Lemons2lemonade

Perhaps this can shed some light on the effects of dopamine and serotonin in pots. Antipsychotic Pharmacotherapy and Orthostatic Hypotension Gugger, James J. CNS Drugs 25. 8 (Aug 2011): 659-71. All antipsychotics are associated with orthostatic hypotension,[1-3] although it is more frequent and severe with certain drugs. The incidence of orthostatic hypotension in patients taking antipsychotics is described below; however, comparison between studies should be done with caution due to significant differences in the demographic profile of each study and differing methods of assessment for orthostasis. The largest source of comparative data comes from the CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness) trial, a large, federally funded study comparing the relative effectiveness and tolerability of second-generation antipsychotics with first-generation antipsychotics (represented by the mid-potency phenothiazine, perphenazine). Table I shows comparative rates of orthostatic hypotension in patients participating in phases I-III of CATIE.[4-8] Among atypical antipsychotics, clozapine and quetiapine had the greatest incidence of orthostatic hypotension, as high as 24% and 27%, respectively, because of a high affinity for the α 1 -adrenoceptor. Table I. Percentage of patients reporting orthostatic faintness in phases I-III of the CATIE trial [Table omitted.] Among the more recently introduced second-generation antipsychotics, iloperidone appears to have the highest incidence of orthostatic hypotension (19.5% compared with 8.3% in patients taking placebo in a pooled analysis of randomized controlled trials),[9] while the incidence of orthostasis with lurasidone and asenapine is less than 2%.[10,11] There are much fewer data on the incidence of orthostatic hypotension with first-generation antipsychotics, although low-potency (i.e. agents with low potency at the dopamine D 2 receptor) phenothiazine antipsychotics such as chlorpromazine and thioridazine are generally considered the most likely to cause orthostatic hypotension.[3] The incidence of orthostasis in a report of 515 patients taking chlorpromazine was 8%[12] and it was 14.7% in a randomized controlled trial.[13] Almost no quantitative data exist for higher-potency phenothiazine antipsychotics (perphenazine, loxapine, trifluoperazine, fluphenazine) and thiothixene,[1,3,14-18] but they are generally considered to infrequently cause orthostatic hypotension. In the pooled analysis of iloperidone studies mentioned above, the incidence of orthostatic hypotension with haloperidol (used as an active control) was 15.3% compared with 8.3% for placebo.[19] Since intramuscular administration generally results in a higher and more rapid elevation of plasma concentrations than oral administration,[20,21] there is likely to be a greater risk of orthostatic hypotension when antipsychotics are administered by the intramuscular route. A large study (n = 2011) evaluated the safety of intramuscular olanzapine relative to other intramuscular antipsychotics (primarily haloperidol). Orthostatic hypotension occurred in 2.4% of patients receiving olanzapine and 4.2% of those receiving any other antipsychotic.[22] Very little data exist for the other intramuscular antipsychotics. In a trial of intramuscular chlorpromazine (dosed at 1 mg/kg with a maximum dose of 100 mg) for the treatment of migraine, 18% (18/100) of patients developed orthostasis.[23] Although the frequency was not defined, orthostasis was the most common adverse effect of chlorpromazine in a trial comparing the efficacy of intramuscular chlorpromazine with intramuscular haloperidol in 50 patients with psychotic agitation; orthostasis was not mentioned as an adverse effect of haloperidol.[24] On iloperidone (the antipshyotic that causes the most OH)from Wikipedia ...acting upon and antagonizing specific neurotransmitters, particularly multiple dopamine and serotonin receptor subtypes. It is considered an ‘atypical’ antipsychotic because it displays serotonin receptor antagonism, similar to other atypical antipsychotics. The older typicalantipsychotics are primarily dopamine antagonists. Iloperidone has been shown to act as an antagonist at all tested receptors. It was found to block the sites of noradrenaline (α 2C ), dopamine (D 2A and D 3 ), and serotonin (5-HT 1A and 5-HT 6 ) receptors. [1] In addition, pharmacogenomic studies identified single nucleotide polymorphisms associated with an enhancedresponse to iloperidone during acute treatment of schizophrenia. [2] What I gather from this, is that OH can be caused by blockage of the serotonin and dopamine receptors. Perhaps this is why ssri's help patients with pots.

I agree with you, we should start compiling them

I was on the metoplerol for a long time and then stopped tolerating it. I now take florinef and like it much better.

Interesting I have a slight nystagmus too. Have you had your potassium levels checked?

I agree with mcblone, tell the doc

It could be the sitting down motion that is making you light headed or that you are urinating when things are already getting bad. I am just the opposite. I feel bad and then have to urinate.

Hi! Thank you for sharing your story! Just an idea, maybe its the car? When I first got sick they thought I might have carbon monoxide poisoning.

I wish I could help too but I am not a fainter. You keep on waking up though sister!

I sure get them!

Alcohol used to stop my fast hr in the beginning. Now, I just flush tremendously and get even worse. It probably is calming down your nerves-- so to speak I'm with katybug on the pina colada!

This sounds to me like your immune system is going wacky. The rash is inflammation, and the fever is also an immunorespone. If your wbc count is low though, that wouldn't make a lot of sense. I know this sounds terrible and I pray to god it is not the case, but you might want to get tested for hiv and leukemia. It also could just be the eds attacking your white blood cells. I would think that the low white blood cell count has a lot to do with whatever it is that is going on. Here is a list of causes http://www.mayoclinic.com/health/low-white-blood-cell-count/MY00162/DSECTION=causes Also I am curious, did the motrin help the rash? I hope you feel better and that this resolves itself. Being sick, especially with a fever is never fun.

High elevation causes the body to increase blood volume i went to Denver though and it took me a few days to adjust. I got pots within 2 months of coming back from my trip in Denver.

I think we potsies should carry this article into the e.r. with us

Sometimes when my arms or legs go numb, I hang them off the bed to get some blood in them. The numbness usually goes away within 30-40 seconds.

I am going through a stage where I'm not sleeping either. It is strange because like Jen, I also am feeling surprisingly rested.

A review of postural orthostatic tachycardia syndrome Sheila Carew, Margaret O. Connor, John Cooke, Richard Conway, Christine Sheehy, Aine Costelloe, and Declan Lyons* Blood Pressure Unit, Mid Western Regional Hospital, Limerick, Ireland Received 4 July 2008; accepted 4 November 2008 Introduction Postural orthostatic tachycardia syndrome (POTS) is defined as a sustained heart rate increase of 30 bpm or increase of heart rate to 120 bpm within the first 10 min of orthostasis associated with symptoms of orthostatic intolerance1–3 and without significant orthostatic hypotension (OH). Patients with POTS are predominately female (4:1) and relatively young,4,5 but can range in age from 15 to 50 years.6 Differences in muscle sympathetic nerve discharge characteristics, in the setting of sympathetic fibre loss associated with POTS, may contribute to the predisposition to and greater prevalence of POTS in female individuals.7 There are no accurate epidemiological studies, but it is estimated that in the USA alone, there are millions of people affected by POTS.8 Pathophysiology Normal physiology of standing When supine, up to 30% of the blood volume is in the thorax. During orthostasis, 300–800 mL of blood is gravitated downwards from the thorax into the abdomen and lower extremities. Most of this pooling into lower limb veins occurs within 10 s. This causes a decrease in venous return to the right side of the heart with a subsequent reduction in the stroke volume and cardiac output. Arterial baroreceptors (carotid sinuses and the aortic arch) and cardiopulmonary mechanoreceptors (heart and lung) detect a reduction in pulse pressure and stroke volume. Compensatory reflexes lead to increased sympathetic nervous system output (peripheral arteriolar vasoconstriction) and reduced parasympathetic nervous system output (reduced vagal tone to the heart with cardio-acceleration). After orthostasis in normal subjects, there is a 10–15 bpm increase in heart rate, systolic blood pressure remains stable, and diastolic blood pressure usually increases (10 mmHg).9 Postural orthostatic tachycardia syndrome Postural orthostatic tachycardia syndrome is a clinical manifestation of multiple underlying mechanisms. It can be divided into a number of overlapping pathophysiological models as follows. Neuropathic This is thought to be associated with partial dysautonomia. The evidence in support of this is as follows: † Distal anhidrosis of the legs is commonly found on thermoregulatory sweat testing and quantitative sudomotor axon reflex testing (up to 50% of POTS patients).4,10 † Ganglionic acetylcholine receptor antibody is positive in between 10 and 15% of the cases.4,11 † There is a blunted increase in post-ganglionic sympathetic nerve discharge (muscle sympathetic nerve activity).12 This peripheral abnormality might reflect partial dysautonomia. Astronauts returning from prolonged exposure to microgravity often display a form of orthostatic intolerance with features similar to POTS.13 This is felt to be due to abnormal muscle sympathetic nerve activity.14 † It is shown that leg arteriolar vasoconstriction is impaired. Therefore, increased arterial inflow can enhance venous filling and cause venous pooling, despite the fact that venous capacitance is normal.

Found this in my research, thought i would share. Sorry about the vertical text, its from a pdf Experimental induction of panic-like symptoms in patients with postural tachycardia syndrome Khurana, Ramesh K . Clinical Autonomic Research 16. 6 (Dec 2006): 371-7. Abstract Patients with postural tachycardia syndrome (POTS) might be misdiagnosed with panic disorder due to shared clinical features. The first aim of our study was to investigate the relationship between symptoms of POTS and panic disorder. The second aim was to delineate clinical features distinguishing symptoms of POTS from panic disorder. A total of 11 patients with POTS and 11 control subjects participated in an IRBapproved, prospective, placebocontrolled study. The experimentally induced panic-like symptoms of POTS were systematically studied using the Acute Panic Inventory (API) questionnaire. The participants answered the questionnaire after each placebo infusion and after each of the three provoking stimuli: head-up tilt test (HUT), isoproterenol infusion (ISI), and sodium lactate infusion (SLI). API responses were summed for each subject at each time point of administration. Individual API symptoms and summed responses were analyzed for statistical significance. All patients with POTS developed symptoms of orthostatic intolerance during HUT. Pharmacologically induced symptoms subjectively mimicked spontaneous symptoms in 5 of 11 patients during ISI and in none of 11 patients during SLI. In contrast, API scores in these patients reached panic threshold in 0 of 11 following HUT, in 4 of 11 following ISI and in 4 of 11 following SLI. Individual symptoms analysis revealed that significant increase in scores was limited to the somatic symptoms of palpitations, dyspnea, and twitching or trembling. In conclusion, the symptoms of POTS are phenomenologically different and clinically distinguishable from panic disorder symptoms Discussion The control results in the current study are consistent with previous studies. Balon and colleagues observed the production of panic symptoms in response to ISI in 4 out of 45 (8.9%) normal control subjects [3]. Liebowitz et al. reported the occurrence of SLI-induced panic in 0–25% of control subjects [23]. Similarly, the current study found that no control subjects reached panic thresholds as compared with baseline API in response to any of the three stimuli. The lack of resemblance of SLI-induced symptoms with spontaneous symptoms and a significant API score elevation above baseline after SLI in only 4 of 11 patients suggest that POTS symptoms cannot be equated with panic symptoms. Both ISI and SLI are considered reliable and valid models of panic-induction. SLI produces panic in panic disorder patients with a sensitivity of 0.85 and specificity 0.77, and ISI provokes panic with less sensitivity and more specificity [2]. It is possible that panic-like episodes occurring with pharmacologic stimuli in POTS patients are associated with a subclinical panic disorder [10], although the lack of similarity between the induced and spontaneous episodes militates against it. Goetz and colleagues (1996) used API questionnaires to evaluate subjective ratings and symptoms in panic disorder patients before and during SLI. Controlling for baseline symptoms levels, these investigators found that the symptoms most strongly associated with panic were desire to flee (0.70), fear of losing control (0.57), afraid in general (0.49), and dyspnea (0.48). These psychological symptoms were determined essential for the diagnosis of lactate-induced panic [15]. Balon and colleagues (1990) compared symptom responses to ISI in subjects with and without panic disorder and found that fear of going crazy, fear of dying, and shortness of breath best discriminated between panic and non-panic [3]. In our POTS patients, neither pharmacologic stimulus produced increased API scores in the cognitive psychological symptoms essential to the diagnosis of panic disorder, such as fear of dying, fear in general, and fear of going crazy. Our POTS patients demonstrated a significant increase in palpitations, dyspnea, and twitching or trembling, which are all somatic symptoms. Palpitations were more prominent with ISI, and trembling or twitching was more prominent with SLI. This study, therefore, does not support the phenomenologic equivalence of panic disorder in POTS patients. The current data suggest that, for a majority of POTS patients, panic-like symptoms are phenomenologically unrelated to panic disorder symptoms. Despite clinical similarities that can lead to misdiagnosis, several characteristics may be helpful in distinguishing POTS patients from panic disorder patients. First, a prior history of panic disorder may be absent in POTS patients. Second, panic-like symptoms in POTS patients are precipitated mostly by change to an upright posture. Third, particular panic symptoms such as fear of dying, fear in general, sense of unreality, and feeling detached are infrequently reported. Fourth, physical and psychophysiological symptoms usually cease with recumbency. Fifth, distinct differences in personality patterns exist between these two groups of patients. A psychological assessment using the Minnesota Multiphasic Personality Inventory questionnaire demonstrated that T scores for manifest anxiety were in the normal range in POTS patients [21]. Sixth, sudomotor and other autonomic abnormalities may be demonstrable in these patients [19]. It is not known why patients with POTS present with panic-like symptoms. POTS may act as organic precipitant of these symptoms as previously described in patients with various medical disorders such as hyperthyroidism and hypoglycemia [33]. These patients may be vulnerable based on innate biological factors and anxiety sensitivity index [5, 16]. 375

Hmm thats interesting. I took metoplerol and celexa at the same time and it made me feel like i weighed a million pounds

I feel like the head pressure indicates a more systemic vasoconstriction problem rather than simply poor vasoconstriction in the abdomen or legs. When we bend over, blood starts pooling in our heads, which means to me that the veins in the head also aren't constricting or returning blood properly. We are like sand timers!!!

Vanderbilt in Tennessee is a good one I hear. They are also doing lots of research. I went to mayo in Arizona. Ramakentesh is really well versed in this and could probably tell you all the doctors and their theories!

Sounds similar to shingles

I've heard that after you exercise, blood goes to to muscles to rebuild them. Makes sense to me, considering I don't get bad until after I exercise.

Naomi, I always ask for 2 liters. It seems to do much more than one. The other thing that seems to really help is a slow dispersal rate from the iv. For example 1 liter per hour with 2 liters total. I have to tell them to slow it down all the time because they think it is pointless and are just trying to get me out of there. If they do it quickly, I seem to urinate it all out. Another thing to note is that the first time they gave me saline was in the hospital. Two bags, slowly, before they wheeled me down for a ttt, as per the cardiologists orders. The ttt still showed pots but my blood pressure went up significantly from the laying sitting standing bp they did in my room that morning--my hr dropped from 170 to 130.

I take florinef and also have the shortness of breath. But I also get my potassium checked regularly and its normal .

Just curious, for everyone, what are the changes that happen that make you feel this way as far as taste, touch, smell, hearing, vision? A lot of people are saying surreal, what is it about the scene that is surreal( the speed of the moment, the lighting, the detail, the placement of objects)?