Path 370 Quiz 4 (CH. 22, 23, 24, 25)

When a client diagnosed with COPD type A asks, "Why is my chest so big and round?", the nurse responds that A. "Loss of elastic tissue in your lungs allows your airways to close and trap air, which makes your chest round." B. "Swelling and mucus in your airways causes air to be trapped in your lungs, which makes your chest round." C. "Coughing caused by your condition has changed the structure of your airways, which makes your chest round." D. "Scar tissue in your lungs makes them stiff and more full of air than usual, which makes your chest round."

A. "Loss of elastic tissue in your lungs allows your airways to close and trap air, which makes your chest round." Loss of elastic tissue in the lungs allows premature airway closure, which traps air, creating a barrel chest. The other answer choices do not describe the pathophysiology that causes barrel chest in persons with COPD type A.

A patient diagnosed with chronic compensated heart failure reports that, "My feet swell if I eat salt but I don't understand why" The nurse's best response is A. "Salt holds water in your blood and makes more pressure against your blood vessels, so fluid leaks out into your tissues and makes them swell." B. "Gravity makes more pressure down by your feet than up at the top of your body, so more fluid leaks into your tissues at your feet and they swell." C. "Salt makes your blood vessels relax and the blood does not flow as fast, so some of it leaks into your tissues and makes swelling." D. "Salt binds to the proteins in your blood and changes the osmotic pressure so more fluid can leak out and stay in the tissues, causing swelling.

A. "Salt holds water in your blood and makes more pressure against your blood vessels, so fluid leaks out into your tissues and makes them swell." Salt holds water in the ECV, thus increasing capillary hydrostatic pressure. Gravity leads to feet swelling, but it does not explain what the patient is asking. Salt does not cause vasodilation, nor does it bind to blood proteins and change osmotic pressure.

What age group has a larger volume of extracellular fluid than intracellular fluid? A. Infants B. Adolescents C. Young adults D. Older adults

A. Infants Infants have a larger volume of extracellular fluid than intracellular fluid. Adolescents, young adults, and older adults have a larger volume of intracellular fluid than extracellular fluid.

The organism that causes pulmonary tuberculosis is A. Mycobacterium tuberculosis. B. Haemophilus tuberculosis. C. Tuberculosis tuberculoci. D. Mycococcidio tuberculosis.

A. Mycobacterium tuberculosis. Mycobacterium tuberculosis causes pulmonary tuberculosis. Haemophilus tuberculosis, Tuberculosis tuberculoci, and Mycococcidio tuberculosis do not cause pulmonary tuberculosis.

Legionnaires disease is characterized by A. Presence of systemic illness. B. Airborne mechanism of communicability. C. Mild symptomatology. D. Resolution with or without antimicrobial therapy.

A. Presence of systemic illness. Legionnaires disease produces system manifestations such as fever, diarrhea, abdominal pain, and pneumonia. The organism that causes Legionnaires disease is transmitted by means of contaminated water. Symptoms are severe, and the disease requires antimicrobial therapy.

Individuals who have chronic bronchitis most often have: A. a productive cough B. normal lung sounds C. a barrel chest D. substantial weight loss

A. a productive cough A productive cough for at least 3 months is the classic sign of chronic bronchitis. People who have chronic bronchitis commonly have abnormal lung sounds resulting from mucus in their airways. Barrel chest is a classic sign of emphysema. Substantial weight loss is characteristic of emphysema, but not of chronic bronchitis.

Manifestations from sodium imbalances occur primarily as a result of A. cellular fluid shifts. B. vascular collapse. C. hyperosmolarity. D. hypervolemia.

A. cellular fluid shifts. Sodium imbalances alter osmolality of fluid compartment leading to osmosis of water from the hypo-osmolar compartment to the hyperosmolar compartment. In brain cells, this leads to swelling or shrinkage of cells, and associated manifestations.

Effects of hypernatremia on the central nervous system typically include A. confusion. B. excitation. C. insomnia. D. hallucinations.

A. confusion. Hypernatremia causes osmotic shrinking of brain cells, which manifests as confusion or coma. Hypernatremia does not usually cause central nervous system excitation, insomnia, or hallucinations.

Signs and symptoms of clinical dehydration include A. decreased urine output. B. increased skin turgor. C. increased blood pressure. D. decreased heart rate.

A. decreased urine output. One clinical manifestation of dehydration is decreased urine output. Skin turgor and blood pressure decrease in clinical dehydration. Heart rate increases in clinical dehydration.

Decreased neuromuscular excitability is often the result of A. hypercalcemia and hypermagnesemia. B. hypomagnesemia and hyperkalemia. C. hypocalcemia and hypokalemia. D. hypernatremia and hypomagnesemia.

A. hypercalcemia and hypermagnesemia. Hypercalcemia and hypermagnesemia result in decreased neuromuscular excitability. Hypomagnesemia, hypocalcemia, and hypomagnesemia result in increased neuromuscular excitability.

Respiratory alkalosis is caused by A. hyperventilation. B. pneumonia. C. chest muscle weakness. D. pulmonary edema.

A. hyperventilation. Hyperventilation causes respiratory alkalosis as a result of loss of carbonic acid. Pneumonia, chest muscle weakness, and pulmonary edema cause carbonic acid to accumulate in the blood and result in respiratory acidosis.

An increase in the resting membrane potential (hyperpolarized) is associated with A. hypokalemia. B. hyperkalemia. C. hypocalcemia. D. hypercalcemia.

A. hypokalemia. Hypokalemia increases the resting membrane potential. Hyperkalemia results in hypopolarization. Hypocalcemia and hypercalcemia do not affect the resting membrane potential.

The body compensates for metabolic alkalosis by A. hypoventilation. B. decreasing arterial carbon dioxide. C. increasing bicarbonate ion excretion. D. hyperventilation.

A. hypoventilation. In metabolic alkalosis, the lungs compensate by hypoventilation to conserve CO2 in the body. Decreasing arterial carbon dioxide would worsen metabolic alkalosis. The respiratory system compensates for metabolic acid and base disturbances; the lungs do not increase bicarbonate ion excretion. Hyperventilation would blow off CO2 and cause respiratory alkalosis.

To best prevent emphysema, a patient is instructed to stop smoking since cigarette smoke A. impairs α1-antitrypsin, allowing elastase to predominate. B. paralyzes the cilia, causing impaired mucociliary clearance. C. predisposes to respiratory infections. D. introduces carcinogens into the lungs.

A. impairs α1-antitrypsin, allowing elastase to predominate. Cigarette smoking impairs α1-antitrypsin, allowing elastase to predominate and destroy lung tissue, causing emphysema. Although cigarette smoking does paralyze cilia, this action predisposes to respiratory infections rather than to emphysema. Although cigarette smoking does predispose to respiratory infections, that is not the mechanism that causes emphysema. Carcinogens introduced by cigarette smoking increase the risk of developing lung cancer, but they are not responsible for emphysema.

Respiratory acidosis is associated with A. increased carbonic acid. B. hypokalemia. C. increased neuromuscular excitability. D. increased pH.

A. increased carbonic acid. Respiratory acidosis causes an excess of carbonic acid that may be because of impaired gas exchange, inadequate neuromuscular function, and impairment of respiratory control of the brainstem. Hypokalemia is associated with alkalosis. Acidosis is associated with decreased neuromuscular excitability. Increased pH is associated with alkalosis; in acidosis the pH is low.

Uncompensated metabolic alkalosis would result in A. increased pH, increased HCO3-. B. increased pH, decreased HCO3-. C. decreased pH, increased HCO3-. D. decreased pH, decreased HCO3-.

A. increased pH, increased HCO3 Metabolic alkalosis is characterized by increased HCO3- and increased pH. HCO3- is a base and would be increased. Decreased pH indicates an uncompensated or partially compensated acidosis.

The finding of ketones in the blood suggests that a person may have A. metabolic acidosis. B. metabolic alkalosis. C. respiratory acidosis. D. respiratory alkalosis.

A. metabolic acidosis. Ketones are produced from breakdown of fat in the body as a result of starvation or lack of ability to utilize glucose in diabetes mellitus. Ketoacids in the blood indicate a very high ketone level in the body, which leads to metabolic acidosis. Ketonuria from high ketones in the blood would not indicate metabolic alkalosis. The respiratory system does not influence ketone level.

When preparing for the admission of a client diagnosed with bronchiectasis, the nurse will A. put a sputum cup and a box of tissues on the bedside table. B. remove the telephone to reduce myocardial oxygen demand. C. add a box of surgical masks to the nursing supplies near the door. D. remove the water pitcher to comply with anticipated fluid restrictions.

A. put a sputum cup and a box of tissues on the bedside table. People who have bronchiectasis have a productive cough, usually with foul-smelling sputum. Bronchiectasis is not contagious or a cardiac condition. Fluid restriction is not part of the treatment for bronchiectasis.

The hypersecretion of mucus resulting for chronic bronchitis is the result of A. recurrent infection. B. destruction of alveolar septa. C. reduced inflammation. D. barrel chest.

A. recurrent infection. Mucus provides a hospitable environment for bacterial colonization and recurrent infection. Destruction of alveolar septa and reduced inflammation are not complications of chronic bronchitis. Hypersecretion of mucus does not contribute to barrel chest.

Emphysema results from destruction of alveolar walls and capillaries, which is because of A. release of proteolytic enzymes from immune cells. B. air trapping with resultant excessive alveolar pressure. C. excessive α1-antitrypsin. D. autoantibodies against pulmonary basement membrane.

A. release of proteolytic enzymes from immune cells. The pathologic changes leading to alveolar destruction are associated with the release of proteolytic enzymes from inflammatory cells such as neutrophils and macrophages. While air trapping occurs in emphysema, the destruction of alveolar walls and capillaries is because of release of proteolytic enzymes. Lack of α1-antitrypsin can result in emphysema. Autoantibodies are not involved in destruction of alveolar walls and capillaries in emphysema.

The electrolyte that has a higher concentration in the extracellular fluid than in the intracellular fluid is _____ ions. A. sodium B. phosphate C. magnesium D. potassium

A. sodium Extracellular fluid has a higher sodium ion concentration than does intracellular fluid. Intracellular fluid has a higher phosphate, magnesium, and potassium ion concentration than does extracellular fluid.

The most definitive diagnostic method for active tuberculosis is acquired via A. sputum culture. B. Mantoux skin test. C. chest x-ray. D. blood culture.

A. sputum culture. The most definitive diagnostic method for active tuberculosis is via sputum culture to identify the acid-fast bacillus. The Mantoux skin test does not distinguish between active infection and past infection. Although a chest x-ray will show characteristic nodules, a sputum culture is the most definitive diagnostic method for active tuberculosis. Unless a patient is septic (infection in the blood), the tuberculosis organism will not be found in the blood.

Airway obstruction in chronic bronchitis is because of A. thick mucus, fibrosis, and smooth muscle hypertrophy. B. loss of alveolar elastin. C. pulmonary edema. D. hyperplasia and deformation of bronchial cartilage.

A. thick mucus, fibrosis, and smooth muscle hypertrophy. Airway obstruction in chronic bronchitis is as a result of thick mucus, fibrosis, and smooth muscle hypertrophy. Loss of alveolar elastin, pulmonary edema, and hyperplasia and deformation of bronchial cartilage are not part of the pathophysiology of chronic bronchitis.

Clinical manifestations of extracellular fluid volume deficit include A. weak pulse, low blood pressure, and increased heart rate. B. thirst, dry mucous membranes, and diarrhea. C. confusion, lethargy, coma, and perhaps seizures. D. cardiac dysrhythmias, paresthesias, and muscle weakness.

A. weak pulse, low blood pressure, and increased heart rate. Clinical manifestations of extracellular fluid volume deficit include weak pulse, low blood pressure, and increased heart rate. Extracellular fluid volume deficit does not cause diarrhea. Confusion, lethargy, coma, and perhaps seizures are associated with osmolality imbalances such as hyponatremia. Cardiac dysrhythmias, paresthesias, and muscle weakness are manifestations of electrolyte imbalances.

Chronic bronchitis often leads to cor pulmonale because of A. ventricular hypoxia. B. increased pulmonary vascular resistance. C. left ventricular strain. D. hypervolemia.

B. increased pulmonary vascular resistance. Chronic bronchitis often leads to cor pulmonale as a result of increased pulmonary vascular resistance when right ventricular end-diastolic pressure increases. Ventricular hypoxia, left ventricular strain, and hypervolemia do not lead to cor pulmonale.

The imbalance that occurs with oliguric renal failure is A. metabolic alkalosis. B. hyperkalemia. C. hypokalemia. D. hypophosphatemia.

B. hyperkalemia. Oliguric renal failure decreases potassium excretion, which causes hyperkalemia. Oliguric renal failure decreases acid excretion and causes metabolic acidosis (not alkalosis). Oliguric renal failure does not cause hypokalemia or hypophosphatemia.

When a parent of a toddler recently diagnosed with pneumococcal pneumonia asks why their child is so much sicker than a classmate was when they were diagnosed with pneumonia, the nurse replies A. "It sounds as if the classmate was just lucky and less exposed at daycare." B. "It sounds like your child has a case of bacterial pneumonia, while the classmate had viral pneumonia." C. "It sounds as if your child is having a severe reaction to bacterial pneumonia. It hits some children harder than others." D. "It sounds as if your child has a case of viral pneumonia, while the classmate had bacterial pneumonia."

B. "It sounds like your child has a case of bacterial pneumonia, while the classmate had viral pneumonia." Viral pneumonia does not produce exudate so the cough is non-productive. In general, symptoms of viral pneumonia are less severe than those of bacterial pneumonia. The uncle's case of viral pneumonia has less acute symptoms than the children's case of bacterial pneumonia. Pneumococcal pneumonia is not necessarily more severe in children. The children most likely have bacterial pneumonia, which is why their symptoms are more acute than the classmate's case of viral pneumonia.

Hyperaldosteronism causes A. ECV deficit and hyperkalemia. B. ECV excess and hypokalemia. C. hyponatremia and hyperkalemia. D. excessive water reabsorption without affecting sodium concentration.

B. ECV excess and hypokalemia. Hyperaldosteronism causes excessive renal retention of sodium and water and excessive potassium excretion, which lead to ECV excess and hypokalemia. Hyperaldosteronism does not cause ECV deficit, hyperkalemia, hyponatremia, or excessive water reabsorption without affecting sodium concentration.

The characteristic x-ray findings in tuberculosis include A. diffuse white-out. B. Ghon tubercles. C. bibasilar infiltrates. D. tracheal deviation.

B. Ghon tubercles. Tuberculosis results in Ghon tubercles that show up as nodules with infiltrates. Diffuse white-out, basilar infiltrates, and tracheal deviation are not characteristic x-ray findings in tuberculosis.

Which disorder is caused by inhalation of organic substances? A. Diffuse interstitial lung disease B. Hypersensitivity pneumonitis C. Sarcoidosis D. Acute respiratory distress syndrome

B. Hypersensitivity pneumonitis Hypersensitivity pneumonitis is caused by inhalation of organic substances that produces an inflammatory immunologic reaction. Diffuse interstitial lung disease is probably related to an immune reaction but not from inhalation of organic substances. Sarcoidosis likely has an immunologic basis, but not from inhalation of organic substances. Acute respiratory distress syndrome is associated with severe trauma, sepsis, and shock.

When exposed to inhaled allergens, a patient with asthma produces large quantities of A. IgG. B. IgE. C. IgA. D. IgM.

B. IgE. During an allergic response, plasma cells produce large quantities of IgE. IgG, IgA, and IgM are not part of the pathophysiology of asthma.

How is a patient hospitalized with a malignant tumor that secretes parathyroid hormone-related peptide monitored for the resulting electrolyte imbalance? A. Serum calcium, Chvostek and Trousseau signs B. Serum calcium, bowel function, level of consciousness C. Serum potassium, Chvostek and Trousseau signs D. Serum potassium, bowel function, level of consciousness

B. Serum calcium, bowel function, level of consciousness Parathyroid hormone increases the plasma calcium concentration, and constipation and lethargy are manifestations of hypercalcemia. Parathyroid hormone increases the plasma calcium concentration, but these are signs of increased neuromuscular excitability, which occurs with hypocalcemia. Parathyroid hormone affects plasma concentration of calcium, not potassium.

Croup is characterized by A. a productive cough. B. a barking cough C. an inability to cough D. drooling, sore throat, and difficulty swallowing.

B. a barking cough Croup is characterized by a barking cough with stridor. A productive cough is not characteristic of croup. Croup is associated with coughing. Drooling, sore throat, and difficulty swallowing are not characteristics of croup.

Viral pneumonia is characterized by A. a productive cough. B. a dry cough. C. exudative consolidation. D. significant ventilation-perfusion imbalance.

B. a dry cough. No exudative fluids are produced. Viral pneumonia does not produce exudates, so the cough is non-productive. Ventilation-perfusion imbalance does not usually occur in viral pneumonia.

Excessive antidiuretic hormone (ADH) secretion can cause _____ concentration. A. increased serum sodium B. decreased serum sodium C. increased serum potassium D. decreased serum potassium

B. decreased serum sodium Excessive ADH stimulates excessive water reabsorption by the kidneys, which dilutes the blood, thus decreasing the serum sodium concentration. Excessive ADH secretion does not cause increased serum sodium or potassium concentrations, or decreased serum potassium concentration.

Lack of α-antitrypsin in emphysema causes A. chronic mucous secretion and airway fibrosis. B. destruction of alveolar tissue. C. pulmonary edema and increased alveolar compliance. D. bronchoconstriction and airway edema.

B. destruction of alveolar tissue. Lack of α1-antitrypsin in emphysema causes destruction of alveolar tissue, as it is a protective enzyme that prohibits proteolytic breakdown of alveolar tissue. Lack of alpha1-antitrypsin does not cause chronic mucous secretion and airway fibrosis, pulmonary edema and increased alveolar compliance, or bronchoconstriction and airway edema.

Early manifestations of a developing metabolic acidosis include A. coma B. headache C. muscle cramps D. short and shallow respirations

B. headache Headache is an early manifestation of a developing metabolic acidosis. Coma is a very late symptom of metabolic acidosis. Muscle cramps are not characteristic of metabolic acidosis. Deep rapid respirations are the compensatory mechanism for metabolic acidosis.

Empyema is defined as an A. exudative bronchitis. B. infection in the pleural space. C. infection localized in the lung. D. infection in the blood.

B. infection in the pleural space. Empyema is infection in the pleural space. Empyema is not exudative bronchitis, localized infection in the lung, or an infection in the blood.

The primary cause of infant respiratory distress syndrome is A. prematurity. B. lack of surfactant. C. maternal illegal drug use during pregnancy. D. umbilical cord compression.

B. lack of surfactant. The primary cause of this disorder is lack of surfactant. While premature infants maydemonstrate this disorder, the actual cause is lack of surfactant. It is a syndrome seen in premature infants. Maternal illegal drug use during pregnancy and umbilical cord compression are not the primary causes of infant respiratory distress syndrome.

Obstructive disorders are associated with A. low residual volumes. B. low expiratory flow rates. C. increased expiratory reserve volume. D. decreased total lung capacity.

B. low expiratory flow rates. Obstructive disorders are associated with low expiratory flow rates. Obstructive disorders are associated with high residual volume. Increased expiratory reserve volume and decreased total lung capacity are not characteristic of obstructive disorders.

Clinical manifestations of moderate to severe hypokalemia include A. muscle spasms and rapid respirations. B. muscle weakness and cardiac dysrhythmias. C. confusion and irritability. D. vomiting and diarrhea.

B. muscle weakness and cardiac dysrhythmias.

The process responsible for distribution of fluid between the interstitial and intracellular compartments is A. filtration. B. osmosis. C. active transport. D. diffusion.

B. osmosis. Distribution of fluid between the interstitial and intracellular compartments occurs by the process of osmosis. Filtration is responsible for the distribution of fluid between the vascular and interstitial compartments. Active transport moves ions across membranes, but does not move water. Diffusion involves movement of particles, not movement of water.

A patient has been hospitalized several times in 6 months with severe ECV depletion and hypokalemia resulting from chronic laxative abuse. Which blood gas results should be relayed to the physician? A. pH in high part of normal range, PaO2 normal, PaCO2 normal, bicarbonate normal B. pH in high part of normal range, PaO2 normal, PaCO2 high, bicarbonate high C. pH in low part of normal range, PaO2 normal, PaCO2 low, bicarbonate low D. pH in low part of normal range, PaO2 normal, PaCO2 normal, bicarbonate normal

B. pH in high part of normal range, PaO2 normal, PaCO2 high, bicarbonate high The laboratory values of pH in high part of normal range, PaO2 normal, PaCO2 high, and bicarbonate high indicate compensated metabolic alkalosis, which is not consistent with increased excretion of bicarbonate in chronic diarrhea from laxative abuse, so you should page the physician. The laboratory values of pH in low part of normal range, PaO2 normal, PaCO2 low, and bicarbonate low indicate compensated metabolic acidosis, which is consistent with increased excretion of bicarbonate in chronic diarrhea from laxative abuse. The other answer options are normal laboratory values.

A patient exhibiting respiratory distress as well as a tracheal shift should be evaluated for A. pneumonia. B. pneumothorax. C. pulmonary edema. D. pulmonary embolus.

B. pneumothorax. Pneumothorax leads to a tracheal shift to the side opposite the pneumothorax. Pneumonia, pulmonary edema, and pulmonary embolus do not lead to tracheal shift.

The person at highest risk for developing hypernatremia is a person who A. self-administers a daily tap water enema to manage a partial bowel obstruction. B. receives tube feedings because he or she is comatose after a stroke. C. has ectopic production of ADH from small cell carcinoma of the lung. D. is receiving IV 0.9% NaCl at a fast rate.

B. receives tube feedings because he or she is comatose after a stroke. Tube feedings are associated with hypernatremia as a result of intake of highly concentrated solution that causes the kidneys to excrete extra water to remove the solute load. Absorption of excessive water from daily tap water enemas would cause hyponatremia. Uncontrolled secretion of ADH causes renal retention of water that leads to hyponatremia. An IV solution of 0.9% NaCl (normal saline) is isotonic.

A person with acute hypoxemia may hyperventilate and develop A. respiratory acidosis B. respiratory alkalosis. C. metabolic alkalosis. D. metabolic acidosis.

B. respiratory alkalosis. Hyperventilation causes much carbonic acid to be blown off, resulting in respiratory alkalosis. Respiratory acidosis is caused by hypoventilation and retention of carbonic acid. Hyperventilation does not cause metabolic acid or base disturbances.

The fraction of total body water (TBW) volume contained in the intracellular space in adults is A. three fourths. B. two thirds. C. one half. D. one third.

B. two thirds. Approximately two thirds of TBW is contained inside the cells. Two thirds, not three fourths, of TBW is contained inside the cells. Two thirds, not one-half, of TBW is contained inside the cells. One-third of the TBW is extracellular in adults.

Which is indicative of a left tension pneumothorax? A. Course crackles throughout the left chest B. Tracheal deviation to the left C. Absent breath sounds on the left D. Respiratory acidosis

C. Absent breath sounds on the left A left pneumothorax results in absent breath sounds on the affected side. Crackles will not be heard because breath sounds are not present. Tracheal deviation occurs on the contralateral side. Pneumothorax results in acute respiratory alkalosis.

Which alterations can lead to edema? A. Decreased capillary hydrostatic pressure B. Increased capillary colloid osmotic pressure C. Decreased lymphatic flow D. Decreased capillary membrane permeability

C. Decreased lymphatic flow Lymphatic obstruction prevents the drainage of accumulated interstitial fluid and proteins, which can lead to severe edema. Decreased capillary hydrostatic pressure would push less fluid into the interstitial space. Increased capillary colloid osmotic pressure would remove fluid from the interstitial space. Decreased capillary membrane permeability would allow less fluid movement into the interstitial space.

A patient who reports an intestinal fistula also reports feeling "weak and dizzy" when she stands. While taking her blood pressure she becomes temporarily unresponsive but quickly regains consciousness when put into a supine position. What nursing interventions will the nurse implement before calling the physician? A. Sit her up again, with proper support, so you can have an accurate upright blood pressure and heart rate to report. B. Give her a drink of water or juice, talk with her to calm her down, and ask if she slept well last night. C. Give her water or juice and some salty crackers and ask if she has had any diarrhea or vomiting. D. Assess small vein filling time, look for ankle edema, and ask if she had any fluid to drink yet today.

C. Give her water or juice and some salty crackers and ask if she has had any diarrhea or vomiting. Her substantial systolic postural blood pressure decreases with tachycardia and syncope when upright are indicators of ECV deficit and she needs salt and water. Your questions will provide information for her physician regarding the origin of the ECV deficit. She fainted the first time when she sat upright and is likely to faint again, given her upright systolic pressure of 77 mm Hg. She needs salt and water to increase her ECV and sleep quality is not directly related to ECV deficit. Ankle edema is a sign of ECV excess.

Allergic (extrinsic) asthma is associated with A. hyporesponsiveness of airways. B. unknown precipitating factors. C. IgE-mediated airway inflammation. D. irreversible airway obstruction.

C. IgE-mediated airway inflammation.

What is the most likely explanation for a diagnosis of hypernatremia in an elderly patient receiving tube feeding? A. Too much sodium in the feedings B. Excess of feedings C. Inadequate water intake D. Kidney failure

C. Inadequate water intake Failure to provide adequate water when a patient is receiving tube feedings could result in hypernatremia. The feedings may have too much sodium, or the patient may be receiving too much feeding solution, but most likely the patient is not receiving enough water. Kidney failure is most likely not the cause of hypernatremia in this patient.

Obstructive sleep apnea would most likely be found in a patient diagnosed with A. myasthenia gravis. B. poliomyelitis. C. Pickwickian syndrome. D. pneumonia.

C. Pickwickian syndrome. Pickwickian syndrome is hypoventilation caused by obesity. Sleep apnea is often a problem in obese individuals. Obstructive sleep apnea is not likely to be found in a patient with myasthenia gravis, poliomyelitis, or pneumonia.

A 3-year-old is diagnosed with starvation ketoacidosis. What signs and symptoms should you anticipate in your assessment? A. Slow, shallow breathing, belligerence, hyperexcitability B. Slow, shallow breathing, numbness and tingling around his mouth C. Rapid, deep breathing, lethargy, abdominal pain D. Rapid, deep breathing, tremors, elevated blood pressure

C. Rapid, deep breathing, lethargy, abdominal pain Rapid, deep breathing, lethargy, and abdominal pain are clinical manifestations of metabolic acidosis and its respiratory compensation. The other answer options are not clinical manifestations of metabolic acidosis and its respiratory compensation.

All obstructive pulmonary disorders are characterized by: A. Hyperresponsiveness. B. Decreased residual volumes C. Resistance to airflow. D. Decreased lung compliance.

C. Resistant to airflow. Obstructive lung diseases are characterized by increased resistance to airflow. Only asthma is characterized by hyperresponsiveness. Increased residual volume is common in obstructive pulmonary disorders. Emphysema is characterized by increased lung compliance caused by a loss of alveoli and elastic tissue.

Which complication of asthma is life threatening? A. Exercise-induced asthma B. Late phase response C. Status asthmaticus D. Mast cell degranulation

C. Status asthmaticus Status asthmaticus is a severe attack unresponsive to routine therapy and can be life threatening if not reversed. Exercise-induced asthma is a form of asthma, rather than a complication of it. The late phase response is part of the pathophysiology of asthma and is not always life threatening. Mast cell degranulation is part of the pathophysiology of asthma and in itself is not life threatening.

Bacterial pneumonia leads to hypoxemia caused by A. cardiogenic pulmonary edema. B. upper airway obstruction. C. accumulation of alveolar exudates. D. interstitial edema.

C. accumulation of alveolar exudates. The inflammatory response to bacterial pneumonia causes accumulation of exudates in the alveoli and impairs oxygenation. Bacterial pneumonia does not cause cardiogenic pulmonary edema. Pneumonia involves lower airway obstruction. Bacterial pneumonia does not lead to interstitial edema.

The major buffer in the extracellular fluid is A. hemoglobin B. albumin C. bicarbonate D. phosphate

C. bicarbonate Bicarbonate is the major buffer in the extracellular fluid. Hemoglobin is in erythrocytes, which are in the vascular compartment, but not in the interstitial portion of extracellular fluid. Albumin is in the vascular compartment, but not in the interstitial portion of extracellular fluid. Phosphate is an important buffer in urine and intracellular fluid.

Signs and symptoms of extracellular fluid volume excess include A. tachycardia B. increased serum sodium concentration. C. bounding pulse. D. increased hematocrit.

C. bounding pulse. Bounding pulse is one of the signs of extracellular fluid volume excess. Tachycardia is one of the signs of extracellular fluid volume deficit. Increased serum sodium concentration is found in hypernatremia. Hematocrit can be decreased with extracellular fluid volume excess.

Cystic fibrosis is associated with A. asthma. B. chronic bronchitis. C. bronchiectasis. D. emphysema.

C. bronchiectasis. Fifty percent of cases of bronchiectasis are associated with cystic fibrosis. Cystic fibrosis is not associated with asthma, chronic bronchitis, or emphysema.

The inward-pulling force of particles in the vascular fluid is called _____ pressure. A. capillary hydrostatic B. interstitial osmotic C. capillary osmotic D. interstitial hydrostatic

C. capillary osmotic Capillary osmotic pressure is the inward-pulling force of particles in the vascular fluid. Capillary hydrostatic pressure is an outward-pulling. The question pertains to vascular fluid rather than interstitial fluid. Interstitial hydrostatic pressure is an outward-pulling force.

Clinical manifestations of hyponatremia include A. weak pulse, low blood pressure, and increased heart rate. B. thirst, dry mucous membranes, and diarrhea. C. confusion, lethargy, coma, and perhaps seizures. D. cardiac dysrhythmias, paresthesias, and muscle weakness.

C. confusion, lethargy, coma, and perhaps seizures. Clinical manifestations of hyponatremia include confusion, lethargy, coma, and perhaps seizures, as they are manifestations of CNS dysfunction. Weak pulse, low blood pressure, and increased heart rate are characteristic of clinical dehydration. Hyponatremia does not cause thirst, dry mucous membranes, and diarrhea. Cardiac dysrhythmias, paresthesias, and muscle weakness are manifestations of electrolyte imbalances.

Total body water in older adults is A. increased because of decreased adipose tissue and decreased bone mass. B. increased because of decreased renal function and hormonal fluctuations. C. decreased because of increased adipose tissue and decreased muscle mass. D. decreased because of renal changes that cause diuresis with sodium excretion.

C. decreased because of increased adipose tissue and decreased muscle mass. Older adults have decreased total body water because of increased adipose tissue and decreased muscle mass. Older adults have increased adipose tissue. Hormonal fluctuations and diuresis with sodium excretion are not characteristic of older adults.

Clinical manifestations of severe symptomatic hypophosphatemia are caused by A. excess proteins. B. renal damage. C. deficiency of ATP. D. hypocalcemia.

C. deficiency of ATP. Clinical manifestations of severe symptomatic hypophosphatemia are caused by a deficiency of ATP. Phosphate is an important component of ATP, which is the major source of energy for many cellular substances. Severe symptomatic hypophosphatemia does not cause excess protein accumulation, damage the kidneys, or cause hypocalcemia.

The nurse provides teaching regarding dietary intake of potassium to avoid an electrolyte imbalance when a patient A. takes very large doses of vitamin D to supplement during chemotherapy for breast cancer. B. has fatty stools from taking an OTC weight loss product that decreases absorption of fat. C. has chronic heart failure that is treated with diuretics. D. experiences anorexia and chronic oliguric renal failure.

C. has chronic heart failure that is treated with diuretics. Chronic heart failure causes increased secretion of aldosterone, which often causes hypokalemia by increasing renal excretion of potassium; most diuretics used to treat heart failure also increase renal excretion of potassium. Vitamin D and malabsorption of fat decreases absorption of calcium, not potassium. Chronic oliguric renal failure causes decreased excretion of potassium. An anorexic patient with chronic oliguric renal failure should not increase dietary potassium.

The patient who requires the most careful monitoring for development of metabolic acidosis is a patient who A. is in the diuretic phase of acute renal failure. B. has had hypokalemia for over a week. C. has had diarrhea for over a week. D. has newly diagnosed Cushing syndrome.

C. has had diarrhea for over a week. Diarrhea causes increased excretion of the base bicarbonate, which can lead to metabolic acidosis. Although the oliguric phase of acute renal failure causes metabolic acidosis, the diuretic phase does not, because the kidneys can still excrete metabolic acids. Hypokalemia is associated with metabolic alkalosis. Cushing syndrome is cortisol excess, which can cause metabolic alkalosis from increased renal excretion of hydrogen ions.

A person who overuses magnesium-aluminum antacids for a long period of time is likely to develop A. hypokalemia. B. hyperkalemia. C. hypophosphatemia. D. hyperphosphatemia.

C. hypophosphatemia. Antacid overuse for a long time can cause hypophosphatemia by binding phosphate in the gastrointestinal tract and preventing its absorption. Magnesium-aluminum antacids do not cause hypokalemia, hyperkalemia, or hyperphosphatemia.

Abnormalities in intracellular regulation of enzyme activity and cellular production of ATP are associated with A. hyponatremia. B. hypocalcemia. C. hypophosphatemia. D. hypokalemia.

C. hypophosphatemia. Phosphate is an important component of ATP. Hypophosphatemia results in decreased ATP to cells. Hyponatremia, hypocalcemia, and hypokalemia do not affect ATP production.

The increased anterior-posterior chest diameter associated with obstructive lung disease is caused by A. increased pulmonary blood flow. B. increased expiratory flow rates. C. increased residual lung volumes. D. decreased chest wall compliance.

C. increased residual lung volumes. Increased residual lung volumes are because of air trapping in obstructive lung disease and cause a barrel chest. Increased pulmonary blood flow does not affect chest diameter. Increased expiratory flow rates would decrease air trapping rather than increase chest diameter. Obstructive lung disease does not involve decreased chest wall compliance. It is increased as a result of loss of alveoli and elastic tissue.

A known cause of hypokalemia is A. oliguric renal failure B. pancreatitis C. insulin overdose D. hyperparathyroidism

C. insulin overdose Insulin overdose causes hypokalemia by shifting potassium into cells. Oliguric renal failure decreases electrolyte excretion. Pancreatitis causes fat malabsorption, which binds calcium and magnesium, but not potassium, in the gastrointestinal tract. Hyperparathyroidism regulates calcium, not potassium.

Diarrhea causes A. respiratory acidosis B. respiratory alkalosis C. metabolic acidosis D. metabolic alkalosis.

C. metabolic acidosis Diarrhea causes metabolic acidosis as the intestinal fluids are rich in bicarbonate ions. Diarrhea causes a metabolic acid-base imbalance and is not related to the respiratory system. Diarrhea involves increased excretion of bicarbonate and causes an acidic condition.

A major cause of treatment failure in tuberculosis is A. resistant organism. B. allergy to drugs used. C. noncompliance. D. immunosuppression.

C. noncompliance. The major cause of treatment failure in tuberculosis is non-adherence to drug therapy. The major cause of treatment failure in tuberculosis is not a resistant organism, drug allergy, or immunosuppression.

Asthma is categorized as a(n) A. restrictive pulmonary disorder. B. infective pulmonary disorder. C. obstructive pulmonary disorder. D. type of acute tracheobronchial obstruction.

C. obstructive pulmonary disorder Asthma is an obstructive pulmonary disorder. Asthma is not a restrictive pulmonary disorder or a type of tracheobronchial obstruction. Although asthma can be associated with infection, it is not an infective pulmonary disorder.

The arterial blood gas pH = 7.52, PaCO2 = 30 mm Hg, HCO3- = 24 mEq/L demonstrates A. metabolic acidosis. B. respiratory acidosis. C. respiratory alkalosis. D. mixed alkalosis.

C. respiratory alkalosis. The high pH, low PaCO2, and normal HCO3indicate respiratory alkalosis. Metabolic and respiratory acidosis would decrease the pH. The HCO3- is normal, so no metabolic imbalance is indicated.

Neuromuscular disorders impair lung function primarily because A. inflammatory events in the lung. B. secondary pneumonia. C. weak muscles of respiration D. inactivity secondary to the disorder.

C. weak muscles of respiration Neuromuscular disorders weaken respiratory muscle function resulting in poor ventilation. Inflammatory events in the lung, secondary pneumonia, and inactivity secondary to the disorder are not the primary reasons neuromuscular disorders impair lung function.

Neuromuscular disorders impair lung function primarily because of A. inflammatory events in the lung. B. secondary pneumonia. C. weak muscles of respiration. D. inactivity secondary to the disorder.

C. weak muscles of respiration. Neuromuscular disorders weaken respiratory muscle function resulting in poor ventilation. Inflammatory events in the lung, secondary pneumonia, and inactivity secondary to the disorder are not the primary reasons neuromuscular disorders impair lung function.

When a parent asks how they will know if their 2-month-old baby, who is throwing up and has frequent diarrhea, is dehydrated, the nurse's best response is A. "Clinical dehydration is the combination of extracellular fluid volume deficit and hypernatremia, so those are the diagnostic criteria." B. "If he doesn't wet his diaper all afternoon and his neck veins look flat when he is lying down, then he is probably dehydrated." C. "If he sleeps more than usual and acts tired when he is awake, then he is probably dehydrated." D. "If the soft spot on the top of his head feels sunken in and his mouth is dry between his cheek and his gums, then he is probably dehydrated."

D. "If the soft spot on the top of his head feels sunken in and his mouth is dry between his cheek and his gums, then he is probably dehydrated." Checking whether the head feels sunken and the mouth is dry between check and gums are useful assessments of ECV deficit in an infant, which is an important part of clinical dehydration. It is true that clinical dehydration is the combination of extracellular fluid volume deficit and hypernatremia, but it does not address the question Mr. Worry is asking. Although the diaper information provides a useful assessment, neck veins are not a reliable assessment in an infant. Drowsiness and fatigue are not reliable assessments for dehydration.

How do clinical conditions that increase vascular permeability cause edema? A. Through altering the negative charge on the capillary basement membrane, which enables excessive fluid to accumulate in the interstitial compartment B. By causing movement of fluid from the vascular compartment into the intracellular compartment, which leads to cell swelling C. Through leakage of vascular fluid into the interstitial fluid, which increases interstitial fluid hydrostatic pressure D. By allowing plasma proteins to leak into the interstitial fluid, which draws in excess fluid by increasing the interstitial fluid osmotic pressure

D. By allowing plasma proteins to leak into the interstitial fluid, which draws in excess fluid by increasing the interstitial fluid osmotic pressure Clinical conditions that increase vascular permeability cause edema by allowing plasma proteins to leak into the interstitial fluid, which draws in excess fluid by increasing the interstitial fluid osmotic pressure. The capillary basement membrane does not change its charge with increased vascular permeability. Increased vascular permeability does not move water into the cells. Increasing the interstitial fluid osmotic pressure would not cause edema.

Which clinical manifestation is not likely the result of a tuberculosis infection? A. Productive cough B. Low-grade fever C. Night sweats D. Cyanosis

D. Cyanosis Cyanosis is not a typical manifestation of tuberculosis infection. A productive cough, low-grade fever, and night sweats are the typical manifestations of tuberculosis infection.

What is likely to lead to hyponatremia? A. Insufficient ADH secretion B. Excess aldosterone secretion C. Administration of intravenous normal saline D. Frequent nasogastric tube irrigation with water

D. Frequent nasogastric tube irrigation with water Sodium is lost from gastric secretions when nasogastric tubes are irrigated with water. The sodium diffuses into the irrigating water and is then lost when the aspirate is withdrawn. Excessive ADH would lead to hyponatremia by retention of water in the body, thus diluting the sodium. Excess aldosterone would increase serum sodium. Normal saline is an isotonic solution and will not alter the serum sodium.

In individuals who have asthma, exposure to an allergen to which they are sensitized leads to which pathophysiologic event? A. Loss of alveolar elastin and premature closure of airways B. Pulmonary edema and decreased alveolar compliance C. Mast cell degranulation that causes decreased surfactant D. Inflammation, mucosal edema, and bronchoconstriction

D. Inflammation, mucosal edema, and bronchoconstriction In asthma, exposure to an allergen causes mast cell degranulation and release of inflammatory mediators that trigger airway inflammation, mucosal edema, and bronchoconstriction. In asthma, exposure to an allergen does not cause loss of alveolar elastin, pulmonary edema and decreased alveolar compliance, or decreased surfactant.

Which assessment would support a diagnosis of Type A COPD rather than Type B COPD? A. Barrel chest, productive cough, cyanosis, very decreased PaO2. B. Noisy breath sounds, fatigue, high PaCO2, overweight. C. Copious sputum, dyspnea, cor pulmonale. D. Normal PaCO2, scant sputum, accessory muscle use, barrel chest.

D. Normal PaCO2, scant sputum, accessory muscle use, barrel chest. Barrel chest and obvious respiratory effort that maintains near normal blood gases are consistent with type A COPD in the early stages. Copious sputum, dyspnea, and cor pulmonale are consistent with type B COPD. Noisy breath sounds, fatigue, high PaCO 2, and overweight are consistent with type B COPD. Barrel chest, productive cough, cyanosis, and very decreased PaO 2 are not consistent with type A COPD.

Emesis causes A. respiratory acidosis B. respiratory alkalosis C. metabolic acidosis D. metabolic alkalosis

D. metabolic alkalosis Emesis causes metabolic alkalosis as the stomach is a major reservoir for acids. Emesis causes a metabolic acid-base imbalance as it is not related to the respiratory system. Emesis involves loss of gastric acid and fluid and causes an alkalotic disruption.

What form of oral rehydration, bottled water or salty broth, is best suited for a patient who is demonstrating signs of clinical dehydration? A. Bottled water, because he is so weak that he might choke on the fluid when he swallows, and water would be less damaging to the lungs than salty soup B. Bottled water, because it will rehydrate his cells C. Salty soup, because he needs nutrition as well as fluid D. Salty soup, because it will provide some sodium to help hold the fluid in his blood vessels and interstitial fluid

D. Salty soup, because it will provide some sodium to help hold the fluid in his blood vessels and interstitial fluid This man has indicators of clinical dehydration and he needs salt to hold the water in his extracellular compartment. Replacing fluids and electrolytes is more important than meeting his nutritional needs now.

Which change in a patient's assessment has the greatest urgency? A. Serum potassium concentration is decreasing; abdominal distention, but denies any difficulty breathing B. Serum calcium concentration is decreasing; reports constipation; is alert and denies any discomfort C. Serum calcium concentration is increasing; reports constipation; is alert and denies any discomfort D. Serum potassium concentration is increasing; has developed cardiac dysrhythmias, but denies any difficulty breathing

D. Serum potassium concentration is increasing; has developed cardiac dysrhythmias, but denies any difficulty breathing Cardiac dysrhythmias from hyperkalemia need rapid attention to prevent potentially life-threatening consequences and are therefore the highest priority for reporting. Certainly you will want to report this symptomatic hypokalemia, but it is not your most urgent priority, because abdominal distention is not rapidly life threatening and you have another patient with cardiac dysrhythmias, which can be life threatening. Certainly you will want to report this hypocalcemia, but it is not your most urgent priority, because there are no signs and symptoms of hypocalcemia and you have another patient with cardiac dysrhythmias, which can be life threatening. Certainly you will want to report this symptomatic hypercalcemia, but it is not your most urgent priority, because constipation is not rapidly life threatening and you have another patient with cardiac dysrhythmias, which can be life threatening.

The assessment findings of a 5-year-old with a history of asthma include extreme shortness of breath, nasal flaring, coughing, pulsus paradoxus, and use of accessory respiratory muscles. There is no wheezing and the chest is silent in many areas. How should you interpret your assessment? A. The signs and symptoms are consistent with asthma; start oxygen and then check to see that your stethoscope is working properly. B. The child probably has consolidated pneumonia; oxygen should be started immediately. C. Since there is not wheezing, asthma is the problem, but oxygen should be started immediately anyway. D. The child may be having such a severe asthma episode that the airways are closed, so start oxygen and get the doctor immediately.

D. The child may be having such a severe asthma episode that the airways are closed, so start oxygen and get the doctor immediately. The airway inflammation, edema, and bronchoconstriction of acute asthma may occlude small airways completely, so that no air is moving, which requires emergency intervention. Alicia has a history of asthma rather than pneumonia. Asthma can occur without wheezing. This is an emergency situation that requires you to start oxygen and notify the physician.

COPD leads to a barrel chest, because it causes A. pulmonary edema. B. muscle atrophy. C. prolonged inspiration. D. air trapping

D. air trapping Destruction of alveolar walls reduces lung elastic recoil, which allows airway collapse during exhalation. Air enters the alveoli during inhalation, but has difficulty escaping during exhalation. When air is trapped in the alveoli, residual volume increases, causing a barrel chest. Destruction of alveolar walls does not cause pulmonary edema, muscle atrophy, or prolonged inspiration.

Renal compensation for respiratory acidosis is evidenced by A. decreased carbon dioxide. B. elevated carbon dioxide. C. decreased bicarbonate ion concentration. D. elevated bicarbonate ion concentration.

D. elevated bicarbonate ion concentration. Elevated bicarbonate ion concentration is evidence of compensation for a respiratory acidosis. The lungs manage the carbon dioxide concentration. Elevated carbon dioxide is evidence of respiratory acidosis, not of compensation for it. Decreased bicarbonate ion concentration would make acidosis worse.

A person who has hyperparathyroidism is likely to develop A. hypokalemia. B. hyperkalemia. C. hypocalcemia. D. hypercalcemia.

D. hypercalcemia. A person who has hyperparathyroidism is likely to develop hypercalcemia, because parathyroid hormone causes calcium to come out of the bones and go to the ECF. Hypokalemia, hyperkalemia, and hypocalcemia are not the result of hyperparathyroidism.

Metabolic alkalosis is often accompanied by A. hypernatremia. B. hyponatremia. C. hyperkalemia. D. hypokalemia.

D. hypokalemia. Hypokalemia often accompanies metabolic alkalosis because it can cause metabolic alkalosis or be caused by it. Metabolic alkalosis and hypernatremia, hyponatremia, and hyperkalemia are not often associated with each other.

Respiratory acidosis may be caused by A. hyperventilation. B. massive blood transfusion. C. tissue hypoxia. D. hypoventilation.

D. hypoventilation. Hypoventilation causes carbonic acid retention and respiratory acidosis. Hyperventilation causes excretion of too much carbonic acid and respiratory alkalosis. The liver metabolizes the citrate in transfused blood into bicarbonate. Tissue hypoxia causes lactic acid production during anaerobic metabolism and metabolic acidosis.

The hallmark manifestation of acute respiratory distress syndrome is A. tachycardia. B hypotension. C. frothy secretions. D. hypoxemia.

D. hypoxemia. The hallmark of acute respiratory distress syndrome is hypoxemia caused by intrapulmonary shunting of blood. Tachycardia, hypotension, and frothy secretion occur in this disorder but are not hallmark.

A patient has a positive Chvostek sign. The nurse interprets this as a sign of A. hypercalcemia. B. hypermagnesemia. C. decreased neuromuscular excitability. D. increased neuromuscular excitability.

D. increased neuromuscular excitability. Positive Chvostek sign indicates increased neuromuscular excitability, which can be caused by hypocalcemia, hypomagnesemia, or other factors. Hypercalcemia and hypermagnesemia cause decreased neuromuscular excitability and do not cause positive Chvostek sign. Hypokalemia and hyperkalemia cause skeletal muscle weakness and do not cause positive Chvostek sign.

Two primary acid-base disorders that are present independently are referred to as A. metabolic acidosis. B. metabolic alkalosis. C. respiratory alkalosis. D. mixed acid-base imbalance.

D. mixed acid-base imbalance. Mixed acid-base disorders occur when two primary acid-base disorders are present independently. They may arise from simultaneous dysfunction of the respiratory system and kidneys. Metabolic acidosis is an acid disorder. Metabolic alkalosis and respiratory alkalosis are base disorders.

A patient with flail chest will demonstrate A. absence of chest movement with breaths. B. no inspiratory breath sounds. C. fluttering chest movements on expirations. D. outward chest movement on expiration.

D. outward chest movement on expiration. Flail chest is demonstrated by paradoxical inward movement on inspiration and outward movement on expiration. Flail chest is not demonstrated by absence of chest movement with breaths, no inspiratory breath sounds, or fluttering chest movements on expiration.

Accumulation of fluid in the pleural space is called A. an abscess. B. pleurisy. C. flail chest. D. pleural effusion.

D. pleural effusion. Pleural effusion is accumulation of fluid in the pleural space. A lung abscess is a circumscribed area of suppuration and lung tissue destruction. Pleurisy is inflammation of the pleura that often manifests with pain on inspiration, fever, and chills. Flail chest is the fracture of several consecutive ribs.

Osmoreceptors located in the hypothalamus control the release of A. angiotensin. B. atrial natriuretic peptide. C. aldosterone. D. vasopressin (antidiuretic hormone, ADH).

D. vasopressin (antidiuretic hormone, ADH). Factors that increase secretion of ADH into the blood include increased osmolality of the blood, which is sensed by osmoreceptors in the hypothalamus. Release of angiotensin, atrial natriuretic peptide, and aldosterone is not controlled by osmoreceptors in the hypothalamus.

Fully compensated respiratory acidosis is demonstrated by a. pH 7.36, PaCO2 55, HCO3- 36. b. pH 7.45, PaCO2 40, HCO3- 28. c. pH 7.26, PaCO2 60, HCO3- 26. d. pH 7.40, PaCO2 40, HCO3- 24.

a. pH 7.36, PaCO2 55, HCO3- 36. Compensation for respiratory acidosis involves conservation of HCO3- in the body; an HCO3- of 36 is a key finding; the normal pH (7.36) indicates compensation. Low HCO3-is not indicative of compensated respiratory acidosis. Low pH indicates no compensation or only partial compensation. Values of pH 7.40, PaCO2 40, and HCO3- 24 are all normal.