Blood gases in asthma

[el_duderino]

---

Members do not see this ad.

Can someone explain how both PaO2 and PCO2 are low during an asthma attack? If you're ventilating enough to end up hypocapnic, how do you also end up hypoxemic?

 

[Kazaki]

During an asthma attack, there's HYPERcapnia because its basically an obstructive disease. So think of it as air can get in but can't leave, you produce the same amount of CO2 so net effect is increased CO2. There's no hypocapnia.
Hypoxemia is easy now. Think of it as a case of chronic bronchitis, you can't get enough air into your lungs because the airways are basically collapsing, so hypoxia 🙂

 

[thehundredthone]

Can someone explain how both PaO2 and PCO2 are low during an asthma attack? If you're ventilating enough to end up hypocapnic, how do you also end up hypoxemic?

Hypoxemia is easy now. Think of it as a case of chronic bronchitis, you can't get enough air into your lungs because the airways are basically collapsing, so hypoxia 🙂

That's actually a great question, and the above response is the common answer but not a complete one. Oxygenation and ventilation are linked but not entirely co-dependent processes. Now, while the intuitive explanation for ABG numbers in asthma is alveolar hypoventilation due to airway obstruction, the real reason for hypoxaemia is the V/Q mismatch. Early studies from the 60s and 80s showed that while beta-agonists reverse airflow obstruction, they do not improve hypoxaemia. In fact, some studies showed that even 100% O2 worsened hypoxemia at least transiently, further lending weight to the mechanism of hypoxic pulmonary vasoconstriction in a V/Q mismatch. Here are a couple of studies that make for good reading: BMJ, 1967 and BMJ Thorax, 1989

During an asthma attack, there's HYPERcapnia because its basically an obstructive disease. So think of it as air can get in but can't leave, you produce the same amount of CO2 so net effect is increased CO2. There's no hypocapnia.

During an asthma attack, hypercapnoea indicates impending or existing respiratory failure due to respiratory muscle fatigue. Remember, asthma is a condition of normalcy with acute exacerbations, hence patients are not chronically hypercapnoeic the way COPD patients are. Asthmatic patients hyperventilate due to hypoxaemic pulmonary responses in order to increase airflow and oxygenation. The by-product of this process is hypocapnoea, since increased ventilation washes out CO2. It is only when the respiratory muscles begin to tire out from the work of breathing that the pCO2 begins to rise, and this is generally an indication for mechanical ventilation.

 

[el_duderino]

That's a great explanation, and makes sense. Thank you.

 

[Kazaki]

Wow! really nice explanation. But I'm a bit confused now

the real reason for hypoxaemia is the V/Q mismatch.

if there's a V/Q mismatch (which there obviously is) shouldn't that create a shunt because hypoxemia in the pulmonary vasculature causes vasoconstriction? So if there's a shunt, where's the blood being shunted towards? All the vessels aren't getting adequate ventilation, so my understanding is that all vessels are constricted

 

[thehundredthone]

if there's a V/Q mismatch (which there obviously is) shouldn't that create a shunt because hypoxemia in the pulmonary vasculature causes vasoconstriction? So if there's a shunt, where's the blood being shunted towards? All the vessels aren't getting adequate ventilation, so my understanding is that all vessels are constricted

Referencing the papers, there is V/Q mismatch but it is not homogenous across the lungs, because ventilation is uneven. Additionally not all areas undergo shunting, most merely see a V/Q mismatch.

 

[worldbeater]

I had asked the same question earlier, I'll dig up the old thread for you: http://forums.studentdoctor.net/threads/ventilatory-drive-in-asthma.1172628/#post-17190624

Patient will present with high CO2 in a prolonged asthma attack in an obstructive pattern/respiratory acidosis (which is more classic and how it presents on practice questions). In a mild case of asthma (something you will see in a clinic), it's due to anxiety and gives a restrictive pattern, increased respiratory rate and blowing off CO2, showing respiratory alkalosis.

 

[thehundredthone]

I had asked the same question earlier, I'll dig up the old thread for you: http://forums.studentdoctor.net/threads/ventilatory-drive-in-asthma.1172628/#post-17190624

Patient will present with high CO2 in a prolonged asthma attack in an obstructive pattern/respiratory acidosis (which is more classic and how it presents on practice questions). In a mild case of asthma (something you will see in a clinic), it's due to anxiety and gives a restrictive pattern, increased respiratory rate and blowing off CO2, showing respiratory alkalosis.

Why do you use the terms obstructive and restrictive patterns?

 

[worldbeater]

Why do you use the terms obstructive and restrictive patterns?

It's just the way we were taught and the CO2/O2 values work out perfectly every time for any respiratory question I have been doing. It keeps my mind organized. I don't think it's mainstream though, because I have gotten weird responses from previous posters on the forum.

 

[thehundredthone]

It's just the way we were taught and the CO2/O2 values work out perfectly every time for any respiratory question I have been doing. It keeps my mind organized. I don't think it's mainstream though, because I have gotten weird responses from previous posters on the forum.

While it may work for your questions (and there are no rules about how you choose to use associations), it's the wrong terminology and using it out loud risks misinformation. Obstructive and restrictive patterns refer to flow volume curves on spirometry, not blood gases. Also, respiratory alkalosis is not related to restrictive disease, other including anxiety and pulmonary embolism also have the same findings. I guess I'm another one with a weird response.

 

[worldbeater]

While it may work for your questions (and there are no rules about how you choose to use associations), it's the wrong terminology and using it out loud risks misinformation. Obstructive and restrictive patterns refer to flow volume curves on spirometry, not blood gases. Also, respiratory alkalosis is not related to restrictive disease, other including anxiety and pulmonary embolism also have the same findings. I guess I'm another one with a weird response

That's fine, I have no issues with it, I appreciate your thoughts. When I am on the wards, I guess I won't use those names of restrictive/obstructive. Maybe it's better to say if in the condition you have a problem breathing in or breathing out. But, they definitely do have a specific pattern that can give you the details that you want when asked by an attending, which can be used. For a patient that has respiratory alkalosis, it all hinges on the patient not able to breathe in normally, so your O2 is decreased, respiratory rate increases, your blowing off CO2 and that gives your increased pH. You can fit anxiety, pulmonary embolism, pregnancy, gram negative sepsis in this pattern. Any bug that affects interstitium, like PJP in an HIV patient(something I was just reading about) will cause a diffusion problem, your O2 will drop, your respiratory rate will increase, and the rest of the pattern will follow. They are all identical. You can literally fit dozens of conditions in this one pattern and it's more powerful to understand as opposed to trying to memorize each disease one by one.

 

[thehundredthone]

That's fine, I have no issues with it, I appreciate your thoughts. When I am on the wards, I guess I won't use those names of restrictive/obstructive. Maybe it's better to say if in the condition you have a problem breathing in or breathing out. But, they definitely do have a specific pattern that can give you the details that you want when asked by an attending, which can be used. For a patient that has respiratory alkalosis, it all hinges on the patient not able to breathe in normally, so your O2 is decreased, respiratory rate increases, your blowing off CO2 and that gives your increased pH. You can fit anxiety, pulmonary embolism, pregnancy, gram negative sepsis in this pattern. Any bug that affects interstitium, like PJP in an HIV patient(something I was just reading about) will cause a diffusion problem, your O2 will drop, your respiratory rate will increase, and the rest of the pattern will follow. They are all identical. You can literally fit dozens of conditions in this one pattern and it's more powerful to understand as opposed to trying to memorize each disease one by one.

Except that pattern is not restrictive, and the majority of conditions you mention don't have an actual mechanical ventilation deficit. Restrictive lung disease specifically refers to a decrease in FEV1 and FVC, where the decrease in FVC is disproportionately greater. This is due to either intrinsic (parenchymal) or extrinsic mechanical restriction in alveolar ventilation either by fibrosis or restricted chest wall (and hence lung) expansion or volume. There is no diffusion or perfusion abnormality in the definition of restrictive lung disease. A restrictive pattern is even more specific, as I said before, to flow volume loops.

In anxiety, pulmonary embolism, sepsis and PJP there is no inability to "breathe in normally". There is no hypoxemia involved in anxiety. The term you want is probably "increased respiratory drive", which applies to most of the conditions you reference. The cause for the increased drive, however, is different. That's what drives the pathophysiology, and thus the management. In sepsis the drive is to compensate for metabolic acidosis, in asthma it is a combination of subjective and real hypoxia, etc. You cannot fix respiratory alkalosis in mild asthma with supplemental O2. You cannot fix it in anxiety or pulmonary embolism with beta agonists. However, you can fix the increased respiratory drive with beta agonists in asthma, anxiolytic therapy (or patience) in anxiety and supplemental O2 along with anticoagulation therapy in pulmonary embolism. All of these will eventually correct their respiratory alkalosis.

It might be an easier thing to remember what conditions are associated with a ventilatory defect that may cause CO2 retention (essentially COPD and acute severe asthma but also decreased respiratory drive from paralysis, drugs, etc.), and classify the rest (everything you mentioned) as being "not those things" rather than calling it a restrictive pattern. Always remember that there is a point at which such oversimplification can hamper your understanding of disease processes, and adversely affect management. When the attending asks whether there is more of a ventilation or a perfusion defect (to know whether supplemental O2 can correct the hypoxemia), the term "restrictive pattern" ceases to work. You have to start thinking about the A-a gradient among other things, it's not as simple as problem breathing in or breathing out (although I get that that by "breathing in" you mean O2 delivery issues in general, ranging from ventilation to perfusion defects).

 

[worldbeater]

The term you want is probably "increased respiratory drive", which applies to most of the conditions you referen

Ok nice, I'll use this from now on.

Always remember that there is a point at which such oversimplification can hamper your understanding of disease processes, and adversely affect management. When the attending asks whether there is more of a ventilation or a perfusion defect (to know whether supplemental O2 can correct the hypoxemia), the term "restrictive pattern" ceases to work. You have to start thinking about the A-a gradient among other things, it's not as simple as problem breathing in or breathing out (although I get that that by "breathing in" you mean O2 delivery issues in general, ranging from ventilation to perfusion defects).

Yeah I agree, I mean at this point I am just learning a general concept to get the answer right on a basic science exam. It's probably premature to say this exact line of logic would work on an actual patient; I am not a resident, you obviously have more real life exposure to patients. Maybe the management will get more complicated on Boards II or Boards III, we will see when I get to that point? Thanks for the post.