Neural control of Breathing Flashcards
Why is there a need to modulate the rate of ventilation?
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 and blood
Diffusion proportional to Surface area D P/ Distance^2
What physiological processes initiate breathing?
Respiratory muscles provide the movement required for ventilation
As respiratory muscles consist of skeletal muscle, they require neural inputs/stimulation to contract
Innervation from motor neurons synapsing from descending spinal tracts provide the contractile signal
Contractile signals are initiated within the brain and descend via spinal tracts, which synapse with lower motor neurons that innervate the respiratory muscle tissue
Which muscles are utilised in quiet/forced inspiration/expiration?
Quiet breathing: Inspiration- Diaphragm Expiration- Elastic recoil Increased/ forced ventilation: Inspiration- External intercostals Accessory- Pectorals, Sternomastoid, Scalene Expiration- Elastic recoil, Internal intercostals Accessory- Abdominals
How does the Central Pattern Generator determine the rate and depth of breathing?
The basic pattern of ventilation is 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)
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
Inputs from higher somatic and emotional centres also feed into the CPG, hence breathing is subject to voluntary control and can be affected by extreme emotional states e.g. panic attacks
However it is impossible to asphyxiate one’s self by holding your breath, as either the urge to breath caused by excess CO2 will be overpowering, or acute hypoxaemia will result in loss of consciousness.
How do central chemoreceptors respond to changes in arterial PCO2?
Central chemoreceptors respond (indirectly) to changes in arterial PCO2
Central respiratory chemo-receptors (CRC) present 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 do not directly respond to changes in blood pH (except via CO2)
How do peripheral chemoreceptors respond to changes in arterial O2, CO2 and pH?
Activates by decreased PaO2, increased PaCO2 and acidaemia
Signal to respiratory centres in medulla (via sensory nerves) to increase ventilation (negative feedback)
What is the hypercapnic drive?
Hypercapnic drive- ventilation is generally proportional to PaCO2
What is the hypoxic drive and when is it important?
Hypoxic drive- hypoxaemia (low PaO2) stimulates increased ventilation
Due to the dominant role of central respiratory chemoreceptors, the level of ventilation is generally proportional to PaCO2 (i.e. is PaCO2 increases, ventilation increases to maintain homeostasis and keep PaCO2 within narrow limits)
pH and PaO2 also affect ventilation- however pH is typically closely linked to CO2 levels, and hypoxic drive (the increased ventilation in response to decreased PaO2) only occurs at very low PaO2
A situation where hypoxic drive takes on a greater role however, is in individuals where severe chronic lung pathology (e.g. COPD) that are unable to ventilate respiratory structures sufficiently.
This results in chronic hypercapnia and hypoxia (type II respiratory failure)
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.
How does ventilation decrease during sleep?
Transition from wakefulness to sleep:
Decreased metabolic rate= decreased respiratory demands
Postural changes alter mechanics of breathing
Decreased SNS and increased PNS tone= decreased HR, BP and CO
Decreased tidal volume, decreased breathing frequency, decreased minute volume
Decreased SaO2 (≈96%), increased PaCO2 (≈7kPa)
Decreased upper airway calibre
What is 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 (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 at the same time) e.g. Cheyne-Stokes respiration
Impact of dysfunction can vary from mild (e.g. sleep apnoea) to severe (permanent cessation), based on the extent of the pathology
What is sleep apnoea and its effects on a person’s health?
Sleep apnoea= temporary cessation of breathing during sleep
Due to obstruction or dysfunction of respiratory system
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
Effects on health:
Tiredness (poor sleep quality)
Cardiovascular complications (stress + increased SNS tone)
Obesity/Diabetes (inflammation + metabolic dysfunction)
What is Cheyne-Stokes respiration?
Cheyne-Stokes respiration (oscillating apnoea and hyperpnoea)
An abnormal pattern of breathing where the control of breathing becomes abnormal so that the system starts to overcompensate
So the person is breathing normally but because of the lack of oxygen from e.g. a high altitude the respiratory system starts
The breathing rate decreases a lot
Eventually the brainstem senses that there’s no oxygen in the body and increases the breathing rate and overshoots increasing it rapidly, where the ventilation increases by too much, excess carbon dioxide has been lost and the pH goes right up
The central chemoreceptors sense this and slow the breathing down
This is a cycle of hypoxaemia and hypocapnia
What is the role of chemoreceptors in regulating respiration?
The CPG receives inputs from central and peripheral chemoreceptors (specialised receptors that detect levels of CO2, O2 and pH) and initiates compensatory changes in ventilation
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 then resulting H+ activates CRCs.
This CRC response to PaCO2 provides the predominant signal involved in regulating ventilation and initiating the urge to breathe
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.
