Acid–base disorders

Normal arterial values: pH 7.35–7.45, PaCO₂ 35–45 mm Hg, HCO₃⁻ 22–26 mEq/L. The middle values, 7.40, 40 and 24, are the reference points for every compensation formula. The three are tied together by the Henderson–Hasselbalch equation: pH depends on the ratio of bicarbonate (set by the kidney) to dissolved CO₂ (set by the lungs), not on either alone.

1. pH: below 7.35 is acidemia, above 7.45 alkalemia.
2. Which variable explains it? In acidemia, a high PaCO₂ points to respiratory acidosis and a low HCO₃⁻ to metabolic acidosis; in alkalemia, a low PaCO₂ means respiratory alkalosis and a high HCO₃⁻ metabolic alkalosis.
3. Expected compensation: calculate what the other variable should be. If the measured value is outside the expected range, a second primary disorder is present.
4. Anion gap (in every metabolic acidosis, and worth calculating in any sick patient): high or normal gap? Correct it for a low albumin.
5. What is left? In a high-gap acidosis compare ΔAG with ΔHCO₃⁻ (delta–delta) to find a hidden metabolic alkalosis or normal-gap acidosis; check the osmolal gap for toxic alcohols.

The clinical signs follow the chemistry. CO₂ dilates cerebral vessels, so respiratory acidosis causes somnolence, headache and raised intracranial pressure, with cyanosis from the accompanying hypoxemia. Respiratory alkalosis lowers ionized calcium (more calcium binds albumin at high pH), so it causes lightheadedness, perioral numbness, Chvostek sign and carpopedal spasm. Metabolic acidosis stimulates central and peripheral chemoreceptors, producing Kussmaul breathing: deep, regular, sighing breaths with a large tidal volume that blow off CO₂ (classic in DKA, but present in any severe metabolic acidosis); acidosis also dilates arterioles (warm skin) and weakens myocardial contraction.

Plasma is electrically neutral, but routine panels measure only some ions. The anion gap is the measured cations minus the measured anions: AG = Na⁺ − (Cl⁻ + HCO₃⁻), normally 12 ± 2 mEq/L in the lecture's units (reference ranges vary by laboratory). The gap is made of unmeasured anions that are always there, mostly albumin, plus phosphate and sulfate.

When an acid HA is added, its H⁺ is buffered by bicarbonate (H⁺ + HCO₃⁻ → H₂CO₃ → H₂O + CO₂), so HCO₃⁻ falls. Its anion A⁻ stays, unmeasured, so the gap rises by about as much as bicarbonate falls: a high-gap acidosis. When bicarbonate itself is lost (diarrhea) or the kidney fails to regenerate or reclaim it (renal tubular acidosis), the kidney retains chloride in its place: Cl⁻ rises as HCO₃⁻ falls, the gap stays normal, and the acidosis is hyperchloremic (normal-gap).

Lecture image

The osmolal gap is measured osmolality minus calculated osmolality (2 × Na⁺ + glucose/18 + BUN/2.8), normally under 10 mOsm/kg. A larger gap means an unmeasured, osmotically active substance. Ethanol raises it without an acidosis; methanol and ethylene glycol raise it early, while the parent alcohol is still present, and then cause a high-gap acidosis as alcohol dehydrogenase converts them to acids.

A metabolic alkalosis needs two things: something that generates it (loss of H⁺ from the stomach or kidney, or a gain of HCO₃⁻) and something that maintains it, because a healthy kidney excretes extra bicarbonate within hours. After vomiting, the maintenance comes from volume contraction and chloride depletion: low volume activates RAAS, aldosterone makes the collecting duct secrete H⁺ and K⁺, the proximal tubule reclaims more bicarbonate, and without chloride the kidney cannot exchange bicarbonate out into the urine. The urine can even be acidic despite alkalemia (paradoxical aciduria).

Diuretics generate an alkalosis two ways: they remove bicarbonate-free fluid around an unchanged amount of bicarbonate (contraction alkalosis), and they deliver more sodium to the collecting duct while aldosterone is high, so H⁺ and K⁺ are secreted. Hypokalemia then sustains the alkalosis by shifting H⁺ into cells.

Suspect a mixed disorder when the pH is normal with abnormal PaCO₂ and HCO₃⁻, when the pH is extreme, or when the compensation calculation misses. The lecture's four examples are below; each calculation shows which number exposes the second disorder.

Work each gas in order. Each step unlocks only when the previous one is right, and every calculation is shown after you commit. Guided cases walks through six gases from the lecture and the simulation. Enter values lets you load a checked example or type your own pH, PaCO₂, HCO₃⁻, Na⁺, Cl⁻ and albumin, then calculate the expected compensation and the anion gap yourself; the tool checks each number and shows the formula with your values substituted.