anciendaze
Senior Member
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At the outset I want to make it clear that this research is dealing with an acute medical crisis that can be life-threatening, not the kind of chronic illness most of us face. That said, I've run into a fair number of people on this forum who have had experiences like mine involving episodes of vasodilatory shock generally unexplained in standard medical practice, and often considered psychological. I've also seen this in close relatives, so I have reason to believe it is genetically transmitted.
A tentative diagnosis of one current problem I have is neurally-mediated hypotension, a form of dysautonomia. What we lack is a good biochemical mechanism which would explain the problem and make this treatable. I am explicitly disavowing the idea that this applies to everyone with "chronic fatigue syndrome".
With that in mind, consider this article on possible interventions in cases of vasodilatory shock with respiratory failure. While you are thinking about this, consider the fact that there are degrees of impairment and we now know there are patients with low vasopressin even when they are not in shock. Those of us who have visited emergency rooms might benefit from emergency medical personnel recognizing that patients with low vasopressin are different. It is also possible to have defects in vasopressin receptors.
Farther afield, could this difference in vasodilation be behind the less dramatic problems of vasodilation of venous return leading to low cardiac fill pressures seen by Systrom's group? Recall that those patients he studied developed dyspnea during exercise. This is not actual vasodilatory shock or respiratory failure, but it certainly sounds related.
A tentative diagnosis of one current problem I have is neurally-mediated hypotension, a form of dysautonomia. What we lack is a good biochemical mechanism which would explain the problem and make this treatable. I am explicitly disavowing the idea that this applies to everyone with "chronic fatigue syndrome".
With that in mind, consider this article on possible interventions in cases of vasodilatory shock with respiratory failure. While you are thinking about this, consider the fact that there are degrees of impairment and we now know there are patients with low vasopressin even when they are not in shock. Those of us who have visited emergency rooms might benefit from emergency medical personnel recognizing that patients with low vasopressin are different. It is also possible to have defects in vasopressin receptors.
Farther afield, could this difference in vasodilation be behind the less dramatic problems of vasodilation of venous return leading to low cardiac fill pressures seen by Systrom's group? Recall that those patients he studied developed dyspnea during exercise. This is not actual vasodilatory shock or respiratory failure, but it certainly sounds related.