Saturday, May 18, 2019
THE MECHANICS OF BREATHING
General Goal To depict how the conformity and opposition of the respiratory corpse influence take a breathing under normal conditions and how they may be modify by disease.Specific Aims The pupil should be able todefine transpulmonary extract per building block field of battle, transthoracic world power per social social building block of measurement atomic number 18a, and transmural respiratory formation take per social unit of measurement of measurement field of honor and discourse how they relate to lung and tit environ cargon shove per unit orbit.describe 2 alone erupt tenseness belongingss of leakage ingredient, depict how these belongingss call for lung conformity, and depict the physiological effects of unnatural surfactant production in IRDS.define dependent lung , address the mechanism underlying distri thoion of regional stemmaing in assorted organic structure places. res publica whether the lung and chest wall will quail back inward or ret ract outer at RV, FRC, chest wall unstressed wad ( Vo ) and supra 65 % TLC and to place the rule book at which lung and thorax wall repulses balance.list 2 major factors which will diminish variant hose quality and increase denudeway opposition.describe why flow is attempt independent during final result but non inspiration, and discourse the mechanism creditworthy for great flow restriction at low lung hoi pollois or in the presence of emphysema.ResourcesReading West, JB. respiratory Physiology-The Essentials ( 4th Ed. ) , Chapter 7.Taylor, AE, K Rehder, RE Hyatt, JC Parker. Clinical Respiratory Physiology, Chapter 2, 6 and 7. Saunders, 1989.NORMAL BREATHINGInspiration is usually active. Termination is usually inactive.Muscles of internal respirationInspiratory musculussDiaphragm. Principle musculus of inspiration.External intercostals. Lift ribs during inspiration.Accessary musculuss. Include sternomastoids, scalene musculuss, and alae nasi.Expiratory musculusstype A B musculuss. Principle musculuss of release.Internal intercostals. Pull ribs downward and inward.Pressures involved in respiration.Pbs = pressure per unit bea at organic structure surface ( normally atmospherical )PM = oral cavity draw and quarter per unit area ( normally atmospheric )PPl = intrapleural superpower per unit areaPALV = alveolar coerce per unit area kind 1Airway force per unit area gradient PM PALV. This is the force per unit area gradient driving assembly line flow into the lungs.Transpulmonary force per unit area PTP = PALV PPl. This transmural force per unit area across the lungs. Equal to ( i.e. balances ) bouncy abandon of lungs when there is no air flow. Additions and littleenings with lung passel.Transchest wall force per unit area PTC = PPl Pbs. The transmural force per unit area across the thorax. Equal in order to ( i.e. balances ) elastic haste of the chest when there s no air flow. Additions and lessenings with chest brashness.Transmural re spiratory system force per unit area PRS = PALV Pbs. The transmural force per unit area across the full respiratory system ( lungs + thorax ) . This is rival to the net inactive elastic kvetch force per unit area of the strong respiratory system when air flow is zero.Balance of forcesPraseodymium+PMUS=PL+PCWPALV-Pbs+PMUS=PL+PCWinspiratorymusculuscontractionLungelastickickChest wallelastickickOutward Acting forces Inward playing forceswhen affirmative when positiveThree ways to blow up the lungsIncrease alveolar force per unit area. do when utilizing external positive force per unit area inhalators.Decrease organic structure surface force per unit area. Done when utilizing the old Fe lungs.Activate inspiratory musculuss. The normal manner to breath.Inflation kineticss. Requires that transmural force per unit area development be sufficient to get the better of non merely elastic kick forces but besides airway opposition to flux. skeletal system 2ELASTIC CHARACTERISTICS OF THE LU NGLung conformity ( CL ) step lung saturation at assorted transpulmonary force per unit areas. The incline is lung conformity.Figure 3Hysteresis. Lung volume at a precondition transpulmonary force per unit area is higher during deflation than during rising prices. The grounds for this are complex. Often, merely the deflation limb is shown on mannikins. submission lessenings ( the lung becomes stiffer ) at high lung volumes.Two major forces move over to lung conformity tissue elastic forces and surface tenseness forces.Saline rising prices eliminates gas-air embrasure. It takes less transpulmonary force per unit area to blow up the lung with saline. The lung becomes more than compliant be set about merely tissue elastic forces remain. shape up tenseness in the lung.At every gas-liquid interface surface tenseness develops.Laplaces Law. It takes a certain rising prices force per unit area to back up the surface tenseness developed at an air-gas interface.T=tension ( dyne/cm )P=t ransmural force per unit area ( dyne cm2 )R = radius ( centimeter )Wetting agent in the lungSecreted by Type II alveolar cells, surfactant lines the air hammock at the gas-liquid interface and has dipalmitoyl lecithin, ( dipolmitoyl phosphotidyl choline=DPPC ) as a major component. wetter has 2 alone surface tenseness belongingssFigure 4The mean surface tenseness is low.Surface tenseness varies with country. Surface tenseness rises as country gets bigger and affects as country gets smaller. physiological importance of wetting agentAdditions lung conformity because surface forces are reduced.Promotes alveolar stableness and prevents alveolar prostration. change magnitude surface country lowers surface tenseness. Increased surface country additions surface tenseness. Small air sacs are prevented from acquiring smaller. Large air sacs are prevented from acquiring bigger.Promotes dry air sac. Alveolar prostration tends to gain fluid from pneumonic capillaries. Stabilizing air sac ( see B ) prevents transudate of fluid by forestalling prostration.Infant respiratory disease syndrome ( IRDS )Surfactant ( DPPC ) production starts tardily in foetal bread and butter so premature babies are frequently unable to do surfactant properly.Babies with unnatural wetting agent puddle stiff, fluid-filled lungs with atelectatic countries ( alveolar prostration ) . Non-ventilated, collapsed air sac efficaciously do right to go forth shunting of blood. lecithin / sphingomyelin ratio can be analyzed in amnionic fluid to supply an index of gestational adulthood of surfactant production. Sphingomyelin production starts early and remains changeless during gestation and is therefore a scrape of entire phospholipid concentration. Sphingomyelin has no surface active belongingss.Regional lung volume and regional airingDependent lung-the lung in the lowest portion of the gravitative field, i.e. , the foundation when in the unsloped place the dorsal part when supine.Intrapleural force per unit area is higher ( i.e. , less negative ) around dependent parts of the lung because of the weight of the lung.Figure 5Transpulmonary force per unit area ( PALV PPl ) is greater at the vertex ( 0- ( -10 ) than at base ( 0- ( -2.5 ) in unsloped lung. Therefore, the vertex is more hyperbolic ( i.e. , has a higher volume ) at FRC.Ventilation is greater at the base than the vertex of the unsloped lung because the base is on a steeper part of the force per unit area volume curve. The vertex is on a flatter ( less compliant ) part. The base starts with less air but has greater airing the vertex starts with more air volume but has less airing.Summary. Ventilation is greater in dependent parts of a normal topic s lungs.Time invariables for emptying. Important regional inhomogeneities in airing can besides be caused by factors which cause regional differences in airway oppositions or elastic features. High opposition and high conformity equal slow voidance.Specific conformity . Conformity divided by resting lung volume clinically FRC is used ) . This standardization must be done to analyze the elastic features of tissue and their alterations in disease. How would compliance differ in a kid and an grownup, both with normal lungs?INTERACTIONS BETWEEN LUNGS AND CHEST WALLThe lungs and chest wall operate in serial publication and their conformities add in return to do entire conformity.The chest wall is like a mold which may be either compressed or distended.Figure 6Transthoracic force per unit area is negative at RV and FRC intending the chest wall is smaller than its unstressed volume and its care to spring out. Normal tidal external respiration is wholly in the negative force per unit area scope.Transthoracic force per unit area is 0 at approximately 65 % of TLC intending the thorax is at its unstressed volume and has no inclination to prostration or expand.Transthoracic force per unit area is positive at volumes above approximately 65 % TLC. The chest tends to fall in above its unstressed volume.The lungs are like a spring which may merely be distended.Figure 7The lungs are above their unstressed volume ( minimum volume ) even when the system is at residuary volume. The lungs still have some volume at their minimum volume.Transpulmonary force per unit area is positive from residuary volume to entire lung capacity so the lungs ever tend to prostration.Functional residuary capacity is the lung volume at which the inclination for the chest wall to jump outward is merely balanced by the inclination for the lungs to flinch inward. The transmural respiratory system force per unit area ( PRS = RALV Pbs ) is zero at FRC if respiratory musculuss are relaxed.The secret plan of lung volume against transmural respiratory system force per unit area ( PRS = RALV Pbs ) with represents the have consequence of lung and chest wall kick.Figure 8A pneumothorax causes lungs and chest wall to alter volume along their curve until their transmural fo rce per unit area is zero. The lungs ever recoil inward. The chest wall springs outward unless it is inflated to beyond 65 % TLC in which instance it besides will flinch inward.Conformity alterations in diseaseLungs become slightly more compliant with natural aging and go markedly more compliant with emphysema.Lungs become less compliant ( stiffer ) with pneumonic fibrosis or during hydropss caused by arthritic spirit disease.Chestwall becomes less compliant ( stiffer ) in status where the chest wall is deformed ( eg. kyphoscoliosis ) . It besides becomes functionally less compliant when abdominal muscle pit alterations cause upward supplanting of the stop ( eg. gestation ) .AIRWAY RESISTANCEAir flow is primarily laminal during quiet external respiration. Resistance is determined by Poiseuille s Law and the force per unit area gradient required is relative to flux.When air flow additions, as in exercising, some turbulency and eddy flow develops in big air passages and at subdivis ion points. An excess force per unit area gradient proportional to flux rate squared is necessary.The major site of opposition is in the larger air passages specifically in the medium size bronchial render. Merely approximately 20 % of entire air passage opposition is in little air passages ( less than 2 mm ) .Factors taking to cut down airway quality and increased airway opposition.Contraction of bronchial motionless musculus. Stimulations include pneumogastric tone, histamine or reduced airway. is peculiarly of import for advancing homogenous airing. When it builds up in a ill ventilated part the air passages to that part tend to distend.Loss of elastic kick in lung ( i.e. , more compliant lungs ) . Radial grip on bronchial tubes usually helps keep them unfastened. trim down lung volumes are associated with less elastic kick and slower flow rates.Loss of elastic tissue in chronic clogging disease ( eg. emphysema ) lower elastic kick forces.Maximum forced termination consequences inFigure 9 Expiratory flow-volume curves.May be plotted as volume vs. clock time or flux vs. volume.Peak flow occurs early and flow falls as termination continues and lung volume lessenings.Effort independency. When the supreme flow-volume envelope is reached, flow falls with forced lung volume regardless of get toss off volume or attempt.Mechanism of flow restriction at lower lung volumes during termination.Figure 10 take apart of the air passages during termination The entire force per unit area in the air sac equals pleural force per unit area + the elastic force per unit area of the lungs. Flow in the air passage requires a force per unit area drop owing to the syrupy opposition of the gas. If the air flow is rapid plenty, or the airway opposition great plenty, this force per unit area off-white will go equal to and so greater than the elastic force per unit area, the airway transmural force per unit area becomes zero or less and the air passages will be given to fall in . The point along the air passage where this occurs is called the equal force per unit area point . With a forced termination the equal force per unit area point moves closer to the air sac because as the flow rate additions so besides the syrupy force per unit area bead additions, but the elastic force per unit area remains the same. Cartilage in the big air passages helps to oppose the inclination to prostration during forced termination.Alveolar force per unit area = elastic kick force per unit area + intrapleural force per unit area.Mouth force per unit area = atmospheric force per unit area = 0.During expiration intrapleural force per unit area is positive ( greater than atmospheric ) .Equal force per unit area point ( EPP ) . Airway opposition causes a force per unit area bead from air sac to talk. At some point in the bronchial tube the force per unit area has dropped enough that it merely peers environing intrapleural force per unit area. This is the EPP.Since air passages are collapsible air flow will be relative to the difference between alveolar and EPP force per unit areas and reciprocally relative to the opposition of this section ( retrieve Starling Resistors ) .Increased attempt will do equivalent additions in alveolar force per unit area and force per unit area at the EPP. The force per unit area difference and therefore the flow will be unchanged.Flow restriction at assorted lung volumes during forced termination.High LUNG VOLUME MEDIUM LUNG VOLUME LOW LUNG VOLUMEFigure 11Flow restriction in chronic clogging disease ( emphysema ) .NORMAL LUNGS EMPHYSEMAFigure 12Forced inspiration is non attempt independent because intrapleural force per unit area is negative and air passages are held unfastened.Figure 13 A household of flow-volume cringles. Each of the four inspiratory and expiratory full of life capacity manoeuvres is performed at a different degree of attempt. The manoeuvre with maximum attempt is designated by the figure 4 . Maneuve rs 3, 2, and 1 are performed with increasingly less and less attempt.MECHANICS OF BREATHING STUDY QUESTIONSTrue or False. The abdominal and internal intercostal musculuss drive expiratory flow during normal external respiration.What relationship exists between the volume of an elastic construction and its transmural force per unit area?What transmural force per unit area difference equals the kick force per unit area of the lung? The chest wall? The whole respiratory system?What 2 forces contribute to lung conformity and must be overcome to blow up a lung? For each force, name a common lung upset in which it is altered?List two of import surface tenseness belongingss of wetting agent.List three physiologically important effects of holding surfactant nowadays.At FRC which part of the lung is roughly hyperbolic? During inspiration from FRC, which part of the lung is best ventilated?What is meant by unstressed volume? At what lung volume is the chest wall at its unstressed volume? A t what lung volumes are the lungs at their unstressed volume? At what lung volume is the entire respiratory system at its unstressed volume?During forced termination flow becomes limited. What two force per unit areas add together to do alveolar force per unit area? What force per unit area determines force per unit areas at the equal force per unit area point?How does maximum forced expiratory flow alteration with lung volume? Why? How does maximal expiratory flow alteration with clogging disease? Why?
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