Chapter 15 - Regulation of Breathing

Kacmarek et al.: Egan’s Fundamentals of Respiratory Care, 11th Edition

MULTIPLE CHOICE

1. Where are the inspiratory and expiratory centers in the brain found?
a. Broca’s area
b. Neurons in the cerebellum
c. Pons
d. No such centers exist

ANS: D
Recent evidence shows that inspiratory and expiratory neurons are anatomically intermingled
and do not necessarily inhibit one another. No clearly separate inspiratory and expiratory
centers exist.

DIF: Recall REF: p. 309 OBJ: 1

2. The medulla oblongata contains which of the following areas?

1. Apneustic center
2. Dorsal respiratory group neurons (DRGs)
3. Pneumotaxic center
4. Ventral respiratory group neurons (VRGs)
a. 1, 2, and 3 only
b. 2 and 4 only
c. 3 only
d. 1, 3, and 4 only

ANS: B
Instead, the medulla contains several widely dispersed respiratory-related neurons, as shown
in Figure 15-1. The DRGs contain mainly inspiratory neurons, whereas the VRGs contain
both inspiratory and expiratory neurons.

DIF: Recall REF: p. 309 OBJ: 1

3. Sensory input to the dorsal respiratory neurons from the lungs, airways, and peripheral
chemoreceptors is provided via which nerves?
1. Glossopharyngeal
2. Phrenic
3. Vagus
4. Trigeminal
a. 1 and 2 only
b. 1, 2, and 4 only
c. 1 and 3 only
d. 2 and 3 only

ANS: C
 The vagus and glossopharyngeal nerves transmit many sensory impulses to the DRGs from
the lungs, airways, peripheral chemoreceptors, and joint proprioceptors. These impulses
modify the basic breathing pattern generated in the medulla.

DIF: Recall REF: p. 309 OBJ: 1

4. To which anatomic structures do the ventral respiratory centers send motor signals during
inspiration?
1. Diaphragm
2. Larynx
3. Pharynx
4. Sternocleidomastoids
a. 1, 2, and 3 only
b. 2 and 4 only
c. 1 only
d. 1, 2, and 4

ANS: A
Some inspiratory VRG neurons send motor impulses through the vagus nerve to the laryngeal
and pharyngeal muscles, abducting the vocal cords and increasing the diameter of the glottis.
Other VRG inspiratory neurons transmit impulses to the diaphragm and external intercostal
muscles.

DIF: Recall REF: p. 309 OBJ: 1

5. Which of the following control the inhibitory neurons that switch off the inspiratory ramp
signal?
1. Apneustic center
2. Pneumotaxic center
3. Pulmonary stretch receptors
a. 1, 2, and 3
b. 1 and 2 only
c. 3 only
d. 2 and 3 only

ANS: D
The inhibitory neurons that switch off the inspiratory ramp signal are controlled by the
pneumotaxic center and pulmonary stretch receptors.

DIF: Recall REF: p. 310 OBJ: 2

6. What centers are located in the pons of the brainstem?

1. Apneustic center
2. Dorsal respiratory neurons
3. Pneumotaxic center
a. 1, 2, and 3
b. 2 and 3 only
c. 1 and 3 only
 d. 1 and 2 only

ANS: C
Figure 15-1 shows two groups of neurons in the pons: (1) the apneustic center and (2) the
pneumotaxic center.

DIF: Recall REF: p. 310 OBJ: 1

7. Failure to switch off the brainstem inspiratory neurons can result in which of the following?
a. Apnea
b. Apneustic breathing
c. Biot’s breathing
d. Cheyne-Stokes breathing

ANS: B
Under such circumstances, the DRG inspiratory neurons fail to switch off, causing prolonged
inspiratory gasps interrupted by occasional expirations (apneustic breathing).

DIF: Recall REF: p. 310 OBJ: 2

8. The pneumotaxic center controls which of the following?

a. Response to changes in blood pH and PCO2
b. Rhythm of the full breathing cycle
c. When inspiration switches off (the inspiratory time)
d. When inspiration switches on (the expiratory time)

ANS: C
The pneumotaxic center controls the “switch-off” point of the inspiratory ramp, thus
controlling inspiratory time.

DIF: Recall REF: p. 310 OBJ: 2 | 3

9. What stimulates the Hering-Breuer inflation reflex?

a. The DRG when it is time to end inspiratory efforts.
b. The stretch of receptors at high lung volumes.
c. The VRG when it is time for inspiration.
d. Very low lung volumes stimulate inspiration.

ANS: B
In adults, the Hering-Breuer reflex is activated only at large tidal volumes (800 to 1000 ml or
more) and, apparently, it is not an important control mechanism in quiet breathing.

DIF: Recall REF: p. 310 OBJ: 4

10. Which statement(s) describe aspects of the Hering-Breuer reflex?

1. It affects the rate and depth of breathing during exercise.
2. It is only activated at large tidal volumes in normal adults.
3. Its impulses travel via the vagus nerve to the dorsal respiratory groups (DRGs).
4. Its receptors are located in the large and small airways.
a. 1 only
 b. 1 and 2 only
c. 2, 3, and 4 only
d. 1, 2, 3, and 4

ANS: D
The Hering-Breuer inflation reflex, described by H. E. Hering and Josef Breuer in 1868, is
generated by stretch receptors located in the smooth muscle of both large and small airways.
When lung inflation stretches these receptors, they send inhibitory impulses through the vagus
nerve to the DRG neurons, stopping further inspiration. In this way, the Hering-Breuer reflex
has an effect similar to that of the pneumotaxic center. In adults, the Hering-Breuer reflex is
activated only at large tidal volumes (800 to 1000 ml or more) and, apparently, it is not an
important control mechanism in quiet breathing. However, this reflex is important in
regulating respiratory rate and depth during moderate to strenuous exercise.

DIF: Recall REF: p. 310 OBJ: 4

11. What is the effect when the deflation reflex is stimulated?

a. A strong inspiratory effort
b. Expiration is initiated
c. Cuts off all inspiratory signals
d. Stimulates the termination of expiration

ANS: A
Sudden collapse of the lung stimulates strong inspiratory efforts (deflation reflex).

DIF: Recall REF: p. 310 OBJ: 4

12. What reflex is associated with the sensory stimulation of the pulmonary stretch receptors that
stimulate a deeper breath upon inspiration?
a. Carotid
b. Head’s paradoxical
c. Hering-Breuer
d. J receptor

ANS: B
If the Hering-Breuer reflex is blocked by cooling the vagus nerve, lung hyperinflation causes
a further increase in inspiratory effort, the opposite of the Hering-Breuer reflex. The receptors
for this reflex are called rapidly adapting receptors, because they stop firing promptly after a
volume change occurs. Head’s reflex may help maintain large tidal volumes during exercise
and may be involved in periodic deep sighs during quiet breathing.

DIF: Recall REF: p. 311 OBJ: 4

13. What receptors are associated with causing coughing, sneezing, and tachypnea when
stimulated?
a. Irritant receptors
b. J receptors
c. Muscle spindles
d. Peripheral proprioceptors
 ANS: A
Rapidly adapting irritant receptors in the epithelium of the larger conducting airways have
vagal sensory nerve fibers. Their stimulation, whether by inhaled irritants or by mechanical
factors, causes reflex bronchoconstriction, coughing, sneezing, tachypnea, and narrowing of
the glottis.

DIF: Recall REF: p. 311 OBJ: 4

14. What negative responses can be elicited by suctioning a patient’s airway?

1. Tachycardia
2. Coughing
3. Laryngospasm
4. Severe bronchospasm
a. 1, 2, and 3 only
b. 2 and 4 only
c. 1 and 3 only
d. 2, 3, and 4 only

ANS: D
Suctioning may result in laryngospasm, coughing, and slowing of the heartbeat. Endotracheal
intubation, airway suctioning, and bronchoscopy readily elicit vagovagal reflexes. Physical
stimulation of the conducting airways, as with suctioning or bronchoscopy, may cause a
severe case of bronchospasm, coughing, and laryngospasm.

DIF: Recall REF: p. 311 OBJ: 4

15. Stimulation of the irritant receptors in the lung can result in which of the following?
1. Bronchoconstriction
2. Coughing
3. Narrowing of the glottis
a. 1 only
b. 1 and 3 only
c. 1, 2, and 3
d. 1 and 3 only

ANS: C
Irritant receptors are responsible for laryngospasm, coughing, and slowing of the heartbeat.
Endotracheal intubation, airway suctioning, and bronchoscopy readily elicit vagovagal
reflexes. Physical stimulation of the conducting airways, as with suctioning or bronchoscopy,
may cause a severe case of bronchospasm, coughing, and laryngospasm.

DIF: Recall REF: p. 311 OBJ: 4

16. Which of the following can cause laryngospasm and bradycardia through a vagovagal reflex?
1. Bronchoscopy
2. Endotracheal intubation
3. Tracheal suctioning
a. 1 only
 b. 1 and 3 only
c. 1, 2, and 3
d. 1 and 2 only

ANS: C
Such reflexes are responsible for laryngospasm, coughing, and slowing of the heartbeat.
Endotracheal intubation, airway suctioning, and bronchoscopy readily elicit vagovagal
reflexes. Physical stimulation of the conducting airways, as with suctioning or bronchoscopy,
may cause a severe case of bronchospasm, coughing, and laryngospasm.

DIF: Recall REF: p. 311 OBJ: 4

17. What receptors cause a rapid shallow breathing pattern when stimulated by pulmonary
disease?
a. Irritant receptors
b. J receptors
c. Muscle spindles
d. Peripheral proprioceptors
ANS: B
C fibers in the lung parenchyma near the pulmonary capillaries are called juxtacapillary
receptors or J receptors. Alveolar inflammatory processes (pneumonia), pulmonary vascular
congestion (congestive heart failure), and pulmonary edema stimulate these receptors. This
stimulation causes rapid, shallow breathing; a sensation of dyspnea; and expiratory narrowing
of the glottis.

DIF: Recall REF: p. 311 OBJ: 4

18. Which of the following can be stimulated by pulmonary J receptors?

1. Edema
2. Inflammatory processes
3. Pulmonary vascular congestion
a. 1 and 3 only
b. 1 only
c. 1 and 3 only
d. 1, 2, and 3

ANS: D
C fibers in the lung parenchyma near the pulmonary capillaries are called juxtacapillary
receptors or J receptors. Alveolar inflammatory processes (pneumonia), pulmonary vascular
congestion (congestive heart failure), and pulmonary edema stimulate these receptors. This
stimulation causes rapid, shallow breathing; a sensation of dyspnea; and expiratory narrowing
of the glottis.

DIF: Recall REF: p. 311 OBJ: 4

19. What receptors are known to cause an increase in ventilation when the patient’s limbs are
moved or cold water is splashed on the patient’s face?
a. Irritant receptors
 b. J receptors
c. Muscle spindles
d. Peripheral proprioceptors

ANS: D
Proprioceptors in muscles, tendons, and joints, as well as pain receptors in muscles and skin,
send stimulatory signals to the medullary respiratory center. Such stimuli increase medullary
inspiratory activity and cause hyperpnea. For this reason, moving the limbs, slapping or
splashing cold water on the skin, and other painful stimuli stimulate ventilation in patients
with respiratory depression.

DIF: Recall REF: p. 311 OBJ: 4

20. Which receptors are primarily responsible for the initial increase in ventilation that occurs at
the beginning of exercise?
a. Carotid chemoreceptors
b. Irritant receptors
c. J receptors
d. Proprioceptors

ANS: D
Proprioceptors in joints and tendons may be important in initiating and maintaining increased
ventilation at the beginning of exercise.

DIF: Recall REF: p. 311 OBJ: 4

21. Adjustment of respiratory muscle contractions to accommodate varying loads is regulated by

which of the following?
a.Medullary respiratory centers
b.Muscle spindle fiber feedback
c.Pontine apneustic center
d.Pontine pneumotaxic center
ANS: B
Muscle spindles in the diaphragm and intercostal muscles are part of a reflex arc that helps the
muscles adjust to an increased load.

DIF: Recall REF: p. 311 OBJ: 4

22. What group of nerve cells senses and responds to changes in the chemical composition of its
fluid environment?
a. Chemoreceptors
b. Gamma-efferent system
c. Muscle spindle fibers
d. Proprioceptors
ANS: A
Hypercapnia, acidemia, and hypoxemia stimulate specialized nerve structures called
chemoreceptors.
 DIF: Recall REF: p. 311 OBJ: 5

23. Where are the peripheral chemoreceptors located?

1. In the arch of the aorta
2. In the bifurcations of carotid arteries
3. On the ventrolateral surfaces of the medulla
a. 1 and 2 only
b. 2 only
c. 2 and 3 only
d. 1 and 3 only

ANS: A
Peripherally located chemoreceptors are found in the fork of the common carotid arteries and
the aortic arch.

DIF: Recall REF: p. 311 OBJ: 5

24. What has the primary responsibility for sensing and responding to changes in blood levels of
CO2?
a. Apneustic centers
b. Central chemoreceptors
c. Peripheral chemoreceptors
d. Pneumotaxic center

ANS: B
Hydrogen ions stimulate highly responsive chemosensitive nerve cells, located bilaterally in
the medulla. Nevertheless, these central chemoreceptors are extremely sensitive to CO2 in an
indirect fashion. Through the hydrolysis reaction, as CO2 increases there is a greater release of
hydrogen ions to which the chemoreceptors respond.

DIF: Recall REF: p. 312 OBJ: 5

25. Which of the following is indirectly responsible for minute-to-minute control of breathing?
a. CO2 levels
b. HCO3 levels
c. Lactate levels
d. Oxygen (O2) levels

ANS: A
As the H+ ions in the CSF are generated in direct relation to the level of arterial PCO2, it is
really the arterial PCO2 that (indirectly) controls primary minute-to-minute ventilation.

DIF: Recall REF: p. 312 OBJ: 5

26. In the face of chronically elevated levels of CO2, what happens to the response mediated by
the central chemoreceptors?
a. It is accentuated or increased.
b. It is muted or decreased.
c. There is no change in the response.
 d. There is no way to predict the body’s response.

ANS: B
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.

DIF: Recall REF: p. 312 OBJ: 5

27. Which of the following causes hypoxic stimulation of the carotid bodies?
1. Large decrease in arterial PO2
2. Large decrease in O2 content
3. CO poisoning
a. 1 only
b. 1 and 2 only
c. 1, 2, and 3
d. 1 and 3 only

ANS: A
When the PaO2 is low carotid body sensitivity to a given [H+] increases; in this way
hypoxemia increases ventilation for any given pH.

DIF: Recall REF: p. 312 OBJ: 6

28. Both anemia and carbon monoxide (CO) poisoning can cause severe hypoxia, yet neither
condition results in a major stimulation of breathing. Why is this so?
a. The peripheral chemoreceptors do not respond to low O2 content.
b. Anemia and CO poisoning depresses the peripheral chemoreceptors.
c. Anemia and CO poisoning depresses the central chemoreceptors.
d. Anemia and CO cause stagnant hypoxia, not hypoxemia.
ANS: A
Because of their extremely high blood-flow rates, the carotid bodies respond to decreased
arterial partial pressure of O2 rather than to an actual decrease in arterial O2 content.

DIF: Recall REF: p. 312 OBJ: 6

29. Stimulation to increase ventilation does not occur until the PaO2 falls below what level?
a. 90 mm Hg
b. 80 mm Hg
c. 70 mm Hg
d. 60 mm Hg

ANS: D
When pH and PaCO2 are normal (pH = 7.40 and PaCO2 = 40 mm Hg), the carotid bodies’
nerve-impulse transmission rate does not increase significantly until the PaO2 decreases to
approximately 60 mm Hg.

DIF: Recall REF: p. 313 OBJ: 6

30. Why does it take approximately 24 hr for a full ventilatory response to develop to acute
hypoxemia?
a. Initial cerebrospinal fluid alkalemia blunts the hypoxic ventilatory stimulus.
b. Peripheral chemoreceptors are slow to respond to decreased blood O2 levels.
c. Renal compensation for respiratory alkalosis increases chemoreceptor sensitivity.
d. A full ventilatory response is not possible until after the muscles become fatigued.
ANS: A
High altitude causes a healthy person’s ventilation to increase because low barometric
pressure decreases the inspired PO2, and thus the arterial PO2, which in turn raises the
sensitivity of peripheral chemoreceptors to hydrogen ions. The resulting increase in
ventilation is less than expected though, because hyperventilation lowers the PaCO2 and raises
arterial pH. The increased pH depresses the medullary respiratory center, counteracting the
excitatory effect of a low PaO2 on peripheral chemoreceptors.

DIF: Recall REF: p. 313 OBJ: 6

31. Which of the following centers responds more strongly to high levels of CO2?
a. Aortic chemoreceptors
b. Carotid chemoreceptors
c. Central chemoreceptors
d. Ventral respiratory centers

ANS: C
For a given increase in PaCO2 or hydrogen ion concentration, the carotid bodies are less
responsive than the central chemoreceptors. The peripheral chemoreceptors account for only
20% to 30% of the ventilatory response to hypercapnia.

DIF: Recall REF: p. 313 OBJ: 6

32. Which respond more rapidly to high levels of CO2?

a. Aortic chemoreceptors
b. Carotid chemoreceptors
c. Central chemoreceptors
d. Ventral respiratory centers

ANS: B
The carotid chemoreceptors respond to increased arterial hydrogen ion concentration more
rapidly than do the central chemoreceptors.

DIF: Recall REF: p. 312 OBJ: 6

33. In the face of hyperoxia, what is the response of the peripheral chemoreceptors to
hypercapnia?
a. There is a decreased drive to breathe.
b. There is an increased drive to breathe.
c. There is insufficient information.
d. There is virtually no response.
ANS: D
 High arterial PO2 (hyperoxia) decreases the peripheral chemoreceptors’ PCO2 sensitivity to
almost zero.

DIF: Recall REF: p. 312 OBJ: 6

34. Coexisting arterial hypoxemia, acidemia, and high PaCO2 (i.e., asphyxia) will have what
effect on the peripheral chemoreceptors?
a. There is a decreased drive to breathe.
b. There is a maximally increased drive to breathe.
c. There is insufficient information to make a determination.
d. There is virtually no response.
ANS: B
Coexisting arterial hypoxemia, acidemia, and high PaCO2 (i.e., asphyxia) maximally stimulate
the peripheral chemoreceptors.

DIF: Recall REF: p. 312 OBJ: 6

35. What happens in chronic hypercapnia?

1. The central chemoreceptive response to CO2 is decreased.
2. The cerebrospinal fluid pH is restored to normal.
3. Responsiveness to increased CO2 is decreased.
a. 1 only
b. 1 and 2 only
c. 2 and 3 only
d. 1, 2, and 3

ANS: D
If PaCO2 rises gradually over time, as might occur in severe COPD because of steadily
deteriorating lung mechanics, the kidneys compensate by increasing the plasma bicarbonate
concentration, keeping the arterial pH within normal limits. As plasma bicarbonate levels
increase, these ions slowly diffuse across the blood-brain barrier, keeping cerebrospinal fluid
pH in its normal range. The central chemoreceptors respond to hydrogen ion concentration,
not the CO2 molecule; thus, they sense a normal pH environment, even though the PaCO2 is
abnormally high.

DIF: Recall REF: p. 314 OBJ: 6

36. When given high concentrations of O2, a patient with chronic hypercapnia may develop a
more serious respiratory acidosis. Which of the following might be contributing to the
patient’s increased PCO2?
1. Worsening ventilation-perfusion (VV/QQ) balance
2. Desensitization of the carotid bodies
3. Removal of the hypoxic stimulus
a. 1 and 2 only
b. 1 only
c. 1 and 3 only
d. 1, 2, and 3
 ANS: C
Nevertheless, the reduction in minute ventilation following O2 breathing in advanced COPD is
not always severe enough to account for the increased PaCO2. Some investigators suggest that
O2 breathing worsens the VV/QQ relationships in the lungs and is responsible for the increase
in PaCO2. Other investigators have suggested that O2-induced hypercapnia is caused by the
combined effects of hypoxic stimulus removal and redistribution of relationships in the
lungs.

DIF: Recall REF: p. 314 OBJ: 7 | 8

37. In what manner would O2 therapy induce worsening mismatch and thus a further
elevation in CO2 in a chronically hypercapnic patient?
a. By improving blood flow to poorly ventilated alveoli
b. By decreasing blood flow to poorly ventilated alveoli
c. Causing bronchoconstriction, which worsens gas flow to low areas
d. Causing bronchodilation, which improves gas flow to poorly ventilated alveoli

ANS: A
Oxygen breathing causes more blood flow to be directed to poorly ventilated alveoli, which
takes blood flow away from well-ventilated alveoli. The key point is that when already under-
ventilated alveoli receive additional blood flow, blood PCO2 rises further. These events can
occur without a fall in overall minute ventilation.

DIF: Recall REF: p. 314 OBJ: 7 | 8

38. How should O2 therapy be administered to chronically hypercapnic patients?

a. Avoid giving any supplemental O2.
b. Give as much O2 as possible (60% to 100%).
c. Withhold O2 until the patient is intubated.
d. Give as much O2 as required to maintain adequate oxygenation.

ANS: D
Oxygen should never be withheld from acutely hypoxemic COPD patients for fear of inducing
hypoventilation and hypercapnia. Tissue oxygenation is an overriding priority; O2 must never
be withheld from exacerbated, hypoxemic COPD patients for any reason. This means the
clinician must be prepared to mechanically support ventilation if O2 administration induces
severe hypoventilation.

DIF: Recall REF: p. 314 OBJ: 8

39. What is the response of a patient with chronic hypercapnia to a sudden acute rise in carbon
dioxide?
a. In almost all of these patients, there will be no response.
b. The patient’s drive to breathe will be increased.
c. This will further depress his or her respiratory centers.
d. This will induce apnea and sudden death.
ANS: B
 Chronic hypercapnia does not mean that the medullary chemoreceptors cannot respond to
further acute rises in PaCO2. A sudden elevation in PaCO2 immediately crosses the blood-
brain barrier into the cerebrospinal fluid, generating H+ ions that subsequently stimulate the
medullary chemoreceptors. This will increase the drive to breathe.

DIF: Recall REF: p. 314 OBJ: 8

40. Which of the following will occur during even strenuous exercise in a normal healthy
individual?
a. Blood gases remain stable.
b. The arterial PCO2 rises.
c. The arterial pH falls.
d. The arterial PO2 falls.
ANS: A
Strenuous exercise increases carbon dioxide production and O2 consumption by as much as
20-fold. Ventilation normally keeps pace with CO2 production, keeping PaCO2, PaO2, and
arterial pH constant. Because arterial blood gases do not change, elevated carbon dioxide or
hypoxia does not stimulate ventilation in healthy individuals during exertion.

DIF: Recall REF: p. 315 OBJ: 11

41. While observing a patient’s breathing, you note that the depth and rate first increase, then
decrease, followed by a period of apnea. Which of the following terms would you use in
charting this observation?
a. Apneustic breathing
b. Biot’s breathing
c. Cheyne-Stokes breathing
d. Paradoxical breathing

ANS: C
In Cheyne-Stokes respiration, respiratory rate, and tidal volume gradually increase and then
gradually decrease to complete apnea (absence of ventilation), which may last several
seconds. Then tidal volume and breathing frequency gradually increase again, repeating the
cycle.

DIF: Recall REF: p. 315 OBJ: 11

42. Which of the following can cause Cheyne-Stokes breathing?

1. Brain injuries
2. Congestive heart failure
3. Metabolic acidosis
a. 1 and 2 only
b. 2 and 3 only
c. 1 and 3 only
d. 1, 2, and 3

ANS: A
 Cheyne-Stokes breathing occurs when cardiac output is low, as in congestive heart failure,
delaying the blood transit time between the lungs and the brain. In this instance, changes in
respiratory center PCO2 lag behind changes in arterial PCO2. For example, when an increased
PaCO2 from the lungs reaches the respiratory neurons, ventilation is stimulated; this then
lowers the arterial PCO2 level. By the time the reduced PaCO2 reaches the medulla to inhibit
ventilation, hyperventilation has been in progress for an inappropriately long time. When
blood from the lung finally does reach the medullary centers, the low PaCO2 greatly depresses
ventilation to the point of apnea. Arterial PCO2 then rises, but a rise in respiratory center PCO2
is delayed because of low blood flow rate. The brain eventually does receive the high PaCO2
signal and the cycle is repeated. Cheyne-Stokes respiration may also be caused by brain
injuries in which the respiratory centers overrespond to changes in the PCO2 level.

DIF: Recall REF: p. 315 OBJ: 11

43. You observe a patient’s breathing pattern as very irregular, with periods of breathing
interspersed with long periods of apnea. Which of the following terms would you use in
charting this observation?
a. Apneustic breathing
b. Biot’s respiration
c. Cheyne-Stokes breathing
d. Kussmaul’s breathing

ANS: B
Biot’s respiration is similar to Cheyne-Stokes respiration, except that tidal volumes are of
identical depth.

DIF: Recall REF: p. 315 OBJ: 11

44. Biot’s respiration is most frequently observed in patients with which of the following?
a. Congestive heart failure
b. Increased intracranial pressure
c. Metabolic acidosis
d. Peripheral nerve disorders

ANS: B
Biot’s breathing occurs in patients with increased intracranial pressure, but the mechanism for
this pattern is unclear.

DIF: Recall REF: p. 315 OBJ: 11

45. What does apneustic breathing indicate?

a. Damage to the cerebrum
b. Damage to the pons
c. Spinal cord transaction
d. Vagal nerve damage

ANS: B
Apneustic breathing indicates damage to the pons.
 DIF: Recall REF: p. 315 OBJ: 11

46. Which of the following are causes of central neurogenic hyperventilation?

1. Head trauma
2. Inadequate brain blood flow
3. Severe brain hypoxia
4. Hypothermia
a. 2 and 3 only
b. 1 and 4 only
c. 2 and 3 only
d. 1, 2, and 3 only

ANS: D
Central neurogenic hyperventilation is characterized by persistent hyperventilation driven by
abnormal neural stimuli. It is related to midbrain and upper pons damage associated with head
trauma, severe brain hypoxia, or lack of blood flow to the brain.

DIF: Recall REF: p. 316 OBJ: 11

47. In patients with closed-head injuries, what may happen in the presence of hypercapnia?
a. High CO2 increases the risk of psychotic events.
b. High CO2 levels cause cerebral vasodilation and improved oxygenation.
c. Severe cerebral vasoconstriction results in anoxia and stroke.
d. Vasodilation causes increased intracranial pressure and possibly stops blood flow.

ANS: D
Increased PCO2 dilates cerebral vessels, raising cerebral blood flow, whereas decreased PCO2
constricts cerebral vessels and reduces cerebral blood flow. In patients with traumatic brain
injury, the brain swells acutely; this raises the intracranial pressure in the rigid skull to such
high levels that blood supply to the brain might be cutoff, causing cerebral hypoxia
(ischemia). That is, high intracranial pressure may exceed cerebral arterial pressure and stop
blood flow.

DIF: Recall REF: p. 316 OBJ: 10 | 11

48. A patient in the emergency room is displaying prolong inspiratory gasps interrupted by
occasional expirations, what serious injury should be suspected on this patient?
1. Pneumotaxic center has been severed.
2. Vagus nerve has been severed.
3. Glossopharyngeal nerve has been severed.
a. 2 and 3 only
b. 1 and 2 only
c. 1 and 3 only
d. 1, 2, and 3

ANS: B
 If a situation occurs where the higher pneumotaxic center and vagus nerves were severed, the
DRG inspiratory neurons would fail to switch off, causing prolonged inspiratory gasps
interrupted by occasional expirations (apneustic breathing). Vagal and pneumotaxic center
impulses hold the apneustic center’s stimulatory effect on DRG neurons in check.

DIF: Application REF: pp. 309-310 OBJ: 3

49. A healthy 33-year-old woman relocates to an area approximately 8000 ft above sea level. On
her first day, she begins to hyperventilate, but in 24 hr she shows signs of recovery. What is
the probable cause of her condition?
a. Hypoxemia-mediated hyperventilation
b. Hypercapnia
c. Hyperoxia-mediated hyperventilation
d. Increased H+

ANS: A
High altitude causes a healthy person’s ventilation to increase because low barometric
pressure decreases the inspired PO2, and thus the arterial PO2, which in turn raises the
sensitivity of peripheral chemoreceptors to H+. The resulting increase in ventilation is less
than expected, though, because hyperventilation lowers the PaCO2 and raises arterial pH.

DIF: Application REF: p. 313 OBJ: 6

50. Why does splashing cold water on the skin stimulate ventilation?
a. It decreases medullary inspiratory activity causing hyperpnea.
b. Hering-Breuer inflation reflex.
c. It increases medullary inspiratory activity causing hyperpnea.
d. J receptor.

ANS: C
Proprioceptors in muscles, tendons, and joints, as well as pain receptors in muscles and skin,
send stimulatory signals to the medullary respiratory center. Such stimuli increase medullary
inspiratory activity and cause hyperpnea. For this reason, moving the limbs, slapping or
splashing cold water on the skin, and other painful stimuli stimulate ventilation in patients
with respiratory depression.

DIF: Recall REF: p. 311 OBJ: 4