Normal PCO2 in life-threatening asthma?

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MedStudentt
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Why would PCO2 be normal in life-threatening asthma? Pathophysiology behind this?
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Spencer Wells
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(Original post by MedStudentt)
Why would PCO2 be normal in life-threatening asthma? Pathophysiology behind this?
Why would it not be normal?

In someone having an asthma attack you'd expect them to hyperventilate. This should result in a respiratory alkaemia (low PaCO2, as the increased minute ventilation results in increase blowing off of CO2.)

If they start to tire (life-threatening asthma), they won't be able to breath as quickly or a deeply. Therefore PaCO2 will rise to normal levels as their minute ventilation falls.

In near-fatal asthma the PaCO2 will be raised, and a respiratory acidaemia will be seen.
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(Original post by Spencer Wells)
Why would it not be normal?

In someone having an asthma attack you'd expect them to hyperventilate. This should result in a respiratory alkaemia (low PaCO2, as the increased minute ventilation results in increase blowing off of CO2.)

If they start to tire (life-threatening asthma), they won't be able to breath as quickly or a deeply. Therefore PaCO2 will rise to normal levels as their minute ventilation falls.

In near-fatal asthma the PaCO2 will be raised, and a respiratory acidaemia will be seen.
Does it affect the A-a gradient?
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Spencer Wells
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Yes
(Original post by Anonymous)
Does it affect the A-a gradient?
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nexttime
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(Original post by Anonymous)
Does it affect the A-a gradient?
(Original post by Spencer Wells)
Yes
Yes, but its probably mainly reduced ventilation right? If its properly near-fatal?
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(Original post by nexttime)
Yes, but its probably mainly reduced ventilation right? If its properly near-fatal?
Yeah, I once got it even as an example of where a 'normal' pO2 would still be very concerning if the patient was on lots of supplemental O2, but ir rarely rarely see it listed as one of the big causes increased gradient. I presume it is because it is only with severe/life threatening asthma that you get significant alveolar hypoventilation?
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(Original post by Anonymous)
Yeah, I once got it even as an example of where a 'normal' pO2 would still be very concerning if the patient was on lots of supplemental O2...
I mean, that would always be concerning surely?

But I guess asthma can be a particularly acute process.

but ir rarely rarely see it listed as one of the big causes increased gradient. I presume it is because it is only with severe/life threatening asthma that you get significant alveolar hypoventilation?
Not really sure on quantification tbh - you do get a lot of distal airway inflammation that will reduce A:a gradient, as well as a bit due to increased mucus production. But then V/Q mismatch is a huge factor too IIRC.
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Spencer Wells
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Asthma primarily results in ventilatory failure (i.e. hypercapnoea) as it nears its terminal phases.
Inflammation of the airways, as well as mucous plugging (the mucociliary clearance tends to be reduced) and airway drying from increased minute ventilation, as well as underlying infection, if present, will contribute to hypoxaemia, and thus an increasing A-a gradient. At this point patients tend to be on high-flow oxygen via facemark, yet remain either hypoxaemic or normoxic (but this is concerning because of the high FiO2, you would expect them to be hyperoxic.) This is an indication to do something about it.

Unfortunately intubating these patients can be fatal. Our ventilators are not sophisticated enough to provide adequate oxygenation/ventilation without causing significant damage to lung tissue, which is often fatal. In addition, because the job of the upper airway is to moisten the air that we breathe, and so much airflow is going past these because of the high respiratory rate, these patients are often hypovolaemic.
Administering anaesthetic drugs (which result in both vasodilatation and myocardial depression) can therefore result in circulatory collapse and cardiac arrest. Combine this with not being able to ventilate such tight lungs and they become massively acidotic (from retained CO2) within seconds to minutes, and die.

This is why I hate intubating asthmatics and will do all I can to avoid doing so.

V/Q mismatch in theory should be autoregulated by the lung. Underventilated lung is going to become hypoxaemic. This will result in hypoxaemic pulmonary vasoconstriction to the affected lung segment, reducing it's blood flow and therefore maintaining V/Q match. This does however result in increased shunt fraction, as deoxygenated blood arrives back at the pulmonary vein.
Last edited by Spencer Wells; 3 years ago
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