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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 Renal dialysis 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: May exhibit: Diarrhea Dark/concentrated urine
May report: Anorexia, nausea/vomiting
cholestyramine (Questran) 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 Discharge plan considerations: DIAGNOSTIC STUDIES Arterial pH: Decreased.35. confusion.. e. . Achieve homeostasis. 4. Physiological balance restored. muscle weakness RESPIRATION May report: May exhibit: Dyspnea on exertion Hyperventilation. rapid breathing) SAFETY May report: May exhibit: Transfusion of blood/blood products Exposure to hepatitis virus Fever. the following interventions are presented in a general format for inclusion in the primary plan of care. NURSING PRIORITIES 1. ECG: Cardiac dysrhythmias (bradycardia) and pattern changes associated with hyperkalemia. Plasma lactic acid: Elevated in lactic acidosis. 3. Anion gap: Higher than 14 mEq/L (high anion gap) or range of 10–14 mEq/L (normal anion gap). 2. Urine pH: Decreased.. Base excess: Negative. delirium.g. 2. Serum glucose: May be decreased or increased depending on etiology. and treatment needs understood. decreased mental function Changes in sensorium. depression. Free of complications. dry mucous membranes NEUROSENSORY May report: May exhibit: Headache. e. tall T wave.5 (in absence of renal disease). coma Decreased deep-tendon reflexes. DISCHARGE GOALS 1. less than 22 mEq/L. prognosis.g. less than 4. Prevent/minimize complications. Kussmaul’s respirations (deep.. alcohol intoxication.g. starvation. less than 7. Bicarbonate (HCO3): Decreased. Serum chloride: Increased. PaCO2: Less than 35 mm Hg. e. Plan in place to meet needs after discharge Because no current nursing diagnosis speaks clearly to metabolic imbalances. drowsiness.May exhibit: Poor skin turgor. Serum potassium: Increased (except in diarrhea. 3. signs of sepsis TEACHING/LEARNING History of alcohol abuse Use of carbonic anhydrase inhibitors or anion-exchange resins. Condition. Provide information about condition/prognosis and treatment needs as appropriate. lethargy. stupor. Serum ketones: Increased in DM. renal tubular acidosis).
. confusion.. Marked dehydration may be present because of vomiting. effects of hypotension.. frequent observation. e. and decreased pH of CNS fluid. strength.g. weakness.g. Monitor I&O closely and weigh daily. diarrhea. and colic) may occur. Assess skin temperature.. Transient respiratory depression may be the result of overcorrection of metabolic acidosis with sodium bicarbonate.. Assess LOC and note progressive changes in neuromuscular status. In the presence of coexisting hyperkalemia. Auscultate bowel sounds. Note: Hypokalemia can occur as acidosis is corrected. color. Observe for altered respiratory excursion. ketoacidosis) occur.g. flaccid paralysis can occur because of hypoxia. Life-threatening cardiovascular collapse may also occur because of vasodilation and decreased cardiac contractility. hyperkalemia. . Therapy needs are based on underlying cause and fluid balance. rate. capillary refill. resulting in premature ventricular contractions (PVCs)/ventricular tachycardia. Be free of symptoms of imbalance. as potassium shifts out of cell in an attempt to correct acidosis. use of side rails. respirations may become depressed. ACTIONS/INTERVENTIONS Acid-Base Management: Metabolic Acidosis (NIC) RATIONALE Independent Monitor BP. sepsis) and hypovolemia (e. vital signs WNL. Evaluates circulatory status. measure abdominal girth as indicated. e. and depth. diarrhea. resulting in systemic shock. GI distress (e. distension. Monitor heart rate/rhythm. tone.. Arteriolar dilation/decreased cardiac contractility (e. movement. Protects patient from injury resulting from decreased mentation/convulsions.g. rapid respirations (Kussmaul’s) may be noted as a compensatory mechanism to eliminate excess acid. tissue perfusion. absence of neurological impairment. Provide seizure/coma precautions. evidenced by hypotension and tissue hypoxia.DESIRED OUTCOMES/EVALUATION CRITERIA—PATIENT WILL: Electrolyte & Acid/Base Balance (NOC) Display serum bicarbonate and electrolytes within normal limits (WNL).g. seizures.g. Decreased mental function. however. 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). e. bed in low position. Deep.
sepsis) promotes correction of the acid-base disorder.. whereas addition of complex carbohydrates will correct acid production from the metabolism of fats. Administer exchange resins and/or assist with dialysis as indicated. DKA.g.1 and other therapies are ineffective or HF develops. Calcium. As acidosis is corrected. Phosphate. May be required as potassium re-enters the cell.2) because sodium bicarbonate can cause rebound metabolic alkalosis.g.g. Modify diet as indicated.ACTIONS/INTERVENTIONS Acid-Base Management: Metabolic Acidosis (NIC) RATIONALE Independent Test/monitor urine pH. D5W/saline solutions. Independent Administer medications as indicated. Monitor/graph serial ABGs. but is used cautiously to correct severe acidosis (pH less than 7. Note: Lactate-containing solutions may be containdicated in the presence of lactic acidosis. Corrects bicarbonate deficit. Choice of solution varies with cause of acidosis. Restriction of protein may be necessary to decrease production of acid waste products. e. drug poisoning. May be given to improve neuromuscular conduction/function.0. . potassium. e. Evaluates therapy needs/effectiveness. e. causing a serum deficit. Neutralizes mouth acids and provides protective lubrication. e. Blood bicarbonate and pH should slowly increase toward normal levels. May be administered to enhance acid excretion in presence of chronic acidosis with hypophosphatemia. highcarbohydrate diet in presence of renal failure or American Diabetes Association (ADA) diet for the person with diabetes. Monitor serum electrolytes. DKA. lemon/glycerine swabs. Addressing the primary condition (e. liver/renal failure.: Sodium bicarbonate/lactate or saline IV.. Kidneys attempt to compensate for acidosis by excreting excess hydrogen in the form of weak acids and ammonia. Provide oral hygiene with sodium bicarbonate washes. May be desired to reduce acidosis by decreasing excess potassium and acid waste products if pH less than 7. serum potassium deficit may occur as potassium shifts back into the cells... as indicated depending on underlying etiology. Collaborative Assist with identification/treatment of underlying cause. low-protein. e.. Potassium chloride.g.g. Replace fluids. Maximum urine acidity is pH of 4.g. Treatment of disorder is directed at mild correction of acidosis until organ(s) function is improved.
.POTENTIAL CONSIDERATIONS: Refer to Potential Considerations relative to underlying cause of acid-base disorder.
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