Pulmonary Physiology: Regulation of Respiration Flashcards

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

A

PCO2 and pH

23
Q

Increases in PaCO2 normally increase

A

Ventilation

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
Q

Ventilation during the awake state is regulated by

A

Chemical and mechanical drives and arousal

26
Q

During sleep we lose the “wakefullness stimulus” this results in

A

Hypoventilation

27
Q

During sleep, respiratory drive is controlled

A

Chemically

28
Q

Can also result with narcotics, COPD, or deep anesthesia

A

Hypoventilation

29
Q

Hypoventilation can be caused by

A

Sleep, narcotics, COPD, and deep anesthesia

30
Q

Occurs with metabolic acidosis due to either peripheral or central chemosensory stimulation

A

Hyperventilation

31
Q

Chemical drive alters ventilation due to a combination of both

A

CO2 drive and hypoxic drive

32
Q

When PaO2 is 100 mm Hg, ventilation is regulated by the level of PCO2 primarily due to stimulation of

A

Central chemoreceptors (some contribution from carotid body)

33
Q

When PaO2 levels decline below 60 mmHg, ventilation is regulated by both

A

PCO2 and PO2

34
Q

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)

A

Hypoxia

35
Q

Hypoxic drive is a result of stimulation of the

A

Carotid body chemoreceptors

36
Q

Hypoxia alone will have what affect?

A

Increased ventilation and decreased PCO2

37
Q

Simultaneous increases in PaCO2 potentiates the increase in 𝑉ventilation at any given PaO2 enhancing the

A

Hypoxic drive

38
Q

H+ does not cross the blood-brain-barrier so metabolic acidosis results in hyperpnea due to stimulation of the

A

Peripheral chemoreceptors

39
Q

Hyperpnea (Ventilatory compensation) decreases PaCO2 and causes a rise in pH and a reduction in

A

Peripheral chemoreceptor drive

40
Q

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

A

Central chemoreceptor drive

41
Q

The ventilatory response to exercise can be broken down into

A

Three phases

42
Q

Characterized by an abrupt increase in ventilation, which reflects the anticipatory response

A

Phase I

43
Q

Gradual increase in ventilation involving a variety of afferents

A

Phase II

44
Q

Steady state of ventilation that reflects a precise matching of ventilation to metabolism

A

Phase III

45
Q

During slow wave sleep, we have

A

Hypoventilation

46
Q

Repetitive episodes of upper airway collapse during sleep, resulting in partial or complete cessation of airflow despite persisting respiratory effort

A

Obstructive sleep apnea

47
Q

The respiratory control centers are located in the

A

Medulla and Pons

48
Q

The brain centers responsible for respiratory rhythm generation and patterning (amplitude and frequency) of the integrated neural output consist of the

A

Pneumotaxic center, apneustic center and the medullary dorsal and ventral respiratory groups

49
Q

There are three major classes of vagal mechanoreceptors. What are they?

A

Slowly-adapting (stretch receptors), rapidly adapting (irritant receptors), and non-myelinated nerve endings (J receptors)