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Intra-arrest Glucose Management

Question# 761

In regards to reversible causes of cardiac arrest, would it be appropriate to consider hypoglycemia as a reversible cause should it fit incident history and after other reversible causes have been addressed?

It seems it was listed as a reversible cause from 2005-2010, but was removed because of worse neurological outcomes. I understand it wouldn't be beneficial to do routinely. However, if I'm not mistaken hypoglycemia can cause Qt prolongation leading to ventricular arrhythmia. Given a history of low oral intake, recent insulin use, perhaps over exertion and/or seizure, family measured BGL while alive, could a dose of D10(or glucagon if no IV/IO access) be considered after all other reversible causes have been addressed with no rosc? Why is it that hypoglycemia is listed as a reversible cause for pediatrics and not adults?


Thank you for your question and thinking out of the box to advocate for your patient(s)!

In short, you’ve nailed it on the head – there is no routine use for intra-arrest glucose (or glucagon). For undifferentiated cardiac arrest there isn't good evidence that measurement or treatment of hypoglycemia makes a difference for outcomes. __

Historically, paramedics used to throw the “coma cocktail” – thiamine, naloxone, and dextrose – to patients in cardiac arrest. It was thought that these were benign medications with limited risks but high potential benefits, but as our training and medical understating has evolved, so too have our treatments. We no longer administer medications empirically.

As you mention, this has been reflected in the most recent iterations of the AHA guidelines. The current AHA guidelines speak to the “H’s and T’s”, or the reversible causes of cardiac arrest. Unfortunately, most of the research looking at intra-arrest glucose controls looks at patients in hospital, a very different population than we see and treat, but the evidence does seem to suggest that it may worsen outcomes and increase mortality in the context of ROSC.

That being said, just because the medication isn’t listed on the ACLS algorithm, doesn’t necessarily mean it’s contraindicated.

If you have a tremendously high index of suspicion that a hypoglycemic event may have preceded the terminal cardiac event, like the patient you outlined in your question, it is certainly reasonable to test and treat if low. In a truly hypoglycemia patient, there MAY be a role of dextrose, provided that those interventions don't interfere with the ones we know make a difference (CPR, defibrillation). In that scenario, document why you checked the sugar and treated if low, and that it didn't interfere with the resuscitation.

There are a couple of things to keep in mind. Namely, an intraarrest peripheral blood glucose will inherently be inaccurate, which is why this metric no longer has value in cardiac arrest. The other is while hypoglycemia causes cerebral deficiency, the myocardium runs primarily on ATP as its energy sources, rather than glucose alone. Dextrose is initially HYPERtonic, but becomes HYPOtonic when metabolized and can further exacerbate cerebral edema.

This means that cardiac arrest due to hypoglycemia is more likely to be the result of brain neuroglycopenia and autonomic dysregulation than direct cardiac action.

It’s proposed that arrythmias in hypoglycemia are the result of reduced glucose in the brain (neuroglycopenia). We know that the brain runs primarily on glucose, so any decrease in glucose or prolonged hypoglycemia can lead to brain damage and death. This in turn can create arrythmias, heart blocks, bradycardia, and eventual death. The cardiac impacts are thus primarily indirect.

There are also direct cardiac impacts. Hypoglycemia can lead to hyperinsulinemia, hypokalemia, which can lead to QTc prolongation and in turn cardiac arrythmias and death. As BGL drops, epinephrine peaks, hypokalemia worsens, QTc prolongation peaks, PVCs and heart blocks occur, norepi peaks, leading to 3rddegree blocks, bradycardia, and sudden death. To further exacerbate it, this autonomic beta stimulation from hypoglycemia, coupled with the epinephrine we routinely administer during cardiac arrest, will further consume glucose and glycogen stores, worsening the state of hypoglycemia, further precipitation this cycle.

Lastly, as we alluded to earlier, HYPERglycemia results in poorer neurological outcomes.

With respect to the discrepancy between PALS and ACLS, there are a couple theories at play. Physiologically, it’s plausible to consider as children have lower glucose stores at baseline. While the adult practitioners infrequently check POC glucose as part of their routine cardiac arrest management, the pediatricians have a different approach as children occasionally present with an undiagnosed metabolic disorder (generally in the first few months of life though), in which hypoglycemia is an important factor can present for the first time in cardiac arrest.

Ultimately, this is a risk/benefit discussion, and in general, the risks far outweigh the potential benefits. If you truly believe hypoglycemia is felt to be the cause of cardiac arrest, and all other priorities have been met, it’s reasonable to test and treat. Otherwise, the routine use of intra-arrest glucose management is not recommended.


25 January 2024

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Please reference the MOST RECENT ALS PCS for updates and changes to these directives.