Understanding cellular energy pathways is directly relevant to clinical nursing. Lactic acidosis occurs when tissues are forced into anaerobic metabolism, and diabetic ketoacidosis (DKA) occurs when cells cannot access glucose and switch to fat metabolism. Both conditions produce metabolic acidosis, a decrease in blood pH caused by accumulation of metabolic acids.
Lactic Acidosis
Cause: Tissue hypoxia forces anaerobic metabolism → pyruvate is converted to lactate + H+. Common triggers: Shock (any type), cardiac arrest, severe anemia, carbon monoxide poisoning, intense exercise. Lab finding: Elevated serum lactate (>2 mmol/L). ABG pattern: Metabolic acidosis, low pH, low HCO₃⁻, normal or low PaCO₂ (respiratory compensation). Treatment: Correct the underlying cause of hypoxia, restore perfusion and oxygenation.
Diabetic Ketoacidosis (DKA)
Cause: Insulin deficiency → glucose cannot enter cells → cells metabolize fat → excess acetyl-CoA → ketone body production. Key signs: Hyperglycemia (>250 mg/dL), ketonuria, Kussmaul respirations (deep/rapid breathing), fruity breath odor (acetone), dehydration. ABG pattern: Metabolic acidosis, low pH, low HCO₃⁻, low PaCO₂ (respiratory compensation). Treatment: IV insulin, IV fluids, electrolyte replacement (especially potassium).
Metabolic vs Respiratory Acidosis
Metabolic acidosis: Caused by accumulation of metabolic acids (lactic acid, ketoacids) OR loss of bicarbonate. pH low, HCO₃⁻ low. Body compensates by hyperventilation (blowing off CO₂). Respiratory acidosis: Caused by CO₂ retention due to hypoventilation (COPD, respiratory depression, airway obstruction). pH low, PaCO₂ high. Body compensates by retaining HCO₃⁻ via kidneys. Key distinction: Look at the PaCO₂, if it matches the pH direction, the problem is respiratory; if HCO₃⁻ matches, the problem is metabolic.
