Paramedicine 101

Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia

01/04/2012 by Rogue Medic 1 Comment

Also posted over at Rogue Medic (now at EMS Blogs) and at Research Blogging. Go check out the excellent material at these sites.

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

This is an interesting study for several reasons. One is the ability of the authors to act out parts of Through the Looking-Glass.^[1] VF and VT are Ventricular Tachycardia and Ventricular Fibrillation.

If life-threatening VF or VT persists despite repeated deﬁbrillation shocks, an additional antiarrhythmic drug is required.^[2]

The next paragraph points out that there is no requirement according to ACLS.

The American Heart Association guideline for advanced cardiac life support (ACLS) states that when VF/pulseless VT persists after two to three shocks plus CPR and administration of a vasopressor, the physician should consider administering an anti-arrhythmic such as amiodarone, and lidocaine may be considered if amiodarone is unavailable.¹ ^[2]

Believing that should consider administering is the same as an additional antiarrhythmic drug is required requires the same lack of illogic as used by the Queen, when instructing Alice to practice believing impossible things.

Then there are the obvious questions. Why compare nikefelant with lidocaine? Why not compare nikefelant with amiodarone? Why not compare nikefelant with an antiarrhythmic that is more effective than amiodarone – procainamide, sotalol, or ajmaline?

Lidocaine is probably used because the IRB (Institutional Review Board) would consider it unethical to have a placebo group. Lidocaine is the placebo, but with less safety than the placebo.

It was by comparing amiodarone with lidocaine that ACLS ended up including amiodarone for VT/VF cardiac arrests. That was a huge boon for Wyeth. We were told that the improved survival to admission was important. We were told that survival studies – the only studies that matter in resuscitation – were being done. We have had only silence since then.

~~We should conclude that amiodarone does not improve survival.~~

No. That is not the right conclusion. If amiodarone produced survival as good as placebo, then that study would have been published and used to justify giving amiodarone. At least we are doing something! That is what people want to believe in.

The only reasonable conclusion is that Wyeth did not publish the results because the survival in the amiodarone group was significantly worse than in the placebo group, or Wyeth stopped the study early, because it was trending toward statistically significant harm from amiodarone.

If the study never reaches statistical significance, they can always rely on there being no proof of harm. That is what we have now and there are plenty of people claiming that no proof of harm means obvious benefit.

Original cartoon

We have a lot of ignorant/willfully ignorant people encouraging us to just give drugs because we cannot prove that these drugs are harmful. We cannot provide evidence that the drugs are harmful, because it is almost impossible to approve a placebo-controlled study to find out. The IRBs claim that it would be unethical to deprive patients of the Standard Of Care, no matter how harmful that Standard Of Care may be. If the IRBs approve a study, the politicians oppose the study.

There were some interesting differences between the lidocaine and nukefalant groups.

The number of shocks before study-drug administration did not differ between the two arms, although epinephrine use before study-drug administration was signiﬁcantly higher in the lidocaine arm (Table 2).^[2]

Epinephrine use
Nikefalant 6/27 – 22.2%
Lidocaine 20/28 – 71.4%
With a p value of <0.001

According to ACLS, an antiarrhythmic should not be considered until after a pressor is considered.

Patients with nifekalant were more likely to have ROSC compared with patients with lidocaine (Table 3). However, there was no difference in 1-month survival or survival to hospital discharge between the nifekalant arm and the lidocaine arm.^[2]

The overall outcome, such as survival rate, of patients with shock-resistant VF or VT is poor regardless of the pharmacological intervention. Nevertheless, termination of VF or VT and recovery of ROSC by nifekalant is important in the initial stage of resuscitation, because we cannot rescue the patients unless VF or VT is converted.^[2]

They assume that the VF/VT will not be converted without a drug.

They assume that converting more VF/VT will lead to more survival even though there continues to be absolutely no evidence to support this hope.

It is reasonable to assume that the short-term thrill of conversion of VF/VT to a better rhythm comes at the expense of long-term harm to the patient.

We need to stop falling for feel good endpoints that encourage us to harm our patients.

If others are NOT helping their patients with these drugs, we want to be NOT helping our patients, too!

Footnotes:

^[1] Through the Looking-Glass
by Lewis Carroll
The Millennium Fulcrum Edition 1.7
CHAPTER V. Wool and Water

‘I can’t believe THAT!’ said Alice.

‘Can’t you?’ the Queen said in a pitying tone. ‘Try again: draw a long breath, and shut your eyes.’

Alice laughed. ‘There’s no use trying,’ she said: ‘one CAN’T believe impossible things.’

‘I daresay you haven’t had much practice,’ said the Queen. ‘When I was your age, I always did it for half-an-hour a day. Why, sometimes I’ve believed as many as six impossible things before breakfast.

^[2] Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia.
Shiga T, Tanaka K, Kato R, Amino M, Matsudo Y, Honda T, Sagara K, Takahashi A, Katoh T, Urashima M, Ogawa S, Takano T, Kasanuki H; Refractory VT/VF, Prospective Evaluation to Differentiate Lidocaine Efficacy from Nifekalant (RELIEF) Study Investigators.
Resuscitation. 2010 Jan;81(1):47-52. Epub 2009 Nov 13.
PMID: 19913983 [PubMed - indexed for MEDLINE]

^[3] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
PMID: 21745533 [PubMed - in process]

Free Full Text PDF Download of In Press Uncorrected Proof from xa.yming.com

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

Filed Under: AHA Guidelines, Cardiac Arrest, Heresy, Pharmacology, Research, Rogue Medic

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

Intraosseous Versus Intravenous Vascular Access During Out-of- Hospital Cardiac Arrest – A Randomized Controlled Trial

12/15/2011 by Rogue Medic 1 Comment

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

For treatment of medical cardiac arrest patients, which is better – IO (IntraOsseous) or IV (IntraVenous) access for medication administration?

Since no medications have ever been demonstrated to improve survival from cardiac arrest (only chest compressions and defibrillation have), the most important consideration will be what method results in the least interruption of compressions and the least interference with defibrillation.

All patients eligible for inclusion in this study had their ﬁrst attempt at vascular access randomized to one of 3 locations: proximal tibial intraosseous, proximal humeral intraosseous, or peripheral intravenous. The proximal tibial insertion site was located medial to the tibial tuberosity, or just below the patella along the ﬂat aspect of the tibia. The proximal humerus insertion site was deﬁned as the greater tubercle of the anterior humeral head 1 cm proximal to the surgical neck of the humerus. Peripheral intravenous catheter placement could occur at any accessible peripheral vein but preferably at the antecubital fossa; the external jugular vein was not an option provided for catheterization.^[1]

Proximal tibial access points.

Proximal humeral access point.
Images credit.

Does this hurt? No. The patients are unresponsive and pulseless (dead), but even live patients and EMS personnel (who have tried this on themselves) report very little pain.

Overall success took into account a failure to maintain initial vascular access during the course of resuscitation, which included needle dislodgement or the inability to successfully administer medications or ﬂuid at any time during the resuscitation.^[1]

Those would interfere with the one claimed benefit – ability to deliver medication.

There was no difference in time to success for either of the intraosseous routes compared with the peripheral intravenous route.^[1]

Click on images to make them larger.

The time to success is interesting. The times for the humeral site are similar to the tibial IO and the IV for placement and first drug administration – at least at the low end of the IQRs (InterQuartile Ranges). The problem is that the upper end of the IQRs is much longer than for the other methods. This is in part due to the low number of patients, which is partially explained by the 13 protocol violations – all in favor of the tibial IO site. The lack of familiarity of paramedics probably also contributes, resulting in much longer times for some of the paramedics.

Finally, there were 13 protocol violations that favored the tibial intraosseous route, which may have been an indicator of bias among paramedics for that route and therefore could have resulted in confounding of the study results.^[1]

It may be that this group of paramedics was much more comfortable with the tibial IO, than with the humeral IO and this led to a greater likelihood of coming up with excuses for protocol violations. This may also have led to the performance differences. I have seen similar differences with the introduction of a new type of IV catheter to some services. There can be a lot of conscious and unconscious resistance to the new method, but after some familiarity develops, things tend to return to normal.

In the literature, intraosseous needle insertions have been linked to local wound infections, osteomyelitis, fat emboli, and compartment syndrome.^18-20 During this study, there was no mechanism in place for EMS or hospital personnel to report complications in the use of the intraosseous device.^[1]

That would be good to know, but this was not one of the goals of the study.

The average weight of patients in the humeral intraosseous group was greater than that of individuals in either of the other 2 arms of the study. This increased weight may have been associated with a difﬁculty in obtaining or maintaining vascular access.^[1]

Weight can be a problem for any method of IV/IO access, so this is a very important limitation.

Weight – mean (SD)

Overall – 97.3 kg (2.7)

Humeral IO – 103.9 kg (6.5)

IV – 97.7 kg (3.8)

Tibial IO – 91.5 kg (3.9)

An average weight of 228.6 pounds (103.9 kg) in the humeral IO group, but only 201.3 pounds (91.5 kg) in the tibial IO group? 27.3 pounds difference (13.8% difference).

That strongly suggests a problem.

The proximal humerus can also prove tenuous during cardiac arrest because it is centered near the upper torso, where resuscitation efforts are occurring, including airway management, ongoing chest compressions, and rescuer interchange. The constant activity creates a tremendous amount of movement and further increases the risk of unintentional needle dislodgement, which was veriﬁed during the debrieﬁng session after each out-of-hospital cardiac arrest, with paramedics frequently citing entanglement of the humeral intraosseous line, leading to dislodgement.^[1]

The peripheral intravenous site is the most commonly used vascular access by all health care providers, yet it proved successful in less than 50% of cases in this study.^[1]

No matter how bad the success of the humeral IO was, the IV success was even worse – less than 50% first attempt success.

Do IOs improve outcomes?

IOs may make it less likely that compressions will be interrupted, but we cannot tell from this study.

IOs may make it more likely that potentially harmful medications will be given.

The most interesting numbers I saw were the total fluid infused – twice as much in the IV group as in either IO group. No explanation is given, other than the possible slower flow rate for an IO. This may help to prevent fluid overload for those patients not in need of having an IV line accidentally left wide open.

There is no evidence that IOs, IVs, tubes, or medications improve survival to discharge with a working brain.

ACLS drug therapy during CPR is often associated with increased rates of ROSC and hospital admission but not increased rates of long-term survival with good neurologic outcome.^[2]

Will this make the Three Stooges Pit Crew concept less of a comedy of errors to implement?

Probably not, but we can hope that the AHA does the right thing and eliminates all of the treatments that don’t work – ventilation, intubation, IV access, IO access, epinephrine, amiodarone, lidocaine, ~~atropine~~ – wait, they actually did remove atropine, so there is hope.

Footnotes:

^[1] Intraosseous Versus Intravenous Vascular Access During Out-of-Hospital Cardiac Arrest: A Randomized Controlled Trial.
Reades R, Studnek JR, Vandeventer S, Garrett J.
Ann Emerg Med. 2011 Dec;58(6):509-16.
PMID: 21856044 [PubMed - in process]

^[2] Medications for Arrest Rhythms
Part 8: Adult Advanced Cardiovascular Life Support
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 8.2: Management of Cardiac Arrest
Free Full Text Article with links to Free Full Text PDF download

Filed Under: AHA Guidelines, Cardiology, Heresy, Pharmacology, 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

How Dangerous is a Long QT Segment on the ECG

11/30/2011 by Rogue Medic 1 Comment

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

There are many things that will lengthen the QT segment, but how much should we worry when the patient has a long QT segment, or when giving the patient a treatment that lengthens the QT segment? Are there some things that, even though they may lengthen the QT segment, may protect the heart from arrhythmia at the same time?

This prospective study was conducted to evaluate the frequency of malignant arrhythmias and to analyse the possible effect of hypothermia on the QTc interval using a continuous Holter ECG during MTH treatment.^[1]

Mild therapeutic hypothermia (MTH in the paper) is one of condition these authors wanted to investigate to find out if it really does cause QT prolongation and if that QT prolongation might be dangerous. Torsades is the arrhythmia that is the main concern. It is potentially lethal, but often responds to magnesium and/or defibrillation. Cardioversion cam be used, if we can get the monitor to synchronize on the spiraling QRS complex, which is not as difficult as some would have us believe.

Torsades. Image credit. This is from a discussion of wide complex tachycardias at EMS 12 Lead.

During the inclusion period between April 2009 and December 2009 a total number of 34 patients were analysed. All patients received mild therapeutic hypothermia treatment after resuscitation according to the current guidelines and regardless of the initial rhythm.^[1]

Out-of-hospital and initial in-hospital treatments were not altered for the study.

The target temperature of 33° C was maintained for 24 h. Intravenous sedation and analgesia were induced in all patients by a combination of midazolam (0.125 mg/kg/h) and fentanyl (0.002 mg/kg/h) with dose adjustment as needed. Muscle relaxation with repetitive administration of pancuronium (0.1 mg/kg) in order to prevent shivering was induced if necessary.^[1]

The interesting part is what they did when they saw these dramatically prolonged QT segments.

They did nothing. We need to learn to be a little less interventionist, when it comes to stable ventricular rhythms.

Post-resuscitation care was uninﬂuenced by the Holter ECG results and the ICU physicians followed the standard operating procedure for cardiac arrest patients. All patients completed the cooling procedure and survived the ﬁrst 48 h. Overcooling (central body temperature lower than 32° C) did not occur in any case, potassium serum levels were closely monitored and supplemented to stay within normal range and to avoid hypokalemia.^[1]

They did keep the potassium in the normal range, which is not something that patients always do outside of the hospital. This is one advantage these patients have over patients being treated for excited delirium, but this is what should be expected with admitted patients.

It isn’t clear if the doctors were blinded to the Holter results, or just did not act on anything they saw. I am interested in which it was.

The number of patients with at least one VT (ventricular tachycardia) was three (8.8%) during MTH and were non-sustained without any additional treatment. Torsade de pointes were not detected.^[1]

In spite of the very long QTc (median 564.47 ms), there were no cases of torsades. There were three cases of VT (≥ 30 seconds of ventricular ectopic beats), but all of these resolved spontaneously.

What happened to the good old days of having to panic and give the antiarrhythmic before the arrhythmia has a chance to go away on its own?

In one patient a maximum of 673.52 ms of QTc interval prolongation was reached after 12 h of 33° C as the highest recorded value without any additional drug treatment causing a QTc prolongation.^[1]

After 24 hours at 33°, the median QTc was 564.47 ms. A QTc longer than 450 is considered prolonged, but some will be comfortable well beyond that.

17 patients (50%) were discharged with a favourable neurological outcome (CPC 1–2) whereas 50% had an unfavourable outcome (CPC 3–5). The overall mortality rate was 38.2%,^[1]

An unfavorable outcome included both death and unfavorable neurological outcomes, so only 11.8% were discharged alive with unfavorable neurological outcomes.

Experimental data showed a stabilization of cell membranes during hypothermia and a higher likelihood of successful deﬁbrillation with a better ROSC rate in a swine model due to hypothermic conditions.^9,10 This indicates that MTH lowers the incidence of arrhythmias rather than raising it. One should keep in mind that more profound hypothermia <30° will increase the risk and therefore temperature should be closely monitored in patients undergoing MTH.^[1]

Hypothermia does appear to protect against arrhythmia, but probably only when the hypothermia is mild.

The green line is at 450 ms, beyond which is considered to be a prolonged QTc.

The blue line is at 550 ms – a level that, if we are to believe those who are most concerned about QTc, is just begging for torsades. The patients’ rhythms should have changed to torsades long before they got to a QTc of 550 ms.

However, a QTc prolongation in elderly emergency patients (QTc ≥450 ms) has been observed in almost 544/1558 patients (35%) in a study by Seftchick et al. The most common comorbidities in this study were structural heart disease, renal failure, and stroke.¹⁴ Five percent of the patients with QTc prolongation died in the emergency department or during hospitalization but none had QTc prolongation or Torsade de pointes listed as a cause of death. Therefore a delay of repolarisation per se seems not necessarily torsadogenic.¹¹^[1]

Will a prolonged QT segment cause torsades?

Maybe, but don’t bet on it, because thaere appear to be many more factors involved, than just the QTc.

Footnotes:

^[1] Severe QTc prolongation under mild hypothermia treatment and incidence of arrhythmias after cardiac arrest–a prospective study in 34 survivors with continuous Holter ECG.
Storm C, Hasper D, Nee J, Joerres A, Schefold JC, Kaufmann J, Roser M.
Resuscitation. 2011 Jul;82(7):859-62. Epub 2011 Mar 15.
PMID: 21482009 [PubMed - in process]

Filed Under: Cardiocerebral resuscitation, Cardiology, Heresy, Pharmacology, Research

Automated external defibrillators and survival after in-hospital cardiac arrest

11/18/2011 by Rogue Medic 2 Comments

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

Yesterday I described the problems with the recent article claiming that corruption was the reason the AHA (American Heart Association) recommended AEDs (Automated External Defibrillators) be placed in non-acute care parts of hospitals.^[1] Today I will look at the study that seems to have inspired the article, even though it came out a year ago.

Does the research claim that there is any suspicion of corruption in the recommendation?

No. The corruption claims appear to be entirely due to the ideological bias of this conspiracy theory site.

Image credit.

Although some studies have shown that AEDs improve survival for out-of-hospital cardiac arrests occurring in certain public locations in which 45% to 71% of cases are treatable with defibrillation,^5,6,7 these devices may be less effective or potentially harmful when used in hospitals where only 1 in 5 hospitalized patients have initial cardiac arrest rhythms that respond to defibrillation.⁸ ^[2]

Is it wrong to look at the research and recommend that the AEDs be used in settings where a manual difibrillator is not available?

No.

Image credit.

The difference between a manual defibrillator and an AED is that the AED will interpret the heart rhythm itself. The nurses and doctors do not need to be able to do this. This makes AEDs ideal for public places where non-medical people can use them to shock a patient out of a fatal heart rhythm. In those settings, AEDs probably save thousands of lives each year.

Image credit.

With a manual defibrillator, there is much greater cost for equipment and for training to be able to identify shockable rhythms. In the hands of someone familiar with resuscitation a manual defibrillator can be used to deliver a shock with only a few seconds of interruption in compressions, while the AED requires almost a minute of interruption. The greatest problem with resuscitation may be interruptions in compressions.^[3], ^[4]

Image credit.

What were the results of the study?

Click on the images to make them larger.

The big benefit from an AED would be when a shockable rhythm is the cause of a cardiac arrest in a less than acute care setting. The nurses are not likely to be certified in ACLS (Advanced Cardiac Life Support). The doctors probably have not treated a cardiac arrest since their last ACLS class. There are no manual defibrillators in that part of the hospital.

While the use of AEDs would require longer interruptions of CPR for the AED to analyze the rhythm, one expectation would be that there would be a significant increase in successful resuscitations of patients with shockable rhythms. According to the data above, only about 1/5 of patients who had the AED applied actually had shockable rhythms ventricular fibrillation of pulseless ventricular tachycardia.

The patients were very well matched for everything that might predispose toward a survival advantage in either group.

Even worse is that the anticipated significant increase in resuscitation of patients with shockable rhythms did not happen.

The good news is that hospitals seem to be doing a great job of defibrillating patients quickly without the AEDs.

The median time to shock is 2 minutes. That is recognizing a pulseless, apneic, unresponsive patient, calling a code, beginning CPR, and getting the defibrillator to the patient, turning it on, and delivering shocks to appropriate patients.

The message from this study appears to be that the hospitals are not experiencing significant delays in delivering shocks without AEDs, so there is not likely to be any benefit from adding AEDs. The possible worsening of outcomes is probably due to complicating the response to resuscitation.

Hospitals are big buildings with a lot of people. Many of these people will experience cardiac arrest. Those are two of the things that suggest that AEDs would improve outcomes.

There is an important difference between hospitals and casinos, airports, and other buildings that showed dramatic increases in survival from cardiac arrest after the addition of AEDs and the training of staff in the use of AEDs.

I started out by asking, Is it wrong to look at the research and recommend that the AEDs be used in settings where a manual difibrillator is not available?

Hospitals already have plenty of manual defibrillators and staff trained to use the defibrillators. While there may be many ways to improve the responses in hospitals, the addition of AEDs does not appear to improve responses to cardiac arrest.

Should the AHA have made this recommendation? The AHA too often goes from no recommendation to permanent part of the treatment guidelines without any transitional phases for assessment of benefits. Their reasoning is understandable. What if this is a treatment that will save thousands, or tens of thousands, of lives? Do we want to delay such a wonderful treatment. Part of me still expects to see the ACLS guidelines printed by Acme.

As with second marriages, the AHA seems to continually expect optimism to triumph over experience. The AHA needs to be more cautious.

It is too easy to implement a plan and too difficult to reverse course. How many of the AHA guidelines worked out as planned? Are we really going to miss out on the next multi-thousand patient life saver? If we don’t play the lottery, are we giving up on a shot at millions? We need to put less emphasis on unproven interventions.

In light of our data, national organizations and hospitals may need to reconsider the use of AEDs in general hospital ward units or develop different strategies for using them.^[2]

Maybe hospitals should donate/sell their AEDs to places/organizations that are more likely to benefit from AEDs. Large buildings, EMS agencies, fire departments, police departments, et cetera.

Footnotes:

^[1] Bad Shock – Automated Devices for Jolting Hearts May Save Fewer Lives in Hospitals
Rogue Medic
Article

^[2] Automated external defibrillators and survival after in-hospital cardiac arrest.
Chan PS, Krumholz HM, Spertus JA, Jones PG, Cram P, Berg RA, Peberdy MA, Nadkarni V, Mancini ME, Nallamothu BK; American Heart Association National Registry of Cardiopulmonary Resuscitation (NRCPR) Investigators.
JAMA. 2010 Nov 17;304(19):2129-36. Epub 2010 Nov 15.
PMID: 21078809 [PubMed - indexed for MEDLINE]

Free Full Text from JAMA with links to Full Text PDF Download

^[3] 60 Year Old Male CC: Sudden Cardiac Arrest
EMS 12 Lead
Article

^[4] Charging the Defibrillator While Continuing Chest Compressions – Part I
Rogue Medic
Article

Filed Under: Cardiac Arrest, Heresy, 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

Sleep quality and fatigue among prehospital providers

10/20/2011 by Rogue Medic 1 Comment

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

Even though many in EMS will tell you that EMS stands not for Emergency Medical Services, but for Earn Money Sleeping, sleep deprivation is a problem for many in EMS, many in medicine, and many in other fields. I am a night person, much more awake and alert at 2 AM, than at 8 AM.

In spite of this, some early to bed, early to rise EMS administrators demand that employees adapt their schedule to the personal preferences of the administrator. This is not only an irrational attitude, but demonstrates such a lack of awareness of what others experience, that working in any patient care setting would be contraindicated.

Sleep deprivation produces impairments in central nervous system (CNS) activities from the most basic functions, such as appetite and temperature regulation, to higher functions, such as memory and vigilance. Sleepiness has been linked to increases in unintentional incidents such as motor vehicle collisons and occupational injuries.^3–5 ^[1]

We should not hesitate to give partial credit to those who insist on having everyone else adapt to their schedules.

Shift workers also tend to have to rely on sleep-inducing agents. A survey of emergency medicine residents revealed that 46% used some kind of sleep agent, including alcohol, benzodiazepines, and muscle relaxants, to fall asleep.⁸ ^[1]

About half of residents, not just EMS personnel, but there is no problem that needs to be addressed. Just gulp down some coffee and put on your war face.

There is some unintentional humor in the study. Probably due to lack of sleep.

We collected 119 completed surveys. Subjects were 54.0% female, and the largest age group was 40 to 49 years (39.3%; Table 1).^[1]

I do consume chocolate to ward off irritability. Maybe that is the 54% of me that is female. Those 40 to 49 years old were the largest group – by weight or volume or something else? I would ask the same about the 54% female, but I know when to not comment. OK, maybe not.

a moderate proportion of subjects reported employment at multiple EMS agencies (34.2%).^[1]

While not the only factor, I would expect that this strongly correlates with sleep deprivation and the resultant negative effects.

I am surprised at the low rate of people working multiple EMS jobs, maybe a lot of them ~~have real jobs~~ work outside of EMS.

The majority of subjects were overweight or obese (84.6%) based on body mass index (BMI).^[1]

Sleep deprivation produces impairments in central nervous system (CNS) activities from the most basic functions, such as appetite and temperature regulation, to higher functions, such as memory and vigilance.^[1]

No connection.

one-fifth reported being told that they have weight problems (22.7%).^[1]

More than 4/5 are obese, but only 1/5 have had a doctor notice this.

Nearly half of the subjects (44.5%) reported experiencing severe fatigue while at work (Fig. 2). The proportion of subjects with severe fatigue increased with years of experience (p < 0.0001),^[1]

A global score >5 suggests poor sleep quality.^[1]

At least this is something that we learn to adapt to, so it should be less of a problem with increased time on the job.

Or not. Maybe the increasing problems at over 20 years indicates an amount of time in EMS that causes more significant damage.

How much of what we do works out as a feedback loop that compounds problems as if we had heart failure?

Image credit.^[2] Click on the image to make it larger.

We know the simple treatments for heart failure – high doses of NTG (NiTroGlycerin) and CPAP (Continuous Positive Airway Pressure).

Maybe the solution to sleep deprivation is something equally simple, such as taking naps or being permitted to sleep when not treating patients.

Even though we have known for decades that NTG and CPAP are the best treatments for acute exacerbation of heart failure, few of us seem to use these treatments. When we do use them, we use homeopathic doses of NTG and we make excuses for not using CPAP.

Will there be any faster adoption of sensible approaches to sleep deprivation?

Will people in EMS be able to make enough to not have to work other jobs?

Federal law limits work hours for many sectors of the transportation industry, including commerical pilots (eight hours of flight time per 24 hours), shipboard personnel on tankers (15 hours per 24 hours), and long-haul truck drivers (14 hours per shift, with a maximum of 11 hours driving).^29–31 ^[1]

Will we only respond to rules set by others?

The mature thing to do would be for us to act first.

One of the reasons I work at my current job is the bosses allow the employees to sleep at any time – as long as calls are covered and other work is accomplished during the shift.

Footnotes:

^[1] Sleep quality and fatigue among prehospital providers.
Patterson PD, Suffoletto BP, Kupas DF, Weaver MD, Hostler D.
Prehosp Emerg Care. 2010 Apr 6;14(2):187-93.
PMID: 20199233 [PubMed - indexed for MEDLINE]

Free Full Text at PubMed Central with links to Free PDF Download

^[2] Prehospital therapy for acute congestive heart failure: state of the art.
Mosesso VN Jr, Dunford J, Blackwell T, Griswell JK.
Prehosp Emerg Care. 2003 Jan-Mar;7(1):13-23. Review.
PMID: 12540139 [PubMed - indexed for MEDLINE]

Free Full Text PDF

Filed Under: Heresy, Research, Risk Management, Rogue Medic

Propofol and the Michael Jackson Effect

10/13/2011 by Rogue Medic

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

One contributing site introduced propofol into its ED 22 months after it began entering patients into the registry. This timing permitted a natural experiment to examine the impact of the use of this drug on physician preferences and patient outcomes in patients undergoing procedural sedation at this site. After the introduction of propofol, all previously available procedural sedation agents remained in the ED formulary and no endorsement for use of propofol over existing medication options was presented to the EPs.^[1]

You should already know the questions I am going to raise – The Michael Jackson Drug? Where did they put all of the dead bodies?

You should also know the response – What dead bodies?

Why do we allow one unusual, dramatically publicized case affect our expectations? Because we don’t stop and think for ourselves.

Minor complications are probably what killed Michael Jackson. Minor complications that should easily have been treated by any First Responder, or any Patient Care Technician, or and Nurse’s Aide in a nursing home. Minor complications that would have resulted in a great big YAWN from anyone with any experience managing airways.

Airway obstruction: responds to repositioning

Anyone who has taken CPR and even vaguely remembers the “Head tilt, chin lift,” method of opening the airway could treat this. No big deal.

Hypoxia: responsive to oxygen

Anyone monitoring the patient’s pulse oximetry could have noticed this and delivered some oxygen to bring the patient’s oxygen saturation back up to the normal range.

This requires only three things –

1. Pulse oximetry measuring equipment.

2. Oxygen (with a means of delivering the oxygen to the patient).

3. A clue.

All of these are part of the minimum equipment that should be present for the use of propofol.

None of these appear to have been present.

Part of the problem with the safety of propofol is that it is deceptive. So many of the complications resolve on their own, that some people will become complacent and not be prepared to deal with the complications, not even the minor complications. Then these minor complications become major life threatening/life ending complications.

How many times did Dr. Conrad Murray administer propofol (and other sedatives) to Michael Jackson, but get away with it because the complications resolved on their own?

Many hospitals only permit anesthesia to administer propofol. The other drugs on this list are much less commonly restricted to just anesthesia. Yet, this most restricted drug, too dangerous for anyone outside of anesthesia, appears to be the safest.

Minor complications dropped from 5.8% to 1.7% when propofol use went from zero percent of procedural sedations to 40% of procedural sedations.

Propofol went from being the least commonly used drug (never used) to the most commonly used drug and the minor complication rate decreased by almost a factor of 3 1/2.

During that period there was an even greater decrease in major complications – from 3.6% they decreased to only 1.0%. This is a decrease by greater than a factor of 3 1/2.

I understand the concern about the ability of people to underestimate the potential for complications, but that is true of all of the drugs that anesthesia does not make a big deal about. By limiting access to the safest drug for procedural sedation, the anesthesia departments are harming patients.

Is propofol a hand grenade or a Holy Grail?

Neither, but it depends on the person using it, which is just a variation of what Paracelsus warned us about medication/poison –

All things are poison and nothing is without poison, only the dose permits something not to be poisonous. – Paracelsus.

There are several possible Michael Jackson effects with propofol.

Patients are choosing more dangerous medications when they need strong sedation.

Doctors should be using propofol with more awareness of the potential complications.

The shortage of propofol seems to have ended, perhaps because propofol was being used less often after the death of Michael Jackson.

Teva
Teva Pharmaceuticals has discontinued their propofol injection.

Hospira – 1-877-946-7747
All presentations: ample levels of inventory to support market demand.
Please check with your wholesaler for available inventory.

APP – 1-888-386-1300
ALL Diprivan and Propofol presentations are sufficiently stocked at wholesalers and distributors nationwide.
Diprivan 1% (20mL, 50mL, and 100mL)
Generic Propofol 1% (20mL, 50mL, and 100mL)
Novaplus Propofol 1% (20mL, 50mL, and 100mL)
Please check with your wholesalers and distribution centers for available inventory.^[2]

If you have not been able to get propofol for your ED (Emergency Department) because of supply issues, that should not be a problem any more.

If you have not been able to get propofol for your ED because of inappropriate restrictions by anesthesia, this study should help to clearly demonstrate that emergency physicians working in community emergency departments are able to use propofol safely. Emergency physicians are safer using propofol than the more conventional medicines – etomidate, fentanyl, and midazolam.

The lesson most people seem to have learned is that propofol is dangerous.

The reality is that propofol may be the safest drug for procedural sedation.

There is also a discussion about this problem of inappropriate restriction of propofol to only anesthesia at Emergency Physicians Monthly –

CMS and Deep Sedation: A Win for Emergency Medicine
by Kevin Klauer, DO, EJD on January 31, 2011
Article

Footnotes:

^[1] Impact of addition of propofol to ED formulary.
Senula G, Sacchetti A, Moore S, Cortese T.
Am J Emerg Med. 2010 Oct;28(8):880-3. Epub 2010 Feb 25.
PMID: 20887909 [PubMed - indexed for MEDLINE]

^[2] Propofol Injection (updated 10/11/2011)
FDA
Current Drug Shortages

Filed Under: Airway Management, Heresy, Pharmacology, Rogue Medic

Paramedicine 101

Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia

Charging the Defibrillator While Continuing Chest Compressions – Part II

Intraosseous Versus Intravenous Vascular Access During Out-of- Hospital Cardiac Arrest – A Randomized Controlled Trial

Does Epinephrine Improve Survival from Cardiac Arrest

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

How Dangerous is a Long QT Segment on the ECG

Automated external defibrillators and survival after in-hospital cardiac arrest

Is IV Bolus Nitro Dangerous – Part II

Sleep quality and fatigue among prehospital providers

Propofol and the Michael Jackson Effect

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