Point well taken. But what is the mechanism of death for “acute alcohol poisoning”? They usually present to the ER having aspirated and gone pulseless non-breather, or gotten hypothermic and done the same, or just given up respiring as a bad job. The patient (usually a college student)drinks a fifth of whiskey in 30 minutes, curls up and dies. I don’t think it’s usually from acute hepatic failure or pancreatitis and resultant shock. Having reviewed the literature (at least the netlit), I’m more confused than usual as to what the actual pathophysiology is. I’m sure the info is out there somewhere, I’m just not finding it. Can you clue in an old fart? Someday you too, will have the opportunity to be out of date!
Grumble, grumble. Back in my day, we had to write progress notes on the backs of shovels with pieces of charcoal, and we liked it!
Hmmm. You’re right. So what the heck is the pathophysiology? My Tintinalli says that “ethanol can cause death directly from respiratory depression, although morbidity and mortality are usually related to unanticipated injury from impaired cognitive function”. So maybe it is just a direct toxic effect on the lungs. OTOH, alocholic ketoacidosis can occur acutely too, depleting glycogen, suppressing insulin, making ketones and getting acidotic. But this usually takes 2-3 days post-binge, no?
I don’t know the answer, and am as confused as ever. Let’s just agree to blame it on the esophageal varices.
And to the OP, my condolences over the loss of your friend.
While I’m looking stuff up in Tintinalli, methanol is found in paints, antifreeze and windshield wiper fluids. In the body, formaldehyde and formic acid accumulate causing metabolic acidosis. Treatment involves preventing the toxic metabolites from forming by inhibiting alcohol dehydrogenase with folate plus ethanol IV or fomepazole (which has 8000 times more affinity than ethanol for ADH), but in severe cases dialysis would also be needed.
Lets see, if one was to become acidotic, that would increase the irritability of the heart…now if one was to have a pre-existing cardiac condition, maybe an accessory pathway, I could possibly see how that could trigger a reaction, but wouldn’t that lead to more of a SVT first?
this is what else I could come across http://202.71.136.146:8080/healthcarehouse/diseases/emerg_em/topic19.htm
Ethanol is a direct CNS depressant that causes decreased motor function and level of consciousness. At high concentrations, ethanol is an anesthetic and can cause autonomic dysfunction (e.g., hypothermia, hypotension), coma, and death from respiratory depression and cardiovascular collapse
heres another great link that elaborates on topic, but comes pretty much to the same conclusion