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.
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.
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.
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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