Last updated on December 31st, 2022 at 11:51 am
Metabolic Alkalosis Nursing Care Plans Diagnosis and Interventions
Metabolic Alkalosis NCLEX Review and Nursing Care Plans
Metabolic alkalosis is characterized by an increased pH and a higher-than-normal plasma bicarbonate level. When bicarbonate levels rise, pCO2 levels must rise as well to keep pH within normal limits.
As a result, when there is metabolic alkalosis, the body compensates by increasing pCO2 and decreasing alveolar ventilation.
Signs and Symptoms of Metabolic Alkalosis
The signs and symptoms of metabolic alkalosis are not always specific, and in some situations, there may be none at all. People suffering from this type of alkalosis frequently complain about the underlying issues causing it. These may consist of:
Symptoms of serious metabolic alkalosis include:
- restlessness
- confusion
- seizures
- Coma
Because metabolic alkalosis reduces ionized calcium concentration, the following indications of hypocalcemia may occur:
- tetany
- Chvostek sign
- Trousseau sign
- change in mental status
Causes of Metabolic Alkalosis
- Loss of gastric acids. This is the most frequent reason for metabolic alkalosis. It is typically affected by vomiting or suction via a nose-feeding tube. Large amounts of hydrochloric acid, a potent acid, are found in gastric secretions. Its depletion causes the blood to become more alkaline.
- Excessive consumption of non-absorbable antacids. Usage of antacids won’t often result in metabolic alkalosis. However, using a nonabsorbable antacid among patients with kidney problems can result in alkalosis. Aluminum hydroxide or magnesium hydroxide are ingredients in non-absorbable antacids.
- Diuretics. Thiazides and loop diuretics both increase sodium chloride excretion in the distal convoluted tubule and the thick ascending loop, correspondingly. Through the depletion of chloride and increased sodium ion transport to the collecting duct, these drugs promote metabolic alkalosis, which increases the secretion of potassium and hydrogen ions.
- Hypokalemia. The hydrogen ions that are normally in the fluid surrounding your cells may go within the cells if you have a potassium deficiency. Because of the absence of acidic hydrogen ions, bodily fluids and blood become more alkaline.
- The reduced blood volume in the arteries. This can result from both liver cirrhosis and a weak heart. The body’s capacity to expel the alkaline bicarbonate ions is compromised by decreased blood flow.
- Organ failure. Failure of a major organ, including the heart, kidneys, or liver, can result in metabolic alkalosis. Potassium levels decrease as a result.
- Genetic conditions. Rarely, metabolic alkalosis may be brought on by an inherited gene. The following five hereditary conditions can result in metabolic alkalosis:
- Bartter syndrome
- Gitelman syndrome
- Liddle syndrome
- Glucocorticoid remediable aldosteronism
- Apparent mineralocorticoid excess
Risk factors for Metabolic Alkalosis
- Severe vomiting. Bicarbonate levels in bodily fluids are elevated in metabolic alkalosis. It can occur under a variety of circumstances. It might be brought on by digestive problems that throw off the acid-base balance in the blood, such as frequent vomiting.
- Critically ill. Metabolic alkalosis is the most prevalent type of acid-base imbalance seen in critically ill patients. Although the effects of acidosis have long been understood, those of severe metabolic alkalosis are only now becoming recognized.
- Patient with NGT. Hydrogen ions can be released through the kidneys or the gastrointestinal tract. Loss of hydrochloric acid-rich stomach secretions in patients with nasogastric (NG) suction causes metabolic alkalosis.
Complications of Metabolic Acidosis
- Electrolyte imbalance. Certain electrolyte levels may fall as a result of metabolic alkalosis. These modifications disturb the acid-base balance in the body. Imbalance in the electrolyte levels include hypophosphatemia, hypokalemia, and hypomagnesemia
- Angina and refractory arrhythmia. Electrolyte and acid-base imbalances are common and potentially serious complications in patients with congestive heart failure. This could be as a result of the neurohumoral activation brought on by the pathophysiological changes in the heart failure state (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), or as a consequence of the adverse side effects of treatment with diuretics, cardiac glycosides, and ACE inhibitors. Hyponatremia, magnesium, and potassium deficiencies are common in people with heart failure; the latter two are crucial for the emergence of cardiac arrhythmias.
- Dehydration. If the alkalosis is caused by prolonged vomiting, severe dehydration and volume restriction are possible.
- Reduced blood supply to the cerebral arteries. causing delirium, seizures, tetany, and impaired mental condition.
- Hepatic Encephalopathy. Metabolic alkalosis can accelerate the development of hepatic encephalopathy in those who are vulnerable by raising ammonia production.
- Hypoventilation. Hypoventilation due to metabolic alkalosis results in hypoxemia, which can be dangerous for patients—especially those with weak respiratory systems—and makes it more difficult to wean patients from mechanical ventilation.
Diagnosis of Metabolic Alkalosis
- Physical Examination. A physical examination can assist determine the cause of metabolic alkalosis. The assessment of hypertension and volume status are both important aspects of the physical examination.To begin the diagnosing process, the doctor will obtain the patient’s medical history and perform a physical examination to assess the symptoms.
- Arterial blood gas. Assessment of respiratory, metabolic, and mixed acid-base problems using pH ([H +]) and CO 2 levels, with or without physiologic compensation (partial pressure of CO 2).
- Urine chloride ion concentration. A urine chloride ion concentration can be obtained if the medical history, physical assessment, drug usage, and presence of hypertension do not reveal the cause of metabolic alkalosis. Low levels of urine chloride ions are typically linked to metabolic alkalosis secondary to volume loss.
- Serum anion gap. The serum anion gap calculation may be used to distinguish between primary metabolic alkalosis and metabolic compensation for respiratory acidosis. As a result of the increased negative charge of albumin and the increased generation of lactate, the anion gap is typically modestly increased in metabolic alkalosis.
- Urine sodium ion concentration. In many cases, especially in those with oliguria, the volume status is assessed by measuring the sodium ion concentration in the urine. In metabolic alkalosis, volume depletion may not, however, result in low urine sodium levels. Serum bicarbonate concentration rises during the first few days following vomiting as a result of the loss of acidic stomach contents. The kidneys make an effort to eliminate extra bicarbonate as sodium or potassium salt. Therefore, despite volume loss, the urine sodium level may be excessively high.
- Plasma renin activity and aldosterone level. Measuring plasma renin activity and aldosterone levels may aid in determining the cause of metabolic alkalosis, particularly in individuals with hypertension, hypokalemic metabolic alkalosis, and renal potassium wasting who are not taking diuretics.
Body’s response to Metabolic Alkalosis
Two of our body organs work to compensate for metabolic alkalosis — The lungs and kidneys.
- Respiratory compensation. When we digest the food we eat into energy in our cells, our bodies create carbon dioxide. The carbon dioxide is absorbed by the red blood cells in our veins and transported to our lungs where it is expelled. Carbonic acid is formed when carbon dioxide gas combines with water in the blood. From there, the carbonic acid breaks into hydrogen and the bicarbonate ion. Ions made of bicarbonate are alkaline. The number of alkaline bicarbonate ions that are carried in our blood can be increased or decreased by altering the rate of breathing. The process is called respiratory compensation, and it occurs automatically in the body. The body responds in this way initially and quickly. Signals are transmitted to lower the rate of respiration to counteract alkalosis.
- Renal compensation. The renal system slowly adjusts by storing bicarbonate to restore pH balance when a patient hypoventilates, causing CO2 retention to occur in the lungs and lowering pH as a result. When hypoventilation is corrected, like with a patient with ventilator-assisted respiratory failure, CO2 levels will fall immediately, while bicarbonate levels will take longer to fall.
Treatment for Metabolic Alkalosis
- Drug therapy. If vomiting occurs, antiemetics should be administered if possible. Gastric acid secretion can be decreased with H2-blockers or more effectively with proton pump inhibitors if sustained gastric suction is required. If necessary, the dose or medication can be withdrawn in patients taking thiazide or loop diuretics. Acetazolamide or a diuretic that spares potassium are other options.
- Chloride-responsive. If volume depletion is present together with chloride-responsive alkalosis, the condition should be treated with an intravenous administration of isotonic sodium chloride solution. Because this type of alkalosis is generally coupled with hypokalemia, use potassium chloride to treat the hypokalemia as well. If chloride-responsive alkalosis occurs in the context of edematous conditions (for example, congestive heart failure [CHF]), utilize potassium chloride rather than sodium chloride to correct the alkalosis and prevent fluid overload. If diuresis is required to rectify the alkalosis, a carbonic anhydrase inhibitor or a potassium-sparing diuretic can be employed.
- Chloride-resistant. The treatment of chloride-resistant metabolic alkalosis is determined by the main cause.
- Diuretics. The potassium-sparing diuretics or aldosterone antagonist diuretics are used to treat metabolic alkalosis. Also, in patients with a syndrome of apparent mineralocorticoid excess, metabolic alkalosis can be treated with potassium-sparing diuretics
- Corticosteroid. Effective treatment in metabolic alkalosis and hypertension in glucocorticoid-remediable hyperaldosteronism.
- Surgery. If an adrenal adenoma or carcinoma is the cause of primary hyperaldosteronism, surgical excision of the tumor should rectify the alkalosis.
Nursing Diagnosis for Metabolic Alkalosis
Metabolic Alkalosis Nursing Care Plan 1
Nursing Diagnosis: Electrolyte Imbalance related to metabolic alkalosis secondary to dehydration, as evidenced by reports of tingling and numbness on extremities, muscle twitching, muscle cramps, fatigue, confusion, and tremors.
Desired Outcomes:
- The patient will have normal serum bicarbonate and electrolyte results.
- The patient will be free from symptoms of imbalance such as the absence of neurological impairment and normal vital signs.
- The patient will perform measures that will help to treat or stop fluid volume loss.
| Metabolic Alkalosis Nursing Interventions | Rationale |
| Assess the patient’s breathing, and note the rhythm, depth, and rate. | Hypoventilation is a compensatory mechanism to save carbonic acid, it carries clear hazards for the patient including hypoxemia and respiratory failure. |
| Assess the patient for signs of dehydration in the oral mucous membranes and skin turgor. | Dehydration symptoms can also be seen on the skin. Elderly patients’ skin loses elasticity, thus it should be examined across the sternum or on the inner thighs to determine skin turgor. It’s possible to see longitudinal furrows surrounding the tongue. |
| Evaluate the patient’s state of consciousness, neuromuscular condition, strength, tone, and movement. | Tingling, numbness, dizziness, restlessness, apathy, and disorientation due to increased pH of CNS fluid are manifestations of a hypersensitive CNS. |
| Monitor the patient’s cardiac rhythm and beat. | Ectopic atrial and ventricular beats, as well as tachy dysrhythmias, could form. |
| Determine the amount and source of the patient’s output. Monitor the patient’s intake and weight daily. | Potassium and HCl are lost in vomiting and GI suctioning, which is helpful in determining the source of ion loss. |
| Encourage the patient to consume foods and liquids that are high in potassium and calcium depending on the blood level, including bananas, cauliflower, dried peaches, figs, wheat germ, canned grapefruit, and apple juice. | When oral intake is possible, it is helpful for replenishing potassium losses. |
| Monitor the patient’s ABGs/pH, serum electrolytes (particularly potassium), and BUN. | Renal function is monitored as the success of the therapy is evaluated. |
| Administer parenteral fluids containing saline solution as directed. | Fluid intake is required to keep hydrated. Depending on the clinical condition, different types and amounts of fluid should be replaced, as well as different infusion rates. Chloride ions will aid in making the blood more acidic to reduce alkalosis. |
| Assist the patient when eating if they are unable to do so on their own and encourage the family to help with feedings as needed. | Patients who are dehydrated may be weak and unable to independently fulfill their recommended intake. |
Metabolic Alkalosis Nursing Care Plan 2
Nursing Diagnosis: Diarrhea related to metabolic alkalosis secondary to acute gastroenteritis, as evidenced by abdominal cramping, frequent defecation, hyperactive bowel sounds, and loose watery stools.
Desired Outcomes:
- The patient will express an understanding of the causes and reason for the treatment of diarrhea.
- The patient will agree to consume at least 1,500 to 2,000 mL of clear liquids to achieve a good skin turgor and normal weight.
- The patient will maintain a normal pattern of bowel functioning.
| Metabolic Alkalosis Nursing Interventions | Rationale |
| Assess the patient for any pain, cramps, indigestion, urgency, loose or watery stools, or symptoms of an overactive bowel. | These assessment results are frequently connected to diarrhea. Patients define diarrhea differently, citing incontinence, increased frequency, the urgency of bowel movements, or loose stool consistency as the main symptoms. Three times per week to three times per day is considered the normal frequency for stools. The main criteria used by doctors to differentiate between acute diarrhea and chronic diarrhea are increased frequency of urination or increased stool weight. |
| Determine the patient’s defecation pattern. | Each person has a different set of bowels. One person’s definition of normal may not apply to another. Treatment will be guided by the evaluation of fecal patterns. |
| Send the patient’s stool for culture as ordered. | Blood, fat, electrolytes, white blood cells, infectious or parasitic organisms, bacterial toxins, and possible etiological organisms causing diarrhea will be identified through testing or stool examinations. |
| Weight the patient daily and note any weight loss. | The body loses a lot of water due to diarrhea. A precise daily weight is a crucial marker of the body’s fluid balance. Over the short term, it has regularly been linked to decreased weight. |
| Analyze the patient’s dietary and behavioral changes. | Regular exercise, healthy food, and excellent health practices can reduce the risk of disease by preventing episodes of diarrhea. |
| Administer the prescribed anti-diarrheal medications for the patient. | The majority of antidiarrheal medications slow down gastrointestinal motility, which increases fluid absorption. Yogurt or probiotic supplements may help to alleviate symptoms by restoring the usual flora in the intestine. |
| Include bulk fiber in the patient’s diet, such as psyllium, cereal, and grains. | Dietary fiber and bulking agents help make the stool thicker by absorbing stool moisture. Some cereal items, dietary supplements, and commercial bulk fiber laxatives all contain psyllium. |
| Encourage the patient to drink 1.5 to 2 L of liquids every 24 hours, plus 200 mL for each loose stool, unless doing so is contraindicated. | Increasing fluid intake is essential, especially if diarrhea is present. Fluid loss can be replaced through increased fluid consumption and liquid meal substitutes. |
Metabolic Alkalosis Nursing Care Plan 3
Nursing Diagnosis: Nausea related to metabolic alkalosis secondary to bowel obstruction, as evidenced by reports of nausea, excessive salivation, gagging sensation, and increased swallowing.
Desired Outcomes:
- The patient will report decreased severity or elimination of nausea.
- The patient will be able to tolerate clear liquids without any nausea.
| Metabolic Alkalosis Nursing Interventions | Rationale |
| Monitor the patient’s daily weights, blood pressure, intake, and output, as well as the skin turgor. | Vomiting, which is frequently accompanied by nausea, can alter a patient’s level of hydration due to fluid loss. |
| Place an emesis basin within the patient’s easy reach. | Vomiting and nausea frequently occur together. If there is a psychogenic component to nausea, keep the emesis basin out of sight but within the patient’s reach. |
| Instruct the patient about proper oral hygiene and offer support. | Anorexia and excessive salivation are linked to this. Maintaining good oral hygiene makes the situation more comfortable and manageable. |
| Reduce unpleasant environmental stimuli and oral intake; use intermittent suctioning with low pressure during NG suctioning; and irrigate the gastric tube with isotonic solutions rather than water if necessary. | Limits HCl, potassium, and calcium losses during digestion. |
| Introduce room temperature soup or bouillon, cold water, ice chips, ginger items, and cold water if tolerated and suitable for the patient’s diet. | This promotes hydration. Whether it’s used to make ginger ale, ginger tea, or chewed as crystallized ginger, ginger helps reduce nausea. It may be difficult to accept hot or cold liquids. |
| Frequently provide the patient with tiny portions of their favorite meals. | This strategy will aid in preserving nutritional status. Some people have more nausea when they are hungry. |
| Inform the patient or caregiver of the best nutritional and liquid options for nausea. | By noting dietary factors to take into consideration when feeling nauseous, patients and caregivers can encourage optimal hydration and nutritional status. |
| Instruct the patient to take their meds exactly as directed. | The frequency of nausea attacks decreases when drugs are taken according to schedule. |
Metabolic Alkalosis Nursing Care Plan 4
Nursing Diagnosis: Ineffective Tissue Perfusion related to metabolic alkalosis secondary to hypovolemia, as evidenced by dryness of the skin, numbness, and altered sensation on extremities, nausea, and cyanosis.
Desired Outcomes:
- The patient will have adequate gastrointestinal perfusion as evidenced by normal blood pressure, tolerance of food intake, regular bowel movements, and absence of stomach pain and distention.
- The patient will exhibit an adequate peripheral perfusion as evidenced by strong peripheral pulses, warm skin temperature with an appropriate capillary refill, and absence of ulcers.
| Metabolic Alkalosis Nursing Interventions | Rationale |
| Assess the patient’s vital signs including the pulse, body temperature, and blood pressure while standing and sitting. | During this process, the nurse can determine if the patient is getting dizzy when changing position, which is a sign of hypovolemia. Pulses are a sign that the specific body part is receiving enough blood flow. A perfusion compromise may be indicated by absent or weak pulses. |
| Assess the patient’s skin and the mucous membranes in the mouth, tongue, and nose for dryness. | This can be a sign of dehydration. |
| Monitor the appearance, temperature, and sensation of all the patient’s extremities. | The color of the extremities should match the ethnic group. An obstruction in the perfusion to the extremity is indicated by pallor, cyanosis, and mottled skin color. |
| Determine the patient’s capillary refill time. | It shouldn’t take more than three seconds for the nail bed to turn pinkish once it has been squeezed. Pale nail beds may indicate inadequate perfusion rather than a blood flow obstruction. |
| Monitor the patient’s fluid balance. | Reduced renal perfusion may be indicated by decreased urine production. Other critical organs, such as the brain perfusion, may not be effectively perfused if the kidneys are not. |
| Evaluate the patient’s intake and output as well as urine clarity and color. | A decline in renal function, and consequently a reduction in renal perfusion, may be indicated by a drop in urine output or a change in color and clarity. |
Metabolic Alkalosis Nursing Care Plan 5
Nursing Diagnosis: Acute Confusion related to metabolic alkalosis secondary to severe dehydration, as evidenced by fluctuation in cognition, increased restlessness, decreased level of consciousness, and sleep disturbances.
Desired Outcome: The patient will regain an average level of consciousness and reality orientation.
| Metabolic Alkalosis Nursing Interventions | Rationale |
| Evaluate the patient’s level of consciousness, neuromuscular condition, strength, tone, and movement; take note of any Chvostek or Trousseau signals. | Tingling, numbness, dizziness, restlessness, apathy, and disorientation due to increased pH of CNS fluid are manifestations of hypersensitive CNS. Tetany may be exacerbated by hypocalcemia (although its occurrence is rare). |
| Orient the patient to the environment, the staff, and any necessary activities. Briefly and concisely present reality. Avoid arguing against incorrect thinking. | To avoid tension and fear, constant and frequent reorienting may be necessary. Reorient the patient to the staff, environment, and procedures. Avoid challenging irrational thoughts because doing so can make delirium and anxiety worse. |
| Analyze and document any potential physiological changes such as infection, changes in temperature, fluid and electrolyte imbalances. | Such modifications need to be reversed because they might be causing confusion. |
| Monitor the patient’s laboratory values. Determine if the patient is having hypoxemia, electrolyte imbalances, BUN/Cr, ammonia levels, serum glucose, infection symptoms, and medication levels including peak/trough as necessary. | Once severe confusion has been identified, the underlying reasons must be found and addressed. Confusion can result from either high or low glucose levels and may also develop from low sodium levels. |
| Limit the patient’s exposure to stimuli. Create a peaceful environment by turning off any unnecessary noise and stimulus. | A disoriented patient may interpret higher amounts of visual and auditory stimuli incorrectly. |
| Establish and maintain an appropriate diet, body temperature, oxygenation (if patients have low oxygen saturation, treat with supplementary oxygen), blood glucose levels, and blood pressure. Maintain normal fluid and electrolyte balance. | Collaborating with the medical staff to treat the underlying causes of confusion. |
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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