Anasthetics (from FA)

[Franksta1118]

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I'm confused about the general principles of anasthetics as outline by FA (page 430 in 2010 version).

Most of it makes sense to me except for "higher AV concentration gradient means more solubility = slower onset of action" Can somebody explain this? What is the solubility referring to (blood or lipid?). I don't understand the principle of how AV gradient would relate to onset of solubility.


Also under "Lungs" it says increased rate and depth of ventilation means more gas tension, that makes sense but is it saying that these anasthetics CAUSE more rate/depth or just that in principle increased rate and depth would increase gas tension?

Thanks

 

[Mr hawkings]

I'm confused about the general principles of anasthetics as outline by FA (page 430 in 2010 version).

Most of it makes sense to me except for "higher AV concentration gradient means more solubility = slower onset of action" Can somebody explain this? What is the solubility referring to (blood or lipid?). I don't understand the principle of how AV gradient would relate to onset of solubility.


Also under "Lungs" it says increased rate and depth of ventilation means more gas tension, that makes sense but is it saying that these anasthetics CAUSE more rate/depth or just that in principle increased rate and depth would increase gas tension?

Thanks

The solubility is in reference to the blood/gas coefficient. The more soluble the gas is in blood, the easier it is for it to cross from alveoli to blood but the longer its going to take to cross from blood to the brain. Since the action of the drug is in the brain, the increased blood solubility means it will take longer to reach its maximal effect. This also means the drug will be redistributed from the brain to other areas in the body just as fast and the action on the brain will be short-lived.

I dont know what AV gradient has to do with th solubility though. It would make sense it they were talking about driving pressue due to the concentration gradient.

As to your second question, both would be true. On one hand, increased vent rate will decrease the time to maximal effect but on the other hand, a lot of these volatile anesthics cause increase vent rate as a side-effect.

Thats how i understood it when it was taught. Someone please correct me if i'm off-base

 

[lord_jeebus]

This is probably a low yield Step I subject, but here's how I think about it.

Let's use two volatile anesthetics for this example:

Desflurane has very low blood solubility. By comparison, Isoflurane is quite soluble.

When you administer inhaled desflurane, because little of it transfers from the alveoli to the blood (because it is not that soluble), the alveolar concentration builds up quickly, and quickly equilibrates with the blood concentration. By contrast, isoflurane is taken up by the blood in significant amounts, removing it from the alveoli, and preventing its concentration there from increasing as quickly.

If you increase ventilation, FA/Fi will increase at a higher rate for all volatile anesthetics. However, this effect is most profound for highly soluble anesthetics. This is because, when an agent is highly soluble, the more agent you deliver, the more is taken up.

If you increase cardiac output, FA/Fi will rise at a lower rate for all anesthetics, because more blood is available to remove the agent from the alveoli. This effect is also most profound for highly soluble anesthetics.

For purposes of testing, Nitrous oxide or Desflurane will likely represent anesthetic agents with low solubility; Methoxyflurane is a stereotypical high solubility agent, but because it is no longer used, Isoflurane may be more likely to appear in this role. If Sevoflurane is tested, know that it is in between.

 

[lord_jeebus]

The solubility is in reference to the blood/gas coefficient. The more soluble the gas is in blood, the easier it is for it to cross from alveoli to blood but the longer its going to take to cross from blood to the brain. Since the action of the drug is in the brain, the increased blood solubility means it will take longer to reach its maximal effect. This also means the drug will be redistributed from the brain to other areas in the body just as fast and the action on the brain will be short-lived.

Yes. An easier way to think about it is that the alveolar and brain concentrations of volatile anesthetics equilibrate quickly, so whatever causes a rapid increase in alveolar concentration will also cause a rapid increase at the site of action.

a lot of these volatile anesthics cause increase vent rate as a side-effect.

Although volatile anesthetics increase respiratory rate, they decrease tidal volume by a proportionally greater amount, leading to decreased minute ventilation.

 

[hyrule]

I'm confused about the general principles of anasthetics as outline by FA (page 430 in 2010 version).

Most of it makes sense to me except for "higher AV concentration gradient means more solubility = slower onset of action" Can somebody explain this? What is the solubility referring to (blood or lipid?). I don't understand the principle of how AV gradient would relate to onset of solubility.


Also under "Lungs" it says increased rate and depth of ventilation means more gas tension, that makes sense but is it saying that these anasthetics CAUSE more rate/depth or just that in principle increased rate and depth would increase gas tension?

Thanks

I also understand everything else except the higher AV concentration gradient part. Anyone care to share some light... as in what do they mean by AV gradient and how it relates to slower onset of action. AV concentration is defined as the solubility of anesthetic in tissues.
I would think that a high solubility in tissues(brain) is what you want, meaning a faster onset. But I'm obviously missing some concept here: that solubility in the brain is inversely related to its rate of effect... which I don't understand.

 

[Mr hawkings]

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[lackli]

I'm also a little confused about the AV concentration gradient being increased means slower onset of action.

The way it makes sense to me is that there is only onset of anesthetic action when tissue is saturated. If the anesthetic has a higher solubility in a tissue, then it takes more anesthetic to saturate the tissue (i.e. a bigger bucket to fill) and thus slower onset of action. If there low solubility in the brain, then the bucket is smaller and the tissue becomes saturated faster and there is faster onset of action.

Is that a good way of looking at it?

 

[engineeredout]

If the AV gradient is low, that means that the difference in concentration between the arterial and venous ends are small, meaning that very little of the drug gets absorbed. Little gets absorbed, means less solubility, means more rapid onset of action (more rapidly equilibrates with the CNS)