flyingsquirrel

There is a list under "test name" and it starts with "CBC". Under that test there are a bunch of things, WBC, RBC, MCH etc and one, "MPV" is indicated as a high level (11.5)-- does anyone know what this means? CBC stands for 'complete blood count'. As other people said MPV is 'mean platelet volume' or the average size of the platelets. Yours is barely high. If your platelet count is normal and you don't have any clotting problems, it's probably just a fluke. Of course, if you are worried, talk to your doctor. Question two. Blood test under the title "diff auto", my "EOS" level is high at 6%. Translation? Less than 5% of your white blood cells should be eosinophils. When this level is elevated it indicates an allergic process or a parasitic infection. In the US it is usually an allergic problem. Question 3, my folate level was high at 21.4 ng/ml, vitamin d and b12 were borderline low-- any idea what that indicates? Could be lots of things, talk to your doctor.

I feel very short of breath when I'm dehyrdrated or lose blood volume. It's amazing how much better I will feel if I push lots of fluids and lots of salt.

I haven't read it, but here's a recent review of the topic... Mustafa HI, Fessel JP, Barwise J, et al. Dysautonomia: perioperative implications. Anesthesiology. 2012;116(1):205-215. http://journals.lww....cations.36.aspx

Start by calling this number 507-538-3270 (general appointment line) and tell them you want to see someone in the 'Heart Rhythm Clinic'. When I first went I think they offered me an appointment in 2 weeks (I couldn't take it and I ended up with one that worked better for my schedule about a month out). Like Issie said, you have to learn how to play the 'Mayo game' if you want to get seen as fast as possible.

And if you're coming to Rochester I can give you some names...

It would be helpful to look at a picture for this, so go here... http://emedicine.med...article/1923077 Go to the 'Gross and Microscopic Anatomy' section, then click on the image that is labled ' Sympathetic and parasympathetic neurotransmitters and receptors'. We are only going to be talking about the top two pathways. So...the top pathway is the parasymathetic pathway. The vagus nerve comes out of the brainstem and travels down towards lots of organs (we only care about the heart right now). It synapses (one neuron meeting another neuron) at a ganglia (a place where synapses happen) very close to the target organ (heart). The neurotransmitter that is used to transmit impulses from the pre-ganglionic neuron to the post-ganglionic neruron is acetycholine (ACh). After ACh serves its purpose in trasmitting the impulse it is quickly broken down by acetylcholinesterase (AChE) and recycled. The impulse travles down the short postganglionic neuron to the target organ (heart) where, again ACh is the neurotransmitter that transmits the impulse, this time to the heart itself. The reason pyridostigmine is used in IST (and I think POTS ) is becasue it is an AChE inhibitor. Parasympathetic transmission is dysfunctional and, in theory, if we can increase the amout of time that ACh spends in the synapse (by delaying its breakdown), we can increase the amount of parasympathetic transmission and slow down heart rate. This sounds great, but remember that people with IST have CRAZY strong sympathetic nervous systems and really wimpy parasympathetic nervous systems (at least when it comes to the parts that feed the heart). ACh is also the neurotransmitter between the pre-ganglionic neuron and the post-ganglionic neuron in the sympathetic pathway. The neurotransmitter between the post-ganglionic neuron and the heart is norepinephrine, which none of us lack for. Because we have an excess of norepi AND this is such a strong pathway to begin with (compared with the parasympathetic) inhibiting ACh breakdown (without any other pharmacologic intervention) has a net effect of INCREASING heart rate in people with IST. (This is not based on any research, this is based on anectodotal experience and physiology.) In order to get a real benefit from pyridostigmine (or any AChE inhibitor), we have to attack the sympathetic side of the problem. The easiest way to do this is with a beta blocker. Even though transmission is increased a the sympathetic ganglion, it is blocked at the beta receptors on the heart. Does this make sense?

Hey Jangle...if you think you have IST, go in through EP cardiology. They will still have you see autonomic neuro and it will be a long wait, but you will be in the system.

Jangle...what you're describing sounds like IST to me. MANY people with a diagnosis of IST (one study said 2/3) do not have a 24 hour average HR over 100. My resting HR is around 88 and my 24 hour average HR was 85 on my last drug-free holter. It is usual for people with IST to drop down to normal HR in their sleep. It bothers me when medical professionals dismiss IST as a 'nusiance disease'. It causes chest pain, shortness of breath, and greatly impacts quality of life. While it is true that in the majority of people it does not lead to any short term complications, in some people (myself included) a sustained high heart rate can cause a tachycardia induced cardiomyopathy which can lead to heart failure. (Usually this can be fully reversed if recognized early and treated with agressive rate control.) The long term consequences of a sustained high heart rate are not clear. Some studies have shown that a high heart rate is an independent risk factor for coronary artery disease and realted heart disease, but the true risk is not clear. Ablations are not recommended for anyone with IST, POTS or not. There are still some people out there recommending and performing them. There are two reasons for this. One is that there is something else going on that a ablation might help with. The second is that they are subscribing to the theory that IST is a primary sinus node abnormality (rather than autonomic dysfunction). There are many studies that show that ablations are initially quite successful, but any that include long term follow-up (1 year+) show recurrence of symptoms and/or the need for a pacemaker. (There is an option for truly intractable cases that involves the complete removal of the sinus node (and sometimes the AV node) and the insertion of a permanent pacemaker.) I would love to try ivabradine as well. IST is notoriously difficult to manage and I don't tolerate beta blockers well (they make me wheeze). Right now the comination of meds I'm on is acutally working quite well. I take a moderate does of a long acting beta blocker (nadolol) to cover the sympathetic side along with pyridostigmine to boost up the parasymathetic side. A note about pyridostigmine...I initially started taking it without a beta blocker and it actually make my heart rate go UP. There is a good physiologic explanation for this if anyone is interested, but once I combined it with a beta blocker it worked great (and all my parasymathetic autonomic testing has completley normalized).

I'll let someone way more qualified cover POTS, but here is what IST looks like clinically: consistently elevated resting heart rate inappropriate rise in heart rate in response to MINOR exertion (not necessarily postural) hypersensitivity (inc heart rate) to beta-agonists (isoproteronol, epinephrine/adrenaline, albuterol, etc) depressed cardiovagal tone (parasymathetic dysfunction) rhythm must be sinus tachycardia (not SVT, etc) I have IST (but not POTS) and my heart rate will rise from minor "exertion" like talking, eating, and walking across a room. (I also run about 8 miles a week.) None of these things are physiologically stressful for my body, it is simply an overreaction of my sympathetic nervous system AND a dysfunction of my parasympathetic system.

Ivabradine and bystolic are two VERY different drugs. Ivabradine is not available in the US or Canada. It is available in Mexico, Europe, and Australia. Bystolic (nebivolol) is a cardioselective beta blocker that also causes nitric oxide release, and therefore vasodilation. Procoralan (ivabradine) is a novel bradycardic agent that blocks If channels to slow the sinus node. It is NOT a beta blocker.

Usually the testing isn't a scheduling problem...it's the doctor appt. Call every day and see if they have anything open sooner. They are used to people doing this.

A series of PVCs that is 7 beats or shorter is considered a "run of PVCs", anything longer than that is V-tach. (Some sources define a run of PVCs as 5 beats or 9 beats.) Other interesting PVC related rhythms are bigeminy (a PVC as every other beat) and trigeminy (a PVC as every third beat). Both of these need immediate attention as they are a sign of significant cardiac irritability.

I use baking soda (sodium bicarbonate) in my water...(1 teaspoon = 1.2 grams of sodium) along with increased dietary salt (sodium chloride). Drinking salty liquids is no more or less hard on your kidneys than eating a similar amount of salt.

Lots of people on the side of the pond still say Holter monitor (named after Norman Holter) although the modern name of the test is 24 (48, etc) hour ambulatory ECG/EKG monitor. ECG/EKG refers to the broad range of tests that look at eletrical rhythms of the heart from single lead rhythm strips, to 12-lead diagnostic quality printouts, to Holters, telemetry, event monitors, etc. ECG=EKG. It doesn't mean anything else in medicine. (unless you are a veternarian...then it can mean equine chorionic gonadotropin...or so says wikipedia.) Even if the graph is not a part of the official report, the data is still there and your physician can access it. They could look through all 24 hours of EKG tracings if they wanted to.

ECG = ElectroCardioGram (english) EKG = ElektroKardioGramm (german) EKG is the original name given to the procedure by Willem Einthoven. While ECG is technically the correct (modern) term in english speaking countries, many traditionalists prefer EKG. A standard Holter test will tell you your maximum, minimum, and average heart rates over the 24 hours. It will also tell you if you had any abnormal rhythms (and specifically what those were). Some Holter software will print out a graph that shows your heart rate over the 24 hours so it is easy to see if your max/min were just a quick peak/valley or if they were sustained. Holters are just EKG, no blood pressure, no anything else.

There are many different protocols for Holter testing and it completley depends on what they are looking for whether you need to go off any of your meds or not. You should definitely ask your GP (who ordered the test), but if they are looking for what your heart is doing over any given 24 hours, generally patients are advised to take the medications they would normally take in those 24 hours in addition to continuing their normal activities. The MOST IMPORTANT thing to do in preparation for Holter testing is TAKE A SHOWER before going to get the monitor put on. You will not be able to shower/bathe/swim until the 24 hours are up. They will probably give you a horribly ugly little bag that goes around your waist or neck to hold the actual monitor. I have found that if I wear a sports bra I can usually hide the monitor in my bra. (also make sure you take your bra OFF while they are putting the monitor on or your will be stuck wearing it for the full 24 hours) Another option is to wear jeans (or other pants with similar front pockets) and a long shirt. Just put the monitor in your pocket and the shirt will cover the wires coming down. (can you tell I've done this a few times?) As for sleeping, I usually just set the monitor on the bed next to me and don't worry about it. If I roll over onto it, I just move it. If you don't want to do this, I would recommend wearing a tight tank top and tucking the monitor and extra wires against your abdomen or back (whichever you don't sleep on).

Yup. A mild rise in heart rate is a normal response to an infection...increased metabolic needs to fight the infection and all that. My heart rate rises out of porportion to other stress (like walking across the room) so it doesn't suprise me that it rises out of porportion to being sick too. A large rise in heart rate, especially when coupled with an increased respiratory rate and/or a decreased blood pressure can be a sign of a serious infection that needs prompt medical attention.

Isoproterenol is not the same thing as adrenaline, although they are both catecholamines. (epinephrine = adrenaline) Isoproterenol's main effect is increasing heart rate. This is the reason it is given in tilt table tests - to increase your heart rate (even more than standing does) to see if they can incduce symptoms. It also causes bronchodilation (similar to albuterol...it used to be used in asthma before there were better drugs). Unlike epinephrine/adrenaline, there is very little direct effect on vascular tone, therefore any effect on blood pressure is solely a result of increased heart rate.

You are correct that estrogen leads to vasodilation (actually estrogen causes an increased release of nitric oxide which causes vasodilation). As far as I can recall, progesterone doesn't have much effect on blood vessels one way or another (but don't quote me on that one).

I drink licorice root tea in addition to eating lots of salt. It seems to help me hold on to salt and fluids longer (and therefore I avoid sudden drops in BP). It also tastes really good, especially with a little milk.

Be careful with bystolic, it DOES cause vasodilation via increased endothelial nitric oxide release.

All beta blocker act on beta 1 receptors (non-cardioselective beta blockers also act on beta 2 receptors). Beta 1 blockers have a variety of actions, the two most important ones are: negative chronotropic effect - slowing down the heart rate negative inotropic effect - decreasing the force with which the heart pumps blood (therefore lowering BP) Generally these effects are fairly evenly balanced with the commonly prescribed beta blockers, however each person will have a slightly different chronotropic and inotropic reaction to any given drug. Also, there may be dose-dependent responses; the blood pressure lowering effects might be seen at a lower dose than the heart rate lowering effects. Any time you lower blood pressure, your body will want to raise your heart rate and constrict your blood vessels in an attempt to compensate. If the beta blocker has not yet taken away your body's ability to increase your heart rate, this is exactly what it will do. I hope this answered your question.

EDIT: please see reply below

This is not a medically recognized syndrome. There is no peer-reviewed research or case reports in the medical literature. The sites on which it is discussed are those devoted to the pseudoscience and propaganda surrounding anti-vaccination. Syndromes and diseases are usually named after the first person to discuss them in the medical literature. As this has not been published in a legitimate scientific journal, I was interested to see how it was named...also two of the three names stood out... Andrew Wakefied is the disgraced physician who published the article in the Lancet that started the anti-vaccine panic/movement. His "research" was later revealed to be fradulent and unethical. The Lancet retracted the article and he lost his medical license. Paul Offit is an infectious disease physican and pediatrician one of the leading proponents of the safety of vaccines. As such he is a frequent target for anti-vaccination groups. His inclusion in the title is ironic, as part of the article cited above purports to explain the syndrome in "simple terms that even Paul Offit can understand." The last name wasn't familiar to me, but a quick google search yielded Alan Phillips JD, a "vaccine rights" lawyer, who fights for your right not to vaccinate your children, thereby turning them into biological weapons. EDIT: I understand what it is like to feel that current medical science has failed to offer answers to our problems, but that is no excuse to fall victim to these snake oil salesmen. They feed off our desperation and need for answers coupled with current medical science's lack of answers for us. We didn't even know that the immune system existed a hundred years ago. Medical science is a constantly evolving field of knowledge. If we don't understand why POTS or MCAS or IST happen, it's because medicine hasn't developed that far yet. If we don't know how to treat them effectively, it's beacuse we haven't yet learned the biochemistry that will allow us to do so.

IV contrast is just yucky stuff. Drink LOTS of fluids. Give your kidneys some help getting the stuff out of your body.