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BiologyHuman Physiology
Match respiratory volumes with their capacities:
A. ERV (Expiratory Reserve Volume) → I. 2500-3000 mL
B. RV (Residual Volume) → II. 500 mL
C. IRV (Inspiratory Reserve Volume) → III. 1000-1100 mL
D. TV (Tidal Volume) → IV. 1100-1200 mL
Options
1
A-III, B-I, C-IV, D-II
2
A-I, B-III, C-II, D-IV
3
A-III, B-IV, C-I, D-II
4
A-I, B-IV, C-II, D-III
Correct Answer
Option 3: A-III, B-IV, C-I, D-II
Solution
1

A. ERV → III (1000-1100 mL): Expiratory Reserve Volume — air forcefully exhaled after normal expiration.

B. RV → IV (1100-1200 mL): Residual Volume — air remaining even after maximum expiration.

2

C. IRV → I (2500-3000 mL): Inspiratory Reserve Volume — additional air forcefully inhaled after normal inspiration. Largest volume.

D. TV → II (500 mL): Tidal Volume — air exchanged in normal quiet breathing. Smallest value.

ERV=1000-1100 mL | RV=1100-1200 mL | IRV=2500-3000 mL | TV=500 mL
Answer: A-III, B-IV, C-I, D-II
Theory: Human Physiology
1. Respiratory Volumes and Capacities

Respiratory volumes are measured by spirometry (using a spirometer). Four basic lung volumes: Tidal Volume (TV): 500 mL — air moved in/out during normal quiet breathing. Inspiratory Reserve Volume (IRV): 2500-3000 mL — additional air forcefully inhaled ABOVE TV. Largest individual lung volume. Expiratory Reserve Volume (ERV): 1000-1100 mL — additional air forcefully exhaled BELOW TV. Residual Volume (RV): 1100-1200 mL — air REMAINING after maximum forceful expiration. Cannot be measured by spirometry (air cannot be expelled). These four volumes account for total lung capacity (TLC = TV + IRV + ERV + RV = approximately 5800-6200 mL). Lung capacities are combinations of two or more volumes: Vital Capacity (VC) = TV + IRV + ERV = 3500-4600 mL. Total Lung Capacity (TLC) = TV + IRV + ERV + RV. Inspiratory Capacity (IC) = TV + IRV. Functional Residual Capacity (FRC) = ERV + RV.

2. Why Residual Volume Cannot Be Measured by Spirometer

RV (Residual Volume) is the air remaining in lungs after maximum forceful expiration. It cannot be measured directly by spirometry because: spirometer measures volumes that can be inhaled/exhaled by the subject. RV remains trapped — cannot be breathed out (airways collapse before all air leaves). RV is important because it prevents alveolar collapse (keeps alveoli partially open between breaths). Methods to measure RV and FRC: Helium dilution technique: subject breathes a known volume of helium-air mixture. Helium mixes with lung air. Known dilution allows calculation of FRC, then RV = FRC - ERV. Body plethysmography (most accurate): subject sits in airtight box. Measures lung volume from pressure-volume changes of box plus subject. Nitrogen washout technique: breathing 100% O2, washing N2 from lungs, measuring N2 exhaled.

3. Dead Space in Respiration

Not all inspired air reaches the alveoli for gas exchange. Anatomical dead space: volume of conducting airways (nose, pharynx, larynx, trachea, bronchi, bronchioles) where no gas exchange occurs. Approximately 150 mL in adults. Effective tidal volume for gas exchange = TV - dead space = 500 - 150 = 350 mL. Alveolar dead space: alveoli that are ventilated but not perfused (no blood flow) — minimal in healthy lungs but increased in pulmonary embolism. Physiological dead space = anatomical + alveolar dead space. Increased dead space: pulmonary embolism (blood clot blocking blood flow to ventilated alveoli), emphysema (alveolar destruction, poor ventilation/perfusion matching), respiratory failure. Alveolar ventilation rate = (TV - dead space) x respiratory rate = (500 - 150) x 12-16 breaths/min = 4200-5600 mL/min. This is the effective ventilation delivering O2 for gas exchange.

4. Breathing Mechanics

Inspiration (active process): diaphragm contracts (descends), external intercostal muscles contract (ribs move up and out) → thoracic volume increases → lung volume increases → intrapulmonary pressure falls below atmospheric pressure → air flows in. Forced inspiration: sternocleidomastoid, scalene muscles (accessory muscles) also contract → even greater thoracic expansion. Expiration (passive during quiet breathing): diaphragm and external intercostals relax → lung elastic recoil → thoracic volume decreases → intrapulmonary pressure rises above atmospheric → air flows out. Forced expiration: internal intercostal muscles and abdominal muscles contract → active compression of thorax. Compliance: a measure of lung expandability = change in volume / change in pressure. High compliance = easily expanded (emphysema). Low compliance = stiff lungs (fibrosis, RDS). Surfactant: reduces surface tension of alveolar fluid → prevents alveolar collapse, increases lung compliance. Deficiency (RDS in premature infants) → stiff lungs → respiratory failure.

5. Gas Exchange — Alveolar and Tissue

Gas exchange occurs by simple diffusion. Driving force = partial pressure gradient. At alveolar membrane: O2: alveolar air PO2 = 104 mmHg. Deoxygenated blood PO2 = 40 mmHg. Gradient = 64 mmHg. O2 diffuses from alveolus into blood. CO2: blood PCO2 = 45 mmHg. Alveolar air PCO2 = 40 mmHg. Gradient = 5 mmHg. CO2 diffuses from blood into alveolus. At tissue level: O2: blood PO2 = 95 mmHg (oxygenated). Tissue PO2 = 40 mmHg. O2 diffuses from blood into tissues. CO2: tissue PCO2 = 45 mmHg. Blood PCO2 = 40 mmHg. CO2 diffuses from tissues into blood. Factors increasing gas exchange: thin alveolar membrane, large surface area (~70 m2), good ventilation-perfusion matching, moist surface.

6. Transport of Oxygen in Blood

O2 transported in two ways: Dissolved in plasma: only 1.5% of total O2 (physically dissolved, proportional to PO2). Bound to haemoglobin: 98.5% of total O2. HbO2 (oxyhaemoglobin) — each Hb molecule carries 4 O2 (one per haem group). Maximum O2 carrying capacity: 1.34 mL O2 per gram of Hb. With normal Hb (15 g/100 mL blood): 20.1 mL O2/100 mL blood. Oxyhaemoglobin dissociation curve: sigmoid shape due to cooperative binding. T state (deoxyHb): low O2 affinity. R state (oxyHb): high O2 affinity. Bohr effect: at low pH (acidic), high CO2, high temperature, high 2,3-DPG → right shift of curve → O2 released more readily. This facilitates O2 delivery to metabolically active (acidic) tissues. Foetal Hb (HbF): higher O2 affinity (left-shifted curve) → facilitates O2 transfer from maternal to foetal blood across placenta.

7. Transport of CO2 in Blood

CO2 transported three ways: Dissolved in plasma: 7-10%. As bicarbonate (HCO3-): 60-70%. CO2 + H2O → H2CO3 → H+ + HCO3- (carbonic anhydrase in RBCs catalyses this). HCO3- exits RBC in exchange for Cl- (chloride shift). H+ buffered by haemoglobin. As carbaminohaemoglobin: 20-25%. CO2 binds to terminal amino groups of haemoglobin. Different from O2 binding site. Haldane effect: deoxyhaemoglobin binds CO2 more readily than oxyhaemoglobin → at tissues (O2 released) → more CO2 binding. At lungs: O2 binds Hb → Hb releases CO2. HCO3- re-enters RBC, combines with H+ → H2CO3 → CO2 + H2O (carbonic anhydrase). CO2 expelled. This whole system maintains blood pH. Normal blood pH: 7.35-7.45. pH < 7.35 = acidosis. pH > 7.45 = alkalosis.

8. Regulation of Breathing

Breathing is regulated by respiratory centres in the brainstem. Medullary respiratory centre: inspiratory centre (DRG — dorsal respiratory group): sets basic rhythm, active during inspiration. Expiratory centre (VRG — ventral respiratory group): active during forced expiration and voluntary breathing. Apneustic centre (lower pons): prolongs inspiration if unchecked. Pneumotaxic centre (upper pons): limits inspiration duration, sets breathing rate. Chemical regulation: Central chemoreceptors (medulla): sense CO2/H+ in CSF (cerebrospinal fluid). CO2 crosses blood-brain barrier → CO2 + H2O → H+ → stimulates breathing. MOST SENSITIVE to CO2 changes. Peripheral chemoreceptors (carotid bodies, aortic bodies): sense PO2, PCO2, pH in blood. Primarily respond to LOW PO2 (hypoxia) below 60 mmHg. Hypercapnia (high CO2): most potent stimulus to breathe. Hypoxia: stimulates peripheral chemoreceptors. Chronic obstructive patients (COPD): may switch to hypoxic drive (chronically high CO2 desensitises central chemoreceptors).

Frequently Asked Questions
1. What are the normal values of all respiratory volumes?
Tidal Volume (TV): 500 mL (normal quiet breathing). Inspiratory Reserve Volume (IRV): 2500-3000 mL (extra air inhaled forcefully). Expiratory Reserve Volume (ERV): 1000-1100 mL (extra air exhaled forcefully). Residual Volume (RV): 1100-1200 mL (air always remaining). Total Lung Capacity (TLC): TV+IRV+ERV+RV = approximately 5800-6200 mL. Vital Capacity (VC): TV+IRV+ERV = approximately 3500-4600 mL. Functional Residual Capacity (FRC): ERV+RV = approximately 2100-2300 mL. Inspiratory Capacity (IC): TV+IRV = approximately 3000-3500 mL. Memory for volumes: RV is between ERV and IRV in size. TV is smallest. IRV is largest.
2. What is vital capacity and what factors affect it?
Vital Capacity (VC) = IRV + TV + ERV = maximum air expelled after maximum inspiration. Normal: 3500-4600 mL in adults. VC is affected by: Age (decreases with age), Sex (males > females by about 20-25%), Height (taller = higher VC), Body position (higher standing than lying), Physical fitness (athletes have higher VC), Lung disease (reduced in restrictive diseases like fibrosis; may be near normal in obstructive diseases). Forced Vital Capacity (FVC): VC exhaled as fast as possible. FEV1 (Forced Expiratory Volume in 1 second): volume exhaled in first second of FVC manoeuvre. FEV1/FVC ratio: normal = >0.70. Obstructive disease (asthma, COPD): FEV1/FVC < 0.70 (airway obstruction limits fast expiration). Restrictive disease (fibrosis, obesity): FEV1/FVC normal or elevated (both FVC and FEV1 reduced proportionally).
3. Why is residual volume important?
Residual Volume (RV) prevents alveolar collapse between breaths. If RV were zero, alveoli would completely collapse during expiration — they would be very difficult to re-expand on inspiration (like trying to inflate a completely deflated balloon vs one with some air already). RV ensures alveoli are always partially open. RV is maintained by: elastic properties of chest wall (chest wall tries to spring outward), surface tension effects of surfactant-lined alveoli. Clinically: increased RV occurs in emphysema (air trapping) and asthma during attack. Decreased RV occurs in restrictive lung diseases (fibrosis, space-occupying lesions). Premature infants: lack surfactant → alveoli collapse → Respiratory Distress Syndrome (RDS). Treatment: exogenous surfactant instillation into airways.
4. What is the difference between ventilation and perfusion?
Ventilation (V): movement of air in and out of lungs. Measured as minute ventilation = TV x respiratory rate = 500 x 12-16 = 6000-8000 mL/min. Alveolar ventilation = (TV - dead space) x rate = 4200-5600 mL/min. Perfusion (Q): blood flow through pulmonary capillaries. Pulmonary blood flow = cardiac output = ~5000 mL/min at rest. V/Q ratio: ratio of ventilation to perfusion in a lung region. Normal V/Q = 0.8 (ventilation slightly less than perfusion). V/Q mismatch: major cause of hypoxaemia. V/Q = 0 (shunt): perfused but not ventilated (pneumonia, atelectasis). V/Q = infinity (dead space): ventilated but not perfused (pulmonary embolism). Gravity effect: V/Q ratio higher at lung apex (ventilation > perfusion) and lower at base. Hypoxic pulmonary vasoconstriction (HPV): areas of low O2 → pulmonary arterioles constrict → blood diverted to better ventilated areas → improves V/Q matching.
5. What is spirometry and what can it diagnose?
Spirometry is the measurement of lung function using a device called a spirometer that measures volumes and flow rates during breathing manoeuvres. Tests: Slow vital capacity (SVC): breathe in maximally then exhale slowly and completely. Measures VC, ERV, IRV. Forced vital capacity (FVC): breathe in maximally then exhale as hard and fast as possible. Measures FVC, FEV1, FEV1/FVC ratio, PEF (peak expiratory flow). Flow-volume loop: displays flow vs volume graphically. Spirometry diagnoses: Obstructive pattern (asthma, COPD, emphysema): FEV1/FVC < 0.70, FVC relatively preserved, flow-volume curve shows concavity in expiratory limb. Restrictive pattern (pulmonary fibrosis, obesity, muscle weakness): FVC reduced, FEV1 reduced, FEV1/FVC ratio normal or elevated, small total lung capacity.
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