Pharmokinetics question

[244913]

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Gents,

I'm finishing up a 4 year hitch as a USAF flight surgeon and starting as a CA-1 this summer, so I've been trying to do some reading on my latest and last deployment from Baby Miller. I'm getting stuck on the pharmokinetics of volatile anesthetics and my question is this:


I understand that P(A) equates with P(br) and therefore relates to both induction and recovery from anesthesia. I also understand that uptake of anesthetic into the blood lowers P(A) which slows onset of induction. Why is this though? Don't you want the anesthetic to diffuse from the alveoli into the blood? How else can the anesthetic get to the L side of the heart and then be pumped systemically to its receptor sites in the brain?


I feel like I am missing some basic concept here because it doesn't make intuitive sense to me.

Also, Miller talks about anesthetic uptake (loss) into pulmonary arterial blood. This seems backwards. Shouldn't the course of anesthetic go from alveoli to capillary interface to venule to pulmonary vein to L side of heart ----> systemic circulation? If it goes into the pulmonary arterial circulation won't it immediately be off-gassed? ie. artery-arteriole-cappillary-alveoli?

I apologize in advance for what is probably an elementary question. Thanks for your insights.

- 61N

 

[pgg]

Not exactly intuitive. The topic comes up periodically, I posted in this old thread explaining it as best I could -

http://forums.studentdoctor.net/showthread.php?t=547016

 

[Idiopathic]

Not exactly intuitive. The topic comes up periodically, I posted in this old thread explaining it as best I could -

http://forums.studentdoctor.net/showthread.php?t=547016

i dont think that explanation is actually true, regardless of how much sense it makes. if you presume that less cardiac output allows for longer transit time in the pulmonary circulation more uptake of anesthetic, this would presumably decrease FA/Fi, which slows inhalation induction. more uptake equals slower induction.

 

[Idiopathic]

also, OP, dont confuse "diffusability" with "solubility". increased solubility creaates more dissolved anesthetic, which doesnt correlate with ability to anesthetize.

i think the low output state has more to do with relative perfusion, i.e. the brain gets a larger percentage of the blood flow in low-output states relative to high-output states...it has very little to do with the pulmonary circulation.

 

[partydoc]

I understand that P(A) equates with P(br) and therefore relates to both induction and recovery from anesthesia. I also understand that uptake of anesthetic into the blood lowers P(A) which slows onset of induction. Why is this though? Don't you want the anesthetic to diffuse from the alveoli into the blood? How else can the anesthetic get to the L side of the heart and then be pumped systemically to its receptor sites in the brain?

Heres my understanding of it:

Yes you want the anesthetic to diffuse from the alveoli to the blood, but you also want it to diffuse from blood to the brain. The idea is that if an agent is more soluble in blood, it is less likely to diffuse into the brain (because it wants to stay in the blood). Leading to longer times for desired amount of anesthetic reaching the brain, and hence longer onset of induction.

Also, Miller talks about anesthetic uptake (loss) into pulmonary arterial blood. This seems backwards. Shouldn't the course of anesthetic go from alveoli to capillary interface to venule to pulmonary vein to L side of heart ----> systemic circulation? If it goes into the pulmonary arterial circulation won't it immediately be off-gassed? ie. artery-arteriole-cappillary-alveoli?

The loss of the gas into the alveolar blood is the amount of gas needed for equilibrium, which must be reached before the gas is going more into the brain than blood (think LeChatlier's from udergrad chem).
It will not be off gassed once it goes into pulm art circulation because it is more soluble in the blood than gas (air).

 

[deleted9493]

Low CO causes a more rapid rise in FA/Fi and will tend to speed induction; this is why giving a beta blocker could theoretically speed an inhalational induction. To the OP, you can greatly simplify thinking about this by considering what is happening at the alveolar level. If FA goes up faster, induction is quickened. Soluble agents will be affected more significantly than insoluble (the insoluble agents will be fast, regardless of CO...again, think rapid rise in FA...they are insoluble in blood!).