orthostatic intolerance is defined by the inability to remain upright without severe signs and symptoms such as hypotension , tachycardia , lightheadedness , pallor , fatigue , weakness , and nausea . orthostatic intolerance appears in many guises including overt dysautonomia , vasovagal syncope , and orthostatic tachycardia ( 1 ) . pots is operationally defined by the presence of symptoms of orthostatic intolerance associated with an increase in sinus heart rate of > 30 beats / min or to a rate of > 120 beats / min during the first 10 min of head up tilt table testing ( 2 ) . we report a case of pots in which we analyze sympathovagal balance during head up tilt testing ( hutt ) . a 36 year old man was referred to our hospital because of palpitations and lypotimia . he experienced presyncope on several occasions in the morning while waking up and when suddenly standing up from a sitting position , but syncope never developed . when he came to our observation , his body weight was 95 kg and his height was 170 cm . ecg showed sinus rhythm of 95 beats / minute without any conduction abnormalities or st - t changes . , atrio - ventricolar slow - fast node re - entry tachycardia was initially suspected . blood pressure was continuously monitored with an arterial tonometer ( sure sign v1 electronics , philips ) placed on the left radial artery , calibrated against oscillometric sphygmomanometer pressure . a continuous electrocardiographic recorder ( holter monitor ela medical synetec ) was also attached for rhythm verification . after resting for 10 min in the supine position , he was positioned upright at an angle of 80 degrees on a tilt table with a footboard for weight bearing . his heart rhythm ( hr ) was 85 beats / min and blood pressure was 130/80 mmhg in the supine position . after 3 min of the tilting , his hr abruptly increased to 150 beats / min and he began to complain of lightheadedness and weakness , but hypotension did not develop . at the end of the passive tilt test for 45 min , he had not experienced syncope or marked hypotension and when he was returned to the supine position , hr quickly went back to normal as it was at the beginning of the test . to analyze the patient s sympathovagal balance during the head - up tilt testing , power spectral analysis of hr variability was performed using the ela medical synetec version 1.10 monitoring system . spectral indices of hr variability were computed by fast fourier analysis for each 2-min interval with 1-min overlap during the passive tilt test . the power spectrum was calculated as high frequency ( hf , 0.150.40 hz ) , low frequency ( lf , 0.050.15 hz ) , and as the ratio of lf to hf power ( lf / hf ) . the changes in hf and lf / hf during the tilt test are shown in figure 1 . 1- changes in high - frequency ( hf ) power and in the ratio of low - frequency ( lf ) to hf power ( lf / hf ) during the passive tilt testing . 
  - changes in high - frequency ( hf ) power and in the ratio of low - frequency ( lf ) to hf power ( lf / hf ) during the passive tilt testing . the lf / hf tended to fluctuate , but it reached a higher level after 25 min of tilting when the patient began to experience symptoms of orthostatic intolerance . we suggested losing weight and increasing fluid intake about every three hours in the day . pots has been described at least since 1940 and usually defined as the development of orthostatic symptoms associated with at least a 30 beat / minute increase in hr or a hr of = />120 beats/ minute , that occurs within the first 10 minutes of standing on upright tilt without orthostatic hypotension ( 2 ) . hutt is the pots diagnosis gold standard ; it is also useful to differentiate diagnosis between pots and neurally mediated syncope ( 3 , 4 ) . in this case report we studied dynamic changes in hr variability during tilt testing in a patient with pots , to understand its physiopathological mechanism . in the present case , lf / hf increased in parallel with the development of orthostatic intolerance without any changes in the hf value . the suggested physiopathologic mechanisms included hypovolemia ( 5 ) , excessive venous pooling while standing ( 6 ) , loss of adequate vascular tone in the lower extremities and beta adrenergic hypersensitivity of cardiac receptors without appropriate baroreflex attenuation ( 7 ) . recently , an increased noradrenergic tone at rest and a blunted postganglionic sympathetic response to standing with compensatory cardiac sympathetic overactivity has been proposed ( 8) . recent genetic studies have demonstrated that a defective gene causes a dysfunction in a norepinephrine transporter protein , producing excessive serum norepinephrine levels . impairment of synaptic norepinephrine clearance could produce a state of excessive sympathetic activation in response to physiologic stimuli ( 9 ) . according to schondorf et al attenuated post - viral panautonomic neuropathy could also be another cause of dysautonomia ( 10 ) . although no previous viral illness was identified in our patient , beta - receptor hypersensitivity may have played an important role in his orthostatic intolerance because this symptom was alleviated by beta - blocker therapy . tilt table testing is useful as a standardized measure of response to postural change in patients with dysautonomic alterations ( 4 ) . in our patient , pots diagnosis before hutt was not easy because the orthostatic intolerance symptoms were compatible with neurally mediated syncope . although there is considerable overlap in the symptoms between pots and neurally mediated syncope , pots symptoms ( blunted postural tachycardia , disabling fatigue , light - headedness , dizziness ) are never associated with significant blood pressure changes in contrast with neurological syncope patients , in whom hypotension is usually present ; this may be due to different degrees of reflex neural inhibition ( 11 ) . in pots , the tachycardia induces a partial and selective reflex inhibition of muscle sympathetic nerve activity , blood pressure is maintained by the faster hr . in neurally mediated syncope , postural change may elicit a stronger neural inhibitory reflex that causes hypotension and bradycardia . for pots patients management it is important to change daily life style , to lose weight , to do mild aerobic exercises , to avoid alcohol excess , dyhydration and prevent hypovolemia while increasing fluid intake , and sleeping with the bed head slightly elevated ( 12 ) . our patient needed pharmacologic therapy with atenolol 100 mg every morning ; his symptoms improved in about thirty days . this case report underlines the usefulness of the head - up tilt testing in differentiating pots from neurally mediated syncope in a patient with orthostatic intolerance . the hrv measure during hutt in a patient with pots studies sympathovagal balance . this analysis confirms in our patient a strongly activated sympathetic tone during a passive tilt with concomitant development of orthostatic intolerance .
the authors present a case of 36 year old male patient with idiopathic postural orthostatic tachycardia syndrome ( pots ) diagnosed during head - up tilt testing . 
 power spectral analysis of heart rate variability ( hrv ) during the tilt test revealed that the ratio of low and high frequency powers ( lf / hf ) increased with the onset of orthostatic intolerance . 
 this analysis confirmed in our patient a strong activation in sympathetic tone .