goldicedance

My guess is this: most of us POTSIES have difficulty taking a shower yet alone a bath. A shower chair is a must. Very warm water is a no-no. I try to finish my shower with a quick splash of much colder water. I also find having a thick terry cloth robe by the shower that I can wrap myself in as well as a big towel for my head. I throw these on after the shower and then plop on the bed to recover--sometimes I even fall asleep. I always have to leave time for this cool dow. As far as hair - long hair would be way to difficult to take care of. Give serious thought to having your hair cut to make things easier on yourself. In the scheme of things, try not to fret about this....things could be alot worse. As far as my life goes, if I had to decide what is worse - POTS or breast cancer survivorship - I would take POTS. The thing with breast cancer, even when you are a survivor, there still lingers in your mind the real possibility that the cancer could return. Lois

M, Sorry you are going to feel rotten. My former (i.e., I moved from Washington and she has since retired) called me this Saturday to see how I was doing. Can you believe that? That's more than virtually any other doctor would do. She retired not only because she wanted to spend more time with her family but she was then experiencing health problems. She had horrible neck pains, headaches, double vison, lightheadedness, and rapid heart rate. It turned out she has a chronic spinal fluid leak. She had a "patch" procedure done in California (she traveled to have it done by this specialist) and is now doing much better. She thinks I should have that checked out. Have you been evaluated for a CSF leak? All that neck surgery makes me think some of that may be going on. Feel better! Lois

Wish you luck at your appointment. I was on Neurontin (gabapentin) from 1995-2005. I slowly increased from a small dose at bedtime to eventually 900/1200/1500. It was prescribed for POTS as well as migraine preventative. Dr. Low at Mayo Rochester confirmed to my internist that large doses of neurotin were needed. In 2005, I switched to Lyrica. My neurologist told me that Lyrica was a "cleaner" drug and that I would not need to keep increasing the dosages of Neurontin. I gained weight from both. Lyrica is really expensive while generic Neurontin - gabapentin - is available and prety cheap. I also have fibromyalgia. I am not sure Lyrica makes a difference in that regard. Lois

Good luck on trying to resolve the problem. Be sure you get the HIDA scan with contrast. I suggest that you check out this site as this topic as come up numerous times. A regular HIDA scan dees not always show a gall bladder as was my case. The scan with contrast did show a great reduction in gb functioning. It also provoked a minor GB pain. The test was not a biggie for me. Lois

AVOID PORT! I had one port in during chemotherapy because my veins were terrible--not only from the chemo but also before the chemo. Always difficut to put in IV during many hospitalizations - even using heat, iv insertion team and pediatric ivs. The risk of infection is too severe with a port! Being a bad stick is generally not a reason!

Mazel tov! Simply fantastic!!!

I'll keep you in my thoughts and wish you complete recovery from your surgery. Be sure you meet with your anethesiiologist before the surgery! That's my only suggestion. BTW - the boots are thes inflatable things that they put on to be sure your legs are pumping and to help prevent blood clot.

Just curious....how many in Potsville have been diagnosed with fibromyaligia? What do you do about/for it? Thanks

Good news! Yeah! You go, Girl!

I first got my pacemaker in 1996 following a sinus node ablation that left me wih bradycardia along with some tachycardia. I then developed junctional tachycardia with which I suffered for about 2 years. I then got an AV node ablation. I have been pacer dependent since 1998. I no longer have that terrible junctional tachycardia. A couple questions: 1 - do you already have 2 leads? when I got my pacer they put in a ventricular lead just in case I would need it down the road. 2 - what brand pacer do you have? I understand that there is a pacer made in Germany (Biotronix) that seems to have some adjustment capability for changes in blood pressure? 3 -how old is your current pacer? if you do not have the ventricular lead, can they add it or do you need to get a new generator? If so, inquire about the Biotronix. Email me if you would like to talk! Good luck, Lois

Suggestion: see about getting your name on the waiting list; in the meanwhile, you can explore other options. Have you though about Mayo JAX? Good luck. Lis

Hi..... I think that your doctor is talking about doing a sinus node ablation and the pacer because,chances are, you will develop bradycardia. If, in fact you have POTS, a sinus node ablation is not a good idea. Chances are if you go that route you may need an AV node ablation as a result of junctional tachycardia. You would then be pacer dependent. That is the route I went down before I was diagnosed with POTS over a decade ago. If you decide to go the pacer route,I would strongly suggest that you be sure they put dual leads in (just in case) as well as explore a pacer made by Biotronix. Let us know how you are doing. Don't be a lurker! Welcome aboard. ois

Beta blockers can sometimes exacerbate asthma! I have asthma and take Labetalol and have had no problems. Lois

This was very interesting. Early on the road to figuring out my problem (back in 1994) my doctor did test me for heavy metal. I would be a little cautious since the doctor doing this research also owns the company that makes the test....posible conflict? It would be interesting if several of us ordered the kit and see what happens.

Hi, Nancy. Check out the article I posted a few weeks ago in which a dentist from University of Maryland Dental School wrote: "Postural orthostatic tachycardia syndrom: Dental treatment considerations." I have since found out that he got his interest in POTS from treating one patient. He decided to look into the literature. I was actually surprised that no one commented on this article. Lois

Childhood symptoms interesting: I could never climb a rope or use those rings. Out of fright!!!!! And, weakness! lol

My astute physician about 8 years ago called to say that this crossed her mind. I was tested, but negative. Lois

Several times (different periods) I had to use my STD benefits. I probably have some language I used as well as additional information. Please message me with specific questions as well as your insurance carrier. I too had an insurance carrier known for their denials. However, I was well armed - included personal information as well as some articles by Dr. Grubb and the Dysautonomia prepared by NIH on the DRF website. I was awarded benefits on my initial application. In fact, there were some provisions providing return to work attempts. Good luck. Don't give up. Remember that you probably know more than the analyst working your claim. Lois

Good luck on your test. For me: HIDA nothing; HIDA with CKK gall bladder attack on table. Why doctors don't order the HIDA CKK the first time is amazing....I guess it is just another example of our health care problems

I take Procrit, but at a very low dose - 10,000 units every 30 days. I can get the injection only if my hematocrit is below 13. I get the Procrit at the Oncologoy Department at Mayo Clinic Jacksonville where I am followed by a hemotologist. This doctor told me that they have virtually discontinued use of Procrit and Aranesp in cancer patients without metastatis. They are concerned about the risk of blood clots coupled with the risk of stimulating cell growth. After having been told and having read the risks, I have decided to move ahead with these injections. The frequency and quantity of the injection is monthly, rather than weekly, and at a much lesser amount. I think it is important for people taking Procrit to be followed by Oncology/Hematology to help avoid untoward events. Lois

You and your family are in my thoughts. I join with the others here in offering condolences as well as hope as you continue your journey in the U.S. Lois

Good for Dr. Rowe. When I first got sick in 1994, my internist pulmonologist investigate many possible causes, including LYME. I even tried IV Rocephin. Good luck to Mack. I take Provigil and find it quite helpful. Lois

I wasn't sure what box to tick. I tried Florinef and under no condition would I take it again. It not only raised by blood pressure too much but it gave me migraine headaches for which I needed hospitalization for several days. When I was taking it, it did help. It was only after a few months that the blood pressure spikes and migraines occured. Frankly, I would give it a try. Why not try it and see what happens? It becomes very difficult to treat POTS if you are not willing to try different drugs and approaches. What works for someone may not work for someone else. Good luck! Lois

I came across this article and thought it would be useful to us POTSIES and our dentists. Perhaps it should also be included in the reference section (excuse me if it already is). I know it is long but I think it is really good. HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS QUICK SEARCH: [advanced] Author: Keyword(s): Year: Vol: Page: -------------------------------------------------------------------------------- J Am Dent Assoc, Vol 137, No 4, 488-493. ? 2006 American Dental Association This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Brooks, J. K. Articles by Francis, L. A.P. Search for Related Content PubMed PubMed Citation Articles by Brooks, J. K. Articles by Francis, L. A.P. Related Collections Practice Management -------------------------------------------------------------------------------- CLINICAL PRACTICE JADA Continuing Education Postural orthostatic tachycardia syndrome Dental treatment considerations John K. Brooks, DDS and Laurie A.P. Francis, RDH ABSTRACT TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES Background. Postural orthostatic tachycardia syndrome (POTS) is a chronic, relatively common autonomic disorder typically affecting younger females. It is distinguished by a dramatic increase in heart rate on the assumption of an upright posture from the supine position. Methods. The authors provide an overview of the demographics, clinical assessment, diagnostic features, differential diagnoses, pathogeneses and medical treatment of patients with POTS, with an emphasis on the clinical treatment of the dental patient affected by the syndrome. Conclusion. Patients frequently exhibit symptoms of lightheadedness, fatigue, palpitations and syncope. Patients with POTS may have Ehlers-Danlos syndrome, mitral valve prolapse, chronic fatigue syndrome or, rarely, the Brugada syndrome. Despite widespread dissemination of information regarding POTS in the medical literature, scant information on it has appeared in dental publications. Practice Implications. Dentists need to be familiar with the clinical features of POTS and be prepared to treat patients at risk of developing syncope. Key Words: Postural orthostatic tachycardia syndrome; autonomic disorder; dental treatment Orthostatic intolerance (OI) refers to a heterogeneous group of disorders of hemodynamic disturbances, characterized by insufficient cerebral perfusion on standing upright or tilting the head upward.1 A common form of OI is orthostatic hypotension, the aberrant physiological response to body position in which patients typically experience a pronounced decline in blood pressure on assuming an upright position. A subset of affected patients may have postural orthostatic tachycardia syndrome (POTS), which is defined as disproportionate increases in cardiac rate of 30 beats per minute within five minutes of moving from a supine to an elevated position, accompanied by at least three orthostatic symptoms.2,3 A prerequisite for a diagnosis of POTS is that patients must be symptomatic for more than three months.4 At times, extreme fluctuations of heart rate are evident, and the rate may accelerate to at least 170 bpm within minutes of elevating from a supine position. Systolic and diastolic blood pressure may suddenly attain dangerously high levels and vacillate greatly, while some patients experience hypotensive episodes and others maintain minimal changes in blood pressure. POTS has been referred to by various names, including neurocirculatory asthenia, mitral valve prolapse (MVP) syndrome, irritable heart, soldier?s heart, idiopathic orthostatic intolerance, orthostatic tachycardia syndrome, postural tachycardia syndrome, hyperadrenergic orthostatic tachycardia and hyperadrenergic orthostatic hypotension. Clinicians have estimated that this syndrome may affect at least 500,000 to 1 million Americans.3,5 There is a decisive 4-6:1 female predilection, with a mean age of 29 years and an age range from 15 to 50 years.4,6 Although numerous articles have been written about POTS, minimal information is available in the dental literature. CLINICAL FEATURES TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES Patients diagnosed with POTS exhibit a myriad of clinical manifestations4,7,8 (Table). Orthostatic symptoms that may occur in at least 75 percent of patients are light-headedness/dizziness, fatigue/weakness, palpitations, exercise intolerance, tremulousness, photosensitivity, shortness of breath and disequilibrium.4,7,8 Awareness of orthostatic symptoms is significant because they may herald the commencement of syncope or near syncope. Fifty-six percent of subjects, in fact, experience syncope.7 View this table: [in this window] [in a new window] TABLE Orthostatic symptoms associated with postural orthostatic tachycardia syndrome.* Patients also may report experiencing chest discomfort, hyperventilation, chills, sleep disruption, reduced vitality, generalized aching, numbing or tingling sensations, dysphagia, frequent urination and lapses of mental acuity.6,7,9 About one-third of affected patients report suffering migraine headaches.10,11 Various gastrointestinal disturbances associated with POTS are diarrhea (75 percent of patients), bloating (72 percent), abdominal cramps (62 percent), constipation (50 percent), early satiety (46 percent) and vomiting (25 percent), and these constitutional changes are more apparent after meals.4 Secretomotor symptoms noted are heat intolerance (58 percent), dry eyes (38 percent) and xerostomia (38 percent).4 Jacob and colleagues7 reported post-prandial flushing in 44 percent of patients. In addition, peripheral appendages may be painful and exhibit pallor, redness, coldness or diaphoresis. Some women may experience cyclic episodes of POTS, often associated with menstruation, leading to fluid loss and weight fluctuations of up to 5 pounds.6 Nearly three-fourths of patients report experiencing flare-ups at random times of the day, while others may become symptomatic with sustained standing, exertion, stress and heat exposure.4 It is of note that some women may become asymptomatic after pregnancy.3 DIAGNOSIS TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES Paramount to establishing an accurate diagnosis of POTS is taking a comprehensive medical history and conducting a thorough physical examination, including a cardiovascular, pulmonary and neurological examination, detailing signs and symptoms specifically with regard to frequency of symptoms and stimuli induction. The box provides a summary of the diagnostic features of POTS. View this table: [in this window] [in a new window] BOX Diagnostic features of postural orthostatic tachycardia syndrome. Head-up tilt-table testing is the main method of evaluating OI. After the patient assumes a supine position in the apparatus, the clinician records his or her baseline blood pressure and heart rate. The clinician then varies the table angulation, usually by 30 and 60 degrees. After administering various drugs, he or she then repeats the blood pressure and heart rate evaluations.12,13 Infusion of isoproterenol, a ?-adrenergic agonist, may immediately provoke exaggerated feelings of cardiac awareness or emotional distress; reversal of these affectations is achieved with administration of propranolol, a ?-adrenergic receptor antagonist.14 Additional assessment of autonomic function may reveal decreased sweat output in the extremities following a thermoregulatory sweat test. Electrocardiographic studies. The results of electrocardiographic studies usually are normal, with the exception of the detection of sinus tachycardia with 24-hour Holter monitoring. The results of echocardiographic investigations otherwise are normal, although 46 to 50 percent of patients with POTS may have MVP with detectable valvular pathosis.7,15,16 Differential diagnosis. Although the development of tachycardia on assuming an upright position is a fundamental diagnostic criterion for POTS, the differential diagnosis is diverse and may involve considerable phenotypic overlap. Orthostatic hypotension is distinguished by a decrease in systolic blood pressure of at least 30 millimeters of mercury or a decrease in diastolic blood pressure of at least 20 mm Hg, without significant alteration of heart rate.10 Neurally mediated (vasovagal) syncope is the result of reflex bradycardia and hypotension, triggered by anxiety, shock, overexertion, aortic stenosis, various drugs and alcohol consumption.17 Chronic fatigue syndrome is noted for its imposing periods of physical and mental exhaustion and headaches; however, a subset of patients may have POTS concurrently.18 MVP may precipitate fatigue, palpitations, chest pain and orthostatic symptoms. Patients with multiple system atrophy and pure autonomic failure exhibit declines in blood pressure in response to exercise. Panic attacks may initiate episodes of hyperventilation comparable to the response to reduced cerebral blood flow apparent in patients with POTS. The Brugada syndrome, a form of right bundle branch block, is noted for the onset of near syncope, palpitations and potentially lethal ventricular tachydysrhythmia, and it may be distinguished from POTS by the electrocardiographic findings and results of pharmacologic provocation with pilsicainide.19 Finally, 75 percent of patients diagnosed with the Ehlers-Danlos syndrome (EDS) manifest symptoms of OI, 58 percent of which are attributable to POTS.20 Establishment of an accurate diagnosis of POTS often is preceded by a protracted sequence of referrals to various medical disciplines, including psychiatry. PATHOGENESIS TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES The pathogenesis of POTS is complex and multi-factorial. Autonomic dysfunction may account for one-half to two-thirds of cases, resulting from reflex parasympathetic withdrawal concomitant with sympathetic stimulation.6,21 In an otherwise healthy person, the gravitational effect on achieving an upright posture produces a sudden reduction in venous return of at least 700 milliliters, which is detected by baroreceptors in the lower extremities. This mediates a central nervous system reflex feedback mechanism that promotes a compensatory norepinephrine discharge from cardiovascular postganglionic axons, thereby maintaining control of arterial pressure without any symptoms.22,23 Patients with POTS, however, exhibit sympathetic denervation of the legs and manifest exaggerated responses to baroreceptor challenges, leading to vasomotor debility. Thus, prolonged standing may result in marked venous pooling from the thorax into the splanchnic bed and lower extremities, with a vast decline in pulse pressure, often leading to cyanotic skin and swelling.24 Hence, insufficient venous return enhances sympathovagal activity, with compensatory cardiac acceleration and blood pressure lability. Another pathophysiological mechanism associated with POTS is ?-adrenergic hyperresponsiveness, with substantial elevations of plasma norepinephrine levels, implicated by such symptoms as tachycardia, palpitations, anxiety and tremulousness on achieving an upright posture.7 A familial predisposition is a salient feature of POTS and is found in at least one-fourth of affected patients.4,25 Other studies have pointed to hypovolemia as an underlying cause of POTS.22,26,27 Interestingly, in approximately 50 percent of cases, the onset of POTS may have been triggered by an antecedent infection, presumably postviral.4,21 In select cases, an autoimmune-mediated process has led to the production of autoantibodies to ganglionic acetylcholine receptors and facilitates autonomic neuropathy.28 Singer and colleagues29 reported a demonstration of an intrinsic sinus node abnormality in a subpopulation of patients with POTS. MEDICAL TREATMENT TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES Treatment of POTS requires a multidisciplinary approach entailing pharmacologic, kinesiologic and dietary strategies correlating to the prevailing clinical deficits. Orthostatic hypotension resulting from peripheral adrenergic failure may be ameliorated with various -adrenergic agonists, such as fludrocortisone, midodrine, clonidine, -methyldopa or phenylpropanolamine.1,15,30 These sympathomimetics and other pressor agents, including ergotamine, dihydroergotamine and octreotide, may promote vasoconstriction in the extremities and splanchnic bed, thereby reducing venous pooling.27 Patients who wear elastic support hose may experience an improvement in venous return.16 In addition, cardiovascular deconditioning through elevation of the patient?s bed (a head-up bed) and physical countermeasures, such as flexing and relaxing the muscles in the extremities, may be beneficial.1,6 A regular mild exercise regimen is expressly advised.1 Tachycardia that occurs in response to ?-receptor supersensitivity may be treated with the ?-adrenergic antagonists propranolol, metroprolol or nadolol,6,31 although their effectiveness has been challenged.1 However, practitioners must consider carefully the appropriateness of using ?-blockers to treat patients who also are affected with mast cell activation disorders.30 When hypovolemia is an etiological factor, patients can maintain homeostasis with ample hydration, high dietary salt intake and use of sodium chloride tablets (in dosages ranging from 10 to 20 grams daily).6,22 Recombinant erythropoietin may improve intravascular volume by increasing the erythrocyte count,32 although its efficacy has been questioned.33 Patients also should avoid ingesting substances that may affect blood pressure, including nitrates, garlic and ginseng, and they should restrict intake of coffee, tea and alcohol. The clinical course of POTS usually is self-limited, with repeated instances of remission and relapse. In an 18-month follow-up study, 80 percent of affected patients reported experiencing clinical improvement, yet only 60 percent regained normal or near-normal functionality (that is, daily activities).4 In severely affected patients, the impaired quality of life may result in undesirable psychosocial consequences, including the inability to work and possible depression.34 DENTAL TREATMENT TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES When treating a patient with a history of POTS, the dentist should assess his or her blood pressure and heart rate before administering local anesthetic, particularly one containing the vasoconstrictor epinephrine or levonordefrin. Judicious use of local anesthetic is essential for patients whose cardiovascular status is not well-maintained, because excessive dosing may promote a pressor response and perhaps initiate a myocardial ischemic event or dysrhythmia.35,36 Nevertheless, inadequate anesthesia may promote endogenous release of epinephrine and risk untoward cardiac events in affected patients who may develop tachycardia or elevated blood pressure at the dental visit. Frequent aspiration during nerve blocks and infiltrations and minimal use of intraligamentary injections will diminish inadvertent intravenous deposition of local anesthetic and possible untoward clinical responses.37 In addition, clinicians should avoid using retraction cord impregnated with epinephrine and select only non?epinephrine-based hemostatic solutions to control localized bleeding. Surgical procedures. Oral and maxillofacial surgical procedures require several modifications. Potential hemodynamic fluctuation during administration of general anesthetic warrants electrocardiographic monitoring and vigilant checking of vital signs. Clinicians can maintain the patient?s blood pressure and heart rate with isoflurane titration and improve vascular tone by administering low doses of phenylephrine. Blood expanders, such as crystalloid, also should be on hand during surgical procedures.38 Postoperative care. Postoperative care should consist of measures to lessen OI, such as providing adequate analgesics to limit the vasopressor response, advising patients to increase fluid levels to avoid dehydration and urging patients to promptly resume their routine physical activities. Because of the potential for impaired mental concentration in patients with POTS, clinicians should provide surgical patients with written postoperative instructions on discharge. Approximately 15 percent of patients with POTS report having drug allergies; consequently, clinicians must conduct a careful pharmacological review before prescribing medications.39 EDS and POTS. Several dental concerns arise when treating patients who have both EDS and POTS. The intrinsic collagen defects associated with EDS may lead to severe, refractory periodontitis. Oral surgical procedures may be complicated by the inherent capillary fragility, which increases the risk of bleeding. Postsurgical hemorrhage may be significant and require the administration of hemostatic agents, such as desmopressin.40 Spontaneous rupture of medium and large blood vessels in the cranium, bowel and gravid uterus is of great concern for patients with EDS subtypes IV and VI.41,42 Ecchymosis formation often is seen after surgery and is induced simply by minor trauma. Delayed wound healing may be apparent, and the increased friability of the mucosa requires that sutures remain in place two to three times longer than usual.43 Hyperextensibility of the joints may lead to recurrent subluxation of the temporomandibular joint and potentiate the need for surgical intervention.44,45 Orthodontic treatment may lead to rapid tooth movement and increased mobility, typically requiring longer retention on completion of the case.46 Antibiotic prophylaxis. In light of the finding that approximately one-half of patients with POTS are diagnosed with MVP,7,15 clinicians must ascertain the need for antibiotic prophylaxis for prevention of bacterial endocarditis in conjunction with invasive dental procedures. The dentist should consult with the patient?s physician to determine valvular incompetency and to obtain the results of echocardiographic studies. If cardiac assessment has revealed significant cardiac regurgitation, the patient must comply strictly with the antibiotic regimen for prevention of endocarditis established by the American Heart Association.47 Fatigue is a predominant feature of POTS and often is associated with chronic fatigue syndrome.48 It may influence adherence to a satisfactory oral hygiene regimen. For these patients, it may be prudent for the dentist to consider more frequent recall appointments. To facilitate tolerance of dental treatment and reduce fatigue, dental offices should schedule patients for shorter, morning procedures and advise them to eat only a small breakfast. Orthostatic intolerance may be minimized with earlier appointments, when ambient temperatures usually are lower. Sleep disturbances commonly affect patients with POTS, and use of hypnotic agents the night before the dental appointment may be advantageous. Patients who feel refreshed are more likely to have improved coping mechanisms. Another vexing problem is the prevalence of xerostomia, which poses a fundamental risk of developing caries, candidiasis and burning mouth syndrome. Successful treatment outcomes may dictate the use of various sialologues and fluoride supplements (including rinses, gels and possibly custom fluoride trays). A heightened perception of anxiety is another clinical finding in patients with POTS, and it may become more pronounced among patients with inherent fears of dental procedures. In these situations, clinicians should consider pre-medication with oral anxiolytics. Because a majority of patients experience photosensitivity8 and may be bothered by the bright overhead light used in the dental operatory, we suggest that they wear darkened eyewear. Patients with POTS are at an increased risk of developing syncope with prolonged standing. Accordingly, it is preferable for them to complete any insurance forms while sitting. When patients are called to the dental operatory, a team member should make an effort to escort them and ensure that they stand up gradually from the seated position. Likewise, at the completion of the dental procedure, a team member should slowly return the supine patient to an upright position and ensure that he or she stands gradually. The dentist must recognize the onset of a syncopal episode and intervene promptly. He or she should place the patient in a completely recumbent position or elevate the patient?s legs slightly above the level of the heart. The dentist or a team member can place a cool, moistened cloth on the patient?s forehead and use aromatic ammonia, which may stimulate a return of consciousness. The dentist should contact the patient?s physician immediately and ask him or her if the patient should make an appointment for reassessment. Any patient who has experienced loss of consciousness or an altered state of alertness should not leave the dental facility unescorted and transportation must be provided. CONCLUSION TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES Dental health care providers should be familiar with the clinical features of POTS and formulate appropriate treatment planning protocols to minimize exacerbation of the patient?s underlying hemodynamic disorder. The medical history should specifically address the signs and symptoms of OI and ascertain whether the patient has various associated conditions, such as EDS, MVP, chronic fatigue syndrome or Brugada syndrome. Routine monitoring of blood pressure and heart rate before and at the end of dental procedures is warranted. Dentists need to be prepared to treat patients at risk of developing syncope. FOOTNOTES Dr. Brooks is a clinical professor, Department of Diagnostic Sciences and Pathology, Baltimore College of Dental Surgery, Dental School, University of Maryland, 666 W. Baltimore St., Baltimore, Md. 21201, e-mail "Oralpath5@aol.com". Address reprint requests to Dr. Brooks. Ms. Francis is in private practice, Mt. Airy, Md. REFERENCES TOP ABSTRACT CLINICAL FEATURES DIAGNOSIS PATHOGENESIS MEDICAL TREATMENT DENTAL TREATMENT CONCLUSION REFERENCES Jacob G, Biaggioni I. Idiopathic orthostatic intolerance and postural tachycardia syndromes. Am J Med Sci 1999;317(2):88?101.[Medline] Novak V, Novak P, Opfer-Gehrking TL, O?Brien PC, Low PA. Clinical and laboratory indices that enhance the diagnosis of postural tachycardia syndrome. Mayo Clin Proc 1998;73:1141?50.[Abstract] Stewart JM. Chronic orthostatic intolerance and the postural tachycardia syndrome (POTS). J Pediatr 2004;145:725?30.[Medline] Sandroni P, Opfer-Gehrking TL, McPhee BR, Low PA. Postural tachycardia syndrome: clinical features and follow-up study. Mayo Clin Proc 1999;74:1106?10.[Abstract] Robertson D. The epidemic of orthostatic tachycardia and orthostatic intolerance. Am J Med Sci 1999;317(2):75?7.[Medline] Low PA, Opfer-Gehrking TL, Textor SC, et al. Postural tachycardia syndrome (POTS). Neurology 1995;45(supplement 5):S19?25.[Medline] Jacob G, Costa F, Shannon JR, et al. The neuropathic postural tachycardia syndrome. N Engl J Med 2000;343:1008?14.[Abstract/Free Full Text] Bonyhay I, Freeman R. Sympathetic nerve activity in response to hypotensive stress in the postural tachycardia syndrome. Circulation 2004;110:3193?8.[Abstract/Free Full Text] Karas B, Grubb BP, Boehm K, Kip K. The postural orthostatic tachycardia syndrome: a potentially treatable cause of chronic fatigue, exercise intolerance, and cognitive impairment in adolescents. Pacing Clin Electrophysiol 2000;23:344?51.[Medline] Low PA, Opfer-Gehrking TL, Textor SC, et al. Comparison of the postural tachycardia syndrome (POTS) with orthostatic hypotension due to autonomic failure. J Auton Nerv Syst 1994;50(2):181?8.[Medline] Mokri B, Low PA. Orthostatic headaches without CSF leak in postural tachycardia syndrome. Neurology 2003;61:980?2.[Abstract/Free Full Text] Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for assessing syncope. American College of Cardiology. J Am Coll Cardiol 1996;28:263?75.[Medline] Grubb BP, Kosinski DJ, Boehm K, Kip K. The postural orthostatic tachycardia syndrome: a neurocardiogenic variant identified during head-up tilt table testing. Pacing Clin Electrophysiol 1997;20:2205?12.[Medline] Frohlich ED, Tarazi RC, Dustan HP. Hyperdynamic ?-adrenergic circulatory state: increased ?-receptor responsiveness. Arch Intern Med 1969;123(1):1?7.[Abstract/Free Full Text] Jacob G, Shannon JR, Black B, et al. Effects of volume loading and pressor agents in idiopathic orthostatic tachycardia. 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