A man with normal lungs and arterial pCOâ‚‚ of 40 mmHg takes an overdose of barbiturates, which half his ventilation but don't change his COâ‚‚ output. What does his arterial pCOâ‚‚ rise to?

Correct Answer: D

Rationale: With ventilation halved (e.g., from 6 L/min to 3 L/min) and CO₂ output unchanged, arterial pCO₂ rises to 80 mmHg (choice D). Normally, pCO₂ = (V̇CO₂ × K) / V̇A, where V̇CO₂ is CO₂ production, K is a constant (≈863), and V̇A is alveolar ventilation. If pCO₂ is 40 mmHg at 6 L/min, V̇CO₂ = (40 × 6) / 863 ≈ 0.278 L/min. Halving ventilation to 3 L/min, new pCO₂ = (0.278 × 863) / 3 ≈ 80 mmHg. Choice A (50) underestimates doubling; B (60) fits a 33% drop; C (70) is arbitrary. Barbiturates depress respiratory drive, reducing V̇A without altering metabolism (V̇CO₂), doubling pCO₂ as ventilation inversely governs it. Thus, D is correct.

Correct Answer: D

Rationale: Choice D is likely correct (no answer provided); vagal afferents, via pulmonary stretch receptors (Hering-Breuer reflex), can prolong inspiration (‘breath-holding') if the pneumotaxic center, which limits inspiration, is destroyed. Choice A is false; vagal input (stretch) inhibits inspiration, not expiration. Choice B is wrong; it doesn't directly excite expiratory neurons. ' vagotomy causes deeper, slower breathing, not gasping (medullary damage does). Choice E (shallow rapid breathing) contradicts vagotomy's effect. Vagal afferents signal lung inflation, inhibiting inspiratory neurons via the medulla. Without pneumotaxic modulation, this can lock inspiration, mimicking breath-holding. Physiologically, D aligns with reflex disruption, making it the most consistent vagal influence description.

Correct Answer: D

Rationale: Choice D is correct (replacing E); normal P₅₀ is ≈26-27 mmHg, the pO₂ at 50% Hb saturation. Choice A is false; HbS has valine replacing glutamic acid (β6 mutation). Choice B is wrong; saturation is the percentage of sites with O₂, not without. ' oxygenated Hb is the R (relaxed) state, not T (tense). Choice E (27 mmHg) is true but redundant here. P₅₀ reflects Hb-O₂ affinity; 27 mmHg is standard at pH 7.4, 37°C, aligning with physiological O₂ unloading. D's accuracy makes it the correct statement.

Correct Answer: D

Rationale: in a blood vessel, P = T/R (Laplace for cylinders), unlike alveoli (P = 2T/R). Choice A is false; alveoli use P = 2T/R (sphere with one surface). Choice B is wrong; soap bubbles (two surfaces) use P = 4T/R. Choice C is true but not the law's direct statement surfactant prevents this. Laplace relates pressure, tension, and radius; vessels (tubular) differ from spherical alveoli. D accurately applies this to vascular physiology.

Correct Answer: B

Rationale: 2,3-DPG levels rise at altitude (hypoxia response), shifting the curve right. Choice A is true; PCO₂ shifts it right (Bohr effect). Choice C is false; deoxy-Hb is tense (T state), not relaxed (R state). Choice D is wrong; CO's affinity is ≈240x, shifting left by reducing available Hb, not curve shape. Altitude adaptation increases 2,3-DPG, aiding O₂ unloading (P₅₀ up), making B the accurate chronic response.