Orthostatic hypotension is defined as a decrease in blood pressure of 20 mm Hg or more systolic or 10 mm Hg or more diastolic within three minutes of standing from the supine position or on assuming a head-up position of 60 degrees during tilt table testing.¹ It is classified as neurogenic or nonneurogenic based on etiology and heart rate response.

With increasing age, there is a normal decline in baroreceptor sensitivity and increase in autonomic neurodegenerative disease.² Orthostatic hypotension occurs in only 5% of middle-aged adults but affects approximately 20% of those 60 years and older.^3–5 Prevalence in nursing homes and geriatric wards is as high as 50% and 68%, respectively.^1,6

Orthostatic hypotension is associated with significant morbidity and mortality, with the greatest risk in those who have comorbidities. Several large meta-analyses reported that orthostatic hypotension is associated with up to a 50% increase in relative risk of all-cause mortality (relative risk [RR] = 1.50; 95% CI, 1.24 to 1.81).^7–9 In middle-aged, community-dwelling patients, it is associated with an increased risk of death (hazard ratio = 1.19 [95% CI, 1.09 to 1.30] to 1.70 [95% CI, 1.40 to 2.00]) after adjustment for other risk factors.^10,11

Orthostatic hypotension is also associated with increased rates of coronary heart disease, myocardial infarction, heart failure, stroke, and falls.^3,8–10 Older people especially are at risk of myocardial infarction and recurrent falls.^12,13 Patients with diabetes mellitus are more likely to develop orthostatic hypotension and have an increased risk of mortality, microvascular and macrovascular complications, and cardiovascular events.^14–18 In the United States, the rate of hospitalizations related to orthostatic hypotension is 36 per 100,000 adults and increases to 233 per 100,000 adults for those 75 years and older.¹⁹

Pathophysiology

Approximately 500 to 1,000 mL of blood pools in the splanchnic circulation and lower extremities when a person stands, causing a decrease in venous return and cardiac output.^2,20–22 Baroreceptors detect decreased stretch and activate the sympathetic nervous system, which elevates the heart rate, bolsters contractility, and increases peripheral resistance through vasoconstriction.^2,21 Baroreceptors also sense decreased blood volume, prompting upregulation of renin release, sodium reabsorption, and vasopressin activity, resulting in enhanced water retention.^2,21 Orthostatic hypotension occurs when there is inadequate intravascular volume or when sympathetic nervous system–mediated vasoconstriction is unable to compensate for gravitational pooling, leading to decreased organ perfusion and associated symptoms ^20,23 (Figure 1).

Clinical Presentation and Evaluation

Symptoms of orthostatic hypotension appear while assuming a standing or upright position and are relieved by returning to a supine position (Table 1).^2,22,24 These symptoms are due to organ hypoperfusion compensation, but they do not have to be present for a diagnosis.^2,5 A history and physical examination aimed at identifying underlying causes of orthostatic hypotension should be performed. Risk factors for orthostatic hypertension are outlined in Table 2.^19,24,25