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Respiratory SOS > Control of Ventilation - lecture 12-1 > Flashcards

Control of Ventilation - lecture 12-1 Flashcards

1
Q

What is hyperventilation?

A

Hyperventilation: breathing that is beyond that required to meet the metabolic needs of the body (i.e. the PaCO2 decreases)

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2
Q

What is hypoventilation?

A

Hypoventilation: Breathing that is less than that required for metabolic needs (i.e. the PaCO2 increases)

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3
Q

What is hyperpnea?

A

Hyperpnea: increased breathing that meets the metabolic needs

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4
Q

What is tachypnea?

A

Tachypnea: increase in the respiratory rate above the normal range (>20 breaths per minute)

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5
Q

What is bradypnea?

A

Bradypnea: decrease in the respiratory rate below normal range (<10 breaths per minute

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6
Q

What is the origin and nature of the respiratory rhythm?

A

Origin: brain stem
Nature: gas exchange

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7
Q

What are the neural components involved in the drive to breathe?

A

Central neural activity
Peripheral sensory neural feedback
Chemical status of blood and CSF

Feedback control helps as well

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8
Q

What are the central controllers of ventilation?

A

Pons, medulla, other parts of brain

brainstem: automatic
Cortex: volitional

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9
Q

Where does the output from the central controllers of ventilation go?

A

Effectors - respiratory muscles

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10
Q

Do respiratory muscles feed back on sensors that help control ventilation?

A

Yes - sensors help determine appropriateness of respiratory effort

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11
Q

What are the sensors involved with control of ventilation?

A

Chemoreceptors - central and peripheral
Upper airway receptors
Pulmonary receptors

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12
Q

What do medullary centers do?

A

Medullary centers are essential and sufficient for automatic rhythmic respiration

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13
Q

What is the dorsal respiratory group? What does it do and how does it provide innervation?

A

Dorsal respiratory group (DRG):

medullary center that provides automatic rhythmic respiration

primarily inspiratory,

provides rhythmic drive to contralateral phrenic motor neurons

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14
Q

What is the ventral respiratory group? What does it do and what does it affect?

A

Ventral respiratory group (VRG):

medullary center that provides automatic rhythmic respiration

primarily expiratory,

provides rhythmic drive to intercostals and abdominal muscles,

regulates the diameter of the upper airway

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15
Q

What is the effect of the pontine centers?

A

Pontine centers exert a major influence on the medullary oscillator, which is erratic and unstable

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16
Q

What are 2 examples of pontine centers?

A

Apneustic center

Pneumotaxic center

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17
Q

What does the apneustic center do?

A

Apneustic center: keeps inspiration in the “on” position

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18
Q

What does the pneumotaxic center do?

A

Pneumotaxic center: facilitates inspiratory off-switching

19
Q

Why is there a burst of inspiratory activity during the expiration phase?

A

Thought to help smooth and control expiratory effort

- could be accentuated in asthma

20
Q

What are the respiratory vagal afferents?

A

Pulmonary stretch receptors
Rapidly adapting receptors
J receptors
Lung C fibers

21
Q

What do the pulmonary stretch receptors do?

A

Slowly adapting pulmonary stretch receptors (PSR) increase activity with increased lung inflation

terminating I, prolonging E

22
Q

Where are the pulmonary stretch receptors located?

A

Located between smooth muscle cells in the airways

23
Q

What mediates the Hering-Breuer inflation reflex?

A

Slowly adapting pulmonary stretch receptors (PSR) increase activity with increased lung inflation - increased firing at large lung volumes will stop inspiration and start expiration to prevent barotrauma

terminating I, prolonging E

24
Q

What do the rapidly adapting receptors do?

A

Rapidly adapting receptors (RAR) respond to the rate of change of inflation, and chemical stimuli

  • increases resp rate
  • stimulated by pneumothorax

promoting I

25
Q

Where are the rapidly adapting receptors located?

A

Located between airway epithelial cells

26
Q

What reflex is mediated by the rapidly adapting receptors?

A

Lung deflation hyperpnea reflex

27
Q

What do J receptors do?

A

J receptors respond quickly to chemicals in the pulmonary circulation and to changes in interstitial fluid volume - i.e. CHF

Tends to promote rapid shallow breathing

28
Q

Where are J receptors located?

A

Located in the alveolar walls, close to capillaries

29
Q

What are the lung c fibers? What do they respond to? What do they do?

A

Lung C fibers are chemoreceptors that respond to histamine , prostaglandins; influence HR, BP, and respiratory rate

30
Q

Where are the lung c fibers located?

A

Located in the larger (bronchial) airways

31
Q

What are the respiratory mechanical afferents?

A

Muscle and chest wall afferents

Airflow flow receptors

32
Q

What are the muscle and chest wall afferents? What kind of info do they provide?

A
  1. Muscle spindles provide length info and influence load compensation
  2. Tendon organs provide muscle tension info
  3. Joint receptors found in the costal-vertebral joint provide information related to rib joint motion
33
Q

What kind of information do the airway flow receptors provide? Where are they found?

A

Airway flow receptors

Found in the upper airway

These are essentially temperature receptors, and the body assesses flow by a decrease in temperature (wind chill) during inspiration.

34
Q

What are the 2 types of respiratory chemoreceptor afferents?

A

Central

Peripheral

35
Q

Where are the central respiratory chemoreceptor afferents located?

A

Near ventral surface of medulla

36
Q

What do the central respiratory chemoreceptor afferents respond to? How fast? What is the result?

A

Respond to changes in PCO2 and pH in the CSF, but stimulation depends on direct interaction with H+ - important

Rapid detection

Stimulation results in increasing tidal volume

37
Q

Where are the peripheral respiratory chemoreceptor afferents located?

A

Carotid and aortic bodies

38
Q

What do the peripheral respiratory chemoreceptor afferents respond to? What is the result?

A

Respond to changes in decreased PaO2 and pH, increased PaCO2
- response increases ventilation

Very weak O2 response until PO2 falls below 60 mmHg, then respiration is increased primarily by increasing f

40% of ventilatory response

39
Q

Why are central chemoreceptors so sensitive to changes in pH? What are central chemoreceptors NOT sensitive to?

A

Central chemoreceptors respond to changes in [H+]

The blood-brain barrier is permeable to CO2

CSF has it’s own carbonic anhydrase (normal pH 7.32)

CSF has a lower protein concentration and therefore a lowered buffering capacity (response and change in pH is quicker)

Not sensitive to PO2 levels

40
Q

Generally, what is the ventilatory response to hypercapnia?

A

Proportional increases in ventilation to ‘blow off’ CO2

- slope of linear line depicting response will be smaller with higher PaO2

41
Q

Generally, what is the ventilatory response to hypoxemia?

A

Quick decline in ventilation after PaO2 passes 40 mm Hg PaO2 threshold

Increased PaCO2 will lead to ventilation being elevated for longer, but ventilation will still decline

42
Q

What can alter the magnitude of the ventilatory response to hypercapnia?

A

Being asleep (slight blunting)
Narcotics (blunts)
Anesthesia

43
Q

What contributes to increased PaCO2 in acute on chronic respiratory failure?

A
  1. Loss of stimulation of the peripheral chemoreceptors leading to reduced ventilation
    - Hypoxemia is partly responsible for driving respiratory rate
  2. Worsening of ventilation-perfusion mismatch
    - Loss of hypoxic vasoconstriction upon administration of 100% O2
  3. Haldane effect
    Administration of 100% O2 results in a higher release of CO2 from hemoglobin and subsequently higher PaCO2 levels
44
Q

Where I left off

A

slide 22, 23

Respiratory SOS (10 decks)

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