Control of Respiration Flashcards

1
Q

What nerve supplies the diaphragm

A

Phrenic Nerve

originates from C3,4,5

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2
Q

Which area of the brain controls breathing and also contains major cardiovascular control?

A

Medulla Oblongata

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3
Q

Name the 2 anatomical components of the medullary respiratory centre

A
  1. Neurons of Dorsal Respiratory Group (DRG)
    - primarily fire during inspiration & hv input to spinal motor neurons that activate respiratory muscles involved in inspiration (diaphragm & external intercostal muscles)
  2. Neurons of Ventral Respiratory Group (VRG)
    - upper part contains respiratory rhythm generator in pre-Botzinger complex
    - rhythm generator composed of pacemaker cells and complex neural network that when acting tgt, set basal respiratory rate
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4
Q

What are the 3 structures that make up the respiratory centre?

A
  1. Medulla (Dorsal Respiratory Group (DRG) & Ventral Respiratory Group (VRG))
  2. Pons (Pontine Respiratory Group (PRG))
  3. Cerebral Cortex (Voluntary Override)
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5
Q

What is the main function of DRG (Dorsal Respiratory Group) and where is it located

A

Location:
-Bilaterally in dorsal portion of medulla

Main function:

  • initiates respiratory rhythm
  • determines timing of respiratory cycle
  • output from DRG to spinal motor neurons that activate diaphragm (Phrenic nerve C3,4,5) and intercostal muscles (intercostal nerves T1-11)
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6
Q

What is the main function of VRG (Ventral Respiratory Group) and where is it located

A

Location:
-each side of medulla, lateral to DRG

Main function:

  • forced expiration by activating motor neurons to cause expiratory muscles to contract
  • respiratory rhythm generator in pre-Botzinger complex of neurons in upper part of VRG. Generator made of pacemaker cells and complex neural network to set basal respiratory rate. Generator activate inspiratory neurons in VRG tht depolarise inspiratory spinal motor neurons to inspiratory muscles contract
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7
Q

What are the 2 parts of the Pontine Respiratory Group (PRG)

A

Penumotaxic Centre

Apneustic Centre

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8
Q

What are the roles of the Pneumotaxic Centre and Apneustic Centre in PRG

A

Pneumotaxic Centre (in upper pons):

  • regulates and can sometimes override apneustic centre
  • ensures smooth transition btwn inspi and expi
  • limits inspi: switches off DRG (inspiratory neurons) signals to prevent hyperinflation so expiration can happen
  • also: increases breathing freq & decreases TV

Apneustic Centre (in lower pons):

  • fine-tuning output of DRG (inspiratory neurons)
  • prolongs inspiration: continues to activate inspiratory neurons to inhibit expiration
  • also: decreases breathing freq & increases TV
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9
Q

What do the Upper Respiratory Tract’s chemo and mechano receptors do?

A

Respond to toxins, irritants and temperature

Nose, nasopharynx, larynx: chemo and mechano receptors: some sense and monitor flow and inhibit the central controller (eg. medullary respiratory centre)

Pharynx: activated by swallowing to prevent respiratory activity from occurring during swallowing to prevent risk of aspiration of food/ liquid

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10
Q

What are the two Pulmonary Stretch Receptors (PSRs) that deal with lung reflexes?
Describe each of them and what they do

A
  1. Slowly Adapting Stretch Receptor (SASRs)
    - myelinated
    - sensitive to inflation/ deflation
    - activated by lung distenesion
    - in airway smooth muscles
    - maintains persistent/ slowly decaying receptor potential during constant stimulus so APs are initiated in afferent neurons during duration of stimulus
    - high activity = inspiration inhibited so expiration begin
    - if inflation maintained, they adapt to low frrq firing
  2. Rapidly Adapting Stretch Receptors (RASRs)
    - myelinated
    - sensitive to TV, frez or lung compliance
    - activated by lung distension and irritants
    - found btwn airway epithelial cells
    - generate a receptor potential & AP at onset of stimulus but quickly stops responding
    - produces brief burst of activity
    - high activity = bronchoconstriction
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11
Q

Describe C Fibres J Receptors that are a part of the mechanical stimulation of respiration

A
  • non-myelinated
  • in capillary walls/ interstitium
  • stimulated by increase in lung interstitial pressure caused by fluid accumulation in interstitium (eg. in occulsion of pulmonary vessel like pulmonary emobolism or left ventricular heart disease and strenous activity)
  • Activity results in: rapid breathing (tachypena), shallow breathing, bronchoconstriction, cardiovascular depression & dry cough
  • also cause sensation of pressure in chest and dyspnea (feeling that breathing is diff and laboured)
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12
Q

What is the role of Central Chemoreceptors that are located in the medulla

A
  • provide excitory input to medullary inspiratory enurons
  • activated when pCO2 in blood is high causing H+ conc in CSF to increase
  • however, blood-brain barrier is relatively impermeable to H+ but CO2 can diffuse through into CSF
  • if arterial pCO2 increase, some of the extra CO2 diffuse into CSF (as bicarb reaction) so more H+ in CSF and change in pH detected by central chemoreceptors
  • Medullary inspiratory neurons stimulated to increase ventilation
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13
Q

What is the role of Peripheral Chemoreceptors (carotid bodies and aortic bodies) located in the neck at the bifurcation of the common carotid arteries and in the thorax on the arch of the aorta.

A
  • in close contact w/ arterial blood but are different from arterial baroreceptor though they are quite close to each other
  • CAROTID: monitor O2 supply to brain, is the predominant peripheral chemoreceptor for respi
  • composed of specialised receptor cells stimulated by decrease of arterial pO2 and increase of H+ conc (CO2 transported in bicarb). Type II cells here release stored neurotransmitters that stimulate carotid sinus nerve when hypoxia (low O2) levels are detected.
  • Provides excitory synaptic input to medullary inspiratory neurons to increase ventilation when high H+ conc
  • not sensitive to small reductions in arterial pO2 but only when it is close to 60mmHg (90% sat) cuz O2 transport in blood not reduced much until pO2 below 60mmHg so not much O2 would be added to blood until that point is reached
  • same for CO cuz CO doesn’t affect am of O2 dissolved in blood or diffusion capacity of lung so arterial pO2 unaltered
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