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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
Where does the voluntary control of resp stem from what is control via
cerebral cortex controlled via pyramidal tracts but limited - bypasses resp centres - short term automatic control will regain precedence especially PCO2
26
What does the limbic system refer to
hypothalamus can influence ventilation fear pain emotion
27
What do chemoreceptors monitor Vascularity
Blood chemistry - PaCO2 - PaO2 - pH highly vascular
28
Is there a lot of O2 removed from blood
Negligible removal of O2 from blood
29
Hypercapnia response
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
Response divide between central and peripheral chemoreceptors
CENTRAL - 80% PERIPHERAL - 20%
31
Peripheral chemoreceptor response
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
What is the initial acute response to an increase in PaCO2
Increased ventilation
33
What is the long-term adaptation of central chemoreceptors
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
What is the only NON-ADAPTING receptor in the body
Peripheral chemoreceptor - decreased PaO2 (hypoxia) drives respiration
35
what happens when there is a prolonged elevation of PaCO2 (50-60 mmHg)
Adaptation of central chemoreceptors
36
What is the driving force for respiration
Peripheral chemoreceptors - PaO2 (hypoxic drive)
37
Why are COPD patients not treated with 100% O2
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
Are central chemoreceptors sensitive to PO2
NO - **_INSENSITIVE_**
39
What do peripheral chemoreceptors mediate When is there a response
Hypoxic response Response when PaO2 drops to 60 mmHg - increased firing in peripheral chemoreceptors - increased resp centre activity - increased ventilation - increased PaO2
40
How does hypoxia stimulate peripheral chemoreceptors
GLOMUS CELLS O2 sensitive K+ channels O2 sensor is on the ECF side
41
Where are slowly adapting stretch receptors located
SM of longer airways
42
What is the stimulus for SARs
Hyperinflation =\> rapid firing continued inflation - slowly adapt to lower firing rate
43
What are the effects of SARs Where do they act
Prolonged expiration and shortened inspiration Act directly on DRG Indirectly on PONS
44
What happens in conditions of altered lung mechanical properties - airway - SAR activity
* Increased airway R - asthma, emphysema, mucus plugs etc * Increased SAR activity slows resp rate by lengthening expiration
45
What is the Hering-Breuer reflex
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
Where are rapidly adapting stretch reflexes/irritant receptors located
between epithelial cells
47
What do RARs respond to
Mechanical and chemical irritant stimuli and to many inflammatory and immunological mediators
48
What are RARs activated by
Lung distension or chemical and particulate irritants - lung oedema - emoblism - dust - cigarette smoke - ammonia
49
What are the 2 effects of RARs
1. Cough 2. Increased inspiration via DRG - increased lung vol
50
Short-term reflex of RAR
Rapidly adapts SAR take over Decreased lung volume
51
What is sleep apnoea
Temporary suspension of breathing
52
What are apnoeic episodes associated with
O2 de-saturation
53
Obstructive sleep apnoea
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
Central sleep apnoea
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
What do the long silent periods of apnoea cause
Increase in PCO2 Decrease in PO2
56
Treatment of sleep apnoea
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
Stimulus for immersion/diving reflex
Contact of head, face, resp tract with cold liquid the colder the water, the stronger the physiological responses
58
Result of immersion/diving reflex
Apnoea Bradycardia Laryngeal spasm Peripheral vasoconstriction (not lungs, heart, brain)
59
Afferent pathways for respiration
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
Importance of immersion reflex
Foetus in utero - breathing practice increases further into gestation Totally immersed in liquid - active immersion reflex
61
Advantages of immersion reflex
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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