A patient with restrictive lung disease will have a relatively normal?

Correct Answer: D

Rationale: Restrictive lung diseases (e.g., pulmonary fibrosis) stiffen lungs, reducing expansion and volumes like forced vital capacity (FVC), which drops below normal (e.g., from 4-5 L to 2-3 L) due to limited inspiratory capacity. Forced expiratory volume in 1 second (FEV1) also decreases proportionally (e.g., from 3-4 L to 1.5-2 L), as less air is available to exhale. However, the FEV1/FVC ratio remains normal or elevated (≥80%) because both values decline similarly, unlike obstructive diseases where FEV1 falls more, lowering the ratio (<70%). Ventilation/perfusion (V/Q) ratio may skew high in restrictive disease (e.g., fibrosis) due to reduced ventilation from stiff lungs, not normal matching. FEV1 and FVC individually are reduced, not normal. The FEV1/FVC ratio's preservation reflects the restrictive pattern impaired volume, not airflow obstruction making it the value least altered relative to healthy norms, a key diagnostic feature in spirometry.

Correct Answer: C

Rationale: Pulmonary vascular resistance (PVR) reflects opposition to blood flow in the pulmonary circulation, influenced by lung volume and vessel mechanics. At high lung volumes (near TLC), extra-alveolar vessels stretch and narrow, and alveolar capillaries compress, increasing PVR. At low volumes (near RV), these vessels are less stretched and more patent, lowering PVR, though this isn't the queried truth. The true statement is that increased PVR can lead to right heart failure, as seen in conditions like pulmonary hypertension or fibrosis, where elevated resistance overworks the right ventricle, causing cor pulmonale. PVR isn't measured by routine pulmonary function tests (e.g., spirometry), which assess airflow and volumes, not vascular pressures cardiac catheterization is required instead. The link to right heart failure is critical, as chronic high PVR elevates pulmonary artery pressure, straining the heart's ability to pump against it, a key pathophysiological consequence distinguishing this option as true amid the others' inaccuracies.

Correct Answer: D

Rationale: In a severe asthma attack, bronchoconstriction obstructs airways, reducing airflow, especially on expiration, causing wheezing. FEV1/FVC decreases (<80%) as FEV1 drops more than FVC due to obstruction, not increases. The ventilation/perfusion (V/Q) ratio in affected areas falls, as ventilation is blocked while perfusion persists, causing hypoxemia (PaO2 60 mmHg vs. 75-100 mmHg normal). Arterial PCO2 (30 mmHg vs. 35-45 mmHg) is lower, not higher, because hypoxemia stimulates hyperventilation via peripheral chemoreceptors, expelling CO2 faster than it builds up, a compensatory response in acute asthma. Inadequate gas exchange lowers PaO2, not PCO2, here. Option D correctly ties low PCO2 to hyperventilation driven by hypoxia, aligning with asthma's physiology where obstruction impairs oxygen uptake but CO2 clearance accelerates with increased respiratory effort.

Correct Answer: D

Rationale: Vital capacity (VC) is the maximum air exhaled after maximal inhalation, measured as inspiratory reserve volume (IRV, ~2-3 L), tidal volume (VT, ~0.5 L), and expiratory reserve volume (ERV, ~1-1.5 L), totaling ~4-5 L via spirometry. Sum of all lung volumes' is total lung capacity (TLC, ~6 L), including RV (~1-1.5 L), not VC. VT plus RV' (~2 L) omits IRV and ERV, far below VC. IRV plus ERV' (~3-4 L) excludes VT, underestimating VC. VC (IRV + VT + ERV) captures the full expirable volume, a key respiratory health metric, distinct from TLC or partial sums, reflecting the lung's functional capacity for deep breathing, widely used in clinical assessment.

Correct Answer: C

Rationale: Lung compliance (C = ΔV / ΔP) measures volume change per pressure unit, correctly defined. It's not maximal during quiet breathing (VT ~500 ml) compliance peaks at moderate volumes, declining near TLC due to stiffness, making that false but not the exception here. The statement more surface tension, more compliance' is incorrect high tension (e.g., no surfactant) reduces compliance by stiffening alveoli, per Laplace's law (P = 2T/r), as in RDS, while low tension increases it. Fibrosis decreases compliance via collagen stiffening true. Emphysema (not listed) raises compliance by elasticity loss. The surface tension error contradicts physiology compliance falls with rising tension, making it the exception, as surfactant's role is to enhance compliance by reducing tension, critical for understanding lung mechanics.