The greatest increase in the physiological dead space would be expected with?

Correct Answer: A

Rationale: Physiological dead space (VD) is the volume of ventilated air not participating in gas exchange, comprising anatomic dead space (conducting airways) and alveolar dead space (non-perfused alveoli). Pulmonary embolism (PE) blocks pulmonary arteries, reducing perfusion to ventilated alveoli, markedly increasing alveolar dead space and thus physiological VD (e.g., from 150 ml to 300+ ml), as large lung regions become wasted ventilation.' Atelectasis collapses alveoli, reducing ventilation and dead space, as unventilated areas don't contribute to VD. Pneumothorax collapses lung tissue, decreasing ventilated volume, not increasing dead space. Bronchoconstriction narrows airways, potentially reducing anatomic dead space slightly, and doesn't directly increase alveolar dead space unless severe hypoxia ensues. PE's perfusion defect creates the greatest VD rise, measurable via increased PaCO2-PECO2 difference, distinguishing it as the most impactful condition among these, reflecting a high V/Q mismatch.

Correct Answer: C

Rationale: Respiratory distress syndrome (RDS) in premature infants arises from immature lungs lacking sufficient surfactant, a phospholipid mixture from type II alveolar cells that reduces alveolar surface tension. Limited surfactant synthesis increases tension, causing alveolar collapse (atelectasis) and low lung compliance lungs become stiff, requiring higher pressures for ventilation, all true features. Positive pressure respirators are standard to maintain oxygenation and prevent collapse, also true. However, the statement about lung compliance being low is universally true in RDS, not the exception. A potential misinterpretation might expect a false statement like alveoli overexpand and burst,' but among these, all align with RDS pathophysiology. If NOT true' implies a trick, low compliance is still consistent, suggesting a contextual error yet, per options, none stand out as false. Assuming standard RDS traits, all are true, but compliance's consistency might confuse; still, it's not the exception intended, requiring re-evaluation of intent. Here, all fit RDS, making C a default choice if misworded.

Correct Answer: B

Rationale: Airway resistance follows Poiseuille's law (R ∝ 1/r^4), but total cross-sectional area governs overall resistance. The trachea, a single tube (~2 cm diameter), has ~3-4 cm² area. Bronchioles, numbering thousands, reach ~300 cm² collectively at terminal stages, yet pale beside alveoli. Alveoli (~300 million) total ~70-100 m² (~700,000-1,000,000 cm²) during inspiration, dwarfing other structures. This vast area slows airflow velocity, reducing resistance to negligible levels at the gas exchange site, where diffusion dominates. Resistance peaks in medium bronchi due to turbulent flow, not alveoli, despite their tiny individual size (~0.2 mm). Trachea and bronchioles handle bulk flow with higher resistance. Alveoli's massive area minimizes resistance, making them the correct choice, critical for efficient ventilation and distinguishing their role from conducting airways.

Correct Answer: B

Rationale: CO2 percentage correlates with PCO2, highest where metabolic CO2 accumulates. Pulmonary arteries carry deoxygenated blood from the right heart to lungs, with PCO2 ~45-46 mmHg venous blood richest in CO2 from tissues, topping the list. Alveolar air equilibrates with arterial blood at ~40 mmHg during gas exchange. Pulmonary veins, post-exchange, carry oxygenated blood with PCO2 ~40 mmHg, arterial levels. Interstitial fluid's PCO2 (~45 mmHg or less) mirrors venous blood or local metabolism but isn't a standard respiratory metric. Systemic arteries (not listed) are also ~40 mmHg. Pulmonary arteries, transporting CO2-rich blood for exhalation, have the highest PCO2, reflecting their pre-exchange role, distinguishing them from oxygenated or equilibrating sites in the respiratory cycle.

Correct Answer: C

Rationale: Functional residual capacity (FRC, ~2.5-3 L) is the lung volume post-normal expiration, a resting state where lung inward recoil balances chest wall outward recoil true for both lung and thorax, but not the focus. The true statement is that at FRC, intra-alveolar pressure equals atmospheric pressure (~760 mmHg), as no airflow occurs (gradient = 0), with muscles relaxed. Intrapleural pressure (IPP) is negative (~-4 mmHg, 756 mmHg) at FRC, not above atmospheric (760 mmHg), maintaining lung expansion false if elevated. Compliance isn't lowest at FRC (not listed). Alveolar-atmospheric equality is a core principle, ensuring rest stability, making it the standout truth, reflecting FRC's role as the ventilatory baseline.