1. Chapter 21 Control of Respiratory
Function

2. Lung Functions Gas exchange Moves O2 into blood Removes CO2 from blood
Barrier immunity
Regulates vasoconstricting substances
Bradykinin
Angiotensin II
Heparin

3. Respiratory System Structures

4. Conducting Airways Move air into the lungs Warm and humidify air
Trap inhaled particles

5. Respiratory Airways Bronchioles Alveoli
Gas is exchanged with the blood.

6. Structure of Airway Walls

7. Respiratory Airways (cont.)

8. Question Which serous membrane lines the thoracic cavity?
Viscera pleura
Parietal pleura
Visceral mediastinum
Parietal mediastinum

9. Answer B. Parietal pleura
Rationale: The organs and walls of the thoracic and abdominal cavities are covered with serous membranes. Visceral membranes cover the organ; parietal membranes line the cavity walls. The two membranes and the space between them allow for ease of movement.
The thoracic cavity is lined by parietal pleura; the lungs are covered by visceral pleura.

10. Respiratory Muscles Diaphragm Accessory muscles of inhalation
External intercostals
Scalene
Sternocleidomastoid
Accessory muscles of exhalation
Internal intercostals
Abdominal muscles

11. Question
True or false?
During inhalation, the diaphragm contracts and flattens.

12. Answer
True
Rationale: The diaphragm is the main muscle of inhalation/inspiration. During inhalation, the diaphragm contracts and flattens (it moves downward in order to accommodate the volume of air you are taking in, allowing space for the lungs to expand).
During exhalation, the diaphragm relaxes and moves back up.

13. Compliance How easily lungs can be inflated depends on
Elastin and collagen fibers
Water content
Surface tension

14. Scenario
A man’s lungs were damaged during a fire, and he developed severe respiratory distress.
The doctor said smoke inhalation had caused an inflammation of his alveoli and destroyed some of his surfactant.
Questions:
What happened to his lung compliance?
Why was he given positive-pressure ventilation?

15. Lung Volumes Tidal volume (TV) Inspiratory reserve volume (IRV)
Expiratory reserve volume (ERV)
Residual volume (RV)

16. Lung Capacities Vital capacity Inspiratory capacity
Functional residual capacity
Total lung capacity

17. Dynamic Lung Function Maximum voluntary ventilation
Forced vital capacity (FVC)
Forced expiratory volume (FEV)
FEV1.0
Minute volume

18. Question
Which measure of lung function indicates the total amount of air that the lungs can hold?
Tidal volume
Functional residual capacity
Vital capacity
Total lung capacity

19. Answer D. Total lung capacity
Ratioanale: Total lung capacity (TLC) is the maximum amount of air that the lungs can hold—everything (volume-wise) at the end of a maximal inhalation (the deepest breath one can possibly take). Normal TLC is approximately 6 L.

20. Gas Exchange Oxygen moves from alveolar air into blood.
Carbon dioxide moves from blood into alveolar air.

21. Ventilation and Perfusion
Scenario:
An inhaled peanut blocks a left primary bronchus.
Questions:
How will the ventilation in the two lungs change?
How will the composition of the air in the two lungs differ?
Which lung should receive more blood?
How should the body alter perfusion of the lungs?

22. Ventilation-Perfusion Mismatching
Blood goes to parts of the lung that do not have oxygen to give it.
Blood does not go to parts of the lung that have oxygen.

23. Ventilation-Perfusion Mismatching (cont.)

24. Question
True or false?
Ventilation-perfusion mismatch results in hypoxia.

25. Answer
True
Rationale: In either case (ventilation without perfusion or perfusion without ventilation), oxygen is not picked up by the capillaries and delivered to the tissues. The result of decreased oxygen at the tissue level is termed hypoxia.

26. Blood Gases—Oxygen Dissolved oxygen = PaO2 or PO2
Normal value greater than 80 mm Hg
Oxygen bound to hemoglobin = oxyhemoglobin
Normal value 95% to 97% saturation

27. Hemoglobin Holds Four Oxygen Molecules
How saturated is this molecule of hemoglobin?
How could a person have a hemoglobin saturation of 95%?

28. Oxygen Capacity Amount of oxygen the blood can hold.
What is the oxygen capacity of normal blood?
What is the oxygen capacity of anemic blood?

29. Oxygen Capacity (cont.)

30. Oxygen Release
If the blood released half of its oxygen to the tissues:
How much oxygen would the normal tissues receive?
How much would the anemic person's tissues receive?

31. Oxygen Release (cont.) Most body tissues have a PO2 of 40 to 60 mm Hg.
How much oxygen does the normal blood release at a PO2 of 40 mm Hg?
The anemic blood?

32. Blood Gases—Carbon Dioxide
Dissolved carbon dioxide = PaCO2 or PCO2
Normal value 35 to 45 mm Hg
Carbon dioxide bound to hemoglobin = carbaminohemoglobin
Carbonic acid  bicarbonate ion and H+
When you exhale, you remove CO2 from your blood and also decrease the amount of carbonic acid, raising your blood pH.

33. Question
True or false?
The relationship between PCO2 and pH is direct.

34. Answer
False
Rationale: The relationship is indirect. As PCO2 levels rise, the amount of carbonic acid in the blood increases, making the pH more acidic (decreasing it).

35. Respiratory Center Control

36. Chemoreceptors Can Adjust Respiration Rate
Central chemoreceptors
Measure PCO2 and pH in cerebrospinal fluid
Increase respiration when PCO2 increases or pH decreases
Peripheral chemoreceptors
Measure PO2 in arterial blood
Increase respiration when PO2 less than 60 mm Hg

37. Scenario You are caring for a COPD client.
He has chronically high PCO2.
He is being given low-flow oxygen and complains all the time that he “needs more air,” so you turn up his oxygen.
Question:
When you check on him later, he is unconscious and not breathing. What happened?

38. Chapter 22 Respiratory Tract Infections,
Neoplasms, and Childhood Disorders

39. Upper Respiratory Viruses in Adults
Common cold
Rhinosinusitis
Influenza

40. The Common Cold Rhinoviruses
Occur in early fall and late spring in persons between ages 5 and 40
Parainfluenza viruses
Occur in children younger than 3
Respiratory syncytial virus
Occur in winter and spring in children younger than 3
Coronaviruses and adenoviruses
Occur in winter and spring

41. Rhinosinusitis (Sinusitis)
Infection or allergy obstructs sinus drainage
Acute: facial pain, headache, purulent nasal discharge, decreased sense of smell, fever
Chronic: nasal obstruction, fullness in the ears, postnasal drip, hoarseness, chronic cough, loss of taste and smell, unpleasant breath, headache

42. Influenza
In the United States, approximately 36,000 persons die each year of influenza-related illness.
Transmission is by aerosol (three or more particles) or direct contact.
Upper respiratory infection (rhinotracheitis):
Like a common cold with profound malaise
Viral pneumonia:
Fever, tachypnea, tachycardia, cyanosis, hypotension
Respiratory viral infection followed by a bacterial infection.

43. Influenza (cont.)

44. Question For which viruses is a 2-year-old most at risk? Rhinoviruses
Parainfluenza viruses
Respiratory syncytial virus (RSV)
All of the above
A and B

45. Answer
E. A and B
Rationale: Slightly older children (≥5 years of age) are at risk for rhinoviral infections. Children under the age of 3 are at risk of infection from both parainfluenza viruses and RSV.

46. Pneumonia—Inflammation of Alveoli and Bronchioles
Typical: bacteria in the alveoli
Lobar: affects an entire lobe of the lung
Bronchopneumonia: patchy distribution over more than one lobe
Atypical
Viral and mycoplasma infections of the alveolar septum or interstitium

47. Pneumonia—Inflammation of Alveoli and Bronchioles (cont.)

48. Tuberculosis
World’s foremost cause of death from a single infectious agent
Causes 26% of avoidable deaths in developing countries
Drug-resistant forms
Mycobacterium tuberculosis hominis
Aerobic
Protective waxy capsule
Can stay alive in “suspended animation” for years

49. Initial TB Infection Macrophages begin a cell-mediated immune response
Takes 3 to 6 weeks to develop positive TB test
Results in a granulomatous lesion
or Ghon focus containing
Macrophages
T cells
Inactive TB bacteria

50. Ghon Complex Nodules in lung tissue and lymph nodes.
Caseous necrosis inside nodules.
Calcium may deposit in the fatty area of necrosis.
Visible on x-rays.

51. Discussion Someone in your class has a positive TB test. Question:
What does this mean?
Are you at risk of infection?

52. Primary TB Primary TB Usually If immune response is isolated in
inadequate, bacteria
Ghon foci
multiply in the lungs
Bacteria
Not
Progressive primary TB
are
contagious
inactive

53. Miliary TB Progressive Primary TB Bacteria may Signs of Bacteria in
Miliary TB lesions look like grains of millet in the tissues.
Meat inspection was introduced to keep them out of the food supply.
Pasteurization of milk was introduced to keep TB out of the milk supply.
Progressive Primary TB
Bacteria may
Signs of
Bacteria in
erode blood
pneumonia
sputum and
vessels and
exhaled
spread through
droplets
the body
MILIARY TB

54. Secondary TB Reinfection from inhaled droplet nuclei
Reactivation of a previously healed primary lesion
Immediate cell-mediated response walls off infection in airways
Bacteria damage tissues in the airways, creating cavities
Signs of chronic pneumonia: gradual destruction of lung tissue
“Consumption”: eventually fatal if untreated

55. Question
Which type of TB may be reactivated if the patient becomes immunocompromised?
Primary
Latent
Miliary
Secondary

56. Answer
D. Secondary
Rationale: Secondary TB, often referred to as reactivation or reinfection TB, may occur if patients are reexposed to TB bacilli (after a primary infection) or if they become immunocompromised (they are unable to contain the infection).

57. Cavitary Tuberculosis

58. Lung Cancer Bronchogenic carcinoma
Arises from epithelial cells lining the lungs
Small cell lung cancer
Non–small cell lung cancer
Large cell carcinoma
Squamous cell
Adenocarcinoma

59. Adenocarcinoma of the Lung

60. Manifestations of Lung Cancer
Changes in organ function (organ damage, inflammation, and failure)
Local effects of tumors (e.g., compression of nerves or veins, gastrointestinal obstruction)
Ectopic hormones secreted by tumor cells (paraneoplastic disorders)
Nonspecific signs of tissue breakdown (e.g., protein wasting, bone breakdown)

61. Respiratory Distress Syndrome
Lack of surfactant; infants are not strong enough to inflate their alveoli.
Protein-rich fluid leaks into the alveoli and further blocks oxygen uptake.
Treatment with mechanical ventilation may cause bronchopulmonary dysplasia and chronic respiratory insufficiency.

62. Question
True or false?
Premature infants are at greater risk of developing respiratory distress syndrome (RDS) than term infants.

63. Answer
True
Rationale: RDS occurs due to a lack of surfactant in the alveoli (the surfactant is produced by alveolar cells and keeps them inflated). Surfactant is typically produced from week 28 (gestational age) through term (40 to 42 weeks). The more premature the infant/neonate, the greater the likelihood that there will be insufficient surfactant to sustain ventilation.

64. Respiratory Obstruction in Children
Increased airway resistance
Extrathoracic airways (upper airways)
Prolonged inspiration; inspirational stridor
Inspiratory retractions as ribs are moved outward and body wall does not expand with rib cage
Intrathoracic airways (lower airways)
Prolonged expiration with wheezing
Rib cage retractions as ribs are pulled inward, but air does not leave lungs

65. Obstructive Disorders
Upper airway
Croup
Epiglottitis
Lower airway
Acute bronchiolitis

66. Question
True or false?
Epiglottitis causes stridor.

67. Answer
True
Rationale: Epiglottitis affects the upper airway (inflammation causes the lumen of the upper airway to become more narrow). When the child inspires, it is difficult to pass air through the narrowed airway. This causes noisy inspiration/stridor.

68. Chapter 23 Disorders of Ventilation and Gas Exchange

69. Hypoxemia PO2 greater than 60 mm Hg Cyanosis
Impaired function of vital centers
Agitated or combative behavior, euphoria, impaired judgment, convulsions, delirium, stupor, coma
Retinal hemorrhage
Hypotension and bradycardia
Activation of compensatory mechanisms
Sympathetic system activation

70. Hypercapnia PCO2 greater than 50 mm Hg Respiratory acidosis
Increased respiration
Decreased nerve activity
Carbon dioxide narcosis
Disorientation, somnolence, coma
Decreased muscle contraction
Vasodilation
Headache; warm flushed skin

71. Question
True or false?
Both hypercapnia and hypoxemia will lead to respiratory failure if untreated.

72. Answer
True
Rationale: In both hypercapnia (PCO2 greater than 50 mm Hg), tissues accumulate carbon dioxide; in hypoxemia (PO2 less than 60 mm Hg), less oxygen is delivered to the tissues. In both cases, gas exchange is impaired, and respiratory failure will result unless the conditions are corrected (with oxygen, mechanical ventilation, etc.).

73. Pleura
Parietal pleura lines the thoracic wall and superior aspect of the diaphragm.
Visceral pleura covers the lung.
Pleural cavity or the space between the two layers contains a thin layer of serous fluid.

74. Pleural Effusion—Fluid in the Pleural Cavity
Hydrothorax: serous fluid
Empyema: pus
Chylothorax: lymph
Hemothorax: blood

75. Scenario Mr. K presents himself with a stab wound.
Now he is having breathing problems, and his breath sounds are diminished on the side with the wound.
His trachea seems to be slanting toward the other side of his chest, and his heart sounds are displaced away from the wound.
He has an increased respiration rate and blood pressure, is pale and sweating with bluish nail beds, and has no bowel sounds.
Question
Explain the effects of the wound.

76. Pneumothorax Air enters the pleural cavity.
Air takes up space, restricting lung expansion.
Partial or complete collapse of the affected lung:
Spontaneous: air-filled blister on the lung ruptures
Traumatic: air enters through chest injuries
Tension: air enters pleural cavity through wound on inhalation, cannot leave on exhalation
Open: air enters pleural cavity through the wound on inhalation and leaves on exhalation

77. Pneumothorax (cont.)

78. Question
True or false?
Open pneumothorax is more life-threatening than tension pneumothorax.

79. Answer
False
Rationale: In open pneumothorax, inhaled air compresses the affected side’s lung, but during exhalation, the lung reinflates somewhat.
In tension pneumothorax, a sort of one-way valve exists— the air enters the affected side during inhalation, but is unable to leave when the patient exhales. Therefore, all of this air exerts increased pressure on the organs of the thoracic cage. Unless the pressure is relieved, tension pneumothorax is fatal.

80. Airway Obstruction in Asthma
Inflammatory mediators
 Airway inflammation
 Increased mucociliary function
 Edema
 Epithelial injury 
 Increased airway responsiveness
 Bronchospasm
 Airflow limitation

81. Extrinsic (Atopic) Asthma
Type I hypersensitivity
Allergen
 Mast cells release inflammatory mediators.
Cause acute response within 10 to 20 minutes
 WBCs enter region and release more inflammatory mediators.
Airway inflammation causes late-phase response in 4 to 8 hours.

82. Bronchial Asthma

83. Intrinsic (Nonatopic) Asthma
Respiratory infections
Epithelial damage, IgE production
Exercise, hyperventilation, cold air
Loss of heat and water may cause bronchospasm.
Inhaled irritants
Inflammation, vagal reflex
Aspirin and other NSAIDs
Abnormal arachidonic acid metabolism

84. Question Which of the following occurs in asthma? Airway inflammation
Bronchospasm
Decreased ability to clear mucous
All of the above

85. Answer D. All of the above
Rationale: Inflammatory mediators lead to airway inflammation, edema of the mucous lining of the airways, bronchospasm, and impaired ability to clear secretions. All of these things cause the airways to narrow during an asthma attack.

86. Chronic Obstructive Pulmonary Disorders
Emphysema
Enlargement of air spaces and destruction of lung tissue
Chronic obstructive bronchitis
Obstruction of small airways
Bronchiectasis
Infection and inflammation destroy smooth muscle in airways  permanent dilation

87. Mechanisms of Airflow Obstruction

88. Mechanisms of COPD Inflammation and fibrosis of the bronchial wall
Hypertrophied mucous glands  excess mucus
Obstructed airflow
Loss of alveolar tissue
Decreased surface area for gas exchange
Loss of elastic lung fibers
Airway collapse, obstructed exhalation, air trapping

89. Emphysema Neutrophils in the alveoli secrete trypsin.
Increased neutrophil numbers due to inhaled irritants can damage alveoli.
α1-antitrypsin inactivates the trypsin before it can damage the alveoli.
A genetic defect in α1-antitrypsin synthesis leads to alveolar damage.

90. Types of Emphysema

91. Chest Wall in Emphysema

92. Chronic Bronchitis Chronic irritation of airways
Increased number of mucous cells
Mucus hypersecretion
Productive cough

93. Pink Puffers Versus Blue Bloaters
Pink puffers (usually emphysema)
Increase respiration to maintain oxygen levels
Dyspnea; increased ventilatory effort
Use accessory muscles; pursed-lip breathing
Blue bloaters (usually bronchitis)
Cannot increase respiration enough to maintain oxygen levels
Cyanosis and polycythemia
Cor pulmonale

94. Question
Which chronic obstructive pulmonary disease primarily affects the alveoli?
Asthma
Emphysema
Chronic bronchitis
Bronchiectasis

95. Answer
B. Emphysema
Rationale: In emphysema, alveolar walls are destroyed. The other chronic pulmonary diseases listed primarily affect the airways.

96. COPD and Blood pH Discussion:
In what range will a COPD client's blood pH fall?
Why?

97. Consequences of COPD COPD  decreased ability to exhale
 Stale air in the lungs
 Low O2 levels  hypoxia
 High CO2 levels  hypercapnia
Which step will cause the central chemoreceptors to increase respiration?
Which will cause the peripheral chemoreceptors to increase respiration?

98. Scenario
A patient with chronic bronchitis has a barrel chest and cyanosis. His pulse oximeter reads 86% oxygenation. His PO2 is 54 mm Hg. His PCO2 is 56 mm Hg.
He is put on low-flow oxygen but complains of shortness of breath. Somebody turns the O2 flow up. He is found in a coma with a PCO2 of 59 mm Hg and blood pH of 7.2.
Questions:
What was the cause of the coma? Why?

99. COPD Consequences
In a COPD client, exhalation is inefficient and O2 levels in the lungs decrease.
If blood goes through the lungs filled with stale air, it will not pick up much oxygen; it might even pick up CO2.
Discussion:
What will the pulmonary arterioles do?
Which side of the heart will be affected? Why?

100. Cystic Fibrosis Recessive disorder in chloride transport proteins
High concentrations of NaCl in the sweat
Less Na+ and water in respiratory mucus and in pancreatic secretions
Mucus is thicker
Obstructs airways
Obstructs the pancreatic and biliary ducts

101. Pathogenesis of Cystic Fibrosis

102. Discussion A client with cystic fibrosis is having
Respiratory problems
Digestive problems, flatulence, steatorrhea, weight loss
Question:
He does not understand why a respiratory disease would cause these problems. How would this be explained to the client?

103. Pulmonary Embolism

104. Pulmonary Hypertension
Secondary
Elevation of pulmonary venous pressure
Increased pulmonary blood flow
Pulmonary vascular obstruction
Hypoxemia
Primary
Blood vessel walls thicken and constrict

105. Pulmonary Arteries

106. Cor Pulmonale
Right-sided heart failure secondary to lung disease or pulmonary hypertension
Decreased lung ventilation
Pulmonary vasoconstriction
Increased workload on the right heart
Decreased oxygenation
Kidney releases erythropoietin  more RBCs made  polycythemia makes blood more viscous
Increased workload on the heart

107. Acute Respiratory Distress Syndrome
Exudate enters the alveoli
Blocks gas exchange
Makes inhalation more difficult
Neutrophils enter the alveoli
Release inflammatory mediators, proteolytic enzymes, reactive oxygen species

108. Mechanisms of Lung Changes in ARDS

109. Question
True or false?
Patients suffering from ARDS will be not necessarily be hypoxemic.

110. Answer
False
Rationale: In ARDS, the alveoli is filled with exudate, decreasing the available surface area for gas exchange. If gas exchange decreases, poorly oxygenated or unoxygenated blood is sent to the tissues (hypoxemia).

111. Causes of Respiratory Failure
Hypoventilation  hypercapnia, hypoxia
Depression of the respiratory center
Diseases of respiratory nerves or muscles
Ventilation/perfusion mismatching
Impaired diffusion  hypoxemia but not hypercapnia
Interstitial lung disease
ALI/ARDS
Pulmonary edema
Pneumonia