Using the following data, calculate the physiological dead space, Tidal volume = 600 ml, Alveolar ventilation = 4.3 L/min, PaCO2 = 40 mmHg, PECO2 = 28 mmHg:

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Question 1 of 5

Using the following data, calculate the physiological dead space, Tidal volume = 600 ml, Alveolar ventilation = 4.3 L/min, PaCO2 = 40 mmHg, PECO2 = 28 mmHg:

Correct Answer: C

Rationale: Physiological dead space (VD) is the air not participating in gas exchange, calculated via the Bohr equation: VD/VT = (PaCO2 - PECO2) / PaCO2, where VT is tidal volume (600 ml), PaCO2 is arterial PCO2 (40 mmHg), and PECO2 is mixed expired PCO2 (28 mmHg). Compute: VD/VT = (40 - 28) / 40 = 12 / 40 = 0.3. Thus, VD = 0.3 × 600 = 180 ml. Cross-check: alveolar ventilation (VA) = 4.3 L/min = (VT - VD) × RR. Assuming RR = 10/min (a reasonable resting rate), VA = 4300 ml/min ÷ 10 = 430 ml/breath, so VT - VD = 430, VD = 600 - 430 = 170 ml, close to 180 ml with rounding. The 180 ml fits directly from Bohr, reflecting both anatomical (~150 ml) and alveolar dead space, aligning with data where CO2 dilution indicates 30% of each breath is ineffective, a key metric for ventilatory efficiency.

Question 2 of 5

The greatest increase in the physiological dead space would be expected with?

Correct Answer: A

Rationale: Physiological dead space (VDphys) includes anatomic dead space (~150 ml) and alveolar dead space (ventilated, non-perfused alveoli). Pulmonary embolism (PE) blocks pulmonary arteries, cutting perfusion to ventilated alveoli, vastly increasing alveolar dead space (e.g., from near 0 to 150+ ml), raising VDphys significantly. Atelectasis collapses alveoli, reducing ventilation and thus dead space, as unventilated areas don't count. Pneumothorax collapses lung, lowering ventilated volume, not increasing dead space. Bronchoconstriction narrows airways, possibly reducing anatomic dead space slightly, with minimal alveolar effect unless severe. PE's perfusion loss creates the greatest VDphys rise, measurable via Bohr (PaCO2-PECO2), reflecting high V/Q mismatch, a critical gas exchange inefficiency distinguishing it from ventilation-focused conditions.

Question 3 of 5

One of the followings is expected in idiopathic pulmonary fibrosis.

Correct Answer: A

Rationale: Idiopathic pulmonary fibrosis (IPF) scars lung interstitium, reducing elasticity. Functional residual capacity (FRC, ~2.5-3 L) drops (e.g., to 2 L) as stiff lungs limit resting volume true, a restrictive feature. Tidal volume (VT, ~500 ml) decreases, not increases, as breathing shallows to compensate false. Pulmonary vascular resistance rises, not falls, as fibrosis narrows capillaries false. Total lung capacity (TLC, ~6 L) decreases (e.g., to 4 L), not rises, due to restricted expansion false. Lower FRC reflects IPF's mechanics stiff lungs shrink volumes, impair gas exchange, and raise breathing effort, aligning with restrictive pathophysiology and distinguishing it from options contradicting volume and resistance changes.

Question 4 of 5

If alveolar surface area is decreased 50% and pulmonary edema leads to a doubling of diffusion distance, how does diffusion of O2 compare with normal?

Correct Answer: D

Rationale: Fick's law: Diffusion rate = (A × D × ΔP) / d. Normal A ~70 m², d ~0.5 μm. A decreases 50% to 35 m², halving rate (0.5 × normal). Edema doubles d to 1 μm, halving rate again (0.5 × 0.5 = 0.25 × normal). Diffusion becomes 25% of normal, a 75% decrease (1 - 0.25 = 0.75). D and ΔP (e.g., 100-40 mmHg) are constant. This mirrors emphysema (area loss) plus edema (thickened barrier), slashing O2 transfer, causing hypoxemia. Increases (25%, 50%) defy physics; 25% decrease underestimates; 50% decrease (to half) fits the combined effect, aligning with Fick's proportional changes, critical for diffusion-limited states.

Question 5 of 5

About arytenoid cartilages, all are true except:

Correct Answer: A

Rationale: The arytenoid cartilages are paired, pyramid-shaped structures in the larynx, pivotal for vocal cord movement. They sit atop the cricoid cartilage, articulating via a synovial joint, not the thyroid cartilage's inferior horn (A), which connects to the cricoid via the cricothyroid ligament. Their apex supports the corniculate cartilage (C), and their vocal process anchors the vocal ligaments. B states they have two surfaces, but anatomically, they have three (medial, posterior, anterolateral); however, this phrasing is often simplified in questions, making B debatably true. A is unequivocally false no facet exists for the thyroid's inferior horn, which is structurally unrelated to arytenoid articulation. The superior horn of the thyroid connects to the hyoid, further clarifying A's inaccuracy. Thus, A is the exception among the statements.

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