Site logo

Acid-Base Imbalances

The human body thrives at a plasma pH range of 7.35 to 7.45. A deviation from these values causes an acid-base imbalance. There are four primary types.

Respiratory alkalosis is characterized by decreased partial pressure of arterial carbon dioxide and increased blood pH. Respiratory acidosis, on the other hand, is the opposite: increased partial pressure of arterial carbon dioxide and decreased blood pH. 

Metabolic alkalosis is characterized by an excessive loss of acid or excessive gain of bicarbonate. Contrastingly, metabolic acidosis comes about as a result of absorbing or retaining too much acid or excessive excretion of bicarbonate. 

Nursing Diagnoses: Respiratory Alkalosis 

May be related to 

  • Ventilation perfusion imbalance (e.g., altered oxygen supply, altered blood flow, altered oxygen-carrying capacity of blood, alveolar-capillary membrane changes)

Possibly evidenced by 

  • Dyspnea 
  • Tachypnea 
  • Changes in mentation 
  • Hypocapnia 
  • Tachycardia 
  • Hypoxia 

Desired outcomes 

  • Demonstrate improved ventilation and adequate oxygenation of tissue as evidenced by ABGs within patient’s acceptable limits and absence of symptoms of respiratory distress
  • Verbalize understanding of causative factors and appropriate interventions
  • Participate in a treatment regimen within the level of ability/situation

Nursing interventions 

Monitor respiratory rate, depth, and effort. Ascertain cause of hyperventilation if possible. Differentiate hyperventilation caused by anxiety, pain, or improper ventilator settings.  Identifies alterations from usual breathing pattern and influences choice of intervention.
Encourage patient to breathe slowly and deeply. Speak in a low, calm tone of voice. Provide safe environment.  May help reassure and calm the agitated patient, thereby aiding the reduction of respiratory rate. Assists patient to regain control.
Assess level of awareness or cognition and note neuromuscular status. Assess strength, tone, reflexes, and sensation.  Decreased mentation (mild to severe) and tetany or seizures may occur when alkalosis is severe.
Demonstrate appropriate breathing patterns, if appropriate, and assist with respiratory aids or rebreathing mask/bag.  Decreasing the rate of respirations can halt the “blowing off” of CO2, elevating Pco2 level and normalizing pH.
Provide comfort measures; encourage use of meditation and visualization. Use tepid sponge bath/cool cloths.  Promotes relaxation and reduces stress. Control and reduction of fever reduces potential for seizures and helps reduce respiration rate.
Provide safety and seizure precautions. Place bed in low position, pad side rails and do frequent observation of the patient.  Changes in mentation, CNS and neuromuscular hyperirritability may result in patient harm, especially if tetany or convulsions occur.
Discuss cause of condition (if known) and appropriate interventions and/or self-care activities.  Promotes participation in therapeutic regimen and may reduce recurrence of disorder.
Assist with identification and treatment of underlying cause.  Respiratory alkalosis is a complication, not an isolated occurrence; addressing the primary condition (hyperventilation of panic attack, organ failure, severe anemia; drug effect, such as with paraldehyde or epinephrine) promotes correction of the disorder and reduces likelihood of recurrence.
Monitor and graph serial ABGs, and pulse oximetry.  Identifies therapy needs and effectiveness.
Monitor serum potassium. Replace as indicated.  Hypokalemia may occur as potassium is lost (urine) or shifted into the cell in exchange for hydrogen in an attempt to correct alkalosis.
Provide sedation and pain medication, as indicated.  May be required to reduce psychogenic cause of hyperventilation.
Administer CO2, or use rebreathing mask as indicated. Reduce respiratory rate and tidal volume, or add additional dead space (tubing) to mechanical ventilator.  Increasing CO2 retention may correct carbonic acid deficit.

Nursing Diagnoses: Respiratory Acidosis

May be related to

  • Ventilation perfusion imbalance (altered oxygen-carrying capacity of blood, altered oxygen supply, alveolar-capillary membrane changes, or altered blood flow)

Possibly evidenced by 

  • Dyspnea with exertion, tachypnea
  • Changes in mentation, irritability
  • Tachycardia
  • Hypoxia, hypercapnia


Desired outcomes 

  • Demonstrate improved ventilation and adequate oxygenation of tissues as evidenced by ABGs within patient’s acceptable limits and absence of symptoms of respiratory distress.
  • Verbalize understanding of causative factors and appropriate interventions.
  • Participate in treatment regimen within level of ability/situation.

Nursing interventions

Monitor respiratory rate, depth, and effort.  Alveolar hypoventilation and associated hypoxemia lead to respiratory distress or failure.
Auscultate breath sounds.  Identifies areas of decreased ventilation (atelectasis) or airway obstruction and changes as patient deteriorates or improves, reflecting effectiveness of treatment, dictating therapy needs.
Note declining level of consciousness.  Signals severe acidotic state, which requires immediate attention. Note: In recovery, sensorium clears slowly because hydrogen ions are slow to cross the blood-brain barrier and clear from cerebrospinal fluid and brain cells.
Monitor heart rate and rhythm.  Tachycardia develops early because the sympathetic nervous system is stimulated, resulting in the release of catecholamines, epinephrine, and norepinephrine, in an attempt to increase oxygen delivery to the tissues. Dysrhythmias that may occur are due to hypoxia (myocardial ischemia) and electrolyte imbalances.
Note skin color, temperature, moisture.  Diaphoresis, pallor, cool or clammy skin are late changes associated with severe or advancing hypoxemia.
Encourage and assist with deep-breathing exercises, turning, and coughing. Suction as necessary. Provide airway adjunct as indicated. Place in semi-Fowler’s position.  These measures improve lung ventilation and reduce or prevent airway obstruction associated with accumulation of mucus.
Restrict use of hypnotic sedatives or tranquilizers.  In the presence of hypoventilation, respiratory depression and CO2 narcosis may develop.
Discuss cause of chronic condition (when known) and appropriate interventions and self-care activities.  Promotes participation in therapeutic regimen, and may reduce recurrence of disorder.
Assist with identification or treatment of underlying cause.  Treatment of disorder is directed at improving alveolar ventilation. Addressing the primary condition (oversedation, lung and respiratory system trauma, pulmonary edema, aspiration) promotes correction of the acid-base disorder.
Monitor and graph serial ABGs, pulse oximetry readings; Hb, serum electrolyte levels.  Evaluates therapy need and effectiveness. Note: Bedside pulse oximetry monitoring is used to show early changes in oxygenation before other signs or symptoms are observed.
Administer oxygen as indicated. Increase respiratory rate or tidal volume of ventilator, if used.  Prevents and corrects hypoxemia and respiratory failure. Note: Must be used with caution in presence of emphysema because respiratory depression or failure may result.
Assist with ventilatory aids: IPPB in conjunction with bronchodilators. Monitor peak flow pressure.  Increases lung expansion and opens airways to improve ventilation, preventing respiratory failure.
Maintain hydration (IV/PO) and provide humidification.  Assists in correction of acidity and thinning and mobilization of respiratory secretions.
Provide appropriate chest physiotherapy, including postural drainage and breathing exercises.  Aids in clearing secretions, which improves ventilation, allowing excess CO2 to be eliminated.
Administer IV solutions such as lactated Ringer’s solution or 0.6 M solution of sodium lactate.  May be useful in nonemergency situations to help control acidosis, until underlying respiratory problem can be corrected.

Administer medications as indicated 

Naloxone hydrochloride (Narcan)  May be useful in arousing patient and stimulating respiratory function in presence of drug overdose and sedation, or acidosis resulting from cardiac arrest.
Sodium bicarbonate (NaHCO3 May be given in small IV doses in emergency situations to quickly correct acidosis if pH is less than 7.25 and hyperkalemia coexists. Note: Rebound alkalosis or tetany may occur.
Potassium chloride (KCl)  Replaces potassium that shifts out of cells during acidotic state. Correction of the acidosis may cause a relative serum hypokalemia as potassium shifts back into cells. Potassium imbalance can impair neuromuscular or respiratory function, causing generalized muscle weakness and cardiac dysrhythmias.
Bronchodilators Helps open constricted airways to improve gas exchange.
Provide low-carbohydrate, high-fat diet (Pulmocare feedings), if indicated.  Helps reduce CO2 production and improves respiratory muscle function and metabolic homeostasis.

Nursing Diagnoses: Metabolic Alkalosis 

Desired outcomes 

  • Display serum bicarbonate and electrolytes WNL.
  • Be free of symptoms of imbalance, e.g., absence of neurological impairment/irritability.

Nursing interventions

Monitor respiratory rate, rhythm, and depth.  Hypoventilation is a compensatory mechanism to conserve carbonic acid and represents definite risks to the individual (hypoxemia and respiratory failure).
Assess level of consciousness and neuromuscular status, strength, tone, movement; note presence of Chvostek’s or Trousseau’s signs.  The CNS may be hyperirritable (increased pH of CNS fluid), resulting in tingling, numbness, dizziness, restlessness, or apathy and confusion. Hypocalcemia may contribute to tetany (although occurrence is rare).
Monitor heart rate and rhythm.  Atrial and ventricular ectopic beats and tachy dysrhythmias may develop.
Record amount and source of output. Monitor intake and daily weight.  Helpful in identifying source of ion loss and potassium and HCl are lost in vomiting and GI suctioning.
Restrict oral intake and reduce noxious environmental stimuli; use intermittent and low suction during NG suctioning; irrigate gastric tube with isotonic solutions rather than water.  Limits gastric losses of HCl, potassium, and calcium.
Provide seizures and safety precautions as indicated. Pad side rails, protect the airway, put bed in low position and frequent observation.  Changes in mentation and CNS or neuromuscular hyperirritability may result in patient harm, especially if tetany or convulsions occur.
Encourage intake of foods and fluids high in potassium and possibly calcium (dependent on blood level), canned grapefruit and apple juices, bananas, cauliflower, dried peaches, figs, and wheat germ.  Useful in replacing potassium losses when oral intake permitted.
Review medication regimen for use of diuretics, such as thiazides (Diuril, Hygroton),furosemide (Lasix), and ethacrynic acid (Edecrin).  Discontinuation of these potassium-losing drugs may prevent recurrence of imbalance.
Instruct patient to avoid use of excessive amounts of sodium bicarbonate.  Ulcer patients can cause alkalosis by taking baking soda and milk of magnesia in addition to prescribed alkaline antacids.
Assist with identification and treatment of underlying disorder.  Addressing the primary condition (prolonged vomiting and/or diarrhea, hyper aldosteronism, Cushing’s syndrome) promotes correction of the acid-base disorder.
Monitor laboratory studies as indicated: ABGs/pH, serum electrolytes (especially potassium), and BUN.  Evaluates therapy needs and effectiveness and monitors renal function.

Administer medications as indicated 

Correcting sodium, water, and chloride defects may be all that is needed to permit kidneys to excrete bicarbonate and correct alkalosis, but must be used with caution in patients with HF or renal insufficiency.

Sodium chloride PO/Ringer’s solution IV unless contraindicated Hypokalemia is frequently present. Chloride is needed so kidney can absorb sodium with chloride, enhancing excretion of bicarbonate.
Ammonium chloride or arginine hydrochloride  Although used only in severe cases, ammonium chloride may be given to increase amount of circulating hydrogen ions. Monitor administration closely to prevent too rapid a decrease in pH, hemolysis of RBCs. Note: May cause rebound metabolic acidosis and is usually contraindicated in patients with renal or hepatic failure.
Acetazolamide (Diamox)  A carbonic anhydrase inhibitor that increases renal excretion of bicarbonate.
Spironolactone (Aldactone)  Effective in treating chloride-resistant alkalosis, e.g., Cushing’s syndrome.
Avoid or limit use of sedatives or hypnotics.  If respirations are depressed, may cause hypoxia and respiratory failure.
Encourage fluids IV/PO.  Replaces extracellular fluid losses, and adequate hydration facilities removal of pulmonary secretions to improve ventilation.
Administer supplemental O2 as indicated and respiratory treatments to improve ventilation.  Respiratory compensation for metabolic alkalosis is hypoventilation, which may cause decreased Pao2 levels or hypoxia.
Prepare patient for and assist with dialysis as needed.  Useful when renal dysfunction prevents clearance of bicarbonate.

Nursing Diagnoses: Metabolic Acidosis

Desired outcomes 

  • Display serum bicarbonate and electrolytes within normal limits (WNL).
  • Be free of symptoms of imbalance, e.g., absence of neurological impairment; vital signs WNL.

Nursing interventions

Monitor BP.  Arteriolar dilation or decreased cardiac contractility and hypovolemia occur, resulting in systemic shock, evidenced by hypotension and tissue hypoxia.
Assess LOC and note progressive changes in neuromuscular status. Note neuromuscular strength, tone, movement.  Decreased mental function, confusion, seizures, weakness, flaccid paralysis can occur because of hypoxia, hyperkalemia, and decreased pH of CNS fluid.
Provide seizure or coma precautions and bed in low position, use of side rails, frequent observation.  Protects patient from injury resulting from decreased mentation and convulsions.
Monitor heart rate and rhythm.  Acidemia may be manifested by changes in ECG configuration and presence of brady dysrhythmias as well as increased ventricular irritability such as fibrillation (signs of hyperkalemia). Life-threatening cardiovascular collapse may also occur because of vasodilation and decreased cardiac contractility. Note: Hypokalemia can occur as acidosis is corrected, resulting in premature ventricular contractions (PVCs) and/or ventricular tachycardia.
Observe for altered respiratory excursion, rate, and depth.  Deep, rapid respirations (Kussmaul’s) may be noted as a compensatory mechanism to eliminate excess acid; however, as potassium shifts out of cell in an attempt to correct acidosis, respirations may become depressed. Transient respiratory depression may be the result of overcorrection of metabolic acidosis with sodium bicarbonate.
Assess skin temperature, color, capillary refill.  Evaluates circulatory status, tissue perfusion, effects of hypotension.
Auscultate bowel sounds, measure abdominal girth as indicated.  In the presence of coexisting hyperkalemia, GI distress (distension, diarrhea, and colic) may occur.
Monitor I&O closely and weigh daily.  Marked dehydration may be present because of vomiting, diarrhea. Therapy needs are based on underlying cause and fluid balance.
Test and monitor urine pH.  Kidneys attempt to compensate for acidosis by excreting excess hydrogen in the form of weak acids and ammonia. Maximum urine acidity is pH of 4.0.
Provide oral hygiene with sodium bicarbonate washes, lemon, glycerine swabs.  Neutralizes mouth acids and provides protective lubrication.
Assist with identification and treatment of underlying cause.  Treatment of disorder is directed at mild correction of acidosis until organ(s) function is improved. Addressing the primary condition (DKA, liver or renal failure, drug poisoning, sepsis) promotes correction of the acid-base disorder.
Monitor and graph serial ABGs.  Evaluates therapy needs and effectiveness. Blood bicarbonate and pH should slowly increase toward normal levels.
Monitor serum electrolytes, especially potassium.  As acidosis is corrected, serum potassium deficit may occur as potassium shifts back into the cells.
Replace fluids, as indicated depending on underlying etiology: D5W/saline solutions.  Choice of solution varies with cause of acidosis: DKA. Note: Lactate-containing solutions may be contraindicated in the presence of lactic acidosis.

Administer medications as indicated

Sodium bicarbonate or lactate or saline IV  Corrects bicarbonate deficit, but is used cautiously to correct severe acidosis (pH less than 7.2) because sodium bicarbonate can cause rebound metabolic alkalosis.
Potassium chloride May be required as potassium re-enters the cell, causing a serum deficit.
Phosphate May be administered to enhance acid excretion in presence of chronic acidosis with hypo phosphatemia.
Calcium May be given to improve neuromuscular conduction and function.
Modify diet as indicated: low-protein, high-carbohydrate diet in presence of renal failure or American Diabetes Association (ADA) diet for the person with diabetes.  Restriction of protein may be necessary to decrease production of acid waste products, whereas addition of complex carbohydrates will correct acid production from the metabolism of fats.
Administer exchange resins and/or assist with dialysis as indicated.  May be desired to reduce acidosis by decreasing excess potassium and acid waste products if pH less than 7.1 and other therapies are ineffective or HF develops.

Nursing Notes

  Contributing Factors Signs, Symptoms, Clinical Manifestations Nursing Diagnoses Medical Management & Nursing Interventions
Respiratory Alkalosis Hyperventilation due to anxiety Hypoxia Improper mechanical ventilation Fever Salicylate poisoning     Light-headedness Inability to concentrate Convulsions+ Chvostek’s sign, nausea, vomiting Muscle twitching Labs indicated (ABG studies reveal abnormal values: >7.45, PaCO2 <35mmHg) Impaired gas exchange Ineffective breathing pattern Ineffective tissue perfusion Acute confusion Risk for injury Institute safety measures for the patient with vertigo or the unconscious patient.Encourage the anxious patient to verbalize fearsAdminister sedation as ordered to relax the patientKeep the patient warm and dryEncourage the patient to take deep, slow breaths or breathe into a brown paper bag (inspire CO2).Monitor vital signsMonitor ABGs, primarily PaCO2; a value <35 mmHg indicates too little CO2 (carbonic acid)
Respiratory Acidosis Chronic obstructive respiratory disordersChest wall trauma, pulmonary edema, atelectasis, pneumothorax, drug overdose, pneumonia, Guillain-Barre syndromeAny condition that results in hypoventilation Increased pulse & respiratory rate Increased blood pressure Mental cloudiness, feeling of fullness in the head WeaknessDull headacheLabs indicated (ABG studies reveal abnormal values: ph <7.35, PaCO2 >45mmHg) Impaired gas exchange Ineffective breathing pattern Ineffective tissue perfusion Acute confusion Risk for injury Institute safety measuresAssist with positioningMonitor I&O and administer fluids as orderedAdminister oxygen and medications for order; monitor hourly vital signs and respiratory status (may requires mechanical ventilation)Monitor ABGs; pH, PaCO2, HCO3
Metabolic Alkalosis Vomiting Gastric suctioning Excessive intake of alkali (antacids, baking soda) Tingling of fingers Dizziness, confusion Tetany Slow, shallow respirations, possibly apneaLabs indicate (ABG studies reveal abnormal values: pH >7.45, HCO3 >26 mEq/L; Urine chloride concentrations help to differentiate between vomiting or diuretic ingestion, or one of the causes of mineralocorticoid excess)     
Metabolic Acidosis KetoacidosisLactic acidosisProlonged fastingSalicylic poisoning Oliguric renal disease Abnormal bicarbonate losses, which can occur in oss of fluid from the lower GI tract from surgery, drains, or severe diarrhea)  HeadacheDrowsiness & confusion WeaknessIncreased respiratory rate & depth Nausea and vomiting Diminished cardiac output with pH <7 (results in hypotensions, cold, clammy skin, cardiac arrhythmias) Labs indicated (ABG studies reveal abnormal values: pH <7.35, and HCO3 >22 mEq/L; serum potassium level reveals hyperkalemia)    

Leave a Comment

We use cookies to improve your experience on our website. By browsing this website, you agree to our use of cookies.

Sign in

Sign Up

Forgotten Password

Job Quick Search