How to manage lactate acidosis in a patient receiving epinephrine (adrenaline) infusion?

Management of Lactate Acidosis from Epinephrine Infusion

Epinephrine-induced lactic acidosis is typically a benign, self-limited phenomenon caused by β2-adrenergic stimulation of aerobic glycolysis rather than tissue hypoxia, and management focuses on continuing epinephrine if clinically necessary while providing supportive care and monitoring for resolution.

Understanding the Mechanism

• Epinephrine causes hyperlactatemia through β2-adrenergic receptor stimulation of aerobic glycolysis (type B lactic acidosis), not tissue hypoperfusion 1, 2
• This mechanism differs fundamentally from type A lactic acidosis caused by tissue hypoxia, making the lactate elevation less clinically concerning 1, 2
• The lactate-to-pyruvate ratio may increase with epinephrine, but this reflects enhanced glycolysis rather than anaerobic metabolism 3
• Resolution typically occurs within 15 hours after epinephrine discontinuation or dose reduction 1

Immediate Assessment Algorithm

Step 1: Rule out true tissue hypoperfusion

• Assess for hypotension (MAP <65 mmHg), hypoxemia (SpO2 <90%), signs of shock (cold extremities, altered mental status, oliguria <0.5 mL/kg/hr), and sepsis 1, 3
• If any of these are present, the lactic acidosis is likely type A (tissue hypoxia) rather than epinephrine-induced 1

Step 2: Evaluate severity of acidosis

• Obtain arterial blood gas to assess pH and bicarbonate 1
• Measure serum lactate level (epinephrine-induced typically 5-10 mmol/L, though can reach 18.6 mmol/L in extreme cases) 1, 2
• Check for other causes: propylene glycol toxicity (if receiving lorazepam or other propylene glycol-containing drugs), metformin use, nucleoside reverse transcriptase inhibitors 4, 2

Step 3: Assess clinical indication for epinephrine

• If epinephrine is being used for anaphylaxis, continue without modification as it is life-saving and has no absolute contraindications 5
• If epinephrine is being used for refractory shock, consider switching to norepinephrine which causes less metabolic derangement 3

Management Strategy

For ongoing anaphylaxis requiring epinephrine:

• Continue epinephrine at necessary doses (intramuscular 0.3-0.5 mg every 5-15 minutes or intravenous infusion 1-10 mcg/min) 5
• Accept the lactic acidosis as an expected and tolerable side effect 1, 2
• Monitor pH and lactate every 2-4 hours to confirm stability or improvement 1

For shock states where epinephrine is being used as vasopressor:

• Switch to norepinephrine as first-line vasopressor, which does not cause the same degree of lactic acidosis 3
• Norepinephrine should be started at 0.1-0.5 mcg/kg/min and titrated to MAP ≥65 mmHg 6
• Ensure adequate fluid resuscitation (minimum 30 mL/kg crystalloid) before or concurrent with vasopressor initiation 6

Supportive care measures:

• Provide supplemental oxygen to maintain SpO2 >94% 5
• Ensure adequate intravascular volume with crystalloid boluses 5
• Monitor vital signs every 15 minutes during acute phase 7
• Avoid sodium bicarbonate administration unless pH <7.1, as bicarbonate therapy can cause hypernatremia, hypervolemia, and paradoxical intracellular acidosis 8

When to Consider Aggressive Intervention

Indications for bicarbonate therapy (use cautiously):

• pH <7.1 with hemodynamic instability despite adequate resuscitation 8
• Administer sodium bicarbonate slowly to avoid complications of hypernatremia and volume overload 8

Indications for renal replacement therapy:

• Severe acidosis (pH <7.0) with lactate >15 mmol/L not responding to supportive care 4
• Concurrent acute kidney injury preventing lactate clearance 4
• Continuous venovenous hemofiltration (CVVH) provides alkali without causing hypernatremia or hypervolemia 8, 4

Critical Pitfalls to Avoid

• Do not discontinue epinephrine during active anaphylaxis due to concern about lactic acidosis—delay in epinephrine administration is associated with anaphylaxis fatalities 5
• Do not assume all lactic acidosis in patients receiving epinephrine is benign—always rule out tissue hypoperfusion, sepsis, and alternative causes 1, 3
• Do not use epinephrine as first-line vasopressor in septic shock—norepinephrine is preferred and causes less metabolic derangement 3
• Do not aggressively treat with bicarbonate—this can worsen outcomes through hypernatremia, volume overload, and paradoxical intracellular acidosis 8
• Do not overlook propylene glycol toxicity in patients receiving continuous lorazepam or diazepam infusions, which can cause severe lactic acidosis requiring fomepizole and dialysis 4

Monitoring and Resolution

• Serial lactate measurements every 2-4 hours to document trend 1
• Arterial blood gases every 4-6 hours if pH <7.2 1
• Expect resolution within 15 hours after epinephrine discontinuation or dose reduction 1
• If lactate continues rising despite epinephrine discontinuation, aggressively search for alternative causes (sepsis, bowel ischemia, liver failure) 1, 2