Episode 16: Getting that sweet ROSC?

Are we giving our patients a sweet chance at ROSC? Or consigning them to a sugary grave? We examine the evidence for and against Dextrose in Cardiac Arrest.

Two renown EMS blogs, Rogue Medic and Mill Hill Avenue Command, have already covered the topic before. But let’s take a deeper look at the evidence for and against Dextrose as well as discuss the cardiac physiology pertaining to Glucose metabolism. We’ll also cover how patients who become hypoglycemic end up going into cardiac arrest in the first place and whether we can accurately detect hypoglycemia in cardiac arrest.

Just like our Narcan podcast, we’re going to science and evidence the crap out of this one.

Here’s a breakdown of the points in this podcast.

  • Myocardial cells don’t use glucose as a primary source of fuel. As little as 4% of myocardial ATP is generated from glucose.
  • Giving dextrose during periods of ischemia increases anaerobic metabolism, promotes the conversion of pyruvate into lactate, causes intracellular acidosis, and may decrease cerebral blood flow, exacerbating cerebral ischemic injury.
  • We can’t accurately determine blood glucose in cardiac arrest using capillary blood glucose. Glucometry using a venous sample without a venous reagent strip is suspect and potentially inaccurate.
  • The largest study to date (Peng, 2015) shows worse overall survival to discharge.
  • The largest study to date (Peng, 2015) shows  worse neurologic outcome.
  • The largest study to date (Peng, 2015) shows no association between dextrose administration and ROSC when propensity-matched analysis was used.
  • Studies show even D5W can worsen outcomes in cardiac arrest.

Here’s the total body of evidence for Dextrose in cardiac arrest resuscitation (click to enlarge)…

Pediatric Hypoglycemia

The above data has been reproduced in accordance with the provisions of 17 U.S. Code § 107 “Fair Use” for the purposes of criticism, comment, and non-commercial educational purposes.

Show Notes

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