Narrative Fallacy

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

Footnotes:

^ ^* This does ignore the obvious problem that both hyponatremia and hypocalcemia are fatal conditions, even though sodium and calcium are toxic. If only there were some kind of medical expert to explain cutting edge toxicology. Somebody like Paracelsus.

^ ¹ Zeno’s paradoxes
Wikipedia
Achilles and the tortoise
Article

^ ² Zeno’s paradoxes
Wikipedia
The dichotomy paradox
Article

^ ³ Thimerosal and the occurrence of autism: negative ecological evidence from Danish population-based data.
Madsen KM, Lauritsen MB, Pedersen CB, Thorsen P, Plesner AM, Andersen PH, Mortensen PB.
Pediatrics. 2003 Sep;112(3 Pt 1):604-6.
PMID: 12949291 [PubMed – indexed for MEDLINE]

Pediatrics has the free full text and free PDF available at their site.
Free Full Text Free PDF

Filed Under: Critical Judgment, EMS EduCast, Heresy, Narrative Fallacy, Science Tagged With: Critical Judgment, Education, Narrative Fallacy, Science

EMS EdUCast – Journal Club 2: Episode 43

Thu, 28 Jan 2010 20:35:00 -0500 by Rogue Medic

A week ago on the EMS EdUCast the topic was resuscitation. The big disagreement was about the IV vs No IV epinephrine study.^[1]

One of the criticisms of the study is that Blair Bigham states that therapeutic hypothermia would lead to improved outcomes. However, the Oslo hospitals started routinely using therapeutic hypothermia only four months after the start of the study. So, almost all of the eligible patients did receive therapeutic hypothermia.^[2] The therapeutic hypothermia study does show a doubling of survival to discharge with good neurological function at one year after discharge, so this does not appear to be any justification for doubting the effectiveness of treatment in Oslo.

Another concern is that PCI (Percutaneous Coronary Angiography or cardiac catheterization) might affect outcomes, but cardiac catheterization was also part of standard treatment in Oslo at the time.

Bill Toon mentions that some of the ambulances are staffed by physicians, but what difference is there between what a physician will do on scene and what a medic will do on scene? Physician staffed ambulances were present at 37% of no IV patients and 38% of IV patients, so this should not have affected either group more than the other.

A concern raised by Rob Theriault was the change in the CPR (CardioPulmonary Resuscitation) and ACLS (Advanced Cardiac Life Support) guidelines during the study period.

Until January 2006, ACLS was performed according to the International Guidelines 2000,¹⁴ with the modification that patients with ventricular fibrillation received 3 minutes of CPR before the first shock and between unsuccessful series of shocks.¹⁵ ^[1]

While they were not using the 2005 guidelines prior to January 2006 in Oslo, they were using a form of CPR that could be described as closer to the 2005 guidelines than the 2000 guidelines. According to the study –

Both groups had adequate and similar CPR quality with few chest compression pauses (median hands-off ratio, 0.15 for the intravenous group and 0.14 for the no intravenous group) and the compression and ventilation rates were within the guideline recommendations (Table 1).^[1]

It appears that the compression interruptions are much less than what we would expect from a similar study done in the US, except where CCR (Continuous Compression Resuscitation or CardioCerebral Resuscitation) is being used correctly.

If you believe, as Blair appears to, that the improved outcomes in the US after the 2005 guidelines are at least partially due to epinephrine, likewise the improvements in the places using CCR, then you anticipate that when the first large enough randomized placebo-controlled study of drugs during cardiac arrest is published, it will show significantly better outcomes for those receiving epinephrine.

I doubt it. I expect something similar to the many studies of traditional treatments that could only be shown to improve surrogate end-points. Surrogate end-points are like alcohol. In moderation, the effects can be pleasant, while intemperate use distorts reality.

Some examples of being misled by surrogate end-points are the routine use of antiarrhythmic medication in post-MI (Myocardial Infarction) patients with PVCs (Premature Ventricular Contractions). The drugs did a great job of getting rid of the nasty looking PVCs, but making the rhythm look better did not improve outcomes. In spite of the wonderfully improved heart rhythms, the fatality rate more than tripled.^[3]

We used to give furosemide (Lasix) to almost all patients presenting with symptoms of CHF (Congestive Heart Failure). Single-mindedly, we would try to remove as much water from CHF patients, because fluid in the lungs is a sign of fluid overload. Research, going back to the 1980s, shows that fluid in the lungs and fluid overload are not the same thing. Giving furosemide causes the body to dump water almost as dramatically as if we gave the patient an enema. Medical directors have responded to research showing harm from furosemide, and many have restricted the use of furosemide.

MAST/PASG (Medical Anti-Shock Trousers/Pneumatic Anti-Shock Garment) was the answer to blood loss. The same argument, that you have to have a pulse to leave the hospital alive, reared its head. Rather than focus on pulses in the ED, medical directors chose the meaningful outcome of more patients leaving the hospital able to care for themselves.

At one point, Buck Feris points out that post-resuscitation care is largely a matter of dealing with the side effects of epinephrine. Blair presents a paper that suggests that there are no post-resuscitation guidelines (not his conclusion). No post-resuscitation guidelines? There is an entire section of the ACLS guidelines on post-resuscitation care.^[4] Just because there is no particular flow sheet to be memorized, does not mean that there are no guidelines. When I taught ACLS, post-resuscitation care was one of the essential parts I covered.

CPR/CCR, defibrillation, potentially reversible causes, and post resuscitation care are the things that make a difference in outcome. Why do we spend so much time on trying to resuscitate people, if we are not going to prepare them to actually deal with what happens after the return of a pulse?

Post-resuscitation care is not just about treating vital signs. Perhaps part of our problem is that we do not see this as part of resuscitation. If we understood this, maybe we would see that giving epinephrine is just about vital signs. Giving epinephrine is not about resuscitation. When we produce a pulse with epinephrine, we need to switch from resuscitation to trying to counter epinephrine toxicity.

Perhaps, if epinephrine were in any way considered good for the heart, I would be less cynical. There are not many drugs more toxic to the heart than epinephrine.

Narrative Fallacy –

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

Free Full Text from NEJM.

Updated 9/14/2012 at 03:00 for formatting.

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Footnotes:

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^[1] Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L.
JAMA. 2009 Nov 25;302(20):2222-9.
PMID: 19934423 [PubMed – in process]

I wrote about this in Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. If you want to read the full text of the study, it is available in PDF at the EMSEdUCast page for this episode.

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^[2] Implementation of a standardised treatment protocol for post resuscitation care after out-of-hospital cardiac arrest.
Sunde K, Pytte M, Jacobsen D, Mangschau A, Jensen LP, Smedsrud C, Draegni T, Steen PA.
Resuscitation. 2007 Apr;73(1):29-39. Epub 2007 Jan 25.
PMID: 17258378 [PubMed – indexed for MEDLINE]

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^[3] Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, et al.
N Engl J Med. 1991 Mar 21;324(12):781-8.
PMID: 1900101 [PubMed – indexed for MEDLINE]

CONCLUSIONS. There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide. Nonlethal events, however, were equally distributed between the active-drug and placebo groups. The mechanisms underlying the excess mortality during treatment with encainide or flecainide remain unknown.

I have written about this in C A S T and Narrative Fallacy and elsewhere.

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^[4] 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Circulation. 2005;112:IV-84 – IV-88.
Part 7.5: Postresuscitation Support
Free Full Text Free PDF

Filed Under: EMS EduCast, Epinephrine, Heresy, Narrative Fallacy, Research Tagged With: Critical Judgment, Epinephrine, Heresy, Narrative Fallacy

2009’s Top Threat To Science In Medicine

Fri, 01 Jan 2010 14:51:30 -0500 by Rogue Medic

Science-Based Medicine, has a post by Dr. Val Jones – 2009’s Top 5 Threats To Science In Medicine.

I do not disagree with the list except, and what would one of my posts be without an except, the number one threat to science in medicine is much more of a problem. Our science education in grade school is where we fail our children. Before they even become adults, they are exposed to all sorts of magical thinking.

Full moons, speaking about something bad increasing the chances it will occur (a jinx), believing that something natural is safer than something manufactured – just because it is not man made, or just a belief in the stereotypical mad scientist bringing about horrors by using the scientific method of inquiry.

That is what science is. Science is a method of inquiry. Science is a tool we use to find out how the world works.

We see something that makes us think. Most people may form an opinion, but not look at this with a method designed to minimize the effect of our biases. And we all have biases.

It seems that there are more patients during a full moon. With a full moon falling at 19:15 GMT (Greenwich Mean Time) this past New Years Eve, this must have been a horrible night of death and destruction. Or was it?

We formulate a hypothesis.

The full moon causes accidents and/or illnesses, or makes accidents and/or illnesses even worse than they would be if there were no full moon.

We figure out what we need to control for to limit our variable to just the possible influence of the full moon. So, let’s look at a study that investigated the effect of a full moon on something that would be very difficult to misinterpret.

We postulated that on full moon days there would be more available moonlight, thus influencing individuals’ activities, and in turn, the propensity for cardiac arrest.^[1]

Interesting. They are not really assuming that the cause of an increase in cardiac arrests would be due to some mystical property of the moon, but that it would be due to more moonlight. fortunately, it does not matter what the actual cause would be for an increase in cardiac arrests, if they set the experiment up properly.

What do they need to do?

This study was a retrospective analysis of a computerized billing database of ED visits.^[1]

The study population consisted of CPR (CardioPulmonary Resuscitation) occurring daily at a cohort of seven hospital ED in northern New Jersey, USA, during the period of 1 January 1988 to 31 December 1998, comprising 4018 days over 11 years. Consecutive patients seen by an emergency physician were included. Emergency physicians see 80–95% of all ED patient visits and the vast majority of cardiac arrest patients. Private physicians see the remainder of the patients.^[1]

Their theory was that the increased moonlight would lead to more activity; more activity would lead to more cardiac arrests; thus there would be more cardiac arrests during a full moon.

Did the investigators prove their hypothesis?

According to their table, which does not reproduce well, there is no increase in cardiac arrest incidence during a full moon. They actually recorded a decrease, but the difference is not statistically significant. The reported statistically significant difference in incidence of cardiac arrest is this. During the new moon, there is less likely to be a cardiac arrest treated by an emergency physician.

There were 2370233 patient visits in the database during the 4018-day (11year) period of study, with 6827 having the primary ICD-9 diagnosis of cardiac arrest.^[2] Table 2 contains the time series regression results. Full moon days were not significantly different from other days (P=0.97). We had an 80% power to identify a difference of 4.5%. However, on average 0.12 fewer CPR occurred on new moon days than on other days (P=0.02). This translates into an average of 6.5% fewer CPR (95% confidence interval 1.3–11.7%) on new moon days than other days. In addition, the results for the potentially confounding variables are presented in Table 2.^[1]

I left part of their original hypothesis off of the initial quote. The stated objective of the study is –

Objective
To determine the effect of the phase of the full and new moon on the variation in the number of daily cardiopulmonary resuscitations.^[1]

In the discussion, they elaborate on their purpose –

Our results show a small but statistically significant decrease in the incidence of CPR with new moon days. We speculate that this may be secondary to a decrease in activity because of less available light on these days, as it has been shown that increased activity is a risk factor for sudden death[39]. Our initial rationale sought to identify and determine the size of any effect on the occurrence of cardiac arrest and its attempted resuscitation (‘CPR’) by lunar influence as a potential insight into an aspect of the occurrence of cardiac arrest. In addition, we sought to identify patient volume variation by lunar cycle potentially to allow for staffing modifications; however, the effect identified did not warrant this.^[1]

This –

We postulated that on full moon days there would be more available moonlight, thus influencing individuals’ activities, and in turn, the propensity for cardiac arrest.^[1]

Becomes –

We speculate that this may be secondary to a decrease in activity because of less available light on these days, as it has been shown that increased activity is a risk factor for sudden death[39] ^[1]

They have found a way to stick with their initial hypothesis by reversing it.

More moonlight does not appear to lead to more cardiac arrests. Why this lack of correlation does not need to be explained is not in the paper. However, the correlation between fewer deaths during a new moon is something that they feel needs to be explained. Haven’t they just misappropriated a Willy Wonka quote? Strike that. Reverse it. Willy Wonka was reversing the meaning of what he was saying. That was the reason he needed to reverse the order.

The authors have not really changed the meaning, only the way they express it. More light/less light leads to more activity/less activity. This leads to more/fewer cardiac arrests.

While I do not dispute the results of this study, I do have a problem with the way they get from Point A to Point C. They seem to travel there by way of a study that shows that more activity leads to more cardiac arrest. Actually the study is of vigorous exertion, not just more activity, but the authors seem to have interpreted the study as couch potatoes live longer. The vigorous exertion study did show –

As expected, the base-line level of habitual exercise significantly attenuated the increase in the risk of sudden death that was associated with an episode of vigorous exertion in both the primary analysis and the three sensitivity analyses. Habitually active men had a much lower risk of sudden death in association with an episode of vigorous exertion than men who exercised less than once a week; however, the most active men’s risk remained significantly elevated during and after vigorous exertion in all analyses.^[3]

There is no suggestion that these episodes of vigorous exertion occurred less frequently during the time of the new moon. According to the hypothesis of the ~~full~~ new moon study, the effect of the new moon should only be at night, when it would make a difference in the amount of available light. This might make more difference in rural areas, than in the suburbs, and more of a difference in suburbs, than in cities, due to the wonders of electrical lighting.

Is there any evidence to support this string of conclusions? I don’t think so.

That does not mean that this hypothesis is incorrect, just that their way of getting there is not supported by the information provided.

One very nice part of this study is the brief review of previous studies and whether they seemed to support, or refute, a connection between various activities and the full moon, but this post is already too long. I will write about other full moon research elsewhere.

Another problem is the way they define a full moon –

We identified full and new moon days that occurred during the study period from the United States National Oceanographic and Aeronautic Administration website. Using this information we created variables for full and new moon days to be used in a regression model of daily CPR, described below.^[1]

So. What is their definition of a new moon, or a full moon? They have not made that clear, but it appears to be limited to one specific day during each lunar cycle.

Using NOAA’s (United States National Oceanographic and Aeronautic Administration’s) website, I found a page that identifies new moons, full moons, and other phases by entering the time period I want to look at. The problem I see is that there is not much detail about how they used this information, or if they were using the same part of NOAA’s website.

Why no discussion of this?

Why no discussion of their definition of new moon and full moon?

If their hypothesis is one that depends on the available light, why does the day before a new moon not count, or the day after, or two days before (or after)?

However, if they are looking for a mystical connection between the full moon and bad events, a case can be made that the full power of the full moon would be on one specific date.

If they are claiming that they are examining the effects of the amount of moonlight, how much difference is there in the amount of moonlight from one day to the next? Where is your cut-off? Why?

I think that their conclusion should be that they find no apparent mystical connection between the full moon and cardiac arrests treated by emergency physicians. Their attempts at explaining their results wander into narrative fallacy, which I have written about here, here, here, here, here, here, here, here, here, and here.

As I have stated before about the way we should look at explanations for scientific results –

Bet that the explanation is wrong.

This is one of the failures of our basic education of students. We do not make this clear to them. Yes, this was where the post started, with the failure of science education in the grade schools.

The media report that a certain study means X, even though the authors of the study may not have suggested that this is true. It is later found that the conclusion popularized by the media is wrong. The blame goes, not to the reporters misrepresenting the science, but to the science. We need to avoid creating explanations that are unsupportable and likely to be found to be in error. We need to stop telling fairy tales. We need to stop talking to media members, who spin research results with misleading explanations.

We have people graduating from high school, but unable to recognize the difference between good science and bad science. Unable to look at a study and determine if there is something there that is meaningful. This continues through college, and even medical school. Number 3 on the list was – Academic Medical Centers, so I am not the only one critical of these ivory towers. The top threat to science in medicine is the lack of understanding of what science is. We fail before the students ever get started. This lack of understanding is due to a lack of education in grade school.

We need to change how we teach science. Some do it well, but the debates on scientific topics in the media suggest that few have been well taught. The ignorant mobs are trying to keep themselves in scientific debates for which they are not even remotely qualified. We need to make it so that more are qualified.

We need to improve our basic science education, because we cannot rely on people from other countries coming here to do the science that we have become too ignorant to handle. Eventually, the destination of smart foreign-born scientists will not be the United States. We do not develop enough of our talent. We remain a scientific power because import talent. We do the same thing with grape pickers and day laborers. These seem to be the jobs that we will no longer do for ourselves. Scientist and day laborer are both looked at as undesirable. We need to change this.

It is in the earlier grades that the problems of bad science education are established. After that point it is a much more difficult task to correct this creeping indoctrination in magical thinking.

I think that this is the number one threat to science in medicine. All of the others only contribute to this.

Magical thinking is a form of corruption. As with other types of corruption, it usually does not start with a cannonball into the deep end, but a gradual acclimatization to more and more corruption. At some point, critical judgment is only a fond memory.

There must have been a time, in the beginning, when we could have said – no. But somehow we missed it. – Tom Stoppard.

We can still fix that problem in education for those in grade school.

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Footnotes:

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^[1] Effect of lunar cycle on temporal variation in cardiopulmonary arrest in seven emergency departments during 11 years.
Alves DW, Allegra JR, Cochrane DG, Cable G.
Eur J Emerg Med. 2003 Sep;10(3):225-8.
PMID: 12972900 [PubMed – indexed for MEDLINE]

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^[2] ICD-9 code definition from the study above

The physicians’ billing department assigns codes according to the International Classification of Diseases, Ninth Revision, and Clinical Modification [International Classification of Disease (ICD)-9 codes]. Patients were included as CPR if they contained any of the ICD-9 codes listed in Table 1 as one of their three primary diagnoses.

Table 1
International Classification of Disease 9 codes
427.4       Ventricular fibrillation
427.41     Ventricular fibrillation
427.5       Cardiac arrest
798.1        Death instantaneous
798.2      Death occurring less than 24h from onset of symptoms
798.9       Death unattended

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^[3] Triggering of sudden death from cardiac causes by vigorous exertion.
Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE.
N Engl J Med. 2000 Nov 9;343(19):1355-61.
PMID: 11070099 [PubMed – indexed for MEDLINE]

Free Full Text from NEJM.

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Alves, D., Allegra, J., Cochrane, D., & Cable, G. (2003). Effect of lunar cycle on temporal variation in cardiopulmonary arrest in seven emergency departments during 11 years European Journal of Emergency Medicine, 10 (3), 225-228 DOI: 10.1097/00063110-200309000-00013

Filed Under: Conventional Ignorance, EMS EduCast, Full Moon, Heresy, Narrative Fallacy, Science, Superstition Tagged With: Conventional Ignorance, Heresy, Narrative Fallacy, Science

Shaggy Comments on Some Research Podcasting Comments

Wed, 30 Dec 2009 01:48:12 -0500 by Rogue Medic

In the comments to Some Research Podcasting Comments, Shaggy wrote,

I am beginning to think our definition of “why” in the educational arena is not the same. If it is, I will just conclude that either one of us is off our rocker. Explaining the importance of a certain treatment modality as well as anything else is considered very important as motivational.

Perhaps that is part of the problem with attaching questionable explanations to the results of research that was not designed to answer these questions.

Should we be more concerned with motivation, than with accuracy?

I could come up with many possible explanations for why something is happening. I would rather say, I don’t know.

Science is much better at showing what does not work, than what does work.

Science is much better at showing what does work, than at explaining why something works.

This was very important when I did occupational safety and health training for the Safety Council in Pa. as the “why” was part of Bloom’s three types of learning, and fell under the affective nicely. Why should you wear PPE?

Because people who do not wear PPE (Personal Protective Equipment) are over-represented in the morbidity and mortality statistics.

Why are safe work practices important?

Because going home to one’s family is more likely, when one follows these safe work practices.

Why is quick and continuous CPR necessary?

Research shows that without quick and continuous CPR, the resuscitation rate is significantly lower.

Maybe it is due to direct compression of the heart. Maybe it is due to increased intrathoracic pressure. Maybe it is due to a rebound effect after compressing the chest. Maybe it is due to some combination of these mechanisms. Maybe it is due to some other mechanism. Maybe it is due to a combination of some other mechanism and one or more of these mechanisms.

What do we need to know?

We need to know that quick and continuous CPR does work.

We do not need to make up stories that will likely be, at best significantly modified, and at worst completely discarded. Do we need to make up these stories just to motivate people to provide good treatment?

Maybe we will know what the mechanism is in a decade. Maybe in two decades. Right now, I think we are just spinning fairy tales to impress others with how smart we think we are. Or has there been research that conclusively shows the complete mechanism for CPR?

Regardless, the important point is that quick and continuous CPR works. How quick and continuous CPR works is not important in deciding whether we should provide quick and continuous CPR.

If you think these questions shouldn’t be answered, I may tend to think you finally went off the ledge.

How did I get on the ledge?

Why was I on the ledge?

How can I know if I fell off the ledge, if I don’t know the answers to the mechanism of my arriving on the ledge?

Then there is the question of whether I was actually on the ledge at all. Last thing I remember, I was nailed to a perch. Nice fish, the perch.

Maybe I just wasn’t motivated to stay on the ledge.

If you think we are talking about two different things, then perhaps you need to clarify for the intellectually challenged like myself.

I think we are talking about the same thing.

I think that we disagree.

On the other hand, I am confident that almost everyone agrees with you.

We need to become much more comfortable with uncertainty.

Narrative Fallacy –

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

Filed Under: EMS EduCast, Heresy, Mythology, Narrative Fallacy Tagged With: Education, Heresy, Mythology, Narrative Fallacy

Some Research Podcasting Comments

Fri, 25 Dec 2009 15:51:00 -0500 by Rogue Medic

This Eve of Christmas Eve both EMS Garage and EMS EduCast.

I Hate People: EMS Garage Episode 67, which is really much more cheerful than it sounds – and it comes with beer recommendations. One warning is that everybody seemed to be having connection problems, so we couldn’t always hear each other. this led to people talking over each other more than usual and pauses, where nobody is talking since they think someone else is still talking. these problems are minor, but do pop up occasionally. Steve Whitehead of The EMT Spot even brings a surreal dimension to the show with mime podcasting.

and

Understanding EMS Research: Episode 42, which may have helped to provide some understanding of research. The problem is that there is far too much to the topic to be covered in one episode. This was expected to be a brief, year end episode. A brief episode? With me on it? What were they thinking?

The other problem is believing that research can be covered effectively and briefly.

A couple of points. I point out that I think that we should start EMS education with research. Only after the students understand research, should we move on to assessment and treatment.

The big disagreement was when we were discussing some of the old discarded EMS myths, which unfortunately have not been discarded everywhere. The old rule of thumb about what pressure is indicated by what pulses, that I wrote about in A Radial Pulse Means a Pressure of At Least . . . ., where I describe the research from the BMJ from 2000^[1] (not 2001 as I stated on the show). There was a bit of discussion of this and somebody mentioned relying on heart rate as an indicator of blood loss. I pointed out that beta blockers and abdominal trauma are two of the confounders of this approach.

The abdominal trauma is something that I will have to do a post on, and I do not have the studies in front of me, but there have been several papers written about surgical patients losing significant amounts of blood, but not becoming tachycardic to indicate the blood loss. Some abdominal surgery patients even became bradycardic with significant blood loss. this is an important problem, because relying on heart rate alone ~~would~~ did cause the continuing uncontrolled bleeding in some of these patients to be missed.

This is something important that we need to be aware of. There are many things that may mislead us in our assessments. The more that we are aware of these confounders, the less likely we are to miss a significant problem. While part of the debate was about whether this happens in the majority of abdominal trauma (it probably does not), this approach is completely irrelevant to developing an awareness of a potentially significant problem. We stress over spinal cord injuries, while the incidence of spinal cord injuries is probably much lower than the incidence of exsanguination due to abdominal trauma that is unrecognized because there is no significant rise in heart rate. The outcome may be more likely to be fatal, as well.

Anyway, my biggest disagreement was when somebody started, based on less information than I already wrote, to try to figure out why this is happening. This is a bad idea.

Why is not important!

When we started to discuss this, that this may be due to vagal stimulus, someone stated that this is just a hypothesis for a study. I don’t have any problem with using that as the hypothesis for a study, but we were not designing a study. We were providing information for educators to use to teach students.

This is exactly where medical myths come from.

The students do not need to know why something works, only that it may work. To suggest anything more than that is suggesting that we know a lot more than we do know.

It is important to know as much about the limitations of our assessments.

It is not important to know why, until after we have a lot of information to support that idea.

Look at where the EMS myths started from. Somebody started explaining why something was happening, or maybe they were only wondering about the cause. Educators got a hold of the idea, and rather than say, I don’t know why, some gave an explanation that was repeated enough to become a myth. A myth that is almost impossible to get rid of, because people want certainty.

Certainty is nice, but it is a problem.

The only certainty in medicine is that we do not know as much as we think we know.

When we start taking explanations for granted, we find that somebody read too much into an observation, or a bunch of observations, or read too much into a study, or a bunch of studies.

This is the same thing that leads the general public to distrust science. We have research that provides limited information, but somebody decides to explain that limited information. If you want to bet on something that is almost a sure thing, here is what you should do.

Bet that the explanation is wrong.

This does not mean that the science was bad, or that the science was wrong, or that the study was not done well, et cetera. It means that somebody took a look at some science and decided to create some fiction, because they assume that they know what they are doing.

The ~~safe bet~~ certain bet is that the explanation is wrong.

The certainty in science and medicine is that our explanations will be wrong. These erroneous explanations will create distrust of science and medicine. these will not be the fault of the researchers, but of those explaining the research.

When we create explanations, we create a narrative – a story. We should start out with, Once upon a time . . . , or something similar, but we don’t. I have discussed this problem with narrative fallacy further in the links listed below. I will write about this more, because this is important.

I do not mean to put down anyone on the show. This is a problem that is almost universal. One of the reasons that it is so common, is that it is natural for us to explain things with stories. When life was simpler, that may have been effective. When the life of someone else is in our hands, we need to be better than that.

Narrative Fallacy –

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

Prepublication History of Manuscript

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Footnotes:

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^[1] Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study.
Deakin CD, Low JL.
BMJ. 2000 Sep 16;321(7262):673-4. No abstract available.
PMID: 10987771 [PubMed – indexed for MEDLINE]

Free Full Text . . . . Free PDF

Filed Under: EMS EduCast, EMS Garage, Heresy, Mythology, Narrative Fallacy Tagged With: Education, Heresy, Mythology, Narrative Fallacy

C A S T and Narrative Fallacy comment from Shaggy

Wed, 22 Jul 2009 18:42:36 -0400 by Rogue Medic

Also posted over at Paramedicine 101. Go check out the rest of what is there.

In the comments to C A S T and Narrative Fallacy, there is a comment by Shaggy:

Sometimes treating the symptoms is all we can do, such as pain management. We as EMS providers cannot set or reduce fractures, but we can sure make the patient feel better as well as treating the pain of an acute abdomen. I know this is not the focus of the post, but I just wanted to throw out there we generally DO treat symptoms and it is usually not a bad thing.^[1]

I agree.

With fentanyl (or even other less effective and less safe pain medicines), we can consistently produce a significant change in the surrogate end point (the level of pain). This is a good thing, because when given by a competent provider, it should not harm the patient. Even the rare cases of harm are outweighed by the benefit to the patient. The goal of our treatment is the surrogate end point, as long as we do not make things worse.

As for requiring a competent provider? There is not any good reason to encourage treatments that do not require a competent provider.

On the other hand, with epinephrine, we can only produce a change in the surrogate end point of the presence of a pulse (ROSC – Return Of Spontaneous Circulation). This is not a good thing, because it does appear to harm the patient. Still, the goal of our treatment is the surrogate end point, as long as we do not make things worse.

Almost all of the things we want to avoid doing to the heart, come in the syringe marked epinephrine.

Do we want to increase the oxygen demand in a heart that may already be hypoxic, ischemic, or infarcted?

A heart that may have arrested due to hypoxia, ischemia, or infarction?

A heart that may have experienced arrhythmia due to hypoxia, ischemia, or infarction?

One of the worst antiarrhythmic medications is epinephrine. Epinephrine is proarrhythmic. Epinephrine causes arrhythmias.

Perhaps the best antiarrhythmic medication we have is oxygen, but epinephrine can increase the demand for oxygen even beyond what can be delivered to the heart by work by working the heart harder. This increases the demand for oxygen still more.

This is bad. This violates that very complex rule of medicine, Oxygen is good.

There are some revisions to that rule, but one revision I do not expect to see is, Increasing oxygen demand, beyond what can be provided, is good.

Increasing oxygen demand, beyond what can be provided, also goes by another name. This name is a catchy one that is most often misused on TV and in the movies. That name is Shock. Most medical people seem to agree that shock is not a good thing. Most post-resuscitation care is focused on preventing/reversing shock, but the administration of epinephrine may be the biggest cause of post-resuscitation shock.

Do we have any reason to believe that real survivors, who received epinephrine, would not have survived without epinephrine?

That is the most important question, isn’t it? Real survivors, as in people who eventually leave the hospital with minimal to no brain damage – neurologically intact.

The answer is, No.

There is no evidence that patients resuscitated after the administration of epinephrine would not have been resuscitated with only BLS treatment.

There is no evidence that patients resuscitated after the administration of epinephrine have better outcomes because of epinephrine. Zero evidence.

Imagine that you are having a heart attack. The heart attack brings on a cardiac arrest.

You are not having a good day.

You are resuscitated, but before resuscitation you were given epinephrine. The epinephrine is acting as if it is Gunnery Sergeant Hartman and you are Private Pyle. He wants you to get up and run, run faster, and keep running.

Why?

That’s what epinephrine does.

Does it care that you were just dead?

No.

Does it care that post-resuscitation care is largely about reversing the effects of epinephrine?

No.

Even in standard doses, this may be the worst medicine you could give to a person having a heart attack, but we increase the dose to ridiculous proportions. We have taken homeopathy, flipped it on its head, and thrown in a bit of Nietzsche. If this doesn’t kill him nothing will. MwaHaHaHaHa

Why?

It is really cool to get a pulse back.

So what if the drug that seems to bring the pulse back also seems to make it go away. We already dropped the patient off at the hospital. If they can’t treat a little iatrogenic shock, maybe they should consider a different line of work. Yeah! That’s the ticket. The hospital did it. It’s the hospital’s fault. Killjoys!

What is the most promising post-resuscitation care? If you pray at the Church of Epinephrine, the most consistent treatment would be something along the lines of stress testing. Of course, nobody does stress testing with 1 mg of epinephrine in a real live person, because that might be expected to lead to murder charges. We only do this to people, who are already dead. Law For Dummies 101 – you can’t kill a person, who is already dead.

Even epinephrine light (dopamine) and epinephrine extra light (dobutamine) are used with a lot of caution in the live patient with a possible heart attack.

Perhaps the AHA has some naturopaths in their midst. Naturopaths will tell you that their treatments are safe, because they are naturally occurring. Epinephrine is a hormone that naturally occurs in the body. So is potassium, which is used to execute people by lethal injection. Natural does not mean safe. Malaria is natural and kills over a million people a year. Natural does not mean good.

With few exceptions, like, antibiotics, medications are usually not able to cure but treat effects and symptoms. Expecting a medication like epi to not only obtain ROSC but heal their heart or any of the multiple causes of cardiac arrest is truly expecting the ridiculous. We usually cannot treat or heal the cause of SCA until we get ROSC. That is the first step or priority.^[1]

I do not expect epinephrine to heal the heart. Epinephrine is toxic to the heart.

The priority is not to make things worse. This should be pretty easy to accomplish with a dead patient. However, we do not have any evidence that we are not making things worse by giving epinephrine.

These are from the EpiPen autoinjector label:

Large doses or accidental intravenous injection of epinephrine may result in cerebral hemorrhage due to sharp rise in blood pressure. DO NOT INJECT INTRAVENOUSLY. Rapidly acting vasodilators can counteract the marked pressor effects of epinephrine.^[2]

ADVERSE REACTIONS
Side effects of epinephrine may include palpitations, tachycardia, sweating, nausea and vomiting, respiratory difficulty, pallor, dizziness, weakness, tremor, headache, apprehension, nervousness and anxiety.
Cardiac arrhythmias may follow administration of epinephrine.

OVERDOSAGE
Overdosage or inadvertent intravascular injection of epinephrine may cause cerebral hemorrhage resulting from a sharp rise in blood pressure. Fatalities may also result from pulmonary edema because of peripheral vascular constriction together with cardiac stimulation.^[2]

Epinephrine is ordinarily administered with extreme caution to patients who have heart disease. Use of epinephrine with drugs that may sensitize the heart to arrhythmias, e.g., digitalis, mercurial diuretics, or quinidine, ordinarily is not recommended. Anginal pain may be induced by epinephrine in patients with coronary insufficiency.

The effects of epinephrine may be potentiated by tricyclic antidepressants and monoamine oxidase inhibitors.

Some patients may be at greater risk of developing adverse reactions after epinephrine administration. These include: hyperthyroid individuals, individuals with cardiovascular disease, hypertension, or diabetes, elderly individuals, pregnant women, pediatric patients under 30 kg (66 lbs.) body weight using EpiPen, and pediatric patients under 15 kg (33 lbs.) body weight using EpiPen Jr.^[2]

While these are from the EpiPen label (300 mcg of 1:1,000 epinephrine for IM injection), not the 1,000 mcg of 1:10,000 epinephrine for IV injection in dead people, the warnings make it pretty clear – this is a dangerous drug in living human beings. It should only be given when the benefits outweigh the risks, such as in anaphylaxis. A dead patient, who is expected to not be dead any more, is probably a poor choice for this treatment.

The only reason that the risk/benefit profile is considered to be positive, is that there is the presumption that patients resuscitated after receiving epinephrine, would not be resuscitated unless they received epinephrine.

There is no evidence to support the hypothesis that epinephrine improves anything other than the speed of return of a pulse. How impatient are we, that we are willing to compromise survival, just for this quick fix?

I do agree science is always changing, and we want it to, because that is how we advance forward. We need to continually ask questions and challenge current practices. I just think that expecting for a miricle drug to treat all the causes of SCA will never happen.^[1]

If we are going to use any treatment, BLS or ALS, we need to demand evidence that the treatment provides more benefit than harm. In cardiac arrest, epinephrine does not have that evidence.

Without that evidence, we need to be very clear that this treatment – epinephrine in cardiac arrest – is only an experimental treatment.

Epinephrine should not be a standard treatment.

Epinephrine is an experimental treatment.

There are some treatments, where we do not have survival data, but we have good enough surrogate end points to justify the use of these treatments. That will be for another post.

BTW, I thought this was an awesome post and should be published in an EMS journal, if anything to inspire logical thinking. We seem to lack that in EMS, always accepting what we are told. Those in EMS who question currently held/traditional practices are often treated as blasphamous heretics.^[1]

Thank you.

Blasphemous heretic?

Gosh. You’re going to make me blush. 😉

Narrative Fallacy –

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

Footnotes:

^ ¹ C A S T and Narrative Fallacy
Rogue Medic
Comments are at the bottom.
C A S T and Narrative Fallacy

^ ² EPIPEN (epinephrine) injection
EPIPEN JR (epinephrine) injection
[DEY]
DailyMed
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Filed Under: Critical Judgment, EMS EduCast, Heresy, Narrative Fallacy, Paramedicine 101 Tagged With: Critical Judgment, Heresy, Narrative Fallacy, Paramedicine 101

C A S T and Narrative Fallacy

Mon, 20 Jul 2009 14:23:15 -0400 by Rogue Medic

Also posted over at Paramedicine 101. Go check out the rest of what is there.

CAST (The Cardiac Arrhythmia Suppression Trial)^[1] was a large scale randomized placebo controlled trial. This was to determine which of the antiarrhythmics would be able to claim the title as the most effective life saving drug on the planet. CAST was one of the most important EMS studies ever done. And CAST wasn’t even an EMS study.

Moricizine vs. encainide vs. flecainide to see what saves the most lives.

Which drug won?

We’re not there, yet.

The experts understood the pathophysiology. They knew how to fix it.

What did the experts see as the problem, pathophysiologically?

After a heart attack, many people will have some extra heart beats. Beats apparently originating in the part of the heart damaged by the heart attack. These are most commonly called PVCs (Premature Ventricular Contractions). 2 PVCs are circled in red below. They are also called VPBs (Ventricular Premature Beats) or even FLBs (Funny Looking Beats), but most commonly PVCs.

After a heart attack (MI or Myocardial Infarction), people with plenty of PVCs (post-MI PVCs) will experience SCA (Sudden Cardiac Arrest) at a higher rate than other people who have had heart attacks, but do not have post-MI PVCs.

That much is accepted. In extrapolating from this. They concluded that if patients with frequent post-MI PVCs were more likely to have SCA, they could prevent SCA by preventing the post-MI PVCs.

Sounds reasonable.

It is reasonable. The problem is that they never tested the theory on a large enough group of people, until CAST, to demonstrate how well the theory worked. At the time, these drugs became the top selling drugs. Sales-wise, they were the Prozac and Viagra of the time. They were a hugely profitable part of the drug market. Yet there was no evidence that they saved lives. Only theory. Only pathophysiology. CAST was designed to show how good they were at saving lives.

Preventing post-MI PVCs is pretty easy. Improving survival is a little more complicated.

Why did people accept that fewer post-MI PVCs is the same as improving survival?

The top electrophysiologists were in agreement about how the heart works. Based on their research showing higher mortality with frequent post-MI PVCs, they told people that this was the best way to save lives.

After a patient had a heart attack, they would record an ECG that showed post-MI PVCs, such as the ECG below.

Then they would give patients the medication. As the medication began to work, the post-MI PVCs went away.

Obviously much better. This is proof that the heart is better and the patient is healthier.

Actually, if the ECG is the face that the heart shows us, this is just a form of Botox for the face of the ECG. We are making it look as it did before the heart attack. Remember, this was just for patients who had a heart attack – post-MI PVCs. The problem is that the antiarrhythmic medications interfere with the conduction system to make the post-MI PVCs disappear. The result of that tinkering is not limited to making the PVCs go away. Some of the other effects are still unclear.

The results of earlier studies were clear that the antiarrhythmic medications made the post-MI PVCs go away. This was viewed as a success. This was only a success at treating a surrogate end point. A surrogate end point is often studied, because it does not require as large a study group as an experiment that is set up to show a difference in meaningful outcome.

What is meaningful outcome?

Survival with a good quality of life.

When we look at all of the drugs that are used in cardiac arrest, we are looking at drugs that have been shown to be effective, at least a little bit, but only at improving surrogate end points. Surrogate end points are appropriate for initial studies, but with widespread use of a treatment, we need to look at meaningful outcomes.

In cardiac arrest, epinephrine is great at getting a heart to beat again (ROSC, or Return Of Spontaneous Circulation). Unfortunately, getting a pulse back, but dying in the hospital, is not a good outcome.^[2] Having the heart rate go from zero to 200 may not not be the best way to calm down a heart that has just experienced SCA, possibly due to overstimulus. This is one of the reasons for the introduction of vasopressin. Vasopressin is less of a stimulant to the heart, less of a cocaine-like jolt to the heart.

In EMS we used to give nifedipine in hypertensive crisis,^[3] because it lowered the blood pressure. It really lowered the blood pressure. The problem was that we were treating a surrogate end point.

Oxygen^[4] is another treatment that many of us give just because of surrogate end points. We seem to be trying to get 110% out of the SpO2, rather than treat the patient. We have not done enough research to know when oxygen is harmful. Hypothermic resuscitation is believed to work by preventing post-resuscitation damage from oxygen.

These are examples of narrative fallacy that were compounded by trusting surrogate end points.

So which drug was best at preventing SCA?

Right up until they stopped the study, the doctors believed that all of them were preventing SCA.

As it turns out, post-MI PVCs do not cause SCA. Post-MI PVCs are indicators of a heart that is more likely to have one, or more, SCAs than hearts without post-MI PVCs.

Getting rid of the post-MI PVCs is no more effective at fixing the heart, than Botox is at making the patient younger. They just make things look better.

Post-MI PVCs are bad and making them go away is good. We are becoming more and more tolerant of PVCs and the patients with post-MI PVCs are not dropping like flies.

In hypertensive crisis, we must lower the pressure right away before we get to the ED. A more controlled lowering of the blood pressure in the ED seems to avoid making the patient worse.

Oxygen. More is better. Perhaps oxygen should be treated as if it is a drug, since oxygen is a drug. Perhaps we should figure out when to give a lot of oxygen, when to give a little oxygen, and when to withhold oxygen.

In CAST the patients receiving the study drugs encainide and flecainide were more than 3 times as likely to die as the patients receiving placebo. These life saving drugs were more than three times as likely to kill the patient.

Three times as deadly as what?

Three times as deadly as placebo.

The title as the most effective life saving drug on the planet, in this case, went to the placebo.

CAST was a study that showed how the top experts, the highest in the hierarchy, can be so sure that they are saving lives that they end up causing more harm than benefit. The greater harm was due to the life saving treatments the experts were promoting.

After the fact, there was a lot of concern about how the experts could have been so wrong. The reality was that these experts didn’t understand the pathophysiology as well as they thought they did.

But why did people listen?

Seeing is deceiving. No more PVCs. What more do you need to know?

–

Narrative Fallacy –

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?