How does respiratory alkalosis occur in pulmonary embolism?

[WanderingGuitarist]

From my understanding, PE causes a dead space. Increased ventilation cannot blow off the extra CO2 due to the wasted ventilation that goes to the healthy alveoli that isn't recieving blood.

So how does alkalosis occur in pulmonary embolism?

Is pulmonary embolism not a true dead space?

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[Dr Blue]

PE causes hypoxia which causes hyperventilation --> decreased pCO2 -->respiratory alkalosis

 

[WanderingGuitarist]

PE causes hypoxia which causes hyperventilation --> decreased pCO2 -->respiratory alkalosis

I get that but from my understanding, in a dead space, hyperventilation can't compensate for the increased paCO2 due to ventilation being wasted on alveoli that are not perfused.

 

[Pepe18]

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[WanderingGuitarist]

It can because in dead space all the blood that is perfusing the lung can have normal gas exchange (whereas shunt has blood not participating in gas exchange). The blood won't flow to the area of obstruction. Since there is more dead space in lung, there is more residual CO2 hanging around in the lung--> this CO2 lowers the PCO2 difference that normally drives CO2 out of the blood.

You compensate by increasing respiration. Breathing faster means bringing more fresh air in, which dilutes the resdiual CO2 left in the dead space--> restoring the drive of CO2 out of the blood. You also get hypoxic vasoconstriction to block vessels, with dilation at well perfused alveoli, which shunt the blood to well ventilated area for exchange

Thanks for your reply! According to Boards and Beyond, he mentions that a true dead space cannot compensate for PCO2 increases due to wasted ventilation.

So what you're saying is that dead spaces can all compensate for PCO2 even though ventilation is wasted? Is the respiratory rate high enough to overcome the wasted ventilation?

Was BoardsBeyond perhaps referring to in theory if no correction has occured?

Sorry for the excessive questions. Pulm is very hard 🙁

 

[Pepe18]

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[WanderingGuitarist]

Yes, because then he goes on to say that PE is more than just a dead space. Severe PE has dead space and then a V/Q mismatch in the area where you dilate arterioles to compensate (V/Q mismatch because those dilated vessels now contain so much blood that is isn't getting fully saturated- so Q is too high for V even though you are hyperventilating.). The V/Q mismatched area is allowing the CO2 to be blown off

I don't like it either. Dead space and shunt are more theoretical concepts that don't exactly play out in real diseases.

Thanks for the reply! Appreciate it 🙂