Lactic Acidosis

Type A versus type B - Type A is hypoperfusion: any shock state (septic, cardiogenic, hypovolemic, obstructive), regional ischemia of a limb or the mesentery, seizures, severe shivering. Type B has no perfusion deficit - liver disease, malignancy, drugs (metformin, epinephrine), TPN, HIV, thiamine deficiency, mitochondrial myopathy, DKA, ethanol. The split decides whether you resuscitate or go hunting for a drug.

A lactate rising intraoperatively - Treat it as an oxygen delivery-consumption mismatch until you disprove it: hypovolemia, low cardiac output, occult hemorrhage, limb or mesenteric ischemia. But hyperlactatemia is not the same thing as acidosis - levels as high as 4 mmol/L may carry no acidosis, and lactate can rise with adequate perfusion and oxygenation.

Do not screen with the anion gap - Elevated lactate with a normal anion gap is well described, and hypoalbuminemia flattens the gap further (expected gap is roughly 2 x albumin in g/dL). Send an actual lactate: bedside analyzers need 0.13 mL and return in under 2 minutes, and samples going to the lab go on ice.

Catecholamine unresponsiveness - Acidemia impairs contractility from about pH 7.2, and below 7.1 the heart no longer responds to catecholamines. Escalating the pressor will not fix that - chase the cause of the acidosis and the perfusion deficit instead.

Drugs that raise lactate - Epinephrine infusions, propylene glycol in IV benzodiazepine formulations (20% to 65% of patients on high-dose benzodiazepine infusions for two days or more), nitroprusside toxicity from cyanide, phenytoin, nitroglycerin, and metformin. A lactate climbing on nitroprusside is a bad sign - stop the drug.

Metformin-associated lactic acidosis (MALA) - Metformin inhibits mitochondrial complex 1 and pyruvate carboxylase, so hydrogen ions accumulate intracellularly and hepatic lactate clearance falls. About 90% is excreted renally unchanged, so renal failure drives accumulation, and hypoglycemia can accompany the acidosis. EXTRIP supports hemodialysis at pH 7.0 or less, lactate over 20 mmol/L, or with shock, renal or hepatic failure, or altered mental status.

Do not take away the compensation - A spontaneously breathing acidotic patient is running Kussmaul respirations to hold the pH up. Induction, paralysis, and default lung-protective settings (rate 10 to 16, low tidal volume) drop minute ventilation and the pH crashes. Set a higher rate or tidal volume to approximate what the patient was generating, and check an ABG early.

Thiamine deficiency - Thiamine is a cofactor for pyruvate dehydrogenase and deficiency is common in the ICU, so consider it when lactate is high without hypoperfusion. Endotoxin raises lactate through the same enzyme block rather than through oxygen deprivation.

Bicarbonate is a last resort - The bicarbonate buffer system barely works at physiologic pH. Sodium bicarbonate generates CO2 that the lungs must clear, raises blood lactate, and binds calcium with a fall in contractility. Marino's threshold is a trial infusion below pH 7.1 - give half the calculated dose, then recheck pH and hemodynamics. THAM and Carbicarb avoid the CO2 load but have not shown a mortality benefit.

D-lactate after bowel resection - A post-op small-bowel-resection patient with an anion gap, encephalopathy, and a normal measured lactate needs a specific D-lactate ordered. Humans make L-lactate and that is all the lab measures; enteric bacteria make the D form.

The arterial gas can mislead you - In low-flow states arterial blood is not a sensitive marker for tissue acid-base status; during CPR an ABG can read near-normal while venous pH is 7.15 with a pCO2 of 70. Under general anesthesia, venous blood from the dorsum of the hand is arterialized enough to substitute for an ABG - pCO2 within about 5 mmHg, pH within 0.03 to 0.04.

Septic shock as the driver - Both the peak lactate and the time it takes to normalize track with mortality, so lactate clearance is the resuscitation target. Source control and antibiotics move that number more than pressor titration does. See Sepsis / Septic Shock.

Lactate accumulates when mitochondria cannot handle the pyruvate presented to them - either because oxygen delivery falls short of demand (type A) or because pyruvate processing is impaired despite adequate perfusion (type B). About 20 mmol/kg/day is produced normally and cleared by liver and kidney, so a persistent lactic acidosis needs excess production plus impaired clearance: cirrhosis, hypothermia, sepsis, severe hypovolemia, severe hypotension. Normal lactate is under 2 mmol/L, 2 to 4 mmol/L is hyperlactatemia, and 4 mmol/L or more is severe.

What makes it your problem at the board is hemodynamic. Contractility starts to fall around a pH of 7.2, and below 7.1 the myocardium stops responding well to catecholamines. Shock with a pH under 7.2 carries roughly 50% mortality, and no survival has been reported once pH falls below 7.0 in a shock state.