Mechanism of Lactate Elevation in Shock
The correct answer is D: Fatty acids cannot be oxidized and glucose is degraded to lactate, which occurs when severe oxygen deprivation forces cells to shift from aerobic to anaerobic metabolism.
Pathophysiology of Hyperlactatemia in Shock
In this elderly patient with peptic ulcer perforation and shock, the severe oxygen deprivation creates a critical metabolic crisis at the cellular level 1, 2:
Primary Mechanism: Anaerobic Glycolysis
- When tissue hypoperfusion occurs, cells cannot complete oxidative phosphorylation because the electron transport chain requires oxygen as the final electron acceptor 3, 4
- Without adequate oxygen, fatty acid oxidation (beta-oxidation) cannot proceed since this process is entirely aerobic and requires functioning mitochondria 5
- Glucose becomes the only available fuel source, but it can only be metabolized through anaerobic glycolysis, which converts glucose to pyruvate and then to lactate instead of entering the Krebs cycle 3, 5
- This represents Type A lactic acidosis, which is directly related to tissue hypoxia and inadequate oxygen delivery 2, 4
Why Other Options Are Incorrect
Option A (Intracellular pH increases) is physiologically backwards—intracellular pH actually decreases (becomes more acidic) due to lactate and hydrogen ion accumulation during anaerobic metabolism 5
Option B (Cells metabolize fatty acids) cannot occur during severe hypoxia because fatty acid oxidation is an exclusively aerobic process requiring oxygen 5
Option C (Glucose metabolized to CO₂ and water) describes normal aerobic respiration, which is precisely what cannot happen during oxygen deprivation 3, 5
Option E (Membrane dysfunction with Na/K changes) describes a secondary consequence of cellular injury but is not the primary mechanism of lactate elevation 6
Clinical Context in Perforated Peptic Ulcer
In this specific clinical scenario 1:
- Hyperlactatemia is a key laboratory finding indicating shock and tissue hypoperfusion in perforated peptic ulcer patients 1, 7
- Lactate normalization is a critical resuscitation target along with MAP ≥65 mmHg and urine output ≥0.5 mL/kg/h 1, 8
- Rapid resuscitation within 1 hour is essential to reduce mortality in these unstable patients 1
Important Caveat
While tissue hypoxia (Type A) is the dominant mechanism in shock states, recognize that not all lactate elevation in sepsis is purely anaerobic 4, 9. Some lactate production can occur through aerobic glycolysis stimulated by catecholamines and Na⁺/K⁺-ATPase activation 9, 6. However, in the acute shock state described in this question with "severe oxygen deprivation," the anaerobic mechanism (Option D) is the primary driver 3, 4.