Bubbletrubble
Contributor
@denisegg: Glad to hear that you're doing OK now.
While it's good that this incident has raised awareness regarding IPE and how little the medical community knows about the various factors in divers which can cause such a condition, I think the involvement of a potential hyperthyroid state should not be discounted. denisegg, what were your thyroid hormone levels at the time of most recent testing (post-incident)?
[Warning: the following section contains medical mumbo-jumbo]
When it comes to circulating thyroid hormone levels, it's very much a "Goldilocks' porridge just right" phenomenon -- bad things can happen when thyroid levels are outside normal limits (too low or too high). It's well-documented in the medical literature that thyroid hormone has significant effects on the heart and blood vessels (via molecular mechanisms involving nitric oxide and endothelium-derived hyperpolarizing factor). Interestingly, thyroid hormone administered in animal tests can cause relaxation of peripheral vessels, which would seem to work in an opposite direction on systemic blood pressure (BP), i.e., drive BP down. However, we know that, if anything, hyperthyroid patients have elevated BP. Cardiologists will tell you that hyperthyroid patients have increased preload to the heart and an elevated heart rate, too. The cause of this is complicated and likely related to shifting blood from the arterial to venous compartment of the vascular system, effectively off-loading the arterial system. At the same time, I believe that the BP sensors (juxtoglomerular cells located on the arterial side) of the renin-angiotensin-aldosterone system will "see" a decreased renal perfusion pressure and respond by trying to increase BP -- thus, creating/exacerbating the hypertensive state. (By the way, this is an oversimplification of how the kidneys control blood pressure and doesn't even mention ADH.) All of this leads to an increase in blood volume and an increase in venous return to the heart.
Perhaps before diving was even attempted, blood volume had expanded. This state, combined with systemic hypertension and the central fluid shifts that occur normally during diving, could have driven excessive fluid to the lungs, leading to IPE. Just reasoning out loud here based on my limited knowledge of medical and dive-specific physiology...
denisegg, I hope that you can hook up with a caring, competent endocrinologist soon. Thank you for sharing your story. Best wishes on your recovery.
While it's good that this incident has raised awareness regarding IPE and how little the medical community knows about the various factors in divers which can cause such a condition, I think the involvement of a potential hyperthyroid state should not be discounted. denisegg, what were your thyroid hormone levels at the time of most recent testing (post-incident)?
[Warning: the following section contains medical mumbo-jumbo]
When it comes to circulating thyroid hormone levels, it's very much a "Goldilocks' porridge just right" phenomenon -- bad things can happen when thyroid levels are outside normal limits (too low or too high). It's well-documented in the medical literature that thyroid hormone has significant effects on the heart and blood vessels (via molecular mechanisms involving nitric oxide and endothelium-derived hyperpolarizing factor). Interestingly, thyroid hormone administered in animal tests can cause relaxation of peripheral vessels, which would seem to work in an opposite direction on systemic blood pressure (BP), i.e., drive BP down. However, we know that, if anything, hyperthyroid patients have elevated BP. Cardiologists will tell you that hyperthyroid patients have increased preload to the heart and an elevated heart rate, too. The cause of this is complicated and likely related to shifting blood from the arterial to venous compartment of the vascular system, effectively off-loading the arterial system. At the same time, I believe that the BP sensors (juxtoglomerular cells located on the arterial side) of the renin-angiotensin-aldosterone system will "see" a decreased renal perfusion pressure and respond by trying to increase BP -- thus, creating/exacerbating the hypertensive state. (By the way, this is an oversimplification of how the kidneys control blood pressure and doesn't even mention ADH.) All of this leads to an increase in blood volume and an increase in venous return to the heart.
Perhaps before diving was even attempted, blood volume had expanded. This state, combined with systemic hypertension and the central fluid shifts that occur normally during diving, could have driven excessive fluid to the lungs, leading to IPE. Just reasoning out loud here based on my limited knowledge of medical and dive-specific physiology...
denisegg, I hope that you can hook up with a caring, competent endocrinologist soon. Thank you for sharing your story. Best wishes on your recovery.
