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.

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].

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.


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