Deconditioning in patients with orthostatic intolerance

Parsaik, Ajay K.; Allison, Thomas G.; Singer, Wolfgang; Sletten, David M.; Joyner, Michael J.; Benarroch, Eduardo E.; Low, Phillip A.; Sandroni, Paola

doi:10.1212/wnl.0b013e31826d5f95

Cited by 99 publications

(78 citation statements)

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“…11 As in all types of orthostatic intolerance, typical exacerbating factors include heat exposure, physical exertion, heavy meals, prolonged recumbency, menses, and drugs such as diuretics and vasodilators. 12 Classic Pathophysiology and POTS Subtypes Exaggerated postural tachycardia may reflect several pathophysiologically distinct mechanisms 2,4,6,8,9,[13][14][15][16] ( Table 1). Based on autonomic testing and plasma norepinephrine (NE) levels, POTS has been classified into several subtypes, including neuropathic and hyperadrenergic POTS 2,13 and, based on measurement of leg venous pressure and calf blood flow, as low-flow, high-flow, and normal-flow POTS.…”

Section: Pots As a Syndrome Of Orthostatic Intolerancementioning

confidence: 99%

“…The term orthostatic intolerance is used to describe a condition in which patients develop symptoms on standing or HUT but do not fulfill the heart rate criteria for the diagnosis of POTS. 4 The diagnostic criteria for orthostatic intolerance and POTS in adults are unsuitable for children and adolescents, and new criteria for these disorders in this age group have been recently proposed.5 POTS is more frequent in women (female:male ratio, 4.5:1), and most cases occur between the ages of 15 and 25 years. Up to 50% of cases have antecedent viral illness, and 25% have a family history of similar complaints.…”

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Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

Benarroch

2012

Mayo Clinic Proceedings

316

354

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Postural tachycardia syndrome (POTS) is defined by a heart rate increment of 30 beats/min or more within 10 minutes of standing or head-up tilt in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. POTS manifests with symptoms of cerebral hypoperfusion and excessive sympathoexcitation. The pathophysiology of POTS is heterogeneous and includes impaired sympathetically mediated vasoconstriction, excessive sympathetic drive, volume dysregulation, and deconditioning. POTS is frequently included in the differential diagnosis of chronic unexplained symptoms, such as inappropriate sinus tachycardia, chronic fatigue, chronic dizziness, or unexplained spells in otherwise healthy young individuals. Many patients with POTS also report symptoms not attributable to orthostatic intolerance, including those of functional gastrointestinal or bladder disorders, chronic headache, fibromyalgia, and sleep disturbances. In many of these cases, cognitive and behavioral factors, somatic hypervigilance associated with anxiety, depression, and behavioral amplification contribute to symptom chronicity. The aims of evaluation in patients with POTS are to exclude cardiac causes of inappropriate tachycardia; elucidate, if possible, the most likely pathophysiologic basis of postural intolerance; assess for the presence of treatable autonomic neuropathies; exclude endocrine causes of a hyperadrenergic state; evaluate for cardiovascular deconditioning; and determine the contribution of emotional and behavioral factors to the patient's symptoms. Management of POTS includes avoidance of precipitating factors, volume expansion, physical countermaneuvers, exercise training, pharmacotherapy (fludrocortisone, midodrine, ␤-blockers, and/or pyridostigmine), and behavioral-cognitive therapy. A literature search of PubMed for articles published from January 1, 1990, to June 15, 2012, was performed using the following terms (or combination of terms): POTS; postural tachycardia syndrome, orthostatic; orthostatic; syncope; sympathetic; baroreceptors; vestibulosympathetic; hypovolemia; visceral pain; chronic fatigue; deconditioning; headache; Chiari malformation; Ehlers-Danlos; emotion; amygdala; insula; anterior cingulate; periaqueductal gray; fludrocortisone; midodrine; propranolol; ␤-adrenergic; and pyridostigmine. Studies were limited to those published in English. Other articles were identified from bibliographies of the retrieved articles. 1,2 According to current criteria for adults, 3 POTS is defined by a heart rate increment of 30 beats/min or more within 10 minutes of standing or head-up tilt (HUT) in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. These criteria may not be applicable for individuals with low resting heart rate. For individuals aged 12 to 19 years, the required increment is at least 40 beats/min.3 The orthostatic tachycardia may be accompanied by symptoms of cerebral hypoperfusion and sympathetic hyperactivity that are reliev...

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Section: Pots As a Syndrome Of Orthostatic Intolerancementioning

confidence: 99%

mentioning

confidence: 99%

Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

Benarroch

2012

Mayo Clinic Proceedings

316

354

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“…Here, we present frequencies of symptoms involving various organ systems as reported by a cohort of POTS patients. Th ere are multiple syndromes of orthostatic intolerance in which patients develop symptoms upon standing, but not all fulfi ll the diagnostic criteria of POTS (7). Th is heterogeneity contributes to the diagnostic and management challenges faced by patients and providers.…”

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confidence: 99%

A Survey-Based Analysis of Symptoms in Patients with Postural Orthostatic Tachycardia Syndrome

Deb¹,

Morgenshtern²,

Culbertson³

et al. 2015

Baylor University Medical Center Proceedings

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“…In contrast, a recent retrospective study showed deconditioning in .90% of patients with POTS after upright exercise testing. 22 This discrepancy may reflect selection bias as well as differences in exercise protocols.…”

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confidence: 99%

Low-dose propranolol and exercise capacity in postural tachycardia syndrome

et al. 2013

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Objective: To determine the effect of low-dose propranolol on maximal exercise capacity in patients with postural tachycardia syndrome (POTS). Methods:We compared the effect of placebo vs a single low dose of propranolol (20 mg) on peak oxygen consumption (VO 2 max), an established measure of exercise capacity, in 11 patients with POTS and 7 healthy subjects in a randomized, double-blind study. Subjects exercised on a semirecumbent bicycle, with increasing intervals of resistance to maximal effort.Results: Maximal exercise capacity was similar between groups following placebo. Low-dose propranolol improved VO 2 max in patients with POTS (24.5 6 0.7 placebo vs 27.6 6 1.0 mL/min/kg propranolol; p 5 0.024), but not healthy subjects. The increase in VO 2 max in POTS was associated with attenuated peak heart rate responses (142 6 8 propranolol vs 165 6 4 bpm placebo; p 5 0.005) and improved stroke volume (81 6 4 propranolol vs 67 6 3 mL placebo; p 5 0.013). In a separate cohort of POTS patients, neither high-dose propranolol (80 mg) nor metoprolol (100 mg) improved VO 2 max, despite similar lowering of heart rate.Conclusions: These findings suggest that nonselective b-blockade with propranolol, when used at the low doses frequently used for treatment of POTS, may provide a modest beneficial effect to improve heart rate control and exercise capacity. Classification of evidence:This study provides Class II evidence that a single low dose of propranolol (20 mg) as compared with placebo is useful in increasing maximum exercise capacity measured 1 hour after medication. Neurology â 2013;80:1927-1933 GLOSSARY BP 5 blood pressure; CI 5 confidence interval; CO 5 cardiac output; HF RRI 5 high-frequency R-R interval; HR 5 heat rate; LF RRI 5 low-frequency R-R interval; MAP 5 mean arterial pressure; POTS 5 postural tachycardia syndrome; SV 5 stroke volume; SVR 5 systemic vascular resistance; VO 2 max 5 peak oxygen consumption.Postural tachycardia syndrome (POTS) is a heterogeneous disorder characterized by sustained tachycardia ($30 bpm) upon standing, unrelated to medications or other medical conditions. 1 Although the underlying cause of POTS remains unclear, several mechanisms have been proposed, including sympathetic activation, hypovolemia, and, more recently, deconditioning.2-4 Indeed, endurance exercise training decreases standing heart rate (HR), restores blood volume, and improves orthostatic tolerance and associated symptoms in POTS. [5][6][7] Another frequently used treatment for POTS is nonselective b-adrenergic blockade with propranolol. 8,9 At low doses, propranolol reduces standing HR and improves orthostatic symptoms. 8,10,11 In contrast, higher doses can more effectively control tachycardia, but do not improve quality of life or orthostatic symptoms. 5,8 Because b-blockers impair exercise tolerance in healthy subjects, 12 this raises the concern that these drugs would counteract the beneficial effects of exercise training in POTS. We hypothesized, however, that by controlling tachycardia, b-blockers ...

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Deconditioning in patients with orthostatic intolerance

Cited by 99 publications

References 14 publications

Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

A Survey-Based Analysis of Symptoms in Patients with Postural Orthostatic Tachycardia Syndrome

Low-dose propranolol and exercise capacity in postural tachycardia syndrome

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