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Resp Physiology > Control of Ventilation > Flashcards

Control of Ventilation Flashcards

1
Q

Where is the basic pattern of breathing generated

A

Medulla oblongata

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2
Q

5 factors involved in sensory input

A
  1. Central chemoreceptors
  2. Peripheral chemoreceptors
  3. Irritant receptors
  4. Muscle stretch receptors
  5. Pulmonary srtetch receptors
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3
Q

What are the 2 discrete areas in the medulla oblongata

A
  1. Dorsal respiratory group
  2. Ventral respiratory group
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4
Q

What is control of breathing influenced by

A

Pneumotaxic centre - expiration

Apneustic centre

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5
Q

DRG NEURONS

  • ______ generator
  • involved in insp or exp
A
  • Rhythm generator
  • Basic resp patter for INSPIRATION
  • repetitive generation of ramps of neural activity
  • results in contraction of inspiratory muscles
  • abruptly shuts off at the end of inspiration (expiration is passive)
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6
Q

Where does the initial AP generation for breathing come from

A

Pre-Botzinger complex

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7
Q

Are DRG neurons stable or unstable

A

Intrinsically unstable

Capable of spontaneous depolarisation

Like the pacemaker of the SA node

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8
Q

How doe DRG neurons fire

A

APs via phrenic and IC nerves - stimulates diaphragm and external intercostals

=> thoracic cavity expands

=> -ve pressure

=> inspiration

Cells stop firing, inspiratory muscles relax, passive exp begins

(some DRG nerves extend into VRG)

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9
Q

What connects peripheral and joint chemoreceptors, lungs and airways to the DRG

A

Sensory impulses are carried in the vagus and glossopharyngeal nerves

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10
Q

What is the VRG responsible for

A

Inspiration and expiration

Augments ventilatory pattern - rhythm i.e. activity of DRG when resp drive is high

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11
Q

What does the VRG provide

A

powerful exp signals to abdominal muscles - ventilation under conditions of high demand (exercise)

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12
Q

Parasympathetic output of the VRG

A

Bronchioles (bronchoconstriction to decrease airflow)

Heart - inhibitory

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13
Q

What is the Pre-Botzinger Complex

A

Interneurons

Part of VRG

Resp rhythm generation

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14
Q

What does the PBC inhibit

A

VRG insp neurons

DRG insp neurons

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15
Q

What does the PBC stimulate

A

VRG exp neurons

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16
Q

2 components of the pontine resp group

A

Pneumotaxic centre

Apneustic centre

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17
Q

4 roles of the pneumotaxic centre

A
  1. Co-ordinates insp -> exp transition
  2. Prevents over-expansion of lungs
  3. Modifies acrtivity in VRG (exp) - directly promotes exp
  4. Modifies activity in apneustic centre - indirectly inhibits its promotion of insp
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18
Q

What switches off the ramping effect of insp

A

pneumotaxic area

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19
Q

What does the apneustic centre modify

A

DRG insp activity

Activates and prolongs insp - deepens breath

  • prolonged excitatory ramps
  • prolonged acitivity in the diaphragm
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20
Q

What is apneusis

Where is apneusis seen

A

Breathing pattern associated with apneustic stimulation

Deep gasping inspiration with a brief, insufficient release

Seen in damage to pons or upper medulla

e.g. stroke/trauma (quadriplegia), ketamine overdose

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21
Q

What neurons are in close proximity in medulla

A

Resp and CVS neurons in close proximity => HR variability in synchrony with resp

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22
Q

_____ ________ in the VRG triggers parasympathetic innervation to the _____ via _____ nerve

A

Nucleus ambiguus in the VRG triggers parasympathetic innervation to the heart via the vagus nerve

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23
Q

What does inspiration trigger

A

inhibitory signals in the nucleus ambiguus and consequently the vagus nerve remains unstimulated

=> HR increases

Conversely, in exp nucleus ambiguus neurons are activated and HR decreases

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24
Q

How does resp sinus arrythmia help with alveolar ventilation and perfusion

A

Improves efficiency of pulmonary gas exchange, which helps to match timing of alveolar ventilation and perfusion

Could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during ebb of perfusion

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25
Q

Where does the voluntary control of resp stem from

what is control via

A

cerebral cortex

controlled via pyramidal tracts but limited

  • bypasses resp centres
  • short term

automatic control will regain precedence especially PCO2

26
Q

What does the limbic system refer to

A

hypothalamus can influence ventilation

fear

pain

emotion

27
Q

What do chemoreceptors monitor

Vascularity

A

Blood chemistry

  • PaCO2
  • PaO2
  • pH

highly vascular

28
Q

Is there a lot of O2 removed from blood

A

Negligible removal of O2 from blood

29
Q

Hypercapnia response

A

Via central chemoreceptors - medulla

Stimulate increased activity from resp centres

Increased ventilation to decrease CO2

Not direct effect of CO2 rather H+

CO2 crosses BBB, H+ does not

Carbonic acid in cerebral spinal fluid

30
Q

Response divide between central and peripheral chemoreceptors

A

CENTRAL - 80%

PERIPHERAL - 20%

31
Q

Peripheral chemoreceptor response

A

PaCO2 increase => acidosis, due to increased [H+]

(not as strong a response as in CNS but 5x faster)

increase in medullary centre activity via glossopharyngeal and vagal nerves

Increase in ventilation => decrease in PaCO2

32
Q

What is the initial acute response to an increase in PaCO2

A

Increased ventilation

33
Q

What is the long-term adaptation of central chemoreceptors

A

Choroid plexus cells (form CSF) add HCO3- to CSF and remove H+ from blood

Added HCO3- to blood => increased CSF pH => inhibition of stimulus for increased ventilation

34
Q

What is the only NON-ADAPTING receptor in the body

A

Peripheral chemoreceptor - decreased PaO2 (hypoxia) drives respiration

35
Q

what happens when there is a prolonged elevation of PaCO2 (50-60 mmHg)

A

Adaptation of central chemoreceptors

36
Q

What is the driving force for respiration

A

Peripheral chemoreceptors - PaO2 (hypoxic drive)

37
Q

Why are COPD patients not treated with 100% O2

A

Potentially removes stimulus for respiration

O2 should not be with-held in hypoxaemic COPD patients as tissue oxygenation is over-riding priority but needs careful monitoring

38
Q

Are central chemoreceptors sensitive to PO2

A

NO - INSENSITIVE

39
Q

What do peripheral chemoreceptors mediate

When is there a response

A

Hypoxic response

Response when PaO2 drops to 60 mmHg

  • increased firing in peripheral chemoreceptors
  • increased resp centre activity
  • increased ventilation
  • increased PaO2
40
Q

How does hypoxia stimulate peripheral chemoreceptors

A

GLOMUS CELLS

O2 sensitive K+ channels

O2 sensor is on the ECF side

41
Q

Where are slowly adapting stretch receptors located

A

SM of longer airways

42
Q

What is the stimulus for SARs

A

Hyperinflation => rapid firing

continued inflation - slowly adapt to lower firing rate

43
Q

What are the effects of SARs

Where do they act

A

Prolonged expiration and shortened inspiration

Act directly on DRG

Indirectly on PONS

44
Q

What happens in conditions of altered lung mechanical properties

  • airway
  • SAR activity
A
  • Increased airway R - asthma, emphysema, mucus plugs etc
  • Increased SAR activity slows resp rate by lengthening expiration
45
Q

What is the Hering-Breuer reflex

A

INFLATION

Activated after large inflation > 1.2 L (exercise)

Lung inflation inhibits further inflation

reflex provided by SAr (afferent limb)

DEFLATION

Lung deflation prevents further deflation

HOWEVER adults have more prominent central responses/signals

46
Q

Where are rapidly adapting stretch reflexes/irritant receptors located

A

between epithelial cells

47
Q

What do RARs respond to

A

Mechanical and chemical irritant stimuli and to many inflammatory and immunological mediators

48
Q

What are RARs activated by

A

Lung distension or chemical and particulate irritants

  • lung oedema
  • emoblism
  • dust
  • cigarette smoke
  • ammonia
49
Q

What are the 2 effects of RARs

A
  1. Cough
  2. Increased inspiration via DRG - increased lung vol
50
Q

Short-term reflex of RAR

A

Rapidly adapts

SAR take over

Decreased lung volume

51
Q

What is sleep apnoea

A

Temporary suspension of breathing

52
Q

What are apnoeic episodes associated with

A

O2 de-saturation

53
Q

Obstructive sleep apnoea

A

Pharynx (usually held open by muscles that relax during sleep) collapses

Caused by excess fat deposits in soft tissue of pharynx or fat masses in the neck

Nasal obstruction

Enlarged tonsils

Large tongue

Certain shapes of palate

Gravity

54
Q

Central sleep apnoea

A

Less common

CNS signal to resp muscles stops completely

Damage to central resp centre or resp neuromuscular junctions

Can trigger seizures or sudden death

55
Q

What do the long silent periods of apnoea cause

A

Increase in PCO2

Decrease in PO2

56
Q

Treatment of sleep apnoea

A

Continuous Positive Airway Pressure

Most common

Keeps airways open by means of pressurised air

Nose or facial mask connective by flexible tube to CPAP machine

57
Q

Stimulus for immersion/diving reflex

A

Contact of head, face, resp tract with cold liquid

the colder the water, the stronger the physiological responses

58
Q

Result of immersion/diving reflex

A

Apnoea

Bradycardia

Laryngeal spasm

Peripheral vasoconstriction (not lungs, heart, brain)

59
Q

Afferent pathways for respiration

A

Via somatic sensory nerves of face and nasal cavity

Very active in infants up to 6 months - survive longer than adults when deprived of O2 underwater

60
Q

Importance of immersion reflex

A

Foetus in utero - breathing practice increases further into gestation

Totally immersed in liquid - active immersion reflex

61
Q

Advantages of immersion reflex

A

Prevents unnecessary resp movements

Relieves workload on the heart - bradycardia, hypotension

BF to vital organs (HLB) - selective vasoconstriction

Resp Physiology (9 decks)

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