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  • Respiratory Physiology Hand Written Notes

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    Dr.G.Bhanu Prakash
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    Respiratory Physiology Hand written notes

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    Respiratory Physiology Hand written notes

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    Respiratory Physiology Hand written notes

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    © All Rights Reserved
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    Segnala contenuti inappropriati
    790 visualizzazioni12 pagine

    Respiratory Physiology Hand Written Notes

    Caricato da

    Dr.G.Bhanu Prakash
    Respiratory Physiology Hand written notes

    Copyright:

    © All Rights Reserved
    Scarica in formato PDF o leggi online su Scribd
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    lot naspirabery physiology Wand, Volumes 2, ‘an capacities KyelationsHp between Inngs R theratic age: at rest (inside tre body) outside tne bedy lang: pulgs ont Hed. nee 7 TC : pats ont TO: palgs io % lun VolAmeS Be eapacites + = with ageing, trayes dacnarse in the lung elestisty op f ResidenS ose lung buf Total lung capacity olsesn’/t change. Volume. —> mone (o also wil capasity decrertes. Janey Volumes By capasihes excapte o Spire mater : measures the out of frelung Resichucel Volume becamge it can’t be blown ang wag. Helium dilution syctem . ale. vite capasit # larger Than femole Lecange oh 3 =m 5 Dlarege body si2e - 2) smengin oP the Ins piratory rawslec , obesity % pregnancy vedas Hn vital capas ity. = Pilomylits , myo patnies , Uytririn Gravis, key phasis, ecoliosi's lung Ciboresis , Infection (in lung) 4 Huids im tre pleural conta VC, And wespiratery Plysibogy slung wachanics G —Pelinihen . soit Qeoe” mechanism ny which air goes in oy out of the fangs D muscles sf Respiration (copmeching forces): A) Muscles of Inspiration: Y Dieephymgim (Quiet) 2) External whaveesto (bicker mnememat) (Quiet) 3) sterng cleidemabtord (forced) ® sealene (forced) B) Muscles of Eypivation: 1) relation of the Inspiratory maccles (dae te lung elaehsty). (Quiet) 2) Interna Intercestels | pur. handle: monement) (orcad) 3) rectus abdeming (forcad) [2\ Auti-strechiny forces ; 1 recoil papenty . £ pro Jung 2) Titsve recictance, 3 Airway & yespiratery pissne resistance , # lung pressures, 5 Intra -alnestar Pressure. Ipffe a HS pleura Pressure. 3) Intra atmos phonic pressure. / traracic = L) Troms. . = Fea. e Aheme) C) Trans Respirator eP « )Trans Respiratery pressing oy (es Continue Elasteity ; mere elastic tis & 4 Compliance F comp ldance. / ® Elsstiaty b Elusitety ty c= AY “AV AP 2g, Fibvosied Lungs ivatory SAM ( both Lunde, CW) eins cae AN BP ERR a “aie Pred i shorts tie Baie ae «TN. Bolaked a lane Cals anh He: chest) D> vesting volume is Syaalt AV BY AP Ga = Potaarah nest wall Farers to be inPlitiny if isofafed form lung alone C which ce iS Resting volume 4 5 siters Cabout 6O%0£ tne no. € Rs ou > 7. oe 2O rel respiratory PWYsiology :surhace i densionk Role of surfactant * alveolar aus - 1 Type T prawmocyte : Pint cols 2) Type Z preemocyte . cuboidal cotls which secrete. surfactant then we hane we surface oner it that ig nespensble foy sur face tension of ean alvedus . , SOD%0dG OSC aO= 80608 Scone el 0950SD0DOG ASH LEVEN ee TR cbtractey Grom abl dlinechin = wet herce = 0 Swe surface teesion reduced surbac altactif 7. exlapt up=> surface tension exisen + becange the surtrte molemules atiractad 2ite by Sicla troy will et polled 40 each oper which cusetne reduction of the surbice Wl oveg . thug cousin§ Clebins Pressune of pra, Alneblas P= Z Tension (1) Yadius (rn) [Fi]. collapsing Pressane is lee becange of large rasius , 3 [BD collapsing pressure is 3 / smahl radivs . ove pecage of = small Alnect drains iKs Pressune into He larger dl the Smell collapses | tre larger intliches ae @ = ventilation |per fusion pdisirurboance which Cage Gas exchanty. dicta’ TA) tre Alneslus rs overventileAad with normal perfasion ee eine he alvialons is wnderventilates with normed Perkasion whiner tra 9s to be exchanged very WEH => carbondted biowd. KTR good lang mp which have multiple alibsli wis large surface Anen but the probham trat small alnrerli hes Ha tendency to cellopse , = Parmetion of Edema in the alvedi :ar tre surface tension inrneates tne collepeing preceme incnerges=s te Shrnked alnertus has the tenclency to Suck nulér fom sar blood capillary tonards the intenstihif space whieh cones tre Permation of Ha Edemeboy alneolt which comge me ffech ne RK tasuPeciont I45 exchange a f= such an alneott due to thickness of he wetsurkece of tra suvhae Area that: loceed abone the alveolus walk ae eur hucetension Causes», ) Alveoli pendency +e callapse 2) formation oF umequad size ef alveol', 3) Ventilation (perfusion disheteance 4) formation of the Blame . these disadvantizeshelned by tne Presence of surfactant (0% falmohily! phesphality| choline) : syntnesized From TYPE IL prenmocyte ands tured as Laminar bedées the by exocytosis trey ane relenged as tubular mylien. Sg fp saader yylien ae | | Q)—pianinar body Fane : J bumi: Tyre TL Preumee ste. 1B che, ai bumin Contin ce esurfactantt meleade is qoy lipid 410% prefein : VaegrempP of Palmotidyed Db group sf — Phesprattayl gusta a 3)i Sfrr af chdline- 3 ocn8 ee 4 apopreteins (A,B, C, 0) =0Psonins. 88S; CBOSS gorners: Ig + albumen pf Surbactant is ampha patric product which hane hydrephatic. component C2scnp of palmotdy!] and pre nest components are hydrophilic $0 surfactant prevent surtace pension by this Puberty, = also surfactant has Ankimicrobaf function by tre Aalp of. apeprotein (A, which Werte as opsonins - ap prefdh (6,0) help in tre surkactant spread opconin over tne surfoce aven | ye Etfects of the surfactants. ) | Surface tension a collapsing Pressure => 27 as Peompliance, = of the (on9 => L work of Inspiratory muscles far byreatumg, So prevent Pteleckasis. ‘collapsing of thaluny, Recpimbory Diskrass eyndvorne 2) Mineola dry map prevent Pulmonary edema, 3) prevent te Unequalizetion oP the almeclay stze , tn Small S\ze Alneelas : Surfactant ConcenMatron "6 More fete Surface Aron whith allowing less surface bencion- in larye site atlmeolass — -- es ee (egg: am oe em pe ae more surface tension Se, it prenent small alnewlag from callapsing & large alveolus from enlarge rnn . Armvestireory plupsiotogy « Asseseins) Pulmonary Panction Cebstretie , Resta) a ebeweHne | by norm ah wincnerse inne Air nay Resistance with normed Ing, paran chef wa BP m FRC PTLC 3) enlarged [ung 4} Pecompliance. Lelaststy 5) Mechanisms of COPD=COAD 4) chronic tenitabion oF ~~ a Ait woujs {exCesine Secretion s) ; 24. chvenic branchibity Y Glastisty caged by smoking Le ») dastruchion of Ha alnedar — -¥ VC Wall : duet P macephage ackivity TRY for carken clearance ;t production 2-4: Emphysema efelastoces ©) chronic. hyperactivity of ta Aivwoy/s Velen Smooth muscles | eg. Asthma AGB) ave chronic 6) can be Acie er chronic L obsirectina ; oe SPifemelery reading T compliance. ReciicHwe, L. 0 1) ncreage inne band Paranchyma with nore Airway 2 Lin FRC ILC a) shrinked lung A) L compliance F elastisy T blosnsty wie wv VRV Presswne withlittle Posy yup | vlad masa eve ented Restnthine: with more @ as un ee eee air gu EVC ie => os | ae EVE, OLEEY FVe BaRer piratory physiology: Cs Pulmonary civculahon + Difference between systemic K Pamonary civemlation + Precean® high 5 low f How (veleaty) slaw, Wigh ves seles wall thickness. more thick. jess ticking pe high, low’ Poa —P Lenessune) sistance 2 Woh, low R= e A (Flow Hi low , high Yi -2F Gempliance : low , hig 07 igh Pressune ue LS Yyetemtc Bas became of IPG Anti graw'ty| eet - vltinonary vs low prediune \ ae \\ LA ~ fo prevent He leaka\ x Ze | a : a / Bp \ ae ot of tra fiWidld edema . bResstanc Pulmonary ecapillies Consimicate mp 1 pressure, GSvot cansariches f / 0 “Sy Resist if forms edema (leakingen of tre Fluids), Saeco at low Oxygen tension pulmonary vesseles consivicate while syctem vesseles Dilates . aX cae ese of * SK pulmonary Vasculou’ Resistance PVR) fi yet? hy “RAP won oP 48-2 yaraTh Sittinte flow Sites 6 ee oft .0-P Pp IS -5 Peal eae i er) Pulmonary Dg ys yee So syctOmic circulation recistan “5s 9-]0 times more tann Pulmonary Civoation WIP Cardiqtoutput Incneaes (darrng Excorsize) iP CO Increases PYR decneages in order to: Dgcod gas exchange 2) Prevent Increased Pressure from Edema borrebion . are 3) Prevent R. Heal ideas awe te Yeducad pressure of te long, gpa by the two mechanicms (capillary Resprebnent & Distension] ave dety Ne Gontivwo ee - mechanitms by which TCO accomackkes PYR , Microcjoulssery cap illaries Reqrument+ capillary DistenSion: in Resting (upright position) ¢ trelower Part oftnalung hat geod pertfasion more than upper segment. Sa ch cardiac. outPat P weanss> Ptelitics of-bicod Passing Huosgyh Pure nay Cirendahrinn => opening B Reqnutment of tre closed microciveubetory channels of tre lung ive adition of toe robe move disteny opened micro civeulabeny channels hich accommolddes the PCO embe p Resistance of the plilmonary cireelution, 2) if Jang Volumes change ( Increase er Decrenge) whet happens te PVR Note: Resting Volumaof tuelung = fanctonl) Recrlanl capa RO. Finetiond) posts of the Aineclsir blood vessles : : D Extn nectar sunpeuncled by Air pockets See try ane subjected fo lung comnective tseue \ pressune— f 2) Alneler , surrounded by prir pockets trey are! OZ qubjected 4s | alncolar pressune. | Ss Daring Inspiration » alnewlay blood vessles Resistomer Imcnaase ( PVR) while Exva | alneolay Lleod vesAas Resistane Decrenses (perk) tng Comed! Dering, Expiration: ExWaalverlw blood veestas conetrweake 2D tncnenge vin the Resictane (PPYR) while alvesley blood VesshOs pi late —> decyaage in re Recictance CL PVR). n alaonary blood vescdles if 3) whack hp pen do PY igefe. palo: PO, pod tre alvester ( lew on77" Ancien) = (H ¥poxia) , f / if we have Moria ew oxygentension) pthe systemic Clrewlacbion, pleod vesseles will dilate morder te bring anova oXY9en and blood wh the site of the hypoxia yy Haas TAL is neal alnertins with nevmel vlood verses, IG] is yee wekbd alnertas with constricded blood vesseler . = when Here is alow Oxygen tension (L Po ) y | of an alnectis imnredictely the cmocth QUs |B of the blood arteriole wall will conshic Blas ies 4 [AS 9 or, and vedu the portusion traards this almerdiyg ~~ unfortnahly tuis puberty of the pulmonary sy tim is dishwirbed by case of high alttade when there, Jenorilized consivich'on of toe, Pulmonary vesselos a ean in patient with chronic CORD Like. sethmaw han algo ts $ chronically which cause. ePPart” Phe gmooth muscles are omshwcded ontre Right Heart + pumb against high Fecistence alvelic mpewhich, cakes Right Heart failure (pulmonary Hyper tvephy Pryst tran Rin Sails Dn we exll this situation 05 Core palronali' epuimonary Hypertension _mechanitm by which Smrotn muscle coivactes whan fe Sconses lew ron (HYperia) , al porfasinm oxygen sensitine channelas ave Kept oper if Oxygen Fercion te yormel when we hare LPY wechseln) OP he Gay wm more ability to contracts, (Vek coll contrac, onygen tens => Cat™ channels oper => = P84, happen Physiologt < cally Ror fetus when the child is dolivayied => f PQ, => dilation of tha pulmo. vesseles mp | PVR sk Bleed ‘Plow Distabuhion af ta ORevent ovens of ta, (e Lung ( Upright pasition) : -ZoreL ; ae iG ee ed ims = Zove. conse gravity apaes the Plow) tie PP continuous Flow (During systole WWiastela) = 2eneL not exist inthe normal healtiy indimoleal pit exists when te, is case of f Cavdlinc output egs: Excarsizing (moves Zonas upward), & in cage of Tdiveclar pressare b Ka 2a), vlawing ail aganict closed mente Le nase =<3> camgas blood Hor +o step inte htermittent Plow Fone yor reduce, tre Continent Plow 2ore. = Zerel canbe prodacad ifwe have hummorhaye oy semare \wjpovlemin whidh causes Zone IE to be converted +e zove L - zee LT canbe Produced (f+ the paent under ave __.Pressune ventilation vintch Conses

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