Cerebral autoregulation is preserved in postural tachycardia syndrome

Abstract

autoregulation is preserved in postural tachycardia syndrome. J Appl Physiol 99: 828 -835, 2005. First published April 28, 2005 doi:10.1152/japplphysiol.00225.2005.-To test whether cerebral autoregulation is impaired in patients with postural tachycardia syndrome (POTS), we evaluated 17 healthy control subjects and 27 patients with POTS. Blood pressure, heart rate, and cerebral blood velocity (transcranial Doppler) were recorded at rest and during 80°h ead-up tilt (HUT). Static cerebral autoregulation, as assessed from the change in cerebrovascular resistance during HUT, was the same in POTS and in controls. The properties of dynamic cerebral autoregulation were inferred from transfer gain, coherence, and phase of the relationship between blood pressure and cerebral blood velocity estimated from filtered data segments (0.02-0.8 Hz). Dynamic cerebral autoregulation of patients with POTS did not differ from that of controls. The patients' dynamic cerebral autoregulation did not change over the course of HUT, despite increased tachycardia suggestive of worsening orthostatic stress. Inflation of military anti-shock trouser pants substantially reduced the tachycardia of patients with POTS without affecting cerebral autoregulation. Symptoms of orthostatic intolerance were reduced in one-half of the patients following military anti-shock trouser pants inflation. We conclude that cerebral perfusion and autoregulation in many patients with POTS do not differ from that of normal control subjects. cerebrovascular circulation; Fourier analysis; hemodynamics THE POSTURAL ORTHOSTATIC TACHYCARDIA syndrome (POTS) is a form of orthostatic intolerance that is characterized by symptoms of lightheadedness, fatigue, palpitations, diminished concentration, blurred vision, tremulousness, shortness of breath, nausea, and impaired cognition that mainly occur during upright posture (5,24,31,33). To qualify for the diagnosis of POTS, these symptoms must occur in conjunction with an increase in heart rate (HR) of Ͼ30 beats/min or a HR Ͼ 120 beats/min within the first 5 min of standing (23)(24)(25)31). The HR increase should be sustained and not associated with orthostatic hypotension (46). Many patients have evidence of hypovolemia (16,26) or exaggerated venous pooling with central hypovolemia (32,48). Inflation of military anti-shock trousers (MAST pants), which prevent venous pooling in the legs, usually causes reversal of the tachycardia (49). The pathophysiology of POTS is poorly understood. Various abnormalities have been described, including the presence of an attenuated autonomic neuropathy (25, 43), increased cardiac norepinephrine spillover (19), impaired norepinephrine transporter (45), or reduced vagal cardiac baroreflex sensitivity (14). Some patients may have evidence of increased sympathetic activity while supine (17, 18), whereas others do not (5).Regardless of pathophysiology, all patients with POTS are significantly disabled by the constellation of symptoms noted above (2).Lightheadedness and impaired concentration while ...

Inconsistent detection of changes in cerebral blood volume by near infrared spectroscopy in standard clinical tests

“…In agreement with other studies from the literature (26,27), significant changes in cerebral blood volume are neither detected by THIi nor by tHbi, which is possibly due to the prompt activation of local myogenic and metabolic compensatory mechanisms (25,38).…”

Neuropeptides and peptide hormones in syncope and orthostatic intolerance

“…However, chronic functional disturbances of ANS-CVS control may also occur, leading to long-standing disability. The most widely recognized example of this is the multi-faceted postural orthostatic tachycardia syndrome (POTS), but other less well recognized conditions almost certainly exist [4,5]. On the other hand, not all forms of 'functional' reflex syncope conditions fit neatly into the 'transient' or 'chronic' categories.…”

“…Additionally, uncommon inflammatory conditions, such as GuillanBarré, may merit consideration. In all of these cases, the essential pathophysiology is transient failure of blood pressure control resulting in self-limited cerebral hypo-perfusion that cannot be fully compensated for by cerebrovascular auto-regulation [4].…”

Posturalinės ortostatinės tachikardijos sindromas

“…Simpatinio aktyvumo padidėjimas -daugelis tyrėjų siūlo simpatinio aktyvumo padidėjimą laikyti pagrindiniu POTS etiologijos veiksniu, remdamiesi keletu klinikinių atvejų: padidėjęs arterinis norepinefrino lygis ramybės metu [7,20,22]; sumažėjęs norepinefrino klirensas [20,23]; padidėjęs širdies susitraukimų dažnis pacientams ramybės būsenoje, lyginant su kontroline grupe [6, 20,22]; neadekvatus širdies susitraukimų dažnio atsakas į izoproterenolio infuziją rodo adrenoreceptorių padidėjusį jautrumą [24].…”

“…Kai kurie simptomai rodo galvos smegenų hipoperfuziją, net esant normaliam arteriniam kraujo spaudimui. Tačiau nėra galutinių įrody-mų dėl nenormalios smegenų kraujotakos ar netinkamos smegenų autoreguliacijos pacientams, sergantiems POTS [22,29]. Simptomai gali atsirasti staiga, dažnai po virusinės infekcijos; kitiems jie pasireiškia be pastebimos priežasties [7,13].…”