Bicarbonate acid-base metabolism

A high amount of bicarbonate is constantly being produced in the body. Degradation of 100 g protein yields approximately 1 mol bicarbonate (= 61 g). Bicarbonate neutralization takes place via the urea cycle too, as the synthesis of 1 mol urea requires 2 mol bicarbonate. Besides the lungs and kidneys, the liver therefore also plays an important role in acid-base metabolism and is partly responsible for pH homoeostasis. 

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. 

Because C02 is a volatile acid, it can rapidly be changed by the respiratory system. If a respiratory acid-base disturbance is present for minutes to hours it is considered an acute disorder while if it is present for days or longer it is considered a chronic disorder. By definition, the metabolic machinery that regulates HC03 results in slow changes in serum bicarbonate and all metabolic disorders are chronic. This means that there are six simple acid-base disorders as outlined in Table 25-1.2... 

Electrolytes Daily doses based on daily maintenance requirements, renal function, gastrointestinal losses, acid-base status, concomitant drug therapy, nutritional and anabolic status Pa lion I has hyponatremia, hypokalemia, hypomagnesemia, and hypophosphatemia, also has low serum bicarbonate concentration, could be component of metabolic acidosis due to sepsis... 

Acid-base disturbances associated with PN usually are related to the patient s underlying condition(s). However, acid-base abnormalities may develop as a result of changes in chloride or acetate concentrations in PN admixtures. Because acetate is converted to bicarbonate in the body, excessive acetate salts in PN can lead to metabolic alkalosis excessive chloride salts in PN can lead to metabolic acidosis. PN should not be used to... 

Metabolic acidosis An acid-base disorder caused by overproduction or accumulation of acid (often lactic acid see lactic acidosis) or a deficit of base (i.e., bicarbonate). 

Less urgent forms of metabolic acidosis - Sodium bicarbonate injection may be added to other IV fluids. The amount of bicarbonate to be given to older children and adults over a 4- to 8-hour period is approximately 2 to 5 mEq/kg, depending on the severity of the acidosis as judged by the lowering of total CO2 content, blood pH, and clinical condition. Initially, an infusion of 2 to 5 mEq/kg over 4 to 8 hours will produce improvement in the acid-base status of the blood. 

Acid-base and electrolyte balance High therapeutic dose especially when used in rheumatic fever, stimulates respiration and causes respiratory alkalosis. Reduction in bicarbonate and potassium level reduces the buffering capacity of the extracellular and intracellular fluid. Hypokalemia may lead to dehydration and hypernatremia. They also interfere with carbohydrate metabolism resulting in accumulation of pyruvic acid and lactic acid. 

It is not yet clear which estimates of the ratio between the levels of protein and of carbohydrate metabolism during hypoxia should be regarded as reliable. It seems likely that the increase in respiratory quotient in freshwater fish to values of 2.5-2.8, as found by Mohamed and Kutty (1983a, 1986), indicates a predominance of protein expenditure over that of carbohydrate. A hypoxic environment shifts the acid-base balance of the fish towards acidosis (Kotsar, 1976), thereby inducing the redistribution of electrolytes, alteration of ion exchange and the activity of Na+-K+-Mg2+-ATPases and alkaline phosphatases. It also leads to an increased level of C02 in the blood, which enhances the bicarbonate buffer system (Kotsar, 1976). In section 2.1, we... 

We see that dihydrogenphosphate will not react with bicarbonate in an acid-base reaction. This also means they are compatible with each other in solution (e.g., blood). Whiles these ions serve other purposes, (e.g., dihydrogen phosphate is the inorganic phosphate in metabolism), both of these ions have acid-base properties and they assist us in maintaining a constant pH. 

In early cardiac arrest, adequate alveolar ventilation is the primary means of limiting carbon dioxide accumulation and controlling the acid base imbalance. With arrests of long duration, buffer therapy is often necessary. Sodium bicarbonate administration for cardiac arrest is controversial because there are few clinical data supporting its use, and it may have some detrimental effects. Sodium bicarbonate can be used in special circumstances (i.e., underlying metabolic acidosis, hyperkalemia, salicylate overdose, or tricychc antidepressant overdose). The dosage should be guided by laboratory analysis if possible. 

Acid-base disturbance. Alkalosis or mixed alkalosis/ acidosis need no specific treatment. Metabolic acidosis is treated with sodium bicarbonate, which alkalinises the urine and accelerates the removal of salicylate in the urine (see p. 97). 

Acid-base disorders Initial metabolic alkalosis (resulting from decreased urea synthesis with reduced bicarbonate consumption) may be superimposed by respiratory alkalosis as an outcome of disorders in lung function. During the further course, metabolic acidosis (with renal insufficiency) and respiratory acidosis (with pulmonary insufficiency) can be expected. In advanced or severe stages of the disease, lactate acidosis may develop in some 50% of all comatose patients owing to restricted gluconeogenesis. 

A woman developed a severe metabolic acidosis and coma after taking nalidixic acid 28 g (14). She was given sodium bicarbonate 600 mmol and developed a respiratory alkalosis with secondary tetany. She recovered consciousness 9 hours later and the acid-base disturbance resolved after 60 hours. 

There is no specific antidote. Supportive care should be instituted for all patients with history of serious boric acid exposure. Substantial recent ingestions may benefit from administration of activated charcoal. Fluid and electrolyte balance, correction of acid/base disturbance, and control of seizures are essential to therapy. Hemodialysis has been successfully used to treat acute boric acid poisoning. Sodium bicarbonate may be used for any metabolic acidosis. 

A description of acid-base balance involves an accounting of the carbonic (H2C03, HCOh COa", and CO2) and noncar-bonic acids and conjugate bases in terms of input (intake plus metabolic production) and output (excretion plus metabolic conversion) over a given time interval. The acid-base status of the body fluids is typically assessed by measurements of total CO2 plasma pH and PCO2, because the bicarbonate/carbonic acid system is the most important buffering system of the plasma. Occasionally, measurement of total titratable acid or base, or other acid and base analytes (e.g., lactate and ammonia [NH3]) is necessary to determine the etiology of an acid-base disorder. 

Most metabolic acid-base disorders develop slowly, within hours in diabetic ketoacidosis and months or even years in chronic renal disease. The respiratory system responds immediately to a change in acid-base status, but several hours maybe required for the response to become maximal. The maximum response is not attained until both the central and peripheral chemoreceptors are fully stimulated. For example, in the early stages of metabolic acidosis, plasma pH decreases, but because H ions equilibrate rather slowly across the blood-brain barrier, the pH in CSF remains nearly normal. However, because peripheral chemoreceptors are stimulated by the decreased plasma pH, hyperventilation occurs, and plasma PCO2 decreases. When this occurs, the PCO2 of the CSF decreases immediately because CO2 equilibrates rapidly across the blood-brain barrier, leading to a rise in the pH of the CSF. This will inhibit the central chemoreceptors. But as plasma bicarbonate gradually falls because of acidosis, bicarbonate concentration and pH in the CSF wih also fall over several hours. At this point, stimulation of respiration becomes maximal as both the central and peripheral chemoreceptors are maximally stimulated. 

Metabolic acidosis is readily detected by decreased plasma bicarbonate (or a negative extracellular base excess), the primary perturbation in this acid-base disorder. Bicarbonate is lost in the buffering of excess acid. Causes include the foUowing ... 

Carbonic acid represents the respiratory component of the buffer pair because its concentration is directly proportional to the PCO2, which is determined by ventilation. Bicarbonate represents the metabolic component because the kidney may alter its concentration by reabsorption, generating new bicarbonate, or altering elimination. The bicarbonate buffer system easily adapts to changes in acid-base status by alterations in ventilatory elimination of acid (PCO2) and/or renal elimination of base (HCO3). 

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