Orthostatic Hypotension in Older and Medically Complex Patients
Orthostatic Hypotension in Older and Medically Complex Patients
There are age- and disease-associated changes in physiology that would be expected to increase the likelihood of hypotension in the face of cardiovascular stressors. Arterial compliance and venous system tortuosity increase. Cardiac hypertrophy associated with aging or hypertension impairs diastolic filling. Renal sodium conservation declines and renin, angiotensin and aldosterone levels are also lower with aging. With standing there is a blunting of the aforementioned hormones, as well as arginine vasopressin. The change in heart rate after hypotensive maneuvers and the maximum heart rate during exercise or isoproterenol infusion are decreased with age and in patients who may be receiving β-adrenergic antagonists. There are also anatomical and physiological changes with age that might reduce the likelihood of hypotension after standing. The vasoconstrictor response of blood vessels to α-agonists probably does not change with normal aging. β-adrenergic-mediated blood vessel relaxation declines despite a normal response to other vasodilators, such as nitroglycerine. Norepinephrine levels in the blood increase with age under both rest and stress conditions. These changes may protect against hypotension with aging. However, it appears that aging increases the risk of hypotension, as studies have shown that diuretic-induced dehydration or drug-induced vasodilation causes greater BP declines in the elderly compared with younger patients. BP declines associated with meals commonly occur in older patients but not in younger patients. Cerebral blood flow declines with increasing age. Hypertension and cerebrovascular disease are also more common in older patients, and both conditions alter cerebral blood flow.
Aging as a Modifier to the Normal Response to Standing
There are age- and disease-associated changes in physiology that would be expected to increase the likelihood of hypotension in the face of cardiovascular stressors. Arterial compliance and venous system tortuosity increase. Cardiac hypertrophy associated with aging or hypertension impairs diastolic filling. Renal sodium conservation declines and renin, angiotensin and aldosterone levels are also lower with aging. With standing there is a blunting of the aforementioned hormones, as well as arginine vasopressin. The change in heart rate after hypotensive maneuvers and the maximum heart rate during exercise or isoproterenol infusion are decreased with age and in patients who may be receiving β-adrenergic antagonists. There are also anatomical and physiological changes with age that might reduce the likelihood of hypotension after standing. The vasoconstrictor response of blood vessels to α-agonists probably does not change with normal aging. β-adrenergic-mediated blood vessel relaxation declines despite a normal response to other vasodilators, such as nitroglycerine. Norepinephrine levels in the blood increase with age under both rest and stress conditions. These changes may protect against hypotension with aging. However, it appears that aging increases the risk of hypotension, as studies have shown that diuretic-induced dehydration or drug-induced vasodilation causes greater BP declines in the elderly compared with younger patients. BP declines associated with meals commonly occur in older patients but not in younger patients. Cerebral blood flow declines with increasing age. Hypertension and cerebrovascular disease are also more common in older patients, and both conditions alter cerebral blood flow.