Prove It: Administering dextrose during cardiac arrest improves outcomes

Understand why dextrose given during prehospital resuscitation from cardiac arrest may actually decrease the chance of survival to hospital discharge


The author has no financial interest, arrangement or direct affiliation with any corporation that has a direct interest in the subject matter of this presentation, including manufacturer(s) of any products or provider(s) of services mentioned.

Medic 23 responds with Engine 14 to a report of a cardiac arrest at a private residence. After a short response, firefighters take over compressions from the wife of a 63 year-old male lying in the kitchen floor. The patient’s initial ECG reveals ventricular fibrillation and the medics respond by delivering a 200 joule countershock. The firefighters immediately resume CPR.

The wife reports the patient awakened about 45 minutes ago, but did not complain of anything before coming into the kitchen to get some coffee. The patient has a history of hypertension, pre-diabetes, and high cholesterol levels (hyperlipidemia). He reportedly took all his medications this morning.

The medics easily insert a supraglottic airway and establish a large bore intravenous line in the patient’s left arm. The PETCO2 reading is 22 mm Hg and the patient remains in VF. The patient’s fingerstick point-of-care glucose reading is 70 mg/dL.

50% dextrose box. (Courtesy photo)
50% dextrose box. (Courtesy photo)

After delivery of a second countershock, the firefighters resume CPR. The patient receives a 1 mg bolus of epinephrine. Although the treatment guidelines in this system do not mention standing order administration of dextrose to patients in cardiac arrest, the system does authorize the drug for hypoglycemic patients with altered mental status. Because this system defines hypoglycemia as a POC glucose reading less than 70 mg/dL, there is some debate about whether the patient should receive dextrose. Ultimately, the medics decide the risk of drug administration is negligible and the potential benefit is significant. After preparing the syringe, they administer 50 mL of 50% dextrose in water.

At the end of the two-minute CPR cycle, the monitor reveals an organized rhythm. The PETCO2 reading jumped to 60 mm Hg. One of the firefighters confirms the presence of a pulse, although the patient shows no signs of regaining consciousness. The 12-lead ECG shows evidence of an inferior wall ST-segment myocardial infarction and the medics activate the STEMI alert. The seven minute transport to the emergency department is uneventful.

In the ED, the patient is hemodynamically stable and the initial ED blood glucose level is 216 mg/dL before transfer to the cath lab. Following balloon angioplasty, the comatose patient is transferred to the intensive care unit to begin targeted temperature management.

On the eighth hospital day, the patient is transferred to a long-term care facility. Although conscious, the patient suffered severe cerebral disability and is dependent on others for daily support.

Study review
Using records from the Get With The Guidelines®-Resuscitation (GWTG-R) registry, researchers in Boston compared survival statistics between patients who received IV dextrose during a resuscitation attempt with those who did not [1]. This study included over 100,000 records of adult patients who suffered a cardiac arrest as an in-patient during a ten-year period in one of 349 participating hospitals in the United States. The primary outcome variable was survival to hospital discharge.

Results
Of the 100,029 patients included in the study, only 4,173 (4.2 percent) received intravenous dextrose during the resuscitation attempt. Overall, 18.6 percent of the study sample survived long enough to be discharged from the hospital. However, patients who received IV dextrose during the resuscitation attempt were significantly less likely to survive to hospital discharge when compared to patients who did not receive dextrose. Even after adjusting for variables known to influence cardiac arrest survival (such as coexisting conditions, initial rhythm and interventions during the arrest), the association between receiving IV dextrose and decreased survival remained.

For those who did survive, administration of dextrose resulted in a greater risk of unfavorable neurologic outcome compared to the control group. This association also remained following multivariate adjustment.

In a subgroup analysis, the researchers examined only those patients with a confirmed diagnosis of diabetes. In this analysis, the administration of dextrose was not associated with increased survival to hospital discharge or favorable neurologic function.

What this means for you
In the early days of EMS, paramedics routinely administered a "coma cocktail" to patients suffering from altered mental status. This practice, consisting of the administration of dextrose, thiamine and naloxone was predicated on the belief that these drugs were essentially harmless but could provide some benefit if the patient actually needed one or more of the medications [2]. Animal studies in the late 1970s began to link hyperglycemia during global brain ischemia to impaired neurological outcomes [3,4] and the blind administration of dextrose began to lose support. More recent human studies have demonstrated the deleterious effects of hyperglycemia on clinical outcomes in critically-ill patients [5] and those with ischemic brain injury secondary to stroke [6,7] or cardiac arrest [8], even in conjunction with targeted temperature management [9-11].

Before 2005, the American Heart Association Emergency Cardiovascular Care Guidelines listed hypoglycemia as a correctable cause of cardiac arrest for the pediatric but not the adult patient [12]. With publication of the 2005 guidelines and without any explanation, the AHA added hypoglycemia to the "H’s and T’s" of possible contributing factors to adult cardiac arrest [13]. However, the 2010 version removed hypoglycemia from the "H’s and T’s" in the adult cardiac arrest algorithm [14] but listed hypoglycemia as a reversible cause of cardiac arrest in the pediatric patient [15]. The latest version of the guidelines follows that same pattern [16,17]. In any case, no version of the guidelines recommends glucose administration unless hypoglycemia is suspected or confirmed.

Hypoglycemia is often confirmed in the out-of-hospital setting using point-of-care glucose testing, in many cases using fingerstick capillary samples. Unfortunately, this method of glucometry may not accurately represent true blood glucose levels in patients who are critically ill. In an emergency department study 32 percent of the hypotensive patients tested were incorrectly categorized as hypoglycemic using fingerstick capillary sampling [18]. One study involving patients in an intensive care unit with true hypoglycemia found the accuracy of capillary sampling to be less than 30 percent when compared to properly calibrated central laboratory measurements [19]. With patient who were receiving CPR, capillary sampling only one-third of the patients identified as hypoglycemic actually were [20]. In fact, in that study, 25 percent of the incorrectly diagnosed patients were actually already hyperglycemic.

Ventricular fibrillation and subsequent ROSC suppresses insulin secretion in animal models resulting in a threefold increase in mean blood glucose levels [21]. This period of hyperglycemia peaks immediately after ROSC with a return to baseline within two to three hours [22,23]. Data from cardiac arrest registry supplemented with blood glucose data demonstrated one characteristic of patients who died during their ICU stay following out-of-hospital cardiac arrest was a significant increase in blood glucose level between the prehospital measurement and the initial hospital admission measurement [24].  This increase occurred despite the fact prehospital personnel did not administer any glucose in the field. Patients who are hyperglycemic after achieving ROSC following cardiac arrest generally have longer recovery times and worsened neurological outcomes [8,25]. 

Interestingly, diabetics themselves may suffer less damage from periods of hyperglycemia following cardiac arrest when compared to non-diabetics [8,26]. Animal models suggest chronic hyperglycemia in diabetics alters the brain’s buffering capacity making them less susceptible to the harmful effects of acidosis [27].

Summary
Through retrospective analysis of registry data, this study suggests that patients who receive glucose in the form of IV dextrose during the prehospital phase of cardiac arrest have a decreased chance of survival to hospital discharge. For those who do survive that long, the administration of intravenous dextrose appears to decrease the chances of good neurological recovery. Point-of-care glucose testing in patients suffering cardiac arrest results in inaccurate reading most of the time, which may prompt EMS personnel to administer glucose in the field.

References

  1. Peng, T. J., Andersen, L. W., Saindon, B. Z., Giberson, T. A., Kim, W. Y., Berg, K., Novack, V., & Donnino, M. W.  (2015). The administration of dextrose during in-hospital cardiac arrest is associated with increased mortality and neurologic morbidity. Critical Care, 19, 160. doi:10.1186/s13054-015-0867-z
  2. Browning, R. G., Olson, D. W., Stueven, H. A., & Mateer, J. R. (1990). 50% dextrose: Antidote or toxin? Annals of Emergency Medicine, 19(6), 683-687. doi:10.1016/S0196-0644(05)82479-5
  3. Myers, R. E., & Yamaguchi, S. (1977). Nervous system effects of cardiac arrest in monkeys: Preservation of vision. Archives of Neurology, 34(2), 65-74. doi:10.1001/archneur.1977.00500140019003
  4. Siemkowicz, E., & Hansen, A. J. (1978). Clinical restitution following cerebral ischemia in hypo-, normo-, and hyperglycemic rats. Acta Neurologica Scandinavica, 58(1), 1-8. doi:10.1111/j.1600-0404.1978.tb02855.x
  5. Al-Tarifi, A., Abou-Shala, N., Tamim, H. M., Rishu, A. H., & Arabi, Y. M. (2011). What is the optimal blood glucose target in critically ill patients? A nested cohort study. Annals of Thoracic Medicine, 6(4), 207-211. doi:10.4103/1817-1737.84774
  6. Gentile, N. T., Seftchick, M. W., Huynh, T., Kruus, L.K., & Gaughan, J. (2006). Decreased mortality by normalizing blood glucose after acute ischemic stroke. Academic Emergency Medicine, 13(2), 174-180. doi:10.1197/j.aem.2005.08.009
  7. Masrur, S., Cox, M., Bhatt, D. L., Smith, E. E., Ellrodt, G., Fonarow, G. C., & Schwamm, L. (2015). Association of acute and chronic hyperglycemia with acute ischemic stroke outcomes post-thrombolysis: Findings from get with the guidelines-stroke. Journal of the American Heart Association, 4(10), e002193. doi:10.1161/JAHA.115.002193
  8. Beiser, D. G., Carr, G. E., Edelson, D. P., Peberdy, M. A., & Hoek, T. L. (2009). Derangements in blood glucose following initial resuscitation from in-hospital cardiac arrest: A report from the national registry of cardiopulmonary resuscitation. Resuscitation, 80(6), 624-630. doi:10.1016/j.resuscitation.2009.02.011
  9. Ettleson, M. D., Arguello, V., Wallia, A., Arguelles, L., Bernstein, R. A., & Molitch, M. E. (2014). Hyperglycemia and insulin resistance in cardiac arrest patients treated with moderate hypothermia. Journal of Clinical Endocrinology and Metabolism, 99(10), E2010-E2014. doi:10.1210/jc.2014-1449
  10. Kim, S. H., Choi, S. P., Park, K. N., Lee, S. J., Lee, K. W., Jeong, T. O., & Youn, C. S. (2014). Association of blood glucose at admission with outcomes in patients treated with therapeutic hypothermia after cardiac arrest. American Journal of Emergency Medicine, 32(8), 900-904. doi:10.1016/j.ajem.2014.05.004
  11. Kim, Y. M., Youn, C. S., Kim, S. H., Lee, B. K., Cho, I. S., Cho, G. C., Jeung, K. W., Oh, S. H., Choi, S. P., Shin, J. H., Cha, K. C., Oh, J. S., Yim, H. W., & Park, K. N. (2015). Adverse events associated with poor neurological outcome during targeted temperature management and advanced critical care after out-of-hospital cardiac arrest. Critical Care, 19(1), 283. doi:10.1186/s13054-015-0991-9
  12. American Heart Association. (2000). Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 10: Pediatric advanced life support. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation, 102(8 Suppl 1), I291-I342. doi:10.1161/01.CIR.102.suppl_1.I-291
  13. American Heart Association. (2005). 2005 AHA guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.2: Management of cardiac arrest. Circulation 112(24 Suppl), IV-57-IV-66. doi:10.1161/CIRCULATIONAHA.105.166557
  14. Neumar, R. W., Otto, C. W., Link, M. S., Kronick, S. L., Shuster, M., Callaway, C. W., Kudenchuk, P. J., Ornato, J. P., McNally, B., Silvers, S. M., Passman, R. S., White, R. D., Hess, E. P., Tang, W., Davis, D., Sinz, E., & Morrison, L. J. (2010). Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 122(suppl 3), S729–S767. doi:10.1161/CIRCULATIONAHA.110.970988
  15. Kleinman, M. E., de Caen, A. R., Chameides, L., Atkins, D. L., Berg, R. A., Berg, M. D., Bhanji, F., Biarent, D., Bingham, R., Coovadia, A. H., Hazinski, M. F., Hickey, R. W., Nadkarni, V. M., Reis, A. G., Rodriguez-Nunez, A., Tibballs, J., Zaritsky, A. L., and Zideman, D. (2010). Part 10: Pediatric basic and advanced life support: 2010 International consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation, 122(16 Suppl 2), S466-S515. doi:10.1161/CIRCULATIONAHA.110.971093
  16. de Caen, A. R., Berg, M. D., Chameides, L., Gooden, C. K., Hickey, R. W., Scott, H. F., Sutton, R. M., Tijssen, J. A., Topjian, A., van der Jagt, É. W., Schexnayder, S. M., & Samson, R. A. (2015). Part 12: Pediatric advanced life support: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 132(18 Suppl 2), S526-S542. doi:10.1161/CIR.0000000000000266
  17. Link, M. S., Berkow, L. C., Kudenchuk, P. J., Halperin, H. R., Hess, E. P., Moitra, V. K., Neumar, R. W., O'Neil, B. J., Paxton, J. H., Silvers, S. M., White, R. D., Yannopoulos, D., & Donnino, M. W. (2015). Part 7: Adult advanced cardiovascular life support: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 132(18 Suppl 2), S444-S464. doi:10.1161/CIR.0000000000000261
  18. Atkin, S. H., Dasmahapatra, A., Jaker, M. A., Chorost, M. I., & Reddy, S. (1991). Fingerstick glucose determination in shock. Annals of Internal Medicine, 114(12), 1020–1024. doi:10.7326/0003-4819-114-12-1020
  19. Kanji, S., Buffie, J., Hutton, B., Bunting, P. S., Singh, A., McDonald, K., Fergusson, D., McIntyre, L. A., & Hebert, P. C. (2005). Reliability of point-of-care testing for glucose measurement in critically ill adults. Critical Care Medicine, 33(12), 2778-2785. doi:10.1097/01.CCM.0000189939.10881.60
  20. Thomas, S. H., Gough, J. E., Benson, N., Austin, P. E., & Stone, C. K. (1994). Accuracy of fingerstick glucose determination in patients receiving CPR. Southern Medical Journal, 87(11), 1072–1075. doi:10.1097/00007611-199411000-00003
  21. Martin, G. B., O’Brien, J. F., Best, R., Goldman, J., Tomlanovich, M. C., & Nowak, R. M. (1985). Insulin and glucose levels during CPR in the canine model. Annals of Emergency Medicine, 14(4), 293–297. doi:10.1016/S0196-0644(85)80089-5
  22. Lennmyr, F., Molnar, M., Basu, S., & Wiklund, L. (2010). Cerebral effects of hyperglycemia in experimental cardiac arrest. Critical Care Medicine, 38(8), 1726–1732. doi:10.1097/CCM.0b013e3181e7982e
  23. Niemann, J. T., Youngquist, S., Rosborough, J. P. (2011). Does early postresuscitation stress hyperglycemia affect 72-hour neurologic outcome? Preliminary observations in the swine model. Prehospital Emergency Care, 15(3), 405–409. doi:10.3109/10903127.2011.569847
  24. Nurmi, J., Boyd, J., Anttalainen, N., Westerbacka, J., & Kuisma, M. (2012). Early increase in blood glucose in patients resuscitated from out-of-hospital ventricular fibrillation predicts poor outcome. Diabetes Care, 35(3), 510–512. doi:10.2337/dc11-1478
  25. Skrifvars, M. B., Pettila, V., Rosenberg, P. H., Castren, M. (2003). A multiple logistic regression analysis of in-hospital factors related to survival at six months in patients resuscitated form out-of-hospital ventricular fibrillation. Resuscitation, 59(3), 319–328. doi:10.1016/S0300-9572(03)00238-7
  26. Monteiro, S., Monteiro, P., Goncalves, F., Freitas, M., & Providencia, L. A. (2010). Hyperglycaemia at admission in acute coronary syndrome patients: Prognostic value in diabetics and non-diabetics. European Journal of Cardiovascular Prevention and Rehabilitation, 17(2), 155–159. doi:10.1097/HJR.0b013e32832e19a3
  27. Hoxworth, J. M., Xu, K., Zhou, Y., Lust, W. D., & LaManna, J. C. (1999). Cerebral metabolic profile, selective neuron loss, and survival of acute and chronic hyperglycemic rats following cardiac arrest and resuscitation. Brain Research, 821(2), 467–479. doi:10.1016/S0006-8993(98)01332-8

Recommended for you

Join the discussion

Copyright © 2020 EMS1. All rights reserved.