How does shock lead to lactic acid production due to inadequate tissue perfusion and oxygen delivery?

From the Guidelines

Shock leads to lactic acid production through a process called anaerobic metabolism, where cells switch to anaerobic glycolysis due to inadequate oxygen delivery, resulting in lactic acid accumulation in the bloodstream 1. When shock occurs, blood pressure drops significantly, causing inadequate blood flow (perfusion) to tissues throughout the body. This reduced perfusion means less oxygen is delivered to cells, creating an oxygen deficit. Without sufficient oxygen, cells cannot perform normal aerobic metabolism through the Krebs cycle and oxidative phosphorylation, which efficiently produces ATP (energy) using oxygen. Instead, cells switch to anaerobic glycolysis, a less efficient process that doesn't require oxygen but produces lactic acid as a byproduct. This metabolic shift allows cells to continue generating some energy during oxygen deprivation, but results in accumulating lactic acid in the bloodstream. The severity of lactic acidosis correlates with the degree of tissue hypoperfusion and is a useful clinical marker for shock severity, as elevated lactate has been shown to correlate with increased mortality in various types of shock 1. Some key points to consider in the management of shock and lactic acidosis include:

• Monitoring lactate levels to assess shock severity and response to treatment 1
• Restoring adequate circulation through fluid resuscitation and vasopressors if needed 1
• Addressing the underlying cause of shock, which might include controlling bleeding, treating infection, or managing cardiac dysfunction 1
• Using lactate-guided resuscitation, which has been shown to reduce mortality in patients with septic shock 1 It is essential to prioritize the management of shock and lactic acidosis to improve patient outcomes, as increased lactate levels are associated with worse outcomes 1.

From the FDA Drug Label

Prolonged administration of any potent vasopressor may result in plasma volume depletion which should be continuously corrected by appropriate fluid and electrolyte replacement therapy If plasma volumes are not corrected, hypotension may recur when LEVOPHED is discontinued, or blood pressure may be maintained at the risk of severe peripheral and visceral vasoconstriction (e.g., decreased renal perfusion) with diminution in blood flow and tissue perfusion with subsequent tissue hypoxia and lactic acidosis and possible ischemic injury.

Shock leads to lactic acid production due to inadequate tissue perfusion and oxygen delivery, resulting in tissue hypoxia. This occurs when there is a decrease in blood flow, causing a reduction in oxygen delivery to tissues, which in turn leads to lactic acidosis.

• Key factors involved in this process include:
  • Decreased renal perfusion
  • Severe peripheral and visceral vasoconstriction
  • Diminution in blood flow and tissue perfusion
  • Subsequent tissue hypoxia 2

From the Research

Mechanism of Lactic Acid Production in Shock

• In shock states, inadequate tissue perfusion and oxygen delivery lead to tissue hypoxia, resulting in anaerobic glycolysis and the production of lactic acid 3.
• Lactic acidosis is a common complication in patients with severe sepsis or septic shock, and is associated with significant morbidity and mortality 3, 4.
• The development of acidemia in critically ill patients is often attributed to reductions in oxygen utilization, which can lead to anaerobic metabolism and lactic acidosis 5.

Factors Contributing to Lactic Acid Production

• Inadequate oxygen delivery to tissues, resulting in tissue hypoxia and anaerobic glycolysis, is a major contributor to lactic acid production in shock states 3, 5.
• Epinephrine-stimulated Na+,K+-ATPase activity in skeletal muscle can also lead to increased aerobic glycolysis and lactate production, even in well-oxygenated tissues 6.
• The severity of shock, as measured by the Society for Cardiovascular Angiography and Intervention (SCAI) shock classification, is also associated with higher lactate levels and worse outcomes 7.

Clinical Implications

• Elevated lactate levels and systemic acidemia are associated with increased mortality in patients with cardiogenic shock 7.
• Lactate clearance and vasopressor use are significant predictors of mortality in severe sepsis patients with lactic acidosis 4.
• The measurement of serum lactate can be useful in diagnosis, monitoring, and prognostication in acute and intensive care settings 3.