Control of respiration Flashcards
what types of muscle are the diaphragm and intercostal muscles and what does this mean?
skeletal muscles
don’t contract unless stimulated by motor neurons
destruction of respiratory motor neurons
destruction or disconnection between origin and respiratory muscles leads to paralysis of respiratory muscles and death - unless artificial respiration
how is respiration initiated?
burst of action potentials in spinal motor neurons to inspiratory muscles
action potentials cease - inspiratory muscles relax, expiration occurs as elastic lungs recoil
exercise and expiration
neurons to expiratory muscles (facilitate expiration) start firing during expiration
control of neurons to respiratory muscles
medulla oblongata (medullary respiratory centre) dorsal respiratory group (DRG) ventral respiratory group (VRG)
DRG neurons
primarily fire during inspiration
input to spinal motor neurons that activate respiratory muscles - diaphragm (phrenic nerve C3,4,5) and external intercostal muscles (intercostal nerves)
VRG neurons
respiratory rhythm generated in pre-Boetzinger complex of neurons in upper VRG - pacemaker cells and neural network, acting together, sets basal respiratory rate
expiratory neurons
most important when large increases in ventilation are required
expiratory muscles contract
quiet breathing
respiratory rhythm generator activates inspiratory neurons in VRG - depolarise inspiratory spinal motor neurons - inspiratory muscles contract
stop firing, relax, passive expiration
increases in breathing
inspiratory and expiratory neurons and muscles alternate in function
pons location and function
above medulla oblongata
sends synaptic input to finetune output of medullary inspiratory neurons and helps terminate inspiration by inhibiting them
apneustic centre
lower pons
finetunes output of medullary inspiratory neurons
terminates inspiration by inhibiting them
pneumotaxic centre
upper pons
modulates activity of apneustic centre
smooths transition between inspiration and expiration
synaptic input from higher areas of the brain
pattern of respiration is controlled voluntarily during speaking, diving, emotions and pain
pulmonary stretch receptors
lie in airway smooth muscle layer
activated by large lung inflation
Hering-Breuer reflex
action potentials in afferent nerve fibres from stretch receptors travel to brain and inhibit medullary activity - feedback from lungs helps terminate inspiration by inhibiting inspiratory nerves in the DRG
only in large tidal volumes
sensitivity of medullary inspiratory neurons
sensitive to inhibition by drugs - barbituates and morphine. death by cessation of breathing
peripheral chemoreceptors
high in neck at bifurcation of common carotid arteries (carotid bodies) and on the arch of aorta (aortic bodies). close to arterial baroreceptors and contact the arterial blood.
composed of specialised receptor cells stimulated by decrease in P02 and increase in [H+] and increased PCO2.
excitory input to inspiratory neurons.
predominant carotid input.
central chemoreceptors
located in medulla.
excitatory synaptic input to medullary inspiratory neurons. #stimulated by increased PCO2 and increased [H+] of extracellular fluid.
control of ventilation by P02
little increase in ventilation until O2 conc is reduced to 60mmHg - after this, there’s a large increase
mediated by peripheral chemoreceptors - increased rate of charging -> increased number of action potentials travelling up afferent nerve fibres and stimulating medullary inspiratory neurons
increased CO2 consequences
increase in alveolar CO2 - diffusion gradient is reversed and arterial CO2 increases
~40mmHG+ arterial CO2 increases ventilation
emphysema and CO2
causes people to retain CO2 - increase in arterial CO2
decreased CO2
removes stimulus for ventilation - metabolically produced co2 accumulates and returns back to normal
CO2 and H+
increased CO2 increases H+
affects peripheral and central chemoreceptors
most important chemoreceptors in regulation of CO2
central - 70% of increased ventilation
effects of increased co2 and decreased o2
potentiate each other’s effects - acute ventilatory response to combined co2 and o2 is greater than sum of individual responses
other symptoms of high blood co2
severe headaches, restlessness, dulling or loss of conciousness
retention of co2
respiratory acidosis
excessive elimination of co2
respiratory alkalosis
metabolic acidosis
increase in H+ not due to primary change in co2
metabolic alkalosis
decrease in H+ not due to primary change in co2
major chemoreceptors involved in altering ventilation in metabolic acidosis/alkalosis + example
peripheral chemoreceptors
addition of lactic acid to the blood (strenuous exercise) causes hyperventilation by mostly stimulation from peripheral chemoreceptors
flow chart of change in H+ conc in blood
production of non co2 acid
increased arterial [H+]
increased firing of peripheral chemoreceptors
increased contraction of respiratory muscles
increaesed ventilation
decreased alveolar and arterial co2
return of arterial [H+] towards normal
chemoreceptors and H+ conc
not involved much due to brain [H+] only increasing a small amount, as it penetrates the blood-brain barrier very slowly
co2 penetrates blood-brain barrier rapidly
decrease of [H+]
ventilation is depressed due to decreased peripheral chemoreceptor output
e.g. loss from vomiting
why is maintenance of normal arterial H+ necessary?
most enzymes of the body function best at physiological pH
