Just a quick question... "Volatile anesthetics permit the use of high inspired concentrations of oxygen." Why?
Thanks!
Thanks!
Just a quick question... "Volatile anesthetics permit the use of high inspired concentrations of oxygen." Why?
Thanks!
Resident. Thanks, pgg!
The context was intraop care for COPD patients.
Better question - is it a good idea to give bad COPD'ers high FIO2's?
Better question - is it a good idea to give bad COPD'ers high FIO2's?
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.
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.
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?
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...
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
Rather than re-type this, I will just post a quote from Tenesma regarding the MYTH of the Hypoxic Drive Theory in COPD patients.
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