Gas Exchange In Lungs Flashcards

1
Q

Gas exchange takes place in the alveoli. The alveoli form what to allow diffusion from air to blood?

A

Air blood barrier

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2
Q
  1. From where does oxygen enter the alveoli?
  2. Where does oxygen dissolve?
  3. What 3 layers does the oxygen have to diffuse through?
  4. The oxygen dissolves where and binds to what?
A
  1. Atmosphere
  2. Alveolar lining fluid
  3. Alveolar epithelium layer, basement membrane and the capillary endothelial cells
  4. It dissolves in plasma and binds to haemoglobin
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3
Q
  1. Approximately, how long does it take for a red blood cell to pass through a capillary? What about during exercise?
  2. Why does the time have to be so quick?
  3. For normal graph on pp02 vs capillary time, there is a steep sigmoid curve. Give a reason to why this graph would become bless steep in diseases like fibrosis
A
  1. At normal = 0.75s, at exercise= 0.25s
  2. Because oxygenation of blood must occur during the brief time taken for red blood cells to flow through pulmonary capillaries
  3. Graph would become less steep due to increased air-blood barrier thickness causing reduced diffusion
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4
Q
  1. What is rate of diffusion proportional to?

2. Explain each of the components involved

A
  1. Rate of diffusion § (surface area)/ distance2 x (Pa-Pc)
  2. Surface area of alveoli; ALF+epithelial+basement membrane+endothelial layer depth; partial pressure gradient between alveolar air and capillary blood
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5
Q
  1. For maximum diffusion, what is best (3)?
  2. What is hypoventilation? Type what respiratory failure?
  3. What is hyperventilation?
  4. What is hypo-perfusion? Type what respiratory failure?
  5. How does emphysema affect diffusion?
  6. How does fibrosis affect diffusion?
  7. How can pneumonia affect diffusion?
A
  1. Increased partial pressure gradient, increased surface area and decreased distance (thickness)
  2. When you don’t breathe in enough to meet demands so levels of carbon dioxide in arterial blood rises more than necessary (hypercapnia) and levels of oxygen in the blood drops. Can cause respiratory acidosis.
    This can be caused by problems controlling intercostal muscles and diaphragm. Type 2 respiratory failure- inadequate ventilation. Reduced oxygen partial pressure in alveoli.
  3. When you breathe too much, more than necessary to meet demands, so levels of carbon dioxide in arterial blood drops below normal. Levels of oxygen in arterial blood rise but only to an extent due to saturation of haemoglobin.
  4. Reduced blood flow to the alveoli so can’t absorb as much oxygen. Type 1 respiratory failure- failure oxygenation, meaning ventilation isn’t the problem, oxygen just doesn’t seem to be entering blood.
    Reduced oxygen partial pressure in capillary.
  5. Reduced surface area due to inflammation
  6. Increased basement membrane thickness
  7. It can cause pulmonary oedema, which increases thickness of fluid layer
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6
Q
  1. What do we do to meet metabolic demands?
  2. Increasing ventilation does what?
  3. How does hypoventilation impair partial pressure gradient?
  4. Decreasing ventilation does what?
  5. What happens to the partial pressure of oxygen in alveoli as ventilation increases?
  6. In hyperventilation, why does the graph for partial pressure of oxygen plateau? What is the saturation partial pressure of oxygen?
  7. What happens to the partial pressure of carbon dioxide as ventilation increases?
A
  1. Increase alveolar ventilation
  2. Increasing ventilation causes a smaller pressure gradient between the atmosphere and the alveoli as more oxygen has entered the alveoli. This increases the partial pressure gradient between the pulmonary capillaries and the alveoli, causing more oxygen to enter blood, allowing gas exchange.
  3. By lowering the partial pressure gradient between alveoli and blood
  4. Decreasing ventilation causes a greater partial pressure gradient between atmosphere and alveoli, meaning there’s a smaller partial pressure gradient between alveoli and blood so less oxygen diffuses in so reduced gas exchange.
  5. Partial pressure of oxygen increases in the alveoli and gets closer to that of the atmosphere
  6. Due to haemoglobin saturation
  7. Partial pressure of carbon dioxide decreases as ventilation increases
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7
Q

Why does blood flow through pulmonary capillaries need to match alveolar ventilation?

A

To enable efficient gas exchange as there’s a maximum amount of oxygen that each unit of blood can carry (saturation).

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8
Q
  1. What does V/Q describe?
  2. What should V/Q usually be? Why?
  3. At rest, ventilation and perfusion are both what? The ratio should be?
A
  1. Relationship between ventilation and perfusion
  2. It should be 1 as 1L of blood can carry 200mL of oxygen; 1L of dry air can carry 200mL of oxygen
  3. 5L/min
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9
Q

What does a V/Q ratio of greater than 1 mean?

A

It means reduced perfusion, so ventilation is greater than perfusion. So we are getting more oxygen to alveoli than oxygen is actually entering the blood. It is hypoperfusion.
This is called ‘physiological dead space effect’ which means the affected alveoli have reduced or no gas exchange. Similar to anatomical dead space.

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10
Q

What does a V/Q ratio smaller than 1 mean?

A

This means perfusion is greater than ventilation so it’s hypoventilation. This is shunt.

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11
Q

What happens if V and Q aren’t matched in individual alveolar units?

A

Gas exchange will be reduced.
In increases partial pressure of carbon dioxide, reflex hyperventilation will be induced to clear the excess carbon dioxide (but oxygen levels won’t rise more than to an extent)

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12
Q
  1. What exist to reduce ventilation-perfusion mismatching?
  2. What does hypoxic vasoconstriction of capillaries do?
  3. What happens if ventilation of specific alveoli decreases?
  4. So where is blood diverted to and why?
  5. What activates this homeostatic mechanism?
  6. Hypoxic vasoconstriction is a protective mechanism but why is it pathological in COPD?
A
  1. Homeostatic mechanisms
  2. Diverts blood flow from poor ventilated alveoli to well ventilated alveoli.
  3. It will cause alveolar carbon dioxide levels to rise and decrease oxygen levels in alveoli so oxygenation falls.
  4. So this reduced partial pressure of oxygen in alveoli induces vasoconstriction, reducing blood flow in alveoli that don’t get enough oxygen from the atmosphere. This is important to match perfusion with ventilation because there’s no point giving blood flow to alveoli who aren’t giving oxygen.
  5. Local hypoxia
  6. If hypoventilation occurs in loads of alveoli, that will cause a lot of vasoconstriction causing increase in resistance with pulmonary vasculture, causing pulmonary hypertension. This can then cause right side of the heart to hypertrophy leading to cardiac failure.
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13
Q

Explain how pulmonary embolism would cause V/Q mismatch

A

Embolism would occlude pulmonary artery supplying a specific part of lung, leading to unperfused alveoli (physiological dead space). This causes the V/Q ratio to go up.
Due to the occlusion, perfusion to other areas increase, so Q becomes greater, decreasing the ratio. So unless ventilation of these alveoli increase to match the perfusion, hypoxia and hypercapnia will occur.

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14
Q
  1. Name 3 things that lead to reduced perfusion of lung reasons, causing an increase in the V/Q ratio
  2. What are the (non functional) affected alveoli called?
  3. Does it respond to oxygen therapy and why?
A
  1. Heart failure which would reduce blood flow to lungs; blocked vessels (pulmonary embolism); loss/damage to capillaries (emphysema)
  2. Physiological dead space
  3. Yes
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15
Q
  1. What is shunt?
  2. What can cause it?
  3. So how does blood travel?
  4. Why does it respond poorly to oxygen therapy?
A
  1. Perfusion without ventilation. V decreases but Q is normal.
  2. Pneumonia, acute lung injury, respiratory distress syndrome, atelectasis
  3. So blood moves from the right side of the heart to the lungs without being oxygenated there and goes to the left side of the heart. This causes hypoxaemia as there’s low oxygen in the arterial system.
  4. No matter how much oxygen you add, that oxygen won’t go to the poorly ventilated alveoli because they won’t take it in so can’t provide oxygen to the capillaries innervating them. So increasing oxygen would just be providing oxygen to other functional areas but they become saturated with oxygen so any more oxygen will have no effect and they end up mixing with the deoxygenated blood from the poor ventilated alveoli so the blood going to the heart will still have some deoxygenated blood.
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16
Q

What does alveolar oxygen partial pressure tell us?

A

Let’s us us determine the cause of respiratory failure - whether it’s due to hypoventilation or poor oxygenation

17
Q
  1. Equation for alveolar oxygen pressure? Write out the complicated one too.
  2. What is RER?
  3. What should the alveolar oxygen pressure be?
  4. What is A-a oxygen gradient?
  5. Ambient air at sea level is the ‘oxygen inspired’. What is the numerical value?
A
  1. Alveolar air content = oxygen inspired - oxygen consumed. It’s basically just comparing oxygen gradient in alveolar and capillary blood.
  2. Respiratory exchange ratio. It’s the relationship between carbon dioxide elimination and oxygen consumption; it’s dependent on substrate used. It’s usually 0.8. The higher the RER, the lower the oxygen consumed. The lower the RER, the greater the oxygen consumed.
  3. It should be less than 2kPa because it’s good for all the oxygen inspired to be used. Bigger than 2kPa means there’s a problem.
  4. The difference between alveolar oxygen partial pressure and the arterial oxygen partial pressure.
  5. 19.74 kPa
18
Q

How can you tell if hypoventilation is contributing to hypoxaemia?

A

If the arterial carbon dioxide partial pressure is more than 6, then you have hypoventilation. At hypoventilation, less oxygen can enter blood as you breathe less so it causes hypoxaemia.

If the arterial carbon dioxide partial pressure is less than e.g 4.9, then you have hyperventilation.

19
Q

How can hypoxaemia and hypocapnia occur simultaneously? (Clinical case)

A

Hypoxia is caused by lack of oxygen going into alveoli (even though there’s increased ventilation as e.g there’s damage to alveoli there).
We get hypocapnia because at increased ventilation (by the mechanical ventilation), more carbon dioxide is being removed so levels of carbon dioxide drops, causing pH to increase.

The patient responding poorly to oxygen therapy is indicative of shunt because not much more of the blood at the well ventilated area can accept oxygen as it’s already saturated so can’t compensate for lack of oxygen in the damaged alveoli so the oxygenated and deoxygenated blood mix.
The mechanical ventilation machine has allowed more carbon dioxide to leave from the well ventilated alveoli (but no more oxygen can enter due to saturation).