Acid-base Compensation is the relative constancy of the acid-base relationship of the internal environment of a living organism, particularly when it comes to the renal system. Also called acid-base balance, acid-base balance, equilibrium of acids and bases. It is an integral part of homeostasis. Quantitatively it is characterized either by the concentration of hydrogen ions in moles per one liter or by the hydrogen pH. The tissues of a living organism are very sensitive to fluctuations in the pH value – outside the permissible range, protein denaturation occurs: cells are destroyed, enzymes lose their ability to perform their functions, and the body can die. Therefore, the acid-base balance in the body is tightly regulated. There are several buffer systems that reversibly bind hydrogen ions and prevent any changes in pH. The bicarbonate buffer system (the most powerful and most controllable among buffer systems) is particularly important: an excess of protons interacts with bicarbonate ions (metabolic alkalosis) to form carbonic acid. Further decrease in the amount of carbonic acid occurs as a result of an accelerated release of carbon dioxide as a result of hyperventilation of the lungs (concentration is determined by the pressure in the alveolar gas mixture.)
There are several approaches for the evaluation and classification of acid-base balance alterations. The physicochemical proposal is the most recent and is based on the difference of strong ions, the total concentration of weak plasma acids and the partial pressure of arterial carbon dioxide. Of great acceptance among anesthesiologists and intensivists, it is a tremendous complex approach, both technical and interpretation. Therefore, in this post, the physiological approach will be used, based on pH, and plasma bicarbonate, which is the simplest, most rigorous and practical way to systematically classify and treat alterations in the acid-base balance.
First of all acid-base disorder must answer three basic questions. The first has to do with what disorder it is. The second, if the secondary response is adequate. The third, about the cause of the disorder. Metabolic acidosis is divided according to the value of the anionic hiatus. Acidosis with increased anionic hiatus: acid gain, endogenous or exogenous, predominates. They are normochloremic acidosis. Acidosis with normal anionic hiatus: the loss of bicarbonate outside the body predominates. They are called hyperchloremic acidosis.
Approximately three-quarters of the value of the anion hiatus correspond to serum albumin, which is an anion, so in the assessment of the anion, hiatus should be taken into account if hypoalbuminemia, as well as other circumstances.
The acid-base balance of the organism is possible thanks to the interrelation of three systems: intracellular and extracellular tampons, which cushion in a minute the acute changes of acid-base balance; respiratory compensation, which starts in minutes and is completed in hours, and renal excretion of excess acids, which takes more time. The total buffer capacity of the organism is about one thousand mMol (forty percent in the extracellular space, and sixty in the intracellular space.)
To plan an adequate treatment, and as in any acid-base disorder, it is essential to identify secondary responses (compensation mechanisms), whether these are adequate or not, and whether there are other acid-base mixed disorders or associated electrolyte disorders.
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In metabolic acidosis, the key aspect of treatment lies in blocking the source of acid production (eg, by providing insulin in diabetic ketoacidosis,) always taking into account the compensations that exist, the rate of acid production and its cause (lactic acidosis due to hypoxia or alcohol intoxication are more serious due to its rapid evolution.) Special caution when planning treatment deserves the detection of hypokalemia since it implies a serious potassium deficit. The replacement of bicarbonate should be very cautious, applied only in certain circumstances (eg, extreme hyperkalemia, potentially fatal drops in pH,) and always assessing the risks and benefits. The only objective is to gain time until the homeostatic mechanisms manage to increase the pH.
To the problem of acidosis due to keto acids caused by insulin deficiency, water deficit, circulating volume deficit, the coexistence of lactic acidosis and potassium deficit, which in turn depends on the duration and magnitude of polyuria secondary to poor glycemic control, and the degree of replacement of losses.
The general treatment plan should include, therefore: Insulin, re-expansion of the extracellular volume, correction of possible potassium deficit, and the decision to administer or not bicarbonate should be valued with great caution. The alterations in the bicarbonate concentration or the partial pressure of carbon dioxide in the arterial blood are accompanied by a compensatory response in the other element. If the compensation is adequate or it will not allow detecting if there is a second or third associated disorder, in what constitute the mixed disorders that are very frequent in clinical practice and that implies a greater severity.
In order to detect mixed disorders, it must be taken into account that a compensation will never be able to normalize the pH. Its treatment and the priority of the actions to follow will depend on the cause and predominant acid-base disorder, always taking into account the associated electrolyte alterations.
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