Increased lactate production |
Increased pyruvate production |
Enzymatic defects in glycogenolysis or gluconeogenesis (as with type 1 glycogen storage disease) |
Respiratory alkalosis, including salicylate intoxication |
Pheochromocytoma |
Beta-agonists |
Sepsis |
Impaired pyruvate utilization |
Decreased activity of pyruvate dehydrogenase or pyruvate carboxylase |
• Congenital |
• Possibly a role in diabetes mellitus, Reye syndrome |
Altered redox state favoring pyruvate conversion to lactate |
Enhanced metabolic rate |
• Grand mal seizure |
• Severe exercise |
• Hypothermic shivering |
• Severe asthma |
Decreased oxygen delivery |
• Shock |
• Cardiac arrest |
• Acute pulmonary edema |
• Carbon monoxide poisoning |
• Severe hypoxemia (PO2 <25 to 30 mmHg) |
• Pheochromocytoma |
Reduced oxygen utilization |
• Cyanide intoxication (decreased oxidative metabolism), which may result from cyanide poisoning or, during a fire, from smoke inhalation of vapors derived from the thermal decomposition of nitrogen-containing materials such as wool, silk, and polyurethane |
• Drug-induced mitochondrial dysfunction due to zidovudine or stavudine |
• Sepsis |
D-lactic acidosis |
Primary decrease in lactate utilization |
Hypoperfusion and marked acidemia |
Alcoholism |
Liver disease |
Mechanism uncertain |
Malignancy |
Diabetes mellitus, including metformin in the absence of tissue hypoxia |
Acquired immunodeficiency syndrome |
Hypoglycemia |
Idiopathic |
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