NCLEX-RN: Medical–Surgical Nursing

Medical–Surgical Nursing: Genitourinary System

Focus topic: Medical–Surgical Nursing

Medical–Surgical Nursing: Acid–Base Regulation

Focus topic: Medical–Surgical Nursing

Medical–Surgical Nursing: Principles of Acid–Base Balance

Focus topic: Medical–Surgical Nursing

A. Acid–base balance is the ratio of acids and bases in the body necessary to maintain a chemical balance conducive to life.
B. Acid–base ratio is 20 parts base to 1 part acid.
C. Acid–base balance is measured by arterial blood samples and recorded as blood pH. Range is 7.35–7.45.
D. Acids are hydrogen ion donors. They release hydrogen ions to neutralize or decrease the strength of the base.
E. Bases are hydrogen ion acceptors. They accept hydrogen ions to convert strong acids to weak acids (for example, hydrochloric acid is converted to carbonic acid).

Regulatory Mechanisms
A. The body controls the pH balance by use of

  • Chemical buffers.
  • Lungs.
  • Cells.
  • Kidneys.

B. The chemical buffer system works fastest, but other regulatory mechanisms provide more reliable protection against acid–base imbalance.

  • A buffer is a substance that reacts to keep pH within normal limits. It functions only when excessive base or acid is present.
  • Chemical buffers are paired (for example, weakly ionized acid or base is balanced with a fully ionized salt).
    a. Pairing prevents excessive changes in normal acid–base balance.
    b. The buffers release or absorb hydrogen ions when needed.
  • The buffer systems in the extracellular fluid react quickly with acids and bases to minimize changes in pH.
    a. Once they react, they are used up.
    b. If further stress occurs, the body is less able to cope.
  • There are four primary buffer systems.
    a. Carbonic acid–bicarbonate—maintains blood pH at 7.4 with ratio of 20 parts bicarbonate to 1 part carbonic acid.
    b. Intracellular and plasma proteins—vary the amounts of hydrogen ions in the chemical structure of the protein (along with liver). They can both attract and release hydrogen ions.

c. Hemoglobin—maintains the balance by the chloride shift. Chloride shifts in and out of red blood cells according to the level of oxygen in the blood plasma. Each chloride ion that leaves the cell is replaced by a bicarbonate ion.
d. Phosphate buffer system—composed of sodium and other cations in association with HPO4– – and H2PO4–; acts like bicarbonate system.

C. Lungs.

  • Next to react are the lungs.
  • It takes 10–30 minutes for lungs to inactivate hydrogen molecules by converting them to water molecules.
  • The carbonic acid that was formed by neutralizing bicarbonate is taken to lungs.
    a. There it is reduced to carbon dioxide and water and exhaled.
    b. When there is excessive acid in the body, the respiratory rate increases to blow off the excessive carbon dioxide and water.
  • When there is too much bicarbonate or base in the body, respirations become deeper and slower.
    a. This process builds up the level of carbonic acid.
    b. The result is that the strength of the excessive bicarbonate is neutralized.
  • Lungs can inactivate only the hydrogen ions carried by carbonic acid. The other ions must be excreted by the kidneys.

D . Cells.

  • They absorb or release extra hydrogen ions.
  • They react in 2–4 hours.

E. Kidneys.

  • Most efficient regulatory mechanism.
  • Begin to function within hours to days as integral part of buffering system.
  • Blood pH is maintained by balance of 20 parts bicarbonate to 1 part carbonic acid.
  • Four processes are involved in acid–base regulation.
    a. Dissociation of H+ from H2CO3 (H+ and HCO3–).
    b. Reabsorption of Na+ from urine filtrate (Na+ and H+ change places).
    c. Formation and conservation of NaHCO3 (Na+ and HCO3–).
    d. NH3 from metabolic process (Krebs cycle) enters kidney’s tubular cell and adds an H+ ion and then exchanges as ammonium with Na+ (Na+ and NH4).
    5. Hydrogen and potassium compete with each other in exchange for Na+ in the tubular urine.
    a. In acidosis, the H+ ion concentration is increased, and K+ ion must wait to be excreted because hydrogen has preference.
    b. In alkalosis, the H+ ion is low and K+ is excreted in larger amounts.
Medical–Surgical Nursing

Medical–Surgical Nursing: Acid–Base Imbalances

Focus topic: Medical–Surgical Nursing

Medical–Surgical Nursing: Metabolic Acidosis

Focus topic: Medical–Surgical Nursing

Definition: Metabolic acidosis occurs when there is a deficit of bases or an accumulation of fixed acids.
A. Changes in pH and serum HCO3.

  • The pH will become acidotic as a result of insufficient base.
    a. It falls below 7.35.
    b. There are either more hydrogen ions or fewer bicarbonate ions present in the blood.
  • The serum CO2 level will be below 22 mEq/L (normal range of CO2 is 26–28 mEq/L).
    a. Serum CO2 measures the amount of circulating bicarbonate.
    b. Serum CO2 acts as a bicarbonate (HCO3) determinant. When serum CO2 is low, HCO3 is lost and acidosis results.

B. Compensatory mechanisms.

  • When compensating for metabolic acidosis, the one clinical manifestation usually observed is the “blowing off ” of excessive acids. This can be noted by a respiratory rate increase.
  • The lungs are the fastest mechanism used to compensate for metabolic acidosis.
    a. If the lungs are involved, as in respiratory acidosis, they cannot function as a compensatory mechanism.
    b. Therefore, the kidneys must take over and the process is much slower.
  • Renal excretion of acid occurs.

C. Laboratory values.

  • The partial pressure of the blood gas carbon dioxide (PCO2) decreases below 35 mm of pressure when the client is compensating. (Normal values: 35–45 mm Hg.)
  • The partial pressure of oxygen (PO2) is usually increased due to increased respiratory rate. (Normal values PO2: 80–100 mm Hg.)
  • The serum potassium level is increased with acidosis, due primarily to the cause of the acidosis.
    a. For example, clients can go into metabolic acidosis from severe diarrhea.
    b. When this condition is present, the potassium moves out of the cell and into the extravascular space due to the dehydration process.
  • Sodium and chloride levels may be decreased. Again, this is usually due to excessive loss through urine or gastrointestinal disorders.
  • Laboratory values when a client is in metabolic acidosis.
    a. pH: < 7.35 (decreased).
    b. HCO3: < 22 mEq/L (decreased).
    c. PCO2: 38–40 mm Hg (normal).

D. Causes of metabolic acidosis (seen particularly in the surgical client).

  • Diabetes—diabetic ketoacidosis.
    a. When insufficient insulin is produced or administered to metabolize carbohydrates, increased fat metabolism results, thus producing excess accumulations of ketones and other acids.
    b. This is the most common problem associated with metabolic acidosis in the surgical client.
  • Renal insufficiency—kidneys lose their ability to reabsorb bicarbonate and secrete hydrogen ions.
  • Diarrhea—excessive amounts of base are lost from the intestines and pancreas, resulting in acidosis.

E. Clinical manifestations.

  • Headache, mental dullness.
  • Drowsiness, confusion.
  • Nausea, vomiting, diarrhea.
  • Coma, twitching, convulsions (late changes).
  • Kussmaul’s respiration (increased respiratory rate due to compensation).
  • Fruity breath (as evidenced in diabetic ketoacidosis as a result of improper fat metabolism).

F. Nursing management.

  • Administer sodium bicarbonate intravenously to alkalize the client and return client to normal acid–base balance as quickly as possible.
    a. Usual dosage: one to three ampules of 50 mEq bicarbonate/ampule.
    b. This is usually the immediate treatment rendered for metabolic acidosis.
  • Administer sodium lactate solution to increase the base level.
    a. Sodium lactate is converted to bicarbonate by the liver.
    b. Lactated Ringer’s IV solution may be used.
  • Administer insulin in ketoacidosis. Insulin moves glucose out of the blood serum and into the cell, thereby decreasing ketosis. Insulin decreases ketones by decreasing the release of fatty acids from fat cells.
  • Monitor laboratory values closely while managing metabolic acidosis.
  • Watch for signs of hyperkalemia and dehydration in the client (oliguria, vital sign changes, etc.).
  • Record intake and output.

Medical–Surgical Nursing: Metabolic Alkalosis

Focus topic: Medical–Surgical Nursing

Definition: Metabolic alkalosis is a malfunction of metabolism, causing an increase in blood base or a reduction of available acids in the serum.
A. Changes in pH and serum bicarbonate (HCO3).

  • The pH will become more alkaline; therefore, it will be above 7.45.
  • Bicarbonate will increase above 26 mEq/L. CO2 measures the amount of circulating bicarbonate or the base portion of the plasma. (A good way to remember these acid–base values is to recall that as the pH increases, so does the HCO3 [and CO2]. The reverse is true for acidosis.)
  • The PCO2 will not change unless the lungs attempt to compensate.
  • Serum potassium and chloride levels decrease, due to the basic cause of the alkalosis, whether it be excessive vomiting or the use of diuretics.

B. Compensatory mechanisms.

  • The lungs attempt to hold on to the carbonic acid in an effort to neutralize the base state; therefore, the rate of respiration decreases.
  • When the lungs are compensating for the alkalotic state, the PCO2 will increase above 45 mEq/L.
  • Renal excretion of bicarbonate occurs.

C. Laboratory values when client is in metabolic alkalosis

  • pH: > 7.45 (increased).
  • HCO3: > 26 mEq/L (increased).
  • PCO2: 38–40 mm Hg (normal).

D. Causes of metabolic alkalosis.

  • Ingestion of excessive soda bicarbonate (used by individuals for acid indigestion).
  • Excessive vomiting, which results in the loss of hydrochloric acid and potassium.
  • Placement of NG tubes that causes a depletion of both hydrochloric acid and potassium.
  • Use of potent diuretics, particularly by cardiac clients. They tend to lose not only potassium but also hydrogen and chloride ions, causing an increase in the bicarbonate level of the serum.
  • Excessive intake of mineralocorticoids.

E. Clinical manifestations.

  • Confusion, dizziness.
  • Nausea, vomiting, diarrhea.
  • Restlessness, irritability, agitation, nervousness.
  • Twitching of extremities, coma, convulsions (late signs).
  • Numbness or tingling of fingers and toes.
  • ECG changes indicate tachycardia, with the T wave running into the P wave.

F. Nursing management.

  • Give Diamox (acetazolamide) to promote kidney excretion of bicarbonate.
  • Administer IV solution of added electrolytes.
    a. Estimate the potassium loss from gastric fluid at 5–10 mEq for each liter lost.
    b. In many institutions, the gastric fluid loss is replaced mL for mL every 2–4 hours.
    c. In other institutions, the approximate electrolyte loss is calculated and this amount is added to the 24-hour IV solution.
    d. Chloride replacement enables renal absorption of NA+ with Cl– and renal excretion of excessive HCO3.
  • Maintain diet of foods high in potassium and chloride (bananas, apricots, dried peaches, Brazil nuts, dried figs, oranges).
  • Administer potassium chloride maintenance doses to clients on long-term diuretics.
  • Give ammonium chloride to increase the amount of available hydrogen ions, thereby increasing the availability of acids in the blood.
  • Check laboratory values frequently to watch for electrolyte imbalance.
  • Watch client for physical signs indicative of hypokalemia or metabolic alkalosis.
  • Keep accurate records of intake and output and vital signs.

Medical–Surgical Nursing: Respiratory Acidosis

Focus topic: Medical–Surgical Nursing

Definition: Respiratory acidosis refers to increased carbonic acid concentration (accumulated CO2 that has combined with water) caused by retention of carbon dioxide through hypoventilation. Differs from metabolic acidosis in that it results from altered alveolar ventilation.
A. Changes in pH, PCO2, and PO2.

  • With an increased acidic state, the pH will fall below 7.35.
  • The PCO2 will be increased above 45–50 mm Hg.
  • The PO2 will be normal (80–100 mm Hg), or it can be decreased as hypoxia increases.
  • The HCO3 will be normal if respiratory acidosis is uncompensated.

B. Compensatory mechanisms.

  • Because the basic problem in respiratory acidosis is a defect in the lungs, the kidneys must be the major compensatory mechanism.
    a. The kidneys work more slowly than the lungs.
    b. Therefore, it will take from hours to days
    for the compensation to take place.
  • The kidneys will retain bicarbonate and return it to the extracellular fluid compartment.
  • The bicarbonate level will be elevated with partial or complete compensation.

C. Laboratory values when client is in respiratory acidosis and compensated acidosis.

  • pH: < 7.35 (decreased).
  • PCO2: > 45 mm Hg (increased).
  • HCO3: 24 mEq/L (normal or increased).

D. Causes of respiratory acidosis.

  • Sedatives.
  • Oversedation with narcotics in postoperative period.
  • A chronic pulmonary disorder such as emphysema, asthma, bronchitis, or pneumonia, leading to
    a. Difficulty in the expiratory phase of respiration, leading to retention of carbon dioxide.
    b. Airway obstruction.
  • Poor gaseous exchange during surgery.

E. Clinical manifestations.

  • Dyspnea after exertion, tachycardia.
  • Visual disturbances.
  • Hyperventilation when at rest.
  • Headache, vertigo, tremors, confusion.
  • Sensorium changes—drowsiness leading to coma (late changes).
  • Carbon dioxide narcosis.
    a. When body has adjusted to higher carbon dioxide levels, the respiratory center loses its sensitivity to elevated carbon dioxide.
    b. Medulla fails to respond to high levels of carbon dioxide.
    c. Client is forced to depend on anoxia for respiratory stimulus.
    d. If a high level of oxygen is administered, client will cease breathing.

F. Nursing management.

  • Turn, cough, and deep-breathe client at least every 2–4 hours as part of general postoperative care. Use oropharyngeal suction if necessary. Maintain semi-Fowler’s position.
  • Encourage the use of the incentive spirometer.
  • When pulmonary complications present a threat, do postural drainage, percussion, and vibration, followed by suctioning.
  • Keep client well hydrated (2–3 L) to facilitate removal of secretions. If client is dehydrated, secretions become thick and more difficult to expectorate.
  • Monitor vital signs carefully, particularly rate and depth of respirations.
  • Monitor arterial blood gases (ABGs) for changes in pH and CO2.
  • Teach pursed-lip breathing to chronic respiratory clients.
  • If oxygen is administered, watch carefully for signs of carbon dioxide narcosis. Usually O2 at 2 L is started.
  • Place client on mechanical ventilation if necessary.
  • Administer aerosol medications through nebulizer treatment.
    a. Bronchodilators (aminophylline)—relieve bronchospasms.
    b. Detergents (Tergemist)—liquefy tenacious mucus.
    c. Antibiotics specific to causative agent.
  • Administer drug therapy.
    a. Sodium bicarbonate IV (0.25 g/kg body weight).
    b. Sodium lactate IV.
    c. Ringer’s lactate IV to replace electrolyte loss.
    d. Potassium to maintain serum levels.

Medical–Surgical Nursing: Respiratory Alkalosis

Focus topic: Medical–Surgical Nursing

Definition: Respiratory alkalosis occurs when an excessive amount of carbon dioxide is exhaled, usually caused by hyperventilation. The loss of carbon dioxide results in a decrease in H+ concentration along with a decrease in PCO2 and an increase in the ratio of bicarbonate to carbonic acid. The result is an increase in the pH level.
A. Changes in pH, PCO2, and PO2.

  • With an increased alkalotic state, the pH will increase above 7.45, indicating there is a decreased amount of carbonic acid in the serum.
  • The PCO2 will be normal to low, as this measures the acid portion of the acid–base system (30–45 mm Hg).
  • The PO2 should be unchanged.
  • The bicarbonate level (HCO3 or CO2 content) should be normal unless the client is compensating.

B. Compensatory mechanisms.

  • Because the basic problem is related to the respiratory system, the kidneys compensate by excreting more bicarbonate ions and retaining hydrogen ions.
  • This process returns the acid–base balance to a normal ratio.

C. Laboratory values when client is in respiratory alkalosis.

  • pH: > 7.45 (increased).
  • PCO2: 35 mm Hg (decreased).
  • HCO3: < 22 mEq/L.

D. Causes of respiratory alkalosis.

  • Hysteria or acute anxiety: Client hyperventilates and exhales excessive amounts of carbon dioxide.
  • Hypoxia: Stimulates client to breathe more vigorously.
  • Following head injuries or intracranial surgery.
  • Increased temperature.
  • Overventilation with mechanical ventilator.
  • Salicylate poisoning.
    a. Stimulation of respiration causes alkalosis through hyperventilation.
    b. Acidosis may occur from excessive salicylates in the blood.

E. Clinical manifestations—increased neuromuscular irritability.

  • Lightheadedness, vertigo, tinnitus, palpitations.
  • Hyperreflexia.
  • Numbness of fingers and toes, tetany.
  • Muscular twitching, convulsions (late changes).
  • Gasping for breath; rapid, deep respirations.

F. Nursing management.

  • Eliminate cause of hyperventilation, instruct client to breathe slowly to decrease CO2 loss.
  • Remain with client and be supportive to reduce anxiety.
  • Use rebreathing bag to return client’s carbon dioxide to self (paper bag works just as well).
  • Provide sedation as ordered.
  • Monitor lab values, especially K+ and HCO3–.
Medical–Surgical Nursing

Medical–Surgical Nursing: System Assessment

Focus topic: Medical–Surgical Nursing

A. Take history to determine presence of renal or urologic problems.
B. Determine use of prescriptions, over-the-counter drugs, and herbs. Many drugs are nephrotoxic.
C. Evaluate urinalysis findings to determine presence of infection, bleeding, or signs of renal failure.
D. Assess (palpate) for kidney pain between last thoracic and third lumbar vertebrae.

  • Severe pain or discomfort may indicate kidney infection, stone, or kidney disease.
  • Kidney enlargement may indicate neoplasm or polycystic disease.

E. Assess pain for location, intensity, and precipitating factors.

  • Arterial pain is related to obstruction and is usually an acute manifestation.
    a. Site of obstruction may be found by tracing the location of radiation of pain.
    b. Pain may be severe and usually radiates down ureter into scrotum or vulva and to the inner thigh.
  • Bladder pain is due to infection and overdistention of the bladder in urinary retention.
  • Testicular pain is caused by inflammation or trauma, and is acute and severe.
  • Pain in the lower back and leg may be caused by prostate cancer with metastasis to pelvic bones.
  • Pain caused by renal disease.
    a. Dull ache in flank, radiating to lower abdomen and upper thigh.
    b. Pain may be absent if there is no sudden distention of kidney capsules.

F. Assess bladder for distention.
G. Examine the urinary catheter drainage for abnormal findings.
H. Evaluate intake and output values; dehydration can lead to infection, calculi formation, and renal failure.
I. Measure vital signs to determine presence of complications.
J. Assess patency of shunts.
K. Assess all body systems for potential alterations as a result of kidney problems.

  • Peripheral edema.
  • Hypertension.
  • Eye disorders.
  • Anemia.
  • Lethargic or irritable condition.
  • Congestive heart failure.

L. Observe for signs and symptoms of fluid and electrolyte imbalances.
M. Evaluate urinary test results for signs of renal abnormalities.
N. Assess client’s feelings about body image.
O. Assess for type of imbalance.

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