Disorders of acid-base balance

We refer to conditions when: or
 * The pH of the internal environment is deviated from the norm (acidemia, alkalemia)
 * there is an excess or lack of acids or bases in the body, i.e. there is a change in the composition of buffers (which may or may not be accompanied by a change in the resulting pH; acidosis, alkalosis).

For the rapid maintenance of pH, the 'bicarbonate buffer is of the greatest importance. One of its components, (HCO3-), has a charge and forms a relatively significant item in the ionogram. Acid-base balance is therefore closely linked to major ion metabolism. In practice, every major disturbance in the acid-base balance will also be accompanied by a disturbance in the mineralogram. Conversely, more significant changes in the ionogram are usually accompanied by a disturbance in the acid-base balance. More on the relationship between acid-base balance and ionogram can be found here.

Respiratory disorders of acid-base balance
If ventilation changes, the partial pressure of carbon dioxide in the blood changes and thus the concentration of conjugated acid of the bicarbonate buffer. Specifically: and conversely
 * hyperventilation accompanied by hypocapnia will lead to respiratory alkalosis
 * hypercapnia caused by ventilatory failure will result in respiratory acidosis.

Metabolic disorders of acid-base balance
As ABR metabolic disorders, we refer to states in which the concentration of bicarbonates (more precisely: standard bicarbonates - see Acid-base balance examination) changes significantly. At the same time, the concentration of one or more main ions always changes, as the bicarbonate anion must be in balance with the other ions of body fluids (more in the chapter Relationships between acid-base balance and ionogram).

Combined disorders of acid-base balance
In practice, one can often encounter a combination of several disorders of acid-base balance. The combination of metabolic acidosis with metabolic alkalosis' is particularly significant: during ABR examination according to Astrup, the individual parameters may be normal or only slightly deviated. Therefore, the combined ABR disorder may not be recognized or may be underestimated. At the same time, a treatment intervention that affects one of the sub-disorders can cause the other disorder to quickly prevail. This can cause a sharp change in the pH of the internal environment and severe metabolic disruption.

Conditions leading to combined ABR disorders are not rare. Typical examples can be:
 * vomiting and diarrhea
 * vomiting leads to hypochloremic alkalosis, diarrhea to acidosis from bicarbonate losses


 * protracted vomiting
 * hypochloremic alkalosis from vomiting is combined with ketoacidosis from starvation and lactic acidosis from insufficient tissue perfusion from hypovolemia


 * hepatorenal failure
 * hepatic metabolic alkalosis is combined with renal acidosis


 * liver failure with respiratory insufficiency
 * severe hypoproteinemia in liver failure leads to pulmonary edema, lactic acidosis develops as a result of hypoxia


 * renal failure with nephrotic syndrome and severe hypoproteinemia
 * renal acidosis from the accumulation of sulfates and phosphates is accompanied by alkalosis in hypoproteinemia

Correction and compensation of acid-base balance disorders
If, for any reason, the ABR is impaired, the organism begins to make efforts to maintain the pH of the internal environment. In essence, ABR fights the original disorder with another disorder that shifts the pH in the opposite direction. We distinguish two groups of such mechanisms:
 * Compensation means that in the event of a metabolic disorder, the pH of the internal environment is maintained by changing respiration. For example, metabolic acidosis is compensated by respiratory alkalosis; the patient will take labored deep breaths ("Kussmaul breathing").
 * We only talk about ``correction'' in the case of ABR metabolic disorders: one metabolic deviation is corrected by another. E.g. a patient with liver failure (and thus metabolic alkalosis) will excrete more bicarbonate through the kidneys and will acidify the urine less.

Corrective and compensatory mechanisms take time to develop. A change in respiration occurs almost immediately after the occurrence of an ABR disturbance. Respiratory compensatory mechanisms then deepen, reaching their maximum in about 12-24 hours. Compensation and correction at the level of the kidneys is much slower - because some transport mechanisms have to be reregulated, which often requires protein synthesis. These mechanisms reach their maximum in five days.

 When arriving at high altitudes, acclimatization takes about five days. The cause of altitude sickness is hyperventilation, which the body tries to counter hypoxia. Effortful breathing, however, will not greatly improve hemoglobin saturation with oxygen - the partial pressure of O2 in the surrounding atmosphere is too low for this, but it leads to respiratory alkalosis. It is alkalosis and ionic imbalance that is the cause of the manifestations of altitude sickness, including cerebral edema, pulmonary edema and tachycardia. Acclimatization consists in over-regulation of the kidneys - essentially in the development of metabolic acidosis, which lasts the mentioned 5 days. It can be accelerated by taking in a large amount of fluids, as the loss of bicarbonates into the urine will increase. As part of the treatment of altitude sickness, the administration of acetazolamide - a carbonic anhydrase inhibitor, which reduces the acidification of the urine - is sometimes recommended (however, more recent work considers the administration of acetazolamide to be of little effectiveness).

Treatment of metabolic acidosis
The basis of the treatment of severe metabolic acidosis is the administration of sodium bicarbonate, either parenterally as part of complex infusion therapy or orally. The advantage of enteral administration is that the organism is left to regulate the absorption of bicarbonates, so there is no need to worry so much about excessive alkalization. On the other hand, this route is slower and less effective, and resorption may be impaired in patients in a more severe condition.

Milder and chronic metabolic acidosis is often corrected by administration of organic acids and their salts. Bicarbonates are actually created only by metabolizing them in the citrate cycle. A condition is good liver function. Lactate (e.g. lactated Ringer's solution for infusion) and citrate (e.g. in oral rehydration solutions used to treat diarrheal diseases) are most commonly used.

If acidosis and acidemia lasted for a long time, it is necessary to adjust the pH of the internal environment slowly.

 It should be remembered that the respiratory center responds to pCO2 as an acid-base sensor: CO2 diffuses from the blood into an environment rich in HCO3 -, so a buffer is created. Its pH depends on the current pCO2. Nerve endings react to the acidity of the environment. With acidosis lasting several days, the respiratory center will be overregulated. A sharp alkalinization of the internal environment could lead to the respiratory center behaving as in hypocapnia - i.e. hyperventilation: breathing would be depressed, even respiratory insufficiency.

Treatment of metabolic alkalosis
The treatment of metabolic alkalosis is most often based on the administration of a physiological solution. While in the blood the concentration of sodium cations is higher than the concentration of chloride anions, in physiological solution both ions are in a 1:1 ratio. By administering a physiological solution, we supply the body with an excess of chlorides. This causes hydrogen carbonates to be displaced in the ionogram and alkalosis is corrected.

Related Articles

 * Relationships between acid-base balance and ionogram
 * Laboratory examination of acid-base balance
 * Acid-base balance