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Metabolic Acidosis and Metabolic Alkalosis

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Metabolic Acidosis and Metabolic Alkalosis 43 Metabolic Acidosis and Metabolic Alkalosis Metabolic Acidosis ing patients. Metabolic alkalosis affects vital biochemical reactions in the body and oxygen delivery by shifting the Metabolic acidosis is caused by increased hydrogen ion oxyhemoglobin dissociation curve leftward (increased or bicarbonate loss. Acute compensation occurs via res- affinity). Hypokalemia induces an intracellular shift of piratory alkalosis. The greatest increase in minute venti- hydrogen ions, causing intracellular acidosis. This usually lation occurs because of lactic acidosis, which is one of reverses with correction of hypokalemia. Volume con- the most common causes of metabolic acidosis in surgi- traction causes a similar shift at the renal level in an cal patients. The initial step in evaluation and treatment attempt to preserve sodium and water. Gastrointestinal of metabolic acidosis is determination of the anion gap losses (nasogastric suction, vomiting) cause a combina- (AG), which is performed using the following equation: tion of hydrogen ion loss, volume contraction, and AG = [Na] − [Cl − HCO3]. The normal anion gap is 8 to hypokalemia, all of which contribute to metabolic 12mEq/L. Elevation of the AG is caused by methanol, alkalosis. Diuresis, either spontaneous or induced, uremia, diabetic ketoacidosis, paraldehyde, isoniazid, causes sodium and chloride losses with reabsorption of lactate accumulation, ethanol, ethylene glycol, and bicarbonate. Hypochloremic, hypokalemic metabolic salicylates. Normal gap acidosis is typically caused by alkalosis with paradoxical aciduria is sometimes seen in gastrointestinal losses, hyperchloremia, and renal tubular surgical patients. This is due to loss of gastric secretions acidosis. The base deficit can also be a marker of with resultant hypovolemia, hypokalemia, and hypo- acid–base status by reflecting the total amount of correc- chloremia. In an attempt to maintain euvolemia, the tion required to restore homeostasis. In the setting of kidney preserves sodium and frequently bicarbonate as lactic acidosis, it may be used as a marker of the degree its anion. Sodium reabsorption occurs at the expense of of hypoperfusion and in guiding resuscitation measures. hydrogen ions, thus acidifying the urine. The treatment of acidosis hinges on treating the The underlying causes must be corrected, particularly primary cause. For lactic acidosis caused by hypoperfu- hypokalemia and hypovolemia. Patients with metabolic sion, this involves correcting the source of volume loss alkalosis are classified as chloride responsive or chloride and administering crystalloid and/or blood products. For unresponsive. A determination of urinary chloride elevated gap acidosis, the treatment is supportive care predicts which treatment will be the most effective. with or without administration of sodium bicarbonate. Low urinary chloride indicates chloride depletion, which The use of bicarbonate in the setting of lactic acidosis should respond to saline, because there is frequently caused by hypoperfusion is detrimental in that it blunts concomitant volume deficit. High urinary chloride the respiratory compensation, leading to cellular acido- typifies chloride-resistant metabolic alkalosis. Treatment sis; it increases the affinity of hemoglobin for oxygen options include acetazolamide, ammonium chloride, and (shifting the dissociation curve leftward); and it elimi- hydrochloric acid administration. The latter condition is nates the utility of using the base deficit to measure the uncommon, but can be present in hyperadrenalism, either effectiveness of resuscitation. endogenous or exogenous. Metabolic Alkalosis Metabolic alkalosis is caused by a loss of hydrogen ions or by the accumulation of bicarbonate. The acute com- pensation is respiratory acidosis in spontaneously breath- 100.
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