Metabolic alkalosis occurs when the body contains excessive amounts of base or alkali. This occurs when there is a loss of acid or hydrogen or a gain in bicarbonate.
A normal pH level is 7.35 – 7.45. An increase above this range is alkalosis. If bicarbonate (HCO3) increases or carbon dioxide (CO2) decreases, alkalosis will occur. The renal system regulates HCO3, so if the kidneys aren’t functioning correctly, bicarbonate is not excreted adequately.
There is also metabolic acidosis, which occurs when there is an excessive accumulation of acid in the body.
In this article:
- Nursing Process
- Nursing Assessment
- Nursing Interventions
- Nursing Care Plans
- Decreased Cardiac Output
- Deficient Fluid Volume
- Deficient Knowledge
- Ineffective Tissue Perfusion
Nursing Process
Nursing management and care for patients with metabolic alkalosis will depend on the cause and severity of the symptoms. For mild cases of metabolic alkalosis, treatment may not be required. Severe cases, however, will require immediate medical attention. Nurses must monitor symptoms and abnormalities, assist with identifying the underlying cause, and initiate appropriate treatment interventions, including intravenous fluids and electrolytes, to correct the imbalance.
Nursing Assessment
The first step of nursing care is the nursing assessment, during which the nurse will gather physical, psychosocial, emotional, and diagnostic data. In this section, we will cover subjective and objective data related to metabolic alkalosis.
Review of Health History
1. Note the patient’s general symptoms.
The patient may manifest symptoms of metabolic alkalosis, including:
- Irritability
- Muscle spasms, cramps, or twitching
- Confusion
- Fatigue
- Tremors
- Arrhythmias
- Paresthesias
- Seizures
- Coma
2. Assess the causative factor.
Causes of metabolic alkalosis include:
- Hypokalemia (intracellular shift of hydrogen)
- Vomiting (loss of GI acid and hydrogen)
- Recent GI surgery
- Nasogastric suctioning
- Excessive use of antacids
- Hypovolemia
- Hyperaldosteronism
- Diuretic use
- Renal failure
- Cystic fibrosis
- Cushing syndrome
- Congenital adrenal hyperplasia (CAH)
- Use of exogenous steroids
- Genetic conditions: Bartter syndrome, Gitelman syndrome, Liddle syndrome
3. Review the patient’s list of medications.
Consuming excessive amounts of certain drugs or supplements can result in metabolic alkalosis. Note the patient’s use of these medications:
- Loop or thiazide diuretics
- Tobacco chewing
- Carbenoxolone
- Fludrocortisone
- Glucocorticoids
- Antacids (magnesium hydroxide)
- Calcium carbonate
4. Consider the patient’s diet.
Chronic licorice ingestion can result in hypokalemia, hypernatremia, and metabolic alkalosis. Baking soda is bicarbonate, and excess ingestion increases the risk of metabolic alkalosis. Inquire about the patient’s dietary habits if a cause is difficult to identify.
Physical Assessment
1. Assess for signs of hypocalcemia.
Metabolic alkalosis lowers the concentration of ionized calcium. Assess for signs of hypocalcemia, including:
- Tetany
- Positive Chvostek sign
- Positive Trousseau sign
- Changes in mental status
- Seizures
2. Assess the cardiovascular status.
Metabolic alkalosis lowers coronary blood flow, causing arrhythmias.
3. Assess vital signs.
The lungs attempt to compensate through hypoventilation to retain CO2 and lower the blood pH, and can result in hypoxemia. Hypertension or hypotension may occur in relation to hypervolemia or hypovolemia.
4. Assess the volume status.
A volume status assessment can predict the risk for metabolic alkalosis. Assessment includes:
- Orthostatic blood pressure changes
- Alterations in heart rate
- Mucous membranes
- Fluid accumulation (edema)
- Skin turgor changes
- Weight changes
- Urine output
Note:
- Chloride-responsive alkalosis = volume depletion.
- Chloride-resistant alkalosis = volume expansion.
5. Assess for signs of self-induced vomiting.
Excessive or self-induced vomiting can cause metabolic alkalosis. Assess for dental caries and enamel degradation in patients with bulimia.
6. Determine the presence of Cushing’s syndrome.
Elevated cortisol levels cause increased sodium reabsorption, hypokalemia, and metabolic alkalosis. Cushing syndrome-related findings include the following:
- Obesity
- Swollen, round, puffy face (moon face)
- Accumulated fat on the back of the neck and between shoulder blades (buffalo hump)
- Excessive hair growth (hirsutism)
- Skin striae with violet color
- Acne
Diagnostic Procedures
1. Review ABGs and electrolytes.
Serum electrolytes and arterial blood gases (ABG) determine the presence of metabolic alkalosis. Metabolic alkalosis is associated with imbalanced electrolytes, and lab results will show hypokalemia and hypochloremia due to decreased fluid volumes.
ABGs will demonstrate:
- pH > 7.45
- pCO2 35-45 mmHg (may be normal or high)
- HCO3 > 26 mEq/L
2. Analyze the urine ion concentration.
Urine sodium ion concentration assesses the volume status in patients with oliguria. Gastric acid loss causes an increased serum bicarbonate concentration. The kidneys try to eliminate excess bicarbonate. As a result, the urine salt level increases despite volume loss.
3. Measure the plasma renin activity and aldosterone level.
These labs can determine the cause of metabolic alkalosis for patients who do not use diuretics.
4. Evaluate the presence of conditions that can increase the risk of metabolic alkalosis.
- Primary hyperaldosteronism: measure the aldosterone levels in a 24-hour urine collection following salt loading.
- Cushing syndrome: measure plasma cortisol:
- At midnight while sleeping
- Free cortisol in a 24-hour urine study
- Dexamethasone suppression test
- Syndrome of apparent mineralocorticoid excess (AME): measure the proportion of cortisol to cortisone metabolites in urine.
- Congenital adrenal hyperplasia: measure the plasma or urine adrenal androgens.
- To rule out diuretic use: screen urine for diuretics for unexplained hypokalemic metabolic alkalosis.
5. Utilize imaging studies.
Imaging studies can assist in diagnosing conditions causing metabolic alkalosis.
- Primary hyperaldosteronism, Cushing syndrome: adrenal imaging studies (CT scan or MRI).
- Renal artery stenosis and kidney-related hypertension: renal Doppler ultrasound, MRI, and renal angiography.
Nursing Interventions
Nursing interventions and care are essential for the patients recovery. In the following section, you will learn more about possible nursing interventions for a patient with metabolic alkalosis.
1. Manage the underlying cause.
Vomiting and diuretic use are the most common causes of metabolic alkalosis. Determine the underlying etiology to manage effectively.
2. Administer medications as prescribed.
- Carbonic anhydrase inhibitors (acetazolamide) inhibit carbonic anhydrase, which reduces the reabsorption of sodium bicarbonate.
- Hydrochloric acid (HCl) is administered IV when alkalosis is severe, and sodium chloride or potassium chloride can’t be administered due to volume overload.
- Potassium-sparing diuretics correct potassium deficiency or fluid and electrolyte imbalance.
- Angiotensin-converting enzyme (ACE) inhibitors prevent aldosterone secretion from the adrenal cortex.
- Potassium supplements correct hypokalemia-related metabolic alkalosis.
- Fluid replacement is for chloride-responsive metabolic alkalosis with hypovolemia.
- Corticosteroids are for hyperaldosteronism, metabolic alkalosis, and hypertension.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in chloride-resistant alkalosis.
3. Stop the vomiting and loss of gastric acid.
Administer antiemetics to prevent vomiting. Nasogastric suction can lead to a loss of gastric acid, which can be reduced through the use of H2-blockers or proton pump inhibitors.
4. Adjust or discontinue diuretics as ordered.
Adjust or discontinue thiazide or loop diuretics. Acetazolamide or a potassium-sparing diuretic are alternatives.
5. Initiate intravenous infusion.
Start a normal saline IV infusion to manage the alkalosis in patients with volume depletion and chloride-responsive alkalosis.
6. Prevent fluid overload.
Administer potassium chloride to treat alkalosis and hypokalemia without causing volume overload in patients with edema or CHF.
7. Assist the patient with dialysis.
Hemodialysis and peritoneal dialysis treat metabolic alkalosis in patients with advanced renal failure by adjusting the dialysate solution.
8. Educate on medication use.
Diuretics may need to be discontinued or reduced if causing too much fluid loss. Antacids commonly contain sodium bicarbonate, and patients who take these excessively are at risk for metabolic alkalosis.
Nursing Care Plans
Once the nurse identifies nursing diagnoses for metabolic alkalosis, nursing care plans help prioritize assessments and interventions for both short and long-term goals of care. In the following section, you will find nursing care plan examples for metabolic alkalosis.
Acute Confusion
Central nervous system symptoms of metabolic alkalosis can range from confusion to coma and affect muscle contraction and sensations.
Nursing Diagnosis: Acute Confusion
Related to:
- Disease process
- Severe dehydration
- Electrolyte imbalances
As evidenced by:
- Altered psychomotor performance
- Decreased level of consciousness
- Muscle twitching
- Tremors
- Numbness and tingling
- Restlessness
- Seizures
Expected outcomes:
- Patient will remain oriented to person, place, and time.
- Patient will maintain a normal level of consciousness without tremors or muscle weakness.
- Patient will not experience a seizure.
Assessment:
1. Assess the patient’s level of consciousness.
The acid-base balance is a delicate system, and slight alterations in pH can result in irritability, confusion, muscle twitching, and more.
2. Assess laboratory values.
ABGs and electrolytes should be monitored closely if the patient is displaying alterations in mental status.
Interventions:
1. Provide reality orientation.
Keeping the patient oriented as needed can help reduce confusion and encourage cooperation with the treatment regimen.
2. Use therapeutic communication and reassurance.
This promotes a trusting relationship with the patient. Reassure family members that confusion is temporary and explain why it is occurring.
3. Limit exposure to stimuli and keep the environment free from excess noise.
Excessive stimulation can aggravate confusion and irritability in patients with metabolic alkalosis.
4. Provide safety against seizures.
Seizures are a risk with metabolic alkalosis. Keep the patient safe in the event of a seizure by preventing injury or aspiration and maintaining a patent airway.
Decreased Cardiac Output
Increased bicarbonate levels in the blood are associated with decreased circulating blood volumes.
Nursing Diagnosis: Decreased Cardiac Output
Related to:
- Electrolyte imbalances
- Alteration in heart rate and rhythm
- Decreased myocardial contractility
- Hypovolemia
- Hypervolemia
- Diuretic misuse
- Increased ventricular filling
- Decreased kidney function
As evidenced by:
- Tachycardia
- Arrhythmia
- Hypotension/hypertension
- Decreased peripheral pulses
- Abnormal heart sounds
- Orthopnea
- Crackles
- Jugular vein distension
- Edema
- Weight gain
- Oliguria
Expected outcomes:
- Patient will manifest adequate cardiac output as evidenced by the following:
- Blood pressure: SBP >90 to <140 mmHg / DBP >60 to <90 mmHg
- Heart rate: 60 to 100 beats/min with a regular rhythm
- Respiratory rate: 12 to 20 breaths/min
- Urine output 0.5 to 1.5 cc/kg/hour
- Absence of abnormal heart sounds
- Patient will adhere to their diuretic regimen to prevent hypokalemia and fluid overload.
Assessment:
1. Monitor blood pressure, heart rate, and rhythm.
Tachycardia is evident even at rest as a compensatory mechanism for decreased ventricular contractility. Orthostatic changes accompany excess or deficient fluid volume. Metabolic alkalosis is a common acid-base abnormality in patients with congestive heart failure (CHF). In the early stages of CHF, hypertension is present due to elevated systemic vascular resistance. As the disease progresses, irreversible hypotension occurs.
2. Monitor oxygen saturation.
A change in oxygen saturation is one of the earliest indicators of reduced cardiac output.
Interventions:
1. Administer medications as ordered.
Heart failure therapy necessitates a complex therapeutic regimen. The cornerstone of treatment includes angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, and diuretics. Aldosterone antagonists, digoxin, and vasodilators may also be prescribed as necessary. Polypharmacy is a challenge for patients with heart failure, but adhering to their treatment plan is crucial to prevent volume overload.
2. Assist in the conduct of diagnostic modalities.
- 12 lead ECG: ST-segment depression and T- wave flattening can develop due to hypokalemia
- Chest x-ray: Cardiomegaly and pulmonary congestion may be observed
3. Take caution with IV fluids.
With CHF, use potassium chloride instead of normal saline to correct alkalosis and hypokalemia and prevent fluid overload. IV HCl can be administered for severe metabolic alkalosis to correct cardiac arrhythmias.
4. Replace with potassium-sparing diuretics.
Thiazide and loop diuretics may need to be replaced with potassium-sparing diuretics to prevent hypokalemia.
Deficient Fluid Volume
Metabolic alkalosis is often caused by severe vomiting, leading to fluid loss and chloride and potassium depletion.
Nursing Diagnosis: Deficient Fluid Volume
Related to:
- Severe vomiting
- Disease process
- Insufficient fluid intake
- Electrolyte imbalances
- Dehydration
As evidenced by:
- Altered skin turgor
- Dry mucous membranes
- Dry skin
- Decreased blood pressure
- Decreased urine output
- Increased body temperature
- Increased heart rate
- Increased urine concentration
- Altered mental status
- Sunken eyes
- Thirst
- Weakness
Expected outcomes:
- Patient will remain free from signs of dehydration, with vital signs within normal limits.
- Patient will demonstrate interventions to manage vomiting and correct fluid loss.
Assessment:
1. Assess for signs of dehydration.
Early signs of dehydration include restlessness, thirst, and inability to concentrate, while the late signs include weak and thready pulse, confusion, and oliguria. These signs occur when the body has compensated fluid loss by moving fluids from interstitial space to the vascular compartment.
2. Assess causative factors contributing to fluid loss.
Fluid loss occurs due to vomiting or diarrhea, which causes metabolic alkalosis due to acid loss, creating an imbalance between acid and bicarbonate. Early identification of the risk factors can help manage and prevent complications.
3. Assess medication use.
Loop diuretics cause the body to excrete potassium which can cause hypokalemia. Excessive consumption of antacids can cause alkalosis since sodium bicarbonate is an ingredient in these medications.
Interventions:
1. Monitor and evaluate electrolyte levels.
Fluid loss in metabolic alkalosis is associated with electrolyte imbalance (hypokalemia and hypochloremia) and will require correction.
2. Administer fluid replacement IV or orally.
If oral fluid intake is difficult due to excessive vomiting, intravenous fluid replacement may be necessary to correct and manage fluid loss in metabolic alkalosis.
3. Monitor the patient’s intake and output.
Decreased urine output can indicate kidney dysfunction, further aggravating metabolic alkalosis if the kidneys cannot reabsorb hydrogen or excrete bicarbonate.
4. Administer medications to treat symptoms.
If severe vomiting or diarrhea is causing hypovolemia and subsequent metabolic alkalosis, administer antiemetics or antidiarrheals to prevent fluid loss.
Deficient Knowledge
Patient education is a vital part of the management of metabolic alkalosis. Patients may need to be made aware of how their medical conditions, medications, or ailments can disrupt their pH.
Nursing Diagnosis: Deficient Knowledge
Related to:
- Unfamiliarity with the medical condition
- Poor health literacy
- Inability to recall information
- Inadequate understanding of information
- Inadequate interest in learning
As evidenced by:
- Inaccurate follow-through of instructions
- Misconceptions about treatment
- Inaccurate statements about alkalosis
- Nonadherence to medication regimen
- Recurrence of alkalosis
Expected outcomes:
- Patient will verbalize an understanding of metabolic alkalosis, its signs and symptoms, possible complications, and treatment regimen.
- Patient will verbalize ways to prevent alkalosis.
Assessment:
1. Assess the health literacy of the patient.
Assessment of health literacy allows accurate care planning and ensures an appropriate teaching approach. Patients with poor health literacy often have poorer health outcomes.
2. Assess the patient’s motivation to learn.
Willingness and motivation to learn impacts health teaching outcomes. If the patient is not cognitively aware, direct teaching towards a support person.
Interventions:
1. Educate the patient about the signs and symptoms of metabolic alkalosis.
Metabolic alkalosis doesn’t always have obvious signs, and the patient may be unaware. The nurse can educate on potential causes and to monitor for changes in alertness, muscle control, or numbness and tingling in the extremities.
2. Discuss medication and alkali ingestion.
Patients who take diuretics are at a higher risk of experiencing metabolic alkalosis from electrolyte imbalances. Educate patients and families that antacids contain sodium bicarbonate, and baking soda is sodium bicarbonate. Excessive ingestion of these can result in metabolic alkalosis.
3. Discuss severe complications with patients with renal failure.
Renal failure prevents the body’s natural buffering system from correcting the acid-base balance. These patients may require dialysis and intense inpatient management.
4. Educate on sources of potassium and calcium.
Electrolytes can be lost with metabolic alkalosis. If the patient can tolerate PO consumption, have them eat dried fruits, potatoes, avocado, and bananas for potassium and cheese, almonds, salmon, and dairy for calcium.
Ineffective Tissue Perfusion
A decrease in blood circulation from hypovolemia and electrolyte depletion leads to inadequate heart, brain, lung, and kidney perfusion.
Nursing Diagnosis: Ineffective Tissue Perfusion
Related to:
- Impaired oxygen transport
- Interruption in blood flow
- Altered bicarbonate levels
- Insufficient knowledge of metabolic alkalosis and its management
As evidenced by:
- Weak or absent peripheral pulses
- Prolonged capillary refill
- Altered sensation
- Peripheral edema
- Muscle twitching
- Muscle cramps and spasms
- Alterations in mental status
- Reduced urine output
- Hypoventilation
Expected outcomes:
- Patient will maintain optimal tissue perfusion as evidenced by the following:
- Strong, palpable pulses
- Capillary refill time of <2 secs
- Absence of edema
- No alterations in sensation
- Urine output 0.5 to 1.5 cc/kg/hour
- Patient will not experience any changes in the level of consciousness.
Assessment:
1. Monitor respiratory status.
Hypoventilation often occurs as a compensatory mechanism for metabolic alkalosis. The respiratory rate will decrease in an attempt to retain CO2 and equalize HCO3 and normalize the blood pH.
2. Monitor urine output.
Urine output is a reliable indicator of renal function. Metabolic alkalosis may occur in patients with kidney disease due to the decreased glomerular filtration rate causing failure to excrete HCO3.
Interventions:
1. Identify the underlying cause.
Treating metabolic alkalosis requires identifying the cause. Diuretics and vomiting are the most common cause of lost acid, resulting in hypovolemia and poor perfusion.
2. Administer isotonic IV solutions as ordered.
Volume expansion is the first step in treating metabolic alkalosis with impaired perfusion.
3. Consider dialysis for chronic kidney disease.
Hemodialysis or peritoneal dialysis can correct metabolic alkalosis in patients with renal failure if they are fluid-overloaded and not responsive to diuretics.
4. Perform neurological checks.
Confusion, seizures, and coma can occur from metabolic alkalosis and electrolyte derangements. Perform neurological checks as ordered.
References
- Ackley, B.J., Ladwig, G.B.,& Makic, M.B.F. (2017). Nursing diagnosis handbook: An evidence-based guide to planning care (11th ed.). Elsevier.
- ACCN Essentials of Critical Care Nursing. 3rd Edition. Suzanne M. Burns, MSN, RRT, ACNP, CCRN, FAAN, FCCM, FAANP. 2014. McGraw Hill Education.
- Alkalosis. MedlinePlus. Reviewed: November 6, 2021. From: https://medlineplus.gov/ency/article/001183.htm
- Brinkman, J. E., & Sharma, S. (2022, July 18). Physiology, metabolic alkalosis – StatPearls – NCBI bookshelf. National Center for Biotechnology Information. Retrieved April 2023, from https://www.ncbi.nlm.nih.gov/books/NBK482291/
- Carpenito, L.J. (2013). Nursing diagnosis: Application to clinical practice. (14th ed.). Lippincott Williams & Wilkins.
- Cleveland Clinic. (2021, May 10). Metabolic alkalosis: Causes, acid-base & electrolyte imbalance. https://my.clevelandclinic.org/health/diseases/21529-metabolic-alkalosis#symptoms-and-causes
- Doenges, M.E., Moorhouse, M.F., & Murr, A.C. (2019). Nursing care plans: Guidelines for individualizing client care across the life span (10th edition). F.A. Davis Company.
- Gulanick, M. & Myers, J.L. (2014). Nursing care plans: Diagnoses, interventions, and Outcomes. (8th ed.). Elsevier.
- Medical-Surgical Nursing: Concepts for Interprofessional Collaborative Care. 9th Edition. Donna D. Ignatavicius, MS, RN, CNE, ANEF. 2018. Elsevier, Inc.
- Metabolic Alkalosis. Journal of the American Society of Nephrology. February 11, 2000. From: https://jasn.asnjournals.org/content/11/2/369
- Physiology, Metabolic Alkalosis. Brinkman JE, Sharma S. [Updated 2022 Jul 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482291/
- Thomas, C. P. (2023, March 30). Metabolic alkalosis workup: Approach considerations, serum anion gap, urine sodium ion concentration. Diseases & Conditions – Medscape Reference. Retrieved April 2023, from https://emedicine.medscape.com/article/243160-workup#showall
- Urso, C., Brucculeri, S., & Caimi, G. (2015). Acid–base and electrolyte abnormalities in heart failure: Pathophysiology and implications. Heart Failure Reviews, 20(4), 493-503. https://doi.org/10.1007/s10741-015-9482-y
