6.15 - Control of Lung Function Flashcards
What nuclei in the medulla oblongata and pons control breathing?
- dorsal respiratory group
- ventral respiratory group
- apneustic centre
- pneumotaxic centre
- pneumonic: DIVE (dorsal inspiration ventral expiration)
What does the dorsal respiratory group do?
- inspiratory centre
- main ‘controller’ of inspiration
- sets the ‘rate’
What does the ventral respiratory group do?
- expiratory centre
- inactive during quiet breathing
- inhibit apneustic centre
What does the apneustic centre do?
- associated with inspiration
- stimulates activity in the dorsal respiratory group (DRG)
- inhibited by pulmonary afferents
What does the pneumotaxic centre do?
- associated with expiration - the ‘inspiratory off switch’
- regulates depth and frequency
Which of the medulla oblongata nuclei inhibit/activate the others?
- dorsal and ventral respiratory groups inhibit each other
- pneumotaxic centre inhibits DRG
- apneustic centre activates DRG
- VRG inhibits apneustic centre
Explain the graph of respiratory pacemaker during quiet breathing.
- APs increase in frequency (apneustic centre) until pneumotaxic centre is activated, which stops inspiration - called ramp potential patterns
- after period of latency, apneustic centre helps program rhythm into dorsal respiratory group
What is the innervation of respiratory muscles like?
- phrenic nerve (motor) key player in innervating diaphragm
- vagus nerve (parasympathetic)
In normal circulation, what are the capillaries like in terms of gaps between the cells?
H2O filled gap junctions but capillaries are thought to be continuous
What are the capillaries like in the blood-brain barrier?
- BBB has tight junctions due to nerve cells which help even more tightly pack endothelial cells together, which restricts what can cross it
- BBB a lot less leaky
- does not allow H+ ions through the membrane
How does CO2 and H2O affect our drive to breathe?
- in capillary: CO2 + H2O –> H2CO3 –> H+ + HCO3-
- the H+ and HCO3- cannot cross the lipid bilayer of endothelial cells (and therefore BBB) as they are charged, but CO2 can
- CO2 crosses into CSF where it reacts with H2O to form carbonic acid, dissociating into H+ + HCO3-
- the H+ interact with afferent fibres in the medulla which send signals to DRG to determine rate and rhythm of breathing
What are the three types of receptors in the airways that affect ventilation?
- irritant receptors
- stretch receptors
- J receptors
What are irritant receptors?
- afferent receptors embedded within and beneath airway epithelium
- cough receptors - detect foreign matter and leads to cough to get rid of it
- leads to cough - involves forceful expiration against a closed glottis with sudden glottal opening and high velocity expulsion of air
What are stretch receptors?
- further down airways down secondary bronchi in tubes that can change size depending on pressure
- excessive inflation of lungs activates pulmonary stretch receptors
- afferent signals to respiratory centres inhibit DRG and apneustic centre and stimulate pneumotaxic VRG
- this inhibits inspiration and stimulates expiration
What are J receptors?
- located next to alveoli
- sensitive to oedema and pulmonary capillary engorgement (leads to high pressure)
- increases breathing frequency after this as the above impede ability of lungs to ventilate and exchange gas e.g. oedema is thick
Describe the graph of volitional apnoea.
- when ventilating, arterial O2 and CO2 remain stable
- when holding breath, arterial O2 decreases and CO2 increases - accumulation of H+ beyond BBB stimulates medulla to breathe in
- CO2 threshold for breathing - once CO2 passes that we start struggling for breath (but can be overcome)
- O2 threshold for blackout - once O2 passes below this, we blackout
How does hyperventilating affect the graph of volitional apnoea?
- increasing ventilation increases arterial O2 and decreases CO2
- once breath is held, CO2 threshold for breathing (struggle phase) is now much closer to O2 threshold for blackout so once you start struggling you may blackout soon after
- using motor cortex going through to control inspiratory muscles to keep them contracted and inhibit/overcome effect of expiratory muscles
What is an acid?
A molecule with a loosely bound H+ ion that it can donate
What is the paradox with acids?
A greater H+ concentration refers to a lower pH
Why must acidity of blood be tightly regulated?
Changes in acidity will alter the 3D structure of proteins (enzymes, hormones, protein channels) which may mean they become less efficient/do not work
What is a base?
- an anionic (negatively charged ion) molecule capable of reversibly binding protons (to reduce the amount that are ‘free’)
- H+A- <–> H+ + A-
- this relationship is an equilibrium - increasing something on one side will push the equation in the opposite direction
How was the buffering capacity of blood discovered?
- by Pitts and Swan who injected a dog with 14M acid that they thought would kill him
- but his blood pH changed very little
- blood has enormous buffering capacity that can react almost immediately to imbalances
How was pH figured out from H+ concentration?
- orders of magnitude difference between H+, Na+, K+: H+ = 0.00000004Eq/L, Na+ = 140Eq/L, K+ = 4Eq/L
- these relatively tiny numbers for [H+] are inconvenient to use
- Sorensen scaled the data using a log10 transformation: log10[H+] = -7.4
- made numbers much more manageable, although negative
- -log10[H+] = 7.4
- the inverse function of log is (10^x), using this we can calculate [H+] from pH
- [H+] = 10^(-pH)
What is alkalaemia?
Higher than normal blood pH
What is acidaemia?
Lower than normal blood pH
What is alkalosis?
Circumstances that decrease H+ concentration and increase pH
What is acidosis?
Circumstances that increase H+ concentration and decrease pH
How is alkalaemia and acidaemia corrected by the body?
- an acidosis causes acidaemia and will need an alkalosis to correct
- an alkalosis causes alkalaemia and will need an acidosis to correct
- changes in ventilation can stimulate a rapid compensatory response to change CO2 elimination and alter pH
- changes in HCO3- and H+ retention/secretion in kidneys can stimulate a slow compensatory response to alter pH
Where are peripheral chemoreceptors located?
- chemoreceptors that sample blood and assess for H+ and CO2 concentration are at bifurcation of carotid arteries in structures called carotid bodies and aortic bodies in aortic arch
- positioned near the carotid baroreceptors (sensitive to changes in blood pressure)
Describe the emotional change to ventilation.
- special senses (taste/smell/hear/sight) and higher brain centres like limbic system elicit emotional response
- this can affect the respiratory control centre in brainstem
- affects breathing rate
- normal situation: motor control > medulla reactivity
How are nerves distributed so that exercise can affect breathing?
- a branch of the efferents from the primary motor cortex that go to skeletal musculature also innervate medulla (to tell brain to start breathing since we are exercising)
- proprioceptive afferents from muscle spindles and Golgi tendons innervate the medulla on the way to the brain - can be shown by cycling someone else’s legs - changes their ventilation as brain recognises big muscles moving = should probably breathe faster
What is the cold shock ventilatory response?
Immersion in cold water (<10oC) results in inspiratory gasp and hyperventilation due to superficial sensory nerve endings in skin –> can lead to death
