Neural control of breathing Flashcards
(25 cards)
why is there a need to modulate the rate of ventilation
-the rate of ventilation adjusted constantly 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 and blood.
In what circumstances does O2 demand and/or CO2 production increase
-demand for O2 (and CO2 production) increases during physical activity
-during infection, injury or metabolic dysfunction:
* rates that had burn injuries had a greater demand of oxygen consumption
how does breathing change to modulate the rate of ventilation
-depends on; tidal volume, dead space volume, breathing frequency
-dead space volume determined by physical structure in resp system
Explain what hapens if the rate of ventilation is increased/decreased
-to increase overall level of ventilation both tidal and breathing frequency increase together, enables to get more O2 into the body
-just increasing ventilation won’t increase O2 supply into body- alongside increases in resp function
-CVS also needed to increase its function to increase overall O2 transport in order to get O2 to respiring tissues.
explain unit volume of blood
unit volume of blood can only be able to carry a finite amount of O2, Hb is 98% saturated so just increasing breathing doesn’t increase O2 supply—> to get more O2 to lung/tissue you need to increase ventilation and cardiac output (exercise)
what physiological process initiates breathing?
1) respiratory muscles provide the movement required for ventilation
2) as resp. muscles consist of skeletal muscle —> they require neural inputs/stimulation to contract
3) innervation from motor neurons synapsing from descending spinal tracts provide the contractile signal.
4) skeletal muscle to contract needs neural input from innovating neuron (motor) they recieve electrical signals from brain to spinal cord and to diaphragm intercostal etc\
5) impulse is from CNS
6) if pathwway is impaired/damaged it will impact on ability for resp. muscle to be activated so impact on ability of individual to breathe
what would happen if the injury was serious
-if injury was serious, C2 above the motor neuuron synapse with spinal cord source and all breathing ability is lost muscle recieving the innocation wouldn’t be able to contract —> if lower than maybe only certain muscles will stop like the diaphragm
explain motor neuron disease
motor neuron disease- individual wouldn’t be able to breathe due to degeneration resp. failure kills them
which muscles are utilised in quiet/force inspiration/expiration
inspiration:
quiet breathing; diaphragm
force inspiration/expiration; external intercostals, pectorals, sternomastoid, scalene
expiration:
quiet breathing; elastic recoil
force inspiration/expiration; elastic recoil (intercostals), abdominals
explain how the basic breathign pattern is generated
-the basis breathing pattern is generated by neuronal systems within the brainstem:
PGR= pontine respiratory group
DRG= dorsal respiratory group
VRG= ventral respiratory group
explain the series of circuitry of neural systems in the brainstem
-extremely dense of complicated network of neural circuits that act as a computer and takes inputs from different parts of the body; different types of input (sensory input, input from chemoreceptors)
-they will tell you how much O2 there is in the blood or how much CO2/what the pH of the blood is
-integrates all this info into resp. pattern
-diaphragm contracts and sends signals to other muscles ; creates resp pattern
How does the central pattern generator determine the rate and depth of breathing?
-the medulla and pons recieve signals about the rate and depth of breathing
-central chemoreceptors (in the brain); detect changes in H+ and CO2 and they send signals to the brain
-peripheral chemoreceptors (in the blood vessels); detect low O2 and high CO2 and H+ and send signals to the lungs to increase breathing
-receptors in muscles and joints
-there are stretch receptos and irritant receptors in the lungs
explain how the CPG integrates data from various neuronal inputs to regulate ventilation
the stimuli affecting ventilation are:
-emotions and voluntary control
the integrating centres are:
-higher brain centres
-limbic system
sensors that detect the stimuli are:
-medullarly chemoreceptors
-carotid and aortic chemoreceptors
-afferent sensory neurones
efferent neurones are:
-somatic motor neurons (inspiration)
-somatic motor neurons (expiration)
effectors are:
-scalene and sternocleidomastoid muscles
-external intercostals
-diaphragm
-internal intercostals
-abdominal muscles
explain how central chemoreceptors respond to changes in arterial PCO2
-central respiratory chemoreceptors (CRC) presents in the medulla indirectly monitor changes in arterial CO2
-although CRC respond to changes in [H+] within cerebrospinal fluid, as H+ does not cross the blood brain barrier. CRC does not directly respond to changes in blood pH (except via CO2)
explain how negative feedback can regulate level of ventilation
by negative feedback able to regulate level of ventilation- if CO2 levels increase so does activation of chemoreceptrs will increase so there will be more acid
explain characteristics of central respiratory chemoreceptors (CRC)
CRC is located within the medulla, indirectly monitors changes in PaCO2 by responding to changes in the pH of the cerebrospinal fluid (CSF). Whilst an increase in PaCO2 will also decrease blood pH, H+ present within arterial blood cannot pass through the blood-brain barrier as they are charged.
-therefore CRC does not respond to blood pH directly —> however arterial CO2 can pass through the blood-brain barrier into the CS, where it will then react to produce carbonic acid
-the resulting H+ activates CRCs. This CRC response to PaCO2 provides the predominant signal involved in regulating ventilation and initiating the urge to breathe
explain characteristics of peripheral chemoreceptors
-peripheral chemoreceptors are located in the blood stream and detect changes in low 02 and high CO2 + H+.
-peripheral chemoreceptors consist of type 1- glomus cells presentt with carotid and aortic bodies, which detect levels of O2, CO2 and pH within arterial blood. Peripheral chemoreceptors are activated by low O2, high CO2 and low pH
-this signals to the medulla centres to increase ventilation
-peripheral chemoreceptors respond to changes in arterial O2, CO2, and pH
explain when carotid bodies and aortic bodies are activated
-activated by decrease in PaO2, increase in PaCO2 and acidaemia
-signal to respiratory centres in the medulla (via sensory nerves) to increase ventilation (negative feedback)
explain what central chemoreceptors repsond to
central chemoreceptors only respond to CO2- hypercapnic drive, controls level of ventilation which is proportional to the CO2 in the body
-whilst oxygen has a role, if manipulate level of O2 in body- has a secondary effect (lesser effect though)
explain the term hypoxic drive
hypoxic drive- chronic resp. disease:
-unable to breathe at a good rate so CO2 builds up and becomes tolerant to CO2 so doesn’t have a lasting effect on their respiration
explain the transition from wakefulness to sleep
-decrease metabolic rate= decrease respiratory demands
-postural changes alter mechanics of breathing
-decrease DNS and increase PNS tone= decrease HR, BP and CO
-decrease tidal volume, decrease breathing frequency, decrease minute volume
-decrease SaO2 (around 96%), increase PaCO2 (around 7kPa)
-decrease in upper airway calibre
explain the pathology associated with dysfunction in central processes that initiate breathing
trauma —> damage to respiratory centres in the brainstem
stroke —> ischaemia- induced brainstem tissue injury
drugs (i.e. opiods) —> suppresson of neural activity
congenital central hypoventilation syndrome
-neonates —-> incomplete development of respiratory centres prior to birth
altitude—> control systems unable to cope with abnormal atmospheric environment (i.e. low O2 and low CO2)
explain the characteristics of sleep apnoea
sleep apnoea= temporary cessation of breathing during sleep
-characterised by >5 episodes per hour lasting >10 secs
-durations of apnoea may be able as 90 secs and the frequency of episodes as high as 160 per hour
effects on health:
-tiredness (poor sleep quality)
-cardiovascular complications
-obesity/ diabetes (inflammation + metabolic dysfunction)
