Respiratory Medical Board Review 2020 Final

[00:00:00]good day everyone i'm tim esternidat from the department of pistology and i was tasked to give you this review on respiratory physiology okay so what i intend to do for the next three hours is discuss to you these 13 concepts which deal with respiratory physiology let's now discuss the first topic which is the changes of auto tension from the atmosphere to the venous blood so this is the first interactive question which of the following occurs to the atmospheric air during ascent to high altitude a is it atmospheric pressure increases b the f i o 2 remains constant c nitrogen concentration remains remains constant and the the inspired oxygen tension increases so what i want you to do is pause the video try to answer it and once you have an answer resume your viewing so let us now discuss the gas composition of atmospheric air which is composed of nitrogen oxygen carbon dioxide and other trace gases here the relative concentration of this gas is 78 is nitrogen 21 is oxygen carbon dioxide is way low at 0.03 percent so if we're going to inhale a tidal volume of 500 cc okay 28 78 of the 500 cc or 390 is nitrogen 21 of the 500 tidal volume or 100 pipe is oxygen so let's now discuss the inspired gas tension of atmospheric air at sea level the atmospheric pressure is 760 millimeters mercury and therefore if we want to compute for the inspired nitrogen gas tension we just multiply 760 with the concentration of nitrogen which is 78 percent and therefore we come out with the inspired nitrogen tension up around 593 so if you want to compute for the gas tension of oxygen in inspired air okay or the pio2 it's 21 times 760 and therefore the inspired air gas tension is 160. now if we add everything up we come out with a total of 760.

[00:02:35]this is based on dalton's law which states that the total pressure is the sum of the partial pressure of the individual gases now let us discuss the changes in atmospheric pressure from sea level here is a graph showing to you the relationship in the x-axis of altitude and the barometric pressure on the y-axis and as you can see based on the relationship okay the greater the altitude the lower is the barometric pressure now here is another graph showing to you now the relationship between the depth between beneath the water surface in the x-axis and barometric pressure in the y-axis again you can see that based on this relationship the greater the depth from sea level the greater is the barometric pressure so if we put this these two graphs in an equation okay you can see that the greater the depth the greater the atmospheric pressure the greater the altitude the lower is the atmospheric pressure now here's a table which will show you the different oxygen tension of inspired air at increasing altitude as we discuss with increasing altitude for example at 7000 feet the barometric pressure decreases to 584 and when we try to compute by the oxygen tension okay we just multiply 580 part times 21 percent so the inspired oxygen tension goes down from 160 to 122. now what will happen with if we further ascend to 36 thousand feet will the pio2 be higher or lower than the 122.

[00:04:24]okay at a higher altitude the barometric pressure decreased further to 170 and 21 of that is 36 percent is 36 millimeters mercury so what i'm driving at is with increasing altitude the pio2 remains constant but the atmospheric pressure decreases and consequently the inspired oxygen tension decreases so let us apply that principle with that of air travel now during international flight k the cruising altitude is around 36 000 feet and at 36 000 feet the barometric pressure is 170 170 the inspired oxygen tension is 36 and this is not compatible with light so what would the airplane manufacturer do they're going to pressurize the cabling pressure to 7000 feet and at 7000 feet the barometric pressure is 580 poor and consequently the inspired oxygen tension is 122 and this is compatible with life thus if we apply that principle of air travel in this table we can see that the crossing altitude is 36 000 feet and the inspired oxygen tension is only 36 and that is not compatible with light so what would the airplane manufacturer do is they're going to pressurize the cabin to 7000 feet and the inspired oxygen tension will be 122 and that is compatible with light thus during air travel the cabin is pressurized to 7000 feet as if the passengers are breathing 15 percent a pile or two let's now move on to deep sea diving and boils law boyle's law states that gas volume varies inversely with pressure pressure times volume is constant and therefore if pressure is going to increase the volume is going to decrease this is illustrated by this carton over here wherein a person is going to dive to 165 bit of salt water notice that the barometric pressure increases from 1 to 6 atmosphere and notice the corresponding decrease in the gas or the lung volume from 100 percent down to around 10 percent and therefore the greater the depth the greater is the barometric pressure the lower the lung volume gas volume is the sudden ascent increases gas volume and this may predispose to borrow trauma and air embolism and this cartoon will illustrate that if for example at 165 feet this is the gas volume and the pay and the diver is going to suddenly ascend the pressure is going to decrease tremendously and the volume or the gas volume is going to increase and may cause structure of the alveoli thus you have barotrauma this air that's going to escape from the alveoli may go to the blood vessels and produce air embolism now in henry's law it states that the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas and therefore the greater the depth the greater the pressure the greater is the molecule in liquid form this is illustrated by this carton over here wherein at sea level for example pip pipe of the 15 nitrogen molecule is in liquid form and when a person dives around 50 meters around 10 of the 15 nitrogen molecule is in the liquid form this is another way of looking at henry's law if for example a person is going to dive around 450 meters the barometric pressure will increase from 760 to 45 60. consequently the nitrogen tension will increase from pipe 93 to 35 56 now nitrogen is a pot soluble substance it crosses the blood-brain barrier it may act as a pulsed neurotransmitter and the diver may manipest with nitrogen macrosis aside from nitrogen causes because of henry's law a deep sea diver may develop decompression sickness which is usually secondary to rapid ascent again if we go back to this illustration here if there will be rapid ascent most of the molecule in liquid form will be converted to a gas sperm it is similar to opening a bottle of coal if you open the bottle of coal there will be a tremendous decrease in pressure here and there will be bubble permission and this is what happens during the compression sickness a rapid ascent will cause bubble formation in all of the tissues including inside the blood vessels producing air embolism thus during deep sea diving a diver may develop biotrauma and air embolism due to boils law he may likewise develop nitrogen causes decompression sickness air embolism due to henry's law so we go back to this question again which of the following occurs to the atmospheric air during ascent to high altitude atmospheric pressure increases that's pulse we know it decreases f io2 remains constant that's true nitrogen concentration remains constant that is likewise true and pio2 increases that is pulse because pio2 is equal to barometric pressure times the oxygen concentration so the correct answer for question number one is f i o two remains constant and nitrogen concentration remains constant moving on to question number two which of the following explains why the arterial oxygen tension is much lower than the alveolar oxygen tension a upper airway humidification of air b low atmospheric pressure c bq relationship in the normal lung and the leptoright shunt due to bronchial circulation again i like you to pause try to answer and then resume now these are the different compartment where oxygen tension may deeper you have atmospheric air then you have air in the airway then you have the alveolar air then you have oxygen in the end capillary oxygen in the pulmonary vein oxygen in the blood in the pulmonary artery oxygen in the tissues oxygen in venus blood oxygen in the pulmonary artery and finally oxygen in mixed venous blood the inspired oxygen tension is 160 while that of the oxygen tension in the airway is 150. the question now is why is there a decrease in the auto tension illustrated here are the functions of the upper and the conducting airway the ambient air or the atmospheric air has a temperature of 22 degrees centigrade and a water vapor pressure somewhere between 0 to 10 millimeters worker as it passes through the upper airway you can see that it is warm and humidified as it goes further into the conducting zone it is further warm and humidified so the cause of the decrease of the auto tension from 160 to 150 is due to the humidification of air by the upper airway and the lower airways conducting zone so from 150 the oxygen tension in the airways goes down to 100 part in the alveolar air the reason for this is the diffusion of oxygen along the ac membrane as mentioned alveolar gas diffuses along the ac membrane into the blood in the pulmonary capillary initially the mixed venous blood is sporty and at equilibrium the end capillary oxygen tension will now be 100 per plus minus 2. if the bq relationship of the respiratory unit is 1 then the end capillary auto tension will be 100 poor however if the bq relationship of the respiratory unit is less than 1 then the auto tension will be less than 100 bar on the other hand if the bq relationship is more than one then the end capillary auto tension will be more than 100 poor on an average the bq relationship of an upright lung is 0.8 and therefore if we average all of the respiratory units and capillary auto tension it is going to be less than 100 from an end capillary auto tension upon 100 plus 2 the arterial oxygen tension now becomes 100 now what is the cost of the decrease from 100 poor to 100 primarily it's due to the presence of shats and these two and the two types of chants could either be albiologians these are the respiratory units with the low bq relationship or the anatomic shunts this is an example of your two anatomic shunts okay you have the bronchial vein to the pulmonary vein and atomic shunt okay the bronchial vein contains the oxygenated blood coming from the bronchial circulation it is at mixed with the oxygenated blood of the pulmonary vein the tibiation vein left ventricle and atomic shunt as shown here the deoxygenated blood coming from the left ventricle drains directly into the left ventricle which contains blood rich in oxygen from the arterial blood of oxygen tension of 100 the tissue auto tension goes down to 23 this is primarily because oxygen is consumed by the nitro mitochondria or oxidative phosphorylation from a 100 arterial oxygen tension the oxygen tension goes down to porti in the venous blood this is primarily because of the oxygen extraction by the tissues so we go back to this second interactive question which of the following explains why the pao2 or the arterial oxygen tension is much lower than the alveolar oxygen tension so it's asking us why is there a difference between the alveolar oxygen tension and the arterial oxygen tension is it due to upper airway humidification of air it is pulse because that will explain while the inspired oxygen tension is different from that of the alveolar oxygen tension is it due to the low atmospheric pressure okay that will not explain the difference between alveolar and arterial the low pio2 will explain the difference between the inspired oxygen tension and the oxygen tension in the airway is the bq relationship of a normal lung yes okay that is responsible why there's a difference between the alveolar oxygen tension and the end capillary auto tension okay as i mentioned earlier the bq relationship of all of the respiratory units on an average is 0.8 and therefore the end capillary auto tension is expectedly to become less than 100 pore now is the left to right shunt due to the bronchial circulation due to bronchial circulation responsible for the difference between the alveolar and the arterial blood okay pulse because it is the right to leptian which is responsible why there's also a difference between the alveolar and the arterial oxygen tension so the correct answer for question number two is the bq relationship of the normal lung now let us move on to the second item which is lung volumes and capacities the third interactive question is that which of the following is equal to functional residual capacity a inspiratory reserve volume plus tidal volume b expiratory reserve volume plus residual volume c total lung capacity minus vital capacity and the vital capacity minus inspiratory capacity again i like you to pause try to answer and then resume tabulated in this slide are the poor lung volumes the mnemonic is either i t e and r number one is inspiratory reserve volume or irb number two is tidal volume or tb number three is expiratory reserve volume or erb and number par is the residual volume or rb i'd like you to pause memorize and then resume so what are the borderline volumes i stands for inspiratory reserve volume t stands for tidal volume e stands for expiratory reserve volume and r stands for residual volume here is the 9-liter collins tracing wherein the x-axis is time y-axis is volume upward deflection of the writing pen is inspiration downward deflection of the writing pen is expiration the amount of air that goes in and out of out of our lungs per breath for normal relaxed breathing is known as your tidal volume it is known as a tidal volume because the inscription it makes in the nine liter collins looks like a tidal wave now it has two reference points this is at end inspiration at an inspiration if we are going to inspire maximally the additional amount of air that we can inspire is logically known as your inspiratory reserved volume now at end expiration if we're going to maximally expire the additional amount of air that we can expire logically is known as expiratory reserve volume the amount of air remaining on our lungs after maximal expiration is known as your residual volume so i want you to pause memorize this figure here then resume once you memorize it because that is essential in the subsequent discussion so let's have a brief review what is number one it is inspiratory reserve volume what is number two it is tidal volume the number three is expiratory reserve volume and number four is residual volume if you combine two or more lung volumes we come out with capacities and there are four lung capacities and the acronym is t v i f okay the burst lung capacity is t which is total lung capacity the second one is v as in vital capacity then we have the i which is the inspiratory capacity and then we have number par which is f which is the functional residual capacity again i like you to pause memorize and resume once you memorize it so what are the portland capacities tbif the first one is total lung capacity the second one is vital capacity the third one is inspiratory capacity and finally we have functional residual capacities so i mentioned to you that if we combine two or more lung volumes we come out with capacity so if we combine all of the poor lung volumes that is known as your total lung capacity if we combine the upper three lung volumes the irb tv and expiratory reserve volume that is known as your vital capacity if we combine the upper tool which is inspiratory reserve volume and tidal volume that is inspiratory capacity and when we combine the lower two which is erb and rb that is functional residual capacity so i want you to pause memorize and resume once you memorize this figure so there are poor lung capacities the mnemonics is tvif the total lung capacity which is composed of the poor lung volumes which is i t e and r then you have your vital capacity which is composed of your three upper lung volumes which is i t and e then you have your inspiratory capacity or ic which is composed of your two upper which is i n t and you have your functional residual capacity or your f r c which is composed of your two lower which is e and r so again i like you to pause memorize then resume okay so let us combine what we have discussed so far you have poor lung volumes which is either and you have poor lung capacities which is tvia okay this stands for total lung capacity which contains the poor lung volumes i t e and r v stands for vital capacity which contains the three upper lung volumes i stands for inspiratory capacity which contains the two upper lung volumes and f stands for functional residual capacity which contains the erb and residual volume again i want you to pause memorize and resume so we go back to this third interactive question which of the following is equal to a part c okay what is our mnemonics either and tvip and we're supposed to have a mental picture of this one okay so if we combine rb and tv that is inspiratory capacity this is pulse erb and rb erb and rb that's functional residual capacity that's right so tlc minus vital capacity dlc minus vital capacity so it's recedible volume this is pulse vc minus ic vc minus ic so that is erb this is pulse so the correct answer is b functional residual capacity is equal to erb plus rb so we move on to the next topic which is elastance and compliance so the part interactive question as us which of the following is equal to the difference between alveolar and atmospheric pressures k a transpulmonary pressure b trans airway pressure c transgestural pressure and the trans-respiratory pressure so i want you to do is pause try to answer and resume once you have another so here are the poor compartment pressures in the respiratory airway so we start up with the airway opening pressure okay then we have the alveolar pressure then we have the pressure inside the pleura which is plural pressure then we have the atmospheric pressure okay again pause memorize and resume the video once you memorize the pore compartment pressures so what are the poor compartment pressure the first one is airway opening the second one is alveolar pressure the third one is intrapleural pressure and the last one is atmospheric pressure so this is another way looking at it so this is the chest wall this is the lung wall and in between that is the pleural cavity okay so that's the mouth opening okay that's the lungs that's the chest wall so what are the poor pressures compartment pressures okay we have the airway opening then we have the alveolar pressure then we have the pleural pressure then finally we have the atmospheric pressure now what are the poor trans pressure okay first one is the trans airway pressure second one is the trans pulmonary or translung pressure third one is the trans chest wall or transthoracic pressure and the part one is the trans respiratory pressure okay so for the ease of memorization for this lecture let's just memorize the trans airway pressure the transpulmonary pressure the trans-chest wall pressure and finally the trans-respiratory pressure so again try to pause memorize and resume the video once you memorize this poor trance pressure the trans pressure is the pressure difference between two compartments okay and therefore the trans airway pressure represents the pressure difference between the trend the airway opening and the alveolar pressure the transpulmonary pressure on the other hand represents the difference in pressure between the alveolar pressure and the intrapleural pressure the trans chest wall pressure represents the difference between the intrapleural pressure and the atmospheric pressure while the trans airway pressure represents the difference between the alveolar and the atmospheric pressure again pause memorize and resume so this is another way of looking at the trans pressure okay what are the poor trans pressure it is the trans airway pressure then you have your transpulmonary pressure then you have your trans chest wall pressure then finally you have your trans respiratory system pressure so the trans airway pressure is the difference between the airway opening and the alveolar pressure the transpulmonary pressure the transplant pressure is the difference between the alveolar pressure and the intraplural pressure okay the trans-chest wall pressure is the difference between the intraplural pressure and the atmospheric pressure while the trans-respiratory system pressure is the difference between the alveolar pressure and now the atmospheric pressure so what is the significance of these trans pressures these trans pressures represent the elastic property of the different organs that comprise the respiratory system okay the transpulmonary pressure which is the difference between the alveolar and the intrapleural pressure represents the elastic property of the lungs the transthoracic pressure i should guess represents the elastic property of the chest wall while the trans-respiratory pressure represents the combined elastic property of both the lungs and the chest wall now if the trans pressure is positive okay it means that the organ is a natural tendency to contract again if the trans pressure is positive it means that the elastic property of that particular organ it wants to contract if the trans pressure is negative okay the elastic property of that particular organ is it wants to expand okay so positive contract negative coolant so which of the following is equal to the difference between the alveolar and the atmospheric pressure a trans pulmonary pressure that's pulse because that's the difference between the alveolar and the pleural cavity pressure the trans airway pressure that is pulsed because that is the difference between the airway opening and the alveolar pressure see the trans chest wall pressure that is the deep that's another pulse because that's the difference between the pleural pressure and the atmospheric pressure and finally we have the trans-respiratory pressure which represents the difference between alveolar and atmospheric pressure moving on to the pip interactive question which of the following statements best describe the elastic property of the respiratory system at frc the lungs have a natural tendency to expand b the chest wall has a natural tendency to contract see the respiratory system is most compliant and the the respiratory system is most elastic so again pause try to answer the question and resume your viewing once you have a tentative answer compliance is the tolerance to the permission and when we talk about lung compliance it is the inflatability of the lungs compliance is computed as a change in volume over the change in pressure the mnemonic is cbp or central venous pressure compliance is computed as a change in volume a change in pressure elastance is the tendency to recoil back to its original configuration when we particularly talk about lung elastance we're talking about resistance to the permission or the collapsibility of the lungs since it is a reciprocal term of compliance elastance is computed as a change in pressure over a change in volume so compliance is the tolerance to the permission and as far as the lung is concerned it is inflatability so for the computation of compliance it's cvp compliance is equal to the change in volume over the change in pressure elastance on the other hand is resistance to the permission or when we particularly talk about lung elastance we're talking about the lungs collapsibility so it is computed as change in pressure over the chains in volume so again kindly pause memorize and resume now let us discuss the origin of the lung elastance or its collapsibility okay one third of the elastic property of the lungs is due to this its elastic tissue content content while two thirds is due to the surface tension now what is surface tension the lungs is composed of millions of alveoli which behaves as a water bubble okay it is lined by a layer of water molecules once these water molecules are exposed to air okay they tend to attract each other and they develop surface tension now this surface tension of the lungs is kepler by the surfactant released by your pneumocytes type two okay so what will happen if the surfactant is going to be low okay if the surfactant is going to be low there's nothing called counteract the surface tension okay and therefore the lung elastic property will be greater now let us now conceptualize elastance compliance with the pressure volume loop or line in the x-axis is plural pressure and the y-axis is volume now during this part of the loop what is happening is the plural pressure is made more negative and air goes into the lungs simultaneously we measure pressure and the volume now in this part of the pressure volume loop the pleural pressure is made less negative and air goes out of the lungs simultaneously pressure and volume are measured now the difference between the inspiratory part of the loop and the expiratory part of the loop is known as your hysteresis and this is due to the surface tension now this is known as your pressure volume loop or line and depending on what mechanical property of the lungs you're talking about okay it may be known as your compliance loop or line or the elastance loop or line now let us now go to the measurement of land compliance or the implicability so as mentioned compliance is computed as change in volume over the chains in pressure so let us compute for the compliance of this black lung here so the change in pressure is from pipe to 7.5 so the change is 2.5 and the change in volume is from 0 to 500 so that is roughly around 500 so 500 over 2.5 that's 200 ml per centimeters of water now let us measure the compliance of this red lung here notice that the compliance is shifted to the right and notice that the slope is less tip okay so the change in pressure is also 2.5 however the change in volume is around 250 ml okay so when we compute for the compliance okay it went down to 100 ml per centimeters water so meaning to say a right ship or a less tip or a flat compliance line means that there's a lower compliance now here's a situation wherein there's a shifting of the compliance line this is normal this is pulmonary fibrosis and this is emphysema in a healthy lung the compliance line is at the normal position it is a normal slope in the report with the normal compliance for a patient with pulmonary fibrosis notice that it is shifted to the right there is less deep slope meaning to say that the lungs are less compliant and therefore a patient with pulmonary fibrosis will have difficulty inspiring now on the other hand a patient with emphysema okay you can see that the compliance line is shifted to the left it has a steeper slope meaning to say that the lungs are more compliant it is easier for the patient to inspire however since the reciprocal term for compliance is elastan it means that the lungs are less elastic less collapsible and therefore patient with pulmonary emphysema is going to have a hard time expiring air now let's discuss elastance without surface tension here's the compliance loop of a lung that is airfield well this is the compliant slope of a lung which is saline pill okay notice that in the compliance loop of the lung which is air peeled there's a difference between inspiratory and expiratory part of the loop which is known as hysteresis and this is due to the air and water interaction which gives rise to surplus tension now in the saline pill lungs okay you can see that there's the loss of hysteresis it is shifted to the left and it is steeper meaning to say that the lungs are more compliant less elastic and this due to the loss of water tension surface tension i mean the loss of the surface tension is on the other hand due to the loss of the air water interaction which is responsible for the surface tension okay let's move on to some nosebleed topics which is the elastic properties of the lungs and the chest wall let us now discuss the compliance of the respiratory system shown in this slide are three relationships wherein the x-axis is trans pressure which could either be either transpulmonary trans-chest wall or trans-respiratory system in relationship to the y-axis which is volume as a percentage of vital capacity this is the compliance line of the lungs is the compliance lung of the chest wall and this is the compliance line of the respiratory system we're going to divide the compliance line of the respiratory system into three parts the first part is from 0 to 25 percent then the second part will be from 25 to 75 and the third part will be 75 to 100 percent so we end up with this figure here so this is the compliance line of the respiratory system we're going to represent this portion from 0 to 25 percent by drawing a straight line this portion here from 25 to 75 by drawing another straight line and from 275 to 100 percent by drawing another straight line here now this one is near a parsi the red one is near residual volume well the blue one is near tlc now make a visual inspection of the three lines the steepest as you can see is the green one which is near frc meaning to say that the respiratory system is most compliant near a part c and when we compare near rb to near frc the red line is less steep and therefore it is less compliant compared to that up near a par c the same can be said about that line near tlc the slope is less and therefore near tlc the the respiratory system is less compliant compared to that of near a part c so what i'm saying is the compliance of the respiratory system is a tri-basic manifestation it is less compliant from zero to 25 percent becoming more compliant from 25 to 75 percent then again less compliant from 75 to 100 percent so this is another way of looking at it now in relationship to the portland volumes and functional residual capacity okay it is less compliant near rb becoming more compliant near frc and again becoming less compliant nil tlc so where do we do our tidal beating we do our tidal greeting k above a part c where the respiratory system is most compliant and therefore it is easier to inflate the lungs and therefore the work of breathing is less so let us review what we have discussed so far with regards the slope and shifting of the compliance curve a right shape of the curve means that the lung is less compliant a lower slope of the line means that the lung is less compliant and near rb and near tlc okay the respiratory system is less compliant so let us now go back again to the significance of the thrust pressure the trans-pulmonary pressure will reflect the elastic property of the lungs the trans-thoracic pressure will reflect the elastic property of the chest wall and the trans-respiratory system pressure will reflect the elastic property of the respiratory system i mentioned if the trans pressure is positive the elastic property of that organ is to contract while if the trans pressure is negative the elastic property of that organ is to expand so let us now discuss the elastic property of the chest wall since we're talking about the chest wall the x-axis will be the transgenic pressure okay while the y-axis will be percent of the vital capacity now let us remember that if the trans-chest wall pressure is positive the elastic tendency of the chest wall is to contract while it appears negative the elastic property of the chest wall is to expand now this is the elastic line of the chest wall let us determine now what is the transgenic pressure at uh zero percent of the vital capacity so it's negative 38 at 30 it's negative 5 at 60 it is zero and at one hundred percent it is positive seven notice that from a lung volume of zero to sixty percent of the vital capacity the trans-chest wall pressure is negative and therefore the elastic tendency of the chest wall is to expand at sixty percent of the vital capacity the trans-chest wall pressure is zero and therefore the chest wall neither wants to expand nor contract beyond 60 percent the transgender pressure is positive and therefore the elastic tendency of the chest wall is collapsed so basically the chest wall has a bipasic elastic tendency and then inflection point will be at sixty percent of the vital capacity so transgender pressure of zero is at sixty percent of the vital capacity so the magic number as far as the elastic tendency of the chest work is concerned it is sixty percent okay it has a by basic elastic tendency below sixty percent it wants to expand while above sixty percent it wants to contract so let us now discuss the elastic property of the lungs since we're talking about the lungs the x-axis will be your trans-pulmonary pressure while the y-axis is still percent of the vital capacity again if the transpulmonary pressure is positive the lungs have a natural tendency to contract while if it is negative the lungs have an elastic tendency to expand now this is the elastic line of the lungs at zero percent of the vital capacity the transpulmonary pressure is positive three at thirty it's positive five and at sixty percent it's positive ten and at one hundred percent it is plus thirty notice that from zero zero percent of the vital capacity till one hundred percent of the vital capacity the transpulmonary pressure is positive and therefore the lungs have an elastic tendency to contract from zero to 100 percent of the vital capacity so basically the lungs have a mono basic elastic tendency it always wants to contract okay so the transpulmonary pressure of zero is not seen in the elastic line of the lungs and therefore the magic number is zero percent of the vital capacity okay above zero percent of the vital capacity the lungs have a natural tendency contract so the lung has a mono basic elastic property okay it as much as possible it wants to contract now let's try to analyze the relationship between the elastic property of the lungs and that of lung volume so this is the elastic line of the lungs as you can see the greater the lung volume is the greater is the transpulmonary pressure the greater the transpulmonary pressure the greater is the elastance the greater is the collapsibility of the lung and the greater is the resistance to the permission or inflammation so putting it in another way the greater the lung volume the greater the transpulmonary pressure the greater the elastance the greater the collapsibility the greater is the resistance to inflation now from a nosebleed topic let us move to a topic which will make you vomit and that is the elastic property of the respiratory system moving on to the elastic property of the respiratory system now the x-axis will be your trans-respiratory pressure again if it is positive the respiratory system has an elastic tendency to contract while if it is negative it has an elastic tendency to expand again the y-axis is still percent of the vital capacity and this is the elastic line of the respiratory system and at zero percent of the vital capacity the trans-respiratory pressure is negative 35 at 30 percent it is zero at sixty percent it is plus ten and at one hundred percent it is plus thirty seven notice that the trans-respiratory pressure from zero to thirty percent of the vital capacity is negative and therefore the respiratory system has an elastic tendency to expand at 30 percent of the vital capacity or a functional residual capacity the trans-respiratory pressure is zero meaning to say it doesn't want to expand nor contract beyond 30 percent or beyond frc the trans-respiratory pressure is positive and therefore the respiratory system has an elastic tendency to collapse and therefore that just like the chest wall the respiratory system has a bi-basic elastic tendency but this time the inflection point is not sixty percent but at thirty percent of the vital capacity or at frc so the transpulmonary pressure of zero is achieved at thirty percent of the vital capacity or frc so when we talk about elastic property of the respiratory system the magic number is 30 of the vital capacity or frc below fprc the respiratory system has an elastic tendency to expand while above a parsi the respiratory system has an elastic tendency to untrack and therefore the respiratory system is a bi-basic elastic tendency and the inflection point is at a part c so let us review what we have been discussing for the past 10 minutes what is the elastic property of the chest wall the lungs in the respiratory system this is the figure which we've been trying to analyze in the x-axis is the transmural pressure and the y-axis is lung volume this time represented as percent of the tlc the green one is the elastic line of the chest wall the red one is the elastic line of the lungs and the black one is the elastic line of the respiratory system in this figure here the green arrow would represent the elastic property of the chest wall while the red arrow would represent the elastic property of the lungs so here is the tabular graph which represents this figure over here okay at 100 percent of the vital capacity the trans-chest wall pressure is positive seven and therefore it wants to contract the trans lung pressure is positive thirty and therefore the lungs would like to contract if the trans-respiratory pressure which is the sum of plus 7 plus 30 is positive 37 and therefore it wants to contract okay so at 100 of the vital capacity the chest wall is an elastic tendency to contract just like the lungs it has an elastic tendency to contract so at one hundred percent of the vital capacity it is plus seven for the trans chest wall it is plus 30 for the transpulmonary pressure and therefore if you sum this boat up it is plus 37 for the respiratory system now at 60 percent of the vital capacity the transgenic pressure is zero and therefore it is neutral the transpulmonary pressure is plus nine and therefore it wants to contract and therefore if you add zero plus nine it is equal to plus nine and therefore the respiratory system elastic pressure is plus nine it wants to contract so at sixty percent of the vital capacity the chest wall neither wants to expand nor contract while the lungs would like to contract at sixty percent of the vital capacity okay the the transgender pressure is zero the lungs uh transpulmonary pressure is plus nine and therefore the respiratory system wants to contract now the most important one is at 30 percent of the vital capacity or the frc notice at frc the transgender pressure is negative pipe it wants to expand while the transpulmonary pressure is plus pipe it wants to contract and therefore when we add it both up it's zero and therefore the respiratory system uh trans pressure is zero it's neutral it neither wants to expand the contract so this is a representation on the elastic property of the respiratory system at functional residual capacity the lungs would like to expand the chest one would like to contract they equalize each other and therefore the trans-respiratory pressure is zero so the lungs would like to contract okay the chest wall would like to expand and therefore they equalize its other the trans-respiratory pressure is zero so the respiratory system would neither like to contract or expand then at zero percent of the vital capacity the transgender wall pressure is negative 38 so the chest wall would like to expand and the transpulmonary pressure is plus three and therefore the lungs would like to contract and when we add it both up that's a negative 35 so the respiratory system has an elastic tendency to expand at zero percent of the vital capacity okay so at zero percent of the vital capacity the chest wall would like to expand while the lungs would like contract okay so the chest wall would like to expand what the lungs would like to contract this is more powerful than this one and therefore the respiratory system would like to expand so let us summarize things at this point with regards compliance of the respiratory system it is most compliant at frc and least compliant at rb and tlc with regards elastic tendency is concerned the lungs have a monobasic elastic tendency as much as possible it wants to contract or collapse the chest wall on the other hand the elastic property is by basic and the inflection point is 60 at greater than 60 percent it wants to contract in less than 60 percent it wants to untrack the respiratory system is likewise the same by basic elastic tendency and the inflection point is now at 30 percent or at a frc okay about 30 it wants to contract and below 30 it wants to expand okay did you survive that are you still alive okay let's move on to the next one what is the origin of the negative intraplural pressure now at f rc you can see here that the chest wall would like to expand and the lungs would like to contract and therefore this opposing elastic properties a negative intrapleural pressure is generated so what is the significance of our fpr c the uprc is known as a relaxed lung volume it is the lung volume or the capacity wherein the elastic property of the chest wall and the lungs equalize each other it is the relaxed lung volume which the respiratory system will try to maintain if the respiratory muscles are relaxing okay so therefore if we inspire maximally up to tlc and we relax our inspiratory muscle on its own the respiratory system will go back to frc even without us expire using our expiratory muscle if we expire maximally down to rb and relax our expiratory muscle on its own because of the elastic property of the respiratory system will go back to frc and this is the basis why expiration is a passive process so when we inspire when we inhale our tidal volume we contract our inspiratory muscle and when we expire we just relax our inspiratory muscle and on its own it is going to go back to a part c so let's go back to this interactive question number pipe which of the following statements best describe the elastic property of the respiratory system at lrc the lungs have a natural tendency to expand that's strong it wants to contract the chest wall has a natural tendency to drag that's again pulse it wants to expand the respiratory system is most compliant okay that's right and the respiratory system is most elastic and that's pulse so the correct answer is the respiratory system is most compliant so let us summarize things at this point there are poor lung volumes the mnemonics is either and their poor lung capacity is its tbi with regards elastance is concerned it is resistance to deformation or as far as the lungs is concerned its collapsibility it is due to one third elastin content and two thirds due to surface tension compliance on the other hand is the tolerance to deformation or the inflatability as far as the lungs are concerned it is computed as central venous pressure its volume over pressure it is plotted by the pressure volume loop or line a right shape means that there is a decreased compliance a decrease in slope means that there is a decrease in compliance there are poor compartment pressures and poor trans pressure the trans pressure would represent the elastic property of a particular organ if it is positive it has an elastic tendency to contract while it is negative it has an elastic tendency to expand the lungs have a monophasic elastic tendency it always wants to collapse the greater the lung volume the greater is the elastic tendency a bipasic elastic tendency is both seen in the chest wall in the respiratory system the inflection point for the chest wall is 60 percent of the vital capacity while that for the respiratory system it's 30 of the vital capacity or at frc the frc has a lot of physiologic significance the elastic recoil of the lung and the chest wall balances each other it is known as the relaxed lung volume or capacity it is the configuration which the respiratory system will maintain if all of the muscles respiratory muscles are relaxed it is the basis while expiration is a passive process during normal quiet breathing let's move on to the port topic which is the mechanics of breathing the sixth interactive question as tabular pressure is most negative at which part of the tidal breathing a startup inspiration b mid inspiration c end of inspiration the mid expiration so i want you to pause try to answer and resume the video once you have a tentative answer let us now discuss the changes during tidal breathing okay at frc the albion air pressure is zero relative to the atmosphere and therefore there is no plop air during inspiration the brain is going to command the chest wall to expand expansion of the chest wall is going to make the alveolar pressure negative relative to the atmosphere since air moves from greater pressure to lesser pressure air will move in during expiration the brain is going to command the inspiratory muscle to relax relaxation of the inspiratory muscle will cause contraction of the thoracic cage this is going to make the alveolar pressure positive relative to the atmosphere and therefore this will cause air to move out into the atmosphere so what i'm driving at is that the alveolar pressure this one is the one that drives air to blow in and out of the lungs now let us discuss the changes during tidal breathing the first thing that's going to change is the plural pressure followed by the alveolar pressure then there will be blow up air then finally there will be increase in lung volume okay at f rc this is our resting lung volume the intrapleural pressure is negative 5 the alveolar pressure is equal to the airway opening pressure that's why there's no blow up air now during inspiration the inspiratory muscle is going to contract this is going to increase the pleural cavity volume the increase in pleural cavity volume is going to decrease the intrapleural pressure and this will make the intraplural pressure more negative so the interpolate pressure becomes more negative and this is transmitted to the alveolar pressure it gradually becomes negative and this will cause an inspiratory blow up air this is going to increase the lung volume the plural pressure negativity progresses and peaks at the end of inspiration the negativity of the alveolar pressure peaks at peak inspiration and gradually returns to zero at end inspiration inspiratory plop peaks at mid inspiration and gradually returns to zero at end inspiration and lung volume period increase and peaks at an inspiration during expiration the inspiratory muscle is going to relax the lung is going to recoil back to a part c and this will cause a diminution in volume and therefore an increase in pressure this increase in pressure will cause less negativity of the intrapleural pressure and therefore the plural pressure becomes less negative the albular pressure becomes positive the expiratory plot starts occurring and the lung volume starts decreasing the plural pressure negativity progressively decreases back acid level in fpr c the positivity of the alveolar pressure peaks at mid expiration and gradually returns to zero at end expiration the same goes with expiratory law it peaks at mid inspiration and gradually returns to n expiration and the lung volume period decreases back to baseline which is functional receivable capacity so these are the changes during tidal breathing as far as the pleural pressure is concerned it assumes iu wave the alveolar pressure assumes a sine wave since the alveolar pressure is the driving pressure per plot the the plot likewise assume a sine wave while that of volume assumes an inverted uv so the pleural pressure is most negative at the end of inspiration the albiota pressure is zero at n inspiration and end expiration it is most negative during mid inspiration in most positive during mid expiration okay the flow is zero at n inspiration and n expiration and it is fastest during mid inspiration and mid expiration and the volume is highest at end inspiration so let us now discuss the respiratory cycle time and the ie ratio in the x-axis is time in the y-axis is volume now this is this is the inspiratory part of the respiratory cycle and it is composed of three phases there are there is inspiration then there's expiration then finally there's a period of noplaw which is known as apnea phase so the period of the respiratory respiratory cycle is divided basically into inspiration and expiration expiration includes the expiration proper and the apnea paste now this is the total time for one respiratory cycle and when we try to see the ratio of the inspiratory time and the expiratory time we can see that normally okay the ie ratio is 1 is to 2 to 3 meaning to say expiration is 2 to 3 times longer than that of inspiration when we increase our respiratory rate the respiratory cycle time decreases the inspiratory time decreases but the expiratory time decreases more and therefore the ie ratio becomes bigger so it becomes one is two one is to two so we go back to this interactive question the algorithm pressure is most negative at which part of the tidal breathing start of inspiration that is pulse because it is zero during mid inspiration that's the correct answer at the end of inspiration no the other pressure is zero at the end of inspiration during mid expiration now it is most positive during expiration so b is the correct answer now let us move on to the big pip topic which is airway resistance so which of the following causes a turbulent airflow pattern a low gas density b slow airflow velocity c a low reynolds number d a large luminal airway diameter so again i'd like you to pause try to answer and resume for number eight it asks us which of the following is accurate with regards to small airway resistance a it contributes highest to total airway resistance b highest at tlc c not dependent on bronchial smooth muscle contraction nd inversely related with lung elastance again i like you to pause try to answer then resume their way resistance is the frictional hindrance to the plow operated by the air passages it is go burn by ohm's law which states that law is directly related to driving pressure while inversely related to airway resistance and therefore the higher the airway resistance the lower will be the flow of air the resistance offered by the airway depends on two factors one the type of plot pattern and two the physical attributes of the airways and the gas which is governed by passover's law the airway is divided by the larynx into your upper airway and to your lower airway the lower airway is actually just a trachea undergoing 23 dichotomous branching ending up with millions of your alveoli the lower airway can be divided further into your respiratory zone that is from airway generation 17 to 23 the structures are with albiolai and their borders gas exchange that's why this is known as your respiratory zone while airway generation one to six they're devoid of alveoli and therefore they're known as the conducting zone because their main job is just to conduct air from the upper airway down into the respiratory zone okay the conducting zone is further divided into your large airways and the small airways small airways anatomically are those with less than two millimeters in diameter they're known as your bronchioles and they're devoid of cartilages they're from airway generation 10 to the 16.

[01:12:42]now let us discuss the airflow pattern the airflow pattern in the upper airway and the conducting zone is by ballplaw and that on the respiratory zone it is a much lower the diffusion type of air block pattern because th that is where the gas exchange occur the bulk block can be further divided into your laminar turbulent and transitional so there are three types of plot pattern the laminar the turbulent and the transitional what will determine what will be the plot pattern will be your reynolds number reynolds number is directly related to the density velocity of airflow the diameter of the conduit and the viscosity of the gases okay the way to memorize this is rn is equal to dbd over this so density velocity diameter over viscosity so this one is the confusing part but the way to memorize it it is alphabetical it is velocity over viscosity now the turbulent flow pattern is assumed if the reynolds number is greater than 2000 the turbulent pattern offers a higher resistance compared to that of a laminar pattern the turbulent pattern is primarily seen in the trachea because the velocity of airflow in the trachea is very high and likewise the diameter of the trachea is very large and therefore the reynolds number will be high more than 2000 causing a turbulent airflow pattern the laminar pattern occurs if the reynolds number is less than one thousand it offers a lower resistance compared to the turbulent pattern and it occurs primarily in the small airways or in the bronchioles this is so because the velocity of airflow in the small airways is slow and likewise the diameter of the bronchioles is likewise small and therefore the reynolds number will be less than 1000 and the plot will be laminar if the reynolds number is between 1000 to 2000 it is going to assume a transitional type of airflow pattern so the bulb load that occurs in the conducting zone can assume three patterns okay in the large airways it is a turbulent blow pattern in the small airways it is a laminar flow pattern and somewhere bit in between is the transitional plow pattern another thing that will determine the airway resistance are the physical attributes of the airways and gas which is governed by passivist law states that airway resistance is directly related to the viscosity of the gas the length of the tube and the radius of the airways the airways radius is dependent on its mucosal thickness the smooth muscle tone and the tethering effect of the lung parenchyma the large airways radius is dependent on the mucosal thickness and the contraction and relaxation of the bronchial smooth muscle the small airways or the bronchioles are devoid of cartilages they're likewise dependent on the mucosal thickness the smooth muscle tone but likewise they are dependent on the tethering effect of the surrounding lang parenchyma so this is a example of the tethering effect of the surrounding lang parenchyma they are devoid of cartilages so they tend to collapse and watch what keeps them patent is the elastic pull of the surrounding lung parenchyma let us now discuss the small airways resistance and its relationship with that of plank volume i want you to go back to this slide which we discuss with regards elastance is concerned and based on this diagram we discussed that the greater the lung volume the greater the transpulmonary pressure the greater is the lung elastance okay so small airways resistance and its relationship with the lung volume okay the small airways is dependent on the tethering effect of the surrounding lung parenchyma what will determine the threatening effect is the elastance of the lungs okay at residual volume there is low lung elastance and therefore the tethering effect is small and therefore the radius is likewise small at tlc since the greater the lung volume the greater the elastance we have a higher lung elastance and therefore there is a greater pull of the small airways and therefore the radius is much greater compared to that of procedural volume and therefore the greater the lung volume the greater the lung elastance or the tethering effect the greater is the radius the smaller is the small airway resistance so that relationship is shown by this graph okay where in the x-axis is volume and the y-axis is airway resistance not notice that the airway resistance is inversely related okay the greater the lung volume the lower is the airway resistance so let us now discuss the distribution of the total airway resistance 50 percent of the total airway resistance is contributed by the nose 30 percent is contributed by the large airways and the parents while only 20 percent is contributed by the bronchials let us now compare the resistance offered by all of the large airways compared to that of the small airways okay based on paso is law which states that the ratios is inversely related to airway resistance we expect that the airway resistance operated by the small airways we will be much larger much bigger compared to the large airways here is a graph which will try to answer to us which offers a greater airway resistance the large or small airways so in the x-axis the trachea the bronchus and the bronchioles and the y-axis is the resistance upward notice contrary to our expectation okay the more distal or smaller airways upper less resistance why is this so okay if we get the radius of the trachea probably it's just it is just this big okay if we get the ratios of all of the bronchioles because their numerous bronchioles we can see that the total luminal radius of all of the bronchioles is much larger and therefore the resistance operated by all of the bronchioles is lower compared to that of the trachea so we go back to this interactive question which the following causes a turbulent airflow pattern so what equation do we need okay it is the reynolds number and reynolds number what's our formula it is dbd over d that is velocity over viscosity okay so low gas density that's pulse the lower the density density the lower the reynolds number we want the higher reynolds number because we're talking about turbulent flow slow airplane velocity again that is pulse low reynolds number again we want a high reynolds number a large luminal airway diameter so if the diameter will go up the reynolds number will go up and that is the correct answer so for number seven a large luminal airway diameter is the correct answer for number eight which of the following is accurate we regard small airway resistance contributes highest to the total airway resistance that's false it is the nose highest at tlc that is pulse because it's inversely related the greater the lung volume the higher the elastance the greater the tethering effect the greater the small airway reduced the lower is the airway resistance it is not dependent on bronchial smooth muscle contraction both the large and the small airways are dependent on bronchial smooth muscle contraction inversely related to lung elastance that's the correct answer the greater the elastance the greater the reduce the smaller is the airway resistance let us now move on to the sixth topic which is the distribution of ventilation which of the following most accurately describe inhalation from rb to tlc the bases are better ventilated from rb to a par c the apices are better ventilated from f rc to tlc at rb the lower lung zones are more compliant than the upper lung zones and d at f rc the lower lung zones are more compliant than the upper lung zone again i'd like you to pause try to answer and then resume so what are the factors that will determine the respiratory units ventilation the greater the resistance k the lower is the ventilation the greater the compliance okay the higher the greater the compliance the higher is the ventilation and therefore the greater the compliance the greater the ventilation the greater the resistance the lower the ventilation between the two what will determine the distribution of ventilation under normal condition is compliance again let us have a brief review a right shape of the compliance curve means that it is less compliant the lower the slope the less compliant is near rb and tlc the respiratory system or the lungs is less compliant now let's compare the compliance of the lung versus that of the albiolus the lungs as an organ is less compliant near rb and tlc against that of a part c it is however composed of several alveoli it is wrong to say that the alveoli of the lung at rb are less compliant than the alveoli of the lung at a par c because there is a regional alveoli compliance differences in the different lung zones what will determine the compliance of the albiolos is its size the alveolar size may vary from almost collapsed moderately descended or maximally distended okay if we try to determine the compliance loop almost collapse alveoli and inflate it okay till maximally distended we're going to have the same compliance loop as that of the lungs okay as you can see here it is most compliant the albiolus is most compliant when it is moderately distended now what are the factors that will determine the configuration of the albiolus whether it's going to be almost collapsed moderately distended or maximally distant the factors that will determine the configuration of the albiolus are the differences in the pressure inside and outside the albiolus the inside pressure is the alveolar pressure and the outside pressure is the intrapleural pressure and we know that the difference between the alveolar and the intrapleural pressure is known as your transpulmonary pressure this is the descending pressure of the alveolus let us now examine the configuration of the alveoli in an upright lung the alveolar pressure is not affected by gravity so it's zero throughout from upper to lower lungs the intraplural pressure on the other hand is affected by gravity it is most negative at the apc and least negative at the basis and therefore if we try to compute for the trans-pulmonary pressure which is the difference between the alveolar and intrapleural pressure zeros minus minus tens plus ten zero minus minus two is plus two we can see that due to the effect of gravity the transpulmonary pressure is more positive in the upper lung zones compared to the lower lung zones and because of this okay the upper lung zones alveoli are more distended than the lower lung zones albioli so let's now analyze the regional lung compliance at residual lung volume so if this is the lung okay this is the configuration of the alveoli okay notice at the bases the alveoli at rb okay are almost collapsed so it's less compliant while at the aps it is moderately distended and therefore more compliant and therefore when we are going to inhale from rb to frc most of the ventilation is going where when we inhale from arbitrary which is better ventilated better the ventilated are the moderately distended and therefore when we inhale from rb to f rc the upper lung zone is better ventilated than the lower lung zone now let us examine now the regional compliance deep compliance of the functional residual capacity at frc you can see at the bases okay the alveoli are moderately distended while the superior partial alveoli are pulled standard and therefore at f r c the lower lung zones alveoli are more compliant than the upper lung zones so if we're going to inhale from frc to tlc we're going to inhale from f rc to dlc which is better ventilated of course which is going to be better better ventilated the one that is more compliant which is moderately extended at the basis so the lower lung zones is better ventilated as we inhale from f r c to t and c so where do we do our tidal breathing we do our tidal reading above f rc so right now our lung bases are better ventilated than the abysses when we do tidal breathing so this is another way of looking at it so when we exhale down to rb and we inhale from rb till to frc the upper is better ventilated however when we inhale from frc to tlc the lower is better ventilated so we go back to this interactive question which of the following most accurately describe inhalation from frc to tlc the bases are better ventilated from when we inhale from rb to a part c that's pulse because it is the abscess the pieces are better ventilated from frc to tlc that's again wrong because we know it is the basis at rb the lower lung zones are more compliant than the upper lung zones that's pulse okay the upper lung zones are more compliant at rb at the upper c the lower lung zones are more compliant than the upper lungs and that's the correct answer so we move on to the seventh topic which is the work of breathing which of the work of breathing component increases in a patient with hyaline membrane disease a the viscous tissue resistance b the airway resistance work of breathing c the non-elastic component and the the elastic component again i like you to pause try to answer then resume let us now discuss the work of breathing during inspiration the inspiratory muscle is going to contract to expand the chest wall which is composed of non-elastic tissue and the lungs which is composed of elastic tissue this is going to create the necessary driving pressure per air to move in against the frictional resistance operated by the airways during expiration on the other hand okay the chest will in the lungs possibly recoil back to f part c and this creates the necessary driving pores per air to move out of the lungs against the frictional resistance offered by the airway so the work of breathing during inspiration can be divided into elastic workout breathing which is the work done to expand the lungs and we have the non-elastic work which is composed of two components to expand the chest wall and likewise to counteract the frictional resistance offered by the airways let us now discuss the work of breathing during expiration during expiration there is no contraction of the muscles it is the elastic recall to a parsy which generates the necessary driving pores and the expiratory muscles only contract if there is increased airway resistance so the work of breathing could be classified as a elastic work of breathing which is the work done to expand the lungs which is composed of elastic tissue the non-elastic work of breathing is composed of two components it is the work done to expand the non-elastic tissues which is otherwise known as the viscose resistance work of breathing and the other component of the non-elastic work of breathing is the work done to counteract the frictional resistance of the airways to the blow up air now 65 percent of the total work of breathing is due to the elastic work of breathing while seven percent accounts for the viscose resistance work of breathing and airway resistance accounts for 28 of the total work of breathing the work of breathing is measured by the pressure volume area okay during inspiration a driving pressure as shown in this illustration is generated from negative two to negative six so that a volume of air as shown in this diagram around 1 liter will go in now during expiration a driving pressure is again generated that's from negative 6 to negative 2 so that the volume of air will move out of the lungs the elastic work of breathing is represented by this area over here oacd o and the viscous resistance workup breathing is likewise embedded in this area over here okay the airway resistance work of breathing on the other hand is represented by o e c f a this is the inspiratory part and that's the expiratory part of the work of breathing okay now under normal conditions there's no work of breathing during expiration it is a passive process the passive recoil of the fprc generates the driving pressure the workout breathing was done during inspiration to expand the respiratory system so that us to create the elastic recoil pressure necessary to expel air out during expiration so normally the total energy expenditure allotted by the work of breathing is only 5 and thus it is so low that we're not aware that we are breathing the work of breathing may be increased in pathological condition elastic workout breathing may be increased in lung diseases or tissue resistance worker breathing may be increased in chest wall diseases examples are hyaline membrane disease congestive heart failure pneumonia scoliosis in hyaline membrane disease there's deficiency of the surfactant and therefore there's increased lung elastance so what's going to happen during increased elastance is the compliance curve is going to shift to the right the inspiratory muscle needs to contract harder from negative 2 to negative 10 or 11 to expand the less compliant respiratory system as you can see the area increases o a c d and likewise the shape of the compliance curve to the right now the airway resistance work of breathing may be increasing asmr copd and you can see here that the loop becomes larger okay so during inspiration okay the inspiratory muscle needs to generate a more negative intrapleural pressure to create a higher driving pressure to per air to go inside the lungs now during expiration okay the expiratory muscles now need to contract to counter the frictional resistance during expiration because the elastic recoil of the lungs back to airports is not enough to generate the necessary driving pressure to propel air out against an increased airway resistance so we go back to this question here which work of breathing component increases in a patient with hyaline membrane diseases okay viscous tissue resistance no it increases during chest wall diseases airway resistance we only see that in asthma or copd or airways diseases non-elastic work of breathing that's wrong because the non-elastic work of breathing is composed of your increased airway resistance workout breathing and likewise increased tissue resistance work of breathing and the correct answer is it's the elastic work of breathing this is usually increased in lung parenchymal diseases so the correct answer is the elastic work of breathing now so let us summarize things at this point here with regards to the mechanics of breathing there will be contraction of the inspiratory muscle which is going to cause changes in the pleural pressure alveolar pressure so there will be air flow and there will be increase in lung volume now during expiration there will be recoil back to a part c the plural pressure becomes less negative the alveolar pressure becomes positive causing expiratory blow and diminution in lung volume under normal condition the ie ratio is one is the two is to three okay the lower arrow is divided to your conducting zone and respiratory zone okay the conducting zone is further subdivided through large and small airways the small airways are devoid of cartilages and therefore they are dependent on the lung elastance tethering effect the lower airway can be can be divided further into conducting zone and the respiratory sound okay in the conducting zone the blow pattern is by ball block and in the large airway it is turbulent while in the small airway it is laminar and somewhere in between it is transitional the airway resistance is dependent on the plot pattern and the physical dimensions or the radius which is dependent on the smooth muscle tone mucosal thickness and the tethering effect now the plot pattern is dependent on the reynolds number and it's dvd over this density velocity diameter over viscosity okay the airway resistance is highest at the nose followed by large and the upper airway in the large airways and the small airways only contributes small area only contributes 20 percent of the total airway resistance due to the effect of gravity on plural pressure the upper lungs on alveoli is more distended than the lower lung zone when we inhale from rb to frc the upper is better ventilated and as we proceed from inhalation from f rc to tlc the lower is better ventilated the work of breathing is measured by the pressure volume area there are three types the elastic workout breathing the non-elastic workout breathing which is further subdivided into your viscous tissue resistance work breathing and the airway resistance work completing the elastic work of breathing accounts for 65 percent of the total work of breathing it is increased in lung parenchymal diseases such as alveolar or interstitial lung diseases the viscous tissue resistance work of breathing accounts for only 7 percent and its increase in chest wall diseases such as in pleural neuromuscular and thoracic cage diseases the airway resistance work of breathing accounts for 28 percent and its increase in airway diseases under normal condition only 5 of the total energy expenditure issues in the work of breathing so we move on to the next topic which is pulmonary circulation question number 11 reads which of the following constrict the pulmonary artery laws a oxygen b nitric oxide c prostaglandin and d thromboxane a2 again i'd like you to pause try to answer and then resume number 12 reads as follows which of the following best describe the pulmonary vascular resistance pbr jutru due to extra alveolar vessels is highest at tlc pbr due to alveolar vessels is highest at rb total pbr is higher in rb than frc and total pbr is higher in frc than in tlc again i like you to pause try to answer and then resume okay this is an overview of the pulmonary and the bronchial circulation okay so the bronchial artery is the branch of the aorta and supplies oxygenated blood to the airways this is drained by the bronchial vein which drains into the pulmonary veins so this is one of the two anatomic shunts in our body this is the pulmonary circulation which is composed of your pulmonary artery the pulmonary capillaries and that of the veins and when it enlarges the pulmonary capillaries we come up with this illustration here okay so this is the site of the gas exchange the albiolo albiolo capillary membrane okay it is a special design the pulmonary capillary it is just composed of a single endothelial cell this is the site of the exchange of fluids and it is burned by sterling's law so let's discuss the fluid movement in the pulmonary microcirculation so this is the pulmonary capillary the hydrostatic forces inside and outside the capillary and their oncotic forces both inside and outside of the capillaries okay some of these forces are filtrating forces some of them are absorbing forces the filtration process are your capillary hydrostatic pressure and your interstitial oncotic pressure while the absorption forces are your interstitial hydrostatic pressure and your capillary oncotic pressure okay the movement of fluid across the ac membrane or the movement of fluid across the capillary under the interstitium is covered by your sterling's equation sterling's equation states that k stands for hydraulic conductivity times the difference between the capillary hydrostatic pressure and the interstitial hydrostatic pressure minus k sigma which is the colloid osmotic reflection coefficient times the difference between the oncotic pressure in the capillaries and the oncotic pressure in the interstitium okay so k reflects the ease of fluid can pass through the membrane sigma would reflect the effectiveness of the solute in generating the osmotic driving process now if this equation starting's equation is positive it means that there's filtration if this equation shows negative meaning that there's absorption now what is the blue with movement in the pulmonary microcirculation under normal condition this is illustrated by this diagram here showing to us the different interstitial and capillary hydrostatic pressure and oncotic pressure and when we substitute those numbers here we can see that the plux is positive so normally there's movement of fluid from the capillaries into the interstitium so there's movement of fluid into the interstitium you have a flux of one now usually there's no fluid accumulation here because those fluid moving out of the pulmonary circulation is immediately drained by the lymphatic vessels okay so normally there's a flux of fluid and the lymphatics prevent its accumulation okay let us now discuss pulmonary edema pulmonary edema occurs if the plux is positive is greater than the lymphatic drainage okay so that may occur if there's increased capillary hydrostatic pressures such as in lab heart failure or fluid overload or there is a decrease in your hydrostatic pressure in the interstitium such as in the expansion pulmonary edema or there may be decreased oncotic pressure in the pulmonary capillaries such as in protein losing the property liver diseases and malnutrition or there may be changes in the k or the sigma okay there may be increase k or a decrease sigma which is usually secondary to inflammation this will cause a positive blocks which may overwhelm the lymphatic drainage so finally there may be lymphatic obstruction okay such as uh it may be blocked by a malignancy or by parasites such as your schistosoma which will cause fluid accumulation in the interstitium okay what are the differences between the pulmonary and the systemic circulation well regards to systemic circulation its main function is for blood supply regulation and the resistance is psi the pressure in the systemic circulation is high and the response to hypoxia is vasodilation it's different in the pulmonary circulation the main function of the pulmonary circulation is for blood oxygenation and carbon dioxide elimination the resistance is low and the pressure is likewise law in the response to hypoxia it is vasoconstriction instead of vasodilation it is vasoconstriction because it's a compensatory mechanism per bq abnormality let us now discuss the pulmonary vascular resistance okay if you want to compute for your pulmonary vascular muscular resistance you can compute it based on ohm's law wherein resistance is equal to the driving pressure over that of blood block now here is at the carton showing to us the different pressures in the pulmonary circulation and in the venous circulation okay so this is the right ventricle giving rise to the pulmonary artery pulmonary capillary pulmonary vein draining into the left atrium so if we want to compute for the pulmonary vascular resistance it's input pressure minus output pressure over that of blood blow okay so the input pressure is pulmonary artery the output pressure is the left atrium and the plot will be your cardiac output coming out of the right ventricle okay and these are the numbers okay and when we substitute that that's how we compute for the pulmonary vascular resistance okay the pulmonary vascular resistance just like your airways is dependent on the physical dimensions of the tube and likewise of the blood so resistance is equal to the viscosity of the blood times the length over that of the radius of your pulmonary blood vessels so aspirin viscosity is concerned it is directly dependent on resistance the higher the hematocrit the higher will be the pulmonary vascular resistance and therefore this is the basis why in some patients with increased pulmonary vascular resistance if they have polycythemia we do plebotomy now what are the factors that will control the radius of the pulmonary blood vessels these are the smooth muscle tone perfusion pressure lung elastance alveolar pressure and lung volume which interacts with each other okay so listed here are substances which dilates the pulmonary blood vessels and which con constricts the pulmonary blood vessels you're supposed to memorize this for the body exam and how are you going to memorize it you just memorize the pure ones okay if the if it is not in the pure ones then it is a constrictor so you just memorize the basal dilator okay if it is not the basal director then you assume it is a basal constrictor okay so how do we memorize the vasodilator the pneumonics is no blood pressure is bad so nitric oxide oxygen bradykinin prostacyclin or prostaglandin i2 beta adrenergic stimulation acetylcholine and dopamine okay these are the factors that will cause smooth muscle relaxation now let us first discuss one of the factors that determines the pulmonary vascular resistance and that is perfusion pressure the pulmonary circulation is a very compliant type of circulation an increase in blood flow is not accompanied by increasing perfusion pressure nor pulmonary vascular resistance this is due to the phenomena of recruitment and accommodation and this will illustrate you what we mean by recruitment and accommodation so initially these blood vessels are open but there is no blood flow as you can see here if there will be increased blood flow okay blood will blow to this open blood vessels okay so that is recruitment this previously blood vessels wherein there's no blood flow is recruited okay the other is accommodation you notice that the blood vessels are not fully distended so if there will be an increase in blood flow okay aside from the recruitment there will be dilation of the blood vessels that is accommodation now there are two types of blood vessels which determine the pulmonary vascular resistance so you have your extra alveoli blood vessels and you have the blood vessels which is exposed to alveolar pressure and we call that the alveolar blood vessels okay the extra alveolar blood vessels are dependent on the lung elastance while the alveolar vessels as i mentioned are dependent on alveolar pressure both lung elastance and alveolar pressure are on the other hand dependent on lung volume and how lung volume affects lung elastance and alveolar pressure are opposite each other that's why the pulmonary vascular resistance relationship to the lung volume is quite complicated so let us now study the relationship between lung volume elastance and extra alveolar vessels regions and you will notice that the relationship between lung volume and extra alveolar blood vessels radius is similar to that of the relationship between lung volume and small airways okay so this is the extra alveolar blood vessels as i mentioned to you it is dependent on the elastance tethering effect on the extra alveolar blood vessels we mentioned that the greater the lung volume the greater is the lung elastance and therefore at rb the elastance is low so the tethering effect on the extra alveolar vessel is quite low so this will be the radius and at tlc where there is a high elastance the tethering effect will be much higher and the radius will be much larger and therefore the greater the lung volume the greater the lung elastance the greater the extra alveolar vessel radius and therefore the lower is the extra alveolar vessel's resistance now let's now examine the relationship between lung volume and the alveolar pressure and the alveolar vessels reduce now the alveolar vessels radius is dependent on the surrounding alveolar pressure the greater the alveolar pressure the greater is the compression the lower is the radius of the alveolar blood vessels so at rb okay there is lesser collapsibility lesser elastance and there will be less alveolar pressure so there will be less compression of the extra alveolar blood vessels okay at tlc there's greater lung elastance so there's greater collapsibility so there's greater alveolar pressure there's a greater compression of the alveolar blood vessels and therefore the radius will be smaller so in essence what's happening is the greater the lung volume the greater the alveolar vessels okay the lower is the alveolar vessels reduce the higher is the alveolar vessel's resistance so it's exactly opposite that of the extra alveolar blood vessels so i mentioned to you that the alveolar vessels is directly related to lung elastance and alveolar vessels is inversely related to the alveolar pressure and both of these are related to the lung volume and therefore as we discussed in the previous two slides this is the relationship the greater the lung volume the greater is the alveolar vessel's resistance and the lower is the extra alveolar vessels resistance the mnemonics is left atrial enlargement lung volume is directly related to alveolar vessels resistance and inversely related to extra alveolar vessels resistance so this is the relationship between lung volume and pulmonary vascular resistance let's start up with the relationship of lung volume in the x-axis and the y-axis we're talking about alveolar vascular resistance okay so the greater the lung volume the greater is the alveolar vessels resistance and when we go to extra alveolar vascular resistance okay the greater the lung volume the lower is the extra alveolar vascular resistance okay your pulmonary vascular resistance is the sum of the resistance offered by your alveolar blood vessels and your extra alveolar blood vessels and you can see if you sum it all up the pulmonary vascular resistance is this u-shaped configuration okay so this one is the extra alveolar blood vessels resistance this one is the alveolar vessels resistance and this one is the total pulmonary vascular resistance and as i mentioned it is u-shaped and the inflection point is that in the frc so the pulmonary vascular resistance total goes down from rb to a par c then begins to rise again from f rc to tlc so in the initial part from the rb to the frc what is predominant is the extra alveolar vascular resistance okay which implements more the total vascular resistance and from frc to tlc what influence more the pulmonary vascular resistance is the alveolar blood vessels receive so let us now go to the effect of gravity on perfusion pressure alveolar pressure and blood block if the perfusion pressure is greater than the alveolar pressure this will become distended and there is going to be blood flow okay but if the alveolar pressure is greater than the perfusion pressure there will be compression and therefore there will be less blood flow in some situation if it is totally collapsed there will be no blood block now the problem now is the perfusion pressure is affected by gravity by while the alveolar pressure is not affected by gravity because of this one there will be a differential in blood flow from top to bottom of the lungs let us now go to the vascular zones of west and let's discuss the principles there are poor zones and we talk about three pressures albiola arterial venus you got to memorize this in alphabetical order albiolar then followed by arterial then the venous pressure the alveolar pressure is not affected by gravity while arterial ambinus are affected by gravity as i mentioned and therefore i like to think as the alveolar as the skipping pressure so in zone 1 the alveolar pressure is greater than the arterial and greater than the venous pressure in zone 2 the arterial is greater than the alveolar and greater than the venus so you see this skip to this one okay in zone 3 the arterial is greater than the venus and greater than the alveolar and in zonpor it's the same arterial is greater than venus greater than alveolar but the extra alveolar blood vessels are collapsed so that's how i memorize the different zones of west so in zone 1 the alveolar is greater than the arterial and greater than the venus this does not exist in the normal lung in zone 2 the arterial is greater than the alveolar greater than the venus and the vessels are partially compressed but there is some blood flow as you can see here with gradually increasing blood flow in sound three the stereo is greater than venus and greater than arterial and notice that the blood vessels are distended that's why you have the greatest blood flow here while in sown part the relationship still the same arterial is greater than nabinos greater than the alveolar and the extra alveolar bladder cells are partially collapsed okay and therefore there is no blood flow at this segment here because it is collapsed so which of the following constrict the pulmonary arterials what is our pneumonic no blood pressure is bad so if it is done if it is not here then it is a constrictor oxygen is in no nitric oxide is in no prostaglandin is in bp thromboxine is not seen here so this is the correct answer this is the basal constrictor which of the following best describes the pulmonary vascular resistance or the pbr our mnemonics is lab atrial enlargement and the total bar pulmonary vascular resistance is u-shaped the inflection point is at f r c so the pbr due to extra alveolar vessels is highest at tlc that is pulse because the greater the lung volume the greater the lower is the extra alveolar blood vessels resistance okay letter b pbr due to alveolar vessels is highest at rb again the grade that's pulse because the greater the lung volume the greater is the alveolar vessel's resistance then total pbr is higher in rb than in frc we looked at with this u-shape and that's right the pbr is higher in rb than at a par c that's the correct answer total pbr is higher in f rc than tlc we know that strong the pbr is lowest at f rc so we move on to the next topic number nine which is alveolar ventilation the respiratory zone starts at which anatomic structure part of the airway wherein the cartilage disappears be 10th generation of the lower airway c 17th generation in the 20th generation again i like you to pause try to answer then resume as i mentioned before the airway is divided by the larynx into your upper airway and the lower airway and your lower airway is just the trachea undergoing 23 dichotomous branching the conducting zone is from airway generation 1 to 16 and the respiratory zone is from airway generation 17 to 23. if for example an individual is going to inhale a tidal volume of 500cc okay 150cc of that will be distributed into your upper airway into your conducting zone and into your respiratory zone wherein there's a high bq relationship and that this is known as your dead space volume okay while the 350 will be distributed to the respiratory zone where it undergoes gas exchange because there's an alveoli and we call that the alveolar space volume so the tidal volume is then the sum of your dead space volume and alveolar space volume the type the volume is usually 5 to 7 mils per ideal body weight in kilograms while the dead space volume is 2.2 ml per actual body weight in kilograms the ba is computed we'll just get the difference between tidal volume and dead space volume and the bd over bt which is the piciologic dead space we just computed as bd over bt so for 60 kilograms times seven so that's approximately 420 ml of tidal volume 60 times 2.2 that's around 132 ml of dead space volume the alveolar space volume is 420 minus 132 that's 288 while the pistol logic dead space is 132 over port 20.

[02:02:38]so for a 70 kilograms we multiply that by seven then that's a wrap 490 but you usually round it up to 500 cc the pistol logic the dead space volume is 150 alveolar space is 350 and the pistol logic dead space ratio is 0.3 what for example will happen to these different parameters if there is going to be respiratory center depression okay what's going to happen is the tidal volume will go down but the anatomic dead space will be maintained and what will be sacrificed will be your alveolar space volume and consequently the pistologic dead space volume physiologic dead space ratio will be higher so let us now discuss alveolar ventilation which has a lot of patient logic significance i mentioned that tidal volume is equal to alveolar space volume plus dead space volume your minute ventilation or your be that is equal to tidal volume times respiratory rate okay so we're going to combine this two equation here so be that is equal to tidal volume which is the sum of alveolar space volume plus dead space volume times respiratory rate okay we're going to multiply rr to this one and therefore we come up with b dot is equal to b a plus r plus bd times r okay this is known as your ba dot this is known as your bd dot okay so be that is equal to ba dot plus bd dot okay so what we're interested with is your b a dot okay that is what is a lot of patio logic significance so we're going to place this on this side of the equation and we're going to transfer this to the other side of the equation so we come out with b dot minus b that equals b a dot okay if we want to expand be that which is tidal volume times rr we come up with the final equation which is tidal volume times rr minus bd dot is equal to ba dot now the ba dot has a lot of significance okay the greater the alveolar ventilation the greater is the auto tension the lower is the co2 tension this is sin in this graph here okay the greater the alveolar alveolar ventilation the greater is the auto tension and the lower is the co2 tension why is that so because alveolar ventilation is the mode of delivery for o2 from the atmosphere into the alveoli into the body alveolar ventilation on the other hand is the mode of elimination of carbon dioxide from the body into the alveoli out into the atmosphere that's why we have this relationship so if the alveolar ventilation will go down the o2 tension will go down while the carbon dioxide tension will go up okay so let's apply that with this equation here so if the tidal volume will go down or the rr will go down or the bd dot will go up the ba dot will go down and consequently the o2 tension will go down while the carbon dioxide tension will go up so the respiratory sound starts at which anatomic structure part of the airways wherein the cartilage disappear that is pulsed those are known as their bronchioles okay the tenth generation of your lower airway that's still part of your conducting zone okay conducting zone is one to 16 and your respiratory zone starts from airway generation 17 to 23. so this is the correct answer okay not the 20th because the respiratory zone starts at 17.

[02:06:55]okay which of the following is both seen in alveolar ventilation and alveolar gas equation ka the paco2 be the pao2 c the carbon dioxide production d r q so i want you to pause try to answer then we're going to resume let's now talk about the two confusing pulmonary equations the alveolar ventilation equation and the alveolar gas equation so there's a ventilation and there's a gas equation alveolar ventilation equation is the relationship between the ba dot which is directly related to the carbon dioxide production of the body or bco2 that over that of alveolar carbon dioxide tension while the alveolar gas equation talks about the o2 tension in the alveoli okay it is equal to the inspired oxygen tension minus the quotient of the alveolar carbon dioxide over that of the respiratory equation let's talk about alveolar ventilation equation in mold more detail okay so again ba dot is directly related to the carbon dioxide production over that of alveolar carbon dioxide okay this is a cos effect relationship this may affect this one or this may affect this one so we rewrite it this way so let's analyze the relationship okay if the carbon dioxide production of the body is constant okay and the ba dot is going to increase what is going to happen to the alveolar carbon dioxide tension it is going to go down okay on the other hand if the carbon dioxide production of the body is going to increase and the individual would like to maintain the alveolar carbon dioxide tension constant the alveolar ventilation needs to increase so that the alveolar carbon dioxide tension will remain constant now let's go to the alveolar gas equation again the alveolar o2 tension is equal to the inspired oxygen tension minus the quotient of alveolar carbon dioxide over that respiratory quotient okay these are the cause variable and this will be the effect variable so for example there will be an increase in alveolar carbon dioxide tension the alveolar auto tension will go down and that's based on dalton's law okay so which of the following is both seen in alveolar ventilation and alveolar gas equation okay what are the two confusing equations okay one is the alveolar ventilation equation so ba that is equal to bco2 over paco2 and the other one is alveolar gas equation so what's the mean variable it is o2 tension in the alveoli which is equal to the pio2 minus the quotient of alveolar carbon dioxide over respiratory ocean so archeo is it mozin no bco2 it's not it's only seen in the alveolar ventilation equation that's false the pao2 is only seen in the alveolar gas equation and the paco2 is both seen in the alveolar ventilation and the alveolar gas equation so that's the correct one so let us move on now to the diffusion along the albiolo capillary membrane which of the following is accurate with regards gas exchange along the alveolar papillary membrane under normal conditions blood stays in the pulmonary capillary four times longer than necessary per carbon dioxide to be adequately removed from the blood b compared to o2 co2 is more depreciable because of a higher molecular weight c during exercise the pulmonary capillary blood transit time is prolonged to promote optimal gas exchange the during tachycardia the pulmonary capillary transit time is shortened and therefore promote hypoxemia okay i'd like you to pause try to answer then resume the diffusion along the ac membrane is governed by the pig's law of diffusion which states that the amount of gas that then that can diffuse along the ac membrane is directly related to the surface area the solubility of the gas the pressure gradient across the ac membrane and inversely related to the thickness of the membrane and the gas molecular weight so this is the relationship of this equation these are the cost variable and this is the effect variable okay so the gray the lower the area the solubility the pressure gradient the thicker the ac membrane is the higher the molecular weight of the gas the lower will be the amount of gas that is going to diffuse along the ac membrane okay which will have an easier time diffusing along the ac membrane the carbon dioxide or the oxygen initially you're going to think that the carbon dioxide is going to have a more difficult time diffusing across the ac membrane because it has a higher molecular weight however the carbon dioxide is much much more soluble than that of oxygen and therefore it diffuses along the ac membrane 20 20 times easier compared to that of oxygen let's now discuss the diffusion of oxygen and carbon dioxide along the ac membrane the alveolar oxygen tension is 104 while the mixed venus auto tension is 40 so the direction of the fusion is towards the blood vessel okay so the blood is going to enter at the venus side and going to traverse the pulmonary capillary and ends up here at the arterial end which is known as the n capillary blood okay notice that the initial net diffusion is from the albiolus to that of the blood in the pulmonary capillary shown by a bigger arrow going this direction against that upper arrow towards going that's direction now at this point here you can see that both arrows are equal in size meaning to say that equilibrium is achieved at this level here and as blood goes from this point till the end capillary there is no net diffusion because equilibrium is already achieved now with regards carbon dioxide is concerned the mixed venus co2 tension is 45 while the alveolar co2 tension is 40 and therefore the net depletion will be towards the albiolus okay notice again that here equilibrium is immediately achieved almost immediately achieved okay as blood enters into the pulmonary capillaries and the rest as it goes through the end capillary there's no net diffusion because equilibrium equilibrium is already achieved okay this is another way of looking at the previous figure the x-axis is the rbc capillary transit time the y-axis there too this is for the auto tension and this is for the carbon dioxide tension in the mixed venous blood or the blood in the pulmonary capillary so initially the auto tension is sporty okay it goes up as gas is diffused oxygen is diffusing from the alveolus into the capillary goes up and equilibrium is achieved at this point at around point 23 seconds and the rest of the time as blood as the blood is traversing the pulmonary capillary there's no change in auto tension because equilibrium is already achieved while per carbon dioxide we we initially started at 45 okay as carbon dioxide diffuses from the blood into the alveoli it decreases in tension and it achieves equilibrium at this point at around 0.7 seconds sorry around point 17 seconds and the rest of the time there's not much change in the carbon dioxide because it is already in a state of equilibrium okay so this is the normal capillary transit time at rest it's around 0.75 seconds and notice that the critical contact time is 0.23 seconds for rbc to be fully oxygenated it needs only to stay around 0.23 seconds out of the 0.75 to be fully oxygenated and the rest of the time we have a large reserve okay so during exercise the reserved time the pulmonary capillary transit time is going to decrease okay but it seldomly decrease below the critical contact time so from 0.75 because of the tachycardia it may go down to 0.5 0.27 but it seldomly goes down to 0.23 to cause hypoxemia so we go back to this question here which of the following is accurate with regards the gas exchange along the ac membrane under normal conditions let's start from below during tachycardia the pulmonary capillary transit time is shortened and therefore promote hypoxemia that is pulse we mentioned it goes down the pulmonary transit time but it seldomly goes down below 0.23 seconds which is the critical attack time during exercise the pulmonary capillary blood transit time is prolonged to promote optimal gas exchange again during exercise there's tachycardia the blood transit time is shortened compared to o2 co2 is more diffusible because of a higher molecular weight based on the pig's equation okay peak slope diffusion that is not true it is because the carbon dioxide is much much more soluble than that of oxygen along the ac membrane and a blood stays in the pulmonary capillary four times longer than necessary for co2 co2 to be adequately removed from the blood and that's the correct answer okay it only needs point 17 seconds per equilibrium and it stays in the blood the blood stays per point 75 seconds so this is the correct answer so let us now move on to the 11th sub topic which is bq relationship which of the following best describe the respiratory units affected by pulmonary embolism a the bq relationship is zero b the alveolar o2 tension is less than 100 part c the alveolar co2 tension is less than 40 and the the respiratory units contribute to the alveolar chant effect i want you to pause try to answer then resume the video which of the following occurs in the lower lung zones respiratory units of an upright lung a hibicu relationship b albiolar shunt effect c auto tension greater than 100 poor in the shunt effect again i like you to pause try to answer then resume the video once you have an answer as i mentioned before what will determine the respiratory units ventilation is compliance and resistance the greater the compliance the greater the ventilation the greater the resistance the lower is the ventilation let us now discuss the ideal bq relationship and to simplify things we're going to think of as the lungs being composed of just two respiratory units the right and the left and the pulmonary artery branching into the right into the left if the minute ventilation is 6 liters 3 liters will go to the right and 3 liters will go to the left if the cardiac output is 6 liters 3 liters will go to the right and 3 liters will go to the left branch of the pulmonary artery okay if we try to compute for the ventilation over perfusion b q 3 over three is equal to one and b q of one is known as your ideal bq that is the bq relationship wherein there's optimal gas exchange from a bq relationship of one okay there may be alteration for example there will be increased airway resistance or diminished compliance of this respiratory unit here and therefore instead of receiving 3 it receives only 2 liters of ventilation 2 over 3 is less than 1 and therefore this type of bq relationship is known as your low pq relationship if for example there's total blockade of the ventilation the of the airways the ventilation now will become zero zero over three is zero and this is known as a b key of zero or a shunt bq relationship on the other side the perfusion may be affected such as there may be partial blockade of the pulmonary artery instead of receiving three it just receives two three over two is more than one and therefore it's known as your high bq relationship or there may be total blockade of the pulmonary artery so the perfusion is now zero three over zero is known as infinity bq now what are the causes of the bq abnormalities low bq okay this could either be a high airway resistance which is going to diminish the ventilation or low compliance which is going to diminish the ventilation such as what you see in pulmonary fibrosis and scoliosis how about the shunt bq okay this may be due to a total obstruction due to a poring body or an extrinsic airway mass producing zero ventilation or there may be at octalectasis collapse it may be extrinsic compression of the alveoli such as in hydrothorax or pneumothorax or a mass which compresses on the alveoli it may also be passive batalectasis such as in the case of hyaline membrane disease wherein there's absence of surfactant okay the albiolai is going to collapse or this may be blooded by fluids as you see in congestion or exudates as you see in pneumonia this diseases will give rise to a shunt bq a high bq relationship can be secondary to the partial obstruction of the blood vessels as you see in pulmonary embolism or during a hypotensive state wherein the profusion will be less than the idl a bq of impinity is seen if there's complete obstruction of the blood vessels as you see in pulmonary embolism wherein the perfusion is going to be zero so three over zero is infinity okay so in copd or asthma what is the primary bq relationship so there will be obstruction in the airways there will be diminution of ventilation and therefore it is a lobby relationship how about the pneumonia what is the bigger relationship so the alveoli will be plotted by exudates and therefore the ventilation will be zero and you have a bq relationship how about in hydrothorax what is the primary bq relationship okay this plural fluid is going to compress on the alveoli it's going to cause collapse of the alveoli and therefore the ventilation will be zero and you have a shunt bq relationship how about pulmonary embolism okay the blood clot will go out to the pulmonary blood vessels diminishing the perfusion or in some extreme cases causing it to be zero and therefore it gives rise either to a high bq relationship or a big u of infinity how about if there is a hypotensive state what will be the primary bq relationship again the q will be affected it will go down so what you're going to have is a high bq relationship so let us discuss the relative ventilation of the different types of the bq relationship in a high bq relationship in infinity you can see that the ventilation is higher than the perfusion so you say that there's a relative hyperventilation in this respiratory unit now in the low bq and the shunt bq you can see that the ventilation is much lower than the perfusion so you may say that there is a relative hypoventilation in this respiratory units with this big u relationship now we go back again to alveolar ventilation we mentioned that the greater the alveolar ventilation the greater is the auto tension the lower is the carbon dioxide tension and therefore if the alveolar ventilation will go down okay the auto tension will go down while the carbon dioxide tension will go up okay so the ideal bq okay you have an optimal gas exchange and therefore the alveolar and blood in the pulmonary capillaries is going to have an auto tension of 100 pore and a co2 tension of 40 okay what is going to happen if you're going to have a relative hyperventilation okay so in relative hyperventilation what will happen to the o2 tension it's going to be higher while the carbon dioxide tension is going to be lower okay higher o2 and lower co2 how about if you have low or shunt bq what will happen to the o2 and co2 tension okay the lower the alveolar ventilation the lower is the auto tension and the higher is the carbon dioxide tension okay so those are the consequences of bq relationship in the auto tension and co2 tension in the alveoli and blood in the pulmonary capillaries so let's have a brief review of what did we discuss so in a big relationship of one the ventilation is matched with the perfusion so the auto tension will be 100 poor and the co2 tension will be 40.

[02:27:44]in the low bq there is relative hypoventilation so the auto tension will be lower while the carbon dioxide will be higher and uh in a 0bq there's much more relative hypoventilation so the auto is much lower okay and the carbon dioxide is much much higher now in a high bq such as in a hypotensive state there's relative hyperventilation so you expect the o2 tension to be greater than 100 pore and the co2 tension to be less than 40.

[02:28:17]however in a b key of infinity okay there's more relative hyperventilation and therefore the old potential will be markedly elevated while the carbon dioxide tension will be markedly low now let us analyze now the bq relationship of the normal lung okay here is the relationship in the x-axis is from the base going to the apex and this is the perfusion notice as one goes from the base to the apieces the perfusion decreases let's do it another way around as you go from the apcs to the base there's increase in the perfusion meaning to say that the lower lung zone is eight times better purpose than the upper lung zone let's now analyze ventilation again from base to apex and ventilation is in the y-axis notice as you go from the apex to the base the ventilation increases meaning to say that the base as you can see here is three times better ventilated than the apcs now which is more affected by gravity you can see that the slope is steeper here so the perfusion is affected more by gravity and because of this it gives rise to regional differences in bq relationship so we combine the two this is ventilation this is perfusion okay notice that in the lower lung zone the ventilation in blue is less than the perfusion in red and therefore the bq relationship is a law bq notice in the a pieces in the upper lung sun the blue which is ventilation is greater than the perfusion and therefore the bq relationship is a high bq here so in the middle you have an ideal bq okay so the auto tension will be one opportu in the upper lung zone you have a high bq so the auto tension will be greater than 100 par and the co2 tension will be less than 40 because there's relative hyperventilation in the upper lung zone while in the lower lung zone you have low bq since you have a relative hypo ventilation the auto tension will be lower while the carbon dioxide will be higher so let us now talk about shunt is a situation wherein blood was not allowed to have gas exchanged with albiolar gas and there are two types the anatomic and the alveolar shan so we already discussed the two types of anatomic shunt now let's shift our attention to albioneration albiologian can occur in a bq relationship of zero or a shunt big q or a low bq relationship in a shunt beak you are a bq relationship of zero notice that in this situation three liters of blood was not given a chance to have gas exchange with air in the alveoli and this situation is known as your true albiologian now in the lobby relationship notice again that not all blood one liter of blood in fact was not given a chance to have gas exchange with gas in the alveoli and this situation is known as your alveolar shunt effect going back to the normal upright lung we know in the lower lung zone we have a low bq relationship and therefore in our lower lung zone we have alveolar shunt effect the total shunt otherwise known as your visual adjection is a combination of your anatomic and alveolar shine it accounts for four percent of the left cardiac output pathological shunt may arise and this may be due to lung diseases which create a low bq relationship or a bigger relationship of zero likewise cardiovascular diseases wherein there's passage of blood from the right to the left heart circulation will give rise to pathologic shunts moving on to dead space ventilation it is a situation where an inspired air is not allowed to have gas exchange with pulmonary capillary blood and there are two types the anatomic dead space and the alveolar dead space the anatomic dead space is composed of your upper airway and the lower airways conducting zone while your alveolar dead space are respiratory units with a bq relationship of infinity or a high bq relationship notice that in a bq of infinity in this drawing here 3 liters of air was not given a chance to have gas exchange with blood in the pulmonary capillary in a high bq not all of the air in the albiolai in fact one liter was not given a chance to have gas exchange with blood in the pulmonary capillary alveolar dead space exists in our normal upright lung we know in the upper lung zone we have a high bq relationship and therefore we have a dollar dead space ventilation in our upper lung zone so the total dead space or your pistologic dead space is composed of the sum of your anatomic dead space and your alveolar dead space and it is usually 150 ml per 70 kilogram individual or 2ml of actual body weight in kilogram so we have our anatomic dead space which is composed of your upper airway conducting zone and you have your alveolar dead space which are the high bq relationship in the upper lung zone the total physiologic dead space k may increase in pathological conditions which may give rise to an increase in our alveolar dead space conditions such as pulmonary embolism or hypotensive state which gives rise to a respiratory unit with a high bq relationship let's now discuss the bq mismatching we got to understand that the respiratory units are connected to each other so from an ideal situation of a bq relationship one pathological condition may set in such as if there is a partial airway obstruction on the right respiratory unit okay instead of receiving 3 it receives 2 liters of ventilation and 2 over 3 is a big relationship of 1.

[02:35:33]now the 1 liter that's supposed to go here is diverted to the other side and therefore it receives 4 liters okay of ventilation over a 3 perfusion 3 liters of perfusion so you have a high bq relationship now in this situation here okay you have a shunt big u or a b q of zero the three that's supposed to go here is diverted to the left side okay and therefore you have six over three and likewise you have a high bq relationship so reba bq or allah bq it indirectly gives rise to a high bq relationship and therefore it increases the alveolar death space moving on to the other side of the illustration pathological condition may occur in the pulmonary circulation such as partial obstruction of the blood vessels such as in pulmonary embolism okay the instead of three it only receives two so you get the big relationship that's three over two that's a big u of greater than one the one liter that's supposed to go here goes to the other side so you have a three over poor bq relationship which is less than one okay in this situation here you have total obstruction of the blood vessels going to the right so the ventilation is zero three over zero i mean the perfusion is zero so three over zero is a big q of infinity the tree that's supposed to go here is diverted to the other side so it gives rise to a bigger relationship of 3 over 6 which is a big u less than 1.

[02:37:14]so a high bq relationship or a bq of infinity indirectly gives rise to a low bq which is going to give rise to alveolar shunt effect now what is the consequences of this bq mismatching under normal condition our pistologic dead space ventilation is due to the ventilation of our anatomic dead space and our alveolar dead space which are located in the upper lung zone now pathological condition may occur which can give rise to big mismatching producing a high or a b of infinity and therefore it adds to alveolar dead space and therefore during vcu mismatching our pistol logic dead space ventilation increases and consequently our alveolar space ventilation decreases which will lead to hypoxemia and hypercapnia so what are the compensatory mechanism for a primarily low bq or a 0bq from an ideal situation okay ventilation problem may occur and it may give rise to a low bq and indirectly give rise to high bq relationship now the compensatory mechanism that is going to be instituted by the respiratory system is in the circulation what's going to happen is there is going to be a hypoxic bus constriction notice that the bq relationship here is low and therefore there will be hypoxemia or hypoxia and the response of the pulmonary circulation will be constrict what will the constriction do notice what's going to happen instead of 3 going here it's going to be 2.5 then partially correcting the log bq here okay likewise the bus constriction here will divert the blood that's supposed to go here towards this side and therefore you're going to have a q of 3.5 and therefore partially correcting the high bq relationship so the hypoxic bus constriction will partially correct the bq mismatching what is then the compensatory mechanism for a primarily high b q or a b q of infinity now from a normal condition there may be perfusion problem there's partial obstruction here so you have a bq relationship that's 3 over 2 or infinity and the blood that's supposed to go here goes here so you have a big relationship of zero what will be the response since the problem is in the perfusion the response will be in the ventilation so what's going to happen is there's going to be bronchoconstriction so instead of three the ventilation in this respiratory unit will be around 2.5 because of the bronchoconstriction partially correcting the high bq relationship from a 3.2 it partially corrects it to 2.5 over 2 and the air that's supposed to go here is directed here so instead of 3 it receives 3.5 so it partially corrects the low bq up three over poor to a partially corrected 3.5 is to poor okay so it partially corrects the bq mismatching so if the primary abnormality is in the ventilation which will give rise to a low b q or a shunt pq the response will be in the circulation in the form of hypoxic vasoconstriction now if the primary beacure abnormality occurs in the perfusion such as in high bq or bq infinity the response will be in the ventilation and there will be bronchoconstriction so the rule of thumb is the other component the v or your q will compensate so going back to this interactive question which of the following best described the respiratory units affected by pulmonary embolism so in pulmonary embolism there may be partial or complete blockade of the pulmonary capillary and therefore it is going to give rise to a high bq or a big u of infinity and where and therefore the bq relationship is zero is wrong okay again we discuss it's supposed to be high or a b key of infinity that'll be other auto tension is less than 100 poor we have relative hyperventilation in a high or a pq of infinity and therefore we expect the oxygen to oxygen tension to be greater than 100 poor okay the alveolar co2 tension is less than 40.

[02:42:12]again we have a relative hyperventilation so we expect the carbon dioxide to be lower and therefore this is the correct answer the respiratory units contribute to alveolar chantipek we only see albion shantipek in a big q relationship that is low bq relationship so that is paulus okay a high or infinity big q gives rise to alveolar dead space so the correct answer is c targolar co2 tension is less than 40. interactive question number 17 which of the following occurs in the lower zone's respiratory unit open upright lung high bq relationship we know in the lower lung zone it has a low bq relationship okay that's false alveolar shanty peck since it is a low bq relationship yes it can give rise to albiola chante auto tension greater than 100 poor since we are below bq we have relative hypoventilation and therefore the auto tension will be less than 100 for shunt bq we don't have a shunt bq in the lower lung zone it is only a low bq relationship the correct answer is alveolar chant effect let us now discuss the second to the last topic which is gas transport which of the following is the correct pix equation vco2 is equal to carjack output times the arterial autocontent bo2 is equal to cardiac output times the mixed venus auto content oxygen consumption is equal to cardiac output minus the difference between the arterial and mixed venous auto content and auto consumption is equal to cardiac output times the sum of the arterial and mixed venus auto content again pause try to answer and resumes once you have an answer so oxygen from the alveoli is transported into the blood into two perms one it's dissolved in physical solution and the other one it is bound to hemoglobin okay if we want to compute for the auto content of arterial blood that is cao2 arterial blood content of oxygen we have to compute for the amount in physical solution and the amount for hemoglobin bound to hemoglobin to compute by the amount in physical solution we multiply.003 times the arterial o2 tension and when we want to compute per the amount of oxygen bound to hemoglobin we use this formula hemoglobin in grams per deciliter times 1.3 per times autosaturation auto saturation is determined by your hemoglobin auto dissociation curve let's analyze this hemoglobin auto dissociation curve in the hemoglobin auto dissociation curve the x-axis is oxygen the y-axis is saturation you can see that the higher the arterial oxygen tension the higher is the hemoglobin o2 saturation but the relationship is not linear it is sigmoidal it is a steep part from 0 to 60 and it has a blood part from 60 and beyond now let me introduce you to the concept of the pppt ppt is the auto tension wherein the hemoglobin is 50 saturation okay so the hemoglobin is 50 saturation so that's what around here so at 50 saturation the arterial auto tension is around 27 okay so normally the pppt is 27 and ppt starterial auto tension wherein the hemoglobin is 50 saturated with oxygen so let us now compute for the oxygen content of arterial blood usually the arterial blood has an arterial auto tension of 95 at 95 you can see that the hemoglobin is 97 saturation so what's the formula how do we compute per the amount of oxygen dissolved in physical solution is point zero zero three times the arterial auto content arterial auto tension so 0.003 times 95 is equal to 0.28 ml how do we compute for the amount bound to hemoglobin okay hemoglobin times one point three port time is auto saturation okay margarine times 1.34 times o2 saturation 15 times 1.34 times uh times 97 that's 19.5 so we sum it all up okay that's around 200 ml per liter of blood so normally the arterial auto content is around 200 ml of blood now let's compute for the auto delivery to the tissue or the do2 delivery of oxygen to the tissue we mentioned that the arterial auto content is 200 ml per liter and the cardiac output is usually 5 to 6 liters so pi times 200 okay the auto delivery is equal to cardiac output times arterial auto content pipe times 200 so normally we're delivering 1000 ml of oxygen per minute to our tissues okay so what are the factors that will affect the auto delivery to the tissues so the do2 is equal to carjack output times ca02 and how do we compute for your cao2 okay it is the amount in physical solution plus bound to hemoglobin what's the formula for in physical solution it's point zero zero three times oxygen tension bound to hemoglobin one point three four times hemoglobin times o2 saturation okay so we come out with these factors that will determine auto delivery so for example there will be a low auto saturation there will be low hemoglobin okay there will be a low oxygen tension or the cardiac output will be low the auto delivery to the tissues will be low now let us now discuss the auto content of mixed venus blood okay it is represented as cvo2 venus blood content of oxygen okay so how much is the oxygen content in venus blood well we use the same formula we cvo2 is equal to in physical solution times hemoglobin but this time we're using venus blood and venus blood has an auto tension of 40 and a saturation of 75 so in physical solution point zero zero three time is sporty bound to hemoglobin the same hemoglobin 15 times one point three poor but this time the saturation is 75 instead of 97 percent so the amount total amount of oxygen in venus blood is 0.12 plus 15 that's roughly around 150 ml per liter of blood okay so the mixed venous blood is a content of 150 ml and if the right cardiac output is 5 liters the amount of oxygen delivered to the pulmonary capillaries is roughly around 750 ml okay so let's now go to oxygen consumption okay if the amount of oxygen delivered to the tissues is 1000 ml per minute and the amount of oxygen leaving from the tissues in the venous blood going into the pulmonary circulation is 750 ml per minute how much was extracted by the tissues so simplistically to compute for the bo2 which is the auto consumption we just get the difference of the amount delivered cardiac output times arterial auto content minus the amount of auto leaving the pulmonary circulation and being delivered to the pulmonary circulation so that's co2 times si binos so this is the peaks equation for the computation of auto consumption okay and we can rewrite it in a short term cardiac output times the difference between the arterial auto content and the mixed venus auto content so which of the following is the correct peaks equation cardiac output times arterial auto content that's pulse that's the auto delivery equation cardiac output times cbo2 that suppose that's the auto delivery to the pulmonary capillaries cardiac output times the difference between arterial and mixed venous blood auto content that's the correct answer it is not cardiac output times the sum of arterial and means venus auto content okay question 19 which of the following is correct with regards a right shape of the hemoglobin auto dissociation curve a hemoglobin affinity to o2 increases b p p rises c hemoglobin rejects carbon dioxide and d associated with the low hydrogen ion content again i like you to pause try to answer and resume once you have an answer so let us now discuss the shifting of the hemoglobin auto dissociation curve now this is the normal position of the hemoglobin auto dissociation curve it may shift to the right or shift to the left okay so at a normal position at a auto tension of 50 the immoglobin is 85 saturated okay an increase in your hydrogen carbon dioxide temperature or 2 3d fiji is going to shift the curve to the right so what will happen if there will be shifting to the right okay again at an oxygen tension of 50 let us see what will be the saturation if the curve is shifted to the right we can see that the saturation is 79 so from 85 when it is shifted to the right it is less saturated so meaning to say that the hemoglobin is rejecting oxygen okay so arise in your 2 3 dpg hydrogen carbon dioxide and temperature will cause the hemoglobin to reject oxygen this will cause a reduction of your auto saturation and this will lead to the right shift of the curve so it is the rule of r now let us see what is going to happen to the p p if the curve is going to shift to the right p t is the auto tension where the hemoglobin is 50 saturated so we we know at 50 saturation and normal position is around 27. what will happen if it is shifted to the right okay when it is shifted to the right we can see that the p50 rises increases from 27 up to 32 so meaning to say arise in your 2 3 h cut is going to cause himoglobin to reject oxygen it is going to lead to a right shape of the curb and this is manifested as a rise in your ppt lowering of your 2 3h cut on the other hand will make hemoglobin labs oxygen okay and therefore leads to the left shape of the curb manifested as lowering up your ppt okay so that's how you're going to remember the shifting to the left and to the right of the hemoglobin auto dissociation curve it is the rule of r's and the rule of l so let us now analyze what is going to happen to the hemoglobin auto dissociation curve during carbon monoxide poisoning as illustrated here during carbon monoxide poisoning okay the carbon monoxide displaces the oxygen and carbon dioxide from the amount of bean and therefore the transport of oxygen and carbon dioxide is severely hampered now aside from that the carbon monoxide is going to displace the hemoglobin auto dissociation to the to the left and therefore in this situation the immunoglobulin labs oxygen and hemoglobin doesn't want to release oxygen so it's a double whammy aside from the carbon monoxide displacing oxygen from the hemoglobin the remaining hemoglobin with bound auto does not want to be released does not want to release the auto to the tissues and therefore there will be severe tissue hypoxia moving on to the unloading of oxygen in the systemic capillaries okay the arterial o2 tension is 95 while in the tissue it is 23 and therefore the pressure gradient papers the movement or the diffusion of oxygen from the arterial blood into the tissues and the amount of oxygen remaining in the venous blood will produce an auto tension of around 40.

[02:57:44]let us now discuss the bourse effect it occurs in the systemic capillaries so this is the rbc with the oxygen bound to the hemoglobin and these are the tissues okay the cells of the tissue okay the cells produce a lot of carbon dioxide and hydrogen and they're going to cause the hemoglobin auto dissociation curve to shift to the right remember 2 3 h cut will cause the curve to shift to the right this will make hemoglobin reject oxygen and the rejection of oxygen will pay for the unloading of oxygen into the tissues let us now discuss internal respiration under normal condition we inspire around 200 ml per minute of oxygen and that 250 ml of oxygen is used by our tissues in aerobic metabolism aerobic metabolism likewise produces 200 ml of carbon dioxide that is subsequently expired by our respiratory system out into the atmosphere okay the ratio of the carbon dioxide production over that of the auto consumption is known as your respiratory ocean okay the ratio of the carbon dioxide production over that of the auto consumption is known as your respiratory exchange ratio okay what's the difference if you get the ratio at the tissue level that is known as your respiratory ocean if you get the tissue in the expired gas that is known as your respiratory exchange ratio so the respiratory quotient okay is equal to the carbon dioxide production of the body over that of the consumption and it's usually 0.8 okay this is uh this side sometimes hard to remember the rq is equal to bco2 over bo2 so it's alphabetical co2 over o2 now normally it's around 0.8 and it may be altered depending on what is the predominant food that we're consuming if it is predominantly carbohydrates the iq becomes 1 proteins it's 0.8 fats becomes lower than 0.8 which is 0.7 so let's now discuss the concept of hypoxemia and hypoxia hypoxemia is low oxygen tension again it's low oxygen tension in the arterial blood hypoxia on the other hand is the inability of the tissue to use oxygen due to either or in low auto delivery or mitochondrial enzyme problems what are the causes of hypoxemia a low arterial autotension a law inspired oxygen such as in high altitude hypoventilation wherein there's cns depression the minute ventilation goes down ac membrane depletion problems such as interstitial lung disease bq mismatching such as in primary lung disease circulation such as your cyanotic heart disease so these are the pipe causes of hypoxemia hypoxia on the other hand slope caused by low auto delivery or a mitochondrial enzyme problem and when we review the auto delivery equation we can see that the cause of low auto delivery could either be a low saturation low hemoglobin low arterial auto tension or hypoxemia a low cardiac output and therefore the low auto delivery as a cause of hypoxia can be further subdivided to that of hypoxiamic hypoxia and the non-hypoxemic hypoxia in the hypoxemic hypoxia this is the cause the low arterial auto tension is the cause of the low auto delivery and the hypoxemia could either be juto what we discussed earlier allo pao2 cns problem ac membrane problem bq mismatch and shunt anomaly so for the non-hypoxamic hypoxia it may be due to a low cardiac output or low hemoglobin so therefore a low cardiac output or hemoglobin problem such as a low hemoglobin level or defective hemoglobin such as in meth hemoglobin mitochondrial enzyme problem is another cause of tissue hypoxia there may be adequate auto delivery but the mitochondria cannot use the deliberate oxygen such as if there's cellular enzyme dysfunction or cyanide poisoning now what are the modes of transport of the carbon dioxide produced by the tissues one is in physical solution either inside the rbc or in the plasma two it can bind to hemoglobin three it can be transported as bicarb which is the predominant form so carbon dioxide binds with hydrogen produce your carbonic acid dissociates into air by carbon hydrogen bicarb moves out of the cell in exchange chloride moves in that's known as your chloride ship it is an osmotically active substance it attracts water and this is the reason why the venus hematocrit is much larger than the arterial hematocrit now let us now discuss how they inspect alden occurs in the pulmonary capillaries and as you know in the pulmonary capillaries the albiolae there's a law co2 tension okay the lossy auto tension is going to shift the hemoglobin auto dissociation curve to the left which means that hemoglobin labs oxygen and therefore oxygen will go and bind to the hemoglobin and displaces carbon dioxide so it is going to be eliminated out into the alveolus into the atmosphere okay so voice effect occurs at the systemic capillaries the stimulus is the high carbon dioxide and the high hydrogen produced by the tissues it cause the hemoglobin auto dissociation curve to shift to the right it makes hemoglobin unloads oxygen okay alden sepec occurs in the pulmonary capillaries the stimulus is a low carbon dioxide okay which caused the moglin hemoglobin dissociation curve to shift to the left okay and therefore hemoglobin loves oxygen okay oxygen will bind to hemoglobin displacing carbon dioxide and therefore this papers carbon dioxide unloading in the pulmonary capillaries so let us analyze the differences between the hemoglobin o2 and the co2 dissociation curve this is the hemoglobin auto dissociation curve it is sigmoidal and therefore the hypoxemia low bq cannot be fully compensated by hyperoxymia of a high bq now this is the mog this is the co2 dissociation curve you can see it is almost linear and because of this the hypercapnia of a low bq can be fully compensated by the hypocapnia of a high bq okay let me illustrate that further so you have your barbecue is matching here okay because of this obstruction it gives rise to a lobby q which gives rise indirectly to a high bq okay let's talk about the oxygen tension because of the lobby q it is hypoxemia on the right side and hypercapnia on the left side and when we try to average this okay the hypercapnia cannot compensate for the hypoxemia and therefore the auto tension will be below the expected average of 100 instead it is 75 because this one cannot fully compensate for this one because the shape of the immunoglobulin auto dissociation curve is linear when we look at the carbon dioxide tension this one is going to have a hypercapnia and this one is going to have a hypocapnia secondary to the high bq relationship and when we average it we come out with the real average of 30 plus 50 divided by 2 is 40.

[03:06:43]meaning to say this one was able to fully compensate for this one because the shape of the co2 dissociation curve is linear so let's discuss this uh 19 interactive question it reads which of the following is correct with regards the right shift of the hemoglobin auto dissociation curve the mongodb infinity to the auto increases actually if there's a right shift among the being is rejecting oxygen that's pulse okay so a right shift is associated with a rise in your ppt okay hemoglobin rejects co2 hemoglobin rejects auto not co2 okay associated with the low hydrogen ion concentration it is a rise in your 2 3 h cot which causes a right shape of your curb so therefore it is not a low hydrogen but a high hydrogen that causes the right shift of the curve okay so the correct answer is ppt rises okay we now go to the last topic which is the controller pretty okay which of the following is the central chemoreceptor most sensitive with arterial autotension arterial carbon dioxide tension csf co2 tension or csf ph so the purpose of the controller perspiration is to establish an automatic rhythm for the contraction of the respiratory muscle this rhythm should match the following the metabolic demands the non-ventilatory events and varying mechanical conditions now let us discuss the respiratory related neurons and there are three types the interneurons which makes interconnection to the other respiratory related neuron the pre-motor neuron which enervates the motor neuron in the motor neuron which innervates the ventilatory muscles so this is another way of looking at the respiratory related interneurons okay you have the motor neurons which innervates the respiratory muscle then you have your pre-motor neurons which enervates the motor neuron then finally you have your interneurons okay which makes interconnections with the other respiratory related neurons okay the first is the ventral respiratory group it is this one okay it contains inspiratory and expiratory neurons and therefore stimulates your inspiratory and expiratory muscles it generates the tidal breathing okay and it is modified by inputs coming from the pontine respiratory center and the dorsal respiratory group the drg which is this one receives sensory information from the chemoreceptors and mechanical receptors it stimulates the brd so that the breathing pattern will change depending on the auto and co2 needs of the individual acid-base balance and other metabolic demands so it is a metabolic feedback for the vrg okay the pontine respiratory center which is this big one here receives sensory information from the higher centers and the peripheral chemoreceptors it inhibits the brg so that the breathing pattern will change during speaking sleeping and exercising okay so the central pattern generator is actually mainly composed of the vrg okay it parts the inspiratory neuron parts in a ramp-like manner stop spiring then you have your expiration so this is the one that is responsible for tidal breathing okay it receives inhibitory signals coming from the pneumotoxic or the pontine center and the dorsal respiratory group such as for example there's metabolic acidosis there's less inhibition from the drg or the pneumotoxic group and therefore the tidal volume will be deeper higher in tidal volume during metabolic acidosis now what are the inputs to the respiratory related neurons shown here the first one is coming from the higher centers this is responsible for the ventilatory accommodation for activities such as speaking playing the musical instrument swallowing and vomiting then you have the respiratory mechanical receptors which detects changes in respiratory mechanical properties such as in congestive heart failure or in asthma then you have those irritant receptors in the airways which is responsible for the change in the ventilatory pattern in the presence of noxious stimuli heavier chemoreceptors which is responsible for the ventilatory adjustments due to the metabolic demands of the body and finally you have the muscles and joint receptors which is responsible for the ventilatory adjustment during different activities let us now discuss the consequences of receptor stimulation stimulation of your stretch receptor located in your airway smooth muscle during inflation will shorten the inspiratory time and increase duration of expiration okay this is known as your herringbroover inflation reflex it is stimulated by inflation and the response is to prevent hyperinflation stimulation of your stretch receptor also located in your airway smooth muscle during depletion is going to trigger a diminution in the duration of your expiration this is known as your herring blow where depletion reflex and this herring blower depletion reflex is stimulated by depletion and the response is to prevent over depletion irritant receptors may be stimulated in the airways epithelial cells the stimulus are your noxious gases allergens lung inflammation and the response will be rapid shallow breathing capping bronchoconstriction or hypersecretion the juxta capillary or the j appearance located in the interstitium near the pulmonary capillaries can become engorged during pulmonary edema and the response pattern response in breathing will be a rapid and shallow respiration their chest wall receptors these are the intrapuzzle fibers in the intercostal muscles which can be stimulated by stretch and this is responsible for the maintenance of our tidal volume now let's discuss the chemoreceptors the peripheral chemoreceptors are very sensitive most sensitive to a low auto tension there's slightly sensitive to high carbon dioxide tension in the low ph the central chemoreceptor on the other hand has a peculiar sensitivity okay so carbon dioxide from the blood will enter and will form carbonic acid and hydrogen it is the diminution in the csf ph which directly stimulates your central chemoreceptors so it is most sensitive to the change in hydrogen ion in the csf brought indirectly by changes in the carbon dioxide so let us look at the respiratory control in action we are familiar with this equation here then let's see how will the respiratory center adjust when there are changes in these variables okay for example there will be pathological conditions which may cause big mismatching and as we mentioned if there's bq mismatching there's increased speciologic dead space ventilation it is going to markedly decrease the alveolar ventilation and consequently lead to hypoxemia and hypercapnia the hypoxemia and hypercapnia is going to stimulate the peripheral and central chemoreceptors and adjustment will be carried out by the ventral respiratory group and the command will be to increase the tidal volume in the respiratory rate this is going to partially correct the low alveolar ventilation and partially correct the hypoxemia and the hypercapnia consequently so that is the setup the purpose of your one of the purpose of your respiratory center so which of the following is the central chemoreceptor most sensitive with po2 no that's not peripheral paco2 well not really it stimulates the central indirectly the csf co2 tension no okay it is actually the csf ph so we go now to the final segment summary the pulmonary vasodilators the mnemonics is not bp is bad there are poor zones of west with three pressures in alphabetical order it's albiola arterial and venus the alveolar is the skipping pressure which gives rise to the poor zones of s zone 1 does not exist in a normal upright lung the greater the lung volume the greater the alveolar pressure the lower is the ab radius the higher is the alveolar vessel resistance the greater the lung volume the greater the elastance the greater is the extra alveolar blood vessels reduce the lower is the extra alveolar blood vessels reduce so the greater the lung volume the higher is the alveolar vessel resistance the greater the blood ball the greater the lung volume the lower is the extra alveolar vascular resistance the total resistance is a combination of your alveolar and extra alveolar and it assumes a u shape the lowest pulmonary vascular resistance is seen at f r c the lower airway is just a trachea undergoing 23 dichotomous branching it is divided to your conducting zone and respiratory sound conducting zone is airway generation 1-16 while respiratory zone is airway generation 17-23 in the large airway it is a turbulent flow while in the small airway it is a laminar flow while in the respiratory zone the blow up air is by diffusion the alveolar ventilation equation as shown here shows to you the relationship between the ba dot and alveolar carbon dioxide tension while the alveolar gas equation shows to you the relationship between the alveolar auto tension and the carbon dioxide tension in the alveoli diffusion equilibrium is achieved at one third of the pulmonary capillary blood transit time we have a lot of reserve for tachycardia okay the ba dot equations is primarily a combination of your b that is equal to tidal volume times r tidal volume is equal to alveolar space volume plus your dead space volume and when we combine both we come up with the equation that ba dot is equal to tidal volume times r minus b delta if there's a relative hyperventilation of the respiratory unit that will lead to a high auto tension and a low co2 tension are used with a low or a shunt pq there there is relative hypoventilation and their secondary to airway and thoracic cage problem while respiratory units with a high or bq of infinity they have relative hyperventilation and they're usually secondary to pulmonary problems so these are the different types of bq of bc 1 produces a normal oxygen and a normal carbon dioxide in a low bq and 0bq there's relative progressive hypoventilation and therefore there is a relative progressive hypoxemia and relative progressive hypercapnia in high bq and a bq of infinity there's a relative increase in hyperventilation and therefore there's a relative increase in the hyperoxemia and a relative decrease in the hypokatnia the upper lung zone is a high bq relationship it is where you find dalviola dead space while in the lower lung zone you have below bq relationship it is where you find the al dollar chant effect the auto content is equal to the amount of oxygen in physical solution and the amount of oxygen bound to hemoglobin the bo2 dot based on the peaks equation is equal to the carjack output times the difference between the arterial auto content and the mixed venus blood auto content the hemoglobin auto dissociation curve is sigmoidal and it follows the rule of r rise in your 2 3 h cut reject makes the moglobin rejects oxygen this will cause a right shape of the curb and this will cause a rise in your p50 the herring brewer inflation and depletion replexes are triggered by inflation and depletion respectively the central chemoreceptors are directly responsive to the csf hydrogen and indirectly responsive to the arterial carbon dioxide tension while the peripheral chemoreceptors are primarily responsive to arterial autotension so with that thank you very much for your attention i hope this review is helpful in the same time enjoyable god bless and make us proud during the board exam