Which of the following structures contains blood with the highest PCO2?

Correct Answer: C

Rationale: PCO2, or partial pressure of carbon dioxide, reflects the concentration of CO2 in blood, highest where metabolic waste accumulates and lowest where gas exchange removes it. The superior vena cava (SVC) carries deoxygenated blood from the upper body back to the heart, rich in CO2 from tissue metabolism, typically with a PCO2 of 45-46 mmHg, making it the highest among the options. Pulmonary veins carry oxygenated blood from the lungs to the heart after CO2 is offloaded in the alveoli, so their PCO2 is low (around 40 mmHg, arterial level). The midportion of pulmonary capillaries is where gas exchange occurs, transitioning from high venous PCO2 to lower arterial levels, averaging less than the SVC. Carotid bodies are chemoreceptors sensing blood gases, not a blood-containing structure, but even arterial blood they monitor has a PCO2 of about 40 mmHg. The SVC, as a major venous return vessel, consistently has the highest PCO2 due to its role in collecting metabolically produced CO2 before pulmonary gas exchange, distinguishing it from the other options.

Correct Answer: B

Rationale: Surfactant, a phospholipid-protein mix from type II alveolar cells, lines alveoli and reduces surface tension of the fluid layer, preventing collapse and easing lung expansion. Normally, water's high surface tension (~72 dynes/cm) pulls alveolar walls inward, but surfactant lowers it (to ~5-10 dynes/cm), stabilizing smaller alveoli per Laplace's law (P = 2T/r). It doesn't increase pleural pressure, which remains negative (~-4 mmHg at rest) to keep lungs expanded surfactant affects intra-alveolar dynamics, not pleural space. It doesn't directly decrease alveolar pressure (typically atmospheric at rest, ~760 mmHg); that's a muscle-driven effect. It makes inspiration easier, not harder, by reducing the work needed to overcome tension, countering collapse tendencies. Pneumothorax relates to pleural breach, not surfactant. Reducing surface tension is the true function, critical for neonatal lung maturation and preventing atelectasis, distinguishing it from pressure or effort-related misconceptions.

Correct Answer: A

Rationale: Work of breathing (WOB) is the energy required to overcome elastic (compliance) and resistive (airway) forces during ventilation. Lung compliance (C = ΔV / ΔP) measures lung stretchability; low compliance (stiff lungs) increases pressure needed for a given volume, raising WOB. Thus, WOB is inversely related to compliance when C decreases, WOB increases, as in fibrosis. During exercise, WOB rises with higher ventilation rates and volumes, not remaining constant. Airway resistance (R) directly affects WOB; higher R (e.g., asthma) increases effort, contradicting not affected.' In pulmonary fibrosis, stiff lungs (low compliance) elevate WOB, not reduce it, unlike emphysema where high compliance might lower elastic work but raise resistive work. The inverse compliance relationship is fundamental, as WOB = ∫P dV, where pressure (P) rises as compliance falls, making this the correct statement reflecting respiratory mechanics.

Correct Answer: A

Rationale: Functional residual capacity (FRC) is the volume in the lungs after a normal expiration, equaling expiratory reserve volume (ERV) plus residual volume (RV). The spirogram shows maximal inhalation to total lung capacity (TLC) and exhalation to RV, with VC (vital capacity) as TLC - RV. RV is given as 1.0 L via helium dilution. FRC = ERV + RV, but without the figure, assume a typical female FRC (~2-3 L). If VC is ~4 L (normal for a young woman) and TLC ~5 L, then after maximal exhalation to RV (1 L), the difference from TLC to FRC includes ERV. Standard ERV is ~1-1.5 L; with RV = 1 L, FRC = 1 + 1 = 2.0 L fits option A, plausible for a smaller female frame. Higher values (2.5-3.5 L) align with larger individuals or males (~3 L). Without exact spirogram data, 2.0 L is reasonable, matching RV + minimal ERV, consistent with helium-derived RV and typical physiology.

Correct Answer: C

Rationale: A stab wound causing pneumothorax allows air into the pleural space, disrupting the negative intrapleural pressure (~-4 to -6 mmHg) that keeps lungs expanded. This equalizes pleural pressure to atmospheric (760 mmHg), eliminating the force opposing lung elastic recoil, which pulls the lung inward to collapse toward the hilum, reducing its volume. Meanwhile, the chest wall's outward recoil, no longer countered by lung tension, causes it to expand outward, increasing thoracic diameter. Thus, the lung collapses and the chest wall expands, a classic pneumothorax feature. Both expanding defies recoil mechanics, fixing at FRC ignores pressure loss, and collapse-collapse misrepresents chest wall behavior. This dynamic reflects the opposing elastic properties unleashed by pleural breach, critical for understanding respiratory compromise and interventions like chest tube placement.