"Dumb questions"

sevo1981 · Jul 23, 2008

Hi everyone. I am a longtime lurker but now a first time poster (just figured out how to do this... sad but true

. I am a new CA-1 and LOVING IT! There are however a LOT of things that don't make sense. Hopefully they will start making sense soon, but in the meantime, I thought this might be a great place to ask some of the "stupid" questions we don't otherwise ask. I'll start with a few.

1. Why don't we do OG/NG suction before RSI if "full stomach" is such a big deal (or do we?????)

2. If the surgery is small and the patient ate something before showing up to the hospital, why don't we just decompress the stomach and move on? (not a good idea for big abd surgeries I understand...)

3. The Lange book talks about how increasing V/Q mismatch leads to slower induction. I thought that increased V/Q mismatch would lead to a higher alveolar conc of anesthetic (since less will be taken up by the pulm circulation) and thus faster induction?

As you can tell, I have a lot to learn. You guys have all helped me a lot already and I want to thank you in advance for the continued support.

Planktonmd · Jul 23, 2008

sevo1981 said:
Hi everyone. I am a long lurker but now a first time poster (just figured out how to do this... sad but true . I am a new CA-1 and LOVING IT! There are however a LOT of things that don't make sense. Hopefully they will start making sense soon, but in the meantime, I thought this might be a great place to ask some of the "stupid" questions we don't otherwise ask. I'll start with a few.

1. Why don't we do OG/NG suction before RSI if "full stomach" is such a big deal (or do we?????)

2. If the surgery is small and the patient ate something before showing up to the hospital, why don't we just decompress the stomach and move on? (not a good idea for big abd surgeries I understand...)

3. The Lange book talks about how increasing V/Q mismatch leads to slower induction. I thought that increased V/Q mismatch would lead to a higher alveolar conc of anesthetic (since less will be taken up by the pulm circulation) and thus faster induction?

As you can tell, I have a lot to learn. You guys have all helped me a lot already and I want to thank you in advance for the continued support.

These are not stupid questions.
1- NG tube before induction on a full stomach can be done if the surgery is an emergency but many times we choose not to do it for patient comfort if we feel sure that the airway is easy.
If the airway looks difficult and it's an emergency then you can make a good case for NG before induction.
You always have to remember that people can still aspirate even with an NG tube in place.
2- I can't think of a logical reason for putting an NG tube in a patient who is undergoing elective surgery just because they had a sandwich on the way to the hospital, NG tubes can not suction cheese burger.
They need to wait.
3- VQ mismatch means you have an increased number of normally ventilated alveoli that are not receiving blood flow.
This means decreased number of alveoli available for gas exchange and it means if the cardiac output remains constant it will take longer to achieve a certain concentration of vapor in the blood because a smaller percentage of the cardiac output is passing through the alveoli during a given period of time.
Does that make sense?

sevo1981 · Jul 23, 2008

Planktonmd said:
3- VQ mismatch means you have an increased number of normally ventilated alveoli that are not receiving blood flow.
This means decreased number of alveoli available for gas exchange and it means if the cardiac output remains constant it will take longer to achieve a certain concentration of vapor in the blood because a smaller percentage of the cardiac output is passing through the alveoli during a given period of time.
Does that make sense?

Thanks so much for all the help! I still don't think I understand though. It makes sense that increased V/Q mismatch decreases conc of anesthetic in the blood. However, does that not mean that it increases the conc of anesthetic in the alveoli? And is the speed of induction not related to alveolar conc and how soon it approaches inspired conc (the same reason why low cardiac output state have FASTER induction). I am missing something big...
Thanks again for all the help!

KungPOWChicken · Jul 23, 2008

Your dead space ventilation is increased when you have a high v/q mismatch. Therefore your ventilation of effective alveoli is decreased and your effective minute ventilation directly influences your speed of induction

toughlife · Jul 23, 2008

sevo1981 said:
Hi everyone. I am a longtime lurker but now a first time poster (just figured out how to do this... sad but true . I am a new CA-1 and LOVING IT! There are however a LOT of things that don't make sense. Hopefully they will start making sense soon, but in the meantime, I thought this might be a great place to ask some of the "stupid" questions we don't otherwise ask. I'll start with a few.

1. Why don't we do OG/NG suction before RSI if "full stomach" is such a big deal (or do we?????)

2. If the surgery is small and the patient ate something before showing up to the hospital, why don't we just decompress the stomach and move on? (not a good idea for big abd surgeries I understand...)

3. The Lange book talks about how increasing V/Q mismatch leads to slower induction. I thought that increased V/Q mismatch would lead to a higher alveolar conc of anesthetic (since less will be taken up by the pulm circulation) and thus faster induction?

As you can tell, I have a lot to learn. You guys have all helped me a lot already and I want to thank you in advance for the continued support.

DUDE! Where do volatile anesthetic agents act? and YES you are missing something BIG. What are they teaching you in residency?

Bertelman · Jul 23, 2008

sevo1981 said:
Thanks so much for all the help! I still don't think I understand though. It makes sense that increased V/Q mismatch decreases conc of anesthetic in the blood. However, does that not mean that it increases the conc of anesthetic in the alveoli? And is the speed of induction not related to alveolar conc and how soon it approaches inspired conc (the same reason why low cardiac output state have FASTER induction). I am missing something big...
Thanks again for all the help!

I think what you are missing is that the lungs are not the site of action for inhaled anesthetics. In V/Q mismatch, the alveoli reach steady state quicker because gas exchange is not happening, i.e. no agent is making it to the brain.

pgg · Jul 23, 2008

sevo1981 said:
Thanks so much for all the help! I still don't think I understand though. It makes sense that increased V/Q mismatch decreases conc of anesthetic in the blood. However, does that not mean that it increases the conc of anesthetic in the alveoli? And is the speed of induction not related to alveolar conc and how soon it approaches inspired conc (the same reason why low cardiac output state have FASTER induction). I am missing something big...
Thanks again for all the help!

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).

Ender · Jul 24, 2008

pgg said:
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).

I was also not clear on this point. Thanks for your help. This is the best explanation that I have either heard or read.

Ender

toughlife · Jul 24, 2008

pgg said:
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).

If you know that, then you can explain everything else without thinking too hard.

sevo1981 · Jul 24, 2008

pgg said:
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).

Thank you SO MUCH! That really helps. No one has been able to explain it this clearly before. Thanks!

epidural man · Aug 4, 2008

sevo1981 said:
1. Why don't we do OG/NG suction before RSI if "full stomach" is such a big deal (or do we?????)

2. If the surgery is small and the patient ate something before showing up to the hospital, why don't we just decompress the stomach and move on? (not a good idea for big abd surgeries I understand...)

Some would argue that having an NG in place increases risk of aspiration as it stents open the LES. In a SBO case, the patient will often have an NG in place. It may be a prudent thing to suck on it a bunch before induction, then remove it before you put them to sleep.

In the pyloric stenotic kids, some guys stick the OG, suck, remove, replace, suck, remove....several times before proceeding.

toughlife said:
DUDE! Where do volatile anesthetic agents act? and YES you are missing something BIG. What are they teaching you in residency?

That's a little harsh......

toughlife · Aug 4, 2008

epidural man said:
Some would argue that having an NG in place increases risk of aspiration as it stents open the LES. In a SBO case, the patient will often have an NG in place. It may be a prudent thing to suck on it a bunch before induction, then remove it before you put them to sleep.

In the pyloric stenotic kids, some guys stick the OG, suck, remove, replace, suck, remove....several times before proceeding.

That's a little harsh......

I know it was harsh and that was the point. I personally believe we need to ensure all residents are learning and learning well. I think our standards and expectations are lower than other specialites and we allow a lack of knowledge and understanding to go on, as long as a resident's technical skills are sufficient to do a case.
That is a great disservice and I make it a point to teach the junior residents to have high expectation of themselves and work hard to learn and showcase their knowledge as the physicians they are.

Otherwise, we are creating yet another generation of stool sitters who are no different than a CRNA.

If you don't know something, go sit down for 30min to an hour and crack a book open and read about it.

You hve to have pride in what you do and what you know. I look to cardiology fellows for inspiration as I see them as very knowledgeale, capable physicians who work hard to learn their craft well.

That is how we need to be. It's time we raise the bar a little and ensure some quality control.

pgg · Aug 4, 2008

toughlife said:
It's time we raise the bar a little and ensure some quality control.

You're right. Every time I run into a med student who wants to "do gas" 'cause it's such a cush life I want to roll him up in a carpet and throw him off a bridge. I think our boards need to be harder and our residencies less stool-oriented.

But I'm not sure how anonymous sarcasm over an internet forum furthers that goal. You're not going to shame someone into reading more, working harder, or just "getting" a concept, the way you might be able to do in person.

The alternative (teaching them something) is more likely to be helpful, and better aligned with the spirit of this forum.

I'm not sure where we should draw the line between spoon feeding trivial information and explaining more difficult or counter-intuitive concepts, but I'm inclined to give the benefit of the doubt to the guy asking the question. It can't all be politics, guns, poker, and alcohol.

sevo1981 · Aug 4, 2008

Thanks for all the help so far. I've been thinking about this and even talking to others. But one question that still remains... yes, gas acts on the brain and is carried there by blood. So why does a high solubility in blood lower the speed of induction? As always, thanks in advance.

loveumms · Aug 4, 2008

pgg said:
You're right. Every time I run into a med student who wants to "do gas" 'cause it's such a cush life I want to roll him up in a carpet and throw him off a bridge. I think our boards need to be harder and our residencies less stool-oriented.

I don't know about making the boards harder. This years in-service exam seemed pretty tough. I do wish that we got more experience with managing multiple rooms in residency. We don't do that, or run the board, at my residency and I'm already worried that when I get out I won't be proficient at either.

drRumi · Aug 4, 2008

toughlife said:
[/B]

I know it was harsh and that was the point. I personally believe we need to ensure all residents are learning and learning well. I think our standards and expectations are lower than other specialites and we allow a lack of knowledge and understanding to go on, as long as a resident's technical skills are sufficient to do a case.
That is a great disservice and I make it a point to teach the junior residents to have high expectation of themselves and work hard to learn and showcase their knowledge as the physicians they are.

Otherwise, we are creating yet another generation of stool sitters who are no different than a CRNA.

If you don't know something, go sit down for 30min to an hour and crack a book open and read about it.

You hve to have pride in what you do and what you know. I look to cardiology fellows for inspiration as I see them as very knowledgeale, capable physicians who work hard to learn their craft well.

That is how we need to be. It's time we raise the bar a little and ensure some quality control.

yea Sevo1981, your such a dumb ***** for asking a question.

i know your a CA1 and all...but damn it...dont be such an idiot as to ask a question. be like toughlife...dont ask questions. he has pride and never asked a question when he was a CA1 ever. when you got a question go read a book. upper residents and attendings are not here to answer your "dumb questions".

pgg · Aug 4, 2008

loveumms said:
I don't know about making the boards harder. This years in-service exam seemed pretty tough.

10-15% of takers nationwide pass the thing after their CA-1 year. I guess it's possible that 1 in 7 people are super-geniuses. It just seems odd to me that being able to pass the exam 1/3 of the way through your training is so common ... it makes me suspicious that the bar isn't set high enough.

nutmegs · Aug 4, 2008

toughlife said:
[/B]

I know it was harsh and that was the point. I personally believe we need to ensure all residents are learning and learning well. I think our standards and expectations are lower than other specialites and we allow a lack of knowledge and understanding to go on, as long as a resident's technical skills are sufficient to do a case.
That is a great disservice and I make it a point to teach the junior residents to have high expectation of themselves and work hard to learn and showcase their knowledge as the physicians they are.

Otherwise, we are creating yet another generation of stool sitters who are no different than a CRNA.

If you don't know something, go sit down for 30min to an hour and crack a book open and read about it.

You hve to have pride in what you do and what you know. I look to cardiology fellows for inspiration as I see them as very knowledgeale, capable physicians who work hard to learn their craft well.

That is how we need to be. It's time we raise the bar a little and ensure some quality control.

Seriously? Chill out. I don't think the first 4 weeks of residency is really the time or place to rag on someone (who is actively trying to learn) for asking ANY question, no matter how "dumb". You are doing nothing to create an open or helpful environment. Consider not posting next time. I plan on asking all the "dumb" questions I have, so get ready.

aredoubleyou · Aug 4, 2008

pgg said:
10-15% of takers nationwide pass the thing after their CA-1 year. I guess it's possible that 1 in 7 people are super-geniuses. It just seems odd to me that being able to pass the exam 1/3 of the way through your training is so common ... it makes me suspicious that the bar isn't set high enough.

One would infer that you therefore believe that
A) a standardized multiple choice exam is a reliable enough tool to confirm that a graduate has sufficient medical knowledge to practice safely, which if flunked can significantly change ones career.

and
B) there should be an inherent flunk rate (as in fact there is with most all standardized tests)

I think the gate keeper should be entrance into residency, not a single exam at the end of residency.

dfk · Aug 4, 2008

toughlife said:
[/B]

I know it was harsh and that was the point. I personally believe we need to ensure all residents are learning and learning well. I think our standards and expectations are lower than other specialites and we allow a lack of knowledge and understanding to go on, as long as a resident's technical skills are sufficient to do a case.
That is a great disservice and I make it a point to teach the junior residents to have high expectation of themselves and work hard to learn and showcase their knowledge as the physicians they are.

Otherwise, we are creating yet another generation of stool sitters who are no different than a CRNA.

If you don't know something, go sit down for 30min to an hour and crack a book open and read about it.

You hve to have pride in what you do and what you know. I look to cardiology fellows for inspiration as I see them as very knowledgeale, capable physicians who work hard to learn their craft well.

That is how we need to be. It's time we raise the bar a little and ensure some quality control.

dude, i'm not here to ruffle feathers, but what is your impression of CRNAs?
totally hatin' in my understanding.

again, you must not think that people other that docs can think for themselves.

you seem as impersonable as you appear...

epidural man · Aug 4, 2008

aredoubleyou said:
One would infer that you therefore believe that
A) a standardized multiple choice exam is a reliable enough tool to confirm that a graduate has sufficient medical knowledge to practice safely, which if flunked can significantly change ones career.

and
B) there should be an inherent flunk rate (as in fact there is with most all standardized tests)

I think the gate keeper should be entrance into residency, not a single exam at the end of residency.

epidural man · Aug 4, 2008

sevo1981 said:
Thanks for all the help so far. I've been thinking about this and even talking to others. But one question that still remains... yes, gas acts on the brain and is carried there by blood. So why does a high solubility in blood lower the speed of induction? As always, thanks in advance.

A gas molecule dissolved in blood that likes to stay dissolved (high solubility) will stay dissolved and not leave the blood in areas of lesser concentration so readily (ie..the brain).

I'm sure that is an over-simplification, but that is how i think of it.

Planktonmd · Aug 4, 2008

sevo1981 said:
Thanks for all the help so far. I've been thinking about this and even talking to others. But one question that still remains... yes, gas acts on the brain and is carried there by blood. So why does a high solubility in blood lower the speed of induction? As always, thanks in advance.

If a vapor is highly soluble then achieving equilibrium is slower since a higher percentage is going to dissolve in the blood and in the CNS and a higher percentage is being eliminated simultaneously.
While an agent with low solubility will achieve equilibrium much faster between the 3 compartments (Alveoli, Blood and CNS) because a smaller percentage is going to dissolve.
Achieving equilibrium is what defines a certain level of anesthesia.

cleansocks · Aug 4, 2008

sevo1981 said:
Thanks for all the help so far. I've been thinking about this and even talking to others. But one question that still remains... yes, gas acts on the brain and is carried there by blood. So why does a high solubility in blood lower the speed of induction? As always, thanks in advance.

(<-- disclaimer: medical student) I've had to think about this all recently too.

To directly answer the question above as I see it, blood acts as a reservoir for the anesthetic agent. If it's more soluble in blood, the anesthetic won't be able to exit the blood as easily when it reaches the brain. Similar concept to oxygen dissociation curve for Hgb - you can oxygenate tissues better when the oxygen can leave the Hgb more easily at the level of the tissue.

The confusing part: Unlike Hgb which has high affinity for O2 in the lungs (getting it into the blood) and low affinity for O2 at the tissues (getting it out of the blood), there is no such curve for anesthetic agents. An anesthetic agent with a high blood-gas partition coefficient (high blood solubility) gets sucked out of the lungs into the blood easily, which theoretically could speed induction, but then it's held onto by the blood more strongly, which theoretically could slow induction. So why isn't it a wash?

The one answer I can think of again analogizes Hgb-O2. When someone is at high altitutude and needs to have MORE O2, what increases? 2,3-BPG, which reduces binding affinity between Hgb and O2. This suggests that the effect of blood preventing an agent from leaving into tissues (ie anesthetic to brain, O2 to tissues) is much more important than the effect of blood being better able to suck in a substance from the lungs.

[confusing thing I just thought of: This concept also supports the reason that increasing CO slows induction. If you increase the amount of blood rushing by the lung, the gas will diffuse into a larger volume of blood, thus there will be a smaller concentration of gas per unit of blood. Thus the gas has a hard time reaching that concentration in blood necessary to "bubble" OUT of it into the brain. But if you think about it, if there is a smaller concentration of the gas in the blood, shouldn't the gas diffuse FASTER from the lung into the blood? Again it COULD be a wash, but the effect of the gas having a hard time ESCAPING from the blood is much stronger than the effect of the gas having an easier time diffusing into the lung, thus slower induction occurs.]

Planktonmd · Aug 4, 2008

cleansocks said:
(<-- disclaimer: medical student) I've had to think about this all recently too.

To directly answer the question above as I see it, blood acts as a reservoir for the anesthetic agent. If it's more soluble in blood, the anesthetic won't be able to exit the blood as easily when it reaches the brain. Similar concept to oxygen dissociation curve for Hgb - you can oxygenate tissues better when the oxygen can leave the Hgb more easily at the level of the tissue.

The confusing part: Unlike Hgb which has high affinity for O2 in the lungs (getting it into the blood) and low affinity for O2 at the tissues (getting it out of the blood), there is no such curve for anesthetic agents. An anesthetic agent with a high blood-gas partition coefficient (high blood solubility) gets sucked out of the lungs into the blood easily, which theoretically could speed induction, but then it's held onto by the blood more strongly, which theoretically could slow induction. So why isn't it a wash?

The one answer I can think of again analogizes Hgb-O2. When someone is at high altitutude and needs to have MORE O2, what increases? 2,3-BPG, which reduces binding affinity between Hgb and O2. This suggests that the effect of blood preventing an agent from leaving into tissues (ie anesthetic to brain, O2 to tissues) is much more important than the effect of blood being better able to suck in a substance from the lungs.

[confusing thing I just thought of: This concept also supports the reason that increasing CO slows induction. If you increase the amount of blood rushing by the lung, the gas will diffuse into a larger volume of blood, thus there will be a smaller concentration of gas per unit of blood. Thus the gas has a hard time reaching that concentration in blood necessary to "bubble" OUT of it into the brain. But if you think about it, if there is a smaller concentration of the gas in the blood, shouldn't the gas diffuse FASTER from the lung into the blood? Again it COULD be a wash, but the effect of the gas having a hard time ESCAPING from the blood is much stronger than the effect of the gas having an easier time diffusing into the lung, thus slower induction occurs.]

Because solubility works both ways: into the brain and out of the brain a highly soluble agent will take longer to reach equilibrium (entering and exiting at a higher rate).
Equilibrium is what defines the anesthetic level.

pgg · Aug 4, 2008

aredoubleyou said:
One would infer that you therefore believe that
A) a standardized multiple choice exam is a reliable enough tool to confirm that a graduate has sufficient medical knowledge to practice safely, which if flunked can significantly change ones career.

I think most would agree that a written exam of some kind is both appropriate and necessary to guarantee a minimum level of knowledge.

My discomfort with the existing system stems not from the failure rate, but the pass rate after just 1/3 of training. These aren't occasional outliers - we're talking >10%.

And not to be too callous, but I would certainly hope that repeated failures to demonstrate a minimum level of knowledge would significantly change one's career, in the direction of not practicing in a risky field of medicine.

aredoubleyou said:
B) there should be an inherent flunk rate (as in fact there is with most all standardized tests)

What's the alternative? No standardized testing?

aredoubleyou said:
I think the gate keeper should be entrance into residency, not a single exam at the end of residency.

I disagree. Admittedly, this is just one study ...

http://www.anesthesia-analgesia.org/cgi/content/full/100/2/502

But this image illustrates two things very well: http://www.anesthesia-analgesia.org/content/vol100/issue2/images/large/36FF1.jpeg

First, that the gatekeepers who select residents are no better than random chance in determining who will be successful residents.

Second, the data suggest that they're a bunch of wusses who are so very reluctant to rate a resident as anything other than "above average" that every single resident winds up with a score in an incredibly narrow range on their 9 point scale. It appears the gatekeepers-turned-evaluators aren't any good at stratification once residency starts, either. The graph of ITE scores is the only one that even slightly resembles objective data. (They have two residents who score in what appears to be the 1st percentile, yet NO residents ever got a subjective score less than a 6 in any area?)

I'm curious what the pass rate is for other specialties 1 year into their 3 or 4 year programs. Maybe every field sees 10-15% (or more) pass a couple years early, and I'm reading too much into the anesthesiology stats.

dillpickles · Aug 5, 2008

I am curious who make toughlife the God of appropriate questions?

Relax tough life, don't we all do the CA-1 year? Or did you skip CA-1?

To the poster - keep on reading and asking questions! Good luck with CA-1 year!

sevo1981 · Aug 5, 2008

Thanks you guys - you have helped tremendously. I really appreciate all the support and understanding. Back to books now (I have been wasting too much time on this board

Thanks again

toughlife · Aug 5, 2008

dfk said:
dude, i'm not here to ruffle feathers, but what is your impression of CRNAs?
totally hatin' in my understanding.

again, you must not think that people other that docs can think for themselves.

you seem as impersonable as you appear...

I think by now you should know why I say what I say. My stand on CRNAs has been the same it was since I first learned about them..especially how committed they are to eradicating anesthesiology and their deliberate and relentless attacks on the specialty via legislative and deceiving campaigns.

How do you expect us to react when the main goal of your organization is to do away with physicians in this specialty and replace them by lesser trained, less educated providers who purport to be equal to physicians in all aspects.

Do you expect residents and anesthesiologists to take this lightly?

If I seem aggressive, mean and relentless towards you and others like yourself, now you know why.

radslooking · Aug 6, 2008

pgg said:
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).

without reading the rest of the thread, and seeing what others wrote, this is an excellent post pgg. Truly worthy of being in a chapter or book. somebody should sticky this.

radslooking · Aug 6, 2008

pgg said:
I think most would agree that a written exam of some kind is both appropriate and necessary to guarantee a minimum level of knowledge.

My discomfort with the existing system stems not from the failure rate, but the pass rate after just 1/3 of training. These aren't occasional outliers - we're talking >10%.

And not to be too callous, but I would certainly hope that repeated failures to demonstrate a minimum level of knowledge would significantly change one's career, in the direction of not practicing in a risky field of medicine.

What's the alternative? No standardized testing?

I disagree. Admittedly, this is just one study ...

http://www.anesthesia-analgesia.org/cgi/content/full/100/2/502

But this image illustrates two things very well: http://www.anesthesia-analgesia.org/content/vol100/issue2/images/large/36FF1.jpeg

First, that the gatekeepers who select residents are no better than random chance in determining who will be successful residents.

Second, the data suggest that they're a bunch of wusses who are so very reluctant to rate a resident as anything other than "above average" that every single resident winds up with a score in an incredibly narrow range on their 9 point scale. It appears the gatekeepers-turned-evaluators aren't any good at stratification once residency starts, either. The graph of ITE scores is the only one that even slightly resembles objective data. (They have two residents who score in what appears to be the 1st percentile, yet NO residents ever got a subjective score less than a 6 in any area?)

I'm curious what the pass rate is for other specialties 1 year into their 3 or 4 year programs. Maybe every field sees 10-15% (or more) pass a couple years early, and I'm reading too much into the anesthesiology stats.

I have to disagree with you here.

First of all, the data showed that nearly all of the people picked for Pitt's program were "successful" residents. What the committee didn't show is that it could deliniate between these 'successful' residents who performed slightly higher or lower. What the process may have done was exclude well those who clearly would underperform. So perhaps the process isn't as bad as you think. (They did not test for this, they basically just said almost all applicants were successful...which may also be a reason why they are bunched up in their assessments of the residents)

I don't think that 10-15 % is unusual at all. You never know who's had prior experience in other fields, had more exposure to difficult cases in ca-1, or who is just plain damn smart and reads a ton.

pgg · Aug 6, 2008

radslooking said:
I have to disagree with you here.

First of all, the data showed that nearly all of the people picked for Pitt's program were "successful" residents. What the committee didn't show is that it could deliniate between these 'successful' residents who performed slightly higher or lower. What the process may have done was exclude well those who clearly would underperform. So perhaps the process isn't as bad as you think. (They did not test for this, they basically just said almost all applicants were successful...which may also be a reason why they are bunched up in their assessments of the residents)

I don't know, the ITE scores they reported were all over the place (from 1st to 98th+ percentiles). 13 of 19 scored over the national mean so it's probably a pretty strong program. But two failed it spectacularly (looks like 1st percentile) and yet neither of those residents ever got a score less than about 6 on any of the subjective evals (one of which is "knowledge"). This suggests to me that however they're coming up with their subjective eval scores, they're not very good at picking out the ones lacking a knowledge base.

Therefore, I'm skeptical that these "gatekeepers to residency" would be superior (alone) to the written/oral boards when it comes to detecting a knowledge-weak candidate for BC. Especially when you consider there may be some secondary gain to polishing their poor residents (flunking someone makes the program look bad).

I think it's very possible to be a good resident who works hard in the hospital, is reliable, has good monkey skills, and can manage most cases in a reasonable manner, all without reading much or acquiring and applying the knowledge that sets us apart from CRNAs. This is where written & oral boards come in, and I think the bar should be set high. How high ... I don't know.

radslooking said:
I don't think that 10-15 % is unusual at all. You never know who's had prior experience in other fields, had more exposure to difficult cases in ca-1, or who is just plain damn smart and reads a ton.

Good point. Anesthesia gets a lot of people doing second residencies and (these days) an above-average cut of applicants in general.

aredoubleyou · Aug 6, 2008

pgg said:
What's the alternative? No standardized testing?

.

I dont have a good answer. I can say that determining that one person is qualified and another person is not qualified to be a consultant in anesthesia based on a multiple choice exam with a fixed fail rate is inherently nonsense - its not measuring against a yard stick, its a moving target that a certain percent will have to fail to make the test valid.

There is almost certainly no way around standardized testing, as subjective evaluations are not only subjective but can have alterior motives as well. But it would be nice (perhaps impossible) to make the exam process compose of multiple exams which assess a safe level of knowledge to practice independently (how the bar is set is a whole different debate) which can be taken repeatedly (within reason) with no inherent flunk rate. This is simmilar to the way we learn and are assessed on procedures - there is not single intubation at the end of residency that you have to hit or you fail and have to wait another year to pass, for example

Regardless, before I ramble on more, its clear that the current standardized test model of normal distributions and inherent flunk rates will not change in the near future.

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