RESP: Neural control of breathing Flashcards
Why must rate of ventilation be modulated?
To match body’s demand for O2 and production of CO2. Adequate absorption of O2 + expulsion of CO2 achieved by maintaining pressure gradients b/w alveoli + blood
In what circumstances does O2 demand/CO2 production increase?
- During physical activity
- Infection, injury or metabolic dysfunction
How does breathing change to modulate ventilation?
As O2 consumption increases, breathing frequency increases, as does ventilation
What does ventilation increases alongside with to increase total O2 transported?
Cardiac output - More blood pumped out = greater perfusion of blood at alveoli, greater V/Q coupling.
What physiological processes initiate breathing? Describe the order of these processes
Respiratory muscles:
- Provide movement required for ventilation
- Consist of skeletal muscle, therefore require neural inputs/stimulation to contract
Innervation:
- Motor neurones synapsing from descending spinal tracts provide the contractile signal.
Order:
Neuronal signal generated in brainstem, signal conducted from CNS to resp muscles via motor neurones, respiratory muscles contract
Which muscles are utilised in quiet/forced inspiration/expiration?
Quiet breathing:
- Inspiration - Diaphragm
- Expiration - Elastic recoil
Increased/ forced ventilation:
- Inspiration
- Respiratory - External intercostals
- Accessory - Sternomastoid, Pectorals, scalene
- Expiration
- Respiratory - Elastic recoil, Internal intercostals
- Accessory - Abdominals
What are the neuronal systems within the brainstem that generate basic breathing pattern?
PRG - Potine respiratory group
DRG - Dorsal respiratory group
VRG - Ventral respiratory group
How does the CPG determine rate + depth of breathing?
Receives inputs from central and peripheral chemoreceptors
Inputs from higher somatic and emotional centres also feed into CPG, hence breathing subject to voluntary control (e.g. it’s by this mechanism that panic attacks lead to hyperventilation)
Central pattern generator consists of:
- Pons
- Medulla oblongata, which divides into:
- Dorsal respiratory group - Responsible for somatic motor neurones (inspiration), acts on:
- Scalene and sternocleidomastoid muscles
- External intercostals
- Diaphragm
- Ventral respiratory group - Responsible for somatic motor neurones (expiration), acts on:
- Internal intercostals
- Abdominal muscles
- Dorsal respiratory group - Responsible for somatic motor neurones (inspiration), acts on:
Sensory receptors:
- Medullary chemoreceptors (detect CO2 level changes), acts directly on CPG, stimulates somatic motor neurones
- Carotid and aortic chemoreceptors (detect changes in O2 and pH levels), send impulse to afferent sensory neurones, which then send impulse to CPG stimulates somatic motor neurones
How do central chemoreceptors respond to changes in arterial PCO2?
- Present in medulla
- Indirectly monitor changes in arterial CO2
- Respond to changes in H+ within CSF, though as H+ cannot cross blood brain barrier, they don’t respond directly to changes in blood pH (except via PaCO2 as CO2 can diffuses across the blood brain barrier)
- Chemoreceptors are activated when they detect high H+ levels (Low pH)
How do peripheral chemoreceptors respond to changes in arterial O2, CO2 and pH?
- Peripheral chemoreceptors consist of type-I glomus cells present within carotid and aortic bodies, detect levels of O2, CO2 and pH within arterial blood
- Activated by ⬇️PaO2, ⬆️PaCO2 and acidaemia (Low pH)
- Signal to respiratory centres in medulla (via sensory nerves) to ⬆️ventilation (negative feedback)
What is the relationship between ventilation and PaCO2?
Generally proportional to one another - This is hypercapnic drive and this is the predominant stimulus for respiration in humans.
How does hypoxaemia affect ventilation?
Stimulates increased ventilation - Hypoxic drive
What happens during the transition from wakefulness to sleep?
- ⬇️metabolic rate = ⬇️respiratory demands
- Postural changes alters mechanics of breathing
- ⬇️tidal volume, ⬇️breathing frequency, ⬇️minute volume
- ⬇️SaO2 (approx 96%), ⬆️PaCO2 (approx 7kPa)
- ⬇️Upper airway calibre
What pathologies are associated with dysfunction in central processes that initiate breathing?
- Trauma - Damage to respiratory centres in brainstem
- Stroke - Ischaemia-induced brainstem tissue injury
- Drugs (opioids etc.) - 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 (low O2 + low CO2). e.g. Cheyne-Stokes respiration
Extent of impact can vary from mild to severe
Describe sleep apnoea
Characterised by >5 episodes per hour lasting >10 seconds
It’s when breathing stops and starts during sleep, and can be due to obstructive issues, or central issues.
Durations of apnoeas may be as long as 90 seconds and frequency of episodes as high as 160 per hour
Effect on health:
- Tiredness (poor sleep quality)
- CVS complications (stress + ⬆️SNS tone)
- Obesity/ Diabetes (inflammation + metabolic dysfunction)
What causes obstructive sleep apnoea?
Caused by temporary blockade of upper respiratory tract. This narrowing and obstruction can be caused by a combination of:
- Increased pressure on neck due to increased, obesity- related, fat deposition
- Individual variation in facial structures displacing the genioglossus (1 of the tongue muscles) into airway
- Fluid moving from legs to head and neck due to recumbent position adopted during sleep, swelling pharyngeal tissues
What causes central sleep apnoea?
Dysfunction in CNS processes that initiate breathing, causing cessation of automated breathing during sleeping (temp or permanently), as pathways initiating breathing no longer function. Examples include:
- Inhibition to the brainstem caused by drugs such as opioids and barbiturates
- Injury to brainstem caused by stroke or trauma
- Congenital defects in brainstem signalling processes (central hypoventilation syndrome, in which individuals lack the capacity to breath whilst asleep)
- Insufficient development of relevant structures and pathways in neonates (infantile central sleep apnoea)
- Hypocapnia (and reduced ventilation) associated with altitude and hypobaric oxygen pressure
How can you differentiate between obstructive and central sleep apnoeas?
Polysomnography by whether diaphragmatic contractions continue during the apnoea.
Obstructive sleep apnoeas are associated with increasing diaphragmatic effort as it tries to overcome the upper respiratory blockade.
In central sleep apnoea, the diaphragm usually fails to respond during periods of apnoea (as there’s temporary cessation of CNS-resp muscle pathway that initiates breathing)
Describe Cheyne-Stokes respiration
It’s a particular abnormal breathing pattern and central sleep apnoea involving oscillating apnoea and hyperpnoea. Periods of apnoea (with resulting hypercapnia and hypoxaemia) stimulate compensatory hyperventilation. However, due to underlying pathological circumastances (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 (and the cycle begins again until it resolves or the individual wakes)
What feedback mechanisms regulate breathing and to what stimuli do they respond?
a. Central chemoreceptors = detect high [H+] in CSF, if HCO3- is high, chemoreceptors won’t be able to detect high H+ in CSF, therefore feedback will rely on peripheral chemoreceptors
b. Peripheral chemoreceptors = HIgh PaCO2 , Low PaO2 and low blood pH
c. Limbic system inputs = Emotional stimuli
d. Stretch receptors = Excessive physical stretch of lungs
