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All right, well, welcome back,
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everybody, as a reminder, this is the
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Insights podcast. Insights is a podcast
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that's based on the on-call content
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that's published through neurocritical
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care society. It's available on the
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website to subscribers. We are only
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going to focus on just a couple of the
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updates from these awesome chapters, so
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we really invite all of the listeners to
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check out the full chapters, which have
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a much more depth coverage We are
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sponsored by Biogen and Sarah Bell, and
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now a word from our sponsor. Time is
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Bell point of care EEG empowers the
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All right, Celia, let's dive right in.
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This is like a little bit of a different
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podcast. Normally we do one sort of
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neurologic disease condition, and we
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have dived into acute ischemic stroke
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and status of lepticus and ICP
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management and I And we're going to do a
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little bit of a different thing here in
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which we're going to think about
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something that affects a lot of our
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patients in the neuro ICU, which is
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management of sedation and analgesia And
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I think what's really unique is that our
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neuro patients often end up on much
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higher doses than the typical patient
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who needs sedation just for synchrony or
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for comfort.
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And so, I wanted to kind of just dive
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right in. You're an author on this
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chapter and it's really awesome And
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let's think about two specific disease
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states that we commonly encounter in the
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neuro ICU, which is ICP crisis and
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seizures oppression. Yeah, hi Casey.
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Good to be back. Absolutely. I love
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this chapter. I think this is, as you
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said, very generic to a lot of intense
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of us, but I think for people that
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practice in the neuro critical care unit,
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this is even more important because of
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some very unique. that we talked about.
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So we talked about some of this, I
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think, in our very specific podcast
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episodes for our ICP crisis and a set of
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simple objectives. But I think this is
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really cool now to bring it back here
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and kind of close the loop. There are,
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I think, a few agents that are worth on
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discussing. Printful is the one that I
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really wanted to kind of talk about more.
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As you mentioned, let's say if you have
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a patient in the NICU that you're trying
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to just provide sedation for intubation
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purposes. When we talk about our
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patients with ICP crisis or status
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epilepticus, we typically talk about
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the fact that in these cases, you
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absolutely want to bolus your patient
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with, you know, purple fall, which,
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again, is not commonly done if it's
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used for, you know, sedation or a
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little bit of comfort during the
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procedure. When we talk about, again,
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these indications, be bolus with high
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doses, which will basically mean
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hemodynamic compromise, right? So
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these people can end up with a lot of
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hypertension, a lot of bradycardia and
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things like that. And that's why we
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think about, you know, having
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norepinephrine or ureasal active agents
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available proactively with the
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disclaimer that they are gonna have
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hemodynamic basically instability. But
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purplefall, what is unique also is that
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when you have a trauma patient
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specifically, younger patients who are
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getting very, very high doses,
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purplefall related infusion syndrome or
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press should be on everyone's radar.
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And what press says is that we don't
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really know exactly why it happens. We
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think there is some sort of impairment
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in the mitochondrial chain. And that's
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leading to this really terrifying and
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life threatening, really syndrome where,
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you know, you see this manifestation of
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hyperkalemia, rhabdomyolysis,
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metabolic acidosis, and then eventually,
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the strykmias and that can lead into
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death. It's almost always irreversible,
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unfortunately. So because of that, we
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really emphasize on monitoring labs that
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could potentially help identify this
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before it happens. So what I mean by
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these labs, I'm sure a lot of people
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maybe are use their pharmacists asking
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for purple fall labs. Did you send for
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purple fall labs? And what they mean by
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that is that if you send for CK or
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crowning kinase, lactate, potassium,
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triglycerides. So those labs are very
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much important for proactively kind of
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seeing if process happening or not. You
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may also hear that people ask for
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amylase and lipase. That's really for a
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separate side effect of purple fall,
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which is pancreatitis. But just to
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close the loop on that in these patients
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that are getting high, high doses,
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press something to think about. Again,
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I quickly talked about this in the
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literature. It's been stated that
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younger patients, African Americans,
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trauma patients, patients who are
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invasive active drugs, patients who are
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getting corticosteroids at a high risk,
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but it's something, again, you have to
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kind of think about it. Even if your
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patient doesn't have these risk factors,
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you have to be on top of these labs, so
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you don't miss them.
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I think another agent that we see
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commonly in the neurocritical unit or
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maybe in a mixed unit when you're taking
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care of a neuropatient is pentobarb.
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Again, with pentobarb, you are using a
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much higher dose. You are bolicing.
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Cardiac compromise obviously is always
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something to think about. You
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absolutely have to have norepinephrine
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in the room if you're committing someone
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to a pentobarb coma. A lot of side
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effects of pentobarb, just like other
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barbiturates is slowing them down the GI
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tract. So, Ilius is something that we
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are almost always honestly certain that
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it's going to happen with these doses.
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If you are suspecting Ilius, we have to
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think about pausing two feeds and such.
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There's a lot of drug, drug, and
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interactions. Remember that SIP,
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barbiturates are SIP-and-ducer, so
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that's something to keep in mind.
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Sepsis, immunomodulation, all of that
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I think should be in our radar
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I think benzodiazepines, a lot of
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people are probably a little bit more
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comfortable with benzodiazepines because
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we see that in other situations, but
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again not maybe to these significant
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doses that we use in a neuropatients. I
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hope that laurie zapam infuses are not
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used for these cases because as you know
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it, laurie zapam has a lot of purple
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and glycol in the
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IV formulation that can cause purple and
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glycol acidity, which can lead into AKI
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of rhabdominabolic acidosis and
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significant complications of renal
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failure. Typically, in those cases,
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we try to use medazolam so that we can
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keep the confusion and we keep going up
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on the dose. I can remember that
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medazolam can accumulate in renal
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failure and that's something to keep in
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mind. But as a general rule, as the
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safest infusion that we can give without
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any purple and glycol in it, that's
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just like another reminder for everyone
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out there there. But those are I think
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some of the highlights. to think about
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and just to remember
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Got it. So, probe will fall when we're
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thinking about, thinking about, you
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know, these doses of 50 to 80, you
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know, for extended periods of time,
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thinking about triglycerides, thinking
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about CK, thinking about hyperclaemia,
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and being really mindful of monitoring
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for those, those lab and those
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metabolic complications, knowing that
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it can cause lactose acidosis and muscle
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breakdown, and this kind of rare
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syndrome. And then, pint of arb, drug
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drug interactions, ilius, it's going
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to be a problem. And then, finally,
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no out-of-hand infusions because that's
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just going to cause AKA. All right,
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got it. All right, the other thing I
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really, really liked about this chapter
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is that even though we are moving away
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from deep hypothermia for just your
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routine cardiac arrest patient, we
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still are using deep hypothermia in some
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cases. And even with more moderate
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hyper, hyperthermia and even just
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beaver prevention, we still have
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patients that have shivering. And so,
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Salia, I was hoping you could walk us
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through. like what should we do for our
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approach to shivering in our
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neuropatients? Yes, absolutely. I
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think it's important to talk about this
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bedside shivering scoring tool that,
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you know, kind of allows our nurses and
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our clinicians to assess the degree of
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shivering the bedside. It goes from
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zero to three, so zero means no
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shivering at all and three is the worst
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shivering that you can have. And the
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idea behind, you know, cinnatives and
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painkillers is that obviously it can
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technically help with changing the
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threshold of shivering, meaning that
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you basically will start shivering at a
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lower temperature, which I thought was
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fascinating. Now, why is it a scoring
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this scoring tool important and helpful?
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It's important because when you have a
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lower degree or a milder degree of
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shivering, you can give a drug that
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correlates. that degree of shivering,
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for example, in the bookshop that we
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have, and also in the Columbia Protocol,
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which I think is really the bible of,
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you know, treatment of shivering. We
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talk about how acetaminophen can be
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given, in my own cases. Something I
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feel like we don't talk about as much
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use for own is also listed, and
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something that I see quite often is that
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people order just a normal ten
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milligrams to eight hour dosing. It's
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important to note that the dosing for
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shivering is a higher dosing. We
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typically talk about 30 milligrams Q8
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for this indication, and then when you
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get to mild to moderate cases of
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shivering, opioids are actually very
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effective, and also dexmatomidine and
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presidex. Now, one surprise when I
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actually was doing some research about
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this is that miperidine, which is not
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an opiate that we commonly use, is the
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most effective opiate when it comes to
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shivering. It can actually reduce your
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shivering threshold by two degrees of of,
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um, that I agree. So, which is huge,
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and I have to admit, in our institution,
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we don't use that agent that much. We
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don't like to use it as much because it
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can cause, you know, neurotoxicity,
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especially invasive renal failure. But
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if you have someone with a normal renal
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function, it's worth probably trying.
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And again, especially if you have a
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patient that they're not, you know,
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neuro is not their main problem They,
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you know, you're doing TTM for other
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indications, which it ultimately ends
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up to be neuroprotection, but just the,
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just the site note that the pheridine is
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pretty effective. And then when you get
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to more severe cases, as we talked
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about with the shivering score, is that
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you could actually use agents like
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purple fall. Obviously at that point,
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your patient will be intubated. They're
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in the ICU setting and things like that
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But if you really want to get to, you
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know, more significant cases where you
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need to Obviously, you can paralyze and
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I'll always remember that when you're
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paralyzing, you have to make sure
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enough pain and sedation management is
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on board and we talked about, you know,
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lower rascals so make sure that patients
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are not aware of their surroundings.
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People are, you know, deeply sedated.
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They're not in pain. They don't
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remember things because that has been
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associated with PTSD Depending on the
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degree of shivering and the score that
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they get, they could get anything from
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acetaminophen all the way to purple fall,
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but it's, it's nice because if you
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objectively assess them, then you can
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give them the agent that they need The
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paradigm is an effective opioid that can
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reduce your shivering threshold by two
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degrees of study grade.
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That's awesome. I think that this is a
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commonly encountered problem and it is
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really nice to use that stepwise
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approach and objective scoring criteria.
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The final thing that we're going to just
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do, you know, maybe just one sort of
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rapid fire purl for is that many, many
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of our patients in the neuro ICU and in
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critical care in general end up totally
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delirious, right? And agitation is a
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major problem. This chapter provides a
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really nice summary of some of the
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agents that can be used to combat ICU
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delirium or agitation, including
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presidex, valproic acid, and
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propranolol. And so maybe just kind of
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one sort of purl to take with each of
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those agents, why you like it, what
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you should look out for. I think if you
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need to extipate people that are
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agitated and you really can't have your,
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you know, fentanyl or other sedating,
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deeply sedating is on board, obviously
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because you're afraid of actually. on
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that. I think prosthetics multiple
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times has shown that people who are
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agitated, and they're very close to
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being extubated, meaning, you know,
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respiratory-wise, mentally, everything,
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like they are ready to be extubated.
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But agitation is the reason for not
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getting them extubated. Bingo,
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prosthetics or dexmatomatine will save
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you and will help you, um, extubate
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those patients. So that's what I think
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about prosthetics or dexmatomatine, I
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should say
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I see you studying, do not bolus
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dexmatomatine or prosthetics. And if
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you do that in the OR, that's, that's
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fine. I just, something that I feel
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like I have to keep saying because not
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only you get the hypertension, but you
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can basically saturate all your
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apotonegus and then you can cause this
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hypertension because now you're actually
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acting on your apple wandersceptors.
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And again, like fat things can happen
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with bolus saying dexmatomatine outside
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of the OLR, so please don't do that. I
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suppose well, peroic acid. I honestly
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am a fan because I think you could have
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all perc acid for someone who's not
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intubated. You could possibly prevent
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someone from getting intubated if
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they're very agitated. The way I like
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to dose it, I think, and we have it in
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the chapter initially, you need a
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loading dose, especially if someone's
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very agitated, 20 to 30 make per kick
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is what we think about. And you heard
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that right. It's really kind of close
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to seizure and status, you know,
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loading doses. And then you could start
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anywhere from 250 to 500
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Q8. Obviously, you have to make sure
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if there aren't a set of penis, not a
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problem Hyperiminemia may be
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an issue. But again, if your patient's
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mental synthesis and very altered, I
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wouldn't chase that. Do not send for a
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serial ammonia levels. And remember,
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usually these patients, when they end
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up on vial peric acid, they're not
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gonna be like seizures patients that you
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are gonna keep them on it. You know,
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studies that we looked at and what we
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put in our chapter, we talk about three
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to seven days. So these are short-term
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kind of getting them through this, you
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know, acute phase that they have,
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delirum, they're agitated because
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they're, you know, they have all these
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other things happening to them. So
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that's just one thing to keep in mind.
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Propranolol is, I think, a very
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interesting idea. I think it's because
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it's so lipophilic, it crosses the
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blood brain barrier, you know, it can
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be helpful with reducing norepinephrine,
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central kind of
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secretion, and that can help with, you
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know, kind of getting that edge off So
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it's been nice. I think it has its
-
utility. Obviously, you have to make
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sure your patient hemodynamically can
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tolerate that because it can cause
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hypertension and bradycardia. I really
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like it in people that are also
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qualified for a beta blocker at baseline.
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I kind of want to switch, you know,
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their actual beta blocker will perform
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all for that timeframe. There is no
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specific dose that I could recommend for
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this specific indication. I think you,
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what we have in the chapters, 10
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milligrams QA, and you kind of see how
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they tolerate it. You can obviously
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always add more of a work rate of
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starting high and kind of. causing
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issues with high doses initially. But I
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think again, this is a very helpful,
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especially in trauma patients, if
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you're also worried about personal, you
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know, hypersynthetic activity, where
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we know that beta blockers may also have
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a role in reducing mortality. So I
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think this population specifically
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trauma patients may really be the
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perfect population to trial this beta
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blocker in.
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That's awesome. Okay. So this was a
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whirlwind chapter And I really invite
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everyone who's listening to actually go
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and read the chapter. There's some
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incredible tables in there. And I think
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it's a very useful just overview for how
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we can best manage these patients and
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the complications to expect and to try
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to prevent as you're using these
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different pharmacological agents. With
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that, any final takeaway pearls?
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I think we covered it all. I wanted to
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kind of echo your
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emphasis here chapter I think is going
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to be really helpful. There's a lot of
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agents we didn't talk about today, you
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know, ketamine, other agents, all
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different types of benzodiazepines,
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such as clobazam. So I think if you
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want more, please go back to the
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chapter and take a look at it.