NEET Breathing and Exchange of Gases Previous Year Questions with Solutions

Mechanisms of breathing vary among different groups of animals depending on their habitats and levels of organization. Lower invertebrates like sponges (Porifera), coelenterates (Cnidaria), and flatworms (Platyhelminthes) exhibit cellular or tissue levels of organization and lack specialized vascular or respiratory organs.

• • Water canal system circulates water past choanocytes and pinacocytes for direct gas exchange.

Earthworms use their moist cuticle (cutaneous respiration, Option 2). Insects have a network of tracheal tubes to transport atmospheric air within the body (Option 3). Aquatic arthropods, molluscs, and fishes use specialized vascularized structures called gills (branchial respiration, Option 4).

• • Option (1) is uniquely correct for sponges.

Sponges exchange O₂ with CO₂ by simple diffusion across their entire body surfaces.

• • Matches official NTA final answer key Option A / (1).

Haemoglobin is a red coloured iron containing pigment present in RBCs. $O_2$ can bind with haemoglobin in a reversible manner to form oxyhaemoglobin. Binding of oxygen with haemoglobin is primarily related to partial pressure of $O_2$. Partial pressure of $CO_2$, hydrogen ion concentration ($H^+$) and temperature are the other factors that interfere with this binding.

In the alveoli, where there is high $pO_2$, low $pCO_2$, lesser $H^+$ concentration and lower temperature, the factors are all favourable for the formation of oxyhaemoglobin. In the tissues, where low $pO_2$, high $pCO_2$, high $H^+$ concentration and higher temperature exist, the conditions are favourable for dissociation of oxygen from the oxyhaemoglobin.

Option (4) directly and correctly captures "High pO₂ and Lesser H⁺ concentration".

Inspiratory Capacity ($IC$) is the total volume of air a person can inspire after a normal expiration, comprising Tidal Volume and Inspiratory Reserve Volume ($IC = TV + IRV$) (D -> III). Expiratory Capacity ($EC$) is the total volume of air a person can expire after a normal inspiration, comprising Tidal Volume and Expiratory Reserve Volume ($EC = TV + ERV$) (A -> II).

Functional Residual Capacity ($FRC$) is the volume of air that remains in the lungs after a normal expiration, including $ERV + RV$ (B -> IV). Vital Capacity ($VC$) is the maximum volume of air a person can breathe in after a forced expiration, encompassing $ERV + TV + IRV$ (C -> I).

A-II, B-IV, C-I, D-III perfectly matches Option (3).

Vital Capacity is defined as the maximum volume of air a person can exhale after a maximal forced inspiration, or the maximum volume of air a person can inhale after a maximal forced expiration:

NCERT defines Vital Capacity: "The maximum volume of air a person can breathe in after a forced expiration. This includes ERV, TV and IRV or the maximum volume of air a person can breathe out after a forced inspiration."

Expiratory Capacity ($EC = TV + ERV$); Inspiratory Capacity ($IC = TV + IRV$); Functional Residual Capacity ($FRC = ERV + RV$); Total Lung Capacity ($TLC = VC + RV = IRV + ERV + TV + RV$).

Binding of oxygen to haemoglobin is a reversible, cooperative oxygenation process governed by the oxygen-haemoglobin dissociation curve. At the pulmonary alveoli: - High $pO_2$ (~104 mm Hg): Provides the steep diffusion gradient driving conformational transition of deoxyhaemoglobin (T-state) into relaxed oxyhaemoglobin (R-state). - Low $pCO_2$ (~40 mm Hg): Minimizes carbamino-haemoglobin formation and prevents carbamylation of N-terminal amino groups. - Lesser $H^+$ concentration (Higher pH ~7.4): Prevents protonation of histidine residues that otherwise stabilize deoxyhaemoglobin (Haldane effect). - Lower Temperature: Exothermic binding of $O_2$ to haem is thermodynamically favoured at lower temperatures.

In metabolically active systemic tissues, the reverse occurs: low $pO_2$, high $pCO_2$, high $H^+$ (acidic lactic/carbonic acid), and elevated temperature facilitate the uncoupling and unloading of oxygen (Bohr effect, rightward shift).

Gas exchange across the alveolar-capillary respiratory membrane proceeds purely by simple passive diffusion governed by partial pressure gradients, gas solubility, and membrane thickness: - Atmospheric Air: $pO_2 = 159\text{ mm Hg}$, $pCO_2 = 0.3\text{ mm Hg}$. - Alveoli: $pO_2 = \mathbf{104\text{ mm Hg}}$, $pCO_2 = \mathbf{40\text{ mm Hg}}$. - Deoxygenated Blood (Pulmonary Artery): $pO_2 = 40\text{ mm Hg}$, $pCO_2 = 45\text{ mm Hg}$. - Oxygenated Blood (Pulmonary Vein / Systemic Arteries): $pO_2 = 95\text{ mm Hg}$, $pCO_2 = 40\text{ mm Hg}$. - Tissues: $pO_2 = 40\text{ mm Hg}$, $pCO_2 = 45\text{ mm Hg}$.

- For $O_2$: Gradient is from alveoli ($104\text{ mm Hg}$) to deoxygenated capillary blood ($40\text{ mm Hg}$), driving rapid influx of oxygen into blood. - For $CO_2$: Gradient is from blood ($45\text{ mm Hg}$) to alveoli ($40\text{ mm Hg}$), driving excretion of carbon dioxide into alveolar air.

The reversible oxygenation of haemoglobin to form oxyhaemoglobin ($Hb(O_2)_4$) is governed by local allosteric modulators: - In Pulmonary Alveoli: Environmental conditions favor maximal oxygen saturation (leftward shift of dissociation curve): 1. High partial pressure of oxygen ($pO_2 \approx 104\text{ mm Hg}$). 2. Low partial pressure of carbon dioxide ($pCO_2 \approx 40\text{ mm Hg}$). 3. Lesser $H^+$ concentration (higher, slightly alkaline pH $\approx 7.4$). 4. Lower body temperature. - In Systemic Tissues: Cellular respiration generates $CO_2$ and lactic acid, creating: 1. Low $pO_2$ ($40\text{ mm Hg}$). 2. High $pCO_2$ ($45\text{ mm Hg}$). 3. High $H^+$ concentration (acidosis). 4. Elevated temperature. - High $[H^+]$ protonates key histidine residues on haemoglobin subunits, stabilizing the low-affinity deoxygenated T-state (Bohr effect) and promoting oxygen dissociation, never formation.

Statement (3) asserts that "Higher H+ conc. in alveoli favours the formation of oxyhaemoglobin." This directly contradicts the Bohr effect and textbook facts; therefore, statement (3) is false and is the correct response.

Inspiration is an active neuromuscular process driven by atmospheric-to-alveolar pressure gradients: - (a) Contraction of Diaphragm: The dome-shaped phrenic-innervated muscular diaphragm contracts and flattens downward, increasing the volume of the thoracic cavity along the antero-posterior axis. - (b) Contraction of External Intercostal Muscles: Intercostal-innervated muscles pull the ribs upward and outward while pushing the sternum ventrally, increasing thoracic volume along the dorso-ventral axis. - Pulmonary Volume Increase: Because the pleura adhere tightly to the thoracic wall via pleural fluid surface tension, any expansion of thoracic volume drives an obligatory increase in pulmonary volume (negating statement (c)). - Intra-Pulmonary Pressure Decrease: According to Boyle’s Law ($P \propto 1/V$), an expansion in pulmonary volume causes intra-pulmonary pressure to drop below atmospheric pressure (negative pressure of approx. $-1\text{ mm Hg}$ to $-3\text{ mm Hg}$), drawing ambient air into the bronchial tree (negating statement (d)).

Only events (a) and (b) occur during inspiration. Statements (c) and (d) describe events occurring during expiration.