Renal
Acid-Base Balance
How the body holds blood pH between 7.35 and 7.45 — buffers, lungs, kidneys
Human enzymes only function within a narrow pH window, so arterial blood is held between 7.35 and 7.45. Three systems defend this range. The bicarbonate buffer (H₂CO₃ ⇌ HCO₃⁻ + H⁺) reacts in seconds. The lungs adjust CO₂ excretion within minutes by changing minute ventilation. The kidneys regenerate bicarbonate and excrete fixed acids over hours to days. A deviation past 6.8 or 7.8 is usually fatal. Disorders are classified as respiratory or metabolic, acidosis or alkalosis, then graded by compensation.
- Normal arterial pH7.35-7.45 (mean 7.40)
- Normal pCO₂35-45 mmHg
- Normal HCO₃⁻22-26 mEq/L
- Main extracellular bufferBicarbonate / carbonic acid
- Henderson-HasselbalchpH = 6.1 + log([HCO₃⁻] / 0.03 × pCO₂)
- Lethal pH range<6.8 or >7.8
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Why acid-base balance matters
- Critical care. Every ICU admission gets an arterial blood gas; trends guide ventilation and resuscitation.
- Diabetes. Diabetic ketoacidosis is defined by pH < 7.3, HCO₃⁻ < 18, and ketones; treatment hinges on the gap closing.
- Toxicology. Methanol, ethylene glycol, and salicylates produce signature acid-base patterns that drive antidote choice.
- Renal medicine. Chronic kidney disease causes a slow metabolic acidosis that accelerates bone loss and muscle wasting.
- Pulmonology. Chronic CO₂ retention in COPD shifts the kidney to defend a higher baseline HCO₃⁻ — over-oxygenation can blunt drive.
- Surgery. Massive transfusion, prolonged tourniquets, and bowel ischemia all generate lactic acidosis that flags reperfusion injury.
- Pediatrics. Pyloric stenosis classically produces a hypochloremic, hypokalemic metabolic alkalosis from vomiting gastric acid.
Common misconceptions
- "Acidosis means pH is low." Acidemia is the low pH; acidosis is the underlying process — a patient can have acidosis with normal pH if a competing alkalosis offsets it.
- "Bicarbonate fixes acidosis." It treats the number, not the cause; in DKA and lactic acidosis it can worsen intracellular pH and cerebral edema.
- "High pCO₂ is always pathological." Permissive hypercapnia is deliberately tolerated in ARDS to protect the lungs from volutrauma.
- "The kidney compensates respiratory disorders quickly." Renal compensation takes days — early in respiratory acidosis the HCO₃⁻ has barely moved.
- "Anion gap is only for diagnosing acidosis." A delta-delta analysis can reveal mixed disorders that the pH alone hides.
- "Lactate equals tissue hypoxia." Lactate also rises from epinephrine, liver failure, metformin, and beta-agonists without anaerobic metabolism.
Frequently asked questions
What sets normal blood pH?
Arterial pH is 7.35-7.45, slightly alkaline. Venous blood runs ~0.03 lower because it carries more CO₂. Intracellular pH is closer to 7.0-7.2. The narrow range matters because protein charge — and therefore enzyme shape and channel gating — depends sharply on pH. Most metabolic enzymes lose activity outside 6.8-7.8, and that range is the practical limit of life.
How does the bicarbonate buffer work?
CO₂ + H₂O ⇌ H₂CO₃ ⇌ HCO₃⁻ + H⁺. When acid is added, bicarbonate consumes the H⁺ and is exhaled as CO₂; when base is added, carbonic acid donates a proton. The buffer is "open" because CO₂ is continuously vented by the lungs and HCO₃⁻ is regenerated by the kidneys, which makes it more powerful than its pKa of 6.1 alone would suggest.
What are the four primary disorders?
Respiratory acidosis (high pCO₂ from hypoventilation — opioids, COPD, neuromuscular weakness). Respiratory alkalosis (low pCO₂ from hyperventilation — anxiety, sepsis, salicylate toxicity, altitude). Metabolic acidosis (low HCO₃⁻ from acid gain or bicarbonate loss). Metabolic alkalosis (high HCO₃⁻ from vomiting, diuretics, hyperaldosteronism).
What is the anion gap?
AG = Na⁺ − (Cl⁻ + HCO₃⁻), normally 8-12 mEq/L. It reflects unmeasured anions. A high anion gap metabolic acidosis (HAGMA) suggests added acid: lactate (shock, sepsis), ketones (DKA, starvation, alcohol), uremia, methanol, ethylene glycol, or salicylates. A normal-gap acidosis points to bicarbonate loss — diarrhea or renal tubular acidosis. The mnemonic MUDPILES is still taught.
How fast does compensation occur?
The lungs respond in minutes — a metabolic acidosis triggers Kussmaul breathing within an hour, dropping pCO₂ by ~1.2 mmHg per 1 mEq/L fall in HCO₃⁻ (Winter's formula). Renal compensation is slower, taking 3-5 days to fully ramp up bicarbonate reabsorption and ammoniagenesis. Mixed disorders are common in ICU patients and require interpreting compensation against expected formulas.
Why is severe acidosis dangerous?
Acidosis depresses myocardial contractility, blunts catecholamine response, causes hyperkalemia by shifting K⁺ out of cells, and impairs coagulation. Below pH 7.0, vasopressors lose potency and arrhythmias appear. Alkalosis is also dangerous — it tightens hemoglobin's grip on oxygen (left-shifts the curve), drops ionized calcium causing tetany, and provokes seizures and arrhythmias.
When do we give bicarbonate?
Sparingly. IV sodium bicarbonate is reserved for severe acidosis (pH < 7.1), tricyclic overdose, hyperkalemia, and selected toxic alcohol poisonings. Routine bicarbonate in cardiac arrest or DKA is no longer recommended — it generates CO₂ that crosses cell membranes faster than HCO₃⁻, paradoxically worsening intracellular acidosis. Treating the underlying cause is the priority.