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
what are the two types of chemorecptors?
central chemoreceprots in medulla
peripherial chemoreceptors in aortic and carotid bodies
why are central chemo receptors important?
they determine 70-75% of breathing impulses hence have a more important dominat role in determining resp rhythmn
how does crc indirectly respond to changes in arterial pco2
where are they located? what do they respond to?
why does it indirectly measure it?
Central respiratory chemoreceptors (CRC) located within the medulla (part of the brainstem) indirectly monitor 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 do not respond to blood pH directly, however arterial CO2 can pass through the blood-brain barrier into the CSF, where it will then react to produce carbonic acid, and the resulting H+ activates CRCs.
how does prc indirectly respond to changes in arterial pco2
what type of cells are in chemoreceptors? what activate the receptors?
Peripheral chemoreceptors consist of type-I glomus cells present 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, and signal to medullar centres to increase ventilation.
what is hypercanic drive?
why is this the case? (think of dominance)
Hypercapnic drive – ventilation is generally proportional to PaCO2
As crc is dominant which respond to H+ dominantly in csf, it generates the stimulus for maintaining a certain level of control of ventilation
hence vemtilation is generally proportional to the level of co2 within the body therefore more co2 means more ventilation to maintain homeostasis and keep PaCO2 within narrow limits
changing level of o2 compared to co2
changing levels of o2 has a secondary effect but is a lesser one compared to co2
Hypoxic drive – hypoxaemia (low PaO2)
when does this occur?
if co2 is maintained at a certain level + manipulate the partial pressure of o2 to be lower, there is a hypoxic drive where it stimulates increased ventilation
only happens at low po2
hypoxic drive in patients
seen in what kind of patients? what is the effect of this?
how will this affect ventilation and resulting effect on this?
individuals with severe chronic lung pathology (e.g. COPD) that are unable to ventilate respiratory structures sufficiently to get rid of adequate co2 hence co2 builds up in body over time becoming chronic
tolerant to that level of co2, no longer produce same effect on stimulatin ventilation. ). Central respiratory chemoreceptor responses are reduced in the presence of chronic hypercapnia due to homeostatic mechanisms that compensate for chronic acidification of the CSF and increase CSF pH back to normal levels, even in the presence of raised PaCO2
In such individuals, the level of ventilation is further reduced, resulting in very low PaO2 and PO2 taking on a predominant role in regulating/initiating ventilation.
ventilation decreases during sleep
why does ventilation decrease?
reasons?
Transition from wakefulness to sleep:
↓metabolic rate = ↓respiratory demands
Postural changes alter mechanics of breathing
↓SNS & ↑PNS tone = ↓HR, BP & CO.
↓tidal volume, ↓breathing frequency, ↓minute volume
↓SaO2 (≈96%), ↑PaCO2 (≈7kPa) hence more tolerant to lower levels of o2 and higher levels of co2
↓upper airway calibre
Pathology associated with dysfunction in central processes that initiate breathing
6 different reasons?
Trauma – damage to respiratory centres in the brainstem (gunshot)
Stroke – ischaemia-induced brainstem tissue injury (less blood supply and tissue death)
Drugs (e.g. opioids) – suppression of neuronal 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), e.g. Cheyne-Stokes respiration
Sleep apnoea
what is it? what is it characterised by? duration and frequency?
temporary cessation of breathing during sleep Characterised by >5 episodes per hour lasting >10 seconds.
Durations of apnoeas may be as long as 90 seconds and the frequency of episodes as high as 160 per hour.
sleep apnoea - effect on health
3 main effects?
Effects on health:
Tiredness (poor sleep quality)
Cardiovascular complications (stress + ↑SNS tone)
Obesity/Diabetes (inflammation + metabolic dysfunction)
Cheyne-Stokes respiration
what is it?
Cheyne-Stokes respiration is a particular abnormal breathing pattern and central sleep apnoea involving an oscillating pattern of apnoea and hyperpnoea.
complications of cheyne-stokes respiration
effect of osciliating patterns?
Periods of apnoea (with resulting hypercapnia and hypoxaemia) stimulate compensatory hyperventilation.
However due to underlying pathological circumstances (e.g. heart failure , brain injury, chemoreceptor dysfunction), the hyperventilatory response overcompensates, producing hypocapnia, respiratory alkalosis and a loss of respiratory drive, resulting in a subsequent period of apnoea
The cycle then begins again until it resolves or the individual is awoken
