Short Of Breath

[lalalisa]

Hello,

I've been really short of breath lately...even without any excursion. Can anyone explain why this happens?

Thanks for any input,

Lisa

[deucykub]

Hi, Lisa:

I'm short of breath any time I exert myself, which means moving at all in any position. I also have asthma (at least that's what the doctors say), but the shortness of breath is there when my asthma is fine. My Electro-Physiologist said the shortness of breath is caused by the tachycardia. When your heart speeds up, your rate of breathing also increases, and you feel short of breath.

That being said - if this is a new symptom for you, you should definitely tell a doctor. I'm seeing a second pulmonologist in April to be sure that all bases are covered and to see if he can figure out where my asthma and POTS overlap. Please be sure to ask a doctor about this if it is new for you.

Take care!

Deucykub

[calypso]

Lisa,

I've been short of breath at rest since my POTS developed and have no explanation as to why. I've had numerous tests -- from pulmonary tests, blood gases, etc., to heart function tests. No abnormalities. But clearly, I feel short of breath all the time. I constantly feel like I won't breathe unless I think about it.

Wish I had ideas/advice for you. I have lived with it for 3-1/2 years now. I can only figure that on some level, it is either an emotional/neurochemical thing (because you can't detect any abnormalities) or it's something you feel but doesn't actually hurt you physically -- because I have had no complications because of it.

Amy

[pamyla]

Hi Lisa,

I've had shortness of breath off and on for many years. In the past year I was diagnosed with multiple tick borne infections and discovered that air hunger is one of the primary symptoms of babesia. With treatment, I've finally seen this symptom diminish.

Anyways, just wanted to chime in because I think in the past I was often too quick to assume my symptoms were 'just pots' and not pursue answers as to why they were occuring. I'd definitely recommend bringing it up to your doctor.

good luck,

Pam

[P SUDIK]

Hi I just can't believe you posted this.I have not been on the forum for a few days,have been in the hospital for the last 3 days.

I have been sob and have had a cough for over 2 wks,new symptoms for me. Wed. afternoon (doing nothing) I could not breath! I went to an Urgent Care close by,didn't want to go to the ER again. Guess what Urgent Care rushed me to the ER. They kept me in Cardiac step down. I could not have any salt or an IV,I said I needed the IV,they said no,that I could be retaining fluid( I was not.) After a cardiogram,echocardiogram,pulminary function test, a barium swallow test ,chest x rays, CT's,I am sure I am forgetting some,oh and a million blood tests, the only thing they knew for sure was that I had a very fast HR.and that my rbc was a little low.

I did not see any docs that I knew,only hospitalists. So I am following up with my pcp and a new EP.

Does anyone think this is POTS? This doc thinks it has something to do with my GERD???,wants me to have an endoscopy. Any Ideas on that? I 'm thinking my bladder muscles and my stomach muscles don't work right ,could this me something like that. The doc did say something about bronchial spasms. Please for give my ramblings,but I am writing what I am thinking. I am still wheezing and coughing,doc does not want me to use inhaler cause it causes my heart to race, anyway I am very confused!!!!! Thanks for listening and would love your opions and suggestions P

[bttrflyamby1981]

The olny thing I have been diagnosed with is POTS, and I too have trouble breathing at times. Mostly I notice it when my heart is beating fast.

[flop]

I'm sure that I've read something recently about shortness of breath and POTS. It was something along the lines of taking deep breaths (not breathing faster) actually causes the blood pressure to rise slightly.

It may well be that we feel breathless when out BPs are low and we have automatically started taking deep breaths to try to raise out BP? The breathlessness is probably because we are breathing fast rather than from a lung problem.

I also wonder, if as a low BP means less blood to our brains (therefore less oxygen to our brains) that that could trigger the breathlessness.

Can't think clearly enough at the moment to postulate further. When I get my surgery over with I will try to find the info on deep breathing and BP changes.

Flop

[Guest tearose]

Heck, I dislike the feeling.

Low blood pressure will give me shortness of breath. Even if I am not being active. I reach for some electrolytes and see if that helps.

[lalalisa]

Hello,

Thanks for everyone's input! It's nice knowing I'm not alone.

Pat - Wow, you have been through a LOT lately. I can't imagine getting all of those tests done in a short period of time - yikes! I don't know what to tell you since I'm not a dr. -- I wouldn't want to steer you in the wrong direction. I really hope you can get some direction from a good dr!

Take care,

Lisa

[deucykub]

Flop - is this article you were referring to?

Hypocapnia and Cerebral Hypoperfusion in Orthostatic Intolerance

I posted this a couple of days ago in the "Patronizing Cardiologist" thread because someone had mentioned the doctor said they were "just hyperventilating."

Hypocapnia (low carbon dioxide) became interesting to me after an arterial blood gas that showed a state of Compensated Respiratory Alkalosis, also called Chronic Alveolar Hyperventilation, which meant that I had been in a state of hyperventilation for so long that my kidneys had compensated to balance my blood's pH. Panic hyperventilation does not last long enough for the kidneys to kick in with compensatory measures; full compensation does not occur for several days! It's also the most common finding in the critically ill.

My doctor looked at the test and said, "ABG looks good." I had done my homework though and said, "But I'm in a state of compensated respiratory alkalosis. That's not normal." He said... "oh yeah, look at that." "What's causing it?" I asked. "Hmm, you're hyperventilating." Thanks, doc, you're a gem, lol.

If I had been hyperventilating in a panic for that long, I would have been in a collapsed heap on the floor.

[flop]

Deucykub,

thanks for posting the link - I must have missed it in the other thread. I hadn't seen that article before. From my quick look at the abstract it seems to be suggesting that hyperventilation causes decreased cerebral blood flow and therefore syncope (i.e. we are all hyperventilating ourselves into collapses - I think not!).

I know that hyperventilation can cause blackouts - there is an infamous video of some German medical students hyperventilating and suddenly standing up from a squatting position to induce syncope (some of them demonstrate a few seizure like movements due to hypoxia).

What I was reading was talking more about deep breaths rather than hyperventilating and was suggesting that the deep breaths were triggered by hypotension and actually helped to improve blood pressure. I think it was in Dr Grubb's book "syncope: mechanisms and management" but I haven't got the book here to look it up (am staying with my Mum before going into hospital tomorrow). I'll try to get my brain fogged memory to remember to look it up for you when I get a chance.

Flop

[deucykub]

Hi, Flop:

I would love to see that article once you are recovered from your surgery and are feeling up to it. Not a minute before, though. Please take it easy after.

The abstract is a bit misleading in the other article. It goes on to say that hyperventilation caused by deep breathing rather than rapid breathing contributes to cerebral hypoperfusion in OI. The deep breathing, as you had said, too, is a compensatory mechanism in response to low blood pressure. Here's the excerpt I found most interesting, which actually states how the hypocapnia in OI is not the result of the same breathing as anxiety (I definitely don't support that hyperventilation IS the cause of our OI and POTS!):

"... However, there are some significant differences between POTS and the hyperventilation syndrome. The respiratory rate and end-tidal CO2 in POTS with the patient at rest are identical to those of control subjects. Hyperventilation that consists of an increased depth without an increased rate only occurs during orthostatic stress. Patients increase their depth of respiration after they develop a transient reduction in BP and a persistent reduction in pulse pressure. An increase in respiratory depth is a well-known mechanism that results in an increase in BP by increasing preload mechanically and by venoconstriction. Deep inspiration also activates a vasoconstrictor reflex with a spinal pathway. Finally, respiratory neurons modulate the rostral ventrolateral medulla and hence vasomotor tone.

Our tentative position is that OI and anxiety-panic states share a common efferent pathway involving sympathetic activation but that they are evoked by quite different mechanisms. Evidence exists to implicate the noradrenergic system in the development of the anxiety-panic state. Even small alterations in noradrenergic function can produce significant cardiovascular, gastrointestinal, and respiratory symptoms in patients with panic disorder that are similar to symptoms experienced by patients with OI. However, the mechanisms evoking those similar symptoms appear to be quite different. OI patients hyperventilate as a compensatory response to OI. However, continued hyperventilation is counterproductive because it causes hypocapnia, which induces a reduction in cerebral perfusion, and worsens symptoms of OI. Furthermore, although a single breath will transiently increase, continued hyperventilation reduces total systemic peripheral resistance, further aggravating OI. For individuals with panic disorder, changes in respiratory rate (ie, hyperventilation) produce panic symptoms rather than being a compensatory phenomenon as seen in patients with OI..."

Good luck with your surgery tomorrow. I'm sure it will be such a relief to rid yourself of those persistent sinus issues! You'll be in my thoughts and prayers.

Take care!

Deucykub

[ramakentesh]

Id like to revisit this post.

primarily because many in the thread state that deep breathing can be a response to low blood pressure and suggesting that this is more likely to be causing the breathlessness exhibited by some POTS patients than a possible hypocapnia.

If you read the article quoted its actually suggesting that the OI patients tested had abnormal CO2 levels and responses to hyperventilation and the result was further hyperventilation causing a worsening of symptoms. The OI patients tested had hyperventilation as a response to orthostatic stress.

The diagnostic criteria for POTS that is becoming increasingly accepted by specialists in these disorders is that POTS occurs without a measurable reduction in blood pressure. Therefore, it is possible that the breathlessness that results in hyperventilation may actually be being caused by mechanisms OTHER than those mearly to stabilise dropping blood pressure (especially when blood pressure doesnt normally drop in POTS - at least in the early stages of orthostatic stress).

It should also be noted that many of the symptoms of POTS are the same as those that would be caused by hypocapnia induced by hyperventilation - anxiety, an overly excited sympathetic nervous system, dizziness, depersonalisation, etc.

Dr J Stewart noted that in a subset of POTS patients designated as Normal Flow POTS - a subgroup of these had significant hypocapnia coupled with excessive vasoconstriction of their hands and feet during orthostatic stress:

http://ajpheart.physiology.org/cgi/content...ract/291/2/H904

Hypocapnia causes cerebral vasoconstriction which has been noted in a variety of studies of POTS - hypocapnia also causes cerebral hypoxia and due to vasoconstriction, reduced blood flow to the brain without a reduction in blood pressure. In short, it alone could possibily account for the symptoms of some POTS patients without blood pooling = and may explain fainting in patients designated as hyperadrenergic.

At the very least breathlessness on a constant basis when considered with the findings of the novak study:

http://stroke.ahajournals.org/cgi/content/abstract/29/9/1876

and another interesting recent article:

http://www.dynamic-med.com/content/6/1/2

[futurehope]

Id like to revisit this post.

primarily because many in the thread state that deep breathing can be a response to low blood pressure and suggesting that this is more likely to be causing the breathlessness exhibited by some POTS patients than a possible hypocapnia.

If you read the article quoted its actually suggesting that the OI patients tested had abnormal CO2 levels and responses to hyperventilation and the result was further hyperventilation causing a worsening of symptoms. The OI patients tested had hyperventilation as a response to orthostatic stress.

The diagnostic criteria for POTS that is becoming increasingly accepted by specialists in these disorders is that POTS occurs without a measurable reduction in blood pressure. Therefore, it is possible that the breathlessness that results in hyperventilation may actually be being caused by mechanisms OTHER than those mearly to stabilise dropping blood pressure (especially when blood pressure doesnt normally drop in POTS - at least in the early stages of orthostatic stress).

It should also be noted that many of the symptoms of POTS are the same as those that would be caused by hypocapnia induced by hyperventilation - anxiety, an overly excited sympathetic nervous system, dizziness, depersonalisation, etc.

Dr J Stewart noted that in a subset of POTS patients designated as Normal Flow POTS - a subgroup of these had significant hypocapnia coupled with excessive vasoconstriction of their hands and feet during orthostatic stress:

http://ajpheart.physiology.org/cgi/content...ract/291/2/H904

Hypocapnia causes cerebral vasoconstriction which has been noted in a variety of studies of POTS - hypocapnia also causes cerebral hypoxia and due to vasoconstriction, reduced blood flow to the brain without a reduction in blood pressure. In short, it alone could possibily account for the symptoms of some POTS patients without blood pooling = and may explain fainting in patients designated as hyperadrenergic.

At the very least breathlessness on a constant basis when considered with the findings of the novak study:

http://stroke.ahajournals.org/cgi/content/abstract/29/9/1876

and another interesting recent article:

http://www.dynamic-med.com/content/6/1/2

Boy, You must spend a lot of time researching. I appreciate your sharing. I had to look up the definition of hypocapnia.

For other dummies like me, hypocapnia means low CO2 in the blood. I have had some tests where the CO2 was an unexplained high. I must have been hyperventilating or was I hypoventilating?

The most useful information for me was from the first article:

Hypocapnia and symptoms of orthostatic hypertension are reversible by CO2 rebreathing.

That means that when I'm in the mall, walking, and am finding myself SOB (short of breath), I'll breathe into my cupped hands to get my CO2 levels down and hopefully return to normal. Thanks for posting the articles.

[firewatcher]

I guess I'm the anomaly. All my tests show chronic hypoxia (low oxygen): increased lung volume, high lung diffusion rate (gas exchange), high red blood cell/hematocrit (which screws with the pulse oximeter reading.) My dyspnea (shortness of breath) is directly correlated to my HR. The higher it goes, the worse it gets.

Of course, the longer I stand, the higher my HR and BP get, put me in motion and it gets even worse! I did a light workout with weights (supposedly anaerobic exercise right? With the leg extensions my HR was 140bpm, with the Lat pull-downs it was 160-180bpm. I was not doing them fast either! Pilates will send my HR above 150bpm for most of the session, even on a BB.)

[ramakentesh]

Your C02 levels might be a more interesting test id reckon. There appears to be a coupling of excessive peripheral vasoconstriction (which appears in the forms of POTS know and hyperadrenergic or in the newer Normal and Low Flow POTS) with elevated C02 levels and cerebral hypoperfusion.

In other words excessive sympo activity is causing an excessive vasoconstrictive response and heart rate and the elevated heart rate is causing hyperventilation somehow and worsening symptoms of OI/POTS when standing.

The hyperventilation in this context isnt purely rapid breathing - it can present with deeper breathing, apneas or other breathing anomalies on standing.

In one of the studies i referenced CO2 rebreathing eased symptoms and in OI symptoms were worsened through hyperventilation while standing.

So perhaps at the end of hte day, Co2 rebreathing may help.