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

- Rogue Medic

Dark Ages of ACLS Comment on Part II of ‘Why Did We Remove Atropine From ACLS?’

 

In the response to Why Did We Remove Atropine From ACLS? Part II is the following from mpatk –
 

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?

 

Valid science requires that we control for as many variables as possible and acknowledge when we cannot adequately control for all relevant variables.

Many people in medicine, perhaps especially those writing guidelines, have ignored that.

The AHA (American Heart Association) is getting better at eliminating the wishful thinking from ACLS (Advanced Cardiac Life Support), but there is still a long way to go. The list of treatments based on wishful thinking is much longer than the list of treatments based on valid evidence of improved outcomes.
 

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.

 

It would be nice to have good evidence to support this, but it is the kind of treatment that is correcting an obvious deficit, so it is not unreasonable without evidence.

We should still try to obtain valid evidence that minimizes the roles of non-ventilation variables.
 

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.

 

I agree with calcium chloride for cardiac arrest that is suspected of being due to hyperkalemia.

I think that dialysis patients should be given 1 gram of calcium chloride as the first treatment after initiation of chest compressions in cardiac arrest.

Again, it would be nice to have good evidence. There are plenty of case reports of cardiac arrest responding to calcium and some other good evidence.[1]
 


Image credit.
 

Similarly, epinephrine seems to have a negative effect; but may be beneficial in e.g. beta-blocker overdose.

 

Are beta blockers competitive antagonists that are reversible with higher doses of what they are supposed to block?

Do you have any evidence?
 

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.

 

Yes.

The problem is that so many treatments have become standards of care/ACLS requirements, that researchers are prevented from randomizing patients to placebo and treatment groups.

The treatment is based on wishful thinking, so all that patients are being deprived of is wishful thinking.

Wishful thinking is dangerous nonsense.

Footnotes:

[1] EMCrit Podcast 32 – Treatment of Severe Hyperkalemia
EMCrit
Podcast page.

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Comments

  1. I do not believe the AHA “insists on looking at all cardiac arrests the same”. If you read the actual course materials rather than just the algorithms, it is clear to me that they differentiate between primary and secondary cardiac arrests, as well as many different etiologies of cardiac arrest.

    The issue, as you have already stated, is the lack of evidence for treatments for the various etiologies of cardiac arrest. The removal of treatments without evidence of benefit is not an implication that all cardiac arrests “are the same”, but rather a tacit admission that the move to evidence based recommendations will cause a vacuum of treatments, as the evidence for those treatments is not currently there.

    This creates an “emperor has no clothes” moment, admitting that long held treatments have no evidence while at the same time attempting to move in the right direction. The issue is that currently the “right direction” can not offer much in the way of evidence.

    For the time being, basing your treament modalities on evidence while at the same time not having that evidence leaves the AHA in a vulnerable place. I can only hope that this vulnerability serves as motivation for more aggressive research to find out what really works.

    For now, if we only know that compressions, electricity, and hypothermia are all that works, then that is all we need to focus on.

  2. I have no idea what the AHA do because it’s irrelevant to me in Australia 🙂 I assume it’s much the same as the ILCOR guidelines, which the ARC (Australian Resuscitation Council) base their guidelines on.

    Basically, ARC guidelines for cardiac arrest look very similar to what I think the AHA ones are – compressions, defib a shockable rhythm, 30:2 compressions:venilations for adults, adrenaline, amiodarone for persistent VF/VT, advanced airway, all the mumbo jumbo.

    There is however a big focus on “detect and correct reversible causes” – the so called 4 H’s and 4 T’s. This seems to make a lot of sense – manage the cardiac arrest (chest compressions, defib) and fix the underlying cause if there is one, and you might actually get a good outcome. It would be nice to see advanced airway/ventilations moved to something to do to correct hypoxia as a reversible cause, rather than on every cardiac arrest, but other than that, it seems to make sense, do some good assessment to the history and clinical findings of your patient to determine if there’s a cause of the arrest, and fix it.

    Thing is, how many of these “fixes” are evidence based? I genuinely don’t know. And how would you come up with studies to test them?

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