METABOLIC ACID-BASE IMBALANCES
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).
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.
Plans of care specific to predisposing factors
Fluid and electrolyte imbalances
Respiratory acidosis (primary carbonic acid excess)
Respiratory alkalosis (primary carbonic acid deficit)
Patient Assessment Database (Dependent on Underlying Cause)
May report: Lethargy, fatigue; muscle weakness
May exhibit: Hypotension, wide pulse pressure
Pulse may be weak, irregular (dysrhythmias)
Jaundiced sclera, skin, mucous membranes (liver failure)
May report: Diarrhea
May exhibit: Dark/concentrated urine
May report: Anorexia, nausea/vomiting
May exhibit: Poor skin turgor, dry mucous membranes
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
May report: Dyspnea on exertion
May exhibit: Hyperventilation, Kussmaul’s respirations (deep, rapid breathing)
May report: Transfusion of blood/blood products
Exposure to hepatitis virus
May exhibit: Fever, signs of sepsis
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
considerations: May require change in therapies for underlying disease process/condition
Refer to section at end of plan for postdischarge considerations
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.
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
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.
DESIRED OUTCOMES/EVALUATION CRITERIA—PATIENT WILL:
Electrolyte & Acid/Base Balance (NOC)
Display serum bicarbonate and electrolytes within normal limits (WNL).
Be free of symptoms of imbalance, e.g., absence of neurological impairment; vital signs WNL.
Acid-Base Management: Metabolic Acidosis (NIC)
Assess LOC and note progressive changes in neuromuscular status, e.g., strength, tone, movement.
Provide seizure/coma precautions, e.g., bed in low position, use of side rails, frequent observation.
Monitor heart rate/rhythm.
Observe for altered respiratory excursion, rate, and depth.
Assess skin temperature, color, capillary refill.
Auscultate bowel sounds; measure abdominal girth as indicated.
Monitor I&O closely and weigh daily.
Arteriolar dilation/decreased cardiac contractility (e.g., sepsis) and hypovolemia (e.g., ketoacidosis) occur, resulting in systemic shock, evidenced by hypotension and tissue hypoxia.
Decreased mental function, confusion, seizures, weakness, flaccid paralysis can occur because of hypoxia, hyperkalemia, and decreased pH of CNS fluid.
Protects patient from injury resulting from decreased mentation/convulsions.
Acidemia may be manifested by changes in ECG configuration and presence of bradydysrhydythmias as well as increased ventricular irritability such as fibrillation (signs of hyperkalemia). Life-threatening cardiovascular collapse may also occur because of vasodilation and decreased cardiac contractility. Note: Hypokalemia can occur as acidosis is corrected, resulting in premature ventricular contractions (PVCs)/ventricular tachycardia.
Deep, rapid respirations (Kussmaul’s) may be noted as a compensatory mechanism to eliminate excess acid; however, as potassium shifts out of cell in an attempt to correct acidosis, respirations may become depressed. Transient respiratory depression may be the result of overcorrection of metabolic acidosis with sodium bicarbonate.
Evaluates circulatory status, tissue perfusion, effects of hypotension.
In the presence of coexisting hyperkalemia, GI distress (e.g., distension, diarrhea, and colic) may occur.
Marked dehydration may be present because of vomiting, diarrhea. Therapy needs are based on underlying cause and fluid balance.
Acid-Base Management: Metabolic Acidosis (NIC)
Test/monitor urine pH.
Provide oral hygiene with sodium bicarbonate washes, lemon/glycerine swabs.
Assist with identification/treatment of underlying cause.
Monitor/graph serial ABGs.
Monitor serum electrolytes, e.g., potassium.
Replace fluids, as indicated depending on underlying etiology, e.g., D5W/saline solutions.
Administer medications as indicated, e.g.:
Sodium bicarbonate/lactate or saline IV;
Modify diet as indicated, e.g., low-protein, high-carbohydrate diet in presence of renal failure or American Diabetes Association (ADA) diet for the person with diabetes.
Administer exchange resins and/or assist with dialysis as indicated.
Kidneys attempt to compensate for acidosis by excreting excess hydrogen in the form of weak acids and ammonia. Maximum urine acidity is pH of 4.0.
Neutralizes mouth acids and provides protective lubrication.
Treatment of disorder is directed at mild correction of acidosis until organ(s) function is improved. Addressing the primary condition (e.g., DKA, liver/renal failure, drug poisoning, sepsis) promotes correction of the acid-base disorder.
Evaluates therapy needs/effectiveness. Blood bicarbonate and pH should slowly increase toward normal levels.
As acidosis is corrected, serum potassium deficit may occur as potassium shifts back into the cells.
Choice of solution varies with cause of acidosis, e.g., DKA. Note: Lactate-containing solutions may be containdicated in the presence of lactic acidosis.
Corrects bicarbonate deficit, but is used cautiously to correct severe acidosis (pH less than 7.2) because sodium bicarbonate can cause rebound metabolic alkalosis.
May be required as potassium re-enters the cell, causing a serum deficit.
May be administered to enhance acid excretion in presence of chronic acidosis with hypophosphatemia.
May be given to improve neuromuscular conduction/function.
Restriction of protein may be necessary to decrease production of acid waste products, whereas addition of complex carbohydrates will correct acid production from the metabolism of fats.
May be desired to reduce acidosis by decreasing excess potassium and acid waste products if pH less than 7.1 and other therapies are ineffective or HF develops.
POTENTIAL CONSIDERATIONS: Refer to Potential Considerations relative to underlying cause of acid-base disorder.