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Firstly, I apologize a bit for the tone of my first posts. Just trying to play the Devil's advocate and I probably got a little carried away. I do want to make it clear that I was not trying to advocate any medical treatment, just presenting an opposing point of view stating that the Dr.s at these clinics are not out of line for running 2L NC.
Dr. 'zilla,
I do have a couple questions.
Firstly, about the COPD patient. I understand the myth of suppression of hypoxic ventilatory drive with O2 administration to the chronically hypercapnic patient, and that this interpretation is largely incorrect. However, it was my impression that it was only the above mechanism that was debunked, but not the presence of the possibility of exacerbating hypercapnia in these patients through multiple mechanisms, including an increase in dead space ventilation (due to loss of compensatory pulmonary vasoconstriction), the Haldane effect, as well as a small decrease in minute ventilation. All of these can take effect within the first hour, which is within the time frame offered in the cases above.
I also understand that most of these patients are at greater risk for hypoxemia than hypercapnia and previously many patients who needed O2 were not getting it due to the traditional teaching that they would stop breathing. However, I interpreted the question as one in which the patient was having increasing chest pain in an acute MI setting, was satting well to begin with, and was not having trouble breathing.
My second question related to the possibility of a deleterious effect of high-flow O2 on cardiovascular function. I know it has been looked at in a few human and animal studies, that high flow O2 can cause coronary vasoconstriction, potentially worsening infarction. Not any real solid evidence that links mechanism with poor outcomes. Just wondering on your opinion?
Thank you
SR
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