COPD and blood pH

[norealname]

Hey guys,
Just struggling with some respiratory mechanisms here and wanted to check if I'm thinking correctly here. I'm just trying to understand how blood pH changes in COPD patients as the disease progresses. Let me know if there's anything wrong with my reasoning.

In the initial stages of COPD, you have low pO2 and high pCO2. the high pCO2 causes chronic respiratory acidosis, with compensation from the kidney. Also, the pO2 here is the main regulator of breathing rate.

In the end-stages of the disease when the sx abruptly exacerbate, pO2 decreases enough to cause excessive stimulation of the carotid bodies --> hyperventilation. The hyperventilation somewhat increases the low pO2, but not nearly enough to return pO2 to normal levels. Also, hyperventilation causes the high CO2 to be blown out rapidly, causing decreased pCO2 --> acute respiratory alkalosis. At this stage, the patient will definitely be hospitalized and be taken care of.

I just want to make sure that when COPD sx exacerbate, an acute uncompensated respiratory alkalosis develops. If i understand this properly, i think i understand pulmonary quite well 🙂

Cheers

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[jdh71]

Hey guys,
Just struggling with some respiratory mechanisms here and wanted to check if I'm thinking correctly here. I'm just trying to understand how blood pH changes in COPD patients as the disease progresses. Let me know if there's anything wrong with my reasoning.

In the initial stages of COPD, you have low pO2 and high pCO2. the high pCO2 causes chronic respiratory acidosis, with compensation from the kidney. Also, the pO2 here is the main regulator of breathing rate.

In the end-stages of the disease when the sx abruptly exacerbate, pO2 decreases enough to cause excessive stimulation of the carotid bodies --> hyperventilation. The hyperventilation somewhat increases the low pO2, but not nearly enough to return pO2 to normal levels. Also, hyperventilation causes the high CO2 to be blown out rapidly, causing decreased pCO2 --> acute respiratory alkalosis. At this stage, the patient will definitely be hospitalized and be taken care of.

I just want to make sure that when COPD sx exacerbate, an acute uncompensated respiratory alkalosis develops. If i understand this properly, i think i understand pulmonary quite well 🙂

Cheers

Chronic lungers will not be able to hyperventilate themselves to a resp. alkalosis. Ventilation is the problem with COPD, for whatever increase in minute ventilation they get from hyperventilation, the volumes they are moving are not going to large enough to make a big difference in pH by itself, especially end stage. In fact, these end stage guys, if they find themselves in a position where they are hyperventilating because of low O2 will also having increasing pCO2 as a result of the exacerbation causing the low O2 in the first place, and will therefore be hypercapnic and acidotic.

EDIT: Your thought process is right concerning asthma though.

 

[IHeartNerds]

A side note: You mention that "pO2 here is the main regulator of breathing rate". Although this is true, this is NOT why you should avoid putting COPDers on 100% O2 when they walk in the door. Try it -- they won't stop breathing. But, their ABG may worsen, since oxygen disregulates local lung hypoxic vasoconstriction in diseased lung units, thereby causing V/Q mismatch.

My mind was blown when a pulm fellow dropped this knowledge on me. I never did believe the whole "respiratory drive" thing.

If the rest of the world already knew, my apologies.

 

[Fuzuli]

A side note: You mention that "pO2 here is the main regulator of breathing rate". Although this is true, this is NOT why you should avoid putting COPDers on 100% O2 when they walk in the door. Try it -- they won't stop breathing. But, their ABG may worsen, since oxygen disregulates local lung hypoxic vasoconstriction in diseased lung units, thereby causing V/Q mismatch.

My mind was blown when a pulm fellow dropped this knowledge on me. I never did believe the whole "respiratory drive" thing.

If the rest of the world already knew, my apologies.

In patients with chronic respiratory acidosis (like COPD), central chemoreceptors that monitor CSF pH (and therefore CO2) levels become insensitive. Therefore, respiratory drive becomes dependent on peripheral chemoreceptors which sense hypoxemia (especially when pO2 < 60 mm Hg). If such a patient were suddenly given %100 FiO2, their peripheral chemoreceptors would be inhibited, which in turn would inhibit the respiratory drive.
Irregardless, oxygen typically (not pathologically) causes vasoconstriction in the pulmonary vascular bed (contrary to other organs). This is why people living in high altitudes can have cor pulmonale.

 

[jdh71]

In patients with chronic respiratory acidosis (like COPD), central chemoreceptors that monitor CSF pH (and therefore CO2) levels become insensitive. Therefore, respiratory drive becomes dependent on peripheral chemoreceptors which sense hypoxemia (especially when pO2 < 60 mm Hg). If such a patient were suddenly given %100 FiO2, their peripheral chemoreceptors would be inhibited, which in turn would inhibit the respiratory drive.
Irregardless, oxygen typically (not pathologically) causes vasoconstriction in the pulmonary vascular bed (contrary to other organs). This is why people living in high altitudes can have cor pulmonale.

I don't think "irregardless" is a word, but you are wrong . . . the "respiratory drive" explanation was disregarded as far back as the 1970's.

Giving a COPDer oxygen creates a shunt as was mentioned before because the increased O2 dialtes blood vessels around poorly ventilated alveoli, and this is why you get a drop pulmonary function.

Check out:

Crossley et al. "Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO sub 2 in intubated patients with chronic obstructive pulmonary disease". Critical Care Medicine. Issue: Volume 25(9), September 1997, pp 1522-1526

And it's corresponding editorial:

"Debunking myths of chronic obstructive lung disease" by Hoyt

*snip*

" . . . It is not clear where this fallacious information comes from, but it seems to enter the medical information database at an early age, at the medical student or resident level, almost like a computer virus corrupting the appropriate function of the equipment. In addition, this myth becomes very difficult to extinguish during the career of the physician, even with clear factual information of long standing. The danger here is that this medical mythology will inappropriately influence treatment decisions in patients . . .

*snip*

The article by Dr. Crossley and colleagues [1] in this issue of Critical Care Medicine is an elegant project capable of debunking the mythological relationship between oxygen and apnea in patients with chronic obstructive lung disease. The authors [1] nicely demonstrate that a substantial dose of oxygen in intubated but spontaneously breathing patients with chronic obstructive lung disease has no effect on PaCO2, deadspace, and respiratory drive. The discussion section of the article [1] is superb. The authors [1] assembled facts from the respiratory physiology literature to demonstrate that oxygen releases hypoxic pulmonary vasoconstriction in chronic obstructive lung disease patients. This release of hypoxic pulmonary vasoconstriction leads to a further mismatch of ventilation and perfusion in chronic obstructive lung disease patients, with a subsequent increase in deadspace. In this situation, minute volume largely stays the same or may increase slightly to eliminate CO2, but the elimination of CO2 has by now become more difficult, as the deadspace has increased . . .

 

[dbth77]

In patients with chronic respiratory acidosis (like COPD), central chemoreceptors that monitor CSF pH (and therefore CO2) levels become insensitive. Therefore, respiratory drive becomes dependent on peripheral chemoreceptors which sense hypoxemia (especially when pO2 < 60 mm Hg). If such a patient were suddenly given %100 FiO2, their peripheral chemoreceptors would be inhibited, which in turn would inhibit the respiratory drive.
Irregardless, oxygen typically (not pathologically) causes vasoconstriction in the pulmonary vascular bed (contrary to other organs). This is why people living in high altitudes can have cor pulmonale.

you managed to get everything wrong in one post

 

[WashMe]

I don't think "irregardless" is a word, but you are wrong . . . the "respiratory drive" explanation was disregarded as far back as the 1970's.

Giving a COPDer oxygen creates a shunt as was mentioned before because the increased O2 dialtes blood vessels around poorly ventilated alveoli, and this is why you get a drop pulmonary function.

Check out:

Crossley et al. "Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO sub 2 in intubated patients with chronic obstructive pulmonary disease". Critical Care Medicine. Issue: Volume 25(9), September 1997, pp 1522-1526

And it's corresponding editorial:

"Debunking myths of chronic obstructive lung disease" by Hoyt

Irregardless is a word (albeit archaic), it means regardless.

 

[jdh71]

Irregardless is a word (albeit archaic), it means regardless.

points to you

"Irregardless is considered nonstandard because of the two negative elements ir- and -less. It was probably formed on the analogy of such words as irrespective, irrelevant, and irreparable. Those who use it, including on occasion educated speakers, may do so from a desire to add emphasis. Irregardless first appeared in the early 20th century and was perhaps popularized by its use in a comic radio program of the 1930s." (link)

 

[Fuzuli]

I don't think "irregardless" is a word, but you are wrong . . . the "respiratory drive" explanation was disregarded as far back as the 1970's.

Giving a COPDer oxygen creates a shunt as was mentioned before because the increased O2 dialtes blood vessels around poorly ventilated alveoli, and this is why you get a drop pulmonary function.

​

I stand corrected, thanks for the info.

you managed to get everything wrong in one post

The only part wrong about my post was saying that hypercapnia created by hyperoxemia is caused by inhibition of peripheral chemoreceptors. But as for the other stuff:

1) There is a thing called respiratory drive, which is mainly controlled by central chemoreceptors under physiologic conditions. There IS also a hypoxic drive. But it's not the reason why there's hyperoxemia associated hypercapnia.
2) Hypoxemia causes pulmonary vasoconstriction, which is an exception (hypoxemia causes vasodilation in other tissues). This is the reason why, like I've said, cor pulmonale can be seen in COPD patients (among with other factors). So the statement that "oxygen disregulates local lung hypoxic vasoconstriction in diseased lung units" is wrong; oxygen acts normally in COPD patients as well. Increase in PO2 causes vasodilation in pulmonary vascular bed, which in turn causes pulmonary shunts and create V/Q mismatch like jdh has said. This seems to be the main pathologic processes underlying the increase in PCO2 in patients who are given increased FiO2.

 

[norealname]

Thanks guys for the great explanations. I really appreciate your input. I also heard about the hypoxic drive being a somewhat outdated theory but wasn't too sure about it.

To Jdh71, why would my explanation fit asthma but not COPD? aren't they both obstructive lung disease and therefore should produce similar symptoms? I'm trying to understand the main difference between all these different obstructive diseases, but I'm still in my MS1, so I'm probably lacking knowledge of pathology to discern between these disorders.

 

[jdh71]

To Jdh71, why would my explanation fit asthma but not COPD? aren't they both obstructive lung disease and therefore should produce similar symptoms? I'm trying to understand the main difference between all these different obstructive diseases, but I'm still in my MS1, so I'm probably lacking knowledge of pathology to discern between these disorders.

The biggest difference between COPD and asthma is the compliance *and elastic recoil of the lung which is shot to hell in COPD, and is largely the the explanation for the pathophysiology of COPD at the anatomoical level. Compliance and elesatic recoil of the lung in asthma is relatively normal (caveat: you can get airway remodeling with lonstanding disease and the wrong medications). So . . . with an acute constriction of the airways as in asthma, you're able to overcome the resistance by recruiting accessory musscles and using mechanical force to overcome the resistance, and thereby maintain a minute ventilation with faster breathing, which can give you the respiratory alkalosis (and you cannot do this with COPD because using more force to exhale, only traps more air because of the floppy airways). So ABGs initially on an acute asthma will likely show an pH >7.4, with low normal pO2, and a low pCO2 . . . this changes as the acute disease progresses.

 

[norealname]

Great! I get it now. Thank you so much!