Compared to a normal individual, a patient with idiopathic pulmonary fibrosis, one of the following is expected to be more than normal?

Correct Answer: B

Rationale: Idiopathic pulmonary fibrosis (IPF) is a restrictive lung disease marked by progressive scarring of the lung interstitium, reducing lung elasticity and function. Total lung capacity (TLC) decreases in IPF because fibrotic tissue stiffens the lungs, limiting their expansion. Forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) are both reduced, but the FEV1/FVC ratio remains normal or elevated, unlike in obstructive diseases. Arterial oxygen partial pressure (PaO2) drops due to impaired gas exchange across thickened alveolar walls, leading to hypoxemia. However, total pulmonary vascular resistance (PVR) increases in IPF as fibrosis compresses and obliterates pulmonary capillaries, narrowing the vascular bed and elevating resistance to blood flow. This increase can strain the right heart, potentially causing cor pulmonale. Among the options, only total pulmonary vascular resistance is expected to be higher than normal, aligning with IPF's impact on the pulmonary vasculature rather than lung volumes or oxygenation, which decline.

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: A

Rationale: Idiopathic pulmonary fibrosis (IPF) scars lung interstitium, reducing elasticity and volumes. Functional residual capacity (FRC), the resting volume (~2.5-3 L normally), decreases in IPF (e.g., to 2 L) as stiff lungs limit expansion, a hallmark of restrictive disease. Tidal volume (VT, ~500 ml) typically decreases, not increases, as breathing becomes shallow due to restricted capacity, often requiring faster rates to maintain ventilation. Pulmonary vascular resistance rises, not falls, as fibrosis compresses capillaries, increasing resistance and risking right heart strain. Total lung capacity (TLC, ~6 L) also drops (e.g., to 4 L), reflecting reduced maximum volume, not higher. Lower FRC aligns with IPF's mechanics stiff lungs reduce resting and total volumes, impair gas exchange, and elevate work of breathing, distinguishing it from options contradicting restrictive physiology.

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.