joyagh

Well, since all the nerves in the body come through the spine (or brain), any spinal damage or head trauma can cause nerve damage. all the organs are part of the autonomic nervous system so if there is damage to the nerves that innervate the heart (nerves that come from T4-8 and the vagus nerve), it can affect the function of the heart/lungs. google-image "autonomic nerve diagram". it will show you which nerves affect which organs and where they come from in the spine.

oh, and there's something called the squatting test which helps identify CAN. this explains a lot to me as my initial symptoms were tachy & dypsnea after bending/squatting chores (laundry, litter box etc) http://www.ncbi.nlm.nih.gov/pubmed/22071282

I found a new neurologist who specializes in dysautonomia and he is going to run more tests for peripheral neuropathy, which he thinks I have - autonomic, motor and somatic. the scary part is, CAN (cardiac autonomic neuropathy) has higher rates of morbidity and mortality in people with diabetes, which I don't have. Sudden cardiac death is a risk. I'm on beta blockers so I guess I'm ok. So to all those docs who say POTS can't kill you - it can if untreated. I'm going to try Alpha Lipoic Adic as I've read it regenerates nerve cells and reduces neuropathy symptoms. I was rear-ended 3 times; once by a car going 60 mph. After he hit me, I hit the guardrail and landed and slammed on the brakes so I wouldn't hit the car in front of me. So i had 3 impacts. I had several spinal injuries from that (1996) and have been fighting recurring pinched nerves in my neck and vertebrae going out of joint. I have stage 2 degen in my neck. My POTS sy started after a flu I had at 4 months pregnant so I thought it was a viral onset, but maybe it was just a perfect storm - virus, pregnancy and nerve damage.

I was just going to post about my car accident and nerve damage and what looks like probable cardiac as well as generalized peripheral autonomic neuropathy causing my POTS sy. I was rear-ended 3 times; once by a car going 60 mph. After he hit me, I hit the guardrail and landed and slammed on the brakes so I wouldn't hit the car in front of me. So i had 3 impacts. I had several spinal injuries from that (1996) and have been fighting recurring pinched nerves in my neck and vertebrae going out of joint. I have stage 2 degen in my neck. I found a new neurologist who specializes in dysautonomia and he is going to run more tests for peripheral neuropathy. the scary part is, CAN (cardiac autonomic neuropathy has higher rates of morbidity and mortality in people with diabetes, which I don't have. Sudden cardiac death is a risk. I'm on beta blockers so I guess I'm ok.

I have noticed that sudafed makes me feel better all around. I feel more focused and calm as well as reduced POTS symptoms. DXM - dextromethorphan (cough suppressant) supposedly helps POTS symptoms too. and ChlorTrimeton and other antihistamines. depends on what you're taking, but cough and congestion meds and antihistamines can def help

although chest pain is not a common symptom for me, when I get gall bladder attacks I get really bad rib cage pain and radiating pain in my back with excruciating pain under my right rib. I don't have the right under-rib pain today, but I wonder if this is gall bladder. It did start after I ate mac & cheese which is when it usually starts. DH insists it's not a heart attack and prob just indigestion. I would have to take myself to ER and it's almost DD's bedtime. wish I had apple cider & vinegar. that'll kill a gall bladder attack in minutes!

I'm a 42 yo woman. This afternoon I developed tightness/pressure and pain in my chest - the whole rib cage area and pain in my mid-back. I am also vaguely nauseaus but hungry and also getting hot & cold sweats. I have a cold and took sudafed but otherwise nothing is unusual. Am I having a heart attack?

It is so hard. I just had a miscarriage and combined with POTS I just didn't want to move, or be around anyone, or be touched. of course my 3 yo DD was EXTRA clingy and demanding, as she always is when she senses I'm not well. I had to get lots of extra sleep to gain rebalance. But it's really hard sometimes. I feel bad b/c I want to parent fully, and I can't physically the way I would have been able to before POTS.

the study was done on sodium ascorbate, so that's what I got. Had to order it from Amazon.

I've read that it's vasoconstriction in the heart arteries, in compensation for hypovolemia.

also, the zoloft didn't make my POTS symptoms worse at all. I guess they can for some ppl but I was fine with it. You might wanna check with your OB/midwife re: Klonopin. If you're breastfeeding or co-sleeping they might not want you on it. (also, it makes me feel more tired, grumpy, dizzy and irritable if I get too much in my system. It has such a long half life that it builds up and causes me a lot of symptoms).

#1. sure - POTS can screw up your neurotransmitters and hormones which are already going through major changes. How far post partum are you? It may be an issue of waiting for the hormones to go back to normal. In the meantime, I think treatment is essential! Have you talked to your OB/midwife? #2. with a panic attack, you'll have emotional fear with the physiological symptoms. with an adrenaline rush you'll ONLY have the physiological symptoms but no mental or emotional fear. #3 - of course. anything that changes your brain chemistry and/or hormone levels will affect POTS, and vice versa, as POTS affects the brain chemicals and hormones. the crying spells might be PPD and might pass, but I think they might need treatment until your hormones even out. That's not a POTS symptom. Cortisol remains high in post partum women for months after delivery and may increase PPD. alot of this may pass in time, but PPD is very serious. #4 - are you nursing? As far as I know Klonopin is not recommended if you're breastfeeding. #5 - Zoloft didn't increase my anxiety at all. In fact, I was so anxious after delivery and it took me 6 months to start zoloft and it helped. SSRI's are a treatment for POTS. I think tricyclic antidepressants are the ones to worry about. I found 50 mg was enough to help, still a small dose. I was SOOOOOOOOOOO paralyzed with fear about taking Zoloft and it really saved me when I got the guts to take it. I personally like my Metoprolol. It helps and doesn't make me tired. You will be sleep deprived with a new baby no matter what, and that will make your POTS and anxiety worse. getting sleep is key, too.

why does the NINDS have the primary symptoms of POTS as lightheadedness and FAINTING? So much other research states that less than 30% of POTS patients faint. This makes dr's think that if you don't faint you are ok. http://www.ninds.nih.gov/disorders/postural_tachycardia_syndrome/postural_tachycardia_syndrome.htm

my POTS developed during pregnancy, and I developed gestational hypertension and pre-eclampsia due to it. I've also had it since delivery 3 years ago. BUT - pregnancy outcomes for POTS patients are no different than for the general population. some people get worse, some get better. my OB & my cardio and endo have said beta blockers are fine in pregnancy. antihistamines can help and are ok. benzos are not ok. ssri's are generally ok under a dr's supervision. I don't know your exact condition, but regular POTS patients can have babies. It might be hard and uncomfortable, but it's not inherently dangerous. Having an infant is probably harder than the pregnancy on you. http://www.ncbi.nlm.nih.gov/pubmed/19659618 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894719/

thanks for all your kind words and support. The HcG is finally out of my system so I feel more like myself, except I had to do a 24 hour urine catch for free catecholamines and creatinine, so i was off my meds for 48 hours, and that kinda sucked. I only knew I was pregnant for about 4 days before I lost it, but I did get very used to the idea and it seemed very real at the time. My cat just died 2 nights ago, so that has superceded the m/c emotions now. But now I'm back on my meds and physically recovering, so it's just the emotional fallout to deal with now. Thanks for the youtube video suggestion. I'll look it up to show DH. Is there one in particular?

I had a miscarriage at 5 weeks pregnant last week. It's pretty much over now. Not sure if I have any HcG in my system anymore - the lab won't get results til Monday. I have been SOOOOOOOOOOOOOO fatigued and exhausted. I've been waiting for it to wear off, but I'm just wiped out and not able to rest. SO many dr's appts - for POTS evals and m/c follow up, and sinus infection and flu shots for DD and vet appts for terminally ill cat. I've been having to get up early and not getting naps, and taking care of 3 yo, household chores and husband: making dinner, grocery shopping, cleaning/laundry, budget/bills, sick cat etc). I haven't lost a large amount of blood (TMI) - just a med/reg menstrual flow. Very little pain as well. I'm just wondering if m/c hits us harder b/c of our existing issues and circulation and other symptoms anyway. I'm just grumpy and irritable b/c I'm so tired and I just wanna sit down and rest and I CANNOT. DH is on my case about being so negative and irritable and complaining. He never understands when I'm not feeling 100%. I'm sure I have some emotional stuff going on from the m/c too, but the fatigue and irritability (short fuse) is really affecting me. Ideas about why this is so difficult?

the following article says sodium ascorbate (from Vit C salts) can help POTS by 50%. any experience with this? http://www.ncbi.nlm.nih.gov/pubmed/21622825

this is an interesting definition; it includes hypovolemic and cardiogenic shock as symptoms for hyperaemia, as well as tachycardia, brady & palps. http://en.wikipedia.org/wiki/Hyperaemia I guess the dyspnea and hyperpnea are part of the symptoms of shock. this pretty much sums up my issues. now I gotta find the cause of hyperaemia and what the metabolic mechanism is.

seems like oxygen would help the subsequent lack of oxygen to the ischemic tissues that result from hyperaemic tissues that shunt blood away from other areas. Seems like hyperaemia and the ischemia that occurs as a result is a metabolic issue. This would make sense for me, I think.

yes, exactly. messed up up, right?! We have the vitals of someone who's bleeding out, or internally, and all the disabling symptoms. but yah, hey, go to work! do chores! get up and pretend to be normal every day!

Active hyperaemia describes my sx/sy so well. and it may explain flushing in those who get POTS flushing. "Active Hyperemia This type of hyperemia is also known as functional hyperemia or exercise hyperemia. It is caused by muscle contraction. Active hyperemia may also result from increase in mental, gastrointestinal or cardiac activity. Collection of the blood in a certain organ results from increase in the blood flow due to increased body metabolism. Active hyperemia is caused by combination of the hypoxia tissue and the production of vasodilator metabolites. Hypoxia tissue is featured by reduced supply of oxygen to the blood vessel tissues which in turn cause increased demand for oxygen. That leads to vasodilation, characterized by widening of the blood vessels that occurs due to process of relaxing the smooth muscle inside the blood vessel walls. Vasodilators are substances that trigger vasodilation and they include ion, nitric oxide, carbon dioxide and adenosine. Reactive Hyperemia This type of hyperemia is also called passive hyperemia and it is caused by blockage in the veins. Blood accumulates in a particular organ in a response to the vein blockage that prevents the normal blood flow. Reactive hyperemia usually occurs after an episode of ischemia such as arterial occlusion. This leads to reduced oxygen level in the blood and increased level of metabolic waste. Blood flow can be blocked if this waste builds up in the body organ. Reactive hyperemia can take place after a tight band is applied to the hand or leg and then removed. Reactive hyperemia may also occur after a coronary occlusion. The longer coronary occlusion lasts reactive hyperemia will be more severe and will last longer. Treatment for Hyperemia Hyperemia is a curable condition. The treatment depends on the type of hyperemia. The disease must be monitored and treated with medications. Hyperemia will not resolve by itself and it must not be left untreated, because it may be harmful to affected person. http://ic.steadyhealth.com/causes_of_hyperemia.html

and of course the norepi/adrenaline surges happen to compensate for the hyperaemia and hypovolemia?

I am so full of questions and have no good doc to ask, so here's another one for ya. Could hyperaemia cause the thoracic hypovolemia that causes POTS symptoms (with or without low blood volume in general)? As if, with any voluntary movement too much blood goes to skeletal muscle and is shunted away from the heart, then there is thoracic hypovolemia, then the high HR/BP/hyperpnea, lightheadedness, spaciness etc. (for me) sets in? before my POTS set in (ever since I had a car accident with spinal injuries) when I was dancing ballet a lot my face would get really red and I'd have to bend over and huff and puff to catch my breath in between combinations. now I'm wondering if this got worse during pregnancy and continues today. Could that be all it is? I guess it's still an ANS disorder. but it'd be an answer. I WANT ANSWERS!!!! http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1464569/

thanks for the info! I guess what I'm thinking is, though, is that maybe we ARE in shock without the blood loss. I mean, the sx/sy are shock, and the aftereffects are draining. Almost like recovering from shock. So it's not like we're going to continue to decline like in shock, unless we continue to do whatever is creating the symptoms (mine are always from mild-mod exertion), but we may be experiencing shock. hence the exhaustion. I am also Hyper-POTS with paroxymal BP - high and low swings with variation in PP. Finally getting EPI levels checked next week.

I posted something similar before, but I continue to be dismayed by how similar my symptoms are to hypovolemic and cardiogenic shock. If I'm not on my BB's, I get either tachy (110-130) with high BP, or tachy with low systolic and high diastolic (narrow pulse pressure) and hyperpnea. My symptoms are exact to the following articles about hypovolemia and cardiogenic shock. EMT's are trained in this but my cardio EP did not seem concerned. I have had cardiac/pulmonary work ups and no pathology is present. my questions is: HOW CAN THIS BE????? "A narrow pulse pressure in a hypovolemic shock patient indicates a decreasing cardiac output (stroke volume) and an increasing peripheral vascular resistance. The decreasing venous volume from blood loss and the sympathetic nervous system attempt to increase or maintain the falling blood pressure through systemic vasoconstriction. This increase in heart rate and myocardial contractility is reflected in the decreasing systolic BP, the increasing diastolic BP and the narrowing pulse pressure. Thus, a blood pressure of 102/88 mmHg no longer appears to be “normal” and requires further assessment of heart rate, respiratory rate and other signs of perfusion, such as the skin color, temperature, condition and the patient’s mental status." http://www.ems1.com/ems-products/education/articles/479223-Blood-Pressure-Assessment-in-the-Hypovolemic-Shock-Patient/ "Early signs include increased heart rate with maintenance of blood pressure even though cardiac output has decreased. As compensatory mechanisms fail, the systolic blood pressure falls and the diastolic pressure increases, causing a narrowed pulse pressure. • Other signs include increased tachycardia; cool, clammy skin; rapid, deep respirations; pulmonary edema (crackles); an S3 gallop; decreased urine output; and impaired level of consciousness." and "Cardiogenic shock occurs primarily as a result of severe left and/or right ventricular dysfunction that results in inadequate cardiac pumping. The most common cause is myocardial infarction; other causes include cardiomyopathy, ventricular rupture, and congenital heart defects. PATHOGENESIS • Decreased contractility results in decreased cardiac output, which causes decreased tissue perfusion that is inadequate to meet basal metabolic requirements. • The sympathetic nervous system and renin-angiotensin system are stimulated as compensatory mechanisms to increase cardiac output. The net result of the activation of compensatory mechanisms is to increase myocardial oxygen demand. This may precipitate further myocardial damage, resulting in a progressive decline in cardiac output." https://docs.google.com/viewer?a=v&q=cache:4FIzEuUFsWsJ:faculty.ksu.edu.sa/73717/Documents/cardiogenic%2520Hypovolemic%2520Shock.doc+&hl=en&gl=us&pid=bl&srcid=ADGEESgBbthiu6qhm-R_NbKX1KeZHRIrHSwgq9Fki7TqhIy5UMXV4Tcvesr9o0knLRogXi2W-uCDefJ0oQsoE2qG3KfeQu55wSuJ7tzxOcLqpD7WI-GWV_zCL39iUWPqzbBkV6j7I_Mw&sig=AHIEtbRKaLcj1eerGMlsc8BdWNL94ms0bg