Classification of acid-base balance disorders

Endogenous and exogenous factors

The causes of ABB shifts are divided into two broad categories.

• Endogenous causes are the most common in clinical practice. They are caused by organ and tissue insufficiency, which disrupts the function of chemical buffer systems and physiological regulators.
• Exogenous causes are associated with the intake of excess acids or alkalis from the outside. These can be medications (e.g., salicylates or acidic solutions for parenteral nutrition containing arginine and histidine, the catabolism of which yields H⁺ ions). Shifts are also caused by toxic substances (methanol, ethylene glycol, paraldehyde, hydrochloric acid) and specific dietary items. For example, high-amino-acid synthetic diets provoke acidosis, while excessive consumption of milk and alkaline mineral waters causes alkalosis.

Criteria for compensation and decompensation

The severity of ABB disorders is determined by how effectively the body's protective systems function. The main reference point is blood pH, the conventional neutral value of which is 7.39.

• Compensated disorders: pH remains within normal limits (7.35–7.45). In compensated acidosis, values range from 7.35 to 7.38, and in compensated alkalosis, from 7.40 to 7.45. A crucial condition for compensation is maintaining the correct proportion between carbonic acid (H₂CO₃) and sodium bicarbonate (NaHCO₃). This ratio must be strictly 20:1, even if the absolute concentrations of the components have changed.
• Uncompensated disorders: buffer reserves are depleted, and pH goes beyond physiological limits. In uncompensated acidosis, the value drops to 7.34 and below; in uncompensated alkalosis, it exceeds 7.46. In this case, both the total amount of bicarbonate buffer components and their ratio are severely disrupted.

Gaseous (respiratory) disorders

This group is based on a primary change in the concentration of carbon dioxide (CO₂), which directly affects the level of carbonic acid.

1. Respiratory acidosis: occurs due to prolonged hypoventilation of the lungs (e.g., during bronchiolar spasm or airway obstruction). Carbon dioxide accumulates in the blood, leading to hypercapnia (pCO₂ above 42 mmHg), and pH decreases.
2. Respiratory alkalosis: develops against the background of hyperventilation (e.g., during mechanical ventilation). The CO₂ level drops, resulting in hypocapnia (pCO₂ of 35 mmHg or less), and pH increases.

Gaseous shifts generally remain compensated for a long time. This is achieved through dynamic changes in alveolar ventilation volume (which increases in acidosis and decreases in alkalosis) and the operation of buffer systems.

Non-gaseous ABB disorders

Here, the triggering factor is a primary change in the bicarbonate level (HCO₃⁻). In non-gaseous acidosis, its concentration decreases, while in non-gaseous alkalosis, it increases.

There are three main groups of non-gaseous disorders:

• Metabolic — associated with the accumulation of excess acidic or alkaline compounds in the body.
• Excretory — occur when renal function is impaired and the kidneys lose the ability to properly excrete acids and alkalis. This group also includes the loss of acidic gastric juice or alkaline intestinal contents.
• Exogenous — caused by the introduction of substances with pronounced acidic or alkaline properties into the body.

Pathogenesis of uncompensated gaseous acidosis

While compensated acidosis proceeds without significant functional alterations, uncompensated acidosis triggers a cascade of severe systemic reactions:

• Respiratory system: respiratory hypoxia increases due to the narrowing of the lumen of small bronchi and bronchioles (smooth muscle spasm).
• Nervous system: cerebral arterioles dilate, leading to pathological arterial hyperemia of the brain tissue, which results in a dangerous increase in intracranial pressure.
• Circulation: in other organs (except the brain), arterioles constrict, conversely. This causes ischemia, microcirculatory disorders, and capillary-trophic insufficiency.
• Tissue metabolism: hypoxemia and tissue hypoxia progress.
• Ionic imbalance: potassium (K⁺) massively shifts into the extracellular fluid, developing hyperkalemia. Simultaneously, hyperphosphatemia and hypochloremia are recorded.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of chemical buffer system depletion in endogenous acidosis
• Pathogenesis of the toxic effects of methanol and ethylene glycol on acid-base balance
• The role of the kidneys in the development of excretory non-gaseous ABB disorders
• Capillary-trophic insufficiency against the background of uncompensated gaseous acidosis
• Mixed and combined ABB disorders: criteria for differential diagnosis

Other topics in "Chapter 13. Acid-Base Disorders"

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