Acid-Base Physiology and ABG Interpretation

pH 7.35–7.45; [H⁺] ≈ 40 nanomolar at pH 7.4 (about a millionth the concentration of sodium).

pH = 6.1 + log([HCO₃⁻] / (0.03 × PCO₂)). Normal: 6.1 + log(24/1.2) = 6.1 + 1.3 = 7.4.

It is an OPEN system: lungs blow off CO₂ without limit and kidneys regenerate HCO₃⁻ without limit, so the buffer is never exhausted.

[H⁺] (nM) ≈ 24 × PCO₂ / [HCO₃⁻]. At pH 7.4, [H⁺] = 40 nM; add ~1 nM for each 0.01 pH unit below 7.4.

Chemical buffers (seconds), respiratory compensation (minutes), renal compensation (hours to days).

~15,000 mmol/day volatile acid (CO₂) from metabolism, plus 50–100 mEq/day fixed acid (sulfuric from methionine/cysteine, phosphoric from phospholipids).

80–90% in the proximal tubule via NHE3; luminal carbonic anhydrase IV splits H₂CO₃, CA II recombines intracellularly, HCO₃⁻ exits via Na⁺/3HCO₃⁻ cotransporter. Reclaims existing base — makes no new base. Blocked by acetazolamide.

α-intercalated cell H⁺-ATPase secretes H⁺ onto a urinary buffer; each buffered H⁺ excreted yields one new HCO₃⁻ into blood via basolateral Cl⁻/HCO₃⁻ exchanger (AE1).

Phosphate (titratable acid, ~1/3, pKa 6.8) and ammonium (~2/3). Free H⁺ alone only takes urine to pH ~4.5, so buffers are essential.

It depends on upregulating glutamine ammoniagenesis in the proximal tubule; NH₄⁺ excretion rises several-fold only over days, unlike near-instant ventilatory change.

1) Acidemia (pH<7.35) or alkalemia (pH>7.45)? 2) Which side drives it — the primary disturbance moves WITH the pH. 3) Is compensation appropriate? Compensation never fully corrects pH; over/undershoot means a second disorder.

Hemoglobin is the main intracellular blood buffer (isohydric shift lets venous blood carry CO₂); bone carbonate dissolves in chronic acidosis, explaining bone disease in CKD and RTA.