Metabolic acidosis compensation

Metabolic acidosis can also result when a person is severely burned. Blood plasma leaks from the circulatory system into the injured area, producing edema (swelling) and reducing the blood volume. If the burned area is large, this loss of blood volume may be sufficient to reduce blood flow and oxygen supply to all the body s tissues. Lack of oxygen, in turn, causes the tissues to produce an excessive amount of lactic acid and leads to metabolic acidosis. To minimize the decrease in pH, the injured person breathes harder to eliminate the excess C02. However, if blood volume drops below levels for which the body can compensate, a vicious circle ensues in which blood flow decreases still further, blood pressure falls, C02 excretion diminishes, and acidosis becomes more severe. People in this state are said to be in shock and will die if not treated promptly. 

Metabolic acidosis and alkalosis result from primary disturbances in the serum H CO., concentration. Respiratory compensation of metabolic disturbances begins within minutes and is complete within 12 hours. 

Metabolic acidosis is characterized by a decrease in serum HC03. The anion gap is used to narrow the differential diagnosis, as this acidosis may be caused by addition of acids (increased anion gap) or loss of HC03 (normal anion gap). The compensation for metabolic acidosis is an increase in ventilation with a decrease in arterial C02. 

Any time an ABG is analyzed it is wise to concurrently inspect the serum chemistry values to calculate the anion gap. The body does not generate an anion gap to compensate for a primary disorder. As such, if the calculated anion gap exceeds 12 mEq/L (mmol/L) there is a primary metabolic acidosis regardless of the pH or the serum HC03 concentration. The anion gap may be artificially lowered by decreased serum albumin, multiple myeloma, lithium intoxication, or a profound increase in the serum potassium, calcium, or magnesium. 

The manifestations of acute severe metabolic acidemia (pH less than 7.15 to 7.20) involve the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. Respiratory compensation may occur as Kussmaul s respirations (i.e., deep, rapid respirations characteristic of diabetic ketoacidosis). 

Failure of compensation is responsible for mixed acid-base disorders such as respiratory acidosis and metabolic acidosis, or respiratory alkalosis and metabolic alkalosis. In contrast, excess compensation is responsible for metabolic acidosis and respiratory alkalosis, or metabolic alkalosis and respiratory acidosis. 

AFE Line AF represents a metabolic acidosis as the HC03 has fallen. Compensation occurs by hyperventilation and the Paco2 falls as shown by line FE. 

The answer is C. Ingestion of an acid or excess production by the body, such as in diabetic ketoacidosis, may induce metabolic acidosis, a condition in which both pH and HCOj become depressed. In response to this condition, the carbonic acid-bicarbonate system is capable of disposing of the excess acid in the form of CO2. The equilibrium between bicarbonate and carbonic acid shifts toward formation of carbonic acid, which is converted to COj and HjO in the RBC catalyzed by carbonic anhydrase, an enzyme found mainly in the RBC. The excess CO2 is then expired by the lungs as a result of respiratory compensation for the acidosis (Figure 1-2). The main role of the kidneys in managing acidosis is through excretion of H" rather than CO2. 

Metabolic acidosis follows, and an increased anion gap results from accumulation of lactate as well as excretion of bicarbonate by the kidney to compensate for respiratory alkalosis. Arterial blood gas testing often reveals this mixed respiratory alkalosis and metabolic acidosis. Body temperature may be elevated owing to uncoupling of oxidative phosphorylation. Severe hyperthermia may occur in serious cases. Vomiting and hyperpnea as well as hyperthermia contribute to fluid loss and dehydration. With very severe poisoning, profound metabolic acidosis, seizures, coma. 

Metabolic acidosis involves a build-up of hydrogen ions in the blood, thus lowering blood pH. Under normal physiological conditions, the kidneys excrete excess hydrogen ions, and release more bicarbonate ions into the bloodstream to buffer the excess acid. However, in renal failure, or in diabetic ketoacidosis, this mechanism either fails, or is unable to compensate to an adequate extent. Hence, metabolic acidosis is usually treated with sodium bicarbonate, either intravenously (1.26% or 8.4% i.v. solution) or orally (typically 1 g three times a day). Sodium bicarbonate 1.26% intravenous solution is isotonic with plasma (and with sodium chloride 0.9%), so may be given in large volumes (1-2 L) by peripheral venous catheter to correct metabolic acidosis and provide fluid replacement at the same time. Sodium bicarbonate 8.4% may only be given by central venous catheter. 

The pH value in the portal vein drops in the case of increased urea synthesis. This decrease corresponds to the consumption of HC03. At the same time, intra-and extrahepatic glutamine synthesis is reduced. When the pH value falls in the blood, corresponding amounts of bicarbonate must be made available for the compensation of metabolic acidosis. This amount of HC03 is then not available for urea synthesis, which results in a curbing of the urea cycle. Additionally, the glutaminase... 

An 11-year-old boy with refractory partial epilepsy who had been taking topiramate 300 mg/day for 13 months developed hyperventilation. He had a hyperchloremic metabolic acidosis with partial respiratory compensation. The hyperventilation and acidosis resolved after the administration of sodium bicarbonate and reduction of the dose of topiramate. 

There are two distinct types of GSH-S deficiency, both associated with mild chronic hemolysis in one type, hemolysis is the only clinical manifestation. In the other, the major clinical features are mental retardation, severe generalized muscle weakness, tremors, incoordination, hemolytic anemia, and metabolic acidosis. This second and much more severe type of GSH-S deficiency is also known as 5-oxopro-linurta or pyroglutamic aciduria. The difference in severity of these disorders reflects the fact that in the mild form, GSH-S deficiency is confined to the RBCs because in this disorder the GSH-S is unstable. GSH-S activity is present in adequate quantity in young RBCs, but it rapidly declines as the cells age, because the cells are unable to synthesize new molecules of GHS-S. Other cells of the body that have nuclei and ribosomes can compensate for accelerated denaturation of GSH-S by synthesizing more. On the other hand, in the severe systemic form of GSH-S deficiency, aE cells of the body have low activities of GSH-S because they cannot form this enzyme in adequate amounts. In both types of GSH-S deficiency, RBCs exhibit notable reduction in GSH concentration. 

Respiratory compensation after correction of metabolic acidosis Others... 

The answer is e. (Murray, pp 15-26.) Pure metabolic acidosis (choice c) or pure metabolic alkalosis exhibits abnormal bicarbonate and normal lung function. Pure respiratory acidosis (choice d) or alkalosis (choice a) is associated with normal renal function (and normal blood acids) with a normal bicarbonate and abnormal Pccv, Thus choices b and e must involve compensation, since both the Pccv and bicarbonate are abnormal. Choice e must represent compensated metabolic alkalosis since the PCO2 is high—if it were compensated respiratory acidosis with a high PcOj, the pH would be low. 

The answer is e. (Murray, pp 298-307. Scriver, pp 1471-1488. Sack, pp 217-218. Wilson, pp 361-384.) In the presence of insulin deficiency, a shift to fatty acid oxidation produces the ketones such as acetoacetate that cause metabolic acidosis. The pH and bicarbonate are low, and there is frequently some respiratory compensation (hyperventilation with deep breaths) to lower the PCO2, as in choice e. A low pH with high PCO2 would represent respiratory acidosis (choices a and b—the low-normal bicarbonate values in these choices indicate partial compensation). Choice d represents respiratory alkalosis as would occur with anxious hyperventilation (high pH and low Peep, partial compensation with high bicarbonate). Choice c illustrates normal values. 

Acid-base status Cannot by itself explain seizure protective effect Nonnal serum pH in patients on KD suggests that metabolic acidosis is compensated Brain pH is normal... 

Respiratory compensation for a primary metabolic acidosis begins rapidly (within 15 to 30 minutes) but does not reach a steady state for 12 to 24 hours after the onset of metabolic acidosis. 

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