A review of hypoglycemia and dextrose treatment in patients with cardiac arrest

Glenn Goodwin; Michael Hinton; Moshe Bengio; Akash Patel; Nicholas Gaeto; Huy Tran; Sanaz Kashan; Tony Zitek

doi:10.15441/ceem.24.305

INTRODUCTION

Hypoglycemia is a cause of cardiac arrest and is associated with an increased risk of death in the critically ill [1]. However, reports of sudden cardiac arrest in hypoglycemic patients are very rare, with a small number of published case reports [2,3]. Results from animal studies indicate that the mechanism by which hypoglycemia causes cardiac arrest seems to be either lethal arrhythmia or seizures with resultant respiratory arrest [4,5]. There is no strong evidence of a causal link between hypoglycemia and fatal arrhythmia in humans, but arrhythmias are thought to occur from sympathetic activation triggered by hypoglycemia, followed by excessive vagal counteraction [6,7].

Medical trainees have long been taught to assess the "Hs (hypovolaemia, hypoxia, hydrogen ion [acidosis], hyperkalaemia/hypokalaemia, hypothermia) and Ts (toxins, tamponade [cardiac], tension pneumothorax, thrombosis [coronary and pulmonary])" when elucidating the cause of cardiac arrest. In 2010, hypoglycemia was removed from the list of “Hs” in the Advanced Cardiac Life Support guidelines because of a lack of evidence [8,9]. However, in our experience, it remains commonplace to check the glucose level with a fingerstick test in patients with cardiac arrest and to administer dextrose if the level is low. In this narrative review article, we review the evidence related to hypoglycemia during cardiac arrest and the use of dextrose in cardiac arrest patients.

SUMMARY OF THE EVIDENCE

Assessment for hypoglycemia in critically ill patients

Overall, the available evidence suggests that fingerstick (capillary) glucose values are not accurate in hypotensive patients, and they may not be accurate in other critically ill patients. Specifically, they are not accurate in cardiac arrest patients.

Atkin et al. [10] performed a prospective comparison of fingerstick glucose values to laboratory values. In hypotensive patients, the mean fingerstick glucose values were 67.5% of the laboratory values. Similarly, in a prospective study, Sylvain et al. [11] found that fingerstick glucose values were not accurate in patients in shock and concluded that fingerstick glucose analysis should not be used in patients with inadequate tissue perfusion.

Hypotension reduces the accuracy of fingerstick glucose levels, as does vasopressor use, according to studies by Pereira et al. [12] and Fekih Hassen et al. [13]. Moreover, fingerstick glucose levels may be inaccurate in other types of critical illness. Critchell et al. [14] found that bedside capillary glucose measurements in intensive care unit patients (not necessarily hypotensive) differed substantially from laboratory glucose values.

Thomas et al. [15] prospectively assessed the accuracy of capillary glucose levels in patients in cardiac arrest. They analyzed both capillary and venous blood samples in a rapid-reagent system and performed laboratory analysis of venous blood to define the true blood glucose level. The researchers found that 5 of the included 50 patients (10%) who seemed to have hypoglycemia on capillary blood assessment were actually not hypoglycemic in laboratory analysis (including 2 patients who were hyperglycemic).

While fingerstick glucose levels are not accurate in patients in cardiac arrest (and in some other critically ill patients), venous blood analysis by a rapid-reagent system or point-of-care device is fairly accurate [11,15].

Animal data regarding dextrose administration during cardiac arrest

In the 1980s, multiple animal studies suggested that the administration of dextrose may be harmful during cardiac arrest. In one study, D'Alecy et al. [16] induced cardiac arrest in two sets of dogs: one set received 1 L of lactated Ringer’s and the other received 1 L of 5% dextrose in lactated Ringer’s. The researchers found that the cohort that received dextrose had significantly worse post-resuscitative neurological outcomes and survivability of at least 24 hours post-resuscitation. A similar study from the 1980s also involved induction of cardiac arrest in dogs that were split into dextrose and non-dextrose groups. All dogs in the non-dextrose group regained significant neurological capabilities (e.g., eating within 24 hours) post-resuscitation, while none of the dogs that received dextrose regained any neurological capabilities [17].

Data regarding dextrose administration during cardiac arrest

While there are no prospective trials assessing dextrose administration during cardiac arrest in humans, multiple retrospective studies show either no benefit or harm from dextrose administration. In a 2015 study, Peng et al. [18] assessed dextrose utilization for in-hospital cardiac arrest patients using the “Get with The Guidelines-Resuscitation” national registry, which amassed 100,029 patients between 2000 and 2010. Of these patients, 4,189 (4.2%) received dextrose during cardiac arrest. Multivariable analysis showed that receiving dextrose was associated with an increased chance of return of spontaneous circulation (ROSC) (relative risk [RR], 1.07; 95% confidence interval [CI], 1.04–1.10) but decreased likelihood of survival to discharge (RR, 0.88; 95% CI, 0.80–0.98) and of good neurologic outcome (RR, 0.88; 95% CI, 0.79–0.99). The only exception was for diabetic patients, for whom there was no significant difference in outcomes.

In 2022, Abramson et al. [19] performed a retrospective study of prehospital cardiac arrest patients and found that survival to hospital discharge with good neurologic outcome did not differ between hypoglycemic patients who received dextrose and those who did not. In particular, 27 of 805 patients (3.3%) treated with dextrose survived with good neurologic outcome compared with 39 of 909 (4.3%) with hypoglycemia who did not receive dextrose. However, the results of this study were limited by unbalanced baseline differences between groups.

In 2023, Wongtanasarasin and Phinyo [20] published a retrospective study that examined emergency department patients who received dextrose during cardiac arrest and those who did not. The study only included patients with blood glucose level of ≤150 mg/dL, as determined by “various point-of-care devices” (it was unclear how often capillary blood samples were used). Dextrose administration during cardiac arrest was not associated with ROSC (adjusted OR [aOR], 1.44; 95% CI, 0.58−3.54), survival to hospital admission (aOR, 1.27; 95% CI, 0.54−3.00), survival to hospital discharge (aOR, 0.68; 95% CI, 0.20−2.29), or favorable neurological status (aOR, 2.21; 95% CI, 0.23−21.42).

DISCUSSION

In this narrative review, we presented evidence that fingerstick glucose levels are not accurate measures of blood glucose during cardiac arrest (or shock). We also provided evidence that dextrose administration may cause neurologic toxicity when administered to patients in cardiac arrest; however, the evidence comes from animal and retrospective studies. Nonetheless, it is unclear if dextrose is beneficial for cardiac arrest even when administered to patients with hypoglycemia --- a concept that may be counterintuitive to some emergency physicians. In reviewing the provided evidence, some additional considerations are warranted.

First, capillary blood flow is compromised in low-flow (shock) states [10,11], and it should not be surprising that capillary blood glucose levels are inaccurate during cardiac arrest. In the studies on this subject described above, the glucose level seemed to be lower by capillary measurement than by venous measurement [10,11,15]; thus, patients who appear to be hypoglycemic (but are not) might receive unnecessary dextrose (which is likely to be harmful). Given that venous blood glucose levels (including those measured on a point-of-care device) are more accurate than capillary blood glucose levels in low-flow states [11,15], we recommend that emergency physicians use venous blood samples with a point-of-care device (if available) to assess the blood glucose level in a cardiac arrest patient. For physicians who do not have means to rapidly analyze venous blood, we recommend using a fingerstick glucose test only in clinical situations where the pretest probability of hypoglycemia is very high (such as in a diabetic who overdosed on their medications).

Notably, it is not clear what level of blood glucose is detrimental to a patient in cardiac arrest. Cardiac myocytes derive most of their energy from fatty acids (not glucose), so the blood glucose level may not be a critical factor to achieving ROSC [21]. Glucose is the main energy supply of the central nervous system, and glycogen stores in the brain are small, so the brain relies on circulating glucose in the blood [22]. Under normal circumstances, a person typically develops neurologic dysfunction when the blood glucose level is <54 mg/dL (3 mmol/L) [23]. However, in cardiac arrest, the metabolic demand of the brain is likely substantially reduced, so a lower blood glucose level may be acceptable.

CONCLUSION

We believe that routine use of fingerstick glucose levels during cardiac arrest should be abandoned. Given the rarity of and uncertainty around hypoglycemia as a cause of sudden cardiac arrest, we recommend only a selective assessment of blood glucose levels in cardiac arrest patients. Although prospective human data are lacking, existing data suggest that dextrose may be harmful to some patients in cardiac arrest. Therefore, we recommend only administering dextrose to cardiac arrest patients if they have severe hypoglycemia confirmed in a venous blood sample (if possible). More research, particularly, a large, randomized-controlled trial investigating the utility and outcomes of dextrose during cardiac arrest, is needed.

NOTES

Author contributions

Conceptualization: GG, NG; Project administration: GG, NG, SK; Supervision: GG, TZ; Writing–original draft: GG, MH, AP, HT; Writing–review & editing: all authors. All authors read and approved the final manuscript.

Conflicts of interest

The authors have no conflicts of interest to declare.

Funding

The authors received no financial support for this study.

Data availability

Data sharing is not applicable as no new data were created or analyzed in this article.

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