J Clin Neurol.  2015 Jul;11(3):220-226. 10.3988/jcn.2015.11.3.220.

Orthostatic Hypotension: Mechanisms, Causes, Management

• Low PA
• Tomalia VA

• KMID: 1894552
• DOI: http://doi.org/10.3988/jcn.2015.11.3.220

Abstract

Orthostatic hypotension (OH) occurs when mechanisms for the regulation of orthostatic BP control fails. Such regulation depends on the baroreflexes, normal blood volume, and defenses against excessive venous pooling. OH is common in the elderly and is associated with an increase in mortality rate. There are many causes of OH. Aging coupled with diseases such as diabetes and Parkinson's disease results in a prevalence of 10-30% in the elderly. These conditions cause baroreflex failure with resulting combination of OH, supine hypertension, and loss of diurnal variation of BP. The treatment of OH is imperfect since it is impossible to normalize standing BP without generating excessive supine hypertension. The practical goal is to improve standing BP so as to minimize symptoms and to improve standing time in order to be able to undertake orthostatic activities of daily living, without excessive supine hypertension. It is possible to achieve these goals with a combination of fludrocortisone, a pressor agent (midodrine or droxidopa), supplemented with procedures to improve orthostatic defenses during periods of increased orthostatic stress. Such procedures include water bolus treatment and physical countermaneuvers. We provide a pragmatic guide on patient education and the patient-orientated approach to the moment to moment management of OH.

Keyword

orthostatic hypotension; baroreflex; supine hypertension; water bolus

MeSH Terms

Activities of Daily Living
Aged
Aging
Baroreflex
Blood Volume
Fludrocortisone
Humans
Hypertension
Hypotension, Orthostatic*
Mortality
Parkinson Disease
Patient Education as Topic
Prevalence
Water
Fludrocortisone
Water

Figure

• 

  Fig. 1 Baroreflex pathways for postural normotension. Baroreceptor afferents (dark blue) synapse at the nucleus of the tractus solitarius (NTS). The vagal component of the baroreflex (green) runs from the NTS to the nucleus ambiguus (NA) and sends efferents to the sinoatrial node (SA) to regulate heart rate. The adrenergic baroreflex pathway (red) runs from the NTS to the caudal ventrolateral medulla (CVLM), and from there to the rostral ventrolateral medulla (RVLM). The adrenergic pathway continues with sympathetic efferents from the RVLM to the interomediolateral thoracic spinal cord, and from there to autonomic ganglia and to the heart, arterioles, and venules (Reprinted from Low and Singer.5 Lancet Neurol 2008;7:451-458, with permission from Elsevier).

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