Medical Mythology | Paramedicine 101

Charging the Defibrillator While Continuing Chest Compressions – Part II

12/27/2011 by Rogue Medic 5 Comments

Also posted over at Rogue Medic (now at EMS Blogs).

Continuing, after a 6 month delay, a discussion of an EMS 12 Lead article from Part I. ACLS (Advanced Cardiac Life Support) recommends charging the defibrillator during compressions. This is no less of a recommendation than giving epinephrine. How many people ignore ACLS guidelines for compressions during charging, but claim that it is evil to disobey anything ACLS recommends on epinephrine, amiodarone, or ventilations?

Analyses of VF waveform characteristics predictive of shock success have documented that the shorter the time interval between the last chest compression and shock delivery, the more likely the shock will be successful.¹⁴¹ A reduction of even a few seconds in the interval from pausing compressions to shock delivery can increase the probability of shock success.¹⁴² ^[1]

Extra pauses in compressions add to the time without compressions.

If the medic/nurse/doctor using a manual defibrillator recognizes a shockable rhythm, why not provide compressions while charging the defibrillator?

Some people will say that this is dangerous.

Image credit.

But if someone accidentally delivers a shock during compressions, people will be killed!

In a systematic review, Hoke et al. summarized 29 reports of accidental deﬁbrillator discharges, of which only 15 occurred during resuscitation attempts.²¹ Symptoms included tingling sensations, discomfort, and minor burns, but no long term effects or major consequences were reported.^[2]

Where are the dead bodies we hear so much about?

Where are the medics/nurses/doctors needing to be defibrillated back to life?

There was only one incident where a shock was delivered while a rescuer was actively performing chest compressions. However, the compression transcript continued without any visible change to CPR administration, suggesting that the rescuer was unaffected by the event. Review of clinical records and audio transcripts revealed no evidence of inadvertent shocks to rescuers. In addition, there was no signiﬁcant difference in the incidence of inappropriate shocks to patients associated with charging during compressions (20.0% vs 20.1%; p = 0.97). ^[2]

In this study, there was one case of a shock being delivered during compressions, but nobody seems to have been affected by this shock.

What happened to the automatic death that ACLS instructors spend so much time describing?

Where is the evidence?

In the current study, charging during compressions decreased median pre-shock pause by over 10 s, which previous studies suggest could have a dramatic effect on clinical outcomes. We previously reported an almost two-fold increase in the chances of successful deﬁbrillation for every 5 s reduction in the pre-shock pause.⁹ Similarly, Eftestøl et al. found that a 10 s hands-off period prior to deﬁbrillation would roughly halve the probability of obtaining ROSC.⁶ ^[2]

The risk to rescuers appears to be minimal, but the possible benefit to patients may be dramatic.

Click on image to make it larger.

The difference in time without compressions is significant.

Interestingly, we found that the most efﬁcient technique with regard to minimizing pauses was not the AHA recommended method of pausing to analyze, resuming CPR to charge, and then pausing again to deﬁbrillate. Rather, charging at the end of every 2 min CPR cycle in anticipation of a shockable rhythm and then pausing only once, brieﬂy, to both analyze and either shock or disarm was associated with signiﬁcantly shorter total pause duration in the 30 s preceding deﬁbrillation. ^[2]

If we see asystole, we do not deliver a shock. We cancel the shock.

If we see PEA (Pulseless Electrical Activity, such as sinus rhythm, sinus tachycardia, sinus bradycardia, or any other non-shockable rhythm), we do not deliver a shock. We cancel the shock.

Cancelling the shock is not going to be the same for each defibrillator, but we do need to know how to cancel the shock for each machine we use. We can read the instructions.

How?

We can turn on the monitor, charge it up to the setting we would use to defibrillate, and try to figure out ways to get the charged defibrillator to turn the shock off. We should already know how to do this.

All that appears to be required is competence. Why is that so difficult?

Why do we keep making excuses for misbehavior?

Footnotes:

^[1] CPR Before Defibrillation
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Rhythm-Based Management of Cardiac Arrest
Defibrillation Strategies
Free Full Text from Circulation with links to Free Full Text PDF

^[2] Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study.
Edelson DP, Robertson-Dick BJ, Yuen TC, Eilevstjønn J, Walsh D, Bareis CJ, Vanden Hoek TL, Abella BS.
Resuscitation. 2010 Nov;81(11):1521-6.
PMID: 20807672 [PubMed - indexed for MEDLINE]

Filed Under: Cardiac Arrest, Heresy, Medical Mythology, Research, Rogue Medic

Does Epinephrine Improve Survival from Cardiac Arrest

12/12/2011 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs).

Even though epinephrine (adrenaline) is used automatically in cardiac arrest, and there is evidence that epinephrine helps to produce a pulse (ROSC – Return Of Spontaneous Circulation), there is no evidence that epinephrine improves the only survival statistic that matters – discharge from the hospital with a brain that still works. There were so many deviations from assignment protocol in their 2009 study,^[1] that the authors decided to examine the results based on what treatment patients actually received. They refer to epinephrine as adrenaline, which is the same drug. I will use adrenaline for consistency.

Our randomized study was analyzed on an intention-to-treat basis.⁴ As expected; some patients in the intravenous group had achieved ROSC before adrenaline could be given, while some in the no-intravenous group received adrenaline for different reasons. For example, it was permitted to place the IV line 5 min after ROSC. If re-arrest occurred, adrenaline could be administered if indicated by the CPR guidelines.⁷ ^[2]

In the no andrenaline group, 37 of the 433 patients did receive andrenaline.

In the adrenaline group, 85 of the 418 patients did not receive andrenaline.

For 3 patients, the authors were unable to tell whether andrenaline was given and these patients were excluded.

This changes the data to 367 patients in the adrenaline group and 481 patients in the no adrenaline group.

Patients in the adrenaline group were more likely to be admitted to hospital and an intensive care unit compared to the no-adrenaline group (OR 2.5 CI 1.9, 3.4 and OR 1.4 CI 1.0, 1.9, respectively). ^[2]

This is nothing new. Patients receiving andrenaline are more likely to have ROSC. All that really matters is what happens after ROSC.

If the patient loses pulses after ROSC, giving more adrenaline may not produce the desired effect – another ROSC.

First look at Table 1. The duration of CPR is much longer with the adrenaline group. Is this because of patients losing pulses?

Click on images to make them larger.

You can also see how few drugs were given to the no adrenaline group. They were not supposed to receive any drugs, but the use of adrenaline was the only criterion for reassigning patients in this reanalysis of the data. Atropine was given to 2% of the no adrenaline group and amiodarone was given to 2%. Was there overlap of these patients? We can’t tell.

The defibrillations were also significantly different. More patients were shocked in the adrenaline group, but more patients in the adrenaline group were in VF (Ventricular Fibrillation) initially. How many of the patients with PEA (Pulseless Electrical Activity) or Asystole developed VF after adrenaline? More shocks were also used for each patient. Was this due to rearrest?

Now looking at Table 2

Adrenaline starts out 2 1/2 times more likely to produce a pulse (ROSC), but a lot of those patients appear to have lost those pulses before admission to the hospital, since Table 2 shows that 69 of the 175 adrenaline patients admitted with CPR (CardioPulmonary Circulation) in progress. Adrenaline wears off in several minutes and produces a lot of undesirable side effects.

More is not better, especially since the doses of adrenaline being given are already many times larger than would be given to any living human.

Most important is the neurological function. I do not want to be resuscitated with only enough neurological function to spend the rest of my life watching reality TV in a long term care facility, or worse. That is not a successful resuscitation.

Adrenaline = 48% admitted to the hospital, but only 6% alive one year later.

No adrenaline = 27% admitted to the hospital, but 12% alive one year later.

Adrenaline (epinephrine) is not just changing the location of death, but is cutting overall survival in half.

Is getting pulses back a good enough reason to kill half of the patients who could survive?

Of the patients admitted to the hospital, 11% of the adrenaline group were discharged with good brain function.

Of the patients admitted to the hospital, 45% of the no adrenaline group were discharged with good brain function.

Of the patients admitted to the hospital, 12% of the adrenaline group were alive one year later.

Of the patients admitted to the hospital, 44% of the no adrenaline group were alive one year later.

The actual use of adrenaline may be a surrogate marker for patients with bad prognosis, but that has previously only been published from studies without a group randomized to not receiving drugs.²¹ ^[2]

There are many limitations of this study, but the authors do not pretend that this is the final answer on adrenaline (epinephrine) in cardiac arrest. They do point out that we are not providing good care by continuing to use adrenaline without studying the outcome that matters – survival with good neurological function.

5% of the no adrenaline group survivors had significant brain damage.

20% of the adrenaline group survivors had significant brain damage.

Maybe the good news is that adrenaline does not produce a lot of survivors.

Droperidol, QT prolongation, and sudden death – what is the evidence – Part I

12/01/2011 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs).

I am continuing to look for evidence that droperidol deserves to be given a ~~scarlet letter~~ black box warning. The authors of this literature review take a look at several articles and some case studies.

Because the outcome of interest, sudden death caused by torsades de pointes, is uncommon and difficult to assess, QT prolongation has become a surrogate marker for potential arrhythmogenicity and is therefore commonly used in research and by regulatory agencies.¹⁸^[1]

Surrogate endpoints are great for making it seem that we know more than we actually do know. When there is not enough information, surrogate end points are a way of saying, If this belief is true, and this other belief is also true, then Treatment Z is safe (or dangerous), or saves X number of lives per year (or kills X number of patients who otherwise would have been expected to live).

The example that I repeatedly use is the Cardiac Arrhythmia Suppression Trial,^[2] which ended up demonstrating that treatment based on the surrogate endpoint of eliminating PVCs (Premature Ventricular Contractions) because they are associated with a higher rate of death actually resulted in tens of thousands of extra deaths.^[3] That is the difference between looking at surrogate endpoints (making assumptions about death rates) and looking at actual death rates.

a consistent relationship between the length of the QT interval and the risk of torsades de pointes or sudden death is not clearly established and might vary from drug to drug and from individual to individual. Hundreds of drugs are known to prolong the QT interval, with widely variable degrees of evidence for clinical dysrhythmias.^16,17 ^[1]

What did the authors find?

Because of the small number of studies and articles identified, we were unable to perform a true systematic review (ie, meta-analysis)²² ^[1]

First, what does the FDA (Food and Drug Administration) label recommend as the dosage of droperidol?

Adult Dosage: The maximum recommended initial dose of droperidol is 2.5 mg I.M. or slow I.V. Additional 1.25 mg doses of droperidol may be administered to achieve the desired effect. However, additional doses should be administered with caution, and only if the potential benefit outweighs the potential risk.^[4]

As if that caution does not apply to the use of every medication.

In one surgical study of 40 patients receiving three weight-based doses of droperidaol, which if given to a 70 kg adult, would be doses of 7 mg, 12.25 mg, and 17.5 mg. Much higher than 2.5 mg. Yes, this is surgery, so what does the FDA recommend about surgical dosing?

Dosage should be individualized. Some of the factors to be considered in determining dose are age, body weight, physical status, underlying pathological condition, use of other drugs, the type of anesthesia to be used, and the surgical procedure involved.^[4]

They certainly were not excluding surgery from their dosing recommendation.

QTc interval prolongation occurred within 1 minute of injection and did not increase with time. Prolongation of the median QTc interval occurred by 37, 44, and 59 ms, respectively, in a dose-dependent fashion; this was also statistically significant (P<.003). ^[1]

Of these patients receiving very high doses, how many died?

No dysrhythmias developed. ^[1]

There was a lower dose surgical study and a long-term psychiatric study. Again, there was QT prolongation, but no arrhythmia (dysrhythmia and arrhythmia are synonyms).

And there is one ED (Emergency Department) retrospective study –

Over a 4-year period, 15,374 patients received 18,020 doses of droperidol. Of the 682 patients who had an ECG performed after droperidol administration, 14 (3.1%) had prolonged QT intervals (defined as >480 ms) without evidence of any bundle branch block. Four of the 14 patients had previously documented prolonged QT intervals not associated with droperidol use. A control group (n=100) who had ECGs performed without the administration of droperidol had a similar incidence of prolonged QT intervals (4.0%). ^[1]

The patients who received droperidol appear to have been less likely to develop QT segment prolongation. With droperidol – 3.1% had QT prolongation. Without droperidol – 4.0% had QT prolongation.

The control group only had 100 patients, so each patient represents 1.0%, but if droperidol is so dangerous there should be more QT prolongation in the droperidol group. Maybe there is something about the way that droperidol is used in the ED that decreases the supposed danger.

These studies do not mean that droperidol is safe, but they do raise questions about the rush to add a black box warning to the droperidol label.

With the black box warning, the FDA essentially says, Lawyers, look here. You don’t have to demonstrate that droperidol is dangerous – we did that for you. Go sue some doctors.

These studies do not support the claim by the FDA that droperidol is dangerous. In Part II, I will continue with the case studies reviewed by the authors.

Footnotes:

^[1] Droperidol, QT prolongation, and sudden death: what is the evidence?
Kao LW, Kirk MA, Evers SJ, Rosenfeld SH.
Ann Emerg Med. 2003 Apr;41(4):546-58. Review.
PMID: 12658255 [PubMed - indexed for MEDLINE]

^[2] 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.

^[3] C A S T and Narrative Fallacy
Rogue Medic
Article

^[4] DROPERIDOL injection, solution
[Hospira, Inc.]
FDA label
DailyMed
Dosage and administration

Filed Under: Cardiology, Heresy, Medical Mythology, Pharmacology, Research, Rogue Medic

Is IV Bolus Nitro Dangerous – Part II

11/09/2011 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs).

Is it safe to treat CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure) with IV (IntraVenous) bolus doses of NTG (NiTroGlycerin or GTN – GlycerylTriNitrate in Commonwealth countries)?

Well, it isn’t too dangerous to study.

all patients received an initial 2-mg intravenous bolus of highdose nitroglycerin, . . . Subsequent 2-mg boluses of high-dose nitroglycerin were permitted every 3 to 5 minutes at the discretion of the treating emergency physician. Repeated administration of high-dose nitroglycerin was allowed for a period of up to 30 minutes, resulting in a maximum potential dose of 20 mg (2 mg every 3 minutes for 30 minutes).^[1]

Those high doses are enough to give a stroke to the doctors, nurses, and medics who think that CHF = Lasix (furosemide), but I am not writing this for people stuck in the 1980s. Most doctors, nurses, and medics appear to realize that nitrates are the most effective medication for CHF. The important question is How aggressive is too aggressive?

What was the effect on heart rate? We want to avoid bradycardia, which is a side effect of too much NTG.

Bradycardia does not seem to be a problem. As with severe pain, there is so much excess that a decrease does not even bring rates down into the normal range.

With respirations, the high dose NTG also only drops the rate to around the upper end of normal. Not exactly the life threat that nitrate alarmists pretend will occur.

We can’t skip blood pressure. This is the terror for those opposed to high doses of nitrates.

What about the hypotension?

If the blood pressure drops, it will stay that way – forever.

If you keep making that face, it will stay that way – forever.

Everybody knows that high doses of NTG will bottom out the blood pressure.

High doses of NTG only rarely cause a significant drop in blood pressure and that resolves spontaneously – just as it does with standard doses of NTG. These patients remained hypertensive, but with their blood pressures much less dangerously elevated than before the high dose IV boluses of NTG.

Maybe they did not give much NTG.

The majority (34.5%) of patients received 3 boluses of high-dose nitroglycerin (Figure 2), and the mean dose of high-dose nitroglycerin administered was 6.5 mg (95% CI 5.2 to 7.8 mg).^[1]

Following the protocol, the doses could have been much higher, but they are reassessing patients prior to giving further doses.

Wouldn’t patients receiving standard doses of NTG by pump would receive similar total doses?

20 μg/minute – 40 μg/minute would receive 0.6 mg – 1.2 mg (600 μg – 1,200 μg) over half an hour (the duration of the experimental dosing). Is there a difference between less than 1 mg and over 6 mg?

I left out one other bit of information. These patients were not just receiving bolus NTG. They were receiving the boluses in addition to IV NTG by pump.

The mean initial and ﬁnal intravenous nitroglycerin infusion rates were 23.6 μ g⁄minute (95% CI 15.4 to 31.9 μ g⁄minute) and 50.2 (95% CI 37.9 to 62.5 μ g/minute) for patients who received high-dose nitroglycerin. The mean initial intravenous nitroglycerin infusion rate for the nonintervention group was 31.7 μ g⁄minute (95% CI 26.0 to 37.3 μ g⁄minute); the ﬁnal intravenous nitroglycerin rate for nonintervention patients was not available.^[1]

The infusion rate for IV NTG started out within the range I gave, but ended up higher than that range, while they were receiving high dose boluses of IV NTG.

Not only are high dose boluses of IV NTG not the instant hypotension/death that some would have us believe, but they can be added to moderate dosing of IV NTG infusions and still not cause problems.

But what were the results?

First the baseline conditions –

Click on the images to make them larger.

I point out that the patients being treated with high dose boluses of IV NTG were much sicker starting out, but I have not shown the improvement.

The primary effectiveness endpoint of endotracheal intubation within 6 hours occurred in 13.8% (95% CI 4.8% to 29.5%) of patients treated with high-dose nitroglycerin and 26.7% (95% CI 15.5% to 40.8%) of the nonintervention patients.^[1]

With high dose IV boluses of NTG 13.8% of patients were intubated.

Without high dose IV boluses of NTG 26.7% of patients were intubated.

High dose IV boluses of NTG cut the intubation rate almost in half.

The primary safety endpoint of cardiovascular complications was 20.7% (95% CI 9.1% to 37.8%) in the high-dose nitroglycerin group (17.2% [95% CI 6.9% to 33.7%] with myocardial infarction and 3.5% [95% CI 0.4% to 15.0%] with symptomatic hypotension) and 28.9% (95% CI 17.3% to 43.1%) of the nonintervention patients (all due to myocardial infarction, with no episodes of symptomatic hypotension).^[1]

With high dose IV boluses of NTG 20.7% of patients had cardiovascular complications –

17.2% had heart attacks.

3.5% had symptomatic hypotension.

Without high dose IV boluses of NTG 28.9% of patients had cardiovascular complications

28.9% had heart attacks.

Zero% had symptomatic hypotension.

By golly, the warnings about hypotension were right!

the occurrence of symptomatic hypotension in the high-dose nitroglycerin group corresponded to a single instance that developed after administration of one 2-mg dose and resolved with a 500-mL ﬂuid bolus, without evidence of further complications.^[1]

As I have stated elsewhere,^[2],^[3] the 500 ml fluid bolus probably was not necessary, since nitrate-induced hypotension resolves spontaneously and without complications.

A rapid and profound decrease in blood pressure was also observed with use of high-dose nitroglycerin, without an associated increase in adverse events. Though encouraging, these results are preliminary, and the next logical step in the evaluation of high-dose nitroglycerin is an adequately powered, multicenter, prospective, randomized, double-blind, comparison trial. According to our investigation, conduction of such a trial seems feasible.^[1]

I keep hearing excuses for why this study is too dangerous to study.

A better conclusion is that it is too dangerous to not study.

Where is the evidence of danger?

Heart failure is one of the five most common admitting diagnoses in the US, so how can we ignore this? More than heart attack. More than asthma. More than almost everything else.

Footnotes:

^[1] Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis.
Levy P, Compton S, Welch R, Delgado G, Jennett A, Penugonda N, Dunne R, Zalenski R.
Ann Emerg Med. 2007 Aug;50(2):144-52. Epub 2007 May 23.
PMID: 17509731 [PubMed - indexed for MEDLINE]

Free Full Text PDF Download from Ferne.org

^[2] Is IV NTG Too Dangerous for EMS
Rogue Medic
Article

^[3] EMS NTG for CHF – Bolus or Infusion – Part II
Rogue Medic
Article

Filed Under: Heresy, Medical Mythology, Pharmacology, Research

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part IV

09/12/2011 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs).

Continuing from Part I, Part II. and Part III.

After assessing what it is that the abdominal pain patients want/expect from a visit to the ED (Emergency Department), how many X-rays it takes to deliver the same radiation as an abdominal CT (Computed Tomographic imaging), whether CTs increase the lifetime risk of cancer, and how many abdominal CTs equal some sort of measure of the radiation exposure of Hiroshima survivors, the authors conclude that people do not understand the risks of radiation.^[1] This study is followed by an excellent editorial.

The easy conclusion from these ﬁndings is, unsurprisingly, that patients are ill informed, and thus efforts to improve their education and awareness should help to mitigate the overuse of imaging and its consequent risks.^[2]

Dr. Wears does not discuss the validity of assuming that there is only one right answer to the questions asked. There is also a podcast discussing this study and discussing the editorial, but the podcast is similarly missing the problem with the study taking for granted that there is a single right answer to the study’s questions.^[3]

First, the “rational person” assumption holds that, given correct information, people should arrive at consistent choices about alternatives (eg, to image or not) based on the net expectation of probabilities and outcomes.²^[2]

If we make rational decisions, why do so many of us smoke?

If we make rational decisions, why do so many of us eat to the point of obesity?

If we make rational decisions, why do so many of us spend so much time watching reality TV?

Dr. Wears cites some of the studies that show that we do not make rational decisions. To insist that we make rational decisions is also irrational. Isolated examples of decisions that appear rational do not mean that a person makes rational decisions any more than a stopped clock being right twice a day means that the stopped clock keeps accurate time.

The authors provide excellent examples of irrationality in one question they present.

Click on images to make them larger.

How a multiple choice question is presented will affect way the answers are chosen.

Why is there no choice for I don’t know?

For most people not familiar with X-rays and CTs, the only honest and rational answer is I don’t know.

When graphing the results, we can further distort the results by making the distances between numbers completely arbitrary. Why present the choices as the Same radiation (the same, or zero difference is 50 x 0), 50 times more (greater by a factor of 50 x 1), 100 times more (greater by a factor of 50 x 2), 250 times more (greater by a factor of 50 x 5), 300 times more (greater by a factor of 50 x 6), and Over 350 times more (greater by a factor of 50 x at least 7).

Why blur the distinction between 100 times and 250 times? When the numbers become blurred, the numbers lose their meaning. When there is no difference in meaning between one number and a number 2 1/2 times as large, are we providing information or are we providing confusion?

We seem to most insist on stripping information of its meaning when we create multiple choice tests. Correct answers become a simple matter of memorization separated from understanding. This is one way to create the protocol monkey – the automaton, whom we claim is rendered harmless by being prevented from thinking. This desire to prevent the use of judgment may be the ultimate irrational decision.

If the difference between 100 and 250 is the same as the difference between 250 and 300, how do we expect anyone to notice differences in dosages? 100 mg – 200 mg – 300 mg – what’s the difference? With memorized answers, the only difference is whether it is graded as correct. With real patients, the differences can be fatal.

We memorize our way to recklessness.

We do not memorize our way to safety.

Previous literature estimates the radiation dose for an abdomen-pelvis CT to be equivalent to 100 to 250 2-view chest series.^2,10-12 For the purpose of this investigation, we used the conservative estimate of 1 abdomen-pelvis CT = 100 2-view chest radiographs.^[1]

I agree with their choice to use the more conservative number, but what this still does not do is put this in a context that helps people to understand. Without understanding something about the radiation exposure of an X-ray, this is an unknown. 10 times an unknown – 100 times an unknown – 1,000 times an unknown – what’s the difference?

Presenting misleading information to medically naive people and proclaiming Eureka! is misleading. We are not finding anything. We are presenting a spectacle, although not as much of one as Archimedes did running naked through the streets (assuming the legend to be true).

The second assumption is that the problem is “out there” in patients, not “in here” in physicians. This might be viewed as a form of the psychologist’s fallacy,³ the idea that although patients’ preferences might suffer from irrationality, ignorance, or irrelevant considerations, ours (physicians’) do not.^[2]

An excellent point that should be extended to researchers.

How much of the problem is in the study design?

What are we measuring?

If the purpose of controlled trials is to examine things objectively, why use a study that seems to ~~depend~~ insist on subjectivity?

I will write more about Dr. Wears editorial later, because it covers a lot of important material on making decisions.

Footnotes:

^[1] Patient perceptions of computed tomographic imaging and their understanding of radiation risk and exposure.
Baumann BM, Chen EH, Mills AM, Glaspey L, Thompson NM, Jones MK, Farner MC.
Ann Emerg Med. 2011 Jul;58(1):1-7.e2. Epub 2010 Dec 13.
PMID: 21146900 [PubMed - indexed for MEDLINE]

Free Full Text from Annals of Emergency Medicine with links to Free Full Text PDF Download

^[2] Risk, radiation, and rationality.
Wears RL.
Ann Emerg Med. 2011 Jul;58(1):9-11. Epub 2011 Apr 2. No abstract available.
PMID: 21459481 [PubMed - indexed for MEDLINE]

^[3] What patients understand about radiation exposure from CTs
David H. Newman, MD, and Ashley Shreve (spelling?)
Annals of Emergency Medicine podcast page
2011 July
Free Podcast in MP3 format

Annals of Emergency Medicine provides a podcast that summarizes the articles published that month. This is an excellent resource. The full July 2011 podcast is – Free Full Podcast in MP3 format. The full archives of Annals of Emergency Medicine podcasts is – Page with links to podcast segments and full month podcasts.

Filed Under: Assessment, Critical Judgment, Education, Heresy, Medical Mythology, Research, Risk Management, Rogue Medic

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part III

09/11/2011 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs).

Continuing from Part I and Part II.

After assessing what it is that the abdominal pain patients want/expect from a visit to the ED (Emergency Department), and how many X-rays it takes to deliver the same radiation as an abdominal CT, they move on to part 3.

Hiroshima?

Use imagery to switch the perspective from the rational to the emotional.

That would be more likely to get an emotional response from an architect.

A person with radiation injuries. That is more likely to produce an emotional response.

Bringing up the imagery of Hiroshima radiation exposure in a study is one way to get us to by-pass the purpose of an objective study, while retaining the appearance of objectivity. Was this the intent of the authors? Probably not, since they got this question from an earlier study. However, they may have appreciated the emotional appeal.

I don’t spend a lot of time examining patients after a CT, but they tend not to have that burned appearance. Visible burns are not the only damage from radiation, so the absence of that burned appearance does not mean that there is no damage.

Berrington de González et al⁴ projected 29,000 excess cancers as a result of the CT scans conducted in 2007.⁴ These cancers are expected to appear in the next 20 to 30 years, with an associated 50% mortality rate. Strategies for decreasing the risks associated with CT imaging include increasing efforts to educate physicians, improving radiation protocols to enable technicians to select the lowest-dose scanning techniques without compromising resolution, and increasing patient awareness of their own radiation exposure by using aids such as FDA medical imaging history cards.^2,8,11,15-18 ^[1]

How much of the risk of radiation is understood well enough to have clear Yes/No answers?

The most important omission is the context.

In what way can the radiation exposure of 2 to 3 CT scans be similar to the radiation exposure of survivors of Hiroshima?

What kind of understanding do these patients have of the varieties of radiation exposure experienced by the survivors of Hiroshima?

We could be asking the patients, How often does a CT make the diagnosis clear in the assessment of undifferentiated abdominal pain?

Or – How often does the CT change the diagnosis for undifferentiated abdominal pain?

This is one question that should be an obvious Yes.

Is it reasonable to disagree with the statement 2 to 3 abdominal CTs over a person’s lifetime can increase the chances of cancer?

This is not quantifying risk, but only stating that it can increase cancer risk.

Let’s turn the statement around and restate what the most popular answer means. 2 to 3 abdominal CTs over a person’s lifetime cannot increase the chances of cancer.

Is anyone really suggesting that?

What would be the basis for such a claim?

Again, would physicians do much better in answering the same questions?

To be continued tomorrow in Part IV.

Footnotes:

Free Full Text from Annals of Emergency Medicine with links to Free Full Text PDF Download

Filed Under: Assessment, Heresy, Medical Mythology, Research, Rogue Medic

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part II

09/10/2011 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs).

Continuing from Part I.

After assessing what it is that the abdominal pain patients want/expect from a visit to the ED (Emergency Department), they move on to part 2.

Second, we attempted to assess patients’ understanding of relative radiation exposure by asking them to compare the amount of radiation exposure from one abdomen-pelvis CT to increasing numbers of 2-view chest radiographs (standard posterior-anterior and lateral chest series).^[1]

And a graph of the responses is here. I added a red bar as an estimate of the responses that were not given because the patients thought that the radiation from a CT is less than the radiation from an X-ray.

When presented as 50 out of 121 who did not answer the question, it seems to be a large percentage, but it is only 50 out of about a thousand patients who did answer the question. Not a large percentage.

The authors included a footnote to the study that produced the numbers they are relying on, but they never specifically cite the X-rays per CT number from that study. This is probably because that study did not produce any simple answer. There is a lot of interpretation of the many factors involved in the study. Even then, the idea that the result can be presented as any simple answer would be misleading.

The simplest answer is in the response of those authors to criticism of their methods.

The concern is that radiation doses from CT are typically 100 times those from conventional x-ray examinations such as chest x-rays or mammograms and that there is now direct epidemiologic evidence of a small but significant increase in the risk of cancer at CT doses.^1-3 Because CT is such a superb diagnostic tool and because individual CT risks are small, the CT benefit–risk balance is generally by far in the patient’s favor.^[2]

Typically?

Is that with any defined size of the error bars?

Because CT is such a superb diagnostic tool and because individual CT risks are small, the CT benefit–risk balance is generally by far in the patient’s favor.

This does not appear to be the message being communicated by the authors of the study I am looking at. When we are dealing with any risks, we should understand the risks, but it does not help to exaggerate the risks.

Again, would physicians do much better in answering the same questions?

Are the answers in this study? Or does this muddy the waters?

To be continued tomorrow in Part III, and maybe Monday in Part IV.

Footnotes:

Free Full Text from Annals of Emergency Medicine with links to Free Full Text PDF Download

^[2] Computed tomography–an increasing source of radiation exposure.
Brenner DJ, Hall EJ.
N Engl J Med. 2007 Nov 29;357(22):2277-84. Review. No abstract available.
PMID: 18046031 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM with links to Free Full Text Comments and Free Full Text PDF Download

Filed Under: Assessment, Heresy, Medical Mythology, Research, Rogue Medic

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part I

09/09/2011 by Rogue Medic Leave a Comment

Also posted over at Rogue Medic (now at EMS Blogs).

How do we make medical decisions?

Do we have any idea of what we are deciding?

How can we improve our decisions?

This study looks at the knowledge of radiation risk among patients with abdominal pain. Some want a CT (Computed Tomographic Imaging), while others may not feel they are better at diagnosis than the doctor. What do they know about the radiation exposure from a CT?

CT is not inherently bad –

Unlike ultrasonography or radiography, CT provides greater level of detail and allows simultaneous imaging of organs, vessels, musculature, and bone. . . . Additional support for the liberal use of abdomen-pelvis CT is that it has been demonstrated to increase emergency physician certainty of diagnosis, decrease the need for emergency surgery from 13% to 5%, and avert up to 24% of proposed hospital admissions.^6,7 ^[1]

On the other hand . . .

there is growing concern that CT is being overused, and it is estimated that 1.5% to 2.0% of all cancers in the United States may now be attributable to the radiation from CT examinations.^2,4 ^[1]

About 1.6 million new cases of cancer are expected this year.^[2]

If correct, that would mean 24,000 to 32,000 new cases of cancer from CT.

About 572 thousand – or almost 0.6 million people are expected to die from cancer this year.^[2]

The new cancers are about 3 times the rate of the deaths. That means that a lot more people are being cured/going into remission, than are dying. (As a side issue – the cures are not due to alternative medicine. However, some of the deaths are due to delays in receiving treatment with real medicine, because of someone’s faith in alternative medicine. If anyone knows of any good research that suggests otherwise, please provide it. Cancer patients would love to have more choices of treatments that really work.)

Even with so much improvement in the treatment of cancer, are we significantly increasing our risk of cancer with little benefit, or no benefit?

We performed a cross-sectional study of adult patients aged 18 years and older who presented to the emergency department (ED) for the evaluation of acute, nontraumatic abdominal pain and assessed their expectations and conﬁdence with increasing diagnostic levels of medical evaluation and their understanding of radiation risk and exposure from abdomen-pelvis CT.^[1]

Part 1 is –

The goals of this investigation were 3-fold. The ﬁrst was to assess patients’ conﬁdence levels with medical evaluations that ranged from a physician-conducted history and physical examination (minimal technology) to one that included a history and physical examination, blood work, and an abdomen-pelvis CT (maximum technology).^[1]

What do patients with abdominal pain want?

Maybe even more than pain medicine, patients seem to want a CT. If that doesn’t provide answers, they want another one. As if radiation will work differently or the body will change or . . . .

Click on the image to make it larger.

Patient conﬁdence in the accuracy of progressive levels of medical evaluation is presented in Table 2. Conﬁdence was lowest for a medical evaluation that was limited to a physician-conducted history and physical examination. The addition of laboratory testing and imaging resulted in a nearly 4-fold increase in conﬁdence, with the highest conﬁdence level in patients who were presented with the option of CT.^[1]

Would physicians be much better at answering the same questions?

To be continued tomorrow in Part II, Sunday in Part III, and maybe Monday in Part IV.

Footnotes:

Free Full Text from Annals of Emergency Medicine with links to Free Full Text PDF Download

^[2] Cancer Facts & Figures 2011
American Cancer Society
Page with link to various forms of information – a Slide Presentation, and Full Text PDF Download

Filed Under: Assessment, Heresy, Medical Mythology, Research, Rogue Medic

Can We Simplify Triage by Using Just GCS

09/08/2011 by Rogue Medic 2 Comments

Also posted over at Rogue Medic now at EMS Blogs. Go check out both sites.

A trauma system must provide the full gamut of available resources to seriously injured patients, but frequent overtriage of patients has financial and administrative ramifications that can ultimately jeopardize trauma system viability.^2,9^[1]

This is an interesting study from 2002, that looks at the possibility of simplifying trauma triage criteria and improving the accuracy of trauma triage criteria, by making it just one trauma triage criterion.

Imagine a system where we intentionally ignore the usual horribly inaccurate trauma triage criteria, such as MOI (Mechanism Of Injury). And these are not even the usual criteria, because this is in a system with criteria already modifieded to avoid a lot of overtriage.

Field criteria for automatic trauma team activation were as follows:

gunshot wound to the torso or neck; gunshot wound to an extremity with loss of distal pulse; identification of a femur, tibial, or spinal fracture; any long bone open fracture; prehospital identification of airway compromise or the need for intubation in the field; systolic blood pressure < 90 mm Hg; heart rate < 60 beats/min or > 130 beats/min; spontaneous respiratory rate < 10 breaths/min or > 30 breaths/min; or paralysis in one or more extremities.

Other than the gunshot wound parameters, mechanism of injury criteria were not routinely used to determine trauma team activation for victims of falls and motor vehicle crashes.^[1]

I like the idea, but the way to assess this is not by hospital admissions.

The principal outcome evaluated in this study was the need for patient hospitalization to treat documented injuries.^[1]

This is the big problem with the study. The authors do admit that this is a limitation, patients may be admitted just for observation. However, the authors do not seem to see the way that GCS can be much more likely to correlate positively with admission. Nowhere else in the study does it mention that they limited this to admissions to treat documented injuries.

If the patient has a GCS of 14, how many doctors will admit the patient overnight, just for observation? How many just for observation patients does it take to affect the data?

The same is true for anything else that might be expected to result in a lot of admission for observation. The possibility of a head injury is so potentially catastrophic, that we have had exponential growth of CT scans of the head, because you can’t be too safe. Head CTs have become so common that we can expect it to increase some cancer rates over the next couple of decades. Just another example of being too safe.

Multivariate stepwise logistic regression analysis was performed to determine which variables within the data set were significant predictors of admission. The dependent variable in the analysis was admission versus nonadmission.^[1]

This is the wrong endpoint. A patient could have been transported to the local not trauma designated hospital and been admitted, as well. If the patient could have been adequately treated at a not trauma designated hospital, should that patient be considered to have appropriately bypassed the not trauma designated hospital just because the patient was admitted to a trauma designated hospital?

Any cause for admission is acceptable. I am being driven to the hospital for a respiratory problem (not yet diagnosed as pneumonia); there is a collision; everybody is uninjured, but the vehicles is not capable of being driven, so I continue to the hospital by ambulance. If I am transported as a trauma, I may expect to be admitted for the pneumonia, not for trauma – but I should expect that I will not be admitted for the lack of injuries due to trauma.

The present study was designed to evaluate traditional triage parameters for predicting hospitalization after MVC. The GCS score was the only prehospital physiologic parameter that provided a clinically relevant and measurable difference between patients who were hospitalized versus those who were discharged from the ED, excluding patients who were in extremis and died shortly after arrival. This reliability was not changed by the presence of positive prehospital anatomic criteria or prehospital airway issues. Three tiers of probability for admission were evident: a very high probability (96%) for GCS score 12, a high probability (73%) for GCS score of 13 to 14, and a relatively low probability (32%) for GCS score of 15. Neither the suspected presence or absence of drugs, alcohol, or a reported loss of consciousness compromised the accuracy of the GCS as a predictor for imminent hospitalization. This is not surprising, because disorientation, belligerence, mild confusion, or history of loss of consciousness does not significantly affect the GCS score. Retrospectively, had a GCS score of 14 been used to trigger trauma team activation, the overall undertriage rate of 19.1% would have improved to 4.4%.^[1]

There is certainly something to consider about this, but the validation needs to be something more objective than admission.

Footnotes:

^[1] A prehospital glasgow coma scale score < or = 14 accurately predicts the need for full trauma team activation and patient hospitalization after motor vehicle collisions.
Norwood SH, McAuley CE, Berne JD, Vallina VL, Creath RG, McLarty J.
J Trauma. 2002 Sep;53(3):503-7.
PMID: 12352488 [PubMed - indexed for MEDLINE]

Filed Under: Assessment, Heresy, Medical Mythology, Rogue Medic

Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia

05/27/2011 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs).

On the most recent episode of the EMS Research Podcast,^[1] Harry Mueller, Bill Toon, and I discuss a recently published paper examining what effect prehospital fentanyl has on hypoxemia or on hypotension.

This study’s objectives were to assess for association between prehospital fentanyl administration and the occurrence of either of the following: hypotension, deﬁned as a drop in systolic blood pressure (SBP) to below 90 mm Hg in a patient at least 5 years of age, or hypoxemia, deﬁned as a drop in peripheral oxygen saturation (SpO₂) to below 90%.^[2]

There were 500 patients and many of them received more than one dose of fentanyl. Several received 6 separate doses of fentanyl.

Even with so many doses given, the mean dose and maximum dose were not that high.^[3]

The median dose of fentanyl per administration was 1.1 µg/kg (IQR 0.8–1.4; range 0.25–3.5 µg); the mean dose was 1.1 µg/kg (SD 0.46). Expressed as a total dose per patient (i.e., summing all doses in a given patient), the median dose was 2.5 µg/kg (IQR 1.7–3.9) with a mean of 3.0 µg/kg (SD 1.8).^[2]

1.1 µg/kg per dose.

The maximum single dose is unusual and is not explained. range 0.25–3.5 µg which should be /kg.

How did one patient receive such a large single dose – 3.5 µg/kg? The thing that makes the most sense (if this was a dosing error) is that this was a small pediatric patient. I carry fentanyl in syringes that contain 100 µg in 2 ml (50 µg/ml), but they might carry vials that have a larger volume. for example, below is packaging for 250 µg in 5 ml (also 50 µg/ml). If an entire vial were given to a 140 kg patient, that would be a dose of 3.5 µg/kg.

Is that what happened?

I don’t know – and that is presuming that this is a dosing error, which may not be valid to presume.

Image credit.^[4]

I like the idea of carrying 10 mg morphine syringes and 100 µg fentanyl syringes. The total dose of each syringe is roughly equivalent in its effect on a patient. Except in very unusual circumstances, even a full 10 mg morphine, or 100 µg fentanyl, is not going to produce significant problems – and that is assuming that there is no judgment going into the dosing of patients.

Should we assume that there is no judgment going into the dosing of patients?

No, but I will get back to this in a little bit.

If this was not a dosing error, it is extremely aggressive dosing. I am comfortable giving a bit more than 1 µg to otherwise healthy trauma patients or burn patients, but I will at least give this a couple of minutes to have some kind of effect and reassess the patient before giving more. Similarly, with morphine, I might give up to 0.15 mg/kg to these same patients. 3.5 µg/kg is about three times higher than I am comfortable with.

Does that make the dose inappropriate?

Without knowing the specifics, we really cannot tell.

Should we assume that there is no judgment going into the dosing of patients?

There are prior data to support the safety of appropriately administered opioids, including fentanyl. The study of Kanowitz et al., although more methodologically rigorous than most reports, is typical in its demonstration of safety: of 2129 patients receiving an opioid (fentanyl), only 12 (0.6%) had a medication-related vital sign abnormality and an intervention was required only once (in a patient who had no sequelae)(8)^[2]

What about in this study?

It is noteworthy that, although the study HEMS program’s fentanyl protocol does not proscribe use of the drug in hypotensive patients, the crew are required to use the agent judiciously (in other words, at the lower end of the recommended dosage range). This means that the safety of fentanyl as demonstrated in the current study may be related to more conservative dosing in unstable patients, but the parallel message is that experienced EMS crews are able to exercise judgment in determining which patients should receive cautious drug dosing.^[2]

Should we assume that there is no judgment going into the dosing of patients?

experienced EMS crews are able to exercise judgment in determining which patients should receive cautious drug dosing.

The authors of this study do not come to the conclusion that EMS crews cannot make dosing decisions independently. The authors come to exactly the opposite conclusion.

What about the hypotension and hypoxemia?

New hypotension (i.e., post-fentanyl SBP < 90 in a patient at least 5 years of age, with pre-fentanyl SBP at least 90) was seen in 28 administrations (2.7% of 1055 administrations, 95% CI 1.8–3.8%).^[2]

Vital signs were measured within ten minutes of each dose of fentanyl (usually within 5 minutes).

Does hypotension developing so soon after fentanyl mean that the fentanyl caused the hypotension?

No.

It is possible that fentanyl did cause the hypotension.

It is possible that fentanyl did contribute to a drop in the blood pressure.

It is possible that fentanyl did not affect the blood pressure at all.

It is possible that fentanyl had the effect of increasing the blood pressure, but that increase was outweighed by something else causing a greater drop in blood pressure.

We do not have enough information to determine what effect fentanyl has on blood pressure in these patients, but we no longer have a good reason for expecting that fentanyl will produce hypotension.

There are many possible side effects of fentanyl, but even in hypotensive patients we should not expect any sudden deterioration in blood pressure with judicious administration of fentanyl by competent EMS personnel.

The authors do make one error here. They use the total number of administrations of fentanyl in their calculation of the rate of new hypotension to come up with 2.7%.

Overall, in 45 cases (4.3% of 1055), fentanyl was administered to patients who were hypotensive.^[2]

Those 45 patients should be excluded from the calculation of new hypotension. Therefore the rate should be 2.8%, rather than 2.7%. This does not change the conclusions in any way. This is just a technicality.

What about those 45 patients who were hypotensive before receiving fentanyl?

In 53% of these cases, hypotension (predictably) remained after the opioid was given—but in 47% of cases in which fentanyl was administered to hypotensive patients, the next SBP exceeded 90.^[2]

About half of the patients who were hypotensive before fentanyl were not hypotensive after fentanyl.

While 45 is a small number of hypotensive patients, how many of us would like to have a treatment for hypotension that is effective on half of our patients?

I am only partly kidding.

We do not know what other treatments were being provided, but how many of these patients may have had changes to their vital signs due to severe pain?

We presume that fentanyl will make vital signs worse, but that is a mistake. We may make less of a mistake with worrying that morphine will cause hypotension, based its potential for histamine release.

What was the effect of fentanyl on vital sign abnormalities in the Kanowitz study of fentanyl?

Of the 2,315 patients who received fentanyl in the field, 66 patients had a vital sign abnormality. Of those 66 patients, three were excluded because they received a sedative in addition to the fentanyl. There were 46 patients who were excluded because their vital sign abnormalities occurred before the administration of fentanyl. Of the 46 patients who had a vital sign abnormality before the administration of fentanyl, 38 patients’ vital signs improved after the administration of fentanyl, eight patients’ vital signs remained the same, and none worsened.^[5]

Of the 46 patients who had a vital sign abnormality before the administration of fentanyl, 38 patients’ vital signs improved after the administration of fentanyl, eight patients’ vital signs remained the same, and none worsened.

It is possible that fentanyl is improving vital signs by decreasing pain.

The problem is that so many of us do not take the pain of others seriously, so we do not expect pain to lead to problems with vital signs.

Does the improvement in vital signs so soon after fentanyl mean that the fentanyl caused the improvement in vital signs?

No.

It is possible that fentanyl did cause the improvement in vital signs.

It is possible that fentanyl did contribute to an improvement in vital signs.

It is possible that fentanyl did not affect the vital signs at all.

It is possible that fentanyl had the effect of worsening the vital signs, but that worsening was outweighed by something else causing a greater improvement in vital signs.

We do not have enough information to determine what effect fentanyl has on vital signs in these patients, but we no longer have a good reason for expecting that fentanyl will frequently produce bad vital signs. Fentanyl was much more likely to be followed by an improvement in vital signs.

We almost forgot about hypoxemia. Hypoxemia is an even bigger concern than hypotension.

What effect did fentanyl have on hypoxemia?

Assessment of the 522 administrations in 279 non-intubated patients revealed no difference in the mean SpO 2 readings before (98.8%, 95% CI 98.5–98.9) and after (98.6%, 95% CI 98.3–99.0) fentanyl administration. There were no instances of hypoxemia in these non-intubated patients receiving fentanyl (one-sided 97.5% CI for 0/279: 0–1.3%).^[2]

Not even a single instance of hypoxemia.

None.

This was such a big concern that one of the helicopter services near me (based in a university hospital) only permitted flight crews to give fentanyl after a patient was intubated.

No tube – no fentanyl.

Myth busted.

We do need to be cautious about the administration of fentanyl to any patient. We should continually monitor ECG, SpO₂, blood pressure, respiratory drive, and level of consciousness. With higher doses we should also continuously monitor waveform capnography.

Fentanyl is safe in the hands of competent EMS providers.

Fentanyl should not require medical command contact for any dose.

Go listen to the podcast.

Contact EMS Research at:
603-397-0367
emsresearchcast at gmail dot com
EMSResearchCast on Twitter
EMS Research at FaceBook

Footnotes:

^[1] Fentanyl Study: EMS Research Episode 9
EMS Research Podcast
Podcast

^[2] Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia.
Krauss WC, Shah S, Shah S, Thomas SH.
J Emerg Med. 2011 Feb;40(2):182-7. Epub 2009 Mar 27.
PMID: 19327928 [PubMed - in process]

Full Text PDF Download at medicalscg.

^[3] Mean, Median, Mode, and Range
Purplemath
Article

It is good to be clear on what the meaning of the terminology. This has the simplest explanation I found in a very brief search.

The “mean” is the “average” you’re used to, where you add up all the numbers and then divide by the number of numbers. The “median” is the “middle” value in the list of numbers. To find the median, your numbers have to be listed in numerical order, so you may have to rewrite your list first.

^[4] FENTANYL CITRATE injection, solution
[Baxter Healthcare Corporation]
FDA Label
DailyMed
How Supplied
Free Full Text FDA Label from DailyMed with links to Free Full Text PDF Download.

^[5] Safety and effectiveness of fentanyl administration for prehospital pain management.
Kanowitz A, Dunn TM, Kanowitz EM, Dunn WW, Vanbuskirk K.
Prehosp Emerg Care. 2006 Jan-Mar;10(1):1-7.
PMID: 16418084 [PubMed - indexed for MEDLINE]

Free Full Text PDF Download from MSTC.

Filed Under: Critical Judgment, EMS Research Podcast, Heresy, Medical Mythology, Pharmacology, Research, Rogue Medic

Charging the Defibrillator While Continuing Chest Compressions – Part II

Does Epinephrine Improve Survival from Cardiac Arrest

Droperidol, QT prolongation, and sudden death – what is the evidence – Part I

Is IV Bolus Nitro Dangerous – Part II

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part IV

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part III

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part II

Patient Perceptions of Computed Tomographic Imaging and Their Understanding of Radiation Risk and Exposure – Part I

Can We Simplify Triage by Using Just GCS

Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia

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