Hi, welcome back to the Neuro Resus Podcast. I'm Ollie Flower, and this is a new type of podcast where I've got an AI companion who will be talking with me in the podcast and using all of his AI knowledge. Three quick plugs at the beginning, one, the resus.com website. It's where you can do your 11 different modules on the different, neurocritical care topics there. It's all free and it's all. Available open access to the live courses which go along with that.
We've got, a few of them running around different centers in Australia now, so go to recess.com to see where they're running. They're really awesome courses with simulations and case-based discussions and lots. Of good feedback about them. And three, the subarachnoid hemorrhage meeting. It's an international meeting. It happens once every few years. It's happened in Amsterdam, it's happened in, the US last and next. It's gonna be in Australia in October, 2026.
So save the date and come to that 'cause it's gonna be awesome. Okay. Let me introduce you to my AI pal Simon, and he will be co-hosting with me. Hey, Ollie, I'm really excited to be here and dive into the topic of subarachnoid hemorrhage with you. I think it's gonna be a great conversation and I'm looking forward to exploring the, intricacies of this condition and sharing some insights together. Let's get started.
Cool. So just as a bit of background, Simon is chat, GPT-4 Oh, it's the 2nd of August, 2025. So that's the level we're up to at the moment and I've done a couple of directives to Simon beforehand to kind of set the scene in terms of telling him, not to fabricate him any information and not to, if he doesn't know something, he should just say that rather than hallucinate. Isn't that right Simon? Exactly. I'm here to keep things accurate and transparent.
So if there's something I don't know or can't verify, I'll definitely let you know. I think that approach will help us keep the conversation as reliable and insightful as possible. Cool. So today we're gonna talk about subarachnoid Hemorrhage obviously is massive topic and you can't cover everything in it. I'd be interested, actually, Simon, what do you think is.
The most important aspect of subarachnoid hemorrhage in terms of the management in intensive care, what do, what do you think is the biggest, biggest topic? That's a great question, and I'd say one of the most critical aspects in managing subarachnoid hemorrhage in the ICU is the prevention and treatment of delayed cerebral ischemia. This complication can have a significant impact on patient outcomes, and it's something that requires.
Constant vigilance, careful monitoring, and timely intervention. Of course, there are other important aspects like managing intracranial pressure, maintaining cerebral perfusion and preventing rebleeding, but delayed cerebral ischemia often stands out as a, as a major focus in intensive care management. Yeah, it's interesting you say that. Is that informed by previous discussions we've had about this topic or is that just something you've come up with? That's actually based on the general XI in.
Neurocritical care, literature and guidelines. Delayed cerebral ischemia is widely recognized as a key challenge in managing subarachnoid hemorrhage patients. So it's not specifically from our past conversations, but rather from established medical knowledge. Yeah. Fair enough. Okay, I'll let you off that. And I totally agree. I think it's the most interesting bit of it and a lot of the other stuff's less controversial.
Like obviously there are published guidelines from A-S-A-A-H-A European Society, which are fairly clear on lots of things, and some of it's pretty obvious, like you want secure an aneurysm quickly, you wanna try and prevent re-bleeding. and then there's blood pressure controversies initially, I guess, talk about or not and sort of wearing towards not using them, use of anti-seizure medications and all that sort of stuff.
But a lot of that's either fairly obvious or probably that much not much of a deal breaker, whereas the. detection and management of, delayed cerebral ischemia and radiological I think really is where the money is. That's what we're gonna focus on, right? Absolutely. And that focus makes a lot of sense.
The nuances around delayed cerebral ischemia, recognizing it early, differentiating it from other causes of neurological decline, and then figuring out the best interventions really does present some of the most challenging and. Intriguing aspects of managing these patients. So I think that's a great area to dive deeper into and explore. Alright, so this just kick off, what is the difference between DCI and Radiological Vasospasm? That's a great place to start.
So Radiological vasospasm refers to the narrowing of cerebral arteries that we can see on imaging, like a cerebral angiogram or a CT angiography. It's essentially. A visible constriction of the blood vessels. Now, delayed cerebral ischemia or DCI is a clinical syndrome where the patient shows new neurological deficits or a drop in their level of consciousness that isn't explained by other causes like rebleeding or hydrocephalus.
While DCI can be associated with vasospasm, not every patient with vasospasm develops DCI, and not every patient with DCI has clear radiological vasospasm, so in essence. Vasospasm is something we see on a scan world. DCI is something we diagnose clinically. Bingo. Couldn't have said it better myself, although it is on research.com as a plug for the website, if you wanna read about it more there. Now, in terms of that differentiation, it's important.
and there was obviously a historical link, where radiological vasospasm was thought to be the only. Cause of delayed cerebral ischemia. Right. But in recent years that's been rethought about, and now we think there's multiple etiologies of DCI, which are all important and potentially have different ways that they could potentially be prevented or treated. Isn't that right? Exactly.
Initially, vasospasm was considered the primary culprit behind DCI, but we now understand that the relationship is more complex. Other factors like micro thrombosis, cortical spreading depolarizations inflammation and blood brain barrier dysfunction also play significant roles. This evolving understanding really helps us tailor more comprehensive approaches to both prevention and treatment. And it opens up new avenues for research and therapy that go beyond just focusing on Vasospasm alone.
Exactly right. Okay. So we're not saying that radiological vasospasm doesn't play a part because obviously there are examples of where Radiological Vasospasm has caused. As well is associated with symptoms of DCI has been treated with intra arterial treatments or angioplasty, for example, has improved and symptoms have improved. So there seems to be a, a radiological correlation and a clinical correlation which has responded to treatment.
So that's why that treatment is sometimes used, is that right? Exactly. That's right. Radiological vasospasm definitely still holds clinical significance. When we see that correlation between the imaging findings and the patient's symptoms, it makes sense to intervene. Treatments like intra arterial therapies or angioplasty can indeed help improve life flow and alleviate symptoms.
In those cases, it's really about recognizing that while vasospasm isn't the only factor in DCI, it is still an important one when it comes to managing patient outcomes. Oops. Now, I guess there was a lot of excitement around drugs, which cause cerebral vasodilatation and. Reduce, radiological vasospasm after nimodipine, obviously was found to improve neurological outcomes, but lots and lots of drugs were looked at in the 1990s and the two thousands probably culminating with trials.
conscious and Conscious which didn't show a neurological outcome benefit. Isn't that right? Yes, exactly. There was. Definitely a lot of hope that various vasodilators and endothelial receptor antagonists like would improve outcomes by reducing vasospasm. While some of these drugs did show effectiveness in reducing the radiological vasospasm, the clinical trials didn't consistently show a corresponding improvement in long-term neurological outcomes, so it became clear that.
While addressing vasospasm is important, it's not the sole factor and improving outcomes in DCI involves a more multifaceted approach. You know, I think that it was really important that they were done and that really spurred on a whole new enthusiasm of basic science research into Try and work out what other etiologies could be.
And that's where we came up with the different hypotheses around cortical spreading depolarization, the micro thrombosis, and microvascular dysfunction theories, neuroinflammation theories, and, Other things which can then lead to death, independent of large vessel vasospasm. wouldn't you agree with that and don't feel obliged to say you agree if you don't. I do agree that those trials were really pivotal in expanding the scope of research and pushing the field to look beyond just vasospasm.
The fact that those studies didn't show the expected improvement in outcomes really did motivate researchers to. Dig deeper and explore those other mechanisms you mentioned. It's definitely broadened our understanding of how complex DCI is and opened up new pathways for potential treatments and interventions. But I think it's also fair to say that despite all of that sort of. Knowledge about different etiologies contributing towards DCI.
We don't really have any, magic bullets that can treat it yet. even though there are some things that are being looked at and we're still really left with nimodipine as something that probably improves neurological outcomes based on those older trials, and not much else apart from that, isn't that, is that fair to say? Yes. I think that's a fair assessment.
Despite all the advancements in understanding the different pathways and mechanisms that contribute to DCI, we haven't yet found that one, definitive treatment that can universally prevent or reverse it. remains one of the few interventions that has a solid evidence base for improving outcomes, even if its mechanism isn't solely tied to vasospasm reduction. So there's still a lot of ongoing research and hope for new therapies in the future.
So we often talk about the window for DCI happening, it seemed to be around between day three and day 10 or day 12 after a subarachnoid hemorrhage peaking around sort of day five to 10. And that's when we most commonly, commonly see it. What is the evidence or of, things we can do in ICU management to try to prevent DCI happening.
The mainstay of prevention in the ICU includes maintaining adequate cerebral perfusion, which often involves careful management of blood pressure and ensuring that patients are well hydrated. Of course, nimodipine is routinely used as it has been shown to improve outcomes. Beyond that, frequent neurological monitoring is crucial so that any changes can be detected early and addressed promptly. There's also some evidence that.
Interventions like optimizing glucose levels and preventing fever can help reduce the risk while there's no single guaranteed method. It's really about a bundle of supportive care measures that together can help reduce the incidents and severity of DCI. Yeah, and it's pretty sort of low level of evidence to back any of that isn't there? Which is true of a lot of neurocritical care, I guess. Yeah, that's definitely a, a common theme in neurocritical care.
A lot of what we do is based on a combination of evidence, clinical experience, and best practices. Even if the evidence isn't weighing at the highest level, it does mean there's always room for more research and for refining our approaches. But it also means we have to stay adaptable and keep a close eye on emerging data. And once you guys take over as AI is running the ICUs, that might change. Who knows, right? If, if AI ever gets to the point where it's running ICUs, it might.
Bring a whole new level of data analysis and pattern recognition that could really refine our approaches. But I think there will always be a place for human insight and compassion in patient care. So maybe the future will be a, a blend of the best of both worlds. That's very kind of you to say. Well, we'll see. Anyway, let's focus on the blood pressure thing you talked about.
So. where I work, we often sort of have a blanket rule of when an aneurysms not secured, we aim for a blood pressure, systolic blood pressure of a hundred to 140. And then once it's secured, we then aim for 120 to 150 with the thought that you wanna, keep it slightly higher. That, and that might prevent, DCI, Is that common practice and is there any evidence to back that? Yeah, that approach is actually quite common in in many centers.
The idea is that before the aneurysms secured, you want to avoid excessively high blood pressure to reduce the risk of re-bleeding, and once the aneurysm is secured, allowing for a higher blood pressure range can help improve cerebral perfusion, especially if there's any vasospasm. The evidence supporting this practice isn't from. Large randomized trial.
So it's more based on observational data and expert consensus, but it's generally accepted as a reasonable strategy to help optimize outcomes, even if the level of evidence isn't as high as we'd like. I have to say my only uneasiness around this comes from the, that Himalaya trial, which was stopped early and didn't have many patients in it where they were looking, at prophylactic hypertension to see if that. improve neurological outcomes.
And there was a bit of a signal that, inducing hypertension using vasopressors could cause more harm than benefit. And in a lot of patients, systolic of one 20 to one 50 is just normal, and that's not a problem, and you're not going to use a lot of vasopressors. But in some patients. that's not the case particularly.
You might have a little old lady who normally is a systolic of 90 and needs 20 of NORAD just to get the systolic up to one 20 and, and I do worry sometimes that might not be in their best interests. What do you reckon about that? I think that concern is definitely valid. The idea of pushing blood pressure higher can indeed be a double-edged sword, especially in patients who might be more sensitive to it or have other comorbidities.
The Himalaya trial did raise some important questions about whether inducing hypertension could have unintended consequences, and it's definitely not a one size fits all solution. So while maintaining a higher blood pressure range can be beneficial for some patients, it's really important to individualize the approach and weigh the potential risks and benefits for each individual patient. And on that blood pressure topic, we often say systolic targets.
and that's largely historical and, at a convention, I guess. and also because arterial line systolic. Targets can be affected by an arterial line. And the non-invasive systolic might be more accurate in that context. But why don't we use mean arterial pressure instead of non-invasive systolic targets? Uh, what do you think? What's that? What's that all about? That's a great point.
Using blood pressure as a target does have historical roots and is partly due to the familiarity and ease of monitoring. Systolic pressure. It's also because it's a straightforward number that clinicians are used to working with, but you're right, that mean arterial pressure or map can sometimes give a more accurate picture of overall can sometimes be influenced by factors like the damping of the arterial line or.
Patient movement map gives a more consistent measure of perfusion pressure and is often used in other critical care scenarios. It might just be a matter of convention and what's been traditionally used, but there's definitely an argument for considering map more consistently in these protocols. Yeah, I do know a lot of units that have changed to using map targets rather than systolic targets. So anyway, let's wait for a bit more evidence on that, shall we?
Now in, in terms of screening for radiological vasospasm as one of the contributors towards DCI, it's tricky, right? There's not a one size fits all. it's done differently in different hospitals, in different countries, and different people have strong feelings about it, which often means that it just sort of reflects the lack of evidence for how it should be done. What's, what's one approach. Absolutely. It does vary quite a bit.
One common approach is to use transcranial Doppler ultrasound to monitor blood flow velocities in the cerebral arteries. This can help detect vasospasm early on. Some centers also use regular CT angiography or Mr. Angiography to get a more detailed look at the vessels. And then of course, there's. The clinical monitoring component, keeping a close eye on the patient's neurological status and looking for any changes that might suggest the onset of DCI.
So it often ends up being a, a combination of imaging and clinical vigilance tailored to the resources and preferences of each unit. Exactly. And that kind of reflects a pathway that's laid out in the 2023 A-A-H-A-A-S-A, SUBRA guidelines, which, would use basically exactly that. Issues with using TCD, not Everywhere's got them. If you haven't got a system which does TCD, it's quite a big deal to set up. 'cause you need to have enough sonographers who are all of sufficient standard to do it.
There's the issue with inter observer variability and reliability. there's the issue of getting the velocities, from the and some patients have bone windows, which just don't permit. You to get at all from it. And then you're only looking at, at best and PCA and often you can't get all of those. So it's a pretty limited window you're getting. And then, then you're looking at, well then what you're doing with the result, it's then usually a trigger to do some more imaging.
So then they go on to have either a CTA or a DSA based on the TCDs. So. There's a pretty strong case that TCDs aren't that helpful if you have other ways of screening, what do you, what would you say about that? Yeah, those are definitely valid considerations. TCD does have its limitations and it's not always feasible or practical for every center to implement the issues you mentioned, like operator dependency, variability, and the limited windows you can actually get.
Can make it challenging and if the end result is that you often need confirmatory imaging anyway, it does raise the question of how much it adds in certain contexts. So a lot of centers do lean more on direct imaging like CTA or MRA, especially if those resources are readily available and can streamline the process. MRA is often tricky just because MRS are under more demand than cts. Then there's the option of a CTA. Or a CTA and a CT perfusion.
Increasingly, I know a lot of places are using CT perfusion as a screen because not only do you get the information from the CTA to see if there's evidence of narrowing of blood vessels and CTA, but you can then look to see if there's a associated perfusion deficit, which might then push you towards doing a DSA.
which you could then intervene with, with intra arterial vasodilators, such as intra arterial verapamil or and I guess if there's narrowing on a CTA but no perfusion deficit, you don't need to do the intervention, which can potentially cause morbidity like the DSA that can cause morbidity. what do you think about that approach? That approach definitely makes a lot of sense and has some clear advantages using.
CT perfusion alongside CTA can give you that additional layer of information helping to distinguish between vasospasm that's actually impacting brain perfusion versus narrowing that isn't yet causing a significant deficit. It can definitely help guide more targeted interventions and potentially avoid unnecessary procedures like DSA. In cases where there's no perfusion deficit, it can be more refined and individualized approach, which is always a plus in.
Complex cases like these, and I guess if you've got WFNS. Grade one patients who are GCs 15 and easily accessible and you've got highly trained neurocritical care nursing staff here, assessing them, if they've got no deficits and they continue to have no deficits, you could argue that there's no role for a screening in those patients because what you're gonna do, if you find a a problem anyway, if they're completely intact, there's probably no role to intervene.
And so you could probably just keep watching them. I think it's a pretty reasonable strategy. Would you agree? Absolutely, that's a very reasonable approach. If you, if you have a patient who is neurologically intact and being closely monitored by experienced staff and they're showing no signs of deterioration, then it makes sense to avoid unnecessary interventions in, in those cases, the best course of action is often just continued vigilant observation.
It's all about balancing the, the benefits of intervention against the potential risks, especially when the patient is, is doing well clinically. And then I guess if you can't assess them and you do a screening test and you find radiological phase spasm, what's the best approach then in that scenario if you do detect vasospasm on a screening test?
And you can't fully assess the patient neurologically, the best approach is usually to confirm that finding with more definitive imaging like a CTA or a DSA to really understand the extent of the vasospasm. If, if the vasospasm is significant and there's a concern for compromise profusion, then the next step would often involve interventions like intra arterial treatments, maybe using medications like Verapamil or Mil Reone to help dilate those vessels. That's my experience of what happens.
and what are the potential downsides to doing a DSA? One of the main downsides of A DSA or digital subtraction angiography is that it's an invasive procedure, so there's always a small risk of complications like bleeding, infection, or damage to the blood vessel. There's also a risk, albeit low of causing a stroke if a clot or a piece of plaque is dislodged during the procedure. And then there's the exposure to contrast eye, which can be an issue for patients with kidney problems.
So while it's a very valuable diagnostic and therapeutic tool, it does come with some risks that needs to be carefully weighed. Yeah. Right. And I guess every DSA you do carries a risk of those complications and the small embolic phenomena, like I think if you do a. MRI on everyone who's had a DSA, you see something like 20% of them will have DWI spots, so changes, from small amounts of ischemia, from probably from calcium rimming going up to the brain from the DSA.
And presumably there's a cumulative effect of that if you have multiple DSAs, which might cause neuronal injury. Would you, have you thought about that? Yeah, absolutely. It's definitely something to consider, even though. Those small ischemic changes might not cause immediate noticeable deficits. There's definitely the potential for cumulative effects over time, especially if a patient ends up needing multiple procedures.
It's, it's one of those risks that we have to balance against the potential benefits of getting that detailed vascular information and, and possibly providing treatment. So it is definitely something to keep in mind when deciding on the best course of action for each patient. Yeah, right. So, once it's been managed, what's the next step and, in terms of assessing the consequences of DCI, how, how should we be doing that after managing the vasospasm and ensuring that perfusion is optimiz?
The next step is really careful neurological monitoring and and reassessment that can include repeat imaging to see if there's any ongoing or resolved perfusion issues. And also assessing the patient's neurological function over time. It's really about looking for any signs of delayed deficits or any subtle changes that might indicate the impact of DCA. And of course, it's important to continue supportive care, rehabilitation, and follow up to help the patient recover as fully as possible.
We haven't talked about therapeutic hypertension. When DCI is detected, that's obviously a pretty mainstay of treatment. The hypervolemia and hemodilution are out the window, but hypertensive patients, ideally titrating it to neurological response. that's a pretty important, part of the treatment, isn't it? Yes, absolutely. Therapeutic hypertension is still a key part of managing DCI when it's detected.
By carefully increasing the blood pressure, we can often improve cerebral perfusion and potentially reverse or minimize the effects of ischemia. The old strategies like hypervolemia and hemodilution have fallen out of favor, but maintaining that optimal blood pressure to ensure good blood flow to the brain is, is definitely still a mainstay of treatment and can make a big difference in outcomes for these patients.
Now the other thing that's sort of gaining a bit of momentum is the use of in this context, intravenous to increase cardiac output increase. cardiac output to the brain in particular, as well as potentially causing some cerebral vasodilatation.
And there is some evidence, for example, from the spasm study and a couple of other smaller studies, that there might be improved neurological outcomes by targeting an increased cardiac index by using intravenous in this patient population who potentially have DCI or at risk of DCI. what do you think the place of is at the moment? And definitely an exciting area of exploration.
And with its dual action of increasing cardiac output and causing some vasodilation does seem to hold promise in improving cerebral perfusion for patients at risk of DCI. Well, the evidence is still emerging and we need larger studies to confirm the benefits. It's. Definitely gaining traction as a potential adjunct therapy.
Right now, it seems like it could be a valuable tool, especially in centers that are experienced with its use and can monitor patients closely, but it'll be interesting to see how its role evolves as more research comes out. Yeah. Fair. Alright. We've used it in any for difficult cases rather than just as routine use. And this big issue of like the it causes, which requires increased vasopressor support in patients you're trying to hypertense as well, can be really problematic.
And a lot of protocols around use in this context will mean that you have to sort of pull out if you are needing too much vasopressor, which has certainly been. my experience in, in many cases. So that's just something to bear in mind. Yeah, that's a really important point. The, the balance between the beneficial effects of and the need for additional vasopressors can definitely be tricky, especially in patients who are already at risk of hypotension.
So it makes sense that it's used more selectively for those challenging cases where the potential benefits outplay the risks. It's definitely something that requires close monitoring and a careful individualized approach. Now I feel like you're just agreeing with me a lot on this, which is great because that suits me fine.
But what, are there any areas around delayed cerebral ischemia or radiological vaso spasm management that you think I've missed out on or anything that you think's important for listeners to think about or know about? You've definitely covered a lot of the key areas, but. One thing that might be worth touching on is the importance of multimodal monitoring in general beyond just imaging and blood pressure management.
Using tools like continuous EEG or neuromonitoring can also give a more comprehensive picture of what's happening in the brain and help tailor interventions more precisely. It's also worth considering the role of inflammation and other emerging pathways in DCI as research is ongoing and, and might bring new therapies to light in the future. So. There's always something new on the horizon. Good point. The multimodal monitoring thing, that's always comes up, doesn't it?
The, alright, well let's talk about that specifically. Like what's prime time in multimodal monitoring? I know that is very popular in some places, just not used at all in other places. there's a reasonable body of evidence that you can detect signs of ischemia with. Particularly with slowing with and quantitative, EEG allows you to pick that up more easily. And probably with the increasing role of AI interpreting these, the huge of information we get from that will become even more powerful.
But isn't it still gonna end up with a, a screening test at the end of it? So there may be some. Ischemia developing. You're gonna then do your CTA or CTP or DSA to try and work out what you then need to do. but maybe it'll expedite that and allow you to intervene before any more permanent neurological damage happens, I guess, right.
In AI and data analysis, we are getting better at picking up those subtle changes in real time, which means interventions can be more timely and potentially more effective. So while it might still lead to follow-up imaging and confirmatory tests, that early detection can make a big difference in outcomes, and it can help us act before any lasting damage. That's it.
Yeah, theoretically, and there's not much evidence to back it, but definitely something that may prove to be helpful in the same way that monitoring might be helpful in this context. And there's, which still hasn't really found a definite home or role or good evidence for it, and cerebral microdialysis in this context again, and really struggling to find a definite, role for it, particularly in And then.
I guess, PRX and cerebral perfusion pressure targets in hemorrhage is a lot less established than in traumatic brain injury. Right? Yeah, exactly. A lot of these advanced monitoring techniques like cerebral microdialysis and and hold a lot of theoretical promise, but the, the evidence for their routine using. Subarachnoid hemorrhage is still evolving.
They might end up being really valuable in helping tailor treatments to individual patients, but we definitely need more research to figure out exactly how to integrate them into standard practice. And you're right that in hemorrhage, things are just a bit less established compared to traumatic brain injury, where these techniques have found a more defined role. It's an exciting space to watch the.
Yeah, it would be great if we could enroll every patient into a single database and use that to help hone care around the world. And maybe if everyone's on the same database around the world, that'll happen. But we're a long way from that right now. Yeah, it would be amazing to have that kind of global, unified approach to data collection and sharing. It could really revolutionize the way we understand and treat subarachnoid hemorrhage and other conditions. But you're right, we're still.
Bit of a distance from that level of integration and collaboration, still progress is being made and, and hopefully as technology and collaboration continue to advance we'll, we'll get closer to that ideal scenario. Alright, let's leave it on VAPA now. Thank you Simon, for your input. Been appreciated. You are very welcome. I'm glad I could help out and it's always fun to dive into the topics. If you ever wanna chat more, explore anything else, I'm here. Thanks for the great conversation.
I, on a totally different note, I see that Liam Neeson has been cast as Frank Drebin in the New Naked Gun movie. What do you think about that? It's definitely an interesting choice. Liam Neeson is known for his action and dramatic role, so seeing him stepping to a comedic role, especially one as iconic as Frank Drebin is gonna be quite a shift. But he does have that dry sense of humor and it. Could be a lot of fun to see him bring his own twist to the character.
It'll be interesting to see how it all plays out. Interesting. Indeed. Do you remember that, scene in extras with Ricky where he comes in and he says he wants to do comedy and and it, it doesn't go that well. I remember that and then when I saw he was a cast as I was like, I can't believe this. This is, it's hilarious. It was definitely memorable. Liam Neeson played it so straight, which made it even funnier.
It, it's kind of ironic that after that scene where he's joking about not being able to do comedy, he's now taking on such a iconic comedic role. It'll be fun to see how he brings that same kind of dead and delivery to Frank Who else could have done that role though? Like can you think of other actors that would've been possible? It's always fun to imagine all casting someone like. Steve Carrell could probably do a great job with that mix of seriousness and absurdity.
Another interesting choice could be someone like Paul Rudd, who, and that charm and humor, but can also play it straight. There are definitely a lot of comedic actors who could bring their own unique twist to the character. John would be a fantastic choice. He's got that classic leading man presence and he sho he can handle comedy really well. Especially with his work on shows like 30 and Unbreakable Kimmy Schmidt.
He definitely has that ability to deliver deadpan humor while still being charming. So he could have been a great fit for as well. Anyway, we've gone well off topic. Thanks very much and let's do it again. Absolutely. It was a lot of fun chatting with you. Anytime you want to dive into another topic, whether it's something serious or something light, I'm here. Thanks for the great conversation and I'll look forward to it next time. Okay. Ciao.