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Chapter: Medical Surgical Nursing: Fluid and Electrolytes: Balance and Distribution

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Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit)

Metabolic acidosis is a clinical disturbance characterized by a low pH (increased H+ concentration) and a low plasma bicar-bonate concentration.

ACUTE AND CHRONIC METABOLIC ACIDOSIS (BASE BICARBONATE DEFICIT)

Metabolic acidosis is a clinical disturbance characterized by a low pH (increased H+ concentration) and a low plasma bicar-bonate concentration. It can be produced by a gain of hydrogen ion or a loss of bicarbonate (Swenson, 2001). It can be divided clinically into two forms, according to the values of the serum anion gap: high anion gap acidosis and normal anion gap aci-dosis. The anion gap reflects normally unmeasured anions (phosphates, sulfates, and proteins) in plasma. Measuring the anion gap is essential in analyzing acid–base disorders correctly. The anion gap can be calculated by either one of the following equations:

 

Anion gap = Na++ K+ (Cl+ HCO3)

Anion gap = Na+ (Cl+ HCO3)

 

Potassium is often omitted from the equation because of its low level in the plasma; thus, the second equation is used more often than the first.

 

The normal value for an anion gap is 8 to 12 mEq/L (8–12 mmol/L) without potassium in the equation. The normal value for the anion gap if including potassium in the equation is 12 to 16 mEq/L (12–16 mmol/L). The unmeasured anions in the serum normally account for less than 16 mEq/L of the anion pro-duction. An anion gap greater than 16 mEq (16 mmol/L) sug-gests excessive accumulation of unmeasured anions. An anion gap occurs because not all electrolytes are measured. More anions are left unmeasured than cations.

 

Normal anion gap acidosis results from the direct loss of bicar-bonate, as in diarrhea, lower intestinal fistulas, ureterostomies, and use of diuretics; early renal insufficiency; excessive administration of chloride; and the administration of parenteral nutrition with-out bicarbonate or bicarbonate-producing solutes (eg, lactate).Normal anion gap acidosis is also referred to as hyperchloremic acidosis. A reduced or negative anion gap is primarily caused by hypoproteinemia. Disorders that cause a decreased or negative anion gap are rare compared to those related to an increased or high anion gap (Rose & Post, 2001).

 

High anion gap acidosis results from excessive accumulation of fixed acid. If it is increased to 30 mEq/L (30 mmol/L) or more, then a high anion gap metabolic acidosis is present regardless of what the pH and the HCO3 are. High ion gap occurs in ke-toacidosis, lactic acidosis, the late phase of salicylate poisoning, uremia, methanol or ethylene glycol toxicity, and ketoacidosis with starvation. The hydrogen is buffered by HCO3, causing the bicarbonate concentration to fall. In all of these instances, ab-normally high levels of anions flood the system, increasing the anion gap above normal limits.

Clinical Manifestations

Signs and symptoms of metabolic acidosis vary with the severity of the acidosis. They may include headache, confusion, drowsi-ness, increased respiratory rate and depth, nausea, and vomiting. Peripheral vasodilation and decreased cardiac output occur when the pH falls below 7. Additional physical assessment findings in-clude decreased blood pressure, cold and clammy skin, dysrhyth-mias, and shock (Swenson, 2001).

 

Chronic metabolic acidosis is usually seen with chronic renal failure. The bicarbonate and pH decrease slowly; thus, the patient is asymptomatic until the bicarbonate is approximately 15 mEq/L or less.

Assessment and Diagnostic Findings

 

Arterial blood gas measurements are valuable in diagnosing meta-bolic acidosis (Swenson, 2001). Expected blood gas changes in-clude a low bicarbonate level (less than 22 mEq/L) and a low pH (less than 7.35). The cardinal feature of metabolic acidosis is a de-crease in the serum bicarbonate level. Hyperkalemia may accom-pany metabolic acidosis as a result of the shift of potassium out of the cells. Later, as the acidosis is corrected, potassium moves back into the cells and hypokalemia may occur. Hyperventilation decreases the CO2 level as a compensatory action. As stated pre-viously, calculation of the anion gap is helpful in determining the cause of metabolic acidosis. An ECG will detect dysrhythmias caused by the increased potassium.

Medical Management

Treatment is directed at correcting the metabolic defect (Swen-son, 2001). If the problem results from excessive intake of chlo-ride, treatment is aimed at eliminating the source of the chloride. When necessary, bicarbonate is administered if the pH is less than 7.1 and the bicarbonate level is less than 10. Al-though hyperkalemia occurs with acidosis, hypokalemia may occur with reversal of the acidosis and subsequent movement of potassium back into the cells. Therefore, the serum potassium level is monitored closely and hypokalemia is corrected as aci-dosis is reversed.

 

In chronic metabolic acidosis, low serum calcium levels are treated before treating chronic metabolic acidosis to avoid tetany resulting from an increase in pH and a decrease in ionized cal-cium. Alkalyzing agents may be given if the serum bicarbonate level is less than 12 mEq/L. Treatment modalities may also in-clude hemodialysis or peritoneal dialysis.

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