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Flashcards in Pulmonary Deck (95):

What are the respiratory and non-respiratory functions of the lung?

Respiratory functions: Gas exchange

Non-respiratory functions:
1. Metabolism (ex: angiotensin II)
2. Air conditioning where the moist mucosa and the increased blood flow warm up the air in the upper airways
3. Blood reservoir
4. Mechanical defense (starts in the upper airways and it prevents the gunk of particles from being stuck and collecting in your lungs)


What are the structural features of the trachea? bronchiole?

Trachea has C-shaped cartilagenous rings that cover the anterior portion. Thus, the posterior side is very flexible.

Also, has mucous secreting cells and epithelium that have cilia. Together, this creates the mucocilary layer which helps to slide air/dust particles back up the airway and out of the body

Bronchioles simply have cartilagenous plates that surround them but these don't really provide as much support, though they allow for increased flexibility. Bronchioles also have a small basement membrane and globet cells that secrete mucous into the lumen of the airway


What are the two zones of the lung? What's the difference b/w the two?

You have the conducting zone and the respiratory zone. The conducting zone is in the upper airways until you reach the terminal bronchioles and this is known as ANATOMICAL DEADSPACE since you have no gas exchange happening here

The lower airways (respiratory bronchioles to alveoli) is known as the respiratory zone and this where you have gas exchange occurring! Also the formation of the alveolar ducts into the alveoli significantly increases the surface area of the respiratory zone


What happens to the cartilagenous rings surrounding the trachea?

As the airways continue to branch further and further and develop their own support, the cartilagenous rings change into plates that surround the bronchioles


What is unique about the respiratory zone?

Has high SA due to the alveoli


What happens to an asthmatic patient's bronchioles?

The bronchiole's have too much overproduction of mucous that can lead to formation of mucous plugs. They also have more mucous secreting goblet cells and they have a thicker basement membrane


What are alveolar pores?

These are small opening b/w individual alveoli that allow for inter alveolar communication and let the lung expand as one giant unit and not as an individualized segment


What happens in emphysema to your alveoli?

The alveoli lose their normal shape and they start to become less honeycomb like and shrivel up

The alveolar walls also thin and wear away...REDUCES SURFACE AREA & thus decreases gas exchagne


What is the dual circulation of the lung?

You have pulmonary circulation that is where gas exchange happens and goes back to the left atria

You have bronchial circulation that supplies the bronchioles w/ the blood supply that they need. This allows for them to be fresh and healthy


What two cells make up the alveolar septum? Function?

The alveolar septum is the wall b/w two alveoli. This is made up of Type I and Type II pneumocytes

Type 1: Majority (95%) and makes up the wall
Type II: Less common but can differentiate into Type I and can also produce surfactant


Why don't our lungs collapse?

1. We have interalveolar dependence due to the honeycomb shape that the alveoli are in. This allows for neighboring alveoli to pull at other alveoli and keep them held up

2. You have surfactant production that reduces the surface tension in the alveoli that you get that you get form the air:liquid interaction


What is adult respiratory distress syndrome?

this is a condition where your surfactant quality is diminished and it's not as good thus you don't reduce the surface area to the extent you would need too. Thus, your lungs are more susceptible to collapse at low pressures

Also you have membrane pealing that prevents efficient gas exchange from occurring


What is your normal anatomical deadspace?

150 ml


What makes up your alveolar gas?

It's a combination of both residual air always stuck in the lungs and inspired air that has made it through the anatomical dead space


What is alveolar ventilation?

Breathing air in and out...specifically the portion that occurs in the respiratory zone where gas exchange happens


What is FEV1? How does the FEV1/FVC ratio differ if you have obstructive lung disease? Restrictive lung disease?

FEV1 is the forced expiration volume that happens in one second...normally the ratio is 0.8 because 80 percent of our expiration happens in that one second

However, in obstructive lung disease, this ratio will be lower since it takes longer for you to expire since you don't have normal lung airflow...decreases the FEV1 and thus decreases the ratio

In restrictive lung disease, you decrease your TLC and this means that you also reduce your FEV1. Therefore, your ratio should be similar though your TLC is reduced


What are some examples of obstructive lung disease?

COPD, asthma, & emphysema


What are some examples of restrictive lung disease?

Anything that impedes the lung's ability to expand fully

Pulmonary fibrosis, chest scarring, neuromuscular disorder, Adult respiratory distress syndrome


How do lung volumes differ for obstructive and restrictive lung disorders?

Obstructive: At lower lung volumes you are more likely to collapse the lung and trap in more air thus you have HIGHER RESIDUAL VOLUME, and thus HIGHER TLC

Restrictive: You can't fully inflate your lungs to normal level and thus you have REDUCED TLC


What is the helium dilution technique? What can it help us calculate?

You take a container with a known concentration and volume of helium and have a person breath this in. Over time it equilibrates with their lung volume. At this point you take the concentration of the helium in the container as new C2 and then you volume is V1 (container volume) and V2 (volume left in lung) which is FRC


How can you maximize your alveolar minute ventilation?

you can maximize this by increasing Tidal volume which can be done by reducing RR

If your tidal volume is unaffected, then you can do it by increasing RR

Also, by decreasing dead space


What is the fowler method?

This is when you give a patient straight up 100 percent oxygen and then you capture their expired breath and plot the percentage of nitrogen captured over time. Note that the nitrogen is usually confined to our alveolar residual volume. Eventually, when this value plateaus, this means you have brought out all the nitrogen. You then draw a vertical line on the graph so that the area about and below the graph are in equal value. The area below the graph is your dead space


What is physiological dead space? How do you get alveolar dead space?

physiological = anatomical + alveolar

you can get alveolar from reduce CO or pulmonary embolism


What happens to you alveolar and arterial CO2 levels as you increase you alveolar ventilation?

If you increase alveolar ventilation, then these levels decrease b/c you're blowing away the CO2


Describe the process of inspiration (mention the effect of intrapleural pressure and transpulmonary and intrapulmonary pressure)

Your brain sends signals to your primary and accessory muscles (if needed) to cause muscle constriction. This leads to expansion of the thoracic wall and increased thoracic volume reduces the intrapleural pressure even more. This causes an increase in the transpulmonary pressure. Also, the alveoli are pulled and expanded, dropping the pulmonary pressure below atmospheric. This leads to air entering your alveoli.


Describe the process of expiration(mention the effect of intrapleural pressure and transpulmonary and intrapulmonary pressure)

Passive process where the diaphragm relaxes and this decreases your thoracic volume, increases intrapleural pressure, and decreases the transpulmonary pressure. Causes air to leave your lung b/c the elastic recoil pushes the alveoli and deflates them (increases pulmonary pressure above atmospheric pressure)


Why is there no airflow at FRC?

Functional residual capacity is the balance b/w lung and chest wall volumes. At this point they both exert the same amount of pressure so there's no airflow!


What is the natural tendency for the lungs and the thoracic wall? Why does this affect the intrapleural pressure?

Lungs want to collapse and the thoracic wall wants to expand...this makes the intrapleural pressure negative during normal breathing


What happens in pneumothorax?

Here you have some puncture that causes the intrapleural pressure to equal atmospheric. Therefore, the transpulmonary pressure is equal to 0. This causes the lung on that side to collapse and the chest wall to expand


What are the two factors that affect ventilation?

Compliance and airway resistance


What are the factors that affect compliance?

1. Elastic content (inverse relationship)
2. Surfactant (direct relationship)
3. Mobility of chest wall (direct relationship)


How does compliance change for pulmonary fibrosis vs emphysema?

Pulmonary fibrosis: there's lower compliance (you're replacing elastin w/ more cells to thicken the alveolar septum and collagen fibers to make the alveoli more rigid)
emphysema: there's more (you're destroying the elastin fibers)


What is hysteresis? What is the primary reason for this?

Hysteresis is the difference b/w the pressure/volume or compliance curves of inspiration and expiration. This is due primarily to surfactant


Why doesn't LaPlace's Law (lower radius = higher pressure) cause movement of air in lungs from high pressure or smaller alveoli into lower pressure/larger alveoli?

.1. Surfactant tends to reduce the surface tension more and more as the radius decreases. This reduced tension decreases the pressure.

2. The alveoli also have interalveolar pores that allow for all the alveoli to further stabilize and stay open!


What is respiratory distress syndrome of the newborn? Treatment (2 means)?

This is when newborns lack adequate surfactant production and thus they don't have fully open alveoli.

Treat by giving them artificial surfactant or via mechanical ventilation


What is FRC?

This is the functional reserve capacity and in normal breathing it's the volume of breath that stays in your lungs when the tendencies of


What are two reasons for chest wall compliance being decreases?

Increased intra-abdominal pressure (ascites or pregnancy)

Reduced normal movement of rib cage (kyphoscoliosis or broken ribs)


Why is the base of the lung more ventilated than the apex?

The apex of the lung has more negative intrapleural pressure due to gravity pulling the lung down. This causes the transpulmonary pressure there to be higher and the alveoli are normally more expanded than at the base. Thus during inspiration, they don't expand as much and the ventilation is lower


Where is perfusion the greatest in the lung?



What causes increases in airway resistance? decreases in airway resistance?

Increase: Bronchoconstriction (histamines, leukotrienes, PNS) and compression of airway

Decrease: Bronchodilation (leukotriene antagonists, SNS (beta 2), and anti-histamines) & low density air (heliox)


What are the two reasons for why lower lung volumes cause increased airway resistance?

1. Traction (less alveoli pull it open and this strength is lower)
2. Reduces transpulmonary gradient (pressure outside > pressure on the inside at low lung volumes so the air way is more likely to constrict/collapse...reduced radius thus more resistance)


Why can forced expiration potentially collapse smaller airways?

This causes your intrapleural pressure to be much more positive and thus in your smaller airways you can potentially exceed the intrapulmonary pressure and cause them to collapse


What are the two types of work in breathing? What do they do?

Resistive work: overcomes tissue or airway obstruction
Elastic work: overcomes loss of elastic recoil in restrictive disorders


What's the difference b/w extrathoracic obstruction and intrathoracic obstruction? How do you differentiate between the two?

Extrathoracic: The flow-volume loop is flatten in inspiration & narrowed. This is b/c you have an obstruction outside the thoracic outlet and during inspiration the tracheal pressure is less then atmospheric pressure causing an obstruction.
ex: vocal cord paralysis & extrathoracic goiter

Intrathoracic: Reduced flow-volume loop for expiration and this is b/c you have an obstruction inside thoracic cavity that causes the tracheal pressure to be less than pulmonary pressure (collapses the airway)
ex: tracheomalcia (problems w/ collagen integrity of the airway causing it to be narrowed and easily collapsable)


How is oxygen primarily transported in our blood? carbon dioxide?

Oxygen is carried mainly through hemoglobin
Carbon dioxide is carried mainly by bicarbonate ions


Compare the solubilities of oxygen and carbon dioxide. How does this affect their diffusion constant?

Oxygen has a much lower solubility than carbon dioxide. This means that oxygen has a lower diffusion constant than carbon dioxide and is not as readily dissolved in the blood


What factors affect a gas's ability to flow through the alveolar:capillary interface?

1. Surface area for diffusion...as this increases, there's higher flow
2. Thickness of membrane...thinner the membrane, then larger the diffusional flow
3. Diffusion constant...higher the constant larger the flow. this is positively related by solubility and negatively related to molecular weight


Define the diffusion classifications of CO, N20, & O2

CO: Diffusion limited b/c when it gets into the blood it immediately gets picked up by hemoglobin and doesn't fall off quickly. Thus, it doesn't really accumulate in the capillaries.

N20: Perfusion limited b/c when it quickly enters the blood and doesn't get picked up by Hb. Thus, within 0.1 seconds it fully saturates the blood and you need the blood to flow and have new blood coming in so that it can pick up more N20

02: normally is perfusion limited but in diseased individuals can become diffusion limited


What are the two components of total diffusion capacity of the lung? What factors affect either component?

Total diffusion capacity = diffusion through the alveolar/capillary membrane + rate of reaction for oxygen combining w/ hemoglobin

Diffusion through membrane can be made worse if the membrane is thickened

Rate of reaction of oxygen w/ hb is based on the alveolar pressure and amount of blood in the lung


In what cases can oxygen diffusion become diffusion limited as opposed to being perfusion limited?

1. Thickened alveolar septum so longer time to diffuse through

2. Severe forms of exercise, especially if you have a lung defect

3. Reduced ambient air oxygen pressure (i.e. higher elevations)


What are three key functions of the pulmonary circulation?

1. Transfer blood to the alveolar:capillary interface and help facilitate gas exchange
2. Provide blood to systemic circulation if needed
3. Metabolism of metabolites such as Bradykinin & Angiotensin


Describe the pulmonary circulation organization in the lungs

pulmonary arteries branch into smaller arteries that follow alongside of larger airways and these continue to branch outward until the end of the terminal bronchioles. The the arteries form a large meshlike capillary sheet that drapes over the alveoli like sheets


Where does the bronchial circulation drain blood to?

It either drains blood into the bronchial veins or the pulmonary veins and brings them back into the right atria or left atria, respectively


Describe the pressure, resistance, and cardiac output from the left and right side

Left and right side have the same cardiac output but left has greater pressure and resistance. Thus the left side of the heart is more muscular


What are two differences b/w the pulmonary and systemic vasculatures (vessel & capillaries)?

1. pulmonary vessels are thinner walled, have more compliance, and dilated. Systemic vessels have more smooth muscles, thicker walls, and more actively controlled

2. Capillaries of the pulmonary form a dense sheet of blood but capillaries of the systemic form networks w/ some connections to distribute blood as needed


What is PAOP? How is it measured? What can it be a good estimate for?

PAOP = Pulmonary arterial occlusion pressure and it is an estimate of left atria pressure, left end-diastolic ventricular pressure, and preload of the heart

This can be measure w/ a pulmonary artery catheter and a balloon at the end that is blown up to create a column of blood in the pulmonary vessels. This can help estimate the pressures


What happens to PVR as arterial and venous pressures increase? Why?

As the pressures increase then they cause previously closed capillaries to open up and also recruit more capillaries. This leads to a reduction in the PVR.

Reduction is fart more for arterial pressure increase than for venous pressure increase


What happens to PVR as blood flow increases? Why?

As blood flow increases, it causes an initial recruitment of capillaries and then an eventual distention of the capillaries, leading to a reduction of the PVR.


What are passive mechanisms and active mechanisms of controlling PVR?

Passive: recruitment of capillaries & capillary distension

Active: Vasoconstriction (localized) upon hypoxia in an alveolus


What happens to PVR as lung volumes increase or decrease?

At TLC, your PVR is the highest it can be b/c your alveoli are fully distended and this compresses the alveolar vessels, causing them to exert more pressure and resistance.

As you decrease your lung volume you reduce you lung volume, until you reach FRC (your lowest PVR).

if you decrease further below this, then the pressure inside of your bronchial airways is soo low that it is compressed by the increased pressure outside of it. Thus you have again an elevation of PVR


What is pulmonary hypertension?

When you have damage or injury to your pulmonary vessels, then you cause remodeling & loss of smooth muscle. This reduces the compliance of the vessels and thus increases the pressure and PVR. This increased resistance can cause increased pressure in the RV and lead to RV hypertrophy.

EVENTUALLY, your cardiac output can also decrease since the RV may push up on the LV and thus lead to reduced filling of the LV or reduced preload


How do low pH and sympathetic stimulation affect pulmonary vessels during hypoxia?

They both cause vasoconstriction and INCREASE PVR


Describe regional vasoconstriction

When you have an alveoli that is occluded it will have lower than normal oxygen partial pressure and larger than normal carbon dioxide partial pressure. In response, your body will vasoconstrict the afferent arteriole entering that capillary bed for the alveoli. This doesn't change pulmonary pressure or PVR since it's localized and allows for more blood flow to the necessary areas of the lung


Describe regional vasoconstriction

When you are at high altitude or have reduced ambient oxygen in the air this leads to a vasoconstriction of all your vessels exposed to the lower oxygen

PVR increases and Pulmonary pressures increase...can cause pulmonary hypertension


Describe the distribution of blood flow through the lungs. What are the three zones?

As you go from the apex to the base, your blood flow or perfusion will increase

Zone 1: this is near the apex and alveolar pressure > arterial pressure > venous pressure...thus you have a certain extent of vasoconstriction of the capillary and this reduces the perfusion...if you have trauma or hemorrhaging then you're more likely to have larger regions of wasted capillaries with 0 perfusion
Zone 2: this is in the middle of the lung and arterial pressure > alveolar pressure > venous pressure. Still not super ideal since the vessel taking blood away from the lung is compressed
Zone 3: This is the base of the lung and arterial pressure > venous pressure > alveolar pressure and this is ideal


In zone 2 and zone 3 what determines the blood flow?

The Alveolar - arterial pressure gradient...remember FLOW = Change in pressure/Resistance. This is independent of the venous pressure gradient


What is fluid flux? How do you increase it?

This is the force in capillaries that causes fluid to be filtered out into the interstitial space.

1. Left heart failure...causes a back up of blood that goes into the pulmonary vessels and increases hydrostatic pressure
2. Reduce protein content in capillaries and decrease oncotic pressure
3. Sepsis that can damage the walls and make them more leaky
4. ARDS where you have low surfactant and thus you have increased surface tension to the alveolar wall and you pull in more water and cause capillaries to leak into the alveolus


What is henry's law?

This states that the amount of gas in the blood is proportional to its solubility and its partial pressure


What is methemoglobin?

This is when you turn a ferrous iron (+2) into ferric iron (+3). This conversion causes hemoglobin to bind oxygen and not let go...causes you to be functionally anemic


What is the structure of hemoglobin? fetal hemoglobin?

hemoglobin normally is 4 subunits (2 alpha and 2 beta)
Fetal hemoglobin is 4 subunits (2 alpha and 2 gamma)


Differentiate b/w oxygen content, oxygen capacity, oxygen saturation, and partial pressure of oxygen

oxygen content = the total amount of oxygen dissolved in blood and found in hb
oxygen capacity = The total amount of oxygen that can bind to your hb
oxygen saturation = percentage of hemoglobin bound by oxygen
partial pressure of oxygen = the amount of oxygen dissolved in the blood


What are the two sections of the oxygen dissociation curve? In which vessel is each section especially important?

1. Plateau region: You're oxygen saturation doesn't drop significantly even w/ drops in your oxygen partial pressure. This is useful in the capillary beds when you are trying to load oxygen.

2. Steep region: This is what's found normally in your veins b/c here small deviations in the partial pressure of oxygen cause huge drops in the oxygen saturation. B/c you want to prioritize unloading your oxygen


What does right ward shift of the oxygen dissociation curve mean? left-ward shift?

right-ward shift = facilitates unloading of oxygen (typically what your venous blood looks like)

left-ward shift = facilitates loading oxygen and holding onto it (typically what your arterial blood looks like)


What is P50? What does a higher or lower number indicate?

P50 is the partial pressure of oxygen needed for there to be 50 percent saturation of your hemoglobin

Higher number = you're more easily unloading oxygen so you're reaching the 50% at a higher than normal partial pressure

Lower number = your no unloading oxygen as readily and holding onto it..this is why you reach the 50% saturation at a lower partial pressure of oxygen


How does an increase or decrease in pH shift the 02 dissociation curve? increase or decrease temperature? Increase or decrease in 2,3-DPG?

pH increase causes leftward shift, pH decrease right
Increase in temp = right, decrease in temp = left
Increase in 2,3-DPG = right, decrease in temp = left


What is the bohr effect?

When you're partial pressure of CO2 increases, you have a right ward shift
When it decreases you have a leftward shift


What is carboxyhemoglobin? How does this affect the oxygen dissociation curve?

This is when hemoglobin binds CO, which has a very strong affinity to it. This prevents hemoglobin from not only letting go of it's currently bound O2 but also from binding any future O2. Causes a leftward shift in the curve since you hold onto O2.

Can cause functional anemia by reducing both the oxygen content and capacity (decreases working hb)


What are four ways of coping w/ the high altitude and decrease in inspired partial O2?

1. Hyperventilate to blow off CO2...as you decrease partial pressure of CO2, then you will increase your alveolar oxygen partial pressure...alveolar gas equation
2. Polycythemia or make more RBC ---> thus while your oxygen saturation decreases, your oxygen content and capacity both increase
3. Respiratory alkalosis --> helps you load your RBC w/ more oxygen at the capillaries and alveoli
4. Increase 2,3-DPG production --> helps unload the oxygen at the tissues more easily


What is the Haldane effect?

As your oxygen partial pressure increases, hemoglobin's affinity to carbon dioxide decreases...this means that you will be able to more easily take on the oxygen


How does the distance b/w capillaries and tissues change with increased demand for oxygen?

As the demand for oxygen increases, then the tissues and capillaries decreases the space b/w them as the tissues recruit and open more capillaries...this helps to increases the tissue partial pressure of oxygen


What is hypoxic hypoxia? Anemic hypoxia? Circulatory hypoxia? Histotoxic hypoxia?

hypoxic hypoxia = low oxygen content or saturation
Anemic hypoxia = low hemoglobin
Circulatory hypoxia = low cardiac output
Histotoxic hypoxia = inability of the cell to consume the oxygen even when it is delivered correctly


What's partial pressure of oxygen and carbon dioxide in inspired air? alveolar gas? mixed venous blood? end-pulmonary artery?

inspired air: O2 is 150 CO2 = 0
Alveolar gas: O2 = 100 and CO2 = 40
Mixed venous blood: O2 = 40 and CO2 = 45
End-pulmonary artery blood: O2 = 100 and CO2 =40 (NOTE THERE MAY BE SOME DEVIATION B/W THE ALVEOLAR AND ARTERIAL O2 partial pressures)


Why does inspired air have more partial pressure of oxygen than alveolar gas

It is dependent upon the consumption of O2 and the replacement by inspired air. In our body, our capillaries consume more than we can replace via inspired air and therefore you have reduce alveolar o2 when compared to the o2 in inspired air


What are 4 causes for hypoxemia?

1. Diffusion limitations that reduce the ability for gas exchange to occur efficiently
2. Abnormal shunts
3. Hypoventilation
4. Severely mismatched Ventilation/Perfusion ratios


Why does our arterial PO2 differ from our alveolar PO2?

1. Diffusion of oxygen through the alveolar membrane into the capillary is not complete and thus you don't get the arterial P02 = alveolar P02

2. We normally have some shunts in our body which then combine w/ normally oxygenated blood and thus cause a lower arterial P02

3. V/Q differences throughout the lung cause perfusion & P02 fluctuations b/w the base and the apex leading to less oxygen in the arteries than in the alveoli


What happens in diffusion limitation? What are three ways in which you can get diffusion limitation based hypoxia?

Diffusion limitation is when diffusion is no longer an efficient process and it takes longer for the blood to be fully oxygenated

1. Thickening of the alveolar:capillary membrane (pulmonary edema or pulmonary fibrosis)
2. Severe exercise/exertion
3. Increasing elevation (decreasing partial pressure of O2 in ambient air)


What is a shunt? What are two normal shunt systems in our body?

Shunt = when you have deoxygenated blood that enters the systemic circulation w/o passing through a ventilated lung...thus this doesn't participate in gas exchange

1. Bronchial veins --> Left atria instead of right atria
2. Coronary veins ---> Thesbian veins ---> Left ventricle


What are three types of intracardiac shunting?

1. Atrial/ventricular septal defects
2. Pulmonary atriovenous fistuals
3. Tetrology of fallot (pulmonary stenosis, overriding aorta, and ventricular septal defect)


Will giving supplemental oxygen to someone w/ shunt help?

No it won't fully help them. Normally, you expect their Pa02 to get to 600, but with this you still have the deoxygenated blood circulating so you only get to 100-105


How does hypoventilation cause hypoxemia? How can you assess if someone has hypoxemia due to this?

Hypoventilation --> Decreases minute ventilation---> increases PaCO2 ---> via the alveolar gas equation causes a drop in PA02

If you give a person 100% oxygen and you note that they are still doing super poorly and their symptoms aren't getting better, then they are hypoventilating...also, will have really high PaCO2 levels.


What can cause hypoventilation?

Damage/injury to respiratory centers
Respiratory muscle weakness/fatigue or nerve injury/spinal cord injury
Obesity that can change lung or chest wall mechanics


What is the V/Q ratio? Why is it important? What does it mean if V/Q 1, & approaching infinity?

It's the ratio of ventilation to perfusion we have in our lungs.
1 means you have a partially occluded vessel that is reducing the perfusion

approaching infinity means you have dead space due to completely blocked vessel


How does V/Q differ across the lung? What's the implication of this for the partial pressures of oxygen and carbon dioxide?

As you get to the base of the lung, ventilation increases but not as much as perfusion. This causes the V/Q ratio to be larger at the base of the lung than at the apex.

This means that at the base of the lung you will have less PO2 and more PCO2 than at the apex.


How do variations in blood flow in the lung lead to the A-a gradient?

The base gets more of the blood flow so the overall arterial oxygen pressure is based heavily on it's low PO2 concentrations (this is due to lower V/Q ratio in the base)


How do O2 concentration differences in the lung lead to the A-a gradient?

The apex has higher P02 concentrations than normal while the base has lower P02 concentrations...however, it's not that much higher, while in the base it's a lot lower. Thus, the apex and higher V/Q regions can't compensate for the lower V/Q regions...this causes the A-a differences