Early Orthostatic Hypotension and Orthostatic Intolerance—More Than an Observation or Annoyance

2017 ◽  
Vol 177 (9) ◽  
pp. 1324 ◽  
Author(s):  
Wolfgang Singer ◽  
Phillip A. Low
2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Chaisith Sivakorn ◽  
Polrat Wilairatana ◽  
Srivicha Krudsood ◽  
Marcus J. Schultz ◽  
Tachpon Techarang ◽  
...  

AbstractImpaired autonomic control of postural homeostasis resulting in orthostatic hypotension has been described in falciparum malaria. However, severe orthostatic intolerance in Plasmodium vivax has been rarely reported. A case of non-immune previously healthy Thai woman presenting with P. vivax infection with well-documented orthostatic hypotension is described. In addition to oral chloroquine and intravenous artesunate, the patient was treated with fluid resuscitation and norepinephrine. During hospitalization, her haemodynamic profile revealed orthostatic hypotension persisting for another three days after microscopic and polymerase chain reaction confirmed parasite clearance. Potential causes are discussed.


2021 ◽  
Vol 8 ◽  
pp. 100071
Author(s):  
Elena M. Christopoulos ◽  
Jennifer Tran ◽  
Sarah L. Hillebrand ◽  
Peter W. Lange ◽  
Rebecca K. Iseli ◽  
...  

Endocrinology ◽  
2010 ◽  
pp. 2063-2082
Author(s):  
Christopher J. Mathias ◽  
Gianluigi Galizia

ESC CardioMed ◽  
2018 ◽  
pp. 2032-2037
Author(s):  
Artur Fedorowski

The impairment of adaptive mechanisms during orthostatic challenge may evoke orthostatic intolerance, a heterogeneous condition, in which the standing position elicits a fall in blood pressure and/or excessive tachycardia, accompanied by a wide spectrum of subjective symptoms such as dizziness, discomfort, nausea, and palpitations. Apart from chronic and potentially debilitating symptoms, orthostatic intolerance may occasionally lead to sudden loss of consciousness and fall injuries. Consequently, orthostatic intolerance should be considered as a possible cause of unexplained syncope. Two main forms of orthostatic intolerance are orthostatic hypotension (OH) and postural orthostatic tachycardia syndrome (POTS). Clinical variants of OH include initial, classical, and delayed forms. The prevalence of OH increases with age, ranging from less than 5% under 40 years to about 20% above 70 years of age, and is higher in chronic diseases, such as hypertension and diabetes, reaching above 35% in Parkinson’s disease and advanced kidney failure. The presence of OH is associated with a higher mortality and an increased incidence of cardiovascular disease, with the majority of patients being asymptomatic in normal conditions. In contrast, POTS affects predominantly young women (70–80%) within an age range of 15–40 years and is usually accompanied by non-specific symptoms: deconditioning, headache, cognitive impairment, and gastrointestinal dysfunction. Management of orthostatic intolerance includes both non-pharmacological and pharmacological methods with limited efficacy in the severe cases. Empirical treatment with vasoactive and volume expanding drugs for OH and POTS, and rhythm controlling therapy for POTS are recommended. Future studies on syndromes of orthostatic intolerance should focus on mechanisms leading to OH and POTS, novel diagnostic methods, and more effective therapeutic options.


ESC CardioMed ◽  
2018 ◽  
pp. 2032-2037
Author(s):  
Artur Fedorowski

The impairment of adaptive mechanisms during orthostatic challenge may evoke orthostatic intolerance, a heterogeneous condition, in which the standing position elicits a fall in blood pressure and/or excessive tachycardia, accompanied by a wide spectrum of subjective symptoms such as dizziness, discomfort, nausea, and palpitations. Apart from chronic and potentially debilitating symptoms, orthostatic intolerance may occasionally lead to sudden loss of consciousness and fall injuries. Consequently, orthostatic intolerance should be considered as a possible cause of unexplained syncope. Two main forms of orthostatic intolerance are orthostatic hypotension (OH) and postural orthostatic tachycardia syndrome (POTS). Clinical variants of OH include initial, classical, and delayed forms. The prevalence of OH increases with age, ranging from less than 5% under 40 years to about 20% above 70 years of age, and is higher in chronic diseases, such as hypertension and diabetes, reaching above 35% in Parkinson’s disease and advanced kidney failure. The presence of OH is associated with a higher mortality and an increased incidence of cardiovascular disease, with the majority of patients being asymptomatic in normal conditions. In contrast, POTS affects predominantly young women (70–80%) within an age range of 15–40 years and is usually accompanied by non-specific symptoms: deconditioning, headache, cognitive impairment, and gastrointestinal dysfunction. Management of orthostatic intolerance includes both non-pharmacological and pharmacological methods with limited efficacy in the severe cases. Empirical treatment with vasoactive and volume expanding drugs for OH and POTS, and rhythm controlling therapy for POTS are recommended. Future studies on syndromes of orthostatic intolerance should focus on mechanisms leading to OH and POTS, novel diagnostic methods, and more effective therapeutic options.


2012 ◽  
Vol 113 (10) ◽  
pp. 1659-1668 ◽  
Author(s):  
Julian M. Stewart

Sympathetic circulatory control is key to the rapid cardiovascular adjustments that occur within seconds of standing upright (orthostasis) and which are required for bipedal stance. Indeed, patients with ineffective sympathetic adrenergic vasoconstriction rapidly develop orthostatic hypotension, prohibiting effective upright activities. One speaks of orthostatic intolerance (OI) when signs, such as hypotension, and symptoms, such as lightheadedness, occur when upright and are relieved by recumbence. The experience of transient mild OI is part of daily life. However, many people experience episodic acute OI as postural faint or chronic OI in the form of orthostatic tachycardia and orthostatic hypotension that significantly reduce the quality of life. Potential mechanisms for OI are discussed including forms of sympathetic hypofunction, forms of sympathetic hyperfunction, and OI that results from regional blood volume redistribution attributable to regional adrenergic hypofunction.


1999 ◽  
Vol 46 (6) ◽  
pp. 691-691 ◽  
Author(s):  
Hidetaka Tanaka ◽  
Hitoshi Yamaguchi ◽  
Reiko Matushima ◽  
Hiroshi Tamai

Sign in / Sign up

Export Citation Format

Share Document