What causes acidosis in the context of shock?

Acidosis in Shock: Pathophysiological Mechanisms

In shock, acidosis primarily occurs due to tissue hypoperfusion leading to anaerobic metabolism and lactic acid production, with additional contributions from hyperchloremia and impaired acid clearance. 1

Primary Mechanisms of Acidosis in Shock

• Tissue Hypoxia: Shock causes widespread reduction in effective tissue perfusion, creating an imbalance between oxygen supply and demand that forces cells to shift to anaerobic metabolism 1

• Lactic Acidosis: Inadequate oxygen delivery to tissues results in anaerobic glycolysis, producing lactate as a byproduct, which is a primary contributor to metabolic acidosis in shock 2

• Impaired Lactate Clearance: Altered liver perfusion during shock can prolong lactate clearance, further exacerbating lactic acidosis 2

• Hyperchloremic Acidosis: Aggressive fluid resuscitation with chloride-rich solutions (normal saline) can lead to hyperchloremia, contributing significantly to the metabolic acidosis seen in shock 3

Types of Acidosis in Shock

• Metabolic Acidosis: The predominant form of acidosis in shock, characterized by:

  • Decreased blood pH (<7.35) 2
  • Reduced serum bicarbonate (<22 mmol/L) 4
  • Elevated blood lactate levels 2
  • Increased base deficit 2

• Respiratory Component: In severe shock, respiratory compensation may be impaired, leading to respiratory acidosis that compounds the metabolic acidosis 2

Clinical Significance of Acidosis Parameters

• Blood Lactate: Serves as a sensitive marker of tissue hypoperfusion and shock severity; elevated levels (>2 mmol/L) indicate tissue hypoxia and correlate with mortality 2

• Base Deficit: An independent predictor of mortality in traumatic hemorrhagic shock; reflects global tissue acidosis due to impaired perfusion 2

• pH Level: Severe acidemia (pH <7.2) combined with elevated lactate (≥5 mmol/L) indicates the highest risk of mortality in cardiogenic shock 5

Specific Acidosis Patterns in Different Shock Types

• Hypovolemic Shock: Initially presents with metabolic acidosis primarily due to lactic acid production from tissue hypoperfusion 1

• Cardiogenic Shock: Features both lactic acidosis from poor tissue perfusion and potential respiratory acidosis if pulmonary edema develops 5

• Septic Shock: Exhibits a complex metabolic acidosis with contributions from:

  • Lactic acidosis from tissue hypoperfusion
  • Hyperchloremic acidosis (often from fluid resuscitation)
  • Increased strong ion gap (unmeasured anions) 3

Clinical Management Implications

• Resuscitation Goals: The primary treatment for shock-induced acidosis is reversing the underlying cause and improving tissue perfusion 6

• Fluid Resuscitation: Consider balanced crystalloid solutions rather than normal saline to minimize hyperchloremic acidosis 3

• Bicarbonate Therapy: Generally not recommended for lactic acidosis with pH ≥7.00, as it may worsen intracellular acidosis and decrease cardiac contractility 6

• Monitoring Parameters: Serial measurements of lactate, base deficit, and pH provide valuable information about shock severity and response to treatment 2

• Prevention of Complications: During resuscitation, avoid hypothermia, hypocalcemia, and worsening acidosis, as these can exacerbate coagulopathy and shock 2