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Pulmonary Physiology

Pulmonary Physiology. Respiratory neurons in brain stem sets basic drive of ventilation descending neural traffic to spinal cord activation of muscles of respiration Ventilation of alveoli coupled with perfusion of pulmonary capillaries Exchange of oxygen and carbon dioxide.

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Pulmonary Physiology

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  1. Pulmonary Physiology • Respiratory neurons in brain stem • sets basic drive of ventilation • descending neural traffic to spinal cord • activation of muscles of respiration • Ventilation of alveoli coupled with perfusion of pulmonary capillaries • Exchange of oxygen and carbon dioxide

  2. Respiratory Centers • Located in brain stem • Dorsal & Ventral Medullary group • Pneumotaxic & Apneustic centers • Affect rate and depth of ventilation • Influenced by: • higher brain centers • peripheral mechanoreceptors • peripheral & central chemoreceptors

  3. Muscles of Ventilation • Inspiratory muscles- • increase thoracic cage volume • Diaphragm, External Intercostals, SCM, • Ant & Post. Sup. Serratus, Scaleni, Levator Costarum • Expiratory muscles- • decrease thoracic cage volume • Abdominals, Internal Intercostals, Post Inf. Serratus, Transverse Thoracis, Pyramidal

  4. Ventilation-Inspiration • Muscles of Inspiration-when contract  thoracic cage volume (uses 3% of TBE) • diaphragm • drops floor of thoracic cage • external intercostals • sternocleidomastoid • anterior serratus • scaleni • serratus posterior superior • levator costarum • (all of the above except diaphragm lift rib cage)

  5. Ventilation-expiration • Muscles of expiration when contract pull rib cage down  thoracic cage volume (forced expiration • rectus abdominus • external and internal obliques • transverse abdominis • internal intercostals • serratus posterior inferior • transversus thoracis • pyramidal • Under resting conditions expiration is passive and is associated with recoil of the lungs

  6. Movement of air in/out of lungs • Considerations • Pleural pressure • negative pressure between parietal and visceral pleura that keeps lung inflated against chest wall • varies between -5 and -7.5 cmH2O (inspiration to expiration • Alveolar pressure • subatmospheric during inspiration • supra-atmospheric during expiration • Transpulmonary pressure • difference between alveolar P & pleural P • measure of the recoil tendency of the lung • peaks at the end of inspiration

  7. Compliance of the lung • V/P • At the onset of inspiration the pleural pressure changes at faster rate than lung volume-”hysteresis” • Air filled lung vs. saline filled lung • Easier to inflate a saline filled lung than an air filled lung because surface tension forces have been eliminated in the saline filled lung

  8. Pleural relationships-lung & chestwall forces

  9. Effect of Thoracic Cage on Lung • Reduces compliance by about 1/2 around functional residual capacity (at the end of a normal expiration) • Compliance greatly reduced at high or low lung volumes

  10. Work of Breathing • Compliance work (elastic work) • Accounts for most of the work normally • Tissue resistance work • viscosity of chest wall and lung • Airway resistance work • Energy required for ventilation • 3-5% of total body energy

  11. Patterns of Breathing • Eupnea • normal breathing (12-17 B/min, 500-600 ml/B) • Hyperpnea •  pulmonary ventilation matching  metabolic demand • Hyperventilation ( CO2) •  pulmonary ventilation > metabolic demand • Hypoventilation ( CO2) •  pulmonary ventilation < metabolic demand

  12. Patterns of breathing (cont.) • Tachypnea •  frequency of respiratory rate • Apnea • Absense of breathing. e.g. Sleep apnea • Dyspnea • Difficult or labored breathing • Orthopnea • Dyspnea when recumbent, relieved when upright. e.g. congestive heart failure, asthma, lung failure

  13. Pleural Pressure • Lungs have a natural tendency to collapse • surface tension forces 2/3 • elastic fibers 1/3 • What keeps lungs against the chest wall? • Held against the chest wall by negative pleural pressure “suction”

  14. Collapse of the lungs • If the pleural space communicates with the atmosphere, i.e. pleural P = atmospheric P the lung will collapse • Causes • Puncture of the parietal pleura • Sucking chest wound • Erosion of visceral pleura • Also if a major airway is blocked the air trapped distal to the block will be absorbed by the blood and that segment of the lung will collapse

  15. Pleural Fluid • Thin layer of mucoid fluid • provides lubrication • transudate (interstitial fluid + protein) • total amount is only a few ml’s • Excess is removed by lymphatics • mediastinum • superior surface of diaphragm • lateral surfaces of parietal pleural • helps create negative pleural pressure

  16. Pleural Effusion • Collection of large amounts of free fluid in pleural space • Edema of pleural cavity • Possible causes: • blockage of lymphatic drainage • cardiac failure-increased capillary filtration P • reduced plasma colloid osmotic pressure • infection/inflammation of pleural surfaces which breaks down capillary membranes

  17. Surfactant • Reduces surface tension forces by forming a monomolecular layer between aqueous fluid lining alveoli and air, preventing a water-air interface • Produced by type II alveolar epithelial cells • complex mix-phospholipids, proteins, ions • dipalmitoyl lecithin, surfactant apoproteins, Ca++ ions

  18. Stabilization of Alveolar size • Role of surfactant • Law of Laplace P=2T/r • Without surfactant smaller alveolar have increased collapse p & would tend to empty into larger alveoli • Big would get bigger and small would get smaller • Surfactant automatically offsets this physical tendency • As the alveolar size  surfactant is concentrated which  surface tension forces, off-setting the  in radius • Interdependence • Size of one alveoli determined in part by surrounding alveoli

  19. Air filled vs. Saline filled lung • Experimentally it is much easier to expand a saline filled lung compared to an air filled lung • In a saline filled lung, surface tension forces are eliminated • Surface tension forces are normally responsible for 2/3 of the collapse tendency of the lung

  20. Static Lung Volumes • Tidal Volume (500ml) • amount of air moved in or out each breath • Inspiratory Reserve Volume (3000ml) • maximum vol. one can inspire above normal inspiration • Expiratory Reserve Volume (1100ml) • maximum vol. one can expire below normal expiration • Residual Volume (1200 ml) • volume of air left in the lungs after maximum expiratory effort

  21. Static Lung Capacities • Functional residual capacity (RV+ERV) • vol. of air left in the lungs after a normal expir., balance point of lung recoil & chest wall forces • Inspiratory capacity (TV+IRV) • max. vol. one can inspire during an insp effort • Vital capacity (IRV+TV+ERV) • max. vol. one can exchange in a resp. cycle • Total lung capacity (IRV+TV+ERV+RV) • the air in the lungs at full inflation

  22. Determination of RV, FRC, TLC • Of the static lung volumes & capacities, the RV, FRC, & TLC cannot be determined with basic spirometry. • Helium dilution method for RV, FRC, TLC • FRC= ([He]i/[He]f-1)Vi • [He]i=initial concentration of helium in jar • [He]f=final concentration of helium in jar • Vi=initial volume of air in bell jar

  23. Determination of RV, FRC, TLC • After FRC is determined with the previous formula, determination of RV & TLC is as follows: • RV = FRC- ERV • TLC= RV + VC • ERV & VC values are determined from basic spirometry • VC, IRV, IC  with restrictive lung conditions

  24. Pulmonary Flow Rates • Compromised with obstructive conditions • decreased air flow • minute respiratory volume • RR X TV • Forced Expiratory Volumes (timed) • FEV/VC • Peak expiratory Flow • Maximum Ventilatory Volume

  25. Airways in lung • 20 generations of branching • Trachea (2 cm2) • Bronchi • first 11 generations of branching • Bronchioles (lack cartilage) • Next 5 generations of branching • Respiratory bronchioles • Last 4 generations of branching • Alveolar ducts give rise to alveolar sacs which give rise to alveoli • 300 million with surface area 50-100 M2

  26. Dead Space • Area where gas exchange cannot occur • Includes most of airway volume • Anatomical dead space (=150 ml) • Airways • Physiological dead space • = anatomical + non functional alveoli • Calculated using a pure O2 inspiration and measuring nitrogen in expired air (fig 37-7) • % area X Ve

  27. Alveolar Volume • Alveolar volume (2150 ml) = FRC (2300 ml)- dead space (150 ml) • At the end of a normal expiration most of the FRC is at the level of the alveoli • Slow turnover of alveolar air (6-7 breaths) • Rate of alveolar ventilation • Va = RR (Vt-Vd)

  28. Autonomic control of airways • Efferent Neural control • SNS-beta receptors causing dilatation • direct effect weak due to sparse innervation • indirect effect predominates via circulating epinephrine • Parasympathetic-muscarinic receptors causing constriction • NANC nerves (non-adrenergic, non-cholinergic) • Inhibitory release VIP and NO  bronchodilitation • Stimulatory  bronchoconstriction, mucous secretion, vascular hyperpermeability, cough, vasodilation “neurogenic inflammation”

  29. Autonomic control of airways • Afferent nerves • Slow adapting receptors • Associated with smooth muscle of proximal airways • Stretch receptors • Involved in reflex control of breathing and cough reflex • Rapidly adapting receptors • Sensitive to mechanical + , protons, low Cl- solutions, histamine, cigarette smoke, ozone, serotonin, PGF 2 • Some responses may be secondary to mechanical distortion produced by bronchoconstriction

  30. Autonomic control of airways • C-fibers (high density) • Contain neuropeptides • Substance P, neurokinin A, calcitonin gene-related peptide • Selectively + by capsaicin • Also activated by bradykinin, protons, hyperosmole solutions and cigarette smoke

  31. Control of Airway Smooth Muscle (cont.) • Local factors • histamine binds to H1 receptors-constriction • histamine binds to H2 receptors-dilation • slow reactive substance of anaphylaxsis-constriction-allergic response to pollen • Prostaglandins E series- dilation • Prostaglandins F series- constriction

  32. Control of Airway Smooth Muscle (cont) • Environmental pollution • smoke, dust, sulfur dioxide, some acidic elements in smog • elicit constriction of airways • mediated by: • parasympathetic reflex • local constrictor responses

  33. Effect of pH on ventilation • Normal level of HCO3- = 24 mEq/L • Metabolic acidosis (HCO3- < 24) will + ventilation • Metabolic alkalosis (HCO3- >24) will – ventilation • Kidney regulates HCO3- • Normal level of CO2 = 40 mmHg • Respiratory acidosis (CO2 > 40) will + ventilation • Respiratory alkalosis (CO2 < 40) will – ventilation • Lung regulates CO2

  34. Pulmonary circulation • Pulmonary artery wall 1/3 as thick as aorta • RV 1/3 as thick as LV • All pulmonary arteries have larger lumen • more compliant • operate under a lower pressure • can accommodate 2/3 of SV from RV • Pulmonary veins shorter but similar compliance compared to systemic veins

  35. Total Pulmonic Blood Volume • 450 ml (9% of total blood volume) • reservoir function 1/2 to 2X TPBV • shifts in volume can occur from pulmonic to systemic or visa versa • e.g. mitral stenosis can  pulmonary volume 100% • shifts have a greater effect on pulmonary circulation

  36. Systemic Bronchial Arteries • Branches off the thoracic aorta which supplies oxygenated blood to the supporting tissue and airways of the lung. (1-2% CO) • Venous drainage is into azygous (1/2) or pulmonary veins (1/2) (short circuit) • drainage into pulmonary veins causes LV output to be slightly higher (1%) than RV output & also dumps some deoxygenated blood into oxygenated pulmonary venous blood

  37. Pulmonary lymphatics • Extensive & extends from all the supportive tissue of lungs & courses to the hilum & mainly into the right lymphatic duct • remove plasma filtrate, particulate matter absorbed from alveoli, and escaped protein from the vascular system • helps to maintain negative interstitial pressure which pulls alveolar epithelium against capillary endothelium. “respiratory membrane”

  38. Pulmonary Pressures • Pulmonary artery pressure = 25/8 • mean = 15 mmHg • Mean pulmonary capillary P = 7 mmHg. • Major pulmonary veins and left atrium • mean pressure = 2 mmHg.

  39. Control of pulmonary blood flow • Since pulmonary blood flow = CO, any factors that affect CO (e.g. peripheral demand) affect pulmonary blood flow in a like way. • However within the lung blood flow is distributed to well ventilated areas • low alveolar O2 causes release of a local vasoconstrictor which automatically redistributes blood to better ventilated areas

  40. ANS influence on pulmonary vascular smooth muscle • SNS + will cause a mild vasoconstriction • 3 Hz to 30 Hz  pulmonary arterial BP about 30% • Mediated by alpha receptors • With alpha blockage response abolished and at 30 Hz. vasodilatation observed as beta receptors are unmasked • Parasympathetic + will cause a mild vasodilatation • (major constrictor effect on pulmonary vascular smooth muscle is low alveolar O2)

  41. Oxygenation of blood in Pulmonary capillary • Under resting conditions blood is fully oxygenated by the time it has passed the first 1/3 of pulmonary capillary • even if velocity  3X full oxygenation occurs • Normal transit time is about .8 sec • Under high CO transit time is .3 sec which still allows for full oxygenation • Limiting factor in exercise is SV

  42. Effect of hydrostatic P on regional pulmonary blood flow • From apex to base capillary P  (gravity) • Zone 1- no flow • alveolar P > capillary P • normally does not exist • Zone 2- intermittent flow (toward the apex) • during systole; capillary P > alveolar P • during diastole; alveolar P > capillary P • Zone 3- continuous flow (toward the base) • capillary P > alveolar P • During exercise entire lung  zone 3

  43. Pulmonary Capillary dynamics • Starling forces (ultrafiltration) • Capillary hydrostatic P = 7 mmHg. • Interstitial hydrostatic P = -8 mmHg. • Plasma colloid osmotic P = 28 mmHg. • Interstitial colloid osmotic P = 14 mm • Filtration forces = 15 mmHg. • Reabsorption forces = 14 mmHg. • Net forces favoring filtration = 1 mmHg. • Excess fluid removed by lymphatics

  44. Basic Gas Laws • Boyle’s Law • At a constant T the V of a given quantity of gas is 1/ to the P it exerts • Avogadro’s Law • = V of gas at the same T & P contain the same # of molecules • Charles’ Law • At a constant P the V of a gas is  to its absolute T • The sum of the above gas laws: • PV=nRT

  45. PV = nRT • P=gas pressure • V=volume a gas occupies • n= number of moles of a gas • R= gas constant • T= absolute temperature in Kelvin(C - 273)

  46. Additional Gas Laws • Graham’s Law • the rate of diffusion of a gas is 1/ to the square root of its molecular weight • Henry’s Law • the quantity of gas that can dissolve in a fluid is = to the partial P of the gas X the solubility coefficient • Dalton’s Law of Partial Pressures • the P exerted by a mixture of gases is =  of the individual (partial) P exerted by each gas

  47. Vapor P of H2O • The pressure that is exerted by the H2O molecules to escape from the liquid to air • Due to molecular motion • Proportional to temperature • At body temperature (37oC) the vapor P of H2O is 47 mmHg.

  48. H2O vapor 3.7 mmHg Oxygen 159 mmHg Nitrogen 597 mmHg CO2 .3 mmHg H2O vapor 47 mmHg Oxygen 104 mmHg Nitrogen 569 mmHg CO2 40 mmHg Atmospheric Air vs. Alveolar Air

  49. Diffusion across the respiratory membrane • Temperature  • Solubility  • Cross-sectional area  • sq root of molecular weight 1/  • concentration gradient  • distance 1/  • Which of the above are properties of the gas?

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