What is the potential increase in blood glucose levels due to cortisol release in cardiac arrest patients?

Blood Glucose Elevation in Cardiac Arrest Patients Due to Cortisol Release

Blood glucose levels in cardiac arrest patients can rise significantly to 180-240 mg/dL (10-13.3 mmol/L) due to stress-induced cortisol release, with non-diabetic patients showing median maximum values of 176 mg/dL and diabetic patients reaching 226 mg/dL. 1

Pathophysiology of Hyperglycemia in Cardiac Arrest

Cardiac arrest represents an extreme physiological stressor that triggers substantial hormonal responses, including:

• Cortisol release: During cardiac arrest, the hypothalamic-pituitary-adrenal axis is activated, leading to cortisol secretion which promotes gluconeogenesis and insulin resistance
• Catecholamine surge: Epinephrine (both endogenous and administered during resuscitation) promotes glycogenolysis and gluconeogenesis
• Relative adrenal insufficiency: Paradoxically, some cardiac arrest patients may have lower than expected cortisol levels for the degree of stress, with studies showing 53% of patients having cortisol concentrations <20 μg/dL during arrest 2

Blood Glucose Ranges Observed

Research data shows distinct patterns of hyperglycemia following cardiac arrest:

• Non-diabetic patients: Median maximum blood glucose of 176 mg/dL (IQR 135-239 mg/dL) 1
• Diabetic patients: Median maximum blood glucose of 226 mg/dL (IQR 165-307 mg/dL) 1
• Survival correlation: In non-diabetics, survival odds decrease when maximum glucose exceeds 240 mg/dL (13.3 mmol/L) 1

Hormonal Response and Timing

The hyperglycemic response typically follows this pattern:

• Initial response: Cortisol levels rise immediately after cardiac arrest, with mean initial serum cortisol concentration of 32.0 ± 33.1 μg/dL 2
• Post-ROSC: Cortisol levels continue to rise significantly from 1 to 6 hours after return of spontaneous circulation (ROSC) 2
• Insulin resistance: Develops during this period, particularly in patients undergoing therapeutic hypothermia 3

Clinical Implications

The hyperglycemia observed has important prognostic and treatment implications:

• Mortality correlation: Higher blood glucose levels between cardiac arrest and initiation of treatment are associated with increased mortality (253 ± 112 mg/dL in non-survivors vs. 192 ± 69 mg/dL in survivors) 3
• ROSC achievement: Hyperglycemic patients (>10 mmol/L or >180 mg/dL) have higher rates of ROSC (68.1%) compared to hypoglycemic patients (≤4.2 mmol/L) who achieve ROSC only 41.9% of the time 4

Management Guidelines

Current guidelines recommend:

• Target glucose range: Maintain moderate glycemic control with target glucose of 144-180 mg/dL (8-10 mmol/L) 5, 6
• Avoid tight control: Do not implement strict glucose control (80-110 mg/dL or 4.4-6.1 mmol/L) due to increased risk of hypoglycemia 5
• Monitoring: Regular glucose monitoring is essential, especially during therapeutic hypothermia which may alter insulin sensitivity 6

Pitfalls and Caveats

Several important considerations should guide management:

• Avoid hypoglycemia: Hypoglycemia (<70 mg/dL or <3.9 mmol/L) is associated with increased mortality and should be strictly avoided 5, 1
• Glucose variability: High glucose variability is associated with worse outcomes, independent of absolute glucose values 5
• Therapeutic hypothermia effects: Hypothermia treatment is associated with higher blood glucose values and increased insulin requirements 5

The relationship between cortisol, glucose levels, and outcomes in cardiac arrest patients highlights the complex metabolic derangements that occur during this critical illness state. Management should focus on moderate glucose control while avoiding hypoglycemia.