2 gets offloaded and oxygen gets onloaded now with that there's uh barometric pressure or actual pressure and we'll talk more about um positive and expiratory pressure and how pressure helps with this process a little bit um in the next unit when we talk about mechanical ventilation but essentially um there's a basic barometric pressure in the lung that also there's a pressure gradient that also helps with this process to move oxygen um onto the blood cells as well so just definitely know that diffusion helps with gas exchange so complications of diffusion with gas exchange so what can impede this gas exchange well we've already talked about a couple things right um if we can't get air into the lungs that's going to be a huge thing so if we can't get air into the lungs and if our lungs are stiff and fibrodic we can't um they can't blow up properly so the two that I really want you guys to focus on for this course is surface area available for diffusion and then the thickness of that alvolar capillary membrane so if you think back to the airway resistance slide and that mucus or sorry that membrane that muscle of the airway is so thickened how much pressure or how hard do you think our patient is going to have to work in order to get gas to diffuse across that really thickened alvolar membrane so even if our lungs aren't blowing up the greatest but now it has a really thickened membrane that that oxygen has to go through um and and then if you add mucus on top of that so now oxygen is having to diffuse through mucus and through this thickened alvolar membrane um you can see how this can severely impair oxygenation in our patients especially when we start talking about pulmonary edema and that interstatial lung disease um also conditions like pneumonia pneumonia is huge um for the the mucus production and that thickened alvolar membrane because of that infectious process and that immune response same thing with our asthmatics right it's more of an immune mediated response so what we uh you know kind of do for these patients obvious is those bronco dilators um for surface area available for diffusion so that's when we talk about that thick um lung so when we blow up our our alvoli or our little balloon what it does is it increases the surface area inside of that little alvoli so basically think about a balloon when it's small it doesn't have much surface area on the inside for gas to exchange as we continue to blow up those alvoli if they're nice and compliant what it does think about a nice giant balloon you're going to have a lot of surface area for oxygen and it's going to thin out that alvolar membrane um for oxygen to freely diffuse across and CO2 to come off so when we don't have good surface area and if we have thickened alvolar capillary membranes that is going to severely affect how gas is diffused across those two things and um oxygen coming off and then CO2 uh or sorry CO2 coming off the red blood cells and oxygen coming back on so how all of this applies to VQ mismatch so when I went to nursing school this was some sort of illusionary like I you know you learn it but you don't fully I feel like sometimes understand it and so this is a very very difficult concept but understanding lung compliance and alvolar membrane and how blood how the heart and lungs are married to each other right is how VQ mismatch occurs so when we talk about VQ mismatch there's a couple different things we have a a couple different things at play here right there can be either be a problem with the lungs there can either be a problem with our circulation or there can be a problem with both which is really really bad and that's what's called our silent units so in figure A here we have this beautiful nice healthy lung where air goes in it blows up to a really nice size we have good blood flow all the way around that uh alvoli through our capillary alvolar like our membrane network that surrounds all of our alvoli so CO2 is coming off nicely and oxygen is diffusing on that is the perfect healthy adult um andor human patient uh airway when we go down to B here well now what happened well now maybe we have some alvolar uh capillary membrane thickening maybe we have a mucus plug here right so because of that our poor little alvoli is all flat and flabby it cannot blow up properly so then what happens here so this is a ventilation mismatch right so we have low ventilation but our perfusion is good however think about what your patient's going to look like so if you have a whole network of alvoli that can't blow up because maybe there's inflammation here maybe there's mucus buildup and so therefore our alvoli either one is blowing up very very small or it can't blow up at all now we have great perfusion our heart is working fine but our lungs are not so CO2 cannot offload and oxygen cannot come onto the blood cell so this is uh something that needs to be fixed very quickly whether we give bronco dilators whether we uh suction out the airway um whether we promote good pulmonary hygiene so our patients need to cough and deep breathe all of these things are going to help our patients um with proper gas exchange so now kind of moving up to C uh now we have a beautiful lung but terrible profusion so again this is how the heart and lungs are married to each other so maybe we have a uh pulmonary embolism here maybe we have plaque buildup which we'll talk more about um in the next unit too when we talk about acute coronary syndrome um but with you know a lot of like high cholesterol or pulmonary uh patients at risk for pulmonary embolism or really just any sort of blood clot anywhere it can you know go to any area of the body well now we have this big beautiful lung but now we have no perfusion so this is a perfusion mismatch so in this case the patient has good air coming in i mean if blood were flowing uh through that alvolar capillary membrane network it you know gas exchange would occur but we can take out again an entire section of lung um perfusion just by having this uh pulmonary embolism here or whatever is blocking the the membrane network and then of course in D uh this is a silent unit so this is where you have uh both respiratory and cardiac issues uh profusion issues so this is basically um a really really bad day so this is an alvoli with no ventilation no profusion co2 cannot come off oxygen cannot come back on if left for a long time this patient would go into cardiopulmonary arrest so when we talk about the KB cycle this is coming back so and I'm going to explain it um in kind of a brief way and how this applies to our respiratory patients and by the way this is going to come back in multiple units cellular respiration matters and you guys probably learned about this I don't know in anatomy physiology or micro whatever but this is very very important because cellular respiration right it's that process where um cells use to produce energy oxygen is a very very important part of this process so how our body produces energy when oxygen is not in the system we go to a very very ineffective way of producing energy and that's anorobic metabolism remember aerobic metabolism means or or respiration whatever you want to it's sometimes called cellular respiration or cellular metabolism right so what happens then is we go to this very ineffective way of producing uh energy which then produces lactate or lactic um which causes a lactic acidosis which we'll talk about here in a little bit when we go through our AGs so yes lactic acidosis uh when we produce it basically it's an oxygen deprived environment and this is going to come back in your shock unit this is going to come back in your cardiac unit so I truly truly want you guys to understand um how this process really affects our patients because if you can break it down to that cellular level it's going to be very helpful in how you actually care um and can and and anticipate patient needs and their uh clinical course all right so during this stage um oxygen helps produce a lot of energy 36 ATP to be exact so one energy um and and that's basically from one glucose molecule if oxygen is present so from one tiny little glucose molecule and with oxygen present in the system we can produce a ton of energy for our bodies this is why oxygen and getting oxygen to our patients is so important again a byproduct of this process is carbon dioxide which we breathe out so removing CO2 is critical because too much of it makes the blood acidic right so if our patients um going back to that VQ mismatch so if our perfusion is fine but our lungs are are you know you we cannot diffuse CO2 off or get oxygen on um or we have some sort of lung disease process like COPD that makes us retain CO2 um our patients can actually become a little bit on the acidic side so when CO2 elevates that is called a respiratory acidosis when lactic acid elevates that is a metabolic acidosis because it's produced through anorobic metabolism again we'll talk more about this in a little bit but removing that CO2 is critical right because otherwise um the blood is going to be acidic and it's going to disrupt normal body functions um when patients can't get enough oxygen to the tissues the body cannot produce enough energy and it produces it very very inefficiently like I just talked about so if oxygen levels drop cells actually switch to anorobic uh respiration aka anorobic metabolism meaning without oxygen so again this also happens due to profusion issues such as VQ mismatches um hypoprofusion states like shock which again this will come back in that unit um which we'll talk about later right and in high metabolic states uh such as sepsis exercise or fever so when we have too much oxygen burning um or we we our bodies have a very high oxygen demand such as it with you know sepsis exercise or fever um this is when our bodies also switch to anorobic respiration or anorobic metab metabolism so you see this sometimes in like really heavy runners um people who have who exercise a lot or who go heavy in the gym um these patients can come in actually in lactic acidosis as well so anorobic respiration or anorobic metabolism only makes two ATP per glucose molecule and produces lactic acid which obviously causes those muscle cramps weakness and if severe lactic acidosis all right normally our bodies can handle especially if anorobic respiration or metabolism happens for a very short time like in running or something like that or in the gym a lot of times this is what causes our muscles to be very very sore so when this happens um basically what uh what happens is uh you know it causes weakness um and then again just that acidosis so aerobic respiration with oxygen remember 36 ATP but with anorobic it's only two this is why our bodies have to work so hard when they when it doesn't get oxygen just to perform regular uh everyday tasks um you know that require energy so the KB cycle can't run without oxygen even though oxygen isn't directly involved in the cycle because it's kind it's sitting out here but oxygen allows the cycle to actually take place inside the mitochondria okay so even though oxygen isn't directly infected in affected in this cycle we cannot produce energy efficiently without it so again this slide is going to come back um through this course in different ways but what you need to know for this unit is that oxygen is needed to keep the whole system running smoothly and impaired profusion or oxygenation to the tissues can happen in several different ways um another factor is oxygenation uh in the very cells that carries oxygen so our red blood cells again going back to unit one anemia can have a profound effect on cellular respiration when it comes to oxygen carrying capacity so I hope that makes sense i hope we're tying in some different concepts and that pathophysiology um of that disease process so as a byproduct um of cellular respiration uh entital CO2 or that carbon dioxide can tell us a lot about ventilation perfusion and even metabolism so just like the last slide this slide is going to come back in multiple units because it is that important so measuring our patient's entital CO2 uh is a real time indicator of how well our patient uh is doing so waveform capnography provides information about both circulation and ventilation before during um and even actually after cardiac arrest um this can actually and we'll talk more about this in units four and five but um you know cardiac or sorry capnography can actually guide some of our cardiac resuscitation efforts so we always want to apply the device early uh in resuscitation but even just in our respiratory distressed patients because it does provide a lot about our clinical decisions it can actually guide a lot of things with our clinical decision-m so if you have a patient um in respiratory distress sometimes just applying an end title um capnography monitor uh really tells us a lot about how CO2 is being eliminated by the lungs so when this occurs you know our patients oxygen might be 90 91 but what is their CO2 level because if they're starting to build up CO2 it does mean that they're um not efficiently removing it from the system they might be getting enough oxygen on but they're definitely not blowing a lot of oxygen out and this is really important in our COPD patients so some waveform capnography devices um in this unit we're really just going to be focusing on the nasal canula version um there is one obviously and we always monitor waveform capnography in an intubated patient uh so that will definitely come back next unit as well when we talk about mechanical ventilation but really waveform capnography is the gold standard for uh monitoring breath by breath how our patient is actually ventilating so when we talk about pulse oxymmetry uh we're actually behind the ball so cap uh pulse occimmetry is actually about 30 to 60 seconds behind what our patient is actually doing in real life okay whereas waveform capnography tells us every single breath how our patient is actually ventilating so a lot of research and actually best patient practices have kind of moved yes oxygen is important SPO2 is important but when we actually guide clinical decisions uh waveform kept and entitle has actually kind of started uh we've started shifting um a lot towards this device so what happens is uh with this device if you've ever seen one in the clinical setting and they have these on the medical surgical floors um and on the crash carts you'll see sometimes um patients on these especially if they're on a PCA pump right because uh we yes we monitor oxygen levels on a PCA pump um but at the facility I work at we actually guide our process but through capnography so our machines our PCA machines actually have this exact capnography device and you screw this into the machine so this is the capnography section of the entitle so the one side goes to So this is your capnography side goes to one nare and then your oxygen actually goes to the other so they're actually only get if you need to turn them on oxygen so you can put this device on and not have any oxygen flow into it so this side will flow oxygen in and this side will actually pick up the CO2 from every single patient breath it has this kind of um little uh catcher what I call it um that kind of hangs down from the patient nose over their mouth just to catch some additional CO2 cuz sometimes our patients like to breathe through their mouth like when they fall asleep or something like that so it just kind of helps pick up that additional CO2 these devices are pretty darn accurate um and like I said we hook these into our PCA pumps because if our patients uh capnography uh or sorry entitle starts rising right because they're not breathing uh efficiently because of too much opioids or whatever so their respiratory rate drops therefore they're holding on to too much CO2 uh the machine actually will not allow them if they push their button it will not allow them to deliver the dose um of that this actually um also picks up their respiratory rate so every time they breathe in the machine not only uh tells them what their entitle is but every time they breathe out it detects a breath and so it it picks up their respiratory rate so if their respiratory rate is too low or their entitle is too high the PCA will is actually programmed not to deliver a dose of their opioid which is actually a really cool thing um technology has come so far so again all of those concepts will be coming back both with opioid overdose CO2 all of that so moving on to everyone's most beloved and favorite topic in the whole wide world arterial blood gases so ABGs I feel like students have either they either get it or they just struggle with this topic so AGs I know you guys have touched base on this i believe it was med surge 2 i believe that you guys did AGS maybe even med surge one so these help determine the quality and the extent of that pulmonary gas exchange and our acidbased status so just like we've been talking about this entire time our uh acidbased balance uh is sometimes uh you know a a product of of oxygen exchange right so we can either have that respiratory component or in the case of that cellular um metabolism without oxygen in the system even if we're breathing okay and ventilating it's not a CO2 issue however if we don't have oxygen in the system our cells can't uh you know produce energy effectively and therefore it would be a metabolic acidosis because of that lactic acid or whatever is building up in the blood causing an acidosis okay so when we talk about AGs there's a few things that we need to know our pH so our pH is just that measure of hydrogen ions 7.4 is neutral okay so a a typical uh a normal pH is 7.35 which is more on the acidic side with that neutral being 7.4 and then on the high end we have 7.45 which is more on the alkaline side okay we also have um our Pa2 so normal Pa2 so when I think of Pa2 really it it's just partial pressure of arterial oxygen just think this is oxygen kind of forget the PA part this is oxygen on an arterial blood gas okay so what's the normal oxygen in our arteries it's going to be 80 to 100 okay and this is millimeters of mercury um and mostly at sea level obviously if we're not at sea level or patients in higher altitudes it's going to be a little bit different however normal is 80 to 100 this is where we want our patients to be for their O2 take off the PA part if that's confusing for you and just look at your O2 now sometimes you'll see an SAO2 this is where I think students get confused when I think of SA think of SPO2 okay so pulse oxymmetry so your Sao2 should be extremely comparable and it's even measured in a percentage of of what how much blood or sorry how much oxygen is attached to your hemoglobin in your blood all right so when I think of Sao2 don't get confused between Pa2 and Sao2 pa is that millimeters mercury 80 to 100 sao2 think SPO2 like your pulse occimmetry um because that's exactly the same thing that it's measuring it's measuring how much oxygen is is attached to the hemoglobin on your blood so normal SAO2 in an arterial sample should be between 93 and 97 which is pretty much where we want all of our patients to lie on an SPO2 anyway so this is extremely comparable number all right so SEO2 is important oxygenation right because it does correspond to your SPO2 and it's basically measures the oxygen supplied to the tissues that is carried by the hemoglobin all right so Pa2 is how much oxygen is floating around in your blood not attached to anything sao2 is how much is actually attached that can actually participate in gas exchange all right but for most of our questions we're only going to look at PA2 however if an enclelex question or one of your questions on your quizzes throws in an SAO2 know the difference of that and essentially how that's going to affect your patients all right so CO2 or PA CO2 again you can knock off the PA if this is confusing for you just know that it's arterial all right so carbon dioxide is that natural byproduct of cellular metabolism which we've already covered you should know this okay we have to blow this off if we don't CO2 is considered an acid so if we're retaining CO2 and CO2 is tied to the lungs all right so if we're retaining CO2 this is because the lungs can't blow it off properly all right so this is a normal mechanism of cellular metabolism co2 is not tied to any sort of met metabolic um acidosis or alkalossis co2 is always tied to the respiratory system because it's whether we can or cannot blow it off properly either we're blowing off too much or blowing off not enough and this is what causes those acidbased disturbances okay so normal CO2 is uh same as your pH it's going to be 35 to 45 so 35 to 45 is kind of a weird numbers in in our body and a lot of things like to be between 35 and 45 all right so Pa CO2 is going to be between 35 to 45 that's going to be our normal okay bicarb so your HCO3 is bicarbonate bicarbonate is a base this is your metabolic function because it's produced in the kidneys so it it's metabolic because it's a direct um metabolic stimulant so the kidneys have to produce by carb so it's it's a base and it's found in the serum and because it's a base too much of it is going to cause an alkalossis because it's a base um too little of it uh so if we're you know not either producing enough because our kidneys aren't functioning properly or we've just produced too much of it and so it this is a finite resource okay our kidneys can't just constantly produce by carb eventually they're going to be like I've had enough and they're no longer going to compensate all right so because it's a hydrogen ion too much by carb and it's processed by the kidneys um is going to cause that alkalossis too little of it is going to cause an an acidosis all right and this is the metabolic process of regulation this is a much slower process so if our patients um have kind of a an initial acidbased disturbance the fastest way to correct that is through your CO2 so this is why respiratory rate is so important in really sick patients because it's going to tell us a lot of different things how many of you guys actually count the respirations you know in a normal healthy person you go in you're like "Yeah they're breathing good it's about 14 16 whatever." Just pick a number that's in there that's like somewhat normal in a patient who's sick or has the potential for deterioration our respiratory rate can tell us a lot about a patient's status and it's something that's a very subtle sign and it's usually one of the first signs because it tells our brain tells our respiratory center that it needs to either pick up the respirations to blow off more CO2 or it it tells us to slow it down to hold on to the CO2 if it's an alkyossis type state okay so this is very very important um that we need to know all right so I know I already went through all of these numbers now how do we actually read and interpret an arterial blood gas result all right so an arterial Oh I didn't tell you the normal of by carb normal by carb is 22 to 26 all right so and that's pretty standard across most laboratory uh results so 22 to 26 is our normal uh HCO3 or our bicarbonate for our kidneys so when we look at a blood gas and it has it listed here how the book wants you to interpret it um you can interpret it a couple different ways some people like to look at the pH first before they look at oxygenation some people like to look it the book tells you to look at oxygenation before the pH so all the oxygenation tells us is so our PAO2 and or our SAO2 what that's going to tell us is is the patient hypoxmic or not hypoxmic means that is is there too little oxygen in the blood system all right so are our tissues uh getting enough oxygen so the answer is going to be yes or no on this are they hypoxmic or not so that's what it wants you to look at after that we're going to look at our pH so our pH our normal is 735 to 745 so with with 74 being neutral right cuz that's right in the middle um is our patient more towards the acidic side or are they more towards the alkyotic side a base all right so this is what we need to look at and then from there we're going to say okay so if if it's normal all right so if it's normal now we're going to look at our CO2 so then we're going to look at our CO2 so our CO2 is is this normal if it's towards the low side all right so that means we are blowing off too much acid which is going to cause um an alkyossis all right i know that's kind of backwards and I'm going to teach you an acronym to help with this so or is it on the high side so this means our respiratory rate is probably too fast all right this is our patients with anxiety they're breathing too quickly they're in pain whatever and they're blowing off too much CO2 or in a metabolic case our our DKers right they're trying to compensate um by blowing off more acid because it's this is a quick way to do it right remember our CO2 is the our respiratory rate is the first one to either increase or decrease to hold on or let go of more CO2 uh to correct quickly or are are is our respiratory rate um too low like in the case of that PCA pump um is our respiratory rate too low and now we're holding on to too much CO2 or is this a COPDer and they can't exhale it good because of poor gas uh diffusion so these are all things to consider because if our CO2 is too high right and so if our pH is low and our CO2 is too high remember CO2 is an acid co2 is an acid so this is how we're going to get rid of it um th that means that it's a respiratory in nature if it's not then then it's usually going to be metabolic and we'll talk more about that here in a little bit so you need to determine what's our CO2 and this is where I think you guys learned the tic-tac-toe method back in maybe med surge one med surge 2 we're going to talk about a different method so now we're going to evaluate our by carb so our by carb is it low high or normal so remember our HCO3 our carb is produced in the kidneys this is going to be a much slower process to fix the problem so is it low high normal too much by carb is going to be on the alkalotic side so it's going to match so if it's high pH is also going to be high if your CO3 or your carb is low if it's metabolic in nature right so if your byarb is low it means we have too little base and therefore we're going to be more on the acidic side so if it's metabolic in nature your pH and your barb are going to match all right so blood gas sample number one and we're going to talk more actually you know what i'm going to bypass this if you guys want to write down these examples you can pause the slideshow here i'm actually going to move on because it's going to make more sense with the compensated and uncompensated okay so this graphic I love this graphic i made this um in Canva or whatever for you guys so so with your pH um so pH is right this is your this is your base so this is right in the middle of that 7.35 to 7.45 so you got your 7.4 anything less than 7.4 so that 7.35 to 7.39 is going to more be more on that acidic side okay so for those of you who kind of get confused about well it's normal but is it acidotic sorry acidotic or alkalotic so this is where um it kind of gets confusing when you have a compensated because your pH is normal but yet nothing else is so we're going to kind of talk more about that too and then of course anything above that 7.4 so 7.41 to 7.45 if it's normal is more on that alkalotic side obviously anything that's outside of that range um that's above that is going to be um abnormal and and on the alkalotic side as well so your pH that 7.35 to 7.45 is normal your CO2 that 35 to 45 and this is going to be your respiratory indicator and we're going to talk more about that too and then your by carb your HCO3 that 22 this says 22 to 28 um I believe your book says 22 to 26 you're going to have different values um depending on your different resources 22 to 26 is is is what I want you guys to to go off of okay so and then your metabolic by carb if there's a question uh I don't think there's any question that's any close to this uh for the different ranges on any of your test questions um but as we go through the problems in this slideshow I think it's it's based off the 28 okay and again every lab is going to be a little bit different and have a little bit different ranges and that's okay 22 to 26 22 to 28 um typical is going to be 22 to 26 per your book okay so with that being said um remember that's your by carb that's your kidneys um it's going to be slower to respond so I use the Rome method now some students use a combination of both the tic-tac-toe and the Rome some students when I teach this are like "Oh my gosh Rome just clicked with me it makes more sense." And some students are like "Nope I'm going to keep using tic-tac-toe." And others just kind of do a myriad of both in between and that's totally fine whatever works for you so when we talk about respiratory and I kind of alluded to this in the previous slide so when our pH is elevated okay so when it's a little bit elevated so more towards that 7.45 either on this end of the spectrum or above and our CO2 is low because remember CO2 is an acid so if we're blowing off too much acid for whatever reason then then it's going to be a respiratory alkyossis okay so pH is high so respiratory opposite so if our pH is high our CO2 is going to be low if it's respiratory in nature okay so with the pH being low so let's say we're more on the acidotic side and our CO2 is elevated so this is where I think more about our COPDers or like in the example I gave before with the PCA pump our respiratory rate is too shallow or too low and we're holding on to CO2 this is an acid it's going to cause an acidosis and if our pH is low it's going to be respiratory in nature so it's going to be a respiratory acidosis now with metabolic it's the opposite right so metabolic is going to be equal so if our pH is high because it's a base so if our pH is more on the basic side and also we have too much base then it's going to be a metabolic alkyossis so both the pH and the bicarb are going to be high now if our pH is low so more on that acidic side of things and our by carb is also low right more kind of on the low end of things we're going to have a metabolic acidosis okay so with that metabolic acidosis uh that's what's going to happen so metabolic acidosis we're going to talk about causes and signs and symptoms and all of those types of things um a little bit later so I don't want to confuse you too much this is all about just reading them right now so metabolic is equal okay so both the pH and the byarb are going to be elevated in a metabolic a uh alkalossis and acidosis so now when we get into compensated versus uncompensated well shoot what are we talking about this is where that 7.4 is very helpful because I'm never going to give you a test question that says your patient has a pH of 7.4 well which way does it go is it more on the alka now in real life you might actually get that and nothing else is normal and then you're like "Well shoot." You're going to have to look at other clinical pictures you are not going to I'm not going to try to trick you like that here so it's always going to be on one end of the spectrum or the other i think where students get confused about acidosis versus alkalossis is if the pH is normal so again if it's that 735 to 739 it's going to be more on that acidic side so you know if you look at your pH and it's normal then it's either one a compensated um something or other or it's just a normal AG okay so this is where you have to look at your other markers in order to determine is this a compensated if your pH is normal now again when you look at these your book always wants you to look at oxygen first and we're going to kind of go through that so uncompensated um and partially compensated so if you look at your pH and it's not normal so it's either on the low end of the spectrum or the high end of the spectrum then you know that uh if your pH is not normal it's either going to be uncompensated or partially compensated so this is where you have to look at your CO2 and by carb um in order to determine if it's fully uncompensated or if it's partially compensated so and I know this is kind of weird where nothing is normal but um so if it's uncompensated either your CO2 or your by carb are going to be normal okay so for instance if your pH is high and your CO or yeah and your CO2 is low and you're in a respiratory alkyossis okay so let's say it's outside of the range so it's 7 um 54 okay so if it's 7.54 and your CO2 is super low like you know 22 or something like that maybe they're having a panic attack and they're just breathing like crazy and they're in this and then they're in this respiratory alkalossis well if their bike if their by carb is normal it's going to be uncompensated this means that your your your kidneys are picking up the slack or or sorry they're not picking up the slack so your body is not compensating so if your if your kidneys are not doing anything and your by carb is still normal then that means it's uncompensated because your kidneys have not yet kicked in to correct this problem and especially in the case of an anxiety patient um this can actually happen quite frequently because anxiety attacks come on very quickly and you can blow off a lot of CO2 very quickly and remember what I said the kidneys sometimes take a minute to kick in and so this is very much a real situation that can happen if you take a blood gas on a patient like this so your pH is not normal but your by carb or your CO2 is normal one or the other has to be normal okay so if your pH isn't normal you're always going to have one that's off if the other one is normal it means it's uncompensated because your body hasn't done anything to fix it yet okay so partially compensated means that nothing is normal so if your pH is out of whack and everything else is out of whack then that means that nothing is normal and it's partially compensated it means that your body is trying to do something but it's not being successful because your pH is not in the homeostasis range okay our bodies love homeostasis it really likes this 7.35 to 7.45 and in normal physiologic function it does everything in its power to keep this tight little range now if nothing is normal that means our bodies are compensating um a little bit but it's not being successful which is why it's partially okay fully compensated means that remember our pH is normal but nothing else is uncompensated our pH is not normal and one or the other and it's uncompensated because our body is just it's not doing what it's supposed to okay so let's do a um let's do a a little problem example here um so completely compensate so sorry uncompensated so remember uncompensated and we're going to kind of talk through this so in your books it always wants you to look at the oxygen first okay so in this case our Pa2 or just our you know regular oxygen that's floating around in our blood 80 to 100 this is 94 well that's normal so okay cool so our patient is not hypoxmic so our pH is on the high side so they're alkalotic okay so okay so why are they alkalotic so now we know that because this is abnormal we're either going to be uncompensated or partially compensated but we have to look at our bicarbon CO2 to to determine that all right so our CO2 is 25 well shoot so now we know because this is high and this is low this is going to be a respiratory alkyossis okay so now we know that we are a respiratory alkyossis okay and we're either uncompensated or partially compensated this is what we know okay so to to determine that the final one by carb well shoot our by carb is normal that means our kidneys have not yet kicked in so our b our kidneys aren't doing their their job yet so we are an uncompensated respiratory alkalossis does that make sense so an uncompensated because our kidneys are like "No we're not going to participate quite yet we're not really doing our thing." We're uncompensated respiratory alkyossis so that's because remember pH is alkalotic the renal system has has not moved out of its range yet to compensate for the primary respiratory disorder okay all right let's do the next little example then we'll do another one so kind of the same same similar thing pa2 well shoot that's normal 80 to 100 cool that's normal so pH well we're a little alkalotic again right because we're above that 7.4 um and we're also out of range all right so so we know we are definitely either in the uncompensated or partially compensated territory because we this is not normal okay so now well why are we not normal so our CO2 is low well our patient's having another panic attack apparently and so they're blowing off way too much CO2 so because this is high and this is low right it's going to be another respiratory alkyossis so now we know it's a respiratory alkyossis and we know that we're either uncompensated or partially compensated so let's figure out which one we are so our by carb is low so it's also decreased so nothing is normal so our pH isn't normal our bicarbs carbs not normal and our CO2 isn't normal so we are a partially compensated respiratory alkalossis okay so let's do the last one here so now again O2 is normal so pH is in that normal range all right so we're still on that alkyotic side though right we're still nearing the alkalossis but we're in range so we know that we are either that this is either a normal AG or it's compensated okay so now we have to look at our other factors to determine is this a normal ABG or is it a compensated AG so if our pH is normal but on the alkalotic side our CO2 is 25 okay so this is not normal so we know that it's on the alkalotic side now that we know that this is not normal so our so we're still gearing towards that respiratory alkyossis right because if our pH is on the upper side but our CO2 is low this is definitely uh a compensated right respiratory alkalossis however um your by carb your by carb is also going to not be normal because our kidneys have finally picked up and said "Okay we're not going to produce any more by carb because um or we're too alkyotic and so we're going to stop producing therefore your by carb drops." Okay so this is a fully compensated respiratory uh alkalossis okay so I want you guys to I'm not going to walk you through these ones i want you guys to either pause the slideshow here and and figure this one out and then I will show you the answer on the next slide all right did you guys get fully compensated respiratory acidosis all right so this one our PAO2 they're they're low this patient's a little hypoxmic okay so the pH of 7.39 so it's a little bit on the acid acidotic side but our CO2 is high so remember pH low CO2 high that's going to be a respiratory problem because a Rome so this is going to be a respiratory acidosis and we know that because the pH is normal it's going to be fully compensated because our bicarb is also out of range so now the kidneys have picked up right our kid the kidneys are doing their job maybe this has been going on for a little bit the kidneys are doing their job and they've started producing more by carb okay oh and I switched slides so go ahead and pause the slideshow here and you guys can do this one on your own as [Music] well all right did you guys get respiratory alkalossis with low saturation uncompensated i don't know why it says low saturation but it does so um because the low saturation because your SAO2 is also out of range so your PO2 is actually okay um it's between that 80 to 100 but your SAO2 is low so this is where your SAO2 does come into play and I think there are maybe one or two quiz questions um either on the quiz midterm or final that has to deal with this okay when we talk about this unit so definitely understand your SAO2 and that's that percentage and it's equivalent to your SPO2 so your actual PO2 is okay but your oxygen saturation so the amount that's attached to the hemoglobin is actually low so um some degree of hypoxmia right so either it's not attaching maybe there's an iron deficiency problem we don't know not neither here nor there this is an AG problem but so pH of 7 uh 7.5 okay so we know that this is uh you know some sort of you know uncompensated something or other whether it's partially um or fully uncompensated and then of course because your CO2 is low so that's what's causing um or sorry your CO2 of 24 i that was not that was weird anyway so the pH is elevated above normal and your P A C2 is below so suggesting that respiratory alkyossis right um and then of course your by carb is still within normal range um uh so it falls within that normal range indicating that there's no significant so this is a uh that uncompensated um respiratory alkalossis okay so hopefully you guys have some i know that was long and we're already an hour in and we haven't gotten past AGs yet but I know a lot of you guys historically struggle with AGS so I really really hope that that makes sense definitely go back and watch that and watch other lectures on AGs as well so now moving into some of the causes and what you're going to see as far as symptoms so respiratory acidosis is characterized right by that inadequate elimination of carbon dioxide we're holding on to too much carbon dioxide so again this can be caused by either ineffect ineffective pulmonary function um either excessive carbon dioxide production or we're just not blowing it off right okay so this is where we have um our cord injuries so we have a patient with respiratory center compromise so I sometimes I think about our patients who overdose right that opioid that PCA example also some sort of over sedation head traumas can be a big one um as far as like like I said our cord injury so you know high cord injuries which we'll talk more more about in our TBI and SCI unit i believe that's in unit 8 or unit 9 um but you know hypoventilation when when we're not breathing enough uh so this is what's going to cause or sorry hypoventilation yes so we aren't breathing enough so we're holding on to that CO2 uh also like lung diseases I've already talked about COPD massive pulmonary embolis where we can't get the CO2 to offload because of that VQ mismatch so these patients are going to be very disnic uh they're going to be restless they're going to have a headache co2 causes a terrible headache um when it's it gets too to be too much are these patients get tacocartic because our hearts and our bodies are trying to be like okay we need to pump blood faster in order to offload this CO2 quicker however if the lungs aren't functioning that's not going to happen these patients can get confused lethargic um as well as with that restless altered mental status changes again these can be patients can be in respiratory distress um they'll eventually have decreased responsiveness because that buildup of CO2 really causes a lot of altered mental status and lethargy as well and then of course we are respiratory alkalossis uh characterized by excessive elimination of carbon dioxide so this is where um I think about these anxiety patients uh these patients are you know panic attacks fear pain hyperventilation is a huge one fever because our respiratory rate elevates in in the presence of fever because uh of that increased metabolic demand um also metabolic issues like thyrotoxyosis salicellates um septacmia that's what can happen and so it anything that's going to increase your respiratory rate um is going to uh and blow off too much CO2 is going to be a respiratory alkyossis so when I think of a respiratory alkalossis and if you've ever seen anybody have a panic attack these patients get terrible paristhesas and tetany to the point where their hands are like um contracted down their arms will contract to their bodies they have terrible muscle cramps um their legs will actually have like horrible charlie horses their feet will pro pr pronounce out which actually just causes more anxiety because they think they're dying um and then you have them blow into a paper bag these are the patients that especially if it's an anxiety pain fear treating their pain um giving them a little Adavan treating their anxiety having them blow into a paper bag to reinhale some of their CO2 those are what's really uh important in these patients so I always think of central nervous system um issues with this where that that tetany the paristhesas they'll start getting numb tingly in fact paristhesas are usually the first symptom that they start getting they'll sweat because they're anxious they have that dry mouth blurred vision these patients eventually sometimes will get confused but definitely you'll see the paristhesas um that tetany those those muscle spasms it can cause cardiac dysriythmias if left to go on for too um they'll get laded they'll get dizzy all of these things are terrible for these respiratory alkalotic patients and again most oftent times when you see this um sure you can see it with like high metabolic demand but I feel like most oftentimes it's going to be your panic attack people so your metabolic acidosis is characterized by excessive production of either nonvolatile so I think of like your DKAs so uh either too much keto ac uh keto ketones um in like a keto acidosis or it's going to be too much lactic production like an a lactic acidosis so with this uh or it's going to be an inadequate concentration of by carb right uh in in the serum so either our by carb is going to be super low or our acids are going to be too high in in for our metabolic acidosis so with this our by carb is usually low because it either stops producing or it's trying to compensate right um and then of course uh so kidney failure can cause this keto acidosis anorobic metabolism um which we've we already kind of talked about that decreased oxygen in the system which produces that lactate um starvation because again our bodies aren't producing energy efficiently um salicellate uh intoxication so because of our salicellate intoxication so our aspirin um it can actually cause a metabolic acidosis a terrible metabolic acidosis and these patients will actually be on by carb drips um because of it um loss of base so diarrhea uh and I can't remember a student had a really good acrony not an acronym but a saying for this so base base from the booty and acid from oh gosh I can't remember it but anyway when we talk about metabolic alkyossis so base from the booty diarrhea okay so you lose base for through diarrhea so that's going to cause a metabolic acidosis so don't get diarrhea and vomiting confused because you're going to when we talk about metabolic alkalossis next that's that's from vomiting but diarrhea based from booty metabolic acidosis Again I feel like headache confusion restlessness le lethargy is going to be characteristic of every single acidbased disturbance but kind of whatever the cause is um is going to be uh some you know kind of your your other issue so if you get like a test question that tells you some symptoms and maybe gives you a diagnosis like ketoacidosis and the patient has cousal respirations with nausea and vomiting um and is confused and restless what what acidbased disturbance are you going to like you know anticipate well it's going to be a metabolic acidosis so those are the types of questions that you other than actually picking apart and and looking at your AGS uh so those are some of the other types of questions that you can you know anticipate with the your AG uh interpretation so again your cousal respiration stuper comr uh stuper coma um nausea vomiting dysriythmias and these are symptoms of metabolic acidosis not causes okay so don't get that confused these are your symptoms so metabolic alkalossis uh characterized by excessive loss of acids or overp production of your bicarbonate so again this is going to be your vomiting nasogastric suctioning okay so nasogastric suctioning is huge this is why when we drop an NG tube for our patients like with our small bowel um there's multiple reasons why we don't have it hooked to continuous suction um one because we don't want that tube to get stuck to the side of the stomach and cause like an ulcer there but two we don't want to over suck too much uh gastric content because our patients need some of that acid in order to maintain acidbased balance so loss of acid uh hypocalemia can actually cause it in fact potassium is one of the main electrolytes that we need to watch for any acidbased disturbance um including uh alkyossis and acidosis our potassium will move freely across our cell membranes anytime um we have an acidbased disturbance so in acidosis usually potassium comes out of the cells and can cause a hyperc calalemia in alkalossis it will move into the cells or you're losing it through fluids and can cause an hypoc calalemia so always just make sure that you're watching um your potassium very closely and I think there is actually a a test question on this about what electrolyte is the most important um and obviously all the electrolytes are important but for sure your potassium is going to be high high on that list also administration of diuretics um can cause an alkalossis as well because you're peeing out a lot of potassium with that um which can actually cause an an alkalossis too um excessive use of bicarbonate so I think of the patients who just chew Tums like crazy um they can actually cause themselves to get a metabolic acidosis because Tums is a base it's a bicarbonate and so they um actually can cause themselves to go into metabolic alkyossis that way as well and then of course you know that excess ingestion of antacids like the Tums which is the same thing but um for the metabolic alkyossis it's a it's similar to your respiratory alkyossis except usually they don't have the paristhesas uh like the that numbness and tingling but they do very much have muscle twitching um metabolic alkyossis is actually worse um because they can actually have really bad seizures with it and actually go into a coma but again with your alkyossis think of that muscle tetany um the twitching the cramps again you're always going to have lethargy weakness with all of these um but definitely the coma the nausea vomiting is going to be a big one too and then the decreased respirations because with those decreased respirations we're trying to hold on to more acid so that's why we actually start getting um we can actually have you know start getting hypercarbic um that way and then causing uh some decreased altered mental status as well all right so moving on to our respiratory diseases hopefully you guys have a good grasp of AGS we spent a lot of time on that and we're going to kind of move through the rest of these slides here so pneumonia pneumonia is an inflammatory response um to basically inhaled or aspirated foreign material so when I think of pneumonia either you have a microorganism that caused it from like a respiratory infection that kind of sat in your lungs and brewed around because either you know you weren't moving around doing good pulmonary hygiene methods or I think of sometimes those little old people who have terrible uh swallow reflexes and who just um you know have like they vomit and they aspirate some of their vomit um or they aspirate while they're eating uh those are big uh risk factors for pneumonia so it does develop when normal pulmonary defense mechanisms are impaired or overwhelmed right so we can't uh either protect our airway and then of course um you know our immune system just isn't it is overwhelmed and it's just fun it's not functioning the most properly so risk factors are going to be colonization either of the oro ferinx aspiration prolonged intubation which we'll talk more about ventilator associated pneumonia uh next unit and then of course host factors so how long has this been going on uh upper respiratory issues is their immune system depleted are they on steroids or some other medication that um you know suppresses the immune system those are all going to take into account for this disease process for developing how we're going to manage this is through antibiotics antibiotics are going to be huge for pneumonia and one of the staples of treating pneumonia as well as good bronchial hygiene therapy so respiratory cultures and sensitivity do need to be done prior to administering antibiotics if possible so we need to collect that send it down to lab uh see what organism that we're dealing with so that way we can tailor our antibiotics to uh destroy that you know microorganism appropriately and then of course supportive therapy most of these patients buy themselves at least a little bit of oxygen preferably humidified because a lot of these patients have terrible secretions and humidifying that oxygen is going to help thin them out so that way they can mobilize them better meaning they can cough it out it's not just going to sit down there and continue to brew occasionally we will need to uh you know intubate these patients and provide them with mechanical ventilation for a short period of time um adequate nutrition is going to be big too getting some protein on board making sure that these patients have the ability to you know regenerate their cells and provide enough energy and then again aggressive pulmonary toileting or bronchial hygiene therapy so we are going to walk these patients if they can we're going to do lots of incentive spometry maybe some chest physiootherapy we need to open up those collapsed alvoli promote good oxygenation and then of course early mobilization is also going to be a staple on top of our antibiotic therapy prevention is going to be strict infection control so how do we prevent pneumonia from occurring in the first place well uh we need good handwashing and of course this is more for our hospitalacquired pneumonia not for our community acquired so for hospitalacquired pneumonia um strict infection control good hand hygiene by all members of the health care team identification of that pathogen um or any pathogen so like if they have MRSA or anything like that being aware of that ahead of time and then of course uh early removal of any invasive lines meaning we're going to get rid of all you know endotrachial tubes NGS anything that can potentially introduce bacteria into the back of that oro fernx and or the airway Okay so diagnostic studies that you can anticipate for these patients are going to be a chest radioraph are big ones uh CBC because we need to look for lucopenia so our high white blood cell count uh we're going to look for lactic acidosis as well because we want to make sure that these patients aren't going septic we're going to get a set of AGS on these patients most likely especially if they're receiving supplemental oxygen or if they're in respiratory distress uh to determine the severity of the illness and and any ensuing hypoxmia and how gas exchange is is doing um we're going to look for our uh you know our Graham stains and our cultures and sensitivities to make sure what organism that we're dealing uh dealing with a lot of times we do like a respiratory film array or that viral testing to look for any sort of respiratory that's more not more for but definitely in your community acquired pneumonia is because those are most likely caused by some sort of respiratory viral illness that happened in the first place so either they had COVID or they had you know RSV or rhino or something along those lines um or just the regular good old corona virus that kind of rolls around every now and then and then of course uh a lot of times especially if they present to the hospital we're going to get a set of blood cultures just to make sure that that infection in their lungs did not ensue to their bloodstream uh those definitions right that community acquired hospitalacquired and then of course ventilator associated pneumonia is what we're going to talk more about next unit however for your community acquired and hospital acquired so community acquired more from those upper respiratory uh infections that kind of just developed out in the community and then it kind of progressed into a pneumonia or your little old ladies or men who aspirated while eating at the nursing home or whatever and then of course your hospitalacquired pneumonia still your little old people aspirating but then of course your infection prevention uh like washing hands and things like that that is not associated with mechanical ventilation okay uh considerations for your older patients uh usual symptoms are going to be feeble fever chills uh white blood cell count sometimes those are absent so these little old people present uh sometimes very uncharacteristic same way that they do with UTI um disease is often latent sometimes they come in maybe just with confusion or high heart rate or Mima's not quite acting herself and she's breathing funny so this is where we have to kind of look at the whole picture and get a good history and physical or sometimes these patients have dementia and they uh can't you know maybe their presentation is a little off anyway prevention for people aed 65 and older so usually we we do recommend the numacle and influenza vaccines for these patient populations so improving pneumonia outcomes uh again I said this before but antibiotics are going to be a cornerstoneaple of pneumonia treatment so antibiotic therapy is the cornerstone of all of our pneumonas whether it be community acquired hospitalacquired or ventilator associated um according to the 2021 surviving sepsis campaigns um initial therapy should be instituted within 1 hour of recognition of sepsis or septic shock so regardless of whether so if they have a pneumonia they definitely have uh some sort and not always sepsis um but they they definitely have an infection present so your book states that if they don't have SERS or sepsis like SERS criteria and I know we talked about that SERS criteria last unit but if they have SERS criteria with a known infection like pneumonia then for sure we need that 1hour bundle we have to get that 1-hour bundle in with that antibiotic administration your book states that chances of survival increase if antibiotics are administered within the 8 hours of admission that is going to be a test question folks so please please please understand that antibiotics are the cornerstone um if they're septic that's a completely different uh you know issue but if your patient comes in with a pneumonia and they're doing okay but regardless chance of survival increases if antibiotics are administered within 8 hours of hospital admission please please please know that because morbidity mortality in these patients especially if they're older can be very high in our in with pneumonia so pumothorax uh pneumthorax is a condition where air enters the space between the lung and the chest wall so we talked about those lovely alvoli and if you have a nasty fibroic alvoli that doesn't blow up very well well if you give it too much pressure sometimes it pops uh pneumthoraxis can also happen from trauma from broken ribs you fall on uh that side or maybe a li a rib punctures a lung sometimes it can be spontaneous uh our tall skinny men are very much uh at high risk for spontaneous pneumothoraxes that's kind of that patient population um definitely not going to be a test question here but I remember back in Enclelex um you know what patient population is more at risk for a you know a spontaneous pumothorax and that's going to be your tall skinny caucasian men are are always your your higher risk population there uh causes uh the lung to partially collapse or completely collapse so therefore it can't expand so you have all of this air buildup you know right around in the outside of this space you get tons of air buildup here and it kind of pushes the lung so your lung will maybe be about this big and it pushes everything to the opposite side um so that's when you start getting that tension pumthorax which we'll talk about here in a second but signs and symptoms of just a regular numo uh sudden onset of acute pleuridic chest pain localized to the affective lung so usually patients will come in this is where again uh everything lives in this cavity your heart your lungs blood flows round and round so all of this is all connected and tied to each other heart and lungs are married so they'll come in maybe they'll have chest pain they'll be disnic uh you know and this is where a good history comes in well did you fall like what what pronounce you know what occurred here if you push on them and it's like reproducible with palpation sometimes it can be from a a rib fracture or you know that uh you'll actually notice that puritic you know they'll kind of say it hurts when I breathe in or whatever um that's usually a good sign that it's more lung related than it is cardiac related uh shortness of breath increased work of breathing tacocardia dispnia um all of these are compensatory mechanisms especially tacicardia to improve cardiac output which we'll talk more about next uh in I believe unit four or five so uneven chest wall movement because this lung and I'm just using this lung as an example uh is blowing up just fine whereas this one is not so you'll see this side of the chest rise and this one will not because if that lung is popped and all of this here is air and that lung has been pushed forward uh the chest will not rise appropriately um so what that will look like on a uh c sorry a radioraph here so this is kind of all lung and I don't know if you guys uh kind of practice reading radioraphs uh or not but tissue usually looks white air is black on a on on any kind of x-ray so and then of course bones are usually white uh in nature and structure and of course it has to do with how much um you know the the depth of the X-ray and things like that so when we take X-ray pictures however with that being said what we want to see uh on these patients are good lung markings so a lot of times when you look at a chest X-ray you can kind of know okay so I see here this is the trachea coming down uh and I don't know if you guys can see this very well but and then we have one branch here and the other branch kind of disappears so you don't really see it um you have here on the good side you have lung markings meaning these kind of interstatial markings meaning that this is like vascule blood flow sometimes it looks a little fluffy meaning that there's some mucus in there but it's kind of black like it's fairly see-through right so you have good lung markings that go all the way out to the edge of the rib cage and down all right so this is the heart um the heart should not be on this side of the chest at least not that far on this side of the chest okay this is the left side so yes the heart lives more on the left however it shouldn't be this far pushed over this is a really bad scenario this is attention pumothorax you'll see on this side um because the lung has popped there are no lung markings and this is all black indicating that there's nothing but air in here and normally I would say yeah air is good in the lungs but air is good in the lungs not in the chest cavity okay so this patient would definitely need um a needle decompression um or they and eventually they're going to need a chest tube this is a huge issue because what's happening is all of this air is pushing all of the chest cavity structures over to one side so the trachea is being impaired the heart is having more pressure put on it which is reducing cardiac output um these patients get very very sick very quickly so we need to release all of this air uh quickly with either either a needle decompression and then we need to prepare for chest tube insertion so when attention numoththorax is relieved the effect is usually very very rapid you're going to get an improvement in oxygen saturation you're going to get a decrease in heart rate because you've just relieved all of that pressure off the heart so it doesn't have to work as hard to maintain cardiac output and you're going to get an increase in blood pressure because you've been compressing the heart for however long with the with the extra air in the chest cavity uh you're decreasing cardia therefore your blood pressure is going to drop and this patient's going to look terrible so once that pneumothorax is relieved again you're going to get an improvement in O2 a decrease in heart rate and an increase in blood pressure that may or may not be a test question so signs and symptoms of that tension numo which we've already kind of talked about a little bit but the hypoxmia that's an early sign so understand your early signs versus your really late signs so just a regular pneumothorax you're you know your patient's going to be hypoxmic might be they be a little bit dysnic they're uh they might be a little tacocartic but now when we start approaching that tension pneumothorax where everything's getting pushed over now they're going to be restless they're going to be apprehensive you might they might even describe it or you might even describe it as the you know feelings of impending doom they're going to go into severe respiratory distress severe tacipia these patients are going to be leaning forward they're going to be tripoding they are not going to look good their cardiac output is going to drop they're going to be pale sometimes they might be diaphoretic they might look like they're on the verge of cardiac arrest and they probably might be okay so these patients absolutely can go into cardiac arrest from this so not too uh concerned i don't want you guys to focus too much on the increasing peak mean airway pressures um but definitely on that cardiovascular collapse okay so you they might be cyanotic you're definitely going to see hypotension and these patients will go into pea uh arrest potentially um if we let this go on for too long so we need to needle decompress quickly and prepare for chest tube insertion so pulmonary embolism is another one of those disease processes that result in a VQ mismatch uh which we talked about way earlier at the beginning of this presentation so this is what's called that physiological shunt right so this happens when air uh or blood or like a it says air uh gets into the alvoli um but blood isn't flowing there to to pick up the oxygen right so we are not getting gas exchange in this lovely little section of the lung so wherever the blood clot has formed so wherever the pulmonary embolism has formed um it's going to cut off blood flow to the entire section of of the lung where gas exchange then is not occurring and not only is gas exchange not occurring but this area the of the lung is actually becoming eskeemic which can cause pulmonary um edema because your in inflammatory markers are going to start going up white blood cells uh things are going to start rushing to that site and causing an edema in that area so this creates a problem obviously where some areas of the lungs have plenty of air but no blood to carry the oxygen to result right so the alvoli might still be blowing up because you're breathing in there's nothing wrong with the lung but it's just not carrying blood out to the rest of the body um another thing that can happen and this is a great graphic for that uh so as a result the body can't get enough oxygen right because we're not onloading an entire section of lung and vascule or sorry uh like circulation um to uh to actually pick up oxygen on this side and depending on where this is so if this is much higher up I mean you can potentially cut off an entire lung in and of itself uh depending on where the pulmonary embolism actually is and gets lodged so because of that carbon dioxide also isn't effectively being removed so when we talk about this and this is a decent graphic um we can actually cause like a right-sided heart failure all right and we'll talk more about that here in just a little bit but because blood flows from you know the right atrium right it comes into the right atria um it goes to the right ventricle and then from the right ventricle it goes through the pulmonary uh you know valve into the vascule so we'll talk more about like afterload um in in unit 4 but essentially what's going to happen is the heart actually has to work harder on the right side to pump blood to the lungs because this blood clot is is creating a resistance that the right heart is now going to have to overcome to pump blood to the lungs so it's actually the heart it's making so this is making the heart work harder to pump blood to the lungs to and not only that but the body knows that it's not getting enough oxygen so a normal compensatory mechanism is going to be tacoc cardia so now the heart is not only working harder on the right side to uh pump blood to the lungs but also now it's having to beat faster as well so our oxygen demand is actually going to go up as well so this can actually cause a right-sided heart failure which we'll talk about here in just a little bit so risk factors for throbo emolism um obviously cancer we talked a little bit about that I believe last unit um prolonged immobilization so we talk about you know long-distance flights long car rides hospital stays people who just sit around and don't do a whole lot pregnancy is a big one because pregnant people just have all kinds of uh vascular issues with increased blood flow uh and things like that contraceptives is a big one as well and hormone replacement so this this is the most tested in enclelex so when you see this uh especially when it comes to pees DVTs blood clots whatever throbo embisms um contraceptives in women are are the most common cause of and biggest risk factor for especially young women on contraceptives and it is the most tested in enclelex so know that and it might be tested here too um inherited blood clotting disorders obviously aphib uh heart failure obesity smoking these all contribute to throbo emolism so blood flow is shunted right from the underper proferused alvoli uh to alvoli that are actually getting good blood flow around the lungs so what happens is uh so this blood flow isn't going here but now it's getting pushed to other areas of the lung because this is happening we can actually cause like a pulmonary congestion so now because profusion is greater to other areas of the lung because blood can't get here so the heart's having to work double time pumping harder on this right side to pump blood to the the lungs uh it's actually making the blood flow to other areas much higher so this can actually cause like capillary leakage around other areas of the lung uh which then will cause like a pulmonary edema as well so now not only is you know the right side of the heart failing because uh it's having to work harder to push blood to other areas but now we're causing like a pulmonary uh we can be causing a pulmonary edema as well which will then uh translate to the left side of the heart right so direct uh physiologic pulmonary changes right include increased minute ventilation which I don't really want you guys to know too much about uh minute ventilation and vital capacity we're not going to focus too much on that um but it's all absolutely going to increase airway resistance right um and we're decreasing diffusion capacity those are the big things so pulmonary embolisms um can lead to core pulmonale core pulmonale is just a really fancy Latin term for right-sided heart failure but it's really good because it describes the relationship between both the heart and the lungs because remember the lungs and the heart are married to each other you really even though they're two separate organs they're very much intertwined so right-sided heart failure um is usually a result of lung dysfunction so it's usually caused by high either blood pressure in the lungs sometimes caused by chronic disease it can be caused by that pulmonary embolism because that right side of the heart has to work harder to overcome that resistance in the lungs in order to pump blood to the lungs therefore it can cause um dilation and stretching um of the uh right chamber of that right ventricle chamber it can also cause hypertrophy meaning that this um muscle wall is going to become thickened therefore it can become stiff and maybe not pump as effectively so what does that do i'm going to introduce a concept here to you guys in unit two that's a cardiac concept but I really want um and I want you guys to understand it because it's going to come back in both units four and in unit 5 um and it's actually going to keep coming back at you throughout the rest of the term and that's afterload so afterload we're going to talk a little bit more about it um like I said in those units but afterload is the force you would think afterload is something like cardiac output cuz that's kind of what it sounds like and this is something that when I went through nursing school again like I I kind I could regurgitate the the knowledge back to you but I didn't really quite understand it so afterload is the force that the heart must overcome to pump blood so we actually want a low afterload a low afterload is going to mean that this you know artery so this is the pulmonary valve um that goes towards uh the you know right and left side of the or sorry of the lungs so when the blood pumps out we want this to be nice and big and full so we want um this to be to have low resistance so when it has low resistance uh think of afterload as resistance so yes afterload I think it's just kind of a misnomer to be honest so when we think of it uh so think of the amount of resistance that this has to overcome so we want this artery to be nice and big and open because then we're going to have low afterload when we have high afterload or high resistance that means it's going to have to work harder in order to eject blood out of there into where it needs to go so the heart is going to have to work harder and that's very very important especially when we start getting into our cardiac units when we start talking about um cardiac output and the factors that affect cardiac output so core pulmonal increased afterload again afterload is just resistance so increased resistance and then that is what the word that I really want you guys to use for afterload so again when the afterload increases um the heart's ability to eject blood is impaired and how I kind of think about this is I think about like a vice so the more we squeeze the more resistance that we are putting on these valves the higher the afterload is going to be so treatment for this is aimed um at decreasing that right ventricular afterload so we need to decrease the resistance in order to improve right ventricular function and of course in the case of like a pulmonary embolism the best way to do that is we need to uh you know dissolve the clot or at least keep the clot from getting bigger which is why a lot of these patients usually end up on some sort of anti-coagulant or if it's bad enough we give them a thrombolytic uh in order to dissolve that clot and and improve afterload so core pulmonale um you guys do need to absolutely know this for the quiz because it's again right-sided heart failure so signs and symptoms of this are going to be JVD so jugular venus distension um peripheral edema so all of this blood that from the right heart because it can't pump very effectively into the lungs is going to start backing up into the body so anytime you have one side of the chamber fill remember it's going to back up to the rest to wherever it goes so right-sided heart failure or core pulmonale is going to back up to the body so that's why we get these big distended neck veins um we get hpatomegaly we'll get acites sometimes um so that liver gets big because it gets congested uh sometimes you'll have shortness of breath and hypoxia uh tacic cardia because the heart is trying to work harder in order to pump blood right um and then of course dizziness and syncope because our our body isn't getting the amount of blood and oxygen that it needs so again the severity of the hemodynamic changes really depends on the size of the PE and how extensive it is um as well as any uh you know pre-existing cardopulmonary conditions so if you imagine an a a good healthy adult who gets a pulmonary embolism especially if it's like a fairly you know even if it's a moderate- sized one these you know a healthy adult is going to do better than somebody with somebody with already heart like already has heart failure or has COPD or has asthma or some other sort of fibrodic lung disease uh these patients just aren't going to do as well with coorbidities which I feel like goes without being said but here we are so PE management uh basically kind of what I alluded to earlier we are going to you know anti-coagulate these patients so heperin is going to be usually our uh drug of choice when we talk about anti-coagulants because heperin is fast so heperin works very very quickly uh treatment with heperin usually continues for at least 5 days um however with that being said we usually start them on anti-coagulants fairly quickly like oral anti-coagulants so the difference between like a warerin and a heperin is heperin is is fast whereas um our warerin takes a little slower because it has to achieve therapeutic blood levels in order for it to become effective right that's why we are always monitoring INR now we have these you know newer ones and I feel like Eloquis is kind of the one that um a lot of physicians and providers are moving towards and I feel like there's a lot of research studies now that say that uh Eloquis is is best practice to use over Warerin just because of its ease of use and efficacy in these patients um and then just without the uh you know high monitoring and things like that too so oral anti-coagulation um should continue for at least 3 to 6 months following a PE um that may or may not be a test question so you guys may want to know that so oral anti-coagulation needs to continue for 3 to 6 months following a PE and again remembering back to unit one the reason that we don't want these patients on Heperin for long periods of time like we try to get them off the Heperin as soon as possible and honestly nowadays um I have seen patients come in with you know extensive pees maybe not huge ones but just a large burden of multiple pees uh we had this truck driver actually come in not that long ago had a ton of pees kind of all over never even started the guy on uh Heperin at all they just started him on Eloquist kept him in the hospital for 5 days and then sent him home so it's kind of crazy uh the things that they do now um and try to get people off hepin because of that risk for heperin induced thrombocyopenia um we want to be very very careful with these patients and that's why they're not on it because if you again if you remember back to unit one uh the chances for hit occur if especially with um patients who are on these for longer than 10 days 5 days is usually kind of max um but practice is changing however your book has not quite caught up with practice so for the purpose of this you know Heperin is still going to be kind of gold standard but just know that if you're in the clinical setting and you see these patients and you're like why is this patient with a pulmonary ambolism not on Heperin well practice is starting to change because there's just better you know it's that whole risk versus benefit thing right so the benefit has to far outweigh the risk um when we talk about signs and symptoms of that pulmonary embolism uh kind of what we've already talked about uh as far as patients with a PE most of the time these patients will go to just a regular med surge floor the reason that a patient would need to go to the intensive care unit is if they have like worsening hypoxmia or hypocapnea um because of spontaneous ventilation whatever uh worsening hypoxmia and hypercapnea if a patient has to go on a mechanical ventilator if they actually did end up having a cardopulmonary arrest because of this PE these are all patients that would then need to go to the ICU uh patients who develop ARDS which we'll talk about here in a little bit too uh the those patients will uh also have to go to the uh ICU so heperin guidelines um so heperin guidelines for this is essentially the the the units usually start at 18 units per kilo you guys do not need to remember this at all just know that generally speaking uh for heperin they usually get a bolus and then we'll usually start them on like a maintenance dose the biggest thing with this is we always want to check for bleeding um we always want to teach our patients about bleeding so definitely go back to unit one where we talked about all of those bleeding risks and the patient education um some of the things that you're going to want to look for and do uh as far as laboratory monitoring these patients are going to have PTTs drawn usually every 6 hours uh practice is also changing in that arena as well where we're also adding on an anti-10A so it's kind of you'll see anti and then X so pretend like the Roman numeral and then A um we actually have changed our guidelines at the hospital that I work at where we'll do an initial uh apt but then we actually titrate our heperin off the anti-10A value um so our protocols have changed a little bit so we use that um just cuz it's a usually a better indicator for kind of where our patients are sitting at for anti-coagulation with the Heperin so we'll still draw an initial PTT and maybe we might do one like the next day or something just to make sure that it's not very out of range but we base our Heperin uh titration and protocols off of the anti-10A and then of course these patients will go home on oral anti-coagulants for up to 3 to 6 months on that so thrombolytic therapy uh thrombolytic therapy is usually only recommended for patients who are at very very high risk of death and from refractory hypotension and hypoxmia from an acute massive PE again thrombolytic therapy is very much a risk versus benefit thing uh these patients when we give them a thrombolytic such as altplays um or TNK or something along those lines these patients are at a huge risk from bleeding to the point where you cannot um start another IV or anything on these patients without having massive bleeding around the site so anytime it's indicated or you think that you might have to give thrombolytic therapy to your patient uh it is important to make sure that they have at least two IVs um that if you they need an NG or any sort of tube or a Foley or whatever it may be all of that has to happen prior to this drug administration because any tube going into this patient um any sort of uh injury or assault can cause massive massive bleeding uh in these patients and we have to be very very careful so huge bleed risk uh to the point where they can just develop spontaneous bleeding like in the brain in fact they have to sign consents or usually some either if the patient is alert and oriented and fine the patient will sign or the patient's uh power of attorney will have to sign a consent to actually receive this drug because of the risks that are associated with it which is why we usually only give it in very very high-risk situations so just for example a patient who would potentially need thrombolytic therapy is maybe this patient has a PE they're already on like high flow oxygen and they're continuing to be hypoxmic so if that's the case remember back to your VQ mismatch so it doesn't matter how much oxygen we throw at this patient there is no blood flow going around that al alvoli so even though the lungs are functioning properly and the little alvoli are blowing up there's no blood surrounding it in order to offload CO2 and onloader oxygen so if that's the case throwing more oxygen at a patient who's already on like high flow oxygen whether it be a non-rebreather or actual high flow nasal canula this is not going to work for them at that point if they continue to go downhill continue to even uh start being hypotensive start having hemodnamic compromise throwing more oxygen at them is not going to help and I say this because if you get a test question that says your patient has a PE and they're already on like a non-rebreather or something along those lines putting you know when it says turn up the oxygen that's not going to help at that point we absolutely have to um talk to the patient or consider a thrombolytic uh in in that case so just make sure that you kind of understand that whole VQ mismatch um the PE when to to to do that's part of that clinical judgment and determining what is going to be best for our patients so IVC filters uh there's I think one or two questions on IVC filters so an IVC filter is recommended to prevent pees in patients with contraindications to heperin therapy so because it's a major risk for bleeding or drug sensitivity maybe in in the a case I can think of is maybe they have like vonilibbrrons or other some sort of hemophilia and so we can't uh give them any type of heperin or anti-coagulant because that can send them into a huge cascade of really terribleness of bleeding um in these patients with hemophilia or something along those lines that's just one example that I can think of of of why a patient would potentially need an IVC filter versus just starting them on anti-coagulation therapy so placement of an IVC filter um is recommended obviously patients with recurring throbo embolism um despite adequate anti-coagulation or uh patients with chronic recurrent embolism uh and pulmonary hypertension so remember with that pulmonary hypertension they can have that because they have COPD or something along those lines where the you know cuz remember COPD is an air trapping disease so it means that what that means is that they have a lot of trouble getting air out right those are the patients who do that ped lip breathing they do that to increase their exhale time so because when they increase their exhale time they can actually force out more air and that's why we teach our COPD patients to pursue when they're in distress because it can actually help with CO2 elimination because they're increasing the amount of time that they exhale normal uh respiratory um you know times are usually 1 second to inhale 2 seconds to exhale and so really if you think about that some of these COPD patients and even asthmatics because it's such an airtrapping disease sometimes it they can suck in a breath in about a second still but now maybe they need a 3-se secondond exhale time or even upwards of a 4 second exhale time so really we're just looking to increase that um and because of that because of that tension in their lungs and all of that air trapping it can actually increase the pressure in their chest when that occurs it can cause a pulmonary hypertension and so that's kind of where I was going with that we'll talk more about um you know intrathoracic uh pressures and things like that when we start talking about mechanical ventilation next unit but that's kind of what that means when we talk about uh current and and and pulmonary hypertension it can also mean like extra fluid and things like that too but just so you know or like leftsided heart failure right because if the left side fails it's going to back up into the lungs so just know that that's kind of what that means um concurrent surgical pulmonary embilctomy or pulmonary endarderectomy so endardctomy just means that they go in and they rotor rooter out um the arteries there okay so routine placement of an IVC filter is not recommended uh for patients who are eligible to be on heperin or some sort of anti-coagulant so again as long as these patients can be anti-coagulated um that's going to be the the primary treatment um IVC filters just know you will come across those uh but they're they're pretty rare and they're really only for patients um who have a lot of contraindications to heperin therapy so do understand that and know um that that's a possibility so going into COPD I know up to this point we've already talked a lot about like COPD and our kind of uh airflow limitation our our air trapping diseases right so COPD falls under that umbrella of uh of airflow limitation um and air trapping so COPD is not fully reversible so that is the difference between COPD and asthma it's still an air trapping disease um but in this case uh it's it it's progressive um so once you kind of have it typically patients get worse they don't usually get better so in COPD it does become harder to breathe over time um because the lungs are damaged they get stiff they get fibroic um and that's usually from uh irritation from harmful particles like gases or cigarette smoke right so COPD involves both the narrowing of the small airways okay so we have that narrowing so we have that airflow limitation and then of course we have damage to the lung tissue itself right so we have decreased uh air flow and decreased lung compliance so all of that really goes to say that these patients can be very difficult to manage in an acute exacerbation so when we talk about that VQ ratio mismatch um is the driving force be behind the hypoxmia in patients with COPD and that's usually regardless of that um and that VQ mismatch is because those little alvoli can't blow up properly and because of that um sometimes we have that air trapping and so with the air trapping only so much can go off so remember with air trapping you know they can breathe in but they don't offload very well so they're are CO2 retainers so what that means is usually oxygen moves from an area of high concentration to low concentration well if they can't blow off the CO2 because their air is trapped in their little alvoli that means that CO2 is in a higher concentration inside those alvoli which means that CO2 is not going to offload from those red blood cells very well because it's not passed through passive diffusion anymore because the concentrations inside the lungs and on the blood cell are more equal and so I hope really that kind of makes sense and everything that we've talked about it's kind of all coming together and why uh because knowing the why is very very important um as a nurse if you it kind of differentiates between just being a a decent nurse and being a great nurse is you have to know the why okay so because of that CO2 does not offload so that's why um this you know that VQ mismatch right so it's and it's more that ventilation side of it not the perfusion so this puts strain on the right side of the heart obviously so COPD patients because of this air trapping and that increased intrathoracic pressure it does put um a lot of strain on the lungs and it puts more pressure in the lungs so these patients have higher pressure in there which then of course makes it harder for that right side of the heart um so it's a big cause of core pulmonal or that right-sided heart failure so any sort of chronic lung disease can cause that core pulmonale right so this puts a lot of strain on it um which of course then makes the right side of the heart chamber bigger hypertrophic like we talked about earlier and then of course um it just doesn't pump as effectively as before so treatments for an acute exacerbation um obviously the cornerstone treatment for these patients is uh inhaled broncoilators uh like albuterol corticosteroids are big on these patients um just to reduce inflammation uh like fluticazone or something along those lines remember we have to be very careful about giving these patients supplemental oxygen for their hypoxmia because they're CO2 retainers and eventually after a very long time um the CO2 becomes the driving force for their respirations so you know in a normal healthy adult patient oxygen is is a driving force for when we take a breath when it triggers our brain to take a breath well in a COPD patient um they live with such high CO2 levels all the time that they almost have a reversal switch um in their brain so their brain now tells them "Hey your CO2 is too high now you need to take a breath." So when we give them a ton of oxygen it can actually depress their respiratory drive which is something that we don't want to happen because they need to offload the CO2 so remember increased respiration rates right just like we talked about with AGs it's going to blow off more CO2 and that's why they become respiratory alkalotic so if we depress a CO2 um retaining patients respiratory drive by giving them increased oxygen well now they're just going to retain more CO2 and we're causing worse of a problem so a short 5-day course usually systemic corticosteroids will usually be put on like a predinazone taper or something along those lines um most oftentimes in a COPD exacerbations we do not give antibiotics um and antibiotics are usually only given um in an acute exacerbation when and I know the picture kind of cut off the words but only when there's compelling evidence that there's actually like some sort of pneumonia or something along those lines so if we have a COPD patient who is having difficulty breathing we do a chest X-ray their x-ray looks kind of fluffy like they might have like a pneumonia or some sort of organism especially along the lines with fever uh and or you know positive respiratory cultures then we're going to be giving them an antibiotic so if we think the patient might have a pneumonia and of course fever is always going to be kind of a key clinical sign here that they're fighting something uh with their immune system and it's not just an exacerbation because of pollen in the air or it's springtime or maybe they you know the air quality sometimes gets really bad i know the last couple summers uh here in Iowa when we had those uh Canada fires um my grandmother has COPD and when the air quality got really she had to stay in her house there was no way she had to Usually she can get off of her oxygen when she's just kind of hanging out around the house but man when we had those uh Canada fires and all that smoke and debris was blowing down and the air quality was really bad she uh really just had to stay inside so a lot of teaching goes into that so indications for ICU admission uh for a COPD patient uh really is going to be that severe dismia with inadequate response to therapy so meaning that these patients are not responding to corticosteroids they're not responding to the bronco dilators um they're still tripoding they're still dismik maybe we have to put them on some sort of non-invasive respiratory uh device like a CPAP or a BiPAP those patients are going to require ICU admission because their um their risk for deterioration is very high not to mention most units will not take CPAP and BiPAP on the medical surgical floor unless it's like a home CPAP or BiPAP but I digress uh changes in mental status is going to be huge because that means that these patients are retaining a lot of of CO2 also sometimes if we do a blood gas and their CO2 is off the charts that's going to also be indicative that hey maybe this patient needs a little bit more respiratory support at least short term meaning that we need to either start them on a CPAP or BiPAP sooner in order to drive the respiratory or sorry drive the CO2 out and control their uh their rate as well so severe or worsening respiratory acidosis despite um oxygen administration obviously any hemodynamic uh instability and then of course the need for non-invasive and or invasive mechanical ventilation so asthma asthma is a long-term lung condition and the difference between asthma and COPD is patients with asthma you can actually correct their airway and it can for the most part go back to normal um when they're not having an actual asthma attack so you know inflammation uh you know and a lot of different causes for this it makes it harder to breathe because those airways obviously become narrow they become inflamed they become more sensitive to whatever it is that is going to trigger them so symptoms are going to include wheezing because remember they're breathing through a straw so it's going to create a lot of adventitious lung sounds wheezing is going to be the the biggest one because they're trying to breathe through that little straw shortness of breath chest tightness these patients um especially if they come in and they are in severe distress and you listen to them and they are tight and you don't hear hardly any air movement that is a really really bad sign and they need an albuterol treatment stat as well as um potentially and usually it's three backtoback nibs we'll reassess we'll give um IV steroids a lot of times especially if they're and a lot of times once you give those three backtoback uh nebulizer treatments You'll actually hear them start to weeze and you'll actually be like "Oh god they sound worse." No they actually sound better because now we've actually opened up their airway to actually produce a weeze the problem before was we weren't hearing any sounds because their airways were so tight that they couldn't even produce a weeze and that is really really bad so a lot of times once you actually open them up they actually what you would think maybe sounds worse but it's not it sounds better so we like to actually hear our patients we if prior they didn't and they were in very uh you know dis you know big-time distress so just make sure that you kind of understand that especially if they look a little bit more relaxed um they still might be in distress but maybe they look a little bit more comfortable they're not as anxious so during that asthma attack the airways may suddenly right tighten bronco constrict they become swollen they fill with mucus make it even harder to breathe um so things that can trigger an asthma exacerbation so definitely understand this exercise can trigger it allergies changes in the weather um or just you know a lot of cold weather uh and other respiratory infections okay so just make sure you understand the causes of this so memory uh trick for this asthma acute attacks that come and go right um there's different levels to an asthma attack so there's that mild to moderate there's the severe and then of course there's that life-threatening so life-threatening is those patients where we I just kind of talked about they have absence of wheezes um and then once you start to open them up oh now they have very loud wheezes okay so that's when you're like they sound worse no they actually sound better um the other thing that once they get to this point a lot of times because they're so hypoxmic their heart rate will start to drop again very very bad sign so we want them tacocartic we want loud wheezes um you know we want them to at least get a couple words out sure they can be agitated uh they can be you know tacipnic this is better than this all right so just make sure to kind of understand that if it's if they're mild to moderate usually they're a little tacocartic um you you might hear a little bit of wheezing uh oftentimes it's just at the exhalation phase like at the end of the expiratory phase um sometimes they might have uh some accessory muscle use but you know most oftentimes it's more of a positioning thing like they'll kind of be leaning forward maybe they might be kind of taking a trying to take that deep breath like usual um they're not usually agitated but they are kind of having that difficulty breathing um and then of course they can talk at least in phrases get a few words out you know they can maybe talk in one sentence and then they have to recover and then maybe they can get another sentence out um that's totally fine so breathlessness even with you know mostly just with walking but when they sit down they're maybe a teeny tiny bit better and then of course with our severe asthmatics like they are breathless even at rest so just kind of understand the difference between those two and again all the things that we've already kind of talked about with uh the absent breath sounds so that silent chest is a priority that is definitely going to be a like enclelex question andor hessie question so that acidosis that air trapping again kind of going back to that prolonged exhalation phase um some of these patients you do not want to intubate an aszmatic if you don't have to because they are very very difficult to manage on a ventilator they're very much better off doing what they need to do uh by themselves with just a little bit of help from medications so patient teaching for these uh for these guys is going to be obviously try to avoid getting sick which you know that's easier said than done um getting cold like going out in severe weather um try to avoid any big strain uh strenuous activity however if you if they do do you know strenuous activity make sure that they have their rescue inhalers and things like that available um maybe even taking meds before they exercise like allergy meds or maybe taking that puff of the albuterol prior to working out um drugs to avoid uh NSAIDs aspirin ibuprofen toridol because those can actually induce bronospasm which will then trigger an asthmatic attack um so those aren't good for asthma uh beta blockers also so beta blockers can actually induce bronco constriction um because remember there's beta cells in both your heart and your lungs so when we talk about that so if if we're giving a beta blocker uh especially if it's not a specific beta blocker for the heart um if it's not just like a beta 1 and most oftent times they you know at least have some degree of effect on all the beta cells both in your heart and your lungs so just know that that those beta blockers can cause bronco constriction uh and so those usually are a no-go drugs to avoid as well so you know looking at your peak flow meters those are going to be a big Enclelex questions as well you're not going to get tested on that for this course but definitely your peak flow meters for some reason Enclelex likes to test on this i'm not sure why but they do so there's that so factors affecting the disease progression uh obviously what age were you when you were diagnosed because the younger you're diagnosed usually the worse your progression of the de disease is going to be what your current treatment is so if you can manage on an inhaler for the most part um then you're doing pretty good if you if it's very rare that you have a big asthma exacerbation um if you maybe have one a year or even one every couple years then you're doing a really good and that's going to actually limit the progression of the disease um effects of symptoms on uh activities of daily living so if you're somebody who can't work out without having an acute asthma exacerbation um then you're probably more likely to have a further progression of the disease so obviously impact on asthma in the patient family just because a lot of these kids are young and sometimes a lot of these kids when they're diagnosed they can kind of grow out of it a little bit because in pediatrics which I'm sure you guys will talk about when you guys talk about respiratory uh pediatric patients have a very uh narrow airway so the narrowest part of their area so so their airway is like cone shaped and so when that happens um they it's very narrow uh at that kind of base of the junctions right at like the crycoid and so what that does is it creates like a like a funnel uh in there and so they have they're more prone to to getting these types of airway diseases especially when they're young as the patient grows up and gets older their airway widens um it gets more cindrilical in shape and so you know they kind of grow out of some of this but at the same time depending on how bad it is when they're young uh these patients can still have a lot of uh symptoms of asthma as they get older and then of course beliefs uh regarding and then not even just beliefs regarding the use of medications but even just affordability of these medications um and the economic impact that it makes on these families so when we talk about management um of these patients uh they should be given extra oxygen right away so they should be put on like a non-rebreather or something along those lines because remember these patients are not like COPDers where they can have reverse um so remember our asthma exacerbations we can actually reverse uh the the lung tissue and like that inflammation fairly quickly and they go back to being normal for the most part it's they don't get like a lot of fibrosis and things like that unless um you know we they have a lot of in inflammation and a lot of uh you know asthma exacerbations to begin with so if the patient isn't getting better with kind of the treatments that we've talked about up to this point so oxygen um aluterol treatments we can start giving the duo um steroids if they're not getting better and still requiring support or high flow oxygen then usually we'll give them magnesium sulfate IV so we'll give them a magnesium over 30 minutes um and that can help to open up the airways as well because it's a bronco uh it helps with like relaxing the bronchioles out so for these patients um again a lot of times if they're you know drowsiness confused that silent chest if we're needing to give them magnesium or they're needing continuous albuterol so if we've given them the backto backto back elbuterol we'll try to wean them off oxygen or at least get them down to like a nasal canula if they can't tolerate that and they're needing um another nebulizer treatment within 2 hours and they can't maintain that Q2hour nebulizer then they have to go to the ICU so that's just one thing that um is kind of what we look at especially in the pediatric population when we're uh talking about asthmatics so acute respiratory failure we got a couple more slides here and then we'll be done i know this was a super long lecture as well uh acute respiratory failure uh it's you you can either have acute hypoxmic meaning we have low O2 we can have um high uh you know CO2 hypercapnic failure or we can have a mix of the two and have both so just kind of understand that either low oxygen or high CO2 is actually a classification of respiratory failure not just distress so our Pao2 is going to be less than 60 and our PA CO2 is going to be greater than 50 so low oxygen levels in the blood um hypoxmia can happen when there are problems with how the body takes and delivers oxygen i feel like we've talked a lot about this throughout this lecture so I'm not going to really hit on that anymore i just really want you guys to understand the definition it's that a pao2 is going to be less than 60 so hypercapnic respiratory failure is basically going to be that signs of hypercapnea remember your pa2 is going to be greater than 50 and they're also going to have that signs of hypercapnea so drowsiness confusion sometimes slur speech altered mental status changes they can have that hand flapping which is this astericsis um I included that on there because it does I think Enclelex will potentially test on that there's there's a good chance that you might get that word and that's kind of hand flapping and that's from um basically kind of like a like a mental status change whether it be hypercapnea sometimes it's uh encphylopathy can cause that hand flapping asterexis and then of course sweating so management of acute respiratory failure uh is going to be kind of similar to everything that we've talked about up until this point so we need to establish an airway we need to give these patients oxygen we need to provide ventilation whether it's non-invasive or uh mechanical really what it is is we need to find out the cause of the respiratory failure and treat that so if they're in respiratory failure because of COPD we need to treat it how we just talked about if they're in respiratory failure because of asthma we need to treat that like we just talked about so we need to figure out the cause and then we need to treat the cause not just the symptoms of course uh if these patients have low fluid balance like if they're uh hypotensive or anything along those lines we need to give them a fluid bololis um we need to optimize cardiac function uh prevent early complications if it's a pneumonia or something like that like we just talked about we need to give antibiotics and like your book says you know better outcomes uh are with pneumonia and antibiotics are if those antibiotics are given within the first eight hours so again anything along those lines we need to find the cause we need to treat it so just know that your patient is going to be uh you know diagnosed as like a failure if their PAO2 is less than 60 and their PA CO2 is greater than 50 all right guys this is the last slide thank you so much for sticking with me i know this was a long one if you have any questions or concerns please email me and let me know