Orthostatic hypotension: managing a difficult problem

Abstract

Orthostatic hypotension (OH) leads to a significant number of hospitalizations each year, and is associated with significant morbidity and mortality among affected individuals. Given the increased risk for cardiovascular events and falls, it is important to identify the underlying etiology of OH and to choose appropriate therapeutic agents. OH can be non-neurogenic or neurogenic (arising from a central or peripheral lesion). The initial evaluation includes orthostatic vital signs, complete history and a physical examination. Patients should also be evaluated for concomitant symptoms of post-prandial hypotension and supine hypertension. Non-pharmacologic interventions are the first step for treatment of OH. The appropriate selection of medications can also help with symptomatic relief. This review highlights the pathophysiology, clinical features, diagnostic work-up and treatment of patients with neurogenic OH.

Keywords: Parkinson’s disease; autonomic failure; autonomic nervous system; droxidopa; multiple system atrophy; orthostatic hypotension; orthostatic intolerance; peripheral neuropathy.

FIG. 1. Examples of Tilt table abnormalities

Panel A is an example of classic neurogenic orthostatic hypotension, during which there is fall in blood pressure within the first 3 minutes of assuming upright posture. Panel B demonstrates initial OH, with a sudden, transient decrease in blood pressure with the upright position, and subsequent recovery. Panel C is an example of delayed orthostatic hypotension, in which the fall in blood pressure occurs after 3 minutes. Panel D is an example of classic orthostatic hypotension in the setting of supine hypertension. Reproduced with permission from Springer Science + Business Media: Clinical Autonomic Research, The relationship between orthostatic hypotension and falling in older adults, 24, 2013, Shaw BH & Claydon VE.

FIG. 2. Distinguishing Vasovagal syncope from Delayed OH

Panel A demonstrates vasovagal syncope. The patient maintains blood pressure and heart rate with upright tilt. After prolonged tilt; there is a sudden, precipitous fall in blood pressure and heart rate. The BP fall was if a boulder fell off of a cliff. Panel B shows a patient with delayed orthostatic hypotension. Note the gradual and progressive fall in blood pressure with head-up tilt that eventually drops to a significant degree. The BP was akin to a boulder rolling down a hill. Reprinted from Electrophysiological Disorders of the Heart, Sanjeev Saksena, Robert S. Sheldon, 985–995, Copyright (2012), with permission from Elsevier.

FIG. 3. Cardiac ¹²³I-metaiodobenzylguanidine (MIBG) scintigraphy scans in patients with Multiple System atrophy (MSA), pure autonomic failure (PAF) and Parkinson’s disease (PD)

MIBG is taken up by intact postganglionic sympathetic neurons. Note that in MSA (Panel A), a “central” autonomic disorder, the cardiac MIBG intake is normal, which is consistent with a preganglionic lesion. In contrast, in PAF (Panel B), a “peripheral” autonomic disorder, and PD (C), cardiac MIBG uptake is decreased, which is reflective of a postganglionic lesion. PD (Panel C) has a cardiac MIBG pattern similar to PAF, suggesting that the autonomic failure in PD is also a “peripheral “ autonomic disorder. Reprinted from Cardiology Clinics, Victor C. Nwazue, Satish R. Raj, Confounders of Vasovagal Syncope Orthostatic Hypotension, 89–100, Copyright (2013), with permission from Elsevier.