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Gaseous Exchange Chapter Notes | Physiology - NEET PG PDF Download

Physical Principles of Gas Exchange

  • Human lungs contain approximately 300 alveoli, each with an average diameter of 0.2 mm.
  • Alveolar walls are extremely thin, allowing close proximity between alveolar gases and pulmonary capillary blood.
  • Gas exchange occurs across the respiratory membrane, which includes the respiratory bronchiole, alveolar ducts, atria, and alveoli, not just the alveoli.
  • The respiratory membrane, also known as the pulmonary membrane, consists of:
    • A thin layer of fluid lining the alveolus.
    • Alveolar epithelium cells.
    • Basement membrane of epithelial cells.
    • A thin interstitial space between the alveolar epithelium and capillary membrane.
    • Capillary basement membrane.
    • Endothelial cells of the capillary.
      Gaseous Exchange Chapter Notes | Physiology - NEET PGUltrastructure of the alveolar respiratory membrane and direction of gas exchange.
  • The average thickness of the respiratory membrane is 0.5 μm (range: 0.2 to 0.6 μm).
  • The total surface area of the respiratory membrane in a healthy adult male is approximately 70 m².
  • Respiratory membrane thickness may increase due to interstitial edema or lung fibrosis.
  • The surface area of the respiratory membrane can decrease due to conditions like pneumonectomy or emphysema (caused by the rupture of many alveoli).
  • The rate of diffusion (D) is governed by the formula:
    • D ∝ (ΔP × A × S) / (d × √M), where:
      • ΔP: Partial pressure difference between the two sides of the diffusion pathway.
      • A: Cross-sectional area of the pathway.
      • S: Solubility of the gas.
      • d: Distance of diffusion.
      • M: Molecular weight of the gas.
  • The diffusion coefficient of a gas is proportional to S / √M, determined by its solubility (S) and molecular weight (M).
  • Assuming the diffusion coefficient of oxygen is 1, the relative diffusion coefficient for CO₂ is ~20, and for carbon monoxide (CO) is 0.81.
  • CO₂ diffuses approximately 20 times faster through the respiratory membrane than O₂ at the same partial pressure due to its higher diffusion coefficient.
  • Lung disorders often result in hypoxemia (low blood O₂ content) rather than hypercarbia (CO₂ retention) because CO₂ diffuses more readily.
  • Alveolar diffusion decreases in emphysema due to reduced effective surface area (A) of the respiratory membrane.
  • Diffusion is also reduced in diseases that increase the diffusion distance (d), such as edema in acute lung injury or fibrosis in interstitial lung diseases.

Capillary Transit Time

  • A red blood cell takes approximately 4 to 5 seconds to travel through the pulmonary circulation at resting cardiac output, with ~0.75 seconds (≈0.8 seconds) spent in the alveolar capillary.
  • The time a red blood cell spends in the pulmonary capillaries is called the capillary transit time.
  • Capillary transit time is calculated using the formula:
    • Mean capillary transit time = (Pulmonary capillary blood volume) / (Pulmonary blood flow).
  • Total blood volume in pulmonary circulation is approximately 450 mL, with 70 mL (range: 60 to 140 mL) located in the pulmonary capillaries.
  • Pulmonary blood flow (PBF) is nearly equal to cardiac output (CO), approximately 5.4 L/min (90 mL/sec) at rest.
  • Normal capillary transit time at rest is approximately 0.8 seconds, calculated from the above formula.
  • An increase in cardiac output reduces capillary transit time.
  • Transit time is critical for determining pulmonary end-capillary PO₂ and diffusing capacity, as it allows partial pressure equilibration between blood and alveolar gases.

Perfusion-Limited and Diffusion-Limited Gas

  • Figure the uptake of N₂O, O₂, and CO in blood relative to their partial pressures and red blood cell transit time in the capillary.
    Gaseous Exchange Chapter Notes | Physiology - NEET PG
  • Perfusion-limited gases (e.g., N₂O and O₂) reach equilibrium with alveolar pressure before exiting the capillary.
  • Diffusion-limited gases (e.g., CO) do not reach equilibrium with alveolar pressure during transit time.
  • Normally, oxygen diffusion equilibrium occurs within 0.25 seconds (1/3 of total transit time), providing a three-fold safety factor.
  • Even if transit time decreases to 0.25 seconds due to high cardiac output, oxygen diffusion equilibrium is achieved.
  • In lung diseases like fibrosis, reduced diffusion capacity may prevent capillary PO₂ from equilibrating with alveolar PO₂ during transit time.
  • N₂O is highly soluble in blood but does not bind to hemoglobin, leading to rapid partial pressure rise and quick diffusion equilibrium regardless of transit time.
  • Changes in diffusing capacity do not affect N₂O uptake; increased uptake requires increased perfusion or cardiac output.
  • N₂O uptake is limited by perfusion, as more red blood cells passing through alveolar capillaries increase uptake.
  • Carbon monoxide (CO) has a 250 times greater affinity for hemoglobin than oxygen, preventing significant partial pressure rise in capillary blood.
  • CO diffusion equilibrium is not achieved during transit time, and uptake depends on diffusing capacity rather than perfusion.
  • Increasing cardiac output does not significantly increase CO uptake.
  • All gas transport in the lung (e.g., O₂, CO₂) is perfusion-limited, except for CO and O₂ under hypoxic conditions.
  • Diffusion-limited gases include CO and O₂ in hypoxic conditions; all other gases, including O₂ under normoxic conditions in healthy lungs, are perfusion-limited.

Diffusing Capacity of Respiratory Membrane

  • Diffusing capacity is defined as the volume of gas that diffuses through the respiratory membrane per minute for a partial pressure difference of 1 mm Hg.
  • Diffusing capacity is directly proportional to the surface area of the alveolocapillary membrane and inversely proportional to its thickness.
  • Diffusing capacity for carbon monoxide (DLCO) is measured as an index of diffusing capacity since CO uptake is diffusion-limited.
  • The general equation for DLCOis:
    • DLCO = (CO uptake in the blood) / (Partial pressure of CO in the alveoli - Partial pressure of CO in blood).
  • CO binds to hemoglobin with high affinity, making the partial pressure of CO in blood effectively zero, except in habitual smokers.
  • The simplified DLCOequation is:
    • DLCO = (CO uptake in the blood) / (Partial pressure of CO in the alveoli).
  • The single-breath method, using a gas mixture with 0.3% CO and 10% helium, is the most common protocol for measuring DLCO.
  • Normal DLCO at rest is approximately 17 mL/min/mm Hg.
  • Oxygen diffusion capacity is 1.23 times that of CO (due to a diffusion coefficient 1.23 times higher), ranging from 21 to 25 mL/min/mm Hg.
  • CO₂ diffusion capacity is approximately 400 to 450 mL/min/mm Hg at rest, increasing to 1200 mL/min/mm Hg during exercise, due to its diffusion coefficient being ~20 times that of O₂.
  • Causes of high and low DLCO:
  • Causes of High D_LCO:
    • Recruitment of blood in alveolar capillary bed (e.g., supine position, hyperdynamic circulation like fever or exercise, bronchial asthma, Muller’s maneuver, left-to-right cardiac shunting, early congestive failure).
    • Miscellaneous causes: polycythemia, alveolar hemorrhage, obesity (cause uncertain), high altitude (due to low FiO₂, increased CO binding with hemoglobin), post-bronchodilation in obstructive disease (6% increase).
  • Causes of Low D_LCO:
    • Decreased surface area for diffusion (e.g., pulmonary resection, emphysema, V/Q mismatch due to pulmonary obstruction).
    • Alveolar capillary membrane disease (e.g., interstitial lung disease like sarcoidosis or connective tissue disease, pulmonary vascular disease like embolism, pulmonary hypertension, vasculitis, alveolar edema, cardiac insufficiency).
    • Miscellaneous causes: anemia, lung cancer, chronic bronchitis, cystic fibrosis.

Gas Transport

Symbols used: P (partial pressure), I (inspired air), E (expired air), A (alveolar), a (arterial), v (venous), v̅ (mixed venous). For example, PIO₂ is the partial pressure of O₂ in inspired air.

Composition of Atmospheric and Alveolar Gases:

  • Atmospheric air exerts barometric pressure (Pbaro) of 736 mm Hg at sea level.
  • Dalton’s law states that Pbaro equals the sum of partial pressures of individual gases: Pbaro = PN2 + PO2 + PCO2.
  • Partial pressure of O₂ (PO2) is calculated as: PO2 = Pbaro × FO2, where FO2 is the fractional concentration of oxygen (21%). Thus, PO2 = 160 mm Hg (736 × 0.21).
  • Inspired air is warmed and humidified, adding water vapor with a partial pressure (PH2O) of 47 mm Hg at 37°C, independent of barometric pressure.
  • Water vapor reduces the total pressure of dry gases in the conducting zone to (Pbaro - PH2O) = (736 - 47) = 689 mm Hg.
  • The formula for partial pressure of inspired air (Pi) is: Pi = (Pbaro - PH2O) × Fi, where Fi is the fraction of inspired dry air (FIO2 = 21%, FIN2 = 79%).
  • Partial pressures in inspired air: PIO2 = (736 - 47) × 0.21 = 145 mm Hg; PIN2 = (736 - 47) × 0.79 = 545 mm Hg.
  • Multicompartment model shows gas compositions:
    • Atmospheric air: N₂ (78.6%, 597 mm Hg), O₂ (20.8%, 159 mm Hg), CO₂ (0.04%, 0.3 mm Hg), H₂O (0.5%, 3.7 mm Hg).
    • Humidified air: N₂ (563 mm Hg), O₂ (149 mm Hg), CO₂ (0.3 mm Hg), H₂O (47 mm Hg).
    • Alveolar air: N₂ (569 mm Hg), O₂ (104 mm Hg), CO₂ (40 mm Hg), H₂O (47 mm Hg).
    • Expired air: N₂ (566 mm Hg, 75%), O₂ (120 mm Hg, 16%), CO₂ (27 mm Hg, 4%), H₂O (47 mm Hg, 6%).
  • Alveolar Gas Equation:
    • Simplified alveolar gas equation for oxygen partial pressure in alveoli (PAO2): PAO2 = PIO2 - (PACO2/ R.Q) + F, where:
      • PACO2: Partial pressure of CO₂ in alveoli (normally 40 mm Hg).
      • R.Q: Respiratory quotient (CO₂ production / O₂ consumption), determined by tissue metabolism in a steady state.
      • F: Small correction factor (~2 mm Hg for air breathing), often ignored.
    • When R.Q = 1, PAO2 = PIO2 - PACO2 = 145 - 40 = 105 mm Hg.

Physiological Shunt

  • Arterial blood partial pressure of O₂ (PaO₂) is 95-98 mm Hg, lower than alveolar PaO2 (100-104 mm Hg) due to venous admixture or physiological shunt.
  • Physiological shunt occurs when well-oxygenated blood from alveoli mixes with less oxygenated blood, primarily from bronchial circulation.
  • Bronchial arteries, branches of the aorta, supply conducting airways with oxygenated blood, and their capillaries anastomose with pulmonary artery-derived capillaries at the respiratory bronchioles, draining partially into pulmonary veins.
    Gaseous Exchange Chapter Notes | Physiology - NEET PGPhysiological shunt.
  • This mixing of partially deoxygenated bronchial blood with oxygenated blood causes a slight reduction in final PO2 compared to alveolar PO2.
  • Shunt flow is calculated based on oxygen content: QT × CaO2 = QS × CvO2 + (QT - QS) × CcO2, where:
    • QT: Total blood flow (cardiac output).
    • CaO2: Oxygen concentration in arterial blood.
    • QS: Shunted blood flow.
    • CvO2: Oxygen concentration in venous blood.
    • CcO2: Oxygen concentration in end-capillary blood.
  • Rearranged shunt equation: QS / QT = (CcO2 - CaO2) / (CcO2 - CvO2).
  • Normal physiological shunt is ~2% of total cardiac output (QT).
  • Shunt fraction increases in pathological conditions like patent ductus arteriosus (PDA) or patent foramen ovale (PFO), allowing systemic venous blood to bypass the lungs.
  • Shunt fractions approaching 50% are life-threatening, requiring aggressive management, such as mechanical ventilation with positive end-expiratory pressure (PEEP) to recruit consolidated or atelectatic alveoli.
  • Hypoxemia in pathological shunts responds poorly to 100% O₂ breathing, as shunted blood bypasses ventilated alveoli, though some arterial PO2 elevation occurs due to oxygen added to ventilated lung capillary blood.

O₂ Transport

Oxygen transport from lungs to tissues occurs via blood circulation and diffusion along a concentration gradient, represented by PO2 differences:

  • Atmospheric PO2: 158-160 mm Hg.
  • Inspired air PO2: 149 mm Hg.
  • Alveolar air PO2: 100 mm Hg.
  • Arterial blood PO2: 95 mm Hg.
  • Venous blood PO2: 40 mm Hg.
  • Tissue interstitial fluid PO2: 40 mm Hg.
  • The gradual decline in PO2 from atmosphere to tissues is called the oxygen cascade.
  • Oxygen exchange from alveolar air to pulmonary capillary blood and from arterial blood to tissues occurs by simple diffusion.
  • Oxygen transport involves three processes:

Uptake of oxygen by pulmonary blood:

  • Alveolar air PO2 is 100 mm Hg, while pulmonary arterial blood PO2 is ~40 mm Hg, driving oxygen diffusion into the blood.

Transport of oxygen in arterial blood:

Oxygen is transported in two forms:

  • Hemoglobin-bound O₂ (99%).
  • Dissolved O₂ (1%).
  • Hemoglobin-bound O₂:
    • Depends on hemoglobin saturation (SO2 or SpO₂), which depends on P_O2.
    • At PO2 = 120 mm Hg, hemoglobin is 100% saturated, carrying 1.39 mL O₂/g of pure hemoglobin (oxygen capacity).
    • In reality, oxygen capacity is ~1.34 mL O₂/g hemoglobin due to inactive hemoglobin derivatives (e.g., methemoglobin, carboxyhemoglobin).
    • 15 g hemoglobin carries 20.1 mL O₂ when fully saturated (1.34 × 15).
    • In arterial blood (PaO₂ = 95 mm Hg), hemoglobin is 97% saturated, carrying 19.5 mL O₂/100 mL blood (20.1 × 97/100).
    • In venous blood (PvO₂ = 40 mm Hg), hemoglobin is 75% saturated, carrying 15.1 mL O₂/100 mL blood.
  • Dissolved O₂:
    • Obeys Henry’s law: Amount dissolved is proportional to P_O2.
    • Dissolved O₂ per 100 mL blood = Solubility of O₂ × P_O2, where solubility is 0.003 mL/mm Hg/dL.
    • In arterial blood (PaO₂ = 95 mm Hg), dissolved O₂ = 0.003 × 95 = 0.285 mL/100 mL.
    • In venous blood (PvO₂ = 40 mm Hg), dissolved O₂ = 0.003 × 40 = 0.12 mL/100 mL.

Total O₂ in 100 mL blood:

  • Arterial blood: 19.5 (Hb-bound) + 0.285 (dissolved) = 19.8 mL.
  • Venous blood: 15.1 (Hb-bound) + 0.12 (dissolved) = 15.2 mL.

Release of oxygen to tissues:

  • Tissues consume ~5 mL O₂/100 mL arterial blood at rest, with a total body oxygen consumption of 250 mL/min (given a cardiac output of 5 L/min).
  • Utilization coefficient = (Oxygen consumed/min) / (Oxygen delivered/min) × 100 = (250 mL/min) / (1000 mL/min) × 100 = 25%.
  • Arterial blood carries ~19.8 mL O₂/100 mL, while venous blood carries ~15.2 mL, delivering ~4.6 mL O₂/100 mL to tissues (0.17 mL dissolved, remainder from hemoglobin).
  • Oxygen loading in lungs per 100 mL blood: whole blood (19.8 mL), hemoglobin solution (19.5 mL), plasma (0.29 mL).
  • In venous blood at P_O2 = 40 mm Hg: whole blood (15.2 mL), hemoglobin solution (15.1 mL), plasma (0.12 mL).
  • Approximately 5 mL O₂ is transported per 100 mL blood from lungs to tissues.

Respiratory Exchange Ratio

  • The respiratory exchange ratio (R) is the ratio of CO₂ output to O₂ uptake at any given time, whether or not equilibrium is reached: R = Rate of CO₂ output / Rate of O₂ uptake.
  • In steady-state conditions, this ratio is called the respiratory quotient (RQ).
  • RQ values:
    • Carbohydrate: 1.00.
    • Fat: 0.70.
    • Protein: 0.82.
    • Mixed diet: 0.825.
  • Extraction ratio = (Oxygen consumption / Oxygen supply) × 100.
  • Arterial blood carries ~20.1 mL O₂/100 mL, and venous blood carries ~15 mL O₂/100 mL, delivering ~5 mL O₂ to tissues.
  • Extraction ratio is ~25% at rest but can increase during exercise.

Oxyhemoglobin Dissociation Curve (OHDC)

  • The OHDC plots the partial pressure of O₂ against the percentage saturation of hemoglobin with O₂, showing a sigmoid shape due to cooperative binding.
  • P50 is the PO2 at which hemoglobin is 50% saturated: 26 mm Hg in arterial blood, 29 mm Hg in venous blood.
  • Key points on the OHDC:
    • PO2 = 0 mm Hg, SO2 = 0% (origin).
    • PO2 = 26 mm Hg, SO2 = 50% (P_50).
    • PO2 = 40 mm Hg, SO2 = 75% (normal mixed venous blood).
    • PO2 = 95 mm Hg, SO2 = 97% (normal arterial blood).
    • PO2 = 100 mm Hg, SO2 = 98% (nearly fully saturated arterial blood).
  • A right shift in the OHDC indicates reduced hemoglobin affinity for O₂, favoring O₂ delivery and increasing P_50.

Factors Causing Displacement Of Oxyhemoglobin Dissociation Curve (OHDC)

Bohr Effect:

  • Changes in blood hydrogen ions or CO₂ affect hemoglobin’s O₂ affinity.
  • Decreased pH (acidosis) reduces O₂ affinity, causing a rightward shift of the OHDC.

Effect of pH:

  • Decreased pH: Direct right shift; indirectly left shift by decreasing 2,3-DPG.
  • Increased pH: Direct left shift; indirectly right shift by increasing 2,3-DPG.

Temperature:

  • Shifts OHDC left in hypothermia and right in hyperthermia.
  • Increased body temperature during exercise contributes to a right shift, alongside increased 2,3-DPG.

2,3-Diphosphoglycerate (2,3-DPG):

  • One 2,3-DPG molecule binds between hemoglobin’s β-chains, stabilizing the T conformation, reducing O₂ affinity, and shifting OHDC right.
  • Formed in the Rapoport-Luebering shunt of glycolysis, with levels determined by synthesis (DPG mutase) and degradation (DPG phosphatase).
  • High pH (alkalosis) enhances DPG mutase and reduces DPG phosphatase, increasing 2,3-DPG levels.

DPG Level with Blood Storage:

  • Storage at <6°C reduces glycolysis to <5% of normal, depleting 2,3-DPG to near zero within 1-2 weeks, shifting OHDC left.
  • Modern preservation solutions (e.g., citrate-phosphate-dextrose) with dextrose, citrate, and adenine/phosphate slow DPG depletion but levels still become negligible within 2 weeks.
  • Post-transfusion, DPG levels reach ~50% of normal within 7 hours and fully recover within 48 hours.
  • Anemia, high altitude, and other factors increase 2,3-DPG levels.

Abnormal Forms of Hemoglobin:

  • Fetal hemoglobin (HbF): Composed of two γ-chains and two α-chains, with lower affinity for 2,3-DPG, causing a left shift (P_50 = 19 mm Hg vs. 26 mm Hg for HbA).
  • Sickle cell anemia: Causes a right shift of OHDC.
  • Thalassemia: Causes a left shift of OHDC.
  • Methemoglobin: Oxidized iron (ferric) increases O₂ affinity in remaining ferrous heme sites, reducing O₂ release and shifting OHDC left.

Carboxyhemoglobin (HbCO):

  • CO binds hemoglobin 250 times more strongly than O₂, though the combination rate is slower.
  • CO binding is slower when displacing O₂ from HbO₂: CO + HbO₂ → HbCO + O₂.
  • High oxygen saturation reduces CO binding rate, utilized in hyperbaric oxygen therapy for CO poisoning.
  • CO reduces hemoglobin’s O₂ carrying capacity, decreases P50, and shifts the OHDC left, partly due to reduced 2,3-DPG.
  • CO affects cellular cytochromes only at 1000 times the lethal dose, so tissue toxicity is not a factor in clinical CO poisoning.

Myoglobin:

  • Present in high amounts in muscles for sustained contraction (e.g., leg and heart muscles).
  • Binds one O₂ molecule per molecule, taking up O₂ readily at low pressure (95% saturated at PO2 = 40 mm Hg vs. 75% for hemoglobin).
  • The oxygen-myoglobin dissociation curve (OMDC) is a rectangular hyperbola, lying left of the OHDC.

Factors Causing OHDC Shifts:

  • Right Shift:
    • Decreased pH, increased CO₂, increased temperature, increased 2,3-DPG, sickle hemoglobin.
    • Increased 2,3-DPG caused by: exercise, high altitude, anemia, alkalosis, inosine, pyruvate, phosphate, thyroid hormones, growth hormone, androgens, hypoxia.
  • Left Shift:
    • Stored blood, fetal hemoglobin (γ-chains don’t bind 2,3-DPG), CO poisoning (partial HbCO saturation), hypothermia, alkalosis, hypocapnia, thalassemia, methemoglobin, cyanide, nitric acid.

Co₂ Transport

  • Arterial blood contains ~48 mL/dL total CO₂; systemic capillaries add ~4 mL/dL, making mixed venous blood ~52 mL/dL.
  • Forms of CO₂ transport:
    • Dissolved CO₂: ~10%.
    • As bicarbonate (HCO₃⁻): ~68%.
    • As carbamino compounds: ~22%.
  • Distribution: ~11% of total CO₂ remains in plasma, ~89% enters red blood cells (RBCs).
  • Table 10.7: Forms of CO₂ Transport:
    • Plasma (~11%): Dissolved CO₂ (5%), carbamino compounds (1%), HCO₃⁻ (5%).
    • RBC (~89%): Dissolved CO₂ (5%), carbamino compounds (21%), HCO₃⁻ (63%).
    • Total: Dissolved CO₂ (10%), carbamino compounds (22%), HCO₃⁻ (68%).
  • Carbamino Compounds:
    • In plasma: CO₂ combines with plasma proteins.
    • In RBCs: CO₂ combines with hemoglobin (Hb).
    • More carbamino compounds form in RBCs due to higher hemoglobin concentration (33 g/dL) compared to plasma proteins (8 g/dL) and hemoglobin’s greater ease of forming carbamino compounds.
  • Bicarbonate (HCO₃⁻):
    • CO₂ diffuses into plasma, dissolves, and reacts with water to form carbonic acid (H₂CO₃), which dissociates into H⁺ and HCO₃⁻: CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻.
      Gaseous Exchange Chapter Notes | Physiology - NEET PG
    • This reaction is slow but accelerated 5000 times by carbonic anhydrase (CA) in RBCs.
    • HCO₃⁻ diffuses out of RBCs in exchange for Cl⁻ via the anion exchanger (AE1), a process called the chloride shift or Hamburger shift.
    • Free H⁺ is buffered by hemoglobin, driving HCO₃⁻ synthesis.
  • In pulmonary capillaries, CO₂ moves from RBCs and plasma into alveolar air, reversing the above reactions; Cl⁻ and H₂O leave RBCs, causing them to shrink.
  • Haldane Effect:
    • Oxygen binding to hemoglobin in pulmonary capillaries displaces CO₂ from blood, enhancing CO₂ transport.
    • Oxyhemoglobin is a stronger acid, reducing hemoglobin’s tendency to form carbaminohemoglobin and releasing H⁺ ions.
    • Released H⁺ binds HCO₃⁻ to form H₂CO₃, which dissociates into H₂O and CO₂, released into alveoli.
    • The Haldane effect is more significant for CO₂ transport than the Bohr effect is for O₂ transport.
  • Significance of Haldane Effect:
    • Figure 10.9 shows CO₂ dissociation curves at P_O2 = 100 mm Hg (lungs) and 40 mm Hg (tissues).
    • At tissues (Point A): PCO2 = 45 mm Hg, CO₂ content = 52 vol%.
    • At lungs (Point B): Haldane effect shifts the curve, reducing CO₂ content to 48 vol% at PCO2 = 40 mm Hg, losing 4 vol% CO₂.
    • Without Haldane effect (Point C), CO₂ content would drop to 50 vol%, losing only 2 vol%.
    • The Haldane effect doubles CO₂ release in lungs and CO₂ pickup in tissues.

Hypoxia

  • Hypoxia: Oxygen deficiency at the tissue level.
  • Hypoxemia: Decreased partial pressure of oxygen (PaO₂) in arterial blood.

Four Categories of Hypoxia (Table 10.8):

  • Hypoxic Hypoxia:
    • Reduced arterial PO2.
    • Causes: High altitude, pneumonia, pulmonary fibrosis, ventilation-perfusion imbalance, venous-to-arterial shunts.
    • Features: Low PaO₂, low PvO₂, decreased (a-v) PO2, decreased dissolved and Hb-bound O₂, stimulates peripheral and central chemoreceptors (if high CO₂), cyanosis present.
  • Anemic Hypoxia:
    • Normal arterial PO2 but reduced hemoglobin available for O₂ transport.
    • Causes: Anemia, CO poisoning, methemoglobinemia.
    • Features: Normal PaO₂, low PvO₂, increased (a-v) PO2, normal dissolved O₂, decreased Hb-bound O₂, peripheral chemoreceptors not stimulated, central chemoreceptors not stimulated, cyanosis rare.
  • Stagnant/Ischemic Hypoxia:
    • Inadequate blood flow to tissues despite normal PO2 and hemoglobin.
    • Causes: Slow circulation (heart failure), shock, hemorrhage.
    • Features: Normal PaO₂, low PvO₂, increased (a-v) PO2, normal dissolved and Hb-bound O₂, peripheral chemoreceptors stimulated, central chemoreceptors not stimulated, cyanosis present.
  • Histotoxic Hypoxia:
    • Adequate O₂ delivery but tissues cannot utilize O₂ due to toxic agents.
    • Causes: Cyanide poisoning.
    • Features: Normal PaO₂, high PvO₂, decreased (a-v) P_O2, normal dissolved and Hb-bound O₂, peripheral chemoreceptors stimulated, central chemoreceptors not stimulated, cyanosis never present.
  • Hypoxic hypoxia is the most common clinical form, often caused by ventilation-perfusion mismatch.
  • Arterial-venous (a-v) oxygen difference increases in stagnant hypoxia (diagnostic) but decreases in histotoxic hypoxia (diagnostic).
  • Peripheral chemoreceptors have high blood flow (2000 mL/100 g/min), meeting O₂ needs via dissolved O₂, so they are not stimulated in anemia or CO poisoning.

Cyanosis

  • Cyanosis is a bluish discoloration of mucous membranes and/or skin.
  • Cyanosis detection thresholds in capillary blood:
    • Deoxyhemoglobin: ≥4 g/dL.
    • Methemoglobin: ≥ 1.5 g/dL.
    • Sulfhemoglobin: ≥ 0.5 g/dL.
  • Central cyanosis may be detectable at SaO₂ of 85%, but in dark-skinned individuals, it may require SaO₂ ≤75%.

Oxygen Treatment Of Hypoxia

  • Oxygen therapy is ineffective for stagnant, anemic, histotoxic hypoxia, and hypoxic hypoxia due to shunting of unoxygenated venous blood past the lungs.
  • Oxygen therapy is highly beneficial for other forms of hypoxic hypoxia.
  • Hyperbaric O₂ Therapy:
    • Effective for: CO poisoning, radiation-induced tissue injury, gas gangrene, severe blood loss anemia, diabetic leg ulcers, slow-healing wounds, and rescue of skin flaps/grafts with marginal circulation.
    • Primary treatment for decompression sickness and air embolism.
  • Neurons are most sensitive to hypoxia, followed by oligodendrocytes, astrocytes, and endothelium.
  • Most sensitive neurons: Pyramidal cells of CA1 hippocampus (Sommer’s sector), Purkinje cells of cerebellum, striatal neurons.
  • Most resistant to hypoxia: Brain stem and spinal cord.
  • Gray matter is more sensitive than white matter.
  • Irreversible damage occurs if no O₂ supply for >5 minutes.
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FAQs on Gaseous Exchange Chapter Notes - Physiology - NEET PG

1. What is the difference between perfusion-limited and diffusion-limited gas exchange?
Ans. Perfusion-limited gas exchange occurs when the amount of gas that can be transferred across the alveolar-capillary membrane is limited by blood flow (perfusion). In contrast, diffusion-limited gas exchange happens when the transfer of gas is limited by the rate of diffusion across the membrane, often due to factors like membrane thickness or gas solubility.
2. How is the diffusing capacity of the respiratory membrane measured?
Ans. The diffusing capacity of the respiratory membrane is typically measured using the single-breath carbon monoxide (CO) uptake test. During this test, a patient inhales a small amount of carbon monoxide, and the amount that diffuses into the blood is measured. This helps in assessing the efficiency of gas exchange in the lungs.
3. What are the primary mechanisms of oxygen transport in the blood?
Ans. Oxygen is transported in the blood primarily in two ways: 1) bound to hemoglobin in red blood cells, which accounts for about 98.5% of oxygen transport, and 2) dissolved in plasma, which constitutes about 1.5% of oxygen transport. Hemoglobin's ability to bind oxygen is influenced by various factors, including pH and carbon dioxide levels.
4. What is the significance of the oxyhemoglobin dissociation curve (OHDC)?
Ans. The oxyhemoglobin dissociation curve illustrates the relationship between the partial pressure of oxygen (PaO2) and the saturation of hemoglobin with oxygen (SaO2). It is crucial for understanding how readily hemoglobin binds to oxygen in the lungs and releases it in the tissues. The shape of the curve can shift due to factors like pH, temperature, and levels of 2,3-bisphosphoglycerate, affecting oxygen delivery to tissues.
5. What are the different ways carbon dioxide is transported in the blood?
Ans. Carbon dioxide is transported in the blood in three main forms: 1) dissolved in plasma (about 7%), 2) as bicarbonate ions (HCO3-) formed through a reaction with water, which accounts for about 70%, and 3) bound to hemoglobin and other proteins (carbamino compounds), making up about 23%. These mechanisms are vital for maintaining acid-base balance and facilitating gas exchange in the lungs.
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,

Objective type Questions

,

practice quizzes

,

past year papers

,

study material

,

Exam

,

video lectures

;