Respiratory adaptations Flashcards

1
Q

Define the Alveolar gas equation

A

PAO2 = PIO2 - Oxygen consumed

PiO2 = (Patm - 47 mm Hg)x FiO2

*(Note: FiO2 is the fraction of inspired oxygen (which is 21% or 0.21 if we are breathing room air))

So, PAO2 = PIO2 - [PaCO2/RQ]

Full equation -
PAO2 = ((Patm - 47 mm Hg)x FiO2) - [PaCO2/RQ]

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2
Q

The Alveolar-arterial O2 gradient (A-a O2 gradient)

A

A-a O2 gradient = PAO2 - PaO2

Step 1: Get the PAO2 from the alveolar gas equation
Step 2: Get the PaO2 from the arterial blood gases

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3
Q

What is the V/Q ration with normal values?

A

V/Q = alveolar ventilation/cardiac output

V/Q = (4 l/min)/(5 l/min)

(here I’ve just used the ‘average’ resting values for each of our parameters)

V/Q = 0.8

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4
Q

When you consider a decrease in the V/Q ratio, all you need to remember is:

A
  • Ventilation is not keeping pace with perfusion.
  • The alveolar oxygen levels will decrease, which will lead to a decrease in arterial oxygen levels (PaO2)
  • The alveolar CO2 levels will increase (we’re not getting rid of it as fast), also leading to an increase in arterial CO2.
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5
Q

To produce an increase in the ventilation-perfusion ratio, I can do one of two things:

A
  1. Increase ventilation (bring in more oxygen to the alveoli, blow off more CO2 from the lungs)
  2. Decrease the perfusion (so the blood takes away less oxygen, delivers less CO2).
    - This will lead to an increase in the PAO2 (and therefore PaO2)cand a decrease in PACO2 and PaCO2

Summarizing, an incease in the V/Q ratio means that ventilation is in excess of the metabolic needs being met by perfusion, so we blow off CO2 (lower PACO2) and increase our PAO2 (and PaO2).

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6
Q

Define alveolar dead space (High V/Q)

A

In a patient, regions of zero blood flow will result from a pulmonary embolism that blocks the blood flow. For the sake of argument, let’s assume that a very little bit of blood can get through. This blood will be very well oxygenated (lots of ventilation, little perfusion) and have a very low CO2. In fact, the arterial blood gases in this situation will approach (but not become) atmospheric (PaO2 ~ 140 mmHg; PaCO2 ~ 0 mmHg). This sounds very good EXCEPT for two things:

  1. Not much blood gets through to these alveoli, so the volume of blood in this condition is very low. However, 5 liters of blood is still coming to the lungs every minute - the blood that can’t get to the area of lung affected by the embolism gets shunted to other parts of the lung (leading to a low V/Q ratio in those parts of the lung).
  2. We wasted energy by bringing ventilation to this area
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7
Q

Define both physiological shunt and anatomical shunt (low V/Q)

A

Physiological shunt: wasting cardiac effort to send the blood to the lungs even though nothing will happen to it as far as oxygen and carbon dioxide go.

Anatomical shunt: occurs when the blood physically doesn’t enter the lungs (e.g. a right-to-left shunt - the blood jumps straight from the right ventricle to the left ventricle without going to the lungs). The end result is the same - some of the arterial blood has very low oxygen and high CO2.

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8
Q

Steps taken by the body to normalize the V/Q ratio:

A

These include:

Hypoxic vasoconstriction: In cases where the V/Q ratio is low (lots of blood or too little ventilation), hypoxic vasoconstriction can occur and cause the blood coming into the area to be directed to other parts of the lung. Decreasing the perfusion of the hypoxic region will raise the V/Q ratio and bring the arterial blood gases closer to what we expect.

Bronchoconstriction: In cases of high V/Q ratio, the bronchi will constrict slightly to increase the resistance and decrease the amount of ventilation coming into an area that is not well perfused (although it won’t shut it down entirely). This limits the amount of alveolar dead space that occurs and minimizes the ‘wasted’ work that occurs with alveolar dead space.

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9
Q

hypoxia refers to

A

inadequate oxygen available for use by the tissues

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10
Q

Anoxia then refers to

A

the total absence of oxygen being delivered to the tissue.

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11
Q

Hypoxemia is the proper term for

A

low oxygen content in the blood

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12
Q

Hypoxic hypoxia:

A

the PaO2 is below normal because either the alveolar PO2 is reduced (e.g environmental reasons such as altitude) or the blood is unable to equilibrate fully with the alveolar air (e.g. as would occur in lung diseases with diffusion impairments such as emphysema or fibrosis).

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13
Q

Anemic hypoxia:

A

In this form of hypoxia, the lungs are in perfect working condition, but the oxygen carrying capacity of the blood has been reduced. As the name implies, anemia is a very effective way of producing anemic hypoxia. Carbon Monoxide produces anemic hypoxia - because it binds to the Hb with such high affinity, preventing oxygen from binding, it reduces the oxygen carrying-capacity of the blood. The tissues do not get sufficient oxygen to maintain their metabolic needs because the blood is not carrying it.

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14
Q

Circulatory hypoxia:

A

In this form of hypoxia the lungs are working just fine and the blood can carry sufficient oxygen. However, the tissue is not receiving sufficient oxygen because the heart cannot pump the blood to the tissue (or the arteries leading to the tissue have been blocked by clots etc…). Sickle cell anemia can lead to circulatory hypoxia as the cells sickle in the blood vessels and block them. (Yes - It also produces an anemic hypoxia as the sickled blood cells are removed from circulation.)

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15
Q

Histotoxic hypoxia:

A

Histotoxic literally means that the cells have been poisoned. In this form of hypoxia, there is no problem getting the oxygen to the tissue - the lungs, blood and circulatory system are all working just fine. However, the tissue is unable to use the oxygen. Cyanide leads to histotoxic hypoxia by poisoning the systems that utilize oxygen to create energy and preventing them from using the oxygen. Even though there is plenty of oxygen there, the cells experience a lack of oxygen and are affected as if there was too little/no oxygen available.

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16
Q

What is the direct stimulus for the central chemoreceptors?

A

Although the central chemoreceptors are responsible for detecting changes in the arterial carbon dioxide levels, they do so by measuring changes in the HYDROGEN ION concentration of the cerebrospinal fluid (CSF).

*Note: This system works because of the presence of carbonic anhydrase within the CSF in the area near the central chemoreceptors.

17
Q

True/False - Peripheral chemoreceptors respond to decreases in O2?

A

True

18
Q

How do the central chemoreceptors reset?

A

The composition of the CSF is going to compensate for the altered CO2. The cells of the choroid plexus are also capable of creating hydrogen ion and bicarbonate from the CO2 in the blood. Unlike the situation near the central chemoreceptors (where the carbonic anhydrase is located in the CSF), the cells of the choroid plexus contain the carbonic anhydrase and can then selectively pump either the hydrogen ion or the bicarbonate into the CSF.

19
Q

What’s the acute response to altitude?

A

Step One - Immediate Responses to Hypoxia: Not surprisingly, the immediate response to hypoxia is mediated through the peripheral chemoreceptors. These begin to increase their firing rate at about a PaO2 of 70 mm Hg and will increase ventilation in response to the hypoxia.

Step Two: An increase in alveolar ventilation will increase the PaO2. The flip side is that, unless metabolic production of CO2 were to change (and we are going to assume it does NOT), this increase in ventilation will lead to a decrease in the PaCO2.

Step Three: The decreased PaCO2 causes a decrease in the firing of the central and central chemoreceptors. This modifies the increase in ventilation we saw initially - the person at altitude has a greater alveolar ventilation than we would if they were at sea level, but it is not as great as the initial increase had produced.

20
Q

The steps involved in acclimatization include:

A

The cells of the choroid plexus are confronted with a CSF pH that is more basic than normal. They then pump more H+ or less HCO3- than under normal conditions into the CSF (as described for John in the early stages of the lung disease). This brings the CSF pH back to the normal range, allowing the peripheral chemoreceptors to drive ventilation in response to the hypoxia. It also means that the central chemoreceptors maintain a PaCO2 that is lower than normal. This accommodation is complete within a couple of weeks.

The hypoxia causes increased release of the hormone erythropoietin from the kidney. If you’ll recall from earlier in the cardiopulmonary section, erythropoietin stimulates the production of red blood cells by the bone marrow. This increase in hematocrit increases the Hb content of the blood, increasing the oxygen carrying capacity of the blood.

The cells of the body also adjust by increasing the number and size of the mitochondria, as well as (if possible) expressing more of the enzymes required for anaerobic glycolysis. These changes allow the cells of the body to make more efficient use of the oxygen that is delivered to them.

21
Q

Effects of Hyperbaric conditions:

A

Not surprisingly, the problems we encounter under hyperbaric conditions are the result of getting too much of the gases in our systems.

  • Development of superoxide and peroxide injures cells.
  • Nitrogen at higher pressure has effects akin to alcohol on neurons in CNS.
  • Air embolism from a closed glottis on ascent