S4 L2 Neural and Chemical control of breathing Flashcards
Reminder:
- Nerve that supplies the diaphragm (and it’s nerve roots)
- Intercostal muscles responsible for inhalation and exhalation?
Diaphragm nerve: Phrenic nerve - from C3, C4, C5
Expiration - Mainly a passive process, by elastic recoil of lungs and chest wall, inner and innermost internal muscles
Inspiration - External intercostal muscles, diaphragm
How is breathing controlled? (where in the brain and name of it) ___ ___ ___
What does the ____ ____ ____ control?
What can it be likened to (analogy)?
How many times does it make the inhalatory intercostal muscles contract a minute? (if not exercing, not pathology…)
Sensory inputs to the ____ ____ ___?
Where is the ____ ____ ____?
Respiratory Pattern Generator
Inputs to the RPG
- State 3…
RPG:
- 2 connections from RPG to ‘two things’ (oppose each other)
ignore blue lines in the diagram
RPG
- How to stop both the inspiratory and expiratory neurones being switched on at the same time?
3 nerves from Inspiratory and Expiratory neurones
Phrenic nerve to diaphragm
Motor neurones to external intercostal muscles
Motor neurones going to internal and innermost intercostal muscles
purple in digram and light green (ignore the rest)
Everything just gone through: inputs to the RPG, inspiratory and expiratory neurones, motor nerves is part of what type of control?
Involuntary:
Somatic but regulated by inputs from autonomic system. (Intercostal muscles are skeletal muscles)
Voluntary part of this system, what does this mean?
What condition is the voluntary part of this system affected in?
Blue in the diagram
Condition - Ondine’s curse: Patient lose ability to regulate breathing involuntarily, can only breath voluntarily. Constantly have to be thinking about breathing! Sleep - will forget to tell the body to breath - so have to be ventilated during sleeping
Summary of whole system
Summary:
- What is included in buffer system
- What are compensatory mechanisms?
Summary:
Link between - Sensors, Respiratory pattern generator, effectors
Chemical Control of Ventilation:
RPG must respond in changes of needs and production of pO2, pCO2, pH
- What does ventilation need to accomodate for?
- Peripheral chemoreceptors sense? how long take to respond?
- Central chemoreceptors sense? how long take to respond?
Accomodate for:
– Maintain adequate oxygen status
– Adjust respirations for changing metabolic status/needs reflected by altered PO2, PCO2, pH (remember that pH is a measure of hydrogen ion concentration – inverse relationship – as H+ levels go up, pH goes down
Peripheral chemoreceptors:
Sense pO2, pCO2 and pH levels (but dominantely, pO2)
Respond in seconds
Central chemoreceptors:
pH and pCO2
Respond in hours
Reminder of the carbonic acid - bicarbonate buffer system, and which organs affect it?
Peripheral chemoreceptors: location, don’t confuse with…, sensitive too…, major function of them…
- Carotid bodies
- Aortic bodies
Peripheral chemoreceptors and pH
- What happens
- HH equation
Aside:
- What happens in hyperventilation?
- What happens in a panic attack?
Summary of Peripheral chemoreceptors:
- 2
- Sensory innervation…
- Most sensitive to changes in…
- Time take to respond?
Central chemoreceptors:
- Location?
- Sense what?
- What can’t they sense?
• Central chemoreceptors
– Specialised neurons located on BRAIN side of Blood Brain Barrier (BBB) -bathed in CSF
– BBB = endothelial cells of blood vessels in brain surrounded by pericytes and foot processes (end feet) of astrocytes to create a highly selective permeability barrier
• Sense increases in arterial PCO2 and—much more slowly—decreases in arterial pH, but not arterial PO2
• When blood-gas parameters nearly normal central chemoreceptors are the primary source of feedback to the brainstem respiratory centres for needed adjustments
• If PCO2 increases suddenly then ventilation increases rapidly - augmenting minute ventilationocesses (end feet) of astrocytes to create a highly selective permeability barrier
• Sense increases in arterial PCO2 and—much more slowly—decreases in arterial pH, but not arterial PO2
• When blood-gas parameters nearly normal central chemoreceptors are the primary source of feedback to the brainstem respiratory centres for needed adjustments
• If PCO2 increases suddenly then ventilation increases rapidly - augmenting minute ventilation
How do chemoreceptors work?
BBB seperates central chemoreceptors in the medulla from arterial blood
BBB has a low permeability to ions such as H+ and HCO3-, but high permeability to small molecules like CO2
Central chemoreceptors and chronic hypercapnia e.g. long-term COPD
- 2 methods of compensation for this
Hypoxaemia (low pO2), Hypercapnia (high pCO2), and Acidosis (low pH), all cause increase in ventilation, which should then cause the following changes in the body..
Can over-oxygenating a patient with COPD (for example) be bad?
Look at PP for some example Q - really helpful
Bad to over-oxygenate: in theory for healthy person it would be fine as can breath carbon dioxide out, but in COPD cant breath the carbon dioxide out as easily, so carbon dioxde stay her in the blood, causing acidity
GW Q:
- How does CO poisoning affect oxygen in the blood?
- For someone with COPD, giving them too much oxygen can be bad because…
How does CO poisoning affect oxygen in the blood?
CO poisoning affects HB levels of O2 and NOT paO2
The peripheral chemoreceptors are only detecting paO2 which would appear normal
COPD:
Lead to high CO2, which is more dangerous than having slightly reduced oxygen levels