General Respirology Flashcards

1
Q

What is hypoxia? How does it differ from hypoxemia?

A

Hypoxia - lack of oxygen delivery to the tissues.

**Hypoxemia - ** low oxygen in the blood, as measured by PaO2

Memory aid: -emia is usually in blood: bacteremia, viremia, etc

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2
Q

What is hypoxemia? How is that different from hypoxia?

A

Hypoxemia - lack of O2 in blood <as></as>

Hypoxia - lack of oxygen delivery to the tissues.

Memory aid: -emia is usually in blood: bacteremia, viremia, etc

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3
Q

What is a normal difference between PAO2 and PaO2?

A

10-20 mm Hg

> that number = problems with gas exchange

low priority: Why 10-20 mm difference?

~ incomplete diffusion

~ ventilation and perfusion not perfectly matched (blood hangs up more in lower part of lung due to gravity)

~ bronchial arterial blood can be collected by veins

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4
Q

So … this normal A-a range (of O2), how is it calculated?

A

<= 10 mm Hg room air (FIO2 = 0.21) in young adults

approximate normal A-a gradient = (Age/4) + 4

ie. A-a range increases with age

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5
Q

What are 5 causes of hypoxemia (decrease of PO2 in blood)?

A
  1. low oxygen content in air (high altritude, bad anesthesia, etc)
  2. low alveolar ventilation - hypoventilation (CNS depression by drugs, inflammation in the brain, disease of resp muscles)
  3. diffusion impairment - increase in distance between alveoli and capillaries (fibrosis)
  4. V/Q (ventillation/perfusion) mismatch
  5. blood shunting (ex. R->L heart shunt)

Memory aid: start from the brain and work your way down (alveolar ventilation (brain or resp muscles), low O2 in air, diffusion impairment (lungs), V/Q mismatch (lungs), shunting (heart)

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6
Q

Explain how low oxygen content affects A-a ratio?

A
  • since less O2 in air, less O2 in blood
  • high altitude
  • accidentally bad anesthesia (bad supply line or content)
  • as PO2 decreases, chemoreceptors pick that up and hyperventilate. consequently PaCO2 decreases as well (hypocapnia)

-> low oxygen in atmosphere - low oxygen in both A and a -> A-a ratio does not change

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7
Q

What is hypocapnia?

A

low PaCO2 (ex. when hyperventillating)

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8
Q

How does low alveolar ventilation influence A-a?

A

low alveolar ventilation - > low O2 in alveoli -> low O2 in arteries

since both A and a are lower, A-a stays normal

reminder: ventilation is not respiration, ventilation is the amount of gas exchange happening in the lungs! V(dot) is minute ventilation in L/min. Ventilation measures the amount of gas traveling through lungs, breaths will not give us that - they can be deep or shallow, but gas volume will give us good idea.

PaCO2 ~ VCO2/VA

Concentration of CO2 in arteries will depend on how much CO2 ventillation is going on, compared to overall alveolar ventilation (as more CO2 flows in, VCO2 increases, so PaCO2 increases, if alveoli ventilate well, VA is high, but PaCO2 is low)

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9
Q

Hypoventilation (reduced alveolar ventilation) is associated with hyper/hypo capnia?

A

Reduced ventilation is associated with hypercapnia (more CO2!)

This is very logical, the less volume you clear in the alveoli, the more CO2 accumulates from the tissues

You can reduce hypercapnia by mechanically ventilating the patient (ventilator), hypoxemia can be corrected with O2 mask.

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10
Q

What are some potential causes of hypoventilation?

A
  • depression of CNS by drugs (ex. narcotics will reduce breathing)
  • inflammation, trauma or hemorrhage in the brainstem (medulla and pons control breathing!)
  • abnormal spinal cord pathway (spinal cord transmits info from chemoreceptors and mechanoreceptors for breathing)
  • desease of the motor neurons of the brainstem/spinal chord
  • disease of the neuromuscular junction
  • disease of the respiratory muscles
  • abnormality of the chest wall
  • upper airway obstruction
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11
Q

How do diffusion abnormalities affect A-a gradient?

A

A-a may be normal at rest in diffusion abnormality, but elevated during exercise (eg. blood flow is slow enough that diffusion is not affected normally (only 1/3 time needed), where is in exercise the flow is too quick and results are seen).

Ex. fibrosis: alveolar O2 is normal, but due to thickening between alveoli and arteries, O2 has hard time diffusing. This is especially noticable during exercise.

Supplemental O2 (FI O2 increased) can stop hypoxemia b/c it increases general PAO2, so more O2 molecues have a chance to travel to blood.

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12
Q

How does ventilation-perfusion inequality (V/Q mismatch) in the lungs influence A-a gradient?

A

Alveolar ventilation is 4L/min and cardiac output is 5L/min

Normal range of the V/Q ratio for the lung is 0.8 -1

Both ventilation and perfusion are gravity dependant; both increase as you move down the lungs. Blood flow changes 5x from top to bottom of lung, but ventilation only changes 2x.

-> At the top of the lungs, there is more ventilation compared to perfusion (easier for gas to be up top, then blood fighting with gravity). At the base of the lungs, there is more perfusion compared to ventilation. -> 0.8 V/Q mismatch is normal, and will change with age as lungs loose elasticity etc

Memory aid:

O2 supplement will help correct hypoxemia b/c it will give more O2 to regions of lung low on O2. A-a would differ since not all O2 in A is getting into a is the definition of Q/V mismatch

Q is flow in physics = perfusion V for ventilation

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13
Q

How does shunting influence A-a gradient? What is meant by shunting?

A

Shunt is a condition in which deoxygenated blood from the venous system is moved to arterial system without receiving O2 from lungs. Shunts occur naturally, but can be result of a disease.

Ex. heart shunt - > septal defect -> blood from right to left, nonoxygenated going into oxygenated left. Ex. Tetralogy of Fallot

Even though A(alveoli) are perfusing ok, arterial O2 (a) would be lower, since shunting contributes deoxygenated venous blood to arterial.

This cannot be corrected with supplemental O2, since this cannot increase O2 in venous blood (it skips lungs!) that mixes with arterial, so aO2 levels will remain constant.

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14
Q

So… what happens in Pulmonary Embolism?

A

in pulmonary embolism, has ventilation (A) but no perfusion (a). Therefore, A-a gradient is very high.

Lungs redirect blood from low perfused to higher perfused areas -> small surface area and more blood -> lower PaO2 -> A-a big

if add O2 - > more O2 to share in overloaded non-embolized areas -> PaO2 improves

V/Q mismatch example (ventilation is there, but blood flow restricted)

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15
Q

Can you summarize 5 causes of hypoxemia, their A-a gradient changes and whether supplemental O2 would help?

A

Try again

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16
Q
A
17
Q

What is the original tissue layer that forms visceral pleura?

A

splanchic mesoderm (memory aid -spleen is inside, visceral pleura is inside, so its splantic rather than somatic = body = outside)

18
Q

What is the original tissue layer that forms parietal pleura?

A

somatic mesoderm (think outside pleura, think somatic)

19
Q

What are the four histological periods in lung formation?

A
  • Pseudoglandular period (like a gland)
    • histological structure resembling a gland, development of pulmonary arteries
  • Canalicular period (17-26 weeks, canaliculus = small passageway)
    • formation of respiratory bronchi and intense growth of pulmonary blood vessels (esp 24-26 weeks = vital)
  • Terminal sacs - think high levels ->23 (26 weeks to birth)
  • Formation of alveoli (32 weeks to 8 years)