Control Of Respiration Flashcards
Carbonic acid equilibrium
CO2 + H2O <—> H2CO3 <—> H+ + (HCO3)-
Carbonic acid equilibrium enzyme
Carbonic anhydrase
Requirement of respiration
- Ensure haemoglobin is as close to full saturation with oxygen as possible
- Efficient use of energy resource
-Regulate PaCO2 carefully
variations in CO2 and small variations in pH can alter physiological function quite widely
Breathing is autonomic
No conscious effort for the basic rhythm
Rate and depth under additional influences
Depends on cyclical excitation and control of many muscles
-Upper airway, lower airway, diaphragm, chest wall
-Near linear activity
-Increase thoracic volume
Input signals to respiratory control centres
Central chemoreceptor a
Voluntary control (cerebrum)
Lung receptors; stretch, J receptors, irritant
Peripheral chemoreceptors: carotid, aortic
Muscle proprioceptors
Respiratory control centres- basic breathing rhythm
Medulla and pons
3 types of Lung receptors
Stretch
J receptors
Irritant
Pons
Pneumotaxic and apneustic centres
Medulla oblongata
Phasic discharge of action potentials
2 main groups:
1. Dorsal respiratory group (DRG)
2. Ventral respiratory group (VRG)
Each are bilateral, and project into the bulbo-spinal motor neuron pools and interconnect
When is DRG active
predominantly active during inspiration
When is VRG active
active in both inspiration and expiration
Central pattern generator
Neural network (interneurons)
Located within DRG/VRG
-Precise functional locations not known
-Start, stop and resetting of an integrator of background ventilatory drive
What does desire to take a breath come from
PaCO2
Inspiration
Progressive increase in inspiratory muscle activation
-Lungs fill at a constant rate until tidal volume achieved
-End of inspiration, rapid decrease in excitation of the respiratory muscles
DRG and VRG prevent over inflation of the lungs
Expiration
Largely passive due to elastic recoil of thoracic wall
-First part of expiration; active slowing with some inspiratory muscle activity
-With increased demands, further muscle activity recruited
-Expiration can be become active also; with additional abdominal wall muscle activity
DRG and VRG prevent over deflation of the lungs
What % influence from PaCO2 on central chemoreceptors
60%
What % influence from PaCO2 on peripheral chemoreceptors
40%
Chemoreceptors
Stimulated by [H+] concentration and gas partial pressures in arterial blood
Brainstem [primary influence is PaCO2]
Peripheral chemoreceptors
Carotids and aorta [PaCO2, PaO2 and pH]
-Significant interaction
Central chemoreceptors
Located in brainstem
Pontomedullary junction
Not within the DRG/VRG complex
Sensitive to PaCO2 of blood perfusing brain (also influenced by PaO2)
Blood brain barrier relatively impermeable to H+ and HCO3-
PaCO2 preferentially diffuses into CSF
Carotid bodies
Bifurcation of the common carotid
Glossopharyngeal (IX) cranial nerve afferents
Aortic bodies
Ascending aorta
Vagal (X) nerve afferents
Peripheral chemoreceptors
Responsible for [all] ventilatory response to hypoxia (reduced PaO2)
Generally not sensitive across normal PaO2 ranges
When exposed to hypoxia, type I cells release stored neurotransmitters that stimulate the cuplike endings of the carotid sinus nerve
Linear response to PaCO2
Interactions between responses
[Poison (e.g. cyanide) and blood pressure responsive]
What are central chemoreceptors sensitive to
PaCO2
What are peripheral chemoreceptors sensitive to
PaO2, PaCO2 and pH
What mediates the response to CO2 by central chemoreceptors
H+ produced during the carbonic acid equilibrium bind to receptors and increase ventilation
Lung receptors
Stretch, J and irritant
Afferents; vagus (X)
Combination of slow and fast adapting receptors
Assist with lung volumes and responses to noxious inhaled agents