control of ventilation Flashcards
explain how respiratory motor movements are affected by the central nervous system
Inspiration
→ occurs via the phrenic (to diaphragm) and intercostal nerves (to external intercostal muscles)
Expiration
→ At rest, expiration is passive so no neural input is required
explain why ventilatory control depends entirely on signalling from the brain (somatic motor neuron input):
severing the spinal cord above the origin of the phrenic nerve (C3-5), breathing ceases.
Describe the location of the two types of chemoreceptors that modulate respiratory centres
also identify the stimuli which activate them:
[1] Central Chemoreceptors
- medulla
- respond directly to H+ (directly reflects PCO2)
- primary ventilatory drive
[2] Peripheral Chemoreceptors
- carotid and aortic bodies
- respond primarily to PO2 (less so to PCO2) and plasma [H+]
- secondary ventilatory drive
List 4 factors involved in changing ‘respiratory drive’ i.e., the rate and depth of breathing:
- Emotion (via the limbic system in the brain)
→ scared, laughing, crying - Voluntary over-ride (via higher centres in the brain)
- Mechano-sensory input from the thorax (e.g. stretch reflex).
- Chemical composition of the blood (PCO2, PO2 and pH) – detected by chemoreceptors.
How do individuals with chronic lung disease (desensitised to PCO2) stimulate ventilation?
They rely on changes in PaO2 to stimulate ventilation through peripheral chemoreceptors
→ Hypoxic Drive
Explain the negative feedback loop that occurs when PCO2 increases in the CSF:
cerebrospinal fluid [H+] goes up
the central chemoreceptors stimulate the respiratory centres to increase ventilation.
PCO2 decreases
Describe the effect of Barbiturates and Opioids on respiratory centres:
depresses respiratory centres
overdose -> respiratory failure -> death
↓ Sensitivity to pH and therefore response to PCO2 (in regards to changes in H+)
↓ PO2 in response to ↓ Peripheral chemoreceptor
Explain how Peripheral Chemoreceptors become important during hypoxia and acid-base imbalance:
if plasma pH falls ([H+] increases)
-> Increased ventilation (metabolic acidosis)
if plasma pH increases ([H+] falls) e.g. vomiting
-> inhibited ventilation (metabolic alkalosis)
Explain how CO2 affects acid-base balance e.g. hypo/hyperventilation:
↑ CO2 in the case of Hypoventilation
-> increased [H+] bringing about respiratory acidosis.
↓ CO2 in case of Hyperventilation
-> decreased [H+] bringing about respiratory alkalosis.
Explain situations where we cannot override involuntary stimuli voluntarily such as PCO2 or [H+]:
Breath-holding
-> passing out due to low levels of O2 and then the brain stem takes control of breathing
Hyperventilation for 30 seconds
-> inhibition of ventilation due to an increase in arterial PO2 or a decrease in arterial PCO2/[H+]
Why does increasing PCO2 in a chamber cause unpleasant and distressing feelings to the subject?
If unable to get rid of CO2
-> distress
breathing in CO2
-> increases PACO2 and thus impairs the partial pressure gradient that normally allows CO2 removal from the pulmonary artery.
CO2 remains in the blood
-> partial pressure gradient at the periphery that pulls CO2 out of cells is also lost
causing CO2 to build up in cells.
what is the major determinant of the degree to which haemoglobin binds (is saturated with) oxygen?
partial pressure of oxygen in the blood.
Ventilatory control is subconscious (autonomous) and involves areas in the pons and medulla, but it can also be voluntary.
what are the 2 nerve groups in the respiratory centres?
[1] Dorsal Respiratory Group of neurons (DRG)
→ Stimulation of inspiratory muscles (diaphragm, external intercostals)
[2] Ventral Respiratory Group of neurons (VRG)
→ Stimulation of tongue, pharynx, larynx, expiratory muscles
→ Maintains a basal tone of contraction to prevent collapse of airways & allows smooth, controlled expiration
