Aug 4, 2016
57
21
Status
Medical Student
I understand COPD patients are mainly dependant on the PO2 levels for the respiratory drive and high flow oxygen supplementation can cause decreased stimulation of peripheral chemoreceptors leading to decreased ventilation.
I came across a statement saying high flow oxygen supplementation INCREASES the physiological dead space, leading to increased V/Q mismatch. How does this happen?
From my understanding, physiological dead space represents the alveoli that are ventilated but poorly perfused.
So if you increase oxygen supplementation, the pulmonary vessels should dilate, increasing the perfusion to these alveoli. Shouldn't that decrease V/Q mismatch?
Can someone explain, please?
 
  • Like
Reactions: lymphocyte
Jul 13, 2016
112
60
Status
Medical Student
There need to be intact vessels there for them to be able to dilate.

In COPD - for instance emphysema, unbalanced proteolytic activity damages the alveolar walls along with the vessels in those walls, so any increase in ventilation increases the V/Q ratio and thus increases dead space.
 

lymphocyte

2+ Year Member
Feb 27, 2015
2,068
3,387
COPD 50/50 Club
Status
Resident [Any Field]
I understand COPD patients are mainly dependant on the PO2 levels for the respiratory drive and high flow oxygen supplementation can cause decreased stimulation of peripheral chemoreceptors leading to decreased ventilation.
I came across a statement saying high flow oxygen supplementation INCREASES the physiological dead space, leading to increased V/Q mismatch. How does this happen?
From my understanding, physiological dead space represents the alveoli that are ventilated but poorly perfused.
So if you increase oxygen supplementation, the pulmonary vessels should dilate, increasing the perfusion to these alveoli. Shouldn't that decrease V/Q mismatch?
Can someone explain, please?
For whatever strange reason, this is my favorite topic in all of medicine, and one of my favourite myths to bust. There's no evidence to support the "respiratory drive" hypothesis, and there's lots of evidence to argue against it. Giving indiscriminate oxygen reverses hypoxic vasoconstriction and drives blood to poor parts of the lung. The Haldane effect plays an important role too. Here's an explanation (and some clinical correlates).

http://forums.studentdoctor.net/threads/copd-50-50-club.1209200/#post-17902945
 
Last edited:

Phloston

Lifetime Donor
7+ Year Member
Jan 17, 2012
3,660
1,353
Osaka, Japan
Oxygen isn't recommended unless the patient is hypoxaemic. There runs the risk of worsening hypercapnea in COPD with excess supplemental oxygen.

UpToDate:

"Supplemental oxygen is a critical component of acute therapy. Because of the risk of prompting worsened hypercapnia with excess supplemental oxygen, administration of supplemental oxygen should target a pulse oxygen saturation (SpO2) of 88 to 92 percent or an arterial oxygen tension (PaO2) of approximately 60 to 70 mmHg [1,32,33]."

"Patients with hypoxemia due to an exacerbation of COPD should receive supplemental oxygen. We suggest that supplemental oxygen be titrated to a target of 88 to 92 percent pulse oxygen saturation, rather than using high-flow, untitrated oxygen (Grade 2B). (See 'Oxygen therapy' above.)"
 
  • Like
Reactions: Paramyxovirus

lymphocyte

2+ Year Member
Feb 27, 2015
2,068
3,387
COPD 50/50 Club
Status
Resident [Any Field]
Oxygen isn't recommended unless the patient is hypoxaemic. There runs the risk of worsening hypercapnea in COPD with excess supplemental oxygen.

UpToDate:

"Supplemental oxygen is a critical component of acute therapy. Because of the risk of prompting worsened hypercapnia with excess supplemental oxygen, administration of supplemental oxygen should target a pulse oxygen saturation (SpO2) of 88 to 92 percent or an arterial oxygen tension (PaO2) of approximately 60 to 70 mmHg [1,32,33]."

"Patients with hypoxemia due to an exacerbation of COPD should receive supplemental oxygen. We suggest that supplemental oxygen be titrated to a target of 88 to 92 percent pulse oxygen saturation, rather than using high-flow, untitrated oxygen (Grade 2B). (See 'Oxygen therapy' above.)"
Just be careful. The key phrase is "critical component." Oxygen is always recommended if you suspect a patient is hypoxic (or is EMS or the nursing staff really supposed to wait for a blood gas to prove a patient is hypoxaemic?). Tissue hypoxia kills much faster than CO2 narcosis. Slap on a pulse ox, bolus up to a reasonable target, and chase CO2 with blood gas (and you really only need the VBG, because it's the trend you're after). Yes, oxygen is probably way overused and hyperoxia seems to be associated with harm in multiple contexts, but acute hypoxia is no bueno, so don't be stingy until you feel safe enough not to be (like when you're on the flat portion of the O2 dissociation curve).

Hafner S, Beloncle F, Koch A, Radermacher P, Asfar P. Hyperoxia in intensive care, emergency, and peri-operative medicine: Dr. Jekyll or Mr. Hyde? A 2015 update. Ann Intensive Care. 2015;5(1):42.

Stub D, Smith K, Bernard S, et al. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction. Circulation. 2015;131(24):2143-50.
 
Last edited:

Phloston

Lifetime Donor
7+ Year Member
Jan 17, 2012
3,660
1,353
Osaka, Japan
Yes, if you suspect hypoxaemia then oxygen is warranted, but if you confirm the patient's gases are normal, you don't need it.
 
OP
P
Aug 4, 2016
57
21
Status
Medical Student
Thank you PowerDan, lymphocyte and Phloston for your feedback! It's very helpful!

I understand how Haldane effect leads to hypercapnea when given high flow supplemental oxygen.
The other mechanism proposed has been "Reversal of hypoxic vasoconstriction" as lymphocyte explained and I read something similar on this article from Pubmed:

"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"?
 

lymphocyte

2+ Year Member
Feb 27, 2015
2,068
3,387
COPD 50/50 Club
Status
Resident [Any Field]
Thank you PowerDan, lymphocyte and Phloston for your feedback! It's very helpful!

I understand how Haldane effect leads to hypercapnea when given high flow supplemental oxygen.
The other mechanism proposed has been "Reversal of hypoxic vasoconstriction" as lymphocyte explained and I read something similar on this article from Pubmed:

"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"?
What's alveolar dead space? "The sum of the volumes of those alveoli which have little or no blood flowing through their adjacent pulmonary capillaries" (West).

So guess what happens when you reverse hypoxic vasoconstriction? You create dead space in other parts of the lung. What were nicely perfused, well-ventilated alveoli are now less perfused--blood is being diverted--and they are less able to exchange gas.

So you create shunt-type problems in relatively damaged lung, but you create dead space in relatively healthy lung. What "wins" in terms of V/Q? Very often dead space, hence the classic picture of hypercapnic hypoxaemia. Welcome to the COPD 50/50 club.
 
  • Like
Reactions: Paramyxovirus
OP
P
Aug 4, 2016
57
21
Status
Medical Student
What's alveolar dead space? "The sum of the volumes of those alveoli which have little or no blood flowing through their adjacent pulmonary capillaries" (West).

So guess what happens when you reverse hypoxic vasoconstriction? You create dead space in other parts of the lung. What were nicely perfused, well-ventilated alveoli are now less perfused--blood is being diverted--and they are less able to exchange gas.

So you create shunt-type problems in relatively damaged lung, but you create dead space in relatively healthy lung. What "wins" in terms of V/Q? Very often dead space, hence the classic picture of hypercapnic hypoxaemia. Welcome to the COPD 50/50 club.
I finally understood what I was looking for. Thank you very much lymphocyte for the wonderful explanation! :)
 
  • Like
Reactions: lymphocyte

nybgrus

5+ Year Member
Jul 20, 2010
376
150
Status
Resident [Any Field]
Sorry that I did not notice @Phloston 's comment here for so long. It has been some crazy busy times for me.

In any case, it seems relatively settled and I completely concur with the ultimate explanations.
 
  • Like
Reactions: Paramyxovirus