A patient with septic shock develops lactic acidosis with a serum lactate of 8 mmol/L. The primary cause of lactate accumulation in distributive shock is:
- A Cellular hypoxia causing pyruvate to be reduced to lactate by LDH when oxidative phosphorylation is insufficient ✓
- B Impaired hepatic lactate clearance due to decreased hepatic blood flow
- C Excess glycogen breakdown releasing glucose that is preferentially converted to lactate
- D Thiamine deficiency in critically ill patients impairing pyruvate dehydrogenase
Correct answer: A. Cellular hypoxia causing pyruvate to be reduced to lactate by LDH when oxidative phosphorylation is insufficient
Explanation
In septic shock, microcirculatory dysfunction and cellular dysoxia (inability of mitochondria to utilize O2 effectively) force pyruvate into anaerobic pathways. With inadequate oxidative phosphorylation, the NADH/NAD+ ratio rises, and LDH reduces pyruvate to lactate to regenerate NAD+ needed for glycolysis. This is Type A lactic acidosis (tissue hypoxia). While hepatic clearance impairment and thiamine deficiency can contribute, the primary driver in acute septic shock is anaerobic glycolysis from tissue hypoxia. Lactate > 4 mmol/L predicts poor prognosis.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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