Acidosis Nursing Diagnosis: A Comprehensive Guide for Nurses

Metabolic acidosis represents a critical health challenge characterized by a significant imbalance in the body’s acid-base equilibrium, specifically marked by an excess accumulation of acid in the bloodstream. This condition arises from several underlying mechanisms, including:

• Reduced kidney function, hindering the excretion of surplus acids.
• Overproduction of acid within the body.
• Excessive loss of bicarbonate, a crucial buffer.

To counteract this imbalance, the body initiates compensatory responses, primarily through the respiratory system. Hyperventilation ensues as the lungs attempt to expel excess carbon dioxide (CO2), aiming to elevate blood pH and restore the bicarbonate to CO2 ratio.

In this article, we will delve into the nursing process for metabolic acidosis, providing a comprehensive guide for nurses to effectively assess, diagnose, and manage patients with this condition.

Nursing Process

The primary objective in managing metabolic acidosis is to effectively correct and sustain a balanced acid-base level within the body. Treatment strategies are centered on addressing the root cause of the imbalance and elevating blood pH, often through the administration of oral or intravenous sodium bicarbonate. Crucially, continuous monitoring of vital signs, laboratory findings, and the patient’s level of consciousness is paramount. This vigilant oversight is essential to gauge the efficacy of the treatment plan and to proactively prevent potential complications.

Nursing Assessment

The initial step in nursing care is a thorough nursing assessment, where nurses collect comprehensive physical, psychosocial, emotional, and diagnostic data. This section will explore both subjective and objective data pertinent to metabolic acidosis.

Review of Health History

1. Document the patient’s presenting symptoms. Metabolic acidosis manifests with a range of symptoms, often linked to the underlying cause. These may include:

• General: Fatigue, generalized weakness, malaise.
• Central Nervous System (CNS): Acute confusion, headache, drowsiness, lethargy, altered mental status.
• Respiratory: Hyperventilation, shortness of breath.
• Cardiovascular: Chest pain, palpitations, hypotension, dizziness.
• Gastrointestinal (GI): Nausea, vomiting, diarrhea, abdominal pain.
• Musculoskeletal: Decreased muscle tone, muscle weakness, reduced reflexes.

2. Identify potential causative factors. A detailed history should explore potential causes of metabolic acidosis, such as:

• Diabetic ketoacidosis (DKA)
• Starvation and malnutrition
• Lactic acidosis (sepsis, hypoperfusion)
• Severe diarrhea and intestinal fluid loss
• Dehydration and hypovolemia
• Renal failure (acute or chronic)
• Renal tubular acidosis (RTA)
• Liver failure and hepatic dysfunction
• Gastrointestinal fistulas and drainage
• Aspirin overdose and salicylate toxicity
• Shock (hypovolemic, septic, cardiogenic)

3. Analyze the patient’s medication history. Certain medications can induce or exacerbate metabolic acidosis. Review the patient’s medication record for:

• Metformin (especially in patients with renal impairment)
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Salicylates (aspirin)
• Valproate
• Isoniazid
• Propofol

4. Inquire about exposure to toxins. Environmental or occupational exposure to certain toxins can lead to metabolic acidosis:

• Methanol (found in fuels, solvents, and windshield washer fluid)
• Ethylene glycol (antifreeze)
• Isopropyl alcohol (rubbing alcohol)
• Butoxyethanol
• Toluene (solvents, paint thinners)

Physical Assessment

1. Evaluate respiratory patterns. Observe for Kussmaul respirations, a characteristic deep, rapid, and labored breathing pattern. This is a significant sign often seen in patients with DKA as the body attempts to compensate for acidosis by expelling CO2.

2. Monitor neurological status for mental status changes. Severe metabolic acidosis can significantly impact neurological function, leading to confusion, disorientation, drowsiness, and progressing to shock and coma. Continuous monitoring of mental status is critical.

3. Regularly assess vital signs. Pay close attention to vital signs for indicators of shock, which can be a consequence of severe metabolic acidosis. Watch for:

• Hypotension (low blood pressure)
• Tachycardia (rapid heart rate)
• Hyperventilation (increased respiratory rate) – the body’s compensatory mechanism.

4. Identify symptoms related to specific underlying conditions. Clinical manifestations of metabolic acidosis can vary depending on the underlying cause.

• Kidney or Liver Failure:

  • Xerosis (dry skin)
  • Pruritus (itching) and scratch marks
  • Pallor (pale skin)
  • Somnolence (excessive sleepiness)
  • Asterixis (flapping tremor, involuntary muscle movement)

• Diabetic Ketoacidosis (DKA):

  • Poor skin turgor (sign of dehydration)
  • Dry mucous membranes
  • Fruity odor on breath (due to ketone production)
  • Rapid and deep breathing (Kussmaul respirations)

Diagnostic Procedures

1. Arterial Blood Gas (ABG) Analysis. ABG testing is crucial for confirming metabolic acidosis and assessing its severity. Interpret ABG results for the following key indicators:

• pH: Decreased (below the normal range of 7.35-7.45), indicating acidemia.
• PaCO2: May be normal or low (below 35 mmHg) as a result of respiratory compensation (hyperventilation).
• HCO3- (Bicarbonate): Decreased (below the normal range of 22-26 mEq/L), indicating a deficit of bicarbonate buffer.

2. Complete Blood Count (CBC). Elevated white blood cell (WBC) count may suggest infection or sepsis, which can be a cause of lactic acidosis.

3. Urinalysis. Urine pH is often acidic (less than 5.0) in metabolic acidosis. Urinalysis can also detect:

• Ketones: Present in DKA and starvation.
• Calcium oxalate crystals: Needle-shaped crystals may be present in ethylene glycol poisoning.

4. Serum Ketone Level. Elevated serum ketone levels strongly suggest DKA or starvation as the cause of metabolic acidosis.

5. Serum Lactate Level. Normal plasma lactate range is 0.5 to 1.5 mEq/L. Elevated levels (above 4-5 mEq/L) indicate lactic acidosis, often seen in sepsis, shock, and severe tissue hypoperfusion.

6. Salicylate and Iron Levels. Measure serum salicylate levels if aspirin overdose is suspected (toxic level > 40-50 mg/dL). Iron levels should be checked if iron poisoning is considered (toxic level > 300 mg/dL), which can also lead to lactic acidosis.

7. Electrolyte Panel. Electrolyte imbalances are common in metabolic acidosis and can be both a cause and consequence. Monitor serum levels of:

• Potassium (K+): Hyperkalemia is frequently observed due to cellular exchange of H+ for K+.
• Sodium (Na+)
• Magnesium (Mg++)
• Phosphorus (PO4—)
• Bicarbonate (HCO3-)
• Chloride (Cl-)

8. Imaging Studies. In some cases, imaging may be needed to assess underlying conditions:

• Abdominal radiographs (KUB): To detect renal stones.
• Computed tomography (CT) scans: For detailed renal imaging and to rule out other abdominal pathology.
• Renal ultrasound: To assess kidney structure and identify obstruction.

9. Electrocardiogram (ECG). Electrolyte imbalances, particularly hyperkalemia, can significantly affect cardiac function and rhythm. ECG monitoring is essential to detect dysrhythmias.

Nursing Interventions

Effective nursing interventions are crucial for the patient’s recovery from metabolic acidosis. These interventions focus on addressing the underlying cause, correcting the acid-base imbalance, and preventing complications.

1. Treat the Underlying Cause. The primary intervention is to identify and treat the root cause of metabolic acidosis.

• Sepsis: Requires prompt and aggressive intravenous antibiotic administration and source control.
• Diabetic Ketoacidosis (DKA): Management involves fluid resuscitation, correction of electrolyte imbalances (especially potassium and sodium), and intravenous insulin therapy.
• Renal Failure: May require dialysis to remove excess acids and waste products.
• Toxin Ingestion: Specific antidotes or treatments are needed depending on the toxin (see detoxification section).
• Dehydration: Fluid replacement with intravenous fluids is critical.

2. Administer Prescribed Medications. Medications play a vital role in correcting metabolic acidosis.

• Alkalinizing Agents: Sodium bicarbonate (NaHCO3) is the primary agent for acute metabolic acidosis. It increases plasma pH and should be administered to maintain pH above 7.20.
• Carbonic Anhydrase Inhibitors: Such as acetazolamide, can promote alkaline diuresis in certain situations, but are less commonly used for acute correction.
• Detoxification Agents (Antidotes): For specific toxin-induced acidosis (see detoxification section below).

3. Sodium Bicarbonate Therapy. Intravenous sodium bicarbonate (NaHCO3) is commonly used to rapidly reverse metabolic acidosis. Dosage is determined by blood pH, serum HCO3- level, and PaCO2. Careful monitoring is essential to avoid overcorrection and alkalosis.

4. Management of Metabolic Acidosis in Chronic Kidney Disease (CKD). Patients with CKD often have chronic metabolic acidosis. Management strategies include:

• Increasing bicarbonate concentration in dialysate solution during hemodialysis.
• Oral sodium bicarbonate supplementation between dialysis sessions.
• Dietary modifications to reduce acid load.

5. Management of Salicylate Toxicity. Treatment for salicylate toxicity includes:

• Alkaline diuresis: Achieved with acetazolamide or intravenous sodium bicarbonate to enhance salicylate excretion in urine.
• Activated charcoal: Multiple doses every 2-4 hours to enhance salicylate elimination from the gastrointestinal tract.
• Hemodialysis: In severe cases of salicylate poisoning.

6. Prepare for Dialysis. Hemodialysis may be necessary for severe metabolic acidosis, especially in cases of:

• Severe toxin ingestion or drug overdose (e.g., methanol, ethylene glycol, salicylates).
• Acute kidney injury (AKI) with inability to excrete acids.
• Severe central nervous system (CNS) depression or coma secondary to acidosis.

7. Initiate Antibiotic Therapy for Sepsis. If septic shock is the underlying cause of lactic acidosis, prompt initiation of broad-spectrum intravenous antibiotics is crucial as part of sepsis management.

8. Potassium Citrate Supplementation for Renal Tubular Acidosis (RTA) Type 1. Patients with RTA type 1 (distal RTA) require daily alkalinizing therapy because their kidneys cannot effectively excrete acids. Potassium citrate is often the preferred agent as it also helps to replace potassium losses.

9. Immediate Detoxification for Toxin Ingestion. Prompt administration of antidotes is critical in toxin-induced metabolic acidosis:

• Ethylene glycol (EG), Diethylene glycol (DEG), and methanol poisoning: Fomepizole is the antidote of choice. It inhibits alcohol dehydrogenase, preventing the formation of toxic metabolites.
• Acetaminophen (Paracetamol) overdose: N-acetylcysteine (NAC) is effective if administered within 8 hours of ingestion to prevent liver damage and metabolic acidosis.

10. Dietary Consultation with a Renal Dietitian. For patients with CKD and chronic metabolic acidosis, referral to a renal dietitian or nutritionist is essential. Dietary education should focus on:

• Reducing acid-producing foods (animal proteins, processed foods).
• Increasing base-producing foods (fruits, vegetables).

11. Patient Education on Acid-Producing and Base-Producing Foods. Educate patients about the impact of diet on acid-base balance.

• Acid-producing foods to limit:

  • Fish and seafood
  • Processed meats (beef, pork, poultry)
  • Eggs
  • Cheese and dairy products
  • Grains (wheat, rice, corn)
  • Alcohol
  • Carbonated beverages

• Base-producing (alkaline) foods to encourage:

  • Fruits (especially citrus fruits, berries, melons)
  • Non-starchy vegetables (leafy greens, root vegetables, cruciferous vegetables)
  • Almond milk
  • Coconut oil
  • Soy products

Nursing Care Plans

Once nursing diagnoses are identified for metabolic acidosis, nursing care plans become essential tools for prioritizing assessments and interventions. These plans guide both short-term and long-term goals of care. Here are examples of nursing care plans for metabolic acidosis, focusing on key nursing diagnoses.

Acute Confusion

Metabolic acidosis can significantly impair neurological function, leading to acid buildup in the brain and causing altered mental status.

Nursing Diagnosis: Acute Confusion

Related Factors:

• Pathophysiological disease process (metabolic acidosis)
• Electrolyte imbalances (hyperkalemia, hyponatremia)
• Impaired cellular metabolism and cerebral oxygenation

As evidenced by:

• Disorientation to person, place, time, and situation
• Lethargy and drowsiness
• Difficulty in attention and concentration
• Inappropriate verbal responses
• Restlessness or agitation
• Altered level of consciousness

Expected Outcomes:

• Patient will regain and maintain orientation to person, place, time, and situation.
• Patient will demonstrate improved alertness, cognitive clarity, and appropriate decision-making ability.

Assessment:

1. Determine and address causative factors of confusion. Identify and treat the underlying cause of metabolic acidosis and contributing factors like electrolyte imbalances, hypoxia, and medications. Assess blood glucose levels, electrolyte levels, ABG results, and perform medication reconciliation.

2. Conduct a comprehensive neurological assessment. Evaluate level of consciousness using Glasgow Coma Scale (GCS), assess pupillary response, motor and sensory function, and cranial nerve function. This helps to differentiate metabolic encephalopathy from other neurological or psychiatric conditions and guides appropriate interventions.

Interventions:

1. Provide frequent reorientation. Due to confusion, repeatedly reorient the patient to their surroundings, time, and situation. Use clear and simple language. Provide visual cues like calendars and clocks.

2. Closely monitor laboratory results and trends. Regularly review and monitor trends in ABGs, electrolyte levels, serum ammonia levels (if liver failure is suspected), and renal function tests. Promptly report and address abnormal values.

3. Explain all procedures and interventions clearly and simply. Patients with confusion may experience increased anxiety and agitation. Clear explanations about nursing care, procedures, and treatments can reduce anxiety and promote cooperation.

4. Ensure adequate sleep and rest periods. Sleep deprivation can exacerbate confusion. Plan nursing care to allow for uninterrupted sleep and rest to promote cognitive recovery. Provide a quiet and comfortable environment.

Ineffective Tissue Perfusion

Acidemia associated with metabolic acidosis impairs oxygen delivery and utilization at the cellular level, potentially leading to ineffective tissue perfusion and shock.

Nursing Diagnosis: Ineffective Tissue Perfusion

Related Factors:

• Increased hydrogen ion concentration in blood (acidemia)
• Hemodynamic instability (hypotension, shock)
• Reduced oxygen-carrying capacity of blood
• Exposure to toxic chemicals impairing cellular respiration
• Renal failure contributing to fluid overload and impaired perfusion

As evidenced by:

• Hypotension (systolic blood pressure < 90 mmHg or MAP < 65 mmHg)
• Tachycardia (heart rate > 100 bpm)
• Tachypnea (respiratory rate > 20 breaths/min)
• Weak or thready peripheral pulses
• Cool, clammy skin
• Prolonged capillary refill time (> 3 seconds)
• Altered mental status (confusion, lethargy)
• Decreased urine output (oliguria)

Expected Outcomes:

• Patient will demonstrate improved tissue perfusion as evidenced by:
  • Systolic blood pressure > 90 mmHg and MAP > 65 mmHg
  • Heart rate between 60-100 beats/min
  • Respiratory rate between 12-20 breaths/min
  • Strong, palpable peripheral pulses
  • Warm and dry extremities
  • Capillary refill time < 3 seconds
• Patient will exhibit improved alertness and stable mental status.

Assessment:

1. Continuously monitor blood pressure trends. Hypotension is a key indicator of ineffective tissue perfusion and can progress to shock in metabolic acidosis. Monitor for progressive hypotension and narrowing pulse pressure, which may indicate worsening perfusion.

2. Assess heart rate, rhythm, and cardiac monitoring. Tachycardia is a compensatory mechanism to maintain cardiac output in hypovolemia and hypotension. Metabolic acidosis-induced hyperkalemia can lead to cardiac arrhythmias, further compromising perfusion. Continuous ECG monitoring is essential.

3. Regularly evaluate neurological status. Changes in mental status, such as drowsiness, confusion, and lethargy, are signs of decreased cerebral perfusion and CNS depression due to acidemia. Frequent neurological checks are crucial.

Interventions:

1. Administer intravenous sodium bicarbonate as prescribed. Sodium bicarbonate is the primary treatment to increase HCO3- levels and correct acidemia, improving blood pH and potentially enhancing tissue perfusion.

2. Aggressively treat hypovolemia and shock. Depending on the underlying cause and severity of shock, interventions may include:

• Intravenous crystalloids (normal saline, lactated Ringer’s) for fluid resuscitation.
• Colloids (albumin) in some cases to increase oncotic pressure.
• Blood products if indicated for blood loss or severe anemia.
• Antibiotics for septic shock.

3. Provide supplemental oxygen therapy as indicated. Administer oxygen via nasal cannula or face mask to improve tissue oxygenation and address hypoxemia related to impaired perfusion.

4. Administer vasopressors as ordered. In severe cases of metabolic acidosis with persistent hypotension and impaired tissue perfusion (shock), vasopressors (e.g., norepinephrine, epinephrine, dopamine, vasopressin) may be necessary to increase blood pressure and improve perfusion to vital organs. Administer vasopressors cautiously and monitor hemodynamic response closely.

Risk for Decreased Cardiac Output

Metabolic acidosis and associated electrolyte imbalances, particularly hyperkalemia, increase the risk of cardiac dysrhythmias and decreased cardiac output.

Nursing Diagnosis: Risk for Decreased Cardiac Output

Related Factors:

• Increased hydrogen ion concentration (acidemia) affecting myocardial contractility
• Alterations in cardiac rhythm due to electrolyte imbalances (hyperkalemia)
• Decreased myocardial contractility secondary to acidemia and electrolyte derangements

As evidenced by:

A risk diagnosis is not evidenced by signs and symptoms as the problem has not yet occurred. Nursing interventions are aimed at prevention.

Expected Outcomes:

• Patient will maintain adequate cardiac output as evidenced by:
  • Stable blood pressure (SBP > 90 mmHg, DBP 60-90 mmHg)
  • Heart rate between 60 to 100 beats/min with regular rhythm
  • Adequate urine output (0.5 to 1.5 mL/kg/hour)
  • Strong and palpable peripheral pulses
• ECG results will demonstrate a normal sinus rhythm without dysrhythmias.

Assessment:

1. Continuously monitor heart rate and rhythm via ECG. Electrolyte imbalances, especially hyperkalemia, are major risk factors for cardiac dysrhythmias. Hyperkalemia is a frequent complication of metabolic acidosis. ECG monitoring is crucial to detect early signs of dysrhythmias.

2. Identify and address causative factors of dysrhythmias and metabolic acidosis. Determine and manage underlying causes of metabolic acidosis, such as DKA, dehydration, renal failure, toxin ingestion, and medication side effects. Correcting the underlying cause is essential to prevent cardiac complications.

Interventions:

1. Review and adjust medications. Identify and discontinue medications that can exacerbate hyperkalemia or cardiac dysrhythmias, if clinically appropriate and ordered by the physician. Examples include potassium-sparing diuretics, ACE inhibitors, and ARBs.

2. Apply continuous ECG monitoring. Patients at risk for decreased cardiac output due to metabolic acidosis should have continuous ECG monitoring to promptly detect and manage dysrhythmias.

3. Exercise caution in treating Renal Tubular Acidosis (RTA) Type 4. RTA type 4 (hyperkalemic RTA) is characterized by metabolic acidosis and hyperkalemia due to impaired renal potassium excretion. Management includes a low-potassium diet and loop diuretics (if renal function permits) to promote potassium excretion. Avoid potassium-sparing diuretics in these patients.

4. Consider dialysis for severe cases. Hemodialysis may be necessary for patients with severe CNS depression, acute kidney injury, or refractory hyperkalemia to correct acidosis, remove toxins, and rapidly reduce serum potassium levels.

Risk for Electrolyte Imbalance

Metabolic acidosis significantly disrupts electrolyte balance, increasing the risk of life-threatening electrolyte imbalances, particularly hyperkalemia.

Nursing Diagnosis: Risk for Electrolyte Imbalance

Related Factors:

• Pathophysiological disease process (metabolic acidosis)
• Compromised regulatory mechanisms (renal dysfunction)
• Endocrine regulatory dysfunction (e.g., in DKA)
• Fluid imbalances (dehydration, fluid overload)
• Effects of metabolic acidosis on cellular ion exchange

As evidenced by:

A risk diagnosis is not evidenced by signs and symptoms as the problem has not yet occurred. Nursing interventions are aimed at prevention.

Expected Outcomes:

• Patient will maintain serum electrolyte levels within normal limits.
• Patient will exhibit stable vital signs and a normal sinus rhythm on ECG, indicating electrolyte balance.

Assessment:

1. Monitor cardiac rate, rhythm, and ECG. Hyperkalemia, a common electrolyte imbalance in metabolic acidosis, can manifest as cardiac irregularities. Monitor ECG for tall, peaked T waves, widening QRS complex, and other signs of hyperkalemia.

2. Regularly assess and monitor electrolyte levels. Obtain and monitor serum electrolyte levels (potassium, sodium, chloride, bicarbonate, magnesium, phosphorus, calcium) at appropriate intervals, as ordered. Prompt identification of imbalances allows for timely intervention.

Interventions:

1. Assess and monitor changes in respiratory patterns. Patients with metabolic acidosis often exhibit hyperventilation (Kussmaul respirations) as a compensatory mechanism to reduce acid load. Monitor respiratory rate, depth, and pattern for signs of respiratory compensation or decompensation.

2. Administer parenteral fluids as indicated and prescribed. Intravenous fluid administration (type and rate) should be carefully prescribed and administered to correct dehydration, improve renal perfusion, and address electrolyte imbalances. Monitor fluid balance closely.

3. Evaluate urinary status and kidney function. The kidneys play a crucial role in compensating for metabolic acidosis by excreting excess hydrogen ions and regulating electrolytes. Assess urine output, urine pH, and monitor renal function tests (BUN, creatinine, eGFR). Decreased urine output may indicate impaired renal compensation or acute kidney injury.

4. Administer medications as indicated and prescribed. Administer oral or intravenous sodium bicarbonate as prescribed to raise blood pH and correct acidosis. Administer electrolyte replacements (e.g., potassium, magnesium) as needed based on laboratory results and physician orders, carefully monitoring for overcorrection.

Risk for Injury

Patients with metabolic acidosis are at increased risk for injury due to weakness, fatigue, confusion, and potential for seizures secondary to electrolyte imbalances and acidemia.

Nursing Diagnosis: Risk for Injury

Related Factors:

• Electrolyte imbalances (e.g., hyponatremia, hyperkalemia)
• Hypoxia and decreased cerebral oxygenation
• Disorientation and altered mental status
• Muscle weakness and impaired coordination
• Fatigue and generalized weakness
• Toxin accumulation and effects on CNS

As evidenced by:

A risk diagnosis is not evidenced by signs and symptoms as the problem has not yet occurred. Nursing interventions are aimed at prevention.

Expected Outcomes:

• Patient will remain free from injury throughout hospitalization and treatment.
• Patient will not experience seizure activity.

Assessment:

1. Identify and assess patient-specific risk factors for injury. Evaluate the patient’s individual risk factors, including:

• Age and developmental stage
• Cognitive awareness and level of consciousness
• Presence of muscle weakness or impaired mobility
• History of falls or seizures
• Use of medications that may increase risk of falls or confusion

2. Assess cognitive status and decision-making ability. Evaluate the patient’s level of confusion, orientation, and ability to follow instructions and make safe decisions. Impaired cognitive function increases the risk of accidents and injuries.

Interventions:

1. Ensure a safe environment to minimize hazards. Implement safety measures to reduce the risk of falls and injuries:

• Keep the bed in the lowest position with side rails up (if appropriate and not contraindicated).
• Ensure bed alarm is activated.
• Keep the call bell within easy reach.
• Remove clutter and obstacles from the patient’s room and path to the bathroom.
• Provide adequate lighting.

2. Assist with ambulation and promote use of assistive devices. Provide assistance with ambulation and transfers, especially if the patient is weak, dizzy, or confused. Encourage the use of assistive devices such as walkers or wheelchairs as needed.

3. Involve patient and family in safety planning and care. Educate the patient and family about the risks of injury associated with metabolic acidosis and involve them in developing and implementing safety measures. Encourage family members to assist with supervision and monitoring, if possible.

4. Implement seizure precautions if indicated. If the patient is at risk for seizures due to electrolyte imbalances or toxin accumulation, implement seizure precautions:

• Pad side rails of the bed.
• Place a padded mat on the floor beside the bed.
• Have suction equipment and oral airway readily available at the bedside.
• Ensure intravenous access is patent for rapid administration of anticonvulsant medications if needed.

References

• Adrogué, H. J., & Emmett, M. (1998). Pathophysiology and management of metabolic acidosis. Journal of Nephrology, 11(Suppl 1), S73-S81.
• Bushinsky, D. A., & Krieger, N. S. (2022). Metabolic Acidosis. Journal of the American Society of Nephrology, 33(7), 1291–1293.
• Emmett, M. (2023). Treatment of Metabolic Acidosis in Adults. UpToDate. Retrieved from https://www.uptodate.com/contents/treatment-of-metabolic-acidosis-in-adults
• Kraft, M. D., & Bressler, K. (2023). Acid Base Balance. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537120/
• Wilkinson, J. M. (2021). Nursing diagnosis handbook. Wolters Kluwer.
• Dochterman, J. M., & Bulechek, G. M. (2004). Nursing Interventions Classification (NIC). Mosby.