20) Neuronal control of breathing

Question 1

Why is the rate of ventilation being modulated constantly?

Answer 1

• It is constantly adjusted to meet the body’s ever changing O2 demand and for the adequate expulsion of CO2
• Adequate absorption of O2 and expulsion of CO2 to/from the body is achieved by maintaining pressure gradients between the body and the alveoli

Question 2

In what circumstances does O2 demand and/or CO2 production increase?

Answer 2

• Demand for O2 (and CO2 production) increases with increased physical activity. As activity increases, ATP production increases to meet increased demand of energy. This means volume of oxygen consumed increases to produce more ATP.
• During injury, infection and metabolic dysfunction. Oxygen demand increases as we get burns or infections and increases further if we suffer from both

Question 3

How does breathing change to modulate ventilation?

Answer 3

• By changing tidal volume (volume of air inhaled during each breathe) and breathing frequency (number of breaths in a unit time) we can change the amount of oxygen we take in and consume

Question 4

How is an overall increase in total O2 transported achieved?

Answer 4

• Whilst increasing ventilation, there are increases in cardiac output to increase total O2 being transported
• Since there is only a finite amount of Hb in circulation only a certain amount of O2 can be carried so hyperventilation will have little effect on O2 delivery
• By increasing cardiac output more blood is being pumped around the body so more O2 is being transported

Question 5

What physiological process initiates breathing?

Answer 5

• Ventilation requires movement of respiratory muscles
• These respiratory muscles are skeletal muscles which require a neural stimuli in order to contract.
• This neural stimuli/signal originates from a series of neuronal circuits in CNS of the brain (the brain stem).
• The brain stem receives different stimuli (e.g. sensory input, chemoreceptor inputs) and generate a respiratory pattern by sending signals at different intervals to the inspiratory and expiratory muscles.
• It does this by travelling down the spinal chord and then down motor neurones that synapse with the spinal chord
• From there it travels into the muscles where they provide a contractile signal for adequate ventilation.
• These signals self/auto generating

Question 6

How can activation of respiratory muscles be impaired?

Answer 6

• Damage to the pathway of electrical stimuli from the brain to the respiratory muscle can impair activation of respiratory muscles.
• This includes damage to the medulla, spinal chord, motor neurone or the muscles themselves
• This has an impact on the ability of the patient to breathe

Question 7

What are the two types of breathing?

Answer 7

• Quiet breathing (at rest)

- Forced inspiration/expiration (when exercising)

Question 8

What are accessory muscles of respiration?

Answer 8

• Muscles that do not have a primary role in respiration but can contribute to respiration when there is high demand for respiration

Question 9

Which muscles are used during quiet breathing?

Answer 9

• Inspiration: Diaphragm

- Expiration: Elastic recoil of the lungs

Question 10

What muscles are used in increased/forced ventilation?

Answer 10

• Inspiration: External intercoastal muscles (and pectorals, sternomastoid, scalene which are accessory muscles)
• Expiration: Elastic recoil, internal intercoastal muscles (and abdominals as accessory muscles)

Question 11

What are different stimuli that determine breathing rate and depth?

Answer 11

• Chemoreceptors: Senses various chemical stimuli (e.g. O2 levels, pH)
• Stretch receptors in the lungs: This ensures the lungs are not over inflated. If inflation volume becomes dangerous an inhibitory signal is sent which stops contraction of the muscle
• Higher centres in the brain: (e.g. emotional centre in the brain)

Question 12

What are the two types of chemoreceptors?

Answer 12

• Central Respiratory Chemoreceptors (CRCs) found in the medulla and are accountable for majority of stimuli sent to the brain
• Peripheral Respiratory Chemoreceptors (PRCs) found in aortic and carotid bodies and are accountable for a small amount of stimuli sent to the brain

Question 13

What do Central Respiratory Chemoreceptors (CRCs) monitor?

Answer 13

• They indirectly monitor changes in arterial CO2
• As blood travels through the cerebral capillaries, CO2 diffuses and passes through the blood brain barrier (barrier between cerebrospinal fluid and blood) into the cerebrospinal fluid
• In the fluid CO2 reacts with H20 to form H2CO3 (carbonic acid) which ionises into H+
• So the chemoreceptor detects changes in [H+] which corresponds to changes in CO2.
• Changing [CO2] can alter the magnitude at which the chemoreceptor is activated

Question 14

How does a change in [CO2] affect CRCs?

Answer 14

• An increase in [CO2] will form more carbonic acid which will dissociate into more [H+]
• This means pH will decrease causing activation of chemoreceptors to increase
• The increased activation of chemoreceptors will cause more stimuli to be sent to the brain stem and so ventilation will increase a greater amount
• As ventilation/breathing increases more CO2 is expelled from the body
• This is an example of negative feedback as the increased stimulus (CO2) elicits a response which causes the stimulus (CO2) to decrease

Question 15

What do Peripheral chemoreceptors respond to?

Answer 15

• Peripheral chemoreceptors respond to changes in pH/H+ (acidaemia), PaO2 and PaCO2
• As signals to these receptors increases, it causes the increased activation
• Increased activation of these receptors sends more stimuli to the brain which causes increased ventilation and increased expulsion of CO2
• It relies on the same negative feedback system as CRCs

Question 16

What is hypercapnic drive?

Answer 16

• Ventilation is proportional to PaCO2

- As CO2 increases, level of ventilation also increases

Question 17

What is hypoxic drive?

Answer 17

• Hypoxaemia (low PaO2/ low levels of O2 in the blood) stimulates increased ventilation
• This drive only kicks in at very low PaO2 levels

Question 18

Why does ventilation decrease during sleep?

Answer 18

• In general there is a lowered metabolic rate so respiratory demand decreases as there is less energy demand so less oxygen demand
• The body becomes more tolerant to low levels of O2 and high levels of CO2
• Sympathetic Nervous System tone decreases and Parasympathetic Nervous System tone increases. This causes HR, BP and CO to decrease
• Tidal volume, breathing frequency and minute volume decreases
• Postural changes alter mechanics in breathing
• Upper airway calibre decreases

Question 19

What pathologies can interrupt the initiation process of breathing?

Answer 19

• Trauma: damage to respiratory centres in the brainstem
• Stroke: ischemia-induced brainstem tissue injury
• Drugs (e.g. opioids): They act on opioid receptors which suppress neuronal activity in the brainstem
• Congenital central hypoventilation syndrome where a person may be born with a brainstem that does not function normally
• 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)

Question 20

How severe are the effect of pathologies on the central processes that initiate breathing?

Answer 20

• Impacts of dysfunction can vary from mild to severe based on the extent of the pathology

Question 21

What is sleep apnoea?

Answer 21

• A condition where a person suffers episodes in their sleep where they stop breathing (for more than 10 secs)
• In the short term it can cause tiredness (poor sleep quality as they are often awoken).
• However over long term it can lead to cardiovascular complications and metabolic complications (e.g. obesity and diabetes)

Question 22

What is Cheyne-Stokes respiration?

Answer 22

• An irregular pattern of breathing where the control of breathing becomes abnormal causing the system to overcompensate in both directions.
• It is caused by change in altitude, chemoreceptor dysfunction and heart failure

Question 23

Explain the progression of Cheyne-Stokes respiration?

Answer 23

• First we experience a state of Hypercapnia (excess CO2 in the blood) or Hypoxaemia (lower levels of O2 in the blood).
• This causes the brain to send additional signals to allow the body to take part in compensatory hyperventilation.
• This compensation becomes excessive and leads to Hypocapnia (low levels of CO2 in the blood) and alkalosis.
• There is a decreased respiratory drive
• As a result the brain sends additional signals to allow the body to take part in compensatory hypoventilation.
• This compensation also becomes excessive and leads back to the state of Hypercapnia and Hypoxaemia we started with