Regarding Pneumothorax, one of the following isn't true?

Correct Answer: D

Rationale: Pneumothorax occurs when air enters the pleural space, disrupting negative intrapleural pressure (~-4 mmHg), causing lung collapse and chest wall expansion. The thorax's diameter increases as the chest wall springs outward due to its elastic recoil. Venous return decreases because positive pleural pressure compresses the vena cava, reducing preload, especially in tension pneumothorax. Vital capacity (VC) drops as the collapsed lung reduces expirable volume (e.g., from 4-5 L to much less). However, lung compliance (C = ΔV / ΔP) doesn't increase it's a lung property (stiffness), not directly altered by pneumothorax. The collapsed lung's volume change per pressure is irrelevant, as it's deflated; compliance may appear effectively zero, but the lung tissue itself isn't more compliant. Increased compliance misrepresents pneumothorax's mechanics, where the issue is pressure loss, not lung elasticity, making this the untrue statement.

Correct Answer: C

Rationale: Physiological dead space (VD) is the air not participating in gas exchange, calculated via the Bohr equation: VD/VT = (PaCO2 - PECO2) / PaCO2, where VT is tidal volume (600 ml), PaCO2 is arterial PCO2 (40 mmHg), and PECO2 is mixed expired PCO2 (28 mmHg). Compute: VD/VT = (40 - 28) / 40 = 12 / 40 = 0.3. Thus, VD = 0.3 × 600 = 180 ml. Cross-check: alveolar ventilation (VA) = 4.3 L/min = (VT - VD) × RR. Assuming RR = 10/min (a reasonable resting rate), VA = 4300 ml/min ÷ 10 = 430 ml/breath, so VT - VD = 430, VD = 600 - 430 = 170 ml, close to 180 ml with rounding. The 180 ml fits directly from Bohr, reflecting both anatomical (~150 ml) and alveolar dead space, aligning with data where CO2 dilution indicates 30% of each breath is ineffective, a key metric for ventilatory efficiency.

Correct Answer: D

Rationale: Residual volume (RV) is the air remaining after maximal expiration (~1-1.5 L), preventing alveolar collapse and measurable via helium dilution or body plethysmography. Tidal volume (VT, ~500 ml) is normal breath size, not post-forceful exhalation. Expiratory reserve volume (ERV, ~1-1.5 L) is extra air exhaled beyond normal expiration, expelled during forced effort, leaving RV. Vital capacity (VC, ~4-5 L) is the maximum exhailable volume (IRV + VT + ERV), excluding RV. RV's persistence reflects lung elasticity and chest wall limits, ensuring some air stays, distinct from volumes tied to active breathing or maximal efforts, making it the correct term for this residual air critical for maintaining lung structure.

Correct Answer: A

Rationale: Physiological dead space (VDphys) includes anatomic dead space (~150 ml) and alveolar dead space (ventilated, non-perfused alveoli). Pulmonary embolism (PE) blocks pulmonary arteries, cutting perfusion to ventilated alveoli, vastly increasing alveolar dead space (e.g., from near 0 to 150+ ml), raising VDphys significantly. Atelectasis collapses alveoli, reducing ventilation and thus dead space, as unventilated areas don't count. Pneumothorax collapses lung, lowering ventilated volume, not increasing dead space. Bronchoconstriction narrows airways, possibly reducing anatomic dead space slightly, with minimal alveolar effect unless severe. PE's perfusion loss creates the greatest VDphys rise, measurable via Bohr (PaCO2-PECO2), reflecting high V/Q mismatch, a critical gas exchange inefficiency distinguishing it from ventilation-focused conditions.

Correct Answer: A

Rationale: Idiopathic pulmonary fibrosis (IPF) scars lung interstitium, reducing elasticity. Functional residual capacity (FRC, ~2.5-3 L) drops (e.g., to 2 L) as stiff lungs limit resting volume true, a restrictive feature. Tidal volume (VT, ~500 ml) decreases, not increases, as breathing shallows to compensate false. Pulmonary vascular resistance rises, not falls, as fibrosis narrows capillaries false. Total lung capacity (TLC, ~6 L) decreases (e.g., to 4 L), not rises, due to restricted expansion false. Lower FRC reflects IPF's mechanics stiff lungs shrink volumes, impair gas exchange, and raise breathing effort, aligning with restrictive pathophysiology and distinguishing it from options contradicting volume and resistance changes.