question about volatile anesthetics

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ngozi

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Just a quick question... "Volatile anesthetics permit the use of high inspired concentrations of oxygen." Why?
Thanks!

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Just a quick question... "Volatile anesthetics permit the use of high inspired concentrations of oxygen." Why?
Thanks!

Hard to know what you're asking without the context, or at what level to frame the answer since it's not clear if you're a student, intern, SRNA, resident, etc.

I'd guess that statement about volatile anesthetics was probably made in comparison to nitrous oxide. Volatile anesthetics are called potent anesthetics because their MAC is very low - just a few percent. This means you can deliver an anesthetic concentration of gas and still give 90%+ oxygen.

Nitrous, with a MAC of 105%, needs to be given in 10s of % to really contribute an effect. This limits the % oxygen you can use - if you're giving 50% nitrous, the best you can do is 50% oxygen.
 
Resident. Thanks, pgg!

The context was intraop care for COPD patients.
 
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Better question - is it a good idea to give bad COPD'ers high FIO2's?

Alright - I see your question and raise you two... Why would it be a bad idea to give someone with "bad COPD" (and btw what's your definition of this - for example are you talking about PFTs, baseline SpO2, home O2, whether they retain or not) a high FiO2 intraop?
Along this line - do you suggest that someone normally on home oxygen who is a known CO2 retainer shouldn't be preoxygenated with 100% O2?
 
Volatile anesthetics achieve an adequate depth of anesthesia at low concentrations. For isoflurane, this is around 1%. For desflurane, it's closer to 6%. That leaves up to 94% of the remaining gas flow reaching the patient to be anything you want, including all oxygen. In this way, volatiles "permit" you to deliver lots of oxygen, and still deliver adequate anesthesia. In contrast, nitrous oxide achieves adequate anesthesia at very high concentrations (the equivalent depth as that described above for iso or des would require hyperbaric, or greater than 100%, nitrous). Xenon requires concentrations of between 30 and 50%. Using either of these would not permit the use of high concentrations of oxygen because the anesthetic itself requires such high concentrations.
 
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Better question - is it a good idea to give bad COPD'ers high FIO2's?

Usually, I wouldn't care too much about their respiratory drive being depressed due to chronic CO2 retention if I'm going to breath for them... Unless it's a super quick procedure.
 
Xenon requires concentrations of between 30 and 50%. Using either of these would not permit the use of high concentrations of oxygen because the anesthetic itself requires such high concentrations.

interesting! I had not heard about Xenon as an anesthetic... Just downloaded a paper about it and will be reading more. Thanks!
 
Alright - I see your question and raise you two... Why would it be a bad idea to give someone with "bad COPD" (and btw what's your definition of this - for example are you talking about PFTs, baseline SpO2, home O2, whether they retain or not) a high FiO2 intraop?
Along this line - do you suggest that someone normally on home oxygen who is a known CO2 retainer shouldn't be preoxygenated with 100% O2?

I can only (try to) answer the first question, as I've never been the primary anesthetist for a "bad COPDer". I would use the parameters of baseline SpO2 and home O2 use as my determinants of "bad" COPD.

My understanding is, if you give "bad COPDers" higher FiO2s (higher than what? I dunno; maybe higher than "necessary," whatever that is) you blow their hypoxic pulmonary vasoconstriction, which is making both shunty and dead-spacey alveoli into alveoli closer to a V/Q = 1. Giving high FiO2's inhibits their HPV, which makes those well-compensated shunty alveoli into seriously-well-perfused but poorly-ventilated (actually V/Q = 0) alveoli, which then diverts blood from those well-compensated dead-space alveoli and turns them into well-ventilated-but-poorly-perfused (V/Q = infinity) alveoli. The effect is, both deadspace and shunt are increased so both your ventilation and oxygenation are hosed.

Well, that said, I might as well shoot for question #2. Preoxygenating with 100% may well cause acute hypercapnia secondary to increased deadspace, and I suppose it could cause acute hypoxemia secondary to increased shunt, but with an ETT, ventilator, and 15L fresh-gas-flows you're more than poised to do something about it :)
 
Usually, I wouldn't care too much about their respiratory drive being depressed due to chronic CO2 retention if I'm going to breath for them... Unless it's a super quick procedure.

its a fine line...

Rather than re-type this, I will just post a quote from Tenesma regarding the MYTH of the Hypoxic Drive Theory in COPD patients.

okay so here is the literature:

The Control of Breathing in Clinical Practice, Caruana-Montaldo, et al, Chest 117/1 Jan., 2000, pages 205-225

Critical Care Medicine September 1997 Editorial “Debunking Myths of Chronic Obstructive Lung Disease”, by Dr. John Hoyt

I quote Dr. Hoyt:

"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, 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.

The basic issue in this story is oxygen. The human body, particularly key organs such as the heart and brain, are not at all forgiving of insufficient supplies of oxygen. Thus, medical decision-making-based on the mythology that oxygen causes apnea and cardiorespiratory arrest in patients with chronic obstructive lung disease by turning off the oxygen respiratory drive-might take the path of withholding or delivering inadequate doses of oxygen to meet the metabolic needs of the patient in respiratory failure. This mistake is generally fatal for the patient, and a treatment tragedy for the misinformed physician.

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.

Most mythological stories are based on some observation, which may be a correct observation but an incorrect interpretation of the events. It is true that the administration of oxygen to a patient with exacerbated chronic obstructive lung disease and acute respiratory failure may lead to an increased CO2. It is true that the hypercarbia may become severe and be associated with cardiorespiratory arrest. The problem is with interpreting the cause of this event. As Dr. Crossley and colleagues [1] indicate, the hypercarbia is caused by release of hypoxic pulmonary vasoconstriction with increased deadspace, and not by down-regulating the hypoxic drive. Thus, one should not fear apnea and cardiorespiratory arrest when giving oxygen to a patient with an exacerbated chronic obstructive lung disease and respiratory failure. Instead, one should be prepared to help the patient eliminate CO2 when deadspace increases. Providing assistance with the elimination of CO2 has been around since the beginning of critical care medicine. It is called mechanical ventilation.

A clear and scientific interpretation of the response to oxygen in a patient with exacerbated chronic obstructive lung disease and acute respiratory failure has always been important, but currently, such an interpretation is essential. As health care transforms itself, a variety of individuals, organizations, and healthcare facilities are attempting to translate medical information into critical pathways. These critical pathways are being used by a wide range of professionals to guide the treatment of patients. The critical pathways must be accurate, and based on the best medical science to protect the life of the patient. A critical pathway for a patient with exacerbated chronic obstructive lung disease and acute respiratory failure based on a down-regulation of hypoxic drive might be constructed to minimize the dose of oxygen to keep the patient breathing spontaneously. However, a critical pathway based on an increase in deadspace and difficulty eliminating CO2 should be constructed to help the patient eliminate CO2 with mechanical ventilation, while meeting the patient's uncompromising physiologic needs for oxygen.

Dr. Crossley and colleagues [1] cite a textbook on respiratory physiology by the British author J. F. Nunn [2]. This book [2], along with the monographs edited by John West on respiratory function and pathophysiology [3,4], has been required reading for anesthesia residents for many years. The books should be read by all physicians caring for critically ill patients. These textbooks create a clear picture of the physiologic changes in lung function that are associated with chronic obstructive lung disease. They allow for the debunking of medical mythology and the appropriate creation of treatment protocols for the management of respiratory failure."

Moral of the story: Harrison's is right and your ER/IM docs telling you this crap are wrong



A good link with more info and an explanation of the physiology of oxygen administration to COPD patients in extremis. This is by an RT and is a little evangelical, but still a good quick overview of the physiology. Enjoy


- pod
 
Since pulmonary hypertension (and bullous emphysema) CAN be complications of COPD, why use N2O at all? Most of the time, I never see PFTs, or the like, on most COPD patients presenting for surgery, but hey..
 
i love how the article says the things you think will happen may happen but not for the reason you think

moral, it can still be dangerous to administer high FiO2 to patients with severe COPD without mechanical ventilation
 
No, the moral is, do not withhold oxygen from COPD patients due to some false fear of making them apneic.

Be aware that an exceedingly small subset of patients may increase their CO2 enough to cause cardio-respiratory depression and require mechanical ventilatory support, but these individuals were working so hard to maintain their razor thin margin of acceptable pO2, prior to your placing oxygen on them, that they almost certainly would have eventually required ventilatory support anyway. I would be willing to bet that these are the same guys that look so obviously bad that when you see them coming through the ER door you reflexively stat page RT to get setup before you even go over to see the patient.

It isn't just semantics on causation of respiratory arrest. The old myth would have you believe that giving oxygen to a large number of COPD patients will cause a large number of respiratory arrests. This simply isn't true. What will happen is that a very small number of the very worst off patients will have a decrease in their work of breathing but MAY go overboard with their own "intrinsic permissive hypercapnia," and require mechanical support.

In our small part of the world maybe it is mostly semantics because we are so facile with mechanical ventilation and most of our patients are not in extremis and are going to get mechanical ventilation for other reasons. However, go into other areas of the hospital and you will quickly get into heated arguments with nurses, paramedics, other docs etc who are convinced that you are killing a patient by providing high FiO2 to a hypoxic COPDer.

- pod
 
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