Norepinephrine

But methylene blue and hydroxycobalamin are non-catecholamine vasopressors.

And they're certainly not considered first-line vasopressors, right? Norepinephrine, first-line vasopressor.

Even epinephrine in some cases.

Phenylephrine, much less commonly used, but something that you could consider.

This is like the inotrope dobutamine epinephrine.

does this as well.

Norepinephrine does this to a small degree, but methylene blue does not affect beta-1.

It is not a catecholaminergic mechanism.

So non-catecholaminergic vasopressors are things like methylene blue and hydroxocobalamin, also vasopressin, um, angiotensin II would be two other ones, all things we've talked about on the channel.

Um, but methylene blue and hydroxocobalamin are non-ca- catecholamine vasopressors, and they're certainly not considered first-line vasopressors, right? Norepinephrine, first-line vasopressor.

Even epinephrine in some cases.

Phenylephrine, much less commonly used, but something that you could consider.

And in REM sleep, the main dreaming stage, one of the most important of these is very low, almost absent.

This particular chemical is called noradrenaline, and it deserves a moment of quiet attention.

Noradrenaline helps us record memories during waking life, sharpening our attention and flagging experiences as significant.

But in REM sleep, its levels drop remarkably low, lower than at almost any other time.

And without it, memories form poorly, weakly, if they form at all.

So dreams, occurring precisely when this memory chemical has retreated, are extraordinarily hard to store.

This low level of noradrenaline is genuinely important to our puzzle, so let us sit with it a little longer.

Noradrenaline is needed to fix memories in place, to give them the durability that lets them survive until morning.

Okay, some advanced clinical applications, which is going to dovetail off some of the stuff we started to talk about.

Norepinephrine is most useful when the main problem is vasodilation with inadequate perfusion pressure, right? Because norepinephrine is primarily alpha-1, and it primarily causes vasoconstriction.

So it's best for the problem of vasodilation because it causes vasoconstriction.

This causes it to work really well in septic shock because that's the dominant hemodynamic problem in septic shock.

So by increasing the diastolic blood pressure, sometimes you'll help improve coronary perfusion of the heart.

And with more blood flow to the heart, that muscle works better.

Norepinephrine does slightly increase contractility through its beta-1 effects.

And the norepinephrine often will increase preload because this is where you get into stressed and unstressed volume.

And in REM sleep, the main dreaming stage, one of the most important of these is very low, almost absent.

This particular chemical is called noradrenaline, and it deserves a moment of quiet attention.

Noradrenaline helps us record memories during waking life, sharpening our attention and flagging experiences as significant.

But in REM sleep, its levels drop remarkably low, lower than at almost any other time.

And without it, memories form poorly, weakly, if they form at all.

So dreams, occurring precisely when this memory chemical has retreated, are extraordinarily hard to store.

This low level of noradrenaline is genuinely important to our puzzle, so let us sit with it a little longer.

Noradrenaline is needed to fix memories in place, to give them the durability that lets them survive until morning.

You know, if your PA pressures take over your blood pressure, cross your blood pressure, you're going to set off a whole different casket of right to left shunting, which then is the death spiral for this patient.

So when in doubt, use Levophed.

You're not a preference.

It's always the drug of choice in all circumstances, period.

And then the ladder.

Noradrenaline first, 0.05 to 0.3 micrograms per kilo per minute, then vasopressin, 1 to 4 units an hour, then methylene blue, 100 milligrams intravenously over 30 minutes, and then high-dose hydroxycobalamin, 5 grams over 15 minutes.

And the warning from the transplant episode still stands.

It absolutely does.

Cytokine absorber on the circuit, with honest acknowledgement that the evidence isn't there yet.

Two arterial lines and climb the vasoplegia ladder.

Noradrenaline, vasopressin, methylene blue, hydroxycobalamin.

But be certain it isn't low output first.

This was a single-center trial in our department with a strong, and I would say almost obsessive, focus on blood pressure management, and keeping the mean arterial pressure above sixty-five is our routine.

Norepinephrine is the first-line vasopressor, and ninety-eight percent of the patients in the trial were given norepinephrine.

This reflects our clinical practice.

The surgeries were also relatively short and low to moderate risk, uh, while it was a trial in patients who wouldn't normally get an arterial catheter.

So the short answer is that there was almost no hypotension left to detect.

Uh, in Bernd's department, in their practice, keeping the MAP above sixty-five is institutional routine.

Norepinephrine, as Bernd outlined, is the first-line vasopressor.

Ninety-eight percent of enrolled patients received it, and the median time-weighted dose was zero point zero five micrograms per kilogram per minute.

And there's chemicals in our brain that are released during these experiences.

Noradrenaline's one.

Um, cortisol is a stress hormone.

There's gobs of hormones that are re-released during stress.