Which of the following is NOT true at FRC?

Correct Answer: B

Rationale: Functional residual capacity (FRC) is the volume of air remaining in the lungs after a normal expiration, representing a balance point where the opposing forces of the lung and chest wall are equal. The elastic recoil of the lung is inward, tending to collapse the lung, while the elastic recoil of the chest wall is outward, tending to expand it. At FRC, these forces cancel each other out, and the lung-thorax system is indeed at rest with no active muscle contraction. However, FRC is not about 75% of total lung capacity (TLC). In a healthy adult, FRC is typically around 2.5-3 liters, while TLC is about 6 liters, making FRC approximately 40-50% of TLC, not 75%. The claim that FRC is about 75% of TLC is significantly overstated and does not reflect physiological norms, making it the statement that is not true at FRC. This misunderstanding could arise from confusing FRC with other lung volumes, but the standard values clearly indicate a lower percentage relative to TLC.

Correct Answer: D

Rationale: Vital capacity (VC) is the maximum volume of air a person can exhale after a maximal inhalation, measured via spirometry as the sum of 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 in adults. It excludes residual volume (RV), which remains after maximal exhalation. Sum of all lung volumes' describes total lung capacity (TLC, ~6 L), including RV, not VC. Tidal volume plus residual volume' (~2 L) is far less than VC, missing IRV and ERV. IRV plus ERV' omits VT, underestimating VC (~3-4 L). The correct definition IRV + VT + ERV captures the full expirable volume, reflecting the lung's functional capacity for deep breathing, a key metric in assessing respiratory health, distinguishing it from TLC or partial volume sums.

Correct Answer: C

Rationale: Lung compliance (C) is the change in lung volume per change in transpulmonary pressure (C = ΔV / ΔP), correctly defined. It's not maximal during quiet breathing (tidal volume ~500 ml); it's tested across a range, peaking at moderate volumes but decreasing at high volumes (e.g., near TLC) due to stiffness. In quiet breathing, compliance operates efficiently but isn't at its maximum. Crucially, compliance is inversely related to surface tension higher tension (e.g., no surfactant) stiffens alveoli, reducing compliance, as in RDS, not increasing it. This statement is incorrect, contradicting Laplace's law (P = 2T/r), where high tension raises collapse pressure, lowering compliance. Fibrosis decreases compliance by stiffening lungs with collagen, and emphysema increases it by destroying elastic fibers both correct. The surface tension error misrepresents surfactant's role, making it the exception among these statements, as compliance falls with rising tension.

Correct Answer: A

Rationale: Airway resistance (R) follows Poiseuille's law (R ∝ 1/r^4), but total resistance depends on cross-sectional area. Later generations (bronchioles) have smaller radii, yet their vast number increases total area (e.g., ~300 cm² vs. trachea's 3-4 cm²), reducing overall R most resistance is in larger airways (trachea, bronchi), where flow is turbulent, making this false. Normally, ~80% of R is in large airways, dropping in smaller ones due to laminar flow and area. Increased R (e.g., asthma) lowers FEV1/FVC (<70%), as FEV1 falls more, a true obstructive sign. Loss of elasticity (emphysema) and bronchoconstriction (asthma) raise R by collapsing or narrowing airways, also true. The false idea of increasing R in later generations misinterprets branching dynamics, where resistance peaks proximally, not distally, aligning with physiological airflow distribution.

Correct Answer: C

Rationale: Asthma, an obstructive disease, features reversible bronchoconstriction, inflammation, and mucus production during attacks. Narrowed airways increase resistance, especially on expiration, when dynamic compression worsens airflow, producing wheezing louder and more prolonged than on inspiration, making that statement false. Work of breathing rises as respiratory muscles (e.g., diaphragm) work harder against resistance and trapped air, a consistent expectation. Bronchodilators (e.g., albuterol) are standard treatment, relaxing bronchial smooth muscle, not contraindicated. FEV1 decreases (e.g., from 80% to 50% predicted) due to obstructed airflow, not increases. Increased work of breathing reflects the effort to overcome narrowed passages, elevating energy expenditure and often leading to accessory muscle use, aligning with asthma's acute physiology where resistance and air trapping dominate, distinguishing it from incorrect options misaligned with clinical presentation.