Fainting Not Due To Tachy

[bjt22]

I don't want to harp, but it sounds as if this doctor is talking in circles and putting up a very defensive argument.

I still recall my friend with what is termed as "malignant VVS" who's heart actually stops when he faints. His doctor noticed that he was hyperventilating, too, when he had an episode. He underwent therapy to avoid this and he did improve...however, that wasn't the genesis of his problem, nor did he doctors ever pretend that it was. The hyperventilation will no doubt make the problem worse and quite likely start a whole new cycle of crash-recover-crash, but other than that, well, I reserve my judgment on this doctor's theories.

[ramakentesh]

Your doctor/specialist is wrong on so many levels. The hyperventilation is related to baroreflex unloading which is a result of POTS rather than its cause. I explained the mechanisms of POTS above and trust me they are based on what the research is telling us, not what one doctor thinks.

Hypocapnia and hyperventilation only occurs in a few POTS patients - in many cerebral vasoconstriction seems to be the result of excess norepinephrine levels.

Honestly, feel free to defend his view, but its based on nothing. People with POTS experience measurable increases in MSNA firing rate and NE levels on tilt even without a reduction of blood pressure and in some cases an increase.

Cerebral vasoregulation is impaired in some forms of POTS

The skeletal muscle pump is impaired in some forms of POTS

excessive vasoconstriction is a hallmark of some forms of POTS

etc.

[yogini]

In addition to what others have said, many POTS patients are NOT hypovolemic and pooling can occur due to autonomic neuropathy. It's very frustratng -offensive, really- that he says yours is due to deconditioning. How is it that many people go from being athletes one day to having pooling the next? It doesn't sound like he understands the mechanics of dysautonomia at all. How did you find this dr?

I still think that tachy doesn't cause fainting - if you faint while your heart is beatin fast, it's because there isn't enough oxygen to the brain. The heart may be beating fast to compensate for this.

On the breathing front, through yoga and breathing exercises I have learned to slow my breaths down to 4-6 breaths/min. It is safe to do when done correctly. But when I don't focus on it, I know breathe a lot faster. I think I was breathing 25 breaths per min before and my breathing has slowed down a lot, even when I don't think about it.

[erik]

Here is the Hyperpnea in Postural Tachycardia website. The Valhalla, NY folks are not crackpot researchers and they happen to be investigating the issue of increased breathing as it relates to POTS. Keep in mind this is related but tangential to what the UofIowa doc is saying... because that doc measured masumeh's pulse and saw no undue increase in pulse upon standing (basically the POTS is gone now though it was there before). As I "read it", that doctor was not claiming hyperventilation to be the cause of POTS... he was suggesting an intervention that will hopefully help.

Here's quote related to the Valhalla study (backed by American Heart Association):

We hypothesize that excessive baroreflex unloading during orthostatic stress (upright positioning) is the initiating event in POTS which results in two additional physiological consequences leading to hypocapnic hyperpnea (low carbon dioxide caused by markedly increased ventilation): a) reduced inhibition of chemoreceptor activity centrally and frank stimulation of peripheral chemoreceptor activity due to sympathetically induced reductions in blood flow to the carotid body. Increased chemoreceptor activity leads to hyperpnea which activates pulmonary stretch receptors.

Study Purpose: In this proposal we address the clinical problem of hyperpnea in orthostatic intolerance and propose a line of investigation which we hope will lead to better understanding of autonomic cardiovascular regulation in postural tachycardia syndrome.

I personally hope that they turn something up that helps understanding and treatment for POTS, syncope, whatever. One thing to note is that they state "hyperpnea which activates pulmonary stretch receptors" which implies that if one can intervene in the hyperpnea, one can mitigate stretch receptor stimulation and perhaps reduce later consequences.

[dsdmom]

I'm going to second yogini's post about autonomic neuropathy and blood pooling. Have you ever been tested for this with a nerve biopsy?

Because if you have autonomic neuropathy, you're going to have blood pooling - and it wouldn't be because you were 'deconditioned.'