Neural Control of Respiration

Question 1

The nervous system controls homeostasis of the respiratory system via controlling.

Answer 1

pH, CO2, & O2

Question 2

Central chemoreceptors detect

Answer 2

arterial (PCO2) pH only

Central chemoreceptors are the most important factor for control of respiratory rate (PCO2).

They are located in the brain. They respond to pH in CSF which is dependent on CO2 that crosses the blood brain barrier. CO2 can cross the blood brain barrier & CSF. It forms carbonic acid which forms acid & decreases the pH which react with the central chemoreceptors.

Question 3

Peripheral chemoreceptors detect

Answer 3

partial pressure of arterial low O2, high CO2, & low pH

In the aortic & carotid bodies (not in the sinuses like in the baroreceptors). The cells in the bodies are called Gloma cells, they respond to hypoxia (low PO2). Low PO2 closes down a potassium channel & the cell depolarizes. Then we open up calcium channels, calcium rushes in & stimulates neurotransmission which activates afferent CN 9 - Glossopharyngeal nerve & sends afferent signals to the brainstem.

Effect of intact or denervated peripheral chemoreceptors on respiratory minute volume. A period of hypoxia lowers O2, increases CO2 and H+, this activates the chemoreceptors and Ventilation increases. Inactivation of the chemoreceptors not only abolishes the response to hypoxia, it reduces Ventilation. This likely results from a toxic effect of hypoxia on the medullary respiratory center.

Question 4

Brainstem generates

Answer 4

basic breathing rhythym

Question 5

2 areas of the medulla (brainstem) responsible for maintaining breathing pattern are

Answer 5

ventral respiratory group neurons VRG

dorsal respiratory group neurons DRG

together they are the central pattern generator

Therefore, breathing is neurogenic, while the heart is myogenic (pattern generated in the SA node).

Question 6

In inspiration: DRG &/or VRG, passive or active, what muscles are used?

Answer 6

The DRG & VRG (motor synapses) are active & synapse with the phrenic (diaphragm) & other synapses innervate spinal nerves which innervate the external intercostals.

See pg. 252-253

Question 7

In expiration: DRG &/or VRG, passive or active, what muscles are used?

Answer 7

The VRG are active & synapse with motor neurons that innervate the internal intercostals (abdominals only during expiration–they are also innervated by VRG).

Question 8

Describe the Hering–Breuer inflation reflex

Answer 8

The Hering–Breuer inflation reflex is a reflex triggered to prevent over-inflation of the lungs. The Hering-Breuer inflation reflex is an inspiratory-stopping reflex of vigorous breathing mediated through the slowly adapting pulmonary stretch receptors via vagal afferents and phrenic efferents. Overinflation triggers vagal afferents.

It is thought not to be important in human adults during normal breathing because the threshold for activating the stretch receptors is not typically reached during eupnea. It becomes important when tidal volume increases during periodic deep breaths (sighs), during exercise and during chronic obstructive pulmonary disease when patients breathe at high lung volume (high FRC) due to increased pulmonary compliance.

During normal breathing, eupnea, the lung is not inflated enough to trigger this reflex. It is triggered during deep breathing.

Question 9

The respiratory control centers, denoted pontine respiratory group and respiratory center are located in the _____ and _____, respectively.

Answer 9

The respiratory control centers, denoted pontine respiratory group and respiratory center are located in the pons (pontine) and medulla, respectively.

These centers establish and modulate the neurogenic respiratory rhythm and receive input from peripheral and central chemoreceptors and also from higher centers in the brain.

See pg. 255

Question 10

What generates the pacemaker activity of the respiratory rhythm?

Answer 10

The VRG also contains the Bötzinger complex (BOT), a cluster of mostly expiratory neurons in the ventro- lateral medulla essential to the generation of pacemaker activity associated with the respiratory rhythm and modulated by afferent input and higher brain centers, but the exact mechanism of rhymicity of breathing is not known. This complex is the target of drugs aimed at stimulating breathing when breathing is depressed, say, by an overdose of opioids.

Therefore, the VRG contains the central pattern generator

Question 11

The DRG & VRG are influenced by the

Answer 11

Pontine respiratory group

The pontine respiratory group (PRG) located in the pons, probably functions to fine-tune the respiratory pattern and modulates the pattern in response to vagal afferents responding to hypercapnea or hypoxia.

Question 12

Rhythmic pattern of breathing is generated in the

Answer 12

Medulla, DRG & VRG, it contains the central pattern generator

In contrast to the myogenic beating of the heart, breathing is neurogenic. The central pattern generator (CPG) for respiration is located in the medullary respiratory center, which is located below the floor of the fourth ventricle of the brain and is comprised of the dorsal respiratory group (DRG) and ventral respiratory group (VRG).

See pg. 257 & 251

Question 13

Describe Cheyne-Stokes respiration

Answer 13

Cheyne-Stokes respiration: an abnormal pattern of breathing characterized by alternating periods of hyperpnea and apnea, each cycle taking from 30 sec to 2 min associated with altered arterial partial pressures of oxygen and carbon dioxide that occur in injuries to the respiratory centers, chronic heart failure, carbon monoxide poisoning, strokes, brain tumors and in newborns with immature respiratory centers, or in some individuals receiving morphine or in some individuals during sleep at high altitude.

See pg. 258

Question 14

Describe Cluster breathing

Answer 14

an abnormal form of breathing associated with stroke, head trauma, pressure, or a lesion in the lower pontine region of the brainstem characterized by closely grouped series of shallow breaths similar in size separated by intervals of apnea and generally indicative of a poor prognosis.

See pg. 258

Question 15

Descibe ataxic breathing

Answer 15

Ataxic breathing, an abnormal form of breathing associated with a lesion in the medullary respiratory center characterized by a completely irregular series of inspirations and expirations with irregular pauses and increasing periods of apnea typically progressing to complete apnea.

See pg. 258

Question 16

Describe Kussmaul breathing

Answer 16

Kussmaul breathing: an abnormal form of deep and labored desperate and gasping breathing associated with severe metabolic acidosis, particularly diabetic metabolic acidosis. In acidosis, a shallow rapid hyperventilation becomes Kussmaul as the acidosis progresses from mild to severe.

Question 17

Alveolar P___ is the major controller of respiratory rate. It is more important than hypoxia in initiating breathing. Increasing PACO2 increases minute _____. However, sensitivity to alveolar PACO2 is _____ by hypoxia.

Answer 17

Alveolar PCO2 is the major controller of respiratory rate. It is more important than hypoxia in initiating breathing. Increasing PACO2 increases minute ventilation. However, sensitivity to alveolar pCO2 is increased by hypoxia.

See pg. 260-262

Question 18

Metabolic acidosis stimulates ventilation and shifts the CO2 sensitivity curve _____. In contrast, sleep slightly shifts the CO2 sensitivity curve _____, with greater _____ shifts seen in chronic obstructive pulmonary disease and by administration of narcotics (opioids) or during deep anesthesia. The reasons these curves shift is because their ______ points change. Ventilation increases @ a constant PCO2, when pH ______. Ventilation increases @ a constant PCO2, when PaO2 ______.

Answer 18

Metabolic acidosis stimulates ventilation and shifts the CO2 sensitivity curve upward. In contrast, sleep slightly shifts the CO2 sensitivity curve downward, with greater downward shifts seen in chronic obstructive pulmonary disease and by administration of narcotics (opioids) or during deep anesthesia. The reasons these curves shift is because their set points change. Ventilation increases @ a constant PCO2, when pH decreases. Ventilation increases @ a constant PCO2, when PaO2 decreases.

See pg. 263-267

Question 19

See pg. 274

Answer 19

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Question 20

______ receptors protect the lung from noxious stimuli, such as dust, chemicals, and cold air. These receptors may trigger coughing, bronchoconstriction, and mucus production when stimulated. ____ and _____ chemoreceptors respond to changes in arterial blood gas composition. Stretch receptors activate during lung _____, whereas _____ capillary receptors respond to capillary engorgement and interstitial edema.

Answer 20

Irritant receptors protect the lung from noxious stimuli, such as dust, chemicals, and cold air. These receptors may trigger coughing, bronchoconstriction, and mucus production when stimulated. Central and peripheral chemoreceptors respond to changes in arterial blood gas composition. Stretch receptors activate during lung inflation, whereas juxtapulmonary capillary receptors respond to capillary engorgement and interstitial edema.

Question 21

Hypoxemia stimulates breathing by a direct effect on the _____ chemoreceptors in the carotid and aortic bodies. _____ chemoreceptors are stimulated by CO2 (or H+).

Answer 21

Hypoxemia stimulates breathing by a direct effect on the peripheral chemoreceptors in the carotid and aortic bodies. Central (medullary) chemoreceptors are stimulated by CO2 (or H+).

Question 22

The decreased Pao2 causes hyperventilation (stimulates breathing) via the ______ chemoreceptors, but not via the ______ chemoreceptors. The decreased Paco2 results from _______ and causes increased pH, which inhibits breathing via the peripheral and central chemoreceptors.

Answer 22

The decreased Pao2 causes hyperventilation (stimulates breathing) via the peripheral chemoreceptors, but not via the central chemoreceptors. The decreased Paco2 results from hyperventilation (increased breathing) and causes increased pH, which inhibits breathing via the peripheral and central chemoreceptors.

Question 23

At high altitude, the Po2 of alveolar air is decreased because barometric pressure is decreased. As a result, arterial Po2 is decreased (

Answer 23

At high altitude, the Po2 of alveolar air is decreased because barometric pressure is decreased. As a result, arterial Po2 is decreased (

Question 24

A lightly anesthetized patient is removed from a ventilator after surgery and the patient fails to breathe for one minute. Which of the following best explains this observation?

Answer 24

The ventilator was set at too high a rate and the patient is hypocapnic.

Question 25

The Hering-Breuer inflation reflex functions to limit the degree of inflation during _____rpnea but not during ____pnea.

Answer 25

The Hering-Breuer inflation reflex functions to limit the degree of inflation during hyperpnea but not during eupnea.

Question 26

Central chemoreceptors respond directly to the _____of the cerebrospinal fluid, whose affinity is affected by ______ diffusing across the blood brain barrier, and then forming carbonic acid which in turn dissociates to bicarbonate and a proton. Therefore ______ is most important for directly stimulating central chemoreceptors.

Answer 26

Central chemoreceptors respond directly to the pH of the cerebrospinal fluid, whose affinity is affected by carbon dioxide diffusing across the blood brain barrier, and then forming carbonic acid which in turn dissociates to bicarbonate and a proton. Therefore pH is most important for directly stimulating central chemoreceptors.

Question 27

Arterial Po2 is sensed by an O2-dependent K+ conductance in glomus cells. A fall in arterial Po2 allows the K+ channel to _____, decreasing K+ efflux and causing membrane ______. ______ activates voltage-gated Ca2+ channels to open and Ca2+ _______.

Answer 27

Arterial Po2 is sensed by an O2-dependent K+ conductance in glomus cells. A fall in arterial Po2 allows the K+ channel to close, decreasing K+ efflux and causing membrane depolarization. Depolarization activates voltage-gated Ca2+ channels to open and Ca2+ influx.