and toxicology case study. So we'll start out with a brief case and then a few questions to follow. It's a 28-year-old man, no other past medical history, brought in by EMS, status post, single gunshot wound to the chest. The FAST, or the focused assessment sonography trauma exam was negative, and then he's stabilized prior to transport to the surgical and trauma ICU. The vitals are as follows. Temperature at 38, he's tachycardic at heart rate 110, and his blood pressure is 130 over 60, respiratory rate 26, and then an O2 sat initially of 92% on room air. His serum creatinine with the initial laboratory values comes back as 2.5, along with that, a urine tox screen initially positive for ethanol, later confirmed with a blood analysis of a BAC of 0.2%. The exam, he's disoriented, confused, and agitated. I would probably say that, you know, based on the patient population at the University of Chicago, that we're seeing in trauma, this would probably fit 75% of the traumas coming in, either single gunshot or multiple, in a similar profile, male or female. And so the initial treatment, after ordering a CEWA scale with intravenous lorazepam, he's given a couple of doses. However, then he has a desaturation, and then O2 sat at 85%, and the ICU team intervenes after upon transfer, and the patient is then intubated. So the first question, which of the following would be initial appropriate management of analgesian sedation or analgo sedation now referred to according to the guidelines? And so choice A, dexmedetomidine infusion, lorazepam infusion B, if you can find it these days, fentanyl intravenous push as needed with propofol infusion, ketamine intravenous push as needed, if you can find that in your hospital these days, and fentanyl intravenous push as needed plus midazolam infusion. So we can go through each of these options, but those are the choices. How many in the group think about choice A, dexmedetomidine infusion? Okay, an option, and you know, we've seen, and now that it's been off patent a number of years, you know, the price has come down, but you know, kind of besides that fact, it's interesting, the initial studies with dexmedetomidine and lorazepam in non-intubated patients really didn't seem to find a difference in the two therapies. There were a couple of smaller studies which showed a decreased lorazepam requirement kind of for breakthrough, but one of the hallmark things of I think in challenges of studying alcohol withdrawal is really kind of focusing on giving appropriate therapy to hit the GABAminobutyric acid receptor or GABA. And I think that's maybe why we haven't seen a greatest effect as we probably would have expected or anticipating rather with dexmedetomidine. And now that the patient's intubated, really we're trying to move towards an analgo-sedation approach, but with the focus on the GABA receptor due to the presence of alcohol that's already in the system. Ketamine, intravenous push could be an option as well, being a N-methyl-D-aspartate antagonist. It's probably more advised to use that in refractory cases as an adjunct, so it can be useful there either as intravenous push or as an infusion, again as an adjunct when other therapies have already been added or maybe have just not come around to getting adequate control of the patient on the mechanical ventilator. And then fentanyl intravenous push as needed with midazolam, again could be an option except the caveat is in the question, you're getting obvious signs and indication of acute kidney injury. So we're trying to avoid a drug that potentially would hang around a little bit longer as midazolam is gonna be cleared renally. But otherwise if it was midazolam PRN, that probably could have been an option too depending on how much control you're getting with the patient. One of the other kind of caveats, so the correct answer would be C, fentanyl intravenous push and then propofol infusion. Propofol, and there are some papers where it was studied even in patients that were, by itself, monotherapy non-intubated. I would advise caution against that. It has been studied and has been used in a different number of sites and globally. But I think the challenge there becomes the monitoring. And so generally, if it's gonna be advised, it would be in an intubated patient. And then you have a balance of some analgesia as well while the patient's intubated. So I did talk about the gabamino butyric acid receptor. The other kind of caveat, and this will come up sometimes, and it can come up in another question, is in regards to lorazepam. And it's a metabolic arrangement. Is anybody familiar with what can happen with high amounts? Or generally, you may not see it with intravenous push as needed dosing, but more as an infusion with lorazepam. Propylene glycol, correct. Yes, and generally, what you could come across, again, at doses probably closer to four to six milligrams an hour. And then again, that one's, it's a little bit easier to remember, you think of it as propofol in terms of the syndrome piece of it, but duration and dose dependent. And so again, higher doses of continuous infusion with the longer duration can make the patient more susceptible to have that. The same type of monitoring in terms of anion gap, acidosis, but the propylene glycol in terms of content, lorazepam would be one of them. The other ones we don't use as often, but the other ones that have quantities of the propylene glycol to kind of think about would be diazepam. Even digoxin intravenous has some, phenytoin and esmolol. And so those are kind of the ones that have the propylene content, but lorazepam being one of the highest. And ketamine, as I had mentioned, could be a nice adjunct. So whenever your other therapies have failed, that can be utilized. And the piece that's not mentioned in the question, but that does come up more practically, and it could in a different question, is the monitoring. So remember initially you're given just some suggestive evidence that it was managed via a CEWA scale. Once a patient becomes intubated, remember obviously the CEWA scale requires a back and forth and an interaction, so to speak. So once a patient is intubated, then there's a fair amount of information and data and literature now that will just support utilizing your RAS score as kind of determining your therapy and a trigger for titration. And so that's perfectly adequate and acceptable. Any questions on, again, the choices for this one? So over the next two days, the serum creatinine improved. However, the agitation only got it slightly better. The notable findings now are a triglyceride of 515 and a lactate of 15. And so the question's asking which of the following statements is correct in terms of what the ICU team is likely observing, that what's going on in the patient. The options, A, pancreatitis, B, additional or worsening alcohol withdrawal, C, rhabdomyolysis, D, propofol infusion syndrome, or E, abdominal compartment syndrome. So in this question, the correct answer is gonna be the propofol infusion syndrome. Even though pancreatitis obviously is a concern and can happen in these patients and can sometimes be a triggering event for an admission, the laboratory values provided, which are absent in terms of identifying that, are not present. But the additional worsening alcohol withdrawal would mean the patient wouldn't be responding at all or not cooperative at all, but you have a little bit of response in terms of giving the propofol infusion, in terms of managing the alcohol withdrawal. And even though the AKI is resolving and you can have worsening of AKI and PRIS or propofol-related infusion syndrome, it makes it less likely that you're gonna have like a rhabdomyolysis and you don't have the other laboratory values indicating. So even though that could be one of the things with propofol infusion syndrome. So it probably hallmarks that, and it's probably common with other types of syndromes. You may have two out of the four. You may not necessarily always have kind of four out of the four kind of findings in terms of the clinical pieces. And so that's something to kind of keep in mind. There wasn't any description of ECG changes, but that would be the other one that would lend itself to kind of going down that road in terms of a diagnosis. Any questions on that? And the resolution is it's supportive care, but it's also withdrawing the agent as quickly as possible. What we found, and this was maybe hallmarked more and it's been now published in a number of papers, but during kind of the height of COVID, large amounts of analgesia, but sedatives were necessary to manage patients on mechanical ventilation. And so it would not be uncommon to get triglycerides in the four or 500s kind of isolated in patients on mechanical ventilation. And this question actually comes up a lot is when to decrease the therapy dose or to kind of eliminate it altogether in terms of a goal of getting it weaned off. In this type of patient, the goal, now that you have a lactic acidosis would be probably to wean it off completely. If you have just, and it's a good kind of teaching point, if you have just an isolated elevated triglyceride level with nothing else, and obviously the patient being able to tell you they have abdominal pain is gonna be probably problematic because you won't necessarily get that type of information. But in just an isolated elevated triglyceride, what we found that worked very well is usually just initially cutting the dose by 50%, your infusion dose, repeating labs the next day. And if it's decreased, cut the infusion dose again, but you can actually still keep it going and running. So you don't have to necessarily kind of abandon the therapy, so to speak, altogether. The one caveat I will say, and that comes up again quite often, is with the dexmedetomidine. You know, recognizing that the initial studies really only looked at it for 24 hours, it's another caveat and kind of important thing to remember is that your alcohol withdrawal patients, on mechanical ventilation or not, once they get kind of tied to the infusion, I'll use that term, it's very difficult to untie them. So you kind of go through this seesaw of titrating down, titrating up, titrating down, titrating up. And then I've kind of termed it, we've kind of iatrogenically created a case scenario withdrawal. And it's obviously very similar, no different than clonidine. So the sooner, if you do have to utilize it, the teaching piece of it is try to have a plan strategically to get it off as soon as possible. Otherwise, you kind of go back in the seesaw of back and forth. Any other questions on the medicines or the syndrome itself? Yeah, so the question is aiming towards if the patient was not, if I understand, not intubated and were to get started on dexamethamidine. A couple of main things is that to be sure that you have actually a true GABA drug, so lorazepam, intravenous, as needed, already documented with the CEWA scale to kind of direct the dosing, that would be first and foremost. If that becomes to escalating dosing amounts or you need something a little bit more acutely, then dexamethamidine can be an adjunct, but I would think even before that, a drug we've started to utilize more in the last several years has been phenobarbital injection, actually. So not as an infusion or a piggyback infusion or anything like that, but intravenous push. So it's significantly lower doses than what's used in status patients or episodes. And the vials, they come in like 65 milligrams, I believe. So doses initially of a 260 milligram intravenous push, and then 130 milligrams twice a day for two days. And I usually suggest a very short duration so that it makes you obviously reevaluate it. But we found that attacking kind of the GABA receptor, so to speak, from all angles has worked a lot better before thinking about adding things like dexamethamidine infusion or ketamine intravenous infusion or IV push. Even though they can be advantageous and the thought process being so you don't have to intubate the patient, what we end up finding is that now once the infusion started, you have to have a strategic plan of how to get it off. Because if you don't, they'll likely or could, and maybe you've already come across this, but they could be in your unit for days. And they're in the unit not because of anything else except a dexamethamidine infusion hanging on the pole. And obviously with throughput and length of stay and surge capacity happening at everyone's hospitals, it's probably important to kind of think of that long-term strategy sooner rather than after it started. But I've not had very good success, and I know a number of people have not. I know it's been published, but to use clonidine and tapers and things like that, what we found is that for some of the patients, at least anecdotally and in what's been published, is they do not tolerate the oral clonidine Q8 very well. And then even worse, we've had patients, believe it or not, and I've kind of seen this unfortunately like with midridrine, where they get started on it and they go on it on the floor. And then there was no plan to get it off. And then they come back to the unit because their blood pressure dropped. So it's like it's thinking beyond just kind of the immediate sense. And we have to do that earlier than we used to, I think. Any side effects of dexamethamidine infusion? Oh, sure. So the side effects of dexamethamidine infusion, the most notable with the infusion are going to be hypotension and bradycardia. It's interesting. The labeling has a bolus dose, which is actually almost exclusively used in the perioperative setting or the operating room. And with the bolus dosing, which is not generally done in the intensive care unit setting as an infusion continuously, but you'll actually see a little bit of hypertension because you'll see peripheral activation of alpha receptors before you'll see the central ones being agonized on. It's actually kind of interesting. When the bolus doses are utilized, you'll actually get a little bit of hypertension, but it's not utilized for like that in alcohol withdrawal management. But it's predominantly going to be hypotension and bradycardia. And in most of the studies, they'll use a trigger of a heart rate less than 50 or so for things like atropine and other alternatives. The only benefit I will say is that if it is observed in the bradycardia and hypotension, if you just shut off the infusion, usually you could see resolution of it pretty quickly. You don't necessarily always have to give an antidote, so to speak. Very good. Thank you. We'll take a—do you want to take like two minutes and—or is it next? You'll proceed? All right. No problem. So we're going to move ahead to the shock and cardiovascular part, and I'm fortunate to have Steve Greenberg, who's going to help me go through this. And again, please jump in if there's something that you want to say or pursue further. So our first case is a 49-year-old using cocaine. He's got hypertension, hyperlipidemia. He last used cocaine five days ago. And as Phil has pointed out, the question is sometimes trying to lead you someplace. So he hasn't used it by history, and the urine tox is also negative. He's presenting with chest pain diaphoresis, and he's diagnosed with a non-ST elevation MI. In addition to aspirin, clopidogrel, and enoxaparin, which of the following medication should be administered within the next 24 hours? And your choices are metoprolol, lorazepam, forapamil, and streptokinase. And again, they've tried to lead you a little bit with the fact that he hasn't used it, and his urine tox is negative. Thank you. OK, and it looks like you all were led in the direction that, or most of you were led in the direction that they wanted to take you. So obviously, in somebody who's used cocaine, we've all been taught that it's got a lot of problems and that you don't want to give unopposed beta blockers in acute intoxication, which is not the case here, because he hasn't used it. And the correct answer is metoprolol. So they're both, again, reminding everybody that, at least in theory, those who present with cocaine induced MIs that you want to avoid giving beta adrenergic blockers initially, because you can get unopposed alpha stimulation. And also, they're highlighting the fact that, in acute intoxication, benzodiazepines are often recommended. But this is not acute intoxication. Farapamil is not a first-line drug for myocardial ischemia. And you don't use lytics for non-STEMI in most cases. So the correct answer here is beta blockers. And you want to jump to the next one or say something about it? Just the fact that, I mean, cocaine is the most common drug of abuse associated with an acute MI. And usually, it's coronary vasospasm. I would say that the half-life of it, it's actually a local anesthetic. I'm an anesthesiologist and intensivist. So we actually use cocaine in the operating room to anesthetize the nose. Thank you. Can you turn on your mic? You guys hear me? Yeah, I think they can. My voice carries. So basically, the half-life is an hour. So as going back to this case, three days or so, it's really not going to be an issue. But when we take patients, critically ill patients, to the operating room with a high risk of cocaine use, that's one of the things we ask. Because we might use drugs that provide that unopposed alpha issue. So it's really something to be very cognizant of in the perioperative area as well. OK, next question. This is a 56-year-old man admitted to the ICU with hypoxemic respiratory failure with an oxygen saturation of 76%. He required intubation. His wife says that he has had heartburn type symptoms for the past three days and became increasingly breathless for an hour before admission. An examination, he has diffused lung rails, elevated jugular venous pressure, and a short, early systolic murmur at the apex. Extremities are cool. ECG demonstrates sinus tach with Q waves and inferior lateral leads and nonspecific SD changes. Chest radiograph demonstrates diffused bilateral infiltrates. And a TT was done, the bedside, showing the left ventricular function is hyperdynamic with a left ventricular ejection fraction of 70% and focal akinesis of the mid and distal inferior lateral inferior segments. Valvular structures were not well visualized. So which of the following is the most appropriate next diagnostic test? A, CT angio of the chest. B, transesophageal echocardiography. C, bronchoscopy with BAL. D, serum procalcitonin level. And E, cardiac nuclear perfusion scan. Go ahead and answer. And we'll talk about it. Great. Okay, going up and down. As more responses come, the sample size gives you a signal. Okay. So, I think we're all done with the response. So, the majority of you got the right answer, which is transesophageal echocardiography. So, let's go through this question. Next slide. So, essentially what this is, is an inferior wall MI. And one of the things that you have to be cognizant of, particularly within the first 24 hours and then up to about three to five days, is a ruptured papillary muscle, which would cause severe MR. And going back to the case in general, you see that the patient has some Q waves in the inferior leads, has some bilateral infiltrates, which would suggest a wide open MR and pulmonary edema, and a hypercontractile left ventricle, which when you have wide open MR, everything is going backwards. So, there's nothing in the left ventricle to pump forward. So, the question would be, is the TTE didn't really show us the mitral valve really well. I mean, I'm surprised that you wouldn't be able to see a wide open MR with a TTE. But again, the images might not be as spectacular as the TE, which is really what we use in the operating room and beyond for a real focal analyzation of the mitral valve. Because again, you can not only see all the specific anterior and posterior leaflets, but you can see the posterior medial and anterior lateral papillary muscles extraordinarily well. So, just as a point to this case, the posterior medial papillary muscle, because it only has the posterior descending artery for circulation, is the most likely one, especially in inferior wall MI, to actually cause a rupture. So, the anterior lateral papillary muscle is supplied by both the circumflex and left anterior descending. So, the one that you're going to primarily see is the posterior medial papillary muscle in terms of rupture. So, again, TTE would be the right choice because it, again, evaluates the mitral valve, although you can still see this on a TTE. So, again, that's why I kind of put that in there that the trans-thoracic echocardiography was done and the views that were elicited weren't spectacular. So, questions about that particular question at all? Any questions? Yeah. So, that requires surgery. Yeah. So, that definitely. And the mortality rate of a papillary muscle rupture is quite high. Yeah. It would depend. You know, sometimes it's replaced, sometimes it's repaired. And then they actually repair the muscle and the cords to the actual valve itself. So, it just depends on the clinical situation. But high mortality rate association. Other questions regarding papillary muscle rupture, inferior wall MI, the specific keys to this? Can you just go back really quick to the question? So, short, early systolic murmur heard at the apex. Again, where do we hear MR? Anybody know where we hear MR the most? If you had your stethoscope, I know we have all of our POCUS equipment now, but. Yeah. And which sternal border going towards the axilla? So, fifth, left intercostal space, midclavicular line coming to the axilla. But again, early systolic murmur. You might hear it, you might not, depending on the gradients between the left ventricle and the left atrium. So, if the left atrial pressure is really high, you're not going to hear a significant, like, a really loud murmur. But if they're not, it's really acute, you will see that significant blow-type murmur. So, okay, we'll go to the next one. Okay, you've got a 55-year-old admitted to the ICU with dyspnea and orthopnea for two weeks. They're ephebrile, heart rate is low, respiratory rate is low, and their pulse ox is adequate. They're awake following commands. They've got a pansystolic murmur, loudest in the fourth intercostal space in the parasternal region. Clear lung sounds. They've got pedal edema. And their labs are listed above. A triple lumen catheter is inserted to obtain a right atrial pressure, which is not something we normally do. And you've got a tracing that we're going to see on the next slide. And Steve really wants to talk about this one. So, I'm going to let him do so once. But the choices are that there's either stenosis or regurgitation in either the mitral or tricuspid valve. And they are asking you to look at A, C, and V waves. And why don't you, since you felt strongly about this, why don't you talk? So, I think the answering is on the next one. But maybe it's worth just talking about when you can look at them and how to find them. Sure. So, this specific waveform correlating with the pressure waveform is actually quite challenging to make out. What you really want to understand is what the A, C, V waves are, and less so the X and Y descents. So, A wave, we're looking at the atria. And we're looking at the right side of the heart. So, this is where that CVP is placed. So, that's the pressure wave. So, the A wave is atrial contraction, right? And the V wave is isofumal contraction of the ventricle and where the tricuspid valve bulges into the right atrium. So, you'll have another pressure upward reflection. The C wave, the V wave, is ventricular emptying. So, you'll have blood. This is during systole. You'll have atrial filling. So, that's the next pop up. So, correlation to the EKG would be the fact that atria, okay, if you have atrial contraction, be right after the P wave, okay? The A, C wave, which is really where we look at end-diastolic volume, occurs at the peak of the R wave of the QRS. And then, actually, the V wave would correlate to after the T wave. So, here, it's very difficult to see that correlation. It almost looks like that big V wave right there, which is the largest upward reflection, is closer to the SQRS. But, again, it's a little bit off in this pressure tracing. But, I can assure you that this is looking at regurgitation, and it's looking at a large V wave during a recurgent valve situation, which, in this particular situation, is on the right side of the heart. So, it would be tricuspid regurgitation. So, just, you know, that one, they should have slowed down the EKG tracing and actually allowed you to see. And I think when you'll take the test, because these are very easily testable questions, unfortunately, even though we don't use them that often, they'll really key into the fact that where is the T wave in relation to the V wave, all right? The other thing, and for this, great, and if you go back just a couple, the other thing to look at, if you don't know the tracing, you might be able to glean the answer by just looking back at the question and the physical exam findings. So, you see a physical exam reveals a pansystolic murmur loudest in the fourth intercostal space in the parasternal region. So, right off the bat, if you hear a pansystolic murmur, okay, you can cross off two out of the four answers, okay? I always say the best way to take tests is to exclude questions. Then you increase your probability, I'm just telling you how to, but you increase your probability of getting an answer right. So, you automatically get A and C. Then, if you think about where the pressure, they're monitoring the pressure, it's on the right side. Well, a CBP will never monitor left-sided pressures. It doesn't get there. You need a PA catheter for that. So, again, crossing out D. So, the only one that's left, without even looking at the tracing, is B. So, just so you know, a lot of these questions, four questions, won't just give you a tracing and have you just be able to interpret the tracing, although that's something that they love testing. But you can also probably glean answers just from some of the physical exam findings. So, that's a perfect example of this question. The one other teaching point I'd make on this, and they don't include this here, you want to read ACV waves, all of them, at end expiration. So, ideally, you'd have a plethysmography tracing to showing this, but it's awfully hard to line all three of them up on something that is poorly reproduced. I oftentimes ask our trainees to put their hands on the patient's chest to see when end expiration is, and then I freeze the actual monitor and make them actually figure out when end-diastolic volume is, which is really the AC interval. It's right between the atrial kick, atrial contraction, and the tricuspid bulging, or if you're looking at the left side of the heart, the microvalve bulging, same kind of thing. So, I try to do that at the bedside so people actually really know how, because the monitor itself actually averages the CVP and wedge pressure tracings over time. So, if you have huge respiratory variations, so on and so forth, that's just an average, and it's probably not accurate what the wedge pressure or CVP are. So, that's it. So, questions about that? Okay. Next patient has an acute MI. He's getting beta blockers, aspirin, and his blood pressure is low. His pulse ox is not tracking. So, low blood pressure, and you can't read something that doesn't show up well peripherally. It also, as an aside, there are lots of other problems with pulse oximetry that we're not going to concentrate on right now. Chances for a favorable long-term outcome will be best with which of the following interventions? And they're asking, do you want to give lytics, intra-aortic balloon pump therapy, rapid cardiac catheterization, or immediate volume resuscitation? And they're asking you for the best of these answers. Okay. We don't have to spend a lot of time on this. Just the, I guess the one thing to point out, lots of people were trained that balloon pumps are helpful in cardiogenic shock. In fact, the only large clinical trial, which is 10 years old, the shock IABP study did not show a difference in outcome. So, many people still put them in. But the best way to reperfuse somebody is to reperfuse them. And so, taking them to the cath lab is correct. All right. So, this is a 77-year-old American man who's admitted to the ICU in the late afternoon for observation after an uneventful, it looks like FEMP bypass. He has a history of diabetes mellitus. He has a history of cardiac disease and coronary artery bypass grafting 10 years ago. The patient has a required intermittent libatal lull and nitroprusside to maintain a systolic blood pressure of less than 160. In the early evening, the patient's noted to become more agitated and is thought to be sundowning, according to the nursing staff. So, throughout the next several hours, the on-call resident gives the patient 30 milligrams of IV haloperidol. So, that's the trigger. The nursing supervisor calls you at 2 a.m. and explains that your patient has just been resuscitated from a chaotic ventricular arrhythmia. Second hint. Review of the patient's admission ECG reveals evidence of a previous myocardial infarction and a prolonged QTC. Third hint. The most likely reason for the arrest is A, cyanide toxicity, B, diabetic cardiomyopathy, C, beta blockade, a patient with autonomic insufficiency, and D, haloperidol. Okay. You guys are acing this. Okay. Any questions about that? That's pretty straightforward. Again, as many of us know, I think that it would have been a little bit more challenging if they would have mixed in some medications that we commonly use in the ICU that cause prolonged QT, which is pretty much every medication that we use. So, this is something we got to be cognizant of. We used a lot of methadone for patients, particularly on ECMO for COVID in the last two years, and we did see significant rise in QT. And one of the things we're always concerned about was torsades de poids. So, that's basically with a prolonged QTC. So, there are a lot of antibiotics, too. Fluoroquinolones are the key ones, azithromycin, fluconazole, some of the antifungals, metronidazole. These are the kind of drugs that you really want to be cluing in. Obviously, haloperidol is the classic one, and this sort of gives it away. There's a chance we might see another one in a few moments. Yes. Yes, do you have a question? I have a question regarding the IV or IM use of haldol. Is there any difference in the outcome of QTC prolongation, or it's all about how much dose we are giving? We have a pharmacist who might be able to be, if you don't mind. Yes. In terms of haloperidol, it's again tied to accumulation. The reports are significantly higher with intravenous use versus oral. With intramuscular, due to the bioavailability, you could still probably get a fair amount of accumulation. So, I would say they're not necessarily equivocal, but probably comparable in terms of occurrence, especially if you get up to look like a total amount of 30 milligrams. But the oral would be significantly less. There's a bioavailability conversion, so it's not necessarily as long. Hence, they now utilize quite a bit of haloperidol deconate, where they'll give the intramuscular every three to four weeks they come in, so they don't have to necessarily get atypical antipsychotics as high a dose as every day. I mean, the only time I've ever actually seen torsades like this is in a patient who is getting antibiotics, particularly fluconazole, and then we're getting antipsychotics on the floor for delirium. So, all these drugs can do it, not just haloperidol. And actually, then, the folks at the bedside, when they call the cardiac arrest, were giving amiodarone, which is the exact wrong drug to give, because that also prolongs the QTC. So, obviously, the right medication we're going to go over in the next couple questions. But that's really—I just haven't—has anybody seen it directly related to Haldol administration without any other medications? You have. Great. How many—how much dosing? Yeah. Right. Okay. Very interesting. Great. Anybody else see it just as an isolated guess? Sixty-one-year-old, recently hospitalized for COPD, who's developing acute severe chest pain, dyspnea, and has persistent ST segment elevation in lead AVR. They're leading you. They're pain-free after dual antiplatelet therapy, heparin, and nitroglycerin. Which of the following diagnoses is most likely? Corporal pulmonary, acute PE, acute pericarditis, acute coronary syndrome due to severe stenosis of the RCA, and acute coronary syndrome due to severe stenosis of the left MCA. Okay, so we've got, we don't often look at EKGs to make now that we have lots of other tools, and this is one where they're trying to, I guess, get you to think about what you might see with EKG findings. So like with many other questions, you can rule out, so pericarditis, you've got the PR changes, depression, and ST segment elevation. Before pulmonary, you usually would see evidence of RVH and right-sided conduction abnormalities, but not an ST segment elevation, and that's what they're leaning to. And so the persistent ST segment elevation is something that you'd see with a really dangerous lesion, the left MCA, and that inferiorly, if the RCA, you'd see inferior ST segment elevation. I have to tell you, this is something that they're trying to lead you to make a point. Hopefully you'll get that point. I'm not sure that I've ever seen this clinically, but it is, that's what they're trying to teach you with this particular finding here. Is there anything you want to add? No, no, no, just, I mean, when you see an isolated ST segment elevation in AVR, it's mainly the proximal LAD, actually, that you're concerned about. So you either kind of know this or you don't, unfortunately. I don't see any other specific hints within the question that would lead you to get the other... Do you so you're asking whether you would see the reciprocal change of the ST elevation lead AVR? Yeah um depending on the timing maybe yes or maybe no I'm not I'm not exactly sure because again this is something we don't see really that often as well. So um I just can tell you that if you have that the distribution is usually in the proximal LAD. It's you know so but you know usually we're looking at uh V1 through V6 you know or 2, 3 AVF or 1 AVL which we know inferior lateral you know depending anterior septal and apical. Okay so 65 year old woman admitted for a subarachnoid hemorrhage presents with dyspnea and substernal chest pain two days after admission. The ECG shows anterior lead ST elevations a troponin elevation which is mildly elevated and then there's no angiographic evidence of obstructive coronary disease or acute plaque rupture. She develops acute blood pressure hypotension of 80 over 60 and is found to have a moderate left ventricular outflow tract obstruction. Which of the following is contraindicated in the treatment of this patient? A. alpha agonists B. beta blockers C. inotropic agents or D. intraortic balloon pumps Does somebody who listed inotropic agents want to explain why they picked the correct answer? Yes. Exactly. Yeah. So, what do you comment, let's take, let's just take dobutamine. What does dobutamine do to cardiac physiology in terms of your heart rate and blood pressure? Say it again. I'm sorry. I can't hear you. Correct. So, you lose that diastolic filling time. If you think about what the best physiology in hypertrophic cardiomyopathy is, something also called systolic anterior motion, which we see when during a microvalve repair, when there's some redundancy in the anterior leaflet, and then there's a sucking sort of a Bernoulli or sort of a sucking of the valve into the outflow track. All that physiology is the same as what they're asking here. And that is, what is the physiology of left ventricular outflow obstruction? And really the treatment for that is slowing the heart rate down. You can increase blood pressure, but not too much using phenylephrine. Phenylephrine would actually be a pretty good drug because it increases blood pressure and lowers or reflex, causes a reflex bradycardia. But what does this patient have? What's the diagnosis without reading the answer there? So they probably have Takotsubo's cardiomyopathy, and we see this a lot. How many of you do neurointensive care? Raise your hand. Nobody? Okay. All right. Well, we see this a lot in subarachnoid or major intracranial hemorrhage patients. And those who have neurologic injury that then subsequently develop Takotsubo's or stress-induced cardiomyopathy have a much higher mortality and morbidity rate than patients that have emotional stress-related Takotsubo's. So what is Takotsubo's? Well, Takotsubo's echocardiographically looks like a ballooned out heart. So you'll have a very apical hypokinetic or achinetic heart, and the base of the left ventricle will contract. So it looks like an outpouching, like an octopus's head. So it kind of goes like this. And when the patients have Takotsubo's related to sort of an emotional stress or catecholamine significant release, those particularly have better prognoses than those patients who develop it from ARDS or hypoxia or an intracranial neurologic injury. So those are really bad prognosticating signs when you develop Takotsubo's. They can actually require intra-aortic balloon pumps and even left ventricular assist devices. In fact, a recent case we had in the operating room, we had a patient undergo a parasophageal hernia repair and came out in cardiogenic shock and clearly thought troponins were way up in the 800 to 900 range. And everybody thought it was, you know, an LAD lesion or something like that. She got a cath, complete clean coronaries. So this patient actually, we ended up putting an impella in her and it took about a week or two for the heart to recover. She got off the impella and got out of the ICU. But that likely was a result of an emotional stress-related response or what we call as Takotsubo's. And she had classic echocardiographic findings that ballooned out apical, achinetic heart with basal sparing. So you might get that on your exam too because it's pretty classic. So tomorrow will be a fair number of questions on neurological issues. So you'll see more of that. The one point, and they didn't take us down here, it's very common to get EKG changes with subarachnoids and you get them in sometimes up to 50 or 60 percent of patients. But the reason that this is not one of those that you ignore is the fact this patient was having symptoms with that. So you've got a 75-year-old admitted to the ICU with shortness of breath, lightheadedness and bradycardia. We've got another EKG question. So get ready. Which of the following is the appropriate next step in his management? And they're asking you whether to ignore it, give atropine, give amiodarone or apply transcutaneous pacing pads. So here's the rhythm. And they're asking you to look at the PR interval and to follow the PR interval and see whether it changes. So which is the most appropriate one? And it looks like you all have tracked the PR interval quite nicely. So it's a Mobitz II, a second degree AV block. The PR interval stayed the same, and it dropped. And it's obviously something that you want to worry about, unlike Winkebach. And so everybody got it right, so I'm not going to spend more time talking about this, unless anybody has questions. OK, during the past several months, after an inferior wall myocardial infarction, a 42-year-old woman reports a frequent fluttering sensation associated with near syncope. She was discharged from the hospital after a myocardial infarction with quinidine for the treatment of paroxysmal atrial fibrillation. Let's just stop there. How many of you have seen quinidine being used for the treatment of paroxysmal AFib in today's world? Raise your hand. I certainly have. So again, that's kind of a trigger. While in the hospital for evaluation, she suddenly becomes dizzy and reports an irregular heartbeat. The tracing shown is obtained, which is the therapeutic agent of choice for this arrhythmia. So this is another one. I think we talked a little bit about this with the haloperidol and the torsades, but that's what this is. And of course the treatment is magnesium. And so, I mean, any questions about that? I think, you know, more commonly, as I said previously, people that are on amiodarone or other drugs that we more commonly use that can really push people over the top and develop a prolonged QT, which then can degenerate into this ventricular, a polymorphic ventricular arrhythmia. So questions about that? I don't wanna belabor it if there aren't any questions. Okay. Again, the fact that no one really has seen the use of quinidine, I haven't seen it in years. You know, this is, again, a little bit out of date, but it just drives home the point that when you have a prolonged QTC and you have this polymorphic ventricular arrhythmia, magnesium is the way to go, one to two grams IV. So you've got a 20-year-old with dilated cardiomyopathy admitted to the ICU. He fails medical management. He started on a biventricular assist device. In the immediate post-op period, the left ventricular device is sent at 70 per minute with driving pressures listed of 180 and negative 45. The RV is set at 70 per minute and the driving systolic pressures are listed here. And the intensivist is called to the bedside. As the patient has a abnormal rhythm, he's awake and following commands. And which of the following is the most appropriate immediate course of action? The most appropriate immediate course of action for managing the abnormal rhythm. And so defibrillation, chest compressions, amiodarone, magnesium, or nothing. In a patient who is awake and following commands with the following EKG and the following blood pressure. So he's breathing, he's got a pulse, he's got a SAT, and he's got a really worrisome EKG in somebody with a biventricular assist device. OK, so they're trying to lead you, and they're giving you a situation that is not common, but not unheard of. I'm not sure that I've seen that, but I mean, yeah. So those of you who pick no intervention is where they're trying to lead you to, that the patient is not having problems with perfusion, with mentation, and they have a functioning biventricular assist device in place that nobody's trying to mess with. So would I be comfortable going home at night and leaving the patient with that rhythm? Maybe not. But they're trying to say that the V-fib that you see is something that you don't need to immediately intervene upon. I mean, again, even the pressures and stuff like that, I mean, usually we would use, usually you look at left ventricular assist devices, you look at speed RPMs. I mean, the fact that they have a negative in driving pressure, this is like basically two ventricles being put into the heart. And so there is no, like, you could take the heart away. It doesn't matter about the irregular heartbeat at all. It's not going to affect cardiac output. That's basically what they're trying to drive home. The reality is, is a lot of times we have one or the other. Left ventricular assist device, we might put in a right ventricular assist device afterwards. But that right ventricle is really important in left ventricular assist devices. Because if you do have an arrhythmia like this without biventricular devices, your RV might suffer from ischemia. And then you lose that right ventricle, which is key to success of cardiac output and your left ventricular assist device. So you usually don't see this type of situation. But again, the big concept is that you have two mechanical devices basically pumping blood and therefore you're not relying at all on the intrinsic or innate function of the heart for cardiac output. OK, so we're on to balloon pumps now. The intra-aortic balloon pump pressure tracing, which you're going to see, is most likely associated with correct timing of the balloon inflation, early balloon inflation, late balloon inflation, early balloon deflation, or late balloon deflation. So we'll see the curve now. Then we'll have you answer the question. Great job. Okay. Excellent. We're going to go home. Yeah. You guys are doing a great job. Just going back, as you can see here, that curve was early balloon inflation. The ones that are really worrisome are early balloon inflation and late balloon deflation. The reason being is the afterload goes up, cardiac output goes down, and myocardial oxygen demand goes up and work goes up as well. That's the actual worst case scenario. The other two, the late balloon inflation or early balloon deflation usually result in a less augmentation of your diastolic blood pressure, which reduces your improvement in coronary perfusion. While those are less concerning because they do less damage to the heart, you're not getting your biggest bang for your buck with your intra-aortic balloon pump. That's basically what this question is showing. You can see the augmentation is actually before the dicrotic notch, which signifies the aortic valve closure. That's where you want assist. You want increased blood pressure to the coronaries during diastole. That's basically what it is. Any questions about that? You guys did really well on the question. Okay. Great. We're on the device part. You've got a 30-year-old who's on peripheral VA ECMO using femoral artery and vein catheters for his worsening cardiogenic shock due to viral myocarditis. During the following week, his native cardiac function appears to be improving. We're giving you another suggestion right there. Although he develops ventilator-associated pneumonia, he started out in antibiotics, and he's got a low PaO2 from the right radial arc line. His O2 sat is 90% on 60% FiO2. They give you part of it, of his vent settings. He's on 7.5 of PEEP, tidal volume of 450, a respiratory rate of 18, which is probably a little high for somebody who's on ECMO, but we won't go there. He's got a right middle lobe and a left lower lobe infiltrate, and post-oxygenator ABG readings show a normal pH, normal PCO2, and a PaO2 of 300, so adequate PaO2. The nurse calls the attending because his sats are going down and his PaO2 is going down. Which of the following is the most appropriate next step in management? So they're giving you these options. You can change out the oxygenator, add a second oxygenator to the circuit. Consider changing to central VA ECMO, increasing the ventilator's FiO2, and converting to veno-venous ECMO. Okay, so actually, Steve and I both agreed that what the majority of you picked was probably a better answer than what they gave. So he's got North-South syndrome. There's another name for this that I'm not ... Harlequin syndrome. Thank you. Harlequin syndrome. And they're telling you that his native heart function, his LV function, is getting better. And there are a number of ways that you can tell that. So on ECMO, it's not pulsatile flow for VA ECMO. So if you start seeing pulsatile flow, it might give you a suggestion that you are starting to get the LV coming back. And the retrograde flow that you normally have from the ECMO can sort of cause a watershed area where you're getting sort of the deoxygenated blood getting mixed with the oxygenated blood. And given that his LV is getting better, it probably makes more sense to think of VA, of switching to VV ECMO. But they are asking you, since you haven't formally assessed the LV, to figure out how well it's working to consider switching to central. What do you want to add, Steve? I mean, I think going to central cannulation for a patient like this is increasing his mortality by an astronomical amount. You have to go into the heart. That's associated with a substantial more amount of bleeding, infection, you name it. So I think there are other ways. You could also do VAV ECMO. So you could still remain peripheral and add another venous cannula. So that would be actually my first choice. The other things you can do in general with North-South syndrome or Harlequin is to increase your ECMO flows and depress the cardiac function by using negative inotropic medications. So then you lower that cardiac output and more of your blood flow and your oxygenated blood is coming from the ECMO machine, which is fem-fem. So I think, yes, central can do it. But that is an extreme situation that is not, I don't think, is a viable real-life situation. I think when you do that, you're thinking the patient may be checking out at this point. The central cannulation stuff that we usually see is post-cardiopulmonary bypass because it's easy. The cannulas are already in the heart. You have an aortic cannula and you already have a venous vena cava cannula. So to put someone on ECMO post-cardiopulmonary bypass in the operating room is just sort of extending the bypass. Doing something like this in the ICU or going to the operating room with this patient is, again, increasing his morbidity and mortality astronomically. So questions about that? Happy to answer anything related to that too. Okay. 75-year-old man presents to the emergency department with acute chest pain that radiates to the back. His initial blood pressure is 160 over 90, and heart rate is 100 beats per minute. ZCG and troponin are negative, and the CT is negative for pulmonary embolus. But there is an evidence of an intimal flap in the descending thoracic aorta. So which is the following most appropriate initial management? A, open surgical repair, B, endovascular repair, C, medical management to achieve heart rate less than 60 and a blood pressure systolic of 100 to 120, or medical management to achieve a heart rate of less than 100 and systolic blood pressure of 120 to 140? Okay, so the answer is keeping that heart rate down to 60 and blood pressure to stop to 100 to 120. How many of you take care of these patients in the medical or surgical ICUs? Okay, if you see, usually the vascular surgeons are involved, they're very particular. It's related to the ACA, AHA guidelines, ACC, AHA guidelines, really trying to drive that wall tension and stress of that aortic flap. So really what you wanna do is start a beta blocker, okay, first, to sort of reduce the pressure over time and then put an afterload agent in. So if the LV ejection fraction's preserved, I usually like to use nicardipine because I really wanna get that pressure down into that sweet spot very quickly. In addition, I'll already have beta blocked the patient. So long-term, it's really challenging as you probably can relate to get these patients in that sweet spot with either oral medications or IV bolus medications. So they end up staying in the ICU for probably longer than we want. And that potentially develops, they develop more complications just from the ICU in general. So I'm getting them on oral medications, Arbetalol and then some afterload vasodilatory medications, ACE inhibitors if their kidneys are okay, so on and so forth, is really good early on in the process because this is a medical management situation for the most part. For the most part, these patients are medically managed. Type A dissections have to go right to the operating room, all right, and that's, again, usually involves the great vessels and proximal to that area. So that's a surgical fixation, that's an emergency surgery. Questions about that at all? The one point I would make on these patients, it's occasionally you'll get somebody who has more than one problem. So you'll have an aortic dissection and you'll have a CVA. And then things get really, so we know exactly what we need to do with these folks. But when you've got one, and this is probably more with type A dissections than type B, but when you're managing those folks post-operatively and they've had both a stroke and they've got a dissection, you need to really thread the needle because you need to have oftentimes permissive hypertension for the brain and you need to medically manage this. And it requires a lot of sort of juggling between two sets of experts who want you to drive the blood pressure in two different directions. That's a great point, John. I mean, it's usually the heart surgeons who are driving that low blood pressure and don't want it to be because of their anastomosis and so on and so forth. And I guess they have a pretty good point because if that anastomosis blows out, you won't have anything to worry about in terms of the stroke. That being said, if you have a watershed area around that stroke, lower blood pressure is a problem. And even going back to the regular patients without a neurologic injury, a lot of times you end up seeing these patients develop renal insufficiency from low blood pressure, acutely lowering this blood pressure to this extreme. And typically I see that these patients get better with time, but because of that low perfusion pressure and the auto-regulatory changes, you don't have enough blood flow. So there are consequences to these recommendations. So you have to be aware of them and know that that may happen down the line as well. So thank you folks. We'll take.

medical conditions

management

case scenarios

trauma patient

acute kidney injury

myocardial infarction

bradycardia

harlequin syndrome

ventricular arrhythmia

aortic dissection

correct management