hi everyone welcome to the third part of our respiratory unit this is acute respiratory distress and mechanical ventilation okay so just as a little bit of review I wanted to put this picture up here of the normal gas exchange unit a reminder that oxygen comes in we breathe it in and uh carbon dioxide is then offloaded what you see here is the alveolus so a single alveoli and you can see that there's a deoxygenated blood comes in and then it is oxygenated and returned to the heart for circulation so this is the basis of gas exchange in the lungs and very important to what we're about to talk about so when stuff starts to go wrong with the lungs one of the things that can happen is called a respiratory failure acute respiratory failure respiratory failure can be divided into two specific types the first one is hypoxemic respiratory failure also known as type 1 respiratory failure and this failure we have low oxygen in the blood now this can be due to cardiac or respiratory causes for example cardiogenic shock ards pneumonia smoke inhalation even hemorrhage basically there is not enough oxygen into the blood the other type of respiratory failure is called hypercapnic respiratory failure or type 2 and this is a failure of the movement of the air in and out of the lungs so this is ventilatory failure now the signs and symptoms between those two sometimes overlap and sometimes don't so let's look at the actual signs and symptoms for hypoxemic respiratory failure the person is generally short short of breath with an increased respiratory rate increased work of breathing their O2 sats are low which can cause altered mental status and hypercapnic respiratory failure the person is also short of breath you'll see them tripod purslip breathing and with decreased deep tendon reflexes they can also have an altered mental status that's usually because sometimes somebody starts with hypercapnic respiratory failure and ends up with hypoxemic or vice versa and therefore we do have a lot of overlap but those are some of the specifics and then there is a third type of respiratory failure which is mixed respiratory failure so as you can tell that would be both so a failure of oxygenation and ventilation so the treatment of all of these respiratory failures does land on some specific things first of all oxygenation we need to apply oxygen to people who are in respiratory failure to make sure that they have oxygen available to be offloaded into the system we mobilize secretions to make sure that they have effective Airway clearance and get anything out of the alveoli so that we can you know expectorate and make sure that gas exchange can occur at that lower level we use medications like bronchodilators steroids diuretics we maintain their mean arterial pressure greater than 65 which is more of a concept under shock but mean arterial pressure basically that's a measure that we can get off of our blood pressure that shows that we have good perfusion to our end organs and then another thing we need to do is make sure that the person has good nutrition these folks are in a hyper metabolic State it's hard work to breathe hard and fast and these people need nutrition so ideally they need to be eating within 24 to 48 hours of presentation okay so respiratory failure we spoke about acute respiratory failure um you can have chronic respiratory failure underlying even hypoxemic and hypercapnic and what happens with these folks is a lot of times they have exacerbations so an exacerbation of hypercapnic respiratory failure would be a common one would be a COPD exacerbation so the difference is how long the signs and symptoms are lasting and you could see that for acute it's within minutes to hours and chronic is longer than that so the next concept I want to discuss with you is something called a VQ ratio so VQ is basically it's ventilation uh is the V which is the air in and out and Q is the perfusion so that's the blood going round and round so for this uh we definitely have normal VQ ratio of 0.8 to 1.2 um and basically we want that to be in that range like if we had a one to one ratio that would mean that ventilation and perfusion were pretty evenly matched so healthy VQ is one and then we do accept a little bit of a range outside of that so 0.8 to 1.2 but not a very big spread what happens with shunting is that we have an area where there's perfusion but no ventilation so remember ventilation is the air in and out so the blood is there but it cannot pick up any oxygen and at that point the the level there is zero so things that would cause that would be like pneumonia you can see them listed here atelectasis a tumor something blocking then the third one is a dead space so this is where we have the air moving in and out but there's no blood to collect it so this means that we're unable to even calculate the VQ ratio so that's a high ventilation and no perfusion so there's uh it's to Infinity so this would be pulmonary embolism cardiogenic shock so we're not perfusing into the lungs thank you those are the main causes and then the fourth if you see down in the right hand corner there that's a silent unit that means that there's no ventilation and there's no preview perfusion so a pneumothorax where the blood supply is clamped down and also the lung is collapsed severe hours it is a terrible thing to have a silent unit none of these are actually good let's take a look at a graphic of it so here you have just exactly what we talked about ventilation perfusion so if you want to pause here you can see some of the different causes you could see the air normally moving out the center would be a normal unit and then on the right we have perfusion well on the right side of the slide so it would be on your left as you're watching this a perfusion without ventilation and on the right would be ventilation without perfusion so we're going to explore the topic of pulmonary shunting just a little bit here basically the lungs are smart okay not as smart as the kidneys but absolutely smart they detect hypoxia and then they vasoconstrict the lungs so this is why any Oxygen given to folks when they're shunting will not reach those areas [Music] imagine if you will you're congested on the Thruway so basically you you need gas there's no gas station and traffic is backed up you get off the Thruway so that's that's basically What's Happening Here that the um deoxygenated blood is going from the right to the left heart without gas exchange [Music] and there's that hypoxia reflex so it's different than peripherally peripherally if we have hypoxia it causes our vessels to dilate but in the lungs it causes them to constrict and this is a life-saving thing sometimes right it's the the lungs basically working to get the best oxygenation so if there's an area that's not working it shuts it down foreign so remember the oxygen never reaches the blood so this is why we give oxygen for respiratory failure because generally there's some measure of relative shunting with our oxygen and this would be absolute shunting so we need to give oxygen regardless oxygen is palliation here we need to work on reversing the cause of the respiratory failure and I wanted to take a moment and uh really let you know something about the abgs which is our pao2 which we talked about normal is 80 to 100. once it gets to 60 to 79 so we're just a hypoxemic in the arterial blood gas it usually doesn't strain the cardiovascular system however we put oxygen to make sure it doesn't moderate hypoxemia is 45 to 59 and this we will end up with massive hypoxia if the system is not able to compensate so we give oxygen there and if our pao2 is under 45 that is severe hypoxemia and associated with tissue hypoxia and needs immediate correction so you can see the common denominator here is once we get under 80 we really want to apply oxygen to prevent bad stuff happening to our patients and this was an interesting question but it says when caring for a client with hypoxemia and right-sided pneumonia the nurse knows to place the client in which of the following positions to improve oxygen saturation so you have left side down right side down semi-fowlers or high Fowlers and in this case if they have a right-sided pneumonia then you want to put them left side down so we increase the blood flow by laying on the unaffected side so good lung down so that's the uh that's the answer to that so now let's start talking about some of the indications for mechanical ventilation so you can see here that it's pretty black and white at NCLEX Hospital right we we have definite times when we would intubate and definite times we wouldn't however what you see out in the actual world will not always mirror this there are many reasons why a person who normally would be on a ventilator isn't including Advanced directives and also their their state right so we want to be able to have people who go on the ventilator who have a chance to come off so those are discussions that the doctors have and we will often delay mechanical ventilation as long as possible if some of our other treatments are working but you can see here in Red so the pao2 is under 55 and we are giving them at least 60 oxygen so the fio2 is 0.6 or 60 oxygen so that means that despite us giving them that oxygen they cannot hold their blood gas or their CO2 is over 50 with a pH less than 7.32 and that's for usually acute deviations if somebody has chronic deviations we do allow a bit more wiggle room in there the respiratory rate if it's over 35 so this means that the person's working very hard to breathe and then a result of any other pulmonary functions tests so what we see clinically in a patient you might see them not breathing or breathing slowly so that is an absolute indication for mechanical ventilation if they are not breathing at all a respiratory respiratory distress with confusion um in fact when the oxygen falls under 55 acutely the short-term memory is altered and the patient actually can experience like a Euphoria and impaired judgment people who are in Shock States so Global hypoperfusion and again if they're just working super hard to breathe then nothing else is working then this might be it so I don't think I want to say anymore on that actually I do want to say something uh there is something to be said about uh decreased oxygenation as well and one of the things I always learned was that the brain softens before the lung so this is just a reminder that sometimes some of the earliest manifestations that we see in a patient revolve around their increased respiratory rate trying to compensate and then that altered mental status sort of agitation um and the other thing I want to mention here is the role of oxygen toxicity so we'll talk about that later as well but we always need to be concerned about oxygen toxicity so we want to use the least amount of oxygen for the least amount of time possible again that's the key what's possible and what's not all right so let's talk about some of the common ventilator settings so this is from your textbook some of the things that you'll normally see you'll see the respiratory rate tidal volume fio2 and then the positive end expiratory pressure so these are just settings uh there's tons more that the respiratory therapist will set and reminder when we talk about mechanical ventilation is that the respiratory therapist is your best friend when it comes to people on the ventilator the respiratory therapist has a degree much like you're seeking right now it's a they have a two-year degree and it's all in respiratory and lung function and Vents and they can be an amazing resource so the normal respiratory rate is set between 12 and 20 for adults you should recognize that as a normal value the tidal volume is based on the patient's weight and usually six to eight milliliters per kilogram and for hours a little bit less and the title volumes how much error is given during each ventilator breath and then the fio2 is the percentage oxygen so room air is around 21 and it could go all the way up to 100. and you can see we usually adjusted off the abgs to keep the O2 level 60 to 80 which is sort of what I talked about before that we don't see a lot of cardiovascular compromise until we get under 60. and then the positive and expiratory pressure that is a little extra that holds the lungs open at the end of expiration so basically it keeps the alveoli from collapsing usually we only need five but with ours we usually need a lot more peep so CMV is also called assist controller AC so basically this is the ventilator doing the work of breathing for the patient so assist control CMV you'll see them written they're exactly the same so this mode is used for patients who require the most support from the ventilator their tidal volume is usually set like we said four to eight 10 MLS per kilogram in that range uh sometimes require decrease due to lung compliance SS control can be used in patients who are spontaneously breathing or not but there's a couple of downsides here so uh people who are on CMV or assist control are more likely to fight the vent so if the patient's body is calling for more tidal volumes or they're not breathing in sync with the machine then the person can absolutely fight the vent they'll have high peaked pressures you'll see their Vital Signs will be skewed and um this can lead to poor outcomes for the patient which is why often when we see fighting the event we look at the need for Sedation and analgesia the most important being sedation and then the other thing is because this is basically oftentimes doing a lot of work for the patient prolonged use ends up decreasing the use of the respiratory muscle so it's actually harder to get the patients off the vents when they are on CNB or assist control foreign other common mode is synchronized intermittent mandatory ventilation so basically uh the machine is a bit smarter here right basically it's allowing the patient to draw the breath and if the patient does not draw the breath then it will provide it for them so this is called the weaning mode usually it causes the patient's respiratory muscles to work more so allows them to sort of exercise their lungs but for weaker or critically ill patients this can actually cause them to tire out easier because again it's causing them to work more but this would be your uh this would be your weaning mode and now a little bit more about Peak you'll hear about people a lot when we talk about respirations and respiratory stuff so peep prevents the alveoli from collapsing and we usually are set around five and we need more than five when we have decreased lung compliance so things like ours severe pneumonias those can cause decreased lung compliance there are some complications with peep the more sort of pressure we leave at the lungs at the end it can actually cause compression of some of the thoracic vessels which decreases venous return so if that's the case anything that increases pressure in the thoracic cavity can lead to a decreased return to the right side of the heart and then barotrauma pneumothorax is always a concern so we can cause the alveoli to rupture and if that's the case then what we see would be basically the same signs and symptoms of a pneumothorax that we've already learned and if that's the case the person may need a chest tube in general we want to avoid High peep but sometimes it's necessary I know there's a couple other types of ventilation that we don't really talk about too much in this course but just to let you know they exist for when we have to worry about more of these um more of these issues with peep we have airway pressure release ventilation and which the expiratory phase is longer than the inspiratory phase but the problem with that is it does cause more pneumothorax and other barotrauma and then we have the high frequency oscillatory ventilation that keeps the people almost constant but also increases the risk of pneumothorax and Barrel trauma so that's the ventilator setting I don't know if you've ever seen that they put it on cream creamies on it quite often it's almost like it's shaking them [Music] now that we've discussed that let's go down to the actual intubation of a patient so we do most places now we'll use video laryngoscopy glidoscope allows us to see and record while we're doing it so you can go back and and take a look but you see there basically this is a laryngoscope that's one folded up and that's uh all the different handles and size blades that one can use so you'll see the doctors asking for the blades the curved ones are Mac blades and the straight ones are called Miller not that you need to know that but [Music] uh the Mac blades I always remember them being curved because they're like an apple like a Macintosh Apple so that's how I remember them so I look real smart in the room if the docs has hand me a Mac and I know what it is so intubation so that's the tools that we use and then let's talk about some of the medications the medications here are very very dangerous medications so you want to know exactly what you're doing with these meds in fact there was just recently a case with a nurse who gave a neuromas neuromuscular blocking agent and basically killed a patient her name was radon devot so the medications we may use some pre-medication so atropine and Lidocaine lidocaine is not normally given you might see it in case of increased intracranial pressure so anytime we're doing any of these Maneuvers we can cause increased pressure so if we have somebody with a head injury or something like that then they'll often give lidocaine so it's not normally given and then we have the induction meds so these are sedatives and anesthetics including automate fentanyl ketamine midazolam and propofol so that's how those are all pronounced and then the paralytics so the nmba's neuromuscular blocking agents so some of those are succinylcholine panturonium and Rock uronium so things we you should know about them is succinyl choline is fast but you can't reverse it you have to wait for it to wear off and Rock uronium takes a little bit longer to work but uh it does have a reversal agent which is the neostigmind so anytime we're starting to consider giving any of these meds especially those neuromuscular blocking agents your concern has to be for the ventilation of the patient because once one of these drugs takes effect they are not going to be able to move a muscle all right those Nimbus or neuromuscular blocking agents basically will make it so they cannot even blink an eye or move a diaphragm so you must be prepared to ventilate the patient we use them sometimes even when the patient's already ventilated so if somebody is really really sick and uh or they're you know they're fighting the vent so much this is why we sometimes will give these but remember if we're not using it we're losing it so increased use of these neuromuscular blocking agents can actually work against the patient so the more sedatives and blocking agents they have on board the less likely they are to be doing their own work of breathing so it can make it very difficult to wean these patients so bear that in mind one of the main ways we intubate somebody is called rapid sequence intubation this is fast it's very effective for emergency Airways and the reason we do rapid sequence intubation is because most people who have an airway emergency don't plan it right they don't plan to say you know at two o'clock today I'm going to go into respiratory distress and need to be put on a mechanical ventilator so I'm going to make sure I'm NPO for you know at least eight hours before so a lot of these are emergency situations so we need to gain immediate control over the airway while making sure we negate the impact of people who have full stomachs or if they have an intact gag reflex so rapid sequence intubation so people people who are already like in a CPR situation we don't do rapid sequence for them they don't need any medications generally because they're they're unconscious and they're basically don't we don't need to do that we're trying to save their life so this is for people who generally were having an emergency situation and still have intact reflexes [Music] so we do an induction agent first to induce unresponsiveness and then we do the neuromuscular blocking agent and that again makes them stop breathing all together so it can be very risky if you have a doc who doesn't know what they're doing or a team who is not communicating well so always remember to make sure that you are bagging this patient with a pvm all right and here is the actual side view of endotracheal intubation if you're not sure what size to grab for the tubes we say it's the rule of Pinky so rule of finger so take the patient's Pinky and that's usually the size that you need it is a this can be pretty dangerous um to make sure you have it in the right area and not too far down if you can see here you could almost put that right down the right bronchus and or in the esophagus uh go through the epiglottis [Music] and then the next thing is how do we check placement once it's there so let's say DACA basically intubates the patient so we usually uh what we'll do is inflate the tube check to make sure the lungs are expanding uh equally check the breath sounds listen over the stomach and I do mine a little different I always listen over the stomach first because if that first breath is in the stomach I want to hear it not after you know the third breath that goes down there uh we have an end title CO2 detector so these are chlorometric detectors so if it's working it should turn yellow like big bird we don't like Barney we like big birds so we don't want purple we want yellow and then we secure the two at this point uh there's potential we could have put a lot of air in the stomach talk to the docs see if anasic gastric tube is indicated plus we'll need some form of uh so decompression initially but then to make sure we're feeding the patient and then we did get the chest x-ray to confirm the two placement yeah you always want to Mark where the tube is at the lip line all right so you always want to know where it's at so if it's at 22 at the lip line you want to document that and that's where it should stay we want to make sure we're checking those cuff pressures for our mechanically ventilated critically ill patients every six to eight hours and we talked about the reasons for that previously sometimes people need a Bite Block to keep them from chewing on the tube obviously we need good oral hygiene and suction of the oral pharynx as needed so if any secretions are kind of lodging in there from that uh repositioning to prevent pneumonia to prevent atelectasis and then of course warming and humidifying of any Oxygen that's given so our ventilators nowadays they take care of that they warm and ventilate the air so some of the the problems with uh mechanical ventilation in general one of them is value trauma which is the title volume is too high and over distend the alveoli the other is Barrow trauma which is um basically elevates the lung pressures sometimes too much peep so if we see signs of Barrow trauma that will be low oxygen levels tachypnea agitation high peak pressures so depending on how much Barrel trauma the person has subcutaneous emphysema is also sign of a barotrauma so what are some of the complications sorry about that complications of of intubation basically the tube itself being in the trachea we have the patient unable to speak we can cause laryngeal's stimulation and increase intracranial pressure and of course the patient could accidentally remove it so people who are acutely ill and on mechanical ventilators you'll often see them with wrist restraints on and if that's the case we don't usually count them as restraints for that reason they are not re they are restraints in the strictest sense but they're not considered restraints per standards because they're to keep the patient alive and not actually trying to restrict their voluntary emotions okay so let's take a moment to talk about the ventilator alarms these are there's a lot of different alarms that will go off some for low pressure some for high some for um minute volumes and for title volume but the the main ones we'll talk about are the um low and the high so the one thing I always want to bring you back to here is no matter what's going on if the ventilator fails for any reason if you cannot figure out the source of an alarm and you cannot ensure that the patient is being adequately oxygenated and ventilated then you have the power to take control of the patient's Airway and bag them yourself while you get some assistance it's never okay to just turn off an alarm and silence an alarm without looking for the cause all right so low pressure the low really means there's a leak somewhere there's a disconnect or an air leak in the circuit so this alarm occurs when the ventilator does not have enough resistance that it's pushing against so if you see a low pressure alarm or hear it things that it could be are um any of the connections most common is that it's literally connected right from the patient so check there first and you know make sure it's on and then uh if it's on then you have to change trace the circuit looking for any disconnection sometimes there's like little caps on things or people are getting um like breathing treatments through the vent they have a little cap cover on that that could have blown off so just check there and if you cannot figure out the cause you can bag the patient get the respiratory therapist involved now high pressure is on the other alarm uh are the other alarm to worry about if these are the uh basically when the machine the ventilator is sensing too much pressure that it's pushing against so um high pressure alarms is usually I think of like a plug right increased airway pressure this could be that the patient's coughing this plug they may have pulmonary edema could be a pneumothorax the patient could be fighting the ventilator and if that's the case we want sedation for the patient you'd want to call and get some atelectasis bronchospasm so what do we do right first and foremost the person just may need to be suctioned they could have Kink tubing if they're biting you can use an oral Airway they have a pneumothorax you need to prepare for a chest tube okay check the abgs if needed so basically most common are going to be secretion suction and biting and fighting remember if something bad is happening you cannot figure it out you can take the airway and bag them yourself [Music] all right so let's talk about suctioning a little different than open suctioning like a trach this would be inline suctioning uh these are great honestly uh these sometimes you'll see them attached to a t piece to a trach but definitely with our mechanically ventilated patients because it allows us to suction the patient without taking them off to then and that allows the peep to continue and that is very important because if we were to disconnect the ventilator any peep that was being given by the ventilator immediately ceases it's better infection control and also protects us okay but the treatment of suctioning is pretty much the same so you definitely want to oxygenate them prior you can turn up the ventilator to a hundred percent and the same thing applies if you see a dysrhythmia or anything happening then you need to stop what you're doing in hyper oxygeny the patient now basic care of somebody with an endotracheal tube is to check that position at least every four hours assessing Their Skin Integrity stability of that securement device thank you auscultate their lung sounds and then do their Oral Care very very frequently [Music] the reason we want to do this is because people who are on a ventilator at high risk for ventilator-associated pneumonia so we know it's ventilator-associated ammonia if it occurs 48 hours after they're intubated so people who get pneumonia from the ventilator they end up with longer hospital stays worse worsening outcomes they are often subjected to many different uh antibiotic resistant organisms and just like we have bundles to prevent against catheter Associated UTIs we also have them to guard against ventilator-associated pneumonia so some of the things we need to do Elevate the head of the bed give them sedation vacations and try and get them weaned off the ventilator chlorhexidine for their Oral Care we need to reposition our patients and then other common care that would be needed would be stress ulcer prophylaxis and DBT prophylaxis so we do not want these folks who are mechanically ventilated to get a stress ulcer so usually on a proton pump and head burger and they should be on anticoagulation as well um okay so now we're going to talk about acute respiratory distress syndrome so with ards basically we lose the ability uh for our alveoli to basically participate in gas exchange the capillary membrane damaged and um more permeable which allows fluid to leak into the alveoli basically makes it like a cotton ball that you dip in water so 10 of all ICU admissions were for ards and this was pre-covered I'm sure the numbers changed with covid 50 mortality rate a sepsis is the most common cause of acute respiratory distress syndrome but there are multiple different causes to it so remember it's it's not necessarily [Music] um a lung issue at its start that's where we see it but it generally it's usually from a systemic disorder but let's talk about a little bit more basically it does result in a lung injury and it could be direct or indirect so some of the indirect sources would mean that the source really isn't the lungs this could be sepsis uh transfusions like trolley people who experience Burns pancreatitis drug overdoses or it could be a direct result of the lung injury and that would be pneumonia aspiration inhalation drowning embolisms but in general whatever has happened usually isn't in an island so what I mean to say by that is the patient is ill all right they have some measure of inflammation in their body and the more inflammation the more likely it is that the the lungs will be damaged so even if that has nothing to do with the lungs it could end up in the lungs and sometimes it does start in the lungs so there's a different phases of Arts we're going to get to those next all right so there are three main phases of Arts you have the exudative phase proliferative and then the fibrotic phase so uh you can pause here to sort of read that but we're going to go into each one of each one so the injury or exudative phase uh basically starts within 24 hours to 72 hours after the initial lung injury so or whatever is happening to cause the problem basically we have a cytokine storm so that's leaking and what do we leak we're leaking fluids and proteins and other substances and proteins draw water into themselves so as a result of this fluid starts to build in the interstitium so early in this phase the person doesn't have altered lung songs or adventitious lung sounds because it's in their interstitium so the alveoli are still functioning but there's fluid in the interstitium but eventually it does cross the alveoli membrane and enter the alveolar space and that leads to the capillary blood not being oxygenated which gives us a mismatch and then starts a shunt which then stimulates more inflammatory and immune systems so as a result of that we end up with a compensation initially but then the patient no longer compensates and the person ends up with decreased oxygenation decreased cardiac output decreased perfusion so they can go into shock which can lead to multiple organ failure or multiple organ dysfunction syndrome foreign death so but it starts with this phase and in this phase the cells that produce surfactant are starting to get damaged so surfactant basically allows for the smooth movement of the alveoli and then there's something called the hilar membrane so basically a high line membrane forms it starts to form in the injury phase and then it really really takes off in the uh in the next phase so how do we start to see some of these signs and symptoms so the injury phase so they're surfactant dysfunction um the hyaline membrane makes everything stiff we have the shunting and here's the kicker the patient is not getting better despite giving them oxygen so what will we see initially we'd see respiratory alkalosis as the respiratory rate increases and causes loss of CO2 in fact the increased respiratory rate is one of the first signs of ards but then as the membrane continues to grow its blocks the CO2 release and then you'll start to see the person retaining CO2 [Music] so after that first phase we go into the second so if that problem continues for one to two weeks after uh then this reparative or proliferative phase continues on lung compliance continues to decline um we have ever increasing inflammation and can have pulmonary hypertension and the goal here is to not progress to the fibrotic phase so if we stop this phase the patient can generally get better if we don't if this phase persists then they end up in the fibrotic phase [Music] and there's the fibrotic phase this is The Chronic relate phase it's two to three weeks after um if the person doesn't recover they their tissue becomes really fibrotic they'll have pulmonary fibrosis so if patients are going to recover it's within six months that they would have the pretty normal lung function but generally it's not possible generally people do not recover from this [Music] so let me just move this guy over here so let's recap ours so basically our O2 is less than 60 of pco2 greater than 50 in a pH less than 7.35 we have a cytokine issue with tumor necrosis factor interleukin-1 and 6 which leads to leakage and pulmonary edema and then decrease surfactant production alveolar collapse so the Hallmark here is increased capillary permeability with hypoxemia unresponsive to oxygenation so chest x-ray would show bilateral infiltrates from white out and this has to occur within 72 hours after whatever lung injury occurs well it's a burn it happens within 72 hours if it's um sepsis it's you know within that time frame and here's your clinical assessment so the initial presentation remember the increased respiratory rate is often the first sign that you'll see very easy to miss that but as it progresses the person could be short of breath tachycardic cough they could be restless you may hear the fine spread scattered crackles thank you but again in the earliest phases you probably won't hear much at all because the fluids in the interstitial it's not until it starts to go into the alveoli that you start to have adventitious lung sounds if you checked an ABG you'd probably find them in respiratory alkalosis with a little bit of mild hypoxemia and the chest x-ray early on doesn't show too much right but then as it progresses we end up with coarse crackles diffuse extensive white outs and at this point the patient is very sick so let's take a look at what a chest x-ray looks like you can see a normal chest x-ray on the left and then ours on the right so the other thing to consider is that basically when we have ards there's the pulmonary edema and that's what you see here if you if you look you can see all of this white out here we have to make sure that it's non-cardiac and origin so to do that we often check this brain naturetic peptide or B and P level and then also an echocardiogram can also distinguish to make sure that it is the lungs that are the problem and not the heart okay so the next thing to consider with ards is the PF ratio so basically it's a quick calculation that allows us to see what's going on with the patient whether they're okay or heading towards ards so we look at the oxygen to percentage oxygen ratio so check the AVG get the pao2 and then the fio2 is whatever oxygen we're giving them and you can see the math that's related to this so in this particular example the oxygenation is at 83 so the pao2 is 83 and at 45 fio2 so make that into a decimal so 0.45 and then divide the pao2 by the fio2 which is 184. so what does that mean though so that comes down to the Berlin definition of ards so for this at uh basically 184 it falls into that moderate ards level so this is the Berlin definition and it means that basically the onset of our illness was within the week that the chest x-ray shows the white outs and the PF ratios under 300 with at least five centimeters of Peep and again that we are holding the heart blameless for this we cannot explain what's happening as being congestive heart failure or fluid overload okay so that's the Berlin definition so what's Let's Talk About ards Management there's the three p's that you have to remember which is prone Peep and permissive hypercapnia so prone is basically uh most of us know what this is now because of because of covid actually when we would see all the patients on ventilators laying on their belly so prone is to put a person laying on their stomach and this basically helps with the positioning the better oxygenation of the lungs peep as well because the we provide peep to keep those alveoli open which allows us to improve oxygenation and then permissive hypercapnia which is a lower tidal volume remember it's never okay if somebody has a TBI or increased intracranial pressure to allow permissive hypercapnia foreign and then a couple things about peep again peep can cause hypotension because of the decreased flow to the right side of the heart so for restricting flow to the input of the heart that we basically restrict flow to the output as well so decrease cardiac output which is related to decreased venous return to the right side of the heart and then Barrow trauma so in irons our peep is usually 10 to 20. normally it's around five so you can see how much more pressure there is that's why we use the decreased title volume because it decreases the amount of Barrow trauma okay so a little bit more management for this uh basically we want to manage any of anxiety by giving them sedation neuromuscular blocking agents steroids because we have a cytokine storm we can do surfactant replacement antibiotics of course diuretics for the pulmonary edema we really don't want to give them a lot of fluids because they're already lung soaked so fluids the less the better we need to concern ourselves with their nutrition within 24 to 48 hours and then of course um any damage from the ventilator itself so some of the complications that occur after Arts again decrease cardiac output dysrhythmias a person could be delirious uh PTSD paralytic ileus hyper metabolism stress ulcers DIC blood clots so do we know how to treat all those I'm hoping at this point we do and remember for Arts the goal and for anybody in mechanical ventilation is to make sure we keep them on the least amount of oxygen possible so that we avoid oxygen toxicity all right and just a little bit more about permissive hypercapnia all right is that our tidal volume being set lower decreases Barrow trauma we cannot use permissive hypercapnia with tbis or increase intracranial pressure and for this our folks are pretty sick so they do generally require IV analgesia and sedation and then the last little thing here's uh here's my fella he's being proned here so we found out with kova that even as people were in early hours before they were on ventilators or anything like that we used to have our patients prone themselves so we'd have to go down the hall and you know say lay on your belly and every two hours we were pruning and again if we use pronine because it allows us to oxygenate the patient better and use less peep it's not an easy thing to do imagine trying to turn that patient with all of his equipment and making sure we're worried about the pressure points that we're creating you could have nerve injury from the way that they're laying so it takes a lot of people usually usually several in fact including a respiratory therapist make sure that the airway is always always secured and then once you have them prone you have to make sure that they're more on the side line position so that the ventilator can do its job all right guys so that is the end of respiratory part three and we've finished with art so I will see you in class