Metabolic Acidosis Nursing Diagnosis and Nursing Care Plan

Last updated on December 31st, 2022 at 11:50 am

Metabolic Acidosis Nursing Care Plans Diagnosis and Interventions

Metabolic Acidosis NCLEX Review and Nursing Care Plans

Metabolic acidosis is one of the acid-base disorders that cause disruptions in the plasma acidity equilibrium. A distinct acidosis is any process that raises the serum hydrogen ion concentration.

Acidosis is divided into two categories: metabolic acidosis, which is controlled by bicarbonate (HCO3), and respiratory acidosis, which involves changes in carbon dioxide.

A decrease in serum bicarbonate of less than 24 mEq/L and an increase in the hydrogen ion concentration in the systemic circulation are the hallmarks of metabolic acidosis. Metabolic acidosis is not a benign condition.

It is rather indicative of an underlying condition that necessitates treatment to reduce morbidity and mortality.

The various causes of metabolic acidosis are divided into four primary categories: (1) increased acid generation, (2) decreased acid excretion, (3) acid consumption, and (4) renal or gastrointestinal (GI) bicarbonate losses.

Signs and Symptoms of Metabolic Acidosis

Most patients with metabolic acidosis are asymptomatic, however some individuals may present with: 

  • confusion
  • fast heartbeat
  • stomach upset
  • headache
  • long and deep breaths
  • loss of appetite
  • vomiting
  • tiredness
  • generalized weakness

Types of Metabolic Acidosis

Healthcare professionals may look for the signs of a particular form of metabolic acidosis to determine what is causing the imbalance.

The existence or absence of an anion gap or the concentration of unmeasured serum anions are used to further categorize metabolic acidosis. According to plasma neutrality, anions must counteract cations in order to keep the charge neutral.

As a result, the sum of the anions bicarbonate and chloride as well as the unmeasured anions, which stand in for the anion gap, balance sodium (Na), the main plasma cation. Lactate and acetoacetate are two unmeasured anions that are frequently among the major causes of metabolic acidosis.

  • Anion gap metabolic acidosis. Anaerobic metabolism and lactic acid buildup are common causes of anion gap metabolic acidosis. Even though lactate appears in many mnemonics for metabolic acidosis differentials, it is vital to remember that this is a consequence of the condition and not a distinct underlying cause.
  • Non-gap metabolic acidosis. Diarrhea and renal tubular acidosis are the main contributors of non-gap metabolic acidosis, which is predominantly caused by bicarbonate loss. Addison’s disease, ureterosigmoid or pancreatic fistulas, acetazolamide use, and hyperalimentation brought on by TPN initiation are additional and less common etiologies.

Cause of Metabolic Acidosis

Metabolic acidosis starts in the kidneys and has several etiologies. Acid accumulation due to increased acid synthesis or acid consumption, decreased acid excretion, or gastrointestinal or renal bicarbonate loss can all contribute to metabolic acidosis. The four main types of metabolic acidosis are as follows:

  • Diabetic acidosis. Individuals with poorly controlled diabetes acquire diabetic acidosis. In these patients, the pancreas does not produce enough insulin leading to the accumulation of ketones and further causes acidemia.
  • Hyperchloremic acidosis. Loss of sodium bicarbonate leads to hyperchloremic acidosis. Sodium bicarbonate is a base that acts as a buffering agent which promotes the efflux of lactate and hydrogen ions from active cells and tissues. This kind of acidosis can be brought on by both vomiting and diarrhea.
  • Lactic acidosis. A buildup of lactic acid in the body can lead to lactic acidosis. Chronic alcohol use, heart disease, cancer, seizures, liver disease, extended oxygen deprivation, and low blood sugar are a few possible causes. Lactic acid accumulation might result from even lengthy exercise.
  • Renal tubular acidosis. When the kidneys are unable to eliminate acidic substances into the urine, renal tubular acidosis results. The blood becomes acidic as a result.

Risk Factors to Metabolic Acidosis

An individual’s risk of metabolic acidosis may be influenced by a number of factors, including:

  • Ketogenic diet. The ketogenic diet is a food regimen high in fat, moderate/low in protein, and extremely low in carbohydrates. This kind of diet stimulates a high production of ketone bodies derived from lipolysis to produce energy. Therefore, a long-term ketogenic diet may induce metabolic acidosis.
  • Renal failure. Healthy kidneys maintain the normal bicarbonate level in the blood and eliminate acid from the body through urine. However, in renal failure, there is insufficient acid removal from the body, which can result in metabolic acidosis.
  • Obesity. Lower serum bicarbonate levels and a higher likelihood of acquiring low bicarbonate levels, a sign of potential metabolic acidosis, are linked to obesity.
  • Dehydration. Extreme dehydration can result in insufficient cardiac output, which leaves a large portion of the tissue with insufficient oxygenation. Lactic acid is produced during the energy-releasing mechanisms when oxygen is not present.
  • Poisoning from methanol or aspirin. Metabolic acidosis brought on by significant methanol consumption is characterized by low serum bicarbonate levels. Due to elevated amounts of lactate and ketone, the anion gap widens. This is most likely the result of formic acid accumulation. Aspirin, on the other hand, causes the uncoupling of oxidative phosphorylation by directly stimulating cerebral respiratory centers and blocking the citric acid cycle. This in turn causes lactic acidosis.
  • Diabetes. When acidic molecules known as ketone bodies accumulate due to uncontrolled diabetes (usually type 1 diabetes), diabetic acidosis (also known as diabetic ketoacidosis and DKA) develops.
  • Poisoning by carbon monoxide. Lactic acidosis will arise from carbon monoxide poisoning because less oxygen can be carried by the circulation. In carbon monoxide poisoning, the amount of oxygen delivered to the tissues is decreased as carbon monoxide molecules attach to oxygen binding sites in hemoglobin.

Complications of Metabolic Acidosis

If left untreated, acidosis can result in the following health issues:

  • Renal stones. Hypercalciuria and hypocitraturia, which are brought on by the systemic metabolic acidosis, also aid in the development of calcium nephrolithiasis.
  • Chronic kidney problems and renal failure. Kidney function declines as acid concentrations rise. Additionally, as kidney function declines, more acid accumulates, further compromising the kidneys.
  • Bone disease. Metabolic acidosis may cause alterations in bone development by directly causing bone to dissolve, promoting osteoclast-mediated bone resorption, suppressing osteoblast-mediated bone formation, and changing blood concentrations or the biological effects of parathyroid hormone and vitamin D.
  • Delayed growth. Human metabolic acidosis is associated with a resistance to the hepatocellular effects of growth hormone and causes a considerable drop in serum IGF-1 levels without any discernible effects on IGF binding protein 3.

Diagnosis of Metabolic Acidosis

Diagnostic procedures for evaluating the presence of metabolic acidosis usually include the following:

  • Comprehensive history and physical examination. A focused history can elicit plausible etiologies of acid-base abnormalities including vomiting, diarrhea, drugs, potential overdoses, and chronic illnesses which predispose an individual to metabolic acidosis (e.g., diabetes mellitus). Indicators specific to each cause are revealed during the physical examination, such as dry mucous membranes in diabetic ketoacidosis patients. Respiratory alkalosis as evidenced by hyperventilation may be present as a compensatory response to aid in the removal of carbon dioxide and to correct the acidemia. However, it must be noted that compensatory reactions do not entirely restore the pH range to its normal state.
  • Anion gap measurement. Metabolic acidosis is diagnosed with a series of blood tests with anion gap measurement being the most common. The difference between the positively and negatively charged electrolytes in the blood is known as the anion gap. A normal anion gap is 12, therefore values above 12 indicate the presence of anion gap metabolic acidosis. In the presence of an anion gap, a delta gap may be determined.
  • Arterial blood gases. Understanding acid-base interpretation is essential for identifying and correcting problems associated with the acid-base equilibrium. An arterial blood gas analyzes the blood pH and concentration of carbon dioxide and oxygen in the blood. Normal blood pH ranges from 7.35 to 7.45, therefore a blood pH less than 7.35 indicates acidemia. The partial pressure of carbon dioxide (pCO2) determines whether an acidosis is respiratory or metabolic in origin.  The pCO2 is higher than 40 to 45 mmHg for respiratory acidosis because of hypoventilation. In contrast, the pCO2 in metabolic acidosis is less than 40 mmHg because it is not the cause of the primary acid-base disturbance. Metabolic acidosis is due to alterations in bicarbonate levels in the blood, therefore the distinguishing laboratory value in metabolic acidosis is a decreased bicarbonate concentration (Normal range: 21 to 28 mEq/L).
  • Urinalysis. A urinalysis may be ordered if metabolic acidosis is suspected. Urinary pH will be determined to determine if acids and bases are eliminated properly by the body.

Treatment for Metabolic Acidosis

The underlying etiology of the acid-base imbalance should be addressed in the management of metabolic acidosis. For sepsis and diabetic ketoacidosis, for instance, sufficient fluid resuscitation and correction of electrolyte imbalances are required. Antidotes for poisoning, dialysis, antibiotics, and the delivery of bicarbonate in specific circumstances are further treatments to take into account. For a detailed explanation of the recommended treatment, refer to the particular conditions.

  • Administration of sodium citrate. With sodium citrate, acidosis brought on by kidney failure can be addressed.
  • Fluid resuscitation and administration of insulin. A patient with diabetic ketoacidosis is treated with the administration of intravenous drip (IV) fluids and insulin to restore normal blood pH.
  • Fluid resuscitation and bicarbonate supplements. Depending on the underlying reason, lactic acidosis therapy options may include bicarbonate supplements, intravenous fluids, oxygen, or antibiotics.
  • Oral sodium bicarbonate. One option for treating hyperchloremic acidosis is to provide sodium bicarbonate orally. Bicarbonate aids in raising the blood pH, making it more alkaline.

Nursing Diagnosis for Metabolic Acidosis

Metabolic Acidosis Nursing Care Plan 1

Risk for Electrolyte Imbalance

Nursing Diagnosis: Risk for Electrolyte Imbalance related to metabolic acidosis secondary to congestive heart failure

Desired Outcomes

  • The patient will display heart rate, blood pressure, and laboratory findings within normal ranges (WNL) for the patient.
  • The patient will demonstrate absence of muscle weakness  and neurological disturbance.
Nursing Interventions for Metabolic AcidosisRationale
Monitor the patient’s heart rate and rhythm.Dysrhythmias in the heart’s atrium and ventricles frequently occur in congestive heart failure (CHF). The electrical pathways of the heart are changed by myocardial strain, fibrosis, and chamber dilation. Patients with HF frequently experience atrial fibrillation. Changes in ECG configuration may also indicate the presence of acidemia. Vasodilation and a reduction in cardiac contractility may also lead to a life-threatening cardiovascular collapse.
Keep an eye out for changes in breathing depth, rate, and excursion.     As a compensatory response to remove excess acid, deep, rapid respirations (Kussmaul’s) may be observed. However, as potassium transfers out of the cell in an effort to correct acidosis, respirations may become depressed.
Evaluate and monitor the capillary refill, skin color, and temperature.     These parameters provide information on the tissue perfusion, hemodynamic state, and consequences of hypotension. Reduced perfusion can cause a cool or clammy sensation when touched, and hypoperfusion in the limb will cause pallor. Identifying indicators of systemic hypoperfusion in the patient will aid in the disease management.
Monitor the patient’s urine output and take note of concentrated and diminishing output.The kidneys try to counteract acidosis by excreting excess hydrogen ions as weak acids and ammonia. The maximum pH of urine is 4.0. Reduced renal perfusion may result in decreased urine production because kidneys retain water and sodium in response to a low cardiac output. Additionally, the patient can grow resistant to diuretics, which would reduce urine output. Normal daytime urine output is low due to fluid shifting into tissues, while nighttime nocturia is caused by enhanced renal perfusion in the supine position.
Observe and monitor the patient’s arterial blood gases (ABGs) and oxygen saturation.In acute circumstances, baseline oxygen saturation is helpful in determining the diagnosis and severity of heart failure Additionally, this reveals information about the heart’s capacity to supply oxygen-rich blood to distal tissues. This also evaluates the effectiveness and need for therapy. In the presence of metabolic acidosis, blood bicarbonate and pH levels should gradually rise to normal ranges.  

Metabolic Acidosis Nursing Care Plan 2


Nursing Diagnosis: Fatigue related to metabolic acidosis secondary to liver cirrhosis as evidenced by reports of a persistent lack of energy and difficulty keeping up with daily activities, reduced performance, and increase in physical complaints.

Desired Outcomes: 

  • The patient will report feeling more energized.
  • The patient will perform activities of daily living (ADLs) and take part in chosen activities at a level appropriate to their ability.
Nursing Interventions for Metabolic AcidosisRationale
Encourage frequent bed rest and chair (recliner) rest when the patient is in a toxic state. Maintain a calm environment and restrict guests as necessary.Energy that is available can be utilized for healing. It is thought that movement and being upright reduce hepatic blood flow, preventing the optimal perfusion to hepatocytes.
Keep an eye out for any return of anorexia, liver sensitivity, and enlargement.  Indicates that the condition has neither improved or has gotten worse. This requires additional rest and a modification to the treatment plan.
Encourage frequent position changes. exemplify and instructThis reduces pressure areas and promotes optimal respiratory function to reduce the risk of tissue breakdown.
Analyze the patient’s description of their level of fatigue, as well as how it has changed over time and whether there are any aggravating or mitigating circumstances.The patient can formulate how much fatigue they are feeling by using a suitable numerical scoring system, such 1 to 10. It is possible to create additional scoring scales using descriptive text or images. The nurse can use this technique to account for changes in the patient’s level of fatigue over time. Determining whether the patient’s level of fatigue is consistent or changes over time is crucial.

Metabolic Acidosis Nursing Care Plan 3


Nursing Diagnosis: Nausea related to metabolic acidosis secondary to diabetic ketoacidosis as evidenced by increased salivation and gagging sensation.

Desired Outcome: 

  • The patient will report reduced severity or elimination of nausea.
Nursing Interventions for Metabolic AcidosisRationale
If vomiting develops or continues for more than 24 hours, alert the patient or caregiver to seek medical attention.Dehydration, an electrolyte imbalance, and nutritional deficits can arise from frequent vomiting.
Check for nausea and any further potential causes of decreased oral intake.    During a diabetic ketoacidosis episode, patients may consume less food or liquid orally. There may be nausea or vomiting as well. The patient might need to be NPO if their level of consciousness has diminished.
Keep track of the patient’s daily weights, blood pressure, intake, and output, as well as measuring skin turgor.Nausea, which is frequently accompanied by vomiting, can alter a patient’s level of hydration due to fluid loss.
To restore circulatory volume as directed, administer isotonic intravenous fluids like 0.9% sodium chloride (normal saline).   Nausea accompanied with vomiting may lead to fluid loss. In line with this, patients with diabetic ketoacidosis may have a 12-liter fluid volume deficit. Vital organs like the kidneys, heart, and brain are significantly at risk for failure because of this large fluid deficit. Therefore, rehydration is necessary to maintain proper organ perfusion.

Metabolic Acidosis Nursing Care Plan 4


Nursing Diagnosis: Diarrhea related to metabolic acidosis secondary to gastroenteritis as evidenced by abdominal pain and cramping, hyperactive bowel sounds, increased frequency of stools, urgency, and loose stool.

Desired Outcomes:

  • The patient’s stool culture will be negative for microorganisms causing gastroenteritis.
  • The patient will pass soft, formed stool no more than three times per day.
Nursing Interventions for Metabolic AcidosisRationale
Encourage the client to consume potassium-rich meals.When a client has diarrhea, the high-potassium stomach contents are excreted out of the body through the gastrointestinal tract and stool, leading to hypokalemia. The potassium may transfer back into the cells once the acidosis is corrected, resulting in a serum potassium deficit.  
Encourage adults to drink more fluids by increasing their consumption to 1.5 to 2.5 liters per day plus 200 ml for each loose stool, unless contraindicated.The most common side effect of gastroenteritis is dehydration. Ideally, it should be avoided by managing fluids properly. Fluids lost in liquid stools are replaced by increased fluid intake. It has been suggested that prompt IV fluid administration may enhance gastrointestinal perfusion, allowing oral feeding to resume sooner, and that enhanced renal perfusion may help treat acidosis and rectify electrolyte imbalances.
Check for stomach pain, cramps, frequent or urgent bowel movements, and loose stools.These assessment results frequently link to diarrhea. When the large intestine is affected by gastroenteritis, the colon is unable to absorb water, which causes the patient’s feces to be extremely watery.
Send the stool of the patient for culture.Stool culture is a test to identify the etiologic agent that caused gastroenteritis.
As directed, administer anti-diarrheal drugs.Diarrhea secondary to gastroenteritis is frequently treated with adsorbent antidiarrheals such as pectin, kaolin, and bismuth salts. These medications cover the gut wall and remove toxins from microorganisms that caused the disease.

Metabolic Acidosis Nursing Care Plan 5

Risk for Decreased Cardiac Output

Nursing Diagnosis: Risk for Decreased Cardiac Output related to metabolic acidosis secondary to chronic kidney disease

Desired Outcomes: 

  • The patient will maintain his/her blood pressure and heart rate within the normal range
  • The patient will manifest strong, equal peripheral pulses and a normal capillary refill time.
Nursing Interventions for Metabolic AcidosisRationale
Prepare the patient for renal replacement therapy such as hemodialysis.Cardiovascular symptoms including hypertension and pericardial effusion may be controlled and prevented by reducing uremic toxins, correcting electrolyte imbalances, and reducing fluid excess.
Monitor the patient’s electrolyte, BUN, and creatinine levels.Electrolyte imbalance can affect cardiac and electrical activity. BUN is usually elevated in chronic kidney disease. Before symptoms become clinically apparent, serum creatinine is slightly elevated in unmonitored patients and progressively increase in the later stage of the disease.
Collaborate in treating the underlying disease or condition, if at all possible.Mild acidosis correction is the goal of disease treatment until organ function is restored. Correction of the acid-base problem is encouraged by treating the underlying illness, such as chronic kidney disease. Interventions including blood pressure control, diabetes management, hyperlipidemia treatment, and avoiding toxins like NSAIDs, intravenous (IV) contrast dye, and aminoglycosides can help stop the progression of chronic kidney disease in its early stages.
Monitor the patient’s blood pressure.Systemic shock, as evidenced by hypotension and tissue hypoxia, results from arteriolar dilatation, reduced cardiac contractility, and hypovolemia.
Administer sodium bicarbonate to the patient.Sodium bicarbonate corrects a bicarbonate deficit. However it must be noted that it should be administered with caution in treating severe acidosis (pH less than 7.2) as it might lead to a rebound metabolic alkalosis.

Nursing References

Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020). Nursing diagnoses handbook: An evidence-based guide to planning care. St. Louis, MO: Elsevier.  Buy on Amazon

Gulanick, M., & Myers, J. L. (2022). Nursing care plans: Diagnoses, interventions, & outcomes. St. Louis, MO: Elsevier. Buy on Amazon

Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2020). Medical-surgical nursing: Concepts for interprofessional collaborative care. St. Louis, MO: Elsevier.  Buy on Amazon

Silvestri, L. A. (2020). Saunders comprehensive review for the NCLEX-RN examination. St. Louis, MO: Elsevier.  Buy on Amazon


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Anna Curran. RN, BSN, PHN

Anna Curran. RN-BC, BSN, PHN, CMSRN I am a Critical Care ER nurse. I have been in this field for over 30 years. I also began teaching BSN and LVN students and found that by writing additional study guides helped their knowledge base, especially when it was time to take the NCLEX examinations.

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