Differential diagnosis of orthostatic hypotension

Abstract

Orthostatic hypotension (OH) is a common clinical manifestation characterized by a significant fall in blood pressure with postural change and is frequently accompanied by debilitating symptoms of orthostatic intolerance. The reported prevalence of OH ranges between 5 and 10% in middle-aged adults with a burden that increases concomitantly with age; in those over 60 years of age, the prevalence is estimated to be over 20%. Unfortunately, the clinical course of OH is not necessarily benign. OH patients are at an increased risk of adverse clinical outcomes including death, falls, cardiovascular and cerebrovascular events, syncope, and impaired quality of life. The differential diagnosis of OH is broad and includes acute precipitants as well as chronic underlying medical conditions, especially of neurological origin. Appropriate diagnosis relies on a systematic history and physical examination with particular attention to orthostatic vital signs, keeping in mind that ambient conditions during diagnostic testing may affect OH detection due to factors such as diurnal variation.

Keywords: Delayed orthostatic hypotension; Initial orthostatic hypotension; Neurogenic orthostatic hypotension; Orthostatic hypotension; Postural orthostatic tachycardia syndrome; Vasovagal syncope.

Figure 1.

Representative blood pressure and heart rate responses to postural change from supine to active stand in (A) classical orthostatic hypotension, (B) delayed orthostatic hypotension, (C) initial orthostatic hypotension, (D) vasovagal syncope, and (E) postural tachycardia syndrome.

Figure 2.

Representative blood pressure (BP) and heart rate (HR) tracings during the Valsalva maneuver in (A) healthy subjects and (B) patients with neurogenic orthostatic hypotension. The Valsalva maneuver is used to evaluate the sympathetic and parasympathetic responses of the baroreflex as an individual forcibly exhales at maximum pressure (~40 mmHg) for 15 seconds. Those with intact autonomic nervous system function are expected to exhibit a specific pattern of physiological responses to the Valsalva maneuver that can be divided into four phases: (I) the mechanical increase in intrathoracic pressure causes a brief increase in BP and decrease in HR; (II, early) the reduction in venous return causes a decrease in stroke volume and BP; (II, late) the baroreflex is activated by the decrease in BP, causing a sympathetically-mediated increase in BP and HR; (III) the pulmonary vascular refills with blood upon termination of the Valsalva maneuver, causing a decrease in BP; (IV) the sudden increase in venous return leads to a compensatory decrease in HR and increase in BP that overshoots baseline BP due to residual sympathetic activity. In patients with impaired autonomic function, as in neurogenic orthostatic hypotension, there is a lack of late phase II BP increase and BP overshoot in phase IV recovery.