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.

That link is no longer available, but the overall page of evidence-based worksheets is available in PDF format here.

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Comments

  1. What does that leave us with?

    Compressions in cardiac arrest.

    Defibrillation in VF cardiac arrest.

    Therapeutic hypothermia after resuscitation.

    The problem is that people (AHA in particular) insist on looking at all cardiac arrests as the same. We don’t treat all forms of shock the same way, why do we do so for cardiac arrest? The only distinction we draw is “shockable vs. non-shockable rhythms”; why not other decision points?

    For example, ventilations are bad….for SCA of cardiac origin; on the other hand, for cardiac arrest secondary to respiratory arrest (e.g. drownings), the ventilations are critical. Sodium bicarbonate isn’t recommended any more….unless it’s a known dialysis patient who missed his dialysis; then bicarb and calcium are life-saving. Similarly, epinephrine seems to have a negative effect; but may be beneficial in e.g. beta-blocker overdose.

    We need to do the research; and we need to mine the data to look for different treatments for different causes rather than trying to cure “cardiac arrest” as a single problem.

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