1. Which, if any, of the lung volumes that you measured would you expect
to change during exercise? How might these changes be accomplished?
Obviously, FVC does not change (it is the maximum possible), and TV increases. There are two possible ways to increase TV: either increase inspiration (top of the curve goes higher) or increase expiration (bottom of the curve goes lower). Because normal breathing involves muscle contraction during inspiration, and no contraction during expiration, most people increase TV by increasing the contraction occurring during inspiration, and leaving the expiration a result of relaxation. As inspiration increases, IRV decreases and EC increases (but ERV and IC remain unchanged). If you begin to forcefully exhale and increase expiration as well, then ERV would decrease and IC would increase.
2. How do characteristics like height, weight, aerobic training or gender
influence lung volumes, esp FVC, in your group?
FVC increases with size (it correlates better with height than with weight), it is smaller in women than in men, and it decreases with age. Aerobic training has little effect on FVC.
3. Why must a person floating on the surface of the water and breathing
through a snorkel increase his tidal volume and/or breathing frequency
if alveolar ventilation is to remain normal?
The snorkel effectively increases the length of the airways and increases the Dead Space (DS). Because VA = (TV - DS) * f, and increase in DS would cause a decrease in VA without a compensatory increase in TV (or f).
4. Look at the following examples of forced expirations. Given
what you know about obstructive and restrictive lung disease, indicate
which patient is normal, which suffers from obstructive disease, and which
suffers from restrictive disease. How do you know?
Patient X is normal; his FVC is large (about 5 L) and his expiration is rapid (so FEV1/FVC is about 80%). Patient Y has obstructive disease; his expiration is slow, so FEV1/FVC is distinctly less than 80%. Although FVC is reduced, it is due to an incomplete expiration; inspiration up to the 5 L mark is normal. Patient Z has restrictive disease; his inspiration is restricted from increasing past 3 L, and his expiration is as fast as normal (FEV1/FVC is about 80%, because both are reduced proportionally).
5. What effect does PaCO2 have on the respiratory control
center? Do your results also suggest how PaO2 might affect
the control center?
An increase in PaCO2 causes the respiratory center to increase ventilation. If the increase is due to apnea, then the increase causes the respiratory center to force an end to the apnea (so breathing resumes). Although the different breathing techniques cause a change in oxygen level (see question #9) as well as a change in carbon dioxide level, the CO2 feedback loop dominates the O2 feedback loop. An investigation of the affect of PaO2 would require an experimental protocol that kept PaCO2 constant, and your experiment did not do that, so your results do not apply to oxygen levels.
6. Why can you stay underwater longer if you hyperventilate first, and
why do some people drown as a result?
By hyperventilating, you expell more CO2 than normal, reducing your starting PaCO2 level. Consequently, it takes longer for PaCO2 to increase to an uncomfortable level, so you can hold your breath and stay underwater longer. Because hemoglobin is well saturated by normal breathing, hyperventilation increases your oxygen supply very little. With a very low starting PaCO2, your oxygen is depleted before the CO2 has reached the unbearable level, and the low oxygen causes you to pass out and drown.
9. How do the three ventilation conditions effect PaO2 and
Compared to the normal levels of PaO2 and PAO2 that result from normal breathing, hyperventilation pulls more oxygen-rich air into your lungs, thereby increasing PAO2, which is in equilibrium with PaO2, so that too increases. However, less than 2% of oxygen carried by arterial blood is dissolved, so the increase in PaO2 has little effect on dissolved oxygen levels, and hemoglobin is already saturated, so the increase in PaO2 has little effect on bound oxygen levels. Breathing with a bag results in a decrease in PAO2, and consequently a decrease in PaO2. Given the hemoglobin saturation curve in your textbook and the value of %O2 that you measured, did you breath with the bag long enough to decrease the PaO2 to a level at which the hemoglobin was not completely saturated?