Poor Studies drive me nutz

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Noyac

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How does a pre-op dose of metoprolol give you less one year MI and more stokes? Physiologically i'm lost.
Did you see the dose?
For the blinded trial, Devereaux randomized 8,351 patients undergoing noncardiac surgery to beta blockadeor placebo. The former received 100 mg of the drug 2-4 hours before surgery and at 6 hours post-operation; starting on post-surgery day 1, the beta blocker group then received 200 mg daily for 30 days, with patients who became hypotensive or bradycardic getting a halved dose.

****, I would be hypotensive and Bradycardic even at half the dose they gave. It’s a stupid study. I’d love to hear these guys defend it.
 
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YES! YES a thousand times YES!
when i signed up for this forum, i was expecting more threads like this.

It's like the scientific method and logical thinkings becomes optional once you specialize in a field.... low level of evidence in the form of expert opinion guides so much of what we practice. It feels like the literature is written by people who barely care about the truth and care more about high impact article and getting published....

Btw has anyone ever read the evidence/rationale on using norepi as the first line pressor in sepsis, suspect at best and laughable IMO.
 
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This has nothing to do with the thread but the title made me do it!

Cowboys' butts drive me nuttttsss.

Sorry.

I couldn't help myself.
 
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The dose is too high for sure, but they did use metoprolol succinate which is approx 2 to 3x more potent than metop tartrate as I recall and depending on the source you read.
So that would make the equivalent bid dose at metop 50mg bid etc
 
Btw has anyone ever read the evidence/rationale on using norepi as the first line pressor in sepsis, suspect at best and laughable IMO.
Can you summarise it a bit? I always thought norepi was a solid choice?
 
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Can you summarise it a bit? I always thought norepi was a solid choice?

The rationale was essentially borne not from the fact that norepi is particularly wonderful, but more from the fact that dopamine (the former standard of care) is actually garbage. I would not hesitate to go first line to epi in a patient whom I suspected had late, decompensated low-output septic shock.


Vasopressors for septic shock

Why Norepinephrine (Levophed) for Septic Shock Instead of Other Vasopressors?

Norepinephrine (Levophed)
is favored as the first-line vasopressor for septic shock in the Surviving Sepsis Guidelines (Grade 1B). Norepinephrine increases mean arterial pressure primarily through vasoconstriction, with little effect on heart rate, stroke volume, and cardiac output; dopamine increases MAP primarily through an increase in cardiac output (by increasing both heart rate and stroke volume). These characteristics make dopamine more likely than norepinephrine to cause potentially harmful tachyarrhythmias.

Norepinephrine and dopamine have been compared directly in at least 6 randomized trials, and less directly in meta-analyses. The Surviving Sepsis Campaign's own (unpublished) pooled analysis of these trials showed a relative risk for death of 0.91 (0.83-0.99) with the use of norepinephrine compared to dopamine as vasopressor therapy for septic shock. A 2012 meta-analysis including randomized and observational trials also concluded dopamine brings an increased risk for death compared with Levophed as a first-line vasopressor for septic shock.

Epinephrine is suggested as the next-line vasopressor after norepinephrine for septic shock, to be added or substituted if norepinephrine is inadequate (Grade 2B). Epinephrine has been compared to norepinephrine in at least 4 randomized trials, with no increase in the risk for death. Epinephrine may increase lactate concentrations by stimulating skeletal muscles' aerobic metabolism, thereby interfering with the use of lactate as a marker of perfusion during treatment of septic shock.

Phenylephrine can decrease stroke volume and is recommended to not be used except as salvage therapy, in known high cardiac output states, or if norepinephrine has caused tachyarrhythmias (Grade 1C).

Vasopressin (or its analogue terlipressin) has been compared to norepinephrine as a vasopressor for septic shock in 9 randomized trials (n=963); vasopressin / terlipressin carried a (non-significant) increased risk of death (albeit a lower risk of tachyarrhythmias) compared to norepinephrine.
 
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The dose is too high for sure, but they did use metoprolol succinate which is approx 2 to 3x more potent than metop tartrate as I recall and depending on the source you read.
So that would make the equivalent bid dose at metop 50mg bid etc
Still too high!!!
 
Perioperative Beta Blockers Trade Fewer MIs for More Deaths

The POISE Trial is just one of these studies that make no sense and actually have great potential to harm pts.
Most of what we call medical "research" would be treated like a joke in any serious mathematics/statistics circles. Beginning with that p(ee) value.

It's just another form of alchemy, but one that looks great on the CV, and with a lot of industrial complex money behind it. Scientifically, it's mostly the blind leading the blind, bull feces disguised as science.
 
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YES! YES a thousand times YES!
when i signed up for this forum, i was expecting more threads like this.

It's like the scientific method and logical thinkings becomes optional once you specialize in a field.... low level of evidence in the form of expert opinion guides so much of what we practice. It feels like the literature is written by people who barely care about the truth and care more about high impact article and getting published....

Btw has anyone ever read the evidence/rationale on using norepi as the first line pressor in sepsis, suspect at best and laughable IMO.
One of the greatest things CCM has taught me is that studies are good mostly for giving me ideas to try (or avoid). Every patient is different. Rigid protocols are for uneducated people, or for lack of a better idea.

Unfortunately, we have this idiotic concept of "standard of care", which is based on "guidelines", which are based exactly on the BS we are criticizing here. That's why I start with the "standard of care", prove it useless, then go to what I think the particular patient's physiology actually needs and will respond to.
 
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The dose is too high for sure, but they did use metoprolol succinate which is approx 2 to 3x more potent than metop tartrate as I recall and depending on the source you read.
So that would make the equivalent bid dose at metop 50mg bid etc

No, it's clinically the same. So you would go from metop 50 bid to succinate 100 qd. Either way, starting at 100 in a beta blocker naive patient is just asking for an assassination.
 
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Wasn't the POISE trial 10 years ago?

And now they are reporting 1 year follow up? Should be 10 year follow up by now.

Very weird.


That trial always brings this to mind:
 
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Can you summarise it a bit? I always thought norepi was a solid choice?

The rationale was essentially borne not from the fact that norepi is particularly wonderful, but more from the fact that dopamine (the former standard of care) is actually garbage. I would not hesitate to go first line to epi in a patient whom I suspected had late, decompensated low-output septic shock.

I stepped away for a bit. But vector covered this pretty well. Also as @FFP said, first line agent should be dependent on the patient being treated, not norepi by default. Why would we have a "first line agent" when the patient we are taking care isn't "standard". What is the point of a first line agent when the first line agent depends on the patient? These "first line agents" are dumbing down medicine into a cookbook, yet it's on the tip of everyone's tongue because having a default feels really comfortable.

Also i have a rant about vasopressin if you go in the private forum and look at the thread i started.

To add more about this discussion, the concept of recommendations also does not breed critical thinking.

To review, the whole idea of recommendations is as follows:

Recommendation grades
1. Strong recommendation: Benefits clearly outweigh the risks and burdens (or vice versa) for most, if not all, patients
2. Weak recommendation: Benefits and risks closely balanced and/or uncertain

Evidence grades
A. High-quality evidence: Consistent evidence from randomized trials, or overwhelming evidence of some other form
B. Moderate-quality evidence: Evidence from randomized trials with important limitations, or very strong evidence of some other form
C. Low-quality evidence: Evidence from observational studies, unsystematic clinical observations, or from randomized trials with serious flaws



In evidence-based medicine, expert recommendation is literally the lowest level of evidence available:

aWjvyZe.jpg


As such, the concept of a 1C recommendation baffles me:
1. Strong recommendation: Benefits clearly outweigh the risks and burdens (or vice versa) for most, if not all, patients
+
C. Low-quality evidence: Evidence from observational studies, unsystematic clinical observations, or from randomized trials with serious flaws

How can the benefit clearly outweigh the risk if we DON'T HAVE ANY GOOD Evidence to say so?
To me, this is saying we have very ****ty evidence, so we are gonna give "a recommendation" to it so we can back up ****ty evidence with the lowers form of evidence...
 
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Most of what we call medical "research" would be treated like a joke in any serious mathematics/statistics circles. Beginning with that p(ee) value.

It's just another form of alchemy, but one that looks great on the CV, and with a lot of industrial complex money behind it. Scientifically, it's mostly the blind leading the blind, bull feces disguised as science.

YES! THIS!

To given the whole picture, the reason why some of our science doesn't pass the rigor of the scientific method is that we often don't have enough resources to get good evidence.

However, we seem to forget when we were taught to be good scientists:

if we don't have any good evidence, we DO NOT RUSH to conclusions.
But not making a conclusion or publishing a negative study isn't sexy in academia. It doesn't get people tenure...

Next thing we know, if we don't have any good evidence, we hold on tighter to the bad evidence and incomplete picture, then entrench our decision in them.

Norepi is an excellent example: we know it's better than dopamine, so we uphold it as the best possible. But just as @vector2 broke it down, those other pressors are not any worse by evidence and all have their uses in specific patients. But how many ICU docs do you know doesn't go to norepi as default because of an expert opinion? and how many people avoid phenylephrine because of this 1C recommendation?
 
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I hesitate to enter into a conversation in a field that is clearly beyond me at this time (starting medical school this fall), but I’ve come to medicine after completing an advanced degree in the natural sciences. I just wanted to chime in from that perspective: while I would hardly consider myself a good statistician, I have found much medical research to be less than robust.

In any case, I love reading the opinions in this forum. Following my stint in the sciences, I’ve worked for the past few years as a paramedic. Despite regular exposure to emergency medicine, I find anesthesiology to be extremely interesting. Keep up the great conversations and case discussions!
 
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YES! THIS!
Norepi is an excellent example: we know it's better than dopamine, so we uphold it as the best possible. But just as @vector2 broke it down, those other pressors are not any worse by evidence and all have their uses in specific patients. But how many ICU docs do you know doesn't go to norepi as default because of an expert opinion? and how many people avoid phenylephrine because of this 1C recommendation?
Not that I am such a genius, but my default is phenylephrine, for the simple reason that I don't put in central lines easily. The patient has to "prove" to me that he needs one. Also, there have been studies where phenylephrine+esmolol didn't have a worse outcome than norepi. And it makes physiologic sense. Where phenylephrine hurts is in the patient with serious heart disease.

I am sure there are many other intensivists whose decisions are not knee-jerk, but adaptive, based on the specific patient's physiology and best interests. I was educated by some of these free thinkers.

I am a strong believer in first do no harm, and that 50% of medicine is bull****, we just don't know which 50%. So I have become a minimalist, and my ICU prophylaxis list doesn't include just SC heparin etc., but also avoiding any iatrogenic complications.

It is indeed not easy, because a lot of bad science has become dogma. Every time I take a step off the beaten path, I have to explain it to the "team", convince some useless busybody "clinical" pharmacist or some surgeon with a god complex, and cover my behind in the notes. A lot of time wasted on convincing people with inferior knowledge and/or IQ (similar to malpractice trial jurors) that I know what I am doing and that it's in the patient's best interest. Especially if there is already some institutional protocol for stupid people in place.
 
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Good
Not that I am such a genius, but my default is phenylephrine, for the simple reason that I don't put in central lines easily. The patient has to "prove" to me that he needs one. Also, there have been studies where phenylephrine+esmolol didn't have a worse outcome than norepi. And it makes physiologic sense. Where phenylephrine hurts is in the patient with serious heart disease.

I am sure there are many other intensivists whose decisions are not knee-jerk, but adaptive, based on the specific patient's physiology and best interests. I was educated by some of these free thinkers.

I am a strong believer in first do no harm, and that 50% of medicine is bull****, we just don't know which 50%. So I have become a minimalist, and my ICU prophylaxis list doesn't include just SC heparin etc., but also avoiding any iatrogenic complications.

It is indeed not easy, because a lot of bad science has become dogma. Every time I take a step off the beaten path, I have to explain it to the "team", convince some useless busybody "clinical" pharmacist or some surgeon with a god complex, and cover my behind in the notes. A lot of time wasted on convincing people with inferior knowledge and/or IQ (similar to malpractice trial jurors) that I know what I am doing and that it's in the patient's best interest. Especially if there is already some institutional protocol for stupid people in place.
l
Not that I am such a genius, but my default is phenylephrine, for the simple reason that I don't put in central lines easily. The patient has to "prove" to me that he needs one. Also, there have been studies where phenylephrine+esmolol didn't have a worse outcome than norepi. And it makes physiologic sense. Where phenylephrine hurts is in the patient with serious heart disease.

I am sure there are many other intensivists whose decisions are not knee-jerk, but adaptive, based on the specific patient's physiology and best interests. I was educated by some of these free thinkers.

I am a strong believer in first do no harm, and that 50% of medicine is bull****, we just don't know which 50%. So I have become a minimalist, and my ICU prophylaxis list doesn't include just SC heparin etc., but also avoiding any iatrogenic complications.

It is indeed not easy, because a lot of bad science has become dogma. Every time I take a step off the beaten path, I have to explain it to the "team", convince some useless busybody "clinical" pharmacist or some surgeon with a god complex, and cover my behind in the notes. A lot of time wasted on convincing people with inferior knowledge and/or IQ (similar to malpractice trial jurors) that I know what I am doing and that it's in the patient's best interest. Especially if there is already some institutional protocol for stupid people in place.


Good luck trying to do anything out of the ordinary with the ICU nurses and their protocols. Using phenyl in a septic patient? "This isn't the standard of care! We need an Aline and central line!"
 
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Good

l



Good luck trying to do anything out of the ordinary with the ICU nurses and their protocols. Using phenyl in a septic patient? "This isn't the standard of care! We need an Aline and central line!"
Well I agree with in a lot of ways, we put in way too many central lines. But I think if a patient needs ICU they will definitely need an art line. So much easier to manage and trend.
And I don't think I would use phenyl in any form of septic patient. If you're septic to my mind you have a bad heart albeit temporarily.
 
Well I agree with in a lot of ways, we put in way too many central lines. But I think if a patient needs ICU they will definitely need an art line. So much easier to manage and trend.
And I don't think I would use phenyl in any form of septic patient. If you're septic to my mind you have a bad heart albeit temporarily.
While some patients may have a sepsis-associated cardiomyopathy (which can be ruled out easily with POCUS), many don't, especially those who would only need low-dose norepi (replaceable with phenylephrine).
 
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Well we're probably splitting hairs here and will never prove either side but I don't think pocus can prove or disprove a cardiomyopathy.

My opinion is purely based on the line of thought that if they're capillaries and vascular tree is leaky during sepsis, then something similiar probably is affecting the heart. A few negligible percent in more robust patients but higher in the weaker ones with cad etc.

Did someone say phenyl plus beta blockers in sepsis?? That doesn't make a lot of sense to me
 
Well we're probably splitting hairs here and will never prove either side but I don't think pocus can prove or disprove a cardiomyopathy.

My opinion is purely based on the line of thought that if they're capillaries and vascular tree is leaky during sepsis, then something similiar probably is affecting the heart. A few negligible percent in more robust patients but higher in the weaker ones with cad etc.

Did someone say phenyl plus beta blockers in sepsis?? That doesn't make a lot of sense to me

sepsis causes a vasodilatory shock. The effect on the heart is the necessary ramping up of the cardiac output to attempt to maintain MAP. Now some cardiac cripples don't exactly tolerate that tachycardic response but it's not from the sepsis, it's the innate disease of the heart itself.
 
Well we're probably splitting hairs here and will never prove either side but I don't think pocus can prove or disprove a cardiomyopathy.

My opinion is purely based on the line of thought that if they're capillaries and vascular tree is leaky during sepsis, then something similiar probably is affecting the heart. A few negligible percent in more robust patients but higher in the weaker ones with cad etc.

Did someone say phenyl plus beta blockers in sepsis?? That doesn't make a lot of sense to me
I did. Phenylephrine for SVR, and esmolol if the tachycardia is still not under control after the neo.

To me, excessive tachycardia is way more harmful in sepsis than phenylephrine.
 
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sepsis causes a vasodilatory shock. The effect on the heart is the necessary ramping up of the cardiac output to attempt to maintain MAP. Now some cardiac cripples don't exactly tolerate that tachycardic response but it's not from the sepsis, it's the innate disease of the heart itself.
Sepsis does produce a cardiomyopathy, which can be pretty severe in some patients, regardless of pre-existing heart disease.

However, I think @Newtwo is overestimating its incidence and impact.
 
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Big butz drive me nutz.
 
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To me, excessive tachycardia is way more harmful in sepsis than phenylephrine.

Why is this not discussed more? the fact that this is a novel concept to many is kinda tellin in how well we've explored our anesthestic or critical options.
 
Septic cardiomyopathy is a bull**** diagnosis.
 
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Why is this not discussed more? the fact that this is a novel concept to many is kinda tellin in how well we've explored our anesthestic or critical options.
I don't think the relationship between revving up the heart (especially in hypotension) and mortality is a novel concept, especially to anybody who understands a whiff of cardiac physiology. We know that beta-blockers are good for survival even in CHF, and this is just the opposite.

The reason phenylephrine is not used more widely is, as usual, dogma (i.e. guidelines, protocols and other BS synonymous with one size fits all). Because of defensive medicine, physicians have stopped "experimenting" on patients, while proper critical care (and not only) is exactly that: finding out what exactly works for that particular patient (trial and error). While cookbook medicine may be good for diseases where one cannot immediately measure the results of one's actions, or one has only one shot (e.g. oncology), it mostly doesn't make sense in most of anesthesiology or critical care, except if one wants to be average.

To me, "average" (i.e. standard of care) is synonymous with bad. Too many people don't get well in the "average" ICUs. The "average" ICU functions like a ward, instead of functioning like an ED or, even better, OR anesthesia. The average ICU patient is seen by the same intensivist maybe twice a day (if he's lucky), and has a lot of semi-amateurs with a say in his care. The sicker the patient, the less we should allow ourselves to be guided by protocols or the average "standard of care", and the more we should keep on trying and measuring what works and what doesn't for that particular patient, every hour of every day. The fact that we don't have PA catheters in most shocked patients anymore, and some are treated almost by ear, is exactly because of those average docs who had no idea how to use it properly, the same way nowadays many so-called intensivists don't even know how to do a focused bedside echo to answer a clinical question. The guidelines are for them, the people who know too little to be open-minded.
 
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The fact that we don't have PA catheters in most shocked patients anymore, and some are treated almost by ear, is exactly because of those average docs who had no idea how to use it properly, the same way nowadays many so-called intensivists don't even know how to do a focused bedside echo to answer a clinical question. The guidelines are for them, the people who know too little to be open-minded.

The reason we don't have PA catheters in all those patients anymore is not because nobody knew how to use them properly, it's because they provided so little additional benefit compared to the risks associated with them. If somebody is brilliant enough to properly use a swan, they are brilliant enough to not need it.
 
The reason we don't have PA catheters in all those patients anymore is not because nobody knew how to use them properly, it's because they provided so little additional benefit compared to the risks associated with them. If somebody is brilliant enough to properly use a swan, they are brilliant enough to not need it.
The benefits depend on the clinical question and the physician. If an intensivist does not know when and how to (not) use a PA catheter, obviously the risks will exceed the benefits (and since the average intensivist belongs to this group, this is what the studies showed). Putting a PA catheter in every septic shock or cardiac surgical patient is about as stupid as not putting it in anybody. For example, not putting a PA catheter in a critical patient with severe PHTN/right heart disease is almost incompetent, about as incompetent as giving fluids/pressors/inotropes based on PA numbers (see many cardiac surgeons even nowadays). The PAC in the ICU can be useful for gross CO/SVR monitoring purposes, especially if one doesn't have good echo windows/skills.

The problem with the average doc is that he's dogmatic and doesn't know the limits and pitfalls of his tools (the PAC is just one example of many). Hence the studies show that the PAC is "useless"; it's mostly the average doc's PAC use that's useless. As useless as, for example, drawing ABGs for base deficit-driven fluid resuscitation. Anyway, I am deviating off-topic here.

P.S. I am one of those "brilliant" docs who rarely needs a Swan. ;)
 
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The problem with the average doc is that he's dogmatic and doesn't know the limits and pitfalls of his tools (the PAC is just one example of many).

100% of physicians believe they are above average (or better) compared to their peers.
 
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100% of physicians believe they are above average (or better) compared to their peers.
I am sure it's something similar to the 93% of car drivers who think they are above average.

Except we do know our board exam percentiles and intensivists get to see each other's therapies and outcomes. ;)
 
100% of physicians believe they are above average (or better) compared to their peers.
I dont know about that statement. I feel I am an average physician when it comes to knowledge. I’m slightly above average in experience mostly because of the years that I’ve been at this.
 
I am sure it's something similar to the 93% of car drivers who think they are above average.

Except we do know our board exam percentiles and intensivists get to see each other's therapies and outcomes. ;)

I don't recall ever seeing anything except pass on the boards. While I assume I got 105% based on extra credit for sheer awesomeness, I have no proof of that.
 
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I'm so tired, I thought this thread said, "Poor students drive me nutz", and I was like wtf?!?!
 
I don't recall ever seeing anything except pass on the boards. While I assume I got 105% based on extra credit for sheer awesomeness, I have no proof of that.

Back in my day you got a % score on the BOARD exam and not just a pass. It was similar to the ITE where a % ranking is assigned to your score.
 
I don't recall ever seeing anything except pass on the boards. While I assume I got 105% based on extra credit for sheer awesomeness, I have no proof of that.

My ABA written exam result and keyword list letter says at the top

Your performance on the ABA written examination is reported as a standardized score on a benchmark scale with a mean of 250 and a
standard deviation of 50. A minimum score of 209 is required to pass the ABA written examination.

And then it lists my score. It doesn't include a percentile but if you're willing to do some handwaving and assume a normal distribution, you could calculate a percentile.

Of course, one of my keywords was "Std Deviation vs. std error calc" so maybe you shouldn't pay any attention to me on this.

Also ... "Ropivacaine stereochemistry" ... "Carbonic anyhydrase: locations" ... "Transplant donor: Hemodynamic mgmt" ... "Strong ion difference" ... it's a wonder I'm allowed to practice.
 
I distinctly remember the percentile being listed on my critical care board results. As in 100% sure. I am pretty sure the percentile was also on my anesthesia written board results, less sure about that though.
 
My ABA written exam result and keyword list letter says at the top



And then it lists my score. It doesn't include a percentile but if you're willing to do some handwaving and assume a normal distribution, you could calculate a percentile.

Of course, one of my keywords was "Std Deviation vs. std error calc" so maybe you shouldn't pay any attention to me on this.

Also ... "Ropivacaine stereochemistry" ... "Carbonic anyhydrase: locations" ... "Transplant donor: Hemodynamic mgmt" ... "Strong ion difference" ... it's a wonder I'm allowed to practice.
Well good thing you do your MOCA, so you can stop threatening patient safety with all those glaring knowledge deficiencies...;)
 
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I love Joe Dirt.

Whoever posted that clip...thanks....I need to watch that show again...maybe show to my kids....they need to experience Joe Dirt as well.

By the way, people are being very critical of studies in medicine.

Doing a good study in medicine is SOOOO difficult....and I don't know what all medical researchers are thinking when they do a study...but most are just trying their damndest to answer a question.

Also, since hierarchy of evidence was brought up...I just have to point out that meta-analysis is NEVER listed on respectable lists (like the one presented here). Level I is always large randomized trials, not "pooled data from a bunch of trials that are likely unrelated and can't be pooled (but let's jam the data together anyway....)"
 
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and I don't know what all medical researchers are thinking when they do a study...but most are just trying their damndest to answer a question.
Nope. Most just want to pad their resumes. Otherwise they would just recognize that they suck at it and stop.

This entire research hysteria would go away the second we would stop promoting people based on it. In the end, we are doctors, not researchers; our measure of success should be our outcomes. If in academia, it should be the quality of our lectures and bedside teaching. (Teachers are not evaluated based on what they publish.) But, hey, when the people running the show have padded resumes, don't teach, and are clinically unimpressive...
 
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Nope. Most just want to pad their resumes. Otherwise they would just recognize that they suck at it and stop.

This entire research hysteria would go away the second we would stop promoting people based on it. In the end, we are doctors, not researchers; our measure of success should be our outcomes. If in academia, it should be the quality of our lectures and bedside teaching. (Teachers are not evaluated based on what they publish.) But, hey, when the people running the show have padded resumes, don't teach, and are clinically unimpressive...

yes, several do to pad their resumes (think meta-analysis).

But FFP, try to come up with a good answer to a clinical question you have with a study....its really difficult.

And then when you do, people won't believe it anyway because they will pick the study apart.

I don't disagree with you, but I also love the line..."walk a mile in someone's shoes."

It's so easy to be critical of others actions....and that applies to everything in life really.
 
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yes, several do to pad their resumes (think meta-analysis).

But FFP, try to come up with a good answer to a clinical question you have with a study....its really difficult.

And then when you do, people won't believe it anyway because they will pick the study apart.

I don't disagree with you, but I also love the line..."walk a mile in someone's shoes."

It's so easy to be critical of others actions....and that applies to everything in life really.

I do not have a problem with not having good data and not knowing what the true best course of actions. One's ego truly has to be curbed to admit we don't have all the answers, specially since we've trained decades to be at our posts. We can still do tons of good with what we know now.

The problem arises when we guard what we were taught in residency or fellowship to be the absolute truths, anything else is blasphemy. That is the currently prevailing sentiment in most of academia, FFP and I both see that and that is why we are critical.

Furthermore, "let's not be critical of others bad practice because good practice is hard" is hardly a good sentiments towards improving patient care. People thinking this way are exactly what drives the current status quo.
 
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