Chapter 14
Regulation of Breathing
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
Learning Objectives
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
Identify where the structures that regulate
breathing are located.
Describe how the inspiratory and expiratory
neurons in the medulla establish the basic
pattern of breathing.
Describe the effect impulses from the
pneumotaxic and apneustic centers in the
pons have on the medullary centers of
breathing.
Identify the effect of various reflexes on
breathing.
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
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Learning Objectives (cont.)
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Describe how the central and peripheral
chemoreceptors differ in the way they regulate
breathing.
State how the central chemoreceptors respond
differently to respiratory and nonrespiratory acidbase disorders.
Describe how the regulation of breathing in
individuals with chronic hypercapnia differs from
the regulation of breathing in healthy persons.
Describe why administering oxygen to patients
with chronic hypercapnia poses a special risk that
is not present in healthy individuals.
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Learning Objectives (cont.)
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

Describe why ascending to a high altitude
has different immediate- and long-term
effects on ventilation.
State why mechanically ventilated patients
with head injuries may benefit from deliberate
hyperventilation.
Describe the characteristics of abnormal
breathing patterns.
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Medullary Respiratory Center
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Rhythmic cycle of breathing originates in
medulla
Higher brain centers, systemic receptors, &
reflexes modify medulla’s output
No truly separate inspiratory & expiratory
centers
Medulla contains several widely dispersed
groups of respiratory-related neurons

These form dorsal & ventral respiratory groups
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Medullary Respiratory Center (cont.)
 Dorsal respiratory groups (DRG)
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
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Composed mainly of inspiratory neurons located
bilaterally in medulla
These neurons send impulses to motor nerves of
diaphragm & external intercostal muscles
DRG nerves extend into VRG not reverse
Vagus & glossopharyngeal nerves bring sensory
impulses to DRG from lungs, airways, peripheral
chemoreceptors, & joint proprioceptors
• Input modifies breathing pattern
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Medullary Respiratory Center (cont.)
 Ventral respiratory groups (VRG)
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
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Contain both inspiratory & expiratory neurons located
bilaterally in medulla
VRG sends inspiratory impulses to:
• Laryngeal & pharyngeal muscles
• Diaphragm & external intercostals
Other VRG neurons send expiratory signals to
abdominal muscles & internal intercostals
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Medullary Respiratory Center (cont.)
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
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Medullary Respiratory Center (cont.)
 Inspiratory ramp
signal

Signal starts low &
gradually increases
to produce smooth
inspiratory effort
instead of gasp
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To abduct the vocal cords and increase the
diameter of the glottis, the ventral respiratory
groups (VRG) inspiratory neurons must send
motor impulses through the
A.
B.
C.
D.
Vagus nerve
Glossopharyngeal nerve
Hypoglossal nerve
Olfactory nerve
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Pontine Respiratory Centers
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Pons modifies output of medullary centers
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2 pontine centers: apneustic & pneumotaxic
Apneustic center
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Functions only identified by cutting connection to
medullary centers
 Apneustic breathing: characterized by long gasping
inspirations interrupted by occasional expirations

Pneumotaxic center
Controls “switch-off,” so controls inspiratory time (IT)
 Increased signals increase RR, while weak signals
prolong IT & large VT (tidal volume)

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Reflex Control of Breathing
 Hering-Breuer inflation reflex

Lung distention causes stretch receptors to send
inhibitory signals to DRG, stopping further
inspiration
• In adults active only on large VT (>800 mL)
• Regulates rate & depth of breathing during moderate to
strenuous exercise
 Deflation reflex

Sudden lung collapse results in hyperpnea as
seen in pneumothoraces
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Which of the following anatomical structures below
does not help control the depth of inspiration?
A.
B.
C.
D.
Apneustic center
Pnuemotaxic center
Vagal nerve
Glossopharyngeal nerve
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Reflex Control of Breathing (cont.)
 Head’s paradoxical reflex
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May maintain large VT during exercise & deep
sighs
May be responsible for babies first breaths at birth
 Irritant receptors
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Stimulated by inhaled irritants or mechanical
factors
Cause bronchospasm, cough, sneeze, tachypnea,
& narrowing of glottis
• Vagovagal reflexes
In hospital, triggered by:
• Suctioning, bronchoscopy, endotracheal intubation
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Reflex Control of Breathing (cont.)
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J-receptors
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Located in lung parenchyma juxtacapillary
Stimulated by pneumonia, CHF, pulmonary
edema
Cause rapid, shallow breathing, dyspnea &
expiratory narrowing of glottis
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Reflex Control of Breathing (cont.)
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Peripheral proprioceptors
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Found in muscles, tendons, joints, & pain
receptors
Movement stimulates hyperpnea.
Moving limbs, pain, cold water all stimulate
breathing in patients w/ respiratory depression
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Reflex Control of Breathing (cont.)
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While a respiratory therapist (RT) is doing a
routine suctioning on a patient, the RT notices that
the patient begins to have a very violent cough,
which pulmonary reflex is responsible for this
response?
A.
B.
C.
D.
Head’s paradoxical reflex
Deflation reflex
Hering-Breuer
Vagovagal reflex
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Chemical Control of Breathing

Body works to maintain proper levels of O2,. CO2,
& pH through mediation of chemoreceptors as it
affects VE
 Central chemoreceptors
• Located bilaterally in medulla
• Stimulated directly by H+ ions, indirectly by CO2



BBB is almost impermeable to H+ & HCO2– but CO2 freely
crosses
In CSF: CO2 is hydrolyzed, releasing H+.
Increased CO2 increases H+ in CSF, causing hyperventilation to
restore
. normal levels pH & CO2
– VA increased 2–3 L/min for each mm Hg rise in PaCO2
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Chemical Control of Breathing (cont.)
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Peripheral chemoreceptors
Located in aortic arch & bifurcations of common
carotid arteries
Peripheral chemoreceptors’ response to ⇓ PaO2
Hypoxemia increases receptors sensitivity for H+
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⇓PaO2 causes ⇑VE for any pH; vice versa.
In
. severe alkalosis, hypoxemia has little affect on VE
Only affected by PaO2, not CaO2 (anemia,
COHb)
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Chemical Control of Breathing (cont.)
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
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Chemical Control of Breathing (cont.)

Peripheral chemoreceptors’ response to ⇓PaO2
(cont.)
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Not significant response until PaO2 falls to ~60 mm Hg
.
• Further falls result in sharp increase in VE
• Meaning: under normal circumstances, oxygen plays no role in
drive to breathe

Hypoxemia—most common cause of hyperventilation
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Peripherally located chemoreceptors (carotid and
aortic bodies) are sensitive to all of the following,
except:
A.
B.
C.
D.
indirectly to hypoxemia
directly to increased H+
indirectly to increased CO2
indirectly to increased H+
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Chemical Control of Breathing (cont.)
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Peripheral chemoreceptors’ response to ⇑PaCO2 &
[H+]
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Less responsive than central chemoreceptors (CCRs)
• One-third of hypercapnic response, but a more rapid response to
changes in [H+]
Hyperoxia: PCRs are almost totally insensitive to changes in
PaCO2; thus any response is due to CCRs
Low PaCO2 renders PCRs almost unresponsive to ⇓PaO2
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If a patient’s PaCO2 started at 45 mmHg and then
rises to 49 mmHg, how much has the patients
alveolar ventilation increased?
A.
B.
C.
D.
2-3 L/min
4-6 L/min
6-9 L/min
8-12 L/min
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Chemical Control of Breathing (cont.)
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Coexisting acidosis, hypercapnia, &
hypoxemia maximally stimulate PCRs
Hypercapnic COPD patients depressed
response to ⇑CaO2
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Chemical Control of Breathing (cont.)
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Control of breathing in chronic hypercapnia .
Sudden rise in PaCO2 causes immediate rise in VE
In slow-rising PaCO2 (severe COPD), kidneys
retain HCO3–, which maintains CSF pH, thus no
hyperventilation response
Hypoxemia seen w/ hypercapnia becomes minuteto-minute breathing stimulus via altered response
to [H+]


Hypoxemia is always present
in severe COPD due to
. .
severe mismatches in V/Q.
Increased FIO2 raises PaO2 making PCR less
sensitive to [H+] resulting in higher PaCO2
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Chemical Control of Breathing (cont.)
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Oxygen-associated hypercapnia
O2 therapy may cause sudden rise in PaCO2 in
severe COPD with chronic hypercapnia
Possible explanations include:


Hypoxic drive is removed (traditional view)
⇑FIO2 may worsen V/Q mismatch
. .
• Hypoxic pulmonary vasoconstriction
is reversed to poorly
ventilated alveoli

⇑FIO2 may make patient susceptible to absorption
atelectasis
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Chemical Control of Breathing
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A COPD patient receiving supplemental O2
develops absorption atelectasis. What is the
probably cause of this patient’s atelectasis?
A.
B.
C.
D.
Nitrogen washout
Hypercapnia
Hypoxemia
Respiratory acidosis
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Chemical Control of Breathing (cont.)
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Oxygen-induced Hypercapnia: KEY POINTS

“COPD” does NOT signify chronic hypercapnia; or
O2 therapy will induce hypoventilation:
• These characteristics are only in end-stage disease
• Present in small percent of COPD patients
 Concern about O2-induced hypercapnia &
acidemia is not warranted in most COPD patients
 O2 should NEVER be withheld in hypoxemic
COPD patients as tissue oxygenation is overriding
priority
 Be prepared to provide MV to rare COPD patient
who does have severe hypoventilation due to
oxygen therapy
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Chemical Control of Breathing (cont.)
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CCR response to acute CO2 increase in
chronic hypercapnia
Acute rises in PaCO2 continues to stimulate
CCRs
Resulting ventilatory response is depressed
due to chemical & mechanical reasons


Increased HCO3– prevents as large a fall in pH, as
would be seen in healthy patient
Abnormal .mechanics impair lung ability to
increase VE
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Ventilatory Response to Exercise
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Strenuous exercise can increase CO2
production & O2 consumption 20-fold

Ventilation normally keeps pace so all ABG values
are held constant
.

Mechanism for increased VE poorly
understood. May be:



CNS sends concurrent signals to skeletal muscles
& to medullary respiratory centers
Joint movement stimulates proprioceptors; send
excitatory signals to medullary centers
May also be due to repeated experience causing
anticipatory changes in ventilation
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Abnormal Breathing Patterns

Cheyne-Stokes respirations (CSR)
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Characterized by cyclic waxing & waning ventilation w/
apnea gradually giving way to hyperpneic
Seen w/ low cardiac output states (CHF)
• Creates lag of CSF CO2 behind arterial PaCO2 & results in
characteristic cycle

Biot’s respiration

Similar to CSR but VT is constant, except during
apneic periods
 Seen in patients w/ elevated ICP
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Abnormal Breathing Patterns (cont.)

Apneustic breathing (previously described)
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Central neurogenic hyperventilation
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Indicates damage to pons
May be caused by head trauma, severe brain
hypoxia, or lack of cerebral perfusion
Central neurogenic hypoventilation

Medulla respiratory centers do not respond to
appropriate stimuli
 Associated w/ head trauma, cerebral hypoxia, &
narcotic suppression
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CO2 & Cerebral Blood Flow (CBF)
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
CO2 plays important role in autoregulation of
CBF mediated through formation of H+
Increased CO2 dilates cerebral vessels; vice
versa
In traumatic brain injury (TBI), brain swells
acutely, raising ICPs > cerebral arterial
pressure (perfusion stops)

Cerebral hypoxia/ischemia
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CO2 & Cerebral Blood Flow (CBF)

Mechanical hyperventilation lowers PaCO2 &
ICP


Controversial—reduces O2 & CBF to injured brain
All agree: must avoid hypoventilation in TBI
patients
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