All right, turn it over for the first neurocritical care question. Good morning. A 52-year-old woman was admitted to the ICU immediately after a middle cerebral artery aneurysm clipping. She has no medical history or surgical history. She's smoked a pack a day for 30 years and is a current smoker. She presented with a ruptured aneurysm and subarachnoid hemorrhage. The initial Hunt and Hess scale was 2, meaning she was drowsy, maybe had a cranial nerve palsy. Her World Federation Neuroelectrical Surgeon scale is 1, which means she had a Glasgow Coma scale of 15. Her modified Fisher score is 3 on presentation, meaning there was thick subarachnoid blood in the middle cerebral artery fissure. She's getting nemotipine to preclude delayed or reduce the likelihood of delayed cerebral ischemia. To optimize cerebral perfusion pressure, which of these should you do? A, hypervolemia and keep the MAP greater than 90, euvolemia, keep the MAP greater than 90, hypervolemia and systolic blood pressure greater than 180, or euvolemia and maintain systolic blood pressure less than 120? So this question is really asking you two things, hypervolemia versus euvolemia, and what do you want the blood pressure to be? If you're Tom Black, three things. Do you like mean arterial pressure? There you go. Select your answers now. It'll be in 10 seconds. They'll show the answers when you press forward. They've made their selection already. They've already made the selection? You can just advance it. The other thing this question is asking, if you're Tom Black, do you want to get into the fight about mean arterial pressure or systolic blood pressure? But that's a whole argument for another day, and we only have the morning. So which of these would you do? Hypervolemia and keep blood pressure greater than 90, some of you said that, euvolemia and mean arterial pressure greater than 90, initiate hypervolemia and hypertension, and euvolemia and blood pressure less than 120. So most of you settled on B, and that would be the best answer here. To go through the answers, so initiating hypervolemia, in general, it's not recommended to start doing hypervolemia before the patient has symptoms of symptomatic vasospasm. It has side effects and prophylactically has no benefit. That's an American Heart Association guidelines for SAH. Most of you picked euvolemia and keep a map of at least 90, and that's the best answer here. Hey, who's changing their answers after we start talking about them? That's cheating. None of you said do hypervolemia and hypertension therapy, again, that is a distractor. That would be appropriate if they told you the patient had acute symptomatic vasospasm, meaning the patient suddenly had a left hemiparesis and was less responsive. That would have been the appropriate response. The question they gave you is of a patient with cervectin hemorrhage who is at risk for vasospasm but doesn't have it at this time. And euvolemia and blood pressure less than 120. You do not want to make patients at risk for vasospasm hypotensive. That makes vasospasm from reduced cerebral perfusion and cerebral infarction more likely. Any questions about this one? If you were to use, if you were to be considering vasospasm, would you use the 180 for systolic or the 90 for MAP as a guide? Hey. Do people remember Tom Black, one of the original intensivists? So there is, in many fields of critical care, there's a discussion about whether or not we should follow MAPs or systolic blood pressure. The neuro field worldwide has generally, generally follows systolic blood pressure. When you look at MAPs and systolic, they are highly correlated with each other. And so the field has picked systolic. Most people would say for hypovolemic therapy, a goal of systolic 180 or MAP 120 would be reasonable. Most people in the field follow systolics. If you look at all the ICH reduction, the blood pressure goal papers for ICH, they also follow systolics. That answer your question? Okay. Any other questions about this one? This is the whole rationale. In case you're interested, these are the references. They're actually, one of my colleagues at Northwestern is rewriting, is updating these subarachnoid hemorrhage guidelines from this 2012 paper. For the record, I wrote a different section in 2012. Okay. So I can take this question. A 49-year-old woman is admitted to the ICU after a Whipple procedure for pancreatic cancer. She's extubated in the operating room and currently in severe pain, moderate level of anxiety after awakening from anesthesia. Which of the following combination of agents is the most appropriate initial treatment for this perioperative patient? Is it A, dexmedetomidine and haloperidol? B, fentanyl and midazolam? C, morphine and etomidate? D, ketorolac and profofol? Or E, fentanyl and dexmedetomidine? You could select your answer now. Still moving. The correct answer here is E, fentanyl and dexmedetomidine. So the principles of management here in a post-operative patient, again, are good analgesia, relief of anxiety, and any other discomfort. So narcotics, opioids like fentanyl, morphine, hydromorphone are commonly what we use. We like to use IV infusion in these patients so we can titrate the narcotic to the comfort of the patient. And certainly, agents like Gatorolac would not be suitable right off the bat. If we want to control someone who's in severe pain, you need to use an IV infusion. And certainly, fentanyl compared to morphine does not have histamine release and therefore is more suitable, particularly if the blood pressure is a little soft. In terms of the anxiety of the patient and trying to control that, we know that if you use benzodiazepines, there's something wrong with using midazolam, per se, but we all know that using benzodiazepines, in general, set up for delirium in many patients and may not be suitable for that purpose. Dexmedetomidine, on the other hand, by continuous infusion, is generally a good agent. It doesn't cause respiratory depression, which we want to make sure we ensure in these patients so that they can cough, they can breathe, they can participate in their respiratory care perioperatively, particularly in this patient who had pancreatic surgery. Things to note about dex, as we spoke about yesterday, bradycardia and hypotension can certainly be associated with dexmedetomidine, but again, this is the best combination agent to use in this patient, fentanyl infusion and dexmedetomidine for controlling severe pain, relieving anxiety without the risk of predisposing the patient to delirium if we're to use benzodiazepines. Again, that would be the best choice to treat this patient. So a little over half of you got this question correctly. And here's your rationale and some references, which we talked about already. Okay. A 73-year-old gentleman presents to the emergency department after an assault. He was struck innumerable times in the head and torso. On arrival, his Glasgow Coma Scale is seven, otherwise hemodynamically stable. He's intubated for area protection. The CT reveals an open frontal skull fracture, small contusion, diffused subarachnoid hemorrhage and a liver lack. In addition to the Glasgow Coma Scale of seven, which of the following is the best indication for the placement of an intracranial pressure monitor? Diffused subarachnoid hemorrhage, an age older than 65 years, a skull fracture, the need for mechanical ventilator support, or the non-operative liver lack? Anybody remember where the Glasgow Coma Scale is from? Where's the Glasgow Coma Scale developed? The original paper is published in 1974, the pre CT era. Billy Joel rules the airwaves. It made my dad's favorite car a 74 Pontiac Catalina. He loved that thing. And there's no CT scans. So what do you do in Glasgow, Scotland on a Saturday night? Everybody drinks. What do you do with a city full of raging drunk people in Glasgow? A lot of trauma. So the Glasgow Coma Scale was the original shorthand to try and figure out who was drunk and who had Dane Bramage. It was never meant to be the scale for all measures of consciousness throughout critical care, although that's ended up what happening. All right, I've stalled enough time. Which is the best one? Let's see how everyone fared here. Actually, the answer is B. This is a tough question, and the guidelines you hear in the next slide, the diffused subarachnoid hemorrhage is actually not a very big deal. In trauma, subarachnoid hemorrhage typically doesn't reduce invasive spasm the way aneurysmal subarachnoid hemorrhage does, and it doesn't do much intracranial pressure. It's usually just subarachnoid blood. It's not a space-occupying clot. I'll show you one of those later this morning. Older people are more comatose, are more likely to have intracranial pressure. The open skull fracture doesn't mandate an ICP monitor. The need for mechanical ventral support, again, really doesn't change it, unless you need very, very high pressures, or you need a PEEP greater than 15, it really doesn't do much intracranial pressure. So really, the major risk factor among these would be the age older than 65 years, would be the relative indication for ICP monitoring. Those of you that practice at centers that do a lot of TBI may be familiar with the main question people are interested in these days is, does brain oxygen tension monitoring, measurement of brain hypoxia, improve outcomes in addition to measuring ICP? And that is the ongoing BOOST-3 clinical trial being run through the NIH SIREN network. So if that's positive, then over the next year, we'll start talking about brain oxygen tension monitoring. You don't have to do ICP monitoring. It's not a class one recommendation. It should be considered. Your friendly neighborhood neurosurgeon may or may not want to put an intracranial pressure monitor. And this is simply part of the discussion. But again, of these, the major risk factor for elevated ICP is the elevated age and coma. Any comments about this question? Yep. Let's get a hand here. Can you use your microphone, please? Yeah. So the answer was B, but then it says age over 40 is part of the guidelines. So I guess my initial thought was, well, it says 65, but the guidelines say 40. So technically, B, I chose it, but it wasn't technically based on the guidelines, it should be 40, right? So it also would have been correct had the answer been age older than 40. But I guess in terms of an exam, if you know the guidelines says age older than 40, but it says 65, technically, it's a wrong answer. No, in the Venn diagram of people older than 65, everyone older than 65 is also older than 40. Probably just thinking about it too much. I don't think they'll give you age over 40 and age over 65 as a choice. They probably would just have either greater than 40 or greater than 65. But I think the risk factor is a slightly older age. Not the traditional 65, but even greater than 40 would be the correct answer. Any other comments? Okay. Move on to the next one. A 41-year-old, a young guy, is admitted to the ICU with a severe traumatic brain injury, Glasgow Coma Scale 4. So this would be, so the worst possible Glasgow Coma Scale is 3. So this is a patient with minimal brain subfunction, probably just extensor posturing. Sustained a motor vehicle accident eight hours ago. Sustained a motor vehicle accident eight hours ago. Ejected through the windshield into a tree. He's afebrile. Heart rate's 56. Stress rate 14. Blood pressure's 114 over 68. His ISP is 16. Which of the following should you do prophylactically? Decompressive craniotomy to relieve pressure. Methylprednisolone. Hypothermia. Or sequential compression devices to prevent deep venous thrombosis. So again, a key in the terminology of the STEM is prophylactically. Which of the following strategies do you need to institute prophylactically in this patient? You Going once, going twice. And the best answer is actually D. Decompressive craniectomy, in patients with refractory elevated intracranial pressure, decompressive craniectomy normalizes ICP as soon as the procedure is done. But outcomes are no better, and actually functional outcomes that follow up are worse for reasons that are not entirely clear. When I asked one of my surgical colleagues what he thought about this prospective randomized clinical trial in the New England Journal, his answer was, the New England Journal of Medicine hates surgery. They might, but that doesn't really explain why decompressive craniectomy didn't work, and it's not the only trial in which it didn't work. Methylprednisolone is a distractor. Of course, you know the principle of neurology. No patient should die without a trial of steroids. TBI is one exception to that. It is the one class one guideline in the Brain Trauma Foundation guidelines. Don't give steroids. It actually makes the outcomes worse, and the patient's more likely to die. Hypothermia does not seem to work for elevated ICP. I'm not sure it works for anything anymore. But sequential compression devices are appropriate, particularly for comatose patients who are unlikely to move very much, and are at a very high likelihood, high risk of deep penis thrombosis and pulmonary emboli. So D was the best answer here. Any other comments? And this is the rationale. Okay. Brain death question. A 53-year-old gentleman presents to the emergency department after a self-inflicted gunshot to the head, causing a devastating bi-hemispheric brain injury. His irreversible coma without any confounding variables. Norma-tensive on mechanical ventilatory support, FII-2 is 0.5, five of PEEP. No brain stem reflexes. No pupils, no eyes, no dolls, no gag, and the rest of it. Given these findings, which of the following would mandate an ancillary test be performed for death by neurological criteria? Cumulonimbus instability requiring pressors. No corneal pharyngeal reflexes. An inability to complete an apnea test. Or the mechanical ventilatory support with an FII of 15, a PEEP of five. As always, RTFQ, read the question. Which would mandate an ancillary test, meaning an apnea challenge, and the exam wouldn't be enough? Going once, going twice. So the best answer here is C. In general, the guidelines for the coverage of brain death require a good reason to be brain dead, you have one here. No brain stem reflexes and apnea. So doing an apnea test, completing one, showing no respiratory effort in the presence of acidemia, is considered diagnostic of death by neurological criteria. Requiring vasopressors is okay. If the patient has a systolic of 100 on two pressors, that's fine, that's not a problem. The absent corneal and pharyngeal reflexes are part of the brain death exam. A patient who meets criteria for brain death will have absent corneal and pharyngeal reflexes. So that's appropriate. And the ventral support is, of course, totally appropriate as well. Any questions about that? Which ancillary tests do you get? If you want to start a ride, ask which ancillary tests should you get. And this is moving back and forth. There's a recent paper, apparently there's a worldwide group of people who argue about brain death criteria that came out last year. EEG is now falling out of favor for brain death declaration. Remember, EEG is on the surface of the cortex, but for brain death, we're really interested in the brain stem and respiratory effort. So EEG often doesn't tell you what's happening in the brain stem, it's too far away from the leads. And EEG is often confounded by all the other machines and other medications needed. Nuclear medicine scanning for lack of intracranial blood flow seems to be making a resurgence. Speck scanning seems to be making a resurgence. And of course, angiography or transcranial doctor looking for no intracranial blood flow are generally considered acceptable tests. Each hospital should have its own policy for brain death. They might vary a little bit from place to place, but they're generally more similar than not. Most places have one or two exams. The current literature is that one exam done by a reliable person is as good as two exams. So most hospitals have dropped the need to do two separate exams. Thank you. Any further comments on that? Expect a brain death question on the board. They love these types of questions. And a lot of discussion from the course lecture would be very helpful. And there's some questions in there as well on that subject, so stay tuned. And these are the references. I have a quick question on that point. Now, as you're doing the brain death test, sometime patient has aspiration during the cardiac arrest and patient is severely hypoxic. And patient probably 100% oxygen, people of eight or 10. We really cannot do a brain death test in those patient because patient is severely hypoxic. Is that correct statement? So most hospital policies ours includes what you should do prior to an apnea challenge. And generally includes pre-oxygenating the patient 100% FiO2 for at least half an hour. And most protocols, including ours, say you have to have a baseline ABG with a starting PaO2 of greater than 200. If you can get to the PaO2 above 200, 100%, meaning the patient doesn't have acute lung injury, you can almost always complete the apnea challenge. If the patient cannot complete an apnea challenge, that's the whole point of this question. If for whatever reason you can't complete it, and that's okay, it happens, patient's aspirate, they have ALI, whatever else, then you have to get an ancillary test to help establish the diagnosis. And which ancillary test you get will depend upon the local resources available and who's available to help read it. For the boards, which are the ancillary tests will they ask? Probably as, so I could never use my privileged position to tell you what's highly likely to show up on the board exam. That being said, this question is written as, which of these situations mandate you get one? They're unlikely to say this one and not the other one's acceptable. They will probably give you some generalities of questions, of tests that are appropriate or wildly inappropriate. Good test questions don't vary from institution to institution so which test you get probably wouldn't make a good question because different tests will be accepted at different hospitals as part of different protocols. So I'm not giving anything away but I wouldn't expect a test, a question to say which one is better, spec scanning, angiography, transcranial Doppler or something else. There was a specific question on that and I think it was in the lecture and the answer was traditional angiography. And they gave you the option of doing CT angiography and the rationale was that based on the national or international guidelines that the traditional angiography was the answer. So that's changing a little bit. This 2020 paper is the paper I was referencing. Traditionally angiography would be considered diagnostic of the donor's cranial blood flow. Although I don't know about you, I sometimes have the angiographers trouble getting them to do angiograms on the live patients, much less the patients that I'm pretty sure are dead already. That would have been the best test, whether or not that's the practical choice for every place, I think that's a different question. Right, and that was just a very specific question that was brought up. That's fair. Are there any, Andrew, any, like some of these biomarkers that are being used, like NLAs and all this other stuff that some centers send and occasionally we do as well. Any role for that? So there's a whole evolving literature of biomarkers for irreversibility of coma and it's whatever stuff leaks out of neurons that we can feasibly measure this year. Neurons specific enolase, N100 proteins, gliofibrillary astrocytes, there's a whole list of long-stuffing neurons that you can send off to a reference lab. All of these generally go along with the idea that the more brain is damaged, the more of these proteins leak out into the serum, the worse the patient is likely to do, but none of them are the sensitivity, in particular the specificity you'd need to want to declare somebody dead. I think they're so recent to unlikely show up on a, maybe on a board examination question. I would think that would be a toughie on a board exam because to my knowledge, there's none of the, there are a bunch of biomarkers in cardiac arrest with ROSC and coma because there's substantial uncertainty about what the prognosis is going to be. That would seem unlikely for brain death where it's still, we have recently reaffirmed it's good reason to be brain dead. Exam consists of brain death, permanent apnea. Quick question along those same lines. So the neuron-specific enolase, sorry, over here. Thank you. There's no cutoff level with brain death that if it's, you know, for sure, yes. All of these, you can draw one of these area, these receiver operating characteristic curves, the area into the C with the area into the curve, and they're all, in all of them, the higher the biomarker, the worse the prognosis, but for brain death, you never want to get that wrong. And no, I've not seen anyone try to declare brain death in a biomarker. I'm not aware of anyone trying to do that. I just didn't know if like a certain level was like, you know, if three of the following out of these five occur, like if that was one of them. It's a reasonable way to think about it. I've not heard of anything like that for brain death. I'm not aware of anything like that on the horizon. Thank you. I certainly wouldn't be the director of the lab that's gonna say someone's dead based upon a lab. It's not a good, don't do that. Raj? So the neuron-specific enolase, I don't know about your center, but for us, it takes approximately three to four days for it to even return. Takes three to four days to come back. Yeah, we have, most of our neurologists rely on it as a trend, so they would order it two days in a row. Generally don't use it from a brain death standpoint, but from an anoxic injury and prognosis standpoint, they would order it two days in a row. Both of those come back in five days. By that time, we were sitting down with the family to have more on the goals of care discussion standpoint. We haven't used it from a brain death. So it sounds like they're almost using it the way we're supposed to use procalcitonin to follow the sepsis burden, looking at trends over time. That's a reasonable way to do it. That is one way to do it. Any other comments? Okay. 75-year-old man with history of stage four lung cancer and advanced emphysema is on mechanical ventilation after a post-viral multilower staph pneumonia. His ICU course is complicated by ARDS, multi-organ failure. It's hospital day 10. He remains on max vent support, deeply sedated and on neuromuscular blockade. His mean arterial pressure is 58 despite norepinephrine at 0.2 mics per kilogram per minute and vasopressin 0.04 units per minute. A family meeting is held to discuss goals of care. His wife and children agree that the patient would not have wanted to be sustained on life support indefinitely given his poor prognosis and are asking the team that advanced life support be removed and that the remainder of his care be focused on comfort measures. Which of the following is the best approach in this end-of-life care scenario? Said A, stop the neuromuscular blocking agent and remove promptly the endotracheal tube while he is still deeply sedated to minimize delay. B, titrate down rather than abruptly discontinue vasopressors. A sudden withdrawal of hemodynamic support may lead to undue discomfort. C, administer opioids using a combination of bolus doses and infusion to treat pain and dyspnea as life support measures are withdrawn. Or D, using judicious doses of benzos with opioids as pharmacologic agents used to treat discomfort frequently hasten death. You can select your answer now. I think 90% of you got the correct answer, which is 91%. C, administering opioids, which generally are our mainstay of treatment at end of life, using bolus doses and infusion as you withdraw life support. It is not ideal to be discontinuing neuromuscular blockers and immediately removing the endotracheal tube. That would not be appropriate, even if you're trying to get the patient to be pronounced sooner. That's not an ideal setting. Vase suppressors are not comfort measures. So stop. There's no need to be tapering vase suppressors. You can just discontinue them. That will not lead to any discomfort to the patient. And I think 9% of you answered judicious doses of benzos, again, fearing that using these agents may create the phenomenon of double effect, where you keep bolusing until you get to a certain point, but you're worried that it might hasten death. But it has now been shown that that actually is not what usually will happen, and that if you are prioritizing the comfort of the patient at end of life, you should not be too concerned that you're hastening death, because your overriding principle in managing this patient at end of life is to provide comfort maximally, rather than worrying about whether you're dropping the blood pressure even more or hastening the respiratory depression in somebody that you might be removing the endotracheal tube. So nowadays, as I'm sure many of your institutions and ICUs, I mean, we have protocol order sets for how to conduct end of life, how do we draw the ventilator, how to titrate the opioids with our nursing staff, with our palliative care teams and our nursing staff. So I don't think this is so much of a concern, from the MD side at least, about what you're doing at the bedside, because these are generally now triggered. Is everybody doing that now, pretty much? Have order sets for end of life care, and how do we draw the ventilator and stop neuromuscular blockade and do all of that? I would think so. And I think 90% of you got this answer correctly. So that's great. And here's your rationale here, which we just talked about. Again, and some references here. There are a few airway questions. I mean, we'll just throw it out there. That came up in the set. So interested in going through some airway sedation questions? Yes? OK. A member of the rapid response team is called to evaluate a patient in respiratory distress. Patient is tachycardic, tachycardic. SpO2 is low at 85 on 100% non-rebreather. His physical exam is notable for only a two-finger breadth tyromental distance and aprognathic upper incisors, very protuberant teat. There's no previous intubation note available, but his history is pertinent for a previous cervical fixation after a traumatic incident. What is the first choice of technique for intubating this patient? It's really asking you the technique for intubation in this patient who has what we all will consider a difficult airway. Is it A, direct laryngoscopy following succinylcholine? Is it B, DL after administering rocuronium? Is it C, video laryngoscopy after rocuronium? D, awake fiber optic assisted intubation? Or E, fiber optic assisted intubation after the administration of rocuronium? So if you could select your answers now. So again, this difficult airway, you have no previous intubation note available. He has a prior cervical fixation after a trauma. What would be the best technique in this patient? It's a nice display of answers here. The correct answer is D, a wake fiber optic assisted intubation. This is a patient with a difficult airway. And there's not a guarantee that if you give somebody a neuromuscular blocking agent that you're necessarily going to be able to intubate this patient successfully. So it would be a little dicey to be giving Soxhenilcholine, Rocuronium, if you can't ensure that you're going to get that airway pretty quickly. So I think the most suitable answer here would be an awake fiber optic intubation. That was on an episode of ER once, I think. Don't parse patients who get the airway. I remember that. And so according to the American Society of Anesthesiology Guidelines for Managing Difficult Airway, there is no standard definition that can be identified in the literature. Difficult airway is a clinical situation in which a conventionally trained anesthesiologist has difficulty with face mask ventilation of the upper airway, difficulty with tracheal intubation, or both. It's really based on patient factors, the clinical setting, and the skill of the physician. This patient can be classified as a difficult intubation. His neck cannot bend. He has a short pyrometal distance and prominent front teeth. Intensivist is often faced with this scenario where only you have a few minutes to decide the method of securing his airway. Neuromuscular blockade, as I mentioned, will not assure that this patient can ventilate by mask if intubation is not successful. Soxhenilcholine may also result in hyperkalemia if the patient has been immobilized for some time. And observational studies have shown that a wake fiber optic assisted intubation for patients with difficult airways is successful anywhere between 88% to 100% of the time. So I think the key here is to have, of course, the most experienced hands and skill, particularly with your anesthesiologist or CRNA in doing this intubation. Recognize your limitations. If you haven't intubated a lot of patients with difficult airways, you don't want to be just thinking you can do rapid sequence and giving neuromuscular blockade and you can't bag mask the patient afterwards because they're now paralyzed. So it's something to be cognizant about. So the correct answer is a wake fiber optic assisted ventilation. And here are your references. Another airway question, 72-year-old man has undergone partial lung resection for squamous cell carcinoma four hours after admission from the PACU to the ICU. He becomes abdundant with partial airway obstruction. His respiratory rate is slow at four. His O2 salt is dropping. He gets six milligrams of epidural morphine and 150 micrograms of epidural fentanyl via a lumbar epidural catheter eight hours before ICU admission. Underlying conditions on the patient are COPD and coronary artery disease with stable angina. And the question for you, which of the following interventions is most appropriate? Is it A, immediate nasotracheal intubation to protect his airway and provide ventilatory assistance? Is it B, immediate orotracheal intubation to protect patency of the airway and provide ventilatory assistance, a technique of intubation, nasotracheal versus orotracheal? C, immediate effective ventilatory support via bag mask while 80 micrograms of naloxone is given via the epidural catheter? Or D, immediate naloxone, 0.4 IV push. So the patient is abdonded, bradypneic, falling sat, he had just gotten epidural morphine, epidural fentanyl, he has COPD. Some more answers are coming in. Correct answer is D, immediate naloxone. And here's your rationale. So this is a patient with delayed ventilatory depression who's abundant after epidural opioids. He had already previously received morphine. So this is a situation where you need to rapidly administer IV naloxone. And I know the dose is listed on your rationale. Can be started at low dose, 2.5 micrograms per kilogram per hour IV infusion. So some might start a little bit lower than that. But again, you need to be cognizant that this is a patient with severe respiratory depression after a large dose of narcotics, and you have to immediately reverse this. Importantly, naloxone, when given epidurally, can be unpredictable and is not an appropriate therapy. And in patients without a full stomach or other significant risk factors for aspiration of gastric contents, effective short-term ventilatory support via mask can often be achieved without having to intubate the patient. Certainly tracheal intubation, whether you go nasal or oral, can be associated with significant morbidity. So you have to first try to reverse with naloxone. And if that's not successful, then, of course, you have to proceed with intubation. The correct answer is immediate naloxone at that dose. And here are your references. Here's another airway question, a 55-year-old man is admitted with community-acquired pneumonia and hypoxia. He's placed on high flow, 100%, 60-liter flow rate. He gets broad-spectrum antibiotics. He continues to deteriorate, worsening tachypnea, hypoxia, and respiratory distress. The decision is made to proceed with tracheal intubation, examining his airway. His mouth opening is greater than 3 centimeters. His neck mobility is normal. His thyromental distance is greater than 6, and his malampati score is 1. Which of the following would be expected if video laryngoscopy, rather than direct laryngoscopy, is used to facilitate this patient's tracheal intubation? So it's a DL versus VL question. Which of the two, if you were to do video laryngoscopy compared to direct laryngoscopy, which of the following would be expected to facilitate this patient's tracheal intubation? A, video laryngoscopy will increase the likelihood of successful intubation on the first attempt. B, it will provide improved glottic view versus direct laryngoscopy. C, video laryngoscopy will reduce post-intubation complications. Or D, video laryngoscopy compared to direct laryngoscopy will reduce the time to successful intubation. The correct answer here is B, vitilaringoscopy will improve glottic view. It has not been shown that using VL versus DL will increase the likelihood that you will have a successful intubation. Again, that's very operator dependent. It will not reduce post-intubation complications as compared to DL, and it will not reduce the time to successful intubation. What it does is improves the view of the glottis and make it more likely that you'll be successful if you have a good view to actually get the endotracheal tube in. So correct answer is B, improve glottic view. Multiple randomized trials use the rationale have shown no benefit of intubation success on the first attempt, whether you're using VL or DL. Furthermore, VL does not improve post-intubation complication rate or reduce the time to successful intubation. It does, however, lead to an improvement in glottic view compared to DL. In a French trial recently published a few years ago now, it was shown that VL was associated with a higher risk, however, of severe life-threatening complications. And although no study has investigated the impact of the type of vitilaringoscopy, the experience of the user and the patient population on the outcome related to the endotracheal intubation. There are some recent studies that actually might suggest that depending on the operator, the complication rate is not as high with VL. So this might be a little older rationale, but again, it's very much dependent on this operator skill. But definitely all you get really is improvement in the view, but no immediate guarantee that you will have a successful intubation just because you're using vitilaringoscopy. And here's your rationale. Okay. Andrew? 24-year-old woman has asthma, comes to the emergency department with coughing, wheezing, and dyspnea. Aggressive treatment with inhaled albuterol and monofilin and steroids is ineffective. She's transferred to the intensive care unit, an endotracheal tube is placed, receives mechanical ventilator support and sedation. Because of dyssynchrony, vecuronium is given as a bolus in infusion. Prior to the administration, percutaneous electrodes are placed in the ulnar nerve with train of four simulation. The patient continues to be dyssynchronous with the ventilator, the train of four finding, the vecuronium infusion is increased, at which time the patient is no longer overbreathing the ventilator, and the train of four twitches, no contractions, which of the following recommendations is most appropriate to evaluate the degree of paralysis? Changing the electrode placement, increasing the train of four current, checking the post-it account, getting a new stimulator, or changing the polarity. So most of you went with increasing the train of four, stimulating current. There's a reasonable way to do this. Again, the definition of a train of four is to monitor the depth of neuromuscular blockade in the sense that you're supposed to get some stimulation with increasing shocks. Generally, deeply paralyzation is one of four. It's present. If there are no twitches, this is generally, if there's no twitch, it means the patient's typically over-paralyzed, or there's too much of a paralytic. There's too much paralytic being infused. Usually, it's not the equipment malfunction that is possible. Usually, increasing it doesn't help very much. Something could increase the post to 10 account. If you can elicit the train of four, usually increasing it doesn't help you as much. So the best answer here would have been, I think the distractor was 60 to 80. So the best answer here was? You want to check the placement or look for? Yes, increasing it from 60 to 80 won't do much. In fact, most, I don't think even, they go up above 60. So the correct answer here was? Generally, A. A, changing the nerve stimulator's electrolytes. Chasing the nerve stimulator, they almost never fail. Replacing the stimulator doesn't help. And again, once it's in place with 60 going to 80 doesn't help you very much. It's a very long rationale. Why don't you dig through this at your leisure? Questions about this? We all use train of four when we give neuromuscular blockade. We're aiming for one twitch, two twitches, three twitches, four twitches for deep paralysis. One, two, three. Anyone else? One to two? I actually haven't used one of these in years. We haven't used one of these in our ICU in years. Certainly for ARDS management in some patients where you're having to deeply sedate and prone and they're still desynchronous with the ventilator and you want to reduce oxygen consumption and preserve diaphragm function, I mean, it's still used. Some of the recent trials have not shown that it definitely improves outcome. And so only low tidal volume ventilation, checking plateau, pressures, and proning have been the only ones that have been definitively shown. But if this was a question from 10 years ago, neuromuscular blockade would have been a yes. But most recently, based on the ROSE trial, that has not proven to be the case.

ICU

cerebral aneurysm

subarachnoid hemorrhage

cerebral perfusion pressure

MAP

hypervolemia

vasospasm

systolic blood pressure

neuro field