Acid-base balance disorders

Acid-base balance disorders are conditions in which:

or
 * the pH of the body's internal environment deviates from the norm (acidemia, alkalemia)
 * there is an excess or deficiency of acids or bases in the organism, ie there is a change in the composition of the buffers (which may or may not be accompanied by a change in the resulting pH; acidosis, alkalosis).

Bicarbonate buffer is of the utmost importance for rapid pH maintenance. One of its components, (HCO3-), has a charge and is a relatively significant part of the ionogram. Acid-base balance is therefore closely linked to the metabolism of major ions. In practice, any major acid-base imbalance will also be accompanied by a disorder in the mineralogram. And conversely, major changes in the ionogram are usually accompanied by an acid-base imbalance. You can find more about the relationship between the acid-base balance and the ionogram here.



Respiratory disorders of the acid-base balance
If the ventilation changes, the partial pressure of carbon dioxide in the blood changes, and therefore also the concentration of the carbonic acid in the bicarbonate buffer changes. Specifically: and conversely
 * hyperventilation accompanied by hypocapnia leads to respiratory alkalosis
 * hypercapnia caused by a ventilation disorder will result in respiratory acidosis.

Metabolic disorders of the acid-base balance
Metabolic acid-base disorders are conditions in which the concentration of bicarbonates changes significantly (more precisely: standard bicarbonates - see Laboratory evaluation of acid-base balance). At the same time, the concentration of one or more major ions always changes, because the bicarbonate anion must be in balance with other ions in the body fluids (more in the chapter Relationship between acid-base balance and ionogram).

Mixed disorders of the acid-base balance
In practice, a combination of several acid-base disorders can be encountered. The combination of metabolic acidosis with metabolic alkalosis is especially important: in the examination for acid-base disorder according to Astrup, the individual parameters may be normal or only slightly deviated. Therefore, the combined acid-base balance disorder may not be recognized or may be underestimated. At the same time, a treatment that affects one of the disorders can cause the other one to prevail quickly. This can lead to a sudden change in the pH of the internal environment and a severe metabolic breakdown.

Conditions leading to combined acid-base balance disorders are not uncommon. Typical examples are:
 * vomiting and diarrhea
 * vomiting leads to hypochloremic alkalosis, diarrhea to acidosis due to bicarbonate losses


 * prolonged vomiting
 * hypochloraemic alkalosis caused by vomiting is combined with fasting ketoacidosis and lactic acidosis due to insufficient tissue perfusion in hypovolemia


 * hepatorenal failure
 * combines hepatic metabolic alkalosis with renal acidosis


 * liver failure with respiratory insufficiency
 * severe hypoproteinemia in liver failure leads to pulmonary edema, hypoxia causes lactic acidosis


 * renal failure with nephrotic syndrome and severe hypoproteinemia
 * renal acidosis from sulfate and phosphate accumulation is accompanied by alkalosis in hypoproteinemia

Correction and compensation of acid-base balance disorders
When the acid-base balance fails for any reason, the body begins to strive to maintain the pH of the internal environment. Ii fights it with another disorder that deflects the pH in the opposite direction. We distinguish two groups of such mechanisms:


 * Compensation means that in the case 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 breathe deeply ("Kussmaul's breathing").


 * We talk about a correction only in the case of metabolic disorders: one metabolic deviation is corrected by another. For e.g. a patient with liver failure (and therefore metabolic alkalosis) will excrete more bicarbonate in the kidneys and the urine will less acidic.

The development of correction and compensation mechanisms takes some time. Respiration changes almost immediately after the disorder occurs. Respiratory compensation mechanisms then deepen, reaching a maximum in about 12 - 24 hours. Compensation and correction at the kidney level are much slower - some transport mechanisms have to be re-regulated, which often requires protein synthesis. These mechanisms reach their maximum in five days.

 When arriving at high altitudes, it is necessary to count about five days of acclimatization. The cause of the alpine disease is hyperventilation, which the body uses to deal with hypoxia. However, strenuous breathing does not improve the oxygen saturation of hemoglobin too much - the O2 partial pressure in the surrounding atmosphere is too low for that, but it does lead to respiratory alkalosis. Alkalosis and ionic imbalance are the causes of alpine disease, which include cerebral edema, pulmonary edema and tachycardia. Acclimatization consists of over-regulation of the kidneys - basically the development of metabolic acidosis, which lasts the mentioned 5 days. It can be accelerated by an intake of large amounts of fluids, as it increases urinary bicarbonate losses. As a part of the treatment of alpine disease, acetazolamide, a carbonic anhydrase inhibitor that reduces urinary acidification, is sometimes recommended (however, recent work considers acetazolamide to be ineffective).

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

Milder and chronic metabolic acidosis is often treated by the administration of organic acids and their salts. Bicarbonates are then formed by their metabolism in the citrate cycle. This is under the condition of good liver function. The most commonly used are lactate (eg Ringer's infusion solution with lactate) and citrate (eg in oral rehydration solutions used to treat diarrhea).

If acidosis and acidemia have lasted for a long time, the pH of the internal environment must be adjusted 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 formed. Its pH depends on the current pCO2. Nerve endings respond to the acidity of the environment. In case of acidosis that lasts several days, the respiratory center is over-regulated. A sudden alkalization of the internal environment could lead to the respiratory center behaving as it does in hypocapnia - hyperventilation: it would lead to respiratory depression, and eventually to respiratory insufficiency.

Treatment of metabolic alkalosis
The treatment of metabolic alkalosis is most often based on the administration of physiological saline. While in the blood the concentration of sodium cations is higher than the concentration of chloride anions, in saline both ions are in a ratio of 1: 1. By administering it, we supply the body with an excess of chlorides. This displaces the bicarbonates in the ionogram and corrects the alkalosis.

Related articles

 * Relationship between acid-base balance and ionogram
 * Laboratory evaluation of acid-base balance
 * Acid-Base balance