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Pulmonary / Lung Function Tests (PFTs)

Pulmonary / Lung Function Tests (PFTs). SURFACTANT. Lipoprotein mixture present in thin layer of fluid lining the alveoli. Consist of surfactant apoprotein , a phospholipid which is dipalmityl lecithin & calcium ions . Secreted by type II alveolar cells. Present at fluid-air interface.

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Pulmonary / Lung Function Tests (PFTs)

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  1. Pulmonary / Lung Function Tests (PFTs)

  2. SURFACTANT • Lipoprotein mixture present in thin layer of fluid lining the alveoli. • Consist of surfactant apoprotein, a phospholipid which is dipalmityl lecithin & calcium ions. • Secreted by type II alveolar cells. • Present at fluid-air interface. • Lowers surface tension of fluid lining the alveoli (surface tension of fluid is inversely proportional to concentration of surfactant).

  3. Role of surfactant During Inspiration During Expiration When lungs shorten, surfactant molecules move together and become concentrated  surface tension is reduced • When alveoli expand, surfactant molecules move apart.

  4. Significance of surfactant • If it is less / absent surface tension will be high (50 dynes / sq. cm) • Depending upon concentration of surfactant, surface tension = 5-30 dynes / sq. cm. • Prevents collapse of alveoli & controls size of alveoli, (specially during expiration, when size decreases). • Increases lung compliance • Keeps alveoli dry • Keeps lungs expanded • Prevent pulmonary edema • Allows fetal lung maturity

  5. Law of Laplace of hollow viscera: P = 2T/R where P is pressure required to keep the viscera expanded, T is surface tension & R is radius

  6. Law of Laplace: Explanation • During expiration, R decreases. If T does not decrease (lack of surfactant)then more pressure (-20 to -30 mmHg) is required to keep the alveoli distended & avoid collapse. • During expiration, force which can keep lungs expanded is negative pressure, which is decreasing, so T must decrease (by adequate surfactant), so that pressure required is not positive pressure, but normal pressure (-2 to -2.5 mmHg).

  7. With or without Surfactant Presence of surfactant Deficiency of surfactant Fluid will move into the alveoli to cause pulmonary edema. More surface tension due to less surfactant. • Fluid will pass from inside to outside . • It is sucked out because of highly negative pressure in interstitium(dry alveoli) -3 mm Hg in alveolus -15 mmHg in alveolus -8 mmHg in interstitium -8 mmHg in interstitium

  8. RDS (Respiratory Distress Syndrome) • Surfactant helps in lung expansion at birth. • If surfactant deficiency  RDS (many areas of collapse in lungs) • In fetal life, its secretion in amniotic fluid begins in 30th week. • By amniocentesis, sample of amniotic fluid is removed & tested for surfactant concentration • Adequate surfactant is index of lung maturitys

  9. Stimulants of surfactant stimulation • Glucocorticoids • Thyroxine • Epinephrine • Contact of air with alveoli

  10. Surfactant deficiency is common in: • Premature babies • Babies born from thyroid deficient mothers • Babies born from diabetic mothers • Babies born from smoker mothers (smoking decreases surfactant secretion)

  11. LUNG COMPLIANCE • Measure of stretch-ability of lungs • Indicates how easily lungs can be expanded • It is change in lung volume per unit change of trans-pulmonary pressure (C = Δ V / Δ P) • Elastance is reciprocal of compliance (E = Δ P / Δ V) .

  12. LUNG COMPLIANCE • The extent to which lungs will expand for each unit increase in transpulmonary pressure (if enough time is allowed to reach equilibrium). • Total compliance of both lungs = 200 ml of air / cm of H2O trans-pulmonary pressure. • When trans-pulmonary pressure increases 1 cm of water, the lung volume, after 10 to 20 seconds, will expand 200 ml.

  13. Compliance diagram

  14. characteristics of the compliance diagram are determined by: • elastic forces of the lung tissue itself and • elastic forces caused by surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces.

  15. Elastic forces of the lung tissue are determined mainly by elastin & collagen fibers in lung parenchyma. In deflated lungs, these fibers are in an elastically contracted and kinked state; when the lungs expand, the fibers become stretched and unkinked, thus elongating and exerting even more elastic force.

  16. When the lungs are filled with air, there is an interface between the alveolar fluid and air in alveoli. In case of saline solution–filled lungs, there is no air-fluid interface; therefore, surface tension effect is not present—only tissue elastic forces are operative.

  17. (Transpleural pr. required to expand air-filled lungs) is 3 x > (Transpleural pr. required to expand saline solution–filled lungs). Tissue elastic forces tending to cause collapse of air-filled lung represent only 1/3 of total lung elasticity, whereas fluid-air surface tension forces in alveoli represent 2/3 of total lung elasticity. The fluid-air surface tension elastic forces of the lungs also increase tremendously when surfactant is not present.

  18. At rest: Quiet inspiration is active, while quiet expiration is passive. So at rest, energy expenditure is on inspiration. 3-5 % of total body energy at rest is used in work of breathing. During Exercise: There is increased rate of pulmonary ventilation & both inspiration & expiration become active. So, energy used in work of breathing increases much. But as total energy expenditure of body also increases very much, so %wise, it remains same, that is 3 – 5 % Work of breathing

  19. 3 types of work of breathing:

  20. Significance: • Not diagnostic of specific pulmonary disease. • Help in differential diagnosis of obstructive & restrictive lung disease. • COPD diseases: Increased resistance to air flow. • Examples: Chronic bronchitis & bronchial asthma. • Restricted Lung Disorders: Fibrosis in inter-alveolar & peri-bronchial tissue  interstitial pulmonary fibrosis  decreased pulmonary compliance but generally without airway obstruction  Prevention of normal lung expansion. • Lung disorders with features of both COPD & restrictive type: Emphysema. • Prognostic information. • Effect of therapeutic measures.

  21. 1. Forced Expiration Time: • Patient is asked to empty his chest as fast as possible after a maximum inspiration. • Normal FET = 3-4 sec. • Increased FET = Obstructive lung disease.

  22. 2. Vital Capacity (VC) • Maximum volume of air breathed out at a slow rate after max. inspiration. • Slow or static VC. • Decreases in obstructive & restrictive lung diseases.

  23. 3. Forced Vital Capacity (FVC): • Volume of air that can be forcefully expelled from the lungs (i.e. within the shortest possible time) after max. inspiration. • Normal or decreased in obstructive lung disease. • Always decreased in restrictive lung disease.

  24. 4. Forced Expiratory Volume-1 (FEV-1) • Volume of air expelled in 1st second during determination of forced vital capacity. • Decreased in obstructive lung disease. • Decreased in those non-obstructive diseases which decrease the vital capacity.

  25. 5. FEV-1:FVC% (FEV-1%) • Characteristically decreased to below 60% in obstructive lung disease & not in restrictive. • Normal or increased in restrictive lung disease. • In obstructive disease, fall in FEV-1 > fall in FVC. • In restrictive disease, fall in FEV-1 and FVC are usually proportional & so FEV-1% remains within normal limits. If fall in FEV-1 is relatively less  FEV-1% will be higher than normal.

  26. 6. Determination of FEV-1: FVC% (FEV-1%) after administering a bronchodilator agent (like isoprenaline): Significance: Can differentiate between reversible & irreversible obstructive lung disease. Reversible: Chronic bronchitis & bronchial asthma. Irreversible: Emphysema.

  27. 7. Determination of Forced Expiratory Flow, 25-75,i-e., FEF 25-75: • Maximum mid-expiratory airflow rate in liters / sec. • Decreased in: Obstructive lung diseases. • Normal / decreased in: Restrictive lung disease.

  28. 8. Peak Expiratory Flow Rate: • Subject breathes out with max. force into the peak flow meter. • Peak flow meter is a hand held device that measures the volume expired in 1st 0.1 sec & gives a reading in liters/min. • PEFR is decreased in obstructive disorders of the lungs.

  29. 9. Respiratory Minute Volume: • Measured by multiplying rate of breathing per minute by tidal volume. • 12 breaths / min x 500 ml / breath • = 12 x 500 • = 6000 ml / min • = 6 L / min

  30. 10. Maximum Voluntary Ventilation Test: • Patient is asked to breathe as deeply and as rapidly as he can for 15 sec. • Volume of air breathed during this time is measured & per min. value is obtained by multiplying it with 4. (as 15 x 4 = 60 sec = 1 min.) • Difficult for the patient. • Only gives FEV1 • Becoming obsolete.

  31. 11. Measurement of Functional Residual Capacity (FRC): • Very accurate method is: Closed circuit helium method. • Helium is inert, insoluble gas (does not cross alveolar –capillary membrane). • A spirometer is filled with max. of 10% helium in air. • Starting point: end-expiratory position. • Patient breathes from closed spirometer system. • CO2 is absorbed by soda lime.

  32. O2 consumed is replaced by adding oxygen to spirometer, whose volume is kept constant. • Due to non-diffusibility of helium into the blood, its volume does not change & remains constant. • As helium in spirometer mixes with air in the lungs, so conc. of gas in the circuit falls to a new level which is determined.

  33. FRC can be calculated by formula: (Initial helium conc.) x (volume of spirometer) = (final helium conc.) x (volume of spirometer + FRC)

  34. 12. Determination of Residual Volume: • R.V = FRC – ERV • It is equal to Functional Residual Capacity minus Expiratory Reserve Volume. • RV is increased in Obstructive lung disease.

  35. 13. Blood Gas Analysis & pH: • Significance: measurement of pH, PCO2 & O2 Saturation of arterial blood give useful information about alveolar ventilation. • Normal values: • pH = 7.4 • PCO2 = 40 mm Hg (measured by introducing CO2 electrode into airway & blood vessel or by infrared) • O2 saturation = 95% (by O2 electrode or applying pulse oximeter to ear lobule).

  36. 14. Diffusing Capacity of Gases: Amount of gas transferred from alveoli to capillary blood per unit time as a function of mean partial pressure gradient. D.C of a gas = amount of its uptake per min. difference between its tension in alveolar air & capillary blood

  37. How to determine Diffusing Capacity of lung: • CO is used to determine lung’s diffusion capacity. SINGLE BREATH TECHNIQUE: CO in a conc. of 0.3% is inspired in 1 single breath. held in lungs for 10 sec & then forcefully expired. Last portion of expired air is collected to determine its CO content. Transfer factor for CO = ml CO transferred / min from alveolar gas to blood (Mean alveolar PCO ) – (Mean capillary blood PCO )

  38. Due to great affinity of CO for Hb, • All CO that passes from alveoli  capillary blood  taken up by Hb  mean capillary blood PCO is so small that it can be neglected.

  39. Decreased Diffusion Capacity: • In diseases causing thickening & separation of capillary & alveolar walls, e.g., 1. Interstitial or alveolar pulmonary fibrosis, 2. Emphysema

  40. Normal Diffusing Capacity: • In bronchial asthma.

  41. D.C OF O2 Vs CO: Diffusion of O2 = 1.23 time that of CO. So transfer factor for O2 = Transfer factor for CO X 1.23

  42. D.C for CO2 Vs O2: • D.C of CO2 = 20.7 x D.C of O2.

  43. Increased Diffusion Capacity: • During Physical Exercise.

  44. Single breath method: CO in a conc. of 0.3% is inspired in a single breath, held in lungs for about 10 sec & then forcefully expired. Gives identical value to steady state method. Steady state method: CO in low conc. is breathed for several minutes. Gives identical value to single breath method. Methods for measuring Diffusion Capacity of Gases:

  45. 15. Measurement of Alveolar Gas Pressure: • Alveolar air can be obtained by asking the subject to expire forcibly & rapidly along a long tube. • The last portion of the expired air was supposed to be a good representative of alveolar air & used to be analyzed for gases. • But it is not a true representative of alveolar air, especially in lung diseases with disturbed ventilation-perfusion ratio.

  46. Arterial blood PCO2 can be taken as a good index of alveolar air PCO2. • Because CO2 diffuses so readily through biological membranes that at any site along the alveolar membrane PCO2 value of air on one side = PCO2 value of blood leaving the pulmonary capillary.

  47. Protective Reflexes: Non respiratory air movement into respiratory tract: • Coughing • Sneezing • Hiccup • Yawning

  48. There are nerve endings in the epithelium of airways called irritant receptors. • These respond to irritants & they may be mechanical as mucus / foreign particle in airways. • It may be chemical,e.g., histamine, bradykinin.

  49. COUGH REFLEX: • Stimuli: Light touch, very slight amount of foreign matter, or chemical irritants (sulphur dioxide gas, chlorine gas). • Cough receptors: on epiglottis, larynx, trachea, bronchi, tonsils. • Afferents: vagus nerve • Respiratory centre: Neuronal circuits of medulla • Events: inspiration followed by forceful expiration. • Purpose: to dislodge the irritants from airways. Expiratory muscles contract during expiration  alveolar pressure becomes very high (up to +100 mm Hg)  irritant is dislodged (velocity of expired air may be 70 – 100 miles / hr.

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