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Human Physiology II · Systems Physiology

Acid-Base Balance

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On this page 7 sections
  1. In 30 seconds
  2. Why this matters
  3. The college version
  4. Eli explains
  5. Worked example
  6. Key takeaway
  7. Study tools

In 30 seconds

The body defends arterial pH near 7.4 against a constant acid load. Chemical buffers—bicarbonate, phosphate, and proteins/hemoglobin—neutralize acid within seconds; the lungs adjust ventilation within minutes to change PCO₂; and the kidneys, within hours to days, secrete H⁺, reabsorb all filtered bicarbonate, and generate new bicarbonate (partly via ). Disturbances are classified by their primary cause (metabolic or respiratory) and direction (acidosis or alkalosis), with compensation moving the other system to return pH toward normal.

Why this matters

Arterial blood gas (ABG) analysis—reporting pH, PCO₂, and HCO₃⁻—is used to identify acid–base disorders, and the is the classic teaching tool for reading those values. Understanding which component changed first (respiratory vs metabolic) and whether compensation has occurred guides interpretation. This is educational context, not guidance: diagnostic criteria, reference ranges, and management vary by institution and jurisdiction, and interpretation of ABGs must be performed by qualified clinicians.

The college version

1. Normal pH and Acid/Base Sources

Normal arterial pH is about 7.35–7.45 (7.40 on average). Acid is produced constantly: as CO₂ (from oxidative metabolism, ~15,000 mmol/day, exhaled) and fixed (nonvolatile) acids from protein metabolism (sulfuric, phosphoric acids) and incomplete fat/carbohydrate oxidation (lactic acid, ketoacids), which the kidneys must excrete. Base equivalents come mainly from dietary plant-based anions and from the body's bicarbonate pool.

2. Chemical Buffers

Buffers are weak acid/base pairs that minimize pH change by absorbing or releasing H⁺. The (CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻) is the main extracellular buffer and is uniquely powerful because both the lungs (CO₂) and kidneys (HCO₃⁻) regulate its components. The (H₂PO₄⁻/HPO₄²⁻) is important in intracellular fluid and in tubular fluid, where "" is excreted. Proteins and hemoglobin are the main intracellular buffers; hemoglobin's histidine residues buffer the CO₂ and H⁺ carried by red blood cells. Buffers act in seconds but cannot eliminate acid—they only blunt its effect.

3. Respiratory and Renal Compensation

changes ventilation to alter PCO₂: rising H⁺ (or CO₂) stimulates chemoreceptors to increase ventilation, blowing off CO₂ and lowering carbonic acid; falling H⁺ depresses ventilation to retain CO₂. This acts in minutes. is slower (hours to days) but definitive: the kidney (1) secretes H⁺ into the tubule via Na⁺/H⁺ exchangers and H⁺-ATPases in proximal and collecting-duct intercalated cells; (2) reabsorbs virtually all filtered bicarbonate (filtered HCO₃⁻ combines with secreted H⁺ to form CO₂, which re-enters the cell and regenerates HCO₃⁻); and (3) generates new bicarbonate by excreting H⁺ bound to urinary buffers—phosphate (titratable acid) and ammonia. Ammoniagenesis in the proximal tubule (glutamine → NH₄⁺ and new HCO₃⁻) is the kidney's main mechanism for adding fresh bicarbonate during chronic acidosis.

4. Acid–Base Disorders and the Davenport Diagram

A primary respiratory disturbance changes PCO₂; a primary metabolic disturbance changes HCO₃⁻. Respiratory acidosis (high PCO₂, e.g., hypoventilation) is compensated by renal HCO₃⁻ retention; respiratory alkalosis (low PCO₂, e.g., hyperventilation) by renal HCO₃⁻ loss. Metabolic acidosis (low HCO₃⁻) is compensated by hyperventilation to lower PCO₂; metabolic alkalosis (high HCO₃⁻) by hypoventilation to raise PCO₂. The Davenport diagram plots plasma HCO₃⁻ against pH, with PCO₂ isobars curving across it: it shows how pH, HCO₃⁻, and PCO₂ move together and distinguishes a compensated disorder (pH near normal but both HCO₃⁻ and PCO₂ abnormal) from an uncompensated one (pH far from normal).

How it works

  1. Buffers (bicarbonate, phosphate, proteins/hemoglobin) blunt acid loads in seconds.
  2. Chemoreceptors sense pH/PCO₂ and adjust ventilation in minutes.
  3. The kidney secretes H⁺, reabsorbs filtered HCO₃⁻, and generates new HCO₃⁻ over hours to days.
  4. Ammoniagenesis and titratable acid excretion carry the acid load into urine while restoring bicarbonate.
  5. The Davenport diagram integrates pH, HCO₃⁻, and PCO₂ to classify any disorder and its compensation.

Common confusions

Do not confuseWithDifference
AcidosisAlkalosisAcidosis = pH below normal; alkalosis = pH above normal
Respiratory acidosisMetabolic acidosisRespiratory = high PCO₂ (lungs); metabolic = low HCO₃⁻ (kidney/metabolism)
Reabsorbed bicarbonateNew (generated) bicarbonateReabsorption reclaims filtered HCO₃⁻; generation adds fresh HCO₃⁻ via ammoniagenesis
CompensationCorrectionCompensation restores pH partly (both values abnormal); correction returns the primary value to normal
Titratable acidAmmonium (NH₄⁺)Both carry H⁺, but NH₄⁺ (ammoniagenesis) is the larger, adaptable pathway

Memory aids

"Buffers Buy time, Breathing is Fast, Kidneys are the Final word." For the equation: pH depends on the Ratio of HCO₃⁻ over CO₂ ("R-O-M: Respiratory = CO₂, Metabolic = HCO₃⁻").

Quick review

Topic Recap

Acid–base balance defends pH ≈ 7.4 through three layers: immediate chemical buffering (bicarbonate, phosphate, proteins/hemoglobin), rapid ventilatory control of PCO₂, and slow renal control of H⁺ secretion, bicarbonate reabsorption, and new-bicarbonate generation via ammoniagenesis. Primary disorders are classified as respiratory (PCO₂) or metabolic (HCO₃⁻) acidosis/alkalosis, and the Davenport diagram maps how pH, HCO₃⁻, and PCO₂ shift with each disorder and its compensation.

Knowledge Check

  1. What is the normal arterial pH, and what are the three buffer systems?
  2. Which organ provides fast (minute-scale) compensation, and which provides slow (hour-to-day) compensation?
  3. What are the two ways the kidney generates "new" bicarbonate?
  4. What is the primary abnormality in respiratory acidosis versus metabolic acidosis?
  5. On a Davenport diagram, what do the curved isobar lines represent?

Answers and Rationales

  1. Normal arterial pH is ~7.4 (7.35–7.45); the buffers are bicarbonate, phosphate, and proteins/hemoglobin.
  2. The lungs compensate fast by changing ventilation (PCO₂); the kidneys compensate slowly by adjusting H⁺ secretion and HCO₃⁻.
  3. New bicarbonate is generated by titratable acid (phosphate-buffered H⁺) excretion and by ammoniagenesis (NH₄⁺ excretion).
  4. Respiratory acidosis is a primary rise in PCO₂ (hypoventilation); metabolic acidosis is a primary fall in HCO₃⁻.
  5. The curved lines are PCO₂ isobars—lines of constant PCO₂ along which metabolic changes (HCO₃⁻ vs pH) move.
Eli, the EliExplains learning guide

Eli explains

The same idea, in plain words

Explain it like I’m 10

Your cells constantly make acid (like the CO₂ you exhale and acids from food and metabolism), yet your blood must stay very close to neutral—just slightly alkaline. The body runs three "cleanup crews" at different speeds: instant chemical sponges (buffers) that soak up acid, a fast ventilation dial that blows off or holds onto CO₂, and a slow but thorough kidney that throws acid out in urine and restores the sponge (bicarbonate) it used.

This is like keeping a pool's pH perfect: buffers are the instant chemicals, breathing is the quick valve, and the kidney is the slow filter that resets everything. It stops being exact because CO₂ is both a waste gas and an acid (carbonic acid), so the lungs and kidneys are yoked together in a two-sided tug-of-war rather than acting independently.

Simple Example

Run up stairs and you breathe hard to blow off the CO₂ your muscles produce, keeping blood from turning acidic. The next day, your kidneys have quietly adjusted how much acid they excrete and how much bicarbonate they keep, locking in the long-term balance.

Worked example

  1. Metabolism produces CO₂ and fixed acids; buffers immediately absorb the added H⁺, preventing large pH swings.
  2. The Henderson–Hasselbalch equation links the system: pH = pKa + log[HCO3-][CO2], where [CO2] = 0.03 × PCO2 (PCO₂ in mmHg); pH depends on the ratio of bicarbonate to dissolved CO₂.
  3. If PCO₂ rises (respiratory acidosis), the lungs respond by ventilating more; the kidneys respond by retaining/generating HCO₃⁻, restoring the ratio and thus the pH.
  4. If HCO₃⁻ falls (metabolic acidosis), ventilation increases to lower PCO₂ (compensation), and the kidneys excrete H⁺ as titratable acid and NH₄⁺ while generating new HCO₃⁻ via ammoniagenesis.
  5. The Davenport diagram visualizes these paired changes: pH on the x-axis, HCO₃⁻ on the y-axis, curved PCO₂ isobars showing that moving along an isobar changes HCO₃⁻ and pH without changing PCO₂ (metabolic), while moving between isobars changes PCO₂ (respiratory).

Key takeaways

  • High yield: Normal arterial pH ≈ 7.4 (range ~7.35–7.45); below = acidosis, above = alkalosis.
  • High yield: Buffers act in seconds, lungs in minutes, kidneys in hours to days.
  • High yield: The kidney reabsorbs essentially all filtered bicarbonate and generates new bicarbonate via ammoniagenesis.
  • High yield: Respiratory disorders = primary PCO₂ change; metabolic disorders = primary HCO₃⁻ change.
  • Compensation drives pH toward normal but never overshoots in a simple disorder.
  • Hemoglobin is the major intracellular/blood buffer; bicarbonate is the major extracellular buffer.

Keep learning

Ready to build on this? Continue to the next lesson.

Study tools & related lessonsYou’ll learn to · Key vocabulary · Related

You’ll learn to

  • State normal arterial pH and the main sources of acid and base in the body.
  • Compare the three chemical buffer systems (bicarbonate, phosphate, proteins/hemoglobin) and their timing.
  • Explain respiratory compensation through ventilation and PCO₂, and renal compensation through H⁺ secretion, bicarbonate reabsorption, and new bicarbonate generation.
  • Classify the four primary acid–base disorders (metabolic/respiratory acidosis/alkalosis) and interpret them on a Davenport diagram.

Key vocabulary

pH
Negative log of [H⁺]; normal arterial ~7.4
Volatile acid
CO₂-derived acid, exhaled by lungs
Fixed (nonvolatile) acid
Non-CO₂ acids from metabolism
Bicarbonate buffer
CO₂/HCO₃⁻ system
Phosphate buffer
H₂PO₄⁻/HPO₄²⁻ pair
Hemoglobin buffer
Protein buffer inside red cells
Respiratory compensation
Ventilation adjusting PCO₂
Renal compensation
Kidney adjusting H⁺/HCO₃⁻
Titratable acid
H⁺ buffered by urinary phosphate
Ammoniagenesis
Glutamine → NH₄⁺ + new HCO₃⁻
Metabolic acidosis/alkalosis
Primary HCO₃⁻ fall/rise
Respiratory acidosis/alkalosis
Primary PCO₂ rise/fall
Davenport diagram
HCO₃⁻ vs pH plot with PCO₂ isobars

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