Neural Control of Breathing Flashcards
How is breathing initiated?
→ Neural activation of respiratory muscles which provide the movement required for ventilation
What do respiratory muscles consist of?
→ Skeletal muscle
What do respiratory muscles require to contract?
→Neural inputs/stimulation to contract
What provides the contractile signal?
→ Innervation from motor neurons synapsing from descending spinal tracts
Which muscles (including accessory muscles) are utilised in quiet/ forced inspiration and expiration?
INSPIRATION:
→quiet breathing: diaphragm
→increased/ forced ventilation: external intercostal muscles (pectorals, sternomastoid and scalene muscles as accessories)
EXPIRATION:
→quiet breathing: elastic recoil
→increased/ forced ventilation: elastic recoil and internal intercostal muscles (abdominal muscles as accessories)
How are basic breathing patterns generated?
→ By neuronal systems within the brainstem
What is the PRG?
→ Pontine respiratory group
→modulate response to hypercapnia, and hypoxia
What is the DRG?
→ Dorsal respiratory group
→stimulates inspiratory movements.
What is the VRG?
→ Ventral respiratory group
→stimulates expiratory movements.
What are the signals that the CPG receives?
→ pH of arterial blood → Amount of CO2 and O2 in arterial blood →Current lung volume → How stretched the lungs are → The CPG(central pattern generator (CPG) integrates data from these various neuronal inputs to regulate ventilation
What does the CPG do with these signals?
→ Integrates data from these neuronal inputs to regulate ventilation
Where are the CRC (central chemoreceptors) found?
→ In the medulla
What do CRC do?
→ Indirectly monitors changes in arterial CO2
Why doesn’t the CRC directly respond to changes in blood pH?
→ Responds to changes in H+ within the cerebrospinal fluid
→ H+ cannot cross the blood brain barrier so CRC cannot directly respond to changes in pH
Where are peripheral chemoreceptors found?
→ In the aortic body and carotid
What do peripheral chemoreceptors detect?
→ Changes in blood oxygen and CO2, but not pH
→ Activated by ↓PaO2, ↑PaCO2 and acidaemia
→ Signal to respiratory centres in medulla (via sensory nerves) to increase ventilation (negative feedback).
What is the hypoxic drive?
→Increased ventilation in response to decreased PaO2
What is sleep apnoea?
→ temporary cessation of breathing during sleep
→ Characterised by >5 episodes per hour lasting >10 seconds.
What are 4 causes of sleep apnoea?
→ Stroke
→ Drugs- suppression of neuronal activity- brainstem function is inhibited
→ Central hypoventilation syndrome
→ Altitude- control systems unable to cope with abnormal atmospheric environment (i.e. low O2 and low CO2), e.g. Cheyne-Stokes respiration
What are the 3 categories of sleep apnoea?
→ Central- when the brain temporarily stops sending signals to the muscles that control breathing
→ Obstructive- muscles that support the soft tissues in the upper airway relax during sleep and block the normal flow of air in and out of the nose and mouth.
→ Mixed
What is Cheyne- stokes respiration?
→ Oscillating hyperpnoea and apnoea
→ Hypercapnia→ Compensatory hyperventilation→ Hypocapnia + alkalosis→ ↓respiratory drive→ Compensatory hypoventilation→
Hypoxaemia
How does Cheyne-stokes respiration occur?
→ Apnoea causes compensatory hyperventilation
→ Hyperventilation overcompensates producing hypocapnia
→the hyperventilatory response overcompensates, producing hypocapnia, respiratory alkalosis and a loss of respiratory drive
Why is it impossible to asphyxiate yourself?
→ Urge to breathe caused by excess CO2 will be overpowering
→ Acute hypoxaemia results in loss of consciousness ( involuntary breathing begings)
Why is there a need to modulate the rate of ventilation?
→ rate of ventilation is constantly adjusted to meet the body’s demand for O2 and production of CO2
In what circumstances does O2 demand and/or CO2 production increase?
→ Demand for O2 (and CO2 production) increases during physical activity…..
→ …..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?
Increases tidal volume
→ breathing frequency
→ increased minute ventilation
How is total O2 transported increased?
→ Ventilation increases alongside cardiac output
→ increased O2 delivery achieved by increasing cardiac output, not PaO2
→ A unit volume of blood can contain finite O2 so just increasing breathing does not increase O2 supply so you need to increase ventilation and cardiac output
What happens to metabolic rate, SNS, PNS tone during sleep?
↓metabolic rate = ↓respiratory demands
→ ↓SNS & ↑PNS tone = ↓HR, BP & CO
What happens to tidal volume, breathing frequency, and minute volume during sleep?
↓tidal volume, ↓breathing frequency, ↓minute volume
What happens to SaO2 and PaCO2 and upper airway calibre during sleep?
↓SaO2 (≈96%), ↑PaCO2 (≈7kPa)
↓upper airway calibre
What are the effects of apnoea on heath?
→ Tiredness (poor sleep quality)
→ Cardiovascular complications (stress + ↑SNS tone)
→ Obesity/Diabetes (inflammation + metabolic dysfunction)- feedback loop
How does the Central Pattern Generator determine the rate & depth of breathing in hyperventilation?
→ increased ventilation rate will remove too much carbon dioxide from their body
→chemoreceptors detect this change,
→send a signal to the medulla, which signals the respiratory muscles →to decrease the ventilation rate so carbon dioxide levels and pH can return to normal levels.
What happens to regulate breathing in someone with diarrhoea and hence acidosis?
→loses a lot of bicarbonate in the intestinal tract,
→decreases bicarbonate levels in the plasma.
→while hydrogen ion concentrations stays the same, blood pH will decrease
→increase ventilation to remove more carbon dioxide to reduce the hydrogen ion concentration
Why do respiratory muscle tissues require nervous stimulation?
All respiratory muscle tissues are of the skeletal type, and so require nervous stimulation in order to contract
How are contractile signals initiated?
→Contractile signals are initiated within the brain
→descend via spinal tracts, which synapse with the lower motor neurons that innervate the respiratory muscle tissue
Which types of responses provides predominant signals involved in regulating ventilation?
CRC response to PaCO2 provides the predominant
Where are type-I glomus cells found?
→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
In what situations does hypoxic drive take on a greater role?
→individuals with severe chronic lung pathology (e.g. COPD) that are unable to ventilate respiratory structures sufficiently
→results in chronic hypercapnia and hypoxia (type II respiratory failure).
Why is central respiratory chemoreceptor responses reduced in chronic hypercapnia?
→due to homeostatic mechanisms that compensate for chronic acidification of the CSF and increase CSF pH back to normal levels
Potential causes of central breathing dysfunction…
- Inhibition the brainstem caused by drugs such as opioids and barbiturates
- Injury to the brainstem caused by stroke or trauma
- Congenital defects in brainstem signalling processes (congenital central hypoventilation syndrome)
- Insufficient development of the relevant structures and pathways in neonates
- Hypocapnia (and reduced ventilation) associated with altitude and hypobaric oxygen pressure.
Limbic system inputs…
Emotional stimuli (e.g. anxiety) acting through the hypothalamus to the medulla and pons
What do central and peripheral chemoreceptors have in common?
Both central and peripheral chemoreceptors function via negative feedback.
