Respiratory Physiology

1. What are 3 lung volumes that can't be measured by spirometry?

*These are RV(Residual Volume),FRC(Functional Residual capacity),TLC(Total Lung capacity).Key to understand all of these is understanding of WHY RV can't be measured and that is pretty simple, because Spirmotery measures how much air you can EXhale/INhale and how fast this processes can carry out, however it can NEVER exactly tell how much air is LEFT inside the lungs and remember that Residual Volume is the amount of air left in the lungs after MAXIMAL expiration.*Then just remember that RV is a component of FRC and TLC, or break down them too and it will make sense, look FRC is basically how much air is left int he lung after NORMAL expiration.(So basically residual volume that is there even with MAXIMAL expiratio+ Amount of air that can be breathed out AFTER Normal expiration which is known as ERV, so remember FRC=RV+ERV) , TLC basically is amount of gas in Lungs after MAXIMAL INspiration and involves RV,ERV,IRV(How much air you can breath in after NORMAL inspiration),TV(air that moves in to the lungs with quiet inspiration), so as you see TLC involves RV, so it is obvious that you can't calculate it with spirometry....Also you can think of TLC as The sum of FRC(RV+ERV) and Inspiratory Capacity(TV+IRV), because remember that TLC=RV+ERV+TV+IRV=FRC( same as:RV+ERV)+IC(same as :TV+IRV), so once again FRC can't be measured by spirometry thus TLC can't me measured by it either...FOR NOW at least Remember RV(Air in the lungs after MAXIMAL expiration),FRC(Volume of gas in the lungs after Normal expiration),TLC(Volume of gas in lungs after Maximal Inspiration) can NOT be measured by spirometry...

VC(Vital Capacity), IC(Inspiratory Capacity), IRV(Inspiratory Reserve Volume)

VC, IC, and IRV can be measured by spirometry, unlike RV, FRC, and TLC which can't be measured due to the limitations of the test.

Explanation

VC, IC, and IRV can be measured by spirometry, unlike RV, FRC, and TLC which can't be measured due to the limitations of the test.

2. How are IRV (Inspiratory reserve volume) and TV (Tidal volume) related?

B. TV is the amount of air that remains in the lungs after forced exhalation.

C. IRV and TV are completely unrelated and do not affect each other.

A. IRV is the maximum amount of air that can be exhaled after the Tidal volume has been exhaled.

*basically IRV is how much air you can INHALE after you Inhaled the Tidal volume, or in other words air that can be breathed in after normal inspiration(During which TIdal volume of around 500ml enters the lungs), so it is not hard to imagine that Inspiratory Capacity(How much air can be breathed IN after normal exhalation) is the sum of Tidal volume +Inspiratory reserve volume.Note that IRV is on average around 4,3 liters while TV is around 500mL, so on average IC should be around 4,8 L.

Inspiratory Reserve Volume (IRV) is the additional air that can be inhaled after a normal inhalation of Tidal Volume (TV). Inspiratory Capacity is calculated as the sum of TV and IRV. Therefore, the correct relationship between IRV and TV is that IRV represents the additional air that can be inhaled on top of the Tidal Volume.

Explanation

Inspiratory Reserve Volume (IRV) is the additional air that can be inhaled after a normal inhalation of Tidal Volume (TV). Inspiratory Capacity is calculated as the sum of TV and IRV. Therefore, the correct relationship between IRV and TV is that IRV represents the additional air that can be inhaled on top of the Tidal Volume.

3. What is the association between ERV and RV in relation to Functional Residual Capacity (FRC)?

ERV/RV=FRC

*Well basically they together make up Functional Residual Capacity(Volume of gas in the lungs after Normal expiration)...it makes perfect sense, look RV is how much air is left in lungs after MAXIMAL expiration, so obviously that air will be there with Normal expiration as well, but with Normal expiration you'd also have additional left overs and that additional volume that stays in lung after Normal expiraiton is ERV(Amount of air that can be still exhaled after normal expiration), so overall TOTAL volume of gas in the lungs after NORMAL expiration would be sum of the air that you can breathe out after normal expiration(ERV) and The amount of air that stays in lungs even after Maximal expiration, so ERV+RV=FRC, and important point is the note that because FRC is made up of RV, it can NOT be measured by spirometry....

ERV x RV = FRC

ERV-RV=FRC

The correct association between ERV and RV to determine FRC is by adding ERV and RV together, not subtracting, multiplying, or dividing them.

Explanation

The correct association between ERV and RV to determine FRC is by adding ERV and RV together, not subtracting, multiplying, or dividing them.

4. What is the difference between IRV and IC in relation to breathing?

IRV is the amount of air that you can breathe in after maximal expiration, whereas IC is the amount of air that you can breathe in after maximal inspiration.

*IRV is amount of air that you can breathe in after normal INSPIRATIONvsIC is amount of air that you can breathe in after normal EXPIRATION...IC actually is made up of IRV + TV(Amount of airt that moves in with quiet inspiration)

IRV is the amount of air that you can breathe in after normal expiration, whereas IC is the amount of air that you can breathe in after normal inspiration.

IRV is the amount of air that you can breathe in after maximal inspiration, whereas IC is the amount of air that you can breathe in after normal expiration.

IRV (Inspiratory Reserve Volume) and IC (Inspiratory Capacity) are both respiratory measurements, but IRV specifically pertains to the additional air that can be inhaled after a normal breath in, while IC represents the total amount of air that can be inhaled after a normal exhale. Understanding the distinctions between these terms is essential in respiratory physiology.

Explanation

IRV (Inspiratory Reserve Volume) and IC (Inspiratory Capacity) are both respiratory measurements, but IRV specifically pertains to the additional air that can be inhaled after a normal breath in, while IC represents the total amount of air that can be inhaled after a normal exhale. Understanding the distinctions between these terms is essential in respiratory physiology.

5. What is the difference between ERV and Vital Capacity?

*ERV is amount of air that you can blow out after normal EXPIRATION(thus reserve after expiration)vsVital Capacity-Maximum volume of gas that can be expired after Maximum Inspiration...thus it makes sense that VC should be composed of Maximum air that can be Inspired after Normal Inspiraiton(IC)+Amount of air that can be exhaled after normal expiraiton...remember that IC is made up of amount of air that enter the lungs with normal inspiration(TV)+amount of air that can enter lungs after Normal inspiration(IRV), so now we get the HY formula, VC=TV+IRV+ERV.<Note that RV is not needed for calculation of VC so it can be measured by Spirometry.Vital capacity normally is around 4.8 liters and if you add to this around 1,2 liters which is Residual volume you would get Total lung capacity which is usually around 6 liters.

ERV is the maximum volume of gas that can be inspired after normal inspiration, while Vital Capacity is the amount of air that can be inspired after maximum expiration.

ERV is the total lung capacity, while Vital Capacity is the amount of air left in the lungs after normal expiration.

ERV is the volume of air that can be inhaled after maximal exhalation, while Vital Capacity is the maximum pressure exerted during exhalation.

ERV is the amount of air that can be blown out after normal expiration, and it is part of the Vital Capacity along with TV and IRV. Understanding this distinction is crucial in respiratory physiology.

Explanation

ERV is the amount of air that can be blown out after normal expiration, and it is part of the Vital Capacity along with TV and IRV. Understanding this distinction is crucial in respiratory physiology.

6. Why is the apex of the healthy lung the largest contributor of alveolar dead space and how can this explain why physiologic dead space increases with V/Q mismatch (such as in PE)?

*Well the thing is that Physiologic dead space is Space that determines basically the Volume of air that doesn't participate in gas exchange, now apices are Most upper parts of lungs and thus blood should overcome more gravitational force to reach them then for lower regions, so when compared to other regions it is Less perfused and with Higher Oxygenation, because the oxygen that enters there from taking in the breath can't properly be exchanged with the venous blood from Pulmonary arteries, because simply less of that deoxygenated blood reaches the Apices, thus LESS of Inspired air participates in gas exchange in the apices of the lungs when compared to Other parts of the lungs, thus apices of the lungs contribute to Physiologic dead space the most...Now thus it makes sense than when you have V/Q defects like PE(when Ventilation is fine but Perfusion-Q is lacking because of the emboli blocking blocking the passage of blood into the space where it is lodged)you would have less volume of inspired air that participates in gas exchange because there is not enough blood supply to exchange it...Now NORMALLY physiologic dead space should be very close to Anatomic deadspace(Conducting zone of respiratory tree that doesn't participate in gas exchange+Small amount of volume that doesn't participate in gas exchange in lung apices), But when Gas exchange is Significantly compromised in RESPIRATORY zone, then Physiologic dead space becomes larger and is called PATHOLOGIC deadspace.

In V/Q mismatch conditions like PE, an increase in ventilation leads to a decrease in physiologic dead space.

Physiologic dead space is mainly determined by the volume of air in the lower lobes of the lungs.

The apex of the healthy lung has the highest blood supply which contributes to the majority of gas exchange.

The correct answer explains that the apices of the lungs are less perfused and have higher oxygenation, leading to less gas exchange and contributing to dead space. In V/Q mismatch like in PE, a decrease in perfusion results in increased dead space rather than improved gas exchange.

Explanation

The correct answer explains that the apices of the lungs are less perfused and have higher oxygenation, leading to less gas exchange and contributing to dead space. In V/Q mismatch like in PE, a decrease in perfusion results in increased dead space rather than improved gas exchange.

7. How can you calculate Physiologic dead space?

Vd=Vt times (PaCO2-PECO2)

Vd=Vt times (PECO2/ PaCO2)

Vd=Vt times (PaCO2/PECO2/PaCO2)

*It is very easy if you know the concept, look physiologic dead space is basically how much of the Inspired air participates in gas exchange, now remember that during quiet inspiration you inspire volume of air known as TIDAL volume(Around 500ml) so now you got to determine how much of this tidal volume didn't participate in gas exchange and that's easy you look at CO2 concentraiton in Arterial blood and you subtract from that CO2 concentration in the EXPIRED air and then you divide this number by CO2 concentraiton in arterial blood, so Vd=Vt times (PaCo2-PECo2/PaCo2)

Physiologic dead space calculation involves understanding the concept of gas exchange and using the formula mentioned in the correct answer to determine the amount of inspired air that does not participate in gas exchange.

Explanation

Physiologic dead space calculation involves understanding the concept of gas exchange and using the formula mentioned in the correct answer to determine the amount of inspired air that does not participate in gas exchange.

8. What are the key concepts to understand the difference between Alveolar and minute ventilation?

Minute ventilation is calculated by dividing Tidal volume by Respiratory rate, while Alveolar ventilation is calculated by adding Physiologic dead space to Tidal volume and then multiplying by Respiratory rate.

*Basically Minute ventilation is How much volume of gas actually enters your Lung PER minute with quiet respiration so all you do is multiply Tidal volume over Respiratory rate(How much you breathe per minute), while Alveolar ventilation measures actually how Much of that air participates in Gas exchange, so all you got to do here is to subtract Physiologic dead space from the Tidal volume and then multiply that number over Respiratory rate.but all they need to give you is respiratory rate and you should be able to calculate both, because Vt=500 while Vd=150, so Ve=500 x RR while Va=350 xRR

Minute ventilation is calculated by multiplying Physiologic dead space by Respiratory rate, while Alveolar ventilation is calculated by dividing Tidal volume by Respiratory rate.

Minute ventilation is calculated by subtracting Tidal volume from Respiratory rate, while Alveolar ventilation is calculated by adding Physiologic dead space to Tidal volume and then dividing by Respiratory rate.

Minute ventilation and Alveolar ventilation are crucial concepts in understanding respiratory physiology. Minute ventilation focuses on the total volume of air entering the lungs per minute, while Alveolar ventilation specifically measures the volume of air participating in gas exchange. Understanding how to calculate both types of ventilation is important for evaluating respiratory function.

Explanation

Minute ventilation and Alveolar ventilation are crucial concepts in understanding respiratory physiology. Minute ventilation focuses on the total volume of air entering the lungs per minute, while Alveolar ventilation specifically measures the volume of air participating in gas exchange. Understanding how to calculate both types of ventilation is important for evaluating respiratory function.

9. What determines combined volumes of Lung and chest wall?

The number of cells in the Lung and chest wall.

The temperature of the Lung and chest wall.

The color of the Lung and chest wall.

*ELASTIC properties of BOTH Chest wall and Lung wall.*Increased elastic recoil means that there is INCREASED tendency of Lungs to collapse INWARD and Increased tendency of Outward Pull of the Chest wall..(it makes sense, think of recoil as ability to return something to "Chilling state", Lung would be normally collapsed without you breathing air into it, while Chest wall would be normally pulled outward, so elastic recoil tries to get back to those states)

The combined volumes of Lungs and chest wall are determined by the elastic properties of both structures. Elastic recoil plays a key role in maintaining the normal physiology of the respiratory system.

Explanation

The combined volumes of Lungs and chest wall are determined by the elastic properties of both structures. Elastic recoil plays a key role in maintaining the normal physiology of the respiratory system.

10. What does the High deltaV/deltaP ratio tell you about stiffness and compliance? How do compliance and this ratio change in Normal aging, Emphysema, Pneumonia, Pulmonary edema, NRDS, and Pulmonary Fibrosis? How does surfactant affect this ratio?

*You should know that Compliance is the change in the VOLUME for given Change in the PRESSURE.<Thus as you Decrease Stiffness you INCREASE compliance...*With Normal aging and Emphysema the Compliance INCREASES and thus the ratio of delta V/deltaP will INCREASE(For same pressure change you get Higher Volume change)...The opposite is true for conditions that increase the stiffness/Decrease the compliance- Conditions like Pulmonary FIBROSIS,ARDS/NRDS,Pneumonia and Pulmonary edema in all of these cases the Compliance decreases and the ratio Decreases too because to get the same Change in the volume you need to develop HIGHER pressure so the ratio of V/P goes down,(Thus We maintain HIGHER POSITIVE pressure for patients with ARDS/NRDS)

Surfactant decreases compliance and increases the deltaV/deltaP ratio.

Compliance decreases with Normal aging and Emphysema.

Pneumonia and Pulmonary Edema increase the Compliance and the deltaV/deltaP ratio.

11. Increased temperature, CO2, H+, and 2,3 BPG all favor the formation of the Taut form of hemoglobin. What does that mean?

Increased temperature and the presence of CO2, H+, and 2,3 BPG have no impact on the binding of O2 to hemoglobin.

*That means that these factors promote formation of DEOXYhemoglobin(Taut,Tense form) which has LOWER affinity to O2 and thus these factors promote RELEASE of O2 from Hemoglobin to Tissues thus dissociation curve switches to the RIGHT, Now Opposite changes for these factors(like in 2,3BPG) would favor formation of RELAXED form known as OXYHEMOGLOBIN and thus Decrease the Unloading of O2 from Hemoglobin(which now has 300 times more affinity for O2 than deoxyhemoglobin) to the tissues, thus Curve shifts to the LEFT.Note that hemoglobin acts as a H buffer(By combining it wit Bicarbonate) and it is made up of 4 Polypeptides(2alpha+2beta), babies have HBF which instead of 2 Beta has 2 Y and that favors HBF of Fetus to steal O2 from lower affinity Hemoglobin(HBA) of mommy.
Don't confuse Right shift with CO2 with LEFT shift with CO.

The Taut form of hemoglobin has higher affinity for O2, resulting in increased oxygenation of tissues.

These factors promote the formation of OXYhemoglobin, resulting in higher O2 affinity and increased release to tissues, shifting the dissociation curve to the left.

Understanding how different factors affect the affinity of hemoglobin for oxygen is crucial for comprehending the oxygen dissociation curve and its shifts.

Explanation

Understanding how different factors affect the affinity of hemoglobin for oxygen is crucial for comprehending the oxygen dissociation curve and its shifts.

12. Exposure to Gas Exhaust, Fires, Gas Heaters...FIRST symptom? SaO2 on Co-oximeter vs Pulse Oximeter...Shift of Oxygen Binding curve, why?

In these exposures you should start thinking about CO poisoning , FIRST symptom is usually HEADACHE and Dizziness, Cherry-red discoloration of skin is classic but onset is later....*Because CO has 200 times higher affinity for hemoglobin that O2 does, it wins the competition for spots and results in Decreased SaO2 which is NOT detected by Pulse oximeter but is Detected by Co-Oximeter...remember only Co-Oximeter can detect decreased SaO2 with presence of Dyshemoglobins(like MetHb/COHb), because less O2 binds hemoglobin we get Decreased Cooperativity and Decreased O2 available for Unloading of O2 into the tissues, thus OBC is SHIFTED to the LEFT, contrast this with CO2 which shifts the curve to the RIGHT by promotion of O2 dissociation from Hemoglobin....Treat with 100% O2 and hyperbaric O2.(You basically want to increase chances of O2 for winning the binding spots by increasing its concentration, remember Competitive inhibitors can be overcome by increasing substrates Sufficiently high)

Increased O2 availability for unloading into tissues due to CO poisoning

CO poisoning results in increased SaO2 on Pulse oximeter

Symptom is usually nausea and vomiting

13. Why might alkalosis result in erythrocytosis?

*Because During alkalosis Ph goes up(H goes DOWN)>Shift of OBC to the LEFT(Less O2 unloading to tissues>Renal Hypoxia>Synthesis of EPO>Comepnsatory Increase in Erythrocyte synthesis.*Decrease in ANYTHING that would normally shif the curve to the Right, will result in shifting to left(Like DECREASED altitude,Decreased Temperature,Decreased Exercise,Decreased H,Decreased CO2,Decreased 2,3 BPG will all shift curve to LEFT while Increase in all of them would give us Shif to right and more O2 unloading to tissues)Once again don't confuse Decreased CO2 which would switch the curve to the left with DECREASED CO which would switch curve to the right(Increase in each obviously has opposite effects)

Because alkalosis results in increased O2 unloading to tissues, reducing the need for erythrocyte production.

Because alkalosis causes a decrease in EPO production, leading to a decrease in erythrocyte synthesis.

Because during alkalosis, there is an increase in pH which directly stimulates erythrocyte production.

Alkalosis leads to a decrease in pH which shifts the OBC curve to the left, resulting in less O2 unloading to tissues and ultimately causing renal hypoxia and an increase in EPO production, leading to erythrocytosis.

Explanation

Alkalosis leads to a decrease in pH which shifts the OBC curve to the left, resulting in less O2 unloading to tissues and ultimately causing renal hypoxia and an increase in EPO production, leading to erythrocytosis.

14. Hemoglobin is a tetramer (2 alpha and 2 beta) and exhibits cooperativity, resulting in a sigmoid shape on the oxygen-hemoglobin dissociation curve. Will it have a higher affinity for O2 when compared to Myoglobin?

Yes, Myoglobin will have a higher affinity for O2 compared to Hemoglobin.

No, Hemoglobin will have a lower affinity for O2 compared to Myoglobin.

*Cooperativity is why Oxygen-Hemoglobin dissociation curve gets SIGMOID <TESTABLE.*Also important to note is that Myoglobin is MONOMER thus it has no multiple binding Sites and thus it can't exhibit Positive Cooperativity, thus it has NO sigmoid curve, HOWEVER remember that it has HIGHER affinity for O2 than hemoglobin A and even higher than Hemoglobin F(Fetal hemoglobin which has less affinity for 2,3BPG and thus has Higher affinity for O2 then HbA)You should be able to identify each on this diagram..Note that impaired cooperation of Hemoglobin by Cyanide,CO is the reason why they Cause LEFT shift of ODC(Less O2 is available on Hemoglobin to Unload it into the tissue), note that they DECREASE O2 binding capacity by occupying their sites on hemoglobin.

No, Hemoglobin will have the same affinity for O2 as Myoglobin.

Cooperativity in Hemoglobin leads to a sigmoid shape on the oxygen-hemoglobin dissociation curve, indicating higher O2 affinity than Myoglobin which lacks multiple binding sites for positive cooperativity.

Explanation

Cooperativity in Hemoglobin leads to a sigmoid shape on the oxygen-hemoglobin dissociation curve, indicating higher O2 affinity than Myoglobin which lacks multiple binding sites for positive cooperativity.

15. Calculate the amount of O2 delivered to tissues given a cardiac output of 5.25, arterial O2 saturation (SaO2), partial pressure of O2 (PaO2), and hemoglobin level.

*Well O2 delivery to tissues=CO x O2 content...O2 Content=O2 binding capacity × Percent saturation + Dissolved O2=(1,34 x Hb x SaO2)+ (0.003 × Pao2)... O2 binding capacity is normally 20.1 because Normal hemoglobin should be around 15 g/dL, 15 x 1,68=20.1.also note that (0.003 × Pao2) represents Dissolved O2.Thus when we have Decreased Hb concentration(Most commonly due to anemia) we would get decreased O2 content and thus decreased O2 delivery to the tissues, However SaO2 and PaO2 can be NORMAL.

O2 content = Hb x SaO2

O2 delivery to tissues = SaO2 - PaO2

Hemoglobin concentration does not affect O2 delivery to tissues

The calculation for O2 content and delivery to tissues involves multiple factors including O2 binding capacity, percent saturation, dissolved O2, and hemoglobin level. Hemoglobin concentration plays a crucial role in determining the amount of O2 delivered to tissues.

Explanation

The calculation for O2 content and delivery to tissues involves multiple factors including O2 binding capacity, percent saturation, dissolved O2, and hemoglobin level. Hemoglobin concentration plays a crucial role in determining the amount of O2 delivered to tissues.

16. Why is the Total O2 content of Blood decreased in cases of CO poisoning or Methemoglobinemia even though Hemoglobin concentration and PaO2 are normal?

The decrease in Total O2 content is due to an increase in the affinity of Hemoglobin for O2 in cases of CO poisoning or Methemoglobinemia.

*Because Total O2 content also depends on % of O2 saturation of Hemoglobin (SaO2) and this is decreased with CO poisoning MetHb but for different reasons, during methhemoglobinemia SaO2 is decreased because Fe3+ can't bind O2 as good as Fe2+ normally would, while with CO poisoning CO occupies binding sites of O2, either way % of O2 on hemoglobin decreases significantly enough to decrease the Total O2 content of blood, however note again that Hemoglobin concentration and PaO2 are NORMAL.

The decrease in Total O2 content is due to a decrease in Hemoglobin concentration caused by CO poisoning or Methemoglobinemia.

The decrease in Total O2 content is due to a decrease in the partial pressure of O2 in the blood (PaO2) caused by CO poisoning or Methemoglobinemia.

In cases of CO poisoning or Methemoglobinemia, the decrease in Total O2 content is primarily due to a decrease in the % of O2 saturation of Hemoglobin (SaO2) caused by the inability of Fe3+ to bind O2 effectively or the occupation of O2 binding sites by CO.

Explanation

In cases of CO poisoning or Methemoglobinemia, the decrease in Total O2 content is primarily due to a decrease in the % of O2 saturation of Hemoglobin (SaO2) caused by the inability of Fe3+ to bind O2 effectively or the occupation of O2 binding sites by CO.

17. Why are lungs unique in their response to hypoxia and what is the significance in pathology?

*Because they need to OXYGENATE the blood not take O2 from it, so when you decrease ALVEOLAR O2 their priority would be to shunt blood to sites where Avelolar O2 is relatively Higher and that will be Done by SELECTIVE vasoconstriction in areas with Lower O2, while this can be good term in short term, In long-term that can result in Concentric Hypertophy of Right ventricle due to increased pressure it has to work against(Increased resistance in Pulmonary arteries due to selective vasoconstriction), This leads to Right Heart failure, and this process of RVH,RHF in response to Pulmonary disease (Like COPD) is called Cor Pulmonale(Often cause of the death, but first RVHF will manifest with Congestion in the systemic venous circulation>Congestive hepatomegaly, Jugular Venous distension,EDEMA)

Alveolar O2 decreases which causes vasodilation in areas with high O2.

Decreased alveolar O2 levels lead to decreased blood flow to the lungs causing decreased resistance in the pulmonary arteries.

Because they need to take oxygen from the blood, not oxygenate it.

18. Emphysema vs Fibrosis: Diffusion/Perfusion limited? Why?

*BOTH result in DIFFUSION limited state(because diffusion is "rate-limiting", problem or what Limits the O2 exchange), in Emphysema because the SURFACE area is Decreased while in Lung Fibrosis because you INCREASE the thickness(Thus gas has to walk trough longer thickness:)

Emphysema and Fibrosis both result in a perfusion limited state.

Emphysema results in a perfusion limited state, while Fibrosis results in a diffusion limited state.

Emphysema and Fibrosis both result in a problem related to oxygen transportation.

19. Calculate Pulmonary Vascular Resistance if you know Pulmonary Capillary Wedge Pressure, Pulmonary artery pressure and Cardiac output.

Pulmonary Vascular Resistance is calculated by subtracting Pulmonary Capillary Wedge Pressure from Pulmonary Artery Pressure.

Pulmonary Vascular Resistance is the same as Pulmonary Artery Pressure.

*PCWP is good approximation for LEFT ATRIAL pressurePressure....Pulmonary Vascular resistance=Pressure in Pulmonary artery - Pressure in LEFT atrium/Cardiac Output...this formula is based on The formula:Resistance(R)=Pressure(P)/Flow(Q), you should be able to play with this formula like calculate Pressure if you know Resistance and Flow, P=QxR

Cardiac Output is not relevant in calculating Pulmonary Vascular Resistance.

To calculate Pulmonary Vascular Resistance, it is the difference between the Pressure in Pulmonary artery and the Pressure in the LEFT atrium divided by Cardiac Output. This formula is a result of the formula: Resistance(R)=Pressure(P)/Flow(Q), where you can manipulate it to solve for different variables.

Explanation

To calculate Pulmonary Vascular Resistance, it is the difference between the Pressure in Pulmonary artery and the Pressure in the LEFT atrium divided by Cardiac Output. This formula is a result of the formula: Resistance(R)=Pressure(P)/Flow(Q), where you can manipulate it to solve for different variables.

20. How do Pulmonary Vascular Resistance and Flow change with different factors?

1)Increased viscocity>Increases Resistance(Directly proportional),Remember Increased Resistance>Decreased Flow(Q=P/R),thus Viscosity of blood is INVERSELY proportional to Blood flow.2)Increased Vessel length >Increases Resistance(Directly proportional)Remember Increased Resistance>Decreased Flow(Q=P/R), thus vessel length is INVERSELY proportional to FLOW.3)Increased diameter in 2 times=increase in radius 4 times...Radius in 4th power is inversely proportional to resistance and thus is directly proportional to Blood flow, in our case Resistance would DECREASE 256 times(4x4x4x4) and Flow would Increase 256 times.

3)Increased diameter in 2 times=increase in radius 4 times...Radius in 4th power is directly proportional to resistance and thus is inversely proportional to Blood flow, in our case Resistance would INCREASE 256 times(4x4x4x4) and Flow would Decrease 256 times.

1)Increased viscocity>Decreases Resistance

2)Increased Vessel length >Decreases Resistance

21. What does R represent and how much is it at sea level when breathing room air? How much is PIo2 under these conditions and what does it represent?

*R is RESPIRATORY QUOTIENT it represents the ratio of CO2 Produced/O2 Consumed.At sea level, breathing room air, it should equal 0.8...PIo2 gives info about Po2 in inspired air and at this conditions it is around 150.so under these conditions all they need to give you is PaCO2 because at sea level,when breathing room air, Alveolar Po2(PAo2)=150-PaCo2/0.8

1. R represents the ratio of O2 Produced/CO2 Consumed. At sea level, when breathing room air, R is 1.2.

2. R represents the ratio of CO2 Produced/O2 Consumed. At sea level, when breathing room air, R is 1.0.

3. R represents the rate of oxygen consumption by the body. At sea level, when breathing room air, R is not significant.

In this question, the important concept is understanding the definitions of R, PIo2, and how to calculate Alveolar Po2. The correct answer explains these concepts clearly and provides the correct calculations. The incorrect answers are designed to test the understanding of these concepts by providing common misconceptions or errors.

Explanation

In this question, the important concept is understanding the definitions of R, PIo2, and how to calculate Alveolar Po2. The correct answer explains these concepts clearly and provides the correct calculations. The incorrect answers are designed to test the understanding of these concepts by providing common misconceptions or errors.

22. Increased difference between Alveolar O2 and Arterial O2 can indicate which conditions, why?

*Increased A-a(PAo2-Pao2) gradient can be seen in FIBROSIS due to Impaired diffusion(more stays in alveoli, less enter the arteries),V/Q mismatch(Like PE, when all the O2 in alveoli can't enter the blood because of block in the pulmonary circulation),Shunts(like Left to right shunts when PaO2 increases and thus the gap between PAo2-Pao2 increases) all listed conditions also lead to HypoXEMIA(Decreased O2 dissolved in plasma,PaO2), but Do Not think that A-a is always increased when you have Hypoxemia, because High Altitude, Respiratory depression/Hypoventilation from Opoid use, can lead to Hypoxemia BUT with NORMAL A-a gradient.

Pulmonary embolism (PE) due to excess O2 in alveoli

High Altitude due to increased oxygen dissolved in plasma

Hyperventilation from anxiety leading to lower A-a gradient

It's important to consider different conditions and their effects on the A-a gradient to determine the correct interpretation.

Explanation

It's important to consider different conditions and their effects on the A-a gradient to determine the correct interpretation.

23. Ischemia vs Hypoxia?

Ischemia is primarily decreased O2 delivery to tissues while Hypoxia is decreased blood delivery to tissues.

*Ischemia is just decreased blood delivery to tissues while Hypoxia is primarily decreased O2 delivery to tissues.Ischemia is marked by decreased venous drainage, while ischemia can often cause Hypoxia(Like decreased cardiac output), it is not equivalent(Decreased O2 dissolved in plasma=Hypoxemia can cause Hypoxia, while it doesn't necessarily indicate Ischemia,however yea conditions that cause HypoXemia are more likely to lead to Hypoxia, but then again this is Not Must either,like CO poisoning,Anemia doesn't affect Po2 but it causes Hypoxia)

Ischemia is marked by decreased O2 dissolved in plasma while Hypoxia is related to venous drainage issues.

Ischemia and Hypoxia both refer to decreased blood delivery to tissues.

24. Is ventilation More in the Apex or the base of the lung?

Ventilation is more in the Apex of the lung

Ventilation is equal in both the Apex and the base of the lung

Ventilation varies depending on the time of day

*Ventilation just like Perfusion is HIGHER at the BASE of the Lung where V/Q=0.6("Extra"perfusion but ventilation is still higher then in bases, its just difference in perfusion is even greater), note because Perfusion is Lower in the apex(V/Q=3)> more O2 can be wasted/used by Bugs like TB....HOWEVER if they ask you about V/Q during exercise, pick number closest to 1, because during exercise Apical capillaries dilate and perfusion(Flow) increases the ratio of Volume/Flow decreases and reaches 1(IDEAL state for gas exchange)

Ventilation is actually higher at the base of the lung due to the V/Q ratio, which is 0.6. This means that there is 'extra' perfusion in the base, but ventilation is still higher than in the apex. The difference in perfusion is even greater. In the apex, where V/Q=3, more O2 can be wasted/used by organisms like TB.

Explanation

Ventilation is actually higher at the base of the lung due to the V/Q ratio, which is 0.6. This means that there is 'extra' perfusion in the base, but ventilation is still higher than in the apex. The difference in perfusion is even greater. In the apex, where V/Q=3, more O2 can be wasted/used by organisms like TB.

25. Compare Pa,PV,PA at the region of lung which has V/Q of 0.6.

PV < Pa < PA

V/Q of 0.6 is compatible with the base of the lung, where gravity increases perfusion more than ventilation and thus V/Q ratio decreases, here you get "Extra perfusion"....Note that PaO2 is partial pressure of O2 in VENOUS blood because Pulmonary arteries carry the VENOUS blood,Pulmonary Veins carry the oxygenated blood towards the Left atrium and PVO2 in this case reflects Partial pressure of oxygen in arterial blood of Pulmonary Veins...SUPER HY At the base of the lung(THIRD ZONE):Pa>PV>PAIt makes sense if you understand that perfusion is "wasted', initially as Venous blood comes in from pulmonary arteries, Lot's of O2 diffuses to it, HOWEVER as blood continues to travel towards the Pulmonary veins, the Perfusion is "wasted" as not enough O2 is in the alveoli to continue giving it to the blood, thus because PAo2 becomes even lower than even PVo2(Excess perfusion Sucks all that O2 from alveoli, but it is still not enough and both PAo2 and PVo2 decrease), then it makes sense that Pvo2 would be <PaO2, well try to understand it but if you can't just memorize it, but KNOW it...

Pa < PV < PA

PA > PV > Pa

The correct order of Pa, PV, and PA at the base of the lung with a V/Q of 0.6 is Pa > PV > PA, due to the excess perfusion at the base leading to lower PaO2 than PV and PAO2.

Explanation

The correct order of Pa, PV, and PA at the base of the lung with a V/Q of 0.6 is Pa > PV > PA, due to the excess perfusion at the base leading to lower PaO2 than PV and PAO2.

26. Under physiologic conditions, which gas is diffusion limited while the others are perfusion limited?

O2 is diffusion limited, CO, CO2, and N2O are all perfusion limited.

N2O is diffusion limited, CO, CO2, and O2 are all perfusion limited.

*ONLY CO is DIFFUSION limited, CO2,O2,N2O are all PERFUSION limited.

CO2 is diffusion limited, CO, O2, and N2O are all perfusion limited.

In this scenario, CO is the only gas that is diffusion limited, meaning its rate of uptake is limited by its ability to diffuse across the alveolar-capillary membrane. CO2, O2, and N2O, on the other hand, are all perfusion limited, where their uptake is limited by blood flow through the pulmonary capillaries rather than the rate of gas diffusion.

Explanation

In this scenario, CO is the only gas that is diffusion limited, meaning its rate of uptake is limited by its ability to diffuse across the alveolar-capillary membrane. CO2, O2, and N2O, on the other hand, are all perfusion limited, where their uptake is limited by blood flow through the pulmonary capillaries rather than the rate of gas diffusion.