Pulmonary Physiology: Regulation of Respiration Flashcards

(49 cards)

1
Q

Activates muscles of breathing via spinal and cranial motor neurons innervating thoracic/abdominal and laryngeal/pharyngeal muscles

A

Central respiratory controller

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2
Q

Feedback from peripheral and central chemoreceptors assess changes in blood and CSF levels of

A

O2, CO2, and pH

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3
Q

Higher brain centers such as those responsible for sleep, wake, exercise, and emotion also regulate

A

Respiratory drive

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4
Q

Terminates inspiration (lung inflation)

A

Peripheral vagal feedback

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5
Q

Located in the rostral third of the pons

-The location of the pneumotaxic center

A

Pontine respiratory neurons (PRG)

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6
Q

Mediates smooth transition from inspiration to expiration by inhibiting inspiratory activity

-Located in PRG

A

Pneumotaxic center

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7
Q

The caudal 2/3 of the pons contains the

A

Apneustic center

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8
Q

In the absence of vagal feedback and the pneumotaxic center inspiratory terminating influences, we see the emergence of an

A

Apneustic breathing pattern (prolonged inspiration)

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9
Q

Contains the neurons responsible for spontaneous rythm generation

A

Medulla

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10
Q

Contains both inspiratory and expiratory neurons

A

PRG (n. parabrachialis and kolliker-fuse n.)

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11
Q

Activation of PRG leads to

A

Rapid, shallow breathing

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12
Q

Contians only inspiratory neurons

A

DRG (in nucleus tractus solitarius)

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13
Q

Contains both inspiratory and expiratory neurons

A

VRG (n. ambiguous, retrofacial n. and n. retroambigualis)

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14
Q

The respiratory “pacemaker” that can initiate rhythm generation

-part of VRG

A

Pre-Bötzinger complex

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15
Q

Respiratory rhythm is generated through a process of reciprocal inhibition between the

A

Inspiratory and expiratory neurons

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16
Q

Peripheral (carotid & aortic bodies) and central (rostroventral medulla) sites that make adjustments in breathing depth and rate based on changes in arterial blood gas tensions and pH

A

Chemoreceptors

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17
Q

Make adjustments in breathing depth and rate based on expansion of the lung and chest as well as irritation of the airways

A

Mechanoreceptors

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18
Q

The carotid body changes its level of activity in response to changes in

A

PaO2, PaCO2, and pH

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19
Q

Carotid body activity increases when PaO2 drops below

A

60 mmHg

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20
Q

Carotid body activity increases when

A

PCO2 increases (pH decreases)

21
Q

Carotid body activity decreases when

A

PCO2 decreases (pH increases)

22
Q

The central chemoreceptors change their activity in response to changes in

23
Q

Increases in PaCO2 normally increase

24
Q

Respiratory diseases which severely impair the ability to excrete CO2 (e.g., severe COPD) result in chronic CO2 retention causing a desensitization of this center and these patients rely on their

A

Hypoxic drive ventilation

25
Ventilation during the awake state is regulated by
Chemical and mechanical drives and arousal
26
During sleep we lose the "wakefullness stimulus" this results in
Hypoventilation
27
During sleep, respiratory drive is controlled
Chemically
28
Can also result with narcotics, COPD, or deep anesthesia
Hypoventilation
29
Hypoventilation can be caused by
Sleep, narcotics, COPD, and deep anesthesia
30
Occurs with metabolic acidosis due to either peripheral or central chemosensory stimulation
Hyperventilation
31
Chemical drive alters ventilation due to a combination of both
CO2 drive and hypoxic drive
32
When PaO2 is 100 mm Hg, ventilation is regulated by the level of PCO2 primarily due to stimulation of
Central chemoreceptors (some contribution from carotid body)
33
When PaO2 levels decline below 60 mmHg, ventilation is regulated by both
PCO2 and PO2
34
Sensed by peripheral (primarily carotid body) chemoreceptors as O2 tension (PaO2) only and not O2 content (CaO2) or saturation (SaO2) (i.e., no response to breathing carbon monoxide)
Hypoxia
35
Hypoxic drive is a result of stimulation of the
Carotid body chemoreceptors
36
Hypoxia alone will have what affect?
Increased ventilation and decreased PCO2
37
Simultaneous increases in PaCO2 potentiates the increase in 𝑉 ventilation at any given PaO2 enhancing the
Hypoxic drive
38
H+ does not cross the blood-brain-barrier so metabolic acidosis results in hyperpnea due to stimulation of the
Peripheral chemoreceptors
39
Hyperpnea (Ventilatory compensation) decreases PaCO2 and causes a rise in pH and a reduction in
Peripheral chemoreceptor drive
40
The reduction in arterial blood PCO2 creates a downhill CO2 gradient from the CSF to the arterial blood which results in an increase in CSF pH and a reduction in the
Central chemoreceptor drive
41
The ventilatory response to exercise can be broken down into
Three phases
42
Characterized by an abrupt increase in ventilation, which reflects the anticipatory response
Phase I
43
Gradual increase in ventilation involving a variety of afferents
Phase II
44
Steady state of ventilation that reflects a precise matching of ventilation to metabolism
Phase III
45
During slow wave sleep, we have
Hypoventilation
46
Repetitive episodes of upper airway collapse during sleep, resulting in partial or complete cessation of airflow despite persisting respiratory effort
Obstructive sleep apnea
47
The respiratory control centers are located in the
Medulla and Pons
48
The brain centers responsible for respiratory rhythm generation and patterning (amplitude and frequency) of the integrated neural output consist of the
Pneumotaxic center, apneustic center and the medullary dorsal and ventral respiratory groups
49
There are three major classes of vagal mechanoreceptors. What are they?
Slowly-adapting (stretch receptors), rapidly adapting (irritant receptors), and non-myelinated nerve endings (J receptors)