Type A vs type B lactic acidosis: split it by mechanism
The same lactate can come from a patient in shock or from one with normal perfusion. Ask one question, is perfusion adequate, to separate type A from type B lactic acidosis.
Chapters (8)
Distinguish type A lactic acidosis (tissue hypoperfusion or hypoxia) from type B (impaired lactate metabolism, drugs, toxins) by mechanism.
The short version
- Lactic acidosis is a high anion gap metabolic acidosis from too much lactate production, too little clearance, or both.
- Type A means poor perfusion or oxygen delivery: tissue starved of oxygen, as in shock or severe lung disease.
- Type B means adequate perfusion with faulty lactate handling: liver failure, thiamine deficiency, drugs such as metformin.
- Thiamine is a cofactor for pyruvate dehydrogenase; without it pyruvate is converted to lactate instead of acetyl CoA.
- Treat the cause. Do not reach for bicarbonate by reflex.
Type A vs type B lactic acidosis: the same lactate, a different problem
Type A vs type B lactic acidosis starts with two patients who both have a lactate of 9 mmol/L. One has a blood pressure of 70/40. The other is sitting up, talking, with a normal pressure. The number is the same; the problem is not.
This lesson splits lactic acidosis into type A and type B by mechanism. Type A is where tissue is short of oxygen. Type B is where lactate handling is faulty despite adequate perfusion.[1][3]
Lactic acidosis, the anion gap and one common definition
The tool we already have is the anion gap: sodium minus chloride and bicarbonate together. Normal is about 12.[2]
normal about 12 mEq/L; potassium is excluded
- Na⁺ 138, Cl⁻ 101, HCO₃⁻ 13
- Cl⁻ + HCO₃⁻ = 101 + 13 = 114
- 138 − 114 = 24
A gap of 24 is a high anion gap metabolic acidosis (HAGMA). Lactate is one of the unmeasured anions behind it.[1][2]
One common definition of lactic acidosis asks for a pH below 7.35 and a lactate above 5 to 6 mmol/L. Other thresholds exist, so this is not the only definition. Smaller rises in lactate are called hyperlactataemia.[1]
Lactate is a balance of production and clearance
Blood lactate is a balance between production and clearance. Lactic acidosis comes from too much made, too little cleared, or both. The liver is the main site of clearance.[1][3]
Type A lactic acidosis: tissue starved of oxygen
In type A the tissues are starved of oxygen. Think shock (hypovolaemic, cardiogenic or septic) or severe lung disease.[1][3][4]
Without enough oxygen, cells make less ATP by oxidative metabolism, so glycolysis speeds up. Pyruvate piles up and is converted to lactate. A poorly perfused liver also clears lactate badly.[1][3]
Type A is the more serious form.[1]
Type B lactic acidosis: adequate perfusion, faulty lactate handling
In type B, perfusion is adequate but lactate handling is faulty. There are three groups: disease states, drugs and toxins, and inborn errors of metabolism.[1][3]
- Liver failure lowers clearance.[1][3]
- Thiamine deficiency is a favourite. Thiamine is a cofactor for pyruvate dehydrogenase, so without it pyruvate cannot be turned into acetyl CoA and is converted to lactate instead.[1][3][4]
- Metformin is the classic drug cause, although the exact mechanism is uncertain.[1][3]
- Regional hypoxia, such as intense exertion or seizures, can raise lactate while global perfusion is fine.[1]
- D-lactate, from gut bacteria after bowel resection, is an oddity: a standard assay misses it.[1]
| Type A | Type B | |
|---|---|---|
| Perfusion | Poor perfusion or oxygen delivery | Adequate perfusion |
| Mechanism | Tissue short of oxygen; glycolysis speeds up and pyruvate becomes lactate | Lactate handling is faulty |
| Examples | Hypovolaemic, cardiogenic or septic shock; severe lung disease | Liver failure, thiamine deficiency, metformin, regional hypoxia, D-lactate |
Treating lactic acidosis: start with the cause
Treatment starts with the cause. Bicarbonate is controversial and can be dangerous in high gap acidosis.[1]
Practice question
Original · USMLE styleA 45-year-old man with long-standing alcohol use disorder is brought to the emergency department because of confusion and rapid breathing. He has eaten very little for 3 days. He has no history of diabetes or bowel surgery. Temperature is 37.0 C (98.6 F), pulse is 104/min, respirations are 28/min, and blood pressure is 124/78 mm Hg. Oxygen saturation is 98% on room air. His extremities are warm and capillary refill time is less than 2 seconds. Examination shows horizontal nystagmus and a wide-based gait. Laboratory studies show:
| Serum Na⁺ | 136 mEq/L |
|---|---|
| Serum Cl⁻ | 100 mEq/L |
| Serum HCO₃⁻ | 11 mEq/L |
| Serum glucose | 88 mg/dL |
| Serum AST | 34 U/L |
| Serum ALT | 28 U/L |
| Serum INR | 1.0 |
| Serum lactate | 11.4 mmol/L |
| Serum beta-hydroxybutyrate | 0.3 mmol/L (normal < 0.5) |
| Arterial pH (room air) | 7.26 |
| Arterial PCO₂ (room air) | 25 mm Hg |
Common questions
What is the difference between type A and type B lactic acidosis?
In type A the tissues are starved of oxygen, from poor perfusion or oxygen delivery. In type B perfusion is adequate but lactate handling is faulty.
What are the causes of type B lactic acidosis?
There are three groups: disease states, drugs and toxins, and inborn errors of metabolism. Examples are liver failure, thiamine deficiency and metformin.
Why does thiamine deficiency cause lactic acidosis?
Thiamine is a cofactor for pyruvate dehydrogenase. Without it pyruvate cannot be turned into acetyl CoA, so it is converted to lactate instead.
Is lactic acidosis a high anion gap acidosis?
Yes. Lactate is one of the unmeasured anions behind a high anion gap metabolic acidosis. The gap is sodium minus chloride and bicarbonate together, and normal is about 12.
Transcript
Read the full narration, by chapter648 words
0:00Same lactate, two very different patients
Two patients. Both have a lactate of nine millimoles per litre. One has a blood pressure of 70 over 40. The other is sitting up, talking, with a normal pressure. Same number, different problem. Today we split lactic acidosis into type A and type B, by mechanism. The objective: tell type A, where tissue is short of oxygen, from type B, where lactate handling is faulty despite adequate perfusion.
0:30The anion gap and the definition of lactic acidosis
First, the tool we already have. The anion gap is sodium, minus chloride and bicarbonate together. Normal is about 12. Say sodium 138, chloride 101, bicarbonate 13. The gap is 24. A high gap metabolic acidosis. Lactate is one of the unmeasured anions behind it. One common definition asks for a pH below 7.35, and a lactate above five to six millimoles per litre.
1:03Lactate: a balance of production and clearance
Now the key idea. Blood lactate is a balance between production and clearance. Too much made, too little cleared, or both. The liver is the main site of clearance.
1:15Type A: oxygen-starved tissue
Type A: the tissues are starved of oxygen. Think shock: hypovolaemic, cardiogenic or septic, or severe lung disease. Without enough oxygen, cells make less ATP by oxidative metabolism, so glycolysis speeds up. Pyruvate piles up, and is converted to lactate. A poorly perfused liver also clears lactate badly. Type A is the more serious form.
1:43Type B: adequate perfusion, faulty handling
Type B: perfusion is adequate, but lactate handling is faulty. There are three groups: disease states, drugs and toxins, and inborn errors of metabolism. Liver failure lowers clearance.
1:56Thiamine and PDH, metformin, regional hypoxia, D-lactate, treatment
Thiamine deficiency is a favourite. Thiamine is a cofactor for pyruvate dehydrogenase, so without it pyruvate cannot be turned into acetyl C o A, and is converted to lactate instead. Metformin is the classic drug cause, although the exact mechanism is uncertain. Regional hypoxia, such as intense exertion or seizures, can also raise lactate while global perfusion is fine. One oddity: D-lactate, from gut bacteria after bowel resection. A standard assay misses it. Treatment starts with the cause. Bicarbonate is controversial, and can be dangerous in high gap acidosis.
2:39Practice question
Your turn. A 45-year-old man with long-standing alcohol use disorder has eaten very little for 3 days. He is confused and breathing fast. Blood pressure 124 over 78, pulse 104, respirations 28, oxygen saturation 98% on room air. His extremities are warm. He has nystagmus and a wide-based gait. Sodium 136, chloride 100, bicarbonate 11, glucose 88. AST, ALT and INR are normal. Lactate is 11.4 millimoles per litre. Serum beta-hydroxybutyrate is normal. Arterial pH is 7.26, PaCO2 25. He has no history of diabetes or bowel surgery. Which of the following best explains his lactic acidosis? A, tissue hypoperfusion from hypovolaemia. B, impaired pyruvate oxidation from a cofactor deficiency. C, accumulation of D-lactate from bacterial overgrowth. D, accumulation of ketoacids from insulin deficiency. E, reduced lactate clearance from acute liver failure. Pause here and decide. The gap is 136 minus the sum of 111, which is 25. High. A is out: his pressure is normal and his extremities are warm. That is not hypovolaemia. C is out: the standard assay already shows lactate, and he has had no bowel surgery. D is out: he has no diabetes, his glucose is 88, and his beta-hydroxybutyrate is normal, so there are no extra ketoacids. E is out: the liver is the main site of clearance, but his AST, ALT and INR are normal. So the answer is B: malnourished, with alcohol use disorder, nystagmus and ataxia, he is thiamine deficient. Pyruvate dehydrogenase stalls, pyruvate becomes lactate, and perfusion is fine.
4:59High-yield recap and next lesson
Three things to keep. One: lactic acidosis is a high gap acidosis, from too much lactate production, too little clearance, or both. Two: type A means poor perfusion or oxygen delivery. Type B means adequate perfusion with faulty metabolism: liver failure, thiamine deficiency, drugs like metformin. Three: treat the cause. Do not reach for bicarbonate by reflex. Next up: DKA and its acid base picture.
Sources
Numbers in the text, e.g. [1], point here- Lactic Acidosis. MSD Manual Professional Version. msdmanuals.com/professional/endocrine-and-metabolic-disorders/acid-base-regulation-and-disorders/lactic-acidosis
- Acid-Base Disorders. MSD Manual Professional Version (anion gap). msdmanuals.com/professional/endocrine-and-metabolic-disorders/acid-base-regulation-and-disorders/acid-base-disorders
- Deranged Physiology. CICM 2002 Paper 2, Question 12 (lactic acidosis). derangedphysiology.com/main/cicm-fellowship-exam/past-papers/2002-paper-2-saqs/question-12
- Lactic acidosis review, J Pediatr Pharmacol Ther 2023. pmc.ncbi.nlm.nih.gov/articles/PMC10731935
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Image credits. Illustrations: Servier Medical Art (smart.servier.com), licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/); adapted (recoloured, outlined, resized): liver, lungs, mitochondrion. All other diagrams are original; example lab values are illustrative.
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-REN-017.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01ABG interpretation, made simple5:35
- EP 02Anion gap explained: high vs normal gap metabolic acidosis5:25
- EP 03Winters' formula: the expected PaCO₂ in metabolic acidosis5:10
- EP 04Delta ratio: find the hidden second acid–base disorder5:09
- EP 05New bicarbonate: how the kidney excretes acid with ammonium5:23
- EP 06High anion gap metabolic acidosis causes, sorted by the anion5:54
- EP 07Osmolar gap: how toxic alcohols hide from the anion gap5:31
- EP 08Urine anion gap: telling diarrhea from RTA5:33
- EP 09Renal tubular acidosis: tell RTA types 1, 2 and 4 apart5:24
- EP 10Metabolic alkalosis: generation, maintenance and urine chloride5:30
- EP 11Vomiting metabolic alkalosis: why the urine turns acid5:36
- EP 12Bartter vs Gitelman: NKCC2, NCC and urine calcium5:21
- EP 13Respiratory acidosis compensation: acute vs chronic5:22
- EP 14Respiratory alkalosis compensation: acute vs chronic5:33
- EP 15Metabolic alkalosis compensation: the expected PaCO₂5:12
- EP 16Salicylate poisoning acid-base: a classic mixed disorder5:31
- EP 17Type A vs type B lactic acidosis: split it by mechanism5:33
- EP 18DKA anion gap explained: from high gap to hyperchloraemic acidosis5:42
- EP 19Acidosis and hyperkalemia: how pH shifts potassium5:43
- EP 20ABG interpretation in 6 steps: the acid-base algorithm5:32
- EP 21Acid-base practice cases: three ABG vignettes, one algorithm5:44