If dead space is one third of the tidal volume and arterial PCO2 is 45 mmHg, what is the mixed expired pCO2?

Correct Answer: B

Rationale: Mixed expired PCO2 (PECO2) reflects CO2 in exhaled air, diluted by dead space ventilation. Given dead space (VD) is one-third of tidal volume (VT), VD/VT = 1/3. The Bohr equation relates physiological dead space to CO2: VD/VT = (PaCO2 - PECO2) / PaCO2, where PaCO2 (arterial PCO2) is 45 mmHg. Substituting: 1/3 = (45 - PECO2) / 45. Solving: 45 / 3 = 45 - PECO2, so 15 = 45 - PECO2, and PECO2 = 45 - 15 = 30 mmHg. This assumes physiological dead space equals anatomic here, as no alveolar dead space is specified. Intuitively, if one-third of each breath doesn't participate in gas exchange (PCO2 ~0 mmHg in inspired air), the expired CO2 is diluted from arterial levels (45 mmHg) to two-thirds strength (30 mmHg), matching the calculation. Options like 45 mmHg imply no dead space effect, while 20 mmHg overestimates dilution. Thus, 30 mmHg aligns with the given ratio and respiratory physiology principles.

Correct Answer: D

Rationale: In a healthy upright individual, regional ventilation varies due to gravity and pleural pressure gradients. At rest, intrapleural pressure (IPP) is more negative at the apex (~-10 cm H2O) than the base (~-2.5 cm H2O) due to lung weight, making apices less compliant (stiffer) and bases more compliant (easier to expand). During quiet breathing (VT = 400 ml, RR = 12/min), the diaphragm's downward pull preferentially ventilates the lower zones, where compliance is higher and initial volume lower, allowing greater volume change (ΔV). Studies (e.g., West) show lower lobes receive ~4 times more ventilation per unit volume than apices. Thus, ventilation is greatest in the lower zones, followed by middle, then upper (Lower > Middle > Upper). Equal ventilation ignores gravity's effect, and Upper > Middle > Lower reverses the gradient. For this boy, VA = (400 - ~120 ml VD) × 12 = ~3.36 L/min, distributed predominantly to the base, making this the best description.

Correct Answer: C

Rationale: Residual volume (RV) is the air left in the lungs after maximal expiration (~1-1.5 L), preventing collapse and measurable only indirectly (e.g., helium dilution). It's not just after tidal expiration that's FRC (~2.5-3 L), including RV plus ERV, making that false. In COPD, RV increases (e.g., to 2-3 L) due to air trapping from obstructed airways and lost elasticity, not decreases. In pulmonary fibrosis, a restrictive disease, RV decreases (e.g., to <1 L) as stiff lungs limit all volumes, including residual air, making this correct. RV doesn't stay constant lifelong aging and disease alter it but in health, it's relatively stable, though this isn't the strongest fit. Fibrosis's reduction reflects restricted lung expansion, contrasting with obstructive hyperinflation, making it the accurate statement amid options misaligned with RV's physiological behavior.

Correct Answer: D

Rationale: Intrapleural pressure (IPP) is the pressure in the pleural space, negative relative to atmospheric (760 mmHg) due to lung (inward) and chest wall (outward) recoil. At FRC, IPP is ~756 mmHg (-4 mmHg); inspiration drops it to ~-6 mmHg, and expiration raises it slightly, but it stays negative in health. It's always less than atmospheric pressure, maintaining lung expansion unless breached (e.g., pneumothorax). It's not just low during inspiration it's consistently subatmospheric. Respiratory muscles adjust IPP but don't equalize it to atmospheric pressure (that's pathological). IPP isn't the alveolar-pleural difference (transpulmonary pressure); it's the pleural cavity's absolute pressure. This constant negativity is vital for lung mechanics, making it the true statement reflecting pleural dynamics.

Correct Answer: D

Rationale: Physiological dead space (VDphys) comprises anatomic dead space (VDanat, ~150 ml, airways) and alveolar dead space (VDalv, non-perfused alveoli). Normally, VDphys ≈ VDanat, but in disease, it's ≥ VDanat due to added VDalv true. Lung diseases (e.g., PE) increase VDphys via VDalv true. High V/Q (ventilation > perfusion, e.g., PE) raises VDphys, as ventilated alveoli lack blood flow true. However, VDphys isn't just alveolar dead space; it's VDanat + VDalv, so equating it to VDalv alone is wrong, omitting the anatomic component always present. This misdefinition skews VDphys's scope, critical for assessing total ventilatory waste, not just alveolar inefficiency, making it the false statement amid accurate descriptions.