(This page is pertinent to both lecture and lab.)
The figures to the right were obtained from the lab meeting at Tuesday at 10:30. Be sure you understand the instructions given to the subject. (Ignore the small decrease near the end of the graph, which occurred after the subject stopped exhaling.)
Our experiment in lab followed the end-tidal CO2 and respiratory rate as our subjects expended progressively more energy on a bicycle ergometer. But before looking at the results, let's review the sensors that influence ventilation.
What is the name of the most important sensor controlling ventilation, where is it found, and what is the factor in the blood that it is monitoring?
The second sensor is the peripheral chemoreceptor. Where is it found? Also, what are two factors in the blood that it monitors?
Now let's look at the correlation between end-tidal CO2 and respiratory rate. The results from our subject in the lab meeting on Tuesday at 10:30 are shown below.
First, observe the end-tidal CO2 when the subject is at low levels of exercise. The subject is averaging a little over 30 mm Hg, which is lower than one would expect, although people vary. But notice at the very beginning it is even lower. This is not unexpected because breathing is so strongly influenced by anticipation. Almost all subjects in the respiratory experiments hyperventilate at first. Notice that the respiratory rate at first is about 15-25 breaths/min. If you measure your own respiratory rate now, your would probably find that it is between 10 and 15 breaths/min. Feedforward effects on the respiratory and cardiovascular system are usually very noticeable. The anticipation ensures that blood gases and the arterial pressure do not change with the onset of exercise in a healthy person.
Observe then that starting between 9 and 10 minutes something is happening. I am sure you know what this is.
So what sensor is driving this increased ventilation?
Finally, observe the data at 15 minutes after the subject has rested for 2 minutes. The respiratory rate has decreased appreciably, but the end-tidal CO2 is about 22 mm Hg. Why is this?
Why is the higher respiratory rate connected to a lower end-tidal CO2?
Does the hyperventilation increase the amount of oxygen in the arterial blood appreciably?
Why are we measuring CO2 at the END of a breath?
Above, we found that end-tidal CO2 is used to estimate the partial pressure of carbon dioxide in alveoli. But where does this lead us?
In a healthy person, can we safely assume that the partial pressure in the alveoli is also a good estimate of the partial pressure in the systemic arterial blood (approximately)?
The sensors controlling respiration respond to the partial pressures of gases on the blood. So what does our experiment with end-tidal CO2 show us about the regulation of breathing?
The figure to the right shows the expected changes in PaO2 and PaCO2 as the level of exercise increases in an exercise tolerance test.
Observe that the PaO2 actually increases somewhat past the lactate threshold (vertical dotted line), while the PaCO2 decreases. This, of course, is not what one expects intuitively. At the extremes of exercise, it feels as if one is struggling to get enough oxygen. In reality, the hemoglobin in blood leaving the lungs is essentially saturated with oxygen at all levels of exercise.
These changes in the blood gases are the result of the great increase in ventilation that results from the addition of lactic acid to the blood.
Why is the reduction in the PaCO2 above the lactate threshold helpful?
Why does the reduced PaCO2 cause alkalosis?
Below is the data from the breath-holding experiment from the lab meeting at 2:30 on Tuesday. Note the overall flow of the experiment: The subject holds his or her breath and we measure the alveolar gases. Then we change one gas, but not the other, and then repeat the breath holding and the measurement of the alveolar gases. We are trying to identify which gas is most important.
|no hyperventilation||85 sec||96||.103||.0703||78.8||53.8|
First notice the alveolar partial pressures in the subject when breathing quietly at rest. The subject was encouraged not to hyperventilate, but it is difficult not to hyperventilate with the whole class watching! All of the subjects hyperventilate a little here, but here there is not much. Without hyperventilation, one would expect approximately 40 mm Hg for the PACO2, although people do vary, as usual. (The oximeter was reading about 2% too high, so the actual values for %Hb are about 2% lower.)
Now notice the partial pressures when the subject "breaks" after breath holding. But is it the O2 or CO2 that is driving the desire to breathe again? To try and answer this, we had the subject hyperventilate, allowing the subject to hold their breath longer.
But what was the point of the hyperventilation?
Notice that the subject held their breath significantly longer after hyperventilation substantially lowered the CO2. This by itself shows the importance of the PaCO2 in determining the desire to breathe after breath holding.
Now notice which gas changed quite a bit, and which one returned nearly to the same value. Hopefully, this is what you would predict. Notice that the partial pressure of oxygen decreased when the breath was held longer, because oxygen was being consumed for a longer time and the hemoglobin saturation dropped. Carbon dioxide, of course, was being produced longer, but it started at a much lower level due to the hyperventilation.
Since the PO2 only fell to 69, it was not quite at a level that would stimulate the peripheral chemoreceptor. So in this subject, it appears that it was only the central chemoreceptor that was causing the subject to stop the breath holding at about a PCO2 of 53 mm Hg.