We'll just do some introductions and then this is our like questions go through the questions kind of thing My name is Kalila Gates. I am pulmonary critical care at Northwestern I'm feeling really old because she was a student and now She'll introduce herself, but she made me feel really old walking in this morning. So no, no, no forever young, right? Hi I'm Sarah Kacoma and I'm anesthesia critical care from Rush University here in Chicago and I know you guys don't know me, but normally my voice is not this low and raspy. So I apologize Which is why I'm wearing a mask And I am just copy I'm the shortest of us all um, but I am pulmonary critical care over at Rush University as well We're going to do some audience Oh I saw the question and then Okay, I gotta go back though cuz I can't see the question on this okay so the first question is in which Scenario, would you use non-invasive ventilation after extubation? We Hmm. We have a 58 year old gentleman with coronary artery bypass grafting This rapid shallow breathing index is 60 on post-op day one You have a 62 year old gentleman with status post esophagectomy who is requiring reintubation on post-op day one We have a 68 year old woman who was intubated three days ago for exacerbation of her COPD or You have a 74 year old man with chameleon acquired pneumonia Who was extubated yesterday and now has worsening respiratory failure? Yeah, it's changing You want to show the correct answer you just click on that little black box Can y'all make that any smaller? All right, let's see, okay, so 81% we're still clocking Oh somebody bailed on us So the correct So the then the big pie is the correct answer I presume Okay, so the majority of you got the correct answer Yeah, I do remember that it is because that We have a person with COPD who is post extubation who is now We're trying to prevent them from being reintubated a is incorrect. Why any ideas? So a they're not they're doing okay, so there's no reason to put non-invasive in the rapid shallow breathing and that's just fine We just need to watch and make sure things are going. Okay B. What is the contraindication in B for non-invasive ventilation? The recent esophagectomy we like to keep that intact And D what's up with D? The data suggests that you're not going to push off the the reintubation using non-invasive inhalation at this point There's already respiratory failure. So there's no need to Prolong the inevitable of reintubation Next question 40 year old person presents with acute onset of shortness of breath History is significant for a recent transatlantic flight He denies any cough fevers chills or chest pain. He has not had any recent episodes of bleeding on Exam. He is in mild distress vital sound signs. He's a febrile heart rate is 110 Respiratory rate is 28 breaths per minute. The blood pressure is 130 over 80 and Oxygen saturation is 88% on room air The exam is significant for left calf swelling. The lungs are clear to auscultation Bilaterally, so which of the following is the most appropriate next step? start therapeutic anticoagulation Send the person down for a CT pulmonary angiogram Push some lytics or check a d-dimer It's like this button as they start You can't see Interesting. Okay. The correct answer is actually to go ahead and start anticoagulation, okay? We know they have a PE. They had a long flight, the calf is swollen, clinically they have a PE. So the best outcome is actually to start anticoagulation. We'll eventually get a CT angiogram to confirm our suspicion, right? But the best next step is actually parental anticoagulation. No indication for systemic therapy. The patient is hemodynamically stable, so there's no reason to push lytics. And the D-dimer offers you nothing but an elevation that does not actually treat the patient. Okay? Questions about that? All right. I think it's me. So in that case, what would you start with? Would you give heparin or would you give just Lominox or what would you do? To do, if it's real much and it's fine, you can do the Lominox load or you can do IV. All right, we'll move on. Seventy-year-old male with end-stage chronic obstructive pulmonary disease presents to the emergency department with acute on chronic dyspnea, hypoxia, and hypercarbia. After an unsuccessful trial of non-invasive ventilation, he is intubated for respiratory failure. Initial ventilator settings are a cyst control volume cycle, tidal volume of 500, respiratory rate set to 20, and he's got an FiO2 of 1.0 or 100%, and a positive end-expiratory pressure or PEEP of 5. He's sedated on propofol to a Richmond agitation sedation scale, score of minus 2. Peak airway pressures are 50, and plateau pressures are 30. Bedside ultrasound shows bilateral lung sliding. On auscultation, he has diffused bilateral wheezes, which of the following is the most likely cause of his elevated airway pressures? Is it A, intrinsic PEEP or auto PEEP, B, pneumothorax, C, endotracheal tube obstruction with secretions, or D, bronchospasm? All right. I'm gonna show our answer. Oh, we still have some changes. Um, but actually the answer is A, probably some auto-peep for this patient. Why the other answers aren't, er, well I guess we can start with why auto-peeping is correct. So he has high peak airway and high plateau pressures. In patients with obstructive lung disease, we know that they're, they need long E times, right, long expiratory times to really blow out all that tidal volume you're delivering them with every breath. So a lot of times we set the ventilator low and slow, right? So low E times, slow respiratory rate. And so this might have been a little bit too high for this patient. Pneumothorax is possible, but he has bilateral lung sliding. He's got, um, so it's at least a little bit less likely. Um, he could have endotracheal, he could have secretions in his ET tube. He could have bronchospasm, but your plats won't necessarily be quite as high. Um, your peak airway pressure will be high, but your plat won't be quite as high. So probably A in this patient, er, um, auto-peep in this patient. Any questions? Yeah, definitely. Exactly, yeah. And so you can have the wheezing more so in the lung tissue itself, right, in the small airways. Um, but I mean he's certainly at risk for bronchospasm, but I don't think that's quite explaining all the, um, elevated plat pressure. All right, um, and the next one. 65 year old man is admitted to the ICU with four days of productive cough, subjective fevers, pleuritic right-sided chest pain, and progressive dyspnea. Exam reveals, uh, he's febrile to 39.1, heart rate of 125, respiratory rate is 22, blood pressure 95 over 40, he's setting 94% on four liters, um, crackles in the gophenia are auscultated at the right lung base, white count is 26 with 20% bands, CT scan with contrast shows a right lower lobe, consolidation in a moderate size, loculated pleural effusion with pleural thickening, peptazo is started and a bolus of IV crystalloid is administered, chest tube is placed, and 750 cc's of purulent fluid is drained. Which of the following would be expected after the administration of intrapleural deoxyribonuclease or DORNASE, um, and tissue plasminogen activator twice per day for three days? Is he at a markedly elevated risk of hemorrhage? Is there going to be increased need for surgical referral? Is there going to be a reduction in mortality? Or is there going to be improved drainage of the infected pleural fluid? Okay, good. Um, so I think the answer that was given in the, um, slide set is incorrect. I think most of you have it right as D, improved drainage of the infected pleural space. Um, this is looking at the MIS, this is a question about the MIS-2 trial back in 2011. Uh, so patients were, here were randomized, uh, patients with empyema here were randomized to intrapleural placebo, uh, TPA alone, DORNASE alone, or TPA and DORNASE, um, twice per day for three days. And so the combination group had a significant reduction in the pleural opacities, um, and also they had improved drainage of their infected pleural space. Uh, they also had decreased need for surgical referral and shorter hospital stays. Um, no difference in mortality and then also no difference in other adverse events like pleural hemorrhage. So, yeah. And so this has become our standard of care, uh, for the initial management for empyema. All right. Let's move this up a little bit. Okay. A 39-year-old woman who has been bedbound presents with tachypnea and shortness of breath. She's intubated and point-of-care ultrasound shows massively dilated right ventricle with decreased right ventricular function. The left ventricle is hyperdynamic but has normal function. There is bowing of the ventricular septum into the left ventricle. The patient's blood pressure continues to drop and the emergency department physician is very concerned that the patient's about to go into cardiac arrest. Which of the following is the next best step in management? A, administer Alteplase over two hours and start unfractionated heparin, um, infusion after the Alteplase infusion has completed. B, administer Tenecteplase over five seconds and start a heparin infusion at the same time. C, start the heparin infusion and send the patient to the CT scanner. Or D, send the patient to the CT scanner, um, of the chest prior to starting antithrombotic therapy. All right, looks like most people have answered. So the answer is going to be B, giving the tenecteplase. So this patient is not doing so great, and it's highly suggestive of acute right heart failure. Given this deteriorating hemodynamics, the correct answer would be to give the tenecteplase over five seconds. An alternative could be the alteplase, but that's a longer infusion. And we're a little bit more worried about impending cardiac arrest. And if you are concerned about impending cardiac arrest, we should not be shipping a patient off to a CT scanner. I think we've all been involved in codes and CT scanners, and let's try to avoid that at all costs. I think that, yeah, this one's still me. OK, a 46-year-old woman presents with a history of lupus and a recent diagnosis of chronic thromboembolic pulmonary hypertension with mild to moderate ventricular dysfunction. She's taking bosentin and warfarin as prescribed by her pulmonologist. She continues to have symptoms of dyspnea on exertion, fatigue, and intermittent episodes of dizziness. She's been referred for a pulmonary endarterectomy. After the procedure, she is transferred to the ICU intubated and sedated. Post-operatively, she develops hypoxia with oxygen saturations of 85%. An arterial blood gas panel shows pH of 7.35, PCO2 of 48, and a PaO2 of 55 on 60% FiO2. Her heart rate is 110 beats per minute, and her blood pressure is 88 over 40. Her cardiac index is 1.8. Pulmonary artery pressures remain moderately elevated at 48 over 18. And a chest x-ray shows bilateral central infiltrate, which of the following is the next best treatment to manage this patient? A, systemic heparin. B, optimization of peak and expiratory pressure. C, dopamine. And D, Lasix. We've got some dopamine lovers in the crowd. So the answer is, I think it was B, optimization of PEEP. So after a pulmonary endarterectomy, most patients have significant improvement in hemodynamics with decrease in pulmonary artery pressure and systemic vasodilatation. Residual pulmonary hypertension will remain in about 20% of patients, and 10% of patients will be concerned for right ventricular dysfunction. Post-operative changes in pulmonary physiology include increased permeability, redistribution of blood flow with temporary alteration of blood flow to newly opened segments, and coagulopathy. All of these increase the risk of prolonged hypoxemia and some residual pulmonary hypertension. So like any patient on a ventilator, the first step is to optimize ventilator settings for lung protective strategy, which is why PEEP is the ultimate answer here. These patients are started on systemic heparin after pulmonary endarterectomy if no bleeding is noted. Dopamine or ionotropic support can be used for right ventricular dysfunction, but with utmost caution, as it can lead to further increase in pulmonary flow and reperfusion edema. ECMO can be used after the procedure as a bridge to recovery in patients with persistent pulmonary hypertension, severe airway hemorrhage, or reperfusion pulmonary edema. So, 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, she developed hypoxemia and requires intubation. She is subsequently diagnosed with ARDS. The next day, she continues to have hypoxemia despite treatment with high flow, not high flow, high FiO2 and low tidal volume ventilation. So, based on that clinical setting, which of the following steps would you take to reduce the risk of mortality? Are you going to switch over to a PRV? Are you going to start inhaled nitric oxide? Are you going to do high frequency oscillatory ventilation? Are you going to consider proning her or not consider? Are you going to prone her or are you going to call an ECMO call? Okay, I pushed the button, did it show, okay, so 91% of you have the correct answer, that is prone positioning. We have a patient who has ARDS, and the question is specifically asking what is going to reduce mortality in this patient, and we already are doing the first thing that's going to be reduced mortality, and that's low tidal volume ventilation. So the only other option, and we'll talk about this a little bit more in the next half hour, that is going to actually impact mortality is prone positioning, and that is the PROSTIVA study that we'll talk about a little bit later. Okay. All right. We have a 60-year-old person who has undergone a craniotomy for meningioma four weeks ago. He comes to the emergency department in moderate respiratory distress with tachypnea, tachycardia, and hypotension. He has been short of breath for the last few days. An initial CT scan shows a saddle PE with large clot burden along with signs of RV strain. Lab analysis shows a metabolic acidosis with a pH of 7.18, a PCO2 of 20, and a PAO2 of 56. And he has been able to maintain oxygen saturation greater than 90% on high-flow nasal cannula. Additional values include an elevated lactate at 9.1, creatinine at 1.73, up from his baseline of 1.01. He has a high potassium at 5.8. His LFTs are elevated. His T billy is 0.8. A PE response team is called. The patient progresses to respiratory and circulatory shock, requiring pressure support with worsening lactic acidosis and hyperkalemia. You do a point-of-care ultrasound, and you see that there is now right ventricular failure. So which of the following is the most appropriate next step in management of this patient? Would you like to do catheter-directed therapy, thrombolytic therapy? Would you like to start IV heparin? Would you like to do mechanical ventilatory support with ECMO? Or would you like to start low molecular weight heparin? This is showing the saddle PE and the right ventricular abnormalities. For sake of time, we'll start. All right, button has started, stop moving. So we want to get him hemodynamically stable. And the way to do that is to initiate, in this situation, what type of ECMO? VA ECMO. So we need respiratory and cardiac support. So we would call the VA ECMO team, we would put him on VA ECMO in the acute next best step setting. And then we can figure out how to bless the clot, whether we're going to do direct TPA or what have you. But in this very acute setting, we do have to do mechanical ventilatory support along with VA ECMO. So that is the rationale for that question. Giago, get me in trouble talking without a microphone. He will be heparinized anyway, but in this acute setting, he is in shock, and so we need and we have the opportunity to temporize him with the ECMO until we can get more definitive management. All right. 82-year-old woman comes to the ER from home with altered mental status, productive cough, shortness of breath. Vital signs include a pulse of 115, a respirate of 40, blood pressure is 90 over 50, and she's setting 78% on room air. She's awake and alert, but she's confused on exam. She's tachypneic and has diffused bronchi. The patient is placed on a non-rebreather mask, and oxygen saturation improves to 94%. X-ray shows multifocal order areas of consolidation. White count is 19 with 10% bands. ABG shows pH 7.35, PCO2 35, PO2 65, bicarb is 18, and her O2 saturation is 90% on 100% non-rebreather. She's transferred to the ICU. What is the next best option in managing this patient's acute hypoxic respiratory failure? Is it keeping her on the non-rebreather since her oxygenation is sufficient, starting her on humidified high-flow oxygen, starting non-invasive positive pressure ventilation, or should we intubate the patient and put her on mechanical ventilation? Okay, correct answer. So actually in this case would probably do B, humidified high-flow oxygen. It's a good starting point. This has been, so essentially these are these high flows of oxygen. You can get up to 60 liters using the system that we have at Rush, but delivering an FIO2 of 100% with 60 liters. Because of these higher flows, there's a little bit of peep and so it helps kind of reduce some of that work of breathing and it might actually reduce the need for patients to be intubated and put on mechanical ventilation. Keeping her on a non-rebreather, probably not the right option. She doesn't get the benefit of the increased flow and typically we don't keep people on non-rebreathers. That's a transition to something else. Non-invasive is an option, but remember this lady is altered. She's got a productive cough, so that may kind of, those are two relative contraindications, right, for non-invasive. And then intubation is still on the table, but I think a reasonable starting point is the humidified high-flow oxygen and then considering intubation if her respiratory status doesn't improve. All right. A member of the rapid response team is called to evaluate a patient in respiratory distress. The patient has tachypnea tachycardia and has an SBO2 of 85% on 100% non-rebreather face mask. On physical examination, the patient's thyromental distance is two finger breaths and he has prognatic upper incisors. There's no previous intubation note available, but his history is pertinent for a previous cervical fixation after a trauma. What is the first choice of technique for intubating this patient? A, direct laryngoscopy following an administration of succinylcholine. B, direct laryngoscopy after administration of rocuronium. C, video laryngoscopy after the administration of rocuronium. D, awake fiber-optic-assisted intubation. E, fiber-optic-assisted intubation after the administration of rocuronium. All right. It looks like everybody has voted here. And the correct answer is D, an awake fibro-optic intubation. I think, you know, we're going to talk about this more, but managing airways in the intensive care unit, safety is always number one priority. So according to the American Society of Anesthesiology guidelines for management of difficult airway, there's no standard definition that can be identified in the literature. A difficult airway is defined as a clinical situation in which a conventionally trained anesthesiologist experienced difficult with face mask ventilation of upper airway, difficulty with tracheal intubation, or both. It is based on patient factors, the clinical setting, and the skills of the physician. This patient can be classified as a difficult intubation on three factors. His neck cannot bend, he has a short thyromental distance, and he has protuberant teeth. is often faced with only a few minutes to decide the method of securing the airway. Neuromuscular blockade will not assure that the patient can be ventilated by a mask if intubation is not successful. Succinylcholine may also result in hyperkalemia if the patient has been immobile for a period of time. Observational studies have shown that an awake fibro-optic assistant intubation for patients with difficult airways is 88-100% successful.

critical care

non-invasive ventilation

pulmonary embolism

auto-PEEP

empyema

ARDS

difficult airways