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.
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.
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.