Regarding dead space, choose the FALSE statement

Correct Answer: C

Rationale: Dead space refers to the portion of the tidal volume that does not participate in gas exchange. Anatomical dead space includes the conducting airways (e.g., trachea, bronchi), while physiological dead space includes both anatomical dead space and any alveolar dead space (alveoli that are ventilated but not perfused). The statement that physiological dead space is the same as alveolar dead space is false because physiological dead space encompasses both anatomical and alveolar components, not just the latter. Measuring physiological dead space involves the Bohr method, which uses mixed expired PCO2, arterial PCO2, and tidal volume, so that statement is true. Mechanical ventilation can increase dead space by adding apparatus dead space (e.g., tubing), and an increased ventilation/perfusion (V/Q) ratio can occur in conditions like pulmonary embolism, where ventilation exceeds perfusion, both of which are accurate. The false statement hinges on the incorrect equivalence of physiological and alveolar dead space, as physiological dead space is a broader concept that includes all non-gas-exchanging volumes, not limited to poorly perfused alveoli.

Correct Answer: B

Rationale: The percentage of CO2 in a structure reflects its PCO2, tied to metabolic production and gas exchange. Pulmonary arteries carry deoxygenated blood from the right heart to the lungs, with a PCO2 of ~45-46 mmHg (venous blood), the highest among options, as it's loaded with CO2 from systemic tissues. Alveolar air has a PCO2 of ~40 mmHg, equilibrated with arterial blood after CO2 diffuses out during respiration. Pulmonary veins, post-gas exchange, carry oxygenated blood with a PCO2 of ~40 mmHg, matching arterial levels. Interstitial fluid's PCO2 varies but approximates venous blood (~45 mmHg) or slightly less, depending on local metabolism, though it's not a standard respiratory measure. Systemic arteries, not listed, also have ~40 mmHg. Pulmonary arteries stand out with the highest CO2 due to their role in transporting metabolically produced CO2 to the lungs for excretion, before alveolar ventilation lowers it, making them the site of peak CO2 concentration.

Correct Answer: C

Rationale: Functional residual capacity (FRC) is the lung volume after a normal expiration (~2.5-3 L), the resting state where lung inward recoil balances chest wall outward recoil. It's the lung's resting volume, but also reflects the thorax's state, though these aren't mutually exclusive options. The key true statement is that at FRC, intra-alveolar pressure equals atmospheric pressure (~760 mmHg), as no airflow occurs (P = 0 gradient), and muscles are relaxed. Intrapleural pressure (IPP) at FRC is negative (~-4 mmHg, 756 mmHg), not more than atmospheric (760 mmHg), due to recoil forces keeping lungs expanded rising above atmospheric only in pathology (e.g., pneumothorax). Lung compliance varies with volume, not lowest at FRC, which is a mid-range point. The equality of alveolar and atmospheric pressure at FRC is a fundamental respiratory principle, ensuring stability at rest, making it the standout true statement.

Correct Answer: D

Rationale: When inspiratory muscles (diaphragm, external intercostals) relax, as after a normal expiration, the lungs reach functional residual capacity (FRC, ~2.5-3 L), the resting volume where lung inward recoil balances chest wall outward recoil. Vital capacity (VC, ~4-5 L) is the maximum exhailable volume after maximal inhalation, requiring active inspiration, not relaxation. Residual volume (RV, ~1-1.5 L) is the air left after maximal expiration, beyond relaxed expiration. Minimal volume' isn't a standard term but might imply RV or zero (collapsed lungs, not natural). FRC is the equilibrium state at rest, with intra-alveolar pressure equaling atmospheric (~760 mmHg), no airflow, and muscles inactive, distinguishing it as the volume post-relaxation, critical for baseline gas exchange and respiratory mechanics.

Correct Answer: B

Rationale: Surfactant, a phospholipid-protein mix from type II alveolar cells, lowers surface tension in alveoli, stabilizing them against collapse. Normally, high surface tension from water (72 dynes/cm) pulls alveoli inward, but surfactant reduces this (to ~5-10 dynes/cm), decreasing the tendency to collapse per Laplace's law (P = 2T/r). It also reduces surface tension forces directly, easing lung expansion. Lower tension decreases lymph flow by reducing fluid shifts into the interstitium from high alveolar pressures. However, lung compliance the ease of expansion increases with surfactant, as lower tension makes lungs less stiff, requiring less pressure for a given volume (C = ΔV / ΔP). Thus, compliance rises, not falls, making it the exception. This increase is vital in neonates and prevents atelectasis, contrasting with the other factors, which diminish as surfactant stabilizes alveoli and reduces mechanical stress, a key adaptation for efficient breathing.