Veynat Labew nit notes Parner, Tldapucicom DeFiition: Serie ot events that fake place in the g expel viable products of concepon out Vagina into outer world enital organs in an cHort to The womb through the 4 patient in labour is called Normal labour (Eutocia) pavturient. 1: Spontaneous in onset 2. Term (33-2 wk) 3. With vertex presentation 4 Withour undue prolongabon Natural termination with minimal aids. Baby ond mother have no complications, Any deviation from the above is called dystociav. PREMONITORY CHANUES oe uy () Lightening: vin fandal height due to formation of Lus and descent of focal presentation {nto pelvis, Causing relieg of symptoms in mother. (2) Show + Cervical mucous plug + show (3) Cervix ripening (4) False labour pains True False 1 in intensity, Frequency, ron-progiessive, does not progressive in intensiny/ Frequency requiar irregular lower abdomen, back tadjates Cangined 1 lower abdomen to Thigh. bag of waters 5 show not reliewed by enema or | relieved medications ective space.INITIATION OF LABOUR PAIN S Si 7 Mechanical theory - uterine distension 2 theories = UuS /ervical sverch Biochemical theory Foetus hypothalamus cRH wet i hui an oe ACH v % PGE 2M, Oxytocin a CRA 7 ; — helps in U progasterone forms estriol active space 4eGurukul In collaboration with NotespaediaGam bibyedudicr & Cell nenbyarc |OrGanization OF Lirt| {BLOOD CIRCULATION nas /& ORGAN SYSTEM <——— AORTA VENA CAVA, ‘ ‘ + oRGANS «= <——— ARTERIES VEINS + + t Tissue = <——— arenes venules ¥ + there uses Ss corsa Exchange (permeobl) a = Celb cna Singer Nicalsew Finid Masasc Medel Nncles 4 Cell gill +15 wm Hack “Many eave pide Rone ho-n5i 55-607 e156 | EEE EEE EE EEE EEE EeePC “AL pds presink excaph Tiglyides Conbuins chaedbnl elycapide yphoophlipds te~Prospao.ina > Main lipid «a feks~ + Heed (flag) ~ Hap ' 2 Tul (Won pa) Hype pd dns 8 yo psp anand Bag? ee ee ere ye a nn + = nt an ae a ous om 6 bilager = Heads Outer surface f f FI Perce. Renan Tails - Taner surface st Teanswenazane Prartns / dnreaans Rorsis. Ea ctn Chanabe ousise ore Proteins ae ct a plasm Proton, . frtoplesmWate : > Universod, solvent ~ Distolves mast charged substances “Hp i polar celue (ast (chs a6 small magnet) ' + Abbrach each other Noch No* + ohm Salt ensly dissdins PAIL sable, pela cubstanvens ane 10 salable, —> HYDROPHILIC > Now ilar sbebances Lipid sdb, + Liropnuse * Dacides ach of dug i Indy Foncrion OF Liens In Cent MiMoRANe| + Rie sacha nagrby 1 Povide Pilly of Ruibly ~ Nosy debe ansabareed aly acide x: Oleic Uni ocd ss Sally: Lipid salable sbdancns cam soy ons oy Fre: Geses (04,60, , 00, Ni de) Cheldal, lodby acide, A ADE Lipid selable hermanes - Sbeaide sf Th : os? TeProteins OF GM. meas “Helps inetromapett ackion of water sulle snbsawees acres cM 1 donee prone avs ee romale (Tal pins) Pompe (se ATP cee. Net mnie, 8 Wober use prosins like Aquaperins / Ho channels bo orees CM Salat i anges AAS Us oo. wae prebins called canvinns Eu: GLUT (Glucose Tamspert) Maker soluble hermones like Tnsubin (51 AA) Eitan ke Ba sce, Naber eal nabs Pon nat ca ete ee Moally end iv mn / Ere: Insulin» Oxybacin, Gvsbin. TSH, CRM , PTH (Hermon) ur GP ALP Ry)=a Thi hed == Thr staid ved, rend om id Mk eat. NON INSULIN D&PENDENT DM:/ IDDM: /OM- IE] J INSULIN DEPENDENT DM/ DIA- = Defock of receptor + Lack of Insulin +@/* Insulin + Insulin level + Insulin resistance, “Tnsubi snatvity ® + The: Wh ess Exercise, Orod hypagycomio drags Ec: Mebformin + Vt: Give Insulin > Others : Moby, LADA 5 Ale ackas ergy, col marker (60), Ankigans Exe: NAC / HLA » ‘t — Mier Wie ey A miceabed els Antigo presenting cls (APE) > SUMMARY : oe unos > Mindy phaphlde —> Bplar¢ Bayer —> Helpless PorEns > Hap Hyp seller Achson chan, paps, cores ,recaplers antigens, naga ceofc Notes Prine Beda Fluids Compaylerert & Herreestayis + 0-tor body wught = Mader Leas nfm plese (la ihe by et) “TEW (Total body wala) (6) oe eae (shy (Suse all old) PA body mcight = coleg oe Ww) lore aql “ECF = BL Tera axecr EGr —™ (Q5/) PLASMA INTERSTITIAL FLUID (157) em) @ Pdnside esse > Preanh bbw vss ce (His) or Tame lad ->(GBlood Calle) > Hap Frm Lap “+ Compaiion same os plasma (glace pt, comdlarly WP alt se eaph oomaprabiné)Sash lor vein INT FLU fF =P27Y vn PLASMA tone + Cobbs of Grit gf Liver A eae ener ore cee eee wasbo ummarg: Au FOE ONE ¥ ONE FORALL Ramon ye dng > Cameer pares Us eennees any fnchion “Al xchange vss serine Sue Noms Seed Emvrmnend: / Mii Saaie Tum sini by Claude Bernard FATHER OF PHYSIOLOGY >The compositions cf Internal Enivonmant salvage maintained the sare -[lORbesTnis (WB. Cannon.) > AL variables ex. HR BP, pl, bmp, glacase Nal ea aves mambaived in normal Fpl ange by bly ean aye 16P = Hypebi, Mtoe, gy < are (B65A6) PHARMA (ceRREcrion) ovement 4 BP - Hypdonsiow —————__+ @ a ake[REGULATORY sveTEMS [ives | FEEDBACK FEEDFORWARD / ANTICIPATORY CONTROL + Comechiows occuvs aber henge +E: BP Regul by Barreca + Gorrecion applied: bore change inv valus of maine variable Value remains same Bet — Barereceptors + BF to @ +B Cd weather > Hyphae - senses More connate Gives butler correction shine bmp. > shivering > Lamp bo counter bask FEEDBACK SYSTEMS lass Cove amp. remains unchanged a Moker achivibios More connmon + Change response ave oppasila low bluase “Bx 1 1Glucase: Tne 24 Nat: Aldosterone: a a4 Cal: PTH “tat 414 8P: Berereceplors 40 Types: Stimulus increase Bu value of change more ~Bes Onghai- 1 Mil yc rfl : mere He sucks ni Auroral, east most fice Orybacin ~ 2 Body head mated goinEtticacy of ngulhery syste + > Given by Gan GAIN = connection ERROR BB via by Omg + & conection t = Gain SE ener b= Gain Baverecpters corrcks by mig Ener = 2mm Gai w $ ANGain = t Cornchion * MF err = 0 Gain ia bly Ba: Kidney in rela regulationqu [iliraticn of Body Fluids Tecumiaues : © Drs Dynan Menon = Comcurbrabion = Amount of dye oe Neha = Coneantraion Aolume Amount of dye + Kear > Conconbrabion Awsunh fe Prince : 1: Add dye (newton davswt Leak out) 2 Tk dita anally in chamber of ccayres same concenbrabion 3 Soall ample il ge cocenbrabon 2 Eiamgle Say woormg Aye Lane! = 19g / CH sooner 400 4g ltl (Abel dys - Ak. encrab) lune = 00g = lob dongle Conse] Ut dye leaks out => Concenbeobin wil fall > does high slur, +s Alm Vb ConeDyes Ussp For Esmiarion : 1 TOW (Teta bly wakes) 9) Hao wader: “050+ Deberium aide J} teorores OH + T,0> Tritium oxide 2) Aninopyrine 2 EOF : Dye held dag Bc Pr Shouldsit onder 10F by rosing call smembrarne, -* Poperbies ~ «Wyo lube a Big sive ead + sai (Plar et rach) | col borane cll by ue a Gueroee (= Gilucate + Fruchoss”) & Manwitel Puasa: + Radicbabelled Albumin, by Todine 1 / + Branis Bow dye Choi labeled 286 A Ler = Tow-Eor 5: INTERSTITIAL Fino = Bor ~ PuasaTeeanscetucar: Povo] a Park eo Arvund | lite Shs sam o all aide tbody cavities / chambers Bin: Phar Fad Synovial Fluid Picard Had Fe Ecratt2+3Oficial Notes Partner GED Tyarspert acres Cll Mer yare lypes of bransport across CM : Active Passive “Again gration “Alng gradient = Low to hig (uphi) “High Low Cdn) sled ars + No enargy neded ~Ea: amps , vesicular bran spart Ex: Difuson Osmosis Grradienb : A~B 450 Are: Pasive 5 Occurs bi gradient present If A+ 8415 , A-B0 + Passive stops wha Baw sno gradient BboA: Active ; Stops whin BuO, A=150 Active stops whew Lhere is me ATP or 100% transport: Prinmary Direc use of ATPs Exe: Pumps 8 wo +> 50 Active Tr adie use wa pumps Ex: Saban syapert Jan prt SaUT-1,2 Nat I” sypert (1x)OMOaTE -Newementcsalvent wake) along se cone throug sami permeable amenbrane “Saale crbaben —v Gen by comalanby /eswelliy perlite per Hlgranm, hangesauth temp, devs ange with bom. (batey) smolriby = Malas ob pr Ube seukion “Eset wal te (28g) w= Veda / coarse | osmale | L Gr) 1000 wiliosmale/ L 6%) 1000 mosnt/ L +A mule Nacl = 58-59 ( 239 + 35-59)) =I mdeNar + | mole ch” (229 + 9854) = Lmoles/L @ Aeswoles /L = For 5, tq (10) > 200 mosm / L Plasmas csmalaniby = 265-285 masm /L (2 300) ~Toicity = solar compared bo plasma (6) 2000 swoson/ L Tovicty Same = Lsotoni Hypertow Hypetonic. Lv Aids 107 Mavwilal Add RB -Thoy will awl agave Ex QL sed for 0-47 Nach solution (Newmal, saline-NS) coahechgiey 5h duxbrose ~ Twibially Lsokonic,, 9 Treveased in hereditary spherocytosis tegegnee nen pees Ex:o7% /0-57 Nach>Estimation of Plasma Osmalarity : © By iat emcentrotion > Cobions = Anions Total Tons = Cations + Anions = 2 Cobions POSM = 2 No*+ Blood glucose + Blod wren, wibrogen Nr: 1 Bled glucose ~Lrgnen i ug camer fo mma /L by dvdng wit 18 2 Bld wren nibrogn IF. gon in-mg /-> comer bo ama /L by dividing with 20 8) Nat = 140 mEq/L Glucose = 40mg! Uren = 28 mg Not 0x2 = 280 Glucose — 90mg! x18 = 5 Ursa a 28 mgil x 26 = 10 Totod. = 295 wasm/L Urea - Gnetfeckive oswole Effective ones olay om one side 6 pull wober (Ex. Nat) ® FPD Method (Freezing Bint Depression Matted)> lesmlar Solution will depress FP by b86'o Tero. ‘ID) FTF Ya osm (500 mosm /L) will freene at -093' — -0486 @ losmelar solution exert osmotic pressure of 224 atm Plasma probes dae obi size exert tle comalariby (around 05-2 mosm/L flow cxmabic pressure = 25 mm Ha called eae Th hep keep Fluid side blood vessels, also play a im Aillration ¢ absorption of Fluid +4 Prins a Liver/ kidney diseases 4 Oncalio pressure = Fluid leaks oat into interstitium called ow oedeana [ELZSIEIEIN [esssssssssnsaszssnszscnszssnssncnsszsnsszansszszeszssessssssussssay, Ou Given by Fick's law Types Single Faciltabed «No comviers used. Ex: 0s /C0s diffusion. To increase vale of transport, carriers or - Depends on cone grand tranaptbrs ae used Ex: GT -.No sodurabional kinlies + High rates bub i deperdo on availa ot carriers > Saburabimal kineticsare) cone. (K) compenitive NON-CoMPETITIVE Was koa B ew cameGRD Cyuililyian & Merbyare etortialy [EFFECT OF K* TF rein reduced esd hyprkalais) > wore Kl come nk due fa more gradient v ae Biger EP (more -ve) -[HYPER POLARIZATION] er cod Ex:-40 mv bo -100 mv sao] EP pe = ~615 lag 120 ty ws ane lg 30 0 Te dad 3 5 EP = 65 Leg 20 = 615g 40 = “If theres high K oudsde hyperkalemia)» loss K* will come ont due bo wore gradient if perkaleia) > i od Lower EP (less -ve) .Exx:-40 mv bo -80mV DEPOLARIZATION. > Hyperkalemia -depdlarizabn > causes Ary Ex: ME, Freshwabtr drowning + 1 release rove deadealls > Hyperkalenio ite £06 changes = Toc ~Caleson quae bo stable wewdhrane > To prevent Arrhytenia“And. Tas blockers to ere: * Loe >Deplarzalio > ala causes past prey Hyphae -Hyprplrizon Lands fo 4 encase anokss gb wastage Flazid pals Ex: Con's gnome DEP valus d: roy oe CI" = -T0 mv —> more oubside , aniow > will create we pelentiok of -0mv Ca. Hoot tom» cabin coming inside il male ve EP = Sign x Pokontial in sv ni + Opa Gl gia . Te cakion is ging enb = -w sign (Ge:X') + Th cabin ging n = re sgn (uC, ne”) + TR enon 6 coneng im ve sg (Ens ch) + Trion gong abo pe Gus) Cation X 1s 100 Howes smoe cubsibe, Pye = 2 Sis 100 bats 2 ag 00 = 260 = RO mv Cabion -> comes inside © sign cL EPye = +120omv© Avion Yi 10 ines snore inside. EPy- = ? ts 10 Hes Lag 1 = 1x 602 6 mV Anton > goes ob bt sgn © EP. tomy ©) Cabion Z is equal inside ¢ onlside > EP = [MEMBRANE POTENTIAL ta 4o “Call swumbrane is seleckivdy permeable, v ~> Ab ait pera bo ee oa They ave called [BiFFDSOLE 18] athens i aac permable by Nat, CPO}, Paine ee They ave called: [NDIFFVSELE TNS “There ts equal distribution of ions azvess cM @ vesb called a.s Gibbs Downaw Equation Ex: Cabions = Anions bub Nat in IGF 4 Nat in ECF 16 i 10 of in EC er cor CATIONS: rs Nat a rms | oor | Proteins“Gibbs Donnan Effect: The dbribubion of dftusble ions is due to Boe presence of mdifusble ions. En lain 1 oan) ~ Du fo the difrnce tw conc, he ional tr bo mv along elecnechamial gradi bo achieve Equlibriune Ex: Na, Cai* 4 Cail wove inside ob * tics to move oub 4 The petonil in the process to EP ( Equilibiom ppletial Lb Lv NERNST EQUATION Paves EP Maraly depend en conc.oF ions. R>Gas constant T > Temporabure b> Nobural lg 2 -+Naleney F> Faraday cantar: cone. inside = +615 cone.oubside EP, stg + 61-8 cone.oubside. EP, cee c cone. insideVoloey: HK OF 92=1 $Me 002 Uy ale | > Thi forall waist Somég/t] — Somég/t | EP a Omv (0 EP, = +615 lag 50 = +CiSleg! atCi50 = Omv 1-0 ‘ igi on ie rt 2 Tt xt ouside = 500 mEq/L ess EP a +615 log 500 = +615 lagi0.n +1541 = +615 nV 50 on EP Values: Nat 60 bo +65 may > Nats cabion ,anove oubside, will move inside and creake +ve value fill Equilibriun, otis cabion more inside, will move oubside and creoke -vo value bill. Euiliniuom (-twv) +Coleulation of EPs : re Nat in cea 180-10 mEq/L Not iw 1oF = 10-14 ameq/L Pyat = +615 log 14 EP at m +615 lag =F O15 lagiO = +6151 = $65 mV‘Nain ECE (hypemabrenia). PEP. Ex: +10 or +60 mV From +60mv Calculation of EP Ket EeF = 38-Sq/L 64) Be? an) KT NGF 0-120 mEq/L (126) ite gt lg A (aki gd tye ata (log 35 =-Leq36) 2-615 0930 =-40mV,Oficial Notes Pariner: MH Yoleyadiacon 0) EE RP Penta across co @ rest (Net tering with channels, cone) > Depend on EP Tons gh mtenubrame permeatiiby (P) ) Pa 0 ft 5 0-9 Abb prmeadle ene 1 Fully porrweable “Th lbs hall imperuale te allons, RMP «0 ~The cali ally / Fray parma bellows , RMP 0 Ex: Tha calli ily prmvabl be Na? (Pai) = +60 mv (soy) J ene Hosea is hily permeable te Ga®*( Pai) = +100, (soy) omy Tha cal is fully prmectle do K"( Pai) = 90 mi (say) } eo mv Tha call is ly prmuable bo C"(Pa) = -10 wv (say) J + Simee our CM ( Neurons , wnascled) are alechively permeable a have non zero PMP )A call i realy permeable fo X,¥,2 ions .Xat20mV ,¥ut4OmV, Za? Si: Frey permeable op X+Y42 =0 60 0 "Za 260nV TF cabin mere inside (lag 3) > 1x 60m + Tf awion, it is mere outside. IF 2 channels blocked -> Create Depolarization ecto space.+ Nemst Equation > EP (Use conc.) >Gualdynen Hedekin Kobe Equation —> RMP >the EP of Prmeabily > Ru = So ot EPayy tip th Ur permeabiy (P) RMP = 5 (EPs X Pd) + (EPs X Per) + (ERX Fa) +E Page % Pas) >A reah, Pap ts obuast 20 (wren Galt) Rue = £(+comv x0) + others = Som + ethers (Kt, ct) Nat has 0 tole im RMP as membrane is ck permeable be Nat @ vest Hence RP depend wily on pervade / Affasble ions Cit ¢ cr) > Kis main Se TF it was permeable be Nat, wat KP > -ve RMP + [ActION POTENTIAL] v Change ply of auncbane Frm ange Lo postive value (towprary) ATP > ActiveTRA AL 6 ) EEE SESS EET 1 Neurons > 10 mV 2 Skeletal @ cardiac snuscle > - 40 mv. | AL-w wat de bo ke a Swodh sauscle = “80% -Thyrid, shade cochlea her eels (~mo to 50:07) 4: Rods 6 cones = 80 be =H0 my 5 RBC = -12miV (clase be zerd)Oficial Notes Parner ee (erchis of (Ye Faevons Arrecrwa RMP * Main fackar for RMP genesis Ki ~Mener ole in RMP gene Dey Raley HF gu bub leas thom Kc dave bo Nag permeatiiey at Par = 1 Cai) Pa = 0-4 Coin) Bug = 002-098 (py low taken zai) ne DN 1 pump < 2 Main amity — , B (domalimas small Fat) Main Bind Not", ATP gh has ArPose aby Blocked by Osan ¢ DeraLis ar, Uroreal Romp >“ Psion all cla bnoalaeral membrane ECE ugh | Coping Rao ~ 2:2 —> Ramps SH oot g 2 KE / Na duannel Paging egpnah grade asin Ar? 4 Apical, — [Pamary Acre Teansronta Tk maintains high Nat im ECF @ bag KT in OF > Help fw RMP GAP by CThrougheub ti) manning te grind “+ FF pump caps = No ATP , Ne RHP > 0 mv > Leche hyperion > 4 ATP Rap acy Damage mens + Bran as very lg demas 10-807. endine energy is used by pp atte 1007 axwobio Jot subrule be hype M i bo hyper (mul ated - hippocampus) > Raspnsile for mas ach bsp dy Ex: Gu, Kidany > Maina cll yams Ex: lb eng (Me Hyp) ‘ nt Production: organele offeced ~ Piet ‘ wt 1 pp acy tote Hh * we in Oe! eo a it Sep a foe a wide ais 81£08~-Cllor olin /lnly ollang ein ove ieee Endenncleaae » Lrveveraible inyng Gl dell / Nereis ecto space,Tt Mel 0, apply meer Pop storks woking 4d reburns bo® Collad Reversie.e Cour Insvey + Collis immertal if obundamb mubvients provided. fx: Hela call culture I “Ya TP anal ny snd ting / sl oman is by tha pap Howes att: depend thie pump This pump OMA by Thy herman Males: 31-42: kab r/o? TE ad lp ganas of RNP dey bab Females 30-35 heal / by | enly 10-207 —> vor eoxe (old pple 4am) + Tk is am cherie; pump > Ramps 5B cur 2G IN -,Neb less of inside the all + Crate ve value hp ne RMP quis RMP = RTD > Nat Kt, er tata) (eed) ey “Tn ype > Pap aps RHP re lard 0 Las -w > DEPLARIZATIO fe Eailily Cause Arey, SecaOficial Notes Partner, nn IPS? EPSP & LON CHANNELS cot Cuanaes In RMP sac Fring lel (-88 3) “Tigger 40 -Deplazakion is Exbany let i aii wale (Prove ATP gsi) “Dep ab sgmapss by Treas is £75? ( xctabry Pb Snaps Rata) “Hype ak synapse by nr rlnae is I95P (Toibitary Pb Snape Rata!) “Wardanono pee ESP 287 by ping Ty Charl ‘NConductance , 1 Resistance 4b t Current (1) Ea: Iy¢ Lye Sp hae by op 8h Eula by ve ce Wain exabalry Tin ons Open Ca¥ chasewels : Ca influx > Depol / EPSP ExsSle P— Stoll 0 lle (sora cart) Make # APs ies view bo 5 1 pain sonsahion erOpen K* chonnals : 1 efx —> Hyperpel / 2057 ae Ex: Opuide Init 5 ell vine J pid recpbor SereaerETIeSSC EY al Leas pen Aoaben rg 4 Dyan dans: C edn —> Hyper /ipp Tibi) Ex: Gagne spinal ord CL chavmel Open K* chav (1058) (58) Ex: Bacloten - Cenbrall Be: CAA mime — faailitabry muscle relaxant > Barbibvrabes Bensadiaepne: cS -> Cause cma, deal rsp depression *Sedatives Muscle nlanend = Amesthesian + Ani eas “hi elyEnhance Hypo “Blac nC hawnls Open 7° cals SA ts (5) ab ly HO Canes) NOMA Receptor © Katowtine / Xenon “ + Ex: Bealurobss — ; en Ue NDA A " : Casbrne VALPROATE : © Nat/ ca!” ch (© NOMN Ngee f : Ebb suxinide @CL/Kt ch (onBs) ae sash pep Ex, Aton DOC for Ex, Absence balers ila Nat / a3" channels open —» Daou. (Excite) 1/1 chavnels open —» Hroesra. (Suit) Ea) A dg Yak io Hf ch. opener > Hypael (Init) Blaed vessel edt muce "cal pevorne “Vadadlation +4 Daslin Eos Miva Ex. Dieu : Ve ot Tnsulinowen A) A dug 0 Clem, chal Mackey —> co J Heart HR, Antiarrhythmic VosodLation, Class HL. Ex. Verapaonil Ex. Dipine8) Local Amsthaios : Black Nat channel Anan. ‘lass 2 Block Nerve fibne—> Lass oF sensation GACross B08 Ea guessoficial Notes Partner qe (clic Petertial “Sao gnasis «Aron Hace > duc to mivimunn Bows Propagation sla fm iia: segment “Fellows “AU or Nowe Law” “Travel along 22am Local / graded paanbial Ex. 1050/6250 / cu? / £70 co. remain ak tw ike of. gunesis 6 dot follow “AUL or Nowe Lave” (0% or 100%) aja eel ap ls increased stimilus = Graded sponse / Elcbrovic. pdentiale Gene Pore “Higher the simulus higher Uae respenae . x. EPSP AY aide, The amplitude of AP remain. canslant under physiological conditions but we can f amplitude OF AP by: 3) Pat autide —s mare Nat enkar + Amplitude t ie Open swore? chanwals —> more Na nko «Amplibude + [Soe 4) Keap chal open for lrg —s mere ta ener «Amplitude t ‘+ Treresed ciulus cant change anpllade ct AP as per Alby Nowe Lew bub ib cam change ee) oNSA node on stimulation t Fag =f HR = Sanson rere ongoing biger sls will wake more APS (1 Freq) =P Sensations — called a [ober Fechner Law] AP I Nevaons) Only occur with Heshald stimulus > 15 wv +L danges RMP from -10 wi bo -55 vv Fring ln Voge gal Wt canes open wrization Start -due bo massive influx of Nat Go bil +38 wv called as spe potential / overshoot Na chavs case 6 dap is over Gogg) Jaan pm 1 gee uk gf ombrane will ela b> RMP (-10wi)-REPOLARIZATION ® @ sm gote ~ Activation gute gel Z7 me gate sh gots ~ Tnactvaion gab, Nat chav- Amother AP cam occur with, ctimulus t AE RMP: om gue dosed, bk gate open Nat cant enter’ LATE REPOLARIZATION = RRP 2-AE Bing lve gate pnb gale open. Wa enters ell > causing Deplasizakion 3: spike +1 open sh clase — Net cant enlar EFOARATION Prati am can ecarr [EARLY REvoLARATON ARPOficial Notes Parner Taper Rehractory Peyieds ea Nat OEPOL + K*—» RePoL. “12 hale ar low compared to Ne chal Corre (leAmsee) “Dang ale praise oh en pet mane pew RAP called at AH a After Hyperpelarization (40m from ~10 m\) “The period of rep. where wunbrane is abo, RMP is ADIBIANERDMpal. (-55 la -10 mi) “ir ole rpy cham ae ced mane ach aur Tawi equine 1 rested by. at = Stimulus: TEED sa | TT-—|ReFRActorY “ARP. + red which tinal cn caus gnu response (onether 48) ~ Gal ered be plc fom Arias alse prevent Tang) Tetons / Tani contraction Doped aly ep. (Me eh apni) RP. + Shrngsimulus cam produce response. —> (19 can eccur agne) + Eclope fs can produce abrrmal conan Ex. Fabra. systole / Eloi bako PVC = Remalure venbricular conraction + Rak prod for ons oF Aria + Lae repel. tear RMP After (crate -somi) | C55 te-10 i> + Lussexctable — | + Move exeable os ib sua ving lve oi> Teranic Contraction “Repealed stimulation makes wuscle ckay ie coubracton period qf fui fo reflex Eas: Auk qrahy scl daring upright pasture ee wire stigaalus —» Ae laa por waliple rpeakad imal Teasing Iepeney = LL — 1080. — 00H —> 10 sinals/ano ose Tomsee = OP “Ceci wuts shone no akony oH: hae Long/ARP Tae CP is inihed in ARP 6 RP cert Se,amalher stmules cam cause conraction only afer wutcle stot relaxing This allows beast by rola ond fillAD ar mma \., Early AD (EAD) AD a Lake AD (LAD) ssamsanensaneneanann: "tap “Tia post nea ring level (55 mv) Last part near Tome More risky Kt ch. blocker will. slow the repl. ft duration oF AD 6 TEAD 1 Frequncy ‘rik o Trades do Piles Aatenignss 1 sgt Ex.Class Tg co Low Glass Te Anlierrhytonc “i WWW = ANoficial Notes Paine ame 11 Jurchion & Excitation Cortyaction coupling mmm (wuss + Newremuscalar Samction. - NAAT ~idhon te val aurons Cea) in ade her fre thay wll las Aaya ak NM due ta La causing Exonytesia Be Mei Nake np (8) ff Opt Nat chan CPD) Conn onl Aselarzaion of alr endplate = [EB] (nd Pate Blea) ae Produces AP ken cress [Fina LEVEL] That APs th ba cling Sareclenoma, (muscle membrane) exile be ndasn Co via Tuber spam Mater End lake + igh pds) AP will trove along extension of sarcolemma, called ax T-tubules # Excite SR vio DHP Cal* Release of Ca? from sR vier Ryanodin Recepkor (RyR) channels Ca cause Exciration Conraaction CovPing wr \ ckEC caronG| By Ca >Co™ bind Troponin - gs diglace,Topemyosin Troponin —Tropemypsin complex prevent contraction by covering bre Actin chains Also called Relaxation Protein “Once brogomyasin is displaced 5 myoin head bind. Acin chains save fr cross bridges Troponin T3240 Troponin T5146 Akon cain ee a ration) ——) Ack ci eee ” tnt LL pe oe To rls rus, CP gous back bo by SER : Smsth ER Ca! My! ATPase pump Alter cB formaion , ATP bind ok Myosin head. ¢ baka by ATPase causes Power stroke - Contraction occur Maggs head big Sa altached. eke chains inward Thread enslaging of cans ¢ shoreing oF wel Re = conTRACTIN This call as Sto Fament Taeoay ~ by Hasday *Sirind, suse ( salad caring) have Daske (A) 6 Ligh (0) band 9% sud TTT“SARCOMERE: Bly Hhe 2 z ins = UNIT OF conTRACTION @-2'2 i) Puneiaeaannies line ale + Contre of T hand - Z Line eat HL zene Active bension in biceps Passive Lenson in biceps TBOTONIG CONTRACTION + Ackive>> Passive => Maveneub accier —» Work done, - dsobenieiconbraxcion, od) Leng ca CEfford) (Loud) (Length change) Load (tension) is save, (Eso = same , Tonio atensiovi) Exesmalking wl . drawing » Werk done = Force x displacennenb = Tension x Length change (AL)ISOMETRIC CONTRACTION] = + Ackive ¢ Passive» No movement» Nolen change» No work done CEfforl)— CLaad) + Teeweic conlraction ( Iso = same ,mebric length) Ex: Pasking against wa “Al conrachios bn a somuvic bu Length change (onevenend) they become ishonio contraction Ew:In systole 1* isovolumetrio: contraction. , Huw if vrricular presure 39 aks pressure (ackive bunsion/effort) ( parasive bansion-/ loa) ‘SL open #6 gjechion occur 4 Vol lang) change = Taconic conbracknOficial Notes Partner. Vetere Ee ectpephuysictegy of Cortinc Ti, uc + V8 Hark 4 sls (EAR oars SEES EEEEEETEEDEEEEE OTA 2 Types Tissue rile Tyla candace Auto thy tlemic. Combractile They marke automatics ARs which brawel, sie pln: SA —+ AV—+ HIS —s Bundle Bramehos Pakage Fibres To-roach muscles L Action Petential ine Cardiac muscle, = Combraction- (a) TTD (Fast AP) RMP fs -80-n0v Spike is +20 bo t30m07 “Firing lel ig ~10 bo-15: ay ecto space,Spike +20mi, Nach, clase (gabe das) Own Phase Early Rapid. Repl KF chopen Caf ch clase, IIREEEBY opal. Phase Late Re Na chen SEED Piahian, 1 Elan by 1 Rai Chases TARP: Prevent from Tetaany Firing lel 15 Anyi Kt Ebflux, = CoP Influx, Las ~domy RMP by Cait chaswncl 40m RMP Phonse, BE ong Acting . ia ma a aware a Cordinc Muscle AP One ee Ee: Neuron fl ek ro ER Kt Oh. Depal. Net the °| Platoon Yar ue Racer Gai th RMP APN NODAL TISSUE} Nl Phase Plateau (Ne Phase 1) = Dap (Phase 0) by Co channelsPhase 6 wot ike RMP oetler bssue (ResHass RMP) Tk move frome ~60aAy to Ao + uP Fig lee -—» Becomaber/ Prapoantiod Geto -to mv). —r Sharh AP Ionic Gass DEaarly closure of KF chaswels change © Leaky el Na chanel — fem aera :Mutor Rale (Hypiplncatin Atiaed- Chi Rapid Col’ chanmels: Make mewbrane reach Fi ‘ita forse tine) 601. Fis 7 palential +a0my Tt cha Bi Oapal pla pike > AP Prasat rteOficial Notes Parner Teacher aml acerrakey & Corductirg Syston GT (MuscLE | NODAL TISSUE | FREBVENDY OF “SPEED oF canovoTiON PULSE GENES erie FES on Ne: | rots osms iat decteman eee) | ee 6 | tae (@ Av Node 40-0 /nin o-05m/s “(Slwest) | soon) tardutog VeBundect nis | 40-co/nin Iafo SN a ste ges toe 0-40 /nin ems Yom F Mn} fe |” 20-tn 4an/s"(Fosteat) aes Compl} ‘Av Node 1s slowush in conduction + Dat bwin Gap jaclions, ¥ dame Tk praduce AV diay (01 suc) —> Pronk wenricwdar tachyeardia in Abril Flutter / Fibrillation 5 ot Saw bl paler in Father woth te dloy- Responsible For AV Back, CO: t PR Iuberal> 02 se Mast common canduction blockAv Delay emsines Alvar Vrricls veer contract at sane bine This haps it proper esa fling whew atvie contract os vorbis won conback allow filng bo take pace * Brine Fibs is Fasest iw conduction Due to max Gap donchons ¢ t die oF flres causing bwer reishance Parkin bres how bale Plateau Phase If Pacemaker Abontiab Phase TZ TARP Make ARs sabamabically “Heda Hse: Hh Plabuanbl hae Faeomater Blane A _\ MN, = Casrdiac Muscle : Plateau but no Pacemaker ee roa Parkin Fibres 5A thede cam make oe 100 APS in 60 Seo. AP iw 6s Minin Hn) - 8h nade will wake AD Well heat. Av node cam make max 6OAP i 60 500 S1AP in tee + TRA node op impulses Av Node becomes the mew Pacemaker Complete, Av Block: (i degres) —> Bundle of His becomes PM for vertriclas ~ Ang iss atest posible Fqveny of dscns ca come PM,* ECG wands aluctrical activity oF mainly muscles as vadal tasue 6 eonducking system axe insulated Eco R ‘vial Depolarization: B T wove: Verbiular Reparation. e 5 RS Complex: Venbriular DeplanzatonOficial Notes Partner GET bndie yd GE Carding Cycle: Tew summary st eveaks sceuring in one Hearh Beat Duration = 08 dee ad ible | Dasa | Contract ¢ Ramp blood | Relax fill Hood. Aer 0.1 see OTe 08. Contract fest enw) a 55 Venbricle 0-3 sue 05st = 0-8 See *Aolual venbviculer diate = 0:53.00 Actual venbicdar speedo = 020 ( 04g = 05sé) bse > Diastale = ax systole Gauss = Divakow obey He “ + ni flark Robi) Eg: WR = coin °. Ouraionsm $0, = (wee © © = 12)nin. Duration = © 208s te HR = 100/ivw '. Durabiany = 60m 0-6 er ‘oo => THR = ¥ Duration,+ THE cause # + T Work dene 204, Demand: + Made porbanh Fucker in Ce demand to HRs 1 HRs. Fa: Symp. Exercise y Aaa, Fear ee Camse 02, Demand Precpie cichamia in cad pants Angina 5 MI (Gt elaion 4 Tal. Tvs) Rearson: Death of bissue cause release of outside : tt Ktoreate current of gery F THR wil reduce duration of both eystele diastole but diastole wherhen mate SF Lass acai ls i “Anal stale ask puto vention dinate muemaen: Verbricular Dioskole “osseeOca Notes Parner: Helrpincne GG Systolic Phase of Cardiac Cycle QE 2Phans OF Cardine Gyles + [ERA Toc] eeoo=4s + Oss + Occur when venice labe diastole + akria, ised. (P- wane) seibed me area Frome: Sexceplarsmic Reticulum Conbrachions: 1 Prssure ave O1IVP called aus ‘oi wove © cose abe Aebive Vera filng (0) m Sy sound Praja incl ns ui Frgquney <20He fal. Ark VENTRICDLAR SYSTOLE] OTE “1 venbriles got dene sad = ARS Compl, Lack bo Replewize i wh te is 1 bo vepolani Hence, POLY is be-voplanine ioe “Mesttricular Depol. —> Ga! raease 5 contraction 1 VP (Veviadar Presure) vital al TVP > Abvial Pressure A are Nie Nate Closure oF AV valves: 5, Sound. Lsovalumebric Contraction : Push AV valves into Rt.abria § tIvP called. ass c-wower (Gonevd) IPVP >> Aorkio Pressure, ‘SL volves opew Av valves descend back into ventric Fe realtone te 2 Paorks Ofarly/ Rapid Fjestion Phase LP rise From 80 mma to 20 wong ‘eaeRVP rise From Hormatly bo 25 raalig =This big vP ease > 13" of Blood. Ejection low / Late Gectiow : “Fall vP deb loss oF Hood in Early Guchion igo “LUE fall from, \2ormmllg bo 80 mmy — {Rapid Goch Rapid Gece \sinw Gute omy be tomy {Rap ue yd ‘geton} RvP Fal from 25 mamtig to 10 mm Hy “Ths vss oly Yat Wed ta be juled se mainly due be forward momentum Atker Bais: fection: > Hho is further Fall inv VP 4 LP < Aorbic: Pressure: RP < Pulmonary Arory Pressure SL vollves close: Sg Sound, Aye Aortic Vadve clase Pub. Valve clase [CRITERIA FOR CLASSIFICATION | lllieazoom Systole Diastole al NN es fe, p95 Gary Mid Lae Scinecata ° + Si Se Syptole +Av dose ® fal. Pe Lsovolumetrio Conbractiow + No Flow vo Lee Sha = ~Siyslale —A9/PS: Mid systalic warmer ye Early Man ow ce ‘tt Hyection ala Labe #4 Flow igi oe ® ([Eekcreo mecHarucaL svoroce } ta a {Pet ca**.. Contraction. AV clase...5)=5,, Ne . Spptole starts From 0. wor) PSL LVET (Ge GuliwRed Opne Ct Vilar Gui Ton) Estimation: EC Pressure Rusard cownds by Phenocasdiogras ceed HSS a Whew aortic valve pew» ft Pressure jeOficial Notes Partner dhe GGttliastelic thase of Cartiac (yl a -18 ventricles got Repalared (T ward) Twawe occur whem vercrck, iv lake systl/ uch Dinclon Ecard bo Endcandums ir @ Intac buark It Toolated fibre: Golly Depa. 6 Repel are Exdecardivan 6 Epicardawe + Dering Rupa, Ca? is pumped bask bo She by Catt= Mg? ATP ance, pump (seges) Regulated. by Phaslanban Relaxation frog dose fy = Pro Diaslol -0:08 se oovdumabric Vorbricdlar Relaration = Daslle Roper - 012 see ote RA by Vena caves: have << tAbrial Pressure due bo Abad: stig f avec wae LA by Pale veins Av Vals open: Avia, Empy : HaVP y-deseanb Enaly Rapid, Passive Venbriculer Fllng Ged) = 54 sound Between 2 fing there is alaast ano Filloeg Bleed is stagnant + DIASTASIS ~ Min amationy ecto space.Abra: ylle = Labo Alive Vevicule Filling (Yard) «55 Sound Veabsgstole = AV values clase. © Iawvolumebric conbrachion SL open Ejection, Suche @ Dinstale 8: St dose @ 1 tay Leowluwcbric Rdsankon, —_ Efe ce Ms [Ts AV open Mid. Diastolic Murmur Op 0 wn ring 8 ea ned lee opm AV close @systole gb Dinatole + 2 parks. Olsorelamubric Pood. (Ve. waawe , Pressure changes) @ V6 change Paid: ( akon in sae Filing in Diaslle) Early “lade C4) ie) ecto space.Oficial Notes Parner Teper GEER eL une Pressure Changes & Vereus Kelty Qin [127711] jestaunssssuusassssussssevessssesessiseveisnseverssveveiassevesssses. 17) 7 + IvP- Jugal Venous Pressure Avalide Avegith v peas Fig av gel 8 fio Ely OBA essary = OV? (Noel bbeon RA ¢ e.g vin) 9 ove eve Candogene /Obdawchie shook, Gembval Venous Pressure: Shook Love : Hypovelamnic, / Distributive shock vue Blood Vol. @ val. bub accumulate im. CVonows Return) — Cold Shack — vessels - Wasrmt shock, = @ RAP = 0-5 ag aaa Clon = 136 cnthao) ®LA Prossure = Powe (Rbmonary Capilany wedge Pressure) f Pcwe —> tition —> fue Orden (525mm)ae es go ni\ he Drenstle Filing occur when AV valves open VSD: LR Shun | =P] pie P< Abviod: Pressure: Pas Systlio Marnuur (vou cuanaes} EDV : End Diastolic Volume + Tks blod filled in ventricle ob Us end of the Diestele +@ 120-130 ml Te dapend. on-— 9 Ventricular Compliance 2 Venous Raburn Bld ening back bo heart + PEDV wil t leads om venkrick evens bof eenbraction sbarts. Hence ik Ws called a Pre Land @ SU: Shrake Values “Tk ts blod pusped by venbricle pur beak +@ the tond Te depend Deov‘)eyocardil Contract OEE : Feet Frackon “Ibis haf bled papel by vel pu bah EF = Shree Vikome x 100 EDV. + @ 657 + The best indicaor of ventricular eHiciney 9 falure is EF d fr they li EF 40-457, @EsY: End Syokelic Veluwe, + This Heed en venlvicle a Ure end af syslale ESV Ebv-Sv + @ 40-50 ml Conse Seemasria : ® Vout. Faure Vol. Filled = £OV too mL oo wd Wh Pompedesv | oan Say Awad LL Pp ls Nol Left = sv aol com (Lov > L650): Ht Leaves sory teed behind 1 Pamped = EF ‘of vol tbFACTORS APETV] DGrrawvity | Poshure + = Min VR: = Shanding > Du bo ves pang in leg veins Max VR Supine —uple Aon a + On padre: ajusnent, He Fak change always oc nv VR a om stand bu (shag) ter, sv co LBP —> Syncope Orthastatic / Postural Hypertension @ deta Muscle Riwup / Peripheral Huaurl/ Anbi Graviby Pump: +The are call muscles —> Compress lag ve a Eq Slows a ey tve *Meck effective diving walking » Jogging eke (cori) @ Venous vans: Prevent bukflew in leg vans @Dusp cusgnaiow : Vry negative ITP ( Deep Inspiration -20 ment) Pills air towards (ereenions- tren) hung Bod bo hea: te‘te gil . (0-Smmty) ‘tens bem Coommig) fp Inerente while welling} @ sagmp. Nerves Do venocawstrichions vier ay receplar tve ¥ too © Deep Finis: Thick Tah ine bg Kop md in compres tve @ Candiae Panu: Exsrks force rom, Fro Vis-a- Fronbe J behind : Vis-a—Terge Heowt COKVR mC >" > aes BodyOficial Notes Parner GD Cayliac bulpul & It’s Applict Arpecty +00: Cardiao Oubpub led purged by each, vonbril pr min TT) EEE EEE EEE PEPE ECHO - Usa of heart + Visualize record all dunes, walla valves How obo ® Dve Duprion MetHod/ InpicaTo Dye Duvrion MeTHoD Co = Amawnbok Dye] 5 Time = Circulation time = 0-5%ee0 Cone. 1 Tie @ TueRMODILATION +I place of dye ld warm valine i used + Also colled Stewart Haswilbow Method + Caleb ct Frm Temp change Dilution methods ave not occuraty if shunts / Fistula /-requrgitadion, prasent @Fions Law, + Fer blood flaw #6 co Fer braiw blood Flow : Kety Methed. co = Titel bry ts cmap per wn Y) O% iFference (svt “iamld « Dfforace m Srl = Svl/io0 el= Ew: (0 I Tikal body & consumption por ni = 960 miler, —» {Dn cnareiev: tape 2000-2500 ml/min, nl/ine (SL /oin) Vom mas} con So anon & 5 0 Say orga consurna 50 lO mine Vo = Sel Organ bleed Flew = 50 1000 mal in © [G0= SV HA] » Sv dtrake Vol.» HR >Heart Rake = 0 wl X 12/ min ®co = 5t/min ie RV BLV om bn cere breadeether — -eLvievs | | ss-cause ning X v “AI las oe oul Bag °Tncorreck a= 5u/min > LY & RV Also SV, EDV, EF, ESV ee, ae same + Bub Prassures ane differnt Lve 2 RvP con SLfmin. a CP one Su/min Ry 26mm Ome Ly R= SL /min, Bedy 60-54) shi)ROL Shum Cyanaic Condition, . Eg Tetrlogy of Flt Tricuspid Abresir aeve Truncus Avberiosus + Lelb Ventricular Faslans (uve): YSV, SEF, co, LAP —> Condigenio Shock. Ace nd by nis liad Pa capris Gegtib tnd or cucing Pl congestion. Orda : Orta + PND Exersional Dyspnae Pine Froty pune ~rapbabiow ab inspirabory ms ob bn any + Right Verbmeular Fulure (eve): 4 Ral How YO Mismatch Opes Accumulation. of Fluid. im side of body causing 5: sbi Oedemo. “ Paid ody eng Span cgi “Ral Ordemar“Hepa slenamagaly stave (315 om Had) » Hepa dager Reflea Ascites Failure of one ventricle comans Failure of other ventricle also —>, FErananghan Grea: Eobmabion ot or (Ge onthapnea Oude, t3¥8) *Miamalah of 60 sanguin om ne side f Lchamia on othoy fu: Tt right heart Fails hangs went gob blood. ¢ Body will congust Tt btt heawk Fails —> Blood owt go to body 4 Cangustion iw lungeGamal Starling Law & Requlation of Stroke Velurc Qa Frank Starling Law (or) Hukero msbeio Regulation ¢ Cheng Ting EDV GV] ; Ev = End Diastolic Velunve Mechamnisen Tey «tv (within init) tSbakching 1 of Muscle Fibre’ Force of Contract at ete dey 7 thai Ties) Achin-Mysine Cros Bridges aa Mas cas bridges ¢ hence max bonson- ob Optimum Lgl (2-2-2408) + Tha if tread swore than, thas foee oF omubraction will decrease * Ow brteling pasve bain aps sing bil mphare /avng of Fle Lingle Tunsion, Relationship Failure, Taba Tension = Active + PassiveFRAN STARLING CURVE] + Lub shih /© Tovabropic Etfosky ar eo) ep (uainly ta") ety 5v( Dumbies Git) teow Tool tase ead Sar EBy (Lens) tore of conbrackon without ype! sock) changing the length tev ab wae EOV * Very high E0v + Ex: Monsive bleed branshusiow 5 AR» MR eke. (tt Pre loud) v Over stretching of muscl, fibre ia LFince of Contractions his ere eerie ies i) ver anu LoHE: Congestive Hoar Fare 5 curr chift ta sight vide Daring Excise : 1VR ue bo muscle, pure» ty symp deep inepurodions obo. Neov v \. Slaw tev vteow tar 1 Pl. Ou ashen A Bload. fog ong be veeciang mucde fee teov (thang) = FS Low tov by NConbrachion 2 Caffeine Thephylie : te AMP 1at* 5 tCenbraction4 Digtalis,Digorine - 82a by @ Na K* pup 4 Buercite 1 Masele mass (LVH) Concentric hyperbplg 5 THR : SV is Teppe / Sbaivade Effeck + iran alsa Is time oC ack ot Cai Rocuulaion: v Nowrachion Bab THR aloe toe demand: Reduce fingOficial Notes Partner. Teac em (aydiac bulpul & Ws Kequlatic [REGULATION OF Co] “Exercise : Bxdy nads more blod How hence Co will increase A to 5 times called Candia, Reserve, @= 20 te 25 L/min Athletes = 30 to 35 L/min Failure = L Reserve ea, ow exertion, wre cecicalin TMAECHANIGM FOR REGULATION] nce ni © SA, = fai Regalo [re ‘in ea, Open calif chanel ee oe ea conte eT Tis we = aa joe Ba het teov Tce: wal ree ainy due to F5.Law “Roding Weis oder pana symp cntrl called ax Vago kone “In Transplanted heart there los of vege tone Hance , Rusting Tachycardia Also soon iny Uv, due te 4 vagal Fone yw.con sv x HR “We Tt by oymg. Dus to LvF for componiation, vn abhltes, tVagnd tone causing Resting Eradycardia, SUK HR = 00 toYGEE cgieral Bleed Flew & Coyr- GT [TvPES oF 61-000 76.525 5 | CER ooo een OO OWhnd Kesoel Vessel + * Large elanstio arterias. Eq, Aovlar + Have elanstio recall * Busehit : During systale ywentrich, canbract to produce waysteli. pressure 5 flow. Alon, rte gohs stretched in spate During diastole, Aorkar will reccil imwards $8 compress blood invide Gives rise to Aortic Diaastalic Prossuae = 80mmty Sisble Gree ts Flow @Malaain blod How in dastle w av Se clase syste bt Gs Diallo ta Pal Ge tere er -, Aery ial Duw to elastic recall *PDA:L->R shunt iw boll, systole 46 diastole called ans Conbinuows Machinery Murenur Aloo im A-V Fistula, Od ge: oni Serasie —> Llc ez. Hardening of rte ‘tear, 108P + 1 PP© Gopocitance Vessel : High: compliance “Thuy sbrolol al scare bled: Acting os Bled Reservoir + Caav store ¢ conten 50-607 of botal blood, “Thay are Systewlo veins “They proven chock iw, ild. to wmederole bleed. lass : T symp. Vode tonshisbew (0) TVR, toworrds heart bo comp: msede bled: ask? Maintain EDV, SV, co 8 @P by @ : + Copaciby 4 ———____ @ vol. + + + > SQ ver Heart Bp Vein [Centar YoU]Oficial Notes Partner Gam Tyes ef Blood Vessels Wirdheysel & Capacitance mmm + Blood Flow Distribution. = ; Organ Blood Flaw lad. Faw /100 ge sony Kidngs t250/mb/min +3 400 wul/t0ogm/ mine(Maa) 15004 Liver (G07) |t500/omb/miw +15 | 100 wel toogre/ min 0g Brain 150 /ub | mine +15 Sombjoogm/min AtRast 20 000- 40,0004 Skeletal Muscles) 800- 1000/4 wiw+ 200) 2-A wl/ loogr/ mire (Win) 4004 Shine Jao famb fine 10-15 web/ cogwe/ mine 250g Heart l250/mul | win +25 too mL/ loogee/ min (bv) co SL fine + Contnay Bluad Flow : 250-nl/aine Dina = Maa Flow Biphasic ew f Systole = Mine Flaw : Contracting -anypcardiun wil squeeze cormany vessts passing Horonghe. Henew 1 Flew. “Almost zero Haw ite Isoveluwwebric: Conbrarciow Systole *Mect dachumia: prone Mase. Infarts (MI) occur in Sub Endacardivoworca notes Parner, MB Hayes GREED Types of Vesyel Capillayicy olan} Copilaries =o recall + Ne smooth muse + Vay permeable for exchange + Simple Squamons endathiliad cells : Capillaries are Fragile, so supported in by Pesicytes = Law Pressure (10-20 ml) + Law Vane ('57 ot blod.) Snag 5 R= Re fe Te Parallel: -—R, ae gta ea tat weet ey 2 eee Ry ste anathor Ry added m parallel Lg 4b 4848 m Re a -o5 Ry sivhen more capillaries ope. Ex: Exercise ~ Resistorce is creased +Arterioles ame auain site of Resistance ecto space,llavies sata ances snstional rein explains du te ions parallel velco few ( Weleciey = Flow rate) cont oft Maw CSA inv aorta, Mace, vwaocy Totter oe, Capilaries Aorta, Min diamabor (5-10Jani)| 24 sna diawacker (25004) "Mad on cae (Se) Mas. sh Min cn Min veloc Maze veloc Aorta, syeely vt An Better exchange Rapid Hood suppy Laminar Hw = | Tanbalnt sow Silene gb Ciconb Noisy #6 Inoue 30 REYNOLD NUMBER” the ee Laminar Flow yrold. Nuneber me >3000 Turbulent Flow ld Number = £1 f = Densil il Ae > 52 bem, = Velocity al Madly — Lew Reynold. Number — = Pens Veloc Most imap, Faschor ‘Slow Velei iy amp ei be Capillaries 45 Sonall atrweys+ Due bo min diameler, few ROCs 5 snore plasma, enter capilaries called a @ Plasnvar Skinoing : Tt results iw low Pov/Hemadecrit in SOSH eZ capil bled Fk Max PV i vercus bod ducts chloride itt / snbiaget Pnomenan: laude ger High, coe, + High Hoeg ~ Exchange al inv RBC TCI im RBC comse osmosis = P86 swallng « Pee tevOficial Notes Partner Fequlaticr. of Kesislarce QD ORE aan aa 6 Artvla:Ho see muscle entoael fale Change Regulate Bled Flow + Maan rusistemee vessels are Arberioles : Due to - Odsecth, Muscles: Mar a per diamaber % > *Vecoandlricion-wmostplicus — ~Macodilabin ~ few shes “fay, Kiduays GT gauss ke.» Bearing ules = bu Shack / Eeareisu + Sueat Glands + bers sLver + Give How iw Diastle+Acrba = Recall (Wind kassel vessel) + Exchange + Captllanien = Pormeable, Cluchange tess) + Shere blaod: Veins m Complamce * (Capacitance vessel) + Regal aed nies = Smad mode (Resilancs sel)“Antrilas offer scheme ob Tissue luvel ( iphery te heart) Hence Hcy aoe mala ike of PR = Pipher Redbone TPR ail t load ow venbricles which ack ondy aller contraction tart, Hunce , called 1s Attor Load: + Works done = Force x Displacesnaac aFxd at “eh te) 2.0 = Prussucre x Melua aa + Miterad PP Loo es) (eo oo tlaed by“Plead + 2 oubconas falters Chuwic Lad: Eg. Exercise in Abblobe | Chronic, HTN) AS / Hoch +, ric: hyperbro ‘AlterLaad, + Concentric, byperbply Orr. allure Hypertrophy - ‘teonntvation = t pressure cru F@/t @/ Pro Load : Dilated. /Eecenbric © v Expond chaybur = tVelumeoficial tes Parner, elaecco GG ervedypanics Bleed Flew Requlatic: [tooo Faw AERDLATION os “Hager Piguillos Equation. aed 5 Fx Blood Flow Pafhessave Gradient = (Arley Pressure Vin Press) Mainly arto Rm Resistance : ALL bak mainly artirieles @ swe Level “Dia eens dn Bhd lw Ft Same C/o > Hea sainbaivs almost Samu Oe bo itnnews Reba iw ll ed ta gps Cae Organs cade Hocr ew Hd Hw by changing their resistence called a Auto regulation of PO rgans wile ware flow at rest : Min resistance Organs wit win Flow af rest : Mar resistance gp Stalte smasces § skin + OHer mast, Resistance f bucome misia vite of PR Re Rast: 2 L100 go fie ~ During Exercise: Flow by 0-40 es ( Max Hei) [ Mae rauguet bled flow“Fa IP = # SBP dus bof SHR, av, too ete) +R [Massive drop R, whiele is tha mainy cause of TFlow— By Aulorgulaon] + Since the snnseles ane aint oF PR = During eve eerie, UPR = YOBP de fo Lome redisbonce [NEGHANIGM OF AVTO REGULATION 00 Exercise + fo, 4 1 Baed Demand: but Poor. Supply 7 Cause tigi” enn PAnaarabic Metabolism Shap Activikye— Fobique Lactic aid, thamp , tp602 , Hyporiar Aube lation steph Fi bmp 49600 » Hype oe Substance P, Aidasis bpH , t hemp. ‘ADP, Ademosian, to* eke. ~ Called as Local: Metabettas Right Shit of 0g Hb Curve * eellaon H pun more Capilarios Toe Release 1 Reviskawce ft Blead Flow“To hing hyp cans neem Poet Ventilation Pret Perfusion Lass wali — Sopa daony Hd sit Jo 09 ich avai Mantas leas ent on porr alec de be vesconabricbm | Ma Rabo + Aukoregulation odsunt in, TL Skiw Langs + Best aukoregulakn ine > Heart s Naw is Adenosine (Vasullaoi) Feit Aerie Mebuelson Hyper ‘pete Comaind) pt, -Vasedibabiow 4 Blocd. FlowOficial Notes Parner GREED Aue yequlaticn ef Bleed Flee + Best aackoregulabions See ime all Heart : Oy Adenosine ‘mainly Braiaw: Aerobic Metabolsvn Oy Hypraie #5 Hypercapwiar pee, Upto (onaitd) Noosodilacion Alensodilacbion Resistance, fem Sit], 9 = Vacasly , b= Lint r= Radios ar tla aa js " ema, Pl veal 18 Temp pelea it ve Mask inp. factor <4! power Taw thy 2m Ly 2" bas eine Le Langer engl > Mane rssh. Stems Vics ae ee Mle Ahr Lead VRpdee Flow tRiyshomie = LI niw + Mone werk = More 0, Demand Vol sane + Pre Load sameofc tes Parner - (QED Wethed ef BP (ytinatier LLL AT + Based om Bernoulli Theorew oni Enargy Perec atontanl fet 7 Padl ony fee ankery #6 make KE =O Toba / Prssare Ena is mearded * BMuthods of 8° Estiwabon + DiRecr INDIRECT vibra erboral cabluter |-Sphuguomanomeler: Recording BF et canons Orn entry ‘Nosh accra bk La | Taken low: Na sed, as ths invasive Karol Katt Sounds » Appear ( PhaceT)=S8P Tt sounds dank diseppear take Dasagper (Man), Phase mulling sounds iv DBP fg AR Pregnancy sAnenniar ce pate bas accurate but mad sid a ibis Non Tends fe give Fal high BP due bo tssne oer 4 sobaToreduce Bais ervor we wuse standard size cuff as per anni si Langtle = #64 oF Mil em, craanbernce Widlly = Ys"4 of Mid arm, draaference Adult ine cuff = 25 om X 125 cm Folée High Falee Low 8° Obese + Shin /ehildeen “Small café ~Leage Calf Si Hard ankevina | -Anscllakng Gap ine EgrArterinseleresis | Hypurlensive + Sound appar dang 0 Paried, + Elect of Gravily: Above Heasb - L BP Belew Heart - BP 1a Foms Hear = BP chang by 0-1 my To remove this emer: «Record. BP in, supine Tie cuff of Heart levelOficial Notes Parner Teac GD Types of BP & Factors Alfecting LY (oS LEED Ogee: @iMo-Hypeatenasion, “Thu dnt vob conbracion *Depund mainly om CO ese: @< tomaily (0-94), <60-Hypebmciow >40- Hyperbension, Tk us duet Elaabio Racal of ee = Depends sail om PR i rte too J emt copies = BP- Depends ew ne. oF bood malecules inside eter ee + too will thsae @ DAP (Outs pape) (Due to mare recoil) But SOP affected amore “1 tht 6 O0P Gut 08P affected, mone by PR changus aus diastole s lenge pidco > 58P PR—> BP @PP (Pulse Pressure) : + Indicode blood How PP =58P-06P| wow {PPA SBP-DEP fe Exercise 198° (Symp) iene 480 (vooudlation ¢ UPR) PPP = t load, supply to mses uvrty of Exercise «PP @Ma/ MAP + Muase Bod Pressure / Meow Areal, Presse © 45-100 nog “This og pss inane ding cxrdine jl Dinca lange (bit) it depends Map = 0BP-+ & PP 5 Da owe, foaeen, = 5B? + 8 Snort = sone (oop 18) axs " = 2008 + 90° S parks sage oe : Ys Sys MOP= $.08P+4.s8P —> -.MOP..% D8P+4.S0P2 = Be Re ~ Ror Total Ph (TR) BP = co KP c Anblgpronsins: HOP = 40 PL i + Radis by ry HL | Vasodilan -Diurebece rece | coe (Nibnadd) ACEI |p Bleck} acer pblocker | + Blocker “ball Recrcin| | veeofc Nees Parner, Peace Sb hegulie TERE] Ts Medulla Rostra Ventre Labial Medulla, (Rvme) Taal 4 Vasa Mobor Centre, NAmbiguons Nts + tSynep bo Heart 6 Vessels + sf Parassymp vibe Vagus tHe t07, 100, top eo a Deus supply vntiles 6 vessels Vogel time top heat V + Vorbis are fat be come out ot Inabion Sarl healing Hmadies: alld 0 wee + 80 te fof mine: io Voricalar Rta + Veg Tnbiit Abr ted Tiss vine Ade Aedes My Rarer, 2.57 tede Reduce Slope of Phase Yue” OAV Node Black 420 Lconducien = 6 Dromobrepi YP Lewatabiliby@ Batonabrpic + MC 4b cve are under conbrel of DENS Higher cenbras: Special situations BP CowbrelEe: Hypethalanaus im Exercie /Emolion, /Fght/ Flt eBaroceplns 4 Chamancepos Mainbain @ BP ee) Cer) Aap cand bus + Shree recaplos mainly ine Arterial walle Thay mainly regula Haat MBP 100 mtg Cath pi) bak mor eve ta BP Tag ak brakes (me Fadbck) - Ty shays. LOP 6 LHR va Duin oF ve ieady hein) vue See vagp ve fadback, \ via: NTS sense BR = Dushackion of OR ¢ Hair ners cause TH BP du fa lees oF VHC Inhibition coed ms Nearer Hyperbnsin Gabssuake wr Le +e ltr nasNere/ [esl MeL! ue En | fesiminte ——FgnCanbid Massage 4H + Locations of BR: fan “Ailes have resling Bradyeardin desks Beg Sag tone 1 Carotid Sinus BR: Bikkrcation of CoA 2 Aorbic Sinus BR” Arcly of Aurkay+ Range BR 51 cota Neo mig oF MBP boy mo Y Akin) Discharge stop Miw ea Max | (mae) Whe, MBP < Comm He Paps ning Ace no lc ebbing 62 Noes skew Mao eo wa @ 2G higher BP oven shun they ack tha BR Chae Kher BP een they @vMc:t8P 4 THR Sanna: 260-100). op eune ot Towards ® Valve aod) ‘eume eove tap ep BP(US reflexes [EBA BRIDGE REFLEX] = weg if nesting HR is low and We que iv fwuids — THR Medu i Aial sticte Stecepttc > t Symp and dinech stimubatiow of SAnode due to RA sbictching by Sv.plucde -BezorD JARscHREFLE = aye (chemo nefier) - caused by Venbreulay chemonecepters . ony giving SV imitate (histamine Capsaicin, Veratidine ete) Stimubatcs Ventricular chemoneceptv Nia vaquencwe roe Brady Candia vee (Hy potonwenn) Apnea (Jem pélang) [SB MaRevetAW ste due to banoneceptns (BR) mainly Seetv iw Bp We ; ,< oe pemiagicnt —_— hamged by Reflex conection patho pradeseet by Be, doug4(SHoek +) VBP > activation of Symp System Via, BR Pe l ee ae Refer tahuycondia, 2 CUSHING REFLEX? —TICT => Compnecsion of Coretnal vessels 1 CNS ischemia ie Dinect tax stimubabcow of Vie Ny stimubaticony of Be ap Partwalaet by vagus yowe tT SHR) - REbIca brady ‘i Candia, if Cut BR kthein newes LE g¥N) Now Wee get CITHRD : No maney’s lato oe Ne 18° SS Ue “CAROTID CLAMPING» - ENS ischerwia 11 BP Canolid BR = Bifurcation o coh B Sinus N- Brain cea VeClamp above Bifurcation) (above BR) STEP sim, LHR Refleabrady candi, BR Braiw damp below Bifurcation) : BR not ctimmated Brain tT Be —> THR een\;) eOfeat Notes Partner Bh iarpechacom EmMiway Classification, ressmres & Mechanics ef Breathing a [WIEBELS AIRWAY CLASSIFICATION ] —iiiiiitttitttttttttttttttttittititii@tsal -Langs are divided om the basis of dvisiow airways into mile parks 23 Gumeraitionss + Trachea : Generation 0 Browehi : Gemeration 1% Termimal Browchisle - Giew 16 Bronchiolas + Respiratory Bronchiole Gem 1, 18,14 sre Alveclar Ducks : Gemerotion 20, 81, 22 se Alves] ‘Gall abvel Aled: Genuration, 2374 a Raph >Exchamae Toner: Gu I be 23 Raspralng Grmchile Alea Conducting Zone: No exchange -Dead space Only Flow eceur Gun 0 to 16 Tracdvea Terminal Bromebvoleradia Terminal: Brwdde “Hanser rschamee [Mase meddle mowsce (aor o Fld) ae -Paglleorvia crag +b is tke tube awhiely Sassi callow How, has eazbiage £ > Brveledlalion Viv Be ceptors Pararsyenparthotio —> Browcho- ccorecbrichiow vir My. BOVLES LAW] + Teod Ga Equation: — [PVamRT] 5 P= Pressure V = Volume RT = Concha body => KH sIF wt , Hen PV one aloo t Tt nacanctant 5 Huw PV Consteml > [PV] : Boys Law tv ve.TPES oF HET) NNO +@ Inapinabion is Active Process bein rcs, Use ATP fer manscle contraction Expands Thora forward faubward | +P 151 Diaphragm ——Exkrnal Intorastals 257 Daphragu dcends L___ (t Verlaan) # Size Tha Curly v + Pressure (Bays lan) + Accossory smusclos : Sturnodeidowwasteid , Scalewe ete. + @ Enpirations is Poassive (No ATP 19 wed for musde contraction) mt is du te dastio recail of lange Forceful Euptodion is Active Process -» It woes ATP for contraction of Aedanaal: Muscas Inter Inerostol Compress hae ff Reduce Site ‘Pressure (Bayles Lani) bac Aon saa prshedinghrge wp[ResrieaToRy PRessvees] aso Niewephere = 160 army Anays oe Sache Bhi duc bs carlage Sha Pl Tw Avda taPa160 Flo /AlalarCaly - Opn Canty ae) IAP at west = Abe, Pressure = Te0 my oF Ora Palabive a ab pressure >TO? angus dain Raspraion: OA Ra = 0/40 mat @Dering Inspiration = 1/159 mg Tran expand —+ Less thar bangs TAP becormas ~ve alls air imeside LIL TAP is zero remo tnd ot nspiabon = 0/10 mi dunagexprabin = +1/> te mg Langs veal 6 compass air msde, ‘Aaak + TAP, becomes tve: Pash air ont bil ZAP is zero againtnd of expiration) Rests — 0/ 160 eumtle 2 layers pearar merge at hime Pal. Cont Plural Comity: Closed cavity Prieto Plea, Cou heron prssure + ETP: Iutrapleuval/ Intra Thoracic Pressure, Always EE] ob mest Brunt (or) 95 be Bom Ho (lonmiy = 136 om Hye)_Stab/ Hse Cheok Opew Cowie — - Air onber Pherae bill ITP is} Proumotharaae saws uoppased sel al aang 1 TTP ach as anchiow pressure #5 will pull Langs oubwards jbowandss theron The bendy of hangs tbo recailinmands 6 cadaper ba ib provid: by ve TTP ok vest “e e ae - % ' [TTP CHANGES DvRING RESPIRATION] OAL rest = -2 mei © quiet inspiration = Gamma (Thoror expands - + 11P; becomes wer -V) guint inp Gammile ( xpande . sien ) ‘AEpancion a ange IAP: becomes ve Ci) fir enter longsDanek inspiration = ~Bmamig « Bath Langs thorax, burn o@ size fl pressure @Foreabul_inaspivadions m -20 mol (eoy 0) 4 Feral exprabon = +20 be +30 mm Fortine jexprakny monccles aeuld be weed , compress thera g M11 — High TAP (Pach ar on freely TIP ob Apex = ~¢/7154 monty Big bat Few albeah sonal bu marmerones alvess T1P ab Bouse = -2/ 7158 ommg Oe te gril an Tine dapdant pak ot ngs FEET Ham Palmanany Pressure + Aeroos lange pressure TPP TAP=3TP) [TPP W Lang Vol + Ab rb a 0-2) = +2 mami Inspiration = = (6) = +5 mmilg Oper Prenmatharan = 0-0-0 milOfeiat Notes Partner ED (onpliac: ae Compliance = Sretchablty | SEE OGTATE OElasbio Tissue, a: Lungs 5 harta, , Rubber baad = Can bo cbretelied Good. Conplanen + Wil rd be @ size Good: Recel Ollgh Compliance Poor Recsil Fg:Emphysemor » Old Age Loss oF Elavsbive Fibre (Xe, Anhi Trypsin, Deficiency’) Poor Recall Rov Expiration ¢& Ai enadt cone out Air Trapping —> Hyprinflaled. Lange Ls Barrel Chast @ Inelastic Tissue iy Fibrosis. “er mpina er ea AL purenchymal Lang dinene cause por conplancr dae bs fois, mthmamaon te ar arel fash = au lain et a CARESS sespnakng ang (00) Al vlumies th eapacitis am poor + Eomphy sma: Higk, ConglianeeObstructive Lang ED. Raor airtlw dus be warrw civways complianen Conmplanee is @/* By Change m Va iid ange Posse Ig Pressure gives vlan o 200 200ml Pog > Combanee = au = @omptance — 00. /mnily (cog) + Am 100 mL /mmtg : Low Conapliane fy ro + Ba 0 wh mami High Compliance Fy: Emphysema LR She = ap0 = 300 ml/min Unit @ompant = $60 Ag» 26a SHE 98 « 2g = 00 lly capa Pes (mtg)[Types oF cowpuiance} O Stabe liawce + @ Langs = 280 wl fom to Langs + Thorax = 130-mb /em 40 laonge + Theta Redace complance dae be inelastic shmuctures “slalio amplanse is muasind by randing prsees gv ves whl aber Ite wel dopant on ois sever FOLD we ean gb Dstt complanea © Qyramic Compliance + Depend ov airway abso erm ova whl pains lvabhing Damien ott ag Tn 0LD—> Less volume coming ub Emp. prawn val Due be high ara vesstanen Op :nn Fabian mig oar fade ingroe Row Prssure Complamce: BL 4 Complanen +010 will show 4 Dynamic, Compliance ( Also RLO) Potabic Complamen ® values ven aint potFst aw reard~ Sakic Complanen See setts eB Ried. mphgsmar: Dyramie Djrami Compliance * at Teall “OLD RAD | OUD [Emphysemar Static |b [@/r | t Dypamic] + | + + Higher complancr + Stable Compliance Single care nso amber + Dynamic Compliance - Double curves Inpnto, “nga ie + Wonk of Breathing : Arco. under curve - [PXV] Higher compliance daning expat dus te surface bonsionOfficial Notes Partner: IM Vetesncadieccom TEND Suyface Tergien ard wifactart a= + Surface Tension? Inward force aching maximally at air fluid interface. Fluid Surface Tension Aluolus Oly Fluid left Surface Tension will try to Collapse alveoli Pull fluid inside ac —_ Ateletasis Pulmonary oedema. * Surface Tension will veduce compliance mainly in imspivakion ° ik causes Difference in mspivation and Expivation Compliance called as Hysteresis > We vemove air inside by filling lungs (cat) with normal saline > No aiv: fluid interaction | Exp > YST= F Compliance — curve Shift to Left side. Insp > also difference in expiration and inspivation is minimal. active spaceAir Filled lung > Hysteresis loop pe oy Dispeeee i" ine fil lungs : i * from Type # preumocytes and Clava cells (mainly surfactant proteins) Eee Make and Release most of Surfactant * Surfactant composition? i) 30% ave phospholipids, main is DPPC (Di Palmitoy! Phosphatidyl Choline) (Lecithin) ii) 30% ave Mutopolysacchavides , proteins. Eq: Fibrin ete. Suvfactant molecules cover water surface and veduce aiv- fluid intevaction —> Decrease ST. Surfactant production starts at 18 -20wks of fetal Life but secretion and action inside alveoli — 28wks onwards. Maximum Secretion and full maturation of lungs > 3U-35.ks. Increased Surfactant by Thyroid, Sex steroids , Glucocorticoids (main), active space.Action of Surfactant 1. Deevease Surface Tension 2. Prevent Pulmonary oedema. 3. Prevent collapse of alveoli mainly in expivation (as alveoli sige decvease Surface molecules comes closey te reduce ST much better) QO Ispivation — Expiration 4. lneveases Compliance 5. Decvease work of breathing - Make Breathing easy = Pre-Term Babies — Less surfactant and Tt Surfactant Atelectasis Pulmonary edema Fuud + Fibrin Ciyaline Membrane make Breathing difficult Pease) called as RDS. (Respivatory Distress Syndrome) active spaceofficat Notes Parner, Yepaedicom mm Pubrvorary Furction Tesh - mmm * PET done by Spivometer. * It vecords inspiratory and expiratory lung volumes and capacities. * Capacities —> Sum of 2 ov move volumes Principle of Spivometry * It records aiv going in and out of lungs but it fail to record the aiy that is nok Coming out of Lungs. &g: Residual volume (ev) 1, TIDAL Votume (Tv) * Normal — Soowl * Ik is aiy going im and out of Lungs in one breath duving normal Tidal Respivation. * Normal tnspivatory volume —> Tv * Normal Expivatovy volume —> Tv 2. INSPIRATORY RESERVE voLUmE (1ev): (@ — 3-3-5t) ° IE is maximum luspivation above and ovey Ty active spaceEnd of Expivation oy Rest. 3. ExPIRATORY RESERVE voLumE (ERv) : (1.3L) * (E & maximum forceful expiration after normal expivation or from Rest position. 4, RESIDUAL VoLUmeE (ev)? (1-2L) * It is Aiv left in Lungs even after maximal forceful expiration. * Since,Rv won't come out Spivometry fails to Prevent collapse during forceful expivation measure it. despite very High (TP + 3omwm Hg 4 Rv wow't come out due to DCA (Dynamic Compression of Airway) active spaceIntya Thoracic Pressure Lavge aivway Thorax * Extra Thoracic Large Airways + Intvathoracic Small Givway * €g: Trachea, Byonchi. * Eg? Bronchioles and Alveolay ducts. * Non compressible and + No cavtilage won collapse due to * $0, High ITP will compress these cartilage. Airways — DCA. * During Forceful expiration , High ITP will close small Intrathovacic airways (ven) before alveoli can collapse. $0, the air in alveoli wont Come out called as Residual volume At Rest Rv ev Closure active spaceOfficial Notes Partner, MM Tlarypcadicom mmm Pulrrerayy Furcticn Test - 2 mmm CLOSING votume (cv) + Ik is from I aivuay Closure in the dependent part of Lungs due to High ITP duving forceful expiration. * IE oceuy in Last part of ERV and when all aivways close , CV and ERV ts over and only Rv left behind. * Closing Capacity (cc) = tv tev Wt is aiv left in Langs after the closure of I airway Ww env ev is part ev (5 Aivway closuve | of ERV All airways close ce Rv * Spivometer fail to give Cv,Rvand Ce. ° For Cv = We use Single Breath N, washout | cv, Dead Space, Estimation “ gy Fowler method FRc. active space* We monitor N2 levels in Expived air. Aiv comes from airways (gives Dead space) then alveoli ~ Initially Aiv comes from all alveoli So, concentyation of Nz tn expived air is constant. The moment Ist Airway close in the dependent part the air from that alveolus won't come out changing the N, comentvation of Expived aiv. This is ew stating point, When no air comes out ,it is end of Cv or ERv both. * ln Obstructive Lung Disease, due to early closure of airways, there is aiv trapping (t Rv, YERv). Also Tee and tev. tu Obstructive eRviv 15 Aivway closure Rv tt active spaceLUNG CAPACITIES t_ INSPIRATORY CAPACITY (Ic) + Le is maximum inspivatory including Tv sce IRveTV , © 35-4 2. ExPIRATORY CAPACITY (EC) + Ub is maxinum Expivatory including Tv + Crervet , @—> be-20 3, FUNCTIONAL RESIDUAL CAPACITY (FRC) * Ak is aiv left in lungs after normal Expiration oy at Rest * Even ERv is left behind alongwith RV. + FROZERVeRV, M—>25L * Volume of Aiv in Lungs at Rest —> ERC OM muscles ave Relaxed J — Hence FRC is called as Relaxation volume. + Ak Rest —> ITP => -2mmlg tap => Ommilg TPP > +2 mmHg called as Relaxation Pressure. active space.+ AE FRE (at Rest) ,the inward vewil of Lung is equal and opposite to outward recoil of chest wall * The opposite recoils will pull both layers of pleuva and expand pleural Cavity ,fall in pressure to cveate Negative I7P. Very good lymphadic drainage of pleural cavity which pull fluid from cavity and maintain Negative ITP always. ESTIMATION OF FRC * Spivometyy fail to gi e FRC as Rv won't come out. © So we use, i) Helium Dilution method mount of Gas ii) N, Washout( Fowler) concentration change method * Eq: Looml Helium given 4 it mix with volume of air in Lungs (FRC) 4 concentration of Helium equal to 4 7. * FRC = looml - loom) = 100x100 = 2600ml = 2:51 ae Khoo 4 active space* In Bullae formation, Eg: Emphysema & less He /N2 enter bullae > under estimation of FRC in Obstructive Lung Disease because trapped aiv won't mix with helium /No Properly. * For FRC estimation in Obstructive Lung Disease we use Plethysmog raphy 4 Based on Boyle's law ina closed chamber, Pv product is constant Puvy 0 PeVe (chamber) (tang) fe VE = K Peve CERO aN, Pressuve measuved against closed glottis. to prevent lung volume to comeout, * If patient ispive —> ¥ Prung , t Pehamber ° IF patient expive —> % Prung > Pohambey AL VITAL CAPACITY + It is maximum inspivation followed by maximum expiration. * Ib depends on i) Strength of Resp muscles i) Lung compliance active spaceMaximum inspiration VvC= IRV +Tv +ERV End of Expivation oy Rest. Maximum Expiration 7 (Rv) Cusow't come out * Normal ve — Male > 4.8L _ Female > 3.2L (Alt values ave 20-307 less infemales dueto smaller thorax to less muscle mass) * Normal vc is move than 80% of expected VC as pe age, sex, Height ete. * Expecked ve —> AL —> Gor is 3-2U * Observed VC —> 3L (less than®) — < 80% W igo aet (itis@®) > 807 active space. Physiologically low ve seen in Females, Old Age, Childven, Shovt stature , Pregnant, obese, Supine etc. VC in Diseases 1 RUD? Restrictive Lung Diseases —> Vv VC due to poor compliance , all volume (ung capacities ave low. 2, OLD? Obstyuctive Lung Diseases. > Normal vc but increased time due to poor aiyflow. — Decreased ve due to air trapping (tev, teev, 4vc) * Eq: Emphysema — vc low Like RLD ,but compliance is high like OLD, pure obstruction with pseudo obstruction. * for Diagnosis of OLD — we use Dynamic Volume aud Capacities. Dynamic Volume and Capacities. eq: Tuc /Fvc — Timed / Forced ve * Ut is VC and Time taken AL in 3sec. — we divide Tve into 3 parts on Time Basis es Fev, ' Fev, Fevs active space* Feu, (Forced Expivatory Volume in 48 sec) ~ lt is aiy expived at the eud of I* sec. aa Duving Tuc — eg: Tue = AL » + Fev, % in OLD but normal Fev,/ im RLD. | Fev,=3L >> Fev > wowwert Fev, into Fev, 7 = Fev, Tve 2t wm child /RLD | x loo (Movmal = 45-807) * Noymal pevson can expive 15-80% of Tvc in IStsec. PARAMETER | NORMAL EMPHYSEMA Expected OLD RUD | (Mixed Features) VALUE ve | aL A@ | ayy | 2e(va) Fev, | 3L tu (+) | 1SW At (i+) Fev, | >5y B45 4b [757 @| 507 Wy) * Best Investigation to differentiate RLD and OLD is FEV, 7% x Normal Record ve ea Novmal WwW Healthy Ru Y Ww Oud active spaceFrow RATES © unit > L/min ov L/sec Forced Expivatory Flow Rate Flow Rates sees A in 26-45% of Expiration FEFR(0-25°/) / PEFR MEFR/FEFR (26-357) (Peak Expivatory Flow Rate) | (Maximum Expivatory Plow Rate) * Ik is maximum Flow Rate * Maximum flow Rate in the middle in the initial (257) of (Gov) of forceful expiration. foweful expiration. * Mainly from Large airways | * From small airways 4 (Diameter < 2mm) Mo BCA DCA occur: Lower value than Perr. *@value of Perr > 5-1St/sec | * @ mere > 3-SL/sec or or _300- 500L/min. '$0-300L/min. * MEFR — Gold Standard for Diagnosis of small airway obstruction. €q: Childhood Asthma. 5, TOTAL LUNG CAPACITIES (TLC) + Uk is sum of alt A Lung volumes (TLC % Lung compliance) active space.* Eg: Emphysema —> Big TLC ,duc to High compliance but poor VC. Catv, beev, birv) Very High Rv and FRC. * Tle = IRVt Ty + ERV4 RV, @— 6-4L . Spivometry fails to give Rv, ce, FRc, TLe FRO= ERv+Rv By Fowlers / Helium method. Rv = FrRc-ERv (Rv Ty Vv . TLezvct+RV eRv = IC+ FRO Rv active spaceOrficiat Notes Partner Haepeudiccom Alveetay,Pulrrerayy Vertilation ard ead Space VENTILATION Cunit > L/min) Minute ventilation / (av) Alveolay ventilation, Pulmonary Ventilation + Ik is aiy going in and out of * Ub is aly getting exchanged per lungs per minutes minute in Langs. * Pus Tux RR (RRI@>9 12-14 Breaths /min) = 5oowl x 12/min = 6000ml = 6L/min * Biv in Airways is not exchanged Fresh aiy (Soom!) N costed as Anatomical Dead space *@> bow * Measuved by o Alveoli All aiv is exchanged. $0, the value of alveolay i) Bohrs Equation (cor) i) Fowler method (N2) exchanged. dead space is Zevo. But if Poor exchange , it will be non-3e70. active spaceTotal ov Physiological Dead Space * Any aiy not exchanged "| eo Anatomical Alveolay * Physiological Dead Space —> Dead Space + Dead Space Physiological Anatomical * In Normal person —> = Dead Space Dead Space * If poor gas exchange , tucreased alveolar Dead Space. (Physiological Ds >> Anatomical Ds) * Alveolay ventilation (av) = (t1v-0s) xer = (S00-150) x 12 /min = 360ml x 12/min = 4200 ml /min = A2L/min. active spaceUcrtitation Hoxfusion Patio andl Applic Aspects V/q RATIO * Indicate Gas exchange Ideal Ratio: Best * ventilation - perfusion Ratio een exchange. + Va = Aix coming for Exchange /min . 4 Blood coming for Exchange /min * if Yq ti — Y/q mismatch. * if Qo — Poor ventilation if iq > 4 — Poor perfusion —> €g: Pulmonary embolism. Oo 6 6 St/min AU /mnin 5t/min Q=5L/min Q=5t/min Qzit/min Va = 5/5= 4 Ya= [5+ 0.2 Wa =Sh 25 Poor ventilation Poor pevfusion * If 3ev0 perfusion —> Q=0 —> Y= 0d Cnfinity) + High V/q > 41 means Airy >> Blood —> Increased Physiological / Alveolar Dead Space active spaceEg: Emphysema — Pabient is Hyperventilating due to Hypoxia (Pursed Lip Breathing) Despite that Hypoxia there is poor gas exchange Because of Destruction of Atveoli and Pulmonary Capillaries. Hence it is the only OLD with Diffusion Defect. * Best lnvestigation for Diffusion Disorder 4 DLCO (diffusion Capacity in Lungs for co) * Meate = 25 m/min/mm Hg * in membrane diffusion disorder it is veduced. * Yq mismatch cause poor gas exchange ¥ 0, Diffusion from Lungs to Blood @eause Hypoxic Hypoxia. (a Pade < 6ommHg) * Allothey Hypoxias (Anemic, Stagnant and Histotoxic) Pad, ® * © Ya for 5 —> v— Alveolar ventilation tung Q— Pulmonary perfusion by RV (Deoxy Blood) Equal to cardiac == Artimin = og (Whole lungs) output (c-0) — SL /min active spaceApex — V/q 1:3 (max.) Base + Ya 0-6 (min) Pevfusion—> Maximum at Base (due to Gravity) veuklation —> Maximum at Base (due to maximum Space / volume available at Base) Compliance — Maximum at Base At Base — Both ventilation and Perfusion are maximum but Perfusion is very high. Compared to ventilation. Hence /Q is minimum. At Apex —> Both ventilation and Perfusion ave poor but Perfusion is very poo. compared to ventilation Here /a is maximum. active space.@. Minimum ¥/Q at Base ? a. Poor ventilation b. Poor Perfusion C. High ventilation — Right statement but nok Right answer d. High perfusion. —_as High ventilation —> max Y/a. @. Maximum Y/@ at Apex 7 a. Poor ventilation b. Poor Perfusion c. High ventilation d. High perfusion. Q. Y/Q variations across bangs ave mainly due to : a) Ventilation changes b) Perfusion changes ©) Gravity 4) Compliance. active spaceQ. Y/a vaviations across lungs ave due to a) Ventilation changes b) Perfusion changes c) Both a) Compliance. Apex Ya -'3 (Air > Blood) Big ove infloted alveoli Poor (Patveoli > Partery > Pvenous > Perfusion Middle Y/q v4 Base V/e- 0.6 Parteny > Paw >Pvenous => zone i —> Waterfall effect (Flow Start) + zone % —> Partery > Pvein > Paiveolar > Maximum Blood flow. (Perfusion) + At Tip of Lung — Yq — 3. : + At Apex Ya-t3 (air > Blood) > Space aslegica in \ Aix not exchanged Properly. So, O2 is left unused in alveoli at apex Maximum PO, at alveoli at apex —> Hence TB (i) ak apical Lobe. active space+ v/a —> 4 Dead space mcvease eT ak ‘On supine / xexo Gravity sushole lung V/q = 0% vemain same 4 ak Base Vg t from 0.6 active space SS * 0-8 whole Lung Y/ammm Partial Pressures fla Gradicrt and Hypexia om * PP Partial Precsuve (Dalton Law) Official Notes Partner: * PP = % of Gas x TP (Total Pressure) $0% -02, 20%-Nz * TP = loo0ommHg * p0z = foommlg Cylinder * pN,= 200 mmHg Total Pressuve = 1000 mmHg * Latm = >Gommig = lookPa (KiloPascal > S-T unit of Pressure) ° 4kPas 7-6 mm Hg PP Values Gos Atmosphere | Alveoli Venous Arterial Blood Pressuve Pressure Blood Systemic = A6ommig | = T6ommiig Systemic —|(Post exchange) 7 Pada Pro, Pao. p% (27) | 150-160 mm: pests 3] oom | Guo-so mamttg| 95 -4emmllg plo, (0.047)| 0.2 wml Paton Py Cor Pa log Aowmunlig Abromallg Aommllg. PN2 (287)! 540-595 540 540 S40 wm Hg Dissolved Nz Dissolved Wa Can come out as Nz bubbles if low pressuve active spacePuor= Sommilg uw tat Bronchial vein Physiological Shunt Ik is mixing of pulmonary vein oxygenated blood with Bronchial vein (Deoxy Blood), Hence, PaO, is < l0ommHg. HYPOXIC HYPOXIA ae * Causes: 4) ventilation disorders ii) Membyane disorders ii) /Q Mismatch iv) Peyfusion mismatch active space* Ppao,- PaO, = Non-xevo due to Physiological shunt called as (A-a) Gradient. —> Novmal = 5-20mmHg. * Hypoxia (v Pao2) with t (A-a) gradient. * Pa0,- Normal but less 02 diffuse to blood causing 1 Pad, hence 41 (A-a Gradient) > €q: i) ® +Oshunt (stood Bypass lungs) ii) Ye mismatch iii) Membrane defect * Hypoxia with normal (A-a) — Ventilation disorders (Hypoventitation) dav = (ttv-1ds) x RR \ Poor exchange A Pa Or po (Ara) = Smmlg => Hypoxia 60 er active spaceOfficial Notes Partner: IM Vltegrcediacom C0 2 ard © 2 Tyargpeyt mm ee * 3 forms of Tyanspovt : i) Dissolved Coo —> 10% —> O4wly. ii) Bicarbonates —> 1S%—> 3ml% [Main] } Total Ami iii) Cavbamino form —> 16% —> 0.6m / €g: i) Cavbamino Hb ii) Carbamino Albumin. OXYGEN TRANSPORT * Sml or 250ml /min — Arterial Blood 3 L> 0, & t \4ml 7% — Total 0, content * looml Blood contain 14 ml O2 at full saturation , Sp02= 007% — Venous Blood | _ : ce a = thant % Cy spo,2 40%) “. Tissue Extvack —> Sml 7 0, at Rest. (move if excercise) * Venous Blood goes to lung —> Lung will Sul / 02 active space.* tom! Blood gives SmI 02 * So0oml Blood gives 250m) Oz Amount of 02 Transported and Blood pumped ' : Heart to au min(Co) Body consumption pey min (stfmin) Casow /min) 10, Supply /mnin = 0 x (A-v) 0, Difference So0oml /min x Smal ‘/- = 5000ml/min x _5_ = 250mI/min 100 — if we excercise = C0 x t(A-v) 0, Difference (62 Supply /onin) . 2oo000ml /min x toml / = 2000ml. * Uforms: (4Hb binds with 40,) i) Hb bound 02 ii) Dissolved 02 Hb bound 02 Dissolved Or 98-947. 1g Hb carry 1-33ml of 02 O3mi active space+ Normal Hb —> 12-16g7% C14) * So, 14g’ Hb will carry Jes 997 Hb: 18.4 ml 7% ~h * 14m) 7 O2 Dissolved 02 : O-3ml 02 * Pad, depend only on Dissolved O2 (Henry Law) not Hb bound 0, * Hence, in Anemia ¥ Hb, ¥ Total 0, but (W) Dissolved 0, and ® Pao.. active spaceOfficial Notes Partner: IM Vlstrcedizcom Oxyger Hereglebir Disseciation Cue RIGHT SHIFT * octurs inTissue: BOHR > tplor > p02 : Hypoxia, Excercise, High Altitude Talycolysis — cause TBPG a * €g. Excercise, High Altitude , Insulin, Thyyvoid Hormone , Glucose , Inosine * # Lactic acid * 42,3 BPG: Bind Rchain of HbA and ° 4 ps Acidosis 0, Release + t Temperature > Acidosis cause Y Glycolysis, 4 2,3 BPG. LEFT SHIFT * occurs im Lungs? HALDANE EFFECT * unloading of Co, and loading of 0, in Hb * HbA bind 0, in Lungs * HbF bind 0, in Placenta : DovBLE HALDANE EFFECT active space+ Factors causing Left Shift = i) t po, ii) V ptor iii) | Temperature iv) V2.3 BPG v) t pH (Atkalosis) vi) Stoved Blood in Blood Bank (low Temp 4c) vil) HbF: 20and 27 Globin chain (No [3 chain) No 2,3 BPG Binding Hence HbF has higher 02 affinity than HbA. $0, HbF can extyact 0, fas maternal HbA. Hence, fetal survival occurs. vii) CO Poisoning? CO has 210 times move affinity for Hb than 0, $0, it is used for Diffusion Studies (Dio) 't form COHb — Carvboxy Hb —> Abnormal Hb which fail to Release 0, to Tissue. (Left Shift) —> Death oceur, — Ik is Anemic Hypoxia. and also Histotoxic Hypoxia as CO inhibit Cyt Puso (Etc) but at So times lethal dose. Hence it is mainly Anemic Hypoxia. active space