Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

2009’s Top Threat To Science In Medicine


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 –

To determine the effect of the phase of the full and new moon on the variation in the number of daily cardiopulmonary resuscitations.


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.


[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]

[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

[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.

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


Shaggy Comments on Some Research Podcasting Comments

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 –

Narrative Fallacy I

How did this happen? – Research

Narrative Fallacy II

CAST and Narrative Fallacy

C A S T and Narrative Fallacy comment from Shaggy

Some Research Podcasting Comments

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

EMS EdUCast – Journal Club 2: Episode 43

Education Problems, Autism, and Vaccines


Some Research Podcasting Comments

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.


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 –

Narrative Fallacy I

How did this happen? – Research

Narrative Fallacy II

CAST and Narrative Fallacy

C A S T and Narrative Fallacy comment from Shaggy

Some Research Podcasting Comments

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

EMS EdUCast – Journal Club 2: Episode 43

Education Problems, Autism, and Vaccines


[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

Prepublication History of Manuscript


C A S T and Narrative Fallacy comment from Shaggy

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.


That’s what epinephrine does.

Does it care that you were just dead?


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


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


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]

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 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.

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 –

Narrative Fallacy I

How did this happen? – Research

Narrative Fallacy II

CAST and Narrative Fallacy

C A S T and Narrative Fallacy comment from Shaggy

Some Research Podcasting Comments

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

EMS EdUCast – Journal Club 2: Episode 43

Education Problems, Autism, and Vaccines


^ 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



C A S T and Narrative Fallacy

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 –

Narrative Fallacy I

How did this happen? – Research

Narrative Fallacy II

CAST and Narrative Fallacy

C A S T and Narrative Fallacy comment from Shaggy

Some Research Podcasting Comments

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

EMS EdUCast – Journal Club 2: Episode 43

Education Problems, Autism, and Vaccines


[1] 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]

Free Full Text Article from N Engl J Med with links to Free Full Text PDF download

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.

[2] Medications for Arrest Rhythms
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Free Full Text Article from Circulation with links to Free Full Text PDF download

To date no placebo-controlled trials have shown that administration of any vasopressor agent at any stage during management of pulseless VT, VF, PEA, or asystole increases the rate of neurologically intact survival to hospital discharge. There is evidence, however, that the use of vasopressor agents favors initial ROSC.

[3] Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudoemergencies?
Grossman E, Messerli FH, Grodzicki T, Kowey P.
JAMA. 1996 Oct 23-30;276(16):1328-31. Review.
PMID: 8861992 [PubMed – indexed for MEDLINE]

Over the past 2 decades, nifedipine in the form of capsules has become widely popular in the treatment of hypertensive emergencies. . . . Given the seriousness of the reported adverse events and the lack of any clinical documentation attesting to a benefit, the use of nifedipine capsules for hypertensive emergencies and pseudoemergencies should be abandoned.

[4] The Oxygen Myth?
Bryan E. Bledsoe, DO, FACEP
JEMS.com Another Perspective
2009 Mar 5

The effects of aging are often due to oxidative stress. Also, some diseases such as atherosclerosis, Alzheimer’s disease, Parkinson’s disease, and others have been linked to oxidative stress and free radical induction. Thus, the evolving thought is that, in some conditions, high concentrations of oxygen can be harmful.


Narrative Fallacy II

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

In the comments to Why Can’t Medics Resuscitate II, anonymous finishes up with this question.

One question. The sole purpose of Epi during arrest is to act as a peripheral vasoconstrictor, thus increasing preload – correct?


I cannot answer this question without writing about narrative fallacy.

How did we get to Narrative Fallacy II, without a Narrative Fallacy I?

I wrote Narrative Fallacy I before Paramedicine 101 was started. You can read it at Narrative Fallacy I. The brief explanation of narrative fallacy is that a narrative fallacy is something that takes the facts, or the information that may be factual, and tries to use this information to explain how that person believes the result is obtained.

Nassim Taleb gives an explanation in his book, The Black Swan.[1] You are given an ice cube and asked to predict what it will look like after sitting on a table at a temperature that will cause it to melt. Not a huge problem. The result will be some kind of puddle.

However, this is not what we are doing. We are presented with the result. From that result (a puddle), we attempt to predict what caused the puddle. We do not know about the ice cube. We do know that an ice cube is one possible cause of a puddle. We also know that many other things could lead to the puddle. This is part of the problem of narrative fallacy. We choose one of many possible explanations that we know about. We choose to ignore the explanations that we think do not fit. We choose to ignore the explanations that we do not know about.

In ten years, or twenty years, we will probably use a different explanation, because we will know more. Does it really matter which erroneous explanation we use, now? The only real use for these explanations is to create more hypotheses to test. The explanation may help in deciding what treatment to give next, although not for a protocol monkey just working his way down the algorithm. Then the explanation does not matter at all.

Some problems:

1. The facts may not be factual. If the result is misunderstood/misinterpreted, then basing the explanation/narrative on that misinformation is not likely to produce an understanding of how something works.

2.The explanation/narrative may fit the facts, but that does not mean that the explanation is the most appropriate for that set of facts. Just about any episode of House M.D. will demonstrate this. As you can clearly see, Dr. House looks up to me. Well, that is one explanation for the picture. It seems to fit the facts, but it doesn’t really fit the facts. After all Dr. House isn’t real, but someday I will be a real boy!
Think of any story with a plot twist. This is based on a narrative fallacy. You have read/watched the story. You have been led to believe that the facts mean one thing, but as the story progresses, you learn that this was due to a misinterpretation. Detective stories are often based on narrative fallacy. Dr. House is based on the fictional detective Sherlock Holmes, so it is no surprise that this is a dominant plot device on the show.

We recognize patterns. Narratives are ways of explaining what might have led to the pattern that we think we are looking at. The pattern may be due to information that we add, due to our biases. The pattern may be due to information that we leave out, because it does not fit with our biases. It is important to recognize patterns. It is important to have ways to evaluate the accuracy of patterns.

3.Now that we have an explanation, we extrapolate from that explanation as if it is a given. Since we all know blah blah blah. Therefore, blahblah blahblah blahblah. blah to blahblah, which everyone knows can be represented as blah2. Clearly, the misinformation is growing at an exponential rate. OK, maybe not so clear and maybe it is not even misinformation, but here is an explanation of narrative fallacy from some of the most accurate observers of narrative fallacy available.


If you have trouble understanding what they are saying, the full text is available here. If that doesn’t work (I am having some linking problems.), scroll to the top of the page and click on Scene 5.

So, why do witches burn?

We need to make sure that we are asking the right questions, rather than questions that reinforce our biases.

Were the villagers interested the truth?


Later on, they would be even more resistant to evidence that the witch is not really a witch. After all, they did burn her, so they have to use some Cognitive DissonanceTM to justify their murder.

So, back to the original question:

One question. The sole purpose of Epi during arrest is to act as a peripheral vasoconstrictor, thus increasing preload – correct?


In the comments, Adam provides the textbook justification of the rationale for giving epinephrine in cardiac arrest. Of course, this is based on the idea that epinephrine works, or that epinephrine behaves as we believe it behaves. This may be true. Or this may be very misleading. Part of the explanation is a major part of why I think epinephrine makes things worse. Too much stimulus. Epinephrine is essentially a heart attack in a syringe. Therefore, it may not be the best choice of treatment for something that is most often the result of a heart attack.

How many of you would knowingly give epinephrine to a patient having a heart attack?

Why are we giving any drug in cardiac arrest? Only one reason – to improve survival to neurologically intact discharge from the hospital and a return to the kind of life the patient had before the cardiac arrest.

When we find a drug that seems to improve outcomes, we feel the need to explain why it helps.

I don’t care.

If the treatment helps, does it matter what the explanation is?

In ten years, or twenty years, we will probably use a different explanation, because we will know more. Does it really matter which erroneous explanation we use, now?

I don’t think so.

What are the chances that in a couple of decades we will be using the same explanation?




Still, we feel this need to come up with some temporary erroneous explanation. Not only that, we criticize those who do not participate in this silliness.

Here is an introduction to an excellent video


The full video is over an hour long. If you enjoy it and understand it, the video is far too short.

Nassim Nicholas Taleb: The Future Has Always Been Crazier Than We Thought

Narrative Fallacy –

Narrative Fallacy I

How did this happen? – Research

Narrative Fallacy II

CAST and Narrative Fallacy

C A S T and Narrative Fallacy comment from Shaggy

Some Research Podcasting Comments

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

EMS EdUCast – Journal Club 2: Episode 43

Education Problems, Autism, and Vaccines


[1] The Black Swan: The Impact of the Highly Improbable
By Nassim Nicholas Taleb

A must read book. If you have anything to do with risk management, then uncertainty/randomness/the unexpected are important parts of what you do. He deals with them better than anyone else. Too many misunderstand his writing, perhaps because they cannot abandon their own biases and accept their lack of control of events. While I find his prose to be awkward (perhaps he does not appear to be awkward, when compared to my writing, so maybe it is just me), his conclusions are essential to the understanding of risk management. Risk management people include any of us who treat patients.
Article about The Black Swan.

TM Cognitive Dissonance
How to harm people with a clear conscience. Fool yourself.


Endotracheal Drug Administration in Cardiac Arrest – comment

Vince of Living La Vida Vince wanted to comment on Endotracheal Drug Administration in Cardiac Arrest. Where he works his Mojo, there are firewalls that do not like him, do not like my blog, or both. He asked me to post this comment. In between, I have responded.

Well, as much as I hate to, you know I cannot resist the urge to ‘poke the gorilla with the stick’, so here goes.

At least this gorilla is not locked up behind a firewall. 🙂

I agree, that given the widespread use of alternative venous access(IO), the ET route of medication administration during resuscitation is most likely of little value [and as you point out potentially harmful-although I would worry just as much about washing the ‘Mr. Bubbles’ away, as making it 😉 ]

A good point that I had not considered to be much of a problem, since I have seen ET drugs given more than occasionally in the ICU.

However, you know my feelings on retrospective studies in general, and this one is particularly horrible! In addition to all the patient disparity between the treatment arms, the ET group was 1.5 times more likely to be in asystole at the onset than the IV group! Might this impact the results? Furthermore, since this was retrospective, the medics doing the treating were not randomizing which patients were going to get ET vs. IV. My guess is that this was most certainly NOT random at all. A myriad of factors such as length of downtime, ability to attain IV access, Single provider vs. double provider etc. etc. etc. may have determined which route a provider chose and would most certainly skew any data.

As much as I am critical of bad research, I do not think this study should be dismissed entirely.

The researchers do make it clear that there are limitations. They discuss these limitations. And the most important reason we should not ignore it is that there is nothing else that is anywhere near as good in looking at ET drug administration in real patients. The patients were not randomized, but they probably did self select for the dosing route that would apply outside of the study. With use of IO (IntraOsseous) needles being common place, we could set up a study that randomizes patients to the IO route or the ET route. This study could be interesting, but would interesting justify doing this study, instead of something that would really matter in EMS?

So I would say that this “study” should be ignored, at least for the purposes of “ruling-out” the potential benefits of ET administration. Poor research is poor research. Trying to make chicken soup out of this chicken-shit is, at best, Quixotic.

This is unfortunately the nature of the beast when it comes to quality research surrounding resuscitation- there is a dearth of good data. Half-truths, anecdotes, bad ideas, and untested theories abound.

The lack of good research should lead us to prohibit this treatment, not permit it.

This study is not of the quality that should be required to advocate for a treatment. The level of evidence needed to eliminate a treatment should be significantly less than the level of evidence needed to recommend a treatment. If there is evidence of harm, you go back to the drawing board and figure out what can be done about the apparent harm. You do not say, Well, it is the standard of care and we need to have much more rigorous evidence to stop using this apparently dangerous treatment, because it is the standard of care.

This is part of my point in Narcan Solves Riddle – Part IV, How did this happen? – Research and Narrative Fallacy I. The level of evidence needed to discourage a treatment should be much lower than the level of evidence needed to treat.

The same is true in looking at an individual patient. We need to be much more rigorous about the things that lead us to be aggressive in treatment, than the things that lead us to be conservative in treatment.

On point of porcine lab testing- it has a valuable place in establishing that for certain formulations, the ET route can provide adequate absorption to approach blood levels established by IV routes – Charlotte and her web notwithstanding. Does this necessarily mean better outcomes? Of course not. Until we get some IRBs with a full compliment of testes*, this is the closest we are ever going to get to scientifically rigorous data on the subject.** (* sarcasm ** not sarcasm)

Perhaps we need to study testes implantation on IRBs.

As far as advocating for treatments because trying to make pigs fly is the closest to real research that we have, I disagree. The pigs do not adequately represent the nursing home patients who appear to be disproportionately selected for this treatment. That is just one of the significant differences. When performing research on other animals, to determine the effect on human animals, some animals are more equal than others. Animal studies do provide evidence to advocate for human testing. They do not provide evidence to advocate for human treatment outside of the well controlled study.

You do make a great point about arbitrary endpoints like presence of a pulse upon arrival.

Thank you.

Consider the pot stirred. It’s been a while! 😉

Always good to think about these things in different ways. For me, the narrative part that does not make sense is this –

Removing ventilation and circulation, just to provide medication, is not good medicine. Especially when the medication is of uncertain benefit when administered by the ideal route.


How did this happen? – Research

Part of the problem with research is the same as the problem with all prediction. We are not good at it. We remember the things we were right about, but we conveniently forget the things we were wrong about.

Nassim Nicholas Taleb[1] describes part of the problem by reversing the situation. Do not try to predict the future, but try to predict the past. Imagine an ice cube placed on a table and try to imagine the way that it will melt. What will the result look like? The result will be a puddle of water.

Now, don’t imagine the situation as one of predicting the future. Imagine you are faced with a puddle of water like the one from the first example. Now, try to imagine what that puddle came from. Was it an ice cube? Was it condensation from a cold glass? Was it something entirely different that produced this puddle? If it did come from a piece of ice, was it an ice cube, a small ice sculpture containing the same amount of water, did some of the water evaporate before you saw the puddle? Is the substance that forms this apparently clear puddle actually water?

When performing research we need to try to control variables, so that we know as much as possible, what happened at each step of the experiment. If we put an ice cube down on a table, then leave, and come back and see a puddle, do we know that the puddle is the result of the ice cube melting? 

No, we do not. Is it reasonable to assume this? Yes, it is a reasonable thing to assume, but research is not about assuming things that are likely. Research is about controlling for all variables, especially those that can easily be controlled for.

When performing research, we need to control everything that we can reasonably control. If we are going to see what happens to an ice cube, we need to sit and watch the ice cube melt. Or we can record the events, so that we can examine the events later. If we are sitting there, watching the ice cube, and somebody comes along, puts the ice cube in a glass with a lot of other ice, puts the glass in the same spot, and the condensation from the glass forms the puddle, we need to know this. This would completely change our results. 

Is this far fetched? It does seem to be, but how do we know until we perform the experiment? If we assume things because we think we already know what is going to happen, then we are fooling ourselves. We can assume all sorts of things, just because the seem like common sense. That is not research. Anybody claiming that it is research is wrong. Unfortunately, this kind of carelessness is not uncommon in EMS research.

Do we really care about an ice cube? No. At least, I do not. This is just a very simple example of how we can assume things in research that will lead to a result that is worse than worthless. Why worse than worthless? Because the resources that could have been used to perform a valid experiment have now been wasted. Because the patients who have been exposed to the experimental treatment will never know if they might have benefited from the study – and neither does anyone else.

Of course the investigators will claim that they were able to demonstrate all sorts of useful information, but this is only because they are incompetent. We should not encourage them.

Actually, we should punish them.

Let’s look at the biggest problem of EMS research – quality.

All sorts of criteria are examined, when performing EMS research. Rarely examined is the quality of the providers participating in the study. Are they typical for the organization? A large enough study can take care of that. Are the providers in the organization representative of excellent, or even just competent, EMS ability? 

To many people, just asking that question is an insult. This should give you a hint of what the answer is for that organization. If they are not constantly questioning their quality, how do they have any idea?

Just because an EMS organization is questioning their quality, does not mean that they are asking the right questions, but it is a good start.

What should we ask?

Was this result from an EMS organization with aggressive medical oversight? Requirements for OLMC (On Line Medical Command) permission are not an example of aggressive oversight. This would better be compared to the Wizard of Oz pulling all kinds of levers and making loud noises to create an impressive spectacle. A spectacle that does not have any substance and is supposed to disguise the reality. We need to avoid the smoke, the mirrors, the man behind the curtain, and look for real indicators of quality.

What can we look for to indicate that an EMS organization is able to provide the kind of quality oversight that would recommend them as a site for evaluation of trauma triage criteria?

If the question is – Can EMS safely triage trauma patients by physical assessment, rather than by mechanism criteria? – then these are some of the questions we should be asking – 

Do they have feedback from the trauma center about patients transported to the trauma center?

If not why not?

HIPAA does not forbid this. 

Do they have feedback from the local hospital about patients transported to the local hospital? 

If not why not?

Again, there is no HIPAA problem, here. If anybody is claiming HIPAA, they are telling you a lie. 

Is the medical director following up on all of the trauma alerts, potential trauma alerts, mechanism alerts, patients who should have gone to a trauma center (which is a huge can of worms on its own – does an ICU admission mean a sick patient or a clueless ED?), . . . ?

If not why not?

Are there continuing education classes available?

If not why not? 

Are opportunities available to spend time in the trauma center performing assessments?

If not why not?

If you believe that Dr. Scalea is correct, that we should not be frugal when it comes to people’s lives (I do agree with this), then why aren’t we making sure that we have excellent EMS providers taking care of these patients? 

Are only trauma center patients deserving of excellent care?

Are only trauma patients deserving of excellent care?

Medical patients require much more critical judgment by EMS. They will only be flown to Shock Trauma when they also have a trauma complaint. Are they unimportant?

Certainly not.

What about feedback on medical patients?

How many pneumonia patients receive furosemide from EMS?

How many pneumonia patients receive furosemide from the hospital?

All that crackles is not CHF.

CHF should not be treated by EMS with furosemide anyway.

This is another way of finding the organizations that not only should not be participating in research, but should not be participating in EMS. 

But this is not trauma and we are only interested in trauma.

Not true. CHF patients are victims of trauma, too. Medical decision making does not limit itself to trauma, or medical, or IV skills, or intubation skills, or . . . . We need to look at the capabilities of those we seek to use as our example of EMS providers. The mediocre need not apply.

If the assessment skills are not common, we need to improve them, so that they become more common. We cannot throw our arms up and whine about it being impractical. This high quality is demonstrated in some EMS organization. 

High quality is not too expensive. If it is considered too expensive, then the organization should be limited to BLS care only.

Narrative Fallacy –

Narrative Fallacy I

How did this happen? – Research

Narrative Fallacy II

CAST and Narrative Fallacy

C A S T and Narrative Fallacy comment from Shaggy

Some Research Podcasting Comments

Shaggy Comments on Some Research Podcasting Comments.

Spine Immobilization in Penetrating Trauma: More Harm Than Good?

EMS EdUCast – Journal Club 2: Episode 43

Education Problems, Autism, and Vaccines


[1] The Black Swan: The Impact of the Highly Improbable
By Nassim Nicholas Taleb
A must read book. If you have anything to do with risk management, then uncertainty/randomness/the unexpected are important parts of what you do. He deals with them better than anyone else. Too many misunderstand his writing, perhaps because they cannot abandon their own biases and accept their lack of control of events. While I find his prose to be awkward (perhaps he does not appear to be awkward, when compared to my writing, so maybe it is just me), his conclusions are essential to the understanding of risk management. Risk management people include any of us who treat patients.
Article about The Black Swan.