Endogenous and Exogenous Factors
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 dysfunction, which impairs chemical buffer systems and physiological regulators.
- Exogenous causes are associated with an excess intake of acids or alkalis from the outside. These can be medications (e.g., salicylates or acidic parenteral nutrition solutions 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 products. For example, synthetic diets with high amino acid doses provoke acidosis, while excessive consumption of milk and alkaline mineral waters leads to 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 the 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 stay at 7.35–7.38, and in compensated alkalosis, at 7.40–7.45. A critical 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 bounds. In uncompensated acidosis, the indicator drops to 7.34 and lower; in uncompensated alkalosis, it exceeds 7.46. In this case, both the total amount of bicarbonate buffer components and their ratio are grossly disrupted.
Respiratory Disorders
This group is based on a primary change in carbon dioxide (CO₂) concentration, which directly affects the level of carbonic acid.
- Respiratory acidosis: occurs due to prolonged alveolar hypoventilation (e.g., during bronchiolar spasm or airway obstruction). Carbon dioxide accumulates in the blood, leading to hypercapnia (pCO₂ above 42 mmHg), and pH decreases.
- Respiratory alkalosis: develops against the background of hyperventilation (e.g., during mechanical ventilation). CO₂ levels drop, causing hypocapnia (pCO₂ 35 mmHg or less), and pH increases.
Respiratory shifts typically remain compensated for a long time. This is achieved through dynamic changes in alveolar ventilation (increasing in acidosis and decreasing in alkalosis) and the action of buffer systems.
Non-Respiratory (Metabolic) Disorders
Here, the triggering factor is a primary change in bicarbonate (HCO₃⁻) levels. In non-respiratory acidosis, its concentration decreases, while in non-respiratory alkalosis, it increases.
There are three main groups of non-respiratory disorders:
- Metabolic — associated with the accumulation of an excess of acidic or alkaline compounds in the body.
- Excretory — occur during renal dysfunction, when the kidneys lose the ability to normally 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 Respiratory 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 small bronchi and bronchioles (smooth muscle spasm).
- Nervous system: cerebral arterioles dilate, resulting in pathological arterial hyperemia of brain tissue, leading to a dangerous increase in intracranial pressure.
- Circulation: in other organs (except the brain), arterioles constrict, leading to ischemia, microcirculatory disorders, and capillary-trophic insufficiency.
- Tissue metabolism: hypoxemia and tissue hypoxia progress.
- Ion imbalance: potassium (K⁺) massively shifts into the extracellular fluid, resulting in hyperkalemia. Concurrently, hyperphosphatemia and hypochloremia are recorded.