Breathing Control

Nervous control of breathing movements
1. Centers
  1. Medulla oblongata
    1. Dorsal respiratory group (DRG)
      1. Inhalation
    2. Ventral respiratory group (VRG)
      1. Exhalation
  2. Pons
    1. Pontine respiratory group (PRG)
      1. Exhalation
    2. Apneustic center
      1. Inhalation & rate
      2. Constant signals to DRG
2. Control of normal quiet breathing – a somewhat passive process
  1. DRG active for 2 sec → impulses to respiratory muscles → inhalation
  2. DRG inactive for 3 sec → no impulse to respiratory muscles → relax → exhalation
  3. RECAP: Inhalation with passive exhalation
3. Control of rapid deep breathing – a more active process
  1. Apneustic center stimulates DRG
  2. DRG stimulates:
    1. Respiratory muscles → inhale
    2. PRG
    3. VRG
  3. PRG inhibits:
    1. Apneustic center
      1. Stops signals to DRG
    2. DRG
      1. Stops inhalation
  4. VRG:
    1. Stimulates respiratory muscles to relax → exhale
    2. Inhibits DRG
  5. When the DRG stops, so do all the inhibitory signals
    1. Allows apneustic center to turn the DRG back on again
    2. The cycle continues
  6. RECAP: Inhalation with forced exhalation
  7. Analogy: “The Useless Box”
    1. Apneustic center = hand flipping switch
    2. DRG = switch to turn on inhalation, PRG, and VRG
    3. PRG/VRG = turn the switch back off
      1. → Exhalation
Chemical regulation of breathing rate
1. Factors
  1. pCO2 in arterial blood
  2. [H+] in arterial blood
  3. Lack of O2 in arterial blood
  4. All based on the Carbonic Acid reaction
    1. CO2 + H2O ←→ H2CO3 ←→ H+ + HCO3–
2. Hypercapnia – pCO2 elevated above normal
  1. Carbonic acid reaction shifts to the right
  2. Increased H+ sends nerve impulses to the respiratory centers in the Medulla Oblongata
  3. Impulses sent to respiratory muscles to increase respiratory rate (hyperpnea)
  4. More exhalation of CO2 = decreased pCO2 in blood
  5. Carbonic acid reaction reverses
  6. Decreased H+ stops nerve impulses
  7. Return to eupnea (normal breathing)
3. Acidosis – high H+ concentration in blood
  1. Respiratory acidosis
    1. Decreased pH caused by increased pCO2 (hypercapnia)
  2. Metabolic acidosis
    1. Increased acid in blood related to metabolic (lactic acid, ketoacids, excess H+)
  3. What happens
    1. Increased H+ in blood
    2. Peripheral chemoreceptors in internal carotid artery send impulses to respiratory center in Medulla Oblongata
    3. Impulses sent to respiratory muscles to increase respiratory rate (hyperpnea)
    4. Decreases CO2 to TRY to decrease acidity of arterial blood
    5. Respiratory acidosis – helps to solve the problem
    6. Metabolic acidosis – process continues until the source of acid is terminated
      1. Respiratory center attempts to alleviate, but can’t completely fix it
4. Hypoxemia – lack O2 in arterial blood
  1. Detected by peripheral chemoreceptors
  2. Signals to Medulla Oblongata
    1. Increase respiratory rate and depth
    2. Increased O2 respiration
  3. Occurs at high altitudes in normal person

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Transcript

In this lesson we’re going to talk about the aspects of our body systems that actually control our breathing.

There are two main things that help control breathing. One is nervous control, which involves breathing centers in the brain stem and nerve signals to the respiratory muscles. We also see chemical regulation where our brain makes changes to our breathing based on chemical concentrations in the blood. We’re going to talk about each of these two things separately and hopefully make them a little easier to understand for you.

First, let’s look at the main breathing centers in the brain. Remember, these breathing centers are in the two parts of the brainstem called the medulla oblongata and the pons. In the medulla we have the dorsal respiratory group or DRG and the ventral respiratory group or VRG. In the pons, we have the pontine respiratory group or PRG and the apneustic center. Now, in this image you’ll see that the apneustic center sends signals to the DRG – which sends signals to the external intercostals and the diaphragm. Remember from the breathing movements lesson that those are the muscles involved in inhalation and normal at rest exhalation. The DRG also sends signals to the VRG if necessary to control the accessory respiratory muscles like the abdominal muscles and the internal intercostals – this would be for rapid or forceful exhalation, like during exercise. You’ll also notice that the pontine respiratory group also sends inhibitory signals back down to the DRG – this becomes a little negative feedback loop to help with our respiratory cycle. So let’s look closer at how these different centers work together for breathing.

Now – during normal quiet breathing, we don’t see that much happening. Basically the DRG is active for 2 seconds, allowing those respiratory muscles to contract, then it’s inactive for 3 seconds, allowing them to relax. Remember that in normal, quiet breathing, our relaxation is actually a passive process. We contract to inhale, then simply relax to exhale. All of this is controlled in the medulla by the dorsal respiratory group. But – if we start to have more active, rapid, deep breathing, we’ve got to do things a little differently.

That’s where the rest of the breathing centers come into play. In rapid, deep breathing, the apneustic center basically starts sending constant signals to the DRG. When the DRG gets stimulated, it sends signals to the respiratory muscles to inhale, just like it normally would. But it is also going to send signals to the PRG and the VRG – so let’s look at what those two centers do. The PRG will actually turn around and inhibit the apneustic center AND the DRG. So basically, the apneustic center turned on the switch (which is the DRG) and the PRG turns right back around and turns them both off again. In just a minute I’m going to give you an illustration that will make this make so much more sense, but remember the DRG also stimulated the VRG, so let’s look at what the VRG is doing. The VRG will stimulate those OTHER respiratory muscles, the abdominal muscles and internal intercostals, to force a more rapid exhalation. And, it, TOO, will turn around and inhibit the DRG. So what the heck – the apneustic center turns on the DRG, the DRG tells us to breathe, and turns on the PRG and VRG, which both turn around and turn the dang DRG off again. Well, again – this is our negative feedback loop. As soon as the DRG is off, these inhibitory signals will also stop – which allows the apneustic center’s constant signals to turn the DRG back on again – it’s a cycle! Let me give you an illustration that will help…

Some of you may have seen this before, or something like it. The hand turns on the switch, the switch makes the box open and the arm come out, which then turns the switch back off. If you google “useless box” or “useless machine” you’ll find dozens of videos, some of them are pretty funny. So how does this relate? The apneustic center turns on the DRG – we inhale (that’s the box opening). That turns on the PRG and VRG (which is the little arm) – which turns the DRG back off again (the switch) and let’s us exhale (the box closes) – then, the apneustic center is now able to turn the drg back on again!

So – the hand is the apneustic center. The switch is the DRG. The box opening is inhalation. The arm is the PRG and VRG. And the box closing is exhalation. Let’s watch it one more time – but you can always come back and watch this over and over to get it!

Breathe in. Breathe out. Breathe in. Breathe out. Remember the apneustic center signals are constant, so once it’s no longer inhibited, it just turns the DRG right back on again! Breathe in. Breathe out. Breathe in. Breathe out. I hope that helped! I love this little box!

Okay, now that you’ve got that. Let’s talk about chemical regulation of breathing. There are three main things that the body will respond to. Changes in the partial pressure of carbon dioxide, written pCO2, changes in hydrogen ion concentration – so this would be like acidosis or alkalosis – and a lack of oxygen. The main factor here for all of this is the carbonic acid reaction. You may have seen this before in chemistry, but this is the basis for most of our acid-base balance in the body. We start with CO2 which gets added to water or H2O. Those together become H2CO3, which is carbonic acid. But, carbonic acid is unstable and will immediately break apart into hydrogen and bicarbonate. As you can see, this reaction could go either way depending on the situation. If we have too much CO2 it will shift to the right to make hydrogen and bicarb. If we want to make more CO2 to try to exhale it, it shifts to the left. So let’s look at a couple of examples of what happens to our breathing because of these reactions.

First we’ll talk about hypercapnia, which is a high partial pressure of carbon dioxide or pCO2. Partial pressure is just the fancy way we measure concentrations of gases. So – if I have a lot of CO2, the carbonic acid reaction or C-A-R shifts to the right. That leads to more hydrogen ion concentration in the blood. THAT sends a signal to the medulla oblongata (which we just talked about) and tells it to increase the respiratory rate. A faster respiratory rate means I’m exhaling more CO2, so my CO2 levels drop. The C-A-R can reverse or stop, so we stop having too much hydrogen, the signals to the medulla stop, and our respiratory rate can return to normal – which remember is called eupnea. So it’s basically a feedback loop, too – too much CO2 – create more hydrogen – tells the brain to breathe faster to get rid of the CO2 – I stop creating more hydrogen – brain signals stop – breathing goes back to normal.

Another time we see basically the same reaction is in acidosis. Acidosis is when we have too much hydrogen in the blood. The only difference here is that that excess hydrogen may not be from this reaction – it might be because of OTHER acids in the blood. Ultimately we see the same response – a signal to the medulla to increase the respiratory rate – and a decrease in CO2 because we’re breathing it all off. The goal here is to shift this back to the left, decrease the acids, and return to normal breathing. But again – remember that this could actually be from a totally different source of acids – so if we don’t actually correct the original problem, then this fast breathing (or tachypnea) will just continue and continue. So – remember in acidosis NOT caused by too much CO2, we always have to correct the source of the problem to fix the patient!

Lastly, the body has peripheral chemoreceptors that respond pretty strongly to low oxygen levels in the tissues, or hypoxia. This will also send signals to the medulla to increase our respiratory rate to try to help us get more oxygen into our system. Now – one thing to note is that at high altitudes, the atmosphere tends to just have less oxygen in it. So when people go up to higher altitudes, like if they’re climbing a mountain or something, we’ll see their respiratory rate increase to try to help them get more oxygen. This is a normal response. Over time, the body will acclimate and the respiratory rate will come down a little – but generally speaking, it stays higher than it would at sea level. I can tell you this from personal experience. I recently moved from South Carolina to Colorado and holy moly. I am always breathing really fast, especially when I work out, just to try to get oxygen!! I went from about 100 feet above sea level to 6500 feet! Definitely feeling the effects of less oxygen, that’s for sure!
Okay, let’s recap. Remember that our bodies have both nervous control and chemical control of our breathing. We have 4 main breathing centers in the medulla oblongata and the pons – the apneustic center, and the dorsal, ventral, and pontine respiratory groups. These help to create a negative feedback loop as the signals cycle around to help create our respiratory cycle of inhalation and exhalation. And the main chemical factors are changes in pCO2, changes in hydrogen concentration, and a lack of oxygen – and a huge contributor to all of this is the carbonic acid reaction. We’re going to talk more about the role of the carbonic acid reaction in the lesson on the respiratory functions of blood, so make sure you check that out.

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