Orthostatic hypotension in older people: considerations, diagnosis and management

Abstract

Orthostatic hypotension (OH) is very common in older people and is encountered daily in emergency departments and medical admissions units. It is associated with a higher risk of falls, fractures, dementia and death, so prompt recognition and treatment are essential. In this review article, we describe the physiology of standing (orthostasis) and the pathophysiology of orthostatic hypotension. We focus particularly on aspects pertinent to older people. We review the evidence and consensus management guidelines for all aspects of management. We also tackle the challenge of concomitant orthostatic hypotension and supine hypertension, providing a treatment overview as well as practical suggestions for management. In summary, orthostatic hypotension (and associated supine hypertension) are common, dangerous and disabling, but adherence to simple structures management strategies can result in major improvements.

Keywords: older; orthostasis; orthostatic hypotension; postural hypotension; supine hypertension.

Fig 1.

Normal haemodynamic changes on standing. a) i) Upon standing, blood pools in the legs, pelvis and gut, resulting in reduced venous return to the heart. ii) Baroreceptors in the aorta and carotid sinus, and mechanoceptors in the lungs and heart detect reduced venous return to the heart. iii and iv) Sympathetic nervous system activation releases noradrenaline into plasma with splanchnic/lower-limb vasoconstriction. The body's physiological response to standing is known as ‘orthostasis’. Adapted with permission from Stop Fainting (www.stopfainting.com). b) Tilt table test: the heart rate (HR) and blood pressure (BP) reflect the normal haemodynamic response to standing on a tilt table. HR/BP are relatively stable on transition from lying to standing. A mild transient fall in BP occurs on reaching upright position, with a transient compensatory HR rise of ∼15%.

Fig 2.

Haemodynamic changes occurring on standing in orthostatic hypotension. a) i) Upon standing, blood pools in the legs, pelvis and gut, resulting in reduced venous return to the heart. ii) Normal compensatory mechanisms for reduced venous return are absent. As a result, vasoconstriction does not occur and noradrenaline is not released into the circulation. iii) Blood continues to pool in the legs, pelvis and gut, leading to a further fall in venous return to the heart. iv) Brain hypoperfusion ensues and, unless the supine position is adopted, syncope occurs. Adapted with permission from Stop Fainting (www.stopfainting.com). b) Tilt table test: the heart rate and blood pressure reflect the physiological responses to standing on a tilt table. Following head-up tilt, the blood pressure falls until syncope is imminent at >10 minutes, at which point the supine position is resumed.

Fig 3.

Physical counter-pressure manoeuvres. Patients should be educated on different physical counter-pressure manoeuvres to employ at the onset of symptoms on standing (a). Tensing lower body muscles while crossing arms and legs (b and c), raising a leg onto a raised surface (d) and squatting (e) can all increase venous return to the heart and raise blood pressure.