A 12 years-old boy has a severe asthmatic attack with wheezing. His arterial pO2 is 60 mmHg and pCO2 is 30 mmHg. His:

Correct Answer: D

Rationale: In a severe asthmatic attack, bronchoconstriction obstructs airways, reducing airflow, particularly during expiration, leading to wheezing. Forced expiratory volume in 1 second (FEV1) drops more than forced vital capacity (FVC), decreasing the FEV1/FVC ratio (normal >80%) due to obstruction, not increasing it. The ventilation/perfusion (V/Q) ratio in affected areas decreases, as ventilation is impaired more than perfusion, causing mismatching and hypoxemia (PaO2 60 mmHg, normal 75-100 mmHg). Arterial PCO2 (30 mmHg, normal 35-45 mmHg) is lower than normal, not higher, because hypoxemia stimulates hyperventilation via peripheral chemoreceptors, increasing respiratory rate to compensate for low oxygen. This overbreathing expels CO2 faster than it accumulates, despite uneven ventilation, contrasting with conditions like COPD where CO2 retention occurs. The lower PCO2 reflects this compensatory mechanism, aligning with asthma's acute physiology where gas exchange inefficiency drives respiratory effort, not CO2 trapping.

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.

Correct Answer: A

Rationale: Air enters the lungs during inspiration per Boyle's law: thoracic expansion lowers intrapulmonary pressure below atmospheric (e.g., 760 to 758 mmHg), creating a pressure gradient driving airflow. Increasing this gradient via stronger diaphragm and intercostal contraction directly boosts inspired volume (e.g., from 500 ml to 600 ml), the primary factor. Increase in action potential' likely means neural impulses to respiratory muscles; more impulses enhance contraction, but this is secondary to the gradient they produce. Combining both overcomplicates pressure is the direct mechanism. Decreasing the gradient reduces flow, opposing the goal. The pressure gradient is the key driver, quantifiable (e.g., 1-2 mmHg for tidal breathing), linking muscle action to volume via physics, distinguishing it as the most impactful factor in ventilation mechanics.