neural control of breathing Flashcards
why is there a need to modulate the rate of ventilation?
how is this achieved?
The rate of ventilation is constantly adjusted to meet the body’s demand for O2 and production of CO2. Adequate absorption of O2 and expulsion of CO2 to/from the body is achieved by maintaining pressure gradients between alveoli & blood.
(breathing as hard as you can all the time is inefficient)
In what circumstances does O2 demand and/or CO2 production increase?
main circumstance and why? other circumstances?
Demand for O2 (and CO2 production) increases during physical activity
↑activity = ↑ATP production = ↑VO2 (VO2 = volume of oxygen consumed)
and during infection, injury or metabolic dysfunction.
VO2 in healthy rats < rats subjected to burns < rats subjected to burns + infection.
How does breathing change to modulate the rate of ventilation?
what does rate of ventilation depend on?
what is dead space volume and what is it determined by?
what is manipulated to increase or decrease ventilation?
rate of ventilation depends on tidal volune, dead space volume and breathing frequency
dead space volume is always the same + determined by the physical structure of the resp system (around 150ml)
other 2 factors are manipulated to increase or decrease ventilation
hence increased ventilation due to increased o2 consumption will have BOTH increased tidal volume + increased breathing frequency
How is ventilation related to cardiac output?
Why is this the case?
Ventilation increases alongside cardiac output to increase total O2 transported
Hb is 98% saturated at rest, hyperventilating alone has little effect on O2 delivery. (o2 stauration doesnt change with increased o2 consumption either)
In healthy, exercising individuals, increased O2 delivery achieved by increasing cardiac output, not PaO2
why does ventialtion alone have little effect on o2 delivery?
RBC can only carry so much o2 which is determined by quantity + conc of haemoglobin (haemoglobin is usally 98% saturated in normal situation) hence increased breathing doesn’t increase o2 supply as blood is already full of o2
hence to get more o2 in body, you need to increase BOTH ventilation and CO (HR increases as o2 consumption increases)
Resp muscles and neural pathway
why do resp muscles need neural pathways?
general pathway?
Respiratory muscles provide the movement required for ventilation.
As resp. muscles consist of skeletal muscle, they require neural inputs/stimulation to contract.
Contractile signals are initiated within the brain and descend via spinal tracts, which synapse with the lower motor neurons that innervate the respiratory muscle tissue
effect on spinal cord injury for breathing
how does location affect effect?
Impact depends on where the injury occured
if very high e.g. c2, then it is above the area the motor neuron synapse goes to any muscle hence all breathing ability is lost
if it is low, maybe only the intercostal muscles could be lost hence preserve some breathing
effect of motor neurone disease on breathing
body won’t be able to carry signal hence can’t innervate the muscle and won’t be able to breathe properly
respiratory failure = cause of death
effect of muscular dystrophy on breathing
muscle degeneration to the point where it is too weak to generate the force necessary to expand the chest + expand the lungs
respiratory failure = cause of death
muscles used for quiet breathing
inspiration and expiration?
inspiration
diaphragm
expiration elastic recoil (not muscles needed)
muscles used for forced inspiration/expiration
Inspiration
resp - external intercostal muscles
acessory - pectorals, sternomastoid, scalene
expiration
resp - elatsic recoild + internal intercostal
accessory - abdominals
How is the the basic pattern of ventilation (i.e. how often to breath and how deep) determined?
where and what determines the pattern?
what does it do?
Determined by a complex system of neurons within the brainstem (the medulla and pons) called the central pattern generator (CPG),
sometimes also referred to as the ‘respiratory pattern generator’ (RPG).
sending and not sending signals to resp muscles to contracts acts as a metronome for breathing
AP generation is autogenerating but different to pacemaker in heart
How does the Central Pattern Generator determine the rate & depth of breathing?
The behaviour of this system is modulated by afferent inputs from various receptors and sensors within the body, which provide feedback regarding the necessary level of ventilation required to maintain healthy CO2, O2, and pH levels.
Different inputs that go to the central pattern generator
4 different inputs?
how do they affect the central pattern generator?
chemoreceptors detecting co2 and H+
stretch receptors in the lung to make sure that you don’t over-inflate the lungs hence if the lungs has too much volume where it becomes dangerous, an inhibitory signal is essential to stop further contraction of the muscle
emotional sense in the brain like the limbic system, intense emotional stimuli e.g panic attack can cause respiratory problems/symptoms therefore increase breathing rate
input from higher centres - breathing to an extent is voluntary as you can choose when you breathe in and out to a certain degree but if you hold your breath and faint, higher centres take control
The CPG integrates data from various neuronal inputs to regulate ventilation
what is the general theory?
waht are the two groups and what do they affect?
Our understanding of how the central pattern generator functions is complex and incomplete. It has been posited that within the medulla there are two, opposing groups of respiratory neurons that signal to different respiratory muscles to initiate inspiration or expiration .
Reciprocal inhibition also exists so that inspiratory neuronal activation signals via interneurons to inhibit expiratory neurons.
dorsal resp group - inspiration
ventral resp group - expiration
