Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory

The Basics:

• Acid-Base depends on the regulation of free H+ ions

• Balance is maintained by chemical buffers, respiratory reaction and kidney reaction.
• ABG analysis is the major diagnostic tool for evaluating acid-base states
• pH: determines the extent of acidity or alkalinity, both of which are measured
• PaCO2: reflects the adequacy of ventilation by the lungs
• Bicarbonate level: reflects the activity of the kidneys in retaining or excreting bicarbonate.
• If hydrogen ion concentration increases, pH decreases (acidosis).
• If hydrogen ion concentration decreases, pH increases (alkalosis).

The DISORDERS

Respiratory Acidosis
is an acid-base imbalance characterized by increased partial pressure of arterial carbon dioxide and
decreased blood pH. The prognosis depends on the severity of the underlying disturbance as well as the
patient’s general clinical condition.
Compensatory mechanisms include
(1) an increased respiratory rate;
(2) hemoglobin (Hb) buffering, forming bicarbonate ions and deoxygenated Hb; and
(3) increased renal ammonia acid excretions with reabsorption of bicarbonate.

Acute respiratory acidosis:

• Associated with acute pulmonary • adult respiratory distress syndrome (ARDS)
edema, • anesthesia/surgery
• aspiration of foreign body, • mechanical ventilators
• overdose of sedatives/barbiturate • excessive CO2 intake (e.g., use of
poisoning rebreathing mask, cerebral vascular
• smoke inhalation, acute laryngospasm accident [CVA] therapy), Pickwickian
• hemothorax/pneumothorax syndrome.
• atelectasis

Chronic respiratory acidosis: Associated with emphysema, asthma, bronchiectasis; neuromuscular

disorders (such as Guillain-Barré syndrome and myasthenia gravis); botulism; spinal cord injuries.
Causes
• Chronic obstructive respiratory • Guillain-Barre syndrome
disorders: emphysema, chronic
bronchitis
• Chest wall trauma
• Pulmonary edema
• Atelectasis
• Pneumothorax
• Drug Overdose
• Pneumonia
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory

Pathophysiology:

Complications

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
• Shock
• Cardiac Arrest

Signs and Symptoms

CNS disturbances: restlessness, confusion, and apprehension to somnolence with fine flapping
•
tremor, or coma.
• Headache
• Dyspnea
• Tachypnea
• Increase in blood pressure
• Mental cloudiness and feeling of fullness in head
• Weakness
Assessment cues are dependent on underlying cause.
ACTIVITY/REST
• May report: Fatigue, mild to profound
• May exhibit: Generalized weakness, ataxia/staggering, loss of coordination (chronic), to stupor
CIRCULATION
• May exhibit: Low BP/hypotension with bounding pulses, pinkish color, warm skin (reflects
vasodilation of severe acidosis)
• Tachycardia, irregular pulse (other/various dysrhythmias)
• Diaphoresis, pallor, and cyanosis (late stage)
FOOD/FLUID
• May report: Nausea/vomiting
NEUROSENSORY
• May report: Feeling of fullness in head (acute—associated with vasodilation)
• Headache, dizziness, visual disturbances
• May exhibit: Confusion, apprehension, agitation, restlessness, somnolence; coma (acute)
• Tremors, decreased reflexes (severe)
RESPIRATION
• May report: Shortness of breath; dyspnea with exertion
• May exhibit: Respiratory rate dependent on underlying cause, i.e., decreased in respiratory
center depression/
• muscle paralysis; otherwise rate is rapid/shallow
• Increased respiratory effort with nasal flaring/yawning, use of neck and upper body muscles
• Decreased respiratory rate/hypoventilation (associated with decreased function of respiratory
center as in head trauma, oversedation, general anesthesia, metabolic alkalosis)
• Adventitious breath sounds (crackles, wheezes); stridor, crowing
KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory

TEACHING/LEARNING
• Refer to specific plans of care reflecting individual predisposing/contributing factors.
Diagnostic Studies
• CONFIRMING DIAGNOSIS: Arterial blood gas (ABG) analysis of
o PaCO2 higher than 45 mm Hg
o pH is below normal range of 7.35 to 7.45
o bicarbonate level is normal (acute) or elevate (in chronic stages)
• Chest X-ray, CT scan can help determine the cause
• ABGs: Pao2: Normal or may be low. Oxygen saturation (Sao2) decreased.
• Paco2: Increased, greater than 45 mm Hg (primary acidosis).
• Bicarbonate (HCO3): Normal or increased, greater than 26 mEq/L (compensated/chronic
stage).
• Arterial pH: Decreased, less than 7.35.
• Electrolytes: Serum potassium: Typically increased.
• Serum chloride: Decreased.
• Serum calcium: Increased.
• Lactic acid: May be elevated.
• Urinalysis: Urine pH decreased.
• Other screening tests: As indicated by underlying illness/condition to determine underlying
cause.
Nursing Diagnosis
The following are the possible nursing diagnosis for Respiratory Acidosis:
• Impaired Gas Exchange
• Ineffective Breathing Pattern
• Ineffective Tissue Perfusion
• Acute Confusion
• Risk for Injury

Nursing Priorities
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.

Discharge Goals
1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.
4. Plan in place to meet needs after discharge.

Nursing Interventions & Considerations

• Remain alert for critical changes in patient’s respiratory, CNS and cardiovascular functions.
Report such changes as well as any variations in ABG values or electrolyte status immediately.
• Maintain adequate hydration.
• Maintain patent airway and provide humidification if acidosis requires mechanical ventilation.
Perform tracheal suctioning frequently and vigorous chest physiotherapy, if ordered.
• Institute safety measures and assist patient with positioning.
• Continuously monitor arterial blood gases.

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory

Respiratory Alkalosis
• is an acid-base imbalance characterized by decreased partial pressure of arterial carbon dioxide
increased blood pH to less than 35 mm Hg, which is due to alveolar hyperventilation.
Uncomplicated respiratory alkalosis leads to decrease in hydrogen ion concentration, which results
in elevated blood pH.
Causes
• Pulmonary Causes:
o severe hypoxemia,
o pneumonia
o interstitial lung disease,
o pulmonary vascular disease and acute asthma.
• Non-pulmonary Causes:
o anxiety
o fever
o aspirin toxicity
o metabolic acidosis
o central nervous system disease
o pregnancy.

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory

Pathophysiology

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory

Complications
• Cardiac arrhythmias
• Seizures
Signs and Symptoms
• Cardinal Sign: Deep Rapid Breathing (40+ bpm)
• CNS and neuromuscular disturbances: lightheadedness, agitation, circumoral and peripheral
paresthesias, carpopedal spasms, twitching and muscle weakness.
• Positive Chvostek’s sign
• Nausea and vomiting
• Muscle twitching

Assessment
CIRCULATION
• May report: History/presence of anemia
• Palpitations
• May exhibit: Hypotension
• Tachycardia, irregular pulse/dysrhythmias
EGO INTEGRITY
• May exhibit: Extreme anxiety (most common cause of hyperventilation)
FOOD/FLUID
• May report: Dry mouth
Nausea/vomiting
• May exhibit: Abdominal distension (elevating diaphragm as with ascites, pregnancy)
• Vomiting
NEUROSENSORY
• May report: Headache, tinnitus
• Numbness/tingling of face, hands, and toes; circumoral and generalized paresthesia
• Lightheadedness, syncope, vertigo, blurred vision
• May exhibit: Confusion, restlessness, obtunded responses, coma
• Hyperactive reflexes, positive Chvostek’s sign, tetany, seizures
• Heightened sensitivity to environmental noise and activity
• Muscle weakness, unsteady gait
PAIN/DISCOMFORT
• May report: Muscle spasms/cramps, epigastric pain, precordial pain (tightness)
RESPIRATION
• May report: Dyspnea
• History of asthma, pulmonary fibrosis
• Recent move/visit to location at high altitude
• May exhibit: Tachypnea; rapid, shallow breathing; hyperventilation (often 40 or more
respirations/minute)
• Intermittent periods of apnea

SAFETY
• May exhibit: Fever
TEACHING/LEARNING
• May report: Use of salicylates/salicylate overdose, catecholamines, theophylline
• Discharge plan DRG projected mean length of inpatient stay: 5.4 days
• considerations: May require change in treatment/therapy of underlying disease
process/condition

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory

Diagnostic Studies
• CONFIRMING DIAGNOSIS: Arterial blood gas (ABG) analysis indicate PaCO2 less than 35 mmHg;
pH elevated in proportion to the fall in PaCO2 (acute) or failing toward normal (chronic).
• Arterial blood gas (ABG) studies reveal abnormal values: pH above 7.45 and partial pressure of
carbon dioxide below 35 mmHg.
• Arterial pH: Greater than 7.45 (may be near normal in chronic stage).
• Bicarbonate (HCO3): Normal or decreased; less than 25 mEq/L (compensatory mechanism).
• Paco2: Decreased, less than 35 mm Hg (primary).
• Serum potassium: Decreased.
• Serum chloride: Increased.
• Serum calcium: Decreased.
• Urine pH: Increased, greater than 7.0.
• Screening tests as indicated to determine underlying cause, e.g.:
• CBC: May reveal severe anemia (decreasing oxygen-carrying capacity).
• Blood cultures: May identify sepsis (usually Gram-negative).
• Blood alcohol: Marked elevation (acute alcoholic intoxication).
• Toxicology screen: May reveal early salicylate poisoning.
• Chest x-ray/lung scan: May reveal multiple pulmonary emboli.
Nursing Priorities
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
Discharge Goals
1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.
4. Plan in place to meet needs after discharge.

Care Setting
This condition does not occur in isolation, but rather is a complication of a broader problem and usually
requires inpatient care in a medical/surgical or subacute unit.
Related Concerns
• Plans of care specific to predisposing • Hyperthyroidism
factors, e.g.: • Fluid and electrolyte imbalances
• Anemias (iron deficiency, pernicious, • Heart failure: chronic
aplastic, hemolytic) • Pneumonia: microbial
• Cirrhosis of the liver • Sepsis/septicemia
• Craniocerebral trauma • Ventilatory assistance (mechanical)
Other Concerns
• Metabolic acidosis
• Metabolic alkalosis
Nursing Diagnosis
• Impaired Gas Exchange • Acute confusion
• Ineffective Breathing pattern • Risk for injury
• Ineffective Tissue perfusion

Nursing Interventions & Considerations

• Be alert for signs of changes in neurologic, neuromuscular or cardiovascular functions.
• Institute safety measures for the patient with vertigo or the unconscious patient.
• Encourage the anxious patient to verbalize fears
• Administer sedation as ordered to relax the patient
• Keep the patient warm and dry
• Encourage the patient to take deep, slow breaths or breathe into a brown paper bag (inspire
CO2).
• Monitor vital signs
• Monitor ABGs, primarily PaCO2; a value less than 35 mmHg indicates too little CO2 (carbonic
acid)

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
Metabolic Acidosis

• is an acid-base imbalance resulting from excessive absorption or retention of acid or excessive

excretion of bicarbonate produced by an underlying pathologic disorder. Symptoms result from
the body’s attempts to correct the acidotic condition through compensatory mechanisms in
the lungs, kidneys and cells.
• Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is
direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is
within normal limits. If the primary problem is the accumulation of organic anions (such as ketones
or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to
correct this imbalance include an increase in respirations to blow off excess CO2, an increase in
ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and
sodium.
• High anion gap acidosis occurs in diabetic ketoacidosis; severe malnutrition or starvation, alcoholic
lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g.,
salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g.,
acetazolamide (Diamox), NH4Cl.
• Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in
renal tubular acidosis, hyperalimentation, vomiting/diarrhea, small-bowel/pancreatic fistulas, and
ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying
drugs (e.g., ammonium chloride).

Care Setting
This condition does not occur in isolation but rather is a complication of a broader problem that may
require inpatient care in a medical-surgical or subacute unit.

Related Concerns
• Plans of care specific to predisposing factors
• Fluid and electrolyte imbalances
• Renal dialysis
• Respiratory acidosis (primary carbonic acid excess)
• Respiratory alkalosis (primary carbonic acid deficit)

Causes
• Anaerobic carbohydrate metabolism
• Renal insufficiency and failure
• Diarrhea and intestinal malabsorption
• ketoacidosis
• lactic acidosis
• prolonged fasting
• salicylate poisoning
• oliguric renal disease
• abnormal bicarbonate losses, which can occur in loss of fluid from the lower GI tract
from surgery, drains or severe diarrhea

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
Pathophysiology

Complications
• Coma
• Arrhythmias
• Cardiac arrest

Signs and symptoms

• headache
• drowsiness and confusion
• weakness
• increased respiratory rate and depth
• nausea and vomiting
• diminished cardiac output with pH below 7, which results in hypotension, cold clammy skin and
cardiac arrhythmias.

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
Assessment

ACTIVITY/REST
• May report: Lethargy, fatigue; muscle weakness
CIRCULATION
• May exhibit: Hypotension, wide pulse pressure
• Pulse may be weak, irregular (dysrhythmias)
• Jaundiced sclera, skin, mucous membranes (liver failure)
ELIMINATION
ADVERTISEMENTS
• May report: Diarrhea
• May exhibit: Dark/concentrated urine
FOOD/FLUID
• May report: Anorexia, nausea/vomiting
• May exhibit: Poor skin turgor, dry mucous membranes
NEUROSENSORY
• May report: Headache, drowsiness, decreased mental function
• May exhibit: Changes in sensorium, e.g., stupor, confusion, lethargy, depression, delirium, coma
• Decreased deep-tendon reflexes, muscle weakness
RESPIRATION
• May report: Dyspnea on exertion
• May exhibit: Hyperventilation, Kussmaul’s respirations (deep, rapid breathing)
SAFETY
• May report: Transfusion of blood/blood products
• Exposure to hepatitis virus
• May exhibit: Fever, signs of sepsis
TEACHING/LEARNING
• History of alcohol abuse
• Use of carbonic anhydrase inhibitors or anion-exchange resins, e.g., cholestyramine (Questran)
Diagnostic Studies
• CONFIRMING DIAGNOSIS: Arterial pH below 7.35 confirms metabolic acidosis. In severe acidotic
states, pH may fall to 7.10 and the partial pressure of arterial carbon dioxide may be normal or
below 34 mmHg. Bicarbonate may be below 22 mEq/L.
• Urine pH: below 4.5 in the absence of renal disease.
• Serum potassium levels: above 5.5 mEq/L from chemical buffering.
• Glucose levels: above 150 mg/dl in diabetics.
• Arterial pH: Decreased, less than 7.35.
• Bicarbonate (HCO3): Decreased, less than 22 mEq/L.
• Paco2: Less than 35 mm Hg.
• Base excess: Negative.
• Anion gap: Higher than 14 mEq/L (high anion gap) or range of 10–14 mEq/L (normal anion gap).
• Serum potassium: Increased (except in diarrhea, renal tubular acidosis).
• Serum chloride: Increased.
• Serum glucose: May be decreased or increased depending on etiology.
• Serum ketones: Increased in DM, starvation, alcohol intoxication.
• Plasma lactic acid: Elevated in lactic acidosis.
• Urine pH: Decreased, less than 4.5 (in absence of renal disease).
• ECG: Cardiac dysrhythmias (bradycardia) and pattern changes associated with hyperkalemia,
e.g., tall T wave.
Nursing Priorities
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
Discharge Goals
1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.
4. Plan in place to meet needs after discharge
Treatment
KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
•Administration of sodium bicarbonate I.V. for severe cases
•Evaluation and correction of electrolyte imbalances and ultimately correction and
management of the underlying cause.
Nursing Interventions & Considerations
• Keep sodium bicarbonate ampules handy for emergency administration.
• Monitor vital signs, laboratory results and level of consciousness frequently.
• Watch out for signs of decreasing level of consciousness.
• Record intake and output accurately to monitor renal function.
• For management of vomiting (common to metabolic acidosis), position the patient to
prevent aspiration.
• Prepare for possible seizures and administer appropriate precautions.
• Provide good oral hygiene after incidences of vomiting. Use sodium bicarbonate washes to
neutralize acid in the patient’s mouth.

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
Metabolic Alkalosis
• is an acid-base imbalance characterized by excessive loss of acid or excessive gain of bicarbonate
produced by an underlying pathologic disorder. Metabolic alkalosis causes metabolic, respiratory, and
renal responses, producing characteristic symptoms. This condition is always secondary to an
underlying cause.
Causes
Metabolic alkalosis results from the loss of acid, retention of base with decreased serum levels of potassium
and chloride. Other causes may include:
• Vomiting • Steroids
• Nasogastric tube drainage or lavage • Use of diuretics
without adequate electrolyte • Hyperadrenocorticism
replacement • Excessive intake of alkali (i.e.,
• Fistulas milk, baking soda, antacid)
Pathophysiology

KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
Signs and Symptoms
Manifestations of metabolic alkalosis result from the body’s attempt to correct the acid-base imbalance,
primarily through hypoventilation. Other manifestations may include:
• Irritability
• Picking at bedclothes (carphology)
• Twitching
• Confusion
• Nausea
• Vomiting
• Diarrhea
• Cardiovascular abnormalities (i.e., atrial tachycardia).
Complications
• Uncorrected metabolic alkalosis may progress to seizures and coma.
Laboratory Studies
• CONFIRMING DIAGNOSIS: Blood pH level greater than 7.45 and bicarbonate levels above 29 mEq/L
confirms Metabolic Alkalosis.
• Urinalysis shows urine pH is usually about 7.0.
• Electrocardiogram may show low T wave, merging with a U wave and atrial or sinus tachycardia.
Care Setting
This condition does not occur in isolation but rather is a complication of a broader problem that may require
inpatient care in a medical-surgical or subacute unit.
Related Concerns
• Plans of care specific to predisposing factors
• Fluid and electrolyte imbalances
• Renal dialysis
• Respiratory acidosis (primary carbonic acid excess)
• Respiratory alkalosis (primary carbonic acid deficit)
Assessment
CIRCULATION
• May exhibit: Tachycardia, irregularities/dysrhythmias
• Hypotension
• Cyanosis
ELIMINATION
• May report: Diarrhea (with high chloride content)
• Use of potassium-losing diuretics (Diuril, Hygroton, Lasix, Edecrin)
• Laxative abuse
FOOD/FLUID
• May report: Anorexia, nausea/prolonged vomiting
• High salt intake; excessive ingestion of licorice
• Recurrent indigestion/heartburn with frequent use of antacids/baking soda
NEUROSENSORY
• May report: Tingling of fingers and toes; circumoral paresthesia
• Muscle twitching, weakness
• Dizziness
• May exhibit: Hypertonicity of muscles, tetany, tremors, convulsions, loss of reflexes
• Confusion, irritability, restlessness, belligerence, apathy, coma
• Picking at bedclothes
SAFETY
• May report: Recent blood transfusions (citrated blood)
RESPIRATION
• May exhibit: Hypoventilation (increases Pco2 and conserves carbonic acid), periods of apnea
TEACHING/LEARNING
• History of Cushing’s syndrome; corticosteroid therapy
KENPOGI
 Handout 12

Acid-Base Disorders

Care of Clients with Problems in Oxygenation, Fluid and Electrolyte Balance, Infectious Inflammation and Immunity
Response, Cellular Aberration NCM 112 Theory
Diagnostic Studies
• Arterial pH: Increased, higher than 7.45.
• Bicarbonate (HCO3): Increased, higher than 26 mEq/L (primary).
• Paco2: Slightly increased, higher than 45 mm Hg (compensatory).
• Base excess: Increased.
• Serum chloride: Decreased, less than 98 mEq/L, disproportionately to serum sodium decreases (if
alkalosis is hypochloremia).
• Serum potassium: Decreased.
• Serum calcium: Usually decreased. Prolonged hypercalcemia (nonparathyroid) may be a
predisposing factor.
• Urine pH: Increased, higher than 7.0.
• Urine chloride: Less than 10 mEq/L suggests chloride-responsive alkalosis, whereas levels higher
than 20 mEq/L suggest chloride resistance.
• ECG: May show hypokalemic changes including peaked P waves, flat T waves, depressed ST
segment, low T wave merging to P wave, and elevated U waves.
Priorities
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as appropriate.
Discharge Goals
1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.
4. Plan in place to meet needs after discharge.
Nursing Diagnosis
The following are the possible nursing diagnosis for Respiratory Acidosis:
• Ineffective Tissue Perfusion
• Acute Confusion
• Risk for Injury
Nursing Interventions & Considerations
• Dilute potassium when giving via I.V. containing potassium salts. Monitor the infusion rate to
prevent damage and watch out for signs of phlebitis.
• Watch for signs of muscle weakness, tetany or decreased activity. Monitor vital signs frequently and
record intake and output to evaluate respiratory, fluid and electrolyte status.
• Observe seizure precautions.

KENPOGI