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Metabolic Acid_base Imbalances

Metabolic Acid_base Imbalances

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Published by Cay Sevilla

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Published by: Cay Sevilla on Jan 27, 2010
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05/19/2012

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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 meansof 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 asoccurs with cardiac arrest).
METABOLIC ACIDOSIS (PRIMARY BASE BICARBONATE [HCO
3
]DEFICIENT)
Metabolic acidosis
(primary base bicarbonate [HCO
3
] 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 highanion 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 (suchas ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct thisimbalance include an increase in respirations to blow off excess CO
2
, an increase in ammonia formation, and acidexcretion (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 initialstage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH
4
Cl. 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 sodiumchloride 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 inpatientcare in a medical-surgical or subacute unit.
RELATED CONCERNS
Plans of care specific to predisposing factorsFluid and electrolyte imbalancesRenal dialysisRespiratory 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 pressurePulse 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, comaDecreased 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 productsExposure to hepatitis virus
May exhibit:
Fever, signs of sepsis
TEACHING/LEARNING
History of alcohol abuseUse 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
DIAGNOSTIC STUDIES
 Arterial pH:
Decreased, less than 7.35.
 Bicarbonate (HCO
3
 ):
Decreased, less than 22 mEq/L.
 Pa
CO
2
:
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 arepresented 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.
 
ACTIONS/INTERVENTIONS
Acid-Base Management: Metabolic Acidosis(NIC)
Independent
Monitor BP.Assess LOC and note progressive changes inneuromuscular 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 asindicated.Monitor I&O closely and weigh daily.
 
RATIONALE
Arteriolar dilation/decreased cardiac contractility (e.g.,sepsis) and hypovolemia (e.g., ketoacidosis) occur,resulting in systemic shock, evidenced by hypotensionand 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 decreasedmentation/convulsions.Acidemia may be manifested by changes in ECGconfiguration and presence of bradydysrhydythmias aswell as increased ventricular irritability such asfibrillation (signs of hyperkalemia). Life-threateningcardiovascular collapse may also occur because of vasodilation and decreased cardiac contractility.
 Note:
 Hypokalemia can occur as acidosis is corrected, resultingin premature ventricular contractions (PVCs)/ventricular tachycardia.Deep, rapid respirations (Kussmaul’s) may be noted as acompensatory mechanism to eliminate excess acid;however, as potassium shifts out of cell in an attempt tocorrect 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 causeand fluid balance.

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