Metabolic Alkalosis

Hypokalemia Contributing Factors

When potassium shifts out of cells to maintain extracellular potassium levels, hydrogen ions shift into the cells to maintain the balance between cations and anions within the cells. The kidneys try to conserve potassium through increased renal excretion, excreting hydrogen ions instead.

Plan for Discharge

When preparing the patient with metabolic alkalosis for discharge, consider the cause of the alkalosis and any underlying factors. For example, provide teaching to the patient and family about the following: • Using appropriate antacids for heartburn and gastric distress • Using potassium supplements as ordered or eating high-potassium foods to prevent hypokalemia if taking a potassium-wasting diuretic or if aldosterone production is impaired • Contacting the primary care provider if uncontrolled or extended vomiting develops.

Severe Alkalosis

an acidifying solution such as dilute hydrochloric acid or ammonium chloride may be administered. In addition, drugs may be used to treat the underlying cause of the alkalosis.

Laboratory and Diagnostic Tests

ABGs Serum Electrolytes Urine pH The ECG patter

Outcomes

Appropriate outcomes will include resolution of the underlying cause and the patient's return to: • Oxygen saturation level of 95% or greater. • Normal or near normal fluid and electrolyte volumes.

Monitor for Impaired Gas Exchange

As a result, the patient is at risk for impaired gas exchange, especially in the presence of underlying lung disease. • Monitor respiratory rate, depth, and effort. Monitor oxygen saturation continuously, reporting an oxygen saturation level of less than 95% (or as ordered). The depressed respiratory drive associated with metabolic alkalosis can lead to hypoxemia and impaired oxygenation of tissues. Oxygen saturation levels of less than 90% indicate significant oxygenation problems. • Assess skin color; note and report cyanosis around the mouth. Central cyanosis, seen around the mouth and oral mucous membranes, indicates significant hypoxia and is a late sign. • Monitor mental status and LOC. Report decreasing LOC or behavior changes such as restlessness, agitation, or confusion. Changes in mental status or behavior may be early signs of hypoxia. • Place in semi-Fowler or Fowler position as tolerated. Elevating the head of the bed facilitates alveolar ventilation and gas exchange. • Administer oxygen as ordered or as necessary to maintain oxygen saturation levels. Supplemental oxygen can help maintain blood and tissue oxygenation despite depressed respirations. • Schedule nursing care activities to allow rest periods. The patient with hypoxemia has limited energy reserves, necessitating frequent rest and limited activities.

Observation and patient interview

Ask the patient about current manifestations such as numbness and tingling, muscle spasms, dizziness, or other symptoms; duration of symptoms and any precipitating factors such as bicarbonate ingestion, vomiting, diuretic therapy, or endocrine disorders; and current medications.

Respiratory System Compensation

Attempts to return the pH to normal by slowing the respiratory rate. Carbon dioxide is retained, and the PaCO2 increases (to greater than 45 mmHg).

Diagnostic tests

Examine test results of ABGs and serum electrolytes.

Physical examination

Examine vital signs, including apical pulse and rate and depth of respirations; muscle strength; and deep tendon reflexes.

Etiology (Simpliflied)

Excessive acid losses due to vomiting or gastric suction Excessive use of potassium-losing diuretics Excessive adrenal corticoid hormones due to: • Cushing syndrome • Hyperaldosteronism • Excessive bicarbonate intake from antacids • Parenteral sodium bicarbonate infusion

Evaluation

Expected outcomes of nursing care relate to restoration of normal body balance. Revisions in the care plan may need to be made if patients do not respond to some aspect of the plan. Nurses may need to follow up with patients released from hospital care to determine whether they are continuing to follow instructions for self-monitoring and self-care.

Health promotion

Focus on teaching patients the risks of using sodium bicarbonate as an antacid to relieve heartburn or gastric distress. Stress the availability of other effective antacid preparations and the need to seek medical evaluation for persistent gastric symptoms. In the hospital setting, carefully monitor laboratory values for patients at risk for developing metabolic alkalosis, particularly patients undergoing continuous gastric suction.

Assessment

Focused assessment data related to metabolic alkalosis are gathered from the patient interview, physical examination, and diagnostic tests.

Risk Factors

Include hospitalization, hypokalemia, and treatment with alkalinizing solutions (e.g., bicarbonate). Can occur in patients of any age, but older adults are at risk because of their delicate fluid and electrolyte status, and treatment focuses on the underlying cause. Young women who practice self-induced vomiting Men and women with chronic hypercapnia respiratory failure are at risk for metabolic alkalosis if their PaCO2 levels are rapidly reduced in mechanical ventilation.

Pharmacologic Therapy

Includes restoring normal fluid volume and administering potassium chloride and sodium chloride solution.

Metabolic Alkalosis in Older Adults

Many older adults can maintain acid-base balance under normal conditions. Metabolic alkalosis may be a consequence of a disorder in older adults. Vomiting may lead to dehydration. Because older adults have a diminished sense of thirst, they can become volume depleted and dehydrated much quicker than younger adults. Metabolic alkalosis results when loss of fluids and volume contraction lower serum potassium. Outcome depends on the nature of the illness and early diagnosis/treatment.

Urine pH

May be low (pH 1-3) if metabolic acidosis is caused by hypokalemia. The kidneys selectively retain potassium and excrete hydrogen ion to restore ECF potassium levels. Urinary chloride levels may be normal or greater than 250 mEq/24 hours.

Etiology

Metabolic alkalosis is a primary problem seen in excessive ingestion of antacids, excessive use of bicarbonate, and lactate administration in hemodialysis. Metabolic alkalosis may also develop from hyperaldosteronism, hypokalemia, hypochloremia, nasogastric suctioning, use of loop diuretics, and vomiting.

Implementation

Nursing care of the patient with metabolic alkalosis is focused on controlling pH while treating the underlying causative disorder and preventing complications.

Serum electrolytes

Often demonstrate decreased serum potassium (less than 3.5 mEq/L) and decreased chloride (less than 95 mEq/L) levels. The serum bicarbonate level is high. Although the total serum calcium may be normal, the ionized fraction of calcium is low.

Monitor for Fluid Volume Deficit

Patients with metabolic alkalosis often have an accompanying fluid volume deficit. • Assess intake and output accurately, monitoring fluid balance. In acute situations, hourly intake and output assessment may be indicated. Urine output of less than 30 mL/hr indicates inadequate tissue perfusion, inadequate renal perfusion, and an increased risk for acute renal failure. • Assess vital signs, CVP, and peripheral pulse volume at least every 4 hours. Hypotension, tachycardia, low CVP, and weak, easily obliterated peripheral pulses indicate hypovolemia. • Weigh daily under standard conditions (time of day, clothing, and scale). Rapid weight changes accurately reflect fluid balance. • Administer IV fluids as prescribed using an electronic infusion pump. If rapid fluid replacement is ordered, monitor for the following indicators of fluid overload: dyspnea, tachypnea, tachycardia, increased CVP, jugular vein distention, and edema. Rapid fluid replacement may lead to hypervolemia, resulting in pulmonary edema and cardiac failure, particularly in patients with compromised cardiac and renal function. • Monitor serum electrolytes, osmolality, and ABG values. Rehydration and administration of potassium chloride affect both acid-base and fluid and electrolyte balance. Careful monitoring is important to identify changes.

ABGs

Show a pH greater than 7.45 and bicarbonate level greater than 28 mEq/L. With compensatory hypoventilation, carbon dioxide is retained and the PaCO2 is greater than 45 mmHg.

The ECG pattern

Shows changes similar to those seen with hypokalemia. These changes may be due to hypokalemia or to the alkalosis.

Potassium Chloride Solution

The potassium restores serum and intracellular potassium levels, allowing the kidneys to conserve hydrogen ions more effectively. Chloride promotes renal excretion of bicarbonate. Sodium chloride solutions restore fluid volume deficits that can contribute to metabolic alkalosis.

Metabolic alkalosis

This bicarbonate excess is characterized by a high pH (>7.45), a high bicarbonate (>28 mEq/L), and PaCO2 higher than 45 mmHg. It may be caused by loss of acid or excess bicarbonate in the body.

Metabolic alkalosis due to loss of hydrogen ions

Usually occurs because of vomiting or gastric suction. Gastric secretions are highly acidic (pH 1-3). When these are lost through vomiting or gastric suction, the alkalinity of body fluids increases. This increased alkalinity results from the loss of acid and from selective retention of bicarbonate by the kidneys as chloride is depleted. (Chloride is the major anion in ECF; when it is lost, bicarbonate is retained as a replacement anion.)

Diagnosis

• Breathing Pattern, Ineffective • Cardiovascular Function, Impaired, Risk for • Fluid Volume: Deficient, Risk for •Injury, Risk for Nursing care of the patient with metabolic alkalosis, as with metabolic acidosis, often focuses on intervention for the primary problem rather than the alkalosis itself. However, the risk for impaired gas exchange is a priority problem, especially with severe metabolic alkalosis.

Clinical Manifestations

• Confusion • Decreasing LOC • Hyperreflexia • Tetany • Dysrhythmias • Hypotension • Seizures • Respiratory failure

Clinical Therapies

• Monitor intake and output closely. • Monitor vital signs, especially respirations and LOC. • Administer ordered IV fluids carefully. • Administer oxygen as ordered. • Treat underlying problem.

Evaluation Outcome

• Patient reports use of antacids that are acceptable for use and that reduce risk of recurrence of metabolic alkalosis. • Patient describes proper self-administration procedure for oral potassium supplements. • Patient describes when to notify provider about changes in daily weight. • Patient's arterial pH returns to normal range. • Patient's serum electrolyte values are within normal range.