Ventilatory drive in asthma

[Jabbed]

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What is the primary stimulatory factor of the respiratory drive in mild asthma (i.e., low pCO2)?

 

[tasar1898]

My guess is a mix of V/Q mismatch ( low ventilation in affected areas ) --> mild hypoxemia + a mild increase in pCO2 due to ''trapped air'' in the affected pulmonary segments ( Mucus plugs and bronchoconstr won't let you move air..)

Maybe someone else knows the exact stimulus

 

[worldbeater]

Asthma is an obstructive disease, you have a problem breathing out. So you will have a high CO2, and that will be your drive to blow it off. CO2 is your respiratory drive.

The only time this isn't the case is with a smoker who has COPD, his CO2 receptors are blunted, so his drive works with the level of oxygen, which is peripheral chemoreceptors (also known as carotid bodies on UWorld, they also give central chemoreceptors as a choice which is wrong, tricky question). This is why in practice, you shouldn't put a COPD patient on oxygen, you will end up putting the patient in a coma because you are screwing with his respiratory drive.

 

[Jabbed]

Asthma is an obstructive disease, you have a problem breathing out. So you will have a high CO2, and that will be your drive to blow it off. CO2 is your respiratory drive.

The only time this isn't the case is with a smoker who has COPD, his CO2 receptors are blunted, so his drive works with the level of oxygen, which is peripheral chemoreceptors (also known as carotid bodies on UWorld, they also give central chemoreceptors as a choice which is wrong, tricky question). This is why in practice, you shouldn't put a COPD patient on oxygen, you will end up putting the patient in a coma because you are screwing with his respiratory drive.

Given that compensated asthma is characterized by respiratory alkalosis, it does not seem logical that CO2 would accumulate and be the driving force for ventilation.

 

[tasar1898]

Probably the central receptors get more sensitized to CO2 , remember that they adapt.. or the peripheral chemoceptors ''sense'' the O2 .. The compensation mechanisms are really complex and in many diseases , still under investigation .. So in a question like this , I guess they will subtly ''point'' you towards an answer

 

[worldbeater]

Given that compensated asthma is characterized by respiratory alkalosis, it does not seem logical that CO2 would accumulate and be the driving force for ventilation.

I am not sure what you mean by compensated asthma, but asthma in general is definitely an obstructive condition and follows an obstructive pattern. You have a build up of mucus and an expiratory wheeze, so obstructive would make sense, right?

I am pretty sure about the respiratory drive works with CO2, can somebody else clarify/confirm this point please?

 

[tasar1898]

What Jabbed is saying is that in mild asthma people tend to hyperventilate and that ''overwhelms'' the obstruction and also produces a respiratory alkalosis ( Low PaCo2 ) , so he is wondering what keeps driving the ventilation to maintain these people in a chronic respiratory alkalosis state.. My guess is either central chemoceptors adapted to ''fire'' at lower PaCo2 , or peripheral chemoceptors firing at the mild hypoxemia(peripheral chemoceptors don't adapt)

 

[Mad Jack]

I'm betting it's direct stimulation of the bronchial C fibers by irritants, which causes bronchoconstriction, mucus secretion, and rapid, shallow breathing. In early asthma, there isn't enough obstruction to offset the reflexive rapid, shallow breathing, so you end up with a respiratory alkalosis initially until the obstruction catches up and you end up with air trapping.

In clinical practice, many patients will also have an anxiety component to their asthma, which further exacerbates their respiratory alkalosis.

 

[tasar1898]

Ahh couldn't remember those damn C fibers...

 

[Mad Jack]

Ahh couldn't remember those damn C fibers...

Don't forget your J receptors either. A lot of people get confused on why people with CHF end up hyperventilating and getting alkalotic even though it's a disease of hypoxia rather than hypoventilation- it's all about those J receptors, and there's not much you can do to fix it except get the fluid out of 'em.

 

[worldbeater]

Ok cool, I missed that mild asthma part. So I'll try to keep in mind the severity of the asthma when figuring out what pattern is occurring. Nice explanation, Mad Jack!