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Hypoglycemia in Cardiac Arrest

It all started with an article that presented a case report of a patient attaining ROSC immediately after the administration of dextrose.

This was problematic because… well… that’s not supposed to happen. Hypoglycemia is not supposed to be one of the immediately reversible causes of cardiac arrest. If you’ll recall the list of ‘Hs’:

  • Hypovolemia

  • Hypoxia

  • Hydrogen Ion (acidosis)

  • Hyper/Hypokalemia

  • Hypothermia

  • and Hypoglycemia (currently only on the PALS AHA list, though)

I would like to present a particular scenario for this blog. You are caring for a diabetic patient known to be hypoglycemic - the glucometer reads “low,” and the patient has a recent history of reduced intake and took insulin shortly before becoming comatose. You have just established IV access, confirmed hypoglycemia via venous sample, and your partner has a D10 infusion ready to administer. However, your cardiac monitor now shows the patient is in VTACH (what is this, a mega-code?). You palpate the carotid artery and do not feel a pulse. You and your partner start CPR and establish all standards of care for a pulseless patient. Are you going to withhold this dextrose infusion, or are you still going to administer it?

The Typical Responses

If I were to ask why you would not give dextrose to a patient in cardiac arrest, what would be your response? I’ve asked many people this question, and I would like to present those reasons first.

  1. Dextrose is contraindicated in cardiac arrest.

  2. You cannot trust point-of-care blood glucose testing in shock states.

  3. The heart does not operate primarily on glucose, it runs on fatty acid oxidation.

  4. Hypoglycemia does not cause cardiac arrest. Therefore, it is not a reversible cause of cardiac arrest.

  5. Hyperglycemia after ROSC results in poor neurological outcomes (most common answer)

Are any of these objections reason enough to withhold dextrose from a known hypoglycemic patient? Let’s discuss each of them and see if they stand up to scrutiny.

1. Dextrose is contraindicated in cardiac arrest

I thought there was some validity to that statement before I started researching. It’s not written anywhere that I can find that you actually should withhold dextrose from any hypoglycemic patient. If the patient has hypoglycemia, dextrose is indicated - there is no mention in any guidelines about the patient’s cardiovascular status (dead or alive).

Legend has it that ACLS had hypoglycemia on the list of Hs until 2010 when it was removed. I went back to the 2010 update to see if the glycemic control section (located only in the ROSC section) had anything to say about this change. Here is a snapshot of the 2010 ACLS update when Hypoglycemia was removed from the Hs list:

While this update does say that hyperglycemia should be avoided due to possible mortality and neurological concerns, it also cites the recommendation for blood glucose to be ideal between 144-180 mg/dL. The update goes even further to say a lower range of 80-110 mg/dL should be avoided due to the risk of hypoglycemia. The talk about hypoglycemia is limited to the setting of ROSC (because they are talking about ICU glycemic control). However, in the short term, that blood glucose at ROSC would be influenced by us if we chose to treat or not treat a known hypoglycemic patient.

In 2020 there was one bullet point about “one small RCT from 2007” that recommended everyone should do what the ICU does and manage patients with the same ROSC glucose ranges. This blurb (along with the previous one) does not say anything about withholding dextrose from a known hypoglycemic patient, it simply states that 150 - 180 is what they consider a safe range for ICU management later on.

I also find it interesting that the 2020 PALS guidelines still have Hypoglycemia as a reversible cause for cardiac arrest on their Hs list:

Does this mean the same diabetic patient receiving dextrose for hypoglycemia during a code when they are 13 years old would not receive that same treatment perhaps just a few years later? Is their biology really so different now? I would say that there seems to be mixed messaging between PALS and ACLS on that aspect of care, but ACLS is mostly just non-specific. In light of new research about hyperglycemia surrounding ROSC, I would speculate that fears surrounding empiric dextrose administration caused ALCS to remove hypoglycemia from the list. I also think it was clinicians who started to believe they couldn’t administer dextrose even when it was indicated because it was removed from that ACLS list.

Another list you may be familiar with is “drugs not recommended for routine use in cardiac arrest,” which does not include dextrose (but includes atropine, sodium bicarbonate, fibrinolysis, and IV fluids, according to that same 2010 update). However, we know those drugs are still given when a specific indication is present. Lists like this warn us that the drugs should not be given routinely or empirically (without a specific, known indication).

Returning to PALS momentarily, a child may present with an arrhythmia, where hypoglycemia would rightfully be on your list for differential diagnosis. However, we also know that hypoglycemia can cause arrhythmias in adults, where correcting the hypoglycemia would also be indicated. But what if that hypoglycemic and bradycardic (or tachycardia) patient were unstable? Perhaps you were not confident you could feel a pulse - is dextrose indicated or not? The decision to do CPR or administer dextrose would then solely depend on the sensitivity of a clinician's fingers to palpate a pulse.

While some will say that PALS includes Hypoglycemia because children have low glucose stores, isn’t the same true for your T1DM patient? These aspects of care are on a spectrum, not arbitrary black-and-white divisions. For all of those who would say that hypoglycemia is not explicitly on the pulseless ACLS algorithm and should not be treated, I would ask them where they read that treating known hypoglycemia was contraindicated. I cannot find any literature to support the practice of withholding dextrose for known hypoglycemia.

2. You cannot trust point-of-care blood glucose testing in shock states.

Capillary samples in hypotensive patients on vasopressors are indeed less accurate than a venous sample. However, how far does this inaccuracy go? If your blood glucose monitor reads "low" (usually less than 20 mg/dL), is the blood glucose actually over something like 70 mg/dL? That's highly unlikely.

Garingarao et al. note, "Glycemic targets for this type of patient [with severe hypoglycemia] should perhaps be less stringent to avoid overtreatment [with insulin] and potentially fatal hypoglycemia."

The difference in capillary testing vs. venous samples in normotensive patients:

The difference in capillary testing vs. venous samples in hypotensive patients:

Venous samples are more accurate, which clinicians would want to consider for a patient in a shock state. The mean bias was 34.9 in the hypotensive group. Even if your patient had a reading below 20 mg/dL (let's say 15, for example), adding 15 to the mean bias of ~35 still gives you a reading of ~50, which is still a level 2 hypoglycemia according to the 2021 ADA standards:

Reference Ranges Classification of hypoglycemia (ADA 2021):

  • Level 1: ≥54 to ≤70 mg/dL; hypoglycemia alert value; initiate fast-acting carbohydrate (e.g., glucose) treatment

  • Level 2: <54 mg/dL; threshold for neuroglycopenic symptoms; requires immediate action

  • Level 3: Hypoglycemia associated with a severe event characterized by altered mental and/or physical status requiring assistance

A 2017 study found a similar difference between mean glucose and capillary samples in critically ill patients:

This isn't even to say that every patient will have an inaccurate measurement in the same direction. You may also have a reading of 45 mg/dL, and the actual value is 10 mg/dL. Likely all we can take away from this is that venous samples are more accurate than capillary samples and that knowing earlier if your patient is hypoglycemic is better than knowing later when their status deteriorates even further.

3. The heart does not operate primarily on glucose, it runs on fatty acid oxidation.

Primarily, yes. However, Lopaschuk et al. (2021) noted that heart failure (and even the cause of heart failure) could alter this metabolism to either favor fatty acid oxidation or glucose oxidation. Heart failure due to diabetes will decrease reliance on glucose, but it doesn't eliminate it. The heart always has some reliance on both glycolysis and glucose oxidation.

It's also worth mentioning that all of the autonomic beta stimulation from hypoglycemia combined with the epinephrine we pump into patients during a cardiac arrest will eat through glucose and glycogen stores throughout the whole body (12). This would leave fewer glucose stores and free glucose available to vital organs, worsening the issue of hypoglycemia. The body needs glucose, even in cardiac arrest, in which high-quality CPR is similar to a shock state in which cardiac output has been cut down to a quarter of its normal level (8).

The next logical question is: Does it even matter what percentage of the heart uses glucose for fuel?

Maybe, but probably not as much as we think when it comes to fatal arrhythmias caused by hypoglycemia. The proposed mechanism for arrhythmias in hypoglycemia has to do with neuroglycopenia (reduced glucose in the brain) and autonomic dysregulation - not just reduced glucose in the heart. The brain has an obligate glucose metabolism, and prolonged hypoglycemia results in brain death (usually the thing we're trying to limit in cardiac arrest).

Most of the brain does not need insulin for glucose transport via GLUT-1 and GLU3 receptors, so insulin resistance in critically ill patients would not impact this (and if insulin resistance were present, the process would require more glucose - not less). Because the brain is so dependent on glucose, irreversible brain damage occurs the longer hypoglycemia is left untreated (Barbara, 2017).

The literature seems to treat hypoglycemia and neurological outcomes as a foregone conclusion. “Although the harmful effects of hypoglycemia on survival and neurological recovery are well established, the BG level above which hyperglycemia would worsen neurological outcome is unknown” (wang et al., 2016).

Time matters when it comes to the treatment of hypoglycemia as far as brain death is concerned. Back in 2004, Auer noted that brain death due to hypoglycemia is not a result of cells becoming starved of glucose but rather an active brain death. "At that time [of EEG flattening in severe hypoglycemia], abrupt energy failure occurs, and the excitatory amino acid aspartate is massively released into the limited brain extracellular space and floods the excitatory amino acid receptors located on neuronal dendrites. Calcium fluxes occur, and membrane breaks in the cell lead rapidly to neuronal necrosis."

If hypoglycemia is not treated in time, hypoglycemic encephalopathy (HE) occurs. Hypoglycemic encephalopathy is characterized by comatose or a prolonged stupor despite normalizing blood glucose levels. This can cause long-lasting mental changes, disability, or even death (Lee et al., 2022).

Considering all this, does hypoglycemia seem like the type of condition that can wait to be corrected?

4. Hypoglycemia does not cause cardiac arrest. Therefore, it is not a reversible cause of cardiac arrest.

We covered in the last section the mechanism by which hypoglycemia would cause cardiac arrest - likely more due to brain neuroglycopenia and autonomic dysregulation than direct cardiac action. Still, I would be remiss if I did not mention Dead in Bed Syndrome since this brings it to a very human level. Jones et al. (2022) systematically reviewed overnight deaths in type 1 diabetes. I found the following rather topical:

"In 1991, the first paper describing the dead-in-bed syndrome was published, describing 22 deaths of children and young adults with type 1 diabetes who were found dead in an undisturbed bed; having been well the previous day, with no diabetes-related complications and with no cause of death found on autopsy. Since then, hypoglycemia has largely been postulated as the cause of the dead-in-bed syndrome, with the current mechanism attributing nocturnal hypoglycemia to fatal cardiac arrhythmias, including QTc interval prolongation and other cardiac arrhythmias."

It doesn't seem that claiming hypoglycemia does not cause cardiac arrest is completely correct. T1DM patients have a 10-fold increase in death over their lifetime, which is attributed to what the literature refers to as "fatal hypoglycemia." Often we read about conditions where the treatment pathway says to 'treat and reverse underlying conditions' - hypoglycemia seems to fall into that category.

I'm not sure where the aversion to saying hypoglycemia kills came from. If a patient has a clot in their coronary artery, which leads to hypoperfusion, ischemia, arrhythmia, and death, it would seem ignorant of me to argue that the clot didn't kill them. This is true even though the arrhythmia crippled their cardiac output, which then caused brain death. Hypoglycemia is not only causing arrhythmia but causes active brain death as well. Why do we attempt to split hairs when discussing a lack of essential energy substrates?

Is hypoglycemia a reversible cause of cardiac arrest? It would seem that it does influence ROSC. The discussion portion of a study entitled "Association between Intra-Arrest Blood Glucose Level and Outcomes of Resuscitation at the Emergency Department: A Retrospective Study" by Wongtanasarasin et al. (2022) had an interesting graph about ROSC and glucose levels.

In the same study, the following was noted at the outset of the Discussion section:

"Our study found that hypoglycemia, defined by intra-arrest BG of less than 100 mg/dL, was associated with lower rates of sustained ROSC. Hypoglycemia was considered one of the reversible causes of cardiac arrest in 2005 guidelines. Later, it was removed in the subsequent guidelines (2010, 2015, and 2020). Moreover, the 2020 guidelines did not address whether BG levels should be assessed during CPR or if intra-arrest hypoglycemia or hyperglycemia should be treated. As shown in our results, it is demonstrated that optimal intra-arrest BG levels were correlated with good clinical outcomes. Several studies found that disturbance of BG regulation after resuscitation from cardiac arrest is common. Recently, a large cohort in Taiwan found that intra-arrest BG less than 150 mg/dL was associated with worse neurological outcomes. Together with our findings, intra-arrest BG could be a marker of resuscitation prognosis."

They continue, "Although we could not draw a causal relationship between variables concerning this study design, normalizing intra-arrest BG was shown to result in good clinical outcomes."

In addition to the case report at the outset of this blog, there was a recent case report by Hui Chong Lau et al. (2022), who noted that their case was another reminder of a life-threatening yet quickly reversible cause of cardiac arrest - hypoglycemia. Again, this was a case of true hypoglycemia, not empiric administration of dextrose as part of some old-school 'coma cocktail.'

Between mechanisms of fatal hypoglycemia, rates of ROSC with certain blood glucose levels, and case reports of hypoglycemic patients achieving ROSC after dextrose administration, I don't think one can claim that hypoglycemia is never a cause of cardiac arrest or that it cannot influence ROSC. If you can't say never, how will you decide which hypoglycemic patients to treat and which not to treat? What data is that selection based on? Perhaps a clinician will leave a patient in a hypoglycemic state out of fear that dextrose administration will cause worse neurological outcomes down the road in the ICU. Let's examine this worry that many clinicians have.

5. Hyperglycemia after ROSC results in poor neurological outcomes (most common answer)

You wouldn’t expect a study entitled “The Administration of Dextrose During In-Hospital Cardiac Arrest is Associated with Increased Mortality and Neurologic Morbidity” (13) to actually encourage the use of dextrose for hypoglycemia during cardiac arrest, but it does. The article states, “Dextrose may be used during cardiac arrest resuscitation to prevent or reverse hypoglycemia.” Okay, that’s cherry-picking, and just because something may be done doesn’t make it right. The next line continues: “However, the incidence of dextrose administration during cardiac arrest and the association of dextrose administration with survival and other outcomes are unknown.”

So, what’s the deal? Does the potential risk of dextrose administration mean we should not be treating hypoglycemia during cardiac arrest? It depends on whether or not the hypoglycemia is known. The study notes several times, and in several different ways, that dextrose is likely to be beneficial in the case of hypoglycemia. All of the following is speaking about cardiac arrest:

  • “The provision of dextrose during cardiac arrest in the absence of confirmed hypoglycemia is not suggested in the current guideline.”

  • “In a truly hypoglycemic patient, the use of dextrose is probably recommended.”

  • “Another potential explanation for our findings [of neuroprotection despite hyperglycemia] is the higher rate of true hypoglycemia in diabetic patients for whom the administration of dextrose would likely be beneficial.”

Discussing the dangers of hyperglycemia seems to distract from the conversation about the dangers of hypoglycemia, especially with some studies casting doubt on the utility of 72-hour glucose ranges following ROSC (13). It would be illogical to say that acute hypoglycemia should not be addressed because hyperglycemia may cause chronic issues (if not well-regulated long-term in the ICU). Is there data suggesting that leaving a patient hypoglycemic would also cause issues? Wang et al. (2020) (pictured and linked below) noted that hypoglycemia was a significant prognosticator for poor neurological outcomes and that patients with blood glucose levels <150 mg/dL did not do well overall. No patients below 70 mg/dL had neurologically intact survival. Of course, correlation does not equal causation, and it would be wrong, based on the study design, to infer that the sole reason for these neurological outcomes was due to glucose. This study, and others I reviewed, postulated that perhaps certain ranges of blood glucose are markers of disease severity. Should we think about glucose similarly to how we think about lactate in the critically ill? Is stress hyperglycemia like high lactate? 🤔 ... Does any of this have anything to do with not treating hypoglycemia? 😆


I find this topic analogous to the subject of PO2. A patient with an OMI or stroke would not be left at a PO2 of 400 mmHg by any responsible clinician, but that doesn't stop the aggressive preoxygenation of these patients to prevent critical desaturation during intubation. The imminent danger of hypoxia outweighs the concern for hyperoxia hours down the road.

Is hypoglycemia a reversible cause of cardiac arrest? I have not been able to prove that this is never the case, so I am forced to say yes. I also cannot provide any argument with evidence to support withholding dextrose from a hypoglycemic patient, dead or alive. After reading through a lot of literature on the deleterious effects of hypoglycemia on the brain and heart, I would go so far as to say that I feel it would be irresponsible to withhold dextrose from a known severely hypoglycemic patient under any circumstance. Perhaps you have a different opinion, but I feel that throwing out treatment for known hypoglycemia due to the potential downstream risks of hyperglycemia is throwing the baby out with the bathwater.

Thank you for reading! This topic has already stirred a lot of conversation online, and I hope that whatever you decide is right for your patients, you're more sure of your stance after reading this blog.

Peer Review

Shane O'Donnell

Personally, this has made me revisit my mental framework surrounding the cardiac arrest. One note about the logistics of BG and cardiac arrest. When patients are not in cardiac arrest, I often obtain my BG samples from a peripheral IV. In cardiac arrest, I frequently obtain IO access as my initial administration line for medications. Regarding patterns, this may cause me to forget to obtain a sample as early as I would in my non-cardiac arrest patient. Given the high potential for increased accuracy, I'll have to alter this in my usual framework.


1. Auer R. N. (2004). Hypoglycemic brain damage. Metabolic brain disease, 19(3-4), 169–175.

2. Barbara, G., Mégarbane, B., Argaud, L. et al. Functional outcome of patients with prolonged hypoglycemic encephalopathy. Ann. Intensive Care7, 54 (2017).

3. Fun, J. R. S., & Chia, M. Y. C. (2020). Hypoglycemic cardiac arrest and rapid return-of-spontaneous circulation (ROSC) with dextrose. The American journal of emergency medicine, 38(9), 1981.e1–1981.e3.

4. Gary D. Lopaschuk, Qutuba G. Karwi, Rong Tian, Adam R. Wende, E. Dale Abel. 2021. Cardiac Energy Metabolism in Heart Failure. Retrieved from:

5. Gray, S. M., Meijer, R. I., & Barrett, E. J. (2014). Insulin regulates brain function, but how does it get there?. Diabetes, 63(12), 3992–3997.

6. Garingarao, C. J., Buenaluz-Sedurante, M., & Jimeno, C. A. (2014). Accuracy of point-of-care blood glucose measurements in critically ill patients in shock. Journal of diabetes science and technology, 8(5), 937–944.

7. Hui Chong Lau, Sze Jia Ng, Subha Saeed, Muhammad Moiz Tahir, Swe Swe Hlaing, Navjot Rai, Rahul Gaiba. 2022. Abstract 15313: Hypoglycemia: The Forgotten "H&T" in Cardiac Arrest.

8. Jiang, L., & Zhang, J. S. (2011). Mechanical cardiopulmonary resuscitation for patients with cardiac arrest. World journal of emergency medicine, 2(3), 165–168.

9. Jones, J., James, S., Brown, F., O'Neal, D., & I Ekinci, E. (2022). Dead in bed – a systematic review of overnight deaths in type 1 diabetes. Diabetes Research and Clinical Practice, 191, 110042.

10. Kalra, S., Mukherjee, J. J., Venkataraman, S., Bantwal, G., Shaikh, S., Saboo, B., Das, A. K., & Ramachandran, A. (2013). Hypoglycemia: The neglected complication. Indian journal of endocrinology and metabolism, 17(5), 819–834.

11. Lee, Y. E., Lee, E. J., Lee, S. E., & Park, J. (2022). Predictors of consciousness improvement in patients with hypoglycemic encephalopathy. Frontiers in Endocrinology, 13.

12. Levy, B., Desebbe, O., Montemont, C., & Gibot, S. (2008). Increased aerobic glycolysis through beta2 stimulation is a common mechanism involved in lactate formation during shock states. Shock (Augusta, Ga.), 30(4), 417–421.

13. Peng, T. J., Andersen, L. W., Saindon, B. Z., Giberson, T. A., Kim, W. Y., Berg, K., Novack, V., Donnino, M. W., & American Heart Association’s Get With The Guidelines®-Resuscitation Investigators (2015). The administration of dextrose during in-hospital cardiac arrest is associated with increased mortality and neurologic morbidity. Critical care (London, England), 19(1), 160.

14. Scott Youngquist , John P Rosborough , and James T Niemann. 2018. Abstract 176: Early Hyperglycemia Following Resuscitation From Cardiac Arrest Does Not Affect 72-Hour Neurologic Outcome in the Swine Model. Retrieved from:

15. Wang, C.-H., Chang, W.-T., Huang, C.-H., Tsai, M.-S., Chou, E., Yu, P.-H., Wu, Y.-W., & Chen, W.-J. (2020). Associations between intra-arrest blood glucose level and outcomes of adult in-hospital cardiac arrest: A 10-year retrospective cohort study. Resuscitation, 146, 103–110.

16. Wang, CH., Huang, CH., Chang, WT. et al. Associations between blood glucose level and outcomes of adult in-hospital cardiac arrest: a retrospective cohort study. Cardiovasc Diabetol15, 118 (2016).

17. Wongtanasarasin, W., Ungrungseesopon, N., & Phinyo, P. (2022). Association between Intra-Arrest Blood Glucose Level and Outcomes of Resuscitation at the Emergency Department: A Retrospective Study. Journal of Clinical Medicine, 11(11), 3067.


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