Biological Chemistry - Berezov, T. T., Korovkin, B. F. 1998

Blood
Blood Buffer Systems and Acid-Base Balance
Disorders of Acid-Base Balance

If the body's compensatory mechanisms fail to prevent shifts in hydrogen ion concentration, acid-base balance is disrupted. This manifests as two opposing states: acidosis and alkalosis.

In acidosis, the concentration of hydrogen ions in the Blood exceeds normal values, leading to a decrease in pH. A drop in pH below 6.8 results in death.

When the hydrogen ion concentration in the blood decreases (corresponding to an increase in pH value), a state of alkalosis occurs. The limit of compatibility with life is a pH of 8.0. In clinical practice, pH values as extreme as 6.8 and 8.0 are virtually never encountered.

Depending on the mechanisms underlying acid-base balance (ABB) disorders, respiratory and metabolic acidosis (or alkalosis) are distinguished.

Respiratory acidosis occurs As a result of a decreased minute ventilation volume (e.g., in Bronchial Asthma, pulmonary edema, emphysema, Pulmonary Atelectasis, mechanical asphyxia, etc.). All these conditions lead to hypoventilation and hypercapnia, i.e., an increase in arterial blood P_CO2. Consequently, the H₂СО₃ content in Blood Plasma increases. Elevated P_CO2 also leads to an increase in plasma HCO₃^- ion concentration due to the Hemoglobin buffer mechanism.

* The alkaline reserve of the blood — the capacity of the blood to bind CO₂ — is investigated using the same Methods as the total CO₂ concentration, but under conditions where blood plasma is equilibrated at P_CO2 = 53.3 hPa (40 mm Hg): the total amount of CO₂ and The amount of physically dissolved CO₂ in the test plasma are determined. Subtracting the second figure from the first yields the value known as the alkaline reserve of the blood. It is expressed in volume percent of CO₂ (volume of CO₂ in milliliters per 100 ml of plasma). In normal humans, this value ranges from 50 to 60 vol. % CO₂.

Patients with pulmonary hypoventilation can rather rapidly develop a condition characterized by a low plasma pH, along with increased concentrations of H₂СО₃ and HCO₃^-. This is precisely respiratory acidosis. Simultaneously with the decrease in blood pH, the urinary excretion of free acids and acids bound in the form of ammonium salts increases.

Metabolic acidosis is the most frequent and severe form of ABB disorders. It is caused by the accumulation of organic acids in Tissues and blood. This type of acidosis is associated with metabolic disturbances and can occur in diabetes, starvation, fever, gastrointestinal tract diseases, and Shock (cardiogenic, traumatic, burn, etc.).

Metabolic acidosis is particularly pronounced in patients with severe diabetes who are not receiving Insulin. The increased acidity is driven by The entry of large amounts of Ketone Bodies into the blood. In response to the continuous production of ketone bodies (ß-hydroxybutyric and acetoacetic acids), the body compensatorily decreases the concentration of H₂СО₃, a proton donor in the bicarbonate buffer system. The reduction in H₂СО₃ concentration is achieved through the accelerated elimination of CO₂ by the Lungs (recall that H₂СО₃ reversibly dissociates into CO₂ and H₂О). However, in severe diabetes, to compensate for acidosis, the lungs must excrete such large amounts of CO₂ that the concentrations of H₂СО₃ and HCO₃^- become extremely low, significantly diminishing the blood's buffer capacity. All of this leads to adverse consequences for the Organism. In metabolic acidosis, urine acidity and urinary ammonia concentration are elevated.

Respiratory alkalosis arises from sharply enhanced pulmonary ventilation, accompanied by the rapid elimination of CO₂ from the body and The Development of hypocapnia (decreased arterial blood P_CO2).

This type of alkalosis may be observed, for example, during the inhalation of pure oxygen, compensatory tachypnea accompanying various diseases, exposure to high-altitude low-pressure environments, and under other conditions.

Due to the reduced carbonic acid content in arterial blood, a shift occurs within the bicarbonate buffer system: a portion of the bicarbonates is converted into carbonic acid. The decrease in HCO₃ concentration occurs with the participation of the hemoglobin buffer mechanism. However, this mechanism cannot fully compensate for the reduction in H₂СО₃ concentration, and hyperventilation can elevate extracellular pH to 7.65 within a matter of minutes. In respiratory alkalosis, the alkaline reserve of the blood decreases.

Metabolic alkalosis develops upon the loss of a large amount of acid equivalents (e.g., intractable vomiting, etc.) and the absorption of basic equivalents of intestinal juice that have not been neutralized by acidic gastric juice, as well as upon the accumulation of basic equivalents in tissues (e.g., in tetany) and in cases of improper correction of metabolic acidosis. In metabolic alkalosis, the plasma HCO₃^- concentration is elevated, and the alkaline reserve of the blood is increased. Compensation for metabolic alkalosis is primarily achieved by reducing the excitability of the respiratory center as pH rises, which leads to a decreased respiratory rate and the onset of compensatory hypercapnia (Table 17.3). Urine acidity and its ammonia content are lowered.

Class="center">Table 17.3. Key simple indicators for assessing acid-base balance

In clinical practice, isolated forms of respiratory or Metabolic Disorders are extremely rare. Determining a complex of ABB indicators helps to clarify The Nature of these disorders and the degree of compensation. In recent decades, sensitive electrodes for the direct measurement of blood pH and P_CO2 have been widely used to study ABB parameters. In clinical settings, it is convenient to use Astrup-type instruments or domestic AZIV and AKOR devices. Using these instruments and appropriate nomograms, the following basic ABB indicators can be determined:

1) actual blood pH — the negative decadic logarithm of the blood hydrogen ion concentration under physiological conditions;

2) actual whole-blood P_CO2 — the partial pressure of carbon dioxide (H₂СО₃ + CO₂) in the blood under physiological conditions;

3) actual bicarbonate (AB) — the bicarbonate concentration in blood plasma under physiological conditions;

4) standard plasma bicarbonate (SB) — the bicarbonate concentration in blood plasma equilibrated with alveolar air and fully saturated with oxygen;

5) whole-blood or plasma buffer bases (BB) — an indicator of the total buffering capacity of the blood or plasma system;

6) normal whole-blood buffer bases (NBB) — the buffer bases of whole-blood at physiological values of pH and alveolar air P_CO2;

7) base excess (BE) — an indicator of the excess or deficit of buffer capacities (BB–NBB).