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Etiology: There are many causes of primary metabolic acidosis and they are commonly classified by the anion gap:
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The ideal treatment for metabolic acidosis is correction of the underlying cause. When urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. The best measure of the level of metabolic acidosis is the Standard Base Excess (SBE) because it is independent of PCO2. If it is decided to administer bicarbonate, the SBE and the size of the treatable space are used to calculate the dose required:
Etiology: Primary Metabolic alkalosis may occur from various causes including:
Prolonged Metabolic Alkalosis may be caused by a number of different mechanisms:
Physiological Response: Adequate hydration normally allows the kidneys to correct the problem. However, in severe cases accompanied by hypokalemia, correction of the hypokalemia may be necessary first.
As with metabolic acidosis, ideal treatment is the correction of the underlying abnormality. More active intervention is occasionally required and various techniques are available. A common transient cause is iatrogenic; correction of acute metabolic acidosis with sodium bicarbonate leaves a residual metabolic alkalosis. Time, hydration, and renal function should gradually correct this.
Contraction alkalosis is one of the easier causes to understand and treat. Dehydration concentrates the body's electrolytes. As the extracellular fluid (pH = 7.4) is on the alkaline side of neutral (pH = 6.8), the relative alkaline mixture of electrolytes is concentrated and shifts the pH to more alkaline value. Rehydration, e.g., with oral fluids or intravenous Ringer's lactate, restores the normal electrolyte concentration and, therefore, the pH.
Other therapies: Intravenous dilute hydrochloric acid is occasionally used but carries the risk of hemolysis. Potassium chloride may also be used unless there is kidney failure. In severe cases which are unresponsive to other measures ammonium chloride may be given (1 to 2 g orally every 4 to 6 hours up to 4 g every 2 hours. It may also given by intravenous infusion (100 to 200 mEq dissolved in 500 to 1000 ml of isotonic saline) in addition to potassium replacement. In severe unresponsive metabolic alkalosis it may be necessary to administer hydrochloric acid or institute peritoneal dialysis.
Specific therapy depends on the underlying pathology. For details visit: E-Medicine (Christie Thomas).
The body's metabolism produces respiratory (carbonic) acid and, in ischemia or cardiorespiratory failure, metabolic (lactic) acid. In emergencies, therefore, urgent correction is most commonly required for metabolic or respiratory acidosis.
The diagram shows an example of a patient with a (pure) metabolic acidosis, SBE = -18 mEq/L. To achieve complete correction for someone weighing 70 kg:
This assumes that the treatable compartment is about 30% of the body, i.e., about 21 liters. Our intention , of course, is to normalize the "Bath Water", i.e., the extracellular fluid, which is 20% of the body (about 14 liters). But, because the injected bicarbonate also equilibrates to some extent with the intracellular fluid, the "treatable volume" is larger.
The full dose returns the metabolic disturbance to about zero. It is customary to give about half the dose which returns the metabolic disturbance about half way back towards normal, i.e., about half way to the zero line. In this case 189 mEq corrects the SBE to -9 mEq/L.
There are several reasons for caution about administering the full calculated dose of bicarbonate:
The bicarbonate is injected initially into the three liter plasma volume instead of the calculated 21 liters of treatable volume (it does not cross the cell membrane to enter the two liters of red cells.) At first, therefore, the dose hugely "over-treats" this small compartment.
When bicarbonate is added to acid it produces CO2 "bubbles". Fortunately, real "bubbles" are not produced in the blood stream. Nevertheless, this vivid picture serves a purpose. It reinforces our understanding: the majority of the injected bicarbonate is converted to carbon dioxide which must then be eliminated by an increase in ventilation.
This initial production of CO2 raises the PCO2 in the plasma and tends to causing relative respiratory acidosis. For each 100 mEq of bicarbonate which is converted, about 2.24 liters of carbon dioxide has to be exhaled, equivalent to ten minutes normal production.
The marked metabolic acidosis here is treated with half the calculated dose. This corrects the metabolic disturbance half way but produces a transient respiratory acidosis. Then, continuing ventilation eliminates the excess CO2 to reach a more modest level of partially compensated metabolic acidosis.
The carbon dioxide which is produced enters the cells freely, unlike the bicarbonate ions which have been administered. Therefore, the added PCO2 inside tends to cause the intracellular fluid to become more acid.
However, direct studies employing nuclear magnetic resonance indicate that this change may be insignificant (Severinghaus, Personal Communication 1986).
The residual effects of bicarbonate are all interelated. Nevetheless, it is helpful to consider them separately as it emphasizes the importance of caution when considering administering bicarbonate.
Sodium Ions: The injected bicarbonate ions are accompanied by sodium ions which will be responsible for a subsequent hypernatremia.
Osmolarity: The hypernatremia will increase the osmolarity of the extracellular fluid. In combination with other therapy, such as intravenous glucose, this hyperosmolarity may be critical and cause coma. In neonates, rapid infusion of bicarbonate may cause intracranial hemorrhage.
Metabolic Alkalosis: Once the underlying pathology causing the metabolic acidosis is corrected, then the bicarbonate therapy will be responsible for a residual iatrogenic metabolic alkalosis.
For all of the above reasons, bicarbonate therapy tends to be reserved for emergencies and situations where indications for therapy are compelling.
Alan W. Grogono
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