Metabolic Acidosis

Start with the gap - Anion gap is sodium minus the sum of chloride and bicarbonate. A high gap points at lactate, ketoacids, or renal failure; a normal gap points at bicarbonate loss - diarrhea, saline infusion, early renal failure, renal tubular acidosis, ureterosigmoid or pancreatic fistula, acetazolamide, or TPN initiation. The specifics live in the High Anion Gap Metabolic Acidosis and Hyperchloremic (Normal Gap) Metabolic Acidosis entries.

Correct the gap for albumin - Expected anion gap is roughly 2 x albumin (g/dL) plus 0.5 x phosphate (mg/dL). A 50% fall in plasma protein can drop the measured gap by up to 75%, so a reassuring gap of 12 in a hypoalbuminemic ICU patient is a real gap being hidden.

Check compensation with Winter's formula - Expected pCO2 = 1.5 x [HCO3] + 8. Measured pCO2 above that means an added respiratory acidosis; below it, an added respiratory alkalosis. Compensation should never return the pH to normal - if it has, a second process is running. Respiratory compensation is nearly immediate, while metabolic compensation for a respiratory disorder takes 6 to 12 hours to appear and days to max out.

Delta gap for hidden disorders - With a gap present, add the delta gap to the bicarbonate: over 30 means a coexisting metabolic alkalosis, under 23 means an additional non-gap acidosis. A normal pH excludes neither, which is why you check the gap even when the pH looks fine.

Do not remove the compensation - Kussmaul respirations are what is holding the pH up. Induction, paralysis, and default ventilator settings drop minute ventilation and the pH falls quickly. Match the minute ventilation the patient was generating and check an early ABG rather than dialing in a textbook rate and tidal volume.

Preop workup - Arterial or venous blood gas with electrolytes, a calculated anion gap, lactate, and renal function; add a salicylate level when overdose is on the table. Under general anesthesia, venous blood from the dorsum of the hand is arterialized enough to stand in for an ABG - pCO2 within about 5 mmHg and pH within 0.03 to 0.04.

Urine anion gap sorts renal from GI - Urine sodium plus potassium minus chloride. Negative means the kidney is appropriately excreting ammonium chloride, so the bicarbonate is being lost from the gut (diarrhea). Zero or positive in the face of an acidosis means the kidney is the problem - renal tubular acidosis or aldosterone deficiency.

Your fluid choice changes the acidosis - Aggressive 0.9% saline resuscitation converts an anion gap acidosis into a hyperchloremic one; consider switching to lactated Ringer's. Follow the ratio of excess gap to bicarbonate deficit rather than the serum bicarbonate, which may never rise even as the patient improves.

Catecholamines and contractility - Below a pH of 7.2 contractility drops, initially offset by the catecholamine release that acidemia itself provokes. Below 7.1 that offset is gone and the heart no longer answers catecholamines, so a pressor-refractory patient with a low pH needs the acidosis addressed, not more norepinephrine.

Bicarbonate on trial only - Reserve it for a pH below about 7.1, and then as a trial: half the calculated dose, then recheck pH and hemodynamics. It converts to CO2, so the patient must have the ventilation to clear it. For an infusion, mix 3 amps (50 mEq each) into 1 L of D5W. It has never been shown to improve outcome.

Potassium during correction - In diabetic ketoacidosis, serum potassium is normal in 74% and elevated in 22% despite depleted total body stores, and it falls once insulin and fluids start. Recheck hourly for the first 4 to 6 hours. See Diabetic Ketoacidosis (DKA).

Mixed pictures are the norm - Metabolic acidosis in an acutely ill patient often sits alongside a respiratory component, and the combination hits harder than either alone. Work the compensation formulas rather than eyeballing the pH. See Respiratory Acidosis.

Metabolic acidosis is a rise in hydrogen ion concentration driven from the bicarbonate side of the buffer system - pH under 7.35 with a serum bicarbonate under 24 mEq/L. Four mechanisms produce it: increased acid production, decreased acid excretion, acid ingestion, and renal or gastrointestinal bicarbonate loss. It is a sign of something else, never a diagnosis on its own, and the anion gap exists to cut that differential in half.

Perioperatively the consequences are cardiovascular and ventilatory. Contractility falls around a pH of 7.2 and the myocardium stops responding to catecholamines below 7.1, while the patient's only compensation is a high minute ventilation that induction and paralysis will take away. Respiratory acidosis is worse than metabolic acidosis at the same pH because CO2 crosses cell membranes far more easily than hydrogen ion does.