With many types of parkinsonian type disease a major cause of patient falling and becoming injured is hypotension - or low blood pressure to the brain.
The more common condition is called orthostatic hypotension. It occurs when the patient changes their physical position such as when they arise from lying down to go to a standing position.
Another condition is called postprandial hypotension. It occurs after a meal has been eaten.
Many age-related physiologic changes affect blood pressure. Numerous studies in Western countries have shown an association between age and blood pressure elevation. But paradoxically, age-related elevations in blood pressure also increase the risk of hypotension. Baroreflex mechanisms regulate systemic blood pressure by resisting transient decreases and damping transient increases in arterial pressure. With age, baroreflex response to both hypertensive and hypotensive stimuli progressively declines. Also, hypertension reduces baroreflex response. Thus, baroreflex function is most impaired in elderly, hypertensive patients. Signs of such impairment include increased lability in blood pressure in response to daily activities and an increased response to hypotensive stimuli, particularly medications.
The diminished baroreflex response may be caused partly by arterial stiffening, which results in damping of baroreceptor stretch and relaxation during changes in arterial pressure. Reduced adrenergic responsiveness by the aged heart may diminish baroreflex-mediated cardioacceleration during hypotensive stimuli. These changes become clinically significant when common hypotensive stresses, such as postural changes, can no longer be offset by compensatory increases in heart rate or vascular resistance.
With age, cerebral blood flow declines. Risk factors for cerebrovascular disease (eg, hypertension, heart disease, diabetes mellitus, and hyperlipidemia) further decrease cerebral blood flow. Thus, elderly patients who have such risk factors may develop cerebral ischemia from even a fairly small drop in blood pressure. Cerebral autoregulatory mechanisms usually compensate for acute reductions in blood pressure. Current data suggest that autoregulation of cerebral blood flow is generally maintained with age, except in certain persons who have symptomatic orthostatic hypotension. Chronic hypertension, however, raises the lowest blood pressure at which autoregulation can maintain cerebral blood flow. Below this level, blood flow may decline, increasing the risk of cerebral ischemia. Although an acute reduction in blood pressure may not be tolerated well by a hypertensive elderly patient, a gradual reduction, using a variety of agents, can be accomplished without compromising cerebral blood flow.
Orthostatic hypotension, a common clinical manifestation of impaired blood pressure homeostasis, occurs in 15% to 20% of noninstitutionalized elderly persons. It is indicated when the patient experiences a 20 mm Hg reduction in systolic blood pressure upon standing upright. The prevalence of orthostatic hypotension increases with age, cardiovascular disease, and basal blood pressure elevation. Many elderly people have wide variations in postural blood pressure, which is closely associated with basal supine systolic blood pressure; ie, when basal supine systolic blood pressure is highest, the decline in postural systolic blood pressure is greatest. Orthostatic hypotension is a significant risk factor for syncope and falls in elderly persons, even those without other evidence of autonomic nervous system dysfunction.
Orthostatic hypotension in the elderly has two distinct clinical presentations: physiologic (attributable to normal aging) and pathologic (attributable to disease).
Physiologic orthostatic hypotension: In healthy elderly persons, this type of hypotension varies dramatically from day to day, is related to blood pressure elevation, and is associated with the exaggerated plasma norepinephrine response to postural change that is characteristic of aging. It often is provoked by common hypotensive stresses, such as volume depletion, ingestion of hypotensive drugs, or Valsalva's maneuver during voiding. Although generally asymptomatic and labile, physiologic orthostatic hypotension may be sufficient to compromise cerebral blood flow and cause dizziness or syncope. Prolonged bed rest may further compromise blood pressure homeostasis, resulting in severe postural hypotension.
Pathologic orthostatic hypotension: Usually symptomatic, this type of hypotension often is associated with postural dizziness or syncope. Acute orthostatic hypotension most commonly results from dehydration during an acute illness. In young patients, excessive cardioacceleration upon standing suggests hypovolemia rather than autonomic dysfunction as the cause of orthostatic hypotension. But in normal elderly persons, cardioacceleration is often blunted, so it may not occur in patients whose orthostatic hypotension results from hypovolemia. A much less common cause of acute orthostatic hypotension is adrenocortical insufficiency accompanied by hyponatremia and hyperkalemia
Causes of Orthostatic Hypotension
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Chronic orthostatic hypotension is usually associated with symptoms of autonomic nervous system dysfunction such as a fixed heart rate, incontinence, constipation, inability to sweat, heat intolerance, impotence, and fatigability.
If no cause is evident, orthostatic hypotension may be primary or idiopathic. Pure autonomic failure (previously called idiopathic orthostatic hypotension) is characterized by lower basal plasma norepinephrine levels in the supine position, no increase in norepinephrine levels upon standing, a lower threshold for the pressor response to infused norepinephrine, and an increased pressor response to tyramine despite the release of less norepinephrine at sympathetic nerve endings. These findings suggest that norepinephrine is depleted from sympathetic nerve endings, resulting in postsynaptic denervation supersensitivity.
Patients with Shy-Drager syndrome have normal levels of circulating norepinephrine and a normal response to infused norepinephrine and tyramine, but their plasma norepinephrine levels do not increase upon standing. This syndrome is associated with neuron degeneration in several areas of the central nervous system, including the corticobulbar, corticospinal, extrapyramidal, and cerebellar systems of the brain, as well as the intermediolateral columns of the spinal cord. Thus, Shy-Drager syndrome is a central nervous system disorder of sympathetic blood pressure control, usually associated with extrapyramidal and cerebellar symptoms.
Disorders of the peripheral autonomic nervous system also cause pathologic orthostatic hypotension. They include insulin-dependent diabetes mellitus, in which severe peripheral neuropathy and other end-organ damage occur, and less common disorders such as amyloidosis, vitamin deficiencies, and neuropathies associated with malignancies, particularly cancers of the lung and the pancreas. Perhaps the most common cause of orthostatic hypotension is the use of medications, such as phenothiazines, tricyclic antidepressants, antianxiety agents, and antihypertensives, including those with central effects (such as methyldopa and clonidine) and those with peripheral effects (such as prazosin, hydralazine, and guanethidine). Because of age-related impairments in ventricular diastolic filling, elderly people depend on adequate venous return to generate a normal cardiac output. Medications that reduce venous return, particularly nitrates and diuretics, commonly produce orthostatic hypotension. With many medications, orthostatic hypotension may result even from usual therapeutic doses.
The clinician should not assume that an elderly person who complains of postural dizziness and light-headedness is suffering from orthostatic hypotension. Rather, blood pressure and pulse rate should be measured after the patient has been recumbent for at least 5 min and after the patient has been standing quietly for 1 min and then for 3 min. A hypotensive response may be immediate or delayed. Prolonged standing or a tilt test may be needed to detect a delayed hypotensive response. Before therapy is initiated, blood pressure should be measured on several occasions to confirm that orthostatic hypotension persists.
The goal of therapy is to reduce or eliminate symptoms; often this can be achieved without completely correcting orthostatic hypotension. Regardless of the cause, orthostatic hypotension should be treated in the stepwise fashion described below.
The first therapeutic considerations include correcting hypovolemia and evaluating the patient's prescription and over-the-counter (OTC) medications to identify a possible cause. A patient with chronic orthostatic hypotension should be instructed to rise slowly after lying in bed or sitting in a chair for a long time. Dorsiflexing the feet before standing often promotes venous return to the heart, accelerates the pulse, and increases blood pressure. Crossing the legs while standing may also help increase blood pressure. A high salt diet aimed at producing a modest weight gain may blunt the symptoms of orthostatic hypotension in many patients. Elastic stockings that cover the calf and thigh and, in some cases, abdominal binders may be effective. Elevating the head of the bed 5° to 20° prevents the diuresis and supine hypertension caused by nocturnal shifts of interstitial fluid from the legs to the rest of the circulation.
If despite these measures, the patient remains symptomatic, medication may be needed. Various drug regimens have been tried, but most have been ineffective or require further study. However, fludrocortisone acetate appears to be effective for most types of orthostatic hypotension. Given in daily doses of 0.1 to 1.0 mg orally until mild peripheral edema develops, this mineralocorticoid increases extracellular fluid and plasma volume and sensitizes blood vessels to the vasoconstrictive effect of norepinephrine. These physiologic changes compensate for the homeostatic impairment that occurs upon rising in most persons with mild to moderately severe orthostatic hypotension. Complications of fludrocortisone therapy include supine hypertension and heart failure. Because hypokalemia can develop with mineralocorticoids, serum potassium should be measured every few months during treatment.
Drugs under study include nonsteroidal anti-inflammatory drugs such as indomethacin, the central alpha2-antagonist yohimbine, the alpha2-agonist clonidine, and beta-adrenergic antagonists that block beta2-vasodilator receptors or have intrinsic sympathomimetic activity, such as pindolol. The central alpha2-antagonist yohimbine can increase central sympathetic nervous system outflow. When such outflow is reduced (as in Shy-Drager syndrome), alpha2-agonists, which inhibit central sympathetic outflow in normal persons, can act on peripheral alpha2-receptors in the veins. This action promotes venoconstriction, thereby increasing venous return. Midodrine, a direct alpha1-agonist, is helpful in some patients with Shy-Drager syndrome or pure autonomic failure.
Various sympathomimetic agents such as ephedrine and phenylephrine have yielded inconsistent results. On the other hand, 250 mg caffeine each morning attenuates orthostatic hypotension in younger patients and can be used afely in the elderly. Ergot alkaloids, including oral ergotamine tartrate and dihydroergotamine given subcutaneously with caffeine, have also been helpful in some patients. In severe cases of orthostatic hypotension that resist traditional approaches, erythropoietin may be useful.
A decline in arterial blood pressure that occurs after a meal. Postprandial hypotension is a clinical abnormality of blood pressure homeostasis in the elderly. Studies of clinically stable, unmedicated elderly patients, both institutionalized and noninstitutionalized, show significant decreases in blood pressure after morning and noon meals; such decreases do not occur in younger persons or in elderly persons who have not just eaten a meal. Up to one third of institutionalized and noninstitutionalized elderly persons have a postprandial blood pressure decline >= 20 mm Hg within 75 min of eating a meal. This decline can be even greater when hypotensive medications are taken before a meal. The incidence of postprandial hypotension is greatest among hypertensive elderly persons and those who have postprandial syncope or autonomic nervous system dysfunction. Postprandial hypotension is probably a common cause of syncope and falls in the elderly. In one study of institutionalized elderly persons, it accounted for 8% of syncopal episodes.
The mechanism of postprandial hypotension is thought to be related to impaired baroreflex compensation for splanchnic blood pooling during digestion. Dysautonomic patients with postprandial hypotension have impaired forearm vasoconstriction, reduced systemic vascular resistance, and abnormal sympathetic nervous system control of heart rate after a meal. Thus, alterations in autonomic control of heart rate and vascular resistance are probably underlying causes of this syndrome.
Postprandial hypotension has two clinical presentations: (1) a physiologic, age-related phenomenon that is rarely symptomatic unless exacerbated by other hypotensive stresses and (2) a more severe pathologic syndrome related to autonomic insufficiency in which more profound hypotension is accompanied by syncope. Blood pressure should be measured before and after meals in geriatric patients who experience postprandial dizziness, falls, syncope, or other cerebral or cardiac ischemic symptoms.
Without clinical trials to evaluate treatments for postprandial hypotension, management is based on common sense. Symptomatic patients should not take hypotensive drugs before meals and should lie down after meals. Reducing dosages of hypotensive drugs and eating small, frequent meals may also help. Recent data suggest that walking after a meal may help restore normal circulation in some patients. This should be attempted only when the patient is under close observation.
Studies of patients with autonomic insufficiency suggest that indomethacin 50 mg q 6 h, caffeine 250 mg with or without dihydroergotamine 6 to 10 µg/kg s.c., or somatostatin 12 to 16 µg s.c. before a meal may ameliorate postprandial hypotension. Caffeine should be given only in the morning so the effect wears off by evening, allowing sleep and avoiding drug tolerance.