Control of Respiration Flashcards
Ventilation vs respiration
Ventilation- process of moving air in and out the lungs (mainly regulated by CO2)
Respiration- the process involved in the exchange of gases between the cells
SEnsor, effectors and controllers
Sensors- chemoreceptors, stretch receptors
Effectors- respiratory muscles
Controller- respiratory centers
Where is central control of breathing?
What does it regulate?
ANS at the medulla and pons (brain stem) as well as cerebral cortex.
Depth of ventilation and frequency
How can you increase frequency and contract/breath size?
Frequency- more AP/minute
Depth- more AP/burst
Generally both of these increase together to increase ventilation
What happens at the respiratory center?
This is the rhythm generator. Burst of AP originate here and conduct down the phrenic nerve stimulating the diaphragm
What happens in the expiratory center?
Normally expiratory is passive process which relies on elastic recoil of lungs and chest wall.
During exercise these neurons fire when inspiration muscles are silent stimulating expiratory muscles
What does the pons control in breathing>
They control the apeustic center which does prolonged inspiration by quick expiration.
this breathing is seen by directly stimulating the apeustic center.or when the connection between the apneustic and pnemotaxic (inhibitory) is severed
What does the pneumotaxic center control
It inhibits apneustic center by terminating inspiration and controls the depth of breathing
The pneumotaxic center can be overridden by temp, emotion and voluntary (breath holding, hyperventilation, speech)
Four things that stimulate ventilation
- Exercise (linear)
- CO2 (linear)
- pH
- O2 (non linear)
List all receptors for breathing
1 Stretch receptors
2Irritant receptors
3 Joint and muscle receptors
4 Juxtacapillary receptors (in alveolar walls and sense engorgement)
5. Chemoreceptors (in medulla)
6. Peripheral receptors (in carotid and aortic)
How do stretch receptors work?
Located in airway walls and they respond to mechanical stretch. When lungs are inflated more than 50% above resting volume further inflation is prohibited
Irritant receptors function and location?
Location- airway epithelium and send afferent signals to vagus nerve.
Stimulated by irritants like smoke, dust, hisamine (released in asthma) and reponses like coughing sneezing and bronchoconstriction
What directly stimulates the central chemorecptors?
H+ in the CSF. H+ isn’t permable to the BBB but CO2 is.
- CO2 diffuses into the CSF where it spontaneously forms carbonic acid which disscoaites into the H+ and HCO3-
Explain the buffer response when H+ is in the CSF
There isn’t really one. Most times protein acts as a buffer, but the lack protein in CSF means any changes in PaCO2 translate to changes in CSF pH
When would we expect increased ventilation
When CO2 increases (so HCO2 and H+ increase) and pH decreases because we want to blow of fthe CO2.
The central chemoreceptors are responding to the increase in H+
Direct and indirect to chemoreceptors
Direct- H+
Indirect- Parteral of CO2 (because of how it crosses BBB and becomes H= and HCO3-)
SHape of central chemorecptors response
Linear- 1 torr increase leads to 4 L.min increase
Very sensitive to small changes in Alveolar
Slope is steeper if hypoxic
Do central chemorecptors adapt? Explain
Yes! After days of sustained change (increase or decrease) in PCO2 Alveolar (edema, COPD or high altitude (low CO2) a non respiratory response regulates CSF and restores H+ back to normal .
When are the central chemocrecptors response lowered? (4)
1 Sleep
- Old ppl.
- Trained athletes
- Drugs (anesthesia)
Important factors about peripheral chemoreceptors
1. What do they respond to? Where? Shape of graph? Adaptation abilities? precentage of ventilation that they are responsible for?
Fast or slow response
1 .Hypoxia- to PP of O2 not the content- so no response in anemia (also respond to hypercapnia (high PCO2 and acidosis(low pH) - overall response elevated when are three are effected
- Carotid!! and aortic arch
- Non linear- small changes in PaO2 only show small change but when PaO2 is below 60 the response is great
- No adaptation
- 20% importance in normal breathing
- Fast response
What happens when the glomes cells in the carotid body are anoxic for 2 mins?
Inhibits K+ channels Leads to a burst of AP Leads to influx of Ca2+ Release of NT More EPSPs Increase info to medullary respiration response
Why does exercise increase ventilation so efficiently?
best guess?
We don’t know! there is no change in PaO2, PaCO2 or pHa.
The response to increase ventilation is almost immediate before blood gases level cans change so it is believed that the response is neurally mediated. The more gradual changes in between may be due to hormonal or blood borne.
Differnece in arterial/venous saturation in
- Normal patient
- Patient that starts with subnormal values
- Arterial should remain fairly constant even with exercise,while venous saturation decreases with exercise but returns to normal almost immediatley
- With dysfunction venous Hb saturation decrease dramatically with exercise because the patient can’t increase CO and muscles only get what the heart delivers. Arterial Hb saturation should remain the same during exercise even if they have heart failure.
** remember PO2 doesn’t change during exercise so can’t increase ventilation***
Effectors
Respiratory receptors get message from medulla and send AP through phrenic to the diaphragm. Diaphrgam gets help from inspiration intercostals, scalene muscles when needed.