#52 Lactate & Lactic Acidosis
On this episode of Critical Care Time, Nick & Cyrus embark on a deep dive into the world of lactic acidosis! As it is the beginning of the academic year, we figured this would be a great topic to demystify and disambiguate for our listeners. We discuss why lactic acidosis matters, and deconstruct all the clinically relevant elements from diagnosis to management, so that you are fully equipped with the tools necessary to conquer your next case of lactic acidosis - or maybe your first!! Ring in this new season of CCT with a banger of an episode and let us know what you think!
Approach to Lactic Acidosis from ICU OnePager.
Key Definitions:
Lactic acid: CH₃CH(OH)COOH → lactate⁻ + H⁺. The H⁺ contributes to metabolic acidosis.
Lactate: The anion measured clinically; non‑toxic and used in gluconeogenesis.
Clinical Threshold: Lactate ≥2 mmol/L + pH <7.35
What is lactic acid?
Lactate is a 3 carbon brake down product of glucose.
Think of your cells as tiny steam engines - they burn fuel, producing heat, and extract useful work.
Normally, cells consume oxygen and turn one molecule of glucose into 6 CO2 molecules and about 30 ATP. This is very efficient (thermodynamic efficiency is about 40%).
Under some conditions however, like when there isn’t oxygen, cells can’t completely metabolize glucose into CO2. Instead of breaking glucose down all the way into CO2, they only break it down half way into pyruvate. Cells need to get rid of all that pyruvate so they convert it to lactate.
Where does lactic acid go?
If lactic acid is produced in muscle and other tissues, it gets metabolized in liver, kidney, and muscle.
Clinical pearl: Because about 70% of lactic acid is metabolized in the liver, ICU patients who have liver failure often have elevated lactate. Patients who have both liver and kidney failure often have markedly elevated lactate.
There is nothing bad intrinsically bad or harmful about lactate.
We all make lactic acid! That’s why our muscles burn during vigorous exercise. RBCs produce lactate constituitively (you wouldn’t want your RBCs to be consuming the oxygen they are transporting!)
Lactic acidosis is normal during vigorous exercise. In a study of six elite rowers doing at 2000m maximal effort erg the mean lactate was 26 mmol/Lduring a 2000 m erg. The lowest recorded pH was 6.74 with a lactate of ~32 mmol/L. This massively elevated lactate is not by itself harmful.
From Neilsen et al 1999.
Why do we care about lactic acid?
Lactic acidosis is bad for two reasons: it can cause a metabolic acidosis and the underlying cause.
A severe lactic acidosis can significantly drop your pH.
Low pH causes enzymes & other cellular processes to work less well.
Acidosis causes cardiac muscle not to pump efficiently. It also causes smooth muscle to relax, dropping vascular tone. This is why we often associate severe acidosis with shock.
To summarize, having a severe acidosis (pH < 7) is bad.
Lactated Ringers and Lactic Acidosis
Sometimes people say “don’t give lactated ringers because it will worsen a lactic acidosis.” This is 99% wrong.
There is a little bit of truth: Because lactated ringers contains lactate, it SHOULD raise your lactate a little. For example, if you gave a 85 kg man 1 L of LR (containing 28 mEq of lactate), you'd expect by lactate to rise by... 0.5 mEq/L
85 kg x 0.6 (water fraction) = 50 L volume of distribution
28 mEq / 50 L = 0.5 mEq/L increase in lactate
So yes giving lactated ringers will raise your serum lactate slightly… about 0.5 mEq/L.
But more importantly that the lactate is the effect on pH.
Remember that LR contains sodium lactate - the conjugate base of lactic acid - this should buffer acidosis and raise pH. Also, because lactated Ringers has a more physiological pH than normal saline, it has less effect on pH. This is much more important than the tiny increase in lactate.
Beware drawing from an LR line—contamination can cause a 400% spurious rise in measured plasma lactate.
Is lactate a good resuscitation endpoint?
You can use it however Lactate‑guided resuscitation trials actually showed more fluids given and worse outcomes.
Classification of Lactic Acidosis: Pathophysiology and Clinical Examples
Type A (Hypoperfusion‑Driven): DO₂ < VO₂
We can break type A (not enough O2) into two categories: decreased delivery of O2 and increased consumption of O2.
Some examples of systemic problems with oxygen delivery include:
severe hypoxemia, low cardiac output (or cardiac arrest), severe anemia.
You can also have impaired oxygen delivery to specific organs/tissues. Like with ischemia to a limb or to bowels.
Examples of increased O2 consumption include:
Vigorous activity - exercise, seizures, increased work of breathing, etc.
Fever - O2 consumption increases by 15% per degree celsius. This means that someone with a fever to 41C has 60% higher O2 consumption.
This is a good reason for fever control!
Type B (Impaired Utilization): Normal delivery but dysfunctional utilization
Impaired utilization can be caused by toxins, vitamin deficiencies, and mitochondrial dysfunction, some infections, and rarely malignancies.
Beta‑2 adrenergic stimulation - from drugs like albuterol and epinephrine - boosts glycolysis and Na⁺/K⁺‑ATPase activity, elevating lactate even without hypoperfusion.
This is a very common cause of rising lactate in the ICU.
The important toxidromes to remember are PRIS (propofol related infusion syndrome), valproic acid, metformin, cyanide, and toxic alcohols.
Drugs like metformin inhibit complex I; propofol infusion syndrome disrupts mitochondria; cyanide blocks complex IV—each leading to lactate accumulation.”
Type D (D‑Lactic Acidosis): Bacterial overgrowth produces D‑isomer
Nature has a strong preference for the “handedness” of certain molecules.
Amino acids are always Left handed, sugars (and DNA/RNA) are almost always right handed
L-lactate (also called S-lactate) is the one produces by our (eukaryotic) cells. Some bacterial break this rule though and make lactate with the opposite chirality. This is called D-lactate.
Lactobacilli are a part of normal flora. Lactobacilli are also used to make all kinds of food: wine, yogurt, cheese, and of course beer! And D-lactate is what makes sourdough sour btw.
Occasionally people can have bacterial overgrowth of lactate producing bacteria. This can cause a high anion gap metabolic acidosis often with neurological symptoms: ataxia, confusion.
Importantly, the standard test for lactate will be normal. A require specialized - usually send out - D‑lactate assay is required for diagnosis.
Diagnostic Approach: Workup and Common Pitfalls
History: shock signs, toxin exposure, GI surgeries, alcohol use. Exam: perfusion, mentation, abdominal findings.
Labs: ABG/VBG with lactate, CMP, LFTs, renal tests, tox screen, D‑lactate if suspicion high.
Don’t reflexively bolus fluids for every elevated lactate; consider clearance issues and drug/metabolic etiologies.
Management Strategies and Pearls
Correct hemodynamics—fluids, vasopressors; antibiotics for sepsis; stop offending agents like metformin.
Replete cofactors: thiamine in alcoholics/TPN, consider biotin if raw‑egg exposure or prolonged antibiotics.
NM: “Monitor lactate alongside perfusion markers; it’s an alert light, not a fault code.”
“Lactate is a check‑engine light—it alerts you to trouble, but you still need the diagnostic manual.
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