Download Respiratory Care Anatomy and Physiology, 3rd

Beachey: Respiratory Care Anatomy and Physiology, 3rd Edition
Chapter 11: Control of Ventilation
Answers to Workbook Questions
Key Terms and Definitions
1. Medulla oblongata—Portion of the brainstem from which rhythmic, cyclical
breathing impulses originate.
2. Pons—Located above the medulla oblongata, portion of the brainstem that is
responsible for regulating the output of the medulla. The two groups of neurons
found in the pons are the apneustic and pneumotaxic centers, known collectively
as the “pontine centers.”
3. Apneustic center—Pontine center thought to be responsible for apneustic
breathing.
4. Pneumotaxic center—Pontine center responsible for controlling the length of
inspiration.
5. Hering-Breuer reflex—Reflex generated by stretch receptors located in smooth
muscle of large and small airways that inhibits further inspiratory efforts when
large tidal volumes are reached.
6. Head’s reflex—Paradoxical reflex to Hering-Breuer reflex that causes increased
inspiratory effort in response to hyperinflation, thought to be helpful in
maintaining large tidal volumes during exercise.
7. Chemoreceptors—Specialized nerve structures that, when stimulated, transmit
impulses to respiratory centers in the medulla.
8. Central chemoreceptors—Specialized nerve cells located in the medulla that are
stimulated by hydrogen ions in cerebral spinal fluid.
9. Peripheral chemoreceptors—Highly vascular tissue also referred to as carotid
bodies (located in the bifurcation of carotid arteries) and aortic bodies (located in
the aortic arch). Peripheral chemoreceptors respond to increased arterial [H+]
regardless of origin.
10. Apneustic breathing—Abnormal breathing pattern characterized by prolonged
inspiratory gasps with occasional expirations.
11. Biot’s breathing—Abnormal breathing pattern characterized by abnormal
respiratory rates with intermittent periods of apnea. May be associated with
lesions of the pons.
12. Cheyne-Stokes breathing—Abnormal breathing pattern characterized by
progressively deeper and faster breathing, followed by decreasing rates and
volumes that result in periods of apnea. May be seen in association with brain
lesions, or in congestive heart failure as a result of delayed blood transit time
between lungs and brain.
Matching
1.
B
A
Apneustic center
Dorsal respiratory group
Copyright © 2013, 2007, 1998 Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.
Answers to Workbook Questions
C
D
Ventral respiratory group
Pneumotaxic center
G
A
F
E
C
D
B
Hering-Breuer reflex
J-receptors
Vagovagal reflexes
Deflation reflex
Slowly adapting receptors
Rapidly adapting irritant receptors
Peripheral proprioceptors
P
C
P
B
P
P
B
P
Respond to arterial carbon dioxide, hypoxia, and hydrogen ions
Are in direct contact with cerebral spinal fluid
Located in the arch of the aorta and bifurcations of the carotid arteries
Respond directly to changes in hydrogen ion concentration
Respond to decreased arterial partial pressure of oxygen
Account for 20–30% of the ventilatory response to hypercapnia
Respond indirectly to changes in PCO2
Hypoxia increases sensitivity to hydrogen ion concentration
11-2
2.
3.
Labeling
A. Pneumotaxic center
B. Nucleus parabrachialis medialis
C. Nucleus Kolliker-Fuse
D. Apneustic Center
E. Dorsal respiratory groups
F. (nucleus tractus solitaries, NTS)
G. Ventral respiratory groups
H. Botzinger’s complex
I.
Nucleus retroambiguus
J.
(caudal and rostral portions)
K. Nucleus ambiguous
L. Pons
M. Medulla oblongata
N. Spinal cord
Short Answer/Critical Thinking Questions
1. The rhythmic spontaneous breathing pattern is caused by nerve impulses
originating in the medulla oblongata. The nerve group containing mainly
inspiratory neurons is known as the dorsal respiratory group while the nerve
group containing both inspiratory and expiratory neurons is known as the ventral
respiratory group.
Copyright © 2013, 2007, 1998 Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.
Answers to Workbook Questions
11-3
2. The Botzinger complex and the pre-Botzinger complex are thought to be
responsible for the basic, rhythmic pattern of breathing. Two theories are
presented to explain rhythm generation: the pacemaker hypothesis and the
network hypothesis. The pacemaker hypothesis suggests that certain medullary
cells have intrinsic pacemaker capabilities, and that these cells drive other
medullary neurons. The network hypothesis suggests that there is a pattern of
interconnections between neurons located throughout the rostral ventral
respiratory group, the pre-Botzinger complex, and the Botzinger complex, and
that these inspiratory and expiratory neurons inhibit one another.
3. After expiration ceases, the inspiratory impulses coming from dorsal and ventral
neurons gradually increase their firing rate, creating a smooth, increasing “ramp”
signal that causes progressively stronger inspiratory muscle contractions, rather
than abrupt inspiratory “gasps.”
4. The pneumotaxic center of the pons and pulmonary stretch receptors are
responsible for controlling the “off switch” of the dorsal respiratory group’s
inspiratory ramp signal, thus inhibiting inspiration. As inspiratory impulses get
stronger, inhibitory neurons also begin to fire with increasing frequency until they
stop, or “switch off,” the inspiratory signal and expiration occurs. A weak signal
from the pneumotaxic center will result in longer inspiratory times and larger tidal
volumes.
5. The apneustic center, if not restrained by the pneumotaxic center, will produce
apneusis, a breathing pattern characterized by prolonged inspiratory gasps. This
type of breathing pattern is generated by severing the connection between the
pneumotaxic and apneustic centers, and also by severing the vagus nerves.
6. Stretch receptors in the smooth muscle of large and small airways are responsible
for the Hering-Breuer reflex, which, like the pneumotaxic center, generates
impulses that act to inhibit inspiration. The difference between them, however, is
that the Hering Breuer reflex is activated only at large tidal volumes. The
pneumotaxic center, then, is responsible for inhibition of inspiration during quiet
breathing, while the Hering-Breuer reflex is more important in regulating rate and
depth of breathing during exercise.
7. A. Vagovagal reflexes result in laryngospasm, bronchospasm, coughing, and
bradycardia. These receptors are found in the epithelium of large airways.
B. J-receptor reflexes are found in the lung parenchyma near pulmonary
capillaries and are stimulated by inflammation (pneumonia), pulmonary vascular
congestion (congestive heart failure), and edema fluid. J-receptors cause rapid,
shallow breathing and a sensation of dyspnea. They are also responsible for the
glottic narrowing that causes expiratory grunting associated with dyspnea.
8. The central chemoreceptors are located the medulla and respond directly to
hydrogen ions. Because the blood-brain barrier is impermeable to hydrogen ions
Copyright © 2013, 2007, 1998 Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.
Answers to Workbook Questions
11-4
but permeable to CO2, elevated arterial CO2 levels will cause CO2 to diffuse
rapidly through the blood-brain barrier into the cerebral spinal fluid (CSF). In the
CSF, CO2 reacts with water to form [H+] and HCO3–. The CSF contains no
buffers, so the generation of [H+] stimulates the chemoreceptors to increase
ventilation within seconds.
9. The peripheral chemoreceptors are responsive to hypoxemia, but unlike elevated
CO2 levels (see Question 8) hypoxemia indirectly increases the drive to breathe.
Peripheral chemoreceptors consist of two areas of vascular tissues known as the
carotid and aortic bodies, which are found, respectively, in the bifurcations of the
carotid arteries, and in the arch of the aorta. Hypoxemia causes peripheral
chemoreceptors in the carotid bodies to become more sensitive to [H+]. When
PaO2 is low, carotid body sensitivity to [H+] increases, stimulating the peripheral
chemoreceptors to fire more rapidly, resulting in increased ventilation. Peripheral
chemoreceptors are also sensitive to arterial CO2 levels.
10. The explanation as to why oxygen administration causes hypercapnic, hypoxemic
patients to hypoventilate is unclear. The traditionally accepted explanation is that
administration of higher oxygen concentrations negates hypoxemia’s stimulatory
effect on the peripheral chemoreceptors. Other investigators believe that oxygen
administration worsens ventilation/perfusion relationships in the lung (due to
pulmonary vasodilation and absorption atelectasis), resulting in elevated blood
PCO2. Finally, some investigators believe that oxygen-induced hypercapnia is due
to a combination of the effects described above.
11. Mechanical hyperventilation of the head injury patient will lower PaCO2, causing
cerebral vasoconstriction, which will decrease cerebral blood flow and
intracranial pressure. The problem with the approach is that the reduction in
cerebral blood flow may cause cerebral ischemia and exacerbate the injury to the
brain. The effect of hyperventilation on cerebral blood flow will diminish after 24
to 48 hours due to the kidney’s compensatory response to hyperventilation (renal
elimination of bicarbonate). A 2005 review of mechanical hyperventilation of the
head injury patient concluded that long-term clinical outcomes were not improved
with the use of hyperventilation therapy. The authors also concluded that
hyperventilation therapy should be considered only in patients with high ICPs,
advising against PaCO2 levels less than 30 mm Hg because of the risk of cerebral
ischemia.
Case Studies
1. The patient may or may not be using excessive pain medication, but the arterial
blood gas report reflects normal baseline values for a patient with chronic
hypercapnia. Although there is a slight upward trend in PO2, PCO2, and [H+], the
values represent a ventilatory status almost identical to the pre-operative state.
PO2 and SaO2 values indicate that the hypoxic drive is probably active. A normally
Copyright © 2013, 2007, 1998 Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.
Answers to Workbook Questions
11-5
functioning central nervous system is confirmed by the patient’s alert mental
status, normal breathing frequency, and normal arterial pH.
Decreases in mental awareness and breathing frequency indicate that the patient’s
PCO2 (and CSF [H+]) has probably risen substantially above his baseline. Oxygen
is flowing at more than twice the rate normally required by the patient and is
suppressing ventilation. The chronically hypercapnic patient is no longer being
driven to breathe by hypoxia, since the SpO2 is now 95% (PaO2 > 60 mm Hg,
within the oximeter’s margin of error) Reducing the oxygen flow rate to the
patient’s normal requirements will allow PO2 to decrease below 60 mm Hg,
stimulating the carotid bodies to drive ventilation. PCO2 will decrease to the
patient’s “normal” level” when alveolar ventilation increases. As CSF PCO2
decreases because of diffusion along the CSF-arterial gradient, CSF [H+] will
decrease and negate the cause of the central nervous system depression.
Key Concept Questions
1. C. The pontine center of the brain serves to fine-tune neural respiratory impulses
originating from the medulla. A spinal cord injury between the pons and medulla
results in an irregular breathing pattern.
2. D. Central and peripheral chemoreceptors are stimulated in response to increased
[H+], which occurs in hypercapnia and acidosis. Hypoxemia stimulates the
carotid bodies in the peripheral chemoreceptors by making them more sensitive to
[H+]. Alkalemia results in decreased [H+], and therefore would not stimulate
ventilation.
3. C. Hypoventilation results in elevated blood CO2 levels, which increase [H+],
dilate cerebral blood vessels, and may increase intracranial pressure, causing
cerebral ischemia.
4. A. Peripheral proprioceptors located in muscles, tendons, and joints send
impulses to the medullary centers to increase inspiratory activity in response to
painful stimuli and movement of the limbs.
Copyright © 2013, 2007, 1998 Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.