Ten Thousand Page Loads

Paramedicine 101 has had over 10,000 page loads and counting. I guess that means some of you are actually reading this stuff. Thank you!

To better understand who we are writing for I would like to open up the comments for this post as a meet and greet. Let us know if you are a student, EMT, paramedic, nurse, or other. Where do you work?

Also, let us know what topics you would like more of.

Thanks for stopping by,

Adam Thompson, EMT-P

Induced Hypothermia Part III

Most recent studies from Pubmed:
[1]Organ injury caused by ischaemia and anoxia during prolonged cardiac arrest is compounded by reperfusion injury that occurs when spontaneous circulation is restored. Mild hypothermia (32-35 degrees C) is neuroprotective through several mechanisms, including suppression of apoptosis, reduced production of excitotoxins and free radicals, and anti-inflammatory actions. Experimental studies show that hypothermia is more effective the earlier it is started after return of spontaneous circulation (ROSC). Two randomised clinical trials show improved survival and neurological outcome in adults who remained comatose after initial resuscitation from prehospital VF cardiac arrest, and who were cooled after ROSC. Different strategies can be used to induce hypothermia. Optimal timing of therapeutic hypothermia for cardiac ischaemia is unknown. In patients who failed to respond to standard cardiopulmonary resuscitation, intra-arrest cooling using ice-cold intravenous (i.v.) fluid improved the chance of survival. Recently, fasudil, a Rho kinase inhibitor, was reported to prevent cerebral ischaemia in vivo by increasing cerebral blood flow and inhibiting inflammatory responses. In future, two different kinds of protective therapies, BCL-2 overexpression and hypothermia,will both inhibit aspects of apoptotic cell death cascades, and that combination treatment can prolong the temporal "therapeutic window" for gene therapy.

[2]AIM OF THE STUDY: Primarily, to investigate induction of therapeutic hypothermia during prehospital cardiopulmonary resuscitation (CPR) using ice-cold intravenous fluids. Effects on return of spontaneous circulation (ROSC), rate of rearrest, temperature and haemodynamics were assessed. Additionally, the outcome was followed until discharge from hospital. MATERIALS AND METHODS: Seventeen adult prehospital patients without obvious external causes for cardiac arrest were included. During CPR and after ROSC, paramedics infused +4 degrees C Ringer's acetate aiming at a target temperature of 33 degrees C. RESULTS: ROSC was achieved in 13 patients, 11 of whom were admitted to hospital. Their mean initial nasopharyngeal temperature was 35.17+/-0.57 degrees C (95% CI), and their temperature on hospital admission was 33.83+/-0.77 degrees C (-1.34 degrees The mean infused volume of cold fluid was 1571+/-517 ml. The rate of rearrest after ROSC was not increased compared to previous reports. Hypotension was observed in five patients. Of the 17 patients, 1 survived to hospital discharge. CONCLUSION: Induction of therapeutic hypothermia during prehospital CPR and after ROSC using ice-cold Ringer's solution effectively decreased nasopharyngeal temperature. The treatment was easily carried out and well tolerated.
[3]Mild resuscitative hypothermia has been shown to improve neurological outcome after cardiac arrest presenting with ventricular fibrillation (VF) due to cardiac causes. We describe the experience of inducing mild hypothermia in three patients with non-cardiac causes of arrest and long delays before a return of spontaneous circulation (ROSC). In one patient, extreme metabolic acidosis due to inadvertent oesophageal intubation complicated therapy, and the role of point-of-care diagnostics in the prehospital setting is briefly discussed. All patients survived to discharge from hospital, and neuropsychological examinations revealed good recovery. It is concluded that mild resuscitative hypothermia may be beneficial also in patients with obvious non-coronary causes for cardiac arrest.
While there is limited research on the topic of induced hypothermia, the research available is heavily in favor of the procedure. When I hear physicians criticize the immaturity of this therapy, I laugh thinking about epinephrine. As RM's last few posts have implied, Epi has been around for quite a while and there is no evidence in support of its use in cardiac arrest protocols. Would those physicians be so critical of Epi?

Above is Wake County's current Induced Hypothermia guideline. Thanks 9-Echo-1. Induced paralysis is only performed in the presence of shivering. Makes sense.

Works cited:

[1][Recent treatment of postischaemic anoxic brain damage after cardiac arrest by using therapeutic hypothermia] Link

[2]Induction of therapeutic hypothermia during prehospital CPR using ice-cold intravenous fluid. Link

[3]Therapeutic hypothermia after prolonged cardiac arrest due to non-coronary causes. Link

C A S T and Narrative Fallacy comment from Shaggy

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.[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. :-)


^ 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



Long QT Syndrome Part II

What is Long QT Syndrome?

Long QT Syndrome (LQTS) is a condition purely diagnosed by an electrocardiogram (ECG). This condition is represented by a long QT interval, hints the name. This represents delayed ventricular repolarization. This condition can be genetic or induced by certain prescribed medications.

How do I detect it?

Easy, as the name implies, measure the QT/QTc interval. The image below shows that the QT interval begins at the very end of the PR Interval, where your isoelectric line will begin another positive or negative deflection, and it ends at the very end of the T wave. Lead II is generally a good place to make your measurement. This may change depending on the R axis.

Normal QT intervals are between 300 & 450ms (0.30 - 0.45 seconds)

An easier way to measure is by looking at your 12-lead diagnostics. While rhythm interpretation may not always be up to par with your monitor; the measurements are usually pretty accurate.

What is the difference between QT & QTc?

The c in QTc stands for corrected. The QTc is the QT interval with a formulated correction based on the patient's heart rate (HR). The faster the HR the shorter the QT interval. The QTc may not always be accurate, but is commonly used for diagnostic purposes. Bazett's formula is used to determine QTc (well according to wikipedia it is).

Why is LQTS bad?

Remember the term refractory period?

Here is your refresher:

The absolute refractory period is the interval during which a second action potential absolutely cannot be initiated, no matter how large a stimulus is applied.

The relative refractory period is the interval immediately following during which initiation of a second action potential is inhibited but not impossible.[1]

Well people with LQTS have a prolonged refractory period, this includes a prolonged relative refractory period. As the definition explains, the relative refractory period tries not to but may invite pre-excitation. What this means is that another beat, from another part of the heart, may occur.

One example of aberrancy due to abnormal refractory period is Ashman's phenomenon. This is an arrhythmia with what is called a "long-short cycle". In atrial fibrillation, you may see a string of QRS complexes with longer R-R intervals (long cycle) followed by a PVC or a run of what looks to be PVCs. This will be followed by QRS complexes with shorter R-R intervals (short cycle). This is caused by pre-excitation during the relative refractory period, and the "PVC" is actually an aberrantly conducted supraventricular complex (bundle branch block pattern). The conduction was delayed due to a busy electrical pathway. Picture a traffic jam in the hearts one lane electrical highway. Below is an example, look at the R-R intervals pre & post premature beat.

Another complication of a longer refractory period is what is known as R on T Phenomenon. This condition may be more severe because it may interfere with hemodynamic stability. A premature complex finds it's home on the tail end of a supraventricular complex and takes over. While the ventricles are attempting to repolarize another focus decides he wants to take over. The best way to do this is by depolarizing while the other pacemaker is repolarizing. Like attacking a sleeping enemy. Below is another image stolen from Google. Those complexes are ventricular in origin.

Another risk associated with LQTS is sudden cardiac arrest. That one doesn't need much explanation. The cause is most likely an arrhythmia brought on by the R on T phenomenon.

More on LQTS to come. If any information I have provided is thought to be inaccurate, please let me know (Tom). I have no problem with being wrong, there is a first time for everything (hopefully sarcasm was detected).

*Once again, all images stolen from Google searches.

C A S T and Narrative Fallacy

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 pot-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 something that 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?


^ 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]

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 Circulation. 2005;112:IV-58 – IV-66.
© 2005 American Heart Association, Inc.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Medications for Arrest Rhythms

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

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 excellent, but over an hour video. If you enjoy it and understand it, the video is far too short.


^ 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.


Why Can't Medics Resuscitate? II

I thought we were working on Why Can't Medics Intubate? Why Can't Medics Resuscitate.

So did I. There I was, just minding my own business, when all of a sudden, out of nowhere SumdoodTM opens this can of worms. I'm completely innocent, I tell you.

OK, now that I have completely exonerated myself offered up this lame excuse, let's take a slightly more organized approach to this resuscitation stuff. I really was trying to ease into it. A shorter than usual post. Just presenting the overview of the study. Not anything in depth. Just putting a toe in the water.

What is state of the art resuscitation?

Even the answer to that is not as simple as it would seem. Several people have mentioned that the use of epinephrine, amiodarone, lidocaine, et cetera, remains in the ACLS (Advanced Cardiac Life Support) guidelines. These critics point out that being in the guidelines is evidence that these treatments have a scientific basis. Surely the AHA (American Heart Association) would not come up with these treatments without a rigorous scientific basis.

Exactly! The AHA wouldn't do that!

Would they?

There is very little high-level evidence for resuscitation therapies, and many traditional treatment recommendations such as the use of epinephrine/adrenaline, are based on animal studies and reluctance to change an existing treatment recommendation until it is proven ineffective or less effective than a novel therapy.[1]

During cardiac arrest, basic CPR and early defibrillation are of primary importance, and drug administration is of secondary importance. Few drugs used in the treatment of cardiac arrest are supported by strong evidence. After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway.[2]

Let me just change what you focus on in reading this paragraph. I am not changing any of the words. People seem to think this paragraph is telling them that the ALS is important. It is not. In stead, look at it this way.

During cardiac arrest, basic CPR and early defibrillation are of primary importance,[2]

What does primary mean in this case?

Primary = more than any other treatment.

and drug administration is of secondary importance.[2]

What does secondary mean in this case?

Secondary = a whole category below any treatment of primary importance.

Few drugs used in the treatment of cardiac arrest are supported by strong evidence.[2]

Surely epinephrine is supported by strong evidence.

No. I'll get to that in a minute. First the change in emphasis.

After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway.[2]

These are so important that they are only things you can do, things you may consider, in addition to the stuff you can consider you may add an advanced airway.

See, they want you to intubate.

The advanced airway can be any alternative airway. The important thing to notice is that this is after you have taken care of the important stuff - continuous compressions and defibrillation. This should never interrupt compressions.

typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital discharge.[3]

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.[4]

See! There is evidence, however, that the use of vasopressor agents favors initial ROSC (Return Of Spontaneous Circulation). That is a good thing. If you don't get pulses back, you can't resuscitate the patient.

It is true, that if you do not get pulses back, you will not resuscitate patients. If we stopped when we got pulses back, declared victory, and paid no attention to what happened after, then epinephrine would be a success.

Epinephrine leads to no real improvement. Epinephrine is a short term fix.

Epinephrine is like cocaine. Cocaine may make the person feel better in the short term, but that is not a good justification for the use of cocaine.

Epinephrine allows a bunch of whackers to high five each other when they get pulses back, even though they are decreasing the chances of long term survival for the patient.

Decreasing the chances for long term survival for the patient?

More patients with pulse, but no more patients surviving, probably means more patients dying in the hospital due to something bad from the epinephrine.

Let's go back to that first quote . . .

The first quote was not from ACLS. Why did you start with that?

Actually, it is. I do not know why it is not included with the rest of the 2005 links.

So, back to that first quote. This shows a big problem with the approach of the people involved.

There is very little high-level evidence for resuscitation therapies, and many traditional treatment recommendations such as the use of epinephrine/adrenaline, are based on animal studies and reluctance to change an existing treatment recommendation until it is proven ineffective or less effective than a novel therapy.[5]

until it is proven ineffective or less effective than a novel therapy.

How much effort is being put into even finding out if it is effective? There is a huge bias toward accepting the traditional treatment. There is no need to provide evidence that epinephrine works. Epinephrine is the traditional treatment.

Traditional means that it has been around a while and is better than the alternative.


Traditional treatments include leeches to remove blood, because medieval doctors were trying to balance the humours in the body. Eventually, people realized that bleeding people to death with the traditional treatment had nothing to do with being effective or with being safe, never mind being both effective and safe.

Until we have evidence that a treatment is both effective and safe, we should not be encouraging widespread use of that treatment.

In cardiac arrest, epinephrine has not been shown to be effective. In cardiac arrest, epinephrine has not been shown to be safe. The presumption of the experts is that epinephrine needs to be shown to be ineffective or less effective than a new treatment. They don't even seem to consider the possibility that epinephrine could be harmful. This kind of bias is inappropriate.

I'm not even getting started on the problems with the typical antiarrhythmic placebos and their significant toxic effects (amiodarone and lidocaine). At least, not yet.


^ TM Sumdood
An often sighted, never captured, never photographed denizen of the world of Ambulance Driver. As with Big Foot, his existence a subject of controversy and exaggeration.
Sumdood: Evil Criminal Mastermind

^ 1 Controversial Topics from the 2005 International Consensus Conference on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations.
Nolan JP, Hazinski MF, Steen PA, Becker LB.
Resuscitation. 2005 Nov-Dec;67(2-3):175-9. No abstract available.
PMID: 16324986 [PubMed - indexed for MEDLINE]

^ 2 Circulation. 2005;112:IV-58 – IV-66.
© 2005 American Heart Association, Inc.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Access for Medications: Correct Priorities

^ 3 Circulation. 2005;112:IV-58 – IV-66.
© 2005 American Heart Association, Inc.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest

^ 4 Circulation. 2005;112:IV-58 – IV-66.
© 2005 American Heart Association, Inc.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Medications for Arrest Rhythms

^ 5 Controversial Topics from the 2005 International Consensus Conference on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations.
Nolan JP, Hazinski MF, Steen PA, Becker LB.
Resuscitation. 2005 Nov-Dec;67(2-3):175-9. No abstract available.
PMID: 16324986 [PubMed - indexed for MEDLINE]


Long QT Syndrome Part I

Long QT Syndrome (LQTS) is thought to be suspect as the cause for more and more deaths. Sudden cardiac arrest and SIDS have been researched as possible consequences of LQTS. Although this electrocardiographic abnormality is very deadly, it is not commonly taught to the prehospital care provider or many other clinicians for that matter.

From Pubmed:
BACKGROUND: Many classes of medications initiated by clinicians can cause adverse events, such as cardiac disturbances. One such adverse outcome is that of acquired long QT syndrome, which can lead to arrhythmias and sudden death. When health care practitioners were surveyed about their knowledge of this condition, 20% indicated they knew very little about long QT syndromes and more than 30% failed to check on current therapy before prescribing QT-prolonging medications. METHODS: A case will be presented to illustrate the importance of understanding this syndrome. RESULTS: The causes and pathophysiology of acquired long QT syndrome are discussed, and the resources for clinicians to obtain more information and growing number of offending medications leading to acquired long QT syndrome are provided. CONCLUSIONS: On-going education is needed to heighten awareness in the health care community to prevent the deleterious outcomes associated with medication induced acquired long QT syndrome.
So let us heighten the awareness of the health care community.

More to come...

Induced Hypothermia Part II

Here are two protocols for induced hypothermia following return of spontaneous circulation (ROSC).

The first protocol (above) is from Wake County EMS. This protocol utilizes external cooling with ice packs and internal cooling via IV with cold saline. A supervisor responds to every cardiac arrest in Wake County and provides the cold saline. They have a small refrigerator in each supervisor vehicle. Wake also utilizes paralytics within this protocol. They use paralysis to bypass shivering; since shivering counteracts hypothermia. A non-depolarizing paralytic to avoid the fasciculations which are a side effect of depolarizing paralytics.

The second protocol (below) is from my own service, Lee County EMS. It is a little more basic and we do not utilize paralytics. We don't monitor temperatures, as of yet, either. We utilize this protocols for post-ventricular fibrillation arrests with ROSC. We have a refrigerator in every ambulance for our Cardizem, Succs, Ativan, and Cold Saline. We use the same cooling measures as Wake. We do not have any data yet, this was just started at the beginning of this year.

Click here to read a 2003 article from Circulation, the journal of the American Heart Association.

Click here for quite a bit of information provided by Wake County EMS

Induced Hypothermia Part I

"Arctic Alert"

If you are in EMS and do any continuing education of your own, or subscribe to one of the few EMS magazines, you have probably heard of induced hypothermia. I first learned of induced hypothermia at a clinical conference in 2007. Brent Myers, the medical director of Wake County EMS was the speaker. This was an Eagles conference topic, so it struck a particular interest with me.

The Concept

Over the years, since the conception of EMS, cardiocerebral resuscitation has been an evolving concept. Treatments have been tried, researched, and protocols have been written and rewritten. The American Heart Association (AHA) has updated their recommendations multiple times. The aim has been to return spontaneous circulation (give the patient their own pulse back). We have successfully discovered what we think works best. BLS before ALS, more chest compressions with less interruptions (see Why Can't Medics Resuscitate by Rogue Medic). The ResQPod has received a class IIA AHA recommendation, and Amiodarone has become the all-in-one dysrhythmic (selective cardiotoxin, thanks AD). More patients are making it to the hospital with a pulse.

But how many more patients are walking out of the hospital?

Almost none. Well until this revolutionary treatment came. The research is still relatively new in the world of medicine, so as you can imagine, it is still a great debate amongst physicians. The research that we do have shows incredible results. In fact, AHA has been recommending the use of induced hypothermia for a few years now.

Okay, what is it?

The treatment is used in hopes to improve cerebral outcome in a post-arrest patient. The hypothermic state is thought to slow cellular metabolism. This slows cerebral hypoxia, necrosis, and anaerobic metabolism which slows impending acidosis.

The Results

Number needed to treat or NNT is simply how many patients it takes to show one with improvement from a specific treatment modality. So if your NNT is 45, as it is with Lopressor (metoprolol), out of 45 STEMI patients treated with Lopressor, only one will show improvement. This is obviously an average and doesn't mean that you can't have two or three of the 45 show improvement.

The NNT for induced hypothermia following return of spontaneous circulation (ROSC) is six. That's right, out of every six patients that have been treated with induced hypothermia, one has walked out of the hospital.

Wake County EMS has done some great research on this topic. Take a look at the graphs below.

The first graph* (above) shows neurological improvement in about 21% more patients when treated with induced hypothermia, and a reduction in mortality of about 22%. Those numbers are incredible.

This second graph* (above) shows an obvious improvement in maintaining ROSC, patients making it to admission, patients being discharged, and neurological improvement.

So why isn't everyone doing this?

The simple answer: It is still a new concept and is not universally accepted despite what research we have.

*All images courtesy of Google searches

Back From ClinCon

I am back from Orlando and ready to start posting again. My team made the finals and took 5th place overall. You have to remember that it is a game, and the winner isn't necessarily someone you would want to take care of you or a loved one. We had a good time and attended quite a few presentations.

I have quite a bit I would like to post about here soon.

Some of what to look forward to:
  • Long QT Syndrome
  • Induced hypothermia
  • More on prehospital immobilization
  • A discussion on stable/unstable vs. symptomatic/asymptomatic
  • More reviews of prehospital research
You may have also noted new authors. Jason Winter and Star of Life Law. I'm not sure how often they will be posting, but I am sure that anything they add will be worth reading. I also have one more author on the way, since the blog isn't becoming as cluttered as I once thought it would. His name is Jason Ausman and he is a critical care/flight medic for my organization. I have been involved in many discussions with this individual and I am certain he will have some great knowledge to add. Please welcome him with the usual scrutiny.

Thanks for stopping by,

Adam Thompson, EMT-P

Why Can't Medics Resuscitate? I

I thought we were working on Why Can't Medics Intubate?

We still are. This is just a change in perspective. A study,[1] not yet published, but available on line, shows part of the problem with resuscitation.

What is that?

As I have stated many times before, we put the ALS (Advanced Life Support) before the BLS (Basic Life Support). We waste time on ALS, that does nothing good for the patient, at the expense of the BLS. The BLS treatments - continuous compressions and rapid defibrillation - have been shown to work. The ALS, well maybe we should start calling ALS Alternative Medicine Life Support.

Alternative Medicine?

We keep making excuses for why ALS does not improve outcomes. Maybe a little homeopathy (pardon the pun), some acupuncture (not on the sternum with the needles), some psychics to talk to the not quite dead, yet . . . .

Ok, OK, what does the study say?

It starts with, SEE EDITORIAL, P. XX., but there is no editorial listed. I think they just realized that this paper would ruffle a feather or two and there will be some ALS apologist will come up with something in a few days.

Editor’s Capsule Summary

What is already known on this topic

Decreased interruption of chest compressions in out-of-hospital cardiac arrest is strongly associated with increased survival in animal models and clinical trials. Little is known, however, about the specific issues that lead to interruptions.

What question this study addressed

What are the frequency and duration of cardiopulmonary resuscitation chest compression interruptions associated with paramedic endotracheal intubation during out-of-hospital cardiac arrest?

What this study adds to our knowledge

In 100 out-of-hospital cardiac arrests, patients' chest compressions were interrupted twice, on average, because of efforts to intubate, with a mean total interruption time of nearly 2 minutes.

How this might change clinical practice

This adds support for the current movement to de-emphasize intubation and delay it until later in resuscitation attempts for out-of-hospital cardiac arrest.

We have been encouraging paramedics to draw people toward the light - the laryngoscope light.

Is there evidence of a benefit of intubation in cardiac arrest treatment?


Intubation in cardiac arrest is as much wishful thinking as epinephrine, lidocaine, bretylium, amiodarone, IV/IO/IC access, et cetera.

Like zombies they follow our voodoo into the ICU as brain dead consumers of massive amounts of resources, but they do not get better.

We know what works - BLS treatments - continuous compressions and rapid defibrillation. We are not satisfied with that, so we come up with things to interfere with the BLS treatments. The above list of ALS treatments have only been demonstrated to be effective at delaying/interrupting/discouraging/interfering with effective treatments.

What has happened to resuscitation rates as ALS has been de-emphasized and more emphasis has been placed on continuous compressions?

They seem to have tripled in most of the places that have cut back on the ALS and emphasized the BLS.


If they were 5%, they are now 15%.

If they were 15%, they are now 45%.

So, why are we still wasting time with ALS?

Maybe we should consider ALS to be a Reversible Cause of continuing Cardiac Arrest.


^ 1 Interruptions in Cardiopulmonary Resuscitation From Paramedic Endotracheal Intubation.
Wang HE, Simeone SJ, Weaver MD, Callaway CW.
Ann Emerg Med. 2009 Jul 1. [Epub ahead of print]
PMID: 19573949 [PubMed - as supplied by publisher]


Why Can't Medics Intubate? Some comments

This was supposed to be a simple question, but not really Why Can't Medics Intubate? I guess I should have anticipated, based on a lot of experience with the topic, that the conversation would not go as planned.

What was the plan?

The plan was not to suggest that few medics can intubate well, or that no medics can intubate well. If there is a difficult prehospital airway, do not expect many anesthesiologists or emergency physicians to volunteer to place the tube. Except for those with an EMS background, these physicians will not be comfortable in this setting. Even in the airway seat of an ambulance, they will feel like fish out of water.

This is not a criticism of anesthesiologists or emergency physicians. When I am being critical of either, or both of them, I will try to make it clear.

Why work in a setting that is uncomfortable? This is something that some people have trouble learning. It was one of my many problems. Trying to prove that you can do something, regardless of the setting, is just a bad idea - and bad patient care. Get the patient to the place where you are most likely to be successful in placing the tube. If you mess around for 10 minutes, in the spot where you found the patient, is there any guarantee that you will place the tube? No. If you move the patient, there is still no guarantee, but you at least give the patient a better shot at a patent airway. And isn't that the goal?

Well, then why not just drop in a King LT, or LMA (Laryngeal Mask Airway), or CombiTube, or some other alternative airway?

No good reason not to. We just are not used to having these alternatives. I have worked places that only had BVM (Bag Valve Mask) and suction as airway alternatives. Other services had the EOA (Esophageal Obturator Airway) - all the problems of intubation and all of the problems of the BVM, but few of the benefits. Things have changed.

And I don't mean that adding RSI (Rapid Sequence Induction) is a new thing. Paramedic RSI has been around since the 1970s. 1970s and new do not belong in the same sentence.

One thing has not changed - medics identify themselves by the ability to intubate.

So why are so many medics so bad at intubation?

Wow! It is almost as if you can read my mind. That is what I was going for.

1. Most medics do not understand intubation anywhere near as well as they believe they do. They have often been taught by similarly limited medics.

2. Most medics are lazy. How often do you see them practicing with a mannequin, or even asking the boss to get a mannequin, so that they can practice? What about asking to get some cadaver lab experience? OR experience? Anyone?

I think the number of medics, who seek this practice is much smaller than the number of medics who can't intubate in these studies. Please provide me with some evidence, if you disagree. In the absence of evidence to the contrary, I maintain that most medics are lazy.

3. We do not know why we intubate.

Less than 8 intubate?

I need to protect the airway.

Dude, I have RSI. I intubate because I can intubate.

What if QA/QI/CYA looks at my chart and gigs me for not intubating the patient?

Et cetera.

Well then, why should we be intubating?

We should only be intubating because we have evidence that it leads to better outcomes for the patient.

We can't even get research that shows that medics can intubate. How are we going to get evidence that patients benefit from intubation?

Actually, there is evidence that medics can intubate. With aggressive medical oversight, high success rates and near zero esophageal intubation rates are not only possible, but should be expected.

This is from one system with aggressive medical oversight.

Our paramedics successfully intubated 95.5% of all the patients receiving succinylcholine. This is comparable to other published success rates for prehospital, paralytic-assisted intubation4-7 (Table 5).

We had a total of six unrecognized esophageal intubations. This rate of 0.4% is similar to the rate of esophageal intubations in other studies of paralyzed patients.2,7

In 1990, we added capnography and a tube aspiration device to all paramedic units. Since 1990, we have had only one case of unrecognized esophageal intubation, a case in which an end-tidal CO2 value of zero was ignored. It is likely that the addition of capnography and a tube aspiration device has, and will, decrease the incidence of unrecognized esophageal intubation.[1]

We feel one critical aspect of our program that has contributed to our success is the combination of excellent training and skill maintenance coupled with strong on-line and off-line medical control. Without this combination, the use of prehospital succinylcholine should not be undertaken.

In our study, prehospital succinylcholine appears to be safe and effective. The next step is a controlled, prospective study utilizing a large single system or multisystem approach. This should include outcome studies to determine not only whether the paralytic agent is safe and effective, but also whether its use affects outcome.[1]

Using systems like this, we need to study the outcomes to see if the effect of intubation is positive. Unfortunately, the outcomes research has generally been in systems that do not seem to have high quality quality. What is the point of studying the outcome of bad airway management? We already know it is bad. What we wonder about is - Why is bad airway management tolerated by those responsible for oversight of airway management?

It appears to be clear that medics can intubate at a rate that would be acceptable in the hospital. We need to stop making excuses for the systems that do not maintain this level of competence.

Still, we need to evaluate the effect of intubation on outcomes.

Not the effect of intubation by National Registry Parrot Medics, but the rate of intubation by competent medics.

If we refuse to evaluate outcomes, we should not be intubating.


^ 1 Prehospital use of succinylcholine: a 20-year review.
Wayne MA, Friedland E.
Prehosp Emerg Care. 1999 Apr-Jun;3(2):107-9.
PMID: 10225641 [PubMed - indexed for MEDLINE]