Transcript
Speaker: Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now your host, Dr. Sergio Zanotti.
Speaker: Post-cardic arrest neurological injury is a common complication of cardiac arrest and a major contributor to poor outcomes.
Speaker: Much attention has been paid to targeted temperature management in post-cardic arrest patients.
Speaker: The evidence for this practice continues to evolve, and we have discussed this topic in previous podcast episodes.
Speaker: Today, we will focus on the other aspects of neurological support in the ICU for post-cardic arrest patients.
Speaker: Our guest is Dr. Ediberto Amorin, a neurologist with subspecialty training in critical care and epilepsy.
Speaker: He has expertise in neurological intensive care, telemedicine, and multimodal brain monitoring with EEG.
Speaker: Dr. Amorin is an assistant professor of neurology at the University of California of San Francisco, Whale Institute of Neurosciences, and directs the Epilepsy and Clinical Neurophysiology Service at the Zuckerberg San Francisco General Hospital.
Speaker: Dr. Amarin's research focuses on coma neuroscience.
Speaker: He has published numerous peer-reviewed studies and co-authored Critical Care Management of Patients After Cardiac Arrest, a scientific statement from the American Heart Association and Neurocritical Care Society earlier this year.
Speaker: Eddie, welcome to Critical Matters.
Speaker: Thanks, Sergio, for inviting me.
Speaker: I'm really excited to talk about this topic.
Speaker: And I think that, as we were discussing before we started recording, a very important topic, an area where there's still a lot to be learned with evidence, but still something that we need to pay a lot of attention to in our cardiac arrest patients in the ICU.
Speaker: And definitely want to hear a little bit of your perspective, not only as a neurointensivist, but also as an expert in seizures and epilepsy.
Speaker: So I would like to start as a way of introduction, maybe with a brief overview of neurological injury and cardiac arrest survivors.
Speaker: What do we see happening to these patients?
Speaker: Absolutely.
Speaker: So there's a lot happening, and I think it's important to think about when it is happening as well, right?
Speaker: Because we think about the no-flow state when the patient is not being resuscitated, right?
Speaker: And then you have the resuscitation efforts where you have a low flow state until you achieve ROSC, return of spontaneous circulation.
Speaker: And there's then concern for reperfusion injury and all the secondary injury that comes after that.
Speaker: So there's a lot of injury that's going to happen in the very beginning, early on.
Speaker: But that's really not the end of the story that can continue for several days.
Speaker: So we think about identifying brain demas.
Speaker: Sometimes you can see that early on the scan when patients come in, but that's also something that may only show up later on when you repeat scans in a few days or development of seizures.
Speaker: They can also develop a few days for after the arrest or with rewarming is a particularly important time to be attentive to that.
Speaker: And there's also a concern for hypoxia, hyperoxia.
Speaker: There's a lot going on.
Speaker: And we think a lot about the monitoring of patients sometimes with traumatic brain injury because there's more literature on that.
Speaker: And sometimes a patient with a cardiac arrest, we're not thinking as actively about this ongoing injury that may happen after the first hit.
Speaker: So I think that's important to think about the first and second hit in cardiac arrest.
Speaker: And I think as we were discussing, Eddie, it's important for people to recognize that there's an initial insult and we're trying to ameliorate the impact of that insult, but there's also secondary insult that can make things worse and what we do or don't do in that post-arrest period, right, from hours to days, can really have an impact on these patients' outcomes.
Speaker: Now, a lot of what
Speaker: non-neurology critical care clinicians think about in this area is targeted temperature management.
Speaker: And we're not going to discuss that in detail.
Speaker: But why do you think this topic is important beyond that for clinicians in the ICU?
Speaker: I'll give us almost like a step back when you think about temperature control, which is the new, new term that resuscitation folks are using now instead of target temperature management, because perhaps we are losing the target, uh, depending on how you read the literature and what your conclusions are from it.
Speaker: But we need to think in the context.
Speaker: So 20 years ago, uh, maybe 30 years ago now, people think that there's not much hope for patients with a cardiac arrest.
Speaker: But that has changed a lot.
Speaker: And if you look at the clinical trials, you know, half or almost half, more than half, depending on the study, a patient recover with good outcomes and good functional recovery.
Speaker: So a lot has evolved and has improved.
Speaker: And I think that has to do with paying attention to intensive care and what we can do to those patients early on, not just with resuscitation efforts, but also what happens in the ICU and how we need to be more hopeful and really
Speaker: push for aggressive care in specific cases because those patients do have the chance to have very good recovery.
Speaker: And we are still now figuring out what type of interventions are needed to help patients achieve better outcomes.
Speaker: So when it comes to temperature control, I think it's very important to think about the bundle of care that comes around temperature control, which goes from frequent neurochecks
Speaker: watching the temperature for swings in temperature, as that's another thing that's important, shivering as a complication, monitoring the brain with EEG, as you may have to have the patient sedated to pursue temperature control, and you're not going to have much of an exam to begin with in many patients, but it might be difficult to identify recovery or demise in the first few days.
Speaker: So those are all things in the bond of care that are important.
Speaker: In terms of what is the right temperature, I think that's still, for some, up to debate.
Speaker: For others, it's clear cut that we should be abandoning at least hypothermia, you know, goals of 33%.
Speaker: and even 36 in some centers and move towards a normal termina.
Speaker: In our hospital, we are still doing hypothermia at 33 and we are part of the ISCAP trial, which is looking at different durations of cooling in patients with cardiac arrest.
Speaker: So there's a lot, I think, to be figured out, particularly in who are the patients that may benefit from temperature control.
Speaker: I think that's still something that has
Speaker: to be investigated.
Speaker: Excellent.
Speaker: And I wanted to, before we start talking about the clinical aspects that you said, all those components that add to good critical care from a neurological perspective in these cardiac arrest patients, in addition to what people are doing or not doing for temperature control,
Speaker: A genesis of a lot we're going to talk about today is this AHA NCS scientific statement that you were part of.
Speaker: Could you just give us a brief high-level overview of that document and how it came about?
Speaker: No, absolutely.
Speaker: I don't speak here as a representative of the American Heart or the Neurocritical Care Society, so this is all my opinion.
Speaker: But the genesis of that document
Speaker: expert consensus was to think critically and carefully about things that we don't necessarily have all the evidence we want available.
Speaker: And the guidelines have a very strict approach to what is a recommendation, then level one, level two, ABCs, you know, may be reasonable.
Speaker: to do this or to do that and in the expert consensus we have the chance to discuss the top topic more broadly and among people who are experts in different areas of resuscitation discuss why we think there is consensus in pursuing one or other type of monitoring or type of intervention and we approach that from all the different systems
Speaker: So we discuss brain resuscitation and management, but we also talk about respiratory GI hematology.
Speaker: So we try to cover all aspects of critical care management of patients who are resuscitated after cardiac arrest.
Speaker: So we just to discuss the specifics, for example, in the brain section, we talk about EEG and seizures, but we even also discuss brain dema management, brain hypoxia, what kind of monitoring should be considered?
Speaker: Should we think about invasive monitoring in what cases?
Speaker: What's the right blood pressure to use?
Speaker: And if you don't have advanced type of monitoring, what would be a reasonable number to pick?
Speaker: So we tried to think with the provider, the bedside provider in mind, and what might be useful information for them to use, particularly in those situations where the level of evidence is not where we want it to be, where it needs to be.
Speaker: We need time to be able to get to the high level of evidence that we want.
Speaker: But in the meantime, we need to make decisions and take good care of patients.
Speaker: So that's really what the goal was of the document.
Speaker: in my view perfect and i think that's a great segue and into the clinical discussion and we'll follow some of the categories of what was discussed from the neurological and support standpoint and we'll start with brain oxygenation and perfusion so in terms of brain oxygenation eddie can you just share with us some of the key determinants of brain oxygenation and maybe give us your perspective on how to practically apply this at the bedside
Speaker: Yes.
Speaker: So I think the difficulty with brain oxygenation and, you know, brain monitoring in general is that it's difficult to put sensors on the brain, in the brain, to know exactly is the brain really hypoxic or not, right?
Speaker: Other body parts, we are used to do that as intensivists and we don't think too much about it.
Speaker: But when it comes to the brain, it's a little bit more complicated.
Speaker: So there are studies that involved
Speaker: invasive parenchymal monitors.
Speaker: That's what we used to do with TBI patients where we have PBT-02, a parenchymal and brain tissue oxygenation monitor.
Speaker: The other measure that's a bit less invasive is usually looking at the jugular venous blood and trying to understand what's the difference in oxygenation from the blood and the vein.
Speaker: So the catheter
Speaker: goes upwards in the jugular towards the brain and you're grabbing the venous sampling right as it exits the brain which is different from a parenchymal probe where you need to drill through the skull and put the probe inside and there are different types of sensors they are fiber optic or have a clark l2o to do that type of monitoring but then it's just me trying to get too specific about the monitors and what it means but that's really important because we felt
Speaker: knowing how you're measuring it is going to be tricky to decide what to do with it.
Speaker: There are other measures that include cerebral oximetry where you use near infrared spectroscopy that's non-invasive.
Speaker: So that's another way to look at kind of a consumption of oxygen as well.
Speaker: The tricky part here is when it comes to hypoxia management is
Speaker: how you're gonna get those sensors in so you have numbers to decide what to do with management, right?
Speaker: I think that's gonna be very center specific.
Speaker: Some places might be more comfortable with that monitoring, may consider that in patients who remain comatose.
Speaker: But the definition,
Speaker: of what patients meet criteria for invasive brain monitoring is really not out there yet.
Speaker: And even for TBI where that's more accepted, there are ongoing studies now to look at that and the BOOST study is specifically looking at PBTO2 goals.
Speaker: Because when we come to invasive monitoring of oxygenation, we tend to aim for a goal of 20.
Speaker: And if it's below that, we may have different maneuvers, we may consider
Speaker: that may be increasing brain perfusion to deliver more oxygen to the brain.
Speaker: We cannot forget to test the probes as well as something that not everybody who is not doing that every day is thinking because those probes may stop working.
Speaker: So you need to do some FL2 challenges to make sure the probes are working.
Speaker: So there's a lot of different things that would be considered
Speaker: in terms of checking the probes and what doing with it, but that's still not clearly defining cardiac arrest.
Speaker: What that would be in a lot of it is borrowed from traumatic brain injury literature, which we still don't know if that's the optimal way to manage those patients or not.
Speaker: So there's a lot to learn yet.
Speaker: And from a very practical perspective, Eddie, I mean, obviously, like you said, some centers have more experience with others and we're still trying to learn from studies what's the best application of all these emerging technologies.
Speaker: But from a very practical standpoint, what are the things that every intensive issue should be worrying about in terms of making sure that we give brain the best chance to have good oxygenation?
Speaker: Yeah, so I think what we've been aiming is to aim for a normal
Speaker: Um, normal saturation, you know, you need to avoid hyperoxia.
Speaker: Um, you know, 92 to 98 has been kind of the set that we're aiming for generally.
Speaker: One discussion is always about where the hemoglobin should be.
Speaker: Right.
Speaker: And depending on the patient population study, people have done different things for other diseases, but we're still recommending the standard hemoglobin A7 as the goal for most patients.
Speaker: Of course, you need to keep in mind a lot of them had cardiac issues, so you may have to modify that goal based on that.
Speaker: And we recommend continuous monitoring of oxygenation.
Speaker: And as well, there's then we get into the specifics of what's the blood pressure that you should target, which may be a segue to another topic of that section, because oxygen delivery also depends on good cerebral perfusion.
Speaker: And that's where perhaps lower map may be deleterious to some patients.
Speaker: Perfect.
Speaker: So before we move on to blood pressure or perfusion, the other aspect I wanted to ask you is in terms of mechanical ventilation, you talked about avoiding hypoxia and hyperoxia and the target that's recommended.
Speaker: Any comments on CO2?
Speaker: Yeah, so we had recent studies looking at hypercarbia.
Speaker: In particular, you know, we have vasodilatation whenever you have higher CO2 and that may improve delivery of oxygen to the brain.
Speaker: But the studies so far have not shown that that was beneficial.
Speaker: And that was, you know, recent publications, this all came out on the New England Journal of Medicine studies on oxygenation and hypercarbia as interventions and they failed to show benefit.
Speaker: So targeting normal car, normal car, you know, where possible probably makes, makes the most sense based on what we know so far.
Speaker: Yeah.
Speaker: So targeting normal levels still is what is, um, preferred at this, at this time.
Speaker: Perfect.
Speaker: I agree.
Speaker: Eddie, in terms of a perfusion or blood pressure, can you just remind us the relationship of mean arterial pressure to what ultimately matters in this discussion, which is cerebral perfusion pressures?
Speaker: Yeah, so I think it's tricky, right, because many of those patients are very sick from a cardiac reason and a very high MAP can be a bit scary to some patients and you need to think about that very carefully.
Speaker: But what we've seen so far in many of the studies is that patients were able to tolerate higher MAPs pretty well.
Speaker: And why do you need your MAP to be high?
Speaker: I think it depends on the...
Speaker: on a few things, but importantly, auto-regulation, right?
Speaker: So if any of us who is walking around goes to a run, we do not have a brain hemorrhage in the middle of our exercise, right?
Speaker: And that's because our body is able to regulate even though our blood pressure, heart rate might be changing.
Speaker: The amount of blood that gets to the brain is stable.
Speaker: So there's vasoconstriction of blood vessels on the brain to
Speaker: avoid your perfusion to get too high and cause issues and brain swelling, hemorrhage.
Speaker: But whenever you have brain injury, and that's very common in cardiac arrest, this ability to regulate how the blood vessels dilate or constrict might be affected and even lost in some cases.
Speaker: Therefore, there's a lot of passive flow on the brain.
Speaker: You need to be very careful.
Speaker: People may have different angles.
Speaker: You may have a shift to the right.
Speaker: and how that, and you may only have auto-regulation in some specific points of the curve.
Speaker: So it can become very complicated, particularly when you have someone that's comatose, that you don't have monitors.
Speaker: And so that's something that you routinely test in traumatic brain injury patients, where we have intracranial monitors.
Speaker: So basically, if we increase the blood pressure, we can see if the intracranial pressure is going up
Speaker: as well.
Speaker: If you lose auto regulation, more blood comes to the brain, therefore your intracranial pressure will rise.
Speaker: So we're able to then adjust our interventions based on the seroperfusion pressure.
Speaker: There's also other ways to look at the optimal seroperfusion where you minimize that relationship of increase in blood flow and ICP because actually you can decrease the ICP
Speaker: if you have good blood flow.
Speaker: So it's not just going in one direction.
Speaker: So you gotta be very careful about that in patients with a significant injury.
Speaker: So that's one of the reasons why the MAP and having a higher MAP, there's some literature indicating that higher MAP may be associated with good outcomes.
Speaker: But again, recent trial, language journal medicine, where we didn't see a benefit on increasing the MAP
Speaker: and this is like patients without intracranial monitors to identify the ideal pressure.
Speaker: So in this study, when you have a map of up to 77 or so on the intervention group, there's no difference with patients with a lower map.
Speaker: And then the practice has been to keep the blood pressure like any ICU patient, the average ICU patient has a map above 65.
Speaker: But in the group,
Speaker: We discussed this and we identified that perhaps a higher MAP may be helpful in some cases and we haven't did not see as much evidence against it in terms of side effects.
Speaker: As long as you take into consideration the patient as a whole and other contradictions of elevated MAP in that situation.
Speaker: And I think obviously it's important to emphasize, like you were saying, Eddie, that with the loss of out of regulation, that curve becomes very linear.
Speaker: So the reperfusion pressure is going to be dependent on MAP.
Speaker: As it goes up, it goes up.
Speaker: And as it goes down, it goes down with no wiggle room.
Speaker: So also you're trying to avoid obviously being on the lower side, right?
Speaker: Where we can't out of regulate to keep the perfusion and cause hypoxia.
Speaker: And that's the idea why in some of these patients, maybe a higher MAP would be better.
Speaker: But the other thing that you talk about, which I thought was very interesting, was this concept of individualizing the target by MAP optimal.
Speaker: Can you talk a little bit more about that and where that is headed?
Speaker: No, absolutely.
Speaker: And
Speaker: That's something that we are still learning how to do because the tools to do that at the bedside are still not as accessible.
Speaker: So to give a parallel, when I'm working in the neuro ICU and I have patients with traumatic brain injury, I find this fascinating.
Speaker: I have a patient that's auto-regulating in the morning, but it's not auto-regulating in the afternoon.
Speaker: And I did the same test.
Speaker: It was just a few hours in between.
Speaker: There is a patient that has a sweet spot and it's a very narrow sweet spot of what the CPP is.
Speaker: So that just reminds us of how dynamic things are and how the different responses of the brain and a combination of things, right?
Speaker: You have your CO2, your oxygen, your intracranial pressure, the amount of edema, your salt status.
Speaker: and how that's all affecting these many factors that drive and contribute to your CPP, your seroprofusion pressure.
Speaker: The CPP opt is a way when you look at the variation of blood pressure over time, and you look at your ICP or CPP as the blood pressure varies and your intrapreneur pressure values vary.
Speaker: And you can also do that not just with intrapreneur,
Speaker: pressure values, but you can also utilize, um, super oximetry.
Speaker: You can also use trascranodopplers.
Speaker: We are really, um, measuring how my, how blood flow is changing over time.
Speaker: And based on that, you identify what's the, um, blood flow that
Speaker: has a better response in this auto-regulation curve.
Speaker: So it's almost, you go, it's a U-shaped curve if you have enough parameters to make that curve available, because your blood pressure needs to vary for you to have a change in parameters and be able to trace the curve with confidence.
Speaker: So if you go all the way to the bottom of that curve, that is your ideal CPP and where you should aim.
Speaker: And that, again, can change over time.
Speaker: So the tricky part is that we don't always have all the gadgets needed to calculate and get information about the pressure on the brain.
Speaker: And even to calculate that, you need to have some computational tools that will kind of put together all those numbers.
Speaker: So I think that is when it becomes a little tricky and there's some software out there that can help you do it.
Speaker: You can try to do it.
Speaker: You know, with the back of the napkin with some numbers available, but that's, you know, difficult to do and to be precise.
Speaker: So ideally you have specialized software that will allow you to calculate what's the optimal superfusion pressure where you minimize increases in ICP related to blood flow.
Speaker: And then you optimize your CPP.
Speaker: And I think it speaks to something that is still not available at the bedside, which is really realizing that a lot of these studies are taking a heterogeneous group of patients and applying two boxes, comparing one to the other, and we might not be able to discern which patients could be harmed and which patients could be helped, and at the end there's no impact.
Speaker: But maybe for every patient, and even as you mentioned, Eddie,
Speaker: During the day that might change, there is an optimal sweet spot that we should be targeting.
Speaker: And hopefully as we get more data and as we get better evidence, we'll be able to tailor that to each patient.
Speaker: But since we don't have that in most of our ICUs, would it be fair, Eddie, to say that based on what we know today,
Speaker: We should start at 65 and above as the floor, and we should really consider, does this patient have a high likelihood or do I have evidence of severe brain injury suggesting loss of autoregulation?
Speaker: And is there any harm or any potential harms of maybe pushing a little bit higher in some of these patients?
Speaker: I think the way you're framing this question is really important.
Speaker: And when people are reading sometimes recommendations, they tend to stick to just one sentence, right?
Speaker: So it's really about the context.
Speaker: And I think you're absolutely right that we should avoid hypotension at all costs.
Speaker: And you should consider a higher map on a patient that has signs of injuries and whether you're worried about if there are no contradictions.
Speaker: So I think that is a reasonable thing to do.
Speaker: And the way I'm seeing it is some centers are starting to also have this invasive type of monitoring or non-invasive monitoring available and they're starting to be more precise on how they decide.
Speaker: So I think that's why I'm excited about those new tools that allow us to do that.
Speaker: But in the meantime, while that's not available, I think this approach is very reasonable.
Speaker: to ask the questions, is there any reason why a higher map is going to harm this patient if I'm worried that they sustained a significant brain injury?
Speaker: And that's where other tools like having EEG available, looking at your scans and your neurological exam may also be helpful on how you decide who may benefit from this decision.
Speaker: Perfect.
Speaker: So I want to talk about edema and ICP.
Speaker: Definitely, I mean, we've all seen CT scan reads or images consistent with diffuse brain edema and cardiac arrest survivors.
Speaker: Usually we take that as a not favorable sign, but there's more to edema probably that we need to learn.
Speaker: Could you give us just a brief overview, Eddie, of the pathophysiology and cardiac arrest and how should we suspect or diagnose it?
Speaker: And what are some of the treatment options that might be considered in some individualized cases?
Speaker: Yeah.
Speaker: So I think we need to think about the type of patient, you know, we have some, some people that progress very rapidly and even on the initial scan, just a few hours after the arrest, you may already see signs of very severe brain dema.
Speaker: We tend to avoid using CT imaging for prognosis early on in, in those patients because of confounding, you may think that the patient has edema, but the
Speaker: edema very early and this often has to do with the resuscitation effort and how long it took and what's the reserve
Speaker: that that patient has.
Speaker: There's actually different degrees of resilience, right?
Speaker: We've seen people that coded for five minutes and have terrible edema, while we've seen people that were coded for 40 minutes and they did okay.
Speaker: So why is it different from patient to patient?
Speaker: So that's something that we don't really understand, but it's something that we need to keep in mind when we look at those patients.
Speaker: And unfortunately, that just complicates the equation.
Speaker: a little bit.
Speaker: And then we need to think about the edema that is happening over time.
Speaker: And that's where we are worried about poor brain perfusion, right?
Speaker: Because that's when you start to have increase in ICP, which is not necessarily yet brain edema.
Speaker: But if you continue to have poor perfusion hypoxia, that might cause secondary brain injury that will lead to cerebral edema.
Speaker: The other thing to keep in mind is some patients are having seizures and have high metabolic demand on the brain during these times.
Speaker: And they may also exacerbate or lower the threshold for critical injury that may contribute to brain dema later on.
Speaker: And because brain dema can be delayed, that's one of the reasons that people wait a few days to get a brain MRI.
Speaker: as a routine practice in most places because you know that if you get an MRI early, you may already see significant injury, but you may miss injury that's progressing over time and delayed lococephalopathy is another complication of cardiac arrest.
Speaker: You need to keep in mind where this imaging can be helpful for diagnosis and then prognostication.
Speaker: But when it comes to acute care,
Speaker: The edema that we see on the scans is kind of a often a late sign.
Speaker: You know, we do constant or frequent pupillary measurements.
Speaker: I think that has been a very helpful tool to have at the bedside.
Speaker: And now we have quantitative measurements of the pupil and that can be an early predictor and also early diagnosis of progression of brain edema.
Speaker: The other tool that we have,
Speaker: at the bedside, and again, just to go back to the physiology, is looking at optic nerve edema, right?
Speaker: We have shortening, so we want to monitor those effects, but unfortunately, they are very late.
Speaker: So that's why I think the discussion on perfusion oxygenation, how to intervene early is really important.
Speaker: um on those patients so we have very early ultra early and then we have delayed that happens over time and that's why we are you know it's hard to in the as an intensivist it's hard to take control the very early injury unless it's like in hospital rest and we do our best there but we are really worried about not doing enough so we want it to be usually pretty aggressive on patients that we're hopeful for a good recovery to prevent
Speaker: this from happening.
Speaker: And can you, so you talked about measuring obviously the pupil diameter over time with pulmonary.
Speaker: You also mentioned the optic nerve.
Speaker: So that's something that's accessible to a lot of our ICUs, right?
Speaker: Just have to learn the expertise of using the ultrasound.
Speaker: Can you comment a little bit more on that?
Speaker: Because I think that's a tool that a lot of people may not be aware or not utilizing.
Speaker: Yes.
Speaker: So popular changes there, there are many papers out there on its prognostic role.
Speaker: And we've seen, uh, when we do that for most of our neuro ICU patients who are in the, do not have a good exam is to track that, um, over time.
Speaker: You can really see changes.
Speaker: And there can also be even like seizures.
Speaker: You can sometimes identify that by popular changes.
Speaker: So I think frequent checks are helpful.
Speaker: on that sense.
Speaker: There's also a lot of interrater errors with qualitative assessment of the pupil and people might not notice.
Speaker: And usually focus are very, paying attention to the size of the pupil and not so much on how much the pupil is moving when you shine a light.
Speaker: And I think that has been one of the key
Speaker: things on using populometry because we can then see that there's a change in this response which is early sign of concern for increase in intracranial pressure in terms of optic nerve ultrasound so
Speaker: That is something that is accessible, but we don't use it too often.
Speaker: And I am still guilty of not doing that day to day in my practice in our ICU.
Speaker: But it's a pretty straightforward tool that we should be using at the bedside more frequently because it's actually very easy to learn how to do the measurements.
Speaker: So it's something that I myself
Speaker: have one of the things I need to do in 2024 after we publish the recommendation is to bring that to my practice and we have some workshops planned with our fellows actually this year.
Speaker: that's a good call of action a challenge for our listeners right i mean we have ultrasounds everywhere now and uh we didn't think we could use it for the lung we can use it for the lung we didn't think we could use it for the brain we can use it for the brain so just learning and applying that at the bedside so so we'll put some some references in the show notes
Speaker: The other thing I wanted to ask you about was ICP specifically, and you did mention a little bit, obviously, as your edema goes up, it is possible that your intracranial pressure will also go up.
Speaker: But when should we suspect elevated ICP in cardiac arrest survivors?
Speaker: And you did talk about some of the changes that can make you suspect that.
Speaker: But also, how do you monitor for that in your practice?
Speaker: And is there anything we can do clinically?
Speaker: Yeah.
Speaker: Yeah, that's a very tricky situation because whenever we see changes in pulmonary response, whenever we see, you know, changes on the optic nerve, when you think about cardiac arrest, you tend to have often more generalized type of edema.
Speaker: So it's not like when you have a stroke.
Speaker: from a bleed or traumatic brain injury that you have a mass lesion that you can intervene on and fix it.
Speaker: And then ICP will come down and you can move on in cardiac arrest.
Speaker: Often there can be a delayed sign of more significant brain edema where interventions may not really necessarily change the ultimate outcome of the patient.
Speaker: So I think that's a big dilemma and why we're really reflecting on our practice
Speaker: of intracranial pressure monitoring, should we be placing bolts in some of those patients to guide our interventions?
Speaker: The tricky part there is like, who should be getting those type of monitors?
Speaker: And we don't know yet if that should be for everybody, right?
Speaker: And just like we are talking about temperature control may not be for everybody, but patients that are with higher concern for
Speaker: brain injury.
Speaker: So people who have longer resuscitation times, people who have a poor exam at the beginning, people who have EEG that's far from a good looking EEG, those perhaps are people who we know have more signs of more significant injury that perhaps we may be able to rescue with more intensive interventions.
Speaker: When you look at the literature, there's not that much out there in terms of measuring ICP with invasive probes in cardiac arrest.
Speaker: But there is a fair amount of patients who do not have an elevation intracranial pressure at all.
Speaker: There are some of those patients that have those very extreme increases in ICP, which related to diffuse brain dema, which may be patients that we
Speaker: might have difficulty having interventions that will clearly improve outcomes.
Speaker: So I think we're still searching for the right patient population that would best benefit from that.
Speaker: But I think looking at your order, neurological injury metrics, including your exam, your EEG, your initial scan, I think that would be helpful in terms of trying to understand who may be a higher risk for developing high ICP
Speaker: down the line.
Speaker: And obviously, there's other guidelines to talk about how to treat edema and high ICP.
Speaker: And in this case, I think it would be very individualized for the patient, but it's still an important discussion to have because it's something that occurs very, very frequently in these patients.
Speaker: The next topic that I wanted to touch on, obviously, something that's very dear to your interest in research and your clinical practice, as well as seizure management.
Speaker: And I wanted to talk about seizures and cardiac arrest survivors.
Speaker: If you could start maybe, Eddie, by giving us an overview of what is seen, and then we can start talking about, okay, how do we look for it and talk a little bit more in detail about seizures
Speaker: types of EEG, what are the advantages, disadvantages, and then about treatment?
Speaker: Yes, I think the EEG in cardiac arrest is really important, not just for prognostic reasons, but really to stratify the types of patients and how they
Speaker: severe injury was.
Speaker: I think one of the things we like to see is if we see a continuous good looking EEG on day one, as soon as we put the EEG on the patient, we feel very reassured, very much more optimistic.
Speaker: And I think, you know, we are always very focused on the poor outcome and what the bad looking EEGs are and what does that mean?
Speaker: but having a good EG is also something that has been very helpful in management of this patient.
Speaker: As we think about all those interventions that we had just been talking about for the last half hour or so.
Speaker: So I'll start with that as a reminder that, you know, there are good things to look for on the patients and not just the bad stuff, which is what I'm going to be talking more about in what has been historically the focus and in critical care in general,
Speaker: And there are clear cut seizures and there's a lot of other things.
Speaker: They're not quite seizures, but that may be bad for you.
Speaker: And I think we're still trying to figure it out what bad for you is and what's the threshold and the threshold is likely going to be different for different patients.
Speaker: So we have the icto interictal continuum, which is those abnormal EEGs to have spikes, epileptic form activity.
Speaker: but they don't quite meet criteria for seizures.
Speaker: And you can see that with sepsis, we can see that with ARDS and many other disorders.
Speaker: And not always treating those things with anti-seizure medications is the right way to go because there's a lot of side effects from those medications and those medications may also affect your clinical exam, which we know is very important when assessing those patients in the ICU.
Speaker: However, if those patterns start to get into high frequency, we know that it means that your brain is having higher metabolism, right?
Speaker: The brain is working harder.
Speaker: And in other diseases, people have shown that whenever you start to get closer to two hertz, you know, more than two spikes per second, you start to have drops in your brain oxygen.
Speaker: You start to have really increased glucose uptake on the pad.
Speaker: And
Speaker: If you have an injured brain to begin with, you need to start to get worried that this could potentially be contributing to the secondary injury we've been talking about, which will affect all the other things as we discussed, ICP, oxygenation.
Speaker: So I think that's why monitoring EEG early is very important, even though the guidelines for prognostication often focus on get all the sedation off, look at the EEG, wait for three days to have a final read on it.
Speaker: The very early EEG is actually very helpful for understanding which patients look good and which patients might start to have changes they're concerning.
Speaker: And particularly, you should not just focus on the
Speaker: Cooling phase after cooling is the re-warming phase is also very important because there's a lot of changes in sedation happening around the time as well.
Speaker: So someone that was in a little bit of purple fall because of the cooling or even normal chermia control or ventilator compliance and you start to get that sedation off to get a good exam, then that person may start to have abnormalities that were being masked by sedation.
Speaker: So that's why close monitoring is very important.
Speaker: In terms of an EEG application, obviously some ICUs have availability for immediate EEG and continuous EEG.
Speaker: Could you comment, Eddie, about the differences and the roles of continuous versus intermittent EEG and also the role, if there is one, between
Speaker: full montage EEG and limited montage EEG which is being pushed a lot I think by a lot of people as an alternative to those centers that might not have the expertise or support that that would provide continuous EEG immediately.
Speaker: Yes, I think the information you get from those two types of monitorings is different and it's really what you do with that information that matters.
Speaker: So if you're just focused on the prognostic aspects of EEG, sometimes intermittent monitoring is just as good, right?
Speaker: Because you're looking for does EEG look good or not on day one?
Speaker: Is it continuous or not?
Speaker: Is it burst suppressed?
Speaker: And then you repeat it on the next day, 24 hours after.
Speaker: Do I see seizures now?
Speaker: Is the EEG more reactive?
Speaker: Is the birth suppression resolved?
Speaker: Did the EEG improve?
Speaker: I think those are important pieces of information that intermittent monitoring can provide.
Speaker: I think the continuous EEG can help you to really see progression of those patterns over time, particularly when you have changes in sedation and other changes in patient care early on that can be informative.
Speaker: And if you're looking for seizures, you may be able to identify those seizures earlier, particularly because many seizures can be non-convulsive.
Speaker: So without EEG, it's hard to tell if that patient is seizing or not.
Speaker: Sometimes it can be very subtle.
Speaker: In cardiac arrest, you have many patients with myoclonus as well, which can be related to the brain and in the cortex and seizures, or it may be what we call subcortical
Speaker: myoclonus, which is not a seizure event.
Speaker: So I think having continuous EEG can be helpful in those times because
Speaker: The malcolin sometimes just happen.
Speaker: And if you already have the AG available, great, you can check on it.
Speaker: If you don't, then you need to get the tech, figure it out.
Speaker: And while you're waiting, you need to make decisions about what you're gonna do with that event, which could be just watching and waiting until you get monitoring to confirm what it is.
Speaker: Or some others may start to treat the patient in interventions, change anesthesia while they're waiting to get that information.
Speaker: In terms of the type of monitoring, in terms of how many channels should you be using, there actually has a lot of literature out there, and I've done studies comparing all the electrodes versus two electrodes versus four electrodes versus eight electrodes.
Speaker: And a limited montage can give you a lot of information because the...
Speaker: Changes in the AG that we see in cardiac arrest are most of the time seen across the brain.
Speaker: So just a few out to us, you're able to catch a lot of the information that we are focused on when it comes to early management, which is is the AG continuous?
Speaker: Is it birth suppressed?
Speaker: Are we seeing periodic discharges that look like seizures, but not quite seizures yet?
Speaker: Are we seeing full blown seizures with the myoclonus?
Speaker: So those are often answered by inter by few channels.
Speaker: You know, from time to time, we do see patients with focal seizures, but that's pretty uncommon.
Speaker: And that's where, when you have a limited EEG might be difficult if the helixels are not in this spot you're looking for, but that is not a common event at all.
Speaker: So to summarize, I think a limited montage can be quite helpful if the full EEG isn't available.
Speaker: And my preference has been to use continuous EEG because of availability in my shot.
Speaker: But intermittent EEG can be quite helpful as well.
Speaker: I think it's really important if you're going to do intermittent EEG to repeat it.
Speaker: So it's not like you do it once and you forget about it.
Speaker: I think having that on day one to kind of determine what's going on with the patient, this patient that's comatose confirmed, there are non-convulsive seizures, but also repeat it as you're rewarming the patient.
Speaker: in the day after.
Speaker: So you can make sure that things have not evolved.
Speaker: And I think also, Eddie, what you mentioned is worth emphasizing or reemphasizing that there are two aspects of applying EEG to our patients in this situation.
Speaker: One is, like you said, prognostic issues.
Speaker: And the other one is trying to figure out if somebody who's not waking up is having seizures that need to be treated, right?
Speaker: And both of those, I think, are very important, but need to be thought of individually.
Speaker: Now,
Speaker: I've seen an evolution over time in cardiac arrest survivors with how we feel about some of these seizures and even status epilepticus where it used to be an ominous sign and like the prognosis was horrible, but that can also be a self-fulfilling prophecy.
Speaker: But I know from what you've shown in some of your talks, but also case reports and other publications that
Speaker: that there is a growing body of evidence, not maybe large randomized trials, because this is very hard to study, that are showing, though, that in some individualized cases, aggressive treatment of these seizures can be associated with improved outcomes.
Speaker: Can you talk a little bit about the treatment aspect of seizures in the cardiac arrest survivor?
Speaker: Yeah, and I think I always think about this, what happened to me as a trainee,
Speaker: So when I was in the very beginning of my residency, I went to see a patient in the cardiac ICU with, um, the faculty and.
Speaker: Visions having myoclonal status and I was told, you know, whenever you see that, that's really a death sentence.
Speaker: There's nothing you can do for this patients.
Speaker: And I think it was a year and a half or maybe two years later, I had someone with the same
Speaker: really the same type of presentation that the family said, oh, we're not ready yet.
Speaker: We would like to do everything we can.
Speaker: He's very young.
Speaker: And then the guy walks out of the hospital.
Speaker: So how do we go from everybody dies to someone that went back to work?
Speaker: So I think to me, that was something that just made me say, whoa, hey, hold on a minute.
Speaker: How can I figure that out?
Speaker: Because it's a pretty serious decision.
Speaker: And if you decide not to treat, or if you decide to treat a little bit, you may be committing that person to an outcome.
Speaker: Of course, we need to be very careful about not over treating patients that have no way of recovery.
Speaker: And that is not a common outcome, right?
Speaker: To have
Speaker: seizures status epileptic is after cardiac arrest and do great.
Speaker: And that's not the majority of the cases.
Speaker: So how to, it's a really a clinical dilemma that we're still trying to figure it out how to approach.
Speaker: I think it's important to understand what's are like bonafide seizures versus just having spikes on the AG.
Speaker: And the Telstar study was very informative, very difficult trial to do that took many years to complete where people pursue treatment of those patterns, the periodic patterns in randomized to no treatment.
Speaker: And what they found is like training those periodic patterns was not helpful at a group level.
Speaker: But when you do some analysis and you look at the patients who actually had high frequency patterns, they were like in the seizure,
Speaker: um part of the spectrum you know the faster type of spikes the the people who didn't get treated they all died while the group who got treatment uh small number of patients did recover and did well so that's just a reminder that we cannot treat all have a blank statement that we should never treat or should treat everybody but we need to be careful about about making that decision and patients to have
Speaker: You know, clear cut seizures, patients who have a background and then they have seizures later on.
Speaker: And that's where people who have seizures on the rewarming phase are actually more likely to be responsive than people who have seizures very early, which.
Speaker: in it kind of makes sense, right?
Speaker: Because it kind of took time for you to develop it.
Speaker: Maybe the injury wasn't as severe as some of those other patients.
Speaker: So I think those are just reminders of how the monitoring is important and how we need to really take into context.
Speaker: What are the other markers of injury?
Speaker: Does this patient have diffuse brain dema on the MRI and reactive pupils or is this someone that has a decent age and then the seizures?
Speaker: came, perhaps those patients have a higher likelihood of recovery and we should more carefully look at them and consider intensive treatment.
Speaker: Is intensive treatment just giving anti-seizure medications, only giving anesthetics?
Speaker: I think we're still trying to learn what that is, but what we've seen is that they tend to be very resistant to anti-seizure medications and you may need to have management with anesthetics
Speaker: in some of those patients.
Speaker: And this is not including the myoclonus piece, which is a separate point that complicates things, but just talking about electrographic seizures and changes on the EEG, there are a lot of different caveats that we need to keep in mind when we're making these decisions and decide how aggressive we want to be.
Speaker: Perfect.
Speaker: The other thing I wanted to ask you was, is there any role for prophylactic anti-seizure medications?
Speaker: Well, that is a good question.
Speaker: And I need to, you know, a disclosure here is that I do have a clinical trial right now that I'm running that's looking at that with the drug perempanil.
Speaker: But putting that to the side, there's no role right now on providing a
Speaker: prophylaxis as soon as a patient gets to the ICU to prevent seizures.
Speaker: So that's not something that's recommended.
Speaker: It's not routine practice.
Speaker: What we do consider is on patients who develop seizures to then start on the seizure medications and see if the patient will respond to that.
Speaker: And depending on that response, decide if additional anti seizure medications are needed or an aesthetics are needed if it is a status epilepticus that's unresponsive to anti seizure medications.
Speaker: But for all comers, that's not something that's recommended right now.
Speaker: And the last thing I wanted to ask you about this specific topic is you did mention myoclonus.
Speaker: And I think this is a source of significant confusion at the bedside.
Speaker: People see any abnormal movement and they call it myoclonus and they immediately assume the patient has no...
Speaker: no good prognosis.
Speaker: But the reality is that we're trying to understand these phenomenon a little bit better.
Speaker: And one of the things that was very instructive for me that I learned from the scientific statement was the new, let's call it terminology classification of how we can think about myoclonus in different ways and how that might have an implication from a therapeutic standpoint.
Speaker: Can you just comment on that briefly, Eddie?
Speaker: Yeah.
Speaker: Yeah.
Speaker: So I think if a patient is having myoclonus of any kind, right, that is because there is some dysfunction on the brain.
Speaker: So of course, if you're having that, you're more likely to have brain injury and patients with myoclonus tend to do worse than people with no myoclonus, if you take that as an isolated factor.
Speaker: But it's very important to understand what type of myoclonus we were talking about.
Speaker: And there's a lot of disagreements in the community about what's the right thing, particularly because of EEG.
Speaker: Because if you have EEG available, as some people may say, that the myoclonus doesn't matter so much, that the EEG gives you most of the information you need.
Speaker: So if you have a good background and you have myoclonus,
Speaker: you know, you shouldn't worry too much about that as a poor prognosis sign, but if you have a flat EEG or a birth suppressed EEG and then myoclonitis, that's a different story.
Speaker: And maybe the EEG is all that you need.
Speaker: But going back to the myoclonitis, I think it's very important to first separate is, is there an EEG correlate to the myoclonitis or not?
Speaker: Because if the myoclonitis is happening without any
Speaker: correlate, you will call that a more subcortical type of myoclonins and those tend to be associated with, again, brain injury, worse outcomes, but there are many people who have good outcomes and good recovery despite having myoclonins early on.
Speaker: Then you have myoclonins associated with EEG changes and that's when it becomes complicated and some of that has to do with the nomenclature that comes from epilepsy.
Speaker: and for myoclonic types of epilepsy and the juvenile myoclonic epilepsy is one of them.
Speaker: And I'm not gonna go into the epilepsy details here, but those are considered seizures by the book.
Speaker: And that's patients who have body jerks, they are associated with changes, spikes on the EEG.
Speaker: So if your EEG is doing something and you have a response to it, that's considered a seizure.
Speaker: But I think we need to look into that, into the context of other things that are happening with the patient.
Speaker: So when it comes to having this correlate on the EEG, you know, by definition, that would be a seizure.
Speaker: But it's different from a standard electrographic seizure where you have evolution, where you have very frequent spikes.
Speaker: And in the sense that those are the
Speaker: events that people are more inclined to treat with anti-seizure medications in a more aggressive fashion than those seizures.
Speaker: They are maloclonal with a jerk and a burst on the EEG or a spike on the EEG.
Speaker: Does that mean that we should not treat patients who have those seizures they are associated with the maloclonals when they're like infrequent?
Speaker: I think the jury is out on that and there has been a tendency not to treat as aggressively patients who have those
Speaker: myoclonic jerks associated with the spikes when they're infrequent, but when they become more frequent, people might decide to treat.
Speaker: I think some of that may also be in the context of patient care, because you may have ventilator desynchrony associated with the myoclonic jerks with or without the electrographic correlate.
Speaker: So that's when we often consider treating them, even if they're not seizures, if there's no EEG changes.
Speaker: And we tend to use anti-seizure medications that are more specific, more generally used for that indication.
Speaker: And levotiracetam, vaporic acid are some of them.
Speaker: We tend to avoid benzodiazepines if we can because it can really impair the exam as any other anti-seizure medication can, but that tends to be more concerning.
Speaker: But I think we still don't know what's the right approach to patients who have myoclonic disease.
Speaker: seizures that do not meet standard criteria for status and epilepticus.
Speaker: So the definitions of that are a little blurry.
Speaker: And I think there is interest now in the community and the epilepsy and the clinical neurophysiology community to try to define that a bit better so you can guide
Speaker: studies, right?
Speaker: Because we need to do studies to decide if this should do anything about it or not.
Speaker: So having better nomenclature, I think would be very important.
Speaker: So we can all agree while we are treating or not treating and make decisions based on that.
Speaker: I think my practice has been to treat and get all the prognostic information.
Speaker: to see if the patient has other signs of brain injury and then decide if we're gonna continue with aggressive care or not.
Speaker: I think the tricky part is when you decide not to treat
Speaker: And then you do all the tests and there's no other significant signs of brain injury.
Speaker: And then you're like, oh, should I have treated or not?
Speaker: And I think that's, again, very tricky and there's no right or wrong way to approach this.
Speaker: It's a very individualized to the patient, to the goals of care.
Speaker: And the clinician team has to discuss all those things with the families to decide.
Speaker: And I think that as we close the discussion, you hit on a very important topic, which I think is a big philosophical divide.
Speaker: A lot of non-neurological trained critical care clinicians have a little bit of a nihilist approach to a lot of these neuro patients.
Speaker: Yes, it's true that the vast majority of cardiac arrest survivors, especially those who don't obviously regain consciousness over time and have all these
Speaker: Signs on EEG and maybe myoclonus and seizures do poorly.
Speaker: But there is a subset of patients that if we are able to identify and treat aggressively, can have better outcomes.
Speaker: We want to avoid having a self-fulfilling prophecy.
Speaker: I didn't do anything at the beginning because I saw bad signs.
Speaker: And of course, the outcome is going to be bad.
Speaker: Right.
Speaker: And on the other hand, we can't be super aggressive forever on everybody because, yes, there's a lot of these patients in which that care is not going to make any difference.
Speaker: And it might cause harm in other ways to patients and families.
Speaker: So one important thing I wanted you to talk as we close, Eddie, is the idea of early triage versus neuroprognostication and maybe talk about what are common pitfalls that we should avoid in these patients.
Speaker: Yeah, and you should stay tuned because the American Heart's coming up with some early triage recommendations soon.
Speaker: And just to put another plug, the ILCOR group also had something a few months ago on brain injury as well, specifically on how to improve outcomes.
Speaker: So there's a scientific statement from ILCOR, which is like international group.
Speaker: So it's not just American Heart, but people from all over the world where they go into some specifics, talk about biomarkers and all those things.
Speaker: So going about early triage, I think the,
Speaker: It's very important not to be overconfident.
Speaker: I think that's something that we all learn, you know, and it's something that you, the more you see, the more careful you are.
Speaker: And I think that's true for many things in medicine, but particularly in neurological injury and recovery.
Speaker: So I think that is something that the more I do this, the more careful I am to be confident and more.
Speaker: I tried to get to look at that problem from different angles.
Speaker: So I think when we assess the patient early on for early triage and the patient has clear diffuse uber edema, herniation, subacronome hemorrhage, something devastating, I think that is important to identify early on.
Speaker: And also keep in mind all the other things are going on with the patient, right?
Speaker: Does this patient need ECPR?
Speaker: Are we going to do ECMO?
Speaker: on someone, how long should we code this patient if they keep having recurrent VTs when something like that happens.
Speaker: So I think that's another reason why trying to get information early can be helpful.
Speaker: My approach has been to be aggressive and try to give everybody the best shot as we get more information and then reassess.
Speaker: So beyond all the cardiovascular in general,
Speaker: critical care things, this early neurological assessment, I just try to keep that information available as is something devastating, as I mentioned, and focus on the acute care and brain monitoring.
Speaker: I think EEG has been something that, of course, I'm biased as a EEG guy, but I found that very helpful, particularly for this early understanding of what direction the care is going.
Speaker: I think one of the pitfalls we have
Speaker: is when we discuss with families, neurology often tends to have that, let's wait three days and I'll talk to you.
Speaker: And for now, just wait.
Speaker: And I think that can be very tough on the families because it just creates a lot of anxiety and it's built up about what's going to happen in three days.
Speaker: And sometimes people...
Speaker: um attach themselves to a test oh the mri is going to happen or let's wait for the mri results we've seen already signs that things are not going the right direction so when it comes to early triage is also very important i think to have continuous communication about how things are progressing as we start to get more information again not to give a self-fulfilling prophecy and decide too early the things you're not going to go well but at least communicate about what's happening
Speaker: to the patient so it doesn't come as a surprise um when things are not going in the right direction for many days to then tell the family that things are not looking good so i think this report and building this communication with families as the multidisciplinary team that we often have when we're taking care of these patients is really important
Speaker: Again, I'm just mainly focused on the neuro side of things today.
Speaker: But when it comes to triage, there's many other factors related to PCI, needs, CPR, and other things that we won't go into much detail because we're going to run out of time.
Speaker: Absolutely.
Speaker: And I think at the end, it's obviously a composite picture, right?
Speaker: But this is a very important aspect and the focus of our discussion today.
Speaker: Well, I think that this has been a wonderful discussion.
Speaker: Eddie, you and the whole AHA NCS group of authors that worked on the scientific statement obviously tackled a very relevant problem for our clinical practice that yet has a lot of unanswered questions, right?
Speaker: But we have to try to provide the best care possible today.
Speaker: And as we learn new things, that care might change.
Speaker: But I think that some of the lessons that I take from our discussion today include to pay attention to every detail that can impact brain oxygenation and perfusion.
Speaker: to think about is this individual patient, would this individual patient need aggressive or other types of brain monitoring?
Speaker: Can I push the MAP up a little bit?
Speaker: Will that help?
Speaker: To really think about the role of EEG, right?
Speaker: If we're not in a neuro ICU that does continuous EEG in everybody, how can I leverage what I have available to
Speaker: in the form of intermittent EEGs with a repeat test or leverage and limited montage EEGs, which I think are much more common today outside of the specialized neuroICUs.
Speaker: And finally, to really think about it's not...
Speaker: yes or no for every for all patients it's some patients need aggressive treatment for their seizures others may not may not have that need and trying to figure that out as a multidisciplinary team i think is ultimately what what what provides the best care for patients and i think it comes back to an old an old truth in medicine that sometimes asking the right questions is the most important thing at the bedside
Speaker: Right.
Speaker: So thank you so much for that discussion.
Speaker: We like to close the podcast, Eddie, with a couple of questions that are unrelated to the clinical topic and to tap into the wisdom of our guest.
Speaker: Would that be OK?
Speaker: Of course.
Speaker: Absolutely.
Speaker: So my first question relates to books.
Speaker: Are there any books or books that have influenced you significantly or books that you have gifted often to other people?
Speaker: That's a good question.
Speaker: You know, right now I'm reading As Real As It Gets is a book about the AIDS start in San Francisco, you know, being in San Francisco, I thought I would need to read more about it.
Speaker: So that has been very interesting reading.
Speaker: In terms of book they have given most out, there's a reason I'm really into biographies.
Speaker: I find fascinating to go back, you know, 300 years, 100 years, 50 years.
Speaker: to see how careers of important people and how that shaped them and how those little things can have big impact.
Speaker: But a recent one, which is in neurology, is the similar Fisher biography that Dr. Kaplan wrote not too long ago.
Speaker: So that's the one I've given to a few folks who have
Speaker: beyond the tree, you know, not necessarily trained by Miller Fisher directly, but trained by people who were trained by them.
Speaker: So third, fourth generation, sometimes neurologists from from that lineage and it was super interesting to learn more about his life and how that shaped who he became.
Speaker: Perfect.
Speaker: And we'll definitely put links to both of these books in the show notes.
Speaker: The second question is, could you share something you changed your mind about over the last couple of years?
Speaker: The last couple of years?
Speaker: I mean, in terms of the last couple of years, I think that is...
Speaker: just a reminder and that's like changed my mind of how important it is to focus on the people around you if they're near or far away just because things can change very quickly and that's something that I've seen in my family with COVID you know people are my age and dad passed away and
Speaker: in a matter of like a week.
Speaker: Um, so I think that was just something that we is a good reminder, um, of how important we need to be and staying in touch with people very frequently, um, and appreciating that and take advantage of long car rides to call people up and see how they're doing.
Speaker: I think that has been something that I changed, um, how I handled that and how I'm much more, have much more intent on doing that than I used to.
Speaker: And I think it's a reminder that good things in life usually take a long time.
Speaker: Bad things happen in an instant, right?
Speaker: And I think it's a very well learned lesson and something very important for all of us.
Speaker: So thanks for sharing that.
Speaker: And the last question, Eddie, is what would you want every intensivist who's listening today to know?
Speaker: It could be a quote of fact, but later unrelated to clinical practice.
Speaker: Yeah, I think to me, one thing that I didn't appreciate as much as a trainee, but when I became an ICU fellow in particular, I realized on how little time we spend, even as intensive it's at the bedside and how it's important to be very in close interactions with our nursing team.
Speaker: I think, and
Speaker: And having a nurse team, nurse led rounds is something that I've witnessed and to me has been very important and something that I think it just serves as a reminder for the clinicians in the team who are not on the bedside all day on how it's important to stay in touch.
Speaker: with your nurses frequently throughout the day and really bringing them in on all important decisions for the patients.
Speaker: I think that is something that to me is very important and I try to pass on to everybody I train with
Speaker: Perfect.
Speaker: And I think this is a good place to stop.
Speaker: I really appreciate you taking the time, Eddie, to share your expertise.
Speaker: Hope to have you back to talk about other neurocritical care topics.
Speaker: As you mentioned, interesting studies and interesting guidelines coming down the pipeline.
Speaker: So again, always a pleasure to learn with you and from you.
Speaker: And thank you so much for sharing your expertise with our audience.
Speaker: Thank you again for the invitation.
Speaker: I really enjoyed the conversation.
Speaker: And hopefully as we come back, we're going to be talking more about precision neurocritical care and how we're going to be moving to provide the right care for the right patient, just like we're doing in other areas of medicine.
Speaker: So I think that that's what we are hoping to do for a cardiac arrest.
Speaker: And I think it's just a matter of time.
Speaker: And that's what we're working on.
Speaker: Thanks, Sergio.
Speaker: Thank you for listening to Critical Matters, a sound podcast.
Speaker: Make sure to subscribe to Critical Matters on Apple or Google Podcasts and share with your network.
Speaker: Sound's transforming the way critical care is provided in hospitals across the country.
Speaker: To learn more, visit www.soundphysicians.com.
