Explore 5-Minute Clinical Consult - view these FREE monographs:
-- The first section of this topic is shown below --
Postural or orthostatic hypotension (OH) represents the failure of cardiovascular reflexes to maintain adequate BP on standing from a supine or sitting position.
- OH is defined as a sustained and persistent drop in systolic BP (SBP) ≥20 mm Hg or diastolic BP (DBP) ≥10 mm Hg within 3 minutes of achieving a standing position, or head-up tilt to at least 60° on tilt table. Delayed OH can infrequently occur with a slow decline in SBP beyond 3 minutes of standing, and may be revealed by extending the period of orthostatic stress (1).
- Characteristic symptoms of OH are recurrent dizziness, lightheadedness, presyncope or syncope with assumption of an upright posture, typically relieved by achieving a recumbent position, and can be incapacitating. In the elderly, OH may be asymptomatic or present with nonspecific complaints of weakness.
Asymptomatic OH is far more common than symptomatic OH, and is an independent risk factor for mortality and cardiovascular disease. OH is also a manifestation of many underlying diseases and may be the initial sign of autonomic failure in many neurologic disorders. The prevalence increases with age, hypertension (HTN), diabetes, and use of antihypertensive medication (2).
80,095 orthostatic-related hospitalizations occurred in the US in 2004; OH was the primary diagnosis in 35%.
~6% of middle-aged persons, and 18% of individuals ≥65 years of age; more common in those living in long-term care facilities (45% vs. 6% living in the community) (2). In those with hypertension, prevalence is 13.4–32.1% (2)
- Elderly, particularly in long-term care facilities
- Multiple comorbidities, including HTN, diabetes, neurodegenerative disorders, and neuropathy
- Polypharmacy (See “Epidemiology” section).
Avoid polypharmacy and monitor drug interactions, maintain adequate fluid balance
- During standing, 500–1,000 mL of blood pools in the lower extremities and the splanchnic vasculature. This reduces cardiac preload, but is opposed by an increase in sympathetic tone and vasopressin release that maintains cerebral perfusion pressure, by increasing peripheral vascular resistance. Impairment of these compensatory mechanisms by autonomic dysfunction, or nonneurogenic causes, such as medications, hypovolemia, or cardiac pump failure, leads to an inability to maintain effective cerebral perfusion pressure. Autonomic dysfunction also impairs proximal tubule renal sodium reabsorption, which contributes to OH through urinary sodium wasting and a consequent reduction in circulating plasma volume. In older people vascular stiffening and decreased baroreceptor sensitivity predispose to OH.
- Supine hypertension (SH), due to baroreflex dysfunction and fluid redistribution upon assuming a horizontal position, is common in patients with OH. Increased renal perfusion pressure in the recumbent position also leads to nocturnal natriuresis, which decreases circulating volume, worsening orthostatic tolerance in the morning.
- Medications (iatrogenic causes):
- Anticholinergics: Benztropine, oxybutynin
- Antidepressants: TCA, MAOIs, SSRIs, and SNRIs
- Antihypertensives: Of classes including diuretics
- Dopamine agonists: Levodopa, bromocriptine, ropinirole, pramipexole
- Insulin (may exacerbate OH in the setting of diabetic neuropathy)
- Narcotics/Sedatives: Morphine, benzodiazepines, barbiturates, promethazine
- Neuroleptics: Chlorpromazine, quetiapine
- Neurotoxic drugs: Amiodarone, vincristine, cisplatin
- Neurogenic causes:
- Idiopathic OH (1/3 of cases of OH)
- Central autonomic nervous system diseases: Familial dysautonomia (rare, childhood), Lewy body dementia, multisystem atrophy (Shy-Drager syndrome), Parkinson disease (PD): 40% of patients with PD have OH. Pure autonomic failure (rare)
- Peripheral autonomic nervous system diseases: Acute autonomic neuropathy and Guillain-Barré syndrome (acute onset, frequently preceded by viral syndrome); alcoholic polyneuropathy; amyloidosis; autoimmune autonomic ganglionopathy (rare); chronic renal failure: Uremic or β-2 microglobulin neuropathy (dialysis). Diabetes: Diabetic autonomic neuropathy (very common). Exposure to neurotoxins. Hereditary sensory and autonomic neuropathies: Dopamine-β-hydroxylase deficiency (rare). HIV neuropathy. Paraneoplastic autonomic neuropathy: SCLC, NSCLC, GI neoplasias, prostate, breast, bladder, kidney, testicle, and ovary. Spinal cord pathologies: Trauma, myelitis, tumors, tabes dorsalis, multiple sclerosis, syringomyelia, infarction, vitamin B12 deficiency
- Nonneurogenic causes:
- Cardiac disorders: Heart failure, arrhythmias, pericardial disease, severe aortic stenosis, idiopathic hypertrophic subaortic stenosis (IHSS), hypertrophic obstructive cardiomyopathy (HOCM), acute aortic regurgitation, acute myocardial infarction
- Intravascular volume depletion: Bleeding, diarrhea, diabetes insipidus, diuretics, poor oral intake, vomiting
- Metabolic: Adrenal insufficiency, hypoaldosteronism, pheochromocytoma, carcinoid syndrome, hypokalemia (severe), hypothyroidism
- Systemic mastocytosis
- Venous pooling: Heat or vigorous exercise, postprandial splanchnic dilation, prolonged recumbency or standing
Commonly Associated Conditions
Diabetes mellitus with neuropathy, uncontrolled HTN and antihypertensive treatment, PD