Metabolic Acidosis

Four basic mechanisms can cause metabolic acidosis

1. Accumulation of metabolic acids 2. Excess loss of bicarbonate 3. An increase in chloride levels 4. Fluid imbalance.

Diagnostic Tests

ABGs, serum electrolytes, and tests as indicated by the underlying primary disorder.

Hyperchloremic acidosis

Can develop when excess of a chloride solution (e.g., NaCl) is infused, causing a rise in chloride concentrations. It also may be related to renal disease or administration of carbonic anhydrate inhibitor diuretics. The anion gap remains normal in metabolic acidosis because of bicarbonate loss or excess chloride.

Kussmaul respirations

Deep, rapid respirations associated with compensatory mechanisms.

High anion gap acidosis.

Excess metabolic acids increase the hydrogen ion concentration of body fluids. The buffering of excess acid by bicarbonate leads to this

Planning

Involves identification and treatment of the underlying cause and restoration and maintenance of acid-base balance.

Hypernatremia

Is a common electrolyte problem that is defined as a rise in serum sodium concentration

Metabolic Acidosis in Older Adults

May be a consequence of diabetes, renal failure, or ketoacidosis. Accidental overdose of salicylic acid (aspirin) may also cause metabolic acidosis. Experience a higher concentration of hydrogen ion in metabolic acidosis, which inversely correlates with serum bicarbonate and PaCO2 May take more medications because of the increased incidence of disease. Diuretics, certain antidepressants, anti-seizure medications, and angiotensin-converting enzyme (ACE) inhibitors may affect acid-base balance in older adults. Outcome depends on the nature of the illness and early diagnosis and treatment.

Cachexia

Wasting with acute weight loss and muscle loss

Clinical Manifestations

• Diminished appetite • Nausea and vomiting • Abdominal pain • Weakness • Fatigue • Headache • General malaise • Decreasing LOC • Dysrhythmia • Bradycardia • Warm, flushed skin • Skeletal problems • Hyperventilation (Kussmaul respirations) • Dyspnea

Clinical Therapies

• Monitor ABG values, intake and output, and LOC. • Position patient to facilitate chest expansion. • Provide oral care for dry mouth. • Administer IV sodium bicarbonate carefully if ordered. • Treat underlying problem as ordered.

Observation and patient interview

Ask the patient about current manifestations, including diminished appetite, nausea, vomiting, abdominal discomfort, fatigue, lethargy, and other symptoms; duration of symptoms and any precipitating factors such as diarrhea and ingestion of a toxin such as aspirin, methanol, or ethylene; chronic diseases such as diabetes or renal failure, cirrhosis of the liver, or endocrine disorders; and current medications.

Hypokalemia

Blood's potassium levels are too low

Accumulation of metabolic acids

Can result from excess acid production or impaired renal elimination of metabolic acids. .

Plan for Discharge

Consider the cause of the acidosis and any underlying factors. Patients who have developed ketoacidosis as a result of diabetes mellitus, starvation, or alcoholism need interventions and teaching to prevent future episodes of acidosis. Diet, medication management, and alcohol dependency treatment are vital teaching areas. When metabolic acidosis is related to renal failure, the patient should be referred for management of the renal failure itself. Patients who have experienced diarrhea or excess ileostomy drainage leading to bicarbonate loss need information about appropriate diarrhea treatment strategies and need to know when to call their primary care provider

Risk Factors

DKA Renal failure Severe sepsis Liver failure Salicylate intoxication Severe Diarrhea Young Women with eating disorders, abuse laxatives, severe diet restriction to the point of cachexia

Acidosis

Depresses cell membrane excitability, affecting neuromuscular function. It also increases the amount of free calcium in ECF by interfering with protein binding. Severe acidosis (pH of 7 or less) depresses myocardial contractility, leading to decreased cardiac output. If kidney function is normal, acid excretion and ammonia production increase to eliminate excess hydrogen ions.

Lactic acidosis

Develops due to tissue hypoxia and a shift to anaerobic metabolism by the cells. Lactate and hydrogen ions are produced, forming lactic acid. Both oxygen and glucose are necessary for normal cell metabolism.

Health Promotion

Discuss management of the underlying disease process (e.g., type 1 diabetes, renal failure) to help patients prevent complications such as DKA and metabolic acidosis.

Evaluation

During the recovery period, frequently monitor pH levels and vital signs, and reassess the patient's condition to revise care plans as necessary.

Physical examination.

Examine mental status and LOC, vital signs including respiratory rate and depth, apical and peripheral pulses, skin color and temperature, abdominal contour and distention, bowel sounds, and urine output.

Early Manifestations

Fatigue, general malaise, diminished appetite, nausea, abdominal pain Resemble those of common viral disorders such as influenza, stress the importance of promptly seeking treatment if these symptoms develop.

Hypovolemia & Metabolic Acidosis

From dehydration will cause metabolic acidosis, contributing to other conditions such as bicarbonate lost in stool, ketones produced with starvation (as seen in eating disorders), ketoacidosis from decreased tissue perfusion, and decreased renal perfusion.

Renal Failure and Metabolic Acidosis

Impairs the body's ability to excrete excess hydrogen ions and form bicarbonate.

Acid-base imbalances and electrolyte balance

In acidosis, potassium is retained as the kidney excretes excess hydrogen ions. Excess hydrogen ions also enter the cells, displacing potassium from the intracellular space to maintain the balance of cations and anions within the cells. The effect of both processes is to increase serum potassium levels. Also in acidosis, calcium is released from its bonds with plasma proteins, increasing the amount of ionized (free) calcium in the blood. Magnesium levels may fall in acidosis.

Reduce Risk for Injury

Mental status and brain function are affected by acidosis, increasing the risk for injury. Nurses working with patients who exhibit altered mental status related to acidosis should: • Monitor neurologic function, including mental status, LOC, and muscle strength. As the pH falls, the resulting decline in mental functioning leads to confusion, stupor, and a decreasing LOC. • Institute safety precautions as necessary: Keep the bed in its lowest position, make sure the call light can be reached, and assign a sitter if necessary. These measures help protect the patient from injury resulting from confusion or disorientation. • Keep clocks, calendars, and familiar objects at bedside. Orient to time, place, and circumstances as needed. Allow significant others to remain with the patient as much as possible. An unfamiliar environment and altered thought processes can further increase the risk for injury. Significant others provide a sense of security and reduce anxiety.

Implementation

Metabolic acidosis affects cardiac output by decreasing myocardial contractility, slowing the heart rate, and increasing the risk for dysrhythmias. The accompanying hyperkalemia increases the risk for decreased cardiac output as well.

Etiology

Metabolic acidosis is rarely a primary disorder; it usually develops during the course of another disease, as follows: • Acute lactic acidosis usually results from tissue hypoxia due to shock or cardiac arrest. • Patients with type 1 diabetes mellitus are at risk for developing DKA. • Acute or chronic renal failure impairs the excretion of metabolic acids. • Diarrhea, intestinal suction, or abdominal fistulas increase the risk for excess bicarbonate loss. • Ingestion of an acidic substance or a substance that can be metabolized to an acid. Conditions that increase nonvolatile acids in the blood (e.g., renal impairment, diabetes mellitus, starvation) Conditions that decrease bicarbonate (e.g., prolonged diarrhea, excessive use of laxatives) Excessive infusion of chloride-containing IV fluids (e.g., NaCl) Excessive ingestion of acids (e.g., salicylates) Cardiac arrest

Nursing Process

Nurses frequently provide care for patients with metabolic acidosis, although the focus of care is usually the underlying disorder (e.g., diabetes mellitus, renal failure) rather than the acidosis itself. For this reason, nurses must know the effects of acidosis and its implications for nursing care.

Teaching for Discharge

Provide teaching to patients and their families about the following: • Using appropriate resources to get medical assistance. • Contacting the primary care provider immediately if the patient experiences dizziness, nausea, vomiting, and fatigue.

Pancreas and Metabolic Acidosis

Secretes bicarbonate-rich fluid into the small intestine. Intestinal suction, severe diarrhea, ileostomy drainage, or fistulas can lead to excess losses of bicarbonate.

Hyperosmolality

The condition especially of a bodily fluid of having abnormally high osmolality.

Collaboration

The focus is on treating the primary disorder, reducing the effects of acidosis on cardiac function, and ensuring adequate oxygenation. Refer to the patient's history for listing of predisposing/contributing factors. Monitor serum electrolytes, especially potassium. Replace fluids as needed. Modify diet as indicated.

Metabolic acidosis

This bicarbonate deficit is characterized by a low pH (<7.35), low bicarbonate (<24 mEq/L), and PaCO2 less than 38 mmHg. It may be caused by excess acid in the body or loss of bicarbonate from the body. When metabolic acidosis develops, the respiratory system attempts to return the pH to normal by increasing the rate and depth of respirations. Carbon dioxide elimination increases, and the PaCO2 falls (to less than 35 mmHg).

Pharmacologic Therapy

To reduce the effects of acidosis on cardiac function, an alkalinizing solution such as bicarbonate may be given if the pH is less than 7.1. Sodium bicarbonate is the most commonly used alkalinizing solution; others include lactate, citrate, and acetate solutions (which are metabolized to bicarbonate). Give alkalinizing solutions intravenously for severe acute metabolic acidosis. Use the oral route for chronic metabolic acidosis. Carefully monitor patients treated with bicarbonate. Rapid correction of the acidosis may lead to metabolic alkalosis and hypokalemia. Hypernatremia and hyperosmolality may develop as well, leading to water retention and fluid overload

Ketoacidosis

When intracellular glucose is inadequate because of starvation or a lack of insulin to move it into cells, the body breaks down fatty tissue to meet its metabolic needs. In this process, fatty acids are released and converted to ketones

Diagnosis

• Cardiac Output, Decreased, Risk for • Electrolyte Imbalance, Risk for • Fluid Volume: Deficient • Fluid Volume: Excess • Falls, Risk for.

Monitor Potential for Excess Fluid Volume

• Monitor and maintain fluid replacement as ordered. Monitor serum sodium levels and osmolality. • Monitor heart and lung sounds, central venous pressure (CVP), and respiratory status. Increasing dyspnea, adventitious lung sounds, a third heart sound (S3) due to the volume of blood flow through the heart, and high CVP readings indicate hypervolemia and should be reported to the healthcare provider. • Assess for edema, particularly in the back, sacral, and periorbital areas. Edema initially affects dependent tissues—the back and sacrum in patients who are bedridden. Periorbital edema indicates more generalized edema. • Assess urine output hourly. Maintain accurate intake and output records. Note urine output less than 30 mL/hour or a positive fluid balance on 24-hour total intake and output calculations. Heart failure and inadequate renal perfusion may lead to decreased urine output. • Obtain daily weights using consistent conditions (same time of day, clothing, and scale). Daily weights are an accurate indicator of fluid balance. • Administer prescribed diuretics as ordered, monitoring the patient's response to therapy. Loop or high-ceiling diuretics such as furosemide can lead to further electrolyte imbalances, especially hypokalemia. This is a significant risk, like that seen during correction of metabolic acidosis.

Implementation in the acute care setting

• Monitor vital signs, including peripheral pulses and capillary refill. Hypotension, diminished pulse strength, and slowed capillary refill may indicate decreased cardiac output and impaired tissue perfusion. Poor tissue perfusion can increase the risk for lactic acidosis. • Monitor intake and output. In particular, patients with eating disorders may attempt to continue self-imposed dietary restrictions. These patients can be resistant to treatment and may try to conceal the true nature of their disorders. • Monitor the ECG pattern for dysrhythmias and changes characteristic of hyperkalemia, such as peaked ↓ waves. Notify the physician of changes. Progressive ECG changes such as widening of the QRS complex indicate an increasing risk of dysrhythmias and cardiac arrest. Dysrhythmias further decrease cardiac output, possibly intensifying the degree of acidosis. • Monitor laboratory values, including ABGs, serum electrolytes, and renal function studies (serum creatinine and blood urea nitrogen [BUN]). Frequent monitoring of laboratory values allows evaluation of the effectiveness of treatment as well as early identification of potential problems.

Expected Outcomes

• Patient maintains pH within normal range. • Patient's vital signs remain within normal range based on age and condition. • Patient maintains adequate oxygenation of tissues. • Patient is able to describe or demonstrate measures to control the disease process to prevent future complications of pH imbalance.

Potential Goals

• Patient will describe and demonstrate preventive measures related to chronic disease process. • pH will remain within normal range. • Disease process causing acid-base imbalance will be controlled to reduce acid production or alkaline loss. • Patient will maintain vital signs within normal range for age and condition. •Patient will maintain baseline cardiac rhythm.