Hypoxic Drive

The hypoxic drive theory is a result of chronic CO2 retention not the other way around. The body has a high CO2, low oxygen, and low pH( whether it's due to respiratory or metabolic) drive to breath. As the body becomes accustomed to chronic CO2 retention the pH normalized(by bicarb increasing or compensating), low oxygen becomes the drive to breath. That is why chronic CO2 retainers are more sensitive to oxygen. hope this helps.

I understand that, its just I've started to realise that the idea of why people with chronic lung disease become CO2 retainers is disputed and what effect this actually has. For instance I found this in the critical care journal:

"There are examples of mythology that float about in the atmosphere of medical information that desperately need to be debunked because they influence the care of patients. One sample of medical mythology is the commonly told story that the administration of oxygen to a patient with chronic obstructive lung disease will shut down the patient's hypoxic respiratory drive and lead to apnea, cardiorespiratory arrest, and the subsequent death of the patient.

It is not clear where this fallacious information comes from, but it seems to enter the medical information database at an early age, 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."

Obvously I will still remain cautious administering O2 to patients with COPD, but still remain unconvinced about the mechanisms behind COPD causing CO2 retention.

A link to a similar article on this topic...

http://home.pacbell.net/whitnack/Why_the_Hypoxic_Drive_Theory_Sucks_Wind.htm.6306

The hypoxic drive theory is a result of chronic CO2 retention not the other way around. The body has a high CO2, low oxygen, and low pH( whether it's due to respiratory or metabolic) drive to breath. As the body becomes accustomed to chronic CO2 retention the pH normalized(by bicarb increasing or compensating), low oxygen becomes the drive to breath. That is why chronic CO2 retainers are more sensitive to oxygen. hope this helps.

The hypoxic drive theory is a result of chronic CO2 retention not the other way around. The body has a high CO2, low oxygen, and low pH( whether it's due to respiratory or metabolic) drive to breath. As the body becomes accustomed to chronic CO2 retention the pH normalized(by bicarb increasing or compensating), low oxygen becomes the drive to breath. That is why chronic CO2 retainers are more sensitive to oxygen. hope this helps.

I will agree that there is alot of controversy. I read the link and did a search and it seems that there is no disagreement on oxygen causing acidosis in chronic hypercapnic's. whether it's from the haldane effect or from desensitized chemoreceptors. oxygen causing acidosis is enough to be very careful with these patients. As for oxygen induced hypoventilation I'll leave it up to the reseachers to determine whether it's a myth or truth.

]This is my understanding on this...

]Every COPDer isn't a CO2 retainer. Look at a room air/2L ABG. If the pH is normal, and the CO2 high... that's a retainer.

]The pH is normal because the body is used to it.

]There are many drives to increase ventilation. Not to breathe... normal breathing is controlled by neurons in the medulla.

]The drive to increase ventilation is a response to correct something. Could be caused by hypoxemia, exercise, or emotional distress.

]The central chemoreceptors, also in the medulla, sense high CO2 and the carotid peripheral chemoreceptors sense low O2.

]The general rule is CO2 > 60 and O2

]Emphysema Pts have air-trapping because of lost compliance (condition) of the lung and alveoli loss. CO2 builds up and they get used to it. As the CO2 sensor is exposed to increased levels it gradually has a lowered response. This leaves the low O2 sensor as the only signal to increase ventilation.

]A chronically hypercapnic person is usually chronically hypoxemic too, and does use the peripheral chemoreceptor responses to breathe... so it is possible to take away the response by keeping the O2 level high, but personally I've never seen it send anyone into respiratory failure. This isn't to say it won't... I've just never seen it. I have found retainers on 4L simple masks* that were semi-conscious but easily arousable once the O2 is removed, and fine on 2L nasal cannula.

]The goal is to maintain the levels that they are used to... a little hypercapnic and a little hypoxic. That's why a sat of 90-92% is acceptable. Just watch the pH.

]And, of course, in an emergency, 100% O2.

]*Masks have to be 6L minimum to prevent CO2 build up.

]This is my understanding on this...

]Every COPDer isn't a CO2 retainer. Look at a room air/2L ABG. If the pH is normal, and the CO2 high... that's a retainer.

]The pH is normal because the body is used to it.

]There are many drives to increase ventilation. Not to breathe... normal breathing is controlled by neurons in the medulla.

]The drive to increase ventilation is a response to correct something. Could be caused by hypoxemia, exercise, or emotional distress.

]The central chemoreceptors, also in the medulla, sense high CO2 and the carotid peripheral chemoreceptors sense low O2.

]The general rule is CO2 > 60 and O2

]Emphysema Pts have air-trapping because of lost compliance (condition) of the lung and alveoli loss. CO2 builds up and they get used to it. As the CO2 sensor is exposed to increased levels it gradually has a lowered response. This leaves the low O2 sensor as the only signal to increase ventilation.

]A chronically hypercapnic person is usually chronically hypoxemic too, and does use the peripheral chemoreceptor responses to breathe... so it is possible to take away the response by keeping the O2 level high, but personally I've never seen it send anyone into respiratory failure. This isn't to say it won't... I've just never seen it. I have found retainers on 4L simple masks* that were semi-conscious but easily arousable once the O2 is removed, and fine on 2L nasal cannula.

]The goal is to maintain the levels that they are used to... a little hypercapnic and a little hypoxic. That's why a sat of 90-92% is acceptable. Just watch the pH.

]And, of course, in an emergency, 100% O2.

]*Masks have to be 6L minimum to prevent CO2 build up.

remember the old saying: treat the pt. i have seen, and i'm sure you have too, many copd-ers become clinically worse with high o2 delivery. i have come on shift to find my copd er in acute distress on 100% and about to code, only to change him over to 4lnc and watch him improve incredibily!

there's the whole oxyhemoglobin curve thing as well. copd-ers are on the right of that curve. they are able to release the o2 quickly off to the cell, but require constant o2 to do that. breathing is work, and respiratory distress brought on by infection or inflammation increases that workload. these pts NEED o2, that is not an issue, the issue seems to be- how much.

in my clinical experience, i have found this to be as individual as the pt. some of us would be ok with a sbp of 98, some of us would be dizzy. some of us could walk around with a hg of 9 and never know it... and again, some of us would be weak. i think the amount of 02 a copd-er requires depends on how much damage has been done to their aveoi over time and the pt's ability to adapt on a cellular level.

give the pt what they need. no more, no less. this seems to be the key with treating copd-ers.