BPK 305 - Lecture 32

respiratory system components

1. central pattern generator

2. sensors

3. integrators

4. effectors

central pattern generator

- in the respiratory control center

- generates a ventilation pattern, and the RCC integrates central and peripheral input information

sensors

to determine PaO2, PaCO2, and arterial [H+] , as well as stretch

respiratory sensors

a. Central chemoreceptors

b. Peripheral chemoreceptors

c. Pulmonary mechanoreceptors

d. Pulmonary sensory nerves

integrators

- automatic and voluntary control

- motor neurons to resp. muscles

effectors

specific respiratory muscles

main areas for respiratory control

1. medulla

2. Apneustic centre

3. Pneumotaxic centre

medulla respiratory centre subgroups

- Dorsal respiratory group

- Ventral respiratory group

where is the dorsal respiratory group?

nucleus tractus solitarius

what does the dorsal respiratory group do?

- process afferent input

- mainly inspiratory neurons

- generate rhythmic activity

where is the ventral respiratory group?

• nucleus retroambiguus

• nucleus retrofacialis

• nucleus paraambiguous

what does the ventral respiratory group do?

- coordinate efferent (motor) output

- inspiratory and expiratory neurons

apneustic center

lengthens inspiration (short expirations and large lung volume)

Pneumotaxic centre

-shortens/inhibits inspiration

- regulates rate and depth of breath

central controllers in the pons

modulate, but are not essential for functional respiration

Central control of ventilation: rhythmicity

Inspiration:

- phrenic nerve output to diaphragm increases over 0.5 - 2s (allows for smooth inflation)

Expiration:

- after a brief burst, phrenic nerve is inactive

central chemoreceptors

• on ventrolateral surface

of medulla

• heavily influenced by CSF pH

neurons stimulated by acidosis

- tend to be

serotonergic (excitatory)

- closely associated with basilar artery

neurons inhibited by acidosis

tend to be GABAergic

what is SIDS sometimes associated with?

reduced

serotonergic fibres in the medulary raphe

what does CSF acidosis do?

- stimulates ventilation

- Strong acute ventilatory response

- respiratory ∆ pHart has greater effect than metabolic ∆ pHart on pHCSF

- due to low BBB permeation by HCO3

what does CSF pH modulate?

sensitivity to PCO2

what does metabolic acidosis do?

increases central

CO2 sensitivity

aortic and coratid bodies

• High perfusion ( 40x > brain/weight )

• Respond to changes in PaO2, PaCO2, pH

what are the aortic and carotid bodies responsible for?

- only sensor for O2

- responsible for ~40% of the ventilatory response to CO2

glomus cells

- sense O2, CO2, H+

- ↑ [H+] (↑CO2) → K+ channel(s) inhibition

- O2-sensitive K+ channel inhibition

- Secretory vesicles containing neurotransmitters

afferent fibres for peripheral chemoreceptors

- carotid sinus nerve and glossopharyngeal (from carotid body)

- vagus nerve (from aoritc body)

peripheral chemoreceptors response to PO2

- ↓ PO2 alone = increased firing frequency of neurons

in the carotid bodies

- ↑ PO2 alone = little effect on firing

- ↑ PCO2 and ↓ pH = ↑ sensitivity to PO2

peripheral chemoreceptor response to PCO2

↑ PCO2 alone = increased firing rate

peripheral chemoreceptor response to pH

↑ H+ alone = ↑ firing rate at all PCO2 values tested

what are carotid bodies sensitive to?

- hypoxia

- both components of respiratory acidosis

- acidosis increases sensitivity to O2

Glomus cell response to ↓PO2, ↑PCO2, ↓pH

- decreased PO2 increases cAMP and increases reduced glutathione

- decreased pH stops Na-H exchanger which increases H+

- increased PCO2 increased H+

- these changes inhibit the K+ channel and increased RMP

- Ca enters the cell an released neurotransmitters on the glossopharyngeal nerve

low PO2 response

- Peripheral chemoreceptors increase

ventilation

- Increases sensitivity to CO2/pH changes

high PaCO2 response

- ↑ ventilation via peripheral & central

chemoreceptors

- Ventilation most sensitive to PaCO2

- Increases sensitivity to PaO2

Hering-Breuer inspiratory inhibitory

reflex

• inspiratory-inhibitory reflex due to increased lung volume

• vagus-to-medulla "off-switch" neurons

• not active in quite breathing in adults

• may regulate tidal volume in in infants

• uses Slowly adapting pulmonary stretch receptors

driving reflex

• cold water activates nasal/facial receptors

• causes breath hold & bradycardia

• protects against aspirating water

sniff reflex

• mechanoreceptors in pharynx / nasopharynx → short & sharp inspiration

• draw material to pharynx for swallow or expectoration

• prevents breathing during swallowing

sigh/yawn

Stimulates surfactant release. Re-opens atelectatic alveoli

Sensory receptors in the tracheobronchial tree

• irritant receptors - cause cough reflex

• stretch receptors - delay next inspiration

somatic receptors

• intercostal muscles, rib joints, tendons

• respond to changes in muscle length and tension

Cheyne-Stokes breathing

• Changing tidal volume and breathing frequency

• Seen with CNS diseases, head trauma, and in

healthy people at altitude

• Likely due to abnormal/slow cerebral blood flow

Apneustic breathing

• Sustained periods of inspiration with

only brief expiration

• Due to loss of inspiratory inhibition

control with CNS damage

sleep apnea

• Unusually prolonged pause in breathing

• Long enough to change PaCO2, PaO2

• Either obstructive or central sleep apnea

• can cause ↑ risk of cardiovascular disease, obsesity, cancer

Ondine's curse

• No automatic breathing control

• aka - Primary Alveolar Hypoventilation

• cause: congenital or brainstem trauma

• usually requires mechanical ventilation or phrenic nerve pacemaker