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 portion of tidal volume (VT) not participating in gas exchange, calculated using the Bohr equation: VD/VT = (PaCO2 - PECO2) / PaCO2, where PaCO2 is arterial PCO2 (40 mmHg) and PECO2 is mixed expired PCO2 (28 mmHg). Plugging in the values: VD/VT = (40 - 28) / 40 = 12 / 40 = 0.3. Since VT is 600 ml, VD = 0.3 × 600 = 180 ml. To verify, alveolar ventilation (VA) is given as 4.3 L/min, and total ventilation (VE) is respiratory rate (RR) × VT. VA = VE - (VD × RR), but we can also derive VD from VA: VA = (VT - VD) × RR. Converting 4.3 L/min to 4300 ml/min and assuming RR from context (e.g., 10 breaths/min aligns with typical resting rates), VT - VD = 4300 / 10 = 430 ml, so VD = 600 - 430 = 170 ml, close to 180 ml, adjusting for rounding. The 180 ml option fits the Bohr calculation directly, confirming it as the physiological dead space, reflecting both anatomical and alveolar components not contributing to CO2 elimination.

Question 2 of 5

Regarding physiological dead space, one of the following is wrong?

Correct Answer: D

Rationale: Physiological dead space (VDphys) includes anatomic dead space (VDanat, ~150 ml, conducting airways) plus alveolar dead space (VDalv, ventilated but non-perfused alveoli). Normally, VDphys ≈ VDanat (~150 ml), but in disease, it's equal to or greater due to added VDalv. Lung diseases like pulmonary embolism increase VDphys by raising VDalv from poor perfusion. A high V/Q ratio (ventilation > perfusion), as in PE, also increases VDphys, as ventilated alveoli lack blood flow. However, VDphys isn't equal to alveolar dead space alone VDalv is just one component. VDphys = VDanat + VDalv, so stating it equals VDalv excludes the anatomic portion, which is always present (e.g., trachea, bronchi). This misdefinition is wrong, as physiological dead space encompasses both, not just wasted alveolar volume, a distinction critical for understanding gas exchange inefficiencies in pathology.

Question 3 of 5

Regarding lung diseases, one of the following is true?

Correct Answer: D

Rationale: In pulmonary fibrosis, a restrictive disease, lung stiffness reduces volumes (FEV1, FVC), but the FEV1/FVC ratio remains ≥80% (normal or higher), as both drop proportionally, unlike obstructive diseases where it's <70% this is true. Airway resistance (R) ∝ 1/r^4 (Poiseuille's law); a 10% diameter increase reduces R dramatically (~40%), not increases it, making that false. COPD (e.g., emphysema, chronic bronchitis) is highly common, not least, due to smoking prevalence. Pulmonary fibrosis doesn't increase airway resistance (an obstructive feature); it reduces compliance, with resistance normal or slightly altered by volume loss. The FEV1/FVC ratio's preservation in fibrosis reflects its restrictive nature, distinguishing it as the true statement, aligning with spirometric patterns and disease mechanics.

Question 4 of 5

Which of the following structures contains blood with the highest PCO2?

Correct Answer: C

Rationale: PCO2, the partial pressure of carbon dioxide, indicates CO2 concentration in blood, highest where metabolic waste accumulates before gas exchange. The superior vena cava (SVC) carries deoxygenated blood from the upper body to the right atrium, with a PCO2 of ~45-46 mmHg venous blood rich in CO2 from tissue metabolism, making it the highest here. Pulmonary veins carry oxygenated blood post-alveolar exchange, with PCO2 lowered to arterial levels (~40 mmHg). Midportion pulmonary capillaries are transitional, where PCO2 drops from venous (~46 mmHg) to arterial (~40 mmHg) during gas exchange, averaging less than SVC. Carotid bodies, chemoreceptors sensing arterial blood (PCO2 ~40 mmHg), aren't blood reservoirs. SVC's role in collecting systemic venous return ensures it carries the most CO2-rich blood before pulmonary offloading, distinguishing it from oxygenated or exchanging sites, reflecting the circulatory path where CO2 peaks prior to exhalation.

Question 5 of 5

At the end of normal quiet expiration, just before the start of inspiration, the lungs are said to be in:

Correct Answer: C

Rationale: Functional residual capacity (FRC) is the lung volume after a normal, quiet expiration (~2.5-3 L), where elastic recoil of the lungs (inward) balances the chest wall (outward), with no muscle activity. Residual volume (RV, ~1-1.5 L) is after maximal expiration, not quiet breathing. Expiratory reserve volume (ERV, ~1-1.5 L) is the extra air forcibly exhaled beyond normal expiration, not the resting state. Inspiratory reserve volume (IRV, ~2-3 L) is additional air inhaled beyond a normal breath, relevant to inspiration. FRC is the resting point before inspiration, maintaining alveolar patency and gas exchange efficiency, with intra-alveolar pressure equaling atmospheric (~760 mmHg). It's distinct from volumes tied to maximal efforts or active phases, reflecting the passive equilibrium critical for respiratory homeostasis.

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