23. Acid Base Control of Respiration Flashcards Preview

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What are the 5 basic elements that feed into the respiratory control centres in the medulla and pons?

After integrating and processing this data, where does the respiratory control centre project to?

Central chemoreceptors, Peripheral chemoreceptors (carotid and aortic), Voluntary control (cerebrum), Mechanoreceptors (stretch, Irritant, J receptors - chemoreceptors), Muscle proprioceptors (e.g. muscle spindles in intercostal muscles)

Via spinal motor neurons and phrenic or other nerves, to diaphragm, intercostals and accessory muscles, and muscles of respiration.


What are the 3 functional components of the respiratory control system?

What is the choroid plexus?

What do the ventricular ependyma cells do?

Sensors (CENTRAL AND PERIPHERAL CHEMORECEPTORS AND PERIPHERAL MECHANORECEPTORS) -> central controller (pons, medulla etc.) -> effectors (respiratory muscles) 

Special tissue within ventricles of brain that has capillaries that allow water and small ions to pass out -> CSF! Fills ventricles and bathes brain.

Regulate CSF secretion from blood.


What are central chemoreceptors? 

What do they detect?

What happens if increased acidity is detected?

Specialised neurons in ventral surface of medulla sensitive to CSF pH.

CO2 diffuses through BBB into CSF -> reacts with H2O = carbonic acid -> converted to H+ and bicarbonate by carbonic anhydrase

Increases stimulation of chemoreceptors -> stimulates neurons in respiratory centres which are close to chemoreceptors in medulla (FB CTRL!) -> increased ventilation which expels more CO2 from lungs and reduced CO2 in blood and pH. 


What is the normal pH of the CSF?

What controls pH in the blood? How is different to in CSF?

How is this system affected in chronic pulmonary disease?


Plasma proteins tend to buffer pH. But CSF contains almost no protein (not filtered through choroid plexus), therefore it has much lower pH buffering capacity than blood. So change in CSF pH for a given change in PCO2 is greater than in blood

Chronically high levels of CO2 in blood, so central chemoreceptors gradually become less sensitive and drive for ventilation from CO2 is reduced.


Describe the 3 types of lung based respiratory receptors.

1. (main) pulmonary stretch receptors in small bronchi and bronchioles - discarge more when lung distended, activity sustrained with lung inflation. Provide off switch to respiratory centre i.e. stops breathing in

2. Irritant receptors - C fibres, mechanoreceptors, lie between airway epithelial cells in trachea and large bronchi, stimulated by noxious gases, cigarette smoke, inhaled dusts and cold air -> fire APs -> cough 

3. J-receptors - chemoreceptors sensitive to fluid in alveoli - respond to pulmonary oedwema, pulomnary emboli, peumonia, congestive heart failure and barotrauma.

NB: proprioveptors can influence respiration too


How do pulmonary stretch receptors work? What is the name of the reflex?

How do irritant receptors work?

How do J receptors work?

Inhibit inspiration when lungs fully inflated (so prevent tissue damage from overinflation). At end of inspiration send APs through vagus afferents to respiratory centres in pons and medulla to inhibit inspiration = The Hering- Breuer inflation reflex.

Detect presence of objects in airways too large to be carried away by mucus -> cough reflex activation

Respond to events such as pulmonary oedema which cause decrease in oxygenation. Stimulate an increase in ventilation and respiration via vagal afferents. 




How would you describe ventilation response to raised PaCO2?

What is the ventilation response curve like with different levels of PCO2 compared to PO2?

Thus what is the main chemical drive to ventilation?

How does hypoxia tie in?

Linear, mainly due to central chemoreceptors. 

As alveolar CO2 increases, breathing rate increases. Also the sensitivity to CO2 is increased in hypoxia. At normal levels of CO2, there is little response of respiratory system until you reach severe hypoxia (alveolar PO2 60mmHg)

Hypercapnia (increase in CO2). Hypoxia on its own does not stimulate breathing until PO2 < 60mmHg

Hypoxia increases sensitivity of the respiratory centres to hypercapnia.


Where are the sensors for hypoxia?

What 3 things do afferent nerves from these receptors respond mainly to?

What do the afferents travel mainly in, and to?

In the peripherial chemoreceptors located in carotid bodies at bifurcation of common carotid arteries, and in aortic bodies above and below aortic arch. Carotid body contains most heavily vascularised tissue in human body.

Reduced PaO2 and plasma pH (and also not as strong to raised PCO2).

Glossopharyngeal nerve (some in vagus) to BS.


What are the 2 types of cells found in the carotid body?

1. glomus type I (chief) cells: derived from neuroectoderm like nerve cells. Release NTs that stim. sensory endings of CNX and CNIX afferents that project to medulla respiratory centres

2. glomus type II (sustentacular) cells: resemble glia - supporting cells


How do type I glomus cells detect hypoxia?

Decrese in PO2 or arterial pH causes depolarisation of cell membrane -> hypoxia leads to inhibition of K+ channels. Inward Na+ leak  = opening of VGCa2+ channels -> ACh and NT release -> act on receptors on afferent nerve gibres adjacent to glomus cell -> AP to respiratory centre.

NB: response increases steeply below pO2 of 60mmHg


Does most of the breathing urge come from central or peripheral chemoreceptors?


What controls respiration?

Central chemoreceptors (CO2)

But if there is arterial hypoxemia the peripheral chemoreceptors become active, and they potentiate the drive from hypercapnia.


Groups of neurons in pons and medulla of BS = respiratory centres: 3 main groups of neurons, the main one is in the medulla -> projects down reticulospinal tract, around margin of ventral horn, to activate diaphragm for inspiration


Where does the phrenic nerve arise, and where does it enter the thorax?

How does it go down the mediastinum?

What does the nerve supply?

In neck from C3-5 roots. Lies on scalenus anterior muscle, enters thorax between subclavian artery and vein.

Anterior to hilum of lung, between pleura and pericardum.

Sensory: diaphragmatic pleura and peritoneum    Motor: diaphragm (only motor supply to diaphragm)


Where do the pH detectors, pulmonary stretch, irritant and J receptors input to?

What does this entitiy then project to?

What happens in the medulla during forced expiration?

NTS on dorsal surface of medulla. 

Dorsal respiratory group which contains cells that fire during inspiration.

Ventral respiratory group in ventral medulla become more active, their axons project down reticulospinal tract and activate internal intercostals.


What 2 regions modulate the respiratory centres and where are they found? 

What do these regions do?

Apneustic centre and pneumotaxic centre in pontine reticular formation.

Apneustic centre prolongs inspiration (e.g. holding breath for swimming)

Pneumotaxic centre modulates (mainly by inhibition) apneustic centre, thus decreasing TV and resp. rate. 



How does the cerebral cortex regulate breathing for vocalisation?

What is cheyne-stokes breathing?

What conditions can it be seen in?

Via pneumotaxic and apneustic centres. (But these centres cannot completely override medulla.)

Sensory input to medulla damaged -> gradual increase in rate and depth of breathing, followed by gradual decrease and temporary stop -> apnoea.

Heart failure, strokes affecting medulla, hyponatremia, traumatic brain injuries and BS tumours. Toxic metabolic encephalopathy. Carbon monoxide poisioning. Morphine administration.


Compare the respiratory responses to CO2 and O2

CO2: PaCO2 most imp. stimulus, most stimulus comes from central chemoreceptors but peripheral can also contribute and their response is faster, response magnified if PaO2 lowered

O2: only peripherial chemoreceptors involved, negligible control during normoxic conditions, control becomes imp at high altitude and in long-term hypoxemia caused by chronic lung disease

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