Flashcards in L8 Control of respiration Deck (10):
What are the main sensory inputs/ output to the respiratory centre of the brain ?
1. The central & peripheral chemoreceptors (+)
2. pulmonary stretch receptors (-)
3. Peripheral receptors ( in muscles ) (+)
4. Input from reticular activation system, cerebral cortex, thalamus
5. Irritant receptor (-)
- phrenic nerve
What are the stimulatory and inhibitory respiratory centers? What is their function ? Location ?
STIMULATORY: ( mainly in medulla oblongata )
1. Dorsal respiratory group ( found in nucleus tractus solitarus )
- responsible on tider respiration ( at rest / mainly inspiration )
2. Ventral respiratory group ( found in ventrolateral region of the medulla )
- responsible on both forced inspiration and expiration
INHIBITORY: (mainly in pons )
What is the effect of oxygen on respiratory response to changes in co2?
The respiratory centre becomes more sensitive and respond to co2 changes if there is hypoxia
Why if you infuse someone with acids he will not hyperventilate immediately?
As 80% of respiration is controlled by central chemoreceptors which senses pH and CO2 in the surrounding brain tissue (brainstem interstitial fluid ) and CSF
However, acids (H+ and HCO3- ) can’t cross BBB rapidly so won’t affect the centre immediately
What does the slope and the position of a curve represent ? How they can be changed ?
1. Slope = sensitivity to CO2 changes ( changed by hypoxia )
2. Position = threshold to start response ( changed by pH )
How glomus cells respond to hypoxia ? What it will release ?
The mechanism is similar to hypoxic vasoconstriction... and it will release ATP and acetylcholine
Why the response to Co2 is linear whereas respond to O2 is curved ?
As Co2 is being sensed by central chemoreceptors directlyso there is no much delay
Whereas O2 is sensed by peripheral chemoreceptors ( glomus bodies ) which will take time to send the impulses to the brain by hering nerve ( by neurons indirectly)
What is the relation between oxygen level and ventilation response ?
At levels of oxygen tension less than 50 mmHg, a further decrease in arterial oxygen tension significantly increases ventilation.
At levels of oxygen tension close to 100 mmHg, changes have little effect on ventilation.
In Cheyne-Stokes breathing, what will increase the delay ?
1. severe reduction in the ejection fraction/cardiac output of the heart
–e.g. severe MI and unconsciousness
2. when there is injury to the brain, other mechanisms that normally buffer that don’t work properly.