Respiratory System — MCQs

Respiratory System Indian Medical PG Practice Questions and MCQs

Question 81: Specific lung compliance is decreased in all of the following conditions EXCEPT:

A. Pulmonary congestion
B. Chronic bronchitis (Correct Answer)
C. Pulmonary fibrosis
D. Decreased surfactant

Explanation: **Explanation:** **Specific Lung Compliance** is defined as compliance per unit lung volume (Compliance/FRC). It is used to standardize compliance across different lung sizes, ensuring that a child and an adult have comparable values. **Why Chronic Bronchitis is the Correct Answer:** In **Chronic Bronchitis**, the primary pathology involves airway inflammation and excessive mucus production rather than significant destruction of the lung parenchyma or changes in elastic recoil. Therefore, **lung compliance remains relatively normal**. In contrast, in Emphysema (the other component of COPD), compliance increases due to the loss of elastic fibers. Since compliance is not decreased in chronic bronchitis, it is the correct "Except" choice. **Why the Other Options are Incorrect:** * **Pulmonary Fibrosis:** This is a restrictive lung disease where the lungs become "stiff" due to excess collagen deposition. This significantly **decreases** compliance. * **Decreased Surfactant:** Surfactant reduces surface tension. A deficiency (e.g., NRDS) increases surface tension, making the alveoli prone to collapse and **decreasing** compliance. * **Pulmonary Congestion:** The presence of excess fluid/blood in the interstitium increases lung stiffness and interferes with alveolar expansion, thereby **decreasing** compliance. **High-Yield Clinical Pearls for NEET-PG:** * **Compliance (C) = ΔV / ΔP.** It is the measure of "distensibility." * **Increased Compliance:** Seen in **Emphysema** (loss of elastic recoil) and **Aging**. * **Decreased Compliance:** Remember the mnemonic **"SCAR"**: **S**urfactant deficiency, **C**ongestion (edema), **A**telectasis, and **R**estrictive lung diseases (Fibrosis). * Specific compliance is a more accurate measure than total compliance when comparing individuals with different lung volumes (e.g., after a pneumonectomy).

Question 82: Natural acclimatization in high altitude is due to what primary physiological change?

A. Increased ventilation
B. Increased oxygen utilization
C. Increase in chest size and decrease in abdominal circumference
D. Decreased partial pressure of oxygen (Correct Answer)

Explanation: **Explanation:** The primary physiological driver for all changes during high-altitude acclimatization is the **decrease in the partial pressure of oxygen ($PO_2$)** in the inspired air. As altitude increases, the barometric pressure falls, leading to a proportional decrease in the $PO_2$ of the atmosphere and, subsequently, the arterial blood ($PaO_2$). This state of **hypobaric hypoxia** acts as the fundamental stimulus that triggers the body’s adaptive mechanisms, such as erythropoiesis and hyperventilation. **Analysis of Options:** * **Option A (Increased ventilation):** While hyperventilation is the *immediate* compensatory response to hypoxia (mediated by peripheral chemoreceptors), it is a **result** of the low $PO_2$, not the primary cause of acclimatization itself. * **Option B (Increased oxygen utilization):** Acclimatization actually involves cellular adaptations to make oxygen utilization more *efficient* (e.g., increased mitochondrial density), but oxygen utilization does not increase; it is often limited by availability. * **Option C (Chest/Abdominal changes):** While native high-altitude dwellers (like Sherpas) may exhibit increased chest dimensions (barrel chest) to accommodate larger lung volumes, this is a long-term developmental adaptation rather than the primary physiological trigger for acclimatization. **High-Yield Clinical Pearls for NEET-PG:** * **Haldane Effect:** The primary stimulus for acclimatization is the low $PO_2$, which leads to the secretion of **Erythropoietin** from the kidneys, increasing RBC count (Polycythemia). * **2,3-BPG:** Levels increase at high altitudes, shifting the Oxygen-Dissociation Curve (ODC) to the **right**, facilitating oxygen unloading at the tissues. * **Pulmonary Hypertension:** Hypoxia causes **hypoxic pulmonary vasoconstriction**, which can lead to Right Ventricular Hypertrophy (RVH) and High-Altitude Pulmonary Edema (HAPE). * **Acid-Base Balance:** Hyperventilation causes respiratory alkalosis; the kidneys compensate by increasing bicarbonate excretion.

Question 83: High oxygen tension in alveoli is due to which of the following?

A. Right to left shunt
B. Ventilation-perfusion mismatch (Correct Answer)
C. Bronchial asthma
D. Inappropriate gas exchange

Explanation: **Explanation:** The correct answer is **Ventilation-perfusion (V/Q) mismatch**. In a normal lung, the V/Q ratio is approximately 0.8. When this ratio increases (V/Q > 1), it indicates that ventilation is high relative to blood flow (perfusion). In the extreme case of **dead space** (V/Q = infinity), ventilation occurs but there is no blood flow to carry oxygen away. Because oxygen is not being removed from the alveoli by pulmonary capillary blood, the alveolar oxygen tension ($P_AO_2$) rises and eventually approaches the partial pressure of oxygen in inspired air ($P_IO_2 \approx 149$ mmHg). **Analysis of Options:** * **Ventilation-perfusion mismatch (Correct):** High V/Q ratios (found typically at the lung apex or in pulmonary embolism) lead to high alveolar $PO_2$ because oxygen delivery to the alveoli exceeds its removal by the blood. * **Right to left shunt:** This involves blood bypassing ventilated alveoli. While it causes low arterial oxygen ($PaO_2$), it does not increase alveolar oxygen tension; in fact, it often leads to a low V/Q ratio. * **Bronchial asthma:** This causes airway obstruction, leading to **decreased** ventilation. A low V/Q ratio results in low alveolar oxygen tension. * **Inappropriate gas exchange:** This is a broad term usually implying diffusion defects or shunts, both of which typically result in hypoxia rather than high alveolar oxygen tension. **High-Yield Pearls for NEET-PG:** * **Apex vs. Base:** The V/Q ratio is highest at the **apex** (~3.0) and lowest at the **base** (~0.6). Therefore, $P_AO_2$ is highest at the apex. * **Dead Space:** V/Q = $\infty$. Alveolar gas composition equals inspired air. * **Shunt:** V/Q = 0. Alveolar gas composition equals mixed venous blood ($P_AO_2 \approx 40$ mmHg). * **West Zones:** High V/Q areas (Zone 1) are physiological dead spaces where alveolar pressure can exceed capillary pressure.

Question 84: Apnoea is defined as:

A. Stoppage of heart beat
B. Cessation of respiration (Correct Answer)
C. Irregular respiration
D. Reduced respiratory rate

Explanation: **Explanation:** **Apnoea** (or apnea) is derived from the Greek word *apnoia*, meaning "without breath." In medical physiology, it is defined as the **temporary cessation of breathing** or the absence of spontaneous respiration. It occurs when the respiratory drive is inhibited or when there is a physical obstruction preventing airflow, leading to a pause in the respiratory cycle. **Analysis of Options:** * **Option B (Correct):** Apnoea specifically refers to the complete stop of airflow. It can be voluntary (breath-holding) or involuntary (e.g., Sleep Apnoea, Deglutition Apnoea during swallowing). * **Option A:** Stoppage of the heartbeat is termed **Asystole** or Cardiac Arrest. While respiratory arrest eventually leads to cardiac arrest, the terms are not synonymous. * **Option C:** Irregular respiration refers to patterns like **Cheyne-Stokes breathing** or **Biot’s respiration**, where the rhythm is inconsistent but breathing has not permanently ceased. * **Option D:** A reduced respiratory rate (typically <12 breaths/minute in adults) is termed **Bradypnoea**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Deglutition Apnoea:** A physiological reflex where respiration is briefly arrested during the pharyngeal stage of swallowing to prevent aspiration. 2. **Sleep Apnoea:** Classified into **Obstructive** (physical airway collapse) and **Central** (loss of ventilatory drive from the brainstem). 3. **Breaking Point:** During voluntary apnoea, the "breaking point" (the urge to breathe) is primarily triggered by **Hypercapnia** (increased $PCO_2$) and secondarily by Hypoxia. 4. **Apnoeic Oxygenation:** The phenomenon where oxygen levels are maintained in the blood despite apnoea, provided the airway is patent and functional residual capacity is filled with 100% $O_2$.

Question 85: What is the normal partial pressure of carbon dioxide in arterial blood?

A. 40 mm Hg (Correct Answer)
B. 37 mm Hg
C. 45 mm Hg
D. 60 mm Hg

Explanation: **Explanation:** The partial pressure of carbon dioxide in arterial blood (**PaCO₂**) is a critical physiological parameter regulated by the balance between metabolic CO₂ production and alveolar ventilation. 1. **Why Option A is Correct:** In a healthy adult at sea level, the normal range for PaCO₂ is **35–45 mm Hg**, with **40 mm Hg** being the standard physiological mean. This value ensures that the blood pH remains within the narrow range of 7.35–7.45. The peripheral and central chemoreceptors are exquisitely sensitive to changes in PaCO₂, adjusting the rate and depth of respiration to maintain this steady state. 2. **Why Other Options are Incorrect:** * **Option B (37 mm Hg):** While within the normal range (35–45), it is not the standard "textbook" value used for physiological calculations or the mean arterial reference. * **Option C (45 mm Hg):** This represents the upper limit of normal arterial CO₂. However, 45 mm Hg is specifically the classic value for **mixed venous blood (PvCO₂)** as it returns to the lungs from the tissues. * **Option D (60 mm Hg):** This indicates significant **hypercapnia** (respiratory acidosis), often seen in Type 2 respiratory failure or severe hypoventilation. **High-Yield Clinical Pearls for NEET-PG:** * **P(A-a)O₂ Gradient:** While we focus on CO₂, remember that the Alveolar-arterial oxygen gradient is a key tool to differentiate causes of hypoxia. * **CO₂ Transport:** Most CO₂ (approx. 70%) is transported as **bicarbonate (HCO₃⁻)**, 23% as carbaminohemoglobin, and 7% dissolved in plasma. * **Haldane Effect:** Deoxygenation of blood increases its ability to carry CO₂; this occurs in systemic tissues. * **Control of Breathing:** The **central chemoreceptors** in the medulla are primarily stimulated by changes in H⁺ concentration derived from PaCO₂, making CO₂ the primary drive for respiration in healthy individuals.

Question 86: The sigmoid shape of the hemoglobin-oxygen dissociation curve is primarily due to which phenomenon?

A. The binding of the first O2 molecule decreases the affinity for subsequent molecules.
B. Hemoglobin can bind to a maximum of two molecules of O2.
C. The cooperative binding of oxygen molecules to hemoglobin. (Correct Answer)
D. All of the above.

Explanation: ### Explanation **1. Why Option C is Correct: The Concept of Cooperativity** The sigmoid (S-shaped) nature of the Oxygen-Hemoglobin Dissociation Curve (OHDC) is a direct result of **positive cooperativity**. Hemoglobin is a tetramer consisting of four polypeptide chains, each with a heme group. * In its deoxygenated state, hemoglobin is in the **T-state (Tense)**, which has a low affinity for oxygen. * When the first molecule of $O_2$ binds, it triggers a conformational change that shifts the molecule into the **R-state (Relaxed)**. * This transition significantly increases the affinity of the remaining heme groups for oxygen, making it progressively easier for the second, third, and fourth molecules to bind. This rapid increase in saturation over a narrow range of $PO_2$ creates the steep portion of the sigmoid curve. **2. Why Other Options are Incorrect** * **Option A:** This is the opposite of the truth. The binding of the first $O_2$ molecule **increases** (not decreases) the affinity for subsequent molecules. * **Option B:** Hemoglobin is a tetramer and can bind up to **four** molecules of $O_2$ (one per heme group), not two. * **Option D:** Since A and B are factually incorrect, "All of the above" is invalid. **3. High-Yield NEET-PG Clinical Pearls** * **P50 Value:** The $PO_2$ at which hemoglobin is 50% saturated (Normal $\approx$ 26-27 mmHg). An increase in P50 signifies a **Right Shift** (decreased affinity). * **Right Shift (CADET, face Right!):** **C**O2 increase, **A**cidosis ($H^+$), **D**PG (2,3-BPG) increase, **E**xercise, and **T**emperature increase. * **Myoglobin:** Unlike hemoglobin, myoglobin is a monomer and lacks cooperativity; therefore, its dissociation curve is **hyperbolic**, not sigmoid. * **Bohr Effect:** The shift of the curve to the right in response to increased $CO_2$ and $H^+$, facilitating oxygen unloading at the tissues.

Question 87: What is the partial pressure for carbon dioxide in the inspired air?

A. 0.3 mm Hg (Correct Answer)
B. 158 mm Hg
C. 100 mm Hg
D. 32 mm Hg

Explanation: ### Explanation The partial pressure of a gas in a mixture is determined by its fractional concentration and the total barometric pressure ($P_{gas} = F_{gas} \times P_{total}$). **1. Why Option A is Correct:** At sea level, the total atmospheric pressure is **760 mm Hg**. Carbon dioxide ($CO_2$) makes up approximately **0.04%** of the dry atmospheric air. * **Calculation:** $0.0004 \times 760 \text{ mm Hg} \approx \mathbf{0.3 \text{ mm Hg}}$. This negligible concentration ensures a steep diffusion gradient between the pulmonary capillary blood ($PCO_2 \approx 46 \text{ mm Hg}$) and the alveoli, facilitating efficient $CO_2$ elimination. **2. Analysis of Incorrect Options:** * **Option B (158 mm Hg):** This is the partial pressure of **Oxygen ($PO_2$)** in inspired (atmospheric) air. It is calculated as $21\%$ of $760 \text{ mm Hg}$ ($0.21 \times 760$). * **Option C (100 mm Hg):** This represents the normal **Alveolar partial pressure of Oxygen ($PAO_2$)**. It is lower than inspired air due to the addition of water vapor and the constant diffusion of $O_2$ into the blood. * **Option D (32 mm Hg):** This is the approximate partial pressure of $CO_2$ in **expired air**. It is higher than inspired air because it includes $CO_2$ cleared from the alveoli, but lower than alveolar $CO_2$ ($40 \text{ mm Hg}$) due to mixing with dead space air. **High-Yield Clinical Pearls for NEET-PG:** * **Humidification:** As air enters the respiratory tract, it is saturated with water vapor ($PH_2O = 47 \text{ mm Hg}$). This dilutes the $PO_2$ from $158 \text{ mm Hg}$ (dry air) to **$149 \text{ mm Hg}$** (humidified tracheal air). * **Alveolar $PCO_2$:** Is typically maintained at **$40 \text{ mm Hg}$**. * **Diffusion Gradient:** $CO_2$ is **20 times more soluble** than $O_2$, allowing it to diffuse rapidly across the respiratory membrane despite a much smaller pressure gradient ($6 \text{ mm Hg}$ for $CO_2$ vs. $60 \text{ mm Hg}$ for $O_2$).

Question 88: What is the typical oxygen saturation in venous blood?

A. 97%
B. 90%
C. 75% (Correct Answer)
D. 46%

Explanation: **Explanation:** The correct answer is **75%**. This value represents the oxygen saturation ($SvO_2$) of mixed venous blood under normal resting conditions. **1. Why 75% is correct:** In a healthy adult at rest, arterial blood is nearly fully saturated with oxygen (approx. 97-100%). As blood passes through systemic capillaries, tissues extract a fraction of this oxygen for metabolism. At rest, the **Oxygen Extraction Ratio (OER)** is typically **25%**. Therefore, 100% (initial) minus 25% (extracted) leaves **75%** of the hemoglobin still saturated with oxygen in the venous return. This corresponds to a partial pressure of oxygen ($PvO_2$) of approximately **40 mmHg**. **2. Why the other options are incorrect:** * **97% (Option A):** This is the typical oxygen saturation of **arterial blood** ($SaO_2$) leaving the lungs. * **90% (Option B):** This value is often considered the "critical threshold" in clinical practice. Below 90%, the oxyhemoglobin dissociation curve enters the steep portion, meaning small drops in $PO_2$ lead to large drops in saturation. * **46% (Option D):** This is a distractor value. **46 mmHg** is the typical partial pressure of Carbon Dioxide ($PvCO_2$) in mixed venous blood, not the oxygen saturation. **Clinical Pearls for NEET-PG:** * **Venous Oxygen Reserve:** The 75% saturation in venous blood acts as a "safety reservoir." During exercise, tissues can increase extraction, causing $SvO_2$ to drop significantly (as low as 25%). * **The P50 Value:** The $PO_2$ at which hemoglobin is 50% saturated is **26.7 mmHg**. * **Mixed Venous Blood:** For accurate measurement, mixed venous blood must be sampled from the **Pulmonary Artery** using a Swan-Ganz catheter, as it represents the average of the entire body's venous return.

Question 89: Anatomical dead space is increased by all EXCEPT:

A. Atropine
B. Halothane
C. Massive pleural effusion (Correct Answer)
D. Inspiration

Explanation: **Explanation:** **Anatomical Dead Space** refers to the volume of the conducting airways (from the nose/mouth down to the terminal bronchioles) where no gas exchange occurs. Its volume is determined by the physical dimensions of these airways. **Why Massive Pleural Effusion is the Correct Answer:** Massive pleural effusion is a restrictive lung pathology. The accumulation of fluid in the pleural cavity exerts extrinsic pressure on the lung parenchyma, leading to **compression atelectasis**. This collapses the small airways and reduces the overall lung volume, thereby **decreasing** the anatomical dead space. **Analysis of Incorrect Options:** * **Atropine:** As an anticholinergic drug, atropine causes bronchodilation. By increasing the caliber (diameter) of the conducting airways, it increases the volume of the anatomical dead space. * **Halothane:** This volatile anesthetic agent has potent bronchodilatory properties. Similar to atropine, it increases the volume of the conducting zone. * **Inspiration:** During inspiration, the expansion of the thoracic cage and the resulting negative intrapleural pressure pull the airways open (traction). This increases both the length and diameter of the bronchi, leading to an increase in anatomical dead space. Conversely, expiration decreases it. **High-Yield Clinical Pearls for NEET-PG:** * **Normal Value:** Anatomical dead space is roughly **2 ml/kg** of body weight (approx. 150 ml in a healthy adult). * **Physiological Dead Space:** Anatomical Dead Space + Alveolar Dead Space. In healthy individuals, it equals anatomical dead space. * **Measurement:** Anatomical dead space is measured by **Fowler’s Method** (Nitrogen washout), while Physiological dead space is measured by **Bohr’s Equation**. * **Factors increasing it:** Upright posture (compared to supine), neck extension, and emphysema (due to airway dilation).

Question 90: The central chemosensitive area responds to changes in:

A. Arterial H+
B. CSF H+
C. Arterial CO2 (Correct Answer)
D. CSF CO2

Explanation: **Explanation:** The central chemosensitive area, located on the ventral surface of the medulla, is primarily responsible for the chemical control of breathing. **Why Arterial CO₂ is the correct answer:** While the central chemoreceptors are exquisitely sensitive to **Hydrogen ions (H⁺)**, these ions cannot cross the blood-brain barrier (BBB). However, **Carbon dioxide (CO₂)** is lipid-soluble and diffuses rapidly across the BBB from the arterial blood into the cerebrospinal fluid (CSF) and interstitial fluid of the brain. Once in the CSF, CO₂ reacts with water (catalyzed by carbonic anhydrase) to form carbonic acid, which dissociates into H⁺ and HCO₃⁻. It is this locally generated H⁺ that directly stimulates the chemoreceptors. Therefore, the **initial change** in the systemic circulation that triggers this central response is a change in **Arterial CO₂**. **Analysis of Incorrect Options:** * **Option A (Arterial H⁺):** H⁺ ions are polar and cannot cross the BBB. Changes in arterial H⁺ primarily stimulate **peripheral chemoreceptors** (carotid and aortic bodies), not central ones. * **Option B (CSF H⁺):** While H⁺ in the CSF is the *direct* stimulus, the question asks what the area responds to in the context of systemic changes. Arterial CO₂ is the primary driver that determines CSF H⁺ levels. * **Option D (CSF CO₂):** CO₂ itself is not the direct stimulant; it must first be converted to H⁺ to activate the receptors. **High-Yield Facts for NEET-PG:** * **Main Stimulus:** The central chemoreceptor is most sensitive to **Hypercapnia** (increased CO₂). * **Oxygen:** Central chemoreceptors do **not** respond to hypoxia; oxygen levels are sensed exclusively by peripheral chemoreceptors. * **Blood-Brain Barrier:** Permeable to CO₂, impermeable to H⁺ and HCO₃⁻. * **Response Time:** Central chemoreceptors provide the main drive for ventilation but are slower to respond than peripheral chemoreceptors.

Practice by Chapter

Mechanics of Breathing

Practice Questions

Pulmonary Ventilation

Practice Questions

Pulmonary Circulation

Practice Questions

Gas Exchange in the Lungs

Practice Questions

Oxygen and Carbon Dioxide Transport

Practice Questions

Control of Breathing

Practice Questions

Respiratory Adjustments in Health and Disease

Practice Questions

High Altitude Physiology

Practice Questions

Diving Physiology

Practice Questions

Respiratory Function Tests

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free