Important: these are LECTURE NOTES written by our colleague Shaimaa, it is not the original sheet.

Transcription

1 Respiratry System Physilgy #6 Lecture ntes Imprtant: these are LECTURE NOTES written by ur clleague Shaimaa, it is nt the riginal sheet. it's imprtant that we dn't waste lts f energy t breathe. the energy we use is very little... the wrk f breathing which is equal t hange f vlume x unit change f pressure change f pressure therefre wuld be mre than expected in increased wrk fr example -1 t drive air way, but t drive air ut is nt k. +1 is nt enugh, +10 means yu havemre breathign wrk the wrk, we use ATP t vercme tw types f frces: elsti frces (70% f wrk), this cmes in tw frms: surface tensin (2/3( and elastic fibers (1/3)... these elastic frces are static ( vs. dynamic) when there is n airflw. secndly, nn-elastic frces which make 30% f the wrk and is f tw frms as well: airway resistance (Which we will talk abut tday) makes up 80% f these frces and tissue viscsity is 20%... elstic frce smanifested when there is n airflw; with airflw yu need additinal frces t drive air in and ut... it is difficult t drive smething vs keeping it at the same place (static vs dynamic)... think f ismetric cntractin f the muscle while carrying smething think f this example: when yua re breathing, yu air inflating the balln and t d this, let's assume it's clsed...t keep it inflated yu need an ppsig frce (the negative pressure) the balln is tending t cllapse with +10, yu need -10 pressure. Hwever let's assume an pen balln and yu have an airway. T drive air in, yu have t vercme the rsitance in the airway... when there is n airflw, yu cancel the airways, yu nly care abut the clapsing tendency f the balln... therefre during airflw, yu have t vercme 1) cllapsing frce f the balln and 2) the airway resistance think f clay: stretching it needs frce, and t return it yu need a frce as well:: nn-elastic... vs. alveli: there is surface tensin = cllapsing frce.

2 Respiratry System Physilgy #6 Lecture ntes therefre tw types f frces... ne is static and anther is dyamic static frces is elastic frces which takes 70% f the ttal wrk and dynamic takes 30% in nrmal cases; and each have tw cmpnents... viscsity will ppse mtin in either directin; cllapsing frces yu shuld apply frce in ne directin and in anther it is passive... dyanminc: 80% airway resistance and 20% frm viscsity... tday we talk abut airway resistance... a persn wh is a chrnic smker: t test his airway resistance due t smking, we perfrm the fllwing: he expired which has 3 phases in a t vs vlume graph 1: he has exhaling, cmpare t the LV: rapid ejectin and filling:: the first part leaves when high flw ccurs... the first 25% f the VC, the first L will leave easily in bth nrmal peple and patients... the last L will leave with difficulty in bth as well. Therefre, the middle 50% is where the difference lies. therefre if we cancel the first and last 25%, we end up cmparing the middle prtin and here we can see thee difference. fr example FEV 1 / FVC = 75% and the nrmal is 80%. 5% is nt that significant, r s it's assumed... but if yu cancel the first and last 25% and just take the middle: mid-mean expiratry flw yu will see the difference here might be duble. This is why this is a mre sensitive test: thef irst was diluted in the first flw and slw flw in the last... yu are taking th emiddle ne. middle vital capacity / t = 3.5 L/ sec nrmal this test is sensitive, but perhaps we can lk at smething mre sensitive. let's take a lung with an intra-pleaural pressure f -8 at the apex and at the base therefre the alveli are mre inflated at the apex than thse in the base that are partially inflated.

3 Respiratry System Physilgy #6 Lecture ntes when yu take 500 ml ventillatin as yu remember frmt he cmpliance curve, at high vlume the lung is nt mpliant. yu cannt inflate an already inflated alveli. which means that mst f the 500 ml ges t the base rather than the apex... therefre, ventillatin f the base is mre than that f the apex. secndly, the heart: it's much easier fr the heart t eject the bld t the base than t apex (due t gravity, in standing psitin).. the perfusint base is mre than that f the apex... these are in their abslute terms, what I care abut is relative. Abslute ventilatin/ perfusin is insignificant, yu care abut the perfusin/v entilatin ratin (and wasted perfusin r ventillatin) let's take a curve f perfusin ging frm the bse t apex (base: max, apex: min) ventilatin is als higher in the base... ventilatin/ perfusin ratin is less than 1 (yu have mre bld in the base) in the apex it is mre than 1, mre ventilatin than perfusin. what des this mean? the apical alvelus: where we have mre ventilatin than perfusin. What wuld yu expect the po2 t be? (emblism: n perfusin, the po2 = 150 (like that f the utside air)... but with a bit f perfusin, it wuld be between , clse t 130 as an example... what wuld be the pco2? Less than 40 and the ph2o: 47 and pn2 = the remaining... let's g dwn t the base where have mre bld the ventillatin. the po2 here wuld be < 100, clse t 90 mmhg. ask the patient t breathe pure xygen (100% xygen)... mst f this xygen is ging t the base because it is higher than that f the base (abslte ventillatin). SEcndly, perfusin f apex is mre than that f the base.... missing infrmatin.

4 Respiratry System Physilgy #6 Lecture ntes when we tak 500 ml, assume 400 ml went dwn and 100 ml abve. the 100 ml are nt ging t dilute the air like thse f the 400 ml, therefre the nitrgen f the 400 ml will decrease... at the end f f tidal vlume, pn f the base < apex. while exhaling, we analyze tw things: nitrgen in expired air + the vlume. --> Vlume vs. nitrgen graph the first phase has n nitrgen, because it is pure xygen f the ADS. then it slwly begins t increase, which cmes frm bth the apex and the base: the air is cming frm bth. But if a persn has slight degree f increased airway resistance, which will clse first? basal r apical brnchiles? the apical are surrunded by mre negatie pressure (-8)... while inspiring, the basal ne will clse, s the last prtin f the air cmes frm the apex, and this air cntains mre nitrgen- yu can see early changes in the airway resistance... s the last increase f nitrgen (clsing pint) cmes frm the apex, and the basal brnchiles clse. clsing vlume, a very sensitive test which can dedict early bstructin in the airways. Befre we understand the clsing vlume, we must als udnerstand ther things the firs tf which is tha tintra-pleural pressure is nt equal at different regins f the lung: at the apex mre negative than the base int he apex means that the alveli at the FRC (befre taking Vt) are already inflated. When yu talk abut already inflated alveli yu g back t the cmpliance curve where the tw ends f hte curve, they are nt cmpliant at small nr large vlumes. Nt cmpliant when the alveli are partially inflated, cmpletely deflated r almst cmpletely inflated: the lung is n lnger cmpliant yu take500 ml which g t the alveli dwn t the base ebcause it is **** due t gravity: mre t the base > apex.

5 Respiratry System Physilgy #6 Lecture ntes mre ventillatin and perfusin at the base but the ratin f v/ p, we will realize that the perfusin is mre in the apex, less at the base. mre air: cmpsitin f the alveli air is clser t that f the air (apex). when yu tkae in 500 ml, 400 ml g dwn (pure xygen), they will dilute the basal air mre because the 400 > 100. S the nitrgen at the end f Vt is less and the apex will be diluted but ina smaller percentage... s yu have tw areaes f high and lw nitrgen and tw different pressures, ne where airways are nt prne t clse (the apex) and the thers are susceptible t clsing if yu make the intra-pleaural pressure less negative if the ther airways are stentic, the airways are prne t clse in the base than that f the apex. when we inhale, pure xygen in the ADS which is als exhaled (pure xygen, nt nitrgen). the air in teh secnd phase: gradualy increase in nitrgen 3rd phase: cnstant level f nitrgen in actuality, it is 4 phases... at te end f expiratin, intra-pleaural pressure less engative and narrwing --> basal airways clse, the air cmes purely frm apex which has higher nitrgen and s suddenly (phase 4) nitrgen rises up... therefre the vlume difference between 3 and 4 is called the clsure vlume: after the basal brnchiles clse, which shuld be 10% f the VC,smetimes nrmal peple reach clsing vlume at the RV:: meaning that the last ml is cming frm the apex and base. but at the age f 40 >10%,c lse t 20% f the VC. we spke f airway resistance... nw, t talk abut the clinical pathlgies: COPD (emphysema -- t much air in the lungs and 2) chrnic brnchitis)...

6 Respiratry System Physilgy #6 Lecture ntes pure airway resistace: brnchial asthma, which becmes chrnic and becmes classified as COPD (early stages are nt COPD) mst f the asthmatic patients recver ttally (90%) especially when they start with the pathlgy at a yung age. emphysema and chrnic brnchitis verlap: every patient suffering frme mphysema has sme srt f chrnic brnchitis, but mst f the clinical picture cmes frm emphysema if the initial pathlgy is that emphysema is a very cmplicated disease becuse it invlves destructin f the alveli, which causes the destructin f the respiratry membrane, the area abailable fr diffusin (surface area), destructin f the capillaries --> destructin f the barrier t be ventillated --> increase pulmnary vascular resistance. the are is reduced, resistance is high... increased resistance, yu must increase driving frce t maintain a nrmal CO, driving frce an be increased by increase pulmnary arterial pressure which nrmally fluctuates between 8-25 mmhg (diastlic and systlic respectively and the mean is 2/4 f the systlic)... pulmnary vascular resistance is nly 1/7th f the systemic vascular resistance and we knw that because delta p/ resistance = Q1 = Q2... Q2 = 100/ TPR... calculatins. s destructin f ne capillary reduces the area, increases resistance, increases pressure, increases afterlad f the RV, increasing its wrk... RV will underg hypertphy and then dilate... RV hypertphy +/- heart failure (which will eventually develp in its absence) due t lung disease/ prblem = rigin will reside in the lung, regardless f the cause is called cr pulmnale... therefre ur issue in emphysema is nt a pure bstructive disease but a cardiac disease: area available fr perfusin is reduced, therefre we must test the diffusin capacity f the lung:: hw much xygen is allwed t diffuse frmt h ealveli t the bld?in this case, the diffusi ncapacity f the lung is less than nrmal... incrase pulmnary vascular resistance/ increased arterial pressure/ enlarged RV.