and we'll start with this one. All righty, so we have a 70-year-old gentleman with in-stage chronic COPD who comes in the ER with acute and chronic dyspnea, hypoxia, and hypercarbia. After an unsuccessful trial of non-invasive ventilation, he is intubated for respiratory failure. His initial vent settings are ACVC, assist control volume control, tidal volume of 500, respiratory rate at 20. His FL2 is 100% with a PEEP set at five. He is sedated on propofol for a Richmond agitation sedation scale of minus two. His peak airway pressures are 50 and his plateau pressures are 30. The bedside ultrasound shows bilateral lung sliding. On auscultation, he has diffused bilateral wheezes. So based on that stem, which of the following is most likely causing his elevated airway pressures? And this, we actually do have a poll everywhere. We have a response. So I think we have to click, no. So is it intrinsic positive end-expiratory pressure, otopeep, pneumothorax, endotracheal tube obstruction with secretions, or bronchospasm? And I don't see anybody at the back table, so I hope this works automatically. Here, click one more time, let's see. Do I click? There we go. Oh, we clicked too many times, but there we go. Oh, very nice. Okay. I'll admit, I initially was like, eh, I don't think it's D, but then we'll talk about why it's not D. All righty, so the correct answer is actually A, and no worries. That's intrinsic positive end-expiratory pressure. And so can we go back to the STEM for a sec? So the thing here, so you heard wheezing, COPD, we're thinking bronchospasm, high peak pressures, okay? But the plateau pressures are borderline, they're not even normal, but they're borderline acceptable. And so the only thing in this, well, not the only thing. So pneumothorax is gonna get you high plateau pressures, that are gonna give you high peak pressures, but we have lung sliding bilaterally, which means there's no pneumothorax. Endotracheal secretions and bronchospasms gonna get you a high peak, but your plateau pressure should be normal. And so in this setting where your peaks are normal and your plateaus are elevated, and so we think, oh, it was 30, it's okay, but 30 is actually not normal, suggesting that there is some intrinsic positive peep or auto-peep that we know of. So that is why A, intrinsic positive in expiratory pressure is actually the correct response. So we've ruled out pneumothorax with our ultrasound, we see bilateral lung sliding, and C will give us low, high peak pressures, but low plateau pressures. C and D would give us that pattern. Any questions about that? And the same thing with bronchospasm. So it'll give you high peak, lower plateaus, and bronchospasm is fitting into this, right? Because you've overrun the time constant of the lung, so there's high airway resistance, and this is a COPD patient, high compliance, so you're not allowing enough time for exhalation before the next breath. And you've got dynamic hyperinflation from auto-peep. You have a question? I think we can rule out or end the auto-peep by just doing the maneuver on the ventilator, so it's. Yeah, you could certainly do that, and if we had waveforms, you'd have known this right off the bat, right? Because with the current ventilator, we don't really have to guess, because I still believe that this person has a bronchospasm. 100%. Because I assume the auto-peep is checked and ruled out. Well, so yes, the patient could have bronchospasm based on the wheezing and the COPD exacerbation, but the bronchospasm alone does not explain the elevated plateau pressure, so that is the caveat in the stem. It's the plateau pressure. We can go to the explanation, which is what we just talked about, but it was the fact that if it was bronchospasm or secretions in the tube, yes, we would have a high peak, but our plateau pressure should not be a major issue. Thank you. Everybody clear? Yeah, other thing is just to explain how to overcome that is by decreasing the tidal volume or decreasing the rate or increasing the IE ratio and those kind of things. If you can explain a little bit, that'll be helpful to you. Yes, so all of those that you just described would actually extend expiratory time. That's how you fix it. So whether you deliver a smaller breath or deliver it faster, whatever you do to shorten the expiratory time or extend the expiratory time, decreasing the respiratory rate would fix that. And eventually, you're right. You treat the bronchospasm, things will get better, but. Yes. So there is still broncho, so, okay. Let's assume that this is, that those numbers were gotten on 60 liters per minute square waveform. Let's make that assumption to make the math easier. So the resistance is still high, right? That'll be a resistance of, I think, 20, if we did the math, peak minus plateau overflow. And so that's still abnormal, it's higher than 15. But if it was just an airway issue, then the plateau should be normal. And that's not the case either. So we have a high peak, we have an elevated resistance, but we also have an elevated plateau, which just, how do we explain all of that? Yes, there is some bronchospasm based on the presentation of COPD exacerbation. However, the plateau pressure being elevated, it has to be some compliance issue, which would be auto-peak or intrinsic peak. So the thing is, maybe you can say, like a peak pressure is 50 and plateau would be, if it is a bronchospasm, the plateau should have been like maybe 20, 25, but it is high, unless there is pneumothorax or something. Yes, but there is no pneumothorax because of the lung sliding on the POCUS exam. Positive lung sliding, lung is up, no pneumothorax. The plateau pressure is kind of unfair. We can hit you right at 30, and you're like, what do I do with that? So that's part of it as well. But 30 is still not normal. We just think of it as normal because anything over 30 makes us a little uncomfortable. But 30 is not normal. Yeah, remember your COPD patients, especially with a lot of emphysema, doesn't have a lot of elastic recoil. So their compliance is actually quite high. So their plateau pressure would probably be 10, 15 normally. The fact that it's at 30 tells you there must be something elevating both. Make sense? Okay, good. And here's a reference for you. So now we have a 36-year-old woman with cervical cancer admitted to the ICU in septic shock. She is adequately resuscitated, but on day two develops hypoxemia, requires intubation. She's diagnosed with acute respiratory distress syndrome. She continues to have hypoxemia despite treatment with a high FiO2, low tidal volume ventilation. Which of the following steps should be taken to reduce her mortality? Okay, key question. Reduce mortality in ARDS. Airway pressure release ventilation, inhaled nitric oxide, high frequency oscillatory ventilation, prone positioning, or ECMO. The voting is open. How do we know when they're done? Well, you guys are nailing this one. And I don't even know that we have to discuss this any further, we did earlier, we talked about the PROSIVA trial. The PO2-FiO2 ratio less than 150 on ARDS lung protective ventilatory support, not making improvements, and prone ventilation will reduce mortality. Here's the reference for you. All righty, so, hello? We have an 82-year-old woman who comes to the ER from home with altered mental status, productive cough, and shortness of breath. Her vital signs include tachycardia at 115, a respiratory rate of 40, blood pressure of 90 over 50, with an oxygen sat of 78% of room air. She's awake and alert, but she is confused. On exam, she is tachypneic and has diffused ronchi. The patient is placed on a NARI breather at 100%, and then her sat is 94% after that. Her portable chest shows multifocal areas of consolidation. White count is elevated at 19,000 with 10% bands. Her ABG is 7.35, 35 CO2, and a PaO2 of 65, with a bicarb of 18. Her excess in saturation is 90% on 100% NARI breather. So this patient is transferred to the ICU. What is the next best option in managing the patient's acute hypoxemic respiratory failure? Do we continue the patient on NARI breather mask? Do we start humidified high-flow oxygen? Do we start non-invasive positive pressure ventilation? Or do we intubate the patient and place her on mechanical ventilation? Someone says C? D, we're still coming in? Okay. All righty, so most of us said B, which is actually the correct answer. So let's talk about it. 100% non-rebreather wasn't working, it's no point to think it's going to work more. High flow nasal cannula has actually been shown to actually improve oxygenation and minimize the need to go further to intubation. How high flow nasal cannula works is because we have humidified high flow nasal cannula. Because we have high flows, 60 liters per minute, we create a reservoir of O2 that we can't get with the 100% non-rebreather. And so you can actually get higher FiO2s with the high flow nasal cannula. In theory, depending on who you talk to, high flow can also provide a small amount of PEEP, depending on who you talk to, anywhere from, I've seen anywhere from 5 to 8 centimeters of water with the PEEP. And also can improve dead space. And so high flow nasal cannula can actually prevent her from moving to intubation. Intubation in this setting is not correct because she does have a mental status, presumably can protect her airway, and you have a potential option to use high flow nasal cannula to try to prevent transitioning to intubation. So that's kind of the way to think about that. Were we following this before COVID, high flow, or were we using positive airway pressure before that? How, for how many years we've been following this high flow strategy? So I think that, go ahead, sorry. No, high flow's been around for 10 years or so. So the heated high flow, high humidity, oxygen, but it has really moved into vogue, not only the later phases of COVID, but because people hate to be on non-invasive ventilation with these tight-fitting face masks. Nobody likes keeping them in place. That's why people went to helmet ventilation to say, maybe this is more tolerable. But I think the high flow nasal cannula, most people tolerate pretty well. And what about, did you say Vapotherm? The B option is Vapotherm, right? That's a brand of high flow, yeah. And then the only other thing is non-invasive ventilation and positive pressure, it's uncomfortable. She is a little bit altered. So it's really not the best positive pressure in the altered patient. And then just perhaps interfering with her ability to clear her secretions. So again, it's what's the best. And in this situation, it would be the high flow nasal cannula. Some references. Now we have a 39-year-old woman who's been bedbound with tachypnea and shortness of breath. She's intubated. The point of care ultrasound shows massively dilated right ventricle and decreased right ventricular function. The left ventricle is hyperdynamic but has normal function. There is bowing of the interventricular septum into the left ventricle. Are we getting the point? The patient's blood pressure continues to drop and the emergency department physician is very concerned that the patient is about to have a cardiac arrest from this underlying condition. So which of the following is the next best step in management? So we can administer alteplase over two hours and then start some unfractionated heparin. We can administer tenecteplase over five seconds, rapid infusion, then start some unfractionated heparin. We can start unfractionated heparin and send the patient for a CT angiogram of the chest. Or we can just send the patient to CT and get the angiogram of the chest and then consider starting antithrombotic therapy. What would you like to do? Like watching election returns, isn't it? The key factor in the stem is that obviously we have this immobilized individual who comes in with what sounds like a scenario for a big PE and in fact has evidence on the ultrasound of RV dysfunction with McConnell's sign. So the ER person is concerned this patient's going to arrest. So do we have two hours to administer our alteplase? Probably not. If it's really that concerning, you want to get something in as fast as you can, five seconds or if you wanted to administer half of your alteplase right up front in the bolus and then continue the rest. But the faster the better is the answer here. And the other important thing is that we don't go for D. If you think somebody has a pulmonary embolus, it's okay to start therapy, whatever the appropriate therapy is, before you get your confirmatory data as long as there's no risk to the therapy you're going to give. So the answer here should be B. And this is basically the discussion that I just gave you that we made an astute diagnosis. We are concerned this patient's not going to be stable enough to not only get a CT scan but to even wait a two-hour infusion of the thrombolytic therapy. So we want to go with a fast protocol, stabilize the patient, and then get them on their therapy. And then we can get our confirmatory CT to confirm that and be done with it. Can you comment on the mechanical thrombectomy? Well that could be an acceptable source, but A, you're going to need to have your angiogram or CT with angiography done already so they know exactly that it's there. And I don't know if your center is set up so that somebody's sitting there in the cath lab saying, okay, send the patient over. Most of the time these people arrive at off hours and you have to call in a cath lab or an interventionalist. So mechanical removal of clot is certainly an alternative procedure for a massive or submassive PE as long as it can be done in reasonable time. And again, the caveat in this case is we think she's going to rest in short order. So that, I think, would eliminate going for a mechanical thrombus removal. And you can still give all this treatment and still consider that option? Yeah. So you can certainly use that as an option. Now this is controversial, so I'm going to do this one. Neither of us wrote this question, so that's a disclaimer right from the start. And we're so glad to have our PharmD in the audience. So here we have a 60-year-old woman with mesothelone-resistant staph aureus, bacteremia without endocarditis. She continues to worsen clinically despite seven days of vancomycin therapy. She's allergic to sulfa. Follow-up cultures on day six of vancomycin therapy remain positive. And here's the susceptibility. So it's MRSA that's resistant to penicillin and oxacillin, resistant to vancomycin, resistant to lenazolid, intermediate-resistant to daptomycin. Which of the following is the most appropriate antimicrobial for this patient? Continue on the vancomycin, quinipristin-dalphopristin, which it's called Sinercid. It's still around, isn't it? Actually I think, I thought King's Pharmaceuticals took it off the market. But I mean, I thought it was, it's not, it's very recently I thought that happened. Okay, so it can go with bacterem, or you can go with calistomethate, also known as calistin. Feel free to vote. You're voting for things you've probably never heard of. Which is why I had Dr. Bok do this question. So remember she's allergic to bacterem, to sulfa, however you could desensitize her. But didn't say that in the stem. So the answer is b. This was a gram-positive antibiotic that, at the same time lenazolid was being developed and daptomycin was being developed, this is being developed, it's a spectrogammon or something like that? Correct, yeah. One of the limitations of why the other drugs came available was that it wasn't as broad as the other, for example, lenazolid and daptomycin, and the other part is that the infusions were generally not well tolerated. Yeah, because a lot of muscle pain, you had to check CPKs on them, and it never really panned out, and I think this must be an old question that has resurrected, but as you saw, this is a terrible MRSA that is resistant to everything else. And the calistin is a gram-negative antibiotic, so we would not have used that for this patient. Yeah, the other is, that's starting to get some data, I know it's not in the question because you can tell it's an older question, is ceftaroline. That was my question, what about it? That would, it could be. That would probably be the modern answer we should replace this with? It'd be the 2022 answer. Okay. Excellent. See, that's why you're in the audience, girl. All right. We have a 65-year-old man admitted to the ICU with four days of productive cough, subjective fevers, pleuritic right-sided chest pain, and progressive dyspnea. On exam, he is febrile at 39.1, heart rate is 125, respiratory rate is 22, with a blood pressure of 95 over 40, satting 94% on four liters, nasal cannula. He has crackles and agophany at the right lung base, his white count is elevated 26,000 with 20% bands. A CT scan of the chest with IV contrast demonstrates a right lower lobe consolidation and a moderate size loculated pleural fusion with pleural thickening. He started on IV zosyn and a bolus of IV crystalloid fluids. A chest tube is placed and we get out 750 cc's of purulent fluid. Which of the following would be expected after the administration of intrapleural deoxyribonuclease DNAs and tissue plasminogen activator twice per day for three days? Would you expect a marked elevated risk of hemorrhage, increased need for surgical referral, reduction in mortality, or improved drainage of infected pleural fluid? We have a gentleman with pneumonia and empyema who we put in a chest tube and we're going to give DNA and TPA. Everybody locked in? Maybe. Alrighty, so the majority of us have the correct answer. It is improved drainage of the infected pleural fluid. Administration of DNA and TPA in the intrapleural space actually does not cause increased risk of hemorrhage. Actually, it reduces the need to go to surgical intervention and it doesn't impact mortality, but it does, again, like help clear out that space. So that, D, is the correct answer. Not significantly to my understanding. There is absolutely a risk of bleeding. Absolutely. He died of bleeding from his pleural space? For the time being, no. I think it is true. Yes there is a risk of bleeding but if you look at the studies comparing the two there wasn't a marked difference between the two. I've clinical practice as you were sharing I've pushed a great amount and have not had significant breathing yep yep I mean it does show the risk but okay we have an 86 year old woman with ventilator associated pneumonia it's necessitating mechanical ventilation that sort of goes together has consistently received a score of 4 on the intensive care delirium screening checklist meaning she has delirium you like questions to tell you exactly what's going on currently she's on lorazepam for sedation at two milligrams per hour which of the following is the best course of action given the above information should we continue lorazepam at two milligrams per hour and titrate the dose down as possible add fentanyl continuous infusion to decrease the lorazepam transition from the raise of ham to dexmedetomidine beginning at point two micrograms per kilogram per hour or discontinue lorazepam infusion and initiate midazolam infusion at two milligrams per hour you it's nice when you know the diagnosis right And C is the correct answer. So we'd like to get rid of the benzos if at all possible and dexmedetomidine is actually a very good alternative and may actually have some benefit for those who have delirium. And here is the rationale. All righty. We have a 35-year-old man who is recovering from ARDS. On ICU day 7, he is alert and cooperative but remains ventilator dependent. He is on pressure support, 14 centimeters of water with a PEEP of 5, FiO2 of 35%. His spontaneous tidal volume is 400 cc. His spontaneous respiratory rate is 22 breaths per minute. He is tolerating full intra-nutrition. His lab values include a hemoglobin that is 9 and no leukocytosis. So based on that data, which of the following is the best next intervention to improve outcomes in this patient? Oh, sorry. Do we transfuse him to get him up to a hemoglobin of 10? Do we institute mobilization and physical therapy? Do we supplement the internal feedings with glutamine? Or do we infuse dexmetomidine nightly for sleep? All right. So that's an easier one. We were talking about it earlier, the importance of mobilization in our critically ill and mechanically ventilated patients. So that's the long drawn out rationale behind we need to get people moving and stronger for improved outcomes. And are all you guys following the ABCDEF bundles of care for approaching your patients in the ICU? I have a feeling that may be another testable area and includes things like mobility. Here's a question you haven't heard before. Here's a 54-year-old man who's diagnosed with infection-related ventilator-associated complication on day 10 of his ICU stay. Initial empiric treatment consists of Piptezo, Levofloxacin, and Vancomycin. Four days later, the tracheal aspirated culture isolates E. coli sensitive to Piptezo. The team discontinues Vancomycin and Levofloxacin. The patient is afebrile. His Y count has decreased to 8,000 from 18,000. For what total antibiotic duration should this patient be treated for his ventilator-associated complication? I should read the days. And actually, we changed the answer to 7 from 8, but not on both slides. And the reason it says 8 is because, remember, the Shastra study was done 8 versus 15. And I told you we just shaved a day off of each. So, you guys nailed that one really well. All right, more talk for our PharmD here. So, we have a 60-year-old, 6-foot-tall man who went for emergent surgery for perforated diverticulum causing septic shock with multiple system organ failure. He currently weighs 80 kilos, 166 pounds. Despite correction of his perforated bowel, he has been unable to be liberated from mechanical ventilation for the past 8 days. His FiO2 requirements are increasing to 60%. The PEEP is at 10. He has developed a new fever and has increasing generalized edema. His medications include Piptezo, Fluconazole, Vomodadine, and Heparin. His OCT reveals no fluid collection or abscess formation. His chest X-ray reveals persistent bilateral infiltrates with increasing oral tracheal secretions. His lab results reveal the following. A white count of 18,000, his platelets are 20,000, his BUN is 28, his creatinine is 1.5. So based on that, which of the following treatments should be eliminated from consideration for this patient? So we have a patient with new ventilator-associated complication. So what should we not consider, daptomycin, lenazolate, televansin, or vancomycin? All righty, so the majority of us got it right. We should not consider daptomycin. Daptomycin does not work when we have concern for a ventilator-associated pneumonia. The pulmonary surfactant actually inhibits daptomycin, so it's not coverage for a ventilator-associated pneumonia. He was already on Zosyn, so he had the gram-negative coverage. We were missing the MRSA coverage with his new symptoms, and so any of the others are fair game. Although I don't know what Tenelovansin. The only other caveat, I thought, with consideration, maybe, and maybe not so much acutely, would be the platelet count with Lennox, but yeah, that's why that one's a little tricky. But I'd agree. You'd avoid daptomycin. But how soon do you get the platelet changes from lenazolid? That was under the impression it takes a little while. It does. It does. It generally, it's more duration-associated, so once you get kind of in that 10- to 14-day range, there's some literature that suggests as soon as seven, but mostly it's going to be like a 10- to 14-day interval before that would be kind of the culprit, if it was going to happen. Was there another question or comment? Yeah, the patient was on fluconazole, too, so Zyvox and fluconazole, they both are QT prolonging agents. We would have to watch it. I would monitor. If I wanted to go with lenazolid, I would monitor the QT, watch it. If I could stop the fluconazole, because there's no evidence of infection otherwise, I would do that and start the lenazolid. To the point, the question was really what's not going to work, and daptomycin is absolutely not going to work in this situation. Exactly. Do you typically check your QTCs daily on patients in your ICU who you have on medications that can affect the QTC? Yeah. I think most of us have been doing that. Even on your monitors, you can now get a representation that correlates pretty well with an ECG. Here's the references. Now we have a 40-year-old man who presents with acute onset of shortness of breath. He has a history significant for a recent transatlantic flight. He denies any cough, fever, chills, or chest pain. He has not had any recent episodes of bleeding. On examination, he is in mild distress. Vital signs show that he's afebrile, heart rate 110, respiratory rate 28, blood pressure 130 over 80, saturating 88% on room air. He's got left calf swelling. His lungs are clear. What is the most appropriate, emphasize most appropriate, next step, do we want to start perineural therapeutic anticoagulation, send him to x-ray for a CT pulmonary angiogram, start systemic thrombolytic therapy, or send off a D-dimer test. Remember, back to a prior discussion. So in somebody who presents with high risk for pulmonary embolism, is that what most of you think is going on here? At least you think he may have a DVT, right? So if there's no contraindication to anticoagulation, we should start anticoagulation first. And they've made a big point of saying no bleeding issues. So the first thing we should do is anticoagulate, and then send him for the CT pulmonary angiogram. Or you can just confirm he's got a DVT. Treatment would be the same. He does not qualify for systemic thrombolytic therapy at this time. And there's really no need to get a D-dimer. Your D-dimer is to help you exclude a DVT or PE in somebody who has a low probability. And this guy is screaming high probability of PE DVT. And here's the explanation of that. Any questions, comments? All righty, so in which of the following scenarios is non-invasive ventilation after extubation most appropriate? We have a 58-year-old gentleman who had a CABG, who now has rapid shallow breathing index of 60 on post-op day one, a 62-year-old gentleman after esophagectomy who required re-intubation on post-op day one, a 68-year-old woman intubated three days ago for exacerbation of chronic obstructive pulmonary disease, or a 74-year-old gentleman with comedic acquired pneumonia who was extubated yesterday and now has worsening respiratory failure. That's actually a really good question. So who are you going to use non-invasive ventilation on? All right, for sake of time, we're going to say that the correct answer is, in fact, C. A, we have an otherwise OK person who is at no risk of extubation failure, so does not require non-invasive ventilation. B, the person had esophagectomy, so actually the esophagectomy is a contraindication to using non-invasive ventilation. C is the classic, this is who it works. You extubate, you go straight to non-invasive ventilation. You don't wait to see how she does. You go from the vent to non-invasive ventilation. And D, I forget what it was, but not non-invasive ventilation. What was D? The pneumonia. Oh, the pneumonia. She's already failed, and so you just need to proceed with re-intubating. She won't do well with, you're not going to prevent her from being re-intubated with non-invasive ventilation. So at that moment when she's already worsening, you just have to go back to mechanical ventilation, invasive mechanical ventilation.

non-invasive ventilation

extubation

intubated

COPD exacerbation

extubation failure

CABG surgery

esophagectomy