Respiratory Failure Overview

All pulmonary diseases jeopardize the function of the lungs. Decreased function could result in respiratory failure. 

To understand respiratory failure better, we need to look at the respiratory system, which the lungs are a part of. 

• The system functions to deliver oxygen to the other organs and get rid of carbon dioxide from the tissue. 
• The lung functions to get oxygen to the blood and get rid of carbon dioxide from the blood.
• Respiratory failure occurs when the lungs cannot adequately add oxygen or remove carbon dioxide from the blood. 
• This obviously makes there be 2 types of respiratory failure, hypoxemic and hypercarbic, also called type 1 and type 2 respectively in the book. 
  • Apparently the type classification is not used very often on the floors, so if you say type 2 respiratory failure, you will be laughed at, but saying hypercarbic respiratory failure will get you the good looking nurse.

So lets compare and contrast…

• Both have low oxygen concentrations in the blood.
• Only hypercarbic has high carbon dioxide concentrations in the blood
• In hypoxemic, it can be either normal or low.
• Hypercarbic respiratory failure has 2 types.
  • Acute: high PaCO2 with low pH (body has not had time to compensate, so you have respiratory acidosis)
  • Chronic: high PaCO2 with normal pH (respiratory acidosis has been compensated for by changes in renal bicarbonate excretion)
• Hypoxemic respiratory failure is characterized by low oxygen saturation (less than 90%) even in the presence of 60% oxygen (normal air is 21%)

Now to better understand these types of respiratory failure, we need to go back over some physiology concepts, namely Alveolar Ventilation and Alveolar-arterial Oxygen Difference.

 Concept #1-Alveolar Ventilation 

• Lungs are represented as a single alveoli
• Remember the conducting airways are dead space.
• The double headed arrow shows ventilation and the larger the arrow the more breathing.
• Also remember the O2, CO2 exchange happens between the alveoli and blood vessels and can be affected by amount of ventilation.

 This shows normal ventilation with normal concentrations (pressures) of gases.

 As a note, the big “A” means alveolar

Little “a” means arterial

Little “mv” means mixed venous, or blood coming from the right atrium before it gets to the lungs.

But what happens if you hyperventilate? 

• You get more oxygen delivered to the alveoli and therefore to the blood. 
• Also, more CO₂ would be washed out of the alveoli and therefore the blood, since they remain at equilibrium. 
• So the P_aO₂ would be above 100 and the PaCO₂ would be below 40.

Now what happens if we hypoventilate

• Not enough oxygen is delivered to the alveoli, so the oxygen tension is down, in this case 60 instead of 100.  The arterial blood will equilibrate, giving a P_aO₂ of 60.
• The CO2 does not get removed adequately from the alveoli so its tension is higher, 80 instead of 40.  So when the blood equilibrates you get a PaCO2 of 80 instead of 40.
• This shows us typical hypercarbic respiratory failure, a low P_aO₂ with a high PaCO2

 So oxygen tension will vary with alveolar ventilation, and CO2 concentration will vary inversely. 

 
That brings us to the next point, alveolar—arterial oxygen difference (gradient).

• It is simply the difference between the oxygen tensions of the alveoli and artery.  It is calculated by taking the alveolar tension and subtracting the arterial O2 tension. 
  • In the case of hypercarbic respiratory failure before,
    • P_AO₂ (60) – P_aO₂ (60) = 0.
• This shows us a key factor of hypercarbic respiratory failure, even though the P_aO₂ is low and the PaCO2 is high, the alveolar—arterial oxygen difference is normal.

So then what about hypoxemic respiratory failure?

• Well they key feature is there is a high oxygen difference.  This can be easily seen in a right to left shunt.
• So below we see two examples, one normal, one with the shunt.

• Above, the lung is totally normal, a normal equilibrium is established, all oxygen tensions are fine, etc.
• Below that, there is a right to left shunt, in this case a mucous plug has blocked ventilation of some of the alveoli, so in essence the blood going by it is being shunted past functional lung, directly to the left artia.  This creates a ventilation perfusion mismatch.
• Part of the alveoli gets hyperventilated, since all of the air goes to that alveoli, to a P_aO₂ up to 110 instead of 100 due to more oxygen delivery and the P_ACO₂ is 30 instead of 40 due to excess removal of CO₂.  However, the other alveoli gets no air, so the venous blood gas tensions do not change.
• When the venous blood from the functional and non functional alveoli mix (assuming an equal mix), the CO₂ concentration equals the average between them.  In this case (45 + 30)/2, which equals 37.5 or 38.
• The oxygen is different.  We see the post capillary O₂ concentration is 55 and not 75, the average of 110 and 40.  So it that a typo?  No, professors are infallible.  So what gives?
• O₂ concentrations are more dependent upon hemoglobin.  So you don’t just average the tensions.  A P_aO₂ of 110 adds very little extra oxygen to the blood, since the hemoglobin is already almost 100% saturated at a P_aO₂ of 100, while a P_aO₂ of 40 is equal to about 75% saturation of hemoglobin.  So if we average the hemoglobin saturations of 100 and 75, we get 88% saturation.  Blood with 88% saturated hemoglobin has an O2 tension of 55.  So it is the hemoglobin that matters.  So what is the alveolar-arterial oxygen difference? 
• PAO2 (110) – PaO2 (55) = 55
• This is now hypoxemic respiratory failure.  This is in fact the way to differentiate between the 2 types of respiratory failure.  If alveolar-arterial difference is abnormally high, it is hypoxemic respiratory failure, if it is normal, it is hypercarbic respiratory failure. (Notice how he stresses this a lot?)

So the previous models are very pure. 

• Everyone’s lungs has a level of alveolar-arterial oxygen difference. 
• It is age dependent. 
• In room air, the difference can be anywhere from 0-25 mmHg, even up to 30. 
• In the book they give us a formula of 2.5 + (.21)age of patient. 
  • But no one uses that, except for maybe the authors. 
  • But just for fun, for Sarada, we take 2.5 +(.21)16, which equals 3.36.
• Peak lung function is found at about age 22, and after that it goes downhill, so at ages 60-70, the normal difference can approach 25 or even 30.

So what else should we know about hypoxemic respiratory failure?

• The causes of hypoxemic respiratory failure are right-to-left shunt, a ventilation perfusion mismatch, and alveolar capillary block (diffusion distance between the alveoli and capillaries is greater) like in interstitial lung disease. 
• The diseases that cause hypoxemic respiratory failure are asthma, interstitial lung disease, COPD, pneumonia, CHF, etc. 
  • Basically anything that alters the balance of ventilation. 

And hypercarbic respiratory failure?

• Again, if you have hypercarbic respiratory failure, you get an oxygen difference within normal ranges, but an increased CO₂ tension. 
• The causes are anything that causes hypoventilation. 
  • Oversedation is a big problem, especially with overzealous house staff that want to keep people ultra relaxed while intubated and get too much sedative.  Also neuromuscular diseases can cause it.

You can also get a combined failure, with a high CO2 and an increased oxygen difference. 

• A good example is someone who has a ventilation-perfusion mismatch who tires out, like an asthmatic who gets fatigued from trying to breathe hard. 
• This creates a hypoventilation of the lungs, which increases P_aCO₂, in addition to the already increased oxygen difference in asthma.

So how do you calculate the alveolar arterial difference?

• 1^st calculate the arterial oxygen and carbon dioxide concentrations.
  • Do this by taking blood from a small artery and measure them.
• But the problem is you also need to measure the alveolar oxygen difference.  It is hard to get a pure sample of alveolar air, since there is that good ole’ dead space there, that affects the sample.
• So we use the alveolar air equation.
• So remember back to when Woody Allen… I mean Dr. Edinger taught us this in physiology.
• Do not worry about memorizing this too much.
• 1^st, assume that total pressure is equal to the pressures of nitrogen, oxygen, carbon dioxide and water.  You assume that the pressure of water is 47 mmHg at body temperature.  You also assume there is good equilibration of CO2 between the alveoli and arterial blood.
• So the formula is…

 The .21 comes from the % of oxygen in inspired air, the PB is total barometric pressure and the R is respiratory quotient, a standard value used to calculate PAO2 from a known PaCO2.

So here are some examples of different types of Respiratory Failures.

In the 1^st example, the calculated gradient is within normal, remember, it can be up to 25 or 30.

The next one is a high gradient with normal PaCO2, giving hypoxemic respiratory failure

The 3^rd has a high PaCO2 with a normal gradient, giving hypercarbic respiratory failure.

The last has both a high PaCO2 and oxygen gradient, giving a combined respiratory failure.

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