1. The conducting division has a relatively thick wall with supportive cartilage, smooth muscle, and a ciliated mucosa. The cartilage keeps it from collapsing, the smooth muscle regulates airflow and dead space, and the mucosa secretes mucus while the cilia propel the mucus upward. The respiratory division must have a thinner wall to allow for gas exchange. It lacks muscle and cartilage, does not secrete mucus, and is not ciliated. Most of its epithelium is simple squamous.

2. Hyperventilation would not significantly affect blood P_o2. The reason is that the blood is already 97% saturated with oxygen even in eupnea, so hyperventilation can add very little. It does, however, expel CO₂faster than it is produced and significantly lowers the blood P_co2. This leads to a rise in blood pH. Emphysema involves a loss of alveolar surface area and thus reduces the uptake of O₂ and release of CO₂. Therefore, the P_o2 is reduced, P_co2 is elevated, and the pH is reduced.

3. As explained in the previous answer, hyperventilation cannot significantly increase the P_o2 of the blood. It does, however, lower the P_co², which delays the time when P_co2 reaches a level that demands resumed breathing. By that time, a person can be dangerously hypoxemic and may faint.

4. His minute respiratory volume is (650 mL/breath)(11 breaths/min) = 7,150 mL/min = 7.15 L/min. With a dead space of 185 mL, his alveolar ventilation rate is (650-185 mL/breath)(11 breaths/min) = 5.12 L/min.

5. In this incident, from an actual case report, the nasoenteric tube was misdirected down the woman's trachea and bronchus instead of her esophagus. It pierced the lung surface, allowing inhaled air to escape into the pleural space. The patient exhibited pneumothorax and atelectasis.

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