Control of Ventilation

Time to give physiology some love! I haven't really posted much about physiology throughout the semester, but since it's my first exam, I guess it's time to get right back to it!

Since I was blogging about respiratory physiology before, I'm going to finish off that topic with this post on control of ventilation.

List the respiratory centres in CNS

There are two main respiratory centres in the central nervous system. They are the pons respiratory centre and the medulla respiratory centre, named after the area where they are found in the brain. The pons respiratory centre can be subdivided into the apneustic centre, which increases the depth of breathing, and the pneumotaxic centre, which decreases depth of breathing. (Note: in PHYL3002 our lecturer just told us that the apneustic centre might not actually exist 0_o) The medullary respiratory centre can be broken down into the dorsal respiratory group (DRG) and ventral respiratory group (VRG). Directly superior to the VRG is the Pre-Bötzinger complex, which is like a pacemaker for the respiratory system. I'll go into more detail on each of these areas throughout the post.

Discuss the generation of the basic rhythm

As I just mentioned, the Pre-Bötzinger complex is the pacemaker and is thus largely responsible for the generation of the rhythm of breathing. It sends signals to the dorsal respiratory group, which causes the diaphragm to contract. These signals don't come all at once- they gradually increase in intensity as an "inspiratory ramp signal." If this didn't happen then all of our breaths would be short and sharp, and we wouldn't be able to do things that require you to control your ventilation, such as talk or play clarinet. Boo.

The DRG is close to the VRG, so when very strong signals are sent to the DRG, they may "spill over" into the VRG. This causes other "accessory" muscles such as the rectus abdominus and internal intercostals to aid in forced expiration. (For more information on muscles involved, please see this post for ANHB2212.)

The pneumotaxic and apneustic centres also influence our breathing. The pneumotaxic centre, as mentioned before, limits our breathing- I remember it as kicking in when breathing is too taxing (pneumotaxic). It can "switch off" the signalling between the DRG and inspiratory muscles. The apneustic centre, however, stops the signal from being "switched off." Normally the pneumotaxic centre dominates, but if the apneustic centre dominates, such as in a condition known as apneusis, the patient may breathe by long inspiratory gasps interrupted by short, brief expirations. (Note: As I mentioned above, one of my lecturers for PHYL3002 has disupted the existence of the apneustic centre.)

Discuss the control of ventilation by P_O2 & P_CO2

When we breathe in, our P_O2 increases and P_CO2 decreases. The opposite is true for when we hold our breath. These differences are the basis of control of ventilation. Changes in our P_O2 and P_CO2 are detected by central and peripheral chemoreceptors.

An increase in P_CO2, as detected by the central chemoreceptors in the medulla, is the main stimulus for increasing our breathing rate. CO₂ can cross the blood brain barrier, where it interacts with water to form H⁺ and HCO₃^-. The H⁺ can be detected by the central chemoreceptors, which then send signals to the respiratory control centres, increasing ventilation. This only occurs up to a point, however: at extremely high P_CO2 levels ( > 70-80 mmHg), the entire brain gets depressed, including the respiratory neurons. Not good.

A decrease in P_O2, as detected by peripheral chemoreceptors in the carotid arteries and aortic arch, can also stimulate an increase in breathing rate. This only happens, however, once P_O2 drops below around 60mmHg, which is pretty rare since normally a rise in P_CO2 would cause us to breathe before this happens. Just like P_CO2, however, if P_O2 drops too low, then the entire brain gets depressed and can't breathe. Another trap to watch out for is that P_O2 is only a measure of dissolved oxygen, and not the total amount (i.e. dissolved oxygen plus oxygen attached to haemoglobin). Hence, in severe anaemia or in carbon monoxide poisoning (where carbon monoxide preferentially binds to haemoglobin rather than oxygen), this respiratory reflex will not kick in and so the patient might die of oxygen deprivation.

Understand exercise induced hyperventilation 

As I'm sure you are well aware, you breathe faster when you exercise. This isn't so much due to changes in P_CO2 or P_O2- during heavy exercise, sometimes our breathing rate is so great that P_CO2 might actually decline or P_O2 might increase. Also, breathing rate often increases before exercise, as a kind of anticipatory response.

Here are some possible mechanisms through which exercise increases ventilation:

• Input from higher cortical centres- this might explain why breathing rate increases before exercise.
• Proprioception- input from receptors in our muscles etc.
• Increase in body temperature
• Secretion of stress hormones such as adrenaline
• Increased sensitivity of chemoreceptors

Now for a quickie on how breathing rates and CO₂ levels fluctuate during and after exercise! As I just mentioned, when you start exercising, or slightly before you start exercising, your breathing rate increases. As your metabolic rate hasn't actually increased yet, you will be blowing off more CO₂ than you are producing, so your CO₂ levels will drop temporarily. As you exercise, your CO₂ production will increase, so eventually your CO₂ levels will be back to normal. When you finish exercising, your breathing will return to normal, but it will be a bit longer before your metabolic rate decreases as well. Hence your CO₂ levels will increase temporarily following exercise.

Discuss other reflexes controlling respiration

There are two main reflexes that you need to know:

1. Hering-Breuer Inflation Reflex: This reflex prevents overinflation of the lungs. Overinflation is picked up by stretch receptors in the smooth muscle of the airways.
2. Irritant Receptor Reflex: This is essentially just coughing or sneezing to get rid of irritants.

And that's it for respiration! Next I'll go back to talking about cardiovascular physiology (which was actually meant to be the first topic after control systems, but I was having issues with the respiratory stuff *cough*Flow-Volume plots*cough*).