New look at hypercapnia
Question:
Thankyou, thankyou and thankyou again Chris, Hacky, Colin, Scooby, Michael and Dr. Mayo. A standing ovation is definitely in order. Chilla
Response:
– Hide quoted text — Show quoted text – Hi, In my problems with asthma an important part was played by the fear of suffocation. Then I cottoned onto Buteyko and found that reduced breathing and acting anti-intuitively brought relief and the slow but steady disappearance of classical symptoms such as attacks, objective shortness of breath and wheeze. Now a new publication has gone even further and proposed that hypercapnia, i. e. above normal carbon dioxide levels in the body may be curative, whereas we all thought that hypercapnia could be the cause of death in status asthmaticus. See: Lancet 1999 Oct 9;354(9186):1283-6 Carbon dioxide and the critically ill–too little of a good thing? Laffey JG, Kavanagh BP [Medline record in process] Permissive hypercapnia (acceptance of raised concentrations of carbon dioxide in mechanically ventilated patients) may be associated with increased survival as a result of less ventilator-associated lung injury. Conversely, hypocapnia is associated with many acute illnesses (eg, asthma, systemic inflammatory response syndrome, pulmonary oedema), and is thought to reflect underlying hyperventilation. Accumulating clinical and basic scientific evidence points to an active role for carbon dioxide in organ injury, in which raised concentrations of carbon dioxide are protective, and low concentrations are injurious. We hypothesise that therapeutic hypercapnia might be tested in severely ill patients to see whether supplemental carbon dioxide could reduce the adverse effects of hypocapnia and promote the beneficial effects of hypercapnia. Such an approach could also expand our understanding of the pathogenesis of disorders in which hypocapnia is a constitutive element. The authors write: "Although hypocapnia [low carbon dioxide] has been assumed to occur as a consequence of many disorders (eg. asthma, systemic inflammatory response syndrome, high-altitutde pulmonary oedema, and ventilator induced lung injury), we propose that hypocapnic alkalosis may be pathogenic. We propose a potentially novel strategy – therapeutic hypercapnia – whereby hypercapnia could be intentionally produced in critically ill patients to provide organ protection." "Acute injury can be caused by hyperventilation: hyperventilation causes hypocapnic alkalosis…….hypocapnia and hyperventilation may be independent causes of bronchopulmonary dysplasia" "Long-term neurological sequalae from exposure to extreme altitude are associated not with exposure to low oxygen concentration, but rather with the generations of extremely low PaCO2 [low carbon dioxide]" In view of this paper Buteyko’s theory that constriction of the airways in asthma is a protective strategy of the body to stop undue loss of carbon dioxide seems all the more plausible, more especially because the attitudes on this ng. If the orthodox interpretation of constriction as the primary target for therapy were correct, there would surely be a different atmosphere without so many detractors and doubters on the one hand and so many almost militant defenders of orthodoxy on the other hand. The Lancet article is of course mainly concerned with emergency medicine, but the insights would seem to apply to an even greater extent for the everyday situation of an asthmatic. It is interesting to note that one paper (Am. Rev. Respir. Dis 1974; 110: 25-33) cited draws attention to a lack of carbon dioxide in an asthmatic as causing increase in airway resistance. Even earlier papers are cited in it dealing with the increase in resistance due to hyperventilation. If it had not been due to the dominating thought of possible suffocation in asthma, a breath therapy based on reduction of the respiratory rate might well have been proposed and used thirty years ago. Couldn’t advocates of orthodox asthma treatment say openly what their views on hypocapnia in asthma are? Cheers, peace and good health, Richard Friedel
Permissive hypercapnea is a method of artificial mechanical ventilation designed to reduce the effects of either hyperinflation or high machine generated pressures (the debate continues) on the lung. This effect (the volume/pressure) causes further damage to the lungs. I agree with the previous responders that this has nothing to do with asthma, and is a method for mechanical ventilation in the ICU, which requires strong sedation and chemical paralysis. P. Mayo, MD, FCCP
Response:
Hi, In my problems with asthma an important part was played by the fear of suffocation. Then I cottoned onto Buteyko and found that reduced breathing and acting anti-intuitively brought relief and the slow but steady disappearance of classical symptoms such as attacks, objective shortness of breath and wheeze.
These symptoms sound more like hyperventilation syndrome than asthma. P.S. I take it that you did not read the article you posted. It was about mechanically ventilated patients – not people breathing on their own. It appears that this mistake was made as a result of your habit of picking articles for a supposed support of a certain position. A compounding factor is the fact that you know nothing about asthma – which causes you to have a difficult time in determining whether an article is or is not relevant. "Usenet is like a herd of performing elephants with diarrhea — massive, diffucult to redirect, awe-inspiring, entertaining, and a source of mind boggling amounts of excrement when you least expect it." Gene Spafford 1992
Response:
Without even having wasted my time reading this article, i will shed a little light on the medical use of "permissive hypercapnia". Essentially many old folks who suffer from COPD and asthma may well be breathing on a hypoxic drive. This drive is not a primary drive, but rather a drive that develops secondary to chronic elevated CO2 levels which in turn is secondary to inneffective ventilation. This inneffective ventilation is casued from several factors, destruction of lung tissue and alveolar surfaces and walls, loss of elasticity of the chest wall and muscles themselves, and in some cases obesity plays a role. Note that a LOW CO2 IS NOT A FACTOR. When attempting to ventilate these patient successfully we sometimes will see one who has elevated ventilating pressures despite all that we are doing. This elevation can lead to further lung damage by, and of itself. Thus, in this case, the trend has been in allowing smaller tdal volumes and lower rates to allow a reduction in intrathoracic pressures. This reduction in volume and rate then also equals a decreased minute ventilation (the amount of gas moved in a minute’s time). Another use is with weaning attempts. A patient maintained at a normal CO2 level will not readily wean from the ventilator if they are physiologically used to an elevated CO2 level. The trick her is then to allow the patient to seek his or her own "norm" and thereby "force" the brain to once again send the signals to breathe. I have seen many patients that were so overventilated for "their" physiological condition, that I put them in CPAP mode and watched them just sit there without breathing for a couple minutes as their CO2 rose….and then voila’….they once again began breathing and went on to being extubated and doing well. permissive hypercapnia can only be accomplished under controlled ventilation, and has NOTHING to do with asthmatics. As I have stated many time before, if a lack of CO2 were the problem, then i would NEVER need to place any of my patients on a vent, nor would any asthmatic ever suffer respiratory failure…..as their attack progressed, and ventilation failed, their CO2 would rise thereby "curing" the problem….but alas it does not, will not, nor could it ever be so. Go back and try to learn a little about the damn disease before you embarass yourself further. Scooby RCP, EMT-P Perinatal-Pediatric Respiratory Specialist This mail is a natural product. The slight variations in spelling and grammar enhance its individual character and beauty and in no way are to be considered flaws or defects.
Response:
Now a new publication has gone even further and proposed that hypercapnia See: Lancet 1999 Oct 9;354(9186):1283-6 Carbon dioxide and the critically ill–too little of a good thing?
Decided to check your reference. http://www.thelancet.com/newlancet/sub/issues/vol354no9186/menu_NOD1…. The Lancet Interactive The Journal Editorial and reviews Review Seminar: Influenza Hypothesis: Carbon dioxide and the critically ill–too little of a good thing? Viewpoint: Continuum of palliative care: lessons from caring for children infected with HIV-1 Viewpoint: Decline in child health in rural Papua New Guinea When you were writing your proof, why did you leave out the point that this paper is a "Hypothesis"? hypothesis: a tentative assumption made in order to draw out and test its logical or empirical consequences You said the authors said, "We hypothesise that therapeutic hypercapnia might be tested". So you are aware that you’re attempting to prove a point with an untested assumption. Correct logical form: This fact, proves this theory. Incorrect: This assumption, proves this theory. Care to post the entire article?
Response:
In my problems with asthma an important part was played by the fear of suffocation. Then I cottoned onto Buteyko and found that reduced breathing and acting anti-intuitively brought relief and the slow but steady disappearance of classical symptoms such as attacks, objective shortness of breath and wheeze. Now a new publication has gone even further and proposed that hypercapnia, i. e. above normal carbon dioxide levels in the body may be curative, whereas we all thought that hypercapnia could be the cause of death in status asthmaticus. See: Lancet 1999 Oct 9;354(9186):1283-6
Well, he is specifically looking at patients on ventilators, and the relationship between permitting higher CO2 levels and ventilator-induced injury. This is a very specific, and somewhat uncommon, medical treatment. His more general focus is the critically ill, not the chronic asthmatic. Although he proposes the possibility of this being related to asthma, he presents absolutely no data to substantiate it having a role in chronic asthma. And, death in asthma results from too little O2, not too much CO2. In view of this paper Buteyko’s theory that constriction of the airways in asthma is a protective strategy of the body to stop undue loss of carbon dioxide seems all the more plausible,
No it doesn’t. First, the authors were speculating WAY beyond their data set; second, they proposed that work needed to be done, not that they already knew the answer. Chris Owens
Response:
Hi, In my problems with asthma an important part was played by the fear of suffocation. Then I cottoned onto Buteyko and found that reduced breathing and acting anti-intuitively brought relief and the slow but steady disappearance of classical symptoms such as attacks, objective shortness of breath and wheeze. Now a new publication has gone even further and proposed that hypercapnia, i. e. above normal carbon dioxide levels in the body may be curative, whereas we all thought that hypercapnia could be the cause of death in status asthmaticus. See: Lancet 1999 Oct 9;354(9186):1283-6 Carbon dioxide and the critically ill–too little of a good thing? Laffey JG, Kavanagh BP [Medline record in process] Permissive hypercapnia (acceptance of raised concentrations of carbon dioxide in mechanically ventilated patients) may be associated with increased survival as a result of less ventilator-associated lung injury. Conversely, hypocapnia is associated with many acute illnesses (eg, asthma, systemic inflammatory response syndrome, pulmonary oedema), and is thought to reflect underlying hyperventilation. Accumulating clinical and basic scientific evidence points to an active role for carbon dioxide in organ injury, in which raised concentrations of carbon dioxide are protective, and low concentrations are injurious. We hypothesise that therapeutic hypercapnia might be tested in severely ill patients to see whether supplemental carbon dioxide could reduce the adverse effects of hypocapnia and promote the beneficial effects of hypercapnia. Such an approach could also expand our understanding of the pathogenesis of disorders in which hypocapnia is a constitutive element. The authors write: "Although hypocapnia [low carbon dioxide] has been assumed to occur as a consequence of many disorders (eg. asthma, systemic inflammatory response syndrome, high-altitutde pulmonary oedema, and ventilator induced lung injury), we propose that hypocapnic alkalosis may be pathogenic. We propose a potentially novel strategy – therapeutic hypercapnia – whereby hypercapnia could be intentionally produced in critically ill patients to provide organ protection." "Acute injury can be caused by hyperventilation: hyperventilation causes hypocapnic alkalosis…….hypocapnia and hyperventilation may be independent causes of bronchopulmonary dysplasia" "Long-term neurological sequalae from exposure to extreme altitude are associated not with exposure to low oxygen concentration, but rather with the generations of extremely low PaCO2 [low carbon dioxide]" In view of this paper Buteyko’s theory that constriction of the airways in asthma is a protective strategy of the body to stop undue loss of carbon dioxide seems all the more plausible, more especially because the attitudes on this ng. If the orthodox interpretation of constriction as the primary target for therapy were correct, there would surely be a different atmosphere without so many detractors and doubters on the one hand and so many almost militant defenders of orthodoxy on the other hand. The Lancet article is of course mainly concerned with emergency medicine, but the insights would seem to apply to an even greater extent for the everyday situation of an asthmatic. It is interesting to note that one paper (Am. Rev. Respir. Dis 1974; 110: 25-33) cited draws attention to a lack of carbon dioxide in an asthmatic as causing increase in airway resistance. Even earlier papers are cited in it dealing with the increase in resistance due to hyperventilation. If it had not been due to the dominating thought of possible suffocation in asthma, a breath therapy based on reduction of the respiratory rate might well have been proposed and used thirty years ago. Couldn’t advocates of orthodox asthma treatment say openly what their views on hypocapnia in asthma are? Cheers, peace and good health, Richard Friedel
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