MSIII Question: Cardiac output effect on uptake of inhalation anesthetics

[castiron]

I am reading the "Inhalation Anesthetics" chapter in Clinical Anesthesiology for my anesthesia rotation and found myself confused on the topic of factors affecting alveolar concentration.

How is it that an INCREASE in cardiac output, which increases the uptake of the anesthetic, actually DELAYS the induction and a DECREASE in cardiac output can actually lead to OVERDOSAGE of anesthetics?

I understand that the partial pressure difference between alveolar gas and venous blood, and the solubility in blood affect the uptake, but cannot seem to wrap my brain why an increase in alveolar blood flow slows induction?


Any help?

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[WholeLottaGame7]

I am reading the "Inhalation Anesthetics" chapter in Clinical Anesthesiology for my anesthesia rotation and found myself confused on the topic of factors affecting alveolar concentration.

How is it that an INCREASE in cardiac output, which increases the uptake of the anesthetic, actually DELAYS the induction and a DECREASE in cardiac output can actually lead to OVERDOSAGE of anesthetics?

I understand that the partial pressure difference between alveolar gas and venous blood, and the solubility in blood affect the uptake, but cannot seem to wrap my brain why an increase in alveolar blood flow slows induction?


Any help?

Conceptually, the way it was explained to me was as follows: pretend you are pissing into a stream (or pouring dye into a stream, whatever). The concentration of piss is going to be lower (slower induction) if the stream you are taking a leak into is the Amazon, the concentration is going to be higher (faster induction) if it's the stream in your backyard.

 

[Ignatius J]

At lower CO states, the partial pressure in your alveoli is exposed to X units of blood for a relative longer period of time than when blood is just pumping through there with higher CO states.

This allows the partial pressure of gas in the blood to approach closer and closer values for the partial pressure of the gas in the alveoli.

Essentially, you are just prolonging the amount of time that the blood is exposed to the gas in the lungs. It then goes to the CNS and takes effect. After that, it is passed back through the lungs where it equilibrates again the best it can. The longer the exposure to the gas in the lungs, the greater the chance of reaching the partial pressure value of the gas in the lungs.

That's how I think of it.

Hope that helps.

 

[btbam]

Conceptually, the way it was explained to me was as follows: pretend you are pissing into a stream (or pouring dye into a stream, whatever). The concentration of piss is going to be lower (slower induction) if the stream you are taking a leak into is the Amazon, the concentration is going to be higher (faster induction) if it's the stream in your backyard.

Yea this is the only way it's ever really made sense to me. I always think of pouring cream into one big cup of coffee and one small cup, the big one will be more "dilute" than the small one (aka high CO).

 

[castiron]

Gotcha! Thanks a lot, that clears it up.

 

[fabfive5]

CLINICALLY it doesn't make much difference....keep that in mind. You overload them so much with gas that these minutia don't come into play...maybe making a few seconds difference.

 

[pgg]

My explanation in this thread:

Speed of induction for inhaled anesthetics can be a bit counterintuitive. At first glance it seems odd that high cardiac output slows induction. This slower induction is explained in some texts as a consequence of alveolar concentration rising more slowly, so I can see where you get the idea that speed of induction is tied to alveolar concentration. It's really not; a threshold concentration of drug in the brain is what makes people go to sleep. Alveolar concentration is assumed to correlate well with blood (and therefore brain) concentration ... and it does under normal conditions. But V/Q mismatch isn't normal, and correlation does not imply causation.

V/Q mismatch isn't good for getting high concentrations of oxygen into the blood, and it isn't good for getting high concentrations of volatile agents into the blood either. Right to left shunts slow induction because blood is bypassing the alveoli and not picking up any volatile agent. Left to right shunts don't affect speed of induction because the blood that actually leaves the heart and goes to the brain is saturated with agent (having passed through the lungs at least once).

The counterintuitive part is understanding why low cardiac output speeds inhalation induction. Remember that concentration of agent in the brain is what makes people go to sleep, so consider how saturated the blood leaving the heart is. 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. (Despite the lower blood concentration, more agent is actually getting picked up in the lungs, so the alveolar concentration doesn't rise as quickly.)

A slower rise in alveolar concentration is a consequence of high CO. Lower blood concentration is also a consequence of high CO.

Don't lose sight of the real issue: actual concentration of the volatile agent in the blood leaving the heart (ie, going to the brain).

 

[RxBoy]

but cannot seem to wrap my brain why an increase in alveolar blood flow slows induction?

Inhaled anesthetic pharmacology is confusing when you compare it to IV pharmacology. You're not alone, it takes some thinking and reading to understand. The one that used to really confuse me was why does a more soluble anesthetic take longer for induction? We tend to think in IV pharmacology because that's all we were taught. Once you understand Gas kinetics/dynamics, it starts to make more sense.

 

[Oh_Gee]

sorry to bump an old thread, but i thought it relevant to post here because this thread popped up when i googled my question

can someone explain how the Alveolar(arterial)-to-venous partial pressure gradient affects uptake? i don't want to just remember the equation ( Uptake = [(λ) × (Q) × (PA − PV)]/Barometric pressure)

. i feel like it would be better if i understand the concept

and also, why does high uptake=slow induction (patient gets effects slower)

 

[deleted171991]

https://forums.studentdoctor.net/threads/uptake-question.1239753/#post-18552440

 

[Adramedstudent]

I am reading the "Inhalation Anesthetics" chapter in Clinical Anesthesiology for my anesthesia rotation and found myself confused on the topic of factors affecting alveolar concentration.

How is it that an INCREASE in cardiac output, which increases the uptake of the anesthetic, actually DELAYS the induction and a DECREASE in cardiac output can actually lead to OVERDOSAGE of anesthetics?

I understand that the partial pressure difference between alveolar gas and venous blood, and the solubility in blood affect the uptake, but cannot seem to wrap my brain why an increase in alveolar blood flow slows induction?


Any help?

When cardiac output will be more, more perfusion will occur, which will lead to fast solubility of the drug, which leads to fast binding of the drug to plasma proteins, even before the required PP of the drug in blood is attained. Induction rate is directly proportional to rate of increase of PP of the drug in blood, hence due to fast dissolving of the drug(it binding to plasma protein) the rate of increase of PP will be low & so, will the induction rate.

 

[Adramedstudent]

sorry to bump an old thread, but i thought it relevant to post here because this thread popped up when i googled my question

can someone explain how the Alveolar(arterial)-to-venous partial pressure gradient affects uptake? i don't want to just remember the equation ( Uptake = [(λ) × (Q) × (PA − PV)]/Barometric pressure)

. i feel like it would be better if i understand the concept

and also, why does high uptake=slow induction (patient gets effects slower)

Your last sentence is wrong. High uptake = Faster induction

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[anbuitachi]

Why does higher solubility increase induction time inhalational? You'd think more are going to brain

 

[dchz]

Your last sentence is wrong. High uptake = Faster induction

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Higher uptake = slower induction if you are talking about uptake in the blood. Because there would be less diffusion to the brain since the molecule is so soluable.


Here is how I would explain it:

Conc (aveola) <=> conc (blood) <=> conc (brain)

It is the amount of gas molecules that DIFFUSES into the brain that causes induction.

All things equal, higher cardiac output causes lower concentrations in the blood. Therefore the lower blood concentrations causes less molecules to diffuse out to the brain. Therefore the brain concentration necessary for induction is achieved slower.

Sure, the increased output might take more molecules to the brain per amount of time. But those molecules are dissolved into the blood and their concentration is lower than their low CO counterparts. Their relative lower concentration in the blood causes less diffusion into the brain to cause a slower induction.

 

[Adramedstudent]

Higher uptake = slower induction if you are talking about uptake in the blood. Because there would be less diffusion to the brain since the molecule is so soluable.


Here is how I would explain it:

Conc (aveola) <=> conc (blood) <=> conc (brain)

It is the amount of gas molecules that DIFFUSES into the brain that causes induction.

All things equal, higher cardiac output causes lower concentrations in the blood. Therefore the lower blood concentrations causes less molecules to diffuse out to the brain. Therefore the brain concentration necessary for induction is achieved slower.

Sure, the increased output might take more molecules to the brain per amount of time. But those molecules are dissolved into the blood and their concentration is lower than their low CO counterparts. Their relative lower concentration in the blood causes less diffusion into the brain to cause a slower induction.

Higher solubility = Slower induction, but
Higher uptake = Faster induction

When cardiac output will be more, more perfusion will occur, which will lead to fast solubility of the drug, which leads to fast binding of the drug to plasma proteins, even before the required PP of the drug in blood is attained. Induction rate is directly proportional to rate of increase of PP of the drug in blood, hence due to fast dissolving of the drug(it binding to plasma protein) the rate of increase of PP will be low & so, will the induction rate.

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[nimbus]

Why does higher solubility increase induction time inhalational? You'd think more are going to brain

Because higher solubility=larger blood reservoir for inhalation agent. You have a larger tank to fill in the blood compartment which takes longer to fill. This causes a delay in attainment of steady state alveolar concentration. Without a high alveolar concentration, you cannot attain high blood or brain concentrations. The more rapidly you can attain high alveolar concentration, the more rapidly you can achieve high brain concentration. Low CO--->less uptake between alveolus and blood--->more rapid rise in alveolar concentration--->more rapid inhalation induction.

 

[nimbus]

When cardiac output will be more, more perfusion will occur, which will lead to fast solubility of the drug, which leads to fast binding of the drug to plasma proteins, even before the required PP of the drug in blood is attained. Induction rate is directly proportional to rate of increase of PP of the drug in blood, hence due to fast dissolving of the drug(it binding to plasma protein) the rate of increase of PP will be low & so, will the induction rate.

For the purpose of this discussion, solubility is not measured in speed but amount. It's not a matter of "fast dissolving" but "more dissolving" which takes longer. More soluble agents have a larger blood compartment. Subtle difference.

 

[Twiggidy]

The first thought should always be

ALVEOLAR CONCENTRATION

That's how inhaled anesthestics are meausred. To get an induction of INHALED anesthetic you have to maintain a high ALVEOLAR concentration. If the inhaled anesthetic has high solubility, it goes into the blood stream quickly, and it becomes difficult to keep an ALVEOLAR concentration.

(Remember, MAC is minimum ALVEOLAR concetration of an inhaled to prevent movement from surgical stimulation)

This "piss in the stream" analogy is perfect

Amazon river = high cardiac output = washing away all the inhaled going to blood stream = slower to get equal concetrationn in blood an alveoli (slow build to MAC) = alveoli concentration stays low = slow induction

Back yard slow moving creek = low CO = gas doesn't wash away fast = faster equal concentration in blood and alveoli = alveoli concentration builds (approaches MAC fast) = alveoli concentration high = fast induction


It took me forever and a few ITE botchings to wrap my head around that

 

[Twiggidy]

For the purpose of this discussion, solubility is not measured in speed but amount. It's not a matter of "fast dissolving" but "more dissolving" which takes longer. More soluble agents have a larger blood compartment. Subtle difference.

And yes, it also relates to solubility of the inhaled agent

A low soluble agent will have a fast induction even at low CO states when compared to a high soluble agent. This is why Sevoflurane is a better inhaled induction anesthetic than isoflurane.

 

[sunealoneal]

I'm reading Duke's right now...

Is this a typo? Or have I been misunderstanding this thread?


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[Iso4ane]

I'm reading Duke's right now...

Is this a typo? Or have I been misunderstanding this thread?

Your book is poorly formatted. What exactly is your question? Your book is correct and as far as I am aware agree with what we been saying. PM if you have to.

 

[sunealoneal]

Your book is poorly formatted. What exactly is your question? Your book is correct and as far as I am aware agree with what we been saying. PM if you have to.

This book says an increase of cardiac output increases the speed onset of volatile induction. Hasn't the everyone here been saying a higher cardiac output slows inhaled gas induction?


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[nimbus]

This book says an increase of cardiac output increases the speed onset of volatile induction. Hasn't the everyone here been saying a higher cardiac output slows inhaled gas induction?


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It doesn't. Increased cardiac output is listed under factors that decrease alveolar concentration and decrease speed of volatile induction. Inappropriate black dot is throwing you off.

 

[pgg]

This book says an increase of cardiac output increases the speed onset of volatile induction. Hasn't the everyone here been saying a higher cardiac output slows inhaled gas induction?

It's poorly formatted -

The line above "increase in cardiac output" says "factors that decrease alveolar concentration or slow onset of volatile induction:"

You understand it correctly

 

[sunealoneal]

I think I need some more coffee. Thanks!


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[Twiggidy]

I think I need some more coffee. Thanks!


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Yeah, they accidentally put a bullet point at "Factors that decrease....." where it shouldn't be. Move that bullet left and the bullets under it a factors that SLOW induction

 

[Iso4ane]

This book says an increase of cardiac output increases the speed onset of volatile induction. Hasn't the everyone here been saying a higher cardiac output slows inhaled gas induction?


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Yeah, I was confused at first too, then my coffee kicked in. What should've tipped you off (and helped tip me off), is that both increases and decreases in minute ventilation was mentioned, which is contradictory, and made me look closer.

 

[Oh_Gee]

I'm reading Duke's right now...

Is this a typo? Or have I been misunderstanding this thread?


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it says "high AND low flow within the breathing circuit"

is that also a typo. those 2 points contradict each other

 

[nimbus]

it says "high AND low flow within the breathing circuit"

is that also a typo. those 2 points contradict each other

High flow--->fast induction
Low flow--->slow induction

Someone please delete that chart. It sucks and it confuses people.

 

[Oh_Gee]

High flow--->fast induction
Low flow--->slow induction

Someone please delete that chart. It sucks and it confuses people.

is that from some review book for residents or something?

 

[MirrorTodd]

is that from some review book for residents or something?

I think it's from Anesthesia secrets.

 

[nimbus]

is that from some review book for residents or something?

No

 

[sunealoneal]

Yeah, I scanned it from Duke's Anesthesia Secrets.

 

[Twiggidy]

Yeah, I scanned it from Duke's Anesthesia Secrets.

Personally I think the only books a resident needs is Baby Miller or Morgan/Mikhail. My attending told me to do this and it really help: Buy 2 copies of either. Keep one at home as your good copy. Take he other and rip all the chapters out and staple each chapter as a separate packet. Take one chapter with you to the OR or OB everyday and read that chapter (whatever service I was on would get the most reads). This way you can read in the OR a bit incognito. Reading in the OR may not be a big deal at some places but at my residency they took it as not paying attention to that case (especially if you're a 1 or 2) even if you were reading anesthesia material. If you read either of those enough you'll have them memorized and that will be extremely helpful for ITE and boards. Just my 2c. In my opinion, the little study books always had mistakes