Which person would be expected to have the largest PAO2-PaO2 gradient? (A stands for alveolar and a-stands for arterial)

Correct Answer: B

Rationale: The PAO2-PaO2 gradient measures the difference between alveolar oxygen (PAO2) and arterial oxygen (PaO2), normally small (~5-10 mmHg) due to efficient diffusion. In pulmonary fibrosis, thickened alveolar walls from scarring impair O2 diffusion, lowering PaO2 (e.g., 60 mmHg) while PAO2 (calculated via the alveolar gas equation, ~100 mmHg at sea level) remains closer to normal, widening the gradient (e.g., 40 mmHg). During exercise in a normal person, increased cardiac output and ventilation match perfusion, keeping the gradient minimal despite higher O2 demand. Anemia reduces oxygen-carrying capacity (low hemoglobin), not diffusion, so PaO2 approximates PAO2, maintaining a normal gradient. At 5000 meters, low atmospheric PO2 reduces both PAO2 and PaO2 proportionately (e.g., PAO2 ~50 mmHg, PaO2 ~45 mmHg), keeping the gradient small. Pulmonary fibrosis uniquely disrupts diffusion, causing the largest gradient, as fibrotic barriers hinder O2 transfer more than ventilation or perfusion issues.

Correct Answer: B

Rationale: Total ventilation (VE) = VT × RR; alveolar ventilation (VA) = (VT - VD) × RR. Initially, T and V have VT = 1000 ml, VD = 200 ml, RR = 20/min. VE = 1000 × 20 = 20 L/min; VA = (1000 - 200) × 20 = 800 × 20 = 16 L/min. For T: VT doubles to 2000 ml, RR halves to 10/min. VE = 2000 × 10 = 20 L/min (constant); VA = (2000 - 200) × 10 = 1800 × 10 = 18 L/min (increases). For V: VT halves to 500 ml, RR doubles to 40/min. VE = 500 × 40 = 20 L/min (constant); VA = (500 - 200) × 40 = 300 × 40 = 12 L/min (decreases). T's larger VT boosts VA despite lower RR, as more air exceeds VD. V's smaller VT reduces VA, as dead space consumes a larger fraction per breath despite higher RR. Option B (T: VE constant, VA increases; V: VE constant, VA decreases) matches, reflecting how VT impacts VA efficiency at fixed VE.

Correct Answer: B

Rationale: Severe respiratory muscle weakness (e.g., in myasthenia gravis) impairs ventilation by weakening inspiratory and expiratory muscles. Tidal volume (VT, ~500 ml normally) decreases due to limited inspiratory force, reducing breath size. Vital capacity (VC, ~4-5 L) drops as maximal inhalation and exhalation are compromised. Oxyhemoglobin saturation falls (e.g., from 95-100% to <90%) as hypoventilation lowers PaO2, causing hypoxemia. Arterial pH may decrease (acidosis) if CO2 retention raises PCO2, but this isn't specified as above normal. However, PCO2 itself (normal 35-45 mmHg) rises above normal (e.g., 50-60 mmHg) due to inadequate CO2 expulsion, a direct result of weak ventilation. Though not listed, if B intended PCO2 (a common mix-up), it fits; otherwise, none are above normal' assuming intent, PCO2's rise is the key abnormality, reflecting ventilatory failure's impact on gas exchange.

Correct Answer: A

Rationale: Total lung capacity (TLC) is the maximum air lungs hold after maximal inspiration, summing residual volume (RV, ~1-1.5 L), expiratory reserve volume (ERV, ~1-1.5 L), tidal volume (VT, ~0.5 L), and inspiratory reserve volume (IRV, ~2-3 L). In adults, TLC averages ~6 L (5-7 L, varying by sex, age, size), per standard physiology (e.g., Guyton). Two liters approximates FRC (~2.5-3 L), the resting volume. Four liters nears vital capacity (VC, ~4-5 L), excluding RV. Nine liters exceeds typical capacity, possibly hyperinflation. Six liters aligns with spirometry plus RV (e.g., helium dilution), reflecting full lung expansion in health, making it the best approximation for a normal human, widely validated across respiratory studies.

Correct Answer: C

Rationale: Surfactant reduces alveolar surface tension, causing hysteresis different inflation vs. deflation pressures in lung P-V curves due to tension dynamics, a true property. It lowers pulmonary resistance by easing expansion, not increasing it false but not queried. Surfactant deficiency is common in preterm neonates (<37 weeks), causing RDS, but in term neonates (≥37 weeks), production is typically mature, making commonly deficient in term-neonates' incorrect RDS is rare at term barring defects. Surfactant indirectly prevents pulmonary edema by stabilizing alveoli, reducing fluid transudation pressure, though not its primary role true enough. The term-neonate error misaligns with developmental physiology, where surfactant sufficiency is expected, distinguishing it as the incorrect statement amid surfactant's established functions.