Why Buffers Are Needed and How They Work
During normal metabolic processes, our body continuously generates a colossal amount of metabolites. Physiologically, acidic products are formed in amounts nearly 20 times greater than basic (alkaline) products. Consequently, systems that provide rapid neutralization, secretion, and excretion of excess acids dominate the body.
Chemical buffer systems act as the first line of defense. These mobile complexes activate immediately when hydrogen ion concentrations change. Their primary mechanism of action is transforming strong acids and bases into weak ones. Due to their specific capacity and high efficiency, they can smooth out moderate fluctuations in acid-base balance within just a few dozen seconds.
Main Chemical Buffers
Total blood buffer capacity is distributed unevenly: erythrocytes provide 57%, and plasma provides 43%. There are four main chemical systems:
- Hemoglobin buffer. The highest-capacity buffer, accounting for more than 50% of the total blood buffer capacity. It functions exclusively inside erythrocytes. Oxygenated hemoglobin (HbO_2) acts as the acidic component—it dissociates roughly 80 times stronger than reduced hemoglobin (Hb), releasing hydrogen ions into the medium and binding cations (primarily potassium). Reduced hemoglobin works as the main basic component. The system's primary task is participating in carbon dioxide transport from tissues to the lungs.
- Bicarbonate buffer. A key buffer of blood and extracellular fluid. In the extracellular environment, it consists of a mixture of carbonic acid and sodium bicarbonate, while inside cells, sodium salts are replaced by potassium and magnesium salts. This is an open system closely associated with external respiration and renal function.
- Protein buffer. The main intracellular buffer, providing about 3/4 of the intracellular fluid's capacity. It consists of weakly dissociating proteins with acidic properties and strong base salts. During acidosis, the mounting excess of acids interacts with protein salts, producing a neutral salt and a weak acid.
- Phosphate buffer. Accounts for about 8% of total capacity. Its role in the blood itself is modest, but it plays a substantial role inside cells and within renal tubules due to high local phosphate concentrations. The alkaline component is sodium monohydrogen phosphate (Na_2HPO_4), and the acidic component is sodium dihydrogen phosphate (NaH_2PO_4).
| Buffer System | Blood Plasma (%) | Erythrocytes (%) |
|---|---|---|
| Bicarbonate | 35 | 18 |
| Hemoglobin | — | 35 |
| Protein | 7 | — |
| Phosphate | 1 | 4 |
Physiological Compensation and ABB Disorders
If chemical buffers cannot cope with the load, physiological (organ) regulatory mechanisms step in. These involve the lungs, kidneys, liver, and gastrointestinal tract. Unlike chemical reactions, organ-level compensation takes significantly longer to achieve an effect—ranging from several minutes to several hours.
Various pathologies trigger specific primary ABB shifts, which the body compensates for via counter-reactions:
- Respiratory acidosis. Primary decrease in pH and increase in carbon dioxide tension (pCO_2). To compensate, the kidneys begin actively retaining bicarbonate (HCO_3^-).
- Respiratory alkalosis. Primary increase in pH and drop in pCO_2. The kidneys respond by enhanced renal excretion of bicarbonate.
- Non-respiratory (metabolic) acidosis. Characterized by a drop in pH and decreased bicarbonate levels. Pulmonary hyperventilation activates to blow off excess carbon dioxide (decreasing pCO_2).
- Non-respiratory (metabolic) alkalosis. Against the background of elevated pH and bicarbonate, the lungs reduce ventilation (hypoventilation) to retain carbon dioxide.
In critical situations (acute heart, respiratory, or renal failure, shock, coma), bones come to the rescue. They function as a massive depot for buffer systems, storing large quantities of carbonic acid salts (calcium, sodium, and potassium carbonates). During acute acid accumulation, bone tissue can provide 30–40% of the body's total buffer capacity.