Aug 4, 2016
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Hello,

I am a medical student and need some help in understanding how does high flow supplemental oxygen in COPD lead to an increase in alveolar dead space?


From my understanding alveolar dead space represents alveoli that are ventilated but poorly perfused and provision of oxygen supplementation should reverse the hypoxic vasoconstriction and lead to better perfusion.


I came across this article in Pubmed which states:


"A high fraction of inspired O2 (FiO2) will increase O2 tension in alveoli with a low level of ventilation, inhibiting hypoxic pulmonary vasoconstriction. As a result, alveoli with relatively impaired ventilation are well perfused, leading to an increase in Va/Q mismatch"


I am confused how can we have high O2 tension in an alveolus that has low level of ventilation? I thought by giving supplemental Oxygen and improving PAO2 (Alveolar partial pressure of oxygen), we improve "Ventilation"?


Can someone clear me on this concept, please?
 
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cbrons

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Because you depress your central respiratory drive (a relatively low level of well compensated hypoxemia is a strong chemical stimulus for maintaining minute ventilation).

Higher arterial O2 also decreases hemoglobin's affinity for CO2 (lookup the Haldane effect).

And like you mentioned, you also lose compensatory hypoxic vasoconstriction in the pulmonary circulation. This increases perfusion of poorly ventilated regions of the lung (V/Q mismatch).

This is why in the hospital, COPDers are kept at an SpO2 of 88-92%.

Today we have one guy who is an end-stage noncomplaint COPDer. Guy walks around with low sats all the time. Of course the nurses will not accept any brief dips into the mid-low 80s on LFNC despite multiple reassurances that he is quite used to it.

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Hernandez

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Because you depress your central respiratory drive (a relatively low level of well compensated hypoxemia is a strong chemical stimulus for maintaining minute ventilation).

Higher arterial O2 also decreases hemoglobin's affinity for CO2 (lookup the Haldane effect).

And like you mentioned, you also lose compensatory hypoxic vasoconstriction in the pulmonary circulation. This increases perfusion of poorly ventilated regions of the lung (V/Q mismatch).

This is why in the hospital, COPDers are kept at an SpO2 of 88-92%.

Today we have one guy who is an end-stage noncomplaint COPDer. Guy walks around with low sats all the time. Of course the nurses will not accept any brief dips into the mid-low 80s on LFNC despite multiple reassurances that he is quite used to it.

Sent from my SM-N910P using SDN mobile
#1 and #2 has nothing to do with changes in alveolar deadspace.

Changes in microvascular tension causing increased perfusion to under ventilated areas increase the relative deadspace.
 

lymphocyte

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Because you depress your central respiratory drive (a relatively low level of well compensated hypoxemia is a strong chemical stimulus for maintaining minute ventilation).

Higher arterial O2 also decreases hemoglobin's affinity for CO2 (lookup the Haldane effect).

And like you mentioned, you also lose compensatory hypoxic vasoconstriction in the pulmonary circulation. This increases perfusion of poorly ventilated regions of the lung (V/Q mismatch).
1. Increased perfusion to poorly ventilated regions of the lung actually creates a shunt-type problem. So it can't be the whole story.
2. What's key: when you reverse hypoxic vasoconstriction, you create dead space in other parts of the lung. Why? Because all that blood is being diverted from relatively well-ventilated alveoli to diseased lung.
3. In the COPD 50/50 Club, the dead-space effect tends to predominate, but you actually have both kinds of V/Q mismatch to varying extent.
4. Yes about the Haldane effect.
5. I wish the central respiratory drive myth would just die. The vast majority of evidence is against it.

Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012;16(5):323.
 
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