CHLORIDE EXCESS (HYPERCHLOREMIA)
Hyperchloremia exists when the serum level exceeds 106 mEq/L (106 mmol/L). Hypernatremia, bicarbonate loss, and metabolic acidosis can occur with high chloride levels. Hyperchloremic metabolic acidosis is also known as normal anion gap acidosis. It is usually caused by the loss of bicarbonate ions via the kidney or the GI tract with a corresponding increase in chloride ions. Chlo-ride ions in the form of acidifying salts accumulate and acidosis occurs with a decrease in bicarbonate ions.
The signs and symptoms of hyperchloremia are the same as those of metabolic acidosis, hypervolemia, and hypernatremia. Tachy-pnea; weakness; lethargy; deep, rapid respirations; diminished cognitive ability; and hypertension occur. If untreated, hyper-chloremia can lead to a decrease in cardiac output, dysrhythmias, and coma. A high chloride level is accompanied by a high sodium level and fluid retention.
The serum chloride level is 108 mEq/L (108 mmol/L) or greater, the serum sodium level is greater than 145 mEq/L (145 mmol/L), the serum pH is less than 7.35, the serum bicarbonate level is less than 22 mEq/L (22 mmol/L), and there is a normal anion gap of 8 to 12 mEq/L (8–12 mmol/L). Urine chloride excretion increases.
Calculation of the serum anion gap is important in analyzing acid–base disorders. The sum of all negatively charged electro-lytes (anions) equals the sum of all positively charged electrolytes (cations) with several anions that are not routinely measured lead-ing to an anion gap. It is based primarily on three electrolytes: sodium, chloride, and bicarbonate or serum CO2. A low aniongap may be attributed to hypoproteinemia, while an elevated anion gap can be due to metabolic acidosis.
Correcting the underlying cause of hyperchloremia and restoring electrolyte, fluid, and acid–base balance are essential. Lactated Ringer’s solution may be prescribed to convert lactate to bicar-bonate in the liver, which will increase the base bicarbonate level and correct the acidosis. Sodium bicarbonate may be given IV to increase bicarbonate levels, which leads to the renal excretion of chloride ions as bicarbonate and chloride compete for combina-tion with sodium. Diuretics may be administered to eliminate chloride as well. Sodium, fluids, and chloride are restricted.
Monitoring vital signs, arterial blood gas values, and intake and output is important to assess the patient’s status and the effec-tiveness of treatment. Assessment findings related to respiratory, neurologic, and cardiac systems are documented and changes dis-cussed with the physician. The nurse teaches the patient about the diet that should be followed to manage hyperchloremia.
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