Chloride (Cl, Cl²) is the most abundant anion in extracellular fluid. It participates with sodium in the maintenance of water balance and aids in the regulation of osmotic pressure. It also contributes to gastric acid (HCl) for digestion and for activation of enzymes. Its most important function is in the maintenance of acid-base balance. In certain forms of metabolic acidosis, for example, serum chloride levels may rise in response to decreased serum bicarbonate levels; this condition is known as hyperchloremic acidosis. If bicarbonate levels fall and serum chloride concentration remains relatively normal, however, a gap between measured cations (i.e., sodium and potassium) and measured anions (i.e., chloride and bicarbonate) occurs. This condition often is called anion gap acidosis (see also section titled "Anion Gap," which follows).

Chloride also helps to maintain acid-base balance through the chloride-bicarbonate shift mechanism, in which chloride ions enter red blood cells in exchange for bicarbonate. Bicarbonate leaves the red blood cells in response to carbon dioxide, which is released from the tissues into venous blood and absorbed into the red blood cells. The carbon dioxide is subsequently converted into carbonic acid, which dissociates into bicarbonate and hydrogen ions. When the bicarbonate concentration in the red blood cells exceeds that of the plasma, bicarbonate diffuses into the blood, and chloride enters the red blood cells to supply the anions necessary for electroneutrality. For this reason, the chloride content of red blood cells in venous blood is slightly higher than that of arterial red blood cells.

Numerous disorders and drugs may alter serum chloride levels (Table 5-24).

• Drugs such as potassium chloride, ammonium chloride, acetazolamide (Diamox), methyldopa (Aldomet), diazoxide (Hyperstat), and guanethidine (Ismelin) may lead to elevated levels.
• Drugs such as ethacrynic acid (Edecrin), furosemide (Lasix), thiazide diuretics, and bicarbonate may lead to decreased levels.

• Routine electrolyte screening in acute and critical illness
• Known or suspected disorder associated with altered acid-base or fluid and electrolyte balance, or both conditions
• Support for diagnosing disorders associated with altered serum chloride levels (see Table 5-24)
• Differentiation of the type of acidosis (hyperchloremic versus anion gap acidosis), with serum chloride levels remaining relatively normal in anion gap acidosis
• Evaluation of the effects of drug therapy on serum chloride levels (see Table 5-24)

Nursing Care Before the Procedure

Client preparation is the same as that for any study involving collection of a peripheral blood sample (see Appendix I).

• Because many drugs may alter serum chloride levels, a medication history should be obtained. It is recommended that those drugs that may alter test results be withheld for 12 to 24 hours before the test, although this practice should be confirmed with the person ordering the study.

A venipuncture is performed and the sample collected in a red-topped tube. The sample should be handled gently to avoid hemolysis and transported promptly to the laboratory.

Nursing Care After the Procedure

Care and assessment after the procedure are the same as for any study involving the collection of a peripheral blood sample.

• Resume any medications withheld before the test.
• Increased levels: Note and report increased levels (hyperchloremia) in relation to increased sodium and decreased bicarbonate, and assess for changes in chloride caused by or resulting in metabolic acidosis.
• Decreased levels: Note and report decreased levels (hypochloremia). Assess for possible cause (vomiting, gastric suction, diarrhea, diuretic medication regimen, chronic lung disease, increased bicarbonate and decreased potassium resulting in metabolic alkalosis).
• Critical values: Notify the physician at once of levels less than 80 mEq/L or greater than 115 mEq/L.