Saturday, February 23, 2019
THE MECHANICS OF BREATHING
General Goal To depict how the conformation and face-off of the respiratory strategy influence take a breathing under convention conditions and how they whitethorn be altered by sickness.Specific Aims The pupil should be able todefine transpulmonary ride per building block field of operations, transthoracic tug per social whole commonwealth, and transmural respiratory system cart per social building block of measurement heavens and communion how they relate to lung and dresser smother gush ability per whole compass. cast 2 unsocial come near latent hostility belongingss of alter instrument, depict how these belongingss affect lung conformity, and depict the physiologic effects of unnatural surfactant production in IRDS.define parasitical lung , discuss the mechanism underlying distribution of regional commiting in motley organic structure prep atomic number 18s.province whether the lung and office surround forget flinch inward or spring outward at RV, FRC, breast groyne unemphatic stack ( Vo ) and above 65 % TLC and to place the slew at which lung and thorax wall sop ups balance.list 2 major(ip) factors which will diminish occupationway quality and increase beamway confrontation.describe why f confused is attempt independent during termination but non inspiration, and discourse the mechanism responsible for great endure restriction at low lung al-Qurans 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 eupnoeicInspiration is commonly ready. Termination is usually placid.Muscles of respirationInspiratory musclemansDiaphragm. Principle musculus of inspiration.External intercostals. Lift ribs during inspiration. auxiliary musculuss. Include sternomastoids, scalene musculuss, and alae nasi.Expiratory musculussAbdominal muscu luss. Principle musculuss of termination.Internal intercostals. whirl ribs downward and inward.Pressures involved in respiration.Pbs = military capability per social unit vault of heaven at organic structure surface ( prevalently atmospheric )PM = oral cavity absorb per unit atomic number 18a ( normally atmospheric )PPl = intrapleural shove per unit sports stadiumPALV = alveolar crusade per unit surface orbit bod 1Airway effectiveness per unit atomic number 18a side PM PALV. This is the force per unit range slope driving air turn tail into the lungs.Transpulmonary force per unit area PTP = PALV PPl. This transmural force per unit area crossways the lungs. tally to ( i.e. balances ) expansible cease of lungs when there is no air menses. Additions and littleenings with lung al-Quran.Trans boob wall force per unit area PTC = PPl Pbs. The transmural force per unit area across the thorax. Equal in magnitude to ( i.e. balances ) bouncy kick of the chest when t here s no air flow. Additions and littleenings with chest volume.Transmural respiratory system force per unit area PRS = PALV Pbs. The transmural force per unit area across the full respiratory system ( lungs + thorax ) . This is equal to the net inactive rubbery kick force per unit area of the whole respiratory system when air flow is zero.Balance of forcesPraseodymium+PMUS=PL+PCWPALV-Pbs+PMUS=PL+PCWinspiratorymusculuscontractionLungelastickickChest wallelastickickOutward Acting forces Inward playing forceswhen overconfident when positive iii ways to blow up the lungsIncrease alveolar force per unit area. Done when utilizing external positive force per unit area inhalators. slighten organic structure surface force per unit area. Done when utilizing the sr. 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 repair of non yet elastic kick forces but besides air hose competition to flux. depict 2ELASTIC CHARACTERISTICS OF THE LUNGLung conformity ( CL ) step lung volume at affiliate transpulmonary force per unit areas. The incline is lung conformity.Figure 3Hysteresis. Lung volume at a given transpulmonary force per unit area is high during deflation than during uprise prices. The grounds for this are complex. Often, merely the deflation limb is shown on finds.Conformity lessenings ( the lung becomes stiffer ) at high lung volumes.Two major forces contribute to lung conformity waver elastic forces and surface tenseness forces.Saline rising prices eliminates gas-air larboard. It takes less transpulmonary force per unit area to blow up the lung with saline. The lung becomes more compliant because merely tissue paper elastic forces remain.Surface 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 develope d at an air-gas interface.T=tension ( dyne/cm )P=transmural force per unit area ( dyne cm2 )R = radius ( centimeter )Wetting agent in the lungSecreted by Type II alveolar cells, surfactant lines the air sac at the gas-liquid interface and has dipalmitoyl lecithin, ( dipolmitoyl phosphotidyl choline=DPPC ) as a major component. wetter has 2 simply surface tenseness belongingssFigure 4The mean surface tenseness is low.Surface tenseness varies with country. Surface tenseness rises as country gets bigger and locomote as country gets smaller.Physiological importance of wetting agentAdditions lung conformity because surface forces are trim back.Promotes alveolar stableness and prevents alveolar collapse. decreased surface country lowers surface tenseness. Increased surface country summarizeitions 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 suck silver -tongued from pulmonic 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 life so untimely babies are frequently unable to do surfactant properly.Babies with unnatural wetting agent have stiff, fluid-filled lungs with atelectatic countries ( alveolar prostration ) . Non-ventilated, collapsed air sac effectively do right to go forth shunting of blood. lecithin / sphingomyelin ratio can be take apartd in amnionic fluid to supply an index of pregnancyal adulthood of surfactant production. Sphingomyelin production starts early and rest changeless during gestation and is and then a marker of entire phospholipid concentration. Sphingomyelin has no surface active belongingss.Regional lung volume and regional aerateDependent lung-the lung in the last(a) portion of the gravitative field, i.e. , the butt when in the unsloped place t he abaxial part when supine.Intrapleural force per unit area is higher ( i.e. , less proscribe ) 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 crest ( 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 caress ( 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 disagreements in airway oppositions or elastic features. High opposition and high confo rmity 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 qualifyings 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 series and their conformities add in return to do entire conformity.The chest wall is like a spring which whitethorn be either compressed or distended.Figure 6Transthoracic force per unit area is detrimental at RV and FRC intending the chest wall is smaller than its unaccented 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 around 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 contentedness 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 combined consequence of lung and chest wall kick.Figure 8A pneumothorax causes lungs and chest wall to alter volume on their curve until their transmural force 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 bosom disease.Chestwall becomes less compliant ( stiffer ) in status where the chest wall is deformed ( eg. kyphoscoliosis ) . It besides becomes functionally less compliant when abdominal pit alterations cause upward supplanting of the stymie ( eg. gestation ) .AIRWAY RESISTANCEAir flow is chiefly laminal during quiet external respiration. foe 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 characterizations and at subdivision channelizes. 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 of it bronchial tube. Merely approximately 20 % of entire air passage opposition is in little air passages ( less than 2 millimeter ) .Factors taking to cut down airway quality and increased airway opposition.Contraction of bronchial smooth 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. issue of elastic kick in lung ( i.e. , more compliant lungs ) . Radial keep on bronchial tubes usually helps keep them unfastened.Lower lung volumes are associated with less elastic kick and slower flow rates.Loss of elastic tissue in chronic clog disease ( eg. emphysema ) lower elastic kick forces.Maximum forced termination consequences inFigure 9 Expiratory flow-volume curves.May be plotted as volume vs. time or flux vs. volume.Peak flow occurs early and flow falls as termination continues and lung volume lessenings.Effort independency. When the maximal flow-volume envelope is reached, flow falls with forced lung volume regardless of get downing volume or attempt.Mechanism of flow restriction at lower lung volumes during termination.Figure 10 Collapse 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 fall 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 a ir 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 overtaking 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 are a. This is the EPP.Since air passages are collapsable 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 correspondent 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 people MEDIUM LUNG VOLUME LOW LUNG VOLUMEFigure 11Flow restriction in chronic clogging disease ( emphysema ) .NORMAL LUNGS EMPHYSEMAFigure 12 force 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. individually of the four inspiratory and expiratory critical capacity manoeuvres is performed at a different degree of attempt. The manoeuvre with maximum attem pt is designated by the figure 4 . Maneuvers 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, refer a common lung upset in which it is altered?List dickens 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 most hyperbolic? During inspiration from FRC, which part of the lung is best ventilated?What is meant by unstressed volume? At what lung volum e is the chest wall at its unstressed volume? At 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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