The body has the remarkable ability to maintain plasma pH within the narrow range of 7.35–7.45. It does so by means of chemical buffering mechanisms by the kidneys and the lungs. Although single acid-base (e.g., metabolic acidosis) imbalances do occur, mixed acid-base imbalances are more common (e.g., metabolic acidosis/respiratory acidosis as occurs with cardiac arrest).
METABOLIC ACIDOSIS (PRIMARY BASE BICARBONATE [HCO3] DEFICIENT)
Metabolic acidosis (primary base bicarbonate [HCO3] deficiency) reflects an excess of acid (hydrogen) and a deficit of base (bicarbonate) resulting from acid overproduction, loss of intestinal bicarbonate, inadequate conservation of bicarbonate, and excretion of acid, or anaerobic metabolism. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium.
High anion gap acidosis occurs in diabetic ketoacidosis; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl.
Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/diarrhea, small-bowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride).
CARE SETTING
This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit.
RELATED CONCERNS
Plans of care specific to predisposing factors
Fluid and electrolyte imbalances
Renal dialysis
Respiratory acidosis (primary carbonic acid excess)
Respiratory alkalosis (primary carbonic acid deficit)
Patient Assessment Database (Dependent on Underlying Cause)
ACTIVITY/REST
May report: Lethargy, fatigue; muscle weakness
CIRCULATION
May exhibit: Hypotension, wide pulse pressure
Pulse may be weak, irregular (dysrhythmias)
Jaundiced sclera, skin, mucous membranes (liver failure)
ELIMINATION
May report: Diarrhea
May exhibit: Dark/concentrated urine
FOOD/FLUID
May report: Anorexia, nausea/vomiting
May exhibit: Poor skin turgor, dry mucous membranes
NEUROSENSORY
May report: Headache, drowsiness, decreased mental function
May exhibit: Changes in sensorium, e.g., stupor, confusion, lethargy, depression, delirium, coma
Decreased deep-tendon reflexes, muscle weakness
RESPIRATION
May report: Dyspnea on exertion
May exhibit: Hyperventilation, Kussmaul’s respirations (deep, rapid breathing)
SAFETY
May report: Transfusion of blood/blood products
Exposure to hepatitis virus
May exhibit: Fever, signs of sepsis
TEACHING/LEARNING
History of alcohol abuse
Use of carbonic anhydrase inhibitors or anion-exchange resins, e.g., cholestyramine
(Questran)
Discharge plan
DRG projected mean length of inpatient stay depends on underlying cause
May require change in therapies for underlying disease process/condition
Refer to section at end of plan for postdischarge considerations
DIAGNOSTIC STUDIES
Arterial pH: Decreased, less than 7.35.
Bicarbonate (HCO3): Decreased, less than 22 mEq/L.
PaCO2: Less than 35 mm Hg.
Base excess: Negative.
Anion gap: Higher than 14 mEq/L (high anion gap) or range of 10–14 mEq/L (normal anion gap).
Serum potassium: Increased (except in diarrhea, renal tubular acidosis).
Serum chloride: Increased.
Serum glucose: May be decreased or increased depending on etiology.
Serum ketones: Increased in DM, starvation, alcohol intoxication.
Plasma lactic acid: Elevated in lactic acidosis.
Urine pH: Decreased, less than 4.5 (in absence of renal disease).
ECG: Cardiac dysrhythmias (bradycardia) and pattern changes associated with hyperkalemia, e.g., tall T wave.
NURSING PRIORITIES
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
DISCHARGE GOALS
1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.
4. Plan in place to meet needs after discharge
Because no current nursing diagnosis speaks clearly to metabolic imbalances, the following interventions are presented in a general format for inclusion in the primary plan of care.
METABOLIC ACIDOSIS (PRIMARY BASE BICARBONATE [HCO3] DEFICIENT)
Metabolic acidosis (primary base bicarbonate [HCO3] deficiency) reflects an excess of acid (hydrogen) and a deficit of base (bicarbonate) resulting from acid overproduction, loss of intestinal bicarbonate, inadequate conservation of bicarbonate, and excretion of acid, or anaerobic metabolism. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium.
High anion gap acidosis occurs in diabetic ketoacidosis; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl.
Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/diarrhea, small-bowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride).
CARE SETTING
This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit.
RELATED CONCERNS
Plans of care specific to predisposing factors
Fluid and electrolyte imbalances
Renal dialysis
Respiratory acidosis (primary carbonic acid excess)
Respiratory alkalosis (primary carbonic acid deficit)
Patient Assessment Database (Dependent on Underlying Cause)
ACTIVITY/REST
May report: Lethargy, fatigue; muscle weakness
CIRCULATION
May exhibit: Hypotension, wide pulse pressure
Pulse may be weak, irregular (dysrhythmias)
Jaundiced sclera, skin, mucous membranes (liver failure)
ELIMINATION
May report: Diarrhea
May exhibit: Dark/concentrated urine
FOOD/FLUID
May report: Anorexia, nausea/vomiting
May exhibit: Poor skin turgor, dry mucous membranes
NEUROSENSORY
May report: Headache, drowsiness, decreased mental function
May exhibit: Changes in sensorium, e.g., stupor, confusion, lethargy, depression, delirium, coma
Decreased deep-tendon reflexes, muscle weakness
RESPIRATION
May report: Dyspnea on exertion
May exhibit: Hyperventilation, Kussmaul’s respirations (deep, rapid breathing)
SAFETY
May report: Transfusion of blood/blood products
Exposure to hepatitis virus
May exhibit: Fever, signs of sepsis
TEACHING/LEARNING
History of alcohol abuse
Use of carbonic anhydrase inhibitors or anion-exchange resins, e.g., cholestyramine
(Questran)
Discharge plan
DRG projected mean length of inpatient stay depends on underlying cause
May require change in therapies for underlying disease process/condition
Refer to section at end of plan for postdischarge considerations
DIAGNOSTIC STUDIES
Arterial pH: Decreased, less than 7.35.
Bicarbonate (HCO3): Decreased, less than 22 mEq/L.
PaCO2: Less than 35 mm Hg.
Base excess: Negative.
Anion gap: Higher than 14 mEq/L (high anion gap) or range of 10–14 mEq/L (normal anion gap).
Serum potassium: Increased (except in diarrhea, renal tubular acidosis).
Serum chloride: Increased.
Serum glucose: May be decreased or increased depending on etiology.
Serum ketones: Increased in DM, starvation, alcohol intoxication.
Plasma lactic acid: Elevated in lactic acidosis.
Urine pH: Decreased, less than 4.5 (in absence of renal disease).
ECG: Cardiac dysrhythmias (bradycardia) and pattern changes associated with hyperkalemia, e.g., tall T wave.
NURSING PRIORITIES
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
DISCHARGE GOALS
1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.
4. Plan in place to meet needs after discharge
Because no current nursing diagnosis speaks clearly to metabolic imbalances, the following interventions are presented in a general format for inclusion in the primary plan of care.
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