Please Help!! understanding the basic of inhalational anesthesia

[ketap]

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hello..i am quiet new to anesthesia..and i am quiet confuse about inhaled anesthetics pharmacokinetics...
1) i understand that the principle is (quote from basics of anesthesia by Miller & Stoelting ) :
"the brain and all other tissues equilibrate with the partial pressure of the inhaled anesthetics delivered to them by arterial blood (Pa) and likewise, the blood equilibrates with the alveolar partial pressure (PA) of the anesthetics.
so , in simpler words: PA~ Pa ~ Pbr "

i do understand that with that equation, we can think : if the PA increased, then the Pa and the Pbr would increase also, and if the PA decrease, the Pa and Pbr would decrease also..so it is very accurate to use PA to control the Pbr.

but what i do not understand is, i've read that : an increased in Cardiac Output, and that means increasing the uptake of anesthetics would prolonged the induction of anesthesia, but a decrease in CO (as in shock) will make the induction faster...why?

i don't understand: though we have a decreased PA, if we have more uptake(CO), won't it increase the partial pressure of the anesthetic gas in the blood (Pa) and eventually increase the delivery of anesthetic gas to the brain and faster the induction? why the textbook said the opposite?

it seems to me that maintaining the alveolar concentration is the most important thing...but won't it be useless, if the Pa is low ,so the Pbr will also low too??

2) and why the uptake will decrease after some period of time?

please help me find the answers and my misunderstanding..thx u

warm regards,

Ketap 🙂

 

[Planktonmd]

Great questions:
The relationship between the speed of induction and cardiac output:
You are partially right, increasing cardiac output increases uptake from the alveoli to the arterial blood but the higher the the uptake from the alveoli the longer it will take to reach equilibrium between the alveoli and the inspired vapor (FA/FI), this equilibrium between alveoli and inspired gases is what determines the speed of induction and this is exactly why increasing cardiac output is going to slow it down, this is by the way also why induction by less soluble agents is faster (the uptake is less)
So, your goal is to reach high alveolar concentration faster and this happens faster if the uptake is less.
The equilibrium between alveoli and inspired gases is an indirect predictor of the equilibrium between brain and blood.

hello..i am quiet new to anesthesia..and i am quiet confuse about inhaled anesthetics pharmacokinetics...
1) i understand that the principle is (quote from basics of anesthesia by Miller & Stoelting ) :
"the brain and all other tissues equilibrate with the partial pressure of the inhaled anesthetics delivered to them by arterial blood (Pa) and likewise, the blood equilibrates with the alveolar partial pressure (PA) of the anesthetics.
so , in simpler words: PA~ Pa ~ Pbr "

i do understand that with that equation, we can think : if the PA increased, then the Pa and the Pbr would increase also, and if the PA decrease, the Pa and Pbr would decrease also..so it is very accurate to use PA to control the Pbr.

but what i do not understand is, i've read that : an increased in Cardiac Output, and that means increasing the uptake of anesthetics would prolonged the induction of anesthesia, but a decrease in CO (as in shock) will make the induction faster...why?

i don't understand: though we have a decreased PA, if we have more uptake(CO), won't it increase the partial pressure of the anesthetic gas in the blood (Pa) and eventually increase the delivery of anesthetic gas to the brain and faster the induction? why the textbook said the opposite?

it seems to me that maintaining the alveolar concentration is the most important thing...but won't it be useless, if the Pa is low ,so the Pbr will also low too??

2) and why the uptake will decrease after some period of time?

please help me find the answers and my misunderstanding..thx u

warm regards,

Ketap 🙂

 

[Planktonmd]

I forgot to answer your second question:
Why the uptake decreases later?
The answer is simple if you understand my first answer, When you reach equilibrium the gradient between inspired vapor concentration (FI) and alveolar vapor concentration (FA) decreases, and this results in slower uptake of the vapor from inspired gases to alveoli.
Remember that gases move from higher concentration to lower.
Very simple.

 

[pgg]

Read this thread, especially post #6.

 

[pgg]

So, your goal is to reach high alveolar concentration faster and this happens faster if the uptake is less.

[...]

this equilibrium between alveoli and inspired gases is what determines the speed of induction

With respect, I think this is the wrong way to approach this conceptually, and I think that fixating on alveolar concentration is why so many people have trouble understanding inhalational induction speed.

OP, alveolar concentration is useful ONLY because it is 1) easy to measure, and 2) roughly approximates gas concentration in the brain. Remember that drug in the brain is what induces people, not drug in the alveolus.

 

[Planktonmd]

You are right, what matters is actually the concentration in the brain but for simplicity we assume that the alveolar concentration does actually reflect the blood concentration and the brain concentration:

The equilibrium between alveoli and inspired gases is an indirect predictor of the equilibrium between brain and blood.

This assumption is usually reasonable except in situations where there is something preventing gas exchange at the alveolar level.
We are basically considering everything between alveoli and brain as one unit exchanging with the inspired gases in the airway.

 

[ketap]

Hello, thx for all the responds 🙂 i'm very happy..thx u so much, but I am very sorry, but I still confuse...

PGG: hi , thanx for the site..great discussion and I am glad u bring it up to my thread..thx u so much 🙂 but yet, I am still confuse...

“High cardiac output = greater volume of blood available to pick up the agent you're pushing into the lungs = lower concentration of agent in the blood “

Why will the increased volume of blood lower the agent's concentration?...doesn't the uptake ( the volume of the agent) increased too, especially for the highly blood soluble agent?or is it because the time for diffusing is decreased with an increased CO?

Plankton,MD, PGG and anyone :

I did understand the answers from Plankton,MD 🙂 but, I am actually having a hard time thinking the steps (algorithm or mechanism) of what happened to the Pa and Pbr of the anesthetic agent with an increased CO...in simpler words, I am confuse about the mechanism of how the increased CO will affect this equation:
PA~Pa~Pbr ?

It seems so hard for me to understand why that equation (so, keeping higher alveolar concentration to achieve high brain concentration) will still work in a condition of an increased CO...if u don't mind, please tell me the mechanism..


Thx u for giving ur time to answer me...and sorry for bothering..
thx u
warm regards, Ketap..🙂

 

[Noyac]

Hello, thx for all the responds 🙂 i'm very happy..thx u so much, but I am very sorry, but I still confuse...

PGG: hi , thanx for the site..great discussion and I am glad u bring it up to my thread..thx u so much 🙂 but yet, I am still confuse...



Why will the increased volume of blood lower the agent's concentration?...doesn't the uptake ( the volume of the agent) increased too, especially for the highly blood soluble agent?or is it because the time for diffusing is decreased with an increased CO?

Plankton,MD, PGG and anyone :

I did understand the answers from Plankton,MD 🙂 but, I am actually having a hard time thinking the steps (algorithm or mechanism) of what happened to the Pa and Pbr of the anesthetic agent with an increased CO...in simpler words, I am confuse about the mechanism of how the increased CO will affect this equation:
PA~Pa~Pbr ?

It seems so hard for me to understand why that equation (so, keeping higher alveolar concentration to achieve high brain concentration) will still work in a condition of an increased CO?if u don't mind, please tell me the mechanism..


Thx u for giving ur time to answer me...and sorry for bothering..

warm regards, Ketap..🙂

Higher CO will remove more agent from alveoli therefore not allowing the conc to rise in the alveoli. Don't think about it in terms of particles of agent present but more in concentration of agent. The higher CO will remove more particles of agent from the alveoli and this in turn keeps the alveolar conc lower.

The greater the alveolar conc the faster the induction.

 

[pgg]

Why will the increased volume of blood lower the agent's concentration?...doesn't the uptake ( the volume of the agent) increased too, especially for the highly blood soluble agent?or is it because the time for diffusing is decreased with an increased CO?

With increasing cardiac output, both the volume of blood passing through the lungs and amount of agent taken up increase. However, the volume of blood increases more than uptake does, so the net result is a lower concentration of agent in the blood leaving the heart (and going to the brain).


Somewhat analagous to the physiologic "anemia" of pregnancy: blood volume and red cell mass both increase, but volume increases more than red cell mass so the net result is a lower hematocrit.

 

[ketap]

With increasing cardiac output, both the volume of blood passing through the lungs and amount of agent taken up increase. However, the volume of blood increases more than uptake does, so the net result is a lower concentration of agent in the blood leaving the heart (and going to the brain). Somewhat analagous to the physiologic "anemia" of pregnancy: blood volume and red cell mass both increase, but volume increases more than red cell mass so the net result is a lower hematocrit.

thx u ,PGG for responding me 🙂 ,i do understand it right now..thx u 🙂 ...so, the high CO will eventually make the concentration of the agent in the blood lower, then... (because concentration is directly proportional to partial pressure), can i say that with the high CO, we will have a lower Pa too? if it can, i'm wondering : how will the alveolar partial pressure (PA) reach the equilibrium with the arterial partial pressure (Pa)? will they equilibrate on a lower partial pressure limit, so the Pa and the Pbr would also equilibrate within lower limit?Am i right? 😕

Hi,noyac..thx u for answering..i am very happy 🙂 but i'm sorry, but I think u misunderstood me...i do know the answer that “keeping the alveolar concentration high will make induction faster.”.and “The higher CO will remove more particles of agent from the alveoli and this in turn keeps the alveolar conc lower”. but, ok..,so the higher CO will keep the alveolar conc lower, but how about the arterial and alveolar partial pressure? What happened to them that causes the induction lower?

I can't find the answers on any books, that's why I posted it in this forum for a discussion..
please help...

and thx u so much for giving your time to answer my questions..🙂

warm regards,
Ketap 🙂

 

[ketap]

hi..why there is no answer to my question? have i think it right? please help..🙁

thx u ,
warm regards, Ketap🙂

 

[Noyac]

Starting to think you are a nurse.

 

[ketap]

noyac: well, i'm not a nurse, i am a med student and i'm now trying to learn about anesthesia..actually i'm not yet learning anesthesia from my teacher, but i will next year....so i am preparing stuffs right now..as i've said before in my first post, that i am new to anesthesia..and that's why i said sorry for bothering...
i am just trying to clarify if my thinking from my last post is right?

(because concentration is directly proportional to partial pressure), can i say that with the high CO, we will have a lower Pa too? if it can, i'm wondering : will the PA and Pa equilibrate on a lower partial pressure limit, so that the Pa and the Pbr would also equilibrate within lower limit?

thx u

warm regards, Ketap