Excessive Heart Rate Response to Orthostatic Stress in Postural Tachycardia Syndrome is not Caused by Anxiety.

2007 ◽  
Vol 18 (2) ◽  
pp. 31-32
Author(s):  
S Masuki ◽  
J H Eisenach ◽  
C P Johnson
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Orthostatic Stress ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia

Excessive heart rate response to orthostatic stress in postural tachycardia syndrome is not caused by anxiety

2007 ◽  
Vol 102 (3) ◽  
pp. 896-903 ◽  
Author(s):  
Shizue Masuki ◽  
John H. Eisenach ◽  
Christopher P. Johnson ◽  
Niki M. Dietz ◽  
Lisa M. Benrud-Larson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mental Stress ◽  
Heart Rate Response ◽  
Lower Body Negative Pressure ◽  
Orthostatic Stress ◽  
Postural Tachycardia Syndrome ◽  
Lower Body ◽  
Venous Pooling ◽  
Postural Tachycardia ◽  
The Relationship

Postural tachycardia syndrome (POTS) is characterized by excessive increases in heart rate (HR) without hypotension during orthostasis. The relationship between the tachycardia and anxiety is uncertain. Therefore, we tested whether the HR response to orthostatic stress in POTS is primarily related to psychological factors. POTS patients ( n = 14) and healthy controls ( n = 10) underwent graded venous pooling with lower body negative pressure (LBNP) to −40 mmHg while wearing deflated antishock trousers. “Sham” venous pooling was performed by 1) trouser inflation to 5 mmHg during LBNP and 2) vacuum pump activation without LBNP. HR responses to mental stress were also measured in both groups, and a questionnaire was used to measure psychological parameters. During LBNP, HR in POTS patients increased 39 ± 5 beats/min vs. 19 ± 3 beats/min in control subjects at −40 mmHg ( P < 0.01). LBNP with trouser inflation markedly blunted the HR responses in the patients (9 ± 2 beats/min) and controls (2 ± 1 beats/min), and there was no HR increase during vacuum application without LBNP in either group. HR responses during mental stress were not different in the patients and controls (18 ± 2 vs. 19 ± 1 beats/min; P > 0.6). Anxiety, somatic vigilance, and catastrophic cognitions were significantly higher in the patients ( P < 0.05), but they were not related to the HR responses during LBNP or mental stress ( P > 0.1). These results suggest that the HR response to orthostatic stress in POTS patients is not caused by anxiety but that it is a physiological response that maintains arterial pressure during venous pooling.

scholarly journals Autonomic dysfunction in post-COVID patients with and witfhout neurological symptoms: a prospective multidomain observational study

2021 ◽  
Author(s):  
Alex Buoite Stella ◽  
Giovanni Furlanis ◽  
Nicolò Arjuna Frezza ◽  
Romina Valentinotti ◽  
Milos Ajcevic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Orthostatic Intolerance ◽  
Neurological Symptoms ◽  
Postural Tachycardia Syndrome ◽  
Symptom Scale ◽  
Autonomic Symptom ◽  
Postural Tachycardia ◽  
Ambulatory Services

AbstractThe autonomic nervous system (ANS) can be affected by COVID-19, and dysautonomia may be a possible complication in post-COVID individuals. Orthostatic hypotension (OH) and postural tachycardia syndrome (POTS) have been suggested to be common after SARS-CoV-2 infection, but other components of ANS function may be also impaired. The Composite Autonomic Symptom Scale 31 (COMPASS-31) questionnaire is a simple and validated tool to assess dysautonomic symptoms. The aim of the present study was to administer the COMPASS-31 questionnaire to a sample of post-COVID patients with and without neurological complaints. Participants were recruited among the post-COVID ambulatory services for follow-up evaluation between 4 weeks and 9 months from COVID-19 symptoms onset. Participants were asked to complete the COMPASS-31 questionnaire referring to the period after COVID-19 disease. Heart rate and blood pressure were manually taken during an active stand test for OH and POTS diagnosis. One-hundred and eighty participants were included in the analysis (70.6% females, 51 ± 13 years), and OH was found in 13.8% of the subjects. Median COMPASS-31 score was 17.6 (6.9–31.4), with the most affected domains being orthostatic intolerance, sudomotor, gastrointestinal and pupillomotor dysfunction. A higher COMPASS-31 score was found in those with neurological symptoms (p < 0.01), due to more severe orthostatic intolerance symptoms (p < 0.01), although gastrointestinal (p < 0.01), urinary (p < 0.01), and pupillomotor (p < 0.01) domains were more represented in the non-neurological symptoms group. This study confirms the importance of monitoring ANS symptoms as a possible complication of COVID-19 disease that may persist in the post-acute period.

scholarly journals The preponderance of initial orthostatic hypotension in postural tachycardia syndrome

2020 ◽  
Vol 129 (3) ◽  
pp. 459-466
Author(s):  
Julian M. Stewart ◽  
Archana Kota ◽  
Mary Breige O’Donnell-Smith ◽  
Paul Visintainer ◽  
Courtney Terilli ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Heart Rate Variability ◽  
Cerebral Blood Flow ◽  
Orthostatic Hypotension ◽  
Pressure Recovery ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia ◽  
Initial Orthostatic Hypotension

Significant initial orthostatic hypotension (IOH) occurs in ~50% of postural tachycardia syndrome (POTS) patients and 13% of controls. Heart rate and blood pressure recovery are prolonged in IOH sustaining lightheadedness; IOH is more prevalent and severe in POTS. Altered cerebral blood flow and cardiorespiratory regulation are more prevalent in POTS. Altered heart rate variability and baroreflex gain may cause nearly instantaneous lightheadedness in POTS. IOH alone fails to confer a strong probability of POTS.

Recent advances in the understanding of the mechanisms underlying postural tachycardia syndrome in children: practical implications for treatment

2016 ◽  
Vol 27 (3) ◽  
pp. 413-417 ◽  
Author(s):  
Xiaochun Zheng ◽  
Yonghong Chen ◽  
Junbao Du
Keyword(s):  
Heart Rate ◽  
Upright Position ◽  
Postural Tachycardia Syndrome ◽  
Postural Orthostatic Tachycardia Syndrome ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Pathophysiological Mechanisms ◽  
Postural Tachycardia ◽  
Β Receptor ◽  
Practical Implications

AbstractPostural tachycardia syndrome is defined by a heart rate increment of 40 beats/minute (bpm) (or a heart rate that exceeds 125 bpm) within 10 minutes of change from the supine position to an upright position in the absence of obvious orthostatic hypotension. There are multiple pathophysiological mechanisms that underlie postural tachycardia syndrome, including peripheral denervation, β-receptor supersensitivity, hypovolaemia, and impaired muscle pump. Some children afflicted with postural orthostatic tachycardia syndrome and hypovolaemic dysregulation have been found to have perturbed renin–angiotensin–aldosterone profile, disturbed vascular endothelial function, and abnormal vasodilation. The hyperadrenergic state in some postural tachycardia syndrome patients is likely a driver for orthostatic tachycardia. Other mechanisms include the presence of treatable autonomic neuropathies. An understanding of these pathophysiological mechanisms might be helpful for the effective treatment of postural tachycardia syndrome.

Case 16: Autonomic Failure or Postural Tachycardia Syndrome?

2019 ◽  
pp. 120-124
Author(s):  
Peter Novak
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia ◽  
Transient Elevation

Small fiber neuropathy is associated with adrenergic failure. Anxiety is common and occasionally can be identified as a transient elevation of heart rate, blood pressure, and cerebral blood flow velocity.

scholarly journals Nitric Oxide and Regulation of Heart Rate in Patients With Postural Tachycardia Syndrome and Healthy Subjects

Hypertension ◽  
2013 ◽  
Vol 61 (2) ◽  
pp. 376-381 ◽  
Author(s):  
Alfredo Gamboa ◽  
Luis E. Okamoto ◽  
Satish R. Raj ◽  
André Diedrich ◽  
Cyndya A. Shibao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Healthy Subjects ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia

scholarly journals Cerebral Blood Flow and Cognitive Performance in Postural Tachycardia Syndrome: Insights from Sustained Cognitive Stress Test

2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Rachel Wells ◽  
Varun Malik ◽  
Anthony G. Brooks ◽  
Dominik Linz ◽  
Adrian D. Elliott ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Stress Test ◽  
Orthostatic Stress ◽  
Postural Tachycardia Syndrome ◽  
Cognitive Stress ◽  
Postural Tachycardia ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

Background The physiology underlying "brain fog" in the absence of orthostatic stress in postural tachycardia syndrome (POTS) remains poorly understood. Methods and Results We evaluated cognitive and hemodynamic responses (cardiovascular and cerebral: heart rate, blood pressure, end‐tidal carbon dioxide, and cerebral blood flow velocity (CBFv) in the middle cerebral artery at baseline, after initial cognitive testing, and after (30‐minutes duration) prolonged cognitive stress test (PCST) whilst seated; as well as after 5‐minute standing in consecutively enrolled participants with POTS (n=22) and healthy controls (n=18). Symptom severity was quantified with orthostatic hypotensive questionnaire at baseline and end of study. Subjects in POTS and control groups were frequency age‐ and sex‐matched (29±11 versus 28±13 years; 86 versus 72% women, respectively; both P ≥0.4). The CBFv decreased in both groups (condition, P =0.04) following PCST, but a greater reduction in CBFv was observed in the POTS versus control group (−7.8% versus −1.8%; interaction, P =0.038). Notably, the reduced CBFv following PCST in the POTS group was similar to that seen during orthostatic stress (60.0±14.9 versus 60.4±14.8 cm/s). Further, PCST resulted in greater slowing in psychomotor speed (6.1% versus 1.4%, interaction, P =0.027) and a greater increase in symptom scores at study completion (interaction, P <0.001) in the patients with POTS, including increased difficulty with concentration. All other physiologic responses (blood pressure and end‐tidal carbon dioxide) did not differ between groups after PCST (all P >0.05). Conclusions Reduced CBFv and cognitive dysfunction were evident in patients with POTS following prolonged cognitive stress even in the absence of orthostatic stress.

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