Chapter 48

1. At sea level, assuming a normal atmospheric pressure of 760 mm Hg, the P_O2 will be 20.9 percent of that, or 159 mm Hg. Therefore the P_O2 at 2,000 meters will be 127 mm Hg. When breathing air at two times the atmospheric pressure, the P_O2 will be 318 mm Hg.

2. Flatworms have a flat, thin body form, so all cells of the body are close enough to the surrounding environment that O₂ and CO₂ can diffuse directly between the cells and the environment. The two components of Fick’s law reflected in these anatomical features are high surface area for diffusion, and minimal path length.

3. As water temperature increases, the O₂ content of water decreases (O₂ solubility decreases with increase in temperature), but since the fish’s body temperature is at equilibrium with the water temperature, its metabolism increases (Q₁₀ effect). Therefore the fish has to ventilate its gills more to satisfy its O₂ needs, and the work of gill ventilation increases O₂ demand even more.

4. In going from sea level to high altitude, the partial pressure of O₂ in the inhaled air decreases, so the partial pressure gradient causing O₂ to diffuse into the body goes down. Since the partial pressure of CO₂ is extremely low at sea level, it does not decrease significantly at high altitude. Therefore the partial pressure gradient for CO₂ diffusing out of the body does not change.

1. If ventilation (water) and perfusion (blood) of the gills are in the same direction (concurrent flow), then the concentration gradient of O₂ across the gills will gradually equilibriate somewhere between the maximum O₂ concentration of the water coming in and the O₂ concentration of the blood coming in. In countercurrent flow, it is possible for the O₂ concentration of the blood leaving the gills to be almost as great as the O₂ concentration of the water entering the gills.

2. An important feature of avian lungs is the parabronchi, which enable air to travel unidirectionally through the lungs. When a bird inhales, the incoming air goes to the posterior air sacs. That fresh air flows into the parabronchi during the next exhalation. The subsequent inhalation causes air in the lungs to flow into the anterior air sacs while fresh air flows into the posterior air sacs. The subsequent exhalation empties the anterior air sacs to the environment while the air in the posterior air sacs enters the lungs. Thus the through-pass of the parabronchi and the bellows action of the air sacs result in continuous, unidirectional flow of air through the avian lungs.

3. The amount of He in the system remains the same but becomes equally distributed in the spirometer and lungs. So the initial amount of He is 0.05 × 30 L = 1.5 L. The final amount of He is still 1.5 L, but it is distributed over 30 L + the person’s FRV. Thus,

   1.5 L = 0.046 × (30 L + FRV)

   1.0 L = 1.38 L + 0.046FRV

   0.12 L = 0.046FRV

   2.61 L = FRV

1. Some premature infants may be born before cells in their alveoli have started to secrete surfactant. Without surfactant, inflation of the lungs requires extra effort to overcome surface tension in the fluid lining the alveoli.

2. There is always tension between the pleural membranes because of the outward pull of the chest wall and the inward pull of the lung tissue. This tension keeps the lungs partially inflated even between breaths. A puncture of the chest wall allows air to enter space between the pleural membranes, equilibrating its pressure with atmospheric pressure. As a result, there is no longer a force maintaining partial inflation of the lungs.

3. The tension between the pleural membranes is maximal at the peak of inhalation because it is maintaining maximum distension of the lung tissue, but once the lungs are filled, air flow ceases and the alveolar pressure is the same as atmospheric pressure.

1. Because of mixing with dead-space air, the maximum P_O2 in the alveoli is about 100 mm Hg, and hemoglobin can fully saturate at that P_O2. The fact that mixed venous blood normally returns to the heart 75 percent saturated means that if the blood flows through any tissue that is very active metabolically, it has a reserve of O₂ that it can off-load to satisfy that local high demand.

2. When the concentration of 1,3-BPG in stored red blood cells decreases, so does the concentration of 2,3-BPG that can be generated by conversion from 1,3-BPG. As a result, the hemoglobin–O₂ binding/dissociation curve shifts to the left. Therefore the O₂ is more tightly bound to the hemoglobin and is not released for use by the respiring cells.

3. The conversion of CO₂ to H₂CO₃ and then to HCO₃^– is a reversible reaction depending on the concentrations of reactants and products. In the respiring tissues the P_CO2 is high and drives the reaction in the red blood cells toward HCO₃^–, which moves into the blood plasma in exchange for Cl^–. In the alveoli, the P_CO2 is low, so this entire suite of reactions is driven in reverse, meaning that the diffusion of CO₂ out of the red blood cells causes HCO₃^– to be moved back into the red blood cells to be converted back to H₂CO₃ and then to CO₂.

1. During tidal breathing, a regular cyclical pattern of firing of respiratory motor neurons in the dorsal respiratory group of the medulla drives muscle contractions of the diaphragm. The need for increased respiratory gas exchange is first met with an increase in the rate of that oscillatory pattern of firing in the dorsal respiratory group, but as the need increases, the ventral respiratory group is recruited and those neurons drive contractions of the intercostal muscles, increasing the volume of air exchanged with each breath.

2. When you go to high altitude, the diffusion gradient for O₂ decreases as atmospheric pressure decreases. However, the diffusion gradient for CO₂ does not change; ambient CO₂ is close to 0 at sea level and also at high altitude. Therefore breathing to satisfy O₂ needs results in a greater loss of CO₂ than at sea level. Since CO₂ is the major stimulus for respiration, respiration slows or ceases until the P_CO2 returns to a level that stimulates breathing.

3. Because the carotid and aortic bodies have high metabolic rates, they are compromised by a decrease in their O₂ supply, whether it is because of decreased blood flow or decreased P_O2 in the blood.

1. Since helium is not absorbed by the respiratory system, the amount of helium remains the same after breathing from the air reservoir as before, but it is distributed in both the reservoir air and the functional residual volume (FRV) of the patient. Using the helium dilution method, we can calculate the FRV.

   0.050 × 30 L = 0.044 (30 L + FRV)

   1.5 L = 1.32 L + 0.044 × FRV

   (1.5 – 1.32)/0.044 = FRV = 4.1 L

   Subtracting the expiratory reserve volume of 1.5 L gives a residual volume of 2.6 L.

2. The patient is always short of breath because the P_O2 in his alveoli is seriously diminished by the stale air in his very large residual volume as well as in his increased FRV during tidal breathing.

1. O₂ available in venous blood:

   Total venous blood = 355 kg × 0.148 × 0.66 = 34.7 kg

   Total venous hemoglobin = 34.7 kg × 0.58 × 0.24 = 4.8 kg

   Total venous O₂ available = 4.8 kg × 1.34 L/kg × 0 .9 = 5.8 L

2. O₂ available in myoglobin:

   Total amount of myoglobin: 355 kg × 0.33 × 44g/kg = 5.2 kg

   O₂ bound to myoglobin: 5.2 kg × 1.34 L/kg = 7 L

3. Total O₂ reserves at beginning of dive:

   2.5 L + 5.8 L + 7.0 L = 15.3 L

4. Maximum sleep episode = total O₂ reserves divided by the diving metabolic rate. So, 5.3 L divided by the rate of O₂ consumption which for a long dive would be 0.0035 L/kg min × 355 kg. So, 15.3L/ 1.24 L/min = 12.3 min, which corresponds well with the observed maximum sleep episode of 13.5 min.

5. A-50

   Assuming the overall dive metabolic rate of 4.5 mL O₂/min kg, the maximum dive time would be 15.31/(0.0045 mL O₂/min × 355 kg) = 10 min, which is much less than the observed dive times.

1. In Figure A, in the 15 minutes that the spiracles were open, the intratracheal O₂ level increased from 19 to 142 mm Hg. In the 22–23 minutes in which the spiracles were closed, the intratracheal level of O₂ dropped from 142 to approximately 37.5 mm Hg. In the approximately 70 minutes that the pupae entered the fluttering phase, the intratracheal O₂ level fluctuated between 37.5 and 18.75 mm Hg. In Figure B, the first chamber’s atmospheric O₂ concentration was 48 mm Hg, but the fluttering phase kept the intratracheal O₂ levels at a fairly consistent 36.75 mm Hg. In the second chamber, the atmospheric O₂ levels were 159 mm Hg. The fluttering phase allowed some fluctuation in the intratracheal O₂ levels, from a high of roughly 38.25 mm Hg to a low of roughly 36 mm Hg. In the third chamber, atmospheric levels of O₂ were almost double normal atmospheric O₂ levels, at 301.5 mm Hg. But the fluttering phase kept the intratracheal O₂ level at an almost constant 30 mm Hg.

2. When the tracheal tubes open, the atmospheric O₂ diffuses into the tubes, bringing the intratracheal O₂ level close to normal atmospheric O₂ levels (159 mm Hg). However, over the approximately 23 minutes that the spiracles are closed, the O₂ levels are slowly depleted as more O₂ is dissolved into the hemocoel and distributed to all of the cells to be used in aerobic respiration. We could predict that this O₂ level would continue to decline, approaching zero, if it were not for the fluttering phase. The fluttering phase appears to allow CO₂ to escape into the atmosphere while also allowing small amounts of O₂ to enter the tracheal tubes and maintain O₂ levels at a fairly constant level.

3. A delicate balance must be maintained between intratracheal O₂ levels and atmospheric O₂ levels. When atmospheric levels of O₂ are normal (middle graph in Figure B), the fluttering phase allows CO₂ release and replacement of O₂ to seek a fairly constant level of O₂ within the trachea. In a low-oxygen environment (first graph in Figure B), the fluttering phase is increased, compared with a normal atmospheric O₂ level. Beginning at a lower level of O₂ at the time of spiracle closure would make it necessary to increase the amount of fluttering to keep O₂ levels at an appropriate intratracheal concentration for adequate aerobic respiration. However, when atmospheric O₂ levels are abnormally high, the fluttering phase is greatly diminished (third graph in Figure B). Opening the spiracles as often as what is seen under normal atmospheric O₂ levels could expose cells to higher than normal O₂ levels. These levels could prove detrimental to insect cells. Therefore decreasing the amount of fluttering would be one way to prevent too much O₂ from entering the tracheal tubes and reaching a toxic cellular level.