Abstract

Orthostatic hypotension (OH) is defined as a persistent, consistent, orthostatic fall in systolic blood pressure of ≥20 mm Hg or diastolic pressure of ≥10 mm Hg by 3 minutes of standing up.1 Acute, unexpected, episodic falls in blood pressure while standing, as in neurocardiogenic syncope, do not satisfy criteria for OH. Medical records for ≈0.4% of all hospitalizations in the United States include OH as a diagnosis, and of these ≈17% have OH as the primary diagnosis.2 OH is associated with increased mortality in middle-aged adults3 and occurs especially commonly in the elderly, with a prevalence in the United States of ≈12%.4 The rate of hospitalization for nonacute OH increases exponentially with age.2 Therefore, as the US population ages, the prevalence of OH and the incidence of OH-related morbidity are likely to increase. OH can be an asymptomatic sign or manifest as symptoms that range from lightheadedness to loss of consciousness. In our experience, patients with OH do not typically present with recurrent syncope because they come to recognize and respond to premonitory symptoms such as generalized weakness, dizziness, fading vision, or lightheadedness that are relieved by lying down. Instead, OH patients often present with orthostatic intolerance and recurrent falls, an important risk factor for hip fracture and head trauma. Moreover, OH often occurs concurrently with supine hypertension, which can be severe.5 The combination of OH and supine hypertension poses a challenging clinical dilemma because the clinician must balance the risk of chronic high blood pressure versus the immediate risk of falls and consequent morbid events. Many causes of OH have been identified. The listing in Table 1⇓ stratifies these in terms of drugs, secondary nonneurogenic causes, secondary neurogenic causes, and primary neurogenic causes. Accordingly, the clinical approach to a patient with OH …

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