Chapter 14 Regulation of Breathing Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc

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

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.

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Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc. 3

Learning Objectives (cont.)

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 acid-base 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.


Learning Objectives (cont.)

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.


Medullary Respiratory Center

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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Dorsal respiratory groups (DRG) 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

Medullary Respiratory Center (cont.)


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Ventral respiratory groups (VRG) 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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Inspiratory ramp signal Signal starts low &

gradually increases to produce smooth inspiratory effort instead of gasp



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.Vagus nerve

B.Glossopharyngeal nerve

C.Hypoglossal nerve

D.Olfactory nerve

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Pontine Respiratory Centers Pons modifies output of medullary centers

2 pontine centers: apneustic & pneumotaxic Apneustic center

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 BreathingHering-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



Which of the following anatomical structures below does not help control the depth of inspiration?

A.Apneustic center

B.Pnuemotaxic center

C.Vagal nerve

D.Glossopharyngeal nerve

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Reflex Control of Breathing (cont.)

Head’s paradoxical reflex May maintain large VT during exercise & deep

sighs May be responsible for babies first breaths at birth

Irritant receptors 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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J-receptors Located in lung parenchyma juxtacapillary Stimulated by pneumonia, CHF, pulmonary edema Cause rapid, shallow breathing, dyspnea &

expiratory narrowing of glottis




Peripheral proprioceptors 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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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.Head’s paradoxical reflex

B.Deflation reflex

C.Hering-Breuer

D.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.)

Peripheral chemoreceptors Located in aortic arch & bifurcations of common

carotid arteries Peripheral chemoreceptors’ response to PaO⇓ 2 Hypoxemia increases receptors sensitivity for H+

⇓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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Peripheral chemoreceptors’ response to PaO⇓ 2

(cont.) 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

. .



Peripherally located chemoreceptors (carotid and aortic bodies) are sensitive to all of the following, except:

A.indirectly to hypoxemia

B.directly to increased H+

C.indirectly to increased CO2

D.indirectly to increased H+

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Peripheral chemoreceptors’ response to ⇑PaCO2 & [H+] 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 PaO⇓ 2



If a patient’s PaCO2 started at 45 mmHg and then rises to 49 mmHg, how much has the patients alveolar ventilation increased?

A.2-3 L/min

B.4-6 L/min

C.6-9 L/min

D.8-12 L/min

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Coexisting acidosis, hypercapnia, & hypoxemia maximally stimulate PCRs

Hypercapnic COPD patients depressed response to CaO⇑ 2


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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 minute-

to-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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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



A COPD patient receiving supplemental O2 develops absorption atelectasis. What is the probably cause of this patient’s atelectasis?

A.Nitrogen washout

B.Hypercapnia

C.Hypoxemia

D.Respiratory acidosis



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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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

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)

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) Indicates damage to pons

Central neurogenic hyperventilation 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



CO2 & Cerebral Blood Flow (CBF)

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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Documents

Chapter 14 Regulation of Breathing Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc