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

- Rogue Medic

Why Did We Remove Atropine From ACLS? Part II

 

Continuing from Part I.

The AHA (American Heart Association) stopped recommendeding use of atropine for the treatment of PEA (Pulseless Electrical Activity) or asystole in the 2010 ACLS (Advanced Cardiac Life Support) guidelines.

There is not much information given, but that little bit of information just makes it more clear that we never had a good reason for making atropine a standard part of ACLS.

One sentence at a time, look at the reasoning –
 

Interventions Not Recommended for Routine Use During Cardiac Arrest
Atropine

Atropine sulfate reverses cholinergic-mediated decreases in heart rate and atrioventricular nodal conduction.[1]

 

There is a hypothetical justification for atropine based on physiology/pathophysiology.

There has been a hypothetical justification for every treatment found to be harmful. That hypothetical justification did not protect patients from real harm.
 

No prospective controlled clinical trials have examined the use of atropine in asystole or bradycardic PEA cardiac arrest.[2]

 

Why was a treatment that had never been demonstrated to improve outcomes recommended and the standard of care?

Without evidence of improved outcomes, should any treatment be used outside of controlled trials?
 

Lower-level clinical studies provide conflicting evidence of the benefit of routine use of atropine in cardiac arrest.34,295,–,304 [1]

 

To translate – Useless information is . . . useless.
 

There is no evidence that atropine has detrimental effects during bradycardic or asystolic cardiac arrest.[1]

 

Is atropine the alternative medicine of cardiac arrest?

This sentence contradicts the evidence review that led to the removal of atropine from the guidelines.

Here is a listing of the evidence that opposes the use of atropine for cardiac arrest.
 


Click on image to make it larger.[2]
 

While the evidence of harm is not great, the evidence of benefit is not great, either.

Evidence of worse outcomes from cardiac arrest is evidence of harm.

There are four studies – three that show a negative correlation with atropine and survival to discharge.

no evidence that atropine has detrimental effects?

The positive studies are also just showing correlation. Poor studies mean poor information. Why were we giving atropine based on poor information?

We were giving atropine based on wishful thinking.
 

Available evidence suggests that routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit (Class IIb, LOE B).[1]

 

We should not include treatments that do not have evidence of therapeutic benefit.
 

For this reason atropine has been removed from the cardiac arrest algorithm.[1]

 

For this reason, atropine should never have been included in the cardiac arrest algorithms.

For this reason, all treatments that do not have evidence of therapeutic benefit should have an expiration date.

If no evidence is provided, the treatment is removed from the guidelines.

This would apply to ventilations, epinephrine (Adrenaline), vasopressin (Pitressin), norepinephrine (Levophed), and phenylephrine (Neo-Synephrine) in cardiac arrest.

This would also apply to amiodarone (Cordarone), lidocaine (Xylocaine), and Magnesium in VF (Ventricular Fibrillation) cardiac arrest.
 

What does that leave us with?

Compressions in cardiac arrest.

Defibrillation in VF cardiac arrest.

Therapeutic hypothermia after resuscitation.

In Part III I will look at the most positive study supporting the use of atropine for cardiac arrest.

Footnotes:

[1] Atropine
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8.2: Management of Cardiac Arrest
Interventions Not Recommended for Routine Use During Cardiac Arrest
Free Full Text from Circulation.

[2] Atropine for cardiac arrest
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Appendix: Evidence-Based Worksheets
Part 8 ALS
ALS-D-024B
Swee Han Lim
Evidence-Based Worksheet Download in PDF format.

.

Epinephrine for V Tach – Instant Death or Effective Treatment?

ResearchBlogging.org
 

The patient has V Tach (Ventricular Tachycardia) with a pulse. After amiodarone is given the patient’s blood pressure drops and the patient becomes unstable. The patient is still awake, so cardioversion would be very painful and these physicians would need to get anesthesia to sedate the patient. I know – that anesthesia requirement is a bad policy and completely unnecessary for the safety of the patient, but it is politics in that facility. However, sedation for emergency cardioversion is very important.

There are other medications that might be effective at terminating V Tach.

What might happen if epinephrine is given?
 

Click on images to make them larger.
 

If take an ACLS (Advanced Cardiac Life Support) class, where the protocolized treatment of arrhythmias is taught, the instructor may tell you that you just killed the patient with epinephrine.

There were three patients treated with epinephrine for V Tach. They were not in the artificial environment of an ACLS class, and had not been taught by the epi for unstable V Tach = death ACLS instructors, so the patients did not know that they were supposed to die.

The physicians treating the V Tach patients had read the ACLS books, as well as a lot of other research on the treatment of arrythmias. The physicians chose to treat these patients with epinephrine.

47 year old male, 125/86 mmHg, heart rate of 170 with the rhythm above. 300 mg amiodarone over 5 min did not get rid of the V Tach, but it did appear to drop the blood pressure to 89/46 mmHg with profuse sweating, but without loss of consciousness. Perhaps that was also true of those taking care of the patient.

1 mg (1,000 μg) of 1:10,000 epinephrine given over less than 60 seconds was followed within 30 seconds by the changes below.
 

 

Heart rate increased to 180, briefly, blood pressure increased to 130/84 mmHg, then the rhythm converted.

Not to V Fib (Ventricular Fibrillation), but to a stable sinus tachycardia at a rate of 110.
 

The side effects of epinephrine were chest discomfort, nausea, and anxiousness.[1]

 

Well, he was only 47, so we got lucky with epinephrine at that young age.

How about a 64 year old male with a heart attack history, low ejection fraction and an AICD (Automated Implantable Cardioverter-Defibrillator), on bisoprolol 10 mg daily and amiodarone 200 mg daily for recurrent NSVT (Non-Sustained V Tach), conscious with a pressure of 85/50 mmHg and now a sustained V Tach at 140 beats/min?

A lower dose of epinephrine was given – 0.5 mg (500 μg) over less than 30 seconds was followed within 30 seconds by an increase of rate from 140 to 148, followed by conversion to a nice slow sinus rhythm.
 

The third patient had V Tach storm, which might seem even less likely to benefit from epinephrine.

A patient with a history of two heart attacks, taking carvedilol (12.5 mg twice daily) and amiodarone (200 mg daily) with an AICD, presenting with a pressure of 90/45 mmHg and a rate of 140+. He received six AICD shocks within 5 minutes in the hospital, but the rhythm returned to V Tach each time. 150 mg amiodarone was given over 15 min and the pressure dropped to 70/40 mmHg. Overdrive pacing was attempted with only a conversion of V Tach to V Fib, which was shocked by the AICD. Within 60 seconds, the V Tach was back. Blood pressure continued to fall to 65/30 mmHg.

Epinephrine was given – 0.5 mg (500 μg) over less than 30 seconds was followed within 30 seconds by an increase in blood pressure to 125/85 mmHg, followed by termination of V Tach within 90 seconds.
 

In cases of drug-resistant poorly tolerated VT, immediate external electrical cardioversion must be attempted. However, there are cases in which VT recurs immediately after the shock, and cardioversion involves the need for anesthesia when the patient is still conscious.[1]

 

Based on the cases reported herein, low doses of IV epinephrine may be able to terminate sustained monomorphic VT, when the arrhythmia is refractory to amiodarone used alone or in combination with beta-blockers and electrical cardioversion.[1]

 

I would not refer to 1,000 μg epinephrine, or even 500 μg, as low dose.

Dr. Scott Weingart discusses the use of epinephrine as a bolus dose pressor, but at much smaller doses.
 

Dose:

0.5-2 ml every 2-5 minutes (5-20 mcg)

No extravasation worries![2]

 

Do not use epinephrine for V Tach without discussing it with your medical director and obtaining permissions, assuming you work some place where the medical director has the authority. If you are a doctor, discuss this with cardiology before using it.

Read the discussion of the many possible confounders in the full text of the paper and learn a bit about cardiology and the ways that physiology misleads us.

Footnotes:

[1] Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia.
Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, Fontaine G.
World J Cardiol. 2012 Oct 26;4(10):296-301. doi: 10.4330/wjc.v4.i10.296.
PMID: 23110246 [PubMed]

Free Full Text from PubMed Central.

[2] Push-Dose Pressors – Podcast 6
EMCrit
Dr. Scott Weingart
Article and podcast.

Bonny, A. (2012). Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia World Journal of Cardiology, 4 (10) DOI: 10.4330/wjc.v4.i10.296

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Examples of Ventricular Tachycardia Caused by Amiodarone – Part I

ResearchBlogging.org
 

How much worse could the patient get if we give amiodarone?

But amiodarone doesn’t cause V Tach (Ventricular Tachycardia). Amiodarone stops V Tach.

Right?

If amiodarone can cause V Tach, shouldn’t someone have told us?
 


Click on image to make it larger.
 

This is a wide complex tachycardia, which should be presumed to be V Tach. The diagnosis of the rhythm as V Tach is supported by the P-wave dissociation and by the history of a heart attack a couple of weeks before. 19 QRS complexes in 5 seconds (multiply by 12 to get the rate for 60 seconds) = 228.

According to ACLS (Advanced Cardiac Life Support) what drug would be indicated for the above rhythm?

For the old timers, let’s throw in a bit of information that is supposed to be important in deciding among the various antiarrhythmics –
 

Transthoracic echocardiography was performed, and the ejection fraction was 34% based on the modified Simpson method.[1]

 

Does the ejection fraction matter in treating wide-complex tachycardia?
 

Note that amiodarone becomes the antiarrhythmic of choice (after failure of adenosine) if the patient’s cardiac function is impaired and the ejection fraction is <40% or there are signs of congestive heart failure.[2]

 

That was only mentioned in the 2000 ACLS guidelines. The 2005 ACLS guidelines and the 2010 ACLS guidelines do not mention ejection fraction in the treatment of V Tach.
 

Do we have good evidence that amiodarone is effective for stable V Tach?
 

Amiodarone has not been studied specifically for the pharmacological termination of hemodynamically stable VT, but it is effective in treating hemodynamically unstable VT and VF.78 81 82 83 84 85 86 87 88 89 90 91 [2]

 

That was written in 2000 and the answer was NO.

Now we have evidence that amiodarone may be effective in about one out of four patients – if we are prepared to wait a half hour, or more. In other words, it is rare for amiodarone to work and rarer still for amiodarone to work before we can get the patient to the hospital.[3],[4],[5]

We do have evidence that amiodarone may be a part of the long-term treatment of unstable V Tach. On the other hand, maybe not.

I do mean long-term treatment, even though these are unstable patients.
 

Twenty-seven (58.5%) of the 46 patients responded to intravenous amiodarone, and an additional 6 patients (13%) showed a late response to amiodarone (Fig. I). Fifteen of the 27 responders (33% of all patients) responded immediately (0 to 2 h), and 26 responded within 72 h . The other patient responded within 84 h (Fig. 2).[6]

 
Up to 84 hours to take effect.

Not exactly an emergency drug.

I have worked some very long shifts. I have never worked an 84 hour shift.

If amiodarone can take 84 hours to work, and the patient is receiving a variety of other treatments during those 84 hours, is it really the amiodarone that is working?

Compared with 84 hours, a less than two hour time to response seems almost instantaneous, but it is not fast for EMS.
 

This patient was treated with oral amiodarone for sustained V Tach during his previous hospital admission for an acute anterior MI (Myocardial Infarction) treated with a stent in the LAD (Left Anterior Descending) coronary artery.

This time he was treated with IV (IntraVenous) amiodarone. The problems began on the first day of IV amiodarone treatment.
 

On the first day of hospitalization, the patients had 10 attacks of pulseless VT treated with successful DC shocks. Occasionally, VT attacks degenerated to ventricular fibrillation.[1]

 

And continued –
 

On the second day of hospitalization, the patient had 14 pulseless VT attacks with successful DC shocks.[1]

 

But the V Tach stopped after the amiodarone was stopped and antithyroid therapy was begun.
 

Thyroid gland toxicity is one of the most important adverse effects of amiodarone and is called amiodarone-induced thyrotoxicosis. Thyrotoxicosis may alter arrhythmia and lead to frequent ventricular tachycardia attacks.[1]

 

All things are poison, and nothing is without poison; only the dose permits something not to be poisonous. – Paracelsus (1493-1541)
 

We do not seem to explain that well in EMS, or even in emergency medicine.
 

All antiarrhythmic agents have some degree of proarrhythmic effects.[7]

 

Amiodarone is one of the most dangerous drugs we carry in EMS.

How much thought do we give to the problems we can cause for our patients with this drug?

How much do we understand about the problems we could be causing when we push medications, such as amiodarone?

Footnotes:

[1] Therapy-resistant ventricular tachycardia caused by amiodarone-induced thyrotoxicosis: a case report of electrical storm.
Erdogan HI, Gul EE, Gok H, Nikus KC.
Am J Emerg Med. 2012 Nov;30(9):2092.e5-7. doi: 10.1016/j.ajem.2011.12.035. Epub 2012 Mar 3.
PMID: 22386340 [PubMed – indexed for MEDLINE]

[2] Amiodarone
2000 ECC Guidelines
Part 6: Advanced Cardiovascular Life Support
Section 5: Pharmacology I: Agents for Arrhythmias
Arrhythmias and the Drugs Used to Treat Them
Hemodynamically Stable Wide-/Broad-Complex Tachycardias
Treatment of Wide-Complex Tachycardias
Free Full Text from Circulation.

[3] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

[4] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306. doi: 10.1111/j.1553-2712.2010.00680.x.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

[5] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

[6] Use of intravenous amiodarone for emergency treatment of life-threatening ventricular arrhythmias.
Helmy I, Herre JM, Gee G, Sharkey H, Malone P, Sauve MJ, Griffin JC, Scheinman MM.
J Am Coll Cardiol. 1988 Oct;12(4):1015-22.
PMID: 3417974 [PubMed – indexed for MEDLINE]

Page with link to Free Full Text Download in PDF format from J Am Coll Cardiol.

This is footnote 84 from the second 2000 ACLS quote.

[7] New Concerns From the International Guidelines 2000 Conference: Impaired Hearts and “Proarrhythmic Antiarrhythmics”
2000 ECC Guidelines
Part 6: Advanced Cardiovascular Life Support
Section 5: Pharmacology I: Agents for Arrhythmias
Arrhythmias and the Drugs Used to Treat Them
Hemodynamically Stable Wide-/Broad-Complex Tachycardias
Free Full Text from Circulation.

Erdogan, H., Gul, E., Gok, H., & Nikus, K. (2012). Therapy-resistant ventricular tachycardia caused by amiodarone-induced thyrotoxicosis: a case report of electrical storm The American Journal of Emergency Medicine, 30 (9), 209200000-2147483647 DOI: 10.1016/j.ajem.2011.12.035

Marill, K., deSouza, I., Nishijima, D., Stair, T., Setnik, G., & Ruskin, J. (2006). Amiodarone Is Poorly Effective for the Acute Termination of Ventricular Tachycardia Annals of Emergency Medicine, 47 (3), 217-224 DOI: 10.1016/j.annemergmed.2005.08.022

Marill, K., deSouza, I., Nishijima, D., Senecal, E., Setnik, G., Stair, T., Ruskin, J., & Ellinor, P. (2010). Amiodarone or Procainamide for the Termination of Sustained Stable Ventricular Tachycardia: An Historical Multicenter Comparison Academic Emergency Medicine, 17 (3), 297-306 DOI: 10.1111/j.1553-2712.2010.00680.x

Tomlinson, D., Cherian, P., Betts, T., & Bashir, Y. (2008). Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emergency Medicine Journal, 25 (1), 15-18 DOI: 10.1136/emj.2007.051086

Helmy, I., Herre, J., Gee, G., Sharkey, H., Malone, P., Sauve, M., Griffin, J., & Scheinman, M. (1988). Use of intravenous amiodarone for emergency treatment of life-threatening ventricular arrhythmias Journal of the American College of Cardiology, 12 (4), 1015-1022 DOI: 10.1016/0735-1097(88)90470-6

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What Does a Moon Landing ECG Look Like?

 

Some interesting ECG from the first people to land on the Moon.

During landing, they were running low on fuel and Buzz Aldrin appears to be showing signs of stress.

 

Click on images to make them larger.
 

The image above is from the following video describing the monitoring of the ECGs of the astronauts.
 

[youtube]PPBF3wgOX9Q[/youtube]
 

The reason this is in the news now is that one of four of the ECGs of Neil Armstrong as he stepped on the Moon was scheduled to be auctioned, but has been pulled due to questions about whether the owners have clear title to these items.[1]

How low on fuel were they? Were they going to crash?

They were just going to have to abort the mission and return to the Command Module, but after years of preparation for a Moon landing, that can be a huge amount of stress.
 


 

“EKG Recordings Taken as Apollo 11 Commander Neil Armstrong Took Man’s First Step on the Moon” and “4:13:24:28 Ground Elapsed Time.” Sheet is signed and inscribed in pencil, “To Paul Jones, The heartbeats that made this accomplishment possible as recorded at MCC on my console. Keep up your heart work. Charles A. Berry M.D.” Presentation also bears a Neil Armstrong autopen signature. Sheet is matted and framed with mission patches from Apollo 7, Apollo 8, Apollo 9, Apollo 10, Apollo 11, Apollo 12, Apollo 13, and two Snoopy patches, to an overall size of 20.75 x 24.75.[2]

 

Look at Buzz Aldrin’s ECG. The rate is about 400 BPM (Beats Per Minute).

Can a human heart beat that fast?

I have seen close to 300 BPM in a febrile infant.

Is the following rate possible for a human?
 


 

The rate is probably not possible.

The reason it looks so fast is most likely because the paper is being fed at a much slower speed than usual.

Conversely, we can get a better idea of what a very fast tachycardia looks like by speeding up the paper feed rate from the standard 25 mm/second to 50 mm/second or by manually pulling the paper through the printer faster than its normal rate.
 

EKG strip, six inches long, taken as Apollo 11 Commander Neil Armstrong took man’s first step on the moon. This is an actual strip of the EKG from Armstrong’s heart monitor at the moment he stepped onto the lunar surface.[2]

 


 

Compare that with a “six second section” of Buzz Aldrin’s ECG during their very low on fuel landing.
 


 

At 12.5 mm/second, this would be a rate of about 200 BPM, faster than the calculated maximum heart rate, but still capable of being a sinus tachycardia that is only associated with minor/moderate symptoms. At 10 mm/second, this would be a rate of about 160 BPM, which I regularly exceed (and recover from without any need for adenosine or cardioversion).
 

[youtube]sTBIr65cL_E[/youtube]
 

Several times you hear them checking with the flight surgeon and receiving a “Go,” each time. A heart rate of 400 should have resulted in something other than a “Go.” A few questions to Buzz Aldrin about how he is feeling would have been prudent.

If I have a patient with a heart rate of 400 and I do not ask a few questions about how the patient is doing, it would probably be because the patient is not capable of communicating. How are you feeling, hummingbird?
 

In general, sinus tachycardia is a response to other factors and, thus, it rarely (if ever) is the cause of instability in and of itself.[3]

 

At EMS 12 Lead, there is an excellent discussion of sinus tachycardia, and the nonsense of assuming that anything faster than 150 BPM is an SVT that needs adenosine or cardiversion.[4] This includes comments from Dr. John Mandrola and Dr. Mark Perrin.
 

Go read it.
 

Footnotes:

[1] Neil Armstrong’s ‘Heartbeat,’ Apollo Joystick Pulled from Auction
by Robert Z. Pearlman, collectSPACE.com Editor
Date: 20 May 2013 Time: 04:34 PM ET
Article

[2] Neil Armstrong’s Heartbeat – EKG Up For Auction
By Patrick Lockerby
May 5th 2013 04:20 PM
Science 2.0
Article

[3] Overview
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Free Full Text from Circulation.

[4] The Trouble With sinus Tachycardia
April 30, 2013
David Baumrind
EMS 12 Lead
Article

.

Another Sinus Tachycardia that F&B Medics Want to Shock

 

In Worst test question ever! – Maybe, I pointed out some of the problems with the way we “educate” people in EMS. The following question was provided with the rhythm above.
 

You are dispatched emergency traffic to the scene of a 24 yo F with “palpitations.” You arrive to find her pale, sweaty and lethargic. You palpate a radial pulse with an extreme rate. You hook her up to the monitor and find the following rhythm? You have a 45 minute transport time. Which of the following is the most appropriate initial treatment for this condition?

1.) Nitroglycerin 0.4mg SL
2.) Immediate synchronized cardioversion
3.) Adenosine 12mg Rapid IV push followed by 20cc NS bolus
4.) Epinephrine 1mg 1:10000 q-3-5m IVP

 

If a test question is so poorly written that there is no justifiable answer, why would anyone competent defend the question?

The answer is that we have dangerous people as “educators” and no really good method of eliminating them from EMS classrooms.

If there are no correct answers, can there be one best answer?

If there are no correct answers, can the most deadly answer possibly be the best answer?

We are supposed to be providing patient care, not making “educators” feel good about being dangerous.

Could the rhythm be atrial flutter?

It is not a bad idea to suspect flutter when the ECG rate is an even fraction of the ≈300 rate that is typical of flutter waves e.g. ≈75, ≈100, and ≈150)?

Is there another wave half way between the P waves seen in this rhythm, which would make both waves F waves?

I do not see any Flutter waves.
 

 

That is the same rhythm. Do you see any F waves?

If the rhythm is sinus, then cardioversion/defibrillation is not going to help, but can make things a lot worse.

We can produce anything from pain to death by shocking this rhythm.

Why would we do that to satisfy an incompetent “educator”?

This might be a good question to identify people who should not be trusted to care for patients. If we are willing to make a choice that is the equivalent of harming patients in order to come up with the one best answer right answer in a testing environment, what might we do when faced with a real patient, but a protocol that we think needs to be followed?

Is cardioversion the way to avoid the QA/QI/CYA spanking?

Should we be trying to figure out how to intervene?

Should we be trying to figure out when to intervene?

If the intervention is a heart-stopping dose of electricity (cardioversion), should we be looking for excuses to shock, or should we be trying to figure out if the patient is likely to benefit from that treatment?

What about this 80+ year old patient, who is pale, and lethargic, but is not confused?
 

 

 
 

Here is a different EMS 12 Lead Facebook post.
 

More ACLS…
Your pt is a 54 yo male found in bed, with AMS. He looks pale, has BP of 84/52 with the rhythm below. No other hx is available right now. What’s the treatment?

 

The earlier post looked like a sinus tachycardia from a rhythm generator. With the HeartSim, to get a good fast narrow complex rhythm use atrial tachycardia and hit the faster button once or twice – that produces a rhythm that is not obviously sinus. There were 25 comments choosing from among the choices given, before there was a comment from someone smart enough to recognize that all of the choices were wrong.

Yes, the National Registry does encourage the fraud of one best answer. Why do medics choose a dangerous treatment, when we know it is dangerous?

We have been taught to choose try to figure out what would be most pleasing to the instructor/evaluator – not to do what is best for the patient.

Why aren’t the instructors/evaluators looking for what is best for the patient?

 
One of the reasons for fewer indefensible answers at EMS 12 Lead is that many of the people following EMS 12 Lead are already medics, nurses, and/or doctors, rather than students looking to please an instructor/evaluator.

This time, there were four good answers before anyone suggested cardioversion, but why are so many of us looking for excuses to use electricity to stop the hearts of patients?

.

Worst test question ever! – Maybe

 

Thank you to David Baumrind of EMS 12 Lead for linking to this here. It probably is not the worst test question ever, but it is very bad.

Read the question, figure out what your response would be, then scroll down for my explanation.
 

You are dispatched emergency traffic to the scene of a 24 yo F with “palpitations.” You arrive to find her pale, sweaty and lethargic. You palpate a radial pulse with an extreme rate. You hook her up to the monitor and find the following rhythm? You have a 45 minute transport time. Which of the following is the most appropriate initial treatment for this condition?

1.) Nitroglycerin 0.4mg SL
2.) Immediate synchronized cardioversion
3.) Adenosine 12mg Rapid IV push followed by 20cc NS bolus
4.) Epinephrine 1mg 1:10000 q-3-5m IVP

-Admin Paul

The original posting was from Exhausted Medic Students ‘R’ Us here.

Go read the original with its hundreds of comments.

 

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All of the answers are completely wrong.
 

ST (Sinus Tachycardia) is the rhythm.

There are clear P waves with consistent PR intervals. It is faster than what some people expect to see from ST, but that is because many of us do not think about what we are learning in EMS.

It is true that the cardiology part of paramedic school is probably the toughest for most people, and we are overwhelmed with new information, but we should be very familiar with this rhythm.

Carry a patient up/down a flight of steps and you may have significant ST – maybe even faster than what is on this strip. If your heart rate is over 150, so what?

Before you have a chance to recover, use the pulse oximeter to measure your heart rate after carrying a patient. You are just checking the accuracy of the machine before applying it to the patient, or before reconnecting it to the patient.
 

1. Nitroglycerin is NOT indicated for palpitations.

NTG is not indicated even for a lot of palpitations. Do you have a protocol for NTG for palpitations?

Ask your medical director how much NTG should be given for palpitations, but don’t be surprised if you are expected to go through some scenarios to demonstrate that you would not really give NTG for palpitations.
 

2. Cardioversion is NOT indicated for sinus tachycardia.

Cardioversion is supposed to cause asystole. During that asystole, it is hoped that the sinus node will become the pacemaker for the patient’s rhythm.

SINUS tachycardia means that the sinus node is already the pacemaker.
 

Cardioversion of sinus tachycardia can only make things worse.
 

Cardioversion of sinus bradycardia can only make things worse.

Cardioversion of any sinus rhythm can only make things worse.
 

3. Adenosine is NOT indicated for sinus tachycardia.

The dose does not matter. The drug is not indicated.

No matter how wrong NTG is for palpitations, adenosine is worse.
 

4. Epinephrine is NOT indicated for sinus tachycardia with a pulse.

How much faster do we want this ST to be? Epinephrine can make it faster.
 

Maybe some people think that the choices should include a vagal maneuver.

No. That would also be wrong.

Calcium channel blocker?

Another wrong.

Beta blocker?

Wrong again.
 

No competent paramedic should attempt to justify any of these answers.

Maybe this is a question to find out just how incompetent people will be to satisfy an authority figure.

One horrible answer is –
 

As a paramedic instructor and a evaluator for National Registry…if my student didn’t cardiovert…I’m failing them.

 

Does the National Registry hire people this ignorant as evaluators?

Yes, but so does every other testing organization. Maybe this guy is lying about being an instructor and evaluator, but this is EMS and we like low standards.

A defender of cardioversion posted the ACLS tachycardia cheat sheet.
 

Click on image to make it larger.

 

Unfortunately, the cheat sheet does not state that we should not shock sinus tachycardia.

If all we know is the cheat sheet, we should consider a career change to explore the exciting world of fast food order fulfillment.

The text of the 2010 ACLS guidelines states –
 

ACLS professionals should be able to recognize and differentiate between sinus tachycardia, narrow-complex supraventricular tachycardia (SVT), and wide-complex tachycardia.[1]

 

A lot of people could not recognize an obvious sinus tachycardia.

Is that the fault of their instructors?

Yes and No.
 

Sinus tachycardia is among the rhythms listed that we are expected to be able to identify.
 

Synchronized cardioversion is recommended to treat (1) unstable SVT, (2) unstable atrial fibrillation, (3) unstable atrial flutter, and (4) unstable monomorphic (regular) VT. Shock can terminate these tachyarrhythmias by interrupting the underlying reentrant pathway that is responsible for them.[1]

 

Sinus tachycardia is not listed among the rhythms that should be shocked.

Here is the important part –
 

If judged to be sinus tachycardia, no specific drug treatment is required. Instead, therapy is directed toward identification and treatment of the underlying cause. When cardiac function is poor, cardiac output can be dependent on a rapid heart rate. In such compensatory tachycardias, stroke volume is limited, so “normalizing” the heart rate can be detrimental.[1]

 

We treat sinus tachycardia by treating the cause.

The cause of sinus tachycardia is never lack of cardioversion.
 

A good test near the end of the cardiology section of paramedic school might include this question to find out if the students have learned anything.

All of the choices are wrong.
 

In medicine, there is not one best answer for all patients.
 

Anyone who says differently is selling something.

Footnotes:

[1] Tachycardia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Cardioversion and Regular Narrow-Complex Tachycardia

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Woman with Risks for Torsades de Pointes Dying within Hours of Leaving the Emergency Department

 

I don’t expect to see this as a headline anywhere, but this possible cause of death something we should be aware of.

Abdominal pain in a patient with many comorbidities. She is given medication and later is found dead at her home.

What drugs was she taking?
 

a Potentially proarrhythmic drugs as classified by the Arizona Center for Education and Research on Therapeutics (www.qtdrugs.org).
b Given during emergency department visit.[1]

 

What risk factors did she have?
 

a Risk factors present in case study.[1]

 

The 12 lead obtained in the ED (Emergency Department) shows a bradycardia with a heart rate of 58 beats per minutes. Bradycardia probably should have been included in the risk factors in this case.

What treatment did she receive that increased her risk of TdP (torsades de pointes)?
 

 

Ondansetron (Zofran)
 

On September 15, 2011, the FDA issued a Medwatch Safety Alert for Zofran (ondansetron) in patients with congenital Long QT syndrome, a heart arrhythmia. The FDA further required GlaxoSmithKline to conduct a thorough QT study to determine the degree to which Zofran may cause QT interval prolongation.[1] On June 29, 2012, the FDA issued an FDA Drug Safety Communication Update entitled New information regarding QT prolongation with ondansetron (Zofran).

The 32-mg high dose of ondansetron (Zofran) has been pulled from the market by the FDA because of concerns about cardiac problems.[15][2]

 

The high dose of 32 mg is more than would usually be given by EMS or in the ED.

In this case, the ondansetron was 8 mg given orally in the ED, so this was a much smaller dose.

What is QT segment prolongation?
 


Image credit.

There is a problem with the image. The ventricles contract during the QRS complex, not during the T wave.
 

Let’s see some torsades.
 


Click on images to make them larger.[3]
 

How do we know that it is TdP?

Because of the long QT segment in the beats preceding the VT (Ventricular Tachycardia).

Does all torsades go away on its own, as the above example did?

No.

 

A medical screening examination was conducted and 8 mg of orally disintegrating ondansetron (Zofran) was administered for persistent nausea and vomiting. A 12-lead electrocardiogram (ECG) completed at triage (Figure 1) was remarkable for left ventricular hypertrophy and QT interval prolongation.[1]

 

This is a patient who should be on a monitor, not necessarily because of the proarrhythmic effects of the drugs she is already taking, but because of the combination with the proarrhythmic drug she has been given in the ED.

 

Shortly thereafter, the patient self-discharged from the emergency department before receiving definitive treatment. Upon making a follow-up phone call, it was discovered that the patient had been found unresponsive in bed approximately 4 hours after leaving the emergency depart[1]

 

Was it the Zofran?

Maybe, but if it was, the ondansetron may only be the straw that broke the camel’s back.

Does that mean that the risks should have been ignored?

No.

Many of the patients we see are the most fragile people in society and we are seeing them when they are at their greatest vulnerability to adverse treatment effects.

The FDA has warned about the QT prolonging effects of ondansetron, so we cannot claim that we could not have known. I have written about this before.[4],[5]

We should be looking for reasons why we should not be giving treatments.

EMS operates under protocols that may state –

If condition X is present, give treatment A, then give treatment B.

ED treatment can be just as protocol driven as EMS treatment.

We have drugs that can be dangerous under certain circumstances.

Should we give any drug without considering the possible drug interactions and adverse events?

If we are not aware of the drug’s possible drug interactions and adverse events, should we be permitted to give the drug?

Ondansetron is one of the drugs I give frequently, but I need to remind myself to consider the possible QT prolonging effects and to look for other QT prolonging drugs and medical conditions.

What other drugs do I carry that can cause QT prolongation?

Amiodarone (Nexterone, Cordarone) is the only drug I carry that is on the Drugs with a Risk of Torsades de Pointes list. Even ondansetron is not on this list. There is less evidence that ondansetron causes torsades, than there is that amiodarone causes torsades.
 

Substantial evidence supports the conclusion that these drugs prolong the QT interval and have a risk of TdP when used as directed in labeling.[6]

 

Oxytocin (Pitocin) and ondansetron are on the Drugs with a Possible Risk of Torsades de Pointes list.
 

Substantial evidence supports the conclusion that these drugs cause QT prolongation but there is insufficient evidence that they, when used as directed in labeling, have a risk of causing TdP.[6]

 

Diphenhydramine (Benadryl) is the only drug I carry that is on the Drugs with a Conditional Risk of Torsades de Pointes list.
 

Substantial evidence supports the conclusion that these drugs prolong the QT interval and have a risk of TdP but only under certain known conditions (e.g. excessive dose, drug interaction, etc.).[6]

 

All of these drugs are generally considered to be safe, because we are ignorant of the adverse events they can cause. TdP is only one adverse event. Amiodarone has other proarrhythmic effects, can cause hypotension,

Then there are the many drugs that may interact with these drugs to prolong the QT segment.

Antibiotics, psychiatric medications (for all kinds of psychiatric conditions – psychosis to depression), erectile dysfunction drugs,

Then why aren’t we seeing large numbers of dead bodies?

These patients have other medical conditions that may lead to death without any TdP or there may not be much TdP caused by these drugs. We do not know.

We do know that thousands, even tens of thousands of patients can die without anyone noticing that the deaths are the effect of a drug.[7]

For example –
 

She was pronounced dead at the scene by emergency care providers. Because of her extensive medical history, the woman’s family declined an autopsy, and her primary physician attributed the death to complications of diabetes mellitus, end-stage renal disease, and hypertension.[1]

 

What was the cause of death?

We do not know.

Given the number of risk factors for TdP, is TdP a likely cause?

Torsades de pointes is no less likely a cause of death than anything listed by the her primary care physician on the death certificate.

This isn’t a multiple choice exam, where someone thinks that there is some mythological one best answer.

This is the real world and all of these conditions probably significantly contributed to her death.

Was ondansetron the final straw?

Maybe.

Footnotes:

[1] Woman with Risks for Torsades de Pointes Dying within Hours of Leaving the Emergency Department.
Pickham D, Sickler K.
J Emerg Nurs. 2011 Dec 2. [Epub ahead of print] No abstract available.
PMID: 22137882 [PubMed – as supplied by publisher]

[2] Ondansetron
Wikipedia
Adverse effects
Article

[3] Etiology, warning signs and therapy of torsade de pointes. A study of 10 patients.
Keren A, Tzivoni D, Gavish D, Levi J, Gottlieb S, Benhorin J, Stern S.
Circulation. 1981 Dec;64(6):1167-74.
PMID: 7296791 [PubMed – indexed for MEDLINE]

Abstract with link to Free Full Text Download in PDF format from Circulation

[4] Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part I
Mon, 02 Jul 2012
Rogue Medic
Article

[5] Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part II
Thu, 05 Jul 2012
Rogue Medic
Article

[6] TdP drug lists
AZCERT.org is now CredibleMedsTM
Web page with links to all lists as pop ups.

[7] 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.

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How do we measure the QT segment when there are prominent U waves?

ResearchBlogging.org
 

This ECG has large T waves, U waves, and P waves, but where does one end and the other begin?

When measuring the QT segment, where do we measure the end of the QT segment and why?

Click on the image to make it larger.
 

Fig. 1 Electrocardiogram demonstrating the phenomenon of T-U fusion.[1]

 

Leads V2 – V4 are the most distinct, but the T wave and the U wave are not distinct from each other. They are connected with no isoelectric line between them. Therefore, the QT segment becomes more of a QTU segment. If the T wave and the U wave did not merge, or fuse, then the QT segment would not include the U wave.
 

Amiodarone is a widely used antiarrythmic drug for various atrial and ventricular arrhythmias. It has the potential to cause prolongation of the QT interval, which, in turn, can increases the incidence of torsade de pointes. Amiodarone is also one of the causes of prominent U waves. The presented case exemplifies the phenomenon of amiodarone-induced T-U fusion and QT prolongation.[1]

 

We seem to forget that any antiarrhythmic drug is also capable of causing arrhythmias. If we alter the conduction system, we can make things better, we can make things worse, or we can produce a combination of both. It is possible to have no effect, but this is more likely just our lack of awareness of the effects we are producing.
 

Amiodarone is also one of the causes of a prominent U wave in the surface electrocardiogram [2]. It blocks the delayed rectifier potassium current, thereby delaying phase 3 of action potential. This repolarization delay may distort T waves and/or produce prominent U waves[3,4].[1]

 

Amiodarone and torsades is a significant, but not well known problem.
 

Proarrhythmia
Like all antiarrhythmic agents, amiodarone I.V. may cause a worsening of existing arrhythmias or precipitate a new arrhythmia. Proarrhythmia, primarily torsades de pointes (TdP), has been associated with prolongation by amiodarone I.V. of the QTc interval to 500 ms or greater. Although QTc prolongation occurred frequently in patients receiving amiodarone I.V., torsades de pointes or new-onset VF occurred infrequently (less than 2%). Patients should be monitored for QTc prolongation during infusion with amiodarone I.V. Combination of amiodarone with other antiarrhythmic therapy that prolongs the QTc should be reserved for patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent.
[2]

 

Here is an explanation of how to measure the QT segment when there is fusion with a prominent U wave.

 

Fig. 2 Panel A represents a magnified segment of lead V 2 of the presented electrocardiogram which demonstrates T, U, and P waves and the phenomenon of T-U fusion.[1]

 
 

Fig. 2 Panel B illustrates the application of the maximum slope intercept method to the U wave to calculate the QTc; the QTc (QT/√RR) is prolonged to 510 milliseconds.[1]

 

If the T wave reaches the isoelectric line, we measure the end of the QT segment at that point. If the T wave runs into the U wave, we should draw the steepest (closest to vertical) line that we can along the descending side of the U wave (Figure 2B).

This makes for a significantly longer QT segment. The longer the QT segment, the greater the risk for torsades appears to be. Torsades is not our friend.[3],[4]

Footnotes:

[1] Amiodarone-induced T-U fusion.
Omar HR.
Am J Emerg Med. 2012 Nov;30(9):2081.e1-2. doi: 10.1016/j.ajem.2011.10.024. Epub 2011 Dec 26. No abstract available.
PMID: 22205017 [PubMed – in process]

[2] AMIODARONE HYDROCHLORIDE injection, solution
[Bedford Laboratories]

DailyMed
Warnings
FDA Label

[3] 47 Year Old Male CC: Crushing Chest Pain
August 11, 2011
EMS 12 Lead
Article

[4] 47 Year Old Male CC: Crushing Chest Pain – Conclusion
August 17, 2011
EMS 12 Lead
Article

Omar, H. (2012). Amiodarone-induced T-U fusion The American Journal of Emergency Medicine, 30 (9), 20810-208100 DOI: 10.1016/j.ajem.2011.10.024

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