Lecture 7 - Control of breathing Flashcards
Why do we need to control our breathing
To maintain normal levels of PaO2 and PaCO2 for metabolic and biocheical stability (e.g. pH)
Despite largely differing demands for O2 uptake and CO2 production, PaO2 and PaCO2 are normally kept with close limits, this is able to happen due to the tight control of ventillation.
What are the three basic elements of breathing?
- Central control in the brainstem which sets pattern/rhythm of breathing and coordinates sensors and effectors to maintain respiratory homeostais
- Sensors - Central/peripheral - these gather information (Chemical and physical), feed back to the controller to allow appropriate changes.
- Effectors - These are respiratory muscles - they adjust ventilation.
General picture of system
Where do the impulses for the automatic process of breathing come from?
And can this system by overriden?
Normal automatic process of breathing originates in impulses that come from the brain stem.
The cortex can overcome the brainstem for voluntary control of breathing.
In what part of the medulla are the respiratory centers?
And what are the three main groups of neurons found here:
The pons and medulla.
Three main groups neurons found in pons & medulla
- Medullary respiratory centre
- Pre-botzinger complex - rhythm generator (pacemaker)
- Dorsal area of respiratory group - inspiration
- Ventral area respiratory group (mainly expiration)
- Apneustic centre (pons) - cuts off inspiration
- Pneumotaxic centre (pons) - fine tuning
main key points of the respiratory centres that you need to understand
- Respiratory centres are in medulla/pons
- Responsible for generating rhythmicity
- Input from chemoreceptors, lung and other receptors and cortex
- Major output via phrenic nerves to diaphragm and intercostals
What are the two types of chemoreceptors found that send signals to the respiratory centres
Central chemo receptors
Peripheral chemoreceptors
These both send afferent signals to the controller to control ventillation to alter PaO2 and PaCO2
Where are the central chemoreceptors found? And, what are they sensitive to? what do they respond to?
CCRs are located need the ventral surface of the medulla. They are sensitive to the PCO2, not PO2, of blood. They respond to changes in pH of the CSF/ECF when CO2 diffuses out of cerebral capillaries.
Where are the peripheral chemoreceptors (PCRs) located, what do they respond to, and how fast do they respond?
PCRs are located in carotid bodies and aortic arch.
The respond to decreased arterial PO2, increased PCO2 and H+. And they respond rapidly.
~90% of O2 response comes from PCRs, and ~20-30% of CO2 response comes from these too.
Remember, CO2 is more dominant in its control over ventillation.
What is the most important stimulus to ventilation?
PaCO2 - under most conditions is the most important stimulus, and is kept within narrow range of +/- 3mmHg.
It’s tightly controlled around 40mmHg.
From which receptors does most of the response to PCO2 come from?
And what factors affect the response to PCO2?
And what increases the respose to PCO2?
Most of the stimulus comes from CCRs (~70-80%), but peripheral chemoreceptors also contribute and they are much faster.
The ventilatory response to PCO2 is reduced by sleep, increasing age, and genetic factors.
The response is exacerbated if PaO2 is lowered.
Describe the ventilatory response to hypoxia
What chemoreceptors are involved
What augments the response
- Only peripheral chemoreceptors are involved in response to hypoxia (they have negligible control during normoxic conditions).
- Their response is augmented by hypercapnia
- hypoxic control becomes important in high altitude, and in long-term hypercapinia caused by chronic lung disease
How does hypercapnia augment the ventilatory affect to hypoxia?
Hypercapnia augments the ventilatory response to stimulation of the peripheral chemoreceptors, such that ventilation is stimulated at PaO2 levels above 60mmHg.
Okay we know what happens to the onset of the ventilatory response to pO2 when hypercapnic conditions, but HOW does this happen?
Why does PaO2 become the principal hypoxic stimulus?
In conditions like chronic bronchitis, emphysema you get CO2 retention. The high PCO2 and acidisos causes an increased HCO3 retention in order to normalise pH.
This means that the pH stimulus for the central chemoreceptor in the medulla is at near normal pH. Which means that the only receptor left to respond is the peripheral chemoreceptors
Therefore hypoventilation, due to increased work of breathing and V/Q mismatch, often makes patients hypoxic which can become the main stimulus to drive ventilation.
How does non-chemical control of breathing occur?
Receptors that are located in the airways and lungs can affect respiration through afferent connections to the respiratory centers from the vagus nerve.
Lung receptors:
- Slowly adapting stretch receptors
- Rapidly adapting stretch receptors
- Juxtacapillary receptors
other receptors
- nose/upper airway, joint/muscle, arterial baroreceptors, pain and temperature