Are you ready to learn about the Regulation of Breathing? I sure hope so because that is what this study guide is all about. The practice questions below correlate with Egan’s Chapter 16, so you can use this information to help prepare for your exams.
This is definitely a topic that you must know as a Respiratory Therapy Student. The good news is — the practice questions listed here are designed to help you develop the knowledge that you need.
So if you’re ready, let’s go ahead and dive right in.
Regulation of Breathing Practice Questions:
1. What is apnea?
The absence of spontaneous breathing.
2. What is the apneustic center?
An anatomically ill-defined, localized collection of neurons in the pons located at the level of the vestibular area that moderates the rhythmic activity of the medullary respiratory centers.
3. What is Biot respirations?
Breathing characterized by irregular periods of apnea alternating with periods in which 4 or 5 breaths of identical depth are taken.
4. What are chemoreceptors?
Sensory nerve cell activated by changes in the chemical environment surrounding it; the chemoreceptors in the carotid artery are sensitive to PCO2 in the blood, signaling the respiratory center in the brain to increase or decrease ventilation.
5. What is Cheyne-stokes respiration?
Abnormal breathing pattern with periods of progressively deeper breaths alternating with periods of shallow breathing apnea.
6. What is the Hering-Breuer inflation reflex?
The parasympathetic inflation reflex mediated via the lungs stretch receptors that appears to influence the duration of the expiratory pause occurring between breaths.
7. What is the pneumotaxic center?
Bilateral group of neurons in the upper part of the pons that rhythmically inhibits inspiration.
8. What are vagovagal reflexes?
Reflexes caused by stimulation of parasympathetic receptors in the airways that can result in laryngospasm, bronchoconstriction, hyperpnea, and bradycardia.
9. What stimulates vagovagal reflexes?
They are often associated with mechanical stimulation, as during procedures such as tracheobronchial aspiration, intubation, or bronchoscopy.
10. Is breathing conscious or automatic activity?
11. Can breathing patterns be consciously changed?
Yes; until willful breathing stops and the neural mechanisms resume.
12. Where does the rhythmic cycle of breathing originate?
It originates in the brain stem, specifically the neurons in the medulla.
13. Do separate inspiratory and expiratory centers exist?
No; the neurons are anatomically intermingled and do not inhibit one another.
14. The medulla contains several widely dispersed respiratory related what?
15. Which respiratory group contains mainly inspiratory neurons?
16. Which respiratory group contains both inspiratory and expiratory neurons?
17. What does DRG stand for?
Dorsal respiratory group.
18. What does VRG stand for?
Ventral respiratory group.
19. What are the characteristics of DRG?
Bilateral in the medulla, send impulses to motor nerves of diaphragm and intercostals, provides main inspiratory stimulus.
20. What modifies the medullas basic breathing pattern?
Sensory impulses that the lungs, airways, peripheral chemoreceptors, and joint proprioceptors have transmitted to the DRG.
21. Do DRG nerves extend into VRG nerves?
Yes, many of them do.
22. Do VRG nerves extend into DRG nerves?
Only a few.
23. What are the characteristics of the VRG?
Bilateral in the medulla, send motor impulses through the vagus nerve to increase the diameter of the glottis, transmitting impulses to the diaphragm and intercostals, send expiratory impulses to the internal intercostals and abdominals.
24. What is the principle of the pacemaker hypothesis?
Medullary cells have intrinsic pacemaker properties which drive other medullary neurons.
25. What is the principle of the network hypothesis?
That rhythmic breathing is the result of a particular pattern of interconnections between neurons dispersed throughout the VRG, the pre-Botzinger complex, and the Botzinger complex; inspiratory and expiratory neurons inhibit one another.
26. Does spontaneous respiration continue if the brain stem is transected above the medulla?
Yes, though it is irregular.
27. Does the pons promote rhythmic breathing?
No; it modifies the output of the medullary centers.
28. What are the two respiratory centers of the pons?
Apneustic and pneumotaxic.
29. What happens when the apneustic center gets severed from the pneumotaxic center and vagus nerve?
DRG neurons fail to switch off, causing prolonged inspiratory gasps interrupted by occasional expirations; aka apneustic breathing.
30. What do strong pneumotaxic signals do?
They increase the respiratory rate.
31. What do weak pneumotaxic impulses do?
They prolong inspiration and increase tidal volume.
32. The apneustic and pneumotaxic centers seem to work together to control what?
The depth of inspiration.
33. Where are the hering-breuer inflation reflex receptors located?
In the smooth muscle of both the large and small airways.
34. Which nerve carries the inhibitory impulses from the hering-breuer reflex receptors to the DRG?
The vagus nerve.
35. Is the hering-breuer inflation reflex an important control mechanism in quiet breathing?
No, this reflex in only activated at large tidal volumes (in adults).
36. Why is the hering-breuer inflation reflex important?
It regulates rate and depth during moderate to strenuous exercise.
37. Rapidly adapting irritant receptors in the epithelium of the larger conducting airways have what?
Vagal sensory nerve fibers.
38. Stimulation of irritant receptors can cause what?
Reflex bronchoconstriction, coughing, sneezing, tachypnea, and narrowing of the glottis.
39. What can stimulate vagovagal reflexes?
Endotracheal intubation, airway suctioning, and bronchoscopy.
40. Airway suctioning and bronchoscopy can cause what?
Severe bronchoconstriction, coughing, and laryngospasm.
41. What is the main trigger of chemoreceptors?
H+ (indirectly CO2).
42. Where are the central chemoreceptors located?
Bilaterally in the medulla.
43. Are the central chemoreceptors in direct contact with arterial blood?
No, they are bathed in the CSF separated by the blood-brain barrier.
44. What is the blood-brain barrier?
The semipermeable membrane that separates the cerebrospinal fluid (CSF) and the blood.
45. How does CO2 effect the central chemoreceptors?
Arterial CO2 easily diffuses across the blood-brain barrier, once inside it reacts with H2O, carbonic anahydrase follows resulting in H+ and HCO3, and the central chemoreceptors are extremely sensitive to H+.
46. Can H+ pass through the blood-brain barrier?
Rarely, it is almost impermeable to H+ and HCO3 so CO2 has to pass through then react with water once its inside.
47. CO2 diffusing from the blood into the CSH increases H+ almost instantly, exciting what?
The chemoreceptors (within seconds).
48. How long does central chemoreceptor stimulation usually last while in respiratory acidosis?
1-2 days, long enough for the kidneys to raise levels of HCO3 in the blood and enough can pass the blood brain barrier to buff the H+.
49. Where are the peripheral chemoreceptors located?
The aortic arch and bilaterally in the bifurcations of the common carotid arteries.
50. The peripheral chemoreceptors increase their firing rates in response to what?
Increased arterial H+ regardless of origin.
51. Which nerve carries impulses from the carotid chemoreceptors to the medulla?
52. Which nerve carries impulses from the aortic chemoreceptors to the medulla?
53. Which peripheral chemoreceptors have more influence over the respiratory center?
Carotid, due to an extremely high rate of blood flow, little time to deposit O2, and exposure to arterial blood 100% of the time.
54. How does hypoxemia affect the peripheral chemoreceptors?
Low O2 makes them more sensitive to H+.
55. Why does decreased PaO2 cause increase ventilation?
Because it makes the carotid chemoreceptors more sensitive to H+, which causes them to fire more frequently.
56. How does increased PaO2 affect the peripheral chemoreceptors?
It makes them less sensitive to H+.
57. Why does increased PaO2 cause a decrease in ventilation?
The carotid chemoreceptors become less sensitive to H+, which causes them to fire less often.
58. When does hypoxemia not have an effect on the carotid chemoreceptors?
In severe alkalemia, because even though the carotid chemoreceptors are more sensitive to H+ there is a lot less in blood at that time.
59. The carotid bodies meet their O2 needs from what?
From dissolved O2 because the flow rate is so fast; therefore it depends less on content and more on partial pressure.
60. When will the nerve-impulse transmissions of the carotid bodies increase when pH and PaCO2 are normal?
When PaO2 decreases to approximately 60 mm Hg.
61. What accounts for the sharpest decrease in O2 content on the O2-Hb equilibrium curve?
A decrease in PaO2 from 60 mm Hg to 30 mm Hg.
62. What percentage do the peripheral chemoreceptors account for in the ventilatory response to Hypercapnia?
63. Which responds more rapidly to increased H+?
64. When peripheral chemoreceptors become insensitive to H+ levels because of high PaO2, what does ventilatory response depend on?
The central chemoreceptors, which are unaffected by hypoxemia.
65. Does a diagnosis of COPD on a patient’s chart automatically mean high PaCO2 or that O2 administration may be associated with hypercapnia?
No, these characteristics are only displayed in severe end-stage disease; a small percentage of patients.
66. Should O2 be withheld from acutely hypoxemic patients with COPD?
No! The fear of hypoventilation and/or hypercapnia does not override oxygenating the tissues.
67. What should you be prepared to do if O2 administration is accompanied by severe hypoventilation?
Support ventilation mechanically.
68. Which breathing pattern occurs when cardiac output is low, as in congestive heart failure, or brain injuries?
69. Why does decreased cardiac output cause Cheyne-stokes?
Because there is a delay in blood transit time between the lungs and the brain.
70. What causes Biot respiration?
Increased intracranial pressure.
71. What can apneustic breathing indicate?
Damage to the pons.
72. Central neurologic hyperventilation is characterized by what?
Persistent hyperventilation driven by abnormal neural stimuli; related to mid-brain and upper pons damage associated with head trauma, severe brain hypoxia, or lack of blood flow to the brain.
73. What are characteristics of central neurogenic hypoventilation?
Unresponsive to ventilatory stimuli; associated with head trauma, brain hypoxia, and narcotic suppression of the respiratory center.
72. CO2 plays an important role in what?
Cerebral blood flow.
73. How does high CO2 affect cerebral blood flow?
It dilates the cerebral vessels increasing blood flow.
74. How does low CO2 affect cerebral blood flow?
It constricts cerebral vessels decreasing blood flow.
75. Why is high intracranial pressure (ICP) bad?
If it exceeds cerebral arterial pressure, blood flow to the brain will stop, leading to cerebral hypoxia (ischemia).
76. Why does decreasing PaCO2 help relieve ICP?
For every 1 mm Hg reduction in PaCO2–> 3% reduction in cerebral blood flow and for every 0.5-0.7 drop in cerebral blood flow–> 1 mm Hg reduction in ICP.
77. Why is mechanical hyperventilation a cause for concern for patients with traumatic brain injuries?
Because with the drop in ICP also comes a drop in cerebral blood flow, which can end up causing ischemia as well.
78. What is the normal ICP?
79. What is the most common cause of hypoxemia?
80. What are dorsal respiratory groups?
They contain mainly inspiratory neurons that are located bilaterally in the medulla.
81. What are ventral respiratory groups?
They contain both inspiratory and expiratory neurons that are located bilaterally in the medulla in 2 different nuclei.
82. Where do DRG neurons send impulses to?
Motor nerves of the diaphragm and external intercostal muscles providing main inspiratory stimulus.
83. Where do VRG send impulses to?
Some send motor impulses through the vagus nerve to laryngeal and pharyngeal muscles increasing the diameter of the glottis/others to diaphragm and external intercostal muscles/other internal intercostal muscles.
84. What are the 2 predominate theories of rhythm generation?
Pacemaker hypothesis and network hypothesis.
85. What is the pacemaker hypothesis?
Certain medullary cells have intrinsic pacemaker properties. These cells drive other medullary neurons.
86. What is the network hypothesis?
Rhythmic breathing is the result of a particular pattern of interconnections between neurons dispersed throughout the rostral VRG, pre-Botzinger complex, and Botzinger complex. Inspiratory and expiratory neurons inhibit one another.
87. Firing rate of DRG and VRG inspiratory neurons increases gradually at the end of what phase?
The expiratory phase.
88. During quiet breathing, inspiratory neurons fire with increasing frequency for approximately how many seconds?
89. After the 2 second firing, then an abrupt switch off occurs allowing expiration to proceed for how many seconds?
90. The inhibitory neurons that switch off the inspiratory ramp signal are controlled by what?
The pneumotaxic center and pulmonary stretch receptors.
91. The pons does not promote rhythmic breathing but rather?
It modifies the output of the medullary centers.
92. Strong pneumotaxic signals increase what?
93. What are the reflexes that have both sensory and motor vagal components?
94. What are the reflexes that are responsible for laryngospasm, coughing, and slowing of the heartbeat?
95. Endotracheal intubation, airway suctioning, and bronchoscopy readily elicit what reflex?
The vagovagal reflexes.
96. What are Proprioceptors?
They send stimulatory signals to the medullary respiratory center, increase medullary inspiratory activity, and cause hyperpnea.
97. The body maintains the proper amounts of oxygen (O2), carbon dioxide (CO2), and hydrogen ions (H+) in the blood mainly by regulating what?
98. Chemoreceptors transmit impulses to the medulla, which will increase what?
99. The stimulatory effect of chronically high CO2 on the central chemoreceptors gradually declines over 1 or 2 days, because?
The kidneys retain bicarbonate ions in response to respiratory acidosis, bringing the blood pH level back toward normal.
100. The peripheral chemoreceptors are?
Small, highly vascular structures known as the carotid and aortic bodies.
101. Peripheral chemoreceptors fire more frequently in the presence of what?
Arterial hypoxemia, because hypoxemia makes them more sensitive to hydrogen.
102. When pH and PaCO2 are normal, the carotid bodies’ nerve-impulse transmission rate does not increase significantly until the PaO2 decreases to what?
About 60 mm Hg.
103. Arterial hypoxemia does not stimulate ventilation greatly until the PaO2 decreases below what?
60 mm Hg.
104. Hypoxia-induced hyperventilation lowers what?
105. People with chronic hypercapnia secondary to advanced COPD have depressed ventilatory responses to acute rises in what?
Arterial CO2, because of their altered acid-base status and partly because their deranged lung mechanics prevents them from increasing their ventilation adequately.
106. The ventilatory response to hypoxemia is greatly enhanced by what?
Hypercapnia and acidemia.
107. A sudden rise in arterial PaCO2 causes an immediate increase in what?
Ventilation, because CO2 rapidly diffuses from the blood into the CSF, increasing the [H+] surrounding the central chemoreceptors.
108. What is Cheyne-Stokes respirations?
The respiratory rate and tidal volume gradually increase and then gradually decrease to complete apnea.
109. When does the Cheyne-stokes respiration pattern occur?
This pattern occurs when cardiac output is low, as in congestive heart failure, delaying the blood transit time between the lungs and the brain. brain injuries in which the respiratory centers over-respond to changes in the PCO2 level.
110. What is Biot’s respiration?
It is similar to Cheyne-Stokes respiration, except that tidal volumes are of identical depth.
111. When does the Biots respiratory pattern occur?
It occurs in patients with increased intracranial pressure.
112. Apneustic breathing indicates damage to what?
113. Central neurogenic hyperventilation is characterized by what?
Persistent hyperventilation driven by abnormal neural stimuli.
114. When does neurogenic hyperventilation occur?
Midbrain and upper pons damage associated with head trauma, severe brain hypoxia, or lack of blood flow to the brain.
115. What is central neurogenic hypoventilation?
Respiratory centers do not respond appropriately to ventilatory stimuli.
116. When does central neurogenic hypoventilation occur?
Associated with head trauma and brain hypoxia, as well as narcotic suppression of the respiratory center.
117. CO2 plays an important role in regulating what?
Cerebral blood flow.
And just like that, you have now made it all the way to the end of our study guide on the Regulation of Breathing. Thank you so much for allowing us to help you along your journey to becoming a Respiratory Therapist.
You can use the practice questions here (along with the other study guides on this website) to boost your knowledge to a whole new level. Thanks again for reading and as always, breathe easy my friend.
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