The primary force responsible for the movement of air into the lungs during inspiration?

Correct Answer: D

Rationale: Inspiration occurs when air moves into the lungs due to a pressure gradient, as per Boyle's law: expanding the thoracic cavity decreases intrapulmonary pressure below atmospheric pressure (760 mmHg to ~758 mmHg), driving air inward. This gradient, the pressure difference between atmospheric and intrapulmonary pressure, is the primary force, created by diaphragm and intercostal muscle contraction. Atmospheric pressure alone isn't a force' but a reference; it's the difference that matters. Muscular spasm implies involuntary action, not the controlled contraction of respiration. Reduced surface tension, via surfactant, aids lung expansion but isn't the driving force it reduces resistance to expansion. Muscle relaxation occurs in expiration, not inspiration. The pressure difference is the fundamental mechanism, quantifiable (e.g., 1-2 mmHg drop suffices for tidal breathing), and directly ties muscle action to airflow, distinguishing it as the essential driver of ventilation.

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.

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.