Couple questions on inhaled anesthetics

[loveoforganic2]

1) Trying to reconcile two things I was taught.

a) Onset is inversely proportional to cardiac output (assuming you maintain cerebral perfusion obviously). This seems to imply inhaled anesthetics are diffusion limited gases

b) Absorption is directly proportional to cardiac output. This seems to imply inhaled anesthetics are perfusion limited gases

I suppose these both could be true if anesthetics are perfusion-limited, and the quicker onset time with decreased cardiac output is a feature of peripheral vasoconstriction in response to the decreased output, but I'd appreciate confirmation on that

2) MAC adjustments related to serum sodium levels - is this a solubility-related effect, an effect of shifts in water distribution, or something else?

TYIA for any help

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[pgg]

Low cardiac output = smaller amount of blood passing through lungs in a given time = more volatile taken up in smaller volume of blood = higher concentration of volatile in the blood leaving the heart. Concentration of agent in the blood leaving the heart and going to the brain is what makes people go to sleep or stay asleep. This is why lower cardiac output speeds inhalation inductions. And also why L --> R shunts don't affect inhalation induction speeds.


IIRC volatiles affect voltage gated sodium channels, increasing permeability to Na and altering membrane excitability. I don't think the hypernatremia --> increased MAC relationship has anything to do with solubility.

 

[loveoforganic2]

Low cardiac output = smaller amount of blood passing through lungs in a given time = more volatile taken up in smaller volume of blood = higher concentration of volatile in the blood leaving the heart. Concentration of agent in the blood leaving the heart and going to the brain is what makes people go to sleep or stay asleep. This is why lower cardiac output speeds inhalation inductions. And also why L --> R shunts don't affect inhalation induction speeds.

Thanks, this concept and cardiac output being proportional to absorption make sense in isolation to me, just not together. What I remember from phys is a spectrum between perfusion limited (increased blood flow is the only way to increase supply to tissue) and diffusion limited (increased alveolar pressure is the only way to increases tissue supply, increased local blood concentration would be inversely proportional to cardiac output) gases, with the difference being whether the alveolar partial pressure of the given gas is able to equilibrate with the arterial partial pressure within the time span of the blood crossing the pulmonary capillary. I think I might have been looking at it as too cut and dry a situation, when you actually have gases that are somewhere in the middle.

IIRC volatiles affect voltage gated sodium channels, increasing permeability to Na and altering membrane excitability. I don't think the hypernatremia --> increased MAC relationship has anything to do with solubility.

Thanks, we've been treating them as "mostly GABAergic + a bunch of other stuff we won't talk about", so that would make sense.

 

[Idiopathic]

Low cardiac output = smaller amount of blood passing through lungs in a given time = more volatile taken up in smaller volume of blood = higher concentration of volatile in the blood leaving the heart. Concentration of agent in the blood leaving the heart and going to the brain is what makes people go to sleep or stay asleep. This is why lower cardiac output speeds inhalation inductions. And also why L --> R shunts don't affect inhalation induction speeds.


IIRC volatiles affect voltage gated sodium channels, increasing permeability to Na and altering membrane excitability. I don't think the hypernatremia --> increased MAC relationship has anything to do with solubility.

yeah people keep saying this but i dont think its true. volatile anesthetic uptake is directly proportional to cardiac output and solubility, so uptake is greater when your cardiac output is high. my theoretical reason why induction is more rapid with low CO states versus high CO states is that blood flow to the brain is relatively preserved in low CO states, so the other organs (muscles/vessel rich group) get less blood flow and take up less anesthetic, leaving the brain to get a higher proportion of volatile, and allowing PA to rise faster since less anesthetic is being taken up and delivered to the rest of the body.

sodium channel conduction is likely a minimal part of the effects of volatile anesthesia, considering your textbooks reiterate that NOBODY KNOWS WHY THEY WORK. likely multifactorial affecting Na/K/GABA/glycine/NMDA/glutamate. i have seen one source that speculates that hypernatremia allows for more vigorous neural conduction even when anesthetized

 

[itokama]

I think the last answer is the right one. Here you have some more text and graphs:

http://books.google.si/books?id=-YI...or decrease the rate of rise od fa/fi&f=false

 

[fakin' the funk]

Low uptake = increased speed of onset, because low uptake = increased rate of rise of Fa/Fi. Low CO states are low uptake states because a relatively small amount of volatile anesthetic in the alveolus is needed to raise the partial pressure in a given amount of time.

 

[Idiopathic]

Low uptake = increased speed of onset, because low uptake = increased rate of rise of Fa/Fi. Low CO states are low uptake states because a relatively small amount of volatile anesthetic in the alveolus is needed to raise the partial pressure in a given amount of time.

but that logic is circular and doesnt explain why you actually get anesthetized. taken to the extreme, a no cardiac output state would equal instantaneous rate of rise for FA/Fi but we wouldnt call that "induction".

its nice to think of for theory, but really it doesnt work this way practically. you need some number of half-times to equilibrate, the higher the global blood flow, the slower it takes to equilibrate in the brain. since nobody actually does it this way, except with kids and their crazy cardiopulmonary dynamics, there really is very little use discussing it outside of memorization for boards.

 

[loveoforganic2]

yeah people keep saying this but i dont think its true. volatile anesthetic uptake is directly proportional to cardiac output and solubility, so uptake is greater when your cardiac output is high. my theoretical reason why induction is more rapid with low CO states versus high CO states is that blood flow to the brain is relatively preserved in low CO states, so the other organs (muscles/vessel rich group) get less blood flow and take up less anesthetic, leaving the brain to get a higher proportion of volatile, and allowing PA to rise faster since less anesthetic is being taken up and delivered to the rest of the body.

This is more or less what I was venturing a guess at as a possible explanation. I had an issue with it when I initially thought of it, but am having a hard time putting the logic back together as to why that was